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HYMS Y4 > KEY ENDOCRINE > Flashcards

KEY ENDOCRINE Flashcards

1
Q

What does mitral stenosis cause?

A

Left atrial hypertrophy.

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2
Q

What does aortic stenosis cause?

A

Left ventricular hypertrophy.

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3
Q

What does mitral regurgitation cause?

A

Left atrial dilatation.

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4
Q

What does aortic regurgitation cause?

A

Left ventricular dilatation.

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5
Q

2 causes of mitral stenosis.

A

Rheumatic heart disease

Infective endocarditis

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6
Q

Murmur caused by mitral stenosis.

A

Mid-diastolic, low-pitched ‘rumbling’ murmur.

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7
Q

Effect of mitral stenosis on S1 sound.

A

Loud S1.

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8
Q

2 associations of mitral stenosis.

A

Malar flush (back pressure of blood in pulmonary system causes increased CO2 and vasodilation).

Atrial fibrillation (as left atrium struggles to push blood through the stenotic valve, causing strain + electrical disruption + fibrillation).

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9
Q

Murmur caused by mitral regurgitation.

A

Pan-systolic, high-pitched ‘whistling’ murmur.

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10
Q

Where does the mitral regurgitation murmur radiate to?

A

The axilla.

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11
Q

What additional heart sound can you hear in mitral regurgitation?

A

Third heart sound (S3).

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12
Q

3 causes of mitral regurgitation.

A

Idiopathic weakening of the valve with age.
IHD
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders (EDS/ Marfan syndrome)

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13
Q

Murmur caused by aortic stenosis.

A

Ejection systolic, high-pitched murmur with a crescendo-decrescendo character.

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14
Q

Where does an aortic stenosis murmur radiate to?

A

The carotids.

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15
Q

Pulse characteristics of a patient with aortic stenosis.

A

Slow rising pulse + narrow pulse pressure

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16
Q

Common complaint with aortic stenosis

A

Exertional syncope due to difficulties maintaining blood flow to the brain

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17
Q

2 causes of aortic stenosis

A

Idiopathic age related calcification

Rheumatic heart disease

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18
Q

Murmur caused by aortic regurgitation

A

Early diastolic, soft murmur ± Austin flint murmur (early diastolic ‘rumbling’ murmur heard at the apex).

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19
Q

Pulse characteristic associated with aortic regurgitation.

A

Collapsing pulse.

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20
Q

2 causes of aortic regurgitation.

A

Idiopathic age related weakness.

Connective tissue disorders (EDS/ Marfan syndrome)

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21
Q

3 causes of Cushing’s syndrome.

A

Exogenous steroids.
Cushing’s disease (pituitary adenoma).
Adrenal adenoma (hormone secreting adrenal tumour).
Paraneoplastic Cushing’s

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22
Q

Most common cause of paraneoplastic Cushing’s?

A

Small cell lung cancer releasing ectopic ACTH.

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23
Q

Test of choice for diagnosing Cushing’s syndrome?

A

Dexamethasone suppression test.

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24
Q

Normal response for the low dose dexamethasone suppression test?

A

Suppression of cortisol release.

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25
Q

Abnormal result for low dose dexamethasone suppression test?

A

Non-suppressed morning cortisol measurement.

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26
Q

If a low dose dexamethasone suppression test is abnormal, what is the next test to be done?

What is the purpose of this test?

A

High dose dexamethasone suppression test to differentiate causes of Cushing’s syndrome.

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27
Q

High dose dexamethasone suppression test result in Cushing’s disease.

A

Cortisol suppressed by higher dose of dexamethasone as pituitary still shows some response to negative feedback.

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28
Q

High dose dexamethasone suppression test result in adrenal adenoma.

A

Cortisol is not supressed (as production is independent from pituitary).

ACTH is suppressed due to negative feedback on hypothalamus and pituitary.

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29
Q

High dose dexamethasone suppression test result in ectopic ACTH secretion.

A

Both cortisol and ACTH are not suppressed as production is independent of hypothalamus and pituitary.

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30
Q

Dose of dexamethasone used in:

1) Low dose suppression test.
2) High dose suppression test.

A

1) 1mg

2) 8mg

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31
Q

Describe the effects of the high dose dexamethasone suppression test on cortisol and ACTH in the following causes:

1) Pituitary adenoma
2) Adrenal adenoma
3) Ectopic ACTH

A

1) Cortisol suppressed + ACTH suppressed.
2) Cortisol not suppressed + ACTH suppressed.
3) Cortisol + ACTH both suppressed.

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32
Q

FBC results in Cushing’s syndrome.

A

Raised WCC
Raised electrolytes
Low potassium (if aldosterone also released from adrenal adenoma).

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33
Q

Cause of primary adrenal insufficiency.

A

Addison’s disease (autoimmune disease where adrenals are damaged)

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34
Q

What is secondary adrenal insufficiency?

A

Inadequate release of ACTH causing less cortisol to be released from adrenals.

Normally caused by loss of or damage to the pituitary gland.

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35
Q

What is Sheehan’s syndrome?

A

Where massive blood loss in childbirth leads to pituitary gland necrosis.

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36
Q

What is tertiary adrenal insufficiency?

A

Inadequate release of CRH.

Normally caused by long term use of exogenous steroids.

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37
Q

Signs of adrenal insufficiency.

A

Bronze hyperpigmentation of the skin + hypotension (normally postural hypotension).

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38
Q

Electrolyte abnormalities in adrenal insufficiency.

A

Hyponatraemia + hyperkalaemia

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39
Q

Investigation of choice for adrenal insufficiency?

A

Short synacthen test.

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40
Q

ACTH level in primary adrenal failure?

A

High.

Pituitary is producing loads of ACTH to try and stimulate adrenals + there is no negative feedback in the absence of cortisol.

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41
Q

ACTH level in secondary adrenal failure?

A

Low.

Adrenal glands are not releasing cortisol as they are not being stimulated by ACTH.

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42
Q

Which antibodies are present in 80% of autoimmune adrenal insufficiency patients?

A

Adrenal cortex antibodies + 21-hydroxylase antibodies.

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43
Q

Result of short synacthen test in primary adrenal insufficiency.

A

Cortisol does not increase (is not double the baseline).

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44
Q

When is ACTH measures in the short synacthen test?

A

Baseline, 30 minutes, 60 minutes.

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45
Q

Management of adrenal insufficiency.

A

Hydrocortisone to replace cortisol.

Fludrocortisone to replace aldosterone.

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46
Q

Sick day rules for adrenal insufficiency?

A

Double corticosteroid dose.

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47
Q

Presentation of Addisonian crisis.

A 
Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
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48
Q

Management of Addisonian crisis.

A 
Intensive monitoring if very unwell
IV hydrocortisone
IV fluids
Correct hypoglycaemia
Monitor electrolytes and fluid balance
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49
Q

TSH level in hyperthyroidism?

A

Low

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50
Q

Only cause of hyperthyroidism where TSH is high?

A

Pituitary adenoma which secretes TSH.

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51
Q

TSH level in hypothyroidism?

A

High (as it is trying to stimulate more thyroid hormone release).

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52
Q

Cause of hypothyroidism where TSH is low?

A

Pituitary/ hypothalamic cause (secondary hypothyroidism).

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53
Q

T3 +T4 levels + TSH levels in hyperthyroidism?

A

T3+T4 elevated.

TSH low.

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54
Q

T3+T4 levels + TSH levels in hypothyroidism?

A

T3+T4 low

TSH high

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55
Q

TSH and T3/T4 levels in the following conditions:

1) Hyperthyroidism.
2) Primary hypothyroidism.
3) Secondary hypothyroidism.

A

1) TSH low, T4/T3 high
2) TSH high, T4/T3 low
3) TSH low, T3/T4 low

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56
Q

Antibodies present in Grave’s disease and Hashimoto’s thyroiditis?

A

Anti-TPO antibodies.

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57
Q

Antibodies present in Grave’s disease alone?

A

TSH receptor antibodies.

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58
Q

Special investigation for hyperthyroidism/ thyroid cancers?

A

Radioisotope scan

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59
Q

Diffuse high uptake on radioisotope scan is found in?

A

Grave’s disease.

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60
Q

Focal high uptake on radioisotope scan is found in?

A

Toxic multi nodular goitre and adenomas.

61
Q

‘Cold’ areas on radioisotope scan can indicate?

A

Thyroid cancer.

62
Q

What causes primary hyperthyroidism?

A

Thyroid pathology where the thyroid produces excessive T3/T4.

63
Q

What causes secondary hyperthyroidism?

A

Pathology in the hypothalamus or pituitary causing the thyroid to produce excessive thyroid hormone due to overstimulation with TSH.

64
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease.

65
Q

Describe Grave’s disease pathophysiology.

A

TSH receptor antibodies > mimic true TSH > stimulate TSH receptors on thyroid > excess TSH production > excess T3/T4 production > negative feedback to hypothalamus and pituitary causes low TSH.

66
Q

2 causes of hyperthyroidism aside from Grave’s disease.

A

Toxic multi nodular goitre.
Solitary toxic thyroid nodule.
De Quervain’s thyroiditis

67
Q

Cause of exophthalmos.

A

Inflammation, swelling and hypertrophy of the tissue behind the eyeball, forcing the eyeball forward.

68
Q

Cause of pre-tibial myoexema.

A

Reaction to TSH antibodies causes deposits of mucin under the skin which cause a discoloured, waxy and oedematous appearance to the skin.

69
Q

Universal features of hyperthyroidism.

A 
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
70
Q

Diffuse goitre + bilateral exophthalmos + pre-tibial myxoedema = ?

A

Grave’s disease - these signs all caused by TSH receptor antibodies.

71
Q

Goitre with firm nodules + >50 = ?

A

Toxic multi nodular goitre.

72
Q

Second most common cause of hyperthyroidism?

A

Toxic multi nodular goitre;

73
Q

Pathophys of toxic multi-nodular goitre?

A

Nodules develop on thyroid that act independently of normal feedback system + continuously produce excessive thyroid hormone.

74
Q

Hyperthyroidism + single nodule (benign adenoma) = ?

A

Solitary toxic thyroid nodule.

75
Q

Fever + neck pain + neck tenderness + dysphagia + hyperthyroidism features = ?

A

De Quervain’s thyroiditis.

76
Q

Management of De Quervain’s thyroiditis?

A

Self-limiting condition

Symptomatic treatment = NSAIDs for pain and inflammation/ beta-blockers for hyperthyroidism symptomatic relief.

77
Q

Signs and symptoms of thyroid storm?

A

Pyrexia + tachycardia + delirium.

78
Q

1st line anti-thyroid drug for hyperthyroidism?

A

Carbimazole.

79
Q

2 regimens that can be used with carbimazole after initial treatment?

A

1) Titration-block (titrate dose to maintain normal levels)

2) Block and replace (block all production and give levothyroxine).

80
Q

2nd line anti-thyroid drug for hyperthyroidism?

A

Propylthiouracil.

81
Q

How does radioactive iodine work?

A

Taken up by thyroid and emits radiation which destroys a proportion of thyroid cells.

82
Q

Side effect of radio iodine treatment?

A

Can leave patient with hypothyroidism requiring levothyroxine replacement.

83
Q

What are the rules for a patient using radio iodine?

A

1) Must not be pregnant + must not get pregnant within 6 months of use.
2) Must avoid close contact with children and pregnancy women for 3 weeks.
3) Limit contact with anyone for several days after receiving the dose.

84
Q

1st line symptomatic control for hyperthyroidism?

A

Propranolol = non-selectively blocks beta receptors.

85
Q

Definitive surgical treatment for hyperthyroidism?

A

Thyroidectomy or removal of toxic nodules.

86
Q

Most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis.

87
Q

Cause of Hashimoto’s thyroiditis?

A

Autoimmune inflammation of thyroid gland.

88
Q

Antibodies associated with Hashimoto’s thyroiditis?

A

anti-TPO antibodies and anti-thyroglobulin antibodies.

89
Q

Most common cause of hypothyroidism in the developing world?

A

Iodine deficiency.

90
Q

2 drugs which can cause hypothyroidism?

A

Lithium (inhibits production of thyroid hormones)

Amiodarone (interferes with thyroid hormone production and metabolism)

91
Q

Cause of secondary hypothyroidism?

A

Most commonly hypopituitarism where pituitary fails to produce enough TSH.

92
Q

General presentation of hypothyroidism?

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Amenorrhoea/ menorrhagia
Constipation
93
Q

TSH and T3/T4 levels in primary hypothyroidism?

A

TSH high, T3/T4 low

94
Q

TSH and T3/T4 levels in secondary hypothyroidism?

A

TSH low, T3/T4 low.

95
Q

Site of pathology in primary hypothyroidism?

A

Thyroid gland

96
Q

Site of pathology in secondary hypothyroidism?

A

Pituitary gland

97
Q

1st line treatment for hypothyroidism?

A

Levothyroxine.

98
Q

Monitoring required when starting levothyroxine?

A

Measure TSH levels monthly until stable.

99
Q

What do you do if TSH level is too high in patients on levothyroxine?

A

Increase dose.

100
Q

What do you do if TSH level is too low in patients on levothyroxine

A

Reduce dose.

101
Q

What happens in hypopituitarism?

A

Decreased secretion of anterior pituitary hormones.

102
Q

What order are anterior pituitary hormones affected in in hypopituitarism?

A

GH > FSH+LH > TSH > ACTH > Prolactin.

103
Q

What is panhypopituitarism?

A

Deficiency in all anterior pituitary hormones.

104
Q

What is Acromegaly?

A

Clinical manifestation of excessive growth hormone.

105
Q

Most common cause of acromegaly?

A

pituitary adenoma.

106
Q

Ophthalmological sign that can be seen in large pituitary adenomas?

A

Bitemporal hemianopia.

107
Q

General signs and symptoms of acromegaly?

A

Prominent forehead and brown (frontal bossing)
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)
Arthritis from imbalanced growth of joints.

108
Q

Management of pituitary adenoma?

A

Trans-sphenoidal removal.

109
Q

3 classes of medications that can be used to block growth hormone?

A

1) Octreotide (somatostatin analogue - blocks GH release).
2) Bromocriptine (DA agonist - blocks GH release)
3) Pegvisomant (GH antagonist used 3rd line).

110
Q

How does GH stimulate excessive bone and soft tissue growth?

A

Through IGF-1.

111
Q

What causes gigantism?

A

Excess GH release before fusion of epiphyseal growth plates.

112
Q

Types of organ dysfunction that can occur in acromegaly?

A

Hypertrophic heart
HTN
T2DM
Colorectal cancer

113
Q

Blood results in acromegaly?

A

High IGF-1.

114
Q

Method of diagnosis of acromegaly?

A

OGTT.

If lowest GH value during OGTT is >1, acromegaly is confirmed.

115
Q

Where is parathyroid hormone produced?

A

Chief cells in the parathyroid glands.

116
Q

Cause of PTH secretion?

A

Hypocalcaemia.

117
Q

4 methods used by PTH to increase blood calcium levels.

A

Increasing osteoclast activity.
Increasing calcium absorption from the gut.
Increasing calcium absorption from the kidneys.
Increasing vitamin D activity.

118
Q

What role does vitamin D do in increasing calcium levels?

A

Increases calcium absorption from intestines.

119
Q

Effects of PTH on vitamin D?

A

Converts Vitamin D into it’s active form, causing further increased absorption of calcium from the intestines.

120
Q

Cause of primary hyperparathyroidism?

A

Uncontrolled PTH production by a tumour.

121
Q

Blood results in primary hyperparathyroidism?

A

High PTH

High Calcium

122
Q

Cause of secondary hyperparathyroidism?

A

Insufficient vitamin D or CKD = low absorption of calcium from intestines, kidneys + bones.

123
Q

Blood results in secondary hyperparathyroidism?

A

High PTH

Low/ normal calcium

124
Q

Cause of tertiary hyperparathyroidism?

A

Persistent secondary hyperthyroidism causing hyperplasia of the parathyroid glands = increased baseline level of PTH secretion.

125
Q

Blood results in tertiary hyperparathyroidism?

A

High PTH

High calcium

126
Q

Most common type of thyroid cancer?

A

Papillary.

127
Q

Thyroid cancer with best prognosis?

A

Papillary.

128
Q

Thyroid cancer associated with MEN 2?

A

Medullary.

129
Q

Thyroid cancer associated with Hashimoto’s thyroiditis?

A

Lymphoma.

130
Q

Bloods associated with primary hyperaldosteronism?

A

Hypertension
Hypokalaemia
Hypernatraemia

131
Q

1st line investigation for primary hyperaldosteronism?

A

Aldosterone/renin ratio

132
Q

Drug that can cause gynaecomastia?

A

Metaclopramide.

133
Q

Drug that can cause hypercalcaemia?

A

Bendroflumethiazide.

134
Q

Dangerous side effect that can be caused by Carbimazole?

A

Agranulocytosis.

135
Q

Define diabetes insipidus.

A

Lack of ADH or lack of response to ADH.

136
Q

What is primary polydipsia?

A

When the patient has normally functioning ADH but is drinking excessive quantities of water = excessive urine production.

137
Q

Brief pathophysiology in nephrogenic diabetes insipidus?

A

Collecting ducts in kidneys do not respond to ADH.

138
Q

Causes of nephrogenic diabetes insipidus?

A

Drugs (lithium)
Mutations in AVPR2 gene that codes for ADH.
Intrinsic kidney disease.
Electrolyte disturbance (hypokalaemia/ hypercalcaemia)

139
Q

Brief pathophysiology of cranial diabetes insipidus?

A

Hypothalamus does not produce any/ sufficient ADH.

140
Q

Causes of cranial diabetes insipidus?

A 
Idiopathic
Brain tumours
Head injury
Brain malformations
Brain infections
Brain surgery/ radiotherapy
141
Q

Clinical features of diabetes insipidus.

A 
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatraemia
142
Q

3 main investigations done in diabetes insipidus?

A

Urine osmolality
Serum osmolality
Water deprivation test (desmopressin stimulation test).

143
Q

1st line investigation for diagnosing diabetes insipidus?

A

Water deprivation test (desmopressin stimulation test).

144
Q

Describe the water deprivation test.

A

Fluid deprivation for 8 hours.
Measure urine osmolality.
Administer desmopressin (synthetic ADH).
Measure urine osmolality 8 hours later.

145
Q

Results for the following in those with diabetes insipidus:

1) Urine osmolality
2) Serum osmolality

A

1) Low

2) High

146
Q

Water deprivation test results in cranial diabetes insipidus?

A

Initial urine osmolality: low.

Urine osmolality after serum ADH: high.

147
Q

Water deprivation test results in nephrogenic diabetes insipidus?

A

Initial urine osmolality: low.

Urine osmolality after serum ADH: low.

148
Q

Water deprivation test results in primary polydipsia?

A

Initial urine osmolality: high.

Urine osmolality after serum ADH: high.

149
Q

Diabetes insipidus management?

A

1) Treat underlying cause.

2) Desmopressin (higher doses required in nephrogenic DI).

HYMS Y4 (8 decks)

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