Term
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Definition
| Competitive and reversible acetylcholinesterase inhibitor, medium duration, acts at the NMJ to increase Ach levels in the synaptic cleft. Used in myasthenia gravis. |
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Term
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Definition
Depolarising blocker of Na+ channels. Competitive agonist of Ach receptors (which are G-protein coupled to Na+ channels).
Phase I block: suxamethonium produces sustained depolarisation of membrane by binding strongly to Ach-receptors at the NMJ.
Phase II block: stays bound as Na+ channels close and enter inactivated state, preventing further depolarisations.
Causes muscle twitches at first. |
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Term
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Definition
| Non-depolarising neuromuscular blocker. Competitive antagonist, blocks Na+ channels, preventing depolarisation. |
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Term
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Definition
Selective Beta 1 antagonist (beta blocker). Decreases effect of sympathetic stimulation on the heart i.e. negative chronotrope and inotrope (decreases transmural pressure); also decreases renal renin output (acts at JGA of kidney) --> decreases CO and BP.
Chronic use decreases TPR
Decreases work of the heart so good for angina (decreases O2 consumption). Also used for supraventricular & ventricular arrhythmias, HF, glaucoma, anxiety.
ADRs- bronchospasm, HF, reduced exercise tolerance, fatigue, heart block, peripheral vasoconstriction, CNS effects (crosses BBB) |
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Term
| Clonidine, alpha-methyldopa |
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Definition
Centrally-acting Alpha 2 agonist. Reduces sympathetic outflow from brainstem (does the same job as NA does- negative feedback).
Reduces BP by reducing chronotropy and inotropy. |
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Term
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Definition
Vasoselective CCB. Inhibits Ca2+ influx through L-type calcium channels (LTCC), causing smooth muscle relaxation of arterioles --> decrease in TPR --> decrease in BP.
Decreases afterload (no effect on venous system so no change in preload), by binding to and stabilising Ca2+ channels in the inactivated state.
Good for HYPERTENSION.
Don't use for angina, as it causes reflex tachycardia
ADRs: extension of drug action (flushing, constipation, hypotension, bradycardia, AV block, HF) |
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Term
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Definition
Cardioselective CCB.
ANGINA (reduces O2 demand)
TACHYARRHYTHMIAS (supraventricular) (Ca2+ channel block more pronounced at higher activity, reduces SAN rate and AVN conduction) Remember that pacemaker cells require slow inward Ca2+ current in order to discharge spontaneously.
ADRs: extension of drug action (flushing, constipation, hypotension, bradycardia, AV block, HF)
Reduces force of contraction (-'ve inotrope) and rate of contraction (-'ve chronotrope)at SAN. Note at AVN it decreases conduction velocity (-'ve dromotrope).
MOA: competes with Ca2+ binding --> promoting inactivated state --> slow channel recovery from inactivation --> increased refractory period. |
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Term
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Definition
Vasodilator Increases cGMP --> protein kinase --> smooth muscle relaxation. Reduces preload and afterload. Good for: angina, HF (reduces afterload --> increase EDV); oedema; reduces O2 demand)
ADRs: extension (flushing, headache, orthostatic hypotension)
Drug interactions: - CCBs - Beta blockers - PDE5 inhibitor (e.g. sildenafil (viagra)- PDE5 terminated cGMP) |
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Term
| Renin (not a drug but good revision) |
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Definition
RAA system.
Low BP/ SNS/ low Na+ --> JGA --> renin --> converts angiotensinogen --> angiotensin I --> angiotensin II -->
- vasoconstriction
- Na+ and H2O retention
- aldosterone (Na+ and H2O retention)
- SNS upregulator
- ADH release
- cardiac & vascular hypertrophy |
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Term
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Definition
Decrease ATII by inhibiting ACE.
This results in
- arteriolar dilation --> reduced afterload
- venous dilation --> reduced preload
- increased bradykinin --> vasodilation (ACE breaks down kinins)
- downregulate SNS and ATII effect on kidney
- reduces aldosterone --> reduces volume
- inhibits cardiac and vascular remodelling (associated with chronic HT, MI, HF)
USED FOR:
- hypertension
- CHF (decreased afterload & preload improves O2 supply/demand ratio)
ARDs:
- cough (bradykinin)
- angioedema
- initial hypotension
- renal issues (e.g. those with impairment) |
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Term
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Definition
ARB (angiotensin II receptor blocker).
Do not cause kinin accumulation --> reduced cough.
Block ATII effect on AT1 receptors --> prevent:
- vascular smooth muscle contraction (causes GI disturbances though)
- aldosterone secretion
- SNS
Doesn't inhibit ATII receptors (which increases NO production --> vasodilation, anti-thrombosis, anti-inflammatory).
USED FOR:
- HT
- HF
ADRs: (well tolerated)
- cough
- hypotension, syncope, headache
- rash
- GI disturbances
- hyperkalaemia (aldosterone causes K+ excretion)
- teratogenic |
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Term
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Definition
Increases inotropy, decreases HR:
1) Inhibits Na+/K+ ATPase. If intracellular Na+ is raised,intracellular Ca2+ accumulates (Na+/Ca++exchanger) --> increased force of contraction.
2) Increases vagal activity to heart --> reduces SAN firing and AVN conduction velocity --> decreases HR.
USED FOR:
- HF
- Rate control e.g. AF
ADRs:
Can cause Ca2+ overload in SR (digoxin toxicity) --> spontaneous release of Ca2+ --> released Ca2+ exits cell through Na2+/Na+ exchanger (1 Ca++ out for every 3 Na+ in) --> net depolarising current--> delayed after-depolarisation --> arrhythmia
Also:
- narrow TI
- interacts with CCBs, beta-blockers, amiodarone, NSAIDS
- nausea, vomiting
- confusion
- interacts with diuretics (that reduce K+): K+ competes with digoxin for binding, so hypokalaemia --> increased digoxin activity |
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Term
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Definition
Class III anti-arrhythmic.
Blocks K+ channels, so prolongs AP --> decreased chance of re-entry.
USED FOR:
- heaps of arrhythmias (supraventricular and ventricular)
> cardiac arrest
> VF/ VT
> AF
ADRs:
- photosensitive skin rashes & decolourisation
- thyroid abnormalities
- pulmonary fibrosis
- corneal deposits
- neurological and GI distubances
- damages veins undiluted |
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Term
| Revision: PGI2 (prostacyclin) |
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Definition
| Synthesised and secreted by endothelial cells. Increases platelet cAMP release (inhibits activation), decreases platelet COX activity --> decreases TXA2 production, therefore reduces platelet aggregation and secretion. |
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Term
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Definition
ANTIPLATELET
Non-selective COX inhibitor --> reduces COX 1 --> reduced TXA2 synthesis --> inhibit platelet aggregation.
Minimal effects on PGI2 because it is synthesised by endothelial cells (which can make more COX since they have DNA hohoho)
ADRs:
- bleeding (GI) |
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Term
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Definition
ANTIPLATELET (if allergic to aspirin)
Non-competitive ADP-receptor antagonist --> prevent action of GpIIb-IIIa receptor --> reduced platelet activation.
Remember: ADP activates platelets by:
1) Causing a conformational change in GpIIb-IIIa complex (fibrinogen receptor)
2) induces binding to fibrinogen
3) platelet aggregation |
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Term
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Definition
Increase action of antithrombin --> inactivates fXa and thrombin (forms an inactive complex with them) --> reduces fibrin formation
ADR:
- bleeding
- HIT (heparin-induced thrombocytopenia). Heparin-dependent IgG activates platelets --> thromboses |
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Term
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Definition
LMWH. Potentiates effect of antithrombin on fXa and thrombin.
Longer duration of action (4-6h), increased bioavailability, fewer ADRs than heparin.
USES:
- prevent DVT
- sometimes MI |
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Term
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Definition
Vitamin K epoxide reductase inhibitor --> prevents gamma-carboxylation of factors 10, 9, 7 and 2 (prothrombin; also proteins C and S --> reduced fibrin.
Takes 24-48h to take effect (cover with Clexane in acute events)
- DVT
- PE
- Stroke
- other thromboembolic states
Reversal:
- withdrawal
- vitamin K adminstration (slow acting)
- Fresh frozen plasma containing clotting factors (fast-acting)
ADRs:
- Very narrow TI
- bleeding
- bruising
- interacts with heaps of drugs (CYP450s, antibiotics which decrease vit K-producing GIT microflora--> increased effect of warfarin) |
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Term
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Definition
Fibrinolytic serine protease.
Increases cleavage of plasminogen --> plasmin --> digestion of fibrin, fibrinogen, other coagulation factors.
Normally synthesised by endothelial cells.
USES:
- ACUTELY in MI, ischaemic stroke
ARDs:
- bleeding |
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Term
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Definition
Osmotic diuretic. Easily filtered, poorly absorbed. Work at whole tubule.
USED FOR: increased ICP
ADRs:
-toxicity (GIT, headaches, hypersensitivity, increased ECV)
- glycerol-like (hyperglycaemia, glycosuria) |
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Term
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Definition
Loop diuretic, most potent. Compete with Cl- for binding, inhibiting Na+K+Cl- co transporter (NKCC2, increase excretion of Na+, K+, Cl-, Mg2+, Ca2+.
USED FOR:
- peripheral & pulmonary oedema (moderate-severe HF)
- hypertension
ADRs:
- hyperuricaemia --> gout
- hypovolaemia --> syncope
- hyponatraemia
- hypokalaemia
- decreased Mg++ and Ca++ |
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Term
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Definition
Thiazide diuretic, acts at DT. Inhibits NaCl cotransporter (competes with aldosterone) --> increases salt excretion.
USED FOR:
- hypertension (front-line use with ACEIs/ARBs, CCBs)
ADRs:
- hyponatraemia --> confusion
- metabolic acidosis (decreased H+)
- hypokalaemia --> arhythmias
- hyperuricaemia --> gout
- impotence
- weakness |
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Term
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Definition
K+ sparing diuretic (weak diuretic). Acts at DT and CD. Aldosterone antagonist (therefore dependent on aldosterone levels).
Aldosterone regulates Na+/K+ pumps (Na+ reabsorption, K+ excretion). Reduces driving force for K+ secretion.
USED FOR:
- hypokalaemia
- liver disease with ascites
- severe HF |
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Term
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Definition
| K+ sparing ddiuretic. Inhibits Na+ channels (associated with aldosterone-dependent Na/K pump), decreasing Na+ reabsorption and decreasing K+ excretion. |
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Term
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Definition
HMG-CoA reductase antagonist --> reduces cholesterol synthesis (from CoA) in the liver --> increased ApoB100 receptors --> increased clearance.
Also slight increase in HDL.
Pleiotropic effects due to PPAR-alpha activation --> reduce inflammation (decrease LDL uptake by macrophages,increase NO).
ADRs:
- myopathy & rhabdomyolysis (decreased Na+/K+ ATPase --> increased Na+ in cells --> burst) - rare but significant
- interacts with CYP-metabolised drugs |
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Term
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Definition
PPAR-alpha activation --> increases FA oxidation in muscle & liver; lipogenesis in liver.
Lowers LDL by shift in hepatocyte metabolism towards FA oxidation.
- increases HDL
- decreases plasma TG and cholesterol. |
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Term
| Cholestyramine and colestipol |
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Definition
Bile acid sequestrants. Positively charged, so bind negavite bile acids in GIT, preventing bile acid reabsorption --> increased cholesterol metabolism to bile acids (and decreased cholesterol absorption) --> decreased cholesterol, increased LDL receptor synthesis, increased LDL clearance.
ADRs:
- resins confined to gut --> bloating, diarrhoea/ constipation |
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Term
| Aims for treatment of an acute MI |
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Definition
Re-establish balance in supply/demand of O2
1) Increase O2 supply
- increase diuration of diastole, decrease coronary resistance
2) Decrease myocardial O2 demand
- decrease HR
- decrease contracility
- decrease wall stress/work (reduce preload and afterload) |
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Term
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Definition
| 1) MONA -Thrombolytics -Antiplatelets (ASAP) -Beta blockers (metoprolol/atenolol)IV > with no evidence of HF, heart block, asthma > decreases O2 demand--> limits infarct size FOLLOW-UP: "Send them home with a SAAB Statins, ACEI's, Antiplatelets/anticoagulants, Beta-blockers, nitrates PCI or CABG |
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Term
| Treatment of NSTEMI and unstable angina |
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Definition
Reduce progression
- antiplatelets (aspirin)
- anticoagulants (LMWH)
- oral nitrates (relieve angina)
- B blockers, ACE Is, statins |
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Term
| Management of stable angina |
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Definition
SNAB
- statins (or fibrates)
- nitrates (sl or oral GTN)
-aspirin (low dose)
- B-blocker (or ACEI)
PCI or CABG |
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Term
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Definition
Oral corticosteroid.
Suppresses pro-inflammatory cytokines, increases anti-inflammatory cytokine production. It increases lipocortin which inhibits inhibits PLA2 --> decreased leukotrienes and PG's.
Reduces inflammation.
ADRs:
- increase glucose, protein catabolism, fat re-distribution
- negative feedback of HPA axis
- osteoporosis (inhibits vit D-mediated Ca2+ absorption, suppresses osteoblasts)
- infection, wound healing prolonged |
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Term
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Definition
Inhhaled cotricosteroid. Increases anti-inflammatory and decreases pro-inflammatory cytokine production.
- Reduces airways inflammation
- inhibits macrophages (reduces antigen response)
- reduces histamine release
- reduces epithelial damage
Extensive 1st pass metabolism --> 1% reaches systemic circulation
To reduce ADRs:
- gargle after use
- large volume spacer
- reduce dose frequency (depending on tests and function) |
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Term
| Acute asthma exacerbation (asthma attack) |
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Definition
"SOS"
Salbutamol
Oxygen
Steroids (high dose prednisone for short course ~5d) |
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Term
| Acute exacerbation of asthma (attack) |
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Definition
"SOS"
Salbutamol
Oxygen
Steroids (high dose oral predisone for ~5days) |
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Term
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Definition
Cromolyn. Is a "mast cell membrane stabiliser"
- reduces release of inflammatory mediators
--> reduces recruitment of inflammatory cells
USES (esp in children):
- exercise-induced asthma
- atopic asthma
- irritant-induced asthma
Mild-moderate asthma |
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Term
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Definition
SABA. RELIEVER.
Selective B2 agonist --> increases cAMP --> inhibits bronchoconstriction, hyperpolarises cells.
Onset: 5-15min
Lasts: 2-5h
USES:
- exercise-induced asthma prevention
ADRs (high doses):
- tremor (activation of skeletal muscle B2 receptors)
- increased HR and force (loss of selectivity)
DON'T USE WITH BETA BLOCKERS |
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Term
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Definition
LABA. Symptom controller
- nocturnal asthma
- exercise-induced asthma
Onset: 10-20min
Duration: 12h |
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Term
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Definition
Xanthine. PDE inhibitor --> inhibits cAMP & cGMP degradation --> increased cAMP, cGMP -->smooth muscle relaxation.
Also adenosine receptor antagonism --> ADRs (GIT, tachycardia, diuresis).
Decreased plasma levels by CYP-metabolised drugs. |
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Term
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Definition
"Atropine-like" - muscarinic receptor antagonist.
Given with B2-agonist (double whammy)
USES:
- asthma
- COPD
ADRs:
- dry mouth
- tachycardia, palpitations...
- urinary retention
- GIT (CONSTIPATION, vomiting)
- blurred vision
- headache |
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Term
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Definition
| Leukotriene receptor antagonists --> inhibits inflammation and bronchoconstriction (though small effects since many other pathways) |
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Term
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Definition
H1 antagonist.
Treatment of nausea & vomiting from motion-sickness, morning sickness (not teratogenic) and stomach irritants.
ADRs:
- drowsiness, sedation (perhaps good)
- headache
Act at vestibular nuclei. |
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Term
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Definition
H1 antagonist.
Treatment of nausea & vomiting from motion-sickness, morning sickness (not teratogenic) and stomach irritants.
ADRs:
- drowsiness, sedation (perhaps good)
- headache
Act at vestibular nuclei. |
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Term
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Definition
Muscarinic antagonists (mAch).
Prophylaxis and treatment of motion sickness, postoperative vomiting.
Interrupts cholinergic transmission between inner ear and vestibular nuclei.
ADRs:
- dry mouth
- blurred vision
- urinary retention
- decreases mental alterness |
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Term
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Definition
5-HT3 antagonist (serotonin)
Acts at CTZ, gut.
Used for postoperative nausea and vomiting, also chemotherapy and radiation.
ADRs (uncommon):
- headache
- constipation |
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Term
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Definition
D2 antagonist. Acts on CTZ and GIT:
- block D2 receptors in CTZ--> increase Ach release from myenteric plexus--> increased motility, good for reflux.
ADRs:
- fatigue, insomnia
- movement disorders |
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Term
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Definition
D2 antagonist. Acts on CTZ and GIT:
- block D2 receptors in CTZ--> increase Ach release from myenteric plexus--> increased motility, good for reflux.
Doesn't cross BBB |
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Term
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Definition
Bulk laxative. Made of polysaccharide polymers which do not get broken down --> attract water --> hydrated mass ---> stretching of GIT--> increased motility
ADRs:
- dehydration (need to take more water) |
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Term
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Definition
Osmotic laxative --> retain fluid, cause distension --> increased motility
ADRs: dehydration |
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Term
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Definition
Osmotic laxitive (disaccharide of fructose + galactose). Cannot be hydrolysed, so poorly absorbed. Hydrolysed by microflora --> traps fluids --> abnormally large volume enters colon --> distension, purgation within 1hr.
ADRs:
- cramps
- flatulence
- diarrhoea
- electrolyte imbalance (dehydration) |
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Term
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Definition
| Faecal softener. Detergent, allows penetration of water into faeces. |
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Term
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Definition
lubrication of faeces.
ADRs:
- reduces fat soluble vitamin absorption
- if inhaled, causes liquid pneumonia |
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Term
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Definition
STIMULANT LAXATIVE. Anthroquinone. - - - Stimulates ENS
- increases H2O and salt secretion by mucosa (partly by irritation) |
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Term
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Definition
Anti-diarrhoeal.
Good for traveller's diarrhoea. Opioid, but doesn't cross BBB.
Activates u-receptors on myenteric plexus --> reduces bowel motility. |
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Term
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Definition
Increases viscosity and adherence of mucus to mucosa --> protective barrier.
USES:
- peptic ulcer
- GORD
Added to antacids |
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Term
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Definition
H2 receptor antagonist (competitive). Inhibits effects of histamine on parietal cells, thus reducing cAMP and H+/K+ exchange.
USED FOR:
- peptic ulcers
- mild GORD
Inhibitor of CYP450s
ADRs:
- diarrhoea
- rash
- headache |
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Term
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Definition
PPI (inhibits H+/K+-ATPase) --> decrease H+ secretion into stomach.
Pro-drugs which are activated by low pH. Acid supression for 24-48h (until new pumps made). Decrease H+ secretion regardless of stimulus.
ADRs (minor)
- headache
- abdo pain (??! really? peptic ulcer maybe...?)
- nausea
- diarrhoea
- constipation |
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Term
| Prostaglandins PGE2 and PGI2 |
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Definition
Decrease acid secretion (decrease cAMP), stimulate HCO3- and mucous production.
NSAIDS that inhibit COX-1 decrease PG formation --> gastric mucosal damage |
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Term
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Definition
Omeprazole
Amoxycillin
Clarithromycin |
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Term
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Definition
5-aminosalicyclate. Anti-inflammatory, believed to inhibit COX and lipogenase pathways; scavenges free radicals.
Used in IBD.
Sulfazine- 5-aminosalicyclate + sulfapyridine (toxic--> ADRs)
Mesalazine- less toxic, newer. |
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Term
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Definition
Anti-inflammatory.
Main drug for IBD.
MOA:
- modulates cytokine levels
- inhibits transcription factor NF-B (prevents cytokine gene expression)
- inhibits PLA2 (phospholipase A2)-> prevents formation of inflammatory messenger molecules.
MANY ADRs |
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Term
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Definition
Thymine base. IMMUNOSUPPRESSANT. Inhibits DNA synthesis --> prevents immune cell proliferation. Use in refractory IBD, or in those intolerant to steroids or mesalazine. Also DMARD (inhibits progression of RA)
ADRs- increased susceptibility to infection |
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Term
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Definition
Quinolone antibiotic. Broad spectrum. Inhibits DNA gyrase.
Good for gram + and esp gram - bacteria:
- E. coli
- Salmonella
- Pseudomonas aeruginosa
- Campylobacter |
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Term
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Definition
| Broad spectrum penicillin. Inhibits cell wall synthesis in non-B-lactamase-producing Gram + and - bacteria (e.g. H.influenzae, E.coli, Salmonella). Most Staph aureus is resistant, but can improve with clavulonic acid (e.g. co-amoxiclav) for penicillinase-producing bacteria. |
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Term
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Definition
For penicillinase-producing penicillin-resistant staphylococci.
MRSA needs to be treated with vancomycin. |
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Term
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Definition
Cephalosporin. Inhibits cell wall synthesis.
Used for:
- meningitis
- pneumonia
- septicaemia |
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Term
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Definition
Bactericidal antibiotic, not absorbed orally. Inhibits peptidoglycan formation, active against most GRAM POSITIVE organisms:
- MRSA
- C. difficile
ADRs:
- renal failure
- hearing loss |
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Term
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Definition
Aminoglycoside antibiotic, inhibits protein synthesis.
Many Gram positive, some Gram negative.
Narrow TI.
USES:
- empiric gram - treatment (life-threatening) e.g. P.aeruginosa.
Synergy with penicillin and vancomycin.
ADRs:
- nephrotoxic
- ototoxic |
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Term
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Definition
Macrolide antibiotic. Alternative to penicillin against Gram +
- streptococci
- staphylococci
- pneumococci
- clostridia
- Mycoplasma pneumoniae
- Legionaire's disease |
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