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Systemic Cardiovascular (Valvular Heart Diseases (Etiology (Developmental…

- - - - Process of formation of atheroma
        
        Endothelial dysfunction: Increased permeability, leukocyte adhesion, monocyte adhesion
        
        Smooth muscle recruitment into the intimate + macrophage activation
        
        Fatty streak macrophages and smooth muscles engulfed in lipids
        
        Fibrofatty atheroma Smooth muscle proliferation, collagen and ECM deposition
      - Epidemiology
        
        Hyperlipidemia
        
        Hypertension
        
        Diabetes
        
        Cigarette smoking
      - Consequences
        
        Vessel thicken --> Lumen narrow --> Poor perfusion --> Ischemia
        
        Loss of elasticity --> Anuerysm --> rupture and haemorrhage
        
        Endothelial changes --> Thrombosis
        
        Acute plaque changes
        
        Myocardial infarction
        
        Cerebral infarction
        
        Aortic aneurysm
        
        Peripheral vascular disease
        
        Chronic plaque changes
        
        Angina
        
        Ischemia in heart, bowel, brain
- - - - Reduced Coronary Flow
        
        Increased myocardial demand (exercise, infection, pregnancy)
        
        Decreased availability of oxygen in blood (Anemia, CO poisoning, pulmonary disease, left to right shunts)
    - - Clinically most dangerous :warning:
        
        Vary in size but normally smaller
        
        Larger lipid core and thinner fibrous cap
        
        More likely to fissure and rupture
        
        Composition is dynamic
    - - Angina Pectoris
        
        Prinzmental angina
        
        Due to arterial spasm, unrelated to physical activity, responds to vasodilator
        
        Unstable angina
        
        Increasing frequent pain, precipitated by lower level of rest, high risk of MI
        
        Stable angina
        
        Relieved by rest or vasodilator, when demand > perfusion
      - Myocardial Infarction
        
        Regional MI
        
        Partial thickness
        
        Full thickness
        
        Circumferential subendocardial infarction
        
        Types of MI by different occlusion
        
        LCA :pen:
        
        Antero-septal
        
        LAD :pen: (40-50%)
        
        Antero-lateral
        
        LCA :pen: (15-20%)
        
        Lateral
        
        RCA :pen: (30-40%)
        
        Posterior
        
        Pathogenesis
        
        Acute plaque event
        
        Thrombus formation
        
        Complete occlusion of lumen
        
        Clinical diagnosis
        
        Severe crushing chest pain
        
        Breathlessness
        
        Sweaty
        
        ECG changes ST elevation
        
        Elevated cardiac enzyme
        
        Morphology
        
        0-12 hours triphenyl tetrazolium chloride test
        
        Necrosed area will not pick up brick red stain
        
        12-24 hours Areas of palor, histologically eosinophils, loss of nucleus, intercellular edema
        
        24-72 hours neutrophils
        
        3-10 days Hyperaemic border around yellow border + granulation tissue
        
        6-8 weeks fibrous scar
        
        Complications
        
        LV failure --> congestive heart failure
        
        Rupture myocardium --> cardiac tamponade
        
        Fibrosis and aneurysm
        
        Thrombus
        
        Conduction system affected --> arrhythmia
        
        Pericarditis --> Dressler's syndrome
        
        Ruptured papillary muscles --> damaged valves
      - Chronic schema heart disease
        
        Narrowing of coronary arteries
        
        Loss of myocardial fibres
        
        Generalised myocardial fibrosis
      - Cardiac death
        
        Lethal arrhythmia from ventricular fibrillation, no infarction
- - - - Left ventricular failure
        
        Causes:
        
        Volume overload (regurg/anaemia)
        
        Pressure overload (hypertension)
        
        Loss of muscle (MI)
        
        Loss of contractility (poisons/myocarditis)
        
        Restricted filling (pericardial effusion)
        
        Conduction problem (Arrhythmia)
        
        Exertional dyspnea / Orthopnoea / Paroxysmal nocturnal dyspnea
        
        Left atrium dilation --> Pulmonary hypertension --> Pulmonary congestion/edema
        
        Hypotension --> Poor tissue perfusion --> Poor tissue oxygenation (kidneys and brain)
      - Right ventricular failure
        
        Causes:
        
        Left sided failure (Most common)
        
        Right valvular problem (stenosis or regurg)
        
        Lung disease
        
        Congestive hepatomegaly
        
        Congestive splenomegaly
        
        Effusions in body cavities
        
        Periphery edema (pitting)
        
        Nocturia (Fluid from legs are return to body while lying down)
    - - Systolic unable to contract and expel sufficient blood, diastolic unable to relax and fill normally, raised filling pressure
- - - - Blood vessels
        
        Atherosclerosis
        
        Arterioloscelrosis
        
        Aneurysm
        
        Hyaline arteriolosclerosis
        
        Benign - Leakage of plasma protein, Hyaline deposition, narrowing
        
        Hyperplastic arteriolosclerosis
        
        Malignant: Onion skin concentric thickening --> smooth muscle deposition --> fibrinoid necrosis of vessel walla
      - Heart
        
        Hypertensive heart disorder
        
        LV pressure overload --> LV hypertrophy
        
        Impaired LV diastolic filling --> Left atrial dilatation --> LV failure
      - Kidney - nephrosclerosis
        CNS - cerebral haemorrhage, cerebra thrombosis
- - - - Myxoid degeneration of valve leaflets
        
        Ballooning of vascular cusps
        
        Associated with Marfan's syndrome :pen:
  - - - Acute phase - 10 days to 6 weeks after pharyngitis, affects younger population, detect by serology testing Ab for streptolysin O. There will be arthritis and carditis
        
        Aschoff bodies :warning: - foci of fibrinoid degeneration surrounded by lymphocyte, collection of cells in between myocardial fibres
      - Chronic phase - damage to heart valves causing stenosis and regurgitation
    - - Fusion of chord tendinae
      - Thickening of heart valve
      - Vegetations along the line of closure of the mitral valve leaflet
    - - Cardiac dilation --> Mitral valve insufficiency --> Heart failure
      - Arrhythmia (due to remodelling of heart valve)
      - Thromboembolic complications (when vegetations dislodge)
      - Infective endocarditis (damaged heart valve can be colonised by bacteria)
  - - - Lead to tissue destruction
        
        Most common: MITRAL and AORTIC
        
        Maybe tricuspid if IV user
      - Types of IE
        
        Acute IE
        
        Normal valves involved
        
        Highly virulent pathogens
        
        Rapid destruction of valves
        
        S. AUREUS :warning:
        
        Subacute IE
        
        Normal commensals bacteria
        
        Due to dental procedure or surgical procedure
        
        STRP VIRIDIANS :warning:
    - - Local
        
        Valve rupture
        
        Myocardial ring abscess
        
        Supparative pericarditis
      - Distant
        
        Embolic organ infarction and abscess formation
        
        Immune complex mediated vasculitis glomerulonephritis
        
        Anemia, splenomegaly
  - - - Fibrinous deposits that are sterile
      - Due to hypercoagulability of blood
- - - - Genetic causes
    - - Systemic causes
    - - Hypertrophic cardiomyopathy
        
        Asymmetric thickening of IV septum
        
        Remodelling, impaired filling during diastolic phase
      - Restrictive cardiomyopathy
        
        No thickening, but deposition of abnormal protein, leading to loss of elasticity
      - Dilated cardiomyopathy
        
        Enlarged LV
        
        Genetic, drugs, alcohol
        
        Impaired systolic function
  - - - Enlarged, flabby myocardium, chambers dilated
    - - Foci of necrosis
        
        Edema between myocardium cells
        
        lymphocyte/eosinophil/granulomatous
        
        Fibrosis
  - - - Left to right shunt
        
        ASD
        
        VSD
        
        PDA (aorta and pulmonary outflow)
      - Right to left shunt
        
        Tetralogy of fallot
        
        Ventricle septal defect
        
        Overriding aorta
        
        Pulmonary stenosis
        
        RV hypertrophy
      - No Shunt
        
        Aortic stenosis
        
        Coarctation of aorta
  - - - Giant cell arteritis
        
        Takayasu's arteritis
    - - Polyarteritis nodosa
        
        Kawasaki disease
    - - ANCA-positive
        
        Wegner's granulomatosis (involves head, neck, kidneys)
        
        Limited Wegner's granulomatosis (involves lungs)
        
        Churg-Strauss syndrome (seen in people with asthma, peripheral eiosinophilla)
      - ANCA-negative
        
        Immune-complex vasculitis
    - - Immune complex related
        
        SLE, polyarteritis nodosa, drug hypersensitivity, virus
      - Non-immune complex related
        
        Antineutrophillic cytoplasmic antibodies (ANCA)
    - - Thrombosis
        
        Haemorrhage
        
        Anuerysm formation