Apr6 M3-GI immunity

Question 1

part of GIT that is very different from the rest of the GIT

Answer 1

oropharynx

• is a large absorptive surface where things are dealt with and absorbed differently
• ex. sublingual meds

Question 2

functions of saliva

Answer 2

• lubricate
• protect against pathogens
• neutralize acids

Question 3

oral manifestations of immune salivation deficiencies

Answer 3

• gingivitis
• fungal infections
• teeth fall out
• periodontal area infections
• esophageal abrasions
• dental caries
• ulcers

Question 4

non infectious ulcers of the mouth: cause

Answer 4

often because not enough saliva production

Question 5

ddx of mouth ulcer

Answer 5

• malignancy
• trauma
• immune deficiency
• infection
• etc

Question 6

oral mucosa immune system components

Answer 6

is part of the MALT
3 sites are
-oral mucosa
-salivary glands
-gingival crevice

Question 7

defensive mechanisms in the oral mucosa

Answer 7

• barrier by squamous epith (tight junctions) + LP
• intraepith dendritic cells (Langerhans cells) = surveillance
• IgA secretion in saliva against invaders
• defensins and pro-inflam cytokines released by EPITH and immune cells

Question 8

most important oral health problem and why

Answer 8

caries

-gingival crevices and other places = places where microbes can stay

Question 9

immune mechanisms at the gingival crevice

Answer 9

• neutrophils clearing microbes and ctly moving from gingival capillaries into the sulcus (crevice)
• are activated by local cytokine prod and co-Rs

Question 10

important thing not to miss on ddx of teeth loss

Answer 10

neutropenia

Question 11

why periodontal attachment is related to neutrophils (not bc neutrophils clear organisms that you necessarily lose your teeth in neutropenia…)

Answer 11

• osteoblasts and osteoclasts are of same lineage as neutrophils
• pathway affecting neutrophils = affects them too

Question 12

mechanical barrier + 1st lines of defense in GIT below oropharynx

Answer 12

• mucosal barrier
• tight junctions
• cilia to keep microbes moving DOWN GIT
• IgA and commensal organisms

Question 13

how pathogens are recognized in the GIT

Answer 13

• TLRs

- NOD-Rs see commensals

Question 14

NOD-R mutation consequence

Answer 14

• higher risk of Crohn’s (IBD)

- don’t see commensal and say it’s ok (regulating (down) the immune system)

Question 15

immune cells inside the mucosal barrier of the GIT

Answer 15

• dendritic cells pick Ags and may go show them at lymph nodes
• T cells INSIDE the intraepith compartment (immunoregulatory + for repair)
• CD8+ T cells can kill infection cells
• IgA neutralizes toxins and prevents virus and bacteria adherence to epith

Question 16

Peyer’s patches def

Answer 16

-sites of active mucosal immune resp in GIT (are in SI, appendix, lymphoid follicles of colon)

Question 17

special cells in Peyer’s patches and what they do

Answer 17

M cells (superabsorbers)

• interact with gut lumen and eat some of everything
• present Ags to lymphocytes AND dendritic cells

Question 18

best way to make sure all the gut is protected against a known Ag

Answer 18

have gut derived lymphocytes that go to blood and lymph circulation of GI mucosa but that also come back to home mucosal sites

Question 19

how do you get lymphocytes to home to mucosal sites in the GIT

Answer 19

homing Rs expressed on T cells recognize chemokines expressed by gut epith cells

Question 20

when is gut inflammation bad and what determines that

Answer 20

ALWAYS BAD

• bad bowel vmvmt
• upset gut
• obstruction
• poor abso
• leaky gut
• perforation
• etc.

Question 21

IPEX (disease where can’t make foxp3+ T reg cells) consequence on GIT

Answer 21

• most immune resp in GIT is tolerant
• you can’t make tolerance
• 1st thing you get i colitis (and is also what kills IPEX pts)
• MAIN PROB IS COLITIS IN IPEX
• also skin problems, primary autoimmune diabetes

Question 22

class 3 MHC molecules fct in GIT

Answer 22

• MIC-A and MIC-B
• role in maintenance of balance in GIT immune system
• infected cells turn on MIC expression
• ALLOWS intraepith lymphs and NK cells to see and kill infected cells

Question 23

c.diff cause and pathology you get

Answer 23

• often bc of Abx use

- pseudomembranous colitis

Question 24

c.diff type of disease

Answer 24

• toxemia (c.diff toxin produced)
• toxin causes leakiness in GIT.
• microbes pass, secretory diarrhea, cells are killed

Question 25

salmonella how affects GIT

Answer 25

• gets in M cells and grows in them and then goes out of them
• infects the next normal cells
• YOU GET DIARRHEA

Question 26

shigellae how infects GIT

Answer 26

gives diarrhea

Question 27

helicobacter pylori how affects GIT

Answer 27

• no problems initially but problems after replicates with time and thrives in high acid environment
• causes ULCERS and ongoing inflammation
• because slow inflammation, not enough stimulus to call enough immune cells

Question 28

long term effects of H pylori infection

Answer 28

• cells keep turning over = higher risk of genetic mutations in lymphocytes
• increased risk of GASTRIC LYMPHOMA

Question 29

definition of colitis

Answer 29

more inflammation in the GIT than T reg cells

Question 30

treatments of IBD and colitis caused by poor regulation

Answer 30

immunosuppressants

Question 31

diverticular disease and associated problems

Answer 31

• outpouching
• diverticulitis = inflammation of outpouching + infection + perforatin
• microbes found are COMMON MICROBES IN THE GIT (but it’s just the place and situation made the immune system unable to tolerate)