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4º Farmacología > Cardiovascular Osmosis > Flashcards

Cardiovascular Osmosis Flashcards

1
Q

What is the common suffix for ACE inhibitors?

A

-pril

e.g. captopril

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2
Q

What is the common suffix for Angiotensin-II receptor blockers?

A

-sartan

e.g. Losartan

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3
Q

________ is an ACE inhibitor that is administered as a prodrug.

A

Enalapril

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4
Q

What is the MOA of Losartan?

A

Competitive antagonism of Angiotensin II Receptors

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5
Q

Angiotensin II Receptor Blockers (ARBs) and thiazide diuretics are both considered choice antihypertensives.

A

first

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6
Q

Which antihypertensives are recommended in patients with diabetes, esp. those with renal complications?

A

Captopril (and other ACE Inhibitors); or angiotensin receptor blockers (like Telmisartan)

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7
Q

The mechanism of action of captopril is ________.

A

ACE inhibition.

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8
Q

What is the MOA of Enalapril?

A

ACE inhibition

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9
Q

What is the MOA of Lisinopril?

A

ACE Inhibition

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10
Q

Captopril, enalapril, and _______ are ACE inhibitors that decrease angiotensin II levels and subsequently decrease GFR by preventing the constriction of efferent arterioles.

A

lisinopril

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11
Q

The mechanism of ______ is to selectively block binding of angiotensin II to AT1 receptor.

A

angiotensin II receptor antagonists

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12
Q

The difference between angiotensin II receptor antagonists and angiotensin-converting enzyme inhibitors is that the former does not increase ______.

A

bradykinin

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13
Q

If angiotensin converting enzyme inihibitors cannot be tolerated, the medication of choice is ______.

A

angiotensin II receptor antagonists

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14
Q

The adverse effects of angiotensin II receptor antagonists are (3) ______.

A

hyperkalemia, decreased glomerular filtration rate, and hypotension.

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15
Q

A 58-year-old man with controlled hypertension presents to the emergency department with a 2 week history of dry, hacking cough. The patient states that the cough is persistent and disruptive, and he finds himself lying down to improve the symptoms, although they usually do not. The patient states that 3 months ago he was switched to a different drug to treat his hypertension, and he is also currently taking a multivitamin for his health. Physical examination is unremarkable, and a plain chest radiograph is obtained which is also unremarkable. The attending physician switches the patient to a different antihypertensive drug in order to improve his symptoms. Which of the following is the most likely mechanism of action for the alternative drug?

A. Decreased production of angiotensin II in the lungs
B. Increased concentration of kinin in the lungs
C. Interference with binding of angiotensin I to its receptor
D. Interference with binding of angiotensin II to its receptor
E. Reduction of serum angiotensin II levels

A

D. Interference with binding of angiotensin II to its receptor

> Angiotensin receptor blockers (ARBs) are used to treat hypertension without causing drug-induced cough or drug-induced angioedema in patients who were previously using angiotensin converting enzyme (ACE) inhibitors.

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16
Q

A 42-year-old man comes to the office for a routine check-up. Medical history includes diabetes mellitus and a long history of smoking. Family history includes coronary artery disease. Temperature is 36.5°C (97.7°F), pulse is 78/min, respirations are 17/min, and blood pressure is 160/89 mm Hg. A repeat blood pressure taken 2 days later shows 143/88 mm Hg. Which of the following is most likely the best initial therapy?

A. Enalapril
B. Furosemide
C. Hydrochlorothiazide
D. Metoprolol
E. Nifedipine

A

A. Enalapril

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17
Q

Which types of diuretics can exacerbate hyperuricemia?

A

Thiazide and loop diuretics

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18
Q

The musculoskeletal toxicity of thiazides includes ______.

A

hyperuricemia/gout

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19
Q

The mechanism of action of thiazide diuretics is the inhibition of ______ at the early distal convoluted tubule.

A

NaCl symporters

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20
Q

What type of diuretic is Indapamide?

A

Thiazide-like diuretic

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21
Q

Thiazides are always used in combination with ______ when treating HF.

A

Furosemide

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22
Q

What is the MOA of thiazide diuretics?

A

Inhibition of NaCl reabsorption at the early distal tubule

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23
Q

How do thiazide diuretics influence serum Ca levels?

A

Increase
(they decrease Ca excretion)

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24
Q

Loop diuretics and ______ are 2 types of diuretics that cause alkalosis due to volume contraction as a result of increased Angiotensin II levels.

A

thiazide diuretics
(ATII increases Na/H exchange in the PCT thereby leading to increased HCO3 reabsorption)

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25
Q

(Medication classes) ______ both cause potassium excretion and a contraction alkalosis.

A

Loop and thiazide diuretics

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26
Q

Which 2 types of diuretics cause alkalosis?

A

Loop; Thiazide

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27
Q

Which is the oral complication of nifedipine?

A

Gingival hyperplasia

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28
Q

What type of vasodilator is Nifedipine?

A

Ca-channel blocker

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29
Q

What type of vasodilator is Nicardipine?

A

Ca-channel blocker

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30
Q

______ are two Ca channel blockers with high vascular selectivity.

A

Nifedipine and nicardipine

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31
Q

______ is a Ca channel blocker with very high vascular selectivity. It is selective for both coronary and cerebral vessels.

A

Nicardipine

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32
Q

______ is a Ca channel blocker that delays labour by blocking uterine Ca channels, thereby decreasing intracellular Ca levels and triggering relaxation of the myometrium.

A

Nifedipine

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33
Q

Amlodipine is a dihydropyridine Ca2+ channel blocker that blocks ______.

A

voltage dependent L-type Ca2+ channels

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34
Q

______ is the prototype dihydropyridine Ca2+ channel blocker.

A

Nifedipine

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35
Q

Which dihydropyridine Ca channel blocker is used in Subarachnoid Hemorrhage to prevent cerebral vasospasm?

A

Nimodipine

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36
Q

The calcium channel blocker class used to treat Raynaud phenomenon is the ______.

A

dihydropyridines (except for Nimodipine)

(Remember, the dihydropyridines primarily act at vascular smooth muscle, not the heart)

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37
Q

Which dihydropyridine Ca channel blocker is similar to nitrates in effect?

A

Nifedipine

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38
Q

______ are a class of Ca2+ channel blockers that preferentially exert their effects on vascular smooth muscle.

A

Dihydropyridines

(Common examples include amlodipine and nifedipine)

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39
Q

A 70-year-old Caucasian man comes to the office for a routine medical check-up. He has not seen a physician for many years because he considers himself to be in good health. His pulse is 74/minute and his blood pressure is 170/100 mm Hg. At this point, the patient is diagnosed with hypertension and is started on antihypertensive medication. During a follow-up visit to the office, a few months after, the patient’s blood pressure is 135/80 mm Hg. However, the physical examination is remarkable for bilateral, symmetrical pitting edema. Which of the following drugs was mostly likely prescribed and caused the edema in this patient?

A. Amlodipine
B. Hydrochlorothiazide
C. Losartan
D. Ramipril
E. Torsemide

A

A. Amlodipine

> Amlodipine is a dihydropyridine calcium channel blocker that works by inhibiting calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells. Is commonly used in the management of hypertension, common adverse effects include peripheral edema, headaches, flushing, and dizziness.

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40
Q

A 75-year-old man comes to the primary care clinic because of tea colored urine for the past 2 weeks. He has been feeling more fatigued for the last few weeks, but denies any other recent changes. He has a history of hyperlipidemia and insulin-dependent diabetes mellitus, as well as a 40-pack-year smoking history. His blood pressure in the room is 201/95 mm Hg. Urinalysis shows 3+ protein and red blood cells. A renal biopsy is obtained and is shown below (“onion skin” appearance).
Which of the following is the most appropriate medication for this patient?

A. Albumin
B. Cisplatin
C. Dexamethasone
D. Epoetin alfa
E. Labetalol

A

E. Labetalol

> Hyperplastic arteriolosclerosis has a characteristic “onion skin” appearance on biopsy of arterioles. It is associated with hypertensive emergencies, which are treated with multiple antihypertensive medications.

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41
Q

______ is an autoimmune-like complication of Hydralazine use.

A

SLE-like syndrome

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42
Q

______ is a vasodilator that can be used to treat HTN in pregnancy.

A

Hydralazine

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43
Q

______ is a vasodilator that is rapidly metabolized into nitric oxide which then causes vasodilation.

A

Sodium nitroprusside

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44
Q

Sodium nitroprusside is a vasodilator that acts on (vasculature) ______.

A

both arterioles and veins

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45
Q

______ toxicity is associated with high doses of the vasodilator, sodium nitroprusside.

A

Cyanide

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46
Q

Following intravenous administration, ______ administration of nitroglycerin has the fastest onset.

A

sublingual

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47
Q

______ is a nitrate with strict oral ROA and long duration of 6-10 hours.

A

Isosorbide Mononitrate

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48
Q

(Drug class) ______ are often given with hydralazine to prevent reflex tachycardia caused by reflex sympathetic stimulation.

A

Beta-blockers

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49
Q

What is the MOA of Hydralazine?

A

Increases cGMP in smooth muscle, thereby causing relaxation (vasodilation)

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50
Q

Which type of blood vessel is preferentially dilated by Hydralazine?

A

Arterioles > veins

51
Q

Hydralazine (increases/reduces) ______ afterload.

A

reduces

52
Q

Which type of drug is commonly co-administered with Hydralazine to prevent reflex tachycardia?

A

Beta-blocker

53
Q

_______ is a vasodilator that can cause Lupus-like syndrome (Drug-induced SLE) as an adverse effect.

A

Hydralazine

> Remember, Drug induced SLE has anti-histone antibodies.

54
Q

______ , nitroglycerine, and sodium nitroprusside are vasodilators that act by increasing cGMP in smooth muscle cells.

A

Hydralazine

55
Q

Sodium nitroprusside is a vasodilator that is used to treat hypertensive emergency and acts by increasing ______ in smooth muscle via the direct release of nitric oxide.

A

cyclic guanosine monophosphate

56
Q

The duration of action of sodium nitroprusside is (short/long) ______.

A

short

57
Q

The clinical use of sodium nitroprusside is ______.

A

hypertensive emergency

58
Q

The mechanism of nitroglycerin is by _______.

A

increasing nitric oxide in vascular smooth muscle, thereby causing an increase in cGMP and smooth muscle relaxation

59
Q

What is the MOA of Isosorbide Dinitrate?

A

Increases NO in vascular smooth muscle, thereby causing an increase in cGMP and smooth muscle relaxation.

60
Q

______ are the type of blood vessels preferentially dilated by nitroglycerin.

A

Veins&raquo_space; arteries

61
Q

______ and Isosorbide Dinitrate are vasodilators that preferentially dilate veins.

A

Nitroglycerin

62
Q

_______ are the treatment for reflex tachycardia resulting from the administration of nitroglycerin.

A

Beta-blockers

63
Q

_______ is an adverse effect of nitroglycerin/isosorbide dinitrate that is commonly seen following industrial exposure to the drug.

A

“Monday Disease”

> Involves the development of tolerance to the drug during the work week (via industrial exposure) and a loss of tolerance over the weekend. Hence when the person returns to work on Monday there is tachycardia, dizziness and headache when they are re-exposed.

64
Q

What adverse effect of Nitroglycerin/Isosorbide Dinitrate is due to industrial exposure to the drug?

A

“Monday Disease”

> Involves the development of tolerance to the drug during the work week (via industrial exposure) and a loss of tolerance over the weekend. Hence when the person returns to work on Monday there is tachycardia, dizziness and headache when they are re-exposed.

65
Q

______ is an adverse effect of Nitroglycerin/Isosorbide Dinitrate that involves the development of tolerance to the drug during the work week (via industrial exposure) and a loss of tolerance over the weekend.

A

“Monday Disease”

> Hence when the person returns to work on Monday there is tachycardia, dizziness and headache when they are re-exposed.

66
Q

_______ is an adverse effect of industrial exposure of nitroglycerin and the development of tolerance during the work week and loss of tolerance over the weekend resulting in tachycardia, dizziness, and headache upon reexposure.

A

“Monday disease”

67
Q

Cyanide toxicity is associated with high doses of the vasodilator _______.

A

nitroprusside

68
Q

A 62-year-old female with hypertension develops drug-induced lupus secondary to hydralazine therapy. You take a biopsy of a lesion on her face (mancha irregular roja, con centro escamoso amarillento) and send it to pathology. Which of the following histopathologic findings in the basal layer of the epidermis is consistent with this diagnosis?

A. Keratinocyte hyperplasia
B. Necrotic histiocytes
C. Lymphocyte necrosis
D. Hydropic degeneration

A

D. Hydropic degeneration

> Hydropic degeneration of the basal layer of the
epidermis is characteristic of lesions in drug-induced lupus.

69
Q

A 68-year-old man comes to the emergency department because of 4 hours of acute onset retrosternal chest pain, radiating to the left arm. It began while he was playing soccer with his grandson. His past history is significant for type 2 diabetes mellitus controlled with insulin, and hypertension controlled with enalapril. Further history revealed that he had ingested a sildenafil tablet yesterday. Physical examination shows a temperature of 37°C (98.6°F), pulse of 69/min, respirations of 18/min, blood pressure of 130/70 mm Hg, and O2 saturation of 95%. An electrocardiogram shows sinus rhythm and ST-segment elevation in leads V4-V6. Which of the following medications is contraindicated for use in this patient for treating his symptoms?

A. Aspirin
B. Atenolol
C. Enoxaparin
D. Morphine
E. Nitroglycerin

A

E. Nitroglycerin

> Nitroglycerin (and other nitrates) are contraindicated in patients with myocardial infarction if a phosphodiesterase inhibitor has been taken in the last 24 hours, due to the risk of inducing severe hypotension.

70
Q

A 78-year-old man with a history of hypertension comes to the emergency department because of severe chest pain while playing chess with his grandson. En route intravenous access is secured and the patient is given a drug that causes whole body vasodilation. He is stable upon arrival. Laboratory tests show normal cardiac enzymes, and a 12-lead electrocardiogram is normal. Prior to administering more prophylactic treatment, which of the following laboratory tests would best monitor the patient’s nitric oxide levels?

A. Methemoglobin levels
B. Plasma nitroprusside concentration
C. Serum thiocyanate levels
D. Urinary cyanide concentration
E. Urinary nitroprusside concentration

A

C. Serum thiocyanate levels

> STL are used to measure the concentration of nitroprusside in the blood. Nitroprusside is a whole body vasodilator used to treat hypertensive crisis.

71
Q

Procainamide is a class _______ antiarrhythmic drug.

A

IA

72
Q

_______ syndrome is an autoimmune-like complication of procainamide use.

A

Systemic lupus erythematosus-like

73
Q

What is the main mechanism of Quinidine action as an anti-arrhythmic?

A

Blockade of activated Na channels

74
Q

What is the effect of Quinidine on the QT interval?

A

Prolongation

75
Q

What is the effect of Quinidine on the automaticity of cardiomyocytes?

A

Decrease

76
Q

_______ is an adverse effect of Quinidine administration and is characterized by autonomic nervous system dysfunction.

A

Cinchonism

77
Q

Quinidine is contradindicated in patients with prolonged _______intervals.

A

QT

78
Q

_______ is used as an antidote for quinidine toxicity because it helps to reverse the cardiotoxic electrocardiographic effects.

A

Sodium lactate

79
Q

_______ is a class IA antiarrhythmic associated with reversible systemic lupus erythematosus-like syndrome.

A

Procainamide

80
Q

Procainamide is an antiarrhythmic that causes a(n) (increase/decrease) _______ in cardiac action potential duration, thus slowing the heart rate.

A

increase

81
Q

Procainamide (increases/decreases) ________ the slope of phase 0 depolarization of the cardiac action potential.

A

decreases

82
Q

What is the main MOA of Flecainide?

A

Blocks activated Na channels

83
Q

The systemic lupus erythematosus-like syndrome caused by procainamide can be diagnosed by finding ______ antibodies in the serum.

A

anti-histone

84
Q

Class IA antiarrhythmics like procainamide block _______ channels in heart.

A

sodium

85
Q

Class _______ sodium channel blockers are contraindicated in structural and ischemic heart disease.

A

Ic

e.g. Flecainide

86
Q

_______ is an adverse effect of Quinidine due to its ability to act as both an anti-muscarinic and alpha blocker.

A

Cinchonism

87
Q

Procainamide (shortens/prolongs) _______ the effective refractory period of cardiac myocytes to cause its effect.

A

prolongs

88
Q

What class of antiarrhythmic is Quinidine?

A

Class IA

89
Q

The systemic lupus erythematosus-like syndrome caused by procainamide is (reversible/irreversible) _______.

A

reversible

90
Q

What class of antiarrhythmic is Disopyramide?

A

Class IA

91
Q

_______ is a class IA antiarrhythmic associated with cinchonism.

A

Quinidine

92
Q

______ is an adverse effect of Quinidine that involves headache and tinnitus.

A

Cinchonism

93
Q

What is the most common side effect of Quinidine?

A

Cinchonism

94
Q

Procainamide causes state (dependent/independent) _______ suppression of heart rate.

A

dependent

95
Q

The QT interval is (shortened/prolonged) _______ by class IA antiarrhythmics like procainamide.

A

prolonged

96
Q

_______ is a Class IA antiarrhythmic that is associated with heart failure as an adverse effect.

A

Disopyramide

97
Q

What class of antiarrhythmic is Mexiletine?

A

Class IB

98
Q

What class of antiarrhythmic is Flecainide?

A

Class IC

99
Q

What class of antiarrhythmic is Propafenone?

A

Class IC

100
Q

_______ is a procainamide-induced arrhythmia that can occur from the drug’s effect of prolonging the QT interval.

A

Torsades de pointes

101
Q

______ is the drug of choice for treating Wolff-Parkinson-White syndrome.

A

Procainamide

102
Q

_______ syndrome is treated with procainamide.

A

Wolff-Parkinson-White

103
Q

A 62-year-old previously healthy man is rushed into the emergency department after experiencing sharp chest pain that radiated down his left arm. En route, prehospital electrocardiography (ECG) shows ST-segment depression, and the patient is administered supplemental oxygen, aspirin and sublingual nitroglycerin. On arrival the patient is stable, however during initial workup the patient’s PO2 drops and his pulse is no longer discernible (see ECG below). The patient is administered a drug which slows the phase 0 upswing and increases the duration of the action potential. Which of the following drugs is most likely to show the desired effects?
A. Flecainide
B. Mexiletine
C. Procainamide
D. Sotalol
E. Timolol

A

C. Procainamide

> is a class Ia antiarrhythmic drug used to treat cardiac arrhythmias including atria fibrillation. It depresses phase 0 and increases the duration of the action potential.

104
Q

A 23-year-old surfer presents to his primary care physician’s office complaining of a new rash that started a week ago and gets worse when he is out in the sun. He also mentions that for the past week he has been experiencing muscle aches and painful joints, which have prevented him from surfing. His medical history is significant for hypertrophic cardiomyopathy, type I diabetes mellitus (DM-I), and acne. In addition, he was diagnosed 3 months ago with Wolff-Parkinson-White (WPW) syndrome. The patient states that he is currently taking procainamide and propranol for WPW, insulin for DM-I, and doxycycline for the acne, and a multivitamin for overall health. Physical examination shows a diffuse rash, pictured below (rash cutáneo). Laboratory analysis shows positive anti-histone antibodies and antinuclear antibodies. Which of the following medications is most likely to cause the patient’s presentation?
A. Doxycycline
B. Insulin
C. Multivitamin
D. Procainamide
E. Propranolol

A

D. Procainamide

105
Q

Beta blockers are class ______ antiarrhythmics and are commonly used to treat supraventricular tachycardias.

A

II

106
Q

Metoprolol acts on phase_______ of the pacemaker cell action potential.

A

4

107
Q

The preferred drug treatments for social phobias are (2) _______.

A

SSRIs and beta-blockers

108
Q

Which class of antiarrhythmics are contraindicated in cocaine users?

A

Class II; Beta-blockers

> There is a risk of unopposed alpha-adrenergic receptor agonist activity (due to the cocaine action) if there is beta-blockade present

109
Q

Which class II antiarrhythmic can exacerbate vasospasm in Prinzmetal angina?

A

Propanolol

110
Q

Saline, _______, and atropine are used for metoprolol overdose.

A

glucagon

111
Q

Metoprolol can cause a (shortened/prolonged) _______ PR interval on ECG.

A

prolonged

112
Q

______ is a Class II antiarrhythmic that has a very short duration of action.

A

Esmolol

113
Q

What is the duration of action of Esmolol?

A

Very short

114
Q

How does the PR-interval change as a response of class II antiarrhythmic action on the AV-node?

A

Elongated PR-interval

> Class II = beta blockers

115
Q

What class of antiarrhythmics are beta-blockers?

A

Class II

116
Q

Which type of drug is commonly co-administered with Hydralazine to prevent reflex tachycardia?

A

Beta-blocker

117
Q

(Drug class) ______ are often given with hydralazine to prevent reflex tachycardia caused by reflex sympathetic stimulation.

A

Beta-blockers

118
Q

Metoprolol acts on cardiac (myocytes/pacemaker cells) _____ to decrease the slope of phase 4.

A

pacemaker cells

119
Q

How do beta-blockers change the PR interval?

A

Elongation

120
Q

Class ________ anti-arrhythmics are beta-blockers.

A

II

121
Q

Beta-blockers are contraindicated in patients that have a PR interval longer than ______ seconds.

A

0.24

122
Q

Beta-blockers cause reduction of cardiac oxygen demand by (elevating/reducing) ________ the heart rate, contractility and blood pressure.

A

reducing

123
Q

Some beta-blockers treat hypertension partly via the inhibition of renin release via ______ adrenergic receptor blocking in the kidneys.

A

beta-1

124
Q

How do beta-blockers change cardiac contractility?

A

Decrease

4º Farmacología (27 decks)

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