Cell Injury, Adaptations and Death Flashcards

1
Q

What is hyperplasia

A

increase in cell NUMBER; occurs in labile and stable cells ; physiologic: female breast at puberty and in pregnancy, after liver partial resection; pathologic: hormonal imbalance stimulate endometrial hyperplasia increase risk for cancer!! , BPH-formation of nodules in prostate gland resulting in urinary obstruction, (not increased risk for cancer)

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2
Q

What is hypertrophy

A

increase in SIZE of cells; physiologic: increased skeletal muscle in weight living, uterus in pregnancy; pathologic: cardiac muscle hypertrophy (enlarged nuclei and myofiber width)

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3
Q

What is atrophy

A

decrease in size of cell due to loss of cell substance; decreased fxn but not death; physiologic: loss of hormonal stimulation (endometrium at menopause), pathologic: decreased functional demand (trauma to peripheral nerve, broken arm)

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4
Q

What is Metaplasia

A

one adult cell type replaced by another that is better able to handle the stress examples: chronic smokers-cells are reprogrammed, from ciliated columnar epithelium to squamous epithelium, acid reflux/Barett Esophagus: squamous epithelium becomes gastric/intestinal type, bone formation in soft tissue, columnar becomes squamous in cervical tissue increasing risk of HPV infeciton

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5
Q

What are characteristics of necrosis?

A

swelling; membrane blebs, breakdown of plasma membrane, organelles, leakage of contents, adjacent inflammation

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6
Q

What are characteristics of apoptosis?

A

condensation of chromatin, membrane blebs, cells shrink, cellular fragmentation, apoptotic bodies, INTACT plasma membrane, no adjacent inflammation

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7
Q

What are the 6 types of necrosis?

A

coagulative, liquefactive, caseous, fatty, gangrenous, fibrinoid

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8
Q

Coagulative necrosis is distinguished by:

A

results from hypoxic or anoxic injury due to ischemia, persistence of dead cells with intact outlines but loss of cellular details, injury denatures both cellular proteins and enzymes, occurs in ALL solid organs EXCEPT brain

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9
Q

Liquefactive necrosis is distinguished by:

A

complete digestion of dead cells, commonly seen with bacterial/fungal infections, PUS, ABCESS, usually happens in brain infarcts, acute polynephritis, no residual tissue is preserved

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10
Q

Caseous necrosis is distinguished by:

A

resembles cheese, fragmented and coagulated cells with loss of tissue architecture, surrounded by a border of inflammatory cells (granuloma), center=necrosis

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11
Q

Fat necrosis is distinguished by:

A

typically seen in pancreas, release of lipases and triglyceries, liquifies fat, smudgy purple areas in microscope-fatty necrosis

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12
Q

intracellular responses to injury

A

decreased ATP, increased ROS, damage to lipids, proteins, loss of cellular components, activation of pro-apoptotic proteins, influx of Ca2+, decreased glycogen, decreased pH, climbing of nuclear chromatin,

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13
Q

Pathologic calcification vs Metastatic calcification

A

dystrophic: damaged tissues with normal serum calcium (aortic valves in elderly, lymph nodes with old TB)-get white gritty deposits; metastatic: normal tissues with hypercalcemia, increased PTH, destruction of bone, Vit D intoxication, renal failure, in lung, kidney, gastric mucosa

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14
Q

Cellular aging is defined by:

A

DNA damage increases with age, decreased cellular replication, progressive shorting of telomeres, lack of telomerase (which usually maintains telomerase length), defective protein homeostasis

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15
Q

What are the four kinds of cellular adaptations?

A

Hyperplasia, hypertrophy, atrophy, metaplasia

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16
Q

what are the two kinds of irreversible injury?

A

necrosis and apoptosis

17
Q

what is acute reversible cell injury characterized by?

A

cellular swelling (hydropic change or vacuolar degeneration in response to distended ER) and fatty change (lipid vacuoles in cytoplasm)

18
Q

what are labile cells?

A

continuously dividing cells; examples: surface epithelia (linings of airways, gastrointestinal tract, skin)

19
Q

what are stable tissues?

A

quiescent; minimal replicative activity normally; examples: parenchyma of most solid organs (live,r kidney, pancreas), endothelial cells, fibroblasts, smooth muscle cells (proliferate in response to injury)

20
Q

what are permanent tissues?

A

non proliferative, neurons, cardiac muscle cells

21
Q

what is hypoxia?

A

inadequate oxygenation of blood, reduced oxygen-carrying capacity of blood

22
Q

what is ischemia?

A

lack of blood supply to the site (coronary artery disease)

23
Q

what is steatosis?

A

fat accumulation-intracellular accumulation of triglycerides, liver enlargement and elevated liver enzymes, often occurs in liver due to alcohol, viral infections, obesity, etc

24
Q

fibrinoid necrosis?

A

deposition of immune complexes in vascular wall, bright pink amorphous appearance, occurs in vasculitis syndromes

25
Q

What is reperfusion and how can it cause injury?

A

restoration of blood flow to ischemic tissue; occurs most frequently in brain and the heart, increased free radical generation, increased leukocytes, plasma proteins and complement (inflammation)

26
Q

subcellular responses to cell injury

A

alterations of the cell resulting in morphology involving specific organelles examples: lipid accumulation, lipofuscin accumulation, lysosomal storage diseases (abnormal enzymes to degrade gangliosides), anthracosis in lung, tattoo (indigestible exogenous substance), mitochondria response to starvation (atrophy), hepatocytes (hypertrophy in response to alcohol)

27
Q

what is kartagener syndrome?

A

immotile cilia due to sterility and lung infections

28
Q

what is hemosiderin?

A

hemoglobin derived pigment containing iron: yellow-brown, occurs where there has been a hemmorage in liver, occurs with increased absorption of iron, transfusion,