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95 Cards in this Set

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Atherosclerotic plaque. This is a mature stable plaque consisting mostly of collagenous fibroconnective tissue. No definite lipid core can be appreciated in this lesion. There is an area of calcification on the right side of the screen. Coronary arteries involved by atherosclerosis can become quite calcified and are sometimes referred to as “pipe stems.” I would estimate that this plaque narrows the lumen by ~70%. The coronary arteries are the vessels next most heavily involved by atherosclerosis after the abdominal aorta.
Histologic section of a coronary artery stained with a trichrome stain which stains collagen blue. This is a typical eccentric plaque with the arrow pointing to an area of the arterial wall which is not involved by the plaque. “F” designates the fibrous cap and “C” designates the lipid core. This plaque narrows the lumen (L) by ~50% and therefore would not have been sufficient to cause angina. In order for a plaque in a coronary artery to result in angina, it is believed that it must narrow the lumen by at least 75%.
Histologic section of a coronary artery from a patient who died with an acute myocardial infarct (MI). The arrow is pointing to an area where the fibrous cap of the plaque has ruptured. Rupture of the fibrous cap has exposed the circulation to thrombogenic material resulting in formation of a superimposed thrombus, which has occluded most of the remainder of the lumen. Note that in the area of rupture, the fibrous cap is rather thin and there is a prominent lipid core. This is the morphologic picture most commonly encountered in individuals who develop an acute transmural MI. Also note, that prior to disruption of the plaque, it would have narrowed the lumen by only ~50%, so that this plaque by itself would in all likelihood not have caused angina pectoris.
Segment of abdominal aorta involved by severe atherosclerosis. The arrows are pointing to several large ulcerated atherosclerotic plaques. Ulcerated plaques can give rise to atheroemboli or thromboemboli. The abdominal aorta is the region of the arterial vasculature most heavily involved by atherosclerosis. For this reason, atherosclerotic aneurysms most frequently occur in the abdominal aorta.
syphilitic aortitis d/t tertiary syphilis.

Syphilis tends to result in inflammation of the vaso vasorum w/ resultant intimal fibrosis and obliteration ofthe lumen (obliterative endarteritis).
This is a section of the heart
"tree-barking"- wrinkled appearance of the intima. Tree-barking is caused by retraction of fibrous scars in the media and is very characteristic feature of syphilitic aortitis.
Small artery exhibiting obliterative endarteritis (endarteritis obliterans).

The lumen is completely obliterated by fibrous tissue. This is the lesion that is seen in the vasa vasorum in tertiary syphilis.
Hyaline arteriolosclerosis in the kidney.

Hyaline arteriolosclerosis is most commonly encountered in individuals with hypertension and diabetes. The walls of the involved arterioles are markedly thickened with resultant narrowing of the lumen. The luminal narrowing can result in ischemia and also exacerbate any underlying hypertension. These lesions are felt to reflect increased extracellular matrix production by the vascular smooth muscle cells
hyperplastic arteriolosclerosis- kidney

concentric laminations resembling the cut surface of an onion "onion skinning". D/t proliferation of vascular smooth muscle cells w/ collagen and basement membrane. Usually seen in MALIGNANT HTN.
Giant cell arteritis

Inflammatory infiltrate can be seen along the internal elastic lamina (black arrows). Thebig cell in the top middle is a Langhan's giant cell. Major concern is that this can lead to blindness in one or both eyes.
Giant cell arteritis

Langhan's giant cells in the bottom middle of the picture and the lumen has been markedly narrowed by intimal fibrosis.
Giant cell arteritis--- in temporal artery

Marked intimal thickening d/t healing w/ fibrosis w/ resultant narrowing of the lumen. The arrow is pointing to an area where the internal elastic lamina has been disrupted.
Polarteritis Nodosa (small artery)

Most characteristic histologic feature is the presence of fibrinoid necrosis. This can result in the rupture (hemorrhage) or weakening (aneurysmal).

Renal arteries are almost always involved and pulmonary arteries are usually spared.
-Common clinical manifestations--> melena or hematochezia and nodular skin lesions.
Varicose veins

Dilated tortuous veins whose valves have become incompetent. Superficial veins in the lower extremities are most commonly involved.

RF: Obesity, Multiple pregnancies and standing occupations.
Stasis dermatitis w/ secondary development of an ulcer d/t severe varices
Saddle emboli

Main pulmonary artery and right and left pulmonary arteries have been opened up. This emboli obstructed the flow of blood to the lungs. Saddle emboli are fatal.
Hemangioma on the tongue.

Benign tumors composed of numerous blood vessels. Vary from bright red to blue depending on the degree of oxygenation of blood w/n the lesion. Occur mc on skin and mucous membranes of the oral cavity and lips. Two types: capillary and cavernous.
Hemangioma- liver

Just beneath the capsule. The liver is the MC location for visceral hemangiomas. Merely incidental findings--- usu not associated with any other effects.
Capillary hemangioma- skin

numerous small capillary-like blood vessels lined by flattened endothelium.
Juvenile hemangioma (capillary) also called strawberry hemangioma.

Most of the cells in the cellular areas are pericytes which are modified smooth muscle cells that surround capillaries. Found on skin of newborn infants and grow rapidly during the 1st few months of life. Fade at 1-3 yrs of age and completely regress in maj of cases by 7 yrs.
infant born w/ large capillary hemangioma of the juvenile type.
Cavernous hemangioma

consists of numerous large dilated BV. They are less common and more likely to involve internal organs than capillary hemangiomas. They do not spontaneously regress and may cause cosmetic problem when on skin.
Cavernous hemangioma

Also named "port wine stains", when shown occuring on one side of the face that are sometimes assoc w/ Sturge- Weber syndrome. If so those cavernous hemangiomas also involve meninges over the brain on the same side of the stain--> mental retardation, seizures, and contralateral hemiplegia.
AIDs pt w/Kaposi Sarcoma

Cutaneous lesions- red to purple in color. AIDs pts w/ KS often have visceral involvement at the time that cutaneous lesions appear. MC- homosexual men. Looks just like basillary angiomatosis w/ AIDs pt.
Kaposi sarcoma

Tumor w/ proliferation of spindle cells w/ numerous small BV and extravasated RBC's. Extravasated RBC's in soft tissue tumor--> think Kaposi!!!
Herpesvirus 8 (KSHV) has been isolated from the tumor cells in 95% KS lesions.
Kaposi sarcoma

largely composed of spindle cells w/ numerous vascular spaces (slit-like). Focal deposits of hemosiderin are present (inside yellow oval) d/t presence of extravasated RBC's in tumor.
Angiosarcome.

MC malignant primary tumor arising in the heart. The tumor (top left) is darker in color because of all the vascular spaces in the tumor. The lighter colored areas are areas of necrosis. There are satellite tumor nodules on the epicardial surface of the heart infiltrating overlying pericardium. Poor prognosis.
Angiosarcoma

highly malignant tumors derived from endothelial cells. MC sites of origin: skin, soft tissue, breast and liver. Vinyl chloride linked to angiosarcomas from the liver.
Angiosarcoma using immunohistochemical stain fo CD31 an endothelial cell marker.

Brown = positive. Factor VIII related antigen (von Willebrand factor) is another endothelial cell marker to confirm angiosarcoma. Very aggressive tumors-local invasion as well as distant metastases. 5-yr survival rate is poor.
Rupture of left ventricular free wall d/t acute myocardial infarct.
- pericardial cavity filled w/ fresh blood (hemopericardium) and creates cardiac tamponade. This is almost invariably fatal-- can occur 3-7 days post MI
Pale yellow area- large acute MI involving the posterior and lateral wall of the left ventricle. Black area in this yellow area= rupture of the left ventricular free wall (cardiac tamponade). In the yellow area there is also a posterior papillary muscle which is also involved by infarct. Occlusion caused by dominant right coronary artery.
white area- old healed MI involving the anterior wall of the left ventricle and anterior portion of the septum- caused by an occlusion of the LAD coronary artery.
MI

Extending from the anterior wall of the left ventricle and into the septum. Center in tan-gray w/ surrounding hyperemia (excess blood vessels supplying this area). Transmural infarction because it extends thru the full thickness of the wall.
acute MI 2-3 days old.

Myofibers have largely lost their nuclei and cross striations indicative of coagulative necrosis. Heavy PMN infiltrate.
Small MI (light pink area)

Area of infarction is completely healed and replaced by dense collagenous fibroconnective tissue. This infarct is 6-8 wks old and could be months or even yrs old.
Healed MI

Stained w/ trichome stain- collagen is blue. Approximately 6-8 weeks post MI, infarcted myocardium is replaced by scar tissue. Scar tissue will restore tensile strength but detract from contractility causing hypertrophy of the muscle around it.
Reperfused infarcted myocardium

infarcted myocardium- loss of nuclei and cross striations w/n the myofibers. BV have been damaged and when area is reperfused the BV leak resulting hemorrhage. The black arrows are pointing to contraction bands which are composed of closely packed hypercontracted sarcomeres (d/t large number of calcium entering the myofibers).
left ventricular aneurysm

Stasis of blood w/n the aneurysm prediposes to the development of the mural thrombus.
Acute infective endocarditis of the aortic valve

caused by Staph aureus and may occur on a previously normal valve,
Infective endocarditis

vegetation is composed of fibrin (pink) w/ large numbers of neutrophils.
Nonbacterial thrombotic endocarditis- mitral valve

there are vegetations along the line of closure of the valve. Do not contain microorganisms or significant numbers of inflammatory cells. Vegetations are small, loosely attaches, nondestructive and along closure of a valve. MC in debilitated pts (cancer or sepsis w/ DIC). Strong assoc w/ MUCINOUS ADENOCARCINOMA
Histologic section of a valve cusp (C) with attached thrombus (vegetation) from a case of NBTE. The thrombus is only loosely attached to the cusp (arrow). There is no inflammation or destruction of the cusp underlying the thrombus. The thrombus (vegetation) is composed principally of fibrin with only very few inflammatory cells and no microorganisms. The vegetations in NBTE may be dislodged from the cusps producing emboli that may result in infarcts in the brain and elsewhere.
Libman-Sacks endocarditis

SLE pts. the vegetations are scattered over the leaflets and are present on the undersurface of the leaflets. Very similar morphologically to acute rheumatic valvulitis.
in RF the vegetations are ____ and are present _______
in Infective endocarditis, the vegetations are ______
in NBTE the vegetations are relatively ____ and present ______
In LSE, the vegetations are relatively ____ and present ______
RF: small, along the closure of the valve
IE: Large, irregular and destructive
NBTE: Small, along the line of closure of the valve and loosely attached
LSE: small, scattered over the leaflets and undersurface of the valve leaflets.
Carcinoid Heart dz

The pale area in the middle are the thickened leaflets and there is an area of mural endocardium just about that exhibiting a plaque like thickening. Thickening of valve leaflets + plaque like thickening of mural endocardium--> characteristic carcinoid heart dz. (right side of heart usually).
Carcinoid syndrome
carcinoid tumor which elaborates serotonin. Serotonin is the mediator believed to be principally responsible for the clinical manifestations of the Carcinoid Syndrome, as well as the cardiac changes seen in Carcinoid Heart Disease. Most patients with the Carcinoid Syndrome have a gastrointestinal carcinoid which has metastasized to the liver.
Carcinoid heart dz

Acid mucopolysaccharides blue-green and elastic tissue black. Endocardial thickening present is d/t deposition of mucopolysaccharides w/n the intima of the endocardium. Left side is usually NOT involve since serotonin is not inactivated in the lungs.
section A: Concentric LVH w/o dilation. (pressure-overloaded),
Section B: normal heart
Section C: hypertrophy w/ dilation. (volume overloaded left ventricle)
left- normal myocardium
right- hypertophy myocardium. Myocyte nuclei have a more rectangular shape
RHD- mitral valve

"fish mouth" stenosis. Arrow is pointing to an area of "commissural fusion" where fibrous tissue has bridged across the commissure and fused the leaflets together--> characteristic of RHD and is NOT present in any other forms of valvular dz.
Calcific aortic stenosis of a congenitally bicuspid aortic valve

sxs in their 50s and 60s
Mitral valve prolapse.

Black arrow--> posterior leaflet of mitral valve has a hooded appearance and is prolapsing into the LA. Chordae tendineae are elongated and thinned out.
Myxomatous degeneration of mitral valve

whitish area--> spongiosa layer of valve leaflet. Very loose appearance (myxomatous) produced by abundant deposition of proteoglycans w/n the ECM.
Large Myxoma- LA

MC primary tumor of the heart (benign). 90% arise w/n atria w/ most of them being in the LA. Can be quite large and exhibit a pedunculated, gelatinous appearing and hemorrhagic mass. They can obstruct the mitral valve and often result in syncopal episodes.
Myxoma

loos myxoid stroma d/t presence of abundant mucopolysaccharides. Nuclei are small and banal appearing (boring, common). Thought to appear from multipotential mesenchymal cells. 10% of peps w/ myxoma have familial syndrome - carney complex- AD, multiple cardiac and extracardiac myxomas, pigmented skin lesions and overactive endocrine.
Necrotizing arteriolitis (fibrinoid necrosis)

Also seen in pts w/ malignant hypertension (>120 diastolic). Deposition of plasma proteins, especially fibrin can develop thrombosis resulting in local infarcs.
Pt w/ Giant Cell Temporal arteritis. Black arrow is pointing at an involved temporal artery which is thickened and somewhat nodular appearing. Often these arteries are tender to palpation.
Giant cell arteritis

Fibrotic thickening of the intima which resulted in a markedly narrowed slit-like lumen. The black arrow is pointing to a giant cell which is contiguous to a degenerated internal elastic lamina.
Takayasu arteritis

Aortic arch angiogram showing narrowing of brachiocephalic, carotid and subclavian arteries. High grade stenosis.
Takayasu arteritis

CS of right carotid artery demonstrating marked intimal thickening w/ minimal residual lumen.
Takayasu arteritis

Hist view of active Takayasu aortitis, illustrating fibrosis of the media w/ Mononuclear inflammation and Langhans giant cells.
Polyarteritis nodosa

There are areas of fibrinoid necrosis involving the inner portion of the vessel wall and the lumen has been obliterated. These walls can rupture acutely or heal w/ a very weak wall and then rupture and cause an aneurysm
Leukocytoclastic Vasculitis

section of skin exhibiting a small vessel in the dermis which is surrounded by infiltrates of neutrophils. These neutrophils typically can be seen to have fragmented nuclei. Fragmented nuclei (karyorrhexis) occuring in leukocytes = leukocytoclasia (hence the name). Usually d/t drugs (esp antibiotics)
Wegner Granulomatosis


There are three nodular lesions, one of which exhibits a large central cavity (yellow arrow). These cavitary lesions resemble mycobacterial or fungal infections, which should always be ruled out in patients who may have Wegener granulomatosis.
Wegner granulomatosis

There is a small artery involved by vasculitis in the bottom right corner of the picture. There are also giant cells in the surrounding lung tissue.
Thromboangiitis obliterans (buerger dz)

The pt dev gangrene over the distal aspect of the 2nd, 3rd, and 4th digits
Thromboangiitis obliterans

Medium sized artery- lumen is occulded by a thrombus. The black arrows point at several microabscesses which are within the thrombus. There is a mixed acute and chronic inflammatory infiltrate which extends out into the surrounding soft tissue.
Left: Gross photo of an abdominal aortic aneurysm (AAA) before it’s been opened up. The arrow is pointing to the site of rupture.
Right: Gross photo of the aneurysm after it’s been opened. A probe marks the site of rupture. The yellow arrow is pointing at the wall of the aneurysm, which is paper thin. The black brace is marking layer upon layer of very thick mural thrombus.
Aortic arch dissection

Intimal tear can be seen and is thought to be the site of origin of the dissection
aortic dissection

Stained for elastin. The * marking the channel of blood which is dissecting thru layers of the media and is called a "dissecting hematoma"
Cystic medial degeneration:

Elastic tissue stain of aortic media from a case of Marfan syndrome. Elastic fibers- black. Note the marked disruption of the elastic tissue fibers w/ areas completely devoid of elastic tissue.
LVH

d/t ventricular outflow tract obstruction
Atherosclerotic plaque rupture w/o superimposed thrombus- rupture of fibrous cap.
Atherosclerotic plaque rupture w/ superimposed thrombus w/ a special fibrin (red) stain
how old is this infarct?
1 day old. There is edema w/ early coagulative necrosis (pyknotic nuclei and hypereosinophilia) and beginning infiltration by neutrophils. Wavy appearance because the normal fiber below contract and pull on the infarcted fibers.
how old is this infarct?
3- days old. This is coagulative necrosis w/ loss of nuclei and cross striations. There is heavy infiltration by neutrophils.
how old is this infarct?
7-10 days. there if infiltration by macrophages which have phagocytized much of the necrotic cellular debris.
how old is this infarct?
3 weeks, viewed w/ a trichrome stain. there is granulation tissue with prominent BV. The wavy blue fibers represent early collagen deposition.
Senile calcific aortic stenosis- involving a previously normal aortic valve having the usually three cusps.
Mitral annular calcification
RHD

high powered few of antischkow cells. These are plump activated macrophages w/ very prominent chromocenters, which are pathognomonic for RF.
Acute rheumatic valvulitis superimposed on chronic RHD- mitral valve

Small vegetations of fibrin called verrucae. Previous episodes of RF have resulted in thickening of the leaflets as well as fusion of some of the chordae tendineae.
RHD

myocardium from a pt w/ RF exhibiting aschoff body.
Mitral valve exhibiting vegetations from a case of subacute endocarditis
acute endocarditis- aortic valve

arrow is pointing to a ring of abscesses which is a potentially very serious complication of acute endocarditis. These ring abscesses can penetrate into the ventricular septum causing conduction disturbances and arrhythmias or can penetrate through the left ventricular free wall resulting in cardiac tamponade.
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (trichrome stain)

Disorganized appearance called "myofiber disarray". Interstitial fibrosis secondary to loss of occasional cardiac myocytes d/t ischemia and apoptosis.
Lymphocytic myocarditis

Pattern usually seen w/ viral myocarditis
Hypersensitivity myocarditis

Numerous eosinphils w/n the inflammatory infiltrate. This pattern is usually seen w/ HSN reactions to various drugs, MC antibiotics
Giant cell myocarditis

scattered giant cells w/ extensive loss of cardiac myocytes. Giant cell myocarditis has a poor prognosis and the cause is unknown.
Chagas dz.

Black arrow is pointing to a myofiber which is distended w/ trypanosomes. Chagas dz- South Am.
Fibrinous pericarditis.

Shaggy appearing fibrinous exudate coating of the epicardial surface of the heart.
Constrictive pericarditis
VSD
Transposition of the great arteries