Cardio/renal Flashcards

0
Q

Verapamil

A
  • Mech: Ca channel blocker (L-type in smooth muscle & heart). Dec. intracell. Ca.
  • Use: angina (atherosclerotic & vasospastic), AV nodal arrhthmias.
  • Tox: constipation, pretibial edema, flushing, dizziness, cardiac depression, hypotension.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Nitroglycerin

sublingual, oral

A
  • Mech: releases NO (which up regs guanylate cyclase which makes more cGMP which activated MLC phosphatase) - relaxes vascular smooth muscle.
  • Use: angina pectoris (SL -> acute, oral ->prophylaxis)
  • Tox: tachy, orthostatic hypotension, headache (vasodilators cause headache).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diltiazem

A

Like verapamil, but w/shorter half life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Nifedipine

A
  • Mech: dihydropyridine Ca channel blocker (these all end in “dipine”, target vascular more so than heart, different than L-type Ca channel blockers). Vascular > cardiac effect.
  • Uses: angina, HTN
  • Tox: like verapamil, less conspitation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Propanolol

A
  • Mech: blocks symp. effect on heart and BP. Reduces renin release.
  • Uses: angina, HTN, arrhythmias, migraine, performance anxiety.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atorvastatin, simvastatin, rosuvastatin

A
  • Mech: inhibit HMG-CoA reductase (cause upreg of LDL receptors)
  • Uses: atherosclerosis
  • Tox: myopathy, hepatic dysfunction, teratogen. (metabolized by P450 system.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Gemfibrozil, Fenofibrate

A
  • Mech: fibrates. PPAR-alpha agonists. Cause inc. in LPL, dec. TG levels in blood.
  • Uses: hypertriglyceridemia
  • Tox: P450 inhibitor, can be toxic w/statins. Hepatic dysfunction, cholestasis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Colestipol, Cholestyramine

A
  • Mech: Prevent reabsorption of bile from GI tract. Cause inc. in LDL receptors b/c liver needs more chol.
  • Use: elevated LDL chol, pruritus.
  • Tox: constipation, bloating.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ezetimibe

A
  • Mech: reduces intestinal absorption of cholesterol.
  • Uses: elevated LDL chol, phytosterolemia.
  • Tox: rare but hepatic dysfunction, myositis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Niacin

A
  • Mech: Dec. VLDL synth, dec. LDL conc., inc. HDL (by dec. its metabolism), inhibits lipolysis in adipose tissue.
  • Uses: Low HDL, elevated VLDL & LDL.
  • Tox: niacin flushing, GI irritation, hepatic toxicity, hyperuricemia, hyperglycemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acetazolamide

A
  • Mech: inhibits CA in PCT. You excrete NaHCO3. You essentially block the formation of the proton you pump out in exchange for Na resorption. Same proton that facilitates bicarb resorption.
  • Uses: glaucoma (it dec. aqeuous humor prod.), mountain sickness, edema w/alkalosis.
  • Tox: causes metabolic acidosis (you spill bicarb, a base), sedation, paresthesias, hyperammonemia in cirrhosis. Sulfa drug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Furosemide,

A
  • Mech: Inhibits the Na/K/2Cl transporter in thick asc. limb of LOH. Causes powerful diuresis and inc. Ca excretion (b/c you lose the positive charge around the tubule which facilitates Ca and Mg resorption).
  • Uses: CHF, pulm edema, severe HTN
  • Tox: metabolic hypokalemic (due to reflex aldo production, resorption of Na, and excretion of K) alkalosis (you spill H in exchange for Na as well). Ototoxicity, hypovolemia, efficacy reduced by NSAIDs. Sulfa drug. Gout.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hydrochlorothiazide

A
  • Mech: inhibit NaCl cotransporter in DCT. (This reduces intracell. Na, which further facilitates resorption of Ca via PTH channel). Causes moderate diuresis and reduced Ca excretion. Nephrogenic diabetes insipidus.
  • Uses: HTN, mild heart failure, SIADH, hypercalciuria w/stones.
  • Tox: metabolic hypokalemic alkalosis, hypercalcemia, hyperlipidemia, hyperuricemia, sulfa allergy. hyponatremia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ethacrynic acid

A

-Mech: loop diuretic w/no sulfur groups.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Spironolactone, eplerenone

A
  • Mech: steroid inhibitors of cytoplasmic Aldo receptors in corticol collecting ducts. Reduce K excretion (potassium sparing).
  • Uses: excessive K loss when using other diuretics. Aldosteronism. CHF.
  • Tox: hyperkalemia (can lead to arrhythmias), gynecomastia (spirinolactone only).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Amiloride, triamterene

A
  • Mech: ENaC channel inhibitor in corticol collecting duct. Reduces Na resorption (aldo upregs ENaC channels). Reduces Na resorption and therefore, K excretion.
  • Uses: excessive K loss w/other diuretics, usually used in combo w/thiazides. hyperaldosteronism, CHF.
  • Tox: hyperkalemia (arrhythmias).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mannitol

A
  • Mech: Causes you to lose water, instead of Na (w/water following) like other diuretics. Inc. tubular osmolarity. Major action is in PCT. Has no pumps to be resorbed.
  • Uses: Reduces intracranial/intraocular pressure. Used ACUTELY.
  • Tox: hyponatremia followed by hypernatremia, headache, nausea, vomiting. Pulm edema, dehydration.
  • Contraindicated in anuria, CHF.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Desmopressin, vasopressin

A
  • Mech: ADH agonists at V1 and V2 ADH receptors - cause insertion of aquaporin channels in collecting tube, reducing water excretion. Vasoconstriction.
  • Uses: pituitary diabetes insipidus
  • Tox: hyponatremia, HTN.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Conivaptan

A
  • Mech: ADH antagonist

- Uses: SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clonidine

A
  • Mech: alpha-2 agonist, in CNS this results in dec. symp outflow.
  • Uses: HTN, ADHD, severe pain, ethanol/opioid withdrawal.
  • Tox: CNS depression (sedation), danger of severe rebound HTN if suddenly stopped, bradycardia, hypotension, respiratory depression, small pupil size.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

alpha-methyldopa

A
  • Mech: alpha-2 agonist
  • Uses: HTN in pregnancy.
  • Tox: can cause hemolytic anemia (safe in pregnancy = binds proteins strongly = can act as hapten), SLE syndrome (also due to hapten quality).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Verapamil, diltiazem

A
  • Mech: L-type Ca channel blocker (heart & vasc.). Moderate vasc. and strong cardiac effects.
  • Uses: HTN, angina, arrhythmias (slows AV node)
  • Tox: Excessive cardiac depression, constipation, AV block, peripheral edema, flushing, dizziness
22
Q

Hydralazine

A
  • Mech: causes release of NO by endothelium. ARTERIOLE dilation.
  • Uses: severe HTN. Used in pregnancy. Freq. given w/beta blockers to block reflex tachy.
  • Tox: Drug induced SLE, compensatory tachy (C/I in angina & CAD), fluid retention, nausea, headache, angina.
  • can be problematic for slow acetylators.
23
Q

Nitroprusside

A
  • Mech: drug itself releases NO (short acting-req constant infusion).
  • Uses: HTN emergency (malignant HTN)
  • Tox: can cause cyanide poisoning b/c it releases cyanide. Hypotension.
24
Q

Fenoldopam

A
  • Mech: D1 agonist. Causes arteriolar dilation (coronary, peripheral, renal, splanchnic vasodilation). Dec. BP and inc. natriuresis.
  • Uses: HTN emergencies.
  • Tox: Excessive hypotension
25
Q

Aliskiren

A
  • Mech: inhibits renin.
  • Uses: HTN
  • Tox: angioedema, renal impairment
26
Q

Captopril, enalapril, linisopril

A
  • Mech: ACE inhibitor (causes inc. in bradykinin), dec. GFR by inhibiting constriction of efferent arterioles.
  • Uses: HTN, CHF, proteinuria, diabetic nephropathy.
  • Tox: CATCHH = cough, andioedema, teratogen, inc. Creatinine (aka dec. GFR), hyperkalemia (need aldo to excrete K), hypotension.
  • C/I in bilateral renal art stenosis.
27
Q

Losartan

A
  • Mech: Blocks AT1 receptor (where Angiotensin 2 binds = on adrenal cortex and vasculature).
  • Uses: HTN
  • Tox: hyperkalemia, teratogen.
28
Q

Neseritide

A
  • Mech: BNP/ANF receptor agonist
  • Uses: acute heart failure
  • Tox: renal damage, hypotension
29
Q

Bosentan

A
  • Mech: Endothelin-1 receptor antagonist. Decreases pulmonary vascular resistance.
  • Uses: Pulm arterial HTN.
  • Tox: hepatic impairment, possible teratogen.
30
Q

NO gas

A
  • Mech: upreg guanylate cyclase -> inc. cGMP -> smooth muscle relax.
  • Uses: pulmonary HTN.
  • Tox: methemoglobinemia, conversion to CO2 (pulmonary irritant).
31
Q

NO synthase activators

A

ACh, histamine

-Mech: inc. IP3 -> inc intracell. Ca -> activates NO synthase which converts arginine to citrulline + NO gas.

32
Q

Cardiac glycoside: digoxin

A
  • Mech: direct inhibition of Na/K pump which indirectly inhibits the Na/Ca antiporter (which pumps Ca out) which results in inc. cytoplasmic Ca, so the SR takes more in, so it gives more out when you contract, so it inc. inotropy.
  • Uses: heart failure, nodal arrhythmias
  • Tox: cholinergic (nausea, vomiting, diarrhea, blurry vision), arrhythmias.
33
Q

Dobutamine

A
  • Mech: beta-1 agonist, inc. inotropy.
  • Uses: CHF
  • Tox: cardiac depression
34
Q

Class 1A: Quinidine, Procainamide, Disopyramide.

A

-inc. AP duration, inc. ERP, inc. QT interval.
-Use: Both atrial and vent. arrhythmias, especially re-entrant and ectopic SVT and VT.
-Tox: Cinchonism (headache, tinnitus with
quinidine), reversible SLE-like syndrome
(procainamide), heart failure (disopyramide),
thrombocytopenia, torsades de pointes due to
inc. QT interval.

35
Q

Class 1B: Lidocaine, Mexiletine, phenytoin

A

-dec. AP duration. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue.
-Use: Acute vent. arrhythmias (especially post-MI), digitalis-induced arrhythmias. 1B is Best post-MI.
-Tox: CNS stimulation/depression, cardiovascular
depression.

36
Q

Class 1C: Flecainide, Propafenone.

A

-Significantly prolongs refractory period in AV node.Minimal effect on AP duration.
-Use: SVTs, including atrial fibrillation. Only as a last
resort in refractory VT.
-Tox: Proarrhythmic, especially post-MI (contraindicated). 1C is Contraindicated in structural and ischemic heart disease.
*last resort. These drugs are never used.

37
Q

Class 2: beta blockers: Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.

A

-Decrease SA and AV nodal activity by dec. cAMP,  dec. Ca2+ currents. Suppress abnormal pacemakers by  dec.
slope of phase 4. AV node particularly sensitive— inc. PR interval. Esmolol very short acting.
-Use: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
-Tox: Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity). Treat
overdose with glucagon.

38
Q

Class 3: K channel blockers: Amiodarone, Ibutilide, Dofetilide, Sotalol.

A

-inc. AP duration, inc. ERP. Used when other
antiarrhythmics fail. inc. QT interval.
-Use: Atrial fibrillation, atrial flutter; ventricular
tachycardia (amiodarone, sotalol).
-Tox:
Sotalol—torsades de pointes, excessive β
blockade.
Ibutilide—torsades de pointes.
Amiodarone—pulmonary fibrosis,
hepatotoxicity, hypothyroidism/
hyperthyroidism (amiodarone is 40% iodine
by weight), corneal deposits, skin deposits
(blue/gray) resulting in photodermatitis,
neurologic effects, constipation, cardiovascular
effects (bradycardia, heart block, CHF).

39
Q

Class 4: CCB: Verapamil, diltiazem.

A
  • dec. conduction velocity, inc. ERP, inc. PR interval.
  • Use: Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
  • Tox: Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).
40
Q

Adenosine

A
  • inc. K+ out of cells = hyperpolarizing the cell and dec. ICa
  • Use: Drug of choice in diagnosing/abolishing supraventricular tachycardia.
  • Very short acting (~ 15 sec)
  • Tox: flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.
41
Q

Magnesium ion

A
  • Effective in torsades de pointes and digoxin toxicity.
  • Mg is structurally very similar to Calcium. So it basically just competes with Ca. But it doesn’t have any of Ca’s effects.
  • Mg also used in premature labor, in seizures - so it basically has competition effect w/Ca.
42
Q

Potassium ion

A

-Increase in all K currents, decreased automaticity,
decreased digitalis toxicity.
-Use: Digitalis toxicity and other arrhythmias if serum K is low.
-Tox: Both hypokalemia and hyperkalemia are associated with arrhythmogenesis. Severe hyperkalemia causes cardiac arrest.

43
Q

Conivaptan

A

ADH antagonist

44
Q

Argatroban, bivalirudin

A

Inhibits activation of thrombin (and therefore fibrin).

  • anti-coagulant used by leeches.
  • Used instead of heparin for anticoagulating patients with HIT (heparin-induced thrombocytopenia)
45
Q

protamine sulfate

A
  • antidote to heparin overdose.

- chemical antagonism.

46
Q

Fresh frozen plasma & IV vitamin K

A
  • antidote to warfarin overdose.
  • IV vitamin K takes long time
  • FFP is immediate.
47
Q

aminocaproic acid (EACA)

A

-inhibitor of fibrinolysis. Given to treat thrombylytic toxicity.

48
Q

Ticlopidine, clopidogrel

A
  • inhibit ADP-induced expression of GpIIb/IIIa
  • anti-platelet
  • Use:
49
Q

Abciximab, eptifibatide, tirofiban.

A
  • Anti-platelet aggregant
  • binds to/blocks GP2a/3b receptor.
  • Use: Acute coronary syndromes & post angioplasty
  • Tox: bleeding, thrombocytopenia
  • this is a hospital type of drug. Not something for chronic management.
50
Q

enoxaparin, dalteparin

A
  • LMW heparin

- better bioavailability and 2–4 times longer half-life. Can be administered subcutaneously and without lab monitoring.

51
Q

Heparins

A

-Complexes with antithrombin III, irreversibly inactivates
the coagulation factors thrombin and factor Xa.
-Use: DVT, PE, MI, unstable angina
-Tox: Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin).

52
Q

Apixaban, rivaroxaban

A
  • Bind and directly inhibit the activity of factor Xa.
  • Use: Treatment & prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with afib.
  • Tox: Bleeding