5 - Autoimmune Conditions

Question 1

What type of hypersensitivity reaction is Grave’s disease and what are the autoantibodies for this disease?

Answer 1

• Type 2
• TSH receptor antibodies

Question 2

Why do patients get exophthalmos in Grave’s disease?

Answer 2

The antibodies are attacking muscles of the eye as the muscles contain TSH receptors. This causes swelling and increased hyularonic acid in the eye so increased osmotic pressure

Question 3

How is Grave’s disease treated?

Answer 3

• Carbimazole: inhibits thyroid peroxidase but be careful as tetarogenic
• Plasmapheresis
• Surgery to remove
• Radioactive iodine
• Beta blockers to help symptoms

Question 4

What type of hypersensitivity reaction is Hashimoto’s disease and what autoantibodies are present?

Answer 4

Type IV

Anti TPO and Anti TG

Question 5

How can we diagnose Hashimoto’s disease?

Answer 5

• Fine needle biopsy to see infiltration of TH1 lymphocytes
• Serum autoantibodies

Question 6

How do we treat Hashimoto’s disease?

Answer 6

Give Levothyroxine and monitor TSH/T4 levels

Question 7

How is the secretion of thyroid hormone regulated?

Answer 7

Question 8

How does carbimazole work?

Answer 8

Question 9

What are the general actions of thyroid hormone and what are the tissue specific effects?

Answer 9

Question 10

What are some common symptoms of SLE and RA?

Answer 10

- Pain: pleuritic chest pain, joint pain (especially hands and wrists)

- Stiffness

- Swelling

- Fatigue

- Fever

Question 11

What is the epidemiology of SLE?

Answer 11

• More common in young Afro-Caribbean females
• Genetic factors important
• Environmental factors like smoking and UV light can be a trigger

Question 12

At what age do most autoimmune diseases develop?

Answer 12

Child bearing aged females 15-45 apart from type I diabetes

Question 13

How do we take a history for autoimmune rheumatic diseases?

Answer 13

• Constitutional symptoms e.g weight loss, fever, night sweats etc

- Glove and Sweater approach

Question 14

What areas of the body should be examined when suspecting an ARD and what should you be looking for?

Answer 14

Question 15

What are some investigations that should be carried out when you suspect SLE?

Answer 15

• Often normal CRP

- Even if bloods normal treat the clinical presentation!!!

Question 16

How should we commence treatment once there is a diagnosis of SLE?

Answer 16

Question 17

What are the 11 criteria for SLE?

Answer 17

A RASH POINTS MEDICAL DIAGNOSIS

Question 18

What is the epidemiology of RA?

Answer 18

• More common in females 3:1
• No race preference
• 1% prevalence
• Genetic and environmental factors (e.g smoking and bad dentition)

Question 19

What is the S factor in rheumatoid arthritis?

Answer 19

Question 20

What tests are done once you suspect RA and what are some autoantibodies in this disease?

Answer 20

Question 21

How is RA treated once it is diagnosed?

Answer 21

Sooner the better to slow progression

Question 22

What are some differentials for this case and what would be the course of treatment if you found of the CRP level was raised?

Answer 22

• Interstitial lung disease due to methotrexate
• Cancer metastases
• Rheumatoid lung nodules
• Pneumonia
• PE
• Do CXR, D dimers (rule out PE), FBC
• Would most likely be pneumonia, don’t give amoxicillin as immunocompromised so can cause C.Diff!!! Give IV co-amoxiclav

Question 23

What are the autoantibodies in rheumatoid arthritis?

Answer 23

- Anti RF: against the rheumatoid factor (Fc part of immunoglobulin G)

• ACPA: anti citrullinated cyclic peptide

Antibodies cause persistent synovitis with systemic inflammation but norma CRP

Question 24

What are some non-articular manifestations of rheumatoid arthritis?

Answer 24

IMPORTANT!!! Rheumatic lung nodules

Question 25

What mediators cause the articular manifestations of rheumatoid arthritis?

Answer 25

**- Progressive, symmetrical, peripheral polyarthritis** - Synovitis and destruction of joints due to the over production of TNF-a. This over production is due to interaction of macrophages and T/B lymphocytes - TNF-a causes an over production of IL-6. Blocking TNF-a and IL-6 can improve synovitis and systemic malaise

Question 26

What information does a D-dimer test provide?

Answer 26

- Used to measure the extent of clotting, it is a breakdown product of fibrin **- Raised:** PE, DVT, malignancy, pregnancy, recent surgergy, infection, stroke, MI **- Negative:** rules out PE

Question 27

What are the differential diagnoses? (especially if when you do a urine dipstick there is blood, protein and nitrates)

Answer 27

- Lupus nephritis - AKI secondary to NSAIDs - Lupus flare - UTI - Issue with glomerulus (blood) Most likely complicated UTI as immunocompromised due to result on dipstick

Question 28

What autoimmune condition does this patient have and why are they more at risk of systemic complications?

Answer 28

**- SLE** - Lack of complement so immune complexes not being opsonised and cleared so more likely to be deposited over the body, e.g kidneys, causing damage

Question 29

What is the pathogenesis involved in SLE and what autoantibody is produced?

Answer 29

**Mainly ANA** **Anti DS-DNA, anti-Ro/La, anti-Sm/RNP** When cells apoptose the cell remnants appear on the cell surface as blebs containing self antigens (e.g DNA and histones) In SLE **removal of blebs by phagocytes in inefficient** so they are transferred to lymphoid tissues where they are taken up by APCs that present self antigens to T cells that activate B-cells

Question 30

What is lupus nephritis?

Answer 30

Occurs in 1/3 of SLE patients and 25% of these reach end stage CKD in 10 years Immune deposits in glomeruli and mesangium (IgG, IgM, IgA, C3, C1q, C4) can be seen on staining and immunofluorescence

Question 31

What medication is given in RA?

Answer 31

- NSAIDs - DMARDs - Steroids - Infliximab and Adalimumab inhibiting TNF-a

Question 32

What are some of the clinical features of SLE?

Answer 32

- Discoid plaques - Skin problems - Kidney problems - Malar rash