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Pathology > Unit 1: Cell Injury and Necrosis I and II > Flashcards

Unit 1: Cell Injury and Necrosis I and II Flashcards

1
Q

Cell injury occurs when?

A
  • cell is unable to adapt to environmental changes and unable to return to full function
  • can be reversible, but can also result in death (apoptosis or necrosis)
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2
Q

Cell types and injury (how long can they go without O2?)

A
  • Neurons= minutes
  • heart/renal epithelial= 30mins-2 hours
  • soft tissue/skeletal muscle= hours
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3
Q

What is involved in cellular injury (what parts of the cell?)

A

membranes, mitochondrial function, protein synthesis, nuclear components, enzymatic processes

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4
Q

Signs of REVERSIBLE cell injury (x6)–4 visible with LM

A
  1. cellular swelling*
  2. cell membrane blebs
  3. detached ribosomes
  4. chromatin clumping*
  5. lipid deposition (fatty change)*
  6. vacuole formation (hydropic change)*

**Can be seen with LM

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5
Q

causes of IRREVERSIBLE cell injury (x6)

–8 total, 5 visible with LM

A
  1. lysosomal rupture
  2. dense bodies in mitochondria
  3. cell membrane rupture
  4. nuclear condensation= Karyolysis* Karyorrhexis* Pyknosis*
  5. vacuolization *
  6. calcification*
  7. increased eosinophilia *
  8. hyalinazation*

**visible with LM

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6
Q

Primary causes of cell injury (x6) and consequence of the injury….

(see pathway of cell injury in notes-Cell injury and necrosis #1)

A
  1. ATP depletion [damages cell membranes]
  2. irreversible mitochondrial damage [causes free radicals to leak out, less ATP synthesis]
  3. Ca+2 homeostasis disrupted [activate degradative enzymes]==>cytoskeletal damage==>nuclear disassembly]
  4. free radical formation [damages membranes]
  5. defect in cell membrane permeability [cause electrolyte imbalance]
  6. DNA/ Protein damage [can lead to cell death]

(Also: pH, physical disruption)

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7
Q

Causes of Cell death

A
  1. Inability to form ATP
  2. Physical disruption of cell membranes (mitochondrial or plasma)
  3. activation of self-digestion enzymes
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8
Q

What can cause ATP to be depleted?

A
  1. Lack of O2 (hypoxia<==ischemia)
  2. lack of substrates
  3. mitochondrial dysfunction
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9
Q

Explain how ATP depletion affects the cell

(ATP depletion results in 3 big things, that then cause more things..)

A
  1. ATP dep Na/K pump not feuled= high Na inside cell==>
    • swelling, blebbing and dilation of membranes, loss of microvilli
    • loss of Ca+2 homeostasis==> activaiton of digestive enzymes
  2. Anaerobic glycolysis for energy==> acidosis==>low pH= chromatin clumping
  3. damage to protein synthesis apparatus ==>
    • ribosomes detach, less protein synthesis ==> lipid deposition (no more lipoprotein)
    • low O2 and glucose==> misfolded proteins (can cause apoptosis)

Notice difference between ATP depletion =cell injury vs interruption of ATP synthesis (damage to mitochondria)= cell death

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10
Q

What damages the mitochondrial membrane?

A

Low O2, high cytosolic calcium, lipase activation, free radical damage

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11
Q

Mitochondrial membrane damage leads to….

A
  1. decreased phospholipid synthesis==> plasma membrane damage
  2. less ATP synthesis==> high Ca==> phospholipase activation==>phospholipid degradation ==> lipid breakdown products have detergent effect==> more membrane damage
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12
Q
  1. What can cause high Ca in cells
  2. What does calcium do?
A
  1. Low ATP (causing pumps to stop working) or physical damage to membranes/organelles (mitochondria and ER)==>Calcium accumulation in cell
  2. high intracellular calcium:
    • activates enzymes: phospholipases, ATPases, proteases, endonucleases
    • induce mitochondrial permeability==> Apoptosis
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13
Q

What is the permeability transition pore? What does it signify

A

disruption of the mitochondrial membrane ==> no electrochemical gradient/ETC==> no ATP production

POINT OF NO RETURN==> CELL DEATH

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14
Q

What can cause increased free radical formation?

A
  1. Infection: neutrophil oxidative burst,
  2. radiation,
  3. chemical exposure (CCl4),
  4. chronic inflammation (ROS, NO)
  5. reperfusion injury,
  6. aging
  7. oxygen toxicity
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15
Q

What specifically do free radicals do to

  1. DNA?
  2. Lipids
  3. Proteins
A
  1. DNA: thymidine dimer formation, single strand breaks
  2. Lipids: peroxidation
  3. Proteins: oxidative modification
    • sulfhydryl x-linking of sulfur AA (cysteine, methionine)
    • polypeptide fragmentation
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16
Q

Protective measures against free radicals

A
  1. Mitochondria: Superoxide dismutase and glutathione peroxidase, catalase,
  2. Membranes: Vit E, A, beta carotene,
  3. ascorbic acid (donno where this chills)
  4. Fenton reaction + glutation peroxidase
  5. transport molecules (Cu, Fe)
17
Q

DNA/protein damage

  1. Etiology
  2. effect
A

DNA/Protein damage

  1. Etiology: free radicals, enzymatic digestion
  2. impaired cellular function==> toxic accumulation in cell and abnormal growth
18
Q

Is ischemia or hypoxia worse—why?

A

Ischemia is worse.

  • Ischemia: hypoxia (low O2), lack of substrates for glycolysis, lactic acid and metabolic waste accumulation
  • Hypoxia: low O2
19
Q

What are causes of hypoxia?

A
  1. ischemia
  2. low SaO2 (oxygen tension
  3. CO poisoning
  4. anemia
20
Q

Chronic inflammation can lead to cancer…How? Examples?

A
  1. chronic inflammation= increased free radical formation= DNA damage==> Dysplasia==> neoplasia
  2. Chronic hep C, smoking, GERD, gastritis
21
Q

Hemochromatosis

  1. Defect
  2. Pathophysiology
  3. Associated diseases
A
  1. Hereditary disease with defect leading to Fe deposition in tissues (heart, liver, pancreas)
  2. Fe causes damage via Fenton reaction= formation of free radicals
  3. Damage results in liver cirrhosis (and cancer), diabetes, heart failure
22
Q

Types of changes that occur in cell within minutes

A
  1. Biochemical = functional loss, arrythmias
23
Q

Changes that occur in hours

A

Ultrastructural- HOURS–need Electron Microscope

  • membrane changes- blebbing, swelling, microvilli distortion, myelin figures
  • mitochondrial- swelling, amourphous densities (phospholipids)
  • ER- detachment of ribosomes, swelling
  • nuclear alterations
24
Q

Changes that occur hours-days

A

Microscopic (light microscope) -hours-days

  • cytoplasmic swelling and pallor
  • hydropic changes (ER swelling and pinching off into small vacuoles)
  • ballooning degeneration= swollen eosinophilic cytoplasm without vacuoles
  • chromatin clumping
25
Q

Changes that occur days- weeks following necrosis

A

Gross changes

  • pallor (can occur in minutes if caused by ischemia)
  • soft= tissue disruption (4 days)
  • raised or depressed
  • Scar= 2+ weeks
26
Q

Alcoholic hepatitis shows

A
  • ballooning degeneration
  • mallory bodies
27
Q

Light microscopy/morphological hallmarks of cell injury (x4)

A
  1. cytoplasmic swelling, pallor (and turgor)
  2. cytoplasmic vacuolization
  3. chromatin clumping
  4. Fatty change (if tissue is involved in lipoprotein synthesis)
28
Q

MORPHOLOGICAL hallmarks of cell death (necrosis)

A
  1. disintegration of nucleus
  2. disruption of cell membranes
  3. digestion of cellular enzymes

==> EOSINOPHILIA and HYALINIZATION of cell==>tissue becomes soft and structure is disrupted

29
Q

Most important feature for identifying necrosis? How does this occur?

A

Loss of nucleus from pyknosis, karyorrhexis, karyolysis

30
Q

Define

  1. Pyknosis
  2. Karyorrhexis
  3. Karyolysis
A

Nuclear changes that indicate NECROSIS

  1. Pyknosis-solid, shrunken basophilic mass. Chromatin is more basophilic
  2. Karyorrhexis- [basophilic] nucleus fragments
  3. Karyolysis-nucleus dissolves into amorphic mass, less basophilic. DNAase activated= dissolution of DNA
31
Q

Autolysis

A
  • autolysis: release of enzymes from lysosomes–activated by calcium
  • irreversible injury that causes morphological change
32
Q

Coagulative Necrosis

  1. LM characteristics
  2. Mechanism
A
  1. LM charactertics of coagulative necrosis
    • karyorrhectic (fragmented) or absent nucleus,
    • eosinophilic cytoplasm,
    • cell outlines preserved,
    • firm tissue (days)==>then softens
  2. Hypoxic cell death (in all tissues but brain)
33
Q

Liquefactive necrosis

  1. LM characteristics
  2. Gross
  3. mechanism
A

liquefactive necrosis

  1. LM changes
    • neutrophils,
    • destructive enzymes from PMNs,
    • tissue architecture destroyed,
    • pus
  2. Gross changes: softening (malacia) yellow/tan color
  3. Causes: G- abscess, ischemia of brain
34
Q

Gangrenous necrosis

  • define
  • causes
  • wet gangrene
A
  • type of coagulative necrosis of multiple tissue layers in limbs
  • Causes: loss of blood supply, frost bite
  • can become wet gangrene if secondary bacterial infection
35
Q

Caseous Necrosis

  • general features
  • gross appearance
  • Light microscope
A

Caseous necrosis

  • type of coagulative necrosis associated with m. tuberculosis.
    • caseating (necrotic center)
    • non caseating (non necrotic center)
  • gross appearance: yellow-white cheese-like material, nodules
  • LM: central area of amorphous eosinophilic granular matter surrounded with epithelioid histiocytes and a lymphocytic mantle. Less distinct cell borders than coag, but more clear than liquefactive.
36
Q

Potts diesease

A

TB in the spine

37
Q

Fat necrosis

  1. features
  2. Light microscope
  3. Gross appearance
A

Fat necrosis- type of coagulative necrosis

  1. soaponifaction from calcium combining with degrading fats and proteins (breast trauma or pancreatitis)
  2. eosinophilic ghost outline of dead adipocytes with basophilic calcium deposits. surrounded by inflammation
  3. white, chalky firm areas–soaponifcation
38
Q

Fibrinoid Necrosis

  1. features
  2. histological appearance
  3. causes?
A

Fibrinoid necrosis- Type III HS reaction.

  1. immune complex depositions within walls of blood vessels with fibrin
  2. looks like fibrin–bright pink hyalinization
  3. polyarteritis nodosa
39
Q

Contraction bands

A

speficif pattern of cardiac myocyte damgage caused by ROS (following repurfusion)

Pathology (7 decks)

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