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
What makes Cushing's syndrome due to an adrenal tumour more likely?
If plasma ACTH is reduced by dexamethasone suppression test but patient is Cushingoid
26
How is an adrenal tumour investigated?
CT adrenal glands, if no mass found then do adrenal vein sampling or adrenal scintography
27
If the ACTH on dexamethasone suppression is low but the patient is still Cushingoid what is the differential?
Pituitary cause | Ectopic ACTH production
28
How do you differentiate between a pituitary cause and ectopic ACTH production?
Give high dose dexamethasone or CRH test. If cortisol is raised then there is a pituitary disease.
29
What is Cushing's disease?
Excess ACTH from anterior pituitary causing Cushing's syndrome
30
What is the problem when using an MRI on pituitary tumours?
Only 70 percent detected as they are very small
31
How is iatrogenic Cushing's syndrome treated?
Stop steroids
32
How is Cushing's disease treated?
Removal of pituitary adenoma | Bilateral adrenalectomy if the source of ACTH is undetectable or recurrent post op
33
How is adrenal adenoma treated?
Adrenalectomy
34
How is adrenal carcinoma treated?
Adrenalectomy + radiotherapy + mitotane (adrenalolytic)
35
How is ectopic ACTH production treated?
Surgery if tumour hasn't spread | Metyrapone, ketoconazole and fluconzole post operatively
36
What is Addison's disease?
Primary adrenocorticoid insufficiency so not enough corticosteroids and adrenocorticoids (e.g. aldosterone) are made
37
What are main causes of Addison's?
80 percent autoimmune TB Adrenal mets Adrenal haemorrhage -Waterhouse Friederichsen syndrome
38
How do Addison's symptoms develop?
Gradually
39
What are the symptoms of Addison's?
``` 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) ```
40
How does aldosterone work?
Regulates BP by acting on distal tubes to enhance sodium and water reabsorption and secrete potassium into urine
41
Which hormone has the opposite function to aldosterone?
ANP
42
Which organ releases ANP?
The heart
43
What the signs of Addison's?
Low BP +/- orthostatic hypotension Hyper pigmentation Other autoimmune conditions such as T1DM, Hashimoto's thyroiditis and vitiligo
44
Why is there hyper pigmentation in Addison's?
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.
45
What is autoimmune polyendocrine syndrome?
Addison's plus at least one of: T1DM, Hashimoto's thyroiditis or vitiligo
46
What is the maintenance therapy of Addison's?
Lifelong hydrocortisone/prednisolone tablets in a dosing regimen that mimics physiological release +/- fludrocortisone (to replace aldosterone)
47
Which features suggest hypoaldosteronism?
Hyponatremia and hyperkalemia
48
Which signs are suggestive of Addison's disease?
``` Hypercalcaemia Hypoglycaemia Eospinophila and lymphocytosis Metabolic acidosis due to hydrogen ion retention Signs of hypoaldosteronism ```
49
On which receptor does aldosterone act?
Na/K pump in the collecting tubule
50
How is Addison's diagnosed?
Synacthen test (ACTH stimulation test) - cortisol levels should not rise when tetracosactide is given
51
What is an Addisonian crisis?
Severe acute adrenal insufficiency
52
What the signs of an Addisonian crisis?
``` Confusion Lethargy Syncope Hyponatremia Hypercalcaemia Severe vomiting and diarrhoea leading to dehydration low BP Hypokalemia Convulsions Fever Penetrating lower body pain ```
53
What is the management of an Addisonian crisis?
Fluids Emergency stat cortisol Fludrocortisone can be given Give emergency pack
54
What is diabetes incipidus?
Extreme thirst due to lack of renal vasopressin (ADH) production
55
How does ADH work?
Increases water reabsorption in the distal tubule and collecting duct by increasing sodium reabsorption across the loop of Henle
56
How is hyponatremia treated?
Fluid restrict and give saline
57
At what point does hyponatremia become severe?
Na
58
What is the link between sodium levels and dehydration?
ECF volume is determined by sodium levels | Salt loss presents earlier than water loss
59
What is an isolated high urea suggestive of?
Upper GI bleed
60
What is an isolated high urea suggestive of in the absence of an upper GI bleed?
ECF depletion
61
What the key clinical signs in hyponatremia?
Postural hypotension Normal JVP Oedema
62
What are the clinical signs of SIADH?
Euvolemic Truly hypotonic plasma Very concentrated urine
63
What is the pathogenesis of SIADH?
Excess ADH from posterior pituitary so excess water retention and dilution of plasma solutes
64
How is SIADH treated?
No saline - already excess H2O Fluid restrict Can give steroids if needed Stop drugs if needed
65
How can you tell there is not renal loss of sodium (and only gut loss) in hyponatremia?
No sodium in the urine
66
What is the diagnosis if the patient has no sodium in the urine with hyponatremia?
SIADH
67
What potential conditions may be present with renal loss of sodium in hyponatremia?
Addisons | Kidney disease causing sodium loss
68
What is Conns syndrome?
Excess ADH production from the adrenal glands (primary aldosteronism)
69
What is the main cause of Conn's?
66 percent - adrenal gland hyperplasia | 33 percent adrenal adenoma
70
How is Conn's diagnosed?
High aldosterone to renin ratio and then do a CT to look for adrenal masses
71
How is Conn's treated?
Spironolactone or eplerenone that blocks ADH function | Adrenalectomy if this doesn't work
72
How does PTH work?
Upregulates osteoclast activity to release calcium into blood from bones
73
How does PTH stimulate osteoclasts?
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
What role does PTH have in regards to vitamin D?
Activates vitamin D in the kidneys | Increases calcium absorption in the gut through this binding via calbindin
75
How does PTH increase renal absorption of calcium?
Acts on distal tubules and collecting tubules to enhance calcium reabsorption
76
How does PTH influence phosphate reabsorption in the kidney?
Decreases phosphate reabsorption in tubular fluid so more lost in urine
77
Why is there only a small drop in phosphate with a rise in PTH?
When bones are broken down some phosphate is released | PTH increases phosphate reabsorption from the kidneys
78
How is PTH secretion stimulated?
Low serum calcium (negative feedback) | High phosphate has some inhibitory effect
79
How is the serum calcium sensed in regard to PTH secretion?
Specific calcium sensing receptors on chief cells
80
Can even slight changes in serum calcium cause maximum PTH secretion?
Yes
81
What is primary hyperparathyroidism?
Hyper function of parathyroid glands themselves causing raised PTH
82
What can cause primary hyperparathyroidism?
Parathyroid adenoma, parathyroid hyperplasia, parathyroid carcinoma (rare)
83
What do bloods tests show in primary hyperparathyroidism?
Raised calcium/ raised PTH/ raised Alk phos/ raised phosphate (unless in renal failure)
84
What would urine tests show in primary hyperparathyroidism?
Raised calcium
85
What symptoms characterise the symptoms of primary hyperparathyroidism?
Stones, moans, groans and psychiatric overtones (kidney stones, hypercalcaemia, constipation, peptic ulcers and depression)
86
What are the less common signs of primary hyperparathyroidism?
``` Thirst and dehydration Abdo pain Pancreatitis Osteoporosis and osteopenia (maybe pathological fractures) Raised BP ```
87
What percentage of primary hyperparathyroidism cases are adenomas?
80 percent
88
What percentage of primary hyperparathyroidism cases are hyperplasia?
20 percent
89
What may be seen on imagining with primary hyperparathyroidism?
``` Subperiosteal cysts Erosions Browns tumours of the phalanges +/- acrosteolysis +/- pepper pot skull ```
90
Which scan is used to diagnose osteoporosis?
DEXA
91
What is the treatment for primary hyperparathyroidism?
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
What are the complications of parathyroid surgery?
Hypoparathyroidism Hoarse voice to recurrent laryngeal nerve damage Low calcium symptoms (hungry bones syndrome)
93
How do blood results look with secondary hyperparathyroidism?
Low calcium and raised PTH
94
What is the treatment for secondary hyperparathyroidism?
phosphate binders and vitamin D +/- cincalet
95
How does cincalet work?
Raises the sensitivity of parathyroid cells to calcium so there is decreased PTH secretion
96
How doe blood results look with tertiary hyperparathyroidism?
Raised calcium with a very high PTH
97
What is the pathogenesis of tertiary hyperparathyroidism?
Prolonged secondary hyperparathyroidism causes the glands to act autonomously after undergoing hyper plastic or adenomatous change
98
In which patients is tertiary hyperparathyroidism more common?
CKD patients
99
What do blood tests show in malignant hyperparathyroidism?
Raised calcium with low PTH
100
What is the pathogenesis of malignant hyperparathyroidism?
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
What can cause elevated prolactin levels?
Micro/macro prolactinoma, anti emetics, anti psychotics, hypothyroidism, pregnancy, lactation, pituitary stalk compression
102
What symptoms may be present in a prolactinoma?
Amenorrhoea, infertility, galactorrhoea and impotence
103
What are the signs of prolactinoma?
Galactorrhoea | Visual field defects due to compression of optic chiasm
104
What do blood tests show in prolactinoma?
Very high prolactin levels Rule out thyroid involvement with TSH (high TSH raises prolactin) MRI of pituitary (MRI more sensitive)
105
Which imaging modality is used to diagnose prolactinoma?
MRI pituitary
106
How is a prolactinoma treated?
Dopamine agonist -bromocriptine, cabergoline, peroglide | Surgery - if pharmacological treatment unsuccessful
107
What symptoms are present in acromegaly?
``` Headaches Arthralgia Sweating Increased ring or shoe size Weakness Diabetes Carpal tunnel syndrome ```
108
What signs are present in acromegaly?
Prognathism, spade hands, prominent supraorbital ridge, bitemporal hemaniopia, hypertension
109
What is the pathogenesis of acromegaly?
Increased growth hormone from pituitary | Usually due to somatotroph derived prolactinoma
110
What makes acromegaly hard to diagnose?
Slow progression and onset of symptoms makes it hard to diagnose early
111
How is a diagnosis of acromegaly made?
IGF 1 screening Glucose tolerance test - GH levels not suppressed enough indicates acromegaly to confirm MRI pituitary
112
How is acromegaly treated?
Somatostatin analogue - octreotide | Surgery
113
What is the blood supply to the thyroid?
Superior and inferior thyroid arteries
114
What is the normal weight of the thyroid?
10 - 20g
115
What is the cellular structure of the thyroid?
Follicular cells around a colloid pool
116
What is the role of C cells in the thyroid?
To produce calcitonin
117
Where is T4 made?
In the thyroid gland - deiodinated in the periphery to T3
118
How does T3 enter cells?
Diffuses through cell membranes
119
How does T3 work?
Binds to nuclear receptors to alter gene transcription
120
What are the roles of T3?
To raise BMR Increase sensitivity to catecholamines Important role in fetal neural development
121
How does thyrotoxicosis affect tendon reflexes?
Brisk reflexes
122
How does hypothyroidism affect tendon reflexes?
Slow relaxing reflexes
123
What heart conditions may be precipitated by thyrotoxicosis?
AF | Palpitations
124
What may be present in the history with thyrotoxicosis?
Other autoimmune conditions
125
What drugs can lead to thyrotoxicosis?
Amiodarone Lithium Interferon Retrovirals
126
What is the first line investigation in thyrotoxicosis and what does it show?
TFTs show high T4/T3 and low TSH
127
What test can be used to confirm a diagnosis of Grave's disease?
Thyroid stimulating immunoglobulin | TPO antibodies
128
Which antibodies are often a marker of autoimmune disease, including Grave's?
Gastric parietal antibodies
129
What is the most common cause of thyrotoxicosis?
Grave's disease
130
Other than Grave's, what else can cause thyrotoxicosis?
``` Toxic multi nodular goitre Toxic adenoma Restrictive thyroiditis Excess iodine (Jod-Basedow) Drugs Thyroid hormone resistance TSH producing tumour (rare) ```
131
What bloods results are seen in thyrotoxicosis due to a TSH producing tumour?
Raised T3/T4 AND raised TSH
132
What is Grave's disease?
``` Autoimmune condition causing one of: thyroid dysfunction (through thyroid stimulating antibodies) opthalmopathy pre tibial myxoedema acropatchy ```
133
How may a goitre appear in Grave's?
Diffuse, smooth goitre with a bruit
134
What are the features of Grave's opthalmopathy?
``` Diplopia Exophthalmos Reduced acuity Tearfulness and grittiness Proptosis Lid lag Loss of colour vision Retraction ```
135
How should Grave's be investigated?
TFTs and MRI orbit (look for periorbital oedema)
136
How is Grave's disease treated?
Steroids | Surgery/radiotherapy may be needed
137
What is the first line treatment for thyrotoxicosis?
Carbimazole (+/- propylthiouracil)
138
What the side effects of carbimazole?
Rash - 1 in 100 agranulocytosis -1 in 1000 sore throat
139
What is the second line therapy for thyrotoxicosis?
Radioiodine abalation
140
What are the potential side effects of using radio iodine?
Radioactivity Hypothyroidism Thyroid eye disease
141
When should surgery be done in thyrotoxicosis?
In the presence of a large goitre
142
What are the potential risks of a thyroidectomy?
Hoarseness of voice due to damage to the recurrent laryngeal nerve Hypothyroidism (+/- hypoparathyroidism)
143
What are common features in a hypothyroid history?
``` Tired Cold Weight gain Dry skin and hair Myxoedema coma ```
144
How do TFTs appear in primary hypothyroidism?
Raised TSH and low T3/T4
145
Which other blood test may appear low in hypothyroidism other than TFTs?
Cortisol
146
Which blood test can confirm Hashimoto's?
TPO antibody positive
147
What are the causes of hypothyroidism?
``` Congenital (1 in 400) Iodine deficiency Hashimoto's Iatrogenic Post partum thyroiditis ```
148
What is the treatment for hypothyroidism?
Levothyroxine (synthetic T4)
149
How does poor levothyroxine compliance show on TFTs?
High TSH with normal T3/T4
150
What are the clinical features of a toxic multi nodular goitre?
``` Thyrotoxicosis Fast growing lump in the neck with sudden enlargement or pain May have retrosternal extension Dysphagia Cough/dyspnoea/stridor ```
151
What primary investigations are relevant in toxic multi nodular goitre?
TFTs Lung function to assess airway compromise CXR (maybe with thoracic inlet views)
152
How is the diagnosis of a toxic multi nodular goitre confirmed?
Ultrasound scan with fine needle aspiration | CT (without contrast)
153
What is the first line treatment in toxic multi nodular goitre?
Watch and wait (especially if comorbidities present)
154
What secondary treatment options for toxic mulitnodular goitre?
Surgery or radioiodine
155
What the specify signs and symptoms of thyroid cancer/neoplasia?
``` Slowly enlarging mass Unilateral Soft and fluctuant mass Asymptomatic History of radiation exposure ```
156
Which investigations should be done in suspected thyroid malignancy?
CXR Calcitonin (raised in medullary thyroid cancer - rare) USS with fine needle aspiration
157
How is thyroid cancer treated?
Near total thyroidectomy with adjuvant iodine 131 abalation (+/- external beam radiotherapy)
158
Which treatment in thyroid cancer will help to confirm the histology?
Near total thyroidectomy
159
What is the post operative treatment following thyroidectomy in thyroid cancer?
High does thyroxine to suppress TSH and therefore recurrence
160
What acts a good tumour marker in thyroid cancer?
Rising serum thyroglobulin
161
What is the role of an iodine tracer in thyroid cancer?
Monitoring
162
What is a non-malignant form of thyroid neoplasia?
Follicular adenoma
163
How is papillary thyroid cancer spread?
Lymphatics
164
How is follicular thyroid cancer spread?
Blood
165
Which thyroid cancer is linked to MEN2?
Medullary
166
In which is it rare to have manifestations in the thyroid?
Lymphoma
167
Which thyroid cancer has the worst prognosis?
Aplastic
168
What is the 10 year disease free rate in papillary and follicular thyroid cancers?
Over 90 percent