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year 3 > Paediatrics Part 1 > Flashcards

Paediatrics Part 1 Flashcards

1
Q

What causes a wheeze

A

Obstruction of airflow within the thorax (heard in expiration)

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2
Q

What is stridor

A

Noise heard during inspiration

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3
Q

What causes stridor

A

Fixed extra thoracic airway obstruction

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4
Q

Investigations for Asthma

A
  1. Peak Expiratory Flow Rate < 80% predicted for height
  2. FEV1/FVC <80% predicted
  3. Concave scooped shape in flow volume curve
  4. Bronchodilator response to beta agonist therapy (15% increase in FEV1 or PEFR)
  5. Spirometry
  6. FeNO
  7. Blood eosinophil levels
  8. IgE
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5
Q

What is FEV

A

How much air a person can exhale during a forced breath in one second

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6
Q

What is FVC

A

Total amount of air exhaled during the FEV test

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7
Q

Name two short acting beta two agonists

A

Salbutamol, terbutaline

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8
Q

Name two long acting beta-2 agonists

A

Salmeterol, formoterol

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9
Q

Name a short-acting anticholinergic

A

Ipratropium Bromide

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10
Q

Name an inhaled corticosteroid

A

Budesonide

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11
Q

Name an oral steroid used in acute asthmatic attakcs

A

Prednisolone

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12
Q

Is serum IgE measured in an asthma diagnosis

A

No

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13
Q

Treatment pathway for asthma

A
  1. Short acting b2

Step 2: Short acting b2 + low dose ICS

Step 3: Short acting b2 + high dose ICS or low dose inhaled steroid + long acting bronchodilator

Step 4: Theophyllines or ipratropoum +/- alternate day steroid.

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14
Q

How is acute severe asthma treated in children >5

A

Sabultamol via nebuliser

Oral Prednisolone (30-40 mg)

Assess after 15 mins and repeat - then ADMISSION

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15
Q

How is acute life-threatening asthma treated

A
  1. Ipratropium via nebuliser (salbutamol 5mg and 0.35mg ipratropium every 20 mins)
  2. Oral Prednisolone or IV Hydrocortisone

Repeat and hospital admission

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16
Q

Acute severe asthma vs life threatening

A

PEF: 33-50% vs <33%

Breathless to speak vs silent chest

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17
Q

Why is FENO measured

A

Produced by eosinophils in the lung alveoli

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18
Q

When are long acting b2 agonists used

A

As prophylaxis

In patients on inhaled budesonide or beclometasone (400 msg.day)

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19
Q

What type of hypersensitivity reaction is asthma

A

Type 1

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20
Q

When is the value of FEV1 normal

A

When it is 80% of the normal predicted value of the patient

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21
Q

What indicates airways restriction

A
  1. Ratio of FEV1/FVC is greater than 0.7 AND FVC is lower than 80% of predicted value
  2. Or just a low FVC
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22
Q

What indicates airways obstruction

A
  1. FEV1/FVC < 0.7 (in other words, they can breathe out fast but obstruction stops them from expelling Total capacity)
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23
Q

Define type I respiratory failure

A

Hypoxia but not hypercapnia

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24
Q

Genetic factors in asthma

A

ADAM33

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25
Q

Three characteristics of asthma

A
  1. Airflow limitation
  2. Airway hyper repsonsiveness
  3. Bronchial inflammation
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26
Q

RF for asthma

A
  1. Atopy
  2. Family history of asthma and atopy
  3. Obesity
  4. Premature birth
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27
Q

Pathophysiology of asthma

A
  1. Inflammed airways react to triggers
  2. Airways narrow and produce excess mucous making it difficult to breathe
  3. Bronchi spasms
  4. Inflammation further narrows airways -> coughing
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28
Q

A child has an X-Ray after a bout of choking, however nothing is seen on the X-Ray despite indications of airway obstruction. What is the likely diagnosis

A

Aspiration of food (food is radiolucent)

Objects are radiopaque

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29
Q

Investigations for foreign body aspiration

A
  1. Indirect signs of obstruction (subglottic density or swelling)
  2. CT Scan
  3. Laryngoscopy to visualise objects
  4. Nasal speculum
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30
Q

Signs of foreign objects in the nose

A
  1. UNilateral, foul-smelling rhinorrhoea

2. Epixstasis (nose bleeds)

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31
Q

Treatment of foreign objects in the nose

A
  1. Blow nose while plugging unobstructed nostril

2. Positive pressure ventilation through the mouth and blocking unobstructed nostril

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32
Q

What is laryngomalacia

A
  1. Congenital abnormality of the laryngeal cartilages
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33
Q

What islaryngomalacia

A
  1. Shortened aryepiglottic folds turn larynx into an omega shape, obstructing airflow
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34
Q

What is contained within the larynx

A

The Vocal Cords

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35
Q

Symptoms of laryngomalacia

A

Inspiratory stridor (worse lying supine)

Breathing difficulties

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36
Q

Diagnosis of laryngomalacia

A

Laryngoscopy or Bronchoscopy

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37
Q

Onset of laryngomalacia

A

few weeks old, self corrects 12-18 months

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38
Q

No infectious causes of rhinitis

A
  1. Allergens
  2. Irritants (cold, dry air, smoke)
  3. Emotional Stress
  4. Excercise
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39
Q

Symptoms of rhinitis

A
  1. Nasal Congestion
  2. Sneezing
  3. Sniffling
  4. Allergic Salute
  5. Conjunctivitis (e.g., allergic shiners)
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40
Q

Diagnosis of rhinitis

A

Symptoms

History of Atopy

Skin test for specific allergens

Specific IgE measurements

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41
Q

Treatment of rhinitis

A

Avoid allergens

Antihistamines
Montelukast
Intranasal steroids

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42
Q

What is montelukast

A

Leukotriene receptor antagonist = relaxation of smooth muscles and reduces inflammation

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43
Q

Causes of infectious rhinitis

A

Virus

  1. Rhinovirus
  2. Influenza virus
  3. RSV
  4. Parainfluenza
  5. Adenovirus

Bacteria:

  1. Strep pneumonia
  2. H. influenzae
  3. Moraxella cattarhalis
  4. Staph aureus

Fungi: Aspergillus in immunocompromised

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44
Q

What is rhinosinusitis

A

Bacteria and fungi can spread to the sinuses and cause inflammation there too

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45
Q

What is the only sinus present at birth

A

Ethmoid

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46
Q

When do maxillary sinuses develop

A

1 month - 1 year of age

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47
Q

When to sphenoid sinuses develop

A

1-2 years of age

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48
Q

When do frontal sinuses devleop

A

After age 10

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49
Q

Symptoms of rhinitis

A
  1. Low grade fever
  2. Low apetite
  3. Congestion
  4. Sneezxing
  5. Nasal discharge
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50
Q

Rhinitis vs rhinosinusitis

A

Low fever vs high grade fever
Nasal Discharge > 10 days
Facial pain or pressure
Voice change

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51
Q

Diagnosis of infectious rhinitis

A
  1. Symptoms

2. Facial X-Ray or CT Scan

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52
Q

Treatment of rhinitis

A

Rest
Fluid
Nasal Irrigation

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53
Q

Treatment of bacterial rhinosinusitis

A

Amoxicillin 10 days

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54
Q

Onset of pharyngitis

A

3-14

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55
Q

Where do pharyngitis infections typically spread to

A

The Tonsils (tonsillopharyngitis)

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56
Q

Symptoms of Viral Tonsillopharyngitis

A
  1. Low grade fever
  2. Sore Throat
  3. Voice Hoarseness
  4. Symptoms of the common cold (nasal congestion, conjunctivitis, cough)
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57
Q

Diagnosis of viral tonsillopharyngitis

A
  1. Erythema and oedema of pharynx and tonsils
  2. No Exudates
  3. Non-Tender Anterior cervical lymphadenopathy
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58
Q

Tonsilopharyngitis vs strep throat

A

Low grade fever vs high grade fever

  1. Sore throat in both
  2. Voice hoarseness in both
  3. common cold symptoms vs none
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59
Q

Diagnosis in viral tonsillopharyngitis vs strep throat

A

Erythema and oedema of pharynx and tonsils in both

No exudates vs Grey-white exudates

Non-tender anterior cevical lymphadenopathy vs tender anterior cervical lymphadenopathy

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60
Q

What criteria is used to identify strep throat

A

Centor Criteria:

C - can’t cough
E - exudates
N - Nodes (tender lymph)
T- Temperature > 38 degrees

OR - Age

3-14 (1)

15-44 (0)

> 44 (-1)

2-3 (test for group a strep)

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61
Q

Testing for group A strep

A
  1. RADT (rapid antigen detection testing)

2. Throat culture

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62
Q

Treatment of Group A strep

A
  1. Penecillin V

2. Amoxicillin

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63
Q

Bacterial tonsillopharyngitis in Children > 10 vs <10

A

> 10:

Peritonsiloar abscess

<10:

Retropharyngeal abscess

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64
Q

Symptoms of tonsilopharyngitis

A
  1. High Fever
  2. Drooling
  3. Dysphagia
  4. Odynophagia (painful chewing)
  5. Muffled voice
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65
Q

Peritonsilar abscess vs retropharyngeal abscess symptoms

A

Trismus (difficulty opening the mouth) vs Torticolis (stiff neck)

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66
Q

Signs of bacterial tonsillopharyngitis upon examination

A
  1. Enlarged tonsils that move the uvula sideways

2. Bulge in posterior pharyngeal wall

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67
Q

Diagnosis of bacterial tonsillopharyngitis

A
  1. Clinical

2. X-ray or CT scan to visualise the abscess

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68
Q

Treatment of tonsillopharyngitis

A

1, Incision and drainage

  1. Ampicillin
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69
Q

Where does a laryngitis infection spread to

A

Laryngotrachobronchitis (CROUP)

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70
Q

Onset of CROuP

A

6 months - 3 years of age

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71
Q

Cause of croup

A
  1. Parainfluenza
  2. RSV
  3. Adenovirus
  4. Infleuzna
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72
Q

Symptoms of croup

A
  1. Prodrome fever and nasal congestion (as it spreads)
  2. Barking cough
  3. Hoarse voice
  4. Inspiratory stridor
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73
Q

Diagnosis of corup

A

Anterior neck X-Ray

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74
Q

Sign found for croup on an X-Ray

A

Subglottic narrowing (steeple sign)

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75
Q

Treatment of Corup

A

Dexamthesone
Cool, humidified air, antipyretics

Repeat doses of racemic epinephrine

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76
Q

Causes of bacterial laryngitis

A
  1. Group A strep
  2. Strep pneumonia
  3. H influenzae

Have a preference for superior portion of the larynx and epiglottis

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77
Q

Symptoms of epiglottitis

A
  1. Rapid onset of high fever
  2. Sore Throat
  3. Hot potato voice
  4. Severe ARDS
    5/ Tripoding to keep epiglottis open
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78
Q

Diagnosis of epiglottiitis

A
  1. Lateral neck x-ray
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79
Q

Treatment of epiglottitis

A

EMERGENCY

Intubation or Tracheostomy

Antibiotics: Ceftriaxone

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80
Q

What lung is usually affected by foreign body aspiration and why

A

Right, because the right bronchi are wide and more vertical.

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81
Q

Non-specific symptoms to foreign body aspiration

A
  1. SUDDEN onset of SOB
  2. Coughing
  3. Gagging
  4. Choking
  5. Drooling
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82
Q

Investigation findings in foreign body aspiration

A

Diminished breath sounds

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83
Q

What anatomical structure usually causes stridor (hint: extrathoracic noise)

A

Trachea (usually when partially obstructed)

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84
Q

What anatomical structures usually cause expiratory wheezing

A
  1. Intrathoracic trachea
  2. Bronchi
  3. Bronchioles
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85
Q

Where will the wheeze be heard

A

Localised the blocked area

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86
Q

In what aspiration cases would no wheeze on stridor be heard

A

When there is complete obstruction (noises only occur with partial obstruction)

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87
Q

Investigations for foreign body aspiration

A
  1. Neck or Chest Radiograph
  2. Chest CT
  3. Bronchoscopy to visualise and remove the object
  4. If it cannot be removed - THORACOTOMY
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88
Q

As food can be radiolucent, what other signs can we see on a neck or chest radiograph for foreign body aspiration

A
  1. Complete Obstruction -> Atelectasis (collapse, partial or complete of the entire lobe) distal to obstruction as its blocking the airway
  2. Partial Obstruction -> Focal Hyperlucency + reduced pulmonary marking distal to obstruction as its blocking the airway like a one way valve.
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89
Q

Symptoms of Asthma

A
  1. Dry Cough
  2. Chest Tightness
  3. SOB
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90
Q

What is characteristic about wheeze findings in Asthma

A
  1. Wheeze is not localised, it happens ALL over both lungs.
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91
Q

Diagnosis of Asthma

A
  1. CXR:
    - Normal but may show diffuse hyper lucency due to airway entrapment
    PFTs: Decreased FEV1 to FVC

FBC: Eosinophils

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92
Q

What kids are affected by acute bronchitis

A

Children UNDER 2

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93
Q

What viruses cause acute bronchitis

A
  1. Influenza A and B
  2. Parainfluenza
  3. Adenovirus
  4. RSV
  5. Rhinovirus
  6. Coronavirus
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94
Q

What bacteria can cause acute bronchitis

A
  1. Bordatella pertussis
  2. Mycoplasma Pneumoniae
  3. Ch;amidyia pneumoniae
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95
Q

Symptoms of Acute Bronchitis

A

Upper respiratory tract infection:

  1. Congestion
  2. Sore Throat
  3. Low Grade Fever

Lower tract:

GOLD: Cough lasting more than 5 days

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96
Q

Ausculattion sounds for acute bronchitis

A
  1. Scattered Rhoncii
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97
Q

What is rhoncii

A

Low pitched wheezing sounds caused by lung secretions

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98
Q

In what conditions is rhoncii heard in

A

COPD

  1. CF
  2. Bronchiectasis
  3. Pneumonia
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99
Q

Three stages of whooping cough

A

Whooping cough is a BRONCHIAL disease:

Catarrhal (1-2 weeks): Mild fever, cough and coryza (cold)

Paroxysmal (2-6 weeks): Violent coughing characteristic of whooping cough (inspiration causes whooping noise)

Convalescent (2-4 weeks): Lessening symptoms that take a whole month to reolve

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100
Q

What other diseases can cause a whooping cough-like syndrome

A

Chlamidyia pneumonia, adenovirus or mycoplasma pneumonia.

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101
Q

Examination of whooping cough

A

Eyes: Subconjunctival haemorrheages

CXR:

Blood counts: Leucocytosis and lymphocytosis

Prenatal swab: bordatella pertussis

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102
Q

Treatment for acute bronchitis

A
  1. Just rest and fluid
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103
Q

Age range of acute bronchiolitis

A

6 months to 2 years

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104
Q

What virus causes acute bronchiolitis

A

RSV (MAINLY)

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105
Q

Symptoms of acute bronchiolitis

A
  1. URTI symptoms: congestion, sore throat, cough and low grade fever
  2. Respiratory Distress:
  • feeding difficulties
  • Episdoes of apnoea
  • 70 breaths/ min (younger than 12 months)
  • 50 breaths/min (older children)
  • O2 saturation < 92%
  • Nasal Flaring
  • Intercostal, subcostal and suprasternal retractions.
  • Cyanosis
  • Lethargic or dehydrated
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106
Q

Risk Factors for Acute Bronchiolitis

A
  1. Being PREMATURE
  2. Younger than 12 weeks
  3. Low birth weight
  4. Didn’t breastfeed
  5. Chronic pulmonary disease
  6. Congenital heart disease
  7. Immmunodeficiency
  8. Neurologic disease that impairs sputum clearance.
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107
Q

Investigations for acute bronchiolitis

A
  1. Pulse Oximetry
  2. CXR: Hyperinflation, atelectasis and consolidation
  3. Nasopharyngeal swab for rapid antigen testing for RSV
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108
Q

Management of acute bronchiolitis

A
  1. Oxygen to push over 92%
  2. Tachypnoea - use an NGT
  3. Nebulised adrenaline for wheeze
  4. Mechanical ventilation
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109
Q

Prophylaxis for acute bronchiolitis

A
  1. Palivizumab (monoclonal antibody for RSV) in those at risk IM.
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110
Q

Onset of early onset Neonatal pneumonia

A

First 3 days of life.

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111
Q

Three main causes of early onset neonatal pneumoniae

A
  1. Group B
  2. Escherichia Coli
  3. Listeria Monocytogenes
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112
Q

Three main causes of late onset neonatal pneumonia (3rd day to 3rd week)

A
  1. Strep pneumoniae
  2. Staph aureus
  3. Strep pyogenes
  4. Adenovirus, parainfluenza, influenza and enteroviruses.
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113
Q

Three main causes of 3 weeks to 6 months pneumonia

A
  1. RSV
  2. Parainfluenza
  3. Adenovirus
  4. Chlamidyia trachoma’s
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114
Q

What distinguishes a C. pneumoniae infection from other strains

A
  1. Afebrile pneumonia of infancy
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115
Q

Three main causes of pneumonia from 6 months to 5 years

A
  1. RSV
  2. Influenza A and B
  3. Parainfluenza
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116
Q

Most common cause of pneumonia in children over 5

A

Atypical bacteria and strep pneumonia

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117
Q

How to differentiate between atypical and strep pneumonia

A
  1. Atypical bacteria causes diffuse pneumonia

2. Strep pneumoniae causes consolidated pneumonia

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118
Q

If a child has travelled and symptoms that last a few weeks, what else should e expected other than pneumonia

A
  1. TB
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119
Q

If a child has recurrent pneumonias or associated GI symptoms, what should be suspected instead of pneumonia

A

CF

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120
Q

If a child has the symptoms for pneumonia but has exposure to farm animals as a history, what should be suspected

A

Q Fever, caused by Coxiella Burnetti

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121
Q

If a child is exposed to Mouse droppings, what pneumonia strain are they suspectible to

A

Hantavirus

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122
Q

Three types of fungal pneumonias found in children

A
  1. Coccidiodomycosis
  2. Histoplasmosis
  3. Blastomycosis
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123
Q

Symptoms of pneumonia

A

Younger:

  1. Fever
  2. Poor Feeding
  3. Lethargy
  4. Apnoea

Older:

  1. Fever
  2. Cough
  3. Tachypnoea

Infection near pleural surface:
Pleuritic chest pain

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124
Q

Symptoms seen in bacterial pneumonia vs viral pneumonia

A

Sudden vs Gradual
More Severe vs Mild
No Upper respiratory symptoms vs upper airway symptoms.

Focal bronchial breath sounds vs diffuse, bilateral sounds.

Crackles in both

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125
Q

Auscultation signs for lobar pneumonia

A
  1. Dullness to percussion
  2. Crackles
  3. Decreased breath sounds
  4. Tactile vocal remits
  5. Bronchial Breathing
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126
Q

What is tactile vocal remits

A

Increased chest vibrations from talking

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127
Q

Pneumonia investigations

A
  1. Sputum
  2. Nasopharyngeal aspirate for viruses in infants
  3. Blood culture
  4. CXR (not routine and only in critical illness)
  5. Pleural fluid aspirate culture and antigen testing
  6. Viral titres
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128
Q

Antibiotic therapy for pneumonia by age

A

<5: Strep pneumonia: Amoxicillin or Co-amoxiclav

> 5: Amoxicillin for mycoplasma pneumoniae

For staph aureus: Amoxicillin with flucloxacillin

Sevre: Co-amoxiclav and cefotaxime

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129
Q

What is the curb-65 criteria for pneumonia

A

C - Confusion
U - Urea > 19mg/DL
R - Resp Rate > 30
B - Systolic BP <90 or Diastolic < 60

65 - Age

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130
Q

Complications of pneumonia

A
  1. Parapneumonic effusion from inflammation

2. Cavitation (empyema) as the infection is localised and has been walled off by the immune system

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131
Q

Atelectasis vs pneumonia

A

X Rays:

Wedge-Shaped
Consolidation with Apex at Hilum
Ipsilateral shift of structures due to volume loss

X Rays:
Normal or increased volume
Conslidation with no apex at hilum
No shift in structure

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132
Q

Lab Tests in pneumonia

A
  1. Elevated WBC
  2. Elevated CRP (more elevated in bacteria than viral)
  3. Blood cultures
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133
Q

Treatment of empyema

A

Urokinase via the chest drain (40,0000 U 12-hourly for three days

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134
Q

Management of TB

A

2 Months: Isoniazid, Rifampicin and Pyrazinamide

THEN 4 months: Isoniazid and Rifampicin

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135
Q

Pulmonary feature of a child with HIV

A

Lymphoid Interstitial Pneumoniitis - responds to steroids

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136
Q

What types of immunodeficiency can cause recurrent infection of the lower airway

A
  1. IgA deficiency
  2. IgG subclass deficiency
  3. Defective cell-mediated immunity
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137
Q

Diagnosis of COVID-19

A
  1. PCR, rapid antigen testing
  2. Oximetry (<91%)
  3. Clinical Frailty Scale
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138
Q

Types of Non-Invasive Ventilatory support for COVID-19

A
  1. High-Flow Nasal Oxygen
  2. Continuous positive airway pressure
  3. Non-Invasive ventilation (masks)
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139
Q

What corticosteroid is given to COVID patients

A

Dexamethasone for 10 days

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140
Q

Treatment of COVID-19 pneumonia in adults

A

Remdesivir for 5 days

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141
Q

Second line treatment for COVID-19 (corticosteroids)

A

Tocilizumab

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142
Q

How long does it take for a neonate to have their first meconium

A

48 Hours

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143
Q

A neonate has not passed meconium within 48 hours, presenting with abdominal distention and refusing to feed. Name three differentials

A

Imperforate Anus
Meconium Ileus
Hirschsprung Disease

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144
Q

What is imperforate Anus

A

A non-patent or tiny anal opening

Sometimes there could be a vesicorectal fistula causing drainage of meconium through the pneis.

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145
Q

What syndrome is associated with an imperforate anus

A

VACTERL SYNDROME

Vertebral Defects
Anal Atresia
Cardiac Anomalies
Tracheoosophageal Fistula 
Esophageal Atresia
Renal Anomalies
Limb Anomalies
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146
Q

Diagnosis of VACTERL Syndrome

A

USS of spine, heart, abdomen and Limbs

NG Tube and Chest X Ray for tracheoosophageal fistula and oesophageal atresia

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147
Q

Treatment of VACTERL syndrome

A

Decompression and Aspiration through an NG tube

  • IV Fluids
  • Nil By Mouth

Perineal Anoplasty - low types

Colostomy - high type

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148
Q

What is Meconium Ileus

A

A sign of cystic fibrosis - where the meconium gets stuck in the terminal ileum.

Might be associated with distended abdomen, tacky, fever if perforated.

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149
Q

Diagnosis of Cystic Fibrosis

A

Abnormal Sweat Test

2 CF-Related Mutations

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150
Q

Investigations for meconium Ileus

A

DRE:
Empty Rectom with No Meconium

Surgical Emergency as it can lead to Bowel Perforation -> peritonitis -> sepsis -> death

Abdominal X-Ray:

  1. Dilated bowel loops proximal to the obstruction.

Soap Bubble appearance.

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151
Q

Sign of meconium peritonitis on an abdominal x ray

A

Calcified intraperitoneal meconium

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152
Q

Treatment of meconium Ileus

A

Decompression - Hypertonic contrast enema to break up meconium

Laparotomy

Perforation = Surgery.

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153
Q

What is Hirschsprung’s disease

A
  1. Meissner’s plexus and Auerbach’s plexus are responsible for smooth muscle contraction and relaxation are missing -> stopping function of the rectum and distal sigmoid colon.

Meconium builds up at the sigmoid and rectum -> megacolon -> perforation.

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154
Q

Diagnosis of Hirschsprung disease

A

Recta Examination -> tight sphincter and explosive release of gas and stool.

Anorectal manometry (dilation of the sphincter with a balloon)

Biopsy to see reduced plea in the mucosa and submucosaa

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155
Q

Treatment of Hirschsprung’s

A

Resection of ganglionic part of colon and reattachment to the rectum

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156
Q

What factors can lead to constipation

A

Dietary:
Low fibre
Decreased fluid

Behavioural:
Anxiety
Fear of painful stools
Embarrassment

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157
Q

What is the problem if a child doe snot poo

A

Water continues to be reabsorbed -> hard stools/

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158
Q

What medications can cause constipation

A
  1. Anticholinergic

2. Iron supplements

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159
Q

What conditions can cause constipation

A
  1. Hypothyroidism
  2. Renal failure
  3. Hypercalcaemia and Hypokalaemia
  4. Spina Bifida and Inflammatory Bowel Disease
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160
Q

Examination findings in constipation

A
  1. Anal fissures (might be withholding during pain)

2. Stool in left abdomen

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161
Q

Investigations for constipation

A
  1. TFTs, BUN and creatinine, Calcium and K+, CRP for inflammatory bowel disease
  2. Abdo X ray or USS
  3. Spinal X Ray or MRI
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162
Q

Treatment of functional constipation

A
  1. Disimpaction using a rectal thermometer
  2. Rectal Glycerin
  3. Prune Juice or osmotic laxatives (propylene glycol) or through an NG tube
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163
Q

Diet modifications for constipation

A
  1. Increase fruit, vegetables and whole grains

2. Ensuring adequate fluid intake.

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164
Q

What structure marks if it is an Upper or Lower GI bleeding

A

Above the ligament of Treitz (suspensory ligament of the duodenum): Oesophagus, stomach and duodenum

Below the ligament of treats: small intestines, large intestines and rectal

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165
Q

WHAT ARE OCCULT GI BLEEDS

A

NO VISIBLE EVIDENCE OF A BLEED: detected by a faecal occult blood test

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166
Q

Symptoms of Upper GI bleeding

A
  1. Haematamesis - Fresh blood indicating ongoing bleed

2. Melena (small amounts of blood that’s passed through the whole GI system)

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167
Q

What is the significance of coffee ground like bleeds in upper GI bleeds

A

Blood has oxidised and bleeding has stopped (old blood)

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168
Q

Symptoms of lower GI bleeds

A
  1. Haematochezia (fresh blood through anus).
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169
Q

First management step in a child with an active bleed complaint

A
  1. Evaluate general appearance (activity, tone, level of consciousness and skin colour, haemodynamic instability)
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170
Q

Symptoms of mild hypovolaemia

A
  1. Slightly dry mouth
  2. Increased thirst
  3. Slightly reduced urine output
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171
Q

Symptoms of moderate hypovolaemia

A
  1. Significantly reduced urine output
  2. Tachycardia
  3. Orthostatic Hypotension
  4. Reduced skin turgour
  5. Dry Mucous Membranes
  6. Irritability
  7. Delayed Cap refill (2-3 seconds)
  8. Deep rests
  9. Indants -> Sunken open fontanelle
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172
Q

Symptoms of severe hypovolaemia

A
  1. Anuria
  2. Hypotension
  3. Cap refill > 3 secs
  4. Cool and Mottled Extremities
  5. Lethargy
  6. Deep Resps
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173
Q

What liver functions are done for GI bleeds

A 
ALT
AST
GGT
Bilirubin 
Albumin

Coagulation studies: Fibrinogen, PT, PTT, INR

Nasogastric Lavage

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174
Q

In well-appearing children, what investigations might be done in a Upper GI bleed

A
  1. Upper Endoscopy
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175
Q

In well-appearing children, what investigations might be done in a Lower GI bleed

A
  1. Colonoscopy
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176
Q

In ill-appearing children, what initial investigation must be done in a or Upper Lower GI bleed

A
  1. 2 Peripheral IV Catheters for fluid resuscitation

2. Blood Transfusion

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177
Q

Signs of fluid overload

A
  1. Crackles
  2. Gallop Rhythm
  3. Hepatomegaly
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178
Q

What is the most common cause of GI bleeds in neonates (<1 month)

A
  1. Maternal Blood Ingestion

Swallowed during delivery or from fissures during breast feeding

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179
Q

How can we check for maternal blood in neonate’s faeces

A

Apt-Downy Test:

Haemolysis of newborn’s stool + NaOH -> Maternal Blood if yellow

If the same = foetal haemoglobin

Spetcrophotometric Assay: shows composition of maternal blood

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180
Q

What can cause anal fissures

A
  1. rectal Thermometers
  2. Birth Injuries
  3. Sexual Abuse
  4. Constipation
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181
Q

Where are anal fissures often found

A

Posterior Midline (MOST OF THE TIME)

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182
Q

What is alarming about a lateral fissure

A

They’re usually caused by infections rather than trauma: Syphilis, HIV or TB

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183
Q

Treatment of anal fissure

A
  1. Heal on own

2. Frequent diaper changes

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184
Q

What can cause food protein-induced proctocolitis

A
  1. Cow’s Milk
  2. Soy Proteins

In Infant formula’s or even through breast milk if mother’s been drinking it

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185
Q

Symptoms of food protein-induced allergic proctocollitis

A
  1. Irritability
  2. Back Arching during feeding
  3. Atopic Dermatitis
  4. Urticaria
  5. Wheezing
  6. Coughing
  7. Vomiting
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186
Q

Diagnosis of food protein-induced allergic proctocollitis

A
  1. In breastfeeding women: Stop mother from drinking milk
  2. In formula feeding: Elemental formulas only with no cow’s milk or soy milk

Then reintroduce cow/soy after 7 days. If it continues, this is a milk allergy and should be stopped again

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187
Q

What can cause GI bleeds if the neonate appears ill and has signs of haemodynamic instability

A

Necrotising enterocolitis: where the portion of the intestines becomes ischaemic and dies from inflammation from pathogens

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188
Q

Where does necrotising enterocolitis usually infect

A

Distal small bowel and the ascending colon and caecum

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189
Q

What babies are most vulnerable to necrotising enterocolitis

A

Premature babies < 1500 g

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190
Q

RF for formula-feeding

A
  1. Loss of protective immunity and bacteria causing flora to be weakened
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191
Q

Onset for necrotising enterocolitis

A

First week of life

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192
Q

Symptoms for necrotising enterocolitis

A
  1. Poor Feeding
  2. Bloating
  3. Bilious Vomiting
  4. Bloody Stools
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193
Q

What is seen on a physical exam for necrotising enterocolitis

A
  1. Abdominal distention
  2. Right lower quadrant mass
  3. Abdo wall erythema
  4. Tenderness
  5. Decreased bowel sounds
  6. Visible intestinal loops

SHOCK

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194
Q

Investigations for necrotising enterocolitis

A
  1. Abdominal Radiograph showing multiple loops of dilated bowel

Pathogonomic pneumatosis intestinalis (air in the bowel wall from bacteria) -> extends to portal veins

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195
Q

Diagnosis of necrotising Enterocolitis

A
  1. Hyponatraemia due to third spacing of fluid
  2. Metabolic acidosis (lactic acid build up from ischaemic bowels)
  3. Thrombocytopenia (DIC)
  4. Neutropenia (sepsis)

Blood cultures for causative pathogens

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196
Q

What criteria is used to classify necrotising enterocolitis

A

Bell’s criteria

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197
Q

Treatment of necrotising enterocolitis

A
  1. Discontinue enteral feeds and switch to parenteral nutrition (Central venous catheter, gastric decompression w/a NG tube)
  2. Benzylpenecillin, metronidazole and gentamicin
  3. Systemic Support: Assisted ventilation

Fluid replacements, inotropes

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198
Q

What is intestinal malrotation with volvulus

A

Twisting of the mesentery around the mesenteric artery

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199
Q

Symptoms of Intestinal Malrotation with volvulus

A
  1. Acute, bilious vomiting
  2. Abdo distention
  3. Bloody diarrhoea
  4. Peritonitis/ sepsis
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200
Q

Diagnosis of Intestinal Malrotation with volvulus

A
  1. USS or abdo x ray in upright position: Distended loops of bowel with air fluid levels
  2. Upper GI contrast series: Spiral shaped duodenum in right lower quadrant instead of left upper quadrant
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201
Q

Treatment of intestinal malrotation with volvulus

A
  1. Stop feeding
  2. FLuid resus w normal saline
  3. NG tube decompression
  4. Vancomycin or Cephalosporins (broad spectrum)
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202
Q

Surgical procedures to untwist the volulus

A

IMMEDIATE laporotomy

LADD’s procedure: straightening out the intestines

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203
Q

What conditions cause GI bleeds between 1 month and 6 years

A
  1. Infectious Colitis
  2. Meckel’s Diverticulum
  3. Intussusception

Rarely: Peptic Ulcer disease and juvenile polyposis

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204
Q

What organisms can cause infectious colitis

A
  1. Shigella
  2. Salmonella
  3. Yersinia
  4. Campylobacter
  5. E. coli
  6. Clostridium Difficile.

CMV
Entamoeba histolytica

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205
Q

Symptoms of Infectious colitis

A
  1. Acute, bloody diarrhoea
  2. fever
  3. Abdo Pain
  4. Cramps
  5. Ill contacts and history of eating undercooked food or takeaways
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206
Q

What complication can result from E. coli

A

Haemolytic Ureamic Syndrome

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207
Q

What is HUS

A

Microangiopathic haemolytic anaemia
Thrombocytopenia
Renal Failure

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208
Q

What organisms can cause infections from eggs or chicken

A

Salmonella or Campylobacter

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209
Q

What organism can cause infections from milk or pork

A

Yersinia

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210
Q

What organism can cause infections from ground meat, cattle and goats

A

E coli

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211
Q

Where can anteamoeba hystolitca infections arise

A
  1. Recent travel to endemic countries and poor sanitation
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212
Q

What organism can cause infections from reptiles

A

Salmonella

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213
Q

Diagnosis for infectious colitis

A
  1. Stool Cultures
  2. PCR
  3. Microscopy for parasites
  4. Rapid stool assay for shigella
  5. Blood CUlture
  6. Check for hypokalaemia
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214
Q

What would be found in HUS

A
  1. Increased BUN
  2. Creatinine
  3. Schistocytes
  4. Haematuria
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215
Q

Treatment for Infectious colitis

A
  1. Rehydration (especially for HUS)

IV if unable to hold down fluids

Oral Rehydration Solution otherwise

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216
Q

If the child has no improvements after 24 hours of Rehydration or Persistent diarrhoea, what should be done

A

Admission to hospital

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217
Q

What diseases can infectious colitis mimic

A

Crohn’s and UC

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218
Q

What is pseudomembranous colitis

A

Caused by an overgrowth of C difficile from antibiotic use, causing inflammation in the large intestines. Yellow white plaques form pseudomembranes on the mucosa.

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219
Q

What is characteristic of Meckel’s Diverticulum

A

RULE of 2s:

  • 2% of the population
  • 2 years age onset
  • 2 x M > F
  • 2 inches long
  • 2 feet of the ileocaecal valve
  • 2 Types of ectopic tissue (gastric mucosa and pancreatic tissue)

The gastric mucosa secretes acid

Pancreatic tissue secretes alkaline pancreatic juices - eroding the wall

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220
Q

Symptoms of Meckel’s Diverticulum

A
  1. USUALLY Asymptomatic

Gastric Mucosa:
- Occult bleeding = iron deficiency

Painless rectal bleeding

Ectopic pancreatic tissue:
- Abdo Pain
Increased serum amylase

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221
Q

Diagnosis of mocker’s diverticulum

A
  1. Laporoscopy in asymptomacti individuals

2. Techetium 99 pertechnate scintigram to detect gastric mucosa outside the stomach

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222
Q

Treatment of mocker’s diverticulum

A

Surgical Resection

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223
Q

What is intussusception

A
  1. Where the proximal portion of the small bowel moves into the distal one.

Causes bowel obstruction and occludes blood supply

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224
Q

Symptoms of intussusception

A

Acute, intermittent colicky abdominal pain that REDUCES when drawing the knees up

Falls asleep between episodes

Nausea and bilious vomiting

If blood supply is compromised: Red current jelly stool (blood + stool + mucous)

Can become necrotic = sepsis

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225
Q

Onset of intussusception

A

3 months to 6 years

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226
Q

Examination findings in intussusception

A
  1. Sausage shaped mass in Right Upper Quadrant
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227
Q

Diagnosis of intussusception

A

. ABDO USS: Shows a target sign (inner circle is the intestines entering the distal segment and outer circle is the distal segment receiving the proximal part )

  1. Abdo X Ray for intestinal obstruction and inteperitoneal gas
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228
Q

When do we suspect intussusception

A

In ANY infant with gastroenteritis who is not getting any better

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229
Q

What does intussusception typically associate with

A

Viral gastroenteritis

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230
Q

What part of the small bowel often is involved in intussusception

A

Enlarged peters patch of the ileum

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231
Q

Treatment of intussusception

A
  1. Resus (IV)
  2. Antibiotics
  3. Analgesia
  4. NGT
  5. Radiological reduction and laparotomy
  6. Barium or water soluble contrast enema
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232
Q

What is Jvenile Polyposis Syndrome

A

SMAD4 gene mutation

Causes multiple hamartomas

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233
Q

Symptoms of JPS

A
  1. USUALLY SYMPOMATIC but there is GI bleeding
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234
Q

Diagnosis of JPS

A
  1. Colonoscpy
  2. Biopsy
  3. Genetic Testing
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235
Q

Treatment of JPS

A

Regular endoscopic monitoring

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236
Q

What condition is duodenal atresia associated with

A

Trisomy 21

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237
Q

Invetigestions of duodenal atresia

A

DOuble bubble sign (gas in stomach and the duodenum

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238
Q

Treatment of duodenal stresia

A

duodenoduodenostomy

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239
Q

What condition may mimic acute appendicitis

A

Mesenteric Adenitis

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240
Q

Two causes of Peptic Ulcers

A

Helicobacter Pylori Infections

NSAIDs

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241
Q

What is a dieulafoy lesion

A

An abnormally dilated artery lining the stomach, more prone to haemorrhages.

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242
Q

Where do mallory-weirs tears often originate

A

Lower 1/3 of the oesophagus and the proximal stomach

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243
Q

Treatment of mallory-weirs tears

A
  1. Thermocoagulation
  2. Endosocpic band ligation

Metoclopromide for vomiting

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244
Q

Treatment of dieulafoy lesions

A

Epinephrine injections

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245
Q

What conditions cause occult GI bleeds

A
  1. IBD
  2. Meckel’s
  3. JP
  4. Peptic Ulcer Disease
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246
Q

Onset of UC

A
  1. 20-30 year olds

2. Gradual and progressive over a few weeks

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247
Q

Extensive colitis vs distal ulcerative colitis

A

UC usually effects the end parts of the large intestines. However, distal includes the descending colon - rectum while extensive involves all the large intestines except for the caecum. Pancolitis is all

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248
Q

Symptoms of UC

A
  1. Fatigue
  2. Fever
  3. Weight Loss
  4. Dyspneoa
  5. Palpitations from iron deficiency anaeia
  6. Bloody diarrhoea
  7. Colicky Diarrhoea Pain
  8. Tenesmus
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249
Q

What is tenesmus

A

The physical feeling you need to shit even if you already just had one

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250
Q

Extraintestinal signs of UC

A
  1. Arthritis
  2. Uveitis
  3. Episcleritis
  4. Skin Lesions: Pyoderma Gangrenosum, erythema nodosum
  5. Primary Sclerosing CHolangitis
  6. Thromboembolisms
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251
Q

Crohn’s vs UC

A

Defecation: Porridge, sometimes steatorrhoea vs Bloody

No Tenesmus vs tenesmus

Continuous involvement vs skip lesions (cobblestone appearance)

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252
Q

Which IBD has noncaseating granulomas (and what does this mean)

A

Crohn’s NOT UC

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253
Q

Complications of UC

A
  1. Forms strictures in the rectosigmoid colon = bowel obstruction
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254
Q

Symptoms of Crohn’s

A
  1. Watery diarrhoea or steatorrhoea
  2. Fistulas between intestines (mass) or interovesical (bladder) = pneumaturia (gas in the urine)
  3. Enterocutaneous fistulas
  4. Phlegmon (localised area of inflammation in bowel wall) -> abscess.
  5. Apthous Ulcers, gingivitis)
  6. Odynophagia, dysphagia
  7. Gallstones -> biliary colic
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255
Q

Differences in extraintetsinal symptoms found in Crohn’s

A

Also forms kidney stones

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256
Q

Most common site of Crohn’s

A

Terminal ileum

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257
Q

Treatment of Crohn’s and UC

A

Oral 5-ASA

Severe symptoms: Oral Prednisolone or IV methylprednisolone

Antibiotics: Metronidazole

Maintenance treatment: azathioprine

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258
Q

Surgery for Uc

A

Total Colectomy and ileostomy: can cause short bowel syndrome (diarrhoea and malnutrition disorders)

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259
Q

Surgery for CD

A

Local surgical resection of localised disease

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260
Q

How to test for H. pylori infection

A

C14 urea breath test

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261
Q

Treatment of H. pylori

A

Amoxicillin, Omeprazole and Clarithromycin/Metronidazole

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262
Q

One faecal test that is positive in IBD

A

Faecal Calprotetcin (released during inflammation)

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263
Q

Where is gluten commonly found

A

Wheat and grains

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264
Q

What substance in gluten causes an immune response during coeliac’s

A

Gliadin

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265
Q

What happens to gluten proteins once reabsorbed at the stomach

A

Broken down by tissue transglutaminase to deaminated gluten proteins

Broken down by macrophages and presented on MHCII

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266
Q

What two anti-bodies are produced in coeliac’s

A

Anti-tTG

Anti-Gladin

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267
Q

Investigations for coeliac’s

A

Villi are flattened

Crypt hyperplasia + shallow crypts

Duodenal biopsy

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268
Q

What virus causes viral gastroenteritis

A

Rotavirus

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269
Q

How is gastroenteritis spread

A

Faecal-oral route

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270
Q

Complications of gastroenteritis

A
  1. Reiter’s syndrome (shigella, campylobacter)
  2. HUS (E.coli and shigella)
  3. Guillain-Barre Syndrome (campylobacter)
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271
Q

Treatment for campylobacter infections

A

Erythromicin

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272
Q

Treatment for c difficile

A

Metronidazole

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273
Q

What is pyloric stenosis

A

Hypertrophy of the circular muscle to produce a tumour

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274
Q

Onset of pyloric Stenosis

A

Third or fourth week of life

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275
Q

Clinical features of pyloric stenosis

A

Non-bilious projectile vomiting or fresh blood from oesophagi’s

Occurs WITHIN an hour of feeding and the baby immediately becomes hungry

  1. Constipation
  2. Dehydration
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276
Q

Diagnosis of pyloric stenosis

A

Test feeding: so breastfeed the baby while the doctor palpates the baby’s abdomen. We should see visible gastric peristalsis passing along the abdomen and tumours are olive shaped masses just above and to the right of the umbilicus

USS

Metabolic alkalosis

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277
Q

Pre-operative management of pyloric stenosis

A
  1. Rehydrate (IV Saline) and KCL

2. Withold feeding

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278
Q

Surgery for pyloric stenosis

A

Ramstedt’s pyloromyotomy: Splijting the thickened pyloric muscle

WITHOLD oral feeds overnight

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279
Q

Signs of dehydration in neonates

A

Sunken fontanelle, dru tongue

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280
Q

Cause of cyclic vomtiing

A

Abdominal Migraines

Manipulative behaviour or mental health issues

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281
Q

What factors cause GORD in infants

A
  1. Slow gastric emptying
  2. Hiatus Hernias
  3. Liquid diet (from milk)
  4. Gastric hyper secretion
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282
Q

Presentation of GORD

A
  1. Regurgitation
  2. Heartburn, difficult feeding with crying
  3. Painful swallowing
  4. Haematemesis

Faltering growth

Resp: Aponea, Hoarseness, cough, stridor and lower respiratory disease (asthma)

Neurobehavioural symptoms: Sandifer’s syndrome (extension and lateral turning of the head, torticolis)

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283
Q

Complication of GORD

A
  1. Barrett’s oesophagus

2. Lower respiratory disease

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284
Q

GORD investigations

A
  1. Upper GI endoscopy
  2. Oeopshageal biopsy
  3. 24 hour oesophageal pH
  4. Barium swallow with fluoroscopy
  5. Radioisotope milk scan
  6. Oesophageal manometry for dysmotility
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285
Q

Treatment of GORD

A
  1. Ranitidine or omeprazole for oesophagi’s
  2. Gaviscon (antacids)
  3. Domperidone
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286
Q

Surgery for GORD

A

Nissen’s fundoplication: creating a sphincter at the bottom

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287
Q

What is achalasia

A
  1. Obstruction of lower oesophageal sphincter
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288
Q

Presentation of achalasia

A
  1. Vomiting
  2. Dyphagia with both liquids and solids
  3. Aspiration
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289
Q

Causes of acute pancreatitis

A

Hep A
Coxsackie B
Mumps

SLE
Kawasaki
HUS
IBD
Hyperlipidaemia

Drugs: Metronidazole

Pancreatic Duct Obstruction: CF

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290
Q

Clinical Features of acute pancreatitis

A

Hypotension
Abdominal Distention
Cullen’s sign (bruising of peri-umbilical area)
grey-Turner’s sign: Bruising of the flanks
Acites
Pleural effusion
Jaundice

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291
Q

Investigations of acute pancreatitis

A

Serum amylase (raised) and deranged LFTs

Abdominal USS and endoscopic retrograde cholangiopancreatography

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292
Q

Complications of chronic pancreatitis

A

DM

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293
Q

Causes of chronic pancreatitis

A 
CF
COngenital ductal anomalies
Sclerosing Cholangitis 
Hyperlipidaemia
Hypercalcaemia
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294
Q

Describe how bilirubin is metabolised

A
  1. Old red blood cells pass through spleen and broken down by macrophages -> heme and global
  2. Heme -> Biliverdin by haemorrhage ocygenase
  3. Biliverdin -> unconjugated bilirubin by biliverdin reductase
  4. Unconjugated bilirubin is lipid soluble
  5. To be water soluble: Bilirubin binds to albumin in blood so it isn’t excreted by kidneys
  6. Unconjugated bilirubin is conjugated by the sinusoidal membranes of hepatocytes -> bile canaliculi -> gallbladder.
  7. Conjugated bilirubin moves into duodenum via ampula of water and is converted by microbes to urobilinogen. 80% -> stercobilinogen which causes brown faeces
  8. 20% of urobilinogen is rebosorbed and sent back to the liver, 10% is excreted by the kidneys and causes yellow urine colour.
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295
Q

What diseases can causes increased haemolytic

A

Haemolytic disease of the newborn
Sickle Cell Anaemia
Glucose 6 phosphate deficiency

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296
Q

What children are particularly susceptible to jaundice

A

Neonates if they’re pre term

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297
Q

Why are preterm babies at a high risk of neonatal jaundice

A

Common in asian newborns: Newborns have high haematocrit but shorter life spans of RBCs.

High RBCs = high levels of unconjugated bilirubin.

Immature UDP glucoronyl transferase so bilirubin conjugation is already imipaured.

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298
Q

What medications can cause neonatal jaundice and why

A

Sulfonamides and ceftriaxone: take up bilirubin binding sites on albumin

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299
Q

How is neonatal jaundice treated

A

non-UV phototherapy: isomerizes unconjugated bilirubin to water-soluble form so it can be excreted.

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300
Q

What can cause breast milk jaundice

A

High levels of glucoronidase in breast milk can deconjugate bilirubin in the intestines. This increases enterohepatic circulation of unconjugated bilirubin -> unconjugated hyperbilirubinaemia

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301
Q

When does breast milk jaundice develop

A

After first 5-7 days of life and peaks after 2 weeks

Whereas physiologic jaundice of newborns occurs within 1 week of life.

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302
Q

What is Gilbert Syndrome

A

Impaired hepatic bilirubin uptake and reduced production of UDP glucoronyl transferase.

LFTs are normal

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303
Q

Consequence of neonatal jaundice

A

Kernicterus: High bilirubin levels in blood can cause brain damage and learning disabilities.

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304
Q

When are intravenous IVIG indicated for neonatal jaundice

A

If rhesus haemolytic disease is present

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305
Q

What is Crigler-Najjar syndrome

A

Complete absence of UDP glucoronyl Transferase

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306
Q

What can cause intrahepatic jaundice

A
  1. Unconjugated +/- conjugated hyperbilirubinaemia
Viral Hep,
Paracetamol overdose, sodium valproate
Wilson's
Alpha 1-antitripsin deficiency 
Hypothyroidism

Budd-Chiari Syndrome
Right sided heart failure

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307
Q

What is budd-chiari yndrome

A

Hepatic veins blocked by a clot causing liver to grow larger

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308
Q

What can cause obstructive jaundice

A
  1. CONJUGATED hyperbilirubinaemia
Biliary atresia
Choledochal cyst 
Primary sclerosis cholangitis
CF
Cholecystitis
Tumours
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309
Q

In emergency treatment of a food allergic reaction, what should be given

A

IM adrenaline

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310
Q

What commonly causes lactose intolerance

A

Post-viral gastroenteritis lactase deficiency (e.g., rotavirus) This is transient and short lasting

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311
Q

Presentation of lactose intolerance

A

Diarhoea
Excessive Flatus
COlics
Stool pH < 5

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312
Q

Presentation of Wilson’s Disease

A

Kayser-Fleischer rings (copper deposits in the eye)

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313
Q

Ivesgtigations for wilson’s

A
  1. Decreased serum copper and caeruloplasmin
  2. 24hr urinary copper excretion
  3. Molecular genetic testing
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314
Q

Treatment of wilson’s

A

Chleation therapy with penecillamine

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315
Q

Presentations of biliary atresia

A

Jaundiced, dark urine, light stools and hepatocplenomegaly

Normal weight and meconium is normal too

Failure to thrive

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316
Q

Onset of biliary atresia

A

2 months

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317
Q

Treatment of biliary atresia

A

Kasai portoeneterostomy

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318
Q

What is an incarcerated inguinal hernia

A

The swelling is irreducible

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319
Q

Initial management of an inguinal hernia

A

Resuscitation and an NGT

  1. AXR: intestinal obstruction
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320
Q

What is a congenital diaphragmatic hernia

A

A hole in the diaphragm.

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321
Q

What are the two types of hiatus hernias

A
  1. Sliding (more common in infants)

2. Rolling

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322
Q

Presentations of inguinal hernias

A
  1. BOYS
  2. Common on the right side due to later descent of the right testis

No symptoms

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323
Q

In what ethnicity are umbilical hernias common

A

Afro-Caribbean children

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324
Q

Marasmus vs Kwshiorkor

A

Severe deficiency of all nutrients and inadequate caloric intake vs normal caloric intake but protein deficiency

Peripheral oedema absent vs peripheral oedema

No hair changes vs sparse hair

Dry skin vs flaky skin

Large appetite vs poor appetite

No submit fat vs reduced subset fat

No fatty liver vs fatty liver

Better prognosis vs worse prognosis

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325
Q

Investigations for kwashiorkor and marasmus

A

Mid-upper arm circumference due to oedema

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326
Q

What can cause vet A deficiency

A

Fat malabsorption states (CF)

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327
Q

What vitamin deficiency can cause rickets

A

Vit D

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328
Q

Causes of Vit D deficiency

A

Low UV light
Fat malabsorption
Hepatic or renal failure

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329
Q

What can cause B12 deficiency

A

Vegan diets
IBD
Pernicious Anaemia

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330
Q

Presentation of B12 deficiency

A
  1. Paraesthesias
  2. Peripheral neuropathy
  3. Macroyctic MEGALOBLASTIC anaemia
  4. Motor weakness
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331
Q

Triad of symptoms in cholecondal cysts

A
  1. INTERMITTENT ABDO PAIN
  2. Jaundice
  3. Right UQ mass
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332
Q

Symptoms of appendicitis

A
  1. Initial periumbilical abdominal pain, with diarrhoea, indigestion and malaise
  2. 48 hours later, localised pain and fever
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333
Q

Two signs of appendicitis

A

McBrurney’s (1/3rd the way from belly button to right anterior superior iliac spine)

Rosving’s sign (palpation of left lower quadrant auses pain in the other side)

Obturator sign: Irritation of obturator interns muscle

Iliopsoas sign: Retrocaecal appendicitis causes pain when extending the right hip

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334
Q

Signs of physical abuse

A
  1. Mark/Bruise
  2. Fractures, Internal Bleeding and Death
  3. Radial Head Subluxation: Nursemaid’s elbow
  4. Burns
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335
Q

Clues of child abuse in patients

A
  1. Repeated hospitalisations with unexplained injuries
  2. History of STId
  3. Explanation is inconsistent with injury severity
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336
Q

What is nursemaid’s elbow

A

Radial Head Sublexation

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337
Q

What do abuse burns usually arise from

A

Forced into hot water: Spared creases in abdomen and palms/soles of the feet

Cigrettes being bumped out

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338
Q

What clotting factors require vit K

A

1972

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339
Q

What is the function of warfarin

A

It blocks Vit K from being in its activate state (blocks via K epoxide reductase), this blocks the extrinsic pathway which requires factor 7 to activate

Then reduces 10 9 and 2 in the intrinsic pathway

Causes 1972 to not be activated

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340
Q

What test is used to measure warfarin pathway

A

PT: extrinsic

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341
Q

What is INR

A

It’s patient’s PT/ control PT (so if it’s 2, it means the patient’s blood takes 2 times longer to clot than the general pop)

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342
Q

What’s a normal INR

A

<1.1

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343
Q

Why is heparin often given at the start of warfarin therapy

A

Because Warfarin can destroy protein C = congenital protein C deficiency.

Causes a state of hyper coagulation (with Va) before anticoagulation occurs.

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344
Q

Name four acyanotic heart defects

A
  1. ventricular septal defect (VSD)
  2. Atrial Septal Defect
  3. Patent Ductus Arteriosus
  4. Coarctation
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345
Q

Name four cyanotic heart defects

A
  1. Tetralogy
  2. Transposition
  3. Truncus Arteriosus
  4. Total Anomalous Pulmonary Venous return
  5. Hypoplastic left heart syndrome
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346
Q

Diagnoses for heart defects

A
  1. ECG
  2. Chest X Ray for suspicion of heart failure
  3. CT or MRI if diagnosis is inconclusive
  4. Cardiac Catheterisation + Angiography if diagnosis remains uncertain after non invasive investigations
  5. Infective endocarditis Prophylaxis (Cyanotic congenital heart disease not fully replier or fully repaired or with existing leaks)
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347
Q

What is the optimal gestational age for screening for congenital heart defects

A

18-22 weeks

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348
Q

What follow up investigation is done if sat levels are <90% in a neonate

A

Urgent Echocardiography

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349
Q

In what conditions should sat levels be repeated hourly

A

IF it remains 90-95% or there is a difference in 3% between the legs and right hand

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350
Q

Pathophysiology of symptoms in Cyanotic defects

A
  1. Oxygenated blood moves from the left ventricle to the right ventricle so no cyanotic symptoms, however this causes pulmonary HTN as extra blood is moving through the pulmonary artery.
  2. However, eventually pulmonary pressure > left ventricle pushing blood, that deoxygenated blood from the right to the left - EISENMENGER SYNDROME
  3. This eventually leads to cyanosis.
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351
Q

What is the most common septal defect

A

Ventricular septal defects

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352
Q

What is different about VSD compared to other cyanotic defects

A

Not related to increased pulmonary vascular resistance

There is just left to right shunting

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353
Q

Ausculttaion Symptoms of VSD on examination

A
  1. Loud, harsh, blowing holosytolic murmur
  2. Palpable thrill
  3. Mid-Diastolic, low pitched rumble from increased blood flow through the mitral valve.
  4. Parasternal heave and a displaced apex beat
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354
Q

Where is the holosystolic murmur in children best heard

A

Lower left sternal border

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355
Q

What is a holosytolic murmur

A
  1. Begins at the first heart sound and continue to the second heart sound
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356
Q

What causes the S1 sound

A

Mitral valve closure (left atrium -> left ventricle) + tricuspid valve closure.

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357
Q

What causes the S2 sound

A

Aortic and pulmonary valve closure

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358
Q

What causes an S2 split sound

A

Inhalation.

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359
Q

Most common cause of an S3 sound

A

Congetsive heart failure

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360
Q

Signs of VSD

A
  1. NO CYANOSIS

2. LFH symptoms: Peripheral oedema, ascites and liver enlargement

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361
Q

Imaging for VSD

A
  1. Transthoracic echocardiography to determine position and size
  2. Doppler echocardiography for magnitude of shunt - GOLD
  3. CXR for Cardiomegaly
  4. ECG for ventricle hypertrophy

Last two not diagnostic but initial investigations

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362
Q

Treatment for small VSD

A
  1. Spontaneous, leave it
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363
Q

Indications for surgical interventions for large VSDs

A
  1. History of endocarditis

2. Left ventricle dysfunction

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364
Q

When are surgical closures of a VSD septum conytraindicated

A

During Severe Pulmonary Hypertension + Eisenmenger’s

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365
Q

Treatment for severe pulmonary hypertension + Eisenmenger’s

A

Bosenten or Sildenafil: Pulmonary vasodilator

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366
Q

Treatment of a small ASD

A

<0.5cm = asymptomatic, leave

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367
Q

What is a large ASD

A

> 2cm

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368
Q

Auscultations of ASD

A
  1. S1: Mid-systolic pulmonary flow
  2. Widened split 2nd sound in all respiratory phases because the extra blood return during inspiration equals out across the atrium. Prolongued emptying of the enlarged right atrium delaying closure.
  3. Short, rumbling, mmid-diastolic murmur in lower sternal border
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369
Q

Signs of ASD

A
  1. Atrial enlargement (chest deformities), Harrison grooves - depression along the sixth and seventh intercostal cartilages.
  2. Signs of heart failure
    3.
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370
Q

Imaging of ASD

A
  1. In children: Transthoracic for size and position of ASD
  2. CXR for heart enlargement and increased pulmonary vascular marking
  3. ECG: Prolongued QRS complex, p > 2.5mm and right axis deviation from hypertrophy
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371
Q

Treatment of ASD

A
  1. Small = spontaneously close in first year of life

2. >1cm = surgical or percutaneous closure

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372
Q

What is the ductus arterioles

A

Opening between the aorta and pulmonary artery

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373
Q

Auscultations of patent ductus arterioles

A
  1. Continuous murmur in second left intercostal space straight after S1
  2. Mid-Diastolic low pitched rumble at apex due to increased blood flow moving through mitral valve.
  3. Systolic thrill radiating across the midclavicular line
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374
Q

Symptoms of patent ductus arterioles

A
  1. COngetsive Failure
  2. Impaired Growth
  3. Bounding peripheral arterial pulses
  4. Wide Pulse Pressure from runoff into pulmonary artery in diastole
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375
Q

Imaging for patent ductus arterioles

A
  1. Echocardiography to visualise and measure ductus
  2. Doppler to see systolic retrograde turbulent flow in the pulmonary artery
  3. Aortic Retrograde flow in diastole
  4. Chest XRAY: Prominent pulmonary artery
  5. Cardiac enlargement
  6. Increased pulmonary vascular markings
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376
Q

ECG findings for patent ductus arterioles

A
  1. Deep Q, Tall R
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377
Q

Treatment of patent ductus arterioles in heaemodynamically stable infants

A
  1. Acetaminophen
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378
Q

Treatment of patent ductus arterioles in unstable infants

A

Surgical ligation or occlusion percutaneously

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379
Q

When in patent ductus arterioles is surgical ligation contraindicated

A

When severe pulmonary vascular obstructive diseases occurs

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380
Q

What is coarctation of aortaa

A
  1. Narrowing of the aorta just where th left subclavian artery branches off, near the ductus arteriosus
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381
Q

Auscultations for coarctation of aorta

A
  1. Short systolic murmur at left sternal border, 3rd and 4th intercostal spaces
  2. Systolic ejection click from bicuspid valve
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382
Q

Symptoms of coarctation

A
  1. Disparity in pulses and blood pressure in arms and legs:

Normal: Femoral pulse occurs slightly before radial pulse.

Radiofemoral delay: Femoral pulse after the radial pulse.

Normal: Systolic in Leggs is 10-20mmHg > arms

Here: Arms has higher systolic pressure than in the legs.

Heart failure and cyanosis.

Tachypnoea

Signs of Heart Failure

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383
Q

Imaging for coarctation

A
  1. ECHO to locate and check valve abnormality
  2. CXR
  3. ECG: Normal in young children
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384
Q

Treatment of mild coarctation

A
  1. Prostaglandin E1 to open ductus and relax tissues
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385
Q

Surgical intervention of coarctation

A
  1. Removing coarctation segment and anastomoses

2. Transcatheter: Balloon and stent angioplasty

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386
Q

Four elements of tetralogy of fallout

A
  1. Pulmonary Stenosis
  2. RVH
  3. Dextraposition of aorta
  4. VSD
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387
Q

Auscultation of tetralogy of fallout

A
  1. Systolic murmur: Crescendo - decrescendo at left sternal border. Preceeded by the clock.

Cause: Turbulence through right ventricular outflow track because of pulmonary stenosis

  1. Systolic thrill
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388
Q

Symptoms of tetralogy of fallout

A
  1. Left anterior hemithorax bulge from RVH
  2. Signs of heart failure
  3. Cyanosis later in life (1st year)
  4. Dyspnoea on mild exertion that is relieved on squatting
  5. Dusky blue skin ray sclerae, clubbing of fingers and toes
  6. PAROXYSMAL HYPERCYANOTIC ATTACKS in 1st -> 2nd years of life.
    7.
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389
Q

What are paroxysmal hyper cyanotic attacks

A
  1. Hyperpneic and restlessness
  2. Cyanosis
  3. Gasping resp
  4. Syncope
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390
Q

Onset of paroxysmal hyper cyanotic attacks

A

Morning or after crying

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391
Q

Complication of paroxysmal hyper cyanotic attacks

A

Progress to convulsions or hemiparesis

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392
Q

Diagnosis of tetralogy of fallout

A
  1. 2D Echocardiography to check extent of overriding aorta, location of RV outflow tract obstruction
  2. CXR: BOOTSHAPED heart and enlarged right sided aorta
  3. ECG: Right Axis deviation from hypertrophy

Prominent R and S

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393
Q

What is characteristic about CXR in tetralogy of fallot

A

BOOTSHAPED heart

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394
Q

Treatment of blue spells

A
  1. Knee-chest positioning
  2. Oxygen therapy
  3. IV Fluid Bolus to increased pulmonary flow
  4. Morphine
  5. IV beta-blockers
  6. IV Phenylephrine
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395
Q

Treatment of heart failure in tetralogy of fallt

A

Digoxin or loop diuretics or complete surgical repair to relieve RV outflow tract obstruction and closure of VSD

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396
Q

What is transposition of the great arteries

A

Usually where the figure of eight systemic/pulmonary blood flow circuit is replacedbby two separate parallel circuits (ie., systemic venous blood possessing through the right side of the heart returns directly to the systemic circulation via a connecting aorta.

Pulmonary venous blood returning to the left side of the heart moves back into the pulmonary circulation via a connecting pulmonary artery.

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397
Q

Clinical features of transposition of the great arteries

A

Within a few hours of life with worsening cyanosis.

Severe hypoxia

398
Q

What is the treatment for transposition of the great arteries

A
  1. Correction of acidosis
  2. Correction of hypoglycaemia
  3. Improve arterial oxygenation using prostaglandin E infusion and balloon atrial septostomy
399
Q

What surgery is done to correct transposition of the great arteries

A

Arterial switch procedure in the first two weeks of life

400
Q

In what condition iss a complete atrioventricular septal defect found

A

Down syndrome

401
Q

Three features of an AV septal defect

A
  1. Large defect from middle of the atrial septum down to the middle of the ventricular septum
  2. Missing bicuspid and tricuspid vallves
  3. Just one common atrioventricular valves guarding the atrioventricular junction
402
Q

ECG findings in complete AVSD

A

Superior axis

403
Q

When is surgery for AVSD offered

A

3 Months

404
Q

What is tricuspid atresia

A

No connection between the right atrium and right ventricle causing venous blood to be diverted to the left side through a patent foramen oval.

405
Q

What is the foramen oval

A

Small opening between the right and left atrium

406
Q

Clinical features of tricuspid atresia

A

Pulmonary blood flow

407
Q

Auscultation findings in transposition of great arteries

A

Single and LOUD S2 sound

Absent murmurs

408
Q

Why is hypoxia only moderate in transposition of great arteries

A

Because the ductus may be patent, allowing some shunting of oxygenated blood from the lungs to the systemic circulation

409
Q

Findings on an echocardiography for transposition of great arteries

A

Egg-Shaped heart

Visualises ductus arteriosus, left ventricular outflow tract obstruction

VSDs

410
Q

Findings on an ECG for tranpsposition of great arteires

A

Right axis deviation

RV hypertrophy

411
Q

What is the balloon atrial septostomy

A

Increases size of foramen ovale

Then corrective surgery

412
Q

What is the corrective surgery for transposition of great arteries

A

Arterial switch operation or rastelli procedure in those with large VSDs

413
Q

What is trunks arteriosus

A

Blood leaves the heart through one main vessel instead of two (the pulmonary artery and the aorta fuse and form one whole vessel).

This causes systemic and pulmonary blood to mix - cyanosis

414
Q

Auscultation findings in truncus arteriosus

A

Loud and Single S2 sound.

Ejection click

Systolic murmur

415
Q

Clinical findings of truncus arterioles

A

Peripheral pulses are accentuated and bounding

Mild cyanosis
Resp distress

416
Q

Clinical investigations for truncus arterioles

A
  1. Echocardiography
  2. Doppler
  3. CXR for cardiac enlargement and right aortic arch (common in third)

ECGs may be normal

417
Q

Treatment of truncus arterioles

A
  1. Diuretics to reduce preload
  2. ACE inhibitors to reduce after load.
  3. Positive pressure ventilation

Definitive: Primary surgical repair.

418
Q

What is aortic stenosis

A
  1. MOST COMMON CAUSE OF Left ventricular outflow obstruction

Thickening of aortic valves

419
Q

RF for aortic stenosis

A

MOST COMMON IN BOYS

420
Q

DLINIDQL FEATURES OF AORTIC STENOSIS

A
  1. ASYMPTOMATIC
  2. MAYBE HEART FAILURE AND COLLAPSE IF SEVERE
  3. Child may complain of syncope and chest pain on exertion
421
Q

Management of aortic stenosis

A

Balloon dilation

Avoid competitive sports

422
Q

What is total anomalous pulmonary venous return

A

This is where the four pulmonary veins are connected to a vessel that is not the left atrium

423
Q

Most common place for total anomalous pulmonary venous return

A

Superior Vena Cava

424
Q

Auscultation findings in TAPVR

A
  1. Systolic Ejetcion Murmur

2. Widely Split second sound

425
Q

Symptoms of TAPVR

A
  1. High pulmonary artery pressure

2. Causes oedema and hypotension -> Symptoms resemble respiratory distress syndrome.

426
Q

TAPVR vs Respiratory distress syndrome

A

Symptoms occur after first 12 hours of life vs immediately after birth

427
Q

Echo findings in TAPVR

A
  1. Abnormal pulmonary venous attachments
  2. Common ascending collecting vein
  3. Dilated superior vena cava
  4. Direct connection between pulmonary venous system and the RA

R->L atrial shunting

428
Q

CXR findings in TAPVR

A
  1. Small Heart
  2. Severe Diffuse Pulmonary oedema
  3. Cardiomegaly
429
Q

ECG findings in TAPVR

A

Right axis deviation

430
Q

Treatment of TAPVR

A
  1. Surgical repair: Wide anastomosis with pulmonary venous confluence.
431
Q

What is hypo plastic Left Heart Syndrome

A
  1. Hypoplasia of the ascending aorta
  2. Hypoplasia of the left ventricle
  3. Maldevelopment of the aortic and mitral valve
  4. This leaves a patent ductus arterioles and ASD
432
Q

Symptoms of hypo plastic left heart syndrome

A
  1. Oxyegnated blood reaching left atrium moves into the right atrium. This mixes with deoxygenated venous blood -> exits the right ventricle to the lungs and then into systemic circulation
433
Q

Auscultation findings of hypo plastic left heart syndrome

A

No murmurs

434
Q

Consequences of hypo plastic left heart syndrome

A

The ductus arterioles closes in first two days of life, causing cariogenic shock:

tachypnoea
2. Dyspnoea
3. Weak Pulse
4. Anuria
Oliguria

Reduction in coronary and cerebral perfusion

435
Q

Treatment of Total Anomalous pulmonary venous connection

A
  1. Surgical anastomosis of the common pulmonary channel to the left atrium, closing the ASD
436
Q

What is hypertrophic obstructive cardiomyopathy

A
  1. Massive left ventricular hypertrophy, where the myocardium is fibroses, resulting in a stiff muscle with decreased distensibility.

This reduces ventricular filling but systolic pumping is maintained til later on.

437
Q

CF for hypertrophic obstructive cardiomyopathy

A
  1. Incidental heart murmur, usually a sudden cause for unexpected death as asymptomatic
438
Q

Treatment of hypertrophic obstructive cardiomyopathy

A
  1. Pacemaker, beta blockers, calcium antagonists

2. Ventricular septal myotome or transplants

439
Q

What malformations are most associated with dextrocardia

A
  1. Pulmonary stenosis, tricuspid atresia, transposition, anomalous venous drainage
440
Q

Most common infective agent in infective endocarditis

A 
Strep viridians (dental)
Staph aureus (catheters)
Group D strep (enterococcus) - GI
441
Q

Examination findings in endocarditis

A
  1. Anaemia
  2. Splinter haemorrheages
  3. Tender nodules in fingers and toes - Osler’s nodes
  4. Erythema in palms and soles of feet (Janeway lesions)
    Finger clubbing later on
  5. Retinal infarcts - roth sports
  6. Necrotic skin lesions and splenomegaly
442
Q

Treatment of endocarditis

A

1, IV Oebecillin or vancomycin for 6 weeks minimum

443
Q

What causes rheumatic fever

A

1, Beta haemolytic streptococcus

444
Q

Ages that typically get rheumatic fever

A

5-15 years old

445
Q

Clinical features of rheumatic fever

A
  1. 2-6 weeks between onset of symptoms and last strep infection (e.g., pharyngitis)
446
Q

What criteria can features of rheumatic fever be categorised under

A

Jones criteria

447
Q

What is jones criteria

A
  1. Pancarditis
  2. Polyarthritis
  3. Erythema marginatum
  4. Syndham’s corea
448
Q

Management of rheumatic fever

A
  1. Bed rest
  2. Aspirin
  3. Corticosteroids
  4. Diuretics
  5. Peecillin V for 10 days
449
Q

What can cause pericarditis

A 
Infections:
Viral: Coxsackie B, EBV
Bacterial: Strep, mycoplasma
TB
Fungal (Histoplasmosis
Parasitic (toxoplasmosis)
Connective Tissue:
RA
RF
SLE
Sarcoidosis

Metabolic:
Hyperuricaemia
Hypothyroidism

450
Q

Clinical feature distinctive of pericarditis

A
  1. Sharp pain exacerbated when lying down

Relieved when sitting or leaning forward - referred to the left shoulder.

451
Q

Management for pericarditis

A
  1. Analgesia for pain relief and ant inflammatory drugs
452
Q

What is constrictive pericarditis

A
  1. Where pericardium inflammation causes the pericardium to become scarred and thickened, making the heart less efficient at pumping blood.
453
Q

Role of the pericardium

A

Fibrous: Keeps heart in the chest cavity
Serous: Forms the cavity which has fluid o let the heart slip as it beats

454
Q

What usually causes pericardial effusion (involving blood)

A

Trauma to the chest: Stabbing

Blunt trauma: Being pushed against an object

MI infarctions: Weakened walls break under pressure

Heart surgery

Aortic dissection

455
Q

Consequence of cardiac tamponade

A

It reduces the amount of space the heart has to expand before contracting again = less CO and leads to hypotension.

456
Q

Features of cardiac tamponade

A
  1. During inhalation systolic BP drops .

Normally: The RV expands and does not affect the left heart volume.

In tomponate, the extra volume pushes the ventricular septum to the left, reducing the stroke volume

Beck’s triad: Distended jugular veins
Hypotension
Distant Heart sounds

457
Q

What is SV

A

The volume of blood pumped out of the LV during each systolic cardiac contraction: End diastolic - End systolic volume

458
Q

What drug can cause myocarditis

A

Adriamycin

459
Q

What infections can cause myocarditis

A

Coxsackie B and EBV

460
Q

Describe the pathway of electrical impulses through the hear t

A

SA Node in right atrium -> walls of right atrium and left atrium via backmann’s bundles

Delayed as it moves to the AV Nodes -> Bundle of His -> purkyje fibres

461
Q

What is the p wave

A

Atrial contraction

462
Q

What is the PR interval

A

Delay before moving to the AV Node

463
Q

What is WPW syndrome

A

Where there is a backdoor entrance from the atria to the ventricles (they usually can only pass through via the AV node)

Through the bundle of Kent -> pre excitation

Signals travel through bundle of Kent AND the bundle of his to cause v strong contractions

This can also result in a reentry circuit, where signals move form bundle of his to the ventricles and back up the bundle of Kent to excite the atrial (atrioventricularr reentrant tachycardia

464
Q

ECG findings for WPW syndrome

A
  1. Short PR interval

QRS prolonged

465
Q

What defines a short PR interval

A

Less than 120 ms

466
Q

What defines a prolonged QRS complex

A

Over 110 ms

467
Q

Symptoms of WPW

A

Atrial arrhythmia: 300BPM and cariogenic shock

468
Q

What is heart block

A

An arrhythmia caused by signals being delayed or blocked (e.g., damage to the nodes)

469
Q

What is a first degree AV block

A

There is a delay in electric conduction but it still makes it through the AV node to the ventricles

PR > 200ms

470
Q

What is Mobitz type 1 second degree block

A

PR gets progressively longer until electric signals are blocked completely (does not make it to the ventricles) -> there is a dropped beat.

471
Q

What is a mobitza type II second degree AV block

A

Fairly random dropped beats, no progressive lengthening of PR interval.

472
Q

What is third degree AV block

A
  1. No signals to ventricles
473
Q

Treatment non heart bloick

A

Atropine to increase heart rate

474
Q

What is the most common abnormal arrhythmia in children

A

Supraventricular tachycardia.

475
Q

Characteristics of innocent heart murmurs in children

A
  1. Systolic in timing never diastolic
  2. Short duration
  3. Inetisifies with increased CO (e..g, fever or exercise)
  4. May change in intensity when changing positions
  5. No thrills
  6. No radiation
    Asymptomatic
476
Q

Types of innocent hear tmurmurs

A
  1. Venous Hum: Machine sound in upper left sternal edge due to great vein flow

Flow murmur: Short systolic murmur: Mid-left sternal edge - from fevers and disappears on itself

477
Q

Likely diagnosis with a continuous apex murmur

A
  1. Mitral regurgitation (seen in cyanotic ehaumatic fever)
478
Q

Likely diagnosis if a continuous murmur is heart in the mid-left sternal edge

A

Tertalogy of fallout

479
Q

Likely diagnosis with an ejection systolic murmur on the upper LSE

A

ASD secundum, fixed split S2

480
Q

Name four cyanotic CHDs

A
  1. Tetralogy of fallout
  2. Transpotiin
  3. Tricuspid atresia
  4. Total anomalous pulmonary drainage.
481
Q

RECAP: BP management pathway

A

<55 and not black:

ACEI or ARB -> ACEi/ARB and CCB -> ACEi/ARB, CCB and thiazide like diuretic -> all + alpha blocker or spironolactone

482
Q

Management of a STEMI

A
  1. Ticagrelor + Aspirin unless high bleeding risk.

High bleeding risk: just aspirin w/without ticagrelor

483
Q

Within how long can a PCI be delivered

A

Within 12 hours of symptoms present .

484
Q

ECG findings in an NSTEMI

A

ST depression

T wave inversion

485
Q

Initial drug therapy for a STEMI

A

300 mg aspirin

486
Q

Mechanism of action of ticagrelor

A

P2y12 inhibitor - stops platelet aggregatio n

487
Q

Mechanism of action of aspirin

A

COX 1 and COX 2 inhibitor: COX 2 is needed to stop prostaglandin production -> anti-inflammatory

488
Q

What does rheumatic fever commonly succeed

A

Strep pharyngitis by strep progenies (strep throat)

489
Q

What valve commonly scars in chronic rheumatic heart disease

A

Mitral -> causes regurgitation and then stenosis

490
Q

Stable vs unstable nagina

A

Unstable: Pain is at rest whereas stable is usually on exertion

491
Q

What is Klinefelter’s syndrome

A

Where a biological male (XY) inherits an extra X chromosome(or a few others)

492
Q

What is the impact of an extra X chromosome in Klinefelter’s

A

Causes less testosterone to be secreted

493
Q

Role of Leydig Cells

A

Respond to LH and covert cholesterol to testosterone

494
Q

What is the role of testosterone in spermatogenesis

A

Testosterone and FSH together cause the Sertoli cells in the seminiferous tubules of the.testes to make more sperm.

495
Q

Describe the negative feedback loop of testosterone

A

Inhibits gNRH and LH from the pituitary glands

496
Q

What cell enhances this negative feedback

A

Sertoli cells which produce inhibin (like how granulose cells produce inhibin to enhance the inhibition of progesterone)

497
Q

How does Klinefelter’s syndrome impact the negative feedback loop of testosterone-LH-GNRH

A
  1. The extra X chromosome stops leading cells from producing testosterone and Sertoli cells from producing inhibin

This causes LH and FSH to increase

Lack of testosterone reduces sperm production and stops testes maturation.

(Each additional X increases oestrogen:testosterone ratio)

498
Q

What cell division phase causes klinefelter’s

A

Extra X chromosome can happen from errors in meiosis (the duplication to sister chromatids).

Meiosis 1: separes the chromosomes into pairs

Meiosis 2: pairs into individual chromatids.

Meiosis 2 doesn’t separate all the pairs

Also:
Failure in equal mitosis can cause excess chromosomes in one cell, so if meiosis II fails again, there are even more X chromosomes that can end up in the gamete (E.g., XXXXY)

499
Q

Onset and symptoms of Klinefelter’s

A 
At puberty:
Hypogonadism (small testes and penis)
Sterile
Tall, long legs, short torso, broad hips and gynecomastia 
Less muscle mass
Less facial and body hair
Weak bones
Low energy levels and IQ points compared to other relatives

Some may live atypical or female gender identities.

500
Q

What diseases does Klinefelter put women at a higher risk of getting

A

Breast Cancer

Osteoporosis

501
Q

Diagnoses of Klinefelter

A

Karyotyping

Amniocentesis

Testosterone, FSH and LH test

502
Q

What is Patau Syndrome

A

A chromosomal disorder where someone inherits an extra copy of chromosome 13 (trisomy 13)

Robertsonian Translocation

503
Q

What cell division error causes pate syndrome and what is this

A

Nondisjunction: where the chromosomes do not split apart causing one cell to get both chromosomes while the other gets none.

So two cells have a chromosome each (24) and two do not (22)

Can also happen in the second step: where the chromosome does not split into individual chromatids.

504
Q

What is mosaicism

A

Where some cells have an extra chromosome and others do not

505
Q

Symptoms of trisomy 13

hint, the disease of the celes

A

Baby:
Microcephaly
Holoprosencephaly (where the prosencephalon fails to divide into two brain hemispheres)
Meningomyelocele

Developmental delay  (LDs)
GI problems: Omphalocele 
Septal herat defects
Polycystic kidney disease 
Cutis Aplasia: Scalp lesions where skin fails to develop 
Microthlmia: Small eyes
Polydactyly 
Cell lip and palate 
Rocker-bottom Feet (smooth feet)
Cyclopia (cyclops - one eye from holoprosencephaly)
506
Q

What is a meningomyelocele

A

Sevre spina bifida where the spinal cord and meninges protrude out of a whole in the back. Only held together by a sack of skin

507
Q

What is an omphalocele

A

Bowel herniates out into the umbilical cord

508
Q

Survival rates of trisomy 13

A

Most babies die before birth: 3 days

5% pass 6 months of life

509
Q

Serum markers for pate

A

1st trimester: Reduced HCG and PAPP-A

2nd trimester: AFP and HCG are normal

Karyotyping through amniocentesis

510
Q

What is Edward’s syndrome

A

A chromosomal disorder where a person inherits an extra copy of chromosome 18

511
Q

Genetic causes for Edwards syndrome

A

Nondisjunction
Robertsonian Translocation
Mosaicism

512
Q

Symptoms of Edwards syndrome

A
  1. LDs
  2. Septal Heart Defect and Patent Ductus Arterioles
  3. Omphalocele
    Oesophageal Atresia
  4. Horseshoe kidneys (where kidneys fuse together)
  5. Pulmonary hypoplasia
  6. Frequent infections
513
Q

How does oesophageal atresia lead to polyhydramnios

A

Swallows less amniotic fluid as its blind ending

514
Q

What tumour are Edwards syndrome people at an increased risk of getting

A

WILMS TUMOUR (Nephroblastoma)

Hepatoblastoma

515
Q

RF for wards syndrome

A
  1. MATERNAL AGE

2. FH

516
Q

RF in Edwards syndrome vs Klinefelter’s

A

Females more commonly effected in Edwards vs males

517
Q

Survival rates of Edwards syndrome

A

Death before birth from central apnoea

518
Q

Investigation findings in edwards

A

Increased nuchal translucency on USS

Polyhydramnios USS

Reduced HCG and PAPP-A

519
Q

What is fragile X Syndrome

A

Named as the edges of the chromosome look pedunculate at the site of mutation

520
Q

Gene involvement in FX syndrome

A

FMR1 - fragile X Mental Retardation 1

Has a trinucleotide repeats where 3 DNA nucleotides are repeated multiple times in a row

This causes DNA polymerase to get confused and then just starts again and recopies the nucleotides from the start again.

521
Q

What is the tricnucleotide repeat found in FX syndrome

A

CGG repeat (>200)

Normal: 5-44

522
Q

Developmental problems of Fragile X chromosome

A
  1. LD
  2. Delayed Speech
  3. Delayed Motor Development (learning to walk at 18 not at 12 motnhs)
  4. Autism, ADHD and seizures
523
Q

Physical features of fragile X

A
  1. Long narrow face
  2. Prominent Jaw and Forehead
  3. Large ears that stick out
524
Q

Why is Fragile X Chromosome less common in females

A

They have a back u[ FMR1 so less penetrance

But can get primary ovarian insufficiency (premature ovarian failure)

525
Q

Symptoms in people with permutation carriers (55-200)

A
  1. Fragile X Associated Tremor ataxia syndrome
    - Intention Tremour, ataxia, memory and cognitive problems

MRI scan

526
Q

Diagnosis of Fragile X Syndrome

A
  1. CGG repeats through DNA test

FMR1 test

Carrier testing in pregnant women

527
Q

What is muscular dystrophy

A

MYTONIC (contracted and unable to relax) DYSTROPHY: poorly noursihed

528
Q

How many types of myotonic dystrophy are there

A

Type 1 (Steinert’s disease)

Type 2

529
Q

Where is the autosomal gene found in MD T1

A

Chromosome 19, long arm

530
Q

What is the autosomal gene in MD T1 called

A

DMPK

531
Q

What genetic error occurs in MD T1

A

A trinucleotide repeat of CTG

532
Q

What is DMPK responsible for

A

Myotonic dystrophy protein kinase: communication between muscle cells, heart and Brian cells

Shuts off

533
Q

Where is the genetic mutation located in MD T2

A

Long arm of chromosome 3

534
Q

What is the gene involved in MD T2

A

CNBP (cellular Nucleic Binding Protein) which controls the genes in muscles of heart and muscles

535
Q

What genetic error causes MD T2

A

Instead of trinucleotide, it’s a tetra nucleotide repeat: CCTG

536
Q

What is repeat expansion in Muscle Dystrophy

A

Increased CTG and CCTG repeats in the affected genes

Caused by slipped ispairing

537
Q

What is slipped mispairing

A

Where the DNA polymerase gets confused and goes back to the beginning and starts again

538
Q

What is the result of repeat expansion

A

Increased number of repeats = earlier and more sever symptoms (ANTICIPATION)

539
Q

How many mutations of DMPK or CNBP are needed to cause disease

A

DMPK: 50 +

CNBP: 75+

540
Q

Onset of symptoms in MD T1

A

Two forms: Congenital and adult form:

Symptoms begin at birth

Adults: Muscle weakness occurs later in life:
facial: Eye dropping, hollow cheeks

Distal Hand muscle weakness
Muscles of lower leg: Foot Drop

541
Q

Onset of symptoms in MD T 2

A

Only presents at adulthood: Milder

Affects proximal muscles of thighs and hips (Can’t walk up stairs or stand up from sitting)

Shoulder and elbow weakness: Can’t pick things up

Myotonia; Sustained muscle contractions, difficulty relaxing muscles after use

Cataracts
Insulin Resistance

542
Q

Diagnosis of MD

A
  1. genetic
  2. EMG
  3. Muscle Biopsy
543
Q

Most common chromosomal disorder among live births

A

Down Syndrome

544
Q

What causes Down syndrome (eugenic error)

A

Nondisjunction of chromsoomes

545
Q

Signs of Down Syndrome

A 
Flat Facial Profile
Upward-slanting palpebral fissures
Epicanthal Folds
Low-Set Ears
Excessive Skin at back of the neck k
A single Transverse Palmar Crease
Clinodactyly (curved fifth finger)
Small nose and mouth 
Large Tongue

HAVING AN EXTRA 21 EFFECTS ALMOST EVERY ORGAN SYSTEM IN THE BODY

546
Q

CV complications of down’s syndrome

A
  1. Endocardial cushion defects (AVSDs)

2. VSDs, ASDs

547
Q

Auscultation sounds in VSDs vs ASDs

A
  1. VSDs: Harsh holosystolic murmur

2. ASDs: Fixed Split S2 Heart Sound

548
Q

Gi Complications of trisomy 21

A

MOST COMMON: Duodenal Atresia = intestinal obstruction

549
Q

Symptoms of Duodenal Atresia

A

BEFORE the MAJOR DUODENAL PAPILLA (where the bile contents are pushed in) = NON-BILIOUS VOMITING

AFTER: BILIOUS VOMITING

550
Q

Onset of duodenal atresia in down syndrome

A

Within hours of being born

551
Q

Abdominal X ray characteristic of duodenal atresia

A

Double Bubble Sign (stomach and duodenum is filled with air)

552
Q

Haematological consequence of trisomy 21

A
  1. Increased risk of Acute Lymphoblastic Leukaemia (ALL)

Acute Myeloblastic Leukaemia (AML)

553
Q

Signs of ALL and AML in children to look out for

A

RECURRENT respiratory tract infections

Anaemia and Laeukopenia on blood tests

Increased 20% blast cells in bone marrow biopsy

554
Q

Urogenital symptoms of down syndrome

A
  1. Males have decreased fertility or even sterility
555
Q

Neurological complication of down syndrome

A
  1. LDs
  2. Early onset Alzheimer’s before 40

Amyloid precursor proteins on chromosome 21, which increases amyloid plaque build up and destroy neurone

556
Q

What is the atlantoaxial instability found in trisomy 21

A

Posterior transverse ligaments in the neck are lax or floppy - responsible for holding the first (atlas) and second (axis) cervical spines.

557
Q

Signs of atlantoaxial instability

A

Reduced cervical spine stability = cervical nerve root compression

Presents with motor symptoms; Weakness in arms and legs or torticolis (head tilting)

558
Q

Prevention of atlantoaxial instability

A

Reduce neck extension

559
Q

What does the combined test consist of for down’s syndrome

A

B-HCG (raised) and PAPP-A (low)

560
Q

What blood test is done for down’s in the second trimester

A 
Alpha feto protein (low)
Beta HCG (high)
Inhibin A (high)
Unconjugated Oestriol (low)
561
Q

When are AFP levels raised

A
  1. Multiple gestations
  2. Open Neural Tube defects
  3. Abdo Wall Defects
562
Q

How is karyotyping for down’s conducted

A

Between 9-11 weeks: Chorionic-villus sampling

Between 15-19 weeks: Amniocentesis

After 20 weeks: Blood test

563
Q

What genetic mutation causes Angelman Syndrome

A

A mutation on chromosome 15, where UBE3A is not expressed and transcribed into E6AP

564
Q

What does UBE3A stand for

A

Ubiquitin-Protein Ligase E3A

565
Q

What is the role of E6AP

A

It tags other proteins with ubiquitin so they get degraded by the proteasome

566
Q

What mechanism regulates what parental gene expresses the UBE3A

A

Imprinting: Usually the mother will express her UBE3A gene, silencing the paternal chromosome with the same gene

Leaves it vulnerable to mutation

567
Q

What genetic process causes the development of angel man syndrome

A

Deletion of hundreds of base pairs on chromosome 15 of the maternal gene

Mutation within the gene to make it effective

Paternal uniparental disomy:
Or just an absent maternal chromosome, resulting in two paternal chromosomes: (that one parent contributed all the chromosomes for that one gene).

Imprinting Defect: Mother’s gene is mistakenly silenced

568
Q

Signs of angel man syndrome

A

Deletion of a gene nearby: OCA2:

Which results in light complexion (compared to the family)

569
Q

Describe how the different mutational processes effect the symptoms seen in Aneglman syndrome

A

Mutations: Asymptomatic

Deletion or Maternal Uniparental disomy causes Prader-Willi syndrome as these also result in changes to nearby genes.

570
Q

Signs of Prader-Willi syndrome in infants

A

Low muscle tone and poor feeding

Delayed development:
Never learn how to speak
Can’t walk properly (walking with arms pronated and flexed legs)

571
Q

Signs of Prader-Willi syndrome in adolescents

A
  1. Overeating
  2. Obesity
  3. Low IQ
  4. Inadequate Genital Development
  5. Fair Complexion
  6. Seizures
  7. Small Head Size
  8. Difficulty w/ sleep
  9. Scoliosis

Triad: LD, Seizures and Ataxia

572
Q

Behaviours in angel man syndrome

A
  1. Happy
  2. Excitable
  3. Hand-Flapping
573
Q

What choromosome is affected in Williams Syndrome

A

Chromosome 7 (microdeletion of 26-28 genes including elastin, these happen randomly occur in gametes)

574
Q

Symptoms of Williams Syndrome

A

Connective Tissue Abnormalities (loss of elastin):

  • Broad Forehead
  • Flat nasal bridge
  • Perioribital puffiness
  • Short upturned nose
  • Long medial cleft
  • Full Lips, Wide Mouth

Narrowing of blood vessels (pulmonary artery stenosis, supravalvular aortic stenosis = heart murmurs + hypertension

They have a cocktail party personality

Cognitive impairement
Weak visual motor and spatial

Anxiety
Phobias
OCD traits

Increased sensitivity to vitamin D: Hypercalcaemia symptoms

Excess calcium then forms kidney stones when excreted

575
Q

Diagnosis of Williams Disease

A

Microarraqy analysis: to check for elastin

FISH

576
Q

Describe the process of iron absorption at the intestinal level

A

Fe3+ -> Fe2+ before being absorbed.

HCL activates Ferrireductase to do this.

577
Q

Other than iron deficiency anaemia, what is another cause for microcytic anaemia in children

A

Lead poisoning from ingesting lead-containing paint in toys.

578
Q

What enzymes does lead inhibit to cause anaemia

A
  1. alpha-ALA
  2. Ferrochelatase
  3. rRNA Degradation

This leads to stippling: build up of substances inside the cell. (basophilic stippling on a peripheral blood smear).

579
Q

What type of inheritance is alpha-thalassaemia

A

Autosomal Recessive

580
Q

Signs of 3 defective alpha genes in thalassaemia

A

HbH Disease:

Causes excess beta chains (4 beta chains in haem).

Damage the red blood cell membrane = haemolytic in bone marrow, extravascular haemolytic in the spleen

Has a very high affinity for oxygen and causes hypoxia in tissues

This causes the bone, live and the kidneys to produce excess RBCs = enlargement of bones, liver and spleen.

Pallor, SOB, fatiguability

Skeletal deformitie, especially skull or face deformities, making them brittle (increased fractures)

Hepatosplenomegaly

581
Q

Signs of 3 defective alpha genes in thalassaemia

A
  1. Hb Bart’s Hydrops Foetalis

Where gamma chains in foetus form tetramers instead.: Very high affinity for oxygen = hypoxia and death

Failed CO

Hepatosplenomegaly = Diffuse and severe oedema all over the foetus (Hydrops fettles). So incompatible with life

582
Q

Blood test results n thalassaemia

A
  1. Reduced Haemoglobin
  2. Microcutic (so reduced MCV)
  3. Reduced mean corpuscular haemoglobin
583
Q

Blood smear result in alpha thalassaemia

A

Target cells

584
Q

Treatment for thalassaemia

A

Iron Chelating Agents

585
Q

What is thalassaemia minor

A

Carriers (heterozygotes)

586
Q

What is thalassaemia mintermedia

A

3 alpha gene deletion (so not complete thalassamia)

587
Q

Pathophysiology of beta thalassaemia

A

Lack of alpha chains causes teranomers of beta chains that deposit and cause inclusion inside the RBCs. Damages the red blood cell membrane = haemolytic in the bone marrow or the spleen.

588
Q

Describe the symptoms of beta thalassaemia

A

Eventually beta chains are broken down and the haemorrhage -> bilirubin + iron (as there is excess beta chains = jaundice and iron causes 2ndary haemochromatosis).

589
Q

Blood tests for beta thalassaemia

A

Reduced Hb, MCV abd MCH

590
Q

When does beta thalassaemia majorr present

A

First year to 18 months of life as hbF drops.

Frontal bossing of skull, maxillary swelling and hepatosplenomegaly.

591
Q

Management of thalassaeia

A

Regular blood transfusion

Desferrioxamine to chelate iron

Splenectoy

Bone marrow transplantation is the only cure.

592
Q

What type of anaemia is hereditary spherocytosis

A

Normocytic

593
Q

What is hereditary spherocytosis

A
  1. Inherited RBC membrane defect causing destabilisation of RBC membrane = excessive haemolytic as the blood cells are faulty
594
Q

Symptoms of hereditary spherocystosis

A
  1. Anaemia, reticulocytosis (lots of premature red blood cells), hyperbilirubinaemia from excessive haemolytic
  2. Splenomegaly
595
Q

What people usually have hereditary spherocystosis

A

Northern European

596
Q

Complications of hereditary spherocystosis

A

Jaundice

597
Q

Diagnosis of Hereditary spherocystossi

A
  1. Reticulocytosis

2. Sphere-shaped (spherical) RBCs.

598
Q

Treatment of hereditary spherocytosis

A

Splenectomy

599
Q

How long do RBCs live for

A

120 days

600
Q

Two types of immune Haemolytic Anaemia

A

Warm (where haemolytic occurs at 37 degrees) and Cold (When people’s blood is exposed to cold temperatures) - 0-10 degrees so when going out in the snow.

601
Q

What causes warm IHA

A

IgG - Warm Agglutinins

602
Q

What antigen do warm agglutinins bind to

A

Rh antigens

NK cells and CD8 T cells bind to Fc receptor and destroy the RBC

603
Q

Symptoms of intravscualer acute cold IHA

A
  1. Intravascular haemolytic leads to Raynaud’s phenomenon.
604
Q

Signs of intravascular IHA

A
  1. Increased haemolytic = increased reticulocytes produced by bone marrow so reticulocytosis (normocytic anaemia)
  2. Lactate Dehydrogenase in killed RBCs leaks = Increased LDH levels

Increased bilirubin from head

In intravascular haemolysis, haemolytic that is bound to haptoglobin is broken down into bile.

Increased haptoglobin and bile

Haemoglobinuria if haptoglobin gets overwhelmed.

Renal insufficiency

605
Q

Where is haemolytic stored

A

In renal tubules as haemosiderin

606
Q

Symptoms of extravascular IHA

A
  1. Haptoglobin is normal

2. No haemoglobin or haemosiderinuria

607
Q

In what children are warm IHAs common in

A 
Precedes:
Viral infetcions
SLE
Lymphomas
Leukaemia
608
Q

What antibiotics can cause warm IHA

A

Penecillin

Cephalosporins

609
Q

What are causes of acute cold IHA in children

A
  1. Viral pneumonia
  2. Mycoplasma
  3. Infectious Mononucleosis
610
Q

Symptoms of haemolytic crisis

A
  1. Bounding HR
  2. SOB
  3. Multiorgan failure from hypoxia

Chronic: fatigue, pallor, sob and jaundice.

611
Q

Treatment of warm IHA

A

Oral Prednisolone

612
Q

What antibody is prevalent in cold IHA

A

IgM

613
Q

What is cold acute IHA also known as

A

Paroxysmal Cold haemoglobinuria as its secondary to infections and vaccines

614
Q

Blood test results in IHA

A
  1. Normocytic aenamia
  2. Reduced haptoglobin
  3. Increased reticulocytes
  4. Increased LDH

Direct Coombs and Antigen testing also

615
Q

Under what three conditions do sickle-shaped Hb molecules clump together

A
  1. Acidosis
  2. Hypoxia
  3. Dehydration
616
Q

Two main consequences of sickle cells

A
  1. Vaso-occlusion

2. Haemolysis: intravascular or extravascular

617
Q

Signs of intravascular haemolyssi

A

Raised haemoglobin and LDH

Increased unconjugated bilirubin as Haptoglobin is reduced

618
Q

Signs of Sickle cell anaemia

A
  1. Increased bilirubin: Scleral Icterus, jaundice and bilirubin gallstones
  2. Anaemia
  3. Reticuloytosis
  4. Expansion of medullary cavities in bone marrow as it increases reticulocyte production (hair on end appaerance on X ray in the skull).
  5. Hepatosplenomegaly

Vasoocclusion:
Tissue ischameia and pain (sickle cell crisis)

Pain starts suddenly and excruciating

Typically affects the same body parts (e.g., bones in hands and feet - dactlyitis or avascular necrosis in the hips, priapism, strokes and mental status changes).

Moyamoya Disease (puff of smoke in lungs)

Haematuria or proteinuria

Acute Chest Syndrome (Chest pain, SOB and cough)

Causes further hypoxia and sickling

Splenic Sequestration: LIFE THRETENING

619
Q

Someone gets a blood test and has a rapid drop in haemoglobin and goes into hypovolaemic shock, what anaemia condition has caused this

A

Splenic Sequestration

620
Q

Chronic complications of sickle cell disease

A
  1. Growth and developmental delay
  2. Learning and Behaviour Issues
  3. Pulmonary HTN
  4. CKD
  5. Auto Splenectomy (fibrosis and shrinkage of the spleen - infections from strep pneumoniae COMMON IN CHILDREN)
621
Q

What precipitates encapsulated organism infections from SCD

A

No vaccination, penecillin V prophylaxis and parvovirus

622
Q

What ENT problems are caused by SCD

A

Adenotonsillar hypertrophy (COMMON)

623
Q

Diagnosis of SCD

A
  1. Raised reticulocytes

2. Hb Electrophoressis GOLD STANDARD

624
Q

What type of anaemia is SCD

A

Microcytic

625
Q

Maintenance treatment of SCD

A
  1. Avoidance
  2. Penecillin V prophylaxis
  3. Oral folic acid
  4. HYDROXYCARBAMIDE to reduce crisis.

Bone marrow transplant

626
Q

What is Diamond-Blackfan syndrome

A
  1. A defect that leads to a reduction in bone marrow RBC production
627
Q

Onset of DBS

A

First year of life as svere anaemia

628
Q

Signs of DBS

A

Cleft palate, deafness, MSK and short stature

629
Q

Blood test findings for DBS

A
  1. REDUCED reticulocytes
630
Q

Treatment of DBS

A

Oral prednisolone

631
Q

What causes transient eyrthroblastopenia of child hood

A
  1. From Parvovirus, EBV, Drugs or hereditary spherocytosis)
632
Q

What is transient eyrthroblastopenia of childhood

A
  1. Slow development of pallor and anaemia

Treatment; Remove underlying causes and transfusion if needed. Rsolves by itself tho

633
Q

Neonatal causes of polycythaemia

A
  1. Hypertransfusion; Delayed cord clamping, twin to twin transfusion , maternal-foetal transfusion

Endocrine: GDM in mother, CAH and neonatal thyrotoxicosis

Maternal: GHTN, Heart Disease

SYndormic: Down syndrome and Dehydration

634
Q

Causes of polycythaemia in older children

A
  1. Polycythaemia rubra
  2. Familial history of high O2 affinity

Secondary to anything causing increased erythropoietin: CHD (REALLY COMMON), Respiratory disease, Chronic obstructive sleep apnoea, chronic alveolar hypoventilation, obesity, altitude, renal cysts/carcinoma, dehydration

635
Q

Consequence of polycythaemia in neonates

A

Hyperviscocity Syndrome: Hypotonia, Congestive heart failure, Tachypnoea, seizures, abnormal renal function and NEC

636
Q

Symptoms of vWD

A
  1. Mucosal bleeding
    Easy Bruising
    Excessive bleeding from dental surgery, trauma and menorrhagia
637
Q

Investigations for vWD

A
  1. APTT raised (as Factor VIII is low in activity), platelet count NORMAL
638
Q

Most common cause of acquired aplastic anaemia

A

Idiopathic

639
Q

What causes aplastic anaemia

A

Bone marrow suppression of RBCs: usually results in pancytopenia

640
Q

What causes paroxysmal nocturnal haemoglobinuria

A

Acquired clonal disorder of marrow cells deficient in glycosylophosphatidylinositol (GPI), which prevents against lysis

641
Q

Investigations results in Paroxysmal nocturnal haemoglobinuria

A
  1. Raised reticulocytes, reduced WBCs and platelets.
642
Q

What is Fanconi’s Anaemia

A
  1. Affects all three haemopoietic cell precursors (lymphoid and myeloid progenitor cells)
643
Q

Presentations of fanconi’s anaemia

A
  1. Bruising or insidious onset anaemia
Short stature
Skin Hyperpigmentation (cafe au lait), skeletal abnormalities)
644
Q

Imvetsigation findings in fanconi’s anaemia

A
  1. FBC: Pancytopenia

Bone Marrow: Hypoplastic, dyserythropoietic or megaloblastic change)

645
Q

Treatment in fanconi’s anaemia

A
  1. RBC transfusion, hearing aids and orthopaedic

Corticosteroids (oxymetholone)

646
Q

What would causes an increase in PT but not in APTT

A

Deficiency of VII, vit K deficiency and warfarin therapy

647
Q

What would causes a stable PT but an increase in APTT

A
  1. Deficiency of VII, IX, XI, XII, haemophilia A, vWD disease,
648
Q

When is a d-dimer test used

A

DVTs

649
Q

What is primary haemostasis

A

Formation of the platelet plug and adhesion to the collagen of the endothelium wall

650
Q

What is haemophilia A

A

Deficiency in factor 8

651
Q

What is haemophilia B

A

Defieincy In factor 9

So they both affect the intrinsic pathway

652
Q

What is an acquired cause of haemophilia

A

Liver Failure.
Vit K deficiency
DIC

653
Q

Presentation of Haemophilia

A
  1. Ecchymosis
  2. Haematomas
  3. Prolongued bleeding after cut or surgery
  4. GI bleeding
  5. Haemturia
  6. Haemarthrosis (joint bleeding), painful, swelling and tender.
  7. Strokes, Increased ICP
654
Q

Investigations in haemophilia

A
  1. Normal platelet count
  2. PT: (7,10,5,2 and 1)
  3. APTT: Intrinsic pathway (12, 11, 9, 8) - 9 and 8 means PTT is prolonged and PT is normal.
655
Q

Treatment of haemophilia

A

Treat with recombinant FVIII product or FVIII inhibitors.

For A ONLY: Desmopresssin (DDAVP), stimulates vWF release and stabilises VIII

656
Q

What is wrong with FVIII inhibitors

A

They diminish the effectiveness over time and cause anaphylaxis

657
Q

What causes Diamond-Blackfan Anaemia

A

Mutations in ribosomes

658
Q

What is important to remember about the investigation results that indicate diamond-blackfan anaemia

A

WBCs and Platelets are normal. Just RBCs affected.

659
Q

What is Scarlet Fever

A

A febrile illness characterised by pharyngitis and a progressive erythematous rash (starting from one area and spreading through the body)

660
Q

Two characteristic symptoms of glomerulonephritis

A

DARK URINE and perirobital oedema

661
Q

First Line Investigation for Slipped Upper Femoral Epiphyses

A

X-Ray of BOTH hips (AP and frog leg views)

662
Q

Describe the pattern of rash seen in Pityriasis Rosea

A

Starts with a Herald’s patch which is a small pink or red oval patch

This then becomes widespread after 2 weeks. These are small red scaly patches all over the body. The rash may be dark brown or black.

663
Q

What is pityriasis Versicolour

A

Golden. light coloured spots (cream) found across the whole back and chest

664
Q

What is an infantile Colic

A

Repeated episodes of excessive or inconsolable crying that lasts for at least 3 hours a day, 3 days a week with no evidence of faltering growth

665
Q

When do infantile colics typically resolve

A

3-4 months of age

666
Q

What virus is most commonly associated with croup

A

Parainfluenza virus

667
Q

How is Respiratory Distress Syndrome Treated

A

DIrect Surfactant replacement

668
Q

Outline the trend of infections caused by poliovirus

A

Initially invades the intestines before travelling into the spinal cord to cause nerve damage

669
Q

How does polio enter the body

A

Through contaminated food and water (faeco-oral)

Droplet infection

670
Q

Pathophysiology of polio

A

Enters the ventral horn of motor neurones, causing inflammation when surrounding immune cells come into the area = DAMAGE

This causes muscle atrophy and becomes weak

671
Q

Types of polio

A

Bulbar Polio = Brainstem problems (speaking and swallowing)

Also stops diaphragmatic breathing

672
Q

What is post-polio syndrome

A

After a neurone innervating a muscle gets damaged, neighbouring neurones form collaterals to reinnervate the muscles. However, ageing causes neurones to die anyways which destroys these neurones and causes muscle dystrophy again

673
Q

Symptoms of Polio

A
  1. HIGH GRADE FEVER
  2. Intense muscle pain from spasm and weakness
  3. Loss of Muscle Reflexes
  4. Paralysis
  5. Develops over a few days
  6. Assymmetric
    AFFECTS LARGER PROXIMAL MUSCLES OF THE LEG FIRST
674
Q

Symptoms of polio in infants

A

Develop acute flaccid paralysis

Breathing difficulties and death

675
Q

Side-effect of the polio vaccine

A

Can cause vaccine- associated paralytic polio from re-activation and mutation of the polio in the vaccine

Also can cause Vaccine Derived Poliovirus (VDPV)

676
Q

Most common cause of Bacterial Meningitis in Infants (under 3)

A

Group B strep
E. coli
Listeria

677
Q

Most common cause of bacteria meningitis in adolescents

A

N. Meningitidis
Strep. pneumoniae
H. Influenza

678
Q

Name two diseases that can spread to the brain and cause acute bacterial meningitis

A
  1. Mycobacterium TB

2. Neurosyphilis

679
Q

What usually causes meningoencephalitis (COMBO)

A

HSV

680
Q

What causes acute encephalitis only

A
  1. Measles (up to 10 years after first infection)

2. VZV

681
Q

Signs of meningitis in infants

A

VERY SUBTLE:

Can just be irritability and poor feeding

682
Q

Name tow signs that are positive in Meningitis and what do they do

A

Kernig’s sign - Flex the hip to 90 degrees and try to extend the knee (pain = positive)

Brudzinski’s sign - Involuntary flexion of the hip when the neck is flexed (positive = pain)

683
Q

In what types of meningitis is protein levels usually elevated (they are normal in some)

A

Bacterial

TB

684
Q

In what type of meningitis is CSF glucose levels normal

A

Viral (low in the others0

685
Q

LONG TERM COMPLICATIONS OF HUS

A
  1. PERSISTENT HYPERTENSION

2. Proteinuria/ AKI

686
Q

What bacteria causes scalded skin syndrome

A

Staph Aureus

687
Q

What is Scalded Skin Syndrome

A

Protease enzymes released by Staph Aureus, causes the skin to be broken and worn down

688
Q

Onset of scalded skin syndrome

A

5 years

689
Q

Presentation of Scalded Skin Syndrome

A
  1. Starts with a generalised patch of erythema -> skin looks thin and wrinkles -> bullae which then fall off to look like scalded skin

Also has b symtoms

690
Q

Management of Scaled Skin Syndrome

A

Admission to hospital

691
Q

Name some abnormalities that need to be checked for in spina bifida before surgery can take place

A

Club feet
Kyphosis
Contractures
Airways

692
Q

What causes congenital hyperinsulinaemia

A

High circulating insulin in foetus’ blood because of DM in the mother (remember hyperglycaemia -> hypoglycaemia due to insulin overload)

693
Q

What are tocolytics

A

Either beta blockers or calcium channel blockers -> delay the contractions in th euterus

694
Q

What is aplasia cutis congenita

A

Loss of the dermal and epidermal layer in the skin (seen in Pate)

695
Q

REMEMBER, ANTIEPLIEPTIC DRUGS ARE MOST COMMONLY STOPPED BECAUSE OF SKIN SENSITIVITY ReACTIONS

A

N/a

696
Q

Scalded skin syndrome vs Toxic Ependermal Necrolysis/Steven-Johnson Syndrome

A

Only affects the upper epidermis and spares the mucous membranes, while toxic epidermal necrolysis affects the dermal-epidermal junction.

697
Q

Are retinoblastoma bilateral or unilateral

A

Bilateral, will come with both pupils being very white during red reflex test

698
Q

What is the weber and rhino’s test and what do they indicate

A

Rinne: Place tuning fork on the mastoid bone and tell the patient to indicate when the sound is no longer being heart. With conductive loss, bone conduction > air conduction (in that, they will be able to hear it for a longer time than usual)

Weber’s test: Place tuning fork on forehead. There should be lateralisation of sound to the affected ear

699
Q

What electrolytes do you need to monitor in Diabetes Type I (DKA)

A

K+! It moves into the cells when insulin is given = hypokalaemia

700
Q

How do we find the volume of IV fluids that are needed to be given in DKA

A

Weight = L

L * 10 (assume 10% fluid deficit in children and young people with DKA)

Divide by 48 hours (as this is being given over 48 hours)

701
Q

What cells produce insulin

A

Beta cells

702
Q

What cells produce glucagon

A

Alpha cells

703
Q

What types of cells are beta and alpha cells

A

Secretory cells arising form the islets of langerhand

704
Q

What is the role of insulin

A

Insulin binds to insulin receptors on muscle and adipose tissues, causeing vesicles (glucose transporters) to fuse with the cell membrane and inserting more glucose channels into the surface = increased uptake of glucose

705
Q

What in the past medical history, would indicate type I Diabetes Mellitus

A

AUTOIMMUNE (as it’s an autoimmune disease): e.g., Hashimoto’s thyroiditis, Vitiligo or Lupus

706
Q

Pathophysiology of Type I Diabetes

A

Immune System attacks the Glutamic Acid Decarboxylase enzymes inside Beta cells = reduction of GABA which is needed to stimulate insulin release.

This decreases the number of beta cells in the islet of Langerhans = less insulin = hyperglycaemia

So, the tissues remain sensitive to insulin, there’s just less insulin secreted

707
Q

Name of the antibodies against beta cells

A

GAD-antibdoies

ANTI-ISLET CELL ANTIBODIES

708
Q

Four clinical symptoms of DM 1

A

Polyphagia (weight loss + increased appetite)
Glycosuria
Polyuria
Polydipsia

709
Q

What causes weight loss in DM 1

A

Lipolysis of adipose tissues

Proteolysis of muscle tissues

This is because glucose can’t get inside cells = lack of nutrition

710
Q

What is the difference between DM 1 and 2

A

Insulin is produced in 2, but tissues do not fully respond

So body starts producing more insulin (compensation phase by beta cells)

Over time, these overworked bet cells get exhausted and die off = insulin levels start to lower.

711
Q

What other substance is also produced by beta cells in conjunction to insulin

A

Amyloid Polypeptide (waste products)

These increase alongside increased insulin production

712
Q

Histology findings in DM 2

A

Amyloid polypeptide aggregates in the pancreas

713
Q

Pathophysiology of Diabetic Ketoacidosis

A

Increased lipolysis in fat tissues = more free fatty acids

These are broken down by the liver to form ketone bodies to supply cells for energy

However, it increases acidity in the blood

714
Q

Why does DKA not happen in DM 2

A

Because insulin is still being produced by the islets (even if it’s low levels), stopping lipolysis

715
Q

Signs of DKA

A
  1. Dehydration
  2. Kussmaul Respiration (sweet and fruity acetone), deep and rapid breaths to reduce acidity

Abdominal Pain, Nausea and Vomiting, Delirium and Psychosis

716
Q

Complications of DKA

A
  1. Acute Cerebral Oedema (as excess glucose increases oncotic pressure, causing water to draw out of the cells and into the ECF
  2. Cardiac Arrhythmia from K+ imbalance
717
Q

Signs of Metabolic Acidosis

A

Reduced pH and Bicarbonates

718
Q

Why do we get Hyperkalaemia in DKA/DM

A

Because insulin is responsible for opening the Na+/K+ co transporter. As there is low insulin, the channels do not open, leaving K+ in the blood

719
Q

Treatment of DKA

A
  1. IV fluids
  2. IV Insulin
  3. IV K+ to prevent hypokalaemia
720
Q

Complication of DM 2

A

Hyperosmolar Hyperglycaemic state

721
Q

What is Hyperosmolar Hyperglycaemic state

A

Where the glucose acts as a solvent, causing water to be drawn out from tissues into the blood = SEVERE dehydration

Can cause coma and death

722
Q

What causes GDM

A

The mother’s inability to produce enough insulin to overcome Placental Human Lactinogen (insulin suppressor)

723
Q

Name two systemic disorders that may cause increased insulin resistance or DM

A

Cushing’s

Glucocorticoids

724
Q

Name two DM 2 medications that can cause weight gain

A

Sulfonylureas (glicazides)

Thiazolidinediones

725
Q

Name one DM 2 medication that may cause weight loss

A

GLP-analogue

726
Q

What DM 2 medication does not cause cardiac problems

A

Thiazolidinediones

727
Q

How are GLP-1 and DPP-IV inhibitors given and how do they work

A

SC injections

GLP-1: Incretins, so they reducee blood sugar

DPP-IV: Stops degradation of GLP-1

728
Q

How much fluid do children need a day

A

Infant: 150ml/kg/Day

Toddlers: 100ml/Kg/Day

729
Q

Name two conditions that may cause dysphagia and thus dehydration in children

A

Cerebral Palsy

Developmental Delay

730
Q

Indications for enteral feeds

A

A person on enteral feeds usually has a condition or injury that stops them from eating by mouth but has a functioning GI tract

731
Q

Types of Enteral feeds

A

NG Tubes: Acute swallowing Pain, Inadequate oral intake (SHORT TERM)

Naso-Jejunal (Delayed Gastric Emptying or STomach/oesophageal pathology) - SHORT TERM

Percutaenous Endoscopic Gastroscopy

Gastrostomy (Head and. neck cancer, Brain Injury) - LONG TERM

Jejunostomy (Gastroparesis, same as NJ but long term) - LONG TERM

732
Q

Management of Dehydration in children

A

Not - Dehydrated: Needs maintenance fluid

Dehydrated: Maintenance + Deficit 50ml/Kg

Shocked: Maintenance + Deficit 100ml/kg + bolus

733
Q

How much glucose should be given to neonates and why

A

IV 10% Glucose as they have high metabolism and no fat reserves

734
Q

Rate at how much IV fluids should be given

A

Day 1 - 60mls/kg/day
2 - 90
3 - 120
4 - 150

735
Q

Formula for weight estimation in children

A

(Age + 4) x 2 = weight in KG

736
Q

What IV Hydration solution is given to children

A

0.9% NaCl + 5% Glucose (+/- KCL, if DKA or Sepsis)

737
Q

How do we calculate the daily (ml/24kg) fluid intake to give to a child

A

First 10kg: 100ml/kg
Next 10kg: 50ml/kg
Every other kg: 20ml/kg

738
Q

How do we correct Fluid Deficit

A

REMEMBER:

Not Dehydrated - Maintenance

Dehydrated (5%) = 50 pls/kg extra

Shocked (10%) = 100mls/kg extra

Formula: Deficit (%) * 10 * Weight

739
Q

Calculate the rate of rehydration fluids that should be given to an 18 months girl, weighing 12kg

  • 4 Days diarrhoea + Vomiting
  • Alert
  • CRT < 2 Secs
  • Dry Lips and Mucosal Membranes
  • Reduced Urine Output
A

First 10kg = 1000mls
Next 2kg = 100mls

Appears to be 5% dehydrated so,

5 x 12 x 10 = 600

600 + 1000 + 100 = 1700

1700/24 = 70.8 ml/hr

740
Q

What is the given fluid bolus in severe dehydration

A

20mls/kg of 0.9% NaCl

741
Q

When would this fluid bolus be reduced to 10

A

Diabetic Ketoacidosis

742
Q

Prenatal causes of Cerebral Palsy

A
  1. Radiation
  2. Infection
  3. Hypoxia
743
Q

What is the main type of cerebral palsy

A

Spastic (70% of cases)

744
Q

What is Spastic Cerebral Palsy

A

Tight/Stiff muscles from damage to the upper motor neurones - impairs the ability to receive GABA (needed to inhibit movements)

Hypertonia

745
Q

Signs of Spastic Cerebral Palsy

A

Scissor Gait (Adductor muscles are constantly flexed)

Tow Walk (As calves are always flexed)

746
Q

What is Dyskinteic Cerebral Palsy

A

Damage to the Basal Ganglia, resulting in involuntary movement (think Huntington’s).

Chorea (Slow and uncontrolled movements moving from muscle to muscle) and Dystoonia (slow and uncontrolled movements)

747
Q

What is Ataxic Cerebral Palsy

A

Damage to the cerebellum, resulting in clumsy and unstable movement and balance

748
Q

Non-Secific symptoms of cerebral palsy

A
  1. Failure to meet milestones
  2. Increased or decreased tone
  3. Problems with co ordination, speech or walking
  4. Feeding or swallowing Problems
  5. LD
749
Q

What structure is damaged to cause kernicterus

A

Basal Ganglia

750
Q

What phototherapy is used in Jaundice

A

Blue Light, 450nm

751
Q

What factor reduces the risk of necrotising entercolitis

A

Breast Milk

752
Q

Signs of Retinoppathy of Prematurity

A

The formation of a fibrous bridge on the retina

Retinal haemorrhages and detachment

753
Q

Treatment of Retinpathy of Prematurity

A

VGEF

Laser Therapy

754
Q

Management of Nocturnal Eneuresis

A

Under 5: Reassurance, that it is likely to resolve without any treatment

If it persists: enuresis alarm and then desmopressin for 7 weeks

755
Q

treatment of Crohn’s (it’s not 5-ASA, that’s for UC)

A

Prednisolone, methylprednisolone or IV Hydrocortisone.

756
Q

First line treatment for GORD in children

A

Aligini acid (1-2 weeks)

If this does not work, a FOUR WEEK trial of a PPI or H2 receptor antagonist should be considered.

757
Q

When are symptoms for croup, the worst?

A

During the night

758
Q

When is croup more common in th year

A

Autumn

759
Q

Scarlet fever vs Kawasaki Disease

A

Scarlet fever also has a strawberry tongue… But affects older children (over 5), while Kawasaki affects under 5.

SCARlet Fever -> Scar from lion licks the sand (rough sandpaper rash) with his strawberry tongue.

The rash in Kawasaki is also started by exposure to light

760
Q

Septic Arthritis vs Transient Synovitis

A

Septic Arthritis would exhibit with >12 WCC and over 40 ESR

761
Q

Name three heart conditions in which a pan-systolic murmur happens

A

Mitral Regurgitation (5th Intercostal space, mid-clavicular line)

Tricuspid Regurgitation 9fifth intercostal space, left sternal border)

VSD - lower left sternal border

762
Q

What three heart conditions have a ejection-systolic murmur

A
  1. Aortic Stenosis (Second intercostal space, right sternal border).
  2. Pulmonary Stenosis (Second Intercostal space, left sternal border)
  3. Hypertrophic Obstructive Cardiomyopathy (fourth intercostal space on left sternal border)
763
Q

Characteristic murmur in ASD

A

Fixed split heart sound

764
Q

Murmur characteristic of patent ductus arteriosus

A

Continuous systolic murmur (machinery/crescendo-decrescendo)

765
Q

Characteristic murmur in Tetralogy of Fallot

A

PULMONARY STENOSIS (Ejection systolic murmur at second intercostal space, left sternal border)

766
Q

What should be done if an innocent heart murmurr gets worse on standing

A

Sent to hospital (innocent murmurs should get quite on standing).

767
Q

In what order does a girl go through puberty

A

Thelarche -> Pubarche -> Growth Spurt -> Menarche (the last phase of puberty)

768
Q

What is a complication of heart surgery (e.g., percutaneous closure of VSDs)

A

Pericardial Effusion

769
Q

What stain is used to check for TB

A

Ziehl-Neelson test

770
Q

How does atopic dermatitis present in the first year of life

A

Confluent erythema, papular, scaly and crusty rash that is mostly present on the head and upper extremities only

771
Q

What is the gold standard test to diagnose lactose intolerance

A

Elevated breath hydrogen levels: This is because lactose-containing products cannot be digested so are metabolised by bacteria to produce H+

772
Q

Signs of poliomyelitis

A

Hypotonia and Hyporeflexia

Neck stiffness

Remember: FLACCID PARALYSIS

773
Q

What are the complications of rhinosinusitis

A

Orbital cellulitis
Meningitis
Osteomyelitis

Which is why rhinosinusitis must be treated

774
Q

What is a consequence of Shaken Baby Syndrome

A

Subdural Haematoma (look out for retinal haemorrhages)

775
Q

What’s a major consequence of Rickets that affects children in the first year of life

A

Seizures: Hypocalcaemic seizures

776
Q

What is the thyroglossal duct

A

A tiny canal that links the thyroid gland and ducts at the front of the neck.

This usually closes in the third month of life (however, this doesn’t close in some people)

777
Q

What is a thyroglossal duct cyst

A

Where the duct fills up with mucous

778
Q

Complication of a thyroglossal duct cyst

A

The cyst can burst open -> Discharging sinus (thyroglossal fistula

Thyroid glands may not migrate down the throat to where they should be = hypothyroidism

779
Q

Examination findings in a thyroglossal duct cyst

A

Moves up when sticking out the tongue

Painless swelling in front, midline of the neck

Refer to surgery (remove the hyoid bone as well)

780
Q

What causes a Branchial cyst

A

Where the second branchial cleft fails to form during foetal development -> Space in the lateral aspect of the neck which can fill with fluid.

781
Q

Where are Branchial cysts found

A

Between angle of the jaw and sternocleidomastoid muscle

782
Q

Examination findings in Branchial cysts

A

Transilluminate with light

783
Q

What is a Branchial Cleft Sinus

A

An abnormal connection fo the branchial cyst to the skin (there will be a small visible hole/discharge from the surface of the skin)

784
Q

What is a normal. healthy foreskin

A

Retracting the foreskin, forms a rose bud on the end (will not fully retract and that’s okay)

785
Q

What is BXO

A

A type of balanitis (white) - similar to Lichen Sclerosis

Affects the glands and scarring of the urethral meatus (urinary retention)

Treatment: Circumcision

786
Q

What does a Smegma cyst look like

A

White swelling under most of the foreskin

787
Q

How do we differentiate between an inguinal hernia or a hydrocele

A

Hydrocele, you can get above the swelling (there is a gap between the swelling and the external inguinal ring).

788
Q

What type of inguinal hernias are more common in children

A

Indirect Inguinal Hernia: Usually caused by abdominal wall defects

Lateral to the inferior epigastric vessels

789
Q

What side do inguinal hernias usually present

A

Right

790
Q

When should a child with an enlarged lymph node, be referred to paediatric surgery

A

> 2cm
Inflamed for over 2 weeks
Enlarging

791
Q

What is different about managing a dermoid cyst found in the midline of the face

A

Possibly connected to CSF, needs to have an MRI before draining

792
Q

Management of an umbilical hernia

A

Leave alone until the age of 5

793
Q

Where are capillary sites taken from:

a) under 6 months
b) Over 6 months

A

Under 6 months - foot

Over 6 months - 3rd or 4th digit

794
Q

Abdominal USS finding in Biliary Atresia

A

Absent Gallbladder or Irregular

Absence of common bile duct

795
Q

At what age can a baby sit up upsupported

A

6 Months

796
Q

At what age can a baby pull themselves to stand

A

9 Months

797
Q

At what age can a baby jump

A

3 Years

798
Q

At what age to children smile spontaneously

A

6 Weeks

799
Q

At what age does a child use a fork and spoon

A

12 month s

800
Q

At what age can a child undress

A

2 Years

801
Q

At what age can a child dress with no help

A

4 Years

802
Q

By what age is not sitting up or walking concerning

A

Not sitting by 1 Year

Not walking by 18 Month s

803
Q

By what age is having no hand preference concerning

A

18 Month s

804
Q

By what age is not smiling concerning

A

3 Months

805
Q

By what age is making no clear words concerning

A

18 Months

806
Q

By what age is no response to carer interactions concerning

A

8 Weeks

807
Q

By what age is still ignoring peers and playing with them concerning

A

3 Years

808
Q

What is the most common type of ASD

A

Ostium Secundum

809
Q

What Are the following ASD types:
a - Ostium Secundum ASD
b - Ostium Primum ASD
c - Sinus venous ASD

A

Ostium Secundum - a hole between two atria

Ostium Primum - Split in one of the leaflets of the mitral valve

Sinus venous ASD: Drainage of the pulmonary veins into the left atrium rather than the right

810
Q

Pathophysiology of Henoch-Schonlein Purpura and lab results

A

IgA are made that directly targets the host’s own endothelial cells

811
Q

What distinguishes Henoch-Schlonlein Purpura over other rashes

A

The purport is palpable above the skin

812
Q

Signs of Henoch-Schonlein Purpura

A

GI Tract: Abdominal Pain

Kidneys: Haematuria
IgA Nephropathy

813
Q

When should Whooping cough be the first suspected infection in a child

A

An acute cough lasting 14 DAYS

  • Paroxysmal cough
  • Inspiratory whoop
  • Post-pertussive vomiting
  • Undiagnosed apnoeitic attacks/cyanosis in young infants
814
Q

What defines compensated shock over late shock

A

Early shock: BP is normal, HR is fast, responsible is fast and they are blue

Late shock:
Hypotension, Bradycardiac, Kussmaul respirations and Anuria

815
Q

What defines clinical shock

A

Pale and cold extremities

CRT >4

816
Q

How do we treat symptomatic hypoglycaemia in neonates

A

Admit to neonatal unit and IV 10% dextrose

Asymptomatic: Encourage normal feeding and monitor glucose

817
Q

When should the PCV vaccine be given

A

3 Months and 12-13 months

818
Q

Rash in Roseola infantum vs Chicken pox

A

Similar pattern of rash, however:

Roseola: Pale pink, macular rash that DISAPPEARS after 48 hours

Chicken Pox: Itchy maculopapular rash that CRUSTS over.

819
Q

When does the Moro Reflex appear and what is it

A

3-4 months:

Head Extension causes abduction followed by adduction of the arms

820
Q

When does the grasp reflex come in and what is it

A

Flexion of fingers when an object is placed into palm

4-5 months

821
Q

What is rooting and when does it present

A

Assists in breast feeding

4 months of age

822
Q

What is stepping and when does it present

A

Walking reflex

2 months of age

Remember:

Some - Stepping (2m)
Meaningful - Moro (4 months)
Reflexes (Rooting - 4m)
Go (grasp 4-5 m)

823
Q

When are children toilet trained

A

3 years of age

824
Q

What would show up on an EEG for infantile spasms

A

Dramatic hypsarrythmia

825
Q

What is an infantile spasm

A

A type of epilepsy involving repeated flexion of the arm/head/trunks followed by extension of the arms.

826
Q

Onset of infantile spasms

A

4-8 months life

827
Q

RF for infantile spasms

A

Male

828
Q

First line therapy of infantile spasms

A

Vigbatrin and ACTH

829
Q

What heart problem is seen in Fragile X Syndrome

A

Mitral Valve Prolapse

830
Q

What is the appearance of a dermoid cyst

A

Multiloculated and heterogenous

831
Q

Where are dermoid cysts usually found

A

Just above the hyoid bone

832
Q

What is a cystic hygroma and where are they usually found

A

Formed from malformation of the lymphatic system, found in the posterior triangle (compared to a branchial cyst which is found at the anterior triangle)

833
Q

What are red sign flags for unwell children

A
  1. Moderate or severe chest wall recession
  2. Does not wake if roused
  3. Reduced skin turgor
  4. Mottled appearance
  5. Grunting
834
Q

Signs of hypernatraemia

A 
Jittery movements
Hypertonia
Hyperreflexia
Convulsions
Drowsiness
835
Q

What conditions are screened for in neonatal blood spot screening

A
  1. Congenital Hypothyroidism
  2. CF
  3. SCD
  4. Phenyketonuria
  5. Medium chain acyl-CoA dehydrogenase deficiency (MCADD)
  6. Maple syrup urine disease
  7. Isolvaleric acidaemia
  8. Glutaric acuduria type I
  9. Homocystinuria
836
Q

What is precocious puberty defined as

A

Under 9 - Male

Under 8 - Female

837
Q

What Genetic condition is associated with Hirschsprung’s Disease

A

Down’s Syndrome

838
Q

Duodenal atresia vs Hirschsprung’s disease in Down’s Syndrome

A

Duodenal atresia does not present with meconium ileus and presents in first feed

Hirschsprung’s disease presents with meconium ileus and presents later.

839
Q

Transient Tachypnoea of the newborn vs Neonatal Respiratory Distress Syndrome

A

NRDS is usually caused by prematurity

transient Tachypnoea of the newborn is usually caused by C-Sections

840
Q

In what children should we expect a UTI in

A

Unexplained fever over 38 degrees

An alternative site of infection but who remain unwell

841
Q

What is the recommended method to sample urine in children

A

Clean Catch

842
Q

What should be done before a suprepubic catheterisation is attempted

A

USS of the abdomen to demonstrate the presence of urine in the bladder

843
Q

In what lab results is a suspicion of a UTI excluded

A

ONLY IF BOTH PYURIA (leucocyte Esterase) and Bacteriuria (Nitrites) are negative. Even if one is positive, you must suspect a UTI

844
Q

In what gender is proteus infection more common

A

Boys

845
Q

How long should a child be observed following antibiotic treatment for a UTI

A

24-48 hours

846
Q

Name three signs of an atypical UTI

A

Poor Urine Flo w
Abdominal Mass
Raised Creatinine

847
Q

Three indications for a micturating Cystourethrogram

A

Vesicourethral Reflux
Bladder
Posterior Urethra

848
Q

Investigation for atypical UTIs

A

DMSA radionuclide imaging to check for renal function (of one kidney relative to the whole renal function) and scarring

Micturating Cystourethrogram

849
Q

When should children be sent to hospital for UTIs

A
  1. Under 3 months
  2. Any child who is systematically unwell
  3. Recurrent UTIs
850
Q

When should preotine:Creatinine ratio be measured

A

First thing in the morning

851
Q

Treatment of Steroid Resistant Nephrotic SYndrome

A

60mg Prednisolone for 4 weeks (standard dose)

852
Q

What is lateral discoid meniscus

A

Instead of the narrow crescent shape seen in a normal meniscus, the lateral meniscus is thicker and fuller = diminished blood supply and weaker capsular attachment.

Because of this, it is more prone to tears

When the knee is stretched, it makes as sound of bouncing bones

853
Q

Diagnostic of a discoid meniscus

A

MRI

854
Q

What is Sever’s Apophysitis

A

Heal pain from sports -> caused by inflammation of the growth plate

855
Q

What can be seen in Accessory Navicular Bone disorders on an X-Ray

A

Plantar medial enlargement of the navicular

856
Q

What is Chondromalacia Patellae

A

The softening of tissue on the underside of the knee cap

Feels full and aching when the knee is flexed

Called ‘RUNNER’S KNEE’

857
Q

First line investigation of bone trauma in children

A

X-Ray (anteroposterior and lateral views)

858
Q

What bone is often broken in chldren

A

Tibia (from unwitnessed falls)

Local tenderness from the tibia shaft - think fracture

859
Q

(ignore trimethoprim card) - what is the first line treatment for upper UTIs

A

IV Ceforoxime for 7 days (for oral, switch to trimethoprim)

860
Q

A child has a UTI, and was unresponsive to IV Ceforoxime, what treatment may we change to and why?

A

IV Meropenem/ Gentamycin

E.Coli is resistent to most penicillins and cephalosporins

This is because E.Coli produces enzymes that destroys beta-lactam antibiotics (penecillins, cephalosporins and Co-Amoxiclav and Tazacin)

861
Q

First line treatment of Osteomyelitis and Septic Arthritis (>3 months)

A

IV Cefuroxime

Treat for 6 weeks ,switching from IV to oral when tolerated

862
Q

What is Usher’s Syndrome

A

Inability of the inner ear and auditory nerves to transmit sensory sound input to the brain (sensorineural hearing loss)

863
Q

Signs of Ushers Syndrome

A

Type 1: Profound Loss, congenital and absent vestibular response

Type 2: Sloping audiogram, congenital and normal vestibular system

Type 3: Progressive variable vestibular system and onset

Accompanied by retinitis pigments

864
Q

Signs of Wardenbergs’ Syndrome

A

Eyes are different colours

Eyes are downwards slanting, making them look wide apart

865
Q

Appearance of teacher collins syndrome

A

Deafness

Followed by underdevelopment of zygomatic complexes (eyes looks sunken)

Conductive hearing loss

866
Q

What is Erythroblastosis Fetalis

A

Rh negative mother previously sensitised to Rh+ cells, causing antibodies to pass through the placenta and haemolytic of the baby’s Rh Positive fetal cells

867
Q

Signs of Erythroblastosis Fetalis

A

Severe Anaemia

Hepatosplenomegaly

868
Q

What ethnicity is most commonly associated with G6PD deficiency

A

Mediterranean and African

869
Q

What is G6PD Deficiency

A

Glutathione is an antioxidant that neutralises free radicals produced from metabolising glucose

G6PD takes the H+ ions away from NADPH that have been reduced by Glutathione reductase

870
Q

How is G6PD deficiency inherited

A

Exclusively affects men as it is X-Linked

871
Q

Signs of G6PD Deficiency

A

jaundice
Dark Tea-Coloured Urine
Back Pain from renal problems

Blood Tests:
Raised reticulocytes
Raised LDH from intracellular hydrolysis
Reduced Haptoglobin 
Raised Bilirubin
872
Q

What is seen on a smear for G6PD deficiency

A

Bite Cells

Heinz Bodies

873
Q

Define Rumination

A

Refrequent regurgitation of ingested food (behavioural)

874
Q

Define Possetting

A

Small Volume vomits during or between feeds in otherwise well children

875
Q

What is Boerhaave Syndrome

A

Oesophageal rupture secondary to forceful vomiting (transmural)

876
Q

Name a bulking agent used for constipation

A

Fybogel

877
Q

Name a stool softener

A

Latculose

878
Q

Define Pa

A
879
Q

What condition in the mother usually causes transposition of the great arteries

A

Diabetes Mellitus 1

880
Q

What is the main cause of cerebral palsy

A

NOT kernicterus (never usually happens in hospitals)

Hypoxic Ischaemic Encephalopathy (from post term and breech deliveries)

881
Q

What chromosome causes DiGeorge Syndrome

A

22

882
Q

Pathophysiology of DiGeorge Syndrome

A

Faulty TBX1 gene:

Stops coding for the third and fourth pharyngeal pouches

883
Q

What do the third and fourth pharyngeal pouches code for

A

Third: Thymus + Inferior Parathyroid Gland

Fourth: Superior Parathyroid Gland

884
Q

Symptoms of DiGeorge

A

Thymic Hypoplasia: Means that T-cells produced in the bone marrow cannot migrate and mature in the thymus = deficiency in mature T cells.

Parathyroid hypoplasia: Means less PTH = hypocalcaemia symptoms

Truncus Arteriosus + Tetralogy of Fallot

Cleft Palate sometimes

885
Q

What type of fractures in babies mayy be non-accidental

A

Non-Motile bone fractures (leg bones, rib fractures)

886
Q

What is the main side effect of Salbutamol

A

Tachycardia

887
Q

First line investigation for suspected volvulus

A

Upper GI contrast study

888
Q

Histology findings of Ewing’s sarcoma

A

Small blue cells with clear cytoplasms on haematoxylin stains

889
Q

What is the onion, osteolytic lesions in Ewing’s sarcoma also described as

A

lamellate periosteal reactions

890
Q

What causes the non-blanching rash in Meningitis and HUS etc

A

Consumption of clotting factors

891
Q

What is a buckle fracture

A

Incomplete fracture of the shaft with bulging of the cortex

892
Q

What fracture is commonly seen in child abuse

A

Spiral Fracture

893
Q

What test is used to differentiate between femoral or tibial length shortening causes in DDH

A

Gallezi Test

894
Q

What are the steps to managing status epileptics

A

FIRST: Buccal Midolazepam or RECTUM Diazepam 10mg

SECOND: IV Lorazepam

Third: IV Phenytoin

895
Q

Changes in doses given of Adrenaline 1:1000 in children suffering from anaphylaxis

A

<6: 150mcg
6-12: 300mcg
>12: 500mcg

896
Q

First line management of a hydrocele

A

Re-assurance, usually goes on it’s own. Incision after 12 months

897
Q

What is one of the most common causes of febrile convulsions in children

A

HSV- 6 : ROSEALA INFANTUM

898
Q

How long should a patient suffering from anaphylaxis be kept in hospital

A

For 6 hours observation, as anaphylaxis can sometimes be bi-phasic.

899
Q

What is milia

A

Loads of white small bumps on the nose of a child or other parts of the face

900
Q

What painkiller is contraindicated in indomethacin treatment for keeping the ductus patent and why?

A

Ibuprofen - antagonises the affect of prostaglandins

901
Q

In what children is a clean catch sample contraindicated to collect urine

A

Babies, young children who won’t pee on command - Urine collection pads instead.

902
Q

Difference in the treatment of hand, foot and mouth disease vs scarlet fever

A

Scarlet fever requires antibiotics

Hand foot in mouth only requires supportive management.

903
Q

Testes
bilateral enlargement = gonadotrophin release from intracranial lesion
unilateral enlargement = gonadal tumour
small testes = adrenal cause (tumour or adrenal hyperplasia)

A

N/a

904
Q

What is McCune Albright syndrome

A

Hyperpigmentation of the skin, contrast to vitiligo

905
Q

What is a complication of chicken pox

A

Necrotising Fasciitis

906
Q

Croup vs Bronchiolitis

A

Bronchiolitis - Barkig cough

Croup - Inspiratory Stridor

907
Q

When is Transient Synovitis common

A

Between 3 and 10 years of age

Anything under, always suspect Septic Arthritis

908
Q

First Line Management of a sudden limp <3 years

A

Urgent Hospital Assessment

909
Q

What is Lumacaftor/Ivacaftor in CF treatment

A

Increases the number of CFTR proteins that integrate into protein surfaces

910
Q

In what children does X-Ray become the first investigation for DDH

A

> 4.5 months

911
Q

When do children talk in small sentences (3-5 words)

A

2.5-3 Years

912
Q

When do children start to respond to their own name

A

9-12 months

913
Q

When do febrile convulsions stop

A

After the age of 5

914
Q

When is the MMR vaccin egiven

A

1 Year

3-4 Years

915
Q

If a child misses their MMR vaccine, when should it be given

A

<10 years: Give MMR vaccine + booster in 3 motnsh

> 10 Years: Give MMR vaccine + Booster in 1 month

916
Q

How does asthma management vary under 5s and over 5s

A

Under 5s:

SABA + 8 week trial of MODERATE-dose ICS

SABA + low dose ICS + LRA

Referral

Over 5s:

SABA

SABA + LOW-dose corticosteroid

SABA + low dose ICS + LTRA

SABA + Low dose ICS + LABA

SABA + MART

SABA + Moderate-dose MART or switch back to moderate dose ICS

917
Q

First line management of cow milk protein allergies

A

Extensive Hydrolysed formula

918
Q

When does an intractable foreskin resolve

A

By 2 years

919
Q

Venous vs Still murmur

A

Venous: Heard below both clavicles

Still: Lower left sternal edge

920
Q

What is the main cause of RDS in neonates

A

Maternal DM

921
Q

How long does a child have to be excluded from school with hand, foot and mouth disease

A

None

922
Q

Most common cardiac problem associated with Duchenne’s

A

Dilated Cardiomyopathy

923
Q

When can children return to school with scarlet fever

A

24 hours after starting antibiotics

924
Q

When should children be reviewed for height restriction by the GP

A

Under 2nd centile

And paediatric review at 0.4 centile

925
Q

When is CPAP or BIPAP indicated

A

When the problem is solely in keeping airways open like RDS.

926
Q

First line intervention of pityriasis Versicolour

A

Ketoconazole shampoo/soap

927
Q

First line intervention for Pityriasis rosea

A

None, self limiting

928
Q

Recovery time in a febrile convulsion

A

1 hour of drowsiness, any more is alarming

929
Q

When is a lumbar puncture in meningitis contraindicated

A

Meningococcal septicaemia

930
Q

What is the appearance of a candidiasis nappy rash

A

Beefy, red well-defined patches

931
Q

What characterises a nappy rash from irritant contact dermatitis

A

Creases are spared

932
Q

Other types of rashes seen in the groin of a neonate

A

Psoriasis: papule would be seen elsewhere too

Seborrhoaic dermatitis: Flaky with scalp involvement

933
Q

Bacterial tracheitis vs Croup

A

Bacterial Tracheitis - does not improve on dexamethasone

Croup does

Both have inspiratory stridor

934
Q

What is the last line medication that would be used to treat cyanosis from CHD

A

Phenylephrine - would cause vasoconstriction, increasing vascular resistance and reducing right to left shunting

935
Q

Symptoms of ADHD

A
  1. Inattention

2. Hyperactivity

936
Q

What is the first line management of a viral induced wheeze

A

Inhaled Salbutamol

937
Q

What is the first line management for Pyloric Stenosis

A

Electrolyte correction

Then Surgery

938
Q

What causes RDS in SCD

A

Aplastic crisis: Tachypnoea, tachycardia in the absence of pain

939
Q

What are morbilliform eruptions

A

Happens in patients being treated with antibiotics (amoxicillin) for Infectious Mononucleosis - generalised maculopapular rash

940
Q

Sepsis vs Diabetic Ketoacidosis

A

Fever vs No Fever

Always consider sepsis in diabetic paediatric patients as UTI’s are more common in them

941
Q

First line treatment for intussusception

A

Air enema

If peritonism is suspected, wanting definitive treatment: Laporoscopic correction/reduction

942
Q

What is the first management step when detecting a murmur in a neonate

A

Wait 24 hours, if after 24 hours of life they still have the murmur, refer for echo

943
Q

Characteristic signs of GORD

A
  1. Back arching
  2. Drawing knees to chest
  3. Initially feeding well and then goes to shit
944
Q

Varicocele vs Hydrocele

A

Varicocele: Pampiniform plexus worm appearance

Hydrocele: Transillumination from build up of fluid in the tunica vaginalis

945
Q

At what age do children eat with a spoon and bowl

A

18 months

946
Q

At what age do children wave goodbye

A

10 months

947
Q

At what age are children pot

A
948
Q

Signs of Pierre Robin sequence

A

Cleft Palate
Retracted Tongue
Small lower jaw

Can only be fed prone

949
Q

What Cardiac disease is common in children who had GDM mothers

A

Transposition of the great arteries

950
Q

Diagnostic of Duchenne’s muscular atrophy

A

Muscle biopsy

951
Q

What are benign rolandic seizures

A

children have a tonic seizure overnight

Usually found sleeping on the floor or messy sheets

952
Q

EEG finding in benign rolandic seizures

A

centro-temporal spikes

953
Q

What is the prognosis of rolandic seizures

A

Most children grow out of it

954
Q

Why is Oxygen contraindicated in neonatal resuscitation

A

oxygen forms free radicals which can cause increased mortality

Just give breaths on air

955
Q

Most common cause of neonatal sepsis

A

E.coli and Strep B

956
Q

What antibiotics are given in neonatal sepsis

A

IV Gentamicin and Benzylpenecillin

957
Q

What is an absolute indication for US of the pelvis

A

ALL babies that were born breach must be given a USS of the pelvis at 6 weeks age

To check for DDH

958
Q

At what age is a pavlik harness sindicated

A

6 weeks +

Anything under is just watchful waiting

959
Q

What should be done to children under 6 with Perthes disease

A

Just observe, keep femoral head within the acetabulum through casts and braces

After that, NSAIDs and physio + Surgery

960
Q

When are sub-optimal o2 levels allowed, only observation is indicated?

A

In the first 10 minutes of life

961
Q

What is a key risk factor for hypoglycaemia

A

Prematurity (will look jittery and irritable)

962
Q

GOLD STANDARD dignosis of pertussis

A

Per Nasal Swab and PCR

963
Q

What vaccines are offered to pregnant women 16-32 weeks?

A

Whooping Cough and Influenza

964
Q

Subdural haemorrhage vs intraventircular haemorrhage

A

IVH - Premature infants

Subdural Haemorrhages - Shaken Baby Syndrome

965
Q

Most common fracture in physical abuse

A

Mid shaft humeral fracture

966
Q

Treatment of strawberry Naevus

A

Topical propranolol but otherwise nothing

967
Q

Name three benign skin problems seen in neonates

A

Erythema neonaturum (white pinpoint papule)
Stork bite/salmon patch (blanches on pressure)
Congenital Dermal Melanocytosis (benign blue spots on the back)

968
Q

What causes ABO incompatibility

A

When the mother is O and the baby is Type A or B

Mother has anti A and B antibodies so causes destruction to baby’s blood

969
Q

Treatment of meconium ileum in CF

A

Therapeutic contrast enema (gastrhogafin)

970
Q

Surgical management of an undescended testes and at what age is this indicated

A

Orchidopexy at 1 year

971
Q

When are inguinal hernias more prominent

A

On crying

972
Q

After what day should medication be given for acute otitis media

A

After 4 days of symptoms

973
Q

When does crying in infantile colics happen the most

A

At night/evening

974
Q

Main viral cause of pneumonia

A

RSV

975
Q

How long should children be off for measles

A

4 Days from onset of rash

976
Q

How long should a child be off from school with Rubella

A

5 Days from onset of rash

977
Q

how long should a child be off from school with Mumps

A

5 Days from onset of swollen glands

978
Q

Conditions that require no exclusion

A 
Conjunctivitis 
Fifth Disease
Roseola
Mononucleosis 
Head Lice
Threadworm
Hand, foot and mouth
979
Q

What does honey injection cause in neonates

A

Infant Botulism

980
Q

What is chorioretinitis

A

Posterior Uveitis

981
Q

First line investigation for asthma

A

Spirometry and Bronchodilator reversibility

Second Line: FeNO + Paek flow diary

982
Q

At what age do children say bye bye

A

12 months

983
Q

What drugs can cause G6PD deficiency

A

Ciprofloxacin
Antimalarials: Primaquins

Sulfonylureas
Sulfonamides

984
Q

Describe the tone of the muscles that characterises Prader-Willi Syndrome

A

Hypotonia

985
Q

Rocker bottom feet in Edward’s vs Patau

A

Rocker bottom feet in Edward’s is usually accompanied by micrognathia

986
Q

Prader willi vs Angelman

A

No hypogonadism or Diabetes/Obesity

Just an ataxic gait with inappropriate laughter (CHARACTERISTIC of Angelman) + Seizures

Both have LDs

987
Q

What hearing test is done at 6-9 months

A

Distraction Test

988
Q

What is the second line treatment for whooping cough if Macrolides are not tolerated

A

Co-Trimoxazole

989
Q

What do the haematoma’s look like in children

A

Bilateral rather than unilateral

990
Q

Define Failure to ThriveWhat BMI indicates possible undernutrition

A

Birthweight < 0.4th Centile

991
Q

How often should children with failure to thrive be monitored

A

Daily < 1 month
Weekly (1-6 months)
Biweekly (6-12m)
Monthly (1 year)

year 3 (25 decks)

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