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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
Q

What is a halo sign, seen on HRCT?

A

Alveolar haemorrhage, seen in invasive pulmonary Asperigllosis

26
Q

How are pts with phagocyte deficiencies managed?

A

Prophylactic Abx, antifungals and immunisations
Surgery
Interferon-g and steroids for CGD
Stem cell transplant

27
Q

What is Di George syndrome?

A

Lack of thymus

28
Q

What defects can cause severe combine immunodeficiency?

A

Stem cells defects or death of developing thrombocytes

29
Q

What disease is caused by defective genes for TCR rearrangement and T cell maturation?

A

Severe combined immunodeficiency and Omenn’s syndrome

30
Q

How do pts with severe combined immunodeficiency present?

A

Failure to thrive
Deep skin and organ abscesses
Decreased lymphocyte count
Increased susceptibility to bacterial, fungal and viral infections

31
Q

How are pts with severe combine immunodeficiency managed in the short and long term?

A

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
Q

What is the outcome of an opportunistic infection is left untreated in a pt with severe combine immunodeficiency disease?

A

Death

33
Q

What complement deficiency is associated with recurrent bacterial infection?

A

C3

34
Q

What can cause decreased production of immune components in secondary ID?

A 
Malnutrition
Infection
Liver disease
Lymphoproliferatife disease
Splenectomy
35
Q

What action does the spleen take against bloodborne pathogens?

A

Opsonises encapsulated bacteria

36
Q

What antibody production function is the spleen involved in?

A

Acute response: IgM production

Long term protection: IgG production

37
Q

Why might a pt need a splenectomy?

A 
Sickle cell anaemia --> infarction
Coeliac disease --> infarction
Infiltration by tumour
Autoimmune haemolytic disease
Trauma
38
Q

How will an asplenic pt present?

A

With encapsulated infections

Overwhelming post-splenectomy infection –> sepsis and meningitis

39
Q

How are asplenic pts managed?

A

Life-long penicillin prophylaxis
Immunisation against encapsulated bacteria
Medic alert bracelet

40
Q

Why are pts w/haematological malignancy more susceptible to infections?

A

Chemo-induced neutropenia
Chemo-induced damage to mucosal barriers
Insertion of vascular catheters used for Tx

41
Q

What should neutropenic sepsis be treated as and how?

A

Acute medical emergency

Immediate empiric Abx and assess septic complication risk

42
Q

How does liver disease cause secondary ID?

A

Decreased synthesis of complement and cytokines

43
Q

What can a cause increased loss or catabolism of immune components in secondary ID?

A

Protein losing conditions such as nephropathy, enteropathy or burns

44
Q

What are immunodeficiencies importantly associated with?

A

Increase in frequency and severity of infections
Autoimmune diseases
Malignancy

45
Q

What will the pattern and type of infections seen in ID always reflect?

A

Immunological defect

46
Q

What lab investigation approaches can be used in secondary ID?

A 
FBC
Test humoral immunity
Test cell-mediated immunity
Test for phagocytic cells
Test for complement components and function
Molecular testing
Gene mutations
47
Q

What definitive tests can be used in investigation of secondary ID?

A

Molecular testing

Gene mutations

48
Q

Why should tonsils and adenoids be large in infection?

A

They consist mainly of B cells

49
Q

What type of ID do recurrent viral and fungal infections indicate?

A

T cell deficiency

50
Q

What type of ID do recurrent bacterial and fungal infections indicate?

A

B cell/ granulocyte deficiency

51
Q

What might a pt with primary ID not present until aged 6 months?

A

Has some protection from maternal IgE antibodies

Semester 3 (50 decks)

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