4. Cellular adaptations
Definition: Reversible changes that take place in a cell in
order for it to survive and function in an abnormal
environment
E.g: changes in size, number or differentiation of cell
9. Pathological
● Hypertrophy of cardiac muscle:
left ventricular hypertrophy in
hypertension or valve defects
● Hypertrophy of smooth muscle:
urinary bladder muscle in benign
prostatic hyperplasia(BPH)
Physiological
● Hypertrophy of skeletal muscles
in bodybuilders, labourers,
athletes
● Hypertrophy of smooth muscle:
uterus in pregnancy due to
estrogen
13. Causes
Can be physiological or pathological
Physiological
Due to hormonal stimulation or compensation
● Breast hyperplasia at puberty, pregnancy and lactation
● Hyperplasia of uterus in pregnancy
● Compensatory hyperplasia: liver grows back after partial
removal(hepatectomy)
14. Pathological
Due to excessive endocrine stimulation or chronic irritation
Can progress to cancer
● Endometrial hyperplasia due to estrogen
● Bladder muscle - BPH
● Chronic injury: skin/oral mucosa
19. Pathological
Local or generalised atrophy
Local:
● Disuse atrophy: atrophy of muscles immobilised in plaster cast or
prolonged bed rest
● Denervation atrophy: muscle atrophy due to nerve damage in
poliomyelitis
● Ischemic atrophy(decreased bloody supply): brain atrophy due to
atherosclerosis of carotid artery
● Pressure atrophy: renal atrophy in hydronephrosis
Generalised:
● Starvation atrophy: malnutrition
27. Cell injury
Definition: a variety of changes of stress that a cell suffers
due to external as well as internal environmental changes.
28. Causes
Cell injury can be due to:
- Reduced oxygen supply(hypoxia)
- Physical agents: trauma, radiation, electric shock
- Chemical agents: heavy metals, chemicals, pollutants, alcohol,
cigarette smoking
- Infectious agents: virus, bacteria, fungi, parasites
- Abnormal immune reactions: autoimmunity, hypersensitivity
reaction
- Nutritional imbalance
- Genetic factors: abnormal genes or chromosomal abnormalities
- Idiopathic: causes is not known
29. Types of cell injury
2 types
Reversible Irreversible
30. Reversible cell injury
If the stimulus is acute and brief or mild, the changes
produced in cell are reversible.
2 patterns seen under microscopy:
● cellular swelling(hydropic)
● Fatty change
31. Cloudy swelling(Hydropic change)
“Due to changes in ion concentration, there is increased water flow
into injured cells, leading to increased water content”
Causes: bacterial toxins, chemical poisons, malnutrition
Organs involved: Kidney, liver, heart and muscle
Gross features:
● organ affected is slightly enlarged due to swelling of cells
● Cut surface: cloudy appearance
Microscopic features:
● Cloudy swelling seen
32.
33. Fatty change(steatosis)
“Abnormal accumulation of triglycerides(lipids) within cells”
Organs affected: liver mainly, heart, muscle, kidney
Causes:
● disorders with liver damage: alcohol abuse, malnutrition,
starvation
● Disorders with hyperlipidemia: obesity, diabetes mellitus,
congenital hyperlipidemia
34. Gross features(fatty liver):
● enlarged liver, yellow, soft, greasy
Microscopy:
● accumulation of fat in small vacuoles in cytoplasm
● Nucleus gets pushed to periphery of cells
38. Irreversible cell injury
Definition: When cell is exposed to continuous injurious
stimulus or if injury is severe, the cell undergoes cell death
2 types of cell death:
● Necrosis(always pathological)
● apoptosis(may be physiological or pathological)
40. Necrosis
Definition: Necrosis refers to the morphological changes
which indicated cell death in a living tissue after an extremely
harmful injury
41.
42. Causes of necrosis
All the causes of cell injury if severe and persistent can cause
necrosis
- Reduced oxygen supply(hypoxia)
- Physical agents: trauma, radiation, electric shock
- Chemical agents: heavy metals, chemicals, pollutants, alcohol,
cigarette smoking
- Infectious agents: virus, bacteria, fungi, parasites
- Abnormal immune reactions: autoimmunity, hypersensitivity
reaction
- Nutritional imbalance
- Genetic factors: abnormal genes or chromosomal abnormalities
- Idiopathic: causes is not known
43. Morphology
General changes seen:
● Increased eosinophilia
● Nuclear changes:
- Pyknosis: shrinking of nucleus - stains deeply
basophilic
- Karyolysis: fading of basophilic staining of nucleus -
“ghost nucleus”
- Karyorrhexis: nucleus breaks into smaller pieces
“Shrinks, fades and breaks up”
45. Types of necrosis
Different morphological patterns of necrosis
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous necrosis
4. Fat necrosis
5. Fibrinoid necrosis
6. Gangrene or Gangrenous necrosis
46. 1. Coagulative necrosis
Outline of dead cells is preserved. Area affected is called “infarct”.
Causes: ischemia(poor blood supply)
Organs affected: heart, kidney, spleen(any organ except brain)
Gross features:
Necrotic tissue appears dry, pale, yellow, soft
Microscopy:
Outline of dead tissue is preserved
47.
48.
49.
50. 2. Liquefactive necrosis/Colliquative necrosis
When dead tissue rapidly undergoes softening and becomes a
thick liquid mass
Causes: - ischemic injury to CNS
- suppurative infections by bacteria
Organs affected: brain, abscess of any organ
Gross: abscess shows cavity containing pus and surrounding wall
with granulation tissue
Microscopy:
Pus: liquefied necrotic cell debris, dead WBCs, macrophages
51.
52. 3. Caseous necrosis
Features of both coagulative and liquefactive necrosis
Caseous means cheese-like
Causes: seen in tuberculosis - hypersensitivity reaction
Organs affected: lung, lymph nodes commonly
Gross:
● necrotic area is yellowish, soft, friable with well-defined borders
Microscopy:
● Lesion called granuloma
● Caseous necrosis in centre, surrounded by epithelioid cells,
53.
54.
55. 4. Fat necrosis
Death of fat tissue due to injury
Causes:
1. Enzymatic: due to acute pancreatitis
2. Traumatic: due to physical injury
Gross:
● Chalky-white areas
Microscopy:
● Fat cells with pale outline, surrounded by inflammatory reaction
56.
57. 5. Fibrinoid necrosis
Special type of necrosis with deposition of pink-staining fibrin-like
material
Causes: immune-mediated vascular injury
Organs affected: arteries, arterioles, glomeruli of kidney
58.
59. 6. Gangrene/Gangrenous necrosis
Definition: massive necrosis with superadded
putrefaction(decomposition)
Putrefaction is decomposition by micro-organisms
Types:
● Dry gangrene
● Wet gangrene
60. 6a. Dry gangrene
Site: affects distal part of limbs(like foot, toe, fingers)
Cause: due to arterial occlusion
Gross features:
● Dry, shrunken, shriveled(mummified) and dark brown/black
● Line of demarcation between the gangrenous area and adjacent
normal skin
Microscopy:
● smudging of soft tissue
● Line of demarcation made of granulation tissue and inflammatory cells
61.
62. 6b. Wet gangrene
Site: affects moist tissues or organs(bowels, lung, mouth), diabetic
foot
Cause: due to venous blockage
Gross features:
● Soft, swollen, putrid, rotten, dark
● No clear line of demarcation
Microscopy:
● Liquefactive necrosis
More dangerous than
dry gangrene ☠
63.
64. DRY GANGRENE WET
Site Limbs Bowels
Example Gangrene due to
atherosclerotic occlusion
Intussusception,
volvulus
Cause Arterial block Venous block
Onset slow sudden
Pathogens Absent Present
Gross features Dry(mummified) Swollen, moist
Line of demarcation Present Not clear
Putrefaction minimal Marked, foul smelling
Spread slow rapid
Prognosis fair poor
65. 6c. Gas gangrene
Special type of gas gangrene caused by infection with gas-
forming anaerobic clostridium bacteria
67. Apoptosis
Definition: it refers to programmed cell death, in which cell
activates enzymes which degrade the cell’s own nucleus and
cytoplasmic proteins
Causes of apoptosis:
1. Physiological
2. Pathological
68. Physiological apoptosis:
E.g:
- Removal of excess cells during development of embryo
- Breakdown of endometrium during the menstrual cycle
- Elimination of neutrophils after immune response
Pathological apoptosis:
E.g:
- Elimination of cells with damaged DNA
- Killing of cells infected by virus
- Elimination of neoplastic cells
69. Morphology
● Cells shrink
● Cytoplasm becomes dense
● Nucleus condenses and fragments
● Formation of cytoplasmic blebs and apoptotic bodies
● Phagocytosis of apoptotic cells/bodies by macrophages
and degradation by lysosomal enzymes
70.
71. Feature Apoptosis Necrosis
Cause Physiological or
pathological
Always pathological
Extent Single cell or small
group of cells
Large group of cells
Nucleus Fragmentation Pyknosis, karyorrhexis,
karyolysis
Cell contents Intact(apoptotic
bodies)
Leak out of cell
Inflammatory
response
Absent Present in surrounding
tissue
Fate of dead cells Ingested by
neighbouring cells
Ingested by
neutrophils and
macrophages
72. References:
● Ramadas Nayak - Textbook of Pathology for
Undergraduates
Questions:
salman.s.ansari92@gmail.com
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scan:
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