Secondary Immunodeficiency Flashcards
When is secondary immunodeficiency most common
In adulthood
What is the first line defence in immunity
The physical barrier
What are the ways which we can disrupt the barrier
Physical distruption: catheter, iv access devices
Pharmacological: PPI use, anti-cholinergic (reduces saliva production)
Surgical: anatomical disruption of barrier
What is splenectomy
Removal of the spleen
In splenectomy what are patients at right of
Overwhelming infeciton from encapsulated bacteria
How do we manage splenectomy
Vaccinate
Prophylactic antibiotics: penicillin or macrolide if allergic
What are the 2 broad types of haematoligical malignancy
Lymphoid malignancy
Myeloid malignancy
How is the normal immune system disrupted in haemoatological malignancy
- 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
What is plasma dyscarsia
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)
In chemotherapy what can happen to the neutrophils
Can decrease to cause neutropenia
How can neutropenia be boosted in chemotherapy
Patient can have g-csf
What is the role of a normal phagocyte
- Migrate to the pathogen
- Recognise the pathogen by antibody/complement receptors
- Phagocytose and internalsie and kill the pathogen
If there is a depletion of phagocyte what is the person prone to
Extracellular bacteria infection
Fungal infection
What are the causes of chronic neutropenia
Autoimmunity
Sequestration in the spleen
Anti gm csf antibodies
Bone marrow failure
What is rituximab
An anti CD20 monoclonal antibody
What id CD20
A protein expressed on all b cells until they become plasma cell
When you give rituxumab what happens to the b cells
They become killed by:
Complement
Inudce antibdy dependent cellular cytoxicity with nk cells
If b cells are killed what does this lead to
B cell aplasia
If you done have b cells what can you not get
Plasma cells
What is the management of secondary immunodeficiency
Vaccination
Antibiotic prophylaxis
Immunoglobulin replacement- ivIG
Stop/treat causative processes
Which immunoglobulin do we give
Igg
To qualify for immunglobulin what are the criterias that you need to meet
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
What example of a drug can be used to block cytokines
Anti tnf
What does tnf alpha cause
Bone erosion
Endothelial activation
Cartilage destruction
Positive feedback to cytokine cascade
What are the ways we can inhibit TNF alpha
Anti tnf:
Inflixamab (monoclon ig)
Entanercept- soluble tnf receptor
What is the aim of anti tnf
To make joints better
What is the consequence of using anti tnf medication
Latent infection e.g latent tuberculosis, therefore by giving anti tnf you can reactivate tb
What are the role of cytokines il1, tnf alpha and il6
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
What is tocilizumab
- Block il-6 receptors to dampen down the sytemic inflammatory resposne
- You do not get stat 3 signalling
- This decreases CRP
What are the consequences of tociluzumab
Infection without CRP
Diverticulitis
Skin and soft tissue infection
What is eculizumab
Block the c5 complement
If eculizumab blocks c5 what does this lead to
Not being able to assemble TCC
What does lack of TCC lead to
Risk for meningococcal and gonococcal infection
