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Anki 3a exports > paediatrics anki 2 > Flashcards

paediatrics anki 2 Flashcards

1
Q

In patients with androgen insensitivity syndrome why don’t female internal organs develop?

A

Testes produce anti-Mullerian hormone-> prevents males from developing upper vagina, uterus, cervix and fallopian tubes

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2
Q

How would hormonal tests look in a patient with androgen insensitivity syndrome?

A

Raised LH
Normal/raised FSH
Normal/raised testosterone (for a male)
Raised oestrogen(for a male)

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3
Q

How is androgen insensitivity syndrome managed?

A

Specialist MDT: paeds gynae, urology, endo, psych
Counselling-generally raised as female
Bilateral orchidectomy(avoid testicular tumours)
Oestrogen therapy
Vaginal dilators/surgery to create an adequate vaginal length

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4
Q

Give some examples of learning disabilities

A

Down’s
ASD and aspergers
Williams
Fragile X
Global developmental delay
Cerebral palsy

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5
Q

How do children with fragile X present?

A

Long thin face
Large protruding ears
Intellectual impariment
Macroorchidism
Social anxiety
ASD features
Mitral valve prolapse

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6
Q

Name some differentials for fragile X

A

ASD(no physical characteristics)
Down’s
Turner’s

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7
Q

How is Fragile X syndrome diagnosed?

A

Genetics-test number of CGC rpeats in FMR1 gen
eCan also be used to detect carriers

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8
Q

How is Fragile X syndrome treated?

A

Behavioural therapy->manage social anxiety and ASD features
SALT for communication
Educational support
Medical management for physical complications

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9
Q

Name some differential diagnoses for Kawasaki disease?

A

Scarlet fever-high fever, strawberry tongue and sandpaper red rash
Measles
Drug reactions
Juvenile rheumaotid arthritis
Toxic schock syndrome

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10
Q

Describe the natural course of Kawasaki disease

A

Acute:
1-2 weeks
Child most unwell with fever, rash and lymphadenopathy

Subacute:
2-4 weeks
Acute sx settle, demasquation and risk of coronary artery aneurysms

Convalescent:
2-4 weeks
Remaining sx settle, coronary arteries may regress

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11
Q

How is measles transmitted?

A

Via droplets from nose, mouth or throat of infected patient

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12
Q

Describe the typical sequence of symptom onset in patients with measles

A

High fever >40 degrees
Coryzal symtpoms
Conjunctivitis
Koplik spots
Rash

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13
Q

Name some differential diagnoses for measles

A

Rubella
Roseola
Scarlet fever

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14
Q

How can rubella be differentiated from measles?

A

Rubella often milder and begins on face then spreads
Measles: Koplik spots

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15
Q

How long after exposure to measles do symptoms develop?

A

10-14 days post exposure

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16
Q

Name some complications of measles

A

Acute otitis media-most common complication
Pneumonia: most common cause of death
Encephalitis: typically 1-2 weeks after onset

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17
Q

How is chicken pox spread?

A

Airborne-direct contact with rasj or breathign in particles form infected person’s cough/sneeze
Can be caught from someone with shingles

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18
Q

How is chicken pox diagnosed?

A

Clinically

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19
Q

How is rubella transmitted?

A

Through respiratory droplets

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20
Q

How is rubella diagnosed?

A

Serology
rubella-specific IgM or rise in IgG in acute and convalescent serum samples

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21
Q

How is rubella treated?

A

Supportive: antipyretics and analgesia
Isolate individuals to prevent spread, escpecially amongst unvaccinated pregnant women

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22
Q

Name some complications of rubella

A

Arthritis
Thrombocytopenia
Encephalitis
Myocarditis

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23
Q

How does diptheria damag the body?

A

Diptheria toxin commonly causes a ‘diptheric membrane’ on tonsils cuased by necrotic mucosal cells
System distribution can produce necrosis of myocardial, neural and renal tissue

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24
Q

How might a patient with diphtheria present?

A

Recent visitor to Eastern europe/russia/asia
Thick, grey white coating on back of throat and tongue
Fever
Sore throat with ‘diphtheric membrane
‘Bulky cervical lymphadenopathy
Neuritis
Heart block

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25
Q

How is a patient diagnosed with diphtheria?

A

Culture of throat swab-Use tellurite or Loeffler’s media

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26
Q

How is diphtheria managed?

A

Intramuscular penicillin
Diphtheria antitoxin

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27
Q

How can scalded skin syndrome be differentiated from toxic epidermal necrolysis(TEN)?

A

Scalded skin syndrome: oral mucosa usually unaffected

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28
Q

Name some differential diagnoses for scalded skin syndrome

A

Toxic Epidermal Necrolysis (TEN): manifests with widespread erythema and necrosis, leading to detachment of the epidermis. It involves mucous membranes, which differentiates it from SSS
S Pemphigus vulgaris: characterised by flaccid blisters and erosions on the skin and mucous membranes; Nikolsky sign is also positive
Bullous Impetigo: typically presents with localized bullae filled with pus, often with surrounding erythema and tenderness

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29
Q

How is scalded skin syndrome diagnosed?

A

Usually clinical
Biopsy can help differentiate from TEN
Cultures: presence of S aureus

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30
Q

How is scalded skin syndrome treated?

A

IV antibiotics: flucloxacillin-inhibits toxin synthesis
Supportive: fluid replacement and pain management
Wound care to prevent secondary infections

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31
Q

How does flucloxacillin treat scalded skin syndrome?

A

Prevents toxin synthesis

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32
Q

How do patients with whooping ocugh present?

A

Spasmodic coughing with a prolonged duration per episode
Inspiratory whooping sound
Rhinorrhoea
Post-tussive vomiting
Apnoeas, especially in infants

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33
Q

Name some consequences of persistent coughing in patient with whooping cough

A

May develop subconjunctival haemorrhages or anoxia leading to syncope or seizures

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34
Q

How do infants with whooping cough often present?

A

Apnoeas

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35
Q

How is whooping cough managed?

A

<6 months: admit
Oral macrolide: clarithromycin, azithromycin etc if cough onset within 21 days
Notify public health
Antibiotic prophylaxis to household contacts
Off school 48hr post abx/21 days from onset of sx

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36
Q

How do macroldies help patients with whooping cough?

A

Don’t alter disease course, byt may alleviate symptoms and minimise transmission

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37
Q

Name 4 enteroviruses

A

Coxsackie A
Coxsackie B
Poliovirus
Echorviruses

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38
Q

How do enteroviruses spread?

A

Faeco-oral or droplet transmission

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39
Q

How do patients with polio present?

A

Most commonly asymptomatic
Minor: flu-like, pain, fever fatigure, headache, vomiting
Major: Acute flaccid paralysis-> bulbar paralysis

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40
Q

How is polio diagnosed?

A

Clinical
Lab: stool, throat swab, CSF analysis

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41
Q

How is polio managed?

A

No cure
Supportive: pain relief, ventilation if breathing difficulties etc
Physio: in cases of paralytic polio
Preventative: vaccination

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42
Q

Name some complications of polio

A

Paralysis, disability and deformities
Respiratory issues: from bulbar polio
Post-polio syndrome: years after initial infection-> muscle weakness, fatigue and pain in previously affected muscles

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43
Q

Name osme viral causes of meningitis

A

Enteroviruses
HSV
HIV

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44
Q

Describe the typical presentation of a child with fifth disease

A

Prodrome of mild fever, coryza, diarrhoea
Characteristic bright red rash on cheeks after a few days-can spread to rest of body but rarely involved palms and soles-peaks after a week then fades

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45
Q

How is fifth’s disease spread

A

Via respiratory route

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46
Q

name some differentials for fifths disease

A

Rubella: presents with a similar rash, but also includes lymphadenopathy and conjunctivitis
Scarlet fever: presents with a similar rash, but also includes a sore throat and a ‘strawberry’ tongue
Roseola: presents with a high fever followed by a rash, but the rash is typically non-pruritic and pink in colour

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47
Q

How is fifth’s disease diagnosed?

A

Usually clinical
Atypical: serological testing for Parvovirus B19
FBC: low reticuloycte

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48
Q

How is pneumonia manged?

A

At home: analgesia, rest, fluids etc
Hospital: IV fluids and oxygen and antibiotics

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49
Q

How is pneumonia in neonates managed?

A

IV fluids
Oxygen
Broad spectrum antibiotics

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50
Q

How is pneumonia in infants managed?

A

IV fluids
Oxygen
Amoxcicillin/co-amoxiclav if severe

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51
Q

How is pneumonia in children aged >5 years managed?

A

IV fluids
Oxygen
Amoxicillin/erythromycin

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52
Q

Name a complication of pneumonia in children

A

Parapenumonic collapse and empyema

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53
Q

How do patients with asthma typically present?

A

Episodic wheeze that is persistent most days and night
Dry cough
SOB
Symptoms worse at night and early morning
Symptoms have trriggers: exercise, pets, dust, cold air, laughing
Interval symptoms

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54
Q

How would you describe a wheeze to a parent?

A

Whistling in chest when your child breathes out

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55
Q

Name some respiratory failure red flags

A

Drowsiness
Cyanosis
Laboured breathing
Lethargy
Tachycardia
Use of accessory muscles

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56
Q

Name some important features to assessing a child presenting with a wheeze

A

Fever
Weight loss
Apnoea
LOC
CYanosis
O2
Hepatomegaly
Breathing: too breathless to feed, hyperinflation/recession, use of accessory muscles, nasal falring, auscultation/percussion
Heart rate >160bpm
Murmur?

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57
Q

Name some causes of a wheeze in children

A

Asthma
Bronchiolitis
Penumonia
Transient early wheezing
Non atopic wheezing
Cardiac failure
Inhaled foreign body
Aspiration of feeds
Cystic fibrosis
Congenital abnormality of lung, airway and heart

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58
Q

How is moderate acute asthma treated?

A

SABA via spacer, 2-4 puffs
Consider oral prednisolone
Reassure

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59
Q

How long do symptoms of croup typically last?

A

48 hours to 1 week

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60
Q

Name some complications of croup

A

Airway obstruction-> trachea intubation
Otitis media
Dehydration form decreased fluid intake
Superinfection resulting in pneumonia

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61
Q

How might a patient with bacterial tracheitis present?

A

High fever
Toxic
Rapidly progressing into airway obstruction and thick airway secretions

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62
Q

How common is bronchiolitis?

A

Most common serious respiratory infection of infancy

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63
Q

Name some causes of bronchiolitis and which is the most common?

A

RSV-80% of cases
Parainfluenza. rhinovirus, adenovirus, mycoplasma pneumoniae

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64
Q

Name some risk factors for bronchiolitis

A

Breastfeeding for <2 months
Older siblings at nursery/school
Smoke exposure
Chronic lung disease of prematurity

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65
Q

How is bronchiolitis diagnosed?

A

Most clinical
Nasopharyngeal aspirate for RSV culture
CXR
If severe: blood gas analysis, continurous O2 monitoring

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66
Q

Name a risk factor for developing bronchiolitis obliterans

A

Lung transplant recipients

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67
Q

If both parents carry the gene for cystic fibrosis, what are the chances the child will have CF?

A

25%

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68
Q

If both parents carry the gene for cystic fibrosis, what are the chances the child will be a carrier?

A

50%

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69
Q

If both parents carry the gene for cystic fibrosis, what are the chances the child won’t have CF or be a carrier?

A

25%

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70
Q

If 1/25 people in UK have CF mutation, what are the cahnces of having a child with CF?

A

1/2500
1/25 x 1/25 x 1/4

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71
Q

How do neonates with cystic fibrosis typically present?

A

Meconium ileus due to viscous meconium
Failure to thrive

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72
Q

How do infants and toddlers with CF typically present?

A

Salty sweat
Faltering growth
Chest infection
Malabsorption

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73
Q

How do older children with CF present?

A

Delayed onset of puberty
Chest infections
Malabsorption

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74
Q

How is CF diagnosed?

A

Screening: neonatal blood spot test: high immunoreactive trypsinogen
Sweat test: high chloride
Genetic testing

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75
Q

How is CF managed?

A

Daily chest physio to clear mucus and prevent pneumonia
Prophylactic antibiotics, bronchodilators and meds to thin secretions
Regular immunisations-> influenza, penumococcla vaccines
Pancreatic enzyme replacement(Creon) and fat soluble vitamin supplementation (ADEK)
Bilateral lung transplant in end stage pulmonary disease

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76
Q

Name some complications of cystic fibrosis

A

Malabsorption and diabetes due to decreased pancreatic enzyme function
Liver failure
Chest infections-> pneumothoraz and life threatening haemoptysis

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77
Q

How does CF cause liver failure?

A

Mucus blocks bile ducts-> bile can’t leave liver

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78
Q

How common is acute epiglottitis?

A

Rare now due to HiB vaccine

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79
Q

How do patients with acute epiglottitis present?

A

Rapid onset and increase in respiratory difficulties
High fever, generally very unwell/toxic
Minimal/absent cough
Soft inspiratory stridorIntesne throat pain
DROOLING
TRIPOD POSITION->leant forward, extending neck, open mouth

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80
Q

Name some differentials for acute epiglottitis

A

Croup
Peritonsillar abscess
Bacterial tracheitis

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81
Q

How do patients with a viral induced wheeze present?

A

Viral illness for 1-2 days preceding onset
SOB
Signs of respiratory distress
Expiratory wheeze throughout the chest

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82
Q

How is multiple trigger wheeze treated?

A

Trial ICS/LTRA for 4-8 weeks

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83
Q

How do patients with otitis media typically present?

A

Otalgia(ear pain)
Fever
Hearing loss
Recent URTI symptoms
Discharge

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84
Q

Name some differential diagnoses for otitis media?

A

URTI
Mastoiditis
Otitis externa
Foreign body

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85
Q

How is otitis media managed?

A

Self-resolving: usually no antibiotics needed, simple analgesia
If no improvement after 3 days: can start antibiotics
In severe cases admit to hospital and antibiotics

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86
Q

Name some complications of otitis media

A

Chronic OM
Tympanic membrane perforation
Meningitis
Mastoiditis
Facial nerve palsy
Labyrinthitis

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87
Q

How can otitis media be prevented?

A

Avoid passive smoking
Avoid flat/supine feeding

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88
Q

How do patients with glue ear typically present?

A

Hearing loss in affected ear

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89
Q

How is glue ear diagnosed?

A

Otoscopy-> dull tympanic membrane with air bubbles or visible fluid level(can look normal), retracted eardrum

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90
Q

Name some of the risk factors for periorbital cellulitis

A

Male
Previous sinus infection
Recent eyelid injury

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91
Q

How do patients with periorbital cellulitis present?

A

Acute onset of red, swollen, painful eye, fever
Eryhtema and oedema of eyelids-> can spread to surrounding skin
Partial/complete ptosis of eye due to swelling
Orbital signs ABSENT(no pain/restriction on movement, proptosis, chemosis etc)

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92
Q

Name some differentials for periorbital cellulitis

A

Orbital cellulitis
Allergic reactions

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93
Q

How is periorbital cellulitis managed?

A

Referral to secondary care assessment
Oral antibiotics usually enough->empirical co-amoxiclav/cefotaxime
May require admission for observation

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94
Q

Name some causes of a squint

A

Idiopathic-most common
Hydrocephalus
Cerebral palsy
Space occupying lesion(retinoblastoma)
Trauma

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95
Q

Name some differential diagnoses for impetigo?

A

Eczema herpeticum
HSV infection
Contact dermatitis
Ringworm

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96
Q

How is impetigo diagnosed?

A

Usually clinically
Skin swab for mc+s in certain cases like recurrent infections or treatment resistant cases

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97
Q

Name some complications of impetigo

A

Sepsis
Glomerulonephritis
Deeper soft tissue infection-cellulitis
Scarring
Post strep glomerulonephritis
Scarlet fever
Staphyloccocus scalded skin syndrome

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98
Q

Name some differentials for toxic shock syndrome

A

Meningococcal scepticaemia
Stevens-Johnson syndrome
Kawasaki disease

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99
Q

How is suspected toxic shock syndrome investigated?

A

Sepsis 6
Throat/wound swabs

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100
Q

How is scarlet fever spread?

A

Via respiratory route-> inhaling or ingesting droplets or direct contact with nose and throat discharge

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101
Q

How is scarlet fever diagnosed?

A

Throat swab
DONT wait for results to start antibiotic treatment

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102
Q

Describe the treament of scarlet fever

A

Oral phenoxymethylpenicillin for 10 days
Azithromycin for penicillin allergy
notifiable disease-report to public health
Keep off school

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103
Q

How long do patients with scarlet fever need to stay off school?

A

Until 24 hours after commencing antibiotics

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104
Q

Name some complications of scarlet fever

A

Rheumatic fever
Post strep glomerulonephritis
Otitis media-most common
Invasive complications-meningitis, bactaraemia etc

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105
Q

How does the ductus venosus close?

A

Immediately after birth-> umbilical cord clamped and no blood flow->closes and becomes ligamentim venosum

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106
Q

How does the ductus arteriosus close?

A

Prostalgandins usually keep it open
Increased blood oxygenation-> drop in circulating prostaglandins->closes
Becomes ligamentum arteriosum

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107
Q

How does the foramen ovale close?

A

First breath->alveoli expand-> decrease pulmonary resistance in right atrium
Left atrial pressure->right atrial pressure->squashes septum and closesSealed shut after a few weeks-> fossa ovalis

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108
Q

Name some differentials for an ejection-systolic murmur

A

Aortic stenosis
Pulmonary stenosis
Hypertrophic obstructive cardiomyopathy

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109
Q

Name some causes/risk factors for a patent ductus arteriosus(PDA)

A

Genetics/related to rubella
Prematurity

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110
Q

How might a patent ductus arterious present in a newborn?

A

Incidentally in neworn exam with murmur
SOB
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

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111
Q

In patients with a PDA that don;t present in childhood, how might they present in adulthood?

A

With heart failure later in life

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112
Q

How is a PDA diagnosed?

A

Echo
Left to right shunt
Hypertrophy of right, left or both ventricles

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113
Q

How are patients with PDA’s managed?

A

Often close soon after birth
Indomethacin/ibuprofen-inhibits prostaglanding synthesis so closes connection
If other CHD that needs surgery-> prostaglandin E1 to keep duct open until after surgical repair

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114
Q

How do NSAIDS work to treat PDA’s?

A

Inhibit prostaglandin synthesis (helps maintain ductal patency)

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115
Q

How might a patient with an atrial septal defect present?

A

Childhood:
SOB
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

Asymptomatic->antenatal scans

Adulthood:
Dsypnoea
Heart failure
Stroke

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116
Q

How are atrial septal defects managed

A

Small: watch and wait
Surgery: transvenous catheter closure or open heart surgery
Medical: anticoagulants like aspiring, warfirin and NOACs

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117
Q

How are patients with critical coarctation of the aorta managed at birth?

A

Prostaglandin E used to keep ductus arteriosus open while waiting for surgery
Surgery to correct coarctation and ligate ductus arteriosus

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118
Q

How are VSDs diagnosed?

A

Typically through antenatal scans or newborn baby check
Can be asymptomatic and present later in life

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119
Q

How are VSD’s managed?

A

Small and asx: watch and wait, may close spontaneously
Surgically: transvenous catheter closure via femoral vein or open heart surgery

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120
Q

How does the VSD contribute to the tetralogy of fallot?

A

Blood can flow between ventricles

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121
Q

How does the overriding aorta contribute to tetralogy of fallot?

A

When right ventricle contracts, aorta is in direction of travel of that blood, greated proportion of deoxygentated blood enters aorta

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122
Q

How does stenosis of the pulmonary valve contribute to tetralogy of fallot?

A

Greater resistance against flow of blood from right ventricle
Blood flows through VSD and into aorta instead of pulmonary vessels
Due to overriding aorta and pulmonary stenosis-> blood is shunted from right to left->cyanosis

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123
Q

How can positional changes improve circulation in tet spells?

A

Older children: squat
Younger children: Bring knees to chest
Increases systemic vascular resistance so encourages blood to enter pulmonary vessels

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124
Q

How is tetralogy of fallot managed in neonates?

A

Prostaglandin infusion to maintain ductus arteriosus: allows blood to flow from aorta back to pulmonary arteries
Total surgical repair-mortality around 5%

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125
Q

How does sodium bicarbonate help treat a tet spell?

A

Buffers any metbaolic acidosis

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126
Q

How is transposition of the great arteries diagnosed?

A

Fetal US-most are picked up antenatally
Echo
CXR-egg on side

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127
Q

Describe the treatment of transposition of the great arteries

A

Prostaglandin E infusion-maintain ductus arteriosus
Balloon septostomy
Definitive: open heart surgery using bypass-arterial switch

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128
Q

How is Ebstein’s anomaly treated?

A

Treat arrhythmias and heart failure
Prophylactic antibiotics to prevent infective endocarditis
Surgical correction: definitive

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129
Q

How is congenital aortic valve stenosis diagnosed and monitored?

A

Echo: GS
Monitoring: echo, ECG, exercise testing

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130
Q

Desrcibe the treatment for congenital aortic valve stenosis

A

Percutaneous balloon aortic valvoplasty
Surgical aortic valvotomy
Valve replacement

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131
Q

Name some complications that can aride from congenital aortic valve stenosis

A

Left ventricular outflow tract obstruction
Heart failure
Ventricular arrhythmia
Bacterial endocarditis
Sudden death-on exertion

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132
Q

How is congenital pulmonary valve stenosis diagnosed?

A

Echo

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133
Q

Name some possible causes of nocturnal enuresis

A

Diabetes-> excessive urination
UTI’s->urgency/frequency
Constipation->compressess bladder

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134
Q

How can haemolytic uraemic syndrome be classified?

A

Secondary/typical
Primary/atypical

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135
Q

Name a differential diagnosis for haemolytic uraemic syndrome and explain how they can be dfferentiated?

A

Thrombotic thrombocytopenic purpura(TTP)
TTP will include symptoms of fever and neurological changes

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136
Q

How is typical haemolytic anaemia managed?

A

Supportive-> fluids, blood transfusions and dialysis if needed
NO antibiotics

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137
Q

How is atypical haemolytic uraemic syndrome managed?

A

Referral to specialist
Treatment with eculizumab(monoclonal antibody)
Plasma exchange may be used in severe cases with no diarrhoea
NO antibiotics

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138
Q

How does eculizumab treat haemolytic uraemic syndrome?

A

Monoclonal antibody-> inhibits the terminal complement pathway

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139
Q

How should urine samples be collected in children with a suspected UTI?

A

Clean catch
Non contaminated collection pad/catheter sample/suprapubic aspiration

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140
Q

Name some complications of a UTI

A

Renal scarring and CKD
Sepsis

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141
Q

How does vesicoureteric reflux result in recurrent UTI’s?

A

Backwards flow carries bacteria up to the kidneys

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142
Q

Give 3 causes of a vesicoureteric reflux

A

Shortened intravesical ureter
Impoperly functioning valve where ureter joins bladder
Neurological disorder affecting the bladder

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143
Q

Name some complicaiton of vesicoureteric reflux

A

Recurrent UTI’s
Pyelonephritis
Renal scarring and UTI’s
Hypertension

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144
Q

Describe the grading of vesicoureteric reflux

A

Grade 1: Incomplete filling upper urinary tract without dilatation
Grade 2: Complete filling +/- slight dilatation
Grade 3: Balloomed calyces
Grade 4: Megaureter
Grade 5: + hydronephrosis

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145
Q

Name some conditions Wilms’ tumour is associated with

A

Beckwith-Wiedemann syndrome
WAGR syndrome(Wilms’, aniridia, GU anomalies, mental retardation)
Denys-Drash syndrome: WT1 gene on CH 11

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146
Q

Name some differential diagnoses for a Wilms’ tumour

A

Neuroblastoma
Mesoblastic nephroma
Renal cell carcinoma->rare in children

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147
Q

Name one poor prognostic factor in a patients with Wilms’ tumour

A

Associations with other genetic conditions

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148
Q

Name some risk factors for cryptorchidism

A

Family history
Small for gestational age
Prematurity
Low brith weight
Maternal smoking in pregnancy

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149
Q

Name some conditions associated with cryptorchidism

A

Cerebral palsy
Wilms’ tumour
Abdominal wall defects

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150
Q

How is cryptorchidism diagnosed?

A

Cinical-physical exam in a supine position

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151
Q

How might a patient with cryptorchidism present?

A

Malpositioned/absent testes/testis
Palpable cryptorchid testis(unable to be pulled into scrotum/returns to higher position after pulling)
Non-palpable testis
Testicular asymmetry/scrotal hyperplasia

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152
Q

Name some differential diagnoses for cryptorchidism

A

Rretractile testis
Intersex conditions

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153
Q

How would a teenager presenting with cryptorchidism be managed?

A

Orchidectomy
Due to a higher risk of malignancy-Sertoli cells degrade after 2 years

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154
Q

Name some complications of hypospadias

A

Difficulty directing urination
Cosmetic and psychological reasons
Sexual dysfunction

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155
Q

Name some complications of phimosis/paraphimosis

A

Recurrent balanoposthitis/UTI’s
Venous congestion, oedema and ischaemia of glans penis

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156
Q

Name some primary causes of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulonephropathy
Membranous nephropathy

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157
Q

How does nephrotic syndrome result in an increased risk of thrombosis?

A

Decreased antithrombin 3, proteins c+s and increase in fibrinogen

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158
Q

How doe nephrotic syndrome result in lower thyroxine?

A

Decreased thyroxine binding globulin-> lowers total(not free) thyroxine

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159
Q

Name some complications of nephrotic syndrome

A

Hypovolaemia->oedema and hypotension
Thrombosis->kiedney leak clotting factorsInfection-> kidenys leak Ig’s and steroid use
Acute/renal failure

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160
Q

Name 2 drugs that can cause minimal change disease

A

NSAIDs
Rifampicin

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161
Q

Name some causes of nephritic syndrome

A

AI:
SLE or Henoch Schonlein purpura
Infections:
post strep
Goodpasture’s disease
IgA nephropathy(Berger’s)
Rapidly progressing glomerulonephritis
Membranoproliferative glomerulonpehritis

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162
Q

Describe the typical presentation of a patient with IgA nephropathy

A

Gross/microscopic haematuria occuring 12-72 hours after an URTI or GI infection
Mild proteinuria
Hypertension

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163
Q

Name some differential diagnoses for IgA nephropathy

A

Post strep glomerulonephritis(weeks post infection not days, IgA deposition)
Henoch Schonlein purpura-> same except systemic IgA complex deposition instead of just kidneys

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164
Q

Name some markers of good prognosis and poorer prognosis of patient with IgA nephropathy

A

Good: frank haematuria
Poor: male, proteinuria, hypertension, smoking, hyperlipidaemia

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165
Q

Name some differential diagnoses for post strep glomerulonephritis

A

IgA nephropathy

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166
Q

Name a complication of post strep glomerulonephritis

A

CKD
Rapidly progressing glomerulonephritis

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167
Q

Goodpastures disease: symptoms, cause,and treatment

A

Symptoms: pulmonary and alveoli haemorrhage
Cause: Anti-GBM antibody deposition
Treatment: Steroids and plasma exchange

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168
Q

Name some causes of rapidly progressinve glomerulonephritis

A

Goodpasture’s
IgA nephropathy
Henoch Schonlein Purpura
Lupus nephritis
Wegener’s granulomatosis

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169
Q

Describe the treatment of rapidly progressive GN

A

Corticosteroids and cyclophosphamide->induce remission
Plasmapharesis->anti GBM disease and severe ANCA associated vasculitis
Supportive: BP control, diet changes, manage fluid overload/electrolyte imbalances
Renal replacement therapy may be required

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170
Q

How can hypogonadism be classified?

A

Primary: testicular failure
Secondary: hypothalamic or pituitary disorders

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171
Q

Give some examples of primary hypogonadism

A

Klinefelter syndrome
Orchitis
Testicular trauma/torsion
Chemo/radioation

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172
Q

Give some examples of secondary hypogonadism

A

Kallmannm syndrome
Pituitary adenomas
Hyperprolactinoma
Anorexia
Opioid use
Glucocorticoid use
HIV/AIDS
Haemochromatosis

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173
Q

Name some differential diagnoses for hypogonadism

A

Depression
Thyroid disorders
CFS

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174
Q

How might hormone levels seem different in those with Klinefelter syndrome?

A

Elevated gonadotrophin levels(FSH, LH etc)
Low testosterone

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175
Q

How is Klinefelter diagnosed?

A

Karyotyping-chromosomal analysis
Hormones will also show high gonadotrophin levels and low testosterone

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176
Q

Describe the treatment of Klinefelter syndrome

A

Testosterone injections-improve many symptoms
Advanced IVF techniques-> fertility options
Breast reduction for cosmesis
MDT input: SALT, OT, physio, educational support

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177
Q

How is Turner’s syndrome diagnosed?

A

Pre-natally: amniocentesis or chorionic villus sampling(CVS)
Definitive: karyotyping after birth

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178
Q

Give some features of Down’s syndrome that aren’t on the face

A

Hypotonia
Pronounced sandal gap
Learning difficulties
Short stature
Congenital heart defects
duodenal atresia
Hirschsprung’s disease

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179
Q

Name some cardiac complications of Down’s sydnrome

A

Endocardial cushion defect
VSD(30%)
Secundum atrial septul defect
Tetralogy of fallot
Isolated PDA

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180
Q

Name some later complications of Down’s syndrome

A

Subfertility
Learning difficultires
ALL
Alzheimer’s
Repeated respiratory infections
Antlantoaxial instability-avoid trampolines
Hypothyroidism
Visual problems: myopia, strabismus, cataracts

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181
Q

How can Down’s syndrome be diagnosed?

A

Antenatal screening: between 10-14 weeks
Combined test: 10-14 weeks: US and maternal bloods
Triple test: 14-20 weeks: maternal blood tests
Quadruple test: 14-20 weeks

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182
Q

Give some examples of muscular dystrophies

A

Duchenne muscular dystrophy
Beckers muscular dystrophy
Myotonic musclar dystrophy

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183
Q

If a mother is a carrier for Duchenne muscular dystrophy and has a child, what it the likelihood that the child will be a carrier or have the condition?

A

If female: 50% chance of being a carrier
If male: 50% chance of having condiiton

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184
Q

How is Duchenne muscular dystrophy managed?

A

Mostly supportive
Oral steroids can slow the progression of muscle weakness
Creatine supplementation can slightly improve muscle stength

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185
Q

How is Becker’s muscular dystrophy different to duchenne muscular dystrophy?

A

Dystrophiin gene less severely affected and maintains some function, symptoms appear later(8-12 years), some patients need wheelchairs in late 20s/30s, others can walk into adulthood

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186
Q

How is William’s syndrome diagnosed?

A

FISH studies(fluorescence in situ hybridization)

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187
Q

Desrcibe the epidemiology of rickets

A

More common in regions of asia and Africa
Asia: lack of sunlight and low vegetable and meat diets
Africa: darker skin pigmentation and reduced vitamin D synthesis

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188
Q

Name some predisposing features to rickets

A

Dietary deficiency of calcium, e.g. in developing countries
Prolonged breastfeeding
Unsupplemented cow’s milk formula
Lack of sunlight

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189
Q

Name some differential diagnoses for transient synovitis

A

Septic arthritis
Ostemyelitis

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190
Q

How is transient synovitis diagnosed?

A

Often clinical diagnosis
Normal basic observations
Normal blood tests with no raised WCC or inflammatory markers
USS: may show effusion, X-ray normal
Joint aspirate: if done should be no bacteria present

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191
Q

How cam mosteomyelitis be classified?

A

Haematogenous spread: commonly occurs in children, spreads from elsewhere(bactaraemia)
Non-haematogneous spread: spreads from adjacent soft tissues/from firect injury/trauma to bone

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192
Q

Name some risk factors for haematogenous osteomyelitis

A

Sickle cell anaemia
IVDU
Immunosuppresion
Infective endocarditis

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193
Q

Name some differentials for osteomyelitis

A

Septic arthritis
Ewing sarcoma
Cellulitis
Gout

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194
Q

Name some risk factors for developing septic arthritis?

A

Pre-existing joint diseases like rheumatoid arthritis
CKD
Immunosuppresive states
Prosthetic joints

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195
Q

Name some complications of septic arthritis

A

Osteomyelitis
Chronic arthritis
Ankylosis

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196
Q

Name some differential diagnoses fro Perthes’ disease

A

Transient synovitis
Septic arthritis
SUFE
JIA

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197
Q

Name 2 complications of Perthes’ disease

A

Osteoarthritis
Premature fusion of the growth plates

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198
Q

How does the femoral head get displaced in Slipped Upper Femoral Epiphysis

A

Displaced posterio-inferiorly

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199
Q

Name some differentials for the diagnosis of slipped upper femoral epiphysis

A

Osteoarthritis
Hip fracture
Specit arthritis

200
Q

How is slipped upper femoral epiphysis diagnosed?

A

AP and lateral(typically frog leg) views are diagnostic: shortened, displaced epiphysis and widened growth plate
Normal blood tests: exclude other causes of joint pain
Technetium bone scam CT, MRI

201
Q

Name some complications of slipped upper femoral epiphysis

A

Osteoarthritis
Avascular necrosis of the femoral head
Chrondrolysis
Leg length discrepancy

202
Q

How is osgood schlatter diagnosed?

A

Moslty clinical
Imaging may be used to rule out other conditions or if symptoms persist

203
Q

How is osgood schlatter managed?

A

Pain control with analgesics and modification of physical activities
NSAIDs for short term relief
Physio; strengthening and stretching exercises for quadriceps or hamstring muscles
If severe: knee brace or cast

204
Q

Name one complication of osgood schlatter

A

Complete avulsion fracture
Tibial tuberosity is separated from the rest of the tibia-> requires surgical intervention

205
Q

Name some risk factors for developing developmental dysplasia of the hip

A

5F’s
Female(6 times mroe likely)
Firstborn
Family history
Frank breech presentation(buttocks or feet first in the womb)
Fluid(oligohydramnios)

206
Q

How might infants with developmental dysplasia of the hip present?

A

Limited hip abduction, especially in flexion
Asymmetry of gluteal and thigh skinfold
Apparent limb length discrepancy

207
Q

How might older children with developmental dysplasia of the hip present?

A

Walking difficulties/limp
Delayed walking
Waddling gait in bilateral cases

208
Q

How is developmental dysplasia of the hips diagnosed?

A

USS of hips
>4.5 months then x-ray

209
Q

Name a complication of Still’s disease

A

Macrophage activation syndrome(MAS)
Severe activation of the immune system with a massive inflammatory response

210
Q

How might a patient with macrophage activation syndrome present?

A

Systemically unwell
DIC
Anaemia
Thrombocytopenia
Bleeding
Non-blanching rash
Life-threatening

211
Q

Name some non-infective differentials for a child wiith a fever for >5 days

A

Still’s disease
Kawasaki disease
Rheumatic fever
Leukaemia

212
Q

How is enthesitis diagnosed?

A

MRI scan-cannot differentiate cause thoguh

213
Q

Name some complications of juvenile idiopathic arthritis

A

Flexion fractures: PT and splinting
Joint destruction: may need prosthesis
Growth failure: chronic disease and steroid use
Anterior uveitis: visual impairment

214
Q

How is torticollis diagnosed?

A

Clinically history and exam-distinguish mechanical vs neuropathic pain

215
Q

Name some differential diagnoses for torticollis

A

Acute disc prolapse
Tonsillitis
Cervical lymphadenopathy
C spine injury
Neurological disorders leading to dystonia

216
Q

Name some redf lag symoptoms in a patient with likely torticollis

A

Neurological symptoms/signs
Malaise, fever, weight loss, unremitting pain affecting sleep
Hx of violent trauma, neck surgery or risk factors for osteoporosis

217
Q

Name some risk factors for adolescent idiopathic arthritis

A

Positive family history
Peak adolescent growth spurt

218
Q

How is scoliosis diagnosed?

A

Clincal exam
Standing x-rays
MRI considered

219
Q

How is discoid meniscus diagnosed?

220
Q

Name one risk factor for AML

A

Ionising radiation

221
Q

Name some poor progmostic factors for AML

A

> 60 years
20% blasts after course of chemo
Cytogenetics: deletions of chromosome 5 or 7

222
Q

How is AML diagnosed?

A

Bloods: leukocystosis
Blood film: blast cells
Bone marrow biopsy: Auer rods

223
Q

How is AML treated?

A

Chemo and targeted therapy
Radiotherapy
Bone marrow transplant
Surgery

224
Q

Name some complications of chemotherapy

A

Failure to treat caancer
Stunted growth and developmetn in children
Infections
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
Tumour lysis syndrome

225
Q

Name 3 non-blanching lesions and how to differentiate between them

A

Petechiae: <3mm-caused by burst capillaries
Purpura: 3-10mm
Ecchymosis: >10mm

226
Q

Name some differentials for a non-blanching rash

A

Leukaemia
Meningococcal scepticaemia
Vasculitis
HSP
ITP
TTP
Traumatic or mechanical(e.g. severe vomiting)
Non-accidental injury

227
Q

How can CML present?

A

Systemic: weight looss, tiredness, fever, night sweats
SplenomegalyB
leeding
Gout
Hyperleukocytosis: visual disturbance, confusion, priapism, deafness

228
Q

How is CML diagnosed?

A

Bloods: leukocytosis (particularly raised myeloid cells), anaemia
Bone marrow testing
Genetics: Philadelphia chromosome

229
Q

How is ALL diagnosed?

A

Leukocytosis on FBC
Blood film and bone marrow: blast cells
Immunophenotyping: differentiate if origin is B or T cell

230
Q

Name some poor prognostic factors for ALL

A

Age <1yr or >10 years
WCC: >20*10^9CNS disease
Non-caucasian
Male

231
Q

How is CLL diagnosed?

A

Blood: lymphocytosis, aanaemia, thrombocytopenia
Blood film: Smudge cells(ruptured WBC’s)
Immunophenotyping: CD5,19,20,23

232
Q

Name some complications of CLL

A

Richter’s transformation
Anaemia
Hypogamaglobulinaemia-> recurrent infections
Warm AI heamolytic anaemia

233
Q

Give aan example of a genetic condition that can predispose a chidl to brain tumours

A

Neurofibromatosis

234
Q

Name some differential diagnoses for a paediatric brain tumour

A

Migraine
Intracranial hypertension
Epilepsy
Meningitis

235
Q

How is a medulloblastoma treated?

A

Surgical resection and chemo

236
Q

Name some differential diagnoses for pyloric stenosis

A

Gastroenteritis
GERD
Infantile colic

237
Q

Name a differential diagnosis for mesenteric adenitis

A

Appendicitis
-Higher grade fever
-Loss of appetite
-Nausea and vomiting
-Elevated WCC
-Focal pain in RLQ

238
Q

How is mesenteric adenitis managed?

A

Usually self limiting-observation and reassurance
Careful safety netting
Surgical: not usually advised, may be needed if appendicitis can’t definitively be ruled out

239
Q

Name some differential diangoses for an intussusception

A

Gastroenteritis
Appendicitis
Volvulus
Meckel’s diverticulum

240
Q

How is intussusception diagnosed?

A

Abdominal USS: ‘target sign’
Can reveal complications

241
Q

How does intestinal malrotation present?

A

Bilious vomiting, often on the first day of life(with volvulus)

242
Q

Name some differentials for a patient wtih intestinal malrotation

A

GERD
Pyloric stenosis
Duodenal atresia
Intestinal obstruction

243
Q

How is malrotation diagnosed?

A

Upper GI contrast study-reveals obstruction point as no contrast will be able to pass
USS
Proximal bowel: corckscrew appearance

244
Q

How is intestinal malrotation managed?

A

Laparotomy
If volvulus present: Ladd’s procedure(includes division of Ladd bands and widening of base of mesentery
Relieve obstruction and correct congenital abnormality

245
Q

Name some risk factors for GORD

A

Preterm delivery
Neurological disorders

246
Q

Name some red flag symptoms in a child with suspected GORD

A

Not keeping down feed(pylroic stenosis/obstruciton)
Projectile vomiting
Haematemesis
Abdominal sdistention
Reduced consciousness, bulging fontanelle or neuro signs
Signs of infection
Rash, angioedema, allergic signs
Respiratory symptoms including apneoas

247
Q

Name some complications for GORD

A

Distress
Failure to thrive
Aspiraiton
Frequent otitis media
Older children: dental erosion

248
Q

If severe complicaiotns and medical treatment is ineffective, what might be considered for a patient with GORD?

A

Fundoplication

249
Q

Describe what might be found on examination of a patient with appendicitis

A

Systemic: pyrexia and tachycardiaLocalised tenderness and guarding in RIF
Tenderness over McBurney’s point(1/3 frmo ASIS to umbilicus)
Rovsing’s sign: RIF pain with palpation of left iliac fossa
Also psoas or obturator sign

250
Q

Name some complications of appendicitis

A

Local abscess formation
Perforation
Gangrene
Postoperative wound infection
Peritonitis

251
Q

How does appendicitis often present in patients under 4 years olf

A

More likely to be atypical and present with perforation

252
Q

Name some complications of biliary atresia?

A

Unsuccessful anastamosis
Progressive liver diease
Cirrhosis with HCC

253
Q

Name some differentials for a febrile convulsion

A

Meningitis
Encephalitis
Electrolyte imbalances causing seizures
Epilepsy

254
Q

How are febrile convulsions managed?

A

If first seizure: admit
Source of fever identified and treated if necessary
Parental educations: appropriate use of antipyretics, don’t sponge child to cool down
Phone ambulance in future if seizure lasts >5 minutes
If recurrent: benzos may be considered-only on advice of specialist(rectal diazepam or buccal midazolam

255
Q

Name some causes of encopresis

A

Spina bifida
Hirschprung’s
Cerebral palsy
Learning disability

256
Q

How might children with constipation present?

A

<3 stools/week
Hard stool that are difficult to pass
Rabbit dropping stools
Abdominal pain
Straining resulting in rectal bleeding
Overflow diarrhoea

257
Q

Name some red flags for constipation in children

A

Not passing meconium within 48hrs of brith(CF/hisrschprung’s)
Neuro signs
Ribbon stool
Vomiting
Abnormal anus/lower back/buttocks
FTT
Acute severe abdo pain and bloating

258
Q

Name some complicaitons of constipation in children

A

Pain
Decreased sensation
Anal fissures
Haemorrhoids
Overflow soiling
Psychosocial morbidity

259
Q

Name some risk factors for developing cerebral palsy

A

Preterm birth
Low birth weight
Multiple birth
Congenital malformations

260
Q

Name some causes of cerebral palsy

A

Antenatal:
cerebral malformation
congenital infection(rubells, toxoplamsosis, CMV)
maternal alcohol/smoking use
Maternal thrombotic disorders
(factor 5 leiden)

Intrapartum:
Birth asphyxia
Trauma

Postnatal:
Intraventricular haemorrhage
Meningitis
Head trauma
Hypoglycaemia
Neonatal sepsis and encephalopathy

261
Q

Name some general symptoms of cerebral palsy

A

Wide variety-delays in reaching developmental milestones, altered tone and weakness
Hand dominance before 18 months
Feeding difficulties
Abdnormal gait

262
Q

Name some associated non-motor symptoms of cerebral palsy

A

Learning difficulties
Epilepsy
Squints
Hearing impairment
GORD

263
Q

Name some differentials for cerebral palsy

A

Muscular dystrophies
Metabolic disorders
Hereditary spastic paraplegia
JIA

264
Q

Name some complications of cerebral palsy

A

Recurrent chest infections->aspiration pneumonias from feeding difficulties
Chornic constipation/incontinence
Visual/hearing impairment
Epilepsy
Behavioural and emotional difficulties
Contractions
GERD

265
Q

Name some differentials for haemolytic disease of the newborn

A

Spherocytosis
G6PD deficiency
Thalassaemia

266
Q

Howw is haemolytic disease of the newborn managed?

A

Intrauterine transfusions if severe anaemia detected in fetus
Early delivery if severe

Postnatal: phototherapy, exchange transfusion to manage high bilirubinImmunoglobulin administration to newborn to prevent further haemolysis

Regular follow up to assess for developmetnal issues

267
Q

Name some complications of haemolytic disease of the newborn

A

Unborn:
Fetal heart failure
Fetal hydrops: fluid retention and swelling
Stillbirth
Newborn:Kernicterus->hearing loss, blindness, vision loss, brain damage, learning difficulties, death

268
Q

Name a complication of a cephalohaematoma

269
Q

How should chest compressions be carried out in children?

A

100-120/min for children and infants
Depth: at least 1/3 depth of chest(4cm infant, 5cm for child)
Children: lower half of sternum
Infants: 2 thumb encircling technique/2 fingers from one hand

270
Q

Name some causes of acute respiratory distress syndrome

A

Infection: sepsis, pneumonia
Major trauma
Aspiration
Pancreatitis
Fat embolism
Drowning
Burns
DIC
Transfusion reactions

271
Q

Name some differentials for acute respiratory distress syndrome

A

Cardiogenic pulmonary oedema
Covid
Bilateral penumonia
Diffuse alveolar haemorrhage

272
Q

How is acute respiratory distress syndrome diagnosed/investigated?

A

CXR: bilateral alveolar infiltrates without other features of heart failure
Arterial blood gases: severity of hypoxemia
Others;Resp viral swabSputum, blood and urine cultures
Serum amylase: screen for pancreatitis
CT cehst

273
Q

Name some differentials for neonatal respiratory distress syndrome

A

Transient tachypnoea of the newborn
Meconium aspiraiton syndrome
Pneumonia

274
Q

How is neonatal respiratory distress syndrome diagnosed/investigated?

A

Usually clinical
CXR: ‘ground glass appearance’
Blood gas: hypoxaemia and hypercapnia

275
Q

How can the risk of neonatal respiratory distress syndrome be reduced in premature infants?

A

Administer glucocorticoids to mother before delivery to enhance surfactant production in the infant

276
Q

Name some complications of neonatal respiratory distress syndrome

A

R->L shunt through collapsed lung or ductus arteriosus
Ventilator use complications->pneumonia, pneumothorax
Pulmonary/intracranial haemorrhage
Necrotising enterocolitis
Bronchopulmoanry dysplasia
Retinopathy of prematurity
Hearing and other neurological impairments

277
Q

Name some neonatal risk factors for neonatal sepsis

A

Late pre-term
Low birth weight <2.5kg
Black race independent risk factor for Group B strep-related sepsis

278
Q

How do patients with neonatal sepsis present?

A

Respiratory distress: grunting, nasal flaring, tachypnoea
Feeding problems
Jaundice
Shock and multi-organ failure
Temperature: not a reliable sign, especiallly in pre-term infants(more likely to be hypothermic)
Seizures
Neurological sx
Discharge from eyes->chlamydia or gonorrhoea
Periumbilical cellulitis
Meningitis: bulging fontanelle, seizures

279
Q

How is neonatal sepsis diagnosed/investigated?

A

Cultures, FBC, CRP
Blood gases
Urine mc+s if late onset sepsis
LP especially if meningitis concern
CXR advised against unless strong suspicion of chest source

280
Q

In a patient with neonatal sepsis, if concerned about meningitis what antibiotic might you consider adding?

A

IV cefotaxime annd IV gentamicin

281
Q

In a patient with neonatal sepsis, if concerned about necrotising enterocolitis what antibiotic might you consider adding?

A

Add metronidazole for anaerobic cover

282
Q

In a patient with neonatal sepsis, if the mother has chorioamnionitis what antibiotic might you consider adding?

A

IV amoxicillin and IV gentamicin to cover for listeria

283
Q

How is transient tachypnoea of the newborn diagnosed/investigated?

A

Clinical
CXR: hyperinflation of lungs and fluid in horizontal fissure

284
Q

How is meconium aspiration syndrome diagnosed/investigated?

A

Mostly clinical
CXR: patchy areas of atelectasis and hyperinflation
ABG
Monitoring of oxygen
CRP, cultures if infection suspected

285
Q

Name some causes of persistent/severe neonatal hypoglycaemia

A

Preterm birth (<37weeks)
Materal diabetes
IUGR
Hypothermia
Sepsis
Inborn errors of metabolism
Nesidioblastosis
Beckwith-Wiedemann syndrome

286
Q

How is gastroschisis investigated/diagnosed?

A

Intrauterine USS, MRI
Labs: increased maternal serum alpha fetoprotein

287
Q

Name some risk factors for gastroschisis

A

Mother’s young age
Exposure to alcohol/tobacco

288
Q

Name some ocmplicaitons of gastroschisis

A

Intestinal inflammation for intrauterine exposure to amniotic fluid
Malabsorption
Infarction of intestinal tube due to compressed blood vessels
Infection

289
Q

Name some conditions associated with exomphalos

A

Down’s syndrome
Edward’s
Patau’s
Beckwith-Wiedemann syndrome

290
Q

Name some risk factors for exomphalos

A

Alcohol/tobacco use in pregnancy
SSRIs
Obesity

291
Q

Name some complications of exomphalos

A

Abdominal cavity malformation
Volvulus
Ischaemic bowel

292
Q

How is exomphalos diagnosed/investigated?

A

Intrauterine USS
MRI
Bloods: MS
AFP
Amniocentesis

293
Q

How does a staged surgical repair work for exomphalos treatment?

A

Sac allowed to granulate and peithelialise over weeks/months-> forms shell
As infant grows-> sac contents can fit inside
Shell removed and abdomen closed

294
Q

Name some complications of intestinal atresia

A

Distention of stomach and duodenum->accumulated fluid
Polyhydramnios(fetus swallows less fluid so more builds up)
Intestinal perforation
Meconium peritonitis

295
Q

Name some of the signs/symptoms of intestinal atresia

A

Polyhdramnios antenatally
Postnatal: distended abdomen and vomiting
Vomiting may be bilious or non-bilious depending on site of atresia

296
Q

How is duodenal atresia diagnosed/investigated?

A

Prenatal USS-> detectable in 3rd trimester: dilated fluid-filled stomach adjacent to dilated duodenum
Postnatal XR: double bubble sign
Physical exam in surgery: apple peel shape of intestines
Amniocentesis for Down’s
Double bubble sign

297
Q

Describe the treatment of duodenal atresia

A

Gastric decompression-> remove fluid from stomach
IV fluid compensation
Surgical reattachment of functional portions of intestines->duodenoduodenostomy

298
Q

Name some differentials for oesophageal atresia and tracheo-oesophageal fistula

A

Congenital diaphragmatic hernia
Duodenal atresia
GORD

299
Q

How is oesophageal atresia diagnosed/investigated?

A

USS antenatally
CXR: coiled NG tube
Echo and renal USS to check for associateed anomalies
Genetics if needed

300
Q

Name some complications of oesophageal atresia and tracheo-oesophageal fistula

A

Anastomotic leak or stricture
Poor feeding and failure to thrive
Reccurence of tracheo-oesophageal fistula
Trachemoalacia
Recurrent chest infections and bronchiectasis
GORD

301
Q

Name some differentials for necrotising enterocilitis

A

Sepsis
Gastroenteritis
Intestinal malrotation with volvulus
Hirschsprung’s disease

302
Q

How is necrotising enterocilitis investigaed/diagnosed?

A

Abdo X-ray
Abdo USS and venous blood gas may also be used

303
Q

Name some preventative strategies for necrotising enterocilitis

A

Encourage breastfeeding in mothers of prem babies
Delayed cord clamping
Antenatal steroids in pre term labour
Treatment of preterm infants with caffeine citrate to prevent bronchopulmonary dysplasia

304
Q

Name some complications of necrotising enterocilitis

A

Perforation and peritonitis
Short bowel syndrome
Sepsis and shock
DIC
Abscess formation

305
Q

How are congenital diaphragmatic hernias diagnosed/investigated?

A

USS in utero
CXR/USS in neonate
Check for other abnormalities including genetics

306
Q

How should bilirubin levels be measures in a neonate?

A

Transcutaenous first
If elevated serum bilirubin

307
Q

Name some complication of neonatal jaundice

A

Related to phototherapy-> loose stools and dehydraiton
Kernicterus

308
Q

Name some complications of kernicterus

A

Damage to nervous system is permanent
Cerebral palsy
Learning difficulties
Deafness

309
Q

Name some complicatons of TORCH infecitons

A

Pre term birth
Delayed devlopment(IUGR)
Physical malformations
Loss of pregnancy

310
Q

How are TORCH infections transmitted?

A

To fetus through placenta
During birth from birth canal
Through breast milk

311
Q

Name some general symptoms of TORCH infections

A

Fever
Lethargy
Cataracts
Jaundice
Reddish-brown spots on skin
Hepatosplenomegaly
Congenital heart disease
Microcephaly
Low birth weight
Hearing loss
Blueberry muffin rash

312
Q

How is CMV transmitted?

A

Direct contact with infected bodily fluids: saliva, tears, mucus, semen and vaginal fluids

313
Q

How is HSV1 transmitted?

A

Oral herpes: oral secretions: kissing, sharing utensils, sharing drinks

314
Q

How is HSV 2 transmitted?

315
Q

How is HSV transmitted to a newborn?

A

Passage through the birth canal

316
Q

Name a consequence of parvovirus B19 in pregnancy

A

Severe reduction in RBC-anaemia in infected newborn-> hydrops fetalis

317
Q

How might newborns with HIV present?

A

Low birth weight
Hepatosplenomegaly
Recurrent bacterial infections-> meningitis and pneumonia

318
Q

How are TORCH infections diagnosed?

A

Prenatal pCR from amniotic fluid: toxoplasmosis, syphilis, B19
CMV: viral culture, IgM, PCR
Rubella: IgM
HSV: viral infections, PCR

319
Q

How is toxoplasmosis treated in pregnancy and infancy?

A

Pregnancy: spiramycin
Infants: pyrimethamine and sulfadiazine

320
Q

How are VZV and HSV treated in pregnancy/neonatology?

321
Q

How is treponema pallidum treated in neonates?

A

Penicillin

322
Q

How is listeriosis investigated/diagnosed?

A

Blood cultures, CSF cultures
Placental or meconium cultures in neonates

323
Q

How is listeriosis prevented in pregnancy

A

Avoid potentially contaminated food products
Cultures if unexplained febrile illness or suspicion of infection

324
Q

How might HSV in neonates be diagnosed/investigated?

A

PCR, virus culture, direct fluorescent testing
MRI brain if suspected encepahlitis

325
Q

How can the risk of bronchopulmonary dysplasia be reduced during pregnancy

A

GAive corticosteroids-betamethasone for premature labour to help speed up lung development

326
Q

How can the risk of bronchopulmonary dysplasia be reduced once born?

A

Use CPAP instead of intubation/ventilation
Caffeine to stimulate respiratory effort
Don’t over-oxygenate

327
Q

How is bronchopulmonary dysplasia diagnosed?

A

CXR and oxygen dependency of infant
Ssleep study to assess o2 sats

328
Q

Name some causes of epilepsy in children

A

Head trauma
Tumours
Infectious diseases
Prenatal injuries
Electrolye disturbances
Developmental disorders
Metabolic disorders

329
Q

How is epilepsy diagnosed/investigated in children?

A

Refer urgently(<2weeks) for paeds assessment after 1st seizure
EEG-doesn’t exclude epilpesy
MRI/CT to rule our structural causes
ECG for cardiac causes
Genome sequencing if onset <2yrs and other features: learning diasbilites etc)

330
Q

Name some complications of epilepsy in children

A

Mood disorders
Status epilepticus
Sudden unexpected death in epilepsy
Developmental delay/regression

331
Q

How are absence seizures diagnosed?

A

EEG: 3Hz, generalized, symmetrical

332
Q

How are absence seizures treated?

A

Ethosuzimide 1st line

333
Q

How is West’s syndorme diagnosed?

A

EEG: hypsarrhythmia
ID underlying cause e.g. tuberous sclerosis, encephalitis etc

334
Q

Describe the treatment of West’s syndrome

A

Vigabatrin 1st line
Poor prognosis

335
Q

How is Dravet’s syndrome diagnosed?

A

Genetic testing

336
Q

Name some causes of global developmental delay

A

Down’s
Fragile X
Rett’s syndrome
Metabolic disorders
Prematurity

337
Q

Name 2 red flags when it comes to development

A

Developmental arrest: initially normal, stops gianing further skills
Developmental regression

338
Q

Name some behaviours that might prompt a referral for developmental delay

A

Doesn’t smile at 10 weeks
Hand preference before 12 month
sCan’t sit unsupported at 12 months
Can’t walk at 18 months

339
Q

Name some causes of gross motor delay

A

CP
Ataxia
Myopathy and muscular dystrophy
Spina bifida
Visual impairment

340
Q

Name some causes of fine motor delay

A

visual impariments(cataracts, retinoblastoma, ambylopia)
Dyspraxia
CP

341
Q

Name some causes of social, emotional and behavioural delay

A

ASD
Neglect
Genetics: Down’s etc
Hearing impairment

342
Q

Name some causes of speech delay

A

Global delay-mchearing impairment
Chronic otitis media with effusion
Environment-lack of stimulus
ASD
Bilingual households

343
Q

Name some key gross motor milestones

A

6-8 months: sits without support
12-15 months: walks unsupported
2 yrs: runs
3-4 yrs: hops on one leg

344
Q

Name some general fine motor and vision milestones

A

Newborn: fix and follow face/light
3 mths: reaches for object
6 mths: palmar grasp, passes objects between hands
9-12 months: pincer grip

345
Q

Name some differentials for retinoblastoma

A

Congenital cataracts
TORCH infection
Congenital rubella-characteristic ‘salt and pepper’ appearance

346
Q

How is retinoblastoma investigated/diagnosed?

A

Ophthalmic exam under general anaesthesia:
dilated fundus exam and UDD B scan(mass-> characteristic)
MIR-> spread
LP/bone marrow biopsy-> if suspicion of extraocular invasion
Genetics

347
Q

Name some conditionas associated with an increased risk of neroblastoma

A

Turner;s
Hirschsprung’s
NF1
Congenital central hypoventilation syndrome

348
Q

How is neuroblastoma diagnosed/investigated?

A

Urine catecholamines-> sensitive and specific: high levels of vanillymandelic acid(noradrenaline breakdown product) and homovanillic acid(adrenaline)
Bloods: pancytopenia, serum catecholamines, LFT’s, LDH
Imaging: abdo USS, if mass: CT/MRI abdomen
Bone scan
Biopsy

349
Q

Name some differentials for neuroblastoma

A

Wilms’ tumour
Rhabdomyosarcoma
Phaeochromocytoma
Other neural crest tumours

350
Q

Name one condition associated with hepatoblastoma

A

Beckweth-Wiedemann syndrome

351
Q

How is hepatoblastoma investigated/diagnosed?

A

AFP: tumour marker
CXR to check for spread
USS
CT/MRI for staging and metastasis
Biopsy

352
Q

Name some differentials for osteosarcoma

A

Ewing sarcoma: elevated ESR and LDH
Chondrosarcoma
Lymphoma of bone

353
Q

How is osteosarcoma investigated/diagnosed?

A

Urgent XR in 25 hrs if child/young person has unexplained bone swelling/pain
-if positive x ray: 48 hour specialist assessment
X-ray: new bony growth and periosteal reaction causing sunburnt appearance
Full body CT: metastasis
Definitive: biopsy

354
Q

Name some poor prognostic factors for osteosarcoma

A

Primary metastasis
Axial/prominent extremity tumour site
Large tumor volume
High serum ALP or LDH

355
Q

How can Ewing’s sarcoma be classified?

A

Low grade restricted to hard coating of bone(A) or local tissues(B)
High grade tissue restricted to hard coating of bone (A) or extending to local tissues(B)
Low or high grade tumour whcih has metastasised

356
Q

Name some differentials for Ewing’s sarcoma

A

Osteosarcoma
Osetomyelitis
Lymphoma

357
Q

How is Ewing’s sarcoma diagnosed/investigated?

A

48 hr Xray if young person with unexplained bone swelling/pain->48 hr assessment if positive
Bloods: FBC and LDH
Xray: onion skin appearance of bone destruction with layers of periosteal bone formation
CT/MRI/PETBone biopsy

358
Q

Name some poor prognostic factors for Ewing’s sarcoma

A

Large tumour burden
High lDH levels
Multiple bony metastasis
Axial localisation age >5yrs
Poor resposne to pre-op chemo

359
Q

Name some risk factors for Hodgkin’s lymphoma

A

EBV
HIV
Immunosuppression
Smoking

360
Q

How is Hodgkin’s lymphoma diagnosed/investigated?

A

Normocytic anaemia, neutrophilia, thrombocytosis, eosinophilia
Raised ESR and LDH
Lymph node biopsy: Reed Sternberg cells cells-diagnostic
CT/PET to stage disease

361
Q

Name some conditions associated with an increased risk of brain tumours

A

Neurofibromatosis
Li-Fraumeni syndrome
Familial adenomatous syndrome
Gorli syndrome

362
Q

How are brain tumours in children diagnosed/investigated?

A

Any child with newly abnormal cerebellar or neurologic function URGENT referral(<48hrs) for suspected brain cancer
MRI/CT to visualise space-occupying lesions
LP&Biopsy

363
Q

Name some commplicaitons of paediatric brain tumours

A

GH deficiency
Cognitive decline
Subsequent brain tumour(risk increased due to radiotherapy)
Osteoporosis and poor mineral density

364
Q

Name some differentials for von Willebrand’s disease

A

Haemophilia-> mc bleeding into joints and muscles

365
Q

How is von Willebrand’s disease diagnosed/investigated?

A

Prolonged bleeding time and APTT
Normal PT and TT
Normal platelet count
Vin willebrand factor level and assay to confirm

366
Q

Name some causes of microcytic anaemia in children

A

Iron deficiency-mc
Thalassaemia
Lead posioning

367
Q

Name some causes of macrocytic anaemia in children

A

Vit B12/folate dficiency

368
Q

Describe the treatment of IDA in children

A

Iron supplements+ diet advice
Vit B12 and folate if needed
Transfusions if severe
Tx underlying disease

369
Q

How is alpha thalassaemia diagnosed/investigated?

A

FBC: microcytic anaemia
Hb electrophoresis-> can be normal, DNA analysis needed to make diagnosis

370
Q

How is beta thalassaemia minor investigated/diagnosed?

A

Microcytosis with only mild anaemia
Blood filmd-target cells and basophilic stippling
Increased RBC
DIAGNOSTIC: Hb electrophoresis: raised HbA2
Ferritin normal/high

371
Q

How is beta thalassaemia najor investigated/diagnosed?

A

Profound microcytic anaemia
Increased reticulocytes
Blood film: marked anisopoikilocytosis, target cells and nucelated RBCs
Methyl blue stains: RBC inclusions with precipitated alpha globin
Electrophoresis-> HbA2 and HbF raised
HbA2 normal or mildly elevated

372
Q

Name some complications of beta thalassaemia major

A

Cardiomyopathy/arrhthymia/failure-AF in older patients
Acute bacterial sepsisrisk increased post splenectomyliver cirrhosis, portal hypertension
Endocrine dysfunction: hypocalcaemia with tetany due to hypoparathyroidismIron overload
Death->usually due to undiagnosed heart failure

373
Q

How can iron overload be prevented?

A

Iron chelating agents: desferrioxamine/deferiprone/deferasirox

374
Q

Name some differentials for sickle cell anaemia

A

Thalassaemia
G6PD deficiency
Haemoglobin C-variant which doesn’t cause sx unlesss combined with HbS variant

375
Q

How is sickle cell disease diagnosed/investigated

A

Diagnostic: Hb electrophoresis
CBC: anaemia
Blood smear: ID sickle shaped cells

376
Q

How is fanconi anaemia diagnosed/investigated?

A

CBC, bone marrow
Chromosome DEB assay
Chromosomal breakage test positive
Cytometric flow analysis

377
Q

How is fanconi anaemia treated?

A

Growth factors(G-CSF)
Androgen therapy
Transfusions
Stem cell transplant
Screen and monitor for malignancies
Family support, genetic counselling

378
Q

Name some complications of fanconi anaemia

A

Neutropenia-> life-threatening infections
Malignancies: myelogenous leukaemias, myelodysplastic syndromes etc
Endocirne derangements
Congenital anomalies

379
Q

Name some differentials for haemophilia

A

Von Willebrand Disease
Factor deficiencies
Platelet disorders
Hamatological malignancies
Vasculitis

380
Q

How is haemophilia investigated/diagnosed?

A

Prolonged APTT with normal bleeding time, PT and thrombine time
Diagnostic: factor 8/9 assay
vWF antigen normal

381
Q

Name a complication of Haemophilia A

A

Up to 1/3 of boys with haemophilia A will develop antibodies to factor 8 tx: worsens bleeding and complicates therapy

382
Q

Name some differentials for ITP

A

Aplastic anaemia
Leukaemia
TTP

383
Q

How is ITP diagnosed/investigated?

A

FBC: isolated thrombocytopenia
Blood film
Inflammatory markers
Bone marrow biopsy-only done if atypical features

384
Q

Name some complications of ITP in children

A

Significant bleeds(3%)
Intracranial haemorrhage(1/300)
Typically occur when plt counts <20 + have pre-existing vascular abnormalities

385
Q

Name some causes of TTP

A

Post-infection: urinary, GI
Pregnancy
Drugs: ciclosporin, OCP, penicillin, clopidogrel, aciclovir
Tumours
SLE
HIV

386
Q

How is TTP investigated/diagnosed?

A

Diagnostic: Low ADAMST13 activity
Urine dpistick: haematuria, non-nephrotic range proteinuria
FBC: normocytic anaemia, thrombocytopenia and raised neutrophil
U&;E: raised urea and creatinine
Clotting normal
Blood film: reticulocytes(secondary to haemolysis) and schistocytes(fragmented RBCs)
D-dimer raised

387
Q

Name some differentials for testicular torsion

A

Epididymo-orchitis
Trauma
Inguinal hernia

388
Q

How is testicular torsion diagnosed/investigated?

A

Clinical
Doppler USS->reduced/absent blood flow to affected testicle-‘whirlpool’ sign
Urinalysis: rule out infection/UTI
Shouldn’t delay treatment to wait for investigations

389
Q

Name some complications of testicular torsion

A

Testicular necrosis
Impaired fertility
Contralateral testicular torsion in 40% of cases without bilateral fixation

390
Q

How does testicular torsion present in neonates?

A

Paainless scrotal swelling whcih does not transilluminate

391
Q

Give some examples of primary sexual characteristics

A

Men: penis, scrotum, testes
Women: vulva, vagina uterus, ovaries

392
Q

Give some examples of secondary sexual characteristics

A

Men: facial hair, testicle/penile enlargement
Women: Pubic hair, breast development, widening of hips

393
Q

How can precocious puberty be classified?

A

Gonadotrophin-dependent precocious puberty(GDPP)
Gonadotrophin independent precocious puberty(GIPP)

394
Q

Name some causes of gonadotrophin-dependent precocious puberty(GDPP)

A

Idiopathic(>90% of cases)
Brian tumours
Cranial radiotherapy
Structural brain damage: hydrocephalus, meningitis, traumatic head injury

395
Q

Name some causes of gonadotrophin-independent precocious puberty

A

Gonadal tumours
Adrenal/liver tumours
Congenital adrenal hyperplasia

396
Q

Name some differentials for precocious puberty

A

Thryoid disorders
Growth hormone excess(acromegaly etc)
McCue-Albright syndrome

397
Q

How is precocious puberty diagnosed/investigated?

A

Measure oestradiol/testosterone levels, adrenal androgens, TFTs and HCG
Brain MRI
Pelvic USS-> ovarian cysts/pathology
Hand and wrist X-rays for bone ageIntra-abdominal imaging if adrenal/hepatic tumour suspected
MRI brain and GnRH stimulation test dependent on initial investigation results

398
Q

Name some complications of precocious puberty

A

Accelerated skeletal development and premature fusion of bone growth plates-> reduced final adult height
Psychological wellbeing

399
Q

How do patients with Kallmann’s syndrome present?

A

Typical: boy with delayed puberty and anosmia(no smell)
Hypogonadism, cryptorchidism
Low sex hormone levels
LFF/FSH low/normal
Normal/above-average height
Cleft lip/palate and visual/hearing defects also seen in some patients

400
Q

Name some differentials for congenital adrenal hyperplasia

A

Adrenocortical tumour
PCOS
Hypothyroidism
Addison’s disease

401
Q

How is congenital adrenal hyperplasia investigated/diagnosed?

A

Bloods: 17-hydroxyprogesterone and ACTH elevated in CAH+ cortisol low
ACTH stimulation testing: gold standard
Genetic testing-to ID specific enzyme too
Imaging: USS to assess internal organs if ambiguous genitalia
Not currently routinely screened for

402
Q

Name some complications of congenital adrenal hyperplasia

A

Growth suppression(premature epiphyseal closure-> high concentration of sex steroids)
Metabolic syndrome(diabetes, obesity, htn)Infertility

403
Q

How is obesity defined in children?

A

BMI >98th centile for their age and sex
Overweight: >91st centile

404
Q

Name some causes of obesity in children

A

Growth hormone deficiency
Endocrine:
Hypothyroidism,
Cushing’s
Down’s
Genetics:
Prader-Willi
Medications: steroids

405
Q

Name some consequences of obesity in childhood

A

Orthopaedic problems: SUFE,, blount’s disease, MSK pain
Psychological consequences: poor self-steem, bullying
Sleep apnoea
Benign intracranial htn
Long term: Increased risk of T2DM, htn, ischaemic heart disease

406
Q

Name some risk factors for congenital hypothyroidism

A

Medication use during pregnancy-e.g. carbimazole
Maternal advanced age
Fhx of thyroid disease
Low birth weight
Pre-term birth
Multiple pregnancies

407
Q

Name some differentials for congenital hypothyroidism

A

Down’s syndrome
Congenital metabolic disorders

408
Q

How is congenital hypothyroidism diagnosed/investigated?

A

Newborn screening: TSH>20mU/L
Elevated TSH and decreased free T4
Imaging: Thyroid USS/radionuclide scan to ID thyroid dysgenesis
Hearing assessment

409
Q

Name some complications of congenital hypothyroidism

A

Irreversible intellectual disability
Sx of hyperthyroidism due to over-replacement of levothyroxine: wt loss, heat intolerance, tachycardia, diarrhoea, palpitations

410
Q

How is pica investigated/diagnosed?

A

FBC: check for anaemiaIron studies
Serum zinc levels
Lead level
Abdo x-ray: ingested foreign objects or GI obstruction
USS/CT if obstruction/perforation suspected
Psych evaluation

411
Q

Name some complications of pica

A

Nutritional deficiencies
GI complications: obstruction, perforation, intestinal parasites
Dental problems
Toxicity: lead poisoning etc
Infections

412
Q

Name a risk factor for eczema

A

Fhx of atopy(asthma, hayfever)

413
Q

How can eczema be classified?

A

Atopic eczema
Allergic contact dermatitis
Irritant contact dermatitis
Seborrheic dermatitis
Venous eczema
Asteatotic dermatitis
Erythrodermic eczema
Pompholyx eczema

414
Q

How is eczema diagnosed?

A

Usually clinical
Patch test: if allergic contact dermatitis
Swabs: if concerned about infection
Bloods: if concerned about infection-total IgE and raised eosiniphils

415
Q

How can eczema be classified in order of severity

A

Mild: areas of dry skin and infrequent itching
Moderate: dry skin, frequent itching and erythema
Severe: widespread, incessant itching and erythema
Infected: weeping, crusted, pustules, fever or malaise

416
Q

Name some complications of eczema

A

Scratching: poor sleep, poor mood, bacterial infection risk
Psycho-social: insecurities, avoid certain activities like swimming
Eczema herpeticum

417
Q

How is eczema herpeticum diagnosed?

A

Swab and Tzanck test

418
Q

How is eczema herpeticum treated?

A

IV aciclovir
Often given concomitantly with antibiotics as concomitant bacterial infection common and difficult to exclude clinically

419
Q

Name some causes of Stevens Johnson syndrome

A

Beta lactams: penicillins and cephalosporins
Sulphonamides
Lamotrigine, carbamazepine, phenytoin
Allpurinol
NSAIDs
OCP
Infectious: HSV, EBV, influenza, hepatitis

420
Q

Name some differentials for Steven-Johnson syndrome

A

Erythema multiforme
Drug rash with eosinophilia and systemic sx(DRESS)

421
Q

How is Steven-Johnson syndrome diagnosed?

A

Usually clinical
Skin biopsy->necrotic keratinocytes and a sparse lymphocytic infiltrate

422
Q

Name some differentials for allergic rhinitis

A

Sinusitis
Nasal polyps
Deviated nasal septum
Common cold

423
Q

How is allergic rhinitis diagnosed?

A

Clinical
Skin prick or blood tests for specific IgE antibodies to ID allergen

424
Q

Name some causes of rashes in children

A

Septicaemia
Slapped cheek
Hand foot and mouth
Measles
Urrticaria
Chickenpox
Roseola
Rubella

425
Q

Name some differentials for urticaria

A

Dermatitis
Drug eruptionsE
rythema multiforme
Vasculitis
AI disorders

426
Q

How is urticaria diagnosed/investigated?

A

Clinical-thorough history and exam
Allergy testing
Bloods: FBC, LFT, TFT, ESR, CRP: rule out underlying systemic diseases
Urinalysis if suspected vasculitis
Skin biopsy
Sx diaries: establish triggers and timings

427
Q

Name some complications of urticaria

A

Resp compromise in severe cases of angioedema involving upper airway
Psych distress and decreased QOL
SE’s from longterm meds

428
Q

Name some different kinds of birth marks

A

Salmon patches/stork-marks
Haemangiomas/strawberry marks
Port wine stains
Cafe-au-lait spots
Blue-grey spots
Congenital moles/naevi

429
Q

How can anaphylaxis be investigated/diagnosed?

A

Serum mast cell tryptase: peak 1 hr post anaphylaxis, remain high for 6 hours
Shouldn’t delay treatment

430
Q

Name some investigations used to iagnose/assess rheumatic fever

A

ECG-prolonged PR
Bloods: FBC, CRP, ESR, cultures
Proof of recent strep infection
CXR-heart failure
Echo-valvular abnormalities

431
Q

Name some complications of rheumatic fever

A

Mitral stenosis-isolated is mc
Mitral regurg
Mixed mitral stenosis and regurgitation
Aortic regurgitation
Aortic stenosis
Tricuspid regurg/stenosis

432
Q

Name some differentials for paediatric heart failure

A

Asthma
Pneumonia
GORD
Anaemia

433
Q

How can infective endocarditis be classified?

A

Acute: Up to 6 weeks
Subacute: 6 weeks-3 months
Chronic: >3 months

434
Q

Name some non-infective causes of infective endocarditis

A

Marantic endocarditis(malignany-pancreatic cancer)
Libman-Sacks endocarditis(SLE)

435
Q

Name some of the symptoms of infective endocarditis

A

Diverse and variable-can be rapid progression or chronically/non-specific
Fever-mc
Night sweats
Anorexia
Weight loss
Myalgia
Headache
Arthralgia
Abdo pain
Cough
Pleuritic pain

436
Q

Name some differentials for infective endocarditis

A

Non-infectious endocarditis
Rheumatic fever

437
Q

How is infective endocarditis diagnosed?

A

Modified Duke criteria
2 major OR one major and 3 minor OR all 5 minor

438
Q

How can you remember the Duke criteria?

A

BE FIVE PM
Major:
Blood cultures
Evidence of endocardial involvement on echo

Minor:
Fever
Immunological phenomena
Vascular phenomena
Echo
Predisposing features
Microbiological evidence

439
Q

Name some indications for surgery in patients with infective endocarditis

A

Haemodynamic instability
Severe heart failure
Severe sepsis
Valve obstruction
infected prosthetic valve
Persistent bactaraemia
Repeated emboli
Aortic root abscess-> PR prolongation on ECG

440
Q

Name some complications of infective endocarditis

A

Acute valvular insufficiency causing heart failure
Neurological sx: stroke, abscess, haemorrhage
Embolic complications-> infarctions of kidneys, spleen or lung
Inffections: osteomyelitis, septic arthritis

441
Q

How is congenital heart block diagnosed?

A

Prenatal scans: fetal bradycardia
ECG: complete dissociation between P waves(atrial contraction) and QRS complexes(ventricular contraction)

442
Q

Name some complications of congenital heart block

A

Fetal hydrops and intrauterine death
Heart failure

443
Q

Name some red flag features when considering a diagnosis of IBS

A

Rectal bleeding
Unexplained/unintentional weight loss
Fhx of bowel or ovarian cancer
Onset after 60 years

444
Q

Name some differentials for IBS

A

IBD
Coeliac
Colorectal cancer

445
Q

Name some parasitic causes of gastroenteritis

A

Cryptosporidium
Entamoeba histlytica
Giardia intestinalis
Schistosoma

446
Q

Name some differentials for gastroenteritis

A

Food poisoningIBS
IBD
Peptic ulcer disease
Bowel obstruction

447
Q

How is gastroenteritis diagnosed/investigates?

A

Clinical
BP
Stool cultures: if immunocompromied, recently travelled abroad, mucus/blood in stool
Urine dip for blood/protein: haemolytic uraemic syndrome
Bloods and blood cultures
Stool cultures if not improving after 7 days

448
Q

How is gastroenteritis caused by salmonella/shigella treated?

A

Ciprofloxacin

449
Q

How is gastroenteritis caused by campylobacter treated?

A

Macrolide like erythromycin

450
Q

How is gastroenteritis caused by cholera treated?

A

Tetracycline

451
Q

How should the spread of gastroenteritis be prevented?

A

Children off school until 48 hours after last episode of vomiting/diarrhoea
Shouldn’t swim in swimmin gpools for 2 weeks after

452
Q

Name some risk factors for developing dehydration in patients with gastroenteritis

A

<1yr
Low brith weight/malnutrition
24 hours: > 2 vomits or >5 diarrhoeal stoolsUnable to tolerate fluids

453
Q

Name some complications of gastroenteritis

A

Dehydration
Lactose intolerance following resolution of gastroenteritis episode
Haemolytic uraemic syndrome

454
Q

Name some risk factors for Crohn’s disease

A

Family history
Smoking : 3 times increased risk
Diets high in refined carbs and fats

455
Q

How is Crohn’s disease diagnosed?

A

Faecal calprotectin: raised
Colonoscopy with biopsy-diagnostic
Anaemia, raised ESR/CRP, thrombocytosis, haematinics and iron studies
Transmural inflammation seen on imaging(MRI)

456
Q

Name some complications of Crohn’s disease

A

Fistulas
Strictures
Abscesses
Malabsorption
Perforation
Nutritional deficiencies
Increased risk of colon cancer
Osteoporosis
Intestinal obstruction and toxic megacolon

457
Q

Name some differentials for Ulcerative colitis

A

Crohn’s
Infectious colitis
Ischaemic colitis

458
Q

How is Ulcerative colitis diagnosed/investigated?

A

Faecal calprotectin
Bloods: raised ESR/CRP, anaemia and raised WCC
Long standing UC: Lead pipe colon on abdo x ray
Colonosopy, barium energy and biopsy

459
Q

Name some indications for urgeent surgery in a patient with Ulcerative colitis

A

Acute fulminant UC
Toxic megacolon with little improvement after 48-72 hours
Sx worsening despite IV steroids

460
Q

Name some acute complications of Ulcerative colitis

A

Toxi megacolon
Massive lower GI haemorrhage

461
Q

Name some long-term complications of Ulcerative colitis

A

Colorectal cancer
Cholangiocarcinoma
Colonic strictures->large bowel obstruction

462
Q

Name 3 things gluten is found in

A

Wheat
Rye
Barley

463
Q

Name some risk factors for coeliac disease

A

Family history
HLA-DQ2 allele
Co-existing AI conditions

464
Q

Name some differentials for coeliac disease

A

IBS
IBD
Lactose intolerance

465
Q

How is coeliac disease diagnosed?

A

Anti TTG IgA antibody and total IgA levels, IgA EMA antibodies
GS: OGD with jejunal biopsy: subtotal villous atrophy

466
Q

Name osme complications of coeliac disease

A

Anaemia(iron, B12 or folate deficiency)
Hyposplenism
Osteoporosis
Enteropathy associated T cell lymphoma(EATL)

467
Q

How can undernutrition be classified?

A

Wasting-low weight for height
Stunting: low height for age
Underweight: low weight for age(can be due to stunting wasting or both)
Micronutrient-related malnutrition: iron, vitamin A or iodine

468
Q

Name some differentials for malnutrition in children

A

Specific genetics: Prader-Willi/Turner
Infectious diseases
Coeliac

469
Q

How might malnutrition be assessed in a child?

A

Accurate measurement of height and weight plotted on growth charts
Bloods to check for anaemia and specific deficiencies
Tests to check for specific organic causes

470
Q

Name some complications of malnutrition

A

More frequent/severe infections
Poor wound healing
Failure to thrive
Reduced muscle mass
Poor bone health-rickets/osteoporosis
Reduced cognition
Leading cause of mortality in children<5yrs globally

471
Q

How can FTT be classified?

A

Organic-medical illness
Non-organic: psycho-social

472
Q

Name some causes of organic FTT

A

GI: GERD, malabsorption like coeliac
Metabolic: thryoid disorders
Chronic: congenital heart disease, CF

473
Q

Name some differentials for FTTQ

A

UTI-common
Laryngomalacia
Pyloric stenosis
CF

474
Q

How should FTT be assessed/investigated?

A

Growth parameters-growht chart
Physical signs of malnutrition-muscle wasint, SC fat loss, brittle hair
Developmental assessment
Investigations for underlying dx: bloods, coeliac screen etc

475
Q

How do patients with Hirschsprung’s disease present?

A

Neonatal: failure/delayed passage of meconium, vomiting
Older children: tx resistant constipation, abdominal distention, poor weight gain

476
Q

How is Hirschsprung’s disease investigated/diagnosed?

A

Abdo x-ray
Rectal biopsy: gold standard

477
Q

Name some differentials for Meckel’s diverticulum

A

Gastroenteritis
Appendicitis
IBD
Intestinal obstruction

478
Q

How is Meckel’s diverticulum investigated/diagnosed?

A

Technetium-99m scan-ID ectopic gastric mucose(if stable)
CT can show intususseption
Ix should not delay tx-dx can be made operatively

479
Q

Name some features indication a Meckel’s diverticulum is high risk

A

Longer than 2cm or narrow neck/fibrotic tissue
Ectopic gastric tissue
Inflamed diverticulum

480
Q

Name some complications for Meckel’s diverticulum

A

Haemorrhage
Intussusception
Obstruction
Ulceration and perforation

481
Q

Describe the symtpoms of toddler’s diarrhoea

A

Stools vary in consistency
Often contain undigested food
>3 loose stools per day

482
Q

How can cow’s milk protein intolerance be classified?

A

Immediate:
IgE mediation: CMPA(allergy)
Delayed: non-IgE mediated(CMPI(intolerance)

483
Q

How is cow’s milk protein intolerance diagnosed/investigated?

A

Eliminate cow’s milk protein from diet for 2-6 weeks and reintroduce-monitor symptoms
Skin prick test
Specific IgE testing

484
Q

Name some differentials for cow’s milk protein intolerance

A

Lactose intolerance
GERD
Eosinophilic oesophagitis

485
Q

How is a choledochal cyst diagnosed?

A

Abdo USS scan-> dilated bile duct
MRCP/ERCP

486
Q

How is a choledochal cyst treated?

A

Surgical removal of cyst and gallbaldder
Liver biopsy at same time to check for damage

487
Q

Name some complications of a choledochal cyst

A

Liver fibrosis/cirrhosis
Cholangitis
Pancreatitis
Cancer of bile ducts

488
Q

Name some complications of neonatal hepatitis

A

If untreated for >6 months risk of chronic liver disease->hepatic cirrhosis-> liver failure

489
Q

How is neonatal hepatitis investigated/diagnosed?

A

USS: check bile ducts for obstruction and correct development
Liver biopsy: multinucelated giant cells
Bloods: high serum bilirubin

490
Q

How can hernias be classified?

A

Location of hernia
Status of bowel

491
Q

Describe the types of hernias when classed by location

A

Umbilical
Epigastric
Inguinal

492
Q

Name some risk factors for hernias in children

A

Low birth weight and prematurity
Family history
Being male-especially inguinal hernias
Connective tissue disorders

493
Q

How are strangulated hernias investigated/diagnosed?

A

Clinically when reducible
USS typically first line-rule out causes of acute abdomen
CT for signs of ischaemia
Bloods for signs of infection

494
Q

Name some complications of a hernia

A

Recurrence of hernia
Stranguled-> bowel ischaemia, necrosis , perforation and sepsis

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