Medicine - Endocrinology Flashcards
(184 cards)
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
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
NAME?
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
NAME?
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
NAME?
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?
#NAME?
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
#NAME?
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?
#NAME?
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?
#NAME?
45
which features in presentation are unique to grave's disease?
#NAME?
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?
#NAME?
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
#NAME?
50
management of a thyrotoxic storm?
#NAME?
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?
#NAME?
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?
#NAME?
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?
#NAME?
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?
#NAME?
70
presentation of DKA?
#NAME?
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?
#NAME?
75
when should blood glucose be checked in T1DM?
#NAME?
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?
#NAME?
80
management of hypoglycaemia in T1DM? if severe?
#NAME?
81
how could a patient in DKA end up hypoglycaemic?
overtreatment with insulin
82
short term complications in T1DM?
#NAME?
83
macrovascular complications in diabetes?
#NAME?
84
microvascular complications in diabetes?
#NAME?
85
nature of neuropathy in diabetes?
- peripheral| - "glove and stocking" distribution
86
infection-related complications in diabetes?
#NAME?
87
what 3 things are used to monitor T1DM?
#NAME?
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?
#NAME?
90
modifiable risk factors for T2DM?
#NAME?
91
how might T2DM present?
#NAME?
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?
#NAME?
97
lifestyle advice given in T2DM?
#NAME?
98
3 main complications to monitor for in T2DM?
#NAME?
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?
#NAME?
104
example of sulfonylurea?
gliclazide
105
MOA of gliclazide?
increases insulin production in pancreas
106
notable side effects of gliclazide?
#NAME?
107
notable side effects of pioglitazone?
#NAME?
108
example of DPP-4 inhibitor?
sitagliptin
109
notable side effects of sitagliptin?
#NAME?
110
notable side effects of GLP-1 inhibitors?
#NAME?
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?
#NAME?
117
describe frontal bossing
prominent forehead and brow bone
118
describe prognathism
large, protruding jaw
119
organ dysfunction caused by GH?
#NAME?
120
management of acromegaly?
#NAME?
121
which drugs can block GH?
#NAME?
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
#NAME?
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?
#NAME?
135
where are juxtaglomerular cells found? what do they do?
#NAME?
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?
#NAME?
140
what is conn's syndrome?
primary hyperaldosteronism
141
causes of conn's syndrome?
#NAME?
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?
#NAME?
145
how is hyperaldosteronism screened for?
work out renin:aldosterone ratio from bloods:- low:high = primary- high:high = secondary
146
investigations for hyperaldosteronism?
#NAME?
147
management of hyperaldosteronism?
#NAME?
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)?
#NAME?
156
symptoms of SIADH? hint: non-specific
#NAME?
157
causes of SIADH?
#NAME?
158
drug causes of SIADH?
#NAME?
159
how is SIADH diagnosed?
#NAME?
160
causes of hyponatraemia?
#NAME?
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?
#NAME?
166
pathophysiology of cranial diabetes insipidus?
hypothalamus not producing ADH for pituitary to secrete
167
causes of cranial diabetes insipidus?
#NAME?
168
presentation of diabetes insipidus? hint: low fluid
#NAME?
169
investigations? hint: findings opp to SIADH
#NAME?
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?
#NAME?
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?
#NAME?
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?
#NAME?
181
management of phaeochromocytoma?
#NAME?
182
TFT results in sick euthyroid syndrome? where is this commonly seen?
#NAME?
183
TFT results in subclinical hypothyroidism?
- high TSH| - NORMAL T4
184
TFT results in pt with poor thyroxine compliance?
- high TSH| - normal T4
