Laboratory: PRACTICALS 3 REVIEWER

Dr. Renan Navarro | April 26, 2019

Transcriber: MBA
LFM
Gastrointestinal Tract
NORMAL ESOPHAGUS and STOMACH, gross

● Take note:
○ Esophagus normally has white-to-tan mucosa
○ Stomach normally has prominent rugal fold
NORMAL ESOPHAGUS
Normal esophagus, endoscopy.
This picture shows the normal
upper GI endoscopic view
demonstrating the transition
from the pale white/pink-to-tan
squamous mucosa of the
esophagus to the darker pink
columnar mucosa of the
stomach at the
gastroesophageal junction.
Histologic Layers:
● Mucosa: stratified non-keratinized squamous
epithelium (→)
● Submucosa: contains minor mucous glands (↑) and
a duct surround by lymphoid tissue (←)
● Muscularis externa: predominantly voluntary
striated muscle to initiate swallowing in the upper
esophagus; involuntary smooth muscle in the lower
esophagus providing propulsive peristalsis of food
and liquid boluses
● Adventitia: not serosa because the esophagus is
not covered by a mesothelial covering
BARRETT ESOPHAGUS
● Gross: From normally pearl white, pale-tan,
mucosal surface, becomes salmon
colored
● Presence of intestinal metaplasia: Normal
squamous epithelial lining is replaced by
cuboidal or columnar epithelium with
goblet cells (metaplastic change),
dysplasia is present.
● Take NOTE: no goblet, no barrett

● Normal lining:
○ upper 2/3 – squamous epithelium
○ Lower 1/3-columnar epithelium
● In Barrett, upper third becomes columnar,
which is more resistant to acidic
environment of stomach.
● Benign
 BARRETT ESOPHAGUS

● Note the columnar epithelium to the left and the squamous epithelium at the
right. Also take note of the goblet cells (arrow) in the columnar mucosa.

● The intestinal metaplasia seen in Barrett results from chronic gastroesophageal

reflux disease (GERD).
● Most serious sequelae of Barrett: ADENOCARCINOMA (secondary to
glandular metaplasia and pronounced dysplasia).
ADENOCARCINOMA of the Esophagus

● Microscopically, note for the several glands infiltrating the muscularis layer
of the esophagus (round to ovoid with sharp lumen, lined by malignant
columnar epithelium).
● Presence of gland-like structures signifies infiltration. Normally, there
should be none.
● Adenocarcinoma is commonly seen in the LOWER 3rd of the esophagus.
ADENOCARCINOMA of the Esophagus

● You can observe here that the tumor has extended beyond muscularis
mucosa to invade the submucosa.
WELL- DIFFERENTIATED SQUAMOUS CELL
CARCINOMA of the Esophagus

Keratin pearl
WELL- DIFFERENTIATED SQUAMOUS CELL
CARCINOMA of the Esophagus
● Clue for malignant transformation:
○ Lacks orderly organization of the keratinocytes (you cannot
distinguish where is the granular layer, or the corneal layer..)
○ Presence of nests of squamous epithelial cells signifies invasion
of dermal layer
○ Presence of keratin pearls (well-differentiated)
○ Intercellular bridges (signifies that there is still adhesion molecules
present between cells)
● Most common site: MIDDLE THIRD
NOTES to Remember for Pathology of the Esophagus
● In Barrett Esophagus, Lower third is prone to metaplasia.
● Adenocarcinoma: LOWER THIRD, glandular structure
● Squamous Cell Carcinoma: MIDDLE THIRD, keratin pearl, NO
glandular structure

● Most common neoplasm of esophagus: LEIOMYOMA

○ Benign
○ Composed of smooth muscle cells

● Most common esophageal malignancy: SQUAMOUS CELL

CARCINOMA followed by ADENOCARCINOMA
Gastrointestinal Stromal Tumor,
Low Grade, Stomach

• GIST (Gastrointestinal Stromal Tumor)

• Origin: Interstitial cells of Cajal
• Microscopically: spindle shaped cells, round to ovoid
• Immunostain to confirm diagnosis: (+) CD117/C-Kit
Gastric Adenocarcinoma, Diffuse Type (Linitis
Plastica)
• Gross:
o Presence of Wall thickening
or hardening
o Maintained anatomical c-
shape when lifted. Normally,
it will sag.
• * Leathery and No infoldings
• Characteristic appearance:
LEATHER BOTTLE

• Microscopy:
o Signet ring cells –
accumulation of
intracytoplasmic mucin
→nucleus is pushed in the
periphery
Chronic Benign Peptic Ulcer
● Grossly:
○ Punched out border (smooth)
○ Round to oval with sharp demarcations
○ Margins at level with surrounding mucosa
○ Smooth/ Clean base
○ Absent overhanging ulcer edge which is present
in malignant ulcers

Histologic Appearance (Four layers of Ulcer):

a) Beneath is a zone of non-specific inflammatory
Additional Notes: infiltrates, neutrophils,
*Most common site: b) In the base of the ulcer, active granulation tissue with
pyloric area in the monocytes,
lesser curvature c) Base and margins have a superficial thin layer of
necrotic fibrinoid debris,
*Most common cause: d) Solid fibrous or collagenized scar. Also note for
H. pylori thickened blood vessel wall.
Chronic Benign Peptic Ulcer

(Four layers of Ulcer):

a) Beneath is a zone of non-specific
inflammatory infiltrates, neutrophils,
b) In the base of the ulcer, active
granulation tissue with monocytes,
c) Base and margins have a superficial
thin layer of necrotic fibrinoid
debris,
d) Solid fibrous or collagenized scar.
Also note for thickened blood vessel
wall.
Chronic Benign Peptic Ulcer

1
2

Layers of Peptic Ulcer

1- thin layer of necrotic fibrinoid debris
2 – zone of non-specific inflammatory infiltrates, predominantly
polymorphonuclear cells (neutrophils)
3 – granulation tissue with monocytes (chronic inflammatory infiltrates)
4 – solid fibrous or collagenized scar
*thickened-wall blood vessel
SMALL INTESTINES: Meckel’s Diverticulum
● True diverticulum
● Involves all layers of GIT (4 layers)
● Presence of outpouchings
● May contain heterotopic rests of
gastric/pancreatic tissue
● Microscopically: presence of
pancreatic acini underneath the
submucosa (not normally there)
● Complications because of
heterotopic rests:
○ Gastric → ulcer
○ Pancreas → autolysis of
adjacent tissues

● Organs of the body with only 3

layers:
○ Gallbladder (no submucosa)
Mixed Hemorrhoids (Gross)

• Dilated veins
• If lined by Squamous epithelium –
external hemorrhoids
• If lined by rectal epithelium –
internal hemorrhoids
• Complications :
- Hemorrhage
- Ulceration
- Thrombosis
- Infection
Microscopically, how will your differentiate internal from external hemorrhoids?
To differentiate external from internal hemorrhoid, begin by looking at the lining of the overlying tissue
(Left) lined by glandular structures (green arrow) = internal hemorrhoids
(Right) lined by squamous epithelium= external hemorrhoids
This specimen is mixed hemorrhoid, as both are present
*Hemorrhoid is just like Varicose veins
Crohn’s Disease vs. Ulcerative Colitis

*Extraintestinal
involvement is
present in both.
*Both can pose a
risk for malignant
transformation, but
take note that this
is only true for
Crohn’s Disease if
there is colonic
involvement.
Crohn’s Disease

Crohn’s Disease:
skipped lesions, can occur
in all parts of GIT, non-
Left picture. Creeping fat (arrow). Upper right.
Skip lesions (circled area) and serpentine ulcers caseating granuloma (*),
(arrow). Lower right. Cobblestone appearance of
mucosa (asterisk) with pus and linear ulcers (arrow)
transmural
Ulcerative Colitis

Ulcerative colitis : exclusive involvement of colon, broad based ulcers and

microscopically presence of plasmalymphocytic infiltrates. Encircled on the right
pictures are crypt abscesses
Irritable Bowel Syndrome (IBS) vs. Inflammatory
Bowel Disease (IBD) (nice to know)
INFLAMMATORY BOWEL DISEASE
Generally, 2 kinds: Crohn’s Disease (CD) and Ulcerative Colitis (UC)

Etiology and Pathogenesis:

1. Genetic Disposition
o NOD2 – susceptible gene in Crohn’s
o 50% concordance rate in monozygotic twins (CD)
o 16% concordance rate in monozygotic twins (UC)
2. Mucosal Immune Responses
o Polarization of helper T-cells to the TH1 type (CD)
o Th17-mediated disease in UC
3. Epithelial defects
o Epithelial tight junction-barrier function
4. Microbiota
o Bacteria = 1012 per ml in the GIT
Irritable Bowel Syndrome (IBS) vs. Inflammatory
Bowel Disease (IBD) (nice to know)
IRRITABLE BOWEL SYNDROME
• No demonstrable pathology
• Chronic relapsing abdominal pain, bloating, changes in bowel habits
• Related to stress (“maybe this can be an illness of medical students” lol)
• Even if symptoms are present, biopsy results will be normal. Hence, clinical
diagnosis should be done.

PATHOLOGY – psychologic stressors, diet, abnormal GI motility, etc. (can’t

pinpoint any particular cause)
CLINICAL FINDING – 20-40 yrs old
PATHOLOGIC FINDING – Normal GIT
DIAGNOSTIC CLINICAL CRITERIA
· Abdominal pain or discomfort at least 3 days per month over 3 months
· Improvement with defecation
· Change in stool frequency and form
POLYPS: NON-NEOPLASTIC vs. NEOPLASTIC
Non-Neoplastic – no dysplasia
o Juvenile/ retention polyp – cystic change, cystically dilated colorectal
glands
o Hyperplastic polyp – non neoplastic, cork-screw appearance of
rectal/colonic glands, tortuous glands

Neoplastic – presence of dysplasia (adenomatous change)

o Tubular Adenoma = with adenomatous change, tubular or round
glands
o Villous Adenoma= with fingerlike structures, dysplasia is obvious,
pseudostratification, visible nucleoli; has the greatest risk for
malignancy
o Tubulo-villous Adenoma= mixture of tubular glands and villous,
dysplasia,
o In Adenomatous polyps, the larger the polyp, the greater risk for
malignant transformation. (↑ SIZE = ↑ risk for MALIGNANCY)
o Recall: “-oma” = BENIGN; thus, Adenomas are benign.
POLYPS: NON-NEOPLASTIC

Juvenile / Retention Polyps

• in children <5y/o
• 80% occur in the rectum
• large; 1-3 cm, rounded, smooth, with a stalk
• cystically dilated glands in abundant lamina propria with
inflammatory cells/ ulceration
POLYPS: NON-NEOPLASTIC

Hyperplastic Polyps
• small (diameter: <5 mm), nipple-like protrusion from mucosa, sessile
• 6th-7th decade; single/ multiple;
• location: rectosigmoid
• composed of well-formed glands & crypts lined by non-neoplastic epithelial
cells with a serrated (saw-toothed) epithelial profile; corkscrew appearance
 POLYPS: NON-NEOPLASTIC

Inflammatory Polyps (not discussed)

• triad of rectal bleeding, mucus discharge, & inflammatory lesion of rectal
wall
• Note the granulation tissue, formation of blood vessels, inflammation, &
sometimes, cystically dilated glands
• cause: impaired relaxation of anorectal sphincter that creates a sharp/ acute
angle at the anterior rectal shell → abrasion & ulceration of mucosa → polyp
o ex: solitary rectal ulcer syndrome
POLYPS: NEOPLASTIC

Tubular Adenoma
• 75% show tubular architecture; most common
• mostly found in the colon
• smooth contour to coarsely lobulated; pedunculated/ sessile
• 1-2.5 cm; branching glands lined by tall columnar epithelium with fibromuscular &
vascular stalk devoid of neoplastic covering epithelium
• may see all degrees of dysplasia
 POLYPS: NEOPLASTIC

Villous Adenoma
• rectum & rectosigmoid
• usually large & sessile (diameter up to 10 cm)
• velvety/ cauliflower-like mass projecting above the normal mucosa
• finger-like papillae (filiform) lined by dysplastic columnar epithelium with
scant lamina propria
• may have varying degrees of dysplasia
• GREATEST RISK FOR MALIGNANCY
POLYPS: NEOPLASTIC

Tubular

Villous

Tubulovillous Adenoma
• contain 25-30% villous architecture
• intermediate between tubular & villous adenomas
COLONIC CARCINOMA/ADENOCARCINOMA

Colorectal Carcinoma, Gross. (L) Fungating mass (encircled). (R)

napkin-ring constriction (arrow).
COLONIC CARCINOMA/ADENOCARCINOMA

Colorectal Carcinoma, Histology. Left sided colonic CA

which appears as a napkin-ring wherein there is constriction
followed by dilation; keratin pearls (arrow)
COLONIC CARCINOMA/ADENOCARCINOMA

Two Important Prognostic Factors of Colonic

Carcinomas: (MUST KNOW!)
1. depth of invasion of tumor
o the more superficial the tumor, the better the prognosis
2. Presence of nodal metastasis

*Additional Notes:
• 98% are adenocarcinoma; may arise from adenomatous polyps
• Common among 60-70 y/o
o now, there are younger cases and are more aggressive, mostly
HNPCC
• more common in affluent countries (may be due to diet)
• LIVER: most common site of metastasis due to portal drainage of
the colon
 CARCINOID TUMOR

Take Note!

• Most common site in

the GIT: small
intestine (jejunum)
• Most common site in
the appendix: tip

Gastrointestinal carcinoid tumor (neuroendocrine tumor).

(A) Carcinoid tumors often form a submucosal nodule
composed of tumor cells embedded in dense fibrous tissue.
(B) High magnification shows the bland cytology that typifies
neuroendocrine tumors. The chromatin texture, with fine and
coarse clumps, frequently assumes a “salt-and-pepper”
pattern. Despite their innocuous appearance, tumors can be
aggressive.
Acute Suppurative Appendicitis
Gross appearance of the appendix shows swollen
and congested, evident by superficial vessels
with minimal to none fibrino-purulent exudates.

Microscopically, the walls shows focal areas of

necrotic mucosa and abundant leukocyctic
infiltrates in the appendiceal wall. Note the
dilated vessels of serosa and
mesoappendiceal filled with RBCs.
Acute Suppurative Appendicitis
• most common acute abdominal condition
• Pathogenetic Factor of Development: associated with obstruction
by fecalith, gallstone (rare), tumor, or ball of worms (seen in the
young) in 50-80% of cases
• in young adults

SIGNS & SYMPTOMS:

• periumbilical pain later localizing at RLQ, fever, tenderness at Mc
Burney’s point, ↑ WBC count
• also vomiting, nausea, difficulty in urination

Diagnosis:
• Look for neutrophilic infiltration of muscularis
o hallmark of acute appendicitis
• Look for lymphocytes and eosinophils in the muscularis layer
o Implies CHRONIC; same as chronic cholecystitis
Hepatobiliary Tree
Gallbladder: Cholelithiasis
Take Note!
Most common type of Gallstone:
- Cholesterol Gallstone

Additional Notes:
Cholelithiasis Risk Factor:
- With both aging and gender,
hypersecretion of biliary
cholesterol appears to play the
major role.
4 F’s for Gallstone risk factors:
Female, Forty, Fat, Fertile

Gross. (Upper) Cholesterol Stone; (Lower)

Pigment Stone
Gallbladder: Cholelithiasis
Type of Gallbladder Stones:
1. CHOLESTEROL
• Yellowish-brown
• radiolucent in x-ray
• Majority of stones
• Contains more than 50% of crystalline cholesterol monohydrate
• More common
2. PIGMENT
• Calcium Salts of Bilirubin
• Appear jet black and usually very small
• A consequence of increased unconjugated bilirubin (unconjugated
hyperbilirubinemia)
• In severe hemolytic anemias, bilirubin will be liberated. Gallstones in
hemolytic patients are of pigment type (because of bilirubin) but
majority of gallstones are cholesterol type.
o BLACK
▪ Radiopaque 50-75%
▪ Found in sterile gallbladder
o BROWN
▪ Radiolucent
▪ Seen in infected hepatic ducts
LIVER: Focal Nodular Hyperplasia
● Not neoplastic but reactive processes
● Benign
● Looks like a cirrhotic liver but it is actually a
central fibrovascular scar with fibrous
bands radiating from it that separates
liver into nodules
● Nodules lack central vein and portal
tracts, while within scars are arterioles,
veins and chronic inflammatory cells
● The most frequent benign solid liver lesion,
(3% of adult population)
● F>M; 90% are women of child bearing age,
two thirds of whom have a history of oral
contraceptive use

Take Note!
Focal Nodular Hyperplasia vs Cirrhosis
• Focal Nodular Hyperplasia – lacks
central vein and portal tracts (distinct
histologic feature)
• Cirrhosis – fibrosis, regenerative nodules
(with portal tracts and central veins),
vascular remodelling
LIVER: Hepatic Adenoma
• True neoplastic tumors
• Rare; develop almost exclusively in young
women during their reproductive years
• Well-differentiated, well-circumscribed
benign tumor with 2-3 cell thick hepatic
cords (**normal: 1-2 cell thick)
• Benign proliferation of hepatocytes forming
glands
• May develop as a result of oral
contraceptive or anabolic steroid use.
• Most important characteristic: Absent
portal tracts in the tumor (sinusoids are the
only one present)
• Usually present as solitary lesion
• Key feature: reticulin framework of the cell
plates is either intact or only focally
decreased

•
Microscopically, hepatic adenoma shows
cords of hepatocytes, with an arterial vascular
supply, and no portal tracts.
LIVER: Hepatic Adenoma vs Focal Nodular
Hyperplasia
Differentiate Hepatic Adenoma from Focal Nodular Hyperplasia:
• Presence of isolated arteries
• Lack of fibrous bands
• A central fibrous zone
• Proliferating bile ductules
• Nodularity

Above indicated are the most helpful features in supporting a diagnosis for
adenoma. Most of these features are not seen in FNH

*next slide shows a table comparison of HA and FNH from Doc L. Cruz’s
lecture
LIVER: Hepatic Adenoma vs Focal Nodular
Hyperplasia
MORPHOLOGIC ADENOMA FOCAL NODULAR HYPERPLASIA
FEATURES
Similar in size, slightly larger or smaller than in Usually normal in size, no significant cytologic
Hepatocytes normal liver; rare tumors show pleomorphism. abnormalities, but foci of cellular pleomorphism
Cytoplasmic glycogen or fat may be present. may be present. Glycogen or fat may be present.
None present (except in variant, or telangiectatic Present in fibrovascular zone, typically at edges of
Bile ductules
adenoma) hepatocytic nodules
Large vessels often seen but without surrounding Abnormal, large, muscular vessels surrounded by
Vessels or other connective tissue zone; small to medium-sized connective tissue stroma
blood-filled spaces isolated hepatic arteries. Peliosis hepatis and
sinusoidal dilation.
Connective tissue Occasional fibrous septa Fibrovascular central zone; myxoid or dense
component collagen; chronic inflammatory infiltrates
Encapsulation May be present, often discontinuous None
Cell plate 1-3 cells wide; “regenerative” appearance 1-3 cells wide; plates may be compressed; foci of
architecture plates >3 cells wide may be present
Normal or slightly decreased; can show acinar Normal staining pattern
Reticulin stain
pattern, particularly in adenomatosis
Age > 10 years, <50 years; almost always female; Young adults, female > male, normal AFP,
normal serum a-fetoprotein (AFP), possible radiographic imaging often demonstrates central
Other features
increased alkaline phosphatase, large lesions prone fibrous zone
to hemorrhage
LIVER: Hepatocellular Carcinoma
• most common primary malignant tumor in
the liver.
• Hallmark of HCC: presence of bile in the
malignant hepatocytes; proves hepatocellular
origin of the metastatic cells
• Microscopically: Tumor islands composed of
trabeculae and sheets of polygonal cells
with large hyperchromatic nuclei and a
prominent nucleolus.
• A high serum AFP level (>1000ng/mL) is
present in almost two thirds of patients with
large HCC tumors.
• Develops over a relatively long period of time
o probably a multistep process that involves
various risk factors, such as chronic
hepatitis, exposure to certain toxic or viral
agents, and genetic alterations
o Most common cause in the Philippines:
Hepatitis B infection
LIVER: Patterns of Hepatic Injury
General Morphologic Features of Hepatic Injury
• NECROSIS
o Zonal Necrosis
▪ Centrilobular (Zone 3)
▪ Midzonal
▪ Periportal – easily affected by infection, and toxins
o Coagulative Necrosis (Hepatocytes)
▪ Usually due to ischemia
o APOPTOSIS (Apoptotic Bodies – Councilman Bodies)
▪ Usually due to viral infections
• DEGENERATION (e.g. fatty change; coagulative change: ground glass
appearance, eosinophilic changes, councilman bodies)
• INFLAMMATION (any type of inflammation of the liver —metabolic or
viral, is called Hepatitis)
• REGENERATION (e.g. cirrhotic changes)
• FIBROSIS
LIVER: Patterns of Hepatic Injury – Piecemeal
Necrosis

• AKA: Interface Hepatitis

• Hallmark of progressive disease
• Chronic inflammatory cells spill out from the portal tract into adjacent parenchyma with
associated necrosis of the hepatocytes of the limiting plate
LIVER: Patterns of Hepatic Injury – Bridging
Necrosis Bridging Necrosis
Necrosis from one portal tract to another
or from portal tract to the central vein
o i.e. necrosis link central veins to
portal tracts or bridge the adjacent
portal tract

This is normal liver at medium power with

zone 1 in periportal region, zone 2 in the
middle of the lobule, and zone 3 in
centrilobular region. A central vein and
a portal triad define the lobule. c = central vein; p = portal tract
LIVER: Patterns of Hepatic Injury

Coagulative Changes in the Liver are

called Eosinophilic Bodies,
Acidophilic Bodies or Mallory
Bodies

Centrilobular Necrosis - centrilobular

region is the area most prone to
metabolic toxins such as those found in
alcoholic liver disease; present in chronic
passive congestion
LIVER: Acute vs Chronic Hepatitis
HISTOPATHOLOGIC FEATURES OF ACUTE AND CHRONIC HEPATITIS
ACUTE
Predominantly Lobular Formation
Lobular Regeneration and Disarray
Ballooning Hepatocyte Degeneration
Apoptotic Bodies (Acidophils)
Kupffer cell aggregates
Mononuclear inflammatory cells, with
Occasional Eosinophils and Neutrophils
Canalicular Cholestasis
Hepatocyte Dropout, Necrosis
CHRONIC
Predominantly Portal Tract Inflammation
Lobular Acidophil Bodies
Mononuclear Inflammatory Cells,
Occasional Plasma Cells
Progressive fibrosis with eventual
Cirrhosis
Portal-based lymphoid aggregates and
Lymphoid Follicle Formation
Interface Hepatitis
Bile Ductular Proliferation
LIVER: Hepatitis B Infection
● AKA: “Serum Hepatitis”
● caused by double-stranded DNA virus
o found in blood and body fluids
o (+) transplacental transmission →
increase risk of hepatocarcinoma

Hepatitis B Virus under Electron Micrograph

Hepatitis B liver; *Councilman bodies
- specific for hepatitis; ground glass
appearance

NOTE! How to differentiate acidophilic bodies

from Councilman bodies?
• They’re the same acidophilic bodies :P
• “Councilman bodies” is a specific term for
acidophilic bodies in A SPECIFIC DISEASE
o Named after the person who discovered
the liver changes in Yellow Fever (he died
of the same disease)
• Practically they’re both the same
LIVER: Hepatitis B Infection
Hepatitis B Virus Structure

● Serum Markers: (very important!)

o HBsAg, HBV-DNA, DNA polymerase, HBc
o HBeAg: Persistence implies continued viral replication, infectivity,
progression to chronic active hepatitis
o HBsAg: levels peak during the acute stages of infection
o Anti-HBe: acute infection has peaked and is on its wane (pa-recovery na)
o IgM Anti-HBc: Recent acute infection;
o (+) transaminases (AST/ALT) – implies continuous destruction of liver cells
LIVER: Hepatitis B Infection
Hepatitis B Serologic Markers

*S=surface; C=core;
Musculoskeletal
Diseases
 OSTEOSARCOMA
• Malignant tumor
• Most common primary malignant tumor
of the bone.
• Age Bracket: 75% occurs in persons
<20 years old (young adults).
• Gross and Radiologic finding:
o Codman’s triangle – indicative of an
aggressive tumor. Triangular shadow
between cortex and raised ends of
periosteum.
o Sunburst pattern
• Microscopically: osteoid and
malignant mesenchymal cells
• Route of metastasis: Hematogenous
spread
Codman’s triangle
• Histogenetic origin: MESENCHYMAL
Radiograph of Osteosarcoma.
Sunburst pattern and Codman’s
triangle (arrows).
OSTEOSARCOMA

Morphology of osteosarcoma. (Gross) Bulky, gritty, and grayish-white

mass with areas of hemorrhage and cystic degeneration. (Histology)
Pleomorphic cells with large, hyperchromatic nuclei. Note the presence of
bizarre hyperchromatic nuclei, and abundant, abnormal mitosis.
 OSTEOID OSTEOMA
TAKE NOTE!
• Radiographic finding: Central nidus
o Size: 2cm or less (if more than 2cm →
OSTEOBLASTOMA)
• Differential diagnosis: Fibrous dysplasia
• Both are benign
• To differentiate: look for Osteoid matrix
elements (absent in fibrous dysplasia)
• First line of med treatment : Aspirin (for pain)

Histologic features of osteoma and

osteoblastoma. Randomly interconnecting
trabeculae of woven bone rimmed by a single
layer of osteoblasts. The stroma is composed of
loose connective tissue with many dilated and
congested capillaries.
 OSTEOCHONDROMA
TAKE NOTE!
• Hallmark tissue: “cartilage cap”

Additional Notes:
• Benign tumor.
• Develop only in bones of
endochondral origin.
• Frequently sessile and have
short stalks that has a
cartilage cap.
• Characterized by the formation
of hyaline or myxoid cartilage.
• Also known as exostosis.
OSTEOCHONDROMA

cartilage cap
CNS
CNS INFECTIONS: Pyogenic Meningitis vs TB
Meningitis
TB Meningitis
Parameters: Pyogenic Meningitis (acute)
(chronic)
CSF Findings: • Elevated WBC count • Elevated WBC count
o Neutrophil present o Lymphocytes and
• Marked protein elevation monocytes present
• Markedly decreased glucose level • Moderate to marked protein
• Lactate >35 mg/dL elevation
• (+) limulus lysate test with g(-) • Decreased glucose level
organism • Lactate >25mg/dL
• (+) gram stains and bacterial • (+) Ziehl-Neelsen test
antigens

Gross Exudates predominantly covers the Exudates predominantly BASAL

Morphology: CONVEXITY of the brain (obliterating cisterns and encasing
cranial nerves); +/- hydrocephalus

NOTES!
Notorious for optic nerve involvement: TB meningitis
Bacterial Meningitis: High protein, low sugar
- evident in both Pyogenic and TB Meningitis which are both bacterial infections.
CNS INFECTIONS: Pyogenic Meningitis vs TB
Meningitis

Exudate in the brain’s convexity Exudate at the base of the brain

-Acute Pyogenic Meningitis -TB Meningitis
CNS HERNIATION: Uncal vs. Tonsillar

Sites of herniation: tonsillar

and transtentorial. The 2
most dangerous and most fatal
due to compression of vital
respiratory centers and
brainstem. Displacement of
brain parenchyma across fixed
barriers can be subfalcine,
transtentorial, or tonsillar (in to
the foramen magnum).

• Herniations - movement of the brain through apertures and natural boundaries as a

result of increased intracranial pressure
o Elevation of the mean CSF pressure above 200mH2O (15mmHg)
CNS HERNIATION: Uncal vs. Tonsillar

Uncal (transtentorial) herniation Tonsilar (cerebellar) herniation

• FATAL: Compresses the • (FATAL)
midbrain • Herniation of the cerebellar
• Herniation of the medial tonsils into the foramen
temporal lobe above the free magnum
edge of the tentorium • Medulla compression
CNS TUMORS: Medulloblastoma

Medulloblastoma:
• (IV/IV)
• Most common in children
• large tumor found exclusively at
cerebellum
• Highly malignant
• Rare to metastasize outside CNS
• Categorized into 4 groups:
1. WNT type - best prognosis
2. SHH type
3. Group 3 - worst prognosis
4. Group 4
CNS TUMORS: Medulloblastoma
Microscopic sections of the tumor
submitted for histopathological
examination shows a neoplasm
composed of sheets of small, round to
oval characteristically “carrot shaped”
(inside the box) cells with poorly
defined margins, scanty cytoplasm and
dense hyperchromatic nuclei. The
stroma is moderately desmoplastic.

Medulloblastoma can present with

numerous neuroblastic (Homer-Wright)
rosettes, i.e. circular arrangements of
tumor cells around a virtual center.

NOTE:
Homer-Wright rosettes: Pseudorosettes- Medulloblastoma
Flexner-Wintersteiner rosettes and fleurettes: True rosettes- Retinoblastoma
CNS TUMORS: Pilocytic Astrocytoma
• I/IV
• Variant of Astrocytoma
• Most common benign tumor in children
• Found in cerebellum, floor & walls of 3rd
ventricle, optic nerves and cerebral
hemispheres
• Usually presents as “child, 10y.o. with
cystic nodule in the cerebellum”

NOTE:
Histologic features of Pilocytic Astrocytoma:
• Brightly eosinophilic, corkscrew-shaped
Rosenthal fibers (yellow arrow)
• PAS (+) eosinophilic granular bodies
(blue arrow)
 CNS TUMORS: Glioblastoma
• IV/IV = poor prognosis
• Most aggressive tumor in adults
• Histologic Hallmarks:
o Necrosis
o Microvascular proliferation
– endothelial cell proliferation

Notice the island of viable tumor cells

encircling the blood vessels in a large
necrotic focus.

viable

Necrotic area
CNS TUMORS: Glioblastoma

The presence of necrosis is one of the histologic hallmarks of glioblastoma. Necrotic areas
are usually seen in serpentine pattern (shown here) or geographic pattern in hypercellular
foci. Tumor cells often aggregate around the periphery of necrotic areas creating
pseudopalisading. Left picture shows a higher magnification of nuclear pseudopalisdaing.
CNS TUMORS: Meningioma
• I/IV = low risk
• Generally benign tumors in adults
• Most Common site: usually attached to
dura (parasagittal)
• Found along
o Any of the EXTERNAL SURFACE of
the brain
o WITHIN the VENTRICULAR
SYSTEM, where they arise from the
stromal arachnoid cells of the choroid
plexus
• Arise from arachnoid meningothelial cells
• Histologic Hallmarks:
o Psamomma bodies
o Whorls of meningothelial cells

Notice the whorled pattern of cell growth

and psammoma bodies (arrow)
CNS TUMORS: Meningioma
 CNS TUMORS: Oligodendroglioma

• I/IV = low risk

• Commonly found among adults in the cerebrum
• Histologically benign but locally infiltrative
• Histologic Hallmarks:
o Fried egg appearance of cells- round nucleus with clear cytoplasm
o Capillaries (chicken-wire appearance) are seen all around, which are
prone to hemorrhage and calcification
CNS HYPERTENSIVE BLEED: Intracerebral
Hemorrhage

(From Batch 2021 trans)

Cause of Intracerebral hemorrhage:
1) Traumatic
2) Non-traumatic
a) Intracerebral - due to Hypertension (HPN), Charcot-Bouchard
microaneurysm, causes lipohyalinosis
b) Subarachnoid - ruptured berry aneurysm
c) Mixed cerebral - subarachnoid, due to rupture vascular formations
d) Blood dyscrasia
e) Tumor bleed
f) Secondary hemorrhage Take Note!
Most common cause of Intracerebral
Bleed: HPN
 end
---------------------- ----------------------
Congrats! You finished it! You’re so awesome!
“Kung may pangarap ka, pag nahihirapan ka na, lagi mong tatandaan
kung ano ba ang pangarap mo at kung kanino ka nangangarap. Pray to
God and He will do the rest. Obstacles make the success sweeter.
Laban lang! #WhateverItTakes”
-Att. Dr. Jean Polido

Laban lang, 2021 Fam!

God bless youuuuuuu!
#RoadtoM.D.
#WhateverItTakes
References:
• Recordings
• 2021 Transes (lec and lab)
• Robbins and Cotran Atlas of Pathology, 3rd ed
• Robbins Basic Pathology, 10th ed.
• pathologyoutlines.com
• webpathology.com
• webpath.med.utah.edu