Pharm-anest, antiarrhythm, chol, DM

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prop of Halothane as anesthetic: high lipid and blood solubility (high potency, slow induction, slow recovery time)
prop of N2O as anesthetic: low blood and lipid solubility--fast induction, low potency
SE inhaled anesthetics: cardiac, respir depression, N/V, increase cerbral BF
toxicity of inhaled anesthetics: halothane=hepatic
methoxyflurane=kidney
enflurane=sz
malignant hyperthermia (rare)
name inhaled anesthetics (6): halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, N2O
how determine potency (formula) for anesthetics: 1/MAC
general prop and use thiopental: IV anesthetic=hi lipid solubility, used induction and short procedures. terminated by redistribution from brain. decr cerbral BF
benzodiazepine used in anesthesia: midazolam (IV anesthetic)
midazolam use, prop: (IV anesthetic, benzodiazepine) commonly for endo, adjunctively with gaseous anesthesias and narcotics. severe postop respir depression and amnesia
midazolam toxicities: severe postop respir depression and amnesia
(a benzo used in endoscopy)
ketamine, type Rx, use: a PCP analog, IV dissociative anesthetic.
SE ketamine: cardio stim, increase cerebral BF,
-disorientation, hallucination, bad dreams
propofol use: IV anesthetic, for rapid induction and short procedures, less post op N than thiopental
Name depolarizing NM blockers: Succinyl choline
stages reversal of depolarizing NM blockers: (succinyl choline)
1. prolonged depolar-no antidote, block is + by - CE
2. repolarized, blocked-use - CE (ie neostigmine)
name nondepolarizing NM block (5): tubocurarine, atracurium, mivacurium, pancuronium, vecuronium
(-curonium, -curium)
reversal atracurium: (a non depol NM block)
an - CE (ie neostigmine, edrophonium)
dantrolene, mech, use (2): tx malignant hyperthermia (caused by inhaled anesthet exc N2O and succinylcholine).
tx neuroleptic malign syndrome
mech: prevent Ca rel from SR skel mscl
name local anesthetics: esters=procaine, cocaine, tetracaine
amides=lidocaine, bupivicaine
mech local anesthetics: block Na channel to binding to specif R on inner portion channel. tertiary amines penetrate mem uncharged, then bind as charged
order of nerve blocked w local anesthetics: small>large diameter, myelyinated>nonmyelinated
small unmyelinated>sm myelinated>large myelinate
loss of sensations w nerve blockade: pain (lose first)>temperature>touch>pressure
SE local anesth, general, 2 specific Rx: bupivicaine=severe cardiac tox
cocaine=arrhyth
HTN
opoiod analges R: act at opoiod receptors
mu=morphine
delta=enkephalin
kappa=dynorphin
dextramethorphan: an opoiod used for cough suppression
loperamide: opoiod used for diarrhea
diphenoxylate: opoiod used for diarrhea
generally opoiods used for 2 things: 1) pain
2) acute pul edema
methadone: an opoiod used in maintenance for addicts
toxicity of opoiods: addiction, respir depression, constipation, miosis (pinpoint), additive CNS depression
tx of opoiod OD: naloxone, naltrexone (opoiod R antagonist)
name NSAIDs: ibuprofen, naproxen, indomethacin
2 effects of NSAIDs: 1) reversibly inhibi COX1,2
2) block PG synthesis
toxicity of NSAIDs: renal damage, aplastic anemia, GI distress, ulcers
2 mech effects of NSAIDs: 1) reversibly inhibi COX1,2
2) block PG synthesis
NSAIDs used for: anti-pyretic, analgesic, anti-inflamm (indomethacin to close PDA)
acetaminophen, how difft NSAID: -rev inhibits COX mostly in CNS (inactiv peripher)
-anti-pyretic, analgesic, no anti-inflamm
toxicity acetaminophen, mech , how tx: hepatic necrosis (depletes glutathione and forms toxic NADQI
(N acetylcysteine antidote)
mechanism of class I anti arrhyth: local anesthetics, decr conduction, esp depolarized. decr slope 4 depolar, increase threshold in abnormal pace
T/F class I antiarrhythm good for fast tachycardias: yes, bc they are state dependent (they selectively depress tissue freq depolarized)
class IA arrhytmics: quinidine, amiodarone, procainamide, disopyramide
class IB arrhytmics: lidocaine, mexiletene, tocainide
mexiletene: class IB arrhytmic
prop of IA arrhyth: increase AP, incr ERP, incr QT
effect both atrial and ventricle
toxicity quinidine: cinchonism
HA, tinnitus, thrombocytopenia, torsades de pointes
toxicity procainamide: (IA) reseversible SLE-like
prop IB arrhyth: decr AP, affect ischaemia or depol Purknje and ventricular
IB used for: acute ventricular (esp s/p MI) and digitalis-induced
pneu for IB Rx: "IB Sancho (Na), I like mex taco"
IB Na, Lidocaine, mexiletene, toacainide
toxicity IB: CNS stim/depress, cardiovas depression
IC arrhyth: flecainide, ecainide, propafenone
propafenone: IC arrhyth
flecainide: IC arrhyth
prop/use IC: no affect AP, useful in VT that ->VF or intractable SVT.
toxicity IC arrhyth: proarrhyth (esp s/p MI)
summary AP duration class I: IA- increase
IB- decrease
IC- no change
what type Rx are II arrhyth?: beta blockers
mech II arrhyth: decr cAMP, decr Ca, suppress abnl by decr slope ph 4. AV node esp sensitive
increase PR interval
how II arrhyth affect intervals: incr PR (as do class IV)
drugs that decr slope ph 4: class I, II arrhyth
name class II arrhyth Rx: propanolol, esmolol (short t1/2), metoprolol, atenolol, timolol
(P MEAT)
toxicity II arrhyth: same as SE beta blockers-impotence, exacerb asthma, CV (bradycardia, AV block, CHF), CNS (sedate, sleep). May mask hypoglycemia
what type Rx III arrhyth: K channel blockers
name III arrhyth: sotalol, ibutilide, bretylium, amiodarone, dofetilide "K IS BAD"
dofetilide: III arrhyth
sotalol: III arrhyth (NOT b blocker!)
amiodarone: both IA and III
prop of III arrhyth: incr AP duration, incr ERP, incr QT. used when others FAIL
which incr QT: IA, III
toxicity sotalol: torsades de pointes, excessive block
toxicity ibtuilide: t de pointes
toxicity bretylium: new arrhythmia, hypotension
toxicity amiodarone: pul fibrosis, hepatotoxic, change thyroid
also corneal deposit, photodermatitis, neuro, constipation, CVS
type Rx is IV arrhyth: Ca blockers
name IV arrhyth: verapamil, diltiazem
prop IV arrhyth: mostly affect AV node, decr conduction, incr ERP, incr PR.
used in prevention nodal arrhythmias
toxicity IV arrhyth: constipation, flushing, edema, CV (CHF, AV block, sinus node depression)
adenosine use arrhyth: diagnose/abolishing AV nodal arrhyth
K+ in arrhyth, mech: depress ectopic pacemakers, esp for digoxin toxicity
Mg use in arrhyth: t de pointes, digoxin toxicity
effect statins: much decr LDL, small decr tg, small incr HDL
problems with statins: expensive, reversible incr LFTs, myositis
effect niacin on lipid: decr LDL, incr HDL, sl decr TG
problems with niacin: red, flushed face which decr w longtime use
names bile acid resins: cholestyramine, colestipol
effect of cholestyramine: decr LDL, slight incr tg
(a bile resin)
problems w bile resins: pts hate-tastes bad, GI discomfort
ezetimibe: cholesterol absorption blocker
effect ezetimibe: decr LDL
toxicity ezetimibe: rare incr LFTs
colestipol: a bile resin
gemfibrozil: a fibrate
effect of fibrates: decr LDL, incr HDL, big decr tg
problem w fibrates: myositis, incr LFTs
mech fibrates: stimulate LPL
what step niacin inhibit: cholesterol being secreted as VLDL
name sulfonylurea: tolbutamide, chlorpropamide, 2nd gen: glyburide, glipizide
mech sulfonylureas: stimulate ins release, closes K channel on beta-cell membrane incr Ca influx
toxicities sulfonylurea: hypoglycemia (more common with gly and glip)
disulfiram-like effects (not with gly and glip)
tolbutamide: sulfonylurea
chlorpropamide: sulfonylurea
mech metformin: inhib gluconeo and incr glycolysis
use of metformin: both DMII, and DMI (doesn't require islet fxn)
SE metformin: lactic acidosis
glitazones, name II: pioglitazone, rosiglitazone
mech glitazone: incr target cell response to insulin (for DMII)
SE glitazone: weight gain, hepatotoxic (troglitazone)
miglitol: a glucosidase inhibitor
mech a-glucosidase inhib: inhibits brush border alpha glucosidases causing delay of hydrolysis, decr postprandial glu
toxicity a-glucosidase inhib: GI disturbance
mech insulin R, effect?: R has tyrosine kinase activity.
mscl-stim glycogen and protein syn
adipose-incr tg storage
toxicity insulin, 2nd use: hypoglycemia (rare hypersensit),
also used for hyperkalemia

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