Autonomic Drug Goals Flashcards

1
Q

where are the cell bodies of parasympathetic neurons located and what are their trajectories

A

Preganglionic cell bodies: craniosacral nuclei

Trajectories: smooth muscle, cardiac muscle and glands

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2
Q

Describe the synthesis, storage, release, and degradation of acetylcholine.

A

synthesis: produced from pyruvic acid in the mitochondria and choline from the choline sodium transporter

stored in the presynaptic neuron vesicles and released via exocytosis into the presynaptic space

Degraded by acetylcholine esterase and recycled back through the choline sodium transporter

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3
Q

subtypes of cholinergic receptors, their anatomical locations, physiological response to ACH, and explain the differences in their signaling mechanisms.

A

M1 (Gq): mediates higher cognitive functions and stimulates the enteric nervous system

M2(Gi): decreases HR and atrial contractility

M3 (Gq): increases exocrine secretions, peristalsis, bronchoconstriction, miosis and increases insulin release (All faucets on)

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4
Q

when do you use direct AChR agonists?

Indirect Agonists?

A

Direct: alleviate neurogenic ileus, increased IP and miosis, produce secretions, bronchial challenge test(methacholine)

Indirect: treatment of myasthenia gravis, postop urinary retention

glaucoma, antidote for atropine, Alzheimer’s

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5
Q

when do you use AChR antagonists?

A

to increase HR/ AV conduction

decrease peristalsis/ secetions ad detrusr tone/ bladder contraction

bronchodilation

mydriasis/ impaired accomodation

decreased eocrine gland secretion

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6
Q

Describe the signs, symptoms, and principles of therapeutics of a patient with anticholinergic toxicity

treatment?

A

dry mouth

flushed skin

thirst

tachycardia

mydriasis

confusion/ agitation

Reverse with Physostigmine

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7
Q

Describe the signs, symptoms, and principles of therapeutics of a patient with excessive cholinergic stimulation

A

All faucets on!!!

similarly seen in organophosphate poisoning

Give Atropine for to block excessive muscarinics and Paralidoxime to regenerate cholinesterases

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8
Q

Compare and contrast the therapeutic uses, mechanism of action, adverse effects, contraindications, and drug interactions of type 5 phosphodiesterase inhibitors and Riociguat

A

MOA of Type5 PDE: increase cGMP to induce smooth muscle relaxation and vasodilation

Sildenafil: smooth muscle relaxation induces erection (Viagra) and pulmonary arterial HTN (Revatio)

Tadalafil: increased cGMP is used to vasodilate pulmonary vasculature in cases of pulmonary arterial HTN (Adcirca) and also improves BPH by increasing smooth muscle relaxation

Riociguat: increased cGMP is used to vasodilate pulmonary vasculature in cases of pulmonary arterial HTN

Avoid use with CYP3A4 inhibitors due to decreased clearance and avoid with Nitro to avoid hypotension an reflex tachycardia

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9
Q

where are the cell bodies of sympathetic neurons located and what are their trajectories

A

origin: thoracolumbar segments
targets: smooth muscle, cardiac muscle, and glands

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10
Q

neurotransmitters released by:

preganglionic sympathetic neurons

postganglionic sympathetic neurons

adrenal medulla.

A

Preganglionic sympathetic neurons: ACh

Postganglionic sympathetic neurons: Norepi in all but sweat glands, which use ACh

Adrenal Medulla: Norepinephrine

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11
Q

synthesis, storage, release, and the termination of action of dopamine, norepinephrine, and epinephrine.

A
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12
Q

autonomic and hormonal control of cardiovascular function and the RAAS system, respectively.

A
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13
Q

anatomical locations of Beta 2 AdR and the physiological response to stimulation

A

Location: smooth muscle, ciliary body of the eye, pancreatic beta cells, skeletal muscle and in the liver

Stimulation: vasodilation, bronchdilation, decreased peripheral vasodilation, increased lipolysis, increased insulin release, increased glycogenolysis, decreased uterine tone, increased aqueous humor production, increased cellular K+ uptake

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14
Q

Anatomical location of Beta 1 AdR and physiologic response to stimulation

A

Location: cardiac muscle and JG apparatus.

Stimulation: Increases, HR, contractility and conduction velocity in the heart and increases renin release in the kidney

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15
Q

Anatomical location of Alpha 1 AdR and physiologic response to stimulation

A

Location: vascular smooth muscle, pupillary dilator muscle of the eye, GI, blader, exocrine glands

Stimulation: increased vasoconstriction/PVR/preload, mydriasis, peristalsis, increased sphincter contraction in the bladder, ejaculation

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16
Q

anatomical locations of Alpha 2 AdR and the physiological response to stimulation

A

Location: blood vessels, eye, pancreatic islet cells, adipose tissue

Stimulation: decreased aqueous humor production, increased platelet aggregation,decreased insulin release, decreased lipolysis

17
Q

Differentiate the second msgrs in alpha 1 ad beta 1 receptors

A

alpha 1= Gq

beta 1= Gs

18
Q

indications and side effects for alpha 1 agonist

A

Indications:

  • orthostatic hypotension/ autonomic insufficiency (Milodrine)
  • Septic/ Neurogenic shock (Norepi)
  • epistaxis/ rhinitis/ rosacea (Oxymetazoline)
  • hypotension, rhinitis, allergic conjunctivitis, open-angle glaucoma, ischemic priapism: phenylephrine

Side effects

HTN, reflex bradycardia, piloerection, urinary retention. schemia / necrosis of distal dgits

19
Q

indications and side effects of Alpha 2 agonists

A

Indications:

  • HTN, ADHD, drug withdrawal: Clonidine
  • HTN in pregnancy: Methyldopa

Side Effects:

CNS suppression, respiratory suppression, bradycardia, hypotension, miosis, rebound HTN, dry mouth

Methyldopa: autoimmune hemolytic anemia and SLE like syndrome

20
Q

indications and side effects of Alpha 1 antagonists

A

Indications:

  • HTN and BPH: Doxazosin, Terazosin
  • BPH and urinary outflow obstruction: Tamsulosin, Alfuzosin, Silodosin
  • HTN and PTSD nightmares: Prazosin
  • Pheochromocytoma: Phenoxybenzamine, Phentolamine

Side Effects:

  • peripheral edema, orthostatic hypotension, retrograde ejaculation, urinary frequency, intraoperative floppy iris syndrome
  • nonselective antagonists: reflex tachycardia and vasodilation
21
Q

indications and side effects of Beta 1 agonists

A

Indications:

  • heart failure, shock, unstable bradycardia: Dobutamine
  • bradycardia/ heart block, cardiac arrest from heart block when pacemaker therapy is unavailable: Isoproterenol

Side Effects:

Tachycardia, arrhythmias, can precipitate MI with CAD

22
Q

indications and side effects of Beta 1 antagonists

A

Indications:

  • CAD, compensated heart failure, ACS, Cardiac arrhythmias,

Side Effects:

bradycardia, bradyarrhythmia, torsades de pointes, worsened heart failure, orthostatic hypotension, CNS depression, hallucinations, high triglycerides, psoriasis

23
Q

indications and side effects of Nonelective Beta 2 antagonists

A

Indications:

  • an alternative to cardioselective beta blockers

Side Effects:

bronchoconstriction, erectile dysfunction, secondary Raynaud phenomenon, hyperglycemia in new-onset diabetes, weight gain, vasoconstriction in patients with PVD