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CC Pathology 1 > Cell injury- reversible & irreversible > Flashcards

Cell injury- reversible & irreversible Flashcards

1
Q

Acute cell swelling

A

-hydropic degeneration; hydropic change; cytotoxic edema; ballooning degeneration

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2
Q

What is highly vulnerable to hypoxia and cell swelling?

A
  • cardiomyocytes
  • proximal renal tubule epithelium
  • hepatocytes
  • endothelium
  • CNS neurons, oligodendrocytes, astrocytes
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3
Q

Definition of acute cell swelling

A
  • early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to H2O overload
  • most common and fundamental expression of cell injury
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4
Q

Etiology of acute swelling

A
  • loss of ionic & fluid homeostasis
  • failure of cell energy production
  • cell membrane damage
  • injury to enzymes regulating ion channels of membranes
    ex. hypoxia, toxic agents
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5
Q

Gross appearance of acute cell swelling

A
  • slightly swollen organ w/ rounded edges
  • pallor when compared to normal
  • cut surface: tissue bulges & can not be easily put in correct apposition
  • slightly heavy
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6
Q

Example of ballooning degeneration resulting in formation of a

A

vesicle (bullae/blister)

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7
Q

Histologic appearance of cellular swelling

A
  • H2O uptake dilutes the cytoplasm
  • cells are enlarged w/ pale cytoplasm
  • may show increased cytoplasmic eosinophilia
  • nucleus in normal position, w/ no morphological changes
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8
Q

Ultrastructural changes of cellular swelling

A
  1. Plasma membrane alterations, such as blebbing, blunting, & loss of microvilli
  2. Mitochondrial changes, including swelling and the appearance of small amorphous densities
  3. Dilation of the ER, w/ detachment of plysomes; intracytoplasmic myelin figures may be present
  4. Nuclear alterations, w/ disaggregation of granular & fibrillar elements
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9
Q

Hydropic change, fatty change (cell swelling)

A

-due to increase uptake of H2O & then to diffuse disintegration of organelles & cytoplasmic proteins

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10
Q

Hypertrophy (cell enlargement)

A

-the cell enlargement is caused by increase of normal organelles

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11
Q

Prognosis of cellular swelling

A
  • depends on the # of cells affected & importance of cells
  • Good (if O2 is restored before the “point of no return”)
  • Poor (progression to irreversible cell injury)
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12
Q

Definition of fatty change

A
  • sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation
  • may be preceded or accompanied by cell swelling
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13
Q

All major classes of lipids can accumulate in cells:

A
  • triglycerides
  • cholesterol
  • phospholipids
  • abnormal complexes of lipids & carbs
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14
Q

Lipidosis

A
  • accumulation of triglycerides & other lipid metabolites (neutral fats & cholesterol) w/in parenchymal cells
  • heart muscle
  • skeletal muscle
  • kidney
  • liver
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15
Q

Etiology of fatty change

A
  • main causes: hypoxia, toxicity, metabolic disorders

- seen in abnormalities of synthesis, utilization &/or mobilization of fat

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16
Q

Pathogensis of fatty change

A
  • impaired metabolism of fatty acids
  • accumulation of triglycerides
  • formation of intracytoplasmic fat vacuoles
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17
Q

Gross appearance of fatty change

A
  • liver: diffuse yellow
  • enhanced reticular pattern if specific zones of hepatocytes are affected
  • edges are rounded & will bulge on section
  • tissue is soft, often friable, cuts easily and has a greasy texture
  • if condition is severe small liver sections may float in fixative or water
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18
Q

Physiologic hepatic lipidosis

A

in late pregnancy (pregnancy toxemia) & heavy early lactation (ketosis) in ruminants

19
Q

Hepatic lipidosis nutritional disorders

A
  • obesity
  • proteins-calorie malnutrition
  • starvation
20
Q

Hepatic lipidosis endocrine dz

A
  • diabetes mellitus

- feline fatty liver syndrome, fat cow syndrome

21
Q

Histologic appearance of fatty change

A
  • well delineated, lipid-filled vacuoles in the cytoplasm
  • vacuoles are single to multiple either small or large
  • vacuoles may displace the cell nucleus to the periphery
22
Q

Prognosis of fatty change

A

-initially reversible: can lead to hepatocyte death (irreversible)

23
Q

Hepatic lipidosis

A

is seen in cats, ruminants, camelids, and mini equines but is rare in dogs and uncommon in other horses

  • more often in obese cats, secondary to anorexia of any cause
  • mortality is high w/o tx
24
Q

Irreversible injury is associated morphologically with:

A
  • severe swelling of mitochondria
  • extensive damage to plasma membranes (giving rise to myelin figures)
  • swelling of lysosomes
25
Q

Cell death

A
  • mainly by necrosis

- apoptosis also contributes

26
Q

Necrosis (AKA Oncosis, Oncotis necrosis)

A

-cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury

27
Q

Necrosis morphologic aspect is due to 2 concurrent processes:

A

-denaturation of proteins
-enzymatic digestion of the cell
(-by endogenous enzymes derived from the lysosomes of the dying cells=autolysis (self digestion))
(-by release of lysosomes content from infiltrating WBCs)
OUTCOME: INFLAMMATION

28
Q

Necrosis Gross Appearance

A

-pale, soft, friable and sharply demarcated from viable tissue by a zone of inflammation

29
Q

Cause of changes of necrotic cells in cytoplasm

A
  • denatured proteins
  • loss of RNA
  • loss of glycogen particles
  • enzyme-digested cytoplasm organelles
30
Q

Appearance of changes of necrotic cells in cytoplasm

A
  • increase binding of eosin (pink)
  • loosing basophilia
  • glassy homogeneous
  • vacuolation and moth eaten appearance
  • calcification may be seen
31
Q

Pattern of tissue necrosis

A
  • may provide clues about the underlying cause

- do not reflect underlying mechanisms but are used by pathologists and clinicians

32
Q

Coagulative (coagulation) necrosis

A

-architecture of dead tissues is preserved (days)
-ultimately the necrotic cells are removed:
~phagocytosis by WBCs
~digestion by the action of lysosomal enzymes of the WBCs

33
Q

Common cause of Coagulative (coagulation) necrosis

A

Ischemia in all solid organs except the brain

34
Q

Liquefactive necrosis

A
  • necrotic architecture is liquefied = liquid

- dead cells are “digested” –> transformation of the tissue into a liquid viscous mass

35
Q

Liquefactive necrosis occurs in

A

-tissue with high neutrophil recruitment and enzymatic release w/ digestion of tissue
-tissues w/ high lipid content
-focal bacterial and occasionally, fungal infections
~microbes stimulate the accumulation of WBCs and the liberation of enzymes from these cells

36
Q

Leukoencephalomalacia

-pathogenesis

A

Ingestion of Fusarium moniliforme containing Fumonisin B1 Toxin-Producing Moldy Corn > Sphingolipid Synthesis Inhibition > Direct Cellular Toxicity > Leukoencephalomalacia

37
Q

Leukoencephalomalacia

-Species affected

A

-horse, also chicken, pig (pulmonary edema)

38
Q

Leukoencephalomalacia necrosis of

A

white matter of cerebral hemispheres, brain stem and cerebellum

39
Q

Necrotic material is frequently creamy yellow bc of the presence of dead WBCs

A

PUS

40
Q

Abscess

A

a localized collection of pus (liquefied tissue) in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue (not in CNS)
-bodies defensive rxn to foreign material

41
Q

2 types of abscesses

A

-septic: (the majority)=infection, release of enzymes from WBCs and infectious agent
-Sterile: process caused by nonliving irritants such as drugs
~likely to turn into firm, solid lumps as they scar, rather than remaining pockets of pus

42
Q

Histolgy of liquefactive necrosis

A
  • loss of cellular detail
  • cells are granular
  • eosinophilic and basophilic debris
  • neutrophil nuclei may dominate nuclear debris
  • no tissue architecture is preserved
43
Q

Gangrenous necrosis

A

not a specific pattern of celll death but begins mostly as coagulative necrosis
-likely due to ischemia

CC Pathology 1 (6 decks)

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