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Pharmacology > Autonomic Drugs > Flashcards

Autonomic Drugs Flashcards

1
Q

What is the general function of cholinomimetic agents and what are potential side effects?

A

Cholinomimetic agents increase cholinergic outflow-> “Wet picture” Parasympathetic: miosis, diarrhea, urination, bronchospasm, lacrimation; Sympathetic: sweating *Can exacerbate COPD, asthma and peptic ulcers (M3 increases bronchoconstriction and gastric acid release)

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2
Q

Which drugs are direct cholinomimetic agonists?

A

Bethanechol, carbachol, methacholine, pilocarpine

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3
Q

Bethanechol - what is the mechanism and action? clinical applications?

A

Direct cholinomimetic agonist Activates bowel and bladder smooth muscle -> increases urination and defication “Bethany, call (bethanechol) me to activate your bowels and bladder.” Uses: postoperative ileus, neurogenic ileus, urinary retention

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4
Q

Carbachol- what is the mechanism and action? clinical applications?

A

Direct cholinomimetic agonist Contricts pupil and relieves intraocular pressure in glaucoma

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5
Q

Methacholine - what is the mechanism and action? clinical applications?

A

Direct cholinomimetic agonist Stimulates muscarinic receptors (M3) in airway when inhaled -> used as challenge test for diagnosis of asthma (exacerbates asthma)

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6
Q

Pilocarpine - what is the mechanism and action? clinical applications?

A

Direct cholinomimetic agonist

Action: Contracts ciliary muscle (open-angle glaucoma), contracts pupillary sphincter (closed-angle glaucoma); resistant to AChE.

Uses: Potent stimulator of sweat, tears and saliva. Open-angle and closed-angle glaucoma

“You cry, drool, and sweat on your pillow”

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7
Q

What is the mechanism for indrect cholinomimetic agonists?

A

Inhibit cholinesterase -> increase synaptic levels of ACh

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8
Q

Which anticholinesterases are used for Alzheimer’s disease? What is the mechanism?

A

Donepezil, galantamine, rivastigmine

Improve cognition and behavior by compensating for decreased ACh from neuronal death. *Does NOT alter progression of disease, only addresses symptoms

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9
Q

Edorphonium - what is the mechanism and clinical use?

A

Indirect cholinomimetic agnoist - anticholinesterase -> increases ACh

Historically used to diagnose myasthenia gravis (very short acting), would relieve MG symptoms for short period of time by increasing ACh

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10
Q

Neostigmine - what is the drug class? what are the clinical uses?

A

-stigmine: anticholinesterase, indirect agonist of ACh

Uses: postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of NMjunction blockade (post-op)

*Does not cross BBB b/c charged*

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11
Q

Physostigmine - drug class? clinical uses?

A

-stigmine: anticholinesterase (indirect ACh agonist)

Used to treat anticholinergic toxicity like atropine overdose, crosses BBB

“Physostigmine “phyxes” atropine overdose

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12
Q

Pyridostigmine - drug class? clinical uses?

A

drug class: -stigmine: anticholinesterase (ACh indirect agonist, cholinomimetic agent)

Used to treat myasthenia gravis (long acting), increases muscle strength, *Does NOT cross BBB, similar to neostigmine

“Pyridostigmine gets rid of myasthenia gravis”

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13
Q

What can cause cholinesterase inhibitor poisoning? What are the symptoms? What is the antidote?

A

Usually caused by organophosphates (parathion, malathion)- components of insecticides–> Farmers

irreversibly inhibit AChE

Symptoms: “wet picture” Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating and Salivation (DUMBBELSS)

Antidote: Atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early)

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14
Q

What is the function of muscarinic antagonists? What are some examples?

A

Function: decrease parasympathetic activity -> mimic sympathetic effects

Examples: Atropine, homatropine, tropicamide, benztropine, glycopyrrolate, hyoscyamine, dicyclomine, ipratropium, tiotropium, oxybutynin, solifenacin, tolterodine, scopolamine

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15
Q

Which muscarinic antagonists are used for the eye? What are the clinical effects?

A

Atropine, homatropine, tropicamide.

Produce mydriasis (dilate pupil during ophthalmic exam) and cycloplegia (paralysis of ciliary muscle-> loss of acommodation)

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16
Q

Benztropine - drug class? clinical use?

A

Muscarinic antagonist

Used for Parkinson disease “Park my Benz” and acute dystonia

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17
Q

Glycopyrrolate - what is the drug class? clinical use?

A

Class: muscarinic antagonist, cannot cross BBB

Parenteral: peroperative use to decrease airway secretions

Oral: treat drooling, peptic ulcers

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18
Q

Hyoscyamine and dicyclomine are muscarinic antagonists use for what application?

A

GI - Antispasmodics for IBS

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19
Q

Which muscarinic antagonists are used to treat COPD and asthma?

A

Ipratropium, tiotropium

Block M3-> decrease bronchoconstriction

“I pray I can breathe soon”

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20
Q

Which muscarinic antagonists are used to treat urinary incontinence and what is the mechanism?

A

Oxybutynin, solifenacin, tolterodine

Muscarinic antagonists are sympathetic mimetics -> relax detrussor muscle -> reduce bladder spasms

21
Q

Scolpamine - what is the drug class and clinical use?

A

Muscarinic antagonist

Used for motion sickeness

22
Q

Atropine - what are the actions, uses and toxicity of the drug?

A

Uses: treat bradycardia and for ophthalmic applications

Actions:

Eye - increase pupil dilation, cycloplegia

Airway - decrease secretions

Stomach - decrease acid secretion

Gut - decrease motility

Bladder - decrease urgency in cystitis

Toxicity: “Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter” Increase body temp (from decreased sweating), increase HR, Dry mouth, dry flushed (vasodilation to decrease temp) skin, cycloplegia, constipation, disorientation

  • Can cause acute angle-closure glaucoma in elderly (mydriasis), urinary retention in men with prostatic hyperplasia, and hypertemia in infants
  • Jimson weed (Datura) -> gardner’s pupil
23
Q

Tetrodotoxin - what is the source? mechanism? symptoms? treatment?

A

Source: ingestion of poorly prepared pufferfish - Japanese delicacy

Mechanism: toxin binds voltage-gated sodium channels in cardiac and nerve tissue -> blocks AP

Symptoms: typical food poisoning symptoms (nausea, vomiting, weakeness) + neuro symptoms: dizziness, paresthesias, loss of deep tendon relfexes

Treatment is supportive

24
Q

Ciguatoxin - what is the source? mechanism? symptoms? treatment?

A

Source: consumption of reef fish (barracuda, snapper, moray eel)

Mechanism: Opens sodium channels -> depolarization

Symptoms: mimic cholinergic poisoning + _*temperture-related dysesthesia (cold feels hot and visversa)*_

Treatment is supportive

25
Q

Scombroid poisoning - what is the source? mechanism? symptoms? treatment?

A

Source: consumption of dark-meat fish (bonito, mackerel, mahi-mahi, tuna) improperly stored at warm temps

Mechanism: bacterial histidine decarboxylase converts histidine -> histamine

Symptoms: Increased histamine -> acute-onset burning sensation of mouth, flushing of face, erythema, urticaria, pruritius, HA. May have anaphylaxis presentation - bronchospasm, angioedema, hypotension

Treatment: antihistamines (loratadine, diphenhydramine) and antianaphylactics if needed (bronchodilators, epinephrine)

26
Q

What are examples of direct sympathomimetics?

A

Albuterol, salmeterol, dobutamine, dopamine, epinephrine, isoproternol, NE, phenylephrine

27
Q

Albuterol, salmeterol: what receptors do they act on and what are the clinical applications?

A

beta2>beta1 –> bronchodilatory effect

Albuterol has shorter t1/2 and is used for acute asthma; salmeterol has longer t1/2 and is used for long-term asthma or COPD control

28
Q

Dobutamine - what is the function and application?

A

Direct sympathomimetic works on: beta1>beta2, alpha

Applications: heart failure (inotropic/contractility >chronotropic/HR), cardiac stress testing

29
Q

Dopamine - what is the function and clinical application?

A

Direct sympathomimetic, works at D1=D2 > beta > alpha

Applications: unstable bradycardia, HF, shock* (increases BP WITHOUT decreasing renal perfusion since D1 relaxes renal vasculature); inotropic and chronotropic alpha effects predominate at high doses

30
Q

Epinephrine - what is the function and clinical application?

A

Function: direct sympathomimetic, beta>alpha at low doses, alpha>beta at high doses

Used for anaphylaxis, asthma, open-angle glaucoma, *stronger effect at beta2 receptor than norepinephrine

31
Q

Isoproterenol - what is the function and application?

A

Direct sympathomimetic: beta1=beta2 *isolated beta agonist

Rarely used clinically (can worsen ischemia), can be used for electrophysiologic evaluation of tachyarrhythmias

32
Q

Norepinephrine - what is the function and application?

A

direct sympathomimetic: alpha1 (vasoconstriction)>alpha2>beta1 (increase renin)

used for hypotension, but decreases renal perfusion so contraindicated with renal problems. Weaker effect at beta2 (vasodilation) than epinehrine

33
Q

Phenylephrine - what is the function and clinical use?

A

direct sympathomimetic: alpha1>alpha2

Used for hypotension (vasoconstriction), ocular procedures (mydriatic), rhinitis (decongestant)

(*does not cause cycloplegia bc under parasympathetic control)

34
Q

What are examples of indirect sympathomimetics and what are their mechanisms of action and clinical uses?

A

Amphetamine: mechanism: increases release of stored catecholamines and prevents reuptake at presynaptic terminal; Uses: narcolepsy, obesity, ADHD

Cocaine: mechanism: prevents reuptake of catecholamines at presynaptic terminal; uses: causes vasoconstriction and local anesthesia

Ephedrine: mechanism: increases release of stored catecholamines; uses: nasal decongestion, urinary incontinence, hypotension

35
Q

What drug class should be avoided in the case of suspected cocaine intoxication?

A

Beta-blockers -> can lead to unopposed alpha1 activation by cocaine and cause severe HTN -> MI, stroke

36
Q

Clonidine - what is the drug class? applications? toxicity?

A

Class: Sympatholytic (alpha2 agonist) inhibits sympathetic outflow: increase alpha2 stimulation -> decreased catecholamine production -> vasodilation, decrease BP, decrease HR

Applications: hypertensive urgency *does NOT decrease renal blood flow, ADHD, Tourette syndrome

Toxicity: CNS depression, bradycardia, hypotension, respiratory depression, miosis

37
Q

alpha-methyldopa: what is the drug class? applications? toxicities?

A

Class: Sympatholytic (alpha2 agonist) inhibits sympathetic outflow: increase alpha2 stimulation -> decreased catecholamine production -> vasodilation, decrease BP, decrease HR

Applications: *HTN in pregnancy

Toxicity: *Direct Coombs positive hemolysis, SLE-like syndrome

38
Q

alpha-blockers: non-selective

What are drug examples and what are their applications and side effects?

A

Phenoxybenzamine (irreversible alpha-blocker) Applications: used preoperatively for pheochromocytoma resection to prevent catecholamine (HTN) crisis; Half-life 24 hours and effects can last 3-4 days

Phentolamine (reversible alpha-blocker) Applications: given to patients on MAOIs (inhibit breakdown of catecholamines) who have eaten tyramine-containing foods (causes toxic build up of catecholamines)

Side effects of both: orthostatic hypotension, relfex tachycardia

39
Q

Which drugs are alpha1 selective blockers? What are their applications and side effects?

A

alpha1 selective blocking drugs with “-osin” ending: prazosin, terazosin, doxazosin, tamsulosin

Applications: urinary symptoms of BPH, PTSD (prazosin), HTN (all except tamsulosin)

Side effects: 1st dose orthostatic hypotension –> symptoms of cerebral hypoperfusion: dizziness, HA

40
Q

Mirtazapine - what is the drug class? application? side effects?

A

drug class: alpha-blocker, alpha2 selective –> increases sympathetic outflow since alpha2 is inhibitory

Application: depression

Side effects: sedation, increases serum cholesterol, increases appetite

41
Q

Beta-blockers: what are examples? what is the mechanism of action?

A

Drugs: end with -lol, -olol for drugs that solely beta-block; -ilol, alol for alpha and beta-blocking drugs

Mechanism: blocking Beta1 -> decrease HR, decrease contractility, decrease renin release -> decrease BP, decrease lipolysis; blocking Beta2 -> decrease HR and contractility, decrease aqueous humor production, decreases intraocular P, bronchoconstriction, increase uterine tone

42
Q

What are the applications of beta-blockers?

A

Angina pectoris: decrease HR and contractility -> decrease O2 consumption

MI: (metoprolol, carvedilol and bisoprolol), decrease mortality

SVT: (metoprolol, esmolol), decrease AV conduction velocity (class II anti-arrhythmic)

HTN: decreases CO and BP via decreased renin secretion (beta1 block on JGA cells)

Glaucoma: (timolol), decrease aqueous humor production and decrease intraocular pressure

43
Q

What are toxic effects of beta-blockers? When should they be avoided?

A

Toxicity: impotence, adverse cardiovascular effects (bradycardia, AV block, HF), CNS adverse effects (seizures, sedation, sleep alterations), dyslipidemia (metoprolol), asthma/COPD exacerbations (via beta2 blockage)

Avoid in cocain users due to risk of unopposed alpha-adrenergic agonist activity -> HTN emergency

44
Q

Which drugs are beta1-selective antagonists? (beta1>beta2)

A

Drugs: acebutolol (partial agonist), atenolol, betaxolol, esmolol, metoprolol (A-M, first half of alphabet)

*Good for patients with co-morbid pulmonary diseases since little antagonism at beta2 (less bronchoconstriction)

45
Q

Which drugs are nonselective beta-blockers? (beta1=beta2)

A

Drugs: Nadolol, pindolol (partial agonist), propranolol, timolol

*Non-selective go from N to Z, second half of alphabet*

46
Q

Which drugs are nonselective alpha and beta antagonists?

A

Carvedilol, labetalol (have modified ending instead of -olol)

47
Q

What is the mechanism of action of Nebivolol?

A

Blocks beta1 receptors –> vasodilation and STIMULATES beta3 receptors –> activates NO synthase

48
Q

What other classes of drugs display antimuscarinic (atropine-like) effects?

A

Antihistamines

TCAs

Antipsychotics

Quinidine

Amantadine

Meperidine

Pharmacology (19 decks)

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