Brainscape's Knowledge GenomeTM

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


See full index

Cardio exam 1 > CCB lecture > Flashcards

CCB lecture Flashcards

1
Q

Ca key role in physiological processes

A

contractility of skeletal, cardiac & smooth muscles

- release of NT from vesicles by exocytosis

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

at resting state, intracellular Ca is

A

low (<0.1micrometers)

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

at resting state, extracellular Ca is

A

10,000 fold higher (~1mM)

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

[Ca] achieved by

A
  • active efflux pumps

- active reuptake into SR

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

mechanisms mediating increase in intracellular Ca

A
  • voltage sensitive Ca channels
  • agonist-mediated Ca release
  • receptor-operated Ca channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

voltage-sensitive Ca channels

A
  • open in response to depolarization of the cell membrane (L-type, T-type, N-type)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

L-type

A

long-lasting large channels (cardiac & smooth muscle cell, SA & AV nodal cells)

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

T-type

A

transient tiny channels

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

N-type

A

neuronal tissue

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

agonist mediated Ca release

A

results from activation of 2nd messengers (IP3) by agonist to release intracellular Ca from storage sites (SR)

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

receptor-operated Ca channels

A

receptor forms a channel & the channel opens when the receptor is occupied by a ligand (NMDA receptor)

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

what initiates contraction of vascular smooth muscle cells?

A

entry of Ca into SMC

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

what initiate contraction of cardiac myocytes?

A

entry of Ca into myocardial cells

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

CCBs inhibit

A

L-type Ca channels-> decreased influx of Ca->

  • < SMC contraction->vasodilation (blood flow)
    • ionotropic effec-> < O2 demand
  • < pacemaker rate of SA node & conduction velocity of AV node-> - chronotropic effect-> < O2 demand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DHP access what channel?

A

CLOSED channel & stabilize it

- mainly act on arterial muscle cells-> VASODILATION

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

non-DHP binds to the

A

OPEN channel & inactivate it & slow down the recovery

-more pronounced effects in the heart

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

“cardio-selective” drugs

A

non-DHP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

“vascular-selective” drugs

A

DHP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

therapeutic uses for CCBs

A

HTN
Angina pectoris
superventricular arrhythmia
migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

main adverse effects of verapamil & diltiazem

A

(non-DHP: Cardio-selective)

  • cardiodepression
  • hypotension, AV node blackade, peripheral edema, elevation of liver enzymes’- HA, flushing, dizziness, constipation
  • caution: inhibition oF CYP3a4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

main adverse effects of amlodipine

A

(DHP: not cardio-selective)

  • edema, dizziness, flushing, palpitation, gingival hyperplasia
  • cardio, CNS, GI side effection
  • long term use may > breast cancer risk
  • caution combining w/ CYP3A4 inhibitors-> hypotenion, kidney failure
22
Q

alpha 1 adrenergic receptor blocker MOA

A

blockage of alpha 1 adrenoreceptors in arteries & veins

- probably blockade of central alpha 1 receptors

23
Q

main ADE of alpha 1 blockers

A

first-dose effect: postural/orthostatic hypotension (alpha 1 receptors in veins)

24
Q

activation of alpha 1 receptors leads to

A

constriction

25
Q

alpha 1 blocker drugs

A

doxazosin
terazosin
prazosin

26
Q

central alpha 2 adrenoreceptor agonist MOA

A
  • activation of central alpha 2 receptors(CV control centers)-> suppression of sympathetic outflow from the brain
  • possible stimulation of presynaptic alpha2-> dec. NE release
  • clonidine: possible interaction with central imidazoline receptors
27
Q

central alpha 2 agonist drugs

A

clonidine
guanfacine
guanebenz
methyldopa

28
Q

clonidine bioavailability

A

100%

- 50% is eliminated in urine unchanged- caution in renal failure

29
Q

clonidine main therapeutic effects

A
  • < BP (central effect)
  • < HR (< sympathetic drive & > vagal tone)
  • < intraocular pressure (used in glaucoma)
30
Q

main adverse effect of clonidine

A
  • sedation & dry mouth
  • sexual dysfunction (due to hyperprolactinemia)
  • bradycardia
  • withdrawal rxn w/ abrupt DC
31
Q

guanfacine (tenex) elimination

A

50% eliminated unchanged in urine

32
Q

guanebenz (wytensin) metabolism

A

100% metabolized in liver

33
Q

methyldopa is similar in structure to

A

tyrosine

34
Q

tyrosine is a precursor for

A

epi & NE

35
Q

what central alpha 2 agonist is a prodrug?

A

methyldopa

36
Q

methyldopa can also be beneficial in

A

preeclampsia

37
Q

peak effect of methyldopa

A

delayed 6-8 hours

duration ~24hrs

38
Q

ADE of methyldopa

A

similar to clonidine + hepatotoxicity & hemolytic anemia

39
Q

methyldopa MOA

A
  • stored in secretory vesicles of adrenergic neurons, substituting NE
  • released into synaptic cleft instead of NE
  • effects similar to clonidine
40
Q

methyldopa needs to be _____ to act

A

transported into CNS

41
Q

what kind of drug is reserpine?

A

sympatholytic

42
Q

what is the first drug that was found to interdere with the function of SNS in humans? (start of antihypertensive therapy)

A

reserpine

43
Q

resperine MOA

A
  • IRREVERSIBLY binds to the vesicular transporter

- BP lowering effects due to both central & peripheral actions

44
Q

reserpine ADE

A
  • > retention of Na & water
  • sedation & inability to concentrate
  • depression & suicidal thoughts
  • caution: should be DC at first sign of depression
45
Q

what kind of drug is hydralazine (apresoline)?

A

direct vasodilation

46
Q

hydralazine MOA

A

direct vasodilation

47
Q

main therapeutics effects of hydralazine

A
  • effective decrease in peripheral resistance (powerful stimulation of SNS->usually combined w/ other drugs)
  • minimal effect on veins-> no postural hypotension
48
Q

Main ADE of hydralazine

A
  • drug induced lupus
  • > retension of Na & H2O
  • HA, flushing, hypotension, tachycardia, angina pectoria
  • caution: aggravation of myocardial ischemia
49
Q

what kind of drug is minocidil (Loniten)?

A

direct vasodilator

50
Q

MOA of minoxidil

A
  • prodrug that needs to be converted to minoxidil sulfate
  • activates ATP-dependent K+ channels in smooth muscles->efflux of K+ from cells-> hyperpolarization-> relaxation of smooth muscle
51
Q

main therapeutic effects of minoxidil

A

dilation of arterioles similar to hydralazine-> decreased PR (powerful SNS stimulation- usually combined w/ other drugs)

52
Q

main ADE of minoxidil

A
  • > retention of Na and water
  • tachycardia, angina pectoris, myocardial ischemia
  • hypertrichosis (hair growth)

Cardio exam 1 (12 decks)

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