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151 Cards in this Set

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**Drugs which prolong the state of inactivation of Na channels:

**DOC for generalized tonic-clonic seizures.

**Treatment of status epilepticus (=diazepam is DOC)

**Treatment of episodic clonic movements following severe head injury
Side Effects:
=gingival hyperplasia
=psychological disturbances
=megaloblastic anemia (interferes w/ folate met.)
Yes--cleft lip/palate
**Treatment of temporal lobe seizures

**DOC for trigeminal neuralgia
**Monitor LFT's especially in young patients or patients w/ treated w/ valproate + other seizure meds

**Can cause an increased release of AVP + potentiate antidiuretic effects of AVP
=dilutional hyponatremia
Phenytoin and phenobarbital cause osteomalacia. How?
**They induce CYP450 --> which increases metabolism of vitamin D and vitamin K
=decreased vitamin D lowers the GI absorption of calcium
=in order to maintain plasma Ca, bone is resorbed
**Metabolized to phenobarbital but probably acts directly on Na channels like phenytoin
=blocks T-type Ca channels in the thalamus

**DOC for absence seizures
What is an absence seizure?
Blank stare, eyelids flutter, 3/sec spike wave rhythms from the thalamus
Baclofen MOA
Interacts w/ GABA (B) receptors linked to K-channels
=enhanced K conductance hyperpolarizes glutaminergic neurons in sc --> prevents release of glutamate onto alpha-motor neurons
=decreased excitation of SPASTIC skeletal muscle
Used to treat spasticity from sc injury, CP, or MS
Dantrolene MOA
**Inhibits release of "trigger" Ca from SR in skeletal muscle
Treatment of spasticity from SC injury, malignant hyperthermia, NMS
Generalized muscle weakness
What blocks NE reuptake?
Desipramine (secondary amine)
What blocks 5-HT uptake?
What blocks BOTH NE and 5-HT reuptake?
=imipramine (tertiary amine)
S/E's of antidepressants:
1) Confusion in the elderly
2) Postural hypotension
=alpha blockade
3) Sedation
=central antimuscarinic effect
4) Urinary retention and tachycardia
=atropine-like effect
5) Fine tremor and AV block
MOA of MAO inhibitors:
**inhibit MAO-A which degrades NE and 5-HT

recall: MAO-B degrades DA
Schizophrenic patient w/ depression
SSRI like fluoxetine
Depressed patient w/ hypotension
SSRI like fluoxetine
Depressed patient being treated w/ an antidepressant suffers from sedation + hypotension
**Could be an MAOI or TCA since BOTH cause sleepiness and hypotension, but pick the TCA because they cause greater orthostatic hypotension than do MAOI's
Small child w/ nocturnal enuresis
Treat w/ TCA for atropine-like effect in urinary bladder
Which NT is involved in OCD?

**Treatment for OCD
=Clomipramine or
Depressed patient w/ CHF is treated w/ digoxin. He is given a TCA.
Inverts or flattens T-wave --> slows conduction in fast fibers so QRS is increased
What are the usual effects when you OD w/ imipramine?
1) Decreased BP
=alpha blockade
2) Increased HR from decreased BP and anticholinergic effects
3) Decreased AV conduction w/ increased Q-T interval
What are the symptoms of serotonin syndrome?
1) Increased BP, HR, and respiration
2) Increased muscle activity
=muscle twitchcing, shivering, myoclonus
=causes hyperthermia and sweating
3) Pupillary dilation
4) Confusion, agitation, hallucinations
What causes the Serotonin Syndrome?
**Results from excessive stimulation of central 5-HT receptors
=caused by an SSRI or a TCA which blocks BOTH NE and 5-HT uptake (i.e. impipramine) ESPECIALLY in patients taking an MAOI
=MAOIs can prevent the degradation of 5-HT in the CNS--> 5HT accumulates in central neurons
Block D2 receptors in the mesolimbic DA pathway
**Least sedating
**Greatest liklihood of EPS
DOC for Tourette's Syndrome
**Effective in treatment of negative symptoms

=must measure CBC weekly
**Prevents emetic effects of D2-receptor stimulation in the CTZ
1) Alpha blockade
2) Muscarinic blockade
3) Central D2 blockade
4) Neuroleptic Malignant Syndrome
What are the effects of an alpha blockade?
=dizziness, orthostatic hypotenstion, increased HR, nasal stuffiness, impotence
What are the effects of a muscarinic blockade?
=dry skin and mouth, mydriasis, increased HR, urinary retion, sedation, hyperprolactinemia, galactorrhea, amenorrhea
Lithium MOA
=Inhibits enzymes important in recycling phosphoinostides

=SO, PIP2 is depleted
What drugs enhance the reabsorption of lithium in the PT causing toxicity?
=Motor and psychiatric distrubances

**Causes NEPHROGENIC DI by inhibiting adenyl cylcase cocupled to V2-ADH receptors in the CD
In a female patient w/ bipolar disease, you must DISCHARGE lithium in the 1st trimester to prevent teratogenesis.
**Called "Ebstein's Anomaly"
=leaflets of mitral valve displaced downward into right ventricle
=tricuspid regurgitation
=right ventricular dysfunction
What are drugs that cause parkinson's-like side effects?
=D2-receptor antagonists like haloperidol, chlorpromazine, trifluperazine
**Precursor of DA which is pumped into the brain via the aromatic amino acid pump
What can interfere w/ the therapeutic action of L-dopa?
**Treatment w/ vitamin B6
=increases peripheral decarboxylation of levodopa --> DOPA
**inhibits DOPA decarboxylase outside the brain to ENHANCE the amount of DOPA taken up by the brain and converted to DA
=central muscarinic receptor blockade
=Central D2 dopamine receptor agonist
=antiviral drug which releases DA centrally
=selective MAO-B inhibitor --> blocks breakdown of DA in CNS
Benefts of Carbidopa + Levodopa
1) Can reduce the dose of DOPA
2) Prevents decarboxylation of DOPA outside of CNS
3) Carbidopa does NOT enter the CNS
4) Carbidopa does NOT attenutate the orthostatic hypotension caused by L-DOPA
What about treatment of a schizophrenic patient w/ levodopa?
=Levodopa can cause the reappearance of psychotic symptoms in a schizophrenic patient w/ parkinsonian symptoms caused by typical antipsychotic drugs (i.e. haloperidol)
What are drugs that INCREASE plasma prolactin?
1) D2-receptor blockers like haloperidol
2) Reserpine
3) Metoclopramide
4) alpha-methyldopa
What are the effects of hyperprolactinemia?
=anovulatory cycles and infertility
=decreased libido/impotence in men
**D2 receptor agonist
=used to treat PD AND
=inhibit prolactin release in hyperprolactinemia

**Reverses infertility caused by hyperprolactinemia
=Oxidized to acetaldehyde by alcohol dehydrogenase
=Acetaldehyde will be degraded to water + CO2 by acetaldehyde dehydrogenase
Kinetics of Ethanol
**Alcohol dehydrogenase is easily saturated w/ low concentrations of ethanol --> SO ethanol is removed by ZERO ORDER KINETICS
=a constant amount of drug/hour
What inhibits acetaldehyde dehydrogenase?
1) Disulfiram
2) Metronidazole
Aldehyde Syndrome
**Build up of aldehyde causes:
=red skin
=pulsating headache
=chest pain
=vertigo, syncope, blurred vision
EtOH and body heat
EtOH enchances the loss of body heat by peripheral vasodilation
A patient is being treated for Giardia and some other infection. They develop n/v and a headache after drinking a beer. Which drug causes this?
Alcoholism causes:
1) Hyperlipidemia + fatty infiltration of the liver
2) Cardiomyopathy, portal HTN, gastric ulceration, esophageal varices
3) Wernicke-Korsakoff Syndrome
What is Wernicke-Korsakoff Syndrome?
**Associated w/ thiamine deficiency
=get paralysis of external eye muscles
=altered mentation
Fetal Alcohol Syndrome
*underdevelopment of mid-facial region
=Flattened face
=Short nose
=Short palpebral fissures

=microcephaly w/ low IQ
=retarded growth
Methanol Toxicity
**Severe visual disturbance
=like being in a snow storm
**Relatively clear sensorium
**Headache, dyspnea, cold digits, GI pain
**Breath smells of formaldehyde
How do you treat this?
**Treat w/ ETHANOL to saturate enzymes which degrade EtOH and MeOH because the TOXIC product of MeOH appears to be a FORMATE COMPOUND produced by the normal breakdown of alcohol and acetaldehyde dehydrogenases
What is the toxic product of ethylene glycol (=antifreeze)?
**Converted to OXALATE
=causes acute renal failure
Amphetamine Toxicity
=Nervousness, restlessness, insomnia
=HTN, tachycardia, hyperthermia
=Toxic psychosis --> paranoid schizophrenia
=weight loss + formication
=tonic-clonic seizures
What about the EYES?
**With early use, you get pupillary DILATION from the release of NE in the radial muscle.
**With PROLONGED use, you get MIOSIS due to depletion of NE
Does amphetamine withdrawl cause delerium tremors (DT's)?
Treatment of ADD and ADHD in children:
Side Effects:
**Can cause:
=depression, insomnia
=loss of appetite + weight loss
Drugs for neonatal apnea
What drug suppresses appetite via the release of NE in the hypothalamus?
What is the effect of MDMA = "ecstacy"?
**can cause degeneration of central 5-HT neurons
=barbiturates, benzos

**Shortened sleep latency--suppression of REM sleep
**Rebound insomnia
**Respiratory depression

=general CNS depressants with a LOW therapeutic indez
**Enhance GABA-A receptor-mediated increase in Cl conductance to HYPERPOLARIZE neurons
=enhances DURATION of channel opening
What about in older patients?
**Can cause a PARADOXICAL excitation.
Which of the barbiturates is the LEAST sedating?
**POOR analgesic activity
=used for the induction of anesthesia
=SHORT duration of action due to redistribution from blood/brain/visera --> skeletal muscle --> fat
CV effects of thiopental:
=Transient decrease in BP w/ reflex increase in HR and dp/dt

**SO, CO is NOT depressed.
=enhances GABA-A-receptor mediated increase in Cl conductance to hyperpolarize neurons
=enhances RATE/FREQUENCY of channel opening
What about in older patients?
**In older patients, drugs have a longer t1/2 due to decreased chlorine
=increased receptor sensitivity to BZ's
So, which benzos are preferred for older patients?

=cleared by glucuronidation rather than CYP450 --> rate of glucuronidation does NOT decrease with age
Which has the shortest t1/2?
=used to treat INSOMNIA

**Greatest risk of rebound insomnia
BENZO Withdrawl Syndrome
=Anxiety, agitation
=Vomiting, sweating, muscle and abdominal cramps
=Myoclonic jerks and convulsions

=used to treat OD w/ Benzo's
=also can precipitate the withdrawl syndrome in patients addicted to benzos
**a non-BZ hypnotic drug
=acts to increase chloride conductance
**Partial agonist at 5-HT-Ia receptors linked to K channels
=causes HYPERPOLARIZATION to suppress neuronal acvitiy
**Slow onset of action conpared to BZ's

**NO sedation or interaction w/ EtOH
=no hypnotic, anticonvulant, or muscle-relaxant effects
Class I

=no medical uses
Class II

=no telephone scripts/refills
Class III

=Rewrite script after 6 months or 5 refills
=Some barbiturates
Class IV

=Rewrite script after 6 months or 5 refills
Class V
Clinically useful opiates are relatively selective for MU receptors--but LARGER doses affect all opiate receptors (=mu, kappa, and delta)
Mu Receptors

=What are the natural agonists?
What causes analgesia?
**Morphine causes analgesia in humans via stimulation of supraspinal mu1 and spinal mu2 receptors
=respiratory depression --> mu2
=decreased GI motility --> mu2
Other Effects of Stimulation at mu receptors?
1) Miosis
2) Euphoria
3) Physical dependence
Kappa Receptors--natural agonists?
Analgesia caused by:
Supraspinal kappa3 and spinal kappa1
Other Effects of Stimulation at kappa Receptors?
=depersonalized feelings
Delta Receptors--agonists?
**Supraspinal and spinal analgesia--SPINAL more important

(recall: at the mu receptors--supraspinal was the dominant effect) is the SUPRASPINAL effect established?
**GABA neuron normally inhibits pain-inhibiting-neurons (PINs)

**Opiates inhibit the GABA neuron
=so no GABA is released onto the PINs = NO inhibition of PINs --> and we get a central descending inhibition of pain pathways
How is the SPINAL effect achieved?
**Opiates block nociceptive stimuli in ascending spinothalmic pathways
=mu2, kappa1, and delta2 stimulation DECREASES NT (glutamate) release
SO, the mu, delta, and kappa receptors are coupled to G-proteins:
**mu and delta --> increased K conductance = HYPERPOLARIZATION

**kappa = decreased Ca conductance
SO, summary of actions of opiates:
1) Analgesia
2) Respiratory Depression
=increase in the threshold CO2 which activates the medullary respiratory center
3) Constipation
4) Miosis
5) Sedation, euphoria, dysphoria, physical dependence
6) Cough suppression
7) Emesis

**Not as much effect on BP or HR in the supine patient
=though, IV morphine can induce histamine release which can DECREASE BP + cause itching/hives
Other adverse CV effect of morphine?
**Can act centrally to cause orthostatic hypotension
What 2 Symptoms does an addict NOT GAIN tolerance to?
1) Miosis
2) Depressed respiration
3) Coma
Which drugs cause LESS depression of respiration?
Symptoms of Opiate Withdrawl:
=Chills, hyperthermia, sweating, + piloerection ("goose flesh")
=n/v, diarrhea
=myalgia, tremor
=anxiety, hostility
Which opiate has the LONGEST DURATION of action?
=active p.o.
=duration of 15-30 hours --> important for keeping addicts OFF morphine
Which drug causes the GREATEST inhibition of respiration?
Whihch has the LEAST POTENTIAL for addiction?

**used to treat diarrhea
DOC for pain and pulmonary edema caused by acute MI
=bc it acts in the CNS to decreases SNS activity
=decreases preload and afterload
A female w/ acute pain from gallstones is treated with morphine. She is in greater pain. WHY?
Morphine contracts the SM of the GB.

recall: opiates can cause SM contraction in the biliary tract + GU tract
Female on methadone has emergent surgery and is treated w/ butorphanol. The patient experiences S/S of opiate withdrawl. Why?
**Butorphanol is a partial agonist at mu receptors--displaces the methadone.
What are the other partial agonists?
Which opiate does NOT cause a dose-related inhibition of respiration?
=the partial agonists pentazocine, butorphanol, and nalbuphine
Newborn baby has respiratory distress depression--why?
Mom recieved an opiate during labor.
Patient w/ MI is treated w/ morphine. WHY?
**Chest and arm pain INCREASE the activity of the sympathetic NS which constricts arterials + venules to increase the preload + afterload
=damaged heart cannot pump increased venous return
=SO, morphine acts centrally to decrease pain and DECREASE sympathetic outflow --> dec. pre/afterload --> improves CO
**The concentration of inspired air which is required to cause a surgical plane of anethesia in 50% of patients

**Measure of anesthetic potency and is INVERSELY related to the oil/gas partition coefficient
Nitrous Oxide
**CANNOT be used for anesthesia because its MAC is >100%
=even if it were 90%, you still couldn't use it --> patient has to breathe at least 20% oxygen to prevent hypoxia
What are drugs that LOWER the MAC (=dose) of volatile anesthetic agents?
1) NO
2) BZ's
3) Opiates
4) Ketamine
5) Barbiturates
6) EtOH
Blood/Gas Partition Coefficient
**Determines rate of onset (induction)/offset of anesthesia
=agents that are POORLY soluble in blood have a RAPID rate of onset/offset
Review --> You are given a question regarding potency or MAC.
**Most POTENT drug has the SMALLEST MAC

**Gas w/ the LOWEST MAC = gas w/ the HIGHEST oil/gas partition coefficeint

**Gas w/ the highest MAC = gas w/ the lowest oil/gas partition coefficient
**An anesthetic gas w/ LOW lipid solubility = HIGH MAC and fast induction and recovery

**An anesthetic gas w/ HIGH lipid solublity = low MAC and SLOW induction and recovery
Second-Gas Effect
**A rapidly absorbed gas INCREASES the rate of uptake of a second gas
=i.e. give 70% nitrous oxide + .78% halothane + 29% oxygen
=the rapid uptake of NO pulls the halothane along w/ it!
THUS, the arterial tension (partial pressure) of halothane rises MORE RAPIDLY when given w/ NO --> what is the NET effect?
**Net effect is 2 fold:
=Steady-state alveolar concentration of halothane is increased
=the MAC of halothane is decreased
What is diffusion hypoxia?
**NO is VERY insoluble in blood
=when its administration is STOPPED, large volumes of NO pour out of the blood into the lungs --> dilutes O2 --> patient becomes hypoxic
When does it occur?
**Occurs in the first 10 minutes after discharge of NO

**Treat patient w/ 100% oxygen
Other Complications of Using NO:
**NO can easily leave the blood and enter ANY air-filled cavity in the body
=i.e. IF the air-filled cavity is non-compliant--sinuses, middle ear--cavity pressure increases --> can cause a RUPTURE of the tympanic membrane or cause n/v after surgery
Factors Controlling the RATE of Induction of Anesthesia:
1) Alveolar ventilation rate
2) Blood/gas partition coefficient
3) Partial pressure of gas in lungs
4) CO
5) Increase in FI = [ ] of gas in inspired air
6) Cerebral blood flow
What does NOT affect this rate?
Factors Controlling the Rate of OFFSET of Anesthesia?
=Blood/gas partition coefficent
=Drug metabolism by the liver
CV Effects of Halothane, Isoflurane, and Enflurane
**Decrease MAP by decreasing either CO or TPR
=IF in the presence of NO, however, they will not decrease BP

**Isoflurane has little effect on CO
Complications after use of Methoxyflurane:
**Causes RENAL FAILURE after surgery via release of fluoride ions.
Ketamine MOA
**Blocks NMDA glutamate receptor coupled to Ca channel
**Produces a dissociative state of consiousness + analgesia + postanesthetic hallucinations

**LEAST LIKELY to suppress respiration.
=all opiates, barbs, benzos, and gaseous anesthetics suppress respiration
Etomidate MOA:
**Enhances GABA-A-mediated chloride conductance to hyperpolarize neurons
**Minimal effect on BP or respiration
**Causes myoclonic movements (=not epilepsy) which can be prevented by pretreatment w/ BENZO's
**Can cause adrenal suppression w/ decrease in plasma cortisol
BP --> no change

Decreased respirations
Increased BP

NC in respirations
BP and respirations no change
DECREASED BP and respirations
What does halothane predispose you to?
**Epi-induced cardiac arrhythmias

**Treat w/ a B-blocker
One more time...what does NO NOT cause?
**NO produces analgesia, amnesia, and mental confusion but NOT anesthesia!