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Pharm > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Diuretic agents mode of action

A

Drugs that increase excretion rate of water

  • mechanism secondary to increased excretion of sodium
  • decrease extracellular fluid volume without reducing plasma volume
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2
Q

Types of diuretics

A
  • Thiazides
  • loop diuretics
  • potassium sparing diuretics
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3
Q

Thiazide mechanism

A

Inhibt NaCl symporter in cortical diluting site of the distal convoluted tubule

  • Increase Na, Cl, and K excretion
  • decrease Ca excretion
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4
Q

Therapeutic uses of thiazides

A

Edema

Hypertension: first choice in treatment of mild to moderate hypertension

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5
Q

Major side effects of thiazides

A
  • Increased distal Na delivery leads to increased K excretion
  • Elevation of plasma renin, Angiotensin II, and aldosterone due to volume and sodium depletion
  • may result in hypokalemia
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6
Q

loop diuretics mechanism of action

A
  • inhibit Na-K-2Cl symporter in thick ascending limb
  • increase Na,Cl excretion
  • increase distal K excretion in exchange for Na reuptake
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7
Q

loop diuretics therapeutic use

A
  • Acute pulmonary edema
  • edema for cardiac, hepatic and renal causes
  • Hypertension refractory to other diuretics
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8
Q

Side effects of loop diuretics

A
  • electrolyte abnormalities (hypokalemia)
  • Worsening of incontinence
  • drugs interaction(NSAIDs and antibiotics)
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9
Q

potassium sparing diuretics mechanism of action

A
  • Inhibit Na reabsorption by principal cells of late distal tubules and collecting ducts
  • Decrease K excretion
  • Act directly on epithelial Na channel(amiloride)
  • act indirectly by antagonism of aldosterone a mineralocorticoid receptor(spironolactone)
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10
Q

Indications of Potassium sparing diuretics

A
  • both types used in combination with thiazides or loop diuretics to decrease hypokalemia
  • Aldosterone receptor antagonists in combo with loop diuretics and ACE inhibitors in heart failure to enhance survival
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11
Q

List the types of sympatholytic

A
  • β blockers
  • CNS Alpha-2 agonists
  • Selective α1 adrenoceptor antagonists
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12
Q

How do the β-blockers work?

A
  • Block cardiac β1 receptors –> decreases HR, contractility and cardiac output
  • Block renal β1 receptors–> Decrease plasma renin, ANG II, and TPR
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13
Q

How is a β-blocker useful for MI

A

Antiarrhythmic, Anti-ischemic, Antiatherogenic, Reverses cardiac remodeling

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14
Q

Why are CNS Alpha-2 agonists not used as a first line?

A

Can be troublesome in elderly patients because orthostatic hypertension and CNS effects

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15
Q

How do selective α1 adrenoceptor antagonists work

A

They block vascular α1 receptors causing vasodilatation, decreased TPR and MAP

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16
Q

When are selective α1 adrenoceptor antagonists used?

A

The yare not used as a fir line for antihypertensive therapy
maybe usedful as adjunctive therapy in resistant hypertension
Adverse effects-Tachycardia, Don’t use in CHF

17
Q

Types of vasodilator agents

A
  • Calcium channel blockers (CCBs)

- alpha-1 antagnoists

18
Q

Target tissue eor CCBs

A
  • Arterial Smooth muscle

- Cardiac tissue

19
Q

Arterial smooth muscle CCB action and adverse effects

A

CCB block L-type voltage gated calcium channels and therefore prevent calcium entry into arterial VSM
-Adverse effects: reflex tachycardia,’ ankle edema due to selective arterial vaso dilatation

20
Q

Cardiac tissue CCB action and drug interaction

A
  • “non-dihydropyridine” CCBs block calcium entry into myocytes
  • drug interactions: may precipitate AV block with drugs that decrease AV node conduction(e.g., Beta-blockers)
21
Q

Direct acting vascular smooth muscle (vasodilator) action

A
  • Binds to and activates potassium channels
  • evokes potassium efflux and cell hyperpolarization
  • prevents calcium-mediated smooth muscle contraction and evokes vasodilation
  • -Triggers baroreflex evoked tachycardia and vasoconstriction -used in combination with beta blockers
22
Q

Agents affecting RAAS

A
  • ACe inhibitors(ACEI)
  • AT1 antagonists(ARBs)
  • Aldosterone antagonists
23
Q

Main types of ACE inhibitors

A
  • Sulfhydryl-containing
  • Dicarboxyl-containing
  • Phosphorous-containing
24
Q

Primary method of clearance of ACE inhibitors

A

Cleared by kidney

25
Q

ACEI adverse effects

A
  • Hypotension- With multidrug therapy
  • Acute renal failure-Volume depletion and bilateral renal artery stenosis
  • hyperkalemia- renal insufficiency, on K-sparing diuretics, diabetic, beta blockers or NSAIDs
  • cough and angioedema(kinen related?)
  • with captopril
26
Q

ACEI contraindications

A
  • Intolerance
    • angioedema and anaphylactoid reactions
    • Anuric renal failure
  • Bilateral renal stenosis
  • Pregnancy
  • Renal insuffiency(Creatinine > 3mg/dL
  • hyperkalemia
  • severe hypotension
27
Q

ARBs description

A
  • non-pepetide AT! competitive antagonist . (10,000 fold more selective for AT1 vs AT2)
  • Cleared by renal and hepatic
  • Antagonizes most biological effects of ANGII
28
Q

Why do ARBs have “insurmountable antagonism”?

A
  • Slow dissociation kinetics
  • AT1 receptor internalization
  • ARB binding at alternative site to AngII
29
Q

ARB vs ACEI

A
  • ARB has comparable effects to ACEI in almost all situations
  • ARBs greater activation of AT1 receptors vs ACEI
  • ARBs permit activation of AT2 receptors
  • ARBs do not increase levels of ACE substrates e.g bradykinin
30
Q

ARB adverse effects

A
  • Less cough & angioedema than ACEI
  • avoid in pregnancy
  • can cause hypotension in patients whose arterial blood pressure or renal function is highly dependent on RAS
  • can cause hyperkalemia in patients with renal disease or in patients taking K supplements or K sparing diuretics
31
Q

Direct renin inhibitor (DRI)pharmacology

A
  • low bioavailability but high affinity and potency is able to compensate
  • peak plasma conc. within 3-6 hrs
  • Half life 20-45 hrs (SS conc in 5-8 days
  • substrate for pgp , which accounts for low absorption.
  • fatty meals decrease absorption
  • elimination mostly as unchanged drug in feces
  • 25% absorbed done in urine as parent drug
32
Q

DRI adverse effects

A
  • Well tolerated
  • diarrhea observed at high does
  • reports of angioedema
  • avoid in pregnancy
33
Q

DRI drug interactions

A
  • Reduces furosemide by 50%

- Plasa levels are incred by Pgp inhibitors

34
Q

Antihypertensive Drug class indications for diabetics

A

All classes

35
Q

Antihypertensive Drug class indications for patients with chronic kidney disease

A

ACEI, ARB

36
Q

Antihypertensive Drug class indications for patients with Drug class indications for patients with heart failure

A

Diuretic, BB, ACEI, ARB, Aldosterone antagonist

37
Q

Antihypertensive Drug class indications for patients post-myocardial infarction

A

BB. ACEI. ARB, aldosterone antagonists

38
Q

Antihypertensive Drug class indications for patients with high CAD risk

A

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Pharm (10 decks)

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