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Peadiatrics > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the clinical difference between laryngomalacia vs. broncho/tracheomalacia?

A

Larygomalacia = most common cause stridor infants and children.
Inspiratory, low-pitched, exacerbated by exertion.
Appear within first 2 weeks of life; increase in severity up to 6 months

Broncho/tracheomalacia = chondromalacia of the central airway, leading to insufficiency cartilage to maintain patency.
Low pitched, monophonic wheeze predominantly during expiration; most prominent over central airways.
Excellent prognosis

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2
Q

What is the significance of biphasic stridor?

A

Suggests fixed proximal airway obstruction, which may be intra- or extrathoracic.

Conversely, VARIABLE inspiratory stridor suggests a less severe, extrathoracic, dynamic obstruction.

DDx of persistent biphasic stridor:

  1. Severe laryngomalacia
  2. Tracheomalacia
  3. Vascular ring (double aortic arch most common form)
  4. Vocal cord paresis (causes hoarse cry)
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3
Q

What is the mutation for CF and its mode of inheritance?

A

Autosomal recessive

Mutation in CFTR (long arm of chromosome 7)
Most common = delta-F508 (3-base pair deletion that leads to loss of a single phenylalanine at position 508; prevents the protein from trafficking to the correct cellular location) (80% cases)

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4
Q

What is the single best predictor of severity in bronchiolitis?

A

Oxygen saturation while breastfeeding

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5
Q

What are the indications for RSV immunoprophylaxis?

A 
Palivizumab 
5 doses (one per month)
  1. Infants born <29 weeks (prophylaxis in first year of life)
  2. BPD infants ( <32 weeks requiring >21% oxygen requirement for at least 28 days); prophylaxis for first year of life
  3. Infants younger than 2 years with BPD who required medical therapy (e.g. supplmental oxygen, gluccocorticoids, diuretics) within 6 months of the anticipated RSV season
  4. Haemodynamically significant heart disease; first year of life
  5. Pulmonary abnormality or neuromuscular disease that impairs ability to clear secretions from lower airways; first year of life
  6. Children <24 months who will be profoundly immunocompromised during RSV season

NOT routine in T21/CF patients

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6
Q

What are the effects of antenatal maternal smoking?

A 
SIDS 
Respiratory infections (pneumonia, bronchitis)
Asthma 
Decreased maximal expiratory flow 
Diabetes mellitus
Atopy 
Otitis media 
Short attention spans
Hyperactivity 
Childhood obesity 
Decreased school performance

NOT associated with decreased lung compliance

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7
Q

Which site of the lung is congenital lobar emphysema affected most?

A

Left upper lobe

Caused by LOCALISED OBSTRUCTION (e.g. congenital deficiency of bronchial cartilage, external compression by aberrant vessels, bronchial stenosis, redundant bronchial mucosal flaps, kinking of bronchus by herniation into the mediastinum)

CXR = radiolucent lobe and mediastinal shift AWAY from affected side

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8
Q

Does infection with pertussis or vaccination confer lifelong protection?

A

No

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9
Q

What type of bacteria is pertussis?

A

Gram-negative coccobacilli
(Bordatella pertussis)

Colonises only ciliated epithelium
Incubation period = 3-12 days
3 stages: catarrhal, paroxysmal, convalescent

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10
Q

What is the difference in symptoms of pertussis in infants <3 months age?

A

They usually do not display classic stages.

  1. Whoop infrequent (lack strength to cause negative intrathoracic pressure)
  2. Cyanosis and apnoea common (more than with viruses)
  3. Paradoxically, cough and whoop can be louder in convalescent phase
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11
Q

When is a pertussis cough worse?

A

At night

Cough is present throughout the day
May be precipitated: yawning, stretching, laughing, yelling, exercise
Triggers: steam inhalation, mist, respiratory irritants

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12
Q

What do you find on CXR and bloods in pertussis?

A

CXR = usually mildly abnormal: perihilar infiltrate or oedema; variable atelectasis. (PTx, pneumomediasium, subcut emphysema rare)

Bloods = leukocytosis (viral); no eosinophilia

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13
Q

Which tests are NOT reliable to test for pertussis?

A

Tests for IgA and IgM pertussis antibody, or antibody to antigens OHER THAN PERTUSSIS TOXIN

Method for confirmation = culture, PCR, and serology.

Results of culture and PCR expected to be positive in unimmunised, untreated children during the CATARRHAL and early PAROXYSMAL stages

*Note: fewer than 20% of culture or PCR tests have positive results in partially or remotely immunised individuals tests in paroxysmal stage

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14
Q

Which patients are at highest risk for pertussis?

A

< 3 months
Premature
Underlying cardiac, pulmonary, muscular or neurologic disorders

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15
Q

What are the characteristics of non-life threatening vs. life-threatening paroxysms in pertussis?

A

LIFE-THREATENING
Apnoea
Respiratory failure

NON-LIFE THREATENING
Duration < 45 sec, red but not cyanosis; tachycardia, bradycardia or desaturation that resolves at end of paroxysm; whooping or strength for brisk self-rescue at end of paroxysm; self-expectorated mucus plug; posttussive exhaustion but not unresponsiveness

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16
Q

What antibiotics are used in pertussis and for what reason? What is the risk of using the antibiotic?

A

Macrolides - azithromycin preferred

Primarily to limit spread of infection

Risk of hypertrophic pyloric stenosis (in neonates treated with orally administered erythromycin); thus azithromycin (but still has risk for PS and azi can cause fatal heart arrhythmias)

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17
Q

What is involved in the CF newborn screen?

A

Two components:

  1. Immunoreactive trypsinogen = enzyme precursor made by pancreas; elevated in CF; damaged pancreatic acinar cells leak into blood
  2. DNA = CFTR mutations

Samples with elevated IRT AND one or two identified CFTR mutations are ‘screen positive’ -> referred for SWEAT TEST to confirm/rule out

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18
Q

Which part of the lungs are changes seen in most commonly with alpha antitrypsin-1 deficiency?

A

Lower lobe predominance

Autosomal recessive
Homozygous -> early onset emphysema (usually occur 4-5th decade of life); 15% with the homozygote Pi(ZZ) phenotype also get progressive liver fibrosis and cirrhosis (manifestation most likely seen in children)

Heterozygotes -> no increase in pulmonary disease unless smoker

*Note: Pi(MM) = normal production protein

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19
Q

What are the XR changes seen in bacterial pneumonia for:

  1. S. pneumoniae
  2. S. pyogenes
  3. H. influenzae
  4. S. aureus
  5. Kleb. pneumoniae

ATYPICAL

  1. M. pneumoniae
  2. Chlamydia pneumoniae
A

S. pneumoniae - pleural effusions, empyema (late)

S. pyogenes (GAS) - pneumatoceles, abscess, empyema

H. influenzae - similar to pneumococcal

S. aureus - pneumatoceles (classic), pneumothorax, empyema, abscess

Klebsiella - (usually in immunosuppressed, prolonged intubation)

Mycoplasma - XR worse than symptoms suggest (headache, fever, pharyngitis prodrome)

Chlamydia - symptoms similar to Mycoplasma

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20
Q

What is the difference on sputum culture between blastomycosis and histoplasmosis?

A

Blastomycosis = Broad Based Budding

Histoplasmosis = narrow-based budding

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21
Q

When is obstruction most severe for intrathoracic vs. extrathoracic obstruction?

A

Intrathoracic - most severe during expiration; relieved during inspiration

Extrathoracic - obstruction increased during inspiration (effect of atmospheric pressure to compress trachea below site of obstruction)

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22
Q

What is the difference in location of obstruction in inspiratory vs. expiratory stridor?

A

Inspiratory stridor = suggests obstruction ABOVE glottis or AT subglottic

Expiratory stridor = suggests obstruction in LOWER trachea (i.e. intrathoracic portion)

(Biphasic suggests glottic or subglottic lesion)

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23
Q

Which part of the lungs is lymphotic interstitial pneumonitis seen most commonly?

A

BIBASILAR infiltrate

Has homogenous ground glass opacities

= most commonly described interstitial lung disease in children
2 general causes:
1) Exaggerated response to inhaled antigens in child with another autoimmune dysfunction
2) Report of primary infection with virus (HIV, EBV)

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24
Q

What are the most common infectious triggers of Steven-Johnson syndrome?

A

Mycoplasma pneumoniae

Cytomegalovirus

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25
Q

What is the most common pulmonary mycosis (fungal infection) in humans?

A

HistoplasMOsis

Transmitted through contaminated birth and bat droppings

CXR - hilar adenopathy and focal alveolar infiltrates

  1. No treatment if acute disease without complications
  2. Itraconazole -> if persistent >4 months or hypoxic
  3. Amphotericin B -> if disseminated
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26
Q

What is the Gram staining for Mycoplasmae?

A

Gram negative

Phylogenetically, should be Gram POSITIVE; however, part of group of bacteria that evolved from Gram Positive but lost their cell walls -> negative

CHARACTERISTICS

  1. Pleomorphic - not cocci/rod; can be either
  2. Intrinsic resistance to beta-lactam agents
  3. Slow culture (‘mulberry’ colonies)
  4. Small - size of viruses
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27
Q

Where is ventilation/perfusion ratio highest in the lungs when the person is standing?

A

APEX of the lung (zone 1)

V/Q ratio is higher in apex when the person is standing than in base of lung (zone 3) because perfusion is nearly absent

However, ventilation and perfusion (SEPARATELY) are highest in the BASE of the lung -> results in comparatively lower V/Q ratio

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28
Q

What is the typical clinical course of Mycoplasma pneumoniae?

A

Gradual onset of headache, malaise, fever and sore throat -> followed by progression of lower respiratory symptoms

Cough = clinical hallmark; worsens during first week of illness

Symptoms generally resolve within 2 weeks, but cough can last up to 4 wks

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29
Q

What two symptoms are unusual with Mycoplasma pneumoniae?

A

Coryza
Gastrointestinal complaints

= suggest VIRAL aetiology

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30
Q

Why is Mycoplasma pneumoniae also known as ‘walking pneumonia’?

A

Clinical findings are often less severe than suggested by patient XR

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31
Q

What part of the lung is most commonly involved in Mycoasplasma pneumoniae, and what are the XR changes?

A

Most common in LOWER lobes

Usually described as interstitial or bronchopneumonic

Bilateral diffuse infiltrates, lobar pneumonia or hilar lymphadenopathy can occur in up to 30% cases

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32
Q

What is the most common extrapulmonary site of Mycoplasma pneumoniae?

A

CNS

Occur 3-23 days after onset respiratory illness (mean =10)

Includes: encephalitis, transverse myelitis, aseptic meningitis, GBS, Bell palsy, post-infectious demyelination, peripheral neuropathy, acute disseminated encephalomyelitis

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33
Q

What is the most common infectious agent associated with Steven-Johnson syndrome?

A

Mycoplasma pneumoniae

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34
Q

What is the best method to diagnose Mycoplasma pneumoniae?

A

PCR testing

-> s&s of 80 to >97%

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35
Q

Why don’t you use IgM antibodies to test for Mycoplasma pneumoniae?

A

High false positive and negative rate

In most cases, IgM antibodies are not detected within the first 1 wk after symptom onset

Can remain IgM positive up to 6-12 mo after infection

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36
Q

How are IgG antibody titers used to diagnose Mycoplasma pneumoniae?

A

4-fold or greater increase in IgG titers between acute and convalescent sera obtained 10 days to 3 weeks apart is DIAGNOSTIC

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37
Q

What antibiotic class is used to treat Mycoplasma pneumoniae?

A

Macrolides

(Erythromycin, clarithromycin, azithromycin)

More effective when started within 3-4 days illness

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38
Q

What does the concept of West zones of the lung describe?

A

Describes areas of lung based upon variations in pulmonary arterial pressure (PaP), pulmonary venous pressure (PvP) and alveolar pressure (AP)

These differences result in a 20 mmHg increase in blood flow found in the base of the lung relative to the apex as a result of gravity in an upright patient

Zone 1 (top) 
AP > PaP > PvP 
Zone 2 (middle) 
PaP > AP > PvP 
Zone 3 (lower) 
PaP > PvP > AP
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39
Q

What is the alveolar gas equation formula?

A

ALVEOLAR GAS EQUATION
Alveolar oxygen partial pressure = [FiO2 x (barometric pressure - partial pressure of water)] - [partial pressure carbon dioxide/ respiratory quotient]

Respiratory quotient = CO2 (eliminated) / O2 (consumed)

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40
Q

What would be the advantage and disadvantage of using plethysmography over helium to determine lung volumes?

A

ADVANTAGE
Helium dilution method underestimates those with airway obstruction

DISADVANTAGE
Large bullae or hiatal hernias may be included in lung volume measurements
Expensive
Claustrophobia

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41
Q

What causes increased vs decreased levels of DLCO

A

= Diffusing capacity of carbon monoxide

DECREASED DLCO
Any condition that reduces lung surface area available for gas diffusion
1. Loss of alveoli or incomplete expansion:(surgery, destruction from disease, atelectasis, pulmonary oedema)
2. Reduction in surface area: emphysema, diffuse fibrosis
3. Decreased pulmonary blood flow: PE, chronic pulmonary hypertension

INCREASED DLCO

  1. Elevated number of binding sites for Hb: polycythaemia, alveolar haemorrhage syndromes, increased pulmonary blood flow (including L->R shunt)
  2. Obesity
  3. Asthma (increases in pulmonary blood capillary volume or extravasation of red cells into alveolus)
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42
Q

What are the changes seen to flow-volume loops in obstructive vs. restrictive lung disease?

A

OBSTRUCTIVE

  1. Decreased expiratory flow rate
  2. Concave scooping of trace in latter half expiration

In EXTRAthoracic obstruction, inspiration curve is decreased; normal expiration curve
In INTRAthoracic obstruction, expiration curve decreased; normal inspiration curve

RESTRICTIVE

  1. Smaller vital capacity (distance on x-axis from start to finish of expiration)
  2. Total lung capacity (TLC) <80%

In INTRAthoracic restrictive disease (parenchymal, interstitial disease), RV is always decreased (distance on x-axis from zero) -> NORMAL RV/TLC ratio
In EXTRAthoracic restrictive disease (obesity, neuromuscular, kyphoscoliosis), can have normal RV, but shape and size similar -> INCREASED RV/TLC ratio

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43
Q

What is the definition of pulmonary (R->L) shunt?

A

Alveoli of lungs are perfused with blood as normal, but VENTILATION IS DECREASED

Shunt = passage of deoxygenated blood from R) of heart to L), without participation in gas exchange in pulmonary capillaries

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44
Q

What is the normal response of vessels to hypoxia in the lungs?

A

Vasoconstriction

When alveoli not ventilated, causes local hypoxia -> vasoconstriction -> blood redirected away from this area to areas which are being ventilated

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45
Q

Which diffuses more easily across alveolar-capillary interface: CO2 or O2?

A

CO2

Thus, in interstitial lung disease, given that CO2 diffuses more easily than O2, there may not be as high a PaCO2

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46
Q

What are examples of R->L pulmonary shunting?

A
  1. Intra-alveolar filling (e.g. pneumonia, pulmonary oedema)
  2. Intracardiac shunt
  3. Vascular shunt (e.g. AVM)

Note that pulmonary embolism = normal ventilation, reduced blood flow
-> an example of INCREASED DEAD SPACE (technically not shunt)

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47
Q

Does carbon monoxide (CO) shift the oxygen-dissociation curve to the left or right?

A

Left

CO binds tightly to Hb (iron moiety of heme with 240x affinity of oxygen) preventing O2 from binding.

Binding of CO causes other oxyHb to bind even more tightly to O2 (shifting cruve to left)
-> i.e. diminishes other three oxygen binding sites to offload oxygen

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48
Q

Does methaemoglobin shift the oxygen-dissociation curve to the left or right?

A

Left

Methaemoglobin = altered state of Hb where ferrous ions (Fe2+) are oxidised to ferric state (Fe3+)

Normally <1.5%

MetHb molecule cannot hold on to O2 or CO2 (unlike CO)
MetHb causes regular ferrous Hb to hold more tightly to O2 (shifting curve to left)

Tx = 100% O2 and methylene blue (artificial electron acceptor to facilitate reduction)

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49
Q

What are the characteristic changes to PFT in obstructive vs. restrictive disease?

A

OBSTRUCTIVE

  1. FEV1 reduced
  2. FVC reduced
  3. Low FEV1/FVC (FEV1 reduced more than FVC)
  4. Reduced FEF25-75
  5. Reduced peak expiratory flow rate (PEFR)

RESTRICTIVE

  1. FVC reduced
  2. FEV1 reduced
  3. FEV1/FVC normal or increased
50
Q

What does a reduced FEF25-75 indicate?

A

Small airways disease

Defined by a reduction in forced expiratory flow at 25-75% of the pulmonary volume and normal spirometry (normal FEV1, FVC and FEV1/FVC ratio)

51
Q

What are the characteristics of FEF25-75%?

A

(Also known as maximal midexpiratory flow rate MMEFR)

  1. Represents flow in smaller conducting airways
  2. Less effort dependent than the other parameters
  3. Particularly useful measurement of milder intrathoracic airway obstruction
  4. Can be reduced by >25% when patient is symptom-free and/or has a normal lung examination and in presence of normal FEV1 and PEFR
  5. Reduction in FEF25-75% can be visually noted as SCOOPING of the flow-volume curve
52
Q

What is the most common clinical diagnosis caused by human metapneumovirus?

A

Bronchiolitis (59%)

Croup (18%)
Asthma exacerbation (14%)
Pnuemonia (8%)

53
Q

Why are macrolides used in CF?

A

mACrolidEs (Azithromycin, Clarithromycin, Erythromycin) have excellent activity against:

  1. Mycoplasma
  2. Chlamydophila pneumoniae
  3. Legionalla pneumophilia

Also:

  1. Reduce virulence properties of Pseudomonas (e.g. biofilm protection)
  2. Contribute to anti-inflammatory effects

Have risk of pyloric stenosis; erythromycin > azithromycin

54
Q

What are the three bacteria seen with high prevalence in CF that are not usually seen in healthy lungs?

A
  1. Staphylococcus aureus
  2. Pseudomonas aeruginosa
  3. Burkholderia cepacia
55
Q

What is the most common complication of CF encountered among individuals school-aged and older?

A

Cystic fibrosis related diabetes (CFRD)

56
Q

When does screening for CF related diabetes start?

A

All patients with CF should under annual screening for CFRD beginning age 10

Screening = OGTT

HbA1c should NOT be used -> low sensitivity for CFRD

57
Q

Why is there a correlation between CF related diabetes and decline in pulmonary function?

A

Development of significant hyperglycaemia favours acquisition of P. aeruginosa and B. cepacia in airways -> adversely affect pulmonary function

Hyperglycemia promotes bacterial growth; causes an exaggerated but less effective inflammatory response

58
Q

What is the difference between night terrors and nightmares?

A

NIGHT TERROR

  1. 5% children, normal development, no long-term effect, most grow out, no association with epilepsy, psychological
  2. Preschool to primary-aged (4-12 years old)
  3. Occur in first few hours of sleep at night (first 1/3 normal sleep)
  4. Starts with sudden scream, thrashing, get up and run around house, sweaty, fast HR, glassy stare
  5. May not recognise parent, unable to be comforted
  6. Last 5-10 minutes, may occur more than once during same night
  7. Does not recall in morning
  8. Strong genetic predisposition; family history sleep walking or night terror
  9. May be worse with fever, illness

NIGHTMARE

  1. Happen in second half of night
  2. Fully wakes up and can remember dream and in morning
59
Q

What is the most common circadian rhythm disturbance in adolescents and young adults?

A

Delayed sleep-wake phase disorder
(‘night-owl’ circadian preference)

7% teenagers
= habitually go to bed and wake up significantly later (>2 hours) -> chronic sleep restriction, impaired day function, increased likelihood depression/psychiatric disorders

Mx = behaviour modification, strategically-timed melatonin (3-5mg in evening 1.5 hours before desired bedtime)

60
Q

What is the name of the neuropeptide that is deficient in narcolepsy (type 1)?

A

Orexin (hypocretin-1)
= essential for maintaining wakefulness
(narcolepsy type 2 not fully understood)

61
Q

What is the age of presentation for narcolepsy?

A

1/3 cases present before age 15 years

Rarely present younger than 5-6 years old

62
Q

What are the features of narcolepsy?

A
  1. Essential = excessive daytime sleepiness
    - > waxing/waning sleepiness, sleep attacks, habitual napping
  2. Cataplexy
  3. Hypnagogic (sleep onset) hallucinations and sleep paralysis
  4. Associated with OBESITY (tends to happen near onset of other symptoms)
  5. Associated with PRECOCIOUS PUBERTY (increased freq in children with narcolepsy)
63
Q

What is the difference between narcolepsy type 1 vs type 2?

A

Type 1 = WITH cataplexy

Type 2 = WITHOUT cataplexy

64
Q

What is the most specific symptom of narcolepsy?

A

Cataplexy
= sudden, transient loss of muscle tone

Weakness or paralysis usually arises in response to strong emotions (laughter, surprise, fright or anticipation of reward) -> range from head/shoulder droop to sudden collapse to floor

Consciousness fully preserved

Episodes last few seconds to 3-5 minutes

65
Q

What is the diagnosis and treatment of narcolepsy?

A

DIAGNOSIS
Characteristic clinical features + nocturnal polysomnography (PSG) and multiple sleep latency test (MSLT)

TREATMENT
= No cure
1. Behavioural and lifestyle modification
2. Stimulant medications (e.g. methyphenidate)
3. Wake-promoting agents (e.g. modafinil)
4. Sodium oxybate (for cataplexy) = CNS depressant

66
Q

What are the types of childhood insomnia?

A
  1. Behavioural-related
    = most common age 0-5

a) related to SLEEP-ONSET
= learned to sleep under certain conditions (e.g. rocking); avoid by putting to slepe when drowsy but still awake, starting at 3/12 age

b) related to INADEQUATE LIMIT SETTING
= common preschool and older
= active resistance, verbal protest and demands at bedtime; can present with nighttime fears to stall; develops from caregiver’s inability to enforce bedtime rules

  1. Psychophysiologic (conditioned)
    = older children and adolescents
    = anxiety specifically about falling asleep; due to heightened emotional arousal; precipitating factors incl poor sleep habits, caffeine, daytime napping
  2. Transient sleep disturbance
    = disruption of sleep schedule (e.g. jet lag, stress)
67
Q

What is the most common site of bronchogenic cysts?

A

Middle mediastinum (65-90%)

Typically single, unilocular and on the RIGHT

= abnormal budding of tracheal diverticulum of foregut (bronchopulmonary foregut malformation) before 16 weeks gestation; lined by secretory respiratory epithelium
Most common cysts in infancy

Do not communicate with tracheobronchial tree

Most often in mediastinum and filled with mucus
Can get infected -> fever, chest pain, cough

Tx = excision; rarely malignant degeneration

68
Q

What are the XR findings of bronchogenic cysts?

A

Usually FLUID filled

Usually do NOT communicate with bronchial tree (therefore not air filled); rather contain water, variable amounts of proteinaceous material, blood products, and calcium oxalate

Occasionally a communication may develop following infection or intervention -> air-filled cystic structure +/- air fluid level

69
Q

What are the XR findings of congenital pulmonary airway malformation?

A

Multicystic AIR-filled lesions
(but can be fluid-filled EARLY on)

Large lesions result in mediastinal sift, depression and inversion of diaphragm

CPAM = multicystic masses of segmental tissue with abnormal bronchial proliferation

5 subtypes: type 1 most common (70%), usually large cysts, one or more dominant

70
Q

What are the types of bronchopulmonary foregut malformations?

A
  1. Congenital pulmonary airways malformation (CPAM)
  2. Pulmonary sequestration
  3. Foregut duplication cysts (bronchogenic, neurenteric and enteric cysts)
  4. Hybrid lesion (CPAM + sequestration)
71
Q

What is the respiratory AIDS-defining illness in children and what are other viral causes?

A

Lymphocytic interstitial pneumonia

= Most commonly described interstitial lung disease in children

VIRAL CAUSES

  1. HIV
  2. EBV
  3. Human T-cell lymphotrophic virus type 1 (HTLV-1)
72
Q

What are the 5 patterns of bacterial pneumonia?

A
  1. Lobar = single lobe/segment of lobe
    - > classic pattern of S. pneumoniae
  2. Bronchopneumonia = involvement of airways and surrounding interstitium
    - > Strep. pyogenes, S. aureus
  3. Necrotising pneumonia
    - > associated with aspiration pneumonia and pneumonia resulting from S. pneumoniae, S. pyogenes and S. aureus
  4. Caseating granuloma
    (Tuberculosis)
  5. Interstitial and peribronchiolar with secondary parenchymal infiltration
    - > severe viral complicated by bacterial
73
Q

What are the two major patterns of viral pneumonia?

A
  1. Interstitial pneumonitis

2. Parenchymal infection with viral inclusions

74
Q

What are the causative organisms of pneumonia in:

  1. Bacteria: neonates vs. infants/children
  2. Viral
A

NEONATES
Bacteria = GBS
Viral = HSV

INFANTS/CHILDREN
Bacteria = Strep. pneumoniae
Virus = RSV

75
Q

What are the typical associations of parainfluenza types?

A

PIV-1 and PIV-2 = croup

PIV-3 = pneumonia, bronchiolitis

PIV-4 = mild URTI, pneumonia, bronchiolitis

76
Q

What is the most common area to be affected by invasive aspergillosis?

A

Lungs (pulmonary aspergillosis)

‘Aspergillosis’ = illness due to allergy, airway or lung invasion, cutaneous infection, or extrapulmonary dissemination caused by species of Aspergillus

Aspergillus = fungus

77
Q

What are the XR findings of pulmonary aspergillosis?

A
  1. Single or multiple nodules +/- cavitation

a) Nodules with surrounding ground glass infiltrates (i.e. ‘halo sign’)
= haemorrhage into the area surrounding fungus

b) Air-crescent sign
= when nodules eventually cavitate

  1. Peribronchial infiltrates +/- TREE-BUD pattern
  2. Patchy/segmental consolidation
78
Q

What is the classic triad of pulmonary aspergillosis?

A
  1. Fever
  2. Pleuritic chest pain
  3. Haemoptysis
79
Q

What are the 4 frequently described XR patterns in Mycoplasma pneumoniae?

A
  1. Bronchopneumonia
  2. Plate-like atelectasis
  3. Nodular infiltration
  4. Hilar lymphadenopathy
80
Q

What is the most common XR finding in Mycoplasma pneumoniae?

A

Peribronchial pneumonia pattern

= thickened bronchial shadow, streaks of interstitial infiltration, and areas of atelectasis

Predilection for LOWER lobes

81
Q

What is the most common XR finding in Legionella pneumonia?

A

Patchy unilobar infiltrates
-> can progress to consolidation

*Note that XR findings are NON-SPECIFIC

82
Q

What is the most common XR finding in PRIMARY pulmonary tuberculosis?

A 
Hilar adenopathy (65%) 
-> usually ipsilated, on RIGHT

OTHER

  1. TUBERCULOMA = when infection becomes localised and a caseating granuloma forms
    - > GHON COMPLEX = when calcifies
  2. Pleural effusions (33%)
  3. Pulmonary infiltrates
    - > perihilar and R)-sided infiltrates = most common

Cavitation uncommon (10-30% only)

*Note that XR often normal

83
Q

Which infection has a predilection for the upper lobe (posterior segment)?

A

POST-PRIMARY pulmonary tuberculosis (seen in 85%)

Post-primary infections are far more likely to cavitate from primary infections

84
Q

What is the gold standard for the diagnosis of restrictive lung disease in children?

A

Reduced total lung capacity (TLC)

i.e. < 80% predicted

85
Q

What is the maximum allowable variation on repeat testing for spirometry?

A

5%

INTRA-instrument repeatability must be <5% or 0.15 L/sec (whichever is greater)

INTER-device reproducibility must be <10% or 0.3L/sec (whichever is greater)

86
Q

What is the gold standard method for recording sleep/wake states and for diagnosing OSA?

A

Overnight polysomnography

87
Q

From polysomnography, what is the definition of:

  1. Apnoea
  2. Hypopnoea
  3. Respiratory effort related arousal (RERA)
A

APNOEA
= >90% decrease in airflow signal that lasting >/= 90% duration of at least 2 normal breaths

a) OBSTRUCTIVE = if there is continued or increased inspiratory effort during the entire period of decreased air flow
b) CENTRAL = if inspiratory effort is absent during the entire period of airflow cessation
c) MIXED = absent respiratory effort during one portion of the event AND presence of inspiratory effort in another portion

HYPOPNOEA
= >/=30% decrease in airflow signal that lasts >/=90% duration of at least 2 normal breaths
Decreased airflow is associated with an arousal, or at least 3% desat

RESP-EFFORT RELATED AROUSAL
= respiratory event (increasing resp effort, flattening of insp portion of nasal pressure waveform, snoring, elevation end-tidal PCO2) that leads to arousal and does not qualify as an apnoea or hypopnoea

88
Q

What is the apnoea hypopnea index cut-off for concern for clinically significant OSA?

A

AHI >1

AHI = number of apnoea plus hypopneas that occur per hour of sleep

89
Q

How do you calculate pulmonary compliance?

A

compliance = (change in VOLUME) / (change in PRESSURE)

e.g. if patient inhales 500mL air, from change of intrapleural pressure from -5cmH2O to -10cmH2O:

compliance = 0.5/(15-(-10)) = 0.1L/cmH2O

90
Q

What are parasomnias, and what are the different types?

A

= episodic behaviours that intrude onto sleep

Sleep terror (40%) 
Sleepwalking (15%) 
Sleep enuresis (25)
91
Q

What are examples of sleep-related movement disorders?

A

= simpler, stereotyped movements are categorised as SLEEP-RELATED MOVEMENT DISOREDERS:

Periodic limb movements of sleep
Sleep-related bruxism
Sleep-related rhythmic movement disorder

92
Q

What are the ages that typical parasomnias or sleep-related movement disorders are seen?

A

INSOMNIA
Behavioural insomnia = 0-5 years
Psychophysiologic insomnia = older children/adolescents

PARASOMNIAS
Sleep terror = 4-12 years
Sleep walking = 8-12 years
Sleep enuresis = 5 years old (15%) -> declines to 5% by 10 years
5 year old = age threshold when most children achieve bladder control

SLEEP-RELATED MOVEMENT DISORDER
Sleep-related bruxism = childhood, decreases with age

93
Q

How do you treat OSA and what are the indications for each?

A

ADENOTONSILLECTOMY
= otherwise healthy children with >/=1+ tonsils and OSA (AHI >1)

POSITIVE AIRWAY PRESSURE
= minimal adenotonsillar tissue, preference for nonsurgical or contraindications

WATCHFUL WAITING
= non-severe OSA confirmed by PSG + reevaluate in 6 months

94
Q

What are some indications for CPAP vs BPAP in children?

A 
CPAP 
1. OSA 
2. Atelectasis 
= expand and recruit alveoli 
3. Cardiogenic pulmonary oedema
= improve gas exchange 
4. Obstructive lung disease 
= reduce air-trapping resulting from lower airway obstruction or constriction 
BPAP 
1. OSA 
2. Neuromuscular 
= helps with inspiration/expiration 
3. Hypoventilation
95
Q

What diseases are contraindications to CPAP?

A
  1. Pneumothorax
    = high pressure may worsen air leak/recurrence
  2. Aspiration risk
    = in patients with copious oral secreations/oral dysfunction
  3. Hypoventilation
    = CO2 retention (blood gas) or elevated end tidal CO2 (PSG)
96
Q

In children with moderate chronic upper airway obstruction, what is the most likely morbidity?

A

Decrements of memory and attention

97
Q

Why are third generation cephalosporins used over penicillins in pneumonia?

A

Provide coverage for beta-lactamase producing agents (H. influenza, M. catarrhalis)

98
Q

What is the PaO2 for 90% sats?

A

60mmHg - think as cut off (from 90% above/below)

PaO2 60 mmHg = 90% sats
PaO2 50 mmHg = ~80% sats
PaO2 25 mmHg = 50% sats

99
Q

What are the changes to oxygen-haemoglobin dissociation curve seen in high altitude?

A

BOTH shift to right, then left

RIGHT = moderate altitude (increased 2,3-DPG)

LEFT = extreme altitude
(much less CO2 in blood)

100
Q

What are the most prevalent pathogens of persistent bacterial infection seen in CF?

A

S. aureus

Pseudomonas aeruginosa

101
Q

What are important pathogens implicated in persistent lung infection in CF patients?

A

S. aureus
Pseudomonas

Burkholderia cepacia 
Stenoprophomonas maltophilia 
Nontuberculous mycobacteria
H. influenzae (non-typeable)
Achromobacter species 
Aspergillus
102
Q

How do you interpret the methacholine challenge test?

A

Dose of methacholine that provokes a 20% drop in FEV1 = PD20

A PD20 of <200-400 microg methacholine is more or less considered a positive test

103
Q

What is the pathophysiological explanation for FEV1 and FVC being reduced in obstruction vs. restrictive disorders?

A

OBSTRUCTIVE
FEV1 = flow impeded by obstruction
FEF25-75% = reduced flow in SMALLER conducting airways
PEFR = reduced as peak flow impeded by obstruction
+/- FVC = gas trapping and hyperinflation

-> gives LOW FEV1/FVC

RESTRICTIVE
FVC = unable to expand lungs as much
FEV1 = initiation of expiratory maneouver is lower

-> gives NORMAL/HIGH FEV1/FVC

104
Q

What spirometry parameter is an established marker of disease progression in cystic fibrosis?

A

FEV1

105
Q

What is the diagnostic criteria for cystic fibrosis?

A

TWO-PRONGED APPROACH:

(A)
Presence of typical clinical features (resp, GI, or GU) 
OR 
History of CF in sibling 
OR 
Positive newborn screening test

PLUS: (lab evidence)

(B)
Two elevated sweat chloride (separate days)
OR
Identification of two CF mutations
OR
Abnormal nasal potential difference measurement

106
Q

What three organisms on culture of lower airway (sputum) strongly suggest CF?

A

S. aureus
P. aeruginosa
Burkholderia cepacia

107
Q

What is the typical cough characteristic in CF?

A

Most prominent upon arising in morning or after activity

108
Q

In a child with rectal prolapse, what diagnosis needs to be considered?

A

Cystic fibrosis (CF)

Causes of rectal prolapse:

  1. Functional constipation and prolonged straining during defacation (most common)
  2. Chronic diarrhoea (enteric/parasitic infection)
  3. CF
  4. Malnutrition
  5. Polyps
  6. Conditions causing muscle floor weakness
109
Q

What is the level that is considered abnormal in sweat testing for CF?

A

> 60 mEq/L

110
Q

What is the most common cause of death for CF?

A

End-stage lung disease

111
Q

What syndrome is associated with subglottic stenosis?

A

Down syndrome
(increased incidence)

Other cause: intubation trauma

112
Q

What are the cardiovascular adverse effects of positive pressure ventilation?

A

DECREASE in cardiac output

Mechanical ventilation -> increased intrathoracic pressure -> decreased venous return (DECREASED PRELOAD) to right heart (dominant), right ventricular dysfunction, and altered left ventricular distensibility -> decreased cardiac output

113
Q

What is the effect of afterload with positive pressure ventilation?

A

DECREASES afterload

Afterload = ventricular wall tension (T) during contraction

T = (transmural pressure x radius) / wall thickness

By increasing pleural pressure, PPV DECREASES transmural pressure and hence DECREASES afterload

114
Q

What is the net effect of decreased afterload and decreased preload on HR with positive pressure ventilation?

A

Normally:

Decrease preload = decrease CO
Decrease afterload = increase CO

Net effect depends on LV contractility!

  1. If normal contractility, PPV tends to decrease cardiac output
  2. If decreased contractility, PPV tends to increase cardiac output
115
Q

Does myocardial oxygen consumption increase or decrease with PPV?

A

Reduced

116
Q

What is the significance of forced inspiration flow/forced expiratory flow 50%?

(i.e. FEF/FIF50)

A

If FEF/FIF50% >1, means inspiratory flow affected more, thus EXTRAthoracic site of obstruction and vice versa

117
Q

What is the normal V/Q ratio?

A

0.8

118
Q

Is ventilation and perfusion higher in the base or the apex of the lung?

A

Base on the lung

However, V/Q is higher at the apex (and lower at the base) as fall in perfusion is higher than fall in ventilation.

119
Q

Does the apex or base of the lung have a lower alveolar CO2 content?

A

Apex

V/Q is higher in apex = low alveolar CO2 and high O2 content

V/Q lower in base = low alveolar O2 and high CO2

120
Q

What are the metabolic changes to blood seen in asthma?

A

Early = respiratory alkalosis
(hyperventilation)

As obstruction worsens and increasing V/Q mismatch, carbon dioxide retention occurs

Late stage = metabolic acidosis (increase WOB, O2 consumption and CO) + respiratory acidosis (resp failure w CO2 retention)

121
Q

What are examples of REM vs. NREM sleep disorders?

A

NREM
Sleep terrors
Sleep walking
Confusional arousals

REM
Nightmares
Sleep paralysis

Peadiatrics (13 decks)

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