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304 > ANS II > Flashcards

ANS II Flashcards

1
Q

parasympathetic effects can be mimicked by..

A
  • muscarinic receptor agonists (carbachol, pilocarpine)

- acetylcholinesterase inhibitors (neostigmine)

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2
Q

parasympathetic effects can be blocked by..

A
  • muscarinic receptor antagonists (atropine)

- skeletal neuromuscular junction blockers (D-tubocurarine)

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3
Q

parasympathomimetics

A

stimulates parasympathetic nervous system

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4
Q

therapeutic uses of parasympathomimetics

A
  • reduce intraocular pressure in glaucoma; facilitate outlflow of aqueous (can cause cataracts with long term use)
  • increase peristalsis of GI tract
  • increase motility of urinary tracts
  • increase salivary secretions
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5
Q

ACh released at the synapse acts for a few milliseconds before..

A

it is metabolized in the synapse

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6
Q

acetylcholinesterase (AChE)

A

metabolize ACh in the synaptic cleft on the outer membrane of the post junctional cell

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7
Q

two types of cholinesterase enzymes

A
  • AChE

- butyrylcholinerterase (BuChE; aka plasma/pseudoChE)

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8
Q

BuChE

A

-located at non-neuronal sites; plasma and liver

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9
Q

Most enzyme inhibitors used clinically … discriminate between the two types of ChE

A

DO NOT

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10
Q

AChE inhibitors

A

increase duration of action of the released ACh at the synapse

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11
Q

3 types of chemical reaction that is produced by cholinesterase

A
  • acetylation
  • carbamylation
  • phosphorylation
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12
Q

acetylation

A

introduce an acetyl group

-acetylated enzyme recovers rapidly

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13
Q

carbamylation

A

enzyme recovers more slowly, 3-4 hours

  • reversible
  • used therapeutically
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14
Q

phosphorylation

A
  • poisons the enzyme
  • irreversible
  • 6 hours
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15
Q

catalytic region of cholinesterase enzyme

A

ser-OH

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16
Q

neostigmine

A

a reversible AChE inhibitor that causes carbamylation

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17
Q

diisopropyl flurophosphate

A

an irreversible AChE inhibitor that causes phorphorylation

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18
Q

2-PAM

A

an oxide that if administered before aging occurs, can bind to and release a phosphate moiety attached to the enzyme during phosphorylation; reversing the enzyme inhibition

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19
Q

donepezil and tacrine (also rivastigmine and galantamine)

A

ChE inhibitors in the CNS that have higher affinity and partition into lipids and cross the blood/brain barrier

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20
Q

ChE inhibitors in the intestine

A

relax sphincters to facilitate peristaltic movement (in postoperative ileum, congenital megacolon)

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21
Q

ChE inhibitors in the bladder

A

treat urinary retention due to atony of smooth muscle

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22
Q

ChE inhibitors in the skeletal muscle neuromuscular junction

A

LOW doses used to treat patients with myasthenia gravis, who have weakness of skeletal muscles
-also used to diagnose it

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23
Q

intermediate doses and high doses ChE inhibitors in skeletal muscle neuromuscular junction

A

i: fasciculations and fibrillations
h: persistent depolarization and muscle paralysis

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24
Q

anti-ChE agents

A

reverse antagonisms by competitive neuromuscular blockers but add to the depolarization and paralysis by succinylcholine and make it worse

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25
Q

muscarinic receptor agonists/ChE inhibitor SIDE EFFECTS

A

increased urinary frequency, diarrhea, vomiting, bradycardia, hypotension, increased salivation, miosis,

26
Q

botulinum toxin

A
  • blocks ACh release

- used to paralyze skeletal muscles

27
Q

clinical uses of botox

A
  • strabismus (unaligned lines of vision),
  • blepharospasm (contracted eyelid)
  • hemifacial spasm
28
Q

cosmetic use of botox

A

to remove facial wrinkles

29
Q

muscarinic cholinergic receptor blockers

A
  • belladonna alkaloids (atropine, scopolamine)

- semisynthetic and synthetic (dicyclomine, ipratropium, oxybutynin)

30
Q

therapeutic uses of muscarinic receptor antagonists

A
  • to treat severe bradycardia
  • cause pupil dilation (used for examination of retina)
  • to treat excessive peristalsis of irritable bowel syndrome
  • decrease gastric acid secretion
  • to treat urinary incontinence
  • block M1 receptors in vestibular apparatus to treat motion sickness
  • inhibit excessive salivary and respiratory tract secretions
31
Q

ipratropium and tiotropium

A

derivatives of atropine that treat COPD

  • administered by inhalation to cause bronchodilation
  • NOT absorbed into systemic circulation
32
Q

trihexyphenidyl and benztropine

A

to treat uncoordinated muscle contraction (Parkinson’s)

33
Q

scopolamine vs atropine

A
  • scopolamine well absorbed orally and reaches brain more readily than atropine
  • scopolamine 1-x more potent at producing CNS effect
  • great fraction of scopolamine present in a unionized form to facilitate absorption through skin
  • scopolamine used for motion sickness as a transdermal patch
34
Q

muscarinic receptor antagonists SIDE EFFECTS

A
  • urinary retention
  • constipation
  • tachycardia
  • dry mouth
  • mydriasis
35
Q

nicotinic cholinergic receptor

A
  • ACh gated sodium channel

- neuromuscular junction blockers

36
Q

two types of neuromuscular junction blockers

A
  • competitive

- depolarizing

37
Q

type of neuromuscular junction blockers based on…

A

electrophysiological differences in their mechanisms of action

38
Q

competitive NM junction blockers

A
  • competitively antagonize the actions of ACh at nicotinic ACh receptors structure different that ACh
  • ex. curare
39
Q

depolarizing agents

A
  • drug occupies and activates nicotinic receptor (agonists) for longer period of time, prevents repolarization
  • structure resembles ACh
  • succinylcholine
40
Q

depolarizing block

A

when depolarizing agents makes muscle fibre refractory to further nerve impulses

41
Q

South Americans and competitive NM blockers

A

native SAmericans used certain plant extracts (d-tubocurarine;strychnos toxifera) as arrow poison that caused muscle paralysis in animals
-curare (generic term)

42
Q

neostigmine, edrophonium, pyridostigmine

A

ChE inhibitors that are used clinically to reverse NM block caused by competitive blockers

43
Q

competitive nm blockers sequence of muscle paralysis

A
  • small rapidly moving muscles first
  • limbs, trunk
  • intercostal muscles
  • diaphragm (respiration stops)

*recovery in reverse

44
Q

competitive nm blockers main side effects

A
  • ganglionic blockade (fall in bp, tachycardia)
  • block of vagal response (increase peristalsis)
  • histamine release (bronchospasm, hypotension, increase bronchial and salivary secretions
45
Q

succinylcholine

A
  • bind to and activates muscle nicotinic receptors
  • short duration of action
  • not metabolized by AChE
  • rapidly hydrolyzed primarily by butyrylcholinesterase in plasma
46
Q

clinical problem with succinylcholine

A

certain patients exhibit several variants of this enzyme, which leads to prolonged and potentially dangerous duration of NM block

47
Q

depolarizing blockers SIDE EFFECTS

A
  • can release K+ rapidly from intracellular sites

- cause hyperkalemia

48
Q

hyperkalemiacan be dangerous in..

A

heart failure patients on digoxin or diuretics

49
Q

malignant hyperthermia

A
  • side effect seen after certain anesthetics and nm blockers (succinylcholine)
  • increase Ca release from SR
  • rigidity, heat production from skeletal muscle, hyperthermia, accelerated muscle metabolism, metabolic acidosis, tachycardia
50
Q

therapeutic uses of NM blockers

A

in surgical anesthesia to obtain relaxation of skeletal muscle, particularly in abdominal wall

51
Q

sympathetic effects can be mimicked by..

A
  • adrenergic receptor agonists (direct)
  • NE uptake blockers (indirect)
  • monoamine oxidase and COMT inhibitors
  • NE releasing agents (indirect)
52
Q

monoamine oxidase and COMT inhibitors

A

delay breakdown of NE and prolong its action

-indirect

53
Q

sympathetic effects can be blocked by..

A

adrenergic receptor antagonists

-ex. prazosin, propranolol

54
Q

termination of NE action at synapse

A

-released transmitter is taken up back into presynaptic nerve terminal by uptake 1

55
Q

uptake 1 blocker

A

increase sympathetic activity

56
Q

baroreceptor

A

control of BP and heart rate

57
Q

epinephrine equipotent at..

A

alpha and beta receptors

58
Q

NE has little activity at..

A

beta 2 receptors

59
Q

isoproterenol

A

most potent sympathomimetic amine; acts exclusively on B receptors

60
Q

therapeutic uses of adrenergic drugs

A
  • allergic reactions/anaphylactic shock (EPIPEN)
  • bronchodilators (asthma)
  • pressor agents (hypotension)
61
Q

therapeutic uses of adrenergic receptor blockers

A
  • hypertension
  • emergency treatment of hypertension
  • hypertension in pheochromocytoma
  • myocardial infarction
  • cardiac arrhythmias
  • migraines
  • benign prostatic hyperplasia
  • glaucoma

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