Resp A-C Flashcards

1
Q

What is the definition of allergic rhinitis?

A

Inflammation of membrane of the nose. Intermittent (<4d/wk, <4wk) or persistent. May be seasonal or perennial.

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2
Q

What is the background of allergic rhinitis?

A

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.

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3
Q

What is the history and exam findings in allergic rhinitis?

A

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.

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4
Q

Which investigations do you use for allergic rhinitis?

A

Skin prick tests, specific IgE.

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5
Q

What is the management of allergic rhinitis?

A

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

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6
Q

What are the complications and prognosis of allergic rhinitis?

A

Poor QOL, problems in school

Most diminish or disappear with age

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7
Q

What is the definition of asthma?

A

Chronic inflammatory airway disease with hyperresponsiveness, bronchial inflammation and variable reversible bronchoconstriction.

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8
Q

What is the background of asthma?

A

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

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9
Q

What is the history and exam findings in asthma?

A

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)

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10
Q

Which investigations do you use for asthma?

A

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.

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11
Q

What is the management of acute asthma?

A

Acute:

ABCDE approach and consider resus transfer if severe.

O SI HAM:

  1. Oxygen, +GET ABG asap
  2. Salbutamol+Ipratropium bromide: try spacer OR Nebulise

· BURST: 10 puffs (or neb) 3 times, back to back within 40 min

  1. Hydrocortisone (IV) or oral prednisolone
  2. 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.

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12
Q

What is the management of chronic asthma?

A

Chronic: Stepwise treatment

  1. SABA (salbutamol)
    • preventer steroid inhaler 200 budesonide
    • add on therapy (LABA/Theophylline +/- increase steroids to 400)
  2. Increase steroid to 800 ug/d
    • oral prednisolone
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13
Q

What are the complications and prognosis of asthma?

A

Decreased growth, psychosocial, risk of death in respiratory distress, increased infections, chest wall deformity

Often remits during puberty. Good prognosis with good treatment.

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14
Q

What’s the definition of acute bronchiolitis?

A

Respiratroy condition characterized by coryza followed by a persistent dry, wheezy cough, breathlessness, poor feeding and hyperinflation of the chest in infants (<1yo).

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15
Q

What’s the background of acute bronchiolitis?

A

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.

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16
Q

What would you see on history and exam in acute bronchiolitis?

A

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)

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17
Q

What investigations would you use in acute bronchiolitis?

A

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

18
Q

What is the management of acute bronchiolitis?

A

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.

19
Q

What are the complications and prognosis of acute bronchiolitis?

A

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.

20
Q

What’s the definition of Chronic lung disease of prematurity (CLD)?

A

Oxygen requirement at corrected age of term with characteristic radiological findings (bronchopulmonary dysplasia)

21
Q

What’s the background of Chronic lung disease of prematurity (CLD)?

A

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.

22
Q

What would you see on history and exam in Chronic lung disease of prematurity (CLD)?

A

Respiratory side well managed by ventilation, but some babies will have poor weight gain, and chronic recession.

23
Q

What investigations would you use in Chronic lung disease of prematurity (CLD)?

A

ABG: compensatory respiratory acidosis.

CXR: characteristic hyperinflation and cystic changes. Determines severity and distinguishes from alectasis, pneumonia or air leak syndrome.

24
Q

What is the management of Chronic lung disease of prematurity (CLD)?

A

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.

25
Q

What are the complications and prognosis of Chronic lung disease of prematurity (CLD)?

A

Increased RSV infection risk (-> ? Pavalizumab?).

Pulmonary HTN -> Cor pulmonale -> HF.

Severely affected children may require life O2 therapy.

26
Q

What’s the definition of Croup (Acute Laryngotracheobronchitis)?

A

Progressive inflammation (larynx -> trachea -> bronchi) secondary to viral infection (parainfluenza, RSV, influenza).

27
Q

What’s the background of Croup?

A

6m-5yos. Occurs in winter months.

Parainfluenza, RSV, Influenza

DD of stridor must be kept in mind. Stridor is present in any condition causing narrowing of subglottal area:

· Epiglottitis: Quick onset drooling, stridor, no cough, toxic

· Anaphylaxis: allergy, exposure, odema

· Foreign body: sudden, clear hx

· Tracheitis: croupy cough, toxic child

· Diphteria: rare, check immunization status

28
Q

What would you see on history and exam in Croup?

A

Coryza: flu feeling, poor feeding and fever for 1-3 days preceding symptoms.

Then…

  1. Laryngitis: barking, croupy cough and hoarse voice
  2. Tracheitis: stridor starting 1-2d after cough
  3. Bronchitis: increased respiratory effort

DO NOT examine throat directly to avoid precipitating obstruction.

Classified with scores 0-3 on 4 categories: Stridor, Recession (subcostal, tracheal tug, severe w/ ac muscle use), Color of skin/cyanosis, Level of consciousness.

Mild <4, Moderate 4-5, Severe>5

29
Q

What investigations would you use in Croup?

A

Clinical diagnosis, seldom blood tests.

30
Q

What is the management of Croup?

A

Mild<4: managed at home with careful observation. Planty of fluid. Paracetamol.

Moderate4-5: Oral steroids and nebulized budesonide improve outcome

Severe>5: Nebulised adrenaline with O2, urgent transfer to PICU for intubation.

31
Q

What are the complications and prognosis of Croup?

A

Upper airway obstruction

Usually lasts 2-3 days but can last weeks.

32
Q

What’s the definition of Cystic fibrosis?

A

Autosomal recessive disease by mutation of chlorine channel gene leading to hyperviscous secretions.

33
Q

What’s the background of Cystic fibrosis?

A

Common genotype in 80% - phenylalanine deletion at chromosome 7q positon 508, coding for abnormal transporter CFTR.

Pathophysiology: Low Cl- and Na+ transport out of cells. This fails to drag water across into mucus secretions, leading to hyperviscosity. Lung is normal at birth but then secretions become viscous. Patients get recurrent Staph areus, H. Inf and Pseudomonas infecitons due to impaired clearance. Pancreatic insufficiency causing early DM, malabsorption and steathorrea due to reduced enzyme delivery.

Epidemiology

1/2500 live births, 1/25 carriers.

34
Q

What would you see on history and exam in Cystic fibrosis?

A

Neonatal: 15% have meconium ileus

Infancy: recurrent chest infections and failure to thrive, delay.

Older: asthma, ABPA (brown sputum with fever and wheeze), sinusitis.

Signs of malnutrition: low muscle mass

Clubbing, hyperinflation, coarse crepitaitons, expiratory rhonchi.

May have jaundice, nasal polyps and rectal prolapse.

35
Q

What investigations would you use in Cystic fibrosis?

A

Sweat test is gold standard, low Na and Cl in sweat.

Lung function: obstructive, low FVC and low FEV FVC ratio.

Guthrie’s test: high serum immunoreactive trypsin

Antenatal test: first trimester CVS / second trimester low intestinal ALP in amniotic fluid.

36
Q

What is the management of Cystic fibrosis?

A

Respiratory: Flucox prophylaxis, nebulized antibiotics (colomycin) when pseudomonas infection, ABPA requires steroids and itraconazole, bronchodilators if asthmatic, nebulized recombinant DNAase used as a mucolytic.

Nutritional: high calorie, high protein diet. Creon (pancreatic enzyme) and vitamin supplementation.

Immunisations: usual schedule and pneumococcal/influenza.

Physiotherapy: twice a day for mucous movement

HLT: if lung function deteriorates,

Gene therapy: viral vectors for CFTR gene replacement with normal CF gene. Still research.

37
Q

What are the complications and prognosis of Cystic fibrosis?

A

Respiratory: L pneumonia, cronchiectasis, cor pulmonale, PTX, haemoptysis.

GI: cirrhosis, portal HTN, DM, obstruction.

Endocrine: DM, low fertility. Psychological.

Median life 40y, children with pseudomonas have higher mortality over 8y.

38
Q

What is anaphylaxis?

A
  • Definition: a severe, life-threatening generalised or systemic hypersensitivity reaction
  • Causes rapid onset compromise of the airway with skin/mucosal signs
39
Q

What is the pathophysiology of anaphylaxis?

A

In children, 85% of anaphylaxis is caused by food allergy
o Most are IgE-mediated reactions
• Other causes: Insect stings, Drugs. Latex, Exercise, Inhalant allergens, Idiopathic
• Most paediatric anaphylaxis occurs in children < 5 years of age, when food allergy is most
prevalent

40
Q

What are the S/S of anaphylaxis?

A

o Airway
▪ Throat and tongue swelling
▪ Difficult breathing and swallowing
▪ Feels throat is closing up
▪ Hoarse voice
▪ Stridor
o Breathing
▪ Shortness of breath
▪ Tachypnoea
▪ Wheeze
▪ Exhaustion
▪ Cyanosis
▪ Respiratory arrest
o Circulation
▪ Pale, clammy
▪ Tachycardia
▪ Collapse
▪ Decreased consciousness
• Skin and/or mucosal changes
o Flushing
o Urticaria
o Angioedema
• Gastrointestinal symptoms
o Vomiting
o Abdominal pain
o Incontinence

41
Q

What is the assessment of Anaphylaxis?

A

• Treat as MEDICAL EMERGENCY
• Assess using ABCDE approach
o Call for help
o Airway: look for and relieve obstruction, swelling, hoarseness, stridor, intubate if
necessary
o Breathing: check if normal, tachypnoea, wheeze, cyanosis, SaO2 <92%
▪ If unresponsive and not breathing normally
• Start CPR immediately
• Ensure help of on the way because advanced life support is essential
▪ If CPR is not required
• Examine chest for signs of airway obstruction
Differential diagnosis:
anaphylaxis
Ÿ Acute asthma attack
Ÿ Faint (vasovagal syncope)
Ÿ Panic attack
Ÿ Breath-holding attack
Ÿ Idiopathic urticaria/angioedema
• Check pulse and blood pressure for circulatory collapse
• Check skin and inside the mouth for urticaria and angio-oedema
o Circulation: pale, clammy, hypotension, drowsy, coma
o Disability: conscious level
o Exposure: urticaria, angioedema

42
Q

What is the management of anaphylaxis?

A

• Place in a comfortable position
o Sitting up if airway and breathing difficult
o Lying flat with/without leg elevation if low bp/feeling faint
o Recovery position if breathing but unconscious
• Give IM adrenaline 1:1000 (as per age-related guidelines)
o Dosage
▪ < 6 years: 150 ug IM
▪ 6 – 12 years: 300 ug IM
▪ > 12 years: 500 ug IM
o Given in the thigh
o Assess response after 5 mins
o Repeat IM injection at 5 min intervals until there has been as adequate response
o Do NOT give IV adrenaline in primary care – but may be given in cases of
cardiopulmonary arrest (specialist only)
• Remove trigger if possible e.g. stinger after a bee sting
• Establish airway
• Give high flow oxygen
• Give IV fluid challenge: 20ml/kg crystalloids
• Chlorpheniramine IM or slow IV
o < 6 months: 250 ug/kg
o 6 months – 6 years: 2.5mg
o 6 – 12 years: 5mg
o > 12 years: 10mg
• Hydrocortisone IM or slow IV
o < 6 months: 25mg
o 6 months – 6 years: 50mg
o 6 – 12 years: 100mg
o > 12 years: 200mg
• Consider salbutamol if wheeze
• Monitor
o Pulse oximetry
o ECG
o Blood pressure
• Observe for 6-12 hours from onset of symptoms as biphasic reactions can occur
• Long term
o Once acute situation has been dealt with, management involves detailed strategies
and training for allergen avoidance, a written management plan with instruction for
treatment of allergic reaction and provision of an adrenaline auto-injector (EpiPen)