Resp A-C Flashcards
What is the definition of allergic rhinitis?
Inflammation of membrane of the nose. Intermittent (<4d/wk, <4wk) or persistent. May be seasonal or perennial.
What is the background of allergic rhinitis?
10% have seasonal, 10% perennial in population. Increasing prevalence.
Parental atopy. More likely in first born children. Associated with allergic conjunctivitis, asthma, otitis media.
Allergen binds to IgE on mast cells leading to chronic inflammation -> hypertrophy in nasal tributaries -> increased production of mucous.
What is the history and exam findings in allergic rhinitis?
Itchy nose, rhinorrhea, itchy eyes, sore throat, cough, bad morning breath.
Allergic nasal crease, purple rims under eyes, infra orbital skin fold, mouth breathing. Pale hypertrophied internal nasal turbinaries.
If polyps, think of cystic fibrosis and aspirin sensitive asthma in older child.
Which investigations do you use for allergic rhinitis?
Skin prick tests, specific IgE.
What is the management of allergic rhinitis?
Avoidance: limit being outside when pollen, shower after getting inside, window filters, wear glasses outside. HDM: covers on sofas and bed, remove cuddly toys, acaricidal spray.
Antihistamines: non sedating, remove itch
Steroid nasal spray: v effective
Decongestants: recommended only in short term due to rebound congestion
LKT receptor antagonists: work in synergy with antihistamines
Immunotherapy: for tolerance, sublingual
What are the complications and prognosis of allergic rhinitis?
Poor QOL, problems in school
Most diminish or disappear with age
What is the definition of asthma?
Chronic inflammatory airway disease with hyperresponsiveness, bronchial inflammation and variable reversible bronchoconstriction.
What is the background of asthma?
10-15% prevalence. More in urban areas.
80% of those who receive a diagnosis symptomatic by age of 5.
FHx of atopy or asthma. ‘Hygiene hypothesis’.
Triggers for attacks: smoking (active or passive) cold, stress, exercise, inhalant allergy.
Pathophysiology: contact with inhalant allergen leds to increased airway receptor responsiveness and constriction of airway. Increased mucous production and cell infiltration
What is the history and exam findings in asthma?
Recurrent nocturnal cough, wheeze (Exercise induced), recurrent URTIs
Assess severity by aksing about frequency and length of attacks, hospital attendance, effect on school.
Expiratory wheeze, anterolateral recession of thorax, accessory muscle use, tachypnea, diminished air entry, tachycardia.
Severe attack: tachycardia, tachypnea, PEF<50%, too breathless to speak
Life threatening attack: cyanosis, silent chest, poor respiratory effors, coma, PEF<33% (BTS guidelines)
Which investigations do you use for asthma?
PEF (in >5yo): bidaily for 14d, large variation in PEF.
CXR: in acute or severe cases to exclude pneumothoras
LFT (spirometry) not in acute phase, to monitor progression and tx. >5y. Obstructive picture: FVC normal or low, FEV/FVC ratio reduced.
What is the management of acute asthma?
Acute:
ABCDE approach and consider resus transfer if severe.
O SI HAM:
- Oxygen, +GET ABG asap
- Salbutamol+Ipratropium bromide: try spacer OR Nebulise
· BURST: 10 puffs (or neb) 3 times, back to back within 40 min
- Hydrocortisone (IV) or oral prednisolone
- Salbutamol IV – SE: decrease K, hyperglycaemia, lactic acidosis
OR Aminophylline IV – SE: cardiac arrhythmias
OR Magnesium sulphate IV – SE: Hypotension
Discharged when PEF>75% on 3-4h inhaler only. Check inhaler technique/adherence.
What is the management of chronic asthma?
Chronic: Stepwise treatment
- SABA (salbutamol)
- preventer steroid inhaler 200 budesonide
- add on therapy (LABA/Theophylline +/- increase steroids to 400)
- Increase steroid to 800 ug/d
- oral prednisolone
What are the complications and prognosis of asthma?
Decreased growth, psychosocial, risk of death in respiratory distress, increased infections, chest wall deformity
Often remits during puberty. Good prognosis with good treatment.
What’s the definition of acute bronchiolitis?
Respiratroy condition characterized by coryza followed by a persistent dry, wheezy cough, breathlessness, poor feeding and hyperinflation of the chest in infants (<1yo).
What’s the background of acute bronchiolitis?
Aetiology
Usually RSV (>75%) but there may be multiple causative agents.
Due to inflammation of the bronchioles with secretion of mucus, necrosis of epithelium and odema of submucosa causing obstruction.
Epidemiology
RF: permaturity, CLD, heart defects, immunodeficiency. Smoking household. Breastfeeding is protective.
What would you see on history and exam in acute bronchiolitis?
History
Cough, breathlessness and wheeze. Hx of coryza. May be too breathless to feed.
Examination
General: mild pyrexia, irritable.
Breathing: tachypnea, recession, nasal flaring and grunting, expriatory wheeze WITH crepitations and crackles (differentiate form asthma/viral induced wheeze by presence of crackles)
What investigations would you use in acute bronchiolitis?
Bloods: not indicated if mild, high WCC, low O2 high CO2, may have low Na due to SIADH.
CXR not indicated in mild disease, may have hyperinflation and right upper lobe collapse, see if any focus of bacterial infection.
Serology for RSV from NPA
What is the management of acute bronchiolitis?
Admission: feeding difficulty, grunting, recession, sats<95%.
Support via:
· Nasal cannula with O2,
· Consider NG or use IV fluids if not feeding.
· Bronchodilators may only have short term benefir.
· Ventilaiton may be necessary if sats <92% despote O2, if there are signs of exhaustion or recurrent aopneas.
Prevention: Pavalizumab (mAb for RSV) in high risk infants.
What are the complications and prognosis of acute bronchiolitis?
Death 0.2%, pICU admission and ventilation in 2%.
Poor feeding for 1 week, persistent cough for 2 weeks. May predispose to further viral induced wheeze in childhood. No clear link with later asthma.
What’s the definition of Chronic lung disease of prematurity (CLD)?
Oxygen requirement at corrected age of term with characteristic radiological findings (bronchopulmonary dysplasia)
What’s the background of Chronic lung disease of prematurity (CLD)?
Aetiology
Occurs in premature infants:
· Barotrauma or volutrauma from PPV at birth
· Low nutritional supplementation at birth
· High O2 levels given at birth
· Secondary free radical production to all the above
Pathophysiology: hypothesized to be related to free radical formation in response to the above stimuli. These disrupt membrane lipids and lead to bad lung development.
Histopathology: interstitial odema, mucosal metaplasia and interstitial fibrosis. Alveoli are overdistended.
Epidemiology
Occurs in premature infants, inversely proportional to gestational age.
What would you see on history and exam in Chronic lung disease of prematurity (CLD)?
Respiratory side well managed by ventilation, but some babies will have poor weight gain, and chronic recession.
What investigations would you use in Chronic lung disease of prematurity (CLD)?
ABG: compensatory respiratory acidosis.
CXR: characteristic hyperinflation and cystic changes. Determines severity and distinguishes from alectasis, pneumonia or air leak syndrome.
What is the management of Chronic lung disease of prematurity (CLD)?
Can not withdraw ventilation as it is necessary for life in preterm infants.
Closely monitor ventilation, maintain pH, pCO2 and pO2 within strict ranges. No evidence for high frequency ventilation.
Nutritional support, parenteral nutrition.
Surfactant therapy at birth in preterm within 2h, early extubation for nasal CPAP in RDS.
Steroids ONLY ot be used in ventilator dependent neonates.