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Pharmacology > Renal I - Inhibitors of RAS > Flashcards

Renal I - Inhibitors of RAS Flashcards

1
Q

Certain ___ syndromes, ____ of the liver, and ___ are associated with excessive body fluid volume and ___.

A

nephritic; cirrhosis; CHF; edema

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2
Q

Two primary classes of pharmacological agents used to modify abnormal body fluid volume status?

What are these used to treat?

A

Modifiers of the renin-angiotensin system and diuretics

CHF, hypertension, cirrhosis, and renal disease

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3
Q

ACE Inhibitors:

Primary action? Duration?

A

Short term effects of reducing body sodium, fluid volume, and BP

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4
Q

What blocks the kidney from forming renin?

What blocks angiotensinogen from being converted to angiotensin I?

A

Beta adrenergic antagonists

Aliskirin blocks conversion to Angiotensin I

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5
Q

What are 2 functions of ACE inhibitors?

A

Block the conversion of Angiotensin I to Angiotensin II

Prevent the breakdown of bradykinin

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6
Q

Where do angiotensin receptor inhibitors act?

A

Block the activation of Angiotensin II on the Adrenal cortex and arterioles

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7
Q

Angiotensin II:

  1. How does it alter peripheral resistance?
  2. What action does it have on noradrenergic transmission?
A
  1. Direct vasoconstriction
  2. Increased NE release/decreased NE reuptake, and increases vascular response
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8
Q

Angiotensin II:

Altered peripheral resistance:

  1. What part of the ANS does it control? Action?
  2. Acts to release ____ from where?
  3. What is the ultimate result?
A
  1. Increases sympathetic discharge in the CNS
  2. Catecholamines from the adrenal medulla
  3. Rapid pressor response
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9
Q

Angiotensin II:

Renal function:

  1. What is its direct effect on renal function?
  2. It stimulates release of ____ from the adrenal cortex. This results in increase ___ reabsorption and increased ___ excretion.
A
  1. Increase Na+ reabsorption in the proximal tubule
  2. aldosterone; Na+; K+
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10
Q

Angiotensin II:

Renal function:

  1. How does it alter renal hemodynamics?
  2. Ultimate result?
A
  1. Direct renal vasoconstriction, enhances NE neurotransmission though increase SNS tone
  2. Slow pressor response
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11
Q

Angiotensin II:

Nonhemodynamic mediated effects on the heart:

  1. Use results in increased expression of?
  2. Use results in increased production of? Synthesis of?
A
  1. Proto-oncogenes
  2. Growth factors; ECM proteins
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12
Q

Angiotensin II:

Hemodynamic mediated effects on the heart:

  1. Results in increased ___ on the heart.
  2. What does it do to the vasculature?
  3. What is the ultimate result?
A
  1. afterload
  2. Increases wall tension
  3. Use of angiotensin II ultimately causes vascular and cardiac hypertrophpy and remodeling
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13
Q

ACE Inhibitors:

Principle effects:

  1. What do they inhibit? What happens to levels of plasma AII?
  2. Other interactions with the renin-angiotensin system?
  3. Bradykinin stimulates ___ biosynthesis. This helps in the reduction of?
A
  1. Inhibit conversion of angiotensin I to angiotensin II; they reduce but do not abolish plasma AII levels
  2. They do not interact directly with other components
  3. prostaglandin; blood pressure
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14
Q

ACE Inhibitors:

3 classes? Which are active vs prodrug?

A

a. sulfhydryl-containing ACE inhibitors - active
b. Dicarboxyl-containing ACE inhibitors - inactive prodrug
c. Phosphorous containing ACE inhibitors - active

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15
Q

Common features of all ACE inhibitors:

  1. All effectively block?
  2. All have similar?
  3. what does this say about current recommendation?
A
  1. All ACEI effectively block the conversion of AI to AII
  2. All ACEI have similar therapeutic indications, adverse-effect profiles, and contraindications
  3. Thus with the above information, there is NO compelling reason to favor one ACE inhibitor over another
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16
Q

Common features of all ACE inhibitors:

What patients are hyper-responsive to ACE inhibitor induced hypotension? What should be done?

A

Patients with elevated plasma renin activity are more suceptible to becoming hypotensive; The initial dose should be reduced in these patients (CHF, Na+ depleted patients etc)

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17
Q

Common features of all ACE inhibitors:

ACE inhibitors are eliminated by the kidney - What does this mean for someone with renal failure? How should medication be altered?

What are the two exceptions to this? Why?

A

Someone with renal failure will have decreased clearance and thus the medication dosage should be lowered

Fosinopril and Spirapril are exceptions to this because they are eliminated by the liver and kidney

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18
Q

What is the main sulfhydryl-containing ACE inhibitor?

What is the main phosphorous-containing ACE inhibitor?

A

Captopril

Fosinopril

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19
Q

What is the main dicarboxyl-containing ACE inhibitor?

Name 7 others?

A

Enalapril

Lisinopril, benazepril, quinapril, moexipril, ramipril, trandolapril, perindopril

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20
Q

What are the therapeutic uses of ACE inhibitors?

A

Hypertension, left ventricular systolic dysfunction, CHF, Acute MI, patients at high risk for CV events, and chronic renal failure

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21
Q

Therapeutic uses of ACE inhibitors:

Hypertension:

  1. What are the principle beneficial effects to the CV system?
  2. What type of hypertension does this not effect? Why?
A
  1. DECREASED: TPR, MAP, DBP and SBP
  2. Ace inhibitors do not reduce the hypertension in primary aldosteronism because this occurs downstream from the ACE effects
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22
Q

Therapeutic uses of ACE inhibitors:

Hypertension:

  1. Long-term fall in systemic BP is caused by what 2 things?
  2. In regards to the graph and renin: line A indicates? B? C?
A
  1. Long term decrease in SBP is due to decreased TPR and left shift in renal pressure-natriuresis
  2. A=normal B=low (due to block of RAAS) C= high
23
Q

Therapeutic uses of ACE inhibitors:

Hypertension Additional effects:

  1. On arterial compliance?
  2. On cardiac function?
  3. On plasma K+ levels?
  4. ACE inhibitors are often combined with?
A
  1. Ace inhibitors cause an increase in arterial compliance
  2. They have no effect on cardiac function
  3. Minimal effects on plasma K+ levels (retention is only seen in patients on supplemental K+/renal impairment/other drugs that decrease K+ excretion)
  4. Ace inhibitors are often combined with diuretics, beta blockers, or Ca++ channel blockers to better control hypertension
24
Q

Therapeutic uses of ACE inhibitors:

Additional effects in hypertension:

  1. What is do they not do that other drugs can cause in the treatment of hypertension?
  2. They are BEST choice for hypertensive patients with? Why?
A
  1. ACE inhibitors do not cause postural hypotension or compromise CV reflexes
  2. They are GREAT for hypertensive patients with diabetes because they have renal protective effects, they improve endothelial function (by blocking A II stimulation of free radicals), and their ability to reduce CV events
25
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

What are the principle beneficial effects?

A

ACE Inhibitors:

a. Prevent/delay the progression of heart failure
b. Decrease the incidence of sudden death and MI
c. Decrease rates of hospitalization
d. Improves quality of life

26
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

  1. The more _____ the ventricular dysfunction, the _____ the benefit of ACEI use.
  2. These should be given to ALL patients with impaired left ventricular systolic function whether or not they have ___ of overt heart failure. The only time they shouldnt be given is?
A
  1. severe; greater
  2. symptoms; ACE inhibitors shouldnt be given for this ONLY if they are contraindicated
27
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

Effects on:

  1. Afterload?
  2. Systolic wall stress?
  3. CO?
  4. Stroke volume?
A
  1. Decrease
  2. Decrease
  3. Increase
  4. Increase
28
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

Effects on:

  1. Arterial compliance?
  2. Heart rate?
  3. Renovascular resistance? RBF?
  4. Natriuresis? How?
A
  1. Increase
  2. Decrease
  3. Decrease resistance and Increase RBF
  4. Increase natriuresis by decreasing aldosterone and direct effect of A II on the kidney
29
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

Effects on:

  1. Body fluid volume?
  2. Results in venodilation with reduced?
  3. Pulmonary arterial pressure?
A

Ace inhibitors

  1. decrease body volume
  2. decreased venous return
  3. decreases pulmonary arterial pressure
30
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

Effects on:

  1. LA/LV filling pressure?
  2. Preload?
  3. Diastolic wall stress?
A

ACE inhibitors:

  1. Decrease left heart filling pressure
  2. decrease preload
  3. decrease diastolic wall stress
31
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

What is one KEY benefit in the treatment of systolic dysfunction associated with chronic CHF?

A

*******ACE INHIBITORS COUNTERACT THE DETRIMENTAL VENTRICULAR REMODELING ASSOCIATED WITH CHRONIC CHF********

32
Q

Therapeutic uses of ACE inhibitors:

Left ventricular systolic dysfunction and CHF:

Chronic exposure of the heart to A II results in stimulation of ____ activity in the ventricle, cardiac ____, and ____ dilation which in turn increases ventricular wall ____. In heart failure ACE inhibitors reduce ventricular ____ and tend to restore the heart to its normal ____ due to the reduction of elevated plasma ___ and ____ levels in CHF.

A

Chronic exposre of the heart to A II results in stimulation of mitotic activity in the ventricle, cardiac fibrosis, and ventricular dilation which in turn increases ventricular wall stress. In heart failure Ace inhibitors reduce ventricular dilation and tend to restore the heart to its normal shape due to the reduction of elevated plasma A II and aldosterone levels in CHF

33
Q

Therapeutic uses of ACE inhibitors:

Acute MI and patients at high risk for CV events:

  1. Unless ____ these should be started immediately during what?
  2. For acute MI, Ace inhibitors can be coadministered with?
A
  1. contraindicated; acute phase of MI
  2. ACE inhibitors can be coadministered with thrombolytics, aspirin, and beta adrenergic antagonists in acute MI
34
Q

Therapeutic uses of ACE inhibitors:

Acute MI and patients at high risk for CV events:

  1. The beneficial effects in acute MI are particularly large in what type of patients?
  2. ACE inhibitors reduce plasma levels of what? What state do they favor?
A
  1. Hypertensive and diabetic
  2. Plasminogen activator inhibitor-1 (PAF-1); they favor a profibrinolytic state
35
Q

Therapeutic uses of ACE inhibitors:

Acute MI and patients at high risk for CV events:

  1. What do they improve in patients with coronary artery disease (CAD)?
  2. Decrease rate of MI, ___, and death in patients with ___ disease or __ even without? (These are high risk patients)
A
  1. Endotheial vasomotor dysfunction (this imbalance of constriction vs dilation of vessels leads to atherosclerosis and is thus improved with ACEI)
  2. stroke; vascular; diabetes; heart failure
36
Q

Therapeutic uses of ACE inhibitors:

Chronic renal failure:

  1. What drugs delay or prevent the progression of renal disease associated with type I diabetes?
  2. Renal protective effects include reduction of injury caused by increased ____ ____ by decreasing BP and decreasing ___ arteriole resistance (which arteriole)
A
  1. Captopril and Lisinopril delay/prevent progression of renal disease associated with type I diabetes
  2. Renal protective effects include reduction of injury caused by increased glomerular pressure by decreasing BP and decreasing efferent arteriole resistance.
37
Q

Therapeutic uses of ACE inhibitors:

Chronic renal failure:

Renal protective effects include improved selectivity of the glomerulous to ____ ____ substances that originally damage the mesangium. This prevents ___ cell proliferation. A reduction in A II may also inhibit excessive?

A

Renal protective effects include improved selectivity of the glomerulous to filter proteinaceous substances that originally damage the mesangium. This prevents mesangial cell proliferation. A reduction in A II may also inhibit excessive mesangial growth

38
Q

ACE Inhibitors and adverse reactions:

Adverse reactions are rare:

  1. Can lead to fetopathic properties in the __/___ trimester related to fetal ____.
  2. Can cause acute renal failure in what 3 conditions? How?
A
  1. Dangerous in the 2nd/3rd trimester related to fetal hypotension
  2. Can cause acute renal failure in bilateral renal artery stenosis, CHF, or volume depletion because A II helps maintain GFR in conditions of low renal perfuction pressure (thus increasing GFR)
39
Q

ACE Inhibitors and adverse reactions:

Who are ACE inhibitors ABSOLUTELY contraindicated in?

A

*** ACE INHIBITORS ARE ABSOLUTELY CONTRAINDICATED IN PREGNANT WOMEN REGARDLESS OF WHETHER THEY SUFFER HYPERTENSION OF PREGNANCY****

40
Q

ACE Inhibitors:

Adverse reactions:

  1. What are four additional side effects (in addition to fetal hypotension and acute renal failure)?
  2. What are VERY RARE side effects?
A
  1. cough, angioedema, hypotension, and hyperkalemia
  2. proteinuria, skin rash, dysgeusia, neutropenia, glycosuria, and hepatotoxicity
41
Q

ACE Inhibitors:

Adverse reactions:

  1. Type of cough? Why is this a concern?
  2. Angioedema causes rapid swelling where? What is the most serious concern?
A

Ace Inhibitors cause:

  1. Dry and bothersome cough; only a serious concern because of patient noncompliance
  2. Angioedematous swelling in the nose, throat, mouth, glottis, larynx, lips, tongue and/or intestine (emesis/diarrhea/pain); Airway obstruction and respiratory distress may lead to death
42
Q

ACE Inhibitors:

Adverse reactions:

  1. How to fix angioedema associated side effects?
  2. Hypotension can occur when? Caution should be used in what patients?
  3. Hyperkalemia is more likely to occur in what patients?
A

ACE Inhibitors:

Adverse reactions:

  1. Fix angioedema by removing drug and it disappears within hours
  2. Hypotension can occur with first dose effect; caution in Na+ depleted/CHF patients as well as patients on multiple antihypertensive drugs (esp diur.)
  3. Hyperkalemia is more likely in patients with renal insufficiency or in patients taking K+ sparing diuretics/K+ supplements/beta blockers or NSAIDS
43
Q

Nonpeptide Angiotensin II receptor antagonists:

Name 7 drugs in order of potency?

Have higher affinity for what receptor as opposed to?

A

candesartan=omesartan > irbesartan=eprosartan > telmisartan=valsartan=EXP3174 (active metabolite of losartan) > losartan

Higher affinity for AT1 vs AT2 receptors

44
Q

Nonpeptide Angiotensin II receptor antagonists:

Pharmacologic effects:

  1. What type of block of the AT1 receptor?
  2. Only reduce BP in what forms of hypertension?
A

Nonpeptide Angiotensin II receptor antagonists:

  1. Competitive block of the AT1 receptor
  2. Only reduce BP in HIGH RENIN forms of hypertension
45
Q

Nonpeptide Angiotensin II receptor antagonists:

Potently and selectively inhibit biological effects of angiotensin II including:

A

Nonpeptide Angiotensin II receptor antagonists inhibit

Contraction of vascular smooth muscle

Rapid/slow pressor responses

Aldosteronse secretion and thirst

Vasopressin and adrenal catecholamine release

Decrease SNS tone and NE neurotransmission

Inhibit cellular hypertrophy and hyperplasia

46
Q

Nonpeptide Angiotensin II receptor antagonists:

The inhibition of biological responses to A II is _____ with ARBs (angiotensin receptor blockers)

A

INSURMOUNTABLE (no amount of AII can overcome the blockade with an ARB)

47
Q

Nonpeptide Angiotensin II receptor antagonists:

ARB vs. ACE inhibitors:

  1. Difference at receptors?
  2. ACE inhibitors may increase ____ levels more than ARBS.
  3. ACE inhibitors increase the levels of a number of ACE _____, including?
A
  1. ARBs reduce more effectively at AT1 and in contrast to ACEI they permit ACTIVATION at AT2
  2. Angiotensin (1-7)
  3. substrates; bradykinin and Ac-SDKP (that promotes toxic anemia)
48
Q

Nonpeptide Angiotensin II receptor antagonists:

Therapeutic uses?

A

Nonpeptide Angiotensin II receptor antagonists:

Used for hypertension, diabetic nephropathy, stroke prophylaxis, CHF, and renoprotective in type II diabetes

49
Q

Nonpeptide Angiotensin II receptor antagonists:

Drugs for diabetic nephropathy?

Drugs for Stroke prophylaxis?

A

Nonpeptide Angiotensin II receptor antagonists:

Diabetic nephropathy - irbesartan and losartan

Stroke prophylaxis - losartan

50
Q

Nonpeptide Angiotensin II receptor antagonists:

Drugs for hypertension?

Drugs for CHF?

A

Nonpeptide Angiotensin II receptor antagonists:

Hypertension - can be treated with ALL ARBS

CHF - valsartan

51
Q

Nonpeptide Angiotensin II receptor antagonists:

Adverse effects of arbs:

  1. Teratogenic - when should it be discontinued?
  2. What can it cause in patients whose BP or renal function is dependent of RAAS?
  3. What can it occur in patients with renal disease?
A

Nonpeptide Angiotensin II receptor antagonists:

​Adverse effects of ARBS:

  1. It should be discontinued before the 2nd trimester
  2. Hypotension, oliguria (low output), progressive azotemia (high level of nitrogenous compounds: urea/creatinine), or acute renal failure
  3. Hyperkalemia
52
Q

Nonpeptide Angiotensin II receptor antagonists:

​Adverse effects of arbs:

  1. Potentiate what?
  2. 2 advantages compared to ACE inhibitors?
A

Nonpeptide Angiotensin II receptor antagonists:

​Adverse effects of arbs:

  1. Potentiate the BP lowering effect of other antihypertensives
  2. They do NOT cause cough and a much lower incidence of angioedema in comparison to ACEI
53
Q

Direct renin inhibitors:

Drug?

Treatment?

Contraindications?

A

Aliskiren is a direct renin inhibitor

It is used for hypertension

Is it contraindicated in patients with diabetes, patients on ACE inhibitors, patients with renal impairement, or patients taking ARBs

Pharmacology (24 decks)

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