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Immunology > Secondary Immunodeficiency > Flashcards

Secondary Immunodeficiency Flashcards

1
Q

When is secondary immunodeficiency most common

A

In adulthood

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2
Q

What is the first line defence in immunity

A

The physical barrier

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3
Q

What are the ways which we can disrupt the barrier

A

Physical distruption: catheter, iv access devices
Pharmacological: PPI use, anti-cholinergic (reduces saliva production)
Surgical: anatomical disruption of barrier

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4
Q

What is splenectomy

A

Removal of the spleen

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5
Q

In splenectomy what are patients at right of

A

Overwhelming infeciton from encapsulated bacteria

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6
Q

How do we manage splenectomy

A

Vaccinate

Prophylactic antibiotics: penicillin or macrolide if allergic

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7
Q

What are the 2 broad types of haematoligical malignancy

A

Lymphoid malignancy

Myeloid malignancy

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8
Q

How is the normal immune system disrupted in haemoatological malignancy

A
  • bone marrow failure due to haematoligical abnormal infiltratve tumour cells
  • chemotherapy that depletes the b cells
  • Chemotherpay that takes out t cells
  • lymph node destruction so relationship between t and b cell cant occur
  • plasma cells targeted by medication
  • higher affinity immunoglobulin can be lost by renal or gi loss
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9
Q

What is plasma dyscarsia

A

In normal blood you have polyclonocal antibodies byt in myeloma you can get monoclonal antibodies that take up the space for polyclonocal response (plasma cell dyscarsia)

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10
Q

In chemotherapy what can happen to the neutrophils

A

Can decrease to cause neutropenia

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11
Q

How can neutropenia be boosted in chemotherapy

A

Patient can have g-csf

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12
Q

What is the role of a normal phagocyte

A
  1. Migrate to the pathogen
  2. Recognise the pathogen by antibody/complement receptors
  3. Phagocytose and internalsie and kill the pathogen
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13
Q

If there is a depletion of phagocyte what is the person prone to

A

Extracellular bacteria infection

Fungal infection

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14
Q

What are the causes of chronic neutropenia

A

Autoimmunity
Sequestration in the spleen
Anti gm csf antibodies
Bone marrow failure

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15
Q

What is rituximab

A

An anti CD20 monoclonal antibody

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16
Q

What id CD20

A

A protein expressed on all b cells until they become plasma cell

17
Q

When you give rituxumab what happens to the b cells

A

They become killed by:
Complement
Inudce antibdy dependent cellular cytoxicity with nk cells

18
Q

If b cells are killed what does this lead to

A

B cell aplasia

19
Q

If you done have b cells what can you not get

A

Plasma cells

20
Q

What is the management of secondary immunodeficiency

A

Vaccination
Antibiotic prophylaxis
Immunoglobulin replacement- ivIG
Stop/treat causative processes

21
Q

Which immunoglobulin do we give

A

Igg

22
Q

To qualify for immunglobulin what are the criterias that you need to meet

A

Igg less than 3g/l
Fail to respond to pneumoccocal vaccination
Fail to get better on 6 months of antibiotic prophylaxis
Underlying cause must be irreversible

23
Q

What example of a drug can be used to block cytokines

A

Anti tnf

24
Q

What does tnf alpha cause

A

Bone erosion
Endothelial activation
Cartilage destruction
Positive feedback to cytokine cascade

25
Q

What are the ways we can inhibit TNF alpha

A

Anti tnf:
Inflixamab (monoclon ig)
Entanercept- soluble tnf receptor

26
Q

What is the aim of anti tnf

A

To make joints better

27
Q

What is the consequence of using anti tnf medication

A

Latent infection e.g latent tuberculosis, therefore by giving anti tnf you can reactivate tb

28
Q

What are the role of cytokines il1, tnf alpha and il6

A

Hypothalamus: to cause fever, rigous and anorexia
Liver: to cause CRP
Bone marrow: increase mobilation of cells e.g neutrophils
Fat and muscle: for metabolism

29
Q

What is tocilizumab

A
  1. Block il-6 receptors to dampen down the sytemic inflammatory resposne
  2. You do not get stat 3 signalling
  3. This decreases CRP
30
Q

What are the consequences of tociluzumab

A

Infection without CRP
Diverticulitis
Skin and soft tissue infection

31
Q

What is eculizumab

A

Block the c5 complement

32
Q

If eculizumab blocks c5 what does this lead to

A

Not being able to assemble TCC

33
Q

What does lack of TCC lead to

A

Risk for meningococcal and gonococcal infection

Immunology (7 decks)

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