Ques med Peads Flashcards

1
Q

What is the most common cause of nephrotic syndrome in children?

A

-Minimal changes disease
-Roughly accounts for 70% of cases of nephrotic syndrome

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2
Q

What is minimal changes disease typically characterised by?

A

-oedema
-frothy urine (excess protein in urine)
-often follows a viral upper respiratory tract infection
-also causes fatigue and weight gain due to fluid retention

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3
Q

Why is it called minimal changes disease?

A

-it is marked by minimal or no changes visible under light microscopy, but more subtle changes can be detected using electron microscopy

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4
Q

What are the investigations that should be carried out in a patient with suspected minimal change disease?

A

-Urine: look for proteinuria, WBC and blood in urine
-Blood tests: low albumin and elevated cholesterol
-Kidney biopsy: only done when patients do not respond to initial treatment to confirm diagnosis

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5
Q

What is the management of minimal change disease?

A

-1st line: Corticosteroids: Prednisolone
-2nd line: Other immunosuppressants e.g. ciclosporin

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6
Q

How to manage oedema and prevent further complication in minimal change disease?

A

-Fluid restriction and reduced salt intake
-In severe cases with significant fluid overload: Administer albumin and furosemide

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7
Q

What is the definition of ITP?

A

-An autoimmune condition with a reduction of circulating platelets leading to easy purport, superficial bleeding into skin, mucotenesous bleeding.

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8
Q

What type of hypersensitivity reaction in ITP and what components are involved?

A

-It is a type II hypersensitivity reaction where by the spleen produces antibodies that are directed against the glycoprotein IIb/IIIa or ib-V-IX complex

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9
Q

What are the main clinical features of vitamin K deficiency?

A

Increased propensity to bruising and if severe enough, internal bleeding

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10
Q

Why are breastfed babies at a bigger risk of vit K deficiency?

A

Breast milk has lower levels of vitamin K compared to formula

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11
Q

Pathogen causing hand foot and mouth disease?

A

Coxsackie virus A16

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12
Q

Diagnosis of rubella?

A

serological testing, look for rubella specific IgM antibodies

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13
Q

What virus is rubella caused by?

A

Rubella tagovirus

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14
Q

What symptoms is rubella characterised by?

A

Fever, coryza, arthralgia, rash (begins on face and moves to trunk, spares the limbs) , lymphadenopathy (classically post-auricular)

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15
Q

How is rubella spread?

A

Through respiratory droplets

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16
Q

How is rubella managed?

A

-Supportive (analgesia and antipyretics)
-Isolate diagnose individual

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17
Q

What is the biggest risk of rubella?

A

Rubella poses a serious risk to unvaccinated pregnant=t women - causing congenital rubella syndrome, which can cause severe fatal abnormalities

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18
Q

What are fatal abnormalities that rubella can cause?

A

-Cataracts
-Deafness
-PAD
-Brian damage

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19
Q

What can be used to confirm glandular fever?

A

A heterophiles antibody “Paul Bunnell’

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20
Q

What is the tretament for bilary atresia?

A

Hepatoportoenterostomy (Kasai procedure): This surgery creates a new pathway from the liver to the gut to bypass the fibrosed bile ducts.

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21
Q

What investigation is used for measles?

A

Diagnosis is primarily achieved by measles-specific IgM and IgG serology, and measles RNA detection by PCR

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22
Q

What is hydrocele?

A

-A pathological accumulation of serous fluid in a sac-like cavity specifically around the testicle
-It typically presents as an enlarged scrotum

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23
Q

What is a nephroblastoma or wilms tumour?

A

-A malignant embryonic tumour originating from the developing kidney.
-It represents the most common abdominal tumour in paediatric patients

24
Q

What are the features of a nephroblastoma?

A

Abdominal mass, abdominal distension, haematuria, and hypertension

25
Q

At what age does a nephroblastoma present?

A

-5 years
-Peak incidence between 3-4 years

26
Q

What are the signs and symptoms of nephroblastoma?

A

-A palpable abdominal mass that does not cross the midline, although it may be bilateral in up to 5% of cases.
-Abdominal distension
-Haematuria
-Hypertension
-Often asymptomatic unless the tumour grows sufficiently large to cause pain or disrupt other abdominal structures.

27
Q

What is the management of nephroblastoma?

A

-Surgical resection
-Adjunctive chemo
-Prognosis - generally excellent 990% 5 years)

28
Q

What are the investigations of a wilms tumour/nephroblastoma?

A

-CT scan of the chest, abdomen, and pelvis (spread disease)
-Definitive diagnosis and staging are confirmed via renal biopsy, which may reveal small round blue cells on histology. (This finding is not exclusive to nephroblastomas)

29
Q

What is seen on USS for intussusception?

A

A classic ‘target’ sign on abdominal ultrasound is seen as concentric echogenic and hypogenic bands, demonstrating the invagination of a bowel segment into an adjacent one.

30
Q

What enzyme deficiency is caused by congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

31
Q

What are the signs of Roseola?

A

-Initial fever lasting upto 5 days with high fevers reaching to 40
-As the fever subsides a blanching, rose-pink macular rash erupts, predominantly over the trunk but may also spread to the face and limbs

32
Q

what is the first step in resuscitating a neonate?

A

The first step is to inflate the lungs by giving 5 breaths via a 250 ml bag-valve mask

33
Q

What is used to stage for puberty?

A

Tanner staging

34
Q

What is slapped cheek syndrome?

A

Erythema infectiosum

35
Q

How does erythema infectiosum present?

A

-initial headache, fever, and cold-like symptoms
-Followed by a rash developing over the following few days; appearing bright red on the cheeks and more lacy in pattern over the rest of the body

36
Q

What is Prader Willi syndrome?

A

-Genetic condition that is inherited by genomic imprinting
- A gene on chromosome 15 is imprinted such that the child only expresses the maternally inherited version of the gene

37
Q

What are the key signs and symptoms of prader willi syndrome?

A

-Hypotonia and poor feeding in infancy
-Developmental delay in early childhood
-Learning disabilities
-Short stature
-Hyperphagia (excessive hunger) and resultant obesity in older childhood. Anecdotal reports suggest that children with Prader-Willi Syndrome may consume non-food items out of excessive hunger.

38
Q

Fitting child - 2 doses of buccal Midazolam, what should be given next?

A

IV Leviteracetam, Phenytoin or Valproate

39
Q

What virus is acute epiglottitis caused by?

A

Haemophilus influenza B (Hib)

40
Q

Down’s syndrome heart abnormality?

A

-Eisenmenger syndrome - due to ventricular septal defect
-Reversal of L-R cardiac shunt to R-L due to pulmonary hypertension

41
Q

What is amniotic fluid embolism?

A

Amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse

42
Q

what is the triad of amniotic fluid embolism ?

A

coagulopathy, hypoxia and hypotension

43
Q

Where is lidocaine injected?

A

Pudneal nerve - pudeneal nerve block

44
Q

What is the regime for medical termiation of pregnancy?

A

-Oral mifepristone 200mg (antiprogesterone)
-Buccal, vaginal, sublingual misoprostol 800mg (prostaglandin analogue) 24-48 hours later

45
Q

How to identify premature rupture of membranes?

A

Actim-PROM vaginal swab detects insulin-like growth factor binding protein-1 (IGFBP-1) in vaginal fluid

46
Q

What causes inguinal hernia in childremn?

A

-Almost always indirect in children and are caused by failure of the processus vaginalis to obliterate
-More commin in boys and on the right

47
Q

What is the first line investigation for asthma?

A

-Spirometry and BDR (bronchodilator reversibility)
-Positive result confirms presence of an obstructive airway pattern

48
Q

Clinical findings in PDA?

A

Collapsing pulse

49
Q

When does moro reflex disappear?

A

6 months
-spread out arms
-pulls arms
-starts crying

50
Q

What is malrotation?

A

Abnormal development of the midgut during embryogenesis, which increases the bowel’s propensity for volvulus and duodenal compression by Ladd bands.

51
Q

How does malrotation present?

A

Bilious vomiting on the first day of life

52
Q

What is the gold standard for malrotation?

A

Upper GI contrast study

53
Q

What is tuberous sclerosis?

A

An autosomal dominant neurocutaneous syndrome typified by cellular hyperplasia, tissue dysplasia, and hamartomas in multiple organs

54
Q

What are the signs and symptoms of tuberous sclerosis?

A

-Neurological: Infantile spasms with hypsarrhythmia as seen on electroencephalogram; seizures/epilepsy
-Skin: Ash leaf macules; shagreen patches; facial angiofibromas; subungual fibromas
-Cognitive: Learning disabilities
-Renal: Angiomyolipomas
-Cardiac: Cardiac rhabdomyomas

55
Q

What kind of reaction occurs when take amoxicillin with glandular fever?

A

Morbilliform Eruption

56
Q
A