Necrosis

Necrosis

Q. 1

Necrosis of cells is due to

 A

Ca’ efflux in cell

 B

Fat deposition in cells

 C

Water imbibition in cells

 D

Enzymatic digestion

Q. 1

Necrosis of cells is due to

 A

Ca’ efflux in cell

 B

Fat deposition in cells

 C

Water imbibition in cells

 D

Enzymatic digestion

Ans. D

Explanation:

Ans. is ‘d i.e., Enzymatic digestion

o Cell injury is reversible upto a certain point, but if the stimulus persists, irreversible injury and ultimate cell death occur.

o There are two principal patterns of cell death :

a Necrosis

q Apoptosis

Necrosis

o Necrosis refers to a spectrum of morphological changes that follow cell death in living tissue.

o Remember this fact Cell death is not due to necrosis rather necrosis (i.e., morphological changes) occurs after cell death  cells placed immediately in fixative are dead but not necrotic. Necrosis only represents the
morphological changes that occur after cell death.

o These morphological changes (necrosis) is the result of 2 concurrent processes :

1. Enzymatic digestion of the cell

q           Enzymes used in the process are derived from two sources :‑

(a)       From the lysosomes of the dead cells themselves (Autolysis)

(b)       From the lysosomes of the immigrant leukocytes (Heterolysis)

2. Denaturation of intracellular proteins

o These processes require hours to develop, So immediatly after cell death there are no detectable necrotic changes. o Necrosis usually effects a group of contigous cells (in contrast to apoptosis that involves death of a single cells), but it can effect single cell also.

o In necrosis, there is diruption of membrane integrity —3 Intracellular contents leak out and elicit inflammation —> Inflammatory changes in the surrounding tissue (By contrast, in apoptosis there is no inflammatory reaction in the tissue).

Morphological changes

o As necrosis follows irreversible injury, the morphological changes are same that have been described in irreversible injury. These are

1.Membrane damage

2.Large flocculent amorphous densities in mitochondria.

3.Intracytoplasmic myelin figures

4.Decreased basophilia and increased eosinophilia due to decreased RNP.

5.Nuclear changes :

          Karyolysis             —> Basophilia of chromatin

          Pyknosis                 —> Nuclear shrinkage

         Karyorrhexis         —> Fragmentation of Pyknotic nucleus.



Q. 2

 Coagulative necrosis is seen in –

 A

Tuberculosis

 B

Fungal infection

 C

Sarcoidosis

 D

Wet gangrene

Q. 2

 Coagulative necrosis is seen in –

 A

Tuberculosis

 B

Fungal infection

 C

Sarcoidosis

 D

Wet gangrene

Ans. A

Explanation:

Ans. is ‘a’ i.e., Tuberculosis

Two distinct variant of coagulative necrosis are:

1.  Dry gangrene

2.  Caseous necrosis (most common cause is TB)


Q. 3

Caseous necrosis in granuloma not found in

 A

Tuberculosis

 B

Leprosy

 C

Histoplasmosis

 D

All

Q. 3

Caseous necrosis in granuloma not found in

 A

Tuberculosis

 B

Leprosy

 C

Histoplasmosis

 D

All

Ans. B

Explanation:

 

Granulomatous Conditions with caseous necrosis :

1. Tuberculosis,                

2. Histoplasmosis,              

3. Coccidiodomycosis       

4. Syphilis

Note – In wegner’s granulomatosis, there is central necrosis in granuloma but it is not caseous necrosis.

Quiz In Between


Q. 4

Fibrinoid necrosis is seen in‑

 A

Polyarteritisnodosa

 B

SLE

 C

HBV

 D

Sarcoidosis

Q. 4

Fibrinoid necrosis is seen in‑

 A

Polyarteritisnodosa

 B

SLE

 C

HBV

 D

Sarcoidosis

Ans. A

Explanation:

Ans. is ‘A’ 

Fibrinoid necrosis

Fibrinoid necrosis is special form of necrosis usually seen in immune reactions involving blood vessels.

It is associated with conditions such as immune vasculitis (e.g. polyarteritis nodosa), malignant hypertensionpreeclampsia, or hyperacute transplant rejection

Common sites undergoing fibrinoid necrosis are, SLEAschoff bodies seen in rheumatic heart disease, Arthus reactionserum sicknesspolyarteritis nodosapoststreptococcal glomerulonephritishyperacutely rejected graftsmalignant hypertension

It is seen in :‑

1)     Immune complex vasculitis

2)     Malignant hypertension.

Deposition of immune complexes, together with fibrin, results in bright pink and amorphous appearance in H & E stain, called fibrinoid (fibrin like).


Q. 5

Trauma to breast causes which type of necrosis ‑

 A

Coagualtive necrosis

 B

Liquefactive necrosis

 C

Caseous necrosis

 D

Fat necrosis

Q. 5

Trauma to breast causes which type of necrosis ‑

 A

Coagualtive necrosis

 B

Liquefactive necrosis

 C

Caseous necrosis

 D

Fat necrosis

Ans. D

Explanation:

Ans. is ‘d’ i.e., Fat necrosis

Fat necrosis

Fat necrosis may be of two types : ‑

Enzymatic fat necrosis

  • This is due to action of lipase on adipose tissue.
  • It occurs most frequently in acute pancreatitis due to leakage of lipase.
  • Depending on the severity of acute pancreatitis, fat necrosis may occur in : – a Adipose tissue contiguous to pancrease, retroperitoneal fat.
  • Adipose tissue in anterior mediastinum.
  • Bone marrow
  • Omental and abdominal fat

Nonenzymatic or Traumatic fat necrosis

  • Occurs due to trauma
  • Is seen in subcutaneous tissue of breast, thigh, and abdomen.

Q. 6

Necrosis with cell bodies retained as ghost cells is ‑

 A

Coagulative necrosis

 B

Liquefactive

 C

Caseous

 D

None

Q. 6

Necrosis with cell bodies retained as ghost cells is ‑

 A

Coagulative necrosis

 B

Liquefactive

 C

Caseous

 D

None

Ans. A

Explanation:

Ans. is ‘a’ i.e., Coagulative necrosis

Quiz In Between


Q. 7

All the following organs likely undergo coagulative necrosis except ‑

 A

Spleen

 B

Heart

 C

Kidney

 D

Brain

Q. 7

All the following organs likely undergo coagulative necrosis except ‑

 A

Spleen

 B

Heart

 C

Kidney

 D

Brain

Ans. D

Explanation:

Ans. is d i.e., Brain

Coagulative necrosis

  • This is most common type of necrosis.
  • This type of necrosis is most frequently caused by sudden cessation of blood flow (ischemia) in organs such as heart (MI), Kidney (ATN), adrenal gland, and spleen.

Note :

  • Brain is the only exception, i.e.,. It is the only solid organ in which ischemia leads to liquifactive necrosis not coagulative necrosis.

Q. 8

Type of necrosis occuring in brain‑

 A

Coagulative

 B

Liquefactive

 C

Fibrinoid

 D

Caseous

Q. 8

Type of necrosis occuring in brain‑

 A

Coagulative

 B

Liquefactive

 C

Fibrinoid

 D

Caseous

Ans. B

Explanation:

Ans. is ‘b’ i.e., Liquefactive

Coagulative necrosis

  • This is most common type of necrosis.
  • This type of necrosis is most frequently caused by sudden cessation of blood flow (ischemia) in organs such as heart (MI), Kidney (ATN), adrenal gland, and spleen.
  • Note : Brain is the only exception, i.e.,. It is the only solid organ in which ischemia leads to liquifactive necrosis not coagulative necrosis.
  • It is also seen with other types of injury e.g., liver necrosis in viral hepatitis, Coagulative necrosis of skin after burns (Thermal injury).
  • Why there is predominant protein denaturation and no enzymatic digestion ?
  • Hypoxia causes intracellular acidosis (has been explained earlier) .1, pH results in denaturation of proteins which includes not only structural proteins but also enzymes —) So, there is no enzymatic digestion.
  • The necrotic cells retain their cellular outline for several days.

Liquefactive necrosis

  • It is the necrotic degradation of tissue that rapidly undergo softening and liquefaction because of the action of hydrolytic enzymes.
  • It occurs after
  1. Infection i.e., suppurative inflammation (most common).
  2. Ischemic necrosis in brain.
  • Note : Brain lacks any substantial supportive stroma, so ischemic necrosis in brain is liquifactive unlike other organs where it is coagulative.
  • Mechanism of liquefactive necrosis —> Microbes stimulates accumulation of inflammatory cells and these cells release lysosomal enzymes.

Caseous necrosis

  • It is a variant of coagulative necrosis.
  • It is most commonly encountered when cell death is attributable to certain organisms e.g., mycobacterium tuberculosis (TB) and fungi (Histoplasma, Coccidioidomycosis).
  • Why is it called caseous necrosis, not coagulative necrosis ?
  • In contrast to coagulative necrosis where tissue architecture is maintained, in caseous necrosis, the tissue architecture is completely obliterated. So, it has been called caseous because of its cheesy white appearance of the area of necrosis.

Q. 9

Caseous necrosis is not found in‑

 A

TB

 B

Histoplasmosis

 C

CMV

 D

Syphilis

Q. 9

Caseous necrosis is not found in‑

 A

TB

 B

Histoplasmosis

 C

CMV

 D

Syphilis

Ans. C

Explanation:

Ans. is ‘c’ i.e.,CMV 

Quiz In Between


Q. 10

Type of necrosis in pancreatitis ‑

 A

Fibrinoid

 B

Coagulative

 C

Fat

 D

Caseous

Q. 10

Type of necrosis in pancreatitis ‑

 A

Fibrinoid

 B

Coagulative

 C

Fat

 D

Caseous

Ans. C

Explanation:

Ans. is ‘c’ i.e., Fat

  • Fat necrosis is seen most frequently in acute pancreatitis due to leakage of lipase.

Fat necrosis

  • Fat necrosis may be of two types : ‑

1. Enzymatic fat necrosis

  • This is due to action of lipase on adipose tissue.
  • It occurs most frequently in acute pancreatitis due to leakage of lipase.
  • Depending on the severity of acute pancreatitis, fat necrosis may occur in : – a Adipose tissue contiguous to pancrease, retroperitoneal fat.
  • Adipose tissue in anterior mediastinum.
  • Bone marrow
  • Omental and abdominal fat

2. Nonenzymatic or Traumatic fat necrosis

  • Occurs due to trauma
  • Is seen in subcutaneous tissue of breast, thigh, and abdomen.

Q. 11

Necrotizing arterioritis with fibrionoid necrosis is ‑

 A

Immediate hypersensitivity

 B

Cell mediated immunity

 C

Antigen-antibody complex mediated

 D

Cytotoxic cell mediated

Q. 11

Necrotizing arterioritis with fibrionoid necrosis is ‑

 A

Immediate hypersensitivity

 B

Cell mediated immunity

 C

Antigen-antibody complex mediated

 D

Cytotoxic cell mediated

Ans. C

Explanation:

Ans. is ‘c’ i.e., Antigen-antibody complex mediated 

  • The principal morphological manifestation of immune (antigen-antibody) complex injury is necrotizing vasculitis with necrosis of vessel wall and intense neutrophilic infiltration.
  • The necrotic tissue and deposits of immune complexes, complement and plasma proteins produce a smudgy eosinophilic deposition that obscures the underlying cellular detail, an appearance termed fibrinoid necrosis.

Quiz In Between



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