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Pharm II Exam 2 > MOA > Flashcards

MOA Flashcards

1
Q

Thioamides- PTU and MMI

A

Prevent hormone synthesis by inhibiting TPO-catalyzed rxns to block iodide organification

Block coupling of iodotyrosines

Drug binds to and inactivates TPO

Slow onset (takes 4- wks to deplete), excreted in urine

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2
Q

Anion Inhibitors- ClO4- and TeO4-

A

Compete with sodium ion transporter for uptake

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3
Q

Iodide

A

Inhibit organification and hormone release and ↓ size of hyper plastic gland

Effect reverses with time (escape) if used alone

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4
Q

Radioactive Iodine

I131

A

Taken orally → rapidly
concentrated in thyroid follicle cells, where
β particles selectively destroy gland w/o injury to adjacent cells →
become euthyroid in 6-8 wks

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5
Q

Biguanides

A

Enhances effects of insulin “sensitizer”

Activates AMP-dependent protein kinase (AMPK) causing ↑ glucose uptake by fat and muscle and ↓ production by liver

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6
Q

Sulfonylureas

A

↑ Insulin release from pancreas beta cells by binding to K+ channel (requires functional beta cells)

Mimic Glucose to Close ATP-sensitive K+ Channels and Stimulate Insulin Secretion

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7
Q

Non-Sulfonylurea Secretagogues (Meglitinides)

A

Mimic glucose to close K+ ch and stim insulin secretion

↑ Insulin release from pancreas beta cells by bindi to beta K+ cells (require fn beta cells)

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8
Q

Thiazolidenediones (TZDs)

A

↑ Insulin sensitivity in target tissues by activating receptor gamma (PPAR-gamma) liganda

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9
Q

GLP-1 Receptor Agonists

A

↑ glucose-dependent insulin secretion

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10
Q

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors

A

Prolong endogenous GLP-1 action

↑ glucose-mediated insulin secretion

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11
Q

α-Glucosidase Inhibitors

A

Stays in intestine and ↓ GI glucose absorption

↓ Postprandial glycemia (must be taken with meal)

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12
Q

Canagliflozin

A

Glucose co-transporter inhibitor

Inhibition of SGLT-2 → suppresses renal glucose re-absorption → lowers blood glucose

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13
Q

Estrogen/progestin combo pill

A

Hypothal
↓ GnRH pulses (P) → no LH surge

Pituitaty
↓ responsiveness to GnRH (combo)

↓FSH/LH release (E) → ↓ follicular devel

Other
thickening of cervical mucus (P) → ↓ sperm penetration

Atrophic endometrium ( P) to implantation

↓ transport of sperm/egg through fallopian tub (combo)

Overall blocks ovulation, atrophies endometrium, thick cervical mucus, altered traans in fallopian tube

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14
Q

Ulipristal

A

Selective

Delays ovulation

Alters cervical mucus and endometrium

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15
Q

Mifepristone

RU486

A

Competitive antagonist

Blocks uterine progesterone receptors → decidual breakdown → blastocyst detachment (↓hCG)

↑ sensitivity of myometrium to PG → contractile, softens cervix

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16
Q

Generally how do combo estrogen/progestins work?

A

by suppressing follicle development, thickening cervical mucus, and inhibiting ovulation

17
Q

Copper IUD

A

reduces sperm motility and viability

18
Q

LNG-IUD

A

inhibits ovulation, thickens cervical mucus, reduces sperm motility and viability

19
Q

Hormonal EC

A

acts by delaying ovulation and may also interfere with sperm migration and fn at all levels of genital tract

20
Q

Tamoxifen

A

Metabolized by CYP2D6 to active metabolites endoxifen and 4- hydroxyTAM that bind to ER-alpha, acting as antagonists in breast tissue to inhibit gene transcription, inhibit cell proliferation and promote apoptosis

Acts as a partial agonist in endometrium to promote endometrial hyperplasia

21
Q

Toremifene

A

Active antagonist at ER-alpha/beta

Does NOT require activation by CYP2D6

Insufficient clinical data at this time, but may act as partial agonist in endometrium to promote endometrial cancer

22
Q

Leuprolide

A

Disrupts normal pulsatile stimulation of GnRH receptor by endogenous GnRH
→ desensitization of GnRH receptor in the pituitary→ ↓ release of FSH and LH from the pituitary→ ↓ estrogen synthesis in the ovaries

23
Q

Anastrozole

A

Reversible inhibitor

Prevent conversion of testosterone to estrogen by inhibiting aromatase (CYP19A1) in adipose tissue

24
Q

Exemestane

A

Suicide inhibitor

Prevent conversion of testosterone to estrogen by inhibiting aromatase (CYP19A1) in adipose tissue

25
Q

Trastuzumab

A

“Armed” monoclonal Ab that has been coupled with DM1 (emtansine)

Ab binds to HER2 extracellular domain IV → Ab is internalized into lysosomal stores → DM1 is released

DM1 is a mitotic spindle poison, binds beta-tubulin to inhibit microtubule polymerization

26
Q

Pertuzumab

A

Monoclonal Ab binds HER2 extracellular domain II to prevent ligand-dependent dimerization with EGFR

27
Q

ALKYLATING AGENTS (Cyclophosphamide and Cisplatin)

A

CCNS drugs

Greatest anti-ca activity in S phase

Bi-functional

Alkylates guanine
residues → produces
interstrand crosslinks

Guanine has abnrml base-pairing w/ thymine during replication → protein miscoding and apoptosis

28
Q

ANTI-METABOLITES

A

CCS drugs (active in S-phase of cell cycle)

Structurally similar to endogenous molecules → act as antagonists of biosynthetic pthwys

Ca cells are more sensitive than nrml cells bc of high growth fraction and higher levels of certain enzymes

29
Q

Methotrexate

A

CCS

Folic acid
analog

Binds to and inhibits
DHFR →
prevents formation of
THF from folate  → prevents
thymidylate, purine &
amino acid synthesis→
interruption of DNA, RNA and protein syntheses
30
Q

5-Fluorouracil

A

CCS

Analog of uracil

Prodrug → converted to 5FdUMP,
which inhibits TS activity which is required for de novo pyrimidine synthesis → slows ca cell replication and causes DNA damage

31
Q

6-Mercaptopurine

A

CCS

HGPRT metabolizes 6 mercap into TIMP →

converted to Thio-dGTP

Thio-dGTP is incorporated
into DNA of replicating
cancer cells→ leading to
apoptosis

32
Q

Vinca Alkaloids (Vinblastine and Vincristine)

A

Binds to β-tubulin→
prevents
polymerization of
microtubules → causes blocking of mitotic spindle formation → tumor cell death

33
Q

Paclitaxel

A

CCS

Binds with high
affinity to β-tubulin and
stabilizes microtubules
(prevents depolymerization)→ cells blocked at G2/M phase

34
Q

Etoposide

A

CCS

Inhibits
topoisomerase II → prevents DNA uncoiling → DNA strand breakage

35
Q

Irinotecan

A

CCS
(CCNS at higher
concentration)

Inhibits topoisomerase I → prevents uncoiling → DNA strand breakage

36
Q

ANTIBIOTICS

A

Insert btwn base pairs of DNA → Δ DNA configuration → strand breakage/ enzyme interference

37
Q

Doxorubicin

A

CCNS

DNA intercalation that
interferes with DNA &
RNA synthesis

Inhibits topoisomerase II→ DNA fragmentation

Free radical formation
→ DNA scission (responsible for cardiotox)

38
Q

Bleomycin

A

CCS

 Intercalation,
scission and
fragmentation of DNA due
to oxidation by a DNAbleomycin-Fe(II)
complex
39
Q

Allopurinol

A

Inhibits XO → prevent uric acid production

Pharm II Exam 2 (7 decks)

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