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101 Cards in this Set

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b)therapeutic uses
c)drug categories (3)
a)inhibits tyrosine hydroxylase in nerve ending so decr in NE over time b/c more can't be synthesized
c)prevention of neuronal release of NE (blockade of NE synthesis leading to NE depletion), indirect adrenolytic
Blockade of NE storage leading to NE depletion drug
a)mechanism (3)
b)drug categories (3)
a1)gets into nerve via passive diffusion
a2)blocks dopamine/NE transport mechanism of uptake into VESICLES
a3)blocks ability of storage vesicles to [] NE
b)prevention neuronal release of NE (blockade of NE storage leading to NE depletion), indirect adrenolytic
Reserpine therapeutic uses
Reserpine adverse effects (6)
1)severe mental depression/incr suicide risk via depleting CNS amines
2)postural hypotension
3)nasal congestion
5)pseudo-parkinsonism b/c depletes CNS dopamine
6)blocks effect of indirect acting adrenomimetics b/c no NE to be released
Formation of "new NT" drug
b)drug categories (3)
a1)results in formation of alpha-methylNE in CNS
a2)this is stored in place of NE
a3)stimulates CNS alpha2 receptors to decr sympathetic tone
b)prevetion of neuronal release of NE (formation of "new NT"), indirect adrenolytic
Alpha-methyldopa therapeutic uses
Adverse effects of Alpha-methyldopa (3)
1)sedation, mental depression (but less than reserpine)
2)postural hypotension (but less than guanethidine)
3)causes hemolytic anemia (but reversible if drug dc'd)
Nicotinic receptors
a)Nm effects...
b)Nn effects...
a)skeletal muscles
Neuromuscluar blocking drug categories (2)
1)competitive antagonists
2)depolarizing antagonists
Neuromuscular blocking drugs competitive antagonist drug (1)
d-Tubocurarine (Curare)
a)sites of axn and axn
b)is a _____ drug
c)@ high doses it...
d)drug category (2)
a)skeletal muscle receptors for ACh (Nm) resulting in muscle paralysis
c)blocks Nn receptors in ANS (including adrenal medulla)
d)neuromuscular blocking drugs, competitive antagonists
Order of blockade of Curare (with time) (4)
1)small moving muscles (finger, toes, eyes)
2)limbs, neck, trunk
3)intercostal muscles
Therapeutic uses of Curare (2)
1)muscle relaxant during surgical anesthesia to facilitate incisions
2)muscle relaxant during electroshock therapy to prevent excessive muscle contration
Adverse effect of Curare (3)
2)hypotension; b/c it releases histamine and blocks nicotinic receptors in ANS
3)bronchospasm b/c it releases histamine
Antidote of Curare and mechanism
b)causes incr in ACh to incr nicotinic receptor stimulation AND it can stim nicotinic receptors directly
Drug interactions (3) w/ Curare and mechanism
1)ether, general anesthetics, antibiotics (all these have muscle relaxant properties)
2)they sequester Ca which causes decr in ACh release
Depolarizing agents (2)
Sites of action of depolarizing agents (2)
1)Selective for Nm @ skeletal muscles
2)autonomic ganglia w/ large doses
b)hydrolysis by ButylChE
Therapeutic uses of depolarizing agents (2)
1)muscle relaxant during surgical anesthesia
2)muscle relaxant during electroshock
Adverse effects of depolarizing agents (6)
1)membranes can't be stimulated by anything but electrical stimuli
3)hypotension b/c of histamine release
4)bronchospasm b/c of histamine release
5)malignant hyperthermia (requires genetic disposition)
6)muscle faciculation after administration
Antidote of depolarizing agents
artificial respiration b/c they cause parital depolarization of membrane
Goals for general anesthesia (5)
Induce reversible state of:
4)muscle relaxation
5)physiological stability to undergo surgery
1st stage of depression in general anesthesia (3)
1)cerebral cortex inhibited
3)loss of consciousness
2nd stage of depression in general anesthesia (4)
1)excitement phase
2)overall increase in sympathetic tone
3)incr BP, HR, respiration, muscle tone
4)cardiac arrhythmias may occur
3rd stage of depression in general anesthesia (3)
1)surgical anesthesia stage
2)progressive CNS depression
3)cardio and respiratory fxn return to normal
4th stage of depression in general anesthesia (3)
1)medullary paralysis
2)overdose of anesthesia
3)cardio and respiratory center inhibited leading to death
Anesthetic that prodcues all stages of anesthesia is called...
complete anesthetic
Induction of anesthesia?
time reqd from consciousness to stage 3
Maintenance of anesthesia?
keep a patient at stage 3
Characteristics of an ideal anesthetic (9)
1)rapid and pleasant induction/emergence
2)easily ID'd changes in depth of anesthesia
3)adequate muscle relaxation
4)absence of toxicity @ normal doses
5)high degree of specificity
6)rapid recovery w/o side effects
8)easy to administer
9)useful for all ages
Routes of Admin of anesthesia (4)
1)inhalation (gases/volatile liquids)
Meyer-Overton theory of mechanism of action of general anesthesia
b/c of correlation b/w lipid solubility and anesthetic potency, axn is due to perturbation (clogging) of cell membrane
Most potent anesthetics
Least potent anesthetic

Nitrous oxide
Why was meyer-overton theory ruled out?
b/c of known enantioselectivity of some general anesthetics
Newer hypothesis's on the mechanism of general anesthesia involve... (4)
specific proteins that modulate membrane ion channels resulting in:
1)hyperpolarized neurons
2)inhibit excitatory synapses
3)enhance inhibitory synapses
Model for general anesthetic based on GABA (2)
1)At GABAa (GABA receptor type a) anesthetics clog it keeping Cl inside the cell, this increases GABA effects in the cell and hyperpolarizes the cell
2)@ GABAb, GABA increases some 2nd messengers that clog GABAb keeping excess K+ in the cell, hyperpolarizing it
Most GABA general anesthetics act where?
What is GABA
inhibitory NT
Other actions of general anesthetics may be mediated by changes in.... (2)
1)increase in inhibitory NT glycine
2)block action of glutamate (excitatory NT)
Anesthetic potency is defined by....
MAC (minimum alveolar [])
minimum alveolar [] reqd to prevent movement in response to surgery in 50% of patients
Measuring MAC requires... (4)
1)easy to measure alveolar []
2)alveolar and brain []s are equal @ equilibrium
3)rapid equilibrium due to high central blood flow
4)MAC does NOT vary with any type of noxious stimulus (surgery type)
MAC can vary in individuals based upon...
MAC values are...
additive w/ different anesthetics
Slopes of dose response curves for general anesthetics are....meaning...

narrow therapeutic index
Nitrous Oxide is classified as a....and why?
incomplete anesthetic b/c it can not get a person to stage 3
Balanced anesthesia?
using several drugs to obtain stage 3
Inhalational anesthetics (6)
1)nitrous oxide
Nitrous Oxide properties (just 5 of many)
1)low potency
2)good analgesic
3)must be used w/ other anesthetics
4)inhibits methionine synthetase (involved in DNA synthesis)
5)not metabolized (exhaled)
Halothane properties (just 5 of many)
1)high potency
2)sensitizes heart to catecholamine
3)dilates vascular beds of skin and brain (contraindicates brain tumor)
4)poor analgesia
5)causes bronchodilation--used to treat status asthmaticus
Isoflurane (3)
1)dilates cerebral vascular bed (contraindicates brain tumor)
2)causes bronchodilation, but leads to cough
3)dilates vascular beds less than halothane or enflurane
Enflurane (2)
1)causes bronchodilation w/o cough
2)used as maintenance NOT induction
used for maintenance b/c of airway irritation leading to cough and salivation
Sevoflurane (2)
1)causes bronchodilation w/o cough
2)MOST effective as a bronchodilator
IV anesthetics (4)
Thiopental properties (5)
1)eliminated by hepatic metabolism and renal excretion
2)hepatic metabolism means in can interact w/ drugs that incr or decr hepatic metabolism
3)cause histamine release
4)respiratory/cardiac depression
5)decr blood pressure by vasodilation
Etomidate (4)
1)does NOT stimulate histamine release
2)eliminated by hepatic metabolism and renal excretion
3)causes pain on injection
4)suppresses adrenocortical stress response by inhibiting corticosteroid production
Ketamine (5)
1)eliminated hepatically or renally
2)produces a cataleptic state termed dissociative anesthesia
3)increases cerebral blood flow (contraindicates brain tumor)
4)causes bronchodilation indirectly
5)blocks glutamate in CNS
Propofol (3)
1)eliminated hepatically and renally
2)causes histamine release
3)causes hypotension by cardiac depression and vascular relaxation
Local anesthetics goal
produce a loss of sensation in localized regions
Overall mechanism of local's (2)
1)block conduction of nerve impulses by inhibiting excitatory Na+ current @ cell membrane
2)incr # of Na+ channels in inactive state
Mechanism steps of local's (4)
1)injected as it's ionized form(+) and free base form
2)free base gets in to cell
3)free base goes back to ionized form
4)block Na channel from inside cell (only ionized form(+) can)
Functional consequences of blocking excitatory Na+ channels (5)
1)Don't change resting membrane potential
2)Decr rate of rise of EPSP
3)Decr rate of risk of AP
4)elevates threshold potential
5)Less overshoot of 0mV than regular AP
What Types of neurons are more susceptible to blockade by locals and what do they control? (3)
a)B fibers- preganglionic efferents
b)C-fibers- postganglionic efferents (motor fxn)
c)C-fibers- pain, temp, touch (sensory fxn)
What type of nerve fibers are more sensitive to blockade by locals?
slow small unmyelinated mediating pain
What type of nerve fibers are less sensitive to blockade by locals?
fast large myelinated that control movement
6 fxns ranked in order of susceptibility to blockade by locals
3)adrenergic vasoconstriction
6)motor fxn
Onset of axn of locals is usually rapid and determined by...(3)
1)molecular size (incr size=incr receptor attachment)
2)lipid solubility (incr solubility=incr access to site of action)
3)degree of ionization (only active in cationic form)
Termination of action of local anesthetics determined by....(2)
1)diffusion out of neurons
2)regional blood flow
Local anesthetics can be used in conjuction w/ a vasoconstriction (like epinephrine) to: (3)
1)prolong effects
2)delay absorption
3)reduce toxicity
Metabolism of local anesthetics via...(2)
1)esters metabolized by esterases in blood/tissues
2)amides metabolized by hepatic enzymes
Applications of local anesthetics... (6 and exp of 3)
1)surface anesthesia
2)infiltration anesthesia (injection into surgical area)
3)nerve block anesthesia (injection into area of nerves that supply surgical area)
4)spinal anesthesia
5)intravenous regional anesthesia (injexn into localized area after removal of blood)
6)Epidural anesthesia
Existence of adverse rxns to locals depends upon...
degree of systemic absorption OR allergy to the local
First local anesthetic discovered was...
Ester local anesthetics (5)
Procaine properties (4)
1)metabolized by plasma esterase
2)release histamine (allergic rxns)
3)requires injection
4)can interfere w/ action of sulfonamides
Benzocaine (2)
1)simplest local
2)used topically ONLY
Chloroprocaine (4)
1)used in situations where systemic absorption would create problems (pregnancy)
2)least toxic of locals
3)can induce DVT
4)contraindicated for intravenous regional block
Amide locals (3)
Prototype for amide locals is...
Lidocaine (3)
2)hepatic metabolism
3)faster, better, longer effects than procaine
4)less likely than procaine to produce allergy
Adrenergic drugs...
a)act on...
b)NE is used to..
c)NE belong to the ___ group of structures
a)SNS or adrenergic nervous system
b)trasmit signals from postganglionic fiber to effector cells
Catecholamine characteristics? (2)
1)adjacent/ortho OH's
2)connected to a benzene
Direct acting adrenergic agonists act via...
bind/activate alpha1/2, beta1/2 receptors
Indirect acting adrenergic agonists act via...
stimulate NE release and prevent its reuptake
Dual/mixed adrenergic agonists act via...
bind to adrenergic receptors and stimulate NE release
NE is a ____ amine
E is a ____ amine
primary amine
methyl/secondary amine
a)catechol (ring and 2 OH's)
c)B-carbon is chiral
ID the parts of this structure (3)
COMT mechanism of breakdown of NE
methylates 3'OH of NE to form inactive methoxyNE
2 break down products of NE and where does each one go?
1)VMA (urine)
2)methoxy-phenylglycol (CNS)
What other pathways are MAO and COMT found in the body
NO WHERE, specific to the NE/E breakdown pathway
2 other enzymes involved in the NE/E breakdown?
1)aldehyde reductase
2)aldehyde deH
Aldehyde reductase, aldehyde deH fxn?
Breaks down SC's of initial NE break down products to form VMA
What is the primary breakdown product of NE/E in the...
a)adrenal medulla
Mechanism of MAO breakdown of NE/E
converts amine to aldehyde
Steps in synthesis of NE (4)
1)Tyrosine to L-dopa via TYROSINE HYDROXYLASE
2)L-dopa to dopamine via AROMATIC L-AA DECARBOXYLASE
3)dopamine taken to vesicle
NE to E via...
Rate limiting enzyme in NE synthesis
tyrosine hydroxylase