Endocrinology Flashcards
1
Q
what is cushing’s syndrome?
A
the signs and symptoms of prolonged abnormal elevated cortisol levels
2
Q
what is cushing’s disease?
A
- where a pituitary adenoma is producing excess ACTH
- a cause of cushing’s syndrome
3
Q
presentation of cushing’s syndrome? (hint: there’s a LOT)
A
- “lemon on matchsticks” (truncal 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
4
Q
causes of cushing’s syndrome?
A
- exogenous steroids
- cushing’s disease
- adrenal adenoma
- paraneoplastic cushing’s
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
6
Q
what is ectopic ACTH?
A
ACTH released from anywhere other than the pituitary
7
Q
diagnostic investigation for cushing’s syndrome?
A
dexamethasone suppression test
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
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
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)
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
12
Q
results of dexamethasone suppression testing in ectopic ACTH production?
A
- neither cortisol nor ACTH suppressed
- it’s from an external source
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)
14
Q
management of cushing’s syndrome? hint: underlying cause
A
- trans-sphenoidal removal of pituitary adenoma
- surgery for adrenal tumour
- surgery for source of ectopic ACTH
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
16
Q
which 2 steroids are deficient in adrenal insufficiency?
A
- cortisol
- aldosterone
17
Q
what is addison’s disease? commonest cause?
A
- primary adrenal insufficiency
- autoimmune is commonest cause
18
Q
what is tertiary adrenal insufficiency? commonest cause?
A
- reduced CRH release from the hypothalamus
- long-term steroid use
19
Q
how can tertiary adrenal insufficiency be prevented?
A
taper down long-term steroids slowly
20
Q
presentation of adrenal insufficiency?
A
- fatigue and weakness (most common)
- nausea
- cramps
- abdo pain
- reduced libido
21
Q
signs O/E of adrenal insufficiency?
A
- bronze hyperpigmentation (addison’s), seen especially in palmar creases
- (postural) hypotension
22
Q
what causes bronze skin in addison’s disease?
A
- increased circulating ACTH
- ACTH stimulates melanocytes
- increased melanin production
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
24
Q
diagnostic test for adrenal insufficiency?
A
short synacthen test
25
what is synacthen?
synthetic ACTH
26
how is the short synacthen test carried out?
- give synacthen at 8am
- measure cortisol at baseline
- then after 30 mins
- then after 60 mins
27
what is the result of the short synacthen test in a healthy person?
cortisol should at least double
28
if cortisol fails to double on the short synacthen test, what does this indicate?
primary adrenal insufficiency (addison's)
29
management of adrenal insufficiency?
- steroid replacements
- hydrocortisone for cortisol
- fludrocortisone for aldosterone
- double doses in acute illness
30
signs of addisonian crisis?
everything low but K+ high
- reduced consciousness
- hypotension
- hypoglycaemia
- hyponatraemia
- hyperkalaemia
- patient looks very unwell
31
triggers of addisonian crisis?
- could be first presentation of addison's disease
- infection
- trauma
- other acute illness
32
management of addisonian crisis?
- IV hydrocortisone 100mg stat
- repeat 6 hourly
- IV fluid resus
- correct hypoglycaemia
- monitor electrolytes and fluid closely
33
TFT findings in hyperthyroidism? hint: different if pituitary source
- low TSH, high if pituitary adenoma
| - high T3 and T4
34
TFT findings in hypothyroidism? hint: different if pituitary / hypothalamic source
- high TSH
- low TSH if pituitary / hypothalamic cause (secondary hypothyroidism)
- low T3 and T4
35
in which conditions are anti-TPO antibodies present?
- grave's disease
| - hashimoto's thyroiditis
36
in which conditions are antithyroglobulin antibodies present?
- grave's disease
- hashimoto's thyroiditis
- thyroid cancer
37
in which conditions are TSH receptor antibodies present?
grave's disease
38
what is the difference between hyperthyroidism and thyrotoxicosis?
- hyperthyroidism describes excessive thyroid hormone production by the thyroid
- thyrotoxicosis means excess of thyroid hormone in the body
39
what is grave's disease? describe the pathophysiology
- autoimmune primary hyperthyroidism
| - TSH receptor antibodies mimic TSH and stimulate the thyroid TSH receptors
40
commonest cause of hyperthyroidism?
grave's disease
41
describe toxic multinodular goitre
nodules develop on the thyroid which keep producing thyroid hormone, independent to the feedback loop
42
what is exophthalmos? which condition is it seen in? what causes it?
- eyeball bulging from socket
- seen in grave's disease
- is a direct reaction to TSH receptor antibodies
43
describe pretibial myxoedema. which condition is it seen in? what causes it?
- discoloured, waxy oedematous skin over shins
- grave's disease
- is a direct reaction to TSH receptor antibodies
44
presentation of hyperthyroidism?
- anxious, irritable
- heat intol, sweating
- tachycardia
- weight loss
- fatigue
- diarrhoea
- sexual dysfunction
45
which features in presentation are unique to grave's disease?
- diffuse goitre without nodules
- bilateral exophthalmos
- pretibial myxoedema
46
which features in presentation are suggestive of toxic mulitnodular goitre?
- goitre with firm nodules felt in neck
| - usually aged 50+
47
describe the presentation in de quervain's thyroiditis?
- viral infection with fever
- neck pain / tenderness
- dysphagia
- hyperthyroidism followed by hypothyroidism
48
prognosis and management of de quervain's thyroiditis?
- self-limiting condition
| - supportive treatment, e.g. NSAIDs, BBs
49
what is the other name for a thyroid storm? describe the presentation of this
- thyrotoxic crisis
- pyrexia
- tachycardia
- delirium
50
management of a thyrotoxic storm?
- fluid resus if needed
- BBs
- propylthiouracil
- hydrocortisone
51
management of hyperthyroidism?
- 1st line: carbimazole
- 2nd: propylthiouracil
- radioactive iodine (drink)
- BB (e.g. propanolol)
- surgery
52
causes of hypothyroidism?
- hashimoto's thyroiditis
- iodine deficiency
- overtreatment of hyperthyroidism
- drugs
- tumours
- infections
- sheehan syndrome
- radiation
53
presentation of hypothyroidism?
- depressed
- weight gain
- fatigue
- dry skin
- coarse hair, hair loss
- fluid retention (oedema, pleural effusions, ascites)
- amenorrhoea
- constipation
54
TFT findings in primary hypothyroidism?
- TSH high
| - T3 and T4 low
55
TFT findings in secondary hypothyroidism?
- TSH low
| - T3 and T4 low
56
management of hypothyroidism?
PO levothyroxine
57
how is levothyroxine treatment monitored?
- measure TSH levels monthly until stable
- if TSH is high, increase levothyroxine dose
- if TSH is low, decrease levothyroxine dose
58
what does "diffuse high uptake" on a radioisotope scan of the thyroid suggest?
grave's disease
59
what does "focal high uptake" on a radioisotope scan of the thyroid suggest?
- toxic multinodular goitre
| - adenoma
60
what do "cold areas" on a radioisotope scan of the thyroid suggest?
thyroid cancer
61
which cells produce glucagon? where are these found?
- alpha cells
| - islets of langerhans in pancreas
62
which cells produce insulin? where are these found?
- beta cells
| - islets of langerhans in pancreas
63
how does insulin reduce blood glucose levels? hint: 2 ways
- causes body cells to absorb glucose to use
| - causes muscle and liver cells to absorb glucose and store it as glycogen
64
what is ketogenesis? when is it done?
- liver converting fatty acids into ketones
| - done when both glucose and glycogen supplies are low
65
what is the normal blood glucose range?
4.4 - 6.1 mmol/L
66
pathophysiology of T1DM?
- pancreas unable to produce enough insulin
- no glucose gets absorbed out of the blood
- causes hyperglycaemia
- autoimmune
67
what is the body's initial response to rising blood ketone levels?
kidneys produce bicarbonate to counteract the acidity
68
how does insulin affect potassium? what happens in DKA? what can happen when DKA is treated?
- 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
69
overall effects of DKA on body?
- hyperglycaemia
- dehydration
- ketosis
- metabolic acidosis (with low bicarbonate)
- potassium imbalance
70
presentation of DKA?
- polyuria
- polydipsia
- N+V
- acetone smell on breath (peardrops)
- kussmaul breathing (deep, laboured breaths)
- dehydration
- hypotension (caused by dehydration)
- altered consciousness
71
diagnostic criteria for DKA?
- blood glucose >11mmol/L
- blood ketones >3mmol/L
- pH <7.3
72
FIG PICK: management of DKA?
- 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)
73
what is the max rate at which potassium can be infused?
10mmol/L
74
patient advice given in long term management of T1DM?
- explain subcut insulin regimes
- monitor carb intake and glucose
- monitor complications
- advice on changing injection site
75
when should blood glucose be checked in T1DM?
- on waking
- after a meal
- before bed
76
what is a typical insulin regime in T1DM?
- background insulin once daily (long-acting)
| - short acting insulin 30 mins before each meal
77
why does the injection site for insulin need to be changed regularly?
risk of lipodystrophy
78
what is lipodystrophy?
the subcut fat hardens from being injected in so much
79
symptoms of hypoglycaemia?
- tremor
- sweating
- irritability
- dizziness
- pallor
80
management of hypoglycaemia in T1DM? if severe?
- first rapid acting glucose (e.g. lucozade)
- then slower acting carbs (e.g. biscuits, toast)
- if severe: IV dextrose and IM glucagon
81
how could a patient in DKA end up hypoglycaemic?
overtreatment with insulin
82
short term complications in T1DM?
- hypoglycaemia
- hyperglycaemia
- DKA
83
macrovascular complications in diabetes?
- CAD
- peripheral ischaemia (diabetic foot)
- stroke
- HTN
84
microvascular complications in diabetes?
- peripheral neuropathy
- retinopathy
- glomerulosclerosis (kidney)
85
nature of neuropathy in diabetes?
- peripheral
| - "glove and stocking" distribution
86
infection-related complications in diabetes?
- UTIs
- pneumonia
- skin infections, esp in feet
- oral / vaginal candida
87
what 3 things are used to monitor T1DM?
- HbA1c
- capillary blood glucose
- flash glucose monitoring (e.g. freestyle libra)
88
what does HbA1c tell us? how often is it checked?
- average blood glucose levels over last 3 months
| - every 3-6 months
89
non-modifiable risk factors for T2DM?
- older age
- non-white ethnicity
- FHx
90
modifiable risk factors for T2DM?
- obesity
- sedentary lifestyle
- high carb diet
91
how might T2DM present?
- fatigue
- polydipsia
- polyuria
- unintentional weight loss
- opportunistic infections
- slow healing
- glucose in urine (on dipstick)
92
when is an oral glucose tolerance test (OGTT) performed?
first thing in the morning, before breakfast
93
what does an OGTT involve?
- take a fasting glucose reading
- then give 75g glucose drink
- then measure glucose again 2 hours later
94
diagnostic criteria for pre-diabetes?
- HbA1c 42 - 47 mmol/L
- fasting glucose 6.1 - 6.9 mmol/L (impaired)
- OGTT 7.8 - 11 mmol/L (impaired)
95
diagnostic criteria for diabetes?
- HbA1c >48mmol/L
- random glucose >11mmol/L
- fasting glucose >7mmol/L
- OGTT >11mmol/L
96
diet advice in T2DM?
- more veg and oily fish
- fewer sugary foods including carbs
- high fibre
97
lifestyle advice given in T2DM?
- diet changes
- exercise and weight loss
- stop smoking
- optimise comorbid conditions (e.g. HTN)
98
3 main complications to monitor for in T2DM?
- diabetic retinopathy
- kidney disease
- diabetic foot
99
what is the target HbA1c for type 2 diabetics on metformin alone?
48mmol/L
100
what is the target HbA1c for type 2 diabetics on more than just metformin?
53mmol/L
101
medical management of T2DM?
- 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
actions of metformin?
- increases insulin sensitivity
| - decreases liver production of glucose
103
notable side effects of metformin?
- diarrhoea
- abdo pain
- lactic acidosis
104
example of sulfonylurea?
gliclazide
105
MOA of gliclazide?
increases insulin production in pancreas
106
notable side effects of gliclazide?
- weight gain
- hypoglycaemia
- increases CVD risk
107
notable side effects of pioglitazone?
- weight gain
- fluid retention
- anaemia
- HF
- bladder cancer
108
example of DPP-4 inhibitor?
sitagliptin
109
notable side effects of sitagliptin?
- GI upset
- URTI
- pancreatitis
110
notable side effects of GLP-1 inhibitors?
- GI upset
- weight loss
- dizziness
- hypoglycaemia (less common)
111
what are the 5 types of insulin? give an example for each
- rapid-acting (novorapid)
- short-acting (actrapid)
- intermediate-acting (insulatard)
- long-acting (levemir)
- combination (humalog 25, 25:75)
112
what causes acromegaly?
an excess of GH
113
where is GH produced in the body?
anterior pituitary gland
114
commonest cause of acromegaly?
pituitary adenoma
115
what visual field defect is seen in pituitary adenoma? why?
- bitemporal hemianopia
| - it compresses the optic chiasm
116
presentation of acromegaly?
- headaches
- bitemporal hemianopia
- frontal bossing
- large nose
- macroglossia
- large hands and feet
- prognathism
- arthritis
117
describe frontal bossing
prominent forehead and brow bone
118
describe prognathism
large, protruding jaw
119
organ dysfunction caused by GH?
- hypertrophic heart
- HTN
- T2DM
- colorectal cancer
120
management of acromegaly?
- trans-sphenoidal removal of pituitary adenoma
- removal of any tumour producing ectopic GH
- meds which block GH
121
which drugs can block GH?
- pegvisomant
- ocreotide (somatostatin analogue)
- bromocriptine (DA agonist)
122
which 2 hormones can inhibit GH?
- somatostatin
| - dopamine
123
which cells produce PTH? where are these found?
chief cells on the parathyroid glands
124
when is PTH secreted?
in response to hypocalcaemia
125
how does PTH increase blood Ca levels? hint: think bone, gut and kidney
- increases osteoclast activity (reabsorbs Ca from bones)
- increases Ca absorption in gut
- increases Ca reabsorption in kidney
- increases vit D activity
126
what causes primary hyperparathyroidism?
excessive PTH being secreted by a tumour on the parathyroid glands
127
management of primary hyperparathyroidism?
surgical tumour removal
128
PTH and calcium levels in primary hyperparathyroidism?
- PTH is high
| - serum calcium is high
129
what causes secondary hyperparathyroidism?
2 main ways:
- vit D deficiency
- chronic renal / liver / failure (mostly CKD)
- bowel disease
130
PTH and calcium levels in secondary hyperparathyroidism?
- PTH is high
| - serum calcium is low
131
what causes tertiary hyperparathyroidism?
prolonged secondary hyperparathyroidism, resulting in parathyroid hyperplasia
132
PTH and calcium levels in tertiary hyperparathyroidism?
- PTH is high
| - serum calcium is high
133
management of tertiary hyperparathyroidism?
surgical removal of some of the excess parathyroid gland
134
main effects of primary hyperparathyroidism? how do these present?
- excessive Ca resorption from bone (osteopenia, fractures)
- excessive Ca excretion by kidneys (renal calculi)
- hypercalcaemia (lots of features)
135
where are juxtaglomerular cells found? what do they do?
- afferent arteriole of glomerulus of nephron
- sense BP
- release renin in response to low BP
136
what is the role of renin?
converts angiotensinogen into angiotensin I
137
where is ACE found in the body? what does it do?
- lungs
| - converts angiotensin I to angiotensin II
138
what is the role of angiotensin II?
stimulates adrenal glands to secrete aldosterone
139
actions of aldosterone?
- increases Na resorption in distal tubules
- increases K secretion in distal tubules
- increases H secretion from collecting ducts
140
what is conn's syndrome?
primary hyperaldosteronism
141
causes of conn's syndrome?
- adrenal adenoma secreting aldosterone (commonest)
- bilateral adrenal hyperplasia
- familial hyperaldosteronism
- adrenal carcinoma (rare)
142
what causes secondary hyperaldosteronism? key finding?
- excess renin, resulting in excess aldosterone
| - high serum renin
143
causes of secondary hyperaldosteronism? hint: renin goes up when kidneys get less blood
- renal artery stenosis
| - renal artery obstruction HF
144
investigations for renal artery stenosis?
- doppler USS
- CT angiogram
- MRA (angiography)
145
how is hyperaldosteronism screened for?
work out renin:aldosterone ratio from bloods:
- low:high = primary
- high:high = secondary
146
investigations for hyperaldosteronism?
- bloods (renin, aldosterone)
- BP (HTN)
- electrolytes (hypokalaemia)
- blood gas (alkalosis)
- CT / MRI (adrenal tumour)
- renal doppler USS (renal artery stenosis)
147
management of hyperaldosteronism?
- treat underlying cause (tumour removal)
- percutaneous renal artery angioplasty (if RAS found)
- aldosterone antagonists (eplerenone, spironolactone)
148
types of hyperaldosteronism?
- primary (conn's syndrome)
| - secondary
149
commonest cause of secondary hypertension?
hyperaldosteronism
150
where is ADH produced?
hypothalamus
151
where is ADH secreted?
posterior pituitary
152
actions of ADH?
water reabsorption in collecting ducts of nephron
153
how much SIADH occur?
- posterior pituitary secreting too much ADH
| - ectopic ADH from a tumour (e.g. SCLC)
154
how does SIADH affect sodium?
- hyponatraemia
| - the excess water dilutes it down
155
how does SIADH affect urine osmolality (and therefore sodium too)?
- high urine osmolality because less water is being excreted (so more concentrated urine)
- high urine sodium because less water in it
156
symptoms of SIADH? hint: non-specific
- headache
- fatigue
- muscle aches
- cramps
- confusion
- severe hyponatraemia (seizures, reduced consciousness)
157
causes of SIADH?
- Small cell lung cancer
- Infection
- Abscess
- Drugs (carbamazepine, SSRIs)
- Head injury
158
drug causes of SIADH?
- thiazide diuretics
- carbamazepine
- antipsychotics
- SSRIs
- NSAIDs
159
how is SIADH diagnosed?
- cannot test specifically for ADH
- euvolaemic O/E
- urine sodium high
- urine osmolality high
- rule out other causes of hyponatraemia
- establish underlying cause
160
causes of hyponatraemia?
- adrenal insufficiency
- diuretic use
- D + V
- burns, fistulas
- excessive sweating
- CKD, AKI
161
investigations in SIADH?
- UEs
- CXR (?pneumonia, lung abscess, cancer)
- CT thorax, abdo, pelvis + MRI brain if suspected cancer
162
management of SIADH?
- 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
major complication of SIADH? how can it happen?
persistent severe hyponatraemia can lead to central pontine myelinolysis
164
pathophysiology of nephrogenic diabetes insipidus?
collecting duct of nephron not responsive to ADH
165
causes of nephrogenic diabetes insipidus?
- drugs, esp lithium
- gene mutation
- intrinsic kidney disease
- hypokalaemia
- hypercalcaemia
166
pathophysiology of cranial diabetes insipidus?
hypothalamus not producing ADH for pituitary to secrete
167
causes of cranial diabetes insipidus?
- idiopathic
- brain tumour
- head injury
- brain malformation
- infection (meningitis, encephalitis, TB)
- iatrogenic (brain surgery, radiotherapy)
168
presentation of diabetes insipidus? hint: low fluid
- polyuria
- polydipsia
- dehydration
- postural hypotension
- hypernatraemia
169
investigations? hint: findings opp to SIADH
- low urine osmolality
- high serum osmolality
- water deprivation test
170
explain the water deprivation test
- no fluid intake for 8 hours
- measure urine osmolality
- give desmopressin (ADH)
- measure urine osmolality again
171
what are the results for the water deprivation test if DI is nephrogenic? what about cranial?
- nephrogenic: urine osmolality initially low and stays low (kidneys not responding to ADH)
- cranial: UO initially low, then high (kidneys can respond to ADH)
172
findings in water deprivation test if the patient has primary polydipsia / is normal?
urine osmolality is normal before even giving desmopressin
173
management of diabetes insipidus?
- treat underlying cause
- desmopressin (synthetic ADH)
- give higher dose if nephrogenic and monitor closely
174
what is a phaeochromocytoma? what does it secrete?
- tumour of chromaffin cells in or out of the adrenal gland
| - secretes adrenaline
175
main association of phaeochromocytoma?
25% are associated with multiple endocrine neoplasia 2 (MEN2)
176
3 x 10% rule of phaeochromocytoma tumours?
- 10% bilateral
- 10% cancerous
- 10% not in the adrenal gland
177
diagnostic investigations for phaeochromocytoma?
- 24h urinary catecholamines
| - plasma free metanephrines
178
why are urinary catecholamines checked in phaeochromocytoma instead of blood levels?
- the adrenaline secretion is in bursts
- blood levels will fluctuate
- 24h urinary ones will give a better idea of total secretion
179
why are plasma metanephrines checked in phaeochromocytoma?
- breakdown product of adrenaline
| - it has a longer half life so less likely to fluctuate than adrenaline
180
presentation of phaeochromocytoma?
- anxiety
- sweating
- headache
- HTN
- tremor
- palpitations
- tachycardia
- paroxysmal AF
181
management of phaeochromocytoma?
- phenoxybenzamine (alpha blocker)
- BBs once established on alpha blocker
- adrenalectomy for tumour removal
182
TFT results in sick euthyroid syndrome? where is this commonly seen?
- low TSH
- low T4
- common in hospital inpatients
183
TFT results in subclinical hypothyroidism?
- high TSH
| - NORMAL T4
184
TFT results in pt with poor thyroxine compliance?
- high TSH
| - normal T4
