Unit 2 Necrosis (2.5-2.6) Flashcards
What are four causes of coagulative necrosis?
- local heat
- local chemicals
- ischemia
- certain bacterial toxins
List 4 outcomes of coagulative necrosis:
- removal through slow digestion
- progression to liquefactive necrosis
- mineralization
- sequestration
A type of coagulative necrosis specific to striated muscle (skeletal or cardiac):
Zenker’s necrosis
What can give necrosis a putrid odor?
exposure to bacteria producing of H2S and methyl mercaptan
Pyknosis -
condensed, solid very basophilic chromatin
Karyorrhexis -
fragmented (may resemble bacteria or other infectious agents)
Karyolysis -
extremely pale nucleus due to dissolution of chromatin
How long after the cell has died before you can see microscopic morphological alterations?
6-8 hours
Why can cytoplasm become eosinophilic (acidophilic)?
due to loss of ribosomal RNA
Why can cytoplasm become basophilic?
chromatolysis of nucleus and diffusion of nuclear DNA
What are the gross characteristics of coagulative necrosis?
characterized by a yellow to grey color (unless filled with blood), firm, friable, and may either bulge or be depressed
What are the microscopic characteristics of coagulative necrosis?
cellular outline discernible, but nuclei in various stages of decomp.; generally stains more acidophilic
What is one of the major take-home points of processes such as vacuolar degeneration, fatty change, or mucoid generation?
reversible and sublethal cell injury
death of living cells in an animal
necrosis
How does necrosis differ from degeneration?
both are the result of cell injury, but the degenerations generally are a stage of change in which there is still some possibility of recuperation
List the order of change seen in a cell following injury:
- biochemical change
- functional change
- morphologic change
What are some of the common causes of necrosis (3)?
hypoxia, ischemia, membrane injury
The heart is a vital organ. So what would you see in a lesion to determine it to be non-fatal (not the true cause of death)?
there was time for morphologic evidence of necrosis to occur (6-8 hours)
Can you see structural change in coagulative necrosis?
not much; can still recognize what tissue it is microscopically
What morphologic changes of the nucleus would you expect to see in coagulative necrosis?
karyolysis, karyorrhexis, pyknosis
Why is calcium important in the final demise of injured cells?
b/c of its role as both an intracellular messenger and enzyme activator
Irreversible cell injury has been simplified into two important features:
failure to restore mitochondrial function and cellular membrane damage
Why is it important that calcium can activate phospholipase A?
destroys cell membranes including the inner mitochondrial membrane
Activation of any other phospholipase as opposed to phospholipase A generates?
arachidonic acid
Substrate for inflammatory mediators which is inhibited by NSAIDs:
arachidonic acid
tissue damage caused when blood supply returns to the tissue after a period of ischemia or hypoxia:
reperfusion injury
includes any molecule with an unpaired electron
free radical
Focal areas of coagulative necrosis due to ischemia:
infarcts
Infarcts most commonly occur secondary to:
thrombosis or thrombeembolism
Loss of adhesion of cell to the extracellular matrix, BM, and neighboring cells by integrins is a common feature of:
necrosis (and is seen to some advantage in coagulative necrosis)
Which part of the hepatic lobule receives blood last?
centrilobular or periacinar region of the lobule
What is the number one reason for passive congestion?
cardiac dysfunction or heart failure
What is the most common pattern of acute liver toxicity?
centrilobular coagulative necrosis
What is an important structure that occurs on the anti-mesenteric surface of the ileum?
Peyer’s patches