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Anti-Hypertensives Flashcards

1
Q

What are the categories established by JNC VIII

A

Normal: <80Prehypertension: 120-139/80-89
Stage 1 hypertension: 140-159/90-99
Stage 2 hypertension: 160+/100+

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2
Q

What are five lifestyle modifications for prehypertensive patients?

A 
Weight reduction
Sodium Intake reduction
Alcohol moderation
DASH diet
Physical Activity
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3
Q

What drugs are initially given to all hypertensive patients with CKD?

A

ACEIs and ARBs

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4
Q

What is the anti-hypertensive agent priority for blacks without CKD?

A

Thiazide diuretics and CCBs

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5
Q

What is the anti-hypertensive agent priority for non-blacks?

A

Thiazide diuretics, ACEIs, ARBs, and CCBs

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6
Q

Describe how bicarbonate is reabsorbed at the proximal convoluted tubule

A

Hydrogen is pumped into the lumen through the Na/H antiporter. Hydrogen combines with bicarbonate to form carbonic acid which is converted to water and carbon dioxide by CA allowing it to enter the tubular epithelial cell. Within the cell CA reforms carbonic acid which dissociates allowing bicarbonate to re-enter the blood stream and hydrogen to be recycled.

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7
Q

Describe how Mg and Ca are reabsorbed in the loop of henle

A

The efforts of the Na/K/2Cl co-transporter and Na/K ATPase serve to increase intracellular potassium causing back diffusion and a positive potential which draws Mg and Ca into the interstitium

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8
Q

What two channels are found in the DCT and what induces the expression of one of them

A

Na/Cl cotransporter and Ca channels

Calcium channels are induced by PTH

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9
Q

Describe how potassium secretion is achieved in the collecting duct

A

Aldosterone induces the expression of ENaC and basolateral Na/K ATPase in the collecting duct. Reabsorption of sodium in the collecting duct leads to an electrochemical gradient causing the loss of potassium.

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10
Q

What is the MOA, prototype, and suffix for carbonic anhydrase inhibitors?

A

MOA - inhibition of membrane and cytoplasmic carbonic anhydrase causing secretion of bicarbonate
Prototype = acetazolamide
Suffix = amide

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11
Q

What are the clinical indications (3) for CAIs?

A

glaucoma, acute mountains sickness, and metabolic alkalosis

Note: note very effective as a monotherapy and often not used

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12
Q

What are the adverse effects (4) of CAIs?

A

Acidosis, kidney stones, parasthesias, and sulfonamide hypersensitivity

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13
Q

What is the MOA, prototypes (2), and suffix (2) for loop diuretics?

A

MOA - these inhibit the Na/K/2Cl co-transporter in the loop of henle
Prototypes - ethacrynic acid and furoseamide (lasix)
Suffix - nide or mide
Note: ethacrynic acid is not a sulfonamide

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14
Q

Describe the relationship of renal secretion rates to the efficacy of loop diuretics

A

These must be in the lumen to be able to inhibit the trifecta transporter

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15
Q

What are the clinical indications (7) for loop diuretics?

A

Heart failure, hypertension, acute renal failure, anion overdose, hypercalcemia, nephrolithiasis, and edema

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16
Q

What are the adverse effects (6) of loop diuretics?

A

Hypokalemia, hypomagnesemia, hypocalcemia, hyperuricemia, ototoxicity, and sulfonamide hypersensitivity

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17
Q

What is the MOA, prototype, and suffix for thiazide diuretics?

A

MOA - inhibition of Na/Cl cotransporter in the DCT
Prototype = hydrochlorothiazide
Suffix = thiazide

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18
Q

What are the clinical indications (4) for thiazide diuretics?

A

Heart failure, hypertension, nephrolithiasis, and nephrogenic diabetes insipidus

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19
Q

What are the adverse effects (7) for thiazide diuretics?

A

hyponatremia, hypokalemia, alkalosis, hyperglycemia, hyperuricemia, hypercalcemia, and sulfonamide hypersensitivity

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20
Q

Describe the MOA of spironolactone

A

Binds and inhibits mineralocorticoid receptors which receive aldosterone.
This is a potassium sparing diuretic
Note: do not require access to the tubular lumen

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21
Q

What are the clinical indications (3) of spironolactone?

A

Hyperaldosteronism, female hirsuitism, and adjunct with potassium-wasting diuretics

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22
Q

What are the adverse effects (3) of spironolactone?

A

Acidosis, hyperkalemia, and anti-androgenic effects

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23
Q

What is amelioride?

A

This is an inhibitor of ENaC.

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24
Q

What are the clinical indications (2) for amelioride?

A

Adjunct with potassium-wasting diuretics and lithium-induced nephrogenic diabetes insipidus

25
What are the adverse effects (2) of amelioride?
Acidosis and hyperkalemia
26
What is the MOA, prototype (2), and suffix for ACEIs?
MOA - inhibits the conversion of AngI to AngII and the degradation of bradykinin Prototypes - captopril and enalapril Suffix - pril
27
What is enalaprilat?
This is the active metabolite of enalapril, which can be given by IV to treat hypertensive crisis
28
What are the clinical indications (5) of ACEIs?
hypertension, heart failure, left ventricular dysfunction, prophylaxis of future cardiovascular events, prophylaxis of nephropathy
29
What are the clinical benefits (3) of ACEIs?
1. Little effect on cardiac function in uncomplicated hypertension 2. Preserves baroreceptors preventing reflexes to changes in posture or physical activity 3. Decreases TPR, and all blood pressures Note: decreased afterload and preload assist in management of heart failure
30
What are the adverse effects (5) of ACEIs?
Cough, angioedema, hyperkalemia, and teratogenesis | Can cause acute renal failure at anytime during therapy
31
What kind of risk factors contribute to acute renal failure in ACEIs?
Any pathology limiting the perfusion of the kidney can result in acute renal failure
32
What effect do ACEIs have on back pressure?
Back pressure is reduced causing a decrease in protein excretion
33
Describe the two angiotensin receptors
AT1 receptors - most common in adults; cause activation of Gq subunit and contraction of smooth muscle cells through IP3 and DAG AT2 receptors - not as common; cause production of bradykinin and nitric oxide
34
What is the MOA, prototypes (2), and suffix of ARBs?
MOA - inhibition of Ang II binding to its receptor; selectively block AT1 receptor and ignore the AT2 receptor. The overall effect is decreased peripheral resistance, decreased renal effects, decreased aldosterone, and decreased cardiac myocyte hypertrophy Prototypes - losartan and valsartan Suffix - sartan
35
What are the clinical indications (5) for ARBs?
Heart failure, hypertension, diabetic nephropathy, prophylaxis post-MI, or prophylaxis for future cardiovascular events Note: Use only when patients are intolerant to ACEIs
36
What are the adverse effects (2) of ARBs?
hyperkalemia and teratogenesis
37
What is aliskrein?
This is a direct inhibitor of renin in the blood. Causes increased in plasma renin, but no increase in renin activity. Note: Contraindicated in pregnancy due to teratogenesis; hyperkalemia
38
Describe the MOA, prototype (2), and suffix for DHP CCBs. Describe how they interact with cardiac myocytes and why this interaction is nullified.
MOA = inhibition of calcium channels in vascular smooth muscle cells Prototype = nifedipine and amlodipine suffix = dipine At low concentrations these will cause vasodilation. At higher concentrations these could effect cardiac myocytes and prolong depolarization. However, the vasodilatory effect would cause reflex tachycardia nullifying this effect.
39
Describe the MOA and prototypes for Non-DHP CCBs. Describe their effect on cardiac myocytes. In light of this effect in which patients should these agents be used and avoided.
MOA = blocking of calcium channels in vascular smooth muscle cells and cardiac myocytes Prototypes = verapamil and diltiazem At cardiac myocytes these have a negative inotropic effect, decrease SA node depolarization rate, and decrease SA node conductivity. These are approved for use in patients with supraventricular tachycardia, but should be avoided in patients on beta blockers or with slowed AV node conduction.
40
Describe the hemodynamic effects (3) of CCBs.
1. Higher affinity for arterioles compared to veins, decreasing postural hypotension 2. Decrease in TPR reduces afterload and oxygen demand of the heart 3. Coronary arteries dilate, reduces angina
41
Describe the pharmacokinetics of CCBs, and then specifically DHPs.
CCBs demonstrate excellent oral bioavailability, but are highly susceptible to the first pass effect. DHPs are normally administered in longer lasting mixtures to avoid the cardiovascular reflexes.
42
What are the adverse effects (2) of DHP CCBs?
ankle edema and excessive hypotension Note: excessive hypotension is avoidable with longer acting preparations
43
What are the adverse effects (2) of Non-DHP CCBs?
Bradycardia and AV node block Note: constipation is seen with verapamil
44
What are the clinical indications (3) for CCBs? what is the caveat to one of these indications?
Hypertension - often cause cardiovascular reflexes and must be administered with another anti-hypertensive (ARBs) Hypertensive emergencies and Angina
45
What is the MOA, clinical indications (2), and adverse effects (3) of minoxidil?
MOA = opens potassium channels on vascular smooth muscle cells causing hyperpolarization of these cells decreasing their contraction rate --> arteriolar dilation Clinical indications = severe hypertension and balding Adverse effects = edema, reflex tachycardia, and hypertrichosis Note: Due to the first two side effects this drug should be administered with a beta-blocker and diuretic
46
What is the MOA, clinical indications (2), and adverse effects (4) of fenoldopam?
MOA = binds to D1 receptors on renal arteries Clinical indications = hypertensive emergencies and post-operative HTN Adverse effects = reflex tachycardia, headaches, flushing, and increased intraocular pressure in glaucoma patients
47
What is the MOA, clincial indications (3), and adverse effects (3) of hydralazine
MOA = induces the release of NO from endothelial cells causing arteriolar dilation only, reducing afterload Clinical indications 1. 1st line agent for HTN in pregnancy when used with methyldopa 2. Heart failure patients along with nitrates 3. Hypertensive emergencies via parenteral administration Adverse effects 1. edema 2. reflex tachycardia 3. lupus-like syndrome
48
What are the MOA, clinical indications (3), and adverse effects (2/3) for nitroprusside and nitroglycerin, respectively?
``` MOA = causes dilation of veins and arterioles decreasing venous return, and decreasing preload. This all reduces the oxygen demand of the heart. Clinical indications = hypertensive crises, heart failure, and angina Adverse effects (nitroprusside) = excessive hypertension and cyanide poisoning Adverse effects (nitroglycerin) = postural hypertension, syncope, and throbbing headaches ```
49
What are the prototypes (5) and selectivity of beta-blockers
Prototypes = carvedilol, lebetalol, metoprolol, atenolol, propanolol Carvedilol, lebetalol, and propanolol are non-selective. Carvedilol and lebetalol also have an effect at the alpha1 receptor Atenolol and metoprolol are cardioselective
50
Describe the clinical indications (3) of beta-blockers
These are not used in many situations unless there is a presence of heart dysfunction: heart failure, MI, or ventricular dysfunction
51
What are the adverse effects (5) of beta-blockers?
Bronchospasm, hyperglycemia, weight gain, erectile dysfunction, and bradycardia Note: many of these effects can be avoided with the use of cardioselective beta blockers
52
What is esmolol and what is it used for?
Esmolol is a cardioseletive beta blocker with rapid onset and duration. Used in peri-operative HTN and hypertensive emergency. Note: Short duration due to metabolism by red blood cell esterases
53
What is the prototype, suffix, clinical indications (2), and adverse effects (2) for alpha1 blockers?
Prototype = prazosin Suffix = azosin Clinical indications = in conjunction with another drug in refractory HTN cases or men with HTN and BPH Adverse effects - orthostatic hypertension and syncope in initial doses
54
Describe the MOA for IV and oral routes of administration, clinical indications (2), and adverse effect (3) for clonidine
Clonidine is an alpha2 agonist. When administered by IV it will cause an increase in blood pressure, followed by a decrease in blood pressure. When given orally it will cause a decrease in blood pressure. Clinical indications - essential hypertension (rarely used) and narcotic, tobacco, or alcohol withdrawal Adverse effects - fatigue, erectile dysfunction, and rebound hypertension
55
What do we use methyldopa for?
Treatment of hypertension in pregnancy
56
Aside from methyldopa and hydralazine what other drug classes can be used in pregnancy?
``` Beta-blockers = labetalol, metoprolol, and pindolol CCBs = nifedipine and nicardipine ```
57
Which vasodilators (7) can be given by IV to treat hypertensive crisis?
Sodium nitroprusside, nitroglycerine, hydralazine, nifedipine, clevidipine, fenoldopam, and enalaprilat
58
Which adrenergic antagonists (4) can be given by IV to treat hypertensive crisis
labetalol, metoprolol, esmolol, and phentolamine
59
What are the effects of decreased bradykinin destruction in ACEI therapy?
Kinins stimulate the production of vasoactive compounds (NO, cGMP, eicosanoids) which oppose the redmodeling effects of AngII on vascular and myocardial tissue. This is thought to be the cause of mortality reduction in ACEI therapy.

CV 2 (7 decks)

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