The Cardiovascular System Flashcards

1
Q

Define atherosclerosis, and desribe the appearance of a simple atheromatous plaque.

A

Atherosclerosis is a condition in which an artery wall thickens as a result of the accumulation of fatty materials within the intimal wall.

The plaque is divided ito three distinct components:

  1. Atheroma - a nodular accumulation of soft, flaky material at the centre composed of macrophage foam cells
  2. Underlying areas of cholesterol crystals
  3. Calcification af the outer base of more advanced lesions
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2
Q

What is this? Describe what is occurring

A

The picture shows a fatty streak. This is the first grossly visible lesion in the development of atherosclerosis, and occur due to aggreagates of macrophages within the intimal layer. They appear in infancy, are asymptomatic and reversible.

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3
Q

What are the 5 hard risk factors for atherosclerosis? What are the soft risk factors

A

Hard risk factors

Male gender (M:F 5:1 <55, 1:1>70), hypercholesterolaemia, smoking, hypertension and diabetes

Soft risk factors

Obesity, physical inactivity, stress, high cholesterol intake, high alcohol intake, homocystinuria (inherited disorder of methionine metabolism) chlamydia pneumonie

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4
Q

What are the complications of atherosclerosis in:

  1. The cardiovascular system
  2. Brain
  3. Lower limbs
  4. Intestine
A
  1. Cardiovascular: Ischaemic heart disease and abdominal aortic aneurysm
  2. Brain: TIAs, cerebral infarction, cardiovascular dementia
  3. Lower limbs: Intermittent claudication, infarction (dry gangrene)
  4. Intestine: Abdominal claudication, infarction
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5
Q

What are the stages of progression from normal artery to atherosclerosis?

A
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6
Q

What is angina, and how does it present?

A

Ischaemia of the heart muscle, usually due to obstruction or spasm of the coronary arteries. Presents with central chest tightness or heaviness, brought on by exertion and relieved by rest. May radiate to arms, neck, jaw or teeth.

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7
Q

There are 5 types of angina. What are they?

A
  1. Stable angina: induced by effort, relieved by rest
  2. Unstable angina: angina of increasing frequency or severity, occuring on minimal exertion or at rest. Greatly increases risk of MI
  3. Decubitus angina: angina on lying flat due to impaired LV function
  4. Variant (Prinzmetal’s): due to coronary varospasm. Patient’s do not have normal risk factors for angina
  5. Nocturnal: occurring at night
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8
Q

What investigations would be carried out for angina?

A
  1. Cardiovascular exam - 4th heart sound during episode occasionally heard. Exclude aortic stenosis
  2. Bloods - check for anaemia, thyrotoxicosis, or hyperlipidaemia
  3. Resting or exercise ECG. ST depression suggests myocardial ischaemia
  4. Cardiac scintigraphy - perfusion scan (at rest or after exercise) with contrast agents can identify regions of ischeamia and CAD
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9
Q

What is the management plan for angina?

A
  1. Adress underlying problems such as anaemia or hyperthyroidism, and manage coexisting conditions (e.g. diabetes, hypercholesterolaemia etc)
  2. GTN can give prompt relief, and beta blockers and calcium channel blockers can be used long term
  3. Lipid lowering therapy in patients with total cholesterol above 4.8 mmol/L
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10
Q

What is a myocardial infarction? Who gets it?

A
  1. Blockage of blood flow to the heart for long enough that part of the heart muscle is damaged or dies
  2. Almost always occurs in patients with coronary atheroma as a result of plaque rupture. The occlusive thrombus has a platelet rich core (white clot) and bulkier surrounding fibrin rich (red) clot
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11
Q

What are the features of an ECG…

  1. Before an MI
  2. Minutes to hours after MI
  3. Days after an MI
  4. Weeks after an MI
  5. Months after an MI
A

A) Normal ECG complex

B) & C) Minutes to hours - ST segment elevation. No change in T waves or QRS complex. Indicates myocardial damage only, not definitive infarction

D) Days - Fall in R Voltage and pathological Q waves appear. T wave inversion

E) One or more weeks - ST segment normal, but abnormal P waves persist. Deep, symmetrical T wave inversion may develop

F) Months - T waves return to normal, abnormal Q waves and reduced R voltage persist

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12
Q

What investigations would be appropriate during an expected MI?

A
  1. ECG
  2. Cardiac markers
  • Creatine Kinase
  • Cardiac specific troponins (Troponin I)
  • Aspartate aminotransferase (AST) and lactate dehydrogenase (LDH)
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13
Q

Order the following markers of MI for the timecourse that they would appear raised following an MI. How specific is each marker?

  1. Troponin I
  2. Creatine Kinase (and cardiac specific CK-MP)
  3. Myoglobin
  4. Lactate dehydrogenase
A
  1. Myoglobin: peaks after 2h. Primary oxygen carrying pigment of muscle tissue - low specificty for MI
  2. Creatine Kinase: peaks after 10 - 24h. Relatively specific when there is no skeletal muscle damage. Returns to normal within 2-3 days
  3. Troponin I: peaks at 12h. Most specific marker for MI, released after 4h. Persists for up to 7 days
  4. LDH: peak at 72h, returns to normal after 10-14 days. Not specific: may also mean cancer, meningitis, HIV.
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14
Q

Myocardial infarctions often involve all 3 coronary arteries and are multifocal. Which coronaries supply which parts of the LV?

A
  1. Left anterior descending - supplies 50% of LV mass on anterior and septal walls
  2. Left Circumflex - supplies 30% ventricular mass on lateral wally
  3. Right - supplies 20% of LV mass on posterior wall
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15
Q

What is the acute management plan for an MI?

A
  1. Initial management with oxygen, analgesia and aspirin. Subsequent management depends on whether there is ST segment elevation
  2. ST segment elevation: primary angioplasty, B blocker and ACE-inhibitor
  3. No ST segment elevation: B blocker, heparin, nitrates
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16
Q

Valvular heart disease can be divded into stenosis, regurgitation and mixed valve disease. What is the difference between each, and what is the underlying pathology?

A
  1. Stenosis - scarring of valve ring or fusion of leaflets, resistance to flow
  2. Regurgitation - scarring of leaflets, gap fails to close
  3. Mixed valve disease - both together
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17
Q

What is rheumatic fever? Which population is most likely to be effected, and which organ systems may be involved?

A

An inflammatory disease developing after an infection with group A streptocossus. Mainly affects children 5 - 15, occurring 14-28 days after strep throat or scarlet fever. May involve heart, joints, skin and brain.

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18
Q

The Duckett Jones criteria are used for the diagnosis of rheumatic fever. There must be two or more major criteria, or one major and two or more minor criteria. What are the major and minor criteria?

A

Major Criteria:

  1. Carditis
  2. Migratory joint polyarthritis
  3. Sydenham’s chorea (involuntary movement from CNS involvement)
  4. Erythema marginatum (see picture)
  5. Subcutaneous nodules

Minor Criteria

  1. Fever
  2. Arthralgia
  3. Previous rheumatic fever
  4. Raised ESR/CRP
  5. Leucocytosis
  6. Prolonger PR interval on ECG
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19
Q

Describe the cardiac pathology of rheumatic fever

A
  1. All three layers of the heart may be affected
  2. Characteristic are Aschoff nodules - granulomatous lesions with a central necrotic area occurring in the myocardium
  3. Warty vegetations may develop on the endocardium, particularly the heart valves
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20
Q

How does the carditis of rheumatic fever manifest?

A
  1. New or changed heart murmurs
  2. Development of cardiac enlargement or failure
  3. ECG changes of pericarditis (raised ST segments) or myocarditis (inverted or flattened T waves)
  4. Transient diastolic mitral murmur
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21
Q

What investigations are performed for expected rheumatic fever?

A
  1. Throat swabs cultured for group A strep
  2. Serological changes may indicate recent streptococcal infection eg. antistrepsolysin O titre
  3. Elevation of inflammatory markers e.g. CRP
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22
Q

What are the 3 causes of aortic valve stenosis?

A
  1. Senile calcific valvular disease - commonest cause, resulting from an inflammatory process with thickening of the subendothelium with adjacent fibrosis
  2. Rheumatic fever - progressive fusion, thickening and calcification.
  3. Congenital bicuspid aortic valve - 1 - 2% of population, calcifies gradually, presents with stenosis during 6th and 7th decades
23
Q

What are the signs and symptoms of aortic stenosis?

A

Symptoms

  1. Ischaemic chest pain (coronaries fill during diastole, this is presented by aortic stenosis)
  2. Dyspnoea
  3. Dizziness
  4. Syncope
  5. Sudden death

Signs

  1. Slow rising pulse
  2. Narrow pulse pressure
  3. Ejection systolic murmur
24
Q

What are the causes of aortic regurgitation?

A
  1. **Rheumatic heart disease and endocarditis (most common) **- abcess formation causes weakning of valve
  2. Marfans
  3. Severe hypertension
  4. Aortitis
  5. Syphiis
25
Q

What are the symptoms and signs of aortic regurgitation?

A

Symptoms

  1. Dyspnoea
  2. Palpitations

Signs

  1. Collapsing pulse
  2. Wide pulse pressure
  3. Early diastolic murmer
  4. Displaced apex beat (due to LV hypertrophy)
26
Q

Describe the pathophysiology of aortic regurgitation.

A

Reflux of blood through the aortic valve into the LV during diastole. There is left ventricular hypertrophy to maintain cardiac output. Due to run-off during diastole, diastolic blood pressure falls and there is reduced coronary perfusion. Ischaemia is exacerbated by hypertrophy.

27
Q

What would the expected findings be in a patient with aortic regurgitation in the following investigations:

  1. Chest X-ray
  2. ECG
  3. Echocardiogram
A
  1. LV enlargemet, possible dilation of the ascending aorta
  2. Apperance characteristic of hypertrophy: tall R waves and inverted T waves in the left sided leads, deep S waves in the right sided leads
  3. Vigorous cardiac contraction and a dilated left ventricle
28
Q

What causes mitral stenosis?

A

Almost all mitral stenosis is due to rheumatic heart fever.

29
Q

Describe the pathophysiology of mitral stenosis?

A
  1. Signiicant reduction in size of valve orifice. Left atrial pressure is increased to maintain cardiac output, causing left atrial hypertrophy and dilation
  2. Consequent increase in pulmonary venous, pulmonary arterial and right heart pressure. This leads to pulmonary oedema
  3. Pulmonary hypertension leads to RV hypertrophy, dilation and failure
30
Q

What are the signs and symptoms of mitral stenosis?

(Clue - they are largely consistent with right heart failure)

A

Symptoms

  1. Dyspnoea
  2. Palpitations (large left atrium favours AF)
  3. Fatigue
  4. Recurrent bronchitis (with a productive, blood-tinged cough)

Signs

  1. Atrial fibrillation
  2. Peripheral cyanosis
  3. Mid-diastolic murmer
31
Q

What would the following investigations show in a patient with mitral stenosis?

  1. Chest X-ray
  2. ECG
  3. Echocardiogram
A
  1. CXR usually shows a generally small heart with an enlarged left atrium
  2. In sinus rhythm, there is a bifid P wave due to delayed left atrial activation. Atrial fibrillation is frequently present
  3. Reduced mitral valve area
32
Q

What are the causes of mitral regurgitation?

A
  1. Rheumatic heart disease (most common)
  2. Mitral annular calcification
  3. Papillary muscle or chordae rupture
  4. Mitral valve prolapse
  5. Endocarditis
  6. LV dilation due to ischaemia (stretches mitral valves, unable to span gap)
33
Q

Describe the pathophysiology of mitral valve regurgitation?

A

Regurgitation between LA and LV. Regurgitation produces left atrial dilation. There is left ventricular enlargement as stroke volume increases to maintain forward cardiac output

34
Q

What are the signs and symptoms of mitral regurgitation?

A

Symptoms:

  1. Dyspnoea (due to pulmonary venous hypertension)
  2. Fatigue (due to reduced cardiac output)

Signs:

  1. Displaced, forceful apex beat and systolic thrill
  2. Pansystolic murmur (due to regurgitation throughout systole)
  3. Prominent third heart sound (blood rushes back into the dilated LV in early diastole)
  4. May be atrial fibrillation
35
Q

What would the following investigations show in a patient with mitral regurgitation?

  1. Chest X-Ray
  2. Electrocardiogram
  3. Echocardiogram
A
  1. Left atrial and left ventricular enlargement
  2. Features of left atrial delay (bifid p-wave) and LV hypertrophy (tall R waves). AF may be present
  3. Dilated left atrium and ventricle. May be specific features of chordal or papillary muscle rupture
36
Q

What is infective endocarditis?

A

Infection (usually bacterial, but can be fungal) of the endocardium. It causes significant morbidity and mortality. It may occur as an acute, fulminating infection (develops suddenly), but more often runs an insidious course and is known as subacute endocarditis.

37
Q

Endocarditis is usually caused by an abnormal cardiac endothelium and the presence of organisms in the bloodstream. How do these factors contribute to the pathology?

A
  1. Abnormal vascular endothelium is usually the result of valvular lesions, creating an area of non-laminar flow, promoting fibrin and platelet deposition. Organisms adhere and grow in small thrombin, leading to more fibrin and platelet deposition and vegetation
  2. Organisms causing endocarditis usually arise from the mouth or skin. Thus, poor oral hygiene, dental procedures, IVDA etc. are risk factors
38
Q

Describe the pathology of infective endocarditis.

A
  1. Infection of predisposed valves (those with pre-existing lesions or prosthetic valves), most commonly aortic and mitral valves leading to regurgitation
  2. Extra-cardiac manifestations such as Janeway lesions and Osler nodes usually resut from embolization or deposition of immune complexes
39
Q

Endocarditis may affect many organs. The most common presentations are with general malaise and the presence of newly diagnosed murmurs. What more infrequent signs may be seen on the hands/skin, and eyes?

A
  1. Clubbing, Osler nodes, splinter haemorrhages, Janeway lesions, petechiae
  2. Roth spots, conjunctival splinter haemorrhage
40
Q

A key diagnostic for endocarditis is blood culture. Which organisms are most likely to be found?

(Clue - mostly skin or dental pathogens)

A
  1. Streptococci (34%) - viridans, bovis
  2. Enterococci (8%) - faecalis, faecium
  3. Staphylococci (42%) - aureus
41
Q

What would be the expected echocardiography finding in a patient with infective endocarditis?

A
  1. Diagnostic through visulization of vegetations, and useful in documenting complications such as valvular dysfunction
42
Q

What is an aneurysm? How is a true aneurysm different from a false aneurysm?

A

An aneurysm is the localized dilatation of the wall of an artery, a vein, or the heart. The chief signs are the formation of a pulsating tumour, and often a bruit heard over the swelling.

A true aneurysm involves all three layers of the vessel wall (intima, media, adventitia)

A false aneurysm is caused by extravasation of blood into extravascular connective tissue, often due to trauma

43
Q

What are the main complications of aneurysms?

A
  1. Rupture
  2. Dissection
  3. Thrombosis
  4. Space occupying lesion
44
Q

What is a Berry aneurysm? What is the main reason for concern for a patient with a Berry aneurysm

A

A berry aneurysm is a saccular aneurysm, resulting from a congenital weakness in blood vessel walls. Berry aneurysms tend to lack tunica media and elastic lamina around the location, and form in areas of brain vasculature which are inherently weak, particularly the Circle of Willis

The main complications of berry aneurysm are stroke, vasospasm and subarachnoid hemorrhage

45
Q

Risk factors for berry aneurysm include conditions causing hypertension, or conditions causing weakning of blood vessel walls. Name some of these conditions.

A

Hypertension

  • Atherosclerosis
  • Renal disease (10 - 30% with autosomal dominant ploycystic kidney disease develop a berry aneurysm)
  • Vasculitis
  • Drugs (eg. cocaine)

Weakning of blood vessel walls

  • Genetic disorders of connective tissue
  • Head trauma
  • Infection
46
Q

What are some of the signs that may precede the rupture of a berry aneurysm?

A
  1. Headaches
  2. Double vision / loss of vision
  3. Eye and neck pain

Rupture is usually spontaneous - warning signs are often absent.

47
Q

What is an arteriovenous malformation? What are the congenital and acquired causes?

A

Abnormal connection between an artery and vein without intervening capillaries. This subjects veins to abnormaly high pressure.

Often of a congenital cause, most likely affecting brain, brainstem or spinal cord, though may be present in lungs.

Acquired AVMs are referred to as arteriovenous fistulae and may be due to:

  1. Rupture of aneurysm into a vein
  2. Trauma
  3. Iatrogenic (e.g. trauma)
48
Q

What are the signs and symptoms of arteriovenous malformation, and what is the main consequence?

A

Usually no symptoms, often an incidental finding. In symptomatic patients, effects will be of a space occupying lesion:

  • Seizure
  • Headache
  • Focal neurological symptoms

Clinical concern: subarachnoid or intracerebral haemorrhage

49
Q

What is vasculitis? What is the difference between primary and secondary vasculitis?

A

Vasculitis is a group of disorders that cause blood vessel (both artery and vein) destruction due to inflammation

Primary vasculitis is cuased by autoimmune attack on endothelial cells, for which the antigen is often unknown

Secondary vasculitis is caused by deposition of circulating immune complexes in the vessel wall and complement activation

50
Q

Primary vasculitis is classified by vessel size. Name whether these diseases effect the large, medium or small vessels.

  1. Polyarteritis nodosa
  2. Wegener’s granulomatosis
  3. Kawasaki disease
  4. Henoch-Schonlein purpura
  5. Giant cell arteritis
  6. Leucocytoclastic vasculitis
  7. Churg-Strauss syndrome
  8. Takayasu arteritis
  9. Microscopic polyangitis
A
51
Q

What is giant cell arteritis?

A

Granulomatous arteritis of aorta and large vesses (e.g. temporal arteries - often interchangeably termed temporal arteritis). Unknown cause, pathology consists of focal inflammation, T-cell and giant cell infiltration and granuloma formation.

52
Q

Who gets giant cell arteritis? What are presenting symptoms?

A

Rare below 55 years, predominantly women

  1. 50% have polymyalgia rheumatica causing muscle pain or stiffness
  2. Severe headache, scalp tenderness and jaw claudication causing pain on eating
  3. Visual disturbances due to ischaemic optic neuropathy. May cause sudden onset blindness (temporary or permanent) with optic artery involvement
53
Q

Giant cell arteritis would be investigated using:

  1. ESR and CRP
  2. Liver biochemistry
  3. Temporal artery biopsy

What would the findings be for each?

A
  1. Raised ESR and CRP
  2. Serum alkaline phosphatase may be raised
  3. Patchy lesions along length of biopsy showing:
  • Intimal hypertrophy
  • Inflammation of intima and subintima
  • Breakup of IEL
  • Giant cells in IEL
54
Q
A