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103 Cards in this Set

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"bladder atony" =
urinary retention (not contracting)

- treated with Bethanechol, which stimulates M3 to contract the bladder => urination
3 second-gen anti-H's:
1. Loratadine

2. Fexofenadine

3. Cetirizine
Amphotericin B = d.o.c. for:
mucormycosis

("fungi of the soil")
Prophylaxis in HIV for these bugs

PCP
(200)

Histoplasma capsulatum
(<150)

Toxoplasma
(<100)

MAC (avium + intracellure)
(<50)
TMP-SMX

Itraconazole

TMP-SMX

Z-pak,


respectively
***Losartan =
ARB

- used in place of ACEI; don't cause cough and don't metabolize bradykinin
in order to work, INH MUST be processed by:
the mycobacteria's catalase-peroxidase
Nifedipine's peripheral vasodilation =>
reflexive tachycardia
Prostacyclin = PGI2; 2 actions:
1. vasodilation

2. inhibition of plat. aggregation
hypoK+ increases pt susceptibility to:
Digoxin (Digitalis) toxicity
3 SE's of Digoxin:
1. AV block

2. V-tach arrhythmias

3. hyperK+
B1-agonists like Dobutamine INCREASE:
myocardial O2 consumption,

by increasing HR
Pyridoxine =
Vit. B6

- nec. with INH, which would otherwise deplete it
Fluticasone =
inhaled corticosteroid
asthma DOES ~~
mucus plugging
"air fluid level" =
abscess on CT, often from anaerobic oral org's AND aerobic org's

- tx with Clindamycin
Bosentan =
competitive antagonist of endothelin r's

- treats primary (idiopathic) PHTN
Li2+ taken by mom =>
Ebstein's phen. in utero

- atrialization of the right ventricle, with tricuspid damage
the Polyenes act by:
binding to the ACTUAL ergosterol

- vs. inhibiting its synth like -allyl amines or -azoles
opioids can cause contraction of:
SM in the Oddi

=> biliary colic, obs.
Dimercaprol is ONLY for:
Lead

- along with EDTA
N-acetylcysteine =
a sulfhydryl group
NF-kB =>
release of cytokines

- seen in Crohn's
Polyethylene glycol =
osmotic laxative

- similar to a nonabsorbable mlcl in the lumen - water will come out via osmosis
3 mech's of Ribavarin, used to treat HCV (+IFNa):
1. lethal hypermutation of HCV RNA

2. direct inhibition of RNAP

3. defective 5' cap of HCV mRNA
Halothane ~~
hepatotoxicity that looks like viral hepatitis
=> hepatocyte death => dec. prot. synth

- replaced with "-fluranes"
Ethanol actually increases:
iron absorption

- worse hemachromatosis in alcoholics
tx for VIPoma =
Somatostatin / Octreotide
INH is metabolized by:
acetylation

=> fast and slow acetylators = biphasic population
tx for prolactinoma =
DOPA agonists like Bromocriptine

- keep it basally inhibited
Octreotide =
Somatostatin analog

- blocks GHRH at ant. pit.

=> no GH
role of B-blockers like Propranolol in hyperthy:

(2)
1. dec. rate of peripheral conversion from T4 to T3

2. negate SNS/B adrenergic r' upregulation by T3
mech of Thionamides (PTU, Methimazole):
1. inhibit peroxidase

2. PTU also decreases peripheral conversion
tx for decreasing exophthalmopathy in pt with Grave's:
corticosteroids
what blood count increases with corticosteroids therapy?
N's

(demargination)

- all other leukocytes dec.
Leuprolide effect is first:
stimulatory,

then quickly inhibitory
**Metformin is absolutely contraindicated in pts with:
renal failure, due to risk of LA accum.

- really, it's contraindicated in a/t that might cause LA - hepatic dysfunction, CHF, sepsis, alcoholism
Metyrapone is a testing drug that blocks:
11-B-hydroxylase,

thereby reducing serum cortisol and stimulating ACTH
**Prolactin INHIBITS:
GnRH

=> hypogonadism

=> anovulation
cat's effect on BP:
**INCREASED** via vasoconstriction
Flutamide =
anti-androgen

- binds TEST *and* DHT r's
Chlorpromazine =
anti-emetic

- D2 blocker
tx of OCD:

(3)
1. SSRIs

Alternatives:

2. Clomipramine (TCA)

and

3. Olanzapine (atypical)
2 meds that treat depression with insomnia:
1. Trazodone

2. Mirtazapine
inhaled anesthetics with inc. lipid solubility can cross the BBB and so are:
MORE potent
2 drugs to treat depression with painful peripheral neuropathy:
1. Amitriptyline (TCA)

2. Duloxetine (SNRI)
mech. of TCA's:

(5)
(+ OD effects)
1. prevent reuptake of NOR and SER
(=> sez's, tremors)

2. blocks central and peripheral Muscarinic r's

3. blocks a1
(=> vasodilation)

4. blocks cardiac fast Na+ chans
(=> arrhythmias, hypotension)

5. H1 blockers
(=> sedation)
OCP's reduce the risk of:
non-hereditary ovarian and endometrial CA's

- multiparity and breast-feeding also dec. ovarian CA risk

(***key is decreased amount of ovulation***)
Argatroban =
DIRECT thrombin inhibitor

- used during HIT
anemia from lead poisoning is the result of:
inhibition of ALAD, ferrochelatase
FGF ~~
angiogenesis, wound repair, embryonic development
ristocetin test:
activates GP2b3a;

nl = plats aggregate, bleeding time and PT dec.

abnl result = NO agg., BT and PT remain high
= vWD
Schilling test: in dietary def. of B12, radiolabeled B12 is:
absorbed in the gut and excreted in the urine in nl amounts (>5%)

(body wants it so bad that it takes it up as much as possible => urine)
GP41 ~~
PENETRATION (fusion)

not attachment (GP120)
Ca2+ blockers used to treat HTN (Amlodipine, Nifedipine) can result in:
facial flushing and *peripheral edema*
2 first-line drugs for the tx of isolated systolic HTN (~elderly):
Dihydropyridine Ca2+ blockers, Thiazides

- ACEI's/ARB's in diabetics
SE of statins (besides myopathy) =
hepatotoxicity
remember that both statins and bile acid sequestrants can cause:
chol. and bile gallstones, respectively
NOR stimulates:
cardiac B1
3 effects of NOR:
1. vasoconstriction via a1 / Gq

2. dec. release of insulin via a2 / Gi

3. inc. contractility via B1 / Gs
1st-line med for tx of essential HTN =
HCTZ
LPL releases:
TG's from carriers,

into tissue
what is heparin's connection to TG's?
it releases LPL's from the endothelium,

resulting in clearance of TG's from the blood
one SE of NO =
conversion to cyanide

=> cyanide toxicity
what's the antidote for cyanide toxicity?
Thiosulfate (Sulfur)
Diazoxide =
arterial vasodilator

- very similar to Hydralazine, except not safe in preg. HTN emergency
Esmolol is short-acting with an immediate onset; upon discontinuation, its effects are:
gone within 20 mins
Fenoldopam =
selective D1-agonist

=> arteriolar dilation, nateurisis

=> dec. BP

- best for HTN with renal insufficiency, b/c it increases renal perfusion
mechanism of ARB's:
block AT-1 r's, thereby inhibiting ATII

(ATII binds AT-1 r's for effect
name of ARB's:
"-sartans"
Cilostazol =
PDE inhibitor
2 effects of Cilostazol:
1. directly dilates arterioles

2. inhibits plat. agg.

(aspirin has only minor vasodilation)
non-lipid effects of Niacin:

(3)
1. vasodilation (flushing)

2. inc. insulin resistance
(hyperglycemia)

3. hyperuricemia
concern when initiating ACEI therapy:
first-dose hypotension

- r.f.'s include hypoNa+, hypovolemia (as per Thiazides), and low BP

- initiate at low doses
1 serious pot. SE of ACEI's =
angioedema, esp of the eyes/tongue/larynx

- due to bradykinin breakdown
4 effects of EPI:
1. inc. HR via B1

2. INC. SBP via B1 and a1

3. dec. DBP at low doses via B2

4. inc. DBP at high doses via a1
pre-tx with Propranolol eliminates the ____ effects of EPI, leaving only
eliminates B1 effects (inc. HR, inc. SBP)

leaving only a1 effects
secretion of PDGF from plat/endo/mP's =>
migration and prolif. of sub-endo SM cells

=> plaque
anaphylactic shock ~~

(4)
1.vasodilation => hypotension

2. bronchoconstriction

3. tachycardia

4. s/ts, rash
Dobutamine ~~
B1-agonist
tx of choice for anaphylaxis =
EPI
a1-agonists like Phenylephrine caused vasoconstriction, => inc. SBP and DBP; inc. Pressure results in:
reflexive vagal tone via baro r's (carotid sinus, aortic arch)

=> dec. HR, conduction
Streptokinase can save someone with MI if given within 6 hrs, but serious SE =
hemorrhage

=> hemorrhagic stroke, bleed out, etc.
Amiloride =
K+-sparing diuretic

- blocks Na+ channels at the CD, like Triamterene
tx of choice for DKA =
insulin and nl saline

- insulin allows body to start using glucose and stop making ketones for energy
=> dec. ketones = inc. serum bicarb
what does Insulin do with K+?
causes it to go INSIDE
best med to increase HDL =
Niacin

(B3)
Fibrates are 1st-line tx for:
hyperTG
best 2 meds for high LDL?
1. Statins

2. Ezetimibe
bile acid resins actually increase:
TG's

- but dec. LDL
(hepatic cholesterol has to be used to re-synthesize bile acids, which increases uptake of LDL FROM circulation)
NOR extravasation =
infused NOR leaking out and causing vasoconstriction of surrounding skin

=> cold skin
Calcium gluconate =
Ca2+, for severe hypocalcemia
Phentolamine =
non-specific alpha blocker

- opposes vasoconstriction
Phenoxybenzamine =
irreversible a1 and a2 antagonist

- used to prevent vasoconstriction/HTN

- can't be overcome with NOR
Phentolamine =
competitive, nonspecific alpha-antagonist
prevention of PE/DVT's =
heparin,

or warfarin
only Statin NOT metabolized by CYP450 =
Pravastatin
inhibiting Statin metabolism = more Statin around =
inc. risk of myopathy and rhabdo

- acute renal failure is a consequence of rhabdo
low Vd = 3-5, ~~

(4)
1. high mlclr weight

2. high charge

3. high plasma protein binding

4. hydrophilic (think plasma)
tachyphylaxis =
decreased effect of nasal decongestants after overuse
(due to negative fb => dec. NOR => vasoconstriction)

- stop the decongestant
cholesterol is nec. to make:
bile acids

- that's why bile acid sequestrants lower circulating chol. - liver has to take it in order to make more bile acid
dec. chol (as per statins) =>
inc. LDL r's on the liver, to take up circulating LDL and make more chol.
m.c.c.o.d. of TCA OD =
arrhythmias/hypotension due to cardiac Na+ chan block
antidote for TCA OD =
NS + HCO3-