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infection and immunity > Allergies And Immunocompromised Hosts > Flashcards

Allergies And Immunocompromised Hosts Flashcards

1
Q

Define hypersensitivity

A

The antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host

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2
Q

What are the 2 phases of allergic reaction?

A

Sensitisation phase - first exposure

Effector phase - re-exposure gives clinical manifestation eg. Anaphylaxis

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3
Q

What are the different types of hypersensitivity reactions?

A

Type 1 - immediate
Type 2 - antibody mediated
Type 3 - immune complex mediated
Type 4 - cell mediated

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4
Q

Describe type 1 hypersensitivity reactions

A

Allergies
Caused by environmental non-infectious antigens (allergens)
IgE produced

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5
Q

Describe a type II hypersensitivity reaction

A

Antibody mediated
Against tissue antigens
IgG/IgM

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6
Q

Describe a type III hypersensitivity reaction

A

Immune complexes mediated

Against soluble antigens

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7
Q

What is atopy?

A

Genetic predisposition of an individual to produce IgE against different allergens

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8
Q

What is a TH1 phenotype?

A

Less likely to get allergies

Protects against

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9
Q

Describe the type of person who is most likely to develop a TH1 phenotypes for allergies

A 
Large family
Live near overstock 
Variable GI flora
Low antibiotic use 
High likelihood of getting parasites 
Poorer sanitation 
(Exposed to more things)
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10
Q

What is the TH2 phenotype for allergies?

A

IgE production

More likely to develop allergies

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11
Q

Describe the type of person more likely to develop an allergy

A 
Urban homes
Small families
GI flora is stable - less diverse
High Abx use
Less likely to get parasites
Good sanitation
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12
Q

Name some common allergens

A 
House dust mites
Animals 
Tree/grass pollens 
Insect venom - wasp/bee stings
Medicines 
Chemicals
Foods
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13
Q

Describe the basis of clinical cross reactivity

A

If you allergic to one thing then you are more likely to become allergic to others

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14
Q

Where are mast cells located?

A

Next to vessels and in mucosal tissue

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15
Q

What enzymes are in mast cells?

A

Tryptase
Chymase
Carboxypeptidase

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16
Q

What are the toxic mediators of mast cells and what do they do?

A 
Histamine 
Heparin 
Toxic to parasites
Increase vascular permeability 
Vasodilation
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17
Q

What happens on the first exposure to an allergen?

A

Antigen specific IgEs start to be made

Coat the mast cells

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18
Q

What happens on the second exposure to allergens?

A

Allergen binds to specific IgEs on mast cells

Causes mast cell activation

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19
Q

What happens when mast cells are activated in the epidermis?

A

Urticaria (hives)
Itchy rash with reddish flare
Vasodilation

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20
Q

What happens following deep dermis activation of mast cells?

A

Angioedema
Non-itchy swelling
Can occur in lips, eyes, tongue and upper resp tract

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21
Q

What effects does the systemic activation of mast cells have?

A 
Hypotension 
Cardiovascular collapse
Generalised urticaria 
Angioedema
Breathing problems
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22
Q

What are the 3 rules for anaphylaxis?

A

Sudden onset of symptoms
Rapidly progressing
At least 2 organ systems involved

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23
Q

What occurs when mast cells are activated in the lungs?

A

Bronchoconstriction

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24
Q

What is the treatment of anaphylactic shock?

A

IM adrenaline

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25
Q

How does adrenaline help with anaphylaxis?

A

Vasoconstriction and increased force of myocardial contraction to increase BP
Bronchodilation
Inhibits mast cell activation

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26
Q

What do we need to monitor in anaphylaxis?

A

Pulse
BP
ECG
Oximetry - O2 sats

27
Q

What percentage of cases will have another anaphylactic response without re-exposure?

A

20%

28
Q

How do we diagnosis allergy?

A

Clinical Hx of atopy, allergens
Blood tests - allergic specific IgE, mast cell enzymes
Skin prick tests - wheel and flare reactions
Challenge tests - for food and drug allergies - risky

29
Q

How do you manage having an allergy?

A 
Allergen avoidance/elimination 
Education 
Medic alert identification
Antihistamines, steroids
Epipens 
Allergen desensitisation/immunotherapy
30
Q

Describe allergen desensitisation/immunotherapy

A

Administration of increasing doses of allergen extracts over a period of years
Hopefully to become desensitised so no longer allergic to these

31
Q

Describe a sickle cell crisis

A

Vaso-occlusive crisis
Painful episodes which can be very severe and can last up to a week
Caused by blocked blood vessels due to the sickle shaped cells
(rigid and sticky)

32
Q

Approximately how many primary immuno deficiencies are there?

A

> 300

33
Q

Why do many PIDs have permanent tissue/organ damage when diagnosed?

A

Takes a long time to diagnose
Often symptoms aren’t specific
Lots of PIDs

34
Q

Define immunocompromised

A

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

35
Q

What are primary immunodeficiencies?

A

Congenital
Due to intrinsic gene defect
Missing protein/cell or non-functional components

36
Q

What is a secondary immunodeficiency?

A

Acquired
Due to an underlying disease/treatment
Decrease production/function of immune components
OR
Increased loss or catabolism of immune components

37
Q

SPUR infections suggests underlying immune deficiency, what does it stand for?

A 
S = severe
P = persistent 
U = unusual (site/microorganism) 
R = recurrent
38
Q

What is a big warning sign for PIDs?

A

Family history of PID

39
Q

What are the limitations of the warning signs for PIDs?

A

Lack of population based evidence
Presentations are all different
Non-infectious manifestations

40
Q

What 3 things in children would lead you to think of PIDs?

A

Family Hx
Failure to thrive
Diagnosis of sepsis

41
Q

What is SCID?

A

Severe combined immunodeficiency
Combined T and B cell problem
15% of all PIDs

42
Q

65% of PIDs are …

A

Antibody deficiencies

43
Q

Give the most common PIDs

A 
Common variable immunodeficiency (CVID)
IgA deficiency 
IgG deficiency 
X linked agammaglubulinaemia 
Neutropenia
44
Q

If a PID manifested at the age of <6 months, what type would you expect it to be?

A

T cell or phagocyte defect

45
Q

If a PID manifested between the ages of 6 months and 5 years, what type would you expect it to be?

A

B cell/antibody or phagocyte defect

46
Q

If a PID manifested at the age of >5 years, what type would you expect it to be?

A

B cell/antibody or complement defect

Or actually a secondary ID

47
Q

Which pathologies suggest complement deficiencies and of which part?

A

Pyogenic infections (C3)
Meningitis/sepsis/arthritis (C5-9)
Angioedema (C1 inhibitor)

48
Q

Phagocytic defects tend to be found in which infections?

A

Skin/mucous infections
Deep seated infections
Invasive fungal infections

49
Q

What pathologies may suggest antibody deficiencies?

A 
Sinoresp infections 
Arthropathies
GI infections 
Malignancies
Autoimmunity
50
Q

What pathologies may suggest T cell defects?

A

Failure to thrive
Deep skin and tissue abscesses
Opportunistic infections

51
Q

What does it mean if people have a weak IgG response to vaccines?

A

Their B cells are affected

52
Q

What do you never give to people with T cell defects?

A

Live vaccines

53
Q

How do you manage PIDs?

A

Supportive - prophylactic Abx, treat infections promptly, nutritional support, CMV negative blood products only, avoid live vaccines
Specific - regular immunoglobulin therapy, haematopoietic stem cell therapy

54
Q

Describe immunoglobulin replacement therapy

A 
IgG from many donors
Make pt immune to the diseases the donors are immune to 
Life long treatment 
Improves quality of life
Can be IV or SC
55
Q

Which conditions have we found that immunoglobulin replacement therapy works against?

A

CVID (common variable)
Bruton’s disease (XLA)
Hyper IgM syndrome

56
Q

Give examples of things that can cause decreased production of immune components

A 
Malnutrition 
Infection
Liver diseases
Lymphoproliferative diseases
Splenectomy
57
Q

What are the functions of the spleen?

A

Clears blood-borne pathogens
Produces antibodies (IgM, IgG)
Splenic macrophages remove opsonised microbes and immune complexes

58
Q

Give some examples of encapsulated bacteria

A

H influenzae
Strep pneumoniae
Neisseria meningitidis

59
Q

What is OPSI?

A

Overwhelming post-splenectomy infection

Sepsis and meningitis

60
Q

What is the management for people without a spleen?

A

Penicillin prophylaxis
Immunisation against encapsulated bacteria a
Medic alert bracelet

61
Q

Why to haematological malignancies increase susceptibility to infections?

A

Chemo induced neutropenia
Damage to mucosal barriers
Vascular catheters

62
Q

What can give a pt an increased loss of immune components?

A

Protein losing conditions - nephropathy, enteropathy (eg. Crohn’s)
Burns

63
Q

Viral and fungal infections suggest which type of immune cell deficiency?

A

T cell

64
Q

Bacteria and fungal infections suggest which immune cell deficiency?

A

B cell
Or
Granulocyte

infection and immunity (9 decks)

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