Anti-hypertensives Flashcards

1
Q

Use of 2 drugs with different mechanisms of action for treatment of hypertension:
A.  Is usually more effective in decreasing BP than
increasing the dose of the first drug
B.  Should be considered for initial therapy in patients with a baseline BP over 20/10 mm Hg above goal
C.  Often allows for lower doses of both drugs
D.  All of the above

A

D. all the above

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2
Q
Which of the following antihypertensive drugs are less
effective as initial therapy in blacks? 
A.  ACEIs
B.  ARBs 
C.  CCBs 
D.  Diuretics
A

A.  ACEIs

B.  ARBs

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3
Q
Which of the following antihypertensive drugs can cause fetal and neonatal morbidity and death? 
A.  ACEIs 
B.  ARBs
C.  Aliskiren 
D.  Beta blockers 
E.  Diuretics
A

A.  ACEIs
B.  ARBs
C.  Aliskiren

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4
Q
One advantage of ARBs over ACEIs for treatment of
hypertension is that they: 
A.  Are significantly more effective 
B.  Are safer for use in pregnancy 
C.  Generally have fewer side effects
D.  Do not cause hyperkalemia 
E.  All of the above
A

C.  Generally have fewer side effects

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5
Q
Which of the following calcium channel blockers usually
cause an initial reflex tachycardia? 
A.  Amlodipine 
B.  Diltiazem
C.  Felodipine
D.  Nicardipine 
E.  Nisoldipine
A

C.  Felodipine
D.  Nicardipine
E.  Nisoldipine

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6
Q
Which of the following drugs should generally be given
with a beta blocker to minimize reflex tachycardia and a
diuretic to avoid fluid retention? 
A.  Clonidine 
B.  Hydralazine 
C.  Prazosin 
D.  Lisinopril 
E.  Valsartan 
F.   Minoxidil
A

B. Hydralazine
F. Minoxidil

*BB Will block reflex tachycardia caused by other classes of antihypertensive agents

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7
Q

BP is the product of what?

A

CO x SVR

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8
Q

Activation of baroreceptor by ____ results in ___

A

stretched by increased vessel tension, increased blood pressure

inhibits sympathetic discharge from medulla resulting in decreased blood pressure

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9
Q

What in control of moment to moment adjustments in BP and what is in control of long-term BP

A

Short: postural baroreceptor reflex arc

long: renal response to perfusion pressure

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10
Q

How do the kidneys control BP?

A
  1. Reduction in renal perfusion pressure (decreased renal blood flow) → increased Na+ and H2O reabsorption via aldosterone (released by action of angiotensin II).
  2. Also increase in renin production → increased angiotensin II → increased vasoconstriction (in addition to release of aldosterone)
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11
Q

describe the major therapeutic classifications and sites of actions for antihypertensives

A
  1. Diuretics —> kidneys (ie. thiazide)
  2. Vasodilators–> vessels (ie. CCBs)
  3. RAAS antagonists–> kidneys, BV (ie. ACEI)
  4. adrenergic inhibitors –> kidneys, CNS, BV, heart (ie. BB, A1 blockers, vasomotor center inhibitors)
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12
Q

When blood pressure is lowered by pharmacologic interventions, homeostatic mechanisms are activated to increase blood pressure - via

A

baroreceptor reflexes–> increase SNS outflow–> vasoconstriction, tachycardia, increased contractility= increase BP

renal perfusion reflexes: increased renin release–> Na/H20 renention = increase BP

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13
Q

Why does moderate-severe hypertension often have to be treated by more than 1 drug?

A
    • rationale being that each agent acts on one of a set of interacting compensatory regulatory mechanisms for blood pressure to increase antihypertensive effect and possibly prevent toxic effect
    • The hypotensive effect resulting from interference with only one mechanism may be diminished by the compensatory response of a second mechanism
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14
Q

What is goal blood pressure

A

Pts under 60, diabetes, CKD: 140/90

pts over 60: 150/90

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15
Q

causes of hypertension

A
  1. Unknown (essential-primary [> 90%])
    2.Identifiable (secondary): renal disease, 1⁰ aldosteronism,
    pheochromocytoma, Cushing’s syndrome, sleep apnea
    3.  Drug-Induced
    -NSAIDs - COX-2 selective inhibitors
    -Sympathomimetics
    -Oral Contraceptives
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16
Q

What are the main classes of initial HTN monotherapy

A
  1. long acting CCBs
  2. ACEI or ARBs
  3. thiazide diuretic

*BB are less used due to adverse CV outcomes (ie. less protection against stroke risk)

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17
Q

Initial monotherapy for hypertension should be based on

A

age and race

  • younger pts respond best to ACEI- ARBs
  • Black patients and elderly patients best to thiazide diuretic or long-acting CCB
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18
Q

Black patients and elderly patients best respond to what hypertension monotherapy

A

Respond best to

  1. thiazide diuretic or
  2. long-acting CCBs as they usually have lower plasma renin activity (PRA) than younger and white patients
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19
Q

younger patients best respond to what hypertension monotherapy

A

ACEIs- ARBs

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20
Q

Switching to second drug has a ___% chance of normotensive response (60-80% initially controlled with a single drug)

A

50%

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21
Q
Responders to a given drug class will do so at \_\_ doses
with \_\_ side effect
A

lower

fewer

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22
Q

Higher doses associated with:

A
  1. more side effects

2. without further significant reductions in blood pressure

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23
Q

What is indicated if not at goal BP with monotherapy

A

combination therapy

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24
Q

What is the preferred combo therapy

A

long acting ACEI + long acting CCB

  • If treated with one as monotherapy, add the other
  • If treated with thiazide diuretic, discontinue and start with ACEI and CCB combination
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25
Q

When should you consider 2 drugs as initial BP therapy?

A

over 20/10 mmHg above goal

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26
Q

What are lifestyle modifications that one can make to treat HTN

A

1 . Keep healthy eating habits: DASH diet - Mediterranean diet - AHA diet - USDA food pattern

  1. Limit sodium intake: no more than 1500 mg/day if BP reduction needed
  2. Stop smoking
  3. Engage in regular physical activity: 3-4 sessions per week of 40 minutes of moderate vigorous activity
  4. Achieve and maintain a healthy weight: if overweight or obese → set goal of 5-10% weight loss in 6 months - can reduce TGs, blood glucose, A1C, and T2DM risk
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27
Q

What are RAAS antagonists

A

ACEI and ARBs

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28
Q

Examples of ACEI (RAAS antagonist)

A
  1. lisinopril
  2. Enalapril
  3. Ramipril
  4. Benazepril
  5. Quinapril
  6. Captopril
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29
Q

what is the MOI of ACEI

A

Inhibits enzyme which converts angiotensin I to angiotensin II

  1. Prevents Ang II-induced vasoconstriction (increased PVR)and aldosterone secretion (increased Na+ retention)
  2. Decreases bradykinin inactivation, increasing its
    vasodilator action
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30
Q

describe the absorption of ACEI

A

well absorbed orally– most have reduced absorption if taken with food

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31
Q

Most ACEI are ___ that are converted to the active metabolite by de-esterification in the liver

A

Prodrugs

exceptions: lisinopril and captopril

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32
Q

Describe the elimination and duration of action of ACEI

A
  1. Active metabolites are eliminated by the kidneys - renal dosing required
    - Exceptions: moexipril and fosinopril
  2. Duration of action generally sufficient to allow once-daily dosing for most agents
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33
Q

Potential SE of ACEI

A
  1. Contraindicated in pregnancy (category C/D in 2nd and 3rd trimester)
  2. DRY COUGH
  3. HYPERkalemia
  4. hypotension (if hypovolemic)
  5. acute renal failure (esp. with renal artery stenosis)
  6. neutropenia and proteinuria with HD captopril
  7. Angioedema
  8. Minor= altered taste sense, skin rash
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34
Q

first-line choice as monotherapy and combination therapy (with calcium channel blocker)

A

ACEI

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35
Q

Particularly effective in young, high-renin patients

A

ACEI (as w/ BB)

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36
Q

Can be used in asthma, diabetes, and CHF

A

ACEI

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37
Q

Clinical trials of ACEI have demonstrated favorable effects when used in patients with ___ and ___

A

diabetes and proteinuric chronic kidney disease

slow progression of diabetic neuropathy and reduce albuminuria

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38
Q

Examples of ARBs (aka AT-1 blockers)

RAAS antagonists

A
  1. Valsartan (diovan)
  2. Losartan (Cozaar)
  3. Olmesartan (Benicar)
  4. Irebesartan (Avapro)
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39
Q

What is the MOI of ARBs (aka AT-1 blockers)

A

selective inhibtion of angiotensin II receptor AT1

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40
Q

What are the advantages of ARBs vs ACEI

A
  1. More complete inhibition of angiotensin action

2. Alternative pathways to form Ang II are NOT blocked by ACEIs (uncertain significance)

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41
Q

What are the disadvantages of ARBs vs ACEI

A
  1. Loss of increased bradykinin actions (vasodilation) that
    result from ACE inhibition
  2. Will not block Ang II actions at non-AT-1 receptors
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42
Q

Describe the PK of ARBs (aka AT-1 blockers)

A
  1. All agents are effective orally with once daily dosing
    except for losartan (twice daily)
  2. Decreased losartan dose necessary in hepatic dysfxn
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43
Q

What are the side effects of ARBs (aka AT-1 blockers)

A
  • similar to ACEI
    1. contraindicated in pregnancy

**NO angioedema or cough (thought to be BK- mediated)

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44
Q

First-line choice as monotherapy and combination therapy. Role for use in hypertensive patients that have responded to ACE inhibitors but had to discontinue ACEI (mostly due to cough).

A

ARBs (aka AT-1 blockers)

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45
Q

Examples of direct renin inhibitors

A
  1. Aliskiren (Tekturna)
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46
Q

What are the MOI of direct renin inhibitors

A

a potent competitive inhibitor of renin → blocks conversion of angiotensinogen to angiotensin I.
-This results in a dose-dependent decrease in plasma renin activity (PRA) and AngI and AngII levels that is associated with a decrease in BP

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47
Q
A patient returns to her physician assistant for routine
monitoring 6 months after her hypertension regimen was modified. Lab results indicated an elevated potassium level. Which agents is most likely responsible for this hyperkalemia? 
A.  Lisinopril 
B.  Chlorthalidone 
C.  Hydrochlorothiazide 
D.  Spironolactone 
E.  Atenolol 
F.  Furosemide 
G. Valsartan
A

A.  Lisinopril
D.  Spironolactone
G. Valsartan

48
Q
A patient with low blood levels of potassium (hypokalemia) would be at increased risk for toxicity from which of the following drugs? 
A.  Lisinopril (an ACE inhibitor) 
B.  Digoxin 
C.  Hydrochlorothiazide 
D.  Propranolol 
E.  Nifedipine
A

B.  Digoxin

49
Q

Advantages of direct renin inhibitors vs ACEI-ARBs

A
  1. Ability to neutralize plasma renin activity when used in combination with ACEIs or ARBs.

(NOTE: ACEIs - ARBs, by decreasing AngII levels, suppress AngII feedback inhibition on renin secretion and increase PRA)

50
Q

Disadvantages of direct renin inhibitors vs ACEI-ARBs

A

Long-term advantages effects need to be established

51
Q

Side effects of direct renin inhibitors

A
  1. GI (diarrhea, abdominal pain)
  2. hyperkalemia

*does not increase BK levels so no angioedema or cough

52
Q

Thus, recommended in patients who are intolerant to other therapies or in combination with other drugs for further blood pressure control

A

direct renin inhibitors

*Blood pressure lowering effect as monotherapy in patients with mild-to-moderate hypertension is commensurate with that of ACEIs and ARBs. Additive effects with a thiazide diuretic or ACEI-ARB.

53
Q

Antihypertensive effects of thiazide diuretics

A
  1. decrease blood volume/CO (short term)

2. decrease PVR (long term)

54
Q

What is the preferred thiazide diuretic for treatment of hypertension? Why?

A

Chlorthalidone is preferred over hydrochlorothiazide

  • more potent w/ longer duration of action w/ single daily dose
  • Used in combination with ACEIs, ARBs, BBs, or CCB
55
Q

Loop diuretic agents are often used when for treatment of hypertension?

A
  1. pts w/ kidney fxn less than 50%
  2. non-responders of thiazide agents
  3. used for volume control in patients with HF or CKD
56
Q

Potassium-sparing diuretic agents are often used when for treatment of hypertension?

A
  1. aldosterone antagonists are useful in certain compelling indications such as HF or post-MI
57
Q

___ will counteract effect of other antihypertensive drugs that cause reflex (often renin-mediated) Na+ retention

A

Diuretics

58
Q

What is the MOI of diuretics used for hypertension

A
  1. Increased Na+ excretion, acutely reducing circulating blood volume. (Blood pressure lowering effect is maintained after blood volume returns to pretreatment levels.)
  2. Reduced intracellular Na+ in arteriolar smooth muscle blocking arteriolar vascular tone
59
Q

Diuretics lowers blood pressure __ mm; often effective alone in treating mild hypertension; some concern with ____

A

10-15mm

deleterious effect on blood lipids [increased cholesterol]

60
Q

Side effects of diuretics when used for treatment of hypertension

A
  1. HYPOKALEMIA (metabolic alkalosis)
  2. uric acid retention (gout attack)
  3. skin rash
  4. HYPERGLYCEMIA
  5. HYPERLIPIDEMIA
  6. HYPERkalemia w/ K+ sparing agents
61
Q

Diuretics for HTN are most useful in what patients?

A
  1. older patients (less risk from long-term changes in blood lipids)
  2. patients with HF
  3. Blacks
  4. slow demineralization in osteoporosis via enhanced renal absorption of Ca2+
62
Q

Diuretics for HTN should be avoided in what patients?

A
  1. sulfa allergy
  2. gout
  3. hyponatremia/hypovolemia
63
Q

NSAIDs can reduce the antihypertensive efficacy of which of the following drug classes?
A.  Diuretics (e.g., hydrochlorothiazide)
B.  ACE inhibitors (e.g., lisinopril)
C.  Alpha-1 blockers (e.g., prazosin)
D.  Calcium channel blockers (e.g., nifedipine)
E.  Beta-blockers (e.g., metoprolol)

A

A.  Diuretics (e.g., hydrochlorothiazide)
B.  ACE inhibitors (e.g., lisinopril)
E.  Beta-blockers (e.g., metoprolol)

64
Q

Examples of CBBs used for HTN

A
  1. Nifedipine
  2. Amlodipine
  3. Felodipine
  4. Diltiazem
  5. Verapamil
65
Q

What is the MOI for CBBS used for HTN

A

Inhibition of L-type Ca++ influx in arterial smooth muscle–> relaxation of vasculature –> decrease PVR

66
Q

Describe the hemodynamic differences exist between CCBs agents

A
  1. Nifedipine (DHP class, i.e., -dipines) most selective
    for vasodilator action on vascular smooth muscle
  2. Verapamil greatest effect on heart (may decrease
    heart rate / cardiac contractility)
    3.  Diltiazem effects are intermediate
67
Q

Available in sustained release forms allowing single daily dosing. Sublingual use for acute hypertension not recommended (tissue ischemia, unpredictable decreases in blood pressure).

A

CCBs

68
Q

Side effects of CCBs for HTN

A
  1. HA
  2. dizziness/ hypotension
  3. flushing
  4. peripheral edema
  5. constipation (ESP. verapamil)
  6. bradycardia, AV block

*Few or no metabolic side effects (hyperglycemia - hyperlipidemia)

69
Q

CCBs are useful to treat HTN in what special populations

A
  1. low renin patients (blacks and elderly)
  2. concomitant angina/ arrhythmias
  3. COPD/asthma/heavy smokers
  4. diabetics
  5. PVD
70
Q
During a routine oral examination, you notice some gum enlargement in your patient.  The patient’s medical history includes the drugs listed below. If this condition is drug-induced the most likely candidate is: 
A.  Albuterol 
B.  Nitroglycerin tablets 
C.  Digoxin 
D.  Verapamil 
E.  Lisinopril 
F.   Hydrochlorothiazide
A

D.  Verapamil

71
Q

First-line choice as monotherapy with ___ CCB and combination therapy

A

long-acting dihydropyridines

72
Q

Examples of direct vasodilators

A
  1. Hydralazine (Apresoline)

2. minoxidil (Loniten)

73
Q

___ traditionally used as third-line, add-on agents in treatment of hypertension.

-Rarely used alone because ____

A

Direct Vasodilators (hydralazine, minoxidil)

their high selectivity for arterial smooth muscle results in reflex action to increase HR / contractility and renin production (Na+ retention) -

*usually used with beta-blocker or diuretic.

74
Q

What is the MOI of direct vasodilators used to treat HTN

A
  1. Hydralazine: dilates arterioles (increases cGMP)
  2. minoxidil: dilates arterioles via opening K channels–> K efflux–> hyperpolarization–> block of vasoconstriction (potentially greater effect than hydralazine)
75
Q

Adverse effects of hydralazine

A
  1. HA
  2. nausea
  3. palpitations
  4. flushing
  5. sweating
76
Q

Reserved for accelerated malignant hypertension unresponsive to conventional therapy (esp., BP over 180/110 and patients with renal insufficiency).

A

Minoxidil

77
Q

Well absorbed orally, available topically as Rogaine® to promote hair growth

A

Minoxidil

78
Q

Side effects of Minoxidil

A
  1. Tachycardia
  2. palpitations
  3. angina
  4. edema
  5. hypertrichosis
  6. HA
  7. sweating
79
Q

What are vasodilators for hypertensive emergencies

A

IV

  1. Sodium nitroprusside (Nipride)
  2. Diazoxide (Hyperstat)

Given parenterally

  1. Labetalol (a/b blocker)
  2. Nicardipine (CCB)
  3. Enalprilat (ACEI)
  4. Fenoldopam (selective D1 receptor agonist)
  5. Esmolol (B1-blocker)
80
Q

What class of drugs are the following agents?

  1. Labetalol
  2. Nicardipine
  3. Enalprilat
  4. Fenoldopam
  5. Esmolol
A
  1. Labetalol (a/b blocker)
  2. Nicardipine (CCB)
  3. Enalprilat (ACEI)
  4. Fenoldopam (selective D1 receptor agonist)
  5. Esmolol (B1-blocker)

*other agents used in hypertensive emergencies parenterally

81
Q

-Infrequent use in hypertensive emergencies - long-acting,
parenterally administered
-  Also available as Proglycem® for use in hypoglycemic
emergencies

A

Diazoxide (hyperstat)

82
Q

how can Diazoxide (hyperstat) be used for hypoglycemic emergiencies?

A

Decreases insulin release from pancreatic β cells via

opening of K+ channels

83
Q

What is the MOI of sodium nitroprusside (nipride)?

A

Dilates arterioles AND venules via nitric oxide (NO)
production
* Very powerful vasodilator

84
Q

When is sodium nitroprusside (nipride) used for HTN?

A

Used by IV infusion in hypertensive emergencies and

severe cardiac failure (e.g., MI)

85
Q

What are associated complications of sodium nitroprusside (nipride) toxicity?

A
  1. accumulation of cyanide metabolite
  2. metabolic acidosis
  3. arrhythmias
  4. hypotension
86
Q

hypotensive actions of beta blockers are related to:

A
  1. negative inotropic activity (β1, heart)
  2. reduction of renin production (β1, kidney).
  3. CNS effects are also possible
87
Q

Examples of Beta blockers used for hypertension

A
  1. Propranolol (Inderal)
  2. Atenolol (Tenormin)
  3. Metoprolol (Lopressor)
  4. Labetalol (Normodyne)
88
Q

Beta blockers have a greater response for BP control in what populations?

A

young, white, hyperkinetic (heart overactive), high renin patients

89
Q

Beta blockers have a compelling indication in pateients with concomitant

A
  1. angina
  2. atrial arrhythmias
  3. HF
  4. post-MI
90
Q

Beta blockers should be avoid in who?

A
  1. asthmatics

2. insulin-dependent diabetics

91
Q

How can A1-blockers control BP?

A

Block of α1 receptors in arterioles and venules (resistance and capacitance vessels) to produce vasodilation. Less reflex tachycardia (no α2 blockade

92
Q

Side effects of Beta blockers

A
  1. Potentiation of congestive heart failure,
  2. bronchospasm in asthmatics,
  3. some CNS disturbances,
  4. sexual dysfunction,
  5. masking of hypoglycemic symptoms,
  6. deleterious effects on blood lipid profile,
  7. abrupt discontinuation may precipitate arrhythmias or myocardial infarctions
93
Q

Side effects of alpha blockers

A

First dose:

  1. syncope;
  2. dizziness,
  3. headache,
  4. lassitude,
  5. nasal stuffiness;

*usually diminish with use

94
Q

NOT recommended for initial monotherapy due to increased risk of heart failure

A

Alpha blockers

95
Q

Examples of Alpha blockers

A
  1. Prazosin (Minipress)
  2. Terazosin (Hytrin)
  3. Doxazosin (Cardura)
96
Q

Advantages of Alpha blockers

A
  1. May be advantageous if hypertensive patient has concomitant benign prostatic hyperplasia (BPH) with urinary symptoms
  2. Absence of CNS depression or bronchospasm (relative to β-blockers),
  3. no adverse blood lipid perturbations (i.e., no hyperlipidemia)
97
Q

The use of epinephrine to treat anaphylactic shock in
may result in an unexpected decrease in blood
pressure if given to a patient who is also taking which
class of antihypertensive agent?

A

A1 blocker (antagonist)

98
Q

Examples of vasomotor center inhibitors

A
  1. Clonidine (Catapres)

2. alpha-methyl Dopa (Aldomet)

99
Q

What is the MOI of Clonidine

A

A2 agonist–> inhibition of central sympathetic outflow

*Mechanism leaves baroreceptor reflex intact (less postural hypotension)

100
Q

Side effects of vasomotor center inhibitors

A
  1. dry mouth and sedation

2. rebound hypertension if rapid withdrawal–> taper

101
Q

Mechanism leaves baroreceptor reflex intact (less postural hypotension); considered as 2nd or 3rd agent

A

vasomotor central inhibitors

102
Q

What is the MOI of alpha-methyldopa?

A

metabolized ot alpha-methyl NE–> which then interferes with peripheral sympathetic function via a reduction of sympathetic outflow from vasopressor centers (acts as post-synaptic α2 adrenergic agonist).

103
Q

Side effects of alpha-methyldopa

A
  1. Overt sedation
  2. impaired concentration
  3. mental depression
  4. impotence
  5. positive Coombs test (predisposition to hemolytic anemia)
104
Q

What med is especially useful for HTN in pregnancy?

A

alpha-methyldopa

105
Q

What are some issues that lead to patient non-compliance?

A
  1. Administered to asymptomatic patient
  2. Provides no direct relief from discomfort
  3. Benefit lies at some future time in preventing disease/death
  4. Drugs can be costly and require frequent administration
106
Q

What class of medication has favorable effects on symptoms in the following comorbid conditions?

  1. BPH:
  2. Essential tremor:
  3. Hyperthyroidism:
  4. Migraine:
  5. Osteoporosis:
  6. Raynaud’s Syndrome:
A
  1. BPH: Alpha blocker
  2. Essential tremor: noncardioselective BB
  3. Hyperthyroidism: BB
  4. Migraine: BB, CCB
  5. Osteoporosis: thiazide diuretic
  6. Raynaud’s Syndrome: DHP CCB
107
Q

What class of medication is has compelling indications (improvement in outcome independent of BP) for the following conditions?

  1. Systolic HF:
  2. Post-MI:
  3. Proteinuric CKD:
  4. Angina:
  5. A/fib/flutter:
A
  1. Systolic HF: ACEI-ARB, BB, diuretic, aldosterone antagonist
  2. Post-MI: ACEI, BB, aldosterone antagonist
  3. Proteinuric CKD: ACEI-ARB
  4. Angina: BB, CCB
  5. A/fib/flutter: BB, non-DHP CCB
108
Q

What class of medication has contraindications for the following conditions

  1. Angioedema:
  2. Bronchospastic disease:
  3. Depression:
  4. Pregnancy:
  5. 2nd-3rd degree heart block:
A
  1. Angioedema: ACEI
  2. Bronchospastic disease: BB
  3. Depression: reserpine
  4. Pregnancy: ACEI-ARB
  5. 2nd-3rd degree heart block: BB, non-DHP CCB
109
Q

What class of medication has adverse effects on the following comorbid conditions

  1. Depression:
  2. Gout:
  3. Hyperkalemia:
  4. Hyponatremia:
  5. Renovascular disease:
A
  1. Depression: BB, clonidine
  2. Gout: diuretic
  3. Hyperkalemia: ACEI-ARB, aldsterone antagonist
  4. Hyponatremia: thiazide diuretic
  5. Renovascular disease: ACEI-ARB
110
Q
Which is an appropriate drug choice for hypertension treatment during pregnancy? 
A.  Lisinopril 
B.  Atorvastatin 
C.  Alpha-methyl dopa 
D.  Aliskerin 
E.  Valsartan 
F.   Hydralazine
A

C.  Alpha-methyl dopa

F.   Hydralazine

111
Q

What special considerations should you make for HTN in the elderly

A

Follow same principles for

general care - lower initial doses may avoid side effects

112
Q

What special considerations should you make for HTN in children and adolescents?

A

Lifestyle interventions strongly recommended. Choice of drugs similar to adults - effective doses are often smaller

113
Q

___, ___, and ___ are preferred medications for the safety of the fetus

A
  1. methyldopa,
  2. β-blockers (labetalol), and
  3. vasodilators (hydralazine)
114
Q

____ should not be used in pregnancy and should be avoided in women likely to become pregnant.

A

ACEIs and ARBs

115
Q

__, __, and ___ do not have the unfavorable effects on blood lipid levels that __ and ___ may have

A

ACEIs, CCBs, and α-blockers

β-blockers or diuretics

116
Q

What antihypertensives are contraindicated in pregnancy?

A
  1. ACEI
  2. ARBs (AT1 blockers)
  3. direct renin inhibitors