2. Cardiovascular Pathology Flashcards
Define heart failure.
L ventricular failure can be divided into systolic and diastolic dysfunction. What are both characterised by? List some things that cause both.
Inability of the heart to pump blood at a rate commensurate with the requirements of the metabolising tissues. Usually develops slowly on background of cardiac hypertrophy but may be acute e.g. MI, acute valve dysfunction. Common (commonest discharge dx in >65yo).
Systolic dysfunction: characterised by reduced ejection fraction and an enlarged LV chamber. Cardiomegaly. Causes: Ischaemic heart disease. Pressure/volume overload e.g. systemic hypertension or AS. Cardiomyopathy.
Diastolic dysfunction: characterised by increased resistance to filling with increased filling pressures. Pliability of myocardium - myocardial cells replaced by tissues not as contractile. Pulmonary congestion. Causes: amyloid, myocardial fibrosis, constrictive pericarditis.
What are the forward or backward effects of heart failure?
What 3 mechanisms occur to compensate for the increased demand on the heart?
What are the consequences from these mechanisms?
Decreased output or damming of blood in venous system.
- Frank-Starling: stretching leads to increased contraction.
- Hypertrophy +/- chamber dilation.
- Activation of neurohormonal systems including NA, RAAS and ANP
May eventually be exceeded
- Heart size/weight increase
- Hypertrophy (increse in cell size) *NOT hyperplasia (increase in number)
- Pressure overload - concentric hypertrophy
- Volume overload - eccentric hypertrophy
- Hypertrophy -> capillary disease -> increase in fibrous tissue -> increased metabolic needs - vicious circle (more hypertrophy -> less adequate blood to it -> ischaemic areas -> replaced by fibrous tissue)—-> failure
What does L sided heart failure cause? (forwards and backwards)
What does R sided heart failure cause?
Define hypertension.
Decreased peripheral pressure and damming of blood in pulmonary circulation. Lungs congested, oedema, accumulation of haemosiderin laden macrophages - leads to dyspnoea, orthopnoea, PND (paroxysmal nocturnal dyspnoea). May affect brain and kidneys if severe (hypoxia).
Usually 20 to LVF, primarily associated wtih severe pulmonary hypertension. If pure liver congested = nutmeg (congestive hepatopathy, pic): centrilobar necrosis and fibrosis; portal vein pressure increase - splenomegaly, ascites. Kidney and brain hypoxia, peripheral oedema.
Elevated BP, >140/>90mmHg. Important risk factor for IHD, CVD, aortic dissection, cardiac and renal failure. Primary 95%, secoondary, benign or malignant/accelerated 5%.
What is the formula for BP?
List conditions from the following categories which could cause HT:
a) renal
b) neurological
c) cardiovascular
d) endocrine
- *BP = CO x peripheral resistance**
- CO affected by blood volume and cardiac factors. PR affected by humoral constrictors/dilators (e.g. angiotensin II/NO), local factors (e.g. pH, hypoxia), neural constrictors/dilators (e.g. α-adrenergic/β adrenergic). Genetic + environmental component.*
a) chronic renal disease, glomerulonephritis, polycycstic kidney disease, renal artery stenosis, vasculitis, renin tumour
b) stress including surgery, psychogenic, raised intracranial pressure
c) coarctation of aorta, systemic vasculitis, increased intravascular volume/CO
d) adenocortical hyperfunction (Cushings (excess cortisol)/Conns (excess aldosterone)), exogenous hormones, phaeochromocytoma (benign adrenal tumour), acromegaly (excessive GH), thyroid disease (hyper/hypo), pregnancy
What a) heart, b) vessel and c) small vessel conditions can cause hypertension?
What is cor pulmonale/pulmonary HT? What are some possible causes?
a) LVH
b) atheroma, aortic dissection, cerebrovascular haemorrhages, degenerative changes e.g fibrointimal thickening
c) hyaline arteriolosclerosis esp kidneys, hyperplastic arteriolosclerosis (onion-skinning - R pic), fibrinoid necrosis in accelerated (L pic)
Enlargement and failure of R ventricle in response to increased vascular resistance from e.g. high BP in lungs or pulmonic stenosis.
Causes: Lung parenchyma disease e.g. COPD, CF, diffuse interstitial fibrosis. Pulmonary vessel disease e.g. recurrent PEs, 10 PH, severe vasculitis. Disorders affecting chest movement e.g. kyphoscoliosis, neuromuscular disease. Disorders causing arterial constriction e.g. hypoxaemia, chronic altitude sickness.
What can cor pulmonale cause?
What is vasculitis?
What is its classification based on?
How do the different types differ?
RV hypertrophy, RA hypertrophy and dilation. Thickened RV (normal <0.5cm). May be tricuspid regurg. Clinical features for RVF + 10 disease. Can be acute or chronic (acute with massive PE). ECG features.
Inflammation of vessel walls. Can be infective or non-infectious (immune complex, ANCA-mediated, direct ab mediated, cell mediated, paraneoplastic or idiopathic).
Pathogenesis or vessel size (pic).
All show vascular injury with mural necrosis and haemorrhage. Localised, organ restricted or systemic. Some are granulomatous (characterised by multinuclear giant cells and epitheloid tissue). 20 ischaemia of down-stream tissue. May cause infarction.
What is polyarteritis nodosa? Where does it commonly occur?
What can it cause?
What are some symptoms of PAN? How is it treated?
Systemic vasculitis of medium arteries. Mainly in young adults. Can be acute/subacute/chronic or episodic. Often spares lungs. Segmental necrotising inflammation of arteries esp renal, cardiac and GI tract. Particularly at branching sites.
Aneurysms, infarcts, haemorrhage. Microscopically transmural inflammation and fibrinoid necrosis. Possible vessel thrombosis. FIbrosis later becoming nodular. Different aged lesions.
Fever, malaise, wt loss, HT, abdo pain and malaena, muscular pains, renal involvment (not gloms), peripheral neuritis. 30% Hep B antigen +. Tx: steroids (e.g. prednisone) and cyclophosphamide. (ANCA -ve. Also small aneurysms are strung like the beads of a rosary = important dx feature)
What is ANCA-related (Anti-neutrophil cytoplasmic antibodies) vasculitis?
What are signs/symptoms/lab findings of Wegener’s granulomatosis (granulomatosis with polyangitis)? (pic - necrosis area on L)
How is it treated?
Some vasculitides are associated with ANCAs: Wegener’s granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis. Systemic/renal limited/other. 85% ANCA +ve. Flu-like illness. Fever, arthralgia, myalgia, purpura, peripheral neuropathy, GI-involvement. May be provoked by drugs e.g. penicillamine, hydralazine.
Affects upper/lower respiratory tract, occular/ear. Face destruction. Necrotising granulomas. Vasculitis. c-ANCA usually +ve. PR3 (The typical ANCAs in GPA are those that react with proteinase 3, an enzyme prevalent in neutrophil granulocytes -> staining pattern).
Aggressive immunosupression with cyclophosphamide (IV/oral) and corticosteroids if pt can tolerate and morphology predicts worthwhile. Untreated 80% 1yr mortality, treated 75% 5yr survival.
What is cardiomyopathy?
Briefly describe the 3 main types of cardiomyopathy.
What typies of cardiomyopathy are the images showing?
Broadly cardic disease resulting from 10 intrinsic myocardial abnormality. Group of diseases that affect the heart muscle. Exclude other causes e.g. ischaemia. Idiopathic or 20 to known cause.
Dilated: ventricles (and atria) enlarge, but wall not v. thick, hypertrophic: ventricle walls thicken and stiffen but no dilation, v. bulky septum, restrictive: venticle walls stiffen but not necessarily thicken.
1) dilated
2) hypertrophic
What happens in dilated cardiomyopathy?
What are the main causes of dilated cardiomyopathy?
What might it lead to?
Progressive cardiac dilation and contractile dysfunction. Big heart (often globular on CXR - can’t define apex well - pic), 4 chamber dilation. Valves/arteries not significantly abnormal. May be thrombi. Micro - myocardial hypertrophy/fibrosis. Any age but esp 20-50
Idiopathic, genetic (30%), post myocarditis, alcohol/other toxicity e.g. doxorubicin, pregnancy associated, haemochromatosis, sarcoidosis (abnormal collections of inflammatory cells that form lumps = granulomas).
Progresive CCF, signs of LVF + RVF, death from failure or sudden death (arrhythmia, b/c conducting system distorted), transplantation.
What happens in hypertrophic cardiomyopathy? (pic)
What usually causes it?
What happens in restrictive cardiomyopathy?
Hypertophic heart, poor diastolic filling, often outflow obstruction, little/no dilation, classically disproportionate thickening of septal myocardium esp subaortic (impinges on LV outflow). Micro hypertrophy, disarray (rather than normal parallel myocetes) and fibrosis.
Usually inherited (familial). Mutation of muscle protein gene esp β-myosin heavy chain. Many different mutations. Leads to poor compliance and reduced LV chamber size +/- outflow obstruction. Clinically heterogeneous, may need surgery.
10 decrease in ventricular compliance, idiopathic, 20 to irradiation fibrosis, amyloid (replacement of normal myocetes with less pliable materials), sarcoid, tumor metastases. Firm ventricles (otherwise normal) with dilated atria. Microscopy may reveal cause.
What is myocarditis?
What are some causes of myocarditis?
What are the symptoms?
What can you see in the histology? (R more zoomed in)
Inflammation of heart muscle causing myocardial injury and not a response to it. May be direct damage or T-cell mediated injury to antigens on myocete surface. Inflammation and myocete necrosis.
Infections: viruses (e.g. enteroviruses, HIV), bacteria (e.g. rickettsiae, chlamydia), fungi, protozoa, helminths.
Immunological: post-viral SLE, drug reactions, transplant rejection
Others: sarcoidosis, giant cell myocarditis
Fatigue, fever, chest discomfort, heart failure, arrhythmias, sudden death. May mimic acute infarct/lead to dilated cardiomyopathy.
L: lots of inflammatory cell infiltrate in some areas and relatively little in others = heterogenous surface. R: lots of inflammatory infiltrate surrounding and killing cardiac myocetes…
What can you see in these 2 histologies? What pathology do they show?
Top: granulomatous inflammation. Necrosis (A). Lots of epitheloid tissue infiltrating. Multinucleated giant cell (ARROW)
Bottom: in kidney, lots of necrotic segments. Necrotising glomerulonephiris.
Pathology: Wegners’s Granulomatosis / Granulomatosis with polyangitis
