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Mechanism of Human Disease > Cell Injury > Flashcards

Flashcards in Cell Injury Deck (23)
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1
Q

Define hyperplasia. Give a physiological and pathological example.

A

increase in the number of cells

  • physio: breast glands increase for lactation during pregnancy
  • patho: high estrogen causes endometrial hyperplasia
2
Q

Define hypertrophy. Give a physiological and pathological example.

A

increase in the size of cells

  • physio: muscle size during weight lifting
  • patho: HTN patients
3
Q

Define atrophy. Give a physiological and pathological example.

A

decrease in cell size

  • physio: low estrogen leading to post-menopausal decrease in endometrial growth
  • patho: muscle atrophy
4
Q

Define metaplasia. Give a physiological and pathological example.

A

cells change from one subset to another in response to stress/injury
- typically, trachea and esophagus are lined with simple columnar cells. cigarette smoking damages these cells and newly forming cells become stratified squamous cells better able to withstand cigarette smoke

5
Q

List cellular adaptations.

A
  • hyperplasia
  • hypertrophy
  • atrophy
  • metaplasia
6
Q

List vulnerable biochemical systems for cellular injury.

A
  • membrane integrity
  • mitochondrial aerobic respiration
  • cellular calcium
  • nuclear integrity
7
Q

List biochemical changes that determine degree of reversible cell injury or cell death.

A
  • ATP depletion
  • reactive oxygen species
  • loss of calcium homeostasis
  • defective cell membrane permeability
8
Q

Describe mechanism of injury via hypoxia.

A

Pathogenesis: decreased O2 => decreased oxidative phosphorylation => decreased ATP => impaired functioning of the Na/K pump => intracellular Na increases => water moves into the cell => swelling

Decreased ATP also => increase in cellular Ca => defective membrane permeability and activated enzymes (CK and LDH)

decreased ATP also => detached ribosomes => impaired protein synthesis => lipid deposition

End result = swelling

9
Q

How can you test for hypoxic injury?

A
  • measure levels of CK and troponin (for MI) as evidence of enzymatic leakage from swollen cells
  • measure lactic acid levels as evidence of anaerobic respiration due to decreased ATP
10
Q

What are defenses against ROS?

A

Vitamin C
Vitamin E
antioxidants

11
Q

Describe mechanism of injury by ROS.

A
  • lesions in DNA
  • crosslinking of proteins
  • oxidation of membranes
  • mitochondrial damage
  • reperfusion injuries
  • metabolism of drugs (CCL3, acetominophen)
12
Q

Describe mechanism of injury via loss of calcium homeostasis

A
  • activation of cellular enzymes
    phospholipases and proteases => membrane degradation
    endonucleases => nuclear damage
    ATPase => decreased ATP
13
Q

List the morphological elements of reversible cellular injury.

A
  • swelling
  • steatosis (fatty changes)
  • myelin
  • ER swelling
  • membrane blebs
14
Q

List morphological characteristics of necrosis.

A
  • presence of leukocytes (mainly neutrophils)
  • increased eosinophilia (more pink due to denaturation of proteins
  • nuclear structural changes (karyolysis, pyknosis, karyhorrhexis
  • occurs in a geography of cells
15
Q

What are structural changes that occur to the nucleus during necrosis?

A
  1. pyknosis: nuclear shrinkage, chromatin condensation
  2. karyorrhexis: fragmented pyknotic nucleus => nucleus disappeared
  3. karyolysis: loss of chromatin due to enzymatic degradation by endonucleases
16
Q

List types of necrosis

A
  • coagulation
  • liquefactive
  • enzyme fat
  • caseous
  • gangrene (dry and wet)
17
Q

Describe coagulation necrosis and its associations, affected cells, and examples.

A

histology: ghost-like remnants of cells without nuclei; intense eosinophilic cytoplasm
affected: solid organs (heart, kidney),

associated with: severe ischemia

example: myocardial/renal infarct

18
Q

Describe liquefactive necrosis and its associations, affected cells, and examples.

A

histology: loss of cellular structure due to bacterial enzymes, accumulation of liquid and debris; unable to tell what the cell is

associated with: bacterial infections, ischemic brain infarct

example: abscesses (collection of neutrophils, dead cells, liquid)

19
Q

Describe caseous necrosis and its associations, affected cells, and examples.

A

histology: granular debris secluded within a granuloma; tissue is soft, white, friable (cheese)

associated with: granulomas

example: tuberculosis lymph node

20
Q

Describe enzymatic fat necrosis and its associations, affected cells, and examples.

A

associated with: focal cell death in pancreas and adjacent fat

example: acute pancreatitis releases enzymes that breakdown surrounding adipose tissue => fatty acids combine with calcium => form soaps

21
Q

Describe gangrene and its associations, affected cells, and examples.

A

def: coagulation (ischemic) necrosis of an extremity, bowel, or gallbladder

wet gangrene = coagulation necrosis + bacterial infection => coagulation necrosis + liquefactive necrosis

22
Q

Define the process of apoptosis.

A
  • regulated cell death characterized by nuclear condensation and fragmentation
  • NOT associated with inflammation
  • phagocytosed
23
Q

Where is apoptosis seen?

A
  • embryonic development
  • hormone dependent physiologic changes (menstrual cycle)
  • proliferating cell populations
  • DNA damage
  • infections
  • accumulation of misfolded proteins