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Respiratory SB > Immunology > Flashcards

Immunology Flashcards

1
Q

what is Kostmann Syndrome

A

Severe chronic neutropenia

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2
Q

clinical presentation of Kostmann syndrome

A

Infections, usually within 2 weeks after birth
Fever
Failure to thrive
Oral ulceration

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3
Q

examples of opsonins

A

Complement C3b
IgG
CRP

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4
Q

what are examples of phagocyte receptors

A

Fc

CR1

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5
Q

features of Chronic granulomatous disease

A 
recurrent deep bacterial infections
recurrent fungal infections
failure to thrive 
Lymphadenopathy and hepatosplenomegaly
Granuloma formation
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6
Q

what is an investigation for chronic granulomatous disease

A

NBT test

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7
Q

defects in what network is linked to susceptibility to intracellular bacteria

A

IL 12 - gIFN

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8
Q

how can phagocyte recruitment be investigated

A

FBC
Presence of pus
Expression of neutrophil adhesion molecules

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9
Q

is there pus is chronic granulomatous disease

A

yes

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10
Q

what is Recricular dysgenesis

A 
Defects of haemopoetic stem cells
Failure of production of;
neutrophils
lymphocytes
monocyte/macrophages
platelets
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11
Q

what is the only treatment of recricular dysgenesis

A

bone marrow transplantation

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12
Q

what is severe combined

immunodeficiency

A

Failure of production of lymphocytes

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13
Q

what are abnormal presentations of SCID

A

unusual skin diseases

family history of early infant death

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14
Q

3-4 month old baby gets infection but is fine after - what disease is this

A

transient hypogammaglobulinaemia of infancy

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15
Q

what is transient hypogammaglobulinaemia of infancy

A

immune systems of 3-4 month old babies slow to mature

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16
Q

what is DiGeorge syndrome

A

development defect of 3rd/4th pharyngeal pouch

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17
Q

features of DiG syndrome

A

Low set ears abnormally folded ears, high forehead,
cleft palate, small mouth and jaw
Hypocalcaemia secondary to hypoparathroidism
Oesophageal atresia
T cell lymphopenia
Complex congenital heart disease

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18
Q

what is the IL12-gIFN network pathway

A

Infected macrophages stimulated to produce IL12
IL12 induces T cells to secrete gIFN
Then gIFN feeds back to macrophages and neutrophils
stimulates production of TNF
activates NADPH oxidase

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19
Q

what is essential investigation in T cell deficiencies

A

HIV test

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20
Q

what is Bruton’s X-linked hypogammaglobulinaemia

A

failure to produce mature B cells
no circulating B cells
no plasma cells
no circulating antibody after first 6 months

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21
Q

what are the 4 types of hypersensitivity reactions

A

Type I: Immediate hypersensitivity
Type II: Direct cell killing
Type III: Immune complex mediated
Type IV: Delayed type hypersensitivity

22
Q

what is angioedema

A

Self-limited, localised swelling of subcutaneous tissues or mucous membranes

23
Q

what is Spontaneous mast cell degranulation

A

Mast cells in the skin become very twitchy, if you touch them they degranulate.

24
Q

what are non-allergic causes of Spontaneous mast cell degranulation

A

drugs - opiates, aspirin, NSAIDS
thyroid disease
idiopathic
physical urticaria

25
Q

what is Samter’s triad

A

asthma, nasal polyps and salicylate sensitivity

26
Q

what test is the gold standard for diagnosing allergy

A

skin-prick test

27
Q

what are anti-histamines

A

H1 receptor antagoinsts

28
Q

what is used in anaphylaxis and how does it work

A

adrenaline

Acts on B2 adrenergic receptors to constrict arterial smooth muscle

29
Q

what are anaphylotoxins

A

Fragments of complement proteins released after activation

increase permeability of blood vessels

30
Q

what are some examples of Type II hypersensitivity diseases

A

Goodpasture’s syndrome
Guillan Barre syndrome
Systemic lupus erythematosus (SLE)

31
Q

what is acute hypersensitivity pneumonitis

A

Immune complexes deposited in the walls of alveoli and bronchioles

32
Q

what causes the wheeze in hypersensitivity pneumonitis

A

inflammation of terminal bronchioles and alveoli caused by activated phagocytes and complement

33
Q

what causes breathlessness in hypersensitivity pneumonitis

A

alveolitis caused by activated phagocytes and complement - results in decreased efficiency of gas transfer

34
Q

what causes malaise, pyrexia in hypersensitivity pneumonitis

A

systemic manifestation of inflammatory response

35
Q

what causes renal dysfunction

A

Deposition of IgG immune complexes

36
Q

what is the mechanism of type 4 hypersensitivity

A

Initial sensitisation to antigen
- generation of “primed” T cells

Subsequent exposure

  • activation of previously primed T cells
  • recruitment of macrophages, other lymphocytes, neutrophils
  • release of proteolytic enzymes, persistent inflammation
37
Q

what is variolation

A

The same organism is being administered as the one that can cause disease, but the route of administration is different

38
Q

when is there active transport of maternal IgG

A

3rd trimester

39
Q

what does breast milk contain especially colostrum

A

IgA

40
Q

what is IgA important for

A

colonisation of infant gi tract

41
Q

what class do all nucleated cells express

A

Class I

42
Q

what cells express Class II

A

Specialised antigen-presenting cells

43
Q

acute cellular rejection mechanism

A

Recognition of donor antigens by CD4+ cells
Activation of CD4+ cells
Production of cytokines
Recruitment and activation of macrophages and neutrophils
Type IV hypersensitivity response

44
Q

what are the symptoms of acute cellular rejection

A

Kidney transplant: Rise in creatinine, fluid retention, hypertension
Liver transplant: Rise in LFTs, coagulopathy
Lung transplant: breathlessness, pulmonary infiltrate

45
Q

hyperacute rejection

A

Rapid destruction of graft within minutes-hours

Mediated by pre-formed antibodies that react with donor cells

46
Q

why would an individual have preformed antibodies against donor cells

A

1) blood group antigens - naturally occurring preformed antibodies, bind surface molecules found on everything
2) HLA antigens - arise through previous exposure

47
Q

when does hyper acute rejection occur

A

recipient has pre-existing anti-donor HLA antibodies

recipient has different blood group

48
Q

what is the difference between hyper acute and acute vascular rejection

A

hyper acute the antibody is already there

vascular rejection antibody is made after transplantation

49
Q

what is chronic allograft failure

A

Cellular proliferation of smooth muscle of vessel wall - leads to blood vessel getting smaller.
Occlusion of vessel lumen

50
Q

what are side effects of immunosuppressive agents

A

Drug toxicity
Infection
Malignancy (cancer)
Atherosclerosis

51
Q

what are examples of side effects of immunosuppressive agents

A

Nephrotoxicity after non-renal transplantation

Ciclosporin associated gingival hypertrophy

52
Q

Form of SCID, causes skin rashes and infection across whole body

A

Graft versus host disease

Respiratory SB (14 decks)

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