Block 1: Cholinergics 4: Nicotinic Agonists And Antagonists

Front 1

Nicotinic agonist effects

Back 1

days of the week: MTWThF
mydriasis
muscle cramps
tachycardia
weakness
twitching
hypertension
hyperglycemia
fasciculation

Front 2

How do Nn receptors differ from Nm

Back 2

Nn are blocked by C6
Nm are blocked by tubocurarine

Front 3

Sequence of transmission at autonomic ganglia

Back 3

ACh --> rapid EPSP (Nn) = main event- depolarization
ACh -> slow IPSP (M2)
ACh -> slower EPSP (M3)
peptide release --> late slow EPSP (peptidergic receptors)

Front 4

two nicotinic agonists

Back 4

nicotine- low conc
and DMPP

Front 5

low conc nicotine effects

Back 5

stimulate Nn --> inc BP, salivation, nausea, vomiting

Front 6

high conc nicotine effect

Back 6

depolarizing blocfk of ganglionic transmission (both parasympathetic and sympathetic!)
also stimulates sensory receptors

Front 7

rapid onset of nausea, salivation, abdominal pain, vomiting, diarrhea, cold sweat, headache, dizziness, distrubed hearing and vision, mental confusion, weakness -->
prostration, dec BP, difficult breathing, weak rapid pulse, convulsions -->
death

Back 7

acute nicotine poisoning = green tobacco sickness

Front 8

action of hexamethonium

Back 8

C6 is a non-depolarizing (as compared to nicotine which was depolarizing) ganglionic blocking drug- no longer used clinically, used to be used for HT

Front 9

How many molecules of ACh are needed to activate Nm

Back 9

2

Front 10

mechanism of action of non-depolarizing Nm blockers

administered?

Back 10

compete with (therefore may be overdcome by) ACh for receptor binding
cause weakness --> flaccid paralysis (muscle contraction can still be caused by direct stimulation)

IV administration

Front 11

pancuronium

Back 11

long acting

Front 12

vecuronium

Back 12

intermediate acting

Front 13

rocuronium

Back 13

intermediate acting

Front 14

atracurium

Back 14

intermediate acting
metabolized by plasma cholinesterase*

Front 15

mivarurium

Back 15

short acting
metabolized by plasma cholinesterase

Front 16

tobucurarin

Back 16

long acting
prototype non-depolarizing Nm blocker
*some ganglionic blockade*- hypotension and tachycardia

Front 17

Mechanism of action of depolarizing Nm blockers

Back 17

activate -> open -> desensitize channel
persist at NMJ because they are resistant to acetylcholinesterase

Front 18

phase I of depolarizing Nm blockers

Back 18

persistant depolarization
fasciculations --> flaccid paralysis
inactivate Na channels
muscle contraction cannot be elicited by direct stimulation

*enhanced by adding ACh

Front 19

phase II of depolarizing Nm blockers

Back 19

flaccid paralysis
end-plate depolarization decreases
muscle repolarizes

Front 20

prototype drug of depolarizing Nm blockers:

administration
onset
duration
metabolism

Back 20

succinylcholine

IV admin
<1 min onset
<5 min duration
metabolized by plasma cholinesterase

Front 21

what may happen if you use succinylcholine in pt's with trauma, burns, nergve damage, renal failure, taking digitalis and diuretics

Back 21

hyperkalemia- potentially life-threatening

Front 22

what may happen if you use succinylcholine in pt's with homozygous mutation for atypical plasma cholinesterase gene?

Back 22

prolonged apnea
can use a dibucaine number plasma cholinesterase test (not routinely used because of low prevalence)

Front 23

what may happen if you use succinylcholine and halothane together or if the pt has a defect in the ryanodine receptor

Back 23

malignant hyperthermia

Front 24

tx malignant hyperthermia

Back 24

dantrolene
(Ryan is the deficient Receptor and Dan is the antiDote)
cooling oxygen
control acidosis

Front 25

5 common uses of succinylcholine

Back 25

muscle relax for abdominal surgery
muscle relax for orthopedic procedures
muscle relax for intubation
muscle relax for bronchoscopy, laryngoscopy, esophagoscopy, etc
prevent trauma during EST

Front 26

would you use more or less inhaled anesthetics while on a non-depolarizing Nm blocker

Back 26

less

Front 27

use more or less local anesthetic while useing non-depolarizing or depolarizing Nm blockers

Back 27

less

Front 28

use more or less Ca channel blockers while using non-depolarizing and depolarizing Nm blockers

Back 28

less

Front 29

what types of antibiotics can cause some neuromuscular blockade

Back 29

aminoglycosides and tetracyclines

Front 30

Two causes of Myasthenia gravis

Back 30

autoimmune- most common
congenital- rare

Front 31

MG sx

Back 31

muscle weakness, abnormal fatiguability
cranial muscles most notable
limb muscles
myasthenic crisis- respiratory distress

Front 32

dx of autoimmune form

Back 32

decremental response of mm to repetitive stimulation of motor neuron
Tensilon test (edrophonium)
Nm antibodies
biopsy

Front 33

tx of MG

Back 33

pyridostigmine (AChE inhibitor)
immunosuppresion
plasmapharesis to remove Nm Ab's
thymectomy (up to 1/2 remission)

Front 34

4 uses of botulinum toxin

Back 34

ocular- strabismus
esophageal- achalasia
vocal cord- spasmodic dysphonia
reverse signs of aging

IRREVERSIBLE ACh release block but muscle reinnervates in 3-6 months so must repeat dose

Front 35

non-depolarizing vs. Phase I vs. Phase II
end-plate potential
onset
dose-dependence
recovery
anticholinesterase
muscle response

Back 35

no effect depolarized repolarized
--- immediate slow
--- low high
--- fast slow
reverse augment reverse
weak--> fascic--> flaccid
flaccid flaccid