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160 Cards in this Set

  • Front
  • Back
hamartoma
Histo. Reveals islands of cartilage and respiratory epithelium
Hamartoma
Gross photos showing the benign lung tumor consisting of mostly cartilage.
Round, coin-like laesions seen on x-ray
Malignant Mesothelioma
Arises from visceral or parietal pleura tumor mass encircles/encases the lung Asbestos exposure is a risk factor
malignant mesothelioma
Arises from visceral or parietal pleura tumor mass encircles/encases the lung Asbestos exposure is a risk factor
Ferruginous bodies
Ferruginous bodies
bronchial carcinoid tumor
Tumors are of neuroendocrine origin and may secrete Serotonin as well as other chemical compounds causing flushing, diarrhea, wheezing, salivation
bronchial carcinoid tumor
Tumors are of neuroendocrine origin and may secrete Serotonin as well as other chemical compounds causing flushing, diarrhea, wheezing, salivation
bronchial carcinoid tumor
Tumors are of neuroendocrine origin and may secrete Serotonin as well as other chemical compounds causing flushing, diarrhea, wheezing, salivation
bronchial carcinoid tumor
Left: spherical, pale mass in lumen of a bronchus Right: histo. Reveals small, rounded, uniform nuclei and moderate cytoplasm Most Common site- appendix
fibrous plaque
fibrous plaque
atherosclerosis of aorta
cholesterol emboli
see needles in middle?
Atherosclerosis on H&E
Foam cells and fibrous tissue
Atherosclerosis
Thickening of walls of artery due to atherosclerosis. Fibrous plaques cause narrowing.
fatty streaks- precursor to Atherosclerosis
Fatty streaks: macrophages w/cholesterol
Result from macrophages taking up LDL and oxidizing it
Atherosclerotic plaque
Atheroma: cholesterol clefts and ulceration with hemorrhage.
cholesterol needles and foam cells
Severe atherosclerosis
Intimal hyperplasia, cholesterol deposits, intimal thickening and ulceration.
Ruptured plaque w/thrombus
Recent thrombus in narrowed coronary artery. Atheromatous plaque – see the cholesterol needles?
see foam cells and cholesterol clefts
Atheroma: accumulation in artery walls made up of foamy macrophages, cell debris, lipid, and fibrous tissue.
atherosclerotic coronary a.
Narrowing of the lumen from an atherosclerotic plaque. Can lead to angina, ischemia, infarction.
bad coronary narrowing
Severe narrowing. Large area of calcification due to long standing atherosclerotic disease – appears bluish on H&E.
Atherosclerotic coronary
Thrombosis and recanalization leaving two small lumens. We know it’s atherosclerotic b/c there are cholesterol clefts and lots of fibrous connective tissue in the walls.
contraction bands
The earliest change histologically seen with acute myocardial infarction in the first day is contraction band necrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Note the many irregular darker pink wavy contraction bands extending across the fibers.
early mi
- Extensive hemorrhage
- The myocardial fibers have dark red contraction bands extending across them.
- The myocardial cell nuclei have almost all disappeared.
- There is beginning acute inflammation.
Another sign of an mi: wavy fibers
Stopped beating due to lack of perfusing
coagulation necrosis
Neutrophils and necrotic fibers.
3-4 day old MI
Lots of inflammatory cells! Myocardial fibers are necrotic and outlines between them barely visible
1-2 week MI
Normal myocardial fibers at top. Marophages between fibers and capillaries.
Little collagenization
Mi w/neutrophilic infiltrate
acute MI
3-5 day mi
Acute MI – dead cells
acute MI
old MI scar tissue
old MI scar
Old MI-
The myocardium beneath the endocardial surface at the top demonstrates pale fibrosis with collagenization following healing of a subendocardial myocardial infarction.

The heart is opened to reveal the left ventricular free wall on the right and the septum in the center.

There has been a remote myocardial infarction that extensively involved the anterior left ventricular free wall and septum.

The white appearance of the endocardial surface indicates the extensive scarring.
Old MI
Acute MI (Right; heavy infiltrate)
Old MI ; collagen)
Both are MI's
Top
The center is tan with surrounding hyperemia.

The infarction is "transmural" in that it extends through the full thickness of the wall.
Bottom
The center of the infarct contains necrotic muscle that appears yellow-tan.
Surrounding this is a zone of red hyperemia.
Remaining viable myocardium is reddish- brown.
Ruptured MI showing coagulation necrosis of the myocardial fibers, and the neutrophils which have come in to be sure the area is not infected with bacteria. Both the cell death itself and the neutrophil enzymes weaken the tissue.
rupture MI
the rupture point, as a deep mark surrounded by brighter red where the blood spread out through the epicardial fat.
ventricular aneurysm (seen) bottom right
Aneurysm: the wall bulges out. The fibrous scar has ballooned out. Stasis allows mural thrombus.
Cor Pulmonale
Any right-heart problem resulting from increased pulmonary vascular resistance (usually poor ventilation, less often fibrosis or primary vascular problems).

The right ventricle undergoes hypertrophy ("Feel that sternal heave!"), dilates, loses its familiar crescent shape and becomes more rounded, and eventually fails. The polycythemia that accompanies hypoxia make the blood more viscous and prone to clot.
Coal Workers Lung
Microscopic pathology
Aggregates of carbon-laden macrophages within a reticulin network
No dense fibrosis
Mild focal stretching of air-spaces ("emphysema") around the bronchiole
Coal Workers Lung
Microscopic pathology
Aggregates of carbon-laden macrophages within a reticulin network
No dense fibrosis
Mild focal stretching of air-spaces ("emphysema") around the bronchiole
Coal Workers Lung
Microscopic pathology
Aggregates of carbon-laden macrophages within a reticulin network
No dense fibrosis
Mild focal stretching of air-spaces ("emphysema") around the bronchiole
Anthracosis (carbon pigment)
Athracosis
Microscopic pathology
What you’re looking for:
Aggregates of carbon-laden macrophages within a reticulin network
No dense fibrosis
Mild focal stretching of air-spaces ("emphysema") around the bronchiole
progressive massive fibrosis
Variously defined to be many nodules 1 cm across or larger and/or one or more circumscribed areas of dense black scar-like tissue, usually in an upper lobe
In the US, in the absence of silicosis, PMF is uncommon, affecting less than 1% of those exposed to coal dust…but there’s plenty of PMF in poor nations
"Fibrosis" is a misnomer because there’s not as much collagen in these lesions as you'd find in a scar or a silicotic nodule (only 20-30% of the lesion is collagen; coal = up to 20% of the lesion)
Etiology of PMF is still obscure, but is probably immune-mediated and caused by the carbon itself
PMF is progressive and lethal; death usually occurs within a few years
No treatment
Progressive Massive Fibrosis (PMF)
Variously defined to be many nodules 1 cm across or larger and/or one or more circumscribed areas of dense black scar-like tissue, usually in an upper lobe
In the US, in the absence of silicosis, PMF is uncommon, affecting less than 1% of those exposed to coal dust…but there’s plenty of PMF in poor nations
"Fibrosis" is a misnomer because there’s not as much collagen in these lesions as you'd find in a scar or a silicotic nodule (only 20-30% of the lesion is collagen; coal = up to 20% of the lesion)
Etiology of PMF is still obscure, but is probably immune-mediated and caused by the carbon itself
PMF is progressive and lethal; death usually occurs within a few years
No treatment
Coal macules in Coal workers lung
progressive massive fibrosis
Dense, black, scar-like tissue
CAplans
Auto-immune disease (rheumatoid arthritis, systemic lupus, scleroderma, polymyositis-dermatomyositis, etc.) with an inorganic pneumoconiosis
Sometimes rheumatoid nodules present in the lungs
CAplans
Auto-immune disease (rheumatoid arthritis, systemic lupus, scleroderma, polymyositis-dermatomyositis, etc.) with an inorganic pneumoconiosis
Sometimes rheumatoid nodules present in the lungs
Silocosis
Tetrahedral crystals of silicon dioxide; tetrahedral configuration essential to fibrogenicity
How silica causes fibrosis (exact mechanism unknown)
Hydroxyl groups on the surfaces of the crystals are arranged to interact efficiently with the -NH3 and -PO4 groups in lipids (contact catalysis)
Free radical formation with peroxidation of membrane lipids is probably also involved
Silocosis
Tetrahedral crystals of silicon dioxide; tetrahedral configuration essential to fibrogenicity
How silica causes fibrosis (exact mechanism unknown)
Hydroxyl groups on the surfaces of the crystals are arranged to interact efficiently with the -NH3 and -PO4 groups in lipids (contact catalysis)
Free radical formation with peroxidation of membrane lipids is probably also involved
Silicosis
Seems mostly to affect macrophages
Classic model: macrophage (sometimes a neutrophil) ingests an inhaled silica particle => taken into phagolysosome => crystal disrupts the phagolysosome membrane, releasing the hydrolytic enzymes and killing the phagocyte => breakdown products of macrophages are chemotactic for other phagocytes and finally promote collagen formation
Current thinking focuses instead on inappropriate production of interleukin 1 and other factors by macrophages following contact with silica
Silocosis
Tends to be worst at the top of the lungs because that’s where more of the air goes
Gross pathology: Pleural adhesions, silicotic nodules, eggshell calcifications in lung and lymph nodes, silicotic nodules around the respiratory bronchioles
Silicotic nodule consists of
Concentric whorls of dense collagen with some silica, surrounded by...
Cellular connective tissue without silica, surrounded by...
Irregular, loose connective tissue with macrophages, epithelioid cells, and abundant silica (continuing growth)
silicosis
silicosis sometimes looks like anthracosis and TB because it is
silicosis on top right is anthracosilicosis
asbtestosis
Gross pathology: Marked pulmonary interstitial fibrosis
Unlike silicosis, fibrosis is diffuse rather than nodular, involving mostly the alveolar septa
Large, dense fibrous plaques form on both parietal and visceral pleura
asbestosis pleural plaques
asbestosis pleural plaques
asbestosis
Asbestos bodies ("ferruginous bodies") are characteristic; golden-yellow beaded rods formed when asbestos (or talc, or other) fibers are coated by protein in the body; most plentiful beneath the pleural surfaces
Granulomas form early in involved areas, but undergo fibrosis by autopsy
asbestosis
Asbestos bodies ("ferruginous bodies") are characteristic; golden-yellow beaded rods formed when asbestos (or talc, or other) fibers are coated by protein in the body; most plentiful beneath the pleural surfaces
Granulomas form early in involved areas, but undergo fibrosis by autopsy
asbestosis
Asbestos bodies ("ferruginous bodies") are characteristic; golden-yellow beaded rods formed when asbestos (or talc, or other) fibers are coated by protein in the body; most plentiful beneath the pleural surfaces
Granulomas form early in involved areas, but undergo fibrosis by autopsy
asbestosis
Asbestos bodies ("ferruginous bodies") are characteristic; golden-yellow beaded rods formed when asbestos (or talc, or other) fibers are coated by protein in the body; most plentiful beneath the pleural surfaces
Granulomas form early in involved areas, but undergo fibrosis by autopsy
mesothelioma
“Spaghetti" microvilli on EM
mesothelioma
Biphasic tumor:
berylliosis
The lesions are practically identical to those of sarcoidosis (i.e., non-caseating granulomas)
berylliosis
The lesions are practically identical to those of sarcoidosis (i.e., non-caseating granulomas)
Farmer's lung
Sensitive to spores from moldy hay, etc.
Non-farmers can get a similar disease from heat-loving bacterial spores in air-conditioners, cardboard, etc
Farmer's lung
farmers lung
(organic pneumonitis)
farmers lung (organic pneumonitis)
World Trade Center Lung
What congenital problem do we see here?
Transposition of Great Vessels
What congenital heart abnormality is this?
VSD
What congenital heart abnormality is this?
VSD
What congenital heart abnormality is this?
VSD
Which shows a congenital abnormality?
ASD: Patent Foramen Ovale
Right: probe patent foramen ovale
Left: Paradoxical embolus: thrombus from R to L
What is wrong with this baby's heart bro?
ASD
Whats going on yo?
ASD
Coarctation of the Aorta
associated w/Turner’s syndrome
Infantile type (PREductal): occlusion proximal to ductus arteriosus (between subclavian a and ductus arteriosus) causes heart failure in womb
Adult type (POSTductal): distal to ductus arteriosus and lower half of body is under-perfused. Branch vessels off aorta get increased blood flow.
whats going on with this heart g?
bicuspid aortic valve
left ventricular hypertrophy
Cardiac hypertrophy: “boxcar” nuclei and thick fibers.
Athlete’s heart. Left ventricle wall is remarkable hypertrophied.
What type of cardiac hypertrophies am I describing?
1. pumping against increased resistance (afterload) but emptying ok. Thick wall, chamber not too dilated, empties
2. Can’t empty properly, Too much blood, refills, or just can’t keep up
Thick wall, chamber very dilated, doesn’t empty
3. Athlete’s heart, Thick wall, chamber can fill and empty well
4. Uneven fiber enlargement, scrambling of fibers.
1. Concentric:
2. Eccentric
3. Physiologic:
4. Hypertrophic cardiomyopathy:
Left side CHF
(from pulmonary edema),
heart slide
Left side CHF
includes pigment laden macrophages
Hypertensive Hypertrophy
heart slide
Pulmonary edema from heart failure: Hemosiderin laden macrophages
What do these three often associate with?
Right sided heart failure
Top right- nutmeg liver
MYOCARDITIS
look for single fiber necrosis
Heart slides
Viral myocarditis
Note infiltration of lymphocytes and plasma cells in the interstitial space (between muscle fibers).  The nuclei and cross striations of the cytoplasm are well preserved.
heart slide
Myocarditis: cellular infiltrate and necrosis
Heart slide
myocarditis, notice the lymphocytes in between muscle fibers
Myocarditis: severe inflammation!
Coxsackie B myocarditis
The interstitial lymphocytic infiltrates shown here are characteristic for a viral myocarditis,.
heart slide
Chagas casuing myocarditis
Accumulation of round granules in the cytoplasm of myocyte.
heart disease
Chagas
Accumulation of round granules in the cytoplasm of myocyte.
heart slides
Chagas, Accumulation of round granules in the cytoplasm of myocyte.
heart
toxoplasmosis
heart
toxoplasmosis
heart
Giant cell myocarditis
heart
Giant cell myocarditis
heart
Giant cell myocarditis
heart
Giant cell myocarditis
heart
dilated cardiomyopathy
Dilated cardiomyopathy: heart is very enlarged and flabby
Dilated L ventricle and fibrosis of subendocardium.
heart
hypertrophyic cardiomyopathy
heart
hypertrophyic cardiomyopathy
heart
hypertrophyic cardiomyopathy
heart
Restrictive-infiltrative-obliterative ("stiff heart"; amyloid) Cardiomyopathy
What do you see here champ?
Hypertrophic Cardiomyopathy - LV Hypertrophy: IV septum is disproportionately thick.
HEART
Amyloid Heart: deposits of pink material b/w myocardial fibers
HEART
Amyloid heart: Congo Red stain – amyloid stains orange red, and w/polarized light has apple-green birefringence
HEART- prussian blue stain
Hemochromatosis, with excessive iron deposition, can occur in the heart as shown here microscopically with Prussian blue iron stain.
The excessive deposition of iron leads to heart enlargement and failure similar to a cardiomyopathy, making hemochromatosis a form of "restrictive" cardiomyopathy.
heart
Pericarditis
heart
(Atrial) myxoma
heart
Metastatic Melanoma
Berry aneurysms
found in brain
AV fistula aneurysms
Tangle of medium vessels
Vein tends to aneurysm
MC in brain can cause
subarachnoid hemorrhage
Shunts blood away from tissues
monckingbergs
vessel
Monckenberg sclerosis
Calcified elastic in vessels
Non-disease
Hyaline arteriolar sclerosis
Narrows lumen of arteriole (can’t dilate or constrict)
4 causes:
↑BP, hyperglycemia, radiation, FSGN (renal)
hyperplastic arteriolar sclerosis
“onion skinning”
Concentric thickening probably endothelial cells failing to apoptose
Hyperplastic Arteriolar Sclerosis
hyperplastic arteriolar sclerosis
“onion skinning”
Concentric thickening probably endothelial cells failing to apoptose
hyperplastic arteriolar sclerosis
“onion skinning”
Concentric thickening probably endothelial cells failing to apoptose
gangrene patient
Polyarteritis Nodosa
Polyarteritis Nodosa
Leukocytoclastic vasculitis
Wegener’s
granulomas and patchy necrosis
sore joints, blood in urine, gangrene
- loss of face
temporal arteritis
Macrophages eat the internal elastic membrane of the external carotid system
pt has headache and aches
temporal arteritis
could cause blindness
Macrophages eat the internal elastic membrane of the external carotid system
pt has headache and aches
temporal arteritis
could cause blindness
Macrophages eat the internal elastic membrane of the external carotid system
temporal artiritis
Takaysu’s Dz- “pulseless dz”
Aorta & its branches thicken
Think granulomas, lymphocytes, plasma cells, fibrosis, and contraction
Kawasaki’s
Kids, fever, Japanese ancestry
Sx:
fever (will last more than five days)
non-purulent conjunctivitis in both eyes
rash
red cracked lips, strawberry tongue
red palms and soles- peeling
a big node in the neck
If it affects coronary a. = deadly
Buerger's Dx
small neurovascular bundles in the extremities become inflamed and undergo thrombosis
Must stop smoking!
Polys touching giant cells within thrombi
Raynaud’s Dz
Spasm & occlusion of arteries in fingers
white "pallor", then red "suffusion", then blue "cyanosis"
Triggered by cold weather
Tx with CCB & gloves!
aortic dissection
Blood pushed through layers of aortic vessel
aortic dissection
Blood pushed through layers of aortic vessel
aortic dissection
Blood pushed through layers of aortic vessel
Thrombophlebitis
Thrombosis of deep vein (usually leg – DVT)
Pain & swelling
Milk leg- cuz of prego
Budd-chiari- of hepatic veins
Trousseau’s migratory thrombophlebitis- affects first one vein, then another– cuz of pancreas cancer
Lymphangitis
Vena Cava Syndrome
Left superiorVC- Compression usually lung cancer HA dusky skin in the head, upper extremities, and upper chest

Right inferiorVC- cancer in para-aortic lymph nodes.Dusky lower bodies and unusual patterns of collateral circulation
angiosarcoma
Karposi’s Sarcoma
In immunocompromised patients with low T count (think AIDS)
Herpes virus 8 is the cause
Will go away if T cell counts get higher
Lymphangioma
lymphangiosarcoma
MC in upper extremities
Starts as purple bruise gets worse
Called Stewart-Treves syndrome – if after mastectomy (olden days complication)
Thrombotic Thrombocytopenic Purpura
Rbc fragments