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1. Write down at least three differences between Apoptosis and Necrosis?

Apoptosis Versus Narcosis
Apoptosis
Predefined cell suicide or programmed cell
death. Natural physiological Process.
Involve one cell at a time.
Cell shrinkage (Dense eosinophilic
cytoplasm)
Pyknosis (Condensation) and Karyorrhexis
(fragmentation) of nuclear material
Formation of membrane blebs and apoptotic
bodies
Phagocytosis of apoptotic bodies by
Macrophages
Caspase dependent pathway
No Inflammation (no immune response)
Necrosis
Premature, unprogrammed cell death always
pathological. Involve many cells
Cell Swelling (Swelling of endoplasmic
reticulum and mitochondria) and membrane
blebs
Pyknosis (condensation), Karyorrhexis
(Fragmentation) and Karyolysis (lysis)of the
nucleus.
Breakdown of the plasma membrane,
organelles (enzymatic digestion), leakage of
cellular contents
Increased eosinophilia, Accumulation of
Myelin figures (whorled precipitated
Phospholipids)
Initiate Inflammation (Strong immune
response)

2. Enlist the four causes of Oedema.

Increased Hydrostatic Pressure
Decreased Plasma Colloidal Osmotic Pressure
Increased Vascular Permeability
Lymphatic Obstruction
Heart Failure / Sodium Retention
3. The three factors that predispose to thrombosis are referred to as "Virchow's triad". What
are the three causes of thrombosis?
A-Damage to the endothelial lining of a blood vessel.
B-Abnormal blood flow (Stasis or turbulence).
C-Increased coagulability of blood, i.e., increased coagulation factors or decrease natural inhibitors.
Hypercoagulability

4. Define jaundice and name its three types.

• Jaundice is a yellow discoloration of the skin and mucous membranes caused by an excess
accumulation of bilirubin in the blood. Jaundice becomes visible when the bilirubin level is
approximately 2 to 3 mg/dL.
• The three main types of jaundice are prehepatic, hepatic, and post hepatic:
 5. What is Infarction? Enlist the two types of infarction?
• Ischemic necrosis of tissue caused by occlusion of either the arterial supply or the venous
drainage in a particular tissue. The 2 most important causes are thrombosis and
thromboembolism. Haemorrhagic (red) infarcts, Anaemic (white) infarcts

6. Define Metaplasia with an example?

• Metaplasia (change in cell type): Replacement of one differentiated cell type with another mature
differentiated cell type that is not normally present in that tissue. E.g in smoker bronchial
columnar epithelium change into squamous epithelium.

Long Questions 08

1. Write down the mechanism of Hypoxic Cell injury.

Hypoxia /
Ischemia

Decrease
ATP

Decreased Failure of Detachment

Anaerobic of Misfolding
activity of calcium
Metabolism Ribosomes of Proteins
sodium pump
Pump
activation of decreased
Decrease Cell death
Decrease pH Increased different Protein
Glycogen
Na+ enzymes synthesis

Decreased activity of
Decreased
cellular enzymes
K+
clumping of
chromatin
Incresed
Ca2+

increased
H2O

2. What is Necrosis and explain all its types thoroughly.

Types or Morphological patterns of necrosis
Classical morphological patterns of necrosis are:
➢ Coagulative Necrosis: Coagulative necrosis is a form of necrosis in which the component cells
are dead, but the basic tissue architecture is preserved for several days. The affected tissues take
on a firm texture, denaturation of cell structural proteins and enzymes without lyses of cell
membrane (cellular structure is preserved), enzymes are denatured and so block the proteolysis
of the dead cells; as a result, an eosinophilic, anucleate cell may persist for days or weeks. E.g.
infarcts that occur in hypoxic injury of any solid tissues, i.e. liver, heart, kidney, except the brain.
• Gross Morphology
• Tissue retains original form & coherent strength
• Firm, pale, dry consistency (visibly distinct from both caseous & liquefactive)
• Will eventually become friable (easily crumbled)
• Often surrounded by a reddened area or hyperemia
• Microscopic Morphology
• Tissue organization remains
• able to recognize
• Cell outline remains with loss of cellular detail
• Nuclear changes
• Cytoplasmic coagulation & hyper eosinophilia
➢ Liquefactive Necrosis: Liquefactive necrosis (or colliquative necrosis) is a type of necrosis that
results in a transformation of the tissue into a liquid viscous mass Infiltration of dead tissue by
large numbers of neutrophils leads to digestion (rather than coagulation) of cell proteins. This
leads to loss of normal tissue architecture. Common in brain.
• Gross Morphology
• A fluid filled cavity in a tissue
• There is a thin line between liquefactive & caseous necrosis
• White to pale tan, brown, red, green colored liquid
• Cream-like consistency
• Foul smelling than coagulative or caseous necrosis
• Microscopic Morphology
• Pink, proteinaceous fluid or hole, if the fluid has already poured out
• Surrounded by inflammatory cells
➢ Caseous Necrosis: Caseous necrosis is a type of cell death that causes tissues to become “cheese-
like” in appearance. The most common cause is tuberculosis, where granulomas form in your
lungs.
• A granuloma is organized and compact immunological structure rich with immune cells, such as
macrophages, monocytes, dendritic cells, neutrophils, epithelioid cells, foamy macrophages, and
multi- nucleated giant cells.
• Granulomas seem to be a defensive mechanism that triggers the body to "wall off" foreign
invaders such as bacteria or fungi to keep them from spreading.
• Gross Morphology
• Dull but slightly greasy & somewhat liquefactive
• Firm, no cohesive strength, usually pale to white (cottage cheese)
• Easily separated with a blunt instrument (like a finger)
• Microscopic Morphology
▪ Loss of all tissue outline (no discernible tissue)
▪ Amorphous, granular debris, mass
 ▪ Infiltrated with macrophages multinucleated giant cells
▪ Often surrounded by fibrous
▪ connective tissue capsules
➢ Fat Necrosis: Fat necrosis is a pattern of necrosis that occurs due to degradation of fatty tissue by
lipases (released from dead cells) to form chalky deposits. This can be seen in acute pancreatitis
(acute inflammation of the pancreas causing necrosis of pancreatic cells and lipase release).
❖ White foci seen on organs due to Saponification.
❖ Saponification: Fatty acids are released via hydrolysis react with Calcium to form chalky
white areas.
➢ Gangrenous Necrosis: A type of coagulative ischemic necrosis. It is usually applied to the lower
leg, which has lost its blood supply and has undergone coagulative necrosis.
❖ Dry gangrene occurs when the blood supply to the tissue is cut off. The area becomes dry,
shrinks, and turns black.
❖ Wet gangrene occurs if bacteria invade this tissue. This makes the area swell, liquefied, and
smell bad.
❖ Gas gangrene when an infection develops deep inside the body and the bacteria responsible
begin releasing gas. which is commonly found with clostridia infection.
• Gross Morphology (Dry Gangrene)
• Tissue is shrunken, wrinkled, leathery, often firm
• Can be pale or darker than normal
• Marginal hyperemia: red line of inflammatory demarcation between infected & normal tissue
• Gross Morphology (Wet Gangrene)
• Swollen, soft, pulpy, dark in color with putrefactive smell
➢ Fibrinoid Necrosis: Fibrinoid necrosis is a specific pattern of irreversible, uncontrolled cell death
that occurs when antigen-antibody complexes are deposited in the walls of blood vessels along
with fibrin. Deposits of these immune complexes, "together with fibrin that has leaked out of
vessels, resulted in a bright pink and amorphous appearance in H&E stains, called fibrinoid
(fibrin-like)