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ENDOCRINE Flashcards

1
Q

Name 3 complications of thyroid surgery

A
  • damage to parathyroid glands can result in hypocalcaemia
  • recurrent laryngeal nerve damage
  • bleeding
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2
Q

What are the ECG findings in hypocalcaemia?

A

Prolonged QT

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3
Q

How does hypocalcaemia present?

A

Muscle cramps

Perioral tingling

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4
Q

When should a second drug be added in T2DM?

A

HbA1c >58 mol/mol

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5
Q

What is the most common cause of hyperthyroidism?

A

Graves disease

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6
Q

Give 4 causes of hyperthyroidism.

A

Graves
Toxic multinodular goitre (Plummer’s disease)
Solitary toxic thyroid nodule
Thyroiditis (De Quervain’s, Hashimoto’s, post-partum and drug-induced)

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7
Q

What is Plummer’s disease?

A

Toxic multinodular goitre

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8
Q

What is a solitary toxic thyroid nodule?

A

Single abnormal thyroid nodule releasing thyroid hormone
Benign adenomas
Treated by surgical removal

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9
Q

What is the difference between primary and secondary hyperthyroidism?

A

Primary - problem with the thyroid

Secondary - problem with hypothalamus/pituitary

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10
Q

What is the pathophysiology of Grave’s disease?

A

Autoimmune - TSH receptor antibodies

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11
Q

What are the risk factors for Grave’s disease?

A

Female

40-60 years

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12
Q

What is thyrotoxicosis?

A

Too much thyroid hormone

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13
Q

What is thyroid storm?

A

Rare medical emergency caused by too much thyroid hormone.

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14
Q

Which drugs can induce thyrotoxicosis?

A

Thyroxine

Amiodarone

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15
Q

What are the signs of hyperthyroidism?

A 
• Sweating and heat intolerance
• Tachycardia
• Weight loss
• Pretibial myxoedema
• Brisk reflexes
Exophthalmos
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16
Q

What are the symptoms of hyperthyroidism?

A

• Anxiety and irritability
• Fatigue
• Frequent loose stools
Sexual dysfunction

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17
Q

What features are unique to Graves disease?

A

Exophthalmos
Pretibial myxoedema
Thyroid acropachy

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18
Q

What are the features of thyroid storm?

A

Pyrexia
Tachycardia
Delirium

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19
Q

What features are unique to toxic multinodular goitre?

A

• Goitre with firm nodules
• Most patients are aged over 50
Second most common cause of thyrotoxicosis (after Grave’s)

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20
Q

What investigations should be done in thyrotoxicosis?

A 
• ↓TSH, ↑T4/↑T3 
• Abs: TSH receptor, TPO 
• ↑Ca, ↑LFTs 
• Isotope scan 
 ↑ in Graves’ 
 ↓ in thyroiditis 
Ophthalmopathy: acuity, fields, movements
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21
Q

What is an isotope scan?

A

Thyroid scans and uptake tests use small doses of radioactive chemicals to create pictures of the thyroid gland.

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22
Q

What is the management of hyperthyroidism?

A

Refer to endocrinology
1st line - carbimazole, normal thyroid function after 4-8 weeks then maintenance dose
2nd line - propylthiouracil
3rd line - radioactive iodine (destroys thyroid cells, hypothyroidism)

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23
Q

Why is carbimazole preferred to propylthiouracil?

A

Propylthiouracil is associated with severe hepatic reactions

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24
Q

What are the two approaches to long-term treatment for hyperthyroidism?

A
  1. Titration block (carbimazole titrated to normal levels)

2. Block and replace (carbimazole + levothyroxine)

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25
Q

What are the requirements for radioactive iodine treatment?

A 
Not pregnant (must not be pregnant within 6 months)
Avoid contact with anyone for 1 week
Avoid children and pregnant women for 3 weeks
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26
Q

What is the management of thyrotoxic storm?

A

Admission
Fluid resuscitation
Beta-blockers

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27
Q

How are beta-blockers used in hyperthyroidism? What is first-line?

A

Control heart rate, reduce anxiety

Propranolol

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28
Q

What is the definitive management of hyperthyroidism?

A

Surgery

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29
Q

What are the complications of thyroid surgery?

A

Recurrent laryngeal nerve damage = hoarseness
Hypoparathyroidism
Hypothyroidism

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30
Q

How long is treatment needed for Grave’s disease?

A

12-18 months

50% relapse –> surgery, radioiodine

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31
Q

What is the most common cause of primary hyperaldosteronsim?

A

Bilateral idiopathic adrenal hyperplasia

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32
Q

What is Cushing’s syndrome?

What is Cushing’s disease?

A

Syndrome: signs and symptoms that develop after prolonged abnormal elevation of cortisol

Disease: pituitary adenoma (tumour) secretes excessive ACTH

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33
Q

Describe the adrenal axis

A

Hypothalamus –> CRH
Pituitary –> ACTH
Adrenals –> mineralocorticoids, glucocorticoids, androgens, catecholamines

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34
Q

What are the features of Cushing’s syndrome?

A 
Round “moon” face
Central Obesity
Abdominal striae
Buffalo Hump (fat pad on upper back)
Proximal limb muscle wasting
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35
Q

What are the physiological effects of high levels of cortisol?

A 
Hypertension
Cardiac hypertrophy
Hyperglycaemia (Type 2 Diabetes)
Depression
Insomnia
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36
Q

How does high-levels of cortisol affect bones and skin?

A

Osteoporosis

Easy bruising and poor skin healing

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37
Q

What are the causes of Cushing’s syndrome?

A

Exogenous steroids (in patients on long term high dose steroid medications)

Cushing’s Disease (a pituitary adenoma releasing excessive ACTH)

Adrenal Adenoma (a hormone secreting adrenal tumour)

Paraneoplastic Cushing’s (SCLC)

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38
Q

What is the most common cause of paraneoplastic Cushing’s?

A

SCLC - ectopic ACTH

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39
Q

What is the first-line investigation for Cushing’s syndrome?

A

Low dose dexamethasone test

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40
Q

Describe the dexamethasone test

A

Low dose - 1mg dexamethasone at 10pm, morning cortisol levels measured to screen for Cushing’s syndrome

If normal or high—> high dose dexamethasone test - 8mg dexamethasone to determine cause of Cushing’s syndrome

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41
Q

What is a normal result from a low dose dexamethasone test?

A

Low cortisol

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42
Q

What is also measured alongside a high dose dexamethasone test?

A

ACTH

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43
Q

What does a high dose dexamethasone test show in pituitary adenoma?

A

Cortisol - low

ACTH - low

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44
Q

What does the high dose dexamethasone test show in adrenal adenomas?

A

Cortisol - high/normal

ACTH - low

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45
Q

What does the high dose dexamethasone test show in paraneoplastic Cushing’s syndrome?

A

Cortisol - high

ACTH - high

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46
Q

What investigations should be done in Cushing’s syndrome?

A
  1. Dexamethasone suppression test (24-hour urinary cortisol can also be done but takes ages)
  2. FBC & U&E (low K)
  3. MRI brain (pituitary adenoma)
  4. Chest CT - SCLC
  5. Abdominal CT - adrenal tumours
47
Q

What is the management of Cushing’s syndrome?

A

The main treatment is to remove the underlying cause (surgically remove the tumour)

  • Trans-sphenoidal (through the nose) removal of pituitary adenoma (depends how big)
  • Surgical removal of adrenal tumour
  • Surgical removal of tumour producing ectopic ACTH
48
Q

What are the 3 types of MEN?

A

MEN type I
MEN type IIa
MEN type IIb

49
Q

What are the features of MEN type I?

A

3 Ps: (MEN1 gene)

Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia

Pituitary (70%)

Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

+adrenal, +thyroid

50
Q

What are the features of MEN IIa?

A

Medullary thyroid cancer

2 Ps: (RET oncogene)

Parathyroid (60%)
Phaeochromocytoma

51
Q

What are the features of MEN IIb?

A

(RET oncogene)

Medullary thyroid cancer

+ 1 P: Phaechromocytoma

52
Q

What is included in a pituitary blood profile?

A 
GH
Prolactin
ACTH
FH
LSH
TFTs
53
Q

What is the most common type of thyroid cancer?

A

Papillary - 70% (mostly young females, excellent prognosis)

54
Q

What are the risk factors for type II diabetes?

A

Non-Modifiable

  • Older age
  • Ethnicity (Black, Chinese, South Asian)
  • Family history

Modifiable

  • Obesity
  • Sedentary lifestyles
  • High carbohydrate (particularly refined carbohydrate) diet
55
Q

What are the symptoms of diabetes type II?

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)
56
Q

When is an oral glucose tolerance test done?

A

in the morning prior to having breakfast

baseline fasting plasma glucose result

giving a 75g glucose drink

measuring plasma glucose 2 hours later

57
Q

What is pre-diabetes?

A

Pre-diabetes is an indication that the patient is heading towards diabetes.

They do not fit the full diabetic diagnostic criteria but should be educated regarding diabetes and implement lifestyle changes to reduce their risk of progressing to diabetes.

They are not currently recommended to start medical treatment at this point.

58
Q

What is the difference between impaired fasting glucose and impaired glucose tolerance?

A

Impaired fasting glucose means that their body struggles to get their blood glucose levels in to normal range, even after a prolonged period without eating carbohydrates.

Impaired glucose tolerance means their body struggles to cope with processing a carbohydrate meal.

59
Q

What is the diagnostic criteria for pre-diabetes?

A

HbA1c: 42-47 mmol/mol

Impaired fasting glucose: 6.1 – 6.9 mmol/l

Impaired glucose tolerance: glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT

60
Q

What is the diagnostic criteria for type II diabetes?

A

HbA1c > 48 mmol/mol

Random Glucose > 11 mmol/l

Fasting Glucose > 7 mmol/l

OGTT 2 hour result > 11 mmol/l

61
Q

How can you counsel a patient with type II diabetes?

A

Diet modification
Risk factors
Monitoring for complications

62
Q

What dietary advice can be given to someone with type II diabetes?

A

Vegetables and oily fish

Typical advice is low glycaemic, high fibre diet

A low carbohydrate may in fact be more effective in treating and preventing diabetes but is not yet mainstream advice

63
Q

How can you optimise risk factors in T2DM?

A

Exercise and weight loss

Stop smoking

Optimise treatment for other illnesses, for example hypertension, hyperlipidaemia and cardiovascular disease

64
Q

Which complications should be monitored in T2DM?

A

Diabetic retinopathy
Kidney disease
Diabetic foot

65
Q

What are the treatment targets for T2DM?

A

48 mmol/mol for new type 2 diabetics

53 mmol/mol for diabetics that have moved beyond metformin alone

66
Q

What is the action of metformin?

A

ncreases insulin sensitivity and decreases liver production of glucose

“weight neutral”

67
Q

What are the side effects of metformin?

A

Diarrhoea and abdominal pain (dose dependent)

Lactic acidosis

Does NOT typically cause hypoglycaemia

68
Q

What are the side effects of pioglitazone?

A 
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
Does NOT typically cause hypoglycaemia
69
Q

What is the most common sylfonylurea?

A

gliclazide

70
Q

What are the side effects of sulfonylureas?

A

Weight gain

Hypoglycaemia

Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy

71
Q

What are the diagnostic criteria for DKA?

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

72
Q

What is the management of DKA?

A

FIGPICK

F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

73
Q

How should you counsel a patient with a new diagnosis of T1DM?

A
  1. Life-long
  2. Glucose monitoring = morning, at each meal, before bed
  3. Insulin treatment = started by a specialist, long-acting, short-acting, lipodystrophy
  4. Short-term complications = hypoglycaemia, hyperglycaemia
  5. Long-term complications = macrovascular, microvascular, infection
  6. Monitoring = HbA1c
74
Q

What are the macrovascular complications of T1DM?

A

Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

75
Q

What are the microvascular complications of T1DM?

A

Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

76
Q

Which infections are common in patients with DM?

A

Urinary Tract Infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis

77
Q

How are C-peptide levels used in the diagnosis of diabetes?

A

When there is a lack of clarity between T1 and T2 e.g. older person presenting with features of T1 and having T2 risk factors e.g. obesity = test C-peptide

C-peptide = low in T1, normal in T2

78
Q

What is subclinical hypothyroidism?

A

TSH raised but T3, T4 normal

no obvious symptoms

79
Q

What is the management of subclinical hypothyroidism?

A

TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range

  • if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine
  • ‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
  • if asymptomatic people, observe and repeat thyroid function in 6 months

TSH is > 10mU/L and the free thyroxine level is within the normal range

  • start treatment (even if asymptomatic) with levothyroxine if <= 70 years
  • ‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
80
Q

How should levothyroxine doses be changed in pregnancy?

A

Increase dose by 50%

Refer to endocrinologist

81
Q

Which medications can reduce the absorption of levothyroxine?

A

Iron supplements

82
Q

What is the screening test for acromegaly?

A

Serum IGF-1 (does not vary throughout the day)

83
Q

Which tests can confirm the diagnosis of acromegaly?

A

oral glucose tolerance test (OGTT) with serial GH measurements

84
Q

What is MODY?

A

Maturity-onset diabetes of the young (MODY) is characterised by the development of type 2 diabetes mellitus in patients < 25 years old

85
Q

What is the optimum treatment for MODY?

A

Sulphonylureas

86
Q

How do Phaeochromocytomas present?

A

triad of sweating, headaches, and palpitations in association with severe hypertension

87
Q

What investigation is used to diagnose a phaeochromocytoma?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

88
Q

What is the definitive management of a phaeochromocytoma?

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

89
Q

What does CRH stand for?

A

Corticotrophin releasing hormone

90
Q

What does ACTH stand for?

A

Adrenocorticotropic hormone

91
Q

What is the function of mineralocorticoids? Give an example of a primary and synthetic mineralocorticoid.

A

Control salt and water balance by promoting sodium and potassium transport.

Primary = Aldosterone
Synthetic = Fludrocortisone
92
Q

What is the function of glucocorticoids? Give an example of a primary and synthetic glucocorticoid.

A

Controls the production and use of sugar/fats and regulates the stress response.

Primary = Cortisol

Synthetic = Hydrocortisone, Prednisolone, Dexamethasone, Beclomethasone

93
Q

What is the function of androgens?

A

Regulate the development of sex characteristics.

94
Q

What is the function of catecholamines? Give an example

A

Fight or flight

Adrenaline (hormone)
Noradrenaline (neurotransmitter)

95
Q

What is adrenal insufficiency?

A

Adrenal glands do not produce enough steroid hormones

96
Q

Which two hormones in particular are lacking in adrenal insufficiency?

A

Cortisol

Aldosterone

97
Q

What is Addison’s disease? What is another name?

A

Adrenal glands have been damaged

Primary adrenal insufficiency

98
Q

What is the most common cause of primary adrenal insufficiency?

A

Autoimmune

99
Q

What is Sheehan’s syndrome?

A

Blood loss during childbirth leads to pituitary gland necrosis

100
Q

What is secondary adrenal insufficiency?

A

Inadequate production of ACTH

101
Q

What is tertiary adrenal insufficiency?

A

Inadequate release of CRH from the hypothalamus - usually due to suddenly stopping long-term steroids

102
Q

What is the presentation of adrenal insufficiency?

A 
• Fatigue
• Nausea
• Cramps
• Abdominal pain
Reduced libido
103
Q

What are the signs of adrenal insufficiency?

A 
Bronze hyperpigmentation (ACTH stimulates melanocytes to produce melanin)
Hypotension
104
Q

What might be found on a U&E blood test in adrenal insufficiency?

A

Hyponatraemia

Hyperkalaemia

105
Q

What test is diagnostic of adrenal insufficiency?

A

Short synacthen test

106
Q

What other blood tests can be done?

A

ACTH

Adrenal autoantibodies - adrenal cortex antibodies & 21-hydroxylase antibodies

107
Q

Describe how the short synacthen test works

A 
Give synacthen (synthetic ACTH) in the morning
Measure blood cortisol at baseline, 30mins and 60 mins after
Cortisol should double, if not = primary adrenal insufficiency (Addison's)
108
Q

Describe how the long synacthen test works

A

Give synacthen over a long period of time
If there is no cortisol response = primary adrenal failure
If there is some cortisol response = adrenal atrophy due to secondary adrenal insufficiency (pituitary problem)

Not really used anymore as can measure ACTH

109
Q

What is the management of Addison’s?

A

Replacement steroids:

  • Hydrocortisone (cortisol replacement)
  • Fludrocortisone (aldosterone replacement)
110
Q

What is an Addisonian crisis?

A

Acute presentation of severe Addison’s

The absence of steroids leads to a life threatening presentation

111
Q

How do patients present with an Addisonian crisis?

A

• Reduced consciousness
• Hypotension
• Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell

112
Q

What can cause Addisonian crisis?

A

First presentation
Infection
Trauma
Acute illness

113
Q

What is the management of an Addisonian crisis?

A

• Intensive monitoring if unwell
• Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours)
• IV fluid resuscitation
• Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

FINALS (26 decks)

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