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MBChB Final Exam Essentials > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Outline the neonatal life support process

A
  1. If pink, give back to mother
  2. If not, rub vigorously
  3. If unsuccessful, start bag and mask ventilation (e.g. Neopuff at 6mmHg)
  4. If not pinking up, add oxygen
  5. Give IV adrenaline 0.3ml 1:1000; followed by 1ml and then an infusion 20ml/kg 0.9% saline
  6. Check glucose
  7. If meconium, suction and wash out oropharynx
  8. Consider endotracheal intubation
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2
Q

What is the scoring system used to assess the progress of life support in the neonate?

A

Apgar Score (monitors vital signs inc. pulse, respirations, tone and colour)

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3
Q

Outline the ABCE approach of neonatal intensive care

A

Airway
Breathing
Circulation
Epithelium (lung/gas exchange, barrier functions of the gut and skin for digestion, keeping out bacteria, intact neuroepithelium lining ventricles and retina)

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4
Q

What common vital signs are monitored in neonatology intensive care?

A

Temperature, BP, pulse, respiration, blood gases, pulse oximetry, U/Es, FBC, weight etc.

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5
Q

List some common problems facing babies on the NICU?

A 
Hypothermia
Hypoxia
Hypoglycaemia
Respiratory Distress Syndrome 
Infection
Intraventricular haemorrhage
Apnoea 
Retinopathy of prematurity 
Necrotising enterocolitis
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6
Q

What is the pathophysiology of intraventricular haemorrhage in preterms?

A

Preterms are at particular risk due to:

1 Unsupported blood vessels in the subependymal germinal matrix
2. Unsupported blood pressure

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7
Q

What are the signs associated with intraventricular haemorrhage?

A

Seizures, bulging fontanelle, cerebral irritability, cerebral palsy.

Many are asymptomatic

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8
Q

What is neonatal apnoea?

A

Neonatal apnoeas are episodes when an infant fails to make any respiratory effort.

They are defined as:

1 .No respiratory efforts for a period of more than 20 sec

  1. A break in respiration of less than 20 sec but associated with bradycardia
  2. Reduction in heart rate of more than 30%
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9
Q

What are some common causes of neonatal apnoea?

A 
Prematurity
Infection
Hypothermia
Aspiration
Congenital heart disease
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10
Q

What is necrotising enterocolitis?

A

Medical condition where a portion of the bowel dies.

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11
Q

What are the signs of necrotising enterocolitis?

A

Poor feeding, bloating, decreased activity, blood in the stool, or vomiting of bile

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12
Q

What is the mortality rate associated with necrotising enterocolitis?

A

25%

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13
Q

What is retinopathy of prematurity?

A

Fibrovascular proliferation of retinal vessels leading to retinal detachment/impaired vision

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14
Q

What are the non-invasive techniques for neonatal ventilation?

(3)

A

CPAP

NIPPV (nasal intermittent positive pressure ventilation)

HFNC

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15
Q

What are the invasive techniques for neonatal ventilation?

3

A

Timed-cycled pressure limited ventilation

Patient-triggered ventilation

High-frequency ventilation

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16
Q

List some complications of long-term ventilation in neonates

A

Lung (pneumothorax, pulmonary haemorrhage, pneumonia)

Airways (upper airway obstruction)

Others (patent-ductus arteriosus, pneumomediastinum

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17
Q

How does neonatal sepsis present?

A

Non-specific and subtle signs

Labile temperature, lethargy, poor feeding, respiratory distress, collapse, DIC

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18
Q

How is neonatal sepsis managed?

A 
ABC approach 
Supportive (ventilation, volume expansion, ionotropes) 
Bloods (FBC, CRP, glucose, cultures) 
CXR
Lumbar puncture

Failure to respond within 24hrs - consider stool samples for virology, throat swab, urine CMV culture

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19
Q

What empirical antibiotics are given in the case of early-onset neonatal sepsis?

What antibiotics would you consider if meningitis or listeria are suspected?

A

Benzylpenicillin and gentamicin

If meningitis is suspected - give ceftriaxone
If listeria suspected (purulent conjunctivitis, maternal infection) - give amoxicillin/ampicillin

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20
Q

What empirical antibiotics are given in the case of late-onset neonatal sepsis?

A

Flucloxacillin and gentamicin

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21
Q

What organism causing late-onset neonatal sepsis associated with central venous catheters in place? How would you treat it?

A

Coagulase-negative Staph.

Vancomycin and discuss removing the catheter

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22
Q

What other type of organism may you consider if treatment with antibiotics fails in the case of late-onset neonatal sepsis?

A

Fungal sepsis

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23
Q

What are the definition of early and late-onset neonatal sepsis?

A

Early ( <3 days)

Late ( >3 days?

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24
Q

List some causes of neonatal seizure

A

Hypoxic-ischaemic encephalopathy (due to antenatal or intrapartum hypoxia)
Infection (meningitis/encephalitis)
Intracranial haemorrhage
Metabolic disorder/disturbance (e.g. hypoglycaemia, hypocalcaemia etc.)
Kernicterus

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25
Q

How are neonatal seizures medically aborted?

A

First line: Phenobarbital
Second line: Phenytoin
Third line: Midazolam et al.

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26
Q

How are neonatal seizures investigated and managed?

A

Rule out reversible causes
Start empirical antibiotics
IV access (FBC, U/Es, LFTs, calcium, glucose, magnesium, blood gases)
Commence cerebral function analysis monitoring
Radiological imaging (CT, MRI cranial US)
Treat prolonged seizures

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27
Q

What is hypoxic-ischaemic encephalopathy?

A

Clinical syndrome of brain injury secondary to hypoxic-ischaemic insult.

Causes could be antepartum (abruption), intrapartum (cord prolapse) or postpartum

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28
Q

What are the signs of hypoxic-ischaemic encephalopathy at birth?

A

Respiratory depression

pH <7 and base excess worse than -12

Encephalopathy develops within 24hrs

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29
Q

How is hypoxic-ischaemic encephalopathy treated?

A

Resuscitation, avoidance of hypothermia, treat seizures and therapeutic hypothermia to reduce death and disability

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30
Q

What is neonatal shock?

A

Shock is an acute state in which circulatory function is inadequate to supply sufficient amounts of O2 and other nutrients to tissues to meet metabolic demands

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31
Q

What are the common causes of neonatal shock?

A

Blood loss (placental haemorrhage, TTTS, lung haemorrhage)

Capillary plasma leaks (sepsis, hypoxia, acidosis)

Fluid loss (diuresis)

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32
Q

What are the signs of neonatal shock?

A

High HR
Low BP
Decreased urine output
Coma

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33
Q

How is neonatal shock managed?

A

ABC
Give colloid 10-20ml/kg IV as needed
Ionotropes e.g. dopamine +/- dobutamine

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34
Q

How common is neonatal jaundice?

A

Very common

60%

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35
Q

Hyperbilirubinaemia (<200micromol/L) after 24hrs is usually described as _________. Meaning benign.

A

Physiological

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36
Q

What are the causes of physiological jaundice in the neonate?

A
  1. Increased bilirubin production
  2. Decreased bilirubin conjugation
  3. Absence of gut flora impedes bilirubin elimination
  4. Breastfeeding
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37
Q

List some causes of visible jaundice within 24hrs of birth

A

Sepsis
Rhesus haemolytic disease
ABO incompatibility
Red cell anomalies (e.g. congenital spherocytosis or G6PD deficiency)

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38
Q

List some causes of common causes of prolonged jaundice?

A 
Breastfeeding
Sepsis 
Hypothyroidism 
Cystic fibrosis 
Biliary atresia
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39
Q

How is prolonged bilirubin treated?

A

Phototherapy

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40
Q

What is kernicterus?

A

Clinical features of acute bilirubin encephalopathy

Symptoms; lethargy, poor feeding, hypertonicity

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41
Q

What are some long term sequelae of kernicterus?

A

Athetoid movements, deafness and decreased IQ

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42
Q

What is Rhesus Haemolytic Disease?

A

When a Rh- mother delvers a Rh+ baby. Leaking of foetal blood into maternal circulation leading to isoimmunisation.

There is a wide clinical spectrum.

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43
Q

Sensitising events in pregnancy include what?

6

A 
Threatened miscarriage
APH
Mild trauma
Amniocentesis 
Chorionic villous sampling 
External cephalic version
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44
Q

What is hydrops fetalis?

A

A severely effected foetus from Rhesus haemolytic disease causing oedema (wit stiff, oedematous lungs.

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45
Q

How is hydrops fetalis managed?

7

A 
Get specialist involved
Correct glucose 
Drain ascites
Correct anaemia 
VIt K correction
Treat heart failure 
Limit IV fluids
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46
Q

What is biliary atresia?

A

Biliary tree occlusion due to congenital angiopathy leading to destruction of extra-hepatic bile ducts

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47
Q

How does biliary atresia present?

A

Jaundiced
Yellow urine
Pale stools
Hepatosplenomegaly

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48
Q

How is biliary atresia treated?

A

Kasai procedure (hepatoportoenterostomy)

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49
Q

What is respiratory distress syndrome?

A

Condition caused by surfactant deficiency leading to atelectasis and respiratory failure

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50
Q

What are the risk factors for developing RDS?

A

Commoner in maternal diabetes, males, 2nd twins and Caesarian sections

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51
Q

What are the signs of RDS?

A 
Increased work of breathing shortly after brith 
Tachypnoea 
Grunting 
Nasal flaring 
Intercostal recession
Cyanosis
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52
Q

How does RDS appear on a Chest X-Ray?

A

Diffuse granular patterns

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53
Q

Give three differentials of RDS

A

Transient tachypnoea of the newborn (resolves pithing 24hrs)
Meconium aspirate
Congenital pneumonia

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54
Q

How is RDS prevented in the antepartum period?

A

Steroid injections given to all women at risk of preterm labour

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55
Q

How is RDS treated?

A

Delay of cord clamping (to promote placenta-foetal transfusion
Give an oxygen/air blend (21%)
Prophylactic surfactant

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56
Q

What is bronchopulmonary dysplasia?

A

A complication of ventilation in RDS causing persistent hypoxia and difficulty weaning off.

Due to barotrauma and oxygen toxicity

Prevented by both antenatal and post-natal steroids, surfactant and high-calorie feeding

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57
Q

What is pulmonary hypoplasia?

A

Suspect in all infants with persisting neonatal tachypnoea, difficulties feeding (particularly if a history of prenatal oligohydramnios)

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58
Q

Describe the appearance of bronchopulmonary dysplasia on a Chest X-Ray.

A

Hyperinflation, rounded radiolucent areas, alternating with thin denser lines

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59
Q

What is meconium aspiration syndrome?

A

Foetal distress in the infant born through meconium-stained amniotic fluid leading to airway obstruction, surfactant dysfunction and pulmonary vasoconstriction.

Treated with surfactant, ventilation, inhaled nitric oxide and antibiotics

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60
Q

What is haemorrhagic disease of the newborn?

A

Occurs 2-7 days postpartum due to a lack of enteric bacteria used to make vitamin K.

Characterised by widespread bleeding and bruising with increased PT and APTT.

Prevention with postpartum 1mg Fit K injection IM

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61
Q

What is DIC? How is it characterised, diagnosed and treated?

A

Disseminated intravascular coagulation (due to NEC or sepsis etc.)

Characterised by petechiae, venipuncture oozing, GI bleeding

Diagnosed by decreased platelets and the presence of schistocytes (fragmented red cells)

Treat the underlying cause, platelet transfusion, cryoprecipitate

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62
Q

What is autoimmune thrombocytopenia?

A

Congenital autoimmune destruction of platelets.

Treated with compatible platelets or irradiated maternal platelets

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63
Q

What are strawberry naevi?

A

Benign vascular malformations develop over few months and then regress. Treat with propranolol if in sensitive area or large

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64
Q

What are milia?

A

1-2mm pearly white/cream papules caused by retention of keratin in the dermis found on forehead, nose, cheeks

Resolve spontaneously

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65
Q

What is erythema toxicum (neonatal urticaria)?

A

Harmless red blotches with central white pustules which come and go in crops. They last approx. 24hrs

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66
Q

What is miliaria crystallina?

A

Prickly heat-like rash develops due to transient sweat-pore disruption

Called milia rubra is there is surrounding flush

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67
Q

What is a stork mark?

A

Capillary dilation of the eyelid, forehead and back of neck.

Blanching and fade over time

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68
Q

What are the signs of suffusion of the face following delivery?

A

Petechial haemorrhage
Facial cyanosis
Subconjunctival haemorrhage

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69
Q

Outline the cause of swollen breasts in the neonate

A

Due to exposure to maternal hormones in utero

May become infected and treated with antibiotics

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70
Q

Outline the process of separation of the umbilicus

A

Dries and separates through a moist base around day seven after delivery.

Can become infected (signs of odour, pus, malaise, erythema)

Rule out patent urachus if failure to close

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71
Q

Outline the causes of a sticky eye in the neonate?

A

Commonly due to blocked tear duct

Swab for ophthalmia neonatourm/chlamydia/gonorrhoea

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72
Q

Outline the causes of a red-stained nappy

A

Usually due to urinary urates but may also be due to blood from the cord or vagina

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73
Q

What is harlequin colour change?

A

Transient and episodic erythema left or right of the midline and contralateral blanching. Self-limiting condition.

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74
Q

List endogenous causes of eczema

A 
Atopic
Seborrhoeic 
Discoid
Pomphylx
Varicose
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75
Q

What is atopic dermatitis?

A

Genetic barrier dysfunction linked to other atopic conditions (asthma, hayfever etc.)

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76
Q

Outline the presentation of atopic eczema in both infants and older children

A

Infants - starts on face/neck and spreads more generally

Older children - flexural pattern predomiantes

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77
Q

What is seborrhoeic eczema?

A

Scaling irritation of the skin. Associated with proliferation of commensal malassezia (yeast)

Often occurring in babies under 3 months and resolving within a year

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78
Q

What is discoid eczema?

A

Scattered annular patchy of itchy eczema

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79
Q

What is pomphylx eczema?

A

Vasicles affecting palms and soles. Intensely itchy

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80
Q

What is varicose eczema?

A

Irritation of the skin associated with oedema and venous insufficiency.

May be complicated by ulceration

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81
Q

List exogenous causes of eczema

A

Allergic contact dermatitis
Irritant contact dermatitis
Photosensitive/photoaggressive dermatitis

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82
Q

Outline the presentation of allergic dermatitis

A

Immediate reaction with severe itching and unresponsive to treatment.

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83
Q

How is allergic dermatitis diagnosed?

A

Blood test - IgE specific to certain common allergens and skin prick testing

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84
Q

Flares of all types of eczema can be associated with what occurances?

A 
Infections
Environment (hot or cold air) 
Pets: if sensitised/allergic
Teething
Stress
Sometimes no cause found
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85
Q

How is eczema managed?

A 
Emollients (lotions, creams or ointments) 
Topical steroids
Calcinurin inhibitors 
UVB therapy
Immunosuppressive medication
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86
Q

Outline the varying strengths of topical steroid creams

A

Mild - hydrocortisone
Moderate - eumovate (25x)
Potent - betnovate (100x)
Very potent (derogate (600x)

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87
Q

What is impetigo?

A

Common acute bacterial skin infection caused by Staph aureus.

Characterised by gold-crusted pustules

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88
Q

How is impetigo managed?

A

Topical antibacterial -fucidin

Oral antibiotic - flucloxacillin

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89
Q

What is molluscum contagiosum?

A

Common benign and self-limiting viral infection fo the molluscipox variety

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90
Q

How is molluscum contagiosum transmitted?

A

Close direct contacts

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91
Q

What si the incubation time of molluscum contagiosum?

A

2 weeks to 6 months

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92
Q

How long can it take for a bout of molluscum contagiosum to clear?

A

Up to 2 years

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93
Q

Describe the molluscum contagiosum lesions

A

Pearly papule with an umbilicated centre

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94
Q

How is molluscum contagiosum treated?

A

Topical 5% potassium hydroxide

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95
Q

What are viral warts?

A

Common, non-cancerous growths of the skin caused by infection with HPV (transmitted by direct contact)

Treated: cryotherapy, topical paint (salicylic acid)

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96
Q

What are viral exanthems?

A

Skin manifestations of viral illnesses(either a reaction to a toxin, damage to the skin or an immune response)

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97
Q

Give some examples of viral exanthems

A 
Chickenpox (varicella-zoster virus) 
Measles (Rubeola virus)
Rubella
Roseola (HSV6)
Erythema infectiosum (provirus B19)
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98
Q

What is the colloquial name of erythema infectiosum?

A

Slapped cheek

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99
Q

What are the features of erythema infectiosum?

A

Erythematous rash on face and lace network rash on trunk/limbs

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100
Q

What rare complications are associated with erythema infectiosum?

A

Aplastic crisis

Risk in pregnancy (spontaneous miscarriage, IUD, hydros fetalis)

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101
Q

Describe the presentation of primary VZV infection?

A

Red papules progressing to vesicles often on the trunk which is intensely itchy and can be accompanied by viral symptoms

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102
Q

What causes hand, foot and mouth disease?

A

Enterovirus (often Coxackie A16)

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103
Q

Outline the presentation of Coxsackie A16 infection?

A

BListers on hand, feet and in the mouth (epidemics in the autumn and summer months)

Self-limiting

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104
Q

What is orofacial granulomatosis?

A

Lip swelling and fissuring with oral mucosal ulcers and tags (cobblestone appearance) often seen in Crohn’s disease

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105
Q

What is erythema nodosum?

A

Skin inflammation that is located in a part of the fatty layer of skin

Resulting in reddish, painful, tender lumps most commonly on the legs below the knees

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106
Q

List some causes of erythema nodosum?

A 
Infections strep. URTI 
IBD
Sarcoidosis 
Drugs (OCP, penicillin)
Idiopathic
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107
Q

What is dermatitis herpetiformis?

A

Rare but persistent immunobullous disease that has been linked to coeliac disease causing itchy blisters in clusters (often symmetrical) on the scalp, shoulders, buttocks, elbows and knees

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108
Q

What is urticaria?

A

Also called hives/wheels

Associated with angioedema with rash lasting from a few minutes up to 24hrs

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109
Q

What are the two types of urticaria?

A

Acute (<6wks)and Chronic (>6wks)

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110
Q

List some causes of urticaria

A

Viral infection
Bacterial infection
Fod/drug allergy
NSAIDs, opiates

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111
Q

How is urticaria treated?

A

Consider triggers and avoid

Antihistamines (desloratadine 1tds)

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112
Q

What common lesions comprise congenital heart disease?

A 
Septal defects (ventricular and atrial)
Patent ductus ateriosus 
Stenosis (pulmonary and aortic) 
Coarctation of the aorta 
Transposition of the Great Arteries 
Tetralogy of Fallot
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113
Q

Congenital heart disease accounts for what percentage congenital conditions?

A

30%

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114
Q

What environmental hazards are associated with congenital heart disease?

A

Drugs (alcohol, amphetamines, cocaine, ecstasy, phenytoin, lithium)

Infections (TORCH and others)

Maternal (DM, SLE)

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115
Q

What chromosomal abnormalities are associated with congenital heart disease?

A

Downs Syndrome (Trisomy 21) 40% AVSD

Edwards Syndrome (Trisomy 18) 80% VSD and PDA

Patau Syndrome (Trisomy 13) 90% VSD and ASD

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116
Q

What congenital heart conditions are associated with the following genetic conditions:

  1. Turner syndrome
  2. Noonan syndrome
  3. Williams syndrome
  4. DiGeorge (22q11 deletion) syndrome
A
  1. Coarctation of the aorta
  2. Pulmonary stenosis
  3. Supravalvular AS
  4. Interrupted aortic arch, truncus arteriosus and tetralogy of Fallot
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117
Q

How is congenital heart disease treated?

A

Surgical correction (fix it)

Medication to improve situation

Palliative procedures e.g. BT shunt, balloon valvo-plasty, prostaglandin infusion, pulmonary banding

Transplantation surgery

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118
Q

How are murmurs characterised?

A

Timing (systolic/diastolic/continuous)

Duration (early/mid/late or ejection/pan-systolic)

Pitch/quality (harsh/soft/vibrstory/pure frequency)

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119
Q

List the four types of innocent murmurs?

A

Stills Murmur (LV outflow murmur)
Pulmonary Outflow Murmur
Venous Hum
Carotid/Brachiocephalic Arterial Bruit

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120
Q

What age does Still’s murmur commonly present?

A

Aged 2-7

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121
Q

Describe the character of Still’s murmur?

A

Soft, systolic; vibratory musical and twangy

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122
Q

Where is Still’s murmur most clearly heard?

A

Apex, left sternal border.

Increases in the supine position and with exercise

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123
Q

What age does a pulmonary outflow murmur commonly present?

A

Age 8-10

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124
Q

Describe the character of a pulmonary outflow murmur

A

Soft systolic; vibratory

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125
Q

Where is pulmonary outflow murmur most clearly heard?

A

Upper left sternal border, well localised and not radiating to the back

Increases in the supine position and with exercise

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126
Q

At what age is a venous hum most likely to develop?

A

Age 3-8

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127
Q

Describe the character of a venous hum

A

Soft and indistinct continuous murmur with diastolic accentuation

128
Q

Where is a venous hum most clearly heard?

A

Supraclavicular and only in the upright position

129
Q

Describe the character and age of onset of a carotid/brachiocephalic arterial bruit

A

Systolic murmur heard in the supraclavicular regions with neck radiation

Decreases on turning the head or extending the neck

Most likely to arise between ages 2-10yrs

130
Q

What are the three main types of ventricular septal defects?

A

Subaortic, perimembranous and muscular

131
Q

How do ventricular septal defects present?

A

Pansystolic murmurs at the lower left sternal edge (sometimes with a thrill)

132
Q

What is Eisenmenger Syndrome?

A

Eisenmenger syndrome refers to any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis

133
Q

How is VSD treated?

A

VSD closure surgery with either:

Amplatzer device or a patch closure

134
Q

How do atrial septal defects present in childhood and in adulthood?

A

Childhood (early on, often incidental finding)

Adulthood (AF, HF, pulmonary hypertension)

135
Q

What does an atrial septal defect sound like on auscultation?

A

Wide fixed splitting of 2nd heart sound with pulmonary outflow murmur.

136
Q

How does pulmonary stenosis present?

A

Asymptomatic in mild stenosis

Moderate/severe - exertion dyspnoea and fatigue

137
Q

What does pulmonary stenosis sound like?

A

Ejection systolic murmur in the upper left sternal border with radiation to the back

138
Q

How is pulmonary stenosis treated?

A

Balloon valvoplasty

139
Q

How does aortic stenosis present?

A

Ejection systolic murmur on the upper right border of the sternum with neck radiation

Often asymptomatic. If severe, reduced exercise tolerance, exertion chest pain and syncope

140
Q

What changes occur to foetal blood circulation at birth?

5

A 
Pulmonary vascular resistance decreases
Systemic vascular resistance increases 
Ductus arteriosus closes 
Foramen vale closes
Ductus venosus closes
141
Q

What type of infants has a higher likelihood of patent ductus arteriosus?

A

Preterm infants

142
Q

How is patent ductus arteriosus treated?

A 
Fluid-restriction / diuretics 
Prostaglandin inhibitors (indomethacin)
Surgical ligation
143
Q

What is transposition of the great arteries/

A

Congenital condition where the aorta arises from the right ventricle and and the pulmonary artery arises from the left.

144
Q

How is transposition of the great arteries treated?

A

Switch procedure

145
Q

What is the tetralogy of Fallot?

Remember PROV

A

A congenital defect characterised by:

Patent ductus arterosus
Right ventricular hypertrophy
Overriding aorta
Ventricular septal defect

146
Q

What are the two indications for enteral feeding/

A

Poor oral intake (e.g. disorder of swallow/suck, prematurity, neurological impairment etc.)

Disorder of digestion and absorption (e.g. cystic fibrosis, short bowel syndrome etc.)

147
Q

What factors need to be considered before initiating enteral feeding?

A 
Quality of life
Psychological factors
Ethics and prognosis
Information and consent
Clinical status
148
Q

List some methods of enteral feeding?

A

PEG tubes (with or without jejunum extension)
NG tube
NJ tube

149
Q

Outline some complications of enteral tubes

A

Infection of stoma site

Over-granulation of stoma site

Buried bumper (he internal bumper of the PEG tube erodes into the gastric wall and lodges itself between the gastric wall and skin)

Tube dislodgement

150
Q

Outline the components of LFTs

A 
Bilirubin
ALT/AST
Alkaline phosphatase 
GGT
Functional tests (coagulation, albumin, blood glucose, ammonia)
151
Q

Outline the types of bilirubin tested in LFTs

A

Total (both conjugated and unconjugated)

Split - direct (conjugated) and indirect (unconjugated)

152
Q

Raised AST/ALT indicates what?

A

Hepatocellular damage (hepatitis)

153
Q

What variables indicated biliary status?

A

Alkaline phosphatase and GGT

154
Q

What are the coagulation tests?

A

Prothrombin time

Activated thromboplastin time

155
Q

What is jaundice?

A

Yellow discolouration of the skin and tissues due to accumulation of bilirubin (visible when total bilirubin is >40-50umol/L)

156
Q

What enzyme is responsible for conjugation of bilirubin?

A

Glucuronic acid glucuronyl transferase

157
Q

What are the three types of jaundice?

A

Pre-hepatic (mostly unconjugated)
Intrahepatic (mixed)
Post-hepatic (mostly conjugated)

158
Q

Jaundice in infants is diagnosed based on the age of the infant. Outline different causes of early, intermediate and prolonged jaundice.

A

Early (<24hrs) - always pathological. Causes include haemolysis and sepsis

Intermediate (24hrs-2wks) - physiological, breast milk, sepsis, haemolysis

Prolonged (>2weks) - extra-hepatic obstruction, neonatal hepatitis, hypothyroidism

159
Q

List two disorders of abnormal conjugation

A

Gilbert’s disease - mild and common

Crigler-Najjar syndrome - rare and severe

160
Q

Why is unconjugated bilirubin potentially dangerous?

A

Unconjugated bilirubin is fat-soluble therefore crosses the blood-brain barrier and deposits in the brain causing kernicterus

161
Q

What are the most common causes of biliary obstruction in infancy?

A

Biliary atresia
Choledochal cyst
Alagille syndrome

162
Q

What is Alagille syndrome?

A

Congenital disorder characterised by intrahepatic cholestasis, dysmorphism and congenital heart disease.

163
Q

List some causes of neonatal hepatitis

7

A 
Alpha-1-antitrypsin disease 
Galactosaemia 
Tyrosinaemia 
Urea cycle defects
Hypothyroidism 
Viral hepatitis 
Parenteral nutrition
164
Q

List some features of chronic liver disease

8

A 
Jaundice 
Epistaxis
Bruising and petechiae
Ascites
Hypotonia
Hepatorenal failure
Peripheral neuropathy
Failure to thrive (malnutrition)
165
Q

Define:

Neonate
Infant
Toddler
Pre-school

A

Neonate <4wks
Infant <1yr
Toddler 1-2yr
Pre-school 2-5yrs

166
Q

Why is breast milk better than formula?

A 
Well tolerated 
Less allergenic 
Low renal solute load
Improves cognitive development 
Reduces infection (macrophages, lymphocytes, lysozymes etc.)
167
Q

What are the different types of specialised formula?

A

For Cows Milk Protein Allergy (either extensively hydrolysed or amino acid-based)

Nutrition dense

Disease-specific (lactose-free, soya milk, calories and calcium)

168
Q

What areas of the brain are associated with wiht nausea and vomiting?

(5)

A

Cerebellum, vomiting centre, tractus solitarius, area postrema and CTZ

169
Q

Outline the four types of vomiting

A

Vomiting with retching
Projectile vomiting
Bilious vomiting
Effortless vomiting

170
Q

Bilius vomiting should always ring alarm bells. What assumption is made about the cause of bilious vomiting until proven otherwise?

A

Due to intestinal obstruction until proven otherwise

171
Q

List some causes of bilious vomiting

A 
Intestinal atresia (newborns)
Malrotation +/- volvulus 
Intersussception 
Ileus 
Crohn's disease with strictures
172
Q

What is volvulus? How does it present?

A

When a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction. Symptoms include abdominal pain, abdominal bloating, vomiting, constipation, and bloody stool.

173
Q

What is intussusception? How does it present?

A

A condition in which one segment of intestine “telescopes” inside of another, causing an intestinal obstruction (blockage).

Usually occuring at the junction of the small and large intestines

Stool mixed with blood and mucus stool
Vomiting, abdominal lump, lethargy, diarrhoea, fever

174
Q

What investigations may help diagnose the cause of bilious vomiting?

A

Abdominal X-Ray (Consider contrast meal)
Surgical laparotomy
Abdominal US

175
Q

What is pyloric stenosis? How does it present?

A

Narrowing of the opening from the stomach to the small intestine (the pylorus).
Symptoms include projectile vomiting without the presence of bile. This most often occurs after the baby is fed.

176
Q

What ultrasound finding can diagnose intussusception?

A

Target sign

177
Q

What characteristic electrolyte imbalance is associated with pyloric stenosis?

A

Metabolic alkalosis
Hypochloriaemia
Hypokalaemia

178
Q

At what age does pyloric stenosis generally become symptomatic?

A

Babies aged 4-12 weeks

179
Q

How does pyloric stenosis typically present?

A

Weight loss
Projectile, non-bilious vomitus
Dehydration and shock

180
Q

How is pyloric stenosis treated?

A

Fluid resuscitation and Ramstedts pyloromyotomy

181
Q

What is gastro-oesophageal reflux disorder?

A

Movement of gastric contents into the oesophagus

182
Q

How can GORD present?

A

GI (vomiting, haematemesis)
Nutritional (feeding problems/failure to thrive)
Respiratory (apnoea, cough, wheeze, chest infections)
Neurological (Sandifer’s syndrome)

183
Q

What is Sandifer’s syndrome?

A

Paroxysmal dystonic movement disorder occurring in association with gastro-oesophageal reflux, and, in some cases, hiatal hernia.

184
Q

How is GORD investigated?

A

pH manography
Upper GI endoscopy
Barium swallow

185
Q

How is GORD treated?

A 
Feed thickeners
Adjust feeding position 
Exclusion diet (milk free)
Nutritional support
Prokinetic drugs 
Acid suppression drugs
186
Q

In severe and refractory GORD, what management option is available?

A

Nissen fundoplication

187
Q

What is the definition of chronic diarrhoea?

A

Four or more stools per day for more than four weeks

188
Q

What is the definition of acute diarrhoea?

A

More than four stools per day for less than one week

189
Q

What are some potential causes of chronic diarrhoea?

A

Motility disturbance (toddler diarrhoea, IBS)

Active secretion (acute infective, IBD)

Malabsorption (food allergy, coeliac disease, cystic fibrosis)

190
Q

What are the four types of diarrhoea?

A

Osmotic
Secretory
Motility
Inflammatory

191
Q

What is the mechanism of motility diarrhoea?

A

Movement of water into the bowel to equilibrate osmotic gradient

192
Q

What is the mechanism of secretory diarrhoea?

A

Intestinal fluid secretion driven by chloride secretion via CFTR transporter

193
Q

What is the mechanism of inflammatory diarrhoea?

A

Malabsorption due to intestinal damage and protein exudate across epithelium

194
Q

What is coeliac disease?

A

Intolerance to gliadin (component of gluten)

195
Q

How does coeliac disease present?

A

Abdominal belatedness, diarrhoea, failure to thrive, constipation, dermatitis herpetiformis

196
Q

What groups of people are more susceptible to coeliac disease?

A

T1DM
Autoimmune thyroid disease
Down’s Syndrome
Family history of coeliac

197
Q

How is coeliac disease tested for?

A

Serological (anti-tissue transglutaminase, anti-endomysial, IgA deficiency)

Duodenal biopsy (villous atrophy)

Genetic testing (HLA, DQ2, DQ8)

198
Q

How is coeliac disease treated?

A

Strict control of diet to avoid gluten

199
Q

What causes constipation?

A 
Poor diet (insufficient fluids or fibre, excessive milk)
Intercurrent illness
Medication (opiates, ondansetron)
FHx
Psychological 
Organic
200
Q

How is constipation treated?

A

Social (explain to parents, improve diet)
Psychological (reduce adverse factors, avoid punitive behaviour, reward good behaviour)
Soften stool

201
Q

Outline the different types of laxatives and their action

A

Osmotic laxatives - lactulose
Stimulant laxatives - senna and pico lax
Isotonic laxatives - movicol

202
Q

What are some telltale signs of constipation in the history?

A 
Poor appetite
irritable 
Lack of energy 
Abdominal pain or distention
Withholding or straining
203
Q

What are the classical symptoms of IBD?

A 
Diarrhoea 
Rectal bleeding
Abdominal pain
Fever
Weight loss
Growth failure
Arthritis
204
Q

What features are predominantly seen in Crohn’s disease?

A

Weight loss

Growth failure

205
Q

What features are predominantly seen in ulcerative colitis?

A

Diarrhoea

Rectal bleeding

206
Q

What aspects of the history are important in the case of IBD?

A 
Intestinal symptoms
Extra-intestinal manifestations
Exclude infection
Family history
Growth and sexual development
Nutritional status
207
Q

What laboratory investigations are important in the diagnosis of IBD?

A

FBC (anaemia, thrombocytosis, raised ESR)

Biochemistry (stool calprotectin, raised CRP, low albumin)

Microbiology (no pathogens)

208
Q

What are the definitive investigations for the diagnosis of IBD?

A

Radiology (MRI, barium meal and follow-through)

Endoscopy (colonoscopy, upper GI endoscopy, mucosal biopsy, capsule endoscopy, enteroscopy)

209
Q

How is IBD treated?

A 
Anti-inflammatories
Immune-suppressive
Biologics
Immunomodulation
Supplementation 
Surgical intervention
210
Q

What features of a history might ring alarm bells with regards to child protection?

A

Late presentation
History changes on repeating
History inconsistent with findings

211
Q

What is the commonest cause of death due to physical abuse?

A

Abrasive head trauma

212
Q

What is the mortality and morbidity associated with abrasive head trauma due to abuse?

A

30%

Half have a residual disability, retinal haemorrhages, neck and cervical spine injury

213
Q

Outline the categories of neglect

A 
Emotional 
Abandonment 
Medical
Nutritional
Educational
Physical 
Failure to provide supervision
214
Q

What is a paediatric fabricated illness?

A

Rare form of child abuse where the guardian/parent induces illness in their child

215
Q

What are the measurements of normal growth/pubertal development?

A

Length (infants)

Height (standing/sitting)

Head circumference (routine in children <2yrs)

Target height and mid-parental height

Bone age (high-quality radiograph)

Growth velocity

Weight

216
Q

How is pubertal stage measured?

A

Tanner statins (breast, genital, pubic/axillary hair and testicular volume)

217
Q

How is testicular volume measured?

A

Prader orchidometer

218
Q

Outline indications for referral to do with growth and development

A 
Extremes of height 
Abnormal high velocity 
History of chronic disease
Obvious dysmorphic syndrome 
Early/late puberty
219
Q

At what ages is puberty considered to be early and late in the different sexes respectively?

A

Boys: Early <9 (rare) and late >14 (common)

Girls: Early <8 and late >13 (rare)

220
Q

What is the most common cause of delayed puberty in boys?

A

Constitutional Delay of Growth and Puberty (CDGP)

221
Q

List causes of delayed puberty

A

Gonadal dysgenesis (Turner 45X, Kleinfelter 47XXY)

Chronic disease (Crohn’s, asthma)

Impaired HPG axis (sept-optic, dysplasia, craniophyringioma, Kallman’s syndrome)

Peripheral (cryptorchidism, testicular irradiation)

222
Q

List two causes of early sexual development

A

Central precious puberty

Precocious pseudopuberty

223
Q

What is central precocious puberty?

A

Early pubertal development (breast/testicular growth) and advanced bone age often due to pituitary lesion

224
Q

What is precocious pseudopuberty?

A

Abnormal sex steroid secretion with low/prepubertal levels of LH/FSH

Clinical picture of secondary sexual characteristics

Need to exclude congenital adrenal hyperplasia

225
Q

What pathology must be excluded in the case of ambiguous genitalia?

A

Congenital adrenal hyperplasia

226
Q

Outline the causes of congenital hypothyroidism

A

Athryeosis (agenesis of the thyroid)
Hypoplastic (dysgenesis of the thyroid)
Ectopic (outside its usual anatomical bounds)

227
Q

What is the most common cause of acquired hypothyroidism?

A

Hashimoto’s thyroiditis

228
Q

What childhood issues can be caused by hypothyroidism?

A

Lack of height gain
Pubertal delay (or precocity)
Poor school performance

229
Q

Outline the presentation of diabetic ketoacidosis?

A 
Nausea and vomiting
Abdominal pain
Sweet-smelling breath
Drowsiness
Rapid, deep, sighing respiration 
Coma
230
Q

List the THINK Symptoms of diabetes

A 
Thirsty
Thinner
Tired
Toilet
Other (blurred vision, candidiasis, constipation, recurring skin infections etc.)
231
Q

List the domains of child development

A 
Gross motor skills
Fine motor skills
Speech and language
Social/personal activities of daily living 
Performance and cognition
232
Q

What is global delay?

A

Delay in two or more of the following domains (motor, language, cognitive, social and emotional)

233
Q

List four assessment tools for development?

A

ASQ (ages and stages questionnaire)

PEDS (parents evaluation of developmental status)

M-CHAT (Autism in toddlers checklist)

SOGS-2 (Schedule of growing skills )

234
Q

What are the red flags for childhood development?

A 
Loss of developmental skills
Concerns about revision/hearing
Floppiness
No speech by 18-24 months 
Asymmetry of movement 
Persistent toe walking
235
Q

List developmental milestones

A

Sit unsupported at 12 months
Walk by 18 months (boys) or 2yrs (girls)
Run by 2.5 years
Hold objects at 5 months
Reach for objects by 6 months
Points to objects to share interest by 2 yrs

236
Q

List some common developmental issues in the motor domain

A

Delayed maturation
Cerebral palsy
Developmental coordination disorder

237
Q

List some common developmental issues in the sensory domain

A

Deafness
Visual impairment
Multi-sensory impairment

238
Q

List some common developmental issues in the language/cognition domain

A

Specific learning impairment

Learning disability

239
Q

List some common developmental issues in the social/communication domain

A

Autism
Asperger syndrome
Elective mutism

240
Q

What formula is used to estimate weight in children?

A

Weight (kg) = 2*(age+4)

241
Q

What is the estimated blood volume of a child?

A

Blood volume (mls) = 80mls/kg

242
Q

What is the average urine output of a child?

A

0.5-1ml/kg/hr

243
Q

What is the volume of insensible loss in children?

A

20mls/kg/L

244
Q

What is the estimated systolic blood plessure for children?

A

Systolic BP (mmHg) = 80 + (2 x age)

245
Q

Outline the change in respiratory rate from the ages of <1 to >10

A

<1yo - 30-40
2-5yo - 25-30
5-10yo - 20-25
>10yo - 15-20

246
Q

Outline the change in heart rate from the ages of <1 to >10

A

<1yo - 110-160
2-5yo - 95-140
5-10yo - 80-120
>10yo - 60-100

247
Q

Outline the change in blood pressure from the ages of <1 to >10

A

<1yo - 70-90
2-5yo - 80-100
5-10yo - 90-110
>10yo - 100-120

248
Q

Under what age is codeine not recommended?

A

<12 years old

249
Q

Outline fluid resuscitation requirements in children

A

20ml/kg bolus 0.9% NaCl

250
Q

Outline fluid maintenance requirements in children

A

4ml/kg for the first 10kg (40ml)
2ml/kg for the next 10kg (20ml)
1ml/kg for every kg thereafter

251
Q

How does appendicitis present?

A

Murphys triad (pain in McBurney’s point, vomiting, fever)

252
Q

What complications can occur in appendicitis?

A

Abscess
Mass
Peritonitis

253
Q

What is non-specific abdominal pain (NSAP?

A

Acute abdominal pain less than one week in duration, for which there is no diagnosis despite investigations and comprises a spectrum of undiagnosed conditions, both somatic and functional, and remains a “diagnosis of exclusion.”

254
Q

What pathologies usually underlie NSAP?

A

Mesenteric adenitis (high temp, URTI, not well)

Pneumonia (sicker than abdominal signs, usually right lower lobe)

255
Q

How is intussusception treated?

A

Penumostatic reduction (try to avoid laparotomy)

256
Q

What is gastroscisis?

A

Type of congenital abdominal wall defect.

Gut eviscerated and exposed

Treated with TPN and primary/delayed closure

257
Q

What is exomphalos?

A

Umbilical defect covered in viscera

Managed with primary/delayed closure

25% post-natal mortality

258
Q

A defect in what structure results in an epigastric hernia?

A

Defect in linea alba above the umbilicus leading to protrusion of preperitoneal fat

259
Q

Outline the common organisms responsible for gastroenteritis in children

(9)

A

Rotavirus, adeno, entero, noro
E.coli, Shigella, Salmonella, Campylobacter
Giardiasis, Amoebiasis

260
Q

Outline the potential presentation of urological conditions in paediatrics

A

Systemic (fever, vomiting, failure to thrive, anaemia, hypertension, renal failure)

Local (pain, changes in urine, abnormal voiding, mass)

Antenatal (asymptomatic, permits immediate postnatal assessment)

261
Q

How are inguinal hernia managed?

A

<1 years old - urgent referral
>1 years old - elective referral and repair

Incarcerated - reduced and repair on the same admission

262
Q

What is a hydrocele?

A

Painless cystic scrotal swelling - increases in size with crying, straining etc.

Managed conservatively until the age of five

263
Q

What is cryptorchidism?

A

Any testis that cannot be manipulated into the bottom half of the scrotum

264
Q

What are the different types of cryptorchidism?

A

True
Retractile
Ectopic
Ascending testis

265
Q

What is the main risk factor for the development of cryptorchidism?

A

Preterm labour

266
Q

What are the indications for orchidopexy?

A 
Fertility - 1% loss germ cells per month of undescent 
Malignancy 
Trauma
Torsion
Cosmetic
267
Q

What is circumcision?

A

Removal of foreskin

268
Q

What are the absolute and relative indications for circumcision?

A

Absolute - balanitis xerotica obliterates (BXO)

Relative (balanoposthitis, religious, UTI)

269
Q

What complications can occur after a circumcision?

A

Bleeding
Meatal stenosis
Fistula
Cosmetic

270
Q

What is acute scrotum?

A

Sudden onset scrotal pain

271
Q

Outline three differential diagnoses for the acute scrotum

A

Torsion
Torsion appendix testis
Epididymitis

272
Q

What can cause epididymitis?

A

Trauma, haematocele, incarcerated, inguinal hernia

273
Q

After 6-8hours of an undiagnosed acute scrotum, what is the best course of action?

A

Explore surgically to recover testis

274
Q

Why do we investigate UTIs in children?

A

Prevent renal scarring and hypertension

275
Q

How does UTI cause renal scarring?

A

Reflux nephropathy and chronic renal failure

276
Q

How is reflux nephropathy managed?

A

Conservative - voiding advice, constipation, fluids

ABx prophylaxis until aged 4 (trimethoprim)

277
Q

What is the definition of a UTI?

A

Pure growth of bacteria >10^5
Pyuria/Dysuria etc.
Systemic upset (fever, vomiting)

278
Q

How is UTI investigated?

A

History and examination (FH, bowels habit, voiding)

USS (hydronephrosis)

Renography (MAG3 for drainage function and reflex, DSMA for function and scarring)

Micturating cystourethrogram (MCUG)

279
Q

What is hypospadias?

A

Urethral meatus on the mental aspect of the penis

280
Q

How is hypospadias managed?

A

Investigated associated anomalies e.g. ambiguous genitalia

US scan

Surgery correction

281
Q

Outline the common features of a history detailing childhood migraine

A 
Associated nausea and vomiting 
Pallor
Photo/phonophobia
Relation to stress/fatigue 
Often positive family history
282
Q

What types of headache history might a child give?

A

Isolated/recurrent acute

Chronic progressive/non-progressive

283
Q

What examinations may be indicated with a child presenting with a headache?

A 
Sinuses, teeth, visual acuity 
Fundoscopy
Visual fields 
Cranial bruit 
Focal neurological signs
Cognitive/emotional status
284
Q

What indications are there for neuroimaging?

A 
Features of cerebellar dysfunction
Features of raised ICP 
New focal deficit e.g. new squint 
Seizures
Personality change 
Unexplained deterioration of school work
285
Q

What presentation would make you consider a neuromuscular junction disorder?

A 
Floppy baby
Slipping from hands
Paucity of movement 
Alert but less motor activity 
Delayed motor milestones 
Able to walk to frequent falls
286
Q

What mutation is associated with Duchenne’s muscular dystrophy?

A

Xp21 dystrophin gene

287
Q

How does Duchenne’s muscular dystrophy?

A

Symmetrical proximal weakness(waddling gait, calf hypertrophy, Gower’s sign positive)

Elevated creatine kinase (>1000U)

Cardiomyopathy and respiratory involvement

288
Q

What is the definition of a seizure/fit?

A

Any sudden attack from whatever cause

289
Q

What is a febrile convulsion?

A

An event occurring in infancy (usually between 3m-5yrs) associated with fever but without evidence of intracranial infection or organic cause

290
Q

What is adolescence?

A

Specific, unique developmental stage occurring between the ages of 11-25

291
Q

What social, emotional and physical changes occur?

A

Social (independence, self-identity, sexual identity)

Emotional (regulation)

Physical (planning, organising, reasoning, abstract thinking)

292
Q

What is the most common childhood malignancy?

A

Leukaemias

293
Q

List some acute complications of chemotherapy

A 
Hair loss
Neausea and vomiting
Mucositis
Diarrhoea/constipation
Bone marrow suppression (anaemia, bleeding, infection)
294
Q

List some chronic complications of chemotherapy

A

Organ impairment
Reduced fertility
Second cancer

295
Q

List some acute complications of radiotherapy

A

Lethargy
Skin irritation
Swelling
Organ inflammation - bowel, lung

296
Q

List some chronic complications of radiotherapy

A

Fibrosis/scarring
Second cancer
Reduced fertility

297
Q

List some oncological emergencies

A 
Sepsis/febrile neutropenia
Raised ICP
Spinal cord compression
Mediastinal mass
Tumour lysis syndrome
298
Q

What are some risk factors for developing febrile neutropenia?

A

ANC <0.5x10^9
Indwelling catheter
Mucosal inflammation
High dose chemotherapy

299
Q

What are the most common organisms associated with febrile neutropenia

A 
Pseudomonas aerignenosa 
E. coli
Enterococci
Staph
Fungi (aspergillus, candida)
300
Q

How does febrile neutropenia present?

A

Fever (or low temp)
Rigors
Drowsiness
Shock

301
Q

OUtline the management of febrile neutropenia

A 
IV access
Bloods 
CXR
Other investigations (urine microscopy, throat swab, LP, viral PCR, CT/USS)
Broad spec. ABx 
Oxygen, fluids, inotropes
302
Q

Describe the presentation of early raised ICP

A

Early morning headache
Tense fontanelle
Nausea/vomiting

303
Q

Describe the presentation of late raised ICP

A 
Constant headache
Papilloedema 
Diplopia
Loss of upgaze 
Reduced GCS
Cushing's triad (Chenyes-Stokes, bradycardia, hypertension)
304
Q

How is raised ICP managed?

A

Dexamethasome if due to tumour

Neurosurgery (ventriculostomy, extra ventricular drain, ventricle-peritoneal shunt) )

305
Q

Outline the pathophysiology of spinal cord compression in paediatric malignancy

A

Invasion from paravertebral disease via intervertebral foramina (CSF seeding or direct invasion)

306
Q

How may spinal cord compression present?

A

Weakness, pain, sensory disturbance, sphincter disturbance

307
Q

How is suspected spinal cord compression investigated?

A

Urgent MRI of spine

308
Q

How is spinal cord compression managed?

A

Dexamethasome to reduce per-tumour oedema

Chemotherapy/spinal decompression surgery

309
Q

How may a mediastinal mass present in the emergency setting?

A

Superior Vena Cava Syndrome

310
Q

List some common causes of superior vena cava syndrome?

A

Lymphoma
Neuroblastoma
Germ cell tumour
Thrombosis

311
Q

How does superior vena cava syndrome present?

A

Facial, neck and upper thoracic plethora (redness)

Oedema, cyanosis, distended veins and reduced GCS

312
Q

How is superior vena cava syndrome investigated?

A

CXR/CT chest

Echocardiogram

313
Q

How is superior vena cava syndrome managed?

A

Keep the patient upright and calm
Urgent biopsy
Definitive treatment is required urgently (chemotherapy and radiotherapy)

314
Q

What is tumour lysis syndrome?

A

Rapid death of tumour cells and release of intracellular contents secondary to treatment

315
Q

What are the biochemical markers of tumour lysis syndrome?

A

Hyperkalaemia
Hyperuraemia
Hyperphosphataemia
Hypocalcaemia

Acute renal failure

316
Q

How is tumour lysis syndrome treated?

A

ECG monitoring
Hyperhydration
Diuretics

Renal replacement therapy (dialysis etc.)

MBChB Final Exam Essentials (18 decks)

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