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26 Cards in this Set

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Drugs used to treat Park Dz
- levodopa = 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 bx B6
increases peripheral decarboxylation of levopdopa to DOPA

- carbidopa = inhibits DOPA (L-aromatic amino acid) decarboxylase outside brain to enhance the amount of DOPA taken up by the brain and converted to DA

- bromocriptine = central D2-dopamine receptor agonist

- amantadine = antiviral drug which release DA centrally

- SELEgiline = SELEctive MAO-B inhibitor, blocks breakdown of DA in CNS

- benztropine = central muscarinic receptor blockade
what enahnces central actions of levodopa in Park Dz?
centrally-acting anticholingergic drugs
carbidopa + levidopa
- 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
S/E of levodopa
can cause reappearance of psychotic Sx (b/c levodopa incr DA) in schizophrenic who developed Park Dz d/t typical antipsychotic like haloperidol
D2-R blockers like haloperidol?
-reserpine
-alpha-methyldopa
-metoclopramide
bromocriptine
D2-dopamine receptor agonist; used to treat PD and inhibit prolactin
release in hyperprolactinemia; reverses infertility caused by hyperprolactinemia
EtOH
- EtOH oxidized to acetaldehyde (via alcohol dehydrogenase)
-acetaldehyde==>water and CO2 (via acetaldehyde dehydrogenase)

- alcohol dehydrogenase easily saturated at low concentrations of ethanol, so ethanol removed by zero-order kinetics = constant AMOUNT of drug/h

- acetaldehyde dehydrogenase inhibited by disulfiram & metronidazole (given to alcoholics to help them stop drinking)
==>build up of acetaldehyde causes peripheral vasodilation (red skin), n/v, pulsating headache, sweating, chest pain, vertigo, syncope, blurred vision, confusion (so you feel like shit if you drink)

- EtOH enhances loss of body heat by peripheral vd (drunk guy on the Titanic)
case: patient being treated for Giardia + some other infection (e.g., bacterial) develops n/v and headache after drinking a beer. Which drug causes this
metronidazole

acetaldehyde dehydrogenase inhibited by disulfiram & metronidazole (given to alcoholics to help them stop drinking); build up of
acetaldehyde causes peripheral vasodilation (red skin), n/v, pulsating headache,
sweating, chest pain, vertigo, syncope, blurred vision, confusion (so you feel like shit if you drink
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.

- (House episode: prison inmate) 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
ethylene glycol
(antifreeze)

converted to aldehydes, acids and oxalate
==>oxalate causes acute renal failure
MDMA (“ecstacy’) = MethyleneDioxyMetAmphetamine
can cause degeneration of central 5-HT neurons
sedative-hypnotic drugs
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.
barbiturates
1) oil: water partition coefficient predicts drug w most rapid onset of action

2) MOA: enhance GABA-A receptor-mediated increase in Cl- conductance to hyperpolarize neurons: enhances duration of channel opening

3) can cause paradoxical excitation in older patients

4) decrease sleep latency, but decrease REM and slow-wave sleep

5) phenobarbital is active when given p.o. and is the least sedating

6) thiopental:
- poor analgesic activity
-used for induction of anesthesia, short duration of action due to redistribution
(blood-brain/viscera ==>skeletal muscle==>fat; thus what decreases concentration is not drug metabolism by liver or kidney, it’s redistribution

-transient decr BP with reflex incr in HR and dP/dT, so CO not depressed
older pts taking benzodiazepines
older patients exhibit incr half-life due to decr clearance
==>incr free plasma concentration from decr plasma protein binding
==>incr receptor sensitivity to BZ’s
==>incr risk of falls and hip fracture
buspirone
anxiolytic but not addictive

1) MOA: a partial agonist at 5-HT1A receptors linked to K+ channel
==>hyperpolarization
==> suppress neuronal activity

2) Slow onset of action compared to BZ's; no sedation or interaction w EtOH

3) No hypnotic, anticonvulsant or muscle relaxant effects
opiates
1) beta-endorphin and enkephalins: effects blocked by naloxone

-depress spinal nociceptive pathways
opiate receptors: mu
natural agonists =
*beta-endorphins,
*enkephalins,
*morphine

Both Mu1 and Mu2==>
-phys dependance
-sedation (incr PSNS)
-miosis (incr PSNS activity from E-W nucleus to sphincter muscle of iris)


ONLY Mu1 (periaquaductal gray)==>
-supraspinal analgesia (Supraspinal Mu1 predominates over spinal Mu2)

(periaquaductal gray is in brain and is thus "supraspinal")

ONLY Mu2 ==>
-spinal analgesia
-decr respiration
-decr GI

Opiate receptors are coupled to G proteins.

-mu and delta= increased K+ conductance = hyperpolarization=inhibitory effect (inhibit CNS)

-kappa= decr Ca++ conductance
=inhibitory effect (inhibit CNS)
opiate receptors:
kappa receptors
natural agonists = dynorphin A and K1

BOTH K1 & K3 cause==>
-sedation
-psychomimesis (Dysphoria=disorientation, depersonalized feelings)

ONLY K1==>
-spinal analgesia
-miosis

ONLY K3==>
-supraspinal analgesia

Opiate receptors are coupled to G proteins.
-mu and delta= increased K+ conductance = hyperpolarization=inhibitory effect (inhibit CNS)

-kappa= decr Ca++ conductance (inhibitory)
delta receptors
natural agonists = enkephalins

BOTH Delta1 & Delta2==>
-supraspinal analgesia

ONLY Delta 2==>
-spinal analgesia

(spinal >> supraspinal)

Opiate receptors are coupled to G proteins.

-mu and delta= increased K+ conductance = hyperpolarization=inhibitory effect (inhibit CNS)

-kappa= decr Ca++ conductance
rhinorrhea, lacrimation,chills, n/v, diarrhea, hyperthermia,
sweating and piloerection (“goose flesh”), myalgia, tremor, urticaria, mydriasis,
anxiety, hostility
opiate withdrawal
DOC for pain and pulmonary edema caused by acute MI
morphine

-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 (via dilation of arteries and veins)

In MI, chest & arm pain incr SNS activity
==>constricts arterioles and venules
==>increase preload and afterload.

-Morphine acts centrally to decrease pain and to decrease
SNS outflow.
==>decreases preload and afterload and improves CO.

-The analgesic effects of morphine also make the patient more comfortable.
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 Mu agonists pentazocine, buprenorphine, nalbuphine ("Partially Blocks Narcotics") can also cause S/S of opiate withdrawal in a patient taking methadone (full Mu agonist)
if preg woman receives an opiate during labor, wht can happen?
newborn has resp depression