Fall 2011 - Gen Path - Test 1 - Cell Death

Front 1

know how ischemia leads to cell death

Back 1

Front 2

define

necrosis

ischemia

hypoxia

infarct

Back 2

Necrosis
- Death of cells prior to death of animal

Ischemia
- Lack of blood flow
- Common cause of necrosis
- Worse than hypoxia

Hypoxia
- Absence of oxygen
- Anytime you have ischemia, you have hypoxia but you can have hypoxia w/o ischemia

Infarct
- Focal area of ischemic necrosis

Front 3

what is the pathogenesis of ischemic cell injury & death

Back 3

Front 4

what is reperfusion injury and how does it cause damage

Back 4

restored blood flow to ischemic tissue increases damage

mechanisms
- reperfusion provides oxygen -> abundant free radicals
- neutrophil infiltration damages viable tissue

Front 5

what are the gross changes associated with cell death

Back 5

bad smells, ewwy-gooeyness...

softening
- must be differentiated from autolysis

color change
- lighter or darker than normal +/- peripheral rxn

ulceration
- only on epithelial or mucosal surfaces (full thickness necrosis)

Front 6

what are the microscopic changes associated with cell death

Back 6

nuclear
- pyknosis (shrunken nucleus)
- karyorrhexis (fragmented nucleus)
- karyolysis (faded or absent nucleus)

cytoplasmic
- increased eosinophilia (loss of ribosomes and alteration of proteins)
loss of internal structures

Front 7

cells do not show signs of death unless _____

Back 7

the animal continues to life for several hours

Front 8

define pyknosis, karyorrhexis, and karyolysis

Back 8

pyknosis
- shrunken, densely basophilic nucleus

karyorrhexis
- fragmented nucleus

karyolysis
- faded or absent nucleus

Front 9

what does normal tissue stain like for H&E

Back 9

hematoxylin
- stains DNA, RNA, and mineral blue

Eosin
- stains proteins pink to red

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cell death

karyolysis (faded or absent nuclei)

bright red area is dead
- loss of ribosomes/ alteration of proteins
- loss of internal structures

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Back 11

cell death

bright red area is dead
- loss of ribosomes/ alteration of proteins
- loss of internal structures

Front 12

Back 12

karyorrhexis
- fragmented nuclei

Front 13

Back 13

pyknosis
- shrunken, densely basophilic nucleus

Front 14

describe the host reaction to necrosis

Back 14

local inflammation
- stimulated by release of cell contents
=> hyperemia (red line surrounding necrotic tissue)
=> leukocyte inflitrate (white line surrounding necrotic tissue)

systemic reaction
- only happens if significant amt of cell contents enter circulation
- systemic inflammatory response syndrome

Front 15

morphologic classification of necrosis

Back 15

coagulative necrosis
- cells and tissues are dead but maintain their architecture
- commonly caused by ischemia (infarct - focal) or toxins (diffuse)


liquefactive necrosis
- complete loss of architecture
- necrotic neutrophils in fluid
- commonly caused by bact infection and/or neutrophilic infiltrate
- abscess (tissue liquefies b/c neut release juices that digest tissue)
- malacia of CNS (not due to bact or neutrophils)


caseous necrosis
- crumbly, cheesy texture
- caused by specific bacterial infections (esp Mycobacterium spp)
- loss of architecture, but tissue is solid and friable
- frequently present at center of granuloma
- ex TB/ caseous lymphadenitis


fat necrosis
- very poor prognosis
- enzymatic: pancreatitis
- firm chalky white spots in abdominal fat, normally clear adipocytes become red (dead) then blue (mineralized), +/- inflammatory rxn
- nutritional/toxic
*fish eating carnivores -> yellow orange fat due to free radical damage
- nutritional/toxic (ruminants)
* firm opaque abdominal fat that may obstruct intestines, less inflammatory than pansteatitis


fibrinoid necrosis
- only in blood vessels
- vessel wall is necrotic and hypereosinophilic (resembels fibrin)
- due to circulating infectious agents, toxins, or hypertension


gangrene (ischemic necrosis)
- dry (coagulative)
- wet (liquefactive)
- gas (necrosis with gas bubbles)

Front 16

what morphoologic classifications of necrosis can occur in any tissue?

which can only occur in fat

which can occur only in blood vessels

Back 16

any tissue
- coagulative
- liquefactive
- caseous

fat only
- fat necrosis

vessels
- fibrinoid necrosis

Front 17

coagulative necrosis

Back 17

coagulative necrosis
- cells and tissues are dead but maintain their architecture
- commonly caused by ischemia (infarct - focal) or toxins (diffuse)

Front 18

liquefactive necrosis

Back 18

complete loss of architecture
- necrotic neutrophils in fluid

commonly caused by bact infection and/or neutrophilic infiltrate

EX:
- abscess (tissue liquefies b/c neut release juices that digest tissue)
- malacia of CNS (not due to bact or neutrophils)

Front 19

caseous necrosis

Back 19

crumbly, cheesy texture

caused by specific bacterial infections (esp Mycobacterium spp)

loss of architecture, but tissue is solid and friable

frequently present at center of granuloma

ex
- TB
- caseous lymphadenitis

Front 20

fat necrosis

Back 20

very poor prognosis

enzymatic: pancreatitis
- firm chalky white spots in abdominal fat
- normally clear adipocytes become red (dead) then blue (mineralized), +/- inflammatory rxn


nutritional/toxic
- fish eating carnivores
- yellow orange fat due to free radical damage
- nutritional/toxic (ruminants)
* firm opaque abdominal fat that may obstruct intestines, less inflammatory than pansteatitis

Front 21

pathogenesis of pancreatitis related fat necrosis

Back 21

pancreatitis

=> release of enzymes (lipases)

=> digestion of abdominal fat into free fatty acids

=> FFA precipitate calcium to form soap (saponification)

see chalky white saponification in abdominal fat

Front 22

pathogenesis of fat necrosis in carnivores that eat fish

Back 22

diet high in rancid fish

=> excess oxidized fats

=> antioxidant deficiency

=> free radical injury of adipose tissue

responsive to Vit E/ Selenium

looks like pancreatitis but with yellow pigment (ceroid)

Front 23

pathogenesis of fat necrosis in ruminants

Back 23

unknown pathogenesis

predisposing factors are grazing fescue, channel island breeds, increasing age

see very firm, opaque abd fat that may obstruct intestines

looks similar to pancreatic fat necrosis but less inflammatory

Front 24

fibrinoid necrosis

Back 24

similar to Beagle-oid or Sadie-oid

only occurs in blood vessels

vessel wall is necrotic and hypereosinophilic (resembles fibrin)

caused by circulating infectious agents, toxins, or hypertension

Front 25

gangrene

Back 25

ischemic necrosis

dry gangrene
- coagulative necrosis
- typically ischemic
- ex: ergotism/ frostbite

wet gangrene
- liquefactive necrosis
- typically involves bacteria
- ex: dog bite

gas gangrene
- necrosis with gas bubbles (formed by certain bacteria)
- ex: blackleg due to Clostridium chauvoei

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Back 26

coagulative necrosis (lower left)

tissue is dead but still see tubules and glomeruli


notice line of inflammation around area of necrosis

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Back 27

coagulative necrosis

notice the line of inflammation around area of necrosis

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Back 28

necrosis

Front 29

Back 29

coagulative necrosis

live hepatocytes on either side and dead hepatocytes down the middle

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Back 30

coagulative necrosis

Front 31

Back 31

liquefactive necrosis (malasia)

In CNS, not always an abscess when see tissue liquefaction
- Call malasia
- See liquefaction with even ischemic damage in CNS
- Not always caused by bacteria

Front 32

what type of cell death is affecting my brain cells right now

Back 32

liquefactive necrosis (aka malasia)

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Back 33

liquefactive necrosis

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Back 34

liquefactive necrosis

notice loss of architecture

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Back 35

liquefactive necrosis

notice loss of architecture

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Back 36

liquefactive necrosis

notice loss of architecture

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Back 37

liquefactive necrosis

notice loss of architecture

Front 38

Back 38

caseous lymphadenitis

Corynebacterium pseudotuberculosis

Front 39

Back 39

caseous lymphadenitis

Corynebacterium pseudotuberculosis

Front 40

Back 40

caseous lymphadenitis

Corynebacterium pseudotuberculosis

Front 41

Back 41

caseous necrosis

Mycobacterium tuberculosis

Front 42

Back 42

caseous necrosis

Front 43

Back 43

caseous necrosis

Front 44

Back 44

enzymatic fat necrosis

pancreatitis => release of enzymes (lipases) => digestion of abdominal fat into FFA => FFA precipitate Ca2+ to form soap

Front 45

Back 45

enzymatic fat necrosis

pancreatitis => release of enzymes (lipases) => digestion of abdominal fat into FFA => FFA precipitate Ca2+ to form soap

Front 46

Back 46

enzymatic fat necrosis

pancreatitis => release of enzymes (lipases) => digestion of abdominal fat into FFA => FFA precipitate Ca2+ to form soap

Front 47

Back 47

nutritional fat necrosis

diet high in rancit fish => excess oxidized fats => antioxidant deficiency => free radical injury of adipose tissue (ceroid pigment in necrotic fat)

usually responsive to Vit E/ Selenium

Front 48

Back 48

nutritional fat necrosis

diet high in rancit fish => excess oxidized fats => antioxidant deficiency => free radical injury of adipose tissue (ceroid pigment in necrotic fat)

usually responsive to Vit E/ Selenium

Front 49

Back 49

nutritional fat necrosis ruminant

unknown pathogenesis but assoc with grazing fescue, genetics, increasing age

Front 50

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nutritional fat necrosis ruminant

unknown pathogenesis but assoc with grazing fescue, genetics, increasing age

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Back 51

dry gangrene - ergotism

coagulative necrosis (usually ischemic)

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Back 52

dry gangrene - ergotism

coagulative necrosis (usually ischemic)

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Back 53

dry gangrene

coagulative necrosis (usually ischemic)

Front 54

Back 54

wet gangrene - liquefactive necrosis

necrosis with inflammation

Front 55

Back 55

gas gangrene

necrosis with gas bubbles

blackleg (clostridium chauvoei)

happens so fast animal dies before cell changes

Front 56

morphologic classifications of necrosis & their causes (quick and dirty)

Back 56

Coagulative Necrosis – ischemia/ toxin

Liquefactive Necrosis - bact

Caseous Necrosis – some bact

Fat Necrosis - pancreatitis

Fibrinoid Necrosis – toxin infection

Gangrene - professor