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Therapeutics II > ACE Inhibitors & Angiotensin Antagonists > Flashcards

ACE Inhibitors & Angiotensin Antagonists Flashcards

1
Q

How do ARBs impact the urate transporter?

A
  • it BLOCKS the urate transporter

- uricosuric effect (increased uric acid excretion, reduces gout risk)

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2
Q

ACE INHIBITOR CONTRAINDICATIONS

A
  • PREGNANCY
  • typically not used in pts with Scr > 2.5 (high doses in pts w/ renal insufficiency may = neutropenia)
  • typically not good in BLACKS
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3
Q

Breakdown of ARB impact

A

blocks AT1 –> blocks release of norepi –> decreases sympathetic action

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4
Q

Renin released due to

A
  1. Drop in BP
  2. Low NaCl in the distal tubule of the kidney
  3. . Activation of specific receptors in JG cells
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5
Q

angiotensin II stimulates the adrenal cortex which

A
  • releases aldosterone

- increases BP

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6
Q

BLOCKED BRADYKININ CAUSES

A
  • PGE2/PGI2 = vasodilation = increased vascular permeability
  • bronchoconstriction = COUGH
  • natriuresis
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7
Q

ARB examples

A
  • losartan (cozaar)

- valsartan (diovan)

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8
Q

angiotensin II can modulate baroreceptor reflex which

A

increases BP WITHOUT reflex bradycardia

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9
Q

Angiotensin II Receptor Type 1 (AT1) Blockers end in

A

-sartans

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10
Q

angiotensin II causes

A

widespread vasoconstriction

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11
Q

Liver releases

A

angiotensinogen

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12
Q

angiotensin II activates thirst center (pituitary gland) which

A
  • causes release of antidiuretic hormone (ADH, vasopressin)
  • drink more –> increase volume
  • increases BP
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13
Q

ADVERSE EFFECTS OF ARBS

A
  • hypotension
  • hyperkalemia («< ACE-Is)
  • teratogenic potential (2nd + 3rd trimester)
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14
Q

Selectively block effects of ANG II does 3 things

A
  1. reduce BP
    * **SANS: inhibit stimulation of NE system (fast pressor effects)
    * **RAAS: reduce secretion of aldosterone (slow pressor effect)
    * **prevent cardiac hypertrophy
  2. reduce renal vasoconstriction
  3. no effects on bradykinin system (cough and angioedema less prevalent)
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15
Q

ACE inhibitor examples

A
  • lisinopril (zestril)
  • enalapril (vasotec)
  • captopril (capote)
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16
Q

enalapril (vasotec)

A
  • prodrug (has ester that needs to be cleaved)

- similar to lisinopril

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17
Q

why ace-inhibitors not good in Blacks

A
  • due to low circulating renin

- but use to treat DN and heart failure

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18
Q

ADH causes

A

aquaporins to move to the collecting duct plasma membrane, which increases water reabsorption

19
Q

AT1 Receptor is blocked by

A

ARBs

20
Q

WHEN BLOCK ACE-I

A

-INCREASES CONCENTRATION OF BRADYKININ

21
Q

SANS definition

A

sympathetic autonomic nervous system

22
Q

Angiotensin Receptor 1 (AT1) coupled to _____ and causes (3 things)

A

Gq GPCR (but also Gi);

  1. vasoconstriction of smooth muscles
    * **PLC –> Ca increase
    * **activation of Ca channels
    * **reduce NO synthesis
  2. Increases BP
    * **increase aldosterone production (adrenal medulla)
  3. Cardiac hypertrophy
23
Q

angiotensin II causes constriction of smooth muscle cells which

A

increases BP

24
Q

captopril (capote)

A
  • useful for supine HTN-orthostatic hypotension
  • short acting (t1/2= < 3 h)
  • side effect = rash
25
Q

angiotensin II does (5 things)

A
  1. stimulates the adrenal cortex
  2. causes constriction of smooth muscle cells
  3. activates thirst center (pituitary gland)
  4. can modulate baroreceptor reflex
  5. causes cardiovascular hypertrophy
26
Q

ACE inhibitors end in

A

-pril

27
Q

inhibition of renin (direct and indirect) contraindications

A
  • PREGNANCY and nursing mothers
  • use with ARBs or ACEIs in pts with kidney impairment or diabetes because of kidney impairment risk, low BP and high K+ in blood
28
Q

RAAS definition

A

renin-angiotensin-aldosterone system

29
Q

CLINICAL USES OF ARBS

A
  • HTN
  • Congestive heart failure
  • diabetic nephropathy
  • stroke prophylaxis
30
Q

ACE INHIBITOR CLINICAL USES

A
  • HTN
  • Heart failure with reduced ejection fraction (left ventricular systolic dysfunction)
  • MI (dampened SNS response)
  • slows down progression of diabetic nephropathy
31
Q

HOW DO ACE INHIBITORS SLOW DOWN PROGRESSION OF DIABETIC NEPHROPATHY

A
  • act on efferent arteriole of the kidney
  • this reduces pressure in the glomerulus
  • diminishes proteinuria
32
Q

lisinopril (zestril)

A
  • most commonly used
  • well tolerated
  • t1/2 = 12h
  • not a pro-drug (available mixed with HCTZ - Zestoretic)
33
Q

Kidney releases

A

renin

34
Q

The release of renin

A

increases BP

35
Q

direct inhibition of renin by

A
  • aliskiren (Tekturna)
  • **10 years old
  • **used alone or in combination to treat HTN
  • **benefit: may decrease carotid arterial stiffness vs HCTZ
36
Q

Indirect inhibition of renin

A

impacts beta 1 blockers (blocks B1-AR mediated release)

37
Q

Mechanism

A
  • enzyme reaction (kidney - renin, liver - angiotensinogen)
  • angiotensin I
  • enzyme reaction (ACE in pulmonary blood)
  • angiotensin II
  • stimulation of adrenal cortex to secrete aldosterone
38
Q

ACE-I ADVERSE EFFECTS

A
  • first dose hypotension (fainting, orthostatic hypotension)
  • hyperkalemia (via aldosterone effect)
  • acute renal failure
  • dry cough
  • angioedema
39
Q

Most relevant diuretics

A
  • thiazides
  • K sparing (aldosterone)
  • loop diuretics
40
Q

Renin is released by ____________ cells in the _______

A

juxtaglomerular; kidney

41
Q

angiotensin-converting enzyme located in

A

pulmonary blood

42
Q

ACE-I drug-drug interactions

A
  • food/antacids reduce bioavailability
  • NSAIDs may reduce effectiveness (renal)
  • K+ supplements
  • may increase plasma levels of digoxin and lithium
43
Q

aldosterone stimulates

A

Na uptake on the apical cell membrane in the distal convoluted tubule and collecting ducts

44
Q

angiotensin II causes cardiovascular hypertrophy which

A
  • increases contraction

- increases BP

Therapeutics II (12 decks)

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