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FPP: pre-midterm > Cell Injury, Adaptations, and Death > Flashcards

Cell Injury, Adaptations, and Death Flashcards

1
Q

What are some etiologies of cell injury?

A

Hypoxia, ischemia, toxins, infectious agents, immunologic reactions, nutritional imbalances, physical agents/trauma, and aging

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2
Q

Which is more severe usually, hypoxia or ischemia?

A

Ischemia; not only is there a deficiency in oxygen, but also a deficiency in nutrient supply and a build up of toxic metabolites

**ischemia= most common cause of cell injury

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3
Q

What is the hallmark of reversible cell injury?

A

Failure of membrane pumps to maintain homeostasis… accumulation of degenerated organelles/lipids results in cell swelling (hydropic change/water coming in, vacuolar degeneration, fatty change)

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4
Q

What is steatosis?

A

Fat accumulation (usually in liver due to cell injury though can happen in heart, muscle, kidney, etc) Can lead to liver enlargement and is REVERSIBLE

*Caused commonly by toxins, obesity, malnutrition, carbon tetrachloride, anoxia diabetes, viral infections

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5
Q

What are the main differences between necrosis and apoptosis?

A

Necrosis

  • major pathway of cell death (more common)
  • uncontrolled
  • in response to toxins, ischemia, etc

Apoptosis

  • occurs with less severe injury/ as a normal process
  • regulated cell death
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6
Q

Define pyknosis

A

Shrinkage and increased basophilia

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7
Q

Define karyorrhexis

A

Fragmentation of the pyknotic nucleus

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8
Q

Define karyolysis

A

Nuclear basophilia disappears due to digestions (by DNase)

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9
Q

What are 3 morphologic changes of cell necrosis?

A
  1. Cytoplasmic changes (increased eosinophilia, homogenous cytoplasm, vacuolation)
  2. Nuclear changes (pyknosis, karyorrhexis, karyolysis)
  3. Dead cells may be completely digested/disappear (debris can be phagocytosed -> resulting fatty acids may calcify)
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10
Q

What is the hallmark of irreversible cell injury?

A

**Membrane damage

  • mitochondrial
  • plasma
  • lysosomal

(enzyme leakage from lysosome/cell -> inflammation)

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11
Q

What does this show?

A 
Dead neurons (left)
\*\*increased eosinophilia and nuclear shrinkage (pyknosis)
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12
Q

What does this show?

A

Vacuolar (hydropic) change in reversible injury (right)

**surface blebs, swelling, and increased eosinophilia (retained nuclei)

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13
Q

What is the most common type of necrosis?

A

Coagulative

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14
Q

What causes coagulative necrosis?

A

Hypoxic/anoxic injury due to ischemia **occurs in all solid organs EXCEPT the brain

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15
Q

How can you identify coagulative necrosis?

A

Persistence of dead cells with intact outlines but with loss of cellular details (e.g. nucleus)

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16
Q

What causes liquefactive necrosis?

A

Commonly seen with bacterial and fungal infections

**exception= brain infarct (liquefactive not coagulative)

(microbes stimulate WBC accumulation which release digestive enzymes -> PUS/abscesses as tissue architecture dissolves)

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17
Q

What causes caseous necrosis?

A

Characteristic of TB infection

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18
Q

How would you identify caseous necrosis?

A

Gross appearance resembles crumbly cheese (fragmented/coagulated cells with loss of tissue architecture)

**usually surrounded by border of inflammatory cells (granuloma)

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19
Q

What causes gangrenous necrosis?

A

NOT a specific type of necrosis; term used for ischemic coagulative necrosis of extremities (and severe necrosis of bowel, appendix, gallbladder, etc)

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20
Q

What is the difference between dry and wet gangrenous necrosis?

A

Wet has liquefactive characteristics due to a bacterial infection also being present

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21
Q

How do you identify gangrenous necrosis?

A

BLACK (e.g. toes, bowel from intussusception)

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22
Q

What causes fat necrosis?

A

Typically seen in the pancreas in acute pancreatitis, can also occur from trauma to fatty tissue (e.g. fat necrosis of breast)

23
Q

How can you identify fat necrosis?

A

Injury releases lipase which liquefies fat, FAs combine with calcium to form chalky white material

24
Q

What causes fibrinoid necrosis?

A

Deposition of immune complexes (antigens and antibodies) in vascular walls

**occurs in vasculitis syndromes (polyarteritis nodosa, giant cell arteritis, etc)

25
Q

How can you identify fibrinoid necrosis?

A

Fibrin-like bright pink amorphous appearance

26
Q

What are the key features of apoptosis?

A

**pathway of regulated cell death:

  • plasma membrane intact
  • cell activated enzymes degrade DNA and proteins
  • no leakage of cell contents -> no inflammation
  • fragments of cell are pinched off (apoptotic bodies)
  • cell fragments consumed by macrophages
27
Q

What are the two causes of apoptosis?

A

Physiologic conditions

  • common during embryogenesis
  • hormone dependent (e.g. breast in pregnancy)
  • turnover of proliferative tissue (e.g. GI epithelium)
  • death of lekocytes after inflammatory response

Pathologic conditions

  • eliminates cells with DNA damage (e.g. secondary to radiation, chemo, etc) if repair fails
  • accumulation of misfolded proteins (e.g. Alzheimer’s)
  • cell injury from viral infection (e.g. HIV)
28
Q

What are the two pathways of apoptosis?

A
  1. Mitochondrial (intrinsic)
  • BH3 sensors activated by cell injury
  • Bcl-2 family effectors released (Bak, Bax)
  • Cytochrome C leaks from mitochondria
  • Cyt C activates caspases
  1. Death receptor (extrinsic)
  • Cells expressing Fas ligand/TNF bind cell surface “death receptors”
  • Adaptor proteins trigger caspase cascade
29
Q

Describe the morphology of apoptosis

A
  • cytoplasmic eosinophilia
  • chromatin condensation/aggregation -> karyorrhexis
  • cell shrinkage -> blebs/apoptotic bodies
  • phagocytosis WITHOUT inflammation (differs from liquefactive necrosis)
30
Q

What factors affect the cell response to injury?

A

Type/cause of injury (ischemia, toxins, infection, etc), and duration/severity of insult

31
Q

What affects the outcome of cell injury?

A

Cell type (e.g. skeletal muscle dies in 2-3 hrs, cardiac muscle in 20-30 min), nutritional/hormonal status, and genetic makeup (e.g. P450s)

32
Q

What are 8 specific examples of causes of cell injury/necrosis?

A
  1. ischemia/hypoxia
  2. reperfusion injury
  3. oxidative stress
  4. chemical/toxic injury (direct and latent)
  5. ER stress
  6. DNA damage
  7. inflammation
33
Q

When simplified (more overlapping irl), what causes apoptosis? Necrosis? Both?

A

Hypoxia, ischemia= necrosis

Mutations, cell stress, infections, radiation= apoptosis

Infections, immunologic disorders= both

34
Q

What is the main difference between ischemia and hypoxia?

A

Both have a reduced supply of oxygen but in hypoxia anaerobic glycolysis continues (ischemia stops aerobic AND anaerobic glycolysis by stopping substrate delivery and removal of metabolites)

35
Q

Where are the two most common places to get reperfusion injury?

A

Brain and heart

36
Q

What are the proposed mechanisms for reperfusion injury?

A
  1. Increased ROS generation with restoration of oxygen flow
  2. Increased leukocytes, plasma proteins, and complement from damaged tissue **inflammation
37
Q

What stresses increase the generation of ROS?

A
  1. absorption of radiant energy (e.g. UV, x-rays, etc)
  2. toxins (e.g. carbon tetrachloride)
  3. reperfusion of ischemic tissues
38
Q

What can result from ROS?

A
  1. membrane damage (lipid peroxidation)
  2. protein breakdown/misfolding
  3. DNA damage/mutations
39
Q

What are the two general mechanisms of chemical injury?

A
  1. Direct toxins (bind to cellular organelle or molecular component) e.g. mercuric chloride binds plasma membrane
  2. Latent toxins (activation, often by liver P450s, results in toxic metabolite) e.g. acetominophen poisoning
40
Q

How does ER stress result in cell injury/necrosis?

A

Misfolded proteins accumulate b/c of increased production or decreased elimination…

  • Normally, misfolded proteins in the ER are ubiquitinated and targeted for destruction.
  • Unfolded protein response is induced if they accumulate (elevated levels then decrease)
  • If more accumulates than the cell can handle (ER stress), apoptosis occurs
41
Q

What are some diseases where misfolded proteins accumulate?

A
  • Cystic fibrosis
  • Tay-sachs
  • Alzheimer’s
  • Huntington’s
  • Parkinson’s
  • Type II diabetes
  • Familial hypercholesterolemia
42
Q

What is the mechanism of apoptosis resulting from DNA damage?

A

With DNA damage, p53 accumulates and stops the cell cycle (to repair DNA)… however if the damage is too great p53 triggers apoptosis

43
Q

Define labile cells

A

Continuously dividing cells (e.g. hematopoietic cells, surface epithelia)

44
Q

Define quiescent

A

Minimal replicative activity normally (stable tissues… can proliferate in response to injury)

e.g. parenchyma of most solid organs, endothelial cells, smooth muscle cells

45
Q

Define permanent tissues

A

Non-proliferative

e.g. neurons, cardiac muscle cells

46
Q

Define hypertrophy… physiologic versus pathologic?

A

Increase in SIZE of cells (results in increase of size of organ)… cells have limites or no capacity to divide

  • Physiologic
    • Increased functional demand
    • e.g. skeletal muscle in weight lifting, uterus in pregnancy
  • Pathologic
    • e.g. cardiac muscle in HTN
47
Q

Define hyperplasia… physiologic versus pathologic?

A

Increase in cell NUMBER

  • Physiologic
    • Female breast at puberty and pregnancy (hormonal)
    • Compensatory liver response after partial resection
    • Connective tissue response with wound healing
  • Pathologic
    • Excessive stimulation by growth factors/hormones
      (e. g. endometrial hyperplasia)
      • REVERSIBLE
      • Increased risk of cancer (exception= benign prostatic hyperplasia)
    • Skin warts with viral infections (e.g. papilloma)
48
Q

Is the enlargement of the uterus during pregnancy hyperplasia or hypertrophy?

A

BOTH

49
Q

Define atrophy… physiologic versus pathologic?

A

Decrease in SIZE of a cell due to loss of cell substance (decreased protein synthesis/increased degradation)

**decreased function but NOT death

  • Physiologic
    • loss of hormonal stimulation (e.g. endometrium in menopause)
  • Pathologic
    • decreased functional demand
    • loss of innervation (e.g. peripheral nerve damage)
    • inadequate nutrition
50
Q

Define metaplasia

A

When one adult cell type is replaced by another (that is better able to handle the stress) **Stem cells differentiate along a new pathway

REVERSIBLE, may be associated with risk of cancer

51
Q

What are two examples of metaplasia?

A
  1. Epithelial
  • ciliated columnar becomes sqaumous epithelium in trachea/bronchi of smokers
  • squamous epithelium becomes gastric/intestinal type in those with reflux **Barrett’s esophagus
  • endocervix: columnar becomes squamous and increases risk of HPV infection
  1. Mesenchymal
    * Bone formation in soft tissue (muscle/connective tissue) at sites of injury
52
Q

What are common examples of intracellular accumulations? What causes them?

A
  • lipid
  • cholesterol (in intima in atherosclerotic plaques in arteries)
  • proteins (neurofibrillary tangles in Alzheimer’s)
  • glycogen
  • pigments (lipofuscin from aging in heart/liver/brain, carbon in lung/lymph nodes from air, melanin, hemosiderin in liver with hemorrhage)

**occurs in acute (lethal) and chronic (on-going) injury as an adaptive response

53
Q

What are the two types of pathologic calcification?

A
  1. Dystrophic
  • non-viable, damaged/dying tissues
  • normal serum calcium
  • gross: white gritty deposits (microscopically basophillic)
  • e.g. atheromas, aortic valves in elderly, lymph nodes with old TB
  1. Metastatic
  • normal tissues
  • hypercalcemia (increased parathyroid hormone, destruction of bone, Vit D intoxication, renal failure)
  • most commonly in interstitial tissues (lung, kidney, gastric mucosa)
54
Q
A

FPP: pre-midterm (19 decks)

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