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Pathology - Quiz 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Distinguish reversible from irreversible cell injury.

A

Reversible: normal cell —injury—> altered cell —recovery—> normal cell

Permanent: normal cell —injury—> permanently altered cell

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2
Q

Identify the cytological changes that are associated with irreversible injury. (4)

A

Increased cytosolic Ca concentration
Mitochondria swelling, Ca precipitates form
Pyknotic nuclei
Apoptosis

Mallory’s hyaline in liver cells damaged by alcohol

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3
Q

Explain how steatosis occurs due to alcohol ingestion. (5 effects)

A

Alcohol gets metabolized to ACETATE, making NADH

  1. Mobilization of FA from body stores
  2. Decreased FA oxidation
  3. Increased TG synthesis
  4. Decreased lipoprotein synthesis
  5. Decreased transport/glycosylation/secretion of VLDL
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4
Q

Name and briefly distinguish 4 types of pathological necrosis.

A
  1. Coagulative necrosis: preservation of the structural outline of dead cells
  2. Liquefactive necrosis: tissue is digested and liquefied
  3. Caseous necrosis: mix of coagulative and liquefactive, seen in TB
  4. Enzymatic fat necrosis: necrosis of fat cells around damaged pancreas
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5
Q

Explain the relationship between hemochromatosis and cirrhosis.

A

Over time, hemochromatosis results in damage to cells due to a variety of mechanisms, including free radical injury
-> Cirrhosis

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6
Q

Name four features of cellular injury that are reversible.

A

Cell swelling: lost ability to regulate Na/K gradient
Loss of eosinophilia
Nuclear chromatin clumps
Lactic acidosis

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7
Q

Explain the role of calcium ions in irreversible cell injury.

A

Injurious agent -> increased cytosolic Ca ->…

  1. Activated phospholipases -> membrane damage
  2. Activated proteases -> disruption of membrane/cytoskeletal proteins
  3. Activated endonuclease -> damaged chromatin
  4. Activated ATPase -> decreased ATP

Key = MEMBRANE DAMAGE

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8
Q

Coagulative necrosis

A

Definition: preservation of the structural outline of dead cells

Mechanism: denaturation of enzymes and structural proteins; inactivation of enzymes prevents autolysis of the cell

  • -Typically caused by ischemia, heavy metals, IR
  • -Characterized by the ‘ghostly’ appearance of cells
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9
Q

Liquefactive necrosis

A

Definition: necrosis resulting in degradation and liquification of tissue
–Usually with extensive acute inflammation (infections)

Mechanism: release of lysosomal enzymes by necrotic cells or release of hydrolytic enzymes by neutrophils

Example: abscess, cerebral infarction (neutrophils come in and digest everything)

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10
Q

Caseous necrosis

A

A combination of coagulative and liquifactive necrosis

  • -Classically associated with TB
  • -Used to describe the amorphous, eosinophilic, acellular material in the center of a granuloma
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11
Q

Gangrenous necrosis

A

The consequence of bacterial colonization of tissue which has already undergone necrosis, usually due to ischemia

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12
Q

Enzymatic fat necrosis

A

Seen in pancreas

Lipases from pancreas, released in acute pancreatitis, digest surrounding fat, causing characteristic yellow flecks

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13
Q

Necrosis

A

Cell death at the level of tissues, often accompanied by an inflammatory infiltrate

Represents the morphologic changes from cell death in living tissues

Effect of enzymatic degradation (primarily by lysosomal enzymes) and denaturation of proteins

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14
Q

Causes of apoptosis (4)

A

Injury: radiation, toxins, free radicals
CTLs
Withdrawal of growth factors, hormones
Receptor ligand interactions (FAS, TNF)

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15
Q

Define steatosis. Is it reversible?

A

Accumulation of fat (triglyceride) in hepatocytes

“Fatty change”

Accumulation of lipid appears as clear circular areas in the cytoplasm of the liver cells

IT IS REVERSIBLE

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16
Q

Hemochromatosis

A

A genetic disease that results in abnormal accumulation of iron in tissues (shows up as brown)

Increased iron absorption results in iron deposition

Secondary damage due to many reasons, including free radical injury

17
Q

Hemosiderosis

A

Abnormal accumulation of iron in tissues due to any cause (shows up as brown)

May be due to a local injury such as old hemorrhage

May be due to systemic cause such as numerous transfusions

18
Q

Ischemia

A

The effect of O2 deprivation on cell function and morphology

19
Q

Infarction

A

Ischemic cell death

Gross manifestation of coagulative (or liquefactive) necrosis secondary to the sudden occlusion of a vessel

Usually wedge–shaped

20
Q

Cirrhosis

A

Cirrhosis is scarring of the liver and poor liver function. It is the final phase of chronic liver disease.

21
Q

Define injury.

A

External or internal challenge to homeostasis

Interferes with normal physiology

Can be external or internal (genetic)

22
Q

Mallory’s hyaline

A

Aggregation of cytokeratin filaments
Dense pink rope-like body in the cytoplasm of hepatocytes
Mark of permanent damage

23
Q

Burkitt lymphoma

A

Malignancy of B lymphocytes with apoptotic cell death of malignant cells and phagocytosis of apoptotic bodies by macrophages

Makes “starry sky pattern”: lightly stained macrophages with apoptotic bodies surrounded by the dense infiltrate of malignant lymphocytes

24
Q

Distinguish white infarcts and red infarcts.

A

White infarcts: circulation is entirely cut off, tissue becomes pale
-Occurs in dense tissue, like heart, kidney, spleen

Red infarcts: hemorrhagic infarcts; occur with dual circulation (in lungs because of bronchial arteries) or if perfusion is immediately restored to the dead tissue (reperfusion infarction)
-Occurs in loose tissue, like lung, bowel, testicle

25
Q

List examples of coagulative necrosis. (3)

A

Myocardial infarction
Renal infarction
Pulmonary infarction

26
Q

List examples of liquefactive necrosis. (2)

A 
Cerebral infarction (stroke)
Necrotizing fungal pneumonia
27
Q

What can cause vaculolar change in the renal tubules? What are the changes seen? (2)

A

Cause: administration of osmotic load (mannitol -> diuresis)
—Aka osmotic nephropathy

Changes:

  • -Swelling of cytoplasm with large numbers of empty-appearving vacuoles
  • -Mostly PCTs affected
28
Q

What can cause steatosis of the liver? (2) What changes are seen in steatosis? (2)

A

Causes: starvation, toxic agents (alcohol)

Changes:

  • -Fat vacuoles in cytoplasm of hepatocytes, especially near central vein
  • -Portal areas are normal/near normal
29
Q

What can cause coagulative necrosis of the adrenal gland? What changes are seen? (5)

A

Cause: ischemic injury

Changes:

  • -Wedge-shaped area of coagulative necrosis
  • -Shadowy outlines of pre-existing cells
  • -Karyolytic (fragmented) or pyknotic nuclei
  • -Hypereosinophilia
  • -Basophilic granular debris along the edge of necrotic zone from necrotic neutrophils
30
Q

What can cause enzymatic necrosis of the pancreas? What changes are seen? (4)

A

Cause: acute pancreatitis

Changes:

  • Marked eosinophilia (saponification, turns blue or red) of fat lobules, with loss of cell detail
  • Large basophilic areas of debris/necrotic cells
  • Necrosis of some normal pancreatic tissue (eosinophilic)
  • Few neutrophils
31
Q

What can cause central necrosis of the liver? What changes are seen? (5)

A

Cause: ischemia, acetaminophen overdose

Changes:

  • -Swelling and loss of eosinophilia in hepatocytes just outside of portal area (reversible change)
  • Increased eosinophilia and shrinkage of hepatocytes near central vein (irreversible)
  • Pyknotic/karyolytic nuclei (ireversible)
  • Few neutrophils present
  • (Sometimes) hemorrhage around central vein

Pathology - Quiz 1 (11 decks)

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