Cardio-Vascular pathology Flashcards
Heart Failure Definition
Inability of heart to pump blood at rate commensurate with the requirements of the metabolising tissues
HF usually develops…
Slowly on background of cardiac hypertrophy
BUT may be acute e.g. MI, acute valve dysfunction
HF Systolic dysfunction causes
Ischaemic heart disease
Pressure or volume overload such as systemic hypertension or AS
Cardiomyopathy
HF Diastolic dysfunction causes
Inability to relax/fill
Amyloid
Myocardial fibrosis
Constrictive pericarditis
HF problems forwards + backwards
Decreased output
Damming of blood in venous system
HF Compensation mechanisms
Frank-Starling law: stretching leads to increased contraction •hypertrophy +/-chamber dilatation
•activation of neurohormonal systems including noradrenaline, RAS and atrial natriuretic peptide
HF Consequences
Heart size/weight increase
•hypertrophy not hyperplasia (sudden death)
•pressure overload -concentric hypertrophy
•volume overload -cavitary dilatation maybe without thickening
•hypertrophy -capillary decrease -increase in fibrous tissue -increased metabolic needs -vicious circle ——> failure
Left sided HF- main features
Decreased peripheral pressure + damming of blood in pulmonary circulation
brain + kidneys affected if severe (hypoxia)
Left sided HF symptoms
Lungs congested
Oedema
Accumulation of haemosiderin laden macrophages in alveoli- leads to dyspnoea, orthopnoea, PND
Right sided HF
Usually secondary to LVF
Primary association with severe pulmonary HT
Right sided HF autopsy
Liver congested- “nutmeg” appearance, centrilobular necrosis + fibrosis
Right sided HF signs
Portal vein pressure increase- splenomegaly, ascites
Kidneys + brain hypoxia, peripheral oedema
Hypertension
Elevated BP Systolic >140, Diastolic >90 Important RF for IHD, CVD (cerebro vascular disease), aortic dissection, cardiac failure, renal failure Primary/essential (95%) Secondary "benign" or "malignant/accelerated" (5%)
Biventricular failure
Both Right and Left side features
Secondary Hypertension causes
Renal
Neurological
Cardiovascular
Endocrine
2dary hypertension- renal
Chronic renal disease Glomerulonephritis Polycystic kidney disease Renal artery stenosis Vasculitis Renin tumour
2dary hypertension- neurological
Stress inducing surgery
Psychogenic
Raised intracranial pressure
2dary hypertension- cardiovascular
Coarctation of aorta
Systemic vasculitis
Increased intravascular vol. or CO
2dary hypertension- endocrine
Adrenocortical hyperfunction (Cushings/Conns) Exogenous hormones Phaeochromocytoma Acromegaly Thyroid disease (hyper or hypo) Pregnancy
BP equation
BP = Cardiac Output x Peripheral Resistance
Hypertension pathological features
LVH
Vessels- atheroma, dissection, cerebrovascular haemorrhage, degenerative changes such as fibrointimal thickening
Small vessels- hyaline arteriolosclerosis esp. kidneys, hyperplastic arteriosclerosis (onion skinning), fibrinoid necrosis in vessel wall
Cor pulmonale
Heart disease consequent to lung disease
Pulmonary HT
High BP in pulmonary circulation
Pulmonary HT/Cor pulmonale causes
Disease of lung parenchyma e.g. COPD, cystic fibrosis, diffuse interstitial fibrosis
Diseases of pulmonary vessels e.g. recurrent PEs, primary PH, severe vasculitis
Disorders affecting chest movement e.g. kyphoscoliosis, neuromuscular disease
Disorders causing arterial constriction e.g. hypoxaemia, chronic altitude sickness
Cor pulmonale
Acute or chronic (acute with passive PE, normally chronic)
See RV hypertrophy, RA hypertrophy + dilatation of both chambers
Tricuspid regurg
Clinical features as of RVF plus primary disease
Thickened R ventricle criteria
Normal <0.5cm
Vasculitis
Inflammation of vessel walls
Infectious or non-infectious
Non-infective are immune complex, ANCA mediated, direct antibody mediated, cell mediated, paraneoplastic or idiopathic
Vasculitis in general
All show vascular injury with mural necrosis and haemorrhage
Localised, organ restricted or systemic
Some are granulomatous
Secondary ischaemia of down-stream tissue
May cause infarction
Polyarteritis nodosa
Systemic vasculitis
Small/medium sized arteries (not veins or smaller vessels)
Often spares lungs
Segmental necrotising inflammation of arteries especially renal, cardiac and GI tract
Branching sites particularly
Polyarteritis nodose diagnosing
Angiogram
See hallmark changes- usually aneurysms
Polyarteritis nodose can lead to
Aneurysms, infarcts, haemorrhage
Microscopically transmural inflammation and fibrinoid necrosis
Possible thrombosis of vessel
After healing, there is fibrosis which later becomes nodular
Lesions of different ages
Polyarteritis nodosa features
Young adults More men than women Acute, subacute or chronic Fever, malaise, weight loss, HT abdo pain + melaena, muscular pains, renal involvement (not gloms), peripheral neuritis 30% have Hep B antigen + Therapy- steroids + cyclophosphamide
ANCA related vasculitis
Systemic/renal limited/other
85% ANCA positive
Flu-like illness
Fever, arthralgia, myalgia, purpura, peripheral neuropathy, GI involvement
May be provoked by drugs (propylthiouracil, penicillamine, hydralazine)
ANCA related vasculitis staining patterns
cytoplasmic and perinuclear (c and p) by IMF
c-ANCA- targeting proteinase r (PR3)
p-ANCA- targeting myeloperoxidase (MPO)
ANCAs in patients without vasculitis
Non-MPO p-ANCA in UC, PSC, autoimmune hep, RA/Felty’s
Wegener’s granulomatosis (aka granulomatosis with polyangitis)
Upper/lower RT Eyes/ears Necrotising granulomas Vasculitis c-ANCA usually Proteinase 3 (PR3) Often have kidney involvement
ANCA treatment
NEED TO BE TREATED- Untreated 80% 1 year mortality
Treated 75% 5 year survival
Aggressive immunosuppression with cyclophosphamide + steroids
Cardiomyopathy
Cardiac disease resulting from primary intrinsic myocardial abnormality
Exclude other causes e.g. ischaemia
Causes are idiopathic or secondary to known cause
3 types (mainly involving left ventricle)- dilated, hypertrophic + restrictive
4th type- arrhythmogenic right ventricular CM
Dilated cardiomyopathy
Progressive cardiac dilatation + contractile dysfunction
Big heart
4 chamber dilatation
Valves/arteries not significantly abnormal
May be thrombi
Microscope -myocardial hypertrophy/fibrosis
Dilated cardiomyopathy features
Idiopathic Genetic 930%) Post myocarditis Alcohol or other toxicity e.g. doxorubicin Pregnancy associated Haemochromatosis Sarcoidosis
Dilated cardiomyopathy patients
any age but usually 20-50 Progressive CCF Signs of LVF + RVF Death from failure or sudden death (arrhythmia) Need transplant
Hypertrophic cardiomyopathy
Hypertrophic heart
Poor diastolic filling
Often outflow obstruction
Little or no dilatation
Classically disproportionate thickening of septal myocardium esp. subaortic
Microscope- hypertrophy, disarray + fibrosis
Hypertrophic cardiomyopathy features
Mutation of muscle protein esp. beta-myosin heavy chain
Most familial
Many diff. mutations
Leads to poor compliance + reduced LV chamber size +/- outflow obstruction
Clinically heterogenous, may need surgery to remove muscle in LV and let blood flow through
Restricted cardiomyopathy
Primary decrease in ventricular compliance
Idiopathic
Secondary to irradiation fibrosis, amyloid, sarcoid, tumour metastases, other
Firm ventricles (otherwise normal) with dilated atria
Microscopy may reveal cause
Myocarditis
Inflammation causing myocardial injury and not a response to it
Infections- viruses (most common) e.g. Coxacjieviruses, enteroviruses, HIV; chlamydia, rickettsiae, bacteria, fungi, protozoa, Helminths
Immunological- post-viral, SLE, drug reactions, transplant rej
Others- sarcoidosis, giant cell mypcarditis
Myocarditis injury
May be direct damage or T cell mediated injury to antigens on myocyte surface
Inflammation and myocyte necrosis
Clinically fatigue, fever, chest discomfort, HF, arrhythmias, sudden death
May mimic acute infarct
May lead to dilated cardiomyopathy
