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1 STEP UW Nephrology > ACEI (amboss and UW) > Flashcards

ACEI (amboss and UW) Flashcards

1
Q

ACEI agents?

A

captopril, enalapril, lisinopril, ramipril, benazepril

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2
Q

ACEI indicatons?

A

Arterial hypertension

Diabetes mellitus (type I and type II)

HF with reduced ejection fraction

History of MI

Nondiabetic chronic kidney disease with proteinuria

Scleroderma-associated hypertensive crisis (even if creatinine is elevated)

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3
Q

Why ACEI used in DM?

A

Nephroprotective indications, such as: Arterial hypertension, Microalbuminuria and proteinuria (especially ≥ 300 mg/g)

Coronary heart disease

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4
Q

ACE inhibitors and ARBs are generally recommended in hypertensive diabetic patients to reduce the risk of cardiovascular events, but they are strongly recommended in diabetic patients with concurrent hypertension and an elevated urinary albumin-to-creatinine ratio (as an indicator for microalbuminuria).

A

.

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5
Q

Why ACEI used in CHD?

A

To reduce the risk of cardiovascular events.

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6
Q

There is minimal evidence to support primary prevention of moderately increased albuminuria in normotensive and normoalbuminuric type I and type II diabetes. Annual screening to identify persistently increased albuminuria is recommended instead. Treatment with a RAAS inhibitor may be considered if albuminuria persists to delay progression towards severely increased albuminuria, especially in patients with type I diabetes, and cardiovascular events

A

.

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7
Q

ACEI has similar effect of what drug?

A

Amyl nitrite is a vasodilator that mimics the effects of ACE inhibitors on the heart.

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8
Q

Why ACEI used in MI?

A

The ability of ACE inhibitors to attenuate ventricular dilatation (remodeling) after an MI is responsible for its survival benefit. Patients will still derive benefit from ACE inhibitors or ARBs if they are not administered immediately after the event.

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9
Q

ACEI mechanism?

A

Mechanism of action: inhibition of ACE → ↓ conversion of angiotensin I to angiotensin II

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10
Q

ACEI effect on GFR?

A

Dilation of efferent arteriole → ↑ renal plasma flow → ↓ GFR → ↓ filtration fraction

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11
Q

ACEI effect on blood pressure? 2

A

↓ Vasoconstriction → ↓ blood pressure

↓ Secretion of aldosterone → ↓ reabsorption of Na+ and water → ↓ blood pressure

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12
Q

ACEI on renin secretion?

A

↑ Renin secretion (due to lack of feedback inhibition) → ↑ angiotensin I

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13
Q

ACEI and bradykinin?

A

↓ Breakdown of bradykinin → ↑ production of arachidonic acid metabolites → ↑ vasodilation → ↓ blood pressure

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14
Q

ACEI on proteinuria and proteinuric CKD?

A

↓ Proteinuria and ↓ progression of proteinuric chronic kidney disease: ↓ intraglomerular hydrostatic pressure attenuates thickening and sclerosis of the GBM

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15
Q

ACEI on preload and afterload?

A

↓ Preload and afterload → ↓ cardiac remodeling after acute myocardial infarction or in chronic hypertensive disease

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16
Q

Increase in bradykinin concentration, which can lead to? 2

A

Dry cough (can be treated by discontinuing ACE inhibitor, consider switching to ARB)

Bradykinin-mediated angioedema due to increased vascular permeability and vasodilation

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17
Q

Why dry cough in bradykinin?

A

The mechanism is not fully understood. However, protussive and proinflammatory effects from local accumulation of bradykinin (and other mediators) in the lung are considered most likely.

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18
Q

Adverse of ACEI?

A

Hypotension

↓ GFR (with ↑ creatinine): can cause AKI in patients with preexisting renal hypoperfusion (e.g., renal artery stenosis, hypovolemia, heart failure)

Hyperkalemia!!!!

Proteinuria

Pemphigus vulgaris (unknown mechanism)

Teratogenicity: renal malformations

Leukopenia

Rash

Taste changes

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19
Q

Early DN effect on glomerular filtration pressure?

A

Elevated glomerular filtration pressure

+ATII further increases glomerular pressure by selective vasoconstriction of the efferent arteriole

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20
Q

Blockage of what decr. glomerular filtration pressure?

A

blockage of ATII, since it increases glomerular pressure by selective vasoconstriction of the efferent arteriole –> lowered glomerular pressure

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21
Q

ACEI use with caution in what condition? and why?

A

In bilateral renal artery stenosis. It leads to decr. renal blood flow –> decr. GFR THEREFORE –> ACTIVATION OF RAAS –> RELEASE OF ATII –> constr. of efferent –> maintain GFR.

ACEI - drop in systemic BP and dilation of efferent.

Drop in BP is no longer high enough to overcome the stenosis –> renal blood flow drops. Due to dilation of efferent –> reduction of intraglomerular filtration pressure -> decr GFR and filtration fraction.

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22
Q

Patients with bilateral and use ACEI are at what risk?

A

Acute renal failure

23
Q

What pressure is reduced in renal artery stenosis?

A

Reduced hydrostatic pressure –> stimulation of ATII –> vasoconstriction –> incr. BP –> incr. renal perfusion

24
Q

In unilateral stenosis normally functioning kidney compensates impaired kidney function.

A

.

25
Q

Why in RAS is normal urinalysis?

A

because glomeruli and tubules functions normally –> no hematuria, proteinuria or casts –> urinalysis is unremarkable

26
Q

Angiotensin-receptor blocker (ARBs, sartans). Agents?

A

valsartan, candesartan, losartan, irbesartan

27
Q

Angiotensin-receptor blocker (ARBs, sartans). Indications?

A

same as ACE inhibitors, mostly used as second-line treatment if ACE inhibitors are not tolerated

28
Q

Direct renin inhibitors. Agents?

A

Aliskiren

29
Q

Direct renin inhibitors.

Indications?

A

Arterial hypertension if both ACE inhibitors and ARBs are not tolerated

30
Q

Angiotensin-receptor blocker (ARBs, sartans). Mechanism?

A

Inhibition of angiotensin II receptor type 1 (AT1 receptor)

31
Q

Angiotensin-receptor blocker (ARBs, sartans). Effect?

A

↓ Vasoconstriction → ↓ blood pressure

↓ Secretion of aldosterone → ↓ reabsorption of Na+ and water → ↓ blood pressure

↑ Renin secretion (compensatory) → ↑ angiotensin I → ↑ angiotensin II

Other effect:
↓ Proteinuria and ↓ progression of proteinuric kidney disease
↓ Cardiac remodeling after acute myocardial infarction or chronic hypertensive disease
No bradykinin elevation (opposed to ACE inhibitors)

32
Q

ACEI vs ATII inhibitors on bradykinin?

A

ACEI - bradykinin levation –> angioedema;

ATII inhibitors –> no bradykinin elevation –> no angioedema

33
Q

Direct renin inhibitors. Mechanism?

A

direct inhibition of renin → ↓ conversion of angiotensinogen into angiotensin I → ↓ angiotensin I and angiotensin II → ↓ angiotensin II → ↓ vasoconstriction

34
Q

Direct renin inhibitors. Effect?

A

↓ Blood pressure

↓ Secretion of aldosterone → ↓ reabsorption of Na+ and water → further ↓ blood pressure

35
Q

ARBS and Direct renin inhibitors adverse?

A 
Angioedema
Hypotension
Hyperkalemia
↓ GFR (with ↑ creatinine)
Teratogenicity
Rash
Diarrhea (direct inhibt)
Leukopenia (ARBS)
36
Q

What kind of kidney injury may occur in patients takins RAAS inhibitors and NSAIDs?

A

Acute kidney injury is a potential side effect of all types of RAAS inhibitors, especially in patients with preexisting kidney disease or in combination with NSAIDs

37
Q

Contraindications for ACE inhibitors and ARBs. Absolute?

A

Hypersensitivity

C1 esterase inhibitor deficiency (due to predisposition to angioedema)

Pregnancy: risk of harm to the fetus (e.g., renal impairment, renal malformations, oligohydramnios, placental insufficiency)

Breastfeeding

38
Q

Contraindications for ACE inhibitors and ARBs. Relative?

A

Aortic stenosis

Renal dysfunction, consider altering dose if GFR < 60 mL/min

Bilateral renal artery stenosis or a solitary kidney: GFR is already decreased and further reduction may lead to acute kidney injury.

39
Q

Contraindications for ACE inhibitors and ARBs. Why mitral stenosis is relative contraindication?

A

These patients may not be able to further increase their stroke volume to compensate for the peripheral vasodilation caused by ACE inhibitors. Severe hypotension may occur.

40
Q

Contraindications for ACE inhibitors and ARBs. Why relative contraindication is Bilateral renal artery stenosis or a solitary kidney?

A

Even patients with advanced renal dysfunction may benefit from treatment with ACE inhibitors, although there might be an initial drop in GFR and increase in creatinine (tolerable up to 30%). Therefore, regular GFR monitoring is required in patients with chronic kidney disease.

41
Q

Contraindications for direct renin inhibitors?

A

Hypersensitivity

Pregnancy

Current treatment with ACE inhibitors or ARBs

42
Q

Interactions. ACE inhibitors and ARBs + other antihypertensive drugs?

A

Other antihypertensive drugs → ↑ hypotensive effect

43
Q

Interactions. ACE inhibitors and ARBs + NSAIDs?

A

NSAIDs → ↓ antihypertensive effect

44
Q

Interactions. ACE inhibitors and ARBs + K sparring diuretics?

A

Potassium-sparing diuretics or other drugs that increase potassium level: ↑ hyperkalemia

45
Q

Interactions. ACE inhibitors and ARBs + allopurinol?

A

Allopurinol: ↑ risk of immunological reactions or leukopenia (not yet fully understood mechanism)

46
Q

Interactions. ACE inhibitors and ARBs.

↑ Level of lithium due to ↓ renal elimination

A

.

47
Q

Interactions. Direct renin inhibitors + ACEI/ARBS?

A

ACE inhibitors or ARBs → ↑ hyperkalemia

DO NOT COMBINE RENIN INHIBITORS + ACEI/ARBS

48
Q

Interactions. Direct renin inhibitors + P-glycoprotein inhibitors?

A

P-glycoprotein inhibitors (e.g., ketoconazole, verapamil, clarithromycin, erythromycin, amiodarone): ↑ aliskiren level

49
Q

When starting an ACE inhibitor or an ARB, monitor what? 3

A

Blood pressure, potassium, and creatinine

50
Q

Combine ACE inhibitors or ARBs with thiazide diuretics to …….

A

offset the risks of hyperkalemia and hypokalemia

51
Q

Starting with low doses (preferably in a controlled setting) is recommended to avoid ……..

A

Starting with low doses (preferably in a controlled setting) is recommended to avoid severe hypotension

52
Q

Drops in blood pressure reduce………

A

Drops in blood pressure reduce renal perfusion

53
Q

What mmHg drop in RENAL ARTERY activates juxtaglomerular apparatus?

A

If the pressure in the RENAL ARTERY falls by more than 10–15 mmHg, proteolytic renin is released from the juxtaglomerular apparatus

54
Q

How RAAS increase BP?

A

2 ways: vasoconstriction and stimulation of the release of aldosterone, which increases the retention of water and sodium

1 STEP UW Nephrology (14 decks)

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