Nimhans Mock 1

NIMHANS - DM Neurology -
Exam Title :
MO...
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QUESTION 1. NDE3MCtTSFVCSEFNICBTQUhBK3NodWJoYW0uc2FoYTQ1MkBnbWFpbC5jb20rOTkzMjE2MD
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A 50 year old man presented to the emergency having woken up blind in his right eye after the
night’s sleep.Three months previously he had been evaluated for headache .An MRI done then
had revealed no abnormality.He was a known hypertensive since 10 years on regular
medications.On examination he had no perception of light in the right eye. Right pupil was
dilated and had no direct light reflex but consensual response to light shown in left eye was
normal .Fundus revealed generalised retinal pallor, swelling of the optic nerve head and
multiple small disc hemorrhages.Field charting was reported to show an altitudinal field
defect.The most likely cause of visual loss in this gentleman is
a) Anterior ischemic optic neuropathy

b) Posterior ischemic optic neuropathy
c) Acute evolved papilledema
d) Central retinal artery occlusion
Correct Answer: A
Your Answer: Unanswered
Explanation
The presentation of this man suggests a vascular etiology for blindness .The visual loss is
neverprominent in papilledema .While central retinal artery occlusion can produce can
produce visual loss of sudden onset ,fundus examination reveals cherry red spot in this
condition unlike what was seen in this patient .Occlusion of opthalmic artery and infarction of
optic nerve head and retina can result from local arteritis.The patient in question probably had
giant cell arteritis a condition commonly associated with anterior ischemic optic
neuropathy.Prognosis for recovery of vision is poor once visual loss sets in.
MORE NIMHANS FACTS- NIMHANS 2000
Medial medullary syndrome results due to occlusion of. ANTERIOR SPINAL ARTERY *****
Medial medullary syndrome is also known as inferior alternating syndrome , hypoglossal

alternating hemiplegia , lower alternating hemiplegia ,or Dejerine syndrome ,
Medial medullary syndrome is due to infarction of the pyramid and contralateral hemiparesis of
the arm and leg, sparing the face, also associated with contralateral loss of joint position sense
and ipsilateral tongue weakness occur.
On side opposite
On side of lesion
lesion
Paralysis of arm and

leg, sparing face;
Paralysis with
impaired tactile and
atrophy of one-half
proprioceptive sense
half the tongue:
over one-half the body:
Ipsilateral twelfth
Contralateral
nerve
pyramidal tract and
medial lemniscus
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Pulmonary wedge pressure is indirectly a Left atrial pressure
The substance found primarily found in tendons is collagen
The specifie substrate for oxidative phosphorylation is ADP
METALLOPORPHYRINS
The important roles these tetrapyrrolic macrocycles play in vital biological processes, in
particular photosynthesis (chlorophyll), oxygen transport (hemoglobin), oxygen activation
(cytochrome), have led to their characterization as ‘pigments of life’.
USU9OIDE=
A 70 year old man presented with limb weakness of 6 months duration .He reported
difficulty in getting up from squatting and climbing stairs and in combing.He also
reported dysphagia with occasional choking.There was no h/o ptosis or diplopia .He
had been recently tested for ‘lung cancer’ one year ago.He was a chronic asthmatic
since childhood and had been on steroid therapy(oral and inhailers) for several
years.On examination, there was no ptosis.He had proximal weakness of all four
limbs.There was no muscle tenderness.He had impaired touch sensation distally and
deep tendon reflexes were absent.Plantar was flexor. The most likely diagnosis
a) Lambert Eaton myasthenic syndrome

b) Polymyositis
c) Myasthenia gravis
d) Steroid induced myopathy
Correct Answer: B
Explanation
The presence of proximal weakness with dysphagia suggests polymyositis as the most likely
diagnosis in this patient.There is no ptosis or diplopia (AI-2006*) and there is no mention of
fatiguability which are characteris of myasthenia gravis.Limb girdle presentation is seen in
10% of myasthenics but again there is no fatiguability in this patient,rather there is a fixed
proximal weakness a feature seen in myasthenics of a very long duration. Limb girdle
presentation is more common in Lambert –Eaton myasthenic syndrome but again there
is distinct fatiguability in such patients.Steroid myopathy can be difficult to differentiate from
polymyositis.However the dysphagia seen in the patient suggests polymyositis rather than
steroid myopathy.Malignancies can predispose to the development of polymyositis as was seen
in this patient .The depressed deep tendon reflex are unusual for polymyositis and indicates
additional neuropathy that may be due to malignancy per se or due to drugs used to treat the
malignancy.
MORE NIMHANS FACTS-NIMHANS 2000
Tumour thought to arise from the chorionic villi
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GTD is the common name for five closely related tumours (one benign tumour , and four malign
ant tumours ):
• The benign tumour

◦ Hydatidiform mole
• The four malignant tumours
◦ Invasive mol e
◦ Choriocarcinoma
◦ Placental site trophoblastic tumour
◦ Epithelioid trophoblastic tumour
◦ The moles were classified as benign or potentially malignant, accordin. to the
criteria of Hertig, while the chorionepitheliomas were divided into
choriocarcinoma, chorioadenoma and syncitioma****** , according to Ewing.
• Endodermal sinus tumor ( EST ), also known as yolk sac tumor ( YST ), is a member
of the germ cell tumor group of cancers . It is the most common testicular tumor in
children under 3, and is also known as infantile embryonal carcinoma .
• The process whereby WBC can squeeze through pores in capillary walls is DIAPE
DESIS
• The fungus which causes the vascular lesion with thrombus formation - MUCOR
[VORICONAZOLE-not useful*****}
• NON ENCAPSULATED BENIGN TUMORS -LEIOMYOMA,CAVERNOUS
HEMANGIOMA,RECTAL ADENOMA
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A patient presented to the emergency department with symptoms of Intracranial infection and a
lumbar puncture was performed.All the following are causes of xanthochromia, in CSF except
a) Rise of CSF protein > 150 mg/dL

b) Hyperbilirubinemia
c) Subarachnoid hemorrhage
d) Traumatic lumbar puncture with RBCs of 1000/cu.mm
Correct Answer: D
Explanation
Xanthochromia has been expanded to include any bloody, brownish, or even cloudy CSF
sample.
Visual inspection may also falsely identify xanthochromia when the CSF is contaminated with
other pigments. This situation has been reported in patients taking rifampin for treatment of
tuberculosis, excessive carotinoid intake from fad dieting, high total CSF protein concentration,
or hepatic jaundice. Elevated CSF protein levels may cause yellowish discoloration of the CSF
because of the presence of albumin-bound bilirubin; this usually requires a protein
concentration in excess of 150 mg/dl******
. Discoloration may be seen at lower protein concentrations if the patient also has jaundice.
Such high protein concentrations are commonly seen in spinal block (Froin's syndrome),
radicular demyelination, carcinomatous meningitis, intracranial neoplasms, and cryptococcal or
tuberculous meningitis*****.
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RBC > 1,00,000 implies large amount of blood that has contaminated the CSF while doing
LP.There will then be contamination with serum bilirubin and lipochromes resulting in
xanthochromia
Bloody Tap SAH
Opening pressure Normal Raises
Serial samples Clearance uniform
Allowed to stand Clots – fibrin webs CSF dilutes the blood & defibrinates
Supernatant with prompt

Clear Xantho chromia due RBC hemolysis
centrifugation
WBC :
1-2 per 1000 Proportion higher
RBC - ratio
Crenation Less common Common
1 mg per 100 Higher protein level due to irritating effect

RBC ratio CSF protein
RBCs of hemolyzed RBCs
MORE NIMHANS FACTS-2000
Sensitivity is a measure of - True positive
Sensitivity
* The term sensitivity was introduced by Yerushalmy.
* The ability of a test to identify correctly all those who have the disease, that is “true
positive”.
Specificity
* The ability of a test to identify correctly those who do not have the disease, that is, “true
negatives”.
* An ideal screening test should be 100% sensitive and 100 % specific
Sandfly acts as a vector to all of the following diseases
Arthropod-borne diseases FOR NIMHANS
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Arthropod Diseases transmitted
1. Mosquito Malaria, filaria, viral

encephalitis (e.g., Japanese
encephalitis), viral fevers
(e.g., dengue, West Nile,
viral haemorrhagic fevers
(e.g., yellow fever, dengue
haemorrhagic fever)
2. Housely Typhoid and paratyphoid

fever, diarrhoea, dysentery,
cholera, gastro-enteritis,
amoebiasis, helminthic
infestations, poliomyelitis,
conjunctivitis, trachoma,
anthrax, yaws, etc
3. Sandfly***** Kala-azar, oriental sore,

* sandfly fever, oraya fever
4. Tsete fly Sleeping sickness
5. Louse Epidemic typhus, relapsing

fever, trench fever,
pediculosis
6. Rat flea Bubonic plague, endemic

typhus, chiggerosis,
hymenolepis diminuta
7. Blackfly Onchocerciasis
8. Reduviid bug Chagas disease
9. Hard tick Tick typhus, viral

encephalitis, viral fevers,
viral haemorrhagic fever,
(e.g., Kyasanur forest
disease), tularemia, tick
paralysis, human babesiosis
10. Soft tick Q fever, relapsing fever
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11. Trombiculid Scrub typhus, Rickettsial-

mite pox
12. Itch-mite Scabies
13. Cyclops Guinea-worm disease, fish

tapeworm (D.latus)
14. Enteric pathogens

Cockroaches
USU9OIDM=
A 75 year old Person is asked to say ‘clog’.When he says,it sounds ‘clong. This type of speech
disturbance is an example of
a) Dysphasia
b) Dysphonia
c) Dysarthia
d) Paraphasia
Correct Answer: B
Explanation
*Dysphasia refers to congenital or developmental languagedisorder and is distinct

from aphasia which is a disorder of language that is acquired secondary to brain
damage.
*Dysarthria refers to disorder of articulation of single sounds.
*Paraphasic speech refers to the presence of errors in the speech output .
*Dysphonia refers to disorder of sound production as would be expected in palatal palsy

when air escapes through the palate on attempting to talk.*****
III nerve palsy associated with contralateral hemiplegla is together known as WEBER
SYNDROME
The syndromes associated with 3 rd nerve are summarised below
Syndrome Feature
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* Site – supr. cerebellar

peduncle
1. Nothnagel’s
syndrome * Effect – Ipsilat 3 rd N
Palsy, contra lateral
cerebellar Ataxia
* Site - Red nucleus
* Effect – Ipsilateral 3 rd
2. Benedict’s N palsy
(AI2007)
+
Controlateral chorea,
athetosis
* Site – Supr. cerebellar

peduncle + Red Nucleus
3. Claudes
* Effect – 1 + 2
* Site – Cerebral peduncle
4. Weber’s * Effect – Ipsilat – 3 rd N.

Palsy +
Contralateral hemiparesis
The etiology of an isolated, pupil-sparing oculomotor palsy is diabetes [AIIMS

NOV-2009***] , hypertension.
STROKE WITHIN POSTERIOR CIRCULATION
P1 Syndromes
* A third nerve palsy with contralateral ataxia (Claude's syndrome) or with contralateral
hemiplegia (Weber's syndrome) may result. If the subthalamic nucleus is involved,
contralateral hemiballismus occurs. Occlusion of the artery of Percheron presents with
paresis of upward gaze and drowsiness, and abulia.
Bilateral proximal PCA occlusion leads to extensive infarction in the midbrain and
subthalamus and presents as coma, unreactive pupils, bilateral pyramidal signs, and
decerebrate rigidity. Occlusion of the penetrating branches of thalamic and thalamogeniculate
arteries is called the thalamic Déjérine-Roussy syndrome and consists of contralateral
hemisensory loss followed by burning pain in the affected areas.
Ataxia telangiectasia is associated with Spino-cerebellar atrophy,LYMPHOMAS and

Athetosis
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Ataxia Telangiectasia
* It is an autosomal recessive [AI - 2012***] disorder, presents with telangiectatic lesions

with deficits in cerebellar function and nystagmus. Associations are pulmonary infections, lym
phomas , leukemias, thymic hypoplasia with cellular and humoral (IgA and IgG2)
immunodeficiencies, premature aging, absent thymus gland and Type 1 diabetes mellitus. His
topathology reveals loss of Purkinje, granule, and basket cells in the cerebellar cortex and
deep cerebellar nuclei. Neuronal loss is also seen in the inferior olives of the medulla, anterior
horn neurons in the spinal cord and of dorsal root ganglion cells associated with posterior
column spinal cord demyelination
* The gene associated is the ATM gene ;it is associated with defective DNA repair.
Heterozygotes are prone for breast cancer.
USU9OIDQ=
A 35 year old lady was admitted in the emergency department with supected seizures.There
was a history of famliy dispute.Measurement of which hormone may help to differentiate a true
and psychogenic seizures
a) Thyroid stimulating hormone (TSH)

b) Prolactin (PRL)
c) Growth Hormone
d) ACTH
Correct Answer: B
Explanation
The differentiation of true and psychogenic seizures is often difficult and the difficulty is
compounded by the fact that the two often co-exist. Psychogenic seizures are non-epileptic
attacks often part of conversion disorder precipitated by a stressful situation.They often
lastlonger than true seizures and may wax and wane over minutes to hours .The behavioural
manifestations of complex partial seizures especially of frontal origin are often bizarre and may
be suspected for psychogenic seizures. A normal EEG does not exclude a true
seizure.Serum levels of PRL are often raised followingtrue seizures in the immediate
30-minute post ictal period in most generalized seizures and many complex partial seizures
and can be of help in some patients.
Viral meningitis with reduced CSF sugar is seen in Coxsackie virus
Hypoglycorrhachia is generally defined as a cerebrospinal fluid glucose concentration of

less than 50 mg/dl or a cerebrospinal fluid/blood ratio of less than 0.50.
HYPOGLYCORRHACHIA is uncommon in central nervous system syndromes of viral etiology,

with the exception of those due to mumps, lymphocytic choriomeningitis, varicella-zoster,herpes
simplex, and eastern equine encephalitis.
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Although hypoglycorrhachia has been found in association with meningoencephalitis due to the
enteroviruses in general,4,7 and specifically Coxsackie B2 2,3 and Coxsackie B5*****
Temporal lobe epilepsy is treated by VALPROATE and carbamazepine
In facial palsy, food accumulated in the mouth due to paralysis of- BUCCINATOR
USU9OIDU=
A 2 year old girl child is brought to OPD with features of hand ringing stereotype movements,
impaired language and communication skills. Her HC is 42 cm. Her birth record shows HC of
35 cm. What is the most likely diagnosis?
a) Asperger syndrome
b) Rett syndrome
c) Fragile x syndrome
d) Colarad syndrome
Correct Answer: B
Explanation
• Asperger syndrome or Asperger's syndrome or Asperger disorder is an autism spectrum

disorder that is characterized by significant difficulties in social interaction
•It differs from other autism spectrum disorders by its relative preservation of linguistic and co
gnitive development
•Asperger syndrome (AS) is one of the autism spectrum disorders (ASD) or pervasive
developmental disorders (PDD), which are a spectrum of psychological conditions that are
characterized by abnormalities of social interaction and communication that pervade the
individual's functioning, and by restricted and repetitive interests and behavior
•Children with AS may have an unusually sophisticated vocabulary at a young age and have
been colloquially called "little professors", but have difficulty understanding figurative language
and tend to use language literally
•Individuals with AS often have excellent auditory and visual perception
•AS is also associated with high levels of alexithymia , which is difficulty in identifying and
describing one's emotions
• Rett syndrome is a neurodevelopmental disorder of the grey matter of the brain that affects
females more commonly than males. The clinical features include small hands and feet and a
deceleration of the rate of head growth (including microcephaly in some).
•People with Rett syndrome are prone to gastrointestinal disorders and up to 80% have
seizures.
•They typically have no verbal skills, and about 50% of individuals affected are not ambulatory .
Scoliosis , growth failure, and constipation are very common and can be problematic.
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•Genetically Rett syndrome (symbolized RTT) is caused by mutations in the gene MECP2 locate
d on the X chromosome and can arise (1) sporadically or (2) from germline mutations
•Brain levels of norepinephrine are lower in people with Rett syndrome. The genetic loss of ME
CP2 changes the properties of cells in the locus coeruleus , the exclusive source of
noradrenergic innervation to the cerebral cortex and hippocampus
•Development is typically normal until 6–18 months, when language and motor milestones
regress, purposeful hand use is lost, and acquired deceleration in the rate of head growth (resu
lting in microcephaly in some ) is seen.
•Hand stereotypes are typical, and breathing irregularities such as hyperventilation,

breathholding, or sighing are seen in many. Early on, autistic-like behavior may be seen.
•The infant with Rett syndrome often avoids detection until 6–18 months
•The syndrome is associated with the expansion of a single trinucleotide gene sequence (CGG)
on the X-chromosome , and results in a failure to express the protein coded by the FMR1 gene,
which is required for normal neural development
•Fragile X is the most common known single gene cause of autism and the most common
inherited cause of intellectual disability
The most common lesion in Wernicke’s encephalopathy is found in the MAMILLARY BODIES
1% of alcoholics develop cerebellar degeneration or atrophy. 1 in 500 develop Wernicke's (oph

thalmoparesis, ataxia, and encephalopathy) and Korsakoff's (retrograde and anterograde
amnesia) syndromes
Wernicke's encephalopathy presents with confusion, ataxia, and diplopia resulting from
inflammation and necrosis of periventricular midline structures, including dorsomedial
thalamus, mammillary bodies, midline cerebellum, periaqueductal gray matter, and trochlear
and abducens nuclei.
Which one of the following is used to halt the process of degeneration of dopaminergic neurons
in striatonigral pathway- VITAMIN E
Prosopognosia is Inability to recognize face
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* The patient Denies the

Anosognosia
existence of hemiparesis
(AIIMS
and even deny ownership
NOV-2011***)
of paralyzed limb.
* It is the inability to
integrate visual
information in the centre of
the gaze with more
peripheral information. It is
described as ‘Misses the
Simultagnosia Forest for the Trees’. It is a
component of Balint’s
syndrome.
* It is due to bilateral
involvement of network for
spatial attention.
* Bilateral or right sided

Dressing
dorsal parietal lobe lesions
Apraxia
is the cause
* Bilateral lesion in
fusiform and lingual gyri of
occipito temporal cortex is
Prosopagnosia
the cause and it presents
with face and object
recognition defects.
* Acute onset of severely

impaired fluency (often
mutism).
* Writing, reading, and

Aphemia
comprehension are intact.
* It is due to partial lesions

of Broca's area or
subcortical lesions.
USU9OIDY=
Hyperkalemic periodic paralysis is caused by which of the following channelopathy
a) calcium channelopathy
b) Sodium channelopathy
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c) Potassium channelopathy
d) Magnesium channelopathy
Correct Answer: B
Explanation
Channelopathies
Sodium channel disorders
Generalized epilepsy with febrile seizure plus -α and β1 subunit
Hyperkalemic periodic paralysis* **** – SCN1a & SCN4a
Paramyotonia congenita- α subunit of SCN4a
Potassium sensitive myotonias.
Potassium channel disorders :
Benign familial neonatal convulsions
Episodic ataxia type 1
Acquired neuromyotonia
Paroxysmal dykinesias
Calcium channel disorders:
Absence epilepsy
Familial hemiplegic migraine
Episodic ataxia type 2
Spinocereberal ataxia type 6 (progressive)
Hypokalemic periodic paralysis
Eaton lambert myesthenic syndrome.
True regarding Cerebral venous sinuses - Transverse sinus is unequal
The transverse sinus is one of the dural venous sinuses and drains the superior sagittal sinus
, the occipital sinus and the straight sinus , and empties into the sigmoid sinus which in turn
reaches the jugular bulb. The transverse sinuses are frequently of unequal size******, wit
h the one formed by the superior sagittal sinus being the larger; they increase in size as they
proceed, from back to center.
Highly variable anatomy. For example one study demonstrated
• 39% hypoplasia of the left sinus

• 31% symmetric
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• 20% aplasia of the left sinus
• 6% hypoplasia of the right sinus
• 4% aplasia of the right sinus
The following drug is avoided in patient with Non ketotic hyperglycemia with seizure - PHENY
TOIN
. Hang up angle reflex is seen in -HYPOTHYROIDISM
All of the following are true regarding Poliomyelitis
a)Maximum recovery after paralysis can occur within months
b. Flaccid paralysis develops during febrile phase of illness
c. Asymmetrical paralysis of proximal leg can occur
USU9OIDc=
Regarding SSRIs which of the following is the correct statement
a) SSRIare useful in mania

b) SSRI blocks reuptake of norepinephrine
c) SSRI causes effect within 2 weeks
d) SSRIare useful in management of Eatingdisorders
Correct Answer: D
Explanation
SSRIs are antidepressants and they are contraindicated in mania*****
.SSRI specifically blocks the reuptake of serotonin (specific serotonin reuptake inhibitors).
SSRIs include
(1) Fluoxetine(2) Fluvoxamine
(3) Paroxetine(4) Citalopram
(5) Escitalopram(6) Sertraline
SSRI have equal efficacy compared to tricyclics and MAOIbut they are superior in causing less
side effects than TCAand MAOI. Cardiac side effects, Anticholinergic and postural hypotension
is less with SSRI.
SSRI has GI side effects and sexual dysfunction.
SSRI are first time antidepressants used not only for depression also for anxiety disorder, Panic
disorder, Phobia, PTSD, Eating disorders ***** and OCD.
All antidepressant shows clinical effect by4 – 6 wks.*****
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HYPOKALEMIA LEADS to paralytic ileus, leads to metabolic alkalosis
Tumour presenting 3 cm. from anal region is treated by CHEMOIRRADIATION
In healing by first intention all of the following occurs
A continuous layer of epidermis forms within 48 hrs
b. Reticulin can be demonstrated in the dermal gap by the 2 nd to 3 rd day
C.By the 4 th week the cellular and vascular elements decrease in number and concentration
Within 24 hours • Neutrophils appear at margins of incision, moving toward fibrin clot •
Epidermis at its cut edges thickens as a result of mitotic activity of basal cells
• Within 24 to 48 hours , spurs of epithelial cells from the both edges migrate and grow
along the cut margins of the dermis, depositing BM components as they move. They fuse in the
midline beneath the surface scab, thus producing a continuous but thin epithelial layer.
1. By day 3, • Neutrophils replaced by macrophages • Granulation tissue progressively

invades incision space • Collagen fibers are now present in the margins of the incision,
but at first these are vertically oriented. • Epithelial cell proliferation continues,
thickening epidermal covering layer
2. By day 5 , • Incisional space is filled with granulation tissue • Neovascularisation is
maximal • Collagen fibrils become more abundant and begin to bridge incision • The
epidermis recovers its normal thickness, and differentiation of surface cells yields a
mature epidermal architecture with surface keratinizatio
3. During the second week • Continued accumulation of collagen and proliferation of
fibroblasts • Leukocytic infiltrate, edema, and increased vascularity have largely
disappeared.
4. By the end of the first month, • Scar comprises a cellular connective tissue devoid of
inflammatory infiltrate, covered now by intact epidermis. • Dermal appendages that have
been destroyed in the line of the incision are permanently lost. • Tensile strength of the
wound increases thereafter, but it may take months for the wounded area to obtain its
maximal strengt
USU9OIDg=
A chronic addict was admitted with symptoms suggestive of Opiate Withdrawal.All of the
following drugs are used in the Treatment of this patient except
a) Methadone
b) Buprenorphine
c) Lofexidine
d) Naloxone
Correct Answer: D
Explanation
Opiate Withdrawal Treatment
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* The principle is to substitute a longer-acting, orally active, pharmacologically equivalent drug

for the abused drug.
* Methadone, buprenorphine (the partial mu agonist) are used. Clonidine, a centrally acting
sympatholytic agent, can be used.. Lofexidine, a clonidine analogue with less hypotensive
effect, is better.
* Methadone for Detoxification is from 2 to 3 weeks to as long as 180 days.
* Buprenorphine is a partial agonist, and produces fewer withdrawal symptoms. Buprenorphine

is superior to the alpha-2-adrenergic agonist clonidine.
* Clonidine relieves lacrimation, rhinorrhea, muscle pain, joint pain, restlessness, and
gastrointestinal symptoms.
* Clonidine or lofexidine are typically administered orally. The side effects are sedation,
lethargy, and dry mouth.
Rapid and Ultrarapid Opiate Detoxification
* The opioid antagonist naltrexone typically is combined with an alpha-2-adrenergic to shorten

the duration of withdrawal. Buprenorphine in combination with naltrexone and clonidine
reduced ROD from 3 to 1 day of detoxification. Ultrarapid opiate detoxification is an
extension of ROD using anesthetics., but it carries risk.
MORE NIMHANS FACTS- NIMHANS 2001
Sine qua non for cerebral cortex- PYRAMIDAL CELLS
IPSP is due to C1- influx
As an example of inhibitory postsynaptic action, consider a neuronal synapse that uses GABA as
its transmitter . At such synapses, the GABA receptors typically open channels that are selectiv
ely permeable to Cl - .***** When these channels open, negatively charged chloride ions can
flow across the membrane
Initiation of impulse starts in- AXON HILLOCK
Melatonin is Serotonergic
.Sprinter’s Energy supply for first 4-5 seconds in 100metrs running race is provided
form CARBOHYDRATE RESERVE
QUESTION 10. NDE3MCtTSFVCSEFNICBTQUhBK3NodWJoYW0uc2FoYTQ1MkBnbWFpbC5jb20rOTkzMjE2M

USU9OIDk=
The antidepressant with reuptake inhibition property of both dopamine and norepinephrine
uptake is
a) Amineptine
b) Nomifensine
c) Amoxapine
d) Mianserine
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Correct Answer: B
Explanation
Nomifensine is a norepinephrine-dopamine reuptake inhibitor developed by a team at Hoechst

AG in the 1960s. i.e. a drug that increases the amount of synaptic norepinephrine and dopamine
available to receptors by blocking the dopamine and norepinephrine reuptake transporters.
Due to the risk of a risk of haemolytic anaemia , the U.S. Food and Drug Administration (FDA)
withdrew approval for nomifensine on March 20, 1992.
*Mucosa in Crohn’s disease shows the appearance of- Cobble stone
*Myophosphorylase deficiency, also known as McArdle's disease, is the most common of the
glycolytic defects to cause exercise intolerance. Exertion can be followed by myoglobinuria and
acute renal failure. Forearm exercise test - An impaired rise in venous lactate is seen in
glycolytic defect. In lactate dehydrogenase deficiency, venous levels of lactate do not increase,
but pyruvate rises to normal.
*Estimation of age examination of teeth is by Gustafson’s method
* Optic atrophy is characteristic feature of poisoning by Methyl alcohol.
The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites forma
ldehyde and formic acid cause severe optic nerve and central nervous system damage.
* Treatment is similar to that for ethylene glycol intoxication with pyridoxine supplements, fom
epizole or ethanol, and hemodialysis. Fomepizole is an alcohol dehydrogenase inhibitor (4-
methyl pyrazole).

USU9OIDEw
A 55 year old man presents with a 10 day history of confusion. His friend mentions that he
drinks 15 units of alcohol a day. Which of the following strongly suggests a diagnosis of
Korsakoff’s psychosis?
a) Absence seizures
b) Delusional beliefs
c) Poor long term memory
d) Auditory hallucinations
e) Confabulation
Correct Answer: E
Explanation
There are six major symptoms of Korsakoff's syndrome:
• ◦ antegrade amnesia- inability to form new memories

◦ retrograde amnesia, severe loss of memories formed before the onset of the
condition
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◦ confabulation that is, invented memories which are then taken as true due to gaps
in memory sometimes associated with blackouts
◦ minimal content in conversation
◦ lack of insight
◦ apathy - the patients lose interest in things quickly and generally appear indifferent
to change.
Thiamine (vitamin B 1 ) deficiency
* Wernicke's encephalopathy presents with confusion, ataxia, and diplopia resulting from
inflammation and necrosis of periventricular midline structures, including dorsomedial
thalamus, mammillary bodies, midline cerebellum, periaqueductal gray matter, and trochlear
and abducens nuclei.
* Prolonged untreated thiamine deficiency can result in an irreversible dementia/amnestic

syndrome (Korsakoff's syndrome). Korsakoff's syndrome - Memory for new events is impaired,
but have normal immediate memory, attention span, and level of consciousness. Mammillary
body atrophy (irreversible)
*1 in 500 develop Wernicke's (ophthalmoparesis, ataxia, and encephalopathy) and Korsakoff's

(retrograde and anterograde amnesia) syndromes.
Parentectomy : A slang term meaning removal of a parent (or both parents) from the child. It
is of relevance to the hospitalization of children.It can be used in
a. Reactive attachment disorder
b. Child abuse
c. Anorexia nervosa
LEIGH disease is due to the accumulation of GLYCOGEN
Mutations of SDHA do not predispose to paraganglioma tumors but instead cause Leigh'
s disease , a form of encephalopathy .
It is most commonly inherited in an autosomal recessive manner OR MITOCHONDRIAL

INHERITANCE.In a few cases of Leigh syndrome due to mutations in nuclear DNA, inheritance
is X-linked recessive
symptoms may include weakness and lack of muscle tone ; spasticity; movement disorders; cere
bellar ataxia ; and peripheral neuropathy.
Mitochondrial DNA Depletion Syndromes
* Mitochondrial DNA depletion syndrome (MDS) includes Leigh's syndrome), PEO, an isolated
myopathy, myo - neuro - gastrointestinal - encephalopathy (MNGIE).

USU9OIDEx
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A 55 year old lady is admitted to a hospital because of cardiac disease.She is on lithium. Even if
her lithium dose remained the same, all of the following would be expected to increase her
plasma lithium level except
a) associated renal disease

b) thiazides
c) low sodium diet
d) caffeine
Correct Answer: D
Explanation
Lithium
Mood stabilising agent
Lithium concentrations are known to be increased with concurrent use of diuretics —

especially loop diuretics (such as furosemide) and thiazides — and non-steroidal anti-
]
inflammatory drugs (NSAIDs) such as ibuprofen and aspirin . Lithium concentrations can also
be increased with concurrent use of ACE inhibitors such as captopril , enalapril , and lisinopril .
There are also drugs that can increase the clearance of lithium from the body, which can result
in decreased lithium levels in the blood. These drugs include theophylline , caffeine *********
**, and acetazolamide . Additionally, increasing dietary s odium intake may also reduce
lithium levels by prompting the kidneys to excrete more lithium
renal failure will increase the level of lithium
Indications
Trt. of acute mania

Prophylaxis of bipolar mood disorder
Others
Schizo affective disorder

Prophylaxis of Unipolar Cyclothymia
Acute depression
Impulsive aggression
Chronic alchoholism
Kleine - levin syndrome
Pharmacokinetics
Rapidly absorbed
Not protein bound
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No metabolism
Entirely by kidneys
Mood of action -Decreasescatecholamine activity Before Starting Therapy
Kidneys-urine routine,
Thyroid-- T4TSH
Heart-ECG
CNS
Dose-900-2100 mg/ d
Side effects
Neurological
Commonest-Tremor-50%
Seizures
Cog wheelrigidity
Delirium
Renal 10-50%
NephrogenicDI
Nephrotic syndrome
CVS
‘T’wavedepression
Endocrine
Hypothyroidism
Weight gain
Pregnancy
Teratogenic
Ebstein’s
Blood Levels
Therapeutic level (acute mania) -0.8 – 1.2 meg/ l
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Prophylactic level (BPD) -0.6 – 1.2 meq/L
Toxic level >2.0meq/L
MORE NIMHANS FACTS-NIMHANS 2001/2002
The surest sign of intrauterine death includes GAS IN AORTA
Oculomotor nerve passes between Superior cerebellar artery and Posterior cerebellar artery
The vagus nerve supplies the large intestine closest up to SPLENIC FLEXURE
PERITONEAL ORGANS
The intraperitoneal organs are the stomach , spleen , liver , bulb of the duodenum , jejun
um , ileum, transverse colon , and sigmoid colon .
The retroperitoneal organs are the remainder of the duodenum , the cecum and ascending
colon , the descending colon , the pancreas , and the kidneys .

USU9OIDEy
Operant condition where paradigm pain stimulus are given to a child for decreasing a certain
undesired behaviour can be classified as:
a) Positive reinforcement
b) Negative reinforcement
c) Punishment
d) Negotiation
Correct Answer: C
Explanation
Behaviour Therapy
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I. Operant Conditioning procedure for Increasing a behaviour Positive reinforcement –

Reward
Negative reinforcement – Punishment is avoided
Modelling
II. Operant conditioning procedures for
Decreasing a behavior
a)Time out
-Reinforcement is withdrawn for
some time
b) Punishment *
c)Satiation
-Undesired response is positively
reinforced
Hysteria – conversion reaction
*Symptoms of motor or sensory function
– suggesting a medical disorder
*Sudden on set
*Symptoms in the presence of psychosocial
stress
*Do not intentionally produce symptoms
* ‘Secondary gain’
-Autonomic system*
-typically not involved
Pulmonary fibrosis is caused by
NItrofurantoin
Methotrexate
Cyclophosphamide
The treatment of choice in the management of acute manic illness is Lithium
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In a patient post myocardial infarction developed atrial fibrillation. Subsequently the ECHO
showed a mural thrombus. The management is by warfarin

USU9OIDEz
Six diseases of animals are caused by prions.In contrast to other prion diseases, Which of the
following is highly communicable
a) Scrapie
b) Mink encephalopathy
c) feline spongiform encephalopathy
d) chronic wasting disease (CWD)
Correct Answer: D
Explanation
MORE NIMHANS FACTS from HARRISON 20th

*Prions also appear to play a role in more common
illnesses such as Alzheimer’s disease (AD) and Parkinson’s disease (PD).
*PrP prions reproduce by binding to the normal, cellular isoform of the prion protein (PrPC) and
stimulating conversion
of PrPC into the disease-causing isoform PrPSc . PrPC is rich in α-helix and has little β-
structure, whereas PrPSc
has less α-helix and a high amount of β-structure . This α-to-β structural transition in PrP is
the
fundamental event underlying this group of prion diseases
*PrP gene located on human chromosome 20.
*Familial CJD (fCJD), Gerstmann-Sträussler-Scheinker (GSS) disease, and fatal familial

insomnia (FFI) are all dominantly inherited prion diseases that are caused by
mutations in the PrP gene
*Iatrogenic CJD (iCJD) seems to be the result of the accidental inoculation of patients
with
prions.
Variant CJD (vCJD) in teenagers and young adults in Europe is the result of exposure
to tainted beef
from cattle with bovine spongiform encephalopathy (BSE).
*Six diseases of animals are caused by prions . Scrapie of sheep and goats is the
prototypic PrP
prion disease. Mink encephalopathy, BSE, feline spongiform encephalopathy, and
exotic ungulate
encephalopathy are all thought to occur after the consumption of prion-infected
foodstuffs.Chronic wasting disease (CWD), a prion disease endemic in deer.
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In contrast to other prion diseases, CWD is highly communicable.
* Both the rods and the PrP amyloid filaments found in brain tissue exhibit similar
ultrastructural
morphology and green-gold birefringence after staining with Congo red dye.
*In FFI, the protease-resistant fragment of PrPSc after deglycosylation has a molecular
mass of 19 kDa, whereas in fCJD and most sporadic prion diseases, it is 21 kDa
*Highly stable amyloids gave rise to stable prions with long incubation times; low-
stability amyloids led to
prions with short incubation times
*The amino acid sequence of PrP encodes the

species of the prion, and the prion derives its PrPSc sequence from the last mammal in
which it was
passaged. This “species barrier” t
o transmission is
correlated with the degree of similarity between the amino acid sequences of PrPC in
the inoculated host and
of PrPSc in the inoculum
*A mutation at codon 178 that results in substitution of asparagine for aspartic acid
produces FF I if a methionine is encoded at the polymorphic residue 129 on the same
allele.
* Typical CJD is seen if the D 1 78N mutation occurs with a valine encoded at position
129 of the same allele
*Accidental transmission of CJD to humans appears to have occurred with corneal

transplantation,
contaminated electroencephalogram (EEG) electrode implantation, and surgical
procedures
*Dura Mater Grafts,human growth hormone (hGH) preparations derived from

human pituitaries can transmit
VARIANT CJD-BSE prions had been transmitted to humans through the consumption
of tainted beef.
NEUROPATHOLOGY-PRIONS
*On light microscopy, the pathologic hallmarks of CJD are spongiform degeneration and
astrocytic gliosis.Generally, the spongiform changes occur in the cerebral cortex,putamen,
caudate nucleus, thalamus, and molecular layer of the cerebellum
*The amyloid plaques of GSS disease are morphologically distinct from those seen in kuru or
scrapie. GSS
plaques consist of a central dense core of amyloid surrounded by smaller globules of
amyloid.The plaques can be distributed throughout the brain but are most frequently found in
the cerebellum .
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*In vCJD, a characteristic feature is the presence of “florid plaques. ” These are composed of a
central core of
PrP amyloid, surrounded by vacuoles in a pattern suggesting petals on a flower
*Most patients (~90%) with CJD exhibit myoclonus
*Dementia with myoclonus can also be due to AD , dementia with Lewy bodies , corticobasal
degeneration , cryptococcal
encephalitis , or the myoclonic epilepsy disorder Unverricht-Lundborg disease
CLINICAL PRESENTATION
*Familial CJD has an earlier mean age of onset than sCJD.
*In GSS disease , ataxia is usually a prominent and presenting feature, with dementia
occurring late in the disease course.
*GSS disease presents earlier than CJD (mean age 43 years) and is typically more slowly
progressive than CJD; death usually occurs within 5 years of onset.
*FFI is characterized by insomnia and dysautonomia; dementia occurs only in the terminal
phase of the illness.
Variant CJD has an unusual clinical course , with a prominent psychiatric prodrome that may
include visual hallucinations and early ataxia, whereas frank dementia is usually a late sign of
vCJD.
LABORATORY TESTS
The only specific diagnostic tests for CJD and other human PrP prion diseases measure PrPSc-
conformation-dependent immunoassay (CDI)
*sCJD On FLAIR sequences and diffusion-weighted imaging, ~90% of patients show increased
intensity
in the basal ganglia and cortical ribboning -can also be seen in viral encephalitis, paraneoplastic
syndromes, or seizures.
*Stress protein 14-3-3 is elevated in the CSF of some patients with CJD
*EEG -The presence of these stereotyped periodic bursts of <200 ms in duration, occurring
every 1–2 s, makes the diagnosis of CJD very
likely.
*Biosafety level 2 practices,
DECONTAMINATION OF CJD PRIONS
*Autoclaving at 134°C for 5 h or treatment with 2 N NaOH for several hours is recommended
for sterilization of
prions
*Amyloid plaques in AD do not correlate with the level of dementia ;****** however, the
level of soluble (oligomeric) Aβ peptide does correlate with memory loss
*The finding that phenothiazines and

acridines inhibit PrPSc formation in cultured cells led to clinical studies of quinacrine in CJD
patient
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USU9OIDE0
Following are true about Tic disorder except
a) More common in girls

b) Motor and vocal tics
c) Age of onset before 7 yrs
d) Motor tic precede vocal tics
Correct Answer: A
Explanation
Tics disorders are common in boys which is characterised by multiple motor or vocal tics
appearing before age of7 years.
Haloperidol or pimozide are preffered treatment.
TIC disorder - Multiple motor tics and one or more vocal tics (Tourette’s disorder [ Tic –
involuntary, sudden, rapid, recurrent, nonrhythmic, stereotyped, motor movements or
vocalisation) .
Haloperidol and pimozide most commonly used
True regarding aortic aneurysm is Thoracic aneurysms have better prognosis
Full thickness graft is indicated in Fascial regions for cosmetic effect
The most common complication of Colle’s fracture is FINGER STIFFNESS
In a trauma patient presenting to the casualty the fluid to be given initially is RL

USU9OIDE1
A patient of Schizophrenia is getting Chlorpromazine, but his auditory hallucinations are not
controlled.The next drug to be given is:
a) Haloperidol
b) Clozapine
c) Sulpride
d) Tianeptin
Correct Answer: B
Explanation
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A 32 year old male presented with painless lymphnode in the cervical region. Lymph node
biopsy shown normal thyroid gland features. But clinically, on palpation thyroid is normal the
diagnosi is LINGUAL THYROID
All are true regarding Myelofibrosis
a. Tear drop poikilocytes
b. Giant abnormal platelets
c. Leucoerythroblastic blood picture
Water hammer pulse is seen in AR
A little girl who was underweight and hypotonic in infancy is obsessed with food, eats
compulsively, and at age 4, sge is already grossly overweight. She is argumentative,
oppositional, and rigid. She has a narrow face, almond – shaped eyes, and a small mouth -
PRADER WILLI SYNDROME

USU9OIDE2
Which of the following is the wrong statement regarding the Hounsfield units
a) Air – 1000 HU
b) Fat- 90 HU
c) Muscle – 50 HU
d) White matter-300
Correct Answer: D
Explanation
CT
Material Hounsefield units
Air 1000*
Lung 300
Fat 90*
Water 0
White matter 30
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Grey matter 40
Muscle 50*
Bone 1000 +*****
*Relative attenuation coefficient
– expressed in Hounsefield unit
Cerebro spinal fluid Is actively secreted by chroidal plexus
“Lesbianism” is also known as -TRIBADISM
EEG pattern in REM sleep is Low amplitude, rapid waves
Plasma ACTH levels are high between these following hours -4.00am-10.00am

USU9OIDE3
Beaded septum sign is seen in Which of the following condition
a) Mitral stenosis
b) Alveolar proteinosis
c) Lymphangitis carcinomatosa
d) Histiocytosis
Correct Answer: C
Explanation
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beaded septum sign
CT scans. —This sign consists of irregular and nodular thickening of interlobular septa
reminiscent of a row of beads . It is frequently seen in lymphangitic spread of cancer and less
often in sarcoidosis
Also seen in sarcoidosis
Unilateral lymphangitis -ca lung
Alveolar proteinosis -crazy pavement
Kerley B line –mitral stenosis
SSRI drug which has less effect on CYP isoenzyme -Sertraline
Choline overdose causes
Fishy body odour
Sweating
Voiding of the bladder
Short acing anticholinesterase is EDROPHONIUM
Antipsychotics are safer in the patient with HYPERTENSION
Adverse effects of INH
Peripheral neuritis
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Hepatitis
Acne
Acneiform eruptions can occur with glucocorticoids, topical or systemic , oral contraceptive
pills, lithium, isoniazid, androgenic steroids, halogens, phenytoin, and phenobarbital

USU9OIDE4
Lateral thoracic meningocoele is seen in
a) Neurofibromatosis
b) Arnold chiary malformation
c) Dandy walker syndrome
d) diastematomyelia
Correct Answer: A
Explanation
Lat. Thor. meningocele -neurofibromatosis Lumbar meningocele - chiary mal-2
Ant sacral meningocele -caudal regression ,neurofibromatosis
Occipital meningocele -chiary type 3
Elimination of avoidable blindness
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According to WHO estimates, about 80% of global blindness is avoidable :
WHO and a Task Force of international NGOs have jointly prepared and launched a common
agenda for global action: " VISION 2020 -- The Right to Sight".
VISION 2020 will be implemented through 4 five-year plans, the first one starting in
2000. The three subsequent phases of implementation will commence in 2005, 2010 and 2015
respectively.
Soil is involved as a mode of transmission by faccoral route in the following
Ancylostomasis
Ascariasis
Hydatid disease
Order of steps involved in CHI – SQUARE test
a. Test the null hypothesis
b.Applying the X2 test
c. Finding the degree of freedom
d.Probability tables
State the null and research/alternative hypotheses.
2. Specify the decision rule and the level of statistical significance for the test, i.e., .05, .01, or
.001. (A significance level of .01 would mean that the probability of the chi-square value must
be .01 or less to reject the null hypothesis, a more stringent criterion than .05.)
3. Compute the expected values.
4. Compute the chi-square statistic.
5. Determine the degrees of freedom for the table.
6. Compare the computed chi-square statistic with the critical value of chi-square; reject the
null hypothesis if the chi-square is equal to or larger than the critical value; accept the null
hypothesis if the chi-square is less than the critical value.
7. State a substantive conclusion

USU9OIDE5
Bare orbit syndrome is seen in which of the following condition
a) Retinoblastoma
b) Neurofibromatosis
c) Enucleation of eye
d) Orbital lymphoma
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Correct Answer: B
Explanation
Bare orbit syndrome is due to absence of greater wing of sphenoid.It is classically observed in
Neurofibromatosis and produces pulsatile Ex-ophthalmosis.Usually associated with plexiform
Neurofibroma of trigeminal nerve. Retinoblastoma showscalcification
Bare orbit sign , is described as a characteristic appearance of orbit, where the innominate
line is absent. The innominate line is a projection of the greater wing of the sphenoid, and its
absence or destruction is responsible for this appearance.
It is the classical frontal radiograph sign of neurofibromatosis type I (NF1). In addition to bare
orbit sign, it is accompanied by egg shaped enlargement of anterior orbital rim, bony defect in
posterior orbit and anteroposterior enlargement of middle cranial fossa .
Bare orbit sign may also be seen in destruction of sphenoid wing, most commonly in neuroblast
oma metastases.
PYROSIS
Seen in reflux esophagitis
May radiate to the neck and the angles of the jaw
Produced by infusion of neural hyperosmolar solutions into the esophagus
The diagnosis is one of elimination, based upon the Rome III criteria : 1) burning retrosternal
discomfort; 2) elimination of heart attack and GERD as the cause; and 3) no esophageal motility
disorders .
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Wilson disease can present as
a. Dystonia
b. Fulminant hepatitis
c. Repeated spontaneous abortion

USU9OIDIw
Cytochrome oxidase enzyme contains which of the following metals in thier chemical structure
a) Iron and Copper

b) Iron and Zinc
c) Copper and Zinc
d) Iron and Manganes
Correct Answer: A
Explanation
Metalloenzymes Iron : Cytochromeoxidase*****, Catalase, Peroxidase, Xanthine oxidase
Copper : Tyrosinase, Cytochrome oxidase*****, SOD, Lysyl oxidase
Zinc : Carbonic anhydrase, Carboxy peptidase,Alcohol dehydrogenase, ALP, Glutamate

dehydrogenase, RNA polymerase
Magnesium : Hexokinase, Enolase, PFK
Manganese : Hexokinase, Enolase
Molybdenum : Xanthine oxidase
Calcium: Lipase, Lecithinase
Most potent anti TB drug -RFM
Risk factors for active tuberculosis among persons who have been infected with tubercle bacilli
-SILICOSIS
Most common cause of postural hypotension is PERIPHERAL NEUROPATHY

NUSU9OIDIx
All of the following statements are correct about metabolism in brain except :
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a) Fatty acids are utilized in starvation

b) 60 % of total energy is utilized during resting stage
c) Ketone bodies are used in starvation
d) Has no stored energy
Correct Answer: A
Explanation
Tissue FED Fasting Starvation
Brain Glucose Glucose Ketone bodies
Heart Fatty acids Fatty acids Ketone bodies
Liver Glucose Fatty acids Amino aicds
Muscle Glucose Fatty acids Fatty acids
Adipose tissue Fatty acid - -
Drug induced SLE seen in
a. Hydralazine
b. Procainamide
c. Isoniazid
The characteristic histopathologic feature of Parkinson's disease is the Lewy body, an eosinop
hilic cytoplasmic inclusion that contains both neurofilaments and alfa-synuclein .
Abdominal aortic aneurysm is common in Males & infrarenal in location
Most common cause of abdominal aortic aneurysm is ATHEROSCLEROSIS
Hyperkalemic periodic paralysis associated with Graves’ disease is seen commonly in A

SIAN MALES
The following are the genetic syndromes associated with DM
a. Prader Willi syndrome
b. Down’s syndrome
c. Klinefelter’s syndrome
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NUSU9OIDIy
Hepotocytes loaded with minimally branched glycogen is seen in which of the following
glycogen storage disorder
a) Von Gierkes disease

b) Tauris disease
c) Cori’s disease
d) Anderson’s disease
Correct Answer: D
Explanation
Anderson’s disease:
Deficiency : defect in Branching enzyme.
Effect : during glycogen synthesis, branching points will not introduced properly leading to
accumulation of abnormal glycogen with minimal branches.
Cori’s disease:
Deficiency : defect in Debranching enzyme.
Effect : during glycogenolysis, branching points will not be broken properly leading to
accumulation of abnormal glycogen with multiple short branches.
Glycogen storage disorders:
Inborn errors of metabolism of glycogen due to which abnormal glycogen gets deposited in
liver, spleen & muscles etc.
Diseases Defective enzyme
Von Gierke’s disease Gluc-6-phosphotase
Pompe’s disease Lysosomal Acid maltase
Limit dextrinosis (Cori’s) Debranching enzyme
Amylopectinoses (Anderson’s) Branching enzyme
Mc Ardle’s Myophosphorylase
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Her’s Liver phosphorylase
Tauris Muscle & RBC Phosphofructokinase
Type VIII Phosphorylase kinase
Glycogen storage diseases presenting with liver involvement and hypoglycemia.
I, III, VI , IV
Muscle involvement:
V, VII, III.
Cardiac involvement:
Pompe’s disease (II)
Drugs used in alcohol addiction are
a. Disulfiram
b. Metronidazole
C.. Fluoxetine
SIADH
Investigations for confirming the diagnosis are 1) low serum osmolality, 2) high urine
osmolality 3) Urine Na + concentration usually >40 mmol/L .
4) Hypouricemia due to the uricosuric state induced by volume expansion 5) absence of
hypothyroidism

NUSU9OIDIz
Set of data which correctly defines restrictive lung disease is :
a) ↑ FRC, ↑ compliance of lung tissue

b) ↑ FEV 1 /FVC, ↓ compliance of lung tissue
c) ↓ FEV 1 /FVC, ↓ compliance of lung tissue
d) ↑ TLC, RVis ↓
Correct Answer: B
Explanation
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Restrictive lung disease
* VC ↓ * FEV1 – Normal * Total lung capacity ↓
* MVV - ↓
* Compliance - ↓
MORE FACTS
Surfactant
Substance %
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Dipalmitoyl phosphatidyl choline 62
Phosphatidyl glycerol 5
Neutral lipids 13
Other phospholipid 10
Protein 8
Carbohydrate 2
* Produced by Type II alveolar epithelial cells * Decreases surface Tension Vital capacity
Increase Decrease
A. Physiological
* Females
A. Physiological * Old age
* Males
* Standing
* Sitting or lying
* Pregnancy
B. Pathological
* Ascites
B Pathological * Pneumothorax, effusion
* Pulmonary fibrosis
Tracheostomy
DECRREASES dead space
Drug of choice in amoebic liver abscess is METRONIDAZOLE
Primary Hypothyroidism is seen in all except [Nim 2005]
a. Iodine deficiency
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b. Iodine excess
c. Lithium
d. Bexarotene
Primary Hypothyroidism is seen in
a. Iodine deficiency
b. Iodine excess
c. Lithium
Therapy with the retinoid X receptor agonist bexarotene is associated with hypothyroidism
caused by decreased pituitary TSH secretion-SECONDARY HYPOTHYROIDISM
ANS -D

NUSU9OIDI0
A 25 YEAR old college student met with an RTA and was admitted in an ICU. He was opening
his eyes on calling and was making incomprehensible sounds. He withdrew his leg on touching.
Calculate the Glascow coma scale
a) 5
b) 6
c) 7
d) 9
Correct Answer: D
Explanation
Glasgow Coma Scale(AI-2006*-AIIMS NOV-2013***)
Eye-opening (E)
* Spontaneous4
* To speech3
* To pain2 * Nil1
Best motor response (M)
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* Obeys6
* Localises5
* Withdraws4 * Abnormal flexion3
* Extensor response2
* Nil1
Verbal response (V)
* Orientated5
* Confused conversation4
* Inappropriate words3 * Incomprehensible sounds2
* Nil1
Coma score = E + M + V
* Minimum3
* Maximum15
HYSTERICAL GAIT DISORDER
Hysterical gait disorders present with abnormal posture with wastage of muscular energy ( asta
sia-abasia) , extreme slow motion, and dramatic fluctuations over time.
Hysterical gait disorder is characterized by
b. Similar presentation like atrophy of the vermis
c. No leg circumduction
d. No hyperreflexia

NUSU9OIDI1
The facilitatory area for micturition is situated in the
a) pontine region
b) midbrain region
c) medulla
d) spinal cord
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Correct Answer: A
Explanation
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Reflex Control
* Fibers in the pelvic nerves are the afferent limb of the voiding reflex, and the parasympathetic
fibers to the bladder that constitute the efferent limb also travel in these nerves. The reflex is
integrated in the sacral portion of the spinal cord- volume of urine in the bladder that normally
initiates a reflex contraction is about 300 to 400 mL.
* The sympathetic nerves to the bladder play no part in micturition.
* The threshold for the voiding reflex, like the stretch reflexes, is adjusted by the activity of
facilitatory and inhibitory centers in the brainstem.
* There is a facilitatory area in the pontine region******* and an inhibitory area in the
midbrain .
* After transection of the brain stem just above the pons, the threshold is lowered and less
bladder filling is required to trigger it
* After transection at the top of the midbrain, the threshold for the reflex is essentially normal.
* There is another facilitatory area in the posterior hypothalamus. Humans with lesions in the
superior frontal gyrus have a reduced desire to urinate and difficulty in stopping micturition
once it has commenced.
Effects of Deafferentation
* When the sacral dorsal roots are cut in experimental animals or interrupted by diseases of the
dorsal roots, such as tabes dorsalis in humans, all reflex contractions of the bladder are
POSITIVE MED PG
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abolished. The bladder becomes distended, thin-walled, and hypotonic, but some contractions
occur because of the intrinsic response of the smooth muscle to stretch.
Effects of Denervation
* When the afferent and efferent nerves are both destroyed, as they may be by tumors of the
cauda equina or filum terminale, the bladder is flaccid and distended for a while.
* The muscle of the "decentralized bladder " becomes active, with many contraction waves
that expel dribbles of urine out of the urethra.
* The bladder becomes shrunken and the bladder wall hypertrophied .
* The reason for the difference between the small, hypertrophic bladder seen in this condition
and the distended, hypotonic bladder seen when only the afferent nerves are interrupted is not
known.
* Three major types of bladder dysfunction are due to neural lesions: (1) the type due to
interruption of the afferent nerves from the bladder, (2) the type due to interruption of both
afferent and efferent nerves, and (3) the type due to interruption of facilitatory and inhibitory
pathways descending from the brain. In all three types the bladder contracts, but the
contractions are generally not sufficient to empty the viscus completely, and residual urine is
left in the bladder.
Effects of Spinal Cord Transection
* During spinal shock, the bladder is flaccid and unresponsive. It becomes overfilled, and urine
dribbles through the sphincters (overflow incontinence).
* After spinal shock has passed, the voiding reflex returns, although there is, of course, no
voluntary control and no inhibition or facilitation from higher centers when the spinal cord is
transected.
* In some instances, the voiding reflex becomes hyperactive, bladder capacity is reduced, and
the wall becomes hypertrophied- spastic neurogenic bladder.
POSITIVE BITS- Renal blood flow is regulated by norepinephrine (constriction, reduction of

flow), dopamine (vasodilation, increases flow), angiotensin II (constricts), prostaglandins
(dilation in the renal cortex and constriction in the renal medulla), and acetylcholine
(vasodilation).
Resistant schizophrenia is treated with CLOZAPINE
LITHIUM SIDE EFFECTS
Agent and Dosing Side Effects
Lithium Common Side Effects
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* Anorexia/diarrhea,
fine tremor, thirst,
polyuria, fatigue,
weight gain, acne,
folliculitis,
neutrophilia,
hypothyroidism
* Blood level is
Starting dose: 300 increased by thiazides,
mg bid or tid tetracyclines, and
NSAIDs
Therapeutic blood
level: 0. 8–1. 2 meq/ * Blood level is
L decreased by
bronchodilators,
verapamil, and
carbonic anhydrase
inhibitors
* Rare side effects: Neur

otoxicity, renal toxicity,
hypercalcemia, ECG
changes

NUSU9OIDI2
Cerebral blood flow is increase in all except
a) chronic anaemia
b) inhalation of 5% carbon dioxide
c) seizures
d) inhalation of hyperbaric oxygen
Correct Answer: D
Explanation
• CBF = CPP / CVR

• The hagen-Poiseuille equation
• Cerebral Blood Flow = Δ P π R4 8 η l
• where: Δ P = cerebral perfusion pressure
• R = radius of the blood vessels
• η = viscosity of the fluid (blood)
• l = length of the tube (blood vessels)
• π = constant, 3.14
• high oxygen consumption of the brain of 3.3ml.100g-1.min -1 (50ml.min-1 in
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• total) which is 20% of the total body consumption
Cerebral blood flow
• In an adult, CBF is typically 750 millilitres per minute or 15% of the cardiac output .
• This equates to 50 to 54 millilitres of blood per 100 grams of brain tissue per minute
• ( ischemia ) results if blood flow to the brain is below 18 to 20 ml per 100 g per minute,
and tissue death occurs if flow dips below 8 to 10 ml per 100 g per minute
• CVR is controlled by four major mechanisms :
• Metabolic control (or 'metabolic autoregulation')
• Pressure autoregulation
• Chemical control (by arterial pCO 2 and pO 2 )
• Neural control
• CBF increases once PaO2 drops below about 6.7kPa so that cerebral oxygen delivery
remains constant.
• Hypoxia acts directly on cerebral tissue to promote the release of adenosine, and in some
cases prostanoids that contribute significantly to cerebral vasodilatation.
• Hypoxia also acts directly on cerebrovascular smooth muscle to produce
hyperpolarisation and reduce calcium uptake, both mechanisms enhancing vasodilatation.
• MORE NIMHANS FACTS-NIMHANS 2005
• Rett’s syndome is characterized by
a. Common in girls
b. Severe mental retardation
c. Hand wringing present
Descending order of types of viruses causing paralytic polio Type 1, type 3, type 2
• Presenting symptom of Normotensive Hydrocephalus is VERTIGO
• Pencil – in – cup deformity is seen in PSORIATIC ARTHRITIS

NUSU9OIDI3
Which of the following nuclei belongs to the General Visceral Efferent column?
a) Facial nerve nucleus

b) Trigeminal nerve nucleus
c) Dorsal nucleus of vagus
d) Nucleus ambiguous
Correct Answer: C
Explanation
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• A, C & D belong to the Special Visceral Efferent Colum (Branchial Efferent Column)
• The nuclei belonging to the General Visceral Efferent column give rise to parasympathetic
fibres, which form the cranial outflow of parasympathetic nervous system. They are four
in number and are situated in the brainstem.
They include
• ◦ Edinger Westphal nucleus (in the midbrain), the fibres of which pass through the
oculomotor nerve to innervate the sphincter papillae and ciliaris muscles.
◦ Superior salivatory and lacrimatory nuclei (in the pons), the fibres of which pass
through the facial nerve to provide secretomotor innervation to submandibular and
sublingual salivary glands and all glands of nasal and oral cavities and lacrimal
gland.
◦ Inferior salivatory nucleus (in the medulla), the fibres of which pass through the
glossopharyngeal nerve to provide secretomotor innervation to parotid gland.
◦ Dorsal vagal nucleus (in the medulla), the fibres of which pass through the vagus
to provide parasympathetic innervation to thoracic viscera and abdominal viscera
down to the midgut. i.e. up to the junction between the right two thirds and left one
third of transverse colon.
The facial nerve has three nuclei.
1.Motor nucleus belongs to the Branchial Efferent (Special Visceral Efferent) column. Its fibres
innervate the muscles derived from the first pharyngeal (branchial) arch mesoderm. I.e.
muscles of facial expression and others.
2.Superior salivatory nucleus belongs to the General Visceral Efferent column. Its fibres
innervate the submandibular and sublingual salivary glands via. Submandibular ganglion and
glands of nasal and oral cavities and lacrimal gland via. Pterygopalatine ganglion.
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3.Nucleus of tractus solitarius belongs to the Special Visceral Afferent column. This nucleus
receives the sensation of taste from the anterior two thirds of tongue via. Facial nerve and, the
Posterior one third of tongue via. Glossopharyngeal and vagus nerves.
The trigeminal nerve has four nuclei. One motor nucleus belonging to the Branchial (Special
Visceral) Efferent column and three sensory nuclei belonging to the General Somatic Afferent
column.
• ◦ Fibres from motor nucleus pass through the mandibular nerve to innervate the
muscles derived from the first branchial arch mesoderm. i.e. muscles of mastication
and others.
◦ Main sensory nucleus receiving touch and pressure sensation from the anterior part
of head.
◦ Spinal nucleus receiving the sensation of pain and temperature from the anterior
part of head.
◦ Mesencephalic nucleus receiving proprioceptive sensation from the muscles of
mastication and other muscles innervated through mandibular nerve.
The nucleus ambiguous is a motor nucleus belonging to the Somatic Efferent column. The IX, X
and XI cranial nerves arise from this nucleus.
In genital TB, the menstrual blood Does not contain tuberculids
In PCOD, Increase LH, increase estrogen
Oral contraceptive pills are contraindicated in
Lactating woman
Patients on sodium valproate
Thyroid disease
Oral contraceptives offer a protective effect against ovarian epithelial tumors and endometrial
cancers and decrease bone fractures and colorectal cancer
Oral contraceptives are contraindicated for cyanotic women because of the enhanced risk of
vascular thrombosis
Oral contraceptives can cause hepatic adenoma, hepatocellular carcinoma and hepatic vein
occlusion (Budd-Chiari syndrome).
Oral Contraceptive Pills
* They act by suppressing ovulation, changing cervical mucus, and altering the endometrium.
The current formulations are made from synthetic estrogens and progestins. The estrogen
component of the pill consists of ethinyl estradiol or mestranol.
* Levonorgestrel is the most androgenic of the progestins and should be avoided in patients
with hyperandrogenic symptoms.
* Contraindications of OC pills are given below
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Absolute
Previous thromboembolic event or stroke
History of an estrogen-dependent tumor
Active liver disease
Pregnancy
Undiagnosed abnormal uterine bleeding
Hypertriglyceridemia
Women aged >35 years who smoke heavily
Disease Risks
Increased
Coronary heart disease
Hypertension
Venous thrombosis—relative risk 4
Stroke
Cerebral vein thrombosis
Cervical cancer—relative risk 2–4 Breast

cancer(mainly BRCA1)
Decreased
Ovarian cancer—50% reduction in risk
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Endometrial cancer—40% reduction in risk

NUSU9OIDI4
Posterior gastric artery is a branch of which of the following artery
a) Left gastric artery

b) Right gastric artery
c) Splenic artery
d) Hepatic artery
Correct Answer: C
Explanation
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IMPORTANT POINTS
1.TORTUOUS ARTERIES :
1.Facial artery, uterine artery, splenic artery, posterior inferior cerebellar artery, lingual artery.
2.BLOOD LESS STRUCTURES :
Cartilage, cornea, lens, epithelium.
3.STRUCTURES WITHOUT LYMPHATICS :
2.Epidermis, Hair, Nails, Cornea, Cartilage central nervous system, bone marrow.
4.PORTAL CIRCULATION :
System of vessels between two capillary beds.
1. Hypothalamic – pituary fortal system.
2. Hepatic system
3. Adrenal, kidney.
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5.VALVELESS VEINS :
Superior vena cava : Inferior vena cava: veins in Head & Neck (Ophthalmic veins) Dural
Sinuses: veetenral veins: Cardiac veins: Pulmonary veins: Hepatic veins: Portal veins: Pelvic
veins: Emissary Veins: Cerebral veins
6.VEINS CARRYING OXYGENATED BLOOD :
1. Pulmonary veins
2. Umbilical veins
7.ARTERIES CARRYING VENOUS BLOOD :
1. Pulmonary artery
2. Umbilical artery
8.SINUSOIDS – lined by endothelium, present in liver, spleen, adrenal, pituitary, lymphnode.
9.THE END ARTERIES : (ARTERY WHICH DO NOT ANASTOMOSE)
Spleen Heart Lungs
Kidneys Metaphysis of long bone Liver
Brain Central branch of cerebral .A
Central artery of Retina
Parts of gastrointestinal tract (vasa recta of mesenteric artery)
The functional end arteries – anastomose, with much smaller arteries. Is not sufficient to
maintain blood supply of the part.
(Coronary arteries)
10.THE ARTERIO-VENOUS ANASTOMOSIS
These are sites where blood is transferred from the arteries to the veins without passing
through capillary plexus.
• The A-V anastomoses lie in organs, whose functions are intermittent. These also help in
temperature regulation.
Skin of apical part of fingers Nose
Lips Ears
Early dumping syndrome
Early dumping takes place 15–30 minutes after meals and consists of crampy abdominal
discomfort, nausea, diarrhea, tachycardia, palpitations, diaphoresis, and rarely, syncope. Ca
use is due to rapid emptying of hyperosmolar gastric contents into the small intestine, leading
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to plasma volume contraction and acute intestinal distention. Vasoactive intestinal
polypeptide, neurotensin, motilin may play a role.
*Late phase dumping takes place 90 min to 3 h after meals. Vasomotor symptoms are light-
headedness, diaphoresis, palpitations, tachycardia, and syncope predominate during this
phase. It is due to hypoglycemia from excessive insulin release.
* Precipitating factors are meals rich in simple carbohydrates (especially sucrose) and high
osmolarity. Ingestion of large amounts of fluids may also contribute.

NUSU9OIDI5
Which of the following muscle is considered as the Abductor of vocal cord
a) Posterior cricoarytenoid
b) Cricothroid
c) Interarytenoid
d) Lateral cricoarytenoid
Correct Answer: A
Explanation
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Glottis – Vocal cord
* Ant 3/5 – intermembranous part
* Post 2/5 – intercartilagenous part
Movement Muscles
* Abduction * Postr. Crico arytenoid*****
* Lateral crico arytenoid * Transverse arytenoid

* Adductors
* Oblique arytenoideus
* Tensor * Cricothyroid * Vocalis
* Relaxors * Thyroarytenoideus
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* Opening inlet of larynx * Thyro epiglotticus
Tit bits * All muscles are supplied by Recurrent laryngeal N except
--> cricothyroid (Ext. larynged N)
* Arteries – <st1>Superior, Inferior thyroid</st1>
* Lymphatics
a) Above vocal cord * Upper deep cervical
* Below vocal cord * Pretracheal, plaryngeal
Nerve supplySensory
-Above the vocal cord – Int. laryngeal N
- Below the vocal cord
– Recurrent laryngeal N
Muscles of Larynx
Action Intrinsic Muscle
Abductor of Vocal Cord Posterior Crico Arytenoid
Thyro arytenoids (external part) Transverse arytenoids

ADDuctor of Vocal Cord
Lateral Crico arytenoids
Tensor of vocal cord Crico Thyroid Thyro Arytenoid (internal part i.e. vocalis )
Openers of Laryngeal
Thyroepiglotti (part of thyro arytenoids)
inlet
Inter arytenoids (oblique part) Inter arytenoids (Posterior oblique part

Closers of laryngeal known as
inlet
Aryepiglottic)
Nerve supply
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Sensory Upto the level of vocal

Motor All intrinsic ms. are supplied by recurrent laryngeal n. folds - Internal laryngeal n.
except for cricothyroid which is supplied by external laryngeal
nerve Below the level of vocal folds -
Recurrent laryngeal n.
Retinal output is mainly from Ganglion cell layer
Suprasellar aneurysms causes BITEMPORAL HEMIANOPIA
GRADENIGO SYNDROME
Syndromes associated with 6th nerve are listed below
Syndrome Effect
Site- Dorsal Pons
Effect
- Ipsilateral lat. Gazepalsy

1. Foville (6 th )
- Ipsilat 7 th N Palsy
- Contralat Lateral
Hemiparesis
Site- Ventral PONS
Effect- Similar to
1. Except eye findings

2. Milard Gubler - LR weakness only instead
of gaze palsy
(Because Abducen fascicles

are involved, not the
nucleus)
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Site- Petrous Apex

(Mastoiditis)
Effect
3. Gradenigo
- Deafness
- Pain
- Ipsilat 6th N Palsy

USU9OIDMw
Tentorium cerebelli is innervated by recurrent tentorial nerve, a branch of
a) Maxillary brach of trigeminal nerve

b) Mandibular branch of trigeminal nerve
c) Ophthalmic branch of trigeminal nerve
d) Trochlear nerve
Correct Answer: C
Explanation
Ophthalmic branch of trigeminal nerve- Cranial nerve V A
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Diabetes mellitus is associated with
a. Down’s syndrome
c. Klinefelter’s syndrome
d. Turner’s syndrome
Most common cause of pleural effusion in HIV patients
A wide variety of infectious and malignant conditions cause pleural effusions in HIV infected
patients, the most common cause in this group was Kaposi's sarcoma
The earliest pathological change in x-ray finding of Ulcerative colitis includes MUCOSAL
GRANULARITY
The earliest feature of multiple sclerosis is OPTIC NEURITIS

USU9OIDMx
Corona radiata of ovum is from which of the following structure
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a) Cummulus ovarius
b) Zona pellucida
c) Formative yolk
d) Follicular cells
Correct Answer: A
Explanation
OVUM
Consists of cell membrane, Nucleus, Cytoplasm and outter coverings
Outter coverings-Zona pellucida and Corona radiata*
Cytoplasm
Ooplasm or yolk
Formative yolk
Nutritive yolkor deutroplasm *
Human oocyte- Microlecithal
(Bird – Macro lecithal)
Follicular cells (Granulosa cells)
layer of flattened epithelial cells
surrounding primary oocyte
outter layer-stratum granulosum
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inner layer-cummulus ovaricus*
Cummulus ovaricus
the outter cells disappear
adjacent to the zona pellucida are arranged radially- Zona radiata*
Granulosa cells (Follicular cells) attached to Zona pellucida elongate forming – Corona
Radiata*
Tit bits
*Zona pellucida disappears by day 5 of devolpment
The clinical feature of normal pressure hydrocephalus is GAIT DISTURBANCE
Drug of choice for social phobia is SSRIs
Treatment : antidepressant medication is the drug of choice.. Selective serotonin reuptake

inhibitors (SSRIs) like Fluoxetine, paroxetine, sertraline are used. Selective serotonin-
norepinephrine reuptake inhibitor (SNRI) venlafaxine also can be used. These drugs should
be started at one-third to one-half of their usual antidepressant dose (5–10 mg fluoxetine, 25–
50 mg sertraline, 10 mg paroxetine, venlafaxine 37. 5 mg). Monoamine oxidase inhibitors
(MAOIs) are also effective mainly in patients with features of atypical depression
(hypersomnia and weight gain). It Typically take 2–6 weeks to become effective.
The drug that is used for Nicotine addiction includes BUPROPION

USU9OIDMy
A body was identied in a forest region with putrefaction.The first organ to putrefy is which of
the following
a) Trachea and larynx

b) Brain
c) Heart
d) Liver
Correct Answer: A
Explanation
Order of Putrefaction
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• Trachea and Larynx
• Stomach, intestine, spleen

• Liver, lungs
• Brain
• Heart
• Kidney, uterus
• Skin, muscle
• Bone
Putrefaction
- Slower in water than air
- Slower in salt water
Side effects of INH
a. Rash
c. Hepatitis
d. Peripheral neuritis
“Seal finger” and “whale finger” are associated with infection of Erysipelothrix.Seal finger
respond to doxycycline
Bites of seals , walruses, and polar bears may cause a chronic suppurative infection known as
seal finger due to Mycoplasma
Foramen spinosum transmits MIDDLE MENINGEAL ARTERIES
Incubation period of Diphtheria is 2-4 DAYS

USU9OIDMz
Person with Eonismattains sexual gratification by which of the following mechanism
a) Getting hurt by partner

b) Seeing a woman nude
c) Fondling female body parts
d) Getting gratification wearing dress of opposite sex
Correct Answer: D
Explanation
DISCUSSION
SEXUAL PERVERSIONS
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SODOMY
SODOMY denotes homosexual penile-anal intercourse.
Heterosexual penile-anal intercourse is called BUGGERY.
The offender is the active agent, the other partner is the passive agent.
If the passive agent is a child, the practice is known as PAEDERASTY.
Habitual passive agents are called CATAMITES, (fairies, gays or queens)
In India, HIJRAS (castrated males) & ZENANAS (male transvestites)
Buccal coitus (sin of Gomorrah)
Buccal-Penile intercourse is called FELLATIO.
The partner who performs the act is called the FELLATOR, and on whom it is performed is the
FELLATEE.
Buccal-vaginal stimulation is referred to as CUNNILINGUS.
Sexual Paraphilias (perversions)
These form a group of psychosexual disorders, which involves involuntary, repetitive, unusual
acts, on which Sexual Arousal and Orgasm are dependent.
Achievement of sexual gratification by means other than natural sexual intercourse.
Fetishism (Fetichism) Sexual focus is on relatively indestructible objects intimately associated

with the human body.
Transvestism : Cross dressing or Eonism.(AIIMS MAY-2014***)
Dressing in the opposite sex, for the purpose of arousal and as an adjunct to masturbation or
sexual intercourse.
Sadism : sexual arousal and orgasm linked to active infliction of injuries or torture of the
sexual partner.
Masochism : sexual excitement linked with passive experience of physical or emotional

humiliation or torture.
Exhibitionism & Voyeurism
They are paired opposite of the Scoptophiic paraphilia.
Exhibitionism involves repeated acts of exposing one’s genitals to a stranger or unsuspected

person
Voyeurism : perversion with desire to observe the genitals or other private parts of the body of
others – Peeping Tom.
FROTTEURISM : Practiced by a male pervert in a crowded place to drive sexual gratification

by rubbing his private parts against a female’s body.
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TROILISM : The pervert gets sexual gratification by inducing his wife to sexual intercourse
with another person and by observing the same.
Necrophilia
Sexual arousal and orgasm can be attained only by intercourse with a corpse,
NECROPHAGIA is an extreme form of Sadism, where in sexual gratification is attained by

tearing out the genitals or other part of the body of a corpse and eating them.
Sec. 297 IPC
Who ever with the intention of offering any indignity to any human corpse, shall be punished
with imprisonment of either description for a term which may extend to one year, or with fine,
or both.
PAEDOPHILIA : Preferential sexual activity with children.
SATYRIASIS : Excessive sexual desire among males. These subjects are liable to commit
sexual offences.
NYMPHOMANIA : Excessive sexual desire among woman.
Indecent assault
Indecent assault generally means sex-linked misbehaviour towards a person of opposite sex or
the same sex.
Any offence committed on a female with the intention or knowledge to outrage her modesty.
Sec. 509 IPC
Whoever, intending to insult the modesty of a woman, utters any word, makes any sound or
gesture, or exhibits any object shall be punished with imprisonment which may extend to one
year .
Kocher Debre Semelaigne Syndrome is a rare syndrome with clinical manifestation of

hypothyroidism associated with pseudomuscular hypertrophy.
The absence of painful spasms and pseudomyotonia differentiates this syndrome from its adult
form, which is Hoffmann syndrome
“Salmon patch” is seen in INTERSTITIAL KERATITIS
Acutely or at the early sign includes painful, photophobic , red and watery eye. This is due to
active corneal inflammation resulting in vascular invasion and stromal necrosis which can be
diffuse or localized. This cause the pinkish discoloration of what was a clear transparent normal
corneal tissue (called Salmon patch of Hutchinson ).
Conjunctival lymphoma is the second most common ocular adnexal tumor and generally
manifests as a salmon -pink patch on the fornix of the eye
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USU9OIDM0
Components of Cannabis includes all except
a) charas
b) bhang
c) Ganja
d) afeem
Correct Answer: D
Explanation
Cannabis preparations.
THE Potency (as

Cannabis
Portions of Plant content (% compared to
preparation
) ‘Bhang)
1.Hashish/ - Resinous exudate from the flowering

8 – 4% 10
Charas tops of cultivated plants
- Small leaves and brackets of

2. Ganja 1 – 2% 2
inflorescence of highly cultivated plants
- Dried leaves, flowering shoots and

3. Bhang 1% 1
cut tops of uncultivated plants
4. Hash oil - Lipid soluble plant extract 15 – 40% 25
The daily production of CSF is 550ML
Circadian rhythm is regulated by Supra chiasmatic nucleus
Vibration sense is carried by Pacinian corpuscles
A widely accepted dogma is that about 15–20% of cardiac output is received by the brain in
healthy adults under resting conditions

USU9OIDM1
Lateral traction test is done in unnatural sexual offences in:
a) Habitual active agent
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b) Pedophilia active agent

c) Bestiality active agent
d) Habitual passive agent
Correct Answer: D
Explanation
Lateral traction test is done in unnatural sexual offences in habitual passive agent.
Lateral buttock traction test is a useful guide as to the patient’s habituation to anal intercourse.
HIV
Treatment guidelines recommend that anyone with a viral load greater than 100,000 copies/mL
of blood should begin treatment.
In mammals, DNA synthesis occurs in -S PHASE
Carnitine deficiency impairs Fatty oxidation
Deficiency of which mineral causes Diabetes mellitus -ZINC
Pramipexole is Dopamine agonist

USU9OIDM2
All are prodrugs EXCEPT
a) INH
b) Nevirapine
c) Metronidazole
d) Mycophenolate mofetil
Correct Answer: B
Explanation
• A prodrug is a pharmacological substance (drug) that is administered in an inactive (or

significantly less active) form. Once administered, the prodrug is metabolised in vivo into
an active metabolite. The rationale behind the use of a prodrug is generally for
absorption, distribution, metabolism, and excretion (ADME) optimization. Prodrugs are
usually designed to improve oral bioavailability,
• Prodrugs can be classified into two types based on their sites of conversion into the final
active drug form: Type I, those that are converted intracellularly (e.g., anti-viral
nucleoside analogs, lipid-lowering statins, antibody-directed/gene-directed enzyme
prodrugs [ADEP/GDEP] for chemotherapy), and Type II, those that are converted
extracellularly, especially in digestive fluids or the systemic circulation (e.g., etoposide
phosphate, valganciclovir, fosamprenavir).
Ø Enalapril is converted by esterase to the active enalaprilat

Ø Valacyclovir is converted by esterase to the active acyclovir
Ø Fosamprenavir is hydrolysed to the active amprenavir
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Ø Levodopa is converted by DOPA decarboxylase to the active dopamine
Ø Chloramphenicol succinate ester is used as intravenous prodrug of chloramphenicol, because
pure chloramphenicol does not dissolve in water
Ø Psilocybin is dephosphorylated to the active psilocin
Ø Heroin is deacetylated by esterase to the active morphine
Ø Codeine is demethylated by the liver enzyme CYP2D6 to the active morphine, as well as
several other compounds that may be active in analgesia
Ø Molsidomine is metabolized into SIN-1 which decomposes into the active compound nitric
oxide
Ø Paliperidone is an atypical antipsychotic for schizophrenia. It's the active metabolite of
risperidone
Ø Mycophenolic acid (INN) (pronounced or mycophenolate******** is an

immunosuppressant drug used to prevent rejection in organ transplantation. It was initially
marketed as the prodrug mycophenolate mofetil (abbreviated MMF) to improve oral
bioavailability. More recently, the salt mycophenolate sodium has also been introduced
Ø Mycophenolate is derived from the fungus Penicillium stoloniferum. Mycophenolate mofetil is
metabolised in the liver to the active moiety mycophenolic acid. It inhibits inosine
monophosphate dehydrogenase, the enzyme that controls the rate of synthesis of guanine
monophosphate in the de novo pathway of purine synthesis used in the proliferation of B and T
lymphocytes.
Ø In general, mycophenolate is used for the prevention of organ transplant rejection.
Ø Its increasing application in treating lupus nephritis has demonstrated more frequent
complete response and less frequent complications
Ø Common adverse drug reactions (≥1% of patients) associated with mycophenolate therapy
include diarrhea, nausea, vomiting, infections, leukopenia, and/or anemia. Mycophenolate
sodium is also commonly associated with fatigue, headache, and/or cough. Intravenous (IV)
administration of mycophenolate mofetil is also commonly associated with thrombophlebitis and
thrombosis. Infrequent adverse effects (0.1–1% of patients) include esophagitis, gastritis,
gastrointestinal tract hemorrhage, and/or invasive cytomegalovirus (CMV) infection
Ø
Nevirapine******** , [not a prodrug******] i s a non-nucleoside reverse transcriptase

inhibitor (NNRTI) used to treat HIV-1 infection and AIDS.
Ø Both nucleoside and non-nucleoside RTIs inhibit the same target, the reverse transcriptase
enzyme, an essential viral enzyme which transcribes viral RNA into DNA. Unlike nucleoside
RTIs, which bind at the enzyme's active site, NNRTIs bind within a pocket termed the NNRTI
pocket.
Ø Resistance to nevirapine develops rapidly if viral replication is not completely suppressed.The
most common mutations observed after nevirapine treatment are Y181C and K103N,
Ø The most common adverse effect of nevirapine is the development of mild or moderate rash
(13%). Severe or life-threatening skin reactions have been observed in 1.5% of patients,
including Stevens-Johnson syndrome, toxic epidermal necrolysis and hypersensitivity.
Ø Nevirapine may cause severe or life-threatening liver toxicity, usually emerging in the first six
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weeks of treatment.
Ø Significant lowering of nevirapine levels occurs with the anti-tuberculosis drug, rifampicin,
and the drugs should not be administered together.
Ø Nevirapine is an inducer of cytochrome P450 isoenzymes CYP3A4 and CYP2B6. It reduces the
levels of several co-administered drugs including the antiretrovirals efavirenz, indinavir,
lopinavir, nelfinavir and saquinavir, as well as clarithromycin, ketoconazole, forms of hormonal
contraception, and methadone
Ø A single dose of nevirapine given to both mother and child reduced the rate of HIV
transmission by almost 50% compared with a very short course of zidovudine (AZT) prophylaxis
Ø Half life45 hours
Metronidazole
Ø
Metronidazole is a prodrug********* . I
Ø
Metronidazole is listed by the International Agency for Research on Cancer (IARC) as
a potential human carcinogen
INHØ Isoniazid is a prodrug******* and must be activated by bacterial catalase. It is

activated by catalase-peroxidase enzyme KatG to form isonicotinic acyl anion or radical. Ø This
mechanism inhibits the synthesis of mycolic acid in the mycobacterial cell wall. Ø Isoniazid is
bactericidal to rapidly-dividing mycobacteria, but is bacteriostatic if the mycobacterium is slow-
growing. Ø Half life0.5-1.6h (fast acetylators), 2-5h (slow acetylators)Ø Adverse reactions
include rash, abnormal liver function tests, hepatitis, sideroblastic anemia, peripheral
neuropathy, mild central nervous system (CNS) effects, drug interactions resulting in increased
phenytoin (Dilantin) or disulfiram (Antabuse) levels and intractable seizures (status epilepticus).
Ø Peripheral neuropathy Ø The N-acetylhydrazine metabolite is believed to be responsible for
the hepatotoxic effects seen in patients treated with isoniazid. The rate of acetylation is
genetically determined. Approximately 50% of blacks and Caucasians are slow inactivators; the
majority of Inuit and Orientals are rapid inactivators. The half-life in fast acetylators is 1 to 2
hours while in slow acetylators it is 2 to 5 hours. Elimination is largely independent of renal
function, however the half-life may be prolonged in liver disease. The rate of acetylation has not
been shown to significantly alter the effectiveness of isoniazid. However, slow acetylation may
lead to higher blood concentrations with chronic administration of the drug, with an increased
risk of toxicity.

USU9OIDM3
All of the following statements about Phenytoin are true, Except
a) Follows saturation kinetics

b) Is teratogenic
c) Is highly protein bound
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d) Stimulates Insulin secretion

Correct Answer: D
Explanation
Phenytoin can cause insulin resistsance* *****

The side effects of common antiepileptics are given below
Drug adverse effect
* Diplopia
* Ataxia
* Phenytoin -Level increased by isoniazid, sulfonamides,
fluoxetine. Half life is 24 h* * Hirsuitism
* Gumhypertrophy
* Ataxia
* Diplopia
* Carbama zepine- Level increased by erythromycin,
* Aplastic Anemia
propoxyphene, isoniazid, cimetidine, fluoxetine. Half life is 10–
17 h * Hepatotoxicity
* Hyponatremia
* Tremor, Ataxia
* Wt. Gain
* Valproic acid -. Half life is 15 hors * Hepatotoxicity
* Alopecia
* Hyperammonemia*
* Lamotrigine. -Half life is25 h * 14 h (with enzyme-inducers)

* Steven. Johnson syndrome
* 59 h (with valproic acid)
* Gabapentin -. Half life is 5-9 hours * Wt. Gain
* Wt. loss* [AIIMS

* Topiramate –also used in Lennox-Gastaut syndrome. Half life
MAY-2006***], glaucoma
is 20–30 h
* Renal stones, hypohydrosis
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* Wt. loss*
* Felbamate - Increases phenytoin, valproic acid, active * Aplastic Anemia
carbamazepine. Half life is 16-20 hours
* Hepatic failure
* Zonisamide-. Half life is 50-68 hours * Renal stones, hypohydrosis
* Lacosamide- Dizziness * Ataxia
* Diplopia
* Vertigo
(PR interval prolongation)
* Half life is 13 hours
Rufinamide used in Lennox-Gastaut syndrome(AIIMS NOV-2013***) * Side effects
* Sedation
* Fatigue
* Dizziness
* Ataxia
* Headache
* Diplopia, ( QT interval prolongation)
* Rufinamide-interactions
* Level increased by valproic acid
* May increase phenytoin
* Half life is 6-10 hours
The lipid lowering drug to be avoided in diabetes as it worsens the glycemic profile NIACIN
All of the following are side effects of Hydralazine
a. Lupus syndrome
b. Rheumatoid arthritis
c. Postural hypotension
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Hydralazine is a potent direct vasodilator that has antioxidant and nitric oxide–enhancing
actions.
* Hydralazine may induce a lupus-like syndrome, and side effects of minoxidil include
hypertrichosis and pericardial effusion .

USU9OIDM4
Which is incorrectely matched for adverse effects?
a) Carbamazepine- Hepatotoxicity
b) Ethosuximide- Bone marrow suppression
c) Lamotrigene – Steven Johnson syndrome
d) Gabapentin – Drug interaction
Correct Answer: D
Explanation
Drugs that are prone to cause hepatotoxicity are Carbamazepine, Valproate & Felbamate.
Blood dyscrasias are induced by Carbamazepine, Ethosuximide & Felbamate. Lamotrigine
causes fatal dermatitis. Gabapentin does not cause drug interaction .
The following cell is involved in LE cell phenomenon- Neutrophil
Firm, warty vegetations along the line of closure of valve is seen in RHD
“Programmed cell death” is known as APOPTOSIS
The toxin responsible for LAthyrism is BOAA
Lathyrism
* neurolathyrism because it affects the nervous system, and in animals as osteolathyrism
The pulse
* Lathyrus sativus is commonly known as “Khesari dhal”
* The seeds of lathyrus have a characteristic triangular shape and grey colour
* diets containing over 30% of this dhal if taken over a period of 2-6 months will result in
neurolathyrism
The toxin
* The toxin present in lathyrus seeds has been identified as Beta oxalyl amino alanine (BOAA)
The disease
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* mainly young men
a) Latent stage:
b) No-stick stage:
c) One-stick stage
d) Two-stick stage
e) Crawler stage
Interventions
a) Vitamin C prophylaxis
b) Banning the crop
c) Removal of toxin
1. Steeping method
* A large quantity of water is boiled and the pulse is soaked in hot water for 2 hours
2. Parboiling
c. Genetic approach: Certain strains of lathyrus contain very low levels of toxin (0.1%)
d. Socio-economic changes

USU9OIDM5
A patient with smear proved malaria was planed for treatment with chloroquine.Chloroquine is
contraindicated in which of the following conditions
a) Pregnancy
b) Epilepsy
c) Psoariasis
d) Psychiatric disorder
Correct Answer: C
Explanation
Antimalarial Contraindication
* Psoariasis
* Chloroquine
* Porphyria
* Primaquine * Connective Tissue disorder
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* Epilepsy
* Mefloquine
* Psychiatric Disorder * Pregnancy
* Pregnancy
* Quinine
* Myasthenia
Tit bits
Mefloquine
* Highly protein bound * In chloroquine resistant falciparum malaria

* Only oral
* Good CSF penetration
* t ½-13-33 days (shortened in acute malaria)
* Contraindicated in
- Epilepsy
- Psychiatric disorder
* Shouldn’t be used with Quinine, Quinidine, b blockers, Calcium channel Blockers
* Mefloquine + chloroquine
→ Seizure s
An elderly man with ataxic hemiparesis, diagnosis is CERBELLAR BLEED
MEDIAL MEDULLARY SYNDROME
Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower

basilar artery) features are listed below
On side opposite
On side of lesion
lesion
Paralysis of arm and

leg, sparing face;
Paralysis with
impaired tactile and
atrophy of one-half
proprioceptive sense
half the tongue:
over one-half the body:
Ipsilateral twelfth
Contralateral
nerve
pyramidal tract and
medial lemniscus
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USU9OIDQw
All are indicators of air pollution except
a) CO2
b) SO2
c) Soiling index
d) Smoke index
Correct Answer: A
Explanation
Air pollutants
* The combination of smoke and fog is called “smog”.
1. Carbon monoxide:
* Environmental concentrations tend to be expressed in terms of 8 hour average

concentrations.
2. Sulphur dioxide:
* When SO 2 combines with water, it forms sulphuric acid; this is the main component of acid
rain.
* A SO 2 concentration of 500 µg/m 3 should not be exceeded over average periods of 10

minutes duration.
* The revision of 24 hour guideline for SO 2 from 125 to 20 µg/m 3 is based on the health
effects.
3. Lead:
* An estimated 80-90 % of lead in ambient air derives from the combustion of leaded petrol.
* Children up to 6 years of age are a population at increased risk.
4. Carbon dioxide:
* Not commonly regarded as an air pollution.*******
5. Hydrocarbons:
6. Cadmium:
* Steel industry, waste incineration, volcanic acition and zinc production seem to account for
the largest emissions.
* Cigarettes may contain from 0.5 to 3 µg cadmium per gram of tobacco.
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7. Hydrogen sulphide:
* Elemental sulphur or sulphur containing compounds come in contact with organic material at
high temperatures.
* The first noticeable effect of hydrogen sulphide at low concentration is its unpleasant odour
Conjunctival irritation is the next subjective symptom.
8. Ozone:
* Ozone at ground level – not to be confused with the ozone layer in the upper atmosphere
* The highest levels of ozone pollution occurs during periods of sunny weather,
* It can caused breathing problems, trigger asthma, reduce lung function and cause lung
diseases.
* The previously recommended limit, which was fixed at 120 µg/m 3 of 8-hour mean, has been
reduced to 100 µg/m 3.
9. Oxides of nitrogen:
* Nitric oxide, which comprises around 95% of nitrogen oxides from a combustion source.
* The current WHO guideline value of 40 µg/m 3 (anuual mean).
10. Polycyclic aromatic hydrocarbons (PAH):
* The examples are Benzo.
a. Pyrene (BaP), Benzanthracene, Benzo
fluoranthene, fluoranthene, Nephthalene etc.
* Produced by incomplete burning of carbon containing material like wood, garbage, coal and
oil.
* PAHs from when materials burn at low temperatures, such as in wood fires and cigarettes.
* BaP is one of the most potent carcinogens among the known PAHs.
* A unit risk for lung cancer for PAH mixture is etimated to be 8.7 x 10 -5 ng/m 3 BaP.
11. Particulate matter:
* Mass and composition tend to divide into two principal groups: coarse particles larger than
2.5 µm in aerodynamic diameter, and fine particles smaller than 2.5 µm (PM 2.5 ) in
aerodynamic diameter.
* The particulate matter of diameter smaller than 2.5 µm are more dangerous.
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* The 2005 AQG set for the first time a guideline value for particular matter (PM) as 10 µg/
m 3 annual mean and 25 µg/m 3 24-hour mean for PM 2.5 and 20 µg/m 3 annual mean
and 50 µg/m 3 24 hours mean for PM 10.
Indoor air pollution
Monitoring of air pollution
* The best indicators of air pollution are sulphur dioxide, smoke and suspended particies.
a. Sulphur dioxide:
b. Smoke or soiling index:(1992-JIP***).
* A known volume of air is filtered through a white filter paper.
* Smoke concetration is estimated and expressed as micrograms/cubic metre of air.
c. Grit and dust measurement.
d. Coefficient of haze.
e. Air pollution index.
The most common malignancy in childhood is ALL
A female child of a mother is diagnosed to have Duchenne’s muscular dystrophy. What

risk does the mother have for her next male child to suffer from similar illness -50%
The most common cause of perinatal mortality is PREMATURITY
The most common pancreatic tumor is ADENOCARCINOMA
Skin lesion characteristic of Lyme’s disease includes ERYTHEMA CHRONICUM MIGRANS

USU9OIDQx
Prevention of first attack of rheumatic activity by early detection & adequate treatment of all
cases of streptococcal pharyngitis is
a) Primordial prevention
b) Primary prevention
c) Secondary prevention
d) Tertiary prevention
Correct Answer: C
Explanation
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(P-31, 37- Park)
Prevention
Levels
-Primary
-Secondary
-Teritiary
Prevention
Levels Features
Primary * Health Promotion * Specific Protection
Secondary * Early Diagnosis and Trt
Teritiary * Disability limitation * Rehabilitation
Primordial Prevention
New concept Prevention in its purest sense
Prevention of devolpment of risk factors
eg – Life style modification (obesity)
Mass education
Primary
Action taken prior to onset of disease Intervention in prepathogenesis phase Types
-Population (mass) strategy
-High risk strategy
eg – improving standard of living to prevent cholera
Secondary
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Action which halts the progress of a disease at its incipient stage and prevents complication
** eg – screening tests and adequate Trt.
Health Promotion *Health education
*Life style modification
*Food fortification
Specific Protection
*Immunisation
*Chemoprophylaxis
*Avoidance of allergy
Any loss or abnormality of psychological physiological or anatomical structure or

Impairment
function (eg :Loss of foot)
Disability Inability to carry out activities because of impairment
As a result of disability, the person experiences certain disadvantages (eg –

Handicap
Unemployment)
The most common site of Berry Aneurysm is Anterior circulation
The most important characteristic feature of breast malignancy in young age is PALPABLE
LUMP

USU9OIDQy
Which among the food toxicants is incorrectly matched
a) Aflatoxins – mycotoxins (storage fungus) produced by Aspergillus flavus, Aspergillus

parasiticus and are hepatotoxins
b) Ergot – this is due to field fungus – claviceps fusiformis and Easily removed by floating
them in salt water
c) Endemic ascites – over all mortality – 80%, causes ascites and jaundice, contamination of
weed seeds of Crotalaria (Jhunjhunia plants) – contain pyrrolizidine alkaloids –
hepatotoxins.
d) Epidemic dropsy – contamination of mustard oil with argemone oil -Sangunarine is the
toxic principle in argemone oil
Correct Answer: C
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Explanation
Endemic ascites – over all mortality – 40%, causes ascites and jaundice******
MORE NIMHANS FACTS
FOOD TOXICANTS
Aflatoxins – mycotoxins (storage fungus) produced by Aspergillus flavus, Aspergillus

parasiticus
These fungi infest food grains like – ground nut, maize, wheat, rice etc.,
Aflatoxins – B1 and G1 – hepatotoxins
More prevalent in Rajasthan and Gujarat
Ergot – this is due to field fungus – claviceps fusiformis
Severe vasoconstriction of capillaries resulting in peripheral gangrene, rarely fatal
Easily removed by floating them in salt water
Endemic ascites – over all mortality – 40%, causes ascites and jaundice******, contaminati
on of weed seeds of Crotalaria (Jhunjhunia plants) – contain pyrrolizidine alkaloids –
hepatotoxins. Prevalent in Madhya pradesh
Epidemic dropsy – contamination of mustard oil with argemone oil
Sangunarine is the toxic principle in argemone oil
Interfers with oxidation of pyruvic acid which accumulates in the blood
Sudden, non inflammatory swelling of legs, with diarrhea, dysnoea, cardiac failure
Tests for the detection of argemone oil – nitric acid test, paper chromatography test (most
sensitive test), detects argemone oil up to 0.0001%
Rheumatoid arthritis commonly affects Cervical spine
Tumor that develops from metaphysis includes Osteosarcoma
EWINGS SARCOMA
Ewing’s Sarcoma(AIIMS-NOV-2010***)
* These tumors form 10-15% of bone sarcomas. Seen mostly in adolescence age group, they
arise from the diaphysis, ( AI-07***) [AIIMS MAY-2014***] and have affinity for flat
bones.They show an Onion peel periosteal reaction with a generous soft tissue mass. On Histo
logy monotonous, small round blue cells are seen [AIIMS MAY-2012***]. D/D include
lymphoma, Embryonal habdomyosarcoma, small cell carcinoma.
* Cytogenic abnormality are Reciprocal Translocation of long arms of 11, chromosome 22.
The surface marker is P 30/32 the product of the myc-2[AIIMS MAY-2012***], gene. A
variant of PNET -peripheral neuroepithelioma is Askin's tumor (chest wall), and
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esthesioneuroblastoma [AI-2012***]. Glycogen-filled cytoplasm detected by staining with
periodic acid–Schiff is characteristic.
* It is very aggressive and considered a systemic disease. Main stay of therapy is

chemotherapy. The Drugs used are Doxorubicin, cyclophosphamide, vincristine,
Dactinomycin, etoposide.
* Lesions below elbow and below mid calf have a 5 yr survival rate 80%. Ewing’s is a
curable tumor even with metastasis in children < 11 yrs.Metastasis usually occurs to the lung,
bone, bone marrow.
The benign and malignant bone lesions have been listed below
Benign Malignant
Cartilage
Common
* Enchondroma
* Multiple myeloma
* Osteochondroma
* Osteosarcoma
* Chondroblastoma
* Chondrosarcoma
* Chondromyxoid
Fibroma * Ewing’s sarcoma
Bone * Malignant fibrous
histiocytoma
* Osteoid Osteoma
Rare
* Osteoblastoma
* Chordoma
Fibrous Tissue
(Notochordal)
* Fibroma
Unknown origin
* Desmoplastic
* Malignant Giant cell
Fibroma
tumor
Vascular
* Adamantinoma
Hemangioma
Vascular
Unknown
Hemangioendothelioma
Giant cell Tumor

USU9OIDQz
The factors that disturb the Hardy Weinburg law of equilibrium is all except
a) Immigration
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b) Gene drift
c) Random mating
d) Natural selection
Correct Answer: C
Explanation
Population genetics
• The study of the precise genetic composition of population.

• Hardy is England and Weinberg in Germany.
• The Hardy-Weinberg law (AIIMS NOV-2011***) states that “the relative frequencies of
each gene allele tends of remain constant from generation to generation”.
Factors which influence the gene frequencies
• The Hardy-Weinberg law assumes that human population is static.

• There are several factors which influence the human gene pool.
(a) Mutation:
• The heterozygotes of sickle cell trait were found to be resistant to falciparum malaria.
• Mutation rates. It is said that each gene has its own characteristic mutation rate which is
estimated anywhere from 104 to 106 per generation.
(b) Natural selection:
(c) Population movements:
(d) Breeding structure
• It practice, however, matings tends to occur selectively.

• This type of mating is called “assortative mating”.
(e) Public health measures.
‘Facial palsy’ in Herpes Zoster infection is seen in Ramsay Hunt syndrome
A pregnant lady of 10 wks, with her sister having a Down’s syndrome baby, wanted to
terminate her pregnancy if her foetus is also having Down’s syndrome. What
investigation is needed- CHORIONCI VILLI SAMPLING
A 24 year old lady with 24 hrs comes with complaints of pain in the right iliac fossa, vomitting,
central dyspareunia, rebound tenderness and with a temperature of 37°C. Pregnancy test
negative. The probable diagnosis is . Acute PID
Scale for sexual maturity is TANNERS STAGING

USU9OIDQ0
A young boy presents with slow athetoid movement with giveaway weakness. The diagnosis is
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a) Dystonia musculorum
b) Niemann –Pick type A
c) Cerebral Palsy
d) Lesch – Nyhan syndrome
Correct Answer: A
Explanation
A condition characterized by focal DYSTONIA that progresses to involuntary spasmodic

contractions of the muscles of the legs, trunk, arms, and face. The hands are often spared,
however, sustained axial and limb contractions may lead to a state where the body is grossly
contorted. Onset is usually in the first or second decade. Familial patterns of inheritance,
primarily autosomal dominant with incomplete penetrance, have been identified.

USU9OIDQ1
All of these are critical components of an FRU except:
a) Surgical intervention availability

b) Newborn care
c) Blood storage facility
d) Laporoscopic services
Correct Answer: D
Explanation
• First referral unit

• Emergency obseteric care
• 1 FRU caters to?
3 Essential elements
• Availability of surgical intereventions

• New born care
• Blood storage facility -24 hrs
• Minimum bed strength- 20-30
• MORE NIMHANS FACTS-NIMHANS 2008
• following acts as a vector of West Nile fever-CULEX MOSQUITO
• A patient aged 50 years, with Down’s Syndrome , presents with difficulty in speech, what
is the diagnosis- Senile dementia Alzhemeimer’s type
• Lesh – Nyhan syndrome
a. Hyperuricemia & Mental retardation
b. Self – Mutilative behaviour
c. Choreoathetosis & Spasticity
d. COMPLETE deficiency of HPRT
•
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USU9OIDQ2
Keratoconus is best treatedwith
a) Contact lens
b) Spherical lens
c) Convex lens
d) Cylindrical lens
Correct Answer: A
Explanation
KERATOCONUS:
1.Munson’s sign : It is a V-shaped conformation ofthe lower lid
produced by the ecstatic cornea in downgaze.
2. Rizutti’s sign . -Lateral illumination of the cornea produces a steeply focused beam of light
near the limbus.
3. Vogt’s striae - Posterior stress lines. These are vertical lines in the deep stroma and
descemet s membrane that parallel the axis of the cornea.
4. Fleischer’s ring -Iron deposits within epithelial layers. The iron
comes from tears and gets accumulated at the junction of normal and
steep cornea or the base of the cone.
5.Epithelial or subepithelial scarring
6.Scissoring of the light reflex on retinoscopy
7.Oil droplet sign of Charleux
Keratometry findings:
Distortion of the mire lines .
A documented increase in corneal curvature over time is a
sensitiveindicator of keratoconus .
A corneal topogram of an eye affected by keratoconus .Blue shows the flattest areas, and red
the steepest.
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Patient had circumduction and loss of ankle jerk might have injury of SCIATIC NERVE
Petechiae, ecchymosis, joint effusion are all symptoms due to the deficiency of VITAMI
NC
The various nutrients, the associated presentation in deficiency states and the dietary
requirements are summarised below
Dietary Level
Nutrient Clinical Finding Associated with
Deficiency
Thiamine Beriberi: neuropathy, muscle weakness and wasting, <0.3 mg/1000 kcal
cardiomegaly, edema, ophthalmoplegia, confabulation
Riboflavin Magenta tongue, angular stomatitis, seborrhea, cheilosis <0.6 mg
Niacin Pellagra: pigmented rash of sun-exposed areas, bright <9.0 niacin equivalents
red tongue, diarrhea, apathy, memory loss,
disorientation
Vitamin B 6 Seborrhea, glossitis convulsions, neuropathy, depression, <0.2 mg

confusion, microcytic anemia
Folate Megaloblastic anemia, atrophic glossitis, depression, <100 microg/d

homocysteine
Vitamin B 12 Megaloblastic anemia, loss of vibratory and position <1.0 microg/d

sense, abnormal gait, dementia, impotence, loss of
bladder and bowel control and increasd homocysteine,
methylmalonic acid levels
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Vitamin C Scurvy: petechiae, ecchymosis, coiled hairs, inflamed <10 mg/d

and bleeding gums, joint effusion, poor wound healing,
fatigue
Vitamin A Xerophthalmia, nightblindness, Bitot's spots, follicular <300 microg/d

hyperkeratosis, impaired embryonic development,
immune dysfunction
Vitamin D Rickets: skeletal deformation, rachitic rosary, bowed <2.0 microg/d

legs; osteomalacia
Vitamin E Peripheral neuropathy, spinocerebellar ataxia, skeletal Not described unless

muscle atrophy, retinopathy [AI-2005***] underlying
contributing factor is
present

USU9OIDQ3
The laser procedure, most often used for treating iris neovascularisation is
a) Goniophotocoagulation
b) Laser trabeculoplasty
c) Panretinal photocoagulation
d) Laser iridoplasty
Correct Answer: C
Explanation
Neovascularization, a pathological change characterized by an uncontrolled growth of vascular

tissue, could occur in various parts of eye, including the cornea, iris, retina, and choroid. The
consequences of neovascularization within these delicate ocular tissues are fibrosis, exudation,
and/or hemorrhage that are responsible for vision loss in many common eye diseases.
The current treatment for many forms of ocular neovascularization involves photocoagulation or
cryotherapy. Pan-retinal or focalphotocoagulation is current standard therapy for diabetic
retinopathy.
Which vitamin excess causes peripheral neuropathy- B 6
A 5 year old child presents with mental retardation seizures, with ligher skin complexion. The
diagnosis is PHENYLKETONURIA
Breast feeding jaundice
a. Pregnanediol may be a factor
b. Free fatty acids can be a cause
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c. Temporary interruption of bilirubin conjugation
d.develops after the first 4-7 days of life

USU9OIDQ4
In the grading of trachoma, trachomatous inflammation – follicular is defined as the presence of
a) 5 or more follicles in the lower tarsal conjunctiva

b) 3 or more follicles in the lower tarsal conjunctiva
c) 5 or more follicles in the upper tarsal conjunctiva
d) 3 or more follicles in the upper tarsal conjunctiva
Correct Answer: C
Explanation
Trachoma control programme started in 1968
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MORE NIMHANS FACTS
TRACHOMA
* a chronic infectious disease of the conjunctiva and cornea, caused by Chlamydia trachomatis
Diagnosis
At least 2 of the following diagnostic criteria
a. follicles on the upper tarsal conjunctiva
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b. limbal follicles or their sequelae, Herbert’s pits
c. typical conjunctival scarring (trichiasis, entropion)
d. vascular pannus, most marked at the superior limbus
* responsible for 0.2 % of visual impairment and blindness in India
Agent factors
AGENT
* C. trachomatis of immune types A,B or C.
* The sexually-transmitted C.trachomatis (serotypes D,E,F,G,H,I,J or K) may be infect, causing

an eye disease
* Morax-Axenfeld diplobacillus is the most innocuos; the Koch-Weeks bacillus is the most
widespread, and the gonococcus the most dangerous
COMMUNICABILITY:
* Trachoma is a disease of low infectivity****
Host factors
AGE
* Two to five years
SEX
* Prevalence equal in younger age groups
* Older age groups, females
Environmental factors
* April-May
Mode of tranmission
* Eye-to-eye transmission
* Direct or indirect contact
Incubation period
* 5 to 12 days
CONTROL OF TRACHOMA
1. Assessment of the problem
* “Blinding trachoma” – as indicated by the presence of
(a) Corneal blindness
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(b) Trachomatous trichiasis and entropion, and
(c) Moderate and severe trachomatous inflammation
2. Chemotherapy
* The antibiotic of choice is 1% ophthalmic ointment or oily suspension of tetracyclines
(a) Mass treatment
* A prevalence of more than 5%****** severe and moderate trachoma in children under 10
years
* The treatment consists of the application twice daily of tetracycline 1% ointment to all
children, for 5 consecutive days each month or once daily for 10 days each month for 6
consecutive months, or for 60 consecutive days
Selective treatment
* The trachoma control programme in India was launched in 1963
* “Health for All by 2000” had set a target of reducing the prevalence of blindness to 0.3%
World Health Organization's Global Campaign
* S-A-F-E strategy :
* Surgery for deformed eyelids
* Periodic mass treatment with azithromycin
* Face washing
* E nvironmental improvements
A 30 year old male, laborer, chronic smoker, alcoholic presents with acute ches pain,
severe back pain, radiation to interscapular area. The diagnosis is Ruptured aortic
aneurysm
Anisocoria that increases in dim light indicates a sympathetic paresis of the iris dilator
muscle. Anisocoria that increases in bright light suggests a parasympathetic palsy.
Mucormycosis causes Invasive sinusitis

USU9OIDQ5
Actions of Inferior rectus are all of the following except
a) Adduction
b) Abduction
c) Depression
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d) Extortion
Correct Answer: B
Explanation
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MORE NIMHANS FACTS
A lesion of the oculomotor nucleus in the rostral midbrain , causes bilateral ptosis because the
levator muscle is innervated by a single central subnucleus. There is also weakness of the
contralateral superior rectus, because it is supplied by the oculomotor nucleus on the other side
[AIIMS MAY 2014***].
The syndromes associated with 3 rd nerve are summarised below
Syndrome Feature
* Site – supr. cerebellar

peduncle
1. Nothnagel’s
syndrome * Effect – Ipsilat 3 rd N
Palsy, contra lateral
cerebellar Ataxia
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* Site - Red nucleus
* Effect – Ipsilateral 3 rd
2. Benedict’s N palsy
(AI2007)
+
Controlateral chorea,
athetosis
* Site – Supr. cerebellar

peduncle + Red Nucleus
3. Claudes
* Effect – 1 + 2
* Site – Cerebral peduncle
4. Weber’s * Effect – Ipsilat – 3 rd N.

Palsy +
Contralateral hemiparesis
Syndromes associated with 6th nerve are listed below
Syndrome Effect
Site- Dorsal Pons
Effect
- Ipsilateral lat. Gazepalsy

1. Foville (6 th )
- Ipsilat 7 th N Palsy
- Contralat Lateral
Hemiparesis
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Site- Ventral PONS
Effect- Similar to
1. Except eye findings

2. Milard Gubler - LR weakness only instead
of gaze palsy
(Because Abducen fascicles

are involved, not the
nucleus)
Site- Petrous Apex

(Mastoiditis)
Effect
3. Gradenigo
- Deafness
- Pain
- Ipsilat 6th N Palsy
Reverse genetics is a method that is used to help understand the function of a gene by
analyzing the phenotypic effects of specific engineered gene sequences .
Reverse genetics usually proceeds in the opposite direction of so-called forward genetic screens
of classical genetics . In other words, while forward genetics seeks to find the genetic basis of a
phenotype or trait, reverse genetics seeks to find what phenotypes arise as a result of particular
genetic sequences.
Serotonin is a derivative of TRYPTOPHAN
The Rate limiting Enzyme for heme Synthesis is . Delta ALA synthase

USU9OIDUw
A patient was on treatment with anticoagulants as he underwent valve replacement.He
presented in the emergency room with history of profuse Epistaxsis. His prescription
revealed dabigartan intake.Which of the following can be used for reversing the
bleeding
a) Idarucizumab
b) Andexanet alfa
c) ciraparantag
d) protamine sulfate
Correct Answer: A
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Explanation
*Anticoagulant reversal should be considered in patients with life-threatening bleeding, such as

intracranial bleeding, if bleeding continues despite supportive measures or if patients require
urgent surgery.
*Idarucizumab is a specific reversal agent for dabigatran.*****
* A monoclonal antibody fragment, idarucizumab binds dabigatran with high affinity to form a
1:1 complex that is then cleared by the kidneys.
*Idarucizumab is given as an intravenous bolus of 5 g. no dosage adjustment required for renal

failure
*Andexanet alfa and ciraparantag are under development for reversal of rivaroxaban, apixaban,
and edoxaban,but not approved
PREGNANCY
As small molecules, the direct oral anticoagulants can all pass through the placenta.
Consequently, these agents are contraindicated in pregnancy, and when used by women of
childbearing potential, appropriate contraception is important. The direct oral anticoagulants
should be avoided in nursing mothers and their safety in children has yet to be established.
MORE NIMHANS FACTS - [Nim DM June 2010]
NEUROLOGICAL TERMS
* HYPERASTHESIA or hypoesthesia refers to a reduction of cutaneous sensation to a specific

type of testing such as pressure, light touch, and warm or cold stimuli; anesthesia, to a
complete absence of skin sensation to the same stimuli plus pinprick;and hypalgesia or analgesi
a, to reduced or absent pain perception (nociception). * Hyperesthesia means pain or increased
sensitivity in response to touch.
* ALLODYNIA describes the situation in which a nonpainful stimulus, once perceived, is

experienced as painful, even excruciating. An example is elicitation of a painful sensation by
application of a vibrating tuning fork.
* HYPERALGESIA denotes severe pain in response to a mildly noxious stimulus, and hyperpat
hia , a broad term, encompasses all the phenomena described by hyperesthesia, allodynia,
and hyperalgesia.
*Following injury and resultant sensitization, normally innocuous stimuli can produce pain
(termed allodynia******[AIIMS-2006] ).
* HYPERPATHIA, a greatly exaggerated pain response to innocuous or mild nociceptive

stimuli, especially when applied repeatedly, is also characteristic of neuropathic pain

USU9OIDUx
Perilymph communicates with subarachnoid space through which of the following
structure
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a) Ductus reuniens
b) Helicotrema
c) Utriculosaccular duct
d) Cochlear aqueduct
Correct Answer: D
Explanation
Explanation
The cochlear aqueduct provides an important communication between the subarachnoid and pe
rilymphatic space . The only outlet from increased intracochlear pressure is via a tear of the
oval or round window membranes.
MORE NIMHANS FACTS
Development and growth of paranasal sinuses
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First
Status of birth Growth radiologic
evidence
* Rapid growth from birth to 3 years and from 4-5 months

Present of birth
Maxillary 7-12 years . Adult size – 15 years after birth
Present of birth
Anterior group:
* 5X2X2 mm
1 year
Ethmoid Reach adult size by 12 years
Posterior group:
5X4X2 mm
Invades frontal bone at the age of 4 years Size

* Frontal Not present 6 years
increases until teens
Reaches sella turcica by the age of 7 years,

* dorsum sellae by late teens and basisphenoid by
Not present 4 years
Sphenoid adult age Reaches full size between 15 years to
adult age
MKT 21,25
Degree of hearing loss
1. Mild 26-40 dB
2. Moderate 41-55 dB
3. Moderately severe 56-70 dB
4. Severe 71-91 dB
5. Profound More than 91 dB
6. Total
Showing results of various tests to differentiate a cochlear from a retrocochlear lesion
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Retrocochlear
Normal Cochlear lesion
lesion
* Pure tone Sensorineural hearing Sensorineural

Normal
audiogram loss hearing loss
* Speech
90-100% Below 90% Very poor
discrimination score
* Roll over
Absent Present Absent
phenomenon
* Recruitment Absent Present Absent
* SISI score 0 – 15% Over 70% 0 – 20%
* Threshold tone
0 – 15 dB Less than 25dB Above 25dB
decay test
* Stapedial reflex Present Present Absent
* Stapedial reflex
Normal Normal Abnormal
decay
Normal interval Normal interval between Wave V delayed or

* BE.R.A
between wave I & V wave I & V absent
Differences between inner and outer hair cells
Inner hair cells Outer hair cells
Total No 3500 12,000
Rows One row Three or four rows
Shape Flask-shaped Cylindrical
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Primarily afferent fibres and very Mainly efferent fibres and very few
Nerve supply
few efferent afferent
Development Develop earlier Develop late
Function Transmit auditory stimuli Modulate function of inner hair cells
Vulner Easily damaged by ototoxic drugs and

More resistant
ability high intensity noise
MORE NIMHANS FACTS- [Nim June Neurosurg 2010]
All of the following statements are true except [Nim June Neurosurg 2010]
a. 60 % body weight in male is water
b. Lean person has more water than obese person
c. Most of the body water is interstitial
d. 50% of body weight is protein and fat
Ans (C)
About two-thirds of total body water is intracellular and one-third is extracellular.

Approximately one-fourth of the ECF is in the plasma and the remainder comprises the
interstitial fluid******
MORE NIMHANS FACTS
*Renin is an enzyme with a molecular mass of
about 40,000 Da that acts on its substrate, angiotensinogen, an α 2 -globulin synthesized by the
liver, to release angiotensin I, a decapeptide, which in turn is converted to angiotensin II (AII),
an octapeptide.
*AII has generalized vasoconstrictor properties, particularly on the renal e ff erent arterioles.
DRUGS ASSOCIATED WITH EDEMA
Nonsteroidal anti-inflammatory drugs
Antihypertensive agents
Direct arterial/arteriolar vasodilators
Hydralazine
Clonidine
Methyldopa
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Guanethidine
Minoxidil
Calcium channel antagonists
α-Adrenergic antagonists
Thiazolidinediones
Steroid hormones
Glucocorticoids
Anabolic steroids
Estrogens
Progestins
Cyclosporine
Growth hormone
Immunotherapies
Interleukin 2

USU9OIDUy
Which of the following bears the maximum pressure during mastication?
a) Pterygomaxillary Buttress
b) Zygomaxillary Buttress
c) Nasomaxillary Buttress
d) Buccomaxillary Buttress
Correct Answer: A
Explanation
Explanation
The vertical buttresses consist of the paired nasomaxillary (NM), zygomaticomaxillary

(ZM) and pterygomaxillary (PM) midfacial buttresses as well as the ramus of the
mandible. These buttresses define the vertical height of the face and provide the bony
support required for mastication.
MORE NIMHANS FACTS
Fracture Maxilla- Le Fort Fracture
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I guerin Lower part of maxilla
II pyramidal Common * Severe Trauma
III * Craniofacial dysfunction
CSF rhinorhea
– Commonest cribriform plate fracture*****
Maxilla fracture
* Malocclusion
* Mobility of maxilla
* Elongation of mid face
* CSF rhinorrhoea – cribriform plate involved *****
Le Fort fractures - types of facial fractures involving the maxillary bone and surrounding
structures in a usually bilateral and either horizontal, pyramidal or transverse way. LeFort
fractures are classic in facial trauma
To qualify for LeFort Fractures the pterygoid plates must be involved. These are seen posterior
to the maxillary sinuses on axial CT and inferior to the orbital rim on coronal slices
Le Fort I fractures (horizontal)
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may result from a force of injury directed low on the maxillary alveolar rim in a downward
direction. It is also known as a Guerin fracture or 'floating palate', and usually involves the
inferior nasal aperture.
The fracture extends from the nasal septum to the lateral pyriform rims, travels horizontally
above the teeth apices, crosses below the zygomaticomaxillary junction, and traverses the
pterygomaxillary junction
Guerin's sign is present characterised by ecchymosis in the region of greater palatine

vessels.
Le Fort II fractures (pyramidal)
may result from a blow to the lower or mid maxilla and usually involve the inferior orbital rim.
Such a fracture has a pyramidal shape and extends from the nasal bridge at or below the
nasofrontal suture through the frontal processes of the maxilla, inferolaterally through the
lacrimal bones and inferior orbital floor and rim through or near the inferior orbital foramen
Le Fort III fractures (transverse)
are otherwise known as craniofacial dissociation and involve the zygomatic arch. These may
follow impact to the nasal bridge or upper maxilla. These fractures start at the nasofrontal and
frontomaxillary sutures and extend posteriorly along the medial wall of the orbit through the
nasolacrimal groove and ethmoid bones
Dishpan Face"
MORE FACTS
Ape face appearance in acromegaly.
LeForte III produces donkey face/ Dish-face deformity.
Lion face in leprosy.

Elephant face in plexiform neurofibroma.
Frog face in ethmoidal tumour.

USU9OIDUz
A 30 year old female with history of singing, vocal abuse and gastrooesphageal efflux
developed nodules at junction of anterior 1/3 rd & middle 3 rd of her vocal cords. What
is treatment of choice?
a) Speech therapy and Proton Pump Inhibitor (PPI)

b) Microlaryngoscopic surgery & CO 2 laser
c) Microlaryngectomy
d) Direct laryngoscopy and biopsy
Correct Answer: A
Explanation
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Explanation
Nodules are typically treated conservatively with voice therapy and behavioral modification
under the guidance of a speech language pathologist. Surgery is reserved for refractory lesions
or in situations where vocal needs are not being met with voice therapy alone.
Treatment of underlying medical problems that affect the voice, such as reflux, allergies, and
sinusitis, may help lessen the severity or occurrence of vocal lesions and enhance vocal hygiene
in general
MORE NIMHANS FACTS
Which one of the following is true about GH? [Nim June 2010]
a. GH secretion increases after exercise, stress and hypoglycemia
b. GH secretion is maximum during evening
c. GH is produced equally in all age groups
d. GH decreases circulating IGF and Somatostatin
GH is the most abundant anterior pituitary hormone
The pituitary GH gene (hGH-N) give rise to 191 amino acids GH.
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Somatostatin [somatotropin-release inhibiting factor (SRIF)] is synthesized in the

medial preoptic area of the hypothalamus and inhibits GH secretion
GH secretion is pulsatile, with highest peak levels occurring at night*****. Hormone

levels in middle age is 15% of pubertal levels******. GH secretion is reduced in obese
individuals.
The majority of action of GH is via IGF-I. The liver is the major source of circulating
IGF-I.
STIMULATORS
Ghrelin
(Gastric derived peptide)
Estrogen
High protein meals
Sleep
Prolonged fasting ******
Dopamine
L-arginine
Apomorphine
Alfa agonist
Ans (A)
MORE NIMHANS FACTS
Growth Hormone Insensitivity is caused by defects of GH receptor structure and are

associated with partial or complete GH insensitivity and growth failure called as
Laron syndrome. This has normal or high GH levels, with decreased circulating GHBP,
and low IGF-I levels.

USU9OIDU0
The muscle relaxant which causes maximum pain in injection site is: which of the following
a) Succinyl choline
b) Vecuronium bromide
c) Cisatracurium
d) Rocuronium bromide
Correct Answer: D
Explanation
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rocuronium bromide can cause intense pain as it is injected*****
NMJ blockers
NON-DEPOLARISING
Bind to Alpha sub units of NMJreceptors and prevent acetylcholine (Ach) from stimulating
receptors.
Effect: compete with Ach for nicotinic receptor binding sites. The blockade is competitive, h
ence muscle paralysis occurs gradually.
Examples include tubocurarine, gallamine, atracurium, vecuronium, mivacurium, rocuronium
and cisatracurium.
These drugs are highly ionised at body pH and contain two quaternary ammonium groups. They
are poorly lipid soluble and poorly protein bound.
Nondepolarizing Muscle Relaxants
• Long acting
◦ Pancuronium
• Intermediate acting
◦ Atracurium
◦ Vecuronium
◦ Rocuronium
◦ Cisatracurium
• Short acting
◦ Mivacurium
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Nondepolarizing Muscle Relaxants
• Atracurium
• Metabolized by
◦ Ester hydrolysis
◦ Hofmann elimination
• Onset 3-5 minutes, duration 25-35 minutes
• Intubating dose 0.5 mg/kg
• MORE NIMHANS FACTS
• Side effects :
histamine release causing hypotension, tachycardia, bronchospasm
Laudanosine toxicity
Rocuronium
• Rocuronium is a monoquaternary amine with a rapid onset and intermediate duration of

action.
• It is 6-8times less potent than vecuronium.
• An intubating dose of 0.6 mg kg produces satisfactory intubating conditions within 60--90
s, and it can be used as an alternative to succinylcholine in larger doses for rapid
sequence intubation.
First Selective Relaxant Binding Agent

SUGAMMADEX
synthetic, gamma-cyclodextrin and is the first and only selective relaxant binding agent (SRBA).
Sugammadex is a unique reversal agent because it encapsulates and then inactivates rocuroni
um and vecuroniu m rather than counteracting their effects. With this innovative mode of
action, it provides rapid reversal of neuromuscular blockade caused by these neuromuscular
blocking agents.
Monitoring Neuromuscular Function
How to monitor?
• Clinical signs
• Use of nerve stimulator
• Clinical signs
• Signs of adequate recovery
◦ Sustained head lift for 5 seconds
◦ Lift the leg (child)
◦ Ability to generate negative inspiratory pressure at least 25 cmH 2 O, able to
swallow and maintain a patent airway
◦ Other crude tests : tongue protrusion, arm lift, hand grip strength
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Evoked responses during depolarizing and nondepolarizing block
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Monitoring Neuromuscular Function
Use of nerve stimulator
• Single twitch : single pulse 0.2 msec

• Tetanic stimulation
• Train-of-four : series of 4 twitch, 0.2 msec long, 2 Hz frequency, administer every 10-15
seconds
• Double burst stimulation
• Post tetanic count
MORE NIMHANS FACTS
Drug interactions: -
1. GA – potentiate competitive blockers – ether, isoflurane potentiate most &Nitrous oxide to

least extent.
2. Flourinated anesthetics predispose to Phase II blockade by Sch.
3. Maligant hyperthermia is more common with sch & halothane or isoflourane used
concomitantly.
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4. Anticholinesterase – reverse competitive blockers. Neostigmine is used.
5. Antibiotics – Aminoglycosides reduce Ach release – potentiate block.
6. CCBs – verapamil – potentiate SMKRs.
7. Diuretics – hypokalemia can enhance block.
Complications of Succinylcholine Administration
Cardiovascular Tachycardia (ganglionics stimulation)
Bradycardia, sinus arrest, junctional rhythm
Hyperkalemia
Fasciculations; myalgia*
Myoglobinuria, elevated plasma creatine phosphokinase
Sustained muscle contraction (myotonic dystrophy, congenital myotonia)
Malignant hyperpyrexia
Masseter muscle rigidity
Prolonged relaxation
Phase II block
Inadequate pseudocholinesterase activity
Increased intraocular pressure*
Increased intracranial pressure*
Increased intragastric pressure*
Histamine release

USU9OIDU1
POYNTING EFFECT (overpressure effect) is associated with which of the following
a) Ether
b) Cyclopropane
c) Nitrous oxide
d) Trichlorethylene
Correct Answer: C
Explanation
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NITROUS OXIDE
• manufactured by heating ammonium nitrate to 250°C

• NH 4 NO 3 » N 2 O + 2H 2 O
• During this process, a number of contaminants may be produced, unless the temperature
is carefully controlled. These include NH 3 , N 2 , NO, NO 2 and HNO 3 , and they are
actively removed by passage through scrubber, caustic soda and water.
• Storage
• French blue cylinders are used to store N 2 O in a liquid phase with its vapour on top at
a gauge pressure of 4400 kPa at room temperature. As the liquid is less compressible
than a gas, the cylinder should be only partially filled.
• The filling ratio is the weight of the fluid in the cylinder divided by the weight of water
required to fill the cylinder. In the UK, the filling ratio for N 2 O is 0.75, but in hotter
climates the filling ratio needs to be 0.67, to avoid cylinder explosion.
• Physicochemical properties
• Molecular weight 44
Boiling point -88°C
Critical temperature 36.5°C
Critical pressure 72 bar
MAC 105%
Partition coefficients Blood/gas 0.47, Oil/gas 1.4
• Fink effect –diffusion hypoxia during recovery.
• POYNTING EFFECT (overpressure effect) ***** – the critical temperature and

pressure of a gas may be affected when it is mixed with another gas. For example, in a
cylinder of Entonox , the new critical temperature of nitrous oxide (known as the
pseudocritical temperature) changes to –6 o C. Therefore, precautions regarding the
cooling of cylinders should be taken into account.
FINK EFFECT – Diffusion hypoxia
MORE NIMHANS FACTS-[Nim June 2010]
Measurement of serum osmolality
In “conventional” units, the calculated serum osmolality (2 × [serum sodium + serum

potassium] +
plasma glucose [mg/dL]/18 + BUN/2.8)

USU9OIDU2
Father of local anaesthesia is which of the following scientist
a) karl coller
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b) Morton
c) john snow
d) H F W Braun
Correct Answer: A
Explanation
Karl Koller (1857-1944), Austrian ophthalmologist. Koller is best known for

introducing cocaine as a local anaesthetic for eye surgery.
MORE NIMHANS FACTS
The impulse propagation is associated with movement of sodium ions inwards and
potasium ions outwards , through their respective channels. The membrane becomes
depolarized. During recovery the ions reverse the direction of their movement across the cell
membrane. Local anaesthetic agents may prevent depolarization and so may prevent
conduction of impulses. It is thought that local anaesthetic drugs exert their effect by
bonding to the internal mouth of the sodium channel . The local analgesic solution preve
nts depolarization of the nerve membrane . As the concentration increases the height of
the action potential is reduced. The firing threshold is elevated, the spread of impulse
conduction is slowed and the refractory period lengthened. Finally nerve conduction is
completely blocked.
MORE NIMHANS FACTS
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LOCAL ANESTHESIA: -
1. Injectable anaesthetic –
Low potency – procaine, chloroprocaine
Intermediate potency – lidocaine, prilocaine
High potency; longer duration of action – tetracaine, bupivacaine, ropivacaine, dibucaine.
1. Surface anaesthetic
1. Soluble –cocaine, lidocaine, tetracaine & beonxinate
2. Insoluble – benzocaine, butamben, oxethazine
2. Others- propranolol, chlorpromazine, H1 anti-histaminics, quinine etc.
Amide-linked – lidocaine, bupivacaine, dibucaine, prilocaine, ropivacaine.
Ester – linked – cocaine, procaine, chloroprocaine, tetracine, benzocaine.
i. Produce more intense, rapidly acting & longer acting anesthesia.
ii. Blind to α1 acid glycoprotein.
iii. Not hydrolyzed by plasma cholinesterase.
iv. Rarely cause hypersensitivity.
Mechanism of Action : - it blocks neuronal axonal membrane sodium channels in its

inactivated states. Thus refractory period of nerve fiber is increased – conduction is blocked.
Factors affecting –
Repeatedly firing neuron is blocked more intensly than a resting nerve. The time of onset of
block depends on the pKa value of LA. Higher the pKa – slower the onset – procaine, tetracaine
& bupivacaine except for chloroprocaine.
Blockade of sodium channels is voltage & time dependent.
It is determined also by type of nerve fiber & its diameter – myelinated fibers are affected more
than unmyelinated.
Atuonomic fibers are more susceptible than somatic fibers.
Order of blockade – pain – temp – touch – deep pressure.
Effect of addition of adrenaline –
1. Prolongs duration of anesthesia.
2. Enhances intensity & reduces systemic side effects – due to reduced systemic absorption.
3. Makes injection more painful.
4. Bloodless field is available for surgery.
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5. Increase tissue edema & necrosis
6. May raise BP & arrhythmia can occur.
Effects: -
1. CNS – cocaine causes stimulation & lignocaine causes depression.
2. CVS – LA are cardiac depressant – hypotension & HR. Bupivacaine produces cardiotoxicity &
Ventricular tachycardia.
3. Blood vessels – direct vasodilatation. Bupivacaine is most & prilocaine is least.
1. Lignocaine – best anesthetic with good surface & injectable anesthesia.
2. Prilocaine – larger volume of distribution. Methamoglobinemia.
3. Eutectic lidocaine / prilocaine – reduction in melting point of 2 solids when mixed. This
increases the penetration of lidocaine – IV cannulation, short dermatological procedures, split
skin graft harvesting.
4. Tetracaine – highly lipid soluble PABA ester –more potent & more toxic – topical application is
used.
5. Bupivacaine- potent, long acting amide derivative useful for nerve block, spinal or epidural
anesthesia. Useful in labor anesthesia. Prolongs QTc – produces arrhythmias. Levobupivacaine
is cardiotoxic metabolite; prone to seizures.
6. Ropivacaine – less cardiotoxic metabolite than bupivacaine.
7. Benoxinate – corneal anesthesia
8. Benzocaine & butamben – PABA derivates – antagonize sulfonamides. Long lasting anesthesia
for mucous membranes & abraded skin surfaces – poor systemic absorption.
Uses –
1. Surface anesthesia
2. Infiltration anesthesia
3. Conduction block
4. Spinal anesthesia
5. Epidural &
6. IV regional anesthesia

USU9OIDU3
Optical density values in Liley’S chart in Zone 3 indicates which of the following
a) Mild disease
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b) Severe disease
c) moderate to severe disease
d) Death within 7-10 days
Correct Answer: D
Explanation
Mild
Zone 2 indicates moderate to severe disease
Zone3- severely affected fetus.Death in 7-10 daysIUT or Delivery indicated.
MORE NIMHANS FACTS-[Nimhans 2013]
REWARD PATHWAY
Neuropathology -the nucleus accumbens is associated with brain reward *****
Deep brain stimulation (DBS) of either the nucleus accumbens or subgenual area 25
elevates mood
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Addictive drugs increase dopamine release in the nucleus accumbens and blockade of
dopamine in the nucleus accumbens can stop the rewarding effects of addictive drugs

USU9OIDU4
In IAP classification of malnutrition,Grade 1 malnutrition implies a weight of which of the
following
a) 71 – 80%
b) 61 – 70%
c) 51 – 60%
d) < 50%
Correct Answer: A
Explanation
Explanation
Degrees of failure to thrive
Weight for age (% of Height for age (% of Weight for height (% of

Degree
median) median) median)
Mild 75 – 90 90 - 95 81 – 90
Moderate 60 – 74 85 - 89 70 – 80
Severe < 60 < 85 < 70
Indicator Interpretation
Indicator of chronic malnutrition, the result of prolonged

Stunting Low height for age
food deprivation and/or illness
Low weight for Suggests acute malnutrition, the result of more recent food
Wasting
height deficit or illness
Combined indicator to reflect both acute and chronic

Underweight Low weight for age
malnutrition.
WHO classification of malnutrition
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Moderate malnutrition Severemalnutrition
Symmetrical edema No Yes (edematous malnutrition)
Weight for height SD score between -2 to -3 SD score < -3 (severe wasting)
Height for age SD score between -2 to -3 SD score <-3 (severe stunting)
IAP classification of malnutrition
Grade of malnutrition Weight for age of the standard (median) (%)
Normal > 80%
Grade I 71 – 80% (mild malnutrition)******
Grade II 61 – 70% (moderate malnutrition)
Grade III 51 – 60% (severe malnutrition)
Grade IV < 50% (very severe malnutrition)

USU9OIDU5
Esophageal atresia with distal Tracheoesophageal fistula belongs to which of the following type
a) Type A
b) Type B
c) Type C
d) Type D
Correct Answer: C
Explanation
Explanation
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In H type TEF, an esophagogram with contrast medium injected under pressure can
demonstrate the defect. Alternatively, the orifice may be detected at bronchoscopy or when
methylene blue dye injected into the endotracheal tube during endoscopy is observed in the
esophagus during inspiration.
Which one of the Interleukins is produced by Th 1 cells? [Nimhans 2013]
a. IL 1
b. IL 2
c. IL 3
c. IL 4
T H 1-type helper T cells - a central role in mediating intracellular killing- IL-2******,

IFN-, IL-3, TNF-alfa, GM-CSF, and TNF-beta
T H 2-type helper T cells - regulatory humoral immunity and isotype switching. IL-3,
-4, -5, -6, -10, and -13
Ans B

USU9OIDYw
POSITIVE MED PG
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All of the following are syndromes associated with obesity except
a) Turner syndrome
b) Carpenter syndrome
c) Prader willi syndrome
d) Klinefelter syndrome
Correct Answer: D
Explanation
Explanation
Body Mass Index (BMI) Classification of obesity in Adults
BMI (kg/m 2 ) WEIGHT STATUS
<18.5 Underweight
18.5–24.9 Normal weight
25–29.9 Overweight
30–34.9 Obese
35–39.9 Moderately obese
40–49.9 Morbid obesity
≥50 Super morbid obesity
Body Mass Index (BMI) Classification of Children and Adolescents
BMI PERCENTILE FOR AGE WEIGHT STATUS
<5th percentile Underweight
5th–84th percentile Normal weight
85th–94th percentile At risk for overweight
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BMI PERCENTILE FOR AGE WEIGHT STATUS
≥95th percentile Overweight
Syndromes associated with obesity:
• Prader-Willi syndrome*****
• Carpenter syndrome*****
• Cohen syndrome
• Cushing syndrome
• Turner syndrome*****

USU9OIDYx
Ipsilateral optic atrophy with contralateral papilloedema is a feature of Which of the following
syndrome
a) Fischer syndrome
b) Foster kennedy syndrome
c) Vogt-kayanagi-Harada syndrome
d) WAGR syndrome
Correct Answer: B
Explanation
Explanation
• Papilloedema is mostly due to raised intracranial pressure. So it is usually bilateral.

Unilateral causes of papilloedema are:
Foster Kennedy Syndrome
• Olfactory or sphenoidal meningiomata & frontal lobe tumors leads to optic atrophy on the
side of lesion (I/L) and papilloedema on the other slide (C/L) due to increase ICT
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Pseudo Foster Kennedy Syndrome
• U.L papilloedema associated with raise ICT (due to any cause) & preexisting optic atrophy
(d/t any other cause)
MORE NIMHANS FACTS-[Nimhans 2013]
Syndrome of inappropriate antidiuretic hormone secretion (SIADH),
* Most common cause of normovolemic hyponatremia is SIAD and there is mild volume-
expansion.
* Hypoosmotic hyponatremia occurs in the setting of an inappropriately concentrated urine

(urine osmolality >100 mosmol/kg) . [AIIMS N0V-2007***]
* It is due to nonphysiologic release of AVP from the posterior pituitary or an ectopic source.
Renal free-water excretion is impaired while the regulation of Na + balance is unaffected.
* The most common causes of SIADH is neuropsychiatric and pulmonary diseases, malignant
tumors, major surgery (postoperative pain), and pharmacologic agents. The commonest drug
causing SIAD is SSRI and the commonest tumor causing is small cell carcinoma
Investigations for confirming the diagnosis are
1) low serum osmolality,
2) high urine osmolality******
3) Urine Na + concentration usually >40 mmol/L .

4) Hypouricemia due to the uricosuric state induced by volume expansion
5) absence of hypothyroidism

USU9OIDYy
Visual pigments of peak spectral sensitivity: 560 nm is which of the following
a) Red cone
b) Blue cone
c) Green cone
d) ALL OF THE ABOVE
Correct Answer: A
Explanation
Explanation
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NIMHANS FACTS
The retina contains three classes of cones, with visual pigments of differing peak spectral
sensitivity: red (560 nm), green (530 nm), and blue (430 nm). The red and green cone pigments
are encoded on
the X chromosome, and the blue cone pigment on chromosome 7. Mutations of the blue cone
pigment are exceedingly rare. Mutations of the red and green pigments cause congenital X-
linked color blindness in 8% of males.

USU9OIDYz
A patient was diagnosed to have Chondroblastoma.All of the following are true
regarding it except:
a) most frequently arise in the epiphyses of long bones

b) Femur is the most common bone affected
c) predominantly in young males (<20 years of age)
d) A joint effusion is seen in ~1/3 of patients
Correct Answer: B
Explanation
Commonest bone involved is humerus*****
Chondroblastomas (or Codman tumours )are rare benign cartilaginous neoplasms that
characteristically arise in the epiphysis or apophysis of a long bone in young patients . Despite
being rare, they are one of the most frequently encoutered benign epiphyseal neoplasms in
skeletally immature patients.
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Epidemiology
Chondroblastomas represent less than 1% of all primary bone tumours, occurring

predominantly in young patients (<20 years of age) . There is a male predilection***** .
Clinical presentation
Clinical presentation is non-specific and may include joint pain, muscle wasting, tenderness,
and swelling/local mass.
Pathology
Microscopically they are composed of chondroblasts, chondroid matrix, cartilage with

occasional giant multi-nucleated cells (which may lead to the incorrect diagnosis of giant cell
tumour ).
Calcium deposition surrounding the chondroblasts, which are typically polyhedral shape,
results in typical "chicken-wire calcification" (pathognomonic)
Aneurysmal bone cysts can be seen secondarily to underlying chondroblastoma.
Distribution
Chondroblastomas most frequently arise in the epiphyses of long bones , with 70%
occurring in the humerus (most frequent) , femur and tibia 9 . ~10% are found in the
hands and feet 7 .
Radiographic features
Chondroblastomas (along with chondromyxoid fibroma ) constitute the “C” in the FEGNOMASH
IC mnemonic for benign appearing cystic lesions
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Plain film
Chondroblastomas are seen as well defined lucent lesions, with either smooth or lobulated
margins and a thin sclerotic rim, arising eccentrically in the epiphysis of long tubular bone such
as the femur, humerus, or tibia or apophysis such as greater trochanter, greater tuberosity,
calcaneus or talus. Internal calcifications can be seen in up to 40-60% of cases . A joint effusion
is seen in ~1/3 of patients******. They range in size from 1-10 cm, with most being 3-4 cm at
diagnosis
CT
Solid periosteal reaction (seen in up to 50% of cases) and internal calcification (calcified matrix
seen in ~1/2 of cases) and cortical breach are also more easily appreciated Endosteal scalloping
may be seen
MRI
These lesions have signal typical of cartilage:
T1: lesion itself is of low to intermediate signal
T2/STIR: lesion is of intermediate to high signal
A.Epiphysis
Common epiphyseal lesions
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Chondroblastoma
Brodies’s abscess
eosinophilic granuloma
Giant cell tumor
Aneurysmal bone cyst
Intra osseous ganglion

USU9OIDY0
One of the following is not an extra medullary intradural tumour
a) meningioma
b) neurofibroma
c) schwanoma
d) Ependymoma
Correct Answer: D
Explanation
xplanation
Ependymoma is Intramedullary******
Explanation
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Commonest intradu.extramed.-neurofibroma
Astrocytoma,ependymoma,intramedullary
Extradural-mets
Myelogram
Brush border-broom stick -extradural Trouser leg - intramedullary
Meniscus,crescent - intradu. extramedullary
Intramedullary Syndromes
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* Intramedullary lesions spare sensation in the perineal and sacral areas ("sacral sparing"), due
to the laminated configuration of the spinothalamic tract with sacral fibers outermost;
corticospinal tract signs appear later.
Extramedullary lesions
* Radicular pain is often prominent, and there is early sacral sensory loss (lateral spinothalamic
tract) and spastic weakness in the legs (corticospinal tract) due to the superficial location of leg
fibers in the corticospinal tract . Extradural are due to malignant lesions. Intradural lesions
are commonly due to benign lesions (neurofibroma being a common cause). Compressive
Myelopathies
* In adults, most neoplasms are epidural in origin, resulting from metastases to the adjacent
spinal bones. Ca breast, lung, prostate, kidney, lymphoma, and plasma cell dyscrasia commonly
metastasis to the vertebra. The thoracic spinal column is most commonly involved; exceptions
are metastases from prostate and ovarian cancer, which occur commonly in the sacral and
lumbar vertebrae. Pain is usually the initial symptom. Plain radiographs and radionuclide bone
scans miss 15–20% of metastatic vertebral lesions. MRI is the investigation of choice.
* Treatment : glucocorticoids, local radiotherapy (3000 cGy administered in 15 daily fractions

initiated as early as possible). Motor deficits, once established for >12 h, do not usually
improve. Intensity-modulated radiotherapy (IMRT), can deliver high doses of focused radiation.
Surgery, either decompression by laminectomy or vertebral body resection is done.
* Most intradural mass lesions are slow-growing and benign like meningiomas,
neurofibromas, chordoma, lipoma, dermoid, or sarcoma. Neurofibromas typically arise near the
posterior root.
* Primary intramedullary tumors present as central cord or hemicord syndromes, often in

the cervical region and are due to ependymomas, hemangioblastomas, or low-grade
astrocytomas.

USU9OIDY1
Which of the following gene abnormalities is associated with excess production of Beta – Globin
chains
a) Promoter region mutation of Beta chain

b) Chain Terminator mutation of Beta chain
c) Splicing mutation of beta chain
d) Deletion of three α chains
Correct Answer: D
Explanation
Explanation
When both alfa alleles on one chromosome are deleted, the locus is called alfa-thal-1; when only
a single alfa allele on one chromosome is deleted, the locus is called alfa-thal-2. AlfaThalasse
mia-2 trait is an asymptomatic, silent carrier state.
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* Alfa-Thalassemia-1 trait resembles beta-thalassemia minor. It is asymptomatic hypochromia

and microcytosis. The RDW is normal.
* Homozygous state for the alfa-thalassemia-1 cis deletion (a deletion that removes both genes
from the same chromosome) (hydrops fetalis) causes total absence of alfa-globin synthesis.
(Fig.114-12). Excess globin forms tetramers called Hb Barts ( 4 ), which has a very high oxygen
affinity.
Beta thalassemia
Beta thalassemia major Beta thalassemia minor
intermedia
* Profound microcytosis and

* Severe anemia , massive
* Similar to major but can hypochromia with target
ineffective erythropoiesis:
survive without chronic cells, mild anemia, mean
hepatosplenomegaly,
hypertransfusion. corpuscular volume is rarely
microcytosis, and elevated HbF
>75 fL
* Factors aggravating anemia –

* Require chronic
infection, onset of puberty, and * Hemoglobin electrophoresis
hypertransfusion therapy-
development of splenomegaly –elevated HbA 2 (3.5–7.5%).
hematocrit of at least 27–30%
and hypersplenism
* Splenectomy if the annual

transfusion requirement
increases by >50%
* Folic acid supplements
* Vaccination with Pneumococcal

vaccine
* Endocrine evaluation – for

glucose intolerance, thyroid
dysfunction, and delayed onset
of puberty
MORE NIMHANS FACTS
Measure Conventional units
Hb 10 grams/deciliter
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RBC 5E+12 cells/liter
MCV = Hct / RBC 80 femtoliters /cell
MCH = Hb / RBC 20 picograms /cell
MCHC = Hb / HCT 25 grams/deciliter

USU9OIDY2
Complications of Allogenic bone marrow Transplantation include all except
a) Chronic graft versus host disease

b) Cataract
c) Infertility
d) Glaucoma
Correct Answer: D
Explanation
Explanation
Complications Following Hematopoietic Cell Transplant
1. * High-dose cyclophosphamide can result in hemorrhagic cystitis.Patients begin

losing their hair 5–6 days posttransplant and by 1 week are pancytopenic.Keratinocyte
growth factor (palifermin) (???AI-2015***) can shorten the duration of
mucositis.Venoocclusive disease of the liver presents with Tender hepatomegaly,
ascites, Jaundice, Fluid retention.Peak on 16 th day.It is seen in 10% of BMT patients.
Mortality is 30%. Treatment is with defibrotide ,a polydeoxyribonucleotide. Most
men become azoospermic, and most postpubertal women will develop ovarian
failure.Cataracts develop in 10–20%******.Aseptic necrosis of the femoral head is seen
in 10% of patients.
Graft-versus-Host Disease
* GVHD developing within the first 3 months posttransplant is termed acute GVHD, while
GVHD developing or persisting beyond 3 months posttransplant is termed chronic GVHD. Acut
e presents Within 3 monthsof Transplant. It presents with erythematous rash, diarrhoea, and
elevated OT/PT. (AI-08♦♦♦)[AIIMS MAY 2007]. Biopsy reveasls Endothelial damage with
lymphocytic infiltration.In skin, the epidermis and hair follicles are damaged; in liver, the small
bile ducts show segmental disruption; and in intestines, destruction of the crypts and mucosal
ulceration. Prevention is by Steroids, Cyclosporine, Tacrolimus, MMF, Methotrexate,
Cyclophosphamide.
Staging
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The staging of acute GVHD is listed below.
Clinical Liver—Bilirubin, (mg/

Skin Gut
Stage dL)
Diarrhea 500–1000 mL/

1 Rash <25% body surface 2–3
d
Rash 25–50% body Diarrhea 1000–1500

2 3–6
surface mL/d
Generalized
3 6–15 Diarrhea >1500 mL/d
erythroderma
4 Desquamation and bullae > 15 Ileus
* Chronic-it occurs m ore common in elderly, unrelated donor, prior acute GVHD. It r esembl
es an autoimmune disorder and presents with malar rash, sicca syndrome, Arthritis and
obliterative bronchiolitis.It is also called as Runts disease. Treatment is with Prednisolone,
cyclosporine, Thalidomide.

USU9OIDY3
During excercise Mr. Ram consumes 1.8L of 02/min. His arterial 02 content is 190ml/l and the
02 content of his mixed venous blood is 130 ml/l calculate his cardiac output.
a) 3.2 L/min
b) 16 L/min
c) 30 L/min
d) 54 L/min
Correct Answer: A
Explanation
Explanation
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FALSE statement about High Anion gap [Nimhans 2013]
a. Seen in uraemia
b. Iron causes high anion gap
c. Hypercholremia present
d. Acidosis is present
An increase in the AG is often due to an increase in unmeasured anions and less commonly is
due to a decrease in unmeasured cations (calcium, magnesium, potassium). The condition
causing high anion gap acidosis are DKA, uremia****, Lactic acidosis, Methanol toxicity,
Starvation and salicylates . [AIIMS MAY-2007***]
Hyperchloremic****** (also called as Nongap) Metabolic
Causes of Non-Anion-Gap Acidosis are diarrhea , [TN-2007***] Renal tubular acidosis,

mineralocorticoid resistance (autosomal dominant PHA I), voltage defect (autosomal dominant
PHA I and PHA II), external pancreatic or small-bowel drainage, ureterosigmoidostomy ,
jejunal loop, ileal loop
Ans C

USU9OIDY4
Regarding Human poverty index,which of the following statements is false
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a) It was introduced in 1987

b) HPI is expressed as percentages.
c) It includes percentage of population not using an improved water source and the
percentage of children under weight for age
d) HPI – 2 includes the following dimensions,Probability at birth of not surviving to age
60Exclusion from the world of reading and communications as measured by percentage of
adults (16 – 65) lacking functional literacy skills
Correct Answer: A
Explanation
Explanation
Human poverty Index – term was introduced in 1997.******
The dimensions for HPI – 1, while HDI measures average achievements in basic dimensions of
human development, the HPI measures deprivation in those dimensions. The dimensions used
in HPI – 1
A long and healthy life vulnerability to death at a relatively early age (probability at birth of not
surviving to age 40.
Knowledge – exclusion from the world of reading and communications.
A decent standard of living – lack of access to overall economic provisioning (percentage of

population not using an improved water source and the percentage of children under weight for
age)
HPI is expressed as percentages.
HPI – 2 measures deprivation in the same dimensions as the HPI – 1 and also captures social
exclusion (as measured by the rate of long-term unemployment 12 months or more)
HPI – 2 includes the following dimensions,
Probability at birth of not surviving to age 60
Exclusion from the world of reading and communications as measured by percentage of adults
(16 – 65) lacking functional literacy skills.
Percentage of people living below the income poverty line
Social exclusion – as measured by the rate of long term unemployment 12 months or more
Gender related development index (GDI) – introduce during the year 1995
Reflects achievements in the basic human development adjusted for gender inequalities
GEM – gender empowerment measure – measures gender inequalities in economic and political
opportunitie

USU9OIDY5
POSITIVE MED PG
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Years of potential life lost (YPLL)- is defined as one that occurs before the age to which a dying
person could have expected to survive -before an arbitrary determined age, usually taken ageis
a) 64 years
b) 68 years
c) 72 years
d) 75 years
Correct Answer: D
Explanation
Indicators OF HEALTH
1. Mortality indicators
a. Crude death rate :
*It is defined as the number of deaths per 1000 population per year in a given community.
b. Expectation of life :
* Life expectancy at birth is “the average number of years that will be lived by those born alive
into a population if the current age-specific mortality rates persist”
c. Age-specific death rates :
d. Infant mortality rate :
* Infant mortality rate is the ratio of deaths under 1 year of age in a given year to the total
number of live births.
e. Child mortality rate :
* number of deaths at ages 1-4 years in a given year, per 1000 children in that age group.
f. Under-5 proportionate mortality :
* It is the proportion of total deaths occuring in the under-5 age group.
g . Adult mortality rate :
* The adult mortality rate is defined as the probability of dying between the age of 15 and 60
years per 1000 population.
h. Proportional mortality rate:
* The simplest measure of estimating the burden of a disease in the community is proportional
mortality rate.
i. Case fatality rate :
* Number of deaths from a specific disease during a specific time period divided by number of
cases of the disease during the same time period, usually expressed as per 100.
j. Years of potential life lost (YPLL)
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* It is defined as one that occurs before the age to which a dying person could have expected to
survive (before an arbitrary determined age, usually taken age 75 years.)

USU9OIDcw
The familial form of Alzheimer's disease is ______ and carried on ______
a) Autosomal dominant; chromosome 21 or chromosome 19

b) Autosomal dominant; chromosome 10 and chromosome 11
c) Recessive; chromosome 21 or chromosome 22
d) Recessive; chromosome 21 or chromosome 9
Correct Answer: A
Explanation
Explanation
Gene in Alzheimers Chromosome
* APP gene 21
* Presenilin 1 14*****
* Presenilin 2 1
* APO ‘Episilon’ 19
* a2 macroglobulin 10
The Molecular Basis for Degenerat ive Dementia
Molecular Susceptibility Pathologic

Dementia Causal Genes (Chromosome)
Basis Genes Findings
APP (21)******, PS-1 (14), PS-2 (1) Amyloid plaques,

(<2% carry neurofibrillary
AD Aβ/tau Apo ε 4 (19)****** tangles, and
these mutations, most often in PS-
1) neuropil threads
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Tau neuronal and

MAPT exon and intron mutations glial inclusions
(17)
FTD Tau H1 MAPT haplotype varying in
(about 10% of familial cases) morphology and
distribution
GRN (10% of familial cases), C9O TDP-43 neuronal

RF72 and glial
inclusions varying
TDP-43 (20–30% of familial cases), rare V in
CP , very
morphology and
rare TARDBP TBK1, TIA1 distribution
FUS neuronal and

glial inclusions
varying in
FUS Very rare FUS
morphology and
distribution
α-Synuclein
α- neuronal
DLB Very rare SNCA (4) Unknown
Synuclein inclusions (Lewy
bodies)
Codon 129
PRNP (20) (up to 15% of patients homozygosity PrP SC deposition,
CJD PrP SC carry panlaminar
for methionine or spongiosiS
valine

USU9OIDcx
A patient was admitted with complaints of pain in the calf muscles which is releived by
movement.A provisional diagnosis of Restless syndrome was made.Restless leg syndrome is
characterized by all of the following except
a) Autosomal reccesive inheritance

b) More common in women
c) Also called as Willis-Ekbom Disease
d) Rotigotine is used for treatment
Correct Answer: A
Explanation
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Explanation
*Restless legs syndrome, or Willis-Ekbom Disease, is a common, chronic, multifactorial,

movement disorder of the limbs in which patients have an irresistible urge to move the legs.
*There is a diurnal pattern of worsened symptoms at night.
*There are two type of Restless Legs Syndrome. Primary Restless Legs Syndrome and
Secondary Restless Legs Syndrome.
Secondary Restless Legs Syndrome can occur secondary to some disorders including:
• Iron deficiency
• End Stage Renal Disease
• Pregnancy
• Diabetes Mellitus
• Rheumatic disease
• Venous insufficiency
• Peripheral neuropathy
• Folate or magnesium deficiency
• Amyloidosis
• Lumbosacral radiculopathy
• Fibromyalgia
• Celiac disease
• Medications have been known to cause or exacerbate the symptoms of Restless Legs
Syndrome. They include antidopaminergic medications (e.g., neuroleptics),
Diphenhydramine, Tricyclic antidepressants (TCAs), Selective serotonin reuptake
inhibitors (SSRIs).
*Women are affected more than men******. . It is threefold more common in pregnant women
* There may be an autosomal dominant inheritance******
*Polymorphisms in genes including BTBD9 and MEIS1 are associated with Restless Legs
Syndrome.
A variety of factors can cause RLS. Iron deficiency is the most common treatable cause, and
iron replacement should be considered if the ferritin level is <75 ng/mL-20 th . Opioids and
benzodiazepines may also be of therapeutic value. Most patients with restless legs also
experience PLMD, although the reverse is not the case.
Medications used
• Dopaminergic agents (eg, pramipexole, ropinirole, bromocriptine, levodopa-carbidopa,

and rotigotine )
• Benzodiazepines (eg, clonazepam)
• Opioids (eg, codeine)
• Anticonvulsants (eg, gabapentin and pregabalin)
• Presynaptic alpha 2 -adrenergic agonists (eg, clonidine)
• Iron salt
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NUSU9OIDcy
A 25 year old lady presented with altered sensorium,hearing loss and acute onset of visual
loss.Her MRI revealed “snowball” lesions in the corpus callosum.Which of the following could
be the possible diagnosis
a) Susac syndrome
b) Multiple sclerosis
c) SLE
d) APLA
Correct Answer: A
Explanation
Explanation
* The possibility of Susac syndrome is raised when a patient presents with one or more
components of the clinical triad (encephalopathy, BRAO, hearing loss) .
*A diagnosis of definite or probable Susac syndrome is based on presence of at least two

components of the triad and documentation of typical “snowball” lesions in the corpus callosum
upon brain MRI. ******
*Susac syndrome is characterized by three main problems: encephalopathy, partial or complete

occlusion of branch retinal artery occlusion, or BRAO and hearing loss
* Susac syndrome primarily affects young women between the ages of 20-40,
*MRI of the brain typically reveals “snowball” lesions in the corpus callosum. All forms require
immunosuppressive treatment while the disease is active.
MORE FACTS
Retinal arterial occlusion also occurs rarely in association with retinal migraine, lupus
erythematosus, anticardiolipin antibodies,
anticoagulant deficiency states (protein S, protein C, and antithrombin deficiency), Susac’s

syndrome - 20 th , pregnancy, IV drug abuse, blood
dyscrasias, dysproteinemias, and temporal arteritis
Anterior Ischemic Optic Neuropathy (AION) This is caused by insufficient blood flow
through the posterior ciliary arteries that supply the optic disc. It produces painless monocular
visual loss that is sudden in onset, followed sometimes by stuttering progression. The optic disc
appears swollen and surrounded by nerve fiber layer splinter hemorrhages AION is divided into
two forms: arteritic and nonarteritic.
The nonarteritic form is most common. .
It is urgent to recognize arteritic AION so that high doses of glucocorticoids can be instituted
immediately to prevent blindness in the second eye. Tocilizumab is an effective alternative to
glucocorticoids for sustained suppression of symptoms of giant cellArteritis-20 th
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Metallosis (chromium, cobalt, nickel) from hip implant failure is a rare cause of toxic
optic neuropathy. Deficiency states induced by starvation, malabsorption, or
alcoholism can lead to insidious visual loss.20 th
Optic disc drusen are calcified, mulberry-like deposits of unknown etiology within the
optic disc, giving rise to “pseudopapilledema

NUSU9OIDcz
Which of the following diseases will NOT cause Proximal Arm/Distal Leg Weakness
(Scapuloperoneal or Humeroperonal) Weakness
a) Emery-Dreifuss muscular dystrophy

b) Inclusion body myositis
c) Facioscapulohumeral muscular dystrophy
d) Ducheene muscular dystrophy
Correct Answer: D
Explanation
Proximal Arm/Distal Leg Weakness (Scapuloperoneal or Humeroperonal)

Weakness
Facioscapulohumeral muscular dystrophy (FSHD)
Scapuloperoneal myopathy and neuropathy
Myofibrillar myopathies
Emery-Dreifuss muscular dystrophy (EDMD)
Bethlem myopathy
Distal Arm/Proximal Leg Weakness
Inclusion body myositis (usually wrist and finger flexors in arms, hip flexors and knee
extensors in legs, and asymmetric)
Myotonic dystrophy (uncommon presentation)
MORE FACTS
Muscle Sti ff ness/Decreased Ability To Relax
Myotonic dystrophy 1 and 2
Myotonia congenita
Paramyotonia congenita
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Hyperkalemic periodic paralysis with myotonia
Potassium aggravated myotonia
Schwartz-Jampel syndrome
Other: rippling muscle disease (acquired and hereditary), acquired neuromyotonia (Isaacs
syndrome), sti ff -person syndrome, Brody disease
Brody myopathy is a hereditary condition that affects the skeletal muscles (muscles used for
movement). Symptoms typically begin in childhood and are characterized by muscle cramping
and stiffening (myopathy) after exercise or other strenuous activity. These symptoms can
worsen in cold temperatures and are usually painless, however, some individuals may have mild
discomfort. Some cases of Brody myopathy are caused by mutations in the ATP2A1 gene
Drug-Induced Myopathies
Drugs Major Toxic Reaction
Lipid-lowering agents Drugs belonging to all three of the
Fibric acid derivatives major classes of lipid-lowering agents
HMG-CoA reductase inhibitors can produce a spectrum of toxicity:
Niacin (nicotinic acid) asymptomatic serum creatine kinase
elevation, myalgias, exercise-induced
pain, rhabdomyolysis, and myoglobinuria.
Glucocorticoids Acute, high-dose glucocorticoid
treatment can cause acute quadriplegic
myopathy. These high doses
of steroids are often combined with
nondepolarizing neuromuscular
blocking agents but the weakness
can occur without their use. Chronic
steroid administration produces

predominantly
proximal weakness.
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Nondepolarizing Acute quadriplegic myopathy can

neuromuscular
occur with or without concomitant
blocking agents
glucocorticoids.
Zidovudine Mitochondrial myopathy with ragged
red fibers
Drugs of abuse All drugs in this group can lead to
Alcohol widespread muscle breakdown,

rhabdomyolysis,
Amphetamines
and myoglobinuria.
Cocaine
Local injections cause muscle
Heroin
necrosis, skin induration, and limb
Phencyclidine
contractures.
Meperidine
Autoimmune toxic myopathy Use of this drug may cause polymyositis
d-Penicillamine and myasthenia gravis.
Amphophilic cationic drugs All amphophilic drugs have the
Amiodarone potential to produce painless,
Chloroquine proximal weakness associated with
Hydroxychloroquine autophagic vacuoles in the muscle
biopsy.
Antimicrotubular drugs This drug produces painless, proximal
Colchicine weakness especially in the setting of
renal failure. Muscle biopsy shows
autophagic vacuoles.
. In myotonic muscular dystrophy type 1 (DM1), distal weakness usually accompanies myotonia,
whereas in DM2, proximal muscles are more affected. Myotonia also occurs with myotonia
congenita (a chloride channel disorder), but in this condition muscle weakness is not prominent.
Myotonia
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may also be seen in individuals with sodium channel mutations (hyperkalemic periodic paralysis
or potassium-sensitive myotonia). Another sodium channelopathy, paramyotonia congenita (PC),
also is associated with muscle stiffness. In contrast to other disorders associated with myotonia
in which the myotonia is eased by repetitive activity, PC is named for a paradoxical phenomenon
whereby the myotonia worsens with repetitive activity. Potassiumaggravated myotonia is an
allelic disorder in which myotonia is brought on by consumption of too much potassium-
containing foods
There are two painful muscle conditions of particular importance, neither of which is associated
with muscle weakness. Fibromyalgia is a common, yet poorly understood myofascial pain
syndrome in which patients complain of severe muscle pain and tenderness, severe fatigue, and
often poor sleep. Serum CK, erythrocyte sedimentation rate (ESR), EMG, and muscle biopsy are
normal . Polymyalgia rheumatica occurs mainly in patients aged >50 years and is characterized
by stiftness and pain in the shoulders, lower back, hips, and thighs . The ESR and CRP are
elevated, while serum CK, EMG, and muscle biopsy are normal .

USU9OIDc0
A patient presented with episodic weakness and was diagnosed to have Myesthenia
gravis.His serology revealed antiMusk antibodies.Which of the following is false
regarding a Myesthenic patient with antiMusk antibodies
a) typically do not experience myasthenic crisis

b) obtain less benefit from anticholinesterase agents than those with AChR antibodies and
may actually worsen
c) MuSK MG is more common in Asians
d) rituximab is not effective
Correct Answer: D
Explanation
Explanation
Myesthenia gravis
*Approximately 20% of patients with MG can be tapered off all immunotherapies
*There does not appear to be a correlation with maximal disease severity and chance for
remission.
*Thymectomy may increase the likelihood of achieving remission in anti-AChR MG, but the
large randomized
trial was too short in duration to examine this endpoint; rather, the results revealed only that
thymectomy
was efficacious and led to less use of glucocorticoids and second line agents. Mortality - 1–2%
range.
*Anti-MuSK patients typically do not experience myasthenic crises*******, but are generally
more difficult to treat than anti-AChR MG. Non-paraneoplastic LEMS is
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usually responsive to immunotherapy and symptomatic treatment with pyridostigmine and 3,4
DAP.
* Juvenile onset MG is uncommon in Western populations but may represent more than half of
cases in Asians. MuSK MG appearts to be more common in the Mediterranean area of Europe
than in northern Europe and is also more common in the northern regions of East Asia ******
* There is a growing body of evidence that rituximab is effective in many MG patients,

especially those with MuSK antibody.****
*Patients with anti-MuSK MG generally obtain less benefit from anticholinesterase agents than
those with AChR antibodies and may actually worsen******
Until recently there was a debate regarding the role of thymectomy in non-thymotous MG, but a
recent large international trial of extended transternal thymectomy in non-thymomatous AChR
antibody positive, generalized MG demonstrated that participants who underwent thymectomy
had improved strength and function, required less prednisone and additions of second line
agents (e.g., azathioprine), and fewer hospitalizations for exacerbations

USU9OIDc1
A patient presented with reccurent attacks of optic neuritis and was diagnosed to have
multiple sclerosis.All of the following drugs are considered as highly effective in the
management of Multiple sclerosis except
a) Natalizumab
b) Fingolimod
c) Ocrelizumab
d) Mitoxantrone Hydrochloride
Correct Answer: B
Explanation
Drugs used in Multiple sclerosis
Highly effective Moderately effective
Natalizumab Fingolimod
Ocrelizumab Interferon β
Alemtuzumab Glatiramer Acetate
Mitoxantrone Hydrochloride Dimethyl Fumarate (DMF)
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Teriflunomide
Daclizumab, a monoclonal antibody against CD25, the α subunit of the interleukin 2 receptor,
was removed from the market in 2018 because of reports of
brain inflammation; it was previously approved for patients who had failed at least two
other therapies
MORE FACTS
Drugs used in Multiple sclerosis
Intravenous I ntramuscular Subcutaneous Oral
Ocrelizumab Interferon 1-Beta Glatrimer acetate Dimethyl fumarate
Natalizumab Fingolimod
Teriflunomid
With three or moretypical T2-weighted lesions, the risk of developing MS after 20 years is
~80%. Conversely, with a normal brain MRI, the likelihood of developing MS is
<20%. Similarly, the presence of two or more Gd-enhancing lesions at baseline is highly
predictive of future MS, as is the appearance of either new T2-
weighted lesions or new Gd enhancement ≥3 months after the initial episode.

USU9OIDc2
Which of the following is incorrect regarding the drugs used in Multiple sclerosis and the
adverse effects
a) Fingolimod - QT prolongation
b) Natalizumab- PML
c) Ocrelizumab-Ca breast
d) Glatimer acetate-toxic epidermal necrolysis
Correct Answer: D
Explanation
Teriflunomide causes toxic epidermal necrolysis or Stevens-Johnson syndrome*****
Fingolimod (Moderately E ff ective)
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*Fingolimod is a sphingosine-1-phosphate (S1P) inhibitor that prevents the egress of

lymphocytes from secondary lymphoid organs such as the lymph
nodes and spleen. Its mechanism of action is probably due to sequestration of lymphocytes in
the periphery, thereby inhibiting their trafficking to the
CNS.
*It is well tolerated, oraly
*First- and second-degree heart block and bradycardia can also occur . A 6-h period of
observation (including electrocardiogram
monitoring) is recommended for all patients receiving their first dose. Other side effects include
macular edema and, rarely, disseminated varicella-zoster
virus (VZV) and cryptococcal infections . Fingolimod can also cause QT prolongation .
DMF is a small molecule and is a Krebs cycle metabolite with anti-inflammatory effects in
psoriasis. Although the precise mechanisms of action of DMF
DMF is a small molecule and is a Krebs cycle metabolite with anti-inflammatory effects in
psoriasis. Although the precise mechanisms of action of DMF
are not fully understood, it seems to modulate the expression of proinflammatory and
anti-inflammatory cytokines
Glatiramer Acetate (Modestly E ff ective)
*Glatiramer acetate is a synthetic, random polypeptide composed of four amino acids (L-
glutamic acid, L-lysine, L-alanine, and L-tyrosine).
*Its mechanism of action may include (1) induction of antigen-specific suppressor T cells; (2)
binding to MHC molecules, thereby displacing bound MBP; or (3) altering the
balance between proinflammatory and regulatory cytokines. Glatiramer acetate reduces the
attack rate (whether measured clinically or by MRI) in RMS.
*glatiramer acetate should be considered as an equally effective alternative to IFN-β in RMS

patients. Its usefulness in
progressive disease is unknown.
*Glatiramer acetate is administered by subcutaneous injection**** .
Mitoxantrone Hydrochloride (Highly Effective)
*Mitoxantrone, an anthracenedione, exerts its antineoplastic action by (1) intercalating into

DNA and producing both strand breaks and interstrand crosslinks,
(2) interfering with RNA synthesis, and (3) inhibiting topoisomerase II (involved in DNA repair).
The FDA approved mitoxantrone .
* Mitoxantrone is indicated for use in patients with rapidly worsening
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MS (defined as patients whose neurologic status remains significantly abnormal between MS

attacks). *
*Mitoxantrone is cardiotoxic . As a result, a
cumulative dose >140 mg/m2 is not recommended*****.
* 12 mg/m2 every 3 months
Daclizumab, a monoclonal antibody against CD25, the α subunit of the interleukin 2 receptor,
was removed from the market in 2018 because of reports of
brain inflammation; it was previously approved for patients who had failed at least two
other therapies
Alemtuzumab (Highly Effective)
*Alemtuzumab is a humanized monoclonal antibody directed against the CD52 antigen that is
expressed on both monocytes and lymphocytes. It causes
lymphocyte depletion (of both B and T cells) and a change in the composition of lymphocyte
subsets.4170
*Because of its toxicity profile, the FDA indicated
alemtuzumab only in patients who have tried and failed at least two other DMTs.
Natalizumab (Highly Effective)
*Natalizumab is a humanized monoclonal antibody directed against the α4 subunit of

α4β1 integrin, a cellular adhesion molecule expressed on the surface
of lymphocytes. It prevents lymphocytes from binding to endothelial cells, thereby preventing

lymphocytes from penetrating the BBB and entering the
CNS. Natalizumab is highly effective in reducing the attack rate and significantly improves all
measures of disease severity in MS (both clinical and MRI).
*Monthly intravenous infusions makes it very convenient for patients.
Treatment with natalizumab is, in general, well tolerated. A small percentage (<10%) of
patients experience
hypersensitivity reactions (including anaphylaxis), and ~6% develop neutralizing antibodies to

the molecule (only half of which persist).
*The major concern with long-term treatment is the risk of PML, a life-threatening condition
resulting from infection by the John Cunningham (JC) virus.
*PML has occurred in ~0.4% of patients treated with natalizumab.
Natalizumab is generally recommended only for JC antibody–negative patients,
*Ocrelizumab (Highly Effective)
*Ocrelizumab is a humanized monoclonal antibody directed against the CD20 molecule present
on the surface of mature B cells. CD20 is not expressed on
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early B-cell precursors or on antibody-producing plasma cells, thus treatment with ocrelizumab
selectively depletes mature B cells while preserving
preexisting humoral immunity and the capacity for B-cell reconstitution by lymphoid stem cells.
*Ocrelizumab rapidly depletes circulating B cells through
antibody-dependent cellular toxicity and complement-dependent cytotoxicity.
*Ocrelizumab targets the same molecule as rituximab, a monoclonal antibody indicated for non-
Hodgkin’s lymphoma and
rheumatoid arthritis, and ofatumumab, indicated for treatment of chronic lymphocytic

leukemia.
* Ocrelizumab 600 mg is administered byintravenous infusion every 24 weeks
*Ocrelizumab is well tolerated with infusion-related reactions
* Rituximab is associated with a very small risk of PML (estimated at <1:25,000/year), thus it is
possible that
ocrelizumab will also carry a nonzero risk. Ocrelizumab may also carry some risk of increased
malignancies including breast cancer, although rituximab is
not associated with an increased risk of malignancy.
Teriflunomide (Modestly E ff ective)
*Teriflunomide inhibits the mitochondrial enzyme dihydro-orotate dehydrogenase, which is a

key part of the pathway for de novo pyrimidine biosynthesis
from carbamoyl phosphate and aspartate. It is the active metabolite of the drug leflunomide
(FDA-approved for rheumatoid arthritis), and it exerts its
anti-inflammatory effects by limiting the proliferation of rapidly dividing T and B cells.
*Consequently, teriflunomide is considered to be cytostatic rather than cytotoxic. Teriflunomide

reduces the attack rate and significantly improves all measures of disease severity in MS
patients.
*It is well tolerated, and its daily oral dosing *****
*treatment with teriflunomide was well tolerated. Teriflunomide rarely causes toxic epidermal
necrolysis or Stevens-Johnson syndrome. *****
*pregnancy category X
* teriflunomide can remain in the bloodstream for 2 years due tohepatobiliary reabsorption.

USU9OIDc3
Motor Nerve Conduction Studies in an axonal degeneration will show all the following except
POSITIVE MED PG
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a) F wave can be absent

b) Conduction block is absent
c) Distal latency is normal
d) Conduction velocity is markedly prolonged
Correct Answer: D
Explanation
El ectrophysiologic Features: Axonal Degeneration Versus Segmental Demyelination
Axonal Segmental
Degeneration Demyelination
Motor Nerve Conduction Studies
Normal (except with CB

CMAP amplitude Decreased
or distal dispersion)
Distal latency Normal Prolonged
Conduction velocity Normal Slow
Conduction block Absent Present
Temporal dispersion Absent Present
F wave Normal or absent Prolonged or absent
H reflex Normal or absent Prolonged or absent
Sensory Nerve Conduction Studies
SNAP amplitude Decreased Normal or decreased
Distal latency Normal Prolonged
Conduction velocity Normal Slow
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Needle EMG
Spontaneous activity
Fibrillations Present Absent
Fasciculations Present Absent
Motor unit potentials
Recruitment Decreased Decreased
Long duration/
Morphology Normal
polyphasic
In general, low-amplitude potentials with relatively preserved distal latencies, conduction

velocities, and late potentials, along with fibrillations on needle EMG, suggest an axonal
neuropathy. On the other hand, slow conduction velocities, prolonged distal latencies and late
potentials, relatively preserved amplitudes, and the absence of fibrillations on needle EMG
imply a primary demyelinating neuropathy. The presence of nonuniform slowing of conduction
velocity, conduction block, or temporal dispersion further suggests an acquired demyelinating
neuropathy (e.g., GBS or CIDP) as opposed to a hereditary demyelinating neuropathy (e.g.,
CMT type 1).

USU9OIDc4
A patient was suspected to have porphyria.Which of the following porphyria is not associated
with peripheral neuropathy
a) acute intermittent porphyria

b) hereditary coproporphyria
c) variegate porphyria
d) Erythropoitic porphyria
Correct Answer: D
Explanation
Porphyria is a group of inherited disorders caused by defects in heme biosynthesis Three forms
of porphyria are associated with peripheral
neuropathy: acute intermittent porphyria (AIP), hereditary coproporphyria (HCP), and

variegate porphyria (VP).*******
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Rare Hereditary Neuropathies
Hereditary Disorders of Lipid Metabolism
Metachromatic leukodystrophy
Krabbe’s disease (globoid cell leukodystrophy)
Fabry’s disease
Adrenoleukodystrophy/adrenomyeloneuropathy
Refsum’s disease
Tangier disease
Cerebrotendinous xanthomatosis
Hereditary Ataxias with Neuropathy
Friedreich’s ataxia
Vitamin E deficiency
Spinocerebellar ataxia
Abetalipoproteinemia (Bassen-Kornzweig disease)
Disorders of Defective DNA Repair
Ataxia-telangiectasia
Cockayne’s syndrome
Giant Axonal Neuropathy
Porphyria
Acute intermittent porphyria (AIP)
Hereditary coproporphyria (HCP)
Variegate porphyria (VP)
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Familial Amyloid Polyneuropathy (FAP)
Transthyretin-related
Gelsolin-related
Apolipoprotein A1-related
MORE FACTS
Adrenomyeloneuropathy
* It is an X - linked dominant disorders caused by mutations in adenosine triphosphate -

binding cassette (ABC) transporter gene. It is a primary axonopathy with secondary
demyelination. Nerve biopsies demonstrate lamellar inclusions in the cytoplasm of Schwann
cells. Very long chain fatty acid (VLCFA) levels (C24, C25, and C26) are increased in the
urine. Adrenal insufficiency is present in two - thirds of patients. Diets low in VLCFAs and
supplemented with Lorenzo's oil (erucic and oleic acids) reduce the levels of VLCFAs and
increase the levels of C22.
Refsum Disease
* The tetrad is (1) peripheral neuropathy, (2) retinitis pigmentosa [AIIMS NOV - 2010***], (3)
cerebellar ataxia, and (4) elevated CSF protein concentration. Other associations are
sensorineural hearing loss, cardiac arrythmias, ichthyosis, and anosmia. It is an autosomal
recessive disease due to mutations in the gene that encodes for phytanoyl - CoA alfa –
hydroxylase [AIIMS NOV - 2008***] (PAHX) or peroxin 7 receptor protein (PRX 7) - serum
phytanic acid levels are elevated. Nerve biopsy demonstrates has onion bulb formation. It is
treated by avoiding phytanic precursors (phytols: fish oils, dairy products) from the diet.
Tangier Disease
* It is due to mutations(AR) in the ATP - binding cassette transporter 1 (ABC1) gene, which
leads to decreased levels of high - density lipoprotein (HDL) cholesterol. Clinical
manifestations are asymmetric multiple mononeuropathies, a slowly progressive symmetric
polyneuropathy predominantly in the legs, a pseudo - syringomyelia pattern with dissociated
sensory loss (abnormal pain/temperature perception but preserved position/vibration in the
arms. There is yellowish - orange tonsil, with splenomegaly and lymphadenopathy. Biochemical
abnormality is increased triacylglycerol levels. Nerve biopsies reveal abnormal accumulation of
lipid in Schwann cells..
Porphyria(AD)
* Three forms of porphyria are associated with peripheral neuropathy: acute

intermittent porphyria (AIP), hereditary coproporphyria (HCP), and variegate
porphyria (VP).

USU9OIDc5
POSITIVE MED PG
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Immune-mediated brachial plexus neuropathy (IBPN) or Parsonage-Turner syndrome is

associated with all of the following except
a) usually presents with an acute onset of severe pain in the shoulder region
b) weakness and often sensory loss occurs
c) primarily involves the suprascapular, long thoracic, or axillary nerves
d) It commonly affects the lower trunk of brachial plexsus
Correct Answer: D
Explanation
Explanation
Immune-mediated brachial plexus neuropathy (IBPN) goes by various terms, including acute
brachial plexitis, neuralgic amyotrophy, and Parsonage-
Turner syndrome. IBPN usually presents with an acute onset of severe pain in the shoulder
region.
However, as the pain dissipates, weakness and often sensory loss are appreciated..
* The most common pattern of
IBPN involves the upper trunk***** or a single or multiple mononeuropathies primarily

involving the suprascapular, long thoracic, or axillary nerves.
Additionally, the phrenic and anterior interosseous nerves may be concomitantly affected
MORE FACTS
* Brachial plexopathies occur in 5% of patients following a median sternotomy and typically

affect the lower trunk*****
Approximately 25% of affected patients have continued pain (postherpetic neuralgia
Standard doses of INH (3–5 mg/kg per day) are associated with a 2%
incidence of neuropathy, whereas neuropathy develops in at least 17% of patients taking in

excess of 6 mg/kg per d. The elderly, malnourished, and “slow
acetylators” are at increased risk for developing the neuropathy. INH inhibits pyridoxal
phosphokinase, resulting in pyridoxine deficiency and the
neuropathy.
[PHN]).
The nucleoside analogues zalcitabine (dideoxycytidine or ddC), didanosine (dideoxyinosine or

ddI), stavudine (d4T), lamivudine (3TC), and antiretroviral
nucleoside reverse transcriptase inhibitor (NRTI) are used to treat HIV infection. One of the
major dose-limiting side effects of these medications is a
predominantly sensory, length-dependent, symmetrically painful neuropathy
The predominant motor neuropathies are listed below
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Motor - predominant neuropathies
Immune neuropathies: acute (Guillain - Barré syndrome); relapsing
Heritable motor - sensory neuropathies
Acute intermittent porphyria
Diphtheritic neuropathy
Lead neuropathy [AIIMS NOV - 2006***]
Brachial neuritis
Diabetic lumbosacralplexus neuropathy (diabetic amyotrophy)
Toxic Neuropathies Secondary to Chemotherapy
Mechanism of Clinical Nerve

Drug EMG/NCS
Neurotoxicity Features Histopathology
Symmetric, S-M,
Axonal degeneration Axonal
large-/
Interfere with of sensorimotor PN;
Vinca alkaloids distal
axonal small-fiber PN;
(vincristine, myelinated and
autonomic
microtubule unmyelinated denervation on
vinblastine, EMG; abnormal
assembly; symptoms
vindesine, fibers; regenerating
common;
impairs axonal clusters, QST, particularly
vinorelbine) vibratory
transport infrequent cranial
minimal segmental
neuropathies demyelination Perception
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Loss of large >

Preferential small myelinated
Low-amplitude or
damage to dorsal unobtainable
and unmyelinated
root ganglia: Predominant fibers;
SNAPs with
large-fiber
? binds to and axonal degeneration normal
Cisplatin cross-links DNA sensory with
CMAPs and EMG;
neuronopathy; abnormal
? inhibits protein small clusters of
synthesis sensory ataxia regenerating
QST, particularly
fibers; secondary vibratory
? impairs axonal
transport segmental
Perception
demyelination
Loss of large >

small myelinated
Symmetric, Axonal
and unmyelinated
Promotes axonal predominantly sensorimotor PN;
fibers;
microtubule distal
sensory PN;
Taxanes axonal degeneration
assembly; large-fiber denervation on
(paclitaxel, with
interferes with EMG; abnormal
modalities
docetaxel) axonal small clusters of
affected more QST, particularly
regenerating
transport than vibratory
fibers; secondary
small-fiber Perception
segmental
demyelination
Abnormalities
consistent with
Length- an axonal sensory

dependent, neuropathy
Bortezomib sensory,
Unknown Not reported with early small-
(Velcade)
predominantly fiber involvement
small-fiber PN
(abnormal
autonomic
studies

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A patient presented with recurrent episodes of optic neuritis and bladder incontinence and was
diagnosed to have multiple sclerosis.Which of the following is the commonest type of Multiple
sclerosis
a) Relapsing or bout onset MS (RMS)

b) Secondary progressive MS (SPMS)
c) Relapsing/remitting MS (RRMS)
d) Primary progressive MS (PPMS)
Correct Answer: A
Explanation
Explanation
Risk factors are Vitamin D deficiency,EBV exposure in childhood and cigarette smoking****
Three clinical types[19 th edition-4] of MS exist
1)Relapsing or bout onset MS (RMS) accounts for 90% of MS cases and is characterized by
discrete attacks of neurological dysfunction that generally
evolve over days to weeks (rarely over hours). . Between attacks, patients are neurologically
stable.
2. Secondary progressive MS (SPMS) always begins as RMS . . SPMS produces a greater

amount of fixed neurologic disability than RMS. For a
patient with RMS, the risk of developing SPMS is ~2% each year.
3. Primary progressive MS (PPMS) accounts for ~10% of cases. These patients do not
experience attacks but rather steadily decline in function from
disease onset . Compared to RMS, the sex distribution is more even, the disease begins later in
life (mean age ~40 years), and disability
develops faster (relative to the onset of the first clinical symptom).
19 TH EDITION
Four clinical types of MS are Relapsing/remitting MS (RRMS - 85%); Secondary progressive

MS (SPMS) always begins as RRMS - risk of developing SPMS is 2% each year;Primary
progressive MS (PPMS) has a steady functional decline, the sex incidence is equal and the
disease begins later in life; Progressive/relapsing MS (PRMS - 5%)
Risk of Developing Multiple Sclerosis (MS)
1 in 3 If an identical twin has MS
1 in 15 If a fraternal twin has MS
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1 in 25 If a sibling has MS
1 in 50 If a parent or half-sibling has MS
1 in 100 If a first cousin has MS
1 in 1000 If a spouse has MS
1 in 1000 If no one in the family has M

USU9OIDgx
The most common nerve involvement in the peripheral neuropathy associated with Glycogen
storage disorder type III-GSDIII- Deficient debranching enzyme activity
a) Ulnar nerve
b) Sural nerve
c) Lateral cutaneous nerve of thigh
d) Median nerve
Correct Answer: D
Explanation
Explanation
GSD III-debrancher enzyme deficiency
*Patients with GSD III present with hepatomegaly, hypoglycemia, short stature, variable
skeletal myopathy, and cardiomyopathy.
*GSD type IIIa involves both liver and muscle. 15% of patients have only liverinvolvement and is
classified as type IIIb.
*Hypoglycemia and hyperlipidemia occur in children.
*Serum creatine kinase (CK) levels - normal levels do not rule outmuscle enzyme deficiency.
* In most patients with type III disease, hepatomegaly improves with age; however,liver fibrosis,
cirrhosis progressing to liver failure, and hepatocellular carcinoma, are noted in many in late
adulthood.*****
*Hepatic adenomas may occur, although less commonly than in GSD I. Left ventricular
hypertrophy, significant scarring of the myocardium, and life-threatening arrhythmias can occur
*The pattern of muscle weakness is variable and both proximal and distalmuscle weakness are
seen.
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*Peripheral neuropathy may become discernible later in life with preferentialmedian nerve
involvement*******.-20 th
* Polycystic ovaries are common .
* Fertility is normal.
More FACTS
Type IX GSD (Liver Phosphorylase Kinase Deficiency)
* The most common subtype is GSD IXa, an X-linked liver PhK deficiency caused by mutations in
the PHKA2 gene, which is also one of the most common liver glycogenoses.
Typically, a child between the ages of 1 year and 5 years presents with
growth retardation and hepatomegaly.
Liver fibrosis has been identified in some patients, including children. Levels of cholesterol,
triglycerides, and liver enzymes are mildly elevated. Fasting ketosis is a feature of the disease.
Lactic and uric acid levels are usually normal. Hypoglycemia may be mild in some but severe
and recurrent in others[20 th ].
*Liver transplantation may be considered in those with severe hepatic involvement
*Other subtypes of type IX GSD include GSD IXb, an autosomal recessive form of liver and
muscle PhK deficiency caused by PHKB mutations.
* GSD IXc, an autosomal recessive form of liver PhK deficiency that often develops into liver
cirrhosis, is due to PHKG2 mutations.
*GSD IXd, a muscle-specific PhK deficiency that causes cramps and myoglobinuria with
exercise, is caused by PHKA1 mutations. The previous reports of cardiac-specific PhK deficiency
is now considered to be a secondary phenomenon, as these patients have mutations in
the PRKAG2 gene. Patients with cardiac PRKAG2 syndrome often present with cardiomyopathy
during infancy. The condition is lethal because of massive glycogen deposition in the
myocardium.
Type IV GSD (Branching enzyme deficiency, Amylopectinosis, Polyglucosan disease or Andersen

disease) is caused by deficiency of branching enzyme activity leading to accumulation of an
abnormal glycogen with poor solubility. The disease is clinically heterogeneous. Individuals
typically present in the first 18 months of life with failure to thrive, hepatosplenomegaly, and
progressive liver cirrhosis leading to death in early childhood. Some patients may develop
hepatic adenomas and hepatocellular carcinoma. GSD IV has extrahepatic manifestations
involving the central and peripheral nervous system as well as cardiac and skeletal muscles.
The adult form is known as adult polyglucosan body disease (APBD) and may present as an
isolated myopathy or with systemic involvement of the central and peripheral nervous system
characterized by neurogenic bladder, peripheral neuropathy, leukodystrophy, and mild cognitive
impairment. Definitive
diagnosis requires demonstration of branching enzyme deficiency in liver, muscle, cultured skin
fibroblasts or leukocytes, or genetic testing of the GBE1 gene. It is likely that life expectancy is
shortened in APBD
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patients though it is yet to be confirmed by long-term natural history studies. Good supportive
care is crucial to improve clinical outcomes.
Liver transplantation may be performed for progressive hepatic failure.
pompes
The disorder encompasses a range of phenotypes. Each includes myopathy but differs in the
age of onset, extent of organ involvement, and clinical severity. The most severe is the infantile
th edition-1] years of age. Infants
form, with cardiomegaly, hypotonia, and death before 2 [19
often present with cardiomyopathy at birth, and develop
a generalized muscle weakness with feeding difficulties, macroglossia, hepatomegaly, and

congestive heart failure due to the rapidly progressive hypertrophic cardiomyopathy.
Adults typically present between the second and seventh decades with slowly progressive
myopathy without overt cardiac involvement. The clinical picture is dominated by slowly
progressive, predominantly proximal limb girdle muscle weakness. The pelvic girdle, paraspinal
muscles, and diaphragm are most seriously affected. Respiratory symptoms include
somnolence, morning headache, orthopnea, and exertional dyspnea. Respiratory failure causes
significant morbidity and mortality in the late-onset form. In rare instances, patients present
with respiratory insufficiency as the initial symptom. Basilar artery aneurysms and dilation of
the ascending aorta have been observed in patients with Pompe disease. Ptosis, lingual
weakness, gastrointestinal dysmotility, and incontinence due to poor sphincter tone are now
being recognized as part of the clinical spectrum. Small-fiber neuropathy, which presents with
painful paresthesia or pins-and-needles sensations, is also seen in some patients with LOPD.
Individuals with advanced disease often require some form of ventilatory support and are
dependent on a walking aid or wheelchair
DIAGNOSIS
The confirmatory step for a diagnosis of Pompe disease is enzyme assay demonstrating deficient
acid α- glucosidase or a gene sequence with two pathogenic mutations in the GAA gene.
Enzyme activity can be measured in muscle, cultured skin fibroblasts, or blood. The latter is
increasingly being used and is very reliable when performed in laboratories with
experience. Prenatal diagnosis using mutation analysis of DNA extracted from fetal cells
obtained by amniocentesis or by measuring GAA enzyme activity in chorionic villi or amniocytes
is available. Carrier detection and prenatal diagnosis, using DNA-based targeted mutation
analysis, are also possible if disease-causing family mutations are already known
The approval of enzyme replacement therapy with alglucosidase alfa in 2006 has changed the
natural history and clinical course of Pompe disease. Other adjunctive treatment options
include dietary modifications, submaximal aerobic exercise, and respiratory muscle strength
training. Gene therapy is under study as another treatment modality.
Pompe disease is now part of the recommended uniform screening panel
Late-Onset Polyglucosan Body Myopathy due to GYG1 Mutations
This is an autosomal recessive, slowly progressive skeletal myopathy caused by mutations in

the GYG1 gene blocking glycogenin-1 biosynthesis. GYG1 mutations results in a reduced or
complete absence of glyogenin-1 which is necessary for glycogen synthesis in muscles. Affected
individuals commonly present with adultonset proximal muscle weakness prominently affecting
the hip and shoulder girdles. Cardiomyopathy and cardiac failure necessitating cardiac
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transplantation is seen. Compared to GSD IV APBD, nervous system involvement has not been
reported although both disorders cause polyglucosan deposition

USU9OIDgy
A 5 day old patient presented with refusal to eat and lethargy progressing to coma.On
evaluation there was acidosis, Increased plasma ammonia and Increased plasma
glutamine. Plasma citrulline is markedly increased.Which of the following enzyme
deficiency could have caused this disease
a) N-acetylglutamate synthase
b) carbamylphosphate synthase 1
c) ornithine transcarbamylase deficiency
d) argininosuccinic acid synthase
Correct Answer: D
Explanation
Explanation
UREA CYCLE DISORDERS
*Deficiencies in urea cycle enzymes are individually rare, but as a group, they affect about 1:3
5,000 [19 th edition- 1:25,000 ] individuals.
*They are all transmitted as autosomal recessive traits, with the exception of ornithine
transcarbamylase deficiency, which is X-linked and the most frequent urea cycle defect*****.
*Infants with classic urea cycle defects present at 1–4 days of life with refusal to eat and
lethargy progressing to coma and death. Milder enzyme deficiencies present with protein
avoidance, recurrent vomiting, migraine, mood swings, chronic fatigue, irritability, and
disorientation that can progress to coma.
*Administration of systemic corticosteroids can precipitate hyperammonemia and can be fatal

in previously asymptomatic individuals.
*The diagnosis requires measurement of plasma ammonia, plasma amino acids, and urine orotic
Acid
*Increased plasma glutamine is seen with all urea cycle defects since ammonia not removed by
the urea cycle in periportal hepatocytes is conjugated to glutamate by glutamine synthase in
perivenous hepatocytes.
* Citrulline is low or undetectable in proximal defects of the urea cycle (N-acetylglutamate

synthase, carbamylphosphate synthase 1, and ornithine transcarbamylase deficiency), with
urine orotic acid being increased only in ornithinetranscarbamylase deficiency.
*Plasma citrulline is markedly increased in argininosuccinic acid synthase deficiency

(citrullinemia type 1), with a milder elevation in argininosuccinic acid lyase deficiency in the
presence of argininosuccinic acid (argininosuccinic aciduria).*******
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Inherited Disorders of Amino Acid Metabolism
Amino
Condition Enzyme Defect Clinical Findings Inheritance
Acid(s)
Dystonia,
DNAJC12 Hydroxylase Co- parkinsonism,
Phenylalanine AR
Deficiency Chaperone intellectual
disability
Intellectual disability,
microcephaly,
Phenylalanine hypopigmented
Phenylketonuria AR
hydroxylase
skin and hairs,
eczema, “mousy” odor
Liver failure, cirrhosis,

Tyrosinemia type rickets, failure to
I Fumarylacetoacetate thrive, peripheral
Tyrosine AR
hydrolase
(hepatorenal) neuropathy, “boiled
cabbage” odor
Palmoplantar
keratosis, painful
Tyrosinemia type
corneal erosions with
II Tyrosine transaminase AR
photophobia,
(oculocutaneous)
intellectual disability
(?)
Hypertyrosinemia with
4-
Tyrosinemia type Hydroxyphenylpyruvate normal liver function,
occasional AR
III
dioxygenase
mental delay
4-
Transient failure to
Hydroxyphenylpyruvate
Hawkinsinuria thrive, metabolic AD
dioxygenase acidosis in infancy
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Ochronosis, arthritis,
Homogentisic acid cardiac valve
Alkaptonuria involvement, coronary AR
oxidase
artery calcification
Hypopigmentation of
Albinism hair, skin, and optic
Tyrosinase fundus; visual AR
(oculocutaneous)
loss; photophobia
Hypopigmentation of
Different enzymes or
Albinism (ocular) optic fundus, visual AR,XL
transporters
loss
Seizures,
ABAT deficiency GABA transaminase intellectual AR
disability, hypotonia
Mild intellectual
Prolidase
Prolidase disability, chronic AR
deficiency
dermatitis
Lens dislocation,
thrombotic vascular
Homocystine Homocystinuria Cystathionine β-synthase disease, intellectual AR
disability, osteoporosis

USU9OIDgz
Budapest consensus criteria is used for clinical diagnosis of which of the following
condition
a) COMPLEX REGIONAL PAIN SYNDROMES (CRPS)

b) Postprandial orthostatic hypotension
c) Postural Orthostatic Tachycardia Syndrome (POTS)
d) Guillian barrie syndrome
Correct Answer: A
Explanation
limb trauma, fractures, myocardial infarction, or stroke can cause CRPS type I*****
Reflex Sympathetic Dystrophy and Causalgia
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* Complex regional pain syndrome (CRPS) types I and II are now called reflex sympathetic
dystrophy (RSD) and causalgia, respectively. CRPS type I(reflex sympathetic dystrophy (RSD)
(AI - 2011***) is a regional pain syndrome that develops after tissue trauma. Examples of
associated trauma include myocardial infarction, minor shoulder or limb injury, and stroke. All
odynia (is the perception of a nonpainful stimulus as painful), hyperpathia (is an exaggerated
pain response to a painful stimulus), and spontaneous pain can occur. CRPS type II
(causalgia) is a regional pain syndrome that develops after injury to a specific peripheral
nerve. CRPS type I (RSD) has three clinical phases. Medicines used in management are
adrenergic blockers, nonsteroidal anti - inflammatory drugs, calcium channel blockers,
phenytoin, opioids, and calcitonin. Stellate ganglion gives temporary pain relief. Symptomati
c Treatment is with Midodrine, a directly acting alfa 1 - agonist that does not cross the blood
- brain barrier. It has a duration of action of 2–4 h.
MORE FACTS-20 th
*Although CRPS type I (RSD) has been classically divided into three
clinical phases, there is little evidence that CRPS “progresses” from one stage to another.
* Currently, the Budapest consensus criteria for clinical diagnosis of CRPS delete staging and
require at least three symptoms and two signs in the following four categories: (1) sensory, (2)
vasomotor, (3) sudomotor/edema, and (4) motor/trophic. Pain (usually burning or electrical in
quality) is the primary clinical feature of CRPS. Limb pain syndromes that do not meet these
criteria are best classified as “limb pain—not otherwise specified.” In CRPS, localized sweating
(increased resting sweat output) and changes in blood flow may produe temperature
differences between affected and unaffected limbs.
The natural history of typical CRPS may be more benign and more variable than previously
recognized. A variety of surgical and medical treatments have been developed, with conflicting
reports of efficacy. Clinical trials suggest that early mobilization with physical therapy or a brief
course of glucocorticoids may be helpful for early CRPS type I or II. Chronic glucocorticoid
treatment is not recommended*****.
Initial Treatment of Orthostatic Hypotension (OH)
Patient education: mechanisms and stressors of OH
High-salt diet (10–20 g/d)
High-fluid intake (2 L/d)
Elevate head of bed 10 cm (4 in.) to minimize supine hypertension
Maintain postural stimuli
Learn physical counter-maneuvers
Compression garments
Correct anemia
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USU9OIDg0
A person sustains spinal cord injury following a road traffic accident. X-ray films indicate a
fracture of T8 vertebra. Which of the following spinal segments is likely to be involved, if you
suspect a lesion of the spinal cord at this level?
a) T7
b) T9
c) T10
d) T11
Correct Answer: D
Explanation
Spinal Cord Levels Relative to the Vertebral Bodies
Spinal Cord Level Corresponding Vertebral Body
Upper cervical Same as cord level
Lower cervical 1 level higher
Upper thoracic 2 levels higher
Lower thoracic 2 to 3 levels higher
Lumbar T10-T12
Sacral T12-L1

USU9OIDg1
According to Revised GCS (2014)-Glascow coma scale, a motor scor of 4 indicates which of the
following
a) Normal flexion
b) Withdraws
c) Localizes
d) obeys
Correct Answer: A
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Explanation
TBI is commonly defined as an alteration in brain function, or other evidence of brain pathology,
caused by an external force, and characterized by the following: (1) any period of loss or
decreased level of consciousness (LOC), (2) any loss of memory for events immediately before
(retrograde) or after (posttraumatic) the injury, (3) any neurological deficits, and/or (4) any
alteration in mental state at the time of injury .-20 th
Glasgow Coma Scale for Head Injury
Eye Opening (E) Verbal Response (V)
Spontaneous 4 Oriented 5
To loud voice 3 Confused, disoriented 4
To Pain 2 Inappropriate words 3
Nil 1 Incomprehensible sounds 2
Nil 1
Best Motor Response (M)
Obeys 6
Localizes 5
Normal flexion-20 th [19 th edition- 4

Withdraws (flexion)]]
Abnormal flexion-20 th [19 th - 3

Abnormal flexion Posturing]
Extension posturing 2
Nil 1
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Note : Coma score = E + M + V. Patients scoring 3 or 4 have an 85% chance of dying or

remaining vegetative, whereas scores >11 indicate only a 5–10% likelihood of death
Note: Revised GCS (2014).

USU9OIDg2
A patient met with a road traffic accident and was diagnosed to have severe brain injury.He did
not have convulsions.Which of the following statement regarding prophylactic antiepileptic
medications is true
a) have no role
b) are given for 48 hrs
c) are given for 1 week
d) are given for 2 weeks
Correct Answer: C
Explanation
SEVER BRAIN INJURY
19 th edition
The use of prophylactic antiepileptic medications has been recommended, but there is
little supportive data
20 TH EDITION
Prophylactic antiepileptic medications are recommended for 7 days and should be discontinued
unless there are multiple seizures postinjury
Bilateral lesions in the fusiform and lingual gyri***** of the occipitotemporal cortex
leads to inability to recognize familiar faces called as prosopagnosia and visual object
agnosi a . The common cause is bilateral infarctions in the territory of the posterior
cerebral arteries
Prosopagnosia- Bilateral lesion in fusiform and lingual gyri of occipito temporal cortex****** is
the cause and it presents with face and object recognition defects

USU9OIDg3
Location of the indicated arrow in internal capsule is
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a) Rubrospinal tract
b) Lateral corticospinal tract
c) Reticulospinal tract
d) Vestibulospinal tract
Correct Answer: A
Explanation
PARINAUDS SYNDROME
Parinaud's Syndrome is also called as dorsal midbrain syndrome . It is a

supranuclear****** vertical gaze disorder from damage to the posterior commissure. It
is a classic sign of hydrocephalus from aqueductal stenosis*****.
Features include loss of upgaze (and sometimes downgaze), convergence-retraction

nystagmus on attempted upgaze, downwards ocular deviation ("setting sun" sign), lid
retraction (Collier's sign*****), skew deviation, pseudoabducens palsy, and light-near
dissociation of the pupils*****.
Pineal Region Tumors
* These typically present with headache, visual symptoms, and hydrocephalus.*****

Patients may have Parinaud's syndrome characterized by impaired upgaze and
accommodation
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USU9OIDg4
Recent work has identified two fundamentally different types of reactive astrocytes that appear
to have
countervailing functions; the terms A1 and A2 astrocytes.A1s might be harmful. In contrast, A2s
up-regulated many neurotrophic factors are protective. Which of the secreted products of
activated microglia, specifically WIIL NOT induce astrocytes to transform to the A1 type
a) IL-1a
b) TGF Beta
c) TNF
d) C1q
Correct Answer: B
Explanation
Explanation
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One characteristic of the response to many types of brain injury is reactive astrocytosis, or the
formation of a glial scar
Recent work has identified two fundamentally different types of reactive astrocytes that appear
to have
countervailing functions; the terms A1 and A2 astrocytes have been proposed, by analogy to
brain
macrophage/microglia M1 and M2 designations
*A1s might be harmful. In contrast, A2s up-regulated many neurotrophic factors are
protective*****
*. A2 astrocytes are induced by ischemia and may serve beneficial functions, including a
contribution to tissue repair after injury.
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*A1 astrocytes are induced in inflammatory and degenerative states, and actively participate in
the injury process.
*Secreted products of activated microglia, specifically IL-1a, TNF, and C1q, induce astrocytes to
transform to the A1 type. *****
*Functionally, A1 astrocytes lose the capacity to phagocytose synapses and myelin debris, and
are strikingly toxic in vitro to various populations of neurons and to mature oligodendrocytes,
Interestingly, OPCs, abundant in active lesions of
multiple sclerosis despite the inflammatory milieu, are resistant to A1 mediated death.
*There is speculation that products of A1 astrocytes could promote damage in
conditions as varied as MS, AD , Parkinson’s disease (PD) , and amyotrophic lateral sclerosis
(ALS) , despite their distinct etiologies and pathologies.
Subject

USU9OIDg5
A patient presented with Head injury and a CTscan revealed a subarachnoid
hemorrhage and was operated upon..He developed increased urine output in the 2 nd
POD.The paramaters were- Bl.urea -20mg;Sr.creatinine-1mg;Sr.sodium-125
mq;sr.K-5mq.What could be the diagnosis
a) Central Diabetes Insipidus

b) Nephrogenic Diabetes Insipidus
c) cerebral salt wasting
d) SIADH
Correct Answer: C
Explanation
*The syndrome of “cerebral salt wasting” is a rare cause of hypovolemic hyponatremia,

encompassing hyponatremia with clinical hypovolemia
and inappropriate natriuresis in association with intracranial disease; associated disorders

include subarachnoid hemorrhage******, traumatic brain injury,
craniotomy, encephalitis, and meningitis
SLEEP FACTS
Polysomnographic profiles define two states of sleep: (1) rapid-eye-movement (REM) sleep and
(2) non-rapid-eye-movement (NREM) sleep. NREM sleep is subdivided into 3 stages ,
characterized by increasing arousal threshold and slowing of the cortical EEG.
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Overall, REM sleep constitutes 20–25% of total sleep****, and NREM stages 1 and 2 are 50–
60%. In infancy, REM sleep may comprise 50% of total sleep time*****, and the percentage is
inversely proportional to developmental age.
The first REM sleep episode occurs in the second hour of sleep*****. More rapid onset of REM
sleep (if <30 min) occurs in endogenous depression, narcolepsy, circadian rhythm disorders, or
drug withdrawal
Characteristic features of sleep in older people include reduction of slow-wave sleep*****,

frequent spontaneous awakenings, early sleep onset, and early morning awakening
* REM sleep is characterized by a low-amplitude, mixed-frequency EEG similar to that

of NREM stage 1 sleep. The EOG shows bursts of REM similar to those seen during
eyes-open wakefulness. Chin EMG activity is absent [AIIMS NOV-2006***] , reflecting
the brainstem-mediated muscle atonia that is characteristic of that state

USU9OIDkw
GLymphatics are associated with which of the follwoing organ
a) Brain
b) Gastrointestinal system
c) Genitourinary system
d) Tongue
Correct Answer: A
Explanation
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Two newly identified lymphatic structures of the CNS are the glymphatic and deep dural
lymphoid systems,
responsible for clearance of debris in the CNS.
*The brain has traditionally been considered to lack a classical lymphatic system, and immune
responses against antigens are
less effectively generated in the CNS than in other organ systems, a concept termed “immune
privilege.” However,
immune privilege status of the brain is only relative and not absolute.
Glymphatic pathways are also likely to represent an important egress pathway for lymphocytes
in the CNS and a route for
lymphocyte encounter with CNS antigens in cervical lymph nodes. In this regard, recent data
indicate that deep
cervical lymph nodes might be a site for antigen-specific stimulation of B-cells in MS .
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*The glymphatic system derives its name from a distinctive architecture involving lymphoid-like
structures and astroglial cells [recognition of its dependence upon glial cells and the similarity
of its functions to those of the peripheral lymphatic system ]
*glymphatic system that likely functions to remove waste products from the brain interstitium
Glymphatic pathways are also likely to represent an important egress pathway for lymphocytes
in the CNS and a route for
lymphocyte encounter with CNS antigens in cervical lymph nodes
*Another fascinating aspect of the glymphatic system is that the transport of fluids and solutes
accelerates with sleep
*Interstitial flow in the CNS is also impaired with aging, possibly related to changes in
astrocytic aquaporin-4
expression
A second recently identified pathway consists of a plexus of small lymphatic-like vessels located
on the external
surface of meningeal arteries and deep dural sinuses (including the sagittal and transverse
sinuses), structures
that exit the brain along the surface of veins and arteries and drain to the deep cervical lymph
nodes

USU9OIDkx
Histopathologic microscopic picture of muscle belongs to which of the following
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a) Polymyositis
b) Myasthenia gravis
c) Scleroderma
d) Dermatomyositis
Correct Answer: D
Explanation
Explanation
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Dermatomyositis
* The cutaneous signs of dermatomyositis may precede or follow the development of myositis
by weeks to years.
* Cases lacking muscle involvement is called as dermatomyositis sine myositis .
* The clinical signs are ,"Heliotrope" erythema, violaceous, flat-topped papules over the dorsal
interphalangeal joints called Gottron's sign or Gottron's papules ,Periungual telangiectasia.
* Sclerodactyly and Raynaud's phenomenon can occur.
* Areas of hypopigmentation, hyperpig-mentation, mild atrophy, and telangiectasia known as

poikiloderma can occur .
* Skin biopsy reveals epidermal atrophy, hydropic degeneration of basal keratinocytes,

edema of the upper dermis, and a mild mononuclear cell infiltrate.
* Direct immunofluorescence microscopy of lesional skin is usually negative.
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* Topical glucocorticoids are used and patients should avoid exposure to ultraviolet
irradiation.
Dermatomyositis presents with Periorbital violaceous erythema is called heliotrope rash. It o

ften involves the hands as erythematous flat-topped papules over the knuckles ( Gottron's sign
) and has periungual telangiectasias.

USU9OIDky
There are some mutations that may be considered ecogenetic, as they typically remain
silent, meaning they do not cause disease, unless an external event occurs.Which of
the followingmutation in mutation in the mitochondrial 12S rRNA gene is associated
with hearing loss but is rapidly exacerbated by exposure to normal dosages of an
aminoglycoside.
a) m.A1555G
b) m.B1555G
c) m.C1555G
d) m.D1555G
Correct Answer: A
Explanation
MITOCHONDRIAL DNA STRUCTURE AND FUNCTION
*mtDNA itself replicates independently of cellular replication.
* Another important feature of the mtDNA replication process is a reduced stringency of

proofreading and replication error correction
* There are some mutations that may be considered ecogenetic, as they typically remain silent,
meaning they do not cause disease, unless an external event occurs.
* One classic example is seen in a common (1:800) mutation in the mitochondrial 12S rRNA
gene, m.A1555G., which is associated with hearing loss but is rapidly exacerbated by exposure
to normal dosages of an aminoglycoside.
Point mutations in the mtDNA gene encoding the 12S rRNA (m.A1555G) result in heritable
nonsyndromic hearing loss. One such mutation causes heritable ototoxic susceptibility to
aminoglycoside antibiotics, which opens a pathway for a simple pharmacogenetic test in the
appropriate clinical settings. This is an example of an eco-genetic disorder in that most people
with this mutation do not develop any symptoms until exposed to an external agent
Another example is strict avoidance of aminoglycosides in the familial syndrome of ototoxic

susceptibility to aminoglycosides in the presence of the mtDNA m.1555A>G mutation of the
12SrRNA encoding gene
MORE FACTS
The mtDNA sequence contains a total of 37 genes, of which 13 encode mitochondrial protein
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components of the ETC . The remaining 22 tRNA- and 2 rRNA-encoding genes are
mitochondria-specific and dedicated to the process of
translating the 13 mtDNA-encoded proteins. The mtDNA itself replicates constantly,

independent of cell division, and requires its own unique
polymerase, referred to as polymerase gamma (polγ), which is encoded by the nuclear

protein POLG

USU9OIDkz
An elevated CSF lactate is a more specific test for mitochondrial disease if there is
central nervous system involvement. Which of the following is a recent marker for the
diagnosis of mitochondrial myopathy
a) Growth Differentiating Factor 15 (GDF15)

b) Glial fribrillary protein
c) Brain derived natriuretic peptide
d) ANP
Correct Answer: A
Explanation
An elevated CSF lactate is a more specific test for mitochondrial disease if there is central
nervous system involvement. The serum creatine kinase may be elevated but is often normal,
even in the presence of a proximal myopathy. Recently, testing for elevated levels of Growth
Differentiating Factor 15 (GDF15) has shown a high degree of sensitivity and specificity in those
with a mitochondrial myopathy, but it is not known yet if the degree of elevation for an
individual patient reflects the severity of the illness or is in any way a marker of disease activity.
Urinary organic and amino acids may also be abnormal, reflecting metabolic and kidney
proximal tubule dysfunction 95% of patients with LHON harbor one of the three mtDNA point
mutations (m.11778A>G, m.A3460A>G, or m.14484T>C).
It is a protein belonging to the transforming growth factor beta superfamily . Under normal
conditions, GDF-15 is expressed in low concentrations in most organs and upregulated because
of injury of organs such as such as liver , kidney , heart and lung
MORE NIMHANS FACTS-2014
Mitral cells are the principal neurons in the olfactory bulb****. There are about 50,
000 in the adult human. They have a primary apical dendrite which extends into a
spherical bundle of neuropil called a glomerulus which receives the input from the
olfactory receptor neurons
Glomeruli
* It is seen in in olfactory bulb . It is a spherical mass of neuropil and recieves input

from unmyelinated axons of receptor cells from olfactory N. The second order neurons
are mitral cells* Axons of mitral cells project into anterior olfactory nucleus and
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amygdala, Prepyriform cortex. Second site for olfactory chemoreception is in
epithelium of vomeronasal organ, which d etect phermones.

USU9OIDk0
Which among the following antiplatelet drugs is a Reversible inhibitor of P2Y12
a) Clopidrogel
b) Prasugrel
c) Ticagrelor
d) Cangrelor
Correct Answer: C
Explanation
The drugs clopidogrel , prasugrel , ticagrelor , and cangrelor bind to this receptor and are
called as antiplatelet agents
ADP RECEPTOR ANTAGONISTS
There are several distinct ADP receptors, classified as P2X1, P2Y1, andP2Y12.*****
The ADP receptor antagonists include the thienopyridines (clopidogrel and prasugrel) and
ticagrelor. All of these drugs target P2Y12, the key ADP receptor on platelets.
Thienopyridines • Mechanism of action The thienopyridines are structurallyrelated drugs

that selectively inhibit ADP-induced plateletaggregation by irreversibly blocking P2Y12*******
Ticagrelor As an orally active inhibitor of P2Y12, ticagrelor differs from the thienopyridines in
that ticagrelor does not require metabolic activation********[NOT A PRODRUG] and it produces
reversible inhibition of the ADP receptor
New agents in advanced stages of development include cangrelor, aparenteral, rapidly acting,
reversible inhibitor of P2Y12. Cangrelor An adenosine analogue, cangrelor binds reversibly to
P2Y12and inhibits its activity. The drug has a half-life of 3–6 min and is givenIV as a bolus
followed by an infusion. When stopped, platelet functionrecovers within 60 min
MORE NIMHANS FACT
NEW ANTIPLATELETS-Vorapaxar An orally active PAR-1 antagonist, vorapaxar is slowly

eliminated with a half-life of about 200 h. ******

USU9OIDk1
Which of the following drug should be stopped 14 days before lumbar puncture
a) Aspirin
b) Heparin
c) Clopidrogel
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d) Ticlopidine
Correct Answer: D
Explanation
GUIDELINES FOR PATIENTS RECEIVING ANTICOAGULANT OR ANTIPLATELT

MEDICATIONS
* Platelet counts; a count of <20,000/Μl is considered to be a contraindication to LP.
Some institutions recommend that the platelet count be >40,000 prior to LP.
* The most common site of bleeding is the epidural space.
Guidelines for some commonly used anticoagulants are summarized below.
Time of stoppage before a

Drug
lumbar puncture
Unfractionated Heparin 2–4 h prior
At least 24 h before the

Low-Molecular-Weight Heparin
procedure.
Spinal puncture is
Warfarin
contraindicated
Aspirin and Nonsteroidal Anti-inflammatory Drugs 10 days for aspirin and for 48 h
(NSAIDs) for NSAIDs.
Ticlopidine 14 days
clopidogrel 7 days prior
Glycoprotein Iib/IIIa Inhibitors, Direct Thrombin

LP avoided
Inhibitors, Oral Factor Xa Inhibitor
* Unfractionated Heparin, Therapeutic Dosing The ASRA 2010 Practice Advisory

recommends discontinuing unfractionated heparin (UFH) 2–4 h prior to removal of spinal or
epidural catheters to minimize risk of hematoma. The half-life of heparin is 60–90 min.
*Low-Molecular-Weight Heparin, should be held for at least 24 h before the procedure.
*Warfarin- Spinal puncture is contraindicated during warfarin therapy.
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*Aspirin and Nonsteroidal Anti-inflammatory Drugs (NSAIDs) . Reversal of drug effect on

platelet function requires stopping the drug for approximately 10 days for aspirin and for 48 h
for NSAIDs.
Ticlopidine/Clopidogrel ASRA guidelines suggest discontinuing ticlopidine 14 days prior to a

spinal or epidural procedure and discontinuing clopidogrel 7 days prior to the procedure.
Abciximab, Eptifibatide, and Other Platelet Glycoprotein Iib/IIIa Inhibitors
ASRA guidelines recommend avoiding spinal or epidural procedures until platelet function is
normal. Similar guidelines are reasonable for performing LP.
Direct Thrombin Inhibitors (e.g., Argatroban, Bivalirudin) ASRA guidelines recommend

against performing spinal or epidural anesthesia in patients receiving thrombin inhibitors.
Oral Factor Xa Inhibitor (e.g., Rivaroxaban)
LP should be avoided in patients receiving this drug

USU9OIDk2
Which among the following combination regarding the channelopathies is not correct
a) Paramyotonia congenital-Sodium Channel

b) Hyperkalemic periodic paralysis- Sodium channel
c) Benign neonatal familial convulsions –K channel
d) Familial hemiplegic migraine 2- Calcium channel
Correct Answer: D
Explanation
Explanation
Examples of Neurologic Channelopathies
Channel
Category Disorder
Type
Episodicataxia-1 K
Ataxias Episodicataxia-2 Ca
Spinocerebellar ataxia-6 Ca
Familial hemiplegic migraine 1 Ca

Migraine
Familial hemiplegic migraine 2 Na
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Benign neonatal familial convulsions K

Epilepsy
Generalized epilepsy with febrile convulsions plus Na
Hyperkalemic periodic paralysis Na

Periodic
paralysis Hypokalemic periodic paralysis Ca
Myotonia ncludec Cl
Myotonia
Paramyotonia congenita Na
Jervell and Lange-Nielsen syndrome (deafness, prolonged QT

Deafness K
interval, and arrhythmia)
Autosomal dominant progressive deafness K
Autoimmune
Kv1
Limbic encephalitis
Kv1
Acquired neuromyotonia
Paraneoplastic Ca (P/Q
Cerebellar ataxia type)
Lambert-Eaton syndrome Ca (P/Q

type)

USU9OIDk3
Which of the following antiepileptic drug acts through opening of K+ Channels
a) lamotrigine
b) topiramate
c) zonisamide
d) ezogabine
Correct Answer: D
Explanation
Antiepileptic drugs appear to act primarily by blocking the initiation or spread The mechanisms
include inhibition of Na+-dependent action potentials in a frequency-dependent manner (e.g.,
phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide, rufinamide),
inhibition of voltage-gated Ca2+ channels (phenytoin, gabapentin, pregabalin), facilitating the
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opening of potassium channels (ezogabine), attenuation of glutamate activity (lamotrigine,
topiramate, felbamate), potentiation of GABA receptor function (benzodiazepines and
barbiturates), increase in the availability of GABA (valproic acid, gabapentin, tiagabine), and
modulation of release of synaptic vesicles (levetiracetam).
Mechanisms of Action of Antiepileptic Drugs
* The mechanism of action of action of various antiepileptic drugs are listed below
* Inhibition of Na + -dependent * Phenytoin, carbamazepine, lamotrigine, topiramate,

action potentials zonisamide, lacosamide, rufinamide
* Inhibition of voltage-gated Ca 2
* Phenytoin, gabapentin, pregabalin
+ channels
* Attenuation of glutamate
* Lamotrigine, topiramate, felbamate
activity
* Potentiation of GABA receptor

* Benzodiazepines and barbiturates
function
* Increase in the availability of * Valproic acid, gabapentin, tiagabine [AIIMS

GABA NOV-2005***]
* Modulation of release of
* Levetiracetam.
synaptic vesicles
Drug adverse effect
* Diplopia
* Phenytoin –Level increased by isoniazid, sulfonamides, * Ataxia

fluoxetine. Half life is 24 h*
* Hirsuitism
* Gumhypertrophy
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* Ataxia
* Diplopia
* Carbama zepine- Level increased by erythromycin,
propoxyphene, isoniazid, cimetidine, fluoxetine. Half life is 10– * Aplastic Anemia
17 h
* Hepatotoxicity
* Hyponatremia
* Tremor, Ataxia
* Wt. Gain
* Valproic acid -. Half life is 15 hors * Hepatotoxicity
* Alopecia
* Hyperammonemia*
* Lamotrigine. –Half life is25 h
* 14 h (with enzyme-inducers) * Steven. Johnson syndrome
* 59 h (with valproic acid)
* Gabapentin -. Half life is 5-9 hours * Wt. Gain
* Wt. loss* [AIIMS

* Topiramate –also used in Lennox-Gastaut syndrome. Half life MAY-2006***], glaucoma
is 20–30 h
* Renal stones, hypohydrosis
* Wt. loss*
* Felbamate – Increases phenytoin, valproic acid, active
* Aplastic Anemia
carbamazepine. Half life is 16-20 hours
* Hepatic failure
* Zonisamide-. Half life is 50-68 hours * Renal stones, hypohydrosis

USU9OIDk4
A patient presented with sudden onset of quadriparesis.His MRI brain revealed
features suggestive of Central Pontine Myelinolysis.Which of the following is false
regarding CPM
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a) quadriplegia
b) pseudobulbar palsy
c) locked in state
d) associated with rapid correction of hypocalcemia
Correct Answer: D
Explanation
Central Pontine Myelinolysis
* This disorder typically presents in a devastating fashion as quadriplegia and pseudobulbar

palsy-locked in state most cases are associated with rapid correction of hyponatremia or with
hyperosmolar states
ANTERIOR CHOROIDAL ARTERY OCCLUSION
Anterior Choroidal Artery (AIIMS NOV-2012***) arises from the internal carotid artery and
supplies the posterior limb of the internal. The complete syndrome of anterior choroidal artery
occlusion consists of contralateral hemiplegia, hemianesthesia (hypesthesia), and homonymous
hemianopia. Anterior choroidal strokes are usually due to situ thrombosis. It is prone for
iatrogenic occlusion during surgical clipping of aneurysms.

USU9OIDk5
Flibanserin, originally developed as an antidepressant, has been approved by the FDA as a
treatment for low sexual desire in
premenopausal women.What is the mode of action of this drug
a) a postsynaptic agonist of serotonin receptor 1A and antagonist of serotonin receptor 2A,

b) a postsynaptic antagonist of serotonin receptor 1A and antagonist of serotonin receptor 2A,
c) a presynaptic agonist of serotonin receptor 1A and antagonist of serotonin receptor 2A,
d) a presynapticantagonist of serotonin receptor 1A and antagonist of serotonin receptor 2A,
Correct Answer: A
Explanation
Flibanserin, originally developed as an antidepressant, has been approved by the FDA as a

treatment for low sexual desire in
premenopausal women. Flibanserin, a postsynaptic agonist of serotonin receptor 1A and

antagonist of serotonin receptor 2A,
increases sexual desire and reduces resultant stress in women with HypoSexual Desire
Disorder (HSDD) with few adverse effects.
Flibanserin may boost sex drive in women who experience low sexual desire and who find the
experience distressing. The drug
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should be discontinued if there is no improvement in sex drive after 8 weeks. Potentially serious
side effects include low blood
pressure, dizziness, and fainting, particularly if it is mixed with alcohol. Other common adverse
events include dizziness, nausea,
fatigue, sleepiness, and insomnia. Health care professionals and pharmacies dealing with
flibanserin have to undergo a
certification process, and patients need to submit a written agreement to abstain from alcohol.
MORE FACTS-NIMHANS 2014
George Phillip Cammann -Famous physician: In 1852 he invented the modern binaural
stethoscope. He never patented it, as he believed the instrument's design should be
freely available
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Review in
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NIMHANS - DM Neurology -

a) Anterior ischemic optic neuropathy

MORE NIMHANS FACTS- NIMHANS 2000

Medial medullary syndrome is also known as inferior alternating syndrome , hypoglossal

Paralysis of arm and

Pulmonary wedge pressure is indirectly a Left atrial pressure

The substance found primarily found in tendons is collagen

The speciﬁe substrate for oxidative phosphorylation is ADP

a) Lambert Eaton myasthenic syndrome

MORE NIMHANS FACTS-NIMHANS 2000

Tumour thought to arise from the chorionic villi

• The benign tumour

a) Rise of CSF protein > 150 mg/dL

Bloody Tap SAH

Opening pressure Normal Raises

Serial samples Clearance uniform

Supernatant with prompt

Crenation Less common Common

1 mg per 100 Higher protein level due to irritating eﬀect

MORE NIMHANS FACTS-2000

Sensitivity is a measure of - True positive

* The term sensitivity was introduced by Yerushalmy.

* An ideal screening test should be 100% sensitive and 100 % speciﬁc

Sandﬂy acts as a vector to all of the following diseases

Arthropod-borne diseases FOR NIMHANS

Arthropod Diseases transmitted

1. Mosquito Malaria, ﬁlaria, viral

2. Housely Typhoid and paratyphoid

3. Sandﬂy***** Kala-azar, oriental sore,

4. Tsete ﬂy Sleeping sickness

5. Louse Epidemic typhus, relapsing

6. Rat ﬂea Bubonic plague, endemic

8. Reduviid bug Chagas disease

9. Hard tick Tick typhus, viral

10. Soft tick Q fever, relapsing fever

11. Trombiculid Scrub typhus, Rickettsial-

12. Itch-mite Scabies

13. Cyclops Guinea-worm disease, ﬁsh

14. Enteric pathogens

*Dysphasia refers to congenital or developmental languagedisorder and is distinct

*Dysarthria refers to disorder of articulation of single sounds.

*Paraphasic speech refers to the presence of errors in the speech output .

*Dysphonia refers to disorder of sound production as would be expected in palatal palsy

MORE NIMHANS FACTS-NIMHANS 2000

The syndromes associated with 3 rd nerve are summarised below

* Site – supr. cerebellar

* Site - Red nucleus

* Site – Supr. cerebellar

* Site – Cerebral peduncle

4. Weber’s * Eﬀect – Ipsilat – 3 rd N.

The etiology of an isolated, pupil-sparing oculomotor palsy is diabetes [AIIMS

STROKE WITHIN POSTERIOR CIRCULATION

Ataxia telangiectasia is associated with Spino-cerebellar atrophy,LYMPHOMAS and

* It is an autosomal recessive [AI - 2012***] disorder, presents with telangiectatic lesions

a) Thyroid stimulating hormone (TSH)

MORE NIMHANS FACTS-NIMHANS 2000

Viral meningitis with reduced CSF sugar is seen in Coxsackie virus

Hypoglycorrhachia is generally deﬁned as a cerebrospinal ﬂuid glucose concentration of

HYPOGLYCORRHACHIA is uncommon in central nervous system syndromes of viral etiology,

simplex, and eastern equine encephalitis.

Temporal lobe epilepsy is treated by VALPROATE and carbamazepine

• Asperger syndrome or Asperger's syndrome or Asperger disorder is an autism spectrum

•Individuals with AS often have excellent auditory and visual perception

•Hand stereotypes are typical, and breathing irregularities such as hyperventilation,