Cellular Adaptation, Inflammation and Repair HS 202

(Laboratory) Trans 3A
Dr. Mark Ang Exam 1
08/14/2018
igv

OUTLINE II. CASE 1: ATROPHY AND METAPLASIA

I. Introduction IX. Case 8: Enzymatic Fat A 65 year old female underwent surgery to remove a benign
II. Case 1: Atrophy And Necrosis tumor of the uterus. The following images show histopathologic
Metaplasia A. Gross Findings findings incidental to the tumor.
A. Atrophy B. Histologic Findings
B. Metaplasia C. Questions A. ATROPHY
C. Questions X. Comparing Morphology Of Histology
III. Case 2: Hypertrophy Forms Of Necrosis • Thin endometrial mucosa
A. Gross Findings XI. Intracellular Accumulations o Blue – tightly packed cells
B. Histologic Findings A. Anthracosis o Pink – Myometrium
C. Questions B. Hemosiderin
• Endometrium
IV. Case 3: Hyperplasia Accumulation
o More glands and spaces
A. Gross Findings C. Melanin In Malignant
o Pallor – edema, less cells
B. Histologic Findings Melanoma
o Gland to stroma ratio – 1:1 (Greater means secretory
C. Questions D. Pathologic Calcification
endometrium or hyperplasia)
V. Coagulation Necrosis E. Fatty Liver
A. Gross Findings XII. Inflammation Uterus
B. Histologic Findings A. Case 1: Appendicitis • Normal Endometrium
C. Questions B. Case 2: o Stains blue due to the affinity of the chromatin to Hematoxylin
VI. Case 5: Coagulation Bronchopneumonia (H&E)
Necrosis C. Case 3: Cholecystitis o Tightly packed cells
A. Gross Findings D. Case 4: Gastric Ulcer o High gland to stroma ratio
B. Histologic Findings E. Case 5: Pulmonary • Atrophic endometrium
C. Questions Tuberculosis o Thinned out
VII. Case 6: Caseation F. Case 6: Suture o Fibrous stroma (middle layer of the second picture)
Necrosis Granuloma o Glands are limited until the base only
A. Gross Findings G. Case 7: Granulation o They also appear small, but are not atypical or dysplastic/
B. Histologic Findings Tissue malignant
C. Questions • Secretory endometrium
VIII. Case 7: Liquefaction o Subnuclear vacuoles – starts releasing glycogen to be released
Necrosis o In preparation for the implantation of the fertilized ovum
A. Gross Findings o Physiologic hyperplasia (serves a function)
B. Histologic Findings
C. Questions

I. INTRODUCTION
Cell Energy Economy
• The cell balances it functions (i.e. secretory, etc.) and it’s ability to
keep itself alive
• Whenever there is imbalance, the cell tries to regain another
equilibrium such that all ATP is well spent
o The cell will always try to adapt
o Otherwise, it will die.
• At the very core of the priority list of functions of a cell, the cell
should always choose to keep itself alive

Must-Know Topics
• Reversible vs. Irreversible changes
• Type of Adaptive changes Figure 1.1 Atrophic Endometrium (scanning)
o Atrophy o Intracellular storage (Melanin,
o Hypertrophy Hemosiderin, Carbon, Calcium,
o Hyperplasia Lipids, Glycogen)
o Metaplasia
o Dysplasia
• Types of Necrosis
o Coagulation o Enzymatic
o Caseation o Fibrinoid
o Liquefactive

Cellular Adaptation
• Any injury can cause adaptive changes
• The more cells divide, the more chances for mutation

Figure 1.2. Atrophic endometrium (HPO)

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Figure 1.3. Normal secretory endometrium (LPO/HPO) Figure 1.5 Normal ectocervix (left) and endocervix (right) at HPO

B. METAPLASIA Metaplastic Cervix

• Replacement of one tissue type by another • Top: Squamous-like (layered, solid-looking)
o Changes into a cell type that is more resistant to the injurious • Bottom: Glands
stimuli • In Figure 1.7, glandular cells are intimately mixed with the
o Human Papilloma Virus cannot infect mature cells metaplastic epithelium (minsan top, minsan bottom)
• Reversible change o We point this out because metaplasia starts with stem cells.
• Example: Squamous Metaplasia o In the image, squamous cells start from underneath of the
o Location: Endocervix glandular epithelium.
o Features immature squamous cells (polygonal) • Metaplastic changes are reactive
o May not mature into its fullest potential (immature squamous
Adaptive changes in the cell are reversible. Remove the stimuli metaplasia)
and the system will go back to the production of the native cells. o The cells are squamous but doesn’t thin out into layers like
normal squamous cells do.
Normal Cervix
• Ectocervix
o Stratified Squamous epithelium (Non-keratinizing)
• Endocervix
o Simple columnar cells
o Lined by mucus producing glandular cells
 Mucin abundant cells
 Nucleus is situated basally

Figure 1.6. Metaplastic Epithelium (Scanning)

Figure 1.4. Normal cervix (scanning)

The transition zone (squamo-columnar junction) is
a favored site for malignancy

Figure 1.7. Metaplastic Epithelium (LPO)

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A. GROSS FINDINGS

Figure 2.1. Gross structure of heart with left ventricular hypertrophy

Figure 1.8. Metaplastic Epithelium (HPO) More than 1.5 cm measurement of heart walls.

C. QUESTIONS B. HISTOLOGIC FINDINGS

Causes of atrophy and metaplasia Normal Cardiac Muscle Cells
• Generally, anything that will lead to the cell’s loss of function would
lead to atrophy (i.e. denervation, disuse)
• Disuse, denervation, lack of hormonal stimulation, ischemia,
irritation, compression/ pressure

Causes most significant for this case

• Low hormonal levels from menopause
• Mass in the uterus (mechanical stressor pushing out the cells),
which can cause damage to its vasculature and physical injury.

Other examples of atrophy and metaplasia

• Types of metaplasia
o Squamous Metaplasia: Protection from physical irritation
o Columnar Metaplasia: Protection from chemical irritation
 mucin will act as a shield
 Reason our esophageal and stomach linings are columnar Figure 2.2. Normal cardiac muscle is smooth and in single straight lines.
(being exposed to acids) I = Intercalated discs; N = nuceli; Arrows = cross trabeculae
• Most common type of metaplasia:
o COLUMNAR TO SQUAMOUS EPITHELIUM Case
o In this case, the benign tumor is causing physical irritation; as • Bigger fibers
such the glandular epithelium wants to be squamous (kasi mas • Bigger Nuclei (Box-Car Nucleus)
makapal yung balat niya making it more suitable against
• Evidence of myocardial hypertrophy at the cellular level
irritation)

Are these adaptive mechanisms reversible or not? Scar

• Adaptive changes in the cell are reversible.
• Remove the stimuli and the system will go back to the production
tissue
of the native cells.

Relationship of metaplasia to dysplasia and neoplasia

• Metaplasia: transformation of one type of tissue to another
(change in phenotype) which may be physiologic or pathologic.
• Dysplasia: Disordered growth and maturation of epithelium.
Anything that forces the cell beyond its capacity will increase the Box-car like
risk for dysplasia nuclei
• Neoplasia: new growth. Occurs when cells lose control of their
physiologic processes.
• Metaplasia and dysplasia are reversible, but neoplasia is
irreversible.
o Sequence: Metaplasia to dysplasia to Neoplasia

Figure 2.3. Myocardial hypertrophy. Left: HPO, Right: LPO

III. CASE 2: HYPERTROPHY
A 32 year old male, previously diagnosed to have rheumatic
fever, consulted for easy fatigability. Chest x-ray showed C. QUESTIONS
cardiomegaly with a cardiothoracic ratio of 0.7. Patient went into heart Causes of hypetrophy
failure and arrested. • Increased workload, hormonal stimulation, nutrition
• Bigger organelles = bigger cells
• Results to a heavier weight

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Causes most significant to the case C. QUESTIONS

• Increased Workload Examples of physiologic and pathologic hyperplasia
o This is detected by mechanoreceptors telling the cells that it • Physiologic: Endometrium, pregnancy, and breasts
should augment the proteins • Pathologic:
o Increases risk for infarction due to increased demand for Name Basic mechanism
oxygen, nutrients etc. Benign Prostatic Excess testosterone, leading to
Hyperplasia difficulty in urination
Other examples of hypetrophy Endometrial hyperplasia Excess estrogen, leading to
abnormal uterine bleeding
• Skeletal muscles
• Uterus (combination of hypertrophy and hyperplasia)
Viral infections (papillomavirus that cause warty growth)
IV. CASE 3: HYPERPLASIA
A 65 year old male was admitted for one month history of Cells capable of undergoing hyperplasia
difficulty in starting urination and dribbling of the urine. At the time of • Labile cells – cells capable of dividing
admission, he developed inability to urinate in spite of urgency and • Example: epithelium: skin, bone marrow cells, GI tract mucosa.
the feel of a distended bladder. Rectal exam revealed a nodule and
enlarged prostate. A prostatectomy was performed. Clinical manifestation in relation to the tissue changes
• Increased prostate volume due to glandular hyperplasia
A. GROSS FINDINGS o Increase in size = compression of the urinary tract
o Dribbling urine: Tfg n he bladder will contract trying to release
the urine, but only little will come out
o The bladder remains full, resulting in the constant urge to urinate
and feeling of distension
• That’s why it’s pathologic, but not necessarily cancer
• It is common among men of older ages (60 y.o. up)

V. COAGULATION NECROSIS
A 40 year old hypertensive multigravida gave birth to a
healthy infant via spontaneous vaginal deliverey at the 33rd week of
gestation. The placenta was submitted for histopathologic
examination.
Figure 3.1 Gross anatomy of a nodular prostate
A. GROSS FINDINGS
• Prostate gland is usually smaller and has no nodules
• Lumen has slit-like shape, which indicates that there is hyperplasia
of the surrounding parenchyma

B. HISTOLOGIC FINDINGS
Nodular Prostatic Hyperplasia
• Proliferation of glands (hyperplasia)
• Thickening of surrounding muscle cells in the glands (hypertrophy)
• Corpora amylacea: round, stone-like concretions

Figure 4.1. Gross structure showing a placental infarct

B. HISTOLOGIC FINDINGS
Viable Villi
• Mature trophoblasts remove their nucleus
• Syncytiotrophoblast extrude nucleus when they mature
* o Other examples of cells that extrude their nucleus once they
mature are skin cells and red blood cells
Infarct leading to Coagulation Necrosis
* • Loss of nuclear detail and staining
o Usually very blue due to chromatin
o May still have an outline
• Generally pink color

Figure 3.2 Nodular Prostatic Hyperplasia (LPO).

Red asterisk: Corpora amylacea
Green asterisk: thicker stromal muscle fibers compared to normal prostate.

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B. HISTOLOGIC FINDINGS
Viable Areas
• The specimen is viable yet inflamed
o This is made evident by the presence and number of
* inflammatory cells
• Blue dots represent nuclei

* Infarct
• Proteins are denaturated
• Chromatin are degraded
• Nuclei cannot be seen in pink side despite visible glomeruli
• Blue dots may be inflammatory cells

Figure 4.2. Viable and infarcted placental villi (LPO)

Red asterisk: Viable Villi, Black asterisk: Infarct

Figure 4.3. Viable and infarcted placental villi (HPO)

C. QUESTIONS
Probable causes of the coagulation necrosis in this case Figure 5.2. Viable and Infarcted Kidney
• Infarct cause by loss of blood flow (ischemia/hypoxia)
• Underlying condition: Preeclampsia
C. QUESTIONS
Is this lesion reversible or not? Causes of the infarct in this case
• Cell death is irreversible.Necrosis is irreversible by its own • Thromboembolism (kidney blood vessel)
definition, since the cell is already dead. o Thrombus travelled to a renal artery and blocked it
o This produced the murmur, indicating that there is a block in the
Organs where coagulation necrosis occur blood supply
• Solid organs at the end of blood supply.
Explanation behind the wedge shaped infarct
o Only have one artery feeding into them.
o Blockage will cause loss of blood flow, causing the necrosis. • As mentioned earlier, this corresponds to the area served by the
blocked BV (Architecture of the blood supply)
VI. CASE 5: COAGULATION NECROSIS
A 15 year old boy with rheumatic heart disease was Explanation for the laboratory findings on the basis of the
admitted for a week’s history of fever. Pertinent in the PE was a tissue change
changing heart murmur. Urinalysis showed positive albumin and • Result: Positive albumin and numerous red blood cells in the
numerous red blood cells. The patient developed acute renal urinalysis
failure and died. An autopsy was performed. • Explanation:
o Due to necrosis of the kidney affecting microstructures such as
A. GROSS FINDINGS the glomerulus and renal tubule cells, there is loss of function.
In this case, filtration.
o Albumin is found because dead cells with proteins spilled in
parenchyma
o RBCs are evident due to destroyed blood vessels
o There is also increased blood flow to compensate the blood lost
by the kidney leading to an increased hydrostatic pressure

VII. CASE 6: CASEATION NECROSIS

A 10 year old boy presented with multiple bilateral cervical
neck lymphadenopathy. Chest x-ray revealed bilateral hilar
Figure 5.1. Gross structure showing a Kidney Infarct
densities. He eventually succumbed to sepsis. The autopsy findings
• Wedge shaped infarct revealed multiple lesions involving the lungs, cervical and hilar
o Represents an area subserved by the blocked artery lymph nodes and testis.
• Red blotches = mini hemorrhages

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A. GROSS FINDINGS
• Caseous = Cheese like
o From the friable white appearance of the area of necrosis
• Encountered most often in foci of tuberculosis infection

Figure 6.3. Tuberculosis Orchitis

C. QUESTIONS
Figure 6.1. Gross structure showing caseation necrosis
Formation of caseation granuloma
seen in Pulmonary Tuberculosis • Chronic inflammatory response to certain organisms (TB)
• Macrophages are activated to form epitheloid macrophages and
B. HISTOLOGIC FINDINGS spherical structures to contain the organism
• Under the microscope, the necrotic area appears as a structureless o Surrounding the sphere are the lymphocytes and plasma cells
collection of fragmented or lysed cells and amorphous granular • Requires intact cell immunity (T-helper cells)
debris enclosed within a distinctive inflammatory border
• This appearance is characteristic of a focus of inflammation known Is caseation necrosis pathognomic for tuberculosis?
as a granuloma • Pathognomic: Characteristic or indicative of a particular disease
o It’s arrangement is in contrast with that of a Mononuclear type or condition (TB)
of inflammation (normal type) • Answer: No, TB does not always have caseation necrosis.
o As mentioned earlier, it is dependent on an intact cell mediated
Granuloma immune response.
• Organized type of chronic mononuclear inflammation  People with HIV do not have it due to poor immune response
• Seen as having a large central caseation with mononucleated giant o Condition may also be found in patients with leprosy, parasitic,
cells or eptheloid histiocytes fungal, and any strange atypical infection the body cannot get
• Cells present rid of using its normal pathways
o Epitheloid histiocytes or activated macrophages  May also be found in autoimmune diseases (Chrohn’s),
 Macrophages may fuse and form multinucleated giant cells sacardosis
 Langhans Type Giant Cells in TB – horseshoe shaped due to
peripheral accumulation of nuclei VIII. CASE 7: LIQUEFACTION NECROSIS
o Lymphocytes and plasma cells surrounding the sphere of A 30 year-old male developed a large, red, swollen and
transformed epithelized histiocytes tender lesion on the left buttock. Excision was performed
• Requires inact cell mediated immunity
o Needs sufficient amount of T-helper cells A. GROSS FINDINGS
• Seen in classical tuberculosis and some fungal infections

Figure 7.1. Gross structure showing an abscess

• Seen usually in focal bacteria or fungal infections

o Microbes stimulate the accumulation of leukocytes and the
subsequent liberation of enzymes from these cells
Figure 6.2. Tuberculosis Lymphadenitis o The release of enzymes leads to the degradation of cells, hence,
the liquefaction
• Pus appears creamy yellow appearance due to the presence of
dead leukocytes or green due to the neutrophil granules
• Hypoxic death of cells within the central nervous system often
manifests as liquefaction necrosis

Chloroma (Solid form)

• Greenish tinge due to pus
o Granules are green in large concentrations
o Pus formed by degenerating neutrophils
• Composed of neoplastic granulocytes

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• Seen in AML – condition where there is proliferation of myeloid

cells Explanation on the clinical and laboratory findings on the
basis of the tissue changes
Abscess formation • Pain caused by essentially digesting one’s self
• Chronic process • Pancreatitis – Elevated lipase and serum amylase
• Implies tissue destruction which leads to scar formation o Lipase and amylase activated before reaching the intestinal
• Leads to the formation of a fibrous wall tract. Results in autodigestion of the pancrease and damage to
o Makes it difficult for drugs to work blood vessels.
o Solution: Drain abscess
X. COMPARING MORPHOLOGY OF
B. HISTOLOGIC FINDINGS FORMS OF NECROSIS
Coagulation Necrosis
• Anucleate cells
• Pink (eosinophilic) cytoplasm
• Structure remains intact
o Injury denatures not only structural proteins but also enzymes
and so blocks the proteolysis of the dead cells
• Inflammatory infiltrates are present
o Seen as nuclei of inflammatory cells in between necrotic tubules

Figure 7.2. Microscopic examination of an abscess

• Structures are not recognizable, slides may be from any organ

C. QUESTIONS
Explain how liquefactive necrosis occurs.
• Neutrophils use enzymes, liquefying everything

Organ/s and/or condition/s where liquefactive necrosis occur

• Brain
• In areas with a very good, active blood flow where you can
phagocytose materials
• Generally, any location where bacterial infections can occur

IX. CASE 8: ENZYMATIC FAT NECROSIS

A 35 year old male had an eating binge and drinking spree
during his brother’s wedding. The next morning, he complained of Figure 9.1. Coagulation Necrosis
severe epigastric pain and was rushed to the hospital. PE showed N = Normal Kidney; I = Infarct
marked marking and tenderness in the upper abdomen. Labs showed
leukocytosis and elevation of serum amylase and lipase. The patient Caseation Necrosis
died after 2 days and an autopsy was performed. • Tissue remains granular or not well digested yet
• Cytoplasm, organelles, and nucler debri remain present
Diagnosis: Acute Pancreatitis • Enclosed within a distinctive inflammatory border

A. GROSS FINDINGS
• White calcified spots in the pancreas
• Enzymatic Fat necrosis leads to the production of free fatty acids
which may undergo saponificanton with high amounts of Calcium
forming white white chalky deposits

B. HISTOLOGIC FINDINGS
• Enzymes get activated prematurely
o Starts digesting the pancreas
• No visible outline (“lusaw”)
• Pale pink amorphous network of remaining collagenous fibers

C. QUESTIONS
Figure 9.2. Caseation Necrosis
Biochemical processes leading to enzymatic fat necrosis
• Injury to the pancreas causes the release of activated pancreatic
Liquefactive Necrosis
enzymes which liquefy fat cell membranes. The released lipases
split the triglyceride esters contained within the fat cells. • Neutrophils are present
Intraperitoneal saponification of calcium by fatty acids in areas of • No visible structure “Lusaw”
fat necrosis form the grossly visible chalky, white nodules, o characterized by digestion of the dead cells
characteristic of fat necrosis
• Alcohol intake and enzymatic fat necrosis:
o Too much alcohol intake causes spasmodic contraction of
pancreatic ducts, which causes stasis
o Also has direct cytotoxic effects on pancreatic acinar cells

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Hemolytic Anemia
• Condition wherein cells are hemolyzed leading to the formation of
hemoglobin and porphyrin ring
• Porphyrin ring (soure of iron) then accumulates in tissues in the
form of hemosiderin
Difference from Lipofuscin
• Hemosiderin exhibits birefringence
• Birefringence: optical property of a material having a refractive
index that depends on the polarization and propagation direction of
light
o According to sir: If you change the polarity of the light, you will
see the hemosiderin granules twinkle
Figure 9.3. Liquefactive Necrosis

Enzymatic Fat Necrosis

• Fat tissue present
• No visible structure “Lusaw”
• Considered liquefactive necrosis of fatty tissue without the
neutrophils

Figure 10.2. Hemosiderin Laden Macrophages

C. MELANIN IN MALIGNANT MELANOMA

• Finer brown granules as compared to hemosiderin
• Seen as melanin caps
o placed over the nucleus: the goal of which is to prevent the UV
rays from penetrating and potentially damaging the nucleus
Figure 9.4. Enzymatic Fat Necrosis
o seen in the keratinocytes of the skin
XI. INTRACELLULAR ACCUMULATIONS
A. ANTHRACOSIS
• Carbon pigment
o Accumulated in alveolar macrophages
o Exogenous pigment, inert in form
• Visible on autopsy
• Location: Lungs

Figure 10.3. Melanin in Malignant Melanoma

Figure 10.1. Anthracosis
D. PATHOLOGIC CALCIFICATION
B. HEMOSIDERIN ACCUMULATION • Abnormal tissue deposition of calcium salts, together with smaller
Hemosiderin amounts of iron, magnesium, and other mineral salts
• Hemoglobin-derived • Has two kinds: (a) dystrophic and (b) dystrophic calcification
• Golden yellow to-brown, granular or crystalline pigment Dystrophic Calcification
• One of the major storage forms of iron • Occurs locally in dying tissues
• Seen in hemochromatosis (iron overload), hemolytic anemia, • Occurs despite normal serum levels of calcium and in the absence
Alzheimer’s disease, endometriotic cyst of derangements in calcium metabolism
• Presence indicates site of chronic repeated hemorrhage • Starts at a necrotic focus
o Endometriotic cyst: repeated bleeding causes the accumulation
of hemosiderin

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Metastatic Calcification Histologic Findings

• Deposition of calcium salts in otherwise normal tissues • Difficult to distinguish parts of the section
• Almost always results from hypercalcemia secondary to some • Aggregates of inflammatory material in periphery of serosa
disturbance in calcium metabolism • Presence of necrotic tissue with hemorrhage
• Normal lymphoid aggregates
o When lymphoid aggregates swell, it can cause congestion,
which can also lead to appendicitis
• Bowel layers (mucosa, submucosa, muscularis, and serosa) are
overrun by inflammatory infiltrate
o Infiltrate is predominantly neutrophil

Figure 10.4. Metastatic Calcification

E. FATTY LIVER
• May be due to excessive alcohol use (Alchoholic Fatty Liver
Disease/AFL) or causes other than excessive alcohol use (Non
Alchoholic Fatty Liver Disease/NAFL)
• Hepatocytes are transformed into round cells completely filled with
lipid droplets

Figure 11.2. Appendix Histologic Findings

Yellow Arrow = Smooth Muscle Fibers
Red Arrow = Neutrophil

Questions
• What is the histologic criterion of diagnosis of Acute
Appendicitis?
o Neutrophils in the muscularis layer
o Inflammatory cells in the mucosa or the serosa layer is not
enough to say thet it is acute appendicitis
 If in the lumen: may be coming from the caecum or patient
may have ulcerative colitis
 If in the serosa: patient may have diverticulitis
• What are the complications of Appendicitis?
Figure 10.5. Fatty Liver o Untreated, appendicitis can lead to rupture, which will cause
peritonitis. This will eventually lead to septic shock and death.
XII. INFLAMMATION o Without rupture, the mesentery can wrap the inflamed appendix
to contain the inflammation and form the phlegmon
A. CASE 1: APPENDICITIS
An 18-year old male presented with abdominal pain of one- B. CASE 2: BRONCHOPNEUMONIA
day duration, initially felt at the epigastric area and became localized A middle-aged male, known alcoholic, was admitted for
at the right lower quadrant. There was associated intermittent difficulty in breathing and high-grade fever. He had been having cough
cramping and one episode of vomiting. and productive of purulent sputum for the past five days.
On admission, the temperature was 39°C was 104 per One week prior to admission, the patient was allegedly
minute. There was tenderness and muscle guarding over the RLQ. sprawled in front of the house with vomitus all over his upper garments.
The WBC count was 15x109/L. An appendectomy was performed. The patient died on the tenth day.
Post-mortem examination of both lungs showed patchy
Gross Findings areas of consolidation, with small pockets of suppurative exudate
• Appendix is enlarged, diameter almost 2cm within the right lung
• Covered with dark brown material
o Fibrinopurulent exudate which is a mixture of inflammatory cells, Gross Findings
hemorrhage, and fibrin • Consolidation of lower lung lobes (dry texture)
• Cut section shows soft wall with fecaloid and purulent material o Lungs become more solid
filling its lumen  Normal lung has air-filled sacs with spongy consistency
• Serosa is dull o Also known as Hepatization
 Has a similar feel to liver upon palpation
o Due to fluid accumulation in lungs
o Neutrophils release their collagenases and proteases
 This enzymes destroy the parenchyma and blood vessels
causing leakage leading to edema and consolidation
• Small pockets of suppurative exudate within the right lung
o Purulent material can be squeezed out
o Alveolar spaces containing neutrophilic exudates
Figure 11.1. Appendix Gross
Yellow Arrow = Fibrinopurulent Exudate

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C. CASE 3: CHOLECYSTITIS
A 50-year old female, obese, and multiparous was admitted
for recurrent right hypochondriac and epigastric pain, sometimes
associated with low grade fever over the last two years. The pain was
noted especially after a heavy meal rich in fat.
Physical examination revealed slight tenderness and
muscle guarding over the right hypochondrium. A cholecystogram
revealed rounded filling defects in the gallbladder. A
cholecystectomy was performed.

Gross Findings
• Rounded filling defects
Figure 11.3. Lungs Gross Findings o Outlines the stones inside the gallbladder
• Wall of gallbladder thickened due to fibrosis
Histologic Findings • Retained its normal pear-shaped configuration, but there are
• Alveolar spaces are flooded by neutrophils and some remnants of fibrous adhesions on the serosal surface
macrophages • Ovoid jet-black caliculi with granular surfaces and brownish yellow
o Neutrophils last for 24-48 hours cores found in lumen
o Monocytes take over during this time • Mucosal surface highly trabeculated
• Presence of distended alveolar spaces
o Compensation for other alveoli that are compromised
• Bronchioles have the same neutrophilic exudates
• Vascular congestion as part of acute response
• Leukocytic alveolitis
• Leukocytes causing inflammation in the alveoli

Figure 11.5. Galbladder Gross Findings showing Cholelithiasis

Yellow Arrow = Caliculi

Histologic Findings
• Not much findings aside from clusters of lymphocytes for chronic
cholelithiasis
o As compared to acute and suppurative inflammation wherein
high number of neutrophils may be seen
Figure 11.4. Lungs Histologic Findings
Red Arrow = Neutrophil
• Thickened wall with spindle cells (fibroblasts) – fibrosis ongoing
Yellow Arrow = Macrophage • Rokitansky ascoff sinuses
Pneumonia o Glandular structures embedded in the muscular layer of the
gallbladder
• Infection inflammation of the lungs
o Invagination of mucosal glands through defects or weak points
• May be caused by aspiration of foreign bodies such as food or in the muscularis coat usually seen in chronically inflammed
transfer of oral microbiota gallbladder
• Alcohol does not cause pneumonia o Formation is caused by herniation during increased pressure
o However, chronic alcoholics are prone to having chronic when gallbladder contracts
subdural hematomas which may decrease sensorium and make o Weak points may be inherent or congenital or may be due to
themselves prone to aspiration repeated inflammation that causes destruction of some parts of
• Acute Pneumonia the muscularis layer
o Refers to acute neutrophilic pneumonia • Inflammatory cells within the wall layers
o Has two kinds: o Predominantly lymphocytes (mononuclear)
 Bronchopneumonia – inflammation is limited to the  Characteristic of chronic inflammation
preibronchial regions  Chronic cholecystitis
 Lobar pneumonia – inflammation affects entire lobe

Questions
• What are the possible outcomes of bronchopneumonia? What
in the history point to an acute inflammatory condition?
o Untreated, septicemia and death
o If treated, fibrosis and scarring
• What are the histologic features seen on the slide that point to
an acute inflammatory process?
o Neutrophils and congested vessels

Figure 11.6. Galbladder Histologic Findings

Yellow Arrow = Rokitansky-Aschoff Sinuses

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Questions o Malignant ulcers – tumors that ulcerated which leave the viable
• What in the histology points to a chronic inflammatory edges of the tumor
processes? o Other characteristics
o Mild mononuclear inflammation consisting of lymphocytes and  Well-demarcated, oval shaped, 2.5cm in size
plasma cells with presence of Rokitansky Ascoff Sinuses  Swollen mucosa over the edge
• What are the disease where the presence of lymphocytes  Mucosa overhanging
connotes an acute inflammation?
o Viral infections Questions
o Hypersensitivity reactions • What are the layers of a peptic ulcer?
o Autoimmune responses o NIGS
• What in the histology points to a chronic inflammatory
D. CASE 4: GASTRIC ULCER process?
A 40-year old male bank executive had been having o Ulcer will characteristically have a mixed type of inflammatory
recurrent epigastric burning for several months. Initial gastroscopy cells
showed an ulcer at the gastric antrum on the lesser curvature. He o Layer of granulation tissue and fibrosis
was given medications of three weeks.  Connotes an attempt to repair which is a hallmark of
There was no relief of symptoms and repeat gastroscopy inflammation
showed no reduction in the size of the ulcer. Antrectomy with • What is the role of Helicobacter pylori in the pathogenesis of
gastroduodenal anastomosis was performed. gastric ulcer?
o Causes chronic infection of the gastric mucosa
Gross Findings o H. Pylori has a lot of virulent factors
• Well-demarcated oval shaped ulcer with 2.5 cm diameter o Initiates an inflammatory response
• With smooth slightly rolled margins into the base o Also associated with the formation of MALToma to diffused large
• Mucosal bed surrounding the ulcer is somewhat edematous b cell lymphoma (more aggressive)
 MALT: Mucosa Associated Lymphoid Tissue
 diffused large b cell lymphoma cannot be treated

E. CASE 5: PULMONARY TUBERCULOSIS

A 10-year old boy was described by his mother as having
been sickly for the last two years, with recurrent cough and low-grade
afternoon fever. Several physicians had treated him either a case of
simple upper respiratory infection or pulmonary tuberculosis.
Significant in the history was that an aunt who took care of the child in
the past had at least two episodes of frank hemoptysis during the past
year.
A few weeks prior to admission, the patient became
Figure 11.7. Gross structure showing Gastric Ulcer
apathetic and less active. Shortly thereafter, the cough became more
distressing and occasionally productive of blood-streaked sputum.
Histologic Findings High fever and labored breathing ensued. On admission, the child was
NIGS cyanotic and he died an hour later.
• Necrosis of the epithelia
• Inflammation – usually a mixture of acute and chronic Gross Finding
• Granulation Tissue – tissue is trying to rebuild itself, new vessels • White areas of consolidation
are being formed o Upon palpation, areas will have firmer consistency compared
• Sclerosis/Fibrosis to adjacent tissue
o Upon squeezing, caseous material escaped the lungs
N • Almost completely consolidated by fibrocaseous lesions which
included tiny grayish nodules and small cavitation
• Regional lymph nodes were enlarged
I • Caseation necrosis

G
Figure 11.8 Layers of ulcers

Ulcer
• Local defect or excavation of the surface of an organ or tissue that
is produced by the sloughing of inflamed necrotic tissue
• Pectic Ulcer Disease Figure 11.9 Pulmonary tuberculosis with visible granuloma formation
o Depending on the appearance of the edge of the ulcer can you
identify if it’s malignant or benign peptic ulcer
o Heat-up-margin – edge that looks similar to stuffed crust pizza

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 Cellular Adaptation, Inflammation and Repair (Laboratory)
HS 202 Exam 1 Trans 3A

Histologic Findings Histologic Findings

• Granuloma • Presence of foreign-body type multinucleated giant cells
o Nodular collection of epithelioid histiocytes – main determinant o “bag of marbles” appearance of nuclei since uclei haphazardly
o Cuff of lymphocytes surrounding histiocytes arranged within the cell.
o Eosinophilic o Foreign body is left undigested (suture remnants)
o Multinucleated Giant Cells may be present • Granuloma secondary to suture
 Langhans-type (Horse-shoe shaped nuclei)
 Foreign-body type
 For foreign bodies Foreign body
 Scattered nuclei
giant type cell
 Touton-type
 For lipid-rich tissues
 Ring shaped nuclei
o Central necrosis is present

suture remnant

Figure 11.12 Suture Granuloma

Figure 11.10 Granuloma formation with central necrosis
Questions
• What are the two types of granuloma based on inciting agent?
o Foreign body granulomas
▪ Incited by relatively inert foreign bodies, in the absence of
T cell-mediated immune responses
▪ Typically, forms around talc, sutures, and other fibers that
are large enough to preclude phagocytosis by
macrophages and do not incite any specific inflammatory
or immune response
o Immune granulomas
▪ Incited by a variety of agents capable of inducing a
persistent T cell-mediated immune response
▪ Hard-to-eradicate agents like persistent microbes or self-
antigens
Figure 11.11 Langhans cell histiocyte with horse-shaped nuclei
G. CASE 7: GRANULATION TISSUE
A 49-year old male complained of a polypoid, ulcerated and
Questions
bleeding mass on the left forefinger. This mass started as a wound
• What is a granuloma? which he got while doing carpentry work at home. Grossly, the mass
o Collection of activated macrophages, often with T- was elevated, and ulcerated with a hemorrhagic base. Histologic
lymphocytes, and sometimes associated with central necrosis sections showed granulation tissue.
o Must have intact immune response to form a granuloma
▪ If a patient has AIDS, there can be no granuloma formation Histologic Findings
• What are other diseases that cause granulomatous • Newly formed capillaries
inflammation? • Fibroblasts
o Foreign bodies that can’t be destroyed
• Mixed inflammatory cells infiltrate (lymphocytes and neutrophils)
o Fungal infections
• Granulation tissue
o Sarcoidosis
o Not a granuloma
o Leprosy
o Active Neovascularization
o Chron’s disease
▪ Still no pericytes which keep the fluids in, causing edema
o Cat-scratch disease
o Fibroblast proliferation
o Mixed inflammatory infiltrate
F. CASE 6: SUTURE GRANULOMA
A 25-year old female underwent excision of a 1-cm in
diameter, firm, movable, non-tender, ill-defined, left breast mass. Four
months later, she had previously undergone excision of a benign
breast mass in the same area. The case was diagnosed as suture
granuloma

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 Cellular Adaptation, Inflammation and Repair (Laboratory)
HS 202 Exam 1 Trans 3A

Figure 11.13 Granulation tissue

Questions
• What is neovascularization?
o Same as angiogenesis.
o New blood vessel formation in pre-existing blood vessels
▪ Neoangiogenesis: vascularization induced by tumor cells
▪ Vasculogenesis: formation of new blood vessels in embryo
• What factors induce neovascularization?
o Cytokines
o PDGF, VEGF
• What are the components of the repair process of tissues
subjected to chronic inflammation?
o Scar formation
o Angiogenesis
o Formation of granulation tissue
o Remodeling of connective tissue

REFERENCES
2021 trans. Pictures from lecture. Robbins Pathologic Basis of
Disease (9th edition).
*Picture heavy af. Print at own discretion.

END OF TRANS

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