Pathophysiology-Ch. 1

Front 1

What are the 5 main disciplines of pathology?

Back 1

Hematology, chemical pathology, immunology, histopathology/cytopathology, microbiology

Front 2

What is the 6th emerging discipline of pathology?

Back 2

Molecular pathology

Front 3

Define homeostasis.

Back 3

The state of balance between opposing pressures operating in and around a cell or tissue.

Front 4

Define steady state.

Back 4

A balance between the intercellular and extrcellular milieu. A state of homeostasis.

Front 5

CSPs

Back 5

Cell Stress Proteins (cytoprotective proteins)

Front 6

Ubiquitin

Back 6

Protein secreted by cells under stress that tags the cell for removal.

Front 7

Lipofuscin

Back 7

Residual bodies (pigment) left over from autophagy that usually build up in skin and cardiac tissues (age spots).

Front 8

Autophagy

Back 8

Cell digests its own organelles. They can utilize the metabolites from the digested parts and excrete the undigested portions through exocytosis.

Front 9

What are the 3 normal adaptive responses of a cell?

Back 9

Increased cell activity, decreased cell activity, and changes in cell morphology

Front 10

Hypertrophy

Back 10

Increased size of cells.

Front 11

Hyperplasia

Back 11

Increased number of cells.

Front 12

Atrophy

Back 12

Decreased size of cell.

Front 13

Involusion

Back 13

Decreased number of cells

Front 14

Apoptosis

Back 14

Programmed cell death.

Front 15

Define metaplasia. Is it reversible?

Back 15

An adaptive mechanism characterized by the change of one cell type into another. Metaplasia is revesible if the stress is discontinued.

Front 16

Pyknosis

Back 16

Damage to the nucleus of a cell, marked by condensation of chromatin. An ultrastructural change present in irreversible cell injury.

Front 17

Karyorrhexis

Back 17

Damage to cell nucleus characterized by fragmentation of the nucleus into smaller particles.

Front 18

Karyolysis

Back 18

Damage to cell nucleus which involves dissolution of nuclear structure and lysis of chromatin by enzymes such as DNAase or RNAase.

Front 19

What are the phases of apoptosis?

Back 19

Induction/Signaling Phase
Effector Phase
Degradation Phase
Phagocytic Phase

Front 20

Explain what happens in the Induction/Signaling Phase of apoptosis.

Back 20

Death signals reach the cell and bind to its receptors.

Front 21

Explain what happens in the Effector Phase of apoptosis.

Back 21

-Cell reaches "point of no return" (irreversible cell damage)
-Cell Executioner Pathway is triggered
-Pro-apoptotic caspases leak from mitochondria
-Executioner's Signal commits cell to die
-Executioner's Sword brings more phagocytic and morphologic changes

Front 22

Explain what happens in the Degradation Phase of apoptosis.

Back 22

-Caspases that have leaked from the mitochondria begin to dismantle cell proteins and DNA.

Front 23

Explain what happens in the Phagocytic Phase of apoptosis.

Back 23

-Clean-up phase
-Cell has undergone enough internal and external change that phagocytes recognize it and destroy it.
-This allows for clean death and the ability for other cells to utilize metabolites from destroyed cell.

Front 24

What are the 4 triggers of apoptosis?

Back 24

*Signal transduction pathway
*Cell damage pathway
*DNA damage/P-53 pathway
*Cell membrane damage

Front 25

Describe the Signal Transduction Pathway.

Back 25

Signal from outside the cell initiate the apoptotic cascade.

Front 26

Describe the Cell Damage Pathway.

Back 26

Involves mitochondrial damage which leaks Ca+ and induces high intracellular Ca+ levels. Free radicals attack mitoch. and/or DNA. Anoxia/hypoxia is induced. T-lymphocytes attack cell.

Front 27

Describe the DNA damage/P-53 pathway.

Back 27

Damaged DNA turns on p-53 gene which makes P-53 protein. P-53 protein checks DNA and can turn on apoptosis by determining if the cell is still viable or not.

Front 28

Describe the cell membrane damage pathway.

Back 28

Cell membrane is damaged and causes activation of cellular enzymes that cause cell death.

Front 29

What are the common etiologies for cell injury?

Back 29

*Hypoxia/anoxia
*Toxic Injury (mercury, chemicals, drugs--dose dependent)
*Pathogens (bacterial, viral, fungal)
*Immune-mediated (organism responds to foreign invaders, but destroys some tissue as well)
*Genetic and Metabolic (inborn enzymatic problems)

Front 30

Describe reperfusion and note why it is a cause of cell injury.

Back 30

Reperfusion is the restoration of blood flow to a tissue after ischemia. The cause for cell injury is that while the blood flow is blocked, anaerobic free radicals build up. Once blood flow is restored the free radicals are washed down stream and cause oxidative damage to other cells.

Front 31

Describe 3 differences in apoptosis and necrosis.

Back 31

*Apoptosis: clean death, programmed death, and mild to moderate ATP depletion.
*Necrosis: unclean death, not programmed death, and severe ATP depletion.

Front 32

What is cell coagulation?

Back 32

Cell coagulation is when a cell is exposed to severe heat or severe chemical exposure. The cell dies all at once, in a sense the cell frys.

Front 33

What factors determine the type of cell injury or death?

Back 33

*Duration/severity of insult
*Cell type
*Age
*Nutrition
*Genetics

Front 34

What types of insults cause necrosis?

Back 34

Severe and sudden insults cause necrosis.

Front 35

Define compesatory hyperplasia.

Back 35

When tissue is removed or damaged other tissue increases activity to compensate for lack.

Front 36

Define nodular hyperplasia.

Back 36

Nests of increased cells in tissue.