Anti-Hypertensives Flashcards

1
Q

What blood pressure figure is considered hypertension?

What blood pressure figure is considered hypertension stage 1?

What blood pressure figure is considered hypertension stage 2?

A

140/90

140-159/90-99

160/100 or more

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2
Q

the actual increase in arterial blood pressure in hypertension is caused by what? what equation should come to mind?

A

an increase in peripheral vascular resistance (PVR) or an increase in cardiac output

BP = CO x PVR

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3
Q

what determines the peripheral vascular resistance?

what determines the cardiac output?

A

the vascular tone

heart rate and stroke volume

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4
Q
  • what is an effective and inexpensive way of reducing venous pressure and CO?
  • what do diuretics do?
  • Reducing blood volume not only reduces central venous pressure, also reduces what?
  • CO is reduced as what other thing is reduced?
A
  • by using drugs that reduce blood volume
  • act on the kidney to enhance sodium and water excretion
  • cardiac output
  • preload
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5
Q

What group of diuretics are preferred for Hypertension?

For thiazides, maximum antihypertensive action is at what dose?

what is an added benefit of these drugs?

What will Toxicity of Thiazides cause?

A

thiazides

lower dose than the diuretic dose

they reduce systemic vascular resistance with long-term use.

  1. hypokalemia
  2. ↓ glucose tolerance and may unmask latent diabetes mellitus
  3. ↑ plasma LDL, cholesterol, and triglycerides
  4. ↑ increased levels of plasma uric acid and precipitate acute gout
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6
Q

Why can beta adrenergic blockers be considered antihypertensives?

A
  1. Decrease CO (block cardiac beta 1 receptors)
  2. inhibit renin release (block beta 1 receptors in JG cells)
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7
Q

what is the Hemodynamic effects of beta blockers in hypertension?

A
  • Heart rate: decreased
  • Cardiac output: decreased
  • Venous tone: unchanged
  • Peripheral vascular resistance: decreased
  • Postural hypotension: negligible
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8
Q

in severe hypertension, how well do beta blockers work?

What is an example of a nonselective compound beta blocker? What are its principal symptoms of toxicity?

what happens when propranolol is discontinued abruptly after prolonged regular use?

A

are useful in preventing the reflex tachycardia that often results from treatment with direct vasodilators

propranolol

toxicity: bradycardia, asthma, peripheral vascular insufficiency, diabetes

result in reflex tachycardia

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9
Q

what is an example of a beta blocker that is cardio-selective beta 1?

what is different of these when compared with propranolol?

A

atenolol and metropolol

they cause less bronchoconstriction

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10
Q

Calcium Channel Blockers (CCBs)act on what receptor?

What Calcium channel blocker drugs are effective in lowering blood pressure?

A

L type Ca++ Channels

Dihydropyridines, Verapamil, diltiazem

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11
Q

Dihydropyridines drugs for lowering blood pressure through calcium channel blocker, are more effective at what?

what may they lead to?

What calcium channel blocker has the most depressant effect?

A

are more selective as vasodilators

may lead to reflex tachycardia

Verapamil

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12
Q

What are the Inhibitors of Renin Angiotensin Aldosterone system (RAAS)?

A
  • ACE Inhibitors (ACEI)
  • Angiotensin Receptor blockers (ARBs)
  • Renin antagonist
  • Aldosterone receptor inhibitor
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13
Q

what are the ACE Inhibitor drugs?

A

Captopril

Enalapril

Ramipril

Benazepril

Fosinopril

Lisinopril

Quinapril

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14
Q

What are the Angiotensin Receptor blockers (ARBs) drugs?

A

Losartan

Valsartan

Candesartan

eprosartan

irbesartan

telmisartan

olmesartan

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15
Q

what is an example drug of renin antagonist?

A

Aliskiren

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16
Q

what is an example drug of Aldosterone receptor inhibitor?

A

spironolactone

elprenone

17
Q

What is the effect of Angiotensin 2 in the myocardium and kidney?

A

there is remodeling:

  • Increased wall-to-lumen ratio in blood vessels
  • Concentric & eccentric hypertrophy
  • Fibrosis
  • Stenosis of intimal surface of blood vessel
    • Due to increased migration and hyperplasia of vascular smooth muscle cells, myocytes, and fibroblasts.
18
Q

What do ACE inhibitors do?

ACE inhibitors are mainly used for what? (drug of choice) Why?

A
  • inhibit the ACE converting enzyme
    • lower BP through vasoconstriction
  • diabetic neuropathy: they diminish proteinuria and stabilize renal function

(they improve intrarenal hemodynamics, with decreased glomerular efferent arteriolar resistance and a resulting reduction of intraglomerular capillary pressure. )

19
Q

What are the adverse effects of ACE inhibitors?

A
  1. Severe hypotension: in patients who are hypovolemic
  2. Dry cough: due to ↑ levels of bradykinin
  3. Acute renal failure: in patients with bilateral renal artery stenosis
  4. Angioedema
  5. Pregnancy category D: cause severe renal pathology in fetus
  6. Drug interactions: Hyperkalemia- if K+ sparing diuretics and ACE inhibitors used at the same time
20
Q

What do Angiotensin receptor blockers do?

what effect do they have on bradykinin metabolism?

Who has more affinity, ACE inhibitors or Angiotensin receptor blockers?

To what patients are angiotensin receptor blockers more benefitial?

A
  • block the angiotensin II type 1 (AT1) receptor
  • none
  • Angiotensin receptor blockers
  • patients with heart failure and chronic kidney disease.
21
Q

What are the adverse effects angiotensin receptor blocker may cause?

A
  1. Noticeably lower incidence of cough
  2. Hyperkalemia
  3. Renal effects
  4. Pregnancy category D
22
Q

what are the 2 types of alpha adrenergic blockers?

A
  • α1-selective drugs
  • Nonselective α-blockers
23
Q

What drugs are alpha-1 selective?

What drugs are non-selective alpha blockers?

A
  • Prazosin, terazosin, doxazosin
  • phentolamine, phenoxybenzamine
24
Q

where do we find alpha 1 receptors?

what side effects can be seen in selective alpha 1 drugs?

In what patients are alpha 1 receptors used mainly?

A

venules and arterioles

postural hypotension

in men with concurrent HTN and benign prostatic hyperplasia (BPH)

25
Q

what do Nonselective α-blockers do?

In what symptoms do they always result in?

When are they used?

A
  • blocks both presynaptic and postsynaptic receptors
  • tachycardia
  • in diagnosis and treatment of pheochromocytoma
26
Q

what are vasodilators?

A

drugs that dilate vessels by acting directly on smooth muscle cells through nonautonomic mechanisms

27
Q

what are the 4 major mechanisms through which vasodilators work?

A
  1. Release of Nitric oxide (NO)
  2. Blockade of Ca2+ channels
  3. Opening of K+ channels
  4. Activation of D1 receptors
28
Q

What vasodilator drugs work by releasing NO?

A
  1. Nitroprusside
  2. Hydralazine
29
Q

What vasodilator drugs work by Blocking Ca2+ channels?

A
  1. Verapamil
  2. Diltiazem
  3. DHP like nifedipine, amlodipine
30
Q

What vasodilator drugs work by opening K+ channels?

A

Minoxidil, diazoxide

31
Q

What vasodilator drugs work by activating D1 receptors?

A

fenoldopam

32
Q

Important

What vasodilators work in veins?

What vasodilators work in arteries?

A

nitrates, ACE Inhibitors, alpha 1 antagonist, nitroprusside sodium

Ca2+ antagonists, hydralazine, minoxidil

33
Q

How does Hydralazine work?

In patients with heart failure and hypertension, hydralazine will work in combination with what other drug?

what major metabolism route will hydralazine use?

A
  • by release of NO and acting as a arteriolar vasodilator
  • nitrates
  • acetylation
34
Q

if a patient is a fast metabolic acetylator, what happens when you give them hydralazine?

what if they are slow acetylators?

A
  • they will have reduced bioavailability (30% bioavailability)
  • they will have more bioavailability (50%)
35
Q

what are the signs of hydralazine toxicity?

A

tachycardia, salt and water retention

Drug induced reversible lupus erythematosus like syndrome:

  • look for arthralgia, myalgia, skin rashes, and fever
36
Q

Drug induced reversible lupus erythematosus like syndrome in hydralazine toxicity will occur in which type of acetylator?

A

slow acetylators

37
Q

when is Minoxidil used? why?

how does it work?

what will you look for if there is minoxidil toxicity?

what is another use for minoxidil?

A
  • for severe HTN since it is an arteriolar vasodilator
  • Acts as a K+ channel opener, causing hyperpolarization and relaxing vascular smooth muscle
  • hypertrichosis/hirsutism (increased hair growth), and tachycardia
  • Rogaine: stimulant of hair growth
38
Q
A