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Medicine Finals > Endocrinology > Flashcards

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?

86
Q

What are the two types of diabetes insipidus?

A

Nephrogenic and cranial

87
Q

Which drug most commonly causes nephrogenic diabetes insipidus?

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?

96
Q

What is the most common type of thyroid cancer?

97
Q

Which thyroid cancer has the best prognosis?

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?

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?

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?

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

Medicine Finals (32 decks)

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