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Final Test: Dynamics II > Sympathomimetics III: Release and Uptake Blockers > Flashcards

Sympathomimetics III: Release and Uptake Blockers Flashcards

1
Q

What are uptake blockers?

A

They elevate sympathetic activity by increasing the concentration of NE at the synapse–allows more receptors to be stimulated for a longer period of time; one mechanism is to increase the release of NE from the pre-synaptic terminal or block the reuptake of NE back into the terminal

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2
Q

What is an amphetamine?

A

amphetamine

dexamphetamine

methamphetamine

phentermine (fastin)

methyphenidate (ritalin)

phenmetrazine (preludin)

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3
Q

What class of drugs were first synthesized in 1920’s?

A

phenylisopropylamines

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4
Q

What are amphetamines?

A

treatment of attention deficit disorder

hyperactivity disorder

narcolepsy

weight loss

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5
Q

What are amphetamines known for?

A

known for their abuse potential

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6
Q

What part of the body do amphetamines stimulate?

A

they stimulate the CNS- cortical and reticular activating systems to increase: wakefulness, altertness, mood, initiative, confidence, elation, euphoria, and concentration ability

fatigue is decreased

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7
Q

What are the examples of amphetamines?

A

1) methamphetamines (speed, ice)
2) 2,5- dimethoxy-4 methylamphetamine (DOM, sTP)
3) methyane-dioxyamphetamine (MDA)
4) methylenedioxymethamphetamine (MDMA, ecstasy, XTC)

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8
Q

How are amphetamines given and how does that affect their absorption?

A

they are well absorbed whether given orally, smoked, sniffed or injected

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9
Q

How do the lack of -OH group impact the function of amphetamines?

A

they lack hydroxyl goups on the phenyl ring thereby increasing bioavailability and duration of action, as COMT cannot methylate the molecule

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10
Q

What structual part of amphetamines and helps with its action?

A

the presence of side chains off the alpha and beta carbons prevents metabolism by MAO; long duration of action

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11
Q

How long is the half life of amphetamines compared to catecholamines?

A

the half-lives of amphetamine are hours compared to minutes of catecholamines

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12
Q

How does the body rid its self of amphetamines?

A

significant amount of drugs are excreted unchanged in the urine; the compounds are weak bases so acidification of the urine will increase the rate of excretion

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13
Q

What is the mechanism of action of amphetamines?

A

it is to elevate the synaptic concentrations of the biogenic amines within the SNS and CNS

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14
Q

How do amphetamines work?

A

they compete with NE, Epi, DA, and 5-HT for binding to the plasma membrane transporters for these neurotransmitters; the amphetamines are substrates for transport into the synaptic terminal

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15
Q

What happens to amphetamines after they enter the nerve terminal?

A

they can displace the endogenous vesicular and non-vesicular pools of neurotransmitter out of the terminal causing release

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16
Q

How does the release of neurotransmitters from the terminal as a result of amphetamines occur?

A

the release can occur via the reversal of the transporters and via diffusion through the membranes

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17
Q

What are some other actions of amphetamines at higher doses?

A

they directly stimulate alpha-receptors and block MAO at higher doses

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18
Q

What do elevation of NE at the synapse lead to?

A

elevations of NE in the synapse lead to stimulation of alpha-receptors in the vasculature and of beta-1 receptos in the heart

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19
Q

What are the side effects of amphetamines?

A

irregular heart beat

irritability, nervousness, a false sense of well being, and insomnia

drowsiness, fatigue, and mental depression after the stimulant effects

following withdrawal-mental depression, nausea and vomitting, stomach cramps, trembling, tiredness, and weakness

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20
Q

What are the drug interactions between amphetamines and alkalizers of the urine (antacids, sodium bicarbonate)?

A

decrease the rate of elmination

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21
Q

What is the drug interaction between inhalation anesthetics and amphetamines?

A

sensitive to the heart to sympathomimetic agents

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22
Q

What is the drug interaction between anti-depressants and amphetamines?

A

they potentiate cardiovascular effects (hypetension and reflex bradycardia)

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23
Q

What is the drug interaction between amphetamines and insulin?

A

increase the risk of hyperglycemia

24
Q

What is the drug interaction between beta blockers and amphetamines?

A

unopposed action of amphetamine and alpha-adrenergic receptors resulting in hypertension and reflex bradycardia

25
Q

What is the contraindication of amphetamines?

A
  • agitation
  • arteriosclerosis
  • cardiovascular disease
  • glaucoma
  • hypertension
26
Q

What are ephedrine and pseudoephedrine?

A

they are related to amphetamines, found primarily in cold prepartions for nasal congestion (Sudafed) usually combined with other cold remedies ; non-prescription but on shelves anymore!! ask pharmacist

27
Q

How is ephedrine/ pseudoephedrine assist in weight loss?

A

OTC preparations containing Ma Hung extract.

28
Q

How is ephedrine/pseudoephedrine and bronchodilator?

A

usually combined with theophylline

29
Q

What mechanism of action ephedrine/pseudoephedrine?

A

release NE withc activates alpha and beta-1 receptors

ephedrine can also stimulate beta-2 receptores directly while pseudoephedrine has little beta-2 action; by now you should know the organ effects

30
Q

What are the side effects ephedrine and pseudoephedrine?

A

nervousness or restlessness

trouble sleeping

pounding heartbeat

increase in blood pressue

31
Q

what are the contraindications ephedrine/pseudoephedrine?

A

angina

arrhythmia

coronary insufficiency

hypertension

32
Q

What is cocaine?

A

its a local anesthetic, most often in dentistry

33
Q

How many people have used cocaine?

A

more than 20 million americans have used cocaine in their life time; around 20% of those are regular users and 25% of those will become addicted (1 miliion)

34
Q

How does cocaine imact the intranasal?

A

cocaine HCl is water soluble and can readily diffuse through the mucous membrane of the nose; it rapidly enter the CNS followed by redistribution to other tissues

35
Q

How does cocaine impact the body when it is smoked or given by IV?

A

cocaine base is heated to an aerosol of particles and vapor is then inhaled directly into the lungs where it enters the bloodstream; cocaine rapidly enters the brain and then is rapidly redistributed, creating the drive for more

36
Q
A
37
Q

How is cocaine broken down?

A

it is metabolized by hepatic and plasma cholinesterases

38
Q

What will speed up the elimination of cocaine?

A

acidification of the urine will speed elimination; cocaine and its metabolites are detectable for 3-4 days in the urine

39
Q

How does cocaine work?

A

it binds to the dopamine, NE, and 5-HT transporters thereby blocking uptake and elevating NT levels in the synapse (similar to the amphetamines)

it is not a substrate and does not enter the terminal to elicit the release of the neurotramitters; it will lead to depletion of the terminal

40
Q

What are the side effects of cocaine?

A

coronary vasoconstriction and myocardial sensitization

arrhythmias

ischemia/stroke

infaracts

endothelial injury-thromus formation

myocarditis and dilated cardiomyopathy

numerous CNS side effects to learn later

41
Q

What are the drug interactions of cocaine with inhalation anesthetics?

A

increased risk of ventricular fibrillation and arrhythmia

42
Q

What are drug interactions of levo and methyldopa and cocaine?

A

cardiac arrhythmia

43
Q

What are drug interaction between cocain and post-ganglionic blockers of hypertension?

A

decreases effect, hypertensive effects

44
Q

What is the drug interaction between cocaine and beta blockers?

A

mutual inhibition of effects as well as unopposed alpha action

45
Q

What is the drug interaction between cocaine and cholinesterase inhibitors?

A

potentiation of cocaine’s effects

46
Q

What is the drug interaction between TCA’s and cocaine?

A

potentiation of cardiocascular effects

47
Q

What is the drug interaction between MAO inhibitors and cocaine?

A

potentiate cardiovascular effects of both drugs

48
Q

What is the drug interaction between sympathomimetics and cocaine?

A

potentiate CNS and cardiovascular problems

49
Q

What is tyramine?

A

it is not used pharmacologically but it is a produce of tyrosine breakdown in the liver and found in various fermented food; its interaction with MAO inhibitors makes it necessary to understand

50
Q

What happens to tyramine levels as it broken down by MAO?

A

significant levels are not attained in normal individuals as tyramine is broken down by MAO; however if MAO is inhibited, the levels of tyramine become significantly elevated.

51
Q

What is the mechanism of action of tyramine?

A

tyramine can enter the presynaptic terminal via uptake by the NE transporter and then into vesicle via the vesicular transporter; oncre inside the vesicle it is converted to octopamine by dopamine-B-hydroxylase ( the enzyme that converts dopamine to NE).

52
Q

What happens to octopamine after it is released?

A

displaces NE from the vesicle where it is released; octopamine does not stimulate the adrenergic receptors

53
Q

What is tyramines interactions with MAO inhibitors?

A

chronic MAO inhibitor use without ingestion of exogenous tyramine leads to a buildup of octopamine in vesicles of sympathetic neurons; when the SNS in activated and vesicules release their contents there is less NE release into the synapse

54
Q

What happens after less NE is relesed into the synapse?

A

this results in a failure to fully activate adrenergic receptors, epecially alpha-1 receptors on the vasculature, which leads to an overall decrease in blood pressure (orthostatic hypotension)

55
Q

What will happen to someone on chronic MAO inhibitor therapy?

A

ingest tyramine a different result is seen, remember the first effect of tyramine is to cause release; thus when tyramine is ingested a large amount of amine is released cause adrenergic receptor stimulation and since MAO is inhibited degradation is prevented

56
Q

Which foods have high levels of tyramine and must be avoid in patients on chronic MAO therapy?

A

cheese

yeast

pickled fish

wine

Final Test: Dynamics II (11 decks)

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