(05) p196 Flashcards
(Sequence of Events in cell injury (for example when caused by hypoxia or ischemia))
(Put these in order)
(part 1)
a. increased glycoloysis, increased intracellular lactate (decreased pH), and depletion of glycogen stores
b. decrease of oxidative phosphorylation and then ATP
c. hypoxia - deficiency of O2
d. net influx of Na+, Ca2+, and H2O with loss of intracellular K+ and Mg2+
e. failure of Na+-K+ pump due to ATP defieciency
c
b
a
e
d
(Sequence of events in cell injury (for example when caused by hypoxia or ischemia)
(part 2)
(put these in order)
a. severe disruption of cell membranes, influx of Ca2+ into mitochondria and cytosol, overall cell enlargement, release of lysozomal enzymes (self digestion) and clearing of the cytosol
b. detachment of ribosomes, clumpking of nuclear chromatin, loss of microvilli, vesiculation of ER
c. irreversible cell injury, cell death (necrosis)
d. swelling of mitochondria, the cytocavitary network (RER, SER, Golgi, and outer nuclear emembrane) and nucleus
d
b
a
c
(types of cell death (necrosis))
- what is often used synonymously with necorsis (cell death due to lethal insult)?
- What is programmed/genetically controlled cell death due to suicide signal?
- consumption of own tissue
- oncosis (onco = swelling/tumor)
- apoptosis
- autophagia
(Oncosis (oncotic necrosis))
- in oncosis
give the series
1-4. starting with severley damaged membranes - what are the next three in sequence?
- what is the type of cell death that occurs after such abnormal stresses as ischemia and chemical injury? Is it always pathologic?
- severely damaged membranes
- lysozomal enzymes enter cytoplasm
- digest cell
- cellular contents leak out
- necrosis; yes
(Necrosis)
(there are distinctive morphologic patterns depending on whether enzyme catabolism or protein denaturation predominates)
1-5. What are the five types?
- caogulation necrosis
- liquefactive necrosis
- caseous necrosis
- gangrenous necrosis
- fat necrosis
(Coagulation Necrosis)
- is it most common?
- charactersitc of what?
(outline of coagulated cell persists for a few days)
- which predominats - protein denaturation or enzymatic digestion?
- injury/intracelluar acidosis denatures enzymatic proteins - causes what?
- necrotic cells are eventually removed by what?
(One form of coagulative necrosis is hyaline degeneration (Zenker’s degeneration) of skeletal/cardiac straiated muscle and smooth muscle
- yes
- hypoxic/ischemic death of cells in all tissues (except brain) - very fatty
- protein denaturation
- block proteolysis
- leukocyte proteolysis and phagocytosis
(Coagulation necrosis)
(Gross Appearance)
- architecture resemles normal tissue, but what two things are different?
- what happens to color?
- firm or soft?
- tissue may be swollen or shrunken
- may you see a local vascular/inflammatory reaction to necrotic tissue
- color and texture
- become more pale (coagulation of cytoplasmic proteins and decreased blood flow)
- firm
- yes
(Coagulation Necrosis)
(Microscopic Appearance)
- is origial cell shape preserved?
(cytoplasm)
- increased or decreased eosinophilia?
- hyalinized (glassy)
3-4. what other two things occur?
(nucleus)
- shrunked and densely bascophilic nuclei
- nuclear framentation
- dissolution of nucleus secondary to DNAases
- yes (dead cells are eosinophilc shadow of original)
- increased (pick up more Hand E)
- vaculoated
- minearlized
- pyknosis
- kayorrhexis
- karyolysis
(check out pics on 219)
(cytoplasmic changes in dead cells)
- what causes loss of differential staining characteristics of nucleus and cytoplasm?
- Massive swelling of what?
3-4. loss of what two things?
- hypereosinophilia of cytoplasm
- cell and cell organelles (with fragmentation)
3 cell to cell contact
- microvilli and cilia
(Liquefactive Necrosis)
- occurs when what predominats?
- in bacterial infections; neutrophils contatin what?
- In what kind of damage of CNS?
(Gross appearance)
- what is appearance of affected tissue?
- in acute inflammation, liquid is often mostly what?
(microscopic appearance)
- may see what?
- enzymatic digestion of necrotic cells
- potent hydrolases
- hypoxic damage
- liquefied to soft, viscous, fluid mass
- dead WBC’s (pus) - abcess
- degenerate neutrophils and/or amorphous necrotic material (or nothing if tissue has flow out)
(don’t see cell outline)
(caseous necrosis)
- typically seen with what?
(gross appearance)
- what does it look like? freqeunctly with what?
(microscopic appearance)
- dead cells persisting as what?
- do necrotic cells retain cellular outline?
- do necrotic cells undergo complete dissolution?
- frequently associated with what kind of inflammmation? plus what?
- bacterial diseases (eg tuberculosis, caseous lymphadentitis)
- grey-white, dry, friable to pasty necrotic material (cottage cheese); dystrophic calcification
- amorphus, coarsely, granular eosinophilic debris
- no
- no
- granulomatous inflammation; thick outer fibrous capsule
(gangrenous necrosis)
- ischemic necrosis of what?
- what is coagulation necrosis of an extremity called?
- what is it called when coagulatave necrosis of dry gangrene is modified by the liquefactive action of saprophytic/putrefacive (live on dead stuff) bacteria?
- what is it called when there are clostridial infections with necrosis and gas prodcution?
- extremities, (limbs, digits, ears) - eg (aspiration pneumonia and mastitis)
- dry gangrene (with subsequent mummification)
- wet gangrene
- gas (“emphysematous”) gangrene (eg. CL. chavoei (black leg))
(fat necrosis)
- distinguished by location in what?
- what is the etiology (four of them)?
(gross appearance)
- what is it?
(microscopic appearance)
- see what in fat tissue?
- often see what kinds of deposits surrounded by inflammatory cells?
- body fat stores
- inflammation (esp pancreatitis), Vit E deficiency, trauma, idiopathic
- firm, white/chalky (saponification)
- areas of necrosis
- basophilic calcium deposits
