Parcialito 11 - Cardiovascular Flashcards
In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.
Large or elastic arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
In these arteries, tunica media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. Examples are the coronaries and renal arteries.
Medium-sized or muscular arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These are the principal control points for regulation of physiologic resistance to blood flow.
Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.
Capillaries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Diameter of an RBC.
7-8 µm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.
Lymphatics(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are small spherical dilatations, typically in the circle of Willis.
Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.
Arteriovenous fistulas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Focal, irregular thickening of the walls of medium and large muscular arteries. Segments of the vessel wall are focally thickened by combination of irregular medial and intimal hyperplasia and fibrosis, causing luminal stenosis.
Fibromuscular dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.
Arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by calcific deposits in muscular arteries, typical in persons older than 50 yrs old. The radiographically visible, palpable calcifications do not encroach on the vessel lumen, and are not clinically significant.
Mockenberg medial calcific sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by intimal lesions called atheromas that protrude into vascular lumina.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Three principal components of an atheromatous plaque.
- Cells (SM cells, macrophages, T cells)
- Extracellular matrix (collagen, elastic fibers, proteoglycans)’
- Intracellular and extracellular lipid, Fibrous cap, central lipid core, neovascularization
(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Non-modifiable risk factors for atherosclerosis. (4)
Increasing age
Male gender
Family history
Genetic abnormalities
(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
Arrange in descending order, based on which blood vessel is most extensively involved in development of atherosclerosis.Popliteal arteries, internal carotid arteries, circle of Willis, coronaries, abdominal aorta
Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 350
Fate of an atheromatous plaque wherein the luminal surface exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
Rupture, ulceration or erosion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.
Atheroembolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atherosclerotic plaque due to increased pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, leading to weakness of the vessel wall.
Aneurysm formation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Most common cause of hypertension.
Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355
This vascular lesion consists of a homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. A major morphologic characteristic in benign nephrosclerosis.
Hyaline arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
Characteristic of malignant hypertension, associated with “onion-skin” concentric, laminated, thickening of the walls of arterioles with luminal narrowing. These laminations consist of smooth muscle cells and thickened duplicated basement membrane.
Hyperplastic arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.
True aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.
False aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.
Arterial dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which are spherical outpouchings, involving only a portion of the vessel wall, varying in size from 5-20cm in diameter and often contain thrombi.
Saccular aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which involve diffuse, circumferential dilation of a long vascular segment, varies in diameter and length, and can involve extensive portions of the aortic arch, abdominal aorta,and iliacs.
Fusiform aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Two most important causes of aortic aneurysms.
Atherosclerosis
Cystic medial degeneration of the arterial media
(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Infection of a major artery that causes weakness to its wall.
Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
This disease can more commonly affects men >50 years old. Lesion usually positioned below the renal arteries and above the aortic bifurcation. Can be saccular or fusiform.
Abdominal aortic aneurysm (AAA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.
Inflammatory AAA(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 358
Atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a Salmonella gastroenteritis. Suppuration further destroys the media, potentiating rapid dilation and rupture.
Mycotic abdominal aortic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Small blood vessels and vasa vasorum show luminal narrowing and obliteration (obliterative endarteritis), scarring of the vessel wall and a dense surrounding rim of lymphocytes and plasma cells that may extend into the media. Characteristic of the tertiary stage of syphilis.
Syphilitic aortitis(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 359
Most common point of origin of an aortic dissection.
Ascending aorta, 10 cms from the aortic valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 360
Most frequent pre-existing histologically detectable lesion in aortic dissection, characterized by elastic tissue fragmentation and separation of the elastic and smooth muscle cell elements of the media by cystic spaces filled with amorphous proteoglycan-rich extracellular matrix.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.
Type A dissections (Stanford)
Type I DeBakey - ascending and descending aorta
Type II DeBakey - ascending aorta only
(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.
Type B dissection / type III DeBakey(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.
Giant cell (Temporal) arteritis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 363
Granulomatous inflammation usually occuring in patients younger than 50 years old. Classically involves the aortic arch, with intimal hyperplasia and irregular thickening of the vessel wall. Origin of great vessels are obliterated causing weakness of peripheral pulses.
Takayasu arteritis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.
Age of patient (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
In this disease, affected blood vessels develop nodular intimal thickening, granulomatous inflammation within the inner media centered on the internal elastic membrane, and fragmentation of the internal elastic lamina. Typically involves temporal and ophthalmic arteries.
Giant - cell/Temporal arteritis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
A systemic vasculitis causing transmural necrotizing inflammation of small to medium sized vessels, with mixed infiltvrate of neutrophils, eosinophils, and mononuclear cells, frequently accompanied by fibrinoid necrosis.Typically involves renal arteries but spares pulmonary vessels.
Polyarteritis Nodosa (PAN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
Arteritis associated with mucocutaneous lymph node syndrome, which usually occurs in children. Coronary arteries can be involved with aneurysm formation or thrombosis. Fibrinoid necrosis usually less prominent.
Kawasaki disease (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 366
Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including cresencteric glomerulonephritis. Associated with c-ANCA.
Wegener granulomatosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367
A necrotizing vasculitis that generally affects capillaries, arterioles and venules, with few or no immune deposits. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with p-ANCA.
Microscopic polyangiitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Eosinophil-rich and granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with p-ANCA.
Churg-Strauss syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Characterized by sharply segmental avute and chronic vasculitis of medium sized and small arteries, predominantly of the extremities. There is acute and chronic inflammation accompanied by luminal thrombosis, containing microabscess composed of neutrophils surrounded by granulomatous inflammation. Strong relationship with cigarette smoking.
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Results from an exaggerated vasoconstriction of digital arteries and arterioles, inducing paroxysmal pallor or cyanosis of the digits of the hands and feet.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects an exaggeration of central and local vasomotor responses to cold or emotion. Structural changes in the arterial walls are absent except late in course when intimal thickening can appear.
Primary Raynaud phenomenon (Raynaud disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects vascular insufficiency of the extremities in the context of arterial disease caused by other entities including SLE, Buerger disease, or atherosclerosis.
Secondary Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Abnormally dilated, tortous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. Veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis. Focal thrombosis and venous valve deformities are common.
Varicose veins (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Most common blood vessels involved in development of varicose veins.
Superficial veins of the upper and lower leg(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Three sites of varices produced in the presence of portal hypertension.
GEJ (Esophageal varices)
Rectum (Hemorrhoids)
Periumbillical veins (Caput medusae)
(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Common and serious complication of of deep vein thrombosis (DVT).
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
The acute inflammation elicited when bacterial infections spread into and through the lymphatics.
Lymphangitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
These are bright red to blue lesions, that vary from a few millimeters to several centimeters in diameter. Unencapsulated aggregates of closely packed, thin-walled capillaries, usually blood-filled and lined by flattened endothelium. Vessels are separated by scant connective tissue stroma.
Capillary hemangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 372
Appears as red-blue, soft, spongy masses 1-2 cm in diameter, which can affect large subcutaneous areas of the face, extremities, and othe body regions. Mass is sharply defined but not encapsulated, composed of large, cavernous, blood-filled spaces.
Cavernous hemangioma(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 372
This form of capillar hemangioma is a rapidly growing peduncular red nodule on the skin, gingival, or oral mucosa, bleeds easily and is often ulcerated.
Pyogenic granuloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
These are round, slightly elevated, red-blue firm nodules, less than 1 cm diameter that can resemble a minute focus of hemorrhage UNDER THE NAIL. Histologically, these are aggregates, nests, and masses of tumor cells intimately associated with branching vascular channels.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
A specialized arteriovenous structure involved in thermoregulation.
Glomus body(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
This lesion is the ordinary “birthmark” and is the most common form of ectasia. Characteristically a flat lesion on the head or neck, ranging in color from light pink to deep purple.
Nevus flammeus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
This non-neoplastic vascular lesion grossly resembles a spider. There is radial, often pulsatile array of dilated subcutaneous arteries or arterioles about a central core, that blanches when pressure is applied to its center.
Spider telangiectasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
An opportunistic infection in immunocompromised persons that manifest as vascular proliferations involving skin, bone, brain and other organs. Characterized grossly by red papules and nodules, or rounded subcutaneous masses. Histologically, there is capillary proliferation with prominent epitheloid EC’s showing nuclear atypia and mitoses. Lesions contain stromal neutrophils, nuclear dust nd purplish granular material.
Bacillary angiomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
Common in patients with AIDS, caused by HHV 8, causing skin lesions ranging from patches, plaques to nodules.
Kaposi sarcoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
These are malignant endothelial neoplasms, with varying histology from plump, anaplastic but recognizable endothelial cells producing vascular channels to widely undifferentiated tumors having solid, spindle cell appearance and producing nondefinite blood vessels.
Angiosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 376
Form of hypertension characterized by systolic pressure more than 200 mmHg or diastolic pressure more than 120 mmHg, renal failure, and retinal hemorrhages and exudates.
Malignant Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 488
The most important independent risk factor for atherosclerosis.
Family history (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 492.
The initial event in the pathogenesis of atherosclerosis
Endothelial injury and dysfunction. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
The major lipoprotein involved in the pathogenesis of atherosclerosis.
LDL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
2 most important causes of endothelial dysfunction
Hemodynamic disturbances and hypercholesterolemia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
The key processes in atherosclerosis
Intimal thickening and lipid accumulation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 496
The major structural component of fibrous cap in an atheromatous plaque
Collagen (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 500
Medial ischemia leading to degenerative changes of aorta, leading to scarring, loss of elastic fibers, inadequate extracellular matrix synthesis, and production of amorphous ground substance. This can be seen in Marfan syndrome and scurvy.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 502
Most common etiology associated with ascending aortic aneurysm
Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 502
A 70 y/o male, hypertensive, present with sudden severe abdominal pain. On physical examination, there is a presence of pulsatile abdominal mass. The most likely diagnosis is:
Abdominal aortic aneurysm(TOPNOTCH)
The most frequent preexisting histologically detectable lesion in aortic dissection
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 504
Presents with sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward.
Aortic dissection(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 505
Most common cause of death in aortic dissection.
Rupture of the dissection into the pericardial, pleural or peririthoneal cavities.(TOPNOTCH) Robbins Basica Pathology, 9th ed., p. 505
A 38 y/o male presents with severe headache and diplopia associated with fever and fatigue. Area along the course of the superficial temporal artery was painful to palpation. Biopsy done revealed intimal thickening of the artery, granulomatous inflmmation of the internal elastic lamina with infiltrate of T cells and macrophages. What is the most likely diagnosis?
Giant cell arteritis (TOPNOTCH)
Patient initially present with fatigue, weight loss and fever and then reduced blood pressure and weak pulses in the carotids and upper extremities, ocular disturbances and neurologic deficits. The most likely diagnosis is:
Takayasu arteritis(TOPNOTCH)
Most common involved blood vessel in Takayasu arteritis.
Aortic arch (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 509
This disease presents with rapidly accelerating hypertension, abdominal pain, bloody stool, myalgia and peripheral neuritis. The most likely diagnosi:
Polyarteritis nodosa(TOPNOTCH)
A 4 y/o female presented with fever and maculopapular rash on her trunk and extremities. This is associated with conjunctival erythema, edema of the hands and feet, and cervical lymph node enlargement. The patient is at risk for what type of blood vessel involvement?
Coronary artery aneurysm which may lead to acute MI. (Case of Kawasaki Disease) (TOPNOTCH)
Patient presents with asthma, allergic rhinitis, palpable purpura, GI bleeding, renal disease, and cardiomyopathy. Histologic findings showed vascular granulomata and hypereosinophilia. The most likely diagnosis is:
Churg-Strauss syndrome(TOPNOTCH)
It presents as a clinical triad of recurrent oral apthous ulcers, genital ulcers, and uveitis.
Behcet Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 511
This disease presents with persistent pneumonitis with bilateral nodular infiltrates, chronic sinusitis, mucosal ulceration of the nasopharynx, and renal disease. Histologic findings of upper respiratory tract lesion showed mucosal granuloma with geographic patterns of central necrosis and vasculitis. The most likely diagnosis:
Granulomatosis with polyangitis/Wegener granulomatosis(TOPNOTCH)
A 30 y/o male, smoker, presents with severe leg pain aggravated by exercise and relieved on rest. It further progressed to extremity ulcerations. What is the most likely diagnosis?
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)
Most imprortant risk factor for DVT
Prolonged immobiliztion resulting in venous stasis. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 514
A 50 y/o male, diagnosed with lung cancer, presented with edema and cyanosis of the head , neck, and arms with cyanosis. This is a case of:
Superior vena cava syndrome (TOPNOTCH)
The most common etiologic agent in lymphangitis.
Group A beta hemolyitc streptococcus. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 515
An autosomal dominant disorder caused by mutations in genes that encode components of TGF-B signaling pathway. Presents with telengiectasia that are widely distributed over the skin and mucus membranes.
Hereditary hemorrhagic telengiectasia/Osler-Weber-Rendu disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 516
Most common type of hemangioma
Capillary hemangioma(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 516
Painful tumors arising from modified smooth muscle cells of arteriovenous structure, most commonly found in the distal portion of the digits.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 517
A 13 year old male dies of a stray bullet to the head on New Year’s Eve. At autopsy, there is a flat yellowish streak seen on the intimal surface of his abdominal aorta, near the bifurcation of the renal arteries. This streak (A) causes minor disturbance in blood flow (B)is expected in his age group (C) is composed of hemosiderin-filled foam cells (D) would have certainly evolved into an atheromatous plaque if he lived to old age
expected in his age group (“fatty streak” (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 348-349)
Early atherosclerotic lesions are usually focal, patchy, and eccentric because (A) there are differences in the vascular hemodynamics at various points (B) the expression of LDL receptors along the blood vessels is varied (C) concentrations of macrophage-activating cytokines are different along blood vessels (D) certain endothelial cells are more sensitive to toxins and hyperglycemia than others
there are differences in vascular hemodynamics at various points (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
A 65 year old diabetic female with poor glycemic control and a 5 year history of intermittent chest pain develops pallor, shortness of breath and diaphoresis. She dies 16 hours later. At autopsy, the left ventricular wall is thickened, with dark mottling of the anterior portion, along with the septum and apex. Which of the following describes the likely histology of her left anterior descending artery? (A) an eccentric atheromatous plaque with a fibrous cap (B) a ruptured fibrous cap with calcifications in the lumen of the vessel (C) a ruptured fibrous cap with thrombus formation (D) complete occlusion of the original lumen by fibrous tissue, with neovascularization in the periphery
a ruptured fibrous cap with thrombus formation (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.351
What is the most common cause of aneurysms?
atherosclerosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
What is the most common site of atherosclerotic aneurysms?
abdominal aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
A 75 year old male with heart failure symptoms of 10 years dies. At autopsy, his aortic trunk is dilated, with fibrous scars and wrinkling of the intima. The aortic valve is also dilated, and the left ventricle is markedly enlarged. Microscopic examination of the aorta shows narrowed or obliterated vasa vasorum to be narrowed, with a dense rim of lymphocytes and plasma cells, some extending into the media. Which of the following can suggest the etiology of the patient’s findings? (A) family history of diabetes (B) chronic alcohol intake (C) history of sexually transmitted infection (D) occupational exposure to benzene
history of sexually transmitted infection (tertiary/cardiovascular syphilis) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.359, 703
A 30 year old female with 3 year history of fever, weight loss and fatigue presents with right eye blindness. PE showed weak pulses in the upper extremities. Which of the following suggests that she has Takayasu arteritis, rather than temporal arteritis? (A) age (B) constitutional symptoms (C) giant cells in the large blood vessels (D) giant cells in the medium blood vessels
age (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364-365
Classic polyarteritis nodosa affects small to medium sized vessels most commonly in which organ? (A) kidneys (B) heart (C) liver (D) GI tract
kidneys (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
A 2 year old boy presents with erythema of the conjunctiva, oral mucosa, palms and soles, with focal erosions. Palpation shows enlarged cervical lymph nodes. He suddenly dies a few hours after ER admission. Autopsy showed marked mononuclear infiltration of his left anterior descending artery, with fibrinoid necrosis and lumen occlusion. What could have prevented this fatal sequela? (A) low dose corticosteroids (B) Hepatitis B vaccine (C) Beta-lactam and aminoglycoside combination (D) intravenous immunoglobulin
intravenous immunoglobulin (Kawasaki disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.366
A 42 year old man with 2 weeks of epistaxis undergoes an intranasal biopsy, which showed chronic granulomatous inflammation with giant cells. Xray showed cavitary lung lesions. He is treated with anti-Koch’s for 6 months, but the epistaxis recurred. He also developed hematuria. Which of the following can help support a diagnosis of Wegener’s granulomatosis, rather than TB? (A) positive P-ANCA (B) positive C-ANCA (C) urinalysis with RBC morphology (D) biopsy of the lung lesion
positive C-ANCA (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367-368
A 27 year old Israeli expat presents with intermittent pain and pallor of the right index and middle fingers, precipitated by smoking and cold temperature. He reports symptomatic relief whenever he stops smoking. What is expected in the arteries of the involved fingers? (A) thrombus with neutrophil aggregates and necrosis (B) histiocytes and giant cells (C) ruptured fibrous cap and underlying foamy cells (D) eosinophils and lymphocytes in the media and intima
thrombus with neutrophil aggregates and necrosis (Buerger disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.368
A 21 year old G1P0, 24 weeks AOG, has a reddish 1.0 cm diameter nodule on her left lower gum. She reports that the nodule appeared at 1 month of pregnancy. A biopsy showed shows capillaries with an acute and chronic inflammatory infiltrate and stromal edema. There is no pleomorphism, necrosis, or atypical mitosis. This nodule (A) can be found in 20% of pregnant women (B) is malignant (C) may spontaneously regress or fibrose after pregnancy (D) is metastatic from an ovarian primary
may spontaneously regress or fibrose after pregnancy (granuloma gravidarum/pregnancy tumor/pyogenic granuloma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.373
A 3 year old female with a large “port wine stain” on the right side of her face has occasional seizures. Further examination showed mental developmental delay. She may also have (A) more extensive vascular malformations (B) multiple colonic polyps (C) color blindness (D) alpha thalassemia
more extensive vascular malformations (Sturge-Weber syndrome) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.374
A 38 year old HIV-positive man has multiple reddish-purple plaques and nodules on his arms and legs. He has never been on antiretroviral therapy. Biopsy of one of the nodules showed sheets of plump spindle cells encompassing small vessels and slit-like spaces, with focal hemorrhage, hemosiderin deposits, lymphocytes, and macrophages. Mitotic figures are common. This neoplasm has been shown to be infected with (A) HPV 16 (B) HHV 8 (C) Hepatitic C (D) HPV 18
HHV8 (Kaposi Sarcoma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
The morphologic and clinical effects of this condition primarily result from progressive damming of blood within the pulmonary circulation. The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-aleolar edema. Hemosiderin-laden macrophages are present.
Left sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hemosiderin laden macrophages are also called _______
Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is usually the earliest and most significant compaint of patients in Left sided HF.
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Most common cause of right sided HF.
Left sided HF(TOPNOTCH)
This is a particularly dramatic form of breathlessness, awakening patients from sleeo with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
The liver is increased in size and weight, a cut section reveals congested red centers of liver lobules surrounded bybpaler, sometimes fatty peripheral regions.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Right-sided HF produces a tense, enlarged spleen, achieving weights of 300-500 grams. Sinusoidal dilation present.
Congestive splenomegaly(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is a hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Most congenital heart disease arise from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These a typically smooth-walled defects near the foramen ovale, usually without associated cardiac abnormalities. Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy and dilation of the pulmonary artery.
Ostium secundum ASD(TOPNOTCH)
Reversal of blood flow through a prolonged (left-to-right shunt) due to pulmonary hypertension, yielding right-sided pressures that exceed those on the left side. This causes unoxygenated blood to go into circulation, causing cyanosis.
Eisenmenger syndrome (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These occur at the lowest part of the atrial septum and can extend to the mitral and tricuspid valves. Abnormalities of the AV Valves are usually present, forming a cleft in the anterior leaflet of the mitral valve or septal leaflet of the tricuspid valve.
Ostium primum ASD(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
In this condition, some of the oxygenated blood flowing from the left ventricle is shunted back to the lungs. Proximal pumonary arteries, left atrium and ventricle may become dilated.
Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
The most common cause of cyanotic congenital heart disease. Heart is large and “boot shaped” as a result of right ventricular hypertrophy.
Tetralogy of Fallot(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
Components of Tetralogy of Fallot.
Pulmonary valve stenosis
Overriding of aorta
Right ventricular hypertrophy
Ventricular septal defect
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa. Right ventricular hypertrophy becomes prominent, while the left ventricle becomes somewhat atrophic.
Transposition of the Great Arteries (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Characterized by tubular narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.
Preductal “infantile” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Aorta is sharply constricted by a ridge of tissue at or just distal to the ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.
Postductal “adult” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib “notching” on xray.
Postductal coarctation of the aorta (without a PDA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
70-75% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest?
90%(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
In this disease the left ventricle may exceed 2.0cm in thickness and the heart may weigh >500 grams. Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”), and increased interstitial fibrosis.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Pathognomonic sign for rheumatic fever,consisting of of a cental zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytes, ocassional plasma cells and plump, activated macrophages.
Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
These cells have abundant cytoplasm and central nuclei with chromatin arrayed in a slender, wavy ribbon (caterpillar cells) which can be found in all three layers of the heart in rheumatic fever. A component of Aschoff bodies.
Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Characterized by organization and subsequent scarring, as a sequelae of rheumatic fever. The mitral (or tricuspid) valve is involved, with leaflet thickening, commisural fission and shortening, thickening and fusiong of the chordae tendinae. Fibrous bridging across valvular commisures create “fishmouth” or “ buttonhole” deformity.
Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Most common valve involved in RHD.
Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405
Major components Jones Criteria for RF.
Carditis
Migratory polyarthritis
Subcutaneous nodules
Erythema marginatum
Syndenham chorea
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Minor components Jones criteria for RF
Fever
Arthralgia
Elevated acute phase reactants (e.g. CRP)
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
How many major and/or minor manifestations are needed to diagnose RF?
Remember: 2012
2 major 0 minor or
1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis of previously normal valves, the most common causative agent is S. aureus.
Acute bacterial endocarditis(TOPNOTCH)
Serious infection characterized by microbial invasion of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues. The heart valves are friable, bulky and potentially destructive.
Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.
Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Most consistent sign of infective endocarditis.
Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Characterized by deposition of sterile, non-inflammatory, nondestructive and small (1mm) masses of fibrin, platelets and other blood components on cardiac valves, along the line of closure of leaflets or cusps.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Sterile vegetations thatvcan develop on the valves of patients with SLE. These are small, granular, pinkish vegetations 1-4mm in diameter and can be located on the undersurface of AV valves, on the cords or endocardium.
Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
The lesions of this disease are distinctive, glistening white intimal plaquelike thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets seen in patients with carcinoid tumors. The lesions are composed of muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix.
Carcinoid heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
Cardiomyopathy which is characterized by progressive cardiac dilation and contractile dysfunction. The heart is characteristically enlarged and flabby, with dilation of all chambers,the ventricular thickness may be less than, equal to or greater than normal.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Characterized by myocardial hypertrophy, abnormal diastolic filling and ventricular outflow obstruction. The heart is thick-walled, heavy and hypercontracting. There is an assymetrical septal hypertrophy described as “banana-like”. Histologically, there is severe myocyte hypertrophy and disarray with interstitial fibrosis.
Hypertrophic cardiomyopathy (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
Mechanism of heart failure in hypertrophic cardiomyopathy.
Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
A common cause of sudden death in young athlethes.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
The ventricles are of approximately normal size or slightly enlarged, the cavities not dilated, and the myocardium is firm. Biatrial dilation is common. Microscopically, there is interstitial fibrosis, varying from minimal to patchy to extensive and diffuse.
Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Mechanism of heart failure in restrictive cardiomyopathy.
Diastolic dysfunction or impaired compliance (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Inflammation of the myocardium.
Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.
Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.
Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis characterized by widespread inflammatory infiltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.
Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.
Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Viruses which account for most cases of myocarditis.
Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Type of pericarditis found in patients with uremia or viral infection. The exudate imparts an irregular apperance to the pericardial surface (bread and butter pericarditis).
Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Normal amount of pericardial fluid in pericardial sac.
30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Serous pericardial effusion can be caused by _________
CHF (congestic Hearts Failure), hypoalbuminemia
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Chylous pericardial fluid can be caused by _______
Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.
Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
The most common tumor of the heart.
Metastatic tumor (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Most common primary tumor of the adult heart.
Myxoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms.
Myxoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most frequent primary tumor of the heart in infants and children. These are generally small gray-white myocardial masses composed of a mixed population of cells, the most characteristic of which are large, rounded or polygonal cells containing numerous glycogen-laden vacuoles separated by strands of cytoplasm, so-called spider cells.
Rhabdomyomas (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
Serosanguinous pericardial effusion can be caused by ________
Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most severe pulmonary changes in congestive heart failure
Accumulation of edema fluid in the alveolar spaces (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Morphologic finding/telltale signs of previous episodes of pulmonary edema
Hemosiderin-laden macrophages (Heart failure cells) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Most common underlying etiology of diastolic failure
Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Group of congenital heart disease characterized by increase pulmonary blood flow but are not initially associated with cyanosis
Left-to-right shunts (ASD, VSD, PDA) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
Most common genetic cause of congenital heart disease
Trisomy 21 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
A 24 y/o female complained of shortness of breath and orthopnea lasting several days. The patient reported having diagnosed since childhood as having “hole in the heart.” Physical exam revealed holosystolic murmur most audible in the left parasternal area accompanied by thrill. Rales were heared in the bilateral lower lung field. The most likely cause of her condition:
VSD (TOPNOTCH)
Most common cause of myocardial ischemia
Obstructive atherosclerotic lesions in the epicardial coronary arteries (TOPNOTCH) Robbins Basic Patholgoy, 9th ed., p. 538
The cause of sudden cardiac death in myocardial infarction
Ventricular arrythmia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 539
Irreversible cell injury in MI occur in how many minutes?
20-40 minutes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Irreversible injury of ischemic myocytes in MI occurs first in what zone in the heart?
Subendocardial zone (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
What blood vessel supply the posterior third of the ventricular septum in majority of the individuals?
Right coronary artery (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Pattern of infarction caused by occlusion of an epicardial vessel
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarction caused by plaque disruption or hypotension, causing circumferential myocardial damage
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as an “ST elevation myocardial infarct”
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as a “non-ST elevation infarct”
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
The typical changes of coagulative necrosis becomes detectable in how many hours of injury?
First 6-12 hours(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 545
Microscopic findings in irreversibly injured myocytes characterized by intensely eosinophilic intracellular stripes composed of closely packed sarcomeres.
Contraction bands (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 546
A 62 y/o obese male had sudden onset of heaviness in the chest, associated with diaphoresis (sudoración excesiva) and dyspnea which started 3 hours prior to consult at the ER. The biomarkers that are most sensitive and specific of myocardial damage that you will request:
Troponins I and T (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 547
A 72 y/o female experienced chest pain and hypotension. A posterior transmural infarct was suspected. Most common complications in this type of infarct
Conduction blocks, right ventricular involvement, or both (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Free wall rupture, expansion, mural thrombi, and aneurysm are common in what type/location of infarct?
Anterior transmural infarct(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Most common cause of rhythm disorder
Ischemic injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 550
A 24 y/o female presents with history of recurrent fever and joint pains accompanied by ECG changes and increased ASO titer in the past 2 years. Physical examination reveals cardiac murmur. What is the clinical impression?
Rheumatic heart disease (TOPNOTCH)
Characteristic anatomic change in Mitral Valve Prolapse (MVP)
Interchordal ballooning of mitral leaflets (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 556
Most frequent mechanism of Sudden Cardiac Death (SCD)
Lethal arrythmia (asystole, ventricular fibrillation) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Earliest microscopic change in systemic hypertensive heart disease
increase in transverse diameter of myocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Most common type of Ventricular Septal Defect (VSD)
Membranous (Interventricular septum) VSD(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 535
The common feature of pulmonary thromboembolism, obstructive sleep apnea, altitude disease, and parenchymal lung disease
Pulmonary hypertension. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 530
A 5 wk old infant presents with tachypnea, diaphoresis, and difficulty feeding. A harsh, continuous, machinery-like murmur was noted upon auscultation. What is the most likely diagnosis?
Patent ductus arteriosus(TOPNOTCH)
Presents with hypertension in the upper extremities, and manifestations of arterial insufficiency such as claudication and coldness. Produce a radiographical visible erosion (notching) of the undersurfaces of the ribs.
Coarctation of the aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 537
Major cause of infective endocarditis among intravenous drug abusers
Staphylococcus aureus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Most common cause of endocarditis of native but previously damaged or otherwise abnormal valves
Streptococcus viridans (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Predominant manifestations of Rheumatic fever (RF)
Carditis and arthritis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Classic hallmark of Infective endocarditis
Vegetations on heart valves(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
A 72 year old hypertensive female last seen apparently well 3 days ago, is found dead in her bathroom with rigor mortis and no signs of foul play. At autopsy, her heart showed left ventricular hypertrophy and a pale tan area at the anteroseptal wall. There are no thrombi in the heart chambers. The valves are unremarkable. Microscopic examination of the pale area showed well-established granulation tissue with new blood vessels and collagen deposition. Neutrophils are rare. She died of (A) an MI that occured 1 hour prior to demise (B) an MI 12 hours prior to demise (C) an MI 2 days prior to demise (D) something else entirely
something else entirely (evolution of morphologic changes in myocardial infarction) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 393
In hypertensive heart disease, there is concentric thickening of the left ventricular wall. A concomitant left atrial dilatation may also be seen due to (A) volume overload from a ventricle with narrowed lumen (B) pressure overload from a ventricle with narrowed lumen (C) cytokines secreted by hypertrophic ventricular myocytes cause atrophy of atrial myocytes (D) cytokines secreted by hypertrophic ventricular myocytes cause metaplasia of atrial myocytes
volume overload from a ventricle with narrowed lumen (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 399
What feature in a stenotic aortic valve suggests rheumatic valvular disease, rather than calcific aortic stenosis? (A) bicuspid valve (B) masses of calcium on the outflow side of cusps (C) fibrotic cusps (D) fusion of the commmissures
fusion of the commisures (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
A 20 year old asymptomatic female is found to have a midsystolic click on her preemployment physical examination. A 2D echo showed mitral valve prolapse. The involved leaflet would show (A) numerous fibroblasts with and dense collagen deposition (B) thinning of the fibrosa layer and myxoid expansion of the spongiosa layer (C) deposition of amorphous material that shows apple-green birefringence when stained with Congo red (D) fibrous stroma with gland-like structures secreting mucin
thinning of fibrosa layer and myxoid espansion of the spongiosa layer (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
A 5 year old male who had a sore throat 3 weeks ago develops fever and joint pains. Auscultation revealed a friction rub, and ASO titers are increased. Which of the following is expected in the patient? (A) friable vegetations on the mitral valve containing fibrin, neutrophils and gram-positive cocci (B) small vegetations on the mitral valve with abundant eosinophils (C) myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (D) myocardium with poorly-circumsccribed aggregates of multinucleated giant cells
myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 403-404
A 19 year old football player dies suddenly during one training session. At autopsy, his heart showed myocardial hypertrophy with disproportionate thickening of the septum, and a narrowed left ventricular lumen. Microscopic examination showed myocyte hypertrophy, myofiber disarray, and interestitial fibrosis. These findings are due to (A) a mutation in one of his genes encoding sarcomeric proteins (B) a silent Coxsackie virus B infection (C) an undisclosed 3 year history of alcohol intake (D) anabolic steroids he has been taking for 6 months
a mutation in one of his genes encoding sarcomeric proteins (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P. 412-413
A 34 year old female on routine checkup is found to have a diastolic murmur. 2D echo showed a pedunculated 3 cm mass in her left atrium attached to the atrial septum. She has no other known masses on workup. She undergoes heart surgery where the atrial mass is resected. Which of the following is its most likely histology? (A) stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (B) sheets of large polygonal cells containing glycogen-containing vacuoles arranged around a central nucleus (C) fascicles of fibroblasts and interspersed collagen bundles (D) sheets of pleomorphic cells lining vascular spaces, some with intracytoplasmic lumens, with atypical mitoses and areas of necrosis
stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 417-418
CARDIOPATOLOGIA ISQUEMICA
Causas
o Aterosclerosis coronaria (90%)
o Arteritis (vasculitis), embolia, vasoespasmo, shock
o Aumento de demanda taquicardia, hipertrofia
o Anemia intensa, cardiopatias cianóticas (reduccion de O2 en la sangre), monox de carbono
Tipos de Angina de Pecho
- Estable: reposo, fármacos vasodilatador
- De prinzmetal: fármacos vasodilatadores
- Inestable: complicación de placa con obstrucción variable.
INFARTO DE MIOCARDIO
Que es?
Destrucción del musculo cardiaco debido a una isquemia grave y prolongada.
Isquemia intensa que dura de 20 a 30 min como minimo, origina un daño irreversible (necrosis) en los miocitos cardiacos.
En un infarto, que se ve en la macro antes de 12h, de 12 a 24h y a lo largo de semanas?
o Menos 12h: no evidente
o 12 a 24h: región de color azul rojizo (sangre estancada y retenida). Después mejor delimitado, color amarillo pardo y blanco.
A lo largo de semanas: evoluciona hacia una cicatriz fibrosa.
En un infarto, que se ve en la micro de acuerdo con el tiempo de evolución?
*granulación y cicatrización son coloración tricomica de masson
En un infarto, que enzimas se elevan?
= isoenzima MB CK (creatinin kinasa)
=› troponina T
- troponina l o mioglobina
=› lactato deshidrogenasa (LDH)
Infarto. Clínica
- Dolor torácico, nauseas, sudoración, disnea
- Cambios ECG
- Elevación enz miocárdicas
Infarto. Cuales pueden ser algunas complicaciones?
- 80-90% complicaciones
Ruptura de la pared ventricular *genera shock cardiogénico
Arritmias
Insuficiencia cardiaca congestiva
Valvulopatias *necrosis
musculopapilar
Pericarditis
Trombosis mural
Aneurisma ventricular
Repetición infarto
Cuales son las características de una lesión por reperfusión?
- Infarto hemorrágico *rojo
- Miocitosen necrosis con bandas de contracción (contracción exagerada de las miofibrillas por alta concentraccion de Ca)
CARDIOPATOLOGIA HIPERTENSIVA
Aumento de la presión arterial, muchas veces es asintomático. Por ser principalemente en las arterias, afecta mas el corazón ………...
Aumento de la presión arterial, muchas veces es asintomático. Por ser principalemente en las arterias, afecta mas el corazón izquierdo.
ESTENOSIS CALFICADA MITRAL
Se dá más en hombres o mujeres?
Mujeres jóvenes
Válvulas blandas, flexibles prolapsadas hacia la AI durante la sístole (clic mesosistolico)
Causas de estenosis aortica
- Cicatrizacion postinflamatoria (cardiopatía reumática)
= Estenosis aortica calcificada senil
-› Calcificación sobre una deformación valvular congénita
Causas de insuficiencia aortica:
Cicatrizacion postinflamatoria (cardiopatía reumática)
Endocarditis infecciosa
Sme de marfan
ENFERMEDAD AORTICA:
Dilatación degenerativa de la aorta
Aortitis sifilítica
Espondilitis anquilosante
Artritis reumatoide
Sme de marfan
FIEBRE Y CARDIOPATÍA REUMÁTICA
Enf inflamatoria aguda, recidivante que aparece …. a ….. semanas post a infeccion por estreptococos del grupo A.
5-15 años
Enf inflamatoria aguda, recidivante que aparece 1 a 5 semanas post a infeccion por estreptococos del grupo A.
5-15 años
FIEBRE Y CARDIOPATÍA REUMÁTICA
LESIÓN CARDIACA AGUDA
Nódulos de aschoff: necrosis fibrinoide rodeada de mononucleares y macrófagos activados (cels de antischkov).
- Pancarditis
- Endocardio: engrosamientos subendocardicos (placas de Mac Callum - AI)
FIEBRE Y CARDIOPATÍA REUMÁTICA
Como es la forma aguda y la cronica? que valvulas son más afectadas?
- Forma aguda: valvulitis con vegetaciones en borde libre. *estenosis
- Forma crónica: engrosamiento fibroso fusión de comisura y cuerdas tendinosas, calcificaciones. *insuficiencia
- 65-70% de los casos solo afectada la valvula mitral, 25% se suma la valvula aortica.
Cual es la diferencia de una miocardiopatia primaria y una secundaria?
Primarias: enfermedades limitadas al musculo cardiaco.
Secundaria: la participación del miocardio es un componente de un padecimiento sistémico o multiorganico. *afectación sistémica que afecta también el corazón *ej: hemacromatosis
MCP dilatada
Cuales son los mecanismos patogenicos y las caracteristicas?
Mecanismos patogénicos:
- Defectos genéticos, bioquímicos o estructurales
- Alcohol
- Periparto
- Miocarditis (viral)
Características:
- Cardiomegalia
- Trombos murales
- Fibrosis intertersticial
- Lesiones microscópicas inespecíficas
MCP VENTRICULAR ARRTIMOGENA DERECHA
Características
Genera arritmias que pueden ser mortales, inicio en la niñes y muerte súbita en el adulto.
Autosómica dominante
Corazón musculoso, hipercontractil, poco distensible con dificultad en relajación diastólica (disfunción diastólica).
Herencia AD
Que es?
MCP Hipertrófica
- Hipertrofia septal asimétrica
- Cavidad en forma de banana
- Obstrucción
- Disposición desordenada de miocitos, hipertróficos y fibrosis, nucleos mas grandes, depósitos de colágeno.
QUE ES?
MCP HIPERTROFICA
Reduce y dificulta el llenado ventricular con disminución del gasto cardiaco. *complicaciones sístole y diástole.
Idiopática o asociada a procesos como fibrosis por radiación, amiloidosis, sarcoidosis, tumores metastásicos o depósito de metabolitos acumulados por alguna enzimopatía congénita.
Que es?
MCP RESTRICTIVA
Se asocia a eosinofilia e infiltración eosinofila en órganos y evolución rápida mortal.\
Que es?
Endocarditis de Loeffler
Ventrículos tamaños normal o un poco aumentados, sus cavidades no dilatadas y el miocardio mantiene una consistencia firme y no es distensible.
Fibrosis intersticial focal o difusa.
Que es?
MCP Restrictiva
Tumores primarios del corazón son raros. 80-90% benignos
Cuales son los benignos y los malignos?
Primarios
- Benignos: mixoma (1o), fibroma, lipoma, rabdomioma, fibroelastoma papilar (2o)
- Malignos: angiosarcoma, rabdomiosarcoma
Caracteristicas de los Mixomas Cardiacos
o Primario mas frecuente en adultos
o Relación con anomalías clonales de los cromosomas 12 y 17.
o 90% estan situados en las aurículas (mixomas auriculares), auricula izquierda
a nivel fosa oval. o 1-10 cm
o Sésiles o pediculados
o Masas duras globulares moteadas por las hemorragias o lesiones blandas translucidas vellosas gelatinosas.
MORFOLOGIA
- Células estrelladas o glubuladas inmersas en abundante sustancia constituida por mucopolisacaridos acidos.
- Estructuras de tipo vascular o glandular
- Hemorragias e inflamación mononuclear.
Que es?
Mixoma cardiaco
Acumulos polipoides subendocardicos de tejido adiposo en VI, AD o tabique, forma de hamartoma.
Que es?
Lipoma - neoplasia benigna
En válvulas derechas de niños e izq de adultos. Proyecciones vellosas de tejido mixoide con musculo liso y fibroblastos, origen trombótico.
Que es?
Fibroelastoma papilar
Neoplasia benigna
Primario mas frecuente en niños de ubicación ventricular. Forma de hamartoma, asociado a esclerosis tuberosa.
Que es?
Rabdomioma
neoplasia benigna
NEOPLASIAS MALIGNAS en el corazón
o Angiosarcoma
o Rabdomiosarcoma
o Metástasis de pulmón, mama melanoma, leucemias y linfomas.
o Mucho infrecuente
Etiologias de las cardiopatias congénitas
Etiología: multifactorial
- alteración genética: monogenicas, proteínas como factor de transcripción, proteínas estructurales, trisomías (21)
- condiciones ambientales: rubeola materna, alcohol, tabaco, hipoxia, fármacos.
- Ausencia de acido fólico
Embriogénesis defectuosa entre la 3a y 8a semana de gestación.
CORTOCIRCUITO IZQ – DER: no pasa por la circulación pulmonar
Sintomas
Cianosis tardia - Hipertrofia VD
Sme de Eisenmenger (HTP con cortocircuito invertido)
CORTOCIRCUITO IZQ – DER
Lugares:
Comunicación interauricular (CIA)
Comunicación interventricular (CIV)
Conducto arterioso permeable (CAP)
Comunicación auriculoventricular
CORTOCIRCUITO DER – IZQ
Sintomas
Hipoxemia con cianosis precoz (nacimiento)
Policitemia (trombosis) *aumento de plaquetas
Acropaquias punta dedos manos y pies
Embolias paradójicas (ACV)
CORTOCIRCUITO DER – IZQ
Lugares
o Tetralogia de Fallot
o Transposición de los grandes vasos
o Tronco arterioso
CARDIOPATÍA CONGÉNITA
Obstrucciones:
o Coartación de aorta
o Estenosis y atresia pulmonar
o Estenosis y atresia aorticas
COMUNICACIÓN INTERAURICULAR
Passaje del torrente sanguíneo desde el septo o
tabique que separa las aurículas.
Que es Ostium primun, ostium secundum y seno venoso?
o Ostium primun: 5%, adyacente a válvulas AV (1)
o Ostium secundum: **90% **Centro, por perforación de fosa oval. (2)
o Seno venoso: 5%, cerca desembocadura VCS (3) *(4) es la VCI
o Asintomáticahasta30años
o Puede producir HTP, es infrecuente
o Anomalía congénita cardíaca más frecuente
Sola (20-30%) o asociada (+ fr)
o 90% porción membranosa del septum, por eso tiene una forma oval
Que es?
COMUNICACIÓN INTERVENTRICULAR
Porque la COMUNICACIÓN INTERVENTRICULAR no genera cianosis? Que es el sindrome de Eisenmenger?
VI ➡️ VD, por eso no genera cianosis
o Con el tiempo, por el aumento de la presión del VD, el flujo puede ser VD ➡️ VI, produciendo cianosis * Sme de Eisenmenger
La sangre pasa desde la aorta hasta la arteria pulmonar, por la mayor presión de la aorta.
Que es?
CONDUCTO ARTERIOSO PERMEABLE
Persistencia anormal post natal
90% Defecto aislado
10% (CIV, coartación de aorta, estenosis de las válvulas pulmonar o aórtica)
Asintomático, soplo en maquinaria
No necesariamente genera cianosis
Que es?
CONDUCTO ARTERIOSO PERMEABLE
- Estenosis de la valvula pulmonar
- Hipertrofia del VD
- Comunicación intraventricular
- Cabalgamiento de la aorta sobre la comunicación intraventricular
Que es?
TETRALOGIA DE FALLOT
Produce cianosis desde el inicio, dado que la circulación derecha pasa directamente a la circulación izquierda, evitando la circulación pulmonar.
Que es?
TETRALOGIA DE FALLOT
TETRALOGIA DE FALLOT
Cuales son las 3 variantes?
TF rosada (sin cianosis): estenosis pulmonar leve.
TF clásica (cianótica): mayor estenosis, shunt der-izq
TF extrema: atresia pulmonar, mucha cianosis
- Aorta sale del VD y Arteria pulmonar del VI.
- Vida posnatal incompatible excepto que exista CIA o CIV.
Que es?
TRANSPOSICIÓN DE GRANDES VASOS
TRONCO ARTERIOSO
Un solo tronco arterial para la aorta y la arteria pulmonar, la sangre del VD y VI se mezcla.
Cianosis importante; HTP
Estrechamiento congénito del diámetro de la aorta, ubicado habitualmente luego de la emergencia de la arteria subclavia
izquierda.
Que es?
COARTACIÓN DE AORTA
o El paciente tiene una buena irrigación de la parte superior del tronco, pero una baja circulación de la parte inferior del tronco.
o Aislado o asociado a otras anomalías (50% valvula aórtica bicúspide)
o Cardiomegalia por sobrecarga crónica.
COARTACIÓN DE AORTA
En la coartacción de la aorta, cual es la diferencia entre con o sin conducto arterioso?
o Con CAP: sintomas después del parto, cianosis en mitad inferior del cuerpo; quirurgia o catéter.
o Sin CAP: asintomático hasta adultez.
Que es atresia de la valvula pulmonar o aortica?
La atresia de las válvulas es una enfermedad congénita del corazón en la cual las válvulas están ausentes o no se formaran correctamente. Como resultado, se produce una obstrucción completa o severa en la salida del ventrículo derecho hacia los pulmones.
Causas de las vasculitis:
o No infecciosa (inmunitaria) +frecuente
o Infecciosa
o Otras: lesión física o químicas (radiación, traumatismos).
Vasculitis de grandes vasos
- Arteritis de células gigantes
- Arteritis de Takayasu
Vasculitis de vasos medianos
- Panarteritis nudosa clásica
- Enfermedad de Kawasaki
Vasculitis de pequeños vasos
- Granulomatosis de Wegener
- Panarteritis microscópica
- Síndrome de Churg-Strauss
- Púrpura de Schönlein-Henoch
- Vasculitis crioglobulinémica esencial
o Forma mas fr em ancianos (dp 50 anos)
o Inflamacion granulomatosa de artérias de gran y pequeno calibre
- Principalmente arterias de la cabeza (temporal, oftálmica y vertebrales).
-› Puede afectar aorta (aortitis de células gigantes
ETIOLOGIA DESCONOCIDA
o Posible reacción inmunitaria LT a Ag desconocidos de la pared vascular.
Que es?
ARTERITIS DE CELULAS GIGANTES
MORFOLOGÍA
o Engrosamiento de la intima
o Inflamación granulomatosa con fragmentación (destrucción) de la elástica
o Linfocitos, macrófagos
o Células gigantes multinucleadas (75%)
o Afectación segmentaria
ARTERITIS DE CELULAS GIGANTES
Vasculitis
CLINICA
Cefalea (mas intensa en trayecto de la temporal), dolor a la palpación
Alteraciones visuales
DX
Biopsia (2-3 cm)
Seriologia
ARTERITIS DE CELULAS GIGANTES
o Vasculitis granulomatosa de arterias de mediano y gran calibre.
o Engrosamiento de la aorta, sobre todo de su cayado y de los grandes vasos, y un estrechamiento importante de la luz en las principales rammas vasculares.
ARTERITIS DE TAKAYASU
ETIOLOGIA Y PATOLOGIA desconocida
o Lesiones aorticas comparten características con la aortitis de células gigantes *pero aparece en menores de 50 anos
ARTERITIS DE TAKAYASU
MORFOLOGIA
o Afecta clásicamente el cayado de la aorta
1/3 se extiende por el resto de la aorta y sus ramas
50% afectación de arteria pulmonar
Arterias renales y coronarias
ARTERITIS DE TAKAYASU
CLINICA
o Disminución de pulsos MMSS
o Alteraciones visuales
o Alteraciones neurológicas
o IAM (art coronarias)
o HTA (art renales)
ARTERITIS DE TAKAYASU
o Enf. generalizada que afecta arterias de pequeño y mediano calibre
o Vasos afectados: riñones, corazón, hígado, tubo digestivo (respeta circulación pulmonar).
o Adultos jóvenes
PANARTERITIS NUDOSA
MORFOLOGIA
o Inflamación necrosante transparietal (neutrófilos, eosinofilos, mononucleares, con necrosis fibrinoide)
o Estadio final: engrosamiento fibroso (a veces nodular) de la pared vascular
o Segmentaria (no toda la circunferencia)
o Ocurre en la ramificación
PANARTERITIS NUDOSA
Vasculitis
CLINICA
Deriva de la isquemia y necrosis de tejidos afectados.
- Malestar, fiebre y adelgazamiento; HTA (afectación renal), dolor abdominal y melenas (tubo digestivo), mialgias y neuritis periférica.
TRATAMIENTO
- Corticoesteroides y ciclofosfamida: remisiones o curación en el 90% de las ocasiones.
PANARTERITIS NUDOSA
o Proceso agudo que afecta lactantes y niños
o Afecta vasos de mediano y gran calibre e incluso de pequenos. *predilección por art. Coronaria
ENF. DE KAWASAKI
o Intensa inflamación de todo el espesor vascular, cicatrizacion engrosamiento obstructivo de la intima.
o Formación de aneurismas, rotura o trombosis (IAM)
o Eritema con erosion oral y conjuntival adenopatías cervicales (sme ganglionar mucocutanea)
Tto: inmunoglobulina, acetisalicilico (ateriopatia coronaria se reduce hasta un 4%).
ENF. DE KAWASAKI
Afecta arteriolas, capilares y vénulas
- cuanto mas pequenos los vasos afectados, mas generalidado son las complicaciones
- Afecta piel, mucosas, pulmones, encéfalo, corazón, tubo digestivo, los riñones y el musculo.
- Glumerulonefritis necrosante (90% de los pacientes) y la capilaritis pulmonar son especialmente frecuentes.
POLIANGEITIS MICROSCÓPICA
(leucocitoclastica)
- Fragmentación de los neutrófilos (vasculitis leucocitoclastica).
- Hemoptisis, hematuria, proteinuria, el dolor o hemarragia intestinal, dolor o debilidad muscular y purpura cutánea palpable.
- ANCA – MPO (p-anca)
POLIANGEITIS MICROSCÓPICA
o Vasculitis necrosante de los vasos de pequeño calibre.
o Relación clásica con asma, rinitis, alergias, hipereosinofilia periférica.
o Lesión vascular aspecto similar a la PAN y poliangitis microscópica mas granulomas y eosinofilos.
Menos de la mitad de los casos ANCA - MPO = p-ANCA
SME DE CHURG-STRAUSS
Triada
- Granulomas necrosantes en VRA (oído, nariz, senos, faringe y laringe), bajas (pulmón) o ambas.
- Vasculitis necrosante o granulomatosa en vasos de pequenos o mediano calibre (ppal pulmones y VRA)
- Nefropatía (glomerulonefritis necrosante focal)
- ANCA PR3 (c-ANCA) +95%
- Mas frecuente en hombres, 40 anos
GRANULOMATOSIS CON POLIVASCULITIS
(WEGENER)
CLINICA
Neumonía persistente en infiltrados nodulares y cavitarios bilaterales (95%), sinusitis crónica (90%), ulceras mucosas de la nasofaringe (75%) y nefropatía (80%).
GRANULOMATOSIS CON POLIVASCULITIS
(WEGENER)
o En grandes fumadores menores de 35 anos
o Inflamación aguda y crónica segmentaria de arterias de mediano y pequeño calibre de miembros (tibial, radial)
o Puede extenderse a venas y los nervios de las extremidades.
o Infiltrado de neutrófilos y trombos con microabscesos
o Dolor, ulceras, gangrena.
TROMBOANGEITIS OBLITERANTE
(ENF. DE BUERGER)
Vasoespasmo miocárdico: miocardiopatía
de …………….
Miocardiopatía de Takotsubo
Vasoespasmo miocárdico: miocardiopatía
de …………….
Miocardiopatía de Takotsubo
HTA: ………. mmHg/ …………. mmHg
HTA: 140 mmHg/ 90 mmHg
HIPERTENSIÓN ARTERIAL
Es un factor de riesgo para que enfermedades?
Cardiopatía isquémica, ACV, IC, Ins. Renal y disección aortica.
HIPERTENSIÓN ARTERIAL
Sin tto: mitad de casos muere por cardiopatía isquémica o ICC y tercera parte por ……...
Sin tto: mitad de casos muere por cardiopatía isquémica o ICC y tercera parte por ACV.
REGULACIÓN DE LA PRESIÓN ARTERIAL
Presión arterial depende de dos variables:
- Gasto cardiaco
- Resistencia periférica
Que disminuye la presión arterial?
↓la resistencia periférica (dilatación):
- Oxido nítrico ↑
- Prostaciclina ↑
- Cininas ↑
- Péptido natriuretico auricular (ANP) ↑
- Factores nerviosos (adrenigenicos) ↓
]Que disminuye la presión arterial?
↓ gasto cardiaco
- Volemia ↓
- PNA↑ (“presión arterial sistólica no invasiva”)
- Frecuencia cardiaca ↓
- Contractilidad ↓
Que aumenta la presión arterial?
↑ gasto cardiaco
- FC↑
- Contracción ↑
- Volemia (aldosterona) ↑
Que aumenta la presión arterial?
↑ resistencia periférica (contracción) *simpático
- Angiotensina II ↑
- Catecolamina ↑
- Tromboxano ↑
- Endotelina ↑
- Factores nerviosos ↑
o Causa desconocida
o Aumento del gasto cardiaco o de la resistencia periférica o ambos
o Alteracion mecanismos renales:
Sitema renina angiotensina
Homeostasis del sodio
Producción de sustancias
vasodepresoras
o Factores genéticos
o Factores ambientales
HTA ESENCIAL (PRIMARIA) – 90-95%
HTA SECUNDARIA
Renal
- Glomerulonefritis aguda,
- nefropatías crónicas,
- enf poliquistica,
- estenosis de la arteria renal,
- vasculitis renal,
- tumores productores de renina.
HTA SECUNDARIA
Endocrina
- Hiperfunción corticosuprarrenal congénita,
- hormonas exógenas,
- feocromocitoma,
- acromegalia,
- hipotiroidismo,
- hipertiroidismo
HTA SECUNDARIA
Cardiovascular
- Coartación de aorta,
- poliarteritis nudosa,
- aumento de vol intravascular
HTA SECUNDARIA
Neurológica
- Psicógena,
- aumento de presión intracraneal,
- apnea del sueño,
- estrés agudo.
- TA mayor 220/ 120 mmHg
- IR, hemorragia y exudados retina
HTA ACELERADA O MALIGNA – 5%
+ fr en hombres y fumadores (raro antes de los 50 anos)
- Debajo de arterias renales y encima de la bifurcación aortica
ANEURISMA DE AORTA ABDOMINAL
Afecta sobre todo a dos grandes grupos:
- Hombres de 40 a 60 anos con antecedente de HTA (mas del 90% de los casos).
- Jóvenes con alteraciones del TC (sme de marfan)
DISECCION AORTICA
DISECCION AORTICA
CLINICA
Dolor precordial con irradiación a espalda y desplazamiento hacia abajo
DISECCION AORTICA
En la disección aortica, cual es la causa más frecuente de morte?
La ruptura exterior de la diseccion hacia las cavidades pericárdica, pleural o peritoneal.
