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M2 Cardiovascular > Hypertension: Pharmacology - Imig > Flashcards

Hypertension: Pharmacology - Imig Flashcards

1
Q

Explain the distribution and relative risk of blood pressure.

A

Blood pressure has a normal distribution; those with elevated BP have exponentially increased risks of stroke and CVD.

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2
Q

Which patient demographic is at highest risk of hypertension (think age, gender)

A

Post-menopausal women.

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3
Q

About 25-30% of US adults have hypertension. About how many of those are not controlling their hypertension? Why?

A

Just over half are uncontrolled, of which many are simply unaware of their hypertension.

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4
Q

Vasodilators

Describe how they decrease blood pressure.

Give some examples.

A

Vasodilators

Directly decrease vascular tone via multiple pathways (NO>>cGMP, K+-ATPase, dopamine antagonism)

Hydralazine, Nitroprusside, Diazoxide, Minoxidil, Fenoldopam

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5
Q

Why are direct arterial vasodilators often coadministered with a beta-blocker?

A

The beta-blocker will counter the resulting baroreceptive reflex (tachycardia, renin release).

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6
Q

What defines a hypertensive crisis?

Distinguish between hypertensive urgency and emergency.

How are they handled?

A

BP >180/120mm Hg.

Urgency features no organ injury. Emergency does (eg encephalopathy, hemorrhage, LV failure, eclampsia, UA, dissecting aneurysm)

Reduce blood pressure (GRADUALLY).

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7
Q

Fill in the blank:

Nitroprusside is a vasodilator that acts mainly on the ____ circulation, producing NO to activate ____. Its major toxicity is ____, made worse by ____.

A

Nitroprusside is a vasodilator that acts mainly on the venous circulation, producing NO to activate GC/cGMP. Its major toxicity is cyanide toxicity, made worse by renal or hepatic injury.

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8
Q

What are the side effects of direct arterial vasodilators? (general AND specific)

With what should they be co-administered?

A

General: Sodium/fluid retention, tachycardia/angina.

Specific: Hydralazine causes lupus-like syndrome, Minoxidil causes hair growth.

Counteract the general SEs with diuretics and beta-blockers.

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9
Q

Calcium Channel Blockers

Describe how they decrease blood pressure.

Give some examples.

A

Calcium Channel Blockers

They decrease vascular tone, and sometimes decrease heart chronotropy/inotropy.

Nifedipine, Amlodipine, Diltiazem, Verapamil.

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10
Q

Distinguish between the mechanisms of actions of DHPs and non-DHP CCBs.

Describe their side effects.

A

DHPs act more on vascular tissue, while non-DHPs act more on heart tissue (decrease HR and AVN conduction).

Both cause flushing and headaches. nonDHPs cause constipation and –Inotropy/AVN conduction, while DHPs (mostly nifedipine) cause edema and “refractoriness”.

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11
Q

Try to recall the locations and effects of the adrenergic receptors: α1, α2, β1, β2.

A

α1 in arterioles (vasoconstriction of skin & splanchnics) & kidneys (increased renin)

α2 in many presynaptic terminals (negative feedback)

β1 in heart (++ino/chrono), kidneys (increased renin)

β2 in lungs (bronchodilation)

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12
Q

a1/a2 Blockers

Describe how they decrease blood pressure.

Give some examples.

A

a1/a2 Blockers

Decrease vascular tone by blocking SNS constriction.

Phenoxybenzamine, Phentolamine.

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13
Q

How are a1 blockers superior to a1/a2 blockers?

Do they competitively or noncompetitively block a1?

When should they be administered?

A

Blockage of a2 blocks negative feedback via the presynaptic receptors; a1 blockers avoid this (net better SNS blocking)

Competitive.

At bedtime to minimize SEs.

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14
Q

a1 Blockers

Give some examples.

Name their side effects (general and specific)

A

a1 Blockers

Prazosin, Terazosin, Doxazosin.

First dose effect results in orthostatic hypotension, dizziness/faintness, palpitations, syncope. Still some reflex tachycardia.

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15
Q

ß-Blockers

Describe how they decrease blood pressure.

Give some examples.

A

ß-Blockers

Block stimulation of renin secretion, as well as heart inotropy/chronotropy.

Propranolol, Metoprolol, Atenolol, Labetalol… about 10 others.

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16
Q

Recall some of the side effects of beta blockers.

What do most of these result from?

Which beta blockers avoid these effects?

A

Glucose intolerance, masked hypoglycemia, bronchospasm, altered lipid profile, CNS depression, impotence, decreased CO/HR…

Many of these result from ß-2 blockage.

The cardioselective beta blockers (metoprolol, atenolol) do not have these effects at low dosage. Better for those with bronchospasm, diabetes, PAD…

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17
Q

Are beta blockers indicated for patients with high-renin HTN?

How does age affect beta-blocker usage?

A

Yes; beta blockers are much more effective in these patients than in those with low renin.

Beta blockers are less effective in older adults, and are best paired with diuretics then.

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18
Q

What category do labetalol and carvedilol fall under?

What are their side effects?

A

These are mixed a1/ß blockers. (competitive inhibitors)

MIld orthostatic hypotension & headaches.

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19
Q

Central a2__ Agonists

Describe how they decrease blood pressure.

Give some examples.

A

Central a2 Agonists

Stop SNS outflow from the vasomotor center (vagal tone predominates).

Clonidine, Guanabenz, a-methyldopa.

20
Q

What are the side effects of central a2 agonists? (general & specific)

A

General: Sodium/fluid retention, depression, orthostatic hypotension/dizziness, rebound upon discontinuation.

Specific: Clonidine has anticholinergic SEs, Methyldopa can cause hepatitis and (rarely) hemolysis.

21
Q

Neuronal/Ganglionic Blockers

Describe how they decrease blood pressure.

Give some examples.

A

Neuronal/Ganglionic Blockers

Stop SNS outflow, this time at the nerve synapse. Multiple mechanisms (usually block release).

Guanethidine, Guanadrel, Reserpine, Trimethaphan

22
Q

Describe the side effects of neuronal/ganglionic blockers (specific & general).

A

General: Decreased CO/HR, diarrhea, fluid/sodium retention (countered with diuretic).

Specific: Reserpine causes sedation/depression and increased gastric acid secretion.

23
Q

Describe some mechanisms by which diuretics produce vasodilation

A
  • decreased Na/water in vessel wall
  • PGI2 and NO release
  • Vascular K channel activation
  • Decrease sensitivity to NE
  • Increase Na-Ca exchange
24
Q

Describe the mechanism of the hypotensive effects of diuretics

A

Exact mechanism unknown

initial: BP drop caused by diuresis
later: chronic hypertensive effect - EC and plasma volume return to near baseline, but PVR is lower than baseline.

25
Q

What are some adverse effects of diuretics?

A
  • electrolyte disturbances
  • hyperglycemia
  • hypotension, orthostasis
  • lipid abnormalities
  • photosensitivity
  • ototoxicity
  • hyperuricemia (gout flares)
26
Q

Describe the general class/mechanism of:

  1. Aliskiren
  2. Lisinopril
  3. Losartan
  4. Spironolactone
A
  1. Blocks conversion of angiotensinogen to angiotensin I
  2. ACE inhibitor
  3. ARB
  4. aldosterone receptor inhibitor
27
Q

Where is ACE (angiotensin-converting enzyme) typically found?

A

Many tissues, primarily endothelial cells and blood vessels

28
Q

Besides converting antiotensin I to angiotensin II, what are some other roles of ACE?

A

block bradykinin degradation

stimulate synthesis of vasodilating substances such as PGE2 and prostacyclin

29
Q

What are some adverse effects of ACE inhibitors?

A
  • cough (bradykinin?)
  • angioedema -> cease therapy immediately (and ARBs)
  • hyperkalemia (especially CKD and DM patients)
  • neutropenia, agranulocytosis, proteinuria, glomerulonephritis
  • acute renal failure
30
Q

What are some adverse effects of ARBs? What adverse effect is observed less often (or less severely) than with ACE inhibitors?

A
  • orthostatic hypertension
  • renal insufficiency
  • hyperkalemia

Less cough than ACE inhibitors (ARBs do not block the breakdown of bradykinin)

31
Q

Compare the roles of AT1 vs. AT2

A

AT1 = ‘bad’

  • vsoconstriction
  • vascular proliferation
  • aldosterone secretion
  • cardiac myocyte proliferation
  • increased sympathetic tone

AT2 = ‘good’

  • vasodilation
  • antiproliferation
  • apoptosis
32
Q

Approximately how long does it take ARBs to reach their maximum effect (model: Losartan)

A

~4-6 weeks

33
Q

What are some adverse effects of aliskiren?

A
  • orthostatic hypotension
  • hyperkalemia
34
Q

ACE inhibitors and ARBs are contraindicated in what patient populations?

A
  • Can cause kidney failure in: severe bilateral renal artery stenosis or severe stenosis to solitary kidney
  • Pregnant women
35
Q

Name some drugs that commonly adversely interact with ACE inhibitors and ARBs

A
  • Medications promoting hyperkalemia
  • Medications sensitive to changes in serum K+
  • Other antihypertensive medications (excessive additive effects)
  • NSAIDs
36
Q

Losartan (and other ARBs or ACE inhibitors) are commonly combined with which other drug to produce a greater antihypertensive effect?

A

HCTZ (or other thiazide diuretic)

37
Q

Describe the basic hypertension treatment algorithm described by JNC7

A
  • Attempt lifestyle modifications
  • If still not at goal (<140/90 mmHg or <130/80mmHz for CKD or DM): drug choices
    • with compelling indications - use compelling indication drugs
    • without compelling indications:
      • Stage 1 hypertension (SBP: 140-159 or DBP 90-99): thiazides, consider ACEI, ARB, BB, CCB, or combo
      • Stage 2 hypertension (SBP>160 or DBP>100): two-drug combo (thiazide + ACEI/ARB/BB/CCB)
38
Q

Describe some lifestyle modifications typicall recommended to decrease hypertension

A
  • reduce weight
  • DASH eating plan
  • dietary sodium restriction
  • increase physical activity
  • reduce alcohol consumption
39
Q

Name the physiological parameters that require monitoring for each:

  • Diuretics
  • beta-blockers
  • RAA drugs
  • CCBs
A
  • Diuretics: blood pressure, BUN/SC, serum electrolytes, uric acid (thiazides)
  • BB: blood pressure, heart rate
  • RAA: blood pressure, BUN/SC, serum K+
  • CCB: blood pressure, heart rate
40
Q

Describe the antihypertensive drug considerations of each of the following special populations:

  1. African Americans
  2. Left ventricular hypertrophy
  3. Elderly
  4. Pregnancy
  5. Children and adolescents
A
  1. Angioedema 2-4x higher prevalance. Response to diuretics + CCB is generally better than ACEI, ARB, or BB.
  2. LVH: aggressive control regresses LVH. However, minoxidil and hydralazine do not help
  3. Elderly (w/ isolated systolic HTN): thiazides and CCBs may be better tolerated
  4. Pregnancy: no ARBs or ACEI. Use methyldopa, BB, and vasodilators (such as hydralazine)
  5. Children/adolescents: no ARBs or ACEI in pregnant or sexually active girls
41
Q

What drug class should always be used as a part of combo therapy for hypertension (unless contraindicated)?

A

thiazide diuretic

42
Q

Define resistant hypertension

A

failure to achieve BP goal on full doses of a 3-drug antihypertensive regimen which includes a diuretic

43
Q

Which drug, used in hypertensive emergencies, carries a risk of thiocyanate and cyanide toxicity?

A

Sodium Nitroprusside

44
Q

Acute heart failure specifically contraindicates what drug(s) commonly used in hypertensive emergencies?

A

Nicardipine, labetalol

also: caution with clevidipine

45
Q

Which hypertensive emergency drug should be used with caution in patients with glaucoma?

What are the caution(s) for Sodium Nitroprusside?

A

Fenoldopam

High intracranial pressure, azotemia, CKD

46
Q

What drug is specifically indicated for eclampsia?

A

Hydralazine

M2 Cardiovascular (40 decks)

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