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Semester 3 > Infection Session 10 > Flashcards

Infection Session 10 Flashcards

1
Q

How long is the delay between onset of symptoms and diagnosis of immunodeficiency which causes high morbidity and mortality?

A

7-9 years

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2
Q

What proportion of pts are diagnosed with immunodeficiency at 18 years or older?

A

> 50%

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3
Q

What percentage of immunodeficiency pts will have permanent tissue/organ damage as a result of being ID?

A

37%

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4
Q

What is the definition of an immunocompromised host?

A

State in which the immune system is unable to respond appropriately and effectively to infectious micro organisms

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5
Q

What is a qualitative immunocompromised host?

A

One defect of component of immune system e.g. HIV causing decreased CD4+ cells

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6
Q

What is a quantitative immunocompromised host?

A

More than one component of immune system defective

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7
Q

What does SPUR stand for in recognition and diagnosis of ID?

A

Severe (life threatening)
Persistent - despite Tx
Unusual - site of infection and causative organism
Recurrent

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8
Q

What is primary ID?

A

Inherited intrinsic defect of the immune system

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9
Q

What is secondary ID?

A

Underlying disease or condition affects immune components

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10
Q

Is primary or secondary ID more common?

A

Secondary

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11
Q

How are primary ID classified?

A

According to which immune component is defective

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12
Q

Which immune component defect causes the majority of primary ID?

A

B cell

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13
Q

Why do primary ID manifest in the first moths of life?

A

Intrinsic defects

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14
Q

What is the most common primary ID needing Tx?

A

Common variable ID where B cells don’t form plasma cells

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15
Q

Under what circumstance is IgA deficiency symptomatic?

A

If B cells don’t form IgA and there is an IgG subclass deficiency due to an unknown defect

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16
Q

What causes Bruton’s disease?

A

Impaired B cell development due to lack of enzyme

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17
Q

What is Hyper-IgM syndrome?

A

Defective CD40 ligand on activated T cells means IgM -X-> IgG so the IgM cannot enter tissues

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18
Q

What inherited intrinsic defects can cause primary ID?

A

Single gene defect
Polygenic
HLA polymorphisms

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19
Q

How does an underlying disease/chronic condition affect immune components?

A

Decreased production
Increased loss
Increase in catabolism

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20
Q

How do pts with primary antibody deficiencies present?

A

Recurrent bacterial URTI and LRTI
GI complications (inc. Giardia infection)
Arthropathies
Increased incidence of autoimmune disease
Increased incidence of lymphoma and gastric carcinoma

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21
Q

How are primary ID pts managed?

A

Prompt/prophylactic Abx
IRT (best Tx)
Manage resp infections and avoid unnecessary radiation

22
Q

Give some examples of phagocyte deficiencies.

A

Cyclic neutropenia
Leukocyte adhesion deficiency
Chronic granulomatous disease
Chediak-Higashi syndrome

23
Q

What happens to neutrophil number in cyclic neutropenia?

A

Decreases every 3/4 weeks

24
Q

How do pts with phagocyte deficiencies present?

A 
Ulcers of skin and mucous membranes
Osteomyelitis
Deep abscesses
Invasive pulmonary aspergillosis
Granulomas
25
What is a halo sign, seen on HRCT?
Alveolar haemorrhage, seen in invasive pulmonary Asperigllosis
26
How are pts with phagocyte deficiencies managed?
Prophylactic Abx, antifungals and immunisations Surgery Interferon-g and steroids for CGD Stem cell transplant
27
What is Di George syndrome?
Lack of thymus
28
What defects can cause severe combine immunodeficiency?
Stem cells defects or death of developing thrombocytes
29
What disease is caused by defective genes for TCR rearrangement and T cell maturation?
Severe combined immunodeficiency and Omenn's syndrome
30
How do pts with severe combined immunodeficiency present?
Failure to thrive Deep skin and organ abscesses Decreased lymphocyte count Increased susceptibility to bacterial, fungal and viral infections
31
How are pts with severe combine immunodeficiency managed in the short and long term?
Short term: no live vaccines, irradiated blood products, aggressive Tx of infections and infection prevention inc. IRT Long term: BM or stem cell transplant, gene therapy
32
What is the outcome of an opportunistic infection is left untreated in a pt with severe combine immunodeficiency disease?
Death
33
What complement deficiency is associated with recurrent bacterial infection?
C3
34
What can cause decreased production of immune components in secondary ID?
``` Malnutrition Infection Liver disease Lymphoproliferatife disease Splenectomy ```
35
What action does the spleen take against bloodborne pathogens?
Opsonises encapsulated bacteria
36
What antibody production function is the spleen involved in?
Acute response: IgM production | Long term protection: IgG production
37
Why might a pt need a splenectomy?
``` Sickle cell anaemia --> infarction Coeliac disease --> infarction Infiltration by tumour Autoimmune haemolytic disease Trauma ```
38
How will an asplenic pt present?
With encapsulated infections | Overwhelming post-splenectomy infection --> sepsis and meningitis
39
How are asplenic pts managed?
Life-long penicillin prophylaxis Immunisation against encapsulated bacteria Medic alert bracelet
40
Why are pts w/haematological malignancy more susceptible to infections?
Chemo-induced neutropenia Chemo-induced damage to mucosal barriers Insertion of vascular catheters used for Tx
41
What should neutropenic sepsis be treated as and how?
Acute medical emergency | Immediate empiric Abx and assess septic complication risk
42
How does liver disease cause secondary ID?
Decreased synthesis of complement and cytokines
43
What can a cause increased loss or catabolism of immune components in secondary ID?
Protein losing conditions such as nephropathy, enteropathy or burns
44
What are immunodeficiencies importantly associated with?
Increase in frequency and severity of infections Autoimmune diseases Malignancy
45
What will the pattern and type of infections seen in ID always reflect?
Immunological defect
46
What lab investigation approaches can be used in secondary ID?
``` FBC Test humoral immunity Test cell-mediated immunity Test for phagocytic cells Test for complement components and function Molecular testing Gene mutations ```
47
What definitive tests can be used in investigation of secondary ID?
Molecular testing | Gene mutations
48
Why should tonsils and adenoids be large in infection?
They consist mainly of B cells
49
What type of ID do recurrent viral and fungal infections indicate?
T cell deficiency
50
What type of ID do recurrent bacterial and fungal infections indicate?
B cell/ granulocyte deficiency
51
What might a pt with primary ID not present until aged 6 months?
Has some protection from maternal IgE antibodies

Semester 3 (50 decks)

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