Drugs

Question 1

• Adjuvant?
• Neoadjuvant?
• Primary?
• Targeted therapy?
• Conventional cytotaxics? Based on?
• Combining agents?
  1. ) DNA damaging agent: Types? (2) Resistance? Risk?
  2. ) Anti-metabolites: Targets? Ex?
  3. ) Topoisomerase interacting agents: Blocks? Risk?
  4. ) Antimicrotubule agents: Effect? Ex?
• These 4 therapies target?

Answer 1

• Chemo after local treatment to kill micrometastases
• Chemo then treatment to make treatment more effective
• Only chemo
• Aim to hit target in tumor cell differently from normal cells
• Hit specific target but not differently from normal cells; tumor cells are closer to apoptosis
• Increase benefits while speading side effects
• Alkylating agents, pt compounds; Increased NER; hemapoietic toxicity
• Products of metabolism; Methotrexate
• Proteins that helps with strand tension; AML and cardiomyopathies
• Increase rigidity or decrease affinity to break MT; Vinca alkaloids
• All cells

Question 2

5. ) Hormonal Agents: Ex? Risks?
6. ) Antibodies: Recognize what? May bring what to targeted cell? Ex? (2)
7. ) Kinase Inhibitors: Low? Works well with? Ex? (2) Do what with cells that don’t respond?

Answer 2

• Tamxifen; altered hormonal signalling
• MArkers on cells; toxic agent; retuximab, herceptin
• Toxicity; CML BCR-ABL; Gleevac/imantinib; use an agent that hits resistant strains

Question 3

• Glucocorticoids: Act on? (2) Overall effect?
• Stress activates? Releases? Activates? Relseases? Acitvates? Releases? (2) Cortisol binds? Same as? Can have what effect?
• Metabolic effects of GC-R? (3)
• Effects of MC-R? (6)
• GC side effects? (7)
• MC side effects? (3)
• Benefits of anti-inflammatory? (2)
• Side effects? (2)
• C11: Hydroxyl? Ketone? What makes it active?
• Can you seperate MCC and GCC? GCC and AI?

Answer 3

• Block COX2; act on lipocortins to break down phospholipase; Decrease LT and PG
• Hypothalmus; CRH; Pituatary; ACTH; AG; MC and GC; GC-R; GC drug; Adrenal supression
• Increased carbs (increase insulin central insulin); protein breakdown AA’s; TG’s –> FFA’s (periphery cortisol wins)
• Incr. Na+, H2O, Edema, BP; Decrease K+, H+
• Adrenal suppression, Cushing Disease, Insomnia, Mood Disturbed, centripital obesity, muscle waste
• Hypertension, hypokelemia, metabolic alkalosis
• Suppress chronic inflammation, autoimmne rxn
• decreased healing, decreased immunoprotection
• Active; inactive; Liver
• Yes; No

Question 4

• Liver glucocorticosteroid metabolism: Enzyme? Active?
• Kidney: Enzyme? Active?
• Fetus has? So? Betemethasone?
  1. ) Cortisol/ Hydrocortisone: GC:MC; Dose type? Potency? Used to treat?
  2. ) Prednisone: Acting? Dose type? GC:MC? Common? Topical activity? Activated by?
  3. ) Methyl Prednisone: Administered how? Gives a? GC:MC?
  4. ) Dexamethasone: Potency? Used for? Provides greatest suprresion of? Acting? Administration routes? (3) GC:MC?
  5. ) Triamcinalone: Potent for? GC:MC? (2) Administration? (2) Acting?
• Large Doses use? Advantage of alternate day?
• How should it be discontinued?

Answer 4

• 11B-HSD1 activates
• 11B-HSD2 Deactivates
• Kidney enzyme but not liver so you can treat moms with GC’s; Can treat fetus with this
• 1:1; Oral; low; Addisons
• Short; oral; 5:1; most common; none; liver
• IV; steroid burst; 5:0
• Most potent; Cerebral Edema; ACTH; Long; topical, injected or oral; 30:0
• Systemic agent/topical; 5:0 (5^3:0 topically); topical or oral; intermediate
• Short acting w/ little MC; minimize adrenal suppression
• Tapered

Question 5

• Sources of PG’s? LT’s?
• Cell membrane + phospholipase =? 2 pathways from there?
• PGI2? (2); PGD/E2? (4); TxA2?
• COX1: Acts how? Mediators? Effects? (4)
• COX 2: Acts how? Mediators? Effects? (5)
• NSAID therapeutic uses? (4) Target? (4) Dose? (4)
• Side effects? (5) Target? (5)

Answer 5

• Leukocytes; plateltes; EC; leukocytes
• Archidonic acid; 5-lipoxygenase –> LT’s; COX 1/2 –> PGG2
• Inhibit pt aggregation, pain; Vasodilation, pain, fever, inflammation; Increase ptt. aggregation
• Homeostatic; PG’s/TXA; Ptt aggreagation, increase mucus in stomach, renal flow, vaso d/c
• Constituative; PG’s; pain, inflammation, fever, reanl, vaso d, utereine contractions
• analgesia - COX2, intermediate; fever - COX2, intermediate; anti-inflamm - COX2, high dose; antithrombotic - COX1, low dose
• GI ulcers - COX1; Bleeding - COX1; Renal dysfunction - COX 1/2; Delay labor - CO2; Increase thrombotic event - COX2

Question 6

1. ) Aspirin: Acts on? Use? (4) Metabolism? Side effects? (5)
2. ) Traditional NSAIDs: Act on? Ex? (3) Use? (3) Side effects? (1)
3. ) Acetamenophen: Acts on? Not? Use? (2) Not? Least likely to effect?
4. ) Celecoxib: Acts on? Effects? (3) Side effects? Except?

Answer 6

• COX1/2 Irreversible; pain, fever, arthritis, decreased clotting; Hydrolyzed by esterase at liver then conjugated; GI upset; bleeding, Reye Syndrome, delay labor, renal failure
• Reversible COX 1/2; Ibprofin, Naproxen, Ketorolac; pain, fever, anti-inflammatory; minimal, maybe kidney failure
• CNS COX2; periphery; Analgesic, antipyretic; NOT anti inflammatory; labor
• COX 2 reversibly, Analgesic, anti-in, antipyretic, no, hypersensitivty due to sulfa