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Pathology I > Reversible VS Irreversible Injury Necrosis & Apoptosis > Flashcards

Reversible VS Irreversible Injury Necrosis & Apoptosis Flashcards

1
Q
Ultra structural = electron microscopy (detecting cell injury)
A
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2
Q

Describe the cell responses to injury depending on the cell type & injury.

A
  1. Adaptation (inc efficiency or productivity)
  2. Degen (diminished functional capacity)
  3. Death
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3
Q

Describe acute cell swelling.

A

-reversible
-early, sublethal manifestation of cell damage
-inc cell size & vol bc H2O overload
-most common expression of cell injury
FIRST Na/K ATPase THEN cell membrane damage

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4
Q

Describe the cells highly vulnerable to hypoxia & cell swelling.

A

-cardiomyocytes
-prox renal tubule epi
-hepatocytes
-endothelium
-CNS neurons

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5
Q

Describe the etiology of acute cell swelling.

A

-loss of ionic & fluid homeostasis
>failure of cell energy prod
>cell membrane damage
>injury to enzymes regulating ion channel of membrane (Na/K ATPase)
-EX: physical/mechanical injury, hypoxia, toxic agents, free radicals, viral organisms, bacterial organisms, immune mediated injury

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6
Q

Describe the pathogenesis of acute cell swelling.

A
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7
Q

Describe the gross appearance of acute cell swelling.

A

-swollen organ w rounded edges
-pallor (pale areas)
-cut surface: tissue bulge & cant be easily put in correct apposition
-heavy ‘wet’ organ

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8
Q

Describe the histologic appearance of cell swelling.

A

-H2O uptake dilute cytoplasm (pale)
-cell enlarged
-inc cytoplasmic eosinophilia
-nucleus in norm position w no morphological changes

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9
Q

Describe epidermis cell swelling.

A

‘Ballooning degen’
-hydropic degen variation
-ex: swine pox virus

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10
Q

Describe the morphological changes of cell swelling.

A
  1. PM alterations
    -blebbing, blunting, loss of microvilli
  2. Mitochondrial changes
    -swelling
    -sm amorphous densities
  3. Dilation of ER
    -detachment of polysomes
    -intracytoplasmic myelin
  4. Nuclear alterations
    -disaggregation of granular & fibrillar elements
    -change in chromatin
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11
Q

Describe what the increase in a size of a cell is due to.

A
  1. Hydropic change, fatty change = cell swelling
    -bc high uptake of H2O & then diffuse disintegration of organelles & cytoplasmic proteins
    -stressed & abnormal
  2. Hypertrophy = cell enlargement
    -bc inc of normal organelles
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12
Q

Describe the prognosis of cell swelling.

A

*depends # of cells affected & imp of cells:
1. Good = if O2 restored before point of no return
2. Poor = progression to irreversible cell injury

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13
Q

Describe fatty changes.

A

-reversible
-sublethal cell damage
-accumulation of lipids in cytoplasm
>TAG, cholesterol/esters, phospholipids, lipids & carbohydrates (lysosomal storage disease)
-may be preceded or accompanied by cell swelling

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14
Q

Describe lipidosis.

A

-accumulation of TAG & other lipid metabolites (neutral fats & chol) in parenchymal cells
>heart, skeletal, muscle, kidney, liver (most common)
-liver (hepatic lipidosis) = alter function bc most central organ to lipid metabolism

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15
Q

Describe the etiology of fatty change.

A

-hypoxia, toxicity, metabolic disorders
-seen in abnormalities of synthesis, utilization or mobilization of fat

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16
Q

Describe the pathogenesis of fatty change.

A

Impaired metabolism of FA -> accumulation of TAG -> formation of intracytoplasmic fat vacuoles

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17
Q

Describe the pathogenesis of fatty liver.

A

Hepatic lipid metabolism results in lipid accumulation if:
1. Excessive delivery of FFA from fat stores/diet
2. Dec oxidation or use of FFA
3. Impaired syn of apoprotein
4. Impaired combination of protein & TAG to make lipoprotein
5. Impaired release of lipoproteins from hepatocytes

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18
Q

Describe the gross appearance of fatty changes.

A

(Fatty liver, hepatic lipidosis/steatosis)
-diffuse yellow if all cells affected
-enhanced reticular pattern if specific zones of hepatocytes affected
-rounded edges & bulge
-soft tissue, friable, cuts easy, greasy
-severe condition = sm liver sections float in fixative/water

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19
Q

Describe the causes of hepatic lipidosis.

A

[reminder: ketones used as alt fuel, made in liver by mitochondria, conversion of acetylCoA from FFA = lipolysis]
1. Physiologic = esp ruminants
-late preg = preg toxemia
-heavy early lactation = ketosis
2. Nutritional disorders
-obesity (inc fat stores)
-protein cal malnutrition (impaired apolipoprotein syn)
-starvation (inc mobilization of TAG)
3. Endocrine disease
-diabetes mellitus (inc mobilization of TAG)
4. Genetic disorders
-niemann pick disease = lysosomal storage disease

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20
Q

Describe the histologic appearance of fatty change.

A

-well delineated, lipid filled vacuoles in cytoplasm
-vacuoles single to multiple, sm or lg, & displace cell nucleus to periphery

21
Q

Describe prognosis of fatty change.

A
  1. Initially reversible
    -can lead to hepatocyte death (irreversible)
  2. Hepatic lipidosis
    -rare in dogs but seen in cats, ruminants, donkeys
    -ID & treat predisposing diseases
    -nutritional support
    -seen in obese cats or secondary to anorexia
    -mortality high w/o treatment
    -oral appetite stim
    -(-) energy balance = take from energy reserves
22
Q

Describe irreversible injury.

A

-swelling of mitochondria & lysosomes
-damage to PM = myelin figures
-myocardium infarcts - 30 to 40 min after ischemia
-cell death: necrosis or apoptosis
-necrotic change seen:
>ultrastructurally <6h
>histo 6-12h
>grossly 1-2d

23
Q

Describe necrosis.

A

-cell death after irreversible cell injury by:
>hypoxia
>ischemia
>direct cell membrane injury
-morphologic due to:
>denature of protein
>enzymatic digestion of cell
—endogenous enzymes from lysosomes of dying cells (autolysis = self digestion)
—release of lysosome content from WBCs (commonly seen w inflammation!)

24
Q

Describe necrosis light microscopy changes.

A
  1. Nucleus
  2. Cytoplasm
    A) cause
    -denature protein
    -loss of RNA & glycogen
    -enzyme digested cytoplasm organelles
    B) appearance
    -inc binding of eosin pink
    -lose basophilia
    -glassy
    -vacuolation/moth eaten
    -calcification
25
Q

Describe necrosis gross appearance.

A

-description: multiple soft, friable, slightly depressed foci w sharply demarcated from viable tissue
-MDx: hepatitis, mutifocal to coalescing, subacute, severe, necrotizing

26
Q

Describe the types of oncotic necrosis.

A
  1. Coagulative necrosis
  2. Caseous necrosis
  3. Liquefactive necrosis
  4. Gangrenous necrosis
  5. Fat necrosis
  6. Fibrinoid necrosis
27
Q

Describe coagulative necrosis.

A

-early response to hypoxia, ischaemia, toxic injury
-denaturation of cell proteins
>structural proteins (maintain cell shape)
>lysosomal protein enzyme (auto digestion delay)
-nucleus show features of necrosis still (pyknosis, karyorrexhis, karyolysis)
>cell outline visible & tissue architecture
-commonly seen in liver, kidney, heart, skeletal muscle
*necrotic cells removed by phagocytes by WBCs & digestion via lysosomal enzymes of WBC

28
Q

Describe an example of coagulative necrosis.

A
29
Q

Describe liquefactive necrosis.

A

-dead cells digested -> transform tissue into liquid
-occurs in:
>tissue w high lipid content (CNS)
>tissue w high neutrophil & enzymatic release w digestion of tissue (abscess)
>focal bacteria & fungal infections
—microbes stim WBC & enzymes

30
Q

Describe liquefactive necrosis examples.

A
31
Q

Describe liquefactive necrosis in sheep.

A

-MDx = bilateral symmetrical encephalomalacia
-Aetiology = toxin from cl. Perfringens (same bacteria from pulpy kidney disease)
-Pathogenesis = overgrowth of intestinal cl perfringens bacteria type D -> release & absorption of epsilon toxin that target endothelial cell in brain & lung -> endothelial necrosis & anoxia/edema of neural parenchyma -> liquefactive necrosis (enterotoxaemia)

32
Q

Describe liquefactive necrosis in horses.

A

‘Leukoencephalomalacia’
-pathogenesis: eat moldy corn containing toxin producing fumonisin B1 (fusarium verticilioides) -> inhibit sphingolipid syn -> accumulation of toxic sphingosine -> direct cell toxicity
-necrosis of white matter of cerebral hemispheres, brain stem, cerebellum

33
Q

Describe gangrenous necrosis.

A

-begins as coagulative necrosis due to ischemia (ex. Frost bite)
-distal extremities (toes, ear, udder, pinna)
-multiple planes of tissue
-dry gangrene = no bacterial superinfection
-wet gangrene = bacterial superinfection, looks liquefactive bc degradative enzymes in bacteria & WBCs

34
Q

Describe caseous necrosis.

A

-cheese like, friable (crumble) white area of necrosis (dead WBCs)
-cause: bacterial infections where bacteria replicate in phagosome
>mycobacterium
>corynebacterium
>fusobacterium
>fungal infections
-compared w coagulation (early stage), caseous is chronic (lytic)
-poorly degradable lipids

35
Q

Describe caseous necrosis gross appearance.

A
36
Q

Describe caseous necrosis histology.

A

-eosinophilic granular cell debris w rim of inflam cells like macrophages
-karyorrhectic basophilic debris & cytoplasmic eosinophilic debris (lytic necrosis)
-dystrophic calcification in center of lesion

37
Q

Describe fat necrosis.

Enzymatic necrosis
A
  1. Enzymatic necrosis
    -activated pancreatic lipases
    -neutral fat (lipase -> TAG)
    -FFA + Ca = saponification (chalky, gritty, white)
    -inflammation
  2. Traumatic necrosis (compression)
    -dystocia
    -SQ in inter muscular fat @ sternum - recumbent cattle
  3. Necrosis of abdominal fat
    -unknown cause
    -mesentery, omentum, retroperitoneum
    -intestinal stenosis
Necrosis of abdominal fat
38
Q

Describe fibrinoid necrosis.

A

-immune reactions w blood vessels
-Ag-Ab complex (type III hypersensitivity) deposited in walls of arteries
-deposit of immune complex + fibrin = fibrinoid (bright pink)

39
Q

Describe apoptosis.

A

-programmed cell death (suicide)
-activate intrinsic enzymes that degrade cell DNA & nuclear & cytoplasmic proteins
-fragments = apoptotic bodies (portion of cytoplasm & nucleus)
-PM & receptors remain intact -> targets for phagocytes

40
Q

Describe apoptosis physiologic VS pathological process.

A
  1. Physiologic (most common)
    -during embryogenesis
    -hormone dependent involution of organs in adult
    -cell deletion in proliferating cell pop
    -delete auto reactive T cell in thymus
    -death of cells after served useful function
  2. Pathologic
    -elim cell injured beyond repair
    -DNA damage
    -misfolded proteins
    -cell death in infections (viral) & neoplastic
    -pathologic atrophy in parenchymal organs after duct obstruction
41
Q

Describe apoptosis morphology.

Arrows point to shrink & condense
A

-cell shrink w inc cytoplasmic density
-chromatin condensation (pyknosis)
-cytoplasmic blebs & apoptotic bodies (fragments)
-phagocytosis of apoptotic cell

Cell not broken, just shrunk
42
Q

Describe apoptosis mechanisms.

A

-activation of capases:
>initiator 9 & 8
>executioner 3 & 6
-Function:
>induce, regulate, execute apoptosis to form apoptotic bodies
(Intrinsic = mitochondria & extrinsic = death receptor)

43
Q

Describe intrinsic VS extrinsic pathway.

A

INTRINSIC
-major mech in mammalian cell
-inc mitochondria permeability & release of pro apoptotic mol into cytoplasm
-cytochrome C = released into cytoplasm & initiate apoptosis
-controlled release by pro & anti apoptotic proteins
>pro: Bak, Bax
>anti: BCL
*BH3 proteins = sense damage/stress
EXTRINSIC
-initiated by death receptors: FasL expressed on self Ag T cells & CD8 cytotoxic T cell
-form binding site w death domain
-FAD -> binds inactive caspase 8 -> active -> apoptosis

44
Q

Describe the removal of apoptotic cells.

A
  1. Apoptotic bodies
    -edible for phagocytes
    -expressed phospholipid in outer membrane to be ID by macrophage receptors
    -coated w Ab & protein of complement (C1q)
  2. Apoptotic cells
    -secrete soluble factors that recruit phagocytes
    -express thrombospondin (adhesive glycoprotein ID by phagocytes)
    -macrophage make protein that bind to apoptotic cell for engulf
45
Q

Describe disorders associated w dysregulated apoptosis.

A
  1. Defective apoptosis & inc cell survival
    -abnormal cell survive
    -cells w mutation in p53 (tumor suppressive gene) subjected to DNA damage & fail to die = mutations -> neoplasia defective DNA repair
    -lymphocytes react against self ag = autoimmune
    -fail to elim dead cells
  2. Inc apoptosis & excessive cell death
    -neurodegenerative = loss of neurons
    -ischemic injury = stroke
    -death of virus infected cell
46
Q

Describe necrosis VS apoptosis.

A
47
Q

Describe reversible VS irreversible cell injury morphologic.

A
48
Q

Describe the other types of cell death.

A
  1. Necroptosis (programmed necrosis)
    -inflam reaction
  2. Pyroptosis
    -fever inducing cytokine IL1

Pathology I (17 decks)

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