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Kim's Drug List > Drugs List > Flashcards

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

Gastric Acid Neutralisation

Uses: Reflux oesophagitis - OTC & prescribed

SE: Mg –> Diarrhoea

Al –> Constipation

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2
Q

Antacids + Alginates

A
  • Sodium Alginate with Sodium Bicarbonate and Calcium Carbonate (Gaviscon)

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

Uses: Reflux oesophagitis - OTC + prescribed

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3
Q

H2 Receptor Antagonists

A
  • Cimetidine
  • Ranitidine

Competitively inhibits gastric H2 receptors to decrease acid secretion.

OTC

Cimetidine inhibits many cytochrome P450 enzymes

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4
Q

Proton Pump Inhibitors

A
  • Omeprazole
  • Lansoprazole

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.

Prescribed drug of choice for reflux oesophagitiss.

More effective than H2 antagonists.

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

Bulk Laxatives

A
  • Methylcellulose
  • Isphagula Husk

Polysaccharide polymers not broken down by normal digestion so retain water in the GI lumen, softening and increasing bulk load and promoting increased motility.

Act over 1-3 days.

First line for constipation & IBS

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6
Q

Stimulant Purgatives (2)

A
  • Bisacodyl

Stimulates rectal mucosa resulting in massmovements - 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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7
Q

Faecal Softeners

A
  • Docusate
  • Arachis oil

Anionic surfactants. Lower surface tension allowing water or fats to enter the stool, softening faeces. Stimulates water & electrolyte secretion into the intestinal lumen

Act 3-5 days

Used for constipation and fissures/piles

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8
Q

Osmotic Laxatives (3)

A
  • 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

SEs: Abdo cramp, gas, flatulence

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9
Q

Oral Rehydration Therapy

A
  • Isotonic/hypotonic solution of glucose and NaCl

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

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10
Q

Opioid Anti-Motility Agents

A
  • Codeine
  • Loperamide

Agonist on mu-opioid receptors in the myenteric plexus. Increases tone and rhythmic contractions of the colon, but diminishes propulsive activity. Pyloric, illocaecal and anal sphincters are contracted

SEs: Chronic use = constipation. Abdo cramps, dizziness

Uses: Acute uncomplicated diarrhoea in adults

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11
Q

Carbonic Anhydrase Inhibitor

A
  • Acetazolomide

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

SE: Also prevents H+ secretion –> metabolic acidosis

Uses: Reduce intraocular pressure in glaucoma (aqueous humour prod. req. HCO3- secretion)

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12
Q

Osmotic diuretic

A
  • Mannitol

Increases the osmolarity of glomerular filtrate thus prevents water reabsorption. Acts mostly where water reabsorption occurs - PCT + descending limb of LOH)

Uses: reducing intracranial pressure + reducing intraocular pressure (glaucoma)

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13
Q

Loop Diuretics

A
  • Furosemide

​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: Hypovolaemia + hypotension, hypokalaemia + hyponatremia, Ototoxicity

Uses: peripheral oedema (chronic heart failure), acute pumonary oedema, Resistant HTN

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14
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.

Notes:

  • 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

SEs: Hyponatraemia/Hypokalaemia, increased plasma uric acid (gout), ED, Hyperglycaemia

Uses: Peripheral oedema (chronic heart failure), hypertension

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15
Q

Potassium Sparing Diuretics

Subclass: Aldosterone Antagonists

A
  • Spironolactone
  • Eplerenone

Weak diuretic alone. Aldosterone antagoniss, 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: Hyperkalaemia, gynaecomastia

Uses:

  • Chronic HF
  • 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.

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16
Q

Potassium Sparing Diuretics

Subclass: ENaC Antagonists

A
  • Amiloride

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

SEs: Hyperkalaemia, Gynaecomastia

Uses:

  • Chronic heart failure
  • Peripheral oedema and ascites caused by cirrhosis
  • Resistant HTN
  • Primary Hyperaldosteronism

Can be used in combination to prevent K+ loss from use of loop/thiazide diuretics

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17
Q

Renin Inhibitor

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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18
Q

Angiotensin-converting Enzyme (ACE) Inhibitor

A
  • Ramipril

Binds to ACE stopping the converstion of Ang I to Ang II so the RAAS system cannot increase BP

SEs: Dry cough (bradykinin build up as not inactivated by ACE), hypotension.

Caution in renal failure - ACE normally constricts efferent arterioles thus ACEI can lead to decreased GFR

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19
Q

Angiotensin-II receptor antagonists

A
  • Losartan
  • Valsartan

Binds to the angiotensin-II receptor, preventing it from working. RAAS cannot increase BP

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20
Q

Aldosterone Antagonist

A
  • Spironolactone

​Antagonist of aldosterone by blocking the mineralocorticoid receptor. Means RAAS cannot increase BP

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21
Q

Thyroid Hormones

A
  • Levothyroxine (Synthetic T4)
  • Liothyonine (Synthetic T3)

Use: Hypothyroidism

Activation of Thyroid Hormone Receptor

Mimics thyroid hormone by binding to incracellular alpha & beta thryoid receptors

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22
Q

Alpha-adrenergic blocker

(to treat altered voiding)

A
  • Doxazosin

Selective alpha 1 adrenergic receptor blocker on bladder neck, urethra. Relaxation smooth muscle —> Urinary flow facilitated

Uses: Urinary retention, BPH/ Overflow Incontinence

SE: Hypotension, Drowsiness, Nausea, Fatigue, Constipation

  • Doxazosin - ZO sounds like GO - makes you GO for a wee*
  • (*Blocks alpha- 1 adrenoreceptors of the sympathetic autonomic nervous system, this relaxes smooth muscles around the bladder (internal and external urinary sphincters) allowing micturition)
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23
Q

Urinary anti-spasmodic; anticholinergic

(Tx of Urinary Incontinence)

A
  • Oxybutinin

MOA: Competitively antagonizes the muscarinic 2/3 acetylcholine receptor leading to reduction of bladder detrusor activity

Use: Urinary Incontinence/ OAB (Urge incontinence)

SE: Blurred vision, Constipation, Dry Mouth, Urinary Retention

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24
Q

B2-Adrenergic Agonists

(tx of airway disease)

A
  • Salbutamol (short acting)
  • Terbutaline (short acting)
  • Salmeterol (long acting)
  • Formoterol (long acting)

Cellular Target: Bronchiolar Smooth Muscle

Molecular Target: Stimulation B2 adrenergic receptors

B2 agonists bind to B2-adrenergic receptors that activate adenylate cyclase. AC increases cAMP levels/ action, 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.

SEs: Tremor, tachycardia, cardiac arrythmia

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25
Q

Anti-cholinergics

(Airways)

A
  • Ipratropium (short acting)
  • Tiotropium (long acting)

Cellular Targets: bronchiolar smooth muscle cells.

Blocks M3 muscarinic ACh receptors. Actives G protein –> Decreases action of PLC:

  • Reducing Ca2+ release into the cytoplasm, reducing smooth muscle contraction causing bronchodilation.

SEs: Dry mouth, constipation, urinary retention

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26
Q

Methylxanthines

A
  • Theophylline
  • Aminophylline

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.

Toxic side effects to must monitor serum - cardic arrythmias + seizures

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27
Q

Leukotriene Antagonists

A
  • Montelukast
  • Zafirlukast

Cellular targer: Eosinophils & Bronchiolar Smooth Muscle

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

SEs: Abdo pain, headache

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28
Q

Glucocorticoids

(Airways)

A
  • Beclomethasone
  • Fluticasone
  • Prednisolone
  • Hydrocortisone

Targets immune cells of the lungs especially macrophages, T-lymps and eosinophils. 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)

SEs: MANY - Moon face, weight gain, osteoporosis, hyperglycaemia

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29
Q

Beta-adrenergic receptor antagonists

(Beta blockers)

A
  • Bisoprolol (Cardioselectiv B1 antag.)
  • Atenolol (cardioselective B1 antag.)
  • Propanolol (B1 & 2 antag.)

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*
  • Blcoked 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

SEs: Dizziness, constipation

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30
Q

Calcium Channel Antagonists

(for heart failure and hypertenison)

A
  • Nifedipine
  • Amlodipine (Dihydropyradine subclass)

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

(Vascular smooth muscle)

SEs: Ankle swelling, palpitations, interact with B-blockers & grapefruit juice

(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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31
Q

Nitrate Vasodilators

A
  • Glycerol trinitrate (GTN)
  • isosorbide mononitrate (ISMN)

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

SE: Headache

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32
Q

Anti-cholinergic

(for emergency bradycardia treatment)

A
  • Atropine

IV. Binds to and blocks muscarinic M2 Ach receptors in the heart. Inhibits effects of cholinergic vagus nerve transmission (normally -ve chronotropic effects). Accelerates repolarisation rate in cardiac muscle cell, so raises heart rate

Uses: Sinus Bradycardia

SE: Dry mouth, Blurred vision, Urinary retention, Constipation

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33
Q

Sympathomimetics

A
  • Noradrenaline (alpha)
  • Dobutamine (beta)
  • Adrenaline (alpha and beta)

Positive inotrope

  • Binds & Stimulates Cardiomyocytes B1 adrenergic receptors
  • Drives heart muscle contraction
  • Resotres function

Uses: Cardiac Arrest

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34
Q

ACE inhibitors

A
  • Ramipril

Inhibits conversion of Ang I to Ang II. Reduces vasoconstriction in peripheral blood vessles –> Reduced afterload –> Lower BP

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

SE: Persistant cough

Notes:

Aldosterone secretions also reduced:

  • Less water retention
  • Less plasma volume
  • Decreased cardiac preload
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35
Q

HMG-CoA Reductase Inhibitors

(statins)

A
  • Atorvastatin
  • Simvastatin

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: CVD prevention WITHOUT affect BP

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36
Q

Neprilysin inhibitors

(used with an ARB drug)

A
  • Sacubitril (used with valsartan)

Neprilysin = Enzyme

Inhibition of natriuretic peptide breakdown –> Promote Water & Sodium excretion

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37
Q

Antiplatelet Drugs (2)

A

Aspirin

  • Blocks enzyme actions of platelet COX enzyme
  • COX required for synthesis Thromboxane A2 production
  • Reduced TXA2 synthesis inhibits platelet activation & thrombus formation
  • SEs: GI bleeding, gastric ulcers due to decreased prostaglandins E2 and I1*
  • Clopidogrel

Binds to and blocks the platelet Adenosive Diphosphate (ADP) receptor, causes decreased platelet activation & therefore thrombus formation

USE: ACS prevention

Can treat CVD without affecting BP

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

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38
Q

Anticoagulants (4)

A
  • Warfarin

​Targets extrinsic pathway which inhibits vitamin K dependent synth of dependent clotting factors 10, 9, 7 and 2 (PT). By inhbiting vitamin K carboxylation of the factors it decreases thrombin production.

WKD TimE = _W_arfarin inhibits vitamin _K_, decreasing Thrombin which is Extrinsic pathway.

Vit K is clotting factors 1972 - 10,9,7,2.

  • Heparin, Unfractioned heparins, low molecular weight heparins

Reversibly bind antithrombin III which inactivates thrombin and FXa.

  • Unfractionated = Inactivated FXa & Thrombin
  • LMWH = Inactivated FXa

HAITTI - _H_eparins activate _A_nti-thrombin 3, Inactivating Thrombin and TenA -Intrisic pathway

  • Dabigatran

Competitive, reversible inhibitor of thrombin

Direct inhibition of thrombin - thrombi cannot convert fibrinogen into fibrin and formation of secondary plug is inhibited

Use: Prophylaxis & Tx of Venous Thromboembolism (2)

Warfarin- “ & ischeamic stroke prevention in AF

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39
Q

Thrombolytics

A
  • Altepase
  • Streptokinase
  • Urokinase

Activates plasminogen to plasmin which digests fibrin and fibrinogen to restore blood flow.

SEs:Arrhythmias, bleeding. Can only use streptokinase one as an immune response is generated againset the bacteria (streptococci) and memory B cells produce anti-streptokinase ABs.

USe: IHD/ ACS

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40
Q

Dopaminergics

(pharma basal ganglia disorders)

A
  • 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.

SEs: Anorexia, drowsiness, hypomania, hypotension, sudden onset sleep, ‘on-off effects’, Arrythmia, Tachycardia

Synthetic more likely to have psych SE

Uses: Parkinsonism. Synthetics used in younger patients

41
Q

Dopa-decarboxylase inhibitor

A
  • Carbidopa
  • Benserazide

​Inhibits dopa-decarboxylase, preventing GI and peripheral metabolism of levodopa meaning more is available to the CNS

Uses: Used with levodopa for Parkinsonism

42
Q

COMT inhibitor

(catechol-O-methyl transferase inhibitor)

A
  • Entacapone
  • Tolcapone

Inhibits COMT in the periphery (outside CNS), reducing dopamine breakdown and allowing for more in the CNS

43
Q

MAOIB Inhibitor

(Monoamine oxidase inhibitors, B form inhibitor)

A
  • Rasagiline
  • Selegiline

Inhibits MAOIB so reducing central metabolism breakdown of dopamine in the CNS

Use: Adjunct with levodopa/carbidopa for Parkonsonism

44
Q

Anticholinergics

(BG disorders)

A
  • Orphenadrine
  • Procyclidine
  • Trihexphenidyl

Muscarinic cholinergic receptor antagonist - in Parkinsons a decrease in dopamine lease to an increase in Ach concentration. Anticholinergics (antimuscarinics) readdress this balance).

SEs: may reduce absorption of levodopa

Uses: Iatrogenic PD (Orphenadrine)

Dystonia (Trihexphendyl & Procyclidine)

45
Q

Dopamine-depleting Drugs

A
  • Tetrabenazine

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.

SEs: Causes depression by decreasing 5HT and NA levels

Uses: Chorea e.g. Huntington’s, Athetosis, Ballismus

46
Q

Weak analgesic/Antipyretic

A
  • Paracetamol

Non-selective COX inhibitor, decreasing prostaglandin production. Also improves peripheral vasodilation (anti-pyretic effects).

  • No PG
  • No prostanoid receptor activation
  • Reduced activation VDNC

SE: Constipation

Interactions: 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.

47
Q

NSAIDs

A
  • Aspirin
  • Ibuprofen
  • Diclofenac
  • Naproxen

COX inhibitors. Decreased prostaglandins so less inflammation

  • Non selective COX inhibitor
  • No PG
  • No prostanoid receptor activation
  • Reduced activation VDNC

Uses: Anti-inflammatory, antipyretic, anticoagulant, analgesic

SEs: GI side effects- gastric ulcers and medication overuse headaches

  • Hypertension, Aspirin not for under 16’s
  • Aspirin –> 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

48
Q

COX-2 selective NSAIDs

A
  • Celecoxib
  • Etoricoxib

MOA: Selective COX 2 Inhibitor –> localised PG bloackage –> No prostanoid receptor activation –> Reduced activation Voltage Gated Na+Channel

  • Directly inhibit COX-2 enzymes - specific for inflammation

USE: Pain, inflammation

SE: Indigestion, Thombosis

Interactions: ACEi, SSRI

49
Q

Weak opioid analgesics

A
  • Codeine
  • Dihydrocodeine

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: analgesia (chronic and acute) and anaesthesia. Nociceptive pain

SEs: Resp depression, decreased GI motility, constipation, tolerance and dependance, nausea

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)

50
Q

Strong Opioid Analgesics

A
  • Morphine
  • Diamorphine

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

SEs: Resp depression, decr GI motility, constipation, tolerance and dependance, N& V, Mood alterations

Interactions: Sedatives

51
Q

Partial/Mixed Agonist opioid analgesics

A
  • Buprenorphrine
  • Pentazocine

Opiod receptor partial agonist @ Mu & Kappa Opioid Receptor and Antagonist at delta

Use: Maintenance therapy, pain relief (moderate to severe)

SE: Constipation, nausea

Interactions: Sedatives

52
Q

Opioid receptor antagonists

A
  • Naloxone (short lasting)
  • Naltrexone (longer lasting)

Compete for the same binding site as opioids, particularly the u receptor so reducing the effect of opioids (Opioid receptor antagonist)

Uses:

1 &2/ Opiod OD, Respiratory depression

2/ Prevent relapse of opiod/ alcohol abuse

SE: Nausea & Tachycardia

53
Q

Drugs used to manage opioid addiction

A
  • Methadone
  • Buprenorphine

Opioid receptor agonists: Methadone = Mu receptor, longer lasting.

Buprenorphine = partial Mu and Kappa R agonist and antagonist at delta

Use: Opiate addiction

SE: Constipation

INteractions: Sedatives

54
Q

Drugs to treat neuropathic pain

+ 4 types of neuropathic pain?

A
  • TCAs (Amitriptyline- NRI, 5HTRI, H1 anatgonist, A1 antagonist, M1 antagonist)
  • Gabapentin (AED) - inhibits VDCC, increases GABA transmission
  • Pregabalin (AED)-Inhibits VDCC, increase GABA transport
  • Carbamazepine (AED)-Sodium channel blocker in inactivated state
    • ​Teratogenic

SE: Dizziness, fatigue

Interactions: Antidepressants

4 types: Phantom limb, trigeminal neuralgia, post-stroke pain, post-herpetic pain (persistent pain after shingles).

Tall Gals Prefer Carbs

55
Q

Tricyclic Antidepressants

A
  • Amitriptyline
  • Nortriptyline
  • Dosulepin
  1. NA reuptake blocker - MAIN action
  2. Serotonin reuptake inhibitor
  3. a1 adrenoreceptor antagonist
  4. H1 receptor antagonist
  5. M1 receptor antagonist

SEs: Anticholinergic syndrome, Sedation (H1 blocker), Dry mouth, constipation (M1 muscarinic blocker), cardiac dysfunction (a1 adrenoreceptor blocker)

56
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A
  • Sertraline
  • Citalopram
  • Fluoxetine

Inhibits 5HT reuptake pump in synaptic cleft so increases 5HT levels.

SEs: Sickness, sleep disorders (insomnia), sexual dysfunction, serotonin syndrome, slow onset. (5S’s), Nausea

Interactions: Lithium, NSAIDs

Seratonin syndrome = Overactiation ANS

  • Hyperthermia
  • CV Problems
  • Aggresion
  • Tremor
  • Rigidity
57
Q

MAOIs

A
  • Moclobemide

Stops breakdown of monoamines in CNS. Increases Na and 5HT levels by inhibiting enzymatic breakdown.

Reversible inhibitor of monoamine oxidase A (RIMA)

  • SEs*: Tachycardia,
  • Postural hypotension, restlessness, convulsions, sleep disorders, Cheese Reaction- increase tyramine which increases NA –> Hypertensive crisis- vasoconstriction. “See People’s Cheese Reaction”
  • Many cross-drug reactions- dont use with SSRIs or TCAs*
58
Q

Atypical Antidepressants

A
  • Reboxetine - NRI, inhibits reuptake of NA, elevating mood
  • Bupropion- Inhibits NA and dopamine reuptake, elevating mood
  • Buspirone - Partial 5HT agonist, reduce activity to increase transmitter levels in the synaptic cleft
  • Agomelatine - Melatonon agonist, increases slow wave sleep patterns.
  • Venlafaxine - 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

59
Q

Mood Stabiliser

A
  • Lithium

MOA Unclear but possible neuronal calicum channel blockade

Uses: Mainly bipolar disorder specturm and Depression- resitant, recurrent unipolar as an adjunct to anti-depressants

Interactions: NSAIDs, ACEi

60
Q

1st generation (classical) Anti-psychotic

A
  • Chlorpromazine
  • Haloperidol

Selective dopamine receptor antagonists - D2. 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

61
Q

2nd generation (Atypical) Antipsychotics

A
  • Amisulpride

​5HT7 and Dopamine (D2) antagonist

  • Risperidone

​5HT2A and Dopamine (D2) antagonist

  • Clozapine

​5HT2A and domapine (D2) antagonist

  • Olanzapine

​​​Selective D2 and 5HT antagonist

  • Quetiapine

​​​Selective D2 and 5HT antagonist

SE: EPS, 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

62
Q

General Anaethetic

A
  • Isoflurane - Unclear
  • Nitrous Oxide - Unclear
  • Sevoflurane - Unclear

SE: Respiratory depression, Irritation of respiratory tract, Bronchospasm, Laryngospasm

  • Propofol - Unclear
  • Ketamine - NMDA (glutamate receptor antagonist)
    • Blocks Ca & Na channels
    • SE: Hallucinations, Raised HR and BP
  • 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

63
Q

Local Anaesthetic

A
  • Lidocaine
  • Bupivacaine
  • Levobupivacaine

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 of LA

Uses: Levobupivicane- Epidural Anaesthesia

64
Q

Neuromuscular blockers

A
  • Suxamethonium (depolarising)
  • Atracurium (non-depolarising)
  • Vecuronium (non-depolarising)
  • Neostigmine - peripheral inhibitor of acetylcholinesterase (depolarising). Also used in MG

Depolarising :

MOA: (non-competitive, agonist) Bind AchR –> Prologned depolarisation (receptor closes & repolarises w/ agonist still bound) –> prevents further depolarisation

  • Fast onset, short duration

AChEi: Increase Ach in junctional cleft, paralysis by overload- all AchR @ max

  • SE: (PNS increase)
    • Bradycardia, Increased secretions & Peristalsis

Non-depolarising - (competitive, agonist):

Binf AChR prevent depolarisation post synaptically. Pre synaptically reduced Ca entry –> Less NT from pre-synaptic vesicle

Notes: Do not cross BBB

  • Slow onset, long duration
65
Q

Drugs used to reverse NMB block

A
  • Sugammadex

Oligosaccharide that forms a complex with NMB, encapsulating and inativating it then removing them from NMJ. ONLY for VECURONIUM

  • Neostigmine

​Peripheral inhibtor of acetylcholinesterase - can reverse non-depolarising blockers by increasing Ach levels so neurone can fire again

  • Use in Myasthenia Gravis
  • SE: Bradycardia
66
Q

Muscle Relaxants/Sedatives/Anxiolytic-hypnotic

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

A
  • Zolpidem (Z drug) - GABA PAM (mechanistically identical to BDZ)
    • USE: Anxiety- short term crisis
  • Temazepam, Diazepam, Lorazepam, Midazolam (BDZ) - GABA PAM Y subunit. Open Cl- channels –> Hyperpolarisation

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.

67
Q

Muscle Relaxants/Sedatives/Anxiolytic-hypnotic

(Think more sedatives but less in anaesthesia in theatre)

A

Dexmedetomidine - a2-adrenergic receptor agonist. Inhibits NA release & terminates pain

USE: Sedation ICU when verbal communication needs to maintained

SE: Bind to a receptor so decrease sympathetic acitivty- Hypotension, Bradycardia

68
Q

Muscle Relaxants/Sedatives/Anxiolytic-hypnotic

(Think more triad of anaesthesia)

A

Afentanil, Fentanil, Remifentanil - Opioid receptor agonists (Mu receptor).

MOA: Decrease opening VDCC, Decrease Ca intracellular store, Decrease exocytosis of transmitter vesicles, Increase of K outflow post synaptically –> Decrease AP & repolarisation time

USE: Sedation but usually Analgesia

SE: Respiratory depression, Miosis, Coma, Tolerance & Addiction

69
Q

Benzodiazepine

(Antagonist)

A
  • Flumazenil

BDZ antagonist - revers bezodiazepine sedatives

70
Q

Anti-Epilepsy drugs (AEDs)

A
  • Sodium Valporate
  • Lamotrigine
  • Carbemazepine

​Block sodium channels in the inactivated state

Use: All types of seizures except absence seizures

SEs: Cognitive impairment, visual impairment, peripheral neuropathy, skin problems

  • Ethosuximide - Ca2+ blocker

​Targets low threshold voltage dependent T-type calcium channels

Use: Absence seizures - first line

71
Q

Benzodiazepines for Epilepsy

A
  • Midazolam - GABA PAM (Y subunit)
  • Lorazepam - GABA PAM (Y subunit)
  • Diazepam - GABA PAM (Y subunit)

GABAA 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.

72
Q

Barbituates (Barb)

A
  • Phenobarbitone- GABA PAM (B subunit)
  • Pentobarbitone- GABA PAM (B subunit)
  • Primidone- GABA PAM (B subunit)

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: Status Epileptics and Primidone Essential Tremor

73
Q

Anticholinesterases

(for dementia)

A
  • Donepezil
  • Galantamine
  • Rivastigmine

Reversible inhibitor of acetylcholinesterase

Use: mild- moderate AD

SE: Nausea & vomiting

74
Q

Glutamate NDMA receptor antagonists

A
  • Memantine

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

75
Q

Antimicrobial/Antiviral drugs for CNS infection

A
  • Ceftriaxone

​Inhibits synthesis of cell walls in bacteria- Bacteriocidal

Use: Bacterial meningitis

SE: CDAD

  • Acyclovir

​Inhibits viral DNA synthesis

Use: viral encephalitis

  • Amoxicillin -

​Induces cell lysis by blocking last stages of cell wall synthesis- Bacteriocidal. Increased uptake by bacteria

USE: Listeriosa Meningitis

USES: CNS and meningococcal infections e.g. menigitis and encephalitis

76
Q

Corticosteroid

(CNS infections)

A
  • Dexamethasone

Glucocorticoid receptor agonist

77
Q

Drugs used to treat hypercalcaemia

A
  • Fluids (normal saline)

​Volume expansion stimulates excretion of Ca2+

  • Furosemide (loop diuretic)

​​Inhibits Na+K+2Cl- transporter keeping Na+ and K+ in the lumen hence it is excreted

  • Calcitonin​

Decreases Ca2+ and PO4 reabsorption in the kidneys, inhibits bone reabsorption by preventing osteoclast action (↓ serum Ca2+ and PO4)

  • Alendronic Acid (bisphosphonates)

Prevents osteoclast bone reabsorption which could further increase serum Ca2+

78
Q

Drugs used in the management of hypocalcaemia

A
  • 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

79
Q

Drugs used in the management of vitamin D deficiency

A
  • Vitamin D (colecalciferol
  • Calcitriol (only in advanced CKD)

Replaces vit D - active form Calcitriol prevents Ca2+ and PO4 excretion from the kidney and increases reabsorption in the intestines.

80
Q

Drugs used to manage osteoporosis

A
  • Alendronic acid (bisphosphonates)

​Prevents osteoclast bone reabsorption. Ruffled boarder impaired. Decrease osteoclast pregenitor development & recruitment. Promote osteoclast apoptosis.

SE: Asymptomatic hypoclacaemia, Osteophageal reaction, GI disturbance, Osteonecrosis, Atypical #

  • Raloxifene (selective oestrogen receptor modulator, SERM)

​Inhiibits the cytokines which recruit osteoclasts thus less bone reabsorption

  • Parathyroid hormone

​Stimulates calcitriol production which prevents Ca2+ and PO4 ecretion from kidney and increases absorption in the intestines

Promote: Osteoblastic differentiation and activity. Inhibit osteoblast apoptosis

SE: Hypercalcaemia, Muscle Cramps, Nausea & Vomiting

  • Denosumab

​MoAb which targest RANKL or RANK receptir so inhibits maturation of osteoclasts so less bone reabsorption. Inhibits OC function, formation & survival

SE: Hypocalcaemia, Diarrhoea, Dysponsea, Constipation

  • Vitamin D
81
Q

Anti-proliferative agents

(DMARDs)

A
  • Methotrexate

​Folic acid antagonist (req for DNA synth) so inhibits the S phase of the cell cycle

  • Azathioprine

​Reduces purine synthesis and reduces DNA synthesis

Both reduce lymphocyte proliferation

SE: Increased infection risk

Teratogenic

GI: Mouth ulcers, Nausea, Diarrhoea

Hair loss

82
Q

Aminosalicylates

(DMARDs)

A
  • Sulphasalazine​
  • Mesalazine

Mechanism unclear - possible COX inhibition

83
Q

Biologics (monoclonal antibodies)

A
  • Infliximab

Anti-TNF cytokine - bind and block proinflammatory function of TNF-alpha

  • Rituximab

Depletion of B-lymphocytes CD20

84
Q

Beta lactams - Penicillins

A
  • Flucoxacillin
    • ​SSTI (use for Staph initially)
    • Bone & Joint infections- Empirical for ^
    • Penicillinase- Resistant
  • Benzylpenicillin
    • ​SSTI (use for strep)
    • Bone & Joint infections- Empirical for ^
  • Amoxicillin
    • ​LRTI
    • Enhanced uptake by bacteria
  • Co-amoxiclav
    • ​Mixed infections (eg: chronic chest)
    • Beca Lactamase Inhibitor
  • Penicillin
    • Tonsillitis

Bactericidal - cell lysis by blocking cell wall synthesis

85
Q

Beta lactams - Carbapenem

A
  • Meropenem

Use: Infections in ITU & Complex, multi drug resistant infections

Bacteriocidal - cell lysis by blocking cell wall synthesis

86
Q

Cephalosporins

A
  • Ceftriaxone

Bacteriocidal - cell lysis by blocking cell wall synthesis

Uses: Bacterial Meningitis, Abdominal sepsis, Ortho infection

SE: CDAD

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

87
Q

Nitroimidazole

A
  • Metronidazole

USE: Anaerobic infecitons- abscess

MOA: Bacteria DNA strucutre & function

88
Q

Macrolides

A
  • Erythromycin

​Bacteriostatic - inhibition of bacterial protein/ RNA synthesis

Uses: URTI, LRTI, SSTI, Atypical LRTI

  • SSTI in place of penicillin
  • Atypical LRTI ie: Legionella
89
Q

Lincosamides

A
  • Clindamycin

Use: SSTI

  • In place of penicilin or where IV access is limited
  • Excellent bioavailability & tissue penetration when taken orally

MOA: Bacteriostatic - inhibition of bacterial & RNA protein synthesis

90
Q

Tetracyclines

A
  • Tetracycline
  • Doxycycline

Bacteriostatic - inhibition of RNA & bacterial protein synthesis

Use: Atypical bacteria lacking cell wall. Eg: Chlamydia, Mycoplasma Rickettsia infections, Typhus

SE: GI Upset- Reflux Oesophagitis, Diarrhoea & Photosensitivity

91
Q

Fluoroquinolones

A
  • Ciprofloxacin

Use: Gram -ve infections

Bacterial DNA strucutre & function

SE: CDAD

92
Q

Oral combination pill contraceptives

A
  • Oestrogen/Progestrogen

Uses: Contraception, Dysmenorrhea, Menorrhagia

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

MOA: Suppresses Ovulation and Reduces LH & FSH Secretion.

Low Oestrogen has negative effect on Anterior Pituitary- Inhibits LH

Progesterone has negative effect on Anterior Pituitary- Inhibits LH & FSH

SE: Breakthrough bleeding, Nausea, Depression, Increased CV Risk (Oestrogen): IHD, Riased BP, THromboembolism, Stroke, Slight Breast Cancer risk w/ long term use

93
Q

Oral mini-pill contraceptives

A
  • Progesterone only

Suppresses ovulation (negative feedback AP for LH and FSH), alters endometrium (inhibits endometrial glands & makes mucus thicker) preventing sperm/egg interaction

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:* Contracpetion, Dysmenorrhagia, Menorrhagia, Emergency contraception
  • Benefits:* can be used instead of COCP when oestrogen is contraindicated
  • SEs:* slight increased risk of thrombotic events (stroke, DVT) and breast cancer. Breakthrough bleeding, Nausea, Vomiting
94
Q

Implants/injectible contraceptives

A
  • Long acting progesterone

Moderate/high dose progesterone causing HPO onhibition suppresses ovulation. Also has mucus/endometrial effects.

SEs: nausea, breakthrough bleeding, depression

95
Q

Hormone Replacement Therapy (HRT)

A
  • Oestrogen alone
  • combined oestrogen and progestin
  • selective oestrogen receptor modulatoes (SERMs( - tamoxifen

Uses: Treats symptoms of menopause- hot flushes, vaginal dryness, sweats, loss of libido and reduces risk of osteoporosis.

MOA: Oestrogen & Progesterone restore the hormone levels. 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.

Combination w/ Progestin avoid cystic endometrial hyperplasia

MOA SERM tamoxifen: Partial Agonist at bone & antagonist & brest & uterine receptors

SEs: Thromboembolism, Stroke. Breakthrough Bleeding, BReast tenderness, Increased breast cancer risk, Increased dementia risk >65yrs

96
Q

Drugs used to induce labour

(vaginal administration)

A
  • Prostaglandin E2 (PGE2; dinoprostone)

Stimulates uterine contraction and cervical ripening

97
Q

Drugs used to augment labour

(IV administration)

A
  • Oxytocin

Oxytocin increases uterine contractions and delivery of the placenta in 3rd stage of labour

Given as an infusion

98
Q

Non-benzodiazepine Hypnotics

A

Zopiclone

MOA: Enhances GABA binding to GABA-A receptors

Use: Insomnia

99
Q

Inhaled analgesics

A

Nitrous Oxide + Oxygen

MOA: unclear

Use: analgesia during childbirth

SE: Decrease synthesis vitamin B12

Kim's Drug List (9 decks)

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