ACE Inhibitors & ARBs Flashcards

1
Q

ACE ending

A

pril
- benazepril, lisinopril, ramipril

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2
Q

ARBs ending

A

sartan
- Irbesartan, losartan, olmesartan, valsartan

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3
Q

general mechanism to RAAS

A

angiotensinogen (Renin) angiotensin 1 (ACE), angiotensin 2

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4
Q

what does angiotensin 2 cause

A

myocardial hypertrophy
increase thrist
increase SNS
increased constriction
aldosterone
- increased NA absorption which leads to water retention
- vascular fibrosis

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5
Q

what is RAAS used for

A

to maintain CO (increase HR, contractility, BP, volume) this is good for short term like trauma but bad for long term like left ventricle ischemia

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6
Q

how do ACEI work

A

inhibiting ACE so blocking the conversion of angiotensin 1 to angiotensin 2

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7
Q

what is Bradykinin

A

vasodilator which is the opposite of angiotensin 2

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8
Q

how do ACEI impact bradykinin

A

when ACE is functioning it degrades bradykinin but when we have an ACEI we get a build up of bradykinin

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9
Q

why is the buildup of Bradykinin important

A

explains the cough and angioedema and also dilates vessels which will decrease blood pressure

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10
Q

how do ARBS work

A

block the angiotensin 2 receptors, there is no harm in having increased angiotensin 2 molecules but ARBS block where the angiotensin 2 molecules work at so we do not get any negative effects

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11
Q

target dosing

A

special predetermined does for diseases that do not have a value or symptom driving the treatment, like heart failure

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12
Q

main side effects of ACEI and ARBS and what differes

A

hypotension, dizziness, renal dysnfunction, hyperkalemia
ACEI only: cough and angioedema

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13
Q

how do ACEI and ARBS affect GFR

A

it normally slightly decreases it which is why it is good for diabetic nephropathy but if you have risk factors like volume depleted, vascoconstricting drugs, or renal vascular disease this can cause your GFR to drop into developing acute renal dysfunction

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14
Q

drug interactions

A

NSAIDS: the chronic use of NSAIDS and ACEI/ARBS can lead to acute renal failure, this is because NSAIDS decrease the pressure by constricting afferent, and ACEI dilates the efferent which lowers the glomerular pressure and the use of these together with extremely decrease the pressure in the glomerulus

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15
Q

what individuals might be at risk for hyperkalemia

A

the use of salt substitutes or potassium supplements which can be seen in patients who have renal failure or heart failure

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16
Q

ACEI are useful for what patients

A

hypertension, diabetes, diabetic nephropathy, post MI, CAD risk

17
Q

what HF patients should get ACEI, all patients with an EF of

A

<40%

18
Q

hypotension is more common with

A

hyponatermia

19
Q

if you have angioedema in the oropharynx

A

this is a medical emergency and that patient should never be put on a ACEI again

20
Q

why do we get an increase in potassium

A

aldosterone isn’t stimulated so we hold onto potassium

21
Q

when should we avoid in pregnancy

A

2nd half: fetal hypotension

22
Q

what other drug is a interaction

A

cyclosporine

23
Q

you may prefer what ARB for patients with gout

A

losartan

24
Q

ARBS

A

Irbesartan
Losartan
Olmesartan
Valsartan

25
Q

ACEI

A

ramipril
lisinopril
benazepril