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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
Describe necrosis gross appearance.
-description: multiple soft, friable, slightly depressed foci w sharply demarcated from viable tissue -MDx: hepatitis, mutifocal to coalescing, subacute, severe, necrotizing
26
Describe the types of oncotic necrosis.
1. Coagulative necrosis 2. Caseous necrosis 3. Liquefactive necrosis 4. Gangrenous necrosis 5. Fat necrosis 6. Fibrinoid necrosis
27
Describe coagulative necrosis.
-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
Describe an example of coagulative necrosis.
29
Describe liquefactive necrosis.
-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
Describe liquefactive necrosis examples.
31
Describe liquefactive necrosis in sheep.
-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
Describe liquefactive necrosis in horses.
‘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
Describe gangrenous necrosis.
-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
Describe caseous necrosis.
-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
Describe caseous necrosis gross appearance.
36
Describe caseous necrosis histology.
-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
Describe fat necrosis.
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
38
Describe fibrinoid necrosis.
-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
Describe apoptosis.
-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
Describe apoptosis physiologic VS pathological process.
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
Describe apoptosis morphology.
-cell shrink w inc cytoplasmic density -chromatin condensation (pyknosis) -cytoplasmic blebs & apoptotic bodies (fragments) -phagocytosis of apoptotic cell
42
Describe apoptosis mechanisms.
-activation of capases: >initiator 9 & 8 >executioner 3 & 6 -Function: >induce, regulate, execute apoptosis to form apoptotic bodies (Intrinsic = mitochondria & extrinsic = death receptor)
43
Describe intrinsic VS extrinsic pathway.
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
Describe the removal of apoptotic cells.
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
Describe disorders associated w dysregulated apoptosis.
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
Describe necrosis VS apoptosis.
47
Describe reversible VS irreversible cell injury morphologic.
48
Describe the other types of cell death.
1. Necroptosis (programmed necrosis) -inflam reaction 2. Pyroptosis -fever inducing cytokine IL1

Pathology I (17 decks)

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