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Endocrinology Flashcards

1
Q

What is the pathophysiology of Type 1 diabetes mellitus (T1DM)?

A

T1DM is a form of diabetes that develops due to immune-mediated destruction of insulin-producing pancreatic beta cells. Without insulin, the body’s cells ‘starve’.

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2
Q

What age does T1DM typically develop?

A

Typically in people under the age of 25 years.

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3
Q

How does T1DM present?

A

Most commonly fatigue, polyuria, polydipsia and weight loss.

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4
Q

Over what time period does T1DM develop over?

A

Can develop over weeks to months.

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5
Q

Some T1DM patients may present critically with what condition?

A

Diabetic ketoacidosis.

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6
Q

How is T1DM diagnosed?

A

Finger-prick glucose monitor.

HbA1c.

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7
Q

What are the diagnostic thresholds for fasting and random blood glucose in symptomatic individuals ?diabetes mellitus?

A

Fasting glucose ≥ 7.0mmol/L.

Random blood glucose ≥ 11.0mmol/L.

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8
Q

What are the diagnostic thresholds for fasting and random blood glucose in asymptomatic individuals ?diabetes mellitus?

A

Fasting glucose ≥ 7.0mmol/L.
Random blood glucose ≥ 11.0mmol/L.
Demonstrated on two separate occasions.

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9
Q

What are the diagnostic thresholds for HbA1c in symptomatic individuals ?diabetes mellitus?

A

HbA1c ≥ 48mmol/mol.

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10
Q

What is HbA1c?

A

Glycated haemoglobin that reflects average blood glucose levels over the previous two-three months.

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11
Q

How is T1DM managed?

A

With regular monitoring of blood glucose and lifelong daily subcutaneous insulin injections.

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12
Q

By what route is insulin administered and where?

A

Subcutaneously typically at the stomach, thighs or buttocks.

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13
Q

What are side effects of subcutaneous insulin use?

A

Injection bruises (rupturing a small capillary when injecting), injection lumps (repeatedly injecting at the same site too often), weight gain and hypoglycaemic episodes.

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14
Q

What increases the risk of hypoglycaemic episodes during insulin use?

A

Imbalance of insulin in relation to food consumed and physical activity undertaken (missing a meal, not eating enough carbohydrates, doing lots of exercise, taking more insulin than needed).

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15
Q

Give four types of insulin.

A

Rapid-acting insulin (before or after meals).
Mixed insulin (mixture of short-acting and long-acting insulin, the number in the name indicates the % that is short-acting).
Intermediate-acting insulin (background insulin taken once or twice a day).
Long-acting insulin (even slower than intermediate and can be taken once per day).

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16
Q

What is typical strength of insulin (units/ml)?

A

100 units/ml.

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17
Q

What is diabetic ketoacidosis (DKA)?

A

A life-threatening complications of diabetes that occurs due to insufficient insulin.

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18
Q

How does DKA present?

A

Abdominal pain, vomiting and reduced consciousness. Patient may also have a high respiratory rate.

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19
Q

What precipitates DKA?

A

Typically precipitated by an illness or stressor. Can occur due to failure to take insulin (more common in the young and vulnerable e.g. homeless).

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20
Q

What investigations should be ordered/undertaken in a patient with suspected DKA?

A

Plasma glucose.
ABG.
Capillary or serum ketones.
Urinalysis.

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21
Q

What does plasma glucose reveal in a patient with DKA?

A

Blood glucose level > 11mmol/L.

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22
Q

What does ABG reveal in a patient with DKA?

A

Metabolic acidosis.

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23
Q

What does serum ketones reveal in a patient with DKA?

A

Ketonaemia > 3mmol/L.

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24
Q

What does urinalysis reveal in a patient with DKA?

A

Positive for glucose (glycosuria) and ketones (ketonuria).

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25
Q

Why do patients with DKA typically have a high respiratory rate?

A

Respiratory compensation for metabolic acidosis (blowing off carbon dioxide).

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26
Q

How is DKA managed?

A

Replace circulating volume with isotonic saline and start an insulin infusion of 0.1 unit/kg/hour.

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27
Q

Under what conditions may a patient develop euglycaemic DKA?

A

Patients taking SGLT2 inhibitors (e.g. canagliflozin). SGLT2 inhibitors cause too much glucose to be lost from urine.

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28
Q

Give five potential complications of DKA?

A

Infection, shock, thrombosis, pulmonary oedema and cerebral oedema.

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29
Q

What is the pathophysiology behind Type 2 diabetes mellitus (T2DM)?

A

High blood sugar, the development of insulin resistance and a relative lack of insulin.

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30
Q

How does T2DM present?

A

Polyuria, polydipsia and unexplained weight loss. Note: many individuals are asymptomatic.

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31
Q

Why do some people with T2DM present with weight loss?

A

Loss of water weight due to polyuria (excess urination).

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32
Q

How is T2DM initially managed?

A

Lifestyle changes such as improved diet, reduced sugar intake, more exercise and weight loss.

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33
Q

What is the target HbA1c for an individual with T2DM managed with lifestyle changes?

A

HbA1c < 48mmol/mol.

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34
Q

What is the first-line pharmacological treatment for T2DM?

A

Metformin.

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35
Q

How does metformin work?

A

Increases insulin sensitivity.

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36
Q

What are the benefits of metformin?

A

Especially useful in overweight patients. Rarely causes hypoglycaemia.

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37
Q

What are the potential side effects of metformin?

A

Gastrointestinal upset (abdominal pain, diarrhoea) and impaired B12 absorption.

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38
Q

What class of drug is metformin?

A

Biguanide.

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39
Q

When should T2DM management progress beyond first-line pharmacological treatment (metformin use)? i.e. HbA1c level

A

If T2DM is uncontrolled (HbA1c > 58 mmol/mol).

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40
Q

What is the next step in the management of T2DM beyond first-line (metformin)?

A

Add a second drug: sulfonylurea (gliclazide), DPP-4 inhibitor (sitagliptin), pioglitazone or SGLT2 inhibitor (canagliflozin).

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41
Q

What is the HbA1c target for an individual with T2DM on two oral antidiabetic agents?

A

HbA1c < 53 mmol/mol.

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42
Q

Metformin use in patients with T2DM is contraindicated in which patients?

A

Those with poor kidney function (eGFR < 30).

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43
Q

When should T2DM management progress beyond two oral antidiabetic agents? i.e. HbA1c level

A

If T2DM is uncontrolled (HbA1c > 58 mmol/mol).

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44
Q

What is the next step in the management of T2DM beyond two oral antidiabetic agents?

A

Add a third drug: sulfonylurea (gliclazide), DPP-4 inhibitor (sitagliptin), pioglitazone or SGLT2 inhibitor (canagliflozin) or consider insulin therapy.

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45
Q

What is the next step in the management of T2DM beyond triple therapy?

A

Consider giving metformin + sulfonylurea + GLP1 mimetic (exenatide). Only continue if there is a reduction of at least 11mmol/mol in HbA1c and weight loss of at least 3% in six months.

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46
Q

How should patients with T2DM be managed while admitted to hospital for acute coronary syndromes?

A

Intravenous insulin infusion with regular blood glucose monitoring.

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47
Q

What class of drug is gliclazide?

A

Sulfonylurea.

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48
Q

How does gliclazide work?

A

Stimulates insulin release.

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49
Q

What is a potential risk of gliclazide/sulfonylurea use?

A

Hypoglycaemia.

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50
Q

What are the potential risks of pioglitazone use?

A

Fractures, bladder cancer, weight gain, fluid, liver impairment.

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51
Q

What class of drug is sitagliptin?

A

DPP-4 inhibitors.

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52
Q

What is a potential risk of sitagliptin/DPP-4 inhibitor use?

A

Acute pancreatitis.

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53
Q

What class of drug is canagliflozin?

A

SGLT2 inhibitors.

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54
Q

What is a potential risk of canagliflozin/SGLT2 inhibitor use?

A

Urinary tract infections including thrush.

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55
Q

What class of drug is exenatide?

A

GLP1 mimetic.

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56
Q

What class of drug can lead to the development of diabetes? How?

A

Steroids. May result in the development of insulin resistance over time.

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57
Q

Hypoglycaemia is defined as a blood glucose level of what?

A

< 4 mmol/L.

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58
Q

The signs/symptoms of hypoglycaemia can be categorised into what two groups?

A

Adrenergic and neuroglycopenic.

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59
Q

What are the adrenergic signs/symptoms of hypoglycaemia?

A

Pallor, perspiration, tremor, tachycardia, anxiety and tingling lips.

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60
Q

What is the mechanism that leads to the development of adrenergic signs/symptoms in hypoglycaemia?

A

Adrenaline and noradrenaline release in response to low blood glucose.

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61
Q

What are the neuroglycopenic signs/symptoms of hypoglycaemia?

A

Confusion, irritability, lethargy, fitting, odd behaviour, slurred speech, coma, hemiparesis.

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62
Q

What is the mechanism that leads to the development of neuroglycopenic signs/symptoms in hypoglycaemia?

A

Direct result of low blood glucose levels in the brain.

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63
Q

Management of hypoglycaemia depends on what factors?

A

Patient conscious level.

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64
Q

How should hypoglycaemia be managed in the conscious, cooperative and able to swallow individual?

A

Give a sugary drink (glucojuice) or glucotabs.

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65
Q

How should hypoglycaemia be managed in the conscious, uncooperative but able to swallow individual?

A

Give glucojel.

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66
Q

How should hypoglycaemia be managed in the unconscious/fitting individual?

A

Give 15-20g of 10% glucose intravenously in those with venous access. Give intramuscular glucagon in those without venous access.

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67
Q

Give four potential complications of diabetes mellitus, other than hypoglycaemia and DKA.

A

Diabetic retinopathy.
Diabetic neuropathy.
Diabetic foot disease.
Hyperosmolar hyperglycaemic state (HHS).

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68
Q

What is diabetic retinopathy?

A

A possible complication of DM that can result in blindness.

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69
Q

How does diabetic retinopathy present?

A

There are often no early warning signs… though some people may complain of blurred vision.

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70
Q

How is diabetic retinopathy investigated?

A

Fundoscopy.

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71
Q

What might fundoscopy reveal in a patient with DM?

A

Cotton wool spots, flame haemorrhages and dot-blot haemorrhages.

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72
Q

How often do diabetics receive eye testing?

A

Annually.

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73
Q

What is diabetic peripheral neuropathy?

A

Peripheral neuropathy is sensory loss in the ‘stocking’ distribution (feet first). Develops due to damaging effect of glucose on nerves.

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74
Q

How is sensation assessed in diabetic individuals?

A

With a monofilament fibre.

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75
Q

What is the first-line treatment for painful diabetic neuropathy?

A

Amitriptyline. Other options include duloxetine, gabapentin or pregabalin.

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76
Q

How might autonomic neuropathy present in diabetic individuals?

A

Postural hypotension (dizziness/light-headedness on standing), gastroparesis (bloating, feeling full).

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77
Q

What is the mechanism behind the development of diabetic foot disease?

A

A combination of peripheral neuropathy and peripheral vascular disease. Neuropathy leads to loss of sensation resulting in abnormal patterns of walking which may develop into pressure areas and skin breaks. Protective sensation is also lost, enabling continuous unconscious trauma. Hyperglycaemia and peripheral vascular disease reduce the individual’s healing potential… allowing damage to progress.

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78
Q

What are the features of hyperosmolar hyperglycaemic state (HHS)?

A

Fatigue, lethargy, nausea + vomiting, altered consciousness, headaches. Cardiovascular features include dehydration, hypotension and tachycardia.

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79
Q

What investigations are used in the diagnosis of HHS?

A

Blood glucose.
Blood ketones.
Venous blood gas.
Serum osmolality.

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80
Q

What does blood glucose reveal in a patient with HHS?

A

Marked hyperglycaemia > 30mmol/L.

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81
Q

What does blood ketones reveal in a patient with HHS?

A

Absence of significant ketonaemia (< 3mmol/L).

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82
Q

What does serum osmolality reveal in a patient with HHS?

A

Significantly raised (> 320 mosmol/kg).

83
Q

What is the management of a patient with HHS?

A

Replace fluid and electrolyte losses by giving intravenous saline.

84
Q

Why is it important not to give insulin initially in the management of HHS?

A

Could precipitate cardiovascular collapse (glucose goes into cell… fluid leaves intravascular space).

85
Q

What is maturity onset diabetes of the young (MODY)? What is the inheritance pattern of MODY?

A

Development of T2DM in patients younger than 25 years. Typically inherited as an autosomal dominant condition.

86
Q

What are the characteristic features of diabetes insipidus (DI)?

A

Large amounts of dilute urine (polyuria) and increased thirst (polydipsia).

87
Q

What are the two categories of diabetes insipidus?

A

Cranial diabetes insipidus and nephrogenic diabetes insipidus.

88
Q

What is the pathophysiology behind cranial diabetes insipidus (include causes)?

A

Lack of antidiuretic hormone production from the posterior pituitary. Causes include post-head injury, pituitary surgery, craniopharyngiomas and haemochromatosis.

89
Q

What is the pathophysiology behind nephrogenic diabetes insipidus (include causes)?

A

Kidney pathology which results in an improper response (insensitivity) to antidiuretic hormone. Causes include genetic (affecting vasopressin receptor), chronic hypercalcaemia, chronic hypokalaemia and lithium use.

90
Q

What investigations might be performed in a patient with suspected diabetes insipidus?

A 
Urine osmolality. 
Serum osmolality. 
Serum glucose. 
Serum sodium. 
Fluid deprivation.
91
Q

What does serum osmolality and urine osmolality reveal in a patient with suspected diabetes insipidus?

A

High serum osmolality and low urine osmolality.

92
Q

How can cranial and nephrogenic diabetes insipidus be differentiated on investigation?

A

Desmopressin response test. In nephrogenic diabetes insipidus urine osmolality will remain low following fluid deprivation and after desmopressin is given. In cranial diabetes insipidus urine osmolality will remain low following fluid deprivation and will be high after desmopressin is given.

93
Q

What is the management of nephrogenic diabetes insipidus?

A

Thiazide diuretics and a low salt, low protein diet.

94
Q

What is the management of cranial diabetes insipidus?

A

Provide desmopressin.

95
Q

What is syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

A

A condition of continuous ADH secretion that leads to reduced urine output.

96
Q

What gland releases antidiuretic hormone?

A

Posterior pituitary.

97
Q

Where is antidiuretic hormone produced?

A

Hypothalamus.

98
Q

By what mechanism does ADH increase water reabsorption?

A

ADH acts on the distal convoluted tubule and collecting duct to cause insertion of aquaporin channels (which increase water reabsorption independent of sodium ions).

99
Q

What is the main complication of SIADH?

A

Water retention leads to an increase in total body water and the development of hyponatraemia.

100
Q

How does SIADH present?

A

Headache, confusion, lethargy, anorexia, seizures and potentially coma.

101
Q

What investigations are used in the diagnosis of SIADH?

A

Urine osmolality.
Serum sodium.
Serum osmolality.

102
Q

The absence of what signs are required for diagnosis of SIADH?

A

Hypovolaemia or oedema. SIADH is a euvolaemic, hypotonic hyponatraemia.

103
Q

How is SIADH managed?

A

Correct underlying cause. In severe hyponatraemia give hypertonic saline cautiously along with furosemide (to avoid fluid overload).

104
Q

Why is it important that hyponatraemia is corrected slowly?

A

There is a risk of osmotic demyelination syndrome if done rapidly.

105
Q

Give potential causes of SIADH.

A

CNS (stroke, subarachnoid haemorrhage, trauma, psychosis).
Malignancy (small cell lung cancer, other lung cancer, neuroblastoma).
Infection (pneumonia, HIV).
Endocrine (hypothyroidism, hypopituitarism).
Drugs (carbamazepine, cyclophosphamide, SSRIs).
Neurosurgery/pituitary surgery.

106
Q

What is the most common type of pituitary tumour?

A

Benign adenomas.

107
Q

The presenting features of pituitary tumours typically develop as a result of what process?

A

Local pressure effects.

108
Q

What is the typical presentation of pituitary tumours?

A

Headache, visual field defects and cranial nerve palsies.

109
Q

How are pituitary tumours investigated?

A

MRI head, visual fields assessment and hormone profile.

110
Q

What is pituitary apoplexy?

A

Rapid pituitary enlargement as a result of a bleed or infarction of a pituitary tumour.

111
Q

How does pituitary apoplexy present?

A

Acute severe headache, ocular palsy, meningism, ophthalmoplegia and reduced consciousness.

112
Q

How is pituitary apoplexy managed?

A

Intramuscular hydrocortisone.

113
Q

What is panhypopituitarism?

A

Deficiency of all anterior pituitary hormones.

114
Q

What hormones are released from the anterior pituitary?

A

Growth hormone, follicle-stimulating hormone, leutinising hormone, thyroid stimulating hormone, adrenocorticotropic hormone and prolactin.

115
Q

What is the presentation of panhypopituitarism?

A

Growth hormone = central obesity, short, osteoporosis, low glucose.
FSH / LH = oligo/amenorrhoea, reduced fertility, low libido.
TSH = hypothyroidism.
ACTH = Addison’s (lethargy, weakness, anorexia, nausea + vomiting).
Prolactin = reduced lactation.

116
Q

What is hyperprolactinaemia?

A

The presence of abnormally high levels of prolactin in the blood.

117
Q

How does hyperprolactinaemia present in females?

A

Galactorrhea, infertility and menstrual disturbances.

118
Q

How does hyperprolactinaemia present in males?

A

Hypogonadism, infertility and erectile dysfunction.

119
Q

What % of females are affected by hypothyroidism in the UK?

A

1-2%

120
Q

What is the most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis.

121
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine insufficiency.

122
Q

What medications can cause hypothyroidism?

A

Lithium, amiodarone, carbimazole.

123
Q

What are the three general features of hypothyroidism?

A

Weight gain (despite loss of appetite), lethargy and cold intolerance (wearing extra clothing).

124
Q

Give six non-general features of hypothyroidism?

A

Skin changes (dry, cold, yellowing). Non-pitting oedema of the hands and face. Hair (dry, coarse). Constipation. Menorrhagia. Decreased deep tendon reflexes.

125
Q

What investigations are used in the diagnosis of hypothyroidism?

A

Thyroid function tests.

126
Q

What are the results of thyroid function tests in an individual with primary hypothyroidism?

A

Thyroid stimulating hormone (TSH) is high.

127
Q

What are the results of thyroid function tests in an individual with secondary hypothyroidism?

A

Thyroid stimulating hormone (TSH) is low/normal.

128
Q

What is the treatment for hypothyroidism?

A

Levothyroxine.

129
Q

What is the most common cause of secondary hypothyroidism?

A

Pituitary gland tumours.

130
Q

How should levothyroxine treatment be altered in pregnant women?

A

Dose should be increased (by 25 micrograms).

131
Q

How should levothyroxine treatment be monitored?

A

Thyroid function tests should be performed every three months until stabilised then yearly thereafter.

132
Q

Give four potential side effects of levothyroxine use.

A

Thyrotoxicosis, reduced bone mineral density, worsening of angina and atrial fibrillation.

133
Q

Which medications may restrict the uptake of levothyroxine and should therefore avoid being taken concurrently?

A

Iron.

Calcium carbonate.

134
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune disease that involves destruction of the thyroid gland.

135
Q

What is a characteristic feature of Hashimoto’s thyroiditis?

A

Goitre (swelling of the thyroid).

136
Q

How can goitre be differentiated from other neck lumps on examination?

A

Goitre moves up and down when swallowing.

137
Q

What is subacute thyroiditis?

A

A self-limiting condition that occurs following viral infection.

138
Q

What are the four phases of subacute thyroiditis and their features?

A

1 - hyperthyroidism, painful goitre, raised ESR (weeks).
2 - euthyroid (weeks).
3 - hypothyroidism (months).
4 - euthyroid.

139
Q

Define hyperthyroidism.

A

A condition of excessive thyroid hormone production by the thyroid gland.

140
Q

Define thyrotoxicosis.

A

A clinical syndrome that occurs due to excessive thyroid hormone levels of any cause.

141
Q

Give three causes of thyrotoxicosis.

A

Grave’s disease.
Toxic multi-nodular goitre.
Amiodarone use.

142
Q

What are the four general features of thyrotoxicosis?

A

Weight loss, restlessness, mania and heat intolerance.

143
Q

Give seven non-general features of thyrotoxicosis?

A

Palpitations, increased sweating, clubbing, diarrhoea, oligomenorrhoea, anxiety and tremor.

144
Q

What investigations are performed in the diagnosis of thyrotoxicosis?

A

Thyroid function tests (TFTs).

145
Q

What are the results of thyroid function testing in patients with thyrotoxicosis?

A

Raised T3 and T4.

Low TSH.

146
Q

What is the most common cause of thyrotoxicosis?

A

Grave’s disease.

147
Q

In addition to the features associated with thyrotoxicosis, how do patients with Grave’s disease present?

A

Exophthalmos.
Ophthalmoplegia.
Pretibial myxoedema.
Digital clubbing.

148
Q

What specific tests may be done in the investigation of Grave’s disease?

A

Raised antithyroid peroxidase.

Raised TSH receptor antibodies.

149
Q

What is the pharmacological management of Grave’s disease?

A

Carbimazole.

Propranolol (for symptom control).

150
Q

What is the mechanism of action of carbimazole in the treatment of Grave’s disease?

A

Carbimazole blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin… reducing thyroid hormone production.

151
Q

What is the most serious potential adverse effect of carbimazole?

A

Agranulocytosis (acute condition of neutropenia)… therefore a full blood count should be obtained following initiation.

152
Q

What condition is indicated by normal/raised parathyroid hormone, raised calcium and low phosphate?

A

Primary hyperparathyroidism.

153
Q

What condition is indicated by raised parathyroid hormone, low/normal calcium and raised phosphate?

A

Secondary hyperparathyroidism.

154
Q

What condition is indicated by raised parathyroid hormone, normal/raised calcium and low phosphate?

A

Tertiary hyperparathyroidism.

155
Q

What is the most important human glucocorticoid?

A

Cortisol.

156
Q

What is Cushing’s syndrome?

A

A collection of signs and symptoms that develops as a result of prolonged exposure to glucocorticoids.

157
Q

How do individuals with Cushing’s syndrome present?

A

Abdominal obesity, thin arms and legs, abdominal striae and round face. In females: anovulation and infertility.

158
Q

What is the name of the test used to confirm the diagnosis in an individual suspected to have Cushing’s syndrome?

A

Overnight dexamethasone suppression test.

159
Q

How is an overnight dexamethasone suppression test performed?

A

Oral dexamethasone is given at 11pm and cortisol levels are measured at 8am.

160
Q

What are the results of an overnight dexamethasone suppression test in an individual with Cushing’s syndrome (vs. an individual without)?

A

Patient’s with Cushing’s show a morning cortisol spike. In patient’s without Cushing’s cortisol production will be suppressed.

161
Q

What are the two categories of Cushing’s syndrome causes?

A

ACTH dependent causes (increased ACTH causes increased cortisol).
ACTH independent causes (increased cortisol irrespective of ACTH).

162
Q

Give two ACTH dependent causes of Cushing’s syndrome?

A

Cushing’s disease.

Ectopic ACTH production such as small cell lung cancer.

163
Q

Give three ACTH independent causes of Cushing’s syndrome?

A

Iatrogenic - corticosteroid therapy.
Adrenal adenoma.
Adrenal carcinoma.

164
Q

What is Cushing’s disease?

A

Pituitary adenoma secreting ACTH leads to adrenal hyperplasia.

165
Q

What is Addison’s disease?

A

A condition of autoimmune destruction of the adrenal glands… leading to reduced cortisol and aldosterone production.

166
Q

How does Addison’s disease present?

A

Lethargy, weakness, anorexia, nausea + vomiting, weight loss, salt-craving, hyperpigmentation. In females: loss of pubic hair.

167
Q

What investigations are performed in the diagnosis of Addison’s disease?

A

Blood pressure, serum glucose, serum sodium, serum potassium, ACTH stimulation test.

168
Q

What does serum glucose reveal in patients with Addison’s disease?

A

Hypoglycaemia.

169
Q

What does blood pressure investigation reveal in patients with Addison’s disease?

A

Hypotension.

170
Q

What does serum sodium and serum potassium reveal in patients with Addison’s disease?

A

Hyponatraemia and hyperkalaemia.

171
Q

What is the definitive investigation for Addison’s disease?

A

ACTH stimulation test (short Synacthen test).

172
Q

What is adrenocorticotropic hormone? What is its function?

A

ACTH is a hormone produced by the anterior pituitary gland that stimulates cortisol release from the cortex of the adrenal gland.

173
Q

How is an ACTH stimulation test performed?

A

Plasma cortisol is measured for baseline. Synacthen (synthetic ACTH) is administered intramuscularly. Cortisol is measured again after 30 minutes.

174
Q

What are the results of an ACTH stimulation test in patients with Addison’s disease?

A

Plasma cortisol will not rise.

175
Q

What is the management of Addison’s disease?

A

Exogenous glucocorticoid therapy (hydrocortisone + fludrocortisone).

176
Q

How should steroid therapy be managed for people with Addison’s disease during an intercurrent illness?

A

Hydrocortisone dose should be double while maintaining the same dose of fludrocortisone.

177
Q

What are the potential causes of an Addisonian crisis?

A

Addisonian crisis may occur due to sepsis or surgery, adrenal haemorrhage or steroid withdrawal.

178
Q

How does Addisonian crisis present?

A

Collapse, shock and pyrexia.

179
Q

What is the management of Addisonian crisis?

A

Hydrocortisone 100mg IM or IV.

180
Q

What is congenital adrenal hyperplasia?

A

Family of disorders characterised by enzyme defects in the pathways that lead to the biosynthesis of cortisol, aldosterone and androgens.

181
Q

What is the inheritance pattern of congenital adrenal hyperplasia?

A

Autosomal recessive.

182
Q

What is the pathophysiology behind congenital adrenal hyperplasia?

A

1 Enzyme defects result in relatively reduced cortisol production. 2 Increased secretion of ACTH via negative feedback. 3 Increased ACTH leads to hyperplasia of the adrenals.

183
Q

Give two forms of classic congenital adrenal hyperplasia.

A

Salt-wasting form.

Simple virilising form.

184
Q

What is the presentation of the salt-wasting form of congenital adrenal hyperplasia?

A

Acute adrenal/Addisonian crisis (collapse, shock, pyrexia) in the first ten days of life.

185
Q

What is the metabolic disturbance associated with congenital adrenal hyperplasia?

A

Hyponatraemic, hyperkalaemic metabolic acidosis.

186
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism.

187
Q

What causes Conn’s syndrome?

A

Bilateral idiopathic adrenal hyperplasia (most common) and adrenal adenoma.

188
Q

What is the presentation of Conn’s syndrome?

A

Muscle weakness/aches. Hypertension.

189
Q

What is the management of Conn’s syndrome?

A

Aldosterone antagonist - spironolactone.

190
Q

What is acromegaly?

A

A condition characterised by excess growth hormone.

191
Q

The majority of cases of acromegaly are caused by what?

A

Pituitary adenoma.

192
Q

How does acromegaly present?

A

Coarse facial appearance, enlargement of hands and feet, large tongue, excessive sweating + oily skin.
Due to pituitary tumour: headaches and bitemporal hemianopia.

193
Q

What investigations are performed in patients with acromegaly?

A

Insulin-like growth factor 1 (IGF-1). MRI head.

194
Q

What does insulin-like growth factor 1 reveal in patients with acromegaly?

A

Raised.

195
Q

What is the management of acromegaly?

A

Surgical: transsphenoidal tumour resection. Medical: somatostatin analogue (octreotide) and growth hormone antagonists (pegvisomant).

196
Q

Patients with acromegaly receive what screening?

A

Annually colonoscopy.

197
Q

What is phaeochromocytoma?

A

A tumour of the adrenal glands that occurs in young people.

198
Q

How do patients with phaeochromocytoma present (inc. obs)?

A

Sweating, anxiety, headaches and palpitations. Hypertension on examination.

199
Q

What investigations are performed in patients with phaeochromocytoma?

A

Urine sample.

200
Q

What does urine sample reveal in patients with phaeochromocytoma?

A

Raised metanephrines.

201
Q

What is the management of phaeochromocytoma?

A

Give phenoxybenzamine (alpha-blocker) before propranolol (beta-blocker).

202
Q

What is the first line investigation in patients with Conn’s syndrome?

A

Plasma aldosterone/renin ratio.

203
Q

In Conn’s syndrome what are the results of a plasma aldosterone/renin ratio?

A

High aldosterone, low renin.

204
Q

What is the most common cause of panhypopituitarism?

A

Non-secreting pituitary macroadenoma.

Finals (11 decks)

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