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
Gastric Acid Neutralisation
Uses: Reflux oesophagitis - OTC & prescribed
SE: Mg –> Diarrhoea
Al –> Constipation
Antacids + Alginates
- 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
H2 Receptor Antagonists
- Cimetidine
- Ranitidine
Competitively inhibits gastric H2 receptors to decrease acid secretion.
OTC
Cimetidine inhibits many cytochrome P450 enzymes
Proton Pump Inhibitors
- 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
Bulk Laxatives
- 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
Stimulant Purgatives (2)
- 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*
Faecal Softeners
- 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
Osmotic Laxatives (3)
- 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
Oral Rehydration Therapy
- 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
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
Carbonic Anhydrase Inhibitor
- 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)
Osmotic diuretic
- 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)
Loop Diuretics
- 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
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.
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
Potassium Sparing Diuretics
Subclass: Aldosterone Antagonists
- 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.
Potassium Sparing Diuretics
Subclass: ENaC Antagonists
- 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
Renin Inhibitor
- 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
Angiotensin-converting Enzyme (ACE) Inhibitor
- 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
Angiotensin-II receptor antagonists
- Losartan
- Valsartan
Binds to the angiotensin-II receptor, preventing it from working. RAAS cannot increase BP
Aldosterone Antagonist
- Spironolactone
Antagonist of aldosterone by blocking the mineralocorticoid receptor. Means RAAS cannot increase BP
Thyroid Hormones
- Levothyroxine (Synthetic T4)
- Liothyonine (Synthetic T3)
Use: Hypothyroidism
Activation of Thyroid Hormone Receptor
Mimics thyroid hormone by binding to incracellular alpha & beta thryoid receptors
Alpha-adrenergic blocker
(to treat altered voiding)
- 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)
Urinary anti-spasmodic; anticholinergic
(Tx of Urinary Incontinence)
- 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
B2-Adrenergic Agonists
(tx of airway disease)
- 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
Anti-cholinergics
(Airways)
- 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
Methylxanthines
- 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
Leukotriene Antagonists
- 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
Glucocorticoids
(Airways)
- 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
Beta-adrenergic receptor antagonists
(Beta blockers)
- 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
Calcium Channel Antagonists
(for heart failure and hypertenison)
- 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.)
Nitrate Vasodilators
- 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
Anti-cholinergic
(for emergency bradycardia treatment)
- 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
Sympathomimetics
- 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
ACE inhibitors
- 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
HMG-CoA Reductase Inhibitors
(statins)
- 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
Neprilysin inhibitors
(used with an ARB drug)
- Sacubitril (used with valsartan)
Neprilysin = Enzyme
Inhibition of natriuretic peptide breakdown –> Promote Water & Sodium excretion
Antiplatelet Drugs (2)
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
Anticoagulants (4)
- 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
Thrombolytics
- 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
Dopaminergics
(pharma basal ganglia disorders)
- 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
Dopa-decarboxylase inhibitor
- 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
COMT inhibitor
(catechol-O-methyl transferase inhibitor)
- Entacapone
- Tolcapone
Inhibits COMT in the periphery (outside CNS), reducing dopamine breakdown and allowing for more in the CNS
MAOIB Inhibitor
(Monoamine oxidase inhibitors, B form inhibitor)
- Rasagiline
- Selegiline
Inhibits MAOIB so reducing central metabolism breakdown of dopamine in the CNS
Use: Adjunct with levodopa/carbidopa for Parkonsonism
Anticholinergics
(BG disorders)
- 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)
Dopamine-depleting Drugs
- 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
Weak analgesic/Antipyretic
- 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.
NSAIDs
- 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
COX-2 selective NSAIDs
- 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
Weak opioid analgesics
- 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)
Strong Opioid Analgesics
- 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
Partial/Mixed Agonist opioid analgesics
- 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
Opioid receptor antagonists
- 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
Drugs used to manage opioid addiction
- 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
Drugs to treat neuropathic pain
+ 4 types of neuropathic pain?
- 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
Tricyclic Antidepressants
- Amitriptyline
- Nortriptyline
- Dosulepin
- NA reuptake blocker - MAIN action
- Serotonin reuptake inhibitor
- a1 adrenoreceptor antagonist
- H1 receptor antagonist
- M1 receptor antagonist
SEs: Anticholinergic syndrome, Sedation (H1 blocker), Dry mouth, constipation (M1 muscarinic blocker), cardiac dysfunction (a1 adrenoreceptor blocker)
Selective Serotonin Reuptake Inhibitors (SSRIs)
- 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
MAOIs
- 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*
Atypical Antidepressants
- 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
Mood Stabiliser
- 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
1st generation (classical) Anti-psychotic
- 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
2nd generation (Atypical) Antipsychotics
- 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
General Anaethetic
- 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
Local Anaesthetic
- 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
Neuromuscular blockers
- 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
Drugs used to reverse NMB block
- 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
Muscle Relaxants/Sedatives/Anxiolytic-hypnotic
(Think more sedatives and one that works in a similar way)
-
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.
Muscle Relaxants/Sedatives/Anxiolytic-hypnotic
(Think more sedatives but less in anaesthesia in theatre)
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
Muscle Relaxants/Sedatives/Anxiolytic-hypnotic
(Think more triad of anaesthesia)
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
Benzodiazepine
(Antagonist)
- Flumazenil
BDZ antagonist - revers bezodiazepine sedatives
Anti-Epilepsy drugs (AEDs)
- 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
Benzodiazepines for Epilepsy
- 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.
Barbituates (Barb)
- 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
Anticholinesterases
(for dementia)
- Donepezil
- Galantamine
- Rivastigmine
Reversible inhibitor of acetylcholinesterase
Use: mild- moderate AD
SE: Nausea & vomiting
Glutamate NDMA receptor antagonists
- 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
Antimicrobial/Antiviral drugs for CNS infection
- 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
Corticosteroid
(CNS infections)
- Dexamethasone
Glucocorticoid receptor agonist
Drugs used to treat hypercalcaemia
- 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+
Drugs used in the management of hypocalcaemia
- 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
Drugs used in the management of vitamin D deficiency
- 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.
Drugs used to manage osteoporosis
- 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
Anti-proliferative agents
(DMARDs)
- 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
Aminosalicylates
(DMARDs)
- Sulphasalazine
- Mesalazine
Mechanism unclear - possible COX inhibition
Biologics (monoclonal antibodies)
- Infliximab
Anti-TNF cytokine - bind and block proinflammatory function of TNF-alpha
- Rituximab
Depletion of B-lymphocytes CD20
Beta lactams - Penicillins
-
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
Beta lactams - Carbapenem
- Meropenem
Use: Infections in ITU & Complex, multi drug resistant infections
Bacteriocidal - cell lysis by blocking cell wall synthesis
Cephalosporins
- 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
Nitroimidazole
- Metronidazole
USE: Anaerobic infecitons- abscess
MOA: Bacteria DNA strucutre & function
Macrolides
- Erythromycin
Bacteriostatic - inhibition of bacterial protein/ RNA synthesis
Uses: URTI, LRTI, SSTI, Atypical LRTI
- SSTI in place of penicillin
- Atypical LRTI ie: Legionella
Lincosamides
- 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
Tetracyclines
- 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
Fluoroquinolones
- Ciprofloxacin
Use: Gram -ve infections
Bacterial DNA strucutre & function
SE: CDAD
Oral combination pill contraceptives
- 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
Oral mini-pill contraceptives
- 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
Implants/injectible contraceptives
- Long acting progesterone
Moderate/high dose progesterone causing HPO onhibition suppresses ovulation. Also has mucus/endometrial effects.
SEs: nausea, breakthrough bleeding, depression
Hormone Replacement Therapy (HRT)
- 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
Drugs used to induce labour
(vaginal administration)
- Prostaglandin E2 (PGE2; dinoprostone)
Stimulates uterine contraction and cervical ripening
Drugs used to augment labour
(IV administration)
- Oxytocin
Oxytocin increases uterine contractions and delivery of the placenta in 3rd stage of labour
Given as an infusion
Non-benzodiazepine Hypnotics
Zopiclone
MOA: Enhances GABA binding to GABA-A receptors
Use: Insomnia
Inhaled analgesics
Nitrous Oxide + Oxygen
MOA: unclear
Use: analgesia during childbirth
SE: Decrease synthesis vitamin B12
