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DD Unit I > DD French drugs tumor drugs > Flashcards

DD French drugs tumor drugs Flashcards

1
Q

Phenobarbital

A

Inducer

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2
Q

Phenytoin

A

Inducer

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3
Q

Carbamazepine

A

Inducer

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4
Q

Rifampin

A

Inducer (remember that it this drug can caused increased clearance of oral contraceptives resulting in increased risk of unplanned uterine parasites)

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5
Q

Ethanol

A

Inducer

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6
Q

St. John?s Wort

A

Inducer

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7
Q

Tobacco smoke

A

Inducer

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8
Q

Nicotine

A

Who knows? But it is apparently not an inducer. This will not be on the test, but note that tobacco smoke is the inducer, not nicotine.

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9
Q

Cimetidine

A

Inhibitor

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10
Q

Erythromycin/Clarithromycin

A

Inhibitor (remember that this drug can decrease the clearance of Lipitor resulting in increased risk of myopathy)

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11
Q

Azole antifungals

A

Inhibitor

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12
Q

Fluoxetine

A

Inhibitor

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13
Q

Grapefruit juice

A

Inhibitor

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14
Q

HIV protease inhibitors

A

Inhibitor

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15
Q

Omeprazole

A

Inhibitor

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16
Q

Ipecac

A

emetic

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17
Q

Activated Charcoal

A

adsorbs toxins

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18
Q

Sorbitol

A

Osmotic cathartic

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19
Q

Polyethylene glycol

A

whole bowel irrigation

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20
Q

N-acetylcysteine

A

Precursor for GSH. Used in acetaminophen toxicity

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21
Q

HOGFACE

A

Mnemonic for remembering inhibitors: HIV protease inhibitors, Omeprazole, Grapefruit, Fluoxetine, Azole fungicides, Cimetidine, Erythromycin/Clathrimycin

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22
Q

PP CREST

A

Mnemonic for remembering inducers: Phenobarbitol, Phenytoin, Carbamazepine, Rifampin, Ethanol, St. John?s Wort, Tobacco smoke

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23
Q

Aspirin

A

COX1/2 inhibitor. ASA, primarily used for anti-clotting properties

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24
Q

tNSAIDs

A

COX1/2 inhibitor. Naproxen, ibuprofen

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25
Q

Acetaminophen

A

COX2 inhibitor. Active in CNS, good for fever suppression

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26
Q

Celecoxib (Celebrex)

A

Selective COX2 inhibitor. Potent. Arthritis treatment, can cause hypertension.

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27
Q

Cortisone

A

Used in GC replacement therapy and emergencies (GC:MC ratio 1:1)

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28
Q

Prednisone

A

Most commonly used for steroid burst therapy (GC:MC ratio 5:1), no topical activity

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29
Q

Methylprednisolone

A

Minimal MC action

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30
Q

Dexamethisone

A

Most potent anti-inflammatory agent, greatest suppression of ACTH, used un cerebral edema and chemo-induced vomiting

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31
Q

Triamcinolone

A

Potent systemic agent with excellent topical activity, no MC action

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32
Q

Cyclophosphamide

A

Chemo - Alkylating agent, crosslinks DNA

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33
Q

Alkylating agent

A

damages DNA, not specific ex. Cylophophamide,

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34
Q

Cisplatin

A

Chemo - Platinum compound, cross-links DNA

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35
Q

Methotrexate

A

Chemo - Antimetabolite, folate analog that is a competitive inhibitor of dihydrofolate reductase which makes purines

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36
Q

5-Fluorouracil

A

Chemo - pyrimidine analog, inhibits DNA sythesis

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37
Q

Topoisomerase interacting agent

A

Chemo - forms double strand breaks, very toxic to heart and bone marrow

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38
Q

Vinblastine/vincristine (Vinca alkaloids)

A

Chemo - Antimicrotubule agents, bind to tubulin and cause depolymerization. Cause nerve damage, muscle damage, neutropenia

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39
Q

Taxanes (paclitaxol, docetaxel)

A

Chemo - Antimicrotubule agents, block mitosis and lead to apoptosis

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40
Q

Tamoxifen, antiandrogens (hormonal agents)

A

Chemo - hormone blockers, used in breast and prostate cancers that depend on hormones for survival

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41
Q

Aromatase inhibitors, GNRH analogs

A

Chemo - hormone production inhibitors, used in breast and prostate cancers that depend on hormones for survival

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42
Q

Rituximab, Trastuzumab/Herceptin, Bevacizumab/Avastin

A

Chemo - antibodies, target cancer cells more specifically (Anti CD21, anti-her2, anti-VEGF, respectively)

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43
Q

Gleevec/Imantinib

A

Chemo - Kinase inhibitor, more targeted against Bcr-Abl, PDGFR, Kit

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44
Q

Dasatinib

A

Chemo - Kinase inhibitor, works in some pts who have become resistant to Gleevec

45
Q

T or F: Prostaglandins and leukotrienes are released from stores of secretory granules.

A

FALSE. They are newly synthesized as needed.

46
Q

Which part of the eicosanoid generating pathway do steroids inhibit?

A

They inhibit phospholipases making arachadonic acid from cell membrane phopholipids.

47
Q

Which part of the eicosanoid generating pathway do non-steroidal anti-inflammatory drugs inhibit?

A

Cyclooxygenase conversion of arachadonic acid to prostaglandins

48
Q

Cox1 or Cox2 or both?- Which pathway promotes inflammation and fever.

A

COX2

49
Q

How do COX1 prostaglandins affect the GI tract?

A

Decrease acid production, increase mucus, increase GI smooth muscle contractions

50
Q

How do COX1 prostaglandins affect platelets?

A

Pro-aggregatory

51
Q

How do COX1 prostaglandins affect the kidneys?

A

Increase renal blood flow, promote diuresis

52
Q

How do COX1 prostaglandins affect the vascular smooth muscle?

A

Increases vasolidation

53
Q

How does COX1 - thromboxanA2 affect smooth muscle?

A

Vasoconstriction

54
Q

Which COX1 pathway product promotes platelet aggregation?

A

thromboxane A2

55
Q

So what will be the consequence of inhibiting COX1?

A

GI: Increased acidity, less mucus, decreased motility. Clotting: Decreased. Kidney: Decreased renal blood flow, less diuresis. Vascular: vasoconstriction or vasodilation depending on inhibition of prostaglandins or thromboxane A2

56
Q

How do COX2 prostaglandins affect the brain?

A

Increase body temperature

57
Q

How do COX2 prostaglandins affect the kidney?

A

Promote renal function - maintenance of RBF

58
Q

How do COX2 prostaglandins affect platelets?

A

Decrease clotting

59
Q

How do COX2 prostaglandins affect the uterus?

A

Increase contractions

60
Q

How do COX2 prostaglandins affect the vasculature?

A

Vasodilation and maintain a patent ductus arteriosus

61
Q

What will be the consequence of inhibiting COX2?

A

Decrease pain and inflammation, decrease fever Kidney: decrease function, Vascular: vasoconstriction, clotting, closed patent ductus arteriosus. Uterine: decrease contraction

62
Q

What is the mechanism of action of aspirin?

A

Irreversibly inhibits COX1 and COX2

63
Q

What is the mechanism of action of tNSAIDs?

A

Reversibly inhibits COX1 and COX2

64
Q

What is the mechanism of action of acetaminophen?

A

Reversibly inhibits COX2 in the CNS

65
Q

What is the mechanism of action of Celecoxib?

A

Reversibly inhibits COX2

66
Q

How is aspirin metabolized?

A

ASA hydrolized by Phase I enzymes followed by SA conjugation by Phase II enzymes. Point being, high doses can saturate Phase II, leading to toxicity

67
Q

T or F: It has been established that NSAIDs are safe to use during pregnancy.

A

FALSE. This has not been established.

68
Q

T or F: Acetaminophen should primarily be used to treat inflammation.

A

FALSE. Primarily use it to treat fever

69
Q

Which NSAID is safest to use during labor?

A

Acetaminophen

70
Q

T or F: tNSAIDs significantly affect platelets.

A

FALSE. Effect is transient and reversible on platelets.

71
Q

T or F: tNSAIDs should primarily be used to treat inflammation.

A

TRUE. They are as effective or superior to ASA and acetaminophen and have few side effects/less toxicity.

72
Q

T or F: NSAIDs are very effective at treating visceral pain.

A

FALSE. Opoids are used to treat visceral pain.

73
Q

What should you be most concerned about in a patient who ODs on tNSAIDs?

A

Renal failure

74
Q

Should aspirin be given to kids? Why or why not?

A

No. They are at risk of developing Reye?s syndrome form it.

75
Q

What pituitary hormone that signals to the adrenal gland does cortisol inhibit?

A

ACTH

76
Q

How does cortisol affect metabolism? (3 things)

A

Inc blood glucose, increase free amino acids (dec protein synth), inc lipolysis and free fatty acids

77
Q

What does aldosterone do?

A

Inc Na reabsorption in the kidney resulting in inc hypertension

78
Q

T or F: Glucocorticoid suppresses T and B cell precursors and division.

A

TRUE

79
Q

T or F: It is safe to give a pregnant woman glucocorticoids.

A

True. 11B-HSD 2 converts active cortisol to inactive cortisone.

80
Q

What is predisone converted to in the liver?

A

Prednisolone (active)

81
Q

Which is the most potent steroidal anti-inflammatory?

A

Dexamethasone

82
Q

What is triamcinolone?

A

Steroidal anti-inflammatory. Excellent topical activity.

83
Q

Of the following, which has the least mineralocorticoid action? The most? a.) Cortisol b.) methylprednisolone c.) prednisone

A

B, A

84
Q

What is a DMARD?

A

Disease-altering anti rheumatic drug. Slow acting.

85
Q

T or F: Steroid anti-inflammatories doses are often determined by trial by error.

A

TRUE

86
Q

What are considerations for steroid use?

A

Large doses (want short acting with little MC), Alternate day schedule, Terminate use gradually to minimize adrenal crisis

87
Q

If you don?t want a topical steroid to have systemic effects, what should you avoid doing?

A

Covering application of steroid with occlusive dressing, apply it over large areas.

88
Q

For local inflammation, what should you do to limit systemic effects?

A

Try to get steroid into the inflamed area - inhalant for lungs, inject into joints, enema for GI diseases, nasal sprays

89
Q

What disorder is caused by high dose GC use?

A

Iatrogenic Cushing?s disease

90
Q

List some side effects of sustained GC treatment?

A

Pituitary suppression, mood disturbance, impaired wound healing, inc risk of infection

91
Q

List some side effects of very long term GC treatment?

A

osteoporosis, cataracts, skin atrophy, growth retardation in children, peptic ulcer

92
Q

Define primary induction chemotherapy.

A

Drug treatment is primary treatment strategy- no surgery or radiation. Often used in palliative care, when there is not other option for complete cure. Rarely, this method will be used to completely cure a cancer depending on the type.

93
Q

Define neoadjuvant chemotherapy.

A

Use of chemo before localized treatment, trying to make that treatment more effective and less damaging.

94
Q

Define adjuvant chemotherapy.

A

Use of chemo in patients after local treatment modalities such as sugary or radiation to kill micrometastases. Goal is to reduce incidence of localized and systemic recurrence after surgery.

95
Q

What is the difference between conventional cytotoxic cancer therapies and targeted therapies?

A

Conventional damage normal cells as well as tumor cells, theory of them largely based on tumor cells being closer to apoptotic threshold, tolerated dose more relevant. Target agents are less toxic and have different resistance mechanisms, aimed at hitting target that is different/faulty in tumor cells but not normal cells.

96
Q

Why do we combine anti-tumor agents?

A

Combine agents that work relatively well on their own to maximize targets, avoid overlapping toxicities, keep treatment as continuous as possible, use drugs at optimal doses.

97
Q

T or F: Chemotherapy has a wide therapeutic window.

A

FALSE

98
Q

T or F: Parmacogenetics is not important in chemotherapy.

A

FALSE

99
Q

What can combining chemo drugs do?

A

1.) Max tumor kill with min toxicity 2.) Treat a great pop of abnormal cells 3.) Slow drug resistance

100
Q

How do cancer cell die?

A

Apoptosis

101
Q

What is the maximally tolerated dose (MTD)?

A

The dose at which you try to treat a patient - max kill and just tolerated by patient

102
Q

What signaling pathway is triggered in apoptosis?

A

Caspases

103
Q

What are the problems with most current chemo drugs?

A

They kill normal cells along with cancer cells and we are not targeting a defect - tumors may have multiple unique defects that make them cancerous

104
Q

How do cancer drugs become chemo resistant?

A

1.) Reduced drug uptake 2.) Reduced apoptotic machinery 3.) Alter cellular target of drug 4.) Increased DNA repair

105
Q

T or F: Tumor stem cells are easily targeted.

A

FALSE

106
Q

What do alkylating agents react with?

A

DNA

107
Q

What causes CML?

A

Genetic translocation that creates the Philadelphia Chromosome

108
Q

What is the most common mechanism of resistance to Gleevec?

A

Mutations that alter drug binding

109
Q

Which anti-tumor agents are associated with neurotoxicity?

A

Antimicrotubule agents

DD Unit I (10 decks)

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