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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

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2
Q

beta-1 receptor ANTAGONISTS - examples

A

beta blockers:
*metoprolol
*carvedilol

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3
Q

beta-1 receptor - functions

A

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

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

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4
Q

beta-2 receptor - function

A

vasodilation

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5
Q

beta-2 receptor AGONISTS - examples

A

*epinephrine
*albuterol
*isoproterenol

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6
Q

beta-2 receptor ANTAGONISTS - examples

A

beta-blockers:
*carvedilol
*labetalol
*propranolol

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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

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8
Q

alpha-1 receptor - function

A

vasoconstriction

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9
Q

alpha-1 receptor AGONISTS - examples

A

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

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10
Q

SELECTIVE alpha-1 receptor ANTAGONISTS - examples

A

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

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11
Q

non-selective alpha-blockers

A

*phentolamine (reversible)
*phenoxybenzamine (irreversible)

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12
Q

alpha-2 receptor AGONISTS - examples

A

*norepinephrine
*epinephrine
*clonidine

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13
Q

alpha-2 receptor ANTAGONSITS - examples

A

*yohimbine
*phenoxybenzamine

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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

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15
Q

beta-blockers in RAS pharmacology

A

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

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16
Q

aliskiren in RAS pharmacology

A

*direct renin inhibitor
*not used

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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

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18
Q

angiotensin-2 receptor blockers (ARBs) in RAS pharmacology

A

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

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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

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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)

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21
Q

spironolactone (aka eplerenone)

A

*blocks aldosterone

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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

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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
non-dihydropyridine calcium channel blockers (CCBs)
*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
nitroprusside MOA
*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
nitroglycerine MOA
*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
nitrates & sildenafil - drug interaction
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
vasodilator drugs - overview
*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
atropine & effects on acetylcholine
*acetylcholine normally results in endothelium-mediated vasodilation *atropine BLOCKS acetylcholine → VASOCONSTRICTION
31
dopamine - overview
*low levels of dopamine circulate in the bloodstream *dopamine itself is a precursor for norepinephrine & epinephrine *there are several different dopamine receptors
32
low-dose dopamine - pharmacology
*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
high-dose dopamine - pharmacology
*at higher doses, dopamine becomes converted to norepinephrine & epinephrine (might as well just give them NE)
34
methyldopa
*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
fenoldopam - MOA
*D1 receptor agonist *dilates systemic vessels, including renal → decreases systemic vascular resistance (SVR) *helps to diurese (eliminate) excess fluid
36
"pressors" to increase blood pressure
*pressors cause vasoconstriction → increase blood pressure *examples: -epinephrine -norepinephrine -dopamine -phenylephrine -vasopressin
37
epinephrine vs. norepinephrine
*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
dose-related effects of epinephrine
*low doses: mostly beta-2 activation *at increasing doses, starts activating alpha-1 → vasoconstriction at higher doses
39
dose-related effects of norepinephrine
*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
antagonists & multi-receptor pressors
*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
beta-blockers in pheochromocytoma
*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
alpha-blockers in pheochromocytoma
*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
pheochromocytoma & pressors - treatment strategy
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
antagonists vs. agonists: acetylcholine receptor
*agonist: acetylcholine (→ vasodilation) *antagonist: atropine (→ vasoconstriction)
45
antagonists vs. agonists: alpha 1 receptor
*agonists: phenylephrine, epi, NE (→ vasoconstriction) *antagonists: phentolamine, phenoxybenzamine, "-azosins" (→ vasodilation)
46
antagonists vs. agonists: beta-2 receptor
*agonists: epi, isoproterenol (→ vasodilation) *antagonists: carvedilol, labetalol, propranolol (→ vasoconstriction)
47
antagonists vs. agonists: calcium channels
*agonist: calcium (→ vasoconstriction) *antagonists: amlodipine, felodipine, diltiazem, verapamil (→ vasodilation)
48
antagonists vs. agonists: angiotensin-2 receptor
*agonist: angiotensin-2 (→ vasoconstriction) *antagonist: angiotensin-2 receptor blockers (ARBs) [end in "-sartan"] (→ vasodilation)
49
ADEs of sudden discontinuation of clonidine
think excessive sympathetic stimulation: *rebound hypertension *diaphoresis *palpitations *anxiety
50
ADEs of digoxin
*yellowish vision *AV block *increased potassium
51
ADEs of ACE inhibitors
*cough *angioedema *increased potassium (because they limit the ability of the kidney to get rid of K)
52
ADEs of ARBs
*increased potassium (because they limit the ability of the kidney to get rid of K)
53
ADEs of sacubitril
*angioedema
54
ADEs of alpha-1 antagonists
*postural hypotension
55
ADEs of beta-blockers
*fatigue (b/c they prevent the conversion of thyroid hormone)
56
vasodilators & reflexive tachycardia
*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)

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