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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
Q

“DUMBBELSS”

A 
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
Q

cyclospasm

A 
excessive accomodation (marked ciliary contraction)
* may be from cholinergic agonists
26
Q

miosis

A

reduction in pupil size due to circular muscle contraction

* may be induced by cholinergic agonists

27
Q

accomodation

A

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
Q

Glaucoma

A

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
Q

Sjogren’s Syndrome

A

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
Q

Atonic/neurogenic bladder & ileus

A

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
Q

Myasthenia Gravis

A

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
Q

Anti-cholinergic overdose

A

ie: atropine, tri-cyclics (anti-depressants), some plants (belladonna, jimson weed)
- -> hallucinations, hyperthermia (esp. in children)
* Antidote: physostigmine (AChE inhibitor)

33
Q

Organophosphate poisoning (OR cholinergic overdose)

A

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
Q

muscarinic AChR antagonists

A
  • block receptor binding, non-selective*
    1. atropine
    2. ipratropium
    3. scopolamine
35
Q

nicotinic AChR antagonists

A

block receptor binding
Ganglionic blockers:
1. mecamylamine 2. trimethaphan (3. Nicotine)
Neuromuscular blockers:
1. cisatracurium 2. rapacuronium 3. succinylamine
4. tubocurarine (5. nicotine)

36
Q

relative CNS distribution of Muscarinic cholinergic antagonists

A
  1. scopolamine (HIGHest)
  2. atropine (~high)
  3. Ipratropium (low)
37
Q

general effects of cholinergic antagonists

A

Induce: “Blind, hot, red, mad”
(mydriasis/cycloplegia, increase temp, confusion/hallucination/delirium… dysregulation & death)

Block: “SLUD” = salivation, lacrimation, urination, defecation

38
Q

mydriasis

A

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
Q

drugs to treat asthma

A 
#1. epinephrine/beta-2 agonists
2. ipratropium ( 2nd choice, if don't tolerate B-2 agonists well)
Also: cysteine-leukotriene inhibitors
40
Q

COPD (chronic obstructive pulmonary disorder)

A

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
Q

depolarizing blockade

A

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
Q

Neuromuscular blockers

A

= 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
Q

phases of depolarizing neuromuscular blockers:

A

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
Q

pharmacokinetic characteristics of neuromuscular blockers

A
  • low distribution to CNS (highly polar)
  • administer by IV (inactive if taken orally)
  • vary in onset time and duration of action*
45
Q

timing of neuromuscular blocker action (onset/offset)

A

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
Q

tubocurarine metabolism pattern

A

(a neuromuscular blocker)
excreted in urine unchanged,
- terminate action w/ re-distribution.

47
Q

rapacuronium metabolism pattern

A

(a neuromuscular blocker)
metabolized by Liver,
– action prolonged w/ hepatic disease

48
Q

succinylcholine metabolism pattern

A

(a neuromuscular blocker)
metabolized by esterases,
– action prolonged if low levels pseudocholinesterase
(aka: plasma cholinesterase/butylcholinesterase;
made in liver but located in plasma)

49
Q

cisatracurium metabolism pattern

A

(a neuromuscular blocker)
metabolized spontaneously
– no specific disease influences on duration of action

50
Q

effects of neuromuscular blockers on cardiovascular system

A

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
Q

Major side effects of Neuromuscular blockers:

A
  1. hyperkalemia
  2. malignant hyperthermia
  3. increase intra-ocular and GI pressures, muscle pain

Pharmacology (8 decks)

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