Path Ntc 1:2

Front 1

relationship among cellular function, cell death and the mophologic changes of cell injury

Back 1

pg 9 graph

Front 2

cell injury =

Back 2

disrupts the ability of cells to maintain homeostasis

Front 3

common areas susceptible to injury in the cell

Back 3

Mitochondria, plasma membrane,ER, nucleus

Front 4

Hypoxia

Back 4

inadequate sulppy of o2 to tissue and individual cells

most common cause is due to ischemia (inadequate blood flow), but it can be:
- erythrocyte impairment
-

Front 5

types of injury

Back 5

hypoxia, physical, chemical, biological (infections), immune reactions, genetic abnormalities, congential (acquired gen abnorm), inadequate nutrition

Front 6

Hypoxia injury

Back 6

-o2= -APT= Na pump impairment= +glycolysis = -Ph

this creates swelling in the cell and Ca accumulates in the cell damaging the cell membrane, inflammatory cells are recruited and there is a release of free radicals

it is reversible when it is just swelling and blood flow is restored in time
it is irreversible when holes are in the plasma membrane, rupture of lysosomes, there is alot of ca in the cell

Front 7

What does ca do in cells?

Back 7

increases permeablitiy of mitochondria, + cytosolic ca activates alot of enz = phospholipases break down plasma membrane, proteases break down the cell and endonucleases breakdown the nuclear membrane

Front 8

Free radical injury

Back 8

superoxide is the major cause in our bodies durring reperfusion of blood to hypoxic tissue

Front 9

Necrosis pg 14

Back 9

breakdown of the plasma membrane organelles and nucleus leakage of contents

Coagulation necrosis: ghost cells
Liquefactive necrosis: tissue turns to liquid and an abscess is a result
Caseous necrosis: combination of the previous 2
gangrene: coagulation necrosis superimposed on bacterial infection

Front 10

Apoptosis

Back 10

progammed cell death

internal initiation (by mitochondria)- loss of growth, dna damage, accumulation of misfolded proteins

External initiation (by death receptors)

these result in a series of caspases are activated then breakdown of different components of the cell then trigger apoptosis

Front 11

Molecular mechanisms controlling apoptosis

Back 11

Initiation: Fas ligand causes trimerization of its receptors. the receptors have death domains and activate capases. TNF same thing but binds to its own receptor. NF-kB can block the cascade and stop the apoptotic process

Control and integration: Cytochrome c is released from the mitochondria and is that major factor in triggering apoptosis

Execution: caspases disrupt both the cytoskeleton and dna of the cell

Front 12

misfolded proteins activated apoptosis

Back 12

pg 17

Front 13

intracellular accumulation

Back 13

pg 18