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Block 4: Pharm > Drugs of the Renin-Angiotensin-Aldosterone System > Flashcards

Drugs of the Renin-Angiotensin-Aldosterone System Flashcards

1
Q

Renin-Angiotensin-Aldosterone System is a very important system in regards to controlling ______.

A

blood pressure

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2
Q

what organ is involved in producing angiotensinogen?

A

liver

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3
Q

Angiotensin II is a very important ______.

A

vasoconstrictor

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4
Q

Angiotensin II is a very important vasoconstrictor, so if you are hypovolemic and the body senses that it needs to increase your blood pressure, you will start trying to convert more angiotensin I to angiotensin II. The enzyme that does this is ACE- angiotensin converting enzyme. And this enzyme is produced where?

A

in the lungs and kidneys

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5
Q

angiotensinogen in the liver gets converted to angiotensin I by Renin, and renin is secreted by the kidneys in response to ____________.

A

adrenergic stimulation (epi, NE, drop in BP)

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6
Q

Angiotensinogen –> angiotensin I–> (___) –>angiotensin II

A

ACE

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7
Q

Why are kidneys controlling BP?

A

angiotensinogen in the liver gets converted to angiotensin I by Renin, and renin is secreted by the kidneys in response to adrenergic stimulation (epi, NE, drop in BP).

Renin responds to juxtaglomerular apparatus in the kidney, that’s what senses the amount of sodium and potassium that we are filtering and absorbing- that’s why kidneys are controlling BP.

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8
Q

angiotensin II causes what 5 things to happen?

A
  1. increased sympathetic activity
  2. sodium and chloride reabsorption, potassium excretion, and water retention
  3. aldosterone secretion
  4. arterioler vasoconstriction = inc. in BP
  5. ADH secretion–> water absorption in collecting duct
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9
Q

ACE also breaks down bradykinin, which is a _______.

A

vasodilator

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10
Q

ACE also breaks down bradykinin, which is a vasodilator. If you don’t need to increase the BP then you don’t need ACE, and if you don’t have ACE then bradykinin will keep - things ________. It is also involved in increasing certain prostaglandin production.

A

vasodilated

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11
Q

If we use ACE INHIBITORS and block ACE, we don’t get angiotensin II made, but we also don’t get breakdown of______.

A

bradykinin

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12
Q

ARBs are angiotensin receptor blockers/ antagonists and bind to receptors to not allow ______ to bind to its receptors on the target tissue.

A

angiotensin II

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13
Q

Aldosterone antagonist (spironolactone) block where aldosterone will bind, so you don’t get activation of the ________.

A

sodium channels

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14
Q

ACE causes _________ (vasoconstriction/vasodilation) and blocks _______ (vasoconstriction/vasodilation)

A

ACE causes vasoconstriction and prevents vasodilation

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15
Q

ACE:
- Cleaves angiotensin I to form _______ (vasoconstrictor)
and Breaks down _______ (vasodilator)

A

angiotensin II

bradykinin

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16
Q

Blocking ACE helps lower BP by reducing vasoconstriction and reducing secretion of _______.

A

aldosterone

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17
Q

ACE inhibitors end in ___.

A

“pril”

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18
Q

most common ACE inhibitor used

A

Lisinopril

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19
Q

Ace inhibitors Actions on CV System

A
  1. Decrease vascular resistance (total peripheral resistance), venous tone, and BP
  2. Reduce preload and afterload (because of vasodilation, which increases cardiac output overall, especially in those with HF or MIs, as well as high BP
  3. Blunt the usual angiotensin II-mediated sympathetic response and aldosterone secretion (BP and cardiac remodeling). By decreasing these things we can prohibit cardiac remodeling in patients with HF, which is why we like to use these drugs in HF and post MI
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20
Q

Ace inhibitors indications for HTN

A

Ace inhibitors are a First-line option or as an add-on to almost every other class except for another renin angiotensin drug, but we do use them with aldosterone antagonists.

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21
Q

Ace inhibitors indications for HF

A

♣ DOC in all stages
♣ Improved morbidity and mortality
♣ One of the first drugs you will prescribe chronically for a pt in HF will be an ace inhibitor

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22
Q

Ace inhibitors indications for MI

A

♣ Should be started immediately after MI
♣ Because of prevention of cardiac remodeling, helping to reduce preload and afterload which reduces work of heart and oxygen demand of heart.

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23
Q

Ace inhibitors indications for DM nephropathy

A

If patient has HTN and diabetes ace inhibitors are good drugs to use because patients with diabetes are susceptible to HTN and nephropathy

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24
Q

all drugs that are Ace inhibitors are “pro drugs” except for what 2?

A

except lisinopril and captopril

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25
Q

Pro-drugs (except lisinopril and captopril) require activation by hydrolysis by
_____ enzymes

A

hepatic

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26
Q

most ACE inhibitors have renal elimination, what things should you monitor?

A

MONITOR BUN/ CREATINE/ GFR

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27
Q

ACE inhibitors ADRs

A
  1. Hypotension
  2. Acute renal failure: especially in renal artery stenosis***
  3. Hyperkalemia
  4. Cough
  5. Angioedema/wheezing
  6. Pregnancy: CI during pregnancy and should stop ASAP if taking
  7. Rash
  8. Extremely rare: dysgeusia (loss of taste), neutropenia, glycosuria, anemia, hepatotoxicity (these are more for FYI)
  9. January 2013: ACEIs linked to hallucinations in elderly (d/c if pt c/o of this)
  10. November 2013: Case report links ACEIs with oral allergy (things they consume) syndrome
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28
Q

ACE inhibitor ADR of hypotension causes a rapid, steep fall in BP. this can occur after initial doses in patients with elevated __________.

A

plasma renin activity

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29
Q

ACE inhibitors are renal protective but also can cause renal damage, main time it causes damage is when someone has underlying ____ problems.

A

renal vascular

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30
Q

If you ever see a sharp spike in BP response after starting an ACE or an ARB, that’s a good indication that patient has what?

A

renal artery stenosis

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31
Q

To monitor the ADR of acute renal failure when using ACE inhibitors, what 2 things should you be watching out for?

A

♣ sudden increase in BP when you start an ACE, because it should fall.
♣ Monitor labs and see creatinine going up then that is also an indication

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32
Q

in regards to the hyperkalemia ADR when using ACE inhibitors, what things should you be cautious about?

A

renal insufficiency, DM, K-sparing diuretics, BBs, NSAIDs

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33
Q

When using ACE inhibitors one ADR is cough, what is this believed to be due to?

A

due to bradykinin and substance P

5-20% of patients described as dry cough

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34
Q

bradykinin and substance P release are thought to be the cause of what 2 ADRs of ACE inhibitors?

A

Angioedema/wheezing

cough

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35
Q

angiodema/wheezing ADR of ACE inhibitors is more likely to happen in what race of patients?

A

black patients

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36
Q

should you use an ace inhibitor in pregnancy?

A

NO

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37
Q

WHY is ACE inhibitors CI in pregnancy?

A

o Fetal hypotension, anuria and renal failure
o Fetal malformations and death
o All drugs that work through renin-angiotensin system are CI in pregnancy because it can cause birth defects and issues with blood supply to developing fetus.

38
Q

January 2013, a study released showed ACEIs linked to hallucinations in ____ patients

A

elderly

39
Q

In November 2013: Case report links ACEIs with ______.

A

oral allergy (things they consume) syndrome

40
Q

What are some extremely rare ADRs of ACEIs?

A

dysgeusia (loss of taste), neutropenia, glycosuria, anemia, hepatotoxicity

41
Q

patients may develop a ______ rash as an ADR when taking ACEIs

A

maculopapular

may be temporary or could resolve with antihistamine

42
Q

If a patient is peeing protein, then there is something wrong with their _____.

A

glomerulus

43
Q

______ is the leading cause of renal disease

A

Diabetes mellitus

44
Q

In patients with type 1 diabetes mellitus and diabetic nephropathy, what drug (ACEI) prevents or delays the progression of renal disease?

A

captopril

45
Q

Renoprotection in type 1 diabetes, as defined by changes in albumin excretion, is also observed in patients using what ACEI?

A

lisinopril

46
Q

The renoprotective effects of ACE inhibitors in type 1 diabetes are in part independent of ______ reduction.

A

blood pressure

47
Q

______ may also decrease retinopathy progression in type 1 diabetics and attenuate the progression of renal insufficiency in patients with a variety of nondiabetic nephropathies.

A

ACE inhibitors

48
Q

there Several mechanisms in the renal protection afforded by ACE inhibitors, what are they?

A
  1. Increased glomerular capillary pressure induces glomerular injury, and ACE inhibitors reduce this parameter both by decreasing arterial blood pressure and by dilating renal efferent arterioles
  2. ACE inhibitors increase the permeability selectivity of the filtering membrane, thereby diminishing exposure of the mesangium (supportive cells) to proteinaceous factors that may stimulate mesangial cell proliferation and matrix production, two processes that contribute to expansion of the mesangium in diabetic nephropathy
  3. Because angiotensin-II is a growth factor, reductions in the intrarenal levels of angiotensin-II may further attenuate mesangial cell growth and matrix production
49
Q
  • If you dilate afferent arteriole and constrict efferent arteriole it will_____ GFR.
A

increase

50
Q

nitric oxide, ANP, dopamine can dilate the _____ arterial

A

afferent

51
Q

Angiotensin II is a vasoconstrictor, it will cause constriction in efferent arteriole and at ____(low or high) doses it can cause afferent constriction.

A

high

52
Q

afferent vasoconstriction _____ GFR

A

decrease

53
Q

afferent vasodilation _____ GFR

A

increases

54
Q

efferent vasoconstriction _____ GFR

A

increases

55
Q

efferent vasodilation _____ GFR

A

decreases

56
Q

ACEIs and ARBS cause efferent _____.

A

vasodilation.

this decreases GFR

57
Q

ANP, NE, and low levels of angiotensin II causes efferent _____.

A

vasoconstriction

this increases GFR

58
Q

NSAIDs and high levels of angiotensin II causes afferent _____.

A

vasoconstriction

decreases GFR

59
Q

ANP, Prostaglandins, DA, Kinins, and NO causes afferent ______.

A

vasodilation

increases GFR

60
Q

the use of ANP, Prostaglandins, DA, Kinins, and NO does what to GFR?

A

increases GFR

61
Q

NSAIDs and high levels of angiotensin II does what to GFR?

A

decreases GFR

62
Q

ANP, NE, and low levels of angiotensin II does what to GFR?

A

INCREASES GFR

63
Q

ACEIs and ARBS does what to GFR?

A

decreases GFR

64
Q
  • ACE/ARB will lower efferent arteriole pressure because it ____.
A

dilates

65
Q

Angiotensin II causes constriction of the efferent arteriole. This helps to maintain adequate glomerular filtration when renal perfusion pressure is___.

A

low

66
Q

Negative Renal Effects of ACEIs (2)

A
  1. Angiotensin II causes constriction of the efferent arteriole
  2. Can induce acute renal insufficiency in patients with:
    o bilateral renal artery stenosis
    o Stenosis of the artery to a single remaining kidney
    o Heart failure
    o Volume depletion owing to diarrhea or diuretics
67
Q

when using ACEIs, you should be careful of DDIs with what 2 drugs?

A
  • Potassium-sparing diuretics and potassium supplementation: increase risk of hyperkalemia
  • NSAIDs: decrease hypotensive effects, increase risk for renal impairment
68
Q

Angiotensin-Receptor Blockers (ARBs)

all end in ______.

A

SARTAN

69
Q

out of all the ARBs,_____has more benefits, it’s once a day and is generic

A

Losartan

70
Q

ARBs: MOA

they are Competitive antagonists of the __________receptors

A

angiotensin II

71
Q

ARBs do NOT affect _______ levels so any ACE produced can degrade this vasodilator

A

bradykinin

72
Q

When using ARBs, You don’t get as much bradykinin (like with ACEIs) so you shouldn’t get as much ________. (2 ADRs of ACEIs)

A

cough or angioedema

73
Q

are ARBs therapeutically identical to ACEIs?

A
  • Technically are NOT therapeutically identical to ACEIs
74
Q

ARBs Can be used in patients who cannot tolerate ACEIs (due to cough)- especially in patients with ___ and _____.

A

Heart failure

MI

75
Q

ARBs uses on the cardiovascular system

A

o HTN: first-line option or add-on
o HF: typically used if ACEI not tolerated
o MI: typically used if ACEI not tolerated
o DM Nephropathy: typically used if ACEI not tolerated

76
Q

All ARBs are ___ active

A

orally

77
Q

ARBs require _____ dosing

A

once-daily

78
Q

______ (first in class) is only agent in class with extensive hepatic metabolism

A

Losartan

79
Q

If pt has underlying liver disease, what ARB should be used?

A

Losartan

80
Q

If pt has underlying liver disease then Loasartan might be best option, but it does help with other medical conditions like ___.

A

gout

81
Q

ARBs ADRs are similar toe ACEs except no ____

A

COUGH

82
Q

should you use ARBs in pregnant patients?

A

NO

83
Q

what is the drug name that is a renin inhibitor?

A

Aliskiren (Tekturna)

84
Q

what is Aliskiren (Tekturna) MOA?

A

direct inhibition of renin

85
Q

What is Aliskiren (Tekturna) be used to treat?

A

HTN

-Not first line, typically used after pt has failed an ACE and an ARB

86
Q

when taking Aliskiren, you should Avoid use with ______, unless prescribed by specialist

A

ACEIs and ARBs

87
Q

when taking Aliskiren, what can decrease absorption of the drug?

A

High-fat meal decreases absorption but in general can be taken without regards to meals

88
Q

Aliskiren is Metabolized via ___ system

A

CYP450

89
Q

Aliskiren: ADRs

A
  • Similar to ACEIs and ARBs
  • Diarrhea with higher doses
  • Hyperkalemia (especially with other drugs that can cause this)
  • Cough
  • Angioedema
  • Pregnancy: Category D (as with ACEIs and ARBs)
90
Q

what is Aliskiren BBW?

A

BBW: can cause injury or death to fetus

91
Q

If using ACEI/ARB plus other drug that stresses kidney, risk of ___increases

A

ADR

o Due to decreased efferent pressure
o Examples: NSAIDs, corticosteroids, diuretics
o MONITOR RENAL FUNCTION: BUN/Cr

92
Q

All ARBs, ACEIs, renin inhibitors should be used with caution in patient with
_____.

A

severe renal impairment

Block 4: Pharm (7 decks)

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