MS 1 Board Exam Reviewer 1

Sympathetic = Adrenergic resembles EPINEPHRINE

Parasympathetic = Cholinergic

Sympathetic Nerve:
Stimulates the sweat glands to produce more
Professor: Cantuba sweat (diaphoresis)
The skin is cold and clammy
Neuro-endocrine: Increases gastric secretion and decreases
- Stressor hypothalamus gastric motility
o Sympatho-adrenal medullary Urinary bladder muscles relax anuria
Diaphoresis Pupils dilate increase in visual acuity
Increase BP
Increase PR o Adrenal-Cortex (secretes
Increase rate and depth in glucocorticoids/steroids,
breathing mineralocorticoids/aldosterone)
Pallor Promote gluconeogenesis
Cold and clammy skin formation of glucose from fats
Anorexia and protein increased
Diarrhea protein catabolism negative
Constipation (-) nitrogen balance
Urinary frequency, oliguria or Weight loss and body weakness
anuria Promotes fluid and sodium
Weight loss and body weakness retention and excretion of
Transient hyperglycemia potassium oliguria
Increase in visual acuity
<400ml of urine output
for 24 hours = Oliguria
Adrenal Glands (located above the kidneys)
<100 ml of urine output
- Secretes cateholamines (in the adrenal
for 24 hours = Anuria
medulla), epinephrine and norepinephrine
o Epinephrine
o Neurohypophyseal
Dilates the coronary arteries,
Posterior pituitary gland
cerebral arteries, pulmonary
ADH and Oxytocin
blood vessels
Anterior FSH, LH, ACTH,
Constricts the peripheral
Melanocyte stimulating
arteries
hormone (MSH), SH
When secreted increases
cardiac output, myocardial
Stress response / SMR / SAMR / GAS
perfusion, and increases PR
Bronchial dilatation
ENDOCRINE SYSTEM
increases respiration
(hyperpnea)
Hypoactive secretion
Constriction of the arteries of
Congenital absence of endocrine glands
the skin decreased blood
Hypoactivity
supply pallor
Idiopathic
Promotes glycogenolysis
breakdown of glycogen to
Hyperactive secretion
glucose in the liver transient
Presence of tumor within or outside the gland
hyperglycemia
 MS 1 Board Exam Reviewer 2

Failure of the liver to deactivate / excrete o Nursing responsibilities when giving

hormones these ADH
Pitressins oily preparations
Decreased amount of pituitary gland give deep IM
- Pituitary dwarfism (dwarf, mentally retarded, lipodystrophy rotate site of
genital atrophy) administration
- Frohlicks syndrome (“Wizened old man”)
- Simmond’s disease Vasopressin Tannate
- Pituitary cachexia Vasoconstrictor increases BP
o Provide commercially prepared growth
hormone Desmopressin Acitate and
o Somatrem / Protropin Lypressin Acetate given
o Somatropin / Humatrope through nasal spray

Increased amount of pituitary gland Clofibrate (Atromid S; Clo 5)

- Acromegaly “epiphyseal line”
- Before closure of the epiphyseal line
=continued growth
- After closure of the epiphyseal line = stopped
growth
- Increased bone thickness
- Hypertrophy of the soft tissue
- Enlargement of the cartilages (enlarged nose,
ears)
- Deepening of the voice
- Prognathism protruding jaw
- Lengthening of the chin
Hypophysectomy – surgical removal of the pitruitary
gland
Somatostatin, Sandostatin, Octreotide/Actreotide
per SQ to control the production of the growth
hormone
Diabetes Insipidus
- Disorder in water metabolism due to the
decreased supply of Anti-diuretic hormone
(ADH)
- Prevents tubular reabsorption of water
- polyuria polydipsia diluted urine
decreased specific gravity increased serum
osmolality increased Na (135 – 145 mEq/L)
o Provide commercially prepared ADH
Pitressin Tannate
Vasopressin Tannate
Desmopressin Acitate
Lypressin Acetate
anti-lipidemic; antidiuretic
effect
SIADH
- Increased production of antidiuretic hormone
(ADH)
- Causes fluid retention (hypervolemia) which
increases the blood pressure and can cause
headache
o Increased renal perfusion and enhances
glomerular filtration rate which
increases urine output (NO LEG EDEMA
CAN BE PRESENT)
- Dilution which causes dillutional hyponatremia
- Decreased osmolarity of fluids into the cells
o Cerebral edema increased ICP
o Cellular overhydration
- Treatment:
o Stop the gland with Cobalt therapy
o Destroy the gland through surgery
o Inhibition of the production of ADH
Demiclocyline / Declomycin
ADRENAL CORTEX
Cushing’s Disease
- Result of hyperactive adrenal cortex
- Presence of moon face – “moon facies”, round
acne and oily appearance
- Hirsutism – hair growth
- Virilism - musculinization
- Buffalo hump
- Increased sugar, salt and sex hormones
 MS 1 Board Exam Reviewer 3

o Symptoms of hyperglycemia Moon - Diagnosed through VMA (Vanillylmandellic

face and Buffalo hump due to abnormal Acid)
fat distribution o Blood 0.2 – 0.9 mg/dl
o Protein catabolism tissue starvation, o Urine 0.2 – 7mg / 24 hours
muscle wasting trunchal obesity –
slender it Parathyroid Hormone (PTH)
o Fluid retention hypervolemia - Necessary for the absorption of Calcium and
increased BP, increased sodium and Phosphorus
decreased potassium - Essential for blood coagulation
o Increased sex hormones virilism, - Regulate cardiac rhythmicity
masculinization, hirsutism - Hypoparathyroidism
o Hypocalcemia
Addison’s Disease o Tetany
- Decreased sugar, salt and decreased sex Unctrollable spasms
hormones (hyperirritability)
o Hypoglycemia (+) Chevostek’s sign (Uilateral
o Decreased fluid retention spasm from the tapping of the
hypovolemia decreased BP, facial nerve)
decreased sodium and increased (+) Troussou’s sign (carpopedal
potassium myocardial irritability spasm as a result from the
dysrhythmias cardiac arrest occlusion using the BP cuff for
o Absence of pubic/axillary hair 1-2 minutes)
- Decreased steroid / glucocorticoid o For calcium supplementation:
o Stimulation of the amount of the Seafoods, cabbage, sardines
pituitary gland ACTH melanocyte NOT MILK, CHEESE OR DAIRY
stimulating effect tan complextion PRODUCTS because they have
“Bronze skinned” HIGH PHOSPHORUS CONTENT
which is dangerous for this type
Conn’s disease of client
- Adenoma benign tumor at the adrenal cortex EGGS ARE NOT ALLOWED AS
- AKA – Primary Aldosteronism WELL
- Hyperactive Calcium carbonate, Lactate,
- Increased production of aldosterone Chloride, Gluconate
Given after meals with
ADRENAL MEDULLA Vitamin D
Vitamin D (dihydrotachysterol
Pheochromocytoma Hytakerol, Calciferol, Calcifidiol,
- Hyperactive production of catecholamines Calcitriol, Tocopherol,
- Signs and symptoms: Menadione, Phytonadione)
o Hypertension
o Headache Isthmus
o Hyperglycemia - T3 – Tri-iodothyronine
o Hypermetabolism - T4 – Thyroxine
o Hyperhidrosis (Profuse sweating) - Thyrocalcitonin
- Treatment
o Cobalt therapy Anterior Piituitary gland trophic area target organ
o Adrenalectomy TSH thyroid gland T3 and T4
ACTH adrenal cortex SSS
 MS 1 Board Exam Reviewer 4

o Only scans the iodine uptake

Diagnostic Tests for Thyroid disorder Hypothyroidism

- PBI (Protein Bound Iodine) - According to onset:
o To evaluate the amount of iodine o Cretinism – onset of hypothyroidism
attached to the protein molecule of the during childhood
blood (4-8 ug%) = microgram percent o Myxedema – onset of hypothyroidism
o 2-3 days before the test, the client during adulthood
should not take any food or drug with - According to cause:
iodine o Primary – thyroid gland (T3 and T4)
- T3 and T4 det o Secondary – anterior pituitary gland
o To evaluate the level of T3 and T4 in the (TSH)
blood (T3 = 70-120 ug%) best influences - Treatment
body metabolism; (T4 = 4.7 – 11 ug%) o Prepare commercially prepared thyroid
o The result is directly proportional to extract thyroid medication
thyroid function Proloid (Thyrodinine)
- TSH test (Thyroid stimulating hormone test) Cytomel
o The result is inversely proportional to Synthroid
thyroid function (0.4-6.11 ug/ml) Euthroid
- BMR (Basal metabolic redetermination) Thyrolar
o O2 consumption at rest Thyrax
o Client should have a good night’s sleep Eltroxine
(rested the whole night with low Thyroxine
anxiety or none at all) Levothyroxine
- TBMR (Theoretical basal metabolic Levothyronine
redetermination)
o Theoretic cal = PP + PR/min – 111 Grave’s disease / Toxic Goiter
o Not conclusive, and not definitive and - LATS (Long-acting thyroid stimulator) gamma
only a hypothetical estimate globulin (iodine accumulation and thyroid
o Normal value (20-30) hyperplasia) Triad symptoms = Goiter, eye
- RAIU (Radioactive Iodine Uptake) signs, hyperthyroidism (elevated T3 and T4)
o Uptake 15-40% o Eye signs:
o Urine 40-80% Exopthalmus (protrusion of the
o Prior to procedure, no food or drugs eyeballs)
with iodine Proptossis (displacement of the
o RAI cocktail 24 hour urine 2-4 eyeball)
hour scanner Lid lag
o Normal uptake of iodine from the 6 Infrequent blinking
millicurees should be 0.9 – 3.8 Fixed stare
millicurees Periorbital edema (edema
o Normal urine excretion of iodine should around the eyelids)
be from 2.4 – 4.8 millicurees (inversely Von Graife (failure of the
proportional in result compared to eyelids to follow the movement
uptake) of the eye when the patient
o HOWEVER THE VALUES VARY looks down)
DEPENDING ON THE AMOUNT o Dalyrimple Sign
INSTILLED INTO THE PATIENT o Hyperthyroidism
- Thyroid scan Voracious
 MS 1 Board Exam Reviewer 5

High metabolism Sub-total thyroidectomy –

Over excitability of the SNS partial removal of the thyroid
Tremors gland
Diaphoresis Thyroid lobectomy – removal of
Palpitation a lobe of the thyroid gland
Nervousness Isthmusectomy – removal of
Constipation (due to the isthmus
SNS stimulation) To prevent hypothyroidism
- EPS anterior pituitary glands after surgery, provide Proloid
- NON-TOXIC GOITER CAN BECOME TOXIC (Thyrodinine) for life
ANYTIME (probably due to stress, infection, o Nursing responsibilities
pregnancy, exposure to cold) Post-operative:
- Treatment modalities: Establish a patent
o Anti-thyroid preparation – prevent the airway through
synthesis of T3 and T4 by blocking the positioning (semi-
utilization of iodine (e.g. Tapazole - fowler)
Methimazole, PTU – Prophylthiouracil,
Neomercazole – Carbimazole) Not HIGH FOWLER
Agranulocytosis because it can cause
To assess for PTU toxicity is tension to the neck
differential count 2nd best is muscles and can strain
CBC the suture line (Collar
line suture / curvilinear
o Iodine preparation – Lugol’s solution, suture) bleeding
Potassium Iodide Saturated Solution
(KISS / SSIK) reduces the vascularity Remind to do deep
and increases the firmness of the gland breathing and coughing
and promote storage of T3 and T4 exercises

o Adrenergic blocking – controls the Promote adequate

symptoms of tremors, HPN, tachycardia nutrition, fluid and
electrolyte balance
o RAI (Radioactive iodine) (after client is fully
awake and return of
o Surgery gag reflex) – gag reflex
Provide high caloric diet to is checked using a
restore the lost glycogen tongue depressor and
reserve and to satisfy the note for the contraction
voracious appetite of the client of the pharyngeal
Provide calm and restful muscle and rising of the
environment palate
Exopthalmus will not regress
before and after surgical After 6-8 hours of
treatment anesthesia, the client
Sistrunk – surgical removal of a should be able to
thyrooglossal cyst urinate (if not, check
Total thyroidectomy – removal the bladder for
of the entire thyroid gland distention)
 MS 1 Board Exam Reviewer 6

Can be caused by
bleeding
Encourage early Tracheobronchial
ambulation to shorten constriction
the convalescent period Laryngospasm
and prevent post- Laryngeal edema
operative complication PREPARE FOR AN
(as soon as the vital EMERGENCY
signs are stable; if still TRACHEOSTOMY /
unstable then START AN ARTIFICIAL
ambulation should be AIRWAY –
discouraged) – remind Tracheostomy set by
to support the head the bedside
and the neck to prevent Thyroid crisis / thyroid storm
flexion and extension Can be caused by pre-
op
o Surgery Complications anxiety/stress/psycholo
Tetany gical effect
Hoarseness (1 accidental Can be caused by post-
recurrent laryngeal nerve operative infection
removed; edema of the glottis)
Aphonia (2 laryngeal Increased T3 and T4 (Hyperthyroidism) anti-thyroid
nerve/bilateral removed) preparation for 3 months Euthyroid state (state of
Will require speech normal thyroid function) Operation (post-op
therapy stress / compensatory mechanism) Increased T3 and
Bleeding T4 (fever and tachycardia) = earliest sign is FEVER due
Pre-op – non- to RESPONSE TO INJURY
administration of
Lugol’s solution Basedoni
Post-op – failure to tie / Parry’s disease
ligate bleeders Thyrotoxicosis
Continuous oozing of
blood that can cause Diabetes (Type 1 – Juvenile, Insulin-dependent / Type 2
airway obstruction - Adult-onset, Non-insulin dependent)
Assess by checking the
dressing; check for Tests for Glycemia
dampness behind the - FBS
neck/nape; listen to the - RBS
complaint/verbalization - PPBS
of the client post-op - Hgt
(complain of tightness - DGTT
around the neck or Tests for Glycosuria
chocking sensation); - BT, CT
evaluate vital signs
(rapid, weak, feeble, Insulin
thread pulse; rapid but - Rapid (10-15 minutes after administration)
shallow RR) o Novolog
Respiratory obstruction o Humalog
 MS 1 Board Exam Reviewer 7

o Aspart - Thiazalidindiones – foster the receptors release

o Lispro preleace of the beta cells (e.g. Pioglitazone,
Rosiglitazone)
- Short (30 minutes – 1 hour onset; 6-8 hours - Contraindications:
duration; given before breakfast) o Pregnancy
o RI (Regular insulin) o Signs of stress
o Humulin R o Allergic reactions
o Crystalline Zinc o Liver disease / kidney disease
o MC Actrapid o Infection (e.g. gangrenous toe)
o Velocuiln o Surgery
o Novolin RV o THESE WOULD REQUIRE A SHIFT TO
- Intermediate THE USE OF INSULIN
o Monotaral
o NPH – Neutral NEUROLOGIC DISORDERS
o Protamine Hagedorn
o Globin Neurological assessment parameters:
o Novulin L - Level of consciousness
o Lente o Both cerebral hemisphere are the
o Humulin N centers for consciousness
- Long o Center for wakefulness is the RAS which
o Ultralente is located at the center of the brainstem
o Lantus o Any structural lesion compressing both
o Glargine hemispheres will cause altered LOC:
o PZI – Protamine Zinc Tumor
o Humulin U Hematoma
Abscess
Route of administration o Metabolic depression
- Subcutaneous Hypoglycemia
- IM Hypoxia
- IV Fluid and electrolyte imbalance
Toxic/chemicals
Diet/Nutrition o Tool/device
- Complex sugars is better for diabetic clients Glasgow coma scale
because it takes time for these sugars to Eye opening
breakdown, but do not remove simple sugars Verbal response
from the diet of the client Motor response
- Exercise will utilize stored insulin and would call GCS = 3-4 deep coma
for a reduced dose to prevent hypoglycemia; if GCS = below 7 and 5-6
dose cannot be reduced then remind patient to coma
take snacks in between o It is possible for a client to have
decorticae and decerebrae at the same
Oral Hypoglycemic Agents time due to both parts of the brain
- Sulfonylureas – stimulates the beta cells to responsible to the reaction are affected
secrete endogenous insulin (e.g. Diabinase, o When checking for pupillary reaction
- Biguanide – increase uptake of glucose in the make use of a opthalmoscope; if not
cells (e.g. Metformin, Glucophage, Phenformin) available then make use of a flashlight
- Alpha-glucosidase inhibitors (Acarbose,
Precose, Glyzet) - Speech of Problem

o Motor speech center is Brochas
o Sensory speech center is Wenickes
o Occipital lobe is for vision
o Temporal is for hearing, balance
o Frontal is for activity, attitudes and
personality
o Aphasia
Motor / expressive – unable to
talk and unable to write =
affectation is in the frontal lobe
Sensory / receptive – unable to
understand written or spoken
words = affectation of the
occipital (visual) or temporal
(hearing) lobe
Global aphasia – combination of
motor/expressive and
sensory/receptive
o Ipsilateral symptoms – on the same side
of the lesion
o Contralateral symptoms – on the
opposite side of the lesion
o Pyramidal tract – controls the fine
motor movement of the body
o Extrapyramidal tract – coarse motor
movement
o Monoplegia – plegia of one extremity
from both sides
o Visual acuity is contralateral
- Gait
o Ataxic gait – unable to remain steady
with feet together = affectation at the
cerebellum
o Dystonic gait – non-directive movement
seen among clients with muscle
atony
o Dystrophic / waddling gait – client
moves with feet apart and with weight
moves from the sides
o Hemiplegic – seen in clients with
disorders of the pyramidal tract (foot
dragging)
o Scissors gait – short, slow steps and legs
are alternating with each other seen
in clients with spastic paralysis
o Steppage gait – high exaggerated steps
affection of the lower motor neuron
MS 1 Board Exam Reviewer 8
- Reflexes
o Knee-jerk
o Bicep
o Tricep
o Babinski – abnormal response is the
fanning of the toes; normal response is
the flexion of the toes
o Chaddocks – squeeze the calf muscle
dorsiflexion of the big toe is pathologic
o Gordons – stroke the inner aspect of
the leg dorsiflexion of the big toe is
pathologic
o Kernigs – flexion and extension of the
lower extremities pain on the
hamstring is pathologic
o Cremasteric – stroke the inner aspect of
the thighs and observe for testes
elevation; make use of a tongue
depressor
o Brudzinski
o Binda
- Coordination
o Romberg’s test – stand with feet
together with closed eyes and
determine if the client will fall to one
side
- Cranial Nerves
Diagnosing a Neurological Disorder
- Lumbar Puncture
o Local anesthesia (Lidocaine, Xylocaine,
Novocaine, Tetracaine HCl, Marcaine
o Positioning – “C” position, shrimp
position, fetal position
o Site of the puncture (L3-L4; L4-L5; L5-
S1) decreased chances of hitting a
spinal nerve which can cause spinal
cord injury
Normal CSF pressure (75-200
mmH20)
- Quickenstedt / Spinal manometric / Spinal
dynamic test
o CSF pressure jugular vein 6-12
seconds
o Tests for sub-arachnoidal obstruction
 MS 1 Board Exam Reviewer 9

o Normal volume of CSF (90-150 ml) o Provide hair shampoo prior and after
o Normal color of the CSF – colorless; procedure
yellow CSF – Xanthochromia / old blood
clot - EMG
o Normal transparency – clear o Measure of the electrical activities of
o CSF CHON = 15-45 mg% elevates will the muscle
result in tumor, multiple sclerosis, o Done to diagnose muscle dystrophy and
gamma globulin peripheral nerve injuries
o CSF glucose = 50-80 mg% glycorakia o Needles attached to the peripheral
(decreased values = CSF infection) muscles that evaluate the muscle at
o CSF chlorides = 118 – 132 mEq/L rest and during activity
(decreased values = CSF infection) o AKA – Jolly’s test / Nerve Conduction
o CSF WBC = 0-8 ml (increased values = Velocity Test (NCV)
leucocytosis)
o CSF gamma globulin = 3-9 % elevates - CT Scan
and can result in multiple sclerosis (IgG) - MRI
- Skull X-ray
- Pneumo-encephalogram (Air / O2)
o During a lumbar pucture aspirate Scanning using Thalium, Technelium and
20ml of CSF and introduce 20ml of O2 Neohydrin all require preparation
O2 will be seen in the brain
Parkinson’s Disease (Paralysis Agitans)
- Cerebral Angiogram - Risk factors:
o Previous history of encephalitis
- Myelogram o Head trauma
o X-ray of the sub-arachnoidal spaces o Smoking
after giving a dye (myodin / o History of atherosclerosis
pantopaque) intraspinous / o Hypertension
intrathecal o Carbon monoxide exposure
o The use of contraceptive spills
- EEG - Neuronal degeneration of the substantia nigra
o Measurement of the electrical activities of the midbrain of the midbrain
of the brain - inhibitory neurotransmitters
o There should be no stimulant or - dopamine
depressant to the client to observe the - impairment of the ________ tract
brainwaves completely o weakness of the muscles
o Do not administer anti-convulsant o mask-like facies
(Phenytoin – dilantin, Na Luminal – - imbalance of voluntary and
Phenodar, Carbamazepine – Tegretol, neurotransmitters
Clonazepam – Klonopin) 24 hours prior o impairement of the muscle response
to EE; HOWEVER IF THE CLIENT IS A for speech (drooling of saliva /
CASE OF EPILEPSY OR SEIZURE THEN microphonia)
THE MEDICATION IS STILL CONTINUED - tremors pin rolling
DESPITE THE PROCEDURE – Prevents - rigidity
Status Epilepticus o cogwheel
o Advise a regular diet prior to procedure, o micrographia
because a state of hypoglycemia can - bradykinesia / dyskinesia (shuffling /
affect the result Propulsince / Festination gait
 MS 1 Board Exam Reviewer 10

- Treated with Levodopa the symptoms) and cholinergic crisis

o Dopar (worsening of the symptoms)
o Larodopa
o Carbidopa – Sinemet - Early stage
o Amantadine HCl – Symmetrel o Weakness of ocular muscles Ptosis
o Trihexyphenidyl – Antane (earliest manifestation), diplopia
o Benztropine Mesylate – Cogentin o Facial and lingual muse
o Biperidine HCl = Akineton “snarling smile”
- Treated with Bromocriptine / Parlodel – Swallowing
stimulates the substancia nigra to release Mastication/chewing
endogenous dopamine
- Treated with MAOI (Monoamine Oxydase
Inhibitor) - Treatment
o Eldepryl o Thymectomy – surgical removal of the
o Seligiline thymus located in the supra sternal
o Carbox notch
- Surgery (Stereotactic Guided) o Thymus gland T cells antibody
o Halanotomy production = removal will stop the
o Pallidotomy antibodies from preventing the
- Nursing care stimulation of the receptors
o Improve muscle strength due to o Thymoma – growth on the thymus
impaired physical mobility gland
o Provide something to hold on to focus o Plasmaphoresis – removal of the
action antibodies of the client to be replaced
o Maintain self-esteem by a donor plasma
o Avoid aspiration o Provide Anti-cholinesterase – increases
o Provide speech therapy or alternative acetylcholine uptake / secretion
communication techniques Watch for cholinergic crisis
o Treat possible constipation Underdose will result in
o Provide safety Myasthenia Crisis
Overdose will result in
Myasthenia Gravis Cholinergic Crisis (decreased
- Auto-immune disorder causing failure in the BP, PR, diarrhea, abdominal
transmission of impulses at the myoneural cramping) – treated with
junction due to a blockage or destruction of the anticholinergics (e.g. Atropine
acetylcholine receptor due to produced Sulfate)
antibodies
Multiple Sclerosis
- Axons release excitatory neurotransmitter - Demyelination of the spinal cord
(Acetylcholine) normally attaches to the - Risk factors:
acetylcholine receptor of the muscle fibers o Auto-immune disease
muscle contraction o Post-viral disease
- In the absence of the excitatory transmission o Stress and pregnancy
muscle atony / weakness o Induced (drugs containing
- Diagnostic test amphetamines – shabu, reducing pills)
o Tensilon Test – used for diagnosing
myasthenia and also for differentiating Risk factors destroys myelin sheath replaced by
between myasthenia crisis (lessening of sclerotic patches of necrotic tissue trigger an
 MS 1 Board Exam Reviewer 11

inflammatory reaction formation of inflammatory o Steroid therapy (anti-inflammatory)

exudates inflammatory edema scarring / fibrosis may reduce the edema around the site
failure of the transmission in electrical impulses of demyelination; HOWEVER THE
- Charcot triad symptoms: SYMPTOMS ARE ONLY RELIEVED BUT
o Ataxic/spastic gait (due to the THE PATHOLOGY IS NOT CURED
demyelination of the cerebellum) o ABCR
Tremors (initially felt in the A – Avonex
lower extremities) B – Betaseron
o Nystagmus / Strabysmus / dysconjugate C – Copoxone
N – movement of the eyes from R – Rebif
side to side PREVENT PROLIFERATION /
S – eye towards the midline PREVENTS THE ACTIVIATION
D – eye away from the midline OF THE T-CELLS
Affects CN III, IV, VI)
Testing eye accommodation is GBS
testing CN III (Occulomotor) - Pathologic changes:
CN IV (Trochlear) – supplies the o Polyradiculoneuritis – demyelination of
superior oblique muscle of the several cranial nerves causing paralysis
eye of the ocular, oropharyngeal and facial
CN VI (Abducens) – supports muscles
the lateral rectus muscle of the o Peripheral neuritis – result of
eye demyelination of the peripheral nerves
o Scanning of Speech ascending paralysis
Result of demyelination of the o Autonomic dysfunction – Over
frontal lobe excitement or under excitement of the
- loss of sensation to pain, touch and pressure SYMPATHETIC and PARASYMPATHETIC
o Demyelination of the parietal lobe nerve fibers
- L-herniettes sign
o Whenever the client bends down, there Incidences: (Epidemiology)
is an electrical stimulation at the lower - Parkinsons more on MEN
trunk - Multiple Sclerosis more on WOMEN
o Demyelination of the mid-cervical - GBS affects BOTH
vertebrae - Myasthenia affects both but early for female
- Behavioral symptoms and late for males
o Euphoria (extremely happy)
o Apathy (unconcerned) CVA / Stroke / Apoplexy
- Cerebral ischemia causing a cerebral infarct
- Diagnosing of Multiple Sclerosis - Cerebral anoxia of more than 4 minutes can
o Done via Lumbar Puncture cause an irreversible brain damage that can
Elevated CSF protein and cause cerebral infarct
elevated Gamma Globulin (IgG) - Causative factors:
o MRI o Occlusive pathology
Evaluates the extent of CVA embolism – can be a result
demyelination of MI, endocarditis,
- Treatment dysrhythmias, embolus from a
o No known management fractured bone, embolus from a
o Supportive / symptomatic treatment malignant cell Sudden onset

CVA thrombosis – can be a
result of DM, atherosclerosis,
hypertension, smoking TIA
(nuchal or nape pain,
paresthesia or tingling
sensation, light-headedness,
syncope, transient loss of
speech, transient loss of
memory)
When TIA takes place,
CVA can occur after 4
weeks
o Hemorrhagic pathology
CVA hemorrhage – can be a
result from a long standing
hypertension, aneurysm
Stress, physical activity
- Signs and symptoms of CVA will depend on the
area of affectation
o There will be symptoms of Increased
intracranial pressure
Earliest manifestation
restlessness with hippus
(alternate dilatation and
constriction of the pupil)
o Papilledema / choked disc
o Projectile vomiting
o Headache / Cephalgia
o Pain in rising and whenever there is a
change in position
- Late signs of increasing intracranial pressure
(ICP)
o Cushing’s triad changes
Increased BP – increased
systolic with normal or
decreased diastolic – WIDENED
PULSE PRESSURE
Decreased PR
Decreased RR
Temperature – initially
increased due to cerebral
metabolism which later
deteriorates
- Causes of increasing intracranial pressure
MS 1 Board Exam Reviewer 12
o Factors that can increase the volume of
CSF (e.g. hydrocephalus, tumor
obstruction of CSF flow)
o Factors that can increase the brain
tissue bulk / brain tissue size (e.g.
meningitis, encephalitis, brain abscess)
o Factors that can increase cerebral blood
flow (e.g. coughing, sneezing, straining)
Increase in pCO2
(hypercabia/hypercapnea)
dilation of cerebral blood vessel
increase in cerebral blood
flow increase in ICP
- Management
o ASA (can cause bleeding; prolonged
prothrombin time)
Common discomfort – GI upset
o Aspilet
o Asperiptin
o Depyridamole
o Ticlopdine / Ticlid
o Clopidogrel / Clavix /Clovix
o Caumadin per orem – antidote Vit K –
is tested with PT
o Heprin SQ, IV – antidote Protamine
Sulfate – tested with PTT
o Streptokinase (Plasminogen activator),
Urokinase, Alteplase, t-PA (tissue type
plasminogen activator), Affokinase
Converts plasminogen to
plasmin causes lysis /
dissolution of the blod clot
Antidote – Aminocaproic acid
(Amicar)
o Cerebral decongestants
Mannitol – hyperosmolar
solution increases urine
output
Dexamethasone (only one that
can cross through the blood
brain barrier) – decreases
cerebral edema decreases
brain tissue bulk and size
o Mechanical ventilation / Ambu bagging
Reduce the level of pCO2
hyperventilation increased
RR (excretes CO2) decreased
 MS 1 Board Exam Reviewer 13

cerebral congestion If patient is to be turned to the

decreased ICP operated side, SHOULD NOT BE
MORE THAN 20 MINUTES
Brain Tumor because it can cause cerebral
- Originating from the brain tissue glioma edema
- From the cranial nerves neuroma DO NOT SUCTION THE CLIENT
- From the brain covering meningioma can increase ICP, mere
- According to location: insertion can trigger coughing
o Supratentorial – cerebrum, anterior 2/3 reflex (increase ICP)
of the brain If necessary,
o Infratentorial – cerebellum, brian stem, OROPHARYNGEAL
posterior 1/3 of the brain SUCTIONING CAN BE
- Earliest indicator of brain tumor DONE (not more than
PAPILLEDEMA 10-15 seconds) ;
- Treatment Nasopharyngeal is not
o Craniotomy done to avoid trauma
o Craniectomy which can cause CSF
o Radiation therapy leakage – HALO SIGN
- Incision Coronal / butterfly (PALE YELLOW RING ON
o Flap, burr hole A GAUZE OR PRESENCE
OF SUGAR IN THE
- Nursing responsibilities DRAINAGE)
o Do not place client in trendelenburg / Do not restrain the client
shock position Do not insert rectal tube, rectal
Abdominal content can thermometer and no manual
compress on diaphragm and extraction of feces can cause
can cause respiratory distress valsalva maneuver and vagal
o If patient has shock, place patient in (parasympathetic) stimulation
SUPINE for adequate cerebral perfusion increase ICP, severe
o Supratentorial surgery place patient hypotension, severe
on head of bed elevated 45 degrees bradycardia
(semi-fowler’s position) for venous Avoid constipation which can
return stimulate straining of the client
o Infratentorial surgery elevate the
bed only within 10-15 degrees (place a Disorders of the blood and blood forming organs
small pillow under the head but DO (Dyscrasia)
NOT PLACE THE CLIENT ON THEIR BACK o Decreased production of different
compression of the brain stem; place blood cells (Pancytopenia)
client on one side = on the unoperated o Overproduction of normal and
side to prevent decompression of brain defective cells
tissue) o Disorder of the spleen
After surgery, it is possible the o Defect in the coagulation mechanism
physician may not return the Hemophilia
bone flap 3-5 days after bone DIC
surgery because any surgery
can cause tissue trauma and - Diagnostic exams:
possible inflammation o CBC, Hgb, Hct
o BT, CT, PT
 MS 1 Board Exam Reviewer 14

o Erythrocyte index - Lymph Node Biopsy

o MCV = Mean corpuscular volume = size - Blood typing
of the RBC = <80 - >94 cu. microns
(microcytic / macrocytic) Types of Anemias (causes)
o MCH = Mean corpuscular hgb = hgb - Decreased erythropoiesis
content, rbc = <22 - >28 o Elements necessary for erythropoiesis:
micromicrograms (hypochromic / Fe – responsible for the
hyperchromic) pigment of the RBC
o MCHC = Mean corpuscular hct Folic Acid – necessary for the
concentration = 30-36 grams / 100 ml maturation of the cell
packed RBC B12 – necessary for the
o Coombs immune bodies adhere synthesis of the nuclei
rbc (hemolysis / agglutination) Vitamin C – necessary for the
o Schilling vitamin B12 absorption of iron
Cyanocobalamine CHON – necessary for the cell
P.o. RAVit B12 24 hour urine wall of the cell
(+, -) B12 o Absence of IRON – Iron Deficiency
(+) – normal Anemia
(-) – pernicious anemia (would Cells are microcytic,
require lifetime parenteral hypochromic (Microcytic,
administration of Vitamin B12) hypochromic anemia)
Gastric mucosa o Deficiency of FOLIC ACID – Folic acid
intrinsic factor B12 anemia
o Bone Marrow (BM) tap / Puncture / Cells are macrocytic,
Aspiration hyperchromic (Macrocytic,
Evaluate size, shape and hyperchromic anemia;
characteristic of the different Megaloblastic Anemia;
blood cells Pernicious anemia)
Poikilocytosis abnormality in
the shape of the cell - Increased hemolysis
Metarubricyte cell – cell with o Rate of RBC destruction is greater than
nuclease at maturity production (Hemolytic anemia)
RBCs do not have o Can be due to greater exposure to
nucleus at maturity ionizing radiation
o Management for BM puncture o Can be post-viral
Position the patient (supine if o Can be due to prolonged use of
anterior and prone or radical if penicillin
posterior) o Can be due to cross matched blood
Apply pressure to dressing at o Sickle-cell anemia falls under this
the site of puncture to prevent category
bleeding
For a child, the femur, uterus or - BM depression
long bones can be used but for o Hypoplastic anemia / Aplastic anemia
adults it cannot be used! o There is depressed / or inadequate
Because as one grows production of RBC or production of
older, the number of immature RBC
marrows in the long
bones decrease - Blood loss
 MS 1 Board Exam Reviewer 15

o Normocytic , normochromic anemia - Avoid cold environment (due to cold

o Can be due to menstruation, surgery intolerance)
- Avoid any sources of infection,
Decreased hemoglobin count reduction in the O2 crowded/congested areas, people with URTI
carrying capacity of the blood tissue hypoxia (due to leukopenia) PLACE CLIENT IN
Brain – restlessness, headache, irritability, REVERSE ISOLATION
syncope - Avoid any form of trauma or injury (due to
Heart – angina pain, increased PR, weakness, bleeding tendencies)
easy fatigability o Encourage the use of soft-bristled
Respiratory – tachypnea (increased RR), toothbrush, electric razors
dsypnea o Avoid constipation, forceful blowing of
GIT – anorexia, angular, angular cheilosis the nose, contact sports
Skin – pallow, brittle hair, intolerance to cold, o Limit the use of parenteral injections (if
brittle nails = spoon shaped koilonychias absolutely necessary, use the sharpest
needle)
Iron Deficiency Anemia - Blood transfusion
- Vinson-plummir syndrome o Packed RBC for decreased
o Dysphagia erythropoietin and increased hemolysis
o Atrophic glossitis o Fresh whole blood for the rest
o Stomatitis (inflammation of the oral - Surgical management
mucosa; also known as MUCOSITIS) o Haemolytic anemia – spleenectomy
- Beefy red tongue (spleen is the source of the abnormal
- Paresthesia – nerve cell degeneration (nerve blood cell)
cells need Vitamin B12 to regenerate) o Hypoplastic anemia / Aplastic anemia –
Bone marrow transplantations
Hemolytic Anemia Syngeneic BM – twin brother or
- Increased hemolysis of RBC sister donor
hyperbilirubinemia jaundice / haemolytic Allogeneic BM – from any
related or unrelated donor (as
Hypoplastic / Aplastic Anemia long as there is a compatible
- BM depression inadequate number of WBC leukocyte-antigen)
production leukopenia (symptoms of Autologous BM – donor is the
infection) / platelet (bleeding, melena, client himself and the BM is
hematuria, ecchymosis) harvested during
remission/absence of
Blood loss symptoms
- Symptoms of hypovolemia
- Hypvolemia (15-25% of the circulating blood Polycythemia Vera
volume is lost; normal blood volume is 4-6 liters - Primary – result of hyperproliferative BM of
unknown cause
Management: - Secondary – result of tissue hypoxia
- Diet high in folic acid and iron
- Iron supplements Tissue hypoxia release of humoral erythropoietin
- Encourage adequate bed rest / reduce energy stimulates BM activity
expenditure - (increased cell acitivity increased cell
o Moderation of physical activity with metabolism increased temperature and
periods of rest weight loss // increased production of basophils
release of histamines pruritus)
 MS 1 Board Exam Reviewer 16

- Onset of the symptoms

increased erythropoiesis o Acute Leukemia – sudden short
- capillary congestion (redness of the skin duration (less than 6 months),
“Plethora”) predominant cells are the immature
- capillary engorgement (bleeding anemia) blast cells
- hemoconcentration o Chronic Leukemia – gradual, long
o HA – dizziness, blurring of vision duration, predominant cells are the
o HPN mature WBC (period of remission and
o Sluggish blood flow thrombus exacerbation)
formation
- compensatory hypertrophy hepa- - Predominant cells
splenomegaly o Acute / chronic lymphocytic Leukemia
o Acute / chronic myelocytic /
- Management myelogenous Leukemia
o Dilute the concentrated blood (increase
Bone Marrow granulocyte myeloblast
fluid intake)
myelocyte NEB
o Avoid venous stasis
o Inhibit BM activity (prepare Bone Marrow non-granulocyte monoblast
administration of Methotrexate / monocyte
Mexate – Antineoplastic / Anti-
metabolites) Lymphoid tissues (non-granulocyte) lymphoblast
o Prepare client for Blood phlebotomy – lymphocytes
opening of the vein to drain the blood Children – Acute Lymphocytic Leukemia

Leukemia Adults – Chronic Myelogenous Leukemia

- Uncontrolled/abnormal proliferation, - Management
multiplication of the immature white blood cells o Chemotherapy
(blast cells)
Multiple Myeloma
- Proliferation - Normal anatomy:
o increased activity of cells o Plasma cells secrete immunoglobulin
increase cell metabolism elevated (CHON) antibodies
temperature - MM
o Proliferation of abnormal plasma cell
o crowd / congest / accumulation in produces dysfunctional immunoglobulin
the BM (join pain and joint swelling) infection / hemoconcentration
/ hinder the production of RBC and (thrombus formation, HPN)
platelet [anemia & thrombocytopenia
bleeding] o Proliferation of abnormal plasma cells
secretion of osteoclast activating
o invade/infiltrate vital organs factor (increases bone destruction or
(splenomegaly, hepatomegaly, bone resorption or demineralization of
increased ICP, renal insufficiency, renal the bone) bone pain (skull >
failure) vertebrae > scapula > pelvis > femur)
calcium losses from the bone (brittle
- immature WBC blast cells prone to bones prone to pathological
infection fracture) // (hypercalcemia

hypercalciuria calcium crystallization
stone formation
- Diagnostic exams
o BM puncture / biopsy (most definitive)
o Bence-Jones Protein (determines
presence of protein in the urine)
most definitive LABORATORY TEST
o CBC with differential count (determines
infection)
o Hematocrit determination
o X-ray of the bones (possible fracture)
o Serum calcium (hypercalcemia)
o Calcium in the urine
Hodgkin’s / Malignant Lymphoma / Lymphosarcoma
- Cancer of the lymphoid organ with proliferation
of the lymphocytes
- Risk factors:
o (+) family history
o Post-viral disease brought about by the
Epstein-barr virus
o Exposure to environmental carcinogen
o Exposure to environmental pollutants
o Gender (incidence is high among males
before age 20 and after age 50)
o (+) Reed-sternberg cells
- Earliest manifestations:
o Painless enlarged lymph nodes
(lymphadenopathy)
- Systemic manifestations:
o Fever
o Weight loss
o Night sweats
- Management for localized enlargement
o Surgical excision and radiotherapy
Non-hodgkin’s lymphoma
- (+) peripheral lymph node enlargement
- (-) Reed-sternberg cells
GI Disorders
Disorders of the Oral cavity – review on your own
Esophageal Disorders:
Achalasia
MS 1 Board Exam Reviewer 17
- Absence / degeneration of the myenteric plexus
or the auerback plexus (no peristalsis –
aperistalsis)
- Food accumulation at the lower end of the
esophagus (Megaesophagus)
- Failure of the cardiac sphincter to relax
(Cardiospasm)
- Signs and symptoms:
o Increased compression at the sternum
due to the accumulation of the food
o Food will decompose at the area of
accumulation and will cause halitosis
o Chemical accumulation due to the
decomposition of food can cause
chemical esophagitis
Dysphagia
Odiphagia / Odinophagia
Pyrosis (heartburn)
Diverticulum
- Pouching / ballooning of a weak wall of the
esophagus
- Risk factor:
o Chronic esophagitis
o Upper abdominal trauma
- If pouching is in the upper 1/3 of the esophagus
Zenker / Pulsion diverticulum
- If pouching is in the middle 1/3 Traction
diverticulum
- If pouching is in the lower 1/3 Epiphrenic
diverticulum
GERD
- Inappropriate relaxation of the lower
esophageal sphincter causing the backflow of
the gastric content into the esophagus
- Risk factors:
o Pregnancy
o Obesity
o Caffeine, coffee intake
o Diet high in fat
o High level of estrogen
o Alcohol
o Smoking
Conservative Nursing Management of Esophageal
Disorders

- Remind to assume an upright position while
eating
- Remind to avoid eating/drinking two (2) hours
before retiring
- Remind to avoid coffee, smoking, alcohol, diet
high in fat
- Maintain an ideal body weight
- Avoid irritants such as spices in the diet
- Take small frequent feeding
- Avoid very hot or very cold drinks
- Render oral care
Specific management:
GERD
o Symptomatic relief
o Increase the pressure at the lower
esophageal sphincter
Use of urecholine
Bethanecol
Domperidone
Zenker Diverticulum
o Surgical removal of the esophageal sac
Traction Diverticulum
o Removal of esophageal sac via
Epiphrenic Diverticulum
o Removal of the esophageal sac via
Achalasia
o Esophagomyotomy – opening or the
division of the esophageal muscle fiber
o Cardiomyotomy – if the division
extends to the cardiac portion of the
stomach
o Hellers
o Nissen Fundoplication – fundus of the
stomach strapped around the sphincter
Meet the nutritional needs after esophageal
surgery is via TPN or Hyperalimentation
o Parenteral administration of nutrients
including glucose, lipids and amino
acids
o Nursing responsibility for client on TPN
Injected using the subclavian
vein because it is the most
stable site due to the shoulder
muscle
If TPN solution is hypertonic
with glucose content of more
MS 1 Board Exam Reviewer 18
than 10% then it is given via
Central line
If to be used for more than 10
days, TPN is given via central
line
Accurate regulation of TPN
(high flow rate will result in
hyperglycemia which can result
in hyperosmolar diuresis
glycosuria polyuria) – (slow
flow rate will result in spoiling
of the TPN because TPN
solutions are only good for 24
hours)
CBG monitoring (to assess the
risk for hyperosmolar diuresis
brought about by
hyperglycemia)
Monitor I and O
Monitor serum electrolytes
Insulin is the ONLY DRUG that
can be incorporated with the
TPN solution
o Most accurate assessment for
effectivity of TPN is BODY WEIGHT
CHANGES
o Assess for venous thrombosis
(manifested by pain and swelling at the
pain, neck or jaw where the TPN
catheter is inserted)
Lower Gastric Disorders:
Peptic Ulcer Disease
- Erosion of a circumscribed area in the GI tract
due to the digestive action of HCl acid and
pepsin
- Gastric ulcer = Rich man’s ulcer
- Duodenal ulcer = Poor man’s ulcer
- Possible sites of PUD (continuously bathed with
pepsin)
o Lower-end of the esophagus
(esophageal ulcer)
o Lesser curvature of the GI tract (gastric
ulcer)
o Upper-end of the duodenum
(duodenual ulcer)
- Protective barriers against pepsin
 MS 1 Board Exam Reviewer 19

o Mucin provides a protective film / “O” – prone to ulcer; high level

coat for the GI tract of pepsinogen which is acted
o Continuous blood supply of the GI tract upon by the gastric acid to form
prevent gastric anoxia pepsin
o Bile and pancreatic enzyme alkalinize “A” – prone to cancer of the
the pepsin to neutralize the acid of the stomach
GI tract
- Even with normal level of acid in the stomach, if - Sign and symptoms
the protective barriers are absent there can still o Gastric ulcer
be a possibility of Peptic Ulcer Disease (PUD) Mid-epigastric burning-knawing
- Changes in PUD pain
o Absence of gastric neutralizer Radiate to left epigastrum
o Gastric anopsia 30 minutes – 2 hours after
- Predisposing factors of PUD: meals
Weight loss
o Poor dietary habit (skipping meals; Food will aggravate
eating fast) – food serves as a buffer for Vomiting will relieve
HCl acid no food = no buffer ; eating Decreased HCl – hypochlorydria
fast = increased acid load into the Hematemesis (coffee ground
duodenum duodenal ulcer vomitus)
o Duodenal ulcer
o Stress (prolonged) parasympathetic Radiating to the right
response (vagal response) increase epigastrum
gastric secretions / motility 2-4 hours after meals
Food relieves the pain
o Ulcerogenic agent (Steroids, NSAIDS, No vomiting occurs
Salycylates) Weight gain
Increased HCl –
o Intake of gastric stimulants hyperchlorhydria
o Personality Melena (black tarry stool)
Type A person – highly
perfectionist, ambitions, - Management
competitive, aggressive o Decrease protein in diet, increase CHO,
individuals increase Fat (Polyunsaturated fat –
o Age vegetable oil, sesame oil)
Gastric ulcer – above 40 years CHON potent secretagogue
of age secretes HCl
Duodenal ulcer – 30-40 years Fat intake stimulate the
old release of enterogastrone
o Sex dereases gastric motility /
Gastric ulcer - BOTH secretion
Duodenal ulcer – MALE o Antacid
o Helicobacter Pylori Constipation AlOH (Amphogel)
o Smoking – nicotine of the smoke – calcium carbonate
destroys the alkalinity of the bile and Laxative Magnesium oxide,
pancreatic enzyme Magnesium hydroxide
o Blood type

Determine if the
antacid can be chewed
or not
Remind the client to
take the antacid with
some amount of water
(otherwise it will only
coat esophagus)
Best given 1 hour after meal, in
between meals or before bed
time (In General: there is no
specific time)
o H2-receptor antagonist
Block the release of histamine
by the parietal cells of the
gastric mucosa (histamine is a
gastric stimulant)
Taken before meals
Given before the antacid
(antacid has a local coating
effect)
o Proton Pump Inhibitor
o Observe for Peptic Ulcer Complication
- Peptic Ulcer Disease Complication
o Perforation – ulcer has invaded the
muscularis of the stomach leakage of
the gastric and intestinal content
causing Peritonitis
o Peritonitis
Upon inspection there is
abdominal distention
Board-like; rigid abdomen
Hypoactive (-) bowel sounds
o Bleeding
o Pyloric obstruction
Vomiting of undigested food;
signs of fluid and electrolyte
imbalances; early satiety
o Intractile ulcer – ulcer not responding
to any forms of management;
symptoms are not relieved
- Treatment for complications
o Gastric Surgery
MS 1 Board Exam Reviewer 20
Billroth I (Sub-total
Gastrectomy with
gastroduodunectomy)
Billroth II (Sub-total
Gastrectomy with
gastrojejenostomy)
Bilroth III (Total Gastrectomy
with Esophago-jejenostomy)
Gastrorraphy (suturing a
perforated stomach)
Antrectomy (removal of the
antrum removal of the
source of gastrin that
stimulates HCl acid secretion)
Vagotomy (removal of the
vagus nerve that supplies the GI
tract = vagal
stimulation/parasympathetic
stimulation increases gastric
secretion and motility) will
result in decreased gastric
secretion and motility
Pyloroplasty (reconstructive
surgery that enlarges the
pyloric opening)
o Billroth procedures indicative for
bleeding
o Billroth III is for cancer of the stomach
o Pyloroplasty is for pyloric obstruction
o Antrectomy and Vagotomy palliative
surgeries that decrease the gastric acid
Post-operative Complications
- Dumping syndrome
o Rapid passage of hyperosmolar solution
into the jejenum causing a:
Local effect that will distend the
jejenum and increase intestinal
motility
Systemic effect of the passage
of the hyperosmolar solution
 MS 1 Board Exam Reviewer 21

causing the passage of the fluid

intravascularly to the jejenum Pathologic lesion
causing shock like symptoms CROHN’S DISEASE ULCERATIVE COLITIS
(hypovolemia) Large submucosal lymph Diffuse mucosal
o Management: node ; Peyers patches ulceration and
Take fluid between meals and give a cobblestone like appearance of an
not with meals mucosa (fissures) ; inflammatory infiltrate
Lie down after eating / eat in Constricted string sign crypt abscess
recumbent position
Take a dry meal Symptoms
No sweets, no food rich in CROHN’S DISEASE ULCERATIVE COLITIS
carbohydrates (CHO take 1-2 RLQ pain Generalized cramping
abdominal pain ; LLQ
hours to fully digest; CHON take
pain
2-4 hours to fully digest)
Diarrhea (3-5 times a day Diarrhea (15-20 times a
Administration of an anti-
containing puss/mucus) day containing
cholinergic to delay gastric puss/mucus/blood)
emptying (Propanthiline Semi-soft to soft stool Liquid-watery stool
Bromide; Propathine) ; formation
Antispasmodic (Bentyl; Rarely bleeds Rectal bleeding
Buscopan)
- Marginal ulcer Management
o Gastric acid comes into contact with the o Symptomatic / supportive
normal mucosa o Rest the GI tract
- Pernicious Anemia Place on NPO
o Reduced gastric acid reduced Start TPN
intrinsic factor malabsorption of o Restore fluid and electrolytes
vitamin B12 o Administer anti-spasmodic, anti-
- Malnutrition diarrheal, NSAIDs, intestinal
o Reduction in gastric capacity antimicrobial (Sulfonamides,
o Requires small-frequent feeding Cotramoxazoles)
o Avoid stimulant in the diet
COLON DISORDERS:
Intestinal Obstruction
Chronic Inflammatory Bowel Disorders – Crohn’s - Mechanical
Disease / Regional Enteritis & Ulcerative Colitis o Occlusion either intraluminally or
extraluminally (inside and outside the
Consider the site of affectation intestines)
CROHN’S DISEASE ULCERATIVE COLITIS Tumor growth
Transmural inflammation Inflammation of the Colon cancer – most
in the ileum (regional) in entire length of the colon common in the recto-
the Small intestine; if in descending colon = sigmoid colon or
the Large intestine it recto-sigmoid colon
descending colon
affects the Ascending
RF for colon cancer
Colon
Ulcerative colitis,
Predisposing factors chronic constipation,
diet high in saturated
CROHN’S DISEASE ULCERATIVE COLITIS
Auto-immune ; Bacterial in origin ; stress fat and protein, diet
hereditary ; allergens low in fiber, presence
 MS 1 Board Exam Reviewer 22

of polyposis (pre-CA
lesions) Acute hemorrhagic pancreatitis
Intussusception - Risk factor:
Volvulous o Alcohol
Diverticulosis o Peneteric ulcer
Adhesion (sticking together of o Drug abuse
the loop of the intestine) o Immunosuppresants
- Neurogenic / Functional o Prolonged use of diuretics
o Absence of peristalsis - Diagnositc tests
Paralytic ileus / adynamic colon o Serum amylase and lipase
Anesthesia effect Lipase is more indicative (Lipase
Peritonitis is solely pancreatic in origin)
Hypokalemia affects Level of serum amylase will only
intestinal tone remain elevated for 3-4 days
- Vascular Level of serum lipase will
o Mesenteric thrombosis remain elevated for 2 weeks
- Management (MORE SPECIFIC)
o Gastric decompression (Gastric tubes)
Levine Enzymatic tests to diagnose Liver Cirrhosis
Salom - SGOT = AST (more on myocardium)
Sump - SGPT = ALT (more on liver)
Evald - SLDH
Moss o Izoenzyme I – elevates in myocardial
o Intestinal decompression (Intestinal insult/damage
tubes) o II – same as I
Miller-Abbott o III – elevates in parenchymal damage
Cantor o IV – elevate when there is liver damage
Harris o V – same as IV
Bakers
o APR / Miles (Abdominal – Perineal T-tube (Surgery)
Resection) - To divert the drainage until edema subsides
Surgical removal of the entire - Prevents peritonitis
colon including the rectum and
anal sphincter T-tube (No surgery)
Permanent use of a colostomy - T-tube colangiography

LIVER Nursing responsibility:

Earliest sign of hepatic coma – (+) asterixes
Earliest symptom of hepatic coma – sleep reversal
Earliest symptom of liver cirrhosis – hepatomegaly
Latest symptom of liver cirrhosis – small contracted
atrophic liver
Increase in unconjugated bilirubin – hemolytic jaundice
Increase in Conjugated bilirubin – obstructive jaundice
Both increase – hepatocellular jaundice
- Place the container IN LINE WITH THE INCISION
because pressure will help in draining the bile
- Make use of karayo gel or powder / corn starch
to prevent skin excoriation
- If bile is increasing, the bile duct is obstructed
(because the bile is not entering the duodenum)
Tonometry
- Measures intra-ocular pressure
- Test to determine Glaucoma
Gonioscopy
 MS 1 Board Exam Reviewer 23

- Test to diagnose the type of glaucoma =

juncture / angle iris and cornea close angle
glaucoma (open angle glaucoma is trabecular
meshwork)
Slit-lamp microscope / Biomicroscope
- Diagnosis for cataract (earliest manifestation
gradual painless loss of vision)

Meiniers disease
- Vertigo
- Unilateral hearing loss
- Tinnitus