Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology FINAL (2nd sem) > B: 32-37 > Flashcards

B: 32-37 Flashcards

(129 cards)

Start Studying
1
Q

Antimetabolites

A
  • CCS (S-phase)
  • pyrimidine antimetabolites:
    • 5FU: inhibits thymidylate synthase, its metabolites incorporates into dna and rna
      • FDUMP : into DNA
      • 5UTP : into RNA
    • cytarabine : activated to cytosine- arabinoside inhibor of DNA polymerases
      • most specific to S-phase out of all antimetab
    • Capecitabine: activated to 5FU
      • oral
  • Folate antimetabolite:
    • Methotrexate : inhibits DHFR
    • Pemetrexed :
  • Purine antimetabolite
    • 6-mercaptopurine : inhibits denovo purine synthesis
      • low oral bioava
      • activated by Hypoxanthine-guanine phosphoribosyl transferase to toxic metabolites
    • thioguanine: inhibits denovo purine synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which drug reduces the toxic effect of Methotrexate?

A

Leucovorin rescue= folinic acid ( rescue therapy: decrease toxic effect)

after administering MTX for 36-48 hrs its terminated before severe toxicity of GI and bone marrow cells –> leucovorin –> accumulates more in normal cells –> rescue of normal cells bcz it bypasses DHFR step in folic acid system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fluorouracil indic.

A
  1. Breast cancer
  2. GI cancer
  3. Head & neck
  4. HCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Methotrexate special SE

A

Pulmonary fibrosis and infiltrates

folate defiency

mucositis, diarhhea

hepatotoxicity

alopecia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Methotrexate indication

A
  1. Breast cancer
  2. Bladder carcinoma
  3. Choriocarcinoma
  4. Head & neck
  5. Primary CNS lymphoma
  6. Non-hodkin lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

6MP indic

A

CML
AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cytarabine ind

A
  1. AML
  2. Non-hodgkin lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

capecitabine ind

A
  1. Breast( metastatic disease resistant to 1st line)
  2. Colon c
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pemetrexed ind

A
  1. Non–small cell lung c
  2. mesothelioma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

5FU toxicity

A
  • ACUTE
    • nausea
    • mucositis
    • diarhhea
  • chronic
    • myelosuppression
    • neurotoxicity
    • alopecia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hepatoxicity side effect occurs with which anti-metabolite?

A
  • MTX: antifolate
  • 6MP: purine antimeta
  • cytarabine: pyrimidine antimetabolite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Alklyting agents

A

Alkylation agents are CCNS drug (CELL CYCLE NON SPECIFIC)

They form reactive molecular species which alkylate nucleophillic groups on DNA bases (Alkalates Guanine N7)

  • Cyclophosphamide- requires hepatic p450 activation,
    • forms DNA cross-links resulting in - of DNA syn & function
  • Cisplatin-
    • cross links DNA strands with platinum
  • Oxaliplatin- for colon cancer
  • Dacarbazine-
    • ​ needs CYP450 for hodgkin lymphoma
  • Temozolomide-
    • ​prodrug: activation in physiologic pH (not hepatic)
    • for Glioblastoma!
  • Bleomycin-
    • complexes with Fe and O2 –> free radicals–> DNA strand termination
    • Anti-tumor antibiotic
    • CCS (G2 phase)
  • Actinomycin D=dactinomycin:
    • ​anti-tumor antibiotic​
    • Inhibits DNA dep-RNA pol, at high doses inhibits DNA SYN

DOCTor!!! ABC!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which is for CNS tumors?

A

Temozolomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give Cyclophosphamide with

A

Mesna to protect the bladder from arecolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cyclophosphamide indication

A
  1. Breast c
  2. Ovarian c
  3. Non-hodgkin lymphoma
  4. Chronic lymphocytic leukemia (CLL)
  5. neuroblastoma

immunosuppressive therapy

CycLo-circle as in breast, ovaryy, CLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cyclophosphamide SE

A
  • myelosupression
  • SIADH
  • HC hemorrhagic cystitis
  • alopecia
  • cardiac dysfunction
  • pulmonary toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cisplatin ind

A
  1. Testicular c
  2. bladder c
  3. ovarian c
  4. lung c

cis all circular organs exp lung

cis - bladderrr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cisplatin SE

A

Neurotoxicity ( Ototoxicity , peripheral
Nephrotoxic

nausea, vomit

NOT ass with myelosupp

*prevent nephrotoxicity by amifostine (free radical scavenger) and saline infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Oxaliplatin ind

A

colon cancer (advanced stage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

oxaliplatin SE

A

Neurotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Dacarbazine ind

A
  • hodgkin lymphoma
  • melanoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Dacarbazine SE

A

Nausea, vomit

Alopecia

skin rash

phototoxicity

myelosupp

Flu-like syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which alkalyting agent is a prodrug

A

temozoloamide

activation in physiologic pH (not hepatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Temozoloamide ind

A

CNS TUMORS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
SE of temozoloamide
nausea vomit myelosupp
26
Bleomycin ind
* CCS drug!!! ( G2 phase) * Anti-tumor antibiotic 1. Hodgkin lym 2. testicular c 3. lymphoma 4. SCC
27
bleomycin mechanism
* mixture of glycopeptides * generates free radical which bind dna --\> strand breaks + inhibit dna synthesis * CCS drug (G2 phase)
28
bleomycin pharmacokinetic
* parenterally * inactivated by tissue amino-peptidases * but some renal clearance. complexes with Fe and O2 \> free radicals \> DNA strand termination
29
bleomycin SE
* pulmonary fibrosis * pneumonitis * hypersensitivity rxn * mucocutaneous rxn * alopecia * hyperpigmentation * blister * hyperkeratosis
30
Alkylation agents are CCS OR CCNS drugs?
ALL are CCNS expect for bleomycin
31
Dactinomycin ( actinomycinD) ind
CCNS Antitumor antibiotic 1. wilms tumor 2. Ewing sarcoma 3. rhabdomyosarcoma 4. Gestational choriocarcinoma
32
Dactinomycin SE
Nausea, vomit myelosuppresion alopecia
33
Topoisomerase inhib.
* **Etoposide**, teniposide- * induces DNA breaks through inhibition of Topo 2 * CCS (late S phase, early G2 phase) * Semi-synthetic derivatives of plant alkaloid- _podophyllotoxin_ * **Irinotecan,** topotecan- * DNA damage by inhibiting Topo 1 ( function: cuts and religates DNA strands) * CCS (S phase) * Semi-synthetic derivative of more toxic _campthothecin_ * **Doxorubicin,** Daunorubicin, epirubicin- * intercalate between DNA bp's, inhibits Topoisomerase 2 * Oxygen frree radicals bind to dna causing strand break * CCNS (anthracyclin) * Anti-tumor Antibiotic _(anthracyclins_) Topo inhibitors make DNA DIE! (dOXO)
34
Doxorubicin indications
1. Breast cancer 2. Ovarian c 3. lymphoma 4. myelomas 5. sarcoma 6. thyroid c
35
Doxirubicin toxicities acute / chronic
* acute: * nausea * arrythmias * chronic * alopecia * myelosupp * cardiomyopathy (CMP) and heart failure
36
what drug is given to protect against doxorubicin cardiotoxicity?
Dexrazoxane = inhibitor of iron-mediated free radical generation may protect against dose-dep form of cardiotoxicity
37
administration of doxorubicin, daunorubicin? metabolism excretion
I.V metabolised in liver products excreted in bile and urine
38
irinotecan mechanism pharmacokinetic
Inhibit topoisomerase 1 resulting in dna damage CCS (S-PHASE) Irinotecan is prodrug converted in liver to active form sn-38 Eliminated in bile and feces genetic variation affects its metabolism (UGT1A)
39
Irinotecan ind
metastatic colorectal c
40
irinotecan SE
nausea, vomit, diarhhea myelosupp(chronic)
41
etoposide mechanism
* CCS (late S-phase, early G2) * derivative of podophyllotoxin * inhibits topoisomerase 2 --\> dna damage
42
etoposide ind
* **Lung cancer** * **non-hodgkin lymphoma** * **gastric c** * germ cell
43
etoposide pharmacokinetic
* oral, distributes well * eliminated via kidney (dose reduction in pts with renal impairment)
44
etoposide se
acute: nausea, vomit chronic: myelosupp, alopecia
45
Microtubule inhib.
* Vinca alkaloid * **Vincristine,** Vinblastine * - inhibit. polym. ALL. Cristine is unstable * Interfere with microtubule _assembly_, resulting in impaired mitosis * Taxane**:** * **Docetaxel**, paclitaxel * Interferes with microtubule _disassembly,_ resulting in impaired mitosis * enhance polym. Breast Lung Overian. DOCtors who pay TAXes stabilize the economy VIN and CRISTINE went to the DOC to pay TAX
46
Vincristine mechanism
* interferes with **microtubule assembly** --\> block formation of mitotiic spindle --\> impaired mitosis * CCS (M phase)
47
vincristine pharmacokinetic
* parrenterally * penetrate most tissue except CSF * Cleared mainly via biliary excretion
48
vincristine ind
1. acute lymphoid leukemia (ALL) 2. Hodgkin lymphoma 3. Non-hodgkin lymphoma 4. wilms tumor 5. neuroblastoma
49
vincristine SE
acute : none chronic: * neurotoxic with peripheral neuropathy * paralytic ileus * myelosupp * alopecia * IADH secretion (inappro adh)
50
Docetaxel mechanism
* CCS (M-phase) * interferes with microtubule diassembly (mitotic spindle)
51
docetaxel, paclitaxel pharmacokinetic
I.V
52
docetaxel ind
Solid tumors * Breast * Ovarian * lung * Gastro-esophageal * prostate * bladder * head & neck
53
docetaxel toxicity
Neurotoxicity Bone marrow depression
54
Hormonal agents
Prednisolone for ALL and Lymphomas Tamoxifen- Estrogen antagonist in breast and CNS , SERM. breast cancer (estrogen sensitive) Anastrazole- aromatase inhib. Goserelin- GnRH agonist , inhibits LH/FSH due to desens. Degarelix- GnRH antagonist for prostate cancer Bicalutamibe- androgen receptor inhibitor prostate. Bi for 2 testicles Octreotide- Somatostatin analog DOG or BAT?
55
prednisolone mechanism
* Activates GC-R alters gene transcription
56
prednisolone indic
* inflammatory conditions * organ transplant * hematologic cancers (leukemia, lymphoma)
57
pharmacokinetic prednisolone
* **duration of activity is longer** than pharmacokinetic half-life of drug _owning to gene transcription effect_
58
prednisolone toxicity
* adrenal suppression * growth inhibition * muscle wasting * osteoporosis * salt retension * glucose-intolerance * behavioral changes
59
tamoxifen mechanism
* Estrogen antagonist in breast & CNS * Estrogen agonist in liver & bone * SERM (selective estrogen modulator) blocks the binding of estrogen to estrogen-sensitive cancel cells in breast.
60
tamoxifen ind
* Prevention and adjuvant treatment of hormone-responsive breast cancer
61
tamoxifen administration
oral
62
tamoxifen SE
* HOT FLUSHES * thromboembolism * endometrial hyperplasia (agonist effect in endometrium) * vaginal bleeding * nausea, vomit
63
anastrazole mechanism
* aromatase inhibitor ( catalyzes conversion of andro-stenedione to estrone)
64
anaztrazole indication
* advanced breast cancer
65
anastrazole toxicity
* nausea * diarrhea * hot flushes * bone, back pain * dyspnea * peripheral edema
66
**Goserelin,** leucoprolide mechanism
* GnRH agonist * synthetic peptide * if administered in constant doses to maintain stable blood levels, they inhibit release of pituitary LH and FSH --\> both androgen and estrogen synthesis decreases
67
goserelin ind
* prostate c * breast * leiomyoma * endometriosis
68
goserelin SE
* headache, nausea * injection site rxn * symptoms of hypogonadism with continuous treatment ( impotence in male)
69
Degarelix mech
* GnRH antagonist: alters release of FSH, LH --\> decreased testestorone synthesis
70
degarelix ind
prostate c
71
degarelix se
headache, vomit nausea
72
Bicalutamide mech
* Androgen receptor antagonist (ANTI-ANDROGEN)
73
Bicalutamide IND
* prostate c
74
Bicalutamide SE
* gynecomastia * hot flush * impotence * hepatotoxic
75
octreotide mech
* Somatostatin receptor agonist * inhibits release of GH, glucagon, insulin , gastrin
76
octreotide ind
* acromegaly * endocrine tumors:(hormone-secreting tumor) * carcinoid * gastrinoma * glucagonoma * isulinoma * VIPoma * acute control of bleeding esophageal varices
77
octreotide pharmacokinetic
* SC * I.V * IM (long acting injection)
78
octreotide SE
* GI * gallstone * bradycardia * cardiac conduction anomalies
79
Small molecule signal transduction inhib.
* Tyrosine kinase inhibitors * **Imatinib**- TK inhib. BCR-ABL for CML. C-kit * **Lapatinib-** TK inhib. HER2 Lap of breast like lack of breast * **Sunitinib-** TK inhib. * **Ibrutinib-** TK inhib like hebrew * EGFR inhibitors * **Gefitinib, Erlotinib**- EGFR antag. NSCLC * mTOR inhibitor * **​Everolimus**- mTOR inhib for renal cancer. renal cancer and mTOR for EVER * proteosome inhibitors (reversible inhibition of 26S) * **Bortezomib** for MM * **Crizotinib**- ALK inhib. Cris speaks Hebrew * **Dabrafenib(BRAF)+Trametinib** for Melanoma Dabra is on the tram and there is a lot of sun * **Tretinoin-** AML and Acne. All trans retinoic acid orally active once/daily Hepatic p450 metabolism Act intracellularly act on mutated, constitutivly active receptors that no longer reply on ligand binding
80
imatinib mechanism
Tyrosine kinase inhibitor * inhibits bcr-abl tyrosine kinase (commonly expressed in CML ass with philadelphia chromosome translocation) and other tyrosine kinases * C-kit tyrosine kinase inhibitor
81
imatinib ind
* CML ( + philedelphia chromosome translocation) * gastrointestinal stromal tumor ( + Ckit tyrosine kinase)
82
imatinib SE
* acute * nausea * vomit * chronic * Fluid retention with ankle and periorbital edema, * diarrhea, * myalgias, * congestive heart failure
83
**Gefitinib, erlotinib** mechanism
EGFR inhibitors (inhibit tyrosine kinase domain)
84
Gefitinib, erlotinib ind
* Gefitinic : Non-small-lung cancer (2nd line) * erlotinib: * Non small lung cancer (2nd line) * pancreatic c (combination therapy)
85
Gefitinib, erlotinib SE
rash (acne like) diarhhea
86
lapatinib mechanism
Tyrosine kinase inhibitor ( HER2/neu and EGFR pathways)
87
lapatinib indication
breast cancer (HER2 positive)
88
lapatinib SE
* rash * diarrhea
89
sunitinib mech
it's a small molecule that inhibits TK receptors. Tyrosine kinase receptor inhibitor ( PDGF-R , VEGF-R) * metabolised by CYP3A4 * elimination: hepatic
90
sunitinib ind
renal cell carcinoma imatinib-resistant GIST
91
sunitinib SE
* diarhhea, nausea, vomit * hypertension * bleeding complications * fatigue
92
Ibrutinib mech
* Tyrosine kinase inhibtor ( Brutons tyrosine kinase in B-cells)
93
ibrutinib ind
* CLL * waldenstrom macroglobulinemia * Mantle cell lymphome * marginal zone lymphoma
94
ibrutinib SE
* URTI * sinusitis * myelosupp
95
Crizotinib mech
* ALK kinase inhibitor * ROS1 oncogene inhibitor
96
crizotinib ind
Non small lung cancer
97
crizotinib SE
Nausea, vomit, diarhhea
98
Bortezomib mechanism
* proteosome inhibitor: Reversibly inhibits chymotrypsin-like activity of the 26S proteasome * ( inhibition result in downregulation of NF-Kbeta signalling pathway)
99
Bortezomib indication
multiple myeloma
100
Bortezomib SE
* acute: * hypotension * edema * GI * chronic * peripheral neuropathy * cardiac dysfunction
101
Dabrafinib and trametinib mechanism
* Dabrafenib : BRAF inhibitor * trametinib : MEK inhibitor USED IN COMBINATION
102
Dabrafinib and trametinib(combo) ind
MELANOMA
103
Everolimus mechanism
* mTOR-inhibitor * Derivative of sirolimus (rapamycin)
104
everolimus ind
* renal cancer * neuroendocrine tumors
105
everolimus SE
stomatitis infections diarhhea
106
T-retinoin - ATRA (all-trans retinoic acid) mechanism
* vitamin A (retinol ) derivative * Differenciating agent: promotes differenciation of promyelocytes (used as adjunct to chemo)
107
T-retinoin ind
* AML (M3 type) acute promyelocytic leukemia * Acne (topical)
108
T-retinoin SE
* Differenciation syndrome : * fever * ARDS * pleural effusion * pericardial effusion * AKI * CNS symptoms
109
Large molecule signal transduction inhib.
* **Trastuzumab-**(emtasnsin) Anti HER2 trust me i cure breast cancer. but cardiotoxic * **Panitumumab**- anti EGFR. colon. Eating panir * **Rituximab**- Anti CD20. CLL, Hodgkins * **Bevacizumab-** Anti VEGF for colon. colon be evacuated from cancer * **INF-a f**or CML, T cell lymphoma, hairy cell leukemia * **Aldesleukin** stimulates T cells for renal cancer. Aldes like aldostrom which works in renal * **Pembrolizumab** activates T cell for melanoma. pembrol sounds like a pimple that rolls on your skin TiP! dont go to RIBA Pal
110
Trastuzumab-(emtansin) mechanism of action
* Monoclonal antibody * GF receptor inhibitor * Inhibits binding of EGF"epidermal GF" to HER2/neu growth receptor. " trust me i cure breast cancer. but cardiotoxic"
111
Trastuzumab-(emtansin) indication
* GF receptor inhibitor 1. HER2/neu receptor positive breast cancer
112
Trastuzumab SE
* Acute: Nausea, vomit, chills, fever, headache * Cardiac dysfunction including heart failure
113
**Panitumumab**, cetuximab mechanism of action
* Anti-EGFR * fully Human monoclonal ANTIBODY
114
**Panitumumab** indication
* Refractory metastatic colorectal cancer NOTE: mutated K-RAS tumors are resistant
115
Panitumumab, cetuximab SE
* nausea, vomit * diarhhea * hypomagnesemia
116
Cetuximab mechanism, indication, SE
* Chimeric monoclonal antibody * GF-r inhibitor ( directed to EC domain of EGFR) * used in COMBO with * + irinotecan+ oxaliplatin for: metastatic colon cancer * +radiation : head & neck cancer * SE: skin rash, hypersensitivity infusion reaction
117
Rituximab mechanism and indication
**Anti CD20 antibody (cell surface antibody)** binds to CD20 in **Non-Hodgkins B cell lymphoma** --\> complement-mediated lysis, direct cytotoxicity, apoptosis CLL,
118
Rituximab SE
* Hypersensitivy rxn 3: serum sickness * Myelosuppression * Infusion-related rxn: 50% of patients * fever * lymphopenia
119
Beva
120
Bevacizumab- mechanism & indication
* Monoclonal antibody * Anti VEGF * Inhibits binding of VEGF to its receptor, resulting in inhibition of tumor vascularization * Indication: * Colorectal c * Breast c * Non-small cell lung c * Renal cancer
121
Bevacizumab SE
* Acute * HTN * infusion rxn * chronic: * Arterial thrombo-embolic event * GI peroforation * wound healing complications * proteinuria
122
Interferon-alpha mechanism , indication
* Endogenous glycoproteins with * **anti-neoplastic,** * **immunosupp** * **& antiviral actions.** * Indication: * CML * Hairy-cell leukemia * T-cell lymphoma
123
Interferon-alpha SE
* Myelosuppression * Neurotoxic
124
Aldesleukin Mechanism, indication
* IL-2 recombinant protein * stimulates growth and differenciation of T cells * Renal cancer * Melanoma
125
Aldesleukin SE
diarrhea hypotension
126
Pembrolizumab mechanism indication
* Humanized monoclonal Ab ( IgG4 isotype) * Immunomodulator (check point protein modulator) * Antibody binds **PD-1 receptor of lymphocytes** ( programmed cell death protein 1) --\> **T-cell activated** (prevent co-inhibitory signal) * activates T cell for **melanoma**. "pembrol sounds like a pimple that rolls on your skin" * Non-small lung cancer
127
Pembrolizumab SE
* Injection site rxn * pneumonitis * inflammation of endocrine glands
128
RA Tx.
Rituximab with Methotrexate
129
Antimetabolites are CCS or CCNS?
CCS

Pharmacology FINAL (2nd sem) (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions