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Pathology 1 - Cell, Tissue, Inflammation > Lectures 2 and 3 - Cell Injury and Necrosis I and II > Flashcards

Lectures 2 and 3 - Cell Injury and Necrosis I and II Flashcards

1
Q

What can cause cell injury?

A
  • Lack of oxygen
  • Lack of nutrients
  • Extreme pH
  • Electrolyte imbalances
  • Toxins
  • Free radical damage
  • Physical disruption
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2
Q

Reversible changes:

A
  • Cellular swelling
  • Cell membrane blebs
  • Detached ribosomes
  • Chromatin clumping
  • Lipid deposition
  • Vacuole formation
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3
Q

Irreversible changes:

A
  • Lysosomes rupture
  • Dense bodies in mitochondria
  • Cell membrane rupture
  • Karyolysis, karyorrhexis, pyknosis
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4
Q

Karyolysis:
Karyorrhexis:
Pyknosis:

A
  • Chromatin dissolves
  • Chromatin breaks
  • Condensation of chromatin (followed by karyorrhexis)
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5
Q

Neurons are damaged in…
Myocardium, hepatocytes, renal epithelium in…
Fibroblasts, epidermis, skeletal muscle in…

A
  • 3-4 min
  • 30 min - 2hr
  • Many hours
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6
Q

3 ways to move from cell injury to cell death:

A
  • Require continuous ATP, so irreparable damage to mitochondria
  • Holes in membranes (ion transport, can’t exclude Ca2+ and Na+)
  • Activation of self-digestion (proteinases, lipases, endonucleases)
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7
Q

List 6 pathways of cell injury:

A
  1. ATP depletion
  2. Irreversible mitochondrial damage
  3. Disrupted Ca2+ homoeostasis
  4. Free radical formation
  5. Defects in cell membrane permeability
  6. Accumulated DNA and protein damage
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8
Q

What can cause ATP depletion?

A

Lack of O2, lack of substrates, decrease in mitochondrial function

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9
Q

What does ATP depletion do exactly?

A
  • Can’t pump out Na+ or maintain Ca2+ homeostasis –> swelling issues
  • Switch to anaerobic glycolysis (lactic acid build-up) –> chromatin clumping
  • Damage to protein synthesis (ribosomes detach RER…lack of O2 leads to misfolded proteins) –> lipid deposition
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10
Q

What produces free radicals?

A

Normal metabolism and neutrophils (superoxide anion), hydrogen peroxide, toxins and environmental agents

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11
Q

What do free radicals do?

A

Cause lipid peroxidation of membranes and formation of thymidine dimers and single-stranded DNA breaks (cancer)

also, chain breakage in proteins

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12
Q

What protects from oxygen free radicals?

A

Catalase, superoxide dismutase, antioxidants and scavengers (Vitamins E and A, ascorbic acid), glutathione peroxidase, binding of metals such as copper and iron

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13
Q

Membrane damage can be caused by a host of things, such as…

A

ROS, decreased O2, increase in cytosolic Ca2+

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14
Q

What is the “point of no return”?

A

Damage to mitochondria and inability to make ATP

…also loss of structural integrity; leakage

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15
Q

List causes of hypoxia:

A
  • ischemia
  • low oxygen tension (hypoxia)
  • CO poisoning
  • severe anemia

Ischemia tends to be more damaging than simple hypoxia (added decrease in delivery of metabolic requirements, and accumulation of metabolic waste)

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16
Q

Hypoxia causes:

A
  • Anaerobic metabolism
  • Impaired Na+ pump
  • Disaggregation of ribosomes
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17
Q

Cancer associated with chronic inflammation examples (ROS):

A
  • chronic hepatitis C
  • smoking
  • gastric reflux, chronic gastritis
18
Q

What is hemochromatosis?

A

Hereditary disease that leads to deposition of iron in many tissues (liver, heart, pancreas, etc.)

  • Chronic tissue damage
  • “Bronze diabetes” - cirrhosis, diabetes, skin pigmentation, heart failure, maybe liver cancer
19
Q

What is reperfusion injury?

A

Re-establishing blood flow to ischemic area may enhance damage initially (ultimately saves tissue)
- O2 converted to ROS, re-establish metabolic pathways that make ROS

Antioxidants help

20
Q

What causes contraction bands?

A

Reperfusion injury, cocaine, chronic catecholamines

21
Q

Carbon tetrachloride yields ROS CCl3- and…

A

Fulminant liver damage and necrosis

  • Lipoprotein synthesis damage –> fatty liver
  • Lipid peroxidation
22
Q

What is the timeline of cell injury?

A
  • Biochemical and functional changes (minutes)
  • Ultrastructural changes (hours)
  • Microscopic changes (hours to days…at least 4 hrs.)
  • Gross tissue changes (days)
23
Q

What is “ballooning degradation” indicative of?

A

Viral illness. Swollen eosinophilic cytoplasm w/o vacuoles

Lymphocytic infiltration.

24
Q

Fatty changes are _______.

A

Reversible! From damage to lipoprotein synthesis. Cells are still intact.

But eventually will die. Alcoholism.

25
Q

Irreversible injury is:

A
  • Enzymatic digestion
  • Denaturation of proteins, lipids, nucleic acids
  • Disruption of membranes
26
Q

What necrotic changes are seen under a light microscope?

A
  • Increased eosinophilia (loss/dissolution of RNA/ribosomes)
  • Hyalinization - glassy/homogenous (loss of glycogen and organelles)
  • Vacuolization
  • Calcification
  • Pyknosis, Karyorrhexis, Karyolysis
27
Q

Pyknosis:

A

Solid, shrunken basophilic mass

Increased basophilia

28
Q

Karyorrhexis:

A

Pyknotic nucleus undergoes fragmentation

29
Q

Karyolysis:

A

Dissolving nucleus into amorphic mass

  • Decreased basophilia
  • Activation of DNAase
30
Q

There is a _____ danger period following MI for rupture when the heart wall is soft

A

4-5 day

31
Q

What are some characteristics of coagulative necrosis?

A

Absent or karyorrhexic nuclei; eosinophilic

Softens after several days

32
Q

Mechanism of coagulative necrosis?

A

Intracellular acidosis denatures proteins and proteolytic enzymes…autolysis minimal and architecture left intact

Characteristic of most hypoxic tissue death, except in brain

33
Q

What are some characteristics of liquefactive necrosis?

A

Infiltration by neutrophils, architecture destroyed, pus

34
Q

What is a special case of liquefactive necrosis?

A

CNS - no collagenous stabilizing tissue (just neurons, astrocytes) so softens, yellow/tan, liquefies

35
Q

What is gangrenous necrosis?

A

Coagulative necrosis associated with loss of blood supply. First dry, usually associated with limbs.

36
Q

What is wet gangrene?

A

Secondary liquefactive necrosis (secondary bacterial infection; often in diabetes)

37
Q

What is caseous necrosis?

A

Type of coagulative; Associated with Mycobacterium and fungal infection (blasto, histo)

Yellow-white, cheese-like material
Often nodules

38
Q

What are characteristics seen in caseous necrosis?

A

Central areas of amorphous eosinophilic granular material

  • Cell outlines indistinct, but not liquefied
  • Macrophages and multinucleated giant cells
  • Granulomatous inflammation

Type IV hypersensitivity

39
Q

What is fat necrosis?

A

Destruction of adipose tissue; uncommon; coagulative

  • Breast (trauma)
  • Pancreatitis (abnormal release of pancreatic lipases)
  • -> saponification
40
Q

What is saponification?

A

Soap formation from calcium and lipids

41
Q

Characteristics of fat necrosis?

A
  • Eosinophilic “ghost” outlines of necrotic adipocytes
  • Basophilic Ca2+ deposits
  • Inflammation
  • No nuclei
42
Q

What is fibrinoid necrosis?

A

Special form; necrosis within walls of blood vessels

  • Immune-mediated vasculitis (Type III)
  • Deposit immune/antibody complexes with fibrin

Pathology 1 - Cell, Tissue, Inflammation (5 decks)

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