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!

1
Q

Antacids

A
  • 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
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2
Q

Antacids + Alginates

A
  • 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: -

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3
Q

H2 Receptor Antagonists

A
  • Cimetidine
  • Ranitidine

MOA: Competitively inhibits gastric H2 receptors to decrease acid secretion. (Cimetidine inhibits many cytochrome P450 enzymes)

  • Use:* Stomach ulcers
  • SE:* Diziness

Interactions: -

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4
Q

Proton Pump Inhibitors

A
  • 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
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5
Q

Pancreatic Enzymes

Name

Use

MOA

A

Name: Pancreatin

Use: Pancreatic insufficiency- CF & Pancreatitis

MOA: Restoration of pancreatix enzymes

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6
Q

Bulk Laxatives

A
  • 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:-

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7
Q

Stimulant Purgatives (2)

A

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
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8
Q

Faecal Softeners

A
  • 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: -

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9
Q

Osmotic Laxatives (3)

A

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
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10
Q

Oral Rehydration Therapy

NOT SURE IF ON LIST

A
  • Isotonic/hypotonic solution of glucose and NaCl

​Exploits ability of glucose to enhance absorption of Na+ and so water.

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11
Q

Opioid Anti-Motility Agents

A
  • 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: -

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12
Q

Carbonic Anhydrase Inhibitor

A

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: -

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13
Q

Osmotic diuretic

A
  • 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: -

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14
Q

Loop Diuretics

A
  • 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

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15
Q

Thiazide Diuretics

A
  • 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
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16
Q

Potassium Sparing Diuretics

Subclass: Aldosterone Antagonists

A
  • 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
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17
Q

Potassium Sparing Diuretics

Subclass: ENaC Antagonists

A
  • 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

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18
Q

Renin Inhibitor

NOT ON Y2

A
  • 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

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19
Q

ACE inhibitors

A

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

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20
Q

Angiotensin-II receptor antagonists/ ARBS

A
  • 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

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21
Q

Neprilysin inhibitors

(used with an ARB drug)

A
  • 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: -

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22
Q

Beta-adrenergic receptor antagonists

(Beta blockers)

A
  • 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

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23
Q

Alpha-adrenergic receptor antagonist (heart or prostate)

A
  • 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

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24
Q

Calcium Channel Antagonists

(for heart failure and hypertenison)

A

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.)

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25
**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**
26
**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:-
27
**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: **Antico****agulation drugs** *_The cloppy dog has 5 limbs (2+3) GPIIb and GPIIIa_*
28
**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
29
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)
30
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: -
31
Anticoagulants- direct FXa inhibitors
**Apixaban, Edoxaban, Rivaroxaban** MOA: **Inhibition FXa in coagulation cascade** Use: **Prophylaxis of stroke from AF; DVT** SE: **Abnormal bleeding** Interactions: **-**
32
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:-
33
**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: -
34
**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**
35
**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**
36
**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:-
37
**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**
38
**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**
39
**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**
40
Mucolytic Name Use MOA
Name: **Dornase Alfa** Use: **CF** MOA: **Synthetic DNAse 1- breakdown of extracellular DNA to reduce sputum viscosity**
41
**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**
42
**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: -
43
**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: -
44
**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:-
45
**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:-
46
**Dopamine-depleting Drugs**
* **Tetrabenazine** MOA: I**nhibits 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: -
47
**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**
48
**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 * "**S**ee **P**eople's **C**heese **R**eaction" *Interactions:* -
49
**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: -
50
**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
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**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: -
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**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: -
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**Mood Stabiliser**
* **Lithium carbonate** MOA**: Unclear but possible neuronal calicum channel blockade** Uses: **B****ipolar disorder** * Depression- resitant, recurrent unipolar as an adjunct to anti-depressants SE: **Tremor, hypothyroidism** Interactions: **NSAIDs, ACEi**
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**Anticholinesterases** **(for dementia)**
* **Donepezil** * **Galantamine** * **Rivastigmine** MOA: **Inhibitor of acetylcholinesterase (reversible)** Use: **mild- moderate AD** SE: **N&V** Interactions: -
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**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: -
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**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
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**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**
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**Benzodiazepine** **(Antagonist)**
* **Flumazenil** MOA: **Antagonises GABA signalling** Use: **Reversal of BDZ signalling** SE:- Interactions:-
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Non-benzodiazepine Hypnotics
**Zopiclone** MOA: **Enhances GABA binding to GABA-A receptors** Use: **Insomnia** SE:- Interactions:-
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**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**
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**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.*
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**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**
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**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**
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**Weak opioid analgesics**
* **Codeine** * **Dihydrocodeine** * Use:* **Mild to moderate pain** * MOA:* **Opioid Receptor Agonist** --\> Decrease opening VDCC--\> Decrease Ca release from intracellular stores --\> Decrease exocytosis of transmitter vesicle and Increasing K outflow (post-synaptic) * SEs:* **Constipation, Nausea** * Resp depression, decreased GI motility, tolerance and dependance * Interactions:* **Sedatives** (Mimic endogenous opioids acting on opioid receptors to modulate pain at all CNS levels. Hyperpolarises the neuron so it is less likely to fire when a stimulus comes through)
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**Strong Opioid Analgesics**
* **Morphine** * **Diamorphine** * **Pethadine** * **Fentanyl** * MOA:* **Opioid Receptor Agonist** --\> Decrease opening VDCC--\> Decrease Ca release from intracellular stores --\> Decrease exocytosis of transmitter vesicle and Increasing K outflow (post-synaptic) * Uses*: Nociceptive **pain- severe** * SEs:* **Nausea,** **Constipation** * Resp depression, decr GI motility, tolerance and dependance, Vomiting, Mood alterations * Interaction:* **Sedatives**
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**Partial/Mixed Agonist opioid analgesics**
* **Buprenorphrine** * **Pentazocine** * MOA:* **Opiod receptor modulation** * Opioid receptor partial agonist @ **Mu & Kappa Opioid Receptor** and Antagonist at delta * Use:* **Moderate-severe pain** * Maintenance therapy * SE:* **Constipation, nausea** * Interaction:* **Sedatives**
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**Opioid receptor antagonists**
* **Naloxone (short lasting)** * **Naltrexone (longer lasting)** MOA: **Opioid receptor antagonist** * Compete for the same binding site as opioids, particularly the u receptor so reducing the effect of opioids Uses: **Opioid OD, Respiratory depresesion** * 2/ Prevent relapse of opiod/ alcohol abuse * SE:* **Nausea & Tachycardia** Interactions: -
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**Drugs used to manage opioid addiction**
* **Methadone** * **Buprenorphine** *MOA:* **Narcotic opioid replacement** (M) * Mu receptor, longer lasting. **Opioid r****eceptor agonist/modulator** (B) * Partial Mu and Kappa R agonist and antagonist at delta * Use:* **Maintenance therapy for opiod addiction.** * B for moderate to severe pain * SE:* **Constipation** * nausea (B) * Interactions:* * **Sedatives**
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**Drugs to treat neuropathic pain** **+ 4 types of neuropathic pain?**
* **TCAs** * **(****Amitriptyline****- NRI, 5HTRI, H1 anatgonist, A1 antagonist, M1 antagonist)** * **Gabapentin** (AED) * MOA: **VDCC antagonist** * increases GABA transmission/ synthesis * **Pregabalin** (AED) * MOA: **VDCC antagonist** * **​**increase GABA transport SE of all: **Dizziness, fatigue** Interactions of all: **Antidepressants** 4 types: Phantom limb, trigeminal neuralgia, post-stroke pain, post-herpetic pain (persistent pain after shingles). Y1 also included * **Carbamazepine** (AED) * MOA: Sodium channel blocker in inactivated state * **​​**SE: Teratogenic
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Inhaled analgesics Name Use MOA SE Interactions
Name: **NO & oxygen mixture** (Gas & air) Use: **Analgesia during childbirth** MOA: **Unclear** SE: **Decreased vitamin B12 synthesis** Interactions: -
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**General Anaethetic**
*Inhaled:* * **Isoflurane** * **Sevoflurane** **​**MOA: **Unclear, possible enhancement of GABA function** SE: **Hypotension** * Respiratory depression, Irritation of respiratory tract, Bronchospasm, Laryngospasm Interactions:- * IV:* * **Propofol** **​**MOA: **Unclear, possible enhancement of GABA function** SE: **Hypotension** Interactions: - * **Ketamine** MOA: **NMDA (glutamate receptor antagonist)** * Blocks Ca & Na channels SE: **Hypotension** * Hallucinations, Raised HR and BP Interactions: - Y1: * Midazolam- GABA PAM y subunit * Can be used with no LOC IV Notes: * Decrease cardiac contracility * Respiratory depression * Decreased CNS function * Reduced sympathetic activity Ketamine/ Midazolam --\> Less CV/ Resp effects
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**Local Anaesthetic**
* **Lidocaine** * **Bupivacaine** * **Levobupivacaine** MOA: **Voltage gated sodium channel blockade.** * Blocks voltage-gated Na+ channels --\> Enter through cell membrane unionioned. Ionised IC space & block inside of Na channel * Not useful in inflamed tissue due to the acidic pH of 'inflammatory soup' reducinng effectiveness Uses: **Local anaesthetic** * Levobupivicane- Epidural Anaesthesia SE: **Rash** Interactions: -
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**Neuromuscular blockers**
Use for all: **Tracheal intubation & mechanical ventilation during surgery** SE: **Hypotension, Skin flushing** Interactions: - * Depolarising* : * **Suxamethonium (depolarising)** MOA: **Initial depolarisation & desensitisation of AChR** * Non-competitive, agonist * Bind AchR --\> Prologned depolarisation (receptor closes & repolarises w/ agonist still bound) --\> prevents further depolarisation * Fast onset, short duration *Non-depolarising* - (competitive, antagonist): * **Atracurium besilate (non-depolarising)** * **Vecuronium (non-depolarising)** MOA: **Competitive antagonist at AChR** * Bind AChR prevent depolarisation post synaptically. Pre synaptically reduced Ca entry --\> Less NT from pre-synaptic vesicle * Do not cross BBB * Slow onset, long duration \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ _Y1:_ **Neostigmine** MOA: Peripheral inhibitor of acetylcholinesterase (depolarising) Use: Also used in MG AChEi: Increase Ach in junctional cleft, paralysis by overload- all AchR @ max SE: (PNS increase) Bradycardia, Increased secretions & Peristalsis
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**Drugs used to reverse NMB block**
Use for all: **Immediate reversal of NMB to reduce post-op pulmonary complications** SE: - Interaction: - * For Non- depolarising:* * **Sugammadex** MOA: **Oligosaccharide that forms a complex with NMB, encapsulating and inativating it then removing them from NMJ** * ONLY for VECURONIUM * For ?Non-depolarising:* * **Neostigmine** MOA: **​Peripheral inhibtor of acetylcholinesterase**- increasing Ach levels so neurone can fire again Use: + **MG** SE: Bradycardia
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**Muscle Relaxants/Sedatives** (Think more sedatives and one that works in a similar way)
Use for all: **Maintain sedation & relaxed muscle tone** ***BDZ and BDZ like*** * **Temazepam**, **Zolpidem** Diazepam, Lorazepam, Midazolam * MOA: **GABA PAM Y subunit**. Open Cl- channels --\> Hyperpolarisation. **Enhanced effects of GABA** * SE: **Drowsiness, Dependence** * Interactions: **Sedatives** ***Alpha-2 agonist*** * **Dexmedetomidine** * MOA: **Alpha-2 agonist inhbits sympathetic activity** * **​**Inhibits NA release & terminates pain signals * SE: **Bradycardia** * Interactions:- ***Opioids*** * **Alfentanil, Fentanil, Remifentanil** * MOA: **Opioid receptor agonist** (Mu receptor) * ​Decreased opening VDCC --\> Decreased release Ca2+ from IC stores --\> Decreased exocytosis of transmitter vesicles. Increasing K outflow post-synaptically * SE: **Constipation, Nausea** * **​**Respiratory depression, Miosis, Conscious depression, Constipation, Addiction/ tolerence * Interactactions: **Sedatives** * **Zolpidem (Z drug) -** GABA PAM (mechanistically identical to BDZ) * USE: Anxiety- short term crisis
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**Beta lactams - Penicillins** (5) General & specific uses, interactions and adverse events
Overall MOA: **Bactericidal - cell lysis by blocking cell wall synthesis** General uses: **Resp infections, Pneumonia, H.Pylori** Adverse Effects: **Rash, Hypersensitivity** Interactions: **Warfarin, Methotrexate** * ***Flucoxacillin*** * **​SSTI** (use for **Staph** initially) * **Bone & Joint infections**- Empirical for ^ * **Penicillinase- Resistant** * ***Benzylpenicillin*** (NOT ON Y2) * **​SSTI** (use for **strep**) * **Bone & Joint infections**- Empirical for ^ * ***Amoxicillin*** * **​LRTI- CAP** * **Enhanced uptake by bacteria** * ***Co-amoxiclav*** * **​Mixed infections** (eg: chronic chest), **UTI**, **Chronic bronchitis** * **Beca Lactamase Inhibitor** * ***Penicillin*** (not on Y2) * **Tonsillitis** **​** * ***Piperacillin-Tazobactam*** * **​HAP** **​** * **Phenoxymethylpenicillin**
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**Beta lactams - Carbapenem**
* **Meropenem** MOA: **Bacteriocidal - cell lysis by blocking cell wall synthesis** Use: **Meningitis, Hospital acquired septicaemia** * Infections in ITU & Complex, multi drug resistant infections SE: **Abdominal pain, Pruritis** Interactions: -
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**Beta lactam- Cephalosporins**
* **Ceftriaxone** MOA: **Bacteriocidal - cell lysis by blocking cell wall synthesis** Uses: **Meningitis**, **Gram negative infections** * Abdominal sepsis, Ortho infection SE: **GI disturbance, Colitis** * CDAD Interactions:- **Warfarin** NOtes: Later generations (like this one) Kill more natural flora & less effective against gram +ve infections. 10% of those with penicillin allergy are allergic to this
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Antifolate Antibiotic MOA Indication Adverse reaction Interaction
**Trimethoprim** MOA: **Inhibition of dihydrofolate reductase** * Nuclotide synthesis (folic acid) prevention Indications: **UTI** (primary care) Adverse Effects: **Rash, GI disturbance** Interactions: **Methotraxate**
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**Fluoroquinolones**
* **Ciprofloxacin** MOA: **Inhibition of DNA gyrase** * Inhibition of bacterial DNA strucutre & function Use: **RTI** * UTI (secondary setting) * Gram -ve infections SE: **Nausea, Convulsions** * CDAD Interactions: **Iron salts, NSAIDS**
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**Macrolides**
* **Erythromycin** * **Azithromycin** **​**MOA: **Inhibition of bacterial protein** **synthesis** * Inhibit translation of mRNA. Inhibit bacterial protein/ RNA synthesis * Bacteriostatic Uses: **Pneumonia** * URTI, LRTI, SSTI, Atypical LRTI * SSTI in place of penicillin * Atypical LRTI ie: Legionella SE: **Gi disturbance, Headache** Interactions: **Digoxin, Theophylline, Statins**
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**Tetracyclines**
* **Doxycycline** * Tetracycline MOA: **Bacteriostatic: Inhibition of bacterial protein synthesis** * Inhibit translation of mRNA. Inhibition of RNA & bacterial protein synthesis Use: **CAP** * Atypical bacteria lacking cell wall. Eg: Chlamydia, Mycoplasma Rickettsia infections, Typhus SE: - * GI Upset- Reflux Oesophagitis, Diarrhoea & Photosensitivity Interactions: -
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Aminoglycoside
**Gentamicin** MOA: **Inhibition of bacterial protein synthesis- bacteriostatic** * Inhibits translation of mRNA. Inhibition of RNA & bacterial protein synthesis Use: **Opthalmic infections** SE:- Interactions:-
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Nitrofuran: Name MOA Indications Adverse reactions
**Nitrofurantoin** MOA: **Bacterial DNA inteference** * Bacterial DNA structure and function inhibition Uses: **UTI** in primary healthcare setting Adverse reactions: **Peripheral neuropathy** Interactions: -
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Glycopeptide
**Vancomycin** MOA: **Inhibition of cell wall synthesis in gram positive bacteria** * Cell wall inhibition Use: **C. Difficile** SE: **Neutropenia, Renal impairment** Interactions: -
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**Nitroimidazole**
* **Metronidazole** MOA: **Inhibition of bacterial DNA synthesis** * Bacteria DNA strucutre & function USE: **Anaerobic bacterial infections: leg ulcers, pressure sores** SE:- Interactions:-
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Antituberculosis drugs Names MOA Adverse reaction
**Rifampicin** & **Isoniazid** for 6 months **Ethambutol** & **Pyrazinamide** for 2 months MOA: * I, E: **Inhibition of mycobacterial cell wall synthesis** * R: **Inhibition of mycobacterial RNA synthesis** Adverse Reaction: **Hepatotoxicity** Interactions: -
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Therapeutic cytokines Name MOA Use Adverse reaction
Name: **Interferon alpha** MOA: **Activation of antiviral intracellular & immune response** Use: **HBV & HCV** Adverse reaction: **Flu-like symptoms, loss of appetite, lethargy, depression** Interactions:-
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DNA polymerase inhibitors ## Footnote Name MOA Use Adverse reaction
**Aciclovir & Ganciclovir** MOA: **Virus replication blockade** * --\> Aciclovir triphosphate. Competitively inhibits viral DNA polymerase incorporates into & terminates growing viral DNA chain & inactivates viral DNA polymerase Use: **HSV** SE: **Nausea & diarrhoea** Interactions: -
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Neuraminidase inhibitors: Name MOA Indication Adverse reaction
**Oseltamvir** MOA: **Prevention of viral budding & infectivity** ​ * Clearves N viron to release from cell thus virion starts to die Indication: **Influenza virus infection** * LRTI acute bronchitis Adverse reaction: **Nausea & vomiting** Interactions:-
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Nucleoside analogues Name MOA Use Adverse reaction
Name: **Ribavirin** MOA: **Disrupts viral RNA synthesis** Use: **HCV, RSV** Adverse reaction: - Interactions:-
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Nucleoside reverse transcriptase inhibitors Name MOA Use Adverse reaction
Name: **Tenofovir** MOA: **Blockade of viral reverse transcriptase function for viral genetic replication** Use: **HIV,** Adverse reaction: **Rash, Stevens-Johnson syndrome** Interactions:-
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Non- nucleoside reverse transcriptase inhibitor Name MOA Use Adverse reaction
Name: **Efavirenz** MOA: **Blockade of viral reverse transcriptase function for viral genetic replication** Use: **HIV** Adverse reaction: **Rash, Stevens-Johnson syndrome** Interactions:-
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Viral protease Inhibitors Name MOA Use Adverse reaction
Name: **Lopinavir** MOA: **Blockade viral protease required for virus particle assembly** Use: **HIV** Adverse reaction: **GI Bleeding** Interactions:-
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Integrase inhibitors Name MOA Use SE Interactions
Name: **Dolutegravir** MOA: **Disrupts integration of HIV genome into host chromosome** Use: **HIV** Adverse reaction: **-** Interactions:-
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Viral fusion inhibitors Name MOA Use Adverse reaction
Name: **Enfuvirtide** MOA: **Blockade of virus fusion to target cell membrane** Use: **HIV** Adverse reaction: **Pacnreatitis** Interactions:-
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Chemokine receptor/ CCR5 antagonist Name MOA Use Adverse reaction
Name: **Maraviroc** MOA: **Blockade of HIV binding to co-factor for cell entry** Use: **HIV** Adverse reaction: **Nausea & diarrhoea** Interactions:-
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Triazole anti-fungal agent Name Use MOA SE Interactions
Name: **Fluconazole** Use: **Candidia infection** MOA: **Disruption of fungal membrane function** SE: **Nausea & abdo pain** Interactions: -
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Blood glucose reducing hormone: Name Use MOA SE Interactions
Name: **Insulin** Use: **DMT1&2** MOA: **Stimulation of glucose uptake by cells** SE: **Hypoglycaemia** Interactions: **Digoxin & Beta blockers**
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Oral Biguanide ## Footnote Name Use MOA SE Interactions
Name: **Metformin** Use: **DMT2** MOA: **Increase insulin sensitivity- decreases hepatic gluconeogenesis, lipolysis, beta oxidation** * Rise in cytosolic [NADH] (from inhibition of mitochondrial glycerol-3-phosphate dehydrogenase) prevents lactate & glycerol --\> glucose SE: **N&V** * Diarrhoea, Lactic acidosis Interactions: **Diuretics, digoxin** Notes- Cardioprotective & anticancer effects
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Sulphonylureas ## Footnote Name Use MOA SE Interactions
Name: **Gliclazide** Use: **DMT2** MOA: **Stimulates pancreatic insulin secretion** * Closes K+ channels (by glucose independent mechanism). Depolarisation results in Ca++ SE: **Hypoglycaemia** Interactions: **Warfarin, NSAIDS**
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Thiazolidinediones ## Footnote Name Use MOA SE Interactions
Name: **Pioglitazone** Use: **DMT2** MOA: **Increases insulin sensitivity in muscle & adipose tissue** * Increases Beta cell preservation SE: **Weight gain,** MI, HF Interactions: NA
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GLP (Glucagon like peptide 1 receptor agonist) Name Use MOA SE Interactions
Name: **Exenatide** Use: **DMT2** MOA: **Incretin analogue- improves glucose control** SE: **Asthenia** * cardiac & cancer effects Interactions: NA
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Dipeptidyl peptidase-4 inhibitor ## Footnote Name Use MOA SE Interactions
Name: **Sitagliptin** Use: **DMT2** MOA: **Reduces inactivation of incretins** SE: **Headache** * cardiac & cancer effects Interactions: NA
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Lipase inhibitor ## Footnote Name Use MOA SE Interactions
Name: **Orlistat** Use: **Obesity especially in DMT2** MOA: **Inhibition of GI uptake of dietary fat** SE: **Oily stools, faecal urgency** Interactions: NA
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**Thyroid Hormones**
* **Levothyroxine (Synthetic T4)** * **Liothyonine (Synthetic T3)** Use: **Hypothyroidism** MOA: **Synthetic hormone-** Activation of Thyroid Hormone Receptor * Mimics thyroid hormone by binding to incracellular alpha & beta thryoid receptors SE: **Diarrhoea, Vomiting** Interactions: **Oral anticoagulation**
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Antiproliferative agent DMARDS (Y2) Name MOA Use SE Interactions
Name: **Methotreaxte** MOA: **Inhibition of dihydrofolate reductase & DNA synthesis for lymphocyte proliferation** Use: **RA** SE: **Nausea,** **Hair loss** * Increased infection risk * Teratogenic; GI: Mouth Ulcers, Nausea, Diarrhoea * Hair loss Interactions: **Warfarin, Corticosteroids**
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Antimetabolite Immunosuprresant ## Footnote Name MOA Use SE Interactions
Name: **Azathioprine** MOA: **Unclear- possible inhibition of DNA synthesis & lymphocyte proliferation** * Purine antagonist Use: **RA & Crohn’s** SE: **Alopecia** * + (increased infeciton risk, teratogenic, mouth ulcers, nausea, diarrhoea) Interactions: N/a
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Cytokine modulators Name MOA Use SE Interactions
Name: **Adalimumab, Etanercept, Infliximab** MOA: **TNF alpha blocker** Use: **RA** SE: **Infections** Interactions: NA
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**Aminosalicylates**
* **Sulphasalazine****​** * **Mesalazine** MOA: **Mechanism unclear - possible COX inhibition. Possible free radical scavenging. T cell supression** Use: **RA, Crohn's** SE: **Nausea** Interactions: **Digoxin & Warfarin**
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**Oral combination pill contraceptives**
* **Desogestrel** & **Ethinyl- estradiol** Uses: **Hormonal Contraception, PCOS** * Dysmenorrhea, Menorrhagia MOA: **Mimics ovulation- reduces FSH** * (Low oestrogen has negative effect on AP inhibiting LH. Progesterone has negative effect on AP- inhibits LH & FSH) * MOA Molecular: Act on Oestrogen & Progesterone Receptors = INTRACEULLAR TRANSCRIPTION FACTORs- ER⍺and ERβ (Oestrogen) and PR-A, PR-B(Progesterone) * Steroid hormones = Hydrophobic molecules therefore diffuse across cell membrane to IC receptors * Hormone binding drives Receptor Activation viadissociation from HSP90 * Active Receptor Dimersform --\> Cell Nucleus & Influence Gene expression SE: **Weight gain, Depression, DVT** * Breakthrough bleeding, Nausea, Depression, Increased CV Risk (Oestrogen): IHD, Riased BP, THromboembolism, Stroke, Slight Breast Cancer risk w/ long term use Interactions:-
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**Oral mini-pill contraceptives**
* **Desogestrel** * **Levonorgestrel** (emergency) MOA: **Mimics ovulation. Reduces LH & FSH. Endometrial changes** * Suppresses ovulation (negative feedback AP for LH and FSH) * Endometrium: Inhibits endometrial growth & makes mucus thicker preventing sperm/egg interaction *Cellular MOA:* * Intracellular Transcription Fractors: PR-A, PR-B * Steroid hormones = Hydrophobic molecules therefore diffuse across cell membrane to IC receptors * Hormone binding drives Receptor Activation via dissociation from HSP90 * Active Receptor Dimers form --\> Cell Nucleus & Influence Gene expression * Uses:* **Hormonal Contracpetion** * Dysmenorrhagia, Menorrhagia, Emergency contraception * SEs:* **Depression** * Slight increased risk of thrombotic events (stroke, DVT) and breast cancer. Breakthrough bleeding, Nausea, Vomiting Interactions: -
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**Implants/injectible contraceptives**
* **Etonogestrel** (long acting progesterone) MOA: **Mimics ovulation: reduces LH & FSH** * Moderate/high dose progesterone causing HPO ihibition suppresses ovulation. Also has mucus/endometrial effects. SEs: **Weight gain, Depression** * nausea, breakthrough bleeding Interactions:-
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**Hormone Replacement Therapy (HRT)**
* **Estradiol** * **Norethisterone** * **Medroxyprogesterone** MOA: **Restore decreased hormone level & function** * Molecules cross membrane and bind to Intraceullar receeptors (INTRACEULLAR TRANSCRIPTION FACTORS)- ERalpha & ERbeta or PR-A & PR B. Binding drives Receptor Acitvation via dissociation from HSP90. Active Receptor Dimer forms --\> Cell nucleus & inflences gene expression. Uses: **Menopause** * Treats symptoms of menopause- hot flushes, vaginal dryness, sweats, loss of libido and reduces risk of osteoporosis. * Combination w/ Progestin avoid cystic endometrial hyperplasia SEs: **Weight gain, Depression** * Thromboembolism, Stroke. Breakthrough Bleeding, BReast tenderness, Increased breast cancer risk, Increased dementia risk \>65yrs Interactions:-
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**Drugs used to induce labour** **(vaginal administration)**
* **Dinoprostone** (Prostaglandin E2 aka PGE2) MOA: **Stimulates cervical ripening** Use: **Delay in labour** SE: - Interactions:-
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**Drugs used to augment labour** **(IV administration)**
* **Oxytocin** MOA: **Stimulate uterine contractions** Use: **Delay in labour** * delivery of the placenta in 3rd stage of labour SE: **Nausea, Arrythmia** Interactions:-
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Antiprogesterone/ PG for medical termination
**Mifepristone with Misoprostol** ## Footnote MOA: **Steroidal antiprogesterone in combination with synthetic PG** Use: Termination in pregnancy SE: GI cramps, Uterine contractions, Vaginal bleeding Interactions: -
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Antifibrinolytic for menorrhagia
**TXA** ## Footnote MOA: Inhibits fibrin clot breakdown by plasmin Use: Menorrhagia SE: Nausea Interactions: -
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NSAID for dysmenorrhoea
**Mefanamic acid** ## Footnote MOA: **Inhibition of PG synthesis** Use: **Dysmenorrhoea** SE: **GI bleeding** Interactions:-
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**Theraputic hormones** (tx bone & calcium homeostasis for increased calcium)
**Calcitonin​** MOA: **Inhibits mobilisation of calcium from bones** * Decreases Ca2+ and PO4 reabsorption in the kidneys, inhibits bone reabsorption by preventing osteoclast action (↓ serum Ca2+ and PO4) Indications: **Osteoporosis, Hypercalcaemia** SE: **Abdominal pain** Interactions: **Antacids**
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Bisphosphonates
Alendronate, Pamidronate MOA: **Inhibits osteoclast function & bone resorption** * Slow rate of bone remodelling: * Absorbed onto hydroxyapatite crystals * When osteoclasts begin to resorb that bone with bisphosphonate, bisphosphonate released & impairs osteoclast ability to form ruffled border to adhere to bony surface & produce protons necessary for bone resorption * Can also decrease osteoclast progenitor development & recruitment * Can promote osteoclast apoptosis Indications: **Osteoporosis, Hypercalcaemia** SE: - Interactions: -
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**Drugs used in the management of hypocalcaemia**
**IV calcium gluconate, Vitamin D, Parathyroid hormone** MOA: **Restoration of calicum levels & metabolism** * IV calcium gluconate * **​**Replaces lost calcium in the body * Vitamin D * vit D in activ form Calcitriol prevents Ca2+ and PO4 excretion from the kidney and increases reabsorption in the intestines Indications: **Hypocalcaemia, Bone loss** SE: **-** Interactions:-
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**Drugs used in the management of vitamin D deficiency**
* **Vitamin D (colecalciferol, calcitriol, 1,25-dihydroxyvitamin D)** MOA: **Restoration vitamin D levels** * Replaces vit D - active form Calcitriol prevents Ca2+ and PO4 excretion from the kidney and increases reabsorption in the intestines. Indications: **Vitamin D deficiency** SE: - Interactions: -
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Selective oestrogen receptor modulators for osteoporosis
Raloxifene MOA: **Stimulation of oestrogen function in bone** * Inhibition of release of Ca from bone & Inhibition of Osteoclast activity * Agonist: stimulate bone formation * Antagonist to receptors in breast & uterine tissue Indications: Prevention of bone fractures SE: Hot flushes Interactions: Warfarin
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Monoclonal antibody (bone & calcium homeostasis)
Denosumab MOA: **Inhibition of osteoclast function & bone resorption** * Monoclonal antibody (similar to OPG which binds to RANKL- from OB to prevent RANKL attaching to RANK on OC) * Inhibits osteoclast formation, function & survival Indications: Osteoporosis SE: Hypocalcaemia Interactions: -
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Treatment for UTI MDR organism | (not on drugs list)
Ertapenem
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Glucocorticoids (in the context of the immune system) ## Footnote Name MOA Use SE Interactions
Name: **Prednisolone, Hydrocortisone, Dexamethasone** MOA: **Intracellular transcription factor interactions, gene expressions (inhibition). Inhibit production of IL-1 to 8 & TNF-alpha** Use: **Suppression of inflammatory diseases (RA, crohn’s, UC)** SE: **Weight gain, Muscle atrophy** Interactions: **PO antidiabetics**
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Calcinerurin Inhibitor ## Footnote Name MOA Use SE Interactions
Name: **Cyclosporin, Tacrolimus** MOA: **Inhibition of T cell signalling- inhibits function or maturation** Use: **Solid organ transplant to prevent rejection & Eczema** SE: **HTN** Interactions: **Aspirin**
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Immune system: Anti-histamine
Name: Chlorphenamine MOA: H1 histamine receptor blockade Use: Hay fever, Urticaria SE: Dry mouth, Sedation Interactions: TCA
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Classical Alkylating agents ## Footnote Name MOA Use SE Interactions
Name: **Cyclophosphamide** MOA: **​Cross linkage and damage to DNA** Use: **Broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions: NA
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Taxanes ## Footnote Name MOA Use SE Interactions
Name: **Paclitaxel, Docetaxel** MOA: **Inhibition of microtubule assembly in mitotic spindle** Use: **Broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions: -
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Vinca alkaloids ## Footnote Name MOA Use SE Interactions
Name: **Vincristine, Vinblastine** MOA: **Inhibition of microtubule assembly in mitotic spindle** Use: **broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions: -
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Antifolates Name MOA Use SE Interactions
Name: M**ethotraxate** MOA: **Inhibition of dihydrofolate reducatase and DNA synthesis** Use: **Broad spectrum of malignancies and RA** SE: **Increased infection risk, Teratogenic, GI: Mouth Ulcers, Nausea, Diarrhoea; Hair loss** Interactions: -
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Antipyramidines Name MOA Use SE Interactions
Name: **Fluorouracil, Cytarabine** MOA: **Inhibition of RNA and DNA synthesis** Use: **Broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions:-
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Antipurines Name MOA Use SE Interactions
Name: **Mercaptopurine, Thioguanine** MOA: **Inhibition of RNA & DNA synthesis** Use: **Broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions: -
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Anthracyclines antibodies Name MOA Use SE Interactions
Name: **Doxorubicin** MOA: **DNA intercalation. Inhibition of RNA & DNA synthesis** Use: **Broad spectrum of malignancies** SE: **Hair loss, bone marrow suppression & nausea** Interactions: -
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Antineoplastic monocolonal antibodies Name MOA Use SE Interactions
Name: **Trastuzumab, Rituximab, Nivolumab** MOA: * **Target cells overexpressing Human epidermal growth factor- 2 (HER2) for tumour reduction & destruction** * **Bind & Block proinflammatory function CD20 on B cells** * **Stimulation of anti-tumor responses via blocking PD-1** Use: * **Early breast cancer** * **Follicular lymphoma, Non-hodgkin’s lymphoma,** Rejection, RA, SLE * **Melanoma** SE: * **Fever and chills** * **Fever and chills** * **-** Interactions: -
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Immunomodulators Name MOA Use SE Interactions
Name: **Lenolidamide** MOA: **Stimulation of T cell response** Use: **Myeloma** SE: **Foetal risk** Interactions: -
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SERMs (anti-neoplastic) Name MOA Use SE Interactions
Name: **Tamoxifen** MOA: **Inhibition of ER function & cell proliferation in breast.** Partial Agonist of Oestrogen Receptors. Inhibition of release of Ca from bone & Inhibition of Osteoclast activity * Agonist: Stimulate bone formation * Antagonist to receptors in: Breast & Uterine tissue Use: **Breast cancer** & osteoporosis SE: * Thromboembolism, Stroke * Breakthrough bleeding, Breast Tenderness * Increased Breast Cancer Risk * Increased Dementia Risk \>65yrs Interactions: -
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LHRH receptor agonist Name MOA Use SE Interactions
Name: **Goserelin** MOA: **Synthetic analogue of LHRH. Activates LHRH receptor function --\> sustained testosterone reduction** Use: **prostate cancer** SE: - Interactions: -
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Oral iron compound ## Footnote Name Use MOA SE Interactions
Name: **Ferrous sulphate** Use: **Iron deficient anaemia** MOA: **Iron Provision** SE: **Constipation** Interactions: **Antacids**
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Water soluable vitamin to treat folate deficient anaemia ## Footnote **Name** **Use** **MOA** **SE** **Interactions**
Name: **Folic Acid (B9)** Use: **Folate deficient anaemia** MOA: **Supports nucleic acid synthesis** SE: - Interactions:-
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Water soluable vitamin to treat pernicious anaemia Name Use MOA SE Interactions
Name: Vitamin B12 parenteral Use: Pernicious anaemia MOA: Enzyme co-factors SE:- Interactions: -
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Class I-IV anti-arrythmic drugs, broadly what are they?
Class I: Sodium channel blockers Class II: Beta blockers Class III: Potassium channel blockers Class Iv: Calcium channel blockers (phenylalkylamine & benzothiazepine subclasses)
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Class I- sodium channel blockers | (include subclasses)
MOA: **Voltage sensitive sodium channels blockage- *prolonged QT interval, increase QRS duration*** SE: **Oedema** Interactions:- **Class 1a:** * *Name*: **Disopyramide, Quinidine** * *MOA extra:* Delays depolarisiation * *Use:* **Ventricular & Supraventricular arrhythmias** **Class 1b)** * *Name*: **Lidocaine** * *MOA extra:* Blocks sodium channel in actively depolaring cells. AP shortened * *Use:* **CPR used IV** **Class 1c)** * *Name*: **Flecainide, Propafenone** * *MOA extra:* Slight reduction in phase 0, no change in AP duration * *Use:* **Paroxysmal AF & ventricular ectopic beats-**"pill in pocket"
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Class II- beta blockers
**Atenolol** (beta-1), **Bisoprolol** (beta-1), **Metoprolol** MOA: **Beta- adrenergic receptor blockade-**reducation in adrenergic effects on rate & intropy Use: **Proplylaxis of paroxysmal atiral tachy or AF** SE: **Hypotension** Interactions: **NSAIDs, Digoxin** *From CVS section* 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
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Class III- Potassium channel blockers
**Amiodarone, Dronedarone, Sotalol** (has so beta blocker activity) ## Footnote MOA: **Potassium channel blockade & caclium channel blocker properties- *prolonged QT interval*** (delay repolarisation) Use: **Supraventricular, nodal & ventricular tacharrythmias, AF** SE: **N&V** Interactions: -
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Class IV: Calcium channel blockers (phenylalkylamine & benzothiazepine subclasses)
**Verapamil, Diltiazem** MOA: **Calcium channel blockade- *reduction of AP & cardiac output*** * Reduces amplitude of phase 2- reduced intracellular calcium thus -ve inotropic on myocytes Use: **SVT (especially paroxysmal)** SE: **Hypotension (verapamil), Constipation (diltiazaem)** Interactions:-
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Cardiac Glycosides
**Digoxin** MOA: **Reduces conductivity of AVN** Use: **Arrythmias- AF, CHF** SE: **Fatigue & Nausea** Interaction:-
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Adenosine
**Adenosine** MOA: **Activates adenosine receptors --\> hyperpolarization & slows conduction through AVN** * Binds A1 receptors in pacemaker tissues. Inhibts AC, reduces cAMP, K+ efflux increases --\> hyperpolarised cells Use: **SVT** SE: **Nausea** Interactions: * CONTRAINDICATED- **obstructive airway disease**
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Antimuscarinic- antiarryhtmetic
**Atropine** MOA: **Blockade of vagal muscarining Ach receptors** * Blocks type M2 Ach receptors on cardiomyocytes * Inhibits PS effects- cholinergic vagus transmission exerting negative chronotropy * Atropine accelerate repolarisation in cardiac muscle Use: **Emergency bradycardia** SE: **Urinary rentention** Interactions:-
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Magnesium
**Magnsium sulphate (IV)** MOA: **Unclear. Aleration of Na+, K+, Ca2+ ion balance via channels & transporters** * Stabalise AP Use: **Emergency arrythmias, IV emergency in asthma** SE: **Electrolyte irregularities** Interactions:-
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Anti emetics H1-receptor antagonist
**Cyclizine** MOA: **Histamine H1 receptor blockade** Use: **Nausea, Vomiting** SE: **Dry mouth, Sedation** Interactions: **Sedatives**
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Anti emetics D2 receptor antagonist
**Domperidone** MOA: **Dopamine D2 receptor blockade in chemoreceptor trigger zone** Use: **Nausea & Vomiting** SE: **Cardiac disease**
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**Urinary anti-spasmodic (anti-muscarinic)**
* **Oxybutinin** MOA: **Competitively** antagonizes the **muscarinic 2/3 acetylcholine receptor** leading to **smooth muscle relaxation** and reduction of bladder detrusor activity Use: **OAB** SE: **Dry Mouth, Tachycardia** (preceded by transient bradycardia) * Blurred vision, Constipation, , Urinary Retention
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Alpha 1 blocker (altered voiding)
Tamulosin ## Footnote MOA: Smooth muscle relxant aciting on bladder neck Indication: BPH, urinary retention SE: Dizziness Interactions: Hypotensive drugs
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Beta-3 agonist
Mirabegron ## Footnote MOA: Stimulates beta-3 adrenergic receptors --\> detrusor smooth muscle relaxation Indication: OAB SE: Bladder pain Interactions: -
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Anti Androgen
**Finasteride** MOA: **Inhibits synthesis of dihydrotestosterone** Use: **BPH** SE: **Impotence** Interactions: -