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PAEDIATRICS > ENDOCRINOLOGY PAEDS > Flashcards

ENDOCRINOLOGY PAEDS Flashcards

1
Q

Normal Blood sugar levels

A

4.4-6.1 mmol/l

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2
Q

How do children with T1DM present?

A

25-50% present with DKA

The rest, triad of symptoms

  • Polyuria
  • Polydipsia
  • Weight loss
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3
Q

Where in pancreas is insulin and glucagon produced

A

Insulin: Beta cells in islets of langerhans

Glucagon: ALpha cells in islets of langerhans

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4
Q

?DM - investigations

A

Baseline bloods
Blood cultures if ?infection
HbA1c (picture of BM over the last 3 months)
TFT and thyroid peroxidase antibodies (TPO) to test for associated autoimmune thyroid disease
Tissue transglutaminase (anti-TTG) ?coeliac
Insulin antibodies, anti-GAD antibodies and islet cell antibodies (antibodies associated with the pancreas and development of type 1 diabetes)

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5
Q

Consequence of injecting insulin into the same spot

A

LIPODYSTROPHY

Subcutaneous fat hardens and prevents absorption of insulin

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6
Q

Basal bonus regime

A

Basal: LONG ACTING INSULIN (e.g. Lantas)
Bolus: SHORT ACTING INSULIN (e.g. actrapid) - usually 3 x per day in between meals

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7
Q

How can a child qualify for an insulin pump on the NHS

A

Needs to be > 12 years old

Have difficulty controlling their HbA1c

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8
Q

Symptoms of hypoglycaemia

A

Hunger, tremor, sweating, irritability, dizziness, pallor

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9
Q

Treatment of hypoglycaemia

A

Mild: Short acting glucose (e.g. lucosade) and long acting carbohydrates (e.g. biscuits/toast)
10-20g glucose

Severe:
IV 10% dextrose 100ml
IM glucagon 1mg

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10
Q

Macrovascular complications of DM

A

Coronary artery disease
Peripheral ischaemia (—>poor healing, ulcers, diabetic foot)
Stroke
HTN

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11
Q

Micro vascular complications

A

Peripheral neuropathy
Retinopathy
Kidney disease

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12
Q

Infection related consequences

A

UTI
Pneumonia
Skin/soft tissue infections
Fungal infections (Oral/vaginal candidiasis for example)

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13
Q

What is DKA

A

Ketones = water soluble fatty acids that can be used as fuel when glucose not available
They are buffered in normal non- diabetic patients, so they don’t become acidotic
T1DM —> extreme hyperglycaemic ketosis —> metabolic acidosis which is life threatening

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14
Q

Main 3 problems of DKA

A
  1. Ketoacidosis: initially kidneys produce bicarbonate to buffer the ketones, then this is used up and blood become acidic
  2. Dehydration: Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. Glucose in urine draws water out with it (OSMOTIC DIURESIS) —> POLYURIA —> dehydration and polydipsia as increases thirst
  3. Potassium imbalance: insulin drives potassium into cells. So without serum potassium can be high, but total body potassium can be low as its not being stored. When starting insulin pt can become hypokalaemic quickly (—> arrhythmias!)
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15
Q

Cerebral oedema in DKA

A

High blood sugar in brain —> water moves from intracellular space to extracellular space —> brain cells shrink and become dehydrated
Rapid correction of dehydration and hyperglycaemia —> rapid shift in water from extracellular space to intracellular space —> oedematous

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16
Q

Management of cerebral oedema in DKA

A

Monitor neurological obs closely
Slow IV fluids
IV mannitol
IV hypertonic saline

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17
Q

DKA presentation

A 
Polyuria
Polydipsia
N&V
Weight loss
Acetone smell on breath 
Dehydration and hypotension 
Altered consciousness
Symptoms of an underlying trigger (e.g. sepsis)
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18
Q

Diagnosing DKA

A

HYPERGLYCAEMIA ( Blood glucose >11 mmol/l)
KETOSIS (blood ketones >3 mmol/l)
ACIDOSIS (pH <7.3)

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19
Q

What’s deficiency in adrenal insufficiency

A

Steroid hormones: particularly cortisone and aldosterone

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20
Q

What is PRIMARY ADRENAL INSUFFICIENCY

A

= ADDISON’S DISEASE

Adrenal glands have been damaged and there is reduced secretion of cortisol and aldosterone

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21
Q

What is SECONDARY ADRENAL INSUFFICIENCY

A

Inadequate ACTH stimulating the adrenal glands (aka not a problem with the glands themselves) —> reduce cortisol levels
Causes: Loss or damage to the pituitary gland - e.g. due to congenital hypoplasia, surgery, infection, radiotherapy, loss of blood supply

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22
Q

What is TERTIARY ADRENAL INSUFFICIENCY

A

Result of inadequate CRH released by HYPOTHALAMUS
E,g, patients being on long term steroids causing suppression of the hypothalamus - when exogenous steroids removed the endogenous steroids not adequately produced (LT steroids should be tapered slowly!)

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23
Q

Features of ADRENAL INSUFFICIENCY in babies

A 
Lethargy
Vomiting 
Poor feeding 
Hypoglycaemia 
Jaundice 
Failure to thrive
24
Q

Features of ADRENAL INSUFFICIENCY in older children

A 
N&V 
Poor weight gain/weight loss 
Anorexia 
Abdo pain 
Muscle weakness/cramps 
Developmental delay 
Addisons: bronze hyperpigmentation (high ACTH stimulates melanocytes)
25
Q

ADRENAL INSUFFICIENCY: investigations

A

U&Es (hyponatraemia and hyperkalaemia)
Glucose (hypoglycaemia)
Cortisol, ACTH, aldosterone and renin levels (prior to administing steroids)

26
Q

Primary vs secondary adrenal insufficiency

27
Q

Short Synacthen Test (ACTH stimulation test) - how does it work

A

Ideally performed in the morning
Synacthen = synthetic ACTH
Blood cortisol measured at baseline, then 30 and 60 mins after administration
Normal: cortisol at least doubles
Abnormal: Failure for cortisol to rise or less than double baseline —> Addison’s disease (Primary adrenal insufficiency)

28
Q

Adrenal insufficiency: Management

A

REPLACEMENT STEROIDS: Titrated to signs, symptoms, electrolytes
HYDROCORTISONE (glucocorticoid) - replaces cortisol
FLUDROCORTISONE (minceralocorticoid) - replaces aldosterone

Does increased during acute illness (to match normal steroid response)

29
Q

Adrenal insufficiency: Monitoring

A 
Growth and development 
BP 
U&Es 
Glucose 
Bone Profile 
Vitamin D
30
Q

Adrenal insufficiency: SICK DAY RULES

A
  • Dose of steroid needs to be increased and given more regularly during acute illness
  • blood sugar monitored closely and eat carbohydrate foods regularly
  • If D&V - need IM injection of steroids at home and might require admission of IV steroids
31
Q

ADDISONIAN CRISIS: Presentation

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia

32
Q

ADDISONIAN CRISIS: Triggers

A

Stopping steroids
Infection/trauma/acute illness
First presentation of adrenal insufficiency

33
Q

ADDISONIAN CRISIS: Management

A

Intensive monitoring if acutely unwell
Parenteral steroids (e.g. IV hydrocortisone)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

34
Q

What is CONGENITAL ADRENAL HYPERPLASIA

A

Deficiency of the 21-hydroxylase enzyme
Causes underproduction of cortisol and aldosterone and overproduction of androgens from birth
Autosomal recessive

35
Q

Action of Aldosterone

A

Acts on kidneys to control balance of salt and water in the blood
Released by adrenal gland in response to renin
Increases sodium re absorption into the blood and potassium secretion into urine
Aka decreases potassium and increases sodium in the blood

36
Q

Pathophysiology of congential adrenal hyperplasia

A

Enzyme that’s deficient (21-hydroxylase) responsible for breaking down progesterone to aldosterone and cortisol
Progesterone is used to create testosterone, so more progesterone —> more testosterone as it is not able to be converted into aldosterone and cortisol

LOW CORTISOL
ABNORMALLY HIGH TESTOSTERONE

37
Q

congential adrenal hyperplasia: PRESENTATION

A

Females: at birth present with virility’s genitalia (ambiguous genitalia) - enlarged clitoris due to testosterone levels

Severe CAH - shortly after birth present with hyponatraemia, hyperkalaemia, hypoglycaemia

Signs/symptoms: poor feeding, vomiting, dehydration, arrhythmias

38
Q

congential adrenal hyperplasia: Presentation in mild cases

A

Symptoms/signs associated to high testosterone levels

Female pt: Tall for age, facial hair, absent periods, deep voice, early puberty
Male pt: Tall, deep voice, large penis, small testicles, early puberty

SKIN HYPERPIGMENTATION - key clue (by product of ACTH production is melanocyte stimulating hormone)

39
Q

congential adrenal hyperplasia: Management

A

CORTISOL REPLACEMENT: usually hydrocortisone
ALDOSTERONE REPLACEMENT: fludrocortisone

Corrective surgery for females with ambiguous genitalia

40
Q

What is GROWTH HORMONE DEFICIENCY?

A

Disruption to the growth hormone axis at the hypothalamus or pituitary gland

41
Q

Explain the GROWTH HORMONE AXIS

A

Hypothalamic-pituitary growth axis
Growth hormone produced by the ANTERIOR PITUITARY gland —> stimulates cell reproduction and growth of organs, muscles, bones and height
Stimulates the release of INSULIN LIKE GROWTH FACTOR (IGF-1) by the liver (important for growth in children and adolescents)

42
Q

CONGENITAL GROWTH HORMONE DEFICIENCY

A

Genetic mutation e.g. GH1 or GHRHR (growth hormone releasing hormone receptor) genes
Or empty sella syndrome (pituitary gland underdeveloped or damaged)

43
Q

ACQUIRED GROWTH HORMONE DEFICIENCY

A

Secondary to trauma, infection, surgery etc.

44
Q

HYPOPITUITARISM / MULTIPLE PITUITARY HORMONE DEFICIENCY

A

When the pituitary does not produce a number of hormones

45
Q

Growth hormone deficiency: PRESENTATION

A

Neonates:

  • Micropenis
  • Hypoglycaemia
  • Severe jaundice

Infants and older children:

  • poor growth, severely slowing from age 2-3
  • SHort stature
  • Slow development of movement and strength
  • Delayed puberty
46
Q

Growth hormone stimulation test

A

Measuring response to medications that normally stimulate the release of GH (e.g. glucagon, insulin, arginine, clonidine)
GH levels monitored for 2-4 hours after administering medication to assess hormonal response

47
Q

Growth hormone deficiency: investigations

A

Growth hormone stimulation test
Test for other associated hormone deficiencies (e.g. thyroid, adrenal deficiency)
MRI brain
Genetic testing (associated genetic conditions e.g. turners syndrome, Prader-Willi syndrome)
X-ray or DEXA scan to determine bone age and help predict final height

48
Q

Growth hormone deficiency: TREATMENT

A

Daily subcutaneous injections of GROWTH HORMONE (SOMATROPIN)
Treatment of other associated hormone deficiencies
Close monitoring of height and development

49
Q

Prevalence of congential hypothyroidism

A

1 in 3000 newborns

50
Q

Common cause of Congenital hypothyroidism

A

Underdevelopment of thyroid gland (dysgenesis)
Fully developed gland that doesn’t produce enough hormones (dyshormonogenesis)

Rarely a problem with the pituitary or hypothalamus

51
Q

Congenital hypothyroidism: presentation

A

Often picked up on NEWBORN BLOOD SPOT SCREENING TEST

  • prolonged neonatal jaundice
  • poor feeding
  • constipation
  • increased sleeping
  • reduced activity
  • slow growth and development
52
Q

Acquired hypothyroidism: causes

A

Autoimmune thyroiditis (hasimotos thyroiditis)

53
Q

Hashimoto’s Thyroiditis: Antibody associations

A

Anti thyroid peroxidase (anti-TPO) and anti-thyroglobulin antibodies

54
Q

Hypothyroidism: Management

A

LEVOTHYROXINE

Fully thyroid function test - TSH, T4, T3

55
Q

Thyroid system

PAEDIATRICS (18 decks)

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