Flashcards in cardiovascular disease 3 Deck (102):
Inflammation of the endocardium of the heart.
2 main forms of endocarditis
– Infective endocarditis (Clinically important).
– Non-infective endocarditis
(Nonbacterial thrombotic endocarditis (NBTE)), Endocarditis of SLE (Libman-Sacks Disease)
what is contained within vegetations of infective endocarditis
– Mixture of thrombotic debris and organisms
where do vegetations of endocarditis occur
Aorta, aneurysmal sacs, blood vessels, prosthetic valves
what type of pathogen causes most endocarditis- bacterial,viral or fungal.
bacterial, although some can be fungal.
acute endocarditis is caused by
highly virulent organisms
lesions produced by acute endocarditis are typically
– Necrotizing, ulcerative, destructive
what is the prognosis of acute endocarditis
low virulence organism
lesions produced by chronic endocarditis are typically
what is the prognosis of subacute endocardditis
cured with antibiotics
risk factors of endocarditis
most common causes- mitral valve prolapse, valvular stenosis, prosthetic valves, unprepared congenital defects, bicuspid AV.
cardiac, valvular problems, rheumatic heart disease.
how does infection get to the heart and cause endocarditis
Dental abnormalities, IVDU, wounds, bowel cancer.
streptococcus viridans from mouth
S aurues from skin
coagulase negative staphylococci- from prosthetic valves
Strep. bovis- endocarditis should prompt investigations for bowel cancer.
vegetation from acute infective endocarditis have what features
• Friable (soft), bulky, potentially destructive.
• Single, multiple and often more than one valve.
• Can erode--- myocardium ------abscess (ring abscess).
• Emboli contain large numbers of virulent organisms
clinical features of infective endocarditis
fever- rapidly developing, fever, chills and weakness.
murmus- common in left sided endocarditis
complications of infective endocarditis
– Immunologically mediated conditions e.g. glomerulonephritis.
– Splinter(in nails) / subungual hemorrhages
– Janeway lesions- • Erythematous or haemorrhagic non-tender lesions on the palms or soles.
– Osler’s nodes- Subcutaneous nodules in the pulp of the digits
– Roth spots- Retinal haemorrhages in the eyes
what does the pneumonic FROMJANE stand for in terms of the clinical presentation of infective endocarditis.
• F – Fever
• R – Roth spots
• O – Osler’s nodes
• M – Murmurs
• J – Janeway Lesions
• A – Anaemia
• N – Nail (splinter) haemorrhage
• E – Emboli (septic)
what are the 2 types of non-infective endocarditis
NBTE- non bacterial thrombolytic endocarditis
Libman sacks endocarditis
what is non bacterial thrombolytic endocarditis aka
what group of patients is non bacterial thrombolytics endocarditis prevelanent in
people who are hypercoaguable
characteristics of vegetations in non-bacterial, thrombolytic endocarditis
small, non destructive, sterol thrombi on valve leaflets
single or multiple.
not invasive/no inflammatory reaction reaction- minimal local effect.
systemic emboli (infects into brain and heart)
what structures do non-bacterial, thrombolytic endocarditis affect
AV valves, chordae, valvular endocardium or mural endocardium of atria and ventricles.
what mediates rheumatic heart disease
immune system following group streptococcal infection.
what presentation is a diagnostic factor if rheumatic fever
Aschoff bodies- diagnostic of RHD.
distinctive cardiac leisons
foci- T cells, plasma cells and macrophages.
Can be found in all 3 cardiac layers-pancarditis
name of vegetations in rheumatic heart disease
which valve is typically affected in rheumatic heart disease and how is it affected
mitral valve stenosis
virtually always involved in chronic disease.
what name if given to the type of stenosis which occurs in rheumatic heart disease
fish mouth, buttonhole.
what is the aetiology of rheumatic fever/RHD
hypersensitivity reaction combines antibody and t cell mediated response.
– Antibodies directed against the M proteins of streptococci
– Cross-react with self antigens in the heart
– CD4+ T cells specific for streptococcal peptides
– Produce cytokines that activate macrophages (e.g. Aschoff bodies)
what criteria is used to diagnose a patient with rheumatic heart disease
Required criteria for diagnosis- 2 major
Required criteria- 1 major and 2 minor.
inflammation of the pericardial sac
main causes of pericarditis
infections- coxscakie virus
bacterial- TB, fungi, parasites
Immunologically mediated processes- Rheumatic fever, SLE, scleroderma, post-cardiotomy, Late post-MI = Dressler’s, drug hypersensitivity
Post-MI (early), uraemia, cardiac surgery, neoplasia, Trauma, radiation
4 different forms of pericarditis
acute, chronic, serous, serofibrinous.
what are the typical components which define acute pericarditis
serous, serofibrinos/fibronous, purulent, haemorrhagic, caseous.
what are the typical components which define chronic pericarditis
what does serous pericarditis produce
inflammtion causes serous fluid accumulation.
what causes serous pericarditis
Caused by non-infectious aetiologies (generally)
– Inflammation in adjacent structures can cause pericardial reaction
– Rarely by viral pericarditis (Coxsackie B / echovirus)
Immunologically mediated processes
– Rheumatic fever, SLE, scleroderma
– Uraemia, neoplasia, radiation
which is the most common type of pericarditis
Serofibrinous/ fibrinous pericarditis.
common causes of serofibrinous/ fibrinous pericarditis.
dresslers syndrome, acute MI, uraemia, radiation, rheumatic fever, SLE, trauma and surgey.
features of serofibrinous/ fibrinous pericarditis.
dry granular, roughend surface, intense inflammatory response.
define dressle's syndrome
what clinical triad does dressler's syndrome involve.
fever, pleuritic chest pain, pericardial effusion.
what causes dresseler's syndrome
Autoimmune reaction to antigens released following myocardial infarction
how long post MI does dresser's syndrome develop
delay of weeks
causes of supparative pericarditis
Features of purulent / suppurative pericarditis
Red, granular, exudate i.e. pus (can be unto 500mls)
inflammation caused by supportive pericarditis can extend to where
what is a consequence of supportive pericarditis
define haemorrhagic pericarditis
blood mixed with serous or supportive effusion
common causes of haemorrhagic pericariditis
Neoplasia (malignant cells in effusion)
Infections (inc TB)Following cardiac surgery ---- cardiac tamponade
common causes of caseous pericarditis
TB or fungal
3 main types of chronic pericadrditis.
what are the features of adhesive pericardiatis.
fibrosis/stringy adhesions obliterates the pericardial cavity
what are the features of adhesive mediastinopericarditis
obliterated pericardial activity with adherence to surrounding structures.
what are the features of constructive pericarditis
Heart encased in fibrous scar – limits cardiac function
clinical features of pericarditis
sharp central chest pain
percadial frictiona rub
Fever, leucocytosis, lymphocytosis, pericardial effusion
what factors exacerbate pericarditis chest pains
exacerbated by: movement, respiration, laying flat
what factors relieve pericarditis chest pains
where does pericardial chest pain radiate to
shoulders and neck
2 complications of pericarditis
pleural effusion and cardiac tamponade
4 types of cardiomyopathy
dilated, hypertrophic, restrictive, arrythmogenic right ventricular cardiomyopathy.
pathogenesis of dilated cardiomyopathy
progressive dilation-contractile dysfunction, heart is enlarged, heavy flabby and cannot contract, myocyte hypertrophy.
causes of dilated cardiomyopathy
genetic- autosomal dominate
alcohol and other toxins- chemotherapy.
SLE, scleroderma, thiamine def., acromegaly, thyrotoxicosis, diabetes
clinical features of dilated cardiomyopathy
at any age
slow progressive signs
fatigue and poor exertional capacity
treatment for dilated cardiomyopathy
long -term ventricular assistance.
what defines hypertrophic cardiomyopathy
what causes a poorly compliant left ventricular myocardium.
• Diastolic dysfunction with preserved systolic function
• Intermittent ventricular outflow obstruction (1/3 cases)
clinical features of hypertrophic cardiomyopathy
• ↓Stroke volume
– Impaired diastolic filling - reduced chamber size / compliance of hypertrophied left ventricle
• Obstruction to the left ventricular outflow
– 25% of patients
• Exertional dyspnoea due to above
• Systolic ejection murmur
– Ventricular outflow obstruction
– Anterior mitral leaflet moves toward the ventricular septum during systole.
complications of hypertophic cardiomyopathy
– Atrial fibrillation
– Mural thrombus formation which can embolization / stroke
– Cardiac failure
– Ventricular arrhythmias
– Sudden death, especially in some affected families
• Most common causes of sudden death in athletes
treatment for hypertophic cardiomyopathy
– Decrease heart rate and contractility - β-adrenergic blockers.
– Reduction of the mass of the septum, which relieves the outflow tract obstruction
in restrictive cardiomyopathy what is the primary cause.
decrease in ventricular compliance.
– Impaired ventricular filling during diastole- decreased ventricular compliance so it cannot fill
in restrictive cardiomyopathy what is the secondary cause.
– Fibrosis, amyloidosis, sarcoidosis, metastatic tumours or deposition of metabolites (inborn errors of metabolism)
define arrythmogenic right ventricular cardiomyopathy
defect in cell adhesion which falls apart when we exercise.
pathogenesis of arrythmogenic right ventricular cardiomyopathy
• RV dilation / myocardial thinning
• Fibrofatty replacement of RV
• Disorder of cell-cell desmosomes.
• Exercise causes the cells detach and die
symptoms of arrythmogenic right ventricular cardiomyopathy
• Silent, syncope, chest pain, palpitations
• Infective (or inflammatory) process àmyocardial injury
causes of myocarditis
• Infections - most cases
– Coxsackie A&B viruses most common
primary cause of arrythmogenic right ventricular cardiomyopathy
clinical features of myocarditis
– Heart failure, arrhythmias and sudden death
– Non-specific symptoms - fatigue, dyspnea, palpitations, precordial discomfort, and fever
– Can mimic acute MI
• Inflammation of the vessel walls
what is the most common form of vasculitis
giant cell arteritis
pathology of giant cell arteritis
– Chronic granulomatous inflammation
– Large to medium-sized arteries
– Esp. in the head (e.g. temporal arteries – AKA temporal arteritis)
– Also vertebral and ophthalmic arteries
morphology of giant cell arteritis
• Intimal thickening
– reduces the lumenal diameter
– Med. granulomatous inflammation
– elastic lamina fragmentation
• Multinucleated giant cells
– 75% of adequately biopsied
clinical features of giant cell arteritis
treatment of giant cell arteritis
– Corticosteroids is generally effective
– anti-TNF therapy in refractory cases
Localised, permanent, abnormal dilatations of a blood vessel
what classifies a anyrsysm
shape- saccular berry, fusiform
what are the different types of anyersyms.
mycotic and false
what is the most common for of anyersysm in the elderly
what are the pain complications of an anyersym
– Rupture causing retroperitoneal haemorrhage
– Embolisation causing limb ischaemia.
define dissecting aneurysms
tear in the wall, blood tracks between intimal and medial layers,
symptoms of a dissecting anyersysm
– Tearing pain in chest radiating to upper left shoulder
define berry anyersym
• Small, saccular lesions that develop in the Circle of Willis
• Develop at sites of medial weakness at arterial bifurcations
what does rupture of a berry anyeursym cause
what does micro and syphilitic aneurysms cause
where do charcot-bouchard aneurysms occur
intracerebral capillaries in hypertensive disease.
define mycotic anyersyms
weakening of the arterial wall secondary to bacterial and fungal infections.
what infection is mostly likely going to cause mycotic anyersyms
sub acute endocarditis
which arteries are commonly affected in mycotic anyersym
define false anyeursym
Blood filled space around a vessel, usually following traumatic rupture or perforating injury
the puncture of which artery commonly presents with a false aneurysm
Peripheral vascular disease can lead to what major consequence