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Semester 3 - Infection > Session 9 - Immunocompromised Host > Flashcards

Session 9 - Immunocompromised Host Flashcards

1
Q

What is the importance of immuno-defiency?

A
  • Immunodeficiency is associated with an increase in the frequency and severity of infections
    • Immunodeficiency is associated with autoimmune diseases and malignancy
    • Failure to recognize and diagnose leads to increased morbidity and mortality
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2
Q

Why is immunodeficiency considered to be subversive?

A

• Long gap between symptom onset and immunodeficiency

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3
Q

Define “immunocompromised”

A

• State in which the immune system is unable to respond appropriately and effectively ot infectious microorganisms

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4
Q

What are two types of defects involved in immunocompromised hosts?

A

Qualitative or quantitative defect of one or more components of the immune system

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5
Q

Give three components of innate immunity which could potentially go wrong?

A
  • Innate barriers
    • Phagocytes
    • Complement
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6
Q

Give three components of adaptive immunity which could potentially go wrong

A
  • B cell
    • Antibodies
    • T cells
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7
Q

Give four features of infections which come about as a result of immunocompromise?

A 
• SPUR
		○ S - Severe
		○ P - Persistent
		○ U - Unusual
		○ R - Reccurent
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8
Q

What are two types of immunodeficiency?

A
  • Primary

* Secondary

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9
Q

What is a primary immunodeficiency?

A

• Intrinsic defect
○ Single-gene disorder
○ Polygenic
○ Polymorphisms

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10
Q

What is a secondary immunodeficiency?

A

• Underlying disease or condition affecting immune components
○ Decreased production

Loss or catabolism

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11
Q

How is a primary immunodeficiency classified?

A

• By the part of the immune system which is damaged

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12
Q

What types of patients are primary immunodeficiency? (age and gender)

A
  • 80% patients <20 yrs

* 70% males (x-linked)

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13
Q

What factors can be affected in a primary immunodeficiency?

A

B cell (50%)
• T cell (30%)
• Phagocytes (18%)
• Complement (2%)

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14
Q

Name three important B cell deficiencies (primary immunodefiency)

A
  • Common variable immunodeficiency
    • IgA deficiency
    • Bruton’s disease
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15
Q

What is the most common type of primary immunodeficiency?

A
  • Common variable immunodeficiency

* Inability of B cells to mature into plasma cells

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16
Q

What does the immunoglobulin/cell levels of someone with B cell CVID look like?

A
  • IgG <5g/l

* IgA and IgM variable

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17
Q

What is the clinically defining feature of IgA deficiency

A
  • IgA <0.05g/l

* B cell unable to switch to IgA

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18
Q

what is the clinically defining feature of Bruton’s disease (3)

A
  • Impaired B cell development
    • IgG <2g/l
    • IgA undetectable
    • Low B cells
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19
Q

How do patients with primary immunodeficiency present?(5)

A
  • Recurrent upper and lower respiratory bacterial infection (bronchiectasis)
    • GI complications including infections
    • Arthropathies
    • Increased incidence of autoimmune disease
    • Increased incidence of lymphoma and gastric carcinoma
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20
Q

How are primary immuno-deficient patients treated? (4)

A
  • Prophylactic antibiotics
    • Immunoglobulin replacement therapy
    • Management of respiratory function

Avoid unnecessary exposure to radiation

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21
Q

What is immunoglobulin replacement therapy and what is its goal?

A
  • IgG >8g/l

* Replacement of immunoglobulin

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22
Q

What is immunoglobulin replacement therapy used to treat?

A

• CIVD

Bruton’s disease

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23
Q

Given two phagocyte deficiencys

A
  • Leukocyte Adhesion Deficiency (LAD)
    • Chronic granulomatous disease (CGD)

Cyclic neutropenia

24
Q

What occurs in Leukocyte Adhesion Deficiency?

A

• Phagocytes cannot adhere to endothelium

25
What occurs in Chronic granulamatous disease?
* Phagocytes can produce respiratory burs | * Granulomas form
26
What is the presentation of someone with a phagocyte deficiency?
* Prolonged and recurrent infection * Ulcers * Abscesses (granuloma) * Invasive aspergillosis
27
What is the management of someone with phagocyte deficiency?
* Prophylactic antibiotic * Interferon-g Steroids
28
How do you recognise someone with phagocyte deficiency?
ABSCESS
29
Name three main T cell deficiencies
* Di George deficiency | * Severe combined Immunodeficiency (SCID)
30
What is DiGeorge syndrome?
* Defect in thymus embryogenesis and incomplete development | * Characterised by lack of thymus
31
Why is DiGeorge syndrome called CATCH-22 Syndrome
``` CATCH 22 • Cardiac abnormalities • Abnormal faces • Thymic hypoplasia • Cleft palate • Hypocalcaemia • MORE SUSCEPTIBLE TO VIRAL AND FUNGAL INFECTIONS ```
32
What is the genetic cause of Catch 22 syndrome/DiGeorge?
• chromosomal abnormalities
33
What is the management of Di George syndrome?
• Neonatal cardiac surgery supplement to correct hypocalcaemia
34
What non-related medical treatment is prohibited in Di George syndrome
• Live vaccines
35
What causes SCID?
• Stem cell defect in g chain used by many T cell receptors Death of developing thymocytes
36
What does SCID look like?
* Failure to thrive * Protracted diarrhoea * Hepato-splenomegaly Low lymphocyte count
37
What is a short term management for SCID?
* aggressive treatment of infections | * Prevention of new infections
38
Give a long term treatment for SCID?
• Bone marrow transplant Gene therapy
39
Name one complement component deficiency
* C1 inhibitor deficiency | * Hereditary angiooedema
40
What are secondary immune deficiencies caused by?
* Malnutritition * Infection * Liver diseases * Lymphoproliferative diseases * Drug induced neutropenia Splenectomy
41
Give three causes of asplenia
* Infarction (SICKLE CELL DISEASE) * Trauma * Autoimmune
42
Give three causes of neutropenia
• Bone marrow infiltration with malignancy Chemotherapy - Cytotoxics and immunosupressants
43
What is the management of neutropenia?
• Treat suspected neutropenic spesis as an acute medical emergency and offer empiric antibiotic therapy immediately Asses patient's risk of septic complications
44
What is the standard presentation of an asplenic patient?
• Susceptibility to encapsulated bacteria ○ Haemophilus influenzae ○ Streptococcus pneumoniae Neisseria meningitidis
45
Why are asplenic patients susceptible to encapsulated bacteria?
* Contains B cells which do not need T cell activation * Encapsulated bacteria difficult to break down and present * Spleen required to clear them
46
What is OPSI?
* Overwhelming post-splenectomy infection | * Causes sepsis and meningitis
47
What is the mangement of an asplenic patient?
* Penicillin prophylaxis * Immunisation against encapsulated bacteria * Patient information; Medic alter bracelet
48
What are the three main immune functions of the spleen?
``` • Removal of blood borne pathogens ○ Encapsulated bacteria • Antibody production ○ Acute response IgM production ○ Long term protection IgG production • Splenic macrophages ○ Removal of opsonized microbes ○ Removal of immune complexes ```
49
Taking a history from a patien
Age - at presentation – Sex – Site(s) and frequency of infection(s) – Type of organism(s) • Viruses and bacteria -> T cell deficiency • Bacteria and fungi -> B cell/granulocytes deficiency – Sensitivity and type of treatment (surgery) – Family history
50
Give two general investigations of ID
* FBC and differential | * Exclusion of secondary immunodeficiency
51
Give four specific investigations for ID
* Test of humoral antibodies * Tests for cell mediated immunity * Tests for phagocytic cells Test for complement
52
What do you test for in cell mediated immunity?
• IgG, IgA, IgM (+/- IgE) • IgG1-4 subclasses • IgG levels to specific previous vaccines tetanus toxoid / HiB / pneumococcus measles , mumps, rubella • Measure antibody in response to “test” immunization
53
Where is CRP produced?
Liver
54
What is the role of CRP in the innate immune response?
CRP acts as an opsonin. | An opsonin binds to the microbial surface leading to enhanced attachment of phagocytes and clearance of microbes.
55
i. What triggers the production of CRP?
Microbial toxins – e.g. endotoxin – triggers the production of cytokines by monocytes and macrophages. These in turn circulate in the blood to the liver where they stimulate the production of the acute phase proteins.

Semester 3 - Infection (14 decks)

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