Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR121 > 3.A-RAAS Inhibitors > Flashcards

3.A-RAAS Inhibitors Flashcards

1
Q

What are the major hormone products of the RAAS?

A

angiotensin II
aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is angiotensin II derived?

A

angiotensinogen–>angiotensin I (via renin)
angiotensin I–>angiotensin II (via ACE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the major actions of angiotensin II?

A

rapid pressor response (vasoconstriction)
slow pressor response (kidney specific effects)
vascular and cardiac hypertrophy and remodelling (effects on heart tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the consequences of low pressure to the kidney?

A

decreased filtration
decreased excretion of toxic substances
decreased tubular pressure–>collapse–>acute renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which cells release renin?

A

juxtaglomerular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 pathways which release renin?

A

intra-renal baroreceptors (low renal pressure)
macula densa (low Na in the loop)
B1 adrenergic receptor pathway (SNS activation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the binding site for renin?

A

angiotensinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where would you find ACE?

A

all over the body on endothelial cell surfaces (angiotensin I to II is automatic in many tissues/organs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the effects of angiotensin II on reno-vascular tissue?

A

vasoconstriction in several tissues
in the kidney it constricts efferent arterioles
-increases glomerular pressure forcing more fluid to be
filtered
-results in rapid increase in GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is aldosterone released?

A

released from adrenal gland following stimulation of the angiotensin-type 1 receptor (AT1) by ANG II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where does aldosterone bind?

A

aldosterone receptors in cells of the distal tubule/collecting tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the actions of aldosterone?

A

reabsorption of Na and excretion of K
-increased activity of ENaCs
-increased synthesis of ENaCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the main mineralocorticoid hormone of the body?

A

aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are ACE inhibitors and where do they act?

A

inhibit ACE activity (ANG I to ANG II conversion)
occurs on endothelial cells throughout circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or false: many ACE inhibitors are prodrugs and are not very potent but have good oral bioavailability

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do all ACE inhibitors end in?

A

-pril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the uses of ACE inhibitors?

A

high blood pressure
-vasodilation and decreased aldosterone secretion

chronic kidney disease
-decreased renal pressure

heart failure and ischemic heart disease
-decreased adverse effects of ANG II and aldosterone on heart
tissue and blood vessels

18
Q

What are some cautions with ACE inhibitors?

A

reduced blood pressure
dry cough (bradykinin accumulation)
risk of hyperkalemia (aldosterone inhibition)
decreased renal perfusion in vulnerable patients

19
Q

What do ARBs stand for?

A

angiotensin receptor blockers

20
Q

Where do ARBs act?

A

inhibit the AT1 receptor (thus blocking actions of ANG II)

21
Q

True or false: the actions of ARBs differ from ACE inhibitors

A

cap
they both block ANG II induced vasoconstriction and aldosterone release (except ARBs have much lower cough due to degradation of bradykinin)

22
Q

What do all ARBs end in?

A

-sartan

23
Q

What are the first line blood pressure agents for people with chronic kidney disease?

A

ACE inhibitors and ARBs

24
Q

What are some of the effects of declined kidney function due to damage?

A

decreased GFR
increased serum creatinine
difficulties excreting fluid and toxins
leakage of proteins

25
Q

How do DRI agents work?

A

bind to the active site of renin to prevent the angiotensinogen to ANG I conversion from happening

26
Q

What is the name of the only DRI available in Canada?

A

aliskiren

27
Q

What do MRAs stand for?

A

mineralocorticoid receptor antagonist

28
Q

How do MRAs work?

A

inhibit the aldosterone receptor

29
Q

What are the names of the MRAs?

A

spironolactone
eplerenone

30
Q

True or false: MRAs are very effective blood pressure agents

A

cap

31
Q

What are the uses for MRAs?

A

resistant hypertension due to aldosterone excess
heart failure (block -ve effects of aldosterone on heart)

32
Q

What are some cautions with MRAs?

A

increased potassium
hormonal effects (partially stimulates progesterone and androgen receptors)

33
Q

What is RAAS?

A

renin-angiotensin-aldosterone system
system that increases blood pressure
RAAS over-activity occurs in many CV conditions

34
Q

What is the major determinant of RAAS activation?

A

renin

35
Q

Where is aldosterone synthesized?

A

synthesized and released from the adrenal gland following stimulation of the AT-1 receptor by ANGII

36
Q

How does aldosterone counteract diuretics?

A

aldosterone promotes the re-absorption of Na while diuretics try inhibit the re-absorption of Na

37
Q

True or false: aldosterone is the only hormone made in the adrenal gland

A

false
the adrenal gland also makes cortisol and dehydroepiandrosterone

38
Q

Aside from ACE, which other enzyme is inhibited by ACE inhibitors?

A

kininase II

39
Q

What does long-standing hypertension increase risk for (in regards to kidney)?

A

chronic kidney disease
-increased pressure can damage glomerulus, damaging filter
function

40
Q

When is ACEI and ARB use considered to be risky?

A

vulnerable people (poor renal blood flow)
-dehydrated
-renal artery stenosis

41
Q

What is a major contraindication for ACEI and ARBs?

A

renal artery stenosis

PHAR121 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions