Pathology 2B Final

Practical Examination
2nd Semester S.Y. 2012-2013 Regular Class
March 11, 2013 Pre-practicals
March 13, 2013 Final Practicals

Compiled by: PikamonMD

Photography by: KingKongMD, DannyBoyMD & J.CoMD

GROSS & SLIDES FOR FINAL PRACTICAL

SLIDES Lymph Node 29. Acute Pyelonephritis with
1. Hemmorhoids with 14. Adenocarcinoma, Renal Abscess
Thrombosis, Anus Peritoneal Seeding 30. Renal Adenocarcinoma
2. Myocardial Infarction 15. Fatty Change, Liver 31. Diabetes Mellitus, Kidney
3. Acute Appendicitis 16. Gout 32. Liver Cirrhosis
4. Chronic Passive 17. Atheroma, Aorta 33. Chronic Cholecystitis
Congestion, Lung 18. Capillary Hemangioma 34. Hepatoma
5. Esophageal Varices 19. Brown Atrophy, Heart 35. Acute Suppurative
6. Cavernous Hemangioma, 20. Lobar Pneumonia Meningitis
Liver 21. Tuberculosis, Lung
7. Lipoma 22. Emphysema, Lung GROSS
8. Fibroadenoma, Breast 23. Simple Endometrial 1. Liver Cirrhosis
9. Hydatidiform Mole Hyperplasia, Uterus 2. Hepatoma
10. Adenocarcinoma, Colon 24. Thyroiditis 3. Hydatidiform Mole
11. Invasive Ductal 25. Thyroid Hyperplasia / 4. Atheroma, Aorta
Carcinoma, Breast 5. Dermoid Cyst, Ovary
12. Squamous Cell 26. Diabetes Mellitus, 6. Leiomyoma, Uterus
Carcinoma, Skin Pancreas
13. Papillary Carcinoma, 27. Carcinoma, Pancreas
Thyroid Metastatic to 28. Schistosomiasis, Appendix
 1. Hemorrhoids with Thrombosis,
Anus
Organ: Anus Etiology: Excessive straining on
Hemodynamic Change: defecation, pregnancy
Thrombosis External Hemorrhoids: collateral
Pathologic Changes: vessels within the inferior
Dilated veins, filled with hemorrhoidal plexus located
thrombus below the anorectal line.
Fibrin layers in the thrombus Internal Hemorrhoids: those that
alternating with platelets & result from dilation of the
blood cells. superior hemorrhoidal plexus
within the distal rectum.
Other dilated veins are either
empty or filled with blood.
Some may have ruptured.
Presence of Line of Zahn in the
thrombus.
 2. Myocardial Infarction
Organ: Heart
Type of Necrosis: Coagulative Necrosis
Hemodynamic change: Infarction
Etiology: Atherosclerosis (most common)
Pathologic Changes:
Separation of myocardial fibers due to edema
Loss of nuclear detail but preservation of cell outlines &
tissue architecture
Result from the denaturation of structural proteins &
enzymes that lyse the dead cells
Cardiac markers: CK-MB, AST, LDH, Troponin I, Troponin T
 3. Acute Appendicitis
Organ: Appendix
Hallmark: Infiltration of Neutrophils, most prominent in the muscularis layer
Type of Inflammation: Acute inflammation
Predominant Inflammatory Cell: Neutrophil
Hemodynamic change: Hyperemia
Etiology:
Children- Lymphoid hyperplasia following viral infection
Adult- Obstruction due to Fecalith Material, Parasitic worms like Ascaris
lumbricoides
Pathologic Changes:
Dilated arterioles and capillaries (more prominent in the lamina propria and
serosa, where the wall is looser)
Loosening of adjacent interstitium indicates edema
Complication of ruptured appendicitis: Peritonitis
4. Chronic Passive Congestion, Lung
Organ: Lungs
Hemodynamic Change: Congestion
Etiology: Left sided heart failure secondary to mitral stenosis
Pathologic Changes:
Fibrosis of the interstitial tissue
Extravasation of blood into the tissues (hemorrhage or
diapedesis in severe congestion)
Hemolysis leads to formation of Heart Failure cells or
Hemosiderin laden Macrophage.
History: Px had RHD with severe mitral stenosis and died of
CHF
 Dilated subepithelial & submucosal veins
with blood stasis

5. Esophageal Varices
Organ: Esophagus
Hemodynamic Change: Congestion
Etiology: Severe hypertension secondary to alcoholic liver cirrhosis
(most common cause)
Pathologic Changes:
Dilated subepithelial & submucosal veins in the distal esophagus
Pathogenesis:Liver cirrhosis (less frequently, portal vein obstruction or
hepatic vein thrombosis) causes portal vein hypertension. Portal
hypertension leads to the opening of porto-systemic shunts that
increase the blood flow into veins at the gastro-esophageal junction
(forming esophageal varices). Esophageal varices are the most
important, since their rupture can lead to massive (even fatal) upper
gastrointestinal hemorrhage.
Complication: Clinically silent until they rupture and produce severe
hematemesis
 6. Cavernous Hemangioma, Liver
Organ: Liver
This lesions constitute 7% of all benign tumors of infancy and
childhood.
Involved in von Hippel-Lindau disease
Pathologic Changes:
Less well circumscribed & more frequently involve deep structures
Red-blue, soft spongy masses 1-2 cm in diameter
Mass is sharply defined but non-encapsulated, composed of large,
cavernous blood-filled vascular spaces
Involves the medium & large size ectatic blood vessels filled w/
blood
With dystrophic calcification
Fails to regress spontaneously
Cell of origin: Endothelial Cell
Complication: Hemorrhage
 7. Lipoma
Most common benign soft tissue tumor in adults
Pathologic Changes:
Painless, soft & well circumscribed
Mature fat cells enclosed in a thin fibrous capsule
Cell of Origin: Adipose tissue (Mesenchymal Cell)
History: Lesion was excised from the thigh of 40
year old woman
 8. Fibroadenoma, Breast
Organ: Breast
Most common benign tumor in
adult females in their 20s and 30s
Cell of origin: Mammary duct type-
epithelium
Etiology: Hormonal changes such as
occur in pregnancy and lactation
may induce hyperplasia of the
epithelial component
Pathologic Changes:
Well circumscribed, painless,
slightly firm, movable, ovoid in
shape, frequently multiple and
bilateral
Mammogram shows dense mass
(Large lobulated
calcifications)
Composed of an overgrowth of
both fibrous & glandular tissue
Thin fibrous capsule enclosing the
growth
There are no intact lobules in the
mass
There is proliferation of fibrous
stroma w/c surrounds the ducts
(pericanalicular) or sometimes
invaginate into the ducts (intra-
canalicular).
Ductal lumen is collapsed &
obliterated
Lining of the ducts may show
compression/hyperplasia
No dilated ducts & no
inflammatory infiltrates
Location of the tumor: Upper-Outer
Quadrant of the Breast
Tumor Marker: CA 15-3
 9. Hydatidiform Mole
Cell of Origin: Trophoblastic cells
Characterized by hydrophic cystic swelling of the chorionic villi w/
hyperplasia & even anaplasia of the chorionic cells
Can occur at any age during the active reproductive period
Usually discovered at 4th-5th month of pregnancy w/ vaginal
bleeding
May arise from a previous normal pregnancy w/ retained placental
tissue/from any ectopic site of pregnancy
May arise from the embryonal part of the ovary
Pathologic Changes:
enlarged chorionic villi w/ hydrophic change of the stroma, no blood
vessel is found, lining is small cytotrophoblast w/ focal areas of
hyperplasia
Rest of the tissues consist decidual cells
Treatment: curretage
Malignant transformation: Choriocarcinoma
Gross specimen:
Delicate, friable mass of thin-walled, translucent, cystic, grape-like
structures consisting of swollen edematous hydrophic villi.
 10.Adenocarcinoma, Colon
Represents an epithelial
malignancy derived from the
mesoderm
2 patterns:
1. Carcinoma of the left side:
ring constriction; shows early
symptoms of intestinal
obstruction
2. Carcinoma of the right side:
grows a polypoid/cauliflower-
like masses/spreading
papillomatous plaques into the
lumen; obstruction does not
iccur due to wide diameter of
cecum
Glands are atypical, lined by
several layers of columnar cells
w/ hyperchromatic nuclei &
pleomorphism
Some glands have invaded the
underlying muscularis layer
Notes from orientation:
- hyperchromatic, no more
secretion (?), loss of polarity,
crowding, layering, increase
number of cells, invasion
Most tumors are composed of
tall columnar cells that resemble
dysplastic epithelium found in
adenomas
The invasive component of
these tumors elicit a strong
stromal desmoplastic response
w/c is responsible for their
characteristic firm consistency
11. Invasive Ductal Carcinoma, Breast
Sheets & nests of anaplastic cells w/ large, irregular nuclei;
strong stromal fibrosis where the cells are enclosed; focal
necrosis is seen; no calcification

appearance of the skin above the mass; nipples were

retracted.
Carcinoma cells form strands & sheets of atypical cells; no
ductal formation is found; fibrosis of stroma
Notes from orientation: malignant glands insinuating in
fibrous stroma; inflammatory cells; glands infiltrate in
adipose tissue; basement membrane is intact;
comedocarcinoma (ducts healed w/ malignant cells; tumor
necrosis at the center); solid tumor cells
12.Squamous Cell Carcinoma, Skin
Most common predisposing factor is chronic exposure to sunlight;
most cases occur in sun-exposed skin
Types:
1. In situ atypical squamous cells replace the normal epidermis
2. Invasive tumor squamous cell invade into the dermis
3. Verrucous fungating but slow growth, deeply invasive w/o
metastasis
Basal layer forms varied sized club-like projections that dip into the
underlying dermis
w/in the masses of cells w/ the central cells showing individual
keratinization or
Cells show hyperchromaticity & some mitotic figures; stroma shows
fibrosis & some dilated blood vessels
 13. Papillary Carcinoma, Thyroid
Metastatic to Lymph Node
CHIEF COMPLAINT: anterior neck lump, w/
enlarged cervical lymph nodes
Produces well formed branches (papilla);
paillary lining containing large nuclei w/c
appears empty
Some nuclei contain granular inclusions;
psammoma bodies
 14. Adenocarcinoma, Peritoneal
Seeding
Anaplastic
No glandular differentiation
 15.Fatty Change, Liver
Organ: Liver
Etiology: Chronic alcoholism, Intoxication of
Chemicals
Mechanism of Lesion:
a. Impaired assembly of Lipoproteins
b. Increased peripheral catabolism of fat
c. Excess NADH + H
This condition is Reversible
 16.Gout
Organ: Synovial joint
Lesion: Tophi formation
Mechanism of lesion: Formation of monosodium urate
crystals in the joints.
Etiology: Increase intake of Purine rich foods, Alcoholism
Microscopic findings:
Urate crystal deposits appearing as slender crystals or
pinkish yellow masses surrounded by macrophages,
fibrosis and giant cells of foreign body type
Laboratory findings:
Elevated serum uric acid
 17.Atheroma, Aorta
Organ: Aorta Hypoxic-ischemic injury such as
Morphological Change: Myocardial Infarction and
Formation of Plaque on the Stroke
Tunica Intima composed of: Microscopic findings:
Cells including smooth muscle Atheromatous plaque
cells, macrophages, and T cells Foamy cells
ECM, including collagen, Cholesterol clefts
elastic fibers, and proteoglycans
Intracellular and extracellular
Pinkish protein material
lipid Gross specimen:
Etiology: Hypercholesterolemia Plaque
Laboratory diagnosis: Total Thrombus
cholesterol of the blood Calcifications
Consequences:
 18.Capillary Hemangioma
Hemangiomas are the most common tumors of
infancy
Chief Complaint: red-blue elevated mass, 0.5 cm
in diameter
Small blood spaces containing RBCs enclosed by
proliferative endothelial cells
Occur in the skin, subcutaneous tissue, & mucous
membranes of oral cavities & lips
Bright red to blue; can be level w/ the skin, or
slightly elevated & have an intact overlying
epithelium
 19.Brown Atrophy, Heart
Thin, atrophic myocardial cells
Stroma is loose w/ areas of fibrous tissue proliferation
Focal areas show replacement of muscle cells by
collagenized tissue
Cells show brownish-yellow granules in the cytoplasm
near the nuclei lipofuscin pigment
Blood vessels are filled w/ blood
Endogenous pigment derived from lipid peroxidation of
the cell membrane of the cellular organelle
 20.Lobar Pneumonia, Lung
Notes from slide orientation:
Alveoli filled w/ inflammatory cells
Predominating cell: Neutrophils
Suppurative inflammation
Blood vessels are congested
Accumulation of fluid in alveoulus
Etiology: Streptococcus pneumoniae
infection
Radiologic examination of the chest
showed densities over the lower lobe,
left lung
WBC count showed leucocytosis w/
polynucleosis
Sputum examination showed gram-
positive cocci in clusters w/ plenty of
pus cells
Type of inflammation: Fibrous
Type of edema: Fibrin-purulent
exudates
4 STAGES:
a. Congestion: vascular engorgement,
intra-alveolar fluid w/ few neutrophils
b. Red hepatization: massive confluent
exudation w/ neutrophils, red cells &
fibrin filling the alveolar spaces
c. c. Gray hepatization: progressive
disintegration of red cells &
persistence of fibrino-suppurative
exudates
d. d. Resolution: consolidated exudates
w/in the alveolar spaces undergoes
passive enzymatic digestion
Diagnostic test: chest x-ray, sputum
exam
Clinical features: abrupt onset of high
fever, shaking chills, mucopurukent
sputum
TX: antibiotics
 21.Tuberculosis, Lung
Etiology: Mycobacterium tuberculosis
Associated w/ TB infection (type IV cell mediated immunity)
Tissue reaction: caseating chronic granulomatous inflammation
Gross: friable w/ cheese like appearance
Histologic: fragmented lysed cells, amorphous cell, granuloma (no
intact cell at center)
Activated macrophages epitheloid cell engulf fuse
mycobacterium resistant
Tubercle: pink, amorphous, granular
langhans -shoe
Pattern of necrosis: caseation necrosis
Chest x-ray showed fibrocaseous densities in the left & right lungs
Post autopsy diagnosis of the case: asphyxiation due to aspiration of
blood clots
 22.Emphysema, Lung
Microscopically, there are
abnormally large alveoli separated 3. Septal capillaries are compressed
by thin septa w/ only focal
centriacinar fibrosis.
Loss of attachments of alveoli to
the outer wall of small airways
Pores of Kohn are so large that
septa appear to be floating/protrude
blindly into alveolar spaces w/ a
club-shaped end
Histologically: large alveoli w/
destroyed alveolar walls; walls
show thinning w/ compressed
capillaries
Pathogenesis:
1. Protease-anti protease mechanism
2. Smoking (tobacco smoke)
Microscopic:
1. Alveolar spaces are enlarged
2. Separated by thing septa
and bloodless
Alveolar wall spaces
(blebs and bullae)
Clinical manifestation: do not appear
unless 1/3 of lung parenchyma is
incapacitated
Dyspnea 1st symptom
Complicastions:
Respiratory acidosis
Coma
Right-sided heart failure
Massive collapse of lungs
secondary to pneumothorax
(rupture of blebs and bullae)
 23. Simple Endometrial Hyperplasia,
Uterus
Chief complaint: irregular menses;
prolonged menstrual period
Thickened endometrium w/
normal sized uterus
Increased number of irregularly
shaped glands of varied sizes;
some are cystically dilated
Lining cells are tall, columnar,
non-secretory w/ no mitosis
Stroma is cellular w/ uniform
stromal cell, few capillaries are
noted
Morphologic change: Hyperplasia
Mechanism of lesion: increased in
number of cells
- Also it is the result of growth-
factor driven proliferation of
cells
Etiology: unopposed estrogen
stimulation
Clinical presentation:
Excessive/Abnormal bleeding
Conditions associated are:
- Obesity
- Menopause
- Prolonged administration of
estrogen
- Polycystic Ovarian disease
Genetic Alteration: PTEN tumor
suppressor gene
Complication: Can lead to
Endometrial Carcinoma
 24. Thyroiditis
Organ: Thyroid
Replacement of thyroid parenchyma by lymphoid cells
& some plasma cells.
Lymphoid cells form lymphoid follicles.
Remnants of thyroid tissue & the follicles contain
colloid or are atrophic.
Slightly swollen cells w/ pinkish, granular cytoplasm
Hurthle cells
Type IV hypersensitivity (cell mediated)
Laboratory diagnosis:
Antibody involved: anti-thyroglobulin antibody
 25.
Disease
Follicular Hyperplasia Histologic description:
Organ: Thyroid Thyroid hyperplasia with
Normal: simple cuboidal
Pathologic: simple columnar, Type II hypersensitivity
colloid lessens, scalloping Antibody mediated
Characterized by a triad of Antibody involved:
clinical findings Thyroid-stimulating
a. Hyperthyroidism due to diffuse, immunoglobulins
hyperfunctional enlargement of TSH-binding inhibitor
the thyroid immunoglobulins
b. Infiltrative ophthalmopathy with Laboratory diagnosis:
resultant exophthalmos
c. Localized, infiltrative
dermopathy, sometimes called
pretibial myxedema
 26.Diabetes Mellitus, Pancreas
Organs : Endocrine Pancreas
Histologic findings:
Reduction in size and number of the
Pancreatic Islets of Langerhans
Fibrosis in the stroma
Amyloid deposits (type 2 DM)
Infiltration by inflammatory cells
(lymphocytes) in the stroma.
Hyperplasia of the islets in non-diabetic
newborns of diabetic mother
Pathogenesis:
Type 1 DM: An autoimmune disease in
which islets destruction is caused
primarily by immune effector cell
reacting aginst endogenous -cell
antigens. The end result of the
destruction of -cells is the decrease
secretion of Insulin leading to decrease in Complications:
rate of glucose transport into certain cells
in the body.
Type 2 DM: The two metabolic defects
that are characterize are (1) decrease
response of peripheral tissues to insulin
(insulin resistance) and (2) -cell
dysfunction that is manifested as
inadequate insulin secretion in the face of
insulin resistance and hyperglycemia.
Signs and Symptoms:
Weight loss
In spite of good/increased appetite
(Polyphagia)
Frequent thirst (Polydipsia)
Frequent urination (Polyuria) w/ no pain
on micturition
Body weakness
Important Laboratory Findings:
+++ urine sugar/glucosuria (diptstick
test)
Diabetic Macrovascular disease
endothelial dysfunction, accelerated
atherosclerosis leading to MI, Gangrene
of the lower etremities, hyaline
arteriosclerosis
Diabetic Retinopathy and Neuropathy
 27.Carcinoma, Pancreas
Usually assymtomatic until nearby tissues have been invaded.
Pancreatic CA involvement in the organ: 60% head, 15% body, 5% tail and
20% diffuse.
Majority are ductal adenoCA
Highly invasive
Host response is desmoplastic reaction (Fibroblast proliferation resulting to
increased interstitium) and lymphocytic infiltration
Histologic findings:
Densely fibrotic stroma
Trapping poorly differentiated adenoCA composed of atypical small
hyperchromatic cells
No Ductal or glandular structures are found
No vascular invasion is seen
Laboratory findings:
Elevated CEA test
 28.Schistosomiasis, Appendix
Etiology: Schistosoma japonicum, S.
mansoni and S. hematobium infection
Organ: Appendix
Signs and symptoms:
Abdominal enlargement
Jaundice
Signs of liver failure
Pathogenesis/Life cycle:
Fork-tailed Cercaria (infective stage)
penetrates (degrades keratin with
water
Becomes Schistosomula and travels to
the lungs and liver where it matures
Mate in the tributaries of the portal vein
(mesenteric or pelvic) where the female
lay ova
Ova erode the intestinal mucosa and are
excreted (diagnostic stage)
Other eggs may deposit in blood
vessels, liver and other organs
Ova excreted in feces hatch in water
which become miracidia and invade the
intermediate host (Oncomelania
quadrasi) where asexual cycle takes
place
Cercaria exits from the snail
Histologic findings:
In ther appendiceal wall, oval ova are
surrounded by fibrosis
Granulomatous tissue reaction
Complications:
Liver involvement (portal hypertension)
leading to ascites, esophageal varices
Lung involvement (cor pulmonale)
leading to Right Sided Heart Failure
Hematuria and granulomatous disease
of the bladder resulting to chronic
obstructive uropathy (S. hematobium
only)
 29. Acute Pyelonephritis with Renal
Abscess
Etiology: caused by bacterial but sometimes shaped areas of suppuration.
viral (polyomavirus) infection whether Distribution of lesion is unpredictable
hematogenous and induced by septicemic and haphazard.
spread or ascending and associated with Damages occur mostly in the poles.
vesico-ureteral reflux
Signs and Symptoms: Laboratory findings:
Dysuria and cloudy urine Urinalysis: +++ albumin, plenty of pus
cells (TNTC) and plenty of bacteria
Lumbar pain (Gram negative bacilli)
Low grade fever Blood: Elevated WBC count with 75%
Pertinent physical examination findings: segmenters and 25% lymphocytes
Positive lumbar punch Treatment:
No abdominal masses Atibiotics
No edema of the eyelids or extremities Antipyretics
Prostate is not enlarged Increase fluid intake
Histologic findings: Complications
Hallmarks: Patchy interstitial suppurative Papillary necrosis
inflammation, intratubular aggregates of Pyonephrosis
neutrophils and tubular necrosis Perinephric abscess
Suppuration may occur as discrete focal
abcesses involving one or both kidneys,
which can extend to a large wedge-
 30.Renal Adenocarcinoma
Most renal cancer are sporadic but Signs and Symptoms:
unusually form of autosomal
dominant familial cancer occur,
usually younger individuals
Von Hippel-Lindau (VPH)
syndrome
Hereditary (familial) clear cell CA
Hereditary papillary CA
Cell of Origin: Tubular epithelium
Risk factors:
Smoking most significant
Obesity particularly in women
Hypertension
Unopposed estrogen therapy in
women
Exposure to asbestos, petroleum,
and heavy metals
Increased incidence in px with
chronic renal failure, acquired
cystic disease and tuberous
sclerosis
Costovertebral pain
Hematuria (the more frequent
attacks of lumbar pain)
Vague abdominal mass and small
blood clots in urine
Histologic findings:
Arise in any portion of the kidney
but more commonly affect poles
Neoplastic cells tend to form
tubules and may invade blood
vessels
May show cystic as well as solid
areas
Most tumors are well differentiated
but some show nuclear atypia with
formation of bizarre nuclei and
giant cells
 31.Diabetes Mellitus, Kidney
Diabetic Nephropathy
Belongs to the classification of DM complications diabetic
microangiopathy .
3 Lesions encountered:
Glumerular
Renal vascular (principally arteriosclerosis)
Pyelonephritis including necrotizing papillitis
Refer to the slide Diabetes Mellitus, Pancreas for other descriptions
Histologic findings:
KW Lesion nodular glumerulosclerosis which is associated with
renal failure
Fibrin cap and capsular drop
Mesangial cell proliferation leads to increasing proteinuria
Basement membrane thickening
 32.Liver Cirrhosis
Pathogenesis: Excessive alcohol intake leads to the liver cell which is transformed into
microvesicular lipid droplets(Steatosis) fibroblastic cell which produces excess collagen
accumulate in the responsible for the formation of fibrosis of the
globules then compress and displace the liver
hepatocyte nucleus to the the Laboratory findings:
continuous alcohol intake, fibrous tissue Elevated B2
develops around the terminal hepatic veins and
extends to the adjacent sinusoids Elevated transaminases
Signs and Symptoms: Elevated alkaline phosphatase
Asymptomatic until later in the course of the Low serum proteins
disease Critical/decreased level of hemoglobin
Jaundice (sclera and skin) Increased hematocrit
Enlargement of the abdomen (ascites) and the Decreased RBC count (Anemia)
legs (pitting edema) Complications:
Malaise Esophageal varices secondary to portal
Body weakness hypertension
Gradual weight loss Ascites
Anorexia Generalized edema
Histologic findings: Gross specimen:
Fibrous proliferation involving the central vein Diffuse nodularity of the surface reflects the
to the portal areas and between portal areas process of nodular regeneration and scarring
Regeneration of the liver cells The greenish tint of some nodules is due to bile
Some fatty change in intact liver cells stasis
Bile stasis in the bile ducts
Inflammatory cells, specially lymphocytes in
the stroma
Ito Cell/ Satellite Cell- Vitamin A storing cell in
 33.Chronic Cholecystitis
May be a sequel to repeated bouts of mild to severe acute
cholecystitis
Develops in absence of antecedent attacks
Conditions usually associated:
Fat
Female
Forty and above
Histologic findings:
Changes in the mucosa and thickness of the wall
Fibrosis in the subepithelial layer
Inflammation and fibrosis extends to the serosal layer
Mucosal outpouching to form Rockitansky Aschoff sinuses
 34.Hepatoma
Also known as liver cell carcinoma/hepatocellular carcinoma
Has less tendency to spread to the blood & lymph nodes
Tends to penetrate the liver capsule & extend the diaphragm
There are malignant liver cells in the stroma; arranged in several
layers of tumor cells (trabecular type); occassional mitotic figures;
cells are surrounded by layer of fibrous tissue
Tumor cells range from well differentiated to highly anaplastic
undifferentiated lesions
Gross specimen:
May appear grossly as
Unifocal (usually large) mass
Multifocal, widely distributed nodules of variable size,
Diffusely infiltrative cancer permeating widely and sometimes
involving the entire liver
 35.Acute Suppurative Meningitis
Histologic description: Exudate is found in the
leptomeninges
Confirmatory test: CSF Culture and sensitivity
a. Neonates: Escherichia coli and Group B Streptococci
b. Adolescent/Adult: Neisseria meningitidis
c. Elderly (Extreme of Age): Listeria monocytogenes and
Streptococcus pneumoniae
d. Immunocompromised and Alcoholics Klebsiella
pneumonia
Destruction of dead cells including inflammatory cell
infiltrates in meningeal wall
Found at subarachnoid space surrounded w/ PMNs
Clinical manifestation: nuchal rigidity, high fever, abnormal
reflexes (positive Babinski sign and sign), Seizure
1. Liver Cirrhosis (Gross)

2. Hepatoma (Gross)
3. Hydatidiform Mole (Gross)
grape-like structures
consisting of swollen
edematous hydrophic
villi

4. Atheroma, Aorta (Gross)

 5. Dermoid Cyst (Gross)

5. Dermoid Cyst (Gross)

Also called Cystic teratoma
Organ: Ovary
Looks like skin due to presence of thin, stratified squamous
epithelium
Notes from orientation:
- Parenchyma consisting of germ layers (ectoderm, mesoderm,
endoderm)
- Predominating components: skin adnexa, stratified squamous
epithelium (w/ lots of keratin)
- Appendages: hair follicle, sebaceous gland, sweat gland, fat nervous
tissue
- Elements: tuffs of hair admixed w sebum (pasty material); bones,
adipose tissue
Most common malignant transformation: Squamous Cell Carcinoma
 6. Leiomyoma, Uterus (Gross)
6. Leiomyoma, Uterus (Gross)
Also called Fibroids
Organ: Uterus (Myometrium)
Most common tumor in women;
occur during the active reproductive No nuclear atypia
life
May regress & calcify
(menopause); may rapidly increase
in size (pregnancy)
Due to excessive estrogenic
stimulation; regarded as endocrine
dependent
Well-differentiated, regular,
spindle-shaped smooth muscle cells
associated with hyalinization
Disseminated peritoneal
leiomyotosis multiple small
nodules in the peritoneum
Histologic:
Cut surface of the mass shows
whorled pattern
Cell of origin: Smooth muscle cells
Presence of smooth muscle growth
where the spindle cells are cut at
different planes
Surrounding intact myometrium
forms a pseudo-capsule around the
mass
Areas of interstitial fibrosis
Locations / Classification:
Submucosal
Intramural most common
Subserosal
Signs and Symptoms:
Abnormal bleeding
Compression of the bladder
Sudden pain
Malignant Transformation:
Leiomyosarcoma