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Met 3b > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Does the pituitary lie outside of the dura?

A

Yes

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2
Q

How can the pituitary be accessed?

A

Through the sphenoid bones

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3
Q

Which artery supplies the posterior pituitary?

A

Inferior hypophyseal artery

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4
Q

Which vein drains the posterior pituitary?

A

Inferior hypophyseal vein

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5
Q

Which hormones are secreted by the posterior pituitary?

A

Vasopressin

Oxytocin

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6
Q

What supplies blood to the anterior pituitary?

A

Capillary plexus with a high concentration of releasing hormones

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7
Q

Which hormones are released by the anterior pituitary?

A

ACTH, TSH, GH, CH, FSH, PRL

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8
Q

What is made in the adrenal cortex?

A

Steroid hormones (cortisol, aldosterone and androgens)

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9
Q

Which histological zones are located in the cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

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10
Q

What is made in the adrenal medulla?

A

catecholamines e.g. adrenaline

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11
Q

What is the role of the HPA axis?

A

Maintains homeostasis in real or perceived stress

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12
Q

On what systems does cortisol act?

A

Metabolic, cardiovascular, immune, CNS

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13
Q

On what receptors do glucocorticoids act on?

A

Glucocorticoid receptors

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14
Q

How is glucocorticoid activity (duration and magnitude) regulated?

A

GR expression

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15
Q

How are GR distributed in the body?

A

Widely through the brain and peripheral tissue

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16
Q

What is Cushing’s syndrome?

A

Excess cortisol

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17
Q

What is the most common cause of Cushing’s syndrome?

A

Iatrogenic administration of steroids

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18
Q

What is the most common cause of Cushing’s syndrome?

A

Raised ACTH usually due to pituitary adenoma (Cushing’s disease)

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19
Q

What are potential endogenous causes of Cushing’s syndrome?

A

Cushing’s disease
Paraneoplastic syndromes
Adrenal adenoma/cancer
Adrenal nodular hyperplasia

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20
Q

How can it be told that Cushing’s syndrome is due to a paraneoplastic cause?

A

ACTH is not surpassed by dexamethasone

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21
Q

What are the symptoms of Cushing’s syndrome?

A 
Weight gain
Mood change
Proximal weakness
Gonadal dysfunction 
Tendon rupture and thickening
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22
Q

What are the signs of Cushing’s syndrome?

A 
Central obesity
Moon face
Buffalo hump
Supraclavicular fat
Muscle atrophy
Purple abdominal striae
Osteoporosis
Raised BP
Raised blood glucose
Infection prone and poor healing
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23
Q

What is the initial test if Cushing’s syndrome is suspected?

A

Midnight cortisol or 24 hr cortisol urine test

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24
Q

How is a diagnosis of Cushing’s syndrome confirmed?

A

Short dexamethasone suppression test - check cortisol at 8am and there is no suppression Cushing’s syndrome

48 hour dexamethasone suppression test - check midnight cortisol

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25
Q

What makes Cushing’s syndrome due to an adrenal tumour more likely?

A

If plasma ACTH is reduced by dexamethasone suppression test but patient is Cushingoid

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26
Q

How is an adrenal tumour investigated?

A

CT adrenal glands, if no mass found then do adrenal vein sampling or adrenal scintography

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27
Q

If the ACTH on dexamethasone suppression is low but the patient is still Cushingoid what is the differential?

A

Pituitary cause

Ectopic ACTH production

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28
Q

How do you differentiate between a pituitary cause and ectopic ACTH production?

A

Give high dose dexamethasone or CRH test. If cortisol is raised then there is a pituitary disease.

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29
Q

What is Cushing’s disease?

A

Excess ACTH from anterior pituitary causing Cushing’s syndrome

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30
Q

What is the problem when using an MRI on pituitary tumours?

A

Only 70 percent detected as they are very small

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31
Q

How is iatrogenic Cushing’s syndrome treated?

A

Stop steroids

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32
Q

How is Cushing’s disease treated?

A

Removal of pituitary adenoma

Bilateral adrenalectomy if the source of ACTH is undetectable or recurrent post op

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33
Q

How is adrenal adenoma treated?

A

Adrenalectomy

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34
Q

How is adrenal carcinoma treated?

A

Adrenalectomy + radiotherapy + mitotane (adrenalolytic)

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35
Q

How is ectopic ACTH production treated?

A

Surgery if tumour hasn’t spread

Metyrapone, ketoconazole and fluconzole post operatively

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36
Q

What is Addison’s disease?

A

Primary adrenocorticoid insufficiency so not enough corticosteroids and adrenocorticoids (e.g. aldosterone) are made

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37
Q

What are main causes of Addison’s?

A

80 percent autoimmune
TB
Adrenal mets
Adrenal haemorrhage -Waterhouse Friederichsen syndrome

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38
Q

How do Addison’s symptoms develop?

A

Gradually

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39
Q

What are the symptoms of Addison’s?

A 
Nausea, vomiting, diarrhoea and sweating
Salt cravings due to sodium loss in urine
Fatigue, light headedness, dizziness
Hyper pigmentation
Muscle weakness and pain
Weight loss
Changes in mood/ personality
Darkening of palmar crease/recent scars (not seen in secondary or tertiary adrenal insufficiency)
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40
Q

How does aldosterone work?

A

Regulates BP by acting on distal tubes to enhance sodium and water reabsorption and secrete potassium into urine

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41
Q

Which hormone has the opposite function to aldosterone?

A

ANP

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42
Q

Which organ releases ANP?

A

The heart

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43
Q

What the signs of Addison’s?

A

Low BP +/- orthostatic hypotension
Hyper pigmentation
Other autoimmune conditions such as T1DM, Hashimoto’s thyroiditis and vitiligo

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44
Q

Why is there hyper pigmentation in Addison’s?

A

Melanocyte stimulating hormone (MCH) and ACTH have the same precursor molecule (POMC). POMC gets cleaved in the anterior pituitary to get MSH, ACTH and beta lipotrophin.

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45
Q

What is autoimmune polyendocrine syndrome?

A

Addison’s plus at least one of: T1DM, Hashimoto’s thyroiditis or vitiligo

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46
Q

What is the maintenance therapy of Addison’s?

A

Lifelong hydrocortisone/prednisolone tablets in a dosing regimen that mimics physiological release
+/- fludrocortisone (to replace aldosterone)

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47
Q

Which features suggest hypoaldosteronism?

A

Hyponatremia and hyperkalemia

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48
Q

Which signs are suggestive of Addison’s disease?

A 
Hypercalcaemia
Hypoglycaemia
Eospinophila and lymphocytosis
Metabolic acidosis due to hydrogen ion retention
Signs of hypoaldosteronism
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49
Q

On which receptor does aldosterone act?

A

Na/K pump in the collecting tubule

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50
Q

How is Addison’s diagnosed?

A

Synacthen test (ACTH stimulation test) - cortisol levels should not rise when tetracosactide is given

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51
Q

What is an Addisonian crisis?

A

Severe acute adrenal insufficiency

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52
Q

What the signs of an Addisonian crisis?

A 
Confusion
Lethargy
Syncope
Hyponatremia
Hypercalcaemia
Severe vomiting and diarrhoea leading to dehydration
low BP
Hypokalemia
Convulsions
Fever
Penetrating lower body pain
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53
Q

What is the management of an Addisonian crisis?

A

Fluids
Emergency stat cortisol
Fludrocortisone can be given
Give emergency pack

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54
Q

What is diabetes incipidus?

A

Extreme thirst due to lack of renal vasopressin (ADH) production

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55
Q

How does ADH work?

A

Increases water reabsorption in the distal tubule and collecting duct by increasing sodium reabsorption across the loop of Henle

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56
Q

How is hyponatremia treated?

A

Fluid restrict and give saline

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57
Q

At what point does hyponatremia become severe?

A

Na

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58
Q

What is the link between sodium levels and dehydration?

A

ECF volume is determined by sodium levels

Salt loss presents earlier than water loss

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59
Q

What is an isolated high urea suggestive of?

A

Upper GI bleed

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60
Q

What is an isolated high urea suggestive of in the absence of an upper GI bleed?

A

ECF depletion

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61
Q

What the key clinical signs in hyponatremia?

A

Postural hypotension
Normal JVP
Oedema

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62
Q

What are the clinical signs of SIADH?

A

Euvolemic
Truly hypotonic plasma
Very concentrated urine

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63
Q

What is the pathogenesis of SIADH?

A

Excess ADH from posterior pituitary so excess water retention and dilution of plasma solutes

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64
Q

How is SIADH treated?

A

No saline - already excess H2O
Fluid restrict
Can give steroids if needed
Stop drugs if needed

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65
Q

How can you tell there is not renal loss of sodium (and only gut loss) in hyponatremia?

A

No sodium in the urine

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66
Q

What is the diagnosis if the patient has no sodium in the urine with hyponatremia?

A

SIADH

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67
Q

What potential conditions may be present with renal loss of sodium in hyponatremia?

A

Addisons

Kidney disease causing sodium loss

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68
Q

What is Conns syndrome?

A

Excess ADH production from the adrenal glands (primary aldosteronism)

69
Q

What is the main cause of Conn’s?

A

66 percent - adrenal gland hyperplasia

33 percent adrenal adenoma

70
Q

How is Conn’s diagnosed?

A

High aldosterone to renin ratio and then do a CT to look for adrenal masses

71
Q

How is Conn’s treated?

A

Spironolactone or eplerenone that blocks ADH function

Adrenalectomy if this doesn’t work

72
Q

How does PTH work?

A

Upregulates osteoclast activity to release calcium into blood from bones

73
Q

How does PTH stimulate osteoclasts?

A

Indirectly, PTH binds to osteoblasts to increase RANKL expression and inhibit osteoprotegrin expression (that normally inhibits the binding of RANKL to RANK). RANKL binding stimulates osteoclast precursors to turn into osteoclasts

74
Q

What role does PTH have in regards to vitamin D?

A

Activates vitamin D in the kidneys

Increases calcium absorption in the gut through this binding via calbindin

75
Q

How does PTH increase renal absorption of calcium?

A

Acts on distal tubules and collecting tubules to enhance calcium reabsorption

76
Q

How does PTH influence phosphate reabsorption in the kidney?

A

Decreases phosphate reabsorption in tubular fluid so more lost in urine

77
Q

Why is there only a small drop in phosphate with a rise in PTH?

A

When bones are broken down some phosphate is released

PTH increases phosphate reabsorption from the kidneys

78
Q

How is PTH secretion stimulated?

A

Low serum calcium (negative feedback)

High phosphate has some inhibitory effect

79
Q

How is the serum calcium sensed in regard to PTH secretion?

A

Specific calcium sensing receptors on chief cells

80
Q

Can even slight changes in serum calcium cause maximum PTH secretion?

A

Yes

81
Q

What is primary hyperparathyroidism?

A

Hyper function of parathyroid glands themselves causing raised PTH

82
Q

What can cause primary hyperparathyroidism?

A

Parathyroid adenoma, parathyroid hyperplasia, parathyroid carcinoma (rare)

83
Q

What do bloods tests show in primary hyperparathyroidism?

A

Raised calcium/ raised PTH/ raised Alk phos/ raised phosphate (unless in renal failure)

84
Q

What would urine tests show in primary hyperparathyroidism?

A

Raised calcium

85
Q

What symptoms characterise the symptoms of primary hyperparathyroidism?

A

Stones, moans, groans and psychiatric overtones (kidney stones, hypercalcaemia, constipation, peptic ulcers and depression)

86
Q

What are the less common signs of primary hyperparathyroidism?

A 
Thirst and dehydration
Abdo pain
Pancreatitis
Osteoporosis and osteopenia (maybe pathological fractures) 
Raised BP
87
Q

What percentage of primary hyperparathyroidism cases are adenomas?

A

80 percent

88
Q

What percentage of primary hyperparathyroidism cases are hyperplasia?

A

20 percent

89
Q

What may be seen on imagining with primary hyperparathyroidism?

A 
Subperiosteal cysts
Erosions
Browns tumours of the phalanges
\+/- acrosteolysis
\+/- pepper pot skull
90
Q

Which scan is used to diagnose osteoporosis?

A

DEXA

91
Q

What is the treatment for primary hyperparathyroidism?

A

Mild - raise fluid intake to prevent stones + avoid thiazide diuretics + reduce intake of calcium and vitamin D
Severe - surgical removal or adenoma or parathyroidectomy - done if high urine or serum calcium, osteoporosis, bone disease, renal stones, decreased GFR and less than 50 years old

92
Q

What are the complications of parathyroid surgery?

A

Hypoparathyroidism
Hoarse voice to recurrent laryngeal nerve damage
Low calcium symptoms (hungry bones syndrome)

93
Q

How do blood results look with secondary hyperparathyroidism?

A

Low calcium and raised PTH

94
Q

What is the treatment for secondary hyperparathyroidism?

A

phosphate binders and vitamin D +/- cincalet

95
Q

How does cincalet work?

A

Raises the sensitivity of parathyroid cells to calcium so there is decreased PTH secretion

96
Q

How doe blood results look with tertiary hyperparathyroidism?

A

Raised calcium with a very high PTH

97
Q

What is the pathogenesis of tertiary hyperparathyroidism?

A

Prolonged secondary hyperparathyroidism causes the glands to act autonomously after undergoing hyper plastic or adenomatous change

98
Q

In which patients is tertiary hyperparathyroidism more common?

A

CKD patients

99
Q

What do blood tests show in malignant hyperparathyroidism?

A

Raised calcium with low PTH

100
Q

What is the pathogenesis of malignant hyperparathyroidism?

A

PTH-rp produced by some squamous cell lung cancers, breast and renal cell carcinomas - this mimics PTH
PTH is low as PTH-rp not detected by assay.

101
Q

What can cause elevated prolactin levels?

A

Micro/macro prolactinoma, anti emetics, anti psychotics, hypothyroidism, pregnancy, lactation, pituitary stalk compression

102
Q

What symptoms may be present in a prolactinoma?

A

Amenorrhoea, infertility, galactorrhoea and impotence

103
Q

What are the signs of prolactinoma?

A

Galactorrhoea

Visual field defects due to compression of optic chiasm

104
Q

What do blood tests show in prolactinoma?

A

Very high prolactin levels
Rule out thyroid involvement with TSH (high TSH raises prolactin)
MRI of pituitary (MRI more sensitive)

105
Q

Which imaging modality is used to diagnose prolactinoma?

A

MRI pituitary

106
Q

How is a prolactinoma treated?

A

Dopamine agonist -bromocriptine, cabergoline, peroglide

Surgery - if pharmacological treatment unsuccessful

107
Q

What symptoms are present in acromegaly?

A 
Headaches
Arthralgia
Sweating
Increased ring or shoe size
Weakness
Diabetes
Carpal tunnel syndrome
108
Q

What signs are present in acromegaly?

A

Prognathism, spade hands, prominent supraorbital ridge, bitemporal hemaniopia, hypertension

109
Q

What is the pathogenesis of acromegaly?

A

Increased growth hormone from pituitary

Usually due to somatotroph derived prolactinoma

110
Q

What makes acromegaly hard to diagnose?

A

Slow progression and onset of symptoms makes it hard to diagnose early

111
Q

How is a diagnosis of acromegaly made?

A

IGF 1 screening
Glucose tolerance test - GH levels not suppressed enough indicates acromegaly to confirm
MRI pituitary

112
Q

How is acromegaly treated?

A

Somatostatin analogue - octreotide

Surgery

113
Q

What is the blood supply to the thyroid?

A

Superior and inferior thyroid arteries

114
Q

What is the normal weight of the thyroid?

A

10 - 20g

115
Q

What is the cellular structure of the thyroid?

A

Follicular cells around a colloid pool

116
Q

What is the role of C cells in the thyroid?

A

To produce calcitonin

117
Q

Where is T4 made?

A

In the thyroid gland - deiodinated in the periphery to T3

118
Q

How does T3 enter cells?

A

Diffuses through cell membranes

119
Q

How does T3 work?

A

Binds to nuclear receptors to alter gene transcription

120
Q

What are the roles of T3?

A

To raise BMR
Increase sensitivity to catecholamines
Important role in fetal neural development

121
Q

How does thyrotoxicosis affect tendon reflexes?

A

Brisk reflexes

122
Q

How does hypothyroidism affect tendon reflexes?

A

Slow relaxing reflexes

123
Q

What heart conditions may be precipitated by thyrotoxicosis?

A

AF

Palpitations

124
Q

What may be present in the history with thyrotoxicosis?

A

Other autoimmune conditions

125
Q

What drugs can lead to thyrotoxicosis?

A

Amiodarone
Lithium
Interferon
Retrovirals

126
Q

What is the first line investigation in thyrotoxicosis and what does it show?

A

TFTs show high T4/T3 and low TSH

127
Q

What test can be used to confirm a diagnosis of Grave’s disease?

A

Thyroid stimulating immunoglobulin

TPO antibodies

128
Q

Which antibodies are often a marker of autoimmune disease, including Grave’s?

A

Gastric parietal antibodies

129
Q

What is the most common cause of thyrotoxicosis?

A

Grave’s disease

130
Q

Other than Grave’s, what else can cause thyrotoxicosis?

A 
Toxic multi nodular goitre
Toxic adenoma
Restrictive thyroiditis
Excess iodine (Jod-Basedow)
Drugs
Thyroid hormone resistance
TSH producing tumour (rare)
131
Q

What bloods results are seen in thyrotoxicosis due to a TSH producing tumour?

A

Raised T3/T4 AND raised TSH

132
Q

What is Grave’s disease?

A 
Autoimmune condition causing one of:
thyroid dysfunction (through thyroid stimulating antibodies)
opthalmopathy
pre tibial myxoedema
acropatchy
133
Q

How may a goitre appear in Grave’s?

A

Diffuse, smooth goitre with a bruit

134
Q

What are the features of Grave’s opthalmopathy?

A 
Diplopia
Exophthalmos
Reduced acuity
Tearfulness and grittiness
Proptosis
Lid lag
Loss of colour vision
Retraction
135
Q

How should Grave’s be investigated?

A

TFTs and MRI orbit (look for periorbital oedema)

136
Q

How is Grave’s disease treated?

A

Steroids

Surgery/radiotherapy may be needed

137
Q

What is the first line treatment for thyrotoxicosis?

A

Carbimazole (+/- propylthiouracil)

138
Q

What the side effects of carbimazole?

A

Rash - 1 in 100
agranulocytosis -1 in 1000
sore throat

139
Q

What is the second line therapy for thyrotoxicosis?

A

Radioiodine abalation

140
Q

What are the potential side effects of using radio iodine?

A

Radioactivity
Hypothyroidism
Thyroid eye disease

141
Q

When should surgery be done in thyrotoxicosis?

A

In the presence of a large goitre

142
Q

What are the potential risks of a thyroidectomy?

A

Hoarseness of voice due to damage to the recurrent laryngeal nerve
Hypothyroidism (+/- hypoparathyroidism)

143
Q

What are common features in a hypothyroid history?

A 
Tired
Cold
Weight gain
Dry skin and hair
Myxoedema coma
144
Q

How do TFTs appear in primary hypothyroidism?

A

Raised TSH and low T3/T4

145
Q

Which other blood test may appear low in hypothyroidism other than TFTs?

A

Cortisol

146
Q

Which blood test can confirm Hashimoto’s?

A

TPO antibody positive

147
Q

What are the causes of hypothyroidism?

A 
Congenital (1 in 400)
Iodine deficiency
Hashimoto's
Iatrogenic
Post partum thyroiditis
148
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (synthetic T4)

149
Q

How does poor levothyroxine compliance show on TFTs?

A

High TSH with normal T3/T4

150
Q

What are the clinical features of a toxic multi nodular goitre?

A 
Thyrotoxicosis
Fast growing lump in the neck with sudden enlargement or pain
May have retrosternal extension
Dysphagia
Cough/dyspnoea/stridor
151
Q

What primary investigations are relevant in toxic multi nodular goitre?

A

TFTs
Lung function to assess airway compromise
CXR (maybe with thoracic inlet views)

152
Q

How is the diagnosis of a toxic multi nodular goitre confirmed?

A

Ultrasound scan with fine needle aspiration

CT (without contrast)

153
Q

What is the first line treatment in toxic multi nodular goitre?

A

Watch and wait (especially if comorbidities present)

154
Q

What secondary treatment options for toxic mulitnodular goitre?

A

Surgery or radioiodine

155
Q

What the specify signs and symptoms of thyroid cancer/neoplasia?

A 
Slowly enlarging mass
Unilateral
Soft and fluctuant mass
Asymptomatic
History of radiation exposure
156
Q

Which investigations should be done in suspected thyroid malignancy?

A

CXR
Calcitonin (raised in medullary thyroid cancer - rare)
USS with fine needle aspiration

157
Q

How is thyroid cancer treated?

A

Near total thyroidectomy with adjuvant iodine 131 abalation (+/- external beam radiotherapy)

158
Q

Which treatment in thyroid cancer will help to confirm the histology?

A

Near total thyroidectomy

159
Q

What is the post operative treatment following thyroidectomy in thyroid cancer?

A

High does thyroxine to suppress TSH and therefore recurrence

160
Q

What acts a good tumour marker in thyroid cancer?

A

Rising serum thyroglobulin

161
Q

What is the role of an iodine tracer in thyroid cancer?

A

Monitoring

162
Q

What is a non-malignant form of thyroid neoplasia?

A

Follicular adenoma

163
Q

How is papillary thyroid cancer spread?

A

Lymphatics

164
Q

How is follicular thyroid cancer spread?

A

Blood

165
Q

Which thyroid cancer is linked to MEN2?

A

Medullary

166
Q

In which is it rare to have manifestations in the thyroid?

A

Lymphoma

167
Q

Which thyroid cancer has the worst prognosis?

A

Aplastic

168
Q

What is the 10 year disease free rate in papillary and follicular thyroid cancers?

A

Over 90 percent

Met 3b (5 decks)

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