Pharm-Part 4

Front 1

Drugs used to treat Park Dz

Back 1

- 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

Front 2

what enahnces central actions of levodopa in Park Dz?

Back 2

centrally-acting anticholingergic drugs

Front 3

carbidopa + levidopa

Back 3

- 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

Front 4

S/E of levodopa

Back 4

can cause reappearance of psychotic Sx (b/c levodopa incr DA) in schizophrenic who developed Park Dz d/t typical antipsychotic like haloperidol

Front 5

D2-R blockers like haloperidol?

Back 5

-reserpine
-alpha-methyldopa
-metoclopramide

Front 6

bromocriptine

Back 6

D2-dopamine receptor agonist; used to treat PD and inhibit prolactin
release in hyperprolactinemia; reverses infertility caused by hyperprolactinemia

Front 7

EtOH

Back 7

- 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)

Front 8

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

Back 8

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

Front 9

alcoholism causes

Back 9

- 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

Front 10

fetal alcohol syndrome

Back 10

flattened face, short nose, short palpebral fissures =
underdevelopment of mid-facial region, microcephaly with low IQ, retarded growth

Front 11

Methanol toxicity

Back 11

- 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

Front 12

ethylene glycol

Back 12

(antifreeze)

converted to aldehydes, acids and oxalate
==>oxalate causes acute renal failure

Front 13

MDMA (“ecstacy’) = MethyleneDioxyMetAmphetamine

Back 13

can cause degeneration of central 5-HT neurons

Front 14

sedative-hypnotic drugs

Back 14

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.

Front 15

barbiturates

Back 15

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

Front 16

older pts taking benzodiazepines

Back 16

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

Front 17

buspirone

Back 17

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

Front 18

opiates

Back 18

1) beta-endorphin and enkephalins: effects blocked by naloxone

-depress spinal nociceptive pathways

Front 19

opiate receptors: mu

Back 19

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)

Front 20

opiate receptors:
kappa receptors

Back 20

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)

Front 21

delta receptors

Back 21

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

Front 22

rhinorrhea, lacrimation,chills, n/v, diarrhea, hyperthermia,
sweating and piloerection (“goose flesh”), myalgia, tremor, urticaria, mydriasis,
anxiety, hostility

Back 22

opiate withdrawal

Front 23

DOC for pain and pulmonary edema caused by acute MI

Back 23

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.

Front 24

tx of female w acute pain from gallstones w morphine causes greater pain. Why?

Back 24

Morphine contracts smooth muscle of gall bladder

Front 25

female on methadone has emergent surgery and is tx w butorphanol; patient
experiences S/S of opiate withdrawal. Why?

Back 25

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)

Front 26

if preg woman receives an opiate during labor, wht can happen?

Back 26

newborn has resp depression