Phase III drug list Flashcards

Question 1

Q

Antacids

Answer

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

Question 2

Q

Antacids + Alginates

Answer

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: -

Question 3

Q

H₂Receptor Antagonists

Answer

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

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

Use:* Stomach ulcers
SE:* Diziness

Interactions: -

Question 4

Q

Proton Pump Inhibitors

Answer

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

Question 5

Q

Pancreatic Enzymes

Name

Use

MOA

Answer

A

Name: Pancreatin

Use: Pancreatic insufficiency- CF & Pancreatitis

MOA: Restoration of pancreatix enzymes

Question 6

Q

Bulk Laxatives

Answer

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:-

Question 7

Q

Stimulant Purgatives (2)

Answer

A

MOA overall: Increase intestinal motility

Indication:* Constipation
SE:* Nausea
Piosulfate
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

Question 8

Q

Faecal Softeners

Answer

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: -

Question 9

Q

Osmotic Laxatives (3)

Answer

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

Question 10

Q

Opioid Anti-Motility Agents

Answer

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

SE: Nausea, Flatulence

(Chronic use = Constipation. Abdo cramps, dizziness)
Interactions:* -

Question 11

Q

Oral Rehydration Therapy

NOT SURE IF ON LIST

Answer

A

Isotonic/hypotonic solution of glucose and NaCl

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

Question 12

Q

Carbonic Anhydrase Inhibitor

Answer

A

Acetazolomide

MOA: Reduce aqueous humour production (req. HCO3- secretion)

Inhibits carbonic anhydrase in PCT to stop the reapsorption of HCO_3^- 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: -

Question 13

Q

Osmotic diuretic

Answer

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: -

Question 14

Q

Loop Diuretics

Answer

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

Question 15

Q

Thiazide Diuretics

Answer

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

Question 16

Q

Potassium Sparing Diuretics

Subclass: Aldosterone Antagonists

Answer

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^{_{+ i}}s 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

Question 17

Q

Potassium Sparing Diuretics

Subclass: ENaC Antagonists

Answer

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

Question 18

Q

ACE inhibitors

Answer

A

Ramipril, Perindopril, Lisinopril, 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

Question 19

Q

Angiotensin-II receptor antagonists/ ARBS

Answer

A

Losartan
Valsartan
Irbesartan
Candersartan

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

Question 20

Q

Renin Inhibitor

Answer

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

Use: HTN

SE; Diarrhoea, Cough

Question 21

Q

Neprilysin inhibitors

(used with an ARB drug)

Answer

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: -

Question 22

Q

Beta-adrenergic receptor antagonists

(Beta blockers)

Answer

A

Bisoprolol (Cardioselectiv B1 antag.)
Atenolol (cardioselective B1 antag.)
Metaprolol (B1 antag)
Propanolol (B1 & 2 antag.)
Labetalol (B1, B2 and Alpha-1 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

Question 23

Q

Alpha 1-adrenergic receptor antagonist (heart or prostate)

Answer

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

Question 24

Q

Alpha 2- adrenergic Agonist

Answer

A

Clonidine

Stimulates alpha 2 receptors causing vasodilation

Use: Acute HTN

SE: Constipation, Dry mouth

Question 25

Q

Calcium Channel Antagonists

(for heart failure and hypertenison)

Answer

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.)

Question 26

Q

Nitrate Vasodilators

Answer

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

Question 27

Q

Selective I(f) Current Inhibitors

Answer

A

Ivabradine

MOA: Inhibition of cardiac I(F) current in SAN

USE: Angina NSR, HF

SE: Bradycardia

Question 28

Q

Sympathomimetics

Answer

A

Noradrenaline (alpha)
Dobutamine (beta)
Adrenaline (alpha and beta)
Metraminol
Isoprenaline

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:-

Question 29

Q

Antiplatelet Drugs (2)

Answer

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, Prasugrel, Ticagrelor

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 (ACS, CVA, Angina)

Can treat CVD without affecting BP

SE: GI irritation & bleeding

Interactions: Anticoagulation drugs

The cloppy dog has 5 limbs (2+3) GPIIb and GPIIIa

Question 30

Q

Anticoagulants (4)

Name the 4 classes

Answer

A

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

Question 31

Q

Anticoagulants- Comarin

Answer

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)

Question 32

Q

Anticoagulants- Direct Thrombin inhibitors

Answer

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: Abnormal bleeding, Bruising

Interactions: -

Question 33

Q

Anticoagulants- direct FXa inhibitors

Answer

A

Apixaban, Rivaroxaban, Edoxaban

MOA: Inhibition FXa in coagulation cascade

Use: Prophylaxis of stroke from AF; DVT

SE: Abnormal bleeding

Interactions: -

Question 34

Q

Anticoagulants- Heparins

Answer

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:-

Question 35

Q

Thrombolytics/ Fibrinolytics

Answer

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: Haemorrhage, Ecchymosis, Hypotension

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: -

Question 36

Q

HMG-CoA Reductase Inhibitors

(statins)

Answer

A

Atorvastatin
Simvastatin
Rosuvastatin

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

Question 37

Q

B₂-Adrenergic Agonists

(tx of airway disease)

Answer

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

Question 38

Q

Anti-muscarinics

(Airways)

Answer

A

Ipratropium (short acting)
Tiotropium, Glycopyrronium, Aclidnium (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:-

Question 39

Q

Methylxanthines

Answer

A

Theophylline
Aminophylline

MOA: Bronchodilator, increases cAMP in smooth muscles via inhibition of PDE

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

Question 40

Q

Glucocorticoids

(Airways)

Answer

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, Throat infections with inhalers

MANY - Moon face, weight gain, osteoporosis, hyperglycaemia

Interactions: Aspirin

Question 41

Q

Leukotriene Antagonists

Answer

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

Question 42

Q

Mucolytic

Name

Use

MOA

Answer

A

Name: Dornase Alfa

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

Name: Carbocisteine

MOA: Cleavage of mucus glycoproteins to reduce sputum viscosity

Use: CF

SE: Gastric Bleeding

Question 43

Q

Dopaminergics

(pharma basal ganglia disorders)

Answer

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

Question 44

Q

Dopa-decarboxylase inhibitor

Answer

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: -

Question 45

Q

MAOI_B Inhibitor

(Monoamine oxidase inhibitors, B form inhibitor)

Answer

A

Rasagiline
Selegiline

MOA: Inhibits MAOI_B breakdown of dopamine in the CNS

Use: PD

Adjunct with levodopa/carbidopa for Parkonsonism

SE: Arrythmia

Interactions: -

Question 46

Q

COMT inhibitor

(catechol-O-methyl transferase inhibitor)

Answer

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:-

Question 47

Q

Anticholinergics

(BG disorders)

Answer

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:-

Question 48

Q

Dopamine-depleting Drugs

Answer

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: PD, Anxiety

Causes depression by decreasing 5HT and NA levels

Interactions: -

Question 49

Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

Answer

A

Sertraline
Citalopram
Fluoxetine

MOA: Inhibits 5HT reuptake pump in synaptic cleft- increases 5HT levels.

Use: Depression/ GAD

SEs: Insomnia, Nausea, Gastric bleeding, Low sodium

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

Question 50

Q

MAOIs Type A

Answer

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: -

Question 51

Q

Tricyclic Antidepressants

Answer

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: -

Question 52

Q

Atypical Antidepressants

Answer

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

Question 53

Q

1st generation (classical) Anti-psychotic

Answer

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: -

Question 54

Q

2nd generation (Atypical) Antipsychotics

Answer

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: -

Question 55

Q

Mood Stabiliser

Answer

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

Question 56

Q

Anticholinesterases

(for dementia)

Answer

A

Donepezil
Galantamine
Rivastigmine

MOA: Inhibitor of acetylcholinesterase (reversible)

Use: mild- moderate AD

SE: N&V

Interactions: -

Question 57

Q

Glutamate NDMA receptor antagonists

Answer

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: -

Question 58

Q

Anti-Epilepsy drugs (AEDs)

Answer

A

For both types:

Use: Epilepsy

SE: Nausea, Blurred vision

Interactions: Macrolide abx

Other drugs: Levetiracetam, Toprimate, Phenytoin. MOA: Decrease neuronal transmission

Sodium Valporate
Lamotrigine (1st line Focal)
Carbemazepine (1st line Focal. Can cause low sodium)

MOA: Block sodium channels in the inactivated state

Use: Epilepsy

All types of seizures except absence seizures (although sodium valproate can be used for this!)

SEs: Cognitive impairment, visual impairment, peripheral neuropathy, skin problems, (hepatotoxicity = valporate)

Ethosuximide - Ca2+ blocker

MOA: Caclium channel blocker

Targets low threshold voltage dependent T-type calcium channels

Use: Absence seizures - first line

Question 59

Q

Benzodiazepines

Answer

A

Midazolam - GABA-A PAM (Y subunit)
Lorazepam - GABA-A PAM (Y subunit)
Diazepam - GABA-A PAM (Y subunit)
Zolpidem (BDZ like): modulation of GABA-A receptor

MOA: GABA-A 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

Question 60

Q

Benzodiazepine

(Antagonist)

Answer

A

Flumazenil

MOA: Antagonises GABA signalling

Use: Reversal of BDZ signalling

SE:-

Interactions:-

Question 61

Q

Non-benzodiazepine Hypnotics

Answer

A

Zopiclone

MOA: Enhances GABA binding to GABA-A receptors

Use: Insomnia

SE:-

Interactions:-

Question 62

Q

Barbituates (Barb)

Answer

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

Question 63

Q

Weak analgesic/Antipyretic

Answer

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.

Question 64

Q

NSAIDs

Answer

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

Answer 65

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

Answer 66

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)

Answer 67

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

Answer 68

A

Buprenorphrine
Tramadol
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

Answer 69

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: -

Answer 70

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

Answer 71

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

Answer 72

A

Name: NO & oxygen mixture (Gas & air)

Use: Analgesia during childbirth

MOA: Unclear

SE: Decreased vitamin B12 synthesis

Interactions: -

Answer 73

A

Sumatriptan, Tomprimate

MOA:

S = Stimulation of 5HT receptors
T= Blockade of voltage gated sodium & potassium channels

Use:

S- Onset

T- Prophylaxis

SE: Flushing, Asthma

Answer 74

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

Answer 75

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: -

Answer 76

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

Answer 77

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

Answer 78

A

Use for all: Maintain sedation & relaxed muscle tone

BDZ and BDZ like

Temazepam, Zolpidem Diazepam, Lorazepam, Midazolam
MOA: GABA-A (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

Answer 79

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

Answer 80

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: -

Answer 81

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

Answer 82

A

Trimethoprim

MOA: Inhibition of dihydrofolate reductase

Nuclotide synthesis (folic acid) prevention

Indications: UTI (primary care)

Adverse Effects: Rash, GI disturbance

Interactions: Methotraxate

Answer 83

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

Answer 84

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, Mycoplasma
- Chlamydia in pregnancy

SE: Gi disturbance, Headache

Interactions: Digoxin, Theophylline, Statins

Affects drugs metabolised by CYP by inhibition thus increasing amount (warfarin, statins)
Caution in drugs that affect QT interval

Answer 85

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
+ve & -ve Bacteria

SE: Photosensitivity

GI Upset- Reflux Oesophagitis, Diarrhoea
Discolouration of tooth enammel in children

Interactions: -

Notes: Do not give in pregnancy, breast feeding or U12

Answer 86

A

Gentamicin

MOA: Inhibition of bacterial protein synthesis- bacteriostatic

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

Use: Opthalmic infections

SE:-

Interactions:-

Answer 87

A

Nitrofurantoin

MOA: Bacterial DNA inteference

Bacterial DNA structure and function inhibition

Uses: UTI in primary healthcare setting

Adverse reactions: Peripheral neuropathy

Interactions: -

Answer 88

A

Vancomycin

MOA: Inhibition of cell wall synthesis in gram positive bacteria

Cell wall inhibition

Use: C. Difficile

SE: Neutropenia, Renal impairment

Interactions: -

Answer 89

A

Metronidazole

MOA: Inhibition of bacterial DNA synthesis

Bacteria DNA strucutre & function

USE: Anaerobic bacterial infections: leg ulcers, pressure sores

SE:-

Interactions:-

Answer 90

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: -

Answer 91

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:-

Answer 92

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: -

Answer 93

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:-

Answer 94

A

Name: Ribavirin

MOA: Disrupts viral RNA synthesis

Use: HCV, RSV

Adverse reaction: -

Interactions:-

Answer 95

A

Name: Tenofovir, Nevirapine

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

Use: HIV,

Adverse reaction: Rash, Stevens-Johnson syndrome

Interactions:-

Answer 96

A

Name: Efavirenz

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

Use: HIV

Adverse reaction: Rash, Stevens-Johnson syndrome

Interactions:-

Answer 97

A

Name: Ritonavir, Lopinavir

MOA: Blockade viral protease required for virus particle assembly

Use: HIV

Adverse reaction: GI Bleeding

Interactions:-

Answer 98

A

Name: Dolutegravir

MOA: Disrupts integration of HIV genome into host chromosome

Use: HIV

Adverse reaction: -

Interactions:-

Answer 99

A

Name: Enfuvirtide

MOA: Blockade of virus fusion to target cell membrane

Use: HIV

Adverse reaction: Pacnreatitis

Interactions:-

Answer 100

A

Name: Maraviroc

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

Use: HIV

Adverse reaction: Nausea & diarrhoea

Interactions:-

Answer 101

A

Name: Fluconazole, Clotrimazole

Use: Candidia infection

MOA: Disruption of fungal membrane function

SE: Nausea & abdo pain

Interactions: -

Answer 102

A

Mebendazole

MOA: Disruption of microtubule assembly in helminth cells

Use: Thread/Hookworm

SE: GI Pain

Answer 103

A

Permethrin

MOA: Inhibits invertebrate neural sodium channels causing pest paralysis

Use: Scabies

SE: Skin irritation

Answer 104

A

Name: Insulin Glarine (LA), Insulin lisper (RA), Insulin aspart (SA)

Use: DMT1&2

MOA: Stimulation of glucose uptake by cells

SE: Hypoglycaemia

Interactions: Digoxin & Beta blockers

Answer 105

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

Answer 106

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

Answer 107

A

Name: Pioglitazone

Use: DMT2

MOA: Increases insulin sensitivity in muscle & adipose tissue

Increases Beta cell preservation

SE: Weight gain, MI, HF

Interactions: NA

Answer 108

A

Name: Exenatide, Liraglutide

Use: DMT2

MOA: Incretin analogue- improves glucose control

SE: Asthenia

cardiac & cancer effects

Interactions: NA

Answer 109

A

Name: Sitagliptin

Use: DMT2

MOA: Reduces inactivation of incretins

SE: Headache

cardiac & cancer effects

Interactions: NA

Answer 110

A

Name: Orlistat

Use: Obesity especially in DMT2

MOA: Inhibition of GI uptake of dietary fat

SE: Oily stools, faecal urgency

Interactions: NA

Answer 111

A

Dapaglifozin, Canaglifozin

MOA: Block renal glucose sodium co-transporter

Use: DMT2

SE: Urosepsis, Genital inflammation

Answer 112

A

Fenofibrate

MOA: Activation of PPAR-alpha transcription factor

Use: Hypercholestrolaemia, Elevated triglycerides

SE: Abdo pain, Flatulance

Answer 113

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

Answer 114

A

Carbimazole, Propylthiouracil,

MOA: Inhibition of TPO enzymes

Use: Hyperthyroidism

SE: Melaena, Sore throat

Answer 115

A

Cabergoline, Bromocriptine

MOA: Stimulation of D2 receptors in pituitary for prolactin synthesis

Use: Hyperprolactinaemia

Se: Cardiac complications

Answer 116

A

Methotrexate

MOA: Inhibition of dihydrofolate reductase and DNA synthesis for lymphocyte proliferation

Use: RA

SE: Nausea, Hair loss

I: Warfarin, Corticosteroids

Answer 117

A

Name: Azathioprine, 6- mercaptopurine

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

Answer 118

A

Name: Adalimumab, Etanercept, Infliximab

MOA: TNF alpha blocker

Use: RA

SE: Infections

Interactions: NA

Answer 119

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

Answer 120

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:-

Answer 121

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: -

Answer 122

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:-

Answer 123

A

Ulipristal

MOA: Stimulation of PG like response in pituitary and endometrium

Use: Emergency contraception

SE: Breast tenderness

Answer 124

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:-

Answer 125

A

Dinoprostone (Prostaglandin E2 aka PGE2)

MOA: Stimulates cervical ripening

Use: Delay in labour

SE: -

Interactions:-

Answer 126

A

Oxytocin

MOA: Stimulate uterine contractions

Use: Delay in labour

delivery of the placenta in 3rd stage of labour

SE: Nausea, Arrythmia

Interactions:-

Answer 127

A

Mifepristone with Misoprostol

MOA: Steroidal antiprogesterone in combination with synthetic PG

Use: Termination in pregnancy

SE: GI cramps, Uterine contractions, Vaginal bleeding

Interactions: -

Answer 128

A

TXA

MOA: Inhibits fibrin clot breakdown by plasmin

Use: Menorrhagia

SE: Nausea

Interactions: -

Answer 129

A

Mefanamic acid

MOA: Inhibition of PG synthesis

Use: Dysmenorrhoea

SE: GI bleeding

Interactions:-

Answer 130

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

Answer 131

A

Alendronate, Pamidronate, Risedronate

MOA: Drives osteoclast apoptosis- 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: - Joint & muscle pain, GI complications

Interactions: -

Answer 132

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:-

Answer 133

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: -

Answer 134

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

Answer 135

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: -

Answer 136

A

Ertapenem

Answer 137

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)

Dexamethasone for cranial imapact/ cerebral oedema

SE: Weight gain, Muscle atrophy

Interactions: PO antidiabetics

Answer 138

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

Answer 139

A

Name: Chlorphenamine, Loratadine

MOA: H1 histamine receptor blockade

Use: Hay fever, Urticaria

SE: Dry mouth, Sedation

Interactions: TCA

Answer 140

A

Mycophenolate

MOA :Inhibition of purine synthesis- anti proliferative

Use: Solid organ transplantation

SE: Infection risk, Thrombocytopenia

Answer 141

A

Filgrastim

MOA: Stimulation of neutrophil production in bone marrow

Use: Neutropenia

SE: Anaemia

Answer 142

A

Acitretin, Isotretinoin

MOA: Activation of intracellular retinoid receptor

Use: Acne, Psoriasis

SE: Teratogenic

Answer 143

A

Name: Cyclophosphamide

MOA: Cross linkage and damage to DNA

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: NA

Answer 144

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: -

Answer 145

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: -

Answer 146

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: -

Answer 147

A

Name: Fluorouracil, Cytarabine

MOA: Inhibition of RNA and DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions:-

Answer 148

A

Name: Mercaptopurine, Thioguanine

MOA: Inhibition of RNA & DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

Answer 149

A

Name: Doxorubicin

MOA: DNA intercalation. Inhibition of RNA & DNA synthesis

Use: Broad spectrum of malignancies

SE: Hair loss, bone marrow suppression & nausea

Interactions: -

Answer 150

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: -

Answer 151

A

Name: Lenolidamide

MOA: Stimulation of T cell response

Use: Myeloma

SE: Foetal risk

Interactions: -

Answer 152

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: -

Answer 153

A

Name: Goserelin

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

Use: prostate cancer

SE: -

Interactions: -

Answer 154

A

Name: Ferrous sulphate

Use: Iron deficient anaemia

MOA: Iron Provision

SE: Constipation

Interactions: Antacids

Answer 155

A

Name: Folic Acid (B9)

Use: Folate deficient anaemia

MOA: Supports nucleic acid synthesis

SE: -

Interactions:-

Answer 156

A

Name: Vitamin B12 parenteral

Use: Pernicious anaemia

MOA: Enzyme co-factors

SE:-

Interactions: -

Answer 157

A

Class I: Sodium channel blockers

Class II: Beta blockers

Class III: Potassium channel blockers

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

Answer 158

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 (VT/ VF)

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”

Answer 159

A

Atenolol (beta-1), Bisoprolol (beta-1), Metoprolol (beta-1), Sotalol

MOA: Beta- adrenergic receptor blockade-reducation in adrenergic effects on rate & intropy

Use: Proplylaxis of paroxysmal atiral tachy or AF

IHD, HF, HTN (step 4)

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

Answer 160

A

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

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

Use: Supraventricular including AF, Nodal, Ventricular tacharrythmias (regular broad complex), CPR (shockable rhythm)

SE: N&V, Hypotension

Interactions: -

Answer 161

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 (narrow QRS regular) (especially paroxysmal)

SE: Hypotension (verapamil), Constipation (diltiazaem)

Interactions:-

Answer 162

A

Digoxin

MOA: Reduces conductivity of AVN

Use: Arrythmias- AF, CHF

SE: Fatigue & Nausea

Interaction:-

Answer 163

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 (narrow QRS regular)

SE: Nausea

Interactions: Dipyridamole

CONTRAINDICATED- obstructive airway disease

Answer 164

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:-

Answer 165

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:-

Answer 166

A

Cyclizine

MOA: Histamine H1 receptor blockade

Use: Nausea, Vomiting

SE: Dry mouth, Sedation

Interactions: Sedatives

Answer 167

A

Domperidone

MOA: Dopamine D2 receptor blockade in chemoreceptor trigger zone

Use: Nausea & Vomiting

SE: Cardiac disease

Answer 168

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

Answer 169

A

Tamulosin

MOA: Smooth muscle relxant aciting on bladder neck

Indication: BPH, urinary retention

SE: Dizziness

Interactions: Hypotensive drugs

Answer 170

A

Mirabegron

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

Indication: OAB

SE: Bladder pain

Interactions: -

Answer 171

A

Finasteride

MOA: Inhibits synthesis of dihydrotestosterone

Use: BPH

SE: Impotence

Interactions: -

Answer 172

A

N-Acetylcysteine

MOA: Restoring & maintaining hepatic intracellular glutathione required for paracetamol detoxifcation

Indication: Paracetamol OD

SE: Oral inflammation

Answer 173

A

Chlordiazepoxide

MOA: Potentiation of GABA-A receptors

Indication: Severe alcohol misuse

SE: Dizzy, Drowsy

Answer 174

A

Clomethiazole

MOA: GABA mimetic, GABA-A receptor agonist

Use: Severe alcohol misuse

SE: Nasal congestion

Answer 175

A

Acamprosate

MOA: GABA mimetic, GABA-A receptor agonist. Possible NDMA receptor antagonist

Use: Severe alcohol misuse

SE: Diarrhoea & Nausea

Answer 176

A

Colchicine

MOA: Inhibition of inflammatory cell motility

Use: Acute gout

SE: Abdo pain, Vomiting

Answer 177

A

Allopurinol, Febuxostat

MOA: Inhibits uric acid synthesis

Use: Gout prophylaxis

SE: Rash

Answer 178

A

Indometacin

MOA: COX enzyme inhibition

Use: Gout

SE: GI toxicity

Answer 179

A

Desmopressin

Use: DI

MOA: Agonist for antidiuretic hormone receptors

SE: Hyponatraemia

Answer 180

A

Leflunomide

MOA: Inhibition of pyrimidine synthesis, reducing DNA & RNA synthesis & lymphocyte production

Use: RA

SE: Teratogenic

Brainscape's Knowledge GenomeTM

Phase III drug 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!

Brainscape's Knowledge Genome^TM