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112 Cards in this Set

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drugs which prolong the state of inactivation of Na+ channels
PVC = phenytoin, valproate, carbamazepine (NB: remember that the Na+ channels exist in three states = activated, inactivated and resting)
DOC for generalized tonic-clonic seizures
phenytoin
phenytoin med use and tx
DOC for generalized tonic-clonic seizures, status epilepticus (diazepam is DOC), tx of episodic clonic movements following severe head injury

non-linear kinetics at large doses, i.e., at large doses elimination not first order
phenytoin S/E
gingival hyperplasia; ataxia, nystagmus, diplopia; psychological disturbances; megaloblastic anemia (interferes w folate metabolism); osteomalacia (responds to vitamin D), teratogenic (cleft lip/palate), not much sedation
DOC for trigeminal neuralgia
carbamazepine
carbamazepine MOA
MOA: prolong the state of inactivation of the Na+ channel = no impulse propagation
carbamazepine med use
tx of temporal lobe seizures, DOC for trigeminal neuralgia
carbamazepine S/E
S/E = monitor LFT’s, esp. in young patients or patients tx w valproate + other seizure meds

5) can cause increased release of AVP and potentiate the antidiuretic effects of AVP; the result is dilutional hyponatremia
Phenytoin and phenobarbital S/E
: induction of CYP450 which increases the metabolism of vit D and vit K (vit K a cofactor for the synthesis of osteocalcin);
Phenytoin and phenobarbital MOA
osteomalacia, decreased vit D lowers the GI absorption of Ca++. In order to maintain plasma [Ca++], bone is resorbed
DOC for absence seizures
ethosuximide
ethosuximide MOA
blocks T-type Ca++ channels in thalamus
baclofen MOA
interacts with GABAB-receptors linked to K+ channels, enhanced K+ conductance hyperpolarizes cells presynpatic membrane of glutaminergic neurons in spinal cord to prevent the release of glutamate onto alpha-motor neurons = decrease efferent excitation of spastic skeletal muscle
baclofen med use
tx of spasticity from spinal cord injury, CP, MS
dantrolene MOA
inhibits release of “trigger” Ca++ from SR in skeltal muscle
dantrolene med use
tx of spasticity from spinal cord injury, malignant hyperthermia, neuroleptic malignant syndrome
dantrolene S/E
generalized muscle weakness
desipramine (DMI), specificty of amine transporter

(know this one)
NE reuptake blocked, secondary amine
fluoxetine, paroxetine, citalopram, fluvoxamine; specificty of amine transporter
5-HT reuptake blocked = SSRI's
imipramine (tertiary amine), cloimpramine, venlafaxine; specificty of amine transporter
both NE & 5-HT reuptake blocked
S/E of antidepressants
FINE TREMOR, confusion in elderly patients, postural hypotension (alpha-blockade), sedation (central antimuscarinic effect), urinary retention and tachycardia (atropine-like effect), fine tremor, AV block (direct toxic effect)
MAO inhibitors are antidepressant because
they inhibit MAO-A which degrades NE & 5-HT (NB: MAO-B degrades DA)
schizophrenic patient w depression
tx w SSRI like fluoxetine
depressed pt w hypotension
tx w SSRI like fluoxetine
Depressed patient being tx w antidepressant suffers from sedation and hypotension
could be MAOI or TCA since both cause sleepiness and hypotension, but pick TCA bx TCA’s cause greater orthostatic hypotension than do MAOI’s
small child w nocturnal enuresis
tx w TCA for atropine-like effect in urinary bladder
Which NT involved in OCD?
5-HT
tx for OCD
clomipramine or SSRI (e.g., fluoxetine)
depresssed patient w CHF tx w digoxin is given TCA
inverts or flattens T-wave, slows conduction in fast fibers so QRS increased
imipramine (tertiary amine which blocks 5-HT & NE uptake1) converted to:
desipramine (secondary amine which blocks NE uptake1)
OD with imipramine:
usual effects are dec BP from alpha-blockade; inc HR from dec BP and anticholinergic effects; decreased AV conduction with inc Q-T interval
serotonin syndrome
results from excessive stimulation of central 5-HT receptors = inc BP, HR and respiration; increased muscle activity (muscle twitching, shivering, myoclonus) causing hyperthermia and sweating; pupillary dilation; confusion, agitation, hallucinations
the serotonin syndrome is caused by
an SSRI (e.g., fluoxetine) or a TCA whch blocks both NE and 5-HT uptake, e.g., imipramine), especially in patients taking an MAOI. MAOI (e.g., phenelzine) prevent the degradation of 5-HT in the CNS, and 5-HT accumulates in the cytoplasm of central 5-HT neurons
Antipsychotic drugs MOA
Block D2-receptors in mesolimbic DA pathway
DOC for Tourette’s syndrome (vocal and motor tics, coprolalia)
haloperidol
haloperidol S/E
least sedating, greatest likelihood of ESP
clozapine med use
effective in tx of negative symptoms; measure CBC weekly w clozapine tx
chlorpromazine prevents
emetic effects of D2-receptor stimulation at CTZ
Antipsychotic drugs S/E's
alpha-blockade = dizziness, orthostatic hypotension, inc HR , nasal stuffiness, impotence
- muscarinic blockade = dry skin & mouth, mydriasis, inc HR, urinary retention, sedation
- central D2-blockade = fine tremor, muscular rigidity, EPS, tardive dyskinesis, hyperprolactinemia, galactorrhea, amenorrhea

- neuroleptic malignant syndrome (vide infra)
Li+ MOA
inhibits enzymes important in recycling phosphoinostides, so PIP2 is depleted
Li+ S/E
- both HCTZ and furosemide enhance the reabsorption of Li+ in the PT causing toxicity

- S/E = tremor, motor and psychiatric disturbances; causes nephrogenic DI by inhibiting adenyl cyclase coupled to V2-ADH receptors in CD

- in a female patient with bipolar dz, must d/c Li+ tx during first trimester to prevent teratogenesis (Ebstein’s anomaly = leaflets of mitral valve displaced downward into right ventricle, tricuspid regurgitation, right ventricular dysfunction)
Drugs which can cause Parkinsonian-like side effects
D2-receptor antagonists like haloperidol, chlorpromazine, trifluperazine
Drugs used to treat PD
levodopa, carbidopa, selegiline, benztropine, bromocriptine, amantadine
levodopa MOA
precursor of DA which is pumped into the brain via the aromatic amino acid pump; tx w vitamin B6 interferes w therapeutic action of levodopa because B6 increases peripheral decarboxylation of levopdopa to DOPA
carbidopa MOA
inhibits DOPA (L-aromatic amino acid) decarboxylase outside brain to enhance the amount of DOPA taken up by the brain and converted to DA
benztropine MOA
central muscarinic receptor blockade
selegiline MOA
selective MAO-B inhibitor, blocks breakdown of DA in CNS
bromocriptine MOA
central D2-dopamine receptor agonist
amantadine MOA
antiviral drug which release DA centrally
carbidopa + levodopa
- can reduce the dose of DOPA
- prevents decarboxylation of DOPA outside CNS
- carbidopa does not enter CNS
- carbidopa does not attenuate the orthostatic hypotension caused by levodopa
levodopa can cause (S/E)
the reappearance of psychotic symptoms in a schizophrenic patient with PD caused by tx w typical antipsychotic drugs (e.g., haloperidol)
Drugs which increase plasma prolactin
-D2-dopamine receptor blockers like haloperidol
- reserpine
- metoclopramide
- alpha-methyldopa
how to treat Parkinson's and reverse hyperprolactinemia
bromocriptine
Ethanol kinetics
oxidized to acetaldehyde by alcohol dehydrogenase; acetaldehyde degraded to water and CO2 by acetaldehyde dehydrogenase
- alcohol dehydrogenase easily saturated a low concentrations of ethanol, so ethanol removed by zero-order kinetics = constant amount of drug/h
acetaldehyde dehydrogenase inhibited by: (2 drugs)
disulfiram & metronidazole; build up of acetaldehyde causes peripheral vasodilation (red skin), n/v, pulsating headache, sweating, chest pain, vertigo, syncope, blurred vision, confusion
patient being treated for Giardia + some other infection (e.g., bacterial) develops n/v and headache after drinking a beer. Which drug causes this rx
metronidazole
Alcoholism causes:
- hyperlipidemia and fatty infiltration of the liver
- cardiomyopathy, portal hypertension, gastric ulceration, esophageal varices
- Wernicke-Korsakoff syndrome - ass w thiamine deficiency - get paralysis of external eye muscles, altered mentation and ataxia
fetal alcohol syndrome
flattened face, short nose, short palpebral fissures = underdevelopment of mid-facial region, microcephaly with low IQ, retarded growth
Methanol toxicity
- severe visual disturbance (“like being in a snow storm”) with relatively clear sensorium, headache, dyspnea, cold digits, GI pain, breath smells of formaldehyde.
- treat w ethanol to saturate enzymes which degrade EtOH and MeOH because toxic product of MeOH appears to be a formate compound produced by the sequential actions of alcohol and acetaldehyde dehydrogenases
ingestion of ethylene glycol from antifreeze
converted to aldehydes, acids and oxalate: oxalate causes acute renal failure
Amphetamine toxicity:
nervousness, restlessness, insomnia, hypertension, tachycardia, hyperthermia, toxic psychosis = paranoid schizophrenia, weight loss, formication, tonic-clonic seizures.
- pupillary dilation from the release of NE in the radial muscle
Use of methylphenidate for tx of ADD and ADHD in children can cause: (S/E)
depression, insomnia, loss of apetite, weight loss, slowed growth rate
to normalize breathing in neonatal apnea
theophylline, aminophylline & caffeine used
phentermine suppresses appetite via
the release of NE in the hypothalamus
MDMA (“ecstacy’) = methylenedioxymetamphetamine - can cause (long term S/E)
degeneration of central 5-HT neurons
All sedative-hypnotic drugs (barbiturates, benzodiazepines, choral hydrate, glutethimide) cause:
dependence, shortened sleep latency, suppression of REM sleep, tolerance, rebound insomnia, respiratory depression. They are NOT analgesic.
oil: water partition coefficient predicts:
drug with most rapid onset (the higher the coefficient the faster it diffuses into the brain)
Barbiturate MOA:
Low therapeutic index/window.

enhance GABA-A receptor-mediated increase in Cl- conductance to hyperpolarize neurons: enhances duration of channel opening
in older pts, Barbiturates can cause:
paradoxical excitation
thiopental MOA and med use:

(know this one)
- used for induction of anesthesia, short duration of action due to redistribution
(blood-brain/viscera -> skeletal muscle- -> fat

- transient decrease in BP with reflex increase in HR and dP/dT, so CO NOT DEPRESSED
Benzodiazepine MOA:
enhance GABAA receptor-mediated increase in Cl- conductance to hyperpolarize neurons; enhances rate of channel opening
Benzodiazepines in older patients
exhibit inc t1/2 due to dec Cl; inc free plasma concentration from dec plasma
protein binding; inc receptor sensitivity to BZ’s = inc risk of falls and hip fracture
with benzodiazepines, less PBPs means:
more effect
benzodiazepines for old people
lorazepam and oxazepam

cleared by glucuronidation in blood rather than CYP450
BZ withdrawal syndrome
anxiety, dysphoria, agitation, insomnia, vomiting, sweating, muscle and abdominal cramps, myoclonic jerks, convulsions. No CV effects!
flumazenil
BZ receptor antagonist; used to tx OD with BZ's; will also precipitate the BZ withdrawal syndrome in a patients addicted to BZ's
zolpidem
a non-BZ hypnotic drug; acts to increase Cl- conductance
Buspirone MOA
a partial agonist at 5-HT1A receptors linked to K+ channel: causes hyperpolarization to suppress neuronal activity
Buspirone effects
anxiolytic but not addictive

Slow onset of action compared to BZ's; no sedation or interaction w EtOH
3) No hypnotic, anticonvulsant or muscle relaxant effects
Drug schedule
Class 1: heroin, LSD, marihuana, mescaline, PCP, psilocybin, MDA, DMT, DET, bufotenine = no med uses

Class 2: opiates, amphetamines, cocaine, some barbiturates, dronabinol
= no tel scripts/refills

Class 3: codeine, opium, some barbiturates = rewrite script after 6 mo or 5 refills

Class 4: BZ’s pentazocine, propoxyphene, phenobarbital = rewrite script after 6 mo or 5 refills

Class 5: diphenoxylate
mu receptors:
- analgesia = supraspinal mu1 in periaqueductal gray and spinal mu2
- morphine causes analgesia in humans via stimulation of supraspinal mu1 and spinal mu2 receptors, but predominant effect is supraspinal mu1
- respiratory depression = mu2
- decreased GI motility = mu2
- miosis = increases PSNS activity from E-W nucleus to sphincter muscle of iris
- euphoria
- physical dependence
supraspinal effect of opiates
a.GABA neuron normally inhibits pain-inhibiting neurons (PIN)
b.Opiates inhibit GABA neuron, so no GABA released onto PIN = no inhibition of PIN = central descending inhibition of pain pathways
c. (inhibitory effect on GABA neurons can explain seizures caused by some opiates like meperidine)
spinal effect of opiates
opiates block nociceptive stimuli in ascending spinothalamic pathways

a.mu2, delta2 & kappa1 stimulation decreases NT release (probaby glutamate) from presynaptic terminal of nociceptive primary afferent
b.mu receptor stimulation creates IPSP (hyperpolarization) in secondary ascending pain transmission neuron
full agonists at mu receptor
“morphine met me finally”

morphine, methadone, meperidine, fentanyl
partial agonists at mu receptor
“partially b-blocks narcotics”

pentazocine, butorphanol, nalbuphine, buprenorphine
toxicity triad of opiates
miosis, coma, depressed respiration
opiate tolerance
tolerance to everything but no tolerance to miosis or constipation
opiate withdrawal
rhinorrhea, lacrimation, chills, n/v, diarrhea, hyperthermia, sweating and piloerection (“goose flesh”), myalgia, tremor, urticaria, mydriasis, anxiety, hostility
diphenoxylate
least potential for addiction; used to tx diarrhea
morphine is DOC for pain and pulmonary edema caused by acute MI bx:
it acts in CNS to dec SNS activity: dec preload and afterload.
tx of female w acute pain from gallstones w morphine causes greater pain. Why?
Morphine contracts smooth muscle of gall bladder
female on methadone has emergent surgery and is tx w butorphanol; patient experiences S/S of opiate withdrawal. Why?
Butorphanol is a partial agonist at mu receptors. The partial agonists pentazocine, nalbuphine and buprenorphine can also cause S/S of opiate withdrawal in a patient taking methadone
which opiate does not cause a dose-related inhibition of respiration
the partial agonists pentazocine, butorphanol and nalbuphine
newborn baby has respiratory depression bx:
mom received an opiate during labor
patient with MI tx with morphine, why?
Chest & arm pain inc the activity of the sympathetic nervous system which constricts arterioles and venules to increase preload and afterload. The damaged heart cannot pump the increased venous return, especially in the face of an increase in afterload. Morphine acts centrally to decrease pain and to decrease sympathetic outflow. Decreased activity of the SNS decreases preload and afterload and improves CO. the analgesic effects of morphine also make the patient more comfortable.
Nitrous oxide N2O cannot be used for anesthesia bx:
Its MAC is 100%. pt must have at least 20% oxygen.
Question re: potency or MAC
Most potent drug has the smallest MAC gas with lowest MAC (most potent) = gas with the highest oil/gas partition coefficient. gas with the highest MAC (least potent) = gas with lowest oil/gas coefficient
factors controlling the rate of induction of anesthesia:
- alveolar ventilation rate
- blood/gas partition coefficient
- partial pressure of gas in lungs
- cardiac output
- increase in FI (concentration of gas in inspired air) = concentration effect = increase dose
- cerebral blood flow
- NOT potency (MAC)
high MAC and fast induction and recovery
an anesthetic gas with low lipid solubility
low MAC and slow induction and recovery
an anesthetic gas with high lipid solubility
second-gas effect
A rapidly absorbed gas inc the rate of uptake of a second gas.Give 70% nitrous oxide + 0.78% halothane + 29% oxygen, and the rapid uptake of nitrous oxide pulls the halothane along with it.
diffusion hypoxia
When N2O is stopped, a large volume of N2O dilutes the oxygen, and the patient becomes hypoxic. Occurs during first 10 min after dc of N2O, tx patient w 100% oxygen
empty air spaces and N2O
If the air-filled cavity is non-compliant (e.g., sinuses, middle ear and cerebral ventricles), intracavity pressure increases. Increased middle ear pressure can rupture the tympanic membrane or cause n/v after surgery.
factors controlling rate of offset of anesthesia
- blood/gas partition coefficient
- hyperventilation
- cardiac output
- drug metabolism by the liver
CV effects - halothane, isoflurance, enflurane
- all volatile agents decrease MAP by decreasing either CO or TPR, but effect to decrease BP is attenuated in the presence of N2O which tends to increase sympathetic activity
- isoflurane has little effect on CO
Ketamine MOA
blocks NMDA glutamate receptor coupled to Ca++ channel (NB: glutamate is an
excitatory NT in the CNS)
Ketamine med use
- produces a dissociative state of consciousness, analgesia and postanesthetic hallucinations
- least likely to supppress respiration (all opiates, barbiturates, BZ’s and gaseous anesthetics suppress respiration)
- MAP via inc CO (inc LV-EDP, dp/dt, HR). Little effect on TPR.
Etomidate MOA:
enhances GABAA-mediated chloride conductance to hyperpolarize neurons
- minimal effect on BP or respiration
Etomidate med use:
- causes myoclonic movements (not epilepsy) which can be prevented by pretx w BZ’s
- can cause adrenal suppression w decrease in plasma cortisol
Which of the following drugs decreases BP and respiration when given i.v.?
1) opiate - BP = nc, dec respir;
2) ketamine - inc BP, respir = nc;
3) etomidate - BP & respir = nc;
4) thiopental - dec BP and respir
Nitrous oxide produces analgesia, amnesia and mental confusion, but does not cause what?
anesthesia!
Halothane predisposes to :
Epi-induced cardiac arrhythmias: tx w beta-blocker.