respiratory_week_5_20190518190157 Flashcards
what is an allergy
IgE mediated antibody response to external antigen (allergen)
what is the role of T lymphocytes in allergy
TH2 cells provide help for B cells to make IgE antibody
what is the role of mast cells in allergy
produce vasoactive substances (histamine typtase, heparin, leukotrienes, prostaglandin, IL-4 and TNFalpha)also express receptors for Fc region of IgE on surface
residual IgE antibodies bind to circulating mast cells via Fc receptor with no great consequence until re-encounter with allergen - what happens
allergen binds to IgE coated mast cells which causes release of vasoactive mediators as well as increased cytokines and leukotriene transcription
what symptoms occur within minutes of release of vasoactive mediators
urticaria (hives, rash, blisters)angiodema (swelling)asthma allergic rhinitis, conjunctivitis anaphylaxis
how to block mast cell activation (management)
mast cell stabilisers (sodium cromoglycate)
how to prevent effects of mast cell activation (management)
antihistamines (H1 receptor antagonists) or leukotriene receptor antagonists (montelukast)
use of anti-inflammatory agents in management
corticosteroids - inhibit formation of inflammatory mediators (platelet activating factor, prostaglandins and cytokines)
how to treat anaphylaxis
self injectable adrenaline - acts on B2 adrenergic receptors to constrict arterial smooth muscle - increases BP and dilates bronchial SM (decreasing airflow obstruction)
how does immunotherapy work
subcutaneous injection of tiny amounts of allergen, gradual increase in dose, immune deviation and this may lead to inhibition of anaphylaxis
what is the onset of type 1 - immediate hypersensitivity (allergy)
seconds (if IgE performed)
what is infectious trigger of type 1
parasites (e.g. schistosomiasis)
what is the environmental trigger of type 1
allergens e.g. dust mite, animal dander, pollen, peanut
what is the adaptive immune mediators of type 1
TH2 cells, B cells, IgE
what is the innate immune mediators of type 1
mast cells, eosinophils
what is onset of type 2 (bound antigen)
seconds (if IgG or IgM is performed)
what is environmental trigger of type 2
immune haemolytic anaemias
what is autoimmune conditions of type 2
graves disease (hyperthyroidism) and good pastures syndrome (bleeding in lungs and kidneys - causes glomerulonephritis and pulmonary haemorrhage)
what is adaptive immune mediators of type 2
B cells, IgG / IgM
what is innate immune mediators of type 2
complement, phagocytes
what is onset of type 3 (immune complex)
hours (if IgG performed)
what is infectious trigger of type 3
post-streptococcal glomerulonephritis
what is environmental trigger of type 3
farmers lung
what is immune conditions of type 3
SLE (lupus) - auto antibodies against nuclear antigens, increase risk of CVDmanagement: limit sun, hydroxychloroquine, corticosteroids, immunosuppressive agents or inhibit B cell proliferation
what is adaptive immune mediators of type 3
B cells, IgG
what is innate immune mediators of type 3
complement, neutrophils
what is onset of type 4 (DTH, delayed hypersensitivity)
2-3 days
what is infectious trigger of type 4
hepatitis B virus
what is environmental trigger of type 4
contact dermatitis, sarcoidosis
what is autoimmune conditions of type 4
type I diabetes, coeliac disease, Rh arthritis
what is adaptive immune mediators of type 4
TH1 cells
what is innate immune mediators of type 4
macrophages
what is harmful autoimmunity (presence of immune response against self tissues)
high titres of auto-antibodies or auto-reactive T cells
what is IPEX syndrome
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)
what is the symptoms of IPEX syndrome
severe infection, intractable diarrhoea, eczema and diabetes
what is treatment and cure of IPEX syndrome
treatment - immunosuppressive drugs or total parental nutritioncure - hematopoetic stem cell transplantation
how can autoimmunity be caused by HLA genes (MHC proteins)
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
how can autoimmunity be caused by genes determining sex
sexual bias in predisposing genetic factors and there is different hormonal influences on lymphocyte function in male and females
what type of autoimmunity is acute rheumatic fever
molecular mimicry (shared antigenic epitopes)
what type of autoimmunity is reactive arthritis following bacterial infection
molecular mimicry - sterile inflammation secondary to bacterial infection, susceptibility associated with inheritance of certain MHC class I, notably HLA-B27
what kind of infections can tigger reactive arthritis
gut infections, sexually acquired infection, viruses and bacteria (streptococcus)
how can autoimmune disorders be caused by antigen sequestration
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
what is examples of immunosuppressive agents
azathioprine, mycophenolate or cyclophosphamide
what is interstitial disease
any disease process affecting lung interstitium (i.e. alveoli, terminal bronchi) and interferes with gas transfer so restrictive lung pattern
what is symptoms of ILD
breathlessness, dry cough
what is sarcoidosis
type 4 hypersensitivity disease, multi system disease, non-caseating granuloma and less common in smokers
what is symptoms of acute sarcoidosis
erythema nodosum, bilateral hilar lymphadenopathy, arthritis, uveitis, parotitis and fever
what is symptoms of chronic sarcoidosis
lung infiltrates (alveolitis), skin infiltrations, peripheral lymphadenopathy, hypercalcaemia
how is sarcoidosis diagnosed
CXR (hilar lymphadenopathy), CT, tissue biopsy (granuloma), pulmonary function, blood test (ACE levels, raised calcium, increased inflammatory markers)
what is the treatment of acute sarcoidosis
self-limiting condition, usually no treatment but steroids if vital organs affected
what is treatment of chronic sarcoidosis
oral steroids usually needed for immunosuppression (azathioprine, methotrexate, anti-TNF therapy)
what is extrinsic allergic alveolitis (hypersensitivity pneumonitis)
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)
what is signs of acute extrinsic allergic alveolitis
cough, breathlessness, fever, myalgiapyrexia, crackles (no wheeze), hypoxia
what does acute extrinsic allergic alveolis look like on chest X ray
widespread pulmonary infiltrates
what is treatment for acute extrinsic allergic alveolitis
oxygen, steroid and antigen avoidance
what is the sings of chronic extrinsic allergic alveolitis
progressive breathlessness an cough, may be crackles, clubbing unusual, small airways, interstitium and occasional granulomas
what does chronic extrinsic allergic alveolitis look like on CXR
pulmonary fibrosis more common in upper zones
what is used in the diagnosis of chronic extrinsic allergic alveolitis
history of exposure, precipitins (IgG antibodies) or lung biopsy if in doubt
what is treatment of chronic extrinsic allergic alveolitis
remove antigen exposure, oral steroids if breathless or low gas transfer
what is signs of idiopathic pulmonary fibrosis (IPF) - most common ILD
progressive breathlessness, dry cough, clubbing, bilateral fine inspiratory crackles
what is results of IPF pulmonary function test
restrictive defect (reduced FEV1 and FVC, high or low ratio, low gas transfer)
what does IPF look like on CXR
bilateral infiltrates
what does IPF look like on CT scan
reticulnodular fibrotic shadowing (worse at lung base and periphery), traction bronchiectasis, honey-combing cystic changes
what is the pathology of IPF
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)
what is treatment of IPF
pirfenidone and nintedanib, oxygen if hypoxic
what is pneumoconiosis
lung disease caused by mineral dust exposureL asbestos, coal workers lung or silicosis
what is simple coal workers pneumoconiosis
CXR abnormality only
what is complicated coal workers pneumoconiosis
progressive massive fibrosis - restrictive pattern with breathlessness
what is caplans syndrome (coal workers)
combination of rheumatoid and pneumoconiosis - pulmonary nodules
what is silicosis
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
where is asbestos found
mining, construction, ship building, boilers and piping
what is the stages in pleural disease caused by asbestos
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
what other diseases can be caused by asbestos
pulmonary fibrosis, partial pleural plaques, bronchial carcinoma (risk multiplies in smokers)
what kind of asbestos is safe and unsafe
serpentine (curved) asbestos safestraight (amphibole) asbestos dangerous
what is respiratory distress in newborn
relative surfactant (phospholipid, apoproteins, production stimulated by steroids) deficiency
what is treatment of respiratory distress in newborn
ventilation, increased O2
what is signs of chronic lung disease in newborn
oxygen requirement beyond 36 weeks plus evidence of pulmonary parenchymal disease on CXR, follows RDS, barotrauma, volume trauma and high inspired O2
when does chronic pulmonary disease heal
heals with growth over 2-3 years - often wheezy
what is a diaphragmatic hernia in a neonatal
neonate with severe breathing difficulty, mostly posterolateral, left sided
what is complication of diaphragmatic hernia
associated pulmonary hypoplasia (pressure on lung bud by hernia - can’t develop well)
what is treatment of diaphragmatic hernia
respiratory control or surgery
what is transient tachypnoea of newborn
high breathing rate often due to presence of lung fluid - grunting shortly after delivery (often delivered by LUSCS for maternal reasons)
what would cystic fibrosis look like in one year old child
1 year old child presenting with prolonged history of cough, loose stools and failure to thrive
what would cystic fibrosis look like in newborn infant
raised immuno-reactive trypsin level on neonatal screening who is also found to be homozygous for F508 gene
respiratory disease caused by which bacteria are the most prominent in cystic fibrosis
staph aureus
what is the stages of asthma management in children
1 - b2 agonists when needed2 - regular inhaled steroids3A - regular inhaled steroids and LABA3B - 3A and leukotriene antagonists 4 - high dose steroids
how does bronchiolitis present
6 week old present with increased work of breathing and possible apnoea, more severe in younger babies, ex prem and family of smokers
what is symptoms of bronchiolitis
tachypnoea (rapid breathing), poor feeding, irritating cough
how does pneumonia present
10 yo with cough, high fever and sputum, previously well, dullness on percussion, increased vocal fremitus and resonance and bronchial breathing
what types of pneumonia on neonates
GBS, e.coli, klebsiella, staph aureus
what types of pneumonia in infants
strep pneumoniae, chlamydia
what types of pneumonia in school age
strep pneumoniae, staph aureus, group A strep, bordetella, mycoplasma, legionella
what is croup and how does it present
viral laryngotracheobronchitis, presents as stridor and barking cough
what is treatment of croup
oral steroids to reduce inflammation
what is rhinitis
acute or chronic inflammation of nasal mucosa - rhinorrohea (runny nose), sneezing, itching, nasal congestion and obstruction
what are the different classifications of allergic rhinitis
seasonal (SAR), perennial (PAR) and episodic (EAR)
what are the steps in allergic rhinitis
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
what is non-allergic rhinitis
does not involve IgE
what are the different causes of non-allergic rhinitis
infectious rhinitishormonal imbalance vasomotor rhinitis (cause idiopathic)non allergic rhinitis with eosinophilia syndrome (NARES)medication e.g. aspirin
what is occupational rhinitis
may involve allergic and non allergic compounds
what does rhinitis and rhinorrhoea do to blood flow and vessels
increased mucosal blood flow, increase blood vessel permeability or both - increases volume of nasal mucosa and cause difficulty breathing in
what is the anti-inflammatory treatment of rhinitis
glucocorticoids (beclometasone, fluticasone and prednisone)
what is the mediator receptor blockade treatment of rhinitis
H1 receptor antagonists (antihistamines - reduce effect of mast cells - e.g. azelastine (nasal) ioratidine, fexofenadinea nd cetirizine)CysLT1 receptor antagonists
what is the nasal blood flow treatment in rhinitis
vasoconstrictors (e.g. oxymetazoline)mimic effect of noradrenaline (activation of a1-adrenoceptors)
what is the anti-allergic treatment in rhinitis
sodium cromoglicate
