NBME 16

176 terms
Luiz_Lima PLUS

Possible causes of blood in

Diverticular disease. Diverticula are small

stool include:

pouches that project from the colon wall. Usually

diverticula don't cause problems, but sometimes
they can bleed or become infected.

Anal fissure . A small cut or tear in the tissue

lining the anus similar to the cracks that occur in
chapped lips or a paper cut. Fissures are often
caused by passing a large, hard stool and can be
painful.
Colitis . Inflammation of the colon. Among the
more common causes are infections or
inflammatory bowel disease.
Angiodysplasia. A condition in which fragile,
abnormal blood vessels lead to bleeding.
Peptic ulcers . An open sore in the lining of the
stomach or duodenum, the upper end of the
small intestine. Many peptic ulcers are caused by
infection with a bacterium called Helicobacter
pylori (H. pylori). Long-term use or high doses of
anti-inflammatory drugs such as aspirin,
ibuprofen, and naproxen can also cause ulcers.
Polyps or cancer . Polyps are benign growths
that can grow, bleed, and become cancerous.
Colorectal cancer is the third most common

cancer in the U.S. It often causes bleeding that is

not noticeable with the naked eye.
Esophageal problems. Varicose veins of the
esophagus or tears in the esophagus can lead to
severe blood loss.
cigarette smoke leads to

increased mucus production but low activity of

cilia and machophage function.

morphine chronic use can be

metabolization of morphine leads to active

lethal due:

metabolites that acumulate.

(eg:Morphine-6-glucuronide (M6G) is a major
active metabolite of morphine, and as such is the
molecule responsible for much of the painrelieving effects of morphine and heroin)

caution of chronic use of

kidney impairment would result in accumulation

morphine in severe ill patients

of the kidney-excreted active agent M6G,

due:

leading to potentially fatal toxicity such as

respiratory depression. The frequent use of
morphine in critically ill patients, and the
common occurrence of kidney failure in this
group implied that M6G accumulation could be a
common

Two major theories of opioid

changes in opioid receptors. One theory

tolerance involve:

purports that receptors undergo changes that

result in decreased receptor activation, or
desensitization, with prolonged exposure to
opioids. The other line of evidence suggests that
opioid receptor down-regulation is at least
partially responsible for the development of
tolerance.
more:
http://www.medscape.com/viewarticle/562216_3

Lamelar bodies where do you

Lungs! lamellar granules (otherwise known as

find?

membrane-coating granules (MCGs), lamellar

bodies, keratinosomes or Odland bodies) are
secretory organelles found in type II
pneumocytes and keratinocytes. Lamellar
granules fuse with the cell membrane and
release pulmonary surfactant into the
extracellular space.
Epidermis!In the upper spinous layer and stratum
granulosum layer of the epidermis, lamellar
bodies are secreted from keratinocytes, resulting
in the formation of an impermeable, lipidcontaining membrane that serves as a water
barrier and is required for correct skin barrier
function. These granules release components
that are required for skin shedding
(desquamation) in the uppermost epidermal
layer, the stratum corneum

what is the 5' untranslated

(also known as a Leader Sequence or Leader

region (5 UTR) ?

RNA) is the region of an mRNA that is directly

upstream from the initiation codon. This region is
important for the regulation of translation of a
transcript by differing mechanisms in viruses,
prokaryotes and eukaryotes

The prokaryotic 5 UTR

the Shine Dalgarno sequence (AGGAGGU),

contains a ribosome binding

which is usually 3-10 base pairs upstream from

site (RBS), also known as

the initiation codon.[5] In contrast, the eukaryotic

5 UTR contains the Kozak consensus sequence
(ACCAUGG), which contains the initiation codon.
[5]

Cap-independent translation
of poliovirus mRNA is
conferred by sequence
elements within the

5 UTR

which allows for translation

An internal ribosome entry site, abbreviated

initiation in an end-

IRES, is a RNA element

independent manner, as part

of the greater process of

The location for IRES elements is often in the

protein synthesis??

5'UTR of Rna virus!, but can also occur elsewhere

In eukaryotic translation,

in mRNAs.

initiation typically occurs at the

5' end of mRNA molecules,
since 5' cap recognition is
required for the assembly of
the initiation complex.
the diference in risk between

treatment rate - control rate

exposed and unexposed

Ie-Ine (incidence of disease/effect.. in exposed to

groups or proportion (%) of

treatment - non exposed_)

disease ocurrences that are

if the risk of lung cancer in smokers is 21% and

attributable to the EXPOSURE.

risk in non smokers is 1%,then 20% of lunk cancer

is attributable to smoking.
AR (attributable Risk)
also AR %: 100x(RR-1)/RR

the proportion of risk

if 2% of patients develop the flu,while 8%

reduction attributable to the

develop without vacine.then RR=2/8=.025 (Ie/Ine)

INTERVENTION as compared

and ...RRR= 1-RR= .75

to control.
the diference in risk (not

control rate - treatment rate.

proportion) atributable to the

(Ine-Ie)

INTERVENTION as compared

ARR

to control

if 8% receive placebo vaccine develop flu X 2%

receive flu vaccine develop flu
8%-2%=6%

presence og genetically

Mosaicism

distinct cell lines in the same

Mccune Albright syndrome

individual.
term and disease example
mutation affecting G ptn

Mccune albright syndrome features

signaling= unilateral cafe au lai

spots
polyostotic fibrous
dysplasia,precocious puberty
multiple endocrine
abnormalities.
lethal if mutation occur before
fertilization (affecting all cells)
mutations arise from mitotic

somatic mosaicism

errors after fertilization and

propagates through multiple
tissues and organs
mutation only in egg or sperm

gonadal mosaicism

cells
one gene contribute to

pleiotropy

different phenotype affecting

(PKU)

multiple organ system

2 hit hypothesis remember

loss of heterozigozity

BRACA1 gene do not always

incomplete penetrance

result in breast ,ovarian cancer

presence of normal and

heteroplasmy

mutated mtDNA resulting in

variable expressivity of
mitocondrial inherited disease
phenotype varyes among

variable expressivity

individuasl with same

phenotype (NF1)
mutations at different LOCI can

LOCUS heterogeneity: albinism

produce similar phenotype

mutations at same LOCI can

allelic heterogeneity: B thalassemia

produce similar phenotype

can result is

unbalanced translocation

miscarriage,stillbirth and
chromossomal imbalance
(down,patau syndrome)
Translocations can be

Reciprocal translocations are usually an

reciprocal (balanced or

exchange of material between nonhomologous

unbalanced) or nonreciprocal

chromosomes. are usually harmless and may be

(robertsonian)(balanced or

found through prenatal diagnosis. However,

unbalanced). give examples?

carriers of balanced reciprocal translocations

have increased risks of creating gametes with
unbalanced chromosome translocations, leading
to miscarriages or children with abnormalities.

2 typer of chromossomal

chromosomal translocations occurring in

reciprocal translocations:

gametogenesis, due to errors in meiosis, and

translocations that occur in cellular division of
somatic cells, due to errors in mitosis. The former
results in a chromosomal abnormality featured in
all cells of the offspring, as in translocation
carriers. Somatic translocations, on the other
hand, result in abnormalities featured only in the
affected cell line, as in chronic myelogenous
leukemia with the Philadelphia chromosome
translocation.

Robertsonian translocation is a

breaks at or near the centromeres of two

type of translocation caused

acrocentric chromosomes(six acrocentric

by

chromosomes: 13, 14, 15, 21, 22 and the Y

chromosome).
The reciprocal exchange of parts gives rise to
one large metacentric chromosome and one
extremely small chromosome that may be lost

from the organism with little effect because it

contains so few genes. The resulting karyotype in
humans leaves only 45 chromosomes, since two
chromosomes have fused together

diseases with congenital

5: Cri du chat syndrome (46 XX or XY,5p-)

MICROscopic deletion of:

7:Williams syndrome

short arm of 5
long arm of 7
microcephaly with intelectual

Cri du chat! cat like cry!

disability,epicantal
folds,cardiac
abnormalities(VSD),
delected region gene of

williams!

elastin, distinctive elfin

fascies,intelec disab, hyper
CALCEMIA (high sensitiity to
vit D) WELL developed verbal
skilss!!extreme friendliness with
strangers! CV problems.
-microdeletion of

-above

chromosome

- turner

-deletion of chromosome:

-CF

-codon deletion

- prader/angelman

-single gene deletion

GRAM + stain 3 divisions:

Cocci
rods(bacilli)
branching filaments

cocci next

catalase

+ staph -> coagulase -> + Aureus

- novobiocin sens: epidermidis X saprophyticus
- strep
rods: CCBL

Clostridium,corynebacterium,bacillus(aerobe),list
eria

Branching filaments

Actinomyces (A naerobe,NOT acid fast) X

Nocardia

GRAM - stain

cocci (diplo)
coccoid rods
Rods
curved rods

maltose fermenter

N meningitis

coccoid rods HP BB

haemophilus, pasteurela, Bordetella pertussis,

Brucella

Rods begins with -

lactose fermenter(pink color)

fast: KEE CS
Klebsiella,E.coli,enteroBACTER
slow: citrobacter, serratia
lactose non fermenter, use oxidase because is
white/colourless!

oxidase - X +

oxidase +: pseudomonas motile encapsuled or

aeromonas hydrophila
oxidase -: next TSI agar

TSI agar (triple sugar iron)

spy!

produces H2S -Black ?

Salmonella

bacterias

proteus
Yersinia
do not produce:

shiiiiiiigella
patient has burning abdominal

duodenal ulcer due arrival of acid food!

pain that occurs 1-2 hours after

usually the pain relieves when patient eats due

patient eats. suspect:

release of pancreatic alkaline secretion

patient has burning abdominal

stomach ulcer due increased acid secreations

pain worsening when eating!

released

fear of eat!
patient wit 6 month history of

bleeding duodenal ulcer

burning abdominal pain that

occurs 1 to 2 hours after he
eats.he also has Black stools
for 2 days!
suspect:
high grade and low grade

low and high differentiation

means:
stage TNM

high stage worst prognosis

T: tumor size ,depth
N:nodules (2 worst)
M: metastasis (worst)

lactose fermenters grow which

Mc conkey: Lactose is key! ->pink colonies

color on Mc conkey?
which color in EMB agar and

EMB(eosin methilene blue|) purple/Black

specifically E.coli ?

colonies and e.coli grows with green sheen

which enzyme is responsible

myeloperoxidase

for the green color of pus and

sputum in bacterial infection?
a blue green heme based
enzyme released from
neutrophil azurophilic granules
and forms hydrochlorus acid(
Bleach)

myeloperoxidase

pigmanet producing bacteria:

Y: actinomyces israelli,S.aureus

yellow (2)

green: pseudomonas aeruginosa ( blue green)

gree

due production of pyocyanin

red

Red: serratia marcescens

condition of urine containing

piuria

white blood cells or pus.

Defined as the presence of 610 or more neutrophils per high
power field of unspun, voided
mid-stream urine
-Can be a sign of a bacterial

piuria

urinary tract infection.

urine which contains white

Sterile pyuria

blood cells while appearing

sterile by standard culturing
techniques.
sterile piuria

sexually transmitted infections, such as

It is often caused by:

gonorrhea, or viruses which will not grow in

bacterial cultures. Sterile pyuria is listed as a side
effect from some medications such as
paracetamol (acetaminophen). Its occurrence is
also associated with certain disease processes,
such as Kawasaki disease and genitourinary
tuberculosis.[2] However, there are many known
causes, including systemic or infectious disease,
structural and physiological reasons, intrinsic
kidney pathology, or drugs.[2]

use monoclonal antibody TNF

PAIR

blockers for: name of drugs:

reumatoid arthritis
names: Adalimu/inflixi/certolizu!

TNF decoy TNF a receptor

Ertanecept

blocker:
main indication of ertanecept

added to metotrexate to treat mod to severe RA

in RA

when Metho failed

Sweating

fever symptoms (above 37 - 98.6F)

Shivering
Headache
Muscle aches
Loss of appetite
Dehydration
General weakness
Hallucinations

High fevers between 103 F (39.4 C) and 106 F (41.1

Confusion

C) may cause:

Irritability
Convulsions
Dehydration
diseases

1- S.mansoni (egg with lateral spine)

1-liver and spleen

Sjaponicum also cause intestinal disease:

enlargement,fibrosis and

(diarrhea,abdominal pain,ulceration)

inflammation (portal

2-S.haematobium (egg with TERMINAL spine)

hypertension)
2-chronic infection can lead to
squamous cell carcinoma of
the bladder and may cause
KATAYAMA fever
(fever,urticaria,angioedema,eo
sinophilia)
praziquantel to treat:

intestinal Nematodes (round) no! give

bendazoles!
use praz! for:
-cestodes(tapeworms) except: neurocist or
echinococcus both albendazole!!

-trematodes(flukes)
1.Cestodes(Tapeworms) give

1.

examples 3

- taenia solium ->intestinal infection (injestion of

2.trematodes

larva) X cisticercosis muscle(ingestion of eggs) or

neurocisticercosis (give albendazol)
-diphylobothrium latum
- echinococcus granulosus give albendazole
2.
schistosoma
clonorchis sinensis
paragommus westermani: live lung: chronic
bronchitis/hemoptisis

1.diphylobothrium latumX

1/2: cestode

2.eccinococcus granulosus X

3. trematode

3.clonorchis sinensis

1/3 from undercooked /raw fish

1.vit B12 deficiency
3.biliary tract inflammation-> pigmented stones,
may cholangiocarcinoma
2. ngestion of eggs from dogs, goes lung and
liver-> hydatid cysts in the liver causing
anaphylaxis if antigens released

Nitrous oxide:

- Has low blood and lipid solubility and thus:

blood and lipid solubility

- Fast Induction & Low Potency

induction and potency:

Isoflurane

Isoflurane

blood and lipid solubility

- Lipid and Blood solubility and thus:

induction and potency:

- Slow Induction & High Potency

relate:

blood/gas is related with onset of action! and

a) blood/gas partitition (or

oil/gas is related to potency

oil/gas) with onset of action,

potency

Blood solubility = Blood/Gas partition

coefficient = solubility = Gas required to

saturate blood =
Slower onset of action.
blood/gas partitition is diretly

indirectly

oy indirectly proportional to
onset of action and
recuperation?
oil/gas partitition is diretly oy

directly

indirectly proportional of
potency?
is there a tendency of

yes! higher potency with slower onset of action.

anesthetics with greater oil/gas

have greater blood/gas
partition?
give prophylatic penicillin daily

encapsulated organisms (S.pneumo first!,

to decrease patientsrisk for

H.Influenza)! due autosplenectomy (howell jolly

infection by:

bodies)

drugs which Concentration in

zero order elimination

plasma decreases linearly with

PEA

time.

phenytoin, ETHANOL,ASPIRIN

rate of elimination is constant

regardless of Cp (constant
amount of drug eliminated per
unit time)
drugs witch decrease
exponentially with time.
rate of elimination is directly
PROPORTIONAL to the drug
concentration!
is a flow dependent
elimination.
there a constant Proportion of

First Order elimination

drug elimined per unit time

if first order elimination in

same proportion! 20%

2hours 12,5 mg decrease to

8mg

10mg, after 2 hours which will

be the concentration?
bacteria mechanism of

1.

resistance for ATB

penicilli G,V

1. penicillinase in bacteria
cleaves the blactam ring

amoxicillin, ampicillin(wider spectrum)

Pipera/ticarcillin (anti pseudo) (may combine wit

penicillins resistant b

b lactamase inhibitors)

lactamases
(oxa/methi,diclo,nafcillin)
bacteria mechanism of

cephalosporins

resistance for ATB

2. structural change in
penicillin binding ptns
(transpeptidases)
bacteria mechanism of

vancomycin

resistance for ATB

3. D ala D ala to D ala d LAC!
(VRE)
bacteria mechanism of

aminoglycosides

resistance for ATB

4. bacterial transferase
inactivate ATB by acetylation,
phosphorilation or adenylation
Bacteria mechanism of
resistance for ATB
5. decrease or increase efflux
out of the bacterial cells by
plasmid encoded transport

tetracycline

pump.
production of a ptn that allows
translation of bacteria to take
place even when ATB is
present within the bacteria.
bacteria mechanism of

chloramphenicol

resistance for ATB

6. plasmid encoded
acetyltransferase inactivates
the drug
bacteria mechanism of

Linezolid

resistance for ATB

7.point mutation of ribossomal
RNA
bacteria mechanism of

macrolides

resistance for ATB

8. methylation of 23 S rRna
binding of 50s prevents
binding of drug
bacteria mechanism of

sulfonamides

resistance for ATB

9.altered enzyme (bacterial
dihydropteroate
synthase),decreased uptake or
PABA synthesis
mechanism of resistance of

Rifamycin

mycobacteria::

monotherapy leads to resistance

mutation reduces drug binding

to RNA polymerase.(mutation
in gene that codes for a DNA
dependent RNA polymerase)
mechanism of resistance of

Isoniazid

mycobacteria:

KAT encodes catalase peroxidase needed to

mutation leading to

convert INH to active metabolite

underexpression of KatC
mechanism of resistance of

cyclovirs

virus for antiviral

1. mutated (thymidine) viral
kinase
mechanism of resistance of

ganciclovir

virus for antiviral

2.mutated (CMV) viral kinase
mechanism of resistance of

Foscarnet

virus for antiviral

does not require activation by viral kinase

3. mutated DNA polymerase

characterized by acute

Reye syndrome

noninflammatory

aspirin use!

encephalopathy
(headache,coma) and fatty
degenerative
liver(hypoglycemia) decreased
beta oxidation! due
mitochondrial enzymes
inhibition!
liver failure after a viral illness,
particularly an upper
respiratory tract infection,
influenza B, varicella, or
gastroenteritis,
H1 blockers! generation?

1.

names contains

DiphENhydramINE,

1. en/ine or en/ate

DimENhydrATE,

2.adine

chlorphENiramINE

2. lorat/fexofenadine
H1 blockers clinical use

both allergy! (second rhinitis! and less sedating

1generation

due low penetration in CNS)

2generation

but first motion sickness,sleep aid (disrupts),

anaphylaxis after stabilization with epinephrine.

expectorants think 2!:

-N acetylcysteine mucolytic!prophylaxis against

induced nephropathy if preexisting renal disease.
-Guaifenesin: EXPECTORANT-thin secretions

cough suppression:think

-opioids:inhibits at CNS level (codeine)

DEXTROmethorphan: antagonizes NMDA
glutamate receptors), synthetic codeine analog!
mild opioid effect if used in excess:constipation

nasal descongestionants

pseudoephedrine and phenylephrine (alpha

adrenergic agonists)
pseu used to makje methamphetamine

AR disease:

the X link disease is seen in 1/100,000 males.which

q square = prevalence

is the expected prevalenve of heterozygous

q = allele frequency

females.

2q = carrier frequency
Allele frequency (q) = the prevalence (q square)
X-linked AR:
Prevalence = allele frequency

Thats why in this question q = 1/100000

q square = q

Carrier state = 2q = 2/100000 = 1/50000

Carrier state for females = 2q

at the initial screening

B10 %

evidence of clamydia

here is no info about how much students have

tracomatis infection is founf in

got the treatment, so consider like a chronic

500 of 2500 student .one year

disease. take out people who had the disease in

later evidence of C tramotis is

people at risk!

found in an additional 200

those 500 who already have it aren't at risk

students which of the

anymore to get it.

following is anual incidence of

c tracomatis infection in this

therefore 200/2000 is the correct answer

population of students
flow rate formula:

- flow velocity X cross sectional area

if fv:20cm/sec and cross area:2cm2 remember to
convert units is L/Min

ohms law to calculate flow

- U=R.i
p1-p2=R.Q(flow)
Q= p1-p2/R

resistance formula:

R= viscosity/radio4
so: Q=p1-p2 x r4 /viscosity

1. hyperproteinemia styates,

viscosity

polycythemia, hereditary
spherocytios increases
2. anemia decreases
have highest total cross

capillaries

sectional area and lowest flow

velocity
organ removal(nephrectomy)

increased TPR and decreased CO

leads to
cm 3

1 ml or 10 -3 L

tanner scale

I prepubertal childhood

I prepubertal childhood
II.pubic hair appears(pubarche);breast buds form
II 8-13 pubic hair

(thelarche)

___________;breast buds________
III pubic hair: darkens/curly! ;breast enlarge;penis
III pubic hair

increase size/lengh

_________;breast___________;penis
increase________

IV penis increase width;scrotal skin/glans, areola

raise

IV penis increase__________;scrotal
skin/glans, areola_;

V adult; areola are no loger raised

V adult; areola

irregular mestrual periods

anovulatory cycles

13/14, after menarche

how S pneumoniae ability to

bhy transformation!

produce capsules (his major

SHN use this ability to take up fragments of Dna

virulence factor)

from environment (eg from cell lysis)

transduction generalized "a

litic phage infecting bacterium!cleaves bacterial

packaging" event by

DNA and parts of both DNA are packaged

together in viral capside to infect another
bacteria.

transduction specialized is a

Lytic Phage! infects bacteria, its viral dna is

"excision event" by:

incomporated in bacterial chromosome! when

phage DNA is EXCISED, flanking bacterial genes
may be excised with it, packaged into viral
capside to infect another bacteria.

which bacteria toxins are

Shiga

encoded by lysogenic phage:

Botulinum

ABCDE

cholera
diphteria
erythrogenci of st pyogenes

the condition may increase the

While most cases of horseshoe kidneys are

risk for:

asymptomatic and discovered upon autops

Kidney obstruction - abnormal

The prevalence of horseshoe kidneys in females

placement of ureter may lead

with Turner Syndrome is about 15%.

to obstruction and dilation of

the kidney.

It can be associated with trisomy 18,13.[5]

Kidney infections - associated

with vesicoureteral reflux.
Kidney stones - deviant
orientation of kidneys
combined with slow urine flow
and kidney obstruction may
lead to kidney stones.
Kidney cancer - increased risk
of renal cancer, especially
Wilms' tumor, transitional cell
carcinoma, and an occasional
case report of carcinoid tumor.
[3] Despite increased risk, the
overall risk is still relatively low.
whats the LH/FSH ratio in

high LH!

POS?

stimulates theca cells to produce androgens

how insulin resistance increase

stimulates theca cells to produce androgens

androgens?
whats does high androgens

high conversion in periphery to estrone due

lead?

aromatase!

androgens are converted to

no, due low FSH!

estradiolin granulosa cells?

what does sex binding

they are in low quantitity due low production by

hormones interfere in level of

the liver leading to higher free levels of

strogens/androgens in blood?

androgens and estrogens in the blood

all are up less FSH

POS

consequences:

1.amenorrhea/oligo, repeated anovulatory

1.high estrogen

cycles-subfertility;

2.high androgen

higher risk of endometrial hyperplasia/cancer

due unoposed estrogen.
2.hirsutism,acne

treat POS

weight reduction
OCP
clomiphene
ketokonazol
spironolactone

why acute alcohol intake

by inhibiting or inducing P450 enzymes to make

protects for acetaminophen

hepatotoxic metabolites!

intake liver injury and chronic

alcohol intake worse live
injury?
oral or depot-injected

progestins (medroxyprogesterone)

contraceptive and also as the

progestin component of
menopausal hormone
replacement therapy to
prevent endometrial
hyperplasia and cancer. is also
used as a treatment for
endometriosis, dysmenorrhea,
and amenorrhea.
decreases growth and
increases vascularization of
endometrium
adjuvant therapy for

exemestane/anastrozole (aromatase inhibitors)

postmenopausal women with

ER+ breast cancer
selective estrogen receptor

clomiphene

modulators

tamoxifen
raloxifene

antagonist at estrogen
receptor in hypothalamus

clomiphene

1 line of infertility due

anovulation
prevents normal feedback
inhibition and increase release
of LH and FSH, which
stimulates ovulation.
may cause Hot flashes,ovarian
enlargement,multipole
pregnancies.
drug to prevent /treat breast

tamoxifen

cancer (ER+)
(also agonist bone,uterus)
drug to prevent breast cancer

Raloxifene

and mainly prevent

osteoporosis *agonist bone)
but antagonist at uterus!
DX: men: Low back

prostatitis

pain,dysuria,urgency,frequency
CD56, chromogranin,

neuroendocrine origin

synaptophysin, and neuronspecific enolase) markers from

bacteria which causes

<35: N.gonorrhea,chlamydia trac

prostatitis

>35: think UTI ( PEcKS

<35 Y

proteus,E.COLI!!!,Klebsiella,Serratia and

>35Y

enterobacter

prostatitis treat:

fluoroquinolones,levo for >4 weeksor

TMP/SMX

is an activator of the intrinsic

Kallikrein

coagulations cascade:

deficienct of kallikrein leads to defective intrinsic

Deficiency leads to increased:

pathway which is measured with PTT ( is

increased in dysfunction of the intrinsic pathway

B1 selective B antagonists

Acetabulol (partial

A to M

agonist),atenolol,esmolol,metoprolol

Non selective B antagonist

Nadolol,Pindolol(partial

N to Z

agonist),propranolol,Timolol

non selective B and alpha

labetalol and carvedilol!

weak B1B2 agonis(partial) acts

acetabulol,pindolol to HTN patients with

as antagonists

bradycardia

non seletive irreversible X

irreversible (PHEnoxbensamine! to

reversible Alpha blockers

PHEochromocytoma
reversible; give to patients using MAO eating
tyramine foods

alpha 1 selective blockers

praz,teraz,doxaz,tamsulosim

(osin) to BPH
alpha 1 selective blockers

Tamsulosin (selective for Alpha 1 a on Prostate!)

(osin) to BPH which does not

does not relax vascular Alpha 1 b receptors on

lower BP!give for normotense

vessels

patients
alpha 2 agonist for ADHD,

clonidine

tourette syndrome
cause CNS
depression,bradycardia,hypoot
ension,respiratory
depression,miosis.
alpha 2 blocher for depression

mirtazapine

but becomes asleep, fat,

hungry!
alpha 2 agonist for HTN in
pregnancy
diect coombs + hemolysis
SLE like syndrome

a methyldopa

name of zone I affected first

periportal zone

by viral hepatitis, ingested

toxins

namoe of zone affected by

intermediate zone

yellow fever
name of zone affected by

pericentral vein (centrilobular)

ISCHEMIA! (high demant of

energy by
Na/Katpase)contains
P450!being most sensible to
metabolic toxins! and alcohol!
(alcoholic hepatitis)
shows micro abscesses within

ulcerative colitis

the crypts and depletion of

mucus from goblet
cells,tenesmus and bloody
diarrhea
which drug upregulate

Fibrates

LPL(lipoprotein lipase)

(high risk of cholesterol gallstones0

increasing blood TG clearance

Myopathy (high risk with statins)

increased cholesterol bile

secretion by decreasing bile
acid formation (inhibition of
cholesterol 7 hydroxilase)
which drug inhibits lipolysis

Vit B3 Niacin

(HSL) at adipose tissues and

red,flushed face decreased by NSAIDS

reduces hepatic VLDL

HyperGLYCEMIA!!:(URICEMIA:((

synthesis?
increases HDL perfect drug!
but side effects:

caution use with statins

ezetimibe,Fibrates

arterial/venous supply above

above:

(superior rectum)

-superior RECTAl (a.)(v.) from IM(a.)(v.)

under pectinate line

(middle/inferior rectum)

under:
-middle RECTAL (a.) from internal iliac (a.)(v.)
directly!
-inferior RECTAL (a.)(v.). from internal pudendal
(a.) from internal iliac

A 57 year old man comes to

A) Inferior mesenteric

the physician because of a 6

B) Internal iliac

month history of progressive

C) Left colic

constipation and a feeling of

D) Pararectal

rectal fullness. Digital rectal

E) Superficial inguinal

examination shows no papable

lesion. Test of the stool for
occult blood is positive.
Colonoscopy shows a mass in
the sigmoid colon. A biopsy
specimen of the mass shows
adenocarcinoma. Metastases
from this mass will most likely
spread via which of the
following lymph nodes?
lymphatic drainage

1.above:

1. above:

-superior rectum: superior RECTAL nodes to

(superior rectumXmiddle

IMesenteric

rectum)

-middle rectal nodes to internal iliac nodes

2. under pectinate line

2. under
-to superficial inguinal nodes

remembre effect of partial

antagonist effect

agonist in presence of full

agonist
P450 inhibitors

Cimetidine

CRACK AMIGOS

Rito NAVIR
Alcohol use acute
CIPROFLOXACIN
KetoconaAZOLES(fluco/itra..)
AMIODARONE
Macrolides (EXCEP AZITRO!)
Isoniazid
GRAPE FRUIT juice
Omeprazole
SULFA
Quinidine!
gingko biloba

P 450 inducers

Phenytoin
Barbiturates
Chronic alcohol
GRISEOFULVIN
RIFANPIN
St johj
green vegetables/ginseng

substrates for P450

statins
anti epilectics
theophiline
OCPs
Ciclosporine/tacrolimus

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