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Cardio > ANS Drugs > Flashcards

ANS Drugs Flashcards

1
Q

Transmitters released at ANS synapses

A

Acetylcholine
Norepinephrine
Dopamine

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2
Q

Which ANS synapses release acetylcholine

A

All preganglionic neurons
All parasympathetic postganglionic neurons
A few sympathetic postganglionic neurons

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3
Q

Which ANS synapses release NE

A

Most sympathetic neurons

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4
Q

Which ANS synpases release dopamine

A

Sympathetic fibers that innervate the renal vasculature and some other vessel beds

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5
Q

What is the predominant tone of the heart?

A

Parasympathetic

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6
Q

Different types of nicotinic receptor?

A

Neuronal – the one at the ans ganglia

Muscular – the one at the NMJ

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7
Q

Different types of muscarinic receptor

A

M2 M4 are coupled to Gi and Go

M1, 3, 5 are coupled to Gq
These activate PLC, which cleave DAG and IP3, which cause Ca release and stimulate PKC

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8
Q

A1 receptor cascade

A

Coupled to Gq. Elevate intracellular Ca 2 and stimulate protein kinase C. Contract smooth muscles. Also cause miosis.

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9
Q

Where do B1 receptors predominate

A

In the heart and in JG cells

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10
Q

Where do B2 receptors predominate?

A

In the vasculature, in bronchial smooth muscle.

Mediate vasodilation and bronchodilation

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11
Q

Where are Dopamine receptors

A

Prominent on the renal vasculature and mediate vascodilation

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12
Q

How is EPI/NE released from adrenals?

A

Behaves with a sympathetic ganglion. ACh released to adrenals, Adrenals release NE and EPI.

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13
Q

Baroreceptor reflex

A

Baroreceptors sense decrease/increase in BP, change heart rate to match .

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14
Q

Sympathetic activity effect on the vasculature

A

Net increase in total peripheral resistance, decrease in venous capacitance.

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15
Q

Where do beta receptors predominate in the vasculature.

A

Coronaries and skeletal muscles (where needed during sympathetic outflow).

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16
Q

Why is renal function preserved in flight/flight?

A

Because DA released in sympathetic outflow on renal vasculature causes vasodilation

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17
Q

Effects of sympathetic activity on the heart

A

Mediated by B1 receptors in ventricles and B2 receptors in the atria/sa node. Positive chronotropy, positive inotropy, positive lusitrophy

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18
Q

How does B stimulation increase chronotropy

A

Increases cAMP, which increases activity of funny current. Drives to threshold quicker

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19
Q

What is the channel that opposes the funny current?

A

GIRK.

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20
Q

How does B stimulation increase AV nodal propagation?

A

Because cAMP activates PKA, which phosphorylates L-type Ca channels, causing them to open and allow more Ca out. More rapid action potential and faster propagation.

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21
Q

How does B stimulation increase inotropy and lusitropy?

A

P the phospholamban. Higher ca in er. More available for release, pushed out of cell quickly.

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22
Q

Epinephrine acts on… and causes…

A

B1, B2, B3, A1, A2 agonist
At high doses causes vasoconstriction (increases mean BP) and increases HR. Direct effects predominate over reflex

At low doses, diastolic BP is decreased because it is more potent at B2 than A1.

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23
Q

Epinephrine at low doses

A

Decreases diastolic BP because epinephrine has great activity at B2 relative to A2. So will dilate.. ya know?

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24
Q

Uses for epi

A

Cardiac arrest, inotropic support.

Acute asthma, analphylaxis.

Prolong action of local anesthetic because causes vasoconstriciton at high doses

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25
Q

NE

A

A1, A2, B1
(no activity at B2)

Increases BP more than Epi.

DECREASES heart rate due to strong pressor effect.

Inotropic effect is still intact.

26
Q

Uses of NE

A

Cardiogenic shock

Septic/hypovolemic shock

27
Q

Adverse effects of NE

A

Severe hypertension, reduced renal flow.

Necrosis and tissue sloughing after IV injection due to extravasation of the drug (look for blanching)!

28
Q

Isoproterenol

A

B1, B2, B3 agonist.

Potent vasodilator (B2).

Increases HR substantially reflex is in same direction as direct, inotropy. Decreases both diastolic and MAP.
Decreases or slightly increases systolic pressure.

29
Q

Uses of isoproterenol

A

Treatment of bradycardia in heart transplant patients.

Can treat some arrhythmias (torsades)

30
Q

Adverse effects of isoproterenol

A

Palpitations, tachycardia, cardiac ischemia, flushing

31
Q

Dobutamine

A

Selective B1 agonist
Structurally resembles dopamine but has little activity at DA receptors.

Inotropy, chronotropy, but ino bigger because B2 dominate at SA.

32
Q

Dobutamine uses

A

Cardiac decompensation after CHF or cardiac surgery. Can cause ventricular ectopic activity.

33
Q

Dopamine

Low dose
intermediate dose
high dose

A

Direct agonist at D1>B2>A

Low Dose; Renal dose activates only D1 receptors. Increase renal blood flow and urine output. Can cause hypotension

Intermediate dose: activates D1 and B1 receptors
Increased renal blood flow, heart rate, cardiac contractility, and CO. Generally no change in TPR. Can cause hypotension

High dose: activates all receptors. Causes vasoconstriction and increased BP.

34
Q

Dopamine uses

A

Treatment of cardiogenic shock especially in oliguric patients.

35
Q

Fenoldopam and use

A

D1 agonist. Dilates peripheral vessles and increases natriuresis. Used to treat severe hypertension and in patients with renal compromise.

36
Q

When NOT to use fenoldopam?

A

In patients with glaucoma.

37
Q

Albuterol

A

Selective B2 agonist.

Used as a bronchodilator for asthma and other pulmonary disease.

Works by increasing cAMP in bronchial smooth muscles which causes relaxation and stabilization of mast cells.

38
Q

Phenylephrine

A

Alpha agonist, only slight affinity for a1. Causes vasoconstriction.

Can be used for hypotension, but much more commonly is used as a decongestant

39
Q

Clonidine

A

Selective A2 agonist.

Decreases sympathetic outflow from the CNS.

Used in management of HTN and hypertensive crisis.

Drowsiness, fatigue, xerostomia

40
Q

Tyramine

A

Not clinically used, but a byproduct of tyrosine metabolism, which is degraded by MAO-A>MAO-B

Evokes release of NE from adrenergic nerves.

Can cause hypertensive crisis.

41
Q

Black Box warning for Beta blockers

A

Abrupt withdrawal from beta blockers can cause angina/MI due to upregulation of receptors. If taken off beta blockers too quickly, heart will be hyperactive and need lots of O2.

42
Q

Who should avoid B blockers

A

Asthmatics (due to possibility of B2 blockade -> bronchospasm)

Also, diabetes patients. Beta blockers can induce hypoglycemia and prevent diabetics from feeling the symptoms of hypoglycemia.

43
Q

Propranolol

A

Non selective B antagonist

Used for angina/svt and vt/pvc/htn/mi/pheochromocytoma

44
Q

Metoprolol

A

Selective B1 antagonist, but can block B2 receptors at the doses used for treating angina.

Used for stable angina/chf/hypertension

45
Q

Pindolol

A

Partial agonist at B1, B2 receptors.
So this has ISA (intrinsic sympathomimetic activity). In the absence of normal agonist, it is an agonist. Acts as a beta antagonist when sympathetic drive is high.

Stimulation in a limited range.

Used for HTN and angina.

NO blackbox warning.

46
Q

Labetalol

A

B1 and A1 antagonist.

Partial agonist at B2 (intrinsic sympathomimetic activity).

Used in hypertensive emergency, especially due to excessive sympathetic activity. Tyramine crisis, pheocromocytoma, methamphetamine.

47
Q

Carvedilol

A

Antagonist at B1 and B2 receptors. But also some A1 receptor blockade, so has vasodilatory effect.

Inhibits cardiac remodeling in CHF. Less effect on glucose metablolism than others.

48
Q

Phentolamine

A

Alpha antagonist with similar activity at A1 and A2.

Causes hypotension, but used to treat hypertensive emergency due to sympathetic overactivity.

49
Q

Parasympathetic effects on the vasculature

A

Vagal activity does not affect vascular tone because they’re not parasympathetically innervated. However. Muscarinic receptors on endothelium causing NO induced vasodilation.

50
Q

Parasympathetic effects on heart

A

Isolated in atria.

51
Q

How does vagal tone decrease chronotropy?

A

Muscarinic receptors on SA node increases current through Girk channels (hyperpolarizing). Funny current intact but more time needed to drive Vm to spike threshold.

52
Q

How does vagal tone decrease lusitropy

A

Reduces cAMP dependent phosphorylation of L-types in AV node causing reduced Ca flow out, makes it slower.

53
Q

Parasympathetic effects on the body

A

Bronchoconstriction, increased secretions, increased GI motility, relaxation of sphincters, contraction of bladder wall, miosis, near vision, miosis, near vision.

54
Q

Acetylcholine

A

Full agonist at MAchR and NAChR.

Degraded very quickly by plasmacholinesterases

55
Q

Bethanecol

A

Muscarinic agonist. Negligible nicotinic activity.

Long duration of action.

Used for urinary retention, neurogenic bladder.

Contraindicated in asthma

56
Q

Nicotine

A

Agonist at nicotinic receptors.

Activates ganglia (both parasympathetic and sympathetic outflow, so produces dominant tone).

Increases BP, Increases HR (due to epi release)

57
Q

Neostigmine/Physostigmine

A

Anticholinesterases. Prevent degrading of ACh in synapse. Used in myesthenia gravis, and atropine poisoning.

Neostigmine can’t cross BBB.

58
Q

Anticholinesterase poisoning (organophosphates)

A

Sludge and the killer B’s

Bronchorrhea, bronchospasm, bradycardia

59
Q

Atropine and scopolamine.

A

Muscarinic antagonists

Hot as a hair, mad as a hatter, dry as a bone.

Used for AV block and for bradycardias.

60
Q

Ipratropium

A

Muscarinic antagonist, inhalation only. Confined to mouth and airways due to quaternary amine. Used to combat acute asthma exacerbation. Also fights bronchospasm associated with COPD.

61
Q

Ganglionic blockers

A

Not used clinically but antagonists of Nn receptors. Functionally denervate targets, so organ specific effects that are opposite to the predominant tone.

Hr increases, BP declines, GI stops moving.

Cardio (23 decks)

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