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Med School Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Hormones released by anterior vs posterior pituitary gland and their function?

A

Anterior:
→ FSH/LH = gamete production
→ TSH = T3/T4 production
→ PRL = milk production, breast development
→ GH = IGF production
→ ACTH = glucocorticoid production
Posterior:
→ ADH = water balance
→ oxytocin = uterine contractions

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2
Q

Outline the thyroid hormonal axis?

A
  • Hypothalamus secretes TRH
  • Pituitary gland secretes TSH
  • Thyroid gland secretes T3 and T4
  • T4 -ve feedback on hypothalamus/pituitary
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3
Q

Ratio of T4:T3 production and clinical relevance?

A

20:1
T4 is a better indicator of thyroid function

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4
Q

Cause of primary vs secondary hyper/hypothyroidism?

A

Primary = thyroid abnormality
Secondary = hypothalamus or pituitary abnormality

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5
Q

Typical TFTs for primary and secondary hypothyroidism and hyperthyroidism?

A

Primary hypothyroidism = high TSH, low T3/T4
Primary hyperthyroidism = low TSH, high T3/T4
Secondary hypothyroidism = low TSH, low T3/T4
Secondary hyperthyroidism = high TSH, high T3/T4

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6
Q

Typical TFTs for subclinical hypothyroidism vs subclinical hyperthyroidism vs sick euthyroid?

A

Subclinical hypothyroidism = high TSH, normal T3/T4
Subclinical hyperthyroidism = low TSH, normal T3/T4
Sick euthyroid = low or normal TSH, low T3/T4

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7
Q

Investigation for thyroid nodule?

A

Thyroid US +/- biopsy

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8
Q

Features of hypothyroidism vs hyperthyroidism?

A

Hypothyroidism = cold, weight gain, fatigue, dry skin/hair, constipation, menorrhagia, carpal tunnel
Hyperthyroidism = warm, weight loss, restlessness, anxiety, tremor, palpitations, hyperhidrosis, diarrhoea, oligomenorrhoea, thyroid acropachy

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9
Q

Triad of thyroid acropachy?

A

Digital clubbing
Swelling of hands and feet
Periosteal new bone formation

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10
Q

Most common cause of hypothyroidism in the developed world vs developing world?

A

Developed world = hashimoto’s thyroiditis
Developing world = iodine deficiency

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11
Q

Features of Hashimoto’s thyroiditis and associated antibodies?

A

Hypothyroid symptoms
Firm, non-tender goitre
PMH autoimmune disease
Antibodies = anti-TPO and anti-Tg

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12
Q

Cancer linked to Hashimoto’s thyroiditis?

A

MALT lymphoma

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13
Q

Treatment for hypothyroidism and dosing guidance?

A

Levothyroxine:
→ elderly or CVD = 25mcg
→ everyone else = 50-100mcg
→ increase dose by 25-50mcg in pregnancy

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14
Q

Monitoring of levothyroxine?

A

TFTs monitored 8-12 weeks after dose change
Aim for TSH 0.5-2.5

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15
Q

Typical TFTs of patient with poor levothyroxine compliance and explain?

A

High TSH, normal T3/T4
→ patient takes medication just before blood test
→ thyroxine (T4) is normal
→ TSH lags reflecting chronic low levels

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16
Q

Drugs which reduce levothyroxine absorption and advice?

A

Iron, calcium
Take 4 hours apart

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17
Q

Management of subclinical hypothyroidism?

A

Offer levothyroxine if:
→ TSH > 10
→ TSH 5.5-10 and symptomatic

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18
Q

Management of myxoedema coma (hypothyroid crisis)?

A

IV fluids + IV levothyroxine + IV corticosteroid

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19
Q

Hypothyroidism after a post-partum haemorrhage?

A

Sheehan syndrome

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20
Q

Most common cause of hyperthyroidism?

A

Grave’s disease

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21
Q

Features of Grave’s disease and assocated antibodies?

A

Hyperthyroid symptoms
Eye disease e.g. exophthalmos
Pretibial myxoedema “orange peel skin”
Thyroid acropachy
Antibodies = anti-TSH receptor and anti-TPO

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22
Q

Investigation and feature of Grave’s disease?

A

Thyroid scinctigraphy
Globally increased iodine uptake

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23
Q

Key lifestyle risk factor for Grave’s disease?

A

Smoking

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24
Q

Treatment for hyperthyroidism?

A

1st line = carbimazole (1st choice) or propylthiouracil (2nd choice)
2nd line = radioiodine therapy
3rd line = surgery
N.B. propanolol is used to block adrenergic symptoms

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25
Q

Management of hyperthyroidism during pregnancy?

A

1st trimester = propylthiouracil
2nd trimester onwards = carbimazole

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26
Q

Major side effect of carbimazole and PPU?

A

Agranulocytosis

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27
Q

Phases and features of subacute (De Quervain’s) thyroiditis?

A

Phase I = hyperthyroidism, painful goitre, flu-like symptoms, raised inflammatory markers e.g. ESR, CRP
Phase II = euthyroid
Phase III = hypothyroidism
Phase IV = euthyroid

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28
Q

Investigation and feature of subacute (De Quervain’s) thyroiditis?

A

Thyroid scintigraphy
Globally reduced iodine uptake

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29
Q

Main drug associated with thyrotoxicosis?

A

Amiodarone

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30
Q

Features of thyrotoxicosis?

A

Fever
Tachycardia
Hypertension
Confusion, agitation
Heart failure (especially in elderly)

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31
Q

Management of thyrotoxicosis?

A

IV propanolol + IV hydrocortisone + propylthiouracil
N.B. IV digoxin if heart failure

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32
Q

Investigation, feature and management of toxic multinodular goitre?

A

Thyroid scintigraphy
Patchy increased iodine uptake
Management = radioiodine therapy

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33
Q

Types of thyroid cancer and most common?

A

Papillary (most common)
Follicular
Medullary
Anaplastic
Lymphoma

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34
Q

Thyroid cancer associated with young females, elderly females, MEN 2, lymph node invasion, vascular invasion, raised calcitonin?

A

Young females = papillary
Elderly females = anaplastic
MEN 2 = medullary
Lymph node invasion = papillary
Vascular invasion = follicular
Raised calcitonin = medullary

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35
Q

Management of papillary and follicular carcinoma?

A

Total thyroidectomy + radioiodine

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36
Q

Outline the parathyroid-thyroid hormone axis?

A
  • Parathyroid gland senses low calcium
  • Chief cells secrete PTH
  • PTH increases calcium
  • Thyroid gland senses high calcium
  • C-cells secrete calcitonin
  • Calcitonin decreases calcium and has negative feedback on parathyroid gland
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37
Q

How does PTH increase and calcitonin decrease calcium levels?

A

PTH = (1) activates osteoclasts, (2) increases calcium re-absorption in kidneys and (3) triggers calcitriol (active vitamin D) formation which increases gut calcium absorption
Calcitonin = inhibits osteoclasts

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38
Q

Features of hypercalcaemia?

A

Bone pain
Renal stones
Constipation
Pancreatitis
Polydipsia/polyuria
Depression

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39
Q

Cause of primary vs secondary vs tertiary hyperparathyroidism?

A

Primary = excess PTH secretion
Secondary = increased PTH secretion in response to low calcium
Tertiary = autonomous PTH secretion after prolonged secondary cause, usually CKD

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40
Q

Blood test features of primary vs secondary vs tertiary hyperparathyroidism?

A

Primary = normal/high PTH, high calcium, low phosphate
Secondary = high PTH, low calcium, high phosphate
Tertiary = high PTH, high calcium, low phopshate, high ALP

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41
Q

X-ray features of hyperparathyroidism?

A

“Pepperpot” skull
Osteopenia
Osteitis fibrosis cystica

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42
Q

Management of hyperparathyroidism?

A

1st line = total parathyroidectomy
2nd line = calcimemetic (e.g. cinacalcet)

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43
Q

Most common cause of hypoparathyroidsm?

A

Parathyroid injury during thyroid/neck surgery

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44
Q

Management of hypoparathyroidism?

A

Vitamin D analogue e.g. alfacalcidol

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45
Q

Features of hypocalcaemia?

A

Tetany e.g. cramps, parasthaesia
Trosseau’s sign (carpal spasm)
Chvostek’s sign (facial twitch)
Psychological disturbance e.g. depression

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46
Q

Which electrolyte is vital for maintaining calcium levels and clinical relevance?

A

Magnesium
→ patient not responding to calcium and vitamin D supplements should have magnesium checked

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47
Q

Features of MEN 1, MEN 2a and MEN 2b?

A

MEN 1 = (3 Ps) parathyroid tumour, pituitary tumour, pancreatic tumour
MEN 2a = (1 M, 2 Ps) medullary carcinoma, parathyroid tumour, phaeochromocytoma
MEN 2b = (2 Ms, 1 P) medullary carcinoma, marfanoid habitus, phaeochromocytoma

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48
Q

Features of a phaeochromocytoma?

A

Hypertension
Headaches
Flushing
Anxiety
Palpitations

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49
Q

Investigation and management of a phaeochromocytoma?

A

Investigation = 24hr urinary metanephrines
Management = alpha-blocker (e.g. phenoxybenzamine) BEFORE beta-blocker (e.g. propanolol) + surgery

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50
Q

Classification of pituitary adenomas?

A

Microadenoma (< 1cm) or macroadenoma (> 1cm)
Functioning (secretory) or non-functioning (no secretion)

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51
Q

Features of pituitary adenoma?

A

Hormonal excess
Hormonal deficit
Headaches
Bitemporal hemianopia

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52
Q

Most common cause of hypopituitarism vs hyperpituitarism?

A

Hypopituitarism = compression of pituitary gland via non-secretory adenoma
Hyperpituitarism = secretory adenoma

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53
Q

Investigation for hypopituitarism and explain?

A

Insulin stress test
→ insulin given, GH and cortisol measured
→ normally GH and cortisol should rise
→ low response indicates hypopituitarism

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54
Q

Most common type of secretory adenoma?

A

Prolactinoma

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55
Q

What normally inhibits prolactin release?

A

Dopamine

56
Q

Features of prolactinoma?

A

Pituitary adenoma symptoms
Amenorrhea
Galactorrhoea
Infertility
Erectile dysfunction

57
Q

Investigation and management of a prolactinoma?

A

Investigation = MRI
1st line = dopamine agonist e.g. cabergoline, bromocriptine
2nd line = trans-sphenoidal surgery

58
Q

Second most common cause of secretory adenoma?

A

GH adenoma

59
Q

What normally inhibits GH release?

A

Somatostatin

60
Q

Features of acromegaly?

A

Pituitary adenoma symptoms
Large “spade-like” hands/feet
Protruding jaw and brow
Interdental spaces
Hyperhidrosis

61
Q

Investigations and management of acromegaly?

A

Investigation = serum IGF-1, OGTT if IGF-1 raised
1st line = trans-sphenoidal surgery
2nd line = somatostatin analogue (e.g. ocreotide)
3nd line = GH antagonist (e.g. pegvisomant), dopamine agonist (e.g. bromocriptine)

62
Q

Types of corticosteroids hormone, where they are produced in the adrenal glands and example?

A

Glucocorticoids (zona fasciculata) = cortisol
Mineralocorticoids (zona glomerulosa) = aldosterone

63
Q

List side effects of glucocorticoids?

A

Osteoporosis
Peptic ulcers
Steroid psychosis
Hyperglycaemia
Cushing’s syndrome
Proximal myopathy
Immunosuppression
Glaucoma, cataracts
Stunted growth in kids

64
Q

List side effects of mineralocorticoids?

A

Fluid retention
Hypertension
Hypokalaemia

65
Q

Effect of cortisol vs aldosterone vs ADH on the kidneys?

A

Cortisol and aldosterone = water and Na retention, K excretion
ADH = water retention, Na and K excretion

66
Q

Cushing’s vs hyperaldosteronism vs Addison’s?

A

Cushing’s = excess CORTISOL
Hyperaldosteronism = excess ALDOSTERONE
Addison’s = lack of CORTISOL AND ALDOSTERONE

67
Q

Classification of Cushing’s syndrome causes?

A

ACTH-dependent e.g. pituitary adenoma, ectopic ACTH
ACTH-independent e.g. adrenal adenoma

68
Q

Features of Cushing’s syndrome?

A

Moon face
Hirsutism
Central obesity
Abdominal striae
Buffalo hump
Thin limbs
Hypertension
Osteoporosis

69
Q

Investigations of Cushing’s syndrome?

A

Overnight low-dose DST
Low-dose 48 hour DST
High-dose 48 hour DST

70
Q

High-dose DST results for Cushing’s causes?

A

ACTH suppressed, cortisol not = adrenal adenoma
ACTH and cortisol suppressed = pituitary adenoma
ACTH and cortisol not suppressed = ectopic ACTH

71
Q

Management of Cushing’s syndrome?

A

Steroid blocker (e.g. metyrapone) + surgery
Replacement steroids post-surgery

72
Q

Most common causes of primary aldosteronism?

A

Bilateral adrenal hyperplasia
Adrenal adenoma (Conn’s syndrome)

73
Q

Features of hyperaldosteronism?

A

Polydipsia/polyuria
Headaches
Hypertension
Hypokalaemia

74
Q

Investigations for primary hyperaldosteronism?

A

Plasma aldosterone:renin ratio
Imaging e.g. CT abdomen
Adrenal vein sampling (to differentiate between unilateral or bilateral pathology)

75
Q

Aldosterone:renin ratio results in primary vs secondary hyperaldosteronism?

A

Primary = high aldosterone, low renin
Secondary = high aldosterone, high renin

76
Q

Management of primary hyperaldosteronism?

A

Adrenal adenoma = surgery
Bilateral adrenal hyperplasia = aldosterone antagonist e.g. spironolcatone

77
Q

Most common cause of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

78
Q

Most common cause of primary hypoadrenalism?

A

Addison’s disease

79
Q

Features of Addison’s disease?

A

Weight loss
Fatigue
Salt craving
Hyperpigmentation
Hypotension
Hypoglycaemia
Hyponatraemia/hyperkalaemia

80
Q

Why can Addison’s present with hypoglycaemia?

A

Cortisol normally increases blood sugar

81
Q

Investigations and management for Addison’s disease?

A

Investigations = short Synacthen test
Management = hydrocortisone + fludricortisone

82
Q

Guidance for unwell patients on steroids?

A

Glucocorticoid dose should be doubled
Mineralocorticoid dose should stay the same

83
Q

Management of Addisonian crisis?

A

IM or IV hydrocortisone
IV saline 0.9% (dextrose if hypoglycaemic)

84
Q

What is pre-diabetes (“impaired glucose tolerance”) and clinical values?

A

Impaired fasting glucose (6.1-6.9) or
Impaired glucose tolerance (7.8-11.0)

85
Q

Cause of T1DM vs T2DM?

A

Type 1 = absolute insulin deficiency caused by autoimmune destruction of pancreatic beta cells
Type 2 = relative insulin deficiency caused by insulin resistance

86
Q

Main features of diabetes?

A

Polydipsia/polyuria
Weight loss (type 1)
Obesity (type 2)

87
Q

Investigations and clinical values for T2DM?

A

If patient is symptomatic:
→ random glucose or OGTT ≥ 11.1
→ fasting glucose ≥ 7.0
→ HbA1c ≥ 48.0
If patient is asymptomatic:
→ above must be demonstrated on 2 occasions

88
Q

HbA1c monitoring guidance and targets?

A

Monitor every 6 months once stable
Lifestyle changes +/- metformin = 48.0
Other anti-diabetic drugs = 53.0

89
Q

What can interfere with HbA1c interpretation and examples?

A

Conditions which shorten RBC lifespan e.g. sickle-cell disease
Conditions which prolong RBC lifespan e.g. IDA, splenectomy

90
Q

Drug options for T2DM?

A

1st line = metformin (+ SGLT-2 inhibitor if known CVD or QRISK > 10%)
2nd line = add DPP-4 inhibitor or pioglitazone or sulfonylurea or SGLT-2 inhibitor
3rd line = metformin + dual therapy of above or insulin
4th line = switch a medication for a GLP-1 mimetic

91
Q

HbA1c level which would prompt addition of 2nd line therapy?

A

≥ 58.0

92
Q

NICE guidance for insulin in T2DM?

A

Start with isophane insulin (intermediate-acting)

93
Q

Antidiabetic medications associated with hypoglycaemia?

A

Sulphonyureas
DPP-4 inhibitors
GLP-1 mimetics
Insulin

94
Q

Metformin mechanism of action and side effects?

A

Mechanism of action = increases insulin sensitivity, decreases hepatic gluconeogenesis
Side effects = GI upset, lactic acidosis

95
Q

Metformin prescribing guidance?

A

Should be titrated up slowly (to reduce GI upset)
If not tolerated, offer modified-release metformin

96
Q

SGLT-2 inhibitor examples, mechanism of action and side effects?

A

Examples = dapagliflozin, empagliflozin
Mechanism of action = inhibits glucose reabsorption in the kidneys
Side effects = weight loss, GU infection

97
Q

Sulfonylurea examples, mechanism of action and side effects?

A

Examples = gliclazide, glipizide
Mechanism of action = increases insulin production
Side effects = weight gain, hypoglycaemia

98
Q

Pioglitazone mechanism of action and side effects?

A

Mechanism of action = reduces peripheral insulin resistance
Side effects = weight gain, hepatotoxic, heart failure, increased risk of bladder cancer

99
Q

DPP-4 inhibitor examples, mechanism of action and side effects?

A

Examples = sitagliptin, alogliptin
Mechanism of action = prevents incretin breakdown
Side effects = GI upset, hypoglycaemia

100
Q

GLP-1 mimetic examples, mechanism of action and side effects?

A

Examples = liraglutide, exenatide
Mechanism of action = increases insulin secretion, inhibits glucagon secretion
Side effects = weight loss, N&V, hypoglycaemia, pancreatitis

101
Q

Outline sick day rules for diabetes mellitus?

A
  • Check blood sugar 4 hourly (or more)
  • Keep well hydrated (aim for 3L/day)
  • Take ALL diabetic medications
    → hold metformin if dehydrated
102
Q

Main factors leading to diabetic foot disease?

A

Diabetic neuropathy
Peripheral arterial disease

103
Q

Drug options for diabetic neuropathy?

A

1st line = amitriptyline, duloxetine, pregabalin, gabapentin
2nd line = another of the above options
N.B. tramadol can be used for exacerbations

104
Q

Drug options for gastroparesis?

A

Metaclopramide
Domperidone
Erythromycin

105
Q

Diabetic nephropathy screening and management?

A

Yearly albumin:creatinine ration (ACR)
ACR > 3 = ACEi/ARB

106
Q

Osmolality calcuation?

A

2(Na) + glucose + urea

107
Q

Outline the pathophysiology of Hyperosmolar Hyperglycaemic State (HHS)?

A
  • Hyperglycaemia increases serum osmolality
  • Body compensates by increased glycosuria
  • Water follows into urine down osmotic gradient
  • Polyuria leading to volume depletion
108
Q

Features of HHS?

A

Progresses over days/weeks
Type 2 diabetics (mostly)
Polyruria/polydipsia
Confusion, fatigue, N&V

109
Q

Biochemical features of HHS?

A

Hyperglycaemia
Raised serum osmolality

110
Q

What inhibits lipolysis and clinical relevance?

A

Insulin
→ T2DM patients still have some insulin so HHS does not present with ketoacidosis

111
Q

Management of HHS?

A

IV fluid replacement
Do not give insulin unless blood glucose stops falling whilst giving IV fluids

112
Q

Complication of giving insulin in HHS?

A

Cerebral pontine myelinolysis

113
Q

Investigations and clinical values for T1DM?

A

If patient is symptomatic:
→ random glucose or OGTT ≥ 11.1
→ fasting glucose ≥ 7.0
If patient is asymptomatic:
→ above must be demonstrated on 2 occasions

114
Q

Why is HbA1c not recommended for diagnosing T1DM?

A

May not reflect a rapid blood glucose increase

115
Q

Additional blood test features of T1DM?

A

Low C-peptide
Anti-GAD, anti-islet cell, insulin antibody

116
Q

T1DM autoantibodies?

A

Anti-GAD
Anti-islet cell
Insulin antibody

117
Q

Management of T1DM?

A

MDI basal-bolus regime (rapid/short mealtime bolus + intermediate/long basal)

118
Q

Give examples of rapid, short, intermediate and long acting insulin?

A

Rapid = aspart (NovoRapid), lispro (Humalog)
Short = Actrapid, Humulin S
Intermediate = isophane
Long = determir (Levemir), glargine (Lantus)

119
Q

Insulin side effects?

A

Weight gain
Hypoglycaemia
Lipodystrophy

120
Q

Management of hypoglycaemia?

A

Mild = 10-20g oral glucose or other fast-acting carbohydrate
Severe = IV dextrose + SC or IM glucagon

121
Q

DVLA diabetes guidance?

A
  • Must inform DVLA if taking insulin
  • Check blood sugars within 2 hours of driving and every 2 hours during long journeys
  • Surrender licence if 1 (group 2) or > 1 (group 1) hypoglycaemic episode requiring medical assistance in the past 12 months
122
Q

Outline the pathophysiology of DKA?

A
  • Lack of insulin leads to uncontrolled lipolysis
  • Adipose tissue breaks down into fatty acids
  • Fatty acids hydrolysed in the liver to ketones
  • Ketones consume HCO3 leading to acidosis
123
Q

Features of DKA?

A

Polydipsia/polyuria
Abdominal pain
Kussmaul’s breathing
Acetone-smelling breath
Drowsiness, coma

124
Q

Biochemical features of DKA?

A

Severe hyperglycaemia
Raised serum osmolality
Hyperketonaemia
Metabolic acidosis
Hypokalaemia

125
Q

Management of DKA?

A

IV 0.9% saline
IV insulin 0.1 unit/kg/hour
→ once glucose < 14.0 add IV 10% dextrose
Correct serum potassium
Continue normal long-acting insulin

126
Q

Complication of fluid replacement in DKA?

A

Cerebral oedema

127
Q

What is maturity-onset diabetes of the young, inheritance and most common form?

A

T2DM in patients < 25
Autosomal dominant
MODY 3

128
Q

Types of diabetes inspidus and cause?

A

Cranial = lack of ADH secretion
Nephrogenic = insensitivity to ADH

129
Q

Water deprivation and DDAVP test results for cranial vs nephrogenic DI?

A

Cranial = low urine osmolality after water deprivation, high urine osmolality after DDAVP
Nephrogenic = low urine osmolality after water deprivation, low urine osmolality after DDAVP

130
Q

Management of DI?

A

Cranial = DDAVP (desmopressin)
Nephrogenic = low salt diet, thiazide diuretics

131
Q

Normal urine osmolality before and after DDAVP in patient with polydipsia/polyuria?

A

Primary polydipsia e.g. excessive drinking

132
Q

General guidance for diabetic management pre- and post-op?

A
  • Variable rate insulin if poor glycaemic control or long surgery meaning more than one missed meal
  • Otherwise, patients should just require their dosage (insulin and/or oral agents) adjusted
133
Q

Only antidiabetic drug which should be omitted on the day of surgery?

A

SGLT-2 inhibitor

134
Q

How to manage once daily vs twice daily insulin pre- and post-op?

A

OD = reduce by 20% (day before + day of)
BD = no change (day before), half morning dose and normal evening dose (day of)

135
Q

Sex hormone levels in Klinefelter’s vs Kallman’s vs androgen insensitivity?

A

Klinefelter’s = high LH, low testosterone
Kallman’s (primary amenorrhoea) = low LH, low testosterone
Androgen insensitivity = high LH, normal/high testosterone

Med School Finals (18 decks)

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