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Foundations Exam 2 > Cellular Responses to Stress > Flashcards

Cellular Responses to Stress Flashcards

1
Q

Hyperplasia

A

Increase in number of cells (result of GF-driven proliferation of mature cells - occur in tissues with capacity to divide)

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2
Q

Hypertrophy

A

Increase in size of cells

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3
Q

Atrophy

A

Decrease in size of cells

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4
Q

Metaplasia

A

Change in structure; reversible change in which one cell type is replaced by another cell type

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5
Q

Physiologic hypertrophy

A

Pregnancy, breast tissue from puberty

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6
Q

Pathologic hypertrophy

A

Excessive of inappropriate actions of a stimulus (like a hormone)

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7
Q

Physiologic atrophy

A

Loss/decrease in hormonal stimulation

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8
Q

Pathologic atrophy

A

Decreased workload, loss of innervation, diminished blood supply, inadequate nutrition

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9
Q

Causes of cell injury

A 
Oxygen deprivation 
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances
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10
Q

Hypoxia

A

Oxygen deprivation in tissues

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11
Q

Hypoxemia

A

Oxygen deprivation in blood

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12
Q

Ischemia

A

Oxygen deprivation

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13
Q

Features of reversible injury

A 
Membrane blebs
Cellular swelling
Mitochondrial changes
Dilation of ER
Nuclear alterations
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14
Q

Irreversible cell injury (death)

A

Necrosis

Apoptosis

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15
Q

Necrosis

A

Result of denaturation of intracellular proteins and enzymatic digestion of the injured cells

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16
Q

Biochemical mechanism in necrosis

A

Mitochondrial damage - less ATP; more ROS
Entry of Ca - increase mitochondrial permeability; activation of cellular enzymes
Membrane damage - Plasma (loss of cell components) or lysosomal (enzymatic digestion of cell components)

17
Q

Coagulative necrosis

A

Happens in solid organs; firm texture; architecture preserved for days (injury denatures structural proteins AND enzymatic proteins so dead cells won’t lyse until leukocytes come in); caused by ischemia

18
Q

Liquefactive necrosis

A

Brain; tissue architecture lost; caused by infection; pus

19
Q

Casseous necrosis

A

Cheese-like appearance; granuloma (injury closed off by activated machrophages); TB infection

20
Q

Fibrinoid necrosis

A

blood vessel; antigen-antibody complexes are deposited in walls of arteries

21
Q

Fat necrosis

A

Saponification (calcium formation)

22
Q

Gangrenous necrosis

A

Usually applied to a limb that has its lost its blood supply; Dry - ischemic; usually coagulative; wet - superimposed infection; liquefactive necrosis

23
Q

Apoptosis

A

Programmed cell death in which cells destined to die activate intrinsic enzymes that degrade the cells’ own DNA and proteins

24
Q

Morphologic evidence of apoptosis

A

Cell shrinkage and chromatin condensation
Pyknotic nuclei
Apoptotic bodies

25
Q

Morphologic evidence of necrosis

A

Increased eosinophilia
Myelin figures
Karyolysis - loss of nuclear material
Pyknosis - nuclear shrinkage and increased basophilia
Karyorrhexis - fragmentation of shrunked nucleus

26
Q

Mitochondrial (intrinsic) pathway

A

Cell injury increases mitochondrial membrane permeability, releasing cytochrome c
Cytochrome C binds to APAF forming apoptosome
Initiator caspase-9 activated, triggers caspase cascade

27
Q

Death receptor (extrinsic) pathway

A

Death receptors engage
Fas binds to it’s ligand and forms a binding site for FADD
FADD binds inactive form of caspase -8
Multiple procaspase-8 come together to cleave and activate each other, trigger apoptosis

28
Q

Initiation phase

A

Some caspases become catalytically active

29
Q

Execution phase

A

Other caspases trigger degradation of critical cellular components

30
Q

Necrosis characteristics

A 
Nuclei digested
Loss of membrane integrity - leaky
Involves larger area of tissue - many cells
Increased inflammation
Always pathologic
31
Q

Apoptosis characteristics

A

Nuclei shrink and fragment
Membrane blebbing with fragmentation of membrane-bound cytoplasm
Involves isolated cells or small groups of cells
Decreased inflammation
Can be physiologic or pathologic

32
Q

Necroptosis

A

Like necrosis - swelling of cell and organelles, release of enzymes, rupture of membrane
Like apoptosis - triggered by genetically programmed signal transduction similar to extrinsic form
DEFENSE AGAINST VIRUSES THAT ENCODE CASPASE INHIBITORS

33
Q

Accumulations

A

Lipid
Protein
Glycogen
Pigments

34
Q

4 main pathways of intracellular accumulation and examples of each

A

Abnormal metabolism - fatty liver (steatosis), hemosiderosis (iron accumulation)
Defect in protein folding and transport - alpha1-antitrypsin mutation
Lack of enzyme that leads to accumulation of endogenous substance - hepatic glycogenosis
Ingestion of indigestible substance leads to accumulation of exogenous substance - anthracosis (pigment accumulation)

35
Q

Pathologic calcification

A

Abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts

36
Q

Dystrophic pathologic calcification

A

Deposition occurs locally in dying tissue (normal serum calcium levels); ex.) atheromas and calcific aortic valves

37
Q

Metastatic pathologic calcification

A

May occur in normal tissues (almost always due to hypercalcemia); consequence of PTH; widely occurs

Foundations Exam 2 (8 decks)

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