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Kim's Drug List > Y2 Drugs List > Flashcards

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
Q

Nitrate Vasodilators

A
  • 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

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26
Q

Sympathomimetics

A
  • 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:-

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27
Q

Antiplatelet Drugs (2)

A

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

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28
Q

Anticoagulants (4)

Name the 4 classes

A
  • Comarin- Warfarin
  • Direct thrombin inhibitors- Dabigatran
  • Direct FXa inhibitors- Apixaban, Edoxaban, Rivarozaban
  • Heparins- Deltaparin, Tinzaparin, Enoxaparin (LMWH), Unfractionated heparin
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29
Q

Anticoagulants- Comarin

A

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)

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30
Q

Anticoagulants- Direct Thrombin inhibitors

A

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: -

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31
Q

Anticoagulants- direct FXa inhibitors

A

Apixaban, Edoxaban, Rivaroxaban

MOA: Inhibition FXa in coagulation cascade

Use: Prophylaxis of stroke from AF; DVT

SE: Abnormal bleeding

Interactions: -

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32
Q

Anticoagulants- Heparins

A

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:-

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33
Q

Thrombolytics/ Fibrinolytics

A
  • 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: -

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34
Q

HMG-CoA Reductase Inhibitors

(statins)

A
  • 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

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35
Q

B2-Adrenergic Agonists

(tx of airway disease)

A
  • 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

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36
Q

Anti-muscarinics

(Airways)

A
  • 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:-

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37
Q

Methylxanthines

A
  • 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

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38
Q

Glucocorticoids

(Airways)

A
  • 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

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39
Q

Leukotriene Antagonists

A
  • 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

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40
Q

Mucolytic

Name

Use

MOA

A

Name: Dornase Alfa

Use: CF

MOA: Synthetic DNAse 1- breakdown of extracellular DNA to reduce sputum viscosity

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41
Q

Dopaminergics

(pharma basal ganglia disorders)

A

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

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42
Q

Dopa-decarboxylase inhibitor

A
  • 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: -

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43
Q

MAOIB Inhibitor

(Monoamine oxidase inhibitors, B form inhibitor)

A
  • Rasagiline
  • Selegiline

MOA: Inhibits MAOIB breakdown of dopamine in the CNS

Use: PD

  • Adjunct with levodopa/carbidopa for Parkonsonism

SE: -

Interactions: -

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44
Q

COMT inhibitor

(catechol-O-methyl transferase inhibitor)

A
  • 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:-

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45
Q

Anticholinergics

(BG disorders)

A
  • 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:-

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46
Q

Dopamine-depleting Drugs

A
  • 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: -

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47
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A
  • 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

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48
Q

MAOIs Type A

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: -

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49
Q

Tricyclic Antidepressants

A
  • 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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50
Q

Atypical Antidepressants

A

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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51
Q

1st generation (classical) Anti-psychotic

A
  • 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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52
Q

2nd generation (Atypical) Antipsychotics

A

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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53
Q

Mood Stabiliser

A
  • 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

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54
Q

Anticholinesterases

(for dementia)

A
  • Donepezil
  • Galantamine
  • Rivastigmine

MOA: Inhibitor of acetylcholinesterase (reversible)

Use: mild- moderate AD

SE: N&V

Interactions: -

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55
Q

Glutamate NDMA receptor antagonists

A
  • 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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56
Q

Anti-Epilepsy drugs (AEDs)

A

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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57
Q

Benzodiazepines

A
  • 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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58
Q

Benzodiazepine

(Antagonist)

A
  • Flumazenil

MOA: Antagonises GABA signalling

Use: Reversal of BDZ signalling

SE:-

Interactions:-

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59
Q

Non-benzodiazepine Hypnotics

A

Zopiclone

MOA: Enhances GABA binding to GABA-A receptors

Use: Insomnia

SE:-

Interactions:-

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60
Q

Barbituates (Barb)

A
  • 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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61
Q

Weak analgesic/Antipyretic

A
  • 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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62
Q

NSAIDs

A
  • 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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63
Q

COX-2 selective NSAIDs

A
  • 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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64
Q

Weak opioid analgesics

A
  • 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)

65
Q

Strong Opioid Analgesics

A
  • 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
66
Q

Partial/Mixed Agonist opioid analgesics

A
  • 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
67
Q

Opioid receptor antagonists

A
  • 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: -

68
Q

Drugs used to manage opioid addiction

A
  • Methadone
  • Buprenorphine

MOA:

Narcotic opioid replacement (M)

  • Mu receptor, longer lasting.

Opioid receptor 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
69
Q

Drugs to treat neuropathic pain

+ 4 types of neuropathic pain?

A
  • 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
70
Q

Inhaled analgesics

Name

Use

MOA

SE

Interactions

A

Name: NO & oxygen mixture (Gas & air)

Use: Analgesia during childbirth

MOA: Unclear

SE: Decreased vitamin B12 synthesis

Interactions: -

71
Q

General Anaethetic

A

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

72
Q

Local Anaesthetic

A
  • 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: -

73
Q

Neuromuscular blockers

A

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

74
Q

Drugs used to reverse NMB block

A

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

75
Q

Muscle Relaxants/Sedatives

(Think more sedatives and one that works in a similar way)

A

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
76
Q

Beta lactams - Penicillins (5)

General & specific uses, interactions and adverse events

A

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
77
Q

Beta lactams - Carbapenem

A
  • 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: -

78
Q

Beta lactam- Cephalosporins

A
  • 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

79
Q

Antifolate Antibiotic

MOA

Indication

Adverse reaction

Interaction

A

Trimethoprim

MOA: Inhibition of dihydrofolate reductase

  • Nuclotide synthesis (folic acid) prevention

Indications: UTI (primary care)

Adverse Effects: Rash, GI disturbance

Interactions: Methotraxate

80
Q

Fluoroquinolones

A
  • 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

81
Q

Macrolides

A
  • 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

82
Q

Tetracyclines

A
  • 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: -

83
Q

Aminoglycoside

A

Gentamicin

MOA: Inhibition of bacterial protein synthesis- bacteriostatic

  • Inhibits translation of mRNA. Inhibition of RNA & bacterial protein synthesis

Use: Opthalmic infections

SE:-

Interactions:-

84
Q

Nitrofuran:

Name

MOA

Indications

Adverse reactions

A

Nitrofurantoin

MOA: Bacterial DNA inteference

  • Bacterial DNA structure and function inhibition

Uses: UTI in primary healthcare setting

Adverse reactions: Peripheral neuropathy

Interactions: -

85
Q

Glycopeptide

A

Vancomycin

MOA: Inhibition of cell wall synthesis in gram positive bacteria

  • Cell wall inhibition

Use: C. Difficile

SE: Neutropenia, Renal impairment

Interactions: -

86
Q

Nitroimidazole

A
  • Metronidazole

MOA: Inhibition of bacterial DNA synthesis

  • Bacteria DNA strucutre & function

USE: Anaerobic bacterial infections: leg ulcers, pressure sores

SE:-

Interactions:-

87
Q

Antituberculosis drugs

Names

MOA

Adverse reaction

A

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: -

88
Q

Therapeutic cytokines

Name

MOA

Use

Adverse reaction

A

Name: Interferon alpha

MOA: Activation of antiviral intracellular & immune response

Use: HBV & HCV

Adverse reaction: Flu-like symptoms, loss of appetite, lethargy, depression

Interactions:-

89
Q

DNA polymerase inhibitors

Name

MOA

Use

Adverse reaction

A

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: -

90
Q

Neuraminidase inhibitors:

Name

MOA

Indication

Adverse reaction

A

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:-

91
Q

Nucleoside analogues

Name

MOA

Use

Adverse reaction

A

Name: Ribavirin

MOA: Disrupts viral RNA synthesis

Use: HCV, RSV

Adverse reaction: -

Interactions:-

92
Q

Nucleoside reverse transcriptase inhibitors

Name

MOA

Use

Adverse reaction

A

Name: Tenofovir

MOA: Blockade of viral reverse transcriptase function for viral genetic replication

Use: HIV,

Adverse reaction: Rash, Stevens-Johnson syndrome

Interactions:-

93
Q

Non- nucleoside reverse transcriptase inhibitor

Name

MOA

Use

Adverse reaction

A

Name: Efavirenz

MOA: Blockade of viral reverse transcriptase function for viral genetic replication

Use: HIV

Adverse reaction: Rash, Stevens-Johnson syndrome

Interactions:-

94
Q

Viral protease Inhibitors

Name

MOA

Use

Adverse reaction

A

Name: Lopinavir

MOA: Blockade viral protease required for virus particle assembly

Use: HIV

Adverse reaction: GI Bleeding

Interactions:-

95
Q

Integrase inhibitors

Name

MOA

Use

SE

Interactions

A

Name: Dolutegravir

MOA: Disrupts integration of HIV genome into host chromosome

Use: HIV

Adverse reaction: -

Interactions:-

96
Q

Viral fusion inhibitors

Name

MOA

Use

Adverse reaction

A

Name: Enfuvirtide

MOA: Blockade of virus fusion to target cell membrane

Use: HIV

Adverse reaction: Pacnreatitis

Interactions:-

97
Q

Chemokine receptor/ CCR5 antagonist

Name

MOA

Use

Adverse reaction

A

Name: Maraviroc

MOA: Blockade of HIV binding to co-factor for cell entry

Use: HIV

Adverse reaction: Nausea & diarrhoea

Interactions:-

98
Q

Triazole anti-fungal agent

Name

Use

MOA

SE

Interactions

A

Name: Fluconazole

Use: Candidia infection

MOA: Disruption of fungal membrane function

SE: Nausea & abdo pain

Interactions: -

99
Q

Blood glucose reducing hormone:

Name

Use

MOA

SE

Interactions

A

Name: Insulin

Use: DMT1&2

MOA: Stimulation of glucose uptake by cells

SE: Hypoglycaemia

Interactions: Digoxin & Beta blockers

100
Q

Oral Biguanide

Name

Use

MOA

SE

Interactions

A

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

101
Q

Sulphonylureas

Name

Use

MOA

SE

Interactions

A

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

102
Q

Thiazolidinediones

Name

Use

MOA

SE

Interactions

A

Name: Pioglitazone

Use: DMT2

MOA: Increases insulin sensitivity in muscle & adipose tissue

  • Increases Beta cell preservation

SE: Weight gain, MI, HF

Interactions: NA

103
Q

GLP (Glucagon like peptide 1 receptor agonist)

Name

Use

MOA

SE

Interactions

A

Name: Exenatide

Use: DMT2

MOA: Incretin analogue- improves glucose control

SE: Asthenia

  • cardiac & cancer effects

Interactions: NA

104
Q

Dipeptidyl peptidase-4 inhibitor

Name

Use

MOA

SE

Interactions

A

Name: Sitagliptin

Use: DMT2

MOA: Reduces inactivation of incretins

SE: Headache

  • cardiac & cancer effects

Interactions: NA

105
Q

Lipase inhibitor

Name

Use

MOA

SE

Interactions

A

Name: Orlistat

Use: Obesity especially in DMT2

MOA: Inhibition of GI uptake of dietary fat

SE: Oily stools, faecal urgency

Interactions: NA

106
Q

Thyroid Hormones

A
  • 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

107
Q

Antiproliferative agent DMARDS (Y2)

Name

MOA

Use

SE

Interactions

A

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

108
Q

Antimetabolite Immunosuprresant

Name

MOA

Use

SE

Interactions

A

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

109
Q

Cytokine modulators

Name

MOA

Use

SE

Interactions

A

Name: Adalimumab, Etanercept, Infliximab

MOA: TNF alpha blocker

Use: RA

SE: Infections

Interactions: NA

110
Q

Aminosalicylates

A
  • Sulphasalazine​
  • Mesalazine

MOA: Mechanism unclear - possible COX inhibition. Possible free radical scavenging. T cell supression

Use: RA, Crohn’s

SE: Nausea

Interactions: Digoxin & Warfarin

111
Q

Oral combination pill contraceptives

A
  • 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:-

112
Q

Oral mini-pill contraceptives

A
  • 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: -

113
Q

Implants/injectible contraceptives

A
  • 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:-

114
Q

Hormone Replacement Therapy (HRT)

A
  • 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:-

115
Q

Drugs used to induce labour

(vaginal administration)

A
  • Dinoprostone (Prostaglandin E2 aka PGE2)

MOA: Stimulates cervical ripening

Use: Delay in labour

SE: -

Interactions:-

116
Q

Drugs used to augment labour

(IV administration)

A
  • Oxytocin

MOA: Stimulate uterine contractions

Use: Delay in labour

  • delivery of the placenta in 3rd stage of labour

SE: Nausea, Arrythmia

Interactions:-

117
Q

Antiprogesterone/ PG for medical termination

A

Mifepristone with Misoprostol

MOA: Steroidal antiprogesterone in combination with synthetic PG

Use: Termination in pregnancy

SE: GI cramps, Uterine contractions, Vaginal bleeding

Interactions: -

118
Q

Antifibrinolytic for menorrhagia

A

TXA

MOA: Inhibits fibrin clot breakdown by plasmin

Use: Menorrhagia

SE: Nausea

Interactions: -

119
Q

NSAID for dysmenorrhoea

A

Mefanamic acid

MOA: Inhibition of PG synthesis

Use: Dysmenorrhoea

SE: GI bleeding

Interactions:-

120
Q

Theraputic hormones

(tx bone & calcium homeostasis for increased calcium)

A

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

121
Q

Bisphosphonates

A

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: -

122
Q

Drugs used in the management of hypocalcaemia

A

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:-

123
Q

Drugs used in the management of vitamin D deficiency

A
  • 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: -

124
Q

Selective oestrogen receptor modulators for osteoporosis

A

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

125
Q

Monoclonal antibody (bone & calcium homeostasis)

A

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: -

126
Q

Treatment for UTI MDR organism

(not on drugs list)

A

Ertapenem

127
Q

Glucocorticoids (in the context of the immune system)

Name

MOA

Use

SE

Interactions

A

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

128
Q

Calcinerurin Inhibitor

Name

MOA

Use

SE

Interactions

A

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

129
Q

Immune system: Anti-histamine

A

Name: Chlorphenamine

MOA: H1 histamine receptor blockade

Use: Hay fever, Urticaria

SE: Dry mouth, Sedation

Interactions: TCA

130
Q

Classical Alkylating agents

Name

MOA

Use

SE

Interactions

A

Name: Cyclophosphamide

MOA: ​Cross linkage and damage to DNA

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: NA

131
Q

Taxanes

Name

MOA

Use

SE

Interactions

A

Name: Paclitaxel, Docetaxel

MOA: Inhibition of microtubule assembly in mitotic spindle

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

132
Q

Vinca alkaloids

Name

MOA

Use

SE

Interactions

A

Name: Vincristine, Vinblastine

MOA: Inhibition of microtubule assembly in mitotic spindle

Use: broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

133
Q

Antifolates

Name

MOA

Use

SE

Interactions

A

Name: Methotraxate

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: -

134
Q

Antipyramidines

Name

MOA

Use

SE

Interactions

A

Name: Fluorouracil, Cytarabine

MOA: Inhibition of RNA and DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions:-

135
Q

Antipurines

Name

MOA

Use

SE

Interactions

A

Name: Mercaptopurine, Thioguanine

MOA: Inhibition of RNA & DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

136
Q

Anthracyclines antibodies

Name

MOA

Use

SE

Interactions

A

Name: Doxorubicin

MOA: DNA intercalation. Inhibition of RNA & DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

137
Q

Antineoplastic monocolonal antibodies

Name

MOA

Use

SE

Interactions

A

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: -

138
Q

Immunomodulators

Name

MOA

Use

SE

Interactions

A

Name: Lenolidamide

MOA: Stimulation of T cell response

Use: Myeloma

SE: Foetal risk

Interactions: -

139
Q

SERMs (anti-neoplastic)

Name

MOA

Use

SE

Interactions

A

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: -

140
Q

LHRH receptor agonist

Name

MOA

Use

SE

Interactions

A

Name: Goserelin

MOA: Synthetic analogue of LHRH. Activates LHRH receptor function –> sustained testosterone reduction

Use: prostate cancer

SE: -

Interactions: -

141
Q

Oral iron compound

Name

Use

MOA

SE

Interactions

A

Name: Ferrous sulphate

Use: Iron deficient anaemia

MOA: Iron Provision

SE: Constipation

Interactions: Antacids

142
Q

Water soluable vitamin to treat folate deficient anaemia

Name

Use

MOA

SE

Interactions

A

Name: Folic Acid (B9)

Use: Folate deficient anaemia

MOA: Supports nucleic acid synthesis

SE: -

Interactions:-

143
Q

Water soluable vitamin to treat pernicious anaemia

Name

Use

MOA

SE

Interactions

A

Name: Vitamin B12 parenteral

Use: Pernicious anaemia

MOA: Enzyme co-factors

SE:-

Interactions: -

144
Q

Class I-IV anti-arrythmic drugs, broadly what are they?

A

Class I: Sodium channel blockers

Class II: Beta blockers

Class III: Potassium channel blockers

Class Iv: Calcium channel blockers (phenylalkylamine & benzothiazepine subclasses)

145
Q

Class I- sodium channel blockers

(include subclasses)

A

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”
146
Q

Class II- beta blockers

A

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

147
Q

Class III- Potassium channel blockers

A

Amiodarone, Dronedarone, Sotalol (has so beta blocker activity)

MOA: Potassium channel blockade & caclium channel blocker properties- prolonged QT interval (delay repolarisation)

Use: Supraventricular, nodal & ventricular tacharrythmias, AF

SE: N&V

Interactions: -

148
Q

Class IV: Calcium channel blockers (phenylalkylamine & benzothiazepine subclasses)

A

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:-

149
Q

Cardiac Glycosides

A

Digoxin

MOA: Reduces conductivity of AVN

Use: Arrythmias- AF, CHF

SE: Fatigue & Nausea

Interaction:-

150
Q

Adenosine

A

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
151
Q

Antimuscarinic- antiarryhtmetic

A

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:-

152
Q

Magnesium

A

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:-

153
Q

Anti emetics H1-receptor antagonist

A

Cyclizine

MOA: Histamine H1 receptor blockade

Use: Nausea, Vomiting

SE: Dry mouth, Sedation

Interactions: Sedatives

154
Q

Anti emetics D2 receptor antagonist

A

Domperidone

MOA: Dopamine D2 receptor blockade in chemoreceptor trigger zone

Use: Nausea & Vomiting

SE: Cardiac disease

155
Q

Urinary anti-spasmodic (anti-muscarinic)

A
  • 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
156
Q

Alpha 1 blocker (altered voiding)

A

Tamulosin

MOA: Smooth muscle relxant aciting on bladder neck

Indication: BPH, urinary retention

SE: Dizziness

Interactions: Hypotensive drugs

157
Q

Beta-3 agonist

A

Mirabegron

MOA: Stimulates beta-3 adrenergic receptors –> detrusor smooth muscle relaxation

Indication: OAB

SE: Bladder pain

Interactions: -

158
Q

Anti Androgen

A

Finasteride

MOA: Inhibits synthesis of dihydrotestosterone

Use: BPH

SE: Impotence

Interactions: -

Kim's Drug List (9 decks)

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