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FPP-MSS > Cell Injury, Adaptations and Death > Flashcards

Cell Injury, Adaptations and Death Flashcards

1
Q

Examples of labile tissues.

A

Hematopoietic cells, surface epithelia (linings of upper airways, gastrointestinal tract, skin etc.)

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2
Q

Examples of stable tissues.

A

Parenchyma of most solid organs (liver, kidney, pancreas).

Endothelial cells, fibroblasts, smooth muscle cells.

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3
Q

Examples of permanent tissues.

A

Neurons
Cardiac myocytes

-Heal with connective tissue

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4
Q

What is cellular hypertrophy?

A

Increase in size of cells = increase in size of organ

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5
Q

Examples of physiologic hypertrophy.

A

Skeletal muscle hypertrophy in weight lifting

Uterus in pregnancy

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6
Q

Examples of pathologic hypertrophy.

A

Cardiac muscle hypertrophy with hypertension

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7
Q

What is hyperplasia?

A

Increase in cell number. Occurs in cells capable of division (labile and stable cells)

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8
Q

Examples of physiologic hyperplasia.

A

Hormonal hyperplasia of female breast at puberty and in pregnancy.
Compensatory hyperplasia of liver after partial resection.
Connective tissue response with wound healing.

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9
Q

Examples of pathologic hyperplasia.

A

Hormonal imbalance stimulating endometrial hyperplasia with menopause.
Benign prostatic hyperplasia (BPH) – formation of nodules in prostate gland.
Skin warts and mucosal lesions associated with viral infections (papilloma virus).

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10
Q

Is enlargement of the uterus during pregnancy hypertrophy or hyperplasia?

A

Both!!

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11
Q

What is atrophy?

A

Decrease in size of a cell due to loss of cell substance. If severe – decreased organ size.

Physiologic cause: loss of hormonal stimulation (endometrium at menopause)

Pathologic cause: decreased functional demand (arm in cast), loss of innervation, inadequate nutrition

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12
Q

What is metaplasia?

A

When one adult cell type is replaced by another adult cell type that is better able to handle a stress.

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13
Q

Explain some examples of epithelial metaplasia.

A

Ciliated columnar epithelium becomes squamous epithelium (trachea/bronchi of smokers)
Squamous epithelium become gastric/intestinal (glandular) type epithelium (distal esophagus in those with reflux)
Columnar becomes squamous in endocervix with increased risk of HPV infection

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14
Q

Explain an example of mesenchymal metaplasia.

A

Bone formation in soft tissue (muscle/connective tissue) at sites of injury.

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15
Q

What constitutes irreversible cell injury?

A

Inability to reverse mitochondrial dysfunction, disturbance of membrane function

Two types: necrosis, apoptosis

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16
Q

Explain necrosis.

A

Cell size enlarges (swells).
Nucleus – pyknosis, karyorrhexis, karyolysis.
Plasma membrane disrupted.
Cellular contents undergo enzymatic digestion, may leak out of cell.
Adjacent inflammation frequent.
Invariably pathologic.

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17
Q

Explain apoptosis.

A

Cell cell is reduced.
Nucleus – fragments into nucleosome-size fragments
Plasma membrane intact but altered structure.
Cellular contents intact, may be released in apoptotic bodies.
No adjacent inflammation.
Often physiologic eliminating unwanted cells.

18
Q

What constitutes reversible cell injury?

A

Fatty change – lipid vacuoles in cytoplasm, from toxic or hypoxic injury, primarily in cells dependent on fat metabolism (i.e. fatty liver secondary to toxins)

Cellular swelling – hydropic change or vacuolar degeneration, from failure of membrane pumps to maintain homeostasis (membrane blebs), vacuoles appear in cells corresponding to distended endoplasmic reticulum.

19
Q

What does a fatty liver look like and why?

A

Yellow color and “greasiness” indicates steatosis.
Hepatocytes are injured resulting in an intracellular accumulation of triglycerides, liver enlargement and elevated liver enzymes.
Clinical manifestations depend upon specific cause and how severe.

20
Q

Why does accumulation occur in a fatty liver?

A

Impairment of microsomal and mitochondrial functions.
Decreased fatty acid oxidation.
Decreased apoprotein formation.
Increased mobilization of fatty acids from periphery.

21
Q

What are some morphologic features of necrosis?

A

Increased eosinophilia, nuclear shrinkage, fragmentation, breakdown of plasma membrane and organelle membranes.

22
Q

Results from hypoxic or anoxic injury due to ischemia.
Persistence of dead cells with intact outlines but with loss of cellular details – denatures cellular proteins and enzymes.
Occurs in all solid organs.

A

Coagulative Necrosis

23
Q

Complete digest of dead cells.
Common with bacterial or fungal infections – stimulate accumulation of WBC, necrotic cells together with acute inflammatory cells = pus.

A

Liquefactive Necrosis

24
Q

What kind of necrosis are brain infarcts?

A

Liquefactive Necrosis

25
Q

Characteristic of tuberculous infection.
Gross appearance resembles cheese.
Fragmented and coagulated cells with loss of tissue architecture.
Usually surrounded by a border of inflammatory cells forming a distinctive patter (granuloma).

A

Caseous Necrosis

26
Q

Term used for ischemic coagulative necrosis of lower or upper extremity.
Also for severe necrosis of other organs (i.e. gangrenous bowel etc)

A

Gangrenous Necrosis

27
Q

Wet gangrene

A

With a bacterial infection – has liquefactive characteristics

28
Q

Typically seen in pancreas in acute pancreatitis – injury to pancreas releases lipase which liquefies fat and splits triglycerides; fatty acids combine with calcium to form chalky white material (saponification).
Can also occur as a result of trauma to fatty tissue with release of lipase’s and triglycerides.

A

Fat Necrosis

29
Q

Deposition of immune complexes in vascular wall.
Fibrin-like – bright pink amorphous appearance.
Occurs in vasculitis syndromes (polyarteritis nodosa, giant cell arteritis etc.)

A

Fibrinoid Necrosis

30
Q

What are some principal targets of cellular injury?

A

Mitochondria: depletion of ATP and increased ROS
Calcium homeostasis: intracellular entry of calcium
Cellular membranes: increase permeability
DNA and cellular proteins: damage to DNA, protein misfolding

31
Q

What injures tissue faster: ischemia or hypoxia?

A

Ischemia – no delivery of substrates for glycolysis, no removal of metabolites by blood flow, ischemia is the most common cause of cell injury.
In hypoxia, anaerobic glycolysis continues

32
Q

What is reperfusion injury?

A

Restoration of blood flow to ischemic tissue that increases cell injury.
Occurs most frequently in brain and heart.
Happens because of increased free radical generation and increased leukocytes, plasma proteins and complement (inflammation).

33
Q

What is a direct toxin?

A

One that binds to cellular organelle or molecule component (mercuric chlorides binds to cell membrane proteins– results in decreased membrane transport and increased membrane permeability)

34
Q

What is a toxic metabolite?

A

A toxin that needs to be activated, often by P-450 oxidases in liver smooth ER (acetaminophen).

35
Q

What is the morphology of apoptosis?

A

Cytoplasmic eosinophilia
Chromatine condensation and aggregation, eventually karyorrhexis
Cell shrinkage with cytoplasmic blebs and apoptotic bodies
Phagocytosis without inflammation

36
Q

What is the intrinsic pathway of apoptosis?

A

Bcl-2 proteins increase permeability of the mitochondria and allow cytochrome C to enter cytoplasm, resulting in caspase activation.

37
Q

What are some sub cellular responses that might be seen in response to injury?

A

Accumulation of abnormal substances (lipofuscin, carbon, iron) in lysosomes, endoplasmic reticulum and mitochondria.

38
Q

What are some cytoskeleton abnormalities that might be seen with injury?

A

Accumulations from toxins: Alcohol-Mallory hyaline in liver

Abnormal organization of microtubules: Kartagener syndrome-immotile cilia, sterility and lung infections

39
Q

Pathologic dystrophic calcification

A 
Non-viable, damaged or dying tissues
Normal serum calcium 
Atheromas, aortic valves in elderly, lymph nodes with TB
White gritty deposits
Basophilic
40
Q

Pathologic metastatic calcification

A

Normal tissues
Hypercalcemia
Increase PTH, destruction of bone, vit D intoxication, renal failure
Commonly in interstitial tissues (lung, kidney, gastric mucosa)

41
Q

What are some characteristics of cellular aging?

A

DNA damage increases (free radicals)
Decreased cellular replication (shortening of telomeres, lack of telomerase)
Defective protein homeostasis (decreases cell survival)

FPP-MSS (17 decks)

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