Oral

candidiasis
Macros : Superficial curdy,
gray-white membranes
that easily wipe off
(pseudomembranous
candidiasis) or painful
erosions (erythematous
candidiasis)
Micros : PAS+ hyphae
within keratin layer in
neutrophilic
background; prominent
inflammatory infiltrate
along the lamina propria
 Oral ulcer
Macros : Single or
multiple, shallow,
hyperemic ulcerations
covered by a thin
exudate with
hyperemic rim
Micros : Initially
mononuclear infiltrate,
then neutrophilic
infiltrate from
secondary bacterial
infection
 Gastric ulcer akut
Macros : 90% < 4 cm, 50% < 2cm,
clean base (due to peptic
enzymes), surrounded by
erythematous mucosa, may see
blood vessel in ulcer base
Micros : Usually < 1 cm, often
multiple, small brown circular
ulcer base (digested blood)
anywhere in stomach.
No induration of margins of
ulcer - abrupt lesions with
normal adjacent mucosa; no
scarring or blood vessel
thickening.
 Gastric ulcer kronik
Macros : Usually sharply punched
out defect with straight walls,
NO heaped up margins.
Size doesnt predict
malignancy.
Micros : Muscle wall replaced by
fibrous tissue. Serosal fibrosis.
Hyperplasia of adjacent lymph
nodes.
Proximal mucosa may be
overhanging.
Distal mucosa may have
ladder-like configuration.
Accompanied by active and
chronic inflammation, unless
NSAID related.
 Proctitis
Macros : Sharply circumscribed, variable
encapsulation
Micros :
Histologically resembles sclerosing
adenosis/fibrocystic change of breast.
Composed of acini and ductal elements
embedded in densely sclerotic stroma
Characteristic finding is presence of large acinar
cells with abundant eosinophilic cytoplasmic
granules
May exhibit ductal epithelial proliferation
ranging from hyperplasia, atypia to DCIS-like
The stroma may show focal adipose tissue,
myxoid change, variable radial scar
Immunohistochemical studies are of limited
value
 Kongenital diapragmatic hernia
Defective closure of
diaphragm, usually
left sided
Hernia sac usually
contains all/part of
stomach
May cause newborn
respiratory
insufficiency
 gastritis
Micros :
Mild: modest edema of lamina
propria, vascular congestion, intact
epithelium, scattered neutrophils,
and hemorrhage in mucosa,
erosions with more severe disease
Moderate / severe: loss of
superficial epithelium above
muscularis mucosa, accompanied
by hemorrhage and variable acute
inflammatory infiltrate and
extrusion of a fibrinopurulent
exudate into the lumen, nearby
epithelium may show regenerative
changes
 Stenosis pyloric
Macros : Thickened pyloric
muscle resembling a fusiform
mass, 3-5 cm, that occludes
the pyloric channel
Micros :
Edema and inflammatory
changes in mucosa or
submucosa
Thickening primarily of
circular muscle, which
terminates abruptly distally
 Necrotizing
enterocolitis
Macros : mild GI disturbance or
fulminant illness with intestinal
gangrene, perforation, sepsis
Micros :
Early: mucosal edema,
hemorrhage, necrosis
Late: hemorrhagic and
gangrenous bowel wall, fibrous
strictures;often pneumatosis
cystoides intestinalis
After recovery, Paneth cell
hyperplasia; colon also shows
metaplastic Paneth cells
 Apendisitis
Macros :
Fibrinopurulent exudate on serosa,
prominent vessels
Lumen may contain blood-tinged pus
Variable perforation, mucosal ulceration,
fecalith or other obstructing agent
Micros :
Mucosal ulceration
Minimal (if early) to dense neutrophils in
muscularis propria with necrosis,
congestion, perivascular neutrophilic
infiltrate
Late: absent mucosa, necrotic wall,
prominent fibrosis, granulation tissue,
marked chronic inflammatory infiltrate in
wall, thrombosed vessels
 Disentri basiler
Patchy lesions with variable villus
abnormality, rarely severe
Increased chronic and acute
inflammatory infiltrate in
epithelium and lamina propria
Small intestinal bacterial
overgrowth: common cause of
chronic diarrhea and
malabsorption with either
villous blunting or normal
duodenal biopsy
 Divertikulitis
Micros : Acute or chronic inflammatory infiltrate
near base of diverticula; occasionally
granulomatous inflammation
 Hirchsprungs disease
Macros : Normal anus but small rectum and
anal canal without stool, dilated proximal
bowel
Micros :
No ganglion cells in submucosal or
myenteric plexus
No / reduced myenteric and muscular
interstitial cells of Cajal in rectosigmoid
colon
Thickening and hypertrophy of
nonmyelinated nerve fibers and muscularis
mucosa
Stercoral ulcers (sharply demarcated
shallow ulcers with mucosal inflammation
due to pressure of feces on obstructed
colon)
Fibromuscular dysplasia of arteries
between normal and diseased colon
Hypoganglionosis: arises between normal
and aganglionic bowel; reduced number of
ganglion cells (such as 10% of normal)
 Hemoroid
Macros :
Clinically four grades:
First degree, anal cushions that slide down past dentate line with straining at stool, that bleed with
defecation
Second, anal cushions that prolapse with straining, but reduce spontaneously
Third, hemorrhoids that remain outside of the anal canal unless manually replaced
Fourth, hemorrhoids that cannot be reduced
Micros :
Dilated, thick walled, congested submucosal vessels and sinusoidal spaces, often with thrombosis;
variable hemorrhage into connective tissue
Dilated spaces may show exuberant vascular proliferation confined to vessel known as papillary
endothelial hyperplasia
Internal hemorrhoids are lined by rectal or transitional mucosa, external hemorrhoids have a
squamous lining
Surface may show ulceration
Pale cells in epidermis resembling Paget cells (pagetoid dyskeratosis) in 68%, prominent in 22%,
likely related to trauma related to prolapse
Examination of hemorrhoids may reveal low or high grade squamous intraepithelial lesions,
invasive squamous cell carcinoma, rectal carcinoma, neuroendocrine tumors, melanoma,
lymphoma, inflammatory bowel disease, nonspecific granulomas, Herpes Simplex Virus infection,
syphilis
 Fissura perianal
Micros :
May be nonspecific; shows ulcerated
transitional or columnar mucosa
with acute and chronic
inflammation, granulation tissue,
reactive and regenerative epithelial
changes or foreign body giant cell
reaction
Anal fissures related to specific
etiology may show epithelioid cell
granulomas as in tuberculosis,
fungal infection or Crohn's disease
Lymphogranuloma venereum and
syphilis induced ulcers may show
intense inflammation rich in plasma
cells
 Fistula perianal
Macros :
Pathologist most commonly receives a fistula resection specimen which looks
either linear or completely maloriented and may have epithelial lining at one of its
edges
The lining may be skin or anorectal mucosa
May be helpful to blunt probe the fistula from the anal mucosal aspect (the
primary opening)
May be challenging to find the primary opening due to chronicity and scarring;
suggest looking at slightly stretched aspect of adjoining mucosa or viewing a small
area with dye that was used to track the fistula during the surgery
There may be many branched secondary openings and therefore a gentle probing
of an unfixed specimen may yield better information
Probing should be followed by longitudinal dissection of fistula with pediatric or
finer scissors along the inserted probe
Reviewing operative notes or preoperative radiological studies may be helpful
It is also helpful to photograph the specimen in an unfixed state and pay attention
to the mucosa adjoining the fistula to look for friable areas or ulcers in a setting of
inflammatory bowel disease
Usually there is limited mucosa; if mucosal ulcers are present, then submit the
entire area of friability and ulceration to exclude dysplasia associated with
inflammatory bowel disease
Must sample ulcerated areas to exclude a rare malignancy
Micros :
Histological features vary based on etiology, duration of disease and
presence of infection
Fistulous tract with mostly fibroconnective tissue with variable
scarring, neutrophilic microabscess, inflammatory granulation
tissue with reactive endothelial cells, fibroblastic proliferation,
granulomas, histiocytic response and foreign body type giant cells
Fibroblastic proliferation may be exuberant and mitotically active,
resembling pseudosarcoma
Focal squamous lining is uncommon
Must exclude viral cytopathic effects especially cytomegalovirus
May obtain special stains for myobacteria and fungal organisms
 Acute viral hepatitis
Clinical :
Phases: incubation, symptomatic preicteric, symptomatic icteric,
convalescence
Peak infectivity is at end of incubation period and early
symptomatic period
Preicteric phase: constitutional symptoms, malaise, fatigue, loss of
appetite; serum-sickness like syndrome in 10% (fever, rash,
arthralgias due to circulating immune complexes), enlarged and
tender liver, elevated serum aminotransferases
Icteric phase: may have abatement of severe symptoms (high fever,
shaking chills, headache, right upper quadrant pain), jaundice due
to conjugated hyperbilirubinemia (dark urine, light stools, pruritis),
increased prothrombin time
Icteric phase common in acute phase of hepatitis A, 50% of
hepatitis B, unusual in hepatitis C
Micros :
Irregular hepatic plates due to variability in hepatocyte size and inflammatory cells
Hepatocyte necrosis, portal and lobular lymphocytic inflammation and
regenerative activity
Hepatocyte death via apoptosis, acidophilic (Councilman-like) body formation,
ballooning degeneration or cytolysis (collapse of reticulin network where cells
have disappeared with appearance of lymphocytes or macrophages)
Infiltrate is usually lymphocytes, most prominent in lobules, then spills over into
periportal hepatocytes (interface hepatitis, more sinusoidal in hepatitis C, CMV,
EBV)
In resolving phase, portal lymphocytes and plasma cells are present with minimal
lobular inflammation
Kupffer cells contain hemosiderin and lipofuscin
Hepatocytes are present in irregularly thickened plates with occasional rosettes
and multinucleation
Report: degree of hepatocellular damage, presence of regenerative activity,
describe inflammatory and stromal response
 Hepatitis kronis :
Clinical :
Patients have a wide spectrum of clinical manifestations, from
asymptomatic to symptomatic decompensated cirrhosis
Many patients are asymptomatic, or have mild non specific complaints
such as fatigue
Physical findings are typically few; may include hepatomegaly or other
stigmata of chronic liver disease, such as palmar erythema
Patients with advanced cirrhosis may develop ascites or esophageal
varices
Serum enzyme levels usually fluctuate, but may be elevated 2x to 10x
Many patients with mild chronic hepatitis C have persistently normal
serum aminotransferase levels
Alkaline phosphatase and bilirubin levels are usually normal, except in
stages of hepatic decompensation
Micros :
Regardless of etiology, chronic hepatitis is characterized by these features, to variable degrees:
Portal inflammation
Interface hepatitis
Parenchymal inflammation and necrosis
Cirrhosis (in many cases)
Portal Inflammation:
A hallmark of chronic hepatitis, ranges from mild and patchy to prominent and diffuse
Lymphocytes are the predominant component, often with variable plasma cells
Minor component is scattered macrophages, neutrophils and eosinophils
Lymphoid follicles may be present, particularly in hepatitis C infection
Interface hepatitis:
Also known as piecemeal necrosis
An important feature of chronic viral hepatitis characterized by:
Mononuclear inflammatory infiltrate involving hepatocytes located at (and disrupting) the limiting plate
Injury or necrosis of periportal hepatocytes
Lobular necroinflammatory activity:
Hepatocyte necrosis is usually variable in severity and spotty in distribution
Apoptotic hepatocytes (acidophil bodies) are usually more centered on periportal areas, and mononuclear
cells tend to cluster around dying hepatocytes
Fibrosis:
Progressive fibrosis of limiting plate leads to enlargement of portal tracts and stellate periportal fibrous
extension
May lead to portal-portal or portal-central fibrous bridging, culminating in cirrhosis, which is usually
micronodular, or mixed micronodular and macronodular type
 Karsinoma hepatoseluler
Macros :
Unifocal, multifocal or diffusely infiltrative soft tumor,
paler than normal tissue, may be green due to bile
Extensive intrahepatic metastases are common
Snakelike masses of tumor may involve the portal vein
(35-80%), hepatic vein (20%) or inferior vena cava
(similar to renal cell carcinoma)
Hemorrhage and necrosis are common
Occasionally tumor is pedunculated (< 1%), usually on
posterior and inferior surfaces of right lobe
Liver usually cirrhotic, often enlarged
Micros :
Patterns are trabecular (most common) with 4+ cells surrounded by layer of
flattened endothelial cells; also clear cell, giant cell, pelioid (vascular lakes),
pseudoglandular (acinar with proteinaceous material or bile in lumina, may
resemble thyroid follicles), sarcomatoid, solid (compact)
Presence of sinusoidal vessels surrounding tumor cells is an important diagnostic
feature
Scanty stroma, from well-differentiated to bizarre (often within same tumor)
Cells are polygonal with distinct cell membranes, abundant granular eosinophilic
cytoplasm, higher N/C ratio than normal, round nuclei with coarse chromatin and
thickened nuclear membrane; may have prominent nucleoli
Common features are portal vein thrombosis, vascular invasion, mitotic figures
Variable: abundant fat, bile (5-33%), bile canaliculi, copper, intracellular hyaline
bodies (round or oval homogeneous eosinophilic hyaline bodies with surrounding
halo containing p62, 9%), intranuclear pseudoinclusions, Mallorys hyaline (Mallory
Denk bodies, 2-25%), no central veins, pale bodies consisting of fibrinogen
mimicking HBsAg-containing ground-glass change (6%); rarely is undifferentiated
Minimal desmoplasia
 Hapatic failure
Usually due to chronic liver disease; causes without overt hepatocellular necrosis are
Reyes syndrome, tetracycline toxicity, acute fatty liver of pregnancy
Symptoms: jaundice, hypoalbuminemia, elevated serum ammonia, fetor hepaticus
(musty body odor due to mercaptans from GI bacteria and methionine), palmar
erythema, spider angiomas, hypogonadism (men), gynecomastia (in men due to
impaired estrogen metabolism and increased serum estrogen)
Complications: multiple organ failure (respiratory failure with pneumonia and
sepsis; renal failure, coagulopathy due to reduction in functional Vitamin K dependent
coagulation Factors II, VII, IX, X
Hepatic encephalopathy: altered consciousness, rigidity, hyperreflexia, asterixis
(nonrhythmic, rapid extension-flexion movements of head and extremities),
associated with elevated serum ammonia
Hepatorenal syndrome: acute renal failure in patients with severe liver disease only;
due to decreased renal perfusion through unknown mechanism; educed urine output,
elevated serum BUN; kidney function improves with improving hepatic function; 80-
95% mortality; borderline renal insufficiency (Creatinine of 2-3 mg/dl) may persist for
months
Hepatic failure
 Pancreatitis
Macros :
Swollen, indurated, edematous or hemorrhagic/necrotic, yellow nodules represent
fat necrosis in pancreas, mesenteric and peritoneal fat
May spread to colon and cause ileus, stenosis, perforation, fistulas
Micros :
Classified as either acute interstitial or acute hemorrhagic types\
Acute interstitial: typically an acute inflammatory cell infiltrate admixed with
edema and fibrinous exudate
Acute hemorrhagic: patchy necrosis typically in a periductal or perilobular
distribution with a sparing of portions of the pancreas; diffuse interstitial edema
due to microvascular leakage, fat necrosis, neutrophils, acinar and blood vessel
destruction, interstitial hemorrhage
Also acinar cell homogenization, ductal dilation with mucinous or squamous
metaplasia, fibroblasts, thrombi in capillaries and venules
Initially neutrophils are present, then macrophages and later lymphocytes
Calcification occurs early and extensively