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Cardiac Flashcards

1
Q

What are the possible interactions of nitrates?

A
  • Not to be used in combination with phosphodisterase inhibitors e.g. viagra (prolongs and enhances hypotensive effect)
  • Anti-hypertensive medication (precipitate hypotension)
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2
Q

What are the side effects of amiodarone?

A
  • ACUTE: Hypotension

Chronic Use

  • Bradycardia, AV block
  • Pneumonitis
  • Hepatitis
  • Photosensitivity, grey discolouration of skin
  • Due to high iodine content, can cause thyroid abnormalities (hyper/hypothyroidism)
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3
Q

What is the mechanism by which furosemide acts?

A
  • Inhibits Na/K/Cl cotransporter in ascending loop of henle → increases electrolytes in lumen → increased diuresis
  • Increased dilation of capacitance veins → reduces preload and increases contractile of overstretched muscle
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4
Q

What are the side effects of thiazide diuretics?

A
  • Hypo - Na/K+ (particularly K+ due to increased Na going to distal tubule → increased exchange with K+ → increased K excretion
  • Arrythmias (due to hypo-K+)
  • Hyperglycaemia, hyperlipidaemia and hypercholesteraemia (increased LDL)
  • Impotence in men
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5
Q

What are the SE of beta blockers?

A
  • Bronchospasm
  • Bradycardia, reduce cardiac contractibility
  • Fatigue
  • Peripheral vascoconstriction - cold extremities and Raynaud’s
  • Headache
  • GI disturbance
  • Sleep disturbance/nightmares/hallucinations
  • Male impotence
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6
Q

What are the side effects of ACEi?

A

Hypotension (part 1st dose)

Persistent dry cough - ACE breaks down bradykinin. Blocking it increases bradykinin.

Hyperkalaemia - lowered aldosterone promotes K+ sparing

Renal failure - particularly in combo with NSAIDs - glomerular arteriole needs to be constricted to maintain filtration

Angiooedma/anaphylactic reactions (rare)

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7
Q

What are the CIs for using clopidogrel?

A
  • Active significant bleeding
  • Elective surgery (stop 7 days prior)

Caution:

  • Kidney and hepatic disease (particularly with active bleeding)
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8
Q

What is the mechanism by which ACEi work?

A
  • Blocks ACE which converts angiotensin I to II (lungs)
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - reduces pheriperhal vascular resistance/afterload
  • Dilates the efferent glomerular arteriole - reduces intraglomerular pressure and slow progression of CKD
  • Reduced aldosterone - promotes water/Na+ excretion - help reduce venous return (reduced preload) - beneficial to HF
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9
Q

What are the indications for beta blockers?

A
  1. IHD - 1st line - angina and ACS - improves symptoms and prognosis
  2. HF - 1st line - improves prognosis by reducing chronic synmpathic stimulation
  3. AF - 1st line - reduces VT and paroxysmal AF - prolonging AV node refrac period and restores sinus R
  4. SVT - 1st line - restores sinus R
  5. HTN - not indicated for intial therapy but for when other medicines e.g. ACEi, diuretics etc fail to work
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10
Q

What time of day should diuretics be taken?

A

In the morning/afternoon - to avoid nocturia

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11
Q

Name some of the possible interactions of digoxin?

A

Thiazide/loop duiretics (reduced K+ - increased risk of toxicity)

AMIODARONE, calcium channel blockers, spirolactone, quinine - increases plasma conc and risk of toxicity

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12
Q

What are the potential SEs for AT1 blockers?

A
  1. Hypotension (part after 1st dose)
  2. Hyperkalaemia (aldosterone promotes K+ excretion)
  3. Renal failure (esp with renal stenosis)

DOES NOT CAUSE PERSISTENT COUGH

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13
Q

How are AT1 blockers excreted?

A

Renally and hepatically

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14
Q

What are the SEs of Aspirin?

A
  • GI irritation/ulceration/haemorrhage
  • hypersensitivity
  • Tinnitus (high, frequent doses)
  • Overdose: hypervent, hearing changes, confusion, convulsions, resp arrest
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15
Q

Name some sytochrome P450 inducers?

A

Phenytoin, carbamezapine, rifampicin

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16
Q

What is the mechanisms by which thiazide diuretics work?

A
  • Act on Na/Cl cotransporter in distal convoluted tubule (block)
  • Prevents Na reabsorption and osmotically associated water - increased diuresis
  • Usually reversed by compensatory changes e.g. RAS system
  • However, also has vasodilatory effect by some unknown mechanism which reduces BP
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17
Q

WHat drug class does furosemide belong to?

A

Loop diuretics

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18
Q

How is aspirin eliminated?

A

Renally

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19
Q

What are the contraindications of ACEi?

A

Acute kidney injury/renal stenosis

Hepatic failure

Caution: Pregnant or breastfeeding; CKD

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20
Q

What are the CIs for aspirin?

A
  • <16 yrs - Reyes syndrome (rare, lifethreatening syndrome affecting liver and brain)
  • Aspirin allergy - hypersensitivity
  • Pregnancy - 3rd trimester - prostaglandin inhibition → premature occlusion of ductus arteriosus
  • Peptic ulcer
  • Gout - may precipitate attack
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21
Q

What are the SEs of potassium diuretics?

A
  • GI upset
  • Hyperkalaemia or hyponatramia
  • Hypotension/dizziness (particularly in combo with loop/thiazide)
  • Urinary symptoms
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22
Q

What type of drug is warfarin?

A

Anticoagulant

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23
Q

What are the contraindications for nitrates?

A
  • Severe aortic stenosis - heart unable to increase Q through narrowed valve to maintain pressure in now dilated vasculature
  • Haemodynamic instability (particularly hypotension)
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24
Q

What are the indications for AT1 blockers?

A

Same as ACEi (for those who cannot tolerate chronic cough associated with ACEi)

  1. HTN
  2. Chronic HF
  3. IHD
  4. Diabetic nephropathy and CKD (proteinuria)
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25
Q

What is the mechanism by which beta blockers work?

A
  • Competitive binder of Beta adrenergic receptors; B1 - Heart; B2 - smooth muscle, blood vessels of ariways
  • Blockage reduces sympathic drive → reduces Myocardia iscahemia by:
    • reducing cardiac contractile force
    • increasing perfusion
    • Reducing conduction speed
  • AF - reduces VT by prolonging AV refractory period
  • HTN - reduces BP by reducing renin (acts on B1 receptor in kidney)
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26
Q

What are the CIs for statins?

A
  • Generally well tolerated
  • Cautioned in: hepatic failure (eliminated by P450 enzymes), kidney failure (excreted by), and pregnancy (foetal development needs cholesterol)
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27
Q

What are the CIs for K+ sparing diuretics?

A
  • Hyperkalaemia/hyponatraemia
  • Severe renal impairment

Cautioned in:

  • Hypokalaemia (unpredictable effects)
  • Volume depletion
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28
Q

How are beta blockers eliminated?

A

Hepatic and renally

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29
Q

What are the indications for amiodarone?

A
  • Tachyarrthymias - AF, A. flutter, SVT, VT, VF - ONLY when other theurapetic options are ineffective/not tolerated/inappropriate
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30
Q
A
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31
Q

What are the SEs of loop duiuretic?

A
  • hypotension/dehydration
  • Low electrolyte states e.g. hypocalcaemia, hyponatramia
  • Gout - urate retention
  • Hearing loss/tinnitus - similar co-trasnporter regulates endolymph in inner ear
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32
Q

What are glyceryl trinitrate and isosorbide mononitrates?

A

Nitrates

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33
Q

What are the side effects of nitrates?

A
  • Flushing
  • Headaches
  • Lightheadedness
  • Sustained use - intolerance (avoid at night to ensure nitrate free period every day)
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34
Q

What class of drug is bendroflumethiazide?

A

Thiazide or thiazide like diuretics

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35
Q

What type of drug is Losartan, candesartan and irbesartan?

A

Angiotensin Receptor blocker (AT1)

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36
Q

When is the best time for statins to be taken?

A

Evening (work best when food intake is lowest)

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37
Q

What class of drug is aspirin?

A

Anti-platelet

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38
Q
A
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39
Q

What are the contraindications for warfarin?

A
  1. Immediate risk of haemorrhage (trauma/surgery)
  2. Pregnancy (1st trimester - teratogenic - cardiac and cranial abnormalities)

Cautioned in hepatic disease - reduced metabolism of drug = increased concentration = increased risk of bleeding

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40
Q
A
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41
Q

What is the mechansim by which digoxin exerts if effect?

A

-vely chronotrophic (reduces HR)

+vely inotrophic (increases contractile force)

AF/A Flutter Increases vagal (parasynpathetic) input → reduces AV conduction → reduces vent tachycardia

HF - directly blocks Na+/K+ ATPase pumps → intracell Na+ increases → intracell Ca2+ increases → increased contractile force

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42
Q

What are the SEs of clopidogrel?

A
  • Significant bleeding
  • GI upset (dyspepsia, diarrhoea, abdo pain)
  • Thrombocytopenia (reduced number and/or function)
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43
Q

What are the CIs for thiazide diuretics?

A
  • Hypo Na/K
  • Gout - reduces uric acid excretion → increases urate retention → precipitates acute gout
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44
Q

What is the mechanism by which warfarin works?

A

Inhibits hepatic production of vitamin K dependent coagulation factors (II, VII, IX, X) and co-factor (Proteins, C, S, Z)

Vitamin K needs to be reduced form for coagulation synthesis - done my vit k epoxide reductase

Warfarin inhibits vit K epoxide reductase

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45
Q

What are the indications for ACEi?

A
  1. First/second line for HTN (reduce stroke, MI, death)
  2. Chronic heart failure - 1st line in improving symptoms/prognosis
  3. Ischameic heart disease - reduce risk of subsequent attacks

Diabetic nephropathy and CKD with proteinuria (reduces prtoeinuria and progression)

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46
Q

What are the CIs for loop diuretics?

A
  • Hypovolaemia/dehydration/hypotension

Cautioned in

  • Hepatic encephalopathy
  • Gout (urate retention)
  • Hypo-Na+/K+
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47
Q

What are the indications for statins?

A
  • Primary prevention of CV disease - >40 yrs with with 10yr risk of CV disease >20%
  • Secondary prevention - 1st line alongside lifestyle changes
  • 1st line for hyperlipidaemia e.g. hypercholestraemia etc
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48
Q

What are the possible interactions of AT1 blockers?

A
  • Avoid with K+ elevating drugs (possible hyperkalemia)
  • Avoid with other diuretics (massive hypotension)

AT1 + NSAIDs increases = potential renal failure

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49
Q

What are the contraindications for digoxin?

A
  • 2nd degree or complete heart block
  • Ventricular arrthymias

Cautioned in:

  • Electrolyte disturbance: particularly K+ (digoxin is a competitor of K= so if there is less K+, digoxin will have greater effect → greater risk of digoxin toxicity
  • Renal failure - eliminated by kidneys → increased chance of digoxin toxicity
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50
Q

What are the indications for furosemide?

A
  1. Acute pulmonary oedema
  2. Fluid overload states - chronic HF, renal disease (nephrotic syndrome), hepatic failure (cirrhosis)
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51
Q

What are the possible interactions of warfarin?

A
  1. Cytochrome P450 inhibitors - reduce metabolism = increased risk of bleeding
  2. Cytochrome P450 inducers - increased metabolism = increased risk of clot
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52
Q

What are the indications for digoxin?

A
  • AF/A flutter (however, mostly superseded by Bblockers/Ca++ channel blockers)
  • 3rd Line for HF (where ACEi, B bnlocker, aldosterone blocker or AT1 blocker are insufficient
53
Q

What are the contraindications for AT1 Blockers?

A
  1. Renal stenosis of AKI
  2. Hepatic failure

Caution in

  1. breastfeeding
  2. Pregnancy
54
Q

What are the possible interactions of amiodarone?

A
  • Loads of drugs!
  • Digoxin
  • Calcium channel blockers
  • Grapefruit juice (inhibits hepatic P450 enzymes - increases amiodarone conc - increases risk of SEs)
55
Q

What class of drug does spirolactone and amiloride belong to?

A

K+ sparing diuretics

56
Q

What are the possible interactions of ACEi?

A

Avoid with K+ elevating drugs (inc supplements/K+ sparing duiretics)

  • Other diuretics - massive hypotension

NSAIDs and ACEi increases risk of renal failure

57
Q

What are the SEs of warfarin?

A
  • Narrow therapeutic index i.e. line between therapeutic (antocoagulation) and SEs (bleeding
    1. Bleeding - minor head injury becomes serious haemorrhage
    2. Spontaneous bleeds e.g. episataxis, retroperitoneal haemorrhage
58
Q

How are thiazide drugs eliminated?

A

Renally

59
Q

What are the indications for nitrates?

A

1 Short acting nitrates (glyceryl trinitrate): TX of acute angina and chest pain associated with ACS - IV infiusion (ACS), GTN spray (stable angina)

  1. Long term nitrates (isosorbide mononitrate) - prophylaxis of angina (where B blockers/calcium channel insufficient/not tolerated) - orally
  2. Tx of pulmonary oedema (+ O2, furosemide)
60
Q

What are the interactions of K+ sparing diuretics?

A
  • K+ elevating drugs/aldosterone antagonists - may cause hyperkalaemia
  • Digoxin/lithium - may alter renal clearance so dose adjustment required
61
Q

What is the mechanism by which amiodarone exerts its effect?

A
  • Blocks Na+, K+ and Ca++ channel blockers and anatognist to A + ß adrenergic receptors
  • Reduces conduction velocity and spontaneous depolarisation
  • Increases resistance to depolarisation (AV node)

AF/A flutter -reduced AV depolarisation = reduce ventricular rate

SVT - breaks circuit and restores sinus rhythm

VT - reduces spontaenous depolarisation

62
Q

What are the interactions of thiazide diuretics?

A
  • NSAIDs reduces effectiveness
  • Avoid combination with other K+ reducing drugs e.g. loop diuretics. If unavoidable, careful electrolyte monitoring
63
Q

What are the potential interactions of beta blockers?

A
  • DO NOT GIVE with non-dihydropyridine calcium channel blockers
  • e.g. verapamil, dilitazem
  • Can increase risk of HF, bradycardia and asytole
64
Q

What are the possible interactions of aspirin?

A
  • Works synergistically with other antiplatelet (e.g. clopidogrel) and anticoagulants (heparin, warfarin) - therefore, icnreased risk of bleeding!
65
Q

What is the mechanism by which clopidogrel works?

A
  • Irreversibly binds to ADP receptor on platelet cell surface
  • Prevents platelet aggregation
  • Reduces risk of aeterial occlusion
  • INDEPENDENT FROM COX pathway - works synergistically with aspirin
66
Q

What are the indications for aspirin?

A
  1. ACS and ischaemic stroke - prevent thrombosis and reduce mortality
  2. Secondary prevention of thrombolytic events in CV, cerebrovascular and peripheral vascular disease
  3. Primary prevention of intracardiac thrombus or embolic stroke in AF where warfarin or NOACs not tolerated
  4. Mild-moderate pain and fever (but other NSAIDs preferred!)
67
Q

What are the indications for potassium sparing diuretics?

A

Combination therapy for Tx/prevention of hypokalaemia associated with thiazide/loop diureticss

68
Q

What is the mechanism by which nitrates work?

A

Nitrates -> NO -> increased cGMP synthesis -> smooth muscle relaxation -> vasodilation of venous and arterial vessels

  • Relaxation of venous capacitance vessels - reduces preload and LV filling
  • Relieves coronary spasm and dilates coronary vessels (improved coronary perfusion)
  • dilates systemic arteries (reduced afterload)
  • OVERALL: reduced myocardial oxygen demand and cardiac work
69
Q

How is digoxin eliminated?

A

Hepatically

70
Q

What class of drugs do atenolol, bisoprolol, propanolol and metoprolol belong to?

A

Beta blockers

71
Q

How should aspirtin be taken?

A
  • Taken with food to avoid GI irritation
72
Q

Name some cytochrome P450 inhibitors

A

Erythromycin

Ciprofloxin

Miconazole

Sodium valporate

Cranberry

Grapefruit juice)

73
Q

What cass of drug is amiodarone?

A

Anti-dysarhythmic

74
Q

What type of drug is rampiril/lisinopril?

A

ACEi

75
Q

What are the indications for thiazide diuretics?

A
  1. 1st line alternative for HTN where Ca+ channel blockers would otherwise be used but not appropriate (e.g. oedema) or HF
  2. Add on therapy for HTN where Ca+ blockers, ACEi and AT1 receptor blockers not appropriately controlling BP
76
Q

What drugs are SELECTIVE beta blockers? (i.e. only B1)

A

Bisoprolol, atenolol, metoprolol

77
Q

Hpw is clopidogrel eliminated?

A

Renally and fecally

78
Q

What are the side effects of digoxin?

A
  • Bradycardia
  • GI Disturbance
  • Rash
  • Dizziness
  • Visual disturbances (blurry/yellow vision)
  • Proarrthymic and low theurapeutic index → digoxin toxicity
  • (On ECG, can cause ST-segment depression - reverse tick sign)
79
Q

What class of drug does clopidogrel belong to?

A

Anti-platelets

80
Q

What isnt aspirin used for primary prevention of CV diseases?

A

Risk:benefit ratio - higher risk of gastric ulceration vs vascular event

81
Q

What is the mechanism by which spirolactone/amiloride works?

A
  • Distal convoluted tubule
  • Blocks epithelium sodium channels
  • Prevents Na+ absoprtion → increases Na+ and H2O excretion and potasiium retention
  • Weak duiretic alone - amiloride usually in combination with other drugs (e.g. co-amilofruse)
82
Q

How should warfarin be taken?

A

Taken around the same time each day (usually evening 18:00 - Paul O’Grady - ‘time for our warfarin!’)

83
Q

What are the contraindiations for amiodarone?

A

Severe hypotension

Active thyroid disease (due to iodine content)

Heart block

84
Q

What are the potential interactions for statins?

A
  • Metabolism by cytochrome P450
  • Cytochrome P450 inhibitors - increase conc of statins and risk of SEs (Erythromycin, ciprofloxin, miconazole, sodium valporate, cranberry and grapefruit juice)
85
Q

What class of drugs are simvastatins, atorvastatin?

A

Statins

86
Q

What are the SEs of statins?

A
  • Generally well tolerated
  • sometimes headache/GI upset

Serious SEs

  • Muscles aches and myalgia
  • Myopathy (SERIOUS)
  • Rhabdomyolysis
87
Q

What are the indications for warfarin?

A
  1. Prevent extention and recurrence of DVTs and PE (collectively VTEs)
  2. Prevent thrombolytic complications from AF and prosthetic valve replacements (Tx = shorterm)

NOT used to prevent arterial thrombosis (MI/thrombolytic stroke) - driven by platelt aggregation

88
Q

What class of drug is digoxin?

A

Cardiac glycoside

89
Q

What are the CI of Beta blockers?

A
  • Asthma - bronchospasm - B2 receptor blockage
  • Heart block

Cautioned in:

  • COPD - safe to use but use selective blockers
  • Haemodynamically instability
  • HF - low dose and increase (too high can imapir cardiac function)
  • Hepatic failure - dose adjustment (elimianted by!)
90
Q

What is the mechanism by which statins work?

A
  • Inhibit HMG CoA Reductase (enzyme that makes statins
  • Reduce cholesterol production from liver
  • Reduce LDL
  • Indirectly reduces triglycerides and increases HDL
  • Slows/reverses atherosclerosis
91
Q

What is the mechanism by which aspirin works?

A

COX inhibitor (irreversible) → reduces pro-aggregratroy factor thromboxane from arachidonic acid → reduces platelet aggregation and risk of arterial occlusion

92
Q

How are ACEi excreted?

A

Renally

93
Q

How are K+ sparing diuretics eliminated?

A

Renally mainly (some hepatic)

94
Q

How are statins eliminated from the body?

A

Hepatitic (Cytochrome P450)

95
Q

What are the indications for clopidogrel?

A

Usually taken in combination with aspirin but can be taken by itself if aspirin intolerated/CI

  • ACS - prevents arterial thrombosis by limiting platelet aggregation
  • Prevents coronary stent occlusion
  • 2º prevention of thrombolytic events in CV, cerebrovascular and peripheral vascular disease
  • Prevent intracardial thrombosis and embolic stroke in AF when warfarin/oral-anticoagulants intolerated/CI
96
Q

What are the possible interactions of clopidogrel?

A
  • Works synergistically with other antiplatelet (e.g. aspirin), anticoagulant (warfarin, heparin) and NSAIDs. Combination can increase risk of bleeding
  • Pro-drug - requires metabolism by hepatic cytochrome P450 to its active for to have anticoagulant effect. P450 inhibitors inhibit clopidogrels activation
97
Q

What are the non-selective beta blockers? (i.e. both B1 and B2 receptors)

A

Propranolol

98
Q

What is the mechanisms by which AT1 (-sartans) blockers work?

A
  • SImilar effect to ACEi - block action of angiotensin II on AT1 receptor
  • Blocking angiotensin II - reduces peripheral vascular resistance (afterload) (lowers BP)

DIlates efferent glomerular arteriole - reduces intraglomerular pressure and slows progression of CKD

Reduces aldosterone - promotes Na+ and H20 ecretion - reduces venous retunr (preload) - beneficial to HF

99
Q

What class of drugs do amlodipine, verapamil, diltiazem, and nifedipine belong to?

A

Calium channel blockers

100
Q

What is the mechanism by which calcium channels exert their action?

A
  • Block L-type calcium channels in vascular system, cardiac system or both
  • Reduces intracellular calcium concentration
  • Vascular - increases relaxation and vasodilation. Reduces BP, thereby reducing AFTERLOAD
  • Cardiac - reduces contractibility, conduction (AV - reduces VT).
  • Overall - reduces myocardial oxygen demand - prevents angina
101
Q

What are the two classes of Ca+ channel blockers? What drugs belong in each class?

A

Dihydropyrines - ampolodipine, nifedipine

Non- dihydropyrines - verapamil

Mixed - diliatazem

102
Q

What are the indications for the use of calcium channel blockers?

A
  1. HTN - 1st and 2nd line - reduce chance of stroke, MI and death
  2. Stable angina - reduced myocardial oxygen demand. Beta blockers main alternative
  3. Supraventricular tachycardia - AF, A flutter, SVT - controls cardiac rate
103
Q

What are the CIs for calcium channel blockers?

A
  1. Unstable angina - increased vasodilation increased reflux, resulting in compensatory increases in HR and hypertension. Increased myocardial work
  2. Severe aortic stenosis - could precipitate collapse
  3. Poor ventricular function - could precipitate or worsen HF (reduces ventricular rate further)
  4. AV conduction delay - could cause heart block
104
Q

What are the side effects of the use of Ca+ channel blockers?

A

Dihydropyrines - due to compensatory increases in HR with reductions in BP

  • flushing, headache, oedema, palpitation

Non-dihyropyrines

  • bradycardia, HF, AV block, constipation

Mixed (diltiazem) - mixed effects! (bit of both…)

105
Q

What are the possible interactions for Ca+ channels blockers?

A
  • Non-dihydropyrines should NOT be used in combination with B blockers (as both are -vely ionotrophic and chronotrophic - could result in heart block, heart failure, bradycardia)
  • Do not combine with grapefruit juice - interact with normal excretion
106
Q

What drug class does alteplase (recombinant tissue plasminogen activatior) and streptokinase belong to?

A

Fibrinolytics/anti-coagulants

107
Q

What is the mechanism for alteplase/streptokinase?

A
  • Activates plasminogen to plasmin
  • Plasmin breaks down fibrous clots and re-canalise occluded vessels
  • Re-perfuses affected tissues, preventing ischaemia and cell death
108
Q

What are the indications for the use of Alteplase/strptokinase?

A
  • Acute ischaemic stroke - if given within 4.5 hrs, will increase chance of patient independence
  • Acute ST elevated MI - reduce mortality if given 12 hrs post onset. However, superseded by percutaneous coronary intervention now
  • Massive PE or haemodynamic instability - reduce clot size and restores normal pulmonary artery pressure
109
Q

What the the CI’s for using alteplase and streptokinase?

A
  • High risk of bleeding e.g. recent trauma/surgery, peptic ulcer, severley high BP, bleeding disorders
  • Acute haemorrhagic stroke
  • Hepatic dysfunction
  • Previous streptokinase Tx - development of anti-streptokinase ABs
110
Q

What are the SEs for alteplase and streptokinase?

A
  • Massive Bleeding
  • Nausea and vomiting
  • Hypotension
  • bruising
  • allergic reaction
  • cardiogenic shock/cardiac arrest
  • Re-perfusion injury to brain and heart - can cause cerebral oedema and arrythmias respectively
111
Q

What are the interactions of alteplase and streptokinase?

A
  • Other anticoagulants and anti-platelets - increased risk of bleeding
  • ACEi - increased risk of anaphylaxis
112
Q

What class of drug do enoxaprin, dalteparin, fondaparinux, and UFH belong to?

A

Heparin

113
Q

What is the mechansim by which heparins work? Specifically UFH, LMWH and fondaprinux.

A
  • Inhibit function of factor Xa and thrombin, preventing blood clot formation and propagation
  • Unfractionated heparin - blocks both
  • LWMHs (i.e. enoxaprin, dalteparin) - blocks both but preferentially factor Xa (preferred for most indications as more stable/predictable)
  • Fondaprinux - blocks Xa only (Tx of ACS)
114
Q

What are the indications for heparins?

A
  • Venous thromboembolism - LWMH 1st line for VTE prohphylaxis and Tx of DVT and PE
  • ACS - fondaprinux and LMWH - 1st line for Tx of ACS - improves re-vascularisation and prevents thrombus progression
  • When warfarin is CI e.g. PREGNANCY
115
Q

What are the contraindications for heparins?

A
  • Increased risk of bleeding e.g. clotting disorders, severe hypotension, recent surgery/trauma
  • Invasive procedures
  • Renal impairment (fondaprinux/LWMH may accumulate)
116
Q

What are the SEs for using heparin?

A
  • Bleeding - especially if combined with other anti-coagulants/anti-platelets
  • Injection site reactions - ?infection
  • Heparin induced thrombocytopenia - rare disorder, low platelets and thrombosis
117
Q

What are the possible interactions of heparins?

A

Combining antithrombolytic drugs increases risk of bleeding

118
Q

How are heparins eliminated?

A

Renally

119
Q

How are fibrinolytic drugs eliminated

A

Hepatically

120
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A
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122
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123
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Drugs (9 decks)

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