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Endocrinology > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

Symptoms of hyperthyroidism

A 
o	Increased basal metabolic rate
o	Tachycardia 
o	Insomnia 
o	Heat intolerance 
o	Diarrhoea 
o	Underweight 
o	Tremors 
o	Amenorrhoea 
o      Pretibial myxoedema
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2
Q

Describe primary hyperthyroidism

A

Pathology is within the thyroid gland

Low TSH, High T4/T3

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3
Q

Describe secondary hyperthyroidism

A

Pathology is within the pituitary gland/hypothalamus

High/normal TSH, High T4/3

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4
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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5
Q

What is Grave’s disease?

A

Autoimmune disorder with TSH receptor autoanitibodies causing diffuse thyroid enlargement/goitre (sometimes with a bruit)

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6
Q

What are the other autoimmune diseases associated with Grave’s disease?

A
  1. Vitiligo
  2. Addisons
  3. T1DM
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7
Q

What is a characteristic symptom of hyperthyroidism?

A

Pretibial myxoedema

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8
Q

Pretibial myxoedema features

A

> 

Pink, purple, brown plaques/nodules on anterior shin 
Bilateral 
Shiny
Firm and non-pittng
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9
Q

What eye features are present in hyperthyroidism?

A

Proptosis (Exophthalmos)

Lid lag

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10
Q

Treatment of hyperthyroidism

A
  1. Beta blockers (for symptomatic relief)
  2. Carbimazole (antithyroid drug)
  3. Radio-iodine
  4. Surgery
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11
Q

What drugs are used for the symptomatic relief of hyperthyroidism?

A

Beta blockers

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12
Q

Carbimazole mechanism of action

A

Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

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13
Q

Carbimazole side effects

A

> agranulocytosis

> crosses the placenta, but may be used in low doses during pregnancy

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14
Q

What is Toxic multinodular goitre?

A

Refers to one or more nodules (typically benign growths) in the thyroid gland that make thyroid hormone without responding to the signal to keep thyroid hormone balanced.

o Older patients (>60)
o Excess thyroid hormone production
o Multiple overactive nodules/follicles

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15
Q

What is a toxic adenoma?

A

o Secretes T3
o Solitary nodule
o Single hot nodule on isotope scan
o Treat with radioiodine

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16
Q

What is another name for Subacute thyroiditis?

A

De Quervain’s thyroiditis

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17
Q

What is Subacute thyroiditis?

A

Self-limiting viral infection

Thyroid function goes from hyperthyroid to hypothyroid to euthyroid

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18
Q

Features of Subacute thyroiditis

A

o Painful goitre
o Fever
o Increased inflammatory markers (CRP)
o Low isotope uptake on scan

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19
Q

What are the features of the isotope scan in Subacute thyroiditis?

A

Low isotope uptake on scan

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20
Q

What are the features of the isotope scan in Toxic adenoma?

A

Single hot nodule on isotope scan

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21
Q

What is a Thyroid crisis/storm?

A

Acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis.

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22
Q

Thyrotoxicosis

A

Excess thyroid hormones in the tissues due to inappropriately high circulating thyroid hormone concentrations.

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23
Q

Symptoms of Thyroid crisis/storm?

A 
>	Temperature >38.5
>	Seizures
>	Vomiting
>	Sweating
>	Extreme restlessness
>	Confusion
>	Jaundice
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24
Q

Treatment of Thyroid crisis/storm?

A
  1. Propranolol
  2. High dose digoxin
  3. Carbimazole
  4. Hydrocortisone/dexamethasone
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25
Q

Complications of Thyroid crisis/storm

A

Shock –> coma –> death

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26
Q

Symptoms of hypothyroidism

A 
o	Decreased basal metabolic rate 
o	Bradycardia 
o	Fatigue 
o	Cold intolerance 
o	Constipation 
o	Overweight 
o	Pale, cold, doughy skin
o	Menorrhagia 
o	Thin, dry hair
o	Carpal tunnel syndrome
o	Hyperlipidaemia 
o	Pitting oedema
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27
Q

Primary hypothyroidism

A

Pathology in the thyroid gland

High TSH, Low T4/3

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28
Q

Secondary hypothyroidism

A

Pathology in the hypothalamus/anterior pituitary

Low/normal TSH, Low T4/3

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29
Q

Most common cause of hypothyroidism

A

Hashimoto’s thyroiditis

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30
Q

Hashimoto’s thyroiditis

A

Autoimmune disorder with autoantibodies against thyroid peroxidase (TPO) - T-cell mediated

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31
Q

Features of Hashimoto’s thyroiditis

A 
o	Increased levels of TPO antibodies
o	Gradual thyroid failure
o	T-cell mediated
o	Goitre 
o	Commoner in older woman
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32
Q

Causes of hypothyroidism

A
  • Hashimoto’s thyroiditis
  • Atrophic thyroiditis
  • Iodine deficiency
  • Previous treatment for hyperthyroidism
  • Sheehan’s syndrome
  • Truama
  • Pituitary tumours
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33
Q

Atrophic thyroiditis

A

Autoimmune disease, less common than Hashimoto’s

Diffuse lymphocytic infiltration of the gland leading to Atrophy & Goitre (hypothyroidism)

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34
Q

Treatment for hypothyroidism

A

Levothyroxine – drug form of T4)

Monitor TFTs every 2 months since treatment commences

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35
Q

Myxoedema coma

A

Medical emergency of hypothyroidism

Unsuspected, untreated or inadequately treated hypothyroidism - Precipitated by illness, drugs

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36
Q

Features of Myxoedema coma

A 
>	Hypothermia
>	Bradycardia
>	Hypotension
>	Hypoglycaemia
>	Hyponatraemia
>	Hypoxia 
>	Hypercapnia
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37
Q

Why are thyroid hormones increased in pregnancy (hyperthyroid)?

A

HcG is a hormone made by the developing foetus and prevents degeneration of the corpus luteum

It mimics TSH and therefore will cause increased T4, which in turn suppresses TSH

Therefore normal TFTs in pregnancy are decreased TSH and increased T4

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38
Q

What is the treatment of hypothyroidism in pregnancy?

A

If pre-existing, must increase levels of thyroxine by 25mcg as soon as pregnancy is suspected

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39
Q

What effect can untreated hypothyroidism have on the unborn baby in pregnancy?

A

Can cause cretinism in baby if untreated

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40
Q

What is the treatment for hyperthyroidism in pregnancy?

A

Treat with propranolol in early pregnancy

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41
Q

What are thyroid adenomas?

A
  • Benign
  • Discrete solitary masses
  • Encapsulated by surrounding collagen cuff
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42
Q

What is the name given to a benign mass in the thyroid?

A

Thyroid adenoma

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43
Q

What are the 4 carcinomas of the thyroid?

A
  • Papillary
  • Follicular
  • Medullary
  • Anaplastic
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44
Q

What is the most common carcinoma of the thyroid?

A

Papillary

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45
Q

What thyroid carcinoma spreads to the lymph nodes (lymphatic spread)?

A

Papillary

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46
Q

Histological features of papillary carcinoma

A

Orphan annie nuclei

Psammoma bodies

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47
Q

Describe papillary carcinoma

A 
o	Young adults
o	Least aggressive
o	Usually solitary nodule
o	Good prognosis
o      Orphan annie nuclei
o      Psammoma bodies
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48
Q

What thyroid carcinoma has hematological spread?

A

Follicular

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49
Q

What is the 2nd most common thyroid carcinoma?

A

Follicular carcinoma

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50
Q

Describe Follicular carcinoma

A

o Usually one nodule
o May have surrounding capsule
o 30-50s
o Haematological spread

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51
Q

Where is medullary carcinoma derived from?

A

Derived by c-cells (calcitonin secretig cells)

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52
Q

What is the condition associated with medullary carcinoma?

A

MEN IIA

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53
Q

Describe medullary carcinoma

A

o Derived by c-cells
o Associated with MEN IIA
o Amyloid deposition
o Aggressive

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54
Q

Describe the features of anaplastic carcinoma

A

o Older patients
o Undifferentiated
o Rapidly growing - can cause dysphagia and stridor
o Very aggressive

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55
Q

What is the most aggressive thyroid carcinoma?

A

Anaplastic

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56
Q

What are the functions of GH?

A 
o	Increased lean body mass
o	Increased energy substrates, glucose and free fatty acids
o	Increased protein synthesis in muscles
o	Decreased fat storage 
o      Acromegaly
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57
Q

What are the features of GH deficiency in children?

A

Growth failure

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58
Q

What are the features of GH deficiency in adults?

A

Osteoporosis

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59
Q

What are the features of excess GH in adults?

A

Acromegaly and diabetes

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60
Q

What are the features of excess GH in children?

A

Gigantism

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61
Q

Investigations for excess GH & acromegaly?

A

Oral glucose tolerance test (OGTT)

MRI pituitary

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62
Q

Features of acromegaly

A 
>	Insidious onset
>	Growth of hands and feet
>	Coarsening of facial features
>	Prominent supra-orbital ridge
>	Wide spread teeth (because jaw enlarges)
>	Macroglossia (large tongue)
>	Headache
>	Hoarse voice 
>	Obstructive sleep apnoea 
>	Joint pain
>	Carpal tunnel syndrome 
>	Acroparaesthesia 
>	Loss of libido
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63
Q

Macroglossia

A

Large tongue

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64
Q

Acroparaesthesia

A

Tingling, pins-and-needles, burning or numbness or stiffness in the hands and feet, particularly the fingers and toes

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65
Q

What hormone suppresses GH?

A

Somatostatin

66
Q

Treatment for acromegaly

A
  1. Surgery
  2. Somatostatin analogue (Octreotide)
  3. Dopamine agonists
  4. Radiotherapy (if surgery is inappropriate)
67
Q

Examples of somatostatin analogues

A

Ocreotide

68
Q

Examples of dopamine agonists

A

Cabergoline or bromocriptine

69
Q

Side effects of Ocreotide (somatostatin analogues)

A

gastritis, gall stones

70
Q

Prolactinoma

A

A noncancerous tumor of the pituitary gland. This tumor causes the pituitary to make too much of a hormone called prolactin. The major effect of prolactinoma is decreased levels of some sex hormones — estrogen in women and testosterone in men.

71
Q

Function of prolactin

A

Causes the breasts to grow and make milk during pregnancy and after birth.

72
Q

Features of Prolactinoma in woman

A 
o	Amenorrhoea or oligomenorrhoea
o	Infertility
o	Galactorrhoea
o	Loss of libido
o	Increased weight
73
Q

Features of Prolactinoma in men

A

o Erectile dysfunction
o Decreased facial hair
o Galactorrhoea

74
Q

Galactorrhoea

A

Milky nipple discharge

75
Q

Treatment of prolactinoma

A

Dopamine agonists (cabergoline)

76
Q

Oligomenorrhoea

A

Infrequent menstrual periods

77
Q

Menorrhagia

A

Heavy or prolonged menstrual bleeding

78
Q

What is the outer layer of the adrenal gland called?

A

zona glomerulosa (secrete mineralocorticoids)

79
Q

What is the middle layer of the adrenal gland called?

A

zona fasciculata (secrete glucocorticoids)

80
Q

What is the inner layer of the adrenal gland called?

A

zona reticularis (secrete androgens)

81
Q

What is the role of the zona glomerulosa?

A

secrete mineralocorticoids

82
Q

What is the role of the zona fasciculata?

A

secrete glucocorticoids e.g. cortisol

83
Q

What is the role of the zona reticularis?

A

secrete androgens

84
Q

An example of a mineralocorticoid

A

Aldosterone

85
Q

Aldosterone function

A

Works on distal convoluted tubule and collecting duct where it increases reabsorption of sodium and increases excretion of potassium

86
Q

What two conditions that arise from the imbalance of aldosterone?

A
  • Conn’s disease

* ADDISON’S DISEASE

87
Q

Conn’s disease

A

Excess aldosterone leading to excess sodium and decreased potassum

88
Q

ADDISON’S DISEASE

A 
Adrenal insufficiency (hypoadrenalism)
Leads to loss of secretion of Cortisol, Aldosterone and Sex hormones
89
Q

What hormones does the medulla release?

A

Adrenaline and noradrenaline in response to increased sympathetic stimulation

90
Q

Presentation of Addison’s disease

A 
o	Fatigue
o	Hyponatraemia 
o	Hyperkalaemia 
o	Hypotension 
o	Weight loss 
o	Nausea 
o	Vomiting 
o	Skin pigmentation
91
Q

Addisonian crisis

A

Serious medical condition caused by the body’s inability to produce a sufficient amount of cortisol. An Addisonian crisis is also known as an acute adrenal crisis.

92
Q

Symptoms of Addisonian crisis

A

o Severe hypotension (postural hypotension)
o Febrile, rapid pulse
o Dehydration
o Often precipitated by trauma or illness

93
Q

Treatment of Addisonian crisis

A
  1. Immediate fluids
  2. IV Hydrocortisone
  3. Dextrose
94
Q

Blood profile of Addison’s disease

A

o Hyponatraemia
o Kyperkalaemia
o High urea

95
Q

Investigations for Addison’s disease

A

Short synacthen test (Synacthen is synthetic ACTH)

So if cortisol increases in response to increased ATCH – it is Addison’s - primary adrenal insufficiency

If cortisol doesn’t increase in response to increased ACTH – it is secondary adrenal insufficiency

96
Q

What investigations should be done if primary adrenal insufficiency is suspected (after a short synacthen test)?

A

If primary adrenal insufficiency is suspected, then do CT/MRI to exclude tumour in adrenals. Also do antibodies (because could be autoimmune)

97
Q

What is the treatment for Addison’s disease?

A

Hydrocortisone (replace glucocorticoid)

Fludrocortisone (replace mineralocorticoid)

98
Q

What conditions are associated with Addison’s disease?

A

Hashimoto’s
Vitiligo
Type 1 DM

99
Q

What is primary conn’s disease?

A

Due to a problem of the adrenal glands themselves, which causes them to release too much aldosterone.

100
Q

What are the causes of primary conn’s disease?

A

Solitary benign adenoma

Bilateral cortical adrenal hyperplasia

101
Q

What is secondary conn’s disease?

A

A problem elsewhere in the body causes the adrenal glands to release too much aldosterone.

102
Q

What are the causes of secondary conn’s disease?

A

Volume depletion

Renal artery stenosis

103
Q

Symptoms in Conn’s disease

A 
o	Hypertension
o	Hypokalaemia 
o	Hypernatraemia 
o	Alkalosis 
o	Polyuria
o	Polydipsia 
o	Muscle weakness and cramps
o	Headaches
o	Non-oedematous
104
Q

What is another name given to Conn’s disease?

A

Hyperaldosteronism

105
Q

Diagnostic test for Conn’s disease

A

Step 1: confirm aldosterone excess
> Measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio)
> If ratio raised (assay dependent) then investigate further with saline suppression test
> Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline confirms PA

Step 2: confirm subtype
> Adrenal CT to demonstrate adenoma
> Sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess

106
Q

Treatment for Conn’s disease

A

Surgical
> Unilateral laparoscopic adrenalectomy
> Only if adrenal adenoma (and excess confirmed in adrenal vein sampling)
> Cure of hypokalaemia

Medical
> In bilateral adrenal hyperplasia
> Use MR antagonists (spironolactone or eplerenone)

107
Q

Cushing’s disease

A

A serious condition of an excess of the steroid hormone cortisol in the blood level caused by a pituitary tumor secreting adrenocorticotropic hormone (ACTH).

108
Q

Causes of Cushing’s dsease

A

Exogenous steroids
Pituitary adenoma (secreting ACTH)
Ectopic ACTH secretion

109
Q

Symptoms of Cushing’s disease

A 
o	Central obesity 
o	Purple striae on abdomen
o	Hirsuitism and acne (in females)
o	Frontal balding (in females)
o	Menstrual dysfunction
o	Moon face
o	Buffalo hump
o	Easy bruising 
o	Proximal myopathy
o	Osteoporosis and fractures
o	Depression
o	Cardiomyopathy 
o	“Lemon on sticks appearance”
110
Q

Investigations for Cushing’s disease

A

Dexamethasone suppression test
> Give oral dexamethasone
> Measure cortisol levels at 0 and 48 hours
> If cortisol remains high, diagnosis is Cushing’s
> If cortisol levels drop, normal response

o 24 hour urinary free cortisol
o Late night salivary cortisol
o Low dose dexamethasone suppression test
o MRI/CT

111
Q

Treatment for Cushing’s disease

A

Trans-sphenoidal removal of the tumour
External pituitary irradiation
Medical therapy
Bilateral adrenalectomy

112
Q

Congenital Adrenal Hyperplasia

A

A group of rare inherited autosomal recessive disorders characterized by a deficiency of 21a hydroxylase deficiency

113
Q

Phaeochromocytoma

A
  • Rare tumour of adrenal medulla

* From chromaffin cells, which secrete Adrenaline and Noradrenaline

114
Q

What is 10% rule of Phaeochromocytoma?

A

o 10% bilateral
o 10% familial
o 10% malignant
o 10% extra adrenal

115
Q

What condition is associated with phaeochromocytoma?

A

MEN II

116
Q

Symptoms of Phaeochromocytoma

A 
Usually young patients
o	Sweating
o	Hypertension
o	Headache
o	Palpitations
o	Flushing
o	Breathlessness
117
Q

Investigations of Phaeochromocytoma

A

3x 24hour urine collections for catecholamines

Abdominal CT/MRI

118
Q

Treatment for Phaeochromocytoma

A

Alpha blockers (phenoxybenzamine – 1st line treatment)
Beta blockers
Surgery
Chemotherapy

119
Q

What is the 1st line drug given in Phaeochromocytoma?

A

Alpha blockers (phenoxybenzamine – 1st line treatment then beta blocker)

120
Q

Why are alpha blockers given before beta blockers in Phaeochromocytoma?

A

Can cause hypertensive crisis

121
Q

Hyperparathyroidism

A

A condition in which one or more of your parathyroid glands become overactive and release (secrete) too much parathyroid hormone (PTH). This causes the levels of calcium in your blood to rise, a condition known as hypercalcemia.

122
Q

Primary Hyperparathyroidism causes

A

Solitary parathyroid adenoma
Carcinoma
Parathyroid hyperplasia

123
Q

Symptoms of Hyperparathyroidism

A
  1. Muscle weakness
  2. Arthralgia
  3. Abdominal pain
  4. Constipation
  5. Renal calculi
  6. Tiredness
  7. Dehydration
    8 Polyuria.
    9/ Polydipsia
  8. Renal stones
  9. Osteoporosis and fractures
  10. Moans, bones, stones and abdominal groans
124
Q

Polyuria

A

excessive urination.

125
Q

Polydipsia

A

extreme thirstiness

126
Q

Investigations for hyperparathyroidism

A
  • Increased parathyroid hormone
  • Increased calcium
  • Decreased phosphate
127
Q

Treatment for primary hyperparathyroidism

A

Surgery

128
Q

Causes of secondary hyperparathyroidism

A
  1. Chronic renal failure
  2. Vitamin D deficiency
  3. Insufficiency calcium in the diet
  4. Excessive magnesium in the diet
129
Q

Blood results in hyperparathyroidism

A
  1. Increased calcium
  2. decreased phosphate
  3. Increased parathyroid hormone
130
Q

Treatment for hyperparathyroidism

A

Increase calcium with supplements

131
Q

Tertiary hyperparathyroidism

A

o Parathyroid glands develop autonomous function
o Keep on producing massive amounts of PTH
o This happens in patients with long term secondary hyperparathyroidism
o So, although calcium levels are increased, PTH is still released

132
Q

Blood results in Tertiary hyperparathyroidism

A

Greatly increased PTH

Increased calcium

133
Q

Treatment for Tertiary hyperparathyroidism

A

Surgery

134
Q

Malignant hyperparathyroidism

A

Parathyroid related protein PTHrP is produced by malignant squamous cell carcinomas - Non-small cell lung cancer, Breast & Renal cancer.

PTHrP mimics PTH resulting in decreased PTH, increased calcium and increased phosphate

135
Q

Primary hypoparathyroidism

A

Decreased PTH secretion due to gland failure. PTH roles is to keep blood calcium level stable

136
Q

Causes of Primary hypoparathyroidism

A

Autoimmune

Digeorge syndrome

137
Q

Blood results in Primary hypoparathyroidism

A
  1. Decreased PTH
  2. Decreased calcium
  3. Increased/normal phosphate
138
Q

Digeorge syndrome

A

Congenital absence of parathyroid glands. Autosomal dominant

139
Q

Treatment for Primary hypoparathyroidism

A

Vitamin d supplements

Calcium supplements

140
Q

Secondary hypoparathyroidism causes

A

Radiation
Post thyroidectomy
Severe hypomagnesaemia

141
Q

Blood results in secondary hypoparathyroidism

A

Low PTH

Increased calcium

142
Q

Pseudohypoparathyroidism

A

A genetic disorder in which the body fails to respond to parathyroid hormone (resistance)

143
Q

Blood results in Pseudohypoparathyroidism

A

Decreased calcium

Increased PTH

144
Q

Features in Pseudohypoparathyroidism

A 
>	Short 4th metacarpals 
>	Round face
>	Short stature
>	Mental retardation
>	Obesity
145
Q

Treatment for Pseudohypoparathyroidism

A

Vitamin D supplements

Calcium supplements

146
Q

Causes of SiADH

A 
o	Cancer (ectopic production of ADH)
o	Meningitis
o	Pneumonia
o	TB
o	Alcohol withdrawal
	Opiates
	Carbamazepine
147
Q

Drugs that cause SiADH

A

Opiates

Carbamazepine

148
Q

Clinical features of SiADH

A 
o	Nausea
o	Dizziness 
o	Light headedness
o	Irritability
o	Collapse
149
Q

Investigations in SiADH

A

Hyponatraemia
Decreased serum osmolarity
Increased urine Osmolarity
Normal renal function

150
Q

Treatment for SiADH

A

Water restriction

Demeclocycline (inhibits action of ADH in kidney)

151
Q

Osmolarity

A

Concentration - e.g increased urine osmolarity is increased urine concentration.

152
Q

Demeclocycline

A

inhibits action of ADH in kidney - used in SiADH

153
Q

Nephrogenic Diabetes insipidus

A

Is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance leads you to produce large amounts of urine.
Due to impaired water re-absorption by the kidneys

154
Q

Causes of cranial Diabetes insipidus

A

Decreased secretion of ADH from posterior pituitary

  • Trauma
  • “DIDMOAD syndrome
155
Q

Causes of nephrogenic Diabetes insipidus

A

Impaired response to ADH in the kidneys

  • Inherited
  • Lithium
  • Chronic renal disease
156
Q

DIDMOAD

A

(DI+DM+optic atrophy+deafness)

157
Q

The two types of Diabetes insipidus

A

Cranial and nephrogenic

158
Q

Clinical features of Diabetes insipidus

A

o Polyuria
o Polydipsea
o Dehydration
o Hypernatraemia

159
Q

Investigations for Diabetes insipidus

A

o Increased sodium
o Increased serum Osmolarity
o Decreased urine Osmolarity (because the kidneys aren’t able to concentrate the urine by reabsorbing the water in nephrogenic)

160
Q

Diagnosis of Diabetes insipidus

A

Water deprivation test - the normal response to deprivation is to increase the action of ADH and produce more concentrated urine

Give desmopressin (synthetic ADH) then measure urine Osmolarity to differentiate between cranial and nephrogenic DI.

161
Q

How to differentiate between cranial and nephrogenic DI?

A

Give desmopressin (synthetic ADH) then measure urine Osmolarity

> 

If urine Osmolarity fails to increase its nephrogenic DI

> 

If urine Osmolarity increases then its cranial DI

Endocrinology (3 decks)

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