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Pharmacology > Lectures: ANS 1-4 > Flashcards

Lectures: ANS 1-4 Flashcards

0
Q

Autonomic system which is REQUIRED for life

A

Parasympathetic (“rest and digest”)

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1
Q

drugs that modulate Acetycholine usually affect which steps of signaling?

A
  1. NT binding to post-synaptic Receptor

2. Acetycholine degradation (in synapse)

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2
Q

Autonomic vs. somatic system organization

+ adrenal pathway

A

Autonomic: 2 neurons to target (CNS—>ganglion —> target)
* Adrenal: CNS —> adrenal medulla to circulation
Somatic: 1 neuron to target

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3
Q

Acetylcholine = NT for what parts of ANS

A
  1. ganglionic neurotransmitter
  2. parasympathetic post-ganglionic to target tissue NT
    * 3. Also: somatic NT to target tissue
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4
Q

Most drugs affecting cholinergic signaling act on:

A
  1. Receptor site for ACh

2. ACh degradation in synapse

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5
Q

Nicotinic cholinergic receptors

A

Ionotropic ligand-gated cation channel,
open when depolarized.
* neuronal subunits (ganglia and adrenal medulla): alpha, beta
* NMJ subunits: alpha, beta, gamma, delta/epsilon
–> mediate neurotransmission at
1. ganglionic synapse of symp, parasymp
2. adrenal medulla
3. neuroeffective (target) synapse for sympathetic ANS

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6
Q

Muscarinic Cholingergic receptor

A

metabotropic, serpentine GPCR
5 subunits: M1, M2, M3, (M4 & M5 = in brain)
* drugs act on all subtypes equally!
–> mediate neurotransmission at “neuroeffective” (target) synapse of parasymp. ANS

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7
Q

norepinephrine

A

primary NT at neuroeffective (end/target) synapse of sympathetic ANS

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8
Q

sympathetic stimulation of adrenal medulla

A
  1. signaled to adrenal medulla by ACh (nicotinic R)
  2. adrenal medulla releases epinephrine into blood
    - -> acts throughout body (endocrine signaling)
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9
Q

pattern of adrenergic signaling

A
  1. NE synthesis
  2. uptake into storage vesicles
  3. release NE (as NT)
    * 4. NE binds to R
    * 5. NE removal = Reuptake
  4. metabolism of NE by COMT
    * drugs mostly act on starred steps
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10
Q

pattern of cholinergic signaling

A
  1. synthesis of ACh
  2. storage in vesicles
  3. release ACh (as NT) into synapse
    * 4. ACh binds to R
    * 5. ACh removal = Degradation
  4. ACh recycling
    * drugs mostly act on starred steps
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11
Q

post-ganglionic sympathetic special case NTs/exceptions:

A

Sympathetic post-ganglionic neurons that do NOT use NE as NT

  1. sweat glands = ACh
  2. some vascular sm. muscle in skeletal muscle = ACh
  3. renal vascular sm. muscle = Dopamine
    * Also: some tissues have mAChRs but No Parasymp. input
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12
Q

main/functional differences between Sympathetic and Parasympathetic pathways

A

Sympathetic:
- NE = reuptake at synapse
- High integration (activates all target organs at 1x)
- ganglia near spinal cord (long POST-ganglionic neurons)
Parasympathetic:
- ACh = degraded at synapse
- low integration (activation to targets = separate/individual)
- ganglia near targets (long PRE-ganglionic neurons)

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13
Q

Homeostatic reflexes

A

autonomic signaling influenced by info relayed to CNS integration central by the (original) ANS effector/target.
(multiple feedback loops)

  • important for determining secondary effects of drugs*
    ie: altering BP initiates feedback loops to heart, etc.
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14
Q

Target tissues w/ muscarininc ACh Rs

A

Parasympathetic: cardiac (decrease HR), sm. muscle (vasodilate), exocrine glands, endothelial cells

Sympathetic: sweat glands (activate)

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15
Q

tissues w/ nicotinic ACh Rs

A

somatic/voluntary: skeletal muscle (activation)

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16
Q

tissues w/ alpha adrenergic Rs

A

sympathetic: vascular smooth muscle (vasoconstrict)

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17
Q

tissues w/ beta adrenergic Rs

A

(sympathetic)
Beta-1 and 2: cardiac muscle (increase contractility & HR)
* beta-2: skeletal muscle vasculature (dilate)

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18
Q

Direct-acting Cholinergic Agonists

A
  1. Acetycholine
  2. Carbechol
  3. Bethanechol (m)
  4. Cevilmeline (m)
  5. Pilocarpine (m)
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19
Q

AcetylcholineEsterase (AChE) inhibitors

A

(= indirect cholinergic agonists)

  1. Echothiophate *irreversible
  2. Edrophomium
  3. Neostigmine
  4. Physostigmine
    * less effect at non-firing sites (where normally no active signaling)
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20
Q

Cholinergic agonists (types, characteristics)

A 
aka: cholinomimetics, 
Useful locally (eye, bladder, NMJ); bad side effects if given systemically. 
Types: direct, indirect, organophosphate antidote
21
Q

non-selective ACh agonists

A

Direct: (2/5) acetylcholine & carbechol

Indirect: (all 4)
echpthiophate, edrophonium, neostigmine, and physostigmine

22
Q

cholinergic agonists DURATION of ACTION

A
  • Seconds: ACh
  • Hours:
    a) Bethanechol, Carbechol, Edrophonium
    b) Cevimeline, Piloocarpine (indirect binding)
    c) neostigmine, physostigmine
  • Days: Echothiophate
23
Q

main effects of direct, non-selective cholinergic agonists

A

Heart: low [ ] –> reflex increase contractility,
high [ ] –> bradycardia
Vasc: vasodilate
GI: increase motility & salivation
Resp: bronchoconstriction, increase secretions
Eye: miosis
Urinary: increase voiding ** also: increase sweating! **

24
"DUMBBELSS"
``` side effects from any/all cholinergic agonists... D: diarrhea U: urination M: miosis Bx2: bronchospasm, bradycardia E: excitation (of sk. mm/fasciculations) L: lacrimation Sx2: sweating, salivating ```
25
cyclospasm
``` excessive accomodation (marked ciliary contraction) * may be from cholinergic agonists ```
26
miosis
reduction in pupil size due to circular muscle contraction | * may be induced by cholinergic agonists
27
accomodation
contraction of the ciliary muscle for near vision, helps decrease intraocular pressure by facilitating outflow of aqueous humor * may be induced by cholinergic agonists
28
Glaucoma
condition of increased intraocular pressure damages retina and optic nerve --> restrict visual field/blindness. Types = "open-" or "closed-angle." Meds: #1 pilocarpine (for emergencies) or echothiophate, timolol, prostaglandins
29
Sjogren's Syndrome
autoimmune destruction of secretory glands in eyes & mouth, - -> dry eyes/mouth, organ dysfunction (renal, lungs, vasc., etc)... * primary = alone, secondary = w/ CT disease Meds: pilocarpine, Cevimeline
30
Atonic/neurogenic bladder & ileus
disruption of normal GI motility/urination, bc of: labor/delivery & surgery (--> opioid analgesics) * may occur w/ megacolon --> lack of: peristalsis, detrusor m. tone, sphincter tone Meds: bethanechol, neostigmine
31
Myasthenia Gravis
autoimmune disease causing loss of nACh Rs @ NMJ only (not at ANS ganglia) --> muscle weakness, esp. w/exercise; ptosis/facial mm. weak Meds: 1. Edrophonium: Dx and evaluate dosing 2. neostigmine: long-term management
32
Anti-cholinergic overdose
ie: atropine, tri-cyclics (anti-depressants), some plants (belladonna, jimson weed) - -> hallucinations, hyperthermia (esp. in children) * Antidote: physostigmine (AChE inhibitor)
33
Organophosphate poisoning (OR cholinergic overdose)
ie: pesticides/insecticides, nerve gases, echothiophate - -> Sx depend on dose: low: DUMBBELSS, med: tight chest, can't walk, invol. urination; high: loss of consciousness, seizures, death * Antidote: Pralodoxime (#1), atropine
34
muscarinic AChR antagonists
* block receptor binding, non-selective* 1. atropine 2. ipratropium 3. scopolamine
35
nicotinic AChR antagonists
*block receptor binding* Ganglionic blockers: 1. mecamylamine 2. trimethaphan (3. Nicotine) Neuromuscular blockers: 1. cisatracurium 2. rapacuronium 3. succinylamine 4. tubocurarine (5. nicotine)
36
relative CNS distribution of Muscarinic cholinergic antagonists
1. scopolamine (HIGHest) 2. atropine (~high) 3. Ipratropium (low)
37
general effects of cholinergic antagonists
Induce: "Blind, hot, red, mad" (mydriasis/cycloplegia, increase temp, confusion/hallucination/delirium... dysregulation & death) Block: "SLUD" = salivation, lacrimation, urination, defecation
38
mydriasis
increase in pupil size due to radial muscle contraction, induced by nicotinic cholinergic antagonists (block ciliary muscle contraction (= parasymp) ==> radial m. = unopposed) *useful for eye exams
39
drugs to treat asthma
``` #1. epinephrine/beta-2 agonists 2. ipratropium ( 2nd choice, if don't tolerate B-2 agonists well) Also: cysteine-leukotriene inhibitors ```
40
COPD (chronic obstructive pulmonary disorder)
chronic, irreversible airflow obstruction and cilia loss -- emphysema (SOB) and chronic bronchitis (increased mucus production and cough) Meds: ipratropium or epinephrine/beta-2 agonists
41
depolarizing blockade
when a receptor is so continuously occupied that post-synaptic membrane stops responding (desensitization) aka: ganglionic OR neuromuscular effect (depends on where) -- too much agonist ==> antagonistic function, passes 1. (agonist effect) to cause 2. (antagonist effect). ie: nicotine on nicotinic AChRs
42
Neuromuscular blockers
= nAChR antagonists that f(x) at NMJ. Non-depolarizing antagonists: (*at low [ ], can be out-competed by AChE inhibitors) 1. cisatracurium 2. rapacuronium 3. tubocurarine Depolarizing agonist (functionally antagonistic, neurom. effect) 4. succinylcholine
43
phases of depolarizing neuromuscular blockers:
Phase I: "prolonged depolarization," acts like agonist. - fasciculations and flaccid paralysis * response augmented by AChE inhibitors (even more ACh to flood Rs) Phase II: gradually repolarize, but resistant to depolarization, * not affected by AChE inhibitors
44
pharmacokinetic characteristics of neuromuscular blockers
- low distribution to CNS (highly polar) - administer by IV (inactive if taken orally) * vary in onset time and duration of action*
45
timing of neuromuscular blocker action (onset/offset)
Onset: Succinylcholine (fastest, 1 min.) < Rapacuronium < Cisatracurium < Tubocurarine (slowest, 6 min.) Duration of Action: succinycholine (shortest, 5 min.) < rapacuronium < tubocurarine < cisatracurium (longest, 1 hr.)
46
tubocurarine metabolism pattern
(a neuromuscular blocker) excreted in urine unchanged, - terminate action w/ re-distribution.
47
rapacuronium metabolism pattern
(a neuromuscular blocker) metabolized by Liver, -- action prolonged w/ hepatic disease
48
succinylcholine metabolism pattern
(a neuromuscular blocker) metabolized by esterases, -- action prolonged if low levels pseudocholinesterase (aka: plasma cholinesterase/butylcholinesterase; made in liver but located in plasma)
49
cisatracurium metabolism pattern
(a neuromuscular blocker) metabolized spontaneously -- no specific disease influences on duration of action
50
effects of neuromuscular blockers on cardiovascular system
Tubocurarine: inhibit cholinergic transmission at adrenal medulla --> hypotension, *reflex: tachycardia Succinylcholine: low = parasymp. stim., high = symp. stim. --> bradycardia (low); hypertension & tachycardia (high) Rapacuronium/Cisatracurium: none.
51
Major side effects of Neuromuscular blockers:
1. hyperkalemia 2. malignant hyperthermia 3. increase intra-ocular and GI pressures, muscle pain

Pharmacology (8 decks)

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