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417 Cards in this Set
- Front
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defintion of anesthetic drugs
|
drugs use to produce surgical anesthesia
|
|
ex. of anesthetic drugs (2)
|
halothane
propofol |
|
definition of anxiolytic/sedative drugs
|
drugs that cause sleep and reduce anxiety
|
|
ex. of anxiolytic/sedative drugs
|
barbiturates
benzodiazepines |
|
definition of antipsychotic drugs
|
drugs that are effective in relieving the symptoms of schizophrenic illness
|
|
ex. of antipsychotic drugs
|
clozapine
chlorpromazine haloperidol |
|
definition of anti-depressant drugs
|
drugs that alleviate symptoms of depressive illness
|
|
ex. of antidepressants (3)
|
MAO inhibitors
TCAs SSRIs |
|
definition of analgesic drugs
|
drugs used clinically to control pain
|
|
ex. of analgesic drugs (2)
|
opiates
carbamazepine |
|
definition of psychomotor stimulants
|
drugs that cause wakefulness and euphoria
|
|
ex. of psychomotor stimulants (3)
|
cocaine
amphetamine caffeine |
|
definition of psychotomimetic drugs
|
drugs that cause disturbance of perception (visual hallucinations) and of behavior in ways that cannot be characterized as sedative or stimulant effects
|
|
ex. of psychotomimetic drugs (3)
|
LSD
mescaline phencyclidine |
|
definition of cognition enhancers
|
drugs that improve memory and cognitive performance
|
|
ex. of cognition enhances (nootropic drugs) (3)
|
AchE inhibitors
NMDA receptor antagonists piracetam |
|
glutamate receptors are found in (3)
|
cortex
basal ganglia sensory pathways |
|
NMDA-R
permeable to (1) blocked by (2) requires (3) as well as (4) to activate it |
1 - Ca+ channels
2 - Mg2+ 3 - glycine 4 - glutamate |
|
D-serine activates NMDA-R via (1) and is released from (2)
|
1 - glycine binding site
2 - astrocytes |
|
selective blocking agents for NMDA channels (3)
|
ketamine
phencyclidine dizoclipine |
|
spermine/spermidine
|
endogenous polyamines
facilitates NMDA channel opening |
|
ifenprodil / eliprodil
|
block spermines
|
|
AMPA-R mediate
|
fast EPSPs in CNS
also found on astrocytes |
|
Kainate-R mediate
|
fast EPSPs in CNS
presynaptic role |
|
NMDA-R mediates
|
slow EPSPs
|
|
metabotropic glutamate R. mediate
|
postsynaptic excitation = inhibition of K+
presynaptic inhibition = inhibition of Ca2+ channels |
|
long term potentiation
|
long lasting enhancement of synaptic transmission that occurs at various CNS synapses following short (conditioning) burst of high frequent presynaptic stimulation
|
|
mechanism of LTP: normal transmission (3)
|
only AMPA-R activated
not enough Glu to activate metabotropic R. NMDA-R inhibited by Mg2+ |
|
mechanism of LTP: after conditioned stimulus
|
enough Glu release to activate metabotropic receptors
NMDA-R unblocked due to depol. --> large influx of Ca2+ activating enzymes |
|
role of NO and AA in LTP
|
serve as retrograde transmitters that increase presynaptic glutamate release
|
|
role of anandamide in LTP
|
suppresses GABA release
|
|
therapeutic interest of Glu-R antagonists
|
reduction of brain injury following damage or stroke
Tx of epilepsy Tx of Alzheimers |
|
examples of glutamate channel blockers (5)
|
ketamine
phencyclidine dizoclipine remacemide memantine |
|
only Glu-R blockers used clinically (2)
- why? (3) |
ketamine
memantine 3 =tendency to cause hallucinations |
|
Glu-R agonists
- act on which R? (1) mechanism (2) use ? (3) |
1 = ampa r
2 = reduce receptor desensitization 3 = improve memory and cognitive performance |
|
examples of Glu-R agonists
|
cyclothiazide (toxic)
piracetam/aniracetam = used in dementia, sensitizes AMPA-R |
|
vigabratrine
|
inhibits GABA transaminase - decreases GABA degradation
Tx. epilepsy |
|
guvacine / nipecotic acid
|
block GABA transport into neurons/astrocytes
|
|
GABAa-R mediates
|
fast postsynaptic inhibition by increased Cl- conductance into post . cell
|
|
muscimol
|
GABAa-R agonist
at receptor site -> from hallucinogenic mushroom |
|
gabaxadol
|
GABAa-R partial agonist
in development as hypnotic drug |
|
alphaxolone
|
steroid anesthetic
GABAa-R agonist at modulatory site |
|
bicucilline
|
GABAa-R antagonist at receptor site (naturally occuring)
--> blocks fast inhibitor synaptic potential in most synapses |
|
gabazine
|
GABAa-R antagonist at receptor site -> synthetic GABA analogue
|
|
picrotoxin
|
blocks GABAa Cl- channel
|
|
tiagibine
|
blocks GABA reuptake
|
|
drugs that mimic GABA (2)
|
gabapentin
pregabalin |
|
GABAb-R actions
|
PRE
inhibits Ca2+ channels (reducing nt release) POST opens K+ channels (reducing post synaptic excitability) |
|
baclofen
|
selective GABAb-R agonist
--> actions not blocked by bicucilline Tx. spasticity and motor disorders |
|
saclofen
|
GABAb-R competitive antagonist
anti-epileptic w/ enhanced cognitive performance --> only experimental |
|
gamma hydroxybutyrate
- what is it? (1) - used by ? (2) and (3) |
1 = natural side produce of GABA synthesis
2 - body builders - increases GH 3 - party goers - euphoria/disinhibition |
|
strychnine
|
convulsant poison
acts on spinal cord blocks synaptic inhibitor response to glycine |
|
B-alanine
|
effects and pattern of distribution similar to glycine
--> NOT blocked by strychnine |
|
tetanus toxin
|
prevents glycine release from inhibitory interneurons in spinal cord
--> reflex hyperexcitability and violent muscle spasms |
|
NE neurons
- located in (1) - project to (2) - release nt (3) - activity increases w/ (4) - stimulates by (5) |
1 = locus ceruleus
2 = cortex, hippocampus, cerebellum 3 - release nt diffusely 4 - behavioral arousal 5 - amphetamine-like drugs |
|
catecholamine hypothesis of depression
|
depression results from functional deficiency of NE in brain, whereas mania from excess NE
|
|
clonidine / methyl-dopa
|
decrease discharge of SNS nerves emerging from CNS
--> lower BP caused by NE |
|
HVA
|
breakdown product of DA
- used as an index of DA turnover and release in human brain |
|
3 main dopamine pathways
|
nigrostriatal (substantia nigra --> corpus striatum)
mesolimbic/mesocortical (midbrain --> nucleus accumbens) tuberohypophyseal (ventral hypothalamus to pituitary) |
|
bromocriptine
|
dopamine agonist, used clinically to suppress prolactin secretion by tumors of pituitary gland
|
|
effect of DA agonists on N/V?
effect of DA antagonists on N/V? |
1 = agonist cause nausea and vomiting
ex. levodopa 2 = antagonists are anti-emetic ex. phenothiazine, metoclopramide |
|
PCPA
|
selectively and irreversibly inhibits tryptophan hydroxylase --> no 5HT made
|
|
5HT cell bodies located in
|
raphe nuclei
|
|
5HT1-R
|
INHIBITORY
1a = autoreceptors (limits rate of firing) 1b/d = presynaptic inhibitors R. in basal ganglia |
|
5HT2-R
|
excitatory postsynaptic effect in cortex and limbic system
|
|
methysergide
|
5HT2-R antagonist
used to Tx migraine |
|
5HT3-R
|
found mainly in area postrema
excitatory inotropic R. |
|
5HT4-R
|
expressed in GI tract and striatum
presynaptic facilitatory effect - Ach release (enhances cognitive performance) |
|
5HT6-R
|
only in CNS
potential targets for improvement of cognition or relief of symptoms of schizo |
|
5HT7-R
|
bound in CNS and blood vessels and GI tract
thermoregulatory functions and endocrine fcns involved in mood, cognition and sleep |
|
hallucinatory effects caused by which 5HT receptor?
|
5HT2a agonists
- loss of cortical inhibition many antipsychotic drugs are 5HT2a antagonsts |
|
Alzheimers results from degeneration of..
|
nucleus basalis of Meynert
|
|
Ach is mainly located in ...
|
forebrain
midbrain brain stem w/ little in cerebellum |
|
which Ach-R are mainly in the brain?
|
M1-R
|
|
cholinergic pathways in the brain are mainly involved in...
|
arousal
learning/memory motor control |
|
xanthenes such as caffeine are antagonists at which receptors?
|
adenosine A-2 R
--> produce arousal and alertness |
|
adenosine
|
neuroprotection
causes: drowsiness, motor incoordination, analgesia and anti-convulsant activity |
|
local anesthetis are (1) w/ pKa btw (2); their activity is (3) dependent and increased at (4); inflamed tissues are often (5) and thus (6)
|
1 = weak bases
2 = 8-9 3 = pH-dependent 4 = increased w/ alkaline pH 5 = acidic 6 = resistant to LA |
|
mechanism of action of local anesthetics
|
block VG Na+ channels, reduce influx of Na+ ions, prevent depolarization = no AP
|
|
ester local anesthetics are degraded by...
|
plasma cholinesterase
half life of 1-2 min (short acting) |
|
amide local anesthetics are degraded by...
|
cytP450 enzymes in liver
longer acting w/ half lives 2-6 hrs |
|
use dependence of local anesthetics
|
depth of block increases w/ AP frequency
- the more channels that are open, the greater the block - LA bind more strongly to inactivated channel |
|
which fibers are preferentially blocked by local anesthetics?
|
small fibers
myelinated (although, usually last bc of size) Adelta and C fibers** --> pain sensation blocked before other modalities |
|
local anesthetis are (1) w/ pKa btw (2); their activity is (3) dependent and increased at (4); inflamed tissues are often (5) and thus (6)
|
1 = weak bases
2 = 8-9 3 = pH-dependent 4 = increased w/ alkaline pH 5 = acidic 6 = resistant to LA |
|
cocaine as local anesthetic
|
rarely used
spray for upper respiratory tract cardio and CNS effects due to block of amine uptake |
|
mechanism of action of local anesthetics
|
block VG Na+ channels, reduce influx of Na+ ions, prevent depolarization = no AP
|
|
procaine
|
LA - first synthetic one, no longer used
|
|
ester local anesthetics are degraded by...
|
plasma cholinesterase
half life of 1-2 min (short acting) |
|
adverse effects of procaine
|
CNS = restlessness, shivering, convulsions, respiratory depression
CV = bradycardia, decreased CO, vasodilation |
|
amide local anesthetics are degraded by...
|
cytP450 enzymes in liver
longer acting w/ half lives 2-6 hrs |
|
lidocaine - uses
|
widely used for local anesthesia
IV use for ventricular dysrhythmias |
|
use dependence of local anesthetics
|
depth of block increases w/ AP frequency
- the more channels that are open, the greater the block - LA bind more strongly to inactivated channel |
|
which fibers are preferentially blocked by local anesthetics?
|
small fibers
myelinated (although, usually last bc of size) Adelta and C fibers** --> pain sensation blocked before other modalities |
|
cocaine as local anesthetic
|
rarely used
spray for upper respiratory tract cardio and CNS effects due to block of amine uptake |
|
procaine
|
LA - first synthetic one, no longer used
|
|
adverse effects of procaine
|
CNS = restlessness, shivering, convulsions, respiratory depression
CV = bradycardia, decreased CO, vasodilation |
|
lidocaine - uses
|
widely used for local anesthesia
IV use for ventricular dysrhythmias |
|
mepivicaine
|
similar to lidocaine
|
|
lidocaine - adverse effects
|
as procaine, but less tendency to cause CNS effects
|
|
tetracaine - uses
|
ester LA
spinal and corneal anesthesia |
|
tetracaine - adverse effects
|
as procaine, but less tendency to cause CNS effects
|
|
bupivicaine
|
longest duration of action
severe cardiotoxicity --> arrhythmias and hypotension |
|
ropivicaine
levobupivicaine |
long duration LA
LESS cardiotoxicity, replacement of bupivicaine |
|
prilocaine
|
amide LA
NOT for obstetric analgesia -> risk of neonatal metHbemia |
|
a1 glycoprotein and LA
|
a1-glycoprotein has high affinity for LA
when amount increases during infection, cancer or autoimmune states --> activity of local anesthetics DECREASES |
|
amethocaine
|
ester-linked LA
|
|
procaine and sulfonamides
|
procaine is metabolized to p-aminobenzoic acid which is a folate precursor -> interferes w/ antibacterial effect of sulfonamides
|
|
CNS adverse effects of LA
|
low dose = depressant
high dose = stimulant --> restlessness --> tremor --> convulsions --> confusion --> extreme agitation --> respiratory depression |
|
Cardio adverse effects of LA
|
myocardial depression
conduction block vasodilation ** cocaine has opposite effects |
|
the lower the MAC, the .... potency
|
higher
|
|
higher the oil partition coefficient (lipid solubility), the .... MAC
|
lower
|
|
high partial pressure of gas in lungs has what effect on anesthetic levels?
|
high PP = more rapid anesthesization
|
|
the greater the ventilation, the .... onset of anesthesia
|
faster
|
|
high pulmonary blood flows, onset of anesthesia is ....
|
reduced
|
|
anesthetic state comprises of (3)
|
LOC
loss of reflexes analgesia |
|
what are the most sensitive brain regions to anesthesia? (2)
|
midbrain reticular formation
--> unconsciousness thalamic sensory relay nuclei --> analgesia |
|
effect of anesthetics on cardio system
|
decrease arterial blood pressure (except N2O)
decrease cardiac contractility |
|
effect of Nitrous Oxide on HR/BP
|
increases HR and BP
|
|
effect of halothane/enflurane on heart
|
myocardial depressants
decrease HR and BP - cause ventricular extrasystoles |
|
older inhalation anesthetics (5)
|
ether
chloroform trichloroethylene cyclopropane methoxyflurane |
|
newer inhalation anesthetics (4)
|
enflurane
isoflurane sevoflurane desflurane |
|
chloroform - toxicity
|
hepatotoxicity
--> free radical formation in liver |
|
methoxyflurance - toxicity
|
fluoride released in metabolism which may cause renal insufficiency after prolonged anesthesia
|
|
halothane anesthesia can rarely results in
|
post-operative hepatitis
|
|
chronic low level exposure to inhalational anesthetics results in
|
liver toxicity (liver disease)
certain types of leukemia spontaneous abortion congenital malformations |
|
xenon
|
inhalational anesthetic
inert gas NO toxicity low potency high cost |
|
adverse effects of halothane
|
1. relaxant effects on uterus - not useful in obstetrics
2. sensitizes heart to NE - dysrhythmias 3. myocardial depressant 4. halothane hepatitis w/ repeated exposure 5. malignant hyperthermia |
|
malignant hyperthermia
|
heat production by skeletal mm. bc of excessive Ca2+ release from SR
--> results in muscle contracture, acidosis, increased BMR, increased body temp |
|
Tx for malignant hyperthermia
|
dantrolene
|
|
adverse effects of nitrous oxide
|
1. diffusional hypoxia - dilutes alveolar PO2
2. prolonged exposure inactivated methionine synthase = bone marrow depression 3. enters gaseous cavities and causes them to expand |
|
adverse effects of enflurane
|
1. renal toxicity - but levels of fluoride are small
2. causes tonic-clonic seizures on induction 3. malignant hyperthermia 4. bronchodilation 5. full mm relaxation - not reversible w/ neostigmine |
|
adverse effects of isoflurane
|
1. coronary vasodilator = hypotension
2. steal phenomenon -> may precipitate MI in patients w/ coronary disease 3. irritant to respiratory tract |
|
adverse effect of desflurane
|
bronchospasm and cough
--> respiratory irritant (not used for induction bc of this) |
|
sevoflurane
|
resembles desflurane
more potent does not irritate respiratory system |
|
neuroleptanesthesia
|
state of deep sedation and analgesia
nitrous oxide + droperidol + fentanyl |
|
thiopental is a (1) drug used as (2) anesthetic, specifically for (3) of anesthesia
|
1 = barbiturate
2 = IV anesthetic 3 = INDUCTION |
|
reduced dose of thiopental needed for induction in (2) conditions
|
1 = malnutrition
2 = liver/ renal disease --> displaced from albumin |
|
adverse effects of thiopental as IV anesthetic (5)
|
1. long hangover -> high lipid solubility
2. no analgesic properties 3. narrow margin of safety 4. tissue necrosis if accidentally injected not in vein 5. poryphria attack |
|
etomidate
|
larger margin of safety than thiopental
preferable in pts. w/ circulatory failure |
|
adverse effects of etomidate (3)
|
1. suppresses adrenal cortex
2. involuntary mvts. during induction 3. post-op nausea/pain at injection site |
|
which anesthetic should you take caution in w/ patients w/ egg+soy allergy?
|
propofol
|
|
benefits of propofol
|
very rapidly metabolized
can be used to maintain anesthesia w/o need for inhalation anti-emetic |
|
adverse effects of propofol
|
30% fall in BP on induction
strong respiratory depression pain at injection site |
|
dissociative amnesia
|
marked sensory loss and analgesia, amnesia and paralysis of mvt w/o LOC
|
|
ketamine
|
blocks NMDA-R
dissociative anesthesia hallucinations common on recovery |
|
action of ketamine on cardio
|
stimulant
--> may lead to increased ICP |
|
midazolam
|
BDZ used adjunctively w/ inhaled anesthetics and IV opioids
|
|
uses of midazolam
|
pre-op sedative
procedures such as endoscopy where full anesthesia is not required |
|
caution w/ midazolam
|
may cause severe cardio-respiratory depression
--> reversible w/ flumazenil |
|
mechanism of action of BDZs
|
increase FREQUENCY of GABAa Cl- channel opening
|
|
main pharmacologic effects of BDZs (5)
|
1. reduction of anxiety and aggression
2. sedation and induction of sleep 3. reduction of mm tone and coordination 4. anticonvulsant action 5. anterograde amenesia |
|
effect of benzo's on sleep
|
decrease time to get to sleep
increase duration of sleep reduce REM sleep (w/ rebound at end) reduce slow wave sleep |
|
which benzo's reduce decerebrate rigidty?
|
clonazepam
flunitrazepam |
|
anti-convulsant effect of benzo's
|
effective against chemically induced convulsions
|
|
clonazepam
|
benzo w/ selective anti-convulsant activity
Tx. of epilepsy |
|
diazepam
|
benzo w/ anti-convulsant activity
Tx. of status epilepticus |
|
benzo overdose
|
prolonged sleep but w/o severe cardio-respiratory depression
- readily reversed w/ flumazenil |
|
side effects of therapeutic benzo use
|
drowsiness
confusion amnesia impaired coordination enhance depressant effects of other drugs such as alcohol |
|
tolerance of benzos
|
increased when used chronically or in high doses
(but apparently not according to prof) |
|
withdrawl signs of benzos
|
anxiety
tremors hyperreflexia seizures --> more common w/ short acting agents |
|
flumazenil
|
benzo competitive antagonist
--> used to reverse effect of benzo overdose --> used to reverse effect of midazolam in anesthesia |
|
buspirone
|
5HT1aR agonist
inhibits D2-R --> only anxiolytic effect do NOT interfere w/ alcohol no rebound effect |
|
side effects of buspirone
|
N/V
headache restlessness tachycardia miosis increased PRL/GH |
|
buspirone used to Tx
|
generalized anxiety disorder
|
|
pentobarbital
|
barbiturate used as anesthetic for lab animals
|
|
phenobarbital
|
barbiturate used to Tx. epilepsy occasionally
|
|
barbiturates induce synthesis of (1) which increases (2)
|
1 = hepatic cytP450 enzymes
2 = increases metabolism of other drugs |
|
mechanism of action of barbiturates
|
increase LENGTH of open time of GABAa Cl- channels
|
|
toxicity of barbiturates (10)
|
tolerance/dependence high
rebound increase in REM "hang over" ataxia speech disturbance increased aggressiveness strong CNS depressive action increased vit. D metabolism increased poryphyrias photosensization |
|
alprazolam
|
BDZ
only one w/ anti-depressant action used to Tx. panic attacks |
|
tetrazepam
|
has muscle relaxant specificity
|
|
hydroxyzine
|
inhibits RAS
antihistamine w/ antiemetic activity good for pts. w/ history of drug abuse |
|
hydroxyzine is used for...
|
sedation prior to dental procedures
Tx. of psychosomatic disorders |
|
toxicity of hydroxyzine
|
sedation
strong atropinic effects myelosuppression slight dependency increased seizures |
|
diol derivatives (3)
|
meprobamate
tybamate phenoglicodol |
|
uses of meprobomate
|
anxiolytic
strong hypnotic/sedative anti-epileptic/sedative |
|
toxicity of meprobomate
|
allergic = bronchospasm , dermatitis
myelosuppression dependence/tolerance episodic euphoria/depression |
|
zolpidem
|
hypnotic drug -> no anticonvulsant or mm relaxant
acts on BDZ-R1 |
|
adverse effects of zolpidem
|
nightmares
agitation headache GI upset dizzines daytime drowsiness |
|
zaleplon
|
same as zolpidem (BDZ-R1)
BUT w/ shorter duration and thus less psychomotor and cognitive effects |
|
eszopiclone
|
Tx. of insomnia
|
|
adverse effects of eszopiclone
|
anxiety
dry mouth headache peripheral edema somnolence unpleasent taste |
|
ramelteon
|
agonist at melatonin MT1/MT2-R
|
|
action of ramelteon
|
induces sleep
maintains circadian rhythm |
|
use of ramelteon
|
used to Tx. insomnia (long term)
|
|
adverse effects of ramelteon
|
dizziness
fatigue somnolence increase PRL |
|
chloral hydrate
|
sedative/hypnotic
-> induces sleep in 30 min, lasts 6 hours |
|
adverse effects of chloral hydrate
|
GI irritant
unpleasant taste synergizes w/ ethanol |
|
ethanol can produce severe CNS depression bc of additive effects w/ (4)
|
1. BDZ
2. antihistamines 3. barbiturates 4. opioids |
|
Tx of choice for withdrawl of ethanol
|
benzo's
|
|
disulfiram
|
Tx. of alcoholism
--> produces conditioned avoidance response |
|
naltrexone
|
long lasting opiate antagonist
used for Tx. of alcohol dependence |
|
nociception
|
acute pain
excessive noxious stimulus gives rise to an intense unpleasant sensation |
|
hyperalgesia
|
chronic pain
increased amt pain associated w/ mild noxious stimulus |
|
allodynia
|
pain evoked by non-noxious stimulus
|
|
electrical stimulation of PAG in rats produces
|
analgesia
|
|
vanilloid receptor (TRPV1) is activated by: (3)
|
capsaicin
temp. higher than 45 C proton conc. less than pH = 5.5 |
|
what is the endogenous ligand for TRPV1 receptor
|
anandamide
|
|
TRPV1 expression is increased in
|
inflammation
-> responsible for hyperalgesia |
|
capsaicin can be used to Tx ?
|
urinary incontinence
--> causes degeneration of primary afferent nerve terminals in bladder |
|
bradykinin
|
potent pain producing substance
--> causes release of PGs which potentiate its action |
|
BK2-R
|
found on nociceptive neurons
- linked to PKC which phosphorylated TRPV1 and opens it |
|
BK1-R
|
upregulated in inflamed tissues
|
|
icatibant
|
BK-2 R antagonist
-> analgesic w/ anti-inflammatory properties |
|
morphine analogues - agonists (3)
|
morphine
diamorphine (heroin) codeine |
|
morphine analogues - partial agonists (2)
|
nalorphine
levalorphan |
|
morphine analogue - antagonist
|
naloxone
|
|
opioid u -R
|
most analgesic effects of opioids
responsible for unwanted side effects, esp. respiratory depression |
|
opioid delta R
|
important in periphery
|
|
opioid k-R
|
analgesia at spinal level
responsible for sedation |
|
mechanism of action of all opioid R
|
Gi = inhibit AC = open K+ channels, inhibit Ca2+ channels
|
|
pharmacologic actions of opioids (8)
|
1. analgesia
2. euphoria 3. respiratory depression 4. suppression of cough reflex 5. nausea/vomiting 6. pupillary constriction 7. constipation 8. hypotension and bradycardia |
|
opioid effect on analgesia
|
reduces affective component of pain
less useful in neuropathic pain |
|
opioid effect on respiratory system
|
respiratory depression even w/ analgesic dose
decrease sensitivity of respiratory centre to PCO2 |
|
2 main opioids used as cough suppressants
|
codeine
dextromethorphan |
|
opioid effect on pupils
|
constriction!!
mediated by u/k-R stimulation of oculomotor nucleus |
|
effects of opioids on GI tract
|
increases GI tone and decreases motility = constipation
contraction of gall bladder but constriction of biliary sphincter |
|
tolerance doesnt affect which two opioid effects?
|
pupillary constriction
constipation |
|
abstinence syndrome to opioids
|
rhinorhea
lacrimation chills goose-flesh muscle aches diarrhea yawning anxiety hostility |
|
what is used to alleviate opioid abstinence syndrome?
|
clonidine
- a2 adrenoreceptor agonist |
|
which agent can reduce opioid tolerance?
|
ketamine
- NMDA-R antagonist |
|
which opioids are less likely to produce dependence?
|
codeine
pentazocine buprenorphine tramadol |
|
diamorphine
|
aka. heroin
rapidly deacetylated to morphine greater lipid solubility more likely to cause dependence |
|
codeine
|
analgesic for mild/moderate pain
anti-tussive no euphoria or addiction constipation! |
|
dihydrocodeine
|
pharm. similar to codeine
|
|
pethidine (meperidine)
|
strong u-R agonist
anti-muscarinic activity euphoric effects causes dependence preferred to morphine in labour |
|
meperidine is metabolized to form (1) which has (2) and (3) effects
|
1 = norpethidine
2 = hallucinogen 3 = convulsant effects |
|
tolerance doesnt affect which two opioid effects?
|
pupillary constriction
constipation |
|
abstinence syndrome to opioids
|
rhinorhea
lacrimation chills goose-flesh muscle aches diarrhea yawning anxiety hostility |
|
what is used to alleviate opioid abstinence syndrome?
|
clonidine
- a2 adrenoreceptor agonist |
|
which agent can reduce opioid tolerance?
|
ketamine
- NMDA-R antagonist |
|
which opioids are less likely to produce dependence?
|
codeine
pentazocine buprenorphine tramadol |
|
diamorphine
|
aka. heroin
rapidly deacetylated to morphine greater lipid solubility more likely to cause dependence |
|
codeine
|
analgesic for mild/moderate pain
anti-tussive no euphoria or addiction constipation! |
|
dihydrocodeine
|
pharm. similar to codeine
|
|
pethidine (meperidine)
|
strong u-R agonist
anti-muscarinic activity euphoric effects causes dependence preferred to morphine in labour |
|
meperidine is metabolized to form (1) which has (2) and (3) effects
|
1 = norpethidine
2 = hallucinogen 3 = convulsant effects |
|
etorphine
|
1000x more potent than morphine
used to immobilize wild animals for research and trapping purposes |
|
nalorphine
|
low doses = competitive antagonist
high doses = analgesic and mimics morphine |
|
naloxone
|
antagonist at all 3 receptors
only lasts few hours, dose must be repeated precipitates withdrawl symptoms in addicts can be used to detect opiate addiction |
|
naltrexone
|
similar to naloxone but longer duration of action
|
|
analeptics aka (1)
used to Tx (2) |
1 = respiratory stimulants
2 = pts in terminal coma or severe respiratory failure |
|
doxapram
|
analeptic
Tx. of acute ventilator failure - less risk of convulsions than others |
|
strychnine
|
blocks glycine R. in spinal cord
|
|
action of strychnine
|
power convulsant - causes violent extensor spasms triggered by minor sensory stimuli
|
|
bicucilline
|
competitively blocks GABAa -R in brain (not spinal cord)
|
|
picrotoxin
|
analeptic - convulsant
blocks Cl- channels of GABA-R (non competitve antagonist) |
|
pentylenetetrazol
|
induces convulsions in experimental models
|
|
amphetamine-related drugs (6)
|
amphetamine
methamphetamine dextroamphetamine methylphenidate MDMA fenfluramine |
|
pharmacologic effects of amphetamines
|
locomotor stimulation
euphoria stereotyped behavior anorexia sympathomimetic - increased HR/BP tremor/mm twitching reduces physical/mental fatigue |
|
effects of the following on amphetamine action:
- 6 hydroxydopamine (1) - a-methyltyrosine (2) - TCAs/MAOi's (3) - reserpine (4) |
1 = abolishes amp. effect
2 = abolishes amp. effect 3 = potentiate amp effects 4 = does not block behavioral amp. effects |
|
which amphetamine drug does NOT cause dependence
|
fenfluramine
|
|
prolonged doses of amphetamines cause.... (1)
abruptly stopped use of amphetamines causes... (2) |
1 = amphetamine psychosis resmembling acute schizo
2 = period of deep sleep, lethargy and depression (even after single dose) |
|
how can you increase excretion of amphetamines?
|
acidification of urine
|
|
methylphenidate
- Tx ? |
ADHD in children
|
|
unwanted side effects of methylphenidate
|
HTN
insomnia anorexia tremors risk of exacerbating schizo risk of dependence |
|
what is a dangerous side effect of methylphenidate
|
can induce heat stroke
--> mm damage and renal failure --> too much ADH secretion, leading to thirst, over hydration and hyponatremia |
|
mechanism of action of cocaine
|
inhibits uptake of NE and DA
--> enhances peripheral effects of SNS nerve activity = psychomotor stimulant effect |
|
effects of cocaine
|
euphoria
increased motor activity magnification of pleasure less stereotyped behaviors, delusions and hallucinations increased BP, HR due to vasoconstriction |
|
adverse effects of cocaine
|
progressive myocardial damage leading to heart failure
impairs brain development in utero high risk of psychological dependence |
|
examples of methylxanthines
|
caffeine
theophylline |
|
clinical use of theophylline
|
bronchodilator in Tx. of sever asthmatic attacks
|
|
pharmacologic effects of methylxanthines
|
CNS stimulation -> reduction of fatigue
diuresis stimulation of cardiac mm relaxation of smooth mm |
|
mechanism of action of methylxanthines
|
inhibit PDE --> increased cAMP levels
A1/A2 adenosine receptor antagonists |
|
mechanism of action of LSD, psilocybin, mescaline
|
5HT2 -R agonists
- at raphe nuclei |
|
do psychotomimetic drugs aka LSD produce addiction or
dependence? (1) what about tolerance? (2) |
1 = no
2 = yes, very quickly |
|
pharmacologic effects of LSD
|
alters perceptions
hallucinations illogical thought processes |
|
mechanism of action of MDMA
|
inhibits monoamine transporters, esp 5HT --> large increase in 5HT followed by depletion
|
|
what is the cause of sudden illness and death w/ MDMA use?
|
acute hyperthermia
-> skeletal mm damage and renal failure |
|
long term effects of MDMA use
|
deleterious effects on memory and cognitive function
--> due to degeneration of 5HT and DA neurons |
|
toxic side effect of chlorpromazine
|
mild jaundice
-> associated w/ elevated ALP |
|
which neuroleptic can be used to Tx. huntingtons?
|
haloperidol
|
|
when to use atypical antipsychotics? (3)
|
1 - if extrapyramidal symptoms are troublesome
2 - if symptom control in inadequte 3 - newly diagnosed patients |
|
when is clozapine reserved for?
|
patients whose condition is inadequately controlled despite use of at least 2 other antipsychotics
|
|
molindone
|
antipsychotic used for Tx. of Tourette's
|
|
toxicity of thioridazine
|
retinal deposits cause visual impairment
high doses - conduction defect |
|
toxicity of zisparidone
|
prolongs QT interval on ECG
|
|
therapeutic plasma conc of Lithium
|
0.6-1.4 mEq/L
|
|
which drug increases the renal clearance of lithium?
|
theophylline
|
|
mechanism of action of Lithium
|
inhibits IP3 and DAG pathway
|
|
lithium used for Tx. of ?
|
bipolar disorder
--> decreases manic behavior and reduces frequency/magnitude of mood swings |
|
lithium is often given concurrently w/ ?
|
anti depressants
|
|
other than lithium, bipolar disorder can be Tx. w/ ?
|
olanzepine
valproic acid (other anti-seizure medications) |
|
Side Effects of Lithium (8)
|
1. tremor/ ataxia
2. sedation/ aphasia 3. thryoid enlargement 4. nephrogenic diabetes insipidus 5. edema 6. acne 7. leukocytosis always present 8. contraindicated in nursing mothers |
|
partial seizures are (1) and show on EEG on (2); they can be experienced as (3), (4), (5) and (6)
|
1 - localized
2 - one hemisphere only 3 - involuntary muscle contraction 4 - abnormal sensory experience 5 - autonomic discharge 6 - effects on mood and behavior |
|
examples of partial seizures
|
jacksonian march
psychomotor epilepsy |
|
traditional drugs used to Tx. partial seizures (3)
|
valproic acid
carbamazepine phenytoin |
|
newer drugs used to Tx partial seizures (3)
|
levetriacetam
tiagabine zonisamide |
|
generalized seizures involve (1) and on EEG (2); characterized w/ (3)
|
1 = whole brain, incl RAS
2 - both hemispheres 3 = LOC |
|
tonic-clonic seizures
- 2 stages |
1 = initial strong contraction of whole musculature (high frequency EEG activity)
2 = 2-4 min of synchronous, violent jerks (EEG = intermittent discharge) |
|
Tx of tonic-clonic seizures
|
valproic acid
carbamazepine phenytoin |
|
absence seizures
|
children
abruptly cease activity - state blankly; pt unaware EEG = rhythmic discharge |
|
Tx of absence seizures (2)
|
ethosuximide
valproic acid **alternatively: clonazepam lamotrigine topiramate |
|
main drug used to Tx. myoclonic seizures
|
valproic acid
|
|
backup drugs in myoclonic seizures
|
clonazepam
levetiracetam lamotrigine zonisamide felbamate |
|
Tx of infantile spasms
|
corticotropin/corticosteroids
|
|
anti-seizure drugs used for Tx of bipolar disorder (4)
|
valproic acid
carbamazepine phenytoin gabapentin |
|
which anti-epileptic drugs enhance activation of GABAa channels?
|
benzos
phenobarbital |
|
inhibits enzyme GABA transaminase
|
vigabatrin
- anti-seizure drug |
|
inhibits uptake of GABA
|
tiagibine
- anti seizure drug |
|
structural analog of GABA
|
gabapentin
|
|
which anti-seizure drugs inhibit Na+ channels?
|
phenytoin
carbamazepine lamotrigine *valproic acid and phenobarbital at high doses |
|
mechanism of action of ethosuximide
|
blocks T type Ca2+ channels (absence seizures)
|
|
mechanism of action of gaba pentin
|
blocks L type Ca2+ channels
|
|
phenobarbital
|
barbiturate w/ greater anti-eplileptic action
- can block both chemically and electrically induced seizures |
|
mechanism of action of phenobarbital
|
blocks Na+ channels, GABA Cl- channels and glutamate R
|
|
phenytoin is effective against (1) induced convulsions
not effect for (2) seizures |
1 = electrically induced
2 = absence seizures |
|
phenytoin metabolism
- mainly bound to (1) - displaced by (2) - causes induction of (3) - metabolism enhanced by (4) - metabolism inihibited by (5) |
1 - albumin in plasma
2 - phenylbutazone, valproic acid, salicylic acid, sulfonamides 3 - hepatic enzymes 4 - phenobarbital, rifampin 5 - cimetidine, isoniazid |
|
side effects of phenytoin (10)
|
1. vertigo
2. nystagmus 3. diplopia 4. headache 5. ataxia 6. hyperplasia of gums 7. hirsutism 8. megaloblastic anemia 9. hypersensitivity 10. teratogen |
|
uses of carbamazepine (3)
|
1 - complex partial seizures
2 - neuropathic pain 3 - bipolar |
|
carbamazepine metabolism can be inhibited by... (2)
|
propoxyphene
valproic acid |
|
side effects of carbamazepine (7)
|
1. diplopia
2. dizziness 3. drowsiness 4. ataxia 5. water retention 6. severe bone marrow depression (rare) 7. hepatic induction of enzymes |
|
carbamazepine accelerates metabolism of ... (4)
|
1. phenytoin
2. warfarin 3. OCP 4. corticosteroids |
|
oxycarbazine
|
prodrug that is metabolized to carbamazepine
--> less toxicity |
|
uses of valproic acid (3)
|
1. infantile epilepsy
2. adolescents w/ grand/petite mal seizures 3. bipolar |
|
valproic acid inhibits metabolism of .. (3)
|
1. phenytoin
2. lamotrigine 3. phenobarbital |
|
side effects of valproic acid (4)
|
1. balding/thinning of hair
2. hepatotoxicity 3. inhibition of drug metabolism 4. teratogen |
|
ethosuximide useful for... (2)
|
PTZ-chemically induced seizures
absence seizures |
|
side effects of ethosuximide (5)
|
1. nausea
2. anorexia 3. lethargy 4. dizziness 5. precipitates tonic-clonic seizures in suseptible pts |
|
mechanism of action of vigabatrin
|
inhibits GABA transaminase = increases GABA content of brain and CSF
|
|
main pro of vigabatrin?
main drawback? |
1 = effective in pts. resistant to other drugs
2 = occurence of depression and psychosis |
|
what is main, serious side effect of lamotrigine?
|
skin rashes
fatal Stephen Johnson syndrome aka. toxic epidermal necrolysis |
|
uses of felbamate
|
limited to severe, refractory seizure states i.e. Lennox-Gestaut syndrome in children
|
|
toxicity of felbamate (2)
|
aplastic anemia
acute hepatic failure |
|
uses of gabapentin (2)
|
1. neuropathic pain
2. add-on therapy w/ other anti-seizure drugs |
|
uses of topiramate
|
add on therapy in refractive cases
|
|
zonisamide
|
sulfonamide (antimicrobial)
used as backup drug in myoclonic seizures and partial seizures |
|
mephenesin
- inhibition of (1) reflex, without affecting (2) reflex - abolishes (3) - used IV to Tx (4) |
1 = polysynaptic withdrawl reflex
2 - tendon jerk reflex 3 - decerebrate rigidty 4 - acute muscle spasm in injury |
|
mechanism of action of baclofen
|
selective agonist at GABAb R
--> inhibits both monosynaptic and polysynaptic reflexes |
|
baclofen used to Tx...
|
muscle spasticity associated w/ MS or spinal injury
|
|
unwanted effects of baclofen
|
drowsiness
motor incoordination nausea |
|
Parkinson's disease is characterized by...
|
loss of DA neurons in substantia nigra
--> loss of inhibitory DA influence on cholinergic neurons, therefore -> increased Ach release in striatum |
|
symptoms of Parkinsons (4)
|
1. tremors
2. bradykinesia 3. muscular rigidity 4. gait |
|
secondary parkinson's can occur after..
|
viral encephalitis
multiple small vascular lesions |
|
do NOT give which drugs to Parkinson's patients? (2)
|
1 = phenothiazines
2 = haloperidol --> block DR receptors (exacerbate) |
|
what is levo-dopa?
|
precursor of DA that is converted in body by dopa-decarboxylase
|
|
side effects of levodopa (6)
|
1. nausea/vomiting
2. cardiac arrthymias 3. orthostatic hypotension 4. on-off phenomena 5. contraindicated in pts w/ history of psychosis 6. mydriasis |
|
on off phenomena
|
in Parkinsons
symptoms may go from akinesia to dyskinesia in a few hours due to changes in levels of levodopa in plasma |
|
carbidopa
- mechanism? (1) - effect? (2) |
1 = dopa decarboxylase inhibitor -> prevents peripheral metabolism of levodopa before it crosses BBB
2 = decreases dose needed of levodopa and decreases side effects |
|
indications for taking levodopa (2)
|
1. divided doses to prevent emetic action
2. take on empty stomach - bc protein interferes w/ absorption |
|
vitamin B6 and levodopa
|
vit B6 increases peripheral breakdown of levodopa
|
|
MAO + levodopa?
|
hypertensive crisis
--> bc of increased catecholamines |
|
effect of levodopa on intraocular pressure
|
INCREASES --> may cause glaucoma or exacerbate it
|
|
mechanism of action of selgeline
|
selective inhibitor of MAO-type b
(degrades DA, not NE/5HT) |
|
use of selegeline
|
adjunct to levodopa in Parkinsons OR newly diagnosed patients
|
|
selegeline metabolism
|
metabolized to dimethylselegiline (neuroprotectice) and amphetamine --> do NOT give past mid afternoon
|
|
side effects of selegiline (5)
|
1. insomnia
2. mood changes 3. dyskinesias 4. GI distress 5. hypotension |
|
selegiline
- take caution when giving with.. (2) |
1 - meperidine (delirium/death)
2. SSRIs (serotonin syndrome) |
|
entacapone/tolecapone
|
COMT inhibitors
--> decrease levels of 3-methyl-O-dopa (which competes w/ levodopa for transport) |
|
uses of entacapone/tolecapone
|
used as adjuncts to levodopa in Parkinsons
--> improve response and increase "on" time |
|
adverse effects of entacapone/tolecapone (6)
|
1. dyskinesias
2. GI distress 3. postural hypotension 4. sleep disorders 5. hallucinations 6. hepatic necrosis in tolecapone |
|
bromocriptine
(pergolide) |
D2-R partial agonist
->increases functional activity of DA nt pathways |
|
clinical use of bromocriptine/pergolide
|
used either alone in Tx. of Parkinsons or in adjunct w/ levodopa
|
|
side effects of bromocriptine (6)
|
1. hallucinations
2. delirium 3. confusion ** not to be used w/ psychotic pts 4. GI upset 5. dyskinesia 6. orthostatic hypotension |
|
what side effect is unique to ergot alkaloids?
|
pulmonary/retroperitoneal fibrosis
erythromelalgia |
|
pramiprexole
ropinirole |
non-ergot dopamine R. agonists
|
|
first line drugs in initial management of Parkinsons
|
pramiprexole
ropinirole |
|
side effects of pramiprexole/ropinorole
|
nausea
hallucinations insomnia dizziness constipation orthostatic hypotension |
|
rotigotine
|
Tx of early stage parkinsons
transdermal patch |
|
amantadine
|
anti-viral used to Tx. Parkinsons
- mechanism unknown |
|
side effects of amantadine (7)
|
1. agitation
2. confusion 3. hallucinations 4. acute toxic psychosis 5. orthostatic hypotension 6. peripheral edema 7. urinary retention |
|
examples of anti-muscarinic agents used to Tx. Parkinsons (4)
|
1. benztropine
2. trihexyphenidyl 3. procyclidine 4. biperiden |
|
anti-muscarinic drugs are contra-indicated in pts w/ (3)
|
1. glaucoma
2. prostatic hyperplasia 3. pyloric stenosis |
|
Alzheimer's Disease is characterized by... (3)
|
1. accumulation of B-amyloid plaques
2. neurofibrillary tangles 3. loss of cortical cholinergic neurons |
|
Ach-E inhibitors used in Tx. of Alzheimer's
|
tacrine
donepezil galantamine rivastigmine |
|
memantine
|
NMDA-R antagonist
|
|
use of memantine
|
neuroprotective against excitotoxicity
--> slows rate of memory loss in Alzheimers - often given in combo w/ AchE inhibitor |
|
riluzole
|
blocks Na+, Ca2+ and Glu channels
--> improved survival time for pts. w/ ALS |
|
mechanism of action of antidepressants
|
potentiate actions of 5HT and/or NE in the brain
|
|
why do antidepressants take 2-4 weeks to develop clinical effects?
|
presynaptic inhibitory receptor densities decrease over time resulting in increased synthesis and release of transmitter
|
|
drug class of choice in Tx. of depression
|
SSRIs
|
|
main SSRIs (6)
|
fluoxetine
citalopram escitalopram fluvoxamine paroxetine sertraline |
|
fluoxetine can alternatively be used to Tx...
|
bulimia
|
|
fluvoxamine can alternatively be used to Tx...
|
OCD
|
|
mechanism of action of SSRIs
|
block reuptake of 5HT = increase conc. of 5HT in cleft = increased POST stimulation
|
|
other therapeutic uses of SSRIs
|
panic disorder
GAD PTSD social anxiety disorder premenstrual dysphoric syndrome |
|
pharmacokinetics of SSRIs
- food increases absorption of (1) - sustained release formula (2) - metabolism? (3) - inhibit which cyp enzyme? (4) - excretion through (5) except (6) is fecal |
1 = sertraline
2 = fluoxetine 3 = hepatic metabolism 4 = cyp2d6 5 = kidneys 6 = paroxetine/sertraline |
|
side effects of SSRIs (8)
|
1. nausea
2. headache 3. anxiety 4. agitation 5. insomnia 6. sexual dysfunction 7. increased risk of suicide in children 8. lower the seizure threshold |
|
SSRI discontinuation syndrome
|
headache, malaise, flu-like symptoms, agitation, irritability, nervousness, palpitations
|
|
serotonin syndrome
|
life threatening syndrome
- severe muscle rigidity - myoclonus - hyperthermia - cardio instability - CNS stimulation - seizures |
|
drugs implicated in serotonin syndrome
|
reaction of SSRIs w/
- MAOis - TCAs -meperidine -MDMA |
|
Tx of serotonin syndrome
|
anti-seizure drugs
muscle relaxants 5HT receptor blockers |
|
venlafaxine
duloxetine |
serotonin-NE reuptake inhibitors
|
|
SNRIs used in Tx of.. (3)
|
1. refractory depression
2. chronic pain associated w/ depression 3. neuropathic pain |
|
mechanism of action of venflaxamine
|
potent 5HT reuptake inhibitor
inhibits NE reuptake at higher doses --> does not have muscarinic or histamine activity |
|
side effects of venflaxamine (6)
|
1. nausea
2. headache 3. sex dysfunction 4. dizziness 5 insomnia 6 high doses = increased HR/BP |
|
mechanism of action of duloxetine
|
inhibits both 5HT/NE reuptake at all doses
|
|
side effects of duloxetine (4)
|
1. GI - nausea, constipation
2. dizziness/insomnia 3. sex dysfxn 4. increased HR/BP |
|
bupropion - mechanism of action
|
weak DA and NE uptake inhibitor
-> atypical anti-depressant |
|
alternative use for bupropion (other than antidepressant)
|
decreases craving and withdrawl symptoms of nicotine use/addiction
|
|
adverse effects of bupropion (6)
|
1. dry mouth
2. sweating 3. nervousness 4. tremor 5. increased risk of seizures at high doses 6. aggravation of psychosis |
|
mechanism of action of mirtazepine
|
enhanced NE/5HT transmission by blocking PRE a2-R and 5HT-R
|
|
adverse effects of mirtazepine (3)
|
1. increases appetite/weight gain
2. sedative 3. autonomic effects |
|
nefazodone
trazadone |
weak inhibitors of 5HT uptake
block POST 5HT2a-R H1 blockers |
|
main adverse effect w/ trazadone
|
priapism
|
|
main adverse effect w/ nefazodone
|
hepatotoxicity
|
|
2nd generation antidepressants (4)
|
amoxapine
bupropion maprotiline trazodone |
|
3rd generation antidepressants
|
mirtazepine
nefazodone venlafaxine |
|
TCAs - tertiary amines (6)
|
imipramine
amitryptaline clomipramine doxepin trimipramine |
|
TCAs - secondary amines (3)
|
desipramine
nortryptaline protryptaline |
|
tetracyclic antidepressants (2)
|
maprotiline
amoxapine |
|
TCAs also block which receptors (3) resulting in (4)
|
1 = a-adrenergic
2 - histamine 3 - muscarinin 4 - SIDE EFFECTS!!! |
|
implications of TCA use
|
moderate to severe depression
- esp. if patient did not respond to SSRIs |
|
alternative uses of imipramine
|
bed-wetting in children
panic attacks ADHD |
|
alternative uses of amitryptaline
|
migraine headaches
chronic pain syndromes |
|
Adverse Effects of TCAs (6)
|
1. sedation, fatigue, confusion (H1 block)
2. sympathomimetic effects (adrenergic block) 3. atropinic effects 4. orthostatic hypotension 5. tremor 6. weight gain |
|
TCAs may exacerbate... (3)
|
1. unstable angina/arrythmias
2. BPH 3. epilepsy |
|
TCAs + MAOis interaction
|
mutual enhancement
= hypertension, increased body temp, convulsions, coma |
|
TCAs + ethanol/benzos/barbs
|
additive CNS depression
--> toxic sedation |
|
TCAs + clonidine/guanethidine/methyldopa
|
decreased anti-hypertensive effects
|
|
TCA manifested by...
|
the 3 C's
cardiotoxicity convulsions coma |
|
examples of MAOIs
|
phenylzine
tranycypromine selegeline |
|
selegeline used to Tx.
|
depression
Parkinsons |
|
indications for MAOIs
|
last line agents for pts/ unresponsive/allergic to TCAs/SSRIs or pts with strong anxiety
- Tx. of phobias - Tx of atypical depressions |
|
MAOi + bupropion
|
seizures
|
|
What must pts. on MAOIs avoid?
|
foods containing tyramine
-> tyramine normally metabolized by MAO -> tyramine has indirect sympathomimetic functions |
|
MAOi + tyramine
|
causes:
occiptal headache stif neck tachycardia nausea HTN cardaic arrhythmias seizures stroke |