Inflammation and Repair

Question 1

What causes inflammation?

Answer 1

Infections, necrosis, foreign bodies (rate crystals from GOUT, cholesterol crystals, and lipids) and immune reactions.

When rate crystals are consumed they cause damage to the membrane of the phagolysosome leading to release of lysosomal enzymes.

Question 2

Recognition of microbes is done by…

Answer 2

TLR (toll like receptors)

Question 3

What are some molecules that indicate cell damage.

Answer 3

Uric acid; DNA break down
Increased ATP; mitochondria break down
Reduced K concentration; plasma membrane damage
DNA in the cytoplasm.

These molecules cause activation of the inflammasome, which causes production of IL-1

Question 4

IL-1: functions

Answer 4

Stimulate histamine
TNF
cause fever indirectly

Question 5

A gain of function of the inflammasome will cause…

Answer 5

auto inflammatory syndromes

Question 6

Acute inflammation major components

Answer 6

Dilation of small vessels, which increases blood flow
Increased permeability, which allows for proteins and leukocytes to leave vessel.
Emigration of leukocytes to activation and elimination of microbes.

Key sign of acute inflammation is the presence of neutrophils

Question 7

Effects of histamine and serotonin

Answer 7

Main regulator of blood dilation in brain is via serotonin, while histamine effects the whole body.
Histamine cause stasis to develop, which allow for transmigration of leukocytes out of BV.

Question 8

Release of histamine is regulated by

Answer 8

physical damage, binding of ab to mast cells, hypersensitivity, and anaphylatoxins.

Question 9

What is exudation? vs ultra filtrate

Answer 9

It is the escape of fluid proteins and leukocytes from vascular tissue into tissue.
Ultra filtrate is considered transudate, which is low protein content with little or no cellular material.

Question 10

Purulent exudate

Answer 10

Pus, which is an exudate rich in leukocytes (neutrophils mainly), debris, and microbes.

Question 11

What are the binding factors/factors for transmigration of leukocytes

Answer 11

Sialyl-lewis X (rolling), CD18/31 (stoping), secretion of collegenase (extravasation).

Question 12

What are the binding factors of endothelium cells for transmigration of leukocytes

Answer 12

P and E selectins (rolling), ICAM-1 and VCAM-1, used for stoping

Question 13

Leukocyte adhesion deficiency

Answer 13

The patient will have recurrent bacterial infections, due to defective inflammation process.

Question 14

Chemotactic molecules

Answer 14

IL-8, C5a, C3a, C4a, and leukotriene B4 (LTB4)

They work by activating GPCR and causing polymerization of actin filaments in direction of concentration.

Question 15

What do corticosteroids do to the inflammation process?

Answer 15

They inhibit the formation of AA by preventing the activation of PLA-2. This prevents the formation of COX products such as PGE-2 (fever), indirectly decreasing IL-1 and TNF formation, also decreasing iNOS formation.

Question 16

PGE-2

Answer 16

Causes vasodilation and increase permeability of capillary, edema formation, chemo attractant for neutrophils, and causes fever

Question 17

PGD-2

Answer 17

Causes vasodilation and increases the permeability of capillary, causes edema formation in neutrophils.

Question 18

PGF-2

Answer 18

contraction of uterine, bronchial smooth muscles, and small arterioles.

Question 19

PGI-2

Answer 19

Potent inhibitor of platelet aggregation and vasodilator

Question 20

TxA-2

Answer 20

Potent platelet aggregator and vasoconstrictor.

Question 21

PGE-1

Answer 21

Used for protection of gastric mucosa

Question 22

LT-B4

Answer 22

potent chemotactic agent for neutrophils and causes generation of ROS and release of lysosomal granules.

Question 23

LT C4, D4, and E4

Answer 23

cause vasoconstriction, bronchospasm, and increased permeability of venues and causing bronchospasm.

Question 24

Lipoxins

Answer 24

Used to suppress inflammation by inhibiting the recruitment of leukocytes by inhibiting chemotaxis and adhesion to endothelium.

Question 25

ROS formed for break down of microbes

Answer 25

Respiratory burst causes the formation of supra-oxide via NADPH oxidase
Dismutase then converts supra-oxide into H2O2
Myeloperoxidase (MPO) then converts hydrogen peroxide into bleach.

Question 26

Secondary Granule content

Answer 26

Lysozymes, collagenase, gelatinase, lactoferrin, plasminogen activator, hisaminase, and alkaline phosphate.

Question 27

Primary granule content

Answer 27

Myeloperoxidase, bacterial factors (lysozymes and defensins), acid hydrolase, and a variety of neutral proteases (cleaves extracellular components and C3 and C5 proteins).

Question 28

NETs (neutrophils extracellular traps)

Answer 28

Extracellular fibrillar network that provides antimicrobial substances, which prevents the spread of microbes by trapping them in fibrils.

Question 29

Tuberculosis

Answer 29

Caseating granuoma and shows signs of giant cells.

Question 30

Leprosy

Answer 30

Acid-fast bacilli in macrophages; non-caseating granulomas.

Question 31

Syphilis

Answer 31

Gumma: plasma cell infiltrate, central cells are are necrotic.

Question 32

Cat-Scratch disease

Answer 32

Rounded stellate granuloma containing central granular debris and recognizable neutrophils,

Question 33

Sarcoidosis

Answer 33

Non-caseating granulomas with abundant activated macrophages

Question 34

Crowns disease (inflammatory bowel disease)

Answer 34

Non-caseating granulomas in the wall of the intestine.

Question 35

Systemic effects of inflammation

Answer 35

Fever (PGE-2), acute phase proteins (CRP,SSA), increased leukocytes, high levels of IL-1 and TNF.

Question 36

Steps of scar formation

Answer 36

Angiogenesis (VEGF)
Granulation tissue formation (fibroblast/connective tissue)
Remodeling connective tissue: remodeling of connective tissue, making scar.
Scar contraction (myofibroblasts)

Question 37

What converts collagen type 3 into collagen type 1 in scars.

Answer 37

Matrix metalloproteinase (MMP’s), requires zinc to function

Question 38

Factors that effect tissue repair

Answer 38

Infection time
Diabetes (abnormal wound healing)
Nutritional status (Vit C)
Glucocorticoids (steroids, inhibits PLA-2)
Mechanical factors
Poor perfusion 
Foreign bodies
Type of injury and extent of injury
Location of injury

Question 39

What does CSF (colony stimulating factor) do?

Answer 39

CSF is responsible for proliferation of progenitor cells in the bone marrow and hematopoietic stem cells.

Question 40

Liver regeneration phases (3)

Answer 40

Priming phase (IL-6, induce GF receptors)
Growth factor phase (HGF and TGF-a, cell cycle stimulation)
Termination phase (restoration to quiescence TGF-B)

Question 41

Healing by First intension

Answer 41

This is only if the damage is on the epithelial layer. Epithelial regeneration and happens if the cut is small and there are few epithelial deaths.
This process takes about a month to fully repair and form scar tissue that contain fibrous unions. This causes tensile strength of the wound to increase.

Question 42

Healing by Second intension

Answer 42

This is if the damage goes beneath the epidermis. This is generally done for large wounds,abscess, ulcerations, and ischemic necrosis.
This process involves the conversation of collagen type 3 to collagen type 1 (2 weeks)
Wound contracture happens here so the scar that is formed is much smaller (5-10% of original size)

Question 43

When does an organ go through fibrosis?

Answer 43

When an organ receives repeated injury such as drinking alcohol, it will recruit macrophages, which will cause destruction of tissue and replacement with fibroblasts, thus making it hard and there is a loss of function.

Question 44

What is a keloid?

Answer 44

Keloids are tissues that have collagen type 3 in excess. This happens because the collagen type is suppose to be converted to type 1, but something happens so the scar grows beyond the area of injury.

Question 45

What is Contracture and how is it obtained?

Answer 45

Contracture is an abnormal formation of collagen tissue, that causes tightening around the palms, soles, and anterior aspect of the thorax. It ends up compromising the movement of joints.
It occurs due to serious burn types of injuries.