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41 Cards in this Set
- Front
- Back
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Iron Replacement
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Fe2+ only:
ORAL - FeSO4 (iron sulfate) or Fe gluconate PARENTERAL - Fe-polymaltose serious is overdose, those with GI irritation must revery to parenteral therapy Also avoid drugs & foods that limit absorption - antacids, foods (phytates & phosphates), ABs (tetracyclines & fluoroquinolones) |
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Folic Acid
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Function: DNA synthesis - (cofactors in dTMP and Purine synthesis)
Sources: green veges, meat Replaces ORALLY - daily, no adverse effects |
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Hydroxocobalamine
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Function - used to make Folic Acid - B12/Cobalamine used for converting Methyl('trapped') FH4 to Formyl FH4. (and hence, dTMP and Purine synthesis)
INTRAMUSCULAR INJECTION of hydroxycobalamine, no adverse effects |
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Drugs used for inadequate production of:
a) RBCs b) Granulocytes c) Platelets |
RBCs - Erythropoetin
deficient in CKD, replaced by s/c injections Granulocytes - G-CSF (Filgrastim) recombinant human granulocyte colony stimulating factor used in those with chemo or bone marrow transplants (low granulocytes) Platelets - Thrombopoetin-mimetic (Romiplostim) used in idiopathic thrombocytopaenic purpura and marrow transplant |
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ANTICOAGULANTS, ANTIPLATELET DRUGS, THROMBOLYTICS
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Anticoagulants
(Warfarin, Heparin) - deplete functional CFs (Dabigatrin/Rivaroxaban) - direct enzyme inihibition Antiplatelets (Aspirin, Clopidogral, Dipyridamole) Thrombolytic drugs (t-PA) |
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Warfarin
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(weak acid) Action - inhibits VKORC1 which 'recycles' vitK from KO to KH2.
Less KH2 (Vit K) decreases PTM carboxylation of glutamic acid in CF 2, 7, 9, 10, Ptn. S and C Adverse effects - bleeding, warfarin skin necrosis, teratogenic Significant Genetic differences in p'kinetics (CYP2C9) and p'dynamics (VKORC1) High ADRs - via: CYP2C9 induction/inhibition, absorption, protein binding, also indirect(T3/4, Oestrogen, ABs, Heparin/antiplatelets) Monitored via INR Reversed by FFP and Vit K |
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Heparin
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(glycosaminoglycan) Action - binds to and helps ATIII (which inactivates thrombin) - less thrombin in thrombin-fibrin clot.
Faster than warfairn. Given Parenterally Used for thrombi/emboli, pregnancy Adverse effects - bleeding, Heparin induced thrombocytopaenia Low MW and Fondaparinux - more specific, longer t1/2, less side effects, more expensive Monitored with APTT (only full unfractionated heparin) |
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Dabigratrin & Rivaroxaban
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Dabigatrin - direct thrombin (IIa) inhibitor
Rovaroxaban - direct Xa inhibitor both oral and new |
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Aspirin
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Acetyl salicylic acid
acetylates COX (which turns AA to PG) - PGs used to make TxA2. Less TxA2 - defective clot formation (only platelets and RBCs have a nucleus - so can't make more COX after inhibition) |
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Clopidogrel
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Blocks ADP receptors on platelets irreversibly
Adverse effects - diarrhoea, nausea, bleeding Prasugrel (same, new) |
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Dipyridamole
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Phosphodiesterase inhibitor - action unknown (less second messenger breakdown in platelets - cAMP & cGMP)
less platelet aggregation & adhesion limited clinical use Patients with TIA where aspirin alone is not preventing them |
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t-PA
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Physiologically activates Plasminogen -> Plasmin
more of it, more plasmin, more breakdown - thrombolysis IV, immediate, esp. AMI |
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CLASSIFICATION OF ANTIARRHYTHMIC DRUGS (Vaughan-Williams)
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Class I - Na+ Channel Blockers
Class II - b-AR Blockers Class III - Prolong ERP (Class IV - Ca2+ Channel Blockers) Adenosine Digoxin |
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Lignocaine
Flecainide |
1) Na+ Channel blockers - slow the rate rise of depolarisation (Phase 0)
each cell takes longer - sum of all delays slower Not widely used anymore - cause arrythmia - slows conduction of 'latent' circuits, timing falls into critical range lignocaine - local anaesthetic |
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b-AR blockers for arrythmia
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Propanolol, Metoprolol (and other -olol's)
Opposite of what happens in SNS 1) Slower conduction - blocks V gated Na channels (also has ligand receptor) , Phase 0 slope lower - sum of all delays (PR interval increases) 2) Lower automaticity - blocks 'leaky' Ca and Na channels - slope lower every cell fires a split second later (slower conduction) and pacemakers fire less often (decr. automaticity) No latent re-entry risk as mainly active in atrial and antrioventricular tissue |
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Amiodarone
Sotalol |
Prolongs ERP
Amiodarone - hugely anti-arrythmic, Toxic Sotalol - b-blocker (also blocks K+ channels) |
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Ca channel blockers as anti-arrythmics
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not used
used as ANTIHYPERTENSIVES |
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Adenosine
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opens K+ channels, lowering resting membrane potential
only IV For Dx of SVT - reverts when given Adverse effects - trasient asystole, bronchospasm Caffeine - adenosine antagonist |
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Digoxin
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Blocks Na/K pump (Na/K ATP'ase)
diminished Na gradient via Na/Ca transporter (which keeps most Ca extracellularly) intracellular Ca is all stored in the SR - therefore, digoxin increases SR stores of Ca 1. Incr in contractility 2. Slower HR (indirect vagus stimulation - slower SA node & conduction) 3. Incr resting membrane potential (due to K+) Uses - atrial tachyarrythmias - slows rate (not ventricular), HF Toxicity - arrythmias (tachy: higher resting membrane and more afterpotentials) neurological (confusion, nausea, xanthopsia) DIGOXIN IS COMPETITIVE WITH POTASSIUM - DO NOT GIVE TO A HYPOKALAEMIC |
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ANTIHYPERTENSIVES
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Initial Rx: (volume first)
1. thiazide diuretic or ACE-I /> AT1 blocker 2. then - add the other (thiazide or ace) 3. add Ca channel blocker 4. add a1 or b AR blocker |
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How does treatment choice of hypertension change with heart failure, diabetes, asthma
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1. HF - ACE-I first as volume reduction and reduced peripheral resistance helps CO
b-blockers reduce mortality 2. ACE-I benefits diabetic renal disease 3. Asthma - has b-blocker risk |
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Calcium channel blocking drugs
(action and effects) |
keeps calcium out of heart and blood vessels - makes them more relaxed
1. reduced action potential duration (but not ERP) - Ca channel opening responsible for prolonged plateau (phase 2) - smaller plateau duration, therefore, reduces cardiac contractility 2. reduced automaticity - on phase 4 leak channels, hence, antiarrythmic Adverse Effects 1. vascular selective (-dipines) - headache, oedema, hypotension 2. cardioselective (verapamil) - bradyarrythmia, HF, hypotension, constipation (not fully selective for myocardial cells, also works on gut) |
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Calcium channel blocking drugs
(names) |
Cardioselective
-verapamil Vascular Selective -dihydropyridines: nifedipine, felodipine, amlodipine Non-selective -diltiazem |
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ACE inhibitors
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-prils
Ramipril, Perindopril (Captopril - grandfather, not used) (Enalapril - not used) ADRs 1. sudden hypotension with first dose (hence, at night) 2. renal failure (fall in GFR as afferent arteriole contraction) 3.cough - bradykinin buildup 4. angioneurotic oedema (neural and bradykinin response) |
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AT1 antagonists
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-sartans
-Candesartan, irbesartan similar to ACE inhibitors but cough and angioneurotic oedema not present (bradykinin adequately broken down by ACE) |
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Blockage of RAAS
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prils and sartans
used for hypertension and heart failure |
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a1-AR blockers for hypertension
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Prazosin
peripheral vasodilatation Adverse effects: reflex tachycardia (so b-block first) peripheral oedema no more reflexes (hypotensive but no postural hypertension reflex) |
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b1-AR blockers for hypertension
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reduce - automaticity, contractility, conduction of heart.
no longer first line for hypertension (used as antiarrythmic) Adverse effects - brochospasm (fatigue, cold peripheries, bradycardia, sleep disturbance) slowly give b-blockers in HF as mortality is usually due to arrythmia, not lower heart work |
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Heart Failure management
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first priority is to lower volume & peripheral resistance (as physiological mech's to maintain BP at the expense of organ perfusion)
1. ACE-I or AT1 blocker 2. Loop diuretic 3. b-AR blocker (arrythmia risk) 4. Digoxin (incr. contractility) 5. Correct cause/risk factors |
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Drug Treatments for Angina
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1. b-blockers
2. verapamil/diltiazam/nefidipine/felodipine/amlodipine 3. nitrates 4. nicorandil |
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Nitrates
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Glyceryl trinitrate (GTN)
Isosorbide (di)nitrate (2nd gen) short - ONER, rapid 1st pass metabolism NO mediated peripheral vasodilation tachyphylaxis |
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Nicorandil
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last resort
NO donor - mediated vasodilation activated K+ channels in vascular smooth muscle (lower memb pot) |
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Immediate management of MI
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1. Analgesia - morphine, nitrates
2. Limit infarct - thrombolysis, ACE inhibit, nitrates, oxygen 3. Arrythmia - b-block 4. Anticoag - aspirin, clopidogrel, heparin 5. Manage acute HF |
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Long term management of MI
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1. Aspirin (recurrent MI)
2. Anticoagulation (recurrent MI) 3. b-block (arrythmia) 4. ACE inhibition (remodelling) |
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Diuretics that prevent Na reabsorption
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1. LOOP (frusemide/bumetanide)
2. early DCT (thiazide/indapamide) 3. late DCT (amiloride/spironolactone) |
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Frusemide/Bumetanide
Thiazide/Indapamide |
Loop diuretics & Early DCT diuretics
all block Cl and Na co-transport on luminal membrane (of K/Cl/Na) Earlier - works better (ie. more Na reabsorbtion prevented) |
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Spironolactone
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analogue of aldosterone (antagonist at the nuclear receptor)
binds to nucleus of late DCT cells and represses transcription of inducable Na/K ATP'ases it's metabolite canrenone does the same hence, less Na reabsorbed and less K+ excreted (K+ sparing) |
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Amiloride
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Blocks Na channel specifically in late DCT
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Mannitol
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simple sugar
not transported across membranes - but passes through glomeruli |
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Explain the mechanism of K+ wasting
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Loop and early DCT diuretics
diuretic causes lower blood volume - detected and so aldosterone released (via RAAS) aldosterone induces Na/K ATPases in late DCT - more Na retention (counter-active) but also more K+ excretion! |
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Diuretic ADRs and Contraindications
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1. Frusemide + Digoxin = BAD, hypokalemia
(any loop diuretic or early DCT) 2. Late DCT + renal failure = BAD, hyperkalemia (K+ retained in RF) 3. Thiazides - uric acid retention (pathway competition) and if severe, gout. (Not with loop, as excreted faster than thiazides) 4. Spironolactone - estrogen effects |
