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M4W1 > CELL INJURY 3: irreversible cell injury - necrosis > Flashcards

CELL INJURY 3: irreversible cell injury - necrosis Flashcards

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1
Q

morphological alterations in reversible cell injury

A
  • cell swelling
  • fatty change
  • plasma membrane blebbing
  • loss of microvilli
  • mitochondrial swelling
  • dilation of ER
  • eosinophilia (red color of cells and tissue)
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2
Q

morphological alterations in irreversible cell injury

A

necrosis (oncotic necrosis):
- unregulated
- energy independent
- eosinophilia (decreased RNA and protein condensation)
- nuclear shrinkage, fragmentation, dissolution

apoptosis (apoptotic necrosis):
- regulated
- energy dependent
- nuclear chromatin condensation
- formation of apoptotic bodies (result from rearrangement of nuclear and cytoplasmic fragments)

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3
Q

types of necrosis

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. gangrenous
  5. fat necrosis
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4
Q

coagulative necrosis common causes, affected tissues, and examples

A

causes:
- hypoxic cell injury (local loss of blood supply)
- ischemia
- bacterial or chemical toxins
- local action of irritating substances

affected tissues:
- liver, heart, kidney, skeletal muscle

observations:
basic tissue architecture preserved temporarily

examples:
- renal infarction
- oak posioning
- ethylene glycol toxicity

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5
Q

infarction

A

necrosis due to ischemia

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6
Q

important nephrotoxins in plants causing renal tubular degeneration and coagulative necrosis

A

cattle:
- oak, acorn (tannins)
- oxalate crystals (rhubarb, sorrel, dock)

cats:
- easter lily

pigs:
- redroot pigweed (phenolic compounds)

dogs:
- raisins/grapes (toxic agent unkown)

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7
Q

bovine oak posioning

A

acute renal tubular necrosis

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8
Q

cat easter lily poisoning

A

acute renal tubular degeneration/necrosis

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9
Q

ethylene glycol poisoning

A
  • in the liver, alcohol dehydrogenase mediates ethylene glycol activation into toxic metabolites - glycolic acid, glycoaldehyde, and glyoxylate
  • glyoxylate causes renal tubule epithelial degeneration
  • glyoxylate can also be metabolized into oxalate which enters the kidneys
  • deposition of oxalate crystals in renal tubules

results in:
- renal tubule obstruction
- mechanical damage
- degeneration and necrosis

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10
Q

important nephrotoxins in heavy metals causing renal tubular degeneration and coagulative necrosis

A
  • mercury
  • lead
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11
Q

important nephrotoxins in chemicals causing renal tubular degeneration and coagulative necrosis

A

ethylene glycol

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12
Q

important nephrotoxins in therapeutic drugs causing renal tubular degeneration and coagulative necrosis

A
  • antibiotics
  • chemotherapeutics
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13
Q

liquefactive necrosis

A

ischemia/toxin induced in CNS

examples:
- thiamine deficiency
- pyogenic bacteria forming abscesses

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14
Q

liquefactive necrosis in the CNS

A

individual neurons initially show coagulation necrosis followed by a liquefactive process affecting the neuroparenchyma

caused by:
- hypoxia or toxin induced neuronal necrosis
which leads to
- enzymatic dissolution of the neuropil (liquefaction) because there is little (or absent) fibrous connective tissue in the CNS (absent fibrous CT is preferred by liquefactive necrosis)
- there is a lack of support for the necrotic tissue
- resulting in a cavity filled with fluid and debris of neuronal membrane lipids
- debris is cleared up by macrophages (gitter cells)

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15
Q

liquefactive necrosis in other tissues

A
  • introduction of pyogenic bacteria
    leads to
  • recruitment of inflammatory cells (mainly neutrophils)
    leads to
  • release of lytic enzymes as a defense mechanisms
    leads to
  • destruction of bacteria & degeneration and necrosis of neutrophils
    results in
  • the formation of an abscess (can be considered a type of liquefactive necrosis)

further:
chronic progression with dehydration
leads to
puss insipissation
which results in
caseous necrosis

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16
Q

neuropil

A

intertwined network of axons, dendrites, and glial cells in the gray matter of the CNS

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17
Q

caseous necrosis

A

dead tissue converted into a granular, friable mass which resembles cottage cheese

chronic lesion seen in any tissue
- often associated with poorly degradable bacterial lipids and contribution of inflammatory cells that die in the process

classic examples:
- mycobacterial infections e.g. Tuberculosis
- Corynebacterium pseudotuberculosis in sheep

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18
Q

microscopic appearance of caseous necrosis

A
  • collection of fragmented/lysed cells with an amorphous granular appearance
  • tissue architecture obliterated, no cell outlines visible (distinct from coagulative necrosis)
  • dystrophic calcification often seen centrally in necrotic areas
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19
Q

Tuberculosis in cattle

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A

inhalation of Mycobacterium bovis causes bacilli within alveolar spaces in the lung which is
phagocytosed by alveolar macrophages
then can go 1 of 2 ways

  1. IDEALLY:
    - bacteria is killed by macrophages
    - infection is stopped
  2. REALITY:
    - inhibition of macrophage bactericidal activity
    - macrophages killed, bacteria spread, propagation of infection
20
Q

Mycobacterium avium intracellulare
avian TB

Study These Flashcards
A

caseating granulomas

21
Q

caseous lymphadenitis (CLA) in sheep and goats
(chronic suppurative lymphadenitis)

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A

Corynebacterium pseudotuberculosis is the causative agent

  • shearing wounds, arthropod bites, conatminated dips
  • spread by ruptured abscesses, oral and nasal secretions
  • incubation period: 3 months - chronic progressive disease
  • ill-thrift
  • carcass condemnation (economic impact)
22
Q

gangrenous necrosis - 3 types and examples

Study These Flashcards
A

3 types:
- dry
- moist
- gas

examples:
- blackleg (Clostridium chauvoei)
- ischemia
- frostbite
- bacterial or other toxins

23
Q

moist gangrene - description, clinical signs, histological findings, and examples

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A

initial lesion is coagulative necrosis, followed by invasion of saprophytic/putrefactive bacteria that produce liquefactive necrosis

clinical signs:
- tissues are red-black, soft, and wet

histological findings:
- coagulative necrosis
- proliferating bacteria
- liquefaction +/- gas bubbles

examples:
- ischemic necrosis of extremities (tight bandage)
- lung necrosis due to inhalation of digesta
- staphylococcal mastitis in cows

24
Q

dry gangrene - description, affected tissues, causes, and gross appearance

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A

coagulation necrosis secondary to infarction with mummification (dehydration)
- peripheral arteriolar vasoconstriction and capillary damage
- typically affects extremities (distal limbs, tail, ears, udder)

injury caused by:
- ingested toxins (ergot and fescue poisoning)
- cold (frostbite)

gross appearance
- shrivelled, dry, black/brown

25
gas gangrene / malignant edema - description, causative agents, and appearance, gross and microscopic
anaerobic bacteria proliferates and produces toxins in tissues - *Clostridium perfringens type A* - *Clostridium septicum* - *Clostridium chauvoei* a.k.a. blackleg - other clostridia (*Cl. sordellii, Cl. novyi type A*) gross and microscopic appearance: - tissues are dark red to black - sero-hemorrhagic exudate - gas bubble formation - coagulation necrosis of muscle
26
black-quarter (blackleg) *Clostridium chauvoei*
spores spread hematogenously from the intestine and lodge into the muscles - remain latent until local tissue trauma with hypoxia occurs - causes anaerobic conditions, spores germinate, and bacterial proliferation occurs with toxin production and release **death usually occurs within 24 hours**
27
blackleg pathogenesis
- spores form when exposed to oxygen - bacteria introduced via inhalation or by abrasions to the skin (tattooes) not a penetrating wound - spores spread hematogenously from the intestine and lodge into the muscles where they remain latent until - local tissue trauma with hypoxia occurs - this causes favorable anaerobic conditions - spores germinate causing bacterial proliferation and toxin production/release
28
fat necrosis and types
specific necrosis of fat types: - enzymatic - traumatic - nutritional - idiopathic
29
enzymatic fat necrosis
adipose tissue necrosis due to leakage of pancreatic enzymes (lipases) is the result of the release of activated pancreatic lipases which causes destruction of peripancreatic adipose tissue - typically associated with acute pancreatic necrosis/pancreatitis
30
traumatic fat necrosis
necrosis caused by crushing of fat; blood vessel compression leads to ischemia of local adipose tissue - pelvic fat in dystocia - sternal fat of recumbent animals
31
nutritional fat necrosis
steatitis/yellow fat disease - consumption of a diet high in polyunsaturated fats and low in antioxidants (vitamin E and selenium) - ROS form and cause lipid peroixdation - adipose tissue more susceptible to ROS damage
32
idiopathic fat necrosis
abdominal fat necrosis of cattle - necrotic fat found in mesentery, omentum, and retroperitoneum
33
early phase cytoplasmic changes in cell death
- cytpolasm becomes homogenous and pink in HE section **increased eosinophilia** 1. decrease/loss of RNA (responsible for cytoplasmic basophilia - blue color) 2. consolidation of cytoplasmic components upon cell collapse (loss of ribosomes from ER) - degradation of cytoplasmic proteins leads to ghost-like appearance of the cell **necrotic cells become individualized** 1. lose adherence to basement membranes and adjacent cells 2. found free in tubules, alveoli, follicles, and other lumens or mucosal surfaces
34
late phase cytoplasmic changes in cell death
cell rupture with loss if integrity and release of cell contents in the extracellular space
35
nuclear changes in cell death
- pyknosis - karyorrhexis - karyolysis - absence
36
pyknosis
- nuclear shrinkage - nuclei shrunken, dark, homogenous, round
37
karyorrhexis
- release of nuclear contents - nuclear envelope ruptured - dark nuclear remnants released into cytoplasm
38
karyolysis
- nucleus very pale - dissolution of chromatin by DNAses
39
absence
completely dissolved or lysed
40
cellular changes in necrosis
- condensation of nuclear chromatin - brightly eosinophilic homogenous cytoplasm - pale ghost-like cells - loss of adherence to neighboring cells or basement membrane
41
examples of necrosis in viral infectious disease
Infectious Bovine Rhinotracheitis (IBR): - Bovine Herpesvirus 1 (BHV-1) Canine parvoviral enteritis: - Canine Parvovirus 2 (CPV-2) Canine infectious hepatitis: - Canine Adenovirus 1 (CAV-1)
42
examples of necrosis in bacterial infectious disease
Tuberculosis (Mycobacteria): - *Mycobacterium tuberculosis* - *M. bovis* - etc. Salmonellosis: - *S. enterica* - serotypes *S. typhimurium*, *S. choleraesuis*, *S. dublin*, etc Clostridial infections: - *Cl. perfringens*, *Cl. difficile*, *Cl. chauvoei*, *Cl. septicum*, etc.
43
Infectious Bovine Rhinotracheitits (Bovine Herpesvirus 1, BHV-1) - presentation/clinical signs
presentation: - transient - acute - febrile illness - severe hyperemia and focal necrosis of nasal, pharyngeal, laryngeal, tracheal, (+/- bronchial) mucosa - diphtheritic membranes: thick plaques of fibrinonecrotic exudate - diphtheritic membranes cover the laryngeal and tracheal mucosa and contribute to secondary bacterial infection after the initial damage to the mucosa
44
canine parvovirus enteritis (Canine Parvovirus 2, CPV-2)
- segmental necrosis and hemorrhage - areas of dark red tissue - variable dilation of intestinal loops - granular texture of serosal surface - initial multiplication in lymphoid tissues - viremia (distribution of virus to crypt epithelial cells in GI tract) - villous atrophy results from inability to replace enterocytes from crypts - necrosis of crypt epithelial cells leads to crypt dilation
45
canine infectious hepatitis (Canine Adenovirus 1, CAV-1) - gross and histologic appearance
gross examination: - liver enlarged and friable - often see fibrin on capsular surface - granular appearance of serosal surfaces of the intestines - gall bladder wall thickened by edema caused by leakage from blood vessels histologic examination: - hepatocyte necrosis and loss - large basophilic intranuclear inclusions in hepatocytes - may also see in endothelial cells
46
possible reactions to necrosis
**inflammatory reaction within viable tissue** - band of inflammatory cells (WBCs) surrounding the areas of necrosis - influx of neutrophils and macrophages into the necrotic tissue - peripheral hyperemia and variable hemorrahge, especially w infarction **digestion and liquefaction of necrotic tissue** - phagocytosis by macrophages - drainage through blood/lymphatic vessels **regeneration of normal tissue or fibrous scarring** - regeneration depends on the tissue type - with fibrous scarring the tissue does not return to its normal structure or function

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