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Endocrine Flashcards

1
Q

What hormones are produced by the anterior pituitary?

A

TSH - thyroid stimulating hormone
GH - growth hormone
ACTH - adrenocorticotrophic hormone
FSH - follicle stimulating hormone
LH - luteinising hormone
Prolactin

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2
Q

What hormones are produced by the posterior pituitary?

A

ADH - antidiuretic hormone
oxytocin
endorphins

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3
Q

Which structure produces hormones that stimulate the pituitary?

A

hypothalamus

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4
Q

What hormone released from the hypothalamus stimulates the release of TSH?

A

TRH - thyrotropin releasing hormone

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5
Q

What is the action of TSH?

A

release of T3 and T4

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6
Q

What is the full name of T3?

A

triiodothyronine

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7
Q

What is the full name of T4?

A

thyroxine

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8
Q

What hormone released from the hypothalamus stimulates the release of ACTH?

A

CRH - corticotropin releasing hormone

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9
Q

What is the action of ACTH?

A

release of cortisol from the adrenal glands

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10
Q

What are the main actions of cortisol?

A

Increases alertness
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism

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11
Q

What hormone released from the hypothalamus stimulates the release of GH?

A

GHRH - growth hormone releasing hormone

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12
Q

What is the main action of GH?

A

release of IGF-1 from the liver

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13
Q

What are the main actions of GH?

A

Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

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14
Q

Where is PTH (parathyroid hormone) released from?

A

parathyroid glands

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15
Q

When is PTH released?

A

when Ca concentration in blood is low

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16
Q

What are the main effects of PTH?

A

increase of Ca in blood by:
- increase in activity and number of osteoclasts - increase in bone resorption
- stimulating calcium reabsorption in kidneys
- stimulating kidneys to convert vit D3 into active form - promotes calcium absorption in the intestines

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17
Q

What is the inheritance pattern of MODY (maturity onset diabetes of the young)?

A

autosomal dominant

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18
Q

What drugs can cause gynaecomastia?

A

spironolactone
digoxin
cannabis
oestrogens
anabolic steroids
GnRH agonists

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19
Q

What is the first line imaging option for thyroid nodules?

A

USS

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20
Q

What are some benign causes of thyroid nodules?

A

multinodular goitre
thyroid adenoma
Hashimoto’s thyroiditis
cysts

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21
Q

What are some malignant causes of thyroid nodules?

A

papillary carcinoma - most common
other carcinomas
lymphoma

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22
Q

What are the risk factors for gestational diabetes?

A

BMI > 30
previous gestational diabetes
first-degree relative with diabetes
family origin with a high prevalence of diabetes

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23
Q

What test is used to screen for gestational diabetes?

A

oral glucose tolerance test (OGTT)

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24
Q

What is the diagnostic threshold for gestational diabetes?

A

fasting glucose > 5.6
2hr glucose > 7.8

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25
What is the management of gestational diabetes?
- new diagnosis - joint diabetes + antenatal clinic within 1 week - advice about diet and exercise - if fasting glucose < 7 -> trial of lifestyle modification for 2 weeks a) if targets not met - start metformin b) targets not met still -> insulin if at the time of diagnosis the fasting glucose level is > 7 mmol/l insulin should be started
26
What is the HbA1C target in T2DM with lifestyle modification only?
48 (6.5%)
27
What is the HbA1C target in T2DM with lifestyle modification + metformin?
48 (6.5%)
28
What is the HbA1C target in T2DM with lifestyle modification + hypoglycaemic drugs?
53 (7%)
29
What is the first line treatment in T2DM?
metformin
30
When should SGLT2 inhibitors be added to T2DM treatment regimen?
if either: - high risk of CV disease - established CV disease - chronic HF
31
What medications should be used if metformin is contraindicated?
chronic HF / CVD risk / established CVD -> SGLT2 monotherapy (-flozin) no CVD risk -> DPP4 (gliptin) or sulfonylurea
32
When is further treatment of T2DM indicated?
HbA1C rises to 58 (7.5%)
33
What are second line treatment options on T2DM?
dual therapy - add another drug, i.e. - metformin + DPP4 (gliptin) - metformin + pioglitazone - metformin + sulfonylurea - metformin +SGLT2 (flozin) - if CVD!!!
34
When is third line therapy indicated in T2DM?
glycaemic control not achieved on dual therapy
35
What are the third line treatment options in T2DM?
add another drug, ie: metformin + DPP-4 inhibitor + sulfonylurea metformin + pioglitazone + sulfonylurea metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met insulin-based treatment
36
How is suspected T1DM investigated?
urine dip - ketones, glucose fasting glucose, random glucose NOT HbA1c (not accurate in T1) low C peptide diabetes specific antibodies
37
What are the diagnostic criteria for symptomatic patients for T1DM?
fasting glucose > 7 random glucose > 11.1
38
What are the diagnostic criteria for asymptomatic patients for T1DM?
fasting glucose > 7 random glucose > 11.1 on 2 separate occassions
39
What is the target for fasting glucose in gestational diabetes?
5.3
40
What is the target for 1 hr and 2hr postprandial glucose in gestational diabetes?
1hr - 7.8 2hr - 6.4
41
What are the sick day rules for patients with T1DM?
DO NOT stop insulin check blood glucose more frequently try to eat / drink carb heavy drink drink at least 3L of fluids
42
What are the sick day rules for patients with T2DM?
stop hypoglycaemic agents restart 24-48 hrs after feeling better, eating and drinking DO NOT stop insulin
43
How is prediabetes defined (HbA1C)?
42-47 mmol (6-6.4%)
44
How is T2DM diagnosed in symptomatic / asymptomatic patients? (glucose levels)
fasting glucose > 7 random glucose > 11.1 if asymptomatic - on 2 separate occassions
45
How is T2DM diagnosed using HbA1c?
> 48 (6.5)
46
What is diabetes insipidus?
either - decreased secretion of ADH from pituitary - cranial DI or - insensitivity to ADH - nephrogenic DI
47
What are some causes of cranial DI?
idiopathic post head injury pituitary surgery infiltrative - e.g. sarcoidosis haemochromocytosis
48
What are some causes of nephrogenic DI?
genetic electrolytes - hypercalcaemia - hypokalaemia lithium tubulo-interstitial disease - obstruction, pyelonephritis, sickle cell
49
What are the features of DI?
polyuria polydipsia
50
What investigations are used in DI?
urine osmolality plasma osmolality - high plasma, low urine osmolality water deprivation test
51
How is nephrogenic DI managed?
thiazides low salt / protein diet
52
How is cranial DI managed?
desmopressin (vasopressin V2 receptor agonist)
53
What is the alternative for patients not tolerating standard release metformin?
modified release metformin
54
What are the 5 components of T1DM management?
HbA1c monitoring - every 3-6 months (< 48) self monitoring of blood glucose - 5-7 fasting - 4-7 before meals insulin - multiple daily injection basal-bolus regimen - twice daily insulin detemir - rapid acting insulin analogues before meals metformin - for BMI >25
55
when do you add SGLT2 to diabetes regime?
if QRISK>10% regardless of HbA1c
56
Which hypoglycaemic drug is contraindicated in (suspected) bladder cancer?
pioglitazone
57
What is the Hba1c target for patients on a drug which may cause hypoglycaemia? (e.g. sulphonylureas)
53
58
What is impaired fastng glucose?
fasting glucose between 6.1 nd 7
59
What is impaired glucose tolerance?
fasting plasma glucose > 7 OGTT between 7.8 and 11.1
60
What is SIADH?
syndrome of inappropriate ADH secretion excessive release of ADH -> water retention, decreased urine production hyponatraemia secondary to dilutional effects of excessive water retention patients are euvolaemic
61
How does ADH work?
increases water reabsorption in collecting ducts -> decreases volume of urine produced
62
What are some causes of SIADH?
malignancy - SCLC neurological - stroke, haemorrhage into cranium infections - TB, pneumonia drugs - SSRIs, sulfonylureas, carbamazepine others - PEEP, porphyrias
63
How is SIADH investigated?
very high urine osmolality in relation to serum osmolality high urine sodium concentration
64
How is SIADH managed?
slow correction fluid restriction ADH antagonists
65
What is Hashimoto's thyroiditis?
chronic autoimmune thyroiditis typically hypothyroidism more common in women
66
What are features of Hashimoto's thyroiditis?
features of hypohyroidism non tender firm goitre anti-TPO antibodies anti-Tg antibodies
67
What is Hashimoto's thyroiditis associated with (other conditions)?
other autoimmune conditions - coeliac, T1DM development of MALT lymphoma
68
What is the most common cause of hypothyroidism in children?
Hashimoto's thyroiditis
69
What is thyroid storm?
life-threatening complication of thyrotoxicosis
70
What are some precipitating factors for thyroid storm?
surgery trauma infection acute iodine load (e.g. CT with contrast)
71
What are the clinical features of thyroid storm?
fever > 38.5 tachycardia confusion, agitation N+V hypertension HF abnormal LFTs
72
How is thyroid storm managed?
symptomatic treatment e.g. paracetamol treatment of underlying precipitating event beta-blockers: typically IV propranolol anti-thyroid drugs: e.g. methimazole or propylthiouracil Lugol's iodine dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
73
What is primary hyperparathyroidism?
excess secretion of PTH -> hypercalcaemia
74
What are the most common causes of primary hyperparathyroidism?
solitary adenoma hyperplasia multiple adenoma carcinoma
75
What are some features of hyperparathyroidism?
hypercalcaemia "Bones, Stones, abdominal groans and psychic moans" - polydipsia, polyuria - depression - anorexia, N+V - peptic ulceration - pancreatitis - bone pain, fracture - renal stones - hypertension
76
What will blood tests show in primary hyperparathyroidism?
raised Ca, low phosphate PTH raised or normal
77
What is the management of primary hyperparathyroidism?
total parathyroidectomy - definitive management calcimimetics
78
What medication used in AF causes thyroid dysfunction (hypo or toxicosis)?
amiodarone
79
What are the main causes of hyperthyroidism?
GIST Graves Inflammation - thyroiditis Solitary toxic nodule Toxic multinodular goitre
80
What is thyroiditis? How does it usually present?
thyroid gland inflammation initial period of hyperthyroidism followed by hypothyroidism
81
What are the main types of thyroiditis?
Hashimoto's De Quervain's postpartum drug-induced
82
What is the presentation of Graves (other than the general symptoms)?
diffuse goitre graves eyes disease pretibial myxoedema thyroid acropachy
83
What is the first line anti-thyroid drug?
carbimazole
84
What is the second line anti-thyroid drug?
propylthiouracil
85
What is a rare, but very serious side effect of both carbimazole and propylthiouracil (anti-thyroid drugs)?
agranulocytosis - very low WBCs makes patients vulnerable to infections
86
How does myxoedema coma typically present?
confusion hypothermia myxoedema
87
What is myxoedema coma associated with?
longstanding hypothyroidism
88
How is myxoedema coma treated?
IV thyroid replacement IV fluid IV corticosteroids
89
What will blood gas show in Cushing's?
hypokalaemic metabolic alkalosis
90
What will blood gas show in Addison's?
hyperkalaemic metabolic acidosis
91
What are the possible causes of hypocalcaemia?
vitamin D deficiency (osteomalacia) chronic kidney disease hypoparathyroidism (e.g. post thyroid/parathyroid surgery) pseudohypoparathyroidism (target cells insensitive to PTH) rhabdomyolysis (initial stages) magnesium deficiency (due to end organ PTH resistance) massive blood transfusion acute pancreatitis
92
How is hypocalcaemia managed?
if severe - IV calcium gluconate
93

Y3 (11 decks)

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