1. Leukoplakia.
LOW
HIGH
2. Fatty liver
LOW
HIGH
3. Kidney amyloidosis (Congo-red
staining)
LOW
HIGH
4. Nutmeg liver (liver in chronic venous
congestion).
LOW
HIGH
5. Lung hemosiderosis.
LOW
HIGH
6. Myocardial infarction
LOW
HIGH
7. Liver infarction.
LOW
HIGH
8. Mixed thrombus.
LOW
HIGH
9. Liver hemosiderosis in hemolytic
anemia.
LOW
HIGH
10. Metastatic calcification in
myocardium.
LOW
HIGH
11. Pigmented nevus of skin.
LOW
HIGH
12. Endometrial adenomatous
hyperplasia.
LOW
HIGH
13. Bronchopneumonia (focal
pneumonia).
LOW
HIGH
14. Lobar pneumonia.
LOW
HIGH
15. Duodenal ulcer.
LOW
16. Suppurative (phlegmonous)
appendicitis
LOW
17. Echinococcus multilocularis in liver
(alveolar hydatid disease)
LOW
18. Trichinella in skeletal muscle.
LOW
19. Miliary tubercles in lung.
LOW
20. Seleroma of larynx.
LOW
21. Hemangioma.
LOW
22. Non-keratinizing squamous cancer.
LOW
23. Gastric adenocarcinoma.
LOW
24. Polymorphocellular sarcoma
(rhabdomyosarcoma).
LOW
25. Melanoma
LOW
26. Coronary artery atherosclerosis.
LOW
27. Alterative-productive myocarditis.
LOW
HIGH
28. Pulmonary emphysema.
LOW
29. Miliary tuberculosis of kidney.
LOW
30. Portal cirrhosis.
LOW
31. Liver in lymphoid leukemia.
LOW
32. Hodgkin's lymphoma.
LOW
HIGH
33. Primarily contracted kidney.
LOW
HIGH
34. Extracapillary (rapidly progressive)
glomerulonephritis.
LOW
35. Chronic pyelonephritis ("thyroid
kidney")
LOW
36. Thyroid gland in Graves'
(Basedow's) disease.
LOW
37. Diabetic glomerulosclerosis.
LOW
38. Kidney in septicopyemia ("embolic
purulent nephritis").
Multiple abscesses in the kidney
cortex, marked congestion in
surrounding tissue. Microbial
emboli in the center of some of
abscesses.
LOW
39. Purulent meningitis.
LOW
40. Focal cardiosclerosis.
LOW
41. Diphtheritic tonsillitis.
LOW
42. Liver lipofuscinosis ("brown
atrophy").
LOW
43. Hashimoto's thyroiditis.
LOW
44. Kidney in cytomegalovirus
infection.
LOW
45. Hyaline membrane disease.
LOW
46. Liver in hemolytic disease of the
newborn.
LOW
47. Spleen in listeriosis.
LOW
48. Kidney cortical necrosis in DIC.
LOW
49. Polycystic kidney disease.
LOW
50. Breast cancer Metastasis to lungs.
LOW
LIST OF GROSS SPECIMENS FOR THE QUIZ
1. Amyloid-lipoid nephrosis
Amyloidosis is a rare disease characterized by a buildup of abnormal amyloid deposits in the body. Amyloid deposits
can build up in the heart, brain, kidneys, spleen and other parts of the body
Lipoid nephrosis is a disease characterized by an insidious onset, a chronic course, edema, oliguria, albuminuria,
changes in the protein and lipoids of the blood, and the deposit of lipoids in the kidney. It occurs alone, or in
combination with diffuse glomerulonephritis, or with amyloid degeneration of the kidney
By definition, there are not glomerular histologic changes or these are subtle (slight mesangial proliferation)
When there is hypercellularity is more probable to find IgM deposits (IgM nephropathy)
2. Hyalinosis of splenic capsule
HYALINOSIS is hyaline degeneration.
Colloquially referred to as “sugar-coated spleen” or “icing-sugar spleen”, it results from the deposition of collagen on
the capsular surface of the spleen, which may occur secondarily to inflammation of the peritoneal cavity. The spleen is
commonly affected and often referred to as sugar-coated spleen. The liver and heart are also sometimes affected and
referred to as frosted liver (or sugar-coated liver) and frosted heart respectively.
3. Pulmonary hemosiderosis
Hemosiderosis is a term used for excessive accumulation of iron deposits called hemosiderin in the tissues. The lungs
and kidneys are often sites of hemosiderosis. Pulmonary hemosiderosis (PH) is characterized by repeated episodes of
intra-alveolar bleeding that lead to abnormal accumulation of iron as hemosiderin in alveolar macrophages and
subsequent development of pulmonary fibrosis and severe anemia
4. Erosive gastritis
Erosive gastritis is gastric mucosal erosion caused by damage to mucosal defenses. It is typically acute, manifesting
with bleeding, but may be subacute or chronic with few or no symptoms.
Erosion: loss of superficial epithelium above muscularis mucosa, accompanied by hemorrhage
Variable changes include acute inflammatory infiltrate, extrusion of fibrinopurulent exudate into lumen, mucosal
sloughing, regenerative changes in nearby epithelium
Severe erosive disease may cause acute GI bleeds
5. Calculous cholecystitis
Calculous cholecystitis develops when the main opening to the gallbladder, the cystic duct, gets blocked by a gallstone
or a substance known as biliary sludge. Biliary sludge is a mixture of bile, a liquid produced by the liver that helps
digest fats, and small cholesterol and salt crystals. Variety of histologic findings, including variable amounts of
mononuclear cell predominant inflammation, mucosal changes including metaplasia, muscular hypertrophy and
transmural fibrosis.
6. Fatty liver (“goose liver”, “foie gras”)
Fatty liver disease (steatosis) is a common condition caused by having too much fat build up in your liver. There are
two types of fatty liver disease: non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease. The primary
risks include alcohol, type 2 diabetes, and obesity. Other risk factors include certain medications such as
glucocorticoids, and hepatitis C. Fatty change represents the intracytoplasmatic accumulation of triglycerides (neutral
fats). At the beginning, the hepatocytes present small fat vacuoles (liposomes) around the nucleus (microvesicular fatty
change). In this stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus.
In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, giving
characteristic signet ring appearance (macrovesicular fatty change). These vesicles are well-delineated and optically
"empty" because fats dissolve during tissue processing. Large vacuoles may coalesce and produce fatty cysts, which
are irreversible lesions. Macrovesicular steatosis is the most common form and is typically associated with alcohol,
diabetes, obesity, and corticosteroids
7. Nutmeg liver (liver in chronic venous congestion)
Nutmeg liver is the pathological appearance of the liver caused by chronic passive congestion of the liver secondary to
right heart failure. The liver appears "speckled" like a grated nutmeg kernel, from the dilated, congested central veins
(dark spots) and paler, unaffected surrounding liver tissue. When severe and longstanding, hepatic congestion can lead
to cirrhosis, a state described as cardiac cirrhosis. Increased pressure in the sublobular branches of the hepatic veins
causes an engorgement of venous blood, and is most frequently due to chronic cardiac lesions, especially those
affecting the right heart, the blood being dammed back in the inferior vena cava and hepatic veins. Macroscopically,
the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver
cells surrounding the central venule of the liver) to become deoxygenated compared to the relatively better-oxygenated
periportal hepatocytes adjacent to the hepatic arterioles. This retardation of the blood also occurs in lung lesions, such
as chronic interstitial pneumonia, pleural effusions, and intrathoracic tumor.
8. Echinococcal liver cyst
Cystic echinocccosis (CE), also known as hydatid disease, is caused by infection with the larval stage of Echinococcus
granulosus, a ~2–7 millimeter long tapeworm found in dogs (definitive host) and sheep, cattle, goats, and pigs
(intermediate hosts). Larval oncospheres are released from eggs and are transported to liver by portal vein,
Oncospheres grow into cysts enlarging at slow pace of about 10 - 15 mm per year. Cysts are composed of
protoscolices and daughter cysts. Hydatid cysts located most often in the liver and lungs, and less frequently in the
bones, kidneys, spleen, muscles and central nervous system.
Liver The histological picture of the hydatid cyst in liver resembled to that in the lung. The cyst had a laminated
membrane revealing presence of numerous protoscolices from within or outside the brood capsule. The cyst wall was
surrounded by the adventitial layer which in turn was surrounded by the inflammatory cells comprising of eosinophils,
mononuclear cells and a few fibroblasts. The adjacent liver parenchyma showed haemorrhages. The laminated cysts
wall was soetimes surrounded immediately by macrophage cell layer followed by a layer of infiltrating cells of
eosinophils and mononuclear cells and then followed by fibroblastic cell layer
9. Cerebral cysticercosis
Cerebral cysticercosis is the result of infestation of the brain with the larval stage of the intestinal tape worm Taenia
Solium. Cysticerci may develop in skeletal and heart muscle, skin, subcutaneous tissues, the lungs, liver, and other
tissues, including the oral mucosa. Grossly these cysts are variably sized ranging from few mm to few cm. and contain
clear fluid. The cyst wall is pearly white and pulpy. Appears like soft coconut pulp. Scolex may be visible inside the
cyst as tiny white nodule. The fluid later turns opaque as the cyst degenerates and finally can be calcified
10. Scleroma
Systemic sclerosis (SSc) is a complex autoimmune connective tissue disease characterized by chronic and progressive
tissue and organ fibrosis with broad patient-to-patient variability. Some risk factors are known and include
combination of persistent Raynaud's phenomenon, steroid hormone imbalance, selected chemicals, thermal, or other
injuries. A scleroma is a hardened patch of tissue in the skin or mucous membranes. It most often forms in the head
and neck. The nose is the most common location for scleromas, but they can also form in the throat and upper lungs
rinous pericarditis (“hairy heart”). Systemic sclerosis is characterized by three distinct pathologic processes: fibrosis,
cellular/humoral autoimmunity, and specific vascular changes. Characterized by fibrosis, inflammation, increased
collagen and vasculitis, Can be part of CREST syndrome (Calcinosis, Raynaud phenomenon, Esophageal involvement,
Sclerodactyly, Telangiectasia)
11. Fibrinous pericarditis (“hairy heart”)
In fibrinous pericarditis, the pericardial texture is rough, granular, and has many fibrous adhesions. There are a number
of possible causes of fibrinous pericarditis, including myocardial infarction, uraemia, rheumatic fever, systems lupus
erythematosis, irradiation of the chest, trauma and (rarely) infections. The pericardium has been opened to display its
visceral and parietal layers and an enlarged heart. Both layers of pericardium are thickened and covered by a thick
shaggy fibrinous exudate.
12. Primarily contracted kidney
A diffusely scarred kidney in which the presence of abnormal fibrous tissue and ischemic atrophy leads to a reduction
in its size. Causes of contracted kidney• Chronic GN (granular appearance) • Chronic pyelonephritis (U-shaped scars) •
Benign nephrosclerosis (V-shaped scars). • Amyloidosis of the kidney. Irregular scarred cortical surface usually at
poles, dilated and blunted calyces, Dilated ureter; retraction and destruction of papillae with "U” shaped scars
13. Hydronephrosis
Hydronephrosis is swelling of one or both kidneys. Kidney swelling happens when urine can't drain from a kidney and
builds up in the kidney as a result. This can occur from a blockage in the tubes that drain urine from the kidneys
(ureters) or from an anatomical defect that doesn't allow urine to drain properly. Thin cortical rim of renal cortex due
to atrophy, more calyceal dilation if incomplete obstruction, since glomerular filtration is not suppressed.
14. Scirrhous gastric cancer
A rare type of stomach cancer that begins in the lining of the stomach and spreads to the muscles of the stomach wall.
This causes the wall of the stomach to become thick, hard, and rubbery, which leads to trouble digesting food. Also
called linitis plastica. The tumor demonstrates an infiltrative behavior, which instead of forming a bulky mass, rather
causes thickening and stiffening of the intestinal wall with foreshortening, luminal stenosis, rigidity and lack of
peristaltic activity (linitis plastica).
15. Uterine cancer
Endometrial cancer is a type of cancer that begins in the uterus. The uterus is the hollow, pear-shaped pelvic organ
where fetal development occurs. Endometrial cancer begins in the layer of cells that form the lining (endometrium) of
the uterus. Endometrial cancer is sometimes called uterine cancer. Endometrial carcinoma most frequently arises in the
corpus proper, but it may also originate in the lower uterine segment. There are no distinctive gross appearances to
differentiate individual subtypes (cell type). In low-volume disease, it is common to find no evidence of residual
disease after diagnostic endometrial curettage. Localized disease manifests as round, polypoid expansile masses that
are friable and often hemorrhagic. Diffuse involvement of the endometrium may show an indurated-appearing surface
without a visible exophytic component. Necrosis and hemorrhage may be seen. Foci of myometrial invasion generally
appear grossly as well-demarcated gray-white areas that are lighter in color than the surrounding uninvolved
myometrium. Extension from the surface lesion is commonly demonstrated.
6. Hodgkin lymphoma in para-aortic lymph nodes
Hodgkin's lymphoma is a type of cancer that affects the lymphatic system, which is part of the body's germ-fighting
immune system. In Hodgkin's lymphoma, white blood cells called lymphocytes grow out of control, causing swollen
lymph nodes and growths throughout the body. 4 subgroups (nodular sclerosis, mixed cellularity, lymphocyte rich,
lymphocyte depleted) with distinct clinical, morphologic and epidemiologic characteristics. nvolves lymph nodes
(cervical > axillary, mediastinal, paraaortic).
Section description:
Effacement of nodal architecture
Nodularity
Mixed inflammatory background (small lymphocytes, neutrophils, eosinophils, histiocytes)
May see scattered large Reed-Sternberg cells with multilobated nuclei and prominent nucleoli
17. Spleen in chronic myeloid leukemia
Splenomegaly is the most common physical finding in patients with chronic myelogenous leukemia (CML).
In more than 50% of the patients with CML, the spleen extends more than 5 cm below the left costal margin
at time of discovery. Splenomegaly, most likely because of extramedullary hematopoiesis, remains one of
the most important prognostic factors in CML patients at diagnosis. While the exact mechanisms leading to
hypersplenism vary somewhat based on the causative aetiology, the underlying pathophysiologic changes are
the same, including splenic congestion and hyper-functioning/hypertrophy. In the case of myeloproliferative
disorders, this is due to a combination of 1) pooling of higher numbers of circulating red blood cells; and 2)
extramedullary haemopoeisis (also known as myeloid metaplasia), which leads to an expansion of splenic
reticular elements.
18. Melanoma metastases in liver
Melanoma usually spreads through the blood circulation to the liver. The majority of liver metastases present as
multiple tumors. Liver metastases are sometimes present when the primary cancer is diagnosed, or it may occur
months or even years after the primary tumor is removed. Metastatic melanoma most often spreads to the lymph
nodes, brain, bones, liver or lungs, and the additional symptoms experienced at this late stage will depend on where the
melanoma has spread. Liver metastases may appear several years after resection of the primary tumor. FNA smears
will show pleomorphic cells with intranuclear inclusions, prominent nucleoli, and cytoplasmic melanin (absent in
amelanotic melanomas). Immunohistochemistry is sensitive and specific for the diagnosis of metastatic melanoma.
Useful markers include HMB-45, S-100 protein, MART-1, and tyrosinase.
19. Aortic atherosclerosis and thrombosis
Thromboembolism may occur when an atherosclerotic plaque from large or medium arteries becomes unstable, and
superimposed thrombi embolize. The thromboemboli tend to be single and tend to lodge in small or medium arteries,
resulting most often in stroke or transient ischemic attack. The surface is somewhat irregular, and there are areas of
pale tan to white admixed with dark red areas. The thrombus often has the outlines of the artery in which it formed.
Development of atherosclerosis follows a predictable path from initiation phase to progression and development of
lipid rich atheromatous plaque to complications leading to ischemic events.
Fatty streaks are flat yellow discoloration in the intima surface
Early plaque is raised yellow, well defined lesion, focal in distribution and irregular in shape
Complicated plaques show ulcers, protrusions and thrombus (
20. Acute myocardial infarction
Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. This is
usually the result of a blockage in one or more of the coronary arteries. In the clinical context, myocardial infarction is
usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. While the vascular
pathogenic mechanism is able to induce mainly coagulative necrosis, which is the specific necrosis of the acute
myocardial infarction, the toxic action of the smoking compounds develops all types of necrosis with myocardial
alterations variably combined among themselves.
The gross morphologic appearance of a myocardial infarction can vary. Patterns include:
• Transmural infarct - involving the entire thickness of the left ventricular wall from endocardium to epicardium,
usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%.
Isolated infarcts of RV and right atrium are extremely rare.
• Subendocardial infarct - multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall.
These do not show the same evolution of changes seen in a transmural MI.
Gross morphologic changes evolve over time as follows:
Time from
Onset
Gross Morphologic Finding
18 - 24 Hours
Pallor of myocardium
24 - 72 Hours
Pallor with some hyperemia
3 - 7 Days
Hyperemic border with central yellowing
10 - 21 Days
Maximally yellow and soft with vascular
margins
7 weeks
White fibrosis
21. Chronic cardiac aneurysm
A ventricular aneurysm is a blood-filled bulge that occurs as a result of an area of weakened tissue in the heart wall. In
most cases, ventricular aneurysms form as a result of damage from a previous heart attack, though they may also be
caused by defects present from birth. Most commonly, the pathogenesis of the aneurysms is due to noninflammatory,
medial degeneration of the elastic aortic wall. However, inflammatory destruction secondary to syphilis, bacterial
infection, noninfectious aortitis, or atherosclerosis can also be causative.
Increased proteolysis of extracellular matrix proteins is probably the mechanism of aneurysm formation, Matrix
metalloproteinase 1(interstitial collagenase), matrix metalloproteinase 2 (gelatinase A), matrix metalloproteinase 3
(stromelysin 1), matrix metalloproteinase 9 (gelatinase B), and matrix metalloproteinase 12 (macrophage
metalloelastase) are capable of degrading essentially all components of arterial wall matrix (elastin, collagen,
proteoglycans, laminin, fibronectin, etc.), and are present in elevated concentrations in aortic aneurysms, while there
are decreased levels of tissue inhibitors of matrix metalloproteinases
Gross description- An aneurysm is commonly defined as a localized dilatation exceeding the diameter of adjacent
normal segments by 50%,
22. Concentric myocardial hypertrophy
Concentric left ventricular hypertrophy is an abnormal increase in left ventricular myocardial mass caused by
chronically increased workload on the heart, most commonly resulting from pressure overload-induced by arteriolar
vasoconstriction as occurs in, chronic hypertension or aortic stenosis. Concentric cardiac hypertrophy occurs in
response to pressure overload and is characterized by thickening of the left ventricle walls and minimal LV dilatation.
Pressure overload occurs during isometric exercises, such as resistance training. There is marked concentric thickening
of the left ventricular wall causing reduction in lumen size
23. Cyst after cerebral hemorrhage
Arachnoid cysts are the most common type of brain cyst. They are often congenital, or present at birth (primary
arachnoid cysts). Head injury or trauma can also result in a secondary arachnoid cyst. The cysts are fluid-filled sacs,
not tumors.
Gross description
Variable size but may be vary large
Thin transparent wall with clear, colorless fluid
Cyst is distinct from leptomeninges and dura
24. Fibroplastic rheumatic endocarditis
This is an infection of the inner lining of the heart, and may occur when rheumatic fever has damaged the heart valves.
a post-infectious sequel of acute rheumatic fever resulting from an abnormal immune response to a streptococcal
pharyngitis that triggers valvular damage.
25. Renal infarctions in periarteritis nodosa
Polyarteritis nodosa is a rare multi-system disorder characterized by widespread inflammation, weakening, and
damage to small and medium-sized arteries. Blood vessels in any organ or organ system may be affected, including
those supplying the kidneys, heart, intestine, nervous system, and/or skeletal muscles. Although the exact cause of
polyarteritis nodosa is not known, it is clear that an attack may be triggered by any of several drugs or vaccines or by a
reaction to infections (either bacterial or viral) such as strep or staph infections or hepatitis B virus. PAN is
characterized by segmental, transmural necrotizing inflammation of muscular arteries, most commonly at points of
bifurcation. Unlike other vasculitic disorders, PAN does not involve postcapillary venules or veins. Lesions in all
stages of development and healing are usually present.
26. Focal pneumonia, fibrinous pleuritis
Depending on which lung lobe is affected, the pneumonia is referred to as upper, middle or lower lobe pneumonia. If
there are several multi-lobe focal inflammations in the lungs, the term focal pneumonia is used. multifocal pneumonia
can be caused by the same things that cause other types of pneumonia—viruses, bacteria, and fungi. The development
of pneumonia requires that a pathogen reach the alveoli and that the host defenses are overwhelmed by microorganism
virulence or by the inoculum size. Fibrinous pleuritis is the most common form of pleuritis. Viral- and bacterialinduced pneumonias will show a fibrinous pleuritis at the beginning and also localized to the areas of the underlying
pneumonia. In viral infections, hemorrhage can occur later on, leading to fibrinous-hemorrhagic pleuritis
27. Lobar pneumonia (gray hepatization stage)
Lobar pneumonia is a form of pneumonia characterized by inflammatory exudate within the intra-alveolar space
resulting in consolidation that affects a large and continuous area of the lobe of a lung. Most cases of lobar pneumonia
are community acquired and caused by Streptococcus pneumoniae. Other causes include Klebsiella pneumoniae,
Legionella pneumophila, Haemophilus influenzae, and Mycobacterium tuberculosis.
Lobar pneumonia is diffuse consolidation involving the entire lobe of the lung. Its evolvement can be broken down
into 4 stages as follows:
Congestion: This stage is characterized by grossly heavy and boggy appearing lung tissue, diffuse congestion,
vascular engorgement, and the accumulation of alveolar fluid rich in infective organisms. There are few red blood cells
(RBC) and neutrophils at this stage.
Red hepatization: Marked infiltration of red blood cells, neutrophils, and fibrin into the alveolar fluid is seen. Grossly,
the lungs appear red and firm akin to a liver, hence the term hepatization.
Gray hepatization: The RBC break down and is associated with fibrinopurulent exudates causing a red to gray color
transformation.
Resolution: Characterized by clearing of the exudates by resident macrophages with or without residual scar tissue
formation.
28. Chronic obstructive pulmonary emphysema
Emphysema, or pulmonary emphysema, is a lower respiratory tract disease, characterised by air-filled spaces
(pneumatoses) in the lung, that can vary in size and may be very large. The spaces are caused by the breakdown of the
walls of the alveoli and they replace the spongy lung parenchyma. Smoking (the main cause) Exposure to air pollution,
such as chemical fumes, dust, and other substances. Irritating fumes and dusts at work. A rare, inherited form of the
disease called alpha 1-antitrypsin (AAT) deficiency-related pulmonary emphysema or early onset pulmonary
emphysema. Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the
terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis.
Gross description
Hyperinflation or ballooning due to entrapment of the air from airway obstruction
Lungs may be overlapping the heart
Upper lobes are more involved
Centriacinar: sparse empty spaces with pigmentation (anthracosis) corresponding enlarged airspaces
Panacinar: airspaces are more or less evenly inflated throughout the secondary lobules
Paraseptal: inflated subpleural airspaces with thin walls
Bullous emphysema
Descriptive term regarding emphysematous lung with visible bullae upon gross examination
Bulla: an air filled space of 1 cm in diameter within the lung which has developed because of emphysematous
destruction of the lung parenchyma
29. Chronic gastric ulcer
A peptic ulcer is a sore on the lining of your stomach, small intestine or esophagus. A peptic ulcer in the stomach is
called a gastric ulcer. The most common causes of peptic ulcers are infection with the bacterium Helicobacter pylori
(H. pylori) and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil, Motrin IB,
others) and naproxen sodium (Aleve). Stress and spicy foods do not cause peptic ulcers. The continuous mucosal
injury due to long-standing infection, leads to atrophy of stomach. This continuous pathological process results in
erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous
replacement.
30. Phlegmonous appendicitis
When an inflamed appendix perforates, the infection is localized by the omentum and bowel loops which present as an
appendiceal mass or phlegmon. Appendiceal phlegmon is considered to be sequelae to acute appendicitis which
presents as an appendiceal mass composed of the inflamed appendix, the adjacent bowel loops, and the greater
omentum. Appendicitis is thought to result from obstruction of the appendiceal lumen, typically by lymphoid
hyperplasia but occasionally by a fecalith, foreign body, or even worms.
Gross description
Gross and microscopic extent of inflammation may not correlate
Inflammation may involve entire appendix or only a segment
Appendix may appear grossly normal when inflammation is limited to the mucosa and submucosa
Appendix appears swollen and erythematous when inflammation extends into the muscularis propria
When the serosa is affected, a purulent exudate appears
Cut surface may show hyperemia or intraluminal or intramural abscess
Appendiceal wall may be completely necrotic in gangrenous appendicitis
Perforation in severe cases
31. Macronodular cirrhosis
Cirrhosis is a condition in which your liver is scarred and permanently damaged. Scar tissue replaces healthy liver
tissue and prevents your liver from working normally. As cirrhosis gets worse, your liver begins to fail.
MACRONODULAR CIRRHOSIS: Larger nodules separated by wider scars and irregularly distributed throughout the
liver usually due to an infectious agent such as viral hepatitis which does not diffuse uniformly throughout the liver.
Gross description
Multiple regenerative nodules throughout the entire liver, separated by bridging fibrosis
32. Biliary cirrhosis
Primary biliary cholangitis, previously called primary biliary cirrhosis, is a chronic disease in which the bile ducts in
your liver are slowly destroyed. Primary biliary cirrhosis is considered an autoimmune disease, which means it is
caused by the body's own immune system mistakenly attacking itself.
Gross description
Hepatomegaly early; cirrhosis late
33. Esophageal varices in portal hypertension
Esophageal varices are enlarged veins in the esophagus. They're often due to obstructed blood flow through the portal
vein, which carries blood from the intestine, pancreas and spleen to the liver. Esophageal varices are abnormal,
enlarged veins in the tube that connects the throat and stomach (esophagus). Causes of esophageal varices include:
Severe liver scarring (cirrhosis). A number of liver diseases — including hepatitis infection, alcoholic liver disease,
fatty liver disease and a bile duct disorder called primary biliary cirrhosis — can result in cirrhosis. Blood clot
(thrombosis). Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the
liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of
blood. The vessels can leak blood or even rupture, causing life-threatening bleeding.
Gross description
Varices may protrude into lumen, mucosa may be normal or inflamed
34. Kidney in acute renal failure
Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney
damage that happens within a few hours or a few days. AKI causes a build-up of waste products in your blood and
makes it hard for your kidneys to keep the right balance of fluid in your body. Causes of kidney failure. Kidney failure
can be the result of several conditions or causes. According to the National Kidney Foundation, the two most common
causes are high blood pressure and diabetes.
35. Chronic pyelonephritis
Chronic pyelonephritis is continuing pyogenic infection of the kidney that occurs almost exclusively in patients with
major anatomic abnormalities. Chronic forms of the condition are more common in people with urinary obstructions.
These can be caused by UTIs, vesicoureteral reflux, or anatomical anomalies. Chronic pyelonephritis is associated with
progressive renal scarring, which can lead to end-stage renal disease (ESRD). For example, in reflux nephropathy,
intrarenal reflux of infected urine is suggested to induce renal injury, which heals with scar formation
Gross description
Irregular scarred cortical surface usually at poles, dilated and blunted calyces
Dilated ureter; retraction and destruction of papillae with "U” shaped scars
36. Rapidly progressive glomerulonephritis (“large mottled kidney”)
Rapidly progressive glomerulonephritis (RPGN) is a disease of the kidney characterized clinically by a rapid decrease
in the glomerular filtration rate (GFR). The most common occurrence is in systemic lupus erythematosus. Other
associated diseases include inflammatory bowel disease, sclerosing cholangitis, autoimmune hepatitis, rheumatoid
arthritis, and Felty syndrome. Pathophysiology comprises a specific set of renal diseases in which an immunologic
mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement
membrane, mesangium, or capillary endothelium.
37. Purulent meningitis
Purulent meningitis refers to inflammation of leptomeninges occurring along with infection of the subarachnoid space
by various purulent bacteria. Clinically, purulent meningitis usually manifests as fever, vomiting, headache, and
meningeal irritation. The most common pathogens are Pneumococcus, Hemophilus influenzae, and Staphylococcus.
Bacterial meningitis is characterized by the entry of bacteria into the cerebrospinal fluid (CSF) and bacterial growth in
this compartment leading to inflammation within the CSF and the adjacent brain tissue.
38. Adrenal hemorrhage (Waterhouse-Friderichsen syndrome)
Waterhouse-Friderichsen syndrome (WFS) is a group of symptoms resulting from the failure of the adrenal glands to
function normally as a result of bleeding into the gland. WFS is caused by severe infection with meningococcus
bacteria or other bacteria, such as: Group B streptococcus. Pseudomonas aeruginosa. Streptococcus pneumoniae.
• Hemorrhagic necrosis of adrenal glands, usually due to bacteremia, classically Neisseria meningitides; also
Pseudomonas aeruginosa, pneumococci, staphylococcus and historically Haemophilus influenzae
•
Less common causes are burns, cardiac failure, hypothermia and birth trauma
Gross description
Glands are enlarged and hemorrhagic with extensive cortical and medullary necrosis
39. Pneumatosis of small intestine in E. coli infection
Pneumatosis intestinalis (PI) refers to the presence of gas within the wall of the small or large intestine. Pneumatosis is
found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular
pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma,
including the trauma of child abuse.
Gross description
Polypoid grape-like masses protrude through mucosa
Soft, bluish and often sessile, "bubble wrap" crackling noise while handling the specimen
40. Diphtheritic colitis in dysentery
Colitis is a chronic digestive disease characterized by inflammation of the inner lining of the colon. Infection, loss of
blood supply in the colon, Inflammatory Bowel Disease (IBD) and invasion of the colon wall with collagen or
lymphocytic white blood cells are all possible causes of an inflamed colon. Pseudomembranous colitis is inflammation
(swelling, irritation) of the large intestine. In many cases, it occurs after taking antibiotics. Using antibiotics can cause
the bacterium Clostridium difficile (C. diff) to grow and infect the lining of the intestine, which produces the
inflammation
Gross description
Yellow-white mucosal plaques or pseudomembranes; may resemble polyps or aphthoid ulcers of Crohn's disease
41. Septic endocarditis
Endocarditis occurs when germs, usually bacteria, enter your bloodstream, travel to your heart, and attach to abnormal
heart valves or damaged heart tissue. Fungi or other germs also may cause endocarditis The pathophysiology of
infective endocarditis comprises at least three critical elements: preparation of the cardiac valve for bacterial
adherence, adhesion of circulating bacteria to the prepared valvular surface, and survival of the adherent bacteria on
the surface, with propagation of the infected vegetation.
Gross description
Vegetations are seen attached to atrial aspect of AV valves and ventricular aspect of semilunar valves in relation to the
line of apposition
Large vegetations may extend into adjacent parts of cusp or leaflets, chordae tendinae or sinus of valsalva
Largest vegetation is seen in fungal infections
Colour varies from red to pink to yellow and may be soft or friable or firm
Surface is smooth, often irregular granular
Lesions may calcify with time after antibiotic treatment
42. Catheter sepsis: thrombo-endocarditis of right atrium предсердия
Non-bacterial thrombotic endocarditis (NBTE) is an uncommon pathological situation, which involves the presence of
bland, fibrin-platelet thrombi. It usually occurs at the endocardium of cardiac valves, in association with endothelial
injury and a hypercoagulative state. Pathological findings showed that NBTE caused by an operative scar on the
endocardium of the right atrium and sustained rheological stress in the right atrium due to compression from pectus
excavatum lead to recurrent thrombus formation.
43. Primary pulmonary tuberculosis complex with a mixed type of progression and
formation of primary cavity
Primary tuberculosis is characterized by a pulmonary parenchymal focus of infection that is typically associated with
regional hilar or mediastinal lymphadenopathy and that develops after initial exposure to tuberculosis. You can get TB
by breathing in air droplets from a cough or sneeze of an infected person. The resulting lung infection is called primary
TB. Most people recover from primary TB infection without further evidence of the disease. The infection may stay
inactive (dormant) for years. TB cavity formation occurs usually in the apices of the lungs or in the apical segment of
the lower lobes.
44. Miliary tuberculosis
Miliary tuberculosis is a potentially life-threatening type of tuberculosis that occurs when a large number of the
bacteria travel through the bloodstream and spread throughout the body. Caused by the airborne bacteria
Mycobacterium tuberculosis. Following exposure and inhalation of TB bacilli in the lung, a primary pulmonary
complex is established, followed by development of pulmonary lymphangitis and hilar lymphadenopathy.
Mycobacteremia and hematogenous seeding occur after the primary infection.
45. Tuberculosis of kidney
Renal TB is typically a disease of young and middle-aged adults. Most cases of renal TB arise by secondary
hematogenous spread of bacilli to the renal cortex from pulmonary lesions either at the time of initial TB infection or
due to late breakdown of an old caseous focus. Tuberculosis of the kidney and urinary tract is, like other forms of the
disease, caused by members of the Mycobacterium tuberculosis complex. The pathogenesis of renal tuberculosis
begins with the initial localization of the tubercle bacilli in the cortical glomeruli causing mechanical stress which lead
to alteration in cell morphology, increased rate of protein synthesis and proliferation of resident glomerular cells as
well as the infiltrating blood borne cells.
Gross description
Multiple cavities filled with yellow friable necrotic material
46. Infantile polycystic kidney disease ("sponge kidney")
Medullary sponge kidney, also known as Cacchi-Ricci disease, is a birth defect where changes occur in the tubules, or
tiny tubes, inside a fetus' kidneys. Consists of fluid-filled kidney cysts that may make the kidneys too big, or enlarged.
caused by a genetic change in the PKHD1 gene and is inherited in an autosomal recessive manner. ARPKD is caused
by mutation in the PKHD1 gene which codes for a protein called fibrocystin. Fibrocystin is thought to have a role in
renal collecting duct and biliary duct differentiation.
Gross description
Markedly enlarged kidneys with smooth surface
Small cysts in cortex and medulla
Dilated channels are perpendicular to cortical surface
Cysts are present in medulla (collecting ducts)
47. Multiple congenital malformations
Multiple congenital anomalies (MCAs) are defined as two or more unrelated major structural malformations that
cannot be explained by an underlying syndrome or sequence. The two most common genetic causes of congenital
anomalies are single-gene defects and chromosomal abnormalities.
48. Hydro-microcephaly in toxoplasmosis
Congenital toxoplasmosis is a disease that occurs in fetuses infected with Toxoplasma gondii, a protozoan parasite,
which is transmitted from mother to fetus. It can cause miscarriage or stillbirth. gondii occurs primarily from ingestion
of inadequately cooked meat containing cysts or from ingestion of oocysts derived from food or water contaminated
with cat feces. Toxoplasma gondii infects a variety of vertebrate hosts, including humans. Transplacental passage of
the parasite leads to congenital toxoplasmosis. A primary infection during the first weeks of gestation causes vertical
transmission at low rate, although it causes major damage to the embryo. Babies born with toxoplasmosis can
develop hydrocephalus, when cerebrospinal fluid that normally circulates through the brain's ventricles backs
up and damages the brain.
49. Multiple uterine fibromyoma
Fibroids range in size from seedlings, undetectable by the human eye, to bulky masses that can distort and enlarge the
uterus. You can have a single fibroid or multiple ones. In extreme cases, multiple fibroids can expand the uterus so
much that it reaches the rib cage and can add weight. Causes: Genetic changes. Many fibroids contain changes in
genes that differ from those in typical uterine muscle cells.
50. Hydatidiform mole
A molar pregnancy — also known as hydatidiform mole — is a rare complication of pregnancy characterized by the
abnormal growth of trophoblasts, the cells that normally develop into the placenta. There are two types of molar
pregnancy, complete molar pregnancy and partial molar pregnancy. A molar pregnancy is caused by an abnormally
fertilized egg
51. Fetal asphyxia
Perinatal asphyxia, or birth asphyxia, results from an inadequate intake of oxygen by the baby during the birth
process — before, during or just after birth. Some causes of birth asphyxia include: Too little oxygen in the mother's
blood before or during birth. Problems with the placenta separating from the womb too soon. Very long or difficult
delivery. The pathophysiology of asphyxia generally results from interruption of placental blood flow with resultant
fetal hypoxia, hypercarbia, and acidosis.
52. Hepatosplenomegaly in hemolytic disease of newborn
Hepatosplenomegaly (HPM) is a disorder where both the liver and spleen swell beyond their normal size, due to one of
a number of causes. infection, such as hepatitis C, syphilis, or sepsis from a significant bacterial infection. chronic liver
disease with portal hypertension. cancers, such as amyloidosis or sarcoidosis. HIV. Hepatosplenomegaly in a young
child can be an ominous physical finding, potentially representing a metabolic, malignant, or infectious process.
Common causes of hepatosplenomegaly in children can be summarized as follows: newborns: storage disorders and
thalassemia. infants: liver unable to process glucocerebroside, which can lead to severe damage to the central nervous
system. older children: malaria, kala azar, enteric fever, and sepsis
53. Cephalohematoma
Cephalohematoma is an accumulation of blood under the scalp. This type of birth injury occurs when pressure on a
baby's head ruptures blood vessels in the scalp. The cause of a cephalohematoma is rupture of blood vessels crossing
the periosteum due to the pressure on the fetal head during birth. During the process of birth, pressure on the skull or
the use of forceps or a vacuum extractor rupture these capillaries resulting in a collection of serosanguineous or bloody
fluid.
54. Wilms’ tumor (nephroblastoma)
Wilms tumor (also called Wilms' tumor or nephroblastoma) is a type of childhood cancer that starts in the kidneys. It is
the most common type of kidney cancer in children. Doctors have found that some Wilms tumors have changes in
specific genes: A small number of Wilms tumors have changes in or loss of the WT1 or WT2 genes, which are tumor
suppressor genes found on chromosome 11. Changes in these genes and some other genes on chromosome 11 can lead
to overgrowth of certain body tissues.
Gross description
Usually large, solitary, spherical mass, sharply demarcated from the renal parenchyma, distorting kidneys contours
In ~10% multinodular
In primarily operated cases, tumor is gray-white or pink-gray in color, lobulated, soft and friable
Some tumors may have a prominent cystic appearance
In pretreated cases, hemorrhage and necrosis are usually extensive