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67 Cards in this Set

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Lecture 155
Lecture 155
3 Parts of local anesthetic
1. Aromatic residue. 2. Intermediate chain (determines degradation. 3. Terminal Amino group
Which types of anesthetics are excreted which way
Amides - out liver. Esters - Broken in blood.
Henderson Hasselbach
pKa - pH = log (BH/B)
TTX-R contain Na1.8 channel, and conduct pain.
Epinephrine and local anesthetic -
Epi increases duration of action. - via decreased blood flow.
Ca and local anesthetic
Ca decreases local anesthetic efficacy.
Local anesthetic site of action
Na channel - a S6 domain IV
Lecture 156
Lecture 156
ACh synthesis enzyme
choline acetyltransferase
Components of the 'Fusion Machine'
Taxin(binds membrane), Brevin(binds vesicle), S-25(interconnects), Tagmin (senses Ca)
Myasthenia Gravis
Auto immune disease w/ reduced # of nicotinic ACh receptors
Lambert Eaton (myasthenic) syndrome
Decrease calcium channels on nerve terminal
Aminoglycoside antibiotics & neuropathy
Aminoglycoside antibiotics block calcium entry into nerve terminal (Also blocked by Mg2+ & other polyvalent cations
3 uses of nondepolarizing blockers
1. Orthopedic manip. 2. Abdominal surgery 3. Bronchoscopy
4 CI's of SUX
1. Burns 2. Cardiac Arrythmia 3. Liver disease/ChE def 4. Long use
2 short term drugs for intubation
1. SUX 2. Rocuronium
3 drugs paralytics pop for duration of surgery
1. Vecuronium 2. Atracurium 3. Pancuronium
Which drug reverses nondepolarizing block
Anticholinesterases (neostigmine) because nondep block is competitive inhib
Which 2 non-dep blockers are excreted by liver
Vecuronium, Rocuronium
Explain adrenergic control of the blood vessels.
Skin and periphery are innevated by sympathetic alpha receptors. Muscles and liver have b2 receptors so they dilate in response to epinephrine
Explain ANS control of sexual function
Parasympathetic: Erection and mucus production, Sympathetic: alpha 2 inhibit erection alpha 1 cause detumescence
Accomodation is controlled by:
Parasympathetic NS
3 classes of drugs that cause orthostatic hypertension
a1 blockers, Adrenergic neuron blockers, ganglionic blockers
How do muscarinic and nicotinic receptors differ?
Muscarinic have are smaller - bind a diff O on ACh
Explain how PS innervation slows heart rate.
Inhibitory G protein - opens potassium channels, resulting in hyperpolarization.
Explain how PS innervation vasodilates
ACh causes release of EDRF --> cGMP
Contraindications to muscarinic agonists
SOAPT - Shock (cardiogenic), obstruction, asthma, peptic ulcers, hyperthyroid
SLUD syndrome
Salivations Lacrimation Urinary Defecation in irreversible acetylcholinesterase inhibitors. Also cause twitching in muscles and CNS effects
Explain AChesterase
Anionic site holds the Ach near to a serine (which partially shares electrons with a nearby histamine) and it's hydrolyzed)
How does edrophonium work?
Blocks the histamine on ChE
How do the nerve gasses work?
Phosphate groups binds to serine in ChE
Treatment of anti-cholinesterase inhibitors?
Atropine + 2-PAM
Explain how Atropine can treat parkinsons
Parkinsons is a misbalance between Dopamine and Ach. Atropine acts to block the Ach and even out the process (in the nigro striatal pathway)
Atropine Toxicity
Dry, Hot, Red, Blind, Mad
CNS cholinergic muscarinic sites
Emesis, Arousal, Memory,
Effects of ganglion blockers
Mostly similar to Atropine, except vasodilation.
Monoamine Oxidase - hyrdolyzes adrenergics in nerve & effector
Hydrolizes adrenergics in effector only.
Uptake 1 vs 2
Uptake 1: High affinity low capacity. Uptake 2: low affinity high capacity
Product of MAO dehydrogenase in periphery
Product of MAO reducatase in CNS
Alpha binding
EPI > NE (no ISO)
Beta binding
ISO > EPI >> NE (NE no effect on B2)
How do Alpha 1 receptors transduce signal?
Phospholipase C --> Inc. Ca. (SOC's & CRAC channel activated too)
How do Beta receptors work?
G-proteins --> cAMP --> PKA
How do Alpha 2 receptors work?
Control channels via G protein (G protien --> Block ATP, Block Ca, open K)
NE receptors
alpha, beta 1
EPI receptors
alpha, beta 1, beta 2
ISO receptors
Beta 1, Beta 2
Principal effects of alpha 2 agonists
Decrease CO, decrease vascular resistance.
How is clonidine used to distinguish b/t pheochromocytoma and essential hypertension?
It will reduce NE in EH not pheo.
Explain the mechanism of tyramine
Indirect acting sympathomimetic. Enters nerve terminal via uptake 1, pushes NE out.
3 problems w/ indirect sympathomimetics
1. Tachyphylaxis. 2. Don't work w/ unptake 1 inhibitors. 3. Hypertensive crisis w/ MAO inhibitor.
Depletion of NE w/ indirect sympathomimetics --> reduced response.
How do ephedrines work?
Work by both indirect actions as well as agonists (esp of B2)
Toxicity of ephedrines
Very high doses --> a1 peripheral vasoconstriciton.
Explain nasal congestions
a1 controlled venous capacitance vessels (erectile) fill, & secrete mucous. Prolonged inhibition blocks the arterioles, and reactive hyperemia occurs.
Nasal Decong. OD
Eventually, dose affects alpha 2 receptors - venoconstriction & damage to nasal mucosa.
What are the primary and secondary treatments for cardifenic shock
Primary: Dobutamine - specific B1. Secondary : Dopamine - Nonspecific Adrenergic (causes vasoconstriction), may worsen myocardial ischemia.
How is yombine an aphrodisiac
Blocks a2 - PARASYMPATHETIC alpha 2 receptors inhibit tumescence.
Contraindications go phosphidiesterase inhibitors
No Nitrates or A1b blockers.
Name three adrenerginic neuron blockers
Bretylium, Reserpine, Guanethidine. (Sympahtolytics)