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

B: 32-37 Flashcards

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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
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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

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3
Q

Fluorouracil indic.

A
  1. Breast cancer
  2. GI cancer
  3. Head & neck
  4. HCC
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4
Q

Methotrexate special SE

A

Pulmonary fibrosis and infiltrates

folate defiency

mucositis, diarhhea

hepatotoxicity

alopecia

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5
Q

Methotrexate indication

A
  1. Breast cancer
  2. Bladder carcinoma
  3. Choriocarcinoma
  4. Head & neck
  5. Primary CNS lymphoma
  6. Non-hodkin lymphoma
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6
Q

6MP indic

A

CML
AML

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7
Q

Cytarabine ind

A
  1. AML
  2. Non-hodgkin lymphoma
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8
Q

capecitabine ind

A
  1. Breast( metastatic disease resistant to 1st line)
  2. Colon c
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9
Q

pemetrexed ind

A
  1. Non–small cell lung c
  2. mesothelioma
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10
Q

5FU toxicity

A
  • ACUTE
    • nausea
    • mucositis
    • diarhhea
  • chronic
    • myelosuppression
    • neurotoxicity
    • alopecia
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11
Q

Hepatoxicity side effect occurs with which anti-metabolite?

A
  • MTX: antifolate
  • 6MP: purine antimeta
  • cytarabine: pyrimidine antimetabolite
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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!!!

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13
Q

Which is for CNS tumors?

A

Temozolomide

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14
Q

Give Cyclophosphamide with

A

Mesna to protect the bladder from arecolin

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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

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16
Q

Cyclophosphamide SE

A
  • myelosupression
  • SIADH
  • HC hemorrhagic cystitis
  • alopecia
  • cardiac dysfunction
  • pulmonary toxicity
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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

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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

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19
Q

Oxaliplatin ind

A

colon cancer (advanced stage)

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20
Q

oxaliplatin SE

A

Neurotoxicity

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21
Q

Dacarbazine ind

A
  • hodgkin lymphoma
  • melanoma
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22
Q

Dacarbazine SE

A

Nausea, vomit

Alopecia

skin rash

phototoxicity

myelosupp

Flu-like syndrome

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23
Q

Which alkalyting agent is a prodrug

A

temozoloamide

activation in physiologic pH (not hepatic)

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24
Q

Temozoloamide ind

A

CNS TUMORS

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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)
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