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CV 2 > Anti-Hypertensives > Flashcards

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
Q

What are the adverse effects (2) of amelioride?

A

Acidosis and hyperkalemia

26
Q

What is the MOA, prototype (2), and suffix for ACEIs?

A

MOA - inhibits the conversion of AngI to AngII and the degradation of bradykinin
Prototypes - captopril and enalapril
Suffix - pril

27
Q

What is enalaprilat?

A

This is the active metabolite of enalapril, which can be given by IV to treat hypertensive crisis

28
Q

What are the clinical indications (5) of ACEIs?

A

hypertension, heart failure, left ventricular dysfunction, prophylaxis of future cardiovascular events, prophylaxis of nephropathy

29
Q

What are the clinical benefits (3) of ACEIs?

A
  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
Q

What are the adverse effects (5) of ACEIs?

A

Cough, angioedema, hyperkalemia, and teratogenesis

Can cause acute renal failure at anytime during therapy

31
Q

What kind of risk factors contribute to acute renal failure in ACEIs?

A

Any pathology limiting the perfusion of the kidney can result in acute renal failure

32
Q

What effect do ACEIs have on back pressure?

A

Back pressure is reduced causing a decrease in protein excretion

33
Q

Describe the two angiotensin receptors

A

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
Q

What is the MOA, prototypes (2), and suffix of ARBs?

A

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
Q

What are the clinical indications (5) for ARBs?

A

Heart failure, hypertension, diabetic nephropathy, prophylaxis post-MI, or prophylaxis for future cardiovascular events

Note: Use only when patients are intolerant to ACEIs

36
Q

What are the adverse effects (2) of ARBs?

A

hyperkalemia and teratogenesis

37
Q

What is aliskrein?

A

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
Q

Describe the MOA, prototype (2), and suffix for DHP CCBs. Describe how they interact with cardiac myocytes and why this interaction is nullified.

A

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
Q

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.

A

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
Q

Describe the hemodynamic effects (3) of CCBs.

A
  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
Q

Describe the pharmacokinetics of CCBs, and then specifically DHPs.

A

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
Q

What are the adverse effects (2) of DHP CCBs?

A

ankle edema and excessive hypotension

Note: excessive hypotension is avoidable with longer acting preparations

43
Q

What are the adverse effects (2) of Non-DHP CCBs?

A

Bradycardia and AV node block

Note: constipation is seen with verapamil

44
Q

What are the clinical indications (3) for CCBs? what is the caveat to one of these indications?

A

Hypertension - often cause cardiovascular reflexes and must be administered with another anti-hypertensive (ARBs)
Hypertensive emergencies and Angina

45
Q

What is the MOA, clinical indications (2), and adverse effects (3) of minoxidil?

A

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
Q

What is the MOA, clinical indications (2), and adverse effects (4) of fenoldopam?

A

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
Q

What is the MOA, clincial indications (3), and adverse effects (3) of hydralazine

A

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
Q

What are the MOA, clinical indications (3), and adverse effects (2/3) for nitroprusside and nitroglycerin, respectively?

A 
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
Q

What are the prototypes (5) and selectivity of beta-blockers

A

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
Q

Describe the clinical indications (3) of beta-blockers

A

These are not used in many situations unless there is a presence of heart dysfunction: heart failure, MI, or ventricular dysfunction

51
Q

What are the adverse effects (5) of beta-blockers?

A

Bronchospasm, hyperglycemia, weight gain, erectile dysfunction, and bradycardia
Note: many of these effects can be avoided with the use of cardioselective beta blockers

52
Q

What is esmolol and what is it used for?

A

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
Q

What is the prototype, suffix, clinical indications (2), and adverse effects (2) for alpha1 blockers?

A

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
Q

Describe the MOA for IV and oral routes of administration, clinical indications (2), and adverse effect (3) for clonidine

A

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
Q

What do we use methyldopa for?

A

Treatment of hypertension in pregnancy

56
Q

Aside from methyldopa and hydralazine what other drug classes can be used in pregnancy?

A 
Beta-blockers = labetalol, metoprolol, and pindolol
CCBs = nifedipine and nicardipine
57
Q

Which vasodilators (7) can be given by IV to treat hypertensive crisis?

A

Sodium nitroprusside, nitroglycerine, hydralazine, nifedipine, clevidipine, fenoldopam, and enalaprilat

58
Q

Which adrenergic antagonists (4) can be given by IV to treat hypertensive crisis

A

labetalol, metoprolol, esmolol, and phentolamine

59
Q

What are the effects of decreased bradykinin destruction in ACEI therapy?

A

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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