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Paediatrics > Paediatrics Endocrinology > Flashcards

Paediatrics Endocrinology Flashcards

1
Q

What is Type 1 diabetes mellitus (T1DM)?

A

Pancreas stops being able to produce insulin (cause is unclear - maybe genetic / triggered by viruses e.g. coxsackie B virus and enterovirus

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2
Q

What is the problem with a lack of insulin?

A

Body cannot take glucose from the blood and use it for fuel - causing hyperglycaemia

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3
Q

What is the aim for blood glucose?

A

4.4 and 6.1 mmol/L

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4
Q

What is insulin produced by?

A

Beta cells in the islets of langerhans in the pancreas

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5
Q

What type of hormone is insulin?

A

Anabolic hormone (building hormone)

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6
Q

How does insulin reduce blood sugar levels?

A

Increases cell uptake of glucose for fuel

Causes liver and muscle cells to store as glycogen

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7
Q

What is glucagon?

A

Hormone which increases blood sugar levels

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8
Q

Where is glucagon made?

A

Alpha cells in the Islets of Langerhans (catabolic hormone)

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9
Q

When is glucagon is released? What does it stimulate?

A

Response to low blood sugar levels to stimulate glycogenolysis (breaking down glycogen into glucose) and gluconeogenesis (converting proteins and fats into glucose)

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10
Q

What is ketogenesis?

A

Conversion of fatty acids to ketones by the liver when there is insufficient supply of glucose and glycogen stores are exhausted such as in prolonged fasting

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11
Q

What are ketones?

A

Water soluble fatty acids which can be used as fuel - can cross blood brain barrier and be used by the brain

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12
Q

What is characteristic for people in ketosis?

A

Acetone smell to breath

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13
Q

How do patients with T1DM present?

A

Diabetic ketoacidosis or hyperglycaemia

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14
Q

What is the classic triad of symptoms of hyperglycaemia?

A

Polyuria (excessive urine)

Polydipsia (excessive thirst)

Weight loss (mostly through dehydration)

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15
Q

What are some less typical presentations of T1DM?

A

Secondary enuresis (bedwetting in a previously dry child)

Recurrent infections

Symptoms are usually present for 1-6 weeks prior to developing DKA - varies significantly

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16
Q

What bloods should be taken with a new diagnosis of T1DM?

A
  • Bloods: FBC, U&Es, formal laboratory glucose
  • Blood cultures for suspected infection (i.e. fever)
  • HbA1c for blood sugar over last 3 months
  • TFTs and thyroid peroxidase antibodies to test for associated autoimmune thyroid disease
  • Tissue transglutaminase (anti-TTG) antibodies for associated coeliac disease
  • Insulin antibodies, anti-GAD antibodies and islet cell antivodies for antibodies associated with destruction of the pancreas and development of type 1 diabetes
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17
Q

What are the management principles for T1DM?

A
  • Subcut insulin regimes
  • Monitoring dietary carbohydrate intake
  • Monitoring blood sugar levels on waking, at each meal and before bed
  • Monitorign for and managing complications both short term and long term
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18
Q

What is the insulin regime for T1DM?

A
  • Background, long acting insulin once a day
  • Short acting inulin injected 30 mins before meals (alternatively can be given by an insulin pump)

Initiated by a diabetic specialist

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19
Q

What can injecting into the same spot cause?

A

Lipodystrophy (subcutaneous fat hardens and prevents normal absorption of insulin)

Check for this if patient is not responding to insulin as expected

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20
Q

What is a ‘basal bolus regime’ for insulin?

A

Basal = injection of long acting insulin e.g. “lantus” typically in evening

Bolus = injection of short acting insulin e.g. actrapid usually 3 times a day (also injected according to number of carbs consumed before every snack)

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21
Q

What is an insulin pump?

A

Small device which continuously infuses insulin at different rates to control blood sugar levels - alternative to basal bolus regime

Insulin is given through a cannula which is inserted under the skin (replaced every 2-3 days and insertion sites rotated

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22
Q

How can a patient qualify for an insulin pump?

A

Child over 12 and have difficulty controlling HbA1c

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23
Q

What are the advantages of an insulin pump?

A

Better sugar control

More flexibility with eating

Less injections

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24
Q

What are the disadvantages of an insulin pump?

A

Difficulties with learning to use pump

Having pump attached at all times

Blockages

Infection

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25
Q

What are the two types of insulin pumps?

A

Tethered pump

Patch pump

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26
Q

What is a tethered pump?

A

Pump + replaceable infusion set

Pump is attached around the waist - controls are usually on the pump itself

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27
Q

What is a patch pump?

A

Sits directly on the skin without any visible tubes

When out of insulin the entire patch pump is disposed of (usually controlled by a separate remote)

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28
Q

What are the short term complications of T1DM?

A

Hypoglycaemia

Hyperglycaemia (DKA)

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29
Q

What is hypoglycaemia?

A

Low blood sugar level caused by too much insulin or not processing carbs correctly e.g. malabsorption, diarrhoea, vomiting and sepsis

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30
Q

What are the typical symptoms of hypoglycaemia?

A

Hunger

Tremor

Swearing

Irritability

Dizziness

Pallor

If severe:

Reduced consciousness

Coma

Death

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31
Q

How is mild hypoglycaemia treated?

A

Rapid acting glucose e.g. lucozade

Slower acting glucose e.g. biscuits / toast to maintain blood sugar when rapid acting glucose is used

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32
Q

How is severe hypoglycaemia treated?

A

IV dextrose (10%) and IM glucagon

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33
Q

What are some other causes of hypoglycaemia?

A

Hypothyroidism

Glycogen storage disease

Growth hormone deficiency

Liver cirrhosis

Alcohol

Fatty acid oxidation deficits (e.g. MCADD)

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34
Q

What is nocturnal hypoglycaemia?

A

Complication of T1DM where the child is sweaty overnight, morning blood glucose levels may be raised - diagnosis can be made by continuous glucose monitoring

Treated by altering the bolus insulin regimes and snacks at bedtime

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35
Q

What is hyperglycaemia different from?

A

DKA

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36
Q

What are the macrovascular complications of T1DM?

A

Coronary artery disease (major cause of death)

Peripheral ischaemia (leading to poor healing, ulcers and diabetic foot)

Stroke

Hypertension

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37
Q

What are some microvascular complications of T1DM?

A

Peripheral neuropathy

Retinopathy

Kidney disease, particularly glomerulosclerosis

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38
Q

What causes the vascular changes in T1DM?

A

Chronic hyperglycaemia causes damage to the endothelial cells of blood vessels causing malfunctioning vessels which are unable to regenerate

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39
Q

What does suppression of the immune system in T1DM cause?

A

UTIs

Pneumonia

Skin and soft tissue infections (especially in feet)

Fungal infections, particularly oral and vaginal candidiasis

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40
Q

What is HbA1c measuring?

A

Glycated haemoglobin - how much glucose is attached to the haemoglobin molecules inside RBCs - reflects average blood glucose over last 3 months

Used to determine how effective interventions are

Blood sample in red top EDTA bottle

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41
Q

What is capillary blood glucose measured with?

A

Glucose meter - used to self-monitor sugar levels

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42
Q

What is flash glucose monitoring (e.g. FreeStyle Libre)

A

Uses a sensor on skin to measure the glucose level of the interstitial fluid in subcutaneous skin

5 minute lag behind blood glucose (so capillary blood glucose needed to check for hypoglycaemia)

User needs a reader to swipe over the sensor

Sensors need replacing every 2 weeks for the FreeStyle Libre system (quite expensive, funding not everywhere)

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43
Q

What is ketogenesis and when does it occur?

A

Liver takes fatty acids and converts to ketones happens when there is an insufficient supply of glucose and glycogen stores

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44
Q

How can ketone levels be measured?

A

Using a urine dipstick and in blood using a ketone meter

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45
Q

What is diabetic ketoacidosis?

A

Metabolic acidosis as a result of extreme hyperglycaemic ketosis (normally ketones are buffered in normal patients so blood doesnt become acidotic)

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46
Q

Why does DKA occur in T1DM?

A

Person isn’t producing enough insulin and not injecting adequate insulin to compensate for this

47
Q

What are the main problems with DKA?

A

Ketoacidosis, dehydration and potassium imbalance

48
Q

Why does dehydration occur in DKA?

A

As glucose is filtered into the urine this draws water out (osmotic diuresis) causes patient to urinate a lot (polyuria) resulting in severe dehydration which stimulated the thirst centre to drink lots of water (polydipsia)

49
Q

What causes the potassium imbalance in DKA?

A

Insulin normally drives potassium into cells

In DKA serum potassium may be normal but total body potassium is low - thus when treatment with insulin starts patients can develop hypoglycaemia which can lead to fatal arrhythmias

50
Q

What is a risk when rapidly correcting dehydration and hyperglycaemia?

A

Cerebral oedema - during DKA dehydration and high blood sugar concentration causes water to move from the intracellular space in the brain to the extracellular space - rapidly correcting this causes brain to swell and become oedematous

51
Q

What should be monitored when correcting DKA?

A

Neurological observations (i.e. GCS) to look for signs of cerebral oedema

Signs of headaches, altered behaviour, bradycardia or changes to conciousness

52
Q

What are the management options of cerebral oedema?

A

Slowing of IV fluids

IV mannitol

IV hypertonic saline

53
Q

How does DKA present?

A

Polyuria

Polydipsia

N&V

Weight loss

Acetone smell to breath

Dehydration and subsequent hypotension

Altered consciousness

Symptoms of underlying trigger (i.e. sepsis)

54
Q

How to diagnose DKA?

A

Hyperglycaemia ( > 11 mmol/l)

Ketosis (blood ketones > 3mmol/l)

Acidosis (pH <7.3)

55
Q

What are the two aspects of correcting DKA?

A

Correct dehydration evenly over 48 hours (corrects the dehydration and dilutes the hyperglycaemia and ketones - too quick = cerebral oedema)

Give fixed rate insulin infusion

56
Q

What are some other important principles of DKA management?

A

Avoid food boluses to minimise risk of cerebral oedema (unless required for resus)

Treat underlying triggers e.g. abx for septic patients

Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/L

Add potassium to IV fluids and monitor

Monitor for signs of cerebral oedema

Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcut insulin

57
Q

What is adrenal insufficiency?

A

Adrenal glands dont produce enough steroid hormones, particularly cortisol and aldosterone (life threatening unless hormones are replaced)

58
Q

What is addison’s disease?

A

Adrenal glands are damaged causing reduced secretion of cortisol and aldosterone aka primary adrenal insufficiency most commonly caused by autoimmune

59
Q

What is secondary adrenal insufficiency?

A

Inadequate ACTH stimulating the adrenal glands causing low levels of cortisol to be released (result of damage to the pituitary gland)

60
Q

What can cause secondary adrenal insufficiency?

A

Congenital underdevelopment (hypoplasia)

Surgery

Infection

Loss of blood flow

Radiotherapy

61
Q

What is tertiary adrenal insufficiency?

A

Result of inadequate CRH release from the hypothalamus usually the result of being on long term steroids (exogenous steroids - longer than 3 weeks) causing suppression of the hypothalamus (long term steroids need to be slowly tapered)

62
Q

What are the features of adrenal insufficiency in babies?

A

Lethargy

Vomiting

Poor feeding

Hypoglycaemia

Jaundice

Failure to thrive

63
Q

What are some features in older children of adrenal insufficiency?

A

N&V

Poor weight gain / weight loss

Anorexia

Abdo pain

Muscle weakness / cramps

Developmental delay or poor academic performance

Bronze hyperpigmentation to skin caused by ACTH (this stimulates melanocytes)

64
Q

What are the investigations for Addison’s Disease?

A

Cortisol / ACTH / aldosterone / renin

U&Es​ (hyponatraemia / hyperkalaemia)

Blood glucose (hypoglycaemia)

65
Q

What is are the results in Addison’s disease (primary adrenal failure)?

A

Low cortisol

Low aldosterone

High ACTH

High renin

66
Q

What are the results in secondary adrenal insufficiency?

A

Low cortisol

Normal aldosterone

Low ACTH

Normal renin

67
Q

What is the short synacthen test (ACTH stimulation test)?

A

Confirms adrenal insufficiency

Performed in the morning - adrenal glands are most fresh

Giving synacthen - synthetic ACTH

Blood cortisol is measured at baseline, 30, 60 minutes (level should at least double)

If no rise then primary adrenal insufficiency (Addison’s disease)

68
Q

What is the treatment of adrenal insufficiency?

A

Replacement steroids:

Hydrocortisone (glucocorticoid) replaces cortisol

Fludrocortisone (mineralcorticoid) replaces aldosterone

69
Q

What is the ‘steroid advice’ for addisons insufficiency?

A

Steroid card and emergency ID tag to inform emergency services

Doses are increased during an acute illness to match the normal steroid response

70
Q

What are paediatric patients with adrenal insufficiency monitored for?

A

Growth and development

Blood pressure

U&Es

Glucose

Bone profile

Vitamin D

71
Q

What are the sick day rules in adrenal insufficiency? (if really unwell with temp over 38 degrees or vomiting and diarrhoea)

A

Increase dose of steroid and given more regularly

Blood sugar needs monitoring closely and eating carby foods

With diarrhoea / vomiting need IM injection of steroid at home and likely required admission for IV steroids

72
Q

What is an Addisonian crisis?

A

Acute presentation of severe Addisons where the absence of steroid homones causes a life threatening presentation

73
Q

How do patients with addisonian crisis present?

A
  • Reduced consciousness
  • Hypotension
  • Hypoglycaemia, hyponatraemia, hyperkalaemia
74
Q

What can trigger an Adrenal crisis?

A

Infection

Trauma

Stopping steroids abruptly

75
Q

What is the management of an Addisonian crisis?

A

Intensive monitoring if they are acutely unwell

Parenteral steroids (i.e. IV hydrocortisone)

IV fluid resus

Correct hypoglycaemia

Careful monitoring of electrolytes and fluid balance

76
Q

What is congenital adrenal hyperplasia?

A

Underproduction of cortisol and aldosterone

Overproduction of androgens

Caused by a congenital deficiency of the 21-hydroxylase enzyme / 11-beta-hydroxylase

Autosomal recessive

77
Q

What is testosterone?

A

Androgen hormone - high levels in men and low levels in women

Promotes male sexual characteristics

78
Q

What do glucocorticoid hormones do?

A

Help body deal with stress, raise blood glucose, reduce inflammation and suppress immune system

79
Q

What is the main glucocorticoid hormone?

A

Cortisol which fluctuates during the day with higher levels in the morning and times of stress

80
Q

When is cortisol released?

A

In response to adrenocorticotropic hormone (ACTH) from anterior pituitary

81
Q

What do mineralcorticoid hormones do?

A

Act on kidneys to control balance of salt and water in blood

82
Q

What is the main mineralcorticoid hormone?

A

Aldosterone

83
Q

Where and when is aldosterone released?

A

Adrenal glandin reponse torenin

84
Q

What does aldosterone do?

A

Increases sodium reabsorption into the blood and potassium secretion into the urine

85
Q

What is the pathophysiology of congenital adrenal hyperplasia?

A

21-hydroxylase enzyme converts progesterone into aldosterone and cortisol - as there is a deficiency then it is instead converted into testosterone

86
Q

How do female patients with CAH present?

A

At birth with ambiguous genitalia (virilised) and enlarged clitoris due to high testosterone levels

87
Q

What are the signs and symptoms of severe CAH?

A

Poor feeding

Vomiting

Dehydration

Arrythmias

88
Q

What are the electrolyte imbalances in severe CAH?

A

Hyponatraemia

Hyperkalaemia

Hypoglycaemia

89
Q

What are the later symptoms of CAH (due to high androgen levels) in men and women respectively?

A

Female

  • Tall
  • Facial hair
  • Absent periods
  • Deep voice
  • Early puberty

Male

  • Tall
  • Deep voice
  • Large penis
  • Small testicles
  • Early puberty
90
Q

What is the ‘textbook clue’ for congenital adrenal hyperplasia?

A

Skin hyperpigmentation because low levels of corticol causes an increase in ACTH (a byproduct of production is melanocyte simulating hormone)

91
Q

What is the management of congenital adrenal hyperplasia?

A

Cortisol replacement with hydrocortisone

Aldosterone replacement with fludrocortisone

Female patients with “virilised” genitals may require corrective surgery

92
Q

Where is growth hormone produced?

A

Anterior pituitary gland

93
Q

What does growth hormone do?

A

Stimulates cell production

Growth of organs, muscles, bones and height

Stimulates release of insulin-like growth factor 1 (IGF-1) by the liver

94
Q

What promotes and supresses the release of GH

A

Promotes = GHRH and Ghrelin

Supresses = Somatostatin

95
Q

What can congenital growth hormone deficiency be caused by?

A

Disruption to the growth hormone axis at the hypothalamus or pituitary gland can be due to a known genetic mutation e.g. GH1 (growth hormone 1) or GHRHR (growth hormone releasing hormone receptor) genes OR sue to empty sella syndromewhere th pituitary gland isunder-developed or damaged

96
Q

What can cause acquired growth hormone deficiency?

A

Secondary to infection, trauma or surgery

97
Q

What is it called when the pituitary does not produce a number of pituitary hormones?

A

Hypothyroidism or multiple pituitary hormone deficiency

98
Q

How does growth hormone deficiency present at birth?

A

Micropenis (in males)

Hypoglycaemia

Severe jaundice

99
Q

How does growth hormone deficiency present in infants and children?

A

Poor growth (stopping / severely slowing from 2-3)

Short stature

Slow development of movement and strength

Delayed puberty

100
Q

What is the growth hormone stimulation test?

A

Giving glucagon, insulin, arginine and clonidine (medications which usually stimulate release of growth hormone) and monitoring the response (every 2-4 hours after)

101
Q

What are the other investigations for growth hormone deficiency?

A

Test for thyroid and adrenal deficiency

MRI brain for structural pituitary / hypothalamus abnormalities

Genetic testing for associated genetic conditions e.g. Turner syndrome and Prader-Willi syndrome

X-ray (usually of the wrist) or a DEXA scan to determine bone age and predict final height

102
Q

What is the treatment of growth hormone deficiency?

A

Daily subcut injections of growth hormone (somatropin)

Treatment of other hormone deficiencies

Close monitoring of height and development

103
Q

What can cause hypothyroidism in children?

A

Congenital / acquired

104
Q

Why is thyroid hormone important in children?

A

Essential for development of brain and body - hypothroidism can cause intellectual disability

105
Q

What can cause congenital hypothyroidism?

A

Underdeveloped thyroid gland (dysgenesis)

Fully developed gland which doesn’t produce enough hormone (dyshormonogenesis)

Cause isn’t clear

106
Q

When is congenital hypothyroidism screened for ?

A

Newborn blood spot screening test

107
Q

How does congenital hypothyroidism present?

A

Prolonged neonatal jaundice

Poor feeding

Constipation

Increased sleeping

Reduced activity

Slow growth and development

108
Q

What is the most common cause of acquired hypothyroidism?

A

Autoimmune thyroiditis aka Hashimoto’s thyroiditis causing autoimmune inflammation of the thyroid gland and subsequent underactivity

109
Q

What is Hashimoto’s disease associated with?

A

Antithyroid peroxidase (anti TPO) antibodies

Antithyroglobulin antibodies

110
Q

What conditions is Hashimoto’s disease associated with?

A

Type 1 diabetes and coeliacs disease

111
Q

What are the symptoms of acquired hypothyroidism?

A

Fatigue and low energy

Poor growth

Weight gain

Poor school performance

Constipation

Dry skin and hair loss

112
Q

What are the investigations for hypothyroisism?

A

TFTs

Thyroid ultrasound

Thyroid antibodies

113
Q

What is the management of hypothyroidism?

A

Levothyroxine orally once a day to replace normal thyroid hormones (titrated based on TFTs and symptoms)

Paediatrics (18 decks)

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