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Endocrinology Flashcards

1
Q

Where is GH produced?

A

Anterior pituitary gland

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2
Q

What is the action of GH?

A

Stimulates cell reproduction and growth of organs, muscles, bones and height
Stimulates release of insulin-like growth factor

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3
Q

Where is IGF-1 released from and what is its action?

A

Released by the liver and promotes growth

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4
Q

What is congenital GH deficiency a result of?

A

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

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5
Q

What are some causes of congenital GH deficiency?

A 
Genetic mutations (e.g. GH1, GHRGHR) 
Empty sella syndrome (underdeveloped pituitary gland) 
Hypopituitarism/ multiple pituitary hormone deficiency
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6
Q

What are some causes of acquired growth hormone deficiency?

A

Secondary to infection, trauma or surgery

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7
Q

How may GH deficiency present in neonates?

A

Micropenis
Hypoglycamia
Severe jaundice

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8
Q

How may older children present with GH deficiency?

A

Poor growth
Short stature
Slow development of movement/ strength
Delayed puberty

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9
Q

What test is done to look for GH deficiency?

A

Growth hormone stimulation test: measuring response to medications that normally stimulate the release of GH.

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10
Q

What other investigations are done when looking at GH deficiency?

A

Test for thyroid and adrenal deficiency
MRI brain (pituitary or hypothalamic abnormalities)
Genetic testing
Xray for bone age

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11
Q

How is GH deficiency managed?

A

Daily subcutaneous injections of GH
Treat other hormone deficiencies
Close monitoring of height and development

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12
Q

What is the pathophysiology of T1DM?

A

Pancreas stops being able to produce insulin (unknown why), meaning cells can’t use glucose, causing hyperglycaemia

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13
Q

What is the ideal blood glucose concentration?

A

4.4-6.1 mmol/ L

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14
Q

Where is insulin produced?

A

Beta cells in the Islets of Langerhans in the pancreas

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15
Q

What kind of hormone is insulin?

A

Anabolic (builiding)

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16
Q

What are the 2 ways insulin reduces blood sugar?

A

Causes cells to absorb glucose from the blood and use it as fuel.
Causes muscle and liver cells to absorb glucose and store it as glycogen.

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17
Q

What kind of hormone is glucagon and where is it produced?

A

Catabolic hormone produced by the alpha cells in the Islets of Langerhans in the pancreas

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18
Q

What occurs during ketogenesis?

A

When there is insufficient supply of glucose and glycogen stores are exhausted, the liver converts fatty acids to ketones to be used as fuel

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19
Q

What percentage of new T1 diabetics present in DKA?

A

25-50%

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20
Q

What is the triad of symptoms that T1 diabetes presents with?

A

Polyuria
Polydipsia
Weight loss

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21
Q

What are some less typical potential presentations of T1 diabetes?

A 
Secondary enuresis (bedwetting in a previously dry child)
Recurrent infections
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22
Q

What bloods should be taken on a new T1 diabetes diagnosis?

A 
FBC
U&E's 
Lab glucose
Blood cultures
HbA1c
TFT's + TPO 
anti-TTG antibodies
Insulin, anti-GAD and Islet cell antibodies
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23
Q

Why are TFT’s and TPO’s done in a newly diagnosed T1 diabetes?

A

To test for autoimmune thyroid disease

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24
Q

Why are anti-TTG antibodies looked for in new T1 diabetes diagnosis?

A

TO test for coeliac disease

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25
Q

Why are Insulin antibodies, anti-GAD antibodies and islet cell antibodies tested for on new T1 diabetes diagnosis?

A

To test for antibodies associated with the destruction of the pancreas and the development of T1 diabetes

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26
Q

What are the different components of T1 diabetes management?

A

Insulin regimes
Monitoring carbohydrate intake
Monitoring blood sugar
Monitoring/ managing complications

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27
Q

When should T1 diabetics check their blood sugar levels?

A

On waking
At each meal
Before bed

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28
Q

What are the different insulin regimes available?

A

Basal- bolus

Insulin pump

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29
Q

What can injecting insulin in the same spot cause?

A

Lipodystrophy- where the subcutaneous fat hardens and prevents normal absorption of insulin

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30
Q

Why should patients cycle their injection sites?

A

To prevent lipodystrophy and ensure effective absorption of insulin

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31
Q

What is the basal part of the basal-bolus regime?

A

Injection of long acting insulin once a day to give constant background insulin

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32
Q

What is the bolus part of the basal-bolus regime?

A

Injection of short acting insulin before meals, and according to the number of carbohydrates consumed with each snack

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33
Q

How do insulin pumps work?

A

Continuously infuse insulin at different rates through a cannula inserted under the skin

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34
Q

How often is the cannula repalced on an insulin pump?

A

Every 2-3 days

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35
Q

What is the criteria needed to qualify for an insulin pump on the NHS?

A

> 12

Have difficulty controlling HbA1c

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36
Q

What are the advantages of an insulin pump?

A

Better blood sugar control
More flexibility with eating
Fewer injections

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37
Q

What are the disadvantages of an insulin pump?

A

Difficulties learning to use it
Having it attached at all times
Blockages in the infusion set
Small risk of infection

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38
Q

What are the two types on insulin pump?

A

Tethered pump

Patch pump

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39
Q

What are tethered pumps?

A

Devices with replaceable infusion sets and insulin. Pump usually has all controls on it and can attach to belt/ pocket ect.

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40
Q

What is a patch pump?

A

Patch attached directly onto body and works via remote. Whole thing needs changing (not just infusion set and location)

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41
Q

What are the short term complications of T1 diabetes?

A

Hypoglycaemia

Hyperglycaemia (& DKA)

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42
Q

What causes hypoglycaemia in diabetes?

A

Too much insulin
Not enough carbohydrates
Not processing carbohydrates properly (malabsorption, diarrhoea, vomiting, sepsis)

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43
Q

What are the typical symptoms of hypoglycaemia?

A 
Hunger
Tremor
Sweating
Irritability
Dizziness
Pallor
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44
Q

How is hypoglycaemia treated?

A

Combination of rapid acting glucose (e.g. lucozade) and slower acting carbohydrates

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45
Q

What are the signs of severe hypoglycaemia?

A

Reduced consciousness
Coma
Death

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46
Q

How is severe hypoglycaemia treated?

A

IV dextrose

IM glucagon

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47
Q

What are other causes of hypoglycaemia?

A 
Hypothyroidism
Glycogen storage disorder
GH deficiency
Liver cirrhosis
Alcohol
Fatty acid oxidation defects
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48
Q

When does hypoglycaemia commonly occur in T1 diabetics and how is this managed?

A

Nocturnal hypoglycaemia

Treat by altering basal-bolus regime and have snacks at bedtime

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49
Q

How is hyperglycaemia managed?

A

Increase insulin dose

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50
Q

What are the different types of long term complications that can occur with T1 diabetes?

A

Macrovascular
Microvascular
Infections

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51
Q

What does chronic exposure to hyperglycaemia do to blood vessels?

A

Damages endothelium, leading to leaky malfunctioning vessels that are unable to regenerate

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52
Q

What does chronic hyperglycaemia to to the immune system?

A

Suppresses it, and creates optimal environment for infectious organisms to thrive

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53
Q

What are the macrovascular complications of T1 diabetes?

A

Coronary artery disease
Peripheral ischaemia (poor healing, ulcers, diabetic foot)
Stroke
Hypertension

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54
Q

What are the microvascular complications of T1 diabetes?

A

Peripheral neuropathy
Retinopathy
Nephropathy

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55
Q

How is T1 diabetes monitored?

A

HbA1c
Capillary blood glucose
Flash glucose monitoring

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56
Q

What is measured on HbA1c?

A

Glycated haemoglobin- reflects average blood glucose over last 3 mnths

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57
Q

How often is HbA1c measured in T1 diabetics?

A

Every 3-6 months to track average blood sugar and assess effectiveness of interventions

58
Q

What is Flash glucose monitoring?

A

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

59
Q

What is the FreeStyle Libre system?

A

Device that sits on upper arm and continuously monitors blood glucose

60
Q

What is the time lag when using flash glucose monitoring?

A

5 minutes

61
Q

What are ketones?

A

Water soluble fatty acids that can be used as fuel

62
Q

How can ketone levels be measured?

A

Urine dipstick

Blood using ketone meter

63
Q

What does hyperglycaemic ketosis do to the blood?

A

Causes metabolic acidosis

64
Q

When does DKA occur?

A

When the patient is not producing adequate and not injecting adequate insulin to compensate

65
Q

What are the key problems in DKA?

A

Ketoacidosis
Dehydration
Potassium imbalance

66
Q

Why do you get dehydrated in DKA?

A

Hyperglycaemia overwhelms the kidneys and causes glucose to be filtered into the urine. This draws water out (osmotic diuresis), resulting in severe dehydration

67
Q

Why do you get potassium imbalance in DKA?

A

Insulin usually drives potassium into cells. Therefore without it potassium stays in the blood

68
Q

What happens to serum potassium in DKA and why?

A

It is either high (due to no insulin driving it into cells) or normal due to kidneys balancing the levels with the amount excreted in the urine

69
Q

What happens to total body potassium in DKA?

A

It is low as none of it is being stored in the cells

70
Q

What can happen when insulin treatment starts in patients with DKA/

A

They can develop severe hypokalaemia, which can lead to fatal arrhythmias

71
Q

What are children with DKA at high risk of developing?

A

Cerebral oedema

72
Q

Why does DKA increase the risk of cerebral oedema?

A

Dehydration + hyperglycaemia cause water to move from the intracellular space in the brain to the extracellular space, causing brain cells to shrink and become dehydrated. Then, the correction with fluids and insulin causes a rapid shift back to the intracellular space, causing the brain to become oedematous

73
Q

What should be monitored closely to look for signs of cerebral oedema when treating DKA?

A

GCS

Headaches, altered behaviour, bradycardia

74
Q

How is cerebral oedema managed?

A

Slowing IV fluids, IV mannitol and IV hypertonic saline

75
Q

How dose DKA present?

A 
Polyuria
Polydipsia
N&V
Weight loss
Acetone breath
Dehydration + hypotension
Altered consciousness
Symptoms of underlying trigger (e.g. sepsis)
76
Q

What is the criteria for diagnosing DKA?

A

Hyperglycaemia (>11mol/l)
Ketosis (>3mmol/l)
Acidosis (ph<7.3)

77
Q

What are the 2 principles of DKA management?

A
  1. Correct dehydration over 48 hours

2. Give fixed rate insulin infusion

78
Q

What other factors should be considered when managing DKA?

A
  • Avoid fluid boluses
  • Treat underlying triggers (Abx for sepsis)
  • Prevent hypoglycaemia with IV dextrose
  • Monitor potassium and add to fluids if needed
  • Monitor for signs of cerebral oedema
  • Monitor glucose, ketones and pH to assess progress
79
Q

What is adrenal insufficiency?

A

Where the adrenal glands don’t produce enough steroid hormones

80
Q

What are the main steroid hormones produces by the adrenal glands?

A

Cortisol and aldosterone

81
Q

What is Addison’s disease?

A

Primary adrenal insufficiency- condition where the adrenal glans have been damaged causing reduction in cortisol and aldosterone secretion

82
Q

What is the most common cause of primary adrenal insufficiency?

A

Autoimmune

83
Q

What is secondary adrenal insufficiency?

A

When there inadequate ACTH stimulating the adrenal glands, resulting in low levels of cortisol being released

84
Q

What is the causes of secondary adrenal insufficiency?

A 
Loss or damage to pituitary gland:
Congenital underdevelopment
Surgery
Infectino
Radiotherapy
Loss of blood flow
85
Q

What is tertiary adrenal insufficiency?

A

The result of inadequate CRH release by the hypothalamus

86
Q

What is the most common cause of tertiary adrenal insufficiency?

A

Long term oral steroids causing suppression of the hypothalamus

87
Q

Why should long term steroids be tapered slowly?

A

If they are withdrawn suddenly, the hypothalamus does not wake up fast enough to produce adequate endogenous steroids.

88
Q

What are the features of adrenal insufficiency in babies?

A 
Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrice
89
Q

What are the features of adrenal insufficiency in older children?

A 
Nausea and vomiting
Weight loss/ poor weight gain
Anorexia
Abdominal pain
Muscle weakness/ cramps
Developmental delay 
Bronze hyperpigmentation in Addison's
90
Q

Why do you get bronze hyperpigmentation in Addison’s?

A

High ACTH levels stimulate melanocytes

91
Q

What investigations should be done with suspected adrenal insufficiency?

A

U&E’s
Blood glucose
Cortisol, ACTH, aldosterone and renin levels
Short synacthen test

92
Q

What will be the results of tests in Addisons disease?

A

Low cortisol
High ACTH
Low aldosterone
High renin

93
Q

What will be the results of tests in secondary adrenal insufficiency?

A

Low cortisol
Low ACTH
Normal aldosterone
Normal renin

94
Q

What is the short synacthen test?

A

Synacthen (synthetic ACTH) given in the morning. Blood cortisol taken at baseline, 30 and 60 minutes after administration.

95
Q

What is a normal result of the short synacthen test?

A

Cortisol level should at least double

96
Q

What does a failure of cortisol to rise indicate in a short synacthen test?

A

Primary adrenal insufficiency

97
Q

How is adrenal insufficiency managed?

A

Replacement steroids

98
Q

What steroid hormones are given to manage adrenal insufficiency?

A

Hydrocortisone to replace cortisol

Fludrocrotisone to replace aldosterone

99
Q

What should patients on steroid hormone be given?

A

Steroid card and emergency ID tag to inform emergency services they are dependent on steroids for life

100
Q

What should be monitored in patients with adrenal insufficiency?

A 
Growth & development
BP
U&E's
Glucose
Bone profile
Vitamin D
101
Q

What should patients on steroids do during acute illness? (Sick day rules)

A

Increase dose of steroids until illness has resolved
Blood sugar monitoring
IM steroid if have diarrhoea or vomiting

102
Q

What is an adrenal crisis?

A

An acute presentation of severe Addisons

103
Q

How does an adrenal crisis present?

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia and hyperkalamia

104
Q

When might adrenal crisis occur?

A

First presentation of Addison’s disease,
Triggered by infection, trauma or other acute illness
Abrupt stopping of long term steroids

105
Q

How do you manage Addisonian crisis?

A

Intensive monitoring
Parenteral steroids
IV fluids
Hypoglycaemia

106
Q

What is congenital adrenal hyperplasia?

A

Underproduction of cortisol and aldosterone, and overproduction of androgens

107
Q

What causes CAH?

A

Autosomal recessive condition causing deficiency of 21-hydroxylase enzyme

108
Q

What type of hormone is testosterone?

A

Androgen

109
Q

What is the action of glucocorticoid hormones?

A

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

110
Q

What is the main glucocorticoid hormone?

A

Cortisol

111
Q

When are cortisol levels higher?

A

In the morning

During times of stress

112
Q

What is cortisol released in response to?

A

ACTH from the anterior pituitary

113
Q

What is the action of mineralocorticoid hormones?

A

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

114
Q

What is the main mineralocorticoid hormone?

A

Aldosterone

115
Q

What is aldosterone released in response to?

A

Renin

116
Q

What is the action of aldosterne?

A

Acts on the kidneys to increase sodium reabsorption in the blood and increase potassium secretion into the urine

117
Q

What is the action of 21-hydroxylase?

A

Enzyme responsible for converting progesterone into aldosterone and cortisol (NOT testosterone)

118
Q

What is progesterone converted into?

A

Aldosterone
Cortisol
Testosterone

119
Q

What is the pathophysiology of congenital adrenal hyperplasia?

A

Defect in 21-hydroxylase enzyme means that there is extra progesterone that cannot be converted to aldosterone or cortisol, so is instead converted to testosterone

120
Q

What are the aldosterone, cocrtisol and testosterone levels in CAH?

A

Low aldosterone & cortisol

High testosterone

121
Q

How does severe CAH present at birth in females?

A

Virilised genitalia

122
Q

What is virilised genitalia?

A

Ambiguous genitalia- enlarged clitoris

123
Q

How do patients with more severe CAH present shortly after birth?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

124
Q

What are the signs and symptoms of severe CAH?

A 
Poor feeding
Vomiting
Dehydration
Arrhythmias
Virilisation
125
Q

When do patients with severe CAH usually present?

A

At birth

126
Q

When do patients with mild cases of CAH usually present?

A

During childhood or after puberty

127
Q

What do the symptoms of mild CAH tend to be related to?

A

High androgen (testosterone) levels

128
Q

How do females with mild CAH usually present?

A 
Tall for age
Facial hair
Absent periods
Deep voice
Early puberty
Hyperpigmentation
129
Q

How do male patients with mild CAH usually present?

A 
Tall 
Deep voice
Large penis
Small testicles
Early puberty 
Hyperpigmentation
130
Q

Why do you get hyperpigmentation in CAH?

A

Pituitary gland responds to low levels of cortisol by producing more ACTH/ A byproduct of ACTH is melanocyte simulating hormone.

131
Q

How is CAH managed?

A

Cortisol replacement with hydrocortisone
Aldosterone replacement with fludrocortisone
Corrective surgery for virilisation

132
Q

What is congenital hypothyroidism?

A

Where the child is born with an underactive thyroid gland or gland that does not produce enough hormone

133
Q

What is dysgenesis?

A

Underdeveloped thyroid gland

134
Q

What is dyshormonogenesis?

A

Fully developed gland that does not produce enough hormone

135
Q

Where is congenital hypothyroidism screened for?

A

Newborn blood spot screening test

136
Q

How may patients with congenital hypothyroidism present if not picked up at screening test?

A 
Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development
137
Q

What is acquired hypothyroidism?

A

Where a child develops an underactive thyroid gland that was previously functioning normally

138
Q

What is the most common cause of acquired hypothyroidism?

A

Autoimmune thyroiditis (Hashimoto’s)

139
Q

What antibodies is Hashimoto’s associated with?

A

anti-TPO and antithyroglobulin

140
Q

What symptoms do you get with Hashimoto’s?

A 
Fatigue
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin/ hair loss
141
Q

How is hypothyroidism investigated?

A

Thyroid function tests
Thyroid USS
Thyroid antibodies

142
Q

How is hypothyroidism managed?

A

Levothyroxine once daily

Paeds (18 decks)

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