Cardio Part 1 Flashcards

Question

What are some useful drugs in atherogenesis?

Answer 1

Aspirin – irreversible inhibitor of platelet cyclo-oxygenase Clopidogrel/Ticagrelor – inhibitors of the P2Y12 ADP receptor on platelets and other drugs with antiplatelet actions Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis PCSK9 inhibitors – monoclonal antibodies that inhibit PCSK9 protein in the liver which leads to improved clearance of cholesterol from the blood.

Answer 2

Specific: an antibody called canakinumab Generic: Colchicine

Answer 3

Atherosclerotic lesions are dynamic - changing with age and health status Environmental factors are key, including genetics Molecular mechanisms in plaques are becoming known and can be targeted with drugs. Major cell types involved in atherogenesis are endothelium, macrophages, smooth muscle cells and platelets Inflammation is critical in the plaque life cycle Stents plus medical therapies have been hugely successful treatments built upon knowledge of the fundamental biology of the vessel wall

Answer 4

one cell layer endothelial layer, nicotine kills the endothelial layers, genetic background might can regenerate in some people that are smoking, but mostly not

Answer 5

in the aortic arch - usually where we see a plaque- change in flow and turbulence will lead to altered endothelial artery function

Answer 6

LDL getting in, making endothelial cells sticky, neutrophil and macrophage gets into the vessels wall, roll along, proliferate, lipid layer is growing, send signals and cells start to multiply and migrate and form fibrous cap, when it get large, enzyme is produced to eat the vessel walls, the blood in the lumen can get in and see a big clot, lead to MI, or can cause partial blockage; or there might be vessels remodelling

Answer 7

This term covers a spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving myocardial infarction (MI) which include Q wave infarction and non-Q wave infarction.

Answer 8

*Clinical classification includes: *Cardiac chest pain at rest *Cardiac chest pain with crescendo pattern *New onset angina *Diagnosis: > history > ECG > troponin (no significant rise in unstable angina)

Answer 9

*ST-elevation MI can usually be diagnosed on ECG at presentation *Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

Answer 10

Pathological Q waves imply a greater extend of MI, R wave is generated by viable myocardial, if you lost the viable cells - pathological Q waves *May also be defined retrospectively as non-Q wave or Q-wave MI on the basis of whether new pathological Q waves develop on the ECG as a result of it *ST elevation MI and MI associated with LBBB are associated with larger infarcts unless effectively treated (and therefore more likely to lead to pathological Q wave formation, heart failure or death)

Answer 11

- Poor R wave progression - ST elevation - Biphasic T wave (up and down)

Answer 12

*Cardiac chest pain *unremitting *usually severe but may be mild or absent *occurs at rest *associated with sweating, breathlessness, nausea and/or vomiting *one third occur in bed at night

Answer 13

Higher risk associated with higher age, diabetes, renal failure, left ventricular systolic dysfunction (elevated NTproBNP level) and other risk factors

Answer 14

*Get in to hospital quickly – 999 call *Paramedics – if ST elevation, contact primary PCI centre for transfer *Take aspirin 300mg immediately *Pain relief

Answer 15

*Make diagnosis *Bed rest *Oxygen therapy if hypoxic *Pain relief – opiates/ nitrates *Aspirin +/- platelet P2Y12 inhibitor *Consider beta-blocker *Consider other antianginal therapy *Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy

Answer 16

1. Normal (clinically silent) 2. Fatty Streak (clinically silent) 3. Fibrous Plaque (Angina Claudication/PAD) 4. Atherosclerotic plaque (Angina Claudication/PAD) 5. Plaque rupture/ Fissure and thrombosis (MI, Ischaemic Stroke, Critical Leg Ischaemia, Cardiovascular death)

Answer 17

- *Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases - *Uncommon causes include *stress-induced (Tako-Tsubo) cardiomyopathy * coronary vasospasm without plaque rupture *drug abuse (amphetamines, cocaine) *dissection of the coronary artery related to defects of the vessel connective tissue *thoracic aortic dissection

Answer 18

* Protein complex regulates actin:myosin contraction *Highly sensitive marker for cardiac muscle injury *Not specific for acute coronary syndrome *May not represent permanent muscle damage * Positive also in: * gram negative sepsis * pulmonary embolism * myocarditis * heart failure * arrhythmias * cytotoxic drugs * …………………and more!

Answer 19

The endothelium is disrupted, exposure to collagen, subendothelium matrix , thrombotic response, ADP is released by platelets after binding, activated platelet has pseudopodia, easier interaction among themselves, platelet aggregation

Answer 20

Aspirin block thromboxane A2, positive feedback loop is reduced, less likely blood clot will occlude the coronary artery Irreversible inactivation of cyclo-oxygenase 1

Answer 21

mimic it as a therapeutic system

Answer 22

High cholesterol is mostly genetic - too much LDL cholesterol, take statin to switch it off since you cant switch off the gene

Answer 23

1. Endothelium produces TPA (Tissue Plasminogen Activator) 2. TPA catalyses the conversion of Plasminogen to Plasmin 3. Plasmin catalyses the conversion of fibrin to fibrin degradation products

Answer 24

1. Clopidogrel 2. Prasugrel 3. Ticagrelor Stop the amplification of platelet activation

Answer 25

P2Y12 inhibitors in combination for aspirin *Increase risk of bleeding so need to exclude serious bleeding prior to administration

Answer 26

Abciximab Tirofiban Eptifibatide

Answer 27

*Only intravenous drugs available *Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS *Increase risk of major bleeding so used selectively *Reducing use globally due to more effective oral antiplatelet therapy *Still useful in STEMI patients undergoing primary PCI to cover delayed absorption of oral P2Y12 inhibitors in these patients (due to opiates delaying gastric emptying)

Answer 28

Used in addition to antiplatelet drugs * Target formation and/or activity of thrombin *Inhibit both fibrin formation and platelet activation * Fondaparinux (a pentasaccharide) used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used * Full-dose anticoagulation used during PCI: options are heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin) or the direct thrombin inhibitor bivalirudin (expensive, not used in Sheffield) *High dose heparin used during cardiopulmonary bypass for CABG surgery

Answer 29

* Initial pain relief if necessary – morphine + metoclopramide, nitrates * Aspirin and P2Y12 inhibitor combination (assuming no contraindications and confirmed diagnosis) * Anticoagulant: fondaparinux or heparin * Consider intravenous glycoprotein IIb/IIIa antagonists for STEMI patient undergoing primary PCI * Anti-anginal therapy – beta blocker, nitrates, calcium antagonist * Secondary prevention – statins, ACEI, beta blocker, other antihypertensive therapy * Heart failure patients – diuretic, ACEI, beta blocker, aldosterone antagonist (spironolactone, epleronone) * Fibrinolytic therapy may be used for acute STEMI if primary PCI not available

Answer 30

Primary PCI - Predilation of occluded coronary artery - Positioning of stent - Deployment of stent - Repeat angiogram after a few months

Answer 31

*Coronary angiography usually performed for patients with troponin elevation or unstable angina refractory to medical therapy * PCI most frequent revascularisation procedure *CABG surgery used in about 10% of patients with NSTE ACS *Uncommonly, patients may have severe diffuse CAD not amenable to revascularisation * Some patients may have no obstructive coronary artery disease due to * Actual diagnosis not ACS * Plaque rupture without significant stenosis and resolution of obstructive thrombus by the time of angiography * Stress-induced (Tako-Tsubo) cardiomyopathy without obstructive coronary artery disease

Answer 32

Clopidogrel is a pro-drug. Activation of clopidogrel via cytochrome P450 enzymes (CYPs) and inactivation, this means the effect of clopidogrel depends on body metabolism, which some of the factors include: * Dose * Age * Weight * Disease states such as diabetes mellitus * Drug-drug interactions e.g. omeprazole and strong CYP3A inhibitors * Genetic variants: CYP2C19 loss-of-function alleles

Answer 33

An oral reversibly-binding P2Y12 antagonist

Answer 34

*Common to all P2Y12 inhibitors: *Bleeding e.g. epistaxis, GI bleeds, haematuria *Rash *GI disturbance *Idiosyncratic *Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel (which are not associated with the same adverse effect but do not have the same evidence for long-term mortality reduction) *Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment

Answer 35

Better outcomes with prasugrel – but many trial limitations and better patients outcomes with ticagrelor in South Yorkshire so still some doubts

Answer 36

P2Y12 inhibitor may be continued for longer than 1 year after ACS if there is a high risk of further ischaemic events in aspirin-treated patients who do not have an excessive risk of life-threatening bleeding

Answer 37

* Make the diagnosis: history, ECG, troponin +/- coronary angiography; consider other diagnoses if uncertain * Pain relief as necessary: opiates (but can delay absorption of P2Y12 inhibitor); nitrates for unstable angina/coronary vasospasm (may be ineffective for MI) * Check no active or recent life-threatening bleeding/severe anaemia * If ST elevation, arrange primary PCI (PPCI) if possible * Initial cardiac monitoring for arrhythmia * Initial antithrombotic therapy: dual antiplatelet therapy (DAPT) + anticoagulant; may use GPIIb/IIIa antagonist for PPCI * Revascularisation if MI or refractory/high risk unstable angina and if feasible * Secondary prevention: DAPT duration individualised; high dose statin (e.g. atorvastatin 40-80mg daily); blood pressure control; beta blocker if LV dysfunction, heart failure or ongoing ischaemia; aldosterone antagonist if heart failure and K+ not high

Answer 38

* Normal weight 280-340 g male, 230-280 g female * Two sides, right thinner than left * Two stage electrical generated contraction * Sarcomere proteins * Contraction initiated by depolarisation and changes to calcium concentration * Protein conformational change – contraction * Removal of calcium (energy dependent) for relaxation to occur

Answer 39

* Atrio-ventricular conduction system – slightly faster conduction * General cardiac myocyte All cells can act as pacemaker Normal cardiac conduction Normal coronary circulation Blood flow through myocardium from aortic root is diastolic

Answer 40

* Normal systolic ejection fraction 60-65% * Failure to transport blood out of heart = cardiac failure * Cardiogenic shock = severe failure * Frank–Starling mechanism and pericardial sac limitations Cardiac/volume increases as venous return increases If you exceed stretch capability of sarcomeres then cardiac contraction force diminishes Myocardial hypertrophy can be an adaptive/ physiological response ~ athletes/pregnancy Hypertrophic response triggered by angiotensin 2, ET-1 and insulin-like growth factor 1, TGF-β >>>> These activate mitogen-activated protein kinase Poor adrenergic sensitisation in cardiac failure Some loss of cardiac myocytes during life is expected but significant loss will impair cardiac contraction.

Answer 41

Left sided cardiac failure – pulmonary congestion and then overload of right side. Right sided cardiac failure with venous hypertension and congestion. Diastolic cardiac failure (HFpEF) ~ Stiffer heart

Answer 42

The heart comprises a single chamber until the fifth week of gestation, then divided by intra-ventricular and intra-atrial septa from endocardial cushions. The muscular intra-ventricular septum grows upwards from the apex of the heart producing the four chambers and allowing valve development to occur.

Answer 43

>> may complicate up to 1% of all live births. = misplaced structures or arrest of the progression of normal structure development. * VSD 25-30% * ASD 10-15% * PDA 10-20% (Patent ductus arteriosus) * Fallots 4-10% (Tetrallogy of fallots) * PS 5-7% * Coarctation 5-7% * AS 4-6% * TGA 4-10% * Truncus arteriosus 2% * Tricuspid atresia 1%

Answer 44

One child with defect increases probability of second child with another defect. * Single genes associated = trisomy 21 (Downs), Turner Syndrome (XO) and di-George Syndrome. * Homeobox genes particularly associated * Infections – Rubella * Drugs – thalidomide, alcohol, phenytoin, amphetamines, lithium, eostrogenic steroids * Diabetes also associated with increased risk of congenital heart disease

Answer 45

* cyanosis, present or absent * whether this occurs from birth ….. or whether it develops later.

Answer 46

* VSD, ASD, PDA, truncus arteriosus, anonymous pulmonary venous drainage, hypoplastic left heart syndrome

Answer 47

* Tetralogy of Fallot, tricuspid atresia

Answer 48

* Complete transposition of great vessels * Coarctation * Pulmonary stenosis * Aortic stenosis * Coronary artery origin from pulmonary artery * Ebstein malformation * Endocaradial fibroelastosis

Answer 49

Initial left – right shunting Pulmonary hypertension right side >> left side shunting associated with right side cardiac failure and right side cardiac hypertrophy

Answer 50

* Probe patent 17% * Paradoxical emboli DVT >>> CNS infarction! * Ostium secundum, 90% variable sized opening = central defect in central septum. * Ostium primum type defect in lower part of septum primum * Other types exist. Eventually produces cardiac arrhythmias, pulmonary hypertension, right ventricular hypertrophy and cardiac failure. Risk of infective endocarditis.

Answer 51

beyond birth, is unusual, since the vessel usually occludes by fibrotic change after vascular spasm as the neonate starts breathing. The left – right side shunting eventually means the lung circulation is overloaded with pulmonary hypertension and right side cardiac failure subsequently. Risk of infective endocarditis. Can be closed surgically, by catheters or by prostaglandin inhibitors (Indomethacin).

Answer 52

Four main features * Pulmonary stenosis * Ventricular septal defect * Dextraposition/over-riding ventricular septal defect * Right ventricle hypertrophy Characteristic boot-shape on radiology and macroscopically. Often associated with other cardiac abnormalities. As a result of the pulmonary stenosis, right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction usually is performed during the first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases.

Answer 53

This involves the aorta coming off the right ventricle and the pulmonary trunk off the left ventricle. Male bias, and particular associated with diabetes. Survival is only possible if there is communication between the circuits and virtually all have an atrial septal defect allowing blood mixing. Treatment = arterial switch with less than 10% overall mortality.

Answer 54

- This is secondary to an excessive sclerosing/obliterating process that normally closes the ductus arteriosus, extending into the aortic wall. - The net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body. - Particularly associated with Turner’s syndrome, and with an association with Berry aneurysms of the brain. * Persistence of the posterior shelf. * Discrepant blood pressures in upper and lower part of the body. - Complications of cardiac failure, rupture of dissecting aneurysm, infective endarteritis, cerebral haemorrhage, stenosis of bicuspid aortic valve (associated). - Treatment = dilatation (stenting) of stenosed segment.

Answer 55

* Secondary endocardial fibroelastosis = a frequent complication of congenital aortic stenosis and coarctation. Profound dense collagen and elastic tissues deposited on endocardial aspect of the left ventricle produces progressive stiffening of the heart and cardiac failure. Similar changes may affect the valves. * Primary endocardial fibroelastosis, may follow a familial pattern. Both are relatively rare.

Answer 56

The normal anatomy of the heart is versed with rightward orientation of the access. It can occur without abnormal positioning of the visceral organs but is usually associated with severe cardiovascular abnormalities. It is more often associated with other organ isomerism.

Answer 57

* Angina (standard, Prinzmetal/unstable, accelerated/crescendo) * Myocardial infarction * Chronic congestive cardiac failure ~ 75% of these patients with dilated/failing hearts reflect ischaemic heart disease * Sudden death Risk factors 1. systemic hypertension 2. cigarette smoking 3. diabetes mellitus 4. elevated cholesterol Also ....obesity, increasing age, male sex, family history, oral contraceptive pill, sedentary life habit, personality features etc

Answer 58

* Atherosclerosis * Thrombosis * Thromboemboli * Artery spasm * Collateral blood vessels * Blood pressure/cardiac output/heart rate * Arteritis Also anaemia, altered oxygen dissociation curve, carbon monoxide, cyanide Increased demand from hypertension, valvular heart disease, hyperthyroidism, fever, thiamin (B1) deficiency, catecholamine stress.... Healthy individual has coronary reserve 4-8 times of resting blood flow Coronary arteries have no resistence in practical terms Constriction/dilation of small intramyocardial branches, < 400 µm diameter. For relatively limited foci of stenosis up to 75% of cross section coronary artery architecture can be lost without impairment of blood flow. At 90% limited blood supply during exercise/demand may be significant.

Answer 59

* Coronary arteritis * Dissecting aneurysm of aorta * Syphilitic aortitis, congenital abnormality of coronary artery origin * Myocardial bridge

Answer 60

* Subendocardial/patchy infarction (type 2) * Transmural infarction. (type 1) Complications of infarcts differ according to which territory has compromised. Dating of myocardial infarction

Answer 61

Followed the development of clot-busting agents and angioplasty techniques. Reperfusion of completely infarcted tissue can produce significant haemorrhage. The reperfusion allows oxygen delivery and a further degree of injury as a result of generation of superoxide radicals etc.

Answer 62

* Arrhythmias (supraventricular and ventricular) * Left ventricular failure – cardiogenic shock. * Generally reflects >40% muscle damage * Extension of infarction, rupture of the myocardium (into pericardial space, between chambers, across papillary muscle insertion)

Answer 63

This is a dilation of part of the myocardial wall, usually associated with fibrosis and atrophy of myocytes. Variable fatty tissue replacement may also occur. The dilatation of the thin walled sac allows blood stasis and thrombosis. Risk of subsequent embolism of such material.

Answer 64

Pericarditis (Dressler syndrome). Inflammation of the sac surrounding the heart (pericarditis). It's believed to occur as the result of the immune system responding to damage to heart tissue or damage to the sac around the heart (pericardium). The damage can result from a heart attack, surgery or traumatic injury. This is a delayed pericarditic reaction following infarction (2-10 weeks). All therapeutic models aim to improve blood supply along the coronary vessels affected, and to restore blood to ischaemic parts of the myocardium. * Thrombolytic enzymes * Percutaneous translumenal coronary angioplasty (PTCA) * Coronary bypass grafting * Other techniques (laser – drill) * Stents * (transplantation)

Answer 65

- WHO classification >140/90 mm Hg. Hypertensive heart disease – reflects cardiac enlargement due to hypertension, and in the absence of other cause. - Compensatory hypertrophy of the heart initially with increased myocyte size, squaring of the nuclei and slight increase of the interstitial fibrous tissue. Initially able to handle the increased workload, eventually the hypertrophy no longer compensates. - Falling amount of oxygen delivery to cardiac myocytes produces further fibrosis and progressive contractile dysfunction. - Often associated with coronary atheroma and ischaemic heart disease – aggravating situation. - Particularly associated with fatal intracerebral haemorrhage.

Answer 66

= Right ventricular hypertrophy and dilatation due to pulmonary hypertension. May reflect an acute event. * Embolisation of material into the pulmonary circuit, but is more common chronically reflecting a variety of lung disorders. * Chronic bronchitis and emphysema * Pulmonary fibrosis * Cystic fibrosis * Recurrent emboli * Primary pulmonary hypertension * Peripheral pulmonary stenosis * Intravenous drug abuse * High altitude * Schistosomiasis * Abnormal movement of the thoracic cage (Pickwickian syndrome, kyphoscoliosis, neuromuscular disorders etc). Classically disproportionate right ventricular hypertrophy as compared with the left. Progressive features of right side cardiac failure with venous overload, peripheral oedema and progressive hepatic congestion.

Answer 67

Group A β-haemolytic streptococcus infection usually upper respiratory tract. Remains a major factor with regard to heart disease in the developing world. Peak age of pathology 9-11 years, but can occur in adults. Development of immunity against the streptococcal pharyngitis produces antibodies that cross react with cardiac myocytes and valvular glycoproteins. This produces localised inflammation and subsequent scarring. Clinical features: Carditis, (cardiomegaly, murmurs, pericarditis and cardiac failure) polyarthritis, chorea, erythema marginatum and subcutaneous nodules. Minor criteria for diagnosis include: previous history of rheumatic fever, arthralgia, raised CRP, ESR and white cell count. Antibodies against group A streptococcal antigens, anti-streptolysin O, anti-DNAse B and anti-hyaluronidase. Symptoms and features diminish after 3-6 months. Some patients die acutely and are shown to have granulomatous foci of inflammation (Aschoff body, Anitchkov cells and some giant cells). There may be pericarditis and endocarditis.

Answer 68

Chronically scarring and deformity produces contracture of the valve and chordae tendinae. These may subsequently calcify and distort blood flow allowing localised thrombosis. They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis. >>> Progressive cardiac dysfunction as a result of the slowly distorting valvular function.

Answer 69

SLE, rheumatoid arthritis, ankylosing spondylitis and other connective tissue disorders.

Answer 70

This is an infective process involving the cardiac valves. Previously subdivided in to acute and subacute forms, both are characterised by high rates of morbidity and mortality. Falling rheumatic fever rates have now meant that the commonest cause in children is congenital heart disease. In adults causes include rheumatic valvular heart, mitral valve prolapse, intravenous drug abuse, prosthetic valves, diabetes, the elderly and pregnancy. Characteristic organisms include streptococci and staphylococci although fungi and atypical bacteria are also recognised

Answer 71

Infection produces rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction. Apart from the sudden development of cardiac failure and septic problems there are other consequences including generation of infected thromboemboli and damage to the kidneys (focal segmental glomerulonephritis FSGS). * Protean symptoms * Fever, anorexia, fatigue * Progressive splenomegaly, petechiae, clubbing * Neurological dysfunction due to mitotic emboli and aneurysms NB Still has 30-40% mortality rate despite antibiotics.

Answer 72

* sterile thrombotic matter deposit on valves with variable degrees of valve dysfunction. * Characteristic in neoplastic conditions. * Degenerative valve disease

Answer 73

May reflect rheumatic aortic valve disease or degenerative processes (senile type). Accelerated in bicuspid aortic valves. Associated with coronary artery disease. Classically 65-80 years age. Nodular calcific deposits in cusps with progressive distortion of valves opening/closure. Obstruction to left ventricle outflow produces pressure overload and cardiac hypertrophy. Risk of sudden cardiac death. Myocardial infarction risk. Increased propensity for infective endocarditis.

Answer 74

Calcification of the mitral valve annulus is usually asymptomatic and of no significance. It does not usually affect the mobile leaflets. However, calcification of the valves, following rheumatic valvular disease or previous inflammation/valvitis, is of significance with either mitral stenosis or regurgitant pathology.

Answer 75

- Describes degeneration of the mitral valves such that the inner fibrosa layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material. The valve cusp bow upwards and may not close adequately producing incompetence/regurgitation. There is an association with sudden cardiac death and a risk of infective endocarditis. Strong association with underlying connective tissue disorders, and Marfan’s syndrome, myotonic dystrophy and other conditions are known to be associated. S3 sound on auscultation – caused by the snap of redundant leaflets as they prolapse into the left atria. ~ 6% of female population, but clearly not all have symptoms.

Answer 76

Reflects inflammation of the myocardium usually associated with muscle cell necrosis and degeneration. Multiple aetiologies although viral myocarditis is the commonest. Direct viral toxicity with associated cell mediated immunity aggravating cell damage. Healing with scarring, but high risk of sudden death.

Answer 77

* Viruses – Coxsackie, Adeno-, Echo, Influenza * Rickettsia – typhus * Bacteria –diphtheria, staphylococcal, streptococcal, borrelia, leptospira * Fungi and Protozoa parasites – toxoplasmosis, cryptococcus * Metazoa - echinococcus Non-infectious causes * Hypersensitivity/immune related diseases – rheumatic fever, SLE, scleroderma, drug reaction, rheumatoid arthritis * Radiation * Miscellaneous – sarcoid, uraemia

Answer 78

Macroscopically dilated with poor muscle movement on specialist investigations. Acute phase shows predominantly lymphocyte infiltrate cutting throughout the myocardium and destroying muscle fibres. Healing phase shows patchy fibrosis with no specific features Symptoms vary from palpitations through to latitude, often in association with an upper respiratory tract infection preceding.

Answer 79

This often causes an inflammatory infiltrate particularly around blood vessels within the myocardium. There may be a predominance of eosinophils.

Answer 80

A very rare highly aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells. Often fatal. Early treatment is transplantation but disease can often recur.

Answer 81

Various types ~ primary cardiac disease with contractile dysfunction and atypical morphology * DCM (Dilated Cardiomyopathy) * HCM (Hypertrophied Cardiomyopathy) * ARVC (arrhythmtic Right Ventricular Cardiomyopathy) * secondary * rare forms

Answer 82

One third familial, but possibly more Most autosomal dominant (AD) but some recessive and X-linked. (Mitochondrial myopathy also recognised) Mutations in several genes are recognised – dystrophin, δ-sarcoglycan, troponin T, β myosin heavy chain, actin, lamin A/C, desmin etc Theory = poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial fibrosis. May also follow a viral myocarditis or an inflammatory myocarditis/toxic myocarditis Pathologically – enlarged, heavy and dilated heart, possibly cardiac weight up to 900 g. Histology shows variable atrophy and hypertrophy increased interstitial tissue occasional inflammatory cells Clinical progression slowly deteriorating cardiac failure, dysrrhythmias and ultimately death.

Answer 83

- Causes – alcohol, increasing prevalence. - - -- Male bias. - Cobalt toxicity - Catecholamines- these are usually derived from exogenous sources, but occasionally pheochromocytoma/paraganglioma. - Micro-infarction ? - Anthracyclines. - Dose dependant toxicity. 550 mg/m2. - Cyclophosphomide - Cocaine - Pregnancy. This may affect up to 1% of females, with a Afro-Caribbean bias. Many recover spontaneously, but one can be left with permanently damaged and dilated heart.

Answer 84

- Many mutations recognised involving β-myosin, myosin binding protein C, troponin T, titin etc. - Proposed mechanism is that HCM is related to defects in force degeneration/ energy usage allowing progressive sarcomeric dysfunction. - Compensatory hypertrophy often occurs. Some mutations are associated with clinical features * β-myosin = cardiac hypertrophic and dysrhythmia * troponin T = risk of sudden death - Asymmetric hypertrophy with distortion of a papillary architecture. - Increased fibrosis in tissues. - Ventricular outflow distortion. - Myocyte disarray. - Variation in small artery substructure. - Many patients have positive family history with cardiac failure and sudden death. - Some present with classic ischaemic heart disease symptoms. - Investigations show high ejection fraction although many apparently are normal. - Investigations include echocardiography and other imaging modalities together with investigation of genetics and family history.

Answer 85

A degenerative condition with progressive dilatation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement. Particularly common in parts of Italy ? 1% of sudden deaths in UK.

Answer 86

This is a group of diseases in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body. 1. Amyloid 2. Endomyocardial disease 3. Storage disease 4. Sarcoid. 1. Amyloid. This can either be amyloid related to the heart (cardiac amyloid) or part of a systemic disorder (amyloidosis AL, AA). Firm enlarged and heavy heart with diffuse infiltration of the protein into the mycyctes, blood vessels and valves. Progressive deterioration with right and left side failure. Classic low voltage ECG. 2. Endomyocardial disease = endomyocardial fibrosis, particularly in African settings and Löeffler endocarditis. This is a temporate region disorder with high grade eosinophilia , rash and progress endocarditis leading to cardiac failure. Characteristically grey-white layer of fibrous tissue extending of the endocardial surfaces of the ventricular cavities. Stiff and poorly compliant ventricle. 3. Storage disease * Glycogen storage disease – type II, III & IV * Mucopolysaccharosis-glycosaminoglycans deposition in cells – Hurler syndrome * Sphingolipidoses – Fabry disease * Haemochromatosis – multiorgan dysfunction with excess iron deposition in multiple tissues. 4. Sarcoid. A chronic granulomatous disease with numerous granulomas of non-caseating giant cell type. May involve the heart producing widespread areas of fibrosis and compensatory hypertrophy. It can produce a restrictive disorder. If it involves the conduction system then this may be the prime pathology of the patients with the risk of sudden death.

Answer 87

with association to long QT syndrome, Brugada syndrome etc. Brugada (brew-GAH-dah) syndrome is a rare but potentially life-threatening heart rhythm condition (arrhythmia) that is sometimes inherited. People with Brugada syndrome have an increased risk of irregular heart rhythms beginning in the lower chambers of the heart (ventricles).

Answer 88

At least 75% of cardiac tumours with bias towards atria. Rather jelly like proliferation of myxoid cells with abundant endothelial vascular channels. Usually produces obstructive symptoms but risk of embolisation. Rhabdomyoma – paediatric tumour with similarity to fetal cardiac cells probably a hamartoma Cardiac sarcomas. These are rare and can show differentiation towards vascular, fibrous and muscle phenotypes. Almost invariably fatal.

Answer 89

Relatively rare clinically, but if adequately sampled at autopsy then tumours of lung, breast, gastro-intestinal tract, melanoma and lymphomas can be found quite regularly.

Answer 90

Serious pericardial effusion – low protein content with few cellular elements. Sero-sanguinous effusion – following trauma, surgery or resuscitation. Haemopericardium – direct bleeding from vasculature wall through the ventricular wall following MI Cardiac tamponade – compression of the heart leading to acute cardiac failure following bleeding in to the pericardial space. Acute pericarditis – often follows viral infection with acute/chronic inflammation of the pericardial surface. Variably fibrinous, purulent or haemorrhagic. Can if severe progress to fibrosis and a restrictive process. NB. Uremia can produce fibrinous pericarditis. NB. Bacterial infection – purulent pericarditis.

Answer 91

* Surfaced by endothelial cells that maintain vascular integrity. * Adhesion to self. * Adhesion to underlying strata. * Leukocyte adhesion molecules. (PSGL-1, VCAM-1, ICAM-1, VLA-4, LFA-1) * Production of vaso active factors (NO, ET1) * Production of prostocyclin and adenine metabolites * Production of factor VIIIa * Production thrombomodulin * Production tissue plasminogen activator and urokanase-like factor * Production of tissue factor, plasminogen activator/inhibitor and factor V * Production of interleukin-1 * Receptors for factor IX and X and low density life of proteins. Growth factor – heparin

Answer 92

Elastic arteries – two elastic laminae. Tunica interna, tunica media, tunica adventitia

Answer 93

Muscular arteries have media with smooth muscle.

Answer 94

Endothelial lining with one or two layers of muscle cells but no elastic tissues.

Answer 95

Blood coagulation occurs when fibrinogen is converted to fibrin.

Answer 96

Clot lysis involves plasminogen being converted to plasmin which then acts on fibrin to produce fibrin degredation products (FDP’s). The process can be inhibited by both plasminogen activator inhibitors and alpha-2 antiplasmin.

Answer 97

A degenerative condition of arteries characterised often by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis. Associated with ischaemic heart disease, myocardial infarction, stroke, peripheral vascular disease etc.

Answer 98

Initiation. Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier. Local cellular proliferation and incorporation of oxidised lipoproteins occurs. Mural thrombi on surface with subsequent healing and repeat of cycle. Adaptation. As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed. This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix. May progress to unstable plaque. Clinical stage. The plaque continues to encroach upon the lumen and runs the risk of haemorrhage of exposure of tissue HLA-DR antigens which may stimulate T cell accumulation. This drives an inflammatory reaction against part of the plaque contents. Complications develop including ulceration, fissuring, calcification and aneurysm change. Pathological stages * Fatty streak. These show macrophages filled with abundant lipid but also smooth muscle cells with fat. * Intimal cell mass. These are collections of muscle cells and connective tissue without lipid – “cushions”. * The atheromatous plaque

Answer 99

Characterised by distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells and a varibly complete endothelial surface. There is local necrotic and fatty matter with scattered lipid rich macrophages. Evidence of local haemorrhage may be seen with iron deposition and calcification. Complicated plaques = Calcification, mural thrombus, vulnerable plaque

Answer 100

* Acute occlusion due to thrombus * Chronic narrowing of vessel lumen with healing of the local thrombus * Aneurysm change * Embolism of thrombus +/- plaque lipid content

Answer 101

Risk factors Hypertension Serum cholesterol level Tobacco smoking Diabetes Increasing age Male > female Inactive and stressful life patterns Homocysteine level CRP (? Infection – Chlamydia, Helicobacter, Herpes )

Answer 102

- Hypertensive vascular disease - Approximately 20-25% of the population will suffer from this. - Racial bias – Afro-Caribbean - Increased risk of aortic aneurysm, stroke, myocardial infarction/rupture - Essential hypertension. - Altered renin-angiotensin system elevates blood pressure by impairing sympathetic output increasing mineralocorticoid secretion and direct vaso-constriction. - It is balanced by atrial natriuretic factor. - In effect the changes to auto-regulation produce an increase in peripheral resistance, that in normality would allow increased blood pressure, diuresis and restoration of normal pressure and volume. - Hypertension, irrespective of the cause, alters blood vessel walls whereby the lumen size is decreased as the wall thickness increases. - Since resistance ~ 1/ r4 => a progressive increase in vascular resistance in hypertensives. - Acquired causes of hypertension - Chronic vascular disease – diabetes, primary elevation of aldosterone, Cushing syndrome, pheochromocytoma, hyperthyroidism, coarctation of the aorta and rennin secreting tumours. - Exogenous (drugs) agents may also be relevant

Answer 103

Hyaline arterosclerosis shows a deposition of basement membrane-like material and accumulation of plasma proteins within the vessel wall. May reflect ageing but it is accelerated in diabetic and hypertensive individuals.

Answer 104

>160/110 mmHg Fibrinoid necrosis of the vessel with local inflammation and focal smooth muscle cell proliferation.

Answer 105

* Mönckeberg medial sclerosis – degenerative calcification of large and medium sized arteries. Usually clinically of no significance. * Raynaud’s phenomenon.** Intermittent bilateral ischaemia of digits/extremities precipitated by motional cold temperature. Accelerated in cases of scleroderma and SLE. May produce distal atrophy and ulceration. * Fibromuscular dysplasia. = Abnormal architecture for the arteries producing variable lumen narrowing and distal poverty of circulation. Particular importance in the renal arteries which produce renal vascular insufficiency and progressive hypertension due to renin-angiotensin stimulation.

Answer 106

An inflammatory and variably necrotic process centred on the blood vessels that may involve arteries, veins or capillaries. Immune background * Deposition of immune complexes * Direct attack on vessels by antibodies * Cell mediated immunity * Viral infection * Serum sickness = model Viral antigens can be found in human vasculitis cases. – HSV, CMV, Parvovirus Small vessel vasculitis is associated with anti-neutrophil cytoplasmic antibodies (ANCA) (perinuclear pANCA, cytoplasmic cANCA). p ANCA ~ myeloperoxidase c ANCA ~ proteinase 3

Answer 107

affects medium and small muscular arteries Male>female Patchy necrotising arteritis with neutrophils, lymphocytes, plasma cells and macrophages. p ANCA+ May thrombose and have distal infarction, or heal with subsequent aneurysms. May involve widespread damage to kidneys, cerebrocirculation, cardiac tissue. Without treatment may prove rapidly fatal.

Answer 108

Leucocytoclastic vasculitis, cutaneous vasculitis, cutaneous necrotising venulitis, systemic hypersensitive angiitis/microscopic polyarteritis Affects the smallest arteries and arterioles Precipitants = drugs (aspirin, penicillin, etc) Infections (streptococci/staphylococci/viral hepatitis, TB, bacterial endocarditis) c/o Palpable purpura Microscopically fibrinoid necrosis and inflammation around small vessels. May also be a feature of collagen vascular disease (lupus/rheumatoid/Sjogren syndrome), Henoch-Schoenlein purpura, dysproteinaemia Some cases reflect neoplasia. 60% p ANCA, 40% c ANCA

Answer 109

Churg-Strauss syndrome is a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA). Allergic granulomatosis and angiitis Strong association with asthma Two thirds positive c/p ANCA Necrotising lesions of small medium arteries, arterioles and veins affecting lungs/spleen/kidney/heart/liver/CAN etc. Granulomatous inflammation with intense eosinophilic infiltrates. Variable fibrinoid necrosis and thrombosis may progress to aneurysm change. Use to have poor prognosis but steroids have improved disease.

Answer 110

- (temporal arteritis/granulomatous arteritis) - Commonest type of vasculitis. - Focal, chronic and granulomatous inflammation of temporal arteries mostly. - Association with polymyalgia rheumatica. - Can involve large arteries (aortic aneurysm/dissection). - Average age 70+. Female bias. - Genetic background with familial history sometimes. * Thickened blood vessel, often palpable. * Granulomatous inflammation involving the full thickness of the wall with macrophages, lymphocytes, plasma cells, neutrophils and occasionally eosinophils. * Giant cells tend to congregate around IEL. Variable necrosis. * Old areas of inflammation show up as focal scars with the fragmentation of elastic laminae. Thrombosis may occur. - Tends to be benign and self-limited but if affects the ocular artery will result in blindness. - Can affect systemic arteries elsewhere with atypical presentation.

Answer 111

This is a vasculitis of the respiratory tract and kidney. It has a male bias, principally around the fifth-sixth decades. 90% ANCA positive, mainly c ANCA. Parenchymal necrosis, vasculitis and granulomatous inflammation with neutrophils, lymphocytes, plasma cell, macrophages and eosinophils. May involve the small arteries and veins. Particularly affects the respiratory tract, kidney and spleen. Lungs = bilaterial pneumonitis with nodular infiltrates that undergo cavitation. Mimic TB. Chronic sinusitis and ulcers of the nasal tissues are common. Kidney = focal necrotising glomerulonephritis which progresses to cresentric glomerulonephritis. Rather protean symptoms initially with pneumonitis/sinusitis. Haematuria and proteinuria are common. May have skin rash, joint pains and neurological changes.

Answer 112

mainly female (90%) classically involves artery of aorta. Asian bias.

Answer 113

Mucocutaneous lymph node syndrome Arteritis principally affecting the coronary arteries. May progress to death due to thrombosis with acute myocardial infarction. Associated with Parvovirus B19 and Coronavirus. Also some cases with staphylococci, streptococci and Chlamydial infection. Generation of antigens that bind to the MHC class II receptors.

Answer 114

- An inflammatory disease of medium and small arteries affecting the distal limbs. - Strong association with tobacco smoking. - Cell mediated hypersensitivity to collagen II and III with impaired endothelium – dependant vasodilatation function. - Neutrophilic infiltrate involving the vessels with subsequent thrombosis and micro- abscess change. - Distal ischaemic symptoms and necrosis. Smoking cessation may lead to remission.

Answer 115

- These are dilated areas of vasculature suggesting either congenital or required weakness of the wall of the vessels. - The incidence rises with age and they are common findings at autopsy and investigations for other pathology. - Described as fusiform, saccular, dissecting and arterio-venous.

Answer 116

>50% dilatation of aortic diameter prevalence rises with age strong association with atheromatous disease familial clustering suggests a genetic component local inflammatory changes can be profound and involve ureters and local nerves. Majority below renal arteries. Vascular thrombosis (lines of Zahn) Clinically abdominal dilatation is initially silent. Fragmentation of the lumenal thrombus leads to distal embolisation and ischaemic damage. Major problem is the risk of aneurysm rupture. Those greater than 5-6 cm diameter increased risk. Prophylactic replacement with Dacron graft or endolumenal prosthesis carries a lower morbidity/mortality risk than waiting for point of rupture.

Answer 117

this rounded berry-like vascular dilatation is particularly common in the cerebral circulation. ~ consequence of longstanding hypertension and/or focal area of weakness within the arterial substructure. Particularly ~ Circle of Willis. >>> Subarachnoid haemorrhage >>> sudden death.

Answer 118

This is a haematoma within the arterial wall with blood entering under pressure from the lumenal surface and dissecting along the length of the media. Often h/o hypertension ?? cystic medial degeneration (Erdheim = age-related) ? Marfan’s syndrome and other connective tissue disorders. Majority occur just above aortic ring * prunes of the large arteries supplying the head * may rupture into local soft tissues, may rupture into pericardium. Double-barrelled aorta if blood re-enters circulation.

Answer 119

inflammatory disease affecting the vasa vasorum. May produce degeneration of the media and subsequent aneurismal change. Wrinkled bark intima ~ ascending aorta.

Answer 120

A varicose vein is an enlarged and torturous vein, principally affecting the superficial leg veins. Risk factors – age, female (pregnancy related), hereditary, posture, obesity Progressive incompetence of valves with further back pressure on venous circuit. Thinning and dilatation of vascular wall in places with patchy calcification. May produce stasis dermatitis with trophic changes to the skin. nb. Other varicose veins – haemorrhoids, oesophageal varices, varicocele

Answer 121

‘Elephantiasis’ – filiarsis Infestation of the lymph nodes and lymphatic vasculature by tropical parasites. Tumour obstruction Surgical clearance (particularly breast surgery) Inherited lymphoedema – Milroy disease

Answer 122

1. Haemangioma. 2. Glomus tumour 3. Haemangioendothelioma 4. Angiosarcoma. 5. Kaposi’s sarcoma Haemangioma. This is a benign proliferation of blood vessel tissue, which varies in name and substructure depending on the site and age of the patient. * Capillary haemangioma – birth marks, ruby spots * Juvenile haemangioma – strawberry haemangioma * Cavernous haemangioma – port wine stains Glomus tumour A benign neoplasm involving the glomus body Composed of vascular channels with proliferation of the glomus cells (neuromyoarterial receptors) mainly affect the hands. Painful! Haemangioendothelioma A vascular tumour of endothelial cells of low grade malignancy. May metastasise to other sites around the body. Angiosarcoma. This is a highly aggressive malignant neoplasm of endothelial cells. Commonly skin, soft tissue, breast, bone, liver and spleen. Rapidly enlarging haemorrhagic tumour with rapid dissemination to other organs. Environmental carcinogens – arsenic and vinyl chloride. Kaposi’s sarcoma Linked to HIV disease and AIDS Associated with human herpes virus 8 (HHV8) Painful purple/brown nodule between 1 and 10 mm diameter. Often on the skin. May progress and disseminate.

Answer 123

Risk factors – * Venous flow stasis from any cause (eg. cardiac failure, chronic venous insufficiency, post operative immobilisation, prolonged bed rest) * Injury (trauma, surgery, child birth) * Hypercoaguability (OCP), pregnancy, cancer, inherited thrombophilic disorders) * Advanced age * Sickle cell disease It is not clear what the true prevalence of deep vein thrombosis actually is within general population or hospital population. However, a variety of features may occur following formation * Lysis * Organisation * Provocation * Embolisation Painful/tender calves may reflect deep vein thrombosis (Homan sign). Treatment = anticoagulants. +/- ? Filter

Answer 124

= the passage of material through the venous or arterial circulations. Commonest process is thrombo-embolus from a deep vein thrombosis. Post operative deep vein thrombosis occurs often following surgery or immobilisation following illness. They are commonly found to embolise in patients beyond the age of 40 years. May be asymptomatic and small. May produce transient dyspnoea for relatively small emboli. May produce focal pulmonary infarction with chest pain, haemoptysis and secondary effusion. Can produce cardiovascular collapse and sudden death (saddle embolus). Paradoxical embolism – embolus that travels through the venous circuit then across from the right to the left side of the heart through a patent foramen ovale. Systemic arterial embolism usually causes infarction of the tissue as the material impacts in the nutrients/oxygen supplying vasculature. Sources * Atherosclerotic plaques, mural thrombus in heart or vasculature * Infective endocarditis * Sites particularly vulnerable – brain, intestine, distal limbs, kidneys and coronary circulation

Answer 125

* Air embolism * Acute decompression sickness * Amniotic fluid embolism * Fat embolism * Bone marrow embolism * Talc/cotton/other material from intravascular injection (drug users)

Answer 126

Mismatch of oxygen demand and supply Commonest reason: IHD

Answer 127

Age Cigarette smoking Family history Diabetes mellitus Hyperlipidemia Hypertension Kidney disease Obesity Physical inactivity Stress Male

Answer 128

Supply: Anemia Hypoxemia Polycythemia Hypothermia Hypovolaemia Hypervolaemia Demand: Hypertension Tachyarrhythmia Valvular heart disease Hyperthyroidism Hypertrophic cardiomyopathy

Answer 129

Exercise cold weather heavy meals emotional stress

Answer 130

Myocardial ischemia occurs when there is an imbalance between the heart's oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply: 1. Impairment of blood flow by proximal arterial stenosis 2. Increased distal resistance eg left ventricular hypertrophy 3. Reduced oxygen-carrying capacity of blood eg anemia

Answer 131

Poiseuille Law p= 8miu L Q/ pie r^4

Answer 132

Crescendo angina (the process from stable angina to unstable angina) Unstable angina (both due to CHD) Prinzmetal’s angina (coronary spasm) – very rare Microvascular angina (Syndrome X) ‘ANOCA’ (angina with apparently normal [main] coronary arteries) Females mostly. Cause unknown.

Answer 133

Incidence Men 35/100,000/y Women 20/100,000/y Prevalence Men 5% (5000/100,000) Women 4% (4000/100,000)

Answer 134

Personal details (demographics, identifiers) Presenting complaint History of PC + risk factors Past medical history Drug history, allergies Family history Social history Systematic enquiry

Answer 135

Chest pain (tightness/ discomfort) *** Breathlessness ** No fluid retention (unlike heart failure) Palpitation (not usually) Syncope or pre-syncope (very rare)

Answer 136

Onset Position (site) Quality (nature / character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment

Answer 137

Myocardial ischemia Pericarditis/ myocarditis Pulmonary embolism/ pleurisy Chest infection/ pleurisy Gastro-oesophageal (reflux, spasm, ulceration) Musculo-skeletal Psychological Dissection of the aorta

Answer 138

Reassure Lifestyle smoking Weight Exercise diet Advice for emergency Medication Revascularisation

Answer 139

History Typical? Atypical? Examination Exacerbating causes Investigation Routine bloods, lipids, ECG Angina? Refer to Cardiology Treat Smoking, Aspirin, B blocker, statin, GTN Diagnostic tests CT Cor Angio Typical or atypical Other non-inv Known CHD and uncertain history Cor Angio If non invasive inconclusive or very high risk

Answer 140

1. CT Coronary Angiography - Good ‘rule-out’ test and at spotting severe disease - Not so good at moderate disease - Anatomical, not functional 2. Exercise Testing - Good functional test But relies upon patient’s ability To walk on a treadmill (useless for elderly, obese, arthritic etc) 3. Myoview Scan - Uses pharmacological stressor (regadenoson) to - Increase HR and CO - Fuzzy pictures: imperfect sensitivity and specificity 4. Stress Echo - Pharmacological stressor - Highly skilled operative required - Seeks regional wall abnormality - Not often used 5. Perfusion MRI - The best of the non invasive tests. Not available everywhere.

Answer 141

Negative Chronotropic (Decrease Heart Rate) Negative Inotropic (Decrease Contractility) Decreased Cardiac Output Decreased O2 demand Side Effects: - Tiredness, Nightmares - Erectile Dysfunction - Bradycardia - Cold hands and feets Contraindications: Severe Bronchospasm, Asthma

Answer 142

- Vasodilators - Decrease BP, Decrease afterload - Decrease venous return, decrease preload Side effect: Headache

Answer 143

- Negative inotropic and chronotropic - Dilate vessels - Decrease BP, Decrease Afterload Side effects: Flushing, Postural Hypotension, Swollen ankles

Answer 144

Antiplatelets Salicylate (Salix = willow tree) Cyclo-oxygenase inhibitor ↓ prostaglandin synthesis, incl. thromboxane ↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic Side Effect: Gastric Ulceration

Answer 145

Decrease blood pressure via RAAS system (Ramipril)

Answer 146

Aspirin GTN β Blocker Long acting nitrate Statin ACE inhibitor Revascularisation: PCI / CABG: MDT meeting Ca++ channel blocker Potassium channel opener Ivabradine

Answer 147

LAD- LIMA Left Anterior Descending Artery use Left Internal Mammary artery Right Coronary Artery - Saphenous vein

Answer 148

PCI Pros: Less invasive Convenient Repeatable Acceptable Cons: Risk stent thrombosis Risk restenosis Can’t deal with complex disease Dual antiplatelet therapy CABG Pros: Prognosis Deals with complex disease Cons: Invasive Risk of stroke, bleeding Can’t do if frail, comorbid One time treatment Length of stay Time for recovery

Answer 149

PCI CABG STEMI ++ - NSTEMI +++ + Stable ++ ++

Answer 150

- Clinical risk factors (hypertension, lipids, diabetes) - Lifestyle risk factors (smoking, diet, physical inactivity) - Environmental risk factors (air pollution, chemicals) - Demographic risk factors (age, sex, ethnicity, genetic) - Psychosocial risk factors (behaviour pattern, depression/anxiety, work "work stress or long working hours", social support)

Answer 151

Friedman & Rosenman (1959) Competitive Hostile Impatient ‘Type A’ Behaviour

Answer 152

Clinical interview - Speech, Answer content - Psychomotor, Non-verbal Questionnaires (for research purposes) - Minnesota Multiphasic Personality Index (MMPI-2) - Cook-Medley Hostility Scale - Jenkins Activity Survey - Bortner Rating Scale - Self-report - poorer predictors

Answer 153

Cognitive: ‘I must always arrive first at work’ reconstructed as ‘As long as I arrive by 9am. I can complete a good days work’ Behavioural: Relaxation, walk at more relaxed pace, reduce work demands Emotional: Learning to relaxation techniques in response to early signs of anxiety or anger

Answer 154

Feelings of anger Annoyance and resentment Verbal or physical aggression

Answer 155

social determinants such as deprivation

Answer 156

Both quantity & quality of social relationships have been found to be related to morbidity and mortality Helps coping with life events Motivation to engage in healthy behaviours Orth-Gomer et al, (1993) Psychosomatic Medicine, - Men (n = 736) 6 year follow up emotional support - close persons ("attachment") extended network ("social integration"). - Both ‘attachment’ and ‘social integration’ were lower in men who developed CHD - Greater incidence of MI and death from CHD

Answer 157

- Observe/explore behaviour patterns - Identify signs of depression/anxiety - Ask questions from assessment tools - Ask patients about their job/occupation - Ask patients about available support (Close contacts and extended network, Physical and Emotional) - Liaise with relevant services (Social Care; Occupational Health)

Answer 158

dont need to test for troponin - angiogram - need bypass thats ST elevation MI (STEMI)

Answer 159

Low Risk Explore history in more detail; other family? No? CP when she runs? No? Then very low probability CHD Discuss stress; follow up sympathetically. Take time. If continues, refer to Cardiology to ‘rule out’ CHD Usually CTCA –ve; occasionally microvascular ETT useful too.

Answer 160

High Risk Chest pain at rest in man with known CHD Very high probability of MI (grey/sweaty) - stent thrombosis? Immediate 999 – don’t waste a second Paramedic ECG – if STE, take straight to cath lab for PPCI If not STE, admit anyway: troponin to look for NSTEMI

Answer 161

1887 in London

Answer 162

A record of the representation of the electrical events of the cardiac cycle. Each event has a distinctive waveform The study of waveform can lead to a greater insight into the the patients' cardiac pathophysiology.

Answer 163

- Arrhythmias - Myocardial ischaemia and infarction - Pericarditis - Chamber hypertrophy - Electrolyte disturbance - Drug toxicity (ie Digoxin and drugs that prolong the QT interval)

Answer 164

- Contraction of any muscle is associated with electrical changes called depolarisation - These changes can be detected by electrodes attached to the surface of the body

Answer 165

SA node - dominant pacemaker with an intrinsic rate of 60-100 beats/minute AV node - backup pacemaker with an intrinsic rate of 40-60 beats/minute Ventricular cells - backup pacemaker with an intrinsic rate of 20-45 beats/min

Answer 166

Electrical impulse that travels towards the electrode produces an upright "positive" deflection.

Answer 167

SA node > AV node > Bundle of His > Bundle branches > Purkinje fibres

Answer 168

P wave - atrial depolarisation QRS wave - ventricular depolarisation T wave - ventricular repolarisation

Answer 169

- Atrial depolarisation + delay in AVjunction ( AV node/ Bundle of His) - Delay allow time for atria to contract before ventricle contract

Answer 170

Horizontal - one small box = 0.04s - one large box = 0.2 s Vertical - one large box = o.5mv

Answer 171

1. Bipolar leads: 2 different points on the body 2. Unipolar lead: One point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart

Answer 172

3 standard limb leads 3 augmented limb leads 6 precordial limb leads

Answer 173

Right arm Left arm Left leg Right Arm (left) to LEft arm (right) - I (o degree) Right Arm (left) to Left leg (down) - II (60degree) Left Arm (right) to Left leg (down) - III (120 degree)

Answer 174

aVR (-150) first quadrant aVL (-30) second quadrant aVF (+90) middle bottom

Answer 175

From fifth intercoastal space, then midclavicular line and mid axillary line V1-V6 measure the heart horizontally v1-v2 septal v3-v4 anterior v5-v6 lateral

Answer 176

1. PR interval should be 120-200 ms or 3-5 little squares. 2. The width of the QRS complex should not exceed 110ms, 3 little squares. 3. The QRS complex should be dominantly upright in Lead 1 and Lead 2. 4. QRS and T wave tend to have the same direction in the limb leads. 5. All waves are negative in lead aVR. 6. The R wave must grow from V1-V4; the S wave must grow from V1-V3 and disappear in V6. 7. The ST segment should start isoelectric except in V1 and V2 where it may be elevated. 8. The P waves should be upright in I and II, and V2-V6. 9.There should be no Q wave or only a small Q less than 0.04s in width in I, II, V2-V6 10. The T wave must be upright in I, II, V2-V6

Answer 177

- always positive in Lead I and Lead II - Always negative in lead aVR - <3 small squares in duration - <2.5 small squares in amplitude - commonly biphasic in lead V1 - Best seen in Lead 2

Answer 178

- Tall (>2.5mm), pointed P waves (P pulmonale)

Answer 179

- Notched/bifid ('M' shaped), P wave (P mitrale) in limb leads

Answer 180

- Bypass the normal slowing process, going straight from atrial to ventricular depolarisation via the Accessory pathway (Bundle of Kent) - WPW condition (Wolff-Parkinson-White syndrome) - short PR wave - will have delta waves

Answer 181

- first degree heart block

Answer 182

- Non-pathological Q waves may present in Lead I, III, aVL, V5, V6 - R wave in lead V6 is smaller than V5 - Depth of the S wave should not exceed 30mm - Pathological Q wave >2mm deep, and 1mm wide, or > 25% of the subsequent R wave

Answer 183

- Sokolow and Lyon criteria - S in V1 + R in V5 or V6 > 35mm - An R wave of 11-13mm (1.1 - 1.3mv) or more in lead aVL is another sign of LVH.

Answer 184

- ST segment is flat (isoelectric) - Elevation or depression of ST segment by 1mm or more - "J"(junction) point is the point between QRS and ST segment

Answer 185

- normal T wave is asymmetrical, first half having a gradual slope than the second - Should be at least 1/8 but less than 2/3 of the amplitude of R - T wave amplitude rarely exceeds 10mm - Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted - T wave follows the direction of QRS deflection

Answer 186

The QT interval is measured in lead aVL as this lead does not have prominent U wave. 1. Total duration of depolarisation and repolarisation 2. QT interval decreases when heart rate increases 3. For HR = 70bpm, QT <0.4s 4. QT interval should be 0.35s- 0.45s 5. Should not be more than half of the interval between adjacent R waves (R-R interval).

Answer 187

- U wave related to after depolarisations which follows repolarisations - U waves are small, round, symmetrical, and positive in lead II, with amplitude <2mm - U wave direction is the same as T wave - more prominent at slow heart rate

Answer 188

Regular Heart Rate - Rule of 300/X - Count the number of big box between 2 QRS complex, and divide 300 by this. Irregular Heart Rate - 10 Second Rule - ECG records 10s of rhythm per page, count the number of beats present on the ECG, and then multiply by 6

Answer 189

- the QRS axis represents overall direction of the heart's electrical activity - Abnormality hints at: > Ventricular enlargement > Conduction blocks (ie hemiblocks) -normal QRS axis from -30 to -90 degree - -30 to -90 is referred to as a left axis deviation (LAD) - +90 to +80 is referred to as a right axis deviation (RAD)

Answer 190

- The quadrant approach - The equiphasic approach

Answer 191

Look at the QRS complex in Lead I and Lead aVF. Determine whether its postive or negative The combination should place the axis into one of the 4 quadrants Lead I on the left, Lead aVF on the upper side, normal axis LAD RAD Intermediate axis

Answer 192

1. Most equiphasic QRS 2. Identified lead lies 90degree away from the lead 3. QRS in this second lead is positive or negative

Answer 193

Phase 0 Na+ in via fast Na channel Phase 1 K+ out via K+ channel Phase 2 Ca+ channel open Ca+ in compensating K+ out Phase 3 K+ out via K+ channel Phase 4 K+ out via K+ channel

Answer 194

- 2 layers - Visceral single cell layer adherent to epicardium - Fibrous parietal layer 2mm thick - Acellular collagen and elastin fibres - 50ml of serous fluid - Great vessels lie within the pericardium - Two layers are continuous - Left atrium is mainly outside the pericardium - Parietal layer has fibrous attachments to fix the heart in the thorax

Answer 195

- Mechanical function restrains the filling volume of the heart - Similar properties to rubber initially stretchy but becomes stiff at higher tension - Thus pericardial sac has a small reserve volume - If this volume is exceeded the pressure is translated to the cardiac chambers - Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount – Tamponade physiology

Answer 196

- How can an effusion get this big? - Chronic accumulation allows adaptation of the parietal pericardium - This compliance reduces the effect on diastolic filling of the chambers - As a result very slowly accumulating effusions rarely cause tamponade

Answer 197

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion Clinical diagnosis made with 2 of 4 from: Chest Pain (85-90%) Friction rub (33%) ECG changes (60%) Pericardial effusion (up to 60% usually mild)

Answer 198

- Viral** (common): Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis). - Bacterial: Mycobacterium tuberculosis (other bacteria rare).

Answer 199

Autoimmune (common): Sjögren syndrome, rheumatoid arthritis, scleroderma, systemic vasculitides Neoplastic: *** Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma). Metabolic: Uraemia, myxoedema Traumatic and Iatrogenic: Early onset (rare): Direct injury (penetrating thoracic injury, oesophageal perforation). Indirect injury (non-penetrating thoracic injury, radiation injury). Delayed onset: Pericardial injury syndromes (common) iatrogenic trauma (e.g.coronary percutaneous intervention, pacemaker lead insertion and radiofrequency ablation). Other: Amyloidosis, aortic dissection, pulmonary arterial hypertension and chronic heart failure.

Answer 200

Difficult to quantify 1% in autopsy series 5% of A&E attendances with chest pain 1% of cases with ST elevation 80-90% of all pericarditis idiopathic Seasonal with viral trends Higher in young, previously healthy patients

Answer 201

1. Chest pain - Severe - Sharp and pleuritic (without constricting crushing character of ischaemic pain) - Rapid onset - Left anterior chest or epigastrium - Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve) - Relieved by sitting forward exacerbated by lying down Other symptoms 2. Dyspnoea 3. Cough 4. Hiccups (phrenic) 5. Systemic disturbance - Viral prodrome, Antecedent fever - Skin rash, joint pain, eye Sx, weight loss (Cause) 6. PMH - Cancer, Rheumatological Dx, Pneumonia, - Cardiac procedure (PCI, ablation), MI

Answer 202

Pneumonia Pleurisy Pulmonary Embolus Chostocondritis Gastro-oesophageal reflux Myocardial ischaemia/infarction** Aortic dissection Pneumothorax Pancreatitis Peritonitis Herpes zoster (shingles)

Answer 203

- Clinical examination > Pericardial rub – pathognomonic, crunching snow > Sinus tachycardia > Fever > Signs of effusion (pulsus paradoxus, Kussmauls sign) 2. ECG 3. Bloods 4. CXR 5. Echocardiogram

Answer 204

- Diffuse ST segment elevation - Concave ST segment – may resemble acute injury pattern of STEMI - No reciprocal ST depression - Saddle shaped - PR depression - Mechanism is epicardial inflammation as adjacent to pericardium ( parietal is inert)

Answer 205

FBC Modest increase in WCC, mild lympocytosis ESR & CRP High ESR may suggest aetiology ANA in young females - SLE Troponin Elevations suggest myopericarditis CXR Often normal in idiopathic Pneumonia common with bacterial Modest enlargement of cardiac silhouette rule out effusion (>300ml to be detectable!)

Answer 206

Sedentary activity until resolution of symptoms and ECG/CRP - Probably only applies to athletes - 3 months NSAID (Ibuprofen 600mg TDS PO 2/52) or Aspirin (750-1000mg BD PO 2/52) Colchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence

Answer 207

Major Fever >38°C Subacute onset Large pericardial effusion Cardiac tamponade Lack of response to aspirin or NSAIDs after at least 1 week of therapy Minor Myopericarditis Immunosuppression Trauma Oral anticoagulant therapy

Answer 208

Most patients with acute pericarditis have a good long-term prognosis Cardiac tamponade rarely occurs in patients with acute idiopathic pericarditis Constrictive pericarditis may occur in 1% of patients with acute idiopathic pericarditis The risk of developing constriction can be classified as: > low (1%) for idiopathic and presumed viral pericarditis > intermediate (2 – 5%) for autoimmune, immune- mediated and neoplastic aetiologies > high (20 – 30%) for bacterial aetiologies, especially with TB and purulent pericarditis 15 – 30% of patients with acute pericarditis will develop recurrence Colchicine reduced recurrence rate by 50%

Answer 209

1. Viral pericarditis - Commonest cause in developed world - Viral serology futile as self limiting illness 2. Purulent bacterial pericarditis and effusion - Staph, strep and pneumococci (Pneumonia, empyema) - Rare <1% - Very sick, high mortality 3. Tuberculous effusion TB pericarditis > 90% HIV +ve in developed countries > 17-40% Constrictive pericarditis - high mortality > Pericardectomy (~50% 5 yr survival) 4. Dressler's syndrome (Post cardiac injury syndromes) Late post MI 1-2 weeks post MI