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Med Sci > Unit 2 B > Flashcards

Unit 2 B Flashcards

1
Q

What is cross tolerance?

A

develop a tolerance to a drug, so you develop tolerance to another drug in the same class

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2
Q

What is cross dependence?

A

a drug can suppress withdraw symptoms caused by cessation of another drug

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3
Q

What is metabolic tolerance?

A

liver produces more enzymes to break down a drug, blood levels will decrease faster

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4
Q

What is pharmacodynamic tolerance?

A

changes in the central nervous system in response to a drug

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5
Q

What is drug sensitization?

A

when a person is hyper-aware of things associated with the drug, inverse of drug tolerance

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6
Q

What is physical dependence?

A

a physical response to stopping the use of a drug

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7
Q

What is Abstinence syndrome?

A

actual set of withdraw symptoms

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8
Q

What is the bond between neurotransmitters and receptors like?

A

ionic, weak, temporary

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9
Q

What are covalent bonds like?

A

strong, permanent

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10
Q

What are the 3 ways drugs can be removed from the synapse?

A

reuptake by glial cells, reuptake by the reuptake channels on the presynaptic cells, enzymatic degradation

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11
Q

What is downregulation of receptors?

A

brain downregulates responses to drug induced reward, shock to your system, receptors become desensitized after repeated use

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12
Q

Explain the concept of stress in terms of withdraw.

A

enhanced stress during withdraw make the person want to use more, CRF is released during withdraw which is what increases the stress

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13
Q

What is CRF?

A

central driver of stress response, amygdala

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14
Q

What percentage of alcohol is absorbed?

A

100%

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15
Q

What is the decline rate of alcohol?

A

around 0.015g% an hour, no half life, 0th order

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16
Q

What is the solubility of alcohol?

A

water soluble, lipid soluble

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17
Q

What happens at the receptors for alcohol?

A

GABA agonist, Glutamate antagonist

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18
Q

What is pavlovian conditioning?

A

outside stimuli or cues causes an automatic drug craving

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19
Q

Explain what happens during withdraw?

A

increase in glutamate activity

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20
Q

What is the effect of alcohol being a glutamate antagonist?

A

decreased memory, cognitive function, overall brain activity

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21
Q

What is the effect of alcohol being a GABA agonist?

A

depressed brain function

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22
Q

What is a biphasic response?

A

acts as a stimulant until BAC of0.05 then depressant effects start, effects the pleasure part of the brain until reaching a certain BAC and then turning into a depressant

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23
Q

What is fatty liver?

A

normal metabolic breakdown of fats is compromised by high levels of alcohol, liver becomes overworked, fat deposits build up in the liver tissue, no signs or symptoms, reversible if a person stops drinking

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24
Q

What is alcoholic hepatitis?

A

acute inflammation of the liver, can be fatal

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25
Q

What is the process of alcoholic hepatitis?

A

bacteria in the gut begins to leak because of intestinal damage due to excessive use of alcohol, bacteria irritates the liver, liver thinks it’s fighting an infection and activates white blood cells to fight it, causes inflammation of the liver and production of scar tissue

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26
Q

What are some symptoms of alcoholic hepatitis?

A

lethargy, nausea, vomiting, abdominal pain

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27
Q

What is alcoholic cirrosis?

A

years of excessive drinking cause a build up of thick fibrous tissue, healthy liver cells are trapped within the scar tissue, liver can’t do it’s job because blood can’t flow through it, becomes irreversible, CHRONIC not acute effect of alcoholism

28
Q

What is portal hypertension?

A

when you don’t have enough healthy liver cells to effectively filter the blood it gets backed up, this causes an increase in pressure in the portal veins leading to the liver

29
Q

What is venous dilation?

A

veins are dilating causing leaks

30
Q

What is ascites?

A

veins leak so much that their capillary fluid accumulates in the abdomen

31
Q

What is esophageal varices?

A

result of portal hypertension, bulging veins in the esophagus, they rupture and people may vomit or throw up blood

32
Q

What is fetal alcohol syndrome?

A

Craniofacial abnormalities, cognitive deficiencies, growth deficiencies,
behavioral issues (most common), there is no cure

33
Q

What are some acute withdraw symptoms?

A

shakes, anxiety, irritability, nausea, craving, vomiting

34
Q

What are treatment options for acute withdraw?

A

Benzos are GABA agonists, they are also used for seizures

35
Q

What are some concerns with benzos?

A

treating an addiction with another drug

36
Q

What do you know about chronic withdraw?

A

cravings can last a lifetime

37
Q

What does Acamprosate do?

A

normalize glutamate activity, partial or weak agonist

38
Q

What does Naltrexone do?

A

opioid antagonist, blocks the high that people experience from alcohol,

39
Q

What does Disulfiram do?

A

inhibits the enzyme acetaldehyde dehydrogenase, causes the accumulation of ACETALDEHYDE, which is toxic and makes people very ill

40
Q

What are the different types of administration for inhalants?

A

sniffing, huffing, bagging

41
Q

What do inhalants do to you?

A

inhibits inhaling oxygen when you take the drug in so you can pass out from the lack of oxygen

42
Q

Effects of inhalants are

A

relaxation, euphoria, disinhibition

43
Q

What are some risks to inhalants?

A

Trauma/Injury (decreased motor control combined with loss of consciousness, Anoxia (lack of oxygen to important tissues, goes on for more than a few minutes you can die), Cardiac Arrhythmia (heart muscle cells needs oxygen, can’t beat normally otherwise)

44
Q

What is nitrous oxide?

A

laughing gas, dentist pain control, safe if used the right way

45
Q

What do you know about anxiety?

A

normal levels are perfectly fine but shouldn’t effect daily life, occurs in amygdala

46
Q

What are barbiturates’?

A

used to treat anxiety in the 60’s but had huge development of tolerance, as metabolic tolerance increased the effective dose increased, causing the margin of safety to be smaller, fatal in overdose, risk for dependency and addiction

47
Q

What is methaqualone?

A

aka Quaalude, caused euphoria and led to addiction and abuse

48
Q

What are benzodiazepines?

A

introduced when barbiturates failed, less addictive and cause less tolerance, Valium, Xanax, Rohypnol

49
Q

What do you know about benzodiazepines half lives?

A

easily absorbed, half lives depend on differences in their metabolites, active metabolites have a much shorter half life

50
Q

What does it mean that benzos are a GABA facilitator?

A

maximizes the natural effects of GABA by acting as a positive allosteric modulator

51
Q

What do you know about withdraw from benzos?

A

you can slowly be tapered off the drug

52
Q

What are the uses of benzos?

A

anticonvulsant, amnestic, anti anxiety but NOT anti depressant, induces sleep, general anesthetic at high dose

53
Q

What are second generation Anti-Insomnia Agents?

A

Zaleplon (Sonata), Zolpidem (Ambien), and Eszopiclone (Lunesta), acts on a single GABA receptor subtype, not antianxiety effects only for sleeping, no tolerance, no withdraw, no loss of receptor sensitivity

54
Q

What does the pineal gland do?

A

synthesizes and releases melatonin, starts in the evening

55
Q

What does the Suprachiasmatic nucleus do?

A

circadian rhythm sets on a 24-hour cycle.

56
Q

What does the Melatonin circadian rhythm do?

A

peaks at the middle of the night, makes you tired

57
Q

What is CBT?

A

cognitive behavioral therapy, help someone fight out the root of their insomnia, most effective way of treating insomnia

58
Q

General anesthetics mechanism of action

A

GABA agonists or dissolves in the cell membrane, aka date rape drug

59
Q

GHB-GABA agonist

A

used by body builders, claimed it increased human growth hormone, euphoria like alcohol without hangover, approved as sleep aid, does not increase human growth hormone

60
Q

CBT in terms of depression

A

effective for mild depression, always helpful, no side effects, can be paired with drug treatment

61
Q

ECT in terms of depression

A

electric convulsive therapy, electrodes are placed on the scalp inducing a seizure, last resort, 80% effective

62
Q

Older antidepressants

A

MAO inhibitors, Tricyclic Antidepressants

63
Q

Tricyclic Antidepressants

A

developed for anti-histaminic purposes but were found to treat depression, many side effects, fatal in overdose

64
Q

MAO Inhibitors

A

lots of side effects, weight gain

65
Q

SSRI’s (Prozac, Escitalopram)

A

selective serotonin reuptake inhibitors, only act as 5-HT reuptake inhibitors, fewer side effects than Tricyclic Antidepressants because they’re more selective, non fatal in overdose, work for 33% of pop, takes awhile for brain to adapt to increased serotonin in the synapse

Med Sci (3 decks)

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