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pharmacology exam 2 > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

afterload

A

-resistance in the aorta/ pulmonary artery.
-increased afterload heart works harder to pump blood out.

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2
Q

preload

A

-pressure from venous system into R side heart by great veins.
-too much preload (excess blood in the heart ) decrease CO. heart cant stretch anymore leading to hypertrophy.

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3
Q

hypertrophic cardiomyopathy HCM

A

-most common form of heart failure in CATS
-excess afterload, increase ventricular pressure leads to venticular concentric hypertrophy
-increased systole
-smaller volume in chamber, muscle is thick

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4
Q

Dilated cardiomyopathy DCM

A

-most common form of heart failure in DOGs
-ecentric hypertrophy
-increased diastolic
-certain breeds predisposed (boxers, pinchers)
-cats develop if low taurine diet.

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5
Q

cardiac insufficiency/ failure

A

-due to reduced stroke volume/ cardiac output caused by: reduced preload, impaired contractility, increased afterload, inadequate valve function, abnormal rates.

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6
Q

heart failure symptoms

A

-cardiomegaly (enlargement)
-LV failure: not filling properly or not enough force to generate SV. blood accumulates in lungs, edema.
-RV failure: blood backs up into great veins, leads to brisket edema, ascites, hepatojugular refelx.
-FAILURE ON ONE SIDE LEADS TO FAILURE ON OTHER SIDE.

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7
Q

positive inotrophic agent
Pimobendan

A

-great for heart failure, extends life in dogs with DCM and mitral valve insifficiency.
-phosphodiesterase inhibitor which increases CAMP, Ca++
-positive inotrope (increase contractility) and arterial vasodilator (decreases afterload)
-increases well being and appetite.

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8
Q

positive inotrophic agent
digoxin

A

-digitalis glycosides isolated from foxglove
-inhibits Na/K atpase (sodium pump)
-increases contractility non selectively
-negative chronotrophic and dromotrophic effects decreases HR, increase CO.
-HIGHLY TOXIC
-increases peripheral tissue perfusion

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9
Q

digoxin mechanism of action

A

-acts on conductor cells to decrease chrono and domotrophy, HR, contractility.
-inhibits Na pump which resets ion gradient in cytoplasm.
-increases Na/Ca exchanegr and leads to ore Ca+ released Ca and contraction.

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10
Q

digoxin effects

A

-increased parasympathetic tone and decreased sympathetic tone (baroreceptor)
-ADE: death, anorexia, vomiting, diarrhea, AV block and arrythmias which can be made worse by hypokalemia.
-so using diaretics which decrease K can make even normal dose toxic.
-hyperkalemia blocks digoxin effects.

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11
Q

B blockers in heart failure

A

-end in LOL
-are useful in HCM and DCM due to inhibition of B1 stimulated renin release.
-B1 selective antagonists are prefered. ex metoprolol

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12
Q

vasodialators in Heart failure

A

-ends in pril
-ACE inhibitors
-enalapril, benzapril, imidipril
-prevent Ang II and Ang I formation by inhibiting angiotensin.
-ang I receptor antagonists (ARB’S) (valsartan or telmisaran)

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13
Q

effects of vasodialators ACE inhibitors and AT1 receptor blockers

A

-cause vasodilation-from no angII, reduce venous and arterial pressure and edema.
-prevent aldosterone release and decrease fluid retention and edema
-enalapril extends life 92% in HR
-Ace inhibitors prevent breakdown of bradykins which can lead to tickle cough

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14
Q

vasodialators best use of treatment/ misc

A

-acute treatment or in severe cases.
-ex. nitroglycerin, sodiul nitripusside break down into NO which can decrease pre and afterload.
-all vasodialators may cause hypotension, refelx tachycardia and activation of the RAAS system.
-best for short term decompensated animals

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15
Q

diuretics in heart failure therapy

A

-pulmonary edema is a huge problem as animal cant breath and is uncomfortable
-best treatment for pulmonary edema
-excessive use can lad to loss of venous return so you need to hydrate
-beware of hypokalemia making digoxin more toxic

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16
Q

digoxin

A

-use: heart failure, but mostly atrial fibrilation
-inhibits Na-L atpase and secondarily increases Ca+
-effects: positive ionotrope, negative chrono and domotrophe

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17
Q

dobuatamine

A

-used in acute treatmentof severe HF
-B1 agonist
-positive ionotrope

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18
Q

pimobendan

A

-best HF drug
-phosphodiasterase inhibitor (PDE3) in heart and BV
-positive inotrope, vasodilator

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19
Q

meteprolol

A

-used for hypertrophic cardiomyopathy
-slows HR and relaxes ventricales for better diastolic filling and increased CO
-B1 blocker.

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20
Q

Enalapril, Benazepril, Imidipril

A

-used for HR, hypertension
-inhibits angiotension converting enzyme
-reduced ang II –> vasodialtion and decreased aldosterone

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21
Q

valsatan, telmisatan

A

-AT1 receptor antagonists
-inhibiting actions of ang II
-causes vasodilation and reduces aldosterone release

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22
Q

nitroglycerine, nitroprusside

A

-used for HF
-exogenous sources of nitric oxide
-venodilation and reduced prelaod

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23
Q

prazosin and hydralazine

A

-used for HF and hypertension
-A1 ardenergic receptor agonsits
-arteriole dialaton and reduced afterload

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24
Q

sildenafil

A

-used for pulmonary hypertension
-phosphodiesterase inhibitor prevent cGMP breakdown.
-vasodilation in the lung and penile circulation and pulmonary pressure

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25
Q

supraventricular tachycardia

A

-any change which decreases the time required for depolarization from the maximal diastolic potential and threshold potential. which causes increased automaticity.

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26
Q

premature venticular contractions ventricular tachycardia

A

-afterdepolarzations from abnormal Ca+ influx into cardiac cells or after phase 3 of ventricular AP.

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27
Q

ventricular tachycardia retrograde condution

A

-unidirectional block and retrograde conduction
-ischemic tissue causes decremental conduction and a one way block

28
Q

antiarrythmics class 1 drugs

A

-Quinidine
Procainamide
Lidocaine
-Na channel inhibitor
-decreses Na and prolongs QRS phase reducing HR and cardiomyocyte excitability
-used for ventricular arrythmias mostly tachycardias

29
Q

anti arrythmic drug class II metaprolol, atenolol

A

-B1 ardenergic receptor antagonists
-Negative chronotrope,
dromotrope & inotrope
-used for supraventicular tachycardias where there is excess sympathetic stimulation

30
Q

aminodarone, bretylium, sotalol

A

-class III antiarythmic
-K channel inhibitor
-decreases K current therby prolonging repolarization phase and reducing heart rate
-used for refractory venticular tachycardias

31
Q

verapramin, dilitazem

A

-class IV anti-arrhythmic
-Ca channel inhibitors
-decreases CA current, negative chronotrophe, slows depolarization in pacemaker cells
-used for supraventricular tachycardias

32
Q

actions of different class 1 anti-arrythmics

A

-class 1A: targets all cardiac cells, including ventricular myocytes
-class 1B targets damaged ventricular myocytes
-class 1C targets all cardiac cells with some preference for conduction cells.

33
Q

Sympathetic nervous system

A

-thoracic and lumbar nerves with short preganglionic and long post ganglionic fibers.
-adrenal medulla secretes NE and EPI into blood.
-chain ganglion response is all or nothing

34
Q

Parasympathetic nervous system

A

-crainial and sacral nerves (vagus is major player)
-long pre and short post ganglionic fibers
-targeted discrete activation

35
Q

autonomic nervous system receptors

A

-Ach activates cholinergic receptors which are muscarinic and nicotinic receptors
-Ne and EPI activate ardenergic receptors which are a and B receptors

36
Q

A1 receptor sympathetic stimulation effects

A

-pupillary dilation
-lacrimal secretion
-Blood vessels: constriction, large SNS stimulation leads to B1 activation in heart and causes dilation.
B2 broncocontriction
-Gi tract: decreased motility
-ejaculation, relax detrusor muscle

37
Q

M2 muscarinic receptor parasympathetic stimulation effects

A

-heart: decrease rate acts on SA node only
decreases contractility, conduction.
-increase lacrimal and salivary secretions
-no PNS innervation in arterioles
-GI: increases motility
-erection

38
Q

ANS signal transduction

A

-Beta receptors increase camp
-phophodiesterase breaks down camp to AMP active form which prolongs the secondary messenger
-Alpha 2 recepor and M2 receptors inhibit camp.
-nitric oxide action M3 on vascular endothelium leads to activation of IP3 and Ca release makes NO acts on smooth muscle and cGMP and causes vasorelaxation.

39
Q

drugs which affect ANS neurotransmission by inhibiting release of neurotransmitter

A

-affecting cholinergic neurotransmission = botulinum toxin
-affecting adrenergic neurotransmission =beryllium

40
Q

drugs which affect ANS neurotransmission by increasing release of a neurotransmitter

A

-affecting cholinergic neurotransmission = black widow spider venom
-affecting adrenergic neurotransmission =amphetamine

41
Q

drugs which affect ANS neurotransmission by inhibiting reuptake of a neutotransmitter

A

-affecting adrenergic neurotransmission =cocaine

42
Q

drugs which affect ANS neurotransmission by inhibiting metabolism of neurotransmitter

A

-affecting cholinergic neurotransmission = cholinesterase inhibitors (neostigmine)
-affecting adrenergic neurotransmission =monoamine oxidase inhibitors

43
Q

acetylcholine and carbachol as cholinergic agonists

A

-direct acting agonists
-non selective cholinergic N=M
-effects everything nitotinic + muscarinic
-large PNS effect

44
Q

nicotine as cholinergic agonist

A

-direct acting agonist
-used pharmacolically in insecticides
-nicotinic sensitive N>M
-receptors in skeletal muscle/ ganglion effects SNS, PNS can lead to muscle twitching

45
Q

muscarine, bethanechol, pilocarpine as cholinergic agonists

A

-muscarinic selective
-M>N
-can stop heart with M
-direct agonist

46
Q

indirect acting cholinergic agonists (AChE inhibitors)

A

-non selective cholinergic N=M
-more PNS can lead to toxicity (SLUD)
-irreversible inhibitors cause ACh accumulation: oraganophosphate, insecticides
-reversible: inhibit: edrophonium, neostigmide=will reverse paralysis in skeletal muscle

47
Q

cholinergic antagonists
-atropine/ipratropium

A

-muscarinic selective M»N
-competative agonists for Ach binding at M.
-treat insecticide poisoning and reduces salivation and resp secretions

48
Q

cholinergic antagonists
-hexamethonium/ trimethaphan

A

-Nn blocker (ganglion blocker)
-cuts out baroreceptor reflex
-dont use in consious animal, used for control of hypotension due to low BP

49
Q

epinephrine and norepinephrine receptor selectivity as ardenergic agonists

A

-EPi: activate all receptors a1,a2,b1,b2
-Ne: all but not B2

50
Q

isopreterenol

A

-ardenergic agoist with (B1=B2).»>a receptor affinity.
-used for heart function a cardiac support drug in emergency

51
Q

dopamine

A

-ardernergic agonist D1>B1>B2>a affinity.
-D1 in renal vasculature so dialates kidneys so animal gets blood flow even in shock.
-loses selectivity at high doses.
-B1 can maintain cardiac function in crashing animals

52
Q

dobutamine

A

-adenergic agonist B1>B2>a
-less peripheral vasodialation and pure B1 heart stumulation

53
Q

phenylephrine

A

-adenergic agonist a1>a2>B
-decongestant, vasoconstriction, decrease secretions

54
Q

clonidine/ xylazine

A

-ardenergic agonist a2>a1>B
-decrease SNS leads to sedation

55
Q

beta 2 agonists

A

-terbutaline, clenbuterol, salbutamol
-used for bronchoconstriction, asthma, can lead to tachycardia
-B2>B1>a

56
Q

alpha antagonists

A

-prazosin a1»»a2
-phenoxybenzamine (reversible)
-phentomaline
-tolazine, atipamezole

57
Q

prazosin

A

-competititve alpha agonist
-very selective a1»»>a2
-a1 in arteries and arterioles cause constriction so this antagonizes it and causes vasodialation
-antihypertensive

58
Q

mixed ardenergic antagonits

A

-labentalol, caredilol
-used in heart failure
-B1=B2>a1>a2
-anti arythmic
-a1 receptor will antagonize compensation from heart failure by decrease Hr and vasoconstriction

59
Q

beta antagonists (B blockers)

A

-anti arrythmic
-metoprolol, acebutolol, atenolol B1»>B2
-good for asthma, cardiac or renal
-for non selective agonists if you block B2 you will inhibit SM relaxation which is a problem in asthma attacks.

60
Q

epi vs Ne injection in the cardio system

A

-NE: a1=a2>B1 leads to a1 vascoconstriction and increased peripheral resistance.
-NE leads to reflex bradycardia.
-EPI: all receptors a1=a2, B1=B2.
-EPI: causes vasodilation and central constriction B2.
-in crashing animal EPI is better because NE can increase pulse rate and decrease heart rate too much. EPIs central vasoconstriction leads to decrease pulse rate.

61
Q

atrial flutter

A

-multple P values on ECG,
-a round circut in the heart so it is always excited leads to AV block.
-can treat with digoxin which helps heart work harder and keeps AV node less excitable and decreases the ventricular rate
-monitor blood levels for signs of toxicity

62
Q

hypertrophic cardiomyopathy treatment

A

-dont use positive ionotrophes (digoxin or pimobendan)
-use B blocker and diuretic instead

63
Q

class 1 antiarrythmics mechansms of action and uses

A

-Na channel blockers
-used for ventricular arrythmias and tachycardias

64
Q

class 2 antiarrythmics mechansms of action

A

b1 antagonists, negative chronotroph, domotroph and ionotroph

65
Q

class 3 antiarrythmics mechansms of action and use

A

-K channel inhibitors, decreases K so prolongs repolarization and reducing HR, prolongs the plateau phase.
-refractory ventricular tachycardias

66
Q

class 4 antiarrythmics mechansms of action

A

-Ca channel inhibitors
-decreases Ca so negative chronotrophy slowing spontaneous depolarization in pacemaker cells.
-used supraventricular arrythmias and hypertrophic cardiomyopathy
-acts similar to class II B blockers
-verapamil, ditiazem
-you do not want these acting anywhere other than the pacemakers if it acts in ventricals in cardiomyocytes it will decrease contractility as a negative side effect.
-do not use in DCM but good more HCM

67
Q

RAAS system and what drugs block it

A

-B-ardenergic antagonists: block renin from kidneys
-ACE inhibitors block ang II formation
-Ang II leads to aldosterone release and vasoconstriction so blocking ang II leads to vasodilation and no aldosterone so not retaining water and less edema.

pharmacology exam 2 (2 decks)

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