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RUSVM Pathology I > Cell Adaptions And Injury > Flashcards

Cell Adaptions And Injury Flashcards

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
Q

What is the histological appearance of cellular swelling

A

Water dilutes the cytoplasm = enlarged and pale cytoplasm

Increase eosinophilia

Nucleus in normal position

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26
Q

What ultrastructural charges occur in cellular swelling?

A

Plasma membrane alterations (blebbing)
Mitochondrial changes
Dilation of ER and detachment of polysomes
Nuclear alterations

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27
Q

What is the difference between hydropic change and hypertrophy? And how do you differentiate the lesions

A

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 .

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28
Q

What pigment provides evidence of previous cell injury?

A

Lipofuscin “wear and tear”

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29
Q

What is sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation?

A

Fatty change (lipidosis)

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30
Q

What are the major types of lipids that can accumulate in cells?

A

Triglycerides
Cholesterol
Phospholipids
Lipid- carbohydrate

31
Q

What are the main causes of fatty change

A

Hypoxia, toxicity, metabolic disorders, and abnormal synthesis/utilization/mobilization of fat

32
Q

What type of cell changes are characterized by diffuse yellow colour, edges bulging , soft, friable, greasy texture?

A

Fatty change

33
Q

In what cases can hepatic lipidosis be a physiological response?

A

Late pregnancy- pregnancy toxemia

Heavy early lactation (ketosis)

34
Q

What nutritional disorders can lead through hepatic lipidosis

A

Obesity
Protein-calorie malnutrition (impaired apolipoprotein synthesis)
Starvation (mobilization of triglycerides)

35
Q

What endocrine diseases can cause hepatic lipidosis?

A

Diabetes mellitus (mobilization of triglycerides)
Feline fatty liver syndrome
Fat cow syndrome

36
Q

What is the histological appearance of fatty change

A

Well-delineated, lipid- filled vacuoles in cytoplasm

May displace cell nucleus to periphery

37
Q

What morphological changes are associated with irreversible cell injury

A

Severe swelling of mitochondria
Extensive damage to plasma membranes
Swelling of lysosomes

38
Q

______________ occurs after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury

A

Necrosis

39
Q

What two cellular processes lead to necrosis?

A

Denturation of proteins

Enzymatic digestion of the cell (autolysis or release of lysosome contents from WBC)

40
Q

An organ that is soft, friable, and sharply demarcated by a zone of inflammation is under going ____________

A

Necrosis

41
Q

What changes can be seen histologically in a necrotic cell?

A

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
Q

What are the 6 types of tissue necrosis?

A 
Coagulative 
Liquefactive 
Gangrenous
Caseous 
Fat 
Fibrinoid
43
Q

What is the common cause of coagulative necrosis

A

Ischemia (

Can occur in all solid organs but the brain

44
Q

How can necrosis be distinguished histologically form autolysis ?

A

Necrotic tissue has a sharp zone of inflammation. Autolysis will not have a clear line

45
Q

On what timeframe are necrotic changes seen?

A

Ultrastructurally- less than 6hours
Histologically - 6-12hrs
Grossly- 24-48hrs

46
Q

Histologically, coagulative necrosis should appear

A

Foci/ localized area of coagulative necrosis (pale nuceli and cells)- architecture of dead tissue is preserved

Rim of leukocytes (basophilic)

Congestion and hemorrhage

47
Q

_____________ necrosis is when cells are digested and transformed into a viscous mass

A

Liquefactive necrosis

48
Q

What types of cells does liquefactive necrosis occur in?

A

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
Q

What is leukoencephalomalacia

A

Necrosis of the white matter of the brain

50
Q

What is leukomelomalacia

A

Necrosis of the white matter of the spinal cord

51
Q

What is polioencephalomalacia

A

Necrosis of the grey matter of the brain

52
Q

What is poliomyelomalacia

A

Necrosis of the grey matter of the spinal cord

53
Q

What can cause leukoenephalomalacia in horses, chickens, or pigs

A

Ingestion of Fusarium verticilioides -> produce Fumosisn B1 toxin -> inhibits sphingolipid synthesis -> direct cellular toxicity

54
Q

What is a abscess? Can abscesses occur in the brain

A

Pus surrounded by a fibrous capsule

Not in CNS - no fibrous CT

55
Q

What are the two types of abscesses?

A

Septic : infection and release of enzymes from WBC and infectious agent (most common)

Sterile: nonliving irritants (eg dugs)

56
Q

What is the histology of liquefactive necrosis

A 
Loss of cellular detail 
Granular cells 
Eosinophilic and basophilic debris 
No tissue architecture preserved 
Many neutrophils
57
Q

What are the two types of generous necrosis

A

Dry - no bacterial infection
Wet-bacterial infection; tissue is wet and liquefactive

Usually begins as coagulative necrosis due to ischemia

58
Q

Friable and white area of necrosis

A

Caseous necrosis

59
Q

Casenous necrosis is usually due to ?

A

Chronic infections
Eg mycobacterium/corynebacterium/fusobacterium and fungal infections

Necrotic debris are dead WBC

60
Q

Histologically, caseous necrosis appears as??

A

Eosinophilic granular cell debris with a rim of inflammatory cells

No tissue architecture

Dystrophic calcification in center of lesion (basophilic)

61
Q

What are the three types of fat necrosis ?

A

Enzymatic
Traumatic necrosis of fat
Necrosis of abdominal fat

62
Q

Describe enzymatic fat necrosis in the pancreas

A

Action of activated pancreatic lipase in “escaped” pancreatic fluid

Free fatty acid and Ca2+ -> calcium soaps (saponificaiton)

=> white and chalky necrosis

63
Q

Form of necrosis usually seen in immune reactions involving blood vessels

A

Fibrinoid necrosis

64
Q

What occurs must occur for formation of fribinoid necrosis

A

Ag-Ab complexes are deposited in the walls of arteries

Immune complexes with fibrin are leaked out of vessels => bright eosinophilic stain

65
Q

Pathway of cell death activated by intrinsic enzymes that degrade the cellular components

A

Apoptosis

66
Q

Apoptotic bodies break into fragments called?

A

Apoptotic bonds

67
Q

How does apoptosis differ from necrosis

A

Apoptosis is programmed cell death (necrosis is not)

Inflammation seen in necrosis and not in apoptosis

68
Q

What are some physiological process where apoptosis is involved?

A

Ebryogenesis
Hormone-dependent involution of organs (thymus and uterus post parturition)
Cell deletion in proliferation
Deletion of auto reactive Tcells

69
Q

What are pathological apoptotic processes

A

TNF or FasL

DNA damage

Accumulation of misfolded proteins

Cell injury eg viral

Pathologic atrophy eg. duct obstruction

70
Q

What cell morphology is seen in apoptosis ?

A

Cell shrinkage with increased cytoplasmic density
Pyknosis - chromatin condensation
Blebbing and apoptotic bodies
Phagocytosis of apoptotic cells by adjacent healthy cells

71
Q

How are apoptotic bodies/cells removed?

A

Bodies: express phospholipids or coated with Ab or complement proteins -> phagocytosed

Cells: secreted factors to recruit phagocytes and express thrombospondidn

72
Q

What disorders can occur with too little apoptosis ?

A

Increased cell survival

P53 mutations -> neoplasia

Self-Ag relative lymphocytes
Failure to remove dead cells
=> autoimmune

73
Q

What disorders can occur with too much apoptosis?

A

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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