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pharmacology > lecture 2 > Flashcards

lecture 2 Flashcards

1
Q

what is CML and what drug was created for it

A

Chronic Myelogenous Leukemia, cancer of the immune systems; Gleevec (Imatinib Mesylate) - to inhibit the BCR-ABL protein

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2
Q

CML is a result of a _______ between chromosomes 9 and 22, forming a _______ chromosome, which makes the fusion mutant protein called BCR-ABL

A

translocation; Philadelphia

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3
Q

The BCR-ABL fusion protein promotes what type of cancer?

A

CML

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4
Q

Gleevec binds to what?

A

ABL (the oncogene/tyrosine kinase)

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5
Q

what’s the mechanism of Gleevec/Imatinib?

A

It binds to the ATP binding site, and blocks the activity of the tyrosine kinase (ABL) that leads to cell division

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6
Q

Why do drugs stop working?

A

Cancer cells will make transporters that make cells resistant to the drugs and work to pump the drug out or don’t even let the drug in (e.g. MDR-1: multi drug resistance, OCT1: organic cation transporter, mutations in ABL)

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7
Q

what is a graded-dose response curve?

A

graphical representation of the relationship btwn the dose/concentration of the drug and the effect it achieves

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8
Q

potency

A

EC50 (effective concentration) - dose required for an individual to experience 50% of the maximum effect

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9
Q

ED50

A

median effective dose - the dose of a drug that can produce a desired or expected response in 50% of the test population

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10
Q

efficacy

A

maximum/Emax response a drug can produce

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11
Q

threshold dose

A

minimum dose at which a drug effect is seen

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12
Q

why is the log graph used for graded dose response curves?

A

convenient scale for low concentrations where the response is changing rapidly with dose - at high conceptrations, where the response changes slowly w dose, the graph is compressed

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13
Q

agonist

A

agent that activates the receptor

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14
Q

partial agonist

A

agent that activates the receptor but doesn’t have as great an efficacy as a full agonist

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15
Q

inverse agonist

A

agent that lowers the activity of a receptor that has some constitutive (intrinsic) activity (e.g. GABA-A receptor, where inverse agonists can bind to the receptor and produce anxiety, which is opposite to normal GABA-A effects) — lowkkkk antagonist

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16
Q

neutral antagonist

A

no effect

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17
Q

antagonist

A

blocks effect of agonist when present

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18
Q

competitive antagonist

A

binds to the receptor at the same site of the agonist

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19
Q

non competitive antagonist

A

binds to different site

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20
Q

allosteric modulator

A

drug that binds to a receptor at a site distinct from the active site, whcih alters the affinity of the receptor for the endogenous ligand. postitive allosteric modulator increase affinity, while negative ones decrease the affinity. (e.g. benzodiazepines increase the effect of GABA)

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21
Q

agonist + competitive antagonist would shift the dose curve in which direction

A

right, you need more of the drug - reduced efficacy, same potency

22
Q

agonist + noncompetitive antagonist would do what to the curve

A

ec50 are very close, so it doesn’t shift as far to the right but there are fewer receptors to respond to the agonist so there’s reduced potency

23
Q

allosteric modulators shift the dose curve which direction and why

A

to the left because it enhances ability of GABA, for example, to open the channels so you need less of it

24
Q

heroin street name and what does it break down into in the brain

A

smack; morphine

25
Q

effects of heroin

A

euphoria, sedation, analgesia (blocking pain passages), respiratory depression, pupillary constriction, constipation, and neonatal abstinence syndrome

26
Q

Mu-opioid receptors are located in the _______ and _______ respiratory centers, leading to respiratory ________

A

brainstem; inhibit; depression

27
Q

neonatal abstinence syndrome (NAS) symptoms

A

excessive crying, slow weight gain, fever irritability, and vomiting

28
Q

opioids can reinforce durg taking behavior by altering activity in the ________ system

A

limbic

29
Q

tolerance

A

with chronic usage, you need more of the drug to get the same effect as you produced with the first usage

30
Q

what is the mechanism of drug tolerance

A

a quicker half life: metabolic or pharmacokinetic tolerance (P450 enzymes) OR an altered cellular response: cellular or pharmacodynamic tolerance (e.g. reduced receptors, modified signal transduction)

31
Q

cross tolerance

A

if tolerance exists for one drug, it will exist for the other drug (LSD and psilocybin)

32
Q

psilocybin is an agonist at what kind of receptors?

A

serotonin! which may help manage treatment-resistant depression

33
Q

reward pathway is also known as

A

mesolimbic dopamine pathway

34
Q

explain the mechanism of morphine-induced rewarding effect

A

the rewarding effect is associated w the stimulation of opioid receptors localized at the GABAergic terminals in the ventral tegmental area (VTA). Morphine inhibits GABA release (we know GABA is inhibits activity) and thus disinhibits the dopaminergic neurons in the nucleus accumbens (NAc).

35
Q

mechanism of opioid receptor agonists

A

opioids inhibit presynaptic calcium influx, decreasing neurotransmitter (GABA) release, and hyperpolarize postsynaptic neurons (via K+ efflux) so that they’re less likely to fire in response to excitatory input — which can lead to addiction

36
Q

naloxone does what and shifts response curve in which direction

A

competitively inhibits opiates; to the right with a much stronger affinity for the opiate receptor

37
Q

tricyclic antidepressants have an “off target” effect as they have

A

antimuscarinic effects

38
Q

therapeutic index

A

the effectiveness of a drug relative to its safety (TD50/ED50) (toxic dose / effective dose)

39
Q

TD50

A

50% reach toxicity

40
Q

LD50

A

half patients die

41
Q

narrow TI drugs

A

warfarin, phenytoin, digoxin, AZT, lithium

42
Q

on-target adverse effects

A

result of drug binding to the intended receptor, but at an inappropriate concentration (e.g. codeine is metabolized to morphine by P450 enzymes in liver, which can vary depending on genetic makeup, bad bc poor metabolizers = poor analgesia); benadryl/diphenhydramide leads to drowsiness, lidocaine can cause seizures if overdose

43
Q

off-target adverse effects

A

caused by drug binding to a target or receptor for which it was not intended (tricyclic antidepressants having antimuscarinic effects)

44
Q

an example of a drug that may produce toxic metabolites

A

acetaminophen and hepatotoxicity

45
Q

HMG CoA reductase inhibitors are also known as what, what are they used for, and what is the on-target adverse effect of it

A

statins; decrease cholesterol levels; muscle toxicity, including rhabdomyolysis

46
Q

rhabdomyolysis

A

when an athlete pushes so hard causing muscle tissue to burst and leak myoglobin, a sticky blood protein that can clog the kidneys

47
Q

SERM (selective estrogen receptor antagonist) drugs and what are they used for

A

Tamoxifex (Nolvadex) used early and advanced ER+ breast cancer - antagonist in breast tissue, but also partial agonist on the endometrium so it has been linked to endometrial cancer; Raloxifene (EVISTA) has estrogenic activity in bone and antiestrogenic activity breast and uterus. Bone decreases resorption and osteoprosois, prevents cancer in breast and uterus (antagonist)

48
Q

OFF-target effects examples

A

The antihistamine terfenadine is a prodrug, generally metabolized to the active form fexofenadine (Allegra) in the liver by P450, but in high doses inhibits a cardiac potassium channel which decreases electrical activity in the heart – led to fatal cardiac arrythmias

49
Q

receptor downregulation

A

prolonged use of many agonists can result in receptor downregulation- e.g. addictive drugs, diazepam (valium). tolerance.

50
Q

receptor upregulation

A

prolonged use of many antagonists can result in receptor upregulation - e.g. dopamine receptor blockers

51
Q

_________ agonists do not cause receptor downregulation

A

partial

52
Q

opioid tolerance

A

downregulation of MORs?

pharmacology (10 decks)

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