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254 Cards in this Set
- Front
- Back
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Which arteries are richest in autonomic nerves?
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Small arteries and arterioles
Important in maintenance of blood pressure! |
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What is the diameter limit for a "small artery"?
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Less than 2mm in diameter
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Endothelial cells contain what kind of bodies? What is found inside these bodies?
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Weibel-Palade bodies
These bodies contain vWF |
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What are the three (3) general steps in the response to vascular injury?
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1. Damage to vessel wall (including endothelium)
2. SMC migration from media to intima w/ dedifferentiation to proliferative (become like fibroblasts; deposit collagen) 3. Proliferation of intimal cells w/ deposition of ECM causes intimal thickening, decreasing the luminal diameter |
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What are two (2) congenital abnormalities of arteries?
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1. Berry aneurysm
2. Arteriovenous Fistula |
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Where are berry aneurysms located?
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Usually @ bifurcation or branching points in the Circle of Willis
ACA and MCA distribution |
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What causes a berry aneurysm?
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Poor development of the musculature in the tunica media, leading to degeneration of the elastic lamina
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What is the worst scenario in a berry aneurysm?
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SUDDEN death in a YOUNG individual
Usually a subarachnoid hemorrhage |
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What are three causes of an AV fistula?
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1. Developmental defect w/ rupture of an arterial aneurysm into a vein
2. Penetrating injuries that pierce a vessel wall 3. Inflammatory necrosis of adjacent vessels |
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What is the clinical significance of an AV fistula?
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RIght sided heart failure!
More blood goes into the right atrium May also rupture |
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What are the three subcategories of arteriosclerosis?
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1. Atherosclerosis
2. Monckeberg medial calcific sclerosis 3. Arteriolosclerosis |
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What five (5) vessels are most commonly associated with atherosclerosis?
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1. Lower AA
2. Coronary arteries 3. Popliteal arteries 4. ICA 5. Circle of Willis |
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What type of arteries does atherosclerosis affect?
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Elastic, and large-to-medium muscular arteries
Does NOT affect small arteries! |
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What is the morphology of an atherosclerotic plaque?
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Fibrous cap = SMC, macrophages, vessels, collagen, proteoglycans
Lipid core = cholesterol, cell debris, foam cells Underlying smooth muscle proliferation of the media |
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What are complications (5) of atherosclerosis?
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1. Calcification
2. Rupture/ulceration 3. Hemorrhage 4. Thrombosis 5. Aneurysm |
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What is a fatty streak?
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An accumulation of lipid-containing macrophages in the intima
Is a PRECURSOR of atherosclerosis |
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What is the main controllable risk factor in atherosclerosis?
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Hyperlipidemia, especially hypercholesterolemia
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Which three increased lipoprotein combinations are most associated with atherosclerosis?
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1. LDL
2. LDL + VLDL 3. Chylomicrons + IDL |
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Which apolipoprotein is associated with HDL?
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ApoA
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Which apolipoprotein is associated with LDL?
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ApoB
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How do you calculate LDL cholesterol?
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Total - HDL - triglycerides/5
tri/5 = VLDL levels |
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What do you look at when you determine the aggressiveness of treatment in atherosclerosis associated with hyperlipidemias?
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LDL cholesterol levels
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What is a desirable total blood cholesterol?
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< 200 mg/dL
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What is a high total blood cholesterol level?
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> 240 mg/dL
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What is a low level of HDL cholesterol?
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< 35 mg/dL
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What is the level of HDL cholesterol that is a negative risk factor for atherosclerosis?
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> 60 mg/dL
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What does hyperhomocysteinemia, stress, C reactive protein, and estrogen deficiency have in common?
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They all are risk factors for developing atherosclerosis
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What is lipoprotein Lp(a)?
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An altered form of LDL that contains a linked apoB-100+apoA
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How do endothelial cells attract monocytes and T-cells to begin the process to form foam cells?
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VCAM1 on endothelial cells binds to monocytes and T-cells
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What four (4) infections may play a factor in atherosclerosis?
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1. Chlamydia pneumoniae
2. Herpes virus 3. CMV 4. H. pylori |
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Describe the mechanism of autoregulation
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An increase in blood flow causes VASOCONSTRICTION to protect tissues against hyperperfusion
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HTN affects what types of arteries?
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Small muscular arteries and arterioles
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What is hyperplastic arteriolosclerosis associated with?
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Malignant HTN!
BP > 160/110 |
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What is the histology of a hyperplastic arteriolosclerosis (chronic and acute cases)?
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"Onion skin" thickening in chronic cases
Fibrinoid necrosis in acute cases |
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What is the histology of benign hyaline arteriolosclerosis?
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Homogenous pink hyaline thickening of arteriole walls
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What are some characteristics of hyaline arteriolosclerosis?
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1. Reflects leakage of plasma components and excessive ECM production
2. Seen in the elderly and diabetics 3. Associated with mild HTN |
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What are three (3) characteristics of Monckeberg Medial Sclerosis?
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1. Degenerative calcification of media of large/medium arteries gives an characteristic X-ray
2. Usually in the ELDERLY 3. ASYMPTOMATIC - no clinical significance! |
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What are four (4) characteristics of Raynaud Phenomenon?
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1. Caused by arterial vasospasm in skin
2. Intermittent painful bilateral attacks of ischemia of fingers or toes precipitated by cold 3. May be isolated, or part of a CT disease (lupus, rheumatoid arthritis) 4. Red-White-Blue |
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What are two (2) complications of fibromuscular dysplasia?
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1. Renal HTN
2. Dissecting aneurysm due to weakening of vessels |
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What type of arteries are affected in fibromuscular dysplasia?
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Large and medium muscular arteries
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Is fibromuscular dysplasia an inflammatory or a non-inflammatory process?
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NON-inflammatory!
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What is the pathology of fibromuscular dysplasia?
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Fibrous tissue metaplasia
(smooth muscle is replaced by fibrous tissue) |
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What are the four (4) pathogenesis of vasculitis?
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1. Deposition of immune complexes
2. Circulating Abs against vessel walls 3. CMI 4. Direct invasion of vessels by infectious pathogens |
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Which vasculitis is associated with HepB (HBsAg-HBsAb immune complexes)?
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Polyarteritis Nodosa
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What type of lesions are associated with polyarteritis nodosa?
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Patchy, fibrinoid necrosis
Vascular involvement is widely scattered |
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What types of arteries does PAN affect?
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Medium and small muscular arteries; large arteries on occasion
IN MULTIPLE ORGANS! |
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How do you treat PAN?
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Steroids, cyclophosphamide
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Which vasculitis is associated with leukocytoclastic vasculitis? What do leukocytoclasts indicate?
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Hypersensitivity (microscopic) polyarteritis
Shows nuclear debris from disintegrating neutrophils |
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What types of arteries does hypersensitivity angiitis affect?
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The smallest arteries and arterioles in multiple organs
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Which vasculitis is associated with a PALPABLE PURPURA?
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Hypersensitivity (microscopic) polyarteritis
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What three (3) things are associated with Churg-Strauss?
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1. Allergic rhinitis
2. Bronchial asthma 3. Peripheral eosinophilia |
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What types of arteries does Churg-Strauss syndrome (allergic granulomatosis) affect?
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Small and medium arteries, arterioles, venules
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What is the most common type of vasculitis?
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Temporal (giant cell) arteritis!
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What patient population does giant cell arteritis affect?
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Elderly (> 50 years of age)
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The pathology of giant cell arteritis involves what three (3) things?
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1. Granulomatous inflammation
2. Fragmented internal elastic lamina 3. Giant cells |
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Which arteries does giant cell arteritis affect?
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1. Temporal
2. Vertebral 3. Ophthalmic 4. Aorta |
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Which are the two most common symptoms in giant cell arteritis?
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1. Headache/throbbing temporal pain
2. Visual symptoms if ophthalmic artery is involved |
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How do you diagnose giant cell arteritis?
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Temporal artery biopsy (however is positive in only 60% of cases)
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What is the treatment for giant cell arteritis?
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Steroids!
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What is the clinical triad for Wegener granulomatosis?
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1. Acute necrotizing granulomas of UPPER RESPIRATORY TRACT
2. Necrotizing/granulomatous vasculitis of SMALL and MEDIUM vessels 3. RENAL DISEASE (glomerulonephritis) |
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Hemoptysis w/ renal disease should indicate which vasculitis?
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Wegener granulomatosis
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Which vasculitis has the strongest association with antineutrophil cytoplasmic antibodies?
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Wegener granulomatosis (90% of them)
Is usually C-ANCA |
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What types of arteries does Wegener granulomatosis affect?
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Small arteries and veins
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Which vasculitis is effectively treated with cyclophosphamide?
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Wegener granulomatosis
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How do you differentiate Takayasu arteritis from giant cell arteritis?
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Giant cell = elderly
Takayasu = young (< 40) women |
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What type of arteries does Takayasu arteritis affect?
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Large arteries, especially the aorta and its branches
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Which vasculitis is associated with "pulseless disease"?
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Takayasu arteritis
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What symptoms are associated with Takayasu arteritis?
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1. Constitutional symptoms
2. Ocular disturbances 3. Intermittent claudication of arms/legs 4. Asymmetric differences in blood pressure |
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What is another name for Kawasaki Disease?
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Mucocutaneous Lymph Node Syndrome
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Which vasculitis characteristically affects the coronary artery?
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Kawasaki Disease
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What is the leading cause of acquired heart disease in children?
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Kawasaki Disease
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What type of patients does Kawasaki disease affect?
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Infants and young children
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Which vasculitis is a response to exogenous substances such as bacterial products and drugs?
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Hypersensitivity (microscopic) polyarteritis
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What are characteristic symptoms of Kawasaki disease?
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1. High fever
2. Rash 3. Conjunctival and oral lesions 4. Lymphadenitis |
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What is the etiology of Kawasaki disease?
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Viral or bacterial etiology
(antibodies directed against EC and SMC) |
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Which vasculitis is associated with smoking?
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Thrombangiitis Obliterans (Buerger Disease)
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Which body part(s) is most affected by Buerger disease?
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Distal arms and legs
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What types of arteries does Buerger disease affect?
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Small and medium arteries of extremities
(tibial and radial arteries!) |
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What separates Buerger disease from atherosclerotic vascular insufficiency?
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Buerger disease has PAIN!
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What are the clinical symptoms of thrombangiitis obliterans?
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1. Intermittent claudication
2. Ulceration and necrosis of digits |
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Which two (2) fungi are most associated with vasculitis?
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1. Aspergillis
2. Mucor |
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Vasculitis can be associated with what other disorders?
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1. Rheumatoid arthritis
2. SLE 3. Anti-phospholipid syndrome 4. Malignancy |
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Which vasculitis affects the large vessels?
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1. Giant cell arteritis
2. Takayasu arteritis |
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Which vasculitis affects the medium vessels?
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1. Polyarteritis nodosa
2. Kawasaki disease 3. Thrombangiitis obliterans |
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Which vasculitis affects the small vessels?
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1. Wegener granulomatosis
2. Churg-Strauss syndrome 3. Microscopic polyangiitis |
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Which vasculitis are associated with p-ANCA?
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1. PAN
2. Churg-Strauss (allergic) 3. Microscopic (hypersensitivity) polyarteritis |
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Syphilitic aneurysms frequently affect which vessel?
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ASCENDING aorta
However, the most common cause of ascending aorta aneurysm remains atherosclerosis |
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What is the #1 cause of aneurysms?
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Atherosclerosis
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What can a dissecting aneurysm be secondary to?
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Marfan syndrome
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What is the characteristic microscopic pathology associated with syphilitic aneurysms?
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Vasa vasorum surrounded by plasma cells and lymphocytes
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Describe the events of thrombosis and embolism in varicose veins.
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Thrombosis is common
Embolism is RARE |
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What is phlebothrombosis?
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Thrombosis w/in a vein
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What is thrombophlebitis?
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Inflammatory changes w/in a vein wall
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Where is the most common site of a phlebothrombosis?
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90% of them occur in the deep leg veins
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What is Homan's sign?
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Pain during forced dorsiflexion of the foot when the knee is flexed to 90 degrees
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What is the major complication of a phlebothrombosis?
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Pulmonary embolism
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What are two (2) special variants of phlebothrombosis?
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1. Phlegmasia alba dolens
2. Migratory thrombophlebitis |
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What is Phlegmasia alba dolens?
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Iliofemoral venous thrombosis that occurs in pregnant women or just following delivery
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What is migratory thrombophlebitis associated with?
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Visceral malignancies - adenocarcinomas especially of the pancreas, colon, lung
Trousseau sign! |
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What is the clinical triad of SVC syndrome?
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1. Dilation of veins of head and neck
2. Cyanosis of head, neck, arms 3. Respiratory distress of pulmonary vessels are compressed |
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What are the clinical features of IVC syndrome?
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1. Marked edema of legs
2. Distension of superficial veins or lower abdomen |
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Which neoplasms are most associated with IVC syndrome?
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Hepatocellular carcinoma, renal cell carcinoma
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What are the two (2) etiologies of IVC syndrome?
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1. Neoplasm w/ obstruction
2. Propagation of a clot from the femoral/iliac veins |
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What is the usual cause of lymphangitis?
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Bacterial infection!
Usually from group A strep |
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What is the clinical presentation of lymphangitis?
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Painful subcutaneous red streaks that represent the inflamed lymphatics
Painful enlarged nodes |
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What are five (5) causes of secondary obstructive lymphedema?
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1. Malignancy
2. Removal of lymph nodes 3. Post-radiation fibrosis 4. Filariasis 5. Post-inflammatory thrombosis |
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What are three (3) causes of primary lymphedema?
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1. Lymphadema Praecox (young females)
2. Milroy's disease (familial faulty development of lymphatics 3. Simple congenital lymphedema |
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How do you differentiate tumorous vascular proliferation from non-tumorous vasoproliferations in inflammation?
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Inflammatory reaction and/or ulceration of overlying epithelium = inflammatory
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How do you separate benign and malignant vascular neoplasms?
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Benign = well-formed channels w/ regular ECs
Malignant = anaplastic cells w/ scant #s of vascular channels |
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What are four (4) types of benign vascular tumors or tumor-like conditions?
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1. Teleangiectasias
2. Angioma 3. Glomangioma 4. Bacillary angiomatosis |
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What are two (2) types of intermediate grade vascular tumors?
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1. Kaposi's Sarcoma
2. Hemangioendothelioma |
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What are three (3) types of malignant vascular tumors?
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1. Hemangiosarcomas
2. Lymphangiosarcoma 3. Hemangiopericytoma |
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What are three (3) types of telangiectasias?
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1. Nevus Flammeus
2. Spider Telangiectasia 3. Osler-Weber-Rendu disease (hereditary hemorrhagic) |
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What is a characteristic of telangiectasias?
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Local dilation of pre-existing vessels gives a focal red lesion
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What is the most common telangiectasia?
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Nevus Flammeus
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What disease is associated with nevus flammeus?
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Sturge-Weber disease
May see a "large facial vascular malformation in a child w/ mental deficiency" |
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What is spider telangiectasia related to?
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Related to INCREASED ESTROGEN
Most common in pregnancy and cirrhosis |
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Is Osler-Weber-Rendu disease dominant or recessive trait?
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Dominant!
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What is the clinical presentation of Osler-Weber-Rendu disease?
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Hemorrhages leading to nosebleeds and bleeds into the intestinal, respiratory, and urinary tract
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What is von Hippel Lindeau disease associated with?
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Cavernous Hemangioma!
Also associated w/ renal neoplasms |
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Are capillary or cavernous hemangiomas deeper and locally destructive?
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Cavernous hemangiomas
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What is the difference b/w a simple and a cavernous lymphangioma?
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Cavernous lymphangiomas are much bigger
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What is a glomus? Where are they located?
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A neuromyoarterial receptor that is sensitive to temperature and regulates arteriolar flow
Found in distal portion of fingers/toes |
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What is a characteristic of a glomangioma?
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Very painful!
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Which benign vascular neoplasm is associated with a Bartonella henselae infection?
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Bacillary angiomatosis!
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How do you treat bacillary angiomatosis?
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Antibiotics (usually macrolides)
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What virus is always associated with Kaposi's Sarcoma?
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KS-associated herpesvirus / human herpesvirus 8
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What is the progression of classic Kaposi's Sarcoma?
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Patch --> Raised plaque --> Nodule
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What are four (4) clinical situations in which you see Kaposi's Sarcoma?
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1. Older men w/ scattered skin lesions
2. African blacks w/ extensive lymph node involvement 3. AIDS patients 4. Transplants w/ immunosuppressive therapy |
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What is a hemangioendothelioma?
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A true vascular neoplasm made up of masses of endothelial cells
An intergrade b/w hemangiomas and hemangiosarcomas |
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What are three (3) causes of hepatic angiosarcoma?
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1. PVC in plastic
2. Arsenicals in pesticides 3. Thoratrust (radioactive contrast agent) |
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What is the etiology of a lymphangiosarcoma?
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Prolonged lymphatic obstruction, as in a mastectomy for breast cancer
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How do you differentiate pericytes from ECs in a hemangiopericytoma?
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Use a silver stain for the basement membrane
Pericytes will be OUTSIDE the basement membrane |
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Where are the most common sites for a hemangiopericytoma?
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1. Lower extremities (thighs)
2. Retroperitoneum |
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What is the clinical presentation (4 things) of left-sided heart failure?
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1. Dyspnea
2. Prerenal azotemia 3. Cerebral hypoxia 4. Atrial fibrillation |
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What three (3) hormone systems are activated in CHF?
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1. Norepinephrine
2. Renin-angiotensin-aldosterone 3. Atrial natriuretic peptide |
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What are heart failure cells?
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Hemosiderin-containing macrophages; provide evidence of previous pulmonary edema
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What pulmonary finding is common in both primary left and right sided heart failure?
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Pleural effusion
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What are four (4) causes of right-sided heart failure?
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1. Left sided heart failure
2. Intrinsic lung disease 3. Congenital R --> L shunts 4. Pulmonic/tricuspid valve disease |
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Engorgement of the systemic and portal systems in right sided heart failure causes what?
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1. Nutmeg liver, hepatomegaly, cirrhosis
2. Congestive splenomegaly, ascites 3. Prerenal azotemia due to congestion and hypoxia 4. Peripheral edema, anasarca 5. Hypoxic encephalopathy |
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What is the #1 cause of ischemic heart disease?
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Atherosclerosis (makes up 95-98% of cases)
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Your patient is an elderly man with heart failure, but no history of angina or myocardial infarction. The cath lab reports narrow coronary arteries.
What is the diagnosis? |
Chronic ischemic heart disease
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What % of a coronary artery needs to be occluded for there to be symptomatic ischemic w/ exertion?
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70-75%
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What % of a coronary artery needs to be occluded for there to be symptomatic ischemic @ rest?
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90%
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What are the 3 major factors in the pathogenesis of ischemic heart disease?
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1. Reduction in coronary artery blood flow
2. The level of myocardial metabolic demands 3. Oxygen content of blood |
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What is the only type of angina that presents with ST elevation on EKG?
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Prinzmetal (vasospam @ rest) angina
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What are the pharmacologic treatments (3) for angina?
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1. Aspirin
2. Beta-blocker 3. Nitroglycerin |
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In a myocardial infarction, how much time does it take for necrosis to occur?
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20-40 minutes
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Explain the exclusivity of transmural infarcts.
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They mainly occur in the left ventricle (97%)
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What are the complications of an anterior heart wall infarction?
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1. Free wall rupture and expansion
2. Mural thrombi 3. Aneurysm |
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What are the complications of a posterior heart wall infarction?
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1. Conduction blocks
2. Right ventricular involvement |
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How long post-infarct will you see a gross dark mottling of the heart tissue?
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12-24 hours
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How long post-infarct will you see a gross yellow-tan softening of heart tissue with a hyperemic border?
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3-7 days
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How long post-infarct will you see a gross gray-white scar?
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2-8 weeks
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How long does a complete scar take to form after a myocardial infarction?
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> 2 months
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When would you first see gross manifestations of a myocardial infarction?
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4-12 hours post-infarct
Will see occasional dark mottling |
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Which cardiac marker shows the earliest increase after an infarction?
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Myoglobin
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The usage of myoglobin as a cardiac marker is limited to what?
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It has a good negative predictive value (negative result is most likely negative)
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How long post-infarct do CK-MB and troponin I levels begin to elevate?
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4-8 hours
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When do CK-MB levels normalize after an infarction?
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3 days
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When do troponin I levels normalize after an infarction?
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5-9 days
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What is the most important hereditary cause of sudden cardiac death?
|
Autosomal dominant long-QT syndrome
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Which is the more common valvular heart disease: valvular stenosis or valvular regurgitation?
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Valvular stenosis (2/3 of cases)
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What is the most frequent cause of mitral stenosis?
|
Rheumatic heart disease
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Which valve is usually never affected in rheumatic heart disease?
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Pulmonic valve
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What kind of inflammation is associated with rheumatic heart disease?
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Pancarditis
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What is an Aschoff body?
|
A central fibrinoid necrosis with degenerating, hypereosinophilic ECM with a rim of T-lymphocytes, plasma cells, and Anitschkow cells
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What are Anitschkow cells?
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Plump activated macrophages w/ slender, wavy ribbon chromatin
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What is a description of the pericarditis associated with rheumatic heart disease?
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"Bread and butter"; the caking up of the butter is the fibrin
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What are the vegetations in rheumatic heart disease composed of?
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1. Fibrin
2. Platelets 3. Inflammatory cells |
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What are the major criteria for diagnosing rheumatic heart disease?
|
1. Polyarthritis
2. Carditis 3. Subcutaneous nodules 4. Erythema marginatum 5. Chorea |
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What are the minor criteria for diagnosing rheumatic heart disease?
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1. Previous rheumatic fever
2. Arthralgia 3. Fever 4. Elevated ESR or CRP 5. EKG changes |
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How long after a group A strep pharyngitis may you see symptoms of rheumatic heart disease?
|
2-3 weeks after infection
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What three (3) serologic tests can you perform to help diagnose rheumatic heart disease?
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1. Antistreptolysin O (used most commonly)
2. Anti-DNAse 3. Anti-hyaluronidase All are proteins made by S. pyogenes |
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How do you treat rheumatic heart disease?
|
1. Treating the strep pharyngitis w/ penicillin
2. Steroids and aspirin if pt is at the acute rheumatic fever stage |
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How is chronic rheumatic heart disease related to acute rheumatic fever?
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It presents w/ severe valvular scarring months or years after acute rheumatic fever
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What will you not see in chronic rheumatic heart disease, but will see in acute rheumatic fever?
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Aschoff bodies
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What is the most common associated dysfunction in chronic rheumatic heart disease?
|
Mitral valve stenosis
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What happens to the valve leaflets in chronic rheumatic heart disease?
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1. Leaflet thickening/calcification
2. Commissural fusion 3. Shortening/thickening/fusion of the chordae tendinae |
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What are five (5) complications of rheumatic heart disease?
|
1. Bacterial endocarditis
2. Mural thrombi 3. CHF 4. Cor pulmonale 5. Adhesive pericarditis |
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What is a complication that is common to all valvular diseases?
|
Bacterial endocarditis
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What is the cause of Libman-Sacks Endocarditis?
|
Systemic Lupus Erythematosus
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What are the characteristics of acute infective endocarditis (3)?
|
1. Occurs on a normal cardiac valve
2. Caused by highly virulent organisms 3. Valve is rapidly destroyed |
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What are the characteristics of subacute infective endocarditis (4)?
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1. Occurs on a previously damaged valve
2. Caused by low virulent organisms 3. Insidious infection; less valvular destruction 4. May see granulation tissue indicative of chronicity |
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What is a common predisposing condition for infective endocarditis among children AND adults?
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Congenital heart disease
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What is absolutely required for there to be infective endocarditis?
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Transient bacteremia
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What is the pathogenesis of an infective endocarditis?
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A) Hemodynamic factors cause the formation of a sterile thrombus made of platelets+fibrin
b) Microorganisms adhere to the thrombus to form a vegetation |
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What are two (2) complications of an infective endocarditis?
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1. Infected thromboemboli
2. Glomerulonephritis |
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What is the most consistent sign in infective endocarditis (especially acute IE)?
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Fever
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What is a symptom secondary to thromboemboli from an infective endocarditis?
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Splinter hemorrhages
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Describe the vegetation in rheumatic heart disease.
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A row of verrucous (warty and small) vegetations along the lines of closure of valve leaflets
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Describe the vegetation in infective endocarditis.
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Large, irregular masses on the valve cusps
Can extend onto the chordae tendinae |
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Describe the vegetations in nonbacterial thrombotic endocarditis.
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Small, BLAND vegetations usually attached @ the line of closure
Only see fibrin and platelets; there is NO inflammation or microorganisms |
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Describe the vegetations in Libman-Sacks endocarditis.
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Small or medium vegetations on either or BOTH SIDES of the valve leaflets
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When might you see a nonbacterial thrombotic endocarditis (marantic endocarditis)?
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1. Malignancy (pancreatic) or other debilitating disease
2. Hypercoagulable state (Trosseau syndrome) |
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What is the most common cause of aortic stenosis?
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Calcific aortic stenosis
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What is the most common degenerative valvular disease?
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Calcific aortic stenosis
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With what valvular disease may you see a "cor bovinum"?
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Calcific aortic stenosis
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Which valvular disease may you see in the elderly, but has no clinical significance?
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Calcification of the mitral valve annulus
Will only see a ring-like opacity on a chest X-ray |
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What is Barlow's Syndrome?
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Late systolic murmer w/ a mid-systolic click
Seen in mitral valve prolapse |
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In which valvular disease may you see a myxomatous degeneration of the valve leaflets?
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Mitral valve prolapse
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What is carcinoid heart disease?
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A systemic syndrome that includes flushing, diarrhea, dermatitis, and bronchoconstriction
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What is a carcinoid?
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A neuroendocrine tumor that resembles a carcinoma
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What is the etiology of carcinoid syndrome?
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High levels of serotonin
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Which side of the heart is affected by carcinoid heart disease?
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The right side!
Fibrous deposits on the tricuspid/pulmonic valves and RV endocardium Carcinoid syndrome = tricuspid insufficiency, pulmonary stenosis |
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When do you see carcinoid heart disease?
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When carcinoid tumors metastasize to the liver
The liver can no longer catabolize the causative mediators |
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What are the four (4) major categories of primary myocardial disease?
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1. Myocarditis
2. Metabolic heart disease 3. Cardiomyopathy 4. Cardiac tumors |
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What is the most common cause of infective myocarditis?
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Viruses!
Coxsackievirus, ECHO, influenza, HIV, CMV |
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What is the most common cause of hypersensitivity myocarditis?
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Drug therapy and transplant rejection
Inflammation usually includes eosinophils |
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What is the most rapidly fatal myocarditis?
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Giant cell myocarditis
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How does hyperthyroidism affect the heart?
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1. Tachycardia
2. Increased CO 3. Angina and cardiac faliure |
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How does hypothyroidism affect the heart?
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1. Bradycardia
2. Decreased CO 3. Impaired contractility |
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What is a non-thyroid cause of metabolic heart disease?
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Beriberi (insufficient vitamin B1)
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Is idiopathic dilated cardiomyopathy a systolic or diastolic dysfunction?
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Systolic dysfunction
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Describe a heart affected by dilated cardiomyopathy.
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Enlarged, flabby, dilation of all chambers, commonly find mural thrombi
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What is the fundamental defect in dilated cardiomyopathy?
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Ineffective contraction!
EF is < 25%, instead of the normal 60% |
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What are the most common drugs that cause secondary dilated cardiomyopathy?
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Alcohol, anthracyclines, cobalt, catecholamines, cyclophosphamide, cocaine
2 A's and 4 C's |
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What are two (2) causes of secondary dilated cardiomyopathy?
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1. Drugs
2. Metabolic disorders (kwashiorkor, storage diseases, acromegaly) |
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What defines hypertrophic cardiomyopathy?
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When cardiac hypertrophy is out of proportion to the hemodynamic load on the heart
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What is the cause of hypertrophic cardiomyopathy?
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Is usually a genetically transmitted mutation affecting sarcomeric proteins (B-myosin heavy chain, cardiac troponin T)
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Describe the heart affected by hypertrophic cardiomyopathy.
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1. Thick walled and heavy
2. Hypercontracting 3. NO ventricular dilation 4. Low stroke volume due to impaired diastolic filling |
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Which primary myocardial disease has a disarrary orientation (oblique and perpendicular) of myocytes?
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Hypertrophic cardiomyopathy
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Which primary myocardial disease has an asymmetric hypertrophy of the IV septum relative to the LV free wall?
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Hypertrophic cardiomyopathy
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When might you see the symptoms of hypertrophic cardiomyopathy?
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During severe exertion
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What is idiopathic hypertrophic subaortic stenosis?
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Obstruction of the ventricular outflow tract by a hypertrophic IV septum
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What are two (2) pharmacologic treatments for hypertrophic cardiomyopathy?
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1. Beta-blockers
2. Calcium channel blockers Reduce contractility and decrease outflow obstruction |
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What are three (3) characteristics of restrictive cardiomyopathy?
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1. Decreased ventricular compliance
2. Limited diastolic filling 3. NORMAL contractility |
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Your patient complains of decreased ventricular compliance, but has normal heart contractility.
What is the diagnosis? |
Restrictive cardiomyopathy
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What is the most common clinical presentation of restrictive cardiomyopathy?
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Right sided heart failure
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What is Loffler Endocarditis?
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A restrictive cardiomyopathy produced by damage via eosinophils
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What are four (4) causes of restrictive cardiomyopathy?
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1. Amyloidosis
2. Endomyocardial disease (i.e. Loffler) 3. Storage diseases 4. Sarcoidosis |
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What is the most common primary tumor of the heart?
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Cardiac myxoma
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Cardiac myxomas most commonly affect where in the heart?
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Left atrium, @ the fossa ovalis
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When do cardiac myxomas become clinically significant?
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When they cause ball-valve obstruction
A type of INTERMITTANT heart failure! |
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What is the most common primary tumor of the heart in infants and children?
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Rhabdomyoma
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Where do papillary fibroelastomas usually grow on the heart?
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Heart valves
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Where are most metastatic tumors located on the heart? Which metastatic tumors commonly affect the heart?
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The pericardium
Lung, breast, GI, lymphoma, leukemia, melanoma |
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What hemodynamic changes in heart valves will you see with pressure?
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Thickening @ the line of closure/edge
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What hemodynamic changes in heart valves will you see with flow/volume?
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Generalized thickening of the valve
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What is the most common type of atrial septal defect?
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A fossa ovalis/ostium secundum type
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What valvular dysfunction do you commonly see with an ostium primum type of ASD? What heart changes will you see with this ASD?
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Mitral regurgitation
LA and RA hypertrophy, CHF |
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What general heart changes will you see with an ASD?
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RA and RV volume hypertrophy
Increased pulmonary flow |
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What general heart changes will you see with a VSD? What heart change will you see with a large VSD?
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RV, LA, LV volume hypertrophy
Large VSD --> RV pressure hypertrophy |
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What general heart changes will you see with a patent ductus arteriosus?
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LA and LV volume hypertrophy
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What general heart changes will you see with pulmonary HTN with shunts?
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Right sided pressure hypertrophy
Left sided volume atrophy |
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What general heart changes will you see with pulmonary stenosis?
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Pressure hypertrophy of RV
Post-stenotic dilation of the pulmonary trunk |
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Where is the narrowing in adult-type coarctation of the aorta? What general heart changes will you see?
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Distal to the subclavian artery
Pressure hypertrophy of LV and sometimes LA, HTN proximal w/ hypotension distal to obstruction, collateral anastamoses |
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Where is the narrowing in fetal-type coarctation of the aorta? What general heart changes will you see?
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Narrowing of the entire transverse arch
Volume hypertrophy and dilation of RA/RV, volume atrophy of LA/LV, dilation of pulmonary arteries, usually an ASD or patent ductus arteriosus |
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In tetralogy of Fallot, what is required of the VSD?
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Must be a "U" shaped VSD confluent w/ the aortic valve
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What is the most common cyanotic form of congenital heart disease?
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Tetralogy of Fallot
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What will you see in the cyanotic form of tetralogy of Fallot?
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1. Pressure hypertrophy of RA and RV
2. Slightly smaller LA and LV 3. R-->L shunt @ ventricular level |
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What will you see in the acyanotic form of tetralogy of Fallot?
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1. Pressure and volume hypertrophy of RV
2. Pressure hypertrophy of RA 3. Volume hypertrophy of LA and LV 4. Enlargement of mitral and aortic orifices 5. L-->R shunt @ ventricular level |
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With which congenital heart diseases may you see cyanosis?
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1. Tetralogy of Fallot
2. Fetal type of coarctation of the aorta |
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With which congenital heart diseases may you see left-sided atrophy?
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1. Pulmonary HTN w/ shunts
2. Fetal type of coarctation of the aorta 3. Slight atrophy w/ cyanotic type of tetralogy of Fallot |
