Week 11

Question 1

Granulomas

• what are they made of?
• why/ how are they made?
• types

Answer 1

• Activated macrophages (activated by cytokines)
• In response to damage, injury, infection to wall off the infection because it can’t be handled the normal way (maybe too big to be phagocytosed)
• foreign body granuloma. immune granuloma, necrotizing vs non-necrotizing granuloma

Question 2

Foreign Body Granuloma

Answer 2

If somebody gets a splinter, their body will try to wall off the foreign body by making a granuloma around it because it can’t get rid of it in any other way. This process doesn’t involve your immune system and isn’t using antigenic substances. Your body can still make a granuloma.

Question 3

Immune granuloma

• what is it
• how does it happen
• problem

Answer 3

• Associated with a persistent T-cell mediated immune response
• Macrophage gets activated by the offending antigen –> activate the T cells which make cytokines (particularly IL-2) –> activates more T-cells and macrophages
• antigen is presumably pathogenic but if it isn’t, the granulomatous process can become more of a problem than the antigen itself.

Question 4

Necrotizing vs non-necrotizing granuloma

- kinds

Answer 4

• Necrotizing has “dead stuff in the middle”

- Caseating refers to it looking like cheese

Question 5

Sarcoidosis

• classic description
• signs/sxs
• Initiating Antigen
• organs can be involved
• how to make dx
• genetics

Answer 5

• non-caseating granulomas
• Typically an African American female w/ family history of Sarcoidosis; in Europe, the patient is likely to be Nordic; Erythema Nodosum
• In a genetically predisposed individual, it is presumed that there is an initiating antigen, although not for sure we suspect antigen is Propionibacterium acnes -> Macrophages present the antigen to the T-cells and then T-cells will release cytokines to activate more macrophages/more T-cells. Activated macrophages will try to fight off the antigen and release other cytokines to recruit more neutrophils.
• All of them!
• documenting granulomatous changes in two organs before making the diagnosis of sarcoidosis (not universal)
• HLA A1 and B8

Question 6

Staging of Sarcoidosis: CXR findings, rate of resolution, prevalence, suggested follow up

• 0
• I
• II
• III
• IV

Answer 6

• Normal, none, 5-10, none
• bilateral hilar adenopathy (only lymphnodes), lung function intact, 55-90%, 50%, every 6 months at first then annually when stable
• bilateral hilar adenopathy w/ pulmonary infiltrates; lung function imparied, 40-70, 25-30, every 3 months
• pulmonary infiltratets w/o hilar adenopathy; 10-20%, 10-12%, every 3 month indefinitely
• pulmonary fibrosis, 0-5%, 5%, every 3 months

Question 7

1 What is this

- kind of cells

Answer 7

High & low-powered images of non-caseating granulomas composed of activating macrophages in the middle of them; they are classically described as having this ring of lymphocytes (T-cells) around them
- CD4 T-cells that release cytokines forming the granulomas

Question 8

2 What is this?

- surrounded by?

Answer 8

• asteroid body in sarcoidosis

- giant cells made up of a bunch of macrophages that are fused in granulomas

Question 9

3 What is this?

Answer 9

shaumann body in sarcoidosis

Question 10

Sarcoidosis Dx 3 criteria

- tests you would order

Answer 10

• compatible clinical and radiological presentation
• Patho evidence of granulomas
• Exclusion of other dx with similar findings (infections/malignancy)
• BAL: increased lymphocytes a nd CD4/8 ratio

Question 11

Management of people with early stage acute sarcoidosis

Answer 11

• no sx so you follow these patients bcuz with early stage people tend to get spontaneously better but if they don’t get better & start progressing that’s when you start considering immune modulation like steroids

Question 12

Other things that cause granulomas

Answer 12

tuberculosis, fungal infections, microbacterial disease, or neoplastic disease