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Medicine > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Kawasaki Disease Presentation

A

Fever >5 days
4/5 of CREAM features
- Conjunctivitis
- Rash
- Edema/Erythema
- Adenopathy (cervical, commonly unilateral)
- Mucosal involvement (strawberry tongue, oral fissures)

Raise Suspicion: prolonged fever and red eyes, hands and feet in a child

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2
Q

Treatment of Kawasaki Disease

A

Aspirin and Intravenous Immunoglobulin (IVIG)

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3
Q

What is pyloric stenosis?

A

Hypertrophy of the pyloric sphincter

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4
Q

Presentation of pyloric stenosis

A

Vomiting after feeds: can be projectile (hitting walls)
O/E: palpable, smooth, olive-sized mass (more obvious during feeding)

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5
Q

Complications of pyloric stenosis

A

Dehydration
Severe vomiting –> acid base abnormality of hypochloremic hypokalemic metabolic alkalosis

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6
Q

Diagnosis of pyloric stenosis

A

Abdominal US

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7
Q

Management of pyloric stenosis

A

Surgical with pyloromyotomy to cut the pyloric sphincter to widen the outlet

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8
Q

What bacteria causes impetigo?

A

Staphylococcal and Streptococcal bacteria
- commonly staphylococcus aureus

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9
Q

Presentation of impetigo

A

Pruritic rash
Golden crust
Face, nose, mouth

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10
Q

Management of impetigo

A

Fusidic acid

Oral flucloxacillin

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11
Q

Intussusception definition

A

Invagination of proximal bowel into a distal segment passing into the caecum through the ileocaecal valve.

The peak ages are between 3 months and 2 years old.

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12
Q

Complications of intussusception

A

Bowel perforation
Peritonitis
Gut necrosis

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13
Q

Presentation of intussusception

A

Severe colicky pain - child characteristically draws up his legs
May refuse feeds
Vomiting may be bile stained
Abdo distension
Sausage-shaped mass may be palpated in the abdomen

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14
Q

Investigations for intussusception

A

‘Target’ sign on abdominal US (concentric echogenic and hypoechogenic bands)

Can also show complications such as free-abdominal air or presence of gangrene.

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15
Q

Management of intussusception

A

Rectal air insufflation or contrast enema (if child is stable)

Operative reduction indicated if:
- failure of non-operative management
- peritonitis or perforation is present
- hemodynamically unstable

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16
Q

Other name for Pertussis

A

Whooping Cough

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17
Q

Cause of Pertussis

A

Bordetella pertussis

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18
Q

Presentation of Pertussis

A

Cough, with prolonged period of coughing per episode
Inspiratory whooping
Rhinorrhoea
Post-tussive vomiting
Apnoeas

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19
Q

Management of Pertussis

A

Macrolides typically first-line
Pertussis is a notifiable disease

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20
Q

Cause of Glandular Fever

A

Epstein Barr Virus (EBV)

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21
Q

Presentation of Glandular Fever

A

Fever
Sore Throat
Fatigue
Hepatomegaly and/or splenomegaly may sometimes be found on palpation

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22
Q

Management of Glandular Fever

A

Supportive
Advise against contact sports and heavy lifting for 1 month to minimise risk of splenic rupture.

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23
Q

What is Hypoxic Ischaemic Encephalopathy (HIE)?

A

Term for brain damage resulting from ante- or perinatal hypoxia

  • lack of oxygen in foetal circulation results in poor supply of oxygen to brain
  • ischaemia results in irreversible brain damage, both from primary neuronal death (immediate) and secondary reperfusion injury (delayed).
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24
Q

Presentation of HIE

A

Depends on the degree of neurological damage

  • Mild: irritability
  • Severe: hypotonia, poor responses, prolonged seizures
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25
Q

Normal Obs at Birth

A

HR: 110-170
RR: 35-55
Systolic BP: 50-70

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26
Q

Normal Obs at 12 months

A

HR: 80-140
RR: 30-40
Systolic BP: 70-100

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27
Q

Normal Obs at 3-5 years

A

HR: 80-130
RR: 20-30
Systolic BP: 70-110

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28
Q

Normal Obs at 6-11 years

A

HR: 70-120
RR: 16-25
Systolic BP: 80-120

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29
Q

Normal Obs at 12-18 years

A

HR: 60-100
RR: 12-22
Systolic BP: 100-120

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30
Q

Indications for Tonsillectomy

A

The indications for tonsillectomy in recurrent tonsillitis are
- seven or more episodes in a single year
- five or more episodes/year in two years
- three or more episodes/year in three years

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31
Q

What is Perthes Disease?

A

Avascular necrosis of the femoral head in children aged 4-8. Disruption of blood flow to the femoral head causes ischaemia.

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32
Q

Presentation of Perthes Disease

A

Gradual onset limp and hip pain.
Pain can also be referred to the knee.
Pain persisting for >4 weeks should raise suspicion

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33
Q

Diagnosis of Perthes Disease

A

Hip X-Ray: shows sclerosis and fragmentation of the epiphysis.

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34
Q

Management of Perthes Disease

A

Depends on extent of necrosis

<50% of the femoral head: can resolve with conservative measures like bed rest and traction.

> 50% of the femoral head: plaster cast keeping the hip abducted or osteotomy may be required. Poorer outcomes and carries ^risk for degenerative arthritis later in life.

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35
Q

What is necrotising enterocolitis?

A

Bowel of premature infant becomes ischaemic or infected

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36
Q

Risk factors for necrotising enterocolitis

A

Prematurity
Low birth weight (LBW)
Non-breast milk feeds
Sepsis
Acute hypoxia
Poor intestinal perfusion

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37
Q

Clinical Features of necrotising enterocolitis

A

First 3 weeks of life
Vomiting (may be bile streaked)
Bloody stools
Abdominal distension
Absent bowel sounds
Signs of systemic compromise inc. acidosis on blood gas

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38
Q

Investigations for necrotising enterocolitis

A

Abdo X-Ray
- dilated bowel loops
- Pneumatosis intestinalis (gas within bowel wall)
- portal venous gas
- Pneumoperitoneum

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39
Q

Management for necrotising enterocolitis

A

NG tube
Broad spectrum Abx
Total parenteral nutrition to rest bowel
IV fluids and ventilation
Surgery to resect necrotic section of bowel may be necessary –> essential if bowel perforation

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40
Q

Complications of necrotising enterocolitis

A

Fatal in 1/5 cases
Long-term implications: having a stoma or short gut syndrome

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41
Q

What anti-depressant is suitable for children?

A

Fluoxetine

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42
Q

What is a Wilm’s tumour?

A

Nephroblastoma
An embryonic tumour from the developing kidney.

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43
Q

Epidemiology of Wilm’s tumour

A

Most common in children <5 years
Peak incidence between 3-4 years of age

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44
Q

Presentation of a Wilm’s tumour

A

Abdo mass that doesn’t cross midline
Abdo distension
Haematuria
Hypertension
Otherwise asymptomatic unless grown large enough to cause pain or infiltrate other abdo structures

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45
Q

Diagnosis of a Wilm’s tumour

A

Suspected nephroblastoma: CT chest, abdomen and pelvis
Definite diagnosis and staging confirmed via renal biopsy
–> small round blue cells may be seen on histology

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46
Q

Management and prognosis of a Wilm’s tumour

A

Surgical options (nephrectomy), chemotherapy and radiotherapy

Excellent prognosis with over >90% 5-year survival rate

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47
Q

In NICU, what consequence of artificial ventilation is routinely screened for?

A

Retinopathy of prematurity

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48
Q

What is Ventricular Septal Defect? (VSD)

A

A birth defect of the heart in which there is a hole in the wall that separates the ventricles of the heart

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49
Q

What murmur is heard in ventricular septal defect?

A

Pansystolic murmur (harsh) best heard at the left lower sternal edge

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50
Q

What vaccines are contra-indicated in a patient with an egg allergy?

A

Yellow Fever
Influenza vaccine - if had been admitted to PICU for egg allergy

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51
Q

What vaccines are contra-indicated for a patient with a history of intussusception?

A

Rotavirus vaccine

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52
Q

What is Turner’s Syndrome?

A

A condition that results in females when one of the X chromosomes is missing or partially missing.

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53
Q

Presentation of Turner’s Syndrome

A

Short stature
Lymphoedema of hands and feet in neonate
Webbed neck
Widely spaced nipples
Delayed puberty
Ovarian dysgenesis causing infertility
Hypothyroidism
Spoon-shaped nails
Congenital heart defects
Normal intellect
Recurrent otitis media

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54
Q

Management of Turner’s Syndrome

A

Growth hormone therapy
Oestrogen replacement to allow development of secondary sexual characteristics

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55
Q

Complications of Turner’s Syndrome

A

^ risk of cardiovascular disease
–> ^ risk of aortic stenosis (from bicuspid valve) and aortic dissection (from coarctation of the aorta)

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56
Q

Chromosomal abnormality seen in Turner’s Syndrome

A

XO karyotype

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57
Q

Most common congenital heart defect seen in Turner’s Syndrome

A

Bicuspid aortic valve (most common)
Coarctation of the aorta

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58
Q

First line pharmacological treatment of ADHD in children >6yo

A

Mehtylphenidate

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59
Q

Rickets results from a deficiency in what?

A

Vitamin D

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60
Q

What is Coeliac disease?

A

A T cell-mediated inflammatory autoimmune disease affecting the small bowel in which sensitivity to prolamin results in villous atrophy and malabsorption

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61
Q

Associations of coeliac disease

A

Positive FHx
HLA-DQ2 allele
Other autoimmune disease (such as type 1 diabetes mellitus)

62
Q

Symptoms of Coeliac Disease

A

Gastro
- abdo pain
- distension
- N&V
- Diarrhoea
- Steatorrhoea

Systemic
- Fatigue
- Weight loss or failure to thrive
- General appearance: pallow, short stature, wasted buttocks, features of vitamin deficiency due to malabsorption (e.g. bruising due to vit K deficiency)
- Dermatitis herpetiformis

63
Q

Diagnosis of Coeliac Disease

A

Stool culture to exclude infection.
First line: Anti-TTG IgA antibody
if +ve, for definitive diagnosis:
Gold standard: OGD and duodenal/jejunal biopsy. Carried out before and after gluten withdrawal.
Histology revelas subtotal villous atrophy, crypt hyperplasia, and intra-epithelial lymphocytes.

64
Q

Complications of Coeliac Disease

A

Anaemia (secondary to iron, B1 or folate deficiency)
Hyposplenism (therefore a susceptibility to encapsulated organisms)
Osteoporosis

65
Q

Causative organism for Hand, Foot and Mouth disease

A

Coxsackie virus A16

66
Q

When is chickenpox no longer infectious?

A

When all the lesions have crusted over

67
Q

What is hydrocephalus?

A

The result of an excess of cerebrospinal fluid (CSF) accumulating in the brain ventricular system.
Puts pressure on the brain parenchyma and can have devastating neurological consequences if not recognised and treated

68
Q

Causes of non-communicating hydrocephalus

A

Something obstruct the flow through the ventricular system:
- a congenital malformation (e.g. stenosis of the aqueduct or a Chiari malformation)
- a tumour or vascular malformation in the posterior fossa
- an intraventricular haemorrhage (premature infants are particularly at risk)

69
Q

Causes of communicating hydrocephalus

A

A failure to reabsorb CSF occurs from an insult to the arachnoid villi.
Examples include meningitis and subarachnoid haemorrhage

70
Q

Presentation of hydrocephalus

A

Enlarged head circumference
Bulging of anterior fontanelle
Distention of veins across the scalp
Late sign: ‘sunsetting’ of the eyes, where upward gaze is limited

71
Q

Diagnosis of hydrocephalus

A

Cranial US (through anterior fontanelle, whilst still open in first few months of life)
or
MRI/CT of the brain

72
Q

Management of hydrocephalus

A

Insertion of a ventriculoperitoneal shunt: to move excess CSF into the abdominal cavity where it is reabsorbed.
Carers should be counselled to look out for signs of a blocked or infected shunt

73
Q

Features of innocent murmurs

A

6 S’s

Soft
Systolic (not all diastolic pathological)
Sensitive (changes w/ child’s position/alongside respiration)
Short (not holosystolic)
Single (no additional sounds)
Small (localised, non-radiating)

74
Q

Presentation of rickets

A

Aching bones and joints
Poor growth and development
Bow leg deformity
Delayed dentition
Weakness
Constipation

75
Q

Neonatal Respiratory Distress Syndrome cause

A

Lack of surfactant
–> surfactant lowers surface tension in alveoli, helping to keep them open
–> lack of, increases surface tension causing alveolar collapse, triggering resp distress
–> made from around 26 wks, but adequate levels not achieved until 35 wks

76
Q

CXR for Neonatal Respiratory Distress Syndrome

A

Ground glass appearance

77
Q

Management of Neonatal Respiratory Distress Syndrome

A

Intratracheal instillation of artificial surfactant.
If preterm delivery expected, give mother glucocorticoids before delivery to ^ surfactant production in baby.

78
Q

Mechanism of Henoch Schonlein Purpura

A

Small vessel vasculitis

79
Q

Presentation of Henoch Schonlein Purpura

A

Purpura or petechiae on the vuttocks and lower limbs
Abdominal pain
Arthralgia
Nephritis (haematuria +/- proteinuria)
May be pyrexial
HSP commonly preceded by a viral upper respiratory tract infection

80
Q

Management of Henoch Schonlein Purpura

A

NSAIDs for analgesia and anti-inflammatory effect
Antihypertensives may be needed to control BP

After episode: regular urine dips for 12 months to check renal impairment

81
Q

What is meconium ileus?

A

A condition where the baby’s first stool is so thick and sticky it causes intestinal obstruction

82
Q

Associations with meconium ileus

A

90% associated with cystic fibrosis
–> calcium channel mutation causes the mucous in the meconium to be excessively thick

83
Q

Presentation of meconium ileus

A

No meconium passed within 48 hours from birth
Signs of intestinal obstruction

84
Q

Diagnosis of meconium ileus

A

Abdo X-Ray: ‘bubbly’ appearance of the intestines with a lack of air-fluid levels

85
Q

Management of meconium ileus

A

‘Drip and suck’
–> IV fluids and stomach drainage with an Ryles tube
Along with enemas to remove the meconium
Surgery may be necessary in severe cases

86
Q

What is coarctation of aorta?

A

A narrowing of the aorta, typically just before the ductus arteriosus

87
Q

Presentation of coarctation of aorta

A

Systolic murmur: typically loudest between the scapulae
Radio-femoral delay
Hypertension
Heart failure

If severe neonates present in shock once the ductus arteriosus closes due to low perfusion after coarctation

88
Q

Associations of coarctation of aorta

A

5% of babies with Turner’s syndrome are born with coarctation of the aorta

89
Q

Management of coarctation of aorta

A

Monitored via echocardiography
Antihypertensives needed for BP if needed
Most cases requiring intervention are corrected via angioplasty and stent insertion

Neonates presenting in shock need prostaglandin to keep the ductus arteriosus patent until the defect is corrected

90
Q

Rash on both cheeks and fever. URTI symptoms.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Slapped Cheek Syndrome/Fifth Disease
  2. Parvovirus B19
  3. Self-limiting & usually resolves within one week
  4. Once rash appears, no longer infectious
91
Q

Blisters on hands and feet. Grey ulcerations in the buccal cavity.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Hand, foot and mouth disease
  2. Coxsackie virus A16
  3. Self-limiting and usually resolves in one week
  4. Do not need to be isolated
92
Q

Coarse ed rash on the cheeks, sore throat, headache fever. Bright red tongue.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Scarlet Fever
  2. Streptococcus species
  3. 10 days of phenoxymethylpenicillin
  4. Infectious until 24 hours after first dose of Abx
93
Q

Erythematous, blanching maculopapular rash all over body. Preceded by a fever, cough and conjunctivitis. White spots inside buccal cavity.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Measles
  2. Measles virus
  3. Self-limiting, immunisation encouraged bc of complications.
  4. Infectious from 4 days before the rash to around 4 days after. Highly infectious
94
Q

Maculopapular vesicular rash that is itchy.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Chicken pox
  2. Varicella zoster virus (human herpes virus 3)
  3. Supportive unless the patient is:
    - a neonate
    - immunocompromised
    - adolescent presenting within first 24 hours of rash onset
    - pregnant
    Then antiviral treatment
  4. Infectious from 1-2 days before the rash until every single lesion has crusted over.
95
Q

Lace-like red rash across the whole body with a high fever.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Roseola
  2. Human Herpes Virus 6
  3. Self-limiting, supportive management
  4. ?
96
Q

Rash beginning on the head and spreading down the trunk. Postauricular lymphadenopathy.

  1. Diagnosis?
  2. Causative organism?
  3. Treatment?
  4. Infectious?
A
  1. Rubella
  2. Rubella virus
  3. Self-limiting, supportive management
    Vaccine exists due to risk of in-utero complications that occur as a result of a pregnant woman being infected.
    4.
97
Q

What is testicular torsion?

A

Emergency
When tissues around the testicle are not attached well. Can cause the testes to twist around the spermatic chord, when this happens it cuts off the blood flow to the testicle.

98
Q

Complications of testicular torsion

A

If not treated immediately can lead to damage to or death of a testicle due to lack of blood supply.
The necrotic testicle must be surgically removed, this can effect fertility.

99
Q

Presentation of testicular torsion

A

Sudden onset, severe pain in one testicle
Often follows minor trauma
High riding in the scrotum
Unilateral loss of cremaster reflex
No relief in pain on elevation of the testicle (negative Prehn’s sign)

100
Q

Management of testicular torsion

A

Expedited surgical exploration with fixation of the testicles with orchidoplexy

101
Q

Presentation of Osteosarcoma

A

Pain and swelling with a prolonged onset are characteristics
Typically occurs in the metaphyses of long bones

102
Q

Diagnosis of Osteosarcoma

A

X-Ray: new bony growth and a periosteal reaction causing a sunburnt appearance.
Signs seen on X-Ray should prompt an urgent full body CT in order to assess for any metastases.
Definitive diagnosis: confirmed using bone biopsy

103
Q

Management of osteosarcoma

A

MDT approach, may include surgery, radiotherapy and chemotherapy

104
Q

Presentation of Ewing’s Sarcoma

A
  • teenagers and young adults
  • pelvis, thigh bone and shin most commonly affected
  • bone pain particularly occuring at night
  • a mass or swelling
  • restricted movement in a joint
105
Q

Investigations for Ewing’s sarcoma

A

X-Ray: lamellated (onion skinning) periosteal reaction visible
MRI: typically shows a large mass w/ evidence of necrosis
Histology: small blue round cells visible w/ clear cytoplasms on haematoxylin and eosin staining

Definitive diagnosis: bone biopsy

106
Q

What is Fragile X syndrome?

A

Genetic condition caused by a CGG trinucleotide repeat in the FMR1 (fragile X mental retardation 1) gene on the X chromosome, affecting synaptic development.

107
Q

Presentation of Fragile X sydrome

A

A long face
Large, protruding ears
Intellectual impairment
Macroorchidism (large testes) - post-pubertal
Social anxiety
Autistic spectrum features

108
Q

Other name for slapped cheek syndrome

A

Fifth disease
Erythema infectiosum

109
Q

What is Hirschsprung’s disease?

A

As the baby develops in utero, the distal colon is not innervated correctly.
The resulting aganglionic colon is shrunken and not able to distend properly.
This causes a back pressure of stool trapped in the more proximal colon.

110
Q

Presentation of Hirschsprung’s disease

A

Present at birth:
- a delay in passing meconium (>48 hours)
- a distended abdomen
- forceful evacuation of meconium after digital rectal examination

111
Q

Diagnosis of Hirschsprung’s disease

A

Rectal suction biopsy

112
Q

Management of Hirschsprung’s disease

A

Definite management: Removal of the section of aganglionic colon and the healthy bowel is pulled through

113
Q

What is patent ductus arteriosus?

A

When the ductus arteriosus remains patent after 4 weeks

114
Q

Presentation of patent ductus arteriosus

A

May be asymptomatic or present with signs of heart failure
Classical murmur: continuous ‘machine-whirring’ murmur throughout the cardiac cycle

115
Q

Management of patent ductus arteriosus

A

Only required if baby is symptomatic.
NSAIDs: inhibit prostaglandins synthesis which normally help maintain ductal patency.
Medical closure of PDAs are more successful in premature babies.
8% will require surgical ligation to close the ductus arteriosus

116
Q

Perinanal/vulval itching in a child
Worse at night
No abnormalities on examination

A

Threadworm

117
Q

1st line treatment of threadworm

A

oral Mebendazole

118
Q

Most common congenital heart defect in infants of diabetic mothers

A

Transposition of the great vessels

119
Q

which anatomical anomaly determines the extent of cyanosis in Tetralogy of Fallot (TOF)?

A

Pulmonary stenosis
- the greater the level of right ventricular outflow obstruction, the less unoxygenated blood reaches the lungs with each beat, the greater the stenosis will be

120
Q

adolescent, localised pain of several months duration with no traumatic event or associated injury and an associated mass on examination

A

Osteosarcoma

121
Q

Cause of congenital heart block

A

Maternal Systemic Lupus Erythematosus (SLE)
–> linked to the presence of maternal anti-Ro and/or anti-La antibodies

122
Q

Most common cause of bacterial meningitis in neonates <3 months

A

Group B strep

123
Q

Most common cause of bacterial meningitis in children >3 months

A

Neisseria meningitidis or Streptococcus pneumoniae

124
Q

Most common viral causes of meningitis

A

Herpes simplex virus (HSV), enterovirus and varicella zoster virus

125
Q

Presentation of meningitis

A

Fever, neck stiffness, vomiting, headache, photophobia, altered consciousness, seizures.

If progressed to meningococcal septicaemia can present with a non-blanching rash

126
Q

Presentation of meningitis is neonates

A

More nonspecific
Symptoms such as hypotonia, poor feeding, lethargy, and a bulging fontanelle

127
Q

Investigations for meningitis

A

Lumbar puncture
- !!never if raised ICP!!
Blood test for meningococcal PCR
Blood cultures

128
Q

Difference between bacterial and viral CSF (meningitis)

A

Appearance: Bacterial = cloudy Viral = clear
Protein: Bacterial = high Viral = mildly raised/normal
Glucose: Bacterial = low Viral = normal
White Cell Count: Bacterial = high neutrophils Viral = high lymphocytes
Culture: Bacterial = bacteria Viral = negative

129
Q

Management of viral meningitis

A

Often supportive
Aciclovir can be used to treat suspected or confirmed HSV or VZV infection

130
Q

Community management of meningitis

A

Suspected meningitis AND a non-blanching rash should receive urgent IM or IV benzylpenicillin prior transfer to hospital

131
Q

Management of bacterial meningitis

A

IV Abx as per local guidelines
Typically, cefotaxime plus amoxicillin in <3 months, ceftriaxone in >3 months

Steroids should be given to reduce chances of complications (Dexamethasone 4 times daily for 4 days >3 months)

132
Q

Complications of meningitis

A

Hearing loss, seizures and epilepsy, cognitive impairment and learning disability, memory loss, cerebral palsy

133
Q

Paediatric Sepsis 6

A

High flow oxygen
Obtain IV/IO access and take blood tests (blood gas, lactate, blood glucose, blood cultures)
Abx: IV or IO
Fluid resuscitation
Involve senior clinicians early
Consider inotropic support

134
Q

Infective causes of encephalitis

A

Most common: HSV (HSV-1 in children, HSV-2 in neonates)
VZV, cytomegalovirus, EBV, enterovirus, and influenza virus

135
Q

Presentation of encephalitis

A

Altered consciousness, altered cognition, unusual behaviours, headache, psychiatric symptoms, acute onset of focal neurological symptoms or seizures, fever

136
Q

Ix for Encephalitis

A

Lumbar puncture: send CSF for viral PCR testing
CT can if LP contraindicated
MRI scan after LP to visualise brain
HIV testing recommended in all patients with encephalitis

137
Q

Management of encephalitis

A

IV antiviral: Aciclovir until results available

Aciclovir for HSV and VZV
Ganciclovir for CMV

138
Q

Complications of encephalitis

A

Lasting fatigue, change in personality/mood, learning disability, headaches, chronic pain, movement disorders, seizures

139
Q

Presentation of mumps

A

Initial period of flu like symptoms involving muscle aches, lethargy, reduced appetite, headache.
Then get parotid gland swelling a few days later

140
Q

Diagnosis of mumps

A

PCR testing on a saliva swab to test for antibodies to mumps virus

NOTIFIABLE DISEASE

141
Q

Managemnet of mumps

A

Supportive with rest, fluids and analgesia
Usually self-limiting and lasts around 1 week

!!Notifiable Disease!!

142
Q

Complications of mumps

A

Pancreatitis, testicular pain, meningitis or encephalitis, sensorineural hearing loss

143
Q

Causative organism for acute epiglottitis

A

Haemophilus influenzae type B (HiB)

144
Q

Symptoms of acute epiglottitis

A

High fever
toxic appearance
drooling
absence of cough
inspiratory stridor
tripod position: immobile/leaning forward with extended neck + open mouth

Unvaccinated

145
Q

Mx of acute epiglottitis

A

do NOT inspect airway

Call senior airway staff to intubate and secure airway
Oxygen + IV Abx (e.g. cefuroxime)

146
Q

Wheeze vs stridor

A

Wheeze:
Monophonic or polyphonic musical sound louder on expiration die to narrowing in lower airway

Stridor:
single note which occurs on inspiration due to upper airway obstruction

147
Q

Differentials for wheeze

A

Asthma
URTI
Bronchiolitis
Allergy
GORD
Foreign body aspiration

148
Q

Differentials for stridor

A

Acute epiglottitis
Croup
Laryngomalacia
Anaphylaxis
Bacterial Tracheitis
Foreign body aspiration

149
Q

Features of diabetic ketoacidosis

A

Polydipsia, polyuria
N+V
Dehydration
Abdo pain
Acetone-smelling breath (‘pear drops’)
Kussmaul breathing
Drowsiness, coma
Hypovolaemic shock

150
Q
A

Medicine (13 decks)

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