Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

YR5 Specialties > Paeds ENDO > Flashcards

Paeds ENDO Flashcards

1
Q

What is the most common cause of CAH?

A

21-hydroxylase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Recall the signs and symptoms of CAH

A

Virilisation of external genitalia
Salt-losing crisis
Tall stature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the best initial investigation to do when there are ambiguous genitalia?

A

USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the confirmatory investigation used to diagnose CAH?

A

Raised plasma 17-alpha-hydroxyprogesterone
Can’t do in a newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What sodium and potassium levels are seen in a salt losing crisis?

A

Hyponatraemia
Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the surgical management option for CAH?

A

For girls there is corrective surgery at early puberty to make the genitalia look more female

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the medical management for CAH?

A

Lifelong hydrocortisone + fludrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How should a salt-losing crisis be managed?

A

IV hydrocortisone
IV saline
IV dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the ‘classical triad’ of symptoms in DM?

A

Polydipsia
Polyuria
Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Recall the diagnostic criteria for DM

A
  1. Sx + fasting >7 OR random >11.1
  2. No Sx + fasting >7 AND random >11.1
  3. No Sx + OGTT >11.1
  4. HbA1c > 6.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What OGTT result is considered ‘impaired’ glucose tolerance?

A

7.8 - 11.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What fasting glucose result is considered ‘impaired’ glucose tolerance?

A

6.1-7.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Recall the 1st and 2nd line options for insulin therapy

A

1st line = multiple daily injection basal-bolus: injections of short-acting insulin before meals, with 1 or more separate daily injections of intermediate acting insulin or long acting insulin analogue

2nd line = continuous SC insulin infusion (pump)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Recall the names of 2 types of long acting insulin

A

Glargine
Determir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Recall the names of 3 types of short acting insulin

A

Lispro
Apart
Glulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why should site of SC insulin injection be regularly rotated in T1DM?

A

Avoidance of lipohypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What should cap glucose be when fasting and after meals?

A

Fasting: 4-7

After meals: 5-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When does annual monitoring for retinopathy/ nephropathy/ neuropathy begin?

A

12 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is DKA managed?

A
  1. Replace fluids: deficit + maintenance requirement
    + K+
  2. After 1-2h, start insulin therapy: infuse at 0.05-0.1 units/kg/hour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of HHS?

A

Weakness, leg cramps, visual disturbances
N+V
MASSIVE DEHYDRATION
Focal neurology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the best option for oral monotherapy in T2DM?

A

Metformin (biguanide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What medications can be added for tx-resistant T2DM?

A

Sulphonylureas (eg glibenclamide)
Alpha-glucosidase inhibitors (eg acarbose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 4 biochemical parameters of DKA

A

Hyperglycaemia >11
Acidosis <7.3
Bicarb <15
Bood ketones >3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is DKA biochemically classified as mild/ mod/ severe?

A

Mild = pH <7.3
Mod = <7.2
Sev = <7.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Recall the volume of fluid resus needed in a DKA emergency?
If shocked: 10mls/kg bolus over 15 mins If not shocked: 10mls/kg bolus over 30 mins
26
How should fluids be replaced following the initial emergency in DKA?
Fluid deficit = 5% if mild-mod DKA, 10% if severe DKA Deficit volume = weight x 10 x deficit% Fluid maintenance: first 10kg = 100ml/kg/day (4ml/kg/h) Next 10kg = 50ml/kg/day (2ml/kg/h) >20kg = 20ml/kg/day (1ml/kg/h)
27
What should be added to all fluids administered in DKA?
40mmol/L K+
28
What is the maintenance requirement of fluids?
First 10kg = 100mls/kg/day (4mls/kg/hour) Next 10kg = +50mls/kg/day (2mls/kg/hour) Every kg above 20kg = +20mls/kg/day (1ml/kg/hour)
29
Recall the % fluid deficit that correlates to each severity of DKA
Mild = 5% Mod = 7% Sev = 10%
30
Calculate the fluid requirement of a 20kg boy in DKA, with pH 7.15, who has already received a 10ml/kg bolus (200ml) over 60 mins
Calculation: (deficit x weight x 10) - initial, "shocked" bolus over 48 hours Deficit if pH = 7.15 = 5% (5 x 20 x 10) = 1000 Initial bolus - 200: 1000-200 = 800 over 48h 800/48 = 17ml/ hour Maintenance = (10 x 100) + (10 x 50) = 1500mls over 24h Total 1900ml over 24h
31
When should insulin therapy be started in DKA?
After 1-2 hours of IV fluid replacement
32
How should insulin dose be calculated?
0.05-0.1 units/ kg/ hour
33
When should dextrose therapy be started in DKA?
When glucose is <14mmol/L
34
Recall 2 important possible complications of DKA with their symptoms
Cerebral odoema: Cushing's triad of raised ICP (bradycarida, HTN, irregular breathing) Hypokalaemia (typically asymptomatic)
35
What is the most common cause of delayed puberty in boys?
CDGP (constitutional delay of growth + puberty)
36
Recall the parameters for referral in growth restriction
If >75th centile, only refer once it drops by >=3 centiles If 25th-75th centile, only refer once it drops by >=2 centiles If <25th centile, refer once centile drops by >=1 centiles
37
What is the definition of delayed puberty in males and females?
Males: no testicular development (<4mL) by age of 14 years Females: no breast development by age 13 years or no period by age 15
38
Recall 3 causes of Constitutional Delay of Growth and Puberty
Chronic disease Malnutrition Psychiatric (eg depression/ AN)
39
Recall some causes of hypogonadotrophic hypogonadism
Hypothalamopituitary disorders: panhypopituitarism, intercranial tumours Kallman's syndrome, PWS Hypothyroidism (acquired)
40
Recall some causes of hypergonadotrophic hypogonadism (high LH ad FSH)
Congenital: cryptochidism (absence of 1 or both testes from scrotum), Kleinfelter's, Turner's Acquired: testicular torsion, chemotherapy, infection, trauma, AI
41
How can delayed puberty be staged in boys vs girls?
Boys: Prader's orchidometer Girls: Tanner's staging
42
What non-gonadotrophin hormones are important to measure as part of initial investigation of delayed puberty?
TSH Prolactin
43
Recall 2 important imaging tests that may be done in investigation of delayed puberty?
Bone age (from wrist x ray) MRI brain
44
How should CDGP be managed?
1st line: reassure + offer observation: fantastic prognosis 2nd line: short course of sex hormone therapy Boys: IM testosterone (every 6 weeks for 6 months) Girls: transdermal oestrogen (6 months) + cyclical progesterone once established
45
How should primary testicular/ ovarian failure be treated?
Boys: regular testosterone injections Girls: oestrogen replacement gradually
46
What are the age parameters for 'early normal' vs precocious puberty?
Early normal: girls = 8-10, boys = 9-12 Precocious: girls = <8, boys = <9
47
What are the different causes of gonadotrophin-dependent vs gonadotrophin-independent precocious puberty?
Gonadtrophin-DEPENDENT: often idiopathic, but may be due to CNS tumours Gonadotrophin-INDEPENDENT: gonadal activation independent of HPG: may be due to ovarian (folllicular cyst, granuloma cell tumour, Leydig cell tumour, gonadoblastoma), or testicular pathology
48
What is premature thelarce?
Isolated breast development before 8 years
49
What does BL enlargement of the testicles indicate before puberty?
Gonadotrophin-dependent precocious puberty (intercranial lesion, ie optic glioma in NF1)
50
What does UL enlargement of a testicle indicate pre-puberty?
Gonadal tumour
51
What does small testes and precocious puberty indicate?
Tumour of CAH (adrenal cause)
52
What is the gold standard investigation for precocious puberty?
GnRH stimulation test
53
If CAH is suspected, what test should be done?
Urinary 17-OH progesterone
54
What is the medical treatment for precocious puberty?
GnRH agonist + GH therapy if gonadotrophin-dependent If gonadotrophin-independent: Testotoxicosis: ketoconazole/ cyproterone CAH: hydrocortisone + GnRH agonist
55
What are the 2 most common causes of dwarfism?
Achondroplasia Hypochondroplasia
56
What is the phenotype of achondroplasia?
Arms + legs short Normal length thorax
57
What is the phenotype of hypochondroplasia
Small stature Micromelia (small extremities) Large head
58
What gene mutation is associated with achondroplasia and hypochondroplasia?
FGFR3 Autosomal dominant mutation
59
Recall some signs and symptoms of osteogenesis imperfecta
Blue sclera Short stature Loose joints Hearing loss Breathing problems
60
Other than short stature, what are the symptoms of achondroplasia?
Hydrocephalus Depression of nasal bridge Marked lumbar lordosis Trident hands
61
What X ray findings may be present in achondroplasia?
Chevron deformity: metaphyseal irregularity Flaring in long bones
62
Recall 4 possible causes of cogenital hypothyroidism, and whether they are inherited or not
Thyroid gland defects (eg missing, ectopic): not inherited Disorder of thyroid hormone metabolism: inherited Hypothalamopituitary dysfunction (eg tumours, ischaemic damage): not inherited Transient hypothyroidism (eg due to maternal carbimazole or Hashimotos, not inherited)
63
Recall some signs and symptoms of congenital hypothyroidism including 3 unique symptoms
Unique: coarse features, macroglossia, umbilical hernia Others: large fontanelles, low temp, jaundice, hypotonia, pleural effusion, short stature, oedema, etc
64
How should congenital hypothyroidism be investigated and treated in an infant?
Pretty much the same as an adult
65
What is the most common cause of acquired primary hypothyroidism?
Hashimoto's AI thyroiditis
66
Recall 2 genetic risk factors for hashimoto's thyroiditis?
Down's Turner's
67
What is the prognosis of growth for children with primary hypothyroidism?
They can catch up
68
What are the signs and symptoms of hyperthyroidism in the foetus?
High CTG trace Foetal goitre on USS
69
What are the signs and symptoms of hyperthyroidism in the neonate?
Same as adult
70
What is the medical management of hyperthyroidism?
Carbimazole/ propothiouracil for 2 years
71
What non-medical management options are there for hyperthyroidism in children?
Radioiodine tx Surgery
72
How is severe obesity, obesity and overweightness defined in children?
Severely obese: 99th centile Obese: >95th centile Overweight: 85th-94th centile
73
What causes impaired skeletal growth in rickets?
Inadequate mineralisation of bone laid down at the epiphyseal growth plates
74
Recall 3 deficiencies that can cause rickets?
Calcium Vit D Phosphate
75
What will an x ray show in Rickets?
Thickened + widened epiphysis Cupping metaphysis Bowing diaphysis
76
What will be the biochemical picture in rickets?
Reduced calcium + phosphate Raised Diagnostic = calcium x phosphate <2.4
77
How can rickets be treated?
Calcium supplements Oral vitamin D2

YR5 Specialties (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions