W2/L11 Flashcards

(17 cards)

1
Q

What are the principle mechanisms of cell injury? (4)

A

Damage to DNA & misfolding of proteins

Disturbance of calcium homeostasis

Damage to cell membranes

Mitochondria ATP depletion & ROS production

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2
Q

Why do cells swell in reversible injury?

A

Failure of the ATP-dependent pumps in plasma membrane

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3
Q

What happens in hepatocytes and myocardial cells when they’re reversibly injured?

A

Fat acuumulation

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4
Q

What are the nuclear changes from DNA breakdown?

A

Pyknosis
Karyorrhexis
Karyolysis

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5
Q

What happens in karyolysis

A

Complete dissolution of the nucleus with reduced basophilia (less purple)

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6
Q

What happens in pyknosis

A

The nucleus becomes small and intensely basophilic (purple)

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7
Q

What happens in karyorrhexis

A

Nuclear fragmentation

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8
Q

What colour is a necrotic cell?

A

Intensely eosinophilic

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9
Q

Why are necrotic cells more eosinophilic? (2)

A

Loss of ribosomal RNA

Increased eosin binding to damaged proteins

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10
Q

What is the histological feature of coagulative nectosis?

A

Ghost outlines

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11
Q

When does coagulative necrosis usually occur?

A

Infarction of solid organs (except brain)

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12
Q

Why does coagulative necrosis occur?

A

Slow enzymatic dissolution

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13
Q

What are the histological features of caseous necrosis?

A

Amorphous granular debris without distinct cell borders

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14
Q

When does caseous necrosis usually occur?

A

In necrotising granulomatous inflammation from TB

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15
Q

Where does liquefactive necrosis usually occur?

A

The brain

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16
Q

What pathology causes fat necrosis?

A

Acute pancreatitis causing release of lipases

17
Q

What’s the result of fat necrosis?

A

Saponification (deposits of chalky white stuff) due to reaction of fatty acids with calcium