drugs to treat Hypertension and HTN urgency/emergency Flashcards

1
Q

lowering blood pressure has been known to do what?

A

Prolong life!

Page Mosaic Theory of hypertension

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2
Q

what is considered the slow but ultimate regulator of blood pressure?

A

Renal blood volume control due to its infinite gain

Kidneys are super important when it comes tp to blood pressure

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3
Q

what are the 2 types of hypertension and their sub groups?

A

Primary Hypertension

  • most common form
  • divided into 3 groups:
  • low renin (AA and elderly)
  • Normal renin
  • High renin
  • no identifiable cause
  • chronic progressive disorder
  • drugs can treat BP but not underlying cause

Secondary Hypertension:

  • has identified primary cause
  • can be cured by treating the cause
  • usually new onset or uncontrolled hypertension in adults
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4
Q

what are the main causes of secondary hypertension?

A
  • Renal parenchymal disease
  • renovascular disease
  • primary aldosteronism
  • obstructive sleep apnea
  • drug or alcohol induced
  • pheochromocytoma
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5
Q

what are the best proven non-pharmacological interventions and preventions of hypertension

A
  • weight loss
  • healthy diet
  • reduced intake of dietary sodium
  • enhanced intake of Potassium
  • physical activity
  • moderation of alcohol
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6
Q

what are the primary agents for oral hypertensive drugs

A
  • Thiazide diuretics
  • ACE inhibitors
  • ARBs
  • CCB dihydropyridines
  • CCB nondihydropyridines
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7
Q

what are the secondary agents of oral antihypertensive drugs?

A
  • loop diuretics
  • K+sparing diuretics
  • aldosterone antagonists
  • Beta blockers cardioselective
  • Beta blockers non cardio selective
  • beta blockers a and b receptor
  • alpha 1 blockers
  • central alpha 2 blockers
  • direct vasodilators
  • direct renin inhibitor
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8
Q

MOA, Effects and Clinical applications of Hydrochlorothiazide?

A

MOA: inhibits sodium reabsorption at the distal tubules by blocking the Na Cl co transporter

Effects:
-increased urinary excretion of Na, H20, K, Mg

Clinical applications:

  • management of hypertension alone or in combination
  • not effective in patients with a low GFR
  • off label calcium nephrolithiasis
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9
Q

Pharmacokinetics and toxicities of Hydrochlorothiazide

A

Pharm: well absorbed

  • excreted in urine
  • half life 6-15 hrs

Toxicities:

  • sulfonamide (hypersensitivity
  • Hypotension
  • hypokalemia
  • hypomagnesemia
  • hyponatremia
  • hypochloremic metabolic alkalosis
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10
Q

what are the other drugs similar to hydrochlorothiazide

A

Chlorothiazide: poor oral absorption

chlorthalidone: longer half life

Metolazone: long acting thiazide diuretic useful in treatment of congestive heart failure

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11
Q

MOA, effects, and clinical applications of Furosemide?

A

MOA: inhibits the Na L 2Cl cotransporter in the TAL of loop of henle
-indirectly inhibits reabsorption of Ca and Mg due to loss of K

Effects:

  • increased H20, Na, Cl, K, Mg, Ca excretion
  • massive fluid removal

CLinical applications:

  • edema associated with HF, Hepatic disease, renal disease
  • decrease preload
  • decrease ECV
  • treeatment of hypertension in patients with a low GFR
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12
Q

Pharmacokinetics and toxicities of furosemide

A

Pharm:

  • elminated in urine
  • short half life

Toxicities:

  • Ototoxicity
  • sulfonamide
  • hypo calcemia, natremia, kaemia, alkalosis
  • hyper glycemia, urcemia
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13
Q

what are the other drugs that act similar to furosemide?

A

Torsemide: longer half life and better oral absorption (thought to be better against HF)

Bumetanide: more predicatble oral absorption

Ethacrynic acid: Non sufonamide loop diuretic
(used for hypersensitivity patients)

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14
Q

MOA, Effects and Clinical applications of Amiloride?

A

MOA: blocks epithelial sodium channels (EnaC) in the collecting ducts and collecting tubules

Effects: small changes in Na excretion

  • blocks K elimination (K sparring)
  • decreased H, Mg, Ca excretion

Clinical applications: counteracts K loss by other diuretics

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15
Q

Pharmacokinetics and toxicites of amiloride

A

Pharm:

  • given orally
  • half life 6-9 hrs
  • ecreted in urine and feces
  • enhances other diuretics

Toxicites:

  • Hyperkalemia (BB warning)
  • hyponatremia
  • hypovolemia
  • dizziness and fatigue
  • nausea vomiting
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16
Q

what is triamterene

A

used similar to amiloride for edema and off level for hypertension, rapidly absorbed, duration of action 6-9 hrs and eliminated as drug metabolites

k+ sparring?

17
Q

MOA, Effects, Clinical applications of Spironolactone

A

MOA:
-Competitive antagonist of aldosterone receptors

Effects:
K+ sparing
-antagonizes pro-fibrotic effects of aldosterone
-decreased exchange of Na and K

Clinical applications

  • counteracts K+ loss induced by other diuretics in treatment of hypertension of heart failure
  • treatment of primary hyperaldosteronism
  • reduce fibrosis in HFrEF and post MI heart failure
  • off label HFpEF, hirutism, acne, treatment of androgenic alopecia
18
Q

Pharm and toxicities of Spironolactone

A

Pharm:

  • long half life
  • slow onset and slow off set
  • enhances the effects of other K+ sparring drugs (ACEI and ARB)

Toxicites:

  • hyperkalemia
  • amenorrhea, hirsutism
  • tumorigen
19
Q

what is eplerenone

A

More selective aldosterone antagonist, approved for use in post-MI heart failure and alone in combination for treatment of hypertension

20
Q

what are the effects of angiotensin II

A

Potent vasoconstrictor

increase extracellular fluid

  • stimulate thirst
  • stimulate aldosterone secretion
  • stimulating ADH secretion

Contributes to cardiovascular remodeling