Essential Drugs Flashcards
Azithromycin
What is it broadly
Class
MoA
Life threatening and QoL adverse reactions and SE
? important patient info
Antibiotic covering Gram + and Atypicals
Class: Macrolide
MoA: Binds to bacterial ribosome and inhibits protein synthesis -> cell growth
Adverse effects: GIT side effects (QoL)
Amoxicillin
What is it broadly
Class
MoA
Life threatening and QoL adverse reactions and SE
? important patient info
Beta lactam antibiotic
MOA: acts on cell wall of bacteria
Metabolism: liver
Excretion: renal (adjust according to GFR)
AE: Hypersensitivity (Beta lactam class effect): Type 1 so angioedema, anaphylaxis, bronchospasm, urticaria
Ceftriaxzone
3rd gen cephalosporin
Useful in bacterial infections and Meningitis (cross BBB good) for Gram pos and gram neg organisms
MoA - inhibit cell wall synthesis
Watch out for penicillin allergies
Adjust in renal impairment
Interaction: Anticoagulant (messes with Vitamin K metab.), NSAIDs (increases risk of bleeding)
AE: NEUROTOXIC, CNS (dizzy, headache), diarrhoea, SJS rarely
Metronidazole
MoA
Indications
Dose considerations
Adverse effects
Class: nitroimidazole derivative antibiotic
MOA: Toxic to DNA, forms highly reactive nitro
radical with anaerobic metabolism Fe:S proteins
Anaerobes
Bacterial vaginosis
C. diff
E. histolyca
G. lamblia
Metabolism: liver (dose adjust)
Excretion: bile, kidney
AE: disulfiram reaction with alcohol, metallic taste, neurotoxic, neutropaenia, INHIBITS WARFARIN METABOLISM
cloxacillin/flucoxacillin
Cloxacillin: resists beta-lactamase from staph
Flucloxacillin: better absorbed PO
Gram positive ONLY
skin and soft tissue infections
class: Beta-lactam antibiotic
Metabolism: liver
Excretion: kidney
AE: class effect of hypersensitivity
Azithromycin
Class: Macrolide
MOA: inhibits protein synthesis (50S ribosome)
Active against Gram +
H pylori, M. avium, chlamydia urtheritis/cervicitis
Allergic to penicillin: azithromycin is substitute
Metabolism: liver
Excretion: bile duct/kidney
AE: nausea, vomiting, diarrhoea
Doxycycline
Class: Tetracycline antibiotic
MOA: inhibit protein synthesis (30S subunit)
Acne, brucellosis, ricketssia
prophylaxis: P. falciparum malaria
Chlamydia (although azithromycin better)
Metabolism: not researched (hm)
AE: teeth discolouration, photosensitivity, n and v, AVOID IN PREG
Gentamicin
an Aminoglycoside covering most gram negative and gram positive Staphs
MoA - interferes with bacterial protein synthesis (binds to 30S ribosomal unit)
AEs - OTOTOXIC!; NEPHROTOXIC
amikacin (just brief overview)
Cotrimoxazole
Sulfonamide Derivative
MoA - both interfere with bacterial folic acid synthesis
its a nasty drug - minimal use outside of HIV (toxo, PCP, isospora) due to toxicity
AE’s - SJS, maculopapular rash, bone marrow suppression, diarrhoea
Electrolytes (inc. K; inc. Na; hypoglycaemia)
Vancomycin
Moxifloxacin
levofloxacin
ciprofloxacin
Warfarin
Unfractionated heparin
A unpredictable heparin but is forgivable
MoA - enhances action of ATT 3
Choice of drug in a pt with high risk of bleeding but not bleeding yet, because you can adjust quick and monitor them
Has antidote - protamine sulphate
Monitor important, monitor until PTT is normal range
Low molecular weight heparin
Aspirin
Class: NSAID, non-selective COX-inhibitor, salicylate
MOA: inhibits thromboxane and prostaglandin synthesis by inhibiting COX enzyme pathway IRREVERSIBLY
LOW DOSE- inhibits thromboxane synthesis only therefore useful in strokes, high dose inhibits both thromboxane and Prostaglandin synthesis (this makes low dose aspirin useful in stroke and MI over other NSAIDs
effectively: antiplatelet, anti-inflam, analgesic
Metabolism: liver
Excretion: kidney
AE: GIT ulcers (inhibits COX-1), BLEEDING
Hypersensitivity: multiple subtypes involving angioedema, urticaria, anaphylaxis, exacerbated respiratory disease, cutaneous disease
Chronic use: nephropathy
CI: malaria, heart failure, kidney failure, asthma
Clopidogrel
Drug class: Antiplatelet, antithrombotic
MOA: prevents aggregation of platelets (ADP binding to P2Y12 receptor)
Metabolism: liver, CYP450
AE: Bleeding
Hypersensitivity: angioedema, urticaria, macpap rash, DRESS
TTP
Contraindications: active bleeding, confirmed hypersensitivity, severe hepatic impairment
alteplase
Class: antithrombotic, tissue plasminogen activator
MOA: activates plasminogen to plasmin, leads to dissolution fibrin clot
Indications: fibrinolytic for acute MI, pulmonary embolism, ischaemic stroke
Metabolism: liver
AE: haemorrhage
CIs: hypersensitivity, gentamicin hypersensitivity, anticoagulant therapy, major surgery previous 3 mnths, HIGH RISK HAEMORRHAGE
drug interactions with coagulation inhibitors: ACE-i, heparin etc
contraindications to aspirin use
- known hypersensitivity
- asthma
- rhinitis
- nasal polyps
- children/teenagers: REYE’s syndrome
Furosemide
Loop diuretic
MoA: inhibits the Na, K, 2 x Cl transporter in the ascending loop
AE’s: OTOTOXICITY, dehydration, metabolic alkalosis, Electrolyte disturbances, sulfa group so Type 2 hypersensitivity
NB: CAN BE USED IN RENAL FAILURE, increase dose in fact, dont use in osteoporosis (causes hypocalcaemia)
Hydrocholothiazide
Thiazide diuretic
MoA: Inhibits the Na Cl pump in the DCT
AE’s - HYPERURICAEMIA AND GOUT, Electrolyte disturbances, hypercalcemia, in high dose = glucose intolerance
Enalapril
Class, MoA, CIs, AE, special considerations
ACE inhibitor
MoA - use brain im not typing it
CI’s - Renal artery stenosis, pregnancy, prev. angioedema, aortic stenosis
AE’s - Hyperkalaemia (decreases aldosterone therefore more K); Hypotension on first dose, drops GFR (watch renal fx and K)
Special considerations: Watch potassium closely, use K sparing diuretic carefully (spiro), watch for angioedema
Spironolactone
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
Carvedilol
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]
Morphine
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)
Tramadol
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
Codeine phosphate
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
Paracetamol
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)
NSAIDs
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
Amitryptilline
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
Carbamazapine
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
COX-1 inhibitors vs COX-2 inhibitors
COX-1: gastric mucosal irritation
eg. indomethacin
COX-2: CVS side effects, but adding aspirin adds gastric mucosa problems
Lopinavir
ARV - protease inhibitor
PK: CYP450 inhibitor (ritonovir)
AE: Inc. in TAGs, inc. cholesterol, diarrhoea