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Y3 > Endocrine > Flashcards

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
Q

What is the management of gestational diabetes?

A
  • 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
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26
Q

What is the HbA1C target in T2DM with lifestyle modification only?

A

48 (6.5%)

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27
Q

What is the HbA1C target in T2DM with lifestyle modification + metformin?

A

48 (6.5%)

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28
Q

What is the HbA1C target in T2DM with lifestyle modification + hypoglycaemic drugs?

A

53 (7%)

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29
Q

What is the first line treatment in T2DM?

A

metformin

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30
Q

When should SGLT2 inhibitors be added to T2DM treatment regimen?

A

if either:
- high risk of CV disease
- established CV disease
- chronic HF

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31
Q

What medications should be used if metformin is contraindicated?

A

chronic HF / CVD risk / established CVD -> SGLT2 monotherapy (-flozin)
no CVD risk -> DPP4 (gliptin) or sulfonylurea

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32
Q

When is further treatment of T2DM indicated?

A

HbA1C rises to 58 (7.5%)

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33
Q

What are second line treatment options on T2DM?

A

dual therapy - add another drug, i.e.
- metformin + DPP4 (gliptin)
- metformin + pioglitazone
- metformin + sulfonylurea
- metformin +SGLT2 (flozin) - if CVD!!!

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34
Q

When is third line therapy indicated in T2DM?

A

glycaemic control not achieved on dual therapy

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35
Q

What are the third line treatment options in T2DM?

A

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

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36
Q

How is suspected T1DM investigated?

A

urine dip - ketones, glucose
fasting glucose, random glucose
NOT HbA1c (not accurate in T1)
low C peptide
diabetes specific antibodies

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37
Q

What are the diagnostic criteria for symptomatic patients for T1DM?

A

fasting glucose > 7
random glucose > 11.1

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38
Q

What are the diagnostic criteria for asymptomatic patients for T1DM?

A

fasting glucose > 7
random glucose > 11.1
on 2 separate occassions

39
Q

What is the target for fasting glucose in gestational diabetes?

A

5.3

40
Q

What is the target for 1 hr and 2hr postprandial glucose in gestational diabetes?

A

1hr - 7.8
2hr - 6.4

41
Q

What are the sick day rules for patients with T1DM?

A

DO NOT stop insulin
check blood glucose more frequently
try to eat / drink carb heavy drink
drink at least 3L of fluids

42
Q

What are the sick day rules for patients with T2DM?

A

stop hypoglycaemic agents
restart 24-48 hrs after feeling better, eating and drinking
DO NOT stop insulin

43
Q

How is prediabetes defined (HbA1C)?

A

42-47 mmol (6-6.4%)

44
Q

How is T2DM diagnosed in symptomatic / asymptomatic patients? (glucose levels)

A

fasting glucose > 7
random glucose > 11.1

if asymptomatic - on 2 separate occassions

45
Q

How is T2DM diagnosed using HbA1c?

A

> 48 (6.5)

46
Q

What is diabetes insipidus?

A

either
- decreased secretion of ADH from pituitary - cranial DI
or
- insensitivity to ADH - nephrogenic DI

47
Q

What are some causes of cranial DI?

A

idiopathic
post head injury
pituitary surgery
infiltrative - e.g. sarcoidosis
haemochromocytosis

48
Q

What are some causes of nephrogenic DI?

A

genetic
electrolytes
- hypercalcaemia
- hypokalaemia
lithium
tubulo-interstitial disease - obstruction, pyelonephritis, sickle cell

49
Q

What are the features of DI?

A

polyuria
polydipsia

50
Q

What investigations are used in DI?

A

urine osmolality
plasma osmolality
- high plasma, low urine osmolality
water deprivation test

51
Q

How is nephrogenic DI managed?

A

thiazides
low salt / protein diet

52
Q

How is cranial DI managed?

A

desmopressin (vasopressin V2 receptor agonist)

53
Q

What is the alternative for patients not tolerating standard release metformin?

A

modified release metformin

54
Q

What are the 5 components of T1DM management?

A

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
Q

when do you add SGLT2 to diabetes regime?

A

if QRISK>10%
regardless of HbA1c

56
Q

Which hypoglycaemic drug is contraindicated in (suspected) bladder cancer?

A

pioglitazone

57
Q

What is the Hba1c target for patients on a drug which may cause hypoglycaemia? (e.g. sulphonylureas)

A

53

58
Q

What is impaired fastng glucose?

A

fasting glucose between 6.1 nd 7

59
Q

What is impaired glucose tolerance?

A

fasting plasma glucose > 7
OGTT between 7.8 and 11.1

60
Q

What is SIADH?

A

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
Q

How does ADH work?

A

increases water reabsorption in collecting ducts -> decreases volume of urine produced

62
Q

What are some causes of SIADH?

A

malignancy - SCLC
neurological - stroke, haemorrhage into cranium
infections - TB, pneumonia
drugs - SSRIs, sulfonylureas, carbamazepine
others - PEEP, porphyrias

63
Q

How is SIADH investigated?

A

very high urine osmolality in relation to serum osmolality
high urine sodium concentration

64
Q

How is SIADH managed?

A

slow correction
fluid restriction
ADH antagonists

65
Q

What is Hashimoto’s thyroiditis?

A

chronic autoimmune thyroiditis
typically hypothyroidism
more common in women

66
Q

What are features of Hashimoto’s thyroiditis?

A

features of hypohyroidism
non tender firm goitre
anti-TPO antibodies
anti-Tg antibodies

67
Q

What is Hashimoto’s thyroiditis associated with (other conditions)?

A

other autoimmune conditions - coeliac, T1DM
development of MALT lymphoma

68
Q

What is the most common cause of hypothyroidism in children?

A

Hashimoto’s thyroiditis

69
Q

What is thyroid storm?

A

life-threatening complication of thyrotoxicosis

70
Q

What are some precipitating factors for thyroid storm?

A

surgery
trauma
infection
acute iodine load (e.g. CT with contrast)

71
Q

What are the clinical features of thyroid storm?

A

fever > 38.5
tachycardia
confusion, agitation
N+V
hypertension
HF
abnormal LFTs

72
Q

How is thyroid storm managed?

A

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
Q

What is primary hyperparathyroidism?

A

excess secretion of PTH -> hypercalcaemia

74
Q

What are the most common causes of primary hyperparathyroidism?

A

solitary adenoma
hyperplasia
multiple adenoma
carcinoma

75
Q

What are some features of hyperparathyroidism?

A

hypercalcaemia
“Bones, Stones, abdominal groans and psychic moans”
- polydipsia, polyuria
- depression
- anorexia, N+V
- peptic ulceration
- pancreatitis
- bone pain, fracture
- renal stones
- hypertension

76
Q

What will blood tests show in primary hyperparathyroidism?

A

raised Ca, low phosphate
PTH raised or normal

77
Q

What is the management of primary hyperparathyroidism?

A

total parathyroidectomy - definitive management
calcimimetics

78
Q

What medication used in AF causes thyroid dysfunction (hypo or toxicosis)?

A

amiodarone

79
Q

What are the main causes of hyperthyroidism?

A

GIST
Graves
Inflammation - thyroiditis
Solitary toxic nodule
Toxic multinodular goitre

80
Q

What is thyroiditis? How does it usually present?

A

thyroid gland inflammation
initial period of hyperthyroidism
followed by hypothyroidism

81
Q

What are the main types of thyroiditis?

A

Hashimoto’s
De Quervain’s
postpartum
drug-induced

82
Q

What is the presentation of Graves (other than the general symptoms)?

A

diffuse goitre
graves eyes disease
pretibial myxoedema
thyroid acropachy

83
Q

What is the first line anti-thyroid drug?

A

carbimazole

84
Q

What is the second line anti-thyroid drug?

A

propylthiouracil

85
Q

What is a rare, but very serious side effect of both carbimazole and propylthiouracil (anti-thyroid drugs)?

A

agranulocytosis - very low WBCs
makes patients vulnerable to infections

86
Q

How does myxoedema coma typically present?

A

confusion
hypothermia
myxoedema

87
Q

What is myxoedema coma associated with?

A

longstanding hypothyroidism

88
Q

How is myxoedema coma treated?

A

IV thyroid replacement
IV fluid
IV corticosteroids

89
Q

What will blood gas show in Cushing’s?

A

hypokalaemic metabolic alkalosis

90
Q

What will blood gas show in Addison’s?

A

hyperkalaemic metabolic acidosis

91
Q

What are the possible causes of hypocalcaemia?

A

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
Q

How is hypocalcaemia managed?

A

if severe - IV calcium gluconate

93
Q
A

Y3 (11 decks)

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