Cell Death

Question 1

3 general types of cell injury and outcomes

Answer 1

reversible injury- cell fully recovers

permanent cell injury- cell survives but is permenantly altered

lethal cell injury- dies d/t injury and causes necrosis

Question 2

steatosis

Answer 2

accumulation of fat in the liver- reversible damage d/t alcohol

effects of hepatic lipid metabolism:

mobilize fatty acids from body stores (outside liver) and brought to liver

decreased fatty acid oxidation, which decreases lipoproteins

increased TG synthesis

decreased transport, glycosylatoin and secretion of VLDL

increased recruitment of inflammatory cells to liver

Question 3

mallorys hyaline

Answer 3

permanent cell injury caused by aggregation of cytokeratin filaments (cytoskeletal abnormality)

appears as dense pink rope like body in cytoplasm of hepatocytes

can be caused by damage from excessive alcohol

can eventually result in scarring and loss of function

Question 4

hemochromatosis

Answer 4

genetic disease that results in abnormal accumulation of iron in tissues (causes secondary damage such as scarring and free radical injury)

seen as brown pigment in a liver HE stain

can be stained blue w/ prussain blue stain- identifies iron

Question 5

hemosiderosis

Answer 5

abnormal accumulation of iron in tissues due to any cause (local injury, hemorrhage, systemic etc.)

Question 6

how is hemochromatosis treated?

Answer 6

blood donation monthly

untreated hemochromatosis will result in cirrhosis and liver failure

Question 7

autophagy

Answer 7

cellular recycling process through degradation of cytoplasmic organelles, proteins, macromolecules

the products of the breakdown are then recycled

plays an important role in cell survival and maintenance- malfunction is linked to disease

Question 8

pompe disease

Answer 8

genetic disease of deficiency in a-glucosidase- needed to breakdown glycogen

results in lysosomal glycogen accumulation, and secondary damage results from excessive glycogen stored in cardiac and skeletal muscle

Question 9

apopotosis stimulants

Answer 9

1 cellular injury from toxins, radiation, free radical, etc. damage dna

2 withdrawal of critical growth factors/hormones

3 receptor initiated interactions (FAS, TNF)

4 cytotoxic t cells

Question 10

apoptotic mechanisms

Answer 10

intrinsic (cell injury, withdrawal of growth hormones) pathways involve regulation via mitochondria. when regulators like BCl2 (antiapoptotic) at the mitochondria are inhibited, capases are activated with cause endonuclease activation and cytoskeleton breakdown, and these are released as apoptotic body

extrinsic pathways skip directly to the caspases in the pathway

Question 11

burkitts lymphoma

Answer 11

starry sky pattern caused by apoptosis

Question 12

early ischemic injury mechanisms

Answer 12

causes a decrease in oxidative phosphorylation, causing a decrease in ATP

cells lose ability to regulate Na/K, and Na enters cells bringing water and Ca with it. K leaves cells

causes swelling, moss of microvilli, ER swelling, myeline figures

also increase glycolysis, which decreases glycogen and pH

damage to ER causes detachment of ribosomes, decreased protein synthesis, and lipid deposition

ALL REVERSIBLE

Question 13

late mechanisms of ischemic injury

Answer 13

influx of Ca causes decreased phospholipid synthesis and increased degradation, which will eventually damage the membrane

the damage to the membrane and decreased pH will activate lysosomes, which will help to break down the nucleus

the accumulation of phospholipid damage, cytoskeletal alterations, and free radicals increase the mitochondrial permiability to Ca, which triggers damage and breakdown of mitochondria

Question 14

role of Ca in cell death

Answer 14

increased cytosolic Ca increase ATPases, phospholipases, proteases, and endonucleases that breakdown ATP, membranes, proteins, and the nucleus

Question 15

mitochondrial changes

Answer 15

mitochondrial change is one of the earliest morphologic changes in cell death

they become porous to water and Ca, appearing w/ swollen and w/ Ca precipitates

ultimately they lose enzymatic systems and cannot recover normal function.

Question 16

cytochrome c

Answer 16

loss of cytochrome c out of the mitochondria is a signal for apoptosis initiation

Question 17

visible cell death timeline

Answer 17

cells die much faster than there are visible markers for its death. may take up to 24-36 hours. affects testing you can do

Question 18

necrosis

Answer 18

cell death at the level of tissues- represents morphologic changes from cell death

cumulative effect of enzymatic degradation of dead cells, lysosomal enzymes, and denatration of proteins

appearance determined by cause of injury, type of tissue, and inflammatory response

Question 19

coagulative necrosis

Answer 19

most common form, in which denatureaiton of cell proteins dominates

ex- infactions (ischemic death)

Question 20

liquefactive necrosis

Answer 20

usually necrosis with extensive inflammation resulting in fairly complete digestion of tissue (liquefication)

ex- abcess, cerebral infarctions

Question 21

wedge shaped infaction

Answer 21

kidneys have end arterial circulation, so they form wedge shaped necrosis b/c cell death increases towards cortex

coagulative necrosis

Question 22

hemorrhagic pulmonary infacrt

Answer 22

occurs b/c there are 2 blood supplies to lung tissue

pulmonary artery becomes blocked by an embolus and long dies, but the broncial artery still passes blood through the tissue, causing it to hemorrhage

coagulative necrosis

Question 23

cerebral infarction

Answer 23

caused by blockage in bran cand causes liquefactive necrosis. causes hemorrhage

Question 24

necrotizing funcal pneumonia w/ abcess formation

Answer 24

abcess is a localized area of liquefactive necrosis (usually d/t infectious organism

in this example, acute inflammation causes liquefactive necrosis in the lung

an occlusion need not occur for an abcess to form

Question 25

caseous necrosis

Answer 25

“cheese-like” appearance of soft, white dead tissue mass

can cause cavitation- whole caused by the liquefication of tissue

found in tuberculosis

Question 26

gangrenous necrosis

Answer 26

result of bacterial colonization of tissue which has already undergone necrosis (ususallty ischmic)

results on liquefactive necrosis superimposed on pre-existing coagulative necrosis

Question 27

fat necrosis

Answer 27

digestive enzymes act on fat, releasing fatty acids, which combine w/ Ca to form soap

associated w/ trauma to pancreas or pancreatitis