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RUSVM Pathology I > Cell Adaptions And Injury > Flashcards

Cell Adaptions And Injury Flashcards

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1
Q

What are the 5 types of cell adaptations?

A 
Atrophy 
Hypertrophy 
Hyperplasia 
Metaplasia 
Dysplasia
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2
Q

Decrease in size/number of cells and their metabolic activity

A

Atrophy

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3
Q

What are causes of atrophy?

A 
Decreased workload
Denervation 
Decreased blood supply/oxygen 
Inadequate nutrition 
Loss of endocrine stimulation 
Aging
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4
Q

What is the difference between atrophy and hypoplasia

A

Atrophy: decrease in size and cell number
Hypoplasia: never achieves full size (incomplete development)

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5
Q

What is aplasia

A

Lack of development of an organ/tissue

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6
Q

Increased size of cells and their functions

A

Hypertrophy

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7
Q

What types of cells are you likely to see hypertrophy as a cell adaptation?

A

Cells with little replication

Cardiomyocyte, skeletal muscle, and neurons

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8
Q

How can cardiac cell adaptations lead to cell injury if the stress is not relieved?

A

Cardiac hypertrophy -> limit beyond which enlargement is able to cope with the increased burden ->Regressive changed–> cardiac failure

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9
Q

An increase in the number of cells of an organ

A

Hyperplasia

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10
Q

Hyperplasia occurs in what types of cells

A

Cells capable of replication

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11
Q

What is most commonly caused by excessive hormonal or growth factor stimulation ?

A

Pathologic hyperplasia

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12
Q

A change in phenotype of a differrentated cell

A

Metaplasia

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13
Q

Metaplasia is an cell adaption in response to ________________ and can result in what changes?

A

Chronic irritation

Decreased function or increase propensity for malignant transformation

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14
Q

Metaplasia is most often seen in what type of cells?

A

Epithelial cells

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15
Q

Abnormal development of cells

A

Dysplasia

Usually epithelial cells

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16
Q

What are the two types of reversible cell injury?

A 
Cellular swelling 
Fatty changes (lipidosis)
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17
Q

What are the two types of irreversible cell injury/death

A

Apoptosis

Necrosis

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18
Q

What is hydro pic degeneration?

A

Acute cell swelling

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19
Q

What cells are highly vulnerable to hypoxia and cell swelling?

A 
Cardiomyocytes 
Proximal renal tubule epithelium 
Hepatocytes 
Endothelium 
CNS neurons, oligodendrocytes, astrocytes
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20
Q

Early, sub-lethal manifestation of cell damage characterized by increased cell size and volume due to H2O overload

A

Acute cell swelling

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21
Q

What is the etiology of acute cell swelling

A

Loss of ionic and fluid homeostasis

  • > failure of cell energy function
  • > cell membrane damage
  • > injury to enzymes regulating ion channels of membrane
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22
Q

What is the pathogenesis of acute cell swelling?

A

Hypoxia (injury) -> decreased ATP production -> Na into cell and K out of cell-> osmotic pressure increases -> water moves into cell -> rupture of ER to form vacuoles -> hydropic degeneration

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23
Q

A tissue that is swollen with round edges, pallor, and slightly heavy compared to normal is characteristic of what cellular change

A

Acute cell swelling

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24
Q

Acute cell swelling of the epidermis is also called?

A

Ballooning dengeneration

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25
What is the histological appearance of cellular swelling
Water dilutes the cytoplasm = enlarged and pale cytoplasm Increase eosinophilia Nucleus in normal position
26
What ultrastructural charges occur in cellular swelling?
Plasma membrane alterations (blebbing) Mitochondrial changes Dilation of ER and detachment of polysomes Nuclear alterations
27
What is the difference between hydropic change and hypertrophy? And how do you differentiate the lesions
Hydropic change- increased uptake water Hypertrophy - enlargement of cell and increased organelles Cannot differentate microscopically Microscopically - hydropic change will have pale cytoplasm and vacuolation. Hypertrophy will be enlarged but, slight disarray but still eosinophilic .
28
What pigment provides evidence of previous cell injury?
Lipofuscin "wear and tear"
29
What is sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation?
Fatty change (lipidosis)
30
What are the major types of lipids that can accumulate in cells?
Triglycerides Cholesterol Phospholipids Lipid- carbohydrate
31
What are the main causes of fatty change
Hypoxia, toxicity, metabolic disorders, and abnormal synthesis/utilization/mobilization of fat
32
What type of cell changes are characterized by diffuse yellow colour, edges bulging , soft, friable, greasy texture?
Fatty change
33
In what cases can hepatic lipidosis be a physiological response?
Late pregnancy- pregnancy toxemia | Heavy early lactation (ketosis)
34
What nutritional disorders can lead through hepatic lipidosis
Obesity Protein-calorie malnutrition (impaired apolipoprotein synthesis) Starvation (mobilization of triglycerides)
35
What endocrine diseases can cause hepatic lipidosis?
Diabetes mellitus (mobilization of triglycerides) Feline fatty liver syndrome Fat cow syndrome
36
What is the histological appearance of fatty change
Well-delineated, lipid- filled vacuoles in cytoplasm | May displace cell nucleus to periphery
37
What morphological changes are associated with irreversible cell injury
Severe swelling of mitochondria Extensive damage to plasma membranes Swelling of lysosomes
38
______________ occurs after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury
Necrosis
39
What two cellular processes lead to necrosis?
Denturation of proteins | Enzymatic digestion of the cell (autolysis or release of lysosome contents from WBC)
40
An organ that is soft, friable, and sharply demarcated by a zone of inflammation is under going ____________
Necrosis
41
What changes can be seen histologically in a necrotic cell?
Pyknosis/karyorrhexis/Karyolysis Increase eosinophilia (denatured proteins) Loosing basophilia (Loss of RNA) Glassy homogenous (loss of glycogen particles) Vacuolation and moth eaten appearance (enzyme-digested cytoplasm organelles) Calcification
42
What are the 6 types of tissue necrosis?
``` Coagulative Liquefactive Gangrenous Caseous Fat Fibrinoid ```
43
What is the common cause of coagulative necrosis
Ischemia ( | Can occur in all solid organs but the brain
44
How can necrosis be distinguished histologically form autolysis ?
Necrotic tissue has a sharp zone of inflammation. Autolysis will not have a clear line
45
On what timeframe are necrotic changes seen?
Ultrastructurally- less than 6hours Histologically - 6-12hrs Grossly- 24-48hrs
46
Histologically, coagulative necrosis should appear
Foci/ localized area of coagulative necrosis (pale nuceli and cells)- architecture of dead tissue is preserved Rim of leukocytes (basophilic) Congestion and hemorrhage
47
_____________ necrosis is when cells are digested and transformed into a viscous mass
Liquefactive necrosis
48
What types of cells does liquefactive necrosis occur in?
Tissues with high neutrophil recruitment and enzymatic release with digestion of tissue Tissue with high lipid content Focal bacteria or fungal infections *typically in CNS)
49
What is leukoencephalomalacia
Necrosis of the white matter of the brain
50
What is leukomelomalacia
Necrosis of the white matter of the spinal cord
51
What is polioencephalomalacia
Necrosis of the grey matter of the brain
52
What is poliomyelomalacia
Necrosis of the grey matter of the spinal cord
53
What can cause leukoenephalomalacia in horses, chickens, or pigs
Ingestion of Fusarium verticilioides -> produce Fumosisn B1 toxin -> inhibits sphingolipid synthesis -> direct cellular toxicity
54
What is a abscess? Can abscesses occur in the brain
Pus surrounded by a fibrous capsule Not in CNS - no fibrous CT
55
What are the two types of abscesses?
Septic : infection and release of enzymes from WBC and infectious agent (most common) Sterile: nonliving irritants (eg dugs)
56
What is the histology of liquefactive necrosis
``` Loss of cellular detail Granular cells Eosinophilic and basophilic debris No tissue architecture preserved Many neutrophils ```
57
What are the two types of generous necrosis
Dry - no bacterial infection Wet-bacterial infection; tissue is wet and liquefactive Usually begins as coagulative necrosis due to ischemia
58
Friable and white area of necrosis
Caseous necrosis
59
Casenous necrosis is usually due to ?
Chronic infections Eg mycobacterium/corynebacterium/fusobacterium and fungal infections Necrotic debris are dead WBC
60
Histologically, caseous necrosis appears as??
Eosinophilic granular cell debris with a rim of inflammatory cells No tissue architecture Dystrophic calcification in center of lesion (basophilic)
61
What are the three types of fat necrosis ?
Enzymatic Traumatic necrosis of fat Necrosis of abdominal fat
62
Describe enzymatic fat necrosis in the pancreas
Action of activated pancreatic lipase in "escaped" pancreatic fluid Free fatty acid and Ca2+ -> calcium soaps (saponificaiton) => white and chalky necrosis
63
Form of necrosis usually seen in immune reactions involving blood vessels
Fibrinoid necrosis
64
What occurs must occur for formation of fribinoid necrosis
Ag-Ab complexes are deposited in the walls of arteries | Immune complexes with fibrin are leaked out of vessels => bright eosinophilic stain
65
Pathway of cell death activated by intrinsic enzymes that degrade the cellular components
Apoptosis
66
Apoptotic bodies break into fragments called?
Apoptotic bonds
67
How does apoptosis differ from necrosis
Apoptosis is programmed cell death (necrosis is not) | Inflammation seen in necrosis and not in apoptosis
68
What are some physiological process where apoptosis is involved?
Ebryogenesis Hormone-dependent involution of organs (thymus and uterus post parturition) Cell deletion in proliferation Deletion of auto reactive Tcells
69
What are pathological apoptotic processes
TNF or FasL DNA damage Accumulation of misfolded proteins Cell injury eg viral Pathologic atrophy eg. duct obstruction
70
What cell morphology is seen in apoptosis ?
Cell shrinkage with increased cytoplasmic density Pyknosis - chromatin condensation Blebbing and apoptotic bodies Phagocytosis of apoptotic cells by adjacent healthy cells
71
How are apoptotic bodies/cells removed?
Bodies: express phospholipids or coated with Ab or complement proteins -> phagocytosed Cells: secreted factors to recruit phagocytes and express thrombospondidn
72
What disorders can occur with too little apoptosis ?
Increased cell survival P53 mutations -> neoplasia Self-Ag relative lymphocytes Failure to remove dead cells => autoimmune
73
What disorders can occur with too much apoptosis?
Excessive cell death Neurodegenerative: lose specific neurons-> mutations and misfolded proteins Ischemic injury Death of virus infected cells

RUSVM Pathology I (17 decks)

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