1.
ATROPHY
TESTIS ATROPHY
TESTIS ATROPHY
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Atrophic tubules are hyalinized and partially lined by Sertoli cells.
TESTIS ATROPHY
Testicular tubules show: Marked loss of germ cells, tall Sertoli cells (blue arrow)
peritubular fibrosis (green arrow ) and interstitial fibrosis (red arrow)
THYROID NORMAL
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THYROID ATROPHY
Are the thyroid follicular
cells dead or alive? Reversible?
Hashimoto’s Thyroiditis ( an autoimmune disease) causes proliferation of
lymphoid follicles (arrow).
QUIZ
BRAIN in ALZHEIMER’S DISEASE
Atrophy, kidney
CHOOSE:
Cell adaptation CHOOSE:
Cell injury Reversible or Irreversible
Cell death
Atrophy, testis
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CHOOSE:
Cell adaptation CHOOSE:
Cell injury Reversible or
Cell death Irreversible
What organ is atrophied?
What is the probable cause?
CHOOSE:
Cell adaptation
Cell injury CHOOSE:
Cell death Reversible or Irreversible
2. HYPERPLASIA
PROSTATE
Both glands and stroma can become
hyperplastic.
Epithelial or stromal predominant
hyperplasia may occur.
PROSTATE – NORMAL GLANDS
HYPERPLASIA – Prostate GLANDULAR
portion
Secretory and basal cell layers proliferate and show papillary infoldings
(arrow)
PROSTATE – NORMAL STROMA
HYPERPLASIA , Prostate STROMAL
portion
HYPERPLASIA, Prostate
NORMAL Palatine Tonsil
B-lymphocytes forming lymphoid follicles are found only in cortical area.
HYPERPLASIA, Palatine tonsil
Increased B-lymphocytic activity causes lymphoid follicles to increase in
number, with germinal centers.
DIFFUSE HYPERPLASIA, THYROID
FOLLICLES
Low power shows prominent infoldings of hyperplastic
epithelium in Grave’s disease, an autoimmune disease.
THYROID HYPERPLASIA
HP shows tall columnar epithelium lining the infoldings. Clear vacuoles
shows increased acitivity of epithelium to produce hormone causing
scalloping out of the colloid.
HYPERTROPHY
Cardiac hypertrophy (LV)
HYPERTROPHY, MYOCARDIUM
3. HYPERTROPHY and
HYPERPLASIA
PREGNANT UTERUS
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NORMAL & GRAVID UTERUS
(Same magnification)
QUIZ
PROSTATIC HYPERPLASIA
CHOOSE:
Cell adaptation
Cell injury CHOOSE:
Cell death Reversible or Irreversible
HYPERPLASIA, Endometrial glands
CHOOSE:
Cell adaptation
Cell injury CHOOSE:
Cell death Reversible or Irreversible
4. METAPLASIA
CERVIX , Squamous cell
CERVIX, Normal
Carcinoma
SQUAMO-COLUMNAR
TRANSFORMATION ZONE
JUNCTION
METAPLASIA, CERVIX
METAPLASIA, Bronchus
METAPLASIA , Esophagus
QUIZ
METAPLASIA,
RESPIRATORY EPITHELIUM
CHOOSE:
Cell adaptation CHOOSE:
Cell injury Reversible or
Cell death
Irreversible?
5. FATTY CHANGE
NORMAL LIVER FATTY CHANGE , Liver
MAIN CAUSES OF FATTY
CHANGE
Metabolic stress – Hypoxia, Kwashiorkor,
Diabetes Mellitus
Toxins - Alcohol, rare drug reactions
Less common:
Reye’s syndrome - microvesicular fatty change
Fatty liver of pregnancy
Fatty change is most
commonly caused by
metabolic stresses &
alcohol.
FATTY CHANGE
SEVERE FATTY CHANGE (STEATOSIS),
Liver
from Alcoholism
CHOOSE:
Cell adaptation
Cell injury
Cell death
FATTY LIVER
HYDROPIC
DEGENERATION
HYDROPIC
NORMAL Renal tubules DEGENERATION, Renal
tubules
CHOOSE:
a) Cell adaptation
b) Cell injury
c) Cell death
STROMAL FATTY
IINFILTRATION, Heart
CHOOSE:
Cell adaptation
Cell injury
Cell death
6. COAGULATION NECROSIS
RENAL TUBULES - COAGULATION NECROSIS –
NORMAL RENAL TUBULES
Coagulation necrosis, kidney
N = Normal
I = Coagulation necrosis
COAGULATION NECROSIS
NORMAL
– Heart
Many nuclei have disappeared. Beginning acute inflammation is seen.
GALLBLADDER - COAGULATION NECROSIS,
NORMAL GALLBLADDER
ACUTE MYOCARDIAL
INFARCTION
Hemorrhagic infarct, intestine
White infarct/ coagulative necrosis
Dry GANGRENE (Frostbite)
Wet GANGRENE
(Ischemia w infection)
6. COAGULATION NECROSIS
ACUTE MYOCARDIAL
INFARCTION
s
Hemorrhagic infarct, intestine in
strangulated hernia
White infarct/ coagulative necrosis,
spleen
COAGULATION NECROSIS – Heart
(ACUTE MYOCARDIAL INFARCTION)
s
RENAL TUBULES - NORMAL
COAGULATION NECROSIS –
RENAL TUBULES
Coagulative necrosis, kidney
HEMORRHAGE
Coagulative necrosis, kidney
GALLBLADDER - COAGULATION NECROSIS,
NORMAL GALLBLADDER
Dry GANGRENE (Frostbite)
Wet GANGRENE
(Ischemia w infection)
7. CASEOUS NECROSIS
CASEOUS NECROSIS
LYMPH NODE LUNG
Granuloma w CASEOUS NECROSIS
(from Histoplasmosis)
NORMAL LUNG
GRANULOMA in TUBERCULOSIS, LUNG
Cells in a granuloma:
Epithelioid cells (modified macrophages), Lymphocytes
GRANULOMA
CASEATING GRANULOMA
Granuloma w CASEOUS NECROSIS
(from Histoplasmosis)
Is caseation present?
Is caseation present?
Is caseation present?
Is caseation present?
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CHOOSE:
Cell adaptation
Cell injury
Cell death Reversible or Irreversible?
8. LIQUEFACTION
NECROSIS
Abscess
LIQUEFACTION NECROSIS
LIQUEFACTION NECROSIS in ABSCESS
Lung abscess
Liver abscess
Cerebral infarct/liquefactive necrosis
Cerebral infarct/liquefactive necrosis
Liquefactive necrosis, brain
9. ENZYMATIC FAT
NECROSIS
ENZYMATIC FAT NECROSIS – Mesenteric fat
ENZYMATIC FAT NECROSIS
showing chalky white areas on pancreas.
ADIPOSE TISSUE, ENZYMATIC FAT
Normal NECROSIS, Omentum
MESENTERIC FAT - ENZYMATIC FAT
NORMAL NECROSIS
TRAUMATIC FAT NECROSIS,
Breast
TRAUMATIC FAT
BREAST - Normal NECROSIS, Breast
QUIZ
What type of necrosis is present?
What type of necrosis is present?
What type of lesion is present?
CHOOSE:
Cell adaptation
Cell injury
Cell death
What type of lesion is present?
CHOOSE:
Cell adaptation
Cell injury
Cell death
What type of necrosis is present in the
field?
What type of lesion is present at the
pointer?
What type of lesion is present at the
pointer?
CHOOSE:
Cell adaptation CHOOSE:
Cell injury Reversible or
Cell death
Irreversible?
What type of lesion is present at the
pointer?
10 EDEMA, CONGESTION &
HEMORRHAGE
EDEMA
EDEMA
BLISTER
R PLEURAL PLEURAL
EFFUSION EFFUSION w
HMGE
PITTING EDEMA
PULMONARY EDEMA
LARYNGEAL EDEMA is life-threatening!
CONGESTION and
HEMORRHAGE
CONGESTION
HEMORRHAGE w
CONGESTION, Lung
neutrophiles
CHRONIC PASSIVE
CONGESTION
CPC, lung w hemosiderin laden macrophages
Carbon pigment in hilar lymph node
Chronic Passive Congestion, Liver
(Nutmeg liver)
CPC, liver
13 HEMORRHAGE
HEMORRHAGE
PETECHIAL
HEMORRHAGE on
epicardium
ECCHYMOSIS
HEMORRHAGE under the toe nail
14 THROMBOSIS
LINES OF ZAHN (True THROMBUS)
Closeup of THROMBUS occluding the main coronary artery
THROMBUS from leg veins occludes main pulmonary artery. .
. . . and becomes adherent to the wall of
pulmonary artery
Pulmonary embolus occludes main pulmonary artery
Pulmonary thrombo-embolus
TUMOR EMBOLUS in a lymphatic vessel
14 ACUTE INFLAMMATION
ACUTE APPENDICITIS
ANATOMIC IDENTIFICATION of ACUTE
INFLAMMATION
VASCULAR
DILATATION
FLUID EXUDATION
CELLULAR
EXUDATION
VASCULAR DILATATION
VASCULAR DILATATION in ACUTE
BRONCHOPNEUMONIA
ACUTE INFLAMMATORY EXUDATE (Cells
& Fluid) w vascular dilatation
in Pneumonia
CELLULAR EXUDATION
CELLULAR EXUDATE is predominantly
NEUTROPHILIC in ACUTE
INFLAMMATION
Margination & Emigration
Emigration
Neutrophils phagocytose Gram+ cocci
FLUID EXUDATION
FLUID EXUDATE may be predominantly
SEROUS
Echocardiogram shows SEROUS EXUDATION in a
confined space PERICARDIAL EFFUSION(PE)
FLUID EXUDATE may be predominantly
FIBRINOUS
FIBRINOUS PERICARDITIS
(“Bread & butter” pericarditis)
Mostly, FLUID EXUDATE is predominantly
CELLULAR (PURULENT EXUDATE)
in bronchi causes purulent sputum
PURULENT EXUDATE on meninges due to
Strep pneumonia
. . .causes obliteration of sulci
ACUTE APPENDICITIS . . .
. . . may rupture to cause . . .
. . . PURULENT PERITONITIS
In SEVERE inflammation, FLUID EXUDATE may
be
RBCs
Fibrin
FIBRINOPURULENT w HEMORRHAGE
Localized suppurative inflammation is seen in
LUNG ABSCESS
. . . and in a Skin PUSTULE
PSEUDOMEMBRANOUS COLITIS with necrosis of
intestinal epithelium, fibrin & inflammatory cells
Pseudomembrane also forms in diphtheria.
Impt to remember: INFLAMMATION is . . .
Without inflammation, life would be
impossible.
14 ACUTE INFLAMMATION
ACUTE APPENDICITIS
ANATOMIC IDENTIFICATION of ACUTE
INFLAMMATION
VASCULAR
DILATATION
FLUID EXUDATION
CELLULAR
EXUDATION
VASCULAR DILATATION
VASCULAR DILATATION in ACUTE
BRONCHOPNEUMONIA
ACUTE INFLAMMATORY EXUDATE (Cells
& Fluid) w vascular dilatation
in Pneumonia
CELLULAR EXUDATION
CELLULAR EXUDATE is predominantly
NEUTROPHILIC in ACUTE
INFLAMMATION
Margination & Emigration
Emigration
Neutrophils phagocytose Gram+ cocci
FLUID EXUDATION
FLUID EXUDATE may be predominantly
SEROUS
Echocardiogram shows SEROUS EXUDATION in a
confined space PERICARDIAL EFFUSION(PE)
FLUID EXUDATE may be predominantly
FIBRINOUS
FIBRINOUS PERICARDITIS
(“Bread & butter” pericarditis)
Mostly, FLUID EXUDATE is predominantly
CELLULAR (PURULENT EXUDATE)
in bronchi causes purulent sputum
PURULENT EXUDATE on meninges due to
Strep pneumonia
. . .causes obliteration of sulci
ACUTE APPENDICITIS . . .
. . . may rupture to cause . . .
. . . PURULENT PERITONITIS
In SEVERE inflammation, FLUID EXUDATE may
be
RBCs
Fibrin
FIBRINOPURULENT w HEMORRHAGE
Localized suppurative inflammation is seen in
LUNG ABSCESS
. . . and in a Skin PUSTULE
PSEUDOMEMBRANOUS COLITIS with necrosis of
intestinal epithelium, fibrin & inflammatory cells
Pseudomembrane also forms in diphtheria.
Impt to remember: INFLAMMATION is . . .
Without inflammation, life would be
impossible.
14 ACUTE INFLAMMATION
ACUTE APPENDICITIS
ANATOMIC IDENTIFICATION of ACUTE
INFLAMMATION
VASCULAR
DILATATION
FLUID EXUDATION
CELLULAR
EXUDATION
VASCULAR DILATATION
VASCULAR DILATATION in ACUTE
BRONCHOPNEUMONIA
ACUTE INFLAMMATORY EXUDATE (Cells
& Fluid) w vascular dilatation
in Pneumonia
CELLULAR EXUDATION
CELLULAR EXUDATE is predominantly
NEUTROPHILIC in ACUTE
INFLAMMATION
Margination & Emigration
Emigration
Neutrophils phagocytose Gram+ cocci
FLUID EXUDATION
FLUID EXUDATE may be predominantly
SEROUS
Echocardiogram shows SEROUS EXUDATION in a
confined space PERICARDIAL EFFUSION(PE)
FLUID EXUDATE may be predominantly
FIBRINOUS
FIBRINOUS PERICARDITIS
(“Bread & butter” pericarditis)
Mostly, FLUID EXUDATE is predominantly
CELLULAR (PURULENT EXUDATE)
in bronchi causes purulent sputum
PURULENT EXUDATE on meninges due to
Strep pneumonia
. . .causes obliteration of sulci
ACUTE APPENDICITIS . . .
. . . may rupture to cause . . .
. . . PURULENT PERITONITIS
In SEVERE inflammation, FLUID EXUDATE may
be
RBCs
Fibrin
FIBRINOPURULENT w HEMORRHAGE
Localized suppurative inflammation is seen in
LUNG ABSCESS
. . . and in a Skin PUSTULE
PSEUDOMEMBRANOUS COLITIS with necrosis of
intestinal epithelium, fibrin & inflammatory cells
Pseudomembrane also forms in diphtheria.
Impt to remember: INFLAMMATION is . . .
Without inflammation, life would be
impossible.
15 CHRONIC NONSPECIFIC
INFLAMMATION
Continued Attempts at
INFLAMMATION HEALING
CHRONIC INFLAMMATION
MORPHOLOGIC FEATURES of
CHRONIC INFLAMMATION
Mononuclear cell infiltration
Cellular Proliferation
(Vascular & fibroblastic)
Chronic Inflammatory Infiltrate
CHRONIC PAROTITIS
. . . and MONONUCLEAR CELLS:
. . . With loss of glandular tissue Lymphocytes, Plasma cells & macrophage
CHRONIC INFLAMMATORY CELLS w
FIBROBLASTS and fibrous extracellular matrix
CHRONIC INFLAMMATORY CELLS
REPAIR or HEALING
a. VASCULAR GRANULATION
TISSUE
b. Fibrovascular Granulation Tissue
c. COLLAGENOUS SCAR
GRANULATION TISSUE on the wall of an
abscess
Granulation tissue in acute myocardial infarction
showing fibroblast & capillaries
Granulation tissue under HP showing fibroblasts
& mononuclear cells
Scarring & adhesions may form bands between lung
& pleura
CHRONIC GRANULOMATOUS
INFLAMMATION
GRANULOMA
CELLS: Epithelioid cells, GIANT CELL – a
lymphocytes, plasma cells, committee of epithelioid
fibroblasts cells
GRANULOMA at the edge of a tubercle
Caseating Granuloma . . . or from Histoplasma
from Tb . . . capsulatum
LANGHAN’S Type FOREIGN BODY Type
GIANT CELL seen in GIANT CELL next to
Tuberculosis aspirated vegetable segment
FOREIGN BODY Type GIANT CELL
REACTION to FOREIGN BODY -
EOSINOPHIILES
REACTION to PARASITE (Filaria)
Granuloma with
Talc crystals used to dilute injected drugs
(seen under polarized light)
HASHIMOTO’S
THYROIDITIS
H
Early, Lymphocytes replace follicles partially.
Hurthle cells line some follicles.
Later, atrophy of follicles, interstitial fibrosis, few
residual chronic inflammatory cells
