DD 1

Question 1

Give 3 examples of PMNs

Answer 1

Neutrophils
Basophils (related to mast cells)
Eosinophils

Question 2

3 examples of Mononuclear cells

Answer 2

Leukocytes
Monocytes
Lymphocytes

Question 3

In acute injuries, are PMNs or mononuclear cells more involved?

Answer 3

PMNs

- produce effect in seconds/minutes

Question 4

In chronic injuries, are PMNs or mononuclear cells more involved?

Answer 4

Mononuclear - (lymphocytes, macrophages, leukocytes)

- ongoing injury

Question 5

What are oxygen free radicals?

Answer 5

chemical species w/ unpaired electron

Question 6

How do oxygen free radicals arise?

Answer 6

H2O2 in the presence of superoxide anion O2- can lead to oxygen free radicals

• generated by too much O2 during O2 poor conditions via intrinsic oxidases and radiation

Question 7

How do oxygen free radicals produce cellular injury?

Answer 7

highly reactive → random oxygen atoms oxidizing (pulling e-) from a variety of things inside cell

Question 8

How does the body get rid of oxygen free radicals?

Answer 8

Via either one of 2 catalases:

1. Superoxide anion, O2- → broken down to H2O2 → broken down by glutathione peroxidase (antioxidant)
2. Oxygen free radicals can also be removed by superoxide dismutase (SOD)

or

Antioxidants (uric acid, Vit E)

Question 9

Where can intrinsic oxidases that generate oxygen radicals be found?

Answer 9

ER of all cells and in PMNs

Question 10

How does ischemia/hypoxia create setting where Oxygen free radical damage causes cell injury

Answer 10

Hypoxia → ischemic injury → Induces txn factor: hypoxia-inducible factor 1 (HIF1 α/β) → Targets genes (EPO, VEGF, glucose transporters, glycolytic enzymes)→ increases ROS

Question 11

Single most important type of injury seen in clinical medicine

Answer 11

Other than cell’s inability to make enough ATP to maintain viability, cell can also produce oxygen radicals.

Question 12

3 ways clinical medicine can produce oxygen radicals

Answer 12

1. O2 therapy
2. Acute inflammation
3. Reperfusion

Question 13

During acute inflammation, which cells have enzymes that can produce oxygen radicals?
-name that enzyme

Answer 13

PMNs
- myeloperoxidase

*hypoxic tissues are infiltrated by PMNs remember?

Question 14

What is reperfusion?

Answer 14

restoring flow of blood to organ/tissue after period of ischemia or hypoxia

Question 15

How can reperfusion (restoring flow of blood to organ/tissue) cause oxygen radicals?

Answer 15

In prolonged ischemia → hypoxanthine is formed via ATP metabolism break down → give back oxygen →Xanthine dehydrogenase is converted to xanthine oxidase → so when you do give them O2→ produces oxygen radicals

Question 16

Which cell death, Necrosis or apoptosis is usually seen in:
ischemia or w/ toxins/chemicals?

With this in mind, would it lead to large or scattered areas of cells dying?

Answer 16

Necrosis

-large area: cells die simultaneously

Question 17

Which cell death, Necrosis or apoptosis is usually seen in:
elevation in intracellular [Ca2+]?

how does death occur?

Answer 17

Necrosis

Ca2+ leaks into cell and Ca2+ storage in ER and mitochondria is released → activates Ca2+ dependent proteases and lipases → cytoplasm dead and swollen → loss in membrane integrity

Question 18

Name 3 ways that Apoptosis is regulated

Answer 18

via:
Ligands + cell surface receptors ( Fas ligand)

Mitochondria activation of caspase (Apoptosis inducing factor AIF)

Nuclear DNA endonuclease

Question 19

coagulative necrosis
What is it?
Example

Answer 19

dead cell remnant “ghost like”

-ie: heart following MI

Question 20

What are three characteristics that you see in smears regarding coagulative necrosis?

Answer 20

more eosinophilic, nucleus shrinks, clumped chromatin deeply basophilic (pyknotic),

fragmented nucleus (karyorrhexis), 
dark condense (pyknotic) clumps break down and disappear (karyolysis)

Question 21

Liquifactive necrosis
What is it?
Example

Answer 21

Dead cell dissolves - lysosomal hydrolases digest cell compartments

Common in: brain + spleen w/ acute infection

Question 22

Caseous necrosis
What is it?
Example

Answer 22

Central portion of infected lymph node is necrotic

Chalky white (like milk casein)

Only in tuberculosis

Question 23

Fat necrosis
What is it?
Example

Answer 23

Necrotic adipose tissue - fats are hydrolyzed into free fatty acids → ppt with Ca2+ →chalky gray material

Common in acute pancreatitis or trauma

Question 24

Reversible biochemical alterations during hypoxic injury

Answer 24

1) ↓ ATP
2) ↓ Na pump (cell swelling)
3) ↑ glycolysis,
4) ↓ pH
5) ↓ protein synthesis

Question 25

Irreversible biochemical alterations during hypoxic injury

Answer 25

1) activation of lysosomal enzymes
2) DNA, protein degradation
3) ↑ Ca 2+ influx

Question 26

5 cardinal signs of injury

Answer 26

1. Calor (heat)
   
   2. Rubor (redness)
   3. Tumor (swelling)
   4. Dolar (pain)
   5. Functio Laesa (loss of function)

Question 27

Which of the 5 cardinal signs of injury can be explained physiologically? how?

Answer 27

Rubor, Tumor and Calor

due to ↑ blood flow, secondary to vasodilation of capillaries and arterioles

Question 28

Exudate
what is it?
What does its presence imply?

Answer 28

Escape of fluid, proteins, and blood cells from vascular system → interstitial tissue/body cavities

Extravascular fluid w/ ↑ protein [ ] → presence implies an increase in permeability of small blood vessels due to tissue injury/inflammation

Question 29

What is another name for interstitial compartment

Answer 29

extravascular compartment or tissue space

Question 30

What type of pressure results in transudate?

Answer 30

increase in hydrostatic pressure and decrease in osmotic pressure.