Y2 Drugs List Flashcards
Welcome to my drugs list deck. They should contain the MOA + usage & side effects that we need to know for every drug on the list. Some cards have ways to remember the drugs/picture prompts... also if there are any mistakes/any could be refined or made better please let me know and ill edit!
Antacids
- Aluminium Hydroxide and Magnesium Hydroxide - Maalox
- Calcium Carbonate and Magnesium Carbonate - Rennie
Uses: Dyspepsia, Heartburn, Reflux oesophagitis, GORD, Peptic Ulcers
MOA: Gastric Acid Neutralisation
SE: Nausea
- Mg –> Diarrhoea
- Al –> Constipation
Antacids + Alginates
- Sodium Alginate with Sodium Bicarbonate
MOA: Anionic polysaccharides - form a viscous gel raft upon binding with water increasing stomach content viscosity this floats to the top of the stomach reducing symptoms. Also contains antacid to neutralise excess acid. Gastric acid neutralisation
Uses: Gastric Reflux, Reflux oesophagitis - OTC + prescribed
SE: Abdominal disention
Interactions: -
H2 Receptor Antagonists
- Cimetidine
- Ranitidine
MOA: Competitively inhibits gastric H2 receptors to decrease acid secretion. (Cimetidine inhibits many cytochrome P450 enzymes)
- Use:* Stomach ulcers
- SE:* Diziness
Interactions: -
Proton Pump Inhibitors
- Omeprazole
- Lansoprazole
MOA: Blockade of parietal cell proton transporters. Irreversibly inhibits H+/K+-ATPase pump, terminal step in acid secretion pathway. Decreases basal and stimulated acid production.
Very specific - inative at neutral pH thus accumulate in secretory canaliculi or parietal cells and are activated in acidic environment.
- Use:* Stomach & duodenal ulcers, Gastric reflux
- SE:* Headache, Diarrohea
- Interactions:* Warfarin
PK:
- Increased doses give disproprtionatley higher increase in [plasma]
- 1/2 life approx 1hr
- Single daily dose affects acid secreions 2-3 days
Pancreatic Enzymes
Name
Use
MOA
Name: Pancreatin
Use: Pancreatic insufficiency- CF & Pancreatitis
MOA: Restoration of pancreatix enzymes
Bulk Laxatives
- Methylcellulose
- Isphagula Husk
MOA: Polysaccharide polymers not broken down by normal digestion so retain water in the GI lumen, softening and increasing bulk load and promoting increased motility. Water retention in lumen –> soften & bulk stools. Act over 1-3 days.
Use: Constipation
SE: -
Interactions:-
Stimulant Purgatives (2)
MOA overall: Increase intestinal motility
- Indication:* Constipation
- SE:* Nausea
- Bisacodyl
Stimulates rectal mucosa resulting in mass movements - defaecation in 15-30 mins
Use: Short courses. W/ Opoids
- Senna
Derivatives anthracene with sugars forming glycosides passes unchanges into colon where bacterial action = release free anthracene derivatives which are absorbed & causes direct effect on myenteric plexus to increase intestinal motility
- Increases activity on distal colon on serosal strain guage
- Chronic use (>3/week for >year) can cause cathartic colon (laxative dependency + req. higher doses) can lead to serious consequences
Faecal Softeners
- Docusate
- Arachis oil
MOA: Anionic surfactants. Lower surface tension allowing water or fats to enter the stool, softening faeces & increasing bulk to aid transit. Stimulates water & electrolyte secretion into the intestinal lumen. Act 3-5 days
Indication: Constipation
SE:-
Interactions: -
Osmotic Laxatives (3)
MOA Overall: Water rention in intestinal lumen
Indication: Constipation
SE: Stomach cramps
Interactions: Antiepileptics
- Saline purgatives - Magnesium sulphate, Magnesium Hydroxide -
Uses: Bowel prep before procedure. Potent, rapid action (1-2hrs)
- Macrogol Uses: Faecal impaction in children, LT management of chronic constipation
Poorly absorbed solutes that maintain increased fluid volume in GI tract by osmosis, accelerating small intestine transit - large fluid volume in colon leads to distension and purgation.
- Lactulose
Semi-synthetic Galactose & Fructose (disaccharide) converted to poorly absorbed monocaccharides by colonic bacteria - Fermentation yields lactic & acetic acid which acts as an osmotic laxative
- Acts 1-3 days
- Uses: Chronic constipation, Hepatic Encephalopathy, Negate effect of opiods
Oral Rehydration Therapy
NOT SURE IF ON LIST
- Isotonic/hypotonic solution of glucose and NaCl
Exploits ability of glucose to enhance absorption of Na+ and so water.

Opioid Anti-Motility Agents
- Codeine
- Loperamide
MOA: Agonist on mu-opioid receptors in the myenteric plexus. Blocks intestinal muscarinic receptors. Increases tone and rhythmic contractions of the colon, but diminishes propulsive activity. Pyloric, illocaecal and anal sphincters are contracted
Uses: Acute uncomplicated diarrhoea in adults
(SEs: RARE. Chronic use = Constipation. Abdo cramps, dizziness)
Interactions: -
Carbonic Anhydrase Inhibitor
Acetazolomide
MOA: Reduce aqueous humour production (req. HCO3- secretion)
- Inhibits carbonic anhydrase in PCT to stop the reapsorption of HCO3- and therefore Na+ so increasing the volume of urine (osmotic balance). Weak diuretic action as only a small amount of sodium is reabsorbed this way
Uses: Reduce intraocular pressure in glaucoma- open and acute close angle
SE: Paraesthesia
- Also prevents H+ secretion –> metabolic acidosis
Interactions: -
Osmotic diuretic
- Mannitol
MOA: Increases the osmolarity of glomerular filtrate thus prevents water reabsorption. Acts mostly where water reabsorption occurs - PCT + descending limb of LOH)
Uses: Cerebral oedema + reducing intraocular pressure (glaucoma), reducing intracranial pressure
SE: Hypotension
Interactions: -
Loop Diuretics
- Furosemide
MOA: Powerful diuretics. Act on thick ascending limb og LOH. Inhibits the Na+K+2CL- co-transporter (competes with Cl- binding). Decreased NaCl reabsorption in thick ascending loop causes decreased osmotic concentration in the medulla thus decreased ADH mediated water absorption.
- Reduced Mg & Ca reabsorption
- Increase in NaCl to DCT. Increase Na uptake by principle cells –> K+ loss –> Metabolic Alkalosis
- Binds to plasma proteins so not filtered but secreted directly into the PCT thus effective in renal impairment/ Nephrotic syndrome.
SEs: Nausea, Dizziness
- Hypovolaemia + hypotension, hypokalaemia + hyponatremia, Ototoxicity
Uses: Oedema, Left ventricular HF
- Acute pumonary oedema, Resistant HTN
Interactions: NSAIDS, ACEi
Thiazide Diuretics
- Bendroflumethiazide
- Indapamide
- Hydrochlorothiazide
- Chlortalidone
(BICH)
Weak/moderate diuresis. Acts on the Early DCT. Inhibits Na+/Cl- co-transporter (competes with Cl- binding). Slower acting but longer lasting than loop diuretics.
- Filtered & not secreted- not good in renal impairment
- Increased NaCl to Distal nephron & decreased blood volume –> Increase K secretion
- Intercalated cells may also secrete H+ –> Alkalosis
Uses: Hypertension, Peripheral oedema (chronic heart failure)
SEs: Electrolyte imbalance, Exacerbation/ precipitation of gout (increased plasma uric acid)
- Hyponatraemia/Hypokalaemia, ED, Hyperglycaemia
- Interactions:* NSAIDS, Digoxin
Potassium Sparing Diuretics
Subclass: Aldosterone Antagonists
- Spironolactone
- Eplerenone
Weak diuretic alone. Aldosterone antagonist, binds to and blocks mineralocorticoid (MR) receptor. Prevents synthesis of ENaC and Na+/K+ATPase activity which stops Na+ reabsorption (and water by osmosis) and reduces K+ secretion into the lumen to K+ is retained.
Notes: Act on Late DCT/ Collecting duct on principle cells (Na/K ATPase)
SEs: GI symptoms, Hyperkalaemia, gynaecomastia
Uses:
- Chronic HF
- Oedema
- Periph oedema +ascites caused by cirrhosis
- Resistant HTN
- Primary Hyperaldosteronism
- Can be used in comination to prevent K+ loss from use of loop/thiazide diuretics.*
- Interactions:*
- NSAIDS
- ACEi
Potassium Sparing Diuretics
Subclass: ENaC Antagonists
- Amiloride
MOA: Weak diuretic alone. ENaC antagonist - blocks ENaC, competes for Na+ binding site thus decreasing luminal permeability to Na+. This causes reduced Potassium secretion into the lumen to potassium is retained
- Can be used in combination to prevent K+ loss from use of loop/thiazide diuretics
Uses:
- Chronic heart failure
- Oedema
- Peripheral oedema and ascites caused by cirrhosis
- Resistant HTN
- Primary Hyperaldosteronism
SEs: GI Symptoms, Hyperkalaemia, Gynaecomastia
Interactions: NSAIDS, ACEi
Renin Inhibitor
NOT ON Y2
- Aliskiren
Inhibits the action of Renin thus stopping formation of Angiotensin I so the RAAS system cannot be used to increas BP
Renin release from granular cells of AA
ACE inhibitors
Ramipril, Captopril
MOA: Binds to ACE inhibiting the converstion of Ang I to Ang II –> Blocks vascocontrictions (reduces afterload) & the RAAS system cannot increase BP
- Caution in renal failure - ACE normally constricts efferent arterioles thus ACEI can lead to decreased GFR
-
Singal Transduction in Smooth Muscle cells:
- Less activation at AG II receptors
- Less increase IP3
- Less Ca release from SR
- Less Ca-Cm
- Less MLCK phosporylation
- Less contraction
- Aldosterone secretions also reduced:
- Less water retention
- Less plasma volume
- Decreased cardiac preload
Use: HTN, Diabetic neuropathy, HF
SEs: Dry cough (bradykinin build up as not inactivated by ACE), Hyperkalaemia, hypotension
Interactions: Lithium, NSAIDS

Angiotensin-II receptor antagonists/ ARBS
- Losartan
- Valsartan
MOA: Blocks angiotensin-renin system. Binds to the angiotensin-II receptor, preventing it from working. RAAS cannot increase BP
Uses: HTN, Diabetic neuropathy, HF
SE: Hypotension, Fatigue
Interactions: Diuretics
Neprilysin inhibitors
(used with an ARB drug)
- Sacubitril, (used with Valsartan)
MOA: Inhibition of natriuretic peptide breakdown –> Promote Water & Sodium excretion
- Neprilysin = Enzyme
Uses: HF with reduced EF
SE: Hypokalaemia, Hypoglycaemia
Interactions: -
Beta-adrenergic receptor antagonists
(Beta blockers)
- Bisoprolol (Cardioselectiv B1 antag.)
- Atenolol (cardioselective B1 antag.)
- Propanolol (B1 & 2 antag.)
MOA: Negative inotropic/ chrontropic agent.
- Competitive inhibitors of adrenaline and noradrenaline at B-adrenoceptor sites. Inhibit sympathetic stimulation of heart muscle.
- Heart Specific: B1 antagonists are selective for the cardiomyocytes: Negative inotropes & chronotropes. Reduce workload on the heart relieving oxygen demand.
-
Molecular Mechanism in the heart:
- Blocked Beta-adrenergic receptors
- Less ATP –> cAMP by Adenylyl Cyclase
- Less Protein Kinase (PK) A activity
- Less release of Ca from SR- Less free Ca inside cell
- Less contraction
Uses: HTN, Stable angina
SEs: Bradycardia, Bronchospasm, Dizziness, constipation
Interactions: NSAIDS, Digoxin

Alpha-adrenergic receptor antagonist (heart or prostate)
- Doxazosin
MOA: Vasodilator, decrease total peripheral resistance
- Selective alpha 1 adrenergic receptor blocker on bladder neck, urethra. Relaxation smooth muscle —> Urinary flow facilitated
- Blocks alpha- 1 adrenoreceptors of the sympathetic autonomic nervous system, this relaxes smooth muscles around the bladder (internal and external urinary sphincters) allowing micturition
Uses: BPH-urinary retention, HTN
SE: Dizziness, Headache. Hypotension, Drowsiness, Nausea, Fatigue, Constipation
Interactions: Hypotensive drugs
Calcium Channel Antagonists
(for heart failure and hypertenison)
Diltiazem
Dihydropyradine subclass
- Nifedipine
- Amlodipine
MOA: Blockade of vascular smooth muscle contraction
- Prevent opening of VGCCs (L type) –> Less Ca influx –> Less binding of Ca to Cm–> As less Ca-Cm complex less phosphrylation MLCK therefore less contraction
-
Notes:
- Does not generally act on veins
- Drives coronary artery dilation- Improves blood flow
- Vasodilatory effect therefore reduced afterload
Use: HTN, Stable angina
SEs: Ankle swelling, Oedema palpitations
Interactions: Beta blockers, Digoxin
(Bind to K-type calcium channels on cardiac and smooth muscle - act on BOTH the heart and vessels. Cause coronary artery dilation. Negative chronotropic effects, negative inotropic effects.)










