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Paediatrics > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is normal fasting glucose

A

3.5 - 5.6 mmol/L

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2
Q

What is normal post prandial glucose

A

< 7.8 mmol/L

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3
Q

What Is prediabetic fasting glucose

A

< 7.0 mmol/L

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4
Q

What is prediabetic post prandial glucose

A

> 7.8 - <11.0 mol/L

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5
Q

What is diabetic fasting glucose

A

equal to or greater than 7.0 mmol/L

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6
Q

What is diabetic post prandial/random glucose

A

equal to or greater than 11.0 mmol/L

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7
Q

What is diabetes

A

A chronic condition characterised by hyperglycaemia

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8
Q

What is Type 1 Diabetes

A

Autoimmune condition characterised by the destruction of B-Cells in the islets of Langerhans therefore no insulin production

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9
Q

What is Type 2 Diabetes

A

Progressive insulin secretory defect:

  • Very low insulin production
  • Insulin Resistance
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10
Q

How do you treat Type 1 diabetes

A

Insulin

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11
Q

How do you treat Type 2 diabetes

A

With Insulin &/or Diet and Exercise

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12
Q

What are the important genetic factors behind Type 1 diabetes

A

Fathers with type I diabetes transmit diabetes to their offspring 2-3 times more frequently than mothers with type I diabetes

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13
Q

What are the important genetic factors behind Type 2 diabetes

A

Type 2 has higher risk of transmission to offspring than Type 1

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14
Q

What does insulin do

A
  • Stimulates uptake of glucose from blood into tissue cells of muscle, kidney and fat
  • Liver: reduces hepatic glucose output by glycogenolysis and reduces gluconeogenesis
  • Regulates the release of glucagon
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15
Q

What does low blood sugar stimulate the release of and what does it do

A

Glucagon - increases hepatic glucose output by increasing glycogenolysis and gluconeogenesis and reduces peripheral glucose uptake

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16
Q

What is a serious consequence of untreated T1DM in children

A

Diabetic Ketoacidosis

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17
Q

What happens in DKA

A
  1. Absent glucose - means there is no regulation of glucagon or Blood Glucose
  2. Glucagon leads to unregulated gluconeogenesis stimulates break down of fat stores leading to the production of fatty acids
  3. These fatty acids are converted in the liver to Ketones
  4. All this leads to increased ketones and glucose in the blood
  5. Ketones lead to acidosis
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18
Q

How does diabetes present

A
  • Weight Loss +/- infection
  • Increased thirst/polydipsia
  • Polyuria
  • Lethargy
  • Poor Growth
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19
Q

What does DKA present with

A

Increased Ketones:

  1. Acidosis- Cellular Dysfunction and Cerebral Oedema, kidney failure
  2. Vomiting - Fluid & Electrolyte depletion leading to cerebral oedema and shock
  3. Osmotic Diuresis - Fluid and Electroltye depletion (large deficits of Na+, K+ and water) leadings to cerebral oedema and shock

Increase Glucose:
1. Osmotic Diuresis - Fluid and Electrolyte Depletion leading to cerebral oedema and shock

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20
Q

How do you manage DKA

A 
Fluid Replacement 
Give IV insulin 
Monitor Glucose hourly 
Monitor electrolytes especially K+ hourly 
Very strict fluid balance 
Hourly neuro obs
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21
Q

What is Hypoglycaemia

A

Deficiency of glucose in the blood stream most commonly caused by insulin therapy

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22
Q

What are the symptoms of hypoglycaemia

A 
Hunger 
Sweating 
Pallor 
Anxious 
Irritable 
Nauseous 
Tachycardia/Palpitations
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23
Q

What can happen if hypoglycaemia is left untreated

A 
Neuroglycopenic Symptoms:
Dizzy
Headache 
Confused
Drowsy 
Personality change 
seirzures/ coma
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24
Q

How is a mild/moderate Hypo managed

A

fast acting carb: Glucose Tablets, Juice/Fizzy drink

Glucogel

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25
Q

How is severe Hypo e.g unconscious managed

A

Glucagon injection IM or SC

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26
Q

What are important things to monitor in someone with diabetes

A

HbA1c - <42 (diabetic >48)
AI screening
Education - alcohol, contraception
Examination - eyes, feet, urine/kidney function, BP, injection sites,

27
Q

What are the causes of Hypothyroidism in children

A

Congenital:
Athyreosis,
Thyroid Dysgenesis,
Thyroid Dyschormonogenesis

Acquired: 
Prematurity, 
Hashimotos Thyroiditis - AI
Hypopituitarism, 
Trisomy 21
Low iodine in developing countries
28
Q

What are the signs of Hypothyroidism

A
  • prolonged neonatal jaundice
  • poor/slow feeding
  • Bradycardia
  • Hypotonia
  • Dry skin
  • inactivity/sleepiness
  • Constipation
29
Q

What can untreated hypothyroidism lead to

A
  • Poor growth and mental development
  • Low IQ
  • Delayed puberty
  • Short Stature
30
Q

How is Hypothyroidism screened and investigated

A
  • All babies screened at newborn blood spot test
  • TSH - High or Low (if pituitary failure)
  • T4 - Low
31
Q

How do you treat Hypothyroidism

A

Levothyroxine

32
Q

What is testicular Torsion

A

When spermatic cord twists cutting off the testicular blood supply causing ishaemia

33
Q

What are the two types of testicular torsion

A

Extravaginal - torsion outside the tunica vaginalis - exclusive to newborns and necrotic at brith needs surgical removal

Intravaginal - twisting of spermatic cord inside tunica vaginalis cutting off blood supply - usually occurs during puberty

34
Q

What are the signs and symptoms of testicular torsion

A

Sudden onset testicular pain and tenderness
Nausea and Vomiting
Testicular exam: Tender and Red

35
Q

How is Testicular Torsion diagnosed and treated

A

US

Prompt surgical untwisting of testicle and sewing of testicle to scrotum

36
Q

What is a factor for undescended testes

A

Prematurity

37
Q

How are undescended testes managed

A

If still undescended by 6 months surgical fixation within the scrotum (orchidopexy)

38
Q

What are risks associated with undescended testes

A

infertility

Neoplasm

39
Q

What is congenital adrenal hyperplasia

A

Usually caused by deficiency of 21 Hydroxylase by a defect on the CYP21 gene

40
Q

What is the pathogenesis of CAH

A

Deficiency of 21 Hydroxylase leads to inadequate production presenting with:

  1. Low levels of cortisol
  2. Increase in ACTH
  3. Adrenal Hyperplasia
  4. Increase in 17 hydroxyprogesterone leading to increase testosterone production

75% will also have aldosterone deficiency/ salt wasting form - as 21 Hydroxylase is needed for it’s synthesis:

  • This is severe
  • Loss of Salt
41
Q

How may they present with Classic CAH

A

Two clinical sub-types of CAH

Salt Wasting Form - Inability to retain salt and water due to deficiency of aldosterone leading to adrenal crisis if not managed:
- Males present: normal at birth (may have small balls, large penis) but a few days after birth present with salt wasting crisis:
> Hyponatraemia
> Hyperkalaemia
> Hypoglycaemia
> Hypovolaemia
> Acidosis
- This presents with symptoms of Failure to Thrive, Vomiting, Dehydration and SHOCK and Collapse

  • Girls present: at birth with ambiguous/Viralised external genitalia
    But genetically female and normal internal female reproductive system, will also have salt water crisis if not diagnosed at birth
Non Salt Wasting Type/Simple Viralising:
Birth:
- Males may appear normal but may have large penis and small testicles
- Females ambiguous/viralised genitalia 
- No symtoms of shock

Both Classical forms will present later:
Both: Precocious Puberty, Excessive body hair, acne, deep voice, short stature and infertility
Girls: Irregular/absent periods

42
Q

How will they present with Salt wasting/non-classical CAH

A

A much milder form which has a later onset than classical:

  • Normal external genitalia in both at birth
  • Precocious Puberty
  • Acne
  • Infertility
  • Females: irregular periods, hirsutism
  • Males: Early beard growth, small balls, large penis
43
Q

How is CAH diagnosed

A
  • plasma 17 hydroxyprogesterone measurement (raised)
  • &/or ACTH stimulation test
    (Low cortisol in blood)
44
Q

How do you manage CAH

A

Lifelong Glucocorticoid replacement therapy:
Glucocortcosteroid - Hydrocortisone
Mineralcorticosteroid (if salt wasting) - Fludrocortisone

Genital Reconstruction Surgery in females with ambiguous genitalia

45
Q

How do you manage Adrenocortical crisis

A 
Hydrocortisone 
IVI Fluids 
Glucose 
Fludrocortisone
Check for Hyperkalaemia - monitor ECG - if hyperkaemia give insulin with glucose infusion
46
Q

How does someone with Androgen Insensitivity Syndrome present

A

Genetically male but ambiguous external genitalia

  • penis doesn’t form or develop
  • No womb or ovaries
  • Fully or partially undescended testicles
47
Q

What can androgen insensitivity syndrome lead to

A

Gender Dysphoria

Give support and advice

48
Q

When is precocious puberty

A

before 8 in girls

before 9 in boys

49
Q

What is used to stage puberty

A

Tanners Staging

50
Q

What is important to note in the tanners stages for boys

A
  1. Enlargement of Testes and slight hair
  2. Enlargement of Penis followed by thick and dark pubic hair
  3. Boys growth accelerates when testes volume reaches 10-12ml
51
Q

What is important to note for the tanners stages for girls

A
  1. Breast development and development of pubic hair
  2. Girls growth accelerates when breasts have started to develop
  3. Stage 4 breast development is prerequisite for menarche
52
Q

What is a genetic disorder characterised by isolated gonadotrophin deficiency

A

Hypogonadothrophic Hypogonadism
Kallmans:
Delayed or Absent Puberty with absent sense of smell
Boys may have micropenis

53
Q

What is Turners Syndrome

A 
Only one normal X chromosome 
Born with oedema of hands and feet 
Short/ Webbed of neck 
Low hairline 
Streak Gonads - Infertility 
CVS malformations 
Renal malformations (horseshoe kidney)
Short Stature
54
Q

What is Klinefelter syndrome

A

Caused by boys being born with extra X - XXY
Language delay/ Learning disability
Primary Hypogonadism/Undesended Testes - Infertility!!!
Small testes/penis and enlarged breasts
Tall
Osteoporosis
Increased risk of breast cancer

55
Q

What causes short stature/ delayed puberty

A
  • Constitutional, Slow maturation (genetic) - most common cause of delayed puberty
  • Idiopathic
  • Environmental – psycho-social
  • Nutrition – pre- or postnatal
  • Chronic disease e.g IBD, coeliac, renal CHD
  • Skeletal disease
  • Turner’s syndrome
  • Endocrine
56
Q

What can cause overgrowth but impaired final height

A 
• Precocious Puberty
• Congenital adrenal
hyperplasia
• McAlbright syndrome
• Hyperthyroidism
57
Q

What can cause overgrowth but increased final height

A
  • Androgen/ or oestrogen deficiency/ oestrogen resistance
  • GH excess
  • Klinefelter syndrome (XXY) • Marfan syndrome
  • (Homocystinuria)
58
Q

What tests should be done for Percocious Puberty

A 
Growth Charts
Puberty Staging 
MRI
Bone Age 
TFTs
LH and FSH
17 hydroxyprogesterone deficiency 
Pelvic US
59
Q

What are the two causes of percosious puberty

A

Central/Gonadotrophin dependent: caused by hypothalamus or pituitary leading to premature release of gonadotrophins
Gonadotrophin Independent: not caused by early release of gonadotrophin e.g tumours, CAH

60
Q

What causes central percocious puberty

how is it diagnosed

How is it managed

A

Causes:
CNS tumours
Idiopathic
Pituitary - Gonadothrophin Releasing Tumours

Diagnosis
Raised LH and FSH
GnRH stimulation test - gold standard (LH&FSH increase after administration of GnRH)

Management:
GnRH agonist
Manage underlying cause

61
Q

What causes peripheral precocious puberty/ Gonadotrophin Independent Percocious Puberty (GIPP).

How is it diagnosed

How is it managed

A
  • ↑ Androgen production, e.g.: Ovarian cyst (most common cause), Congenital adrenal hyperplasia
  • ↑ Estrogen production, e.g.: HCG-secreting germ cell tumors (e.g., granulosa cell tumor)
    ↑ β-HCG production: e.g., hepatoblastoma
  • Primary hypothyroidism
  • Obesity-related precocious sexual development due to compensatory hyperinsulinemia (caused by increased insulin resistance in obesity)

Diagnosis:
High oestrogen or Testosterone production depending on tumour
Low FSH and LH
GnRH stimulation test - no change

Management:

  • Remove Tumour
  • Treat CAH
  • Ovarian cyst should resolve itself
62
Q

What is Prader - Willi

A

Caused by a deletion in the paternally inherited chromosome 15 or maternal uniparental disomy (both copies of 15 come from mother but both turned off due to imprinting) causes:

  • Neonatal hypotonia and poor feeding
  • Moderate Mental Retardation
  • Hyperphagia and obesity
  • Small genitalia
63
Q

What is Angle-mans Syndrome

A

Caused by a deletion in the Maternally inherited chromosome 15 or paternal uniparental disomy causes:

  • “Happy puppet” unprovoked laughing/clapping
  • Microcephally
  • Mental retardation
  • Seizures
  • Ataxia
  • Broad based gait

Paediatrics (13 decks)

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