Cardiovascular pathology 3 Flashcards
INFECTIVE ENDOCARDITIS
Definition and Aeitology
Inflammation of the endocardium – ie - lining of the heart inflamed, mainly involves the valves
Typical lesion = “vegetation” on valves 2main forms: Infective endocarditis and Non-infective endocarditis.
Epidemiology: Can occur in normal heart with highly virulent organisms
(-> Acute, aggressive ) but more common is on background of Structural abnormality of valves or myocardium
With organisms of lower virulence (->Sub-acute infective endocarditis = not so nasty)
Including: Rheumatic heart disease was major cause. More common causes now: MV prolapse, Valvular stenosis (calcification etc), Artificial (prosthetic) valves, Unrepaired and repaired congenital defects and Bicuspid AV.
Infective endocarditis:
Aeitology and pathogenesis
Any route of bacteria into the blood stream e.g. Dental abnormalities, IVDU, wounds, bowel cancer.
Streptococcus viridans from the mouth Endocarditis in native but damaged / abnormal valves 50-60% cases
S. aureus from the skin: 10% to 20% of cases overall esp. IVDU
Coagulase-negative staphylococci (e.g. S. epidermidis): Commonly infect prosthetic heart valvesy: Dental disease, catheters, GI procedures, bowel malignancy, soft tissue infections
Pathogenesis: Colonization / invasion of heart valves or heart chamber endocardium by a microbe
Vegetations made of thrombus and organisms. Destroy underlying heart or vascular tissues (eg aorta): aneurysmal sacs -> abscesses local and distant (emboli) -> Septic infarcts or mycotic aneurysms
Most cases bacterial. Fungi / other classes can also cause
Key clinical features infective endocarditis
Most consistent sign, Rapidly developing fever, chills, weakness
Can be slight or absent, particularly in the elderly.
Non-specific symptoms, May be only presentation Loss of weight / flu-like syndrome.
Murmurs. 90% of patients with left-sided IE . New valvular defect or represent a pre-existing abnormality.
Complications: Immunologically mediated conditions e.g. glomerulonephritis
Clinical manifestations (micro-thromboemboli)
Splinter / subungual hemorrhages
Janeway lesions.
Rheumatic fever
Definition + epidemiology
Acute, immunologically mediated, multi-system inflammatory disease following group A streptococcal pharyngitis
Epidemiology: Rare in developed world because of improved diagnosis / treatment. 15 million in developing countries (Africa, Middle and Far East in particular) / poor Western populations. Age – Typically children 5 - 15
Rheumatic fever aeitology and features
Aetiology: group A streptococcal pharyngitis
Features: Vegetations called veruccae. Mitral valve changes are classical . Virtually only cause of mitral stenosis
Leaflet thickening. Virtually always involved in chronic disease. MV only in most cases cases. Aortic valve in 25% of cases. Tricuspid valve / pulmonary valves – uncommon. Fibrous bridging of valvular commissures & calcification
“FISH MOUTH” or “buttonhole” stenoses
Rheumatic fever pathogenesis + clinical features
to hypersensitivity reactions. = Combined antibody and T-cell mediated response
to self-antigens in the heart. Group A strep (pharyngitis) -> antibodies AND T cells (which make cytokines that activate macrophages (e.g. Aschoff bodies) -> Cross react with self-proteins in the heart.
Left atrium dilates –> mural thrombi form -> embolise. Right ventricular hypertrophy
CARDIOMYOPATHY
heart muscle disease and strictly speaking is of uncertain cause
Pathogenesis
Uknown aeitiology
Pathogenesis: Heart Failure (abnormal muscle cannot cope with workload). Emboli, Arrhythmias (Disruption of electrical conduction pathways)
4 types of cardiomyopathy
1) Dialated progressive dialation
Contractile (systolic) dysfunction, Heart enlarged, heavy, flabby (dilation of chambers), Myocyte hypertrophy with fibrosis. Associations: Genetic (20 – 50% cases) Autosomal dominant (mainly), Cytoskeletal proteins gene mutation. Alcohol (10-20%) and other toxins E.g. chemotherapy. Others: SLE, scleroderma, thiamine def., acromegaly, thyrotoxicosis, and diabetes.
Epidemiology: Any age but commonly 20 – 50
Clinical features: Slow progressive signs / symptoms of CCF, SoB, fatigue, and poor exertional capacity
5 year survival = ~ 25% (like the ejection fraction. Death due to CCF, arrhythmia / embolism (intra-cardiac thrombus). Treatment: Cardiac transplantation , Long-term ventricular assist (can induce regression).
2) Hypertrophic
Defined by myocardial hypertrophy. Thick-walled, heavy, poorly compliant left ventricular myocardium: Diastolic dysfunction with preserved systolic function, Intermittent ventricular outflow obstruction (1/3 cases). 100% genetic.
Clinical features: Decreased Stroke volume: Impaired diastolic filling - reduced chamber size / compliance of hypertrophied left ventricle. Obstruction to the left ventricular outflow in 25% of patients, Exertional dyspnoea due to above and Systolic ejection murmur. Ventricular outflow obstruction. Anterior mitral leaflet moves toward the ventricular septum during systole.
Complications: AF, thrombus, cardiac failure. Treat by decreasing heart rate and contractility
3) Restrictive
Rare, primary disease in ventricular compliance. Ventircals normal size but myocardium firm and non-compliant
4) Arrythmogenic right ventricular cardiomyopathy (dysplasia)
Genetic disease (A.D.), ~1 in 5000. RV dilation / myocardial thinning
Fibrofatty replacement of RV. Disorder of cell-cell desmosomes
Exercise cells detach and die. Silent, syncope, chest pain, palpitations. Sudden cardiac death – young / exercise
PERICARDITIS
definition and etiology
Definition: Inflammation of the pericardial sac.
Aetiology: Infections: viruses, bacteria, Autoimmune: rheumatic fever, SLE, scleroderma, late post MIS. Other: surgery, neoplasia, trauma, radiation.
Pericarditis pathogenesis and clinical features
Acute pericarditis (inflamed): Serous, Serofibrinous / fibrinous, Purulent / suppurative, Haemorrhagic, Caseous. Chronic pericarditis (stuck down): Adhesive, Adhesive mediastinopericarditis, Constrictive pericarditis.
Inflammation causes clear ‘serous’ fluid accumulation
Caused by non-infectious aetiologies (generally). Inflammation in adjacent structures can cause pericardial reaction. Rarely by viral pericarditis (Coxsackie B / echovirus)
Autoimmune: Rheumatic fever, SLE, scleroderma
Other: Uraemia, neoplasia, radiation
Key clinical features: Sharp central chest pain…characteristics, Exacerbated by : movement, respiration, lying flat, Relieved : sitting forwards, Radiating : shoulders / neck, Differentials : angina, pleurisy
Pericardial friction rub, Fever, leucocytosis, lymphocytosis, pericardial effusion
Complications – pericardial effusion / cardiac tamponade
MYOCARDITIS
Definition: Inflammation of myocardium.
Epidemiology: Varies, depends on cause
Aetiology: Infections (HIV), immune mediated e.g. transplant rejection and others e.g. sarcoidosis.
Pathogenesis: Infection or inflammatory trigger–> cytokines, cytotoxic damage, damage myocytes
Myocytes +/or endothelium malfunction. Electrical problems / mechanical problems / clotting problems
Key clinical features: Chronic heart failure, sudden death, arrhythmias, chest pain.
VASCULITIS- GIANT CELL ARTERITIS ONLY
Definition: Chronic granulomatous inflammation of large to small sized arteries, principally in the head
Aetiology: Exact cause not known but broadly speaking the end stage problems are immune mediated
Epidemiology: Most common form of vasculitis. Older individuals in US / Europe (>50).
Pathogenesis: Chronic granulomatous inflammation –> NARROWS ARTERY –> ISCHAEMIA –> CELL DAMAGE Esp. in the head (e.g. temporal arteries – AKA temporal arteritis). Also vertebral and ophthalmic arteries. Ophthalmic arterial involvement. Permanent blindness. Giant-cell arteritis is a medical emergency requiring prompt recognition and treatment – early recognition is VITAL! Also occurs in other vessels Eg aorta (giant-cell aortitis).
Key clinical features: Rare < 50 years, vague symptoms e.g. fatigue, weight loss. Facial pain or headache. Superficial temporal artery (painful to palpation). Jaw claudication
Diagnosis - biopsy and histologic, Segmental disease Hence 2- to 3-cm length of artery
Treatment: Corticosteroids is generally effective anti-TNF therapy in refractory cases
