Y2 Drugs List Flashcards
Welcome to my drugs list deck. They should contain the MOA + usage & side effects that we need to know for every drug on the list. Some cards have ways to remember the drugs/picture prompts... also if there are any mistakes/any could be refined or made better please let me know and ill edit!
Antacids
- Aluminium Hydroxide and Magnesium Hydroxide - Maalox
- Calcium Carbonate and Magnesium Carbonate - Rennie
Uses: Dyspepsia, Heartburn, Reflux oesophagitis, GORD, Peptic Ulcers
MOA: Gastric Acid Neutralisation
SE: Nausea
- Mg –> Diarrhoea
- Al –> Constipation
Antacids + Alginates
- Sodium Alginate with Sodium Bicarbonate
MOA: Anionic polysaccharides - form a viscous gel raft upon binding with water increasing stomach content viscosity this floats to the top of the stomach reducing symptoms. Also contains antacid to neutralise excess acid. Gastric acid neutralisation
Uses: Gastric Reflux, Reflux oesophagitis - OTC + prescribed
SE: Abdominal disention
Interactions: -
H2 Receptor Antagonists
- Cimetidine
- Ranitidine
MOA: Competitively inhibits gastric H2 receptors to decrease acid secretion. (Cimetidine inhibits many cytochrome P450 enzymes)
- Use:* Stomach ulcers
- SE:* Diziness
Interactions: -
Proton Pump Inhibitors
- Omeprazole
- Lansoprazole
MOA: Blockade of parietal cell proton transporters. Irreversibly inhibits H+/K+-ATPase pump, terminal step in acid secretion pathway. Decreases basal and stimulated acid production.
Very specific - inative at neutral pH thus accumulate in secretory canaliculi or parietal cells and are activated in acidic environment.
- Use:* Stomach & duodenal ulcers, Gastric reflux
- SE:* Headache, Diarrohea
- Interactions:* Warfarin
PK:
- Increased doses give disproprtionatley higher increase in [plasma]
- 1/2 life approx 1hr
- Single daily dose affects acid secreions 2-3 days
Pancreatic Enzymes
Name
Use
MOA
Name: Pancreatin
Use: Pancreatic insufficiency- CF & Pancreatitis
MOA: Restoration of pancreatix enzymes
Bulk Laxatives
- Methylcellulose
- Isphagula Husk
MOA: Polysaccharide polymers not broken down by normal digestion so retain water in the GI lumen, softening and increasing bulk load and promoting increased motility. Water retention in lumen –> soften & bulk stools. Act over 1-3 days.
Use: Constipation
SE: -
Interactions:-
Stimulant Purgatives (2)
MOA overall: Increase intestinal motility
- Indication:* Constipation
- SE:* Nausea
- Bisacodyl
Stimulates rectal mucosa resulting in mass movements - defaecation in 15-30 mins
Use: Short courses. W/ Opoids
- Senna
Derivatives anthracene with sugars forming glycosides passes unchanges into colon where bacterial action = release free anthracene derivatives which are absorbed & causes direct effect on myenteric plexus to increase intestinal motility
- Increases activity on distal colon on serosal strain guage
- Chronic use (>3/week for >year) can cause cathartic colon (laxative dependency + req. higher doses) can lead to serious consequences
Faecal Softeners
- Docusate
- Arachis oil
MOA: Anionic surfactants. Lower surface tension allowing water or fats to enter the stool, softening faeces & increasing bulk to aid transit. Stimulates water & electrolyte secretion into the intestinal lumen. Act 3-5 days
Indication: Constipation
SE:-
Interactions: -
Osmotic Laxatives (3)
MOA Overall: Water rention in intestinal lumen
Indication: Constipation
SE: Stomach cramps
Interactions: Antiepileptics
- Saline purgatives - Magnesium sulphate, Magnesium Hydroxide -
Uses: Bowel prep before procedure. Potent, rapid action (1-2hrs)
- Macrogol Uses: Faecal impaction in children, LT management of chronic constipation
Poorly absorbed solutes that maintain increased fluid volume in GI tract by osmosis, accelerating small intestine transit - large fluid volume in colon leads to distension and purgation.
- Lactulose
Semi-synthetic Galactose & Fructose (disaccharide) converted to poorly absorbed monocaccharides by colonic bacteria - Fermentation yields lactic & acetic acid which acts as an osmotic laxative
- Acts 1-3 days
- Uses: Chronic constipation, Hepatic Encephalopathy, Negate effect of opiods
Oral Rehydration Therapy
NOT SURE IF ON LIST
- Isotonic/hypotonic solution of glucose and NaCl
Exploits ability of glucose to enhance absorption of Na+ and so water.
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/107/a_image_thumb.png?1555575996)
Opioid Anti-Motility Agents
- Codeine
- Loperamide
MOA: Agonist on mu-opioid receptors in the myenteric plexus. Blocks intestinal muscarinic receptors. Increases tone and rhythmic contractions of the colon, but diminishes propulsive activity. Pyloric, illocaecal and anal sphincters are contracted
Uses: Acute uncomplicated diarrhoea in adults
(SEs: RARE. Chronic use = Constipation. Abdo cramps, dizziness)
Interactions: -
Carbonic Anhydrase Inhibitor
Acetazolomide
MOA: Reduce aqueous humour production (req. HCO3- secretion)
- Inhibits carbonic anhydrase in PCT to stop the reapsorption of HCO3- and therefore Na+ so increasing the volume of urine (osmotic balance). Weak diuretic action as only a small amount of sodium is reabsorbed this way
Uses: Reduce intraocular pressure in glaucoma- open and acute close angle
SE: Paraesthesia
- Also prevents H+ secretion –> metabolic acidosis
Interactions: -
Osmotic diuretic
- Mannitol
MOA: Increases the osmolarity of glomerular filtrate thus prevents water reabsorption. Acts mostly where water reabsorption occurs - PCT + descending limb of LOH)
Uses: Cerebral oedema + reducing intraocular pressure (glaucoma), reducing intracranial pressure
SE: Hypotension
Interactions: -
Loop Diuretics
- Furosemide
MOA: Powerful diuretics. Act on thick ascending limb og LOH. Inhibits the Na+K+2CL- co-transporter (competes with Cl- binding). Decreased NaCl reabsorption in thick ascending loop causes decreased osmotic concentration in the medulla thus decreased ADH mediated water absorption.
- Reduced Mg & Ca reabsorption
- Increase in NaCl to DCT. Increase Na uptake by principle cells –> K+ loss –> Metabolic Alkalosis
- Binds to plasma proteins so not filtered but secreted directly into the PCT thus effective in renal impairment/ Nephrotic syndrome.
SEs: Nausea, Dizziness
- Hypovolaemia + hypotension, hypokalaemia + hyponatremia, Ototoxicity
Uses: Oedema, Left ventricular HF
- Acute pumonary oedema, Resistant HTN
Interactions: NSAIDS, ACEi
Thiazide Diuretics
- Bendroflumethiazide
- Indapamide
- Hydrochlorothiazide
- Chlortalidone
(BICH)
Weak/moderate diuresis. Acts on the Early DCT. Inhibits Na+/Cl- co-transporter (competes with Cl- binding). Slower acting but longer lasting than loop diuretics.
- Filtered & not secreted- not good in renal impairment
- Increased NaCl to Distal nephron & decreased blood volume –> Increase K secretion
- Intercalated cells may also secrete H+ –> Alkalosis
Uses: Hypertension, Peripheral oedema (chronic heart failure)
SEs: Electrolyte imbalance, Exacerbation/ precipitation of gout (increased plasma uric acid)
- Hyponatraemia/Hypokalaemia, ED, Hyperglycaemia
- Interactions:* NSAIDS, Digoxin
Potassium Sparing Diuretics
Subclass: Aldosterone Antagonists
- Spironolactone
- Eplerenone
Weak diuretic alone. Aldosterone antagonist, binds to and blocks mineralocorticoid (MR) receptor. Prevents synthesis of ENaC and Na+/K+ATPase activity which stops Na+ reabsorption (and water by osmosis) and reduces K+ secretion into the lumen to K+ is retained.
Notes: Act on Late DCT/ Collecting duct on principle cells (Na/K ATPase)
SEs: GI symptoms, Hyperkalaemia, gynaecomastia
Uses:
- Chronic HF
- Oedema
- Periph oedema +ascites caused by cirrhosis
- Resistant HTN
- Primary Hyperaldosteronism
- Can be used in comination to prevent K+ loss from use of loop/thiazide diuretics.*
- Interactions:*
- NSAIDS
- ACEi
Potassium Sparing Diuretics
Subclass: ENaC Antagonists
- Amiloride
MOA: Weak diuretic alone. ENaC antagonist - blocks ENaC, competes for Na+ binding site thus decreasing luminal permeability to Na+. This causes reduced Potassium secretion into the lumen to potassium is retained
- Can be used in combination to prevent K+ loss from use of loop/thiazide diuretics
Uses:
- Chronic heart failure
- Oedema
- Peripheral oedema and ascites caused by cirrhosis
- Resistant HTN
- Primary Hyperaldosteronism
SEs: GI Symptoms, Hyperkalaemia, Gynaecomastia
Interactions: NSAIDS, ACEi
Renin Inhibitor
NOT ON Y2
- Aliskiren
Inhibits the action of Renin thus stopping formation of Angiotensin I so the RAAS system cannot be used to increas BP
Renin release from granular cells of AA
ACE inhibitors
Ramipril, Captopril
MOA: Binds to ACE inhibiting the converstion of Ang I to Ang II –> Blocks vascocontrictions (reduces afterload) & the RAAS system cannot increase BP
- Caution in renal failure - ACE normally constricts efferent arterioles thus ACEI can lead to decreased GFR
-
Singal Transduction in Smooth Muscle cells:
- Less activation at AG II receptors
- Less increase IP3
- Less Ca release from SR
- Less Ca-Cm
- Less MLCK phosporylation
- Less contraction
- Aldosterone secretions also reduced:
- Less water retention
- Less plasma volume
- Decreased cardiac preload
Use: HTN, Diabetic neuropathy, HF
SEs: Dry cough (bradykinin build up as not inactivated by ACE), Hyperkalaemia, hypotension
Interactions: Lithium, NSAIDS
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/132/a_image_thumb.png?1556024829)
Angiotensin-II receptor antagonists/ ARBS
- Losartan
- Valsartan
MOA: Blocks angiotensin-renin system. Binds to the angiotensin-II receptor, preventing it from working. RAAS cannot increase BP
Uses: HTN, Diabetic neuropathy, HF
SE: Hypotension, Fatigue
Interactions: Diuretics
Neprilysin inhibitors
(used with an ARB drug)
- Sacubitril, (used with Valsartan)
MOA: Inhibition of natriuretic peptide breakdown –> Promote Water & Sodium excretion
- Neprilysin = Enzyme
Uses: HF with reduced EF
SE: Hypokalaemia, Hypoglycaemia
Interactions: -
Beta-adrenergic receptor antagonists
(Beta blockers)
- Bisoprolol (Cardioselectiv B1 antag.)
- Atenolol (cardioselective B1 antag.)
- Propanolol (B1 & 2 antag.)
MOA: Negative inotropic/ chrontropic agent.
- Competitive inhibitors of adrenaline and noradrenaline at B-adrenoceptor sites. Inhibit sympathetic stimulation of heart muscle.
- Heart Specific: B1 antagonists are selective for the cardiomyocytes: Negative inotropes & chronotropes. Reduce workload on the heart relieving oxygen demand.
-
Molecular Mechanism in the heart:
- Blocked Beta-adrenergic receptors
- Less ATP –> cAMP by Adenylyl Cyclase
- Less Protein Kinase (PK) A activity
- Less release of Ca from SR- Less free Ca inside cell
- Less contraction
Uses: HTN, Stable angina
SEs: Bradycardia, Bronchospasm, Dizziness, constipation
Interactions: NSAIDS, Digoxin
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/127/a_image_thumb.png?1549365476)
Alpha-adrenergic receptor antagonist (heart or prostate)
- Doxazosin
MOA: Vasodilator, decrease total peripheral resistance
- Selective alpha 1 adrenergic receptor blocker on bladder neck, urethra. Relaxation smooth muscle —> Urinary flow facilitated
- Blocks alpha- 1 adrenoreceptors of the sympathetic autonomic nervous system, this relaxes smooth muscles around the bladder (internal and external urinary sphincters) allowing micturition
Uses: BPH-urinary retention, HTN
SE: Dizziness, Headache. Hypotension, Drowsiness, Nausea, Fatigue, Constipation
Interactions: Hypotensive drugs
Calcium Channel Antagonists
(for heart failure and hypertenison)
Diltiazem
Dihydropyradine subclass
- Nifedipine
- Amlodipine
MOA: Blockade of vascular smooth muscle contraction
- Prevent opening of VGCCs (L type) –> Less Ca influx –> Less binding of Ca to Cm–> As less Ca-Cm complex less phosphrylation MLCK therefore less contraction
-
Notes:
- Does not generally act on veins
- Drives coronary artery dilation- Improves blood flow
- Vasodilatory effect therefore reduced afterload
Use: HTN, Stable angina
SEs: Ankle swelling, Oedema palpitations
Interactions: Beta blockers, Digoxin
(Bind to K-type calcium channels on cardiac and smooth muscle - act on BOTH the heart and vessels. Cause coronary artery dilation. Negative chronotropic effects, negative inotropic effects.)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/128/a_image_thumb.png?1555923438)
Nitrate Vasodilators
- Glycerol trinitrate (GTN)
- isosorbide mononitrate (ISMN)
MOA: NO release –> Smooth muscle relaxation
- Metabolised to release Nitric Oxide (NO) which stimulates soluble guanylate cyclase. Increases cGMP in vasc. smooth muscle cells. Drives dephosphorylation of MLC via activation of MLC Phosphatase causing vascular smooth muscle relaxation.
- Heart Effects: Can act to dilate arteries AND veins. Venodilation decreases preload. Coronary artery dilation increases blood and oxygen supply to the myocardium. Promote moderate arteriolar dilation- reduces cardiac afterload
Use: Acute angina pectoris, HF
SE: Headache, Hypotension
Interactions: Antihypertensives
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/129/a_image_thumb.png?1556024432)
Sympathomimetics
- Noradrenaline (alpha)
- Dobutamine (beta)
- Adrenaline (alpha and beta)
MOA: Adrenergic stimulation increased inotropy
- Positive inotrope: Binds & Stimulates Cardiomyocytes B1 adrenergic receptor –> Drives heart muscle contraction –> Resotres function
Uses: Cardiac Arrest, Cardiogenic shock
SE: Arrythmia
Interactions:-
Antiplatelet Drugs (2)
Aspirin
- Inhibition of thromboxane synthesis
- Blocks enzyme actions of platelet COX enzyme. COX required for synthesis Thromboxane A2 production. Reduced TXA2 synthesis inhibits platelet activation & thrombus formation
Clopidogrel
- Inhibition of platelet activation by ADP
- Binds to and blocks the platelet Adenosive Diphosphate (ADP) receptor, causes decreased platelet activation & therefore thrombus formation
USE: Primary & Secondary relief for CVD, Anticoagulant prophylaxis, ACS prevention
- Can treat CVD without affecting BP
SE: GI irritation & bleeding
Interactions: Anticoagulation drugs
The cloppy dog has 5 limbs (2+3) GPIIb and GPIIIa
Anticoagulants (4)
Name the 4 classes
- Comarin- Warfarin
- Direct thrombin inhibitors- Dabigatran
- Direct FXa inhibitors- Apixaban, Edoxaban, Rivarozaban
- Heparins- Deltaparin, Tinzaparin, Enoxaparin (LMWH), Unfractionated heparin
Anticoagulants- Comarin
Warfarin
MOA: Inhibition of vitamin K epoxide reductase
- Targets extrinsic pathway which inhibits vitamin K dependent synth of dependent clotting factors 10, 9, 7 and 2 (1972) (PT)
- By inhbiting vitamin K carboxylation of the factors it decreases thrombin production
USE: DVT, Prophylaxis of stroke from AF
SE: Abnormal bleeding
Interactions: NSAIDS, Diuretics, (many others)
Anticoagulants- Direct Thrombin inhibitors
Dabigatran
MOA: Competitive, reversible inhibitor of thrombin
- Direct inhibition of thrombin - thrombi cannot convert fibrinogen into fibrin and formation of secondary plug is inhibited
Use: Prophylaxis of VTE post-surgery
SE: -
Interactions: -
Anticoagulants- direct FXa inhibitors
Apixaban, Edoxaban, Rivaroxaban
MOA: Inhibition FXa in coagulation cascade
Use: Prophylaxis of stroke from AF; DVT
SE: Abnormal bleeding
Interactions: -
Anticoagulants- Heparins
Deltaparin, Tinzaparin, Enoxaparin (LMWH), Unfractionated Heparin
MOA: Reversibly bind antithrombin III which inactivates thrombin and FXa.
- Unfractionated = Inactivated FXa & Thrombin
- LMWH = Inactivated FXa
Use: Prophylaxis of VTE & PE
SE: Abnormal bleeding
Interactions:-
Thrombolytics/ Fibrinolytics
- Altepase
- Streptokinase
- Urokinase
MOA: Activates plasminogen to plasmin for proteolytic breakdown of thrombus fibrin (digests fibrin and fibrinogen to restore blood flow).
Use: MI, Ischaemic stroke
SEs: N/A
- Arrhythmias, bleeding. Can only use streptokinase once as an immune response is generated againset the bacteria (streptococci) and memory B cells produce anti-streptokinase ABs.
Interactions: -
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/137/a_image_thumb.png?1549366234)
HMG-CoA Reductase Inhibitors
(statins)
- Atorvastatin
- Simvastatin
MOA: Inhibition of mavelonate pathway required for cholestrol synthesis
- HMGCR enzyme is essential & rate-limiting in cholesterol synthetic pathway
- HMGCR Inhibitors reduce circulating cholesterol levels, Promote uptake of excess cholesterol from bloodstream into liver
Use: Hyptercholetrolaemia, Risk of CVD & Stroke
- CVD prevention WITHOUT affect BP
SE: Myalgia
Interactions: Verapamil, Macrolides
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/133/a_image_thumb.png?1549365757)
B2-Adrenergic Agonists
(tx of airway disease)
- Salbutamol (short acting)
- Terbutaline (short acting)
- Salmeterol (long acting)
- Formoterol (long acting)
MOA: Dilates bronchial smooth muscle
- Cellular Target: Bronchiolar Smooth Muscle
- Molecular Target: Stimulation B2 adrenergic receptors
- B2 agonists bind to B2-adrenergic receptors –> activation associated G protein –> increases action adenylate cyclase. AC increases cAMP levels/ action in cytoplasm, activting protein kinase A (PKA). PKA :
- Drives Ca2+ –> Storage vesicles
- Inactivates MLCK by reducing phosphyrlation –>
- This ^ plus less Ca2+ in Cytoplasm –> reducation in smooth muscle contraction resulting in relaxation of smooth muscle in the airway.
Use: Asthma. Reversible airway obstruction
SEs: Tremor, tachycardia, cardiac arrythmia
Interactions: Diuretics
Anti-muscarinics
(Airways)
- Ipratropium (short acting)
- Tiotropium (long acting)
MOA: Blocks muscarining receptors –> bronchiol dilation
- Cellular Targets: Bronchiolar smooth muscle cells.
- Blocks M3 muscarinic ACh receptors.
- Actives G protein –> Decreases action of PLC: reduces ca release from IC stores
- Reducing Ca2+ release into the cytoplasm, reducing smooth muscle contraction causing bronchodilation.
Use: Acute asthma, Bronchospasms in COPD
SEs: Dry mouth, constipation, urinary retention
Interactions:-
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/123/a_image_thumb.png?1556790613)
Methylxanthines
- Theophylline
- Aminophylline
MOA: Bronchodilator, increases cAMP in smooth muscles
- Cellular targets: bronchiolar smooth muscle cells.
- Mollecular targets: Blockage PDE
- Binds to B2 adrenergic receptor. Activation associated G protein. Increases action Adenylate cyclase- covnverts ATP –> cAMP in Cytoplasms. This is normally inactivated by phosphodiesterase (PDE).
-
Durgs block PDE sustains cAMP levels activating PKA
- Drives Ca2+ into storgae vesicles
- Inactives MLCK by reducing phosphorylation
- Less Ca2+ in cytoplasm and reduced phosphorylation MLCK–> Smooth muscle relaxtion–> bronchodilation.
Use: Acute asthma, Reversible airways obstruction
SE: Headache, Nausea
Interactions: Antidepressants, Salbutamol
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/124/a_image_thumb.png?1549365156)
Glucocorticoids
(Airways)
- Beclomethasone
- Fluticasone
- Prednisolone
- Hydrocortisone
MOA: Reduction of inflammation & mucus production
- Cellular target: Lung immune cells- Macrophages, T-lymps and eosinophils.
- Molecular target: Intracellular GR
- Activates the glucocorticoid receptor (GR) which interacts with selected nuclear DNA sequences and influences the expression of g=key genes:
- Repression of pro-inflammatory mediators (TH2 cytokines)
- Expression of anti-inflammatory products (B2 adrenoceptors)
Use: Asthma, Allergic rhinitis
SEs: Cough
- MANY - Moon face, weight gain, osteoporosis, hyperglycaemia
Interactions: Aspirin
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/126/a_image_thumb.jpg?1549365417)
Leukotriene Antagonists
- Montelukast
- Zafirlukast
MOA: Blockade of leukotriene receptors
- Cellular targer: Eosinophils & Bronchiolar Smooth Muscle
- Molecular target: Blocks CysLT1 leukotriene receptors.
- This reduces the inflammatory response in early and late phases of asthma
- Additive effect when used with other drugs (eg: inhale glucocorticoids)
- No evidence of effect on remodelling
Use: Asthma, Allergic rhinitis
SEs: Abdo pain, headache
Interactions: Phenobarbital
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/125/a_image_thumb.jpg?1549365316)
Mucolytic
Name
Use
MOA
Name: Dornase Alfa
Use: CF
MOA: Synthetic DNAse 1- breakdown of extracellular DNA to reduce sputum viscosity
Dopaminergics
(pharma basal ganglia disorders)
MOA: Increases dopamine synthesis & dopaminergic function
Levodopa (DA precursor)
- Levodopa converts to dopamine as dopamine does not cross BBB - restores activity in the nigrostriatal pathway.
Pramipexole (synthetic agonist)
Ropinirole (synthetic agonist)
Rotigotine (synthetic agonist)
- DA Receptor agonist
- Synthetic dopamine agonists stimulate D2 receptors on striatal neurons improving dopaminergic transmission.
Use: PD
- Synthetics used in younger patients
SEs: Confusion, Agitiation
- Anorexia, drowsiness, hypomania, hypotension, sudden onset sleep, ‘on-off effects’, Arrythmia, Tachycardia
- Synthetic more likely to have psych SE
Interactions: MOAI
Dopa-decarboxylase inhibitor
- Carbidopa
- Benserazide
MOA: Stops breakdown of levadopa in periphery by inhibiting dopa-decarboxylase
- preventing GI and peripheral metabolism of levodopa meaning more is available to the CNS
Uses: PD
- Used with levodopa for Parkinsonism
SE: Confusion, Agitation
Interactions: -
MAOIB Inhibitor
(Monoamine oxidase inhibitors, B form inhibitor)
- Rasagiline
- Selegiline
MOA: Inhibits MAOIB breakdown of dopamine in the CNS
Use: PD
- Adjunct with levodopa/carbidopa for Parkonsonism
SE: -
Interactions: -
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/141/a_image_thumb.jpg?1549366584)
COMT inhibitor
(catechol-O-methyl transferase inhibitor)
- Entacapone
- Tolcapone
MOA: Blockade of dopamine precursor breakdown by inhibition of COMT
- Inhibits COMT in the periphery (outside CNS), reducing dopamine breakdown and allowing for more in the CNS
Use: PD
SE: N&V
Interactions:-
![](https://s3.amazonaws.com/brainscape-prod/system/cm/288/620/140/a_image_thumb.jpg?1549366458)
Anticholinergics
(BG disorders)
- Orphenadrine
- Procyclidine
- Trihexphenidyl
MOA: Muscarinic cholinergic receptor antagonist
- in Parkinsons a decrease in dopamine lease to an increase in Ach concentration. Anticholinergics (antimuscarinics) readdress this balance).
Use: PD (especially iatrogenic), Muscle rigidity, SE of anti-psychotics
- Iatrogenic PD (Orphenadrine)
- Dystonia (Trihexphendyl & Procyclidine)
SEs: Dry mouth, Constipation
- may reduce absorption of levodopa
Interactions:-
Dopamine-depleting Drugs
- Tetrabenazine
MOA: Inhibits VMAT2 within basal ganglia, preventing uptake of DA into vesicles
- Depletes serotonin, noradrenaline and dopamine. Dopamine is req for fine motor movement, so inhibition is helpful for kyperkinesis.
Uses: Huntington’s
- Athetosis, Ballismus, Chorea
SEs: -
- Causes depression by decreasing 5HT and NA levels
Interactions: -
Selective Serotonin Reuptake Inhibitors (SSRIs)
- Sertraline
- Citalopram
- Fluoxetine
MOA: Inhibits 5HT reuptake pump in synaptic cleft- increases 5HT levels.
Use: Depression/ GAD
SEs: Insomnia, Nausea
- Sickness (nausea) sleep disorders- insomnia, sexual dysfunction, serotonin syndrome, slow onset. (5S’s)
- Seratonin syndrome = Overactiation ANS
- Hyperthermia
- CV Problems
- Aggresion
- Tremor
- Rigidity
Interactions: Lithium, NSAIDS
MAOIs Type A
- Moclobemide
MOA: Inhibits MAO A (in CNS) –> decreases breakdown of Na &5HT
- Reversible inhibitor of monoamine oxidase A (RIMA)
Use: Depression
SEs: Tachycardia
- Cheese reaction: Postural hypotension, restlessness, convulsions, sleep disorders,
- Cheese Reaction- increase tyramine which increases NA –> Hypertensive crisis- vasoconstriction
- “See People’s Cheese Reaction”
Interactions: -
Tricyclic Antidepressants
- Amitriptyline
- Nortriptyline
- Dosulepin
MOA: Na & 5HT reuptake inhibitor in synaptic cleft. a1 adrenoreceptor antagonist, H1 receptor antagonist, M1 receptor antagonist
Use: Depression, Neuropathic pain
SEs: Anticholinergic syndrome
- Sedation (H1 blocker)
- Dry mouth, constipation (M1 muscarinic blocker)
- cardiac dysfunction (a1 adrenoreceptor blocker)
Interactions: -
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Atypical Antidepressants
Overall Use: Depression
Interactions & SE: -
Reboxetine
- NRI
Bupropion
- Inhibits NA and dopamine reuptake
Buspirone
- Partial 5HT1a agonist reduce activity to increase transmitter levels in the synaptic cleft
Agomelatine
- Melatonon agonist, increases slow wave sleep patterns.
Venlafaxine
- ?NRI
- SNRI - Inhibits reuptake of 5HT & Na
Mirtazapine
-
a2-adrenergic antagonist
- SE: Postural hypotension, Sleep disorder, Bronchoconstriction, Decreased HR
Ruboxetine- Depression
Venlafaxine- GAD/ PSTD/ Depression
Busprione- GAD/ OCD/ Depression
Mirtazapine- Depression
Bupropion: Depression following smothin cessation
1st generation (classical) Anti-psychotic
- Chlorpromazine
- Haloperidol
MOA: Selective dopamine receptor blockade/ antagonists
- Also affect H1, M1 and a1
Use: Schizophrenia
SEs: Blurred vision, Tremor, EPS, Hypotension
- Tardive Dyskinesia (disabling involuntary movements)
- Tongue Twisiting, Choreiform movements
- Extrapyramidal symptoms
- Slowed movement
- Tremor
- Akasthisia,
- Sedation
- Neuroleptic malignant syndrome:
- Altered consciousness, Hyperthermia, Tachycardia, Incontinence
- M1 receptor: Dry mouth, Constipation, Blurred vision
- H1 receptor: Weight gain, Sedation
- D2 Receptor: Slow movement, Rigidity, Prolactin elevation
- Alpha1 Receptor: Hypotension, Drowsiness
Interactions: -
2nd generation (Atypical) Antipsychotics
MOA overall: Selective D2 dopamine & 5HT receptor blockade
Use: Schizophrenia
- Amisulpride
5HT7 and Dopamine antagonist
- Risperidone
5HT2A and Dopamine antagonist
- Clozapine
5HT2A and domapine antagonist
- Olanzapine
Selective D2 and 5HT antagonist
- Quetiapine
Selective D2 and 5HT antagonist
SE: Hypotension, EPS (- less likely: Akathisia, Tremor, Slowed movement, Sedation)
- Neuroleptic Malignant Syndrome: Hyperthermia, Tachycardia, Altered Conciousness, Incotinence
- D2 Anatagonist: Rigidity, Slow speech, Stiffness, Tremor
- 5HT antagonist: Consiptation, Somnolence, Weight gain, Dizziness
Interactions: -
Mood Stabiliser
- Lithium carbonate
MOA: Unclear but possible neuronal calicum channel blockade
Uses: Bipolar disorder
- Depression- resitant, recurrent unipolar as an adjunct to anti-depressants
SE: Tremor, hypothyroidism
Interactions: NSAIDs, ACEi
Anticholinesterases
(for dementia)
- Donepezil
- Galantamine
- Rivastigmine
MOA: Inhibitor of acetylcholinesterase (reversible)
Use: mild- moderate AD
SE: N&V
Interactions: -
Glutamate NDMA receptor antagonists
- Memantine
MOA: VD blocker of NMDA receptors (NMDA NAM)
- Interferes with glutamate mediated cell death as prevents Calcium getting into cell
Use: Moderate to severe AD
SE: Constipation & Hypertension
Interactions: -
Anti-Epilepsy drugs (AEDs)
For both types:
Use: Epilepsy
SE: Nausea, Blurred vision
Interactions: Macrolide abx
- Sodium Valporate
- Lamotrigine
- Carbemazepine
MOA: Block sodium channels in the inactivated state
Use: Epilepsy
- All types of seizures except absence seizures
SEs: Cognitive impairment, visual impairment, peripheral neuropathy, skin problems
- Ethosuximide - Ca2+ blocker
MOA: Caclium channel blocker
- Targets low threshold voltage dependent T-type calcium channels
Use: Absence seizures - first line
Benzodiazepines
- Midazolam - GABA PAM (Y subunit)
- Lorazepam - GABA PAM (Y subunit)
- Diazepam - GABA PAM (Y subunit)
- Zolpidem (BDZ like)
MOA: GABA PAM Y subunit- opens Cl- channels –> Cl- influx –> Hyperpolarisation. Enhanced effects of GABA
- GABA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present.
Use: Epilepsy, Acute seizures
SE: Drowsiness, Dependence
Interactions: Sedatives
Benzodiazepine
(Antagonist)
- Flumazenil
MOA: Antagonises GABA signalling
Use: Reversal of BDZ signalling
SE:-
Interactions:-
Non-benzodiazepine Hypnotics
Zopiclone
MOA: Enhances GABA binding to GABA-A receptors
Use: Insomnia
SE:-
Interactions:-
Barbituates (Barb)
- Phenobarbitone- GABA PAM (B subunit)
- Pentobarbitone- GABA PAM (B subunit)
- Primidone- GABA PAM (B subunit)
MOA: GABA PAM Beta subunit. Enhanced effects of GABA
- GABA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present.
Use: Epilespy, Acute seizures
- Status Epileptics
- Primidone Essential Tremor
SE: Drowsiness, Fainting
Interactions: Sedatives, Anticoagulants
Weak analgesic/Antipyretic
- Paracetamol
Use: Mild-moderate pain & fever
MOA: Unclear- possible COX inhibitor in CNS
- No PG –>
- No prostanoid receptor activation –>
- Reduced activation VDNC
SE: Constipation
Interaction: Warfarin
In OD - conjugation (phase II metab.) pathway is saturated, phase I metab yields toxic metabolite NAPBQI which in high levels is toxic to hepatocytes –> liver failure.
NSAIDs
- Aspirin
- Ibuprofen
- Diclofenac
- Naproxen
Use: Mild- moderate pain, Inflammation
MOA: Non selective COX inhibitors. Blockade prostaglandins synthesis so less inflammation
- Non selective COX inhibiton –> No PG –> No prostanoid receptor activation –> Reduced activation VDNC
SEs:
- GI side effects- gastric ulcers and medication overuse headaches
- HTN
-
Not for under 16’s
- Reye’s Syndrome: Following viral infection asprin can cause RS (Fatty deposits in liver and brain)
- NSAID intoxication: Salicylism (high dose of acute or chronic NSAID ingestion. Classic symptom = Tinnitus)
Interactions: Diuretics, ACEi
COX-2 selective NSAIDs
- Celecoxib
- Etoricoxib
- Use:* Inflammation, Nociceptive pain
- MOA:* Selective COX 2 Inhibitor –> No PG –> No prostanoid receptor activation –> Reduced activation Voltage Gated Na+Channel. Localised Pg blockade
- SE:* Indigestion, Thombosis
Interactions: ACEi & SSRI