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Question 1

the 5 cardinal signs of inflammation?

Answer 1

pain, redness, swelling, loss of function, and heat

Question 2

3 components of acute inflammation

Answer 2

1. vascular dilation (more blood flow to area)
2. endothelial activation (edema by protein leakage)
3. neutrophil activation and migration

Question 3

transudate vs exudate, regarding leakage

Answer 3

transudate = increased hydrostatic pressure, thus fluid leaks out

exudate = protein and fluid leakage

Question 4

What mediators lead to vasodilation?

Answer 4

prostaglandins, NO and histamine

Question 5

what mediators increase permeability

Answer 5

histamine, serotonin, bradykinin, leukotrienes

Question 6

what mediators help with chemotaxis and leukocyte recruitment

Answer 6

cytokines, chemokines, leukotrienes, bacterial products

Question 7

what mediators lead to fever

Answer 7

prostaglandins and cytokines

Question 8

what mediators lead to pain

Answer 8

prostaglandins and bradykinin

Question 9

what mediators lead to tissue damage

Answer 9

NO, leukocyte enzymes, and reactive oxygen species

Question 10

pyrogenic bacteria? examples?

Answer 10

promote purulent inflammation

example: acute appendicitis, lobar pneumonia

Question 11

components of purulent exudate and fibrous exudate?

Answer 11

purulent = mainly neutrophils, with few macrophages and fibrin

fibrous = mainly fibrin with few neutrophils

Question 12

serous inflammation?

Answer 12

In this pattern of acute inflammation the main tissue response is accumulation of fluid with a low plasma protein and cell content (transudate)

can be seen in response to a burn and in serous membrane-lined cavities

Question 13

outcomes of acute inflammation?

Answer 13

1. resolution (occurs when CT framework is intact)
2. healing by fibrosis (damage to CT framework or tissues cannot regenerate)
3. abscess formation (collection of pus due to extensive tissue damage or pyrogenic bacteria)
4. progression to chronic inflammation

determined by severity of damage, the capacity of cells to duplicate, and type of tissue damage

Question 14

acute vs chronic abscess

Answer 14

acute = Expansion is limited by organization & repair at the margins of the abscess

chronic = The abscess may become encapsulated by
granulation & fibrous tissue

Question 15

what cells are seen in chronic inflammation

Answer 15

plasma cells, lymphocytes, macrophages, eosinophils, and fibroblasts

Question 16

Chronic Granulomatous Inflammation

Answer 16

A granuloma is a cellular attempt to contain a persistent agent that is difficulty to eradicate

seen to have epithelioid macrophages and giant cells

foreign body giant cells: nuclei are central

langhans giant cells: nuclei are in periphery

Question 17

Tuberculosis Granuloma

Answer 17

due to mycobacterium tuberculosis

morphology: 
central necrosis
epithelioid macrophages  
langhans giant cells 
lymphocytes

Question 18

Oxidative phase of the PPP?

Answer 18

irreversible reactions
forms NADPH and pentose phosphate
enzyme is G6PD

pathway:
1. glucose 6-phosphate is converted to 6-phosphogluconate by G6PD (regulated step)

2. 6-phosphogluconate is converted to ribulose 5-phosphate by 6-phosphogluconate dehydrogenase

Question 19

non-oxidative phase of PPP

Answer 19

reversible reactions
takes place when pentoses are not needed

pathway:
1. Xylulose 5-P is converted to glyceraldehyde 3-P by transketolase. ribose is converted to sedoheptulose 7-P by same enzyme
2. glyceraldehyde 3-P is converted to fructose 6-P by transaldolase. Sedoheptulose 7-P is converted to erythrose 4-P (same enzyme)
3. erythrose 4-P is converted to glyceraldehyde 3-P by transketolase

Question 20

how is ribulose 6-P converted to ribose 5-P

Answer 20

isomerase

Question 21

How is ribulose 5-P converted to xylulose 5-P

Answer 21

epimerase

Question 22

what does transketolase need in order to function?

Answer 22

TPP or thiamine as a coenzyme

those with beriberi have low thiamine; which can be tested by transketolase activity

Question 23

Uses of NADPH

Answer 23

1. detoxification of hydrogen peroxide and reactive oxygen species
2. phagocytosis in WBC’s

Question 24

phagocytosis in WBC’s pathway?

Answer 24

1. oxygen is converted to superoxide by NADPH oxidase (respiratory or oxidative burst)
2. superoxide is converted to hydrogen peroxide by superoxide dismutase
3. H2O2 can be converted to HOCl by myeloperoxidase

H2O2 can also go through the fenton reaction to create hydroxyl radicals

HOCl is toxic to fungi

HOCl and hydroxyl radicals are toxic to bacteria

Question 25

Chronic granulomatous disease

Answer 25

NADPH oxidase deficiency

severe persistent fungal and bacterial infections due to defective respiratory burst

Question 26

Myeloperoxidase deficiency

Answer 26

increased risk of fungal infections

normal respiratory burst, but decreased HOCl formation

Question 27

RBC detoxification of H2O2

Answer 27

H2O2 is converted to water by glutathione peroxidase
(the hydrogen is donated by reduced glutathione or GSH)
selenium containing enzyme

oxidized glutathione (GS-SG) can be converted back to the reduced form by glutathione reductase

Question 28

how does acute hemolysis occur and signs?

Answer 28

G6PD deficiency (X-linked recessive)
Heinz bodies are seen in the RBC’s
accumulation of reactive species

increased bilirubin (yellow eyes) 
less hemoglobin and brown/red urine 

sulfonamides and some antimalarial drugs lead to increased oxidative stress, thus acute hemolysis may occur.

Question 29

what does catalase do?

Answer 29

found in the peroxisome

uses hydrogen peroxide for detoxification

Question 30

ALS or amyotrophic lateral sclerosis

Answer 30

10 percent of the time this disease can be due to a deficiency in the enzyme SOD (superoxide dismutase)

Question 31

Candida albicans

Answer 31

more likely to get recurrent infections from this fungi when one has a myeloperoxidase deficiency

reduced formation of HOCl

Question 32

NO and cell defense

Answer 32

NO synthase can convert NO to peroxynitrite

can kill invading bacteria

Question 33

rate-limiting step of the PPP?

Answer 33

G6PD

lack of this enzyme leads to the impairment of NADPH formation.
RBC is not protected form oxidative damage