L3 Inflammation

Question 1

acute inflammation

Answer 1

hours to weeks
rapid onset
neutrophil driven
prominent vascular response 
innate immunity 
immediate reaction to tissue injury

Question 2

chronic inflammation

Answer 2

persistent reaction to tissue injury
slow response
less prominent vascular response 
duration weeks to years
cell-mediated immunity 
mononuclear cell predominance (lymphocytes, plasma cells, and monocytes)

Question 3

acute inflammation causes

Answer 3

microbial infection, tissue necrosis, physical agents, chemical irritants, immune mediated hypersensitivity

Question 4

chronic inflammation cuases

Answer 4

foreign body, autoimmune disorders, persistent tissue injury and acute inflammation, primary granulomatous disease, and microorganisms resistant to phagocytosis or intracellular killing (mycobacteria, viruses, fungi and some parasites)

Question 5

inflammation is usually beneficial but it can definitely cause morbidity and mortality example being

Answer 5

fatal acute pneumonia

Question 6

cardinal signs of inflammation

Answer 6

rudor - redness 
tumor - swelling 
dolor - pain 
calor - heat
functio laesa - loss of function

Question 7

vasoactive mediators of edema can be _________ and _______ derived and work to increase membrane permeability and increase vasodilation

Answer 7

cell or plasma

Question 8

cell derived vasoactice mediators

Answer 8

1. mast cells- histamine
2. platelet cells - serotonin
3. epithelium - nitric oxide, prostaglandins, platelet activating factor
4. inflammatory cells- prostaglandins, platelet activating factor, and leukotrienes

Question 9

plasma derived vasoactive mediators

Answer 9

1. hageman factor activation- 1. kallikrein kinin system (KK cells) - kinin (bradykinin) 2. clotting/fibrinolytic system- fibrin split products
2. complement system activation

Question 10

inflammatory mediators

Answer 10

vasoactive mediators (leading to edema) and chemotactic factors (leading to acute and or chronic inflammation)

Question 11

mechanisms of phagocytosis and cell killing

Answer 11

1. C3b receptor and Fc receptor attach to antigens on bacteria
2. respiratory burst

Question 12

oxidative burst- order of events

1.

Answer 12

1. molecular oxygen reduced by NADPH oxidase produces superoxide anion (o2) enzyme NADPHA oxidase

Question 13

oxidative burst- order of events

2.

Answer 13

2. generation of hydrogen peroxide enzyme superoxiide dismutase

Question 14

oxidative burst- order of events

3.

Answer 14

3. hydroxyl radical (OH) attacks DNA

Question 15

oxidative burst- order of events

4.

Answer 15

4. hypochlorous acid (HOCL) has many toxic effects

enzyme myeloperoxidase

Question 16

chronic granulomatous disease

Answer 16

inherited disorder of phagocytic cells, results from an inability of phagocytes to produce bactericidal superoxide anions because lack NADPH oxidase, cannot break down bacteria because cannot form needed h2o2 and superoxide

Question 17

aphagocytic cells are unable/able to kill catalase positive microorganisms because they can/cannot break down hydrogen peroxide

Answer 17

unable; can

Question 18

catalase negative microorganisms can/cannot be killed in people with chronic granulomatous disease

Answer 18

can because they produce H2O2

Question 19

migration out of vessels

Answer 19

macrophages send chemokines to inflame the blood vessel near the region of infection causing inflammatory cells to leave the blood vessel

Question 20

fibrinous exudate

Answer 20

full of fibrin and edema fluid

Question 21

fibrosis

Answer 21

end product of inflammation, scar tissue has not healed properly, fibroblast have laid down collagen

Question 22

granulation tissue

Answer 22

end product of inflammation where the developing wound healing and repair, rebuilding new capillaries

Question 23

granulomatous inflammation

Answer 23

specialized form of chronic inflammation where your body cannot get rid of the infection/organism/substance so forms a dense accumulation mononuclear phagocytes surrounded by a collar of lymphocytes

Question 24

What is not considered a purpose or role of inflammation? 
generate inflammatory mediators
localize/eliminate pathogenic insult
promote local tissue damage
repair injured tissue compartment
restore normal physiology

Answer 24

promote local tissue damage

Question 25

When compared to monocytes/macrophages, which is the most appropriate statement to describe neutrophils? are longer lived controls Mycobacterium tuberculosis communicates with T-cells antigen-presenting cell with MHC class II receptors first to extravascular space in response to infection

Answer 25

first to extravascular space in response to infection

Question 26

In oxygen-dependent killing of neutrophils, superoxide anion and hydrogen peroxide, respectively, are generated by which enzymes for the respiratory burst? catalase and lysozyme glutathione peroxidase and sulfhydryl oxidase lactoferrin and gelatinase myeloperoxidase and flavin reductase NADPH oxidase and superoxide dismutase

Answer 26

NADPH oxidase and superoxide dismutase

Question 27

Q1. Which of the following cytokines are most likely involved in the early stages of acute inflammation? IL-4, IL-5, IL-13 IL-1, TNF-alpha, IL-6 Interferon beta & gamma Terminal complement proteins Cytokines are only involved in chronic inflammation

Answer 27

IL-1, TNF-alpha, IL-6

Question 28

``` Q2. The physician seeing the child is concerned of a developing abscess. If an aspirate (with a needle and syringe) is obtained from the area of swelling, the inflammatory cells likely to be present in greatest numbers are: Mononuclear cells Dendritic cells B (Antibody producing) Cell Basophils Neutrophils ```

Answer 28

Neutrophils

Question 29

Q3. Signs that this process was progressing to chronic inflammation would be: Decrease in collagen (extracellular matrix) Increase in arteriolar dilation Increase in monocytes Increase in histamine This process can not progress to chronic inflammation

Answer 29

Increase in monocytes

Question 30

Q5. CJ who has Chronic Granulomatous Disease (CGD) is not at increased risk of serious infections due to Streptococcus pneumoniae (in contrast to Staphylococcus aureus, Aspergillus, and select other organisms). Why? S. pneumoniae is a catalase-negative organism which can produce hydrogen peroxide Streptococci are not affected by oxygen radicals The structure of the thin cell wall and outer membrane make it more susceptible to lysis S. pneumoniae is a catalase-positive organism which can destroy oxygen radicals Antibody produced from immunization counteract the cytochrome defect

Answer 30

S. pneumoniae is a catalase-negative organism which can produce hydrogen peroxide