Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
38 Cards in this Set
- Front
- Back
What are the indirectly acting sympathiomimetic amine drugs?
|
Amphetamine
methamphetamine methylphenidate |
|
Alternative drug to amphetamines to treat narcolepsy?
|
Modafinil (provigil)
|
|
Amphetamines are considered what schedule drug?
|
II: high abuse potential and high propensity to cause psychological dependence
|
|
What is the amphetamine structure like?
|
A catecholamine x more lipid soluble--rapidly penetrates the BBB
|
|
What does NH4Cl- have to do with amphetamines?
|
It acidifies the urine and increases its rate of elimination. Used in detox.
|
|
What is the mechanism of action for amphetamines?
|
1. Pentrates the neuron terminal by diffusion and riding the amine transporters
2. It displaces amines in the vesicles (NE, DA, 5-HT); b/c it is a weak-base and disrupts pH. 3. The displaced amines leave the terminal via reverse uptake by the transporters. OVERALL: Massive release of NE and DA (>5-HT) into the synaptic cleft |
|
What is the ph of amphetamines?
|
pKa: 9.9= weak base b/c an amine
|
|
What are the respective effects of massive release of DA and NE?
|
DA= "high" and addictive properties (reward pathway)
NE=sleep-supressing effect |
|
What are the SE of amphetamines in the periphery?
|
a and B Adrenergic Receptors (NE): increase atrial pressure and tachycardia
|
|
What are the CNS SE of amphetamines?
|
*inc. alertness
*delayed sleep *anorexia *dec. fatigue *euphoria *inc. motor and speech activity |
|
What is the rebound phenomemon with amphetamines?
|
After the Major CNS effects: period of depression, hypersomnia, depression
|
|
What are the effects of amphetamines at high doses?
|
*psychotic state-sim. to paranoid schizo.
*can trigger convulsions *severe HTN and stroke |
|
How do you treat amphetamine OD/toxicity?
|
*nitroprusside or a-blocker if BP severely elevated
*Sedative drugs |
|
What are the therapeutic uses of Amphetamines?
|
*hypersomnia=narcolepsy
*obesity |
|
What are the drugs used to treat narcolepsy?
|
Amphetamines= D-amphetamine or methylphenidate (i.e. ritalin)
Modafinil=not amphet. tx's narc |
|
What drugs are used to treat cataplexy component of narcolepsy?
|
clomipramine(TCA) or fluoxetine (SSRI) (anti-depressants)
|
|
What are the drugs used to treat obesity?
|
Orlistat (pancreatic lipase inhibitor)
Sibutramine (meridia)-inhibit NE and serotonin re-uptake |
|
What is Sibutramine?
|
It is a selective NE and serotonin re-uptake inhibitor that does not affect DA. Used as an anorectic drug for severe obesity.
|
|
What is methylphenidate?
|
Piperidine derivative of amphetamine.
(Ritalin) tx-ADHD |
|
What are alternative tx for ADHD?
|
TCA-deipramine, clonidine, atomoxetine(related to clonidine)
|
|
What is the mechanism of action of cocaine?
|
Blocks uptake of DA, NE and 5-HT. Increase synaptic levels of the amines.
|
|
What is crack?
|
is cocaine base. Very lipid soluble and smokable
|
|
What are the clinical uses of cocaine?
|
A local anesthetic-nasal and oral made in a form that will not enter the CNS
|
|
What is the action of DA receptor antagonists in a cocaine patient?
|
I.e: Neuroleptics
*alleviate the cocaine-induced psychosis, and the convulsions but do not change Peripheral toxic sx |
|
What drug is used to stop cocaine convulsions?
|
Diazepam IV (benzo)
|
|
What are methylxanthines?
|
Alkaloids found in tea, coffee, cocoa and other plants.
|
|
What are the 3 main effects of theophylline and caffeine in the CNS?
|
1. increased alertness
2. respiratory stimulation 3. convulsive potential at high dose |
|
What is the mechanism of action for methylxanthines?
|
1. Low dose: (teas) competitive inhibition of CNS adenosine A1 and A2 receptors.
2. High does: (theophylline-asthma) inhibit PDE and inc. cAMP. |
|
What is the function of adenosine in the brain?
|
Depresses neuronal function by activating A1R coupled to K-channels. Post and Pre-syn. Presyn= inhibition of NT release
|
|
Where are the A2 receptors located?
|
A2R-high conc. in the striatum-role in motor function.
|
|
What are the medical uses of methyxanthines?
|
1. Primary apnea of prematurity (caffeine or theophylline)- b/c of weak hypoxia chemoreflexes that can't overcome adenosine in brainstem.
2. Asthma tx- high doses the bronchodilatory effect |
|
How would you describe the nicotine compound?
|
*lipid-soluble drug well absorbed by the skin and mucosa.
*Activates nicotinic R |
|
What is the mechanism of Nicotine at low doses?
|
Activate N-R in autonomic ganglia, lungs/airways and CNS--largely a presynaptic receptor--inc. release of DA by depolarization of the terminals
|
|
What are the effects of Nicotine at high doses?
|
N acts on all nicotinic receptors and produces a depolarizing blockade and receptor desenesitization at autonomic ganglia and NMJ. EFFECT: peripheral CVS collapse, muscle weakness, resp. failure->death
|
|
what are the SE of Nicotine at low doses?
|
*Nausea-stim lung,airway affer. and area posterma
*inc. respiration (carotid chemo) *tremor, inc. alertness, fac. memory and attention, muscle relax (?via renshaw cell activation of SC) *activ auto ganglia (both) and adrenal medulla--GI and CVS |
|
What is the half-life of nicotine?
|
2hrs, heavy smokers titrate blood in narrow lmits
|
|
Clinical uses of nicotine?
|
Treatment of addiction by replacement therapy.
|
|
What are the major groups of Stimulants?
|
1. Indirect acting sympathiomemetic amines: amphetamines, methyphenidate, cocaine
2. Methylxanthines 3. Nicotine |