Respiratory Flashcards

Question

ARDS Management

Answer 1

Generally need ICU admission Reverse Hypoxia Organ support Treat the cause Possible evidence for prone positioning and muscle relaxation

Answer 2

Hypersensitivity reaction in response to colonisation of resp tract with Aspergillus fumigatus

Answer 3

Unlikely to occur in those without risk factors Asthma - thick mucus in airways makes it harder to clear fungus CF - impaired mucous clearance and airways inflammation Atopy history - Aspergillus acts as antigen inducing TH2 cells to produce eosinophils Other possible risk factors: 1. HLA associations - DR2 or DR5 2. IL-10 promoter polymorphisms 3. CFTR gene mutations 4. Surfactant protein polymorphisms

Answer 4

In those with risk factors inhalation of spores trigger a T1HS reaction. Aspergillus acts as antigen stimulating TH2 cells to secrete cytokines. These promote IgE and IgG synthesis - these enhance eosinophil production and survival. These cause mediator release and vasoldiation with bronchoconstriction Inflammation causes mucus production, airways hyperreactivity and bronchiecstasis.

Answer 5

New or worsening cough with inc sputum (brown / black) Wheeze Blood (inflammation and bronchiecstasis) Chest Pain Weight loss fever Occasionally may get associated chronic rhinosinusitis (allergic aspergillus sinusitis) To diagnose 1. Skin Test - positive hypersensitivity to fungus - not specific 2. Bloods - IgG and IgE against fungus. Serum total IgE. Eosinophilia (steroids mask this) 3. CXR (Upper / middle lobe infiltrates). CT

Answer 6

Initially - Steroids and adjunctive antifungal (if very poor functional status) Remission - Maintenance of inhaled steroids If cannot be weaned off of steroids without remission - Faily oral steroids and omalizumab (anti IgE therapy)

Answer 7

Bronchiectasis - mostly central Fibrosis Reps failure Pulm HTN Side effects related to steroids.

Answer 8

Genetics + Env + Immunological Env - allergens, resp infections, tobacco, occupational exposure. Antenatal smoking and RSV infection in pregnancy. Immune - Asthma is the imabalance of immune response. This leads to cytokine production (IL 4,5 and 13) which causes eosinophilic inflammation and IgE production.

Answer 9

"Chronic inflammatory disorder secondary to T1HS" Airway inflammation - pro-inflammatory mediators cause airway oedema, mucuous and constriction. Bronchoconstriction - contraction of smooth muscle secondary to mediatiors Hyper-responsiveness - excessive narrowing of airways to stimuli. Mucous production and airway remodelling - chronic inflammation leads to changes in the airway wall. These include subepithelial fibrosis, inc msucle muss, gland hypertrophy and angiogenesis.

Answer 10

1. Intermittent - less than once a week. Normal Pulm function between episodes. Nocturnal symptoms less than 2x a month 2. Mild Persistent - More than once a week but less than once a day. More than 2x a month nocturnally. Normal Pulm function tests. 3. Moderate Persistent - Daily with the use of SABA. Nocturnal symptoms more than once a week FEV1 and PEFR netween 60-80% predicted 4. Severe Perisistent - Continuous daily symptoms limiting activity. Under 60% predicted pulm function

Answer 11

FeNo - fractional exhaled nitric oxide. This is produced by nitric oxide synthase and one of these rises when there is rise in eosinophils. Over 17 - All need FeNO and BDR 5-16 = all should have BDR. FeNo if there is normal spirometry or obstructive but with normal BDR Under 5 - clinical judgement

Answer 12

FeNO - over 40ppb or 35 in kids FEV1/FVC under 70% BDR - improvement of 12% FEV1 or 200ml in adults. 12% or more in kids only.

Answer 13

Step up each time not controlled or if symptoms more than 3x a week / night time waking 1. SABA 2. SBA and low dose ICS 3. SABA + low does ICS + LTRA 4. SABA + low dose ICS +LABA continue LTRA if worked) 5. Switch ICS and LABA for MART (includes the low dose ICS) 6. increase MART to mod dose ICS 7. Add either ICS to high dose (not as MART), LAMA / theophylline or specialist referral Low dose ICS - under 400mcg budenoside Mod - 400-800mmcg High os over 800mcg

Answer 14

Status asthamticus - severe persistent Asthma attack Pneumonia COPD Pneumothorax Osteoporosis - steroids Anxiety and depression

Answer 15

Irreversibly dilated Bronchi + chronic Bronchial Inflammation and infection Can be localised (one lobe) or generalised A deficit of mucociliary clearance +/- immune function = microorganisms acquisition, colonisation and infection = chronic inflammation = dilation and thickening or bronchi = bronchial wall oedema = more infection = cycle repeats

Answer 16

Idiopathic - 45% Post infection Immunodeficiency COPD Connective tissue disorders ABPA Ciliary issues Asthma IBD Aspiration A1AT Pinks yellow Nail syndrome congenital malformation

Answer 17

Chronic Producitve couch + recurrent chest infections up to 50% may have haemoptysis Other: Chest Pain GORD - 20-40% Rhinosinusitis On exam: Crackles clubbing and wheeze Investigation - CXR, Sputum culture. High res CT (best) On CT: 1. Bronchoarterial ratio over 1 - this is signet ring sign (lumen is alrger than artery) 2. Lack of tapering - bronchi should get smaller as they get closer to periphery 3. Bronchus visible within 1cm of pleural surface Once diagnosed: 1. Bloods - IgE, FBC and investigate for ABPA. Serum IgG and IGA + IgM - screen for immunodeficiency

Answer 18

Diffuse interstitual lung disease which affects distal brocnhioles, alveolar ducts + wall. Unknown cause 50-60 y/o with cough, SoB, fever and malaise with no response to abx. Leukocytosis on bloods and elevated ESR and CRP. Bilateral patchy or diffuse consolidation / ground glass on imaging Treat as watch and wait or high dose steroids if severe

Answer 19

Small to medium vasculitis. Pathogenesis: 1. Prodromal allergic phase - asthma 2. Eosinophilic phase - tissue infiltration with eosinophils - gastroenteritis / pneuomonia 3. Vasculitic phase - endothelial damage - purpura, neuropathy and organ damage Unknown cause but thought to be related to genes, env, immune (pANCA + high IgE) with infection can trigger

Answer 20

Also called Hypersensitivity Pneumonitis. Induced by immune response to rpt inhalation of antigens Farmers lung, bird fanciers lung, Malt workers lung or issues with air conditioning Acutely present with - 4-8 hour after expsosure - cough fever, malaise and SoB. Reslves after 1-2 days Chronic - cough, weight loss, clubbing and pulm fibrosis

Answer 21

Antigen Exposure - small particles that can reach alveoli Sensitisation - particles are processed by APC (antigen presenting cells) and present to T lymphocytes. These become activate and release cytokines. Acute Inflammatory reaction - On re-exposure an inflammatory response is mounted. Leads to neutrophilic infiltration in alveoli leading to alveolitis. There is increased vasc permeability causing fluid accumulation in alveoli (impaired gas exchange) Chronic Inflammation and Fibrosis - Repeated exposure causes lymphocytic alvooelitis and granuloma formation. Causes pulm fibrosis

Answer 22

Bloods FBC - normocytic anaemia and inc WCC ABG Imaging CXR HRCT - can be normal. Lung function - acute phase it is restrictive. In chronic will turn into obstructive Management Avoid causative agent Steroids - note IPF is not steroid responsive. In EAA these need to be tapered down.

Answer 23

Farmers Lung - Saccharopolyspora rectivirgula Malt - Aspergillus Clavatus Mushroom - Thermophillic