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Therapeutics P2 > Exam 2 lecture 6 > Flashcards

Exam 2 lecture 6 Flashcards

1
Q

BP formula

A

CO X PR

cardiac output x peripheral resistance

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2
Q

what are two direct effects of NE

A

On heart- Increase HR
on kidney- Renin release (RAAS)

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3
Q

How does renin release affect BP

A

Rennin release can affect BP

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4
Q

what receptors does NE act on in the heart.

A

B-1 receptors

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5
Q

Renin inhibitor stops what step

A

Angiotensinogen to angiotensin I

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6
Q

ACE inhibitor stops what step

A

Angiotensin I to angiotensin II

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7
Q

How does B1 activation affect CO

A

increases it

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8
Q

do RAAS blockers affect BV and SV?

A

yes

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9
Q

why do alpha blockers matter for SV

A

they reduce peripheral resistance

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10
Q

How is renin release activated in the kidney

A

When we have low Na or low BP

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11
Q

Where is ACE released from

A

Lungs

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12
Q

Where is angiotensinogen released from

A

Liver

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13
Q

What does aldosterone secretion do

A

Increase Na retention

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14
Q

How does angiotensinogen affect BP

A

increases it

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15
Q

What is renins substrate

A

angiotensinogen

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16
Q

What is the product for Renin and angiotensinogen

A

angiotensin I

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17
Q

What kind of molecule is Angiotensin I? What is it a substrate for?

A

Angiotensin I is a peptide.
Angiotensin I is a substrate for ACE

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18
Q

What does ACE do to Angiotensin I

A

Converts it to Angiotensin II

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19
Q

What are the two targets for Angiotensin II

A

1) Producing vasoconstriction, increasing BP
2) aldosterone secretion, increasing NA and H20 retention, increasing BP

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20
Q

What do ACE inhibitors target? WHat do ARBs target?

A

ACE inhibitor targets ACE
ARBs target Angiotensin II

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21
Q

ARB acronym. WHat does it block

A

Angiotensin receptor blcoker. Blocks Angiotensin II

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22
Q

Additional action of ACE

A

Works on bradykinin

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23
Q

Is bradykinin active? Is Angiotensin I active

A

ANgiotensin I is inactive and Angiotensin II is actove. ACE inhibitors stop the activation of angiotensin I

Bradykinin is active. ACE cleavs it and makes it inactive. ACE makes it inctive. ACE inhibitors keep t active

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24
Q

Bradykinin use

A

Goes through prostaglandin to cause vasodilation

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25
Q

How does ACE affect bradykinin

A

When ACE deactivates bradykinin, it blocks vasodilation. Causing vasocinstriction and increasing BP.

ACE inhibitors stop this inactivation of bradykinin

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26
Q

What causes and stops angiotensinogen to angiotensin

A

Renin causes it

Renin inhibitors stop it

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27
Q

What causes and stops angiotensin I to angiotensin II

A

ACE causes

ACE inhibitors stop

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28
Q

ACE inhibitor drug names end in

A

-pril

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29
Q

Name some ACE inhibitor drugs

A

Benzapril
Captopril
Enalapril
Lisinopril
Ramipril

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30
Q

What blocks angiotensin II to aldosterone

A

ARB

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31
Q

Name ARB drugs

A

-sartans
Losartan
candesartan
Valsartan
irbesartan

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32
Q

What blocks aldosterone reaching target cell

A

aldosterone antagonist (spironolactone)

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33
Q

What cells release renin

A

Juxtaglomerular cells in kidney

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34
Q

How is angiotensinogen degraded

A

angiotensinogen->angiotensin I->angiotensinII->angiotensin III.

Angiotensin III is the inactive product

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35
Q

name a renin inhibitor drug

A

Aliskiren

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36
Q

Aliskiren MOA

A

It is a renin inhibitor that stops formation of ANG I from angiotensinogen

37
Q

What is a contraindication for all RAAS drugs (renin inhibitors, ACE inhibitors, ARBs)

A

Pregnant and nursing

38
Q

Ace inhibitor drugs all end in

A

-Pril

39
Q

What is the most potent ACE inhibitor

A

Enalapril

40
Q

What is something all ACE inhibitors share in common with each other

A

They are prodrugs (except lisinopril)

41
Q

What are the 3 ACE inhibitor classes

A

Sulfhydryl containing
Dicarboxyl containing
Phosphorous containing

42
Q

Sulfhydryl containing ACE inhibitor prototype

A

Captoptril

43
Q

Dicarboxyl containing ACE inhibitor prototype

A

enalapril

44
Q

Phosphorous containing ACE prototype

A

Fosinopril

45
Q

Most commonly used ACE inhibitor

A

Lisinopril

46
Q

Which ACE inhibitor is not a prodrug

A

Lisinopril

47
Q

What is enalaprils name when active? ROA? Prodrug or not?

A

Enalaprilat

Oral and IV

Prodrug

48
Q

Captoptril pro drug or no? side effects?

A

Not pro drug

may cause rashes

49
Q

How can we tell if an ACE inhibitor is active or a prodrug from a structure

A

If the structure has two carboxylate groups, it is ACTIVE

50
Q

How is enalapril activated? How can we tell the structure apart

A

Esterase cleaves it and activates it.

has ester group and carboxylic acid group

51
Q

How can we differentiate captopril structurally

A

sulfohydryl (HS group)

52
Q

How can we tell fosinopril apart from the other ACe inhibitors

A

Has phosphate group

53
Q

What do ACE inhibitors do

A

Reduce vasoconstriction and reduce myocardial mitogenic actovity

54
Q

1st line tx for HTN

A

ACE and ARB

55
Q

Demographics of who ACE inhibitors and ARBs could benefit most

A

Works least on african american

56
Q

ACE inhibitors side effects

A

Dry cough, Angioedema, hyperkalemia

57
Q

NSAID and ACE inhibitor inhibitor worry

A

NSAIDs may lower effectiveness

58
Q

Why is cough and angioedema a side effect for ACE inhibitors but not ARBS (AT1)

A

Cough and angioedema caused by bradykinin pathway. ARBs do not affect this pathway.

59
Q

how do NSAIDs affect ACE inhibitors

A

NSAIDs block the production of prostaglandins. This lowers the hypotensive effect of ACE

60
Q

ARBs all end with? also known as

A

-SARTANS

AT1 receptor blockers

61
Q

MOA of ARBs

A

Block angiotensin I receptors with a much higher affinity for AT1 versus AT2

62
Q

Are ARBs more selective for AT1 or AT2

A

AT1

63
Q

least potent ARB? most potent ARB?

A

least- losartan
most- candesartan and omesartan

64
Q

Main ARBs

A

Losartan and Valsartan

65
Q

Recognize the ARB scaffold

A

phenyl ring attatched to imidazoline

66
Q

How to differentiate Valsartan and Losartan structurally

A

Valsartan has an Isopropyl group (looks like a V)
Losartan has an OH group (LOHsartan)

67
Q

T/F Even though losartan is the least potent ARB, Losartans metabolite is as potent as valsartan

A

True

68
Q

in what order do we try ACE and ARBs

A

ACE 1st, then ARB

69
Q

Clinical use of ARBs

A

HTN 1st line, use if ACE do not work or are not tolerated

70
Q

Adverse effects of ARBs? COntraindicated in

A

Hyperkalemia

pregnant and nursing women (just like the other RAAS drugs)

71
Q

ARBs and ACEs do not work well in african americans yes or no

A

True

72
Q

Aldosterone MOA and drug bnames

A

Spironolactone and eplerone

MOA
-potassium sparring diuretic

73
Q

adverse effects of spironolactone

A

Hyperkalemia
Gynecomastia

74
Q

1st line drugs for HTN

A

Diuretics (thiazides)
ACE inhibitors
ARBs
CCBs

In no particular order

75
Q

2nd line drugs for HTN

A

Loop diuretics
sympatholytics (B and A blockers)
Direct renin inhibitor

76
Q

Two thiazide drugs

A

Chlorthalidone
Hydrochlorothiazide

77
Q

Where do thiazides work? what transorter does it use?

A

DCT
Uses Na-CL transporter

78
Q

Do thiazides work well in african americans?

A

Good for AFrican americans
Not good for diabetes patients

79
Q

Side effects of Thiazides

A

Hyperkalemia, Hyperuremia, Hypercalcemiia

80
Q

Why are loop diuretics not 1st line?

A

Single doses are potent but very short acting

81
Q

Drugs to avoid in pregnancy

A

ACE inhibitors
ARBs
Direct renin inhibitors
Aldosterone antagonists

82
Q

B blocker end with
Alpha blockers end with
ACE inhibitors end with
Angiotensin II receptors end with

A

B blockers- LOL

Alpha blockers-AZOSIN

ACE inhibitors- PRIL

ARBs- SARTAN

83
Q

renin inhibitor drug name

A

Aliskiren

84
Q

Aldosterone drugs

A

Spironolactone
Epelrone

85
Q

Thiazide drug name

A

Chlorothalidone
Hydrochlorothiazide

86
Q

Alpha 2 agonist drug names

A

Clonidine
Methyldopa

87
Q

Dopamine receptor agonist drug name

A

Fenoldopam

88
Q
A

Therapeutics P2 (41 decks)

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