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respiratory_week_5_20190518190157 Flashcards

1
Q

what is an allergy

A

IgE mediated antibody response to external antigen (allergen)

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2
Q

what is the role of T lymphocytes in allergy

A

TH2 cells provide help for B cells to make IgE antibody

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3
Q

what is the role of mast cells in allergy

A

produce vasoactive substances (histamine typtase, heparin, leukotrienes, prostaglandin, IL-4 and TNFalpha)also express receptors for Fc region of IgE on surface

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4
Q

residual IgE antibodies bind to circulating mast cells via Fc receptor with no great consequence until re-encounter with allergen - what happens

A

allergen binds to IgE coated mast cells which causes release of vasoactive mediators as well as increased cytokines and leukotriene transcription

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5
Q

what symptoms occur within minutes of release of vasoactive mediators

A

urticaria (hives, rash, blisters)angiodema (swelling)asthma allergic rhinitis, conjunctivitis anaphylaxis

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6
Q

how to block mast cell activation (management)

A

mast cell stabilisers (sodium cromoglycate)

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7
Q

how to prevent effects of mast cell activation (management)

A

antihistamines (H1 receptor antagonists) or leukotriene receptor antagonists (montelukast)

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8
Q

use of anti-inflammatory agents in management

A

corticosteroids - inhibit formation of inflammatory mediators (platelet activating factor, prostaglandins and cytokines)

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9
Q

how to treat anaphylaxis

A

self injectable adrenaline - acts on B2 adrenergic receptors to constrict arterial smooth muscle - increases BP and dilates bronchial SM (decreasing airflow obstruction)

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10
Q

how does immunotherapy work

A

subcutaneous injection of tiny amounts of allergen, gradual increase in dose, immune deviation and this may lead to inhibition of anaphylaxis

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11
Q

what is the onset of type 1 - immediate hypersensitivity (allergy)

A

seconds (if IgE performed)

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12
Q

what is infectious trigger of type 1

A

parasites (e.g. schistosomiasis)

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13
Q

what is the environmental trigger of type 1

A

allergens e.g. dust mite, animal dander, pollen, peanut

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14
Q

what is the adaptive immune mediators of type 1

A

TH2 cells, B cells, IgE

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15
Q

what is the innate immune mediators of type 1

A

mast cells, eosinophils

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16
Q

what is onset of type 2 (bound antigen)

A

seconds (if IgG or IgM is performed)

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17
Q

what is environmental trigger of type 2

A

immune haemolytic anaemias

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18
Q

what is autoimmune conditions of type 2

A

graves disease (hyperthyroidism) and good pastures syndrome (bleeding in lungs and kidneys - causes glomerulonephritis and pulmonary haemorrhage)

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19
Q

what is adaptive immune mediators of type 2

A

B cells, IgG / IgM

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20
Q

what is innate immune mediators of type 2

A

complement, phagocytes

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21
Q

what is onset of type 3 (immune complex)

A

hours (if IgG performed)

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22
Q

what is infectious trigger of type 3

A

post-streptococcal glomerulonephritis

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23
Q

what is environmental trigger of type 3

A

farmers lung

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24
Q

what is immune conditions of type 3

A

SLE (lupus) - auto antibodies against nuclear antigens, increase risk of CVDmanagement: limit sun, hydroxychloroquine, corticosteroids, immunosuppressive agents or inhibit B cell proliferation

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25
Q

what is adaptive immune mediators of type 3

A

B cells, IgG

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26
Q

what is innate immune mediators of type 3

A

complement, neutrophils

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27
Q

what is onset of type 4 (DTH, delayed hypersensitivity)

A

2-3 days

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28
Q

what is infectious trigger of type 4

A

hepatitis B virus

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29
Q

what is environmental trigger of type 4

A

contact dermatitis, sarcoidosis

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30
Q

what is autoimmune conditions of type 4

A

type I diabetes, coeliac disease, Rh arthritis

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31
Q

what is adaptive immune mediators of type 4

A

TH1 cells

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32
Q

what is innate immune mediators of type 4

A

macrophages

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33
Q

what is harmful autoimmunity (presence of immune response against self tissues)

A

high titres of auto-antibodies or auto-reactive T cells

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34
Q

what is IPEX syndrome

A

caused by single gene defect mutation in FOXP3 which essential for development of regulatory T cellsresults in failure of peripheral tolerance (inactivation of self-reactive lymphocytes)

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35
Q

what is the symptoms of IPEX syndrome

A

severe infection, intractable diarrhoea, eczema and diabetes

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36
Q

what is treatment and cure of IPEX syndrome

A

treatment - immunosuppressive drugs or total parental nutritioncure - hematopoetic stem cell transplantation

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37
Q

how can autoimmunity be caused by HLA genes (MHC proteins)

A

complex genetic interplay AD’s has been associated with different variants of the HLA genes, particularly, class II genes which are presented on antigen presenting cells

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38
Q

how can autoimmunity be caused by genes determining sex

A

sexual bias in predisposing genetic factors and there is different hormonal influences on lymphocyte function in male and females

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39
Q

what type of autoimmunity is acute rheumatic fever

A

molecular mimicry (shared antigenic epitopes)

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40
Q

what type of autoimmunity is reactive arthritis following bacterial infection

A

molecular mimicry - sterile inflammation secondary to bacterial infection, susceptibility associated with inheritance of certain MHC class I, notably HLA-B27

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41
Q

what kind of infections can tigger reactive arthritis

A

gut infections, sexually acquired infection, viruses and bacteria (streptococcus)

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42
Q

how can autoimmune disorders be caused by antigen sequestration

A

brain, eyes and testes never normally exposed to immune system but if injury occurs and immune cells reach these tissues then abnormal, hyper-responses will take place causing damage

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43
Q

what is examples of immunosuppressive agents

A

azathioprine, mycophenolate or cyclophosphamide

44
Q

what is interstitial disease

A

any disease process affecting lung interstitium (i.e. alveoli, terminal bronchi) and interferes with gas transfer so restrictive lung pattern

45
Q

what is symptoms of ILD

A

breathlessness, dry cough

46
Q

what is sarcoidosis

A

type 4 hypersensitivity disease, multi system disease, non-caseating granuloma and less common in smokers

47
Q

what is symptoms of acute sarcoidosis

A

erythema nodosum, bilateral hilar lymphadenopathy, arthritis, uveitis, parotitis and fever

48
Q

what is symptoms of chronic sarcoidosis

A

lung infiltrates (alveolitis), skin infiltrations, peripheral lymphadenopathy, hypercalcaemia

49
Q

how is sarcoidosis diagnosed

A

CXR (hilar lymphadenopathy), CT, tissue biopsy (granuloma), pulmonary function, blood test (ACE levels, raised calcium, increased inflammatory markers)

50
Q

what is the treatment of acute sarcoidosis

A

self-limiting condition, usually no treatment but steroids if vital organs affected

51
Q

what is treatment of chronic sarcoidosis

A

oral steroids usually needed for immunosuppression (azathioprine, methotrexate, anti-TNF therapy)

52
Q

what is extrinsic allergic alveolitis (hypersensitivity pneumonitis)

A

type III hypersensitivity reaction (restrictive)caused by thermophilic actinomycetes (farmers lung, malt workers, mushroom workers) avian antigens (bird fanciers lung) and drugs (gold, bleomycin, sulphasalazine)

53
Q

what is signs of acute extrinsic allergic alveolitis

A

cough, breathlessness, fever, myalgiapyrexia, crackles (no wheeze), hypoxia

54
Q

what does acute extrinsic allergic alveolis look like on chest X ray

A

widespread pulmonary infiltrates

55
Q

what is treatment for acute extrinsic allergic alveolitis

A

oxygen, steroid and antigen avoidance

56
Q

what is the sings of chronic extrinsic allergic alveolitis

A

progressive breathlessness an cough, may be crackles, clubbing unusual, small airways, interstitium and occasional granulomas

57
Q

what does chronic extrinsic allergic alveolitis look like on CXR

A

pulmonary fibrosis more common in upper zones

58
Q

what is used in the diagnosis of chronic extrinsic allergic alveolitis

A

history of exposure, precipitins (IgG antibodies) or lung biopsy if in doubt

59
Q

what is treatment of chronic extrinsic allergic alveolitis

A

remove antigen exposure, oral steroids if breathless or low gas transfer

60
Q

what is signs of idiopathic pulmonary fibrosis (IPF) - most common ILD

A

progressive breathlessness, dry cough, clubbing, bilateral fine inspiratory crackles

61
Q

what is results of IPF pulmonary function test

A

restrictive defect (reduced FEV1 and FVC, high or low ratio, low gas transfer)

62
Q

what does IPF look like on CXR

A

bilateral infiltrates

63
Q

what does IPF look like on CT scan

A

reticulnodular fibrotic shadowing (worse at lung base and periphery), traction bronchiectasis, honey-combing cystic changes

64
Q

what is the pathology of IPF

A

usual interstitial pneumonia pattern, sub pleural and basal fibrosis, heterogenous fibrosis in alveolar walls and honeycombing (terminally lung structure replaced by dilated spaces surrounding fibrous walls)

65
Q

what is treatment of IPF

A

pirfenidone and nintedanib, oxygen if hypoxic

66
Q

what is pneumoconiosis

A

lung disease caused by mineral dust exposureL asbestos, coal workers lung or silicosis

67
Q

what is simple coal workers pneumoconiosis

A

CXR abnormality only

68
Q

what is complicated coal workers pneumoconiosis

A

progressive massive fibrosis - restrictive pattern with breathlessness

69
Q

what is caplans syndrome (coal workers)

A

combination of rheumatoid and pneumoconiosis - pulmonary nodules

70
Q

what is silicosis

A

caused by inhalation of crystalline silica dust (mining, foundry, glass or boiler workers) and is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs

71
Q

where is asbestos found

A

mining, construction, ship building, boilers and piping

72
Q

what is the stages in pleural disease caused by asbestos

A

1) benign pleural plaques - asymptomatic 2) acute asbestos pleuritic - fever, pain, bloody PE3) PE and diffuse pleural thickening - restrictive impairment 4) malignant mesothelioma - incurable pleural cancer - presents with chest pain and PE

73
Q

what other diseases can be caused by asbestos

A

pulmonary fibrosis, partial pleural plaques, bronchial carcinoma (risk multiplies in smokers)

74
Q

what kind of asbestos is safe and unsafe

A

serpentine (curved) asbestos safestraight (amphibole) asbestos dangerous

75
Q

what is respiratory distress in newborn

A

relative surfactant (phospholipid, apoproteins, production stimulated by steroids) deficiency

76
Q

what is treatment of respiratory distress in newborn

A

ventilation, increased O2

77
Q

what is signs of chronic lung disease in newborn

A

oxygen requirement beyond 36 weeks plus evidence of pulmonary parenchymal disease on CXR, follows RDS, barotrauma, volume trauma and high inspired O2

78
Q

when does chronic pulmonary disease heal

A

heals with growth over 2-3 years - often wheezy

79
Q

what is a diaphragmatic hernia in a neonatal

A

neonate with severe breathing difficulty, mostly posterolateral, left sided

80
Q

what is complication of diaphragmatic hernia

A

associated pulmonary hypoplasia (pressure on lung bud by hernia - can’t develop well)

81
Q

what is treatment of diaphragmatic hernia

A

respiratory control or surgery

82
Q

what is transient tachypnoea of newborn

A

high breathing rate often due to presence of lung fluid - grunting shortly after delivery (often delivered by LUSCS for maternal reasons)

83
Q

what would cystic fibrosis look like in one year old child

A

1 year old child presenting with prolonged history of cough, loose stools and failure to thrive

84
Q

what would cystic fibrosis look like in newborn infant

A

raised immuno-reactive trypsin level on neonatal screening who is also found to be homozygous for F508 gene

85
Q

respiratory disease caused by which bacteria are the most prominent in cystic fibrosis

A

staph aureus

86
Q

what is the stages of asthma management in children

A

1 - b2 agonists when needed2 - regular inhaled steroids3A - regular inhaled steroids and LABA3B - 3A and leukotriene antagonists 4 - high dose steroids

87
Q

how does bronchiolitis present

A

6 week old present with increased work of breathing and possible apnoea, more severe in younger babies, ex prem and family of smokers

88
Q

what is symptoms of bronchiolitis

A

tachypnoea (rapid breathing), poor feeding, irritating cough

89
Q

how does pneumonia present

A

10 yo with cough, high fever and sputum, previously well, dullness on percussion, increased vocal fremitus and resonance and bronchial breathing

90
Q

what types of pneumonia on neonates

A

GBS, e.coli, klebsiella, staph aureus

91
Q

what types of pneumonia in infants

A

strep pneumoniae, chlamydia

92
Q

what types of pneumonia in school age

A

strep pneumoniae, staph aureus, group A strep, bordetella, mycoplasma, legionella

93
Q

what is croup and how does it present

A

viral laryngotracheobronchitis, presents as stridor and barking cough

94
Q

what is treatment of croup

A

oral steroids to reduce inflammation

95
Q

what is rhinitis

A

acute or chronic inflammation of nasal mucosa - rhinorrohea (runny nose), sneezing, itching, nasal congestion and obstruction

96
Q

what are the different classifications of allergic rhinitis

A

seasonal (SAR), perennial (PAR) and episodic (EAR)

97
Q

what are the steps in allergic rhinitis

A

1) inhalation increases specific IgE2) IgE binds to mast cells and basophils3) re-exposure cause made cell and basophil degranulation4) release of mediators (histamine, cysLTs, tryptase, prostaglandins) causing itching, sneezing, rhinorrhoea and nasal congestion5) delayed response by recruitment of lymphocytes and eosinophils to nasal muscosa contribute to congestion

98
Q

what is non-allergic rhinitis

A

does not involve IgE

99
Q

what are the different causes of non-allergic rhinitis

A

infectious rhinitishormonal imbalance vasomotor rhinitis (cause idiopathic)non allergic rhinitis with eosinophilia syndrome (NARES)medication e.g. aspirin

100
Q

what is occupational rhinitis

A

may involve allergic and non allergic compounds

101
Q

what does rhinitis and rhinorrhoea do to blood flow and vessels

A

increased mucosal blood flow, increase blood vessel permeability or both - increases volume of nasal mucosa and cause difficulty breathing in

102
Q

what is the anti-inflammatory treatment of rhinitis

A

glucocorticoids (beclometasone, fluticasone and prednisone)

103
Q

what is the mediator receptor blockade treatment of rhinitis

A

H1 receptor antagonists (antihistamines - reduce effect of mast cells - e.g. azelastine (nasal) ioratidine, fexofenadinea nd cetirizine)CysLT1 receptor antagonists

104
Q

what is the nasal blood flow treatment in rhinitis

A

vasoconstrictors (e.g. oxymetazoline)mimic effect of noradrenaline (activation of a1-adrenoceptors)

105
Q

what is the anti-allergic treatment in rhinitis

A

sodium cromoglicate

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