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Sketchy Pharmacology Notecards > Autonomics > Flashcards

Autonomics Flashcards

1
Q

What are the 3 kinds of muscarinic receptors and where are they found?

A

M1, M2 and M3M1 is found in CNS and enteric nervous systemM2 is primarily in heart, decreases heart rate only at the SA nodeM3 is at the glands, bladder and smooth muscles of the eye

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2
Q

Explain M1 MOA.

A

M1 Gq - activate IP3-DAG cascade –> increased intracellular calcium;

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3
Q

Explain M2 MOA.

A

M2 is Gi, decreases cAMP

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4
Q

Explain M3 MOA.

A

M3 is Gq - activate IP3-DAG cascade –> increased intracellular calcium;

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5
Q

What happens in an intact endothelium when muscarinic agonist is administered

A

Vasodilation

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6
Q

What happens vasculature without endothelium when muscarinic agonist is administeredWhat disease is this phenomenon associated with?

A

Vasoconstriction by increasing intracellular Ca in the smooth musclesAtherosclerosis

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7
Q

Bethanecol

A

Used to treat non-obstructive gastrointestinl dysmotility (e.g. post-op ileus, neurogenic ileus - like from spinal cord injury, congenital megaocolon) and urinary retention. Muscarinic agonist increase the secretory ability and motility of the gut

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8
Q

Pilocarpine

A

Pilocarpine - increases salivation (treats fry mouth - sjograns) and treats glaucoma by contracting the ciliary muscles, facilitating the outflow of aqueous humor and causing pupillary constriction ; causes accommodation of lens

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9
Q

How is acute angle glaucoma treated?

A

For acute angle glaucoma it is important to cause contraction of sphincter papillae muscle which leads to pupillary constriction, pilocarpine can be used to achieve this

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10
Q

What are the 3 places where nicotinic receptors are found?

A

Autonomic ganglia, skeletal muscle motor end plates, and adrenal gland (post ganglionic organ)

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11
Q

MOA of nicotinic receptors?

A

transmembrane polypeptides that act as ion channels (influx of positive ions –>depolarization of skeletal muscles

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12
Q

What drug is used for smoking cessation

A

Very clean = Vernicline

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13
Q

Carbachol

A

Carbachol - both muscarinic and nicotinic agonist, causes pupillary constriction (useful in acute angle-closure glaucoma)

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14
Q

What are indirect cholinomimetics?

A

ACh esterase inhibitors

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15
Q

What is one disease that involves the use of indirect cholinominetics to increase ACh at the NMJ?

A

Myasthenia Gravis - antobodies against the ACh receptors are made

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16
Q

What are the different kinds of indirect cholinomimetics?

A

Quaternary, tertiary and phosphate derivatives. Quaternary cannot cross the BBB hence their effects are more peripheral, tertiary have more central effects

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17
Q

What are the examples of quaternary AChEI?

A

NeostigminePyridostigmineEdrophonium

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18
Q

What is the use of neostigmine?

A

Can reverse nondepolarizing neuromuscular blockade after surgery (removing effects of anesthesia); like urinary retention after surgery

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19
Q

What are the uses of pyridostigmine?

A

Long-term treatment for MG; only symptomatic treatment

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20
Q

What is the use of edrophonium?

A

Diagnosis of MG since it has a very short half life.

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21
Q

Describe the test that is done to dx MG?

A

It is called the tensilon testPt comes with worsening MG symptoms: 1. could be over treated (cholinergic crisis - too much ACh) or 2. could be undertreated (Myastenia crisis)If give edrophonium and symptoms get better, then undertreated/Myasthenia crisis

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22
Q

Give an example of tertiary AChEI? What are its uses?

A

Physostigmine, used for more of its central CNS effects since it can cross the BBB

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23
Q

Name two plants which are known to cause atropine poisoning.

A

Belladonna flower and Jimson’s weed, Jimson’s weed is also called Gardner’s mydriasis

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24
Q

Name drugs that are specific for nicotinic receptors at the NMJ?

A

Tubocurarine, Pancuronium, Cisatracurium

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25
Q

Explain the MOA of succinylcholine.

A

Nicotinic Ach receptor AGONIST; like an analogue of ACH, causes phase 1 block; potentiates depolarization

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26
Q

What is the most common cause of ACh esterase inhibitor toxicity?

A

Insecticide poisoning/occupational expsure

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27
Q

Name organophosphate AChEI

A

Parathion, Malathion, Echothiophate

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28
Q

What kind of paralysis does these cause? What does over activation of ACh receptors at the NMJ lead to?

A

Flaccid paralysis

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29
Q

What can be used to reverse ACh toxicity? What is its limitation?

A

Pralidoxime - reverses organophosphate toxicity; regenerates acetylcholinesterase at muscarinic AND nicotinic receptors - reverses cholinergic toxicity, including flaccid paralysis.However it cannot enter CNS, ONLY PERIPHERAL, ineffective once organophosphate -cholinesterase complex has occurred, a process called aging.

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30
Q

What drug can be used to reverse central and peripheral ACh toxicity?

A

Atropine - reverses both peripheral and central muscarinic toxicity from organophosphate poisoningHowever, it cannot reverses neuromuscular blockade/paralysis since it is only a muscarinic antagonist

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31
Q

Name drugs used in Alzheimer’s disease.

A

GalantamineRivastigmineDonepezil

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32
Q

Explain the MOA of atropine.

A

Non selective competitive antagonist of M1, M2 and M3

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33
Q

What are atropine’s effects on eyes?

A

Mydriasis and cycloplegia (inability to accommodate for near vision due to ciliary muscles paralysis)

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34
Q

What is the main muscarinic receptor found in CNS

A

M1

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35
Q

What are the effects of scopolamine?What is it used for?

A

prevent sea sickness/motion sickness as it crosses BBB and inhibits central M1 receptors, important to know that this is a property shared by most of the muscarinic antagonists.

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36
Q

What is the role of muscarinic antagonists in Parkinsons’ disease and other CNS diseases?

A

M1 receptors are found in CNS, it turns out that reduction in muscarinic transmission in the CNS is helpful in Parkinsons disease

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37
Q

What is the role of muscarinic antagonist in post MI treatment?

A

Block parasympathetic activation of M2 receptors on SA and AV nodes, normally parasympathetic tone to the heart determines the HR and blocking this tone can increase HR which is important usually after post MI - increased HR (tachycardia), increased AV conduction (treatment for heart block)

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38
Q

What is the role of muscarinic antagonist in heart block treatment?

A

Used for heart block therapy: Heart block can occurs when there is a delay or decreased electrical transmission to the ventricles through the AV nodes, this can be caused by numerous pathologies, IV atropine can be administered to reverse heart block in these patients since muscarinic receptor antagonists increase AV conduction

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39
Q

What is the role of anti muscarinics in COPD treatment?

A

Smooth muscles and secretory glands in the airway receive vagal innervation modulated by M3 receptors, anti muscarinic agents can be used to cause dilation of the airways and reduce secretions.

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40
Q

Name the drugs that are used in COPD

A

Ipratropium - M3 muscarinic antagonist for COPD, INHALED, bronchodilation –> decreased secretionsTiotropium - M3 muscarinic antagonist for COPD, INHALED, bronchodilation –> decreased secretions; longer bronchodilation; can be given once a day for COPD

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41
Q

Name the anti muscarinics used for urinary incontinence treatment?

A

Oxybutynin - M3 muscarinic antagonist, for incontinence, relaxes smooth muscle in ureters and bladder wallTolterodine - M3 muscarinic antagonist, for incontinence, relaxes smooth muscle in ureters and bladder wall

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42
Q

Benztropine

A

Benztropine - centrally acting M1 muscarinic antagonists, treatment for parkinson’s tremor and rigidity (loss of dopamine in basal ganglia) - blocks excess cholinergic activity, no effect on bradykinesia

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43
Q

Trihexyphenidyl

A

Trihexyphenidyl - centrally acting M1 muscarinic antagonists, treatment for parkinson’s tremor and rigidity (loss of dopamine in basal ganglia) -blocks excess cholinergic activity, no effect on bradykinesia

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44
Q

How can antipsychotics cause drug induced Parkinson’s?

A

Antipsychotic drugs are known to cause extrapyramidal side effects, antipsychotic agents stop dopaminergic transmission, just like in Parkinson’s disease so they cause similar symptoms- dystonia, akathisia

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45
Q

What are the side effects of anti muscarinics?

A

o Hot as a hare: antimuscarinics inhibit M3 receptors, sweat glands –> decreased sweating –> hyperthermiao Dry as a cracker: decreased salivation and lacrimation –> dry mouth and eyeso Blind as a bat - mydriasis and cycloplegia –blurred vision high pressure as a kettle Vignette: lady has Bradycardia after MI, then give atropine, comes back with eye pain –> induced acute angle closure glaucomao Mydriasis –> decreased outflow of aqueous humor –> acute angle closure glaucoma o Mad as a hatter - cross BBB –> antagonize M1 receptors –> sedation, agitation, hallucination, coma (esp in old pts)

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46
Q

What are alpha and beta receptors coupled to intracellularly?

A

Alpha 1,2 beta 1,2 -> QISSAlpha 1 is coupled to Gq, Alpha 2 is Gi, Beta 1 and 2 is Gs

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47
Q

What are the effects of alpha 1 activation?

A

Gq –> IP3 DAG cascade – increased calcium - activate smooth muscle –> increase in peripheral arterial resistance (vasoconstriction in arteries AND veins)

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48
Q

What are the effects of alpha 2 activation?

A

Gi, decrease cAMP, these are sympatholytics, Inhibit neurotransmitter release at presynaptic receptors at the adrenergic and cholinergic nerve terminals

49
Q

What are the effects of beta 1 activation?

A

Gs - increase cAMP; receptors are found on cardiac myocytes and JGA cells in kidneys

50
Q

What are the effects of beta 2 activation?

A

Gs - protein kinase A – relaxation of smooth muscles

51
Q

What places is alpha 1 receptor found and what are its effects?

A

Venoconstriction –> hypovolemic or distributive shock to maintain COAlpha 1 receptors dilated pupils (dilator pupillae), causes mydriasisThey also cause constriction of urethra and prosthetic sphincter - causes urinary retention

52
Q

Describe the effects of alpha 1 receptors on vasculature

A

” Increases systolic pressure (arteriolar constriction)” Increased MAP (increase in SVR)” Increased diastolic pressure (venous constriction)” Increase in MAP stretch in baroreceptors==> REFLEXIVE increase in vagal tone –> BRADYCARDIA

53
Q

Name an alpha 1 agonist and state its use

A

Phenylephrine alpha-1 agonist - vasoconstriction – helps nasal congestion, mydriasis - activates alpha 1 at pupillary dilator muscle, able to use at eye docPhenylephrine is also administered systemically as IV for hypovolemic shock

54
Q

Explain how diabetic neuropathy patients respond to alpha 1 agonist treatment.

A

Patients with diabetic neuropathy have reduced autonomic function so they cant elicit reflexes like reflex bradycardia upon administration of phenylephrine

55
Q

What is the treatment of septic shock

A

Septic shock - give phenylephrine and norepinephrine increase SVD and venous return to treat distributive/hypovolemic shock)

56
Q

What is NE selective towards?

A

Agonist on alpha>beta1 agonist, MOSTLY alpha 1 and alpha 2

57
Q

State the effects of NE on vasculature

A

” Increase systolic pressure (alpha 1 arteriolar constriction)” Increase MAP (increased SVR)” Increased diastolic pressure (alpha venous constriction)” Reflexive bradycardia” Increased cardiac contractility (beta 1)” Increased Pulse pressure = diff between systolic and diastolic (beta-1 increase in contractility)

58
Q

State the systemic effects of stimulating alpha 2 receptors other than decreasing catecholamine secretion into the synaptic cleft?

A

Alpha 2 cells are expressed on pancreatic islet cells - decreases insulin releaseDecreased lipolysis and release of fatty acidsCiliary body in eye - decrease aqueous humor production

59
Q

Name an alpha 2 receptor agonist and its use

A

Brimonidine - alpha 2 agonist - decreases aqueous humor production, used for chronic open angle glaucoma

60
Q

Describe the effects of beta 1 agonist

A

Increase in inotropy and chronotropy of the heart, increase in renin release

61
Q

Describe the effects of beta 2 receptors

A

Vasodilation in coronary and skeletal muscle vasoDILATION –> decreases SVRDecreases diastolic pressureActivates lipolysis and release of free fatty acidsIncreased gluconeogenesis at liverIncreased insulin release and usageIncreased aqueous humor production at ciliary muscle

62
Q

What is a side effect of increased insulin release other than hypoglycemia

A

Drives potasium into cells - hypolkalemia due to increased insulin, insulin drives K into the cells

63
Q

Name beta 2 receptors agonists used in obstetrics

A

Ritodrine - Beta 2 agonists relax uterine smooth muscle, to prevent premature laborTerbutaline - Beta 2 agonists relax uterine smooth muscle, to prevent premature labor

64
Q

Dobutamine

A

DobutamineBeta1>beta2 agonistSounds like Do-beta 1” Increase HR” Increase contractility” Increased CO” Vasodilation - decreases SVR - effects minimal since minimal beta 2 activity” Increases systolic pressure (beta 1 increase in CO)” Increased pulse pressure = diff between systolic and diastolic (beta 1 increase in contractility” Decrease diastolic pressure (beta 2 arteriolar dilation)” Increases contractility and CO to treat cardiogenic shock - Acute HF, cardiogenic shock” Helped to use if pt cant tolerate stress test

65
Q

Isoproterenol

A

IsoproterenolBeta1=beta2 agonistBeta 1 - “ increased HR, “ increased contractility Beta 2 - “ Vasodilation” decreases SVR “ decreases diastolic pressure (Beta 2 vasodilation and decreased SVR)” also relax the uterus so can delay premature labor, Terbutaline and Ritodrine are used for this, they are potent beta 2 agonistsDecrease MAP (beta-2 decrease SVR)Decreased diastolic (beta-2 arteriolar dilation)Increase pulse pressure = diff between systolic and diastolic - beta 1 increase in contractility

66
Q

Explain the effects of epinephrine at low dose

A

Low dose - primarily beta effects - bronchiodilation (beta 2)” Diastolic pressure decrease - beta 2 dilation” Elevated HR (beta 1)” Increased cardiac contractility (beta 1)

67
Q

Explain the effects of epinephrine at high dose

A

High doses - Alpha domiates” Vasoconstriction” Increases systolic pressure (alpha-1 arteriolar constriction)” Increase MAP (alpha-1 increase in SVR)Increase pulse pressure (beta1 increase in contractility)For anaphylactic shock = Increase SVR, bronchodilation

68
Q

Name chatecholamines

A

Epinephrine, norepinephrine, dopamine

69
Q

Explain the synthesis of dopamine and NE

A

Tyrosine = amino acid precursor to catecholamines - transported to nerve terminalTyrosine –> L-DOPA –> dopamineDopamine –> norepinephrine (inside the vesicle) by dopamine beta hydroxylase

70
Q

How is dopamine and NE transmission terminated

A

Dopaminergic transmission is terminated either by diffusion of dopamine out of the synapse or by reuptake of dopamine, several medication like the one’s used in ADHD and depression inhibit this reuptake, thereby increasing the transmission of dopaminergic neuronsNET transports norepinephrine (and dopamine, DAT) back into the presynaptic neuron

71
Q

Explain the MOA of cocaine

A

Cocaine-it is an indirect sympathomimetics that inhibits NET and DAT, increasing dopamine and NE concentration at the synapse, reuptake inhibitor

72
Q

Explain how does cocaine exhibit anesthetic effect?

A

It is a potent vasoconstriction and hence causes local anesthesia

73
Q

What are the peripheral effects of cocaine?

A

Peripheral stimulation –> sympathetic stimulation: hypertension, tachycardia, mydriasis

74
Q

What are the central effects of cocaine?

A

Central stimulation –> arousal, addiction, seizures

75
Q

What is the hallmark of cocaine toxicity?How does it present in a vignette?How is cocaine toxicity managed?

A

Hallmark of cocaine toxicity is coronary vasospasm leading to acute MITypical vignette: agitation, pupillary dilation, hypertension, tachycardia, usually it is taken up by injecting, snorting or ingesting so a vignette may mention mucosal atrophy, nasoseptal perforation (due to vasoconstriction) –> can lead to coronary vasospasm and MIManagement of cocaine intoxication is usually supportive but we need to know that we should not give them beta blocker as it will lead to unopposed alpha stimulation leading to severe hypertension

76
Q

Ephedrine

A

Ephedrine - releases stored catecholaminesUse: nasal decongestion, urinary incontinence, hypotension

77
Q

Metyrosine

A

Metyrosine (my tire)- tyrosine analog, prevents conversion of tyrosine to L-DOPA

78
Q

Atomoxetine

A

Atomoxetine - selective NET inhibitor, used for for ADHD

79
Q

What is the role of VMAT

A

VMAT (vesicular monoamine transporter) - catecholamine are transported by VMAT into presynaptic vesicle

80
Q

Reserpine

A

Reserpine - inhibits VMAT, depleting neurotransmitter stores

81
Q

Explain the MOA of Amphetamines, what are their effects and what is a clinical use of them?

A

Amphetamines - reuptake inhibitor, releases stored catecholamines; displace catecholamines (NE, dopamine) into synapse, they have a mood elevating effect that explains their wide spread abuse, makes them alert and increased attention also treats ADHD

82
Q

Methylphenidate

A

Methylphenidate - amphetamine derivative, treats ADHD, suppress appetite

83
Q

Modafinil

A

It is a stimulant, used for treating narcolepsy, suppress appetite

84
Q

Explain D1 MOA and what are its effects? Where is it found?

A

D1 – Gs (increased cAMP) –> increased renal blood flow

85
Q

Explain D2 MOA and where is it found?

A

D2 – GiFound in CNS

86
Q

What are the adrenergic effects of dopamine?

A

High dose - activate alpha 1 receptors (pressor effects)Low dose - activate beta 1 receptors (cardiac activation)

87
Q

What are the effects of alpha 2 agonists?

A

Alpha-2 agonists decrease sympathetic tone –> reduced BP (sympatholytic), act directly at the CNS, when alpha 2 agonists are given systemically given it is the central effects of alpha 2 receptors that dominate, causing reduced sympathetic outflow from the CNS

88
Q

Clonidine

A

Alpha 2 agonists, reduces blood pressure by reducing sympathetic tone, treats hypertension, hypertensive urgency, ADHD refractory to stimulants

89
Q

What neurological problem is also treated with alpha 2 agonists and why?

A

Alpha 2 agonists are also used to treat tourette’s syndrome, alpha 2 agonists such as clonidine are preferred over neurological agents as they don’t cause extrapyramidal side effects as most of the neurological agents cause.

90
Q

Alpha methyldopa

A

Alpha 2 agonist - analog of L-dopa, causes the synthesis of alpha norpei that acts on central alpha 2 receptors to reduce blood pressure, similar to clonidine, treats hypertension (primarily gestational hypertension)

91
Q

What is a side effect of methyldopa

A

Causes lupus like syndrome

92
Q

Taxanadine

A

Taxanadine - muscle relaxant, it is also a centrally acting alpha 2 agonist

93
Q

What is one alpha antagonist clinical use other than treating HTN or HTN crisis?

A

Alpha antagonists can be used to treat cocaine toxicity since we can’t use beta blockers due to the risk of unopposed alpha 1 effect leading to HTN crisis

94
Q

Phentolamine MOA and state its 1 clinical use

A

Phentolamine - reversible (short acting) alpha-1 and alpha-2 receptor antagonist, causes vasodilation (alpha 1)Phentolamine can be used to treat cocaine induced hypertension and manage cocaine toxicity, remember that the hallmark of cocaine overdose is systemic vasoconstriction that can lead to end organ failure and death

95
Q

Phenoxybenzamine

A

irreversible (covaletly bonds) alpha-1 and alpha-2 receptor antagonist

96
Q

What does wine and aged cheese contain? How can this lead to a hypertensive crisis in people on antipsychotics?How can this be treated?

A

Wine and aged cheese contain the sympathomimetic agent tyramine which is metabolized by MAO-AMAO-inhibitors, for example drugs used for depression - can prevent metabolism of tyramine –>this can lead to hypertensive crisis due to systemic distribution of tyramine. This is treated with alpha blockers - phentolamine)

97
Q

Explain the treatment of pheochromocytoma using alpha blockers.

A

Phenochromocytoma - catecholamine secreting tumor of adrenal medulla Catecholamine excess can cause headaches, hypertension, palpitations, sweating use alpha blockers (e.g. phenoxybenzamine is used days before surgery and phentolamine is used intraoperatively) preoperatively to control BP

98
Q

What are the side effects of alpha antagonists?

A

Orthostatic hypotensionAlpha blocker induced hypotension causes reflex tachycardia

99
Q

What is the main use of alpha 1 antagonists?

A

Alpha 1 antagonists reduce smooth muscle contraction - relax smooth muscles in urethra and prostate, treats BPH. They are especially useful for patients with both hypertension and BPH

100
Q

Name alpha 1 antagonists

A

“-osin” alpha-1 selective antagonistsPrazosinTerazosinDoxazosinTamsulosin

101
Q

What is another use of parazosin?

A

Can also be used for PTSD treatment, helps with the associated sleep disorder and nightmares seen in PTSD

102
Q

Name an alpha 2 antagonist and state its use

A

Mirtazapine - atypical antidepressant with antagonist effect at alpha 2 and other receptors; enhances serotonin secretion, treats depression

103
Q

Where are beta receptors present in the heart and what are their 2 functions?

A

Beta 1 are distributed all over the cardiac tissue, blocking these receptors will cause a decrease in inotropy. On the other hand beta 1 receptors are also located at SA and AV nodes causing a decrease in chronotropy!

104
Q

What happens when beta 1 receptors are blocked at the SA node?

A

Bradycardia

105
Q

What happens when beta 1 receptors are blocked at the AV node?

A

Heart block

106
Q

Name beta 1 selective antagonists

A

Beta-1 selective antagonists - A-BEAMAtenololBextaxololEsmololAcebutololMetoprolol

107
Q

What is the main adverse effect of beta 1 antagonist?

A

It can exacerbate heart block

108
Q

When exactly are beta blockers particularly helpful? Do they improve mortality and morbidity of HF patients like loop diuretics do?

A

Acute treatment of MI and other acute coronary syndromes (ACS), cardioselective beta blockers are the first line therapy in management of acute cardiac symptoms such as angina, acute MI, NSTEMI etc Beta blockers are known to help reduce mortality and morbidity in chronic heart failure patients by inhibiting cardiac remodeling, ironically they are also known to exacerbate and precipitate heart failure since pumping function of the heart in stress is often maintained by catecholamines

109
Q

Carvedilol

A

Carvedilol = also useful chronic HF pts - nonselective beta blocker and alpha-1 blocker

110
Q

What are the other 2 CV pathologies where beta blockers are particularly helpful?

A

Acute management of aortic dissection (IV)Hypertrophic obstructive cardiomyopathy, in this disease the hypertrophy of the left ventricle does not only inhibit ventricle filling but also obstructs the outflow tract of the blood, this can sometimes acute hemodynamic collapse, beta blockers are useful in these situations to decrease HR and increase diastolic filling time

111
Q

Timolol

A

Topical non-selective beta blockers (timolol – topical!) -treats glaucoma (antagonize beta 2 receptors in ciliary epithelium - decease production of aqueous humor production

112
Q

What are the 3 uses of beta blockers other than treating heart conditions?

A

Migraine prophylaxis, Thyroid stormBeta blockers treat essential tremor

113
Q

What is a thyroid storm and how is it treated?

A

Beta blockers blocks increased sympathetic activity, catecholamine surge is a serious complication of thyroid toxicoses, it presents as agitation, delirium, fever, tachyardia - propranolol, prednisone and propylthiouracyl (three P’s) are used to treat this, so they can also used for symptomatic management of Grave’s disease, Beta blockers will NOT reverse exophthalmos

114
Q

Explain the management of acute aortic dissection and what drug is used for this?

A

Acute aortic dissection, in aortic dissection treatment usually involved rapidly lowering blood pressure to 120/100 mm Hg which differs from treatment of other cardiovascular complications where the blood pressure is lowered more slowlyLabetelol

115
Q

Labetolol and its other uses

A

Labetalol = nonselective beta blocker and alpha 1 blocker;vasoldilation (alpha 1)Hypertension in pregnancyIV for hypertensive emergency (not just in pregnancy)

116
Q

Acebutolol

A

Acebutolol - selective beta 1 antagonist with partial agonist activity

117
Q

Pindolol

A

Pindolol - nonselective beta blocker with partial agonist activity

118
Q

How can we overcome the adverse effects of beta blockers?

A

Some of the most adverse effects of beta blockers such as heart failure, heart block and bradycardia can be overcome with Glucagon - treats beta blocker toxicity - stimulates heart via glucagon receptors which are not being blocked by beta blockers

Sketchy Pharmacology Notecards (14 decks)

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