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YEAR 5: Immunopathology > IMMUNO: Secondary immune deficiencies and HIV infection Pt.1 > Flashcards

IMMUNO: Secondary immune deficiencies and HIV infection Pt.1 Flashcards

1
Q

What are some manifestations of immune deficiencies?

A
  1. Infections
  2. Autoimmune and allergic disease
  3. Persistent inflammation
  4. Cancer
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2
Q

Which childhood infection can cause secondary immune deficiency?

A

Measles - immune defect lasts from months to years

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3
Q

What are the common causes of secondary immune deficiencies?

A
  1. Malnutrition - most common worldwide
  2. Measles
  3. TB
  4. HIV
  5. SARS-CoV-2
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4
Q

What are some drugs/therapies that can cause immunodeficiency?

A

Small molecules

  • Steroids
  • Cytoxic drugs - methotrexate/azathioprine,
  • Antiepileptics - phenytoin/ carbamazepine/ levetiracetam
  • Calcineurin inhibiors - tacrolimus,
  • DMARD (sulphasalazine)

JAK inhibitors - ruxolitinib, tofacitinib

Biologic and cellular therapies

  • Anti-CD20
  • Anti-TNF (TB)
  • CAR-T cell therapies
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5
Q

Which B cell lymphoproliferative disorders are most associated with immune deficiency?

A
  • Multiple myeloma
  • CLL
  • NHL
  • MGUS
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6
Q

What is the 2 characteristics of Goods’ syndrome?
What are the consequences of its immunodeficiency disorder?

A

Characteristics

  • Thymoma
  • Immunodeficiency due to hypogammaglobulinemia

Consequences

  • B and T cells absent
  • CMV/ PJP / muco-cutaneous candida infections
  • Autoimmune disease disease e.g. pure red cell aplasia, myasthenia gravis, lichen planus
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7
Q

Which haematological cancers cause immunodeficiency and how?

A

B and plasma cell cancers

  • Antibody deficiency
  • Leukopenia
  • Treatment (cytotoxic chemotherapy)
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8
Q

How do you evaluate secondary immune deficiency?

A
  1. Infection history, unusual childhood complications of illness, reaction to vaccines, loss of schooling
  2. PMH of other illness e.g. lymphoma, bronchiectasis, lymphoma/cancers, TB, hep B/C.
  3. FH of infection/AI/cancer
  4. Medication history
  5. Vaccine history e.g childhood, pneumococcal, flu vaccines
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9
Q

How do you ‘FISH’ for immunodeficiency?
What % of immunodeficiencies will be picked up this way?

A
  1. FBC - Hb <10g/L, neutrophil, lymphocyte, platelet counts
  2. Immunoglobulins (IgG, IgA, IgM, IgE)
  3. Serum complement (C3, C4) - immune complex disease or lupus
  4. HIV test (18-80years)

This will pick up 85% of immune defects

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10
Q

What are the other first line investigations for immunodeficiency after FISH?

A
  • Renal and liver profile
  • Calcium and bone profile
  • Total protein and albumin
  • Urine protein/creatinine ratio
  • Serum protein electrophoresis
  • Serum free light chains
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11
Q

What clinical situations can cause reduction in

  • IgG only
  • IgG and IgM
  • IgG and IgA
A

IgG - Protein-losing enteropathy, prednisolone >10mg/day

IgG and IgM - B cell neoplasm, rituximab

IgG and IgA - Primary antibody deficiency

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12
Q

Which vaccine-related tests can be used as a second line test for immune deficiencies?
What is the management if these are deranged?

A

Measure concentration of vaccine antibodies (provided they were previously vaccinated)

  • Tetanus toxoid- protein antigen detection
  • Pneumovax vaccine - carbohydrate antigen detection (for all 23 serotypes or to individual pneumococcal serotypes).

If low… offer Pneumovax II and tetanus immunisation to test immune function.
Failure to respond to this is a criteria for receipt of IgG replacement therapy for secondary antibody deficiency syndromes.

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13
Q

How is serum protein electrophoresis useful in immunodeficiency diagnosis? What can be missed on SPE (electrophoresis)?

A
  • Serum proteins are separated by charge. Discrete bands are formed for each immunoglobulin as they bind by immunofixation
  • Monoclonal proteins can indicate MGUS, MM etc.
  • SPE can miss free light chain disease (seen in 20% of MM) so must measure these separately
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14
Q

What are monoclonal protein bands associated with on SPE (electrophoresis)?

A

If monoclonal proteins are found this can be associated with:

  1. MM
  2. WMG (Waldenström Macroglobulinemia - IgM)
  3. NHL
  4. MGUS
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15
Q

How can lymphocyte subsets be investigated in suspected immunodeficiency?

A

Flow cytometry - quantifies subsets based on surface antigens

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16
Q

What is the management of secondary immune deficiency?

A
  1. Treat cause
  2. Advise exposure reduction
  3. Immunisation of patient and household contacts
  4. Education to treat bacterial infection promptly (excluded from antimicrobial stewardship rules) e.g. co-amoxiclav 625mg TDS for 10-14 days, rather than 375mg for 5-7 days
  5. Prophylactc antibiotics for confirmed recurrent bacterial infection
17
Q

What are the indications for secondary antibody deficiency syndrome IgG replacement?

A

Unreversable hypogammaglobinaemia

OR

Hypogammaglobinaemia associated with treatment/post-treatment/cancer (e.g. cytoxic or biologic therapy, NHL/CLL/MM)

AND

  1. Recurrent infections despite continuous ABx for 6 months
  2. IgG <4g/L
  3. Failure of vaccine response to pneumococcal/other polysaccharide vaccine
18
Q

Man with reduced IgG and IgM on predisolone 5mg and rituximab what is the cause of the deficiency

A

Rituximab

(predisolone <10mg should not have such an impact)

19
Q

How many people live with HIV in UK?
What % are virally suppressed in the UK?

A
  • >100,000 living with HIV in the UK
  • Infections incidence fallen by 70% in the last 4-5 years
  • ~70% those on ART have undetectable viral load
20
Q

What kind of virus is HIV?

A
  • Double-stranded RNA retrovirus
  • Lentivirus (genus of retrovirus) - slow evolution of disease
21
Q

Describe the lifecycle of HIV-1.

A
  • Binds to CD4 and then to chemokine co-receptor CCR5 or CXCR4
  • vRNA converting into DNA by reverse transcriptase
  • vDNA integrated into host genome
  • vDNA transcribed to viral mRNA
  • vRNA translated to viral proteins
  • Packaging and release of mature virus
22
Q

Where did HIV-1 originate?

A

Chimpanzees

Lineages M, N, O and P present

  • M lineage transmission occurred in Cameroon in 1910-1930 initially, spread along the Congo river into Kinshasa in 1960 and became pandemic
  • M lineage consists of 9 subtypes and 40 recombinant forms
23
Q

What is the natural history of HIV-1 infection as defined by viral replication?
What are the 3 phases?
When is risk of transmission greatest?
When is viral diversity greatest?

A
  1. Acute
  2. Latent stage (asymptomatic but progessive)
  3. AIDS

Risk of transmission - greatest in acute phase, then in the AIDS phase

Viral diversity greatest in the AIDS phase

24
Q

What drives viral diversity in HIV? What are the implications of this?

A

Viral diversity due to

  • Error-prone nature of HIV reverse transcriptase
  • Short generation time of viral cycle
  • Length of infection

Leads to…

  • Emergence of drug resistance
  • Evasion of immune system

Need to use combination therapies

25
Q

What is the life expectancy of those living with HIV and taking HAART?

A

80yrs = male

81yrs = female

YEAR 5: Immunopathology (25 decks)

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