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Year 2 MBChB > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the causes of hypoparathyroidism?

A

Di George Syndrome
Malignancy
Autoimmune destruction of parafollicular cells

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2
Q

How does hypoparathyroidism present?

A

Cramp & tetany of muscles

Pins & needles

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3
Q

What is Chvostek’s sign?

A

Twitching of facial muscle when tapping nerve

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4
Q

What is trousseaus signs?

A

Inflamm of BP cuff over sys BP for a period of time –> tetany of hand muscles

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5
Q

What are the blood cell changes in hypoparathyroidism?

A

Decreased PTH
Decreased calcium
Increased phosphate

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6
Q

How is hypoparathyroidism managed?

A

Calcium & vitamin D supplements

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7
Q

Describe the pathophysiology of pseudohypoparathyroidism?

A

Caused by genetic receptor abnormality –> PTH resistance –> PTH receptor cannot be stimulate –> increased serum PTH levels –> hypocalcaemia –> even more PTH

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8
Q

What are the complications of pseudohypoparathyroidism?

A 
Subcut calcification 
Mental retardation 
Brachydactyly 
Obesity 
Bone abnormalities
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9
Q

What is the DEXA score for osteopenia?

A

1-2.5

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10
Q

What is the DEXA score for osteoporosis?

A

> 2.5

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11
Q

Disease: low calcium, low phosphate, high ALP, high PTH

A

Osteomalacia

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12
Q

Disease: high calcium, low phosphate, high ALP, high PTH

A

Primary hyperparathyroid

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13
Q

Disease: low calcium, high phosphate, high ALP, high PTH

A

CKD

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14
Q

Disease: normal calcium, normal phosphate, normal PTH, high ALP

A

Pagets

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15
Q

What effect does PTH have on the bone?

A

Increases resorption resulting in increased serum calcium

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16
Q

What do osteoclasts do?

A

Bone resorption

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17
Q

What do osteoblasts do?

A

Bone formation

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18
Q

Which bone is the porous type?

A

Trabecular

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19
Q

Which bone is the dense type?

A

Cortical

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20
Q

What effect does PTH have on the kidney?

A

Causes Vit D activation

Tubular reabsorption resulting in increased calcium and less phosphate

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21
Q

When is calcitonin secreted?

A

In extreme hypercalcaemia

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22
Q

What is primary hyperparathyroidism caused by?

A

Overactivity of the gland

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23
Q

What is secondary hyperparathyroidism?

A

Physiological response to low calcium

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24
Q

What is tertiary hyperparathyroidism?

A

Autonomous gland after chronic secondary

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25
Q

What are the features of hyperparathyroidism?

A

Stones, bones, moans and abdominal groans

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26
Q

How is hyperparathyroidism diagnosed?

A

Increased calcium
Increased PTH
Increased urinary calcium

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27
Q

What are the features of hypercalcaemia?

A

Muscle weakness, constipation, stones, moans

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28
Q

What is the management of hyperparathyroidism?

A

Adenoma excision
Avoid lots of calcium and vitamin D
High fluid diet

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29
Q

What is pheochromocytoma?

A

Tumour of the sympathetic paraganglia cells

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30
Q

What syndrome in pheochromocytoma assoc with?

A

MEN 2

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31
Q

What is the classic triad of pheochromocytoma?

A

Hypertension, sweating, headaches

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32
Q

What are the features of phaechromocytoma?

A

Hypertension, arrhythmia, sweating, pallor, headaches, anxiety

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33
Q

How is phaechromocytoma investigated?

A

Urinary catecholamines, CT/MRI, MIBG

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34
Q

How is phaeochromocytoma managed?

A

Atenolol, phenoxybenzamine, chemotherapy

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35
Q

What is Addison’s?

A

Glucocorticoid insufficiency

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36
Q

When should Addison’s be considered?

A

Worsening symptoms on thyroxine, Unexplained hypos in T1DM

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37
Q

What is the presentation of addisons?

A

Fatigue and weakness, anorexia, N&V, bronze skin, salt cravings, hypotension, loss of pubes

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38
Q

How is Addison’s managed?

A

Hydrocortisone

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39
Q

How is Addison’s investigated (including findings)?

A

Low sodium, low potassium, short synacthen test: no cortisol spike

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40
Q

What are the two types of cushings syndrome?

A

ACTH dependent and independent

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41
Q

What causes ACTH dependent cushings?

A

Adenoma in pituitary

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42
Q

What causes ACTH independent cushings?

A

Adrenal adenoma, nodular hyperplasia

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43
Q

How does Cushing’s present?

A

Moon face, striae, easy bruising, muscle wasting, central obesity, dysthymia, bone pain

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44
Q

How is Cushing’s investigated?

A

Low dose dex test,
High dose dex suppression,
Measure ACTH, DEXA scan

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45
Q

What happens to low dose dexamethasone test in Cushing’s?

A

> 50nmol

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46
Q

What is the HDDS for in Cushing’s?

A

To determine if pituitary (50%)

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47
Q

What are the ACTH levels in Cushing’s (dependent on source)?

A

< 300 in pituitary
< 1 adrenal
> 300 ectopic

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48
Q

How is Cushing’s managed?

A

Metyrapone, ketoconazole, surgery (trans-sphenoidal, bilateral adrenalectomy

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49
Q

What is the management of bilateral adrenal hyperplasia?

A

Eplerenone

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50
Q

What is Conn’s syndrome?

A

Adrenal adenoma (tumour in zona glomerulosa –> excess aldosterone)

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51
Q

What are the features of Conn’s?

A

Hypertension, hypernatraemia, hypokalaemia

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52
Q

How is Conn’s investigated?

A

Aldesterone:renin saline suppression

Usually incidental finding

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53
Q

What does the zona glomerulosa produce?

A

Aldosterone

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54
Q

What does aldosterone do?

A 
Sodium retention  (hence water swell) 
Increases BP
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55
Q

What does the zona fasciculata produce?

A

Cortisol

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56
Q

What controls the zona fasciculata?

A

ACTH

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57
Q

What controls the zona glomerulosa?

A

RAAS

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58
Q

What does the zona reticularis?

A

DHEA

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59
Q

What controls the zona reticularis?

A

ACTH

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60
Q

What does the medulla of adrenals produce?

A

Adrenaline + noradrenaline

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61
Q

What are the adrenalines derived from and where?

A

Tyrosine in chromaffin cells

62
Q

What is the medulla of the adrenals controlled by?

A

Sympathetic stimulation

63
Q

State the layers of the adrenal (from superficial to deep)

A

Connective tissue, z. glomerulosa, z. fasciculata, z. reticularis, medulla

64
Q

What is the thyroid attached to?

A

Thyroid cartilage and upper end of trachea

65
Q

What do follicular cells produce?

A

Thyroglobulin

66
Q

What do parafollicular cells produce?

A

Calcitonin

67
Q

What is T3 made up of?

A

2 x MIT

68
Q

What is T4 made up of?

A

MIT + DIT

69
Q

Which thyroid hormone is more biologically active?

A

T3

70
Q

Where is T4 converted and what to?

A

T3 in the liver and kidneys

71
Q

High TSH + low T4?

A

Primary hypothyroidism

72
Q

Low TSH + low T4?

A

Secondary hypothyroidism

73
Q

Low TSH + high T4?

A

Thyrotoxicosis

74
Q

High TSH + normal T4?

A

Subclinical hypothyroidism

75
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

76
Q

What are the features of Hashimoto’s thyroiditis?

A

Hypothyroidism: weight gain, constipation, leathery, cold intolerance etc
Firm non-tender goitre

77
Q

How is Hashimoto’s thyroiditis investigated?

A

High TSH, low T3 & T4, Anti-TPO antibodies

78
Q

How is Hashimoto’s thyroiditis managed?

A

Thyroid replacement - levothyroxine

79
Q

What is De Quervains thyroiditis?

A

Follows viral infection and presents with hyperthyroid

80
Q

What are the phases of De Quervains thyroiditis?

A

Hyperthyroid, raised ESR, painful goitre (3-6 weeks), euthyroid (1-3 weeks), hypothyroid (weeks - months), return back to normal

81
Q

How is De Quervains thyroiditis investigated?

A

Iodine uptake scan - globally decreased

82
Q

How is De Quervains thyroiditis managed?

A

Self limiting, NSAIDs for pain, severe: steroids

83
Q

What is toxic multi nodular goitre?

A

Autonomous nodules in thyroid which produce T3 & T4

84
Q

What are the features of toxic multi nodular goitre?

A

Everything in overdrive (hyperthyroid),
Asymmetrical nodular goitre,
Tremor,
Moist, smooth skin

85
Q

How is toxic multi nodular goitre investigated?

A

iodine uptake scan - patchy uptake,
Low TSH, high T3 &T4,
USS

86
Q

How is toxic multi nodular goitre managed?

A

Radioiodine therapy

Surgery

87
Q

What is the most common cause of thyrotoxicosis?

A

Graves

88
Q

What are the features of Graves?

A

Goitre,
Exopthalmus,
Pretibial myxoedema,
Hyperthyroidism; weight loss, heat intolerance, anxiety, diarrhoea, palpitations, tachycardia

89
Q

How is graves investigated?

A

Low TSH, high T3 & T4,

Anti-TSH

90
Q

What is the management of Graves?

A

Carbimazole, PTU,
Surgery,
Radioiodine therapy

91
Q

What is an important complication of carbimazole?

A

Agranulocytosis

92
Q

What is the HbA1c target?

A

7% or below - 48mmol

93
Q

What are the side effects of metformin?

A

Vomiting & diarrhoea, rash, lactic acidosis

94
Q

How much does metformin reduce the HbA1c by?

A

15-20mmol

95
Q

What effect does metformin have on weight?

A

neutral

96
Q

What is the basic mode of action of metformin?

A

Increased insulin sensitivity

97
Q

What is the basic mode of action of sulphonylureas?

A

Increases pancreatic release - must produce at least some

98
Q

Does sulphonylureas have any effect on T2DM complications?

A

Microvascular prevention

99
Q

What are the side effects of sulphonylureas?

A

Hypos, weight gain

100
Q

When should sulphonylureas be avoided?

A

In severe hepatic and renal failure

101
Q

What effect do TZDs have on T2DM complications?

A

Macrovascular prevention

102
Q

What are the side effects of TZDs?

A

Hypos, weight gain, doubles risk of heart failure

103
Q

What is the management of mild hypoglycaemia?

A

Glucose tabs

104
Q

What is the management of moderate hypoglycaemia?

A

dextrogel

105
Q

What is the management of severe hypoglycaemia?

A

IV glucose 10%

106
Q

What random blood glucose measurement may indicate diabetes?

A

> 11.0

107
Q

What fasting BG is normal?

A

< 5.6

108
Q

What fasting BG indicates pre diabetes (impaired fasting glucose)?

A

5.6 - 6.9

109
Q

What fasting BG indicates diabetes?

A

> 6.9

110
Q

What oral glucose tolerance test result is normal?

A

< 7.8

111
Q

What oral glucose tolerance test result indicates impaired glucose tolerance?

A

7.8 - 11

112
Q

What oral glucose tolerance test result indicates diabetes?

A

> 11.0

113
Q

What is the most common thyroid cancer?

A

Papillary

114
Q

What is medullary thyroid cancer?

A

Cancer of parafollicular cells - secretes calcitonin

115
Q

Which thyroid cancer carries the worst prognosis?

A

Anaplastic

116
Q

What is the histology of papillary thyroid cancer?

A

papillary projections and pale empty nuclei

117
Q

Does papillary cancer metastasise commonly?

A

Lymph nodes yes

118
Q

How do follicular adenomas usually present?

A

Solitary thyroid nodule

119
Q

How is follicular carcinoma and adenoma differentiated?

A

microscopically capsular invasion is seen in carcinoma

120
Q

Does follicular carcinoma metastasise?

A

Yes, vascular invasion predominantly

121
Q

Who gets anaplastic thyroid cancer?

A

Old ladies

122
Q

What is ineffective against thyroid cancer?

A

Chemotherapy

123
Q

What is part of MEN 1?

A

Pituitary adenoma, parathyroid hyperplasia, pancreatic cancer

124
Q

What is part of MEN 2a?

A

Parathyroid hyperplasia, medullary thyroid cancer, phaeochromocytoma

125
Q

What is part of MEN 2b?

A

Neuromas, Marfanoid features, Medullary thyroid cancer, phaechromocytoma

126
Q

What does the anterior pituitary produce?

A

Gonadotrophins, GH, PRL, TSH, ACTH

127
Q

What does the posterior pituitary produce?

A

Oxytocin & ADH

128
Q

What is the initial management of hypercalcaemia?

A

Saline

129
Q

What is the medical management of pheochromocytoma?

A

Alpha blocker > beta blocker

130
Q

What is the most common cause of Addison’s?

A

Autoimmune adrenalitis

131
Q

What is the HbA1c in pre diabetes?

A

42-47

132
Q

What are the features of Klinefelters?

A

Tall, infertility, small testes, gynaecomastia, no secondary sexual characteristics

133
Q

What drugs can cause a raised PRL?

A

Metoclopramide, domperidone

134
Q

What is used to monitor response to treatment in hypothyroid?

A

TSH

135
Q

What test is used to differentiate between T1 and T2 DM?

A

C-peptide

136
Q

When should another drug be added in diabetes?

A

HbA1c > 58 (7.5%)

137
Q

What are the features of HHS?

A

Increased serum osmolality, no ketosis, hyperglycaemia

138
Q

What are causes of HHS?

A

Illness, dehydration

139
Q

What is the first line management of a prolactinoma?

A

Bromocriptine, cabergoline

140
Q

Bone thing steroids increase risk of

A

Osteonecrosis, osteoporosis

141
Q

What is the BP target in T2DM if there is no organ damage?

A

140/80

142
Q

What is the Bp target in T2DM if there is organ damage?

A

130/80

143
Q

What is the management of DKA?

A

Fluid resus, insulin infusion, potassium replacement

144
Q

What is the management of HHS?

A

Fluid resus, allow time before insulin

145
Q

What happens to steroid doses in Addisons if they get ill?

A

2 x hydrocortisone, normal fludrocortisone

146
Q

What HbA1c is diagnostic of diabetes?

A

> 6.5%

147
Q

What does the ABG/electrolytes show in Cushing’s?

A

Hypokalaemia metabolic alkalosis

148
Q

What is an easily modifiable risk factor for thyroid eye disease?

A

Smoking

149
Q

What do SGLT2s increase your risk of?

A

Thrush, urine infections

150
Q

What is the optimal treatment in HNF1A-MODY?

A

Sulphonylureas

151
Q

What are the levels in sick euthyroid?

A

TSH -/raised, low T3 & T4

152
Q

What is the treatment for post menopausal women with a fracture (endocrinologically)?

A

Bisphosphonates

Year 2 MBChB (8 decks)

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