Page 1

Class of Drug

Name

Acetylcholine Bethanecol Directly Acting Cholinomimetics Pilocarpine

Pharmacokinetics Degraded by Achesterase and recycled t½=3-4hrs limited access to brain t½=3-4hrs not Ach-esterase substrate

Physostigmine Indirectly acting Cholinomimetics Anticholinesterase

Neostigmine

t½=30mins ANS>NMJ

Ecothiopate (organophosphorous compounds) Trimetaphan

IV

Hexamethonium

Cholinoceptor Antagonists

Neuromuscular blocking drugs (nondepolarising)

MOA

Clinical Use

Stimulates muscarinic and nicotinic receptors

None – stimulates all autonomic ganglia

Muscarinic agonist, especially M3(glands)

↑Bladder emptying + GI motility

Muscarinic partial agonist

Glaucoma (local admin)

Reversible AChE inhibitor. Block active site with carbamyl group. Reactivated by hydrolysis

Glaucoma (local), Atropine poisoning

Irreversible AChE inhibitor. Phosphorylates enzyme (stable)

Glaucoma (local)

Nicotinic ion channel blockers (incomplete, use dependent) [Ganglion Blocking]

Atropine

I.V. after MI

Muscarinic antagonist

Hyoscine (Anti-emetic)

Transdermal patch, oral, I.V.

Muscarinic antagonist. Acts at vestibular nucleus, NST, vomiting centre.

Tropicamide Ipratropium bromide

Local

Muscarinic antagonist

Inhalation

Muscarinic antagonist

I.V. (↑ charged) doesn’t cross BBB/ placenta. Not metabolised. Excreted 70% urine, 30% bile.

Competitive AChR antagonist at NMJ. 70-80% block necessary. Graded block – greater block further away from endplate.

Tubocurarine

Myasthenia gravis

Major Effects

Pupil constriction aids fluid drainage Low: ↑Muscarinic effects Moderate: ↑ANS SLUDGE BBB

[Insecticides] To induce hypotension during surgery Anti-hypertensive (not in use) Parkinson’s disease, IBS, MI (↓motility+secretions) Anaesthetic premedication, prevents motion sickness (not during) Examination of retina Asthma, obstructive airway disease Relaxation of skeletal muscle during surgery. ↓ need for anaesthetic and permits artificial ventilation.

Hypotension, vasodilation, ↓Renin secretion. Cholinergic balance in basal ganglia Sedation at mild doses, bronchodilation Pupil dilation Bronchodilation Flaccid paralysis – eye muscles, face, limbs, diaphragm

Side Effects

ST 1

General Muscarinic: Salivation, ↑bronchial + GI secretions, blurred vision, sweating, hypotension, bradycardia. General Muscarinic Higher doses - ↑all ANS, depolarising block Excitation, convulsions, unconsciousness, resp depression, death. Antidote: Pralidoxin BBB ↓↓ ANS function. Death due to targeting skeletal muscle. ↓ Secretions, pupil dilation, ↓GI tone, bronchodilation Mild doses – agitation, ↓sweating, ↓secretions, Cylopegia, CNS disturbance, drowsiness, mydriasis, constipation at high doses Poisoning: Hyperactivity -> CNS depression. Hot, Dry, Blind, Mad: Treat with anticholinesterase Hypotension (↓TPR, histamine release), reflex tachycardia, bronchospasm, excessive secretions, apnoea – must assist respiration. Can be reversed by anti AChE


Class of Drug

Name

(nondepolarising)

Atracurium

Depolarising Neuromuscular Blockers

SNS Agonists (sympathomimetics) Direct

MOA

Clinical Use

See above

See above

AChR agonist. 2 ACh molecules. Steady influx of Na+ means inactivation remains closed, as potential cannot fall below threshold.

Brief procedures – tracheal intubation, dislocations.

Adrenaline

I.V., I.M., local Poor oral absorption. DOA – mins – quickly degraded

Non-selective (α<β)

Anaphylactic shock, COPD, heart block management, spinal anaesthesia, prolong DOA of local anaesthesia, glaucoma

Phenylephrine

Resistant to COMT, not MAO. Usually local admin

Selective α1 agonist

Vasoconstrictor, mydriatic, nasal decongestant

Clonidine

Oral, I.V.

Selective α2 agonist ↓Sympathetic tone by presynaptic NA inhibition

Hypertension, migraine

Isoprenaline

Resistant to Uptake 1 and MAO. t½=2hrs I.V.

Suxamethonium

Dobutamine

Salbutamol SNS Agonists (sympathomimetics) Indirect

Tyramine

Pharmacokinetics Duration – 15-60m Spon Decompose Not broken down by AChE. Hydrolysed by Pseudocholinesterases. DOA – 3-7mins

t½=2min, rapid COMT degradation. I.V. Resistant to COMT, MAO, Uptake 1. I.V., oral, inhalation In cheese, wine, soy sauce. Extensive 1st pass metabolism, short half life. No BBB

Selective β1+β2 agonist

Selective β1 agonist

Selective β2 agonist Weak non-selective agonist Competitive Uptake1 inhibitor MAO Competitor. Displaces NA from vesicles into cytosol causing NA leak from cell.

Heart block, cardiogeneic shock, acute heart failure, MI (No longer for asthma) Heart block, cardiogeneic shock, acute heart failure, MI Asthma Threatened uncomplicated premature labour -

Major Effects

Side Effects

ST 2

Histamine: Bronchospasm, Excessive Secretion + HypoT

Flaccid paralysis

Bronchodilation, suppression of mediators, ↑HR + contractility, ↑TPR, vasoconstriction Pupil dilation, restricts blood to prevent mucus production ↓Sympathetic outflow from brainstem

Muscle pain, loss of K+, bradycardia Secretions: ↓ mucus, thicker CVS: cold extremities tachycardia, palpitations, arrhythmias,  stroke & pulmonary oedema Muscle: Tremor CVS effects

Reflex tachycardia, dysrhythmias No reflex tachycardia Bronchodilation, inhibition of mediators

Reflex tachycardia, tremor. Caution in cardiac patients, hyperthyroidism and diabetics

-

Hypertensive crisis “Cheese Reaction” when taking MOA inhibiting drugs


Class of Drug

Indirect sympathomimetic, Drug of abuse, Local Anaesthetic

Name

Pharmacokinetics

Cocaine

Smoked – absorbed quickly, slow orally, nasally. Well absorbed. Readily crosses BBB. Degraded by plasma + hepatic esterases. 90% protein bound t½=30mins. Excreted in urine.

Propranolol Atenolol SNS Antagonists

Not for Asthmatics

Labetolol

Drugs affecting rennin – angiotensin – aldosterone system Calcium

Prevents re-uptake of Dopamine in NAcc. Blocks voltage gated Na+ channels.

β1 antagonist β1+α1 antagonist α1+α2 antagonist

Prazosin Doxazosin

Methyldopa

Uptake 1 inhibitor. Prevents NA reuptake therefore ↑ Synaptic Activity

β1+β2 antagonist

Phentolamine

False Transmitters

MOA

Not degraded by MAO. Doesn’t cross placenta

Hypertension, Arrhythmias, Angina, Glaucoma Not used

Taken up by NA neurones, forms false transmitter. Less active on α1, more active on α2. Accumulates in neurone.

Hypertension (in pregnancy)

Losartan

Non-competitive antagonist of Angiotensin 1 receptors. Phenylakylamine

Anxiety

Inhibits Enzyme (Renin) Inhibit opening of L-type

Hypertension, heart failure, post-MI, diabetic nephropathy, renal insufficiency. Hypertension. Patients with heart failure that cannot tolerate ACEIs Experimental Angina, Hypertension,

Side Effects

ST 3

Euphoria, excitement, ↑motor activity, tachycardia, vasoconstriction, ↑BP, HR, platelet activation, tremors, convulsions, resp depression (medullary centres), death

Do not co-administer with Adrenaline

Hypertension

Inhibit ACE, prevent conversion of angiotensin I to angiotensin II

Major Effects

Local anaesthetic in ophthalmology.

α1 antagonist

Enalapril, Captopril

Aliskiren Verapamil

Clinical Use

↓CO, + BP during exercise ↓CO, effect on airways only in high doses ↓TPR, no change in CO ↓BP, TPR, reflex ↑CO/HR

Bronchoconstriction, Cardiac Failure, Hypoglycaemia Fatigue, Cold Extremities, Bad Dreams ↑ NA release due to α2 blockade, reflex tachycardia, ↑ GI motility, diarrhoea

↓BP/, ↓CO, VD dramatic hypotension, ↓LDL and ↑HDL Renal blood flow well maintained – good in renal failure.

Dry mouth, postural hypotension, sexual dysfunction, sedation Hepatitis-like damage.

Prevent vasoconstriction →↓TPR→↓BP

Hypotension, dry cough, angioedema, hyperkalaemia, renal failure

Postural hypotension

Less extensive than ACE inhibitors ↓ HR (AV) and

AV block, bradycardia, heart


Class of Drug

channel Antagonists

Βeta-Blocker

Name

Pharmacokinetics

MOA

Diltiazem

Benzothiazepine

calcium channels. Causes arterial vasodilatation

Amlodipine

Dihydropyridines

Atenolol Glyceryl Trinitrate

Organic Nitrates

Nicorandil Isosorbide Mononitrate Adenosine Amiodarone Dronedarone

Anti-arrhythmics

st

No longer 1 line Hypertensive Extensive 1st pass metabolism. t½=30mins, sublingual, oral. Latter 2 longer transdermally. t½ = 20-30s I.V. t½ = 10-100days D: Less toxic but less effective

Ivabradine

α-blockers + sympatholytics

SVT, atrial fibrillation

contractility.

failure, constipation

Angina, Hypertension Hypertension

↓ cardiac workload

Flushing, headaches, hypotension, ankle oedema

Angina, Cardiac dysrhthmias, HF, Thyrotoxicosis, Glaucoma, Mirgane

-ve Chronotropic & inotropic Control/Correct Dysrhythmia

Bronchoconstriction, heart block, bradycardia, fatigue, cold extremities, nightmares, hypoglycaemia in diabetics

Angina

Improve myocardial oxygen demand

Hypotension, headache, flushing, Tolerance – Eccentric dosing. Chest pain, SoB, dizziness, nausea. Accumulates in skin, lungs, thyroid. Photosensitive skin rash, pulmonary fibrosis. Amiodarone and verapamil ↓digoxin excretion and tissue binding. Immune antibody available for toxicity. AV block and ectopic pacemaker.

Release NO→venodilation ↓venous return. Weak antiplatelet, coronary artery VD Opens K+ channels→ arterial dilation. Also NO donor. Acts on A1 receptors to slow conduction through AV node

Terminate SVT, safer than verapamil

Complex ion channel blocker

SVTs and ventricular tachyarrhythmias.

t½=40hrs

Atrial fibrillation, relief of symptoms in heart failure.

↓Ventricular rate, ↑contractility. Slows conduction through AVn

CI: post-MI, sick sinus syndrome; cardiogenic shock;

Blocks If channel – Na/K channel in sinoatrial node

Angina (w/ normal sinus rhythm)

Slows HR

Dobutamine Cardiac Intropes

Major Effects

Inhibit Na+/K+ pump. ↑intracellular Na+ →↑Ca2+ via Na+/Ca Exchange → +ve inotropic effect. Central Vagal Stimulation -> -ve chronotropic

Digoxin (Cardiac Glycosides)

β1 Antagonist

Clinical Use

Milrinone Doxazosin Prazosin Phenoxybenzamine

β1 selective agonist Phosphodiesterase Inhibitor: Prevents cGMP breakdown

Positive Inotroic: ↑ Force of Contractions

Competitive α1 antagonist

Postural Hypotension

Irreversible α1 antagonist

Pheochromocytoma (w/ β-blockers)

Side Effects

ST 4

Bradycardia, 1 degree Heart block, Ventricular & SVA Decrease chronic heart failure survival rate

Tachycardia


Class of Drug

Name

Centrally Acting Sympatholytics

Clonidine Mononidine

Vasoconstrictor

Sumitriptan

Cannabis

Drugs of abuse

Cocaine

Nicotine

Disulfiram

Pharmacokinetics

MOA α2 adrenceptor agonist Imadazoline agonist 5HT1D agonist. Vasoconstriction of large arteries, inhibits trigeminal nerve transmission.

Inhalation 50% Oral 10-15% ↑½2hr duration t½=7days (remains in fat tissues). Metabolised in liver – active metabolite 11-hydroxy-THC. Enterohepatic cycling. 25% urine, 65% Bile IV. Oral. Nasal. Inhalation t½=20-90min Plasma/Liver Choliensterase Inhalation 20% absorbed. Distributes rapidly in tissues. Elimination t½=23hrs. Metabolised in liver to cotinine.

Endogenous cannabinoid receptors (hippocampus, cerebellum, cortex, basal ganglia CB1, immune cells CB2). Anandamide is endogenous agonist. Inhibit GABA interneurones in VTA → disinhibition of dopaminergic projection.

Clinical Use

Major Effects

Hypertension

↓ Sym outflow from Brain

Ecgonine Methyl Ester, Benzoylecgonine Inhibits reuptake of dopamine in NAcc Nicotinic receptor agonist. Sympathetic activation via peripheral receptors or directly on brain. Binds to nicotinic receptors on dendrites of VTA neurones →↑ firing rate.

-

Acetaldehyde dehydrogenase inhibitor. Causes build up of acetaldehyde.

Aversion therapy for recovering alcoholics.

ST 5

Coronary vasoconstriction – do not use in patients with coronary disease.

Migraine Attacks

Abuse

Side Effects

Effects on perception, depression of cognition, slow reaction times, defects in short term memory, ↑ satiety, motor incoordination

Tachycardia, vasodilation → reddening conjunctivae, postural hypotension and fainting, immunosuppressant, respiratory effects (tar, carcinogens), psychosis due to loss of anterior cingulated cortex → loss of inhibition and more primitive actions

VC, ↑ Sym, ↑ Euphoria/Disphoria, HR, ↓ Cerebral Heightened Energy, Blood flow + Insomnia, Restlessness, hyper-pyrexia in Talkative, Violence, Anorexia CNS -> Epilsepy CVS: ↑Sym : ↑ HR, BP, SV, vasoconstriction, blood coagulation, LDL, VLDL, FFA, risk of atherosclerosis, MI, CVD, stroke. ↓ oxygen carrying capacity HDL Metabolic: ↑metabolic rate, ACTH, cortisol, ↓appetite Neurological: ↓risk of Parkinson’s & Alzheimer’s Acetaldehyde build up: None when alcohol not flushing, present. tachycardia, panic, distress.


Class of Drug

Drugs of abuse

Name

Alcohol

Warfarin

Anticoagulants

Heparin LMWH

Aspirin (also NSAID) Antiplatelet agents

Clopidogrel

Abciximab

Pharmacokinetics

MOA

Oral. 20% stomach, 80% SI. Substantial 1stPM – saturation kinetics. 90% metabolised, 10% excreted unchanged by lungs. 85% metabolised in liver, 15% Gut Oral, absorbed quickly. Delayed Effect for 12-16hrs. t½=4-5days. 99.99% Plasma protein bound, hepatic metabolism by CYP450. Poor oral absorption. Given S.C./ I.V. short t½. Saturation kinetics. LMWH has longer t½ and no saturation kinetics.

↑ GABA mediated inhibition (sedative effects) Inhibition on Ca2+ entry → ↓ NT release. Inhibition of NMDA receptor function (memory loss?) Major action on cortex, RAS, corpus callosum, hypothalamus, hippocampus, cerebellum, basal ganglia.

Oral, highly plasma protein bound Oral. Peak plasma conc at 4hrs, effect delayed 4 days. I.V. Binds rapidly to platelets and cleared with platelets. t½=24-48hrs.

Inhibits the activation of vitamin K → Prevents synthesis of clotting factors II, VII, IX, X.

Clinical Use

Major Effects

Antagonist of GpIIb/IIIa receptor (monoclonal antibody)

ST 6

CNS: Depressant, ↓sensory function, concentration, motor function, reaction time, coordination. ↑confidence, euphoria, memory loss. Coma, resp failure. Dementia, degeneration of cerebellum, neuropathy, myopathy, Wernicke-Korsakoff syndrome. CVS: Vasodilation, flushing, ↓Ca2+ entry, ↑prostaglandins, ↓thrombosis risk/ heart disease - ↑HDL, ↓plaque formation, ↓thromboxane, ↓platelet aggregation. Chronic Liver: Fatty Liver -> Hepatitis -> Cirrhosis. Oesophageal Varice. Endo: ↑ACTH, ↓Testosterone -> Feminisation. Foetal Development. Haemorrhage, teratogenicity. Drug interactions with: Prevention/ treatment • Drugs inhibiting/ of DVT, PE, prevent inducing CYP450 clotting during Anticoagulant • Drugs which displace haemodialysis/ bypass warfarin from albumin surgery. • Drugs inhibiting platelet function

Activated antithrombin III which inhibits factor Xa and thrombin by active serine binding. LMWH has less action on thrombin Irreversible COX-1 (and slight COX-2) inhibitor. Acetylates active site. Prevents TXA2 and PGE2 production. Pro-drug inhibits fibrinogen binding to GpIIb/IIIa receptors.

Side Effects

Bleeding, thrombocytopenia, osteoporosis, hypersensitivity. Reversal by protamine I.V., binds to give inactive complex. Prevention of high risk cardiovascular patients. Analgesic, antipyretic, anti-inflammatory Aspirin sensitive patients Acute Coronary Syndromes, with heparin and aspirin to prevent ischaemia in unstable angina.

Analgesic, antipyretic, antiinflammatory, antiplatelet. Prevents platelet aggregation

GI sensitivity (ulceration, bleeding, perforation). ↓Creatinine clearance, ↑bleeding time, BronchoC Bleeding, GI haemorrhage, diarrhoea, rash, rarely neutropenia. Bleeding, immunogenic.


Class of Drug

Name Streptokinase

Fibrinolytics Alteplase

Statins

Fibrate Misc

Simvastatin Pravastatin Benzafibrate Gemfibrozil Nicotinic Acid Ezetimibe

Diuretics Mannitol Acetazolamine

Frusemide (Loop diuretic)

Bendrofluazide (Thiazide) Amiloride (Potassium Sparing Diuretics)

Pharmacokinetics

MOA

Clinical Use

Major Effects

Binds to plasminogen and Acute MI - ↓mortality activates - conformational I.V. 30-60 min (additive with aspirin), Recombinant tPA – works infusion acute thrombotic stroke Break down clot better on plasminogen bound (3hrs), DVT, PE arterial to fibrin than soluble → clot t½=12-18mins thromboembolism sensitive. Activates Plasmin HMG-CoA reductase Patients with high inhibitors. ↓cholesterol ↓Total cholesterol, blood Oral production in the liver. ↑ LDL cholesterol, pressure, diabetes or receptors on hepatocytes → LDL, TGs. ↑HDL MI. ↓ LDL in blood. Ligand for PPAR-α -> ↓10% LDL ↑10% First Line for high TG ↑lipoprotein lipase activity HDL ↓30%TG ↓VLDL release -> ↓ 30-50% TG. ↓ 10-20% Cholesterol + ↑HDL Glucuronidation Inhibits cholesterol Combination Therapy Activiated absorption Pharmacologically inert. Filtered by glomerulus, not Prevent acute renal reabsorbed. ↑osmolarity of tubular fluid →↓water failure (given in clinical ↑Urine volume reabsorption setting due to ↑osmol) Inhibit intra+extracellular carbonic anhydrase. ↓ Used in glaucoma, ↑Urine volume, HCO3 reabsorption →Na++H2O reabsorption ↓.↑Na+ metabolic alkalosis, & and ↑K+,Na+ and delivery to DCT→↑K+ loss. renal stones. HCO3 excretion. Acute pulmonary Inhibitor of Na+/2Cl-/K+ pump. ↑ Urine Oral, onset 1hr, oedema, oedema due (Triple Transporter in Asc volume~15DOA 4-6hrs. to heart failure, renal or Limb). Dilutes interstitium 30%, ↑Na+, K+, Tubular secretion, hepatic disease. →↓concentrating power of Cl-, Ca2+, Mg2+ ~50% metabolised. Hypercalcaemia/ collecting duct. excretion. hyperkalaemia. Inhibitors of Na+/Cl- pump at Congestive heart ↑Urine volume Oral, onset 1-2hrs, DCT, →↑Na+ delivery to failure, hypertension, 5-10%. DOA 8-12hrs. collecting duct →↓water nephrogenic diabetes ↑Na+,K+,Cl-,Mg2+ Tubular secretion. reabsorption. ↑K+ loss due to insipidus!?, severe excretion. ↓Ca2+ + compensation for Na resistant oedema. excretion. + + + Poor orally. Onset Blocks Na channel in Na /K With other diuretics to ↑urine vol 5%. 6hrs. DOA 24hrs. exchange mechanism. ↑Na+ prevent K+ loss ↑Na+,H+, uric + Excreted and ↓K loss. acid loss. unchanged.

Side Effects

ST 7

Bleeding, GI haemorrhage, stroke. Allergy Bleeding, GI haemorrhage, stroke. Not antigenic RARE: Myalgia, muscle cramps, myopathy, rhabdomyolysis, acute renal failure Not for Pregenant Women. A number of UE Electrolyte imbalance (hypernatraemia: nausea, vomiting, Pul Oe) ↑ECF vol K+ loss, metabolic acidosis. Metabolic alkalosis, hypovolaemia, hypotension, hypokalaemia. K+ loss, diabetes mellitus (interferes with insulin secretion), metabolic alkalosis. Hyperkalaemia, metabolic acidosis.


Class of Drug

Anti-emetics (see also antimuscarinics: Hyoscine)

Gastric and duodenal ulcers

Name

Pharmacokinetics

MOA

Clinical Use

Major Effects

Spironolactone

Oral, onset/DOA – days. Filtered by glomerulus.

Aldosterone antagonist. Blocks Na+/K+ exchanger in DCT. ↑K+ retention.

↑urine vol 5%. ↑Na+,H+, uric acid loss.

Hyperkalaemia, gynaecomastia, menstrual disorders, testicular atrophy.

Promethazine

Oral. Onset in 12hrs, peak effect 4hrs, DOA 24hrs.

Competitive antagonist of H1>muscarinic>D2 receptors. Acts centrally at NST, vestibular nucleus and vomiting centres

Heart failure, hypertension to prevent K+ loss with diuretics. Motion sickness, normally prophylactically. Disorders of labyrinth, morning sickness, pre-/post-operatively.

Also relief of allergic symptoms, anaphylaxis, night sedation.

Dizziness, tinnitus, fatigue, sedation (excitation in excess), convulsions, general anti-muscarinic.

Metoclopramid e

Oral, rapid absorption, Extensive 1stPM. I.V. Crosses BBB and placenta.

Dopamine receptor antagonist (D2>>H1>>M). Acts centrally at CTZ.

Nausea & vomiting associated with toxins, e.g. uraemia, radiation sickness, GI disorders, chemotherapy.

↑ GI motility and gastric emptying.

Drowsiness, dizziness, extrapyrimidal reactions (children – Parkinsonian-like) Hyperprolactinaemia. anxiety, ↓bioavailability when co-administered.

Ondansetron

Oral, well absorbed, excreted in urine.

5HT3 receptor antagonist. Blocks visceral afferents and CTZ.

Chemotherapy (cisplatin), radiation sickness and postoperatively.

Prevents nausea & vomiting associated with toxins and pain

Headache, flushing and warmth, constipation.

Oral. DOA 23days. Enteric coated for slow release. Oral, well absorbed.

Targets anaerobic bacteria and protozoa Broad spectrum Inhibits bacterial tRNA translocation Irreversible inhibitor of H+/K+ pump. Weak base that accumulates in canaliculi and is activated by acid. Histamine receptor antagonists

Antibiotics e.g. Metronidazole Amoxycillin Clarithromycin

Gastric and duodenal ulcers: PPIs H2 antagonists Gastric and duodenal ulcers: Cytoprotective drugs

Omeprazole Cimetidine Ranitidine Bismuth chelate Sucralfate Misoprostal

Strong negative charge in low pH. Binds to positive charge groups to form gel-like complex. Limits H+ and pepsin getting to ulcer. PG agonist (analogue of PGE1)

Triple therapy for ulcers, GORD.

↓acid secretion by 90%

Triple therapy for ulcers, GORD

↓acid secretion by 60% ↑PGs, mucus, HCO3 secretion. ↓ Helicobacter pylori Maintains mucus barrier, ↓acid secretion

Co-prescribed with oral NSAIDs

ST 8

Metronidazole interferes with alcohol metabolism

Elimination of Helicobacter pylori as part of triple therapy.

Triple therapy, resistant cases

Side Effects

Rare Rare. Likely relapse after withdrawal. CYP450 inhibitor Constipation ↓Absorption of drugs and nutrients Diarrhoea, abdominal cramps, uterine contractions. Do not give in pregnancy


Class of Drug

Name

Ant-Acids

Ant-Acids Al3+ & Mg2+

Respiratory Drugs (Salbutamol & ipratropium)

Pharmacokinetics

Aminophylline

Oral, I.V.

Salmeterol

Long-acting 12hrs Powder Inhalation

Ibuprofen

Oral

NSAIDs (Aspirin) Celecoxib

Other analgesic

Paracetamol

Opiates Morphine

Codeine Heroin

Oral. Conjugated with glutathione in liver.

Oral 40-50% absorption~30mins Metabolised in liver, excret urine. Oral. 5-10% converted to morphine in liver. Oral 50-100% absorption, I.V. Metabolised by plasma esterases. Excreted in urine.

MOA

Clinical Use

Neutralises acid, ↑ gastric pH, ↓ Pepsin activity Phosphodiesterase inhibitor. Prevents breakdown on cAMP → prolonged smooth muscle relaxation.

Non-ulcer dyspepsia Reduce duodenal ulcer Asthma

Relaxation of airway smooth muscle.

β2 receptor agonist

Asthma. COPD

Longer than Salbutamol

Reversible COX-1 and COX2 inhibitor.

Analgesic, antiinflammatory, antipyretic

Selective reversible COX-2 inhibitor →↓ risk of ulceration (can still inhibit HCL secretion with COX-1)

Patients at high risk of GI side effects, and asthmatics. Those taking NSAIDs longterm.

Not fully known. Restricted to nervous tissue. May inhibit COX during conversion (peroxidation) of PGG2 to PGH2 Bind to μ, κ, δ G-protein receptors. ↑K+ loss & ↓Ca2+ entry. • Analgesia: μ, κ receptors in dorsal horn of spinal cord, ↓pain perception. μ, κ receptors on PAG (actually inhibit GABA interneurones) , ↑ pain tolerance. μ, δ receptors in NRPG to↑ pain tolerance.

Major Effects

Side Effects

ST 9

GI sensitivity (ulceration, bleeding, perforation). ↓Creatinine clearance, bronchoconstriction (lower incidence than aspirin) Antiinflammatory

Mild-moderate pain relief

Analgesic, antipyretic

Pain relief, anti-tussive

Analgesic

Euphoria

More lipid soluble → brain faster. Quickly metabolised → more addictive

↑ Risk cardiovascular events and MI. glutathione depletion → build up of N-acetyl-pbenzoquinoneimine → oxidation of hepatic enzymes → liver failure. Treat with acetylcysteine or oral methionine (oxidises their thiol groups instead) • Respiratory depression • nausea and vomiting • ↓ GI motility • pupil constriction • histamine release (itching, urticaria, rarely hypotension) • Dependence and withdrawal


Class of Drug

Opioid antagonists IBD Glucocorticoids

Name

Pharmacokinetics

Fentanyl

Oral, buccal, intranasal, dermal, 50-100% absorption. Metabolised in liver – oxidation. Excreted in urine.

Methadone

t½=24hrs

Naloxone

I.V. high dose, short acting

Prednisolone Fluticasone Budesonide Sulfasalazine

IBD Aminosalicylates

IBD Immunosuppressants

Mesalazine Olsalazine Azathioprine

Tapered dose Topical admin – fluid or foam enemas (high 1stPM) Suppositories, enemas, pH dependent release capsules (SI), slow release microsphere (small and large bowel) Pro-drug, activated by flora. Metabolised by Xanthine oxidase

MOA

Clinical Use

Major Effects

Side Effects

ST 10

Very lipid soluble. Oxidised metabolites may be active

• Euphoria: μ receptors inhibit GABA neurones in VTA →↑ Dopamine in NAcc • Cough: inhibit cough centre, and afferents from larynx • Resp depression: μ2 receptors inhibit central chemoreceptors in medulla Opioid receptor antagonist Intracellular GC receptor agonist. Positive TFs for antiinflammatory proteins or negative TFs for inflammatory proteins. ↓influx inflammatory cells. ↓antigen presentation, cell proliferation ↓Eicosanoids, free radicals, cytokines, leukocyte infiltration. Broken down to sulfapyridine and 5-ASA by gut flora. 5-ASA molecule alone 2 5-ASA molecules linked Active component is purine analogue →interferes with DNA synth →prevents cell division. Enhances T-cell apoptosis

Wean heroin addicts

Most lipid soluble → dissipates into fat very quickly.

Treatment of opiate overdose Reduces need for surgery. Treats severe active disease

Precipitates withdrawal symptoms ↓ vasodilation, swelling, cell recruitment + tissue damage

Osteoporosis, ↑gastric ulceration, suppression HPA axis, diabetes, hypertension, infection, Cushing’s syndrome Caused by sulfapyridine

Maintenance of remission (no immunosuppressive actions) Effective in UC, not Crohn’s

Antiinflammatory

Maintenance of remission in Crohn’s. Also somewhat effective in UC

↓Antibody + cell immune responses, infiltration, proliferation

Few Bone marrow suppression. Do not administer with xanthine oxidase inhibitors (allopurinol) → blood disorders


Class of Drug

Name

Infliximab

Pharmacokinetics

MOA

Clinical Use

Major Effects

I.V. (now also S.C.) t½=9days

Monoclonal anti-TNF antibody. ↓activation of TNF receptors, inactivates TNF bound to receptors. Inhibits inflammatory responses downstream

Crohn’s disease – people with refractory disease and fistulae. Most effect in young or colonic CD

↓cytokines, leukocyte infiltration. ↑Tcell apoptosis, complement lysis of TNFexpressing cells

Spinal cord muscle relaxant, Spasmolytic for stroke, MS patients

↓Tone from upper motor neurones

None, used experimentally

Convulsant

GABAA agonist: Clhyperpolarisation -> IPSP GABAB agonist. Mimics presyn action of GABA (Gs proteins) to 1.↓Ca2+ influx and ↓NT release from excitatory neurones 2. ↑K+ conductance -> Hyperpolarisation Competitive GABAA antagonist Competitive GABAB Antagonists

Muscinol GABA related drugs

Baclofen

(Sodium Valporate, VIgabatrin) Bicuculline Phaclofen Saclofen Phenobarbitone

Amobarbital Barbiturates

Thiopentone

t½=20-25hrs

Bind to BARB subunit of GABAA receptor. Enhance GABA linkage between GABA, GABA modulin and BZ subunits. ↑GABA binding to GABA subunit (not reciprocated). At high concs, direct opening of Cl- channel. → ↑Duration of channel openings. Also ↓glutamate transmission

Anti-convulsant Sedative/hypnotic, severe intractable insomnia

General anaesthetic

Non-selective CNS depressant, other membrane effects also

Side Effects

ST 11

↑TB, infections, septicaemia, malignancy, demyelinating disease, heart failure. Can be immunogenic – given with azathioprine. Only in clinical setting due to anaphylaxis

Low margin of safety – resp depression, lethal overdose (alkaline diuresis can be used to↑ excretion), ↓REM sleep →hangover effects. Potentiate other CNS depressants, develop tolerance (pharmacokinetic and tissue), dependence and withdrawal (insomnia, anxiety, tremor, convulsions, death) CYP450 inducers


Class of Drug

Name

Diazepam Benzodiazepine

Temazepam Oxazepam Other hypnotics Other anxiolytics

Chloral Hydrate

Pharmacokinetics Oral, I.V. for status epilepticus. Protein bound. Wide distn. Metabolised in liver. Excreted in urine t½=32hrs. Metabolised to Temazepam t½=8hrs. Metabolised to Oxazepam t½=8hrs. Metabolised in liver to trichloroethanol (active component)

Propanolol

MOA

Bind to BZ subunit of GABAA receptor. Enhance GABA linkage between GABA, GABA modulin and BZ subunits, ↑GABA binding to GABA subunit (reciprocated effect). → ↑Frequency of channel openings

Unknown. May be related to alcohol Improves physical symptoms

Clinical Use

Anti-convulsant, antispastic, anxiolytic (long acting) Wide safety margin. Don’t depress respiration or induce liver enzymes.

“Remove anxiety without impairing mental or physical activity”

Sedatives, hypnotics (short acting)

Reduce mental/physical activity/ induce sleep

Slow onset (days/weeks)

5-HT1A receptor agonist.

Anxiolytic

L-DOPA

Broken down by DD, 95% in periphery

Precursor to dopamine. Dopa-decarboxylase converts to Dopamine in nerve terminal

Treats hypokinesia, rigidity, tremor

Carbidopa

(w/ L-DOPA: Sinamet)

Inhibitor of peripheral DD Peripherally acting Dopamine receptor antagonist

Domperidone Bromocriptine (Pergolide, Ropinerol) Deprenyl (Selegiline) Resagiline

Doesn’t require conversion – used when there are fewer neurones (R – promotes antiapoptosis genes – Early Trials)

Dopamine receptor agonists Selective MAO-B inhibitor. Inhibits breakdown of dopamine only in dopaminergic areas of CNS

Given with L-DOPA to prevent periphery bd Given with L-DOPA to prevent nausea Longer DOA than LDOPA, more sustained, fewer dyskinesias. Given with L-DOPA Early stages of disease, or with LDOPA (↓required dose, ↓side effects)

Side Effects

ST 12

Sedation, confusion, ataxia. Potentiate other CNS depressants. Tissue tolerance occurs. Dependence and withdrawal less intense than BARBs. ↑In plasma if used with other highly protein bound drugs.

Wide margin of safety In hospitals as with children and hypnotic elderly “Stage Fright”: Tachycardia β1, Tremor β2

Buspirone

Antiparkinsonian

Major Effects

↑ Dopamine ↑half life of LDOPA & ↓ UE Prevents CTZ stimulation ↑ Stimulation of Dopamine receptors ↑Dopamine

If overdose -> rousible sleep, give I.V. flumazenil (competitive BZ antagonist) Few Fewer than benzodiazepines (especially sedative ones). Possible future alternative Acute: Nausea and vomiting, hypotension, psychological effects (schizophrenia-like) Chronic: Dyskinesias, on-off effects. ↓ Effectiveness. [[Madopar – L-DOPA + Benserazide]] Confusion, dizziness, nausea, vomiting, hallucinations, constipation, headache, dyskinesias Nausea, vomiting, hypotension, confusion, agitation


Class of Drug

Neuroleptics (typical) Neuroleptics (atypical)

Name

Pharmacokinetics

Entacapone

Peripherally acting

Tolcapone

CNS and peripheral

Phenothiazine Chlorpromazin e Haloperidol Sulpiride Clozapine Nitrous oxide

General Anaesthetics (inhalation)

General Anaesthetics (Intravenous)

Local Anaesthetics (Cocaine)

Halothane Enflurane Etomidate Propofol

Lidocaine

Delayed effect, take weeks to work. Initially ↑dopamine synthesis and receptors. ↓Over time Rapidly eliminated Brain ↔ Blood ↔ Alveoli. All very lipid soluble, so slow into blood, fast into brain Metabolised in liver. No excretion from lungs t½= 2hrs Well absorbed from mucous membranes (any ROA) 70% protein bound. Hepatic dealkylation

MOA

Clinical Use

Major Effects

COMT inhibitors, prevent breakdown of dopamine. COMT in periphery converts L-DOPA→3-0-MD, which compete for same mechanism to cross BBB.

↓Required dose of L-DOPA. More potent than MAO inhibitors

↑Dopamine in CNS.→ ↑bio-availability of L-DOPA

D2 Dopamine-like receptor antagonists. Most block many other receptor types (5-HT) Relatively non-selective between D1 and D2, but high affinity for D4 ↓NMDA (glutamate) receptor function Potentiate GABAA and glycine receptor function. No subunit selectivity. Inhibit nicotinic Ach receptors Bind somewhere on GABAA receptor and ↑activity. More effective on β subunits. β3 in spinal cord→ suppression of reflexes, α5 hippocampus→ amnesia Voltage gated Na+ channel blocker. Weak base, crosses connective tissue into nerve, into neurone. Becomes ionised with proton inside neurone, blocks open Na+ channel to prevent Na+ influx

Schizophrenia. Treat positive but not negative symptoms (due to D1 Dopamine deficit) To maintain anaesthesia (IV Propofol maintained by Enflurane gas) To induce anaesthesia. Suppress coughing, airway excitation. More potent than inhalation anaesthetics Surface anaesthetic, minor surgery, limb surgery, dental surgery, spinal anaesthesia, epidural.

Side Effects

ST 13

Anti-emetic (CTZ), anti-histamine (block H1 receptors), acute dyskinesias - reversible on withdrawal, controlled by anticholinergics Tardive dyskinesias (20-30%) – made worse by withdrawal, only overcome by ↑neuroleptic (months or years of treatment). Incidence ↓with atypical neuroleptics. Hyperprolactinaemia, lactation. Anti-muscarinic Loss of consciousness, Difficult to induce suppression of anaesthesia, less potent than reflex responses I.V. anaesthetics. Amnesia, analgesia Loss of consciousness, suppression of Difficult to control when in the reflex responses bloodstream. Elimination Amnesia, slower than from lungs analgesia ↓Generation and CNS: stimulation, conduction of restlessness, confusion, a.p.s. tremor (paradoxical, may Selective for block inhibitory systems) small, nonCVS: myocardial depression, myelinated vasodilation, ↓BP fibres


Class of Drug

Cytotoxic Drugs 1. Alkylating Agents

2. Antimetabolites

Name

Pharmacokinetics

MOA

Cyclophosphamide (mephalon, chloramibucil)

Pro-drug, hydroxylated by CYP450 -> Phosphoramide Mustard + Acrolein

Carbonium ion is reactive group, bind irreversibly to DNA, RNA, proteins. Main target is N7 of guanine, but most have other targets Folate antagonist. Prevents purine synthesis Pyramidine Analogue – interferes with 2’deoxythymidylate synthesis Purine Analogue Interferes w/ topoisomerase II  Transcription Causes fragmentation of DNA chains. Acts on nondividing cells. Metal chelating Inhibits topoisomerase II, preventing DNA/ RNA synth Bind to tubulin, prevents Spindle Formation. Arrests mitosis at metaphase Inhibits topoisomerase II, preventing DNA synthesis. Inhibits mitochondrial function Inhibits ribonucleotides reductase Causes guanine inter-strand links MAO inhibitor. Inhibits DNA/RNA synthesis and interferes with mitosis at interphase. Alkylates N7 + O6 of Guanaine

Methotrexate Fluorouracil

3. Cytotoxic antibiotics

Azathioprine Actinomycin D (Dactinomycin) Bleomycin

I.V.

Doxorubicin 4. Plant alkaloids

5. Misc

Vincristine [Vinca Alkaloid]

NOT I.T.

Etoposide

[A Podophyllotoxin]

Hydroxyurea Cisplatin

Procarbazine

Activated by CYP450

Clinical Use

Major Effects

Side Effects

ST 14

Intra/inter-chain links interfere with transcription/ replication

Stops cells dividing

Kills cells Cancer, immunosuppressants at lower doses

Stops cells dividing

• Myelotoxicity (↓leukocytes, ↑infections) • ↓healing • ↓growth in children • Sterility • Teratogenicity • Hair loss • Nausea and vomiting.


Class of Drug

Antibacterial Drugs affecting Folate

Name

Pharmacokinetics

Sulphamethoxazole Sulphonamides

Oral, readily absorbed. Peak plasma conc 4-6hrs

Trimethoprim Tetrahydrofolate production inhibitor

Oral, fully absorbed. ↑concs in lungs and kidney. ⅔ each drug protein bound

β-lactam Penicillin Antibacterial affecting Peptidoglycan Synthesis Cephalosporins

Cephalexin (O) Cefuroxine (P) Cefotaxime (P) Tetracyclines

Antibacterial affecting Protein Synethesis

Widely distributed in body fluids. Crosses placenta. Only crosses BBB when meninges inflamed. 90% renal tubular secretion Some oral, most I.M./ I.V. Widely distributed in body fluids. Cross placenta + BBB. Mostly renal tubular secretion Oral (sometimes parenterally). Chelate metal irons → ↓absorption with foods. Enter most body fluids. Excretion from bile (Doxycycline all bile) + renal filtration

MOA Structural analogue of Paminobenzoic acid. Competitive inhibitor of dihydropteroate (enzyme of folic acid synthesis) Folate antagonist. Inhibits dihydrofolate reductase in bacteria (See Methrotrexate – Cancer)

Irreversible inhibitors of a trans-peptidation enzyme that cross-links peptide chains to form peptidoglycan cell wall

β-lactam antibiotic Inhibits transpeptidase

Clinical Use

Major Effects

UTI and Resp TI Synergistic effects Pneumocystis carinii in AIDS patients

Resistance greater than penicillins. Altered binding sites, ↓penetration

Hypersensitivity to Sulphonamide

Bactericidal

Bactericidal

Bacterial meningitis Actively transported into bacteria. Interrupt protein synthesis. Compete with tRNA for A binding site -> inhibits mRNA-tRNA

Gram+ and -, mycoplasma, rickettsia, chamyldia, some spirochaetes and protozoa. Resistance largely due to efflux

ST 15

Mild – nausea, vomiting, headache. Severe – hepatitis, hypersensitivity, bone marrow suppression Nausea, vomiting, skin rashes

Sequential Blockers Co-trimoxazole

Resistance by βlactamases (give with inhibitors e.g. clavulanic acid) Also ↓permeability of cell membrane and altered binding sites

Side Effects

Hypersensitivity – skin rashes, fever, anaphylactic shock. GI disturbances.

Hypersensitivity, similar to penicillin. Nephrotoxicity, alcohol intolerance. Diarrhoea if oral.

Bacteriostatic

GI disturbances. Can cause bone deformities in children. Do not give when pregnant. Some phototoxicity (Demeclocycline & Minocycline) and vestibular disturbances. High doses give anti-anabolic effect. Do not give if renal function impaired - accumulation


Class of Drug

Name

Antimycobacterial agents

t½ = 2hrs Oral. Widely distributed in tissues and fluids. Crosses BBB. 30-50% protein bound. Metabolised in liver. 10% renally excreted unchanged t½=2hrs. Polar, not absorbed orally. I.M./ I.V. minimal protein binding, doesn’t enter cells, cross placenta or BBB. Excreted by glomerular filtration

MOA

Clinical Use

Major Effects

Gram+ and -. Resistance due to enzyme production. Plasmid mediated.

Bacteriostatic

Inhibit protein synthesis. Bind to 30S subunit, alter codon: anticodon recognition → production of defective proteins

Gram+ and -. Resistance by enzyme inactivation (plasmid mediated). Also failure of penetration, binding site mutations.

Bactericidal (enhanced by agents interfering with cell wall synth)

Isoniazid

Oral, readily absorbed. Widely distributed, crosses BBB. Metabolism involves acetylation

Not fully understood. Passes into mammalian cells – effective against intracellular bacteria. Inhibits mycolicacids (cell wall components)

Tuberculosis and leprosy. Penetrates to necrotic, tuberculous lesions.

Bacteriostatic on resting cells, bactericidal on dividing cells

Rifampicin

Oral, widely distributed. Excreted in bile and urine. Undergoes enterohepatic cycling. Metabolites retain activity

DNA-dependent RNA polymerase inhibitor in prokaryotes. Enters phagocytic cells

Mycobacteria and other Gram + and many gram - species

Pyrazinamide

Oral, widely distributed, crosses BBB. Excreted by glomerular filtration

Inactive at pH7, tuberculostatic at low pH. Effective against intracellular organisms in acidic phagolysosomes

Gentamicin Aminoglycoside

Side Effects

ST 16

Hypersensitivity. GI disturbances. Inhibits protein synthesis. Binds to 50S ribosome subunit, inhibits transpeptidation.

Chloramphenicol

Antibacterial affecting Protein Synethesis

Pharmacokinetics

Pancytopenia (Bone marrow suppression), Grey baby syndrome – vomiting, diarrhoea, flaccidity, low temp + ash grey –> 40% mortality. Requires active transport enter, which Chloramphenicol can block. Progressive Ototoxicity, Reversible nephrotoxicity Loading Doses.

Slow metabolisers have a better therapeutic response (t ½ = 3hr vs 1.5hr)

Infrequent (<4%), skin eruptions, fever, GI disturbances

Bacteriostatic

Arthralgia, GI disturbances, Malaise + fever


Class of Drug

Name

Nystatin Antifungal agents

Pharmacokinetics

No absorption across mucus membranes

Miconazole

I.V. infusion if systemic. Oral if GI. Short half life

Acyclovir

Oral, I.V., topical. 20% GI absorption. Widely distributed, ½ crosses BBB. Excreted by filtration+ secretion

Antiviral agents Zidovudine

Phenytoin Anti-convulsants

Carbamazepine

Oral, 1stPM gives 60-80% bioavailability. Also I.V. Crosses BBB. Metabolised with glucuronide in liver. 20% excreted unchanged in urine t½=12-40hrs. Hepatic oxidation, hydroxylation. Renal excretion. Saturation kinetics. 70-90% protein bound t½=36hrs (↓with chronic treatment). Hepatic oxidation, conjugation. Can auto-induce

MOA Binds to cell membrane, forms a pore →ion channel, interferes with permeability and transport. Greater avidity for ergosterol(fungi, protozoa) Blocks ergosterol synthesis by enzyme inhibition → altered fluidity, interfering with enzymes on membrane Converted to monophosphate by viral TK, then to triphosphate by host TK. This is viral DNA pol substrate and is a chain terminator Trhymidine analogue -> Reverse transcriptase inhibitor. Similar to acyclovir. Triphosphate form terminates chain.

Clinical Use

Major Effects

Stops cell division, prevents hyphae formation

Infrequent, GI disturbances, pruritis, blood dyscrasias Minimal. Local inflammation in I.V. infusion, nausea, headache.

Herpes simplex, also CMV Resistance due to change in viral TK

Enters cells by passive diffusion

ST 17

Rare. Nausea, vomiting, rash

Infections of skin and GI tract

Patients with HIV/AIDS Resistance due to progressive accumulating mutations in reverse transcriptase

Side Effects

↓incidence of opportunistic infection, ↓viral load, ↓risk of transmission from mother to baby Accidental Exposure

Common: Anaemia, Neutropenia Uncommon: GI disturbance, skin rash, insomnia, fever, headache, abnormal liver function, Repeated: Confusion, anxiety, depression, flu-like symptoms

Partial epilepsy and status epilepticus

Rash, vasculitis, fever, hepatitis, ataxia, sedation, gingival hypertrophy, folate deficiency, depression, hirsutism, peripheral neuropathy. CYP450 inducer, easily displaced from proteins

Partial and secondary generalised seizures

Rash, hepatitis, nephritis, ataxia, dizziness, sedation, diplopia, Vit K def, depression, impotence, osteomalacia, hyponatraemia Hepatic enzyme inducer

Voltage gated Na+ channel blocker


Class of Drug

Anti-convulsants

Anti-Convul

Phenytoin

Name

Pharmacokinetics

Valproate

Clinical Use

Major Effects

Side Effects

t½=4-12hrs. Hepatic oxidation, conjugation

Enhance GABA mediated inhibition (possibly inhibits GABA metabolism)

Wide spectrum, partial or generalised seizures

Vigabatrin

t½=6-8hrs, but longer DOA

GABA-T inhibitor – prolongs action of GABA inhibition

Little, some infantile spasms

Lamotrigine

t½=29hrs. Hepatic glucuronidation (no phase 1) t½= ↑by valporate to 60hrs, ↓PHT/CBZ to 15hrs

Voltage gated Na+ channel blocker

Wide spectrum, partial or generalised seizures

Drug

Effect on Anti-convulsants

Drug

Amiodorone, Isoniazid

Phenytoin Metabolism Inhibitor → ↑PHT

Warfarin

Displaces phenytoin from protein bound -> only use near safn Displaces protein bound & inhibits metabolism → easy toxicity Induces metabolism Inhibits epoxide-hydrolase → 4x (VGA) ↑ CBZ-epoxide

AEDs (Lamotrigine) corticosteroids, cyclosporin Oral Conceptative w/ oestrogen AEDs (PHT, VPA, LTG)

Reduce levels of others

Inhibits metabolism x2-3 CBZ

OCP

Inform patients

Warfarin

↓ [Warfarin]

AED

↑ [PHT, PB, LTG]

Carbamzepine

↑ CBZ-epoxide

Aspirin

PHT, PB VPA LTG Macrolide antibiotics (Erythomycin) Ca2+ Channel blockers (Diltiazene / Verapamil) Fluoxetine Hepatic Enzyme Inducers e.g. PHT, PB, CBZ Antacids Some NSAIDs, Aspirin, phenylbutazone

↑ 2x CBZ (Nifedipine -> no effect)

Effect of Drug on X Induces CYP450 -> ↓ [warfin]. Monitor INR closely. Induces CYP450 -> ↓ [conc]. ↓ Efficacy (50ug eostradiol req)

May ↑CBZ levels ↓ [Valproate] May impair absorption Displaces VPA from albumin -> Toxicity

ST 18

Hepatic toxicity (young), pancreatitis, drowsiness, encephalopathy, tremor, blood dyscrasias, hair loss, weight gain, PCOS Potent CYP450 inhibitor Visual field defects (retinopathy) ~40%. No CYP450 involvement Well tolerated, rash, headache, blood dyscrasia, ataxia, diplopia, dizziness, sedation, insomnia, mood disturbance. No CYP450 involvement

Sodium Valporate

Valproate

Carbamazepine

MOA

Year 2 Drug Table - ST  

Year 2 Drug Table - ST

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