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57 Cards in this Set

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atropine and scopolamine
competitively blocked all five subtypes of the muscarinic receptors
M1, M3, and M5

g-protein...
linked to phospholipase C
M2 and M4

g protein...
linked in an inhibitory manner with adenyl cyclase
M2 mainly acts in the
stomach and heart

(nerves and smooth muscle)
M3 (M2b) mainly acts in the
glands

(smooth muscle, endothelium)
M1, M4, and M5 mainly act in the
nerves and CNS
Dicyclomine
a muscarinic receptor antagonist

antispasmodic
Trihexylphenidyl
muscarinic receptor antagonist
Benztropine
a muscarinic receptor antagonist

Parkinson's
Gallamine
a muscarinic receptor antagonist

MNJ blocker
nicotinic receptor structure
5 subunit Na+/K+ ion channels
Nm

Nicotinic receptor, the muscle type
end plate receptor; located at the skeletal muscle neuromuscular junction

5 subunit Na+/K+ ion channels

the mechanism: Na+, K+ depolarizing ion channel
Nn

Nicotinic receptor, the neuronal type
ganglion receptor

location: postganglionic cell body, dendrites

alpha and beta subunits only

the mechanism: Na+, K+ depolarizing ion channel
Nn and Nm are structurally different enough (5 units vs. 2 units) so...
that semi-selective antagonists exist for ganglia and for the MNJ
Atropine
prototypical muscarinic blocker

found in common plant, jimson weed
Signs of atropine poisoning
interruption of normal cholinergic tone to end organs which intensifies sympathetic effects in same end organ
Effects of atropine poisoning
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)
Cycloplegia
blurred vision

an effect of atropine poisoning
Ipatropium
bronchodilator...by blocking muscarinic receptor

for asthma
Tiotropium
bronchodilator (acts longer)...by blocking muscarinic receptor

used for asthma
Scopolamine
anti-cholingergic

used as an anesthetic adjunct to decrease bronchial secretions and to induce amnesia
Scopolamine transdermal patches
anti-cholingergic
used for motion sickness
Perenzipine
muscarinic receptor blocker
used to manage peptic ulcers
Dicyclomine
used to induce constipation in people with irritable bowel syndrome

muscarinic receptor blocker
When overdose of atropine in children
ice baths for fever
When overdose of atropine in adults
restrains and observation for self-destructive acts

catheterize
succinylcholine
only depolarizing blocker at the MNJ in clinical use
Ach and nicotine...although classed as agonists
can produce depolarizing blockade at nicotinic receptors
Phase 1 block
the the persistent occupation of the receptor (nicotinic) causes prolonged depolarization in which the receptor does not respond to any stimulus
Phase 2 block
where the receptor (nicotinic) is desensitized to agonists but will respond to other stimuli(depolarization-desensitization block)
structure of succinylcholine
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
administration of succinylcholine
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
Clearance of succinylcholine
only depolarizing blocker at the MNJ in clinical use

cleared by plasma ChE...patients lacking this enzyme are paralyzed for many hours
What muscles are relaxed first with succinylcholine
large muscles of the chest and abdomen fasciculate first (postoperative pain) and then become flaccid
Malignant hyperthermia caused by succinylcholine
rare patients experience this

caused by uncontrolled release of Ca++ from the sarcoplasmic reticulum
Dantrolene
muscle relaxant that decreases intracellular calcium

used with bicarbonate and ice baths in order to treat muscle rigidness, acidosis, and high fever
What synergizes with succinylcholine
anesthetic gases and aminoglycoside antibiotics
Curare

(d-tubocurarine)
prototype nondepolarizing blocker at MNJ

little used today

produces competitive and reversible block
never give curare or such a drug to...
unanesthetized patients, and never let a patient emerge from anesthesia before reversing the paralysis with neostigmine
Pancuronium
competitive nondepolarizing MNJ blocker

aminosterol

cleared by renal excretion
Bad in renal disease
Pancuronium

competitive nondepolarizing MNJ blocker
Rocuronium
competitive nondepolarizing MNJ blocker

cleared by liver metabolism

aminosterol
Vercuronium
competitive nondepolarizing MNJ blocker

cleared by liver metabolism

aminosterol
Cisatracurium
competitve nondepolarizing MNJ blocker

benzoisoquinoliniums

cleared by the liver and plasma esterases even though they are nondepolarizers
Okay in both renal disease and liver disease
cisatracurium
Bad in liver disease
rocuronium and vercuronium
How competitive nondepolarizing MNJ blockers affect muscles...
small muscles affected before large ones (opposite of succinylcholine)
The effects of competitive nondepolarizing MNJ blockers reversed with...
neostigmine

(this will increase ACh...a carbamate ChE inhibitor)
The side effects of competitive nondepolarizing MNJ blockers
(pancurium, rocuronium, vercuronium, and cisatracurium)

tachycardia, hypertension, histamine release; interactions with anesthetics and aminoglycosides
One ganglionic blocker
NONDEPOLARIZING COMPETITIVE

Trimethaphan
Trimethaphan
only ganglionic blocker in clinical use

nondepolarizing competitive
Actions of trimethaphan
blocks all ganglia, but is used for its effects on sympathetic ganglia

used for emergency control of hypertensive crisis or surgery for aortic aneurysm
Effects of trimethaphan
dissipated in minutes

cleared by the liver
Side effects of trimethaphan
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
Botulism toxin
blocks the neuronal release of ACh
Activity of botulism toxin
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
Botulism toxin...most toxic molecule known...other uses:
1. BoTox: to remove facial wrinkles and prevent hyperhydrosis

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