ILA- resp + cardio Flashcards

1
Q

A two year old girl called Emily is brought in with a barking cough, noisy breathing and a hoarse cry. Her mother says that she has been unwell for a few days with coryza. Generally, Emily is a healthy child and she is up to date with her immunisations. Her weight is 12 kg. On examination, Emily has a harsh stridor at rest with an intermittent barking cough. She has a lowgrade fever of 37.8°C. Her oxygen saturations are 94% in air. What is the differential diagnosis? - whats most likely?

A
Croup aka viral laryngotracheobronchitis!! - most likely
Epiglottitis 
Bacterial trachetitis – bad one  
Foreign body  
Diphtheria  
Laryngemalacia  
Subglotic stenosis  
Allergic laryngeal angioedema – seen in anaphylaxis and recurrent croup- quite common, floppy,  
Inhalation smoke/fumes
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2
Q

What is stridor? How is it different from wheeze?

A

Stridor is an upper respiratory problem caused by extra thoracic obstruction in upper airway. It is an inspiration sound. Sounds harsh and musical.

wheeze high pitched, on exhalation, obstuctive cause in lower airways

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3
Q

What is the diagnositic features of croup?

A

6 months to 6 years
Has mild fever, harsh stridor, difficulty breathing, hoarse voice (due to inflamm of vocal cords) and barking cough (due to trachel odema and collapse) which fits with croup
Followed an event of coryza

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4
Q

What are the sx of croup?

A
Over days 
Coryza procedes 
Barking cough, severe 
Can drink 
Unwell 
Low grade fever 
Harsh stridor 
Hoarse voice
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5
Q

What are the sx of epiglottitis?

A
Over hours 
Bacterial  
Cough slight/absent 
Drools saliva 
tripod position - lean foward and extend neck when seated
Very unwell 
High grade fever 
Soft stridor 
Muffled voice with reluctance to speak
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6
Q

When examining child with stridor, what must you not do and why?

A

Must avoid doing an exam of the throat using a spatula as can lead to total airway obstruction, (laryngospasm) unless resuss equipment is on hand

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7
Q

What is the usual cause of croup, and when is it most prevalent (age and time of year and day)?

A

Cause – viral usually – parainfluenza most common, then rhinovirus, RSV and influenza
Most prevalent age is 2 yrs
Most common in autumn – when go back after holidays to school
Symptoms are worse at night

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8
Q

What is the first-line treatment for croup?

A

Steroids - cortico - dexqa or pred - PO if poss but otherwise IM/ budesonide by nebs

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9
Q

Child with croup deteriorates and saturations drop to 86%. How should she be managed now?

A
Nebulised adrenaline (epinephrine) is usually reserved for patients in moderate-to-severe distress. Crash call.  
Can give burnside nebs as well mixed.  
If dropping sats with stridor means obstruction is indicated (dropping sats for wheeze is normal)  - May need emergency tracheotomy if don’t recover
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10
Q

Jake is a six month old child who has been referred by his GP with difficulty in feeding and breathing and a dry cough with coryza. He has been unwell for the past two days but has become worse overnight. He was born at term with no difficulties. His birth weight was 3.2kg. On examination, Jake has a low grade fever of 37.8o C and peripheral cyanosis, with oxygen saturations of 88% in air. He has a hyper-inflated chest with tachypnoea and intercostal recession. There are widespread crepitations and wheeze bilaterally on auscultation. What is the most likely diagnosis?

A

Bronchiolitis – infant, dry cough, tachypnoea, recession, hyperinflated chest, crackles, wheeze
Difficulty feeding due to coryzal – indicates viral
Bronchiolitis indicated by crepitations rather than viral induced wheeze

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11
Q

What is the differential diagnosis of wheezy child?

A

Bronchiolitis
Viral induced wheeze
Atypical pneumonia
More acute – anaphylaxis or foreign body

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12
Q

What are the most common causative organisms of bronchiolitis? What is the most common?

A

RSV - most common
Parainfluenza
Rhinovirus
adenovirus

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13
Q

What risk factors for bronchiolitis?

A
CF
Premature – bronchopulmonary dysplasia 
CHD 
Any other underlying lung condition – chronic lung disease  
Immunodeficiency  
Parents smoking
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14
Q

Which investigation would you order for bronchiolitis?

A

Pulse oximetry
Viral throat swabs for respiratory viruses ! – confirm RSV- associated bronchiolitis obliterates and want to keep RSV patients separate from non RSV patients (RSV very infectious)

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15
Q

How is bronchiolitis treated?

A
supportive
Oxygen 
Fluids 
NGT if still cant feed 
Anti pyrexials  
CPAP if severe  
Ribavarin – anti RSV monoclonal antibody if very severe
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16
Q

How can bronchiolitis be prevented and in what categories of patients would this be done?

A

How can bronchiolitis be prevented and in what categories of patients would this be done?
Airborne spread, prevented by palavizumab in IM over winter – for those with CLD or BPD or pulmonary hypophysis or congenital heart disease or immunodeficiency

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17
Q

child with bronchiolitis was diagnosed with cystic fibrosis (CF) by the neonatal screening test taken on day six of life. Does this change the diagnosis or the management of bronchiolitis?

A

Might need PT and abx

More likely to need IV as can’t clear their excretions

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18
Q

What test confirms CF?

A

Newborn blood spot test – IRT levels (immunoreactibe trypsin)
In older do sweat test for sodium and chloride - will be an excess of both

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19
Q

What conditions are picked up on the newborn screening test?

A

CF
Congenital hypothyroidism
SCD
Metabolic inherited eg PKU – don’t need to learn their names just be aware we test for some metabolic conditions

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20
Q

What is the pattern of inheritance for CF?

A

Autosomal recessive

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21
Q

What is the pathophysiology behind CF and which organ systems are affected?

A

CFTR defect –> cAMP chloride channel found in membrane of epithelial cells.
Prevents absorption of chloride –> so less sodium is absorbed
Dehydrated pancreas, biliary, reproductive, liver, bowel and lungs
Dehydration of the airway surfaces reduces mucociliary clearance and favours bacterial colonisation, local bacterial defences are impaired by local salt concentrations and bacterial adherence is increased by changes in cell surface glycoproteins.
Increased bacterial colonisation and reduced clearance produce inflammatory lung damage due to an exuberant neutrophilic response involving mediators such as IL8 and neutrophil elastase.

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22
Q

How does CF present clinically at different ages?

A

Newborn: screening, meconium ileus (thick meconium – delay in passing stool due to obstruction- distension, comit, constipated)
Infancy: Prolonged jaundice neonate, poor growth, recurrent chest infections, malabsorption – due to pancreatic enzyme insufficiency
Young child : bronchiectasis, rectal prolapse, nasal polyp, sinusitis
Older child: DM, portal htn and cirrhosis, distal obstruction, pneumothorax, sterility

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23
Q

Management of CF?

A

PT for mucus clearance
Continuous prophylactic abx for resp infections eg flucloxacillin – chronic psuedomnoas infection
Nebs saline to increase sputum clearance
May have portacath for easier IV access
Lung transplant for end stage CF disease
Pancreatic replacement enzymes and high calories meal
Ursodeoxycholic acid to help bile movement

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24
Q

A six-week-old infant is referred to hospital with a three-week history of progressive wheeze, poor feeding, and poor weight gain. She now appears short of breath especially towards the end of feeds. She was born at term with no difficulties. Her routine neonatal examination was normal. What is the differential diagnosis?

A
VSD 
Asd 
Pda  
Bronchiolitis  
Reflux  
Immunodeficiency 
Tracheo/laryngomalacia
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25
Q

On examination, six week old who is progressive FTT, SOB, appear coryzal, is apyrexial and her oxygen saturations are 96% in air. Her femoral pulses are normal. There is a palpable thrill on the chest wall and on auscultation, there is a harsh pansystolic murmur, loudest at the left sternal edge. Jessie is tachypnoeic with some intercostal and sternal recession. There are fine crepitations audible in both lung fields. The liver is just palpable at 3cm below the costal margin. What is the most likely diagnosis and why?

A

VSD – progressive SOB, faltering growth after 1 week old; tachyponea; nsystolic murmur on L sternal edge; hepatomegaly and crackles and SOB (heart failure) ; No fever ; femoral pulses fine – indicates PDA unlikely

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26
Q

What investigations would you request for VSD and what would they show?

A

CXR – cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings, pulmonary oedema, Kelley b lines
ECG – biventricular hypertrophy
Echo – shows anatomy, hemodynamic effects, pulmonary htn

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27
Q

Management of VSD?

A

Diuretics combined with captopril - Furosemide for heart failure
Surgery between 3-6 months to prevent eisenmengers
Manage faltering growth with high calorie meal

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28
Q

What are other causes of heart failure in neonates and infants and older children?

A

Neonates –hypoplastic L heart syndrome, severe aortic stenosis, severe coarction of the aorta, interruption of the aortic arch
Infants – VSD, AVSD, persistent ductus arteriosus
Older- eisenmengers, rheumatic heart disease, cardiomyopathy
any age- increased free or pre load and anaemia and sepsis

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29
Q

How does a left to right shunt present and what are the types?

A

SOB

Eg ASD, VSD, PDA

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30
Q

How does a right to left shunt present and what are the types?

A

Cyanosis

Eg tetrology of fallot, TGA

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31
Q

How does common mixing present and what are the types?

A

SOB and cyanosis

Eg AVSD, complex congenital heart disease

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32
Q

What are differentials in a child with a wheeze?

A

viral episodic wheeze, asthma, bronhciolitis, foreign body aspiration, cystic fibrosis, pneumonia

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33
Q

How does bronchiolitis present?

A

<18 m
Coryzal symptoms precede a dry cough, SOB, recession crackles, hyperinflated chest, fever, wheeze, WONT feed due to coryzal sx will be mouh breathing and therefore cannot breastfeed

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34
Q

ix and mx for bronchiolitis?

A

Do pulse oximetry. Only do more if in resp failure.

Give oxygen, fluids, NGT feed

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35
Q

describe the presentation of a viral induced wheeze

A

Under 5s
Thought to be due to smaller airways eg RF include second hand smoke or prematurity
Episodic in nature, occurs each time have viral infection eg common cold
No interval symptoms

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36
Q

mx of VIW

A

No benefit from inhaled steroids but may use PO

Use bronchodilators, if that doesn’t work add ipratropium, then add montelukast. Give oxyegn.

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37
Q

What are the sx of asthma?

A

wheeze, dry cough, SOB, chest tight, worse at night and early morning, Fhx or person hs atopy

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38
Q

What ix are done for asthma?

A

PEFR or spirometry. Usually variability shown. Diagnosis shown by improvement on values with bronchodilator. - 12% improvement shows variability and is typical of asthma

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39
Q

pathophysiology of asthma

A

Bronchial inflammation, hypersensitivity, airway narrowing -pathophysiology

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40
Q

signs of moderate vs severe vs life threatening asthma attack?

A

mod:Able to talk in sentences;
Arterial oxygen saturation (SpO2) ≥ 92%;
Peak flow ≥ 50% best or predicted;
Heart rate ≤ 140/minute in children aged 1–5 years; heart rate ≤ 125/minute in children aged over 5 years;
Respiratory rate ≤ 40/minute in children aged 1–5 years; respiratory rate ≤ 30/minute in children aged over 5 years.

severe: Can’t complete sentences in one breath or too breathless to talk or feed;
SpO2  140/minute in children aged 1–5 years; heart rate > 125/minute in children aged over 5 years;
Respiratory rate > 40/minute in children aged 1–5 years; respiratory rate > 30/minute in children aged over 5 years.

life threatening:
Peak flow

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41
Q

mx of acute asthma attack?

A
  1. Supplementary high flow oxygen- 1 puff every 30-60 s of salbutamol up to a max of 10 puffs 4 hrly
  2. nebulised salbutamol (add on MgSO4)
  3. nebulised ipratropium bromide (add on MgSo4)
  4. Oral prednisone (1mg per kg for 3 days)/ IV hydrocortisone if not swallowing

SECOND LINE - send to PICU (already do this if its life-threatening)
5. IV magnesium sulphate

  1. IV Salbutamol
  2. IV aminophylline
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42
Q

What is the mx of chronic asthma?

A

Mild step 1: SABA
Step 2: preventor: ICS 200mcg starting dose
Step 3: add on: over 5- LTRA then LABA -less than 5 – LTRA only (montelukast)
OVER 5:
step 4: MART regime
Step 5: increase inhaled steroid dose to 800mcg/ day or consider theophylline or referral
If fail to respond – consider adherence, choice drugs, environment, diagnosis

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43
Q

what are examples of the asthma preventer drugs?

A

Inhaled steroids: beclamethasone, budesonide, fluticasone, mometason
Inhaled cromones: sodium cromoglycate

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44
Q

what are examples of the asthma reliever drugs?

A

Beta agonists: salbutamol, terbutaline

Ipratropium bromide : anticholinergic bronchodilators

45
Q

what are examples of the asthma add on drugs?

A

Long acting beta agonists: salmeterol, formoterol
Leukatriene receptor antagonists: montelukast
Theophyllines eg aminophylline
Oral steroids eg prednisolone
Omalizumab (anti IgE)

46
Q

How do spacers work?

A

LV spacer via mouth –> swallow to GI tract/ some just goes straight to lungs —> absorb to gut —> liver, first pass activation –> systemic circulation —-> lung absorbs

47
Q

long term SE of ICS?

A

adrenal suppression, growth suppression (though should not effect ultimate height)

48
Q

give some examples of some upper vs lower airway infections

A

Upper – rhinitis (viral), otitis media, tonsillitis, pharyngitis- sore throat (viral), laryngitis (viral), common cold (coryza), acute otitis media, sinusitis (uncommon)
Lower- bronchitis, croup (viral), epiglottitis (bacterial), tracheitis, bronchiolitis (viral), pneumonia

49
Q

What are the conducting vs respiratory airways?

A

conducting – nose, pharynx, larynx, trachea, bronchi, bronchioles – continuous passageway for air to move in and out of lungs

Respiratory airways - respiratory bronchioles, alveolar ducts, and alveoli. - gas exchange

50
Q

What are the differentials for stridor in a child?

A
  • Croup
  • Epiglottitis
  • Bacterial Tracheitis
  • Diphtheria
  • Laryngomalacia
  • Inhaled foreign body
  • Angioedema /
    anaphylaxis
51
Q

summarise croup

A
Mostly viral - paraflu!!
6 months to 6 yrs of age 
Sx: Harsh and loud stridor, self limiting, barking seal like cough, harsh stridor, recession, worse at night, hoarse voice  
Spring/autumn 
mx Steroids!
52
Q

summarise epiglottitis

A

Cause by Hib
1-6 yrs
Acute, life threatening
Sx: Painful throat, cant swallow saliva – drool, fever, soft stridor, minimal or absent cough
DO NOT look at epiglottis as can cause total airway obstruction and death

53
Q

most common causitive pneumonia organism in newborns vs infants vs 5+?

A

Newborn: group B strep
Infant: RSV, strep pneumoniae (most common), Hib, pertussis and chlamydia
5+: mycoplasma pneumoniae, strep pneumoniae, chlamydia pneumoniae
Hib and GBS is prior to vaccine

54
Q

atypical cause of penumonia?

A

chlamydia, pseudomonas, E.coli, measle, varicella

55
Q

presentation pneumonia?

A
fever
irritable
poor feed
cough (uncommon in neonates)
SOB
preceding URTI
pain (older children)
56
Q

What are signs of resp distress?

A

Cyanosis in severe cases.
Grunting.
Nasal flaring. In children aged under 12 months this can be a useful indicator of pneumonia
Marked tachypnoea
head bobbing
Chest indrawing (intercostal and suprasternal recession).
Other signs such as subcostal recession, abdominal ‘see-saw’ breathing and tripod positioning.
Reduced oxygen saturation (less than 95%).

57
Q

When should penunonia be considered in <3 yrs?

A

Bacterial pneumonia should be consider in under 3s when there is a fever with chest recession and a RR of above 50

58
Q

How may pneumonia appear on CXr?

A

On CXR: A dense or fluffy opacity that occupies a portion or whole of a lobe or lung that may or may not contain an air bronchograms

59
Q

mx for penumonia?

A

Neonates – IV Broadspectrum abx

Older children 1st line – Amoxicillin
2nd line erythromycin

Add co-amoxiclav if associated with influenza

Macrolides (the mycins) will cover the atypical pneumonias.

60
Q

what is empyema?

A

complication of pneumonia where pus collects in pleural space

61
Q

What is acute bronchitis?

A

inflammation of mucous membranes of the bronchial tubes.

usually caused by infections, allergens or asthma

62
Q

sx of acute bronchitis?

A

coryzal sx; fever; wheeze, cough 7-14 day hx

63
Q

What are differentials for bronchitis?

A

asthma and pneumonia (CXR and lung function tests rule out)

64
Q

chronic bronchitis vs bronchiectasis?

A

bronchial deformity in bronchiectasis is saccular or fusiform; in acute and chronic bronchitis, it is cylindrical.
both present the same and caused by chronic inflammations

65
Q

how does bronchiectasis present?

A

wet cough, crackles, recurrent pneumonia, haemoptysis

66
Q

How does the fetal circulation work?

A

Maternal blood in placenta –> umbilical vein –> Inferior VC –> RA –> (some blood will not go into foramen ovalis and goes to pulmonary artery and to lungs but that will mostly be bypassed by the patent ductus arteriosus which takes it straight to the aorta) foramen ovalis –> LA –> LV –> aorta–> umbilical artery –> circulates to body (head and neck first etc)

67
Q

What happens at first breath to the circulation?

A

First breath –> adrenaline released –> fluid out of lungs –>oxygenation –> inflates lungs –> resistance to pulmonary blood flow falls –> volume of blood to lungs increases

68
Q

What does the umb. artery clamping do to the circulation?

A

Umbilical artery clamped –> increases aortic pressure and decreases RA pressure as there is no longer blood from placenta –> change in pressure due to this plus the above closes the foramen ovale

69
Q

when does the ductus arteriosus shut?

A

1-2 days of life, when it does so it can leave the babies with some CHD in severe condition as they were dependent on the duct.

70
Q

How does heart failure present?

A

Heart failure: SOB, sweaty, poor feed, FTT, recurrent chest infections, tachypnoea/cardic, enlarged heart, murmur, hepatomegaly, cool peripheries

71
Q

What added sx does R sided HF cause?

A

oedema

72
Q

What are causes of HF?

A

Causes of HF: coarction of aorta, AS, (neonates- obstruction) VSD, AVSD, PDA, (infants-high pulmonary flow) Eisenmenger, rheumatic heart disease, cardiomyopathy (older children- L or R HF)

73
Q

What are examples of L to R shunts?

A

ASD, PDA, VSD, AVSD

74
Q

What are the ix of L to R shunts?

A

CXR (find signs for HF). ECG, echo. If they have RV hypertrophy that will be seen on ecg

75
Q

What is the mx of L to R shunts?

A

stabilise, increase caloric intake, NGT, diuretics, ACE-I, surgery to occlude the shunt

76
Q

How does ASD present?

A

Asymptomatic when young
Sx: fixed and widely split S2, SOB, ejection systolic murmur in pulmonary area
Sx older children: also have fixed splitting, palpitations (RA dilation causing SAN damage)

77
Q

Why does ASD have an ejection systolic murmur?

A

this is due to the blood travelling from higher to lower p and therefore moving from the L side to the R side and there therefore being more blood outflow with systole in the PA

78
Q

What is the pathophysiology of PDA?

A

Aorta –> PA –> increased p blood to the lungs –> epithelial changes –> SOB –> less feeds -> fail to thrive

79
Q

How does PDA present?

A

Symptoms: continuous murmur (pansystolic, machinery) in pulmonary area, best heard in clavicle, hepatomegaly, oedema, thrill, gallop rhythm, active precordium, SOB, FTT

80
Q

Why does PDA present with a pansystolic murmur?

A

as pressure is higher in the aorta than the pulmonary artery in both systole and diastole so the sound carries on through both;

81
Q

How does VSD present?

A

SOB, pansystolic murmur in LLSE, poor feed, FTT, tachypnoea, hepatomegaly, oedema, thrill, gallop rhythm

82
Q

What is VSD associated with?

A

IE

83
Q

What is AVSD associated with?

A

T21

84
Q

How does AVSD present?

A

Sx: poor feeding, FTT, tachypnoea, tachycardia, active precordium, thrill, gallop rhythm, hepatomegaly, Oedema, murmur from the regurg

If it is complete the baby will be cyanosed, there will be no murmur, pulmonary htn

85
Q

What are examples of stenosis of valves in children + their mx?

A

Coarctation of the aorta
aortic stenosis
pulmonary stenosis
Mx: monitor; dilation via stent or balloon

86
Q

how does Coarctation of the aorta present?

A

Weak femorals compared to brachials and feel for radio femoral delay, this is because the upper limbs are getting more blood due to the location of the coarctation after the upper limb vessels
Discrepancy between upper and lower BP
Ejection systolic murmur at upper sternal edge and collateral heard

87
Q

mx of Coarctation of the aorta ?

A

Mx: monitor and if severe may need a stent/surgical repair

88
Q

how does AS present?

A

Weak pulses, thrill in suprasternal and carotid area
Ejection systolic murmur in aortic area (RUSB)
Compensatory LV hypertrophy due to a thickened valve and trying increase blood outflow

89
Q

How does PS present?

A

Ejection systolic murmur on upper left sternal edge which radiates to the back with the pulmonary branches
Right ventricular heave due to compensatory RV hypertrophy

90
Q

What are differentials for cyanosis in the newborn?

A

Cyanosis can be caused by: persistent pulmonary htn of the newborn, heart problems, infection, metabolic errors, respiratory disorders

If saturated well and appear normal cyanosis is likely due to a structural heart problem

91
Q

emergency mx of cyanotic heart disease?

A

ABCDE

prostaglandins

92
Q

What is transposition of the great arteries?

A

Arteries on wrong side of the heart which means non oxygenated blood from the body keeps going around the body on the R side and the blood keeps circulating around the lungs on the left creating two closed circuits.

93
Q

how does transposition of the great arteries present?

A

shock, cyanosis, acidosis. Present with this a few mins/hrs after birth

94
Q

ix for transposition of the great arteries?

A

Ix: echo essential to see wrong position

95
Q

mx for transposition of the great arteries?

A

Mx: mix the blood in an emergency by opening the foramen ovale via balloon septostomy, then later replant the arteries

96
Q

what is tetralogy of fallot?

A

Has a large VSD, overriding of the aorta, pulmonary stenosis –> obstruction of outflow tract resulting in RV hypertrophy

97
Q

How does tetralogy of fallot present?

A

Sx: hypercyanotic spells, squatting on exercise, clubbing, ejection systolic murmur, cresendo, decrescendo

98
Q

Mx for tetralogy of fallot?

A

Mx: propranolol for cyanotic spells, do BT shunt repair at 6-9 months
Screen for 22q deletion

99
Q

How does tetralogy of fallot appear on a CXR?

A

CXR: boot shaped heart

100
Q

Which syndromes are associated with which congental heart defects?

A
Turner’s = coA, AS 
T21= AVSD, VSD, ToF 
Noonan’s = ASD, PS 
22q 11.2 deletion = ToF 
7q11.23 = AS, PS
101
Q

what is rheumatic fever?

A

Associated with heart defects

secondary to strep infection or scarlett efevr

102
Q

What is the mneumonic for the diagnostic jones criteria for rheumatic fever?

A
major criteria: JONES
Joint involvement
O - looks like herart for myocarditis
Nodules (SC)
Erythema marginatum
Sydenham chorea

(+ positive cultures)

103
Q

What is a MART regime?

A

MART treatment consists of a single inhaler containing both ICS and a fast-acting LABA

104
Q

What is laryngomalacia?

A

This is congenital stridor aka floppy larynx

Part of the larynx above the vocal cords (the supraglottic larynx) is structured in a
way that allows it to cause partial airway obstruction.

Chronic stridor on inhalation, when the larynx flops across the airway as the infant
breathes in.

A characteristic “omega” shape epiglottis on
Bronchoscopy.

105
Q

Describe the difference between pleural effusion and oedema

A

Effusion = accumulation fluid in pleural space either due to 1) too much fluid or 2) lack of clearance (sometimes proteins move in w the fluid) - sx: Sx: dull percussion, decreased chest wall movement, decreased breath sounds around fluid, SOB

oedema = Fluid in alveoli and interstitium -Sx: SOB, orthopnoea in L sided HF (as pulmonary congestion increases with lying down), cough up pink frothy sputum

106
Q

Describe primary spontaneous pnuemothorax

A

A pneumothorax happens when air leaks out of the lung. It becomes trapped in the space between the outside of the lung and the ribcage. The air can squash the lung and cause some or all of the lung to collapse.

Patients affected by PSP tend to be tall. Marfan’s syndrome or a Marfan’s habitus increases the risk.

Examination of the chest:
May show that the affected side moves less than the normal side.
The trachea is deviated away from the side of collapse, especially in tension pneumothorax.
Percussion reveals hyper-resonance over the collapse.
Breath sounds are reduced or absent over the affected area.
CXR: density on unaffected side; elvated hemithorax on unaffected side, mediastinal shift to unaffected side

107
Q

Describe heart block poem

A

If the R is far from P then you have a first degree
longer, longer, longer drop then you have a wenkebach
if some Ps dont get though then you have a mobitz 2
if Ps and Qs dont agree then you have a 3rd degree

108
Q

bundle branch block on ecg?

A

LBBB: WILLIAM
RBBB: MARROW

109
Q

Describe innocent heart murmur in child + its mx

A

soft, systolic, L sternal edge, no other sx, usually after viral illness
wait 6 months and then check again to see if resolved