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44 Cards in this Set
- Front
- Back
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Plasma Homocysteine
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•Risk factor for athlerosclerosis
•Can be caused by low folate and vitamin B intake •Is seen in alcoholics |
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Mockenberg Calcification
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•In muscular arteries
•Older than 50 years old •Calcific deposits •Often palpable •Not clinically significant |
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Clinical Manisfestations of Athlerosclerosis
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Coronary Heart Disease:
•MI •Angina •Congestive heart failure •Sudden cardiac death Abdominal Aortic Aneurysm Cerebral Vascular Disease •Stroke •Transient Ischemic Attack •Chronic Ischemic Encephalopathy Peripheral Vascular Disease •Claudication (pain in legs from ischemia) •Ischemic Bowel Disease •Gangrene |
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Malignant Hypertension
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•210/120
•Necrotizing Arteriolitis: deposits of fibrinoid and acute necrosis of the vessel wall (from definition of hyperplastic atherosclerosis) Can lead to: •Renal Failure •Left Ventricular Failure •Hypertensive Encephalopathy |
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Complications of Hypertension
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•Large Blood Vessels: Atherosclerosis
•Small Blood Vessels: Hyaline and Hyperplastic Arteriosclerosis •Heart: Left Ventricular Hypertrophy and Hypertensive cardiomyopathy that leads to IHD and MI •Kidney: Nephrosclerosis •Eyes: Hypertensive retinopathy •Brain: Hemorrhage and Infarction |
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Morphology of Hyaline Atherosclerosis
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•Homogenous, pink hyaline thickening of the walls of the arterioles with loss of underlying structural details and with narrowing of lumen
•Leakage of plasma components across vascular endothelium and increasing extracellular matrix production by smooth muscle cells •Endothelial Injury is attenuated by chronic hemodynamic stress from hypertension or from metabolic stress from diabetes |
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Morphology of Hyperplastic Atherosclerosis
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•Onion skin, concentric laminated thickening of the walls of the arterioles with progressive narrowing of the lumen
•Necrotizing arteriolitis: deposits of fibrinoid and acute necrosis of the vessel wall |
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Vasculitis
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Inflammation and necrosis of the blood vessels, including arteries, veins and capillaries
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What are the targets of p-ANCA and c-ANCA?
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p-ANCA: myeloperoxidase
c-ANCA: proteinase-3 |
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Clinical Features of Giant Cell (Temporal) Arteritis
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•Age of 50 and above
•M:F 1:1 Symptoms: •Vague fever •Weight loss •Fatigue •Facial Pain •Headache •Diplopia •Progressive hazy vision •Loss of vision |
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Morphology of Giant Cell (Temporal) Arteritis
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•Focal, nodular thickening with reduction of lumen
•Granulomatous inflammation of intima and inner media •Giant cells, mononuclear cells •FRAGMENTATION OF INNER ELASTIC LAMINA! |
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Clinical Features of Takayasu Arteritis
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•Most common in females < 40 years
•Ocular changes, retinal hemorrhages, blindness, visual disturbances •Pulseless disease •Low BP in upper limb •Neurologic defects such as hemiparesis, dizziness, focal weakness •Coldness/numbness of fingers |
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Morphology of Takayasu Arteritis
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•Irregular thickening of aorta or branch vessel wall with intimal wrinkling and narrowing of lumen
•Mononuclear inflammation of the media accompanied by granulomatous change leading to patchy necrosis of media •Collegenous fibrosis involving all layers of vessel wall |
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Polyarteritis Nodosa Features
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•Systemic Vasculitis
•Spares Pulm. Circulation •Transmural necrotizing inflammation of small or medium sized muscular arteries •Typically involves renal and visceral arteries Arterioles, Capillaries, Venules not affected 30% of patients have HBV antigen in serum No Glomerulonephritis |
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Morphology of Polyarteritis Nodosa
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Gross:
•Distribution of lesions in descending order: Kidney, heart, liver, GIT Microscopy: •Acute stage: transmural inflammation, fibronoid necrosis of the inner half of the vessel wall •Later stages: Inflammation is replaced by fibrous thickening of the vessel wall All stages of activity can occur simultaneous, even in same artery! |
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Clinical Features of Kawasaki Disease
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•Fever
•Conjunctival and Oral Erythema •Edema of Hands and Feet •Skin Rash with Desquamation •Enlargement of Cervical Lymph Nodes Associated with Mucocutaneous Lymph Node Syndrome |
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Morphology of Kawasaki Syndrome
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Can range from:
•Severe destruction of all constituents of the wall by a segmental necrotizing process with moderate fibrinoid change and dense infiltrate to... •Mild changes involving intima only Acute vasculitis can lead to aneurysm formation and associated thrombosis with MI |
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Clinical Features of Buerger's Disease
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•Affects males usually
•Smoking is a huge risk factor •Claudication •Severe progressive pain on exercise or on rest •Chronic ulceration of the toes, feet, fingers followed by gangrene •Cold sensitivity •Superficial phlebitis •Distal Ichemic Necrosis |
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Morphology of Buerger's Disease
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•Acute and chronic inflammation permeating arterial walls, followed by thrombosis of lumen
•Thrombus contains small microabscesses marked by a central focus of neutrophils surrounded by granulomatous inflammation |
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Clinical Features of Wegener's Granulomatosis
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•Persistent pneumonitis with bilateral nodular and cavity infiltrates
•Chronic sinusitis •Mucosal ulceration of the nasopharynx •Evidence of renal disease Limited WG has no renal involvement |
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Morphology of Wegener's Granulomatosis
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Classic Triad:
•Acute necrotizing granulomas of upper and lower resp. tract •Focal necrotizing or granulomatous vasculitis affecting small to medium sized vessels, most prominent in lungs and upper airways but affecting other sites as well •Renal disease in the form of necrotizing, often crescentric glomerulitis Grossly: •Ulcerative lesions of the nose, pharynx, palate. •In the lungs, dispersed focal necrotizing granulomas coalesce to produce nodules that may undergo cavitations Microscopy: •Areas of necrosis rimmed by lymphocytes, plasma cells, macrophages and giant cells associated with necrotizing vasculitis •Lesions undergo progressive fibrosis and organization |
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Morphology of Aortic Aneurysm
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•Complicated atherosclerotic lesions with destruction of the normal arterial wall and its replacement by fibrous tissue
•Thickened and focally inflamed adventitia |
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Morphology of Syphilitic Aneurysms
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•Tree bark appearance - wrinkling of aortic intima
•Aortic valve ring dilation resulting in valvular insufficiency •Aortic valvular insufficiency leads to cor bovinum (left ventricle hypertrophy) |
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Clinical Features of Syphiltic Aneurysms
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• Encroachment on the mediastinal structures
– Respiratory difficulties. – Difficulty in swallowing. – Persistent cough due to pressure on recurrent laryngeal nerve • Pain caused by erosion of the ribs or vertebrae. • Valvular incompetence (aortic regurgitation) leading to left ventricular hypertrophy, cardiac ischemia due to obstruction to coronary ostia. • Rupture of the aneurysm. • Most common cause of death - heart failure due to aortic regurgitation. |
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Morphology of Left Heart in Left Heart Failure
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Hypertrophied and dilated, so it is thin
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ECG in Myocardial Infarction
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Elevated ST segment and Inversion of the T wave
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Morphology of Chronic Ischemic Heart Disease
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Grossly:
•Enlarged and heavy heart due to hypertrophy and dilation •Discrete gray white scars of healed previous infarcts •Patchy fibrous thickening of mural endothelium Microscopy: •Myocardial hypertrophy •Diffuse endothelial vacuolization (myocytolysis) •Scars of previously healed infarcts |
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Morphology of Hypertensive Heart Disease
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•Concentric hypertrophy of Left Ventricle
•Long Standing Cases - right ventricular hypertrophy and dilation Microscopy: •enlarged myocytes, containing large, hyperchromatic boxcar shaped nuclei |
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Causes of Chronic Cor Pulmonale
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•COPD most common
•IPF •CF •Marked obesity |
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Morphology of Acute Rheumatic Fever
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•Myocarditis - Hallmark is presence of Aschoff bodies within connective tissue of heart
•Endocarditis - Edematous and thickened valves with foci of fibronoid necrosis •Pericarditis - fibrinous pericarditis |
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Morphology of Calcific Stenosis
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Leaflets are rigid and deformed by irregular calcified masses. Calcium deposits lie behind the valve cusps and extend into Sinus of Valsalva
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Morphology of Mitral Valve Prolapse
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Gross:
•Soft, enlarged mitral valve cusps which leads to ballooning of cusps into atrium during systole •Ruptured chordae tendinae •Dilated mitral annulus Microscopy: •Excessive amounts of loose, edematous faintly basophilic ground substance within the middle layer of the valve leaflet and chordae Most patients are asymptomatic |
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Morphology of Infective Endocarditis
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Gross:
– Bulky, friable vegetations that may obstruct the valve orifice – Rapid destruction of the valves – rupture of the leaflets, chordae tendineae, papillary muscles – Ring abscess – abscesses in perivalvular myocardium Microscopy – Large number of organisms mixed with fibrin and blood cells – Minimal inflammatory response |
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Morphology of Subacute Endocarditis
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Gross:
– Vegetations are less friable – Associated with less valve destruction – Ring abscesses uncommon Microscopy – Presence of granulation tissue – Fibrosis, calcification – Chronic inflammatory infiltrate |
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Clinical Features of Infective Endocarditis
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Acute bacterial endocarditis:
– High grade fever with chills – Features of septicemia Subacute bacterial endocarditis: – Low grade fever; malaise – Weight loss – Changing cardiac murmurs – Splenomegaly – Clubbing of fingers |
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Morphology of Marantic Nonbacterial Thrombotic Endocarditis
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Gross:
– Multiple, small nodules along the line of closure – Mitral valve – most commonly affected Microscopy: – Nodules are composed of eosinophilic material (fibrin) and a delicate layer of aggregated platelets – No inflammation or fibrosis |
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Libman-Sacks Endocariditis
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Patients have SLE, vegetations on both sides of valve
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Morphology of Viral Myocarditis
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Gross – dilated heart, may be normal
• Cut surface – mottled surface due to hemorrhages and pale flabby myocardium • Interstitial inflammation -mainly lymphocytes and a few plasma cells • Focal necrosis of myocytes adjacent to inflammatory cells |
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Giant Cell Myocarditis
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Look for granulomatous inflammation with giant cells. Usually in patients with SLE
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Morphology of Dilated Cardiomyopathy
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– Dilation and hypertrophy of all the chambers
– heart is enlarged, flabby, and heavy (2-3 times normal weight) – Dilation and poor contractile dysfunction – mural thrombosis - embolization – Bag like heart Microscopy: • M/E – myocytes are hypertrophied with enlarged nuclei • Interstitial and endocardial fibrosis • Small subendocardial scars replace individual cells – reflect healing of necrotic myocytes |
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Clinical Features of Dilated Cardiomyopathy
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• Fundamental defect is ineffective contraction
• Ejection fraction is < 25% (normal 50-65%) • 20-60 year – most common • Progressive congestive heart failure refractory to therapy • Death usually occurs due to progressive cardiac failure or arrhythmias |
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Morphology of Hypertrophic Cardiomyopathy
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• Gross – massive myocardial hypertrophy without ventricular dilation
• Asymmetric septal hypertrophy – most prominent in the subaortic region – idiopathic hypertrophic subaortic stenosis • On cross section – banana-like configuration of ventricular cavity Microscopy: • Extensive myocyte hypertrophy – transverse myocyte diameter is 40 µM (normal 15 µM) • Myofiber disarray - haphazard arrangement of hypertrophied, abnormally branching myocytes • Interstitial and replacement fibrosis •Myocardium does not relax |
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Clinical Features of Hypertrophic Cardiomyopathy
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• Exertional dyspnea
• Angina or MI • Sudden death – due to arrhythmias |
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Clinical Features of Restrictive Cardiomyopathy
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• Loss of ventricular compliance
• Systole is not forceful • Exertional dyspnea, fatigue, chest pain Complications: – Arrhythmias – Congestive heart failure |
