Cardiovascular pathology I

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  • Created by: z
  • Created on: 19-03-16 19:13

Athersclerosis

  • sites (most to leats common)
    • abdomial aorta
    • coronary arteries
    • popliteal arteries
    • desc thoracic aorta
    • internal carotids
    • circle of willis
  • pathogenesis
    • fatty streak in children
    • athermatous plaques develop through life
    • become symptomatic middle age or later
  • conseqeunces:
    • MI/IHD/sudden death/stroke/CVA
    • gangrene of extremities, gut ischaemia
    • AAA - rupture
    • haemorrhage into placque
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Atheromatous plaque

  • structure
    • fibrous cap
    • cells (smooth m. and inflamm)
    • lipid
    • CT and ECM
  • stable plaque:
    • thick fibrous cap
  • unstable plaque:
    • no thick cap; at risk of rupture/fissure causing emboli +/- thrombosis
  • RFs or atherosclerosis
    • no modifiable: age, male, FHx, genetic abnormality
    • modifiable: high lipids, HTN, smoking, DM
  • pathogenesis theory:
    • "response to injury hypothesis"
    • chronic inflam response of arterial wall inititated by chronic endothelail injury
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Ischaemic heart disease

  • imbalance b/w supply and demand for oxygenated blood in the heart
  • 90% due to atehrosclerosis of coronary artery disease
    • 10%: congenital herat disease, anameia, lung disease
  • aggravated by anything that incr demand or decr supply:
    • hypertrophy, hypotension, hypoxaemia, incr HR
  • risk of IHD w/ athersclerosis dep on:
    • no. of vessels affected (usually > 1)
    • distribution (prox LAD, prox LCX, entire RCA)
    • degree of narrowing (75% reduction in x-sctional area= critical stenosis)
  • 4 syndromes of IHD
    • MI (myocyte necrosis, see elevated creatinine kinase [3d] and troponins [7-10d] w/in 4-8hrs); angina pectoris (NO necrosis); chronic IHD; sudden cardiac death
  • NB most dangerous lesions are 50-755 stenosis w/ lipid rich core and minimal fibrous cap- do not produce angina,high risk of rupture/fissure w/ no collaterals or preconditioning has occurred
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Myocardial infarction

  • transmural
    • full wall thickness
    • assoc w/ acute thrombosis/occlusion of vessel
    • occ due to vasospasm or emboli
    • on distribution of singl eartery
  • subendocardial
    • inner 1/3-1/2 of myocardium
    • may extend being territory of singl eartery
    • subendocardial zone is least perfused thus most at risk w/ reduced coronary flow
    • usually critical stenosis but no acute plaque change
  • histologically can see from 4 hrs
  • macroscopically can see from 12 hrs
  • NB blood supply
    • LAD: apex, anterio LV, anterior IVS
    • LCX: lat LV 
    • RCA: inferior/posterior LV, posterior IVS, RV
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Myocardial infarction II

  • early reperfusion
    • salvages sublethally injured myocytes and minimise infarct size
    • risk of reperfusion injury
    • despite salvage some myocytes may not function for several days: "stunned myocardium"
    • repetitive short lived ischaemia may be protective (preconditioning)
  • complications:
    • contractile dysfnction > heart failure > cardiogenic shock
    • arrythmias
    • myocardial rupture
      • in free wall: tamponade/ in IVS: L to R shunt
      • papillary muscle: acute severe mitral regurg
    • pericarditis early or in weeks (Dressler syndrome= AI)
    • mural thrombus (emoboli risk)
    • ventricular aneurysm
    • progressive late heart failure
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Heart failure

  • failure of heart as a pump
  • adaptive mechanisms to prevent/postpone failure
    • dilation (incr preload due to Frank-Starling mechanism)
    • hypertrophy (incr size of myocytes)
    • activation of neurohumoral mechanisms
      • NA released by adrenergic cardiac nerves > incr HR
      • activation of RAA system > maintain renal function
      • release of atrial natriuretic peptide (ANP) due to high BP > aldosterone antagonist
  • causes:
    • usually systolic dysfunction (poor contarction)
    • oc diastolic dysfunction (stiff walls unable to fill properly)
  • L HF > pulmonary oedema, organ ischaemia (impaired renal function)
    • occurs in most forms of heart disease
  • R HF > organ ischaemia, peripheral oedema, congestion of organs, ascites/pleural effusion
    • usually secondary to LHF
    • pure R HF is uncommon (cor pulmonale)
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Hypertensive heart disease

  • response of herat to increased demands
    • systemic hypertension
    • pulmonary hypertension = cor pulmonary
  • hypertension leads to hypertrophy which causes:
    • myocardial dysfunction
    • cardiac dilation
    • CCF
    • sudden death
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Systemic hypertensive heart disease

  • Dx criteria
    • LV hypertrophy (concentric) + Hx/pathologucal evidenc of HTN
  • Presentation:
    • asymptomatic > ECG 
    • AF (w/ LA enlargement)
    • CCF
  • gross morphology
    • circumferential LV hypertrophy
    • NO lV dilation
    • incr heart weight
    • thick wall (> stiff > impaired filling > LA enlargement)
  • histology
    • incr myocyte size
    • incr nuclear size
    • interstitial fibrosis
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Cor pulmonare

  • pulmonary hypertensive heart disease
  • secondary to pulmonary HTN
    • due to abnormality of lungs/pulmonary vasculature
    • must exclude 2nd to 
      • congenital heart disease
      • disease of left heart
  • acute presenation:
    • sudden incr in pulm BP
      • e.g. massive PE
      • see dilation of RV, no hypertrophy
  • chronic:
    • prolonged pr overload
    • RV hypertrophy
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