DD French drugs tumor drugs Flashcards
1
Q
Phenobarbital
A
Inducer
2
Q
Phenytoin
A
Inducer
3
Q
Carbamazepine
A
Inducer
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)
5
Q
Ethanol
A
Inducer
6
Q
St. John?s Wort
A
Inducer
7
Q
Tobacco smoke
A
Inducer
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.
9
Q
Cimetidine
A
Inhibitor
10
Q
Erythromycin/Clarithromycin
A
Inhibitor (remember that this drug can decrease the clearance of Lipitor resulting in increased risk of myopathy)
11
Q
Azole antifungals
A
Inhibitor
12
Q
Fluoxetine
A
Inhibitor
13
Q
Grapefruit juice
A
Inhibitor
14
Q
HIV protease inhibitors
A
Inhibitor
15
Q
Omeprazole
A
Inhibitor
16
Q
Ipecac
A
emetic
17
Q
Activated Charcoal
A
adsorbs toxins
18
Q
Sorbitol
A
Osmotic cathartic
19
Q
Polyethylene glycol
A
whole bowel irrigation
20
Q
N-acetylcysteine
A
Precursor for GSH. Used in acetaminophen toxicity
21
Q
HOGFACE
A
Mnemonic for remembering inhibitors: HIV protease inhibitors, Omeprazole, Grapefruit, Fluoxetine, Azole fungicides, Cimetidine, Erythromycin/Clathrimycin
22
Q
PP CREST
A
Mnemonic for remembering inducers: Phenobarbitol, Phenytoin, Carbamazepine, Rifampin, Ethanol, St. John?s Wort, Tobacco smoke
23
Q
Aspirin
A
COX1/2 inhibitor. ASA, primarily used for anti-clotting properties
24
Q
tNSAIDs
A
COX1/2 inhibitor. Naproxen, ibuprofen
25
Acetaminophen
COX2 inhibitor. Active in CNS, good for fever suppression
26
Celecoxib (Celebrex)
Selective COX2 inhibitor. Potent. Arthritis treatment, can cause hypertension.
27
Cortisone
Used in GC replacement therapy and emergencies (GC:MC ratio 1:1)
28
Prednisone
Most commonly used for steroid burst therapy (GC:MC ratio 5:1), no topical activity
29
Methylprednisolone
Minimal MC action
30
Dexamethisone
Most potent anti-inflammatory agent, greatest suppression of ACTH, used un cerebral edema and chemo-induced vomiting
31
Triamcinolone
Potent systemic agent with excellent topical activity, no MC action
32
Cyclophosphamide
Chemo - Alkylating agent, crosslinks DNA
33
Alkylating agent
damages DNA, not specific ex. Cylophophamide,
34
Cisplatin
Chemo - Platinum compound, cross-links DNA
35
Methotrexate
Chemo - Antimetabolite, folate analog that is a competitive inhibitor of dihydrofolate reductase which makes purines
36
5-Fluorouracil
Chemo - pyrimidine analog, inhibits DNA sythesis
37
Topoisomerase interacting agent
Chemo - forms double strand breaks, very toxic to heart and bone marrow
38
Vinblastine/vincristine (Vinca alkaloids)
Chemo - Antimicrotubule agents, bind to tubulin and cause depolymerization. Cause nerve damage, muscle damage, neutropenia
39
Taxanes (paclitaxol, docetaxel)
Chemo - Antimicrotubule agents, block mitosis and lead to apoptosis
40
Tamoxifen, antiandrogens (hormonal agents)
Chemo - hormone blockers, used in breast and prostate cancers that depend on hormones for survival
41
Aromatase inhibitors, GNRH analogs
Chemo - hormone production inhibitors, used in breast and prostate cancers that depend on hormones for survival
42
Rituximab, Trastuzumab/Herceptin, Bevacizumab/Avastin
Chemo - antibodies, target cancer cells more specifically (Anti CD21, anti-her2, anti-VEGF, respectively)
43
Gleevec/Imantinib
Chemo - Kinase inhibitor, more targeted against Bcr-Abl, PDGFR, Kit
44
Dasatinib
Chemo - Kinase inhibitor, works in some pts who have become resistant to Gleevec
45
T or F: Prostaglandins and leukotrienes are released from stores of secretory granules.
FALSE. They are newly synthesized as needed.
46
Which part of the eicosanoid generating pathway do steroids inhibit?
They inhibit phospholipases making arachadonic acid from cell membrane phopholipids.
47
Which part of the eicosanoid generating pathway do non-steroidal anti-inflammatory drugs inhibit?
Cyclooxygenase conversion of arachadonic acid to prostaglandins
48
Cox1 or Cox2 or both?- Which pathway promotes inflammation and fever.
COX2
49
How do COX1 prostaglandins affect the GI tract?
Decrease acid production, increase mucus, increase GI smooth muscle contractions
50
How do COX1 prostaglandins affect platelets?
Pro-aggregatory
51
How do COX1 prostaglandins affect the kidneys?
Increase renal blood flow, promote diuresis
52
How do COX1 prostaglandins affect the vascular smooth muscle?
Increases vasolidation
53
How does COX1 - thromboxanA2 affect smooth muscle?
Vasoconstriction
54
Which COX1 pathway product promotes platelet aggregation?
thromboxane A2
55
So what will be the consequence of inhibiting COX1?
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
How do COX2 prostaglandins affect the brain?
Increase body temperature
57
How do COX2 prostaglandins affect the kidney?
Promote renal function - maintenance of RBF
58
How do COX2 prostaglandins affect platelets?
Decrease clotting
59
How do COX2 prostaglandins affect the uterus?
Increase contractions
60
How do COX2 prostaglandins affect the vasculature?
Vasodilation and maintain a patent ductus arteriosus
61
What will be the consequence of inhibiting COX2?
Decrease pain and inflammation, decrease fever Kidney: decrease function, Vascular: vasoconstriction, clotting, closed patent ductus arteriosus. Uterine: decrease contraction
62
What is the mechanism of action of aspirin?
Irreversibly inhibits COX1 and COX2
63
What is the mechanism of action of tNSAIDs?
Reversibly inhibits COX1 and COX2
64
What is the mechanism of action of acetaminophen?
Reversibly inhibits COX2 in the CNS
65
What is the mechanism of action of Celecoxib?
Reversibly inhibits COX2
66
How is aspirin metabolized?
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
T or F: It has been established that NSAIDs are safe to use during pregnancy.
FALSE. This has not been established.
68
T or F: Acetaminophen should primarily be used to treat inflammation.
FALSE. Primarily use it to treat fever
69
Which NSAID is safest to use during labor?
Acetaminophen
70
T or F: tNSAIDs significantly affect platelets.
FALSE. Effect is transient and reversible on platelets.
71
T or F: tNSAIDs should primarily be used to treat inflammation.
TRUE. They are as effective or superior to ASA and acetaminophen and have few side effects/less toxicity.
72
T or F: NSAIDs are very effective at treating visceral pain.
FALSE. Opoids are used to treat visceral pain.
73
What should you be most concerned about in a patient who ODs on tNSAIDs?
Renal failure
74
Should aspirin be given to kids? Why or why not?
No. They are at risk of developing Reye?s syndrome form it.
75
What pituitary hormone that signals to the adrenal gland does cortisol inhibit?
ACTH
76
How does cortisol affect metabolism? (3 things)
Inc blood glucose, increase free amino acids (dec protein synth), inc lipolysis and free fatty acids
77
What does aldosterone do?
Inc Na reabsorption in the kidney resulting in inc hypertension
78
T or F: Glucocorticoid suppresses T and B cell precursors and division.
TRUE
79
T or F: It is safe to give a pregnant woman glucocorticoids.
True. 11B-HSD 2 converts active cortisol to inactive cortisone.
80
What is predisone converted to in the liver?
Prednisolone (active)
81
Which is the most potent steroidal anti-inflammatory?
Dexamethasone
82
What is triamcinolone?
Steroidal anti-inflammatory. Excellent topical activity.
83
Of the following, which has the least mineralocorticoid action? The most? a.) Cortisol b.) methylprednisolone c.) prednisone
B, A
84
What is a DMARD?
Disease-altering anti rheumatic drug. Slow acting.
85
T or F: Steroid anti-inflammatories doses are often determined by trial by error.
TRUE
86
What are considerations for steroid use?
Large doses (want short acting with little MC), Alternate day schedule, Terminate use gradually to minimize adrenal crisis
87
If you don?t want a topical steroid to have systemic effects, what should you avoid doing?
Covering application of steroid with occlusive dressing, apply it over large areas.
88
For local inflammation, what should you do to limit systemic effects?
Try to get steroid into the inflamed area - inhalant for lungs, inject into joints, enema for GI diseases, nasal sprays
89
What disorder is caused by high dose GC use?
Iatrogenic Cushing?s disease
90
List some side effects of sustained GC treatment?
Pituitary suppression, mood disturbance, impaired wound healing, inc risk of infection
91
List some side effects of very long term GC treatment?
osteoporosis, cataracts, skin atrophy, growth retardation in children, peptic ulcer
92
Define primary induction chemotherapy.
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
Define neoadjuvant chemotherapy.
Use of chemo before localized treatment, trying to make that treatment more effective and less damaging.
94
Define adjuvant chemotherapy.
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
What is the difference between conventional cytotoxic cancer therapies and targeted therapies?
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
Why do we combine anti-tumor agents?
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
T or F: Chemotherapy has a wide therapeutic window.
FALSE
98
T or F: Parmacogenetics is not important in chemotherapy.
FALSE
99
What can combining chemo drugs do?
1.) Max tumor kill with min toxicity 2.) Treat a great pop of abnormal cells 3.) Slow drug resistance
100
How do cancer cell die?
Apoptosis
101
What is the maximally tolerated dose (MTD)?
The dose at which you try to treat a patient - max kill and just tolerated by patient
102
What signaling pathway is triggered in apoptosis?
Caspases
103
What are the problems with most current chemo drugs?
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
How do cancer drugs become chemo resistant?
1.) Reduced drug uptake 2.) Reduced apoptotic machinery 3.) Alter cellular target of drug 4.) Increased DNA repair
105
T or F: Tumor stem cells are easily targeted.
FALSE
106
What do alkylating agents react with?
DNA
107
What causes CML?
Genetic translocation that creates the Philadelphia Chromosome
108
What is the most common mechanism of resistance to Gleevec?
Mutations that alter drug binding
109
Which anti-tumor agents are associated with neurotoxicity?
Antimicrotubule agents
