Essential Drugs Flashcards

Question

Spironolactone

Answer 1

K sparing diuretic MoA: Aldosterone antagonist, inhibits the NaK (K out, Na in) pump in the collecting duct SE's: HYPERKALAEMIA (especially when used with ACEi) [DO NOT give if K>5 or creat. >120] Oestrogen things: Hirsutism, men boobies, sex. dysfunction

Answer 2

Class: Beta blocker as well as alpha blocking activity MoA: Non-selective beta and alpha blocking activity, slows HR, SV and CO, also causes vasodilation life-threatening: WATCH for asthma!, anything that makes heart slow (AV block, long PR, HR <60), hypotension is CI not essential - [Uses in CHF: dec. pulmonary capillary pressure, dec. HR, dec. systemic vascular resistance Uses in HPT: reduces CO, dec. tachycardia (beta agonist induced and orthostatic), vasodiltion, decreased perpheriral resistance, decreased renal pressure and renin activity]

Answer 3

Class: opioid MOA: mu-opioid receptor agonist Metabolism: glucuronidation (UDP) Excretion: urine Histamine release: vasodilatation, itching, bronchoconstriction AE: nausea & sedation (go away), constipation, resp depression (decrease brainstem responsiveness to CO2 and rhythmicity) Caution: Hepatic and renal impairment, elderly, pregnancy near term, lactation, neonates, decreased pulmonary reserve (COPD and acute asthma)

Answer 4

Class: opioid (weak) MOA: mu-receptor agonist, inhibit serotonin and noradrenaline reuptake synergistic with paracetamol Metabolism: Liver (CYP2D6) Excretion: Renal Drug interactions: carbamazapine induces its metabolism predisposes to serotonin syndrome, be aware of giving with SSRIs, MAOIs AEs: nausea, sedation, constipation, resp depression, less abuse potential however CYP2D6 variants: slow metaboliser: poor analgesia but constipation fast metaboliser: resp depression, coma and death

Answer 5

Class: weak opioid MOA: weak affinity for mu-opioid receptor (agonist) Metabolism: liver CYP2D6 Excretion: AE: morphine CYP2D6 variants: slow metaboliser: poor analgesia but constipation fast metaboliser: resp depression, coma and death

Answer 6

class: acetaminophen is actual name, analgesic drug (not anti-inflam like NSAIDs), antipyretic MOA: inhibits prostaglandin synthesis centrally (some COX inhibition peripherally) Metabolism: liver Excretion: renal AEs: Hepatotoxicity (NAPQI metabolite is toxic!), nephropathy (also seen with aspirin and NSAIDs)

Answer 7

Class: NSAIDs MOA: inhibit COX-pathway, effectively preventing synthesis of prostaglandins from arachidonic acid COX-1 selective: inhibit prostaglandins associated with gastric mucosal protection, platelet aggregation COX-2 selective: inflam prostaglandins inhibited Metabolism: liver Excretion: kidney/bile AE: Bronchoconstriction: avoid in asthma Fluid retention Nephropathy and ARF Bleeding Hypersensitivity Dyspepsia and peptic ulceration Hepatotoxicity CI: hypersensitivity, active peptic ulceration, Malaria Caution: bleeding disorders, renal or hepatic impairment, heart failure, hypertension, asthma, history dyspepsia

Answer 8

Class: TCA antidepressant, also analgesic, anxiolytic, sedative MOA:increases noradrenergic or serotonergic neurotransmission by blocking the norepinephrine or serotonin transporter (NET or SERT) at presynaptic terminals, antihistamine effect good if have sleep and anxiety disorder Metabolism: liver (including CYP3A4) Excretion: kidney AEs: fast, irregular heartbeat, DILI, dry mouth, blurred vision, weight gain, constipation orthostatic hypotension, dizziness, sedation: alpha adrenergic blockade

Answer 9

Class: anticonvulsant MOA: inhibits sodium channel firing Indications: trigeminal neuralgia, Bipolar 1, epilepsy, post herpetic neuralgia metabolism: CYP450 inducer and substrate excretion: kidney Beware: drug drug interactions (example treating neuropathic pain and on ARVs

Answer 10

COX-1: gastric mucosal irritation eg. indomethacin COX-2: CVS side effects, but adding aspirin adds gastric mucosa problems

Answer 11

ARV - protease inhibitor PK: CYP450 inhibitor (ritonovir) AE: Inc. in TAGs, inc. cholesterol, diarrhoea

Answer 12

ARV - InSTI AE: Insomia PK: It depends on CYP450 (conc. dec. by rif.) Messes with renal tubular secretion of creat. - inc. creat. levels but GFR is not affected, so its not a problem NB: HIGH genetic barrier to resistance

Answer 13

ARV - NNRTI Low genetic barrier to resistance SE's: Neuropsych SEs, RASH AND HEPATOTOXICITY PK: CYP450 metabolised - it is an INDUCER!

Answer 14

ARV - NNRTI PK : CYP450 inducer! AE: Rash and Hepatoxicity (WORSE than efavirenz) Low genetic resistance barrier

Answer 15

ARV - NRTI PK - CYP450 inducer or substrate Renally excreted NB: Interacts with other nephrotoxic drugs (Cyclosporins, aminogly.) AE - NEPHROTOXICITY, OSTEOPAENIA Special shiii: Also treatment for Hep B

Answer 16

Antifungal MoA - inhibits fungal CPY450 and therefore STOPS FUNGAL CELL WALL SYN. PK: Renally excreted - needs DOSE ADJUSTMENT Inhibits CYP450!!!! AE: Hepatotoxic, Neurotoxic

Answer 17

ARV - NRTI PK - Renally elim. DOSE ADJUST ? interacts with sorbital AE - FEW! : LACTIC ACIDOSIS (class effect) In resistance: CRIPPLES VIRUS so we leave it in 2nd line even if resistance (M184V) developed

Answer 18

Anti-TB MoA: Stops cell MEMBRANE synthesis PK: Metabolised in liver (CI in severe hepatic failure) AE: Arthralgia, Hyperuricaemia, ?Rash, HEPATOXIC I REPEAT HEPATOXIC Special Shiii : It kills PERSISTERS - good drug

Answer 19

Antifungal MoA - Causes membrane leakage of cell content and consequent cell death Prevent Mortality PK - RENALLY METABOLISED! AE - NEPHROTOXIC Thrombophlebitis Anaemia and LOW HypoK, HypoMg

Answer 20

Anti-TB (And Ethionamide) MoA - stops mycolic acid synthesis in cell wall (cell wall syn.) PK: Liver metabolised, elim in kidney AE: Neurotoxic, Hepatotoxic, Peripheral neuropathy, Hypersensitivity reaction (Rash, hepatitis)

Answer 21

Anti-TB MoA - Bacteriostatic, inhibits cell wall synthesis PK - renal elimination AE - UVEITIS!!!! (cant give in < 8y/o) Rash Hyperuricaemia peripheral neuropathy NO DILI!

Answer 22

Class: Anti TB MoA - Inhibit RNA polymerase PK - potent CPY450 INDUCER! therefore lots of drug interactions AE - Type 2 antibody mediated hypersens. reaction with haemolysis etc. INTERSTITIAL NEPHRITIS: drug hypersensitivity reaction Gives RED URINE Also causes haem issues - anaemia, thrombocyto. DILI! flu syndrome skin itching, rash Special: It kills persisters in high dose

Answer 23

Class: CNS depressent MOA: enhances GABA, inhibits glutamate, enhances euphoria associated with opioids and endogenous cannabinoids Toxicity: hypoglycaemia, hypothermia, metabolic acidosis, electrolyte disturbances, cardiac arrhythmias, aspiration, ototoxic and gastric irritation causes vomiting Treat: reverse side effects, give thiamine if chronic alcohol abuse, haemodialysis if severe Metabolism: saturable, in liver distributes to all cells in body so affects ALL systems eg testicular atrophy, anovulation, immunosuppression, cardiomyopathy Withdrawal symptoms: excitatory-increased BP, tachycardia, seizures, tremors, sweating

Answer 24

Drug class: stimulant MOA: indirect acting sympathomimetic, increases dopamine, serotonin and noradrenaline euphoria, but less intense than cocaine & lasts longer paranoia, hyperthermia, tachycardia, hyperytension, palpitations, loss of appetite, anxiety, insomnia very lipophilic and can cross BBB eg: methylphenidate, ephedrine Metabolism: liver-CYP2D6 Withdrawal symptoms: sedation, depressed mood, overeating AEs: Hallucinations, anorexia, hyperthermia (serotonin)

Answer 25

Class: stimulant MOA: inhibits dopamine reuptake, prolongs action of dopamine within synapse Effects: euphoria, tachycardia, palpitations, insomnia, decreased appetite, local vasoconstriction Adverse effects: risk of intracranial haem, ischaemic stroke, MI, arrhythmia, seizures withdrawal symptoms: mild

Answer 26

Drug class: cannabinoid MOA: acts on cannabinoid receptors, decrease dopamine inhibition Leads to: euphoria, relaxation daily use assoc. with anxiety attacks, hallucinations and psychosis relieves N &V associated with chemo, appetite stimulant abrupt cessation: restless, irritable, agitation, insomnia, cramps Treat with benzos Metabolism: liver (CYP450)

Answer 27

Class: opioid MOA: mu-agonist, inhibit GABA neurons, leads to euphoria, pupillary miosis, conjunctival injection, decreased resp rate and bradycardia, absent bowel sounds. Pulm oedema, aspiration pneumonia, rhabdomyolysis in OD Greater availability and higher potency than morphine short-acting TOLERANCE Withdrawal: nausea, vom, diarrhoea Insomnia, myalgia (u receptors, u agonists relieve this), sweating, mydriasis, lacrimation, rhinorrhoea, agitation tachycardia, raised BP (NE affects)

Answer 28

Class: Sulfonylurea all the gli.......... Glimepiride: preferred in elderly Glibenclamide: avoid in elderly MOA: relies upon residual Beta cell function in pancreas. Promotes insulin secretion from these cells & stimulates their growth, enhances beta cell sensitivity to glucose, reduces GLUCAGON release Metabolism: liver, CYP450 Excretion: renal (beware low GFR) AEs: Hypoglycaemia (esp if old, renal impairment, irreg meals), weight gain CI: severe hepatic impairment, pregnancy, avoid if renal impairment eGFR less than 60

Answer 29

benzos anticonvulsants (except phenytoin) eg. carbamazapine beta blockers clonidine (alpha 2 agonist) disulfiram: build up of acetaldehyde which makes you feel crap Naltrexone (as seen with opioid withdrawal and dependence)

Answer 30

benzos anticonvulsants (except phenytoin) eg. carbamazapine beta blockers clonidine (alpha 2 agonist) disulfiram: build up of acetaldehyde which makes you feel crap Naltrexone (as seen with opioid withdrawal and dependence)

Answer 31

1. Mannitol 2. Corticosteroids 3. Heparin 4. Aspirin/NSAIDs (renal impairment)

Answer 32

Class: antimalarial MOA: prevents nucleic acid synthesis, protein synthesis and glycolysis in P. falciparum ONLY IF IV ARTESUNATE UNAVAILABLE Loading dose very NB, over 4 hrs, IV then 10mg/kg slow infusion over 8 hrs Metabolism: liver Excretion: needs to be dose adjusted in renal failure (adjust maintenance dose, not loading dose) NB AE: hypoglycaemia, arrhythmias Not ideal drug: 3 times a day, metallic taste

Answer 33

Class: antimalarial MOA: blocks asexual forms malaria parasite First line Does not need to be dose adjusted in renal and hepatic impairment (unlike quinine) Give 3 doses 12 hrs apart before starting oral therapy Metabolism: liver (CYP2A6-beware amiodarone, isoniazid) AE: delayed haemolysis (1 week plus, non immune patients eg. non-endemic areas, children, hyperparasitaemia)

Answer 34

Class: antimalarial Prevents asexual parasite AND sexual gametocyte stages that can infect mosquito oral, twice a day for 3 days, dose adjust according to weight Maximise absorption: fat better tolerated, 3 days only instead of 7 for quinine fist line for uncomplicated malaria Metabolism: CYP450, beware rifampicin and efavirenz CI: allergic, less than 5kg (usually iv anyway because vulnerable), severe malaria (at least 3 doses IV before transitioning to oral AL), pregnant in 1st trimester

Answer 35

Latent phase, need to add Primaquine (everyday for 14 days, NOT IN PREGNANCY)

Answer 36

Mefloquine (weekly). Start at least one week before entering a malaria area, take once weekly while there and for four weeks after leaving the malaria area, OR Doxycycline (daily). Start one day before entering a malaria area, take daily while there and for four weeks after leaving the malaria area, OR Atovaquone-proguanil (daily). Start one to two days before entering malaria area, take daily while there and for seven days after leaving the area.

Answer 37

epilepsy psych arrhythmias infant less than 5kg

Answer 38

Pregnancy. Children under eight years of age. Caution in travellers with myasthenia gravis.

Answer 39

renal impairment pregnancy; lack of data though

Answer 40

1. Benzo IV: diazepam, clonazepam, lorazepam Buccal: Loraz, midaz IM: loraz, clonaz PR: diaz Then IV infusion phenytoin/ phenobarb in kids Still not working: intubate and give thiopental(barb)/propofol infusion BUT NB: phenobarb and thiopental are barbs and INDUCE metabolism of phenytoin so infusion of phenytoin may become subtherapeutic

Answer 41

Class: anticonvulsant MOA: enhances GABA, prolongs inactivation Na channels Autoinduces itself after 2 weeks at maximal induction PK: potent inducer CYP450 Metabolism: CYP450 in liver AEs: BM suppression: aplastic anaemia, agran Hypersensitivity Cerebellar symptoms: ataxia, vertigo Induces metabolism of tramadol?

Answer 42

Phenos and carbamazapine

Answer 43

Class: Barbiturate, anticonvulsant MOA: enhances action of GABA metabolism: liver, also potent inducer CYP450, induces metabolism of phenytoin AE: hyperactivity in kids, sedation (goes away), systemic hypersensitivity

Answer 44

1. Glucocorticoids 2. Thiazide diuretics 3. Atypical antipsychotics 4. ARVs (Protease inhibitors) 5. I need to check this but tacrolimus?

Answer 45

Protophane or Humulin N once or twice dly/ usually @ night not after 10pm takes 2-4 hrs to work, lasts 16-24 hrs

Answer 46

actrapid works within 30 min, take 30 min before meal stops working after 2-4 hrs

Answer 47

Mix short acting and intermediate acting insulin diff proportions eg. 30/70 Given twice daily. First dose before breakfast, second after supper covers mealtime and basal insulin requirements ACTRAPHANE

Answer 48

Basal bolus mimics normal insulin secretion in beta cells Combo: pre-meal short acting insulin (bolus) that you give before each meal (30 min) plus long-acting insulin used/or intermediate?: protophane/Humulin N at BEDTIME no later than 10pm 50:50 ratio

Answer 49

0.6 units/kg body weight

Answer 50

Class: hormone, protein so needs to be given subcut as degraded in GIT if given orally MOA: increases glucose entry into cell, stimulates lipogenesis, protein synthesis, glycogenesis and glycolysis, basically prevents hyperglycaemia and increases glucose storage, utilisation Secreted by Beta cells in pancreas Metabolised in KIDNEY AE: weight gain, accumulation of fat at drug IM site, HYPOGLYCAEMIA

Answer 51

Class: Biguanide MOA: reduces hepatic gluconeogenesis & glycogen metabolism, also reduces beta oxidation does not really enhance lipogenesis, raises HDL Metabolism; it actually isnt metabolised in liver so liver safe! Excretion: excreted unchanged in urine-NB GFR needs to be monitored AE: GIT, LACTIC ACIDOSIS (inhibits conversion lactate to glucose), reduced B12 absorption NO WEIGHT GAIN, HYPOGLYCAEMIA Does not effect insulin secretion CI: eGFR below 30, raised creatinine, CCF

Answer 52

Mefloquine (neuropsych)

Answer 53

Novolog, apidra, Humalog

Answer 54

beware ace-inhibitors and spironolactone because they can cause hyperK+ Other drugs affected by renal failure: Erythropoietin-renal failure and anaemia Activated Vit D

Answer 55

beware propanolol: drug with extensive first pass metabolism rather chose drugs that are metabolised via conjugation instead of CYP450

Answer 56

be aware: GFR slows down and so does hepatic metabolism (opposite of pregnancy) 1. anticonvulsants 2. hypnotics 3. morphine 4. NSAIDs 5. Warfarin

Answer 57

losartan anything sartan basically remember know benefits of bradykinin such as renal vasodilation

Answer 58

any drugs that help you to relax eg. diazepam, midazolam alcohol

Answer 59

SEIZURES ataxia, nystagmus, slurred speech

Answer 60

Class: anticoagulant MOA: increases activity antithrombin 3 shorter half-life, quick to switch on and off PROs: has antidote (protamine sulphate), quick to start/stop, have to monitor PTT so can pick up on bleeding quick beware concurrent use of NSAIDs, anticoagulants monitor internal coag pathway: aPTT

Answer 61

Class: anticoagulant MOA: increase activity antithrombin 3, inhibits Factor 10A AND 2A (thrombin) No need for monitoring, longer half life so danger if there's a bleed, no antidote renal clearance, do not give if end stage renal disease AE: bleeding CI: heparin induced thrombocytopaenia

Answer 62

class; anticoagulant MOA; competes with Vit K, inhibits factors 2,7,9,10 Also inhibits Protein c, s and z: hypercoag state in first few days as these are body's natural anticoagulants First inhibits natural anticoagulants then acts on coagulants Takes 48-72 hrs to work because natural clotting factors in blood need time to be destroyed. Therefore need to give heparin. Warfarin skin necrosis NB (warfarin destroys protein s and c resulting in formation tiny clots in vessels) Antidote: fast: FFP, PCC, slow: Vit K monitor external coag pathway (INR) Highly protein bound CI: do not give with alcohol, pregnant, recent intracranial haemorrhage, cirrhosis (liver unable to synthesise albumin and clotting factors so more predisposed to bleeding), known coagulation defects

Answer 63

NB just to remember that heparins do not thrombolyse, they just prevent further formation if clot Bleeding Osteoporosis Alopecia Thrombosis Heparin induced thrombocyopaenia

Essential Drugs Flashcards

(88 cards)