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Pharmacology > 10) Hypertension and Anti-Hypertensives > Flashcards

10) Hypertension and Anti-Hypertensives Flashcards

1
Q

Hypertension is recognized as a major risk factor for several potentially lethal cardiovascular conditions, including

A
  • Myocardial infarction
  • Heart failure
  • Stroke
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2
Q

Elevated systolic pressure is considered

A
  • 120-130 mmHg
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3
Q

Stage 1 hypertension systolic pressure

A
  • 130/80 to 140/89 mmHg
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4
Q

Stage 2 hypertension systolic pressure

A
  • 140/90 mmHg +
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5
Q

Systemic vascular resistance (SVR)

A
  • Resistance to blood flow offered by all of the systemic vasculature
  • Excluding the pulmonary vasculature
  • AKA total peripheral resistance
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6
Q

SVR is determined by mechanisms that cause

A
  • Vasoconstriction which increase SVR
  • Vasodilation which
    decrease SVR
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7
Q

Although SVR is primarily determined by changes in blood vessel diameters, changes in

A
  • Blood viscosity also affect SVR
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8
Q

Cardiac output (CO)

A
  • Amount of blood pumped by the heart per minute

- Amount of work performed by the heart in response to the body’s need for oxygen

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9
Q

Drugs used in hypertension

A
  • Diuretics
  • Sympathoplegics
  • Vasodilators
  • Angiotensin antagonists
  • Renin inhibitors
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10
Q

Sympathoplegics are blockers of

A
  • A/B receptors
  • Nerve terminals
  • Ganglia
  • CNS sympathetic outflow
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11
Q

Vasodilator examples

A
  • Calcium blockers
  • Parenteral vasodilators
  • Older oral vasodilators
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12
Q

Angiotensin antagonist examples

A
  • ACE inhibitors

- Receptor blockers

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13
Q

The diuretics most important for treating hypertension are

A
  • Thiazides (eg, chlorthalidone, hydrochlorothiazide)

- Loop diuretics (eg, furosemide)

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14
Q

Nephron (basic structural unit of the kidney) function

A
  • Regulate concentration of water and soluble substances (like Na+) by filtering the blood
  • Reabsorbs what is needed
  • Excretes the rest as urine
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15
Q

Segments of the nephron

A
  • PCT: Proximal convoluted tubule
  • TAL: Thick ascending loop of Henle
  • DCT: Distal convoluted tubule
  • CCT: Cortical collecting duct
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16
Q

Diuretics acting on PCT

A
  • Carbonic anhydrase inhibitors (acetazolamide)
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17
Q

Diuretics acting on TAL

A
  • Loop diuretics (furosemide)
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18
Q

Diuretics acting on DCT

A
  • Thiazides (hydrochlorothiazide)
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19
Q

Diuretics acting on CCT

A
  • K+ sparing diuretics (spironolactone)
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20
Q

Duretics modify

A
  • Salt secretion
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21
Q

Drugs that modify water excretion

A
  • Osmotic diuretics (mannitol: also modifies salt excretion)
  • ADH agonists (desmopressin)
  • ADH antagonists (conivaptan)
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22
Q

Loop diuretics

A
  • Furosemide, Bumetanide, Torsemide (all sulfonamide derivatives)
  • Ethacrynic acid (not a sulfonamide)
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23
Q

Loop diuretics usually induce

A
  • Hypokalemic metabolic alkalosis

- Large amounts of sodium are presented to the collecting tubules, potassium wasting may be severe

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24
Q

Loop are very efficacious. They can cause

A
  • Hypovolemia

- Cardiovascular complications

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25
Q

Distal convoluted tubule

A
  • Pumps Na+/Cl- out of the lumen of the nephron via the
    Na+/Cl– carrier (NCC)
  • Channel is target of thiazide diuretics
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26
Q

Calcium is also reabsorbed in the DCT under the control of

A
  • Parathyroid hormone (PTH)
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27
Q

Thiazides are sulfonamide derivatives; the ones that lack typical thiazide ring in their structure are therefore considered

A
  • Thiazide-like which also contain sulfonamide
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28
Q

Because they act in a diluting segment of the nephron, thiazides may reduce

A
  • Excretion of water and cause dilutional hyponatremia
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29
Q

Loop diuretic names

A
  • Bumetanide
  • Bumex
  • Furosemide
  • Lasix
  • Torsemide
  • Ethacrynic acid
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30
Q

Bumetanide and Bumex metabolism

A
  • Partially hepatic, then urine excreted
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31
Q

Furosemide and Lasix metabolism

A
  • Mainly renal
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32
Q

Torsemide metabolism

A
  • Mainly hepatic
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33
Q

Ethacrynic acid metabolism

A
  • Partially hepatic
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34
Q

Thiazide diuretic names

A
  • Chlorothiazide

- Hydrochlorothiazide

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35
Q

Chlorothiazide and hydrochlorothiazide metabolism

A
  • Not metabolized

- Excreted unchanged in urine

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36
Q

Thiazide-like diuretic names

A
  • Chlorthalidone
  • Indapamide
  • Metolazone
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37
Q

Chlorthalidone and Metolazone metabolism

A
  • Not metabolized

- Excreted unchanged in urine

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38
Q

Indapamide metabolism

A
  • Hepatic
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39
Q

Loop diuretic side effects

A
  • LFT increased
  • Hypomagnesemia
  • Hypokalemia
  • Hypocalcemia
  • Photosensitivity
  • Nephrotoxicity
  • Ototoxicity (dose-related)
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40
Q

Thiazide-like diuretic side effects

A
  • Hypokalemia
  • Hypercalcemia
  • Hypercholesterolemia
  • Hypertriglyceridemia
  • Increase LDL
  • Azotemia
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41
Q

Diuretic side effects (shared by both kinds)

A
  • Fluid and electrolyte loss
  • Hypovolemia (dehydration)
  • Hypotension
  • Hyperglycemia
  • Hyperuricemia
  • Hypochloremia
  • Hyponatremia (dilutional)
  • Metabolic alkalosis
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42
Q

Final segment of the nephron

A
  • Cortical collecting tubule

- Controlled by aldosterone

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43
Q

Aldosterone

A
  • Steroid hormone secreted by the adrenal cortex

- Responsible for sodium reabsorption (2–5%)

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44
Q

The reabsorption of sodium occurs via

A
  • Epithelial sodium channels (ENaC)

- Accompanied by loss of potassium or hydrogen ions

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45
Q

The collecting tubule is the primary site of

A
  • Acidification of the urine

- Last site of potassium excretion

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46
Q

The aldosterone receptor and the sodium channels are sites of action of the

A
  • Potassium-sparing diuretics
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47
Q

Reabsorption of water occurs in the

A
  • Collecting tubule

- Under the control of antidiuretic hormone (ADH)

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48
Q

Most diuretics act from the

A
  • Luminal side of the membrane (except aldosterone receptor antagonist group)
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49
Q

Aldosterone receptor antagonist group (diuretics)

A
  • Spironolactone and eplerenone
  • Enter the collecting tubule from the basolateral side
  • Bind to cytoplasmic aldosterone receptor
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50
Q

Carbonic anhydrase inhibitor (Acetazolamide) method of action

A
  • Inhibit carbonic anhydrase
  • In proximal tubule, bicarbonate reabsorption is blocked and Na+ is
    excreted with HCO-
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51
Q

Carbonic anhydrase inhibitor (Acetazolamide) toxicities/interactions

A
  • Metabolic acidosis

- Hyperammonemia in cirrhosis

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52
Q

Loop diuretics

(furosemide, bumetanide and torsemide, ethacrynic acid) method of action

A
  • Inhibit Na+/K+/2Cl- transporter in thick ascending limb of loop of Henle
  • Cause powerful diuresis and increased Ca2+ excretion
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53
Q 
Loop diuretics
(furosemide, bumetanide and torsemide, ethacrynic acid) toxicities/interactions
A
  • Metabolic hypokalemic alkalosis
  • Ototoxicity
  • Hypovolemia
  • Efficacy reduced by nonsteroidal anti- inflammatory drugs
  • Sulfonamide allergy
54
Q

Thiazide diuretics Hydrochlorothiazide, chlorthalidone (thiazide-like) method of action

A
  • Inhibit Na+/Cl- transporter in distal convoluted tubule

- Cause moderate diuresis and reduced excretion of calcium

55
Q

Thiazide diuretics Hydrochlorothiazide, chlorthalidone (thiazide-like) toxicities/interactions

A
  • Metabolic hypokalemic alkalosis
  • Early hyponatremia
  • Increased serum glucose, lipids, uric acid
  • Efficacy reduced by nonsteroidal anti-inflammatory drugs
  • Sulfonamide allergy
56
Q

K+- sparing diuretics (Spironolactone, eplerenone) method of action

A
  • Steroid inhibitors of cytoplasmic aldosterone receptor in cortical collecting ducts
  • Reduce K+ excretion
57
Q

K+- sparing diuretics (Spironolactone, eplerenone) toxicities/interactions

A
  • Hyperkalemia

- Gynecomastia (spironolactone only)

58
Q

K+- sparing diuretics (Amiloride, triamterene) method of action

A
  • Inhibitor of ENaC epithelial sodium channels in cortical collecting duct
  • Reduces Na+ reabsorption and K+ excretion
59
Q

K+- sparing diuretics (Amiloride, triamterene) toxicities/interactions

A
  • Hyperkalemia
60
Q

Osmotic diuretics (Mannitol) method of action

A
  • Osmotically retains water in tubule by reducing reabsorption in proximal tubule, descending limb of Henle’s loop, and collecting ducts
  • In the periphery, mannitol extracts water from cells
61
Q

Osmotic diuretics (Mannitol) toxicities/interactions

A
  • Hyponatremia followed by hypernatremia

- Headache, nausea, vomiting

62
Q

Angiotensin converting enzyme inhibitor (ACEI) names

A
  • Enalapril
  • Captopril
  • Ramipril
  • Lisinopril
  • Benazepril
  • Trandolapril
  • Others
63
Q

There is sufficient evidence that proves that ACEI and ARB reduce

A
  • Progression of CKD (chronic kidney disease)
64
Q

ACE inhibitors reduce the activity of

A
  • Renin-angiotensin-aldosterone system (RAAS)
65
Q

RAAS is activated in response to

A
  • Fall in blood pressure (hypotension) or salt-water

imbalance of the body

66
Q

Renin

A
  • Released by kidney
  • Enzyme that changes angiotensinogen (a protein made in the liver)
    to angiotensin I
67
Q

ACE (Angiotensin converting enzyme) converts

A
  • Angiotensin I into angiotensin II
68
Q

The system increases blood pressure by

A
  • Increasing the amount of salt and water the body retains

- Action of angiotensin as a vasoconstrictor

69
Q

Inhibition of ACE side effects

A
  • Hypotension /dizziness
  • Increase serum creatinine/ renal impairment
  • Hyperkalemia
70
Q

Inhibition of enzymes other than ACE side effects

A
  • Cough caused by elevated bradykinin level due to ACE inhibition can be a cause of dry cough, angioedema and/or rash, hypotension, and inflammation-related pain
71
Q

Other side effects of ACEI

A
  • Neutropenia, agranulocytosis
  • GI: N/V/D
  • Impotence
  • Taste change
72
Q

Angiotensin II receptor blockers (ARB) names

A
  • Valsartan
  • Telmisartan
  • Losartan
  • Irbesartan
  • Olmesartan
  • Candersartan
  • Others
73
Q

ARBs are AT1-receptor antagonists

A
  • Block the activation of angiotensin II AT1 receptors
74
Q

Blockage of AT1 receptors directly causes

A
  • Vasodilation
  • Reduces secretion of vasopressin
  • Reduces production and secretion of aldosterone
75
Q

Hepatically metabolized ARBs

A
  • Losartan
  • Valsartan
  • Irbesartan
  • Telmisartan
  • Eprosartan
76
Q

Hepatically mixed with renally metabolized ARBs

A
  • Candesartan
  • Olmesartan
  • Azilsartan
77
Q

Clinical effects of ACEI and ARB

A
  • Relax the efferent arteriole
  • Lowers intra-glomerular pressure
  • Reduces GFR
78
Q

Advantage of ARB over ACEI

A
  • Doesn’t block type II AgII receptors
  • Maintains antiproliferative effect
  • Bradykinin is converted to kinin, so no dry cough as side effect
79
Q

Blockage of AT1 receptor side effects

A
  • Hypotension /dizziness
  • Increase serum creatinine/ renal impairment
  • Hyperkalemia
80
Q

Aliskiren (Tekturna)

A
  • Direct renin inhibitor

- Taken once a day

81
Q

Aliskiren (Tekturna) method of action

A
  • Renin inhibitor
  • Renin is the first enzyme in the RAAS that cleaves angiotensinogen to
    angiotensin I
82
Q

Aliskiren (Tekturna) side effects

A
  • Hyperkalemia
  • Angioedema
  • Low blood pressure
  • Cough, diarrhea and headaches
83
Q

Aliskiren (Tekturna) metabolism

A
  • Unchanged in urine and feces
84
Q

Sympathoplegics that act in CNS

A
  • Alpha2-selective agonists (eg, clonidine, methyldopa)
85
Q

Alpha 2-selective agonists (eg, clonidine, methyldopa) cause a decrease in

A
  • Sympathetic outflow by activation of α2 receptors in the CNS
  • Both drugs may cause sedation
86
Q

Alpha 2-selective agonist CNS activity

A
  • Readily enter the CNS when given orally
87
Q

Alpha 2-selective agonists reduce blood pressure by

A
  • Reducing cardiac output and vascular resistance
88
Q

Major compensatory response of alpha 2-selective agonists

A
  • Salt retention
89
Q

Sudden discontinuation of clonidine causes

A
  • Rebound hypertension

- May be severe

90
Q

Methyldopa occasionally causes

A
  • Hematologic immunotoxicity

- Hemolytic anemia

91
Q

Hemolytic anemia

A
  • Disorder in which red blood cells are destroyed faster than they can be made
92
Q

Adrenoreceptor blockers

A
  • Alpha-1 blockers

- Beta blockers

93
Q

Alpha1-selective agents (eg, prazosin, doxazosin, terazosin)

A
  • Moderately effective antihypertensive drugs

- Reduce vascular resistance and venous return

94
Q

Alpha 1 receptor is found in

A
  • Blood vessels
  • Sphincters of the GI
  • Eye
  • Genitourinary (uterus)
95
Q

Nonselective α blockers (phentolamine, phenoxybenzamine) are of no value in

A
  • Chronic hypertension because of excessive reflex tachycardia
96
Q

Alpha 1-selective adrenoceptor blockers cause

A
  • Orthostatic hypotension, especially with the first few doses
  • Also relax smooth muscle in the prostate (useful in benign prostatic hyperplasia)
97
Q

Beta blockers are used very heavily in the treatment of

A
  • Hypertension
98
Q

Beta blocker examples

A
  • Propranolol is the prototype

- Atenolol, metoprolol, and carvedilol are among the most popular

99
Q

Beta blocker effects

A
  • Reduce cardiac output

- Chronic use may decrease vascular resistance

100
Q

Chronic use of beta blockers may cause a decrease in vascular resistance as a result of

A
  • Reduced angiotensin levels

- β blockers reduce renin release from the kidney

101
Q

Vasodilators

A
  • Drugs that dilate blood vessels by acting directly on smooth muscle cells
102
Q

Vasodilators act by four major mechanisms

A

1) Blockade of calcium channels
2) Release of nitric oxide
3) Activation of D1 dopamine receptors through Gs
4) Opening of potassium channels (which leads to hyperpolarization)

103
Q

4 major vasodilators

A

1) Calcium channel blockers
2) Nitrates, Nitroprusside, hydralazine
3) Fenoldopam
4) Minoxidil, diazoxide

104
Q

Effective vasodilators

A
  • Calcium channel blockers

- Verapamil and diltiazem also reduce cardiac output in most patients

105
Q

Two types of CCB

A
  • Dihydropyridine (DHP) with nifedipine as the prototype

- Non-DHP

106
Q

DHP names

A
  • Amlodipine
  • Felodipine
  • Isradipine
  • Nicardipine
  • Nifedipine
  • Nimodipine
  • Nitrendipine
107
Q

DHP mechanism

A
  • High vascular selectivity (reduces SVR and BP)

- Can lead to reflex cardiac stimulation (tachycardia and increased inotropy)…can offset beneficial effects

108
Q

DHP side effects

A
  • Flushing
  • Headache
  • Excessive hypotension
  • Edema
  • Reflex tachycardia
  • Long-acting dihydropyridines (e.g., extended release nifedipine, amlodipine) reduce reflex responses
109
Q

Non-DHP names

A
  • Verapamil

- Diltiazem

110
Q

Verapamil (non-DHP) mechanism

A
  • Selective for the myocardium, less effective as a systemic vasodilator drug
  • Indication for treating angina (by reducing myocardial oxygen demand)
111
Q

Diltiazem (non-DHP) mechanism

A
  • Intermediate between verapamil and dihydropyridines in its selectivity for vascular calcium channels
  • Able to reduce arterial pressure without producing the same degree of reflex tachycardia of dihydropyridines
112
Q

Non-DHP side effects

A
  • Bradycardia
  • Impaired electrical conduction (e.g., atrioventricular nodal block)
  • Depressed contractility
113
Q

Hydralazine and Minoxidil

A
  • Older vasodilators

- More effect on arterioles than veins

114
Q

Hydralazine

A
  • Acts through the release of nitric oxide from endothelial cells
  • Rarely used at high dosage
115
Q

Hydralazine is rarely used at high dosage because of

A
  • Hydralazine-induced lupus erythematosus

- Reversible upon stopping the drug

116
Q

Minoxidil

A
  • Potassium channel opener that hyperpolarizes and relaxes vascular smooth muscle
117
Q

Minoxidil can cause

A
  • Hirsutism, so it is also available as a topical agent for the treatment of baldness
118
Q

Minoxidil use/mechanism

A
  • Extremely efficacious
  • Reserved for severe hypertension
  • Diazoxide has the same mechanism of action, but is less preferred because of the high side effects
119
Q

Hydralazine metabolism

A
  • Hepatic

- DOA = 12h

120
Q

Hydralazine side effects

A
  • Hydralazine-induced Lupus like syndrome
  • Blood dyscrasias
  • Hypotension
  • Peripheral neuritis (pyridozine treatment is needed here)
  • Flushing; orthostatic hypotension
121
Q

Minoxidil metabolsim

A
  • Hepatic

- DOA = 2-5 days

122
Q

Minoxidil side effects

A
  • Fluid retention; sodium/ water retention; weight gain
  • Increase serum creatinine and liver enzymes
  • US Box warning: pericarditis
  • Syncope; sinus tachycardia
  • Hypertrichosis
123
Q

Diazoxide (thiazide derivative but lacks diuretic properties) DOA

A
  • Less than 8h
124
Q

Diazoxide side effects

A
  • Hyperosmolar coma
  • Hypotension, tachycardia
  • Headache
  • Pancreatitis
  • Hirsutism
  • Hyperglycemia
  • Sodium retention
  • Blood dyscrasias (thrombocytopenia; neutropenia; decrease hematocrit
  • Blurred vision
  • Gout
125
Q

Parenteral vasodilators used in hypertensive emergencies

A
  • Nitroprusside
  • Diazoxide
  • Fenoldopam
126
Q

Nitroprusside mechanism

A
  • Releases nitric oxide (from the drug molecule itself) - Increases cyclic guanine monophosphate (cGMP) concentration
  • Increases relaxation in vascular smooth muscle
  • Dilates arterial resistance vessels more than venous vessels
127
Q

Dopamine D1 receptor activation by fenoldopam causes

A
  • Prompt, marked arteriolar vasodilation
128
Q

Nitroprusside properties

A
  • Brand = Nitropress
  • DOA = 10 min
  • Short-acting agent
  • Light-sensitive
129
Q

Fenoldopam properties

A
  • Brand = Cortopam
  • DOA = 1h
  • Metabolism = hepatic
130
Q

Nitroprusside and Fenoldopam shared side effects

A
  • Flushing
  • Headaches
  • Hypotension
  • Tachycardia
131
Q

Nitroprusside side effects

A
  • Methemoglobinemia
  • Hypothyroidism
  • Can release cyanide ions
132
Q

Fenoldopam side effects

A
  • Increase liver enzyme

Pharmacology (27 decks)

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