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PHARMACOLOGY > Module 03: Pharmacology of Hypertension (Lecture) (Part 01) > Flashcards

Module 03: Pharmacology of Hypertension (Lecture) (Part 01) Flashcards

1
Q

This condition is characterized when the systolic blood pressure (SBP) values of 130mmHg or more and the diastolic blood pressure (DB) is more than 80 mmHg.

A

Hypertension

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2
Q

This is delineated as one of the most common chronic medical condition characterized by a persistent elevation of arterial blood pressure.

A

Hypertension

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3
Q

Describe hypertension as a studied topic.

A

Hypertension has been among the most studied topics of the previous century and has been one of the most significant comorbidities contributing to the development of stroke, myocardial infarction, heart failure, and renal failure.

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4
Q

Describe how the definition and categories of hypertension have evolved over the years.

A

The definition categories of hypertension have been evolving over the years, but there is a consensus that persistent BP readings of 140/90 mmHg or more should undergo treatment with the usual therapeutic target of 130/80 mmHg.

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5
Q

Under the data of the JNC8 Blood Pressure Classification and Categories, what is the range of a normal blood pressure in systolic and diastolic blood pressure?

A

SBP: <130 mmHg
DBP: <85 mmHg

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6
Q

Under the data of the JNC8 Blood Pressure Classification and Categories, what is the range of a high-normal blood pressure in systolic and diastolic blood pressure?

A

SBP: 130 to 139 mmHg
DBP: 80 to 89 mmHg

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7
Q

Under the data of the JNC8 Blood Pressure Classification and Categories, what is the range of grade 1 hypertension in systolic and diastolic blood pressure?

A

SBP: 140 to 159 mmHg
DBP: 90 to 99 mmHg

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8
Q

Under the data of the JNC8 Blood Pressure Classification and Categories, what is the range of grade 2 hypertension in systolic and diastolic blood pressure?

A

SBP: >160 mmHg
DBP: >100 mmHg

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9
Q

Under the data of the ACC/AHN HTN Blood Pressure Classification and Categories, what is the range of a normal blood pressure in systolic and diastolic blood pressure?

A

SBP: <120mmHg
DBP: <80 mmHg

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10
Q

Under the data of the ACC/AHN HTN Blood Pressure Classification and Categories, what is the range of an elevated blood pressure in systolic and diastolic blood pressure?

A

SBP: 120 to 129 mmHg
DBP: <80 mmHg

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11
Q

Under the data of the ACC/AHN HTN Blood Pressure Classification and Categories, what is the range stage one hypertension in systolic and diastolic blood pressure?

A

SBP: 130 to 139 mmHg
DBP: 80 to 89 mmHg

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12
Q

Under the data of the ACC/AHN HTN Blood Pressure Classification and Categories, what is the range stage two hypertension in systolic and diastolic blood pressure?

A

SBP: >140 mmHg
DBP: >90 mmHg

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13
Q

Under the data of the ACC/AHN HTN Blood Pressure Classification and Categories, what is the range of a hypertensive crisis in systolic and diastolic blood pressure?

A

SBP: >180 mmHg
DBP: >120 mmHg

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14
Q

Under the data of the Blood Pressure Classification for Adult Filipinos, what is the range of a normal blood pressure?

A

<120/80 mmHg

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15
Q

Under the data of the Blood Pressure Classification for Adult Filipinos, what is the range of borderline hypertension?

A

120 to 138/80 to 89 mmHg

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16
Q

Under the data of the Blood Pressure Classification for Adult Filipinos, what is the range of hypertension?

A

> 140/90 mmHg

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17
Q

These are a class of drugs that are used to treat hypertension (high blood pressure).

A

Antihypertensives

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18
Q

This kind of therapy seeks to prevent complications of high blood pressure, such as stroke, heart failure, kidney failure, and myocardial infarction.

A

Antihypertensive therapy

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19
Q

Evidence suggests that the reduction of blood pressure by 5 mmHg can decrease the risk of what:

A

(1) Decrease the risk of stroke by 34%
(2) Decrease the risk of ischemic disease by 21%
(3) And can reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.

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20
Q

What are the four (4) drug classes of hypertensives utilized to treat high blood pressure (hypertension)?

A

(A) A: Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) and Angiotensin II Receptor Blockers (ARBS), Alpha Blockers
(B) B: Beta Blockers
(C) C: Calcium Channel Blockers (Central Antagonists)
(D) D: Diuretics

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21
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

ACE Inhibitors

A

Drug Name: “pril”
Examples: Lisinopril and Enalapril
Mechanism of Action: Inhibit ACE
Main Effect on BP: Decrease SVR and SV

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22
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

Angiotensin II Receptor Blockers (ARBs)

A

Drug Name: “sartan”
Examples: Losartan and Valsartan
Mechanism of Action: Block Angiotensin II Receptors
Main Effect on BP: Decrease SVR and SV

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23
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

Alpha Blockers

A

Drug Name: “osin”
Examples: Doxazosin and Terazosin
Mechanism of Action: Block Alpha Receptors
Main Effect on BP: Decrease SVR

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24
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

Beta Blockers

A

Drug Name: “lol”
Examples: Metoprolol and Labetolol
Mechanism of Action: Block Beta Receptors
Main Effect on BP: Decrease HR and SV

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25
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

Calcium Channel Blockers (CCBs)

A

Drug Name: “dipine”
Examples: Amlodipine and Nicardipine
Mechanism of Action: Block Calcium Channels
Main Effect on BP: Decrease SVR

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26
Q

Based on the Antihypertensive Drug Class:
State the drug name, the mechanism of action, the main effect on blood pressure and list some examples.

Diuretics

A

Drug Name: “ide”
Examples: Furosemide and Hydrochlorothiazide
Mechanism of Action: Facilitate Diuresis
Main Effect on BP: Decrease SV

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27
Q

What is the suffix for ACE inhibitors?

A

pril

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28
Q

What is the suffix for Angiotensin II Receptor Blockers (ARBs)?

A

sartan

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29
Q

What is the suffix for Alpha Blockers?

A

Selective Alpha 1 Blockers: osin and zosin
Nonselective Alpha 1 Blockers: mine (Phentolomine and Phenoxybenzamine)

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30
Q

What is the suffix for Beta Blockers?

A

lol

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31
Q

What is the suffix for Calcium Channel Blockers?

A

Dihydropyridines: dipine
Non-dihydropyridines: Verapamil and Diltiazem

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32
Q

What is the suffix for diuretics?

A

ide

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33
Q

Why can and ARB be chosen over an ACE?

A

Indications of ACEIs and ARBa are similar. An ARB may be chosen over an ACE in patients with (or at high risk for) ACE induced side effects such as cough or angioedema.

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34
Q

What is a common side effect of ACE inhibitors that may lead to switching to an ARB?

A

ACE inhibitors may cause a persistent cough, which is not typically seen with ARBs.

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35
Q

How can combining RAAS inhibitors with other antihypertensive medications improve patient compliance?

A

Some RAAS inhibitors are formulated in combination with other antihypertensives, like hydrochlorothiazides, allowing patients to take a single pill for better medication compliance.

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36
Q

What are the FDA-approved indications for the use of ACEIs and ARBs?

A

(A) Hypertension (first line agent), especially for patients who also have:
(B) Type II diabetes mellitus
(C)Chronic kidney disease (CKD)
(D) Coronary artery disease (CAD)
(E) Diabetic nephropathy
(F) heart failure with reduced ejection fraction (HFrEF)
(I) STEMI: Treatment within 24 hours improves survival of hemodynamically stable patients.

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37
Q

What are the off label uses of ACEIs and ARBs?

A

(A) Non-ST elevation acute coronary syndrome (ACS)
(B) Stable coronary artery disease (CAD)
(C) Proteinuric coronary kidney disease (CKD)
(D) Post transplant erythrocytosis in renal transplant recipients

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38
Q

Under RAAS Inhibitors, mortality benefits are see in patients with what?

A

(A) Hypertension
(B) Heart failure
(C) Acute Myocardial Infarction
(D) Stroke
(E) Diabetes Mellitus

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39
Q

Are ACE inhibitors (ACEIs) and ARBs generally used together?

A

No, ACEIs and ARBs are generally not used together, except in rare cases typically managed by nephrologists.

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40
Q

ACEIs and ARBs are frequently combines with what:

A

(A) Diuretics (most commonly hydrochlorothiazide)
(B) Calcium Channel Blockers

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41
Q

What is a common combination of ARB and diuretic?

A

Losartan + hydrochlorothiazide (HCTZ) is a common combination, marketed as Hyzaar.

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42
Q

Name a combination of ARB and calcium channel blocker (CCB).

A

(A) Amlodipine + olmesartan is a combination marketed as Azor.
(B) Telmisartan + amlodipine is marketed as Twynsta.
(C) Valsartan + amlodipine is marketed as Exforge.

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43
Q

Why are ARBs often better tolerated than ACEIs?

A

ARBs have fewer side effects compared to ACEIs, making them more likely to be taken by patients.

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44
Q

This drug acts by inhibiting the conversion of angiotensin I to angiotensin II thereby decreasing the vasoconstrictor effect of angiotensin II and the aldosterone production secondary to angiotensin II stimulation.

A

Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors)

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45
Q

ACEIs block what?

A

They block the degradation of bradykinin causing vasodilation.

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46
Q

Based on the physiologic effects of Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors), it decreases peripheral vascular resistance via:

A

(A) Decreasing angiotensin II levels
(B) Increasing Bradykinin
(C) Decreasing efferent resistance in the kidney

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46
Q

Based on the physiologic effects of Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors), what happens when there is a decrease in angiotensin II levels?

A

There will be a reduction in
(A) Vasoconstriction
(B) Sympathetic activity
(C) Na+ and water reabsorption in the kidney (direct effect)
(D) Aldosterone secretion

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47
Q

How do ACE inhibitors affect bradykinin levels?

A

ACE inhibitors increase bradykinin levels, leading to vasodilation but also increasing the risk of cough and angioedema.

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48
Q

This effect of ACE inhibitors reduces proteinuria and helps stabilize renal function, particularly in patients with chronic kidney disease (CKD).

A

Decrease efferent arteriole resistance

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49
Q

This is the prototype ACE inhibitor drug, acting as a potent and specific inhibitor of peptidyl-dipeptidase.

A

Captopril (Capoten)

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50
Q

What is the mechanism of action of captopril?

A

Captopril blocks the conversion of angiotensin I to angiotensin II, suppressing the renin-angiotensin system and inhibiting pressure responses to exogenous angiotensin.

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51
Q

This is a vasoconstrictor and an important regulator of arterial blood pressure.

A

Captopril

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52
Q

What are the primary indications for captopril use?

A

(A) Essential renovascular hypertension (usually administered with other drugs, particularly thiazide diuretics)
(B) Congestive Heart Failure (CHF) in combination with other drugs
(C) Nephropathy, including diabetic nephropathy

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53
Q

In what conditions is captopril particularly useful when combined with other drugs?

A

Captopril is used in CHF, particularly with
(A) Cardiac glycosides
(B) Diuretics
(C) B-adrenergic blockers

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54
Q

Captopril is characterized to improve the survival of patients with what?

A

Left ventricular dysfunction following myocardial infarction

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55
Q

What is the initial oral dose of ACE inhibitors for hypertension?

A

12.5 mg - 25 mg, given twice or three times a day (BID-TID), which may increase to 50 mg BID-TID at 1-2 week intervals.

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56
Q

What is the usual dosage range for ACE inhibitors in hypertension?

A

The usual range is 25 mg - 150 mg BID-TID, with a maximum of 450 mg per day.

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57
Q

What is the dosing strategy for malignant hypertension when using ACE inhibitors?

A

The initial dose is 25 mg, increasing every 2 hours until the desired blood pressure is achieved, not exceeding 450 mg/day.

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58
Q

What is the recommended dose of ACE inhibitors for left ventricular dysfunction post-myocardial infarction (MI)?

A

The initial dose is 6.25 mg (single dose), then 12.5 mg TID, increasing to 25 mg TID over several days, and eventually 50 mg TID. This can begin 3 days post-MI.

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59
Q

How quickly do ACE inhibitors generally take effect after administration?

A

ACE Inhibitors have a relatively quick onset of action (15 to 60 minutes)

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60
Q

Describe the bioavailability of ACE inhibitors?

A

Prodrugs have higher bioavailability compared with active drugs.

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61
Q

What is the peak time and duration of action for most ACE inhibitors?

A

Peak time is about 1 hour, with a duration of action lasting 6-12 hours.

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62
Q

How are ACE inhibitors distributed in the body?

A

Most ACE inhibitors have minimal protein binding, are well distributed, and cross the placental barrier. They are excreted in breast milk in small amounts.

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63
Q

How are Angiotensin Receptor Blockers (ARBs) metabolized?

A

ARBs undergo extensive hepatic metabolism.

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64
Q

How much ARBS are excreted as feces? State in percentages.

A

60%

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65
Q

How much ARBS are excreted as urine? State in percentages.

A

35% approximately 4% as unchanged drugs

66
Q

What is the plasma half-life range for Angiotensin Receptor Blockers (ARBs)?

A

The plasma half-life varies from 2 to 24 hours, following a biphasic pattern (2 hours and 6 to 9 hours average).

67
Q

How are ACE inhibitor prodrugs metabolized?

A

ACE inhibitor prodrugs are activated via hydrolysis in the liver, with about 50% undergoing this process.

68
Q

How are ACE inhibitor active drugs metabolized?

A

Active drugs are unchanged.

69
Q

How are ACE inhibitors excreted?

A

Excreted primarily in the urine (kidneys) at 50% unchanged.

70
Q

What is the plasma half-life of ACE inhibitors, and how does it change in renal disease?

A

The plasma half-life varies from 2 to 24 hours, and it increases 2 hours in renal disease.

71
Q

What are the significant adverse effects and toxicity of ACE inhibitors?

A

(A) Cough, dyspnea and bronchospasm
(B) Hypotension and postural hypotension
(C) Tachycardia
(D) Angina
(E) Impotence
(F) Dysuria nocturia polyuria frequency
(G) Increase BUN, creatinine or oliguria
(H) Hypersensitivity
(I) Angioedema
(J) Hyperkalemia

72
Q

These drugs bind to and inhibit the angiotensin II type 1 receptor and are indicated to treat hypertension, congestive heart failure, and diabetic nephropathy.

A

Angiotensin II Receptor Antagonist (ARBs)

73
Q

What is the effect of Angiotensin Receptor Blockers (ARBs) on angiotensin II activity?

A

ARBs decrease angiotensin II activity.

74
Q

Based on the physiologic effects of Angiotensin Receptor Blockers, what happens when there is a decrease of angiotensin II activity?

A

There will also be a reduction in:
(A) Vasoconstriction
(B) Sympathetic activity
(C) Na+ and water reabsorption in the kidney
(D) Aldosterone secretion

75
Q

Do ARBs have any effect on bradykinin?

A

No, ARBs do not affect bradykinin levels.

76
Q

This is an angiotensin receptor blocker used to treat hypertension and diabetic nephropathy and is used to reduce the risk of stroke.

A

Losartan (Cozaar)

77
Q

What are the main indications for losartan (Cozaar)?

A

Losartan is used to treat hypertension, diabetic nephropathy with elevated serum creatinine and proteinuria in patients with type 2 diabetes and hypertension- , and to reduce the risk of stroke, especially in patients with left ventricular hypertrophy.

78
Q

At what age is losartan indicated for treating hypertension?

A

In patients older than 6 years old

79
Q

This is indicated to treat hypertension and to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy.

A

Losartan with hydrochlorothiazide

80
Q

What are the absolute contraindications of Angiotensin Receptor Blockers (ARBS)?

A

(A) History angioedema
(B) Pregnancy (2nd and 3rd trimester) and lactation (pregnancy category D)
(C) Patients with diabetes should not use both a DRI (aliskiren) and an ACE or ARB

81
Q

What are the relative contraindications of Angiotensin Receptor Blockers (ARBS)?

A

(A) Patients with abnormal renal function.
(B) Aortic stenosis (ACEIs and ARBs are afterload reducers and can lead to severe hypotension
(C) Dehydration or hypovolemia
(D) Patients taking other medications that may lead to hyperkalemia (e.g. K+ sparing diuretics)

82
Q

What is the recommended oral dose of losartan for hypertension when used alone?

A

50 mg/day

83
Q

What is the recommended oral dose of losartan for hypertension when used in combination with diuretics?

A

25 mg/day

84
Q

What is the recommended maintenance oral dose of losartan for hypertension?

A

25mg to 100mg per day

85
Q

What is the initial dose of losartan for hypertension with left ventricular hypertrophy?

A

50 mg/day.

86
Q

What is the recommended combination therapy for hypertension with left ventricular hypertrophy using losartan?

A

Start with 50 mg/day of losartan, add hydrochlorothiazide 12.5 mg/day, and/or increase losartan to 100 mg/day, then increase hydrochlorothiazide to 25 mg/day if needed.

87
Q

What are the significant adverse effects and toxicity of angiotensin receptor blockers?

A

(A) Hypotension or postural hypotension
(B) Dysrhytmias or 2nd degree AV Block
(C) Angina or myocardial infarction
(D) Impotence
(E) Nocturia, Polyuria, Frequency, UTI
(F) Increase BUN, Creatinine, Oliguria (renal failure)
(G) Dizziness, insomnia, confusion, tremors, and headache
(H) Diarrhea, dyspepsia, anorexia, and vomiting
(I) Anemia
(J) Gout
(K) Cramps or myalgia
(L) Angioedema

88
Q

These are drugs that block the activity of catecholomines, primarily norepinephrine (NE).

A

Anti-adrenergic drugs

89
Q

What are the two (2) major types adrenergic receptors?

A

(A) Alpha Receptors
(B) Beta Receptors (There are several subtypes of each)

90
Q

Adrenergic drugs can be classified according to their specificity for the different receptors, with the major classes including:

A

(A) Selective beta-1 receptor blockers
(B) Nonselective beta-blockers
(C) Mixed alpha- and beta-blockers
(D) Selective alpha-1 receptor blockers
(E) Nonselective alpha-blockers

91
Q

These act by depleting or inhibiting the release of catecholomines from the peripherial nerve ending or altering response at alpha-1 and alpha-2 receptor sites. VASODILATORS.

A

Peripherally-acting selective antihypertensives

92
Q

How do peripherally acting alpha blockers work in the treatment of hypertension?

A

They act by depleting or inhibiting the release of catecholamines from peripheral nerve endings or altering the response at alpha 1- and alpha 2-receptor sites.

93
Q

What is the primary physiologic effect of peripherally acting alpha blockers?

A

They cause vasodilation, which helps to lower blood pressure.

94
Q

These are found in smooth muscle throughout the body, including bronchial, vascular, intestinal, and bladder walls.

A

Alpha-1 receptors

95
Q

What role do alpha-1 receptors play in the cardiovascular system?

A

Alpha-1 receptors play a major role in determining vascular tone and increase afterload by decreasing systemic vascular resistance (SVR).

96
Q

Alpha-1 receptor antagonists cause what:

A

(A) Vasodilation
(B) Relaxation of bladder muscles - improved micro-nutrition

97
Q

This is is an alpha-1 antagonist marketed by Pfizer, first approved by the FDA in 1988.

A

Prazosin (Minipress)

98
Q

What off-label use has prazosin been studied for recently?

A

Prazosin has been studied for its benefits in controlling symptoms of post-traumatic stress disorder (PTSD), especially for reducing nightmares.

99
Q

What are the primary indications for prazosin?

A

Prazosin is indicated for hypertension, benign prostatic hyperplasia (BPH), and off-label for PTSD.

100
Q

Prazosin can be given alone or with other antihypertensive drugs, including what:

A

(A) Diuretics
(B) Beta-adrenergic blocking agents

101
Q

Can prazosin negatively impact lung function?

A

Does not negatively impact lung function, and therefore may be used to manage hypertension in patients who are asthmatic or patients with COPD.

102
Q

What are the contraindications of alpha blockers?

A

(A) Angina, hypotension, orthostatic hypotension, and syncope
(B) Geriatric patients
(C) Pregnancy and lactation (pregnancy category C)
(D) Hypersensitivity
(E) Priapism
(F) Ocular surgery (sp. Cataract)

103
Q

What are the precautions of alpha blockers?

A

(A) Children
(B) Hepatic Disease

104
Q

What is the initial oral dose of prazosin for adults?

A

1 mg BID to TID (may increase dose if further control is needed)

105
Q

What is the usual dose range of prazosin for adults?

A

2 to 20 mg/day, with a maximum dose of 40 mg/day (doses above 20 mg/day typically do not increase effectiveness).

106
Q

What is the initial dose of prazosin for hypertensive urgency, especially in crises associated with increased circulating catecholomines?

A

10 to 20 mg orally, with the option to repeat the dose after 30 minutes if needed.

107
Q

Why must the dosage of prazosin be adjusted for elderly patients?

A

Elderly patients may be more sensitive to the hypotensive and adverse effects of prazosin, requiring dosage adjustments.

108
Q

What are the significant adverse effects and toxicity of alpha blockers?

A

(A) Orthostatic hypotension
(B) Syncope and or dizziness
(C) Drowsiness
(D) Headache
(F) Fatigue
(G) Palpitations or Rebound hypertension
(H) Nasal congestion
(I) GI distress
(J) Edema
(L) Priapism (prolonged erection)
(M) Blurring of vision

109
Q

These drugs competitively inhibit beta-adrenergic receptors.

A

Beta-blockers

110
Q

What is the difference between nonselective and cardioselective beta-blockers?

A

Nonselective beta-blockers bind to both beta-1 (B1) and beta-2 (B2) receptors, while cardioselective beta-blockers only bind to B1 receptors.

111
Q

Can you name examples of cardioselective (B1) beta-blockers?

A

Metoprolol (Betaloc, Lopressor) and bisoprolol (Cardicor) are examples of cardioselective beta-blockers.

112
Q

Can you name examples of nonselective (B1 and B2) beta-blockers?

A

Propranolol (Inderal) and carvedilol (Carvid) are examples of nonselective beta-blockers.

113
Q

These are located in the sinoatrial (SA) node, atrioventricular (AV) node, atrial and ventricular muscle, and kidneys.

A

Beta-1 receptors

114
Q

These are located in blood vessels, bronchi, the gastrointestinal tract, uterus, liver, and urinary system.

A

Beta-2 receptors

115
Q

What are the anti-arrhythmic effects (class 2 anti-arrhythmic drugs) based on the physiologic effects of beta blockers?

A

(A) Negative chronotropic effects (HR)
(B) Negative dromotropic effects
(C) Prolonged refractory period
(D) Membrane stabilizing activity (MS and intrinsic sympathomimetic activity (ISA) do not have a major impact on anti-arrhythmic potency

116
Q

What happens when there are negative dromotropic effects based on the physiologic effects of beta blockers?

A

(A) Delays speed and ability to instigate an action potential
(B) Decreases conduction velocity

117
Q

How does beta-1 (B1) blockade affect oxygen demand and contractility?

A

(1) Decreases heart rate
(2) Decreases contractility
(3) Decreases afterload
(4) Decreases blood pressure

118
Q

How does beta-1 blockade indirectly improve oxygen supply?

A

Beta-1 blockade prolongs diastole, improving perfusion and indirectly increasing oxygen supply.

119
Q

What are the physiologic effects of beta-2 (B2) blockade?

A

Beta-2 blockade causes vasodilation and bronchoconstriction.

120
Q

Which beta-blocker exhibits alpha-1 (A1) blockade, and what is the effect?

A

Carvedilol exhibits alpha-1 blockade, which further reduces afterload by decreasing systemic vascular resistance (SVR).

121
Q

What is the effect of beta-blockers on the ECG?

A

Beta-blockers cause PR prolongation on the ECG.

122
Q

What are the absolute contraindications of beta blockers?

A

(A) Asthma
(B) Uncompensated HF and or cardiogenic shock
(C) 2nd or 3rd degree heart block

123
Q

What are the relative contraindications of beta blockers?

A

(A) Individuals prone to hypoglycemia or diabetes
(B) Hypotension
(C) Peripheral artery disease (PVD)
(D) Liver or kidney disease
(E) Pheochromocytoma (untreated with alpha blockade)
(F) MG
(G) Hyperthyroidism

124
Q

What is the recommended initial oral dose of beta-blockers for hypertension in adults?

A

50 mg BID or 100 mg/day, with the option to increase to 200 to 450 mg in divided doses.

125
Q

How is the extended-release (XR) form of beta-blockers administered?

A

XR tablets are given once daily.

126
Q

What is the initial dose of beta-blockers for hypertension in geriatric patients?

A

Initially, 25 mg/day, with the dose increased weekly as needed.

127
Q

The symptoms of this include bradycardia, hypotension, myocardial depression, cardiogenic shock, ventricular dysrhythmias, mental status changes (delirium, coma, seizures), bronchospasm, and hypoglycemia.

A

Beta-blocker overdose

128
Q

Although beta blockers are generally safe, overdose can produce symptoms of toxicity within ____________.

A

Two hours (almost always within 6)

129
Q

These drugs inhibit both alpha-1 and beta-adrenergic receptors, preventing their stimulation, which leads to vasodilation and a reduction in blood pressure.

A

Combined alpha and beta adrenergic receptor inhibitors

130
Q

Can you name examples of combined alpha & beta blockers?

A

Labetalol (Trandate) and carvedilol (Carvid, Coreg) are examples of combined alpha & beta blockers.

131
Q

What are the absolute contraindications of alpha and beta blockers?

A

(A) Hypersensitivity to Beta Blockers
(B) Asthma
(C) Uncompensated Heart Failure and or cardiogenic shock
(D) 2nd and 3rd degree heart block
(E) Sinus Bradycardia

132
Q

What is the recommended oral dose of combined alpha & beta blockers for hypertension?

A

100 mg BID, which may be given with a diuretic, and can be increased to 200 mg BID after 2 days. The maximum dose is 2,400 mg/day in divided doses.

133
Q

Under the recommended oral dose of combined alpha & beta blockers for hypertension, it can be increased to 200 mg BID after 2 days and can continue to increase every:

A

1 to 3 days

134
Q

How are combined alpha & beta blockers administered for hypertensive crisis via IV bolus?

A

20 mg IV bolus over 2 minutes, with repeated doses of 40-80 mg every 10 minutes, not exceeding 300 mg.

135
Q

How is the IV infusion for hypertensive crisis administered using combined alpha & beta blockers?

A

200 mg in 160 ml D5W (1:1 dilution), running at 2 ml/min (2 mg/min).

136
Q

Under IV infusion for hypertensive crisis administered using combined alpha & beta blockers, when should you stop the infusion?

A

Stop the infusion once the desired BP is achieved, and repeat every 6-8 hours if needed.

137
Q

How are combined alpha & beta blockers metabolized?

A

They are extensively metabolized in the liver.

138
Q

How are combined alpha & beta blockers excretion?

A

(A) 55-60% in the urine
(B) 12-27% recovered in the feces

139
Q

What is the plasma half-life of combined alpha & beta blockers, and do they pass into breast milk?

A

The plasma half-life is 1.7-6.1 hours, and they do pass through into breast milk.

140
Q

What is the pharmacologic class of calcium channel blockers that binds more selectively to vascular smooth muscle calcium channels?

A

Dihydropyridines.

141
Q

What is the primary effect of dihydropyridine calcium channel blockers?

A

Vasodilation

142
Q

What side effect can dihydropyridine calcium channel blockers cause due to their vasodilatory action?

A

Reflex tachycardia (amlodipine)

143
Q

This primarily affect heart contractility and conduction, with less vasodilation and no reflex tachycardia.

A

Non-dihydropyridines

144
Q

What are the two main subclasses of non-dihydropyridine calcium channel blockers?

A

Benzothiazepine and Phenylalkylamine.

145
Q

They act as myocardial depressants with some effect on vascular smooth muscles, primarily affecting the heart.

A

Benzothiazepine (as a cardiac depressant and a vasodilator)

146
Q

Can you give an example of a benzothiazepine calcium channel blocker?

A

Diltiazem

147
Q

They act as strong myocardial depressants by acting on cardiac myocytes with minimal effect on vascular smooth muscle.

A

Phenylalkylamine

148
Q

Can you give an example of a phenylalkylamine calcium channel blocker?

A

Verapamil.

149
Q

What are the physiologic effects of calcium channel blockers?

A

(A) Smooth muscle relaxation (especially vascular muscles) leading to systemic vasodilation
(B) Reduced myocardial contractility
(C) Decreased atrioventricular node conduction velocity
(D) Decreased automaticity (SA node effect)

150
Q

How do calcium channel blockers affect cardiac afterload and blood pressure?

A

They reduce cardiac afterload, lowering blood pressure, especially in hypertension. Dihydropyridines have the greatest effect, followed by diltiazem and verapamil.

151
Q

What is the inotropic effect of calcium channel blockers on the heart?

A

They reduce myocardial contractility, resulting in a negative inotropic effect, lowering cardiac output and blood pressure.

152
Q

Which calcium channel blockers are most effective in reducing oxygen demand in angina patients?

A

Verapamil and diltiazem.

153
Q

How do calcium channel blockers affect atrioventricular (AV) node conduction?

A

They decrease AV node conduction velocity, leading to a negative dromotropic effect, useful in treating supraventricular arrhythmias.

154
Q

What is the effect of calcium channel blockers on the sinoatrial (SA) node?

A

They decrease automaticity, producing a negative chronotropic effect, which lowers heart rate, cardiac output, and blood pressure.

155
Q

Which calcium channel blockers are associated with negative chronotropic and dromotropic effects?

A

Verapamil and diltiazem

155
Q

What are the contraindications to non-dihydropyridine calcium channel blockers?

A

(A) Heart failure with reduced ejection fraction
(B) Sick sinus syndrome
(C) 2nd and 3rd-degree AV block
(D) Supraventricular tachyarrhythmias with an accessory pathway (e.g., Wolff-Parkinson-White syndrome)
(E) Avoid combining with beta-blockers

156
Q

What are the contraindications to dihydropyridine calcium channel blockers?

A

(A) Moderate to severe aortic stenosis
(B) Hypertrophic obstructive cardiomyopathy

157
Q

What are the significant adverse effects of dihydropyridine calcium channel blockers?

A

(A) Headache (due to cerebral vasodilation)
(B) Reflex tachycardia (especially with short-acting nifedipine)
(C) Hypotension
(D) Flushing
(E) Peripheral edema (dose-dependent, usually with amlodipine)
(F) Gingival hyperplasia

158
Q

What are the significant adverse effects of non-dihydropyridine calcium channel blockers?

A

(A) Constipation (dose-dependent)
(B) Fatigue
(C) Bradycardia
(D) Atrioventricular (AV) nodal block
(E) Worsening of cardiac output
(F) Gingival hyperplasia

159
Q

They decrease blood pressure by diminishing sympathetic outflow from the vasomotor center, reducing peripheral vascular resistance.

A

Centrally acting alpha-2 adrenergic agonist

160
Q

These are antihypertensives that decrease blood pressure by diminishing sympathetic outflow from the vasomotor center. VASODILATORS.

A

Centrally acting alpha-2 adrenergic agonist

161
Q

What are examples of centrally acting alpha-2 adrenergic agonists?

A

(A) Methyldopa (Aldomet)
(B) Clonidine (Catapres)
(C) Guanabenz

PHARMACOLOGY (9 decks)

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