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RCS > L2, L4- Cholinergic Drug Overview > Flashcards

L2, L4- Cholinergic Drug Overview Flashcards

1
Q

compare direct and indirect cholinergic agonists

A

Direct- binds and activates muscarinic or nicotinic receptors

Indirect- inhibits AChE

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2
Q

therapeutic direct acting cholinergic drugs preferentially bind (nicotinic/muscarinic) receptors

A

muscarinic

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3
Q

list the direct effects of ACh on the cardiovascular system (ignore dosing)

A

-vasodilation (M3)

  • dec cardiac rate (M2)
  • dec rate of conduction in SA and AV nodes (M2)
  • dec force of heart contraction (M2)
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4
Q

compare the cardiovascualar effects of ACh administered at low and high doses

A

Low: dec BP due to vasodilation (M3) –> reflex tachycardia: baroreceptors overpower low dose ACh

High: dec BP due to vasodilation (M3), bradycardia (M2): ACh effect&raquo_space; baroreceptors

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5
Q

describe the effects of ACh on the following:

1) vasculature
(2) eyes (x2
(3) inc secretions from what glands?
(4) lungs
(5) heart
(6) GI tract
(7) bladder

A

1- (endothelial cells) NO release => vasodilation and dec BP
2- miosis (iris: pupil constriction), lens accommodation (ciliary muscle)
3- salivary, sweat, lacrimal glands
4- bronchial constriction and inc secretions
5- dec HR, dec conduction velocity
6- inc tone, peristalsis, secretions + sphincter relaxation
7- detrusor muscle contraction + relaxation of sphincter
(Note- erections for males, variable effects on uterus for females)

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6
Q

describe the effect of large doses of ACh given with atropine

A

-atropine is a muscarinic antagonist
-=> ACh produce a nicotinic response: inc BP, vasoconstriction
-due to stimulation of SNS ganglia and Epi. release via adrenal medulla stimulation
(Note- must be a significantly large dose)

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7
Q

what are the two forms choline agents come in and what does it indicate about its effects

A
  • quaternary ammonium: polar, doesn’t cross BBB

- tertiary amine: nonpolar, crosses BBB (acts on CNS)

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8
Q

list the 4 choline esters

A
  • ACh
  • methacholine
  • carbachol
  • bethanechol
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9
Q

compare ACh metabolism with the rest of the choline esters

A
  • ACh is metabolized rapidly (by plasma BChE and AChE, 5-20 sec)
  • methacholine, carbachol, bethanechol are more resistant to hydrolysis by cholinesterases
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10
Q

list the generalized adverse effects of muscarinic agonists

A
  • sweating
  • salivation
  • flushing
  • low BP
  • nausea, abdominal pain, diarrhea
  • bronchospasm
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11
Q

describe the effect of nicotine at low doses

A
  • ANS ganglia stimulation via depolarization => simultaneous SNS/PSNS activation
  • CV (SNS): inc BP, HR
  • GI/GU (PSNS): n/v/d, voiding of urine
  • Secretions from SNS/PSNS
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12
Q

describe the effect of nicotine at high doses (and symptom of acute poisoning)

A
  • ANS ganglia blockade + neuromuscular blockade
  • Poisoning: n/v/d, abdominal pain, salivation, cold sweat, mental confusion, weakness’ BP falls, weak pulse => death via paralysis of respiratory muscles or central respiratory failure
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13
Q

compare the mechanisms of action of 3 types of anti-cholinesterases (aka the type of binding)

A

1) edrophonium: reversible non-covalent binding with AChE (short-lived: 2-10 mins)
2) carbamates: covalent binding with AChE (.5-6 hrs)
3) organphosphates: AChE phosphorylation => extremely stable covalent bond + very slow hydrolysis

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14
Q

organophosphates will (1) cholinesterases, which will in turn undergo a process called (2) in order to (3)

A

1- phosphorylate
2- ageing
3- strengthens the phosphorus-enzyme bond

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15
Q

compare the effects of low and high doses of liposoluble anti-cholinesterases

A

Low- inhibition => CNS activation

High- convulsions –> coma + respiratory arrest

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16
Q

describe the effects of anti-cholinesterases on the cardiovascular system (moderate and toxic doses)

A

-activates both SNS/PSNS + activates AChRs on cardiac and vascular smooth muscle

  • PSNS effects in the Heart (at moderate doses): negative chronotropic / dromotropic / ionotropic effects => fall in CO, modest bradycardia
  • SNS effects on vasculature (at moderate doses): inc systemic vascular resistance and BP

-Toxic doses: marked bradyardia, significant dec in CO, hypotension

17
Q

describe the effects of anti-cholinesterases in the NMJ

A
  • inc strength of contraction

- used to reverse action of non-depolarizing neuromuscular blockers (+ myasthenia gravis Tx)

18
Q

(1) drugs related to ACh can be used in Alzheimer’s disease, this includes the following, (2), and has the purpose to (3)

A
  • AChE inhibitors: donepezil, rivastigmine, galantamine

- slows the progression of Alzheimer’s, but does not reverse or treat it

19
Q

(1) can be used to split the phosphorous-enzyme (P-AChE) bond made by organophosphates if given before (2). This is usuful in the treatment for (3).

A

1- pralidoxime
2- ageing
3- organophosphate insecticide poisoning (cholinesterase regenerator)
(Note- given after muscarinic antagonist like atropine)

20
Q

list the types of cholinergic antagonists

A
  • muscarinic receptor antagonists
  • nicotinic receptor antagonists: ganglion blockers (Nn) and NMJ blockers (Nm)
  • presynaptic acting drugs (M2)
21
Q

list the effects of atropine on the following:

(1) eyes
(2) GI
(3) GU
(4) secretions

A

1- mydriasis, cycloplegia (ciliary muscle paralysis - loss of accommodation)
2- reduced gastric motility
3- dec hypermotility of bladder
4- dec salivary (dry mouth), dec sweat (=> hyperthermia), dec lacrimal (dry eyes) secretions

22
Q

list the effects of atropine on the cardiovascular system at low and moderate/high doses

A

Low: presynaptic M2 receptor blockade increases ACh release => bradycardia

Moderate/High: atrial M2 receptor blockade => tachycardia; cutaneous vasodilation

23
Q

list the adverse effects of atropine

A
  • dry mouth (no salivary secretion), blurred vision (mydriasis, cycloplegia), sandy eyes (no lacrimal secretion), tachycardia (atrial M2 blockade), constipation (dec GI motility), urinary retention (inc bladder relaxation)
  • CNS effects (b/c tertiary amine): restlessness, confusion, hallucinations, delirium —> depression, collapse of circulatory / respiratory systems —> death
24
Q

what are the contrindications of using antimuscarinic agents

A
  • angle closure glaucoma
  • Pts with prostatic hypertrophy (worsens urinary retention)
  • elderly: sensitive to neurological changes (especially dementia patients)
25
Q

list the 2 mechanisms of nicotinic ganglion blockers

A

1) prolonged depolarization (nicotine is agonist –> antagonist effects with prolonged exposure)
2) AChR-N antagonism (hexamethonium, mecamylamine)

26
Q

what are the uses for ganglion blockers (nicotinic antagonists)

A

rarely used because there are many more selective autonomic agents available

27
Q

list the effects of ganglionic blockade on the following:

(1) vasculature
(2) heart
(3) eyes
(4) GI tract
(5) bladder
(6) sweat glands
(7) salivary glands

A

1- (α1) vasodilation, venodilation, hypotension
2- (M2) inc HR
3- (M3) mydriasis, cycloplegia
4- (M3) reduced tone/motility, constipation, dec secretions
5- (M3) urinary retention
6- (M3) anhydrosis
7- (M3) xerostomia (dry mouth)

28
Q

xerostomia =

A

dry mouth (absent salivary flow)

29
Q

what is the biggest risk with using depolarizing blockers and what can be used to prevent it

A

(succinylcholine)

  • Malignant hyperthermia: excessive Ca++ release from SR
  • usually from combination of succinylcholine + halogenated anesthetic
  • Tx with dantolene –> prevents Ca++ release from SR
30
Q

(1) is prevents the synthesis of ACh by blocking (2) which functions to (3)

A

Hemicholium-3: blocks CHT (Na+/choline symporter), prevents uptake of choline necessary for ACh synthesis

31
Q

(1) prevents the storage of ACh by blocking (2) which functions to (3)

A

Vesamicol: blocks VAChT (H+/ACh antiporter), prevents ACh storage w/in vesicles

RCS (29 decks)

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