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Y4 Paediatrics > ILOs 1 > Flashcards

ILOs 1 Flashcards

1
Q

Give some causes of global developmental delay

A

Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders

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2
Q

Give some causes of gross motor delay

A

Cerebral palsy
Ataxia
Myopathy
Spina bifida
Visual impairment

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3
Q

Give some causes of fine motor delay

A

Dyspraxia
Cerebral palsy
Muscular dystrophy
Visual impairment

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4
Q

Give some causes of speech and language delay

A

Specific social circumstances, for example exposure to multiple languages or siblings that do all the talking
Hearing impairment
Learning disability
Autism
Cerebral palsy
Neglect

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5
Q

Give some causes of social delay

A

Emotional and social neglect
Parenting issues
Autism

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6
Q

What are the main types of pneumothorax seen in children?

A

spontaneous pneumothorax:

  1. primary spontaneous pneumothorax (PSP): Occurs without underlying lung disease, often in tall, thin, young individuals, associated with the rupture of subpleural blebs or bullae
  2. secondary spontaneous pneumothorax (SSP): Occurs in patients with pre-existing lung disease, such as asthma, CF and pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor

traumatic pneumothorax

iatrogenic pneumothorax

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7
Q

What are the sxs and signs of a simple pneumothorax?

A

Symptoms tend to come on suddenly:
dyspnoea
pleuritic chest pain

Signs
hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia

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8
Q

What is a tension pneumothorax?

A

a severe pneumothorax

occurs when a one way valve is created between the lung and the pleura, which leads to an accumulation of air within the pleural cavity = increase in intrathoracic pressure

results in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse

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9
Q

What are the signs of tension pneumothorax?

A

tracheal deviation away from the side of the pneumothorax
hypotension, tachycardia, tachypnoea
quiet heart sounds
cyanosis

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10
Q

Management in primary pneumothorax without shortness of breath, and <2cm in size?

A

discharge and review

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11
Q

Management of pneumothorax with a rim of air >2cm or clinically short of breath (SOB)?

A

Chest drain insertion

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12
Q

What is the safe triangle for chest drain insertion?

A

The triangle is located in the mid axillary line of the 5th intercostal space.

It is bordered by:
Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla.

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13
Q

How can you find out a chest drain is in the right place without doing a CXR?

A

Chest drain swinging: water level rises on inspiration, falls on expiration

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14
Q

How should a suspected tension pneumothorax be investigated and managed?

A

A tension pneumothorax should not be investigated if suspected but should be immediately decompressed with a needle (14G needle, 2nd intercostal space)

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15
Q

How can poisoning of unknown origin be investigated?

A

can consult NPIS or TOXBASE for advice

Blood tests, such as toxicological investigations, FBC, U&Es, LFTs, glucose, clotting and arterial blood gases

urine drug screen

ECG

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16
Q

How can poisoning of unknown origin be managed?

A

can consult NPIS or TOXBASE for advice

Activated charcoal can bind to the poison and prevent absorption - up to 1 hour after ingestion

Alkalinisation of the urine for salicylate poisoning

Haemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, and sodium valproate

Antidotes (if available) may be given for certain poisons

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17
Q

Give some key clinical features of malnutrition in children

A

High susceptibility to infections
Slow or poor wound healing
bradycardia, hypotension, and hypothermia
Depleted subcutaneous fat stores
Low skeletal muscle mass

In children, other indicators of undernutrition include:
Wasting: low weight for height
Stunting: low height for age
Underweight: low weight for age

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18
Q

Give some complications of malnutrition

A

Impaired immunity (increased risk of infections)
Poor wound healing
Growth restriction in children
Unintentional weight loss, specifically the loss of muscle mass
Multi-organ failure
Death

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19
Q

What signs should you look for on examination of a malnourished child?

A

shock: lethargic or unconscious; with cold hands, slow capillary refill (> 3 s), or weak (low volume), rapid pulse and low blood pressure
signs of dehydration e.g. decreased skin turgor
severe palmar pallor
bilateral pitting oedema
eye signs of vitamin A deficiency

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20
Q

What is Marasmus?

A

overt loss of adipose tissue and muscle as a result of total calorie insufficiency

children appear emaciated, weak and lethargic, and have associated bradycardia, hypotension, and hypothermia

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21
Q

What is Kwashiorkor?

A

‘the sickness of the weaning’ - often occurs on cessation of breastfeeding
severe protein deficiency with fair caloric intake
hypoalbuminaemia may cause bilateral pitting oedema and distended abdomen due to ascites

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22
Q

How should you assess a malnourished child?

A

detailed dietary history and physical examination

anthropometric measurements (including weight, length, and head circumference in younger children)

skinfold thickness and mid-upper-arm circumference (MUAC)

U&Es, LFTs, serum albumin levels

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23
Q

How should you manage a malnourished child?

A

treat hypoglycaemia
treat / prevent any hypothermia
rehydrate
refeed slowly with regular refeeding bloods

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24
Q

How should you dx and tx hypoglycaemia in a child?

A

take capillary BM - blood glucose below < 3 mmol/litre = hypoglycaemia

Give 50 ml of 10% glucose solution orally or by nasogastric tube
If the child is unconscious, treat with IV 10% glucose at 5 ml/kg

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25
Q

How can you dx and mx hypothermia in a child?

A

If the axillary temperature is < 35 °C or does not register on a normal thermometer, assume hypothermia. When a low-reading thermometer is available, rectal temperature (< 35.5 °C) confirms hypothermia

Re-warm the child: Make sure the child is clothed (especially the head); cover with a warmed blanket and place a heater or lamp nearby, or put the child on the mother’s bare chest or abdomen (skin-to-skin)

treat for potential hypoglycaemia and infection

Feed immediately and again every 2 hours

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26
Q

What atrial septal defects may be seen in children?

A

Ostium secondum : septum secondum fails to fully close, leaving a hole in the wall

Patent foramen ovale: foramen ovale fails to close (although this not strictly classified as an ASD)

Ostium primum: septum primum fails to fully close, leaving a hole in the wall. This tends to lead to atrioventricular valve defects

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27
Q

What are the potential complications of ASDs in children?

A

Stroke in the context of venous thromboembolism
Atrial fibrillation or atrial flutter
Pulmonary hypertension and right sided heart failure
Eisenmenger syndrome - reversal of left to right shunt due to pulmonary hypertension

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28
Q

What may be heard on auscultation of an ASD?

A

mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound (doesn’t change with inspiration or expiration)

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29
Q

How may ASDs present in children?

A

may be picked up on antenatal screening / newborn examination

may be symptomatic:
Shortness of breath
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure or stroke

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30
Q

How can ASDs be managed?

A

should be referred to a paediatric cardiologist for ongoing management

If the ASD is small and asymptomatic, watching and waiting can be appropriate

can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery

anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke

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31
Q

What conditions are commonly associated with VSDs in children?

A

Down’s Syndrome and Turner’s Syndrome

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32
Q

What is the usual direction of flow of blood in a VSD? What may this cause?

A

from left to right

patient remains acyanotic but too much blood flow into the lungs may cause right sided overload / right heart failure

pulmonary hypertension may cause reversal of the shunt (Einsenmengers syndrome)

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33
Q

What sxs may VSDs present with?

A

Poor feeding
Dyspnoea
Tachypnoea
Failure to thrive

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34
Q

What may be heard on auscultation of the chest of a patient with a VSD?

A

pan-systolic murmur more prominently heard at the left lower sternal border in the third and fourth intercostal spaces

may be a systolic thrill on palpation

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35
Q

How should VSDs be managed?

A

referred to paediatric cardiologist

small VSDs with no symptoms or evidence of pulmonary hypertension / HF can be watched and often close spontaneously

can be corrected surgically using a transvenous catheter closure via the femoral vein or open heart surgery

increased risk of infective endocarditis in patients with a VSD =antibiotic prophylaxis should be considered during surgical procedures

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36
Q

Give some symptoms of aortic stenosis

A

fatigue, shortness of breath, dizziness and fainting

sxs typically worse on exertion as the outflow from the left ventricle cannot keep up with demand

severe aortic stenosis will present with heart failure within months of birth.

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37
Q

Describe the murmur heard in aortic stenosis

A

ejection systolic murmur heard loudest at the aortic area (second intercostal space, right sternal border)

It has a crescendo-decrescendo character and radiates to the carotids

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38
Q

Besides a murmur, what might you find on examination of aortic stenosis?

A

Ejection click just before the murmur
Palpable thrill during systole
Slow rising pulse and narrow pulse pressure

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39
Q

How can aortic stenosis be investigated and managed?

A

gold standard for dx is an echocardiogram

monitoring with regular echos, exercise testing and ECGs

Mx options:
Percutaneous balloon aortic valvoplasty
Surgical aortic valvotomy
Valve replacement

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40
Q

Give some complications of aortic stenosis

A

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

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41
Q

What conditions may be associated with congenital pulmonary valve stenosis?

A

Tetralogy of Fallot
William syndrome
Noonan syndrome
Congenital rubella syndrome

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42
Q

Give some signs of pulmonary stenosis found on examination

A

Ejection systolic murmur heard loudest at the pulmonary area (second intercostal space, left sternal border)
Palpable thrill in the pulmonary area
Right ventricular heave due to right ventricular hypertrophy
Raised JVP with giant a waves

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43
Q

How should pulmonary stenosis be investigated and managed?

A

ix = echo

mild = watch and wait

symptomatic = balloon valvuloplasty via a venous catheter
(femoral vein > IVC > right side of the heart > pulmonary valve)

44
Q

Allergic rhinitis is a condition caused by an IgE-mediated type 1 hypersensitivity reaction, where environmental allergens cause an allergic inflammatory response in the nasal mucosa.

How can it be classified?

A

Seasonal, for example hay fever
Perennial (year round), for example house dust mite allergy
Occupational, associated with the school or work environment

45
Q

Presentation of allergic rhinitis?

A

Runny, blocked and itchy nose
Sneezing
Itchy, red and swollen eyes
personal / family hx of atopy

46
Q

How can allergic rhinitis be managed?

A

Avoid the trigger : hoovering, changing pillows regularly and good ventilation of the home for dust mite allergy; staying indoors during high pollen counts for hay fever; minimising contact with pets that trigger

Non-sedating antihistamines e.g. cetirizine, loratadine and fexofenadine

Nasal corticosteroid sprays such as fluticasone and mometasone

Referral to paediatric allergy specialist if unmanageable

47
Q

Good technique for using nasal spray?

A

Hold the spray in the left hand when spraying into the right nostril and vice versa. Aim to spray slightly outward, away from the nasal septum. Do NOT sniff at the same time as spraying, as this sends the mist straight to the back of the throat.

48
Q

What is urticaria? How can it be managed?

A

local or generalised superficial swelling of the skin
pale, pink raised skin, also called ‘hives’ or ‘wheals’
pruritic

mx:
non-sedating antihistamines are first-line
prednisolone is used for severe or resistant episodes

49
Q

Give some causes of acute urticaria

A

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

50
Q

Give some causes of AKI

A

prerenal: hypovolaemia secondary to diarrhoea/vomiting, sepsis

renal: glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN)
rhabdomyolysis

post-renal: kidney stone in ureter or bladder

51
Q

Give some sxs and signs of AKI

A

reduced urine output
pulmonary and peripheral oedema
arrhythmias (deranged electrolytes)
features of uraemia (e.g. pericarditis or encephalopathy)

52
Q

What causes ARPCKD?

A

mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6

53
Q

How does ARPCKD present?

A

oligohydramnios and polycystic kidneys seen on antenatal scans

lack of amniotic fluid can lead to Potter syndrome: dysmorphic features such as low set ears, a flat nasal bridge, skeletal abnormalities, pulmonary hypoplasia, and respiratory failure shortly after birth

54
Q

What complications may children with ARPCKD face in later life?

A

Liver failure and portal htn due to liver fibrosis
Progressive renal failure
Hypertension due to renal failure
Chronic lung disease

55
Q

What is Multicystic dysplastic kidney (MCDK)?

A

where one of the baby’s kidneys is made up of many cysts while the other kidney is normal, normally diagnosed on antenatal ultrasound scans

often the cystic kidney will atrophy and disappear before 5 years of age

having a single kidney can put the person at risk of UTI, hypertension and CKD

56
Q

What is nephritis?

A

inflammation within the nephrons of the kidneys. It causes:
Reduction in kidney function
Haematuria
Proteinuria

57
Q

What are the two most common causes of nephritis in children?

A

post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease)

58
Q

How does post-streptococcal glomerulonephritis present? Mx?

A

occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis caused by Streptococcus pyogenes

may be hx of tonsillitis, positive throat swab results or anti-streptolysin antibody titres found on blood test

supportive mx, may use antihypertensive medications and diuretics for complications

59
Q

What will you see on histological examination of renal biopsy for Berger’s disease?

A

IgA deposits and glomerular mesangial proliferation

60
Q

Outline the presentation and mx of IgA nephropathy (Berger’s disease)?

A

Frank haematuria following upper resp tract infection in young person
related to Henoch-Schonlein Purpura, which is an IgA vasculitis

Mx: supportive treatment of the renal failure and immunosuppressant medications such as steroids and cyclophosphamide to slow the progression

61
Q

What is Haemolytic uraemic syndrome (HUS)?

A

thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from either E. coli or Shigella

classic triad of:
Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)

62
Q

How does HUS present?

A

Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:

Fever
Abdominal pain
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion, lethargy

63
Q

How does HUS present on investigation?

A

FBC (thrombocytopenia), U&Es (deranged), creatinine
peripheral blood smear = broken red cells
blood culture to rule out septicaemia

64
Q

How should HUS be managed?

A

hospital admission and supportive management with treatment of:

Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

65
Q

How does oral candidiasis present in children?

A

white or creamy patches on the tongue, inner cheeks, gums, tonsils, or roof of the mouth. These patches may be painful or cause discomfort while eating or drinking = reduced feeding / avoidance behaviours

66
Q

How can oral candidiasis in kids be managed?

A

Topical antifungals are considered first-line therapy for mild-to-moderate cases of oral candidiasis:

Nystatin suspension
Miconazole gel

67
Q

Cellulitis is a bacterial infection of the dermis and subcut tissues most commonly caused by infection with Streptococcus pyogenes.

How does it present?

A

commonly occurs on the shins, usually unilateral

erythema (generally well-defined margins but some cases may present with diffuse erythema)

blisters and bullae may be seen

swelling

systemic upset: fever, malaise, nausea

68
Q

How is cellulitis diagnosed and managed?

A

clinical dx - no ix required

oral flucloxacillin as first-line treatment for mild/moderate cellulitis
oral clarithromycin or doxycycline if penicillin allergic

69
Q

Conjunctivitis is the most common eye problem presenting to primary care. It is characterised by sore, red eyes associated with a sticky discharge.

How does it present differently if bacterial or viral?

A

Bacterial conjunctivitis
Purulent discharge
Eyes may be ‘stuck together’ in the morning

Viral conjunctivitis
Serous discharge
Recent URTI
Preauricular lymph nodes

70
Q

How can infective conjunctivitis be managed?

A

normally a self-limiting condition that usually settles without treatment within 1-2 weeks

topical antibiotic therapy e.g. Chloramphenicol drops (given every 2-3 hourly initially)

advice should be given not to share towels

school exclusion is not necessary

71
Q

How can herpes simplex infection present?

A

primary infection: may present with a severe gingivostomatitis
cold sores
painful genital ulceration

72
Q

How can herpes simplex infection be managed?

A

gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
cold sores: topical aciclovir
genital herpes: oral aciclovir

73
Q

Falciparum malaria is the commonest, and most severe, type of malaria. Describe the key presenting features

A

Feature of severe malaria:
hypoglycaemia
acidosis
temperature > 39 °C
severe anaemia
schizonts on a blood film
parasitaemia > 2%

74
Q

What are the major complications of severe falciparum malaria?

A

hypoglycaemia
cerebral malaria: seizures, coma
acute renal failure
acute respiratory distress syndrome (ARDS)
DIC

shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse

75
Q

First line tx for uncomplicated falciparum malaria?

A

WHO guidelines recommend artemisinin-based combination therapies (ACTs) as first-line therapy

examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine

76
Q

First line tx for complicated falciparum malaria?

A

a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state
- IV artesunate or IV quinine dihydrochloride

if parasite count > 10% then exchange transfusion should be considered

77
Q

What is the most common cause of non-falciparum malaria?

A

Plasmodium vivax

78
Q

How does non-falciparum malaria present?

A

general features of malaria: fever, headache, myalgia, anaemia, hepatosplenomegaly, jaundice

Plasmodium vivax/ovale: cyclical fever every 48 hours, hypnozoite stage so may relapse following treatment.

Plasmodium malariae: cyclical fever every 72 hours, associated with nephrotic syndrome.

79
Q

How should non-falciparum malaria be treated?

A

in areas which are known to be chloroquine-sensitive then WHO recommend either chloroquine
in areas which are known to be chloroquine-resistant an ACT should be used

patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse

80
Q

How is a diagnosis of malaria made?

A

malaria blood film - sent in an EDTA bottle (red)
Need 3 samples over 3 consective days to exclude malaria due to 48 hour lifecyle

can also do:
FBC, U&Es, LFTs, glucose, coagulation
CT head

81
Q

What bacteria commonly cause acute otitis media?

A

Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis

82
Q

How may otitis media present?

A

otalgia - children may tug or rub their ear
fever, coryza
hearing loss
ear discharge may occur if the tympanic membrane perforates

83
Q

Findings on otoscopy for otitis media?

A

bulging tympanic membrane → loss of light reflex
opacification or erythema of the tympanic membrane
perforation with purulent otorrhoea

84
Q

How should otitis media be managed?

A

generally a self-limiting condition that does not require an antibiotic prescription, only analgesia

abx if:
Symptoms lasting more than 4 days
Systemically unwell
Younger than 2 years with bilateral otitis media
Perforation and/or discharge in the canal

5-7 day course of amoxicillin is first-line

85
Q

Complications of otitis media?

A

mastoiditis
meningitis
brain abscess
facial nerve paralysis

86
Q

Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the orbital septum, within the orbit. What are the risk factors?

A

Childhood (mean age of hospitalisation 7-12 yrs)
Lack of Hib vaccination
Previous sinus infection
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection

87
Q

How may orbital cellulitis present?

A

Redness and swelling around the eye
Eyelid oedema and ptosis
Proptosis
Severe ocular pain
Ophthalmoplegia/pain with eye movements
Visual disturbance

88
Q

How can you differentiate between orbital and peri-orbital (pre-septal) cellulitis?

A

reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis

89
Q

How should orbital cellulitis be investigated?

A

Complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema

FBC– WBC elevated, raised inflammatory markers

Blood culture and swab (most common bacterial causes – Streptococcus, Staph aureus, HiB)

CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis

90
Q

How should orbital cellulitis be managed?

A

admission to hospital for IV antibiotics

91
Q

What ix can be done for children with recurrent infections?

A

FBC
Immunoglobulins: B cell disorders
Complement proteins: complement disorders

Antibody responses to vaccines, specifically pneumococcal and haemophilus vaccines
HIV test

Chest x-ray for scarring from previous chest infections

Sweat test for CF
CT chest for bronchiectasis

92
Q

Severe combined immunodeficiency (SCID) is the most severe condition causing immunodeficiency, with absent or dysfunctioning T and B cells. How does it present?

A

Persistent severe diarrhoea
Failure to thrive
Opportunistic infections e.g. severe and later fatal chickenpox, PJP and cytomegalovirus
Unwell after live vaccinations such as the BCG, MMR and nasal flu vaccine
Omenn syndrome

93
Q

What is the genetic cause of most cases of SCID?

A

mutation in common gamma chain on the X chromosome that codes for interleukin receptors on T and B cells

X-linked recessive inheritance

94
Q

What is Omenn syndrome?

A

rare cause of SCID, autosomal recessive inheritance

abnormally functioning and deregulated T cells that attack the tissues in the fetus

erythroderma
alopecia
Diarrhoea, failure to thrive
lymphadenopathy
hepatosplenomegaly

95
Q

How can SCID be managed?

A

treating underlying infections
immunoglobulin therapy
sterile environment
avoiding live vaccines
haematopoietic stem cell transplantation

96
Q

What is Selective Immunoglobulin A Deficiency?

A

most common immunoglobulin deficiency

patients have low levels of IgA and normal levels of IgG and IgM

tendency to recurrent mucous membrane infections, such as LRTIs

97
Q

What is Common variable immunodeficiency?

A

genetic mutation in the genes coding for components of B cells = deficiency in IgG and IgA

recurrent respiratory tract infections
unable to develop immunity to infections or vaccinations
prone to immune disorders such as RA and cancers such as non-Hodgkins lymphoma

98
Q

What is X-linked agammaglobulinaemia?

A

X-linked recessive condition

results in abnormal B cell development and deficiency in all classes of immunoglobulins

99
Q

What is DiGeorge syndrome?

A

22q11.2 deletion syndrome
An underdeveloped thymus gland = inability to create functional T cells

C – Congenital heart disease
A – Abnormal facies (characteristic facial appearance)
T – Thymus gland incompletely developed
C – Cleft palate
H – Hypoparathyroidism and resulting Hypocalcaemia
22nd chromosome affected

100
Q

Important mx step in patients with complement deficiencies?

A

Vaccination against encapsulated organisms

101
Q

Rubella, also known as German measles, is a viral infection caused by the togavirus. What features does it present with?

A

prodrome, e.g. low-grade fever
rash: maculopapular, initially on the face before spreading to the whole body, usually fades by the 3-5 day
lymphadenopathy: suboccipital and postauricular

102
Q

Complications of rubella?

A

arthritis
encephalitis
myocarditis
thrombocytopaenia

103
Q

What is the FEVER PAIN criteria for diagnosis of tonsilitis?

A

Fever over 38°C
Purulence (pharyngeal/tonsillar exudate).
Attend rapidly (3 days or less)
severely Inflamed tonsils
No cough or coryza

0-1 = no abx
2-3 = consider abx
4-5 = abx almost definitely indicated

104
Q

What abx are given if indicated in tonsillitis ?

A

if antibiotics are indicated then either phenoxymethylpenicillin or erythromycin (if the patient is penicillin allergic) should be given

7 or 10 day course should be given

105
Q

Potential complications of tonsillitis?

A

Peritonsillar abscess or neck abscess
Acute otitis media
Acute sinusitis
Acute post-streptococcal glomerulonephritis
Streptococcal toxic shock syndrome
Scarlet fever
Acute rheumatic fever

106
Q

How does staphylococcal toxic shock syndrome present?

A

fever
hypotension
diffuse erythematous rash
desquamation of rash, especially of the palms and soles

involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)

107
Q

How is staphylococcal toxic shock syndrome managed?

A

removal of infection focus (e.g. retained tampon)
IV fluids
IV antibiotics

Y4 Paediatrics (17 decks)

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