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MBBS Y5 > Medicine - Endocrinology > Flashcards

Medicine - Endocrinology Flashcards

1
Q

what is cushing’s syndrome?

A

the signs and symptoms of prolonged abnormal elevated cortisol levels

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2
Q

what is cushing’s disease?

A
  • where a pituitary adenoma is producing excess ACTH| - a cause of cushing’s syndrome
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3
Q

presentation of cushing’s syndrome? (hint: there’s a LOT)

A

obesity with proximal limb muscle wasting)
- abdo striae
- “moon face” (rounded)
- “buffalo hump” (fat pad on back)
- HTN
- T2DM or hyperglycaemia
- depression
- insomnia
- osteoporosis
- easy bruising
- poor skin healing

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4
Q

causes of cushing’s syndrome?

A
  • exogenous steroids
  • cushing’s disease
  • adrenal adenoma
  • paraneoplastic cushing’s
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5
Q

what is paraneoplastic cushing’s? commonest cause of this?

A
  • when a tumour releases ACTH but it is NOT in the pituitary
  • SCLC is commonest cause
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6
Q

what is ectopic ACTH?

A

ACTH released from anywhere other than the pituitary

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7
Q

diagnostic investigation for cushing’s syndrome?

A

dexamethasone suppression test

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8
Q

how is a dexamethasone suppression test carried out?

A
  • patient takes a dose of dexamethasone at night
  • cortisol and ACTH measured in the morning
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9
Q

how is the result of a dexamethasone suppression test interpreted?

A
  • normal cortisol and ACTH suggest cushing’s syndrome
  • if result is abnormal for a low dose test, do a high dose test next
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10
Q

results of dexamethasone suppression testing in adrenal adenoma?

A
  • ACTH suppressed but cortisol NOT supressed
  • this is independent of the pituitary (which produces cortisol)
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11
Q

results of dexamethasone suppression testing in pituitary adenoma?

A
  • cortisol and ACTH both suppressed
  • pituitary still functioning somewhat normally
  • this is cushing’s disease
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12
Q

results of dexamethasone suppression testing in ectopic ACTH production?

A
  • neither cortisol nor ACTH suppressed
  • it’s from an external source
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13
Q

investigations in cushing’s syndrome? hint: don’t forget ectopic causes

A
  • dex suppression test
  • 24h urinary free cortisol (high)
  • FBC (raised WCC)
  • UEs (K+ low if aldosterone also being secreted)
  • MRI brain (pit adenoma)
  • CT chest (SCLC)
  • CT abdo (adrenal adenomas)
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14
Q

management of cushing’s syndrome? hint: underlying cause

A

NAME?

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15
Q

what can be done about adrenal tumours which cannot be removed?

A

remove both adrenal glands and give lifelong replacement steroid hormones instead

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16
Q

which 2 steroids are deficient in adrenal insufficiency?

A
  • cortisol| - aldosterone
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17
Q

what is addison’s disease? commonest cause?

A
  • primary adrenal insufficiency| - autoimmune is commonest cause
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18
Q

what is tertiary adrenal insufficiency? commonest cause?

A
  • reduced CRH release from the hypothalamus| - long-term steroid use
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19
Q

how can tertiary adrenal insufficiency be prevented?

A

taper down long-term steroids slowly

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20
Q

presentation of adrenal insufficiency?

A

NAME?

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21
Q

signs O/E of adrenal insufficiency?

A
  • bronze hyperpigmentation (addison’s), seen especially in palmar creases- (postural) hypotension
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22
Q

what causes bronze skin in addison’s disease?

A

NAME?

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23
Q

investigations and findings in adrenal insufficiency? hint: most are on bloods

A
  • UEs (low Na+, high K+) - early morning cortisol - short synacthen test (diagnostic)- ACTH levels (high in addison’s, low in secondary insufficiency)- adrenal cortex antibodies (autoimmune)- 21-hydroxylase antibodies (autoimmune)- CT / MRI adrenals
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24
Q

diagnostic test for adrenal insufficiency?

A

short synacthen test

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25
Q

what is synacthen?

A

synthetic ACTH

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26
Q

how is the short synacthen test carried out?

A
  • give synacthen at 8am - measure cortisol at baseline- then after 30 mins- then after 60 mins
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27
Q

what is the result of the short synacthen test in a healthy person?

A

cortisol should at least double

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28
Q

if cortisol fails to double on the short synacthen test, what does this indicate?

A

primary adrenal insufficiency (addison’s)

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29
Q

management of adrenal insufficiency?

A

NAME?

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30
Q

signs of addisonian crisis?

A

everything low but K+ high- reduced consciousness - hypotension- hypoglycaemia - hyponatraemia- hyperkalaemia - patient looks very unwell

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31
Q

triggers of addisonian crisis?

A
  • could be first presentation of addison’s disease- infection- trauma - other acute illness
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32
Q

management of addisonian crisis?

A
  • IV hydrocortisone 100mg stat - repeat 6 hourly - IV fluid resus- correct hypoglycaemia - monitor electrolytes and fluid closely
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33
Q

TFT findings in hyperthyroidism? hint: different if pituitary source

A
  • low TSH, high if pituitary adenoma| - high T3 and T4
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34
Q

TFT findings in hypothyroidism? hint: different if pituitary / hypothalamic source

A

NAME?

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35
Q

in which conditions are anti-TPO antibodies present?

A
  • grave’s disease| - hashimoto’s thyroiditis
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36
Q

in which conditions are antithyroglobulin antibodies present?

A
  • grave’s disease- hashimoto’s thyroiditis- thyroid cancer
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37
Q

in which conditions are TSH receptor antibodies present?

A

grave’s disease

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38
Q

what is the difference between hyperthyroidism and thyrotoxicosis?

A

NAME?

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39
Q

what is grave’s disease? describe the pathophysiology

A
  • autoimmune primary hyperthyroidism| - TSH receptor antibodies mimic TSH and stimulate the thyroid TSH receptors
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40
Q

commonest cause of hyperthyroidism?

A

grave’s disease

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41
Q

describe toxic multinodular goitre

A

nodules develop on the thyroid which keep producing thyroid hormone, independent to the feedback loop

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42
Q

what is exophthalmos? which condition is it seen in? what causes it?

A
  • eyeball bulging from socket- seen in grave’s disease- is a direct reaction to TSH receptor antibodies
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43
Q

describe pretibial myxoedema. which condition is it seen in? what causes it?

A
  • discoloured, waxy oedematous skin over shins- grave’s disease- is a direct reaction to TSH receptor antibodies
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44
Q

presentation of hyperthyroidism?

A

NAME?

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45
Q

which features in presentation are unique to grave’s disease?

A

NAME?

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46
Q

which features in presentation are suggestive of toxic mulitnodular goitre?

A
  • goitre with firm nodules felt in neck| - usually aged 50+
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47
Q

describe the presentation in de quervain’s thyroiditis?

A

NAME?

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48
Q

prognosis and management of de quervain’s thyroiditis?

A
  • self-limiting condition| - supportive treatment, e.g. NSAIDs, BBs
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49
Q

what is the other name for a thyroid storm? describe the presentation of this

A

NAME?

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50
Q

management of a thyrotoxic storm?

A

NAME?

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51
Q

management of hyperthyroidism?

A
  • 1st line: carbimazole - 2nd: propylthiouracil - radioactive iodine (drink)- BB (e.g. propanolol)- surgery
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52
Q

causes of hypothyroidism?

A
  • hashimoto’s thyroiditis - iodine deficiency - overtreatment of hyperthyroidism- drugs - tumours- infections - sheehan syndrome - radiation
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53
Q

presentation of hypothyroidism?

A

NAME?

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54
Q

TFT findings in primary hypothyroidism?

A
  • TSH high| - T3 and T4 low
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55
Q

TFT findings in secondary hypothyroidism?

A
  • TSH low| - T3 and T4 low
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56
Q

management of hypothyroidism?

A

PO levothyroxine

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57
Q

how is levothyroxine treatment monitored?

A

NAME?

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58
Q

what does “diffuse high uptake” on a radioisotope scan of the thyroid suggest?

A

grave’s disease

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59
Q

what does “focal high uptake” on a radioisotope scan of the thyroid suggest?

A
  • toxic multinodular goitre| - adenoma
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60
Q

what do “cold areas” on a radioisotope scan of the thyroid suggest?

A

thyroid cancer

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61
Q

which cells produce glucagon? where are these found?

A
  • alpha cells| - islets of langerhans in pancreas
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62
Q

which cells produce insulin? where are these found?

A
  • beta cells| - islets of langerhans in pancreas
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63
Q

how does insulin reduce blood glucose levels? hint: 2 ways

A
  • causes body cells to absorb glucose to use| - causes muscle and liver cells to absorb glucose and store it as glycogen
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64
Q

what is ketogenesis? when is it done?

A
  • liver converting fatty acids into ketones| - done when both glucose and glycogen supplies are low
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65
Q

what is the normal blood glucose range?

A

4.4 - 6.1 mmol/L

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66
Q

pathophysiology of T1DM?

A

NAME?

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67
Q

what is the body’s initial response to rising blood ketone levels?

A

kidneys produce bicarbonate to counteract the acidity

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68
Q

how does insulin affect potassium? what happens in DKA? what can happen when DKA is treated?

A
  • insulin causes cells to absorb potassium- in DKA, serum potassium is high or normal because there’s not enough insulin so none of it is being absorbed, but the kidneys carry on excreting it - however, total body potassium is low - treating with insulin can cause a severe hypokalaemia
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69
Q

overall effects of DKA on body?

A

NAME?

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70
Q

presentation of DKA?

A

NAME?

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71
Q

diagnostic criteria for DKA?

A
  • blood glucose >11mmol/L - blood ketones >3mmol/L- pH <7.3
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72
Q

FIG PICK: management of DKA?

A
  • Fluids (IV fluid resus)- Insulin infusion - Glucose (monitor closely, consider dextrose)- Potassium (monitor 4-hourly and correct)- Infection (treat underlying triggers)- Chart (check fluid balance)- Ketones (monitor them)
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73
Q

what is the max rate at which potassium can be infused?

A

10mmol/L

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74
Q

patient advice given in long term management of T1DM?

75
Q

when should blood glucose be checked in T1DM?

76
Q

what is a typical insulin regime in T1DM?

A
  • background insulin once daily (long-acting)| - short acting insulin 30 mins before each meal
77
Q

why does the injection site for insulin need to be changed regularly?

A

risk of lipodystrophy

78
Q

what is lipodystrophy?

A

the subcut fat hardens from being injected in so much

79
Q

symptoms of hypoglycaemia?

80
Q

management of hypoglycaemia in T1DM? if severe?

81
Q

how could a patient in DKA end up hypoglycaemic?

A

overtreatment with insulin

82
Q

short term complications in T1DM?

83
Q

macrovascular complications in diabetes?

84
Q

microvascular complications in diabetes?

85
Q

nature of neuropathy in diabetes?

A
  • peripheral| - “glove and stocking” distribution
86
Q

infection-related complications in diabetes?

87
Q

what 3 things are used to monitor T1DM?

88
Q

what does HbA1c tell us? how often is it checked?

A
  • average blood glucose levels over last 3 months| - every 3-6 months
89
Q

non-modifiable risk factors for T2DM?

90
Q

modifiable risk factors for T2DM?

91
Q

how might T2DM present?

92
Q

when is an oral glucose tolerance test (OGTT) performed?

A

first thing in the morning, before breakfast

93
Q

what does an OGTT involve?

A
  • take a fasting glucose reading- then give 75g glucose drink- then measure glucose again 2 hours later
94
Q

diagnostic criteria for pre-diabetes?

A
  • HbA1c 42 - 47 mmol/L- fasting glucose 6.1 - 6.9 mmol/L (impaired)- OGTT 7.8 - 11 mmol/L (impaired)
95
Q

diagnostic criteria for diabetes?

A
  • HbA1c >48mmol/L- random glucose >11mmol/L- fasting glucose >7mmol/L- OGTT >11mmol/L
96
Q

diet advice in T2DM?

97
Q

lifestyle advice given in T2DM?

98
Q

3 main complications to monitor for in T2DM?

99
Q

what is the target HbA1c for type 2 diabetics on metformin alone?

100
Q

what is the target HbA1c for type 2 diabetics on more than just metformin?

101
Q

medical management of T2DM?

A
  • 1st line: metformin - 2nd: add add sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor- 3rd: metformin + sulfonylurea + GLP-1 mimetic- 4th: metformin + insulin
102
Q

actions of metformin?

A
  • increases insulin sensitivity| - decreases liver production of glucose
103
Q

notable side effects of metformin?

104
Q

example of sulfonylurea?

A

gliclazide

105
Q

MOA of gliclazide?

A

increases insulin production in pancreas

106
Q

notable side effects of gliclazide?

107
Q

notable side effects of pioglitazone?

108
Q

example of DPP-4 inhibitor?

A

sitagliptin

109
Q

notable side effects of sitagliptin?

110
Q

notable side effects of GLP-1 inhibitors?

111
Q

what are the 5 types of insulin? give an example for each

A
  • rapid-acting (novorapid)- short-acting (actrapid)- intermediate-acting (insulatard)- long-acting (levemir) - combination (humalog 25, 25:75)
112
Q

what causes acromegaly?

A

an excess of GH

113
Q

where is GH produced in the body?

A

anterior pituitary gland

114
Q

commonest cause of acromegaly?

A

pituitary adenoma

115
Q

what visual field defect is seen in pituitary adenoma? why?

A
  • bitemporal hemianopia| - it compresses the optic chiasm
116
Q

presentation of acromegaly?

117
Q

describe frontal bossing

A

prominent forehead and brow bone

118
Q

describe prognathism

A

large, protruding jaw

119
Q

organ dysfunction caused by GH?

120
Q

management of acromegaly?

121
Q

which drugs can block GH?

122
Q

which 2 hormones can inhibit GH?

A
  • somatostatin| - dopamine
123
Q

which cells produce PTH? where are these found?

A

chief cells on the parathyroid glands

124
Q

when is PTH secreted?

A

in response to hypocalcaemia

125
Q

how does PTH increase blood Ca levels? hint: think bone, gut and kidney

126
Q

what causes primary hyperparathyroidism?

A

excessive PTH being secreted by a tumour on the parathyroid glands

127
Q

management of primary hyperparathyroidism?

A

surgical tumour removal

128
Q

PTH and calcium levels in primary hyperparathyroidism?

A
  • PTH is high| - serum calcium is high
129
Q

what causes secondary hyperparathyroidism?

A

2 main ways:- vit D deficiency- chronic renal / liver / failure (mostly CKD) - bowel disease

130
Q

PTH and calcium levels in secondary hyperparathyroidism?

A
  • PTH is high| - serum calcium is low
131
Q

what causes tertiary hyperparathyroidism?

A

prolonged secondary hyperparathyroidism, resulting in parathyroid hyperplasia

132
Q

PTH and calcium levels in tertiary hyperparathyroidism?

A
  • PTH is high| - serum calcium is high
133
Q

management of tertiary hyperparathyroidism?

A

surgical removal of some of the excess parathyroid gland

134
Q

main effects of primary hyperparathyroidism? how do these present?

135
Q

where are juxtaglomerular cells found? what do they do?

136
Q

what is the role of renin?

A

converts angiotensinogen into angiotensin I

137
Q

where is ACE found in the body? what does it do?

A
  • lungs| - converts angiotensin I to angiotensin II
138
Q

what is the role of angiotensin II?

A

stimulates adrenal glands to secrete aldosterone

139
Q

actions of aldosterone?

140
Q

what is conn’s syndrome?

A

primary hyperaldosteronism

141
Q

causes of conn’s syndrome?

142
Q

what causes secondary hyperaldosteronism? key finding?

A
  • excess renin, resulting in excess aldosterone| - high serum renin
143
Q

causes of secondary hyperaldosteronism? hint: renin goes up when kidneys get less blood

A
  • renal artery stenosis| - renal artery obstruction HF
144
Q

investigations for renal artery stenosis?

145
Q

how is hyperaldosteronism screened for?

A

work out renin:aldosterone ratio from bloods:- low:high = primary- high:high = secondary

146
Q

investigations for hyperaldosteronism?

147
Q

management of hyperaldosteronism?

148
Q

types of hyperaldosteronism?

A
  • primary (conn’s syndrome)| - secondary
149
Q

commonest cause of secondary hypertension?

A

hyperaldosteronism

150
Q

where is ADH produced?

A

hypothalamus

151
Q

where is ADH secreted?

A

posterior pituitary

152
Q

actions of ADH?

A

water reabsorption in collecting ducts of nephron

153
Q

how much SIADH occur?

A
  • posterior pituitary secreting too much ADH| - ectopic ADH from a tumour (e.g. SCLC)
154
Q

how does SIADH affect sodium?

A
  • hyponatraemia| - the excess water dilutes it down
155
Q

how does SIADH affect urine osmolality (and therefore sodium too)?

156
Q

symptoms of SIADH? hint: non-specific

157
Q

causes of SIADH?

158
Q

drug causes of SIADH?

159
Q

how is SIADH diagnosed?

160
Q

causes of hyponatraemia?

161
Q

investigations in SIADH?

A
  • UEs- CXR (?pneumonia, lung abscess, cancer)- CT thorax, abdo, pelvis + MRI brain if suspected cancer
162
Q

management of SIADH?

A
  • treat underlying cause- commonly drug cause - stop the drug- fluid restriction 500ml-1L (correct Na)- tolvaptan (ADH receptor blocker)- demeclocycline (ABx which inhibits ADH)
163
Q

major complication of SIADH? how can it happen?

A

persistent severe hyponatraemia can lead to central pontine myelinolysis

164
Q

pathophysiology of nephrogenic diabetes insipidus?

A

collecting duct of nephron not responsive to ADH

165
Q

causes of nephrogenic diabetes insipidus?

166
Q

pathophysiology of cranial diabetes insipidus?

A

hypothalamus not producing ADH for pituitary to secrete

167
Q

causes of cranial diabetes insipidus?

168
Q

presentation of diabetes insipidus? hint: low fluid

169
Q

investigations? hint: findings opp to SIADH

170
Q

explain the water deprivation test

A
  • no fluid intake for 8 hours - measure urine osmolality- give desmopressin (ADH)- measure urine osmolality again
171
Q

what are the results for the water deprivation test if DI is nephrogenic? what about cranial?

172
Q

findings in water deprivation test if the patient has primary polydipsia / is normal?

A

urine osmolality is normal before even giving desmopressin

173
Q

management of diabetes insipidus?

174
Q

what is a phaeochromocytoma? what does it secrete?

A
  • tumour of chromaffin cells in or out of the adrenal gland| - secretes adrenaline
175
Q

main association of phaeochromocytoma?

A

25% are associated with multiple endocrine neoplasia 2 (MEN2)

176
Q

3 x 10% rule of phaeochromocytoma tumours?

A
  • 10% bilateral- 10% cancerous- 10% not in the adrenal gland
177
Q

diagnostic investigations for phaeochromocytoma?

A
  • 24h urinary catecholamines| - plasma free metanephrines
178
Q

why are urinary catecholamines checked in phaeochromocytoma instead of blood levels?

A
  • the adrenaline secretion is in bursts- blood levels will fluctuate- 24h urinary ones will give a better idea of total secretion
179
Q

why are plasma metanephrines checked in phaeochromocytoma?

A
  • breakdown product of adrenaline| - it has a longer half life so less likely to fluctuate than adrenaline
180
Q

presentation of phaeochromocytoma?

181
Q

management of phaeochromocytoma?

182
Q

TFT results in sick euthyroid syndrome? where is this commonly seen?

183
Q

TFT results in subclinical hypothyroidism?

A
  • high TSH| - NORMAL T4
184
Q

TFT results in pt with poor thyroxine compliance?

A
  • high TSH| - normal T4

MBBS Y5 (27 decks)

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