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C TO REVISE - PHASE 3A > PAEDS - INFECTION/ALLERGY, MSK/DERM AND EXTRA CONDITIONS > Flashcards

PAEDS - INFECTION/ALLERGY, MSK/DERM AND EXTRA CONDITIONS Flashcards

1
Q

MENINGITIS
What are the most common causes of bacterial meningitis?

A
  • Neonates = GBS or listeria monocytogenes
  • 1m–6y = N. meningitidis (gram -ve diplococci), S. pneumoniae (gram + ve cocci chain), H. influenzae
  • > 6y = meningococcus + pneumococcus, rarely TB
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2
Q

MENINGITIS
What is the difference between Kernig’s and Brudzinski signs?

A
  • Kernig = pain/unable to extend leg at knee when it’s bent
  • Brudzinski = involuntary flexion of hips/knees when neck flexed
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3
Q

MENINGITIS
What are some complications of meningitis?

A
  • Hearing (sensorineural) loss is key complication
  • Seizures + epilepsy, cerebral abscess, encephalitis + hydrocephalus
  • Cognitive impairment, cerebral palsy + LD
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4
Q

MENINGITIS
What is the management of bacterial meningitis?

A
  • Supportive = correct shock with fluids, oxygen if needed
  • <3m = IV cefotaxime + amoxicillin (cover listeria from ?pregnancy)
  • > 3m = IV ceftriaxone + IV dexamethasone to reduce frequency + severity of hearing loss + neuro damage (NOT before 3m)
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5
Q

SEPTICAEMIA
What are the causes of septicaemia?

A
  • Most common = N. meningitidis
  • Neonates = GBS or gram -ve organisms from birth canal
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6
Q

MEASLES
What is measles?

A
  • Infection with measles virus (Morbillivirus) via droplets (highly contagious)
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7
Q

RUBELLA
What is the clinical presentation of rubella?

A
  • Mild prodrome (low-grade fever, sore throat, coryza)
  • Pink maculopapular rash starts on face then spreads down to cover whole body
  • Rash not itchy in children but is in adults
  • Suboccipital + postauricular lymphadenopathy
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8
Q

RUBELLA
What are some complications of rubella?
How can it be reduced?

A
  • Rare but > encephalitis, arthritis, myocarditis + thrombocytopenia
  • Congenital rubella syndrome > cataracts, CHD + sensorineural deafness
  • Avoid pregnant women, school exclusion 4d from rash, ensure vaccinated
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9
Q

MUMPS
What is mumps?
How does it occur?

A
  • RNA paramyxovirus, occurs in winter + spring, spreads via resp droplets where virus replicates in epithelial cells
  • Virus accesses parotid glands before further dissemination
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10
Q

MUMPS
What are some complications of mumps?

A
  • Viral meningitis + encephalitis
  • Orchitis (usually unilateral, may reduce sperm count + lead to infertility)
  • Pancreatitis
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11
Q

SLAPPED CHEEK
What are some complications of slapped cheek syndrome?

A
  • Aplastic crisis (most serious) more common in chronic haemolytic anaemias like sickle cell, thalassaemia + in immunocompromised
  • Vertical transmission can lead to foetal hydrops + death due to severe anaemia
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12
Q

TOXIC SHOCK SYNDROME
Give some examples of multi-organ dysfunction in toxic shock syndrome

A
  • GI = D+V
  • CNS = confusion
  • Thrombocytopenia
  • Renal failure
  • Hepatitis
  • Clotting abnormalities
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13
Q

HIV
When should HIV be suspected?

A
  • Persistent lymphadenopathy
  • Hepatosplenomegaly
  • Recurrent fever
  • Parotitis
  • Serious, persistent, unusual, recurrent (SPUR) infections
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14
Q

HIV
How should HIV be managed?

A
  • Antiretrovirals based on viral load + CD4 count
  • Co-trimoxazole prophylaxis (PCP)
  • ?Additional vaccines but not BCG as live
  • Regular follow up, check development, psychological support
  • Safe sex education when older
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15
Q

TUBERCULOSIS
What is the pathophysiology of tuberculosis (TB)?

A
  • Lung lesion + (mediastinal) lymph nodes = Ghon or primary complex
  • Primary infection > caseating granulomas followed by period of dormancy with ?reactivation (secondary TB)
  • If immune system unable to cope it disseminates > miliary TB
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16
Q

VACCINATIONS
What vaccines are attenuated?

A
  • MMR, BCG, nasal flu, rotavirus + Men B
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17
Q

ALLERGY
What is an allergy?
Give examples

A
  • Hypersensitivity reaction initiated by specific immunoglobulins
  • Food allergy, eczema, allergic rhinitis, asthma, urticaria, insect sting, drugs, latex + anaphylaxis
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18
Q

ALLERGY
Define hypersensitivity

A

Objectively reproducible symptoms/signs following a defined stimulus at a dose tolerated by a normal person

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19
Q

ALLERGY
Give an example of a type 1hypersensitivity reaction

A
  • acute anaphylaxis,
  • hayfever
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20
Q

ALLERGIC RHINITIS
What are the different types of antihistamines that can be taken for allergic rhinitis?

A
  • Non-sedating = cetirizine, loratadine
  • Sedating = chlorphenamine (Piriton) + promethazine
  • Nasal may be good option for rapid onset Sx in response to trigger
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21
Q

ANAPHYLAXIS
What investigation confirms anaphylaxis?

A
  • Serum mast cell tryptase within 6h of event = mast cell degranulation
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22
Q

IMMUNE DEFICIENCY
What are the 6 types of immune deficiency?

A
  • T-cell defects
  • B-cell defects
  • Combined B- + T-cell defects
  • Neutrophil defect
  • Leucocyte function defect
  • Complement defects
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23
Q

IMMUNE DEFICIENCY
What are some investigations for immune deficiency?

A
  • FBC (WCC, lymphocytes, neutrophils)
  • Blood film
  • Complement
  • Immunoglobulins
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24
Q

IMMUNE DEFICIENCY
What prophylaxis should be given in immune deficiency?

A
  • T-cell + neutrophil = co-trimoxazole for PCP, fluconazole for fungal
  • B-cell = azithromycin for recurrent bacterial infections
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25
Q

IMMUNE DEFICIENCY
What is the management of immune deficiency?

A
  • Prompt, appropriate + longer Abx courses
  • Screen for end-organ disease (CT scan)
  • Ig replacement therapy if antibody deficient
  • Bone marrow transplantation for SCID, chronic granulomatous disease
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26
Q

WHOOPING COUGH
What are some complications of pertussis?

A
  • Pneumonia
  • Convulsions
  • Bronchiectasis
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27
Q

POLIO
what is the pathophysiology?

A
  • transmitted via faecal-oral route
  • incubation period is 3-30 days + can be excreted for up to 6 weeks
  • replicates in nasopharynx + GI tract and can spread to CNS where it can affect anterior horn cells, motor neurons and the brainstem
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28
Q

POLIO
what is the clinical presentation?

A

90-95% of cases are asymptomatic
fatigue
fever
nausea and vomiting
diarrhoea
sore throat
headache
photophobia

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29
Q

POLIO
what are the clinical features of a more serious polio infection?

A

acute flaccid paralysis (AFP)
- initially fatigue, fever N+V
- asymmetrical lower limb weakness and flaccidity

can progress to life-threatening bulbar paralysis and respiratory compromise

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30
Q

POLIO
what are the investigations?

A
  • virus culture from stool, CSF or pharynx
  • CSF analysis
  • serum antibodies to poliovirus
  • MRI of spinal cord
  • EMG of affected limb(s)
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31
Q

POLIO
what is the management?

A
  • supportive care with rehydration and neurological monitoring
  • physiotherapy
  • intubation and ventilation for respiratory paralysis
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32
Q

POLIO
what are the complications?

A

post-poliomyelitis syndrome (PPS) - this usually occurs years after the initial infection
- demonstrates the same features as polio infection
- treated in the same way as polio

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33
Q

DIPHTHERIA
what is the cause?

A

Corynebacterium diphtheriae

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34
Q

DIPHTHERIA
what is the clinical presentation?

A
  • sore throat
  • low grade fever
  • dysphagia, dysphonia, dyspnoea and croupy cough can occur in serious illness
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35
Q

DIPHTHERIA
what is the management?

A
  • hospitalisation, isolation
  • diphtheria anti-toxin
  • antibiotic (procaine benzylpenicillin)
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36
Q

DIPHTHERIA
what is the management for close-contacts?

A

prophylactic antibiotics - erythromycin

diphtheria toxoid immunisation

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37
Q

CHICKEN POX
How long is it contagious for?

A

Contagious 4d before rash + until lesions crusted (often 5d)

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38
Q

GLANDULAR FEVER
What are the complications of glandular fever?

A
  • Splenic rupture,
  • haemolytic anaemia,
  • chronic fatigue,
  • EBV associated with Burkitt’s lymphoma
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39
Q

TUBERCULOSIS
When diagnosing TB, what would you see on sputum MC&S?

A

Acid fast bacilli stain red with Ziehl-Neelson stain on Lowenstein-Jenson culture medium

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40
Q

TUBERCULOSIS
When diagnosing TB, what would you see on CXR?

A
  • Patchy consolidation,
  • pleural effusions,
  • hilar lymphadenopathy
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41
Q

ALLERGY
Define atopy

A

Personal/familial tendency to produce IgE in response to ordinary exposures to allergens (triad = eczema, asthma + rhinitis)

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42
Q

ALLERGY
Give an example of a type 2 hypersensitivity reaction

A
  • autoimmune disease,
  • haemolytic disease of newborn,
  • transfusion reaction
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43
Q

ALLERGY
Give an example of a type 3 hypersensitivity reaction

A
  • SLE,
  • RA,
  • HSP,
  • post-strep glomerulonephritis
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44
Q

ALLERGY
Give an example for of a type 4 hypersensitivity reaction

A
  • TB,
  • contact dermatitis
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45
Q

OSTEOMYELITIS
What are some investigations for osteomyelitis?

A
  • FBC (Raised WCC), raised ESR/CRP, blood cultures, bone marrow aspiration MC&S
  • XR can be normal
  • MRI is best imaging to establish Dx
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46
Q

OSTEOMYELITIS
What is the management of osteomyelitis?

A
  • IV empirical Abx (flucloxacillin or clindamycin if allergy) until sensitivities back
  • Amoxicillin, cefotaxime or ceftriaxone if <4y + suspect H. influenzae
  • ?Surgical drainage or debridement of infected bone
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47
Q

JIA
What is the criteria for a clinical diagnosis of JIA?

A
  • Onset before 16y with no underlying cause
  • Joint swelling/stiffness
  • > 6w in duration to exclude other causes (i.e. reactive)
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48
Q

JIA
How does systemic JIA (Still’s disease) present?

A
  • Subtle salmon-pink rash
  • High swinging fevers
  • Lymphadenopathy, weight loss, muscle pain, splenomegaly
  • Pleuritis, pericarditis + uveitis
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49
Q

JIA
What are the investigations for systemic JIA?

A
  • Antinuclear antibodies (ANA) + rheumatoid factor = NEGATIVE
  • Raised inflammatory markers = CRP/ESR, platelets + serum ferritin
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50
Q

JIA
How might enthesitis-related arthritis present?

A
  • Sx of psoriasis (psoriatic plaques, nail pitting, dactylitis) or IBD
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51
Q

JIA
What are some complications from JIA?

A
  • Chronic anterior uveitis > severe visual impairment
  • Flexion contractures of joints
  • Growth failure + constitutional problems like delayed puberty
  • Osteoporosis
52
Q

OSTEOPOROSIS
What are the causes of osteoporosis?

A
  • Inherited = osteogenesis imperfecta, haematological issues
  • Acquired:
    – Drug induced (Steroids)
    – Endocrinopathies (hypoparathyroidism)
    – Malabsorption
    – Immobilisation (disabilities)
    – Inflammatory disorders
53
Q

OSTEOGENESIS IMPERFECTA
What are some associations with osteogenesis imperfecta?

A
  • Conductive hearing loss (otosclerosis)
  • Blue/grey tinted sclera due to scleral thinness
  • Valvular prolapse, aortic dissection > aortic incompetence
  • Hernias
  • ‘Wormian bones’ = skull feels like bubble wrap (wiggly black lines on skull XR)
54
Q

RICKETS
What are some risk factors for rickets?

A
  • Darker skin (need more sunlight)
  • Lack of exposure to sun
  • Poor diet or malabsorption
  • CKD as kidneys metabolise vitamin D to active form
55
Q

RICKETS
What are the symptoms of rickets?

A
  • Bone pain, swelling + deformities
  • Muscle weakness + poor growth (gross motor delay)
  • Pathological or abnormal #
  • May have hypocalcaemic convulsions or carpopedal spasm
56
Q

RICKETS
What are some bone deformities seen in rickets?

A
  • Bowing of legs, knock knees
  • Harrison sulcus = indentation of softened lower ribcage at site of attachment of diaphragm
  • Rachitic rosary = ends of ribs expand at costochondral junctions causing lumps along chest
  • Craniotabes = soft skull with delayed closure of sutures + frontal bossing
  • Expansion of metaphyses (esp. wrist)
57
Q

RICKETS
What are some investigations for rickets?

A
  • Serum biochemistry
  • FBC + ferritin (Fe anaemia), inflammatory markers
  • Kidney, liver + TFTs, malabsorption screen (anti-TTG)
  • Autoimmune + rheumatoid tests
  • XR required to diagnose
58
Q

RICKETS
What would serum biochemistry show in rickets?

A
  • Low = calcium + phosphate
  • High = ALP + PTH
  • 25-hydroxyvitamin D levels deficient (<25nmol/L)
59
Q

RICKETS
What might an XR show in rickets?

A
  • Osteopenia (radiolucent bones)
  • Cupping
  • Fraying of metaphyses
  • Widened epiphyseal plate
60
Q

PSORIASIS
What is the pathophysiology of psoriasis?

A
  • Chronic autoimmune condition where abnormal T-cell activation > hyperproliferation of keratinocytes + so psoriatic skin lesions
61
Q

PSORIASIS
What is the clinical presentation of psoarisis?

A
  • Koebner phenomenon = new plaques of psoriasis at sites of skin trauma
  • Residual pigmentation of skin after lesions resolve
  • Auspitz sign = small points of bleeding when plaques scraped off
  • Nail changes (pitting + onycholysis)
62
Q

PSORIASIS
What is the management of psoriasis?

A
  • 1st line = topical steroids, topical vitamin d analogues (calcipotriol)
  • 2nd line = UV phototherapy
  • 3rd line = immunosuppression with methotrexate or biologics
63
Q

NAPPY RASH
What is the management of nappy rash?

A
  • Highly absorbent nappies
  • Maximise time not wearing + ensure dry before replacing nappy
  • Change nappy + clean skin ASAP
  • Water or gentle alcohol-free products to clean
  • Topical imidazole if candida
64
Q

SCOLIOSIS
what are the causes?

A
  • idiopathic = most common
  • congenital = usually from congenital structural defect of the spine e.g. spina bifida
  • secondary = neuromuscular imbalance (cerebral palsy, muscular dystrophy), disorders of bone or connective tissues
65
Q

SCOLIOSIS
what conditions can cause scoliosis?

A

cerebral palsy
muscular dystrophy
birth defects
infections
tumours
marfan syndrome
down syndrome

66
Q

TORTICOLLIS
what are the causes of congenital torticollis?

A
  • congenital muscular torticollis (CMT) = usually noticed in 1st month after birth. It causes shortening + fibrosis of sternocleidomastoid (can have palpable mass)
  • malformed cervical spine
  • spina bifida
67
Q

TORTICOLLIS
what are the causes of acquired torticollis?

A
  • MSK = muscle spasm
  • infection = URTI, otitis media, dental infection, pharyngeal infection
  • atlantoaxial rotatory fixation
  • inflammation = juvenile idiopathic arthritis
  • neoplasm = CNS tumours
68
Q

OSGOOD SCHLATTERS
what are the risk factors?

A
  • male gender
  • age - 12-15 in boys, 8-12 in girls
  • sudden skeletal growth
  • repetitive activities such as jumping and sprinting
69
Q

SEPTIC ARTHRITIS
what is the criteria for diagnosing septic arthritis?

A

Kocher’s modified criteria /5, ≥3 is likely
–Temp>38.5
– Raised CRP/ESR/WCC
– Non-weight bearing

70
Q

JIA
What is the immunology of polyarticular JIA?

A

If rheumatoid factor +ve = seropositive (tend to be older children)

71
Q

JIA
what is the immunology of oligoarticular JIA?

A

ANA +ve but RF -ve

72
Q

JIA
What is it associated with?

A
  • HLA-B27 gene
  • Prone to anterior uveitis = ophthalmology referral
73
Q

JIA
What causes reactive arthritis?

A

Post STI (chlamydia) in older children or Salmonella, Campylobacter

74
Q

OSTEOGENESIS IMPERFECTA
What is the pathophysiology?

A

Defects in type 1 collagen protein which is essential for the structure + function of bone, as well as skin, tendons + other connective tissues

75
Q

RICKETS
What are some sources of vitamin D?

A

Sunlight, fortified cereals, eggs, oily fish

76
Q

PSORIASIS
What are the causes?

A
  • HLA-B13,
  • environmental triggers (alcohol, stress, group A strep)
77
Q

JIA
How does macrophage activation syndrome present?

A
  • Acutely unwell with DIC,
  • febrile,
  • anaemia,
  • thrombocytopenia,
  • bleeding,
  • non-blanching rash,
  • low ESR
78
Q

JIA
What is the management of macrophage activation syndrome?

A

Life-threatening = supportive + steroids

79
Q

TONSILLITIS

What criteria can be used to distinguish if tonsillitis is bacterial or viral?

A

CENTOR –
- Tonsillar exudate, tender ant. cervical lymphadenopathy, fever, absence of cough (≥3 ?strep)
FeverPAIN score –
- Fever, Purulence, Attend rapidly (3d after Sx), severely Inflamed tonsils, No cough/coryza (2–3 consider delayed, ≥4 consider Abx)

80
Q

TONSILLITIS

What is the main complication of tonsillitis?

A
  • Quinsy (peritonsillar abscess)
81
Q

TONSILLITIS

What is the management of tonsillitis?

A
  • 1st line = Phenoxymethylpenicillin
  • if penicillin allergic = erythromycin

- Tonsillectomy last resort if quinsy (in 6w), recurrent severe (≥5/year) or OSA

82
Q

TONSILLITIS

How does quinsy present?

A

Severe sore throat (unilateral), uvula deviation, lockjaw

83
Q

TONSILLITIS

What is the management for quinsy?

A

Incision + drainage + IV Abx

84
Q

INTESTINAL MALROTATION
What can contribute to the obstruction in intestinal malrotation?
How may it present?

A
  • Ladd bands may cross the duodenum

- Obstruction or obstruction with compromised blood supply

85
Q

INTESTINAL MALROTATION

What is the investigation + management of intestinal malrotation?

A
  • Urgent upper GI contrast study is Dx, abdo USS

- Urgent surgical correction = Ladd’s procedure rotates bowel anti-clockwise

86
Q

ABDOMINAL MIGRAINE
What is the acute management of abdominal migraine?
What is the prophylaxis?
What is a caution?

A
  • Sumatriptan + paracetamol ± NSAID (ibuprofen)
  • Pizotifen (serotonin receptor antagonist) or propranolol
  • Withdraw pizotifen slowly as can cause depression, anxiety, poor sleep + tremor
87
Q

FUNCTIONAL DYSPEPSIA

What is functional dyspepsia?

A
  • Epigastric pain, early satiety, bloating + postprandial vomiting
88
Q

FUNCTIONAL DYSPEPSIA

What is the management of functional dyspepsia?

A
  • C-13 Urea breath test for H. pylori + upper GI endoscopy if Sx recur, if normal = Dx
  • Hypoallergenic diet
  • Eradicate H. pylori if suspected with triple therapy > omeprazole, amoxicillin + metronidazole or clarithromycin
89
Q

NEPHRITIC SYNDROME
What antibodies would you screen for?
What would renal biopsy show in IgA nephropathy?

A
  • Anti-dsDNA if SLE, ANCA in vasculitides

- IgA deposits + glomerular mesangial proliferation

90
Q

VARICOCELE
What is a varicocele?
Which side is most likely?
How does it present?

A
  • Abnormal dilatation of the testicular veins
  • L sided due to angle of L testicular vein entering the L renal vein
  • ‘Bag of worms’, dragging or aching sensation, associated with subfertility
91
Q

VARICOCELE

What is the management of varicocele?

A
  • Confirm with USS + Doppler studies

- Conservative unless pain

92
Q

DIABETES MELLITUS

What is the physiology of insulin?

A
  • Lowers blood glucose by stimulating uptake from blood into muscle, kidney + fat cells as well as targeting the liver to convert glucose to glycogen
93
Q

DIABETES MELLITUS

What are some negatives about insulin therapy in general?

A
  • Lipohypertrophy (rotate site)
  • Risk of hypoglycaemia
  • Weight gain
94
Q

DIABETIC KETOACIDOSIS

How does the body respond to ketoacidosis?

A
  • Initially, kidney produces bicarbonate to counteract but this is used up > acidotic
  • Hyperglycaemia overwhelms the kidneys + glucose starts being filtered into the urine + draws water out with it in the process (osmotic diuresis) leading to polyuria + severe dehydration, stimulating thirst centre (polydipsia)
95
Q

DIABETIC KETOACIDOSIS

What is the effect on potassium in DKA?

A
  • Kidneys excrete K+ in urine so overall body K+ is low so when treatment with insulin starts can develop severe hypokalaemia as insulin drives K+ into cells
96
Q

DIABETIC KETOACIDOSIS

What is the clinical presentation of DKA?

A
  • Smell of acetone on breath (pear drops)
  • Vomiting, dehydration, abdominal pain
  • Hyperventilation due to acidosis (Kussmaul’s breathing)
  • Drowsiness, coma + hypovolaemic shock
97
Q

DIABETIC KETOACIDOSIS

What are some investigations for DKA?

A

Diagnosis –
- Glucose >11mmol/L
- Blood ketones >3mmol/L
- Blood gas pH <7.3 or bicarb <15mmol/L (metabolic acidosis)
ECG = signs of hypokalaemia (U waves, small/absent T, long PR, ST depression)
- U+Es + creatinine show dehydration, hypokalaemia

98
Q

DIABETIC KETOACIDOSIS

What are some complications of DKA?

A
  • Cerebral oedema (neuro obs)
  • VTE
  • Hypokalaemia > arrhythmias
  • AKI
99
Q

DIABETIC KETOACIDOSIS

How do you calculate how dehydrated someone is in DKA?

A
  • 5% if pH 7.2–7.29 or bicarbonate <15 (mild)
  • 7% if ph 7.1–7.19 or bicarbonate <10 (mod)
  • 10% if pH <7.1 or bicarbonate <5 (severe)
100
Q

DIABETIC KETOACIDOSIS
What fluids do you give in DKA for…

i) shock?
ii) not shocked but needs fluids?
iii) maintenance?

A

i) 1st bolus = 0.9% NaCl 20ml/kg, subsequent 10ml/kg, do NOT subtract bolus from deficit
ii) 0.9% NaCl 10ml/kg over 1 hour, DO subtract bolus from deficit
iii) 0.9% NaCl with 40mmol/L KCl (20mmol in 500ml bag)

101
Q

HYPOGLYCAEMIA

What are some hypo phenomena?

A
  • Hypo unawareness
  • Reactive hypoglycaemia (after meal)
  • Somogyi = post-hypoglycaemic hyperglycaemia
  • Dawn phenomena = morning rise in blood sugar
102
Q

APNOEA OF PREMATURITY

What is apnoea of prematurity?

A
  • Periods where breathing stops spontaneously for >20s (or shorter periods with oxygen desaturation or bradycardia
  • Common, esp <28w
103
Q

APNOEA OF PREMATURITY

What is the management of apnoea of prematurity?

A
  • Gentle tactile stimulation when alerted by apnoea monitors
  • Resp stimulant like IV caffeine
  • May need CPAP if frequent
104
Q

IV HAEMORRHAGE

What is the management of intraventricular haemorrhage?

A
  • Cranial USS
  • Sx relief with removal of CSF by LP or ventricular tap
  • Ventriculoperitoneal shunt may be needed for hydrocephalus
105
Q

RETINOPATHY
What is the pathophysiology of retinopathy of prematurity?
What may this lead to?

A
  • Affects developing blood vessels at junction of the vascular + non-vascularised retina
  • Retinal blood vessel formation is stimulated by hypoxia so hyperoxic insult can prevent this
  • Retina responds with vascular proliferation which may progress to retinal detachment, fibrosis + blindness
106
Q

RETINOPATHY
What are some risk factors for retinopathy of prematurity?
What is the clinical presentation?

A
  • Use of high oxygen conc, very LBW (<1.5kg), premature babies <32w
  • Plus disease describes other findings like tortuous vessels + hazy vitreous humour
107
Q

RETINOPATHY

What is the management of retinopathy of prematurity?

A
  • Regular eye screening by ophthalmologist for susceptible preterm infants (<1.5kg or <32w), must visualise all retinal areas
  • Transpupillary laser photocoagulation to halt + reverse neovascularisation
108
Q

NEONATAL CONJUNCTIVITIS
What is neonatal conjunctivitis?
What is the management?

A
  • Common starting day 3–4
  • Usually just cleaning with water or saline
  • More troublesome discharge or redness of eye may be staph/strep so topical Abx eye ointment like neomycin
109
Q

NEONATAL CONJUNCTIVITIS
In terms of neonatal conjunctivitis, how would…

i) gonococcal infection
ii) chlamydia infection

present and what is the management of both?

A

i) Purulent discharge, conjunctival injection, eyelid swelling, within 48h
– Gram stain, IV ceftriaxone + cleanse frequently (can lose vision)
ii) Purulent discharge, eyelid swelling, 1-2w
– Immunofluorescent staining, PO erythromycin for 2w

110
Q

SIDS

What are some major risk factors for SIDS?

A
  • Baby sleeping prone
  • Parental smoking (during pregnancy or in same room)
  • LBW + prematurity
  • Sharing a bed
  • Hyperthermia (over wrapping) or head covering (blanket moving)
111
Q

SIDS

What are some other risk factors for SIDS?

A
  • M>F
  • Low socioeconomic status
  • Infant pillow use
  • Maternal drug use
112
Q

SIDS

What are some protective factors from SIDS?

A
  • Breastfeeding
  • Room (NOT bed) sharing
  • Use of dummies
113
Q

SIDS

What is the management of SIDS?

A
  • Following cot death screen siblings for sepsis + inborn errors of metabolism
  • Infants sleep on backs, ‘feet-to-foot’ position
  • Do not smoke near them
  • Bedroom for first 6m
114
Q

NUTRITION

What are the advantages of breastfeeding?

A
  • Free
  • Helps bonding
  • Lactational amenorrhoea
  • Reduces risk of NEC in preterm infants + SIDS
  • Antibodies to protect neonate against infection
  • Reduced maternal risk of breast + ovarian cancer
115
Q

NUTRITION

What are the disadvantages of breastfeeding?

A
  • Breast milk jaundice
  • Unknown intake so ?eating adequately
  • Discomfort for mother
  • Transmission of drugs or infections to baby
  • Insufficient vitamin D + K (reason for vitamin K IM injection at birth)
116
Q

ROSEOLA INFANTUM
What is roseola infantum?
How is it spread?

A
  • Caused by human herpes virus 6+7

- Classically most children infected by age 2, often from oral secretions of a family member

117
Q

COMMON KNEE ISSUES
What is chondromalacia patellae?
How does it present?
What is the management

A
  • Softening of the cartilage of the patellar, common in teenage girls
  • Anterior knee pain on walking up/downstairs + rising from prolonged sitting
  • Usually responds to physiotherapy
118
Q

COMMON KNEE ISSUES
What is…

i) osteochondritis dissecans?
ii) patellar subluxation?

A

i) Pain after exercise with intermittent swelling

ii) Medial knee pain due to lateral subluxation of the patellar, knee may give way

119
Q

ACHONDROPLASIA

What is the clinical presentation of achondroplasia?

A
  • Short stature from marked shortening of limbs + fingers
  • Large head with frontal bossing + depression of nasal bridge
  • ‘Trident’ hands + marked lumbar lordosis
120
Q

ACHONDROPLASIA

What are some complications of achondroplasia?

A
  • Foramen magnum stenosis > cervical cord compression + hydrocephalus
  • Recurrent otitis media (cranial abnormalities)
  • Obstructive sleep apnoea
  • Obesity
121
Q

HEAD LICE

What is the management of headlice?

A
  • Dimeticone 4% or malathion 0.5% lotions, leave overnight then wash off (repeat 7d later to kill any head lice hatched since)
  • Special fine combs + wet combing (bug-busting) every 3–4d for 2w
122
Q

SCABIES

What is scabies?

A
  • Infestation of mites (Sarcoptes scabiei) that burrow under skin + lay eggs
  • Can take 8w for Sx (delayed type 4 hypersensitivity reaction)
123
Q

SCABIES
What is the clinical presentation of scabies?
Classic location?
When would you suspect it?

A
  • Very itchy burrows, papules + vesicles (may be track marks from mites)
  • Classic location between finger webs, can spread to whole body
  • Suspect if child + family itching
124
Q

HYPERTHYROIDISM

What is the management of hyperthyroidism?

A
  • 1st line = carbimazole or propylthiouracil (either dose titration or block + replace with thyroxine)
  • Radioiodine can be used too
  • May need subtotal thyroidectomy to give permanent remission
  • Beta-blockers for symptomatic relief
125
Q

THREADWORMS
What causes threadworms?

A

Enterobius vermicularis

126
Q

THREADWORMS
How is it treated?

A

Single dose mebendazole + hygiene measures for WHOLE family

C TO REVISE - PHASE 3A (11 decks)

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