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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
What type of bacteria are associated with abscess formation?
Pyogenic (staph, strep, pseudomonas)
26
What type of necrosis causes muscle tissue to be grossly pale, shiny, and swollen
Zenker's
27
Bacteria that cause: 1) blackleg 2) malignant edema
1) Clostridium chauvoei | 2) Clostridium septicum
28
What type of necrosis is grossly opaque/white, solid/firm, and somewhat granular
fat necrosis
29
Panniculitis
inflammation of fat
30
What type of necrosis is caused by saprophytic bacteria
moist gangrene
31
What type of necrosis is grossly: swollen, soft and pulpy; usually darkly colored and putrid odor
Moist gangrene
32
Which type of necrosis will present with large bacilli microscopically
moist gangrene
33
What type of necrosis is common in tissue extremities (i.e. lower fluid content and temp)
Dry gangrene
34
What type of necrosis appears grossly cool, shriveled, leather-like, and discolored
dry gangrene
35
What type of necrosis requires anaerobic conditions?
gas gangrene
36
What usually causes gas gangrene?
clostridial infections
37
What 4 factors determine the outcome of necrosis?
1) types of cells affected 2) location of cells 3) number of cells affected 4) rate at which cells are affected
38
Liquefaction and removal occurs when?
liquefaction is slow
39
Liquefaction with cyst formation occurs when
fluid accumulated faster than it can be removed
40
When do you see liquefaction with abscess formation?
when the necrosis is caused by pyogenic bacteria
41
Abscess Phlegmon Carbuncle
1) localized collection of pus from liquefaction of tissue 2) inflammation of SQ connective tissue 3) large abscess with multiple draining tracts
42
coagulative and caseation necrosis usually lead to
encapsulation without liquefaction
43
with encapsulation without liquefaction, what makes up the capsule
fibrous connective tissue
44
What is the outcome of necrosis in tissues that border free surfaces?
sloughing
45
Erosion Ulcer Slough
1) doesn't penetrate basement membrane (no scar) 2) does penetrate BM 3) large area of necrosis; scarring
46
When the necrotic area is replaced by connective tissue
replacement by scar
47
Autolysis Heterolysis Putrefaction
1) break down by lysosomal enzymes 2) breakdown by bacterial enzymes 3) invasion by saprophytic bacteria
48
List cells/tissues in order of death (first-->last)
neurons-->muscle-->organ cells-->chondrocytes
49
1) Cooling of body 2) Gravitational blood migration 3) muscle contraction
1) algor mortis 2) livor mortis 3) rigor mortis
50
T/F: The most active muscles with undergo rigor first
True
51
What are 2 reasons for rigor mortis?
1) depleted ATP prevents myosin release from actin | 2) increased cytosolic Ca causes muscle stimulation
52
How does pseudomelanosis occur?
putrefactive bacteria make H2S which then combines with iron--> iron sulfide which discolors the tissue black
53
what 5 things can signal apoptosis
``` embryogenesis lack of growth factors receptor-ligand interaction granzymes (from T cells) injurious agents ```
54
How is the extrinsic apoptotic pathway initiated? What caspase is activated?
Binding of death receptor (i.e. TNF) | Caspase 8
55
The intrinsic apoptotic pathway involves was organelle?
mitochondria
56
Intrinsic apoptosis: 1) what molecules leak from the mitochondria? 2) what caspase is activated?
1) Cytochrome C and apoptosis inducing factor (AIF) | 2) caspase 9
57
How do macrophages recognize apoptotic bodies?
They express phosphatidylserines on their outer surface
58
What are the 4 ways cells can adapt?
hypertrophy hyperplasia metaplasia atrophy
59
What kind of cells undergo hypertrophy?
Those that cannot divide or undergo little replication
60
Two types of hypertophy
1) physiologic (increased workload) | 2) compensatory (due to loss or obstruction)
61
Cell Types: 1) labile cells 2) permanent cells 3) stable cells
1) commonly proliferate (i.e. epithelium) 2) little to no proliferation 3) intermediate proliferation (bone)
62
When one cell type replaces another
metaplasia
63
Two causes of metaplasia
chronic damage | vitamin A deficiency
64
Atresia
congenital absence of normal orifice or closure of a hollow tubular organ
65
Which organs are most commonly affected by water accumulation?
liver and kidney
66
What protein is necessary for the formation of lipoprotein?
apoprotein
67
What are the two mechanisms that lead to fatty liver?
increased delivery of FA to hepatocyte | Decreased mobilization of lipids from hepatocyte
68
What two methyl donors are needed for lipoprotein synthesis?
Choline and methionine
69
Which are antiapoptotic and which are pro-apoptotic? 1) Bcl-2, Bcl-x 2) Bak, Bax, Bim
1) anti | 2) pro
70
More severe water accumulation is called
hydropic degeneration
71
Two causes for glycogen accumulation?
prolonged/severe hyperglycemia | excessive glucocorticoids
72
Sphingolipidoses: 2 form and what enzyme is deficient with each?
GM1--Beta-galactosidase GM2--beta-hexosaminidase A
73
What cell type is usually affected by accumulation of complex carbs and lipids
neurons
74
Glycoproteinoses: what enzyme is deficient? Causes accumulation of what residues?
Alpha-mannosidosis accumulation of N-acetylglucosamine residues
75
Mucopolysaccharidoses: defective catabolism of?
glycosaminoglycans (GAGs)
76
Sphingolipidoses, Glycoproteinoses, and Mucopolysaccharidoses are examples of what?
inherited storage diseases
77
Locoweed toxicity is an example of?
Induced storage disease
78
What is the toxic component in locoweed plants?
swainsonine
79
In locoweed toxicity, swainsonine is a potent inhibitor of?
a-mannosidase
80
Caused by cellular uptake of excessive amount of protein
hyaline droplet degeneration
81
These can be seen in a urinalysis and are indicitive of glomerular damage
albuminous casts
82
Epithelial hyaline is an indication of what?
previous inflammation
83
Extracellular hyaline found in the walls of damaged blood vessels
Fibrinoid
84
Main components of fibrinoid
fibrin and immunoglobuin
85
a proteinaceous substance deposited along basement membranes and between cells
amyloid
86
Two types of amyloid? which is more common in vet med?
1) AL amyloid | 2) AA amyloid (more common)
87
Where is AA amyloid derived from?
SAA (serum amyloid-associated) protein
88
Where does SAA come from? Stimulus?
From liver; chronic inflammation (IL-1, IL-6)
89
What special stain can you use for amyloid?
congo red
90
Describe the breakdown of purines with gout:
Adenine-->hypoxanthine-->xanthine-->uric acid Guanine-->xanthine-->uric acid
91
What is mucinous degeneration? where does it occur?
serous atrophy of fat coronary groove of heart and mesenteric fat
92
What substance can give fat a yellow appearance?
carotenoids
93
what pigment forms from coal/carbon dust?
Anthracosis
94
What is melanosis
when melanin is found in tissues that are not normally pigmented
95
Special stain to see the Fe in hemosiderin?
Prussian blue
96
Which is not a true pigment?
Hematin
97
Wear and tear pigment/aging pigment
lipofuscin
98
Which type of calcification is secondary to necrosis?
Dystrophic calcification
99
What type of calcification is associated with hypercalcemia?
Metastatic
100
Some causes of hypercalcemia?
primary hyperparathyroid, hypervitaminosis D, renal disease

Pathology (6 decks)

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