ADAPTIVE CHANGE Etiology: Increased workload of the heart
Endometrial Hyperplasia, Uterus Pathogenesis:
Brown Atrophy, Heart
Left Ventricular Hypertrophy, Heart
ENDOMETRIAL HYPERPLASIA
Organ:UTERUS
Disease/Diagnosis: Endometrial Hyperplasia
Type of Adaptation/Pathological Change:
Hyperplasia
Etiology/Mechanism of adaptive change: Prolonged
and unopposed estrogenstimulation
Pathogenesis: Increased estrogen →increased
proliferation of endometrial glands
Micro: Non –Atypical Hyperplasia*; increased gland-
to-stroma ratio; cysticallydilated glands; increased
endometrial folds
Gross: Swiss-cheese like appearance
Predisposing factors: Menopause, prolonged
administration of estrogenic agents, PCOS
(Polycystic Ovary Syndrome)
Clinical Manifestation: Menorrhagia(excessive
menstrual bleeding), metorrhagia(uterine bleeding
at irregular intervals)
Diagnostic Test: Endometrial Biopsy
Treatment/Management: Progesterone Therapy,
Hysterectomy
What is the characteristic gross finding of this
lesion?
BROWN ATROPHY
Organ:HEART (myocardium)
Disease/Diagnosis: Brown Atrophy of the Heart
Type of Adaptation/Pathological Change: Atrophy
Type of Injury: Reversible
Etiology: Aging(senile atrophy); malnutrition
Pathogenesis: Decreased blood supply →decreased
synthesis of cellular building blocks and increased
breakdown of cellular organelles →reduction in size
Gross: Reduction in the size of the heart, chocolate
myocardium
Micro: atrophic myocardial cells; widened
interstialspaces; brownish lipofuscin pigments*
(residual autophagicbodies) located at cytoplasm
perinuclear (near nucleus) due to lipid peroxidation
Clinical Manifestation: Weight loss; seen in the heart
of aging patients, severe malnutrition and cancer
cachexia
Pathway: ubiquitin-proetosomepathway
Complication: terminal cancer
LEFT VENTRICULAR HYPERTROPHY
Organ:HEART
Disease/Diagnosis: Left Ventricular Hypertrophy
Type of Adaptation/Pathological Change:
Hypertrophy
Type of Injury: Irreversible
a.Increased workload →mechanical stretch of cardiac muscles
→activation of mechanical sensors →induce production of GFs
and agonist
b.Activation of signal transduction pathways involved in
hypertrophy and signaling downstream of G-protein-coupled
receptors
c.Activation of transcription factors →increased synthesis of
muscle protein
Gross: thickened left ventricle (normal = 1.3-1.5 cm)
Micro: Increased tissue mass of myocardial fibers
Clinical Condition/Complication: Heart Failure
Lab Dx: Chest X-Ray
Genetic alteration: Increased Atrial Natriuretic Peptide
REVERSIBLE INJURY
Cellular Swelling, Kidney
Fatty Change, Liver
CELLULAR SWELLING
Organ: KIDNEY
Disease/Diagnosis: -
Type of Injury: Reversible
Etiology: ATP depletion / hypoxia
Pathogenesis: Decreased oxygen supply →decreased ATP
synthesis →failure of energy dependent ion pumps (Na-K
pump) in the plasma membrane →increased influx of sodium
→water influx
Gross: Increased weight, turgor and pallor of kidney
Micro: Tubules with dilated epithelial cells; small clear
vacuoles in cytoplasm due to hydrophobic change or vacuolar
degeneration
Lesion: Cellular swelling –first manifestation of all cellular
injury
Fatty Change
Organ: LIVER
Disease: Steatosis
Etiology: Excessive alcohol intake; obesity
Pathogenesis: impaired synthesis/catabolism →excessive
accumulation of triglyceride within the hepatocytes
Micro: eosinophilic granular cytoplasm, fat vacuoles*, signet
ring-like cells
Gross: enlarged greasy liver with a pale yellow appearance
Type of Reversible Injury: Fatty change
Clinical Condition: Jaundice, ascites
Clinical Presentation: Generally asymptomatic, fatigue,
malaise, right upper quadrant discomfort
Lab Dx: Mild elevations of serum bilirubin and alkaline
phosphatase; Elevated alanine transaminase (ALT) and
aspartate transaminase (AST)
Treatment: Diet Modification
Fatty Change
Pathologic Cholesterol Accumulations:
atherosclerosis (blood vessels), xanthomas (tumor in
skin and tendons), cholesterolosis(galbladder),
Niemann-Pick disease, type C (multiple organs)
Give the complete histologicbasis of this lesion?
Fat vacuole with Triglyceride inside
IRREVERSIBLE INJURY
CoagulativeNecrosis: Myocardial Infarction, Heart
CaseationNecrosis: Tuberculosis, Intestine and
Lungs
Myocardial Infarction
Organ:Heart
Diagnosis: Myocardial Infaction
Disease / Clinical Condition: Atherosclerosis
Type of Injury: Irreversible
Types of Necrosis: CoagulativeNecrosis
Etiology: Ischemia due to blood vessel obstruction
Pathogenesis: Ischemia →Denaturation of structural
proteins and enzymes
Micro: Loss of nuclei*; preservation of the
myocardial architecture (coagulative necrosis);
presence of lipofuscin granules; Pale myocardial
cells, striations are lost; wavy fibers at the periphery
of infarcted area; pyknotic(shrunken) nuclei;
karryorhexis(nuclear fragmentation),
karyolysis(disappearance of nuclei)
Gross: Decreased heart size with necrosis;
thickening of LV and decreased weight of the heart
Clinical Presentation: Chest pain, rapid weak pulse,
hypotension, SOB
Lab Dx: CK-MB, TropI and T(specific); ECG: ST
elevation and T wave inversion
Treatment: Thrombolytic agents,
PercutaneousTransluminalCoronary Angiography
*Earliest histological change: within 24 hours
*Most pronounced ischemia: Subendocardium
Pigment: Lipofuscin
Infarct: White Infarct
Hemodynamic Change: Thrombus
Tuberculosis
Organ: Lungs (apex) / Intestine (ileum)
Disease/Diagnosis: Tuberculosis of the Lungs /
Intestine
Type of Injury: Irreversible
Type of Necrosis: CaseationNecrosis
Lesion: Tubercle
Types of Inflam: Chronic
GranulomatousInflammation
Etiology: Foci of Tuberculosis infection secondary to
acid-fast bacilli Mycobacterium tuberculosis
Pathogenesis: effects of Type IV hypersensitivity /
CD4+T cells
Micro: Granuloma with entralareas of caseation necrosis in
submucosa; presence of epitheloidcells*, multinucleated
Langhansgiant cells in the periphery; foreign body giant cells;
nucleus arranged haphazardly
Gross: Foci of the TB lesions on the apex, parenchymal
scarring; formation of cyst leading to cavitation; cheese-like
appearance
Clinical Manifestation: Cough and purulent sputum
production, often with blood streak
Lab Dx: AFB Microscopy; Chest Radiograph (radiologic
analysis)
Treatment: RIPE (Rifampin, Isoniazid, Pyrazinamide,
Ethambutol
CELLULAR ACCUMULATIONS
Uric Acid: Gout, Olecranon Bursae
Cholesterol: Atheroma, Aorta
Pigment Accumulation: Hemosiderin-laden Macrophages in
Chronic Passive Congestion, Lungs
Uric Acid: Gout
Organ: OLECRANON BURSAE
Disease/Diagnosis : Gouty Arthritis
Etiology: Primary: Idiopathic (90%); Secondary due to
underlying dse(10%)
Pathogenesis: Overproduction or reduced excretion, or both
of uric acid →hyperuricemia→precipitation of monosodium
urate crystals in joint →tissue injury and inflammation
Gross: Swollen and inflamed joint, tophus* (aggregates of
urate crystals) which may appear in articular cartilage,
ligaments, tendons and bursae
Micro: Dissolved monosodium urate crystals surrounded by
reactive fibroblast mononuclear inflammatory cells and
foreign body giant cells
Intracellular Accumulation: Monosodium Urate Crystals
Lesion: Tophus
Clinical Condition: Gouty Arthritis
Clinical Presentation: Severe pain, swelling, erythemaof
involved joint
Lab Dx: arthrocentesis, serum BUN(Blood Uric Acid) Level, x-
ray (to rule out osteoarthritis)
Treatment: NSAIDS, colchicine, allopurinol
Cholesterol: Atheroma
Organ: Aorta (tunica intima)
Disease/Diagnosis: Atherosclerosis
Lesion: Atheroma at Tunica Intima; fatty streaks (earliest)
Intracellular Accumulations: Cholesterol
Etiology: Hypercholesterolemia (Risk factor)
Pathogenesis: Risk factors (hyperlipidemia, etc.) →chronic
endothelial injury (intimal thickening) →endothelial
dysfunction →LDL accumulation in vessel wall →macrophage
activation & smooth muscle recruitment →macrophages &
smooth muscle cells engulf lipid →smooth muscle cell
proliferation, collagen & ECM deposition →extracellular &
intracellular lipid accumulation →atheroma
Gross: White yellow plaques
Micro: Fatty Streak –earliest lesion in
atherosclerosis;
Fibrous Cap –composed of smooth muscle cells and
dense collagen
Cholesterol clefts* –lipid filled foamy macrophages
Cells: Lipid-laden macrophages (foam cells), T cells
and smooth muscle cells
Most Common Location: lower abdominal aorta
Clinical Condition: Atherosclerosis
Clinical Presentation: Chest Pain, SOB, fatigue,
weakness
Treatment: Statins
If the abnormal deposits found in this tissue section
is located in the dermis, what is this called?
XANTHOMAS
Hemosiderin-laden Macrophages : CPC, Lungs
Organ:Lungs
Disease/Diagnosis: Chronic Passive Congestion
Site: Alveolar capillaries
Etiology: Left sided heart failure
Pathogenesis: LSHF –damming back of blood from
left side of the heart to lungs–congestion of alveolar
capillaries –increased hydrostatic pressure –fluid
leaks out into interstitial space
Gross: Enlarged, boggy, heavy with fuidoozing out
when squeezed
Micro: Congested alveolar capillaries; intra alveolar
transudate –finely granular, pale pink material, heart
failure cells or hemosiderin-laden macrophages
Pigment accumulation: Hemosiderin
Clinical Presentation: Chest pain, SOB
Lab Dx: Chest X-Ray check BNP
Treatment: Diuretics(Lasix), Vasodilators
Hemodynamic Change: Edemadue to increased
hydrostatic pressure –excessive interstitial fluid
which accumulates in alveolar space and
Congestiondue to increased blood volume,
decreased blood outflow from tissue, passive
INFLAMMATION AND REPAIR
Acute Inflammation: Acute Appendicitis, Appendix
Chronic Inflammation: Chronic Pyelonephritis,
Kidney
Chronic Granulomatous Inflammation:
Tuberculosis, Intestine and Lungs
Repair: Post Necrotic Cirrhosis, Liver
Acute Appendicitis
Organ: APPENDIX
Disease/Diagnosis: Acute Appendicitis
Etiology: 50-80% due to overt luminal obstruction
usually caused by small stone-like mass of stool or
fecalith
Pathogenesis: progressive increase in intraluminal
pressure that compromise the venous outflow
Obstruction →stasis of luminal contents favoring bacterial
proliferation(usually E. coli)→ischemia and inflammation
→tissue edema and neutrophilic infiltration of the lumen,
muscular wall and peri-appendicealsoft tissue
Periappendicitis: Neutrophilsin the periphery
Predominant Inflammatory Cells: Neutrophils
Location : Muscularis
Micro: Infiltration of the muscularispropriaby
polymorphonuclearcells, particularly neutrophils; Hyperemia –
dilated serosal blood vessel, increased in oxygenated blood,
lumphoidnodules with germinal center
Gross: yellow-tan exudates, swollen appendix, hyperemia
Location of Lesion: Muscularis
Clinical Presentation: periumbilical pain at RLQ, nausea,
vomiting, increased WBC count, deep tenderness at
McBurney’spoint
Lab Dx: NeutrophilicLeukocytosis
Treatment: Appendectomy
Hemodynamic Change: Hyperemia
Type of Inflammation: Acute Suppurative Inflammation
Chronic Pyelonephritis
Organ: KIDNEY
Disease/Diagnosis: Chronic Pyelonephritis
Etiology: Repeated bouts of renal inflammation and scarring
due to infections (85% due to gram negative bacilli)
Pathogenesis: Bacterial colonization of the distal urethra
→entry into bladder →ascending infection →acute
polynephritis→repeated bouts + obstruction →chronic
pyelonephritis
Micro: Atrophic tubules*; interstitial fibrosis; mononuclear
cells (lymphocyte and macrophages); thyroidization–dilated
tubules with flattened epithelium with a colloid like material
resembling thyroid
Gross: Irregular scarred kidney, involves calysesand pelvis
Clinical Presentation: Back pain, fever, pyuria, poluuria,
bacteriuria
Lab Dx: Urinalyis, IV pyelogram, ultrasound
Treatment: Dialysis
Type of inflammation: Chronic Inflammtion
Most common cause: E. coli
Chracteristic Cells: Mononuclear cells (Lymphocyte and
plasma cells)
Tuberculosis
Organ: LUNGS (apex) / INTESTINE (ileum)
Disease/Diagnosis: Tuberculosis of the Lungs / Intestine
Type of Injury: Irreversible
Type of Necrosis: Caseation Necrosis
Lesion: Tubercle
Types of Inflam: Chronic GranulomatousInflammation
Etiology: Foci of Tuberculosis infection secondary to acid-fast
bacilli Mycobacterium tuberculosis
Pathogenesis: effects of Type IV hypersensitivity / CD4+T cells
Gross: Foci of the TB lesions on the apex, parenchymal
scarring; formation of cyst leading to cavitation; cheese-like
appearance
Micro: Granuloma with entralareas of caseation
necrosis in submucosa; presence of epitheloid cells*,
multinucleated Langhansgiant cells in the giant cells
in the periphery; foreign body giant cells; nucleus
arranged haphazardly
Antibody: CD4+ Cells
Lesion: Tubercle
Predominant Inflammatory Cell: Lymphocyte
Clinical manifestation: Cough and purulent sputum
production, often with blood streak
Lab Dx: AFB Microscopy; Chest
Radiograph(radiologic analysis)
Treatment: R.I.P.E. (Rifampin, Isoniazid,
Pyrazinamide, Ethambutol)

Post-Necrotic Cirrhosis
Organ: LIVER
Disease/Diagnosis: Post-Necrotic Cirrhosis of the
Liver
Etiology: chronic hepatitis Infection (HBV and HCV),
non alcoholic fatty liver disease, alcoholic liver
disease
Pathogenesis: diffused transformation of the liver
into regenerative parenchymal nodules surrounded
by fibrous bands and variable degrees of porto-
systemic shunting
Micro: Diffuse fibrosis which eventually link portal
tracts; Regenerating hepatocytessurrounded by
fibrous bands
Gross: Nodules (bridging fibrous septa and
regenerating hepatocytes); limp, wrinkled organ
Clinical Presentation: Cirrhosis may remain clinically
silent for many years until complications of portal
hypertension –ascites and esophageal varices;
anorexia
Lab Dx: increased serum bilirubin and alkaline
phosphate, liver biopsy
Complication: liver carcinoma
The nodules in this lesion represents what aspect of
the healing process?
--Bridging fibrous septa and regenerating
hepatocytes which form nodules