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Pharm Block 4: Cardio drugs > Pharm_Merged > Flashcards

Pharm_Merged Flashcards

1
Q

What non-drug item can increase the risk of statin adverse events?

A

Grapefruit juice

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2
Q

What is the function of chylomicrons?

A

Exogenous lipoprotein: Transport of dietary fat, cholesterol and bile acids from intestine to liver

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3
Q

What is the route of administration for all thrombolytic agents?

A

IV

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4
Q

Describe the elimination of beta blockers

A

Liver: Propranolol, carvedilol, metoprololKidney: atenolol, nadolol, sotalol

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5
Q

What is the difference between mexiletine and lidocaine?

A

Mexiletine is an orally active lidocaine analogue with a much longer half life-Used off label for chronic pain

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6
Q

What are the side effects of verapamil and diltiazem?

A

Bradycardia

CHF

Heart block

Hypotension

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7
Q

What are the actions of cAMP in cardiac muscle?

A

Opens L-type Ca2+ channels

Increased reuptake of Ca into SR

Increased pacemaker current

Increased rate of conduction

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8
Q

Where in the body are nitrates most effective?

A

Systemic circulation

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9
Q

What is the mechanism of action of lomitapide?

A

Inhibition of MTP enzyme, preventing the formation of chylomicrons by enterocytes and VLDLs by hepatocytes

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10
Q

What is the mechanism of action of eplerenone?

A

Aldosterone antagonist

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11
Q

What are the factors that limit fibrinolysis?

A

Fibrin crosslinking by factor XIIIa Antiplasmin content in and around fibrin clot

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12
Q

Is warfarin plasma bound?

A

Yes, 97% bound to albumin This gives warfarin a long half life

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13
Q

What are the products of platelet activation and endothelial interaction?

A

Prostaglandin derivatives

Endoperoxides

Thromboxanes

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14
Q

Which thrombolytic agents are used for pulmonary embolism?

A

Streptokinase and urokinase

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15
Q

What are the most commonly used beta blockers?

A

Metoprolol Atenolol

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16
Q

What transporter is responsible for liver uptake of statins?

A

OATP2

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17
Q

Where do diuretics have to get to in order to be effective?

A

They must reach the tubular fluid in order to be effective

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18
Q

What is the only cholesterol absorption inhibitor drug?

A

Ezetimibe

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19
Q

What is the affect of arginine analogs (ex: NMMA)?

A

Inhibition of the conversion of arginine to citrulline decreases formation of NO

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20
Q

What is the typical non-selective beta blocker?

A

Propranolol

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21
Q

What are the contraindications for mannitol?

A

CHF, renal failure, pulmonary edema *CHF and RF reduce glomerular filtration, pulmonary edema would be exacerbated

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22
Q

Describe the pharmacokinetics of amiloride

A

Long half life (21h) Secreted into tubule via OBTExcreted unchanged by kidney

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23
Q

What are the side effects of all beta blockers?

A

Bradycardia

Impotence

Increased TGs

Decreased HDLs

Hyperglycemia

Impaired exercise tolerance

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24
Q

What is the mechanism of action of the statins?

A

HMG-CoA reductase inhibitors Competitive inhibition of the rate limiting enzyme of cholesterol biosynthesis. SREBP is activated leading to increased LDLR gene expression, increased LDL clearance

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25
Q

What is the difference in vasodilator drugs used for acute versus chronic CHF?

A

Acute CHF drugs (nitroprusside, nitroglycerin) are given IV and have rapid onset of actionChronic CHF drugs (ACEi’s, ARBs, hydralazine, minoxidil, prazosin, LCZ696) are given orally and have slower onset of aciton

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26
Q

What are the contraindications for fibrate usage?

A

Pregnant/lactating women Hepatic dysfunction (drug is hepatotoxic) Renal dysfunction (drug renally excreted) Gall bladder disease

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27
Q

Describe the pharmacokinetics of spironolactone

A

Slow onset, takes days for effect Liver metabolism to several active metabolites

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28
Q

How does the Ca2+ reabsorption differ between loop diuretics and hydrochlorothiazide?

A

Loop diuretics decrease Ca2+ reabsorption whereas hydrochlorothiazide increases Ca2+ reabsorption

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29
Q

What are the main factors that promote fibrinolysis?

A

Plasminogen content of clot

tPA content/activity in and around clot

Protection of bound plasmin from antiplasmin

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30
Q

How does glutathione affect vascular pathology?

A

In CVD and DM, glutathione levels are reduced. This leads to increased vascular pathology due to increased NO.

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31
Q

What are the side effects of ivabradine?

A

Luminous phenomena, bradycardia, AV block

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32
Q

List the class IB anti-arrhythmic drugs

A

Lidocaine Mexiletine

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33
Q

Describe the population variation of clopidogrel and prasugrel

A

Prasugrel has less population variation than clopidogrel. A significant portion of the population is non-respondant to clopidogrel due to a polymorphism.

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34
Q

What levels of LDL and TG are considered “very high”?

A

LDL > 190 mg/dLTG > 500 mg/dL

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35
Q

What are the clinical indications for spironolactone?

A

Primary and secondary hyperaldosteronism

Liver cirrhosis (drug of choice)

Hypertension

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36
Q

What are the mechanical effects of digitalis glycosides?

A

Increased contractility-increased velocity of shortening, force of contraction, ventricular emptying-Decreased ESV and EDV

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37
Q

Contraindications of ACE inhibitors

A

Pregnancy

Bilateral renal stenosis

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38
Q

Describe the contents of light and dark granules

A

Light: PF4, beta-thromboglobulin, PDGF

Dark: Ca2+, Serotonin, ATP/ADP

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39
Q

Describe the effect of gain of function and loss of function mutations in the PCSK9 gene

A

Gain of function: high LDL levels, increased risk for CVD

Loss of function: low LDL levels, decreased risk for CVD

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40
Q

How does hepatic cirrhosis cause systemic edema?

A

Increased pressure in sinusoids leads to exudate, ascites Decreased albumin production decreases oncotic pressure, RAA system activated, Na retention

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41
Q

What is the major danger of anti-arrhythmic drugs?

A

The do not act specifically, and can end up depressing conduction in normal cells leading to drug-induced arrhythmias -Dosage, HR, acidosis, electrolytes and ischemia all impact the effect

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42
Q

Diuretics primarily prevent Na+ ________________

A

Diuretics primarily prevent Na+ entry into the tubule cells

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43
Q

What is the mechanism of action of bile acid-binding resins?

A

Bind to negatively charged bile acids to prevent small intestinal reabsorption, thus leading to excretion of bile acids via feces. Increased bile acid production –> decrease cholesterol levels

LDLR is upregulated leading to increased LDL clearance

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44
Q

What are the clinical uses of heparin?

A

Therapeutic, surgical and prophylactic ANTICOAGULATION Unstable angina Adjunct therapy with thrombolytic drugs Thrombotic and ischemic strokes

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45
Q

What are the side effects of nitrates?

A

Exaggeration of therapeutic effects: -orthostatic hypotension-reflex tachycardia-headacheTolerance can also develop

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46
Q

What is ranolazine?

A

New class of antianginal drugs with a unknown mechanism

Inhibits pFOX, decreasing beta oxidation

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47
Q

What are the adverse effects of amiloride?

A

Hyperkalemia (exacerbated by NSAIDs)GI upset: NVD Muscle cramps CNS: headache, dizziness

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48
Q

What is acutely decompensated CHF?

A

Acute CHF superimposed on the setting of chronic CHF

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49
Q

Which CCB has the strongest negative inotropic and chronotropic effects?

A

Verapamil has the strongest inotropic and chronotropic effects

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50
Q

How are statins excreted?

A

ALL statins are excreted via bile and feces after glucoronidation by UGT1A1/1A3 in the liver

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51
Q

Describe the effect of metoprolol on exercise performance

A

Decreases variation in heart rate and reduces ischemic changes in response to exercise

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52
Q

What lab test is used to monitor warfarin therapy?

A

PT is used to monitor warfarin and its effect on the extrinsic pathway

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53
Q

What are the causes of hyperlipidemia?

A

Genetics: familial genetic disorder

Lifestyle: diet, obesity, alcohol, smoking, age, physical inactivity

Diseases: T2 DM, hypothyroidism

Drugs: antiviral, antipsychotics, corticosteroids, oral contraceptives

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54
Q

What are the ions secreted in the collecting ducts?

A

K+ and H+ are secreted in the collecting ducts

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55
Q

How is thrombolytic therapy useful for MI patients?

A

Many MI patients have thrombi formed in the coronary vessels. Thrombolytic therapy is used to try to get rid of the fibrin-rich occlusion

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56
Q

What are the interactions with anti-Xa drugs?

A

Anti-Xa drugs are potent CYP3A4 inhibitors

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57
Q

What are the indications for dronedarone?

A

Atrial fibrillation/flutter

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58
Q

Which diuretic drugs most profoundly increase urinary K+?

A

Loop + thiazide combo

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59
Q

What are the non-pharmacological therapies for acute CHF?

A

PCI/surgical therapy: revascularization and/or valve repair

Ultrafiltration

Intra-aortic balloon pump

Ventricular assist devices

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60
Q

Location of action of acetazolamide

A

Proximal convoluted tubule

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61
Q

What are the non-pharmacologic anti-arrhythmic therapies?

A

Vagal maneuvers

Radiofrequency ablation/Cryoablation

Electrical cardioversion

Implantable cardioverter-defibrillators

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62
Q

Describe the cardiac conduction system

A

The sinoatrial node is the pacemaker, and is located in the wall of the right atrium. The SA stimulus spreads across the atria to the AV node, which has a 150ms delay. The his-Purkinje system then rapidly depolarizes the ventricles leading to cardiac contraction

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63
Q

What is bivalirudin?

A

A synthetic antithrombin that is a combination of hirudin and a tripeptide used for anticoagulation during stent placement and angioplasty

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64
Q

What are the contraindications for bile acid resins?

A

Type III dysbetalipoproteinemia Raised TGs (risk for pancreatitis)

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65
Q

What is the mechanism of action of the beta blockers?

A

Decreased 1) cardiac contractility 2) Cardiac Output3) renin secretion

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66
Q

Major side effect of diltiazem

A

Bradycardia

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67
Q

What is the function of plasmin?

A

Plasmin is the major fibrinolytic enzyme. Breaks down fibrinogen and fibrin.

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68
Q

What are the indications for beta blockers?

A

Prevent recurrent infarct, sudden death after MI

Exercise-induced arrhythmias

AFib, AFlutter, AV nodal reentry

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69
Q

What is the mechanism of action of mipomersen?

A

This oligonucleotide reduces the expression of apoB leading to reduced production of VLDLs by hypatocytes

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70
Q

What is the indication for Ciostazol?

A

Management of intermittent claudication

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71
Q

What are the adverse effects of procainamide?

A

Ganglion blocking properties

Hypotension

Anticholinergic effect

Induce torsade de pointes

Lupus erythematosus syndrome from chronic use (30% of patients)

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72
Q

Clinical use of nitrates

A

Angina pectoris

Hypertensive emergencies

CHF

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73
Q

What are the drugs that treat hypertriglyceridemia?

A

Niacin

Fibrates (gemfibrozil, fenofibrate)

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74
Q

What are the drug interactions for potassium sparing diuretics?

A

NSAIDs ACE inhibitors with ARBs

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75
Q

What are the adverse effects of lidocaine?

A

Least cardiotoxic Class I drug Can cause hypotension Local anesthetic properties: paresthesias, tremors, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions

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76
Q

What regulates the H2O permeability of the collecting duct?

A

In the presence of ADH, the collecting ducts are permeable to H2O due to aquaporin insertion

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77
Q

What drugs are vasodilators used for treating HTN?

A

Hydralazine Minoxidil Nitroprusside

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78
Q

What is the major action of angiotensin II?

A

Profound vasoconstriction

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79
Q

Which antiplatelet drugs must be given via IV?

A

The GP IIb/IIIa inhibitors are the only antiplatelet drugs not given orally

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80
Q

Describe the function of vasoactive intestinal peptide

A

VIP causes vasodilation and also functions as a neuromodulator

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81
Q

Describe the mechanism of action of niacin

A

COMPLEX-decreases release of FFAs, decreasing FA synthesis-increases HDL via increased apoA1-decreased macrophage recruitment to lesions-decreased thrombosis risk by decreasing Lp(a)-decreased VLDL production, increased clearance

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82
Q

What are the treatment objectives for acute CHF?

A

Early recognition and treatment Decrease symptoms - Reduce pulmonary congestion: loop diuretics, venodilators, nesiritide-Increase CO: –Increase contractility: beta blockers, phosphodiesterase inhibitors –Reduce afterload: nitroprusside

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83
Q

What is the mechanism of action of the loop diuretics?

A

Block the Na/K/2Cl cotransporter which increases urinary water, Na, K, Ca, and Mg excretion- Also dilates venous system and renal vasodilation mediated by PGs

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84
Q

What are the clinical indications for furosemide?

A

Acute PE Edema w/ CHF Acute hypercalcemia, hyperkalemia Hypertension

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85
Q

What are the NO levels in septic shock?

A

NO levels are markedly increased in septic shock.LPS induces NOS-2 to produce NO, leads to hypotension and shock

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86
Q

Mechanism of action for Losartan

A

Angiotensin II receptor blocker Mediates vasoconstriction and sodium retention

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87
Q

Describe the ionic movements in the distal convoluted tubule

A

Transporters: lumenal Na/Cl symporter, basolateral Na/K ATPase and Na/Ca antiporter

Na gradient drives Na/Cl symporter-Ca absorption regulated by PTH

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88
Q

Are Calcium channel blockers used for CHF patients?

A

No. Contraindicated for CHF due to negative inotropic effects

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89
Q

What class of drugs does dabigatran interact with?

A

Proton pump inhibitors

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90
Q

How do ACE inhibitors affect renal function in diabetics?

A

Preserve renal function

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91
Q

What is the ECG manifestation of treatment with amiodarone, dronedarone, and sotalol?

A

QT prolongation on the EKG

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92
Q

What are the clinical indications of amiloride?

A

Edema Hypertension Used in combo with other diuretics to minimize K+ loss

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93
Q

What is the effect of excessive production of angiotensin II?

A

Hypertension and disorders of hemodynamics

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94
Q

What is the route of administration for warfarin?

A

Oral

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95
Q

What are the general pharmacological strategies used to treat hyperlipidemia?

A

Decrease in LDL (Primary targets) Increase HDL (secondary) Decrease TG (secondary)

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96
Q

What are the main regulators of prostacyclin and thromboxane synthesis?

A

Endothelial lining Lipoproteins and other blood components Diet, drugs, hemodynamics

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97
Q

How is heparin therapy monitored?

A

Heparin therapy is carefully monitored using APTT Target APTT is 2-2.5x baseline

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98
Q

What are the indications for the anti-Xa drugs?

A

Stroke prevention in AFib patients

Prophylaxis of DVT

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99
Q

Where is ACE primarily located in the body?

A

On the luminal structure of the endothelial cells throughout the vasculature

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100
Q

What is the mechanism of action for mannitol?

A

Osmotic diuretic (holds water in tubule) that acts in the water permeable segments of the nephron (proximal tubule, descending loop, collecting ducts +ADH)

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101
Q

What are the drug interactions with thrombolytic agents?

A

Antiplatelet drugs, heparins and dextrans

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102
Q

What are the side effects of potassium sparing diuretics?

A

Hyperkalemia Gynecomastia

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103
Q

How is heparin metabolized?

A

25% excreted in urine Some metabolized in liver by heparinases Mast cells take up heparin Endothelium binds heparin

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104
Q

Warfarin is an analogue of _________

A

Vitamin K Warfarin and Vit K have similar chemical structures

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105
Q

What is the indication for dabigatran?

A

Stroke prevention in AFib patients

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106
Q

What are the clinical uses of LMW heparin

A

DVT: Prophylaxis and treatment Acute coronary syndromes management Anticoagulation during procedures

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107
Q

What is the difference between clonidine and guanfacine?

A

Guanfacine has a longer half life, less chance for rebound hypertension

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108
Q

What are the 4 major vasoactive peptides that have important roles for regulating hemodynamics?

A

Angiotensin Kinins Endothelins Vasopressin

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109
Q

How do thiazide diuretics cause hypercalcemia?

A

Inhibition of Na/Cl cotransporter decreases intracellular [Na+], producing a bigger gradient for the Na/Ca antiporter on the basolateral membrane. More Ca gets pumped out of the cells (reabsorption), leading to hypercalcemia

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110
Q

What is the treatment for severe hypercholesterolemia?

A

Drug therapy: reduce LDL using a statin in order to decrease risk of atherosclerosis

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111
Q

What are the clinical advantages of LMW heparin

A

Better bioavailability, longer duration of action, less bleeding, lesser thrombocytopenia

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112
Q

What are the thiazide drugs other than hydrochlorothiazide and how to the differ?

A

Chlorothiazide: 1/10 potency, short half life

Metolazone: 10x potency, long half life

Indapamide: 20x potency, longer half life, liver metabolism

Chlorthalidone: same potency, Longest half life

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113
Q

Describe the pharmacology of omega 3 fatty acid

A

Contains acids that compete with AA in the PG pathway in order to inhibit the effects of TXA2

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114
Q

What drug interactions are associated with loop diuretics?

A

NSAIDs Aminoglycosides

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115
Q

What are the main side effects of warfarin?

A

Bleeding due to hypoprothrombinemia (ecchymoses, purpura, hematuria, hemorrhage)

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116
Q

What is argatroban?

A

A synthetic anti-thrombin agent used as an anticoagulant alternative to heparin for patients with heparin induced thrombocytopenia

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117
Q

What additional risk must be considered for diabetic patients taking beta blockers

A

Masked hypoglycemia Epinephrine is released when glucose is low, but its effect is blocked so the typical hypoglycemic symptoms may not present

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118
Q

What are antithrombin concentrates clinically used for?

A

Congenital antithrombin deficiency Sepsis and DIC

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119
Q

Describe the formation of atherosclerosis starting with endothelial injury

A

Endothelial injury allows LDL to enter vessel wall. LDL is oxidized and then taken up by macrophages, which convert to foam cells that promote SMC migration and proliferation as well as ECM synthesis. Foam cells release debris leading to fatty streak formation.

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120
Q

How do loop and thiazide diuretics cause metabolic alkalosis?

A

Lumen negative potential (increased Na and Cl-) enhances H+ efflux from the intercalated cells. More HCO3- is therefore reabsorbed, leading to alkalosis

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121
Q

What are the adverse effects of beta blockers?

A

Bradycardia, reduced exercise capacity, heart failure, hypotension, AV block Bronchospasm Lowered glucose, lowered HR

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122
Q

What effect do inducers of CYP3A4 have on statin therapy?

A

Inducers of CYP3A4 reduce plasma concentrations and thus reduce clinical efficacy of statins

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123
Q

What is the main loop diuretic?

A

Furosemide (Lasix)

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124
Q

When is methyldopa most often prescribed?

A

Pregnancy with hypertension

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125
Q

What drugs interact with anti-platelet drugs?

A

Thrombolytic agents Heparin/LMW heparin/Oral anticoagulants Warfarin Antithrombin agents

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126
Q

What is the mechanism of action of heparin?

A

Inhibits action of Xa, IIa, XIIa, Xia (2,10,11,12) by binding to ATIII and increasing ATIII affinity for these factors

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127
Q

What is the metabolite of procainamide?

A

NAPA, which has class III activity

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128
Q

What is the mechanism of action of icatibant?

A

B2 receptor inhibitor May be useful for hypotension and myocardial hypertrophy

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129
Q

What are the therapeutic uses of vitamin K?

A

-Antidote for drug-induced hypoprothrombinemia -Intestinal disorders and surgery -Hypoprothrombinemias in newborns

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130
Q

Describe the interaction between sildenaphil and nitrates

A

Strong adverse reaction that can cause severe hypotension. Both drugs result in increased cGMP levels leading to relaxation

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131
Q

What is the mechanism of action of sildenafil (viagra)?

A

Inhibition of phosphodiesterase Increases cGMP levels (by preventing conversion to GMP) leading to increased relaxation

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132
Q

What condition worsens adverse effects associated with mannitol?

A

AEs predominate if filtration is impaired because mannitol cannot reach the tubule without filtration

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133
Q

What is the effect of urotensin?

A

Vasoconstriction of arterial bedsIncreased in patients with end stage heart failure

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134
Q

Describe the mechanism of action of nitrates

A

Nitrates cause endothelium independent smooth muscle relaxation by activating GC to increase cGMP, dephosphorylates myosin light chains Decreased venous return, decreased LV wall tension, reduced afterload and direct coronary artery vasodilation

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135
Q

What are the 4 major classes of drugs that reduce LDL levels?

A

Statins Bile acid-binding resins Cholesterol absorption inhibitors PCSK9 inhibitors

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136
Q

What are the endogenous modulators of heparin action?

A

ATIII Heparin cofactor II Tissue factor pathway inhibitor (TFPI) Platelet factor 4 (PF4)

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137
Q

Which drugs are the ADH antagonists?

A

Demeclocycline: tetracycline antibiotic Lithium: psych drug for mania Vaptans

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138
Q

What are the loop diuretics other than furosemide and how do they differ?

A

Bumetanide (40x potency, shorter half life, liver metabolism) Torsemide (longer half life, duration, better oral absorption, liver metabolism) Ethacrynic acid (different structure, used w/ hypersensitivity, BAD AEs)

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139
Q

In addition to ACE inhibitors blocking Ang II production, what other peptides are inhibited?

A

Bradykinin metabolism is blocked by ACE inhibitorsLeads to hypotension

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140
Q

Which direction does the concentration gradient favor for Na+, Ca2+ and K+?

A

Na+: InCa2+: InK+: Out

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141
Q

What are the drug interactions for thiazides?

A

NSAIDs and beta blockers

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142
Q

What adverse effects are associated with amiodarone?

A

Bradycardia and heart block Pulmonary toxicity, hepatic toxicityPhotodermatitisCorneal microdepositsBlocks T4 to T3Hypo/hyperthyroidisms

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143
Q

What are the side effects of nifedipine?

A

Reflex tachycardia: major adverse effectPeripheral edemaHypotension

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144
Q

Describe the ionic movements in the thick ascending limb

A

Transporters: Na/K/2Cl cotransporter moves cations in from lumen, Na/K ATPase basolateral, K+/Cl- cotransport basolateral 1) ATPase maintains Na gradient to drive NaKCl cotransporter 2) K+ enters from both sides and diffuses back into lumen through channel creating a positive lumenal charge 3) Positive lumenal charge repels Mg and Ca promoting paracellular diffusion

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145
Q

What is the difference between amiodarone and dronedarone?

A

They are structural analogs, but dronedarone does not have iodine atoms attached

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146
Q

What is the effect of calcitonin gene related peptide (CGRP)?

A

Hypotension and tachycardia

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147
Q

Do PCSK9 inhibitors work if statins are also being used?

A

Yes. They decrease serum LDL even in the presence of maximally tolerated statin drugs.

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148
Q

What enzymes synthesize NO?

A

Nitric oxide synthase family of enzymes (three isoforms)

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149
Q

What drugs interact with loop diuretics

A

Aminoglycosides Anticoagulants (increased effect)Beta blockersDigoxinNSAIDsQuinidineSulfonureasSteroids

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150
Q

Describe the adverse events associated with statins

A

The most serious adverse effects are muscular: rhabdomyolysis, myalgia, myopathy Others:GI disturbances, Liver enzyme increase,T2DM

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151
Q

What are the CA inhibitors other than acetazolamide?

A

Dichlorphenamide: 30x potencyMethazolamide: 5x potencyDozolamide: topical ocular use

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152
Q

How do loop and thiazide diuretics cause hypokalemia?

A

Increased tubular Na+ and Cl- creates a more negative lumen potential, which promotes K+ efflux from principal cells

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153
Q

What is a contraindication for dabigatran?

A

Renal failure Dabigatran is 100% cleared by the kidney

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154
Q

What diuretic therapies are recommended for CHF?

A

Spironolactone to prevent hypokalmeia induced heart problems ACE inhibitors (increase K) may be used with thiazide or loop diuretics

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155
Q

Why are vasodilators beneficial for CHF patients?

A

Reduced afterload due to reduced systemic vascular resistance allows for increased SV and CO

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156
Q

What is the mechanism of action of acetazolamide?

A

Reversibly inhibits carbonic anhydrase, thus inhibiting the reabsorption of HCO3- in the proximal tubule

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157
Q

What is the most common side effect of heparin and related drugs?

A

Bleeding

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158
Q

What is the mechanism of action of clopidogrel?

A

Selective inhibition of the ADP receptor, leading to inhibition of platelet aggregation

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159
Q

What adverse events are associated with fibrates?

A

Gallstones Myopathy, Rhabdomyolysis

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160
Q

What are the vaptans and how do they differ?

A

V2 (kidney) receptor antagonists: tolvaptan, mozavaptan, lixivaptanV1a (vascular smooth muscle) and V2 antagonist: conivaptan

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161
Q

Describe the dose dependence of statins

A

Decreases in LDL are dose dependent, but there larger doses increase adverse events more than they improve therapeutic effect

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162
Q

What specific beta blockers are used for chronic CHF therapy?

A

Carvedilol Metoprolol Bucindolol

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163
Q

What are the clinical applications of antiplatelet drugs?

A

Cerebrovascular disease (TIA, stroke) Coronary artery disease (MI, unstable angina) Saphenous vein coronary artery bypass grafts Peripheral vascular disease Small vessel disease Prevention of thrombosis on artificial surfaces

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164
Q

What are the adverse effects associated with mannitol

A

Caused by increased plasma osmolarity, water leaves cells, Na follows -Acute pulmonary edema -Dehydration -Headache, nausea, vomiting

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165
Q

What are the clinical indications for hydrochlorothiazide?

A

Hypertension CHF Prevent kidney stones by reducing Ca2+ excretion

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166
Q

What are the main NO donor drugs?

A

Nitroglycerine Hydralazine L-Arginine

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167
Q

Why doesn’t adenosine kill patients?

A

It has an extremely short half life, so its effects are short lived

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168
Q

What drugs interact with Thiazides?

A

Anticoagulants (decreased effect) Beta blockers Carbamazepine Digoxin NSAIDs Quinidine

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169
Q

What are the major thiazide diuretics?

A

Hydrochlorothiazide Chlorthalidone

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170
Q

What are the contraindications for statin therapy?

A

Pregnancy, nursing mothers and women who may become pregnant Patients with liver disease

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171
Q

What inotropic agents are used to treat CHF?

A

Beta agonists: dobutamine, dopamine, isoproterenol and norepinephrine Phosphodiesterase inhibitors: inamrinone, milrinone *These drugs increase cAMP levels

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172
Q

How is BP affected by NO levels?

A

Decreased NO levels may result in an increased BP

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173
Q

What are the indications for verapamil?

A

Lowers heart rate and increases PR interval Used for supraventricular arrhythmias (drug of choice) Re-entry arrhythmias/tachycardias Slowed ventricular rate in atrial flutter/fibrillation

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174
Q

What is the route of administration of heparin?

A

IV or subcutaneous Not absorbed orally or rectally

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175
Q

What is the mechanism of action of the fibrates?

A

Ligands for the PPAR-alpha transcription factorPromotes expression of genes involved with lipoprotein structure, function and metabolism

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176
Q

What is the effect of dipyridamole?

A

Coronary vasodilatation

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177
Q

What coagulation factors does warfarin act on?

A

II, VII, IX, X

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178
Q

What adverse events are associated with ezetimibe?

A

Flatulence and diarrhea

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179
Q

What is the function of angiotensinase?

A

Breaks down angiotensin II and III into small fragments

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180
Q

What are the major ionic fluxes associated with each phase of the action potential?

A

Phase 0: Na and Ca inPhase 1: Transient K outPhase 2: Plateau from Ca2+ inPhase 3: K+ outPhase 4: resting membrane (K+ permeable, but K in = K out)

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181
Q

What are the bile acid binding resin drug names?

A

Cholestryramaine Colestipol Colesevelam

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182
Q

What is a unique side effect of nitroprusside?

A

Cyanide poisoning

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183
Q

What are the 3 subclasses of class I antiarrhythmic drugs and how do they differ?

A

IA: intermediate kinetics, APD prolonged IB: fast kinetics, APD decreased IC: slow kinetics, APD unchanged

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184
Q

What is the clinical effect of omega-3 fatty acids?

A

Lowers TG levels, increases HDL, may increase LDL

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185
Q

What is Bosentan?

A

A non-selective ET antagonist available orally and IV Inhibits endothelin

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186
Q

What drugs interact with bile acid resins?

A

Many. Do not give drugs at same time as resins (Stagger doses to avoid interactions)

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187
Q

What are the activators of plasmin?

A

t-PA, urokinase, streptokinase Factor XIIa

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188
Q

Describe the composition of lipoprotein particles

A

Lipid membrane made of phospholipids and cholesterol Hydrophobic core containing TGs and cholesterol esters Apolipoproteins, structural proteins and ligands for particle uptake

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189
Q

How do CA inhibitors cause hypokalemia?

A

Increased tubular HCO3- makes lumen potential more negative. This electrogradient increases K+ efflux from principal cells into the tubule and thus increased K+ excretion, hypokalemia

190
Q

How does diuretic treatment differ between chronic right heart failure and acute left heart failure?

A

Right: oral loop diuretics Left: IV loop diuretics (Emergent situation)

191
Q

What are the two pathways of arachadonic acid metabolism?

A

Cyclooxygenase pathway to form PGs Lipoxygenase pathway to form LTs

192
Q

What are the major natriuretic peptides?

A

ABC: Atrial NP Brain NP C-type NP

193
Q

What is the difference between prazosin, terazosin, and doxazosin?

A

Terazosin and doxazosin have longer half lives than prazosin

194
Q

What effect does NO have on platelet function?

A

NO is a potent inhibitor of platelet adhesion, activate and aggregation NO also regulates release of 5HT, growth factors and TXA from platelets

195
Q

What pharmacological changes are beneficial in order to correct cells with abnormal automaticity?

A

Reduced phase 4 slopeIncrease max EmIncrease threshold potentialIncrease action potential durration

196
Q

What channels/receptors are affected by propafenone?

A

Potent Na+ channel blocker Also blocks K+ channels Weak beta blocking activity

197
Q

What class of drugs does warfarin belong to?

A

Vitamin K antagonists (VKAs)

198
Q

Describe the pharmacokinetics of mannitol

A

Not orally absorbed, so given IV to reach kidneyHalf life is 1.2 h

199
Q

What is fondaparinux?

A

Pentasaccharide Complexes with ATIII in order to inhibit factor Xa Used for management of DVT

200
Q

Compare the clinical benefits of angiotensin receptor antagonists and ACE inhibitors

A

They are basically identical: decreased function of angiotensin II

201
Q

What commonly precipitates rhabdomyolysis in patients taking statins?

A

High statin dose OR drug interaction Drugs that inhibit CYP3A4 (cyclosporins, macrolides, ketaconazole)

202
Q

Describe the role of kinins in pain

A

Promote redness, local heat, swelling and painPain is produced via nociceptive afferents in the skin and viscera

203
Q

What are the major adverse effects associated with niacin?

A

Skin flushing, itching Inhibited uric acid secretion can cause gout Can exacerbate peptic ulcer disease

204
Q

Compare the potency of kinins to histamine

A

Kinins are 10x more potent than histamine

205
Q

What factors effect the dose of oral anticoagulants?

A

Nutrition, anemia, liver disease, biliary obstruction, drugs

206
Q

What are the main effects of thrombolytic therapy?

A

Reduce thrombus size Reduce fibrinogen levels Increase fibrinogen and fibrin degradation products Antiplatelet activators

207
Q

What adverse events are associated with acetazolamide?

A

Metabolic acidosis (due to chronic excretion of HCO3-) Hypokalemia (acute effect) Calcium phosphate stones (due to high pH in tubule) Drowsiness, paresthesias and hypersensitivity

208
Q

What molecules increase the production of angiotensinogen?

A

Corticosteroids Estrogens Thyroid Hormones Angiotensin II

209
Q

List the class IC anti-arrhythmic drugs

A

Flecainide Propafenone

210
Q

What are the kinin receptors,?

A

B1 and B2B1 are the main receptors that are responsible for the kinin biological effectsB2 are targeted by drugs to block bradykinin

211
Q

What are the processes targeted by anti-angiotensin II drugs?

A

Block renin secretion/action Inhibit ACE function Block angiotensin receptors

212
Q

What is LCZ696?

A

A combination of valsartan (ARB) and sacubitril (Neprilysin inhibitor) Valsartan blocks the AT1a receptor on cardiac and vascular smooth muscle Sacubitril causes vasodilation and reduced ECF volume via sodium excretion

213
Q

Patients with what conditions should NOT be treated with beta blockers?

A

Asthma, COPD Diabetics: may mask tachycardia associated with hypoglycemia

214
Q

High TG levels lead to an increased risk of what disease?

A

High TGs increase risk of pancreatitis

215
Q

What is the major effect of nitrates?

A

Dilation of venous capacitance vessels

216
Q

List the class IA anti-arrhythmic drugs

A

Procainamide Quinidine Disopyramide

217
Q

What are the therapeutic uses of niacin?

A

Lower plasma cholesterol and TG Used in patients with familial combined hyperlipidemia and familial dysbetalipoproteinemia

218
Q

What are the angiotensin antagonist drugs?

A

Saralasin Losartan Valsartan

219
Q

What are the adverse effects of flecainide?

A

Increased mortality in patients with Vtach, MI, and ventricular ectopy

220
Q

Why are quinidines rarely used?

A
  • They have many adverse events in and out of the heart- Ganglion blocking & hypotension (worse than procainamide) - Anticholinergic effects require combo therapy with drug slowing AV conduction - Induce VFib, torade de pointes - Chronic use causes cinchonism
221
Q

What are the targets for inhibiting NO?

A

1) L-arginine derivatives (L-NMMA, L-NAME) 2) Inhibit NOS synthesis 3) Inhibit binding of arginine to NOS 4) NO scavengers

222
Q

What are the names of the orally active ACE inhibitors?

A

Captopril Enalapril

223
Q

What are the effects of cAMP in cardiac muscle?

A

Inotropy, lusitropy, chronotropy, dromotropy

224
Q

Which anti-hypertensive drugs are not used as first line drugs of choice?

A

Centrally acting agonists Alpha adrenergic blockersBeta blockersVasodilators

225
Q

What is the mechanism of action of PCSK9 inhibitors?

A

PCSK9 inhibitors are human antibodies that are specific for the PCSK9 protein. They bind PCSK9 and prevent its interaction with LDLR. Result: increased expression of LDLR

226
Q

What is the major ion transporter in the thick ascending limb?

A

Na+/K+/2Cl- cotransporter pumps these cations out of the lumen

227
Q

What is the function of kallikrein?

A

Converts HMW kininogen to bradykinin, leading to vasodilation and hypotension

228
Q

Which ADP receptor inhibitors are prodrugs that require liver transformation?

A

Ticlopidine, Clopidogrel and prasugrel

229
Q

How does the relative ratio of cholesterol:TG differ between LDL and HDL?

A

LDL: 60% cholesterol, 25% TGHDL: 20% cholesterol, 5% TG, 35% phospholipid

230
Q

What are the side effects of the thiazide diuretics?

A

HyponatremiaHyperglycemiaIncreased LDL/HDLHypokalemia

231
Q

What are the 4 categories of NO donor drugs?

A

Ultra short (fastest acting) Short Intermediary Long (slowest acting)

232
Q

What effect do bile acid-binding resins have on LDL, HDL and TGs?

A

Modest reduction of LDL No effect on HDL Small increase in TGs

233
Q

What are the adverse effects of hydrochlorothiazide?

A

Hyponatremia, hypokalemia Dehydration Metabolic alkalosis Hyperuricemia Hyperglycemia Hyperlipidemia (LDL) Weakness, fatigue, paresthesia, hypersensitivity

234
Q

Describe the steps that lead to the production of angiotensin III

A

Renin converts angiotensinogen to angiotensin IACE converts Angiotensin I to II (II is the active form)II is degraded into III

235
Q

What is the molecular mechanism of amiodarone?

A

Blocks K+ and Na+ channels, Ca++ channels weakly, and beta receptors

236
Q

What are the major substances reabsorbed and secreted in the proximal convoluted tubule?

A

Reabsorbed: NaHCO3, NaCl Secreted: organic acids and bases

237
Q

Describe use-dependent/state-dependent drug action

A

A drug binding with high affinity to the active and inactive channel, but dissociating from the resting channelsThis in theory targets depolarized cells that are involved with tachyarrhthmias while leaving unaffected cells alone

238
Q

What is phenoxybenzamine used for?

A

Treating HTN in patients with Pheochromocytoma

239
Q

Side effects of verapamil

A

Constipation Bradycardia

240
Q

What are the two classes of Ca channel blockers?

A

Dihydropyridines: nifedipine, nitrendipineNon-dihydropyradines: benzothiazepine (diltiazem) and phenylalkylamine (verapamil)

241
Q

What advantages does lisinopril have over enalopril?

A

Easily absorbed Not metabolized, excreted unchanged by kidney

242
Q

What are the side effects of beta blockers?

A

Bronchospasm Peripheral vasospasm Exaggerated cardiac effects: bradycardia, heart blockCNS effects: insomnia, depression, fatigue

243
Q

What is a clinically important difference between Pravastatin and the rest of the statins?

A

Pravastatin is not metabolized by CYP450, unlike the other statins Fewer associated adverse events (decreased incidence of rhabdomyolysis)

244
Q

What is the general effect of vasopressin?

A

Increased BP via increased renal resorption of water

245
Q

What are the calcium channel blockers used for angina?

A

Dihydropyridines: nifedipine, nicardipine, amlodipineVerapamilDiltiazemBepridil

246
Q

What are the other names of angiotensin converting enzyme (ACE)?

A

Peptidyle dipeptidaseKininase II

247
Q

What are the treatment objectives for chronic CHF?

A

Early recognition of ventricular dysfunction Prevent ventricular remodeling Decrease symptoms: decrease congestion, increase CO Prolong survival

248
Q

What drugs interact with K+ sparing diuretics?

A

ACE inhibitors NSAIDs

249
Q

Describe the mechanism of renal disease causing systemic edema

A

2 Pathways:1) Urinary loss of albumin decreases plasma oncotic pressure2) reduced GFR leads to renal Na retention, water retention

250
Q

What class of drugs may interact with CCBs?

A

Beta blockersUse together with caution

251
Q

How does the action potential from a cardiac pacemaker cell differ from a ventricular cell?

A

Pacemaker cells do not have rapid depolarization caused by fast sodium channelsPacemaker cells also have spontaneous phase 4 depolarization unlike the ventricles

252
Q

What is Niseritide and what is it used for clinically?

A

Niseritide is a recombinant form of BNP Used to treat CHF by inducing vasodilation and natriuresis

253
Q

Describe the drug interaction between gemfibrozil and statins

A

Gemfibrozil inhibits OATP2 transporter, which decreases statin uptake by the liver. This leads to increased statin concentration in the blood and increased risk of myopathy, rhabdomyolysis Also inhibits glucoronidation leading to increased systemic levels of statin

254
Q

What are the endothelin receptors?

A

ET-A and ET-B

255
Q

What is the mechanism of action for spironolactone?

A

Competitive inhibition of aldosterone receptor -Also anti-androgenic, decreases testosterone synthesis

256
Q

What fragments are formed by plasmin degradation of stabilized fibrin?

A

Fragments X, Y, D and E These products form D-dimers, hallmarks of DVT and DIC

257
Q

Location of action of thiazides

A

Distal convoluted tubule

258
Q

What are the anti-Xa drugs?

A

Apixaban Edoxaban Rivaroxaban

259
Q

What are the nonpharmacological treatments for chronic CHF?

A

Surgical therapy Left ventricular assist devices Biventricular pacing Cardiac transplantation

260
Q

What factors increase the risk for arrhythmia?

A

Digitalis treatment General anesthesia Acute MI

261
Q

What is the treatment of warfarin overdose?

A

-Replacement of factors II, VII, IX, X via whole fresh blood infusion of frozen plasma -Recombinant factor VIIa -Vitamin K

262
Q

What are the side effects of digitalis?

A

VERY NARROW THERAPEUTIC WINDOW Causes DADs and abnormal automaticity, arrhythmias

263
Q

From where in the AP do EAD’s originate? How are DAD’s different?

A

EAD’s originate from the plateau phase, more often in slow heart ratesDAD’s originate from the resting potential, more often in high heart rates

264
Q

What is the major difference between metoprolol and atenolol?

A

Metoprolol crosses the BBB, atenolol does not

265
Q

What are the side effects of the loop diuretics?

A

Dehydration/hyponatremia Hypokalemia Impaired diabetes control Increased LDL/HDL Ototoxicity

266
Q

What are the indications for procainamide?

A

Atrial and ventricular arrhythmias (rarely used today)Drug of second or third choice for post-MI ventricular arrhythmias (lidocaine, amiodarone are preferred)

267
Q

What complications are associated with thrombolytic therapy?

A

Bleeding, re-occlusion, stroke

268
Q

What are the side effects of the lipophilic beta blockers?

A

Insomnia Chronic fatigue

269
Q

Location of action of ADH antagonists

A

Collecting ducts

270
Q

Describe the size of heparin

A

Heterogenous Molecular weight varies between 2kDa and 40kDa

271
Q

Increased LDL is associated with what disease?

A

Increased LDL is associated with an increased risk of cardiovascular disease

272
Q

What are the classes of anti-arrhythmic drugs?

A

I: Na+ channel blockers II: beta blockers III: Prolong action potential duration IV: Ca++ channel blockers Other

273
Q

How are HDL levels associated with TG levels?

A

Elevated TGs are associated with decreased HDL (good cholesterol)

274
Q

What is the mechanism for bile acid resins increasing TG levels?

A

bile acids normally suppress endogenous TG synthesis, so the resins decrease bile acid levels leading to increased TG synthesis

275
Q

Describe the states of the Na+ channels in cardiomyocytes

A

3 states, differing based on the conformation of the m (activation) and h (inactivation) gates. Resting: m closed, h open Activated: m and h open, only occurs for 1-2msec Inactivated: m open, h closedThe channels are restored from inactivated to resting state with time and/or voltage

276
Q

What CCBs shouldnt be used to treat chronic hypertension?

A

Short acting CCBs put chronic HTN patients at high risk for MI

277
Q

Which CCB has the strongest vasodilatory effect?

A

Nifedipine

278
Q

Describe the ionic movements in the intercalated cells of the collecting tubule

A

H+ secreted into tubular lumen by proton pumpHCO3- reabsorbed into circulation by HCO3-/Cl- countertransport on basolateral membrane

279
Q

When are vasodilators used for?

A

Used in combo for patients not responding to first line treatment for HTN

280
Q

How does the handling of LDL change in hypercholesterolemia?

A

LDL levels are too high in hypercholesterolemia The LDLR-lysosome degradation of LDL cannot keep up with the high LDL levelsLDL is no longer targeted to peripheral cells, which can lead to the development of atherosclerosis

281
Q

What pharmacokinetic parameter makes amiodarone treatment complicated?

A

Complex half life, takes very long to clear because it accumulates in several organs

282
Q

What is the mechanism of action for ACE inhibitors preventing ventricular remodelling?

A

1) Ang II is a cardiomyocyte growth factor and fibroblast mitogen 2) Inhibit RAA system 3) Decreased wall stress

283
Q

Describe where heparin is found naturally within the body

A

Found in mast cell granules with histamine and serotonin

284
Q

What are the ACE inhibitor drugs?

A

Captopril Enalapril Lisinopril

285
Q

What is the indication for lidocaine?

A

Post-MI arrhythmias Ventricular tachycardia and fibrillation after cardioversion with ischemia/infarction **Selectively inhibits conduction in depolarized cells

286
Q

Which NOS isoforms are inducible, which are constitutively active?

A

NOS-2 is inducible NOS-1, NOS-3 are constitutive

287
Q

How is kallikrein related to the coagulation cascade?

A

Plasma prekallikrein is also known as Fletcher factor, which promotes the intrinsic pathway of coagulation. Factor XIIa also increases kallikrein production

288
Q

What is adenosine used for?

A

Conversion of paroxysmal supraventricular tachycardia to sinus rhythm

289
Q

What is the major contraindication for losartan treatment?

A

Pregnancy Causes fetal renal failure

290
Q

Is antiplatelet monotherapy typically used?

A

No, dual antiplatelet therapy is often used because single target therapy is not sufficient.

291
Q

Describe the structure and function of the juxtaglomerular apparatus

A

Cells from distal convoluted tubule and glomerular afferent arteriole containing osmoreceptors (macula densa) and mechanoreceptors (JG cells) that regulate the RAA system via renin release

292
Q

What is the mechanism of action of dipyridamole and cilostazol?

A

Phosphodiesterase inhibitors

293
Q

Location of action of mannitol

A

Proximal convoluted tubule

294
Q

What are the most used beta blockers for exertional angina?

A

Cardioselective: atenolol and metoprolol

295
Q

How is warfarin metabolized?

A

Liver: hydroxylated in hepatic ER into inactive compound

296
Q

What are the anatomical input(s) and output(s) to the kidney?

A

Input: renal artery Outputs: renal vein and ureter

297
Q

What is the main oral anticoagulant prescribed in the US?

A

Warfarin

298
Q

What are the indications for amiodarone?

A

Oral:Recurrent ventricular tachycardia or fibrillation Atrial fibrillation IV: cardiac arrest, termination of Vtach, fibrillation

299
Q

What are the inhibitors of plasmin?

A

Aminocaproic acid, PAI-1, TAFI, alpha2 antiplasmin, alpha2 macroglobulin

300
Q

What are the main pharmacological mechanisms for anti-arrhythmic drugs?

A

Na+ channel blockadeBlockade of sympathetic autonomic effectsProlong the effective refractory periodCa++ channel blockade

301
Q

What are the most widely used NO donor drugs?

A

Nitrates Denitrated to release NO, cause smooth muscle relaxation

302
Q

What are the beneficial effects of NO?

A

Smooth muscle relaxation Vasodilation Immune regulation Anesthetic effects Anti-atherosclerotic responses

303
Q

How many amino acids are found in angiotensinogen, angiotensin I, and angiotensin II?

A

Angiotensinogen: 14 Angiotensin I: 10 Angiotensin II: 8

304
Q

How does triamterene differ from amiloride?

A

10x less potent than amiloride with a much shorter half life

305
Q

What is the general mechanism of anti-platelet drugs?

A

Inhibition of primary hemostatic plug formation, aggregation, activation and release mechanisms

306
Q

What is ivabradine?

A

Funny current inhibitor Newest anti-anginal drug

307
Q

What is the pathway that NO acts on?

A

NO interacts with the guanyl cyclase which converts GTP to cGMPThis leads to vasodilation

308
Q

What are the indications for acetazolamide treatment?

A

Diuretic therapy (used in combination) Glaucoma (reduce intraocular pressure) Urinary alkalinization (treat overdose, stones) Acute mountain sickness

309
Q

List the components of the nephron in order that filtered fluid traverses the nephron

A

Glomerulus Proximal convoluted tubule Loop of henle (thin descending and ascending, thick ascending) Distal convoluted tubule Collecting ducts

310
Q

How do fibrates affect levels of TG, LDL, HDL?

A

Large reduction in TG Mild reduction in LDL Mild increase in HDL

311
Q

What is the effect of ACE inhibitors on bradykinin levels?

A

Bradykinin levels are increased by ACE inhibitors due the inhibition of kininase II Leads to hypotension

312
Q

What are the sympatholytic drugs used to treat hypertension?

A

Clonidine and Guanfacine Methyldopa *Both are alpha 2 agonists

313
Q

What are the pathological effects of NO?

A

Production of free radicals Nitrosation Irritant effects

314
Q

What is the mechanism of action of monteleukast and zafirleukast?

A

Leukotriene receptor inhibitors

315
Q

What diuretics are used to treat acute CHF?

A

FurosemideThiazides

316
Q

What class of anti-hypertensive is the best choice for uncomplicated hypertension therapy?

A

Diuretics

317
Q

What are the side effects of clonidine?

A

Sedation Dry mouth Dermatitis Rebound hypertension

318
Q

What is the mechanism of action of warfarin?

A

Inhibit II, VII, IX, X by preventing carboxylation of glutamic acid, thus preventing Ca2+ binding

319
Q

How does the kidney control ECF volume?

A

Adjusting NaCl and H2O excretion by altering nephron permeability, regulating ion channels

320
Q

Which diuretic drugs most profoundly increase urinary NaCl?

A

Loop agents + thiazides comboLoop agent monotherapy

321
Q

Describe the pharmacokinetics of heparin

A

PK of heparin is dose dependent Higher doses, longer half life

322
Q

What is the function of lipoprotein lipase?

A

Cleaves off free fatty acids from triglycerides of lipoproteins

323
Q

Describe the pharmacokinetics of acetazolamide

A

Good oral absorption Effect begins ~30 minutes, lasts 12 hours Renal secretion via OAT

324
Q

What is the mechanism of action of ezetimibe?

A

Inhibits NPC1L1 (protein for uptake of dietary and biliary cholesterol in small intestine) Reduces VLDL and LDL production and increases LDLR

325
Q

CCBs should not be given to patients with what condition?

A

Contraindicated for patients with conduction disturbances, heart failure

326
Q

How are beta blockers beneficial for treating arrhythmias?

A

Heart rate is reduced, thus decreasing intracellular Ca overload, pacemaker currents are slowed

327
Q

What drugs are used to counteract the effects of thrombolytic agents?

A

Epsilon amino caproic acid (EACA)Tranexemic acidAprotonin

328
Q

Is the thin descending limb H2O permeable or impermeable?

A

Permeable Water is reabsorbed from the lumen leading to concentration of the tubular fluid

329
Q

What are the contraindications for thiazides?

A

Hypokalemia

330
Q

How does warfarin cause necrosis?

A

Impaired functionality of protein C due to inhibition of gamma carboxylation of glutamic acid

331
Q

Location of action of furosemide

A

Thick ascending limb

332
Q

What is the antagonist of heparin?

A

Protamine: very basic protein derived from fish sperm Combines with heparin to form stable salt with no anticoagulant activity 1:1 antagonism

333
Q

Describe the general mechanism of action of vasoactive peptides?

A

Act on cell surface receptors (GPCRs) leading to production of second messengers or opening of ion channels

334
Q

What is the general goal of anti-arrhythmic therapy?

A

Reduce ectopic pacemaker activity and/or modify conduction characteristics to disable re-entry circuits

335
Q

How are beta blockers useful for chronic CHF treatment?

A

Increased survival due to reduced LV deterioration Mechanism: reduced HR and blocking deleterious effects of chronic sympathetic stimulation

336
Q

What are the drugs that inhibit GPIIb/IIIa receptors?

A

Tirofiban Eptifibatide Abciximab

337
Q

What amino acid is digested to produce endogenous NO?

A

arginine

338
Q

What are the clinical indications of mannitol?

A

-Maintenance/Increase of urine volume (Renal failure, drug overdose) -Reduce intracranial/intraocular pressure (doesn’t cross BBB or enter eye, so it pulls fluid out)

339
Q

What are the drug therapies for exertional angina?

A

Nitrates CCBs Beta blockers Ranolazine Ivabradine

340
Q

Describe the pathway for Na+ and HCO3- absorption in the proximal convoluted tubule

A

Transporters: Na/H antiport on lumenal side, Na/HCO3- on basolateral side 1) Na enters cells via antiporter down gradient and is pumped out via Na/K pump 2) HCO3- is converted to CO2 and H2O in the tubules by CA, which then can diffuse into the cell 3) CO2 and H2O combine to form H+ and HCO3- via intracellular CA 4) HCO3- pumped out of cell into blood

341
Q

How does eplerenone differ from spironolactone?

A

Same MOA, but does not inhibit testosterone binding, so it has decreased side effects Much more expensive

342
Q

What can alter the rate of phase 4 depolarization in cardiac pacemaker cells?

A

Hypokalemia, beta stimulation, and acidosis increase the rate of depolarization, thus reaching threshold fasterBeta blockade, vagal stimulation decrease the depolarization thus reaching the threshold slower

343
Q

What do all arrhythmias result from?

A

1) disturbed impulse formation 2) disturbed impulse conduction 3) a combination of both

344
Q

Side effects of nifedipine

A

Acute tachycardia Peripheral edema

345
Q

What is the effect of neurotensin?

A

Vasodilation, hypotension, increased vascular permeability, hyperglycemia and inhibition of gastric motility

346
Q

How is INR calculated?

A

INR is a normalized PT value INR = PT_patient / PT_normalcontrol

347
Q

What was the original parent compound for diuretic drugs?

A

Sulfanilamide (an antibiotic) that causes metabolic acidosis and alkaline urine (NaHCO3 diuresis)

348
Q

What effect does ezetimibe have on TG levels?

A

Ezetimibe does not raise TG levels (unlike bile acid resins)

349
Q

What are the side effects of the non-selective beta blockers?

A

Increased airway resistance

350
Q

How do calcium channel blockers affect the action potential?

A

Slower AP upstroke, slowed conduction velocityInhibition of Ca influx during AP and also during diastole

351
Q

Describe the ionic movements in the principal cell of the collecting tubule

A

Na and water reabsorbed with ADH presentK secreted via K+ channels Basolateral Na/K ATPase Aldosterone regulates Na/K ATPase and channel expression

352
Q

What is the mechanism of action of amiloride and triamterene?

A

Blocks Na+ channels in the principal cells, thus decreasing the driving force for K+ efflux K+ sparing

353
Q

Which diuretic drugs most profoundly increase urinary NaHCO3- ?

A

Carbonic anhydrase inhibitors

354
Q

How does membrane potential alter the availability of sodium channels?

A

Fewer channels are available at higher potentialsChannels close between -55 and -75 mV

355
Q

What side effects are associated with reserpine?

A

Depression/suicidal ideationsNasal congestion

356
Q

What is the definition of a diuretic?

A

a substance/drug that increases the discharge of urine

357
Q

What is the effect of neuropeptide Y?

A

Vasoconstriction, mediates hypertensive responses

358
Q

What are the anatomic sites of blood pressure control?

A

1) Arterioles 2) Veinous capacitance 3) Heart 4) Kidneys: RAA system

359
Q

Why are diuretics useful for acute CHF?

A

Reduced preload and pulmonary venous pressureIncreases oxygenation

360
Q

What primarily drives Na+ reabsorption throughout the tubule epithelial cells?

A

The Na/K ATPase pump on the basolateral membrane keeps a low [Na+] and a high [K+] inside the cells

361
Q

What vascular beds are affected by bradykinin?

A

Heart, liver, kidney, intestine, skeletal muscles, liver

362
Q

What is the primary determinant of the refractory period?

A

Action potential duration

363
Q

What is the main side effect of the eicosanoids?

A

Hypotension

364
Q

Location of action of K+ sparing diuretics

A

Collecting ducts

365
Q

What are some causes of diuretic resistance?

A

NSAID useCHF or chronic renal failureNephrotic syndromeHepatic cirrhosis *Overcome via increased dose, decreased interval, add another drug

366
Q

What is the mechanism of action for reserpine?

A

Blocks VMAT, preventing NE concentration in vesicles

367
Q

What is Lp(a) and how are Lp(a) levels related to risk of atherosclerosis?

A

Lp(a) is a lipoprotein that prevents thrombolysis (competitive inhibition of thrombolysis pathway) Decreased levels are associated with decreased risk for atherosclerosis

368
Q

Should anti-arrhythmic drugs be used in patients with asymptomatic or minimally symptomatic arrhythmias?

A

No. Increased mortality is associated with anti-arrhythmia treatment

369
Q

How does time affect success of thrombolytic therapy?

A

Older clots are less susceptible to the lytic action of thrombolytic agents

370
Q

What drugs prevent ventricular remodeling?

A

ACE inhibitors, ARB’s, LCZ696 Beta blockers Aldosterone antagonists (spironolactone)

371
Q

Which angiotensin is most pharmacologically and pathologically active?

A

Angiotensin I

372
Q

What are the potassium sparing diuretics?

A

Aldosterone receptor blocker: Spironolactone, Eplerenone ENaC blocker: Triamterene, Amiloride

373
Q

In what situations should K+ sparing diuretics be avoided?

A

Hyperkalemia Patients on drugs (ACEi’s) or with diseases (DM, renal insufficiency) that could cause hyperkalemia

374
Q

What is the effect of vasopeptide inhibitors (omapatrilat, sampatrilat, fasidotrilat)?

A

Enhanced vasodilation, reduced vasoconstriction and increased sodium excretion Mechanism: increased levels of natriuretic peptides and decreased formation of Ang II

375
Q

What are the main drug-drug mechanisms leading to inhibition of warfarin’s effect?

A

Decreasing absorption of warfarin Increasing metabolism of warfarin

376
Q

How does edema form?

A

If filtration exceeds lymphatic drainage, edema formsUnbalanced starling forces

377
Q

What are the main drug-drug mechanisms leading to potentiation of warfarin’s effect?

A

Causing vit K deficiency (ABX) Displacing warfarin from albumin Decreasing clotting factor synthesis Decreasing metabolism Antiplatelet aggregating properties

378
Q

Is warfarin safe to give to pregnant women?

A

No. Warfarin passes the placental barrier and can cause fetal malformation

379
Q

Describe the drug interactions with fibrates

A

Strong protein binders, can displace other albumin bound drugs leading to increased concentrations of other drugs in unbound, active form Major rxn between gemfibrozil and statins (fenofibrate does not affect statin levels)

380
Q

Elevated triglycerides are an independent risk factor for what diseases?

A

Atherosclerosis Cardiovascular disease Pancreatitis (at very high TG levels >500mg/dL)

381
Q

What is the mechanism of action of hydrochlorothiazide?

A

Inhibition of the Na/Cl cotransporter on the lumenal side of the distal tubule

382
Q

What are the symptoms of cardiac arrhythmias?

A

Wilde range from asymptomatic to severe hemodynamic consequences with reduced cardiac output and death

383
Q

What does natriuretic mean?

A

Increased Na+ excretion-In addition to diuretics increasing urine output, many also increase Na+ excretion (natriuretic)

384
Q

What are the indications for flecainide and propafenone?

A

Supraventricular arrhythmias in patients with otherwise normal hearts

385
Q

What are the contraindications for acetazolamide?

A

Cirrhosis because serum NH3 is elevated by both liver failure and increased tubule pH

386
Q

Describe the therapeutic uses of ezetimibe

A

Used to lower LDL in hypercholesterolemia Used in combination with statin to decrease LDL using a lower dose of statin (decrease side effects)

387
Q

Describe the pharmacokinetics of furosemide

A

Rapid oral absorption with a short half life, short durationRenal secretion via OAT

388
Q

What are the major recombinant tissue plasminogen activator drugs?

A

Alteplase, reteplase, and tenecteplase

389
Q

Describe the structure of chemically synthesized heparin

A

Composed of pentasaccharide Mimics the sequence repeats found in natural heparin in order to maintain ATIII interaction

390
Q

What is the mechanism of action of argatroban, bivalirudin and hirudin?

A

Directly inhibits IIa (thrombin)

391
Q

Describe the chemical structure of heparin

A

Strongly acidic mucopolysaccharide with repeating units of sulfated glucuronic acid and sulfated glucosamine

392
Q

What are the clinical uses of warfarin?

A

Prophylaxis for thrombotic disorders Treatment of established thrombus

393
Q

Where are defibrinogenating agents found in nature?

A

Snake venom

394
Q

What are the two types of calcium channel blockers and how do they differ?

A

Dihydropyridines: selective for smooth muscleNon-dihydropyridines: smooth muscle and cardiac pacemakers

395
Q

What are the absolute contraindications of thrombolytic therapy?

A

Intracranial bleeding Massive hemmorhage

396
Q

What channels are not present in pacemaker cells that are found in normal myocytes?

A

Fast sodium channels

397
Q

What regulates NaCl permeability of the collecting duct?

A

Aldosterone

398
Q

What are the 3 main categories of thrombolytic agents?

A

Urokinase Streptokinase Recombinant tissue plasminogen activators

399
Q

What role does PCSK9 play in hypercholesterolemia?

A

PCSK9 is a secreted enzyme responsible for controlling the levels of LDLR expressed on liver cells. Binds to LDLR, triggers internalization and degradation of LDLR

400
Q

What is the mechanism for diuretics causing hypokalemia and metabolic alkalosis?

A

The Na+ concentration in the lumen of the collecting duct is increased. A net negative lumenal charge drives K+ and H+ out of cells into lumen to be excreted.

401
Q

Describe how diuretics reach the tubular fluid

A

Mannitol is filtered across the glomerulus Most others are secreted via organic acid/base transporters in the proximal tubule

402
Q

Explain reverse use/state-dependence

A

Class III anti-arrhythmics have the least effect at fast heart rates, which is when their effects are most needed

403
Q

What is the effect of substance P?

A

Vasodilation via release of NO

404
Q

What adverse effects are associated with ADH antagonists?

A

hypernatremia, thirst, dry mouth, hypoteension, dizziness

405
Q

What is the mechanism of action of digitalis glycosides?

A

Inhibit the Na/K ATPase pump which increase the Na inside the cell, this leads to increased activity of the Na/Ca exchanger, bringing more Ca into the cell and more Ca stored in the SR

406
Q

What are the actions of heparin?

A

Plasma clearing Neutralization of vascular lining Release of tissue factor pathway inhibitor (TFPI)

407
Q

Which NOS isoform is considered “bad” and is a target for drugs?

A

NOS-2 (the inducible isoform)

408
Q

What is the treatment for moderate hypercholesterolemia?

A

Therapeutic lifestyle change is sufficient if there is a low cardiovascular risk

409
Q

What is the general effect of endothelins?

A

Vasoconstriction

410
Q

Side effects of ACE inhibitors

A

Hyperkalemia Dry cough Angioedema

411
Q

Describe the clinical use of bile acid resins

A

Not typically used when statin therapy is an option, but are used in combination for aggressive reduciton of LDL. Statins are contraindicated in children, and women who are lactating/pregnant, so bile acid resins are a useful statin alternative

412
Q

Do angiotensin receptor antagonists have any effect on the actions of ACE?

A

No

413
Q

In what situations are adrenomodulin levels increased?

A

Intense exercise Hypertension Renal failure Septic shock

414
Q

What role does NO play for organ transplant patients?

A

NO is cytoprotective, prevents cellular and platelet adhesion. Dietary arginine supplements are helpful for transplant patient management

415
Q

What are the major side effects associated with NO drugs?

A

Hypotension

416
Q

What is desmopressin?

A

A vasopressin analogue drugUsed for diabetes insipidus, hemophilia and vWF disease (increases VIII), and dental procedures

417
Q

What is the most common electrolyte disorder in hospitalized patients? How is this treated?

A

Hyponatremia*Corrected with AVP receptor antagonists (vaptans)

418
Q

What is the risk with aspirin resistance?

A

May cause recurrent ischemic vascular events in patients taking low dose aspirin

419
Q

What are the main classes of antiplatelet agents?

A

1) Aspirin 2) COX inhibitors 3) NSAIDs 4) ADP receptor inhibitors 5) Dipyridamole 6) Cilostazol 7) GPIIb/IIIa inhibitors 8) Prostacyclin analogue

420
Q

How does re-entry occur?

A

A unidirectional block must be presentA loop is formed from conduction down a normal branch that can loop retrograde through the block slowly and then trigger another impulse down the normal branch

421
Q

What are the eicosanoids?

A

Monteleukast Zafirleukast Zieuton

422
Q

Describe the balance between PGI2 and TXA2 and how it is modulated

A

Healthy individuals should COX pathways that favor PGI2 over TXA2 in order to prevent clotting. Aspirin blocks TXA2 formation in order to tip the balance in favor of PGI2

423
Q

What are the major pharmacologic actions of nitric oxide?

A

Smooth muscle relaxation Decreased cell adhesionInflammatory response

424
Q

What are the indications for ADH antagonists?

A

SIADHeuvolemic or hypervolemic hyponatremiaCHF

425
Q

What are the new drugs developed for the treatment of homozygous familial hypercholesterolemia?

A

Lomitapide and Mipomersen

426
Q

What is the effect of NO on ischemic and reperfusion injury?

A

NO has been shown to protect against ischemic and reperfusion injury

427
Q

What is the effect of statins on concentrations of LDL, HDL, and TGs?

A

Significant reduction of LDL Modest increase in HDL Modest decrease in TGs

428
Q

What effect does niacin have on TGs, LDLs and HDLs?

A

Reduce TGs moderately reduce LDLs moderately increase HDLs (most effective drug to raise HDL)

429
Q

What are the most commonly used nitrates for angina?

A

NitroglycerinIsosorbide mono/dinitrate

430
Q

Why is it beneficial to prolong Na+ channel recovery time for arrhythmia treatment?

A

Prolonging recovery time may prevent re-entry, block tachycardia and prevent premature beats from occurring by decreasing the likelihood that a new action potential will fire

431
Q

What happens if NaCl intake > output?

A

Edema developsThis happens in heart failure, renal failure

432
Q

Describe the endogenous pathway of lipoprotein metabolism

A

VLDL –> IDL –> LDLLDL delivers cholesterol to the periphery or back to the liver

433
Q

Describe the NO treatment for pulmonary hypertension

A

Inhaled to improve cardiopulmonary function Essentially a low dose of viagra (INOmax)

434
Q

Describe the effect of class I anti-arrhythmic drugs

A

Reduced conduction velocity by blocking fast sodium channels, reduces the rate and magnitude of phase 0 depolarization

435
Q

What antiplatelet drugs are used to treat asthma?

A

Zafirleukast and ZieutonTreatment for “aZZma”

436
Q

What are the first line drugs of choice for treating hypertension?

A

Diuretics Calcium channel blockers ACE inhibitors Angiotensin receptor blockers

437
Q

What are the main protective roles of HDL against atherosclerosis?

A

1) Antioxidant activity: PON1 enzyme 2) Inhibit endothelial adhesion molecules 3) Prevent formation of foam cells 4) Promote reverse cholesterol transport

438
Q

What are the nonpharmacological treatments of angina pectoris?

A

Exercise training Angioplasty Atherectomy Stents Intra-aortic balloon counterpulsation CABG

439
Q

What are the major calcium channel blockers and which class do they fall in?

A

Nifedipine: dihydropyridine Diltiazem: nondihydropyridineVerapamil: nondihydropyridine

440
Q

What are the adverse effects associated with bile acid resins?

A

Very few side effects because they are not absorbed or metabolized (remain in GI tract)- GI disturbances- Impaired absorption of fat soluble vitamins

441
Q

How does the bioavailability of LMW heparin differ from native heparin?

A

LMW heparin has 100% bioavailability unlike native heparin which has ~30% bioavailability

442
Q

What is the indication for ancrod?

A

fibrinolytic agent used to treat strokes

443
Q

What adverse effects are associated with verapamil?

A

Vasodilation and negative inotropy can cause hypotension, fibrillation in patients with Vtach-AV block-Heart block-Constipation, nervousness, peripheral edema

444
Q

What is hirudin?

A

A thrombin inhibitor derived from leaches Used for anticoagulation in thrombocytopenic patients

445
Q

What ion is reabsorbed in the distal convoluted tubule and what regulates this reabsorption?

A

Ca2+ is reabsorbed in the DCT in the presence of PTH

446
Q

Side effects of hyralazine

A

Tachycardia Angina aggrevation Fluid retention NSAIDs can reduce effectiveness

447
Q

What are the systemic effects of digitalis glycosides?

A

Increased COIncreased renal perfusion Decreased sympathetic tone

448
Q

What is the mechanism of action of Prazosin?

A

Selective alpha 1 antagonist

449
Q

What site do anti-platelet have activity in that anticoagulants do not?

A

The arterial circulation

450
Q

What adverse events are associated with spironolactone?

A

Hyperkalemia (K+ sparing) Metabolic acidosis (H+ sparing) Gynecomastia, amenorrhea, impotence, decreased libido GI upset, ulcers CNS: headache, confusion, fatigue

451
Q

What type of lipid is considered “bad” cholesterol? What about “good” cholesterol?

A

LDL is bad cholesterolHDL is good cholesterol

452
Q

Compare the potency of angiotensin II and norepinephrine

A

Angiotensin II is 40x more potent than NE

453
Q

Are nitrates used prophylactically?

A

Yes. They can be used as treatment or prophylaxis for exertional angina.

454
Q

What affect does spironolactone have on potassium levels and pH?

A

Sparing of K+ and H+ due to aldosterone inhibition -The negative lumenal charge is prevented because Na remains in lumen

455
Q

What are the clinical uses of calcium channel blockers?

A

Angina PectorisHypertensionArrhythmiasHypertrophic cardiopyopathyMigraineRaynaud’s phenomenon

456
Q

What is the relationship between ammonia excretion and urine pH?

A

Inversely related Increased urine pH (like due to acetazolamide treatments) will decrease ammonia excretion, thus increasing serum ammonia

457
Q

What is the typical selective beta 1 blocker?

A

Esmolol

458
Q

Describe the pharmacokinetics of hydrochlorothiazide

A

Good oral absorption, renal elimination Short half life (2.5 h)

459
Q

What are the contraindications for beta blockers?

A

Acute CHF Bradycardia, heart block Peripheral vascular disease Insulin-dependent diabetes mellitus Sexual impotence Bronchospasm

460
Q

What are the PCSK9 inhibitor drug names?

A

Alirocumab Evolocumab

461
Q

What are contraindications for potassium sparing diuretic treatment?

A

RAS inhibitors

462
Q

What is the general effect of the kinins?

A

Vasodilation, hypotension

463
Q

What adverse effects are associated with furosemide?

A

Hyponatremia, kypokalemia, hypomagnesemia Dehydration Metabolic alkalosis Mild hyperglycemia

464
Q

How do baseline LDL levels affect the effectiveness of statins?

A

Statins are effective at reducing CHD risk irrespective of the initial baseline LDL. They are the drug of choice for primary and secondary CHD prevention

465
Q

Do the new oral anticoagulants require coagulation monitoring?

A

No.

466
Q

What are the “good combinations” of drugs used to treat hypertension?

A

Thiazide/Loop diuretic + K+ sparing diuretic Thiazide with beta blockersCCBs with ACEi’s

467
Q

What is reverse cholesterol transport?

A

Transport of cholesterol from periphery back to the liver where it can be secreted as bile

468
Q

What are the “bad combinations” of drugs used to treat hypertension?

A

ACEi’s with K+ sparing diuretics ACEi’s with ARBs have no advantage in diabetics

469
Q

What is the target of Dabigatran?

A

Factor IIa (thrombin)

470
Q

What are the side effects of heparin?

A

Hemorrhagic complications Heparin induced thrombocytopenia Osteoporosis –> fracture risk Alopecia (loss of hair)

471
Q

What are the diuretics empirically derived from sulfanilamide and how do they work?

A

Acetazolamide (CA inhibitor) Dichlorphenamide (CA inhibitor) Disulfamoylchloraniline (most commonly used diuretic today)

472
Q

What are the most widely used ADP receptor inhibitors?

A

Clopidogrel and prasugrel

Pharm Block 4: Cardio drugs (1 decks)

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