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
How can lymphoma be investigated?
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
26
How can lymphoma be staged?
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
27
Treatment if lymphoma is with chemotherapy and possibly radiotherapy. Describe the prognosis and potential complications
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
28
Outline the pathophysiology of sickle cell disease
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.
29
Give some complications of sickle cell disease
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)
30
What is sickle cell crisis?
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
31
What is acute chest syndrome?
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
How can acute chest syndrome be managed?
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
What is the general mx of sickle cell disease?
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
How should a child with newly diagnosed T1DM be investigated?
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
How should T1DM in kids be managed?
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
What are the advantages and disadvantages of insulin pumps ?
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
Sxs of hypoglycaemia in children?
hunger, tremor, sweating, irritability, dizziness and pallor more severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated
38
Mx of hypoglycaemia in children?
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
Give some complications of T1DM
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
How may DKA present?
Polyuria, Polydipsia, WL (poor diabetic control) Nausea and vomiting Dehydration and hypotension Altered consciousness Acetone smell to their breath
41
How can DKA be diagnosed?
Hyperglycaemia (i.e. blood glucose > 11 mmol/l) Ketosis (i.e. blood ketones > 3 mmol/l) Acidosis (i.e. pH < 7.3)
42
How should DKA be managed?
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
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?
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
What is the most common cause of acquired hypothyroidism in kids? How does it present?
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
How is Hashimoto's thyroiditis managed in kids?
managed by paediatric endocrinology IX: full thyroid function blood tests (TSH, T3 and T4), thyroid ultrasound and thyroid antibodies. Levothyroxine orally OD
46
Which children should be given Vit D supplementation?
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
How does thyrotoxicosis present? mx?
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
Causes of hyperthyroidism?
“GIST” mnemonic: G – Graves’ disease I – Inflammation (thyroiditis) S – Solitary toxic thyroid nodule T – Toxic multinodular goitre
49
What is diabetes insipidus?
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
Give some causes of cranial DI
idiopathic post head injury pituitary surgery hereditary haemochromatosis
51
Give some causes of nephrogenic DI
genetic lithium tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
52
How does can diabetes insipidus be investigated and managed?
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
Autoimmune hepatitis is a rare cause of chronic hepatitis (inflammation in the liver). Which type more commonly affects children?
Type 2 usually affects children or young people, more commonly girls It presents with acute hepatitis with high transaminases and jaundice.
54
What autoantibodies are seen in Type 2 autoimmune hepatitis?
Anti-liver kidney microsomes-1 (anti-LKM1) Anti-liver cytosol antigen type 1 (anti-LC1)
55
How can Type 2 autoimmune hepatitis be managed?
Treatment is with high-dose steroids (e.g., prednisolone). Other immunosuppressants are also used, particularly azathioprine.
56
What can cause acute liver failure?
paracetamol overdose alcohol viral hepatitis (usually A or B) acute fatty liver of pregnancy
57
What features may acute liver failure present with?
jaundice coagulopathy: raised prothrombin time hypoalbuminaemia hepatic encephalopathy renal failure is common ('hepatorenal syndrome')
58
What is Fetor hepaticus?
sweet and fecal breath - sign of liver failure
59
how does IBD present?
Diarrhoea Abdominal pain Rectal bleeding Fatigue Weight loss
60
What are the differentiating features of Crohn's disease?
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
What are the differentiating features of UC?
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
What associated conditions may be seen in patients with IBD?
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
When is the usual onset for UC and Crohn's?
UC: 15-25 years and 55-65 years Crohn's: late adolescence and early adulthood
64
How can suspected IBD be investigated?
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
Most common disease pattern in UC and Crohn's?
UC- proctitis Crohn’s- ileitis
66
What is seen on histology in Crohn’s?
Inflammation in all layers from mucosa to serosa increased goblet cells granulomas
67
What is seen on histology in UC?
No inflammation beyond submucosa crypt abscesses depletion of goblet cells and mucin
68
How can Crohn's disease be managed?
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
How can UC be managed?
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
What is Hypoxic ischaemic encephalopathy (HIE)? What can cause it?
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
What is Henoch Schonlein Purpura? How should it be managed?
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
Ix for HSP?
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
What is reactive arthritis?
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
How should reactive arthritis be investigated?
Joint aspiration Synovial fluid is sent for microscopy, culture and sensitivity testing for infection, and crystal examination for gout and pseudogout.
75
How should reactive arthritis be managed?
symptomatic: analgesia, NSAIDS, intra-articular steroids sulfasalazine and methotrexate are sometimes used for persistent disease symptoms rarely last more than 12 months