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Immunology > Clinical Context of Immunology > Flashcards

Clinical Context of Immunology Flashcards

1
Q

What are 4 clinical features of Graves disease?

A
  • Heart Palapatations
  • Excessive sweating
  • Weight loss
  • Muscle Weakness
  • Exophthalmos
  • Increased in BMR
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2
Q

What is the type of Hypersensitivity in Graves’ Disease?

A
  • Type 2 hypersensitivity.
  • IgG antibodies against TSH receptor which mimic the hormone by stimulating the thyroid gland to produce thyroid hormones
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3
Q

What are the treatments available for Graves’ Disease?

A

Anti-thyroid drugs – Carbimazole

Radioactive iodine – to destroy thyroid cells

Surgery (thyroidectomy or sub-total thyroidectomy

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4
Q

What is the risk to the newborn of a woman with Graves’ Disease?

A

TSI can cross the placenta and act on the thyroid gland on the baby causing symptoms within the new-born. Can cause neonatal Graves’ disease

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5
Q

What are the features of Hashimoto’s Disease?

A
  • Weight Gain
  • Lethargy
  • Cold intolerance
  • Bradycardia
  • Dry skin
  • Hoarse Voice
  • Constipation
  • Slow reflexes
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6
Q

What are 2 autoantibodies in Hashimoto’s Disease?

A
  • Anti-thyroglobulin antibody

* Anti-thyroid peroxidase antibody

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7
Q

What is a thyroid biopsy likely to show in Hashimoto’s Disease?

A
  • Infiltrate of lymphocytes (CD4+ and CD8+)

- Plasma cells (with is a mature B cell producing a single antibody).

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8
Q

What is the treatment for Hypothyroidism and how is it monitored?

A

-Replacement therapy with Thyroxine
-Monitor clinically
TSH levels should return to normal and can be monitored

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9
Q

What is the main auto antibody found in blood test for Rheumatoid Arthritis?

A

-Autoantibodies to the Fc portion of immunoglobulin G (rheumatoid factor)

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10
Q

What other autoantibodies can occur in RA?

A
  1. Anti-Cyclic Citrullinated Peptide (anti-CCP). Also referred to as Anti-citrullinated protein antibody (ACPA)
  2. Antinuclear Antibodies
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11
Q

What are the main findings in relation to joint in Rheumatoid Arthritis?

A
  • Chronic Symmetrical Polyarthritis
  • Synovitis
  • Joint destruction
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12
Q

What is the pathophysiology of the changes to joints found in RA?

A
  • There is persistent synovitis, causing chronic symmetrical polyarthritis with systemic inflammation.
  • There is over-activation of the inflammatory process. Chemoattractant produced in the joint recruit circulating inflammatory cells
  • Over-production of tumour necrosis factor (TNF) leads to synovitis and joint destruction. Interaction of macrophages and T and B lymphocytes drives this over-production.
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13
Q

What can occur in lungs of patient with RA?

A

Nodules

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14
Q

What are other non0articular manifestations of RA

A
  • Pericarditis
  • Anaemia
  • Leg ulcers
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15
Q

What is the treatment for Rheumatoid Arthritis?

A

DMARDs

  • Sulfasalazine
  • Methotrexate
  • Hydroxychloroquine
  • Leflunomide

Steroids

  • Prednisolone
  • Methylprednisolone
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16
Q

What is the type of hypersensitivity reaction in Systemic Lupus Erythematosus?

A

-Mainly Type 3

17
Q

What is the pathophysiology of SLE?

A
  • When cells die by apoptosis, the cellular remnants appear on the cell surface as small blebs that carry self antigens.
  • These antigens include nuclear constituents (e.g. DNA and histones), which are normally hidden from the immune system.
  • In people with SLE, removal of these blebs by phagocytes is inefficient, so that they are transferred to lymphoid tissues, where they can be taken up by antigen-presenting cells.
  • The self antigens from these blebs can then be presented to T cells, which in turn stimulate B cells to produce autoantibodies directed against these antigens.
18
Q

What are the immunological consequences of SLE?

A

The combination of availability of self-antigens and failure of the immune system to inactivate B cells and T cells that recognize these self-antigens (i.e. a breakdown of tolerance) leads to the following immunological consequences.

  • Development of autoantibodies that either form circulating complexes or deposit by binding directly to tissues.
  • Activation of complement and influx of neutrophils, causing inflammation in those tissues.
  • Abnormal cytokine production
19
Q

What are the main auto-antibodies to SLE?

A

-Antinuclear antibodies

This includes: Anti DNA (or anti double stranded DNA).

20
Q

What other autoantibodies can occur in SLE?

A
  • Anti-Sm antibodies
  • Antiphospholipid antibodies
  • Complements
21
Q

What are 3 features of SLE?

A
  • Butterfly rash on face
  • Photosensitivity
  • Urticaria
  • Vasculitis
  • Purpura
22
Q

What might you find in a full blood counts of a patient with SLE?

A
  • Anaemia
  • Low white cell count
  • Low platelet count
23
Q

If there is evidence of haemolytic anaemia what test of the blood might help to confirm the autoimmune nature of the anaemia?

A

Blood Test: Coombs’ Test

24
Q

What are 3 other body organs/systems that can be affected in SLE?

A
  • Pericarditis
  • Abdominal pain
  • Renal disease
  • Myositis
25
Q

What are the treatment principles of SLE?

A
  • Lifestyle modification, use of sunscreen
  • DMARDS: Hydrochloroquine, Azathioprine, Mycophenolate
  • Use of steroids: Prednisolone, Methyl Prednisolone
  • In severe cases: IV Cyclophosphamide

Immunology (9 decks)

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