Brainscape's Knowledge GenomeTM

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


See full index

Cardiology Exam > Vascular Physiology 4 > Flashcards

Vascular Physiology 4 Flashcards

1
Q

beta-1 receptor AGONISTS - examples

A

*epinephrine
*norepinephrine
*isoproterenol
*dopamine
*dobutamine

*phosphodiesterase inhibitors (MOA: inhibition of breakdown of cAMP by blocking phosphodiesterase → cAMP sticks around longer)
-ex: milrinone

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

beta-1 receptor ANTAGONISTS - examples

A

beta blockers:
*metoprolol
*carvedilol

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

beta-1 receptor - functions

A

*increases heart rate (chronotropy)
*increases contractility (inotropy)

note: there are NO beta-1 receptors in blood vessels

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

beta-2 receptor - function

A

vasodilation

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

beta-2 receptor AGONISTS - examples

A

*epinephrine
*albuterol
*isoproterenol

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

beta-2 receptor ANTAGONISTS - examples

A

beta-blockers:
*carvedilol
*labetalol
*propranolol

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

beta-blockers - overview & naming conventions

A

*can help to SLOW DOWN heart rate
*usually end in “-lol”:
-if name starts with A-M, selective for Beta-1
-if name starts with N-Z, non-selective (blocks Beta-1 and 2)

EXCEPTIONS:
*carvedilol and labetalol are non-selective beta-blockers which also block alpha-receptors
*pindolol and acebutolol increase sympathetic activity

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

alpha-1 receptor - function

A

vasoconstriction

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

alpha-1 receptor AGONISTS - examples

A

*epinephrine
*norepinephrine
*phenylephrine (alpha-1 only)

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

SELECTIVE alpha-1 receptor ANTAGONISTS - examples

A

*end in “-zosin”:
-prazosin
-terazosin
-doxazosin

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

non-selective alpha-blockers

A

*phentolamine (reversible)
*phenoxybenzamine (irreversible)

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

alpha-2 receptor AGONISTS - examples

A

*norepinephrine
*epinephrine
*clonidine

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

alpha-2 receptor ANTAGONSITS - examples

A

*yohimbine
*phenoxybenzamine

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

alpha-2 receptor - functions

A

*when activated, alpha-2 receptors INHIBIT NEUROTRANSMITTER RELEASE (esp. norepinephrine) from presynaptic neurons
*alpha-2 is a feedback receptor

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

beta-blockers in RAS pharmacology

A

*decrease renin release due to SNS stimulation (blocks NE)

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

aliskiren in RAS pharmacology

A

*direct renin inhibitor
*not used

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

ACE inhibitors in RAS pharmacology

A

*end in “-pril (lisinopril, captopril)
*INHIBIT angiotensin-converting enzyme (ACE) → inhibiting production of angiotensin 2 (a vasoconstrictor) → taking away a vasoconstrictor
*INCREASES BRADYKININ (potentiating the effect of a vasodilator)

note - some people develop a cough with ACE inhibitors; some develop angioedema

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

angiotensin-2 receptor blockers (ARBs) in RAS pharmacology

A

*end in “sartan” (losartan, etc)
*only block AT1

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

effects of BNP (nesiritide) as pharmacology

A

*renal: get rid of sodium & fluid through urine; inhibits renin release
*adrenal: inhibits aldosterone release
*heart: prevents maladaptive hypertrophy
*blood vessels: relaxes both arterial and venous tone
*DECREASES PRELOAD & AFTERLOAD

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

sacubitril - MOA

A

*neprilysn is an enzyme that breaks down BNP and ANP
*sacubitril INHIBITRS NEPRILYSN → BNP and ANP stay around much longer (potentiates the effects of BNP and ANP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

spironolactone (aka eplerenone)

A

*blocks aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

calcium channel blockers - MOA

A

*prevent influx of calcium into vascular smooth muscle → less calcium available to facilitate actin-myosin crosslinks → PREVENTS VASOCONSTRICTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

minodoxidil - MOA

A

*opens potassium channels → potassium leaves the cell → hyperpolarization of cell → more DIFFICULT TO OPEN VOLTAGE-GATED CALCIUM CHANNEL → PREVENTS VASOCONSTRICTION

24
Q

dihydropyridine calcium channel blockers (CCBs)

A

*end in “-dipine”
*block calcium channels in VASCULAR SMOOTH MUSCLE
*examples: felodipine, amlodipine

25
Q

non-dihydropyridine calcium channel blockers (CCBs)

A

*block calcium channels in HEART & BLOOD VESSELS (and everywhere else)
*great at slowing heart rate, but may decrease calcium influx → decrease inotropy
*examples: verapamil, diltiazem

26
Q

nitroprusside MOA

A

*nitroprusside is a powerful arterial & venous DILATOR
*decreases afterload and preload
*SPONTANEOUSLY DEGRADE to give off NITRIC OXIDE → increased cGMP → relaxation
*also gives off CYANIDE, which goes to liver and gets converted to thiocyanate, which is secreted in the urine

27
Q

nitroglycerine MOA

A

*nitroglycerin (and isosorbide) are a powerful VENOUS DILATOR with some arterial dilation at higher doses
*significantly decreases PRELOAD
*requires enzymatic conversion with ALDEHYDE DEHYDROGENASE → nitric oxide → increased cGMP → relaxation

28
Q

nitrates & sildenafil - drug interaction

A

nitrates & sildenafil do NOT mix:

*nitroglycerin increases cGMP
*sildenafil blocks phosphodiesterase (cGMP is normally broken down by phosphodiesterase)
*giving nitroglycerin to someone who has taken sildenafil in the past 1-2 days → increased cGMP with inability to break it down → may lead to life threatening HYPOTENSION/very low vascular tone

29
Q

vasodilator drugs - overview

A

*venodilators: nitrates [decrease PRELOAD]

*mixed vasodilators: nitroprusside, ACE inhibitors/ARBs, alpha-receptor blockers, alpha-2 agonist, sacubitril, nesiritide

*arterial dilators: hydralazine, minoxidil, calcium channel blockers [decrease AFTERLOAD]

30
Q

atropine & effects on acetylcholine

A

*acetylcholine normally results in endothelium-mediated vasodilation
*atropine BLOCKS acetylcholine → VASOCONSTRICTION

31
Q

dopamine - overview

A

*low levels of dopamine circulate in the bloodstream
*dopamine itself is a precursor for norepinephrine & epinephrine
*there are several different dopamine receptors

32
Q

low-dose dopamine - pharmacology

A

*at low doses, dopamine activates D-receptors:
-at D1 in renal arteries → renal artery dilation (may help eliminate extra fluids)
-D receptors in the heart → increased contractility & elevated heart rat

33
Q

high-dose dopamine - pharmacology

A

*at higher doses, dopamine becomes converted to norepinephrine & epinephrine (might as well just give them NE)

34
Q

methyldopa

A

*safest medication to lower blood pressure during pregnancy
*acts in 2 ways:
1) inhibits DOPA decarboxylase → prevents synthesis of dopamine, NE, and epi
2) gets converted to alpha-methyl-norepinephrine → activates alpha-2 receptor → prevents NE release

35
Q

fenoldopam - MOA

A

*D1 receptor agonist
*dilates systemic vessels, including renal → decreases systemic vascular resistance (SVR)
*helps to diurese (eliminate) excess fluid

36
Q

“pressors” to increase blood pressure

A

*pressors cause vasoconstriction → increase blood pressure
*examples:
-epinephrine
-norepinephrine
-dopamine
-phenylephrine
-vasopressin

37
Q

epinephrine vs. norepinephrine

A

*epi: beta1 & beta 2 > alpha1 (boards love you to know that epi binds to beta2)

*NE: alpha1 = beta1 (boards love you to know that NE binds to alpha 2)

38
Q

dose-related effects of epinephrine

A

*low doses: mostly beta-2 activation
*at increasing doses, starts activating alpha-1 → vasoconstriction at higher doses

39
Q

dose-related effects of norepinephrine

A

*NE initially binds to alpha-2 → decreased endogenous NE and epi → decreased HR
*after time, NE starts activating alpha-2
*NE causes increased SYSTOLIC & DIASTOLIC BP

40
Q

antagonists & multi-receptor pressors

A

*when many different receptors are available, the pressors bind to the ones available based on their affinity for it
*when an ANTAGONIST (ex. beta blocker, alpha blocker) blocks certain receptors, it forces the pressors to bind to the ones that are available:
-when a BETA-BLOCKER is given, all the available epi/NE bind to alpha-1 receptors → vasoconstriction & increased BP
-when an ALPHA-BLOCKER is given, all the available epi/NE bind to beta receptors → decreased BP

41
Q

beta-blockers in pheochromocytoma

A

*when giving a beta-blocker to someone with an epinephrine-secreting tumor (pheochromocytoma) → excess epi/NE activate alpha-1 → unopposed alpha vasoconstriction → severe hypertension

42
Q

alpha-blockers in pheochromocytoma

A

*when giving an alpha-blocker to someone with an epinephrine-secreting tumor (pheochromocytoma) → excess epi/NE activate beta-2 → DECREASED BP, EVEN LOWER THAN WHAT IT WOULD NORMALLY BE

43
Q

pheochromocytoma & pressors - treatment strategy

A

1) give phenoxybenzamine FIRST to block alpha-receptors (irreversibly)
2) next, give non-selective beta blockers right before surgery

*these measures prevent hypertensive crisis during the operation from epinephrine release when the surgeon has to touch the tumor

44
Q

antagonists vs. agonists: acetylcholine receptor

A

*agonist: acetylcholine (→ vasodilation)

*antagonist: atropine (→ vasoconstriction)

45
Q

antagonists vs. agonists: alpha 1 receptor

A

*agonists: phenylephrine, epi, NE (→ vasoconstriction)

*antagonists: phentolamine, phenoxybenzamine, “-azosins” (→ vasodilation)

46
Q

antagonists vs. agonists: beta-2 receptor

A

*agonists: epi, isoproterenol (→ vasodilation)

*antagonists: carvedilol, labetalol, propranolol (→ vasoconstriction)

47
Q

antagonists vs. agonists: calcium channels

A

*agonist: calcium (→ vasoconstriction)

*antagonists: amlodipine, felodipine, diltiazem, verapamil (→ vasodilation)

48
Q

antagonists vs. agonists: angiotensin-2 receptor

A

*agonist: angiotensin-2 (→ vasoconstriction)

*antagonist: angiotensin-2 receptor blockers (ARBs) [end in “-sartan”] (→ vasodilation)

49
Q

ADEs of sudden discontinuation of clonidine

A

think excessive sympathetic stimulation:
*rebound hypertension
*diaphoresis
*palpitations
*anxiety

50
Q

ADEs of digoxin

A

*yellowish vision
*AV block
*increased potassium

51
Q

ADEs of ACE inhibitors

A

*cough
*angioedema
*increased potassium (because they limit the ability of the kidney to get rid of K)

52
Q

ADEs of ARBs

A

*increased potassium (because they limit the ability of the kidney to get rid of K)

53
Q

ADEs of sacubitril

A

*angioedema

54
Q

ADEs of alpha-1 antagonists

A

*postural hypotension

55
Q

ADEs of beta-blockers

A

*fatigue (b/c they prevent the conversion of thyroid hormone)

56
Q

vasodilators & reflexive tachycardia

A

*when we give a medication (vasodilator) which drops our systemic vascular resistance (SVR), then our body responds by increasing cardiac output via INCREASED HEART RATE (tachycardia)

Cardiology Exam (52 decks)

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