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Drug Action II > Exam II Memorize > Flashcards

Exam II Memorize Flashcards

1
Q

UGT1A1 is required for?

a. bile elimination
b. ammonia elimination
c. transcellular transport
d. Transporting drug into the hepatocyte

A

a

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2
Q

valve disease:

A

valve cannot fully close

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3
Q

aneurysm:

A

bulged blood vessel

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4
Q

cardiomyopathy:

A

thickening of myocardium, harder to pump blood

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5
Q

pulmonary stenosis:

A

pulmonary valve is too small, narrow, or stiff

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6
Q

statin enters enterocyte via which transporters?

a. SLCO2B1 & SLC15A1
b. UGT1A1 & UGT1A3
c. ABC1 & ABCG2
d. OATP1B1 & OATP1B2

A

a

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7
Q

once transported into enterocyte, statin is metabolized by which two enzymes into active and inactive metabolites?

a. CYP2C3/5
b. CYP3B4/5
c. CYP3A4/5
d. CYP1A2/3

A

c

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8
Q

both statin and its metabolites enter hepatocyte via which transporter?

a. UGT1A1
b. SLC15A1
c. SLCO2B1
d. UGT1A3

A

c

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9
Q

Statin in liver is metabolized by?

A

various CYP enzymes

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10
Q

statin metabolites are further metabolized by?

A

UGT1A1/3 or UGT2B7

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11
Q

statin is transported out of liver or transported to renal cell and eliminated by which transporters?

a. ABC1 & ABCG2
b. UGT1A1 & UGT1A3
c. SLCO2B1 & SLC15A1
d. OATP1B1 & OATP1B2

A

a

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12
Q

where can genetic variation occur during PK factors of statin?

A

elimination transporters or transportation transporters such as SLCO2B1

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13
Q

which transporter is responsible for stain uptake and transport out of liver?

A

OATP1B1

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14
Q

what does the *5 SNP in the SLCO1B1 gene do?

what does it increase the risk of?

A

produces a less efficient OATP1B1 protein and is less able to xport statins to liver
inc risk of CVD instead of reducing risk of CVD

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15
Q

which enzymes metabolize the prodrug clopidogrel into its first metabolite?

A

cyp2C19, 3A4, and A12

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16
Q

which enzyme is required for clopidogrel activation?

A

paraoxonase-1 (PON1)

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17
Q

how does clopidogrel work as an antiplatelet?

A

prevent ADP binding to P2Y12 platelet receptor

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18
Q

in the colon, what happens if APC is mutated?

A

causes colon cells to hyperproliferate

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19
Q

what gene is activated in response to hyperproliferation of the colon cells?

A

ras

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20
Q

what does ras do during proliferating colon cells?

A

localizes cells into one area to generate adenoma

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21
Q

what is the p53 gene and what happens to the colon if its mutated?

A

tumor suppressor gene

adenoma becomes carcinoma

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22
Q

once a carcinoma develops in the colon, and there’s a mutation in the DCC gene, what happens?
what is the DCC gene?

A

cancer becomes invasive and spreads

DCC is a tumor suppressor gene

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23
Q

what genetic condition causes APC mutation in colon?

a. Hereditary Non-Polyposis (HNP)
b. Categorical Autonomic Polyposis (CAP)
c. Familial Adenomatous Polyposis (FAP)

A

c

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24
Q

which two drugs treat colon cancer?

A

5FU and irinotecan

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25
Q

what does 5FU bind to causing inhibition of the enzyme resulting in inhibition of DNA synthesis

A

thymidylate synthase (TS)

26
Q

most of 5FU is eliminated by which enzyme?

A

dihydropyrimidine dehydrogenase

27
Q

if FU is converted to FUMP, what is the result?

A

RNA damage

28
Q

if FU is converted to a diff metabolite, what is the result?

A

DNA damage

29
Q

MIR27A inhibits coding gene DPYD which produces DPD.

A

.

30
Q

what happens in the mutation of DPD?

what is the result?

A

a guanine is changed to adenosine at exon 14 causing a deletion of the entire exon, leaving only exon 13&15
DPD cannot effectively metabolize 5-FU leading to toxicity

31
Q

what happens in the mutation of thymidylate synthesis? (normal vs mutated TS)

A

normal TS has 2 tandem repeats, when FU acts on TS it decreases TS activity and causes good antitumour response
mutated TS has 3 tandem repeats which will increase TS activity causing poor antitumour response

32
Q

which metabolite of irinotecan causes antitumour activity?

A

SN-38

33
Q

which two enzymes convert irinotecan to SN-38?

A

CES1 and CES2

34
Q

mutations in ABC xporters modifies toxicity of drug

A

.

35
Q

metabolism of irinotecan is dependent on CES1 & CES2 mutations

A

.

36
Q

UGTs convert SN-38 to?

A

SN-38G

37
Q

UGT1A1 polymorphims can predict toxicity in cancer pts

A

.

38
Q

how do UGT1A1 polymorphims affect irinotecan therapy?

A

mutation which dec. expression of UGT which slows down glucuronidation causing toxicity symptoms

39
Q

mercaptopurine is a treatment for acute lymphoblastic leukemia. it is converted into its active metabolite thioguanine nucleotides via which enzyme?

A

hypoxanthine phosphoribosyl transferase (HPRT)

40
Q

meracptopurine is also converted into its inactive metabolite via which enzyme?

A

thiopurine S-methyl-transferase (TPMT)

41
Q

chronic myelogenous leukemia: which gene causes it? what protein does this gene produce? what does the protein do?

A

BCR-ABL, bcr-abl protein, the protein increases leukemic cells

42
Q

what treatment inhibits bcr-abl protein?

A

imanitib

43
Q

what enzyme does imanitib inhibit? how does it inhibit bcr-abl protein?

A

tyrosine kinase inhibitor

bins to bcr-abl site where ATP would bind inhibitng proliferation

44
Q

what does herceptin do?

A

stops HER2 receptors from signaling cancer cells to grow

45
Q

which two proteins are overproduced in alzeimers?

A

amyloid and tau

46
Q

APOE3 & APOE4 allow neurons to grow and inhibit inflammation of glial cells

A

.

47
Q

mutations in APOE3/4 inhibit neuron growth

A

.

48
Q

causes of parkinsons occur due to polymorphisms of?

A

DRD2, COMT, & SLC6A3

49
Q

what is phenytoin? how does it work? what encodes it?

A

treatment for parkinsons. inhibits neuronal sodium channels

SCN genes

50
Q

G6PD, RBCs only way to protect from infection. deficiencies cause? it also effects the way certain drugs work, such as-

A

hemolytic anemia

antibacterial, antipyretics, antimalaria

51
Q

treatment drug for tuberculosis?

A

isoniazid (INH)

52
Q

isoniazid is metabolize by?

A

NATs

53
Q

what is the goal of non viral gene therapy?

A

insert DNA into target cells

54
Q

severe combined immunodeficiency disease (SCID) is caused by a deficiency in?

A

adenosine deaminase

55
Q

how is SCID treated?

A

implant normal ADA gene into retrovirus and infect T cells

56
Q

what is ornithine transcarbamylase deficiency (OTC)?
what happens?
what is the treatment? how does it work?

A

urea cycle disorder
liver unable to remove ammonia
sodium benzoate=> binds to ammonia and increases elimination

57
Q

what causes cystic fibrosis?

A

mutation in cystic fibrosis transmembrane conductance regulator (CFTR) gene

58
Q

what gene therapy treatment is used for CF?

A

adenovirus

59
Q

what does the CFTR gene do?

A

regulates fluid excretion

60
Q

what is p53?

A

DNA repair enzyme

61
Q

what happens if the ras gene is mutated?

A

cannot regulate cell division, causes non-stop mitosis

Drug Action II (10 decks)

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