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
Dolutegravir
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
Efavirenz
ARV - NNRTI
Low genetic barrier to resistance
SE’s: Neuropsych SEs, RASH AND HEPATOTOXICITY
PK: CYP450 metabolised - it is an INDUCER!
Nevirapine
ARV - NNRTI
PK : CYP450 inducer!
AE: Rash and Hepatoxicity (WORSE than efavirenz)
Low genetic resistance barrier
Tenofovir
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
Fluconazole
Antifungal
MoA - inhibits fungal CPY450 and therefore STOPS FUNGAL CELL WALL SYN.
PK: Renally excreted - needs DOSE ADJUSTMENT
Inhibits CYP450!!!!
AE: Hepatotoxic, Neurotoxic
Lamivudine
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
Pyrazinamide
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
Amphoterrible B
whoops sorry Amphotericin B
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
Isoniazid
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)
Ethambutol
Anti-TB
MoA - Bacteriostatic, inhibits cell wall synthesis
PK - renal elimination
AE - UVEITIS!!!! (cant give in < 8y/o)
Rash
Hyperuricaemia
peripheral neuropathy
NO DILI!
Rifampicin
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
Ethanol
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
Methamphetamines
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)
Cocaine
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
Cannabis
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)
Heroin
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)
Benzodiazepines
Sulfonylurea
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
Medical management alcohol withdrawal
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)
Medical management alcohol withdrawal
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)
4 drugs contraindicated for malaria
- Mannitol
- Corticosteroids
- Heparin
- Aspirin/NSAIDs (renal impairment)
Quinine
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
Artesunate
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)
artemether lumefantrine
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
P.ovale and P. vivax
Latent phase, need to add Primaquine (everyday for 14 days, NOT IN PREGNANCY)
malaria prophylaxis
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.
contraindications to mefloquine
epilepsy
psych
arrhythmias
infant less than 5kg
contraindications to doxycycline
Pregnancy. Children
under eight
years of age.
Caution in travellers
with myasthenia
gravis.
contraindications for atovaquone-proguanil
renal impairment
pregnancy; lack of data though
how to treat status epilepticus
- 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
Carbamazapine
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?
which 3 anticonvulsant drugs have similar structure and are cross-reactive with risk of hypersens reaction
Phenos and carbamazapine
Phenobarb
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
diabetogenic drugs
- Glucocorticoids
- Thiazide diuretics
- Atypical antipsychotics
- ARVs (Protease inhibitors)
- I need to check this but tacrolimus?
Intermediate acting insulin
Protophane or Humulin N
once or twice dly/ usually @ night not after 10pm
takes 2-4 hrs to work, lasts 16-24 hrs
short acting insulin
actrapid
works within 30 min, take 30 min before meal
stops working after 2-4 hrs
Biphasic insulin
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
what is preferred insulin regimen
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
initial total daily insulin dose
0.6 units/kg body weight
Insulin
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
Metformin
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
which antimalarial drug is only used for prophylaxis and not treatment?
Mefloquine (neuropsych)
rapid acting insulin
Novolog, apidra, Humalog
prescribing tips in renal failure
beware ace-inhibitors and spironolactone because they can cause hyperK+
Other drugs affected by renal failure:
Erythropoietin-renal failure and anaemia
Activated Vit D
prescribing tips hepatic failure
beware propanolol: drug with extensive first pass metabolism
rather chose drugs that are metabolised via conjugation instead of CYP450
which drugs to avoid in elderly
be aware: GFR slows down and so does hepatic metabolism (opposite of pregnancy)
- anticonvulsants
- hypnotics
- morphine
- NSAIDs
- Warfarin
examples of arbs
losartan
anything sartan basically
remember know benefits of bradykinin such as renal vasodilation
which drugs cause anterograde amnesia
any drugs that help you to relax
eg. diazepam, midazolam
alcohol
how does phenytoin toxicity present
SEIZURES
ataxia, nystagmus, slurred speech
unfractionated heparin
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
low molecular weight heparin
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
Warfarin
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
adverse effects heparin
NB just to remember that heparins do not thrombolyse, they just prevent further formation if clot
Bleeding
Osteoporosis
Alopecia
Thrombosis
Heparin induced thrombocyopaenia
