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ANS Flashcards

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0
Q

M1,M2,M3: G-protein activation

A

M1 and M3: Gq - Phospholipase C

M2: Gi

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1
Q

Sympathetic vs. parasympathetic

A

Sympathetic: t1-L2, short preganglionic (ACh nicotinic), long post (Epi)
Parasympathetic C1-C8 + L3-S5, long preganglionic (ACh) short post (muscarinic ACh)

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2
Q

M2 receptor locations

A 
M2 is the heart of med school)
M2 - Gi (decrease cAMP) 
- SA node
- AV node
- cardiac myocytes
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3
Q

M1/M3: location and activation

A

Phospholipase C

  • vascular sm. muscle
  • sm. muscle of GI (walls, sphincters)
  • GI secretions
  • urogenital: bladder walls, sphincters, uterus, seminal vesicles
  • eye: iris, ciliary muscle, lacrimal glands
  • M1 are CNS
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4
Q

Direct muscarine agonists

A

Non-selectively activates M1,2 and 3. Cevimaline is more selective for M3 (civilized people drive M3s)
Choline esters:
- methacholine: asthma diagnosis
- carbachol: glaucoma(constricts pupils) meiosis induction
- bethanachol: urinary retention/GI dysmotility

Alkaloids:

  • pilocarpine (muscarine analog) xerostomia
  • cevimaline - glaucoma, miosis induction
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5
Q

Cholinergic effects:9 DUMBBELLS

A 
Blurred vision
N/V/D
Sweating 
Hypersalivation
Flushing
Bradycardia
Reflex tachycardia 
Bronchoconstriction
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6
Q

Natural alkaloid amines:

A

in NAAM the AK shot (antagonize) AT you with a SCOPE)
Direct muscarinic antagonists: nicotinic ACh poisoning, N/V (motion sickness)
Atropine, scopolamine
Tertiary amines : high CNS penetrance
Quaternary amines: lower CNS penetrance than tertiary

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7
Q

Atropine

A

No selective muscarinic antagonist

  • antidote for muscarinic ACh toxicity
  • bronchi, salivary and sweat glands most effective
  • ACLS algorithm
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8
Q

Scopolamine

A

Nonselective muscarinic antagonist

  • Substantial CNS effects
  • prevention of motion sickness N/V
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9
Q

Benzotropine and triphenidyl

A
  • M1 selective
  • decrease tremor in early Parkinson’s (park your benz, with the triprop logo, benzs are thrilling cars)
  • treat extra pyramidal symptoms
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10
Q

hyoscyamine and dicyclomine

A
  • Nonselective muscarinic antagonist (hyoscyamine)
  • M1/3 selective (dicyclomine)
  • decreases GI motility in IBS
    (hyo rode a cycle back from the bathroom)
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11
Q

Tertiary and quaternary amines: indications for urinary incontinence

A 
Urinary incontinence
- high M3 selectivity tertiary amines:
    ~ Darifenacin
    ~ solifenacin 
- low M3 selectivity tertiary amines:
    ~ oxybutynin
    ~ tolterodine
    ~ fesoterodine
- quaternary amines
    ~ Trospium
  (Don't Soil (high) Old Trousers For (low) the 4th Time (quaternary))
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12
Q

Quaternary amines for COPD/asthma

A
  • Nonselective muscarine antagonists
  • first line for COPD
  • not first line for emergency management of airways
    Ipratroprium (brats are short and high energy: short acting, muscarinic agonist) and tiotropium (long acting)
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13
Q

Direct nicotinic agonist

A

Acetylcholine/nicotine: agonists (Varen Succed DAN: direct nicotinic agonists)

  • varenicline (partial nicotinic agonist)
  • succinylcholine (paradoxical action: brief fasiculation followed by flaccid paralysis)
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14
Q

Direct nicotinic agonist toxicity: cause

A 
nicotine and varenicline
Nicotine: 
- acute
    ~ N/V/D
    ~ Cardiac (HTN, arrythmias) 
    ~ CNS: seizures, depolarizing blockade 
- chronic CV and GI risk
Varenicline
- nausea
- CNS: insomnia, abnormal dreams psych
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15
Q

Direct nicotinic agonist toxicity: succinylcholine

A
  • paralysis (prolonged)
  • malignant hyperthermia
  • myopathy
  • hyperkalemia (continue depolarization causes continuous efflux of K)
    (Hypnotize My Mind Please)
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16
Q

AChE inhibitors: general

A

Indirect cholinergic agonist (inhibits degradation in the synapse)
- treatment for myasthenia gravis (edro, neo and phyo caused ester agony)
- edrophonium (short acting: non-covalent bond)
- neostygmine
- phyostigmine
~ stigmines: nonlabile covalent bond long lasting (Stygmines styck around)

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17
Q

Organophosphate poisoning: MOA and trt

A
  • Covalent bonding
  • muscarinc and nicotinic toxicity
  • trt: atropine and pralidoxamine (ACH antagonism and AChE regeneration)
    (spray at toxic at bugs: atropine + pralidoxamine)
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18
Q

Central AChE inhibitors (DRG): examples (3), indications, toxicities

A
  • indicated in dementia esp. Alzheimer’s
  • relatively selective for CNS AChE (DRG)
  • toxicity: GI, dizziness, bradycardia, hepatotoxicity
  • e.g.
    ~ Donepezil
    ~ galantamine
    ~ rivastimine
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19
Q

Adrenergic receptor: general

A

G-protein linked

  • a1: Gq (Phospholipase C)
  • a2: Gi (decrease cAMP)
  • B1/2: Gs (increase cAMP)
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20
Q

Dopamine pathway

A

Tyrosine -THB-> L-dopa -pyridoxal phosphate-> dopamine -vitamin C-> norepi -s-adenysylmethionine-> epi

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21
Q

Catecholamine affinity

A 
NE: high for a1/2 and lower for B1
Epi: dose dependent
- low dose B predominates 
- high dose a predominates 
DA: also dose dependent 
- low dose: dopamine 
- moderate dose: high affinity to B1, lower for a1 and dopamine
- high dose: a1 over B1
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22
Q

Alpha Agonists

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A

a1: vasoconstriction
- systemic: phenylepherine, midorine
- local: phenylepherine, oxymetazoline, tetrahydrazoline

a2: negative feedback on central and peripheral adrenergic *note-even though its adrenergic, stimulating it decreases symp.
- neurons - decrease NE release/sympathetic outflow
- Clonadine, methyldopa, dexmedetomidine, tizanidine

AA is for potheads) (sMoking local POT causes agony, Come To My Drugstore: drugstore will help you take less)

23
Q

Non-selective alpha antagonists

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A

Phenoxybenzamine (irreversible)
Phentolamine (reversible)
- pro-op pheo management
(NSAA popt into space to get iron from a meteor)

24
a1-antagonists
- inhibit vasoconstriction (a1med) and prostate sm. muscle contrxn. - terazosin - tamulosin Alpha An: a ninja
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Clinical indications for a1 inhibitors
- blockade of a1 vasoconstriction, vascular and prostatic for BHP and 2nd line for HTN - terazosin, doxazosin, prazosin - a1a antagonist: tamulosin for BHP - risk of hypotension alpha: elite ninjas Put Tangos Down)
26
a2 antagonists:
Minimal clinical utility: increases sympathetic outflow | - mirtazapine (antidepressant) exhibits central a2 antagonism as one MOA
27
Non-selective B agonist: 1
Isoproteronol (terrornol) - B1: increases HR/contractility (B1) - B2: induces vascular and bronchial sm. muscle realaxation - rarely clinically used: tachyarrythmias, palpitations Doberman causes terror
28
B1 adrenergic AGonist
Dobutamine: - enatiomers have competing B1 and a1 effects -> B1 antagonism - causes positive inotropy with minimal increase in HR and without vasoconstriction (Doberman causes terror, less hr increase/vasodilation) BAG): they put 1BAG over the dobermans head to make it less frightening)
29
Clinical indications for dobutamine and toxicity
Phamacological Cardiac stress test Acute decompensating heart failure Cardiogenic shock Toxicity: arrythmias, HTN and tremors
30
B2 adrenergic agonists: short and long acting
``` (2 Bags of alcohOL) Short: albuterol et al - 5-15 min onset; 3-4 hour duration - acute asthma trt (1st line) - COPD, hyperkalemia (2nd line) (IV albuterol) ``` Long: salmeterol et al - 15-50 minute onset; 12-24 hour duration - chronic asthma trt (prevents bronchospasm)
31
B3 - adrenergic agonists
Mirabegron (miraBegron, Bladder, Beta = 3) - over active bladder - toxicity: HTN, Tachycardia - drug interactions: CYP3A4, 2D6
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B blockers: 4 types
Non-selective B1 selective Selective vasodilators Sympathomimetics
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Non-selective B antagonists
Tim antagonized the Pro and got kicked in the Nads. The boys (beta) lolled) LOLs: propranolol, nadolol, timolol - B1 blockade: decreases heart contractility - decrease in renin release - B2 blockade: many non-cardiac symptoms, tremor and glaucoma - highly lipophilic, on the way out for CV indications
34
Vasodilation B blockers:
a/B blockers: carvedilol, labetalol - vasodilation - more commonly used for CV indications B blockers with NO (nitrous oxide) effect: Nebivolol - B1 selective - increases NO release from endothelium - NO B Nebivolol
35
B- sympathomimetics
they pinned a medal on the ace mime Acebutolol, pindolol - partial B1 agonist with or without B2 activity - for PTs. With CV indications who can't tolerate Beta blockade - rarely used (less effective than full antagonists)
36
Indications for B blockers
HTN: 1st line only for PTs. With additions CV indications Ischemic HD Chronic HF Arrythmias
37
B blocker toxicity
``` CV: - bradycardia, or block - hypotension - worsening of acute HF Peripheral - bronchospasm - masked hypoglycemia - worsening PVD - impotence CNS - fatigue - depression (assoc with lipophilicity) Decreaseed exercise tolerance Management of overdose: IsoproTERRORnol, glucagon ```
38
Catecholamine storage inhibitor: use, MOA, toxicities
Reserpine - irreversible inhibitor of VMAT - depletes: norepi, epi, serotonin and dopamine - used to be used for HTN - toxicities: depression, anxiety, psychosis
39
Catecholamine Storage inhibitors
MOA: promotes release of stored catecholamines | clinical indication: ADHD, narcolepsy, obesity (phentermine only)
40
False neurotransmitters:
Tyramine: many food and drug interactions with MAOIs - in beer, wine, aged cheese, live, fave beans - displaces NE -> can lead to HTN crisis Tyr is a false god, but encountering him will raise your BP
41
Storage inhibitors: mixed action sympathomimetics; MOA, Indications (mimics are false: pseudo)
Ephedrine, pseudoephedrine - MOA: Nonselective a/B agonist - enhanced norepi release - MOA: decongestant (Sudafed)
42
Catecholamines reuptake inhibitors
``` Amy and Velna were a pain when they cockblocked atom from picking up Sarah Tonin because atom was hyper) Cocaine: potent NET inhibitor - c-II controlled substance Atomoxerine - less potent that cocaine - used to trt ADHD - minimal CV risk (Clonadine like effect) SSRIs/SNRIs - amitriptyline (SS) - venlafaxine (SN) - for depression and neuropathic pain ```
43
MAOIs: function, interactions, SE
MOA: inhibition of MAO increases available catecholamines for release - effects both a and B receptors - interaction with tryramine -> HTN crisis - serotonin syndrome ~ anti-depressants and seretonergic meds (tramadol, meperidine, dex, St. John wort) ~ hyperthermia, HTN, myoclonus, rigidity, autonomic instability, and mental status changes
44
Chol
Direct ACh agonist: choline esters - carbachol - bethanachol
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Receptor locations: a1
Iris radial smooth muscle Vascular smooth muscle; skin, mucosa, viscera GI/UG sphincters, (contraction: pressure builds) Pilomotor - Gq (act Phospholipase C - IP3/DAG)
46
Receptor locations: a2
GI walls: activation (auto receptors decrease sympathetic flow) Sympathetic preganglionic auto receptors (decrease NE) (MAIN) Pancreatic islet cells (decrease secretion) - Gi (decrease cAMP)
47
B1 receptor locations
Heart (increase contractility, CO) Kidneys: (increase renin release-> increase BP) - Gs (increase cAMP)
48
B2 receptor locations
- AIRWAY: vaso/bronchodilation - All other Sm. muscle - Gs (increase cAMP)
49
M1: receptor location
CNS, parasympathetic | - Gq (Phospholipase C-> IP3/DAG)
50
M2 receptor locations
Heart | -Gi (decrease Phospholipase C - IP3/DAG)
51
M3 receptor locations
Et al | - Gq (act Phospholipase C - IP3/DAG)
52
Zosin
Alpha-1 antagonists
54
Cycloplegia
- Loss of parasympathetic accommodation reflex | - blurred vision sans Diplopia
82
ANS receptor for which there are no drugs (or of little clinical significance)
Nonspecific alpha agonist Alpha-2 Antagonist Beta-2 Antagonist
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