Chemotherapy Flashcards
Describe the classification of anti-arrhythmic drugs
Class I (sodium channel blocker): IA e.g. Quinidine, Procainamide - moderate change in phase 0 IB e.g. Lidocaine - little change in phase 0 IC e.g. Flecainide - marked change in phase 0 Class II (B blockers) e.g. Propanolol, Bisoprolol - block sympathetic activity, decrease phase 4 depolarisation and automaticity Class III (potassium channel blocker) e.g. Amiodarone - prolong depolarisation, increase AP duration and ERP Class IV (calcium channel blockers) e.g. Verapamil, Diltiazem - block L type calcium channels, most effective at SA and AV nodes, decrease phase 4 depolarisation and conduction velocity
List some ADRs of anti-arrhythmic drugs
Class I - dizziness, GI disturbances, hypotension, pro-arrhythmic, sudden death
Class II - bronchospasm,hypotension
Class III - pulmonary fibrosis, hepatic injury, increased LDLs, hypothyroidism, photosensitivity
Class IV - asystole, constipation
List what anti-arrhythmic drugs you would use with particular arrhythmias
AF - class IA, IC, II, III, digoxin VF - class IB Sinus tachycardia - class II, IV SVT - class IA, IC, II, III, IV, adenosine WPW - class IC, III Reentrant - class II, IV Vagal bradycardia - atropine Toursades des Pointes - magnesium Class III has a wide spectrum of use
Explain the mechanism of some additional anti-arrhythmic drugs such as adenosine, digoxin and atropine
Adenosine - slows AV conduction
Digoxin (cardiac glycoside) - slows AV condition and heart rate
Atropine (selective muscarinic antagonist) - speeds up AV conduction
List the sites of action of chemotherapy drugs
Chemotherapy drugs interrupt: DNA synthesis DNA DNA transcription/duplication Mitosis
Understand the concept of the log kill ratio in chemotherapy
Chemotherapeutic agents kill a constant fraction of cells (first order kinetics) rather than a specific number of cells after each dose
Low growth fraction (solid cancer tumours) respond poorly to chemotherapy and need to be removed by surgery
High growth faction (disseminated cancers) respond well to chemotherapy
Refinish the main cytotoxic chemotherapeutic groups and actions at their targets: antimetabolites, DNA alkylators/intercalators, mitotic inhibitors (spindle poisons)
Antimetabolites e.g. Methotrexate - can’t produce purines, 5-FU - can’t synthesis DNA
Alkylating agents e.g. Platinum based, nitrogen mustards - directly damage DNA, impair replication by cross linkages
Intercalating agents - inhibit DNA replication, insert themselves between bases of DNA –> kinking/uncoiling
Spindle poisons e.g. Vinca alkaloids - prevent spindle formation, Taxanes - promote assembly, prevent disassembly
Appreciate the range of factors influencing pharmacokinetics in chemotherapy including routes of delivery and drug resistance
Absorption - compliance, gut problems
Distribution - weight loss, low body fat, ascites
Elimination - liver and renal dysfunction, other medication
Protein binding - low albumin, other drugs
List some important chemotherapy DDIs
Vincristine + itraconazole (anti-fungal)
5-FU + warfarin
Methotrexate + penicillin, NSAIDs
Be aware of clinical monitoring assessing therapeutic improvement and minimising ADR risk
Monitor response of cancer, drug levels, organ damage
Understand the concept of the fractional cell kill hypothesis
Multiple drug administration leads to decreased number of cells surviving
Bone marrow cells repair faster than tumour cells
List some common ADRs of chemotherapy
Acute renal failure due to rapid tumour lysis
DIC
Vomiting due to central chemoreceptor trigger zone
Alopecia (avoid via scalp cooling)
Skin toxicity - irritation, thrombophlebitis of veins, extravasation
Mucositis
Cardiotoxicity
King toxicity - pulmonary fibrosis
Be able to describe the targets of drug action on the cardiovascular system
Decrease phase 4 slope/increase AP threshold
Decrease conduction velocity/increase ERP
