Paeds Resp Flashcards

1
Q

What is the difference between wheeze and stridor?

A

Wheeze is an obstruction of the lower respiratory tract and stridor is obstruction outside of the chest. Wheeze is heard as a continuous whistling noise heard more on expiration. Stridor is a high-pitched sound heard more in inspiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three main causes of a wheeze?

A

Viral induced wheeze
Asthma
Persistent infantile wheeze - happy wheezers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the differentials for an acute wheeze?

A

Foreign body: Sudden onset wheezing, choking, stridor

Pneumonia: Auscultatory crackles, Fever

Bronchiolitis: Seasonal pattern, Nasal flaring & Intercostal recessions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the differentials for a chronic wheeze?

A

Asthma: Episodic pattern, Cough &Response of bronchodilators

CF

Vascular ring: Exacerbated by neck flexion & Relieved by neck hyperextension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the three main differentials for stridor?

A

Croup

Epiglottitis

Bacterial tracheitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What suggests croup in a child presenting with stridor?

A

Seasonal pattern
Barking cough
Temp <38.5
Harsh rasping stridor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What suggests Epiglottitis in a child presenting with stridor?

A

Stridor
Drooling - due to inability to swallow
Sudden onset over hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What suggests Bacterial tracheitis in a child presenting with stridor?

A

High fever
Appears very ill
Rapidly progressive airway obstruction + thick secretions
Caused by staph aureus
IV Abx and intubation/ventilation if required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When is the peak incidence of croup?

A

6 months to 3 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the RFs for croup?

A

Young

Male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the aetiology of croup?

A

Parainfluenza virus types 1 or 3
RSV
Influenza A and B
Adenovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the clinical presentation of croup?

A
Barking cough
Stridor
Hoarse voice
Respiratory distress (Tracheal tug, Chest recessions, Tachypnea)
Lethargy 
Symptoms worse at night 
Agitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What investigations would you do in suspected croup?

A

CRP
FBC
U+Es

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you manage croup?

A
Single dose of oral dexamethasone 0.15mg/kg
Nebulised adrenaline 
Temporary relief of symptoms
Supportive 
Kept calm 
O2 therapy if required 
Call ENT/Anaesthetist = airway support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is epiglottitis?

A

Intense swelling of the epiglottis causing upper airway obstruction
Caused by h. Influenzae - which is now vaccincated against
Very acute onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the presentation of epiglottitis?

A

Sore throat in a septic looking child
Child unable to speak or swallow (drooling)
Sitting upright, immobile with open mouth to optimise airway
Soft inspiratory stridor, increases resp distress, little or no cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you manage epiglottitis?

A

Do not examine throat is suspected
Call anaesthetics and ENT surgeon
IV cefotaxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is whooping cough?

A

Pertussis (also known as whooping cough) is an upper respiratory tract infection (URTI) characterised by a severe cough. Bordetella pertussis is the typical aetiological agent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the presentation of pertussis?

A

Catarrhal stage (Coryza for 7 days)
Inspiratory whoop (forced inhalation against a closed glottis)
Spasms of cough – worse at night, cause vomiting, cyanosis, epistaxis and subconjunctival haemorrhages.
Paroxysmal phase 3-6 weeks but can persist for months (100 day cough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What investigation do you undertake in pertussis?

A

Nasal swab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you manage pertussis?

A

< 1 month old Azithromycin 5 days
>1 month old Azithromycin/ Erythromycin 7 days or Trimethoprim for 7 days if abx resistance
School exclusion

22
Q

What is bronchiolitis?

A

Most common LRTI in children
Increases incidence in winter
90% 1-9 months
7 day

23
Q

What is the aetiology of bronchiolitis?

A

Respiratory syncytial virus (RSV) accounts for the majority of cases, although rhinovirus, human metapneumovirus, influenza, parainfluenza, and adenovirus can all cause bronchiolitis as well.

24
Q

What are the RFs for bronchiolitis?

A

Breast fed for less than 2 months
Smoke exposure
Having siblings at school/ nursery
Chronic lung disease due to prematurity

25
Q

What is the pathophysiology of bronchiolitis?

A

Proliferation of goblet cells causing excess mucus production
IgE mediated type 1 allergic reaction causing inflammation
Bronchiolar constriction
Infiltration of lymphocytes causing submucosal oedema
Infiltration of cytokines and chemokines

26
Q

What is the presentation of bronchiolitis?

A
History: 
Low grade fever 
Nasal congestion 
Rhinorrhoea 
Cough 
Feeding difficulty 
Examination: 
Tachypnoea 
Grunting 
Nasal flaring 
Intercostal, subcostal or supraclavicular recessions 
Inspiratory crackles 
Expiratory wheeze 
Hyperinflated chest 
Cyanosis or pallor
27
Q

What are the differentials for bronchiolitis?

A
Pneumonia 
Croup 
CF 
Bronchitis 
HF - hard to diagnose.
28
Q

What are the investigations for bronchiolitis?

A

Pulse oximetry
Enzyme-linked immunosorbent assay (ELISA) rapid antigen detection or reverse transcriptase polymerase chain reaction (RT-PCR) of nasal swab (RT-PCR more sensitive but not available everywhere yet)
Chest X-ray (not necessary for diagnosis)

29
Q

What is the management of bronchiolitis?

A

Supportive:

Humidified O2
NG feeds
Fluids

30
Q

What is the prophylaxis treatment for bronchiolitis?

A

Palivizumab.

Palivizumab is a humanised monoclonal antibody that binds to the F protein of respiratory syncytial virus (RSV) and inhibits viral infection and replication.In the first year of life, the AAP recommends prophylaxis for infants born before 29 weeks, or preterm infants with chronic lung disease of prematurity; or infants with haemodynamically significant congenital heart disease; or infants with pulmonary abnormalities or neuromuscular disease that impairs the ability to clear secretions from the upper airways.

31
Q

What is the pathophysiology of asthma?

A

Chronic inflammatory disorder of lower airways secondary to hypersensitivity
Reversible airway obstruction
Atopy, genetic predisposition and environmental factors all effect bronchial inflammation.

Pathophysiology:
Bronchial inflammation 
  a) Oedema 
  b) Excessive mucus production → mucous plug 
  c) Infiltration with cells 

Bronchial hyperresponsiveness
a)Exaggerated twitchiness to inhaled stimuli

Airway narrowing
a) Reversible airflow obstruction (peak flow variability )

Symptoms

a) Wheeze
b) Cough
c) Breathlessness
d) Chest tightness

32
Q

What are the clinical features of asthma?

A
Intermittent dyspnea 
Sputum production 
Disturbed sleep (quantify by nights/ weeks)
Wheeze
Nocturnal Cough 
Diurnal variation 
Decreased exercise tolerance
33
Q

What are the investigations for asthma?

A

Clinical symptoms
Spirometry: FEV1:FVC < 70%
Bronchodilator reversibility – FEV1 improvement by 12% or more
FeNO >= 35ppb
CXR: May show hyperinflation. Helps distinguish from other cardiac and pulmonary diseases such as cardiac failure, bronchiectasis, or situs inversus.

34
Q

What suggests a severe asthma attack?

A

In < 5’s
Sats <92%, unable to talk, HR >140, RR >40 use of accessory neck muscles

In > 5’s
Sats <92%, PEF <50%, unable to complete sentences, HR >125, RR >30 use of accessory neck muscles

35
Q

What suggests a life-threatening asthma attack?

A

In < 5’s
Sats <92%, silent chest, bradycardic, poor resp effort, altered consciousness, cyanosed

In > 5’s
Sats <92%, PEF <33% silent chest, bradycardic, poor resp effort, altered consciousness, cyanosed

36
Q

What is the acute management of asthma?

A
ABCDE
High flow O2
Salbutamol nebs 
Back to back if severe (in HCU environment) 
SE Hypokalemia (drives K+ out of cells) 
IV hydrocortisone 
Or oral if tolerated 
Ipratropium Bromide Nebs 
Magnesium Sulphate IV 
Call ICU 
Salbutamol IV 
Arrhythmias 
ECG monitoring
37
Q

What is the chronic management of asthma?

A

AVOID TRIGGERS & EDUCATION

Step 1: short acting beta agonist (Salbutamol)
If this is needed more than once a day or three times a week then move to…

Step 2 : Inhaled corticosteroid (beclometasone dipropionate (BDP), budesonide, and fluticasone propionate)

Step 3: increase corticosteroid and add LABA ( Salmeterol or formoterol)

Step 4: Add ons (montelukast, theophylline and omalizumab)

38
Q

What causes CF?

A

Mutation in the gene of the long arm of chromosome 7 in the region 7q31.2
Most common inherited disease in white populations
Much less common in afro-caribbean and Asian people
Prevalence is 1 in 2500 new-born
9000 people currently with CF in UK

39
Q

What is the pathophysiology of CF?

A

Mutations in chromosome 7 which codes for CF transmembraneous conductance regulator protein, a chloride channel and regulatory protein found in epithelial cell membranes in lungs, pancreas, GI and reproductive tract.
Decreased transport of chloride and/or CFTR affected ions, such as sodium and bicarbonate, leads to an alteration in viscosity and tenacity of mucus produced at the epithelial surfaces and to increased salt concentration in sweat gland secretions.

40
Q

How does CF affect each system?

A

Respiratory Tract:
Chloride ion movement and sodium reabsorption is affected in the defective cells.
This rescues the amount of water in secretions which results in reduced airways surface liquid (ASL)
ASL = impt component of mucociliary escalator → impedes mucous clearance
Provides a niche for bacterial growth (bacterial are protected against host immune system and antibiotics)

Pancreas
Pancreatic insufficiency → CF related DM

GI Tract
Small intestine secretes viscous mucous which can cause bowel obstruction in utero
In utero CF causes cholestasis - leading to neonatal jaundice
This can cause intestinal obstruction syndrome and CF related liver disease in later life

Reproductive tract
98% of men are infertile
Congenital absence of the vas deferens

41
Q

What are the clinical features of CF in neonates?

A

Meconium Ileus
Screening identifies the majority of cases (Guthrie test)
Failure to Thrive
Prolonged neonatal jaundice

42
Q

What are the clinical features of CF in infancy?

A

Failure to thrive
Recurrent chest infections
Pancreatic insufficiency - steatorrhoea

43
Q

What are the clinical features of CF in childhood?

A

Rectal prolapse
Nasal polyps (high indication it is CF)
Sinusitis

44
Q

What are the clinical features of CF in adolescence?

A

Pancreatic insufficiency - DM
Chronic lung disease
DIOS, gallstones, liver cirrhosis.

45
Q

What is seen on examination in CF?

A

Hands: finger clubbing
Face: nasal polyps
Chest: hyperinflated, crepitations, portacath (indwelling vascular access device)
Abdomen: fecal mass (if constipated/DIOS) may have a scar from ileostomy (meconium ileus)

46
Q

What investigations would you do for CF?

A

Clinical history and FH of disease are key diagnostic features.
Sweat sodium measurement > 60mmol/L
Blood DNA analysis of gene defect
Radiology showing features of CF
Absent vas deferens and epididymis
Blood immunoreactivity tyrosine levels.
Genetic screening for the carrier state together with counselling should be offered to those with a family history of CF.

47
Q

What is the management of CF?

A

Should be managed by MDT, parents should be involved as part of the team as well.
No cure for CF: the aims of treatment are to minimize progression of the disease (early identification of infection) and maintain adequate nutrition and development.

Nutrition – strong link between good nutrition and good development/ prognosis for CF

Education to improve QoL, good nutrition and prompt treatment of exacerbations

Clearly explaining diagnosis and providing written information and support information
Lifelong and life limiting condition

General care
Stopping smoking, vaccinations

Oxygen therapy if necessary

Antibiotic treatment:
70% of adults with CF have Pseudomonas infection in sputum
Nebulised antipseudomonal antibiotic therapy helps improve lung function and decreases risk of relevant exacerbations

Drug therapy:
B2 agonists
Inhaled corticosteroids
Purely symptomatic relief

Airway clearance:
Twice daily physiotherapy is needed 
Inhalation of recombinant DNAse (Reduces viscosity of mucous)
Hypertonic saline by inhalation
Amiloride - inhibits sodium transport
Acetylcysteine

Non-invasive ventilation
Improves symptoms in chronic respiratory failure

Treat pancreatic insufficiency

48
Q

What is the aetiology of paediatric pneumonia?

A
Bacterial:
Strep Pneumonia 
H influenzae (vaccinated against)
Staph aureus / klebsiella
TB
Mycoplasma  
Viral:
 RSV 
Influenza A and B 
Parainfluenza 
HIV (Bacterial infection remains major cause of fitness)
49
Q

What are the clinical features of pneumonia?

A
Fever 
Cough 
Rapid breathing 
Lethargy 
Poor feeding 
‘Unwell child’ 

Resp distress:
Use of accessory muscles (Sternocleidomastoid, trapezius, abdominal)
Head bob
Recessions (Tracheal tug, Subcostal, Intercostal, Sternal)
Nasal flaring
Audible sounds (Stridor, wheeze)
Tachypneic, Tachycardic

Older children:
Pleural pain 
Crackles 
Bronchial breathing 
Expiration and inspiration sound the same
50
Q

What investigations do you do for pneumonia?

A

Sputum sample:
MC+S

CXR:
Consolidation

51
Q

What is the management of pneumonia?

A

1st line:
Oral amoxicillin
Target bacteria cell wall

2nd line:
Clarithromycin

Atypical - Macrolide:
Inhibits protein synthesis of bacteria.

52
Q

What is bacterial bronchitis?

A

Persistent inflammation of the lower airways driven by chronic infection
Chronic wet cough in children

Caused by:
Haemophilus influenzae
Moraxella catarrhalis

Tx:
High dose antibiotics - co=amoxiclav (4+ weeks)
Physiotherapy
Thought to be a precursor to bronchiectasis (permanent dilatation of the bronchi)