Cholinergic Ii

Front 1

atropine and scopolamine

Back 1

competitively blocked all five subtypes of the muscarinic receptors

Front 2

M1, M3, and M5

g-protein...

Back 2

linked to phospholipase C

Front 3

M2 and M4

g protein...

Back 3

linked in an inhibitory manner with adenyl cyclase

Front 4

M2 mainly acts in the

Back 4

stomach and heart

(nerves and smooth muscle)

Front 5

M3 (M2b) mainly acts in the

Back 5

glands

(smooth muscle, endothelium)

Front 6

M1, M4, and M5 mainly act in the

Back 6

nerves and CNS

Front 7

Dicyclomine

Back 7

a muscarinic receptor antagonist

antispasmodic

Front 8

Trihexylphenidyl

Back 8

muscarinic receptor antagonist

Front 9

Benztropine

Back 9

a muscarinic receptor antagonist

Parkinson's

Front 10

Gallamine

Back 10

a muscarinic receptor antagonist

MNJ blocker

Front 11

nicotinic receptor structure

Back 11

5 subunit Na+/K+ ion channels

Front 12

Nm

Nicotinic receptor, the muscle type

Back 12

end plate receptor; located at the skeletal muscle neuromuscular junction

5 subunit Na+/K+ ion channels

the mechanism: Na+, K+ depolarizing ion channel

Front 13

Nn

Nicotinic receptor, the neuronal type

Back 13

ganglion receptor

location: postganglionic cell body, dendrites

alpha and beta subunits only

the mechanism: Na+, K+ depolarizing ion channel

Front 14

Nn and Nm are structurally different enough (5 units vs. 2 units) so...

Back 14

that semi-selective antagonists exist for ganglia and for the MNJ

Front 15

Atropine

Back 15

prototypical muscarinic blocker

found in common plant, jimson weed

Front 16

Signs of atropine poisoning

Back 16

interruption of normal cholinergic tone to end organs which intensifies sympathetic effects in same end organ

Front 17

Effects of atropine poisoning

Back 17

1. delirium, hallucinations
2. blindness (mydriasis, photophobia, blurred vision (cycloplegia))
3. Dry mouth, block of sweating
4. Red: prostaglandins, fever, anhidrosis
5. Hot: anhidrosis, CNS?

(other effects: urinary retention...block of detrussor muscle...bronchodilation, and tachycardia)

Front 18

Cycloplegia

Back 18

blurred vision

an effect of atropine poisoning

Front 19

Ipatropium

Back 19

bronchodilator...by blocking muscarinic receptor

for asthma

Front 20

Tiotropium

Back 20

bronchodilator (acts longer)...by blocking muscarinic receptor

used for asthma

Front 21

Scopolamine

Back 21

anti-cholingergic

used as an anesthetic adjunct to decrease bronchial secretions and to induce amnesia

Front 22

Scopolamine transdermal patches

Back 22

anti-cholingergic
used for motion sickness

Front 23

Perenzipine

Back 23

muscarinic receptor blocker
used to manage peptic ulcers

Front 24

Dicyclomine

Back 24

used to induce constipation in people with irritable bowel syndrome

muscarinic receptor blocker

Front 25

When overdose of atropine in children

Back 25

ice baths for fever

Front 26

When overdose of atropine in adults

Back 26

restrains and observation for self-destructive acts

catheterize

Front 27

succinylcholine

Back 27

only depolarizing blocker at the MNJ in clinical use

Front 28

Ach and nicotine...although classed as agonists

Back 28

can produce depolarizing blockade at nicotinic receptors

Front 29

Phase 1 block

Back 29

the the persistent occupation of the receptor (nicotinic) causes prolonged depolarization in which the receptor does not respond to any stimulus

Front 30

Phase 2 block

Back 30

where the receptor (nicotinic) is desensitized to agonists but will respond to other stimuli(depolarization-desensitization block)

Front 31

structure of succinylcholine

Back 31

two molecules of ACh joined together

functions just like ACh at the MNJ

doesnt get to ganglia

REMEMBER: succinylcholine is the only depolarizing blocker at the MNJ in clinical use

Front 32

administration of succinylcholine

Back 32

remembern: the only depolarizing blocker at the MNJ in clinical use

given as iv. bolus or controlled drip to titrate to desired degree of relaxation

effects within a minute and bolus lasts only 5-7 minutes

Front 33

Clearance of succinylcholine

Back 33

only depolarizing blocker at the MNJ in clinical use

cleared by plasma ChE...patients lacking this enzyme are paralyzed for many hours

Front 34

What muscles are relaxed first with succinylcholine

Back 34

large muscles of the chest and abdomen fasciculate first (postoperative pain) and then become flaccid

Front 35

Malignant hyperthermia caused by succinylcholine

Back 35

rare patients experience this

caused by uncontrolled release of Ca++ from the sarcoplasmic reticulum

Front 36

Dantrolene

Back 36

muscle relaxant that decreases intracellular calcium

used with bicarbonate and ice baths in order to treat muscle rigidness, acidosis, and high fever

Front 37

What synergizes with succinylcholine

Back 37

anesthetic gases and aminoglycoside antibiotics

Front 38

Curare

(d-tubocurarine)

Back 38

prototype nondepolarizing blocker at MNJ

little used today

produces competitive and reversible block

Front 39

never give curare or such a drug to...

Back 39

unanesthetized patients, and never let a patient emerge from anesthesia before reversing the paralysis with neostigmine

Front 40

Pancuronium

Back 40

competitive nondepolarizing MNJ blocker

aminosterol

cleared by renal excretion

Front 41

Bad in renal disease

Back 41

Pancuronium

competitive nondepolarizing MNJ blocker

Front 42

Rocuronium

Back 42

competitive nondepolarizing MNJ blocker

cleared by liver metabolism

aminosterol

Front 43

Vercuronium

Back 43

competitive nondepolarizing MNJ blocker

cleared by liver metabolism

aminosterol

Front 44

Cisatracurium

Back 44

competitve nondepolarizing MNJ blocker

benzoisoquinoliniums

cleared by the liver and plasma esterases even though they are nondepolarizers

Front 45

Okay in both renal disease and liver disease

Back 45

cisatracurium

Front 46

Bad in liver disease

Back 46

rocuronium and vercuronium

Front 47

How competitive nondepolarizing MNJ blockers affect muscles...

Back 47

small muscles affected before large ones (opposite of succinylcholine)

Front 48

The effects of competitive nondepolarizing MNJ blockers reversed with...

Back 48

neostigmine

(this will increase ACh...a carbamate ChE inhibitor)

Front 49

The side effects of competitive nondepolarizing MNJ blockers

Back 49

(pancurium, rocuronium, vercuronium, and cisatracurium)

tachycardia, hypertension, histamine release; interactions with anesthetics and aminoglycosides

Front 50

One ganglionic blocker

Back 50

NONDEPOLARIZING COMPETITIVE

Trimethaphan

Front 51

Trimethaphan

Back 51

only ganglionic blocker in clinical use

nondepolarizing competitive

Front 52

Actions of trimethaphan

Back 52

blocks all ganglia, but is used for its effects on sympathetic ganglia

used for emergency control of hypertensive crisis or surgery for aortic aneurysm

Front 53

Effects of trimethaphan

Back 53

dissipated in minutes

cleared by the liver

Front 54

Side effects of trimethaphan

Back 54

because its used in hypertensive crisis or surgery for aorti aneurysm, its side effects are orthostatic hypotension, urinary retention, constipation, impaired accommodation of lens of the eye (mostly parasympathetic blockade but at ganglionic level)

remember: trimethaphan is the only ganglionic blocker in clinical use and it is nondepolarizing competitive

Front 55

Botulism toxin

Back 55

blocks the neuronal release of ACh

Front 56

Activity of botulism toxin

Back 56

interferes with docking proteins on the interior of the nerve membrane

1. if vesicles can't dock properly, they can't release the neurotransmitter
2. interruption of somatic motor nerve transmission leads to flaccid paralysis
3. interruption of transmission at muscarinic sites produces some signs linke atropine poisoning, but no CNS effects

Front 57

Botulism toxin...most toxic molecule known...other uses:

Back 57

1. BoTox: to remove facial wrinkles and prevent hyperhydrosis

2. in strabismus, blepharospasm, spasmocid torticollis, achalasia, and anal fissures