Cell Injury Flashcards
(135 cards)
1
Q
Describe the gross appearance of acute cell swelling
A
Swollen organ with rounded edges
Pallor when compared to normal
When cut surface - tissue bulges
Heavy “wet” organ
2
Q
Histologic effects of Liquefactive Necrosis
A
Loss of cellular detail
Granular cells
Eosinophillic and basophillic debris
Neutrophil nuclei may dominate
No tissue architecture preserved
3
Q
Niemann Pick Disease
A
Lysosomal Storage disease
4
Q
Caseous necrosis is typically related to (acute/chronic) disease.
A
Caseous necrosis is typically related to (acute/chronic) disease.
5
Q
Cellular contents in Necrosis vs Apoptosis
A
Necrosis: Enzymatic digestion; may leak
Apoptosis: Intact; released in apoptotic bodies
6
Q
T/F: Apoptosis induces inflammation
A
False
7
Q
Which (Necrosis or Apoptosis) causes inflammation
A
Necrosis
8
Q
Liquefactive Necrosis occurs in
A
Tissues with high neutrophil recruitment and enzymatic release with digestion of tissue
Tissues with high lipid content
Focal bacterial /fungal infections
9
Q
MDx
A
Bilateral, symmetrical encephalomalacia
10
Q
MDx
A
Multifocal caseous pneumonia
11
Q
Sterile Abscess
A
Process caused by non living irritants such as drugs, likely to turn into firm, solid lumps as they scar
12
Q
Cell size in Necrosis vs Apoptosis
A
Necrosis - Enlarged
Apoptosis - Reduced
13
Q
Example of cell injury
A
Acute Cell Swelling
14
Q
Executioner caspases
A
3 and 6
15
Q
Abscess
A
Localized collection of pus in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue
16
Q
Cell death can occur by what two processes
A
Necrosis
Apoptosis
17
Q
Cytochrome C
A
Essential for life; released into cytoplasm to initiate suicide program of apoptosis
18
Q
Pyknosis
A
Nuclear shrinkage - DNA condenses into shrunken basophilic mass
19
Q
MDx
A
Hepatitis, multifocal to coalescing, subacute, severe, necrotizing
20
Q
Cellular changes due to acute cell swelling
A
Dilution of cytoplasm
Cells enlarged
Increased cytoplasmic eosinophilia
21
Q
Example of cell injury
A
Acute Cell Swelling
_________________________
Ballooning degeneration resuling in formation of a vesicle
22
Q
Apoptosis has a physiologic or pathologic role?
A
Often physiologic - may be pathologic after some forms of cell injury
23
Q
Example of cell injury
A
Liquefactive Necrosis
24
Q
Changes of necrotic cells in cytoplasm
A
Increased binding of eosin
Loosing basophillia
Glassy homogeneous
Vacuolation and moth eaten appearance
+/- Calcification
25
Possible mechanisms resulting in lipid accumulation
Excessive delivery of FFA from fat stores or diet
Decreased oxidation or use of FFAs
Impaired synthesis of apoprotein
Impaired combination of protein and triglycerides to form lipoproteins
Impaired release of lipoproteins from hepatocytes
26
Apoptotic Bodies
Fragments of apoptotic cells that contain portions of the cytoplasm and nucleus
27
Intrinisic apoptotic pathway initiated by
withdrawal of growth factors or hormones
28
Cause
Vitamin E/ Selenium Deficiency
29
Etiology
Vesicular exanthema of swine virus - Calicivirus
30
Infarct
localized area of coagulative necrosis
31
Example of cell injury
Acute Cell Swelling
32
Name of Disease
Blackhead
33
Cells that are highly vulnerable to hypoxia and cell swelling
Cardiomyocytes
Proximal Renal Tubule Epithelium
Hepatocytes
Endothelium
CNS Neurons, Oligodendrocytes, Astrocytes
34
Gangrenous Necrosis
Not a specific pattern of cell death but begins mostly as coagulative necrosis, usually applied to distal extemities and involves multiple planes of tissue
35
Dry Gangrene
No bacterial superinfection; tissue appears dry
36
Saponification
Free Fatty Acids + Ca → Ca Soaps
37
Septic Abscess
Infection, release of enzymes from WBC and infectious agent
38
Example of cell injury
Fatty Change
39
Example of cell injury
Necrosis
40
Acute cellular swelling and fatty chage are considered to be (reversible/irreversible) cell injuries.
Acute cellular swelling and fatty chage are considered to be (**reversible**/irreversible) cell injuries.
41
Disease
Caseous lymphadenitis
42
Dystocia and Recumbent Cattle can cause what type of necrosis
Fat necrosis
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Traumatic Fat Necrosis
43
Liquefactive necrosis typically occurs in the ____________ system.
Liquefactive necrosis typically occurs in the **central nervous** system.
44
\_\_\_\_\_\_\_\_\_ occurs when there is an abnormality of synthesis, utilization and/or mobilization of fat.
**Fatty Change** occurs when there is an abnormality of synthesis, utilization and/or mobilization of fat.
45
Etiology
Histomonas melegridis
46
Only form in which triglycerides can be transported out of hepatocytes
Lipoproteins
47
Extrinsic Apoptotic Pathway
Death-Receptor Initiated Pathway
48
Example of cell injury
Liquefactive Necrosis
49
Necrosis of Abdominal fat in cattle is of what cause
Unknown cause
50
Acute Cell Swelling
Early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to H2O overload
51
Etiology of Fatty Change
Hypoxia
Toxicity
Metabolic Disorder
52
Acute cell swelling is typically due to
Acute cell swelling is typically due to **loss of ionic and fluid homeostasis**
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Failure of cell energy production
Cell membrane damage
Injury to enzymes regulating ion channels of membranes
53
MDx
Multifocal hemorrhagic polyomyelitis
54
Prognosis of acute cellular swelling depends on
Prognosis of acute cellular swelling depends on **the number of cells affected and importance of cells**
55
Physiologic causes of hepatic lipidosis
Pregnancy toxemia
Ketosis
56
Etiology
Sarcocystis neurona
57
Three types of fat necrosis
Enzymatic Necrosis
Traumatic Necrosis
Necrosis of Abdominal Fat
58
Describe the morphology of apoptosis
Cell shrinkage, Increased cytoplasmic density
Chromatin condensation
Formation of cytoplasmic blebs and apoptotic bodies
Phagocytosis
59
Fatty Change
Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
May be preceded or accompanied by cell swelling
60
Example of cell injury
Wet Gangrene
61
Lipofuscin in a cell is evidence of
Lipofuscin in a cell is evidence of **previous injury**
62
Enzymatic Necrosis
Action of activated pancreatic lipases in escaped pancreatic fluid
63
Histologic appearance of fatty change
Delineated, lipid filled vacuoles in the cytoplasm
May displace nucleus to the periphery
64
Karyolysis
Nuclear fading - chromatin dissolution due to action of DNAases and RNAases
65
Plasma membrane in Necrosis vs Apoptosis
Necrosis: Disrupted
Apoptosis: Intacted, altered structure
66
Morphologic necrosis due to 2 concurrent processes
Denaturation of proteins
Enzymatic digestion of the cell
67
Pathogenesis of fatty change
Impaired metabolism of fatty acids → Accumulation of triglycerides → Formation of intracytoplasmic fat vacuoles
68
DDx
Equine Herpes Virus 1
Rabies
West Nile Virus
69
Prognosis of fatty change
Initially reversible but can lead to irreversible hepatocyte death
70
Liquefactive Necrosis
Dead cells are "digested" - transformed from tissue to liquid viscous mass
71
Ketone Bodies
Alternative fuel for cells
Produced in liver by mitochondria
72
Example of cell injury
Fatty Change
73
Possible causes of caseous necrosis
Mycobacterium
Corynebacterium
Fusobacterium
Fungal infections
74
Example of cell injury
Fatty change
75
Etiology
Corynebacterium pseudotuberculosis
76
Bcl Family Proteins
Pro and Anti- Apoptotic
Control release of cytochrome C
77
Clinical manifestations of lipidosis are most commonly detected as alterations in ________ function because it is most central to lipid metabolism.
Clinical manifestations of lipidosis are most commonly detected as alterations in **liver** function because it is most central to lipid metabolism.
78
Increase in cell size can be due to
Cell Swelling
Cell Enlargement
79
Necrosis
Cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury
80
Anti-Apoptotic Proteins
Bcl-2 Bcl-X, Mcl -1
81
Example of cell injury
Fibrinoid Necrosis
82
Disorders associated with too little apoptosis
Cells with p53 mutation
Lymphocytes that react against self-Ag
Failure to eliminate dead cells
83
Fibrinoid necrosis occurs when
Fibrinoid necrosis occurs when **Ag-Ab complexes are deposited in walls of arteries**
84
Disease
Polioencephalomalacia
85
Caseous necrosis is associated with poorly degradable _________ of bacterial origin.
Caseous necrosis is associated with poorly degradable **lipid** of bacterial origin.
86
Pro-Apoptotic Proteins
Bim, Bid, Bad
Bak, Bax
87
Initiator caspases
8 and 9
88
Example of cell injury
Dry gangrene
89
A good prognosis is possible with acute cell swelling if
A good prognosis is possible with acute cell swelling if **oxygen is restored before the "point of no return"**
90
Common cause of coagulative necrosis
Ischemia in all solid organs except brain
91
Fibrinoid Necrosis
Special form of necrosis usually seen in immune reactions involving blood vessels
92
Intrinisic Apoptotic Pathway
Mitochondrial Pathway
93
Leukoencephalomalacia causes
Necrosis of white matter of cerebral hemispheres, brain stem and cerebellum
94
Endocrine causes of hepatic lipidosis
Diabetes mellitus
Feline Fatty Liver Syndrome
Fat Cow Syndrome
95
Caseous Necrosis
Friable white area of necrosis, necrotic debris represents dead WBCs
96
Coagulative Necrosis
Architecture of dead tissues is preserved, ultimately the necrotic tissue is removed by phagocytosis or digestion by action of lysosomal enzymes of WBC
97
Apoptosis
Pathway of cell death
98
Irreversible cell injury is associated morphologically with
Severe swelling of mitochondria
Extensive damage to plasma membrane
Swelling of lysosomes
99
Hisologic effects of caseous necrosis
Eosinophilic granular cell debris
Rim of inflammatory cells
Obliterated tissue architecture
Dystrophic calcification in center of lesion
100
Leukoencephalomalacia Pathogenesis
Ingestion of Fusarium moniliforme containing Fumonisin B1 Toxin Producing Moldy Corn → Sphingolipid Synthesis Inhibition → Direct Cellular Toxicity → Leukoencephalomalacia
101
Disorders associated with too much apoptosis
Neurodegenertive disease
Ischemic injury
Death of virus infected cells
102
Example of cell injury
Fat necrosis
103
Example of cell injury
Caseous Necrosis
104
Wet Gangrene
Bacterial superinfection occured, tissue looks wet and liquefactive by actions of degradative enzymes in the bacteria and the attracted WBC
105
Example of cell injury
Coagulative Necrosis
106
The most common and fundamental expression of cell injury is \_\_\_\_\_\_\_\_\_\_\_.
The most common and fundamental expression of cell injury is **acute cell swelling**.
107
A frequent outcome of necrosis is \_\_\_\_\_\_\_\_\_\_\_.
A frequent outcome of necrosis is **inflammation**.
108
Describe the gross appearance of fatty change
Diffuse yellow
Enhanced reticular pattern if specific zones affected
Edges rounded and bulge on section
Tissue soft, friable and cuts easily with greasy texture
May float in fix/water
109
MDx
Multifocal necrohemorrhagic myelitis
110
Nutritional causes of hepatic lipidosis
Obesity
Protein - Calorie Malnutrition
Starvation
111
2 types of abscesses
Septic
Sterile
112
Karyorrhexis
Nuclear fragmentation - pyknoic nucli membrane ruptures and nucleus undergoes fragmentation
113
Disease
Equine Leukomyelitis
114
Disease
Leukoencephalomalacia
115
Disease
Tuberculosis
116
Most frequent causes of acute cell swelling
Hypoxia
Toxic agents
117
Patterns of tissue necrosis
Coagulative necrosis
Liquefactive necrosis
Gangrenous necrosis
Caseous necrosis
Fat necrosis
Fribrinoid necrosis
118
Example of cell injury
Coagulative Necrosis
119
Example of cell injury
Liquefactive necrosis
120
Polioencephalomalacia can be caused by
Thiamine deficiency diet
Increased ruminal thiaminase activity
Administration of thiamine analogs
High levels of sulfur in diet
Lead toxicity
Thiaminase containing plants
121
Lipidosis
Accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells
122
Example of cell injury
Enzymatic Fat Necrosis
123
Apoptosis can occur during what two types of processes
Physiologic
Pathologic
124
Pus
Necrotic material, frequently creamy yellow because of the presence of dead WBCs
125
Necrosis has a physiologic or pathologic role?
Invariably pathologic - culmination of irreversible cell injury
126
Abscesses result due to
Abscesses result due to **the body's defensive reaction to foreign material**
127
Nucleus in Necrosis vs Apoptosis
Necrosis: Pyknosis → Karyorrhexis → Karyolysis
Apoptosis: Fragmented
128
Describe the gross appearance of necrosis
Pale, soft, friable
Sharply demarcated by zone of inflammation
129
Example of cell injury
Necrosis
130
Conversion of acetyl coA from fatty acid oxidation causes
Lipolysis
131
Extrinisic apoptotic pathway initiated by
Receptor- ligand interactions
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Fas
TNF Receptor
132
Major classes of lipids that can accumulate in cells
Triglycerides
Cholesterol/ Cholesterol Esters
Phospholipids
Complexes of Lipids and Carbohydrates
133
Species affected by Leukoencephalomalcia
Horse
Chicken
Pig
134
Ultrastructural changes of acute cell swelling
Plasma membrane alterations
Mitochondrial changes
Dilation of the ER
Nuclear alterations
135
Disease
Nutritional Myopathy
White Muscle Disease
