The Cardiovascular System Flashcards
Define atherosclerosis, and desribe the appearance of a simple atheromatous plaque.
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:
- Atheroma - a nodular accumulation of soft, flaky material at the centre composed of macrophage foam cells
- Underlying areas of cholesterol crystals
- Calcification af the outer base of more advanced lesions
What is this? Describe what is occurring
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.
What are the 5 hard risk factors for atherosclerosis? What are the soft risk factors
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
What are the complications of atherosclerosis in:
- The cardiovascular system
- Brain
- Lower limbs
- Intestine
- Cardiovascular: Ischaemic heart disease and abdominal aortic aneurysm
- Brain: TIAs, cerebral infarction, cardiovascular dementia
- Lower limbs: Intermittent claudication, infarction (dry gangrene)
- Intestine: Abdominal claudication, infarction
What are the stages of progression from normal artery to atherosclerosis?
What is angina, and how does it present?
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.
There are 5 types of angina. What are they?
- Stable angina: induced by effort, relieved by rest
- Unstable angina: angina of increasing frequency or severity, occuring on minimal exertion or at rest. Greatly increases risk of MI
- Decubitus angina: angina on lying flat due to impaired LV function
- Variant (Prinzmetal’s): due to coronary varospasm. Patient’s do not have normal risk factors for angina
- Nocturnal: occurring at night
What investigations would be carried out for angina?
- Cardiovascular exam - 4th heart sound during episode occasionally heard. Exclude aortic stenosis
- Bloods - check for anaemia, thyrotoxicosis, or hyperlipidaemia
- Resting or exercise ECG. ST depression suggests myocardial ischaemia
- Cardiac scintigraphy - perfusion scan (at rest or after exercise) with contrast agents can identify regions of ischeamia and CAD
What is the management plan for angina?
- Adress underlying problems such as anaemia or hyperthyroidism, and manage coexisting conditions (e.g. diabetes, hypercholesterolaemia etc)
- GTN can give prompt relief, and beta blockers and calcium channel blockers can be used long term
- Lipid lowering therapy in patients with total cholesterol above 4.8 mmol/L
What is a myocardial infarction? Who gets it?
- Blockage of blood flow to the heart for long enough that part of the heart muscle is damaged or dies
- 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
What are the features of an ECG…
- Before an MI
- Minutes to hours after MI
- Days after an MI
- Weeks after an MI
- Months after an MI
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
What investigations would be appropriate during an expected MI?
- ECG
- Cardiac markers
- Creatine Kinase
- Cardiac specific troponins (Troponin I)
- Aspartate aminotransferase (AST) and lactate dehydrogenase (LDH)
Order the following markers of MI for the timecourse that they would appear raised following an MI. How specific is each marker?
- Troponin I
- Creatine Kinase (and cardiac specific CK-MP)
- Myoglobin
- Lactate dehydrogenase
- Myoglobin: peaks after 2h. Primary oxygen carrying pigment of muscle tissue - low specificty for MI
- Creatine Kinase: peaks after 10 - 24h. Relatively specific when there is no skeletal muscle damage. Returns to normal within 2-3 days
- Troponin I: peaks at 12h. Most specific marker for MI, released after 4h. Persists for up to 7 days
- LDH: peak at 72h, returns to normal after 10-14 days. Not specific: may also mean cancer, meningitis, HIV.
Myocardial infarctions often involve all 3 coronary arteries and are multifocal. Which coronaries supply which parts of the LV?
- Left anterior descending - supplies 50% of LV mass on anterior and septal walls
- Left Circumflex - supplies 30% ventricular mass on lateral wally
- Right - supplies 20% of LV mass on posterior wall
What is the acute management plan for an MI?
- Initial management with oxygen, analgesia and aspirin. Subsequent management depends on whether there is ST segment elevation
- ST segment elevation: primary angioplasty, B blocker and ACE-inhibitor
- No ST segment elevation: B blocker, heparin, nitrates
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?
- Stenosis - scarring of valve ring or fusion of leaflets, resistance to flow
- Regurgitation - scarring of leaflets, gap fails to close
- Mixed valve disease - both together
What is rheumatic fever? Which population is most likely to be effected, and which organ systems may be involved?
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.
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?
Major Criteria:
- Carditis
- Migratory joint polyarthritis
- Sydenham’s chorea (involuntary movement from CNS involvement)
- Erythema marginatum (see picture)
- Subcutaneous nodules
Minor Criteria
- Fever
- Arthralgia
- Previous rheumatic fever
- Raised ESR/CRP
- Leucocytosis
- Prolonger PR interval on ECG
Describe the cardiac pathology of rheumatic fever
- All three layers of the heart may be affected
- Characteristic are Aschoff nodules - granulomatous lesions with a central necrotic area occurring in the myocardium
- Warty vegetations may develop on the endocardium, particularly the heart valves
How does the carditis of rheumatic fever manifest?
- New or changed heart murmurs
- Development of cardiac enlargement or failure
- ECG changes of pericarditis (raised ST segments) or myocarditis (inverted or flattened T waves)
- Transient diastolic mitral murmur
What investigations are performed for expected rheumatic fever?
- Throat swabs cultured for group A strep
- Serological changes may indicate recent streptococcal infection eg. antistrepsolysin O titre
- Elevation of inflammatory markers e.g. CRP
What are the 3 causes of aortic valve stenosis?
- Senile calcific valvular disease - commonest cause, resulting from an inflammatory process with thickening of the subendothelium with adjacent fibrosis
- Rheumatic fever - progressive fusion, thickening and calcification.
- Congenital bicuspid aortic valve - 1 - 2% of population, calcifies gradually, presents with stenosis during 6th and 7th decades
What would the expected findings be in a patient with aortic regurgitation in the following investigations:
- Chest X-ray
- ECG
- Echocardiogram
- LV enlargemet, possible dilation of the ascending aorta
- Apperance characteristic of hypertrophy: tall R waves and inverted T waves in the left sided leads, deep S waves in the right sided leads
- Vigorous cardiac contraction and a dilated left ventricle
What would the following investigations show in a patient with mitral stenosis?
- Chest X-ray
- ECG
- Echocardiogram
- CXR usually shows a generally small heart with an enlarged left atrium
- In sinus rhythm, there is a bifid P wave due to delayed left atrial activation. Atrial fibrillation is frequently present
- Reduced mitral valve area
What is infective endocarditis?
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.
What is an aneurysm? How is a true aneurysm different from a false aneurysm?
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
What is a Berry aneurysm? What is the main reason for concern for a patient with a Berry aneurysm
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
What is an arteriovenous malformation? What are the congenital and acquired causes?
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:
- Rupture of aneurysm into a vein
- Trauma
- Iatrogenic (e.g. trauma)
What are the signs and symptoms of arteriovenous malformation, and what is the main consequence?
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
What is vasculitis? What is the difference between primary and secondary vasculitis?
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
Primary vasculitis is classified by vessel size. Name whether these diseases effect the large, medium or small vessels.
- Polyarteritis nodosa
- Wegener’s granulomatosis
- Kawasaki disease
- Henoch-Schonlein purpura
- Giant cell arteritis
- Leucocytoclastic vasculitis
- Churg-Strauss syndrome
- Takayasu arteritis
- Microscopic polyangitis
What is giant cell arteritis?
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.
Who gets giant cell arteritis? What are presenting symptoms?
Rare below 55 years, predominantly women
- 50% have polymyalgia rheumatica causing muscle pain or stiffness
- Severe headache, scalp tenderness and jaw claudication causing pain on eating
- Visual disturbances due to ischaemic optic neuropathy. May cause sudden onset blindness (temporary or permanent) with optic artery involvement
