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103 Cards in this Set
- Front
- Back
"bladder atony" =
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urinary retention (not contracting)
- treated with Bethanechol, which stimulates M3 to contract the bladder => urination |
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3 second-gen anti-H's:
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1. Loratadine
2. Fexofenadine 3. Cetirizine |
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Amphotericin B = d.o.c. for:
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mucormycosis
("fungi of the soil") |
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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 |
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***Losartan =
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ARB
- used in place of ACEI; don't cause cough and don't metabolize bradykinin |
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in order to work, INH MUST be processed by:
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the mycobacteria's catalase-peroxidase
|
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Nifedipine's peripheral vasodilation =>
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reflexive tachycardia
|
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Prostacyclin = PGI2; 2 actions:
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1. vasodilation
2. inhibition of plat. aggregation |
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hypoK+ increases pt susceptibility to:
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Digoxin (Digitalis) toxicity
|
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3 SE's of Digoxin:
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1. AV block
2. V-tach arrhythmias 3. hyperK+ |
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B1-agonists like Dobutamine INCREASE:
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myocardial O2 consumption,
by increasing HR |
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Pyridoxine =
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Vit. B6
- nec. with INH, which would otherwise deplete it |
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Fluticasone =
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inhaled corticosteroid
|
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asthma DOES ~~
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mucus plugging
|
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"air fluid level" =
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abscess on CT, often from anaerobic oral org's AND aerobic org's
- tx with Clindamycin |
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Bosentan =
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competitive antagonist of endothelin r's
- treats primary (idiopathic) PHTN |
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Li2+ taken by mom =>
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Ebstein's phen. in utero
- atrialization of the right ventricle, with tricuspid damage |
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the Polyenes act by:
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binding to the ACTUAL ergosterol
- vs. inhibiting its synth like -allyl amines or -azoles |
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opioids can cause contraction of:
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SM in the Oddi
=> biliary colic, obs. |
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Dimercaprol is ONLY for:
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Lead
- along with EDTA |
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N-acetylcysteine =
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a sulfhydryl group
|
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NF-kB =>
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release of cytokines
- seen in Crohn's |
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Polyethylene glycol =
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osmotic laxative
- similar to a nonabsorbable mlcl in the lumen - water will come out via osmosis |
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3 mech's of Ribavarin, used to treat HCV (+IFNa):
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1. lethal hypermutation of HCV RNA
2. direct inhibition of RNAP 3. defective 5' cap of HCV mRNA |
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Halothane ~~
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hepatotoxicity that looks like viral hepatitis
=> hepatocyte death => dec. prot. synth - replaced with "-fluranes" |
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Ethanol actually increases:
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iron absorption
- worse hemachromatosis in alcoholics |
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tx for VIPoma =
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Somatostatin / Octreotide
|
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INH is metabolized by:
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acetylation
=> fast and slow acetylators = biphasic population |
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tx for prolactinoma =
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DOPA agonists like Bromocriptine
- keep it basally inhibited |
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Octreotide =
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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 |
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mech of Thionamides (PTU, Methimazole):
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1. inhibit peroxidase
2. PTU also decreases peripheral conversion |
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tx for decreasing exophthalmopathy in pt with Grave's:
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corticosteroids
|
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what blood count increases with corticosteroids therapy?
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N's
(demargination) - all other leukocytes dec. |
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Leuprolide effect is first:
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stimulatory,
then quickly inhibitory |
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**Metformin is absolutely contraindicated in pts with:
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renal failure, due to risk of LA accum.
- really, it's contraindicated in a/t that might cause LA - hepatic dysfunction, CHF, sepsis, alcoholism |
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Metyrapone is a testing drug that blocks:
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11-B-hydroxylase,
thereby reducing serum cortisol and stimulating ACTH |
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**Prolactin INHIBITS:
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GnRH
=> hypogonadism => anovulation |
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cat's effect on BP:
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**INCREASED** via vasoconstriction
|
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Flutamide =
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anti-androgen
- binds TEST *and* DHT r's |
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Chlorpromazine =
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anti-emetic
- D2 blocker |
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tx of OCD:
(3) |
1. SSRIs
Alternatives: 2. Clomipramine (TCA) and 3. Olanzapine (atypical) |
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2 meds that treat depression with insomnia:
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1. Trazodone
2. Mirtazapine |
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inhaled anesthetics with inc. lipid solubility can cross the BBB and so are:
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MORE potent
|
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2 drugs to treat depression with painful peripheral neuropathy:
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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) |
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OCP's reduce the risk of:
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non-hereditary ovarian and endometrial CA's
- multiparity and breast-feeding also dec. ovarian CA risk (***key is decreased amount of ovulation***) |
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Argatroban =
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DIRECT thrombin inhibitor
- used during HIT |
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anemia from lead poisoning is the result of:
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inhibition of ALAD, ferrochelatase
|
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FGF ~~
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angiogenesis, wound repair, embryonic development
|
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ristocetin test:
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activates GP2b3a;
nl = plats aggregate, bleeding time and PT dec. abnl result = NO agg., BT and PT remain high = vWD |
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Schilling test: in dietary def. of B12, radiolabeled B12 is:
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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 ~~
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PENETRATION (fusion)
not attachment (GP120) |
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Ca2+ blockers used to treat HTN (Amlodipine, Nifedipine) can result in:
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facial flushing and *peripheral edema*
|
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2 first-line drugs for the tx of isolated systolic HTN (~elderly):
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Dihydropyridine Ca2+ blockers, Thiazides
- ACEI's/ARB's in diabetics |
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SE of statins (besides myopathy) =
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hepatotoxicity
|
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remember that both statins and bile acid sequestrants can cause:
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chol. and bile gallstones, respectively
|
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NOR stimulates:
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cardiac B1
|
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3 effects of NOR:
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1. vasoconstriction via a1 / Gq
2. dec. release of insulin via a2 / Gi 3. inc. contractility via B1 / Gs |
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1st-line med for tx of essential HTN =
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HCTZ
|
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LPL releases:
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TG's from carriers,
into tissue |
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what is heparin's connection to TG's?
|
it releases LPL's from the endothelium,
resulting in clearance of TG's from the blood |
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one SE of NO =
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conversion to cyanide
=> cyanide toxicity |
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what's the antidote for cyanide toxicity?
|
Thiosulfate (Sulfur)
|
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Diazoxide =
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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 =
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selective D1-agonist
=> arteriolar dilation, nateurisis => dec. BP - best for HTN with renal insufficiency, b/c it increases renal perfusion |
|
mechanism of ARB's:
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block AT-1 r's, thereby inhibiting ATII
(ATII binds AT-1 r's for effect |
|
name of ARB's:
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"-sartans"
|
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Cilostazol =
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PDE inhibitor
|
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2 effects of Cilostazol:
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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 |
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concern when initiating ACEI therapy:
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first-dose hypotension
- r.f.'s include hypoNa+, hypovolemia (as per Thiazides), and low BP - initiate at low doses |
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1 serious pot. SE of ACEI's =
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angioedema, esp of the eyes/tongue/larynx
- due to bradykinin breakdown |
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4 effects of EPI:
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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 |
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pre-tx with Propranolol eliminates the ____ effects of EPI, leaving only
|
eliminates B1 effects (inc. HR, inc. SBP)
leaving only a1 effects |
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secretion of PDGF from plat/endo/mP's =>
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migration and prolif. of sub-endo SM cells
=> plaque |
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anaphylactic shock ~~
(4) |
1.vasodilation => hypotension
2. bronchoconstriction 3. tachycardia 4. s/ts, rash |
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Dobutamine ~~
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B1-agonist
|
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tx of choice for anaphylaxis =
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EPI
|
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a1-agonists like Phenylephrine caused vasoconstriction, => inc. SBP and DBP; inc. Pressure results in:
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reflexive vagal tone via baro r's (carotid sinus, aortic arch)
=> dec. HR, conduction |
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Streptokinase can save someone with MI if given within 6 hrs, but serious SE =
|
hemorrhage
=> hemorrhagic stroke, bleed out, etc. |
|
Amiloride =
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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
|
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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 =
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Ca2+, for severe hypocalcemia
|
|
Phentolamine =
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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-
|