Systemic Pathology - Cardiovascular - Heller

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  1. Congestive Heart Failure
    • An end-stage manifestation of many processes that impede the heart’s ability to function.
    • Cardiac output insufficient
    • Heart first adapts by increasing size/mass, but eventually fails
  2. Why does the heart fail?
    • Failure of the pump.
    • An obstruction to flow
    • Regurgitant flow
    • Disorders of cardiac conduction.
    • Disruption of the continuity of the circulatory system
  3. Congestive Heart Failure
    • Usually chronic inability to deliver needs associated with congestion of organs
    • Can be acute after fluid overload, MI, acute valvular function, etc
    • Characterized by diminished cardiac output, systolic dysfunction (forward failure), or damming back of blood in the venous system, diastolic failure with insufficient filling (backward failure), or both.
    • Not a disease
    • End stage of many processes
    • May be left or right sided, or both
    • Degree of dysfunction and whether compensated or not best evaluated outside of heart.
  4. Heart failure
    • Initially heart can compensate by release of catecholamines, myocyte hypertrophy.
    • Hypertrophy due to adaptive molecular and cellular remodelling
    • Enlargement later pathologic w/ ineffective function/structure. May have arrhythmias
    • Later when compensation fails see dilatation
  5. Left sided failure
    • Ischemia due to MI
    • Hypertension
    • Aortic stenosis
    • Mitral regurgitation
  6. Forward failure
    • Systolic dysfunction
    • Tissue hypoxia
  7. Left sided failure
    • Heart can’t keep up w/ venous return from lungs
    • Increase back pressure into lungs leads to pulmonary congestion and edema
    • Lungs heavy/wet (Rales)
    • Micro: Lungs show congestion, edema, and hemosiderin-laden alveolar macrophages in alveoli “heart failure cells”
    • Decreased renal perfusion activates renin-angiotensin-aldosterone system, leads to retention of salt and water, worsening pulmonary edema
    • Hypoxic encephalopathy
  8. Symptoms
    • Dyspnea on exertion
    • Paroxysmal nocturnal dyspnea
    • Orthopnea - sit up straight
    • Hemoptysis - cough up blood
    • Rales - sound
  9. Signs
    • Hypoxic encephalopathy
    • Renal underperfusion causes Renin-aldosterone to kick in, worsening pulmonary edema
    • Azotemia
  10. Micro
    Myocyte hypertrophy w/ boxcar nuclei (enlarged and rectangular in shape)
  11. Right sided failure
    • Usually due to left sided failure.
    • Backup from left into lungs overloads right heart
    • Heart cannot accept normal systemic return
    • “cor pulmonale” - right heart failure due to pulmonary hypertension.
    • Pulmonary edema not prominent
  12. Relaxation failure
    • Diastolic dysfunction
    • Congestion and stasis of systemic organs
  13. Right sided failure - manifestations
    • Right heart can’t keep up w/systemic return
    • Systemic & portal venous congestion and edema
    • Chronic passive congestion of the liver (nutmeg liver)
    • Splenomegaly
    • Distended neck veins
    • Deep leg vein thrombosis, stasis dermatitis
    • Pedal and pretibial edema, +/- pitting
    • Anasarca - total-body edema, most serious
    • Pericardial, pleural effusions, ascites
  14. Cardiomyopathies
    • Intrinsically sick heart
    • Primary abnormality of myocardium
    • Wide array of etiologies: inflammation, immune, genetic, metabolic, idiopathic
    • Dilated, hypertrophic, restrictive based on morphology and function
    • Traditionally, exclude ischemic, although “ischemic cardiomyopathy” is a term used by some for CHF associated w/ CAD
  15. Dilated, hypertrophic, restrictive Cardiomyopathies ??
    • dilated: LV LA dilated; small portion is genetic
    • Hypertrophic: 100% genetic; LV hypertrophic, LA dilated
    • Restrictive: LV normal, LA dilated
  16. Dilated cardiomyopathy
    • Most common pattern (90%)
    • Heavy, flabby heart w/ dilated chambers.
    • Histology - variable myocyte hypertrophy, boxcar nuclei, and interstitial fibrosis
    • Poor contractility leads to increased end-systolic, and diastolic volumes, leading to dilatation
    • Slow onset CHF
    • Poor ejection fraction
    • Mitral regurgitation
    • Arrhythmias
    • Embolism
    • Death within 5 years not rare
  17. Etiologies of DCM:
    infection (myocarditis), cardiotoxic drugs/chemicals (ETOH), nutritional disorders, genetic (25-35%), pregnancy (probably multifactorial), autoimmune, idiopathic
  18. Although dilated and hypertrophic cardiomyopathies differ greatly in subcellular basis and morphologic phenotypes, they share a common set of clinical complications - heart failure, sudden death, atrial fibrilation, stroke.
  19. Hypertrophic cardiomyopathy
    • Marked LVH without dilatation leads to resistence to diastolic filling with hypercontracted heart and contracted slit-like ventricle (“banana-like”)
    • 50% familial (autosomal dominant), 50% sporadic
    • Asymmetrical thickening, often in subaortic region of septum, even thicker than the wall.
    • Classic young athlete sudden death
    • Histological characteristics - disarray (dilated CM is more organized), extreme hypertrophy (boxcar), and branching of myocytes; interstitial fibrosis
    • Manifestations
    • •Angina
    • •Atrial fibrillation w/ possible thromboembolism
    • •Mitral infective endocarditis
    • •Ventricular arrhythmias
    • •Sudden death
  20. Restrictive Cardiomyopathy
    • Essentially normal sized heart, dilated atria
    • Reduced ventricular compliance due to stiffening of wall and failure of relaxation leads to resistance to diastolic filling.
    • Systolic function unaffected, hence no hypertrophy
    • Etiologies - Radiation injury/fibrosis, amyloidosis, sarcoidosis, idiopathic, inborn errors of metabolism, metastatic tumors
    • If not idiopathic, see specific pathology of the causative disease
  21. Amyloid Restrictive Cardiomyopathy
    • red stain -> apple green
    • Amyloid infiltration around myocytes
  22. Myocarditis
    • Myocardial Inflammation
    • Cause but not a response to myocardial injury (ie in MI)
    • Coxackieviruses A and B and other enteroviruses probably account for most of the cases.
  23. Active phase of Myocarditis
    • Normal or dilated; some hypertrophy may be present.
    • Ventricular myocardium - flabby, mottled by pale foci or minute hemorrhagic lesions.
    • Interstitial inflammatory infiltrate and focal necrosis of myocytes adjacent to the inflammatory cells - diagnosis
    • The lesions may be diffuse or patchy.
    • Mural thrombi may be present in any chamber.
  24. Congenital Heart Disease
    • Abnormalities of the heart/great vessels present at birth
    • Most common heart disease in children
    • May be associated with genetic syndromes such as trisomy 13,18, 21, XO
    • May be caused by a genetic abnormality
    • May be environmental, ex Rubella syndrome
  25. Two basic functional categories
    • Shunt (L->R, R->L, or both)
    • Obstruction to flow
  26. Non-cyanotic shunt
    • L->R, not bypassing lungs, overloading instead, more common
    • Increased pulmonary flow -> increased pulmonary pressure/volume -> pulmonary hypertension -> RVH -> heart failure, cor pulmonale
    • Not initially cyanotic, but can become later
    • When pulmonary pressure equals systemic, can have reversal of shunt from right to left, leading to cyanosis
  27. Most Common L to R shunt
    • Atrial septal defect (ASD)
    • Ventricular septal defect (VSD)
    • Patent ductus arteriosus (PDA)
    • {Atrioventricular canal (endocardial cushion defect)
    • Coarctation of the aorta}
  28. ASD
    • Usually asymptomatic until adulthood
    • Complications include
    • • Pulmonary hypertension
    • • Cardiac failure
    • • Paradoxical embolization - thrombus crossing over; right atrial clot going to systemic circulation instead of pulmonary
  29. VSD
    • Most common congenital heart lesion
    • If small may be asymptomatic and close spontaneously
    • If large, generally presents from birth
    • Membranous VSD and Muscular VSD (towards the bottom of the heart)
  30. AV canals
    • Endocardial cushion defect
    • A combination of ASD and VSD
    • One giant AV valve, not normal
    • Most common in trisomy 21, down syndrome
  31. Patent Ductus Arteriosus
    • In fetus, blood goes from pulmonary artery to aorta, bypassing the lungs
    • Should close off and become a fibrous band soon after birth
    • If stays open after birth, since the systemic pressure is higher, the flow goes from aorta to pulmonary, overloading the lungs, causing pulmonary hypertension.
    • Long term risk of CHF (small channel)
  32. Cyanotic shunt
    • Deoxygenated blood from right bypasses lungs, goes to left, hence early cyanosis
    • •Tetralogy of Fallot
    • •Transposition of the great vessels
    • •Truncus arteriosus
  33. Tetralogy of Fallot
    • Right ventricular outlet obstruction (subpulmonic stenosis)
    • Ventricular septal defect
    • Right ventricular hypertrophy
    • Big overriding aorta - due to ventricular hypertrophy
  34. Transposition of the great vessels
    • Two closed systems.
    • Need communication to survive - ASD, VSD, PDA
  35. Truncus arteriosus
    • One vessel coming off the heart, different patterns
    • Always accompanied by VSD
  36. Obstruction to flow
    • Abnormal narrowing of chambers, valves or blood vessels.
    • - Coarctation of aorta - Higher association with turner’s syndrome, 45 XO
    • - Pulmonary stenosis or atresia
    • - Aortic stenosis or atresia
  37. Obstruction to flow
    • Early life - Depending on severity of obstruction and associated cardiac lesions, patients may present with congestive heart failure, severe acidosis, or poor perfusion to the lower body.
    • Beyond infancy - usually asymptomatic. may present with hypertension, headache, nosebleed, leg cramps, muscle weakness, cold feet, or neurological changes. Also differential of pulses - Collaterals
  38. Blood vessels
    • All vessels except capillaries share a three-layered architecture, inner to outer:
    • - Endothelium lined intima
    • - Surrounding smooth muscle media
    • - Supportive adventitia - some capillaries
    • Composition of a vessel (smooth muscle cell and matrix content) vary according to hemodynamic demands (e.g., pressure, pulsatility) and functional requirements.
    • Composition influences the nature and consequences of pathologic injuries.
  39. Response of Vascular Wall Cells to Injury
    • All vessels are lined by endothelium
    • Endothelial cells in specific vascular beds have special features that allow for tissue-specific functions (e.g., fenestrated endothelial cells in renal glomeruli).
    • Injury (of almost any type) to the vessel wall results in a stereotyped healing response involving smooth muscle cell proliferation, extracellular matrix deposition, and intimal expansion.
    • Excessive thickening of the intima may result in luminal stenosis and vascular obstruction.
  40. Aneurysms
    • A dilatation
    • Localized abnormal dilatation of vessel or heart
    • May be saccular (outpouching) or fusiform (pointy) in shape
    • May be after trauma, congenital (eg berry aneurysm), infection (eg syphilis, mycotic), or relating to systemic diseases
  41. Berry Aneurysm
    • Intracranial saccular aneurysm
    • Develop at branch points of Circle of Willis
    • If rupture
    • - Most common cause of significant subarachnoid hemorrhage
    • - 25-50% mortality
    • - SEVERE SUDDEN headache
  42. The most common aneurysm are the aortic aneurysm, below the renal arteries.
  43. Clinical effects
    • Compress nerves, bones, viscera
    • Rupture - massive hemorrhage, fatal
    • Obstruct renal arteries
    • Thromboembolism to leg arteries
  44. False aneurysm
    • Hematoma covered by extravascular connective tissue, extravasation of blood.
    • More likely to burst than other types of aneurysm.
  45. Dissection
    tear in intima + extravasation of blood
  46. Abdominal Aortic Aneurysm - Risk Factors
    • Hypertension
    • Connective tissue abnormality (eg Marfan)
    • Atherosclerosis - weakening the vessel
    • Cystic medial degeneration (sometimes w/ Marfan, sometimes independent; w/ snapped elastic fibers)
  47. Abdominal Aortic Aneurysm - Outcomes
    • Rupture into peritoneal cavity or retroperitoneum
    • Obstruction w/ ischemia - usually w/ smaller vessels
    • Embolism of atheroma or mural thrombus - Stroke, loss of limb possible
    • Impingement on adjacent structure, eg ureter or vertebra
    • Abdominal “tumor”
  48. Outcomes of Aortic Dissection
    • AD can occur de novo or as consequence of aneurysm
    • Creation of a false channel within the muscular wall of the aorta. May not have aneurysmal dilatation
    • Expanding hematoma
    • Often starts near ascending aorta, near valve
    • Often ruptures outwards w/ catastrophic hemorrhage
    • Ripping or tearing chest pain as lesion extends
    • Can develop hemopericardium with cardiac tamponade
    • Can rupture inwards (“double barrel aorta”, “chronic dissection”)
  49. Vasculitis Syndromes (vasculitides)
    • Inflammation of vessel walls
    • Variety of causes
    • Most common:
    • • Direct injury to vessels by infectious organisms
    • • Immune-related inflammation
  50. Immune-related vasculitis - mechanisms
    • Immune complex formation with damage
    • Anti-neutrophil cytoplasmic autoantibodies (ANCAs) directed against enzymes in neutrophil granules
    • - p-ANCA against myeloperoxidase (p=perinuclear)
    • - c-ANCA against proteinase (c=cytoplasmic)
    • Antiendothelial cell antibodies
    • Autoreactive T-cells
  51. Large vessel vasculitis
    • Giant cell arteritis
    • Takayasu arteritis
  52. Giant Cell (Temporal) Arteritis
    • Most common vasculitis syndrome
    • Cause unknown, possibly a T cell mediated immune response to an unknown antigen in vessel wall
    • Genetic. Increased in HLA-DR4 branches of the carotid, esp. temporal & opthalmic
    • Destructive granulomatous inflammation
    • of the vessel wall
    • CD4+ T cells
    • Fragmentation of internal elastic lamina
    • Usually giant cells
    • Inflammation -> intimal thickening -> stenosis +/- thrombosis
    • Classic female >50 w/ severe headache and radiating facial pain
    • 50% ocular sx due to involvement of opthalmic artery. Treat early to prevent blindness
    • About 50% w/ flu-like syndrome + joint stiffness: polymyalgia rheumatica
  53. Takayasu’s Arteritis
    • Granulomatous inflammation of large arteries branching from aortic arch
    • Luminal occlusion
    • Blindness, neurological impairment, undetectable upper extremity pulses
    • Young females
  54. Medium-sized vessel vasculitis
    • • Polyarteritis nodosa (PAN)
    • • Kawasaki disease
    • • Thromboangiitis obliterans (Buerger disease)
  55. PAN
    • Segmental necrotizing inflammation of vessels, most often of kidney, heart, liver.
    • Lungs spared.
    • • Acute inflammation, necrosis and thickening of vessels
    • • Can get aneurysms, ruptures
    • • Young adults
    • • Fever, ischemia of involved organs.
    • • Can die of acute renal failure
  56. Kawasaki disease (mucocutaneous lymph node disease)
    • • Involves coronary arteries
    • • Usually children under 4
    • • Systemic symptoms, fever, eye and mouth mucous membrane redness/erosion, red palms, soles, skin rash, cervical adenopathy
    • Coronary aneurysms (beading) and death possible
  57. Buerger disease (Thromboangiitis obliterans)
    • • Acute & chronic inflammation of arm and leg vessels
    • • Can spread from arteries to veins, nerves
    • • Big association w/ cigarettes
    • Ulcers/gangrene of extremities
  58. Small vessel vasculitis
    • • Wegner’s granulomatosis
    • • Churg Strauss syndrome (allergic granulomatous angiitis)
    • • Leukocytoclastic vasculitis
  59. Wegener’s Granulomatosis
    • small to medium-sized vessel disease
    • Cause unknown, c-ANCA in 95% of patients
    • Classic Triad:
    • • Necrotizing/granulomatous inflammation of small to medium sized vessels
    • • Necrotizing granulomas of upper/lower respiratory tract including ear, sinuses, oral cavity
    • • Necrotizing glomerulonephritis
    • Male > Female
    • 5th decade
    • Persistent pneumonitis w/ bilat cavitary and nodular infiltrates
    • Chronic sinusitis, mucosal ulcerations of nasopharynx, renal disease
    • Variety of other sx.
    • Strawberry Gingiva
  60. Churg-Strauss Syndrome
    • Allergic angiitis and granulomatosis.
    • Nose, sinuses, lungs, heart, intestine and nerves.
    • May also affect the kidneys, muscles, or joints.
    • Associated with asthma and eosinophils.
  61. Leukocytoclastic vasculitis
    Inflammation of the small vessels of the skin
  62. Vasculitis associated w/systemic disorder - Henoch Schönlein purpura
    • • Purpura of extensor surfaces of arms, legs, buttocks
    • • Abdominal pain, vomitting, intestinal bleeding
    • • Nonmigratory arthralgia
    • • Renal abnormalities
    • • Necrotizing vasculitis of small dermal vessels
  63. Vasculitis in summary
    • Inflammation of vessel walls.
    • Frequently associated with systemic manifestations (including fever, malaise, myalgias, and arthralgias) and organ dysfunction that depends on the pattern of vascular involvement.
    • Can result from infections; more commonly has immunologic basis, including immune complex deposition, formation of antineutrophil antibodies (ANCA), or T cell responses to vascular wall antigens.
    • Different forms tend to specifically affect vessels of a particular caliber and location, and the clinical manifestations depend on the pattern of vessel involvement.
  64. Reynaud’s phenomenon
    • Exaggerated vasoconstriction of arteries and arterioles in the extremities, particularly the fingers and toes, but also occasionally the nose, earlobes, or lips.
    • Primary exaggerated central and local vasomotor responses to cold or emotion; it affects 3% to 5% of the general population and has a predilection for young women.
  65. Varicose Veins
    • Abnormally dilated, elongated, tortuous veins.
    • Prolonged increased intraluminal pressure predisposes, eg. long periods of standing, pregnancy.
    • Can occur anywhere, 3 important clinical sites:
    • - superficial veins of legs;
    • - anorectal venous plexus;
    • - esophagus.
  66. Varicose veins of legs
    • Upper & lower superficial veins.
    • Most common location.
    • Increase w/age, obesity, female, pregnancy.
    • Venous dilatation, valve incompetence, stasis, congestion/edema, thrombosis (not the one in the deep vein), stasis dermatitis and varicose ulcers.
    • Resultant impaired circulation leads to risk of infection and impaired wound healing.
  67. Anorectal venous plexus
    • A K A hemorrhoids.
    • Type depends on the place of origin relative to the dentate line.
    • Above - internal hemorrhoids.
    • Below - external hemorrhoids.
    • Above and below - mixed hemorrhoids.
  68. Esophageal varices
    • A complication of portal hypertension in cirrhosis.
    • Rupture may cause fatal hematemesis.
  69. Caput Medusae
    Abdominal varicose capillaries.
  70. Thrombophlebitis & Phlebothrombosis.
    • 90% deep leg veins;
    • Risk factors include cardiac failure, neoplasia (secretion induce clotting; paraneoplastic syndrome), pregnancy, obesity, postoperative status, prolonged bedrest or immobilization, genetic hypercoagulability;
    • Trousseau sign - migratory thrombophlebitis as a paraneoplastic syndrome, esp with pancreas, colon, lung cancers.
  71. Signs and Symptoms of deep vein thrombosis.
    • Early, none;
    • Edema, cyanosis, dilated superficial veins, heat, redness, tenderness, swelling, pain, possible;
    • Homan sign - pain on forced dorsiflexion of foot.
    • Phlegmasia alba dolens - iliofemoral thrombosis with pregnancy;
    • Risk of pulmonary embolism.
  72. Superior vena cava syndrome;
    • Neoplasms that compress or invade the superior vena cava;
    • Bronchogenic carcinoma, mediastinal lymphoma, or other space-occupying lesions in the mediastinum such as aortic aneurysms.
    • Marked dilation of the veins of the head, neck, and arms with cyanosis.
    • Pulmonary vessels can also be compressed, inducing respiratory distress.
  73. Lymphangitis;
    • Acute inflammation elicited by the spread of bacterial infections into lymphatics; Group A β-hemolytic streptococci is the most common agent, although can be any microbe.
    • Lymphatics are dilated and filled with an exudate of neutrophils and monocytes; the infiltrates can extend through the vessel wall, and in severe cases, can produce cellulitis or focal abscesses.
    • Red, painful subcutaneous streaks (the inflamed lymphatics), and painful enlargement of the draining lymph nodes (lymphadenitis).
    • If bacteria are not successfully contained within the lymph nodes, subsequent escape into the venous circulation can result in bacteremia or sepsis.
  74. Lymphedema;
    • Primary lymphedema - isolated congenital defect (simple congenital lymphedema) or familial Milroy disease (heredofamilial congenital lymphedema), which results in lymphatic agenesis or hypoplasia.
    • Secondary or obstructive lymphedema - blockage of lymphatic by tumors, node-removing surgery, radiation, filariasis (Elephantiasis), postinflammatory.
    • Increases hydrostatic pressure in distal lymphatics and causes increased interstitial fluid accumulation.
    • Peau d'orange (orange peel) look skin - Persistent edema and subsequent deposition of interstitial connective tissue thus affect the overlying skin, typically the skin overlying breast cancers after tumor cells clog the draining lymphatics.
    • Ulcers - may develop due to inadequate tissue perfusion.
    • Rupture of dilated lymphatics (e.g., secondary to obstruction from a tumor) leads to milky accumulations of lymph, eg. chylous ascites (abdomen), chylothorax, and chylopericardium.
  75. Vascular neoplasms can be endothelial-derived (e.g., hemangioma, lymphangioma, angiosarcoma) or can arise from cells that support or surround blood vessels (e.g., glomus tumor, hemangiopericytoma).
  76. Vascular tumor summary;
    • Vascular ectasias are not neoplasms, but rather dilations of existing vessels.
    • Vessel neoplasms can derive from either blood vessels or lymphatics, and can be composed of endothelial cells (hemangioma, lymphangioma, angiosarcoma) or other components of vascular wall cells.
    • Mostly benign (e.g., hemangiomas), some intermediate, locally aggressive (e.g., Kaposi sarcoma), and others are highly malignant (e.g., angiosarcoma).
    • Benign tumors typically form obvious vascular channels lined by normal-appearing endothelial cells.
    • Malignant tumors are more often solid and cellular, exhibit cytologic atypia, and lack well-defined vessels.
  77. Vascular Tumors and Tumor-Like Conditions - Benign Developmental and Acquired Conditions;
    • Hemangioma;
    • - Capillary hemangioma ;
    • - Cavernous hemangioma (large);
    • - Pyogenic granuloma (in mouth);
    • Lymphangioma ;
    • - Simple (capillary) lymphangioma;
    • - Cavernous lymphangioma (cystic hygroma);
    • Glomus tumor;
    • Vascular ectasias;
    • - Nevus flammeus ;
    • - Spider telangiectasia (arterial spider) ;
    • - Hereditary hemorrhagic telangiectasis (Osler-Weber-Rendu disease);
    • Reactive vascular proliferations;
    • Bacillary angiomatosis.
  78. Intermediate Grade Neoplasms;
    • Kaposi sarcoma;
    • Hemangioendothelioma.
  79. Malignant Neoplasms;
    • Angiosarcoma;
    • Hemangiopericytoma.
  80. Hemangiomas;
    • Capillary - congenital ones can regress spontaneously;
    • Cavernous;
    • Pyogenic granulomas - capillary hemangiomas; rapidly growing, red, pedunculated, lesions on skin, gingival, or oral mucosa. They bleed easily and are often ulcerated.
  81. Lymphangiomas;
    • Capillary;
    • Cavernous lymphangiomas (cystic hygromas)
    • - typically in the neck (common in Turner syndrome) or axilla of children; more rarely in the retroperitoneum.
    • - occasionally enormous (up to 15 cm in diameter) and may fill the axilla or produce gross deformities about the neck (disfiguring webbed neck in Turner).
    • Margins are indistinct and unencapsulated even though not malignant, making definitive resection difficult.
  82. Glomus tumor;
    • Painful;
    • Arising from modified smooth muscle cells of the glomus bodies, arteriovenous structures involved in thermoregulation.
    • Distal portion of the digits, especially under the fingernails.
    • Excision is curative.
  83. Nevus flammeus
    • “birthmark”, the most common form of vascular ectasias; light pink to deep purple, flat, head or neck, composed of dilated vessels. Most ultimately regress spontaneously.
    • "Port wine stain" - a special form. Tends to grow during childhood, thickens the skin surface, and does not fade with time.
  84. Bacillary angiomatosis;
    • Vascular proliferation in immunocompromised hosts caused by opportunistic gram-negative bacilli of the Bartonella family.
    • Lesions can involve the skin, bone, brain, and other organs.
    • Two species are implicated:
    • - B. henselae - lives on domestic cat; causes cat-scratch disease (a necrotizing granulomatous disorder of lymph nodes) in immunocompetent hosts.
    • - B. Quintana - transmitted by human body lice; the cause of “trench fever” in World War I.
  85. Morphology Bacillary angiomatosis.
    • Characteristic cutaneous lesion.
    • Acute neutrophilic inflammation and vascular (capillary) proliferation. Silver stain demonstrates clusters of tangled bacilli.
  86. Kaposi sarcoma (KS);
    • Intermediate grade vascular neoplasm caused by human herpes virus 8, highly associated with AIDS.
    • Classic KS - found in older men of Mediterranean, Middle Eastern, or Eastern European descent (especially Ashkenazic Jews); uncommon in U.S. It can be associated with malignancy or altered immunity, but not AIDS.
    • Endemic African KS - HIV-negative individuals.
    • Transplant-associated KS.
    • AIDS-associated (epidemic) KS is an AIDS-defining illness, and worldwide, it represents the most common HIV-related malignancy.
    • Show spindle cells.
  87. Epithelioid hemangioendothelioma;
    • Adults;
    • Around medium- and large-sized veins.
    • Extremely variable clinical behavior
    • Mostly cured by excision, but up to 40% recur, 20% to 30% eventually metastasize, and perhaps 15% of patients die of their tumor.
  88. Angiosarcoma;
    • Older adults;
    • May occur at any site, but mostly skin, soft tissue, breast, and liver.
    • Hepatic angiosarcoma - associated with carcinogenic exposures, including arsenic (e.g., in pesticides), Thorotrast (a radioactive contrast agent formerly used for radiologic imaging), and polyvinyl chloride (a widely used plastic); Long latency.
    • Can arise in the setting of lymphedema, classically in the ipsilateral upper extremity several years after radical mastectomy (with lymph node resection); the tumor presumably arises from lymphatic vessels (lymphangiosarcoma).
    • Can be induced by radiation.
    • Locally invasive and can readily metastasize; 5-year survival rates approach 30%.
    • Histology - Atypia of endothelial cells; hyperchromatic.

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Author:
neopho
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324883
Filename:
Systemic Pathology - Cardiovascular - Heller
Updated:
2016-11-26 21:07:24
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Systemic Pathology - Cardiovascular - Heller
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