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Week 5 Flashcards

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1
Q

What type of hypersensitivity reaction is Sarcoidosis?

A

Type IV (cell-mediated, delayed), disease of unknown cause

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2
Q

What pharmacological options are available in allergic reactions?

What about anaphylaxis?

A

Sodium cromoglycate - mast cell stabiilisers

Anti-histamines - H1 receptor antagonists

Leukotriene receptor antagonists - e.g. montelukast

Corticoseroids - anti-inflammatory effect

Anaphylaxis - IM adrenaline, acts on ß2 adrenoreceptors to constrict arterial smooth muscle and dilate bronchial smooth muscle

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3
Q

ILD is a very general grouping of diseases. What are some of these?

A

IPF - unknown origin

Sarcoidosis - multi-system granulomatous disorder, unknown origin

Hypersensitivity pneumonitis - allergic origin

Pneumoconiosis - occupational, mineral dusts

Connective tissue disease - Rheumatoid Arthritis (Type IV HS, autoimmune)

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4
Q

What do inflammatory mediators cause to happen in asthma, and how does this present clinically?

A

Muscle spasm - bronchoconstriction, wheeze

Mucosal inflammation - mucosal secretions and oedema, resulting in sputum production

Inflammatory cell infiltrate - lymphocytes and eosinophils invade, sputum appears yellow

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5
Q

What test can be done to determine acute anaphylaxis?

A

Tryptase test - peaks 1-2 hours after exposure to allergen

A rise in this mast cell-derived mediator only occurs in anaphylaxis

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6
Q

Where do B cells become activated?

A

They are presented with antigen in lymph nodes

Co-stimulation with this and T cells = rapid proliferation

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7
Q

Name some common respiratory problems in children

A

Croup

Respiratory Distress of the Newborn

Congenital diaphragmatic hernia

CF

Asthma

Bronchiolitis

Childhood pneumonia

TB

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8
Q

What are the secondary lymphoid organs?

A

This is where lymphocytes produced in the primary lymphoid tissues become activated

  • ​lymph nodes
  • tonsils
  • spleen
  • Peyer’s patches (lymphoid tissue found in the ileum)
  • mucosa-associated lymphoid tissue (MALT)
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9
Q

What is Bruton’s X-linked hypogammaglobulinaemia?

A

Failure to produce mature B cells, meaning…

  • No circulating B cells
  • No plasma cells
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10
Q

How would you test for Sarcoidosis?

What classical sign would be seen on a tissue biopsy taken from the lung of someone with Sarcoidosis?

A

Disease of exclusion…

  • tuberculin skin test
  • CXR
  • CT scan
  • tissue biopsy
  • lung function tests
  • blood tests

Classically presents with non-caseating granulomas (unlike TB, which is caseating)

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11
Q

What is Type III Hypersensitivity?

A

Immune-complex mediated

Antibodies in the presence of excess antigen form complexes that become trapped in vessels, joints and glomeruli

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12
Q

Croup - definition, clinical presentation, treatment

A

Definition

  • AKA laryngotracheobronchitis
  • Usually of viral origin, most commonly caused by parainfluenza, also caused by Influenza A+B, measles, RSV and adenovirus

Presentation

  • Young children
  • Stridor, barking cough
  • Difficulty breathing, usually worse at night

Treatment

  • Oral steroids to reduce inflammation
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13
Q

What is the most common cause of SCID?

A

X-linked SCID

Cause in 45% of all types of SCID

Mutation in a component of the IL2 receptor, resulting in an inability to respond to cytokines ⇒

  • failure of T cell and NK cell development
  • production of immature B cells
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14
Q

How do glucocorticoids treat asthma?

A

Decrease formation of Th2 cytokines (IL-4 and IL-5) and cause apoptosis

Prevent production of IgE

Reduce number of mast cells and decrease Fc epsilon expression

Prevent allergen-induced influx of eosinophils into the lungs and cause apoptosis

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15
Q

Names some types of Hypersensitivity Pneumonitis. What type of Hypersensitivity is this?

A

Types

  • Farmer’s Lung
  • Bird Fancier’s Lung
  • Cheese Worker’s Lung
  • etc. etc.

Type III Hypersensitivity - immune complexes form in the lungs and cannot be cleared

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16
Q

What are the 3 complement activating pathways?

What are the 4 things that happen following complement activation?

A

Classical - Antigen + Antibody + C1 complex (C1+C4-C2=C3)

Mannose-binding Lectin - MBL+Mannose-positive microbe

Alternative - Spontaneous C3 cleavage

4 things

  • Opsonisation
  • Direct killing (MAC)
  • Chemotaxis
  • Solubilisation of immune complexes
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17
Q

What cytokine released by CD4+ve cells triggers differentiation into Th2 helper cells?

A

IL-4

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18
Q

What do CD4+ve T cells do? What MHC do they recognise?

A

Immunoregulatory function

  • provide co-stimulatory signals to activate CD8 T cells and B cells
  • produce cytokines
  • regulate other lymphocytes and phagocytes

Recognise peptides presented on HLA class II molecules

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19
Q

What type of Hypersensitivity reaction is Hypersensitivity Pneumonitis? Examples?

A

Type III (immune-complex deposition)

Bird fanciers lung

Farmer’s lung

Cheese monger’s lung etc.

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20
Q

What are the primary lymphoid organs? What occurs here?

A

Bone marrow

  • Both B and T cells are created here, but only B cells mature here

Thymus

  • T cells mature here
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21
Q

Once differentiated, which interleukins does Th2 release? What are their functions?

A

IL-4, IL-5 and IL-13

IL-5 is involved in eosinophil recruitment

IL-4 and IL-13 are involved in mast cell recruitment

All three are involved in B cell maturation into plasma cells, which produce IgE

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22
Q

What substances do mast cells release? Both pre-formed and synthesised on demand

What are eosinophils important for?

A

Pre-formed

  • Histamine
  • Tryptase
  • Heparin

Synthesised on demand

  • Leukotrienes
  • Prostaglandins
  • Cytokines (incl. IL-4 and TNF alpha)

Important in parasite defence and wound healing

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23
Q

How is the complement pathway regulated?

A

Through negative feedback

Solubilisation of immune complexes that triggered the cascade in the first place switches off the process

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24
Q

Type III hypersensitivity treatment

A

Decrease inflammation - corticosteroids

Decrease antibody production - immunosuppression

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25
IPF - treatment
Steroids and immunosuppressants **do not** change the course of the disease New antifibrotic drugs - **Pirfenidone** and **Nintedanib**. Don't reverse the disease, just slow the progression Lung transplants in younger patients, give oxygen if hypoxic Median survival following IPF diagnosis is 4 years
26
What act as opsonins?
Complement (C3b) Antibodies Acute phase proteins e.g. CRP
27
Where are complement proteins produced?
In the liver
28
What are some key features of taking an allergic history?
Time, recurrence, symptoms What's the trigger? Is there a personal/family history of allergy? Does removal of the trigger improve the condition?
29
What is SCID? Clinical presentation
Severe Combined Immunodeficiency Defects in lymphoid precursors, meaning lymphocytes cannot be produced Clinical presentation * unwell by 3 months old * persistent diarrhoea * failure to thrive * infections of all kinds are common * "Unusual skin disease" * **Graft versus Host Disease** - colonisation of empty bone marrow by maternal lymphocytes * Family history of early infant death
30
Hypersensitivity Pneumonitis - acute presentation and treatment
Presentation * cough * breathlessness * fever * myalgia * crackles, no wheeze! * CXR shows widespread infiltrates * Typically occurs **several hours after exposure to allergen** (flu-like) Treatment * Oxygen * Steroids * Antigen avoidance
31
What is atelectasis?
Collapse/closure of a lung due to impaired or absent gas exchange. Usually unilateral, can be single lobes or whole lungs
32
What complement factors are involved in chemotaxis?
C3a C5a
33
What has happened here?
Diaphragmatic hernia 1/2400 births Most common on the left side
34
What is Type I Hypersensitivity?
Immediate hypersensitivity, as in allergic reactions IgE-mediated response to external antigen Very common Includes... * Asthma * Hayfever * Food and drugs allergies * Angioedema * Animal allergies
35
What is the chief component of photochemical smog?
Ozone (O3)
36
What are T lymphocytes involved in the defence against?
Intracellular pathogens Viruses
37
Systemic Lupus Erythematosis is a Type _ Hypersensitivity reaction
Type III Antibodies are produced against the contents of cell nuclei, complexes form Results in complement activation, inflammation, chemotaxis etc. Presents as a rash, renal impairment, fever due to complex deposition in small blood vessels and glomeruli
38
What is the classical radiological sign seen in Chronic Hypersensitivity Pneumonitis?
Honeycombing and air-trapping due to extensive fibrosis
39
Name some types of pneumoconiosis
Asbestosis Silicosis Berylosis Stanosis
40
What is DiGeorge syndrome? Where is the chromosomal abnormality?
Developmental defect of the 3rd/4th pharyngeal pouch, **deletion of chromosome 22q11** Causes a **failure of thymic development** Clinical presentation * "funny looking kid" - cleft palate, low set ears, high forehead, small mouth and jaw * congenital heart defects * psychiatric disorders * Recurrent/frequent viral, bacterial and fungal infections
41
Clinical presentation of chronic Sarcoidosis?
Lung infiltrates Skin infiltrations Peripheral lymphadenopathy Hypercalcaemia Other organs affected
42
What bacteria is most likely to cause pneumonia in the following age groups? Neonates Infants School Age
Neonates * *E. coli, Klebsiella, Staph aureus*, Guillan-Barre Syndrome Infants * *Strep pneumoniae, Chlamydia* School age * *Strep pneumoniae, Staph aureus*, Group A strep, *Bordetella, Mycoplasma, Legionella*
43
Clinical presentation of acute sarcoidosis?
Erythema nodosum Bilateral hilar lymphadenopathy Arthritis Uveitis, parotitis Fever
44
What are some clinical examples of Type II hypersensitivity reactions in... Blood cells Kindeys Nervous System Endocrine System Skin
Blood - transfusion reaction, autoimmune haemolytic anaemia Kidneys - Goodpasture's syndrome Nervous system - Guillan-Barre Endocrine system - Grave's disease
45
Sarcoidosis - treatment
Acute - usually self-limiting, steroids can be given if vital organs are affected Chronic - steroids required, as well as immunosuppression (azathioprine, methotrexate, anti-TNF therapy)
46
What are the clinical features of a Type I Hypersensitivity reaction?
Occurs quickly following exposure May be associated with one or more organ system Presentation is influenced by site of contact Threshold for reactions may be influenced by outside factors e.g. exercise, temperature, alcohol etc.
47
Type IV Hypersensitivity - examples, both autoimmune and non-autoimmune
Autoimmune * Type 1 diabetes * Psoriasis * Rheumatoid arthritis Non-autoimmune * TB * Sarcoidosis * Leprosy * Cellular rejection of solid organ transplant
48
Name some B cell maturation defects
SCID - failure of lymphocyte precursors X-linked agammglobulinaemia - failure of B cell maturation CVID - Failure of IgG production (low leves of IgA and IgM also seen) X-linked hyper IgM syndrome (failure of T cell co-stimulation) Selective IgA deficiency - failure of IgA production
49
What are the features characteristic of early and late stage ILD? What is acute ILD exemplified by?
Early - alveolitis - injury with inflammatory cell infiltration Late - fibrosis Acute ILD is exemplified by Acute Respiratory Distress Syndrome
50
What % of babies is Respiratory Distress of the Newborn seen in?
1% of all births
51
Why does SCID not present for the first 3 months?
Maternal IgG acts to protect the neonate during this time peroid. NB - even normal babies can get infections at 3-4 months if their immune system is slow to mature.
52
Hypersensitivity Pneumonitis - chronic presentation and treatment
Presentation * Progressive breathlessness over years * May be crackles, clubbing is rare * CXR shows pulmonary fibrosis, **most commonly in the upper zones** * Lung function tests show restrictive pattern Treatment * As with acute, but **make sure antigen is removed**
53
What is the gold standard of testing for allergies? What needs to be kept in mind?
Skin-prick test Drugs can influence the response * antihistamines should be discontinued for at least 48 hours prior to testing * corticosteroids have no influence on skin prick tests
54
Other than IgE-mediated allergic reactions, what are some other causes of spontaneous mast cell degranulation?
Drugs - opiates, aspirin, other NSAIDs Thyroid disease Ideopathic Physical urticaria i.e. in response to heat/pressure
55
What is the name of the condition that asbestosis exposure predisposes to? How long does it take to develop?
Mesothelioma 20-30 years
56
What's the most common ILD?
Ideopathic Pulmonary Fibrosis (IPF)
57
What might be the cause of low levels of IgA, IgG and IgE? How might this present?
Common variable immunodeficiency (CVID) Presents with... * Recurrent bacterial infections, often with severe end-organ damage * Bronchiectasis * Persistent sinusitis * Recurrent GI infections Disease mechanism of CVID is unknown
58
What commonly used drug might asthmatics need to be careful of? What could this result in in severe cases?
**Aspirin**-induced asthma - affects approximately 20% of asthmatics Characterised by wheeze up to 3 hours after ingestion Triggered by a few NSAIDs, especially ibuprofen and diclofenac **Samter's Triad -** 2-3% of asthmatics, presents as asthma, nasal polyps and salicylate sensitivity (present in aspirin, other NSAIDs and some food stuffs)
59
What receptor do mast cells express? What causes the degranulation of mast cells?
Fc episolon receptor 1 (FceR1), binds to Fc region of IgE antibodies IgE binds to mast cells with no great consequence, until it **re-encounters the allergen.** This causes disruption of the mast cell membrane and release/synthesis of mediators
60
Mnemonic for remembering types of hypersensitivity?
A, B, C, D A - Type I - Allergic reaction B - Type II - antiBody C - Type III - immune Complex D - Type IV - Delayed
61
Reticular Dysgenesis (again) - what is it?
Defects in haematopoetic stem cells Unable to generate... * neutrophils * lymphocytes * monocytes/macrophages * platelets Fatal, unless corrected with bone marrow transplant
62
What do CD8+ve T cells do? What What MHC do they recognise? What are they particularly important in defending against?
Function * Specialised cytotoxic T cell * Kills via * pore-forming - perforin * triggering apoptosis * secreting cytokines Recognise peptides presented on **HLA class I molecules** Particularly important in defending against viral antigens and tumours
63
What is Type II Hypersensitivity?
Direct cell killing - antibody binds to cell-surface antigen, resulting in complement activation and opsonisation
64
Which resp diseases CANNOT be treated with steroids?
Sleep apnoea Uncomplicated infection IPF
65
What is Type IV Hypersensitivity?
Delayed type, mediated by T cells Imbalance in immune response
66
IPF - clinical presentation
Progressive breathlessness Clubbing, bilateral basal crackles Restrictive lung pattern Bilateral infiltrates on CXR CT scan shows **honeycombing**

Respiratory (11 decks)

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