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Pathology > Exam 1--Cell Injury > Flashcards

Exam 1--Cell Injury Flashcards

1
Q

Most common cause of cell injury

A

hypoxia

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2
Q

How does endotoxin lead to shock?

A

causes changed in blood vessels and coagulation system

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3
Q

2 outcomes of cell overworking/overstimulation?

A

1) cell adapts and changes

2) becomes exhausted and dies

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4
Q

What determines a cell’s response to an injury? (3 things)

A

1) type of injury
2) duration of injury
3) severity

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5
Q

what 3 things determine the OUTCOME of cell injury?

A

1) cell type
2) cell state
3) adaptability of injured cell

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6
Q

5 Most important targets of cell injury

A

1) aerobic respiration
2) cell membrane integrity
3) protein synthesis
4) cytoskeleton
5) genetic apparatus

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7
Q

T/F: cellular function is lost long before cell death occurs

A

True

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8
Q

Increases in cytosolic Ca leads to activation of what 4 types of enzymes?

A

1) ATPases
2) Phospholipases
3) proteases
4) endonucleases

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9
Q

Cell susceptibility to hypoxia:

1) high
2) intermediate
3) low

A

1) neurons
2) myocardium, heptocytes
3) fibroblasts, skeletal muscle

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10
Q

What are 3 sources of free radicals?

A

1) absorption of radiant energy
2) normal metabolism
3) enzymatic conversion of chemicals and drugs

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11
Q

2 ways free radicals cause damage

A

1) lipid peroxidation of membranes

2) oxidation of cellular proteins

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12
Q

Describe lipid peroxidation of membranes

A

free radicals attack and modify the double bonds in unsaturated fatty acids

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13
Q

Describe oxidation of cellular proteins

A

free radicals modify the sulfhydral group which results in protein-protein cross linking

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14
Q

How do cysteine and glutathione prevent free radical damage?

A

enter reactions with free radicals to stabilize them and prevent damage

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15
Q

How does catalase prevent free radical damage

A

breaks hydrogen peroxide into water and oxygen

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16
Q

What 3 GENERAL things change with necrotic tissue?

A

Color, strength, and odor

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17
Q

Karyorrhexis vs. Karyolysis

A

Karyorrhexis–nucleus broken apart and ruptured nuclear envelope
Karyolysis–nuclear chromatin degraded, hollow nuclear membrane

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18
Q

What type of necrosis is grossly firm, dry, and often pale (but can be red/black)

A

Coagulative

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19
Q

What type of necrosis is associated with LOSS of tissue architecture?

A

Caseation

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20
Q

What type of necrosis is grossly: dry but greasy, easily crumbles, and is white/grey or yellowish

A

Caseation

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21
Q

Main cause of caseation necrosis?

A

Mycobacterial spp.

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22
Q

What are 3 outcomes of caseation necrosis?

A

encapsulation
mineralization
liquefaction

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23
Q

What makes a cyst different from an abscess?

A

Cyst is lined by epithelial cells (source of the fluid)

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24
Q

Why does the CNS only undergo liquefactive necrosis?

A

nervous tissue is high in lipids and low in proteins to coagulate

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25
Q

What type of bacteria are associated with abscess formation?

A

Pyogenic (staph, strep, pseudomonas)

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26
Q

What type of necrosis causes muscle tissue to be grossly pale, shiny, and swollen

A

Zenker’s

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27
Q

Bacteria that cause:

1) blackleg
2) malignant edema

A

1) Clostridium chauvoei

2) Clostridium septicum

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28
Q

What type of necrosis is grossly opaque/white, solid/firm, and somewhat granular

A

fat necrosis

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29
Q

Panniculitis

A

inflammation of fat

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30
Q

What type of necrosis is caused by saprophytic bacteria

A

moist gangrene

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31
Q

What type of necrosis is grossly: swollen, soft and pulpy; usually darkly colored and putrid odor

A

Moist gangrene

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32
Q

Which type of necrosis will present with large bacilli microscopically

A

moist gangrene

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33
Q

What type of necrosis is common in tissue extremities (i.e. lower fluid content and temp)

A

Dry gangrene

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34
Q

What type of necrosis appears grossly cool, shriveled, leather-like, and discolored

A

dry gangrene

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35
Q

What type of necrosis requires anaerobic conditions?

A

gas gangrene

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36
Q

What usually causes gas gangrene?

A

clostridial infections

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37
Q

What 4 factors determine the outcome of necrosis?

A

1) types of cells affected
2) location of cells
3) number of cells affected
4) rate at which cells are affected

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38
Q

Liquefaction and removal occurs when?

A

liquefaction is slow

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39
Q

Liquefaction with cyst formation occurs when

A

fluid accumulated faster than it can be removed

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40
Q

When do you see liquefaction with abscess formation?

A

when the necrosis is caused by pyogenic bacteria

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41
Q

Abscess
Phlegmon
Carbuncle

A

1) localized collection of pus from liquefaction of tissue
2) inflammation of SQ connective tissue
3) large abscess with multiple draining tracts

42
Q

coagulative and caseation necrosis usually lead to

A

encapsulation without liquefaction

43
Q

with encapsulation without liquefaction, what makes up the capsule

A

fibrous connective tissue

44
Q

What is the outcome of necrosis in tissues that border free surfaces?

A

sloughing

45
Q

Erosion
Ulcer
Slough

A

1) doesn’t penetrate basement membrane (no scar)
2) does penetrate BM
3) large area of necrosis; scarring

46
Q

When the necrotic area is replaced by connective tissue

A

replacement by scar

47
Q

Autolysis
Heterolysis
Putrefaction

A

1) break down by lysosomal enzymes
2) breakdown by bacterial enzymes
3) invasion by saprophytic bacteria

48
Q

List cells/tissues in order of death (first–>last)

A

neurons–>muscle–>organ cells–>chondrocytes

49
Q

1) Cooling of body
2) Gravitational blood migration
3) muscle contraction

A

1) algor mortis
2) livor mortis
3) rigor mortis

50
Q

T/F: The most active muscles with undergo rigor first

A

True

51
Q

What are 2 reasons for rigor mortis?

A

1) depleted ATP prevents myosin release from actin

2) increased cytosolic Ca causes muscle stimulation

52
Q

How does pseudomelanosis occur?

A

putrefactive bacteria make H2S which then combines with iron–> iron sulfide which discolors the tissue black

53
Q

what 5 things can signal apoptosis

A 
embryogenesis
lack of growth factors
receptor-ligand interaction
granzymes (from T cells)
injurious agents
54
Q

How is the extrinsic apoptotic pathway initiated? What caspase is activated?

A

Binding of death receptor (i.e. TNF)

Caspase 8

55
Q

The intrinsic apoptotic pathway involves was organelle?

A

mitochondria

56
Q

Intrinsic apoptosis:

1) what molecules leak from the mitochondria?
2) what caspase is activated?

A

1) Cytochrome C and apoptosis inducing factor (AIF)

2) caspase 9

57
Q

How do macrophages recognize apoptotic bodies?

A

They express phosphatidylserines on their outer surface

58
Q

What are the 4 ways cells can adapt?

A

hypertrophy
hyperplasia
metaplasia
atrophy

59
Q

What kind of cells undergo hypertrophy?

A

Those that cannot divide or undergo little replication

60
Q

Two types of hypertophy

A

1) physiologic (increased workload)

2) compensatory (due to loss or obstruction)

61
Q

Cell Types:

1) labile cells
2) permanent cells
3) stable cells

A

1) commonly proliferate (i.e. epithelium)
2) little to no proliferation
3) intermediate proliferation (bone)

62
Q

When one cell type replaces another

A

metaplasia

63
Q

Two causes of metaplasia

A

chronic damage

vitamin A deficiency

64
Q

Atresia

A

congenital absence of normal orifice or closure of a hollow tubular organ

65
Q

Which organs are most commonly affected by water accumulation?

A

liver and kidney

66
Q

What protein is necessary for the formation of lipoprotein?

A

apoprotein

67
Q

What are the two mechanisms that lead to fatty liver?

A

increased delivery of FA to hepatocyte

Decreased mobilization of lipids from hepatocyte

68
Q

What two methyl donors are needed for lipoprotein synthesis?

A

Choline and methionine

69
Q

Which are antiapoptotic and which are pro-apoptotic?

1) Bcl-2, Bcl-x
2) Bak, Bax, Bim

A

1) anti

2) pro

70
Q

More severe water accumulation is called

A

hydropic degeneration

71
Q

Two causes for glycogen accumulation?

A

prolonged/severe hyperglycemia

excessive glucocorticoids

72
Q

Sphingolipidoses: 2 form and what enzyme is deficient with each?

A

GM1–Beta-galactosidase

GM2–beta-hexosaminidase A

73
Q

What cell type is usually affected by accumulation of complex carbs and lipids

A

neurons

74
Q

Glycoproteinoses: what enzyme is deficient? Causes accumulation of what residues?

A

Alpha-mannosidosis

accumulation of N-acetylglucosamine residues

75
Q

Mucopolysaccharidoses: defective catabolism of?

A

glycosaminoglycans (GAGs)

76
Q

Sphingolipidoses, Glycoproteinoses, and Mucopolysaccharidoses are examples of what?

A

inherited storage diseases

77
Q

Locoweed toxicity is an example of?

A

Induced storage disease

78
Q

What is the toxic component in locoweed plants?

A

swainsonine

79
Q

In locoweed toxicity, swainsonine is a potent inhibitor of?

A

a-mannosidase

80
Q

Caused by cellular uptake of excessive amount of protein

A

hyaline droplet degeneration

81
Q

These can be seen in a urinalysis and are indicitive of glomerular damage

A

albuminous casts

82
Q

Epithelial hyaline is an indication of what?

A

previous inflammation

83
Q

Extracellular hyaline found in the walls of damaged blood vessels

A

Fibrinoid

84
Q

Main components of fibrinoid

A

fibrin and immunoglobuin

85
Q

a proteinaceous substance deposited along basement membranes and between cells

A

amyloid

86
Q

Two types of amyloid? which is more common in vet med?

A

1) AL amyloid

2) AA amyloid (more common)

87
Q

Where is AA amyloid derived from?

A

SAA (serum amyloid-associated) protein

88
Q

Where does SAA come from? Stimulus?

A

From liver; chronic inflammation (IL-1, IL-6)

89
Q

What special stain can you use for amyloid?

A

congo red

90
Q

Describe the breakdown of purines with gout:

A

Adenine–>hypoxanthine–>xanthine–>uric acid

Guanine–>xanthine–>uric acid

91
Q

What is mucinous degeneration? where does it occur?

A

serous atrophy of fat

coronary groove of heart and mesenteric fat

92
Q

What substance can give fat a yellow appearance?

A

carotenoids

93
Q

what pigment forms from coal/carbon dust?

A

Anthracosis

94
Q

What is melanosis

A

when melanin is found in tissues that are not normally pigmented

95
Q

Special stain to see the Fe in hemosiderin?

A

Prussian blue

96
Q

Which is not a true pigment?

A

Hematin

97
Q

Wear and tear pigment/aging pigment

A

lipofuscin

98
Q

Which type of calcification is secondary to necrosis?

A

Dystrophic calcification

99
Q

What type of calcification is associated with hypercalcemia?

A

Metastatic

100
Q

Some causes of hypercalcemia?

A

primary hyperparathyroid, hypervitaminosis D, renal disease

Pathology (6 decks)

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