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Y4 Paediatrics > ILOs 2 > Flashcards

ILOs 2 Flashcards

1
Q

How is TB investigated?

A

The Mantoux test is the main technique used to screen for latent tuberculosis. (interferon-gamma blood test may be used if risk of false negatives)

Chest x-ray
upper lobe cavitation is the classical finding of reactivated TB
bilateral hilar lymphadenopathy

Sputum smear
3 specimens are needed, rapid and inexpensive
stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain)
all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)

Nucleic acid amplification tests (NAAT)
allows rapid diagnosis (within 24-48 hours)
more sensitive than smear but less sensitive than culture

Sputum culture
the GOLD STANDARD investigation
more sensitive than a sputum smear and nucleic acid amplification tests
can assess drug sensitivities
can take 1-3 weeks

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2
Q

How is active TB managed?

A

Initial phase - first 2 months (RIPE)
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

Continuation phase - next 4 months
Rifampicin
Isoniazid

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3
Q

How is latent TB managed?

A

latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

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4
Q

Adverse effects of TB drugs?

A

rifampicin:
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

isoniazid:
liver enzyme inhibitor
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis

pyrazinamide:
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

ethambutol:
optic neuritis: check visual acuity before and during treatment

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5
Q

Presentation of TB?

A

Gradually worsening symptoms

Lethargy
Pyrexia and night sweats
Weight loss
Cough +/- haemoptysis
Lymphadenopathy
Erythema nodosum

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6
Q

What are Viral Exanthemas?

A

An “exanthem” is an eruptive widespread rash
Originally there were six “viral exanthemas”:

First disease: Measles
Second disease: Scarlet Fever
Third disease: Rubella (AKA German Measles)
Fourth disease: Dukes’ Disease
Fifth disease: Parvovirus B19
Sixth disease: Roseola Infantum

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7
Q

How can parvovirus B19 present?

A

asymptomatic

pancytopaenia in immunosuppressed patients

aplastic crises e.g. in sickle-cell disease
parvovirus B19 suppresses erythropoiesis for about a week

hydrops fetalis
parvovirus B19 in pregnant women can cross the placenta

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8
Q

How does parvovirus B19 cause hydrops fetalis? Mx?

A

parvovirus B19 in pregnant women can cross the placenta in pregnant women
this causes severe anaemia due to viral suppression of fetal erythropoiesis → heart failure secondary to severe anaemia → the accumulation of fluid in fetal serous cavities (e.g. ascites, pleural and pericardial effusions)
treated with intrauterine blood transfusions

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9
Q

What is the most common causative organism for viral gastroenteritis in kids?

A

rotavirus

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10
Q

Viral gastroenteritis is a self-limiting condition which lasts <14 days. The most common symptoms include:

A

Acute diarrhoea: passage of 3 or more stools per day, for a duration of less than 14 days
Watery and non-bloody
blood in the stool = suspicion of Shiga-toxin producing E-coli or Campylobacter infection

Vomiting

Mild fever : >38°C in children under 3 months old should raise suspicion of bacterial pathology
Any child under 3 months old with a temperature >38°C should be urgently admitted to hospital

Abdominal pain

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11
Q

What can cause anaemia in infancy?

A

Physiologic anaemia of infancy causes most cases of anaemia in infancy.

The other causes of anaemia in infants are:
Anaemia of prematurity
Blood loss
Haemolysis
Twin-twin transfusion

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12
Q

What can cause haemolysis in infancy?

A

Haemolytic disease of the newborn (ABO or rhesus incompatibility)
Hereditary spherocytosis
G6PD deficiency

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13
Q

What causes physiologic anaemia of infancy?

A

There is a normal dip in haemoglobin around 6-9 weeks of age in healthy term babies. High oxygen delivery to the tissues caused by the high haemoglobin levels at birth cause negative feedback. Production of erythropoietin by the kidneys is suppressed and there is reduced production of Hb by the bone marrow.

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14
Q

What causes anaemia of prematurity?

A

Less time in utero receiving iron from the mother
Red blood cell creation cannot keep up with the rapid growth in the first few weeks
Reduced erythropoietin levels
Blood tests remove a significant portion of their circulating volume

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15
Q

What causes haemolytic disease of the newborn?

A

When a mother is Rhesus negative and the foetus is Rhesus positive, the mother’s immune system will recognise the rhesus D antigen of the foetus as foreign and produce antibodies (sensitisation).

During subsequent pregnancies, the mothers anti-D antibodies can cross the placenta. If that foetus is rhesus positive, these antibodies attach themselves to the red blood cells of the fetus and causes the immune system of the fetus to attack = haemolysis, causing anaemia and high bilirubin levels

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16
Q

How can haemolytic disease of the newborn be investigated?

A

direct Coombs test (DCT) can be used to check for immune haemolytic anaemia

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17
Q

Give some sxs of anaemia

A

Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions

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18
Q

Give some signs of anaemia

A

Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate

Signs of specific causes of anaemia:
Koilonychia: iron deficiency
Angular chelitis :iron deficiency
Atrophic glossitis:iron deficiency
Brittle hair and nails : iron deficiency
Jaundice: haemolytic anaemia
Bone deformities: thalassaemia

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19
Q

How can anaemia in children be investigated?

A

FBC for haemoglobin and MCV
Reticulocyte count
Bilirubin (raised in haemolysis)
Ferritin (iron deficiency)
B12 and folate

Blood film

Direct Coombs test (autoimmune haemolytic anaemia)

Haemoglobin electrophoresis (haemoglobinopathies)

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20
Q

What can cause hyposplenism?

A

splenectomy
sickle-cell
coeliac disease, dermatitis herpetiformis
Graves’ disease
SLE

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21
Q

What may be seen on a blood film of a hyposplenic patient?

A

Howell-Jolly bodies
siderocytes

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22
Q

What are the risk factors for developing lymphoma?

A

EBV
Immunosuppression
Solid organ transplant
Prev cancer tx

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23
Q

How may lymphoma present?

A

Weight loss, Night sweats, Fevers (‘B’ sxs, associated with worse prognosis)

Non-tender lymphadenopathy is the most common examination finding
Mediastinal lymphadenopathy may present with cough, wheeze or other difficulty in breathing, and occasionally SVC obstruction or airway compromise

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24
Q

ddx for lymphoma?

A

reactive lymphadenopathy
leukaemia
metastatic cancer

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25
Q

How can lymphoma be investigated?

A

FBC
U&Es: tumour lysis syndrome can occur before treatment begins in lymphomas with rapid cell turnover
LDH (lactate dehydrogenase) levels are usually elevated

Imaging
USS
CXR may be required if there are symptoms of mediastinal node involvement.
A full body CT to determine extent of disease

Biopsy
Lymph node biopsy

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26
Q

How can lymphoma be staged?

A

Lugano Classification

Stage 1: single group of lymph nodes or a single organ
Stage 2: 2 or more groups of lymph nodes or organs on the same side of the diaphragm
Stage 3: lymph nodes or organs on both sides of the diaphragm
Stage 4: diffuse involvement of lymph nodes and organs such as the liver and bones

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27
Q

Treatment if lymphoma is with chemotherapy and possibly radiotherapy. Describe the prognosis and potential complications

A

The majority of children will recover completely, with Hodgkin’s lymphoma carrying a more favourable prognosis than non-Hodgkin’s lymphoma

Complications:
tumour lysis syndrome
neutropenia
alopecia
sub-fertility

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28
Q

Outline the pathophysiology of sickle cell disease

A

autosomal recessive condition affecting the gene for beta-globin on chromosome 11

One abnormal copy of the gene = sickle-cell trait
Two abnormal copies = sickle-cell disease

abnormal variant called haemoglobin S (HbS) results in sickle-shaped red blood cells.

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29
Q

Give some complications of sickle cell disease

A

Anaemia
Increased risk of infection
CKD
Sickle cell crises
Acute chest syndrome
Stroke
Avascular necrosis in large joints such as the hip
Pulmonary hypertension
Gallstones
Priapism (painful and persistent penile erections)

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30
Q

What is sickle cell crisis?

A

when the flow of blood is blocked to an area because the sickled cells have become stuck in the blood vessel- often very painful

can occur spontaneously or triggered by dehydration, infection, stress or cold weather

supportive mx

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31
Q

What is acute chest syndrome?

A

complication of sickle cell when the vessels supplying the lungs become clogged with red blood cells

presents with fever, shortness of breath, chest pain, cough and hypoxia

CXR will show pulmonary infiltrates

medical emergency!!!

32
Q

How can acute chest syndrome be managed?

A

Analgesia
IV fluids
Antibiotics if indicated
Blood transfusions

Incentive spirometry using a machine that encourages effective and deep breathing

Respiratory support with oxygen, non-invasive ventilation or mechanical ventilation

33
Q

What is the general mx of sickle cell disease?

A

Avoid triggers for crises, such as dehydration
Up-to-date vaccinations
Antibiotic prophylaxis to protect against infection, typically with penicillin V (phenoxymethylpenicillin)
Hydroxycarbamide (stimulates HbF)
Crizanlizumab
Blood transfusions for severe anaemia
Bone marrow transplant can be curative

34
Q

How should a child with newly diagnosed T1DM be investigated?

A

FBC, U&Es
blood glucose and HbA1c

Thyroid function tests and thyroid peroxidase antibodies (TPO) to test for associated autoimmune thyroid disease

Tissue transglutaminase (anti-TTG) antibodies for associated coeliac disease

Insulin antibodies, anti-GAD antibodies and islet cell antibodies

35
Q

How should T1DM in kids be managed?

A

basal bolus SC insulin regime
long acting insulin, such as “Lantus”, typically in the evening, short acting insulin, such as “Actrapid”, usually three times a day before meals

or insulin pump (Tethered / Patch pump)

Monitoring dietary carbohydrate intake
Monitoring blood sugar levels on waking, at each meal and before bed
Monitoring for and managing complications

36
Q

What are the advantages and disadvantages of insulin pumps ?

A

advantages: better blood sugar control, more flexibility with eating and less injections

disadvantages: difficulties learning to use the pump, having it attached at all times, blockages in the infusion set and a small risk of infection

37
Q

Sxs of hypoglycaemia in children?

A

hunger, tremor, sweating, irritability, dizziness and pallor
more severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated

38
Q

Mx of hypoglycaemia in children?

A

rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits or toast

oral glucose not safe = IV dextrose (2mg/kg bolus followed by a 5mg/kg/hour infusion)
or intramuscular glucagon

39
Q

Give some complications of T1DM

A

Macrovascular Complications:
Coronary artery disease
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

Microvascular Complications:
Peripheral neuropathy
Retinopathy
Nephropathy

Infection Related Complications
UTIs
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis

40
Q

How may DKA present?

A

Polyuria, Polydipsia, WL (poor diabetic control)
Nausea and vomiting
Dehydration and hypotension
Altered consciousness
Acetone smell to their breath

41
Q

How can DKA be diagnosed?

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

42
Q

How should DKA be managed?

A

Correct dehydration evenly over 48 hours -correcting it faster increases the risk of cerebral oedema

Give a fixed rate insulin infusion

Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l
Add potassium to IV fluids and monitor serum potassium closely

Treat underlying triggers

Monitor for signs of cerebral oedema
Monitor glucose, ketones and pH to assess their progress and determine when to switch to SC insulin

43
Q

Congenital hypothyroidism is where the child is born with an underactive thyroid gland.

It can be the result of an underdeveloped thyroid gland (dysgenesis) or a fully developed gland that does not produce enough hormone (dyshormonogenesis).

How does it present?

A

screened for on the newborn blood spot screening test. Where it is not picked up a birth, patients can present with:

Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development

44
Q

What is the most common cause of acquired hypothyroidism in kids? How does it present?

A

autoimmune thyroiditis, also known as Hashimoto’s thyroiditis (association with T1DM and coeliac disease)

antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies

Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss

45
Q

How is Hashimoto’s thyroiditis managed in kids?

A

managed by paediatric endocrinology

IX: full thyroid function blood tests (TSH, T3 and T4), thyroid ultrasound and thyroid antibodies.

Levothyroxine orally OD

46
Q

Which children should be given Vit D supplementation?

A

all children aged 6 months - 5 years

babies fed with formula milk do not need to take a supplement if they are taking more than 500ml of milk a day, as formula milk is fortified with vitamin D

47
Q

How does thyrotoxicosis present? mx?

A

Most cases caused by Grave’s disease
TSH down, T4 and T3 up
thyroid autoantibodies

Weight loss
Restlessness, anxiety, tremor
Heat intolerance
Palpitations, tachycardia
Diarrhoea

mx = carbimazole and BB

48
Q

Causes of hyperthyroidism?

A

“GIST” mnemonic:

G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

49
Q

What is diabetes insipidus?

A

a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

presents with polyuria and polydipsia

50
Q

Give some causes of cranial DI

A

idiopathic
post head injury
pituitary surgery
hereditary haemochromatosis

51
Q

Give some causes of nephrogenic DI

A

genetic
lithium
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

52
Q

How does can diabetes insipidus be investigated and managed?

A

Investigation
high plasma osmolality, low urine osmolality
(urine osmolality of >700 mOsm/kg excludes DI)
water deprivation test

Mx
cranial = desmopressin (synthetic ADH)
nephrogenic = thiazides and low salt/protein diet

53
Q

Autoimmune hepatitis is a rare cause of chronic hepatitis (inflammation in the liver).

Which type more commonly affects children?

A

Type 2 usually affects children or young people, more commonly girls

It presents with acute hepatitis with high transaminases and jaundice.

54
Q

What autoantibodies are seen in Type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

55
Q

How can Type 2 autoimmune hepatitis be managed?

A

Treatment is with high-dose steroids (e.g., prednisolone). Other immunosuppressants are also used, particularly azathioprine.

56
Q

What can cause acute liver failure?

A

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

57
Q

What features may acute liver failure present with?

A

jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)

58
Q

What is Fetor hepaticus?

A

sweet and fecal breath - sign of liver failure

59
Q

how does IBD present?

A

Diarrhoea
Abdominal pain
Rectal bleeding
Fatigue
Weight loss

60
Q

What are the differentiating features of Crohn’s disease?

A

N – No blood or mucus (PR bleeding is less common)
E – Entire gastrointestinal tract affected (from mouth to anus)
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)

61
Q

What are the differentiating features of UC?

A

C – Continuous inflammation
L – Limited to the colon and rectum
O – Only superficial mucosa affected
S – Smoking may be protective (ulcerative colitis is less common in smokers)
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis

62
Q

What associated conditions may be seen in patients with IBD?

A

Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)

Pyoderma gangrenosum (rapidly enlarging, painful skin ulcers)

Enteropathic arthritis (a type of inflammatory arthritis)

Primary sclerosing cholangitis (particularly with ulcerative colitis)

Red eye conditions (e.g., episcleritis, scleritis and anterior uveitis)

63
Q

When is the usual onset for UC and Crohn’s?

A

UC: 15-25 years and 55-65 years
Crohn’s: late adolescence and early adulthood

64
Q

How can suspected IBD be investigated?

A

Bloods:
* FBC for haemoglobin (low in anaemia) and platelet count (raised with inflammation)
* U&Es and LFTs can show low albumin in severe disease (protein is lost in the bowel)
* CRP
* TFTs for hyperthyroidism as a cause of diarrhoea
* anti-TTG for coeliac disease

Stool microscopy and culture
Faecal calprotectin
Colonoscopy with multiple intestinal biopsies

65
Q

Most common disease pattern in UC and Crohn’s?

A

UC- proctitis
Crohn’s- ileitis

66
Q

What is seen on histology in Crohn’s?

A

Inflammation in all layers from mucosa to serosa
increased goblet cells
granulomas

67
Q

What is seen on histology in UC?

A

No inflammation beyond submucosa
crypt abscesses
depletion of goblet cells and mucin

68
Q

How can Crohn’s disease be managed?

A

ESR can be used to assess disease progression

first-line management strategy for the induction of remission is glucocorticoids
Azathioprine or mercaptopurine is used first-line to maintain remission

Managing complications:
MRI is the investigation of choice for suspected perianal fistulae- provides visualisation of the course
Wound swab can be used for recurrent abscesses

69
Q

How can UC be managed?

A

Options for inducing remission:
Aminosalicylate (e.g., oral or rectal mesalazine) first-line
Corticosteroids (e.g., oral or rectal prednisolone) second-line

Options for maintaining remission in ulcerative colitis are:
Aminosalicylate (e.g., oral or rectal mesalazine) first-line
Azathioprine
Mercaptopurine

70
Q

What is Hypoxic ischaemic encephalopathy (HIE)? What can cause it?

A

occurs in neonates as a result of hypoxia during birth, can lead to permanent damage to the brain, causing cerebral palsy

Causes:
Maternal shock
Intrapartum haemorrhage
Prolapsed cord, causing compression of the cord during birth
Nuchal cord, where the cord is wrapped around the neck of the baby

71
Q

What is Henoch Schonlein Purpura? How should it be managed?

A

an IgA mediated small vessel vasculitis

classically presents with abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs

Patients with active Henoch-Schonlein purpura: blood pressure and urinanalysis should be monitored to detect progressive renal involvement

tx is usually supportive

72
Q

Ix for HSP?

A

Full blood count and blood film for thrombocytopenia, sepsis and leukaemia
Renal profile for kidney involvement
Serum albumin for nephrotic syndrome
CRP for sepsis
Blood cultures for sepsis
Urine dipstick for proteinuria
Urine protein:creatinine ratio to quantify the proteinuria
Blood pressure for hypertension

73
Q

What is reactive arthritis?

A

HLA-B27 associated seronegative spondyloarthropathy

develops following an infection where the organism cannot be recovered from the joint

warm, swollen and painful joint, typically presents after gastroenteritis or STI

74
Q

How should reactive arthritis be investigated?

A

Joint aspiration

Synovial fluid is sent for microscopy, culture and sensitivity testing for infection, and crystal examination for gout and pseudogout.

75
Q

How should reactive arthritis be managed?

A

symptomatic: analgesia, NSAIDS, intra-articular steroids
sulfasalazine and methotrexate are sometimes used for persistent disease
symptoms rarely last more than 12 months

Y4 Paediatrics (17 decks)

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