Endocrinology Flashcards

1
Q

What are the two main causes of hypercalcaemia?

A

Primary Hyperparathyroidism

Malignancy e.g. multiple myeloma, bone metastasis

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2
Q

How does hypercalcaemia present?

A

Bones, stones, moans, groans

Bone pain/fracture
Renal calculi / renal colic
Depression

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3
Q

How does hypercalcaemia show on an ECG?

A

Short QT interval

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4
Q

How is hypercalcaemia treated?

A

Rehydration with normal saline

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5
Q

What are the causes of hypocalcaemia?

A

Vitamin D deficiency
Chronic kidney disease
Primary hypoparathyroidism
Pseudohypoparathyroidism

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6
Q

How does hypocalcaemia present?

A

Tetany - muscle twitching/cramping
Parasthaesia

Trousseau’s sign
Chvostek’s sign

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7
Q

How does hypocalcaemia show on an ECG?

A

Prolonged QT interval

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8
Q

How is hypocalcaemia managed?

A

IV Calcium Gluconate

10ml of 10% over 10 minutes

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9
Q

What is Cushing’s Syndrome?

A

The signs and symptoms due to prolonged cortisol excess

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10
Q

What is Cushing’s Disease?

A

Increased cortisol due to a pituitary adenoma secreting ACTH

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11
Q

How does Cushing’s Syndrome present?

A

Moon face
Central obesity
Proximal limb wasting
Buffalo hump

Hyperglycaemia
Hypertension
Osteoporosis
Depression

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12
Q

What are ACTH dependent causes of Cushing’s?

A

Cushing’s Disease

Ectopic ACTH secreted from small cell lung cancer

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13
Q

What are ACTH independent causes of Cushing’s?

A

Steroids
Adrenal adenoma
Adrenal carcinoma

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14
Q

How is Cushing’s Syndrome investigated?

A

Overnight Dexamethasone suppression test

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15
Q

What is seen on 8mg Dexamethasone suppression test for Cushing’s Disease?

A

Suppressed ACTH, suppressed cortisol

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16
Q

What does it mean if the 8mg Dexamethasone suppression test suppresses ACTH but not cortisol?

A

ACTH independent Cushing’s - adrenal adenoma, adrenal carcinoma

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17
Q

What does it mean if both ACTH and cortisol are still high after 8mg Dexamethasone suppression test?

A

Ectopic ACTH production e.g. from small cell lung cancer

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18
Q

What is the main cause of primary hypoadrenalism?

A

Addison’s disease

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19
Q

What are causes of secondary adrenal insufficiency?

A

Due to the pituitary not producing enough ACTH - may be due to surgery/trauma/radiotherapy

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20
Q

What is tertiary hypoadrenalism?

A

Hypothalamus not producing enough corticotrophin releasing hormone - usually due to long term steroid use

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21
Q

How does adrenal insufficiency present?

A

Lethargy, weakness

Weight loss

Salt-craving

Hypoglycaemia

Hyponatraemia

Hyperkalaemia

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22
Q

How is adrenal insufficiency investigated?

A

Short synacthen test - Synacthen given and cortisol levels measured before and after (Synacthen is synthetic ACTH and stimulates adrenal hormone release)

Can also measure 9am cortisol

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23
Q

How is hypoaldrenalism managed?

A

Hydrocortisone + fludrocortisone

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24
Q

How does an Addisonian crisis present?

A
Hypotension
Hypoglycaemia
Reduced consciousness
Hyponatraemia
Hyperkalaemia
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25
Q

How is an Addisonian crisis managed?

A

100mg stat hydrocortisone

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26
Q

What are the two main causes of hyperaldosteronism?

A
Adrenal adenoma (conn’s syndrome)
Bilateral idiopathic adrenal hyperplasia
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27
Q

How does hyperaldosteronism present?

A

Hypertension

Hypokalaemia- may present as muscle weakness

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28
Q

How is bilateral adrenal hyperplasia managed?

A

Aldosterone antagonist (Spironolactone)

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29
Q

How does type 1 diabetes present?

A

Polyuria
Polydipsia
Weight loss

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30
Q

What blood glucose is needed to diagnose type 1 diabetes?

A

Fasting >7

Random >11.1

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31
Q

What autoantibodies can be seen in T1DM?

A

Anti-GAD
Insulin autoantibodies
Islet cell antibodies

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32
Q

How is type 1 diabetes managed?

A

Insulin therapy

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33
Q

How does DKA present?

A
Polyuria
Polydipsia
Dehydration 
Abdominal pain
Kussmaul breathing
Acetone smelling breath
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34
Q

What lab results are seen in DKA?

A

Raised ketones
Raised blood pH (metabolic acidosis with raised anion gap)
Raised glucose
Low bicarbonate

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35
Q

How is DKA managed?

A

1) fluid resus with 0.9% sodium chloride
2) IV Insulin at 0.1 units/kg/hour
3) potassium replacement

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36
Q

What are modifiable risk factors for T2DM?

A

Obesity
Sedentary lifestyle
High carb diet

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37
Q

What are non-modifiable risk factors for T2DM?

A

Ethnicity
Family history
Old age

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38
Q

How is T2DM investigated?

A

Fasting glucose >7
Random glucose >11.1
HbA1c >48

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39
Q

How is T2DM managed?

A

1) Metformin
2) add: Sulfonylurea/gliptin/pioglitazone/SGLT-2 inhibitor
3) add another
4) insulin

Add another if HbA1c is above 58

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40
Q

What are side effects of Metformin?

A

Diarrhoea
Abdominal pain
Lactic acidosis

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41
Q

When is Metformin contraindicated?

A

Chronic kidney disease

Recent MI

Alcohol abuse

Note: stop Metformin in acidosis

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42
Q

Which diabetic drug can cause hypoglycaemia?

A

Sulfonylurea (keep HbA1c at 53)

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43
Q

What are side effects of sulfonylurea?

A

Weight gain

Hypoglycaemia

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44
Q

Which diabetic drug is CI in pregnancy and breastfeeding?

A

Sulfonylurea

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45
Q

What are side effects of a gliptin (DPP4 inhibitor)?

A

Symptoms of URTI

GI tract upset

Pancreatitis

NOT THAT EFFECTIVE

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46
Q

What are side effects of a pioglitazone e.g. Thiazolidinedione?

A

Weight gain

Increased risk of bladder cancer (CI in bladder cancer)

Fluid retention

Increased risk of fractures

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47
Q

How does hypoglycaemia present?

A
Sweating
Shaking
Anxiety
Hunger
Nausea
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48
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

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49
Q

How does hypothyroidism present?

A
Weight gain
Menorrhagia
Cold intolerance
Constipation 
Dry skin
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50
Q

What autoantibodies are seen in Hashimoto’s?

A

Anti-thyroglobulin antibodies

Anti-TPO antibodies

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51
Q

How is hypothyroidism managed?

A

Levothyroxine

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52
Q

What are side effects of levothyroxine?

A

Hyperthyroidism

Reduced bone mineral density
(osteoporosis)

Worsening of angina

AF

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53
Q

What medications interact with levothyroxine?

A

Iron tablets and calcium carbonate

Allow 4 hours gap

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54
Q

What TFTs are seen in hypothyroidism?

A

High TSH

Low T3/T4

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55
Q

What is the most common cause of hyperthyroidism?

A

Graves’ disease

56
Q

How does hyperthyroidism present?

A
Weight loss
Mania
Heat intolerance
Excessive sweating
Oligomenorrhea
Pretibial myxoedema 
Diarrhoea
57
Q

What autoantibody is seen in Graves’ disease?

A

Anti-TSH antibodies

58
Q

What extra symptoms are seen in Graves’ disease?

A

Exophthalmos

Pretibial myxoedema

59
Q

What are other causes of hyperthyroidism?

A

Toxic multinodular goitre

Solitary toxic thyroid nodule

Subacute thyroiditis

60
Q

What is the presentation of subacute thyroiditis?

A

Hyperthyroidism after a viral infection
Self-limiting

TENDER goitre

61
Q

How is hyperthyroidism managed?

A

1) symptomatic relief with propranolol
2) anti-thyroid drug: Carbimazole
3) radioactive iodine
4) thyroidectomy

62
Q

What is a thyroid storm?

A

Life threatening complication of hyperthyroidism

Precipitated by illness/surgery/trauma

63
Q

How does thyroid storm present?

A

High-grade fever

Confusion/agitation

Hypotension

Tachycardia

Nausea and vomiting

Treated with = Propranolol + Steroid (e.g. Hydrocortisone) + Anti-thyroid drug (Carbimazole/Propylthiouracil)

64
Q

How is thyroid storm managed ?

A

Propranolol + Steroid (e.g. Hydrocortisone) + Anti-thyroid drug (Carbimazole/Propylthiouracil)

65
Q

What is the role of parathyroid hormone?

A

Increased calcium by:

Increasing calcium reabsorption

Inhibiting osteoclasts

Stimulating kidneys to convert vitamin D3 to calcitriol

66
Q

What is primary hyperparathyroidism? What is the most common cause?

A

Usually due to an adenoma of the parathyroid gland

67
Q

What lab results are seen in primary hyperparathyroidism?

A

High parathyroid hormone
High calcium
Low phosphate

68
Q

What is secondary hyperparathyroidism?

A

High parathyroid hormone due to:
Reduced dietary intake of vitamin d
Chronic kidney disease

High PTH
normal calcium

69
Q

What is tertiary hyperparathyroidism?

A

After there has been secondary hyperparathyroidism for a long time.
Causes hyperplasia of the parathyroid.
Once underlying cause is treated, still increased PTH

High PTH, high calcium

70
Q

What are the symptoms of hyperparathyroidism?

A
Same symptoms of hypercalcaemia
Bones, groans, stones, moans
Bone pain/fractures
Renal stones
Depression
71
Q

What is the main cause of hypoparathyroidism?

A

Usually secondary to thyroid surgery

72
Q

How does hypoparathyroidism present?

A

Presents with hypocalcaemia

Tetany - muscle twitching/cramping

Parasthesia

Chvostek’s sign – twitching of facial muscles in response to tapping over facial nerve

Trousseau’s sign - carpopedal spasm of the hand and wrist occurs after an individual wears a blood pressure cuff inflated over their systolic blood pressure for 2 to 3 minutes

73
Q

What is pseudohypoparathyroidism?

A

Target cells are not sensitive to PTH

High PTH

Low calcium

74
Q

What is Acromegaly?

A

Excess growth hormone

75
Q

What is the main cause of acromegaly?

A

Pituitary adenoma

76
Q

What are features of acromegaly?

A

Large tongue

Large nose

Large hands and feet

Protruding jaw

Prominent forehead

Skin tags

Excess sweating

Symptoms of tumour - headaches, bitemporal hemianopia

77
Q

What is the initial investigation conducted in acromegaly?

A

Insulin-like growth factor

78
Q

What next test is conducted for acromegaly if ILGF-1 is positive?

A

Oral glucose tolerance test

79
Q

How is acromegaly managed?

A

Trans-sphenoidal removal of pituitary tumour

If surgery not suitable - somatostatin analogue e.g. octreotide

80
Q

What is a pituitary adenoma?

A

A benign pituitary tumour

81
Q

How does a pituitary adenoma present?

A

Symptoms of excess hormone being produced (prolactin, growth hormone or ACTH to cortisol)

Symptoms of pituitary tumour (hypopituitarism, bitemporal hemianopia, headaches)

82
Q

What is a prolactinoma?

A

A prolactin secreting pituitary adenoma

83
Q

How does a prolactinoma present?

A

In women - amenorrhoea, galactorrhoea, infertility

In men - impotence, lack of libido, galactorrhoea

84
Q

How is a prolactinoma managed?

A

Dopamine agonists - bromocriptine or cabergoline

If this fails - trans sphenoidal removal

85
Q

What is diabetes insipidus?

A

Low ADH

86
Q

What are the two types of diabetes insipidus?

A

Nephrogenic and cranial

87
Q

Which drug most commonly causes nephrogenic diabetes insipidus?

A

Lithium

88
Q

How does diabetes insipidus present?

A

Polyuria and polydipsia

89
Q

Does diabetes insipidus have high or low urine osmolality?

A

Low urine osmolality

90
Q

How is diabetes insipidus investigated?

A

Fluid deprivation test

No fluid for 8 hours - test urine osmolality

Then give desmopressin and Check again in 8 hours

Cranial DI - urine osmolality high after giving desmopression
Nephrogenic DI - urine osmolality still low

91
Q

How is diabetes insipidus treated?

A

Cranial - desmopressin

Nephrogenic - thiazide diuretics

92
Q

What is SIADH?

A

Excess ADH

93
Q

What electrolyte imbalance is seen in SIADH?

A

Hyponatraemia

94
Q

What do you have to be careful of when treating severe hyponatraemia?

A

Central pontine myelinosis

95
Q

How is SIADH treated?

A

Tolvaptan

96
Q

What is the most common type of thyroid cancer?

A

Papillary

97
Q

Which thyroid cancer has the best prognosis?

A

Papillary

98
Q

What is a phaeochromocytoma?

A

Adrenal tumour secreting catecholamines (adrenaline and noradrenaline)

99
Q

How is phaeochromocytoma treated?

A

Definitive management - surgery

1) stabilise patient with alpha blocker - Phenoxybenzamime
2) then beta blocker - propranolol

100
Q

Which type of thyroid cancer is associated with increased calcitonin?

A

Medullary

101
Q

Why do you have to be careful with fluid resus in DKA in children and young adults?

A

Can cause cerebral oedema

102
Q

How does cerebral oedema present?

A

Headache, irritability, visual disturbances, confusion

103
Q

Which diabetes drug is associated with weight loss?

A

SGLT-2 inhibitor ( -gliflozin)

104
Q

What is the main side effect of carbimazole?

A

Agranulocytosis

105
Q

What does HbA1c need to be to add another diabetic drug to someone who has T2DM?

A

58 or over

106
Q

What are macro vascular complications of diabetes?

A

Coronary artery disease

Peripheral ischaemia

Stroke

HTN

107
Q

What are micro vascular complications of diabetes?

A

Peripheral neuropathy

Retinopathy -proliferative

Nephropathy - glomerulonephritis

108
Q

What is gastroparesis? How is it managed?

A

Complication of diabetes

Delayed gastric emptying - food held in stomach longer than usual

Causes nausea/vomiting

Abdominal pain

Feeling of fullness/bloating

Management = Domperidone/Metoclopramide

109
Q

What is subclinical hypothyroidism? How is subclinical hypothyroidism managed?

A

Raised TSH but normal T3/T4

If TSH 4-10:
If under 65 + symptomatic = Levothyroxine.
Otherwise - watch and wait

If TSH >10
Under 70 = Levothyroxine
Older than 70 = watch and wait

110
Q

What is the action of aldosterone?

A

Increases sodium+water absorption

Increases potassium excretion

Increases BP

111
Q

How can diabetes be diagnosed in a patient with haemoglobinopthy?

A

Oral glucose tolerance testing

Can’t do HbA1c because of haemaglobin

112
Q

Which drugs can cause gynaecomastia?

A

Spironolactone
Digoxin
Finasteride
Goserelin

113
Q

What are causes of gynaecomastia? (Non-drug)

A
Physiological – normal in puberty
Kallman’s/Klinefelter’s
Testicular failure
Liver disease
Testicular cancer
Drugs
114
Q

What happens to C-peptide levels in T1DM?

A

Low

115
Q

What is bitemporal hemianopia and what can cause this?

A

Loss of vision in both eyes on temporal side

Due to damage to the optic chiasm - due to tumours e.g. pituitary tumour

116
Q

What is the role of ADH?

A

Increased water absorption at the DCT and collecting duct

117
Q

What is the role of aldosterone?

A

Increased sodium reabsorption

Increased potassium excretion

Increases BP

118
Q

Why does hypocalcaemia occur in CKD?

A

Decreased renal production of vitamin D –> Decreased calcium absorption

119
Q

How is postpartum thyroiditis managed?

A

Watch and wait

120
Q

What are the three types of multiple endocrine neoplasia?

A

MEN type I = 3 P’s
Hyperparathyroid, pituitary, pancreas (insulinoma, gastrinoma)
Hypocalcaemia

MEN type IIa
2 P’s - parathyroid + phaeochromocytoma
Medullary thyroid cancer

MEN type IIb
1 P - Phaeochromocytoma
Marfanoid body habits

121
Q

What is pituitary apoplexy?

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

122
Q

What are precipitating factors of a pituitary apoplexy?

A

HTN
Pregnancy
Trauma
Anticoagulation

123
Q

What are features of a pituitary apoplexy?

A

Sudden onset headache similar to that seen in subarachnoid haemorrhage

Vomiting

Neck stiffness

Visual field defects: classically bitemporal superior quadrantic defect

Extraocular nerve palsies

Features of pituitary insufficiency
e.g. hypotension/hyponatraemia secondary to hypoadrenalism

124
Q

How is pituitary apoplexy diagnosed?

A

MRI Head

125
Q

How is pituitary apoplexy managed?

A

Urgent steroid replacement
Careful fluid balance

Definitive = surgery

126
Q

Which visual defect is seen in pituitary apoplexy?

A

Classically bitemporal superior quadrantic defect

Bitemporal superior quadrantinopia

127
Q

What is sick euthyroid syndrome?

How is it managed?

A

Everything low - TSH, T3, T4
Or TSH inappropriately normal with low T3 and T4

No thyroid abnormality

No treatment needed - usually recovers after recovery from systemic illness

128
Q

What is carcinoid syndrome? How does it present?

A

A rare, slow growing malignant tumour that develops in the neuroendocrine system

Usually from liver mets

Abdominal pain
Diarrhoea
Flushing
Bronchospasm

129
Q

How is carcinoid syndrome diagnosed?

A

Raised urinary 5-HIAA

130
Q

How is carcinoid syndrome managed?

A

Octreotide (somatostatin analogue)

131
Q

How is pheochromocytoma diagnosed?

A

24 hour urinary collection of metanephrines

132
Q

What is a myxoedema coma? How does it present?

A

Complication of untreated hypothyroidism

Confusion
Hypothermia
Bradycardia
Hyporeflexia
Seizures
133
Q

How is myxoedema coma managed?

A

IV thyroid replacement + IV hydrocortisone (until co-existing adrenal insufficiency has been excluded)

134
Q

How is hyperaldosteronism investigated/diagnosed?

A

First line investigation for hyperaldosteronism = Plasma aldosterone/renin ratio

If abnormal –> CT Abdomen, adrenal venous sampling (To differentiate cause).

135
Q

What is the diagnostic criteria for hyperosmolar hyperglycaemic state?

A
  1. Hypovolaemia
  2. Hyperglycaemia (No ketonaemia or acidosis)
  3. High serum osmolality
136
Q

How is hyperosmolar hyperglycaemic state managed?

A

Mainstay = 0.9% Sodium Chloride
This will reduce hyperglycaemia and treat serum osmolality

Check serum osmolality frequently

Can add insulin but only once glucose is no longer dropping with just fluids