1
Q
Front
A
Back
2
Q
Heart failure leads to activation of the renin–angiotensin–aldosterone system via two mechanisms: ______ and ______.
A
1) Increased renin release by juxtaglomerular cells due to diminished renal perfusion pressure; 2) Renin release promoted by sympathetic stimulation and β receptor activation.
3
Q
Which hormone is a potent vasoconstrictor formed from angiotensin I by ACE?
A
Angiotensin II
4
Q
High levels of angiotensin II and aldosterone have what direct detrimental effects on cardiac muscle?
A
Remodeling, fibrosis, and inflammatory changes
5
Q
Which standard pharmacotherapy in HFrEF blocks the enzyme that cleaves angiotensin I to angiotensin II?
A
ACE inhibitors
6
Q
ACE inhibitors diminish the inactivation of which potent vasodilator?
A
Bradykinin
7
Q
Fill in the blank: Vasodilation in ACE inhibitor therapy occurs due to ↓ ______ and ↑ ______.
A
↓ Angiotensin II, ↑ Bradykinin
8
Q
By reducing angiotensin II levels, ACE inhibitors decrease secretion of ______.
A
Aldosterone
9
Q
Clinical scenario: A 65-year-old man with HFrEF shows improved cardiac output after starting a drug that decreases vascular resistance and venous tone. Which class of drug is responsible?
A
ACE inhibitors
10
Q
ACE inhibitors blunt the usual angiotensin II–mediated increase in ______ and ______ seen in HF.
A
Epinephrine, aldosterone
11
Q
True/False: ACE inhibitors improve clinical signs and symptoms of HF but have no effect on survival.
A
False (They improve survival)
12
Q
Patients with the lowest ______ show the greatest benefit from ACE inhibitors.
A
Ejection fraction
13
Q
ACE inhibitors may be used in combination with which drugs depending on HF severity?
A
Diuretics, β-blockers, digoxin, aldosterone antagonists, hydralazine/isosorbide dinitrate
14
Q
Clinical scenario: A patient post-myocardial infarction is prescribed a long-term drug that improves survival and prevents LV remodeling. Which drug class?
A
ACE inhibitors
15
Q
Name two non-HF conditions where ACE inhibitors are also indicated.
A
Hypertension, recent myocardial infarction (or high risk for cardiovascular event)
16
Q
Adverse effects of ACE inhibitors include ______, ______, ______, ______, and rarely ______.
A
Postural hypotension, renal insufficiency, hyperkalemia, persistent dry cough, angioedema
17
Q
Which adverse effect of ACE inhibitors is due to bradykinin accumulation?
A
Persistent dry cough
18
Q
Potassium levels must be monitored when ACE inhibitors are used with ______, ______, or ______.
A
Potassium supplements, potassium-sparing diuretics, aldosterone antagonists
19
Q
Which lab value must be monitored in patients with underlying renal disease taking ACE inhibitors?
A
Serum creatinine
20
Q
Fill in the blank: ACE inhibitors are ______ and should not be used in pregnant women.
A
Teratogenic
21
Q
Clinical scenario: A hypertensive pregnant woman is accidentally prescribed lisinopril. What is the major risk to the fetus?
A
Teratogenicity
22
Q
Front
A
Back
23
Q
ARBs are competitive antagonists of which receptor?
A
Angiotensin II type 1 receptor
24
Q
Fill in the blank: ARBs provide more complete blockade of ______ action compared to ACE inhibitors.
A
Angiotensin II
25
Why do ARBs provide more complete blockade than ACE inhibitors?
Because ACE inhibitors inhibit only one enzyme producing angiotensin II
26
Do ARBs affect bradykinin levels?
No
27
Clinical scenario: A patient with HFrEF develops persistent dry cough and angioedema on lisinopril. Which drug class is the best substitute?
ARBs
28
True/False: ARBs are therapeutically identical to ACE inhibitors.
False (They are similar but not identical)
29
Although ARBs have a different mechanism of action than ACE inhibitors, their actions on ______ and ______ are similar.
Preload, afterload
30
Main indication of ARBs in HF patients is as a substitute in those with ______ or ______ due to ACE inhibitors.
Severe cough, angioedema
31
Besides heart failure, ARBs are also used in treatment of ______.
Hypertension
32
Adverse effects of ARBs resemble which other drug class?
ACE inhibitors
33
ARBs have a lower incidence of ______ and ______ compared to ACE inhibitors.
Cough, angioedema
34
Like ACE inhibitors, ARBs are contraindicated in ______.
Pregnancy
35
Clinical scenario: A 70-year-old woman with HFrEF and hypertension cannot tolerate ACE inhibitors due to severe cough. What is the next best drug class?
ARBs
36
37
Patients with advanced heart disease have elevated aldosterone levels due to ______ stimulation and reduced ______ of the hormone.
Angiotensin II stimulation, hepatic clearance
38
Spironolactone is a direct antagonist of which hormone?
Aldosterone
39
Fill in the blank: Spironolactone prevents ______ retention, myocardial ______, and ______.
Salt, hypertrophy, hypokalemia
40
Eplerenone is a competitive antagonist of aldosterone at ______ receptors.
Mineralocorticoid
41
Which aldosterone antagonist has fewer endocrine side effects and why?
Eplerenone, due to reduced affinity for glucocorticoid, androgen, and progesterone receptors
42
Aldosterone antagonists are indicated in patients with more severe stages of ______ or ______ and recent myocardial infarction.
HFrEF, HFrEF
43
Clinical scenario: A patient with severe HFrEF post-MI is prescribed a mineralocorticoid receptor antagonist to reduce remodeling and improve survival. Which drug is most commonly used?
Spironolactone
44
True/False: Eplerenone is less likely than spironolactone to cause gynecomastia.
True
45
Front
Back
46
Although β-blockers have negative inotropic activity, what long-term effects do they produce in HF?
Improved systolic functioning and reverse cardiac remodeling
47
What system’s chronic activation do β-blockers counteract in HF?
Sympathetic nervous system
48
Fill in the blank: β-blockers decrease ______ rate and inhibit release of ______ in the kidneys.
Heart, renin
49
Which neurotransmitter’s deleterious effects on cardiac fibers are prevented by β-blockers?
Norepinephrine
50
List three β-blockers that have shown benefit in HF.
Bisoprolol, carvedilol, long-acting metoprolol succinate
51
Which β-blocker is nonselective and also blocks α-adrenoreceptors?
Carvedilol
52
Bisoprolol and metoprolol succinate are selective antagonists of which receptor subtype?
β1
53
Clinical scenario: A patient with HFrEF is prescribed a β-blocker that reduces mortality but initially worsens symptoms. What is the rationale?
Long-term β-blockade improves remodeling and survival despite short-term symptom exacerbation
54
β-blockade is recommended for all patients with which type of HF?
Chronic, stable HF
55
True/False: Bisoprolol, carvedilol, and metoprolol succinate reduce morbidity but not mortality in HFrEF.
False (They reduce both morbidity and mortality)
56
Treatment with β-blockers in HF should be started at ______ doses and ______ titrated.
Low, gradually
57
Both carvedilol and metoprolol are metabolized by which cytochrome P450 isoenzyme?
CYP2D6
58
Inhibitors of CYP2D6 may do what to carvedilol and metoprolol levels?
Increase drug levels and risk of adverse effects
59
Carvedilol is also a substrate of which efflux transporter?
P-glycoprotein (P-gp)
60
Fill in the blank: Increased effects of carvedilol may occur if coadministered with ______ inhibitors.
P-gp
61
Clinical scenario: A patient on carvedilol starts amiodarone and verapamil. What risk increases?
Excessive AV conduction slowing and bradycardia
62
Which other drug classes must β-blockers be used with caution due to AV conduction slowing?
Amiodarone, verapamil, diltiazem
63
Front
Back
64
What is the main role of diuretics in HF?
Relieve pulmonary congestion and peripheral edema
65
Diuretics reduce symptoms of volume overload such as ______ and ______.
Orthopnea, paroxysmal nocturnal dyspnea
66
Fill in the blank: Diuretics decrease plasma volume and venous return (______), reducing cardiac workload and oxygen demand.
Preload
67
How may diuretics decrease afterload?
By reducing plasma volume, thereby decreasing blood pressure
68
Which class of diuretics is most commonly used in HF?
Loop diuretics
69
Loop diuretics are particularly useful in HF patients who require ______ or who have ______.
Extensive diuresis, renal insufficiency
70
Clinical scenario: A patient with HF and renal insufficiency develops severe fluid overload. Which diuretic class is most appropriate?
Loop diuretics
71
What is a major risk of loop diuretic overdose?
Profound hypovolemia
72
True/False: Diuretics improve survival in HF.
False (They do not improve survival; only relieve symptoms)
73
When should diuretics be used in HF management?
Only to treat signs and symptoms of volume excess
74
75
Dilation of venous blood vessels leads to decreased cardiac ______ by increasing venous capacitance.
Preload
76
Which class of drugs is commonly used as venous dilators in HF?
Nitrates
77
Arterial dilators, such as hydralazine, reduce systemic ______ and decrease ______.
Arteriolar resistance, afterload
78
Clinical scenario: A patient with HF is intolerant of ACE inhibitors and β-blockers. Which drug combination may be used to improve symptoms?
Hydralazine and isosorbide dinitrate
79
A fixed-dose combination of hydralazine and isosorbide dinitrate has been shown to improve symptoms and survival in which patient population?
Black patients with HFrEF on standard therapy
80
Common adverse effects of hydralazine/isosorbide dinitrate combination include ______, ______, and ______.
Headache, hypotension, tachycardia
81
Which rare autoimmune condition has been associated with hydralazine use?
Drug-induced lupus
82
Front
Back
83
What is the general effect of positive inotropic agents on cardiac contractility and output?
Enhance contractility and increase cardiac output
84
Fill in the blank: The inotropic action of positive inotropes is due to increased ______ concentration in cardiac cells.
Cytoplasmic calcium
85
True/False: All positive inotropes that increase intracellular calcium improve survival in HFrEF.
False (most reduce survival, except digoxin at low dose)
86
Which positive inotrope is the exception used chronically in HFrEF?
Digoxin
87
Positive inotropes other than digoxin are used mainly in what clinical setting?
Short-term, inpatient setting
88
Digitalis glycosides are derived from which plant?
Foxglove (Digitalis)
89
Which digitalis glycoside is most widely used in HF?
Digoxin
90
Which digitalis glycoside is seldom used due to very long duration of action?
Digitoxin
91
Why is digoxin considered risky in therapy?
It has a low therapeutic index
92
Mechanism: Digoxin inhibits which enzyme to increase intracellular calcium?
Na+/K+-ATPase
93
Fill in the blank: Inhibition of Na+/K+-ATPase reduces the ______ gradient, impairing the Na+/Ca2+ exchanger and increasing intracellular Ca2+.
Na+
94
Clinical scenario: A patient on digoxin has resting membrane potential shifted to –70 mV instead of –90 mV. What risk does this pose?
Increased membrane excitability and arrhythmias (toxicity)
95
What effect does digoxin have on vagal tone?
Enhances vagal tone
96
By slowing AV node conduction, digoxin is useful in treating ______.
Atrial fibrillation
97
What neurohormonal effect is seen with low-dose digoxin?
Inhibition of sympathetic activation
98
Target serum concentration of digoxin in HFrEF for benefit is ______ ng/mL.
0.5 to 0.8
99
At higher serum digoxin concentrations, what happens to mortality?
Mortality likely increases
100
Is digoxin indicated in diastolic HF or right-sided HF?
No, unless atrial fibrillation or flutter is present
101
True/False: Mild to moderate HF patients usually require digoxin as first-line therapy.
False (they respond to ACE inhibitors, β-blockers, aldosterone antagonists, vasodilators, diuretics)
102
What early GI symptoms may indicate digoxin toxicity?
Anorexia, nausea, vomiting
103
Classic visual disturbance in digoxin toxicity is ______.
Yellowish vision (xanthopsia)
104
What electrolyte imbalance predisposes to digoxin toxicity?
Hypokalemia
105
Why does hypokalemia increase digoxin toxicity risk?
Both compete for the same binding site on Na+/K+-ATPase
106
Clinical scenario: A patient on digoxin and furosemide presents with ventricular tachycardia. What is the likely cause?
Digoxin toxicity due to diuretic-induced hypokalemia
107
What antibody treatment can be used for severe digoxin toxicity?
Digoxin immune Fab
108
Digoxin is a substrate of which efflux transporter?
P-glycoprotein (P-gp)
109
Which drugs increase digoxin levels by inhibiting P-gp?
Clarithromycin, verapamil, amiodarone
110
Which other drugs must digoxin be used cautiously with due to AV conduction slowing?
β-blockers, verapamil, diltiazem
111
Front
Back
112
Which β-adrenergic agonist is the most commonly used inotropic agent other than digoxin?
Dobutamine
113
Fill in the blank: β-Adrenergic agonists improve cardiac performance by positive inotropic effect and ______.
Vasodilation
114
Mechanism: β-adrenergic agonists increase intracellular ______, leading to more calcium entry.
cAMP
115
Clinical scenario: A patient with acute decompensated HF is started on IV dobutamine. What is the expected effect on contractility?
Increased contractility (positive inotropy)
116
True/False: Dopamine and dobutamine are used chronically in HFrEF patients for survival benefit.
False (short-term only)
117
Which phosphodiesterase inhibitor is used as an inotrope in refractory HF?
Milrinone
118
Mechanism: Milrinone increases intracellular cAMP by inhibiting ______.
Phosphodiesterase
119
Fill in the blank: Both β-adrenergic agonists and milrinone increase intracellular calcium and therefore ______.
Contractility
120
What is the major risk of long-term milrinone therapy?
Increased mortality
121
Is short-term IV milrinone associated with increased mortality in patients without CAD?
No
122
In which patients may IV milrinone provide symptomatic benefit?
Refractory HF patients
123
Order of therapy: What is usually the first drug introduced in overt HF for volume overload?
Loop diuretic
124
Fill in the blank: After diuretic optimization, ______ inhibitors (or ARBs if not tolerated) are added and titrated.
ACE
125
True/False: Historically, β-blockers were added only after ACE inhibitors were optimized.
True (but now both are initiated together in low doses)
126
In current practice, patients with newly diagnosed HFrEF are often started on both ______ and ______ after stabilization.
ACE inhibitor and β-blocker
127
Why are ACE inhibitors and β-blockers titrated slowly in HF therapy?
To increase tolerability and prevent decompensation
128
Which drugs are added if symptoms persist despite optimal ACE inhibitor and β-blocker?
Digoxin, aldosterone antagonists, hydralazine + isosorbide dinitrate
129
Clinical scenario: A patient with persistent dyspnea despite ACE inhibitor and β-blocker therapy. What next-line agents may help?
Digoxin, aldosterone antagonists, hydralazine + isosorbide dinitrate
130
Stage-based therapy: As HF progresses, is monotherapy or polytherapy usually required?
Polytherapy
Pharma Post-mids
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