3. Cell Physiology
Cell membrane: Semi-permeable membrane with pumps
for ionic / osmotic homeostasis
Nucleus: Nucleolus (synthesis of ribosomal RNA)
Mitochondria: Oxidative phosphorylation (main source of
ATP)
Endoplasmic reticulum (ER), Ribosomes and Golgi
Apparatus: Protein synthesis and transport
Lysosome: Endocytosis, phagocytosis and pinocytosis
followed by degradation
Peroxisome: Catalase and oxidase enzymes, metabolism
of H2O2 fatty acid
8. Reversible Cell Injury
Occurs when
environmental changes
exceed the capacity of
the cell to maintain
normal homeostasis
But if the stress is
removed or the cell
withstands the assault
the injury is reversible
9. Irreversible Cell Injury
If the stress remains
severe, the cell injury
becomes irreversible and
leads to cell death
11. Mechanisms of Cell Injury
Defects in membrane permeability
Mitochondrial damage ˃ Depletion of ATP
Accumulation of oxygen-derived free radical
(Oxidative stress)
Influx of intracellular calcium and loss of calcium
homeostasis
12. Mechanisms Of Cell Death
Physiological, as in cell life cycle
Necrosis: Morphologic changes seen in dead cells within
living tissue
Autolysis: Dissolution of dead cells by the cells own
digestive enzymes
Apoptosis: Programmed cell death
“Apoptosis is a pathway of cell death that is induced by a
tightly-regulated suicide program in which cells destined
to die activate enzymes that degrade the cell’s own
nuclear DNA and nuclear and cytoplasmic proteins”
13. Cell Injury Signs
Morphological
Swelling
Dystrophy
Dysplasia
Necrosis
Autolysis
Functional
Decrease in function
Cellular
Increase in permeability
Cytoplasmic enzymes
leakage to the blood
Metabolic derangements
Injury mediators
Synthesis impairments
Electrolyte balance
disorders
14. Fatty Change
Occurs in:
Hypoxic injury
Toxic or metabolic injury
Appearance of lipid vacuoles in the cytoplasm
Swelling of cells is reversible
In cells involved in and dependent on fat metabolism
Hepatocytes
Myocardial cells
15. Pigmentation
Endogenous
Lipofuscin – ageing pigment
Melanin – in melanocyte
Hemosiderin – aggregates of ferritin
Accumulation of bilirubin
Too much produced (e.g., hemolysis)
Not processed (e.g., cirrhosis)
Outflow blocked (e.g., choledocholithiasis)
Exogenous
Anthracosis (cigarette smoking; urban living)
Tattoo
16. Calcification
Abnormal tissue deposition of calcium salts
Dystrophic
• Patients have a normal calcium level
• Calcification affects previously damaged tissue
(Ageing or damaged heart valve)
Metastatic
• Patients have an elevated level of serum calcium
Causes: Hyperparathyroidism, bony metastases, RF
Atherosclerosis (common)
Aortic stenosis (uncommon)
- Calcification is not routinely reversible
Tricuspid valve - Calcification
17. Amyloidosis
A group of diseases characterised by extracellular
depostion of fibrillar proteinaceous substance called
amyloid
Has morphological appearance, staining properties and
physical structure but with variable protein or biochemical
composition
Deposits intracellularly and extracellularly
18. Amyloidosis of Heart
Heart is involved in systemic amyloidosis
Advanced cases.. restrictive cardiomyopathy, arrhythmias
Gross: heart enlarged, surface pale, translucent and waxy
Epicardium, endocardium and valves show tiny nodular
deposits of amyloid
Microscopy: Amyloid deposits in and around coronaries
In primary amyloidosis, deposits of AL are seen around
myocardial fibres in ring like formations (ring fibres)
In localised form, deposits are seen in left atrium and
interatrial septum
19. Necrosis
Result of denaturation of intracellular proteins and
enzymatic digestion of the lethally injured cell
Necrotic cells are unable to maintain membrane integrity
Lysosomal enzymes digest the necrotic cells
Dead cells may ultimately become calcified
Coagulative
Liquefactive
Caseous
Fat
Gangrenous
Fibrinoid
20. Coagulative Necrosis – Kidney
A localized area of coagulative
necrosis is called an infarct
Gangrene - Coagulative
necrosis involving multiple
tissue planes
21. Caseous Necrosis – Tuberculosis
collection of fragmented or lysed cells
and amorphous granular debris
enclosed within a distinctive
inflammatory border
Fat Necrosis – Mesentry
Focal areas of fat destruction,
typically resulting from release of
activated pancreatic lipases
22. Fibrinoid - Artery
When complexes of antigens
and antibodies are deposited
in the walls of arteries
Liquifactive Necrosis – Cerebrum
Digestion of the dead cells, resulting
In transformation of the tissue into a
liquid viscous mass