Cardiology Flashcards

1
Q

Abciximab - MOA, use and risk

A

Monoclonal antibody that irreversibly binds to the GPIIb/IIIa glycoprotein receptors
This prevents final common pathway of platelet activation/ aggregations
Used to prevent thrombosis/ restenosis in patient’s undergoing stenting for unstable angina. Also Glycoprotein (GP) IIb/IIIa inhibitors are often used as a rescue or bailout therapy to manage complications arising during percutaneous coronary intervention, rather than as prophylactic treatment. Usually used where there is a high thrombus burden.
Main risk is thrombocytpaenic haemorrhage. For this reason you only use is once. Can be reversed by platelet administration.
Examples of simililar drugs include tirofiban and eptifibatide

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2
Q

Adenosine
MOA, use, side effects, which patient’s should not be given adenosine?

A

Purine nucleoside with short half life of 8-10 seconds
Acts via adenosine receptors, activating K+ channels in SAN and AVN.
Used to terminate SVT and is used to diagnostically distinguish SVT from VT. Duration of action is significantly increased by conocurrent use of dipyridamole.
Makes you feel as if you are going to die - anxiety, bronchospasm, flushing, chest tightening.
AVOID IN ASTHMA.

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3
Q

Amiodarone
Drug class
MOA
Side effects
Monitoring

A

Class III antiarrhythmic that works via blockade of the rectifier voltage gated K+ channels during repolarisation phase (III) of cardiac action potential. Also has sodium blockade action and beta blocking activity (dirty drug).
Use: Treatment of tachyarrhythmias, like VF, AF, flutter and WPW. Used generally second line.
Risks:
Long QT syndrome as you are stretching out the cardiac action potential –> TDP
Increased effects of Warfarin and Digoxin
Thyroid (hyper or hypo)
Slate grey rash
Lung fibrosis
Liver dysfunction
Thrombophlebitis
Corneal deposits
Photosensitivity
Parasthesias
Monioring: LFTs, CXR and TFTs before treatment. U&Es need to be monitored regularly to look at potassium levels.

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4
Q

What are the different classes of antiarrhythmics?

A

I: Sodium channel blockers
II: Beta blockers
III: Potassium channel blockers
IV: CCBs and miscellaneous

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5
Q

Calcium channel blockers

A

Promotes vasodilation, reduces myocyte contractility and delays cardiac action potential.
Indications: HTN, Angina, class 4 antiarrythmics (AF, atrial flutter) and Raynaud’s phenomenon. .
Risks: Swollen legs, reflex tachycardia, flushing, bradycardia, constipation, hyperprolactinaemia, gum hypertrophy
Contraindications: Heart failure and bradycardia

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6
Q

Examples of common calcium channel blockers

A

Dihydropiridines all end in dipine and are specific to the peripheral vessel smooth muscle. E.g. Amlodipine, Felodipine, Nicardipine, Nifedipine. Uses: HTN, cardiac vasospasm, Raynaud’s Phenomenon and subarachnoid haemorrhages.

Non-dihydropirines are more specific to the heart. E.g. Diltiazem or Verapamil so are used as class IV antiarrhythmics in treatment of atrial fibrillation and flutter. Also used for angina.

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7
Q

Nicorandil

A

Vasodilatory drug - works via nitrate action AND as a potassium channel openeer.
Contraindicated - hyperkalaemia, hypotensive shock, LV failure, pulmonary oedema
Very common to get headache (50% people), flushing and dizziness

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8
Q

Aliskiren

A

Direct renin inhibitor (inhibits conversion of angiotensinogen to angiotensin 1). Treatment of essential HTN either alone or in combination with ARBs/ACEi

Main risks: Renal impairment, hyperkalaemia. Beware of using it with other drugs that cause hyperkalaemia.

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9
Q

ACE inhibitors

A

Reduces mortality in:
- Heart failure
- MI
- Diabetic nephropathy

Contraindications:
- Bilateral funtional renal artery stenosis
- Severe renal impairment

Main SE are dry cough, hyperkalaemia and hypotension

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10
Q

ARBs

A

Examples: Losartan, Candesartan, Irbesartan, Valsartan

Improved survival in:
- HTN
- Cardiac failure
- MI
- Diabetic nephropathy

Risks: cough (less common than ACEi) and cannot be used in bilateral renal artery stenosis (same as ACEi)

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11
Q

Examples of thrombolysis agents and main contraindications

A

Streptokinase, Alteplase, Reteplase, Tenecteplase

Absolute: Active bleeding, intracranial neoplasm, history of brain haemorrhage/stroke, pregnancy, aortic dissection, head trauma, BP > 200/120

Relative: Anticoagulation, bleeding disorders, prolonged CPR, recent surgery, predictable intracardiac thrombus (AF + mitral stenosis), active diabetic retinopathy, INR>1.8

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12
Q

Ticagrelor

A

Platelet aggregation inhibitor that works via P2Y12 inhibition. Used to reduce long term stroke risk after MI.

Uses:
- Medical management of STEMI/ NSTEMI where PCI is inappropriate
- Typically given for 1 year
- Dont give in combination with an anticoagulant

Risks: Dyspnoea and bradycardia (adenosine like action). Don’t give to patients with a high bleeding risk.

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13
Q

Bivalirudin

A

Direct thrombin inhibitor, given IV during pPCI alongside a bailout GPi (e.g. Abciximab)

Main benefit is reduced bleeding compared to other drugs (hence NICE guidelines recommended if femoral access being used) but main risk is increased stent thrombosis.

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14
Q

Clopidogrel

A

300-600mg given as loading dose for primary PCI
75mg given as part of DAPT for 1 year post MI (if you are not using Ticagrelor). 600mg has been found to achieve platelet aggregation more quickly and is appropriate for STEMI.

MOA: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.

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15
Q

Prasugrel

A

MOA: Prasugrel is a thienopyridine, an irreversible antagonist of the ADP P2Y12 receptor.

More potent than Clopidogrel, given only for those undergoing PCI according to NICE guidelines. Don’t give if >75, weighing <60kg, previous stroke/TIA.

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16
Q

Fondaparinux
Use
MOA, who should NOT be given it?

A

Fondaparinux selectively binds to antithrombin III.

Don’t give if:
- About to undergo PCI
- Low weight
- Poor renal function
- High bleeding risk

Fondaparinux is given for NSTEMI for 1 week prior to non-urgent PCI.

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17
Q

Indapamide mechanism of action

A

Indapamide is a thiazide-like diuretic drug used in the treatment of hypertension, as well as decompensated heart failure.

NOTE: preferred to bendroflumethiazide in treatment of HTN

18
Q

Digoxin

A

MOA: Digoxin is a cardiac glycoside that increases the force of myocardial contraction and reduces conductivity within the atrioventricular (AV) node.

Note: You an get a ‘reversed tick’ ST depression in inferolateral leads with digoxin therapy, but can also indicate toxicity

Uses: AF, Atrial flutter, heart failure

Digoxin toxicity
- Don’t diagnose on Digoxin level alone as this can be normal
- Can get almost any arrhythmia including heart block and atrial arrhythmias
- Typically: severe bradycardia, hypotension, hyperkalaemia, anorexia, nausea/vomiting, yellow vision (xanthopsia), diarrhoea, gynaecomastia

Predisposing factors to Digoxin toxicity:
- Hypokalaemia and any drugs causing hypokalaemia (e.g. thiazides)
- Hypomagnesia
- Hypercalaemia
- Amiodarone
- Quinine
- Calcium antagonists
- Renal failure
- Hypothyroidism

Management
- Digibind
- Correct hypokalaemia
- Correct arrhythmias

19
Q

Flecainide

A

MOA: Class 1c antiarrhythmic - works via sodium channel blockade to inhibit the upstroke of the cardiac action potential. Reduces heart rate and contractility.

Uses: cardioversion in SVT/AF, ventricular arrythmias, pre-exitation syndromes

Risks: DONT USE after an MI or in heart failure - can be pro arrhythmic in these patients.

Side effects: vertigo, visual disturbance

20
Q

What causes a prolonged PR?

A

Delayed conduction through the AV node

Normal variant
Athleticism
Hyperkalaemia
Drugs: BB, CCB, Digoxin, Amiodarone
Inferior MI
Mitral valve surgery

21
Q

Statins

MOA
Risks
Target cholesterol levels

A

MOA - HMG co-reductase inhibitors, which is the enzyme normally most active during sleep. Also will upregulate LDL receptors and decrease HDL receptors

Main risk is rhabdomyolysis in 10-20% of patients. Worse if renally impaired or combined with a fibrate.
DON’T combine with clarithromycin.

Aim total cholesterol <4mmol/L and LDL <2mmol/L

22
Q

Ivabradine

A

Acts as a funny current inhibitor (an inward sodium channel) found predominantly in the SAN. It results in a reduced resting heart rate.

Uses: Angina and heart failure. Can avoid the symptoms attributed to reduced peripheral blood flow with beta blockers.

Note that the algorithm for angina states to try a BB or CCB as first line. If this doesn’t work, try either Ivabradine, Nicorandil, Ranolazine or ISMN monotherapy second line).

Risks: Don’t use with concurrent BB or CCB. Avoid in sick sinus syndrome.

23
Q

Thiazide and Thiazide-like diuretics

Examples
MOA
Uses
Risks/ SE

A

Thiazides = Bendroflumethiazide or Metolazone
Thiazide-like = Indapamide or Chlortalidone

They work by inhibiting sodium resorption at the DISTAL CONVOLUTED TUBULES - via the NaCl symporter. Potassium will be lost as a result.

Uses: Thiazides really only used for mild heart failure now, although loops are still first line. Indapamide and other thiazide-like diuretics are third-line for HTN.

Adverse effects: hyponatraemia, hyPERcalcaemia, hypokalaemia, hypotensive/dehydration symptoms, gout, impotance

Rare: Agranulocytosis, thrombocytopenia, photosensitivity, pancreatitis.

24
Q

Noval oral anticoagulants

A

Apixaban and Rivaroxaban
Factor Xa inhibitors
Now first line for AF/ VTE

Dabigatran
Direct thrombin inhibitor. Main thing to remember is it shouldnt be used if Creatinine Clearance <30 and it can be reversed via administration of Idaricizumab.
Liscenced for following uses:
- VTE prevention post knee/hip surgery
- Non-valvular AF as long as following criteria met: previous thromboembolic disease, LVEF<40, NYHA 2 or above, age >75 or age>65 but coexistant diabetes, CAD or HTN.

IMPORTANT CONTRAINDICATIONS: Don’t give DOACs to those with antiphospholipid syndrome (can increase thromboembolic events) and efficacy with prosthetic heart valves has not been established so persist with Warfarin.

25
Q

CYP450 inducers

A

CYP450 inducers will increase the metabolism of a given drug and therefore DECREASE the effect. This can take several days to occur.

Can be remembered by mneumic PC BRAS

Phenytoin
Carbemazepine
Barbituates
Rifampicin
Alcohol (chronic)
St John’s Wort and Smoking

26
Q

CYP450 inhibitors

A

CYP450 inhibitors will decrease the metabolism of a drug, therefore it stays longer in the system and the effect is potentiated. The effect is immediate.

Can be remembered via mneumonic AOD DEVICES

Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazide
Ciprofloxacin
Ethanol (acute)
Sulfonamide

27
Q

Drug induced lupus

Who gets it?
Main symptoms
Main precipitants

A

Associated with the HLA-DR4 gene
Equal incidence in men and women

Athralgia, butterfly rash, pleurisy

Lots! But remember beta blockers, hydralazine, phenytoin, antipsychotics, antibiotics

28
Q

Drug induced lupus

Who gets it?
Main symptoms
Main precipitants

A

Associated with the HLA-DR4 gene
Equal incidence in men and women

Athralgia, butterfly rash, pleurisy

Lots! But remember beta blockers, hydralazine, phenytoin, antipsychotics, antibiotics

29
Q

Carbimazole

A

Inhibits a peroxidase enzyme that catalyses several steps in the conversion of tyrosine to thyroid hormone.

Used for hyperthyroidism, takes at least 6 weeks to reduce symptoms. May need to give the patient beta blockers in the meantime.

Risks: Agranulocytosis in the first 6 weeks of therapy. Patients should be advised to seek medical help if they get a sore throat. Don’t use in pregnancy - risk of neonatal goitre.

30
Q

Exanatide

A

Binds to, and activates, the GLP-1 (glucagon-like peptide-1) receptor to increase insulin secretion, suppresses glucagon secretion, and slows gastric emptying.

Used in combination with Metformin or sulphonylurea (or both).

Given subcutaneously.

Risks: delayed gastric emptying can cause dyspepsia or altered bowel habit.

31
Q

Ciclosporin

MOA
Adverse features

A

Immunosuppressant. Reduces T cell proliferation via reduction of IL-2 release. ALso works as a calcineurin inhibitor.

Uses: Post organ transplant, RA, psoriasis, UC, pure red cell aplasia

Adverse effects: (note how everything is increased - fluid, BP, K+, hair, gums, glucose)
Nephrotoxicity
Hepatotoxicity
Fluid retention
HTN
Hyperkalaemia
Hair growth
Gingival hyperplasia
Impaired glucose tolerance
Hyperlipidaemia
Risk of severe infection

32
Q

Which drug causes acute tubular necrosis?

A

Gentamicin, statins, anti-freeze, chemotherapy (cisplatin)

Death of tubular epithelial cells in renal tubules. Characteristic sign is AKI and ‘muddy brown casts’ in urine.

33
Q

How do you manage bleach ingestion?

A

If completely asymptomatic, you can trial a period of fluid and observation.

Otherwise, urgent oesophago-gastroduodenoscopy and IV PPI.

34
Q

Features of methanol poisoning
How is it managed?

A

(1) Effects associated with alcohol poisoning (intoxication & nausea)
(2) Specific visual effects of which pathology not understood. Blindness, possibly due to accumulation of formic acid.
(3) Metabolic acidosis with high anion gap (MUDPILES)

Management:
- Fomepizole - competitive inhibitor of alcohol dehydrogenase
- Can alternatively give ethanol
- Haemodialysis may be needed
- Cofactor therapy with folinic acid reduces ophthalmological complications

35
Q

Carbon monoxide poisoning

A

Causes a left shift in the oxygen dissociation curve –> early plateau
Pulse oximetry will be falsely high as it can’t distinguish oxyhaemoglobin from carboxyhaemoglobin

Symptoms: headache, nausea, vertigo, confusion, weakness
Severe toxcity: pink skin, high fevers, arrythmias, EPS, coma, death

ECG shows cardiac ischaemica
VBG: shows carboxyhaemoglobin>10%, or in severe cases>30%

Management:
- 100% high flow oxygen via non-rebreathe until all symptoms have resolved
- Hyperbaric chamber a possibility if specialist advises

36
Q

Ciprofloxacin - MOA and risks

A

Quinolone antibiotic - inhibit DNA synthesis. Other quinolones include levofloxacin.

Risks:
- Lowered seizure thereshold in epilepsy
- Tendon damage / rupture - increased if taking steroids
- Long QT
- Teratogenic
- Don’t give to breastfeeding women
- Avoid in G6PD

37
Q

Features of Lithium toxicity

Why is lithium prone to toxicity?
Symptoms
Precipitants
Management

A

Lithium has a narrow therapeutic range and a long half life. It is excreted by the kidneys.

Symptoms:
- Course tremor (fine tremor at therapeutic levels)
- Hyperreflexia
- Confusion
- Polyuria
- Seizure –> coma

Precipitants:
- Dehydration
- Renal failure
- Diuretics, especially thiazides
- ACEi/ARBs
- NSAIDs
- Metronidazole

Management:
- Mostly rehydration with normal saline
- Haemodialysis in extreme cases

38
Q

Macrolide antibiotics - examples, MOA, uses and risks

A

Examples: Erythromycin, Clarithromycin, Azithromycin

MOA: bacteriostatic, inhibit bacterial protein synthesis

Uses: Infections, but also Erythromycin used in gastric paresis to encourage gastric emptying

Risks:
- QT prolongation
- GI Side effects
- Cholestatic jaundice
- PY450 inhibitor - don’t use with statins or increased risk of rhabdomyolysis

39
Q

What are the two phases of drug metabolism?

A

Phase 1 reactions: Oxidation, reduction, hydrolysis. Generally performed by P450 enzymes - e.g. alcohol dehydrogenase.

Phase 2 reactions: conjunction. Products typically excreted in urine or bile

40
Q

What is meant by first pass metabolism?

A

A phenomenon whereby the concentration of a drug is greatly reduced before it reaches systemic circulation due to hepatic metabolism. As a result, much larger doses are needed orally.

Examples:
- Aspirin, ISMN, GTN, Propanolol, Verapamil
- Hydrocortisone, testosterone

41
Q

What is meant by zero-order kinetics?

A

A phenomenon whereby the concentration of a drug does not affect the metabolic rate, because the metabolic pathways have become saturated. Explains why you fail a breathaliser if you’ve been drinking the night before.

Examples:
- Phenytoin
- Salicylates (Aspirin)
- Heparin
- Alcohol