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MBChB > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What hormones are released from the anterior pituitary?

A

ACTH
TSH
LH/FSH
GH

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2
Q

What hormones are released from the posterior pituitary?

A

Prolactin

ADH

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3
Q

What visual disturbance is caused by compression of the optic chiasm?

A

Bitemporal hemianopia

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4
Q

What are the different types of pituitary tumours?

A

Non-functional
Functional
Other

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5
Q

What are the effects of functional pituitary tumours?

A

Prolactin - prolactinoma
GH - acromegaly
ACTH - Cushing’s disease
TSH - TSHoma

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6
Q

Give three examples of ‘other’ pituitary tumours

A

Craniopharyngioma
Pituitary cancer
Rathke’s cyst

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7
Q

Describe non-functional pituitary tumours

A 
Most common (25%)
No hormonal releases
Mass effects
- visual field defects
- headache
- stops other pituitary hormones working
- eye movement problems due to involvement of cranial nerves --> blurred vision
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8
Q

How should non-functioning pituitary tumours be investigated?

A

Imaging - MRI
Visual field assessment
Measure pituitary hormones

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9
Q

How should non-functioning pituitary tumours be managed?

A

Surgery - protection of vision

Radiotherapy

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10
Q

Describe hypopituitarism

A

Failure of the (anterior) pituitary
Can affect a single hormonal axis or all hormones (panhypopituitarism)
Leads to secondary gonadal/thyroid/adrenal failure
Need multiple hormone replacement

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11
Q

In hypopituitarism, what hormonal replacement therapy should always be started first?

A

Hydrocortisone

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12
Q

Give some potential causes of hypopituitarism

A 
Tumours
Radiotherapy
Infarction/haemorrhage (apoplexy)
Infiltrate (sarcoid)
Trauma
Lymphocytic hypophysitis
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13
Q

What are potential causes of high prolactin?

A

Prolactinomas
Physiological - pregnancy, breast feeding
Drugs that block dopamine
Stalk effect - loss of inhibitory dopamine

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14
Q

Give examples of drugs that block dopamine

A

Tricyclics
Antiemetics
Antipsychotics

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15
Q

What is a prolactinoma?

A

Pituitary tumour that secretes prolactin

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16
Q

What are the clinical features of a prolactinoma?

A 
Galactorrhoea
Headaches
Mass effects
Visual field defects
Amenorrhoea/erectile dysfunction
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17
Q

Describe the diagnosis of prolactinoma

A 
Serum prolactin (>6000)
MRI pituitary
Test remaining pituitary function
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18
Q

Describe the treatment of a prolactinoma

A

Medical:
Dopamine agonist - cabergoline, bromocriptine

Surgical:
VF compromised
Failure of medical therapy

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19
Q

Describe the association of prolactinomas and pregnancy

A

Pituitary gland get bigger in pregnancy - increase in prolactin production

Dopamine agonists are contraindicated
[Prolactin] is unhelpful
Monitor visual fields if macroprolactinoma

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20
Q

Describe acromegaly

A

Pituitary tumour secreting growth hormone post puberty

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21
Q

What are the clinical features of acromegaly?

A 
Sweats and headaches
Alteration of facial features
Increased hand/feet size
Visual impairment
Cardiomegaly
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22
Q

Describe the diagnosis of acromegaly

A

Glucose tolerance test (glucose should suppress GH)
Measure IGF-1 (GH stimulates liver to produce IGF-1)
MRI

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23
Q

Describe the management of acromegaly

A

Surgery - first line to debulk tumour

Drugs:
Somatostatin analogue - octreotide (before and after surgery)
Dopamine agonist
GH receptor antagonist (Pegvisomant)

Radiotherapy - residual tumour/ongoing symptoms

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24
Q

Describe Cushing’s disease

A

Pituitary tumour secreting ACTH

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25
Q

What are the symptoms of Cushing’s disease?

A 
Weight gain 
Thin skin 
Easy bruising
Hypertension
Osteoporosis
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26
Q

How can Cushing’s disease be diagnosed?

A

Try to suppress ACTH by dexamethasone suppression therapy

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27
Q

Describe the management of Cushing’s disease

A

Surgery first line

If fails or inappropriate:
Bilateral adrenalectomy
Medical therapy - metyrapone, ketoconazole
Radiotherapy

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28
Q

Describe TSHoma

A

Rare pituitary tumour releasing TSH

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29
Q

What TFT results are associated with TSHoma?

A

High TSH

High fT4

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30
Q

What are the two types of Diabetes Inspidus?

A

Central

Nephrogenic

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31
Q

What are potential central causes of diabetes insidius?

A 
Idiopathic
Trauma
Pituitary tumour
Pituitary surgery
Pregnancy
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32
Q

What are the clinical features of diabetes inspidus?

A

Polydipsia

Polyuria (>3L/d urine output)

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33
Q

Describe the diagnosis of diabetes inspidus

A

Try to stimulate the release
Water deprivation test
Assess ability to concentrate urine with ADH (nephrogenic won’t)

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34
Q

What is diabetes inspidus?

A

ADH deficiency

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35
Q

Describe the treatment of diabetes inspidus

A

Treat underlying cause

ddAVP (spray, tablets, injection)

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36
Q

What are the layers of the adrenal cortex, and what does each layer produce?

A

Zona Glomerulosa = aldosterone
Zona Fasciculata = cortisol
Zona Reticularis = androgens

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37
Q

What cells are located in the adrenal medulla, and what do they produce?

A

Chromograffin cells

Catecholamines

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38
Q

What features are commonly associated with primary aldosteronism (Conn’s syndrome)?

A

Hypertension

Hypokalaemia

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39
Q

What biochemistry is associated with primary aldosteronism (Conn’s syndrome)?

A

High aldosterone
Low renin
Very high aldosterone:renin ratio

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40
Q

What medications should be stopped if a patient is thought to have primary aldosteronism (Conn’s syndrome)?

A

Beta blockers

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41
Q

What medications can be used in patients who have primary aldosteronism (Conn’s syndrome)?

A

Alpha blockers
Verapamil
Hydralazine

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42
Q

How is primary aldosteronism (Conn’s syndrome) diagnosed?

A

Saline suppression test
2L of saline over 4 hours (should suppress aldosterone production)
4h aldosterone >470pmol/l = highly suspicious

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43
Q

Describe the management of primary aldosteronism (Conn’s syndrome)

A

Surgical:
Unilateral laparoscopic adrenalectomy - if adrenal adenoma
Cures hypokalaemia
Cures HTN in 30-70%

Medical:
MR antagonist (spironolactone/eplerenone)
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44
Q

What are the clinical features associated with Cushing’s syndrome?

A 
Hirsutism
Striae
Proximal myopathy
Plethora
Easy bruising
HTN
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45
Q

Describe the diagnosis of Cushing’s syndrome

A

24h urinary free cortisol
Dexamethasone suppression testing
Late night salivary cortisol (cortisol should be at its lowest levels during the night)

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46
Q

What are the causes of Cushing’s syndrome?

A

ACTH dependent:
Pituitary adenoma = Cushing’s disease
Ectopic ACTH
Ectopic CRH

ACTH independent:
Adrenal adenoma
Adrenal carcinoma
Nodular hyperplasia

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47
Q

What is the mode of inheritance of congenital adrenal hyperplasia?

A

Autosomal recessive

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48
Q

Define congenital adrenal hyperplasia

A

Range of genetic disorders relating to defects in steroidogenic genes

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49
Q

What is the most common gene which is mutated in congenital adrenal hyperplasia?

A

CYP21 (21 hydroxylase)

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50
Q

What happens to hormone levels in congenital adrenal hyperplasia?

A

Aldosterone and cortisol not produced

Increased androgen and 17-OH progesterone

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51
Q

What are the effects on males and females in congenital adrenal hyperplasia?

A

Males: adrenal crisis (hypotension, hyponatraemia), early virilization

Females: ambiguous genitals

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52
Q

What is the management of congenital adrenal hyperplasia?

A

Mineralocorticoid and glucocorticoid replacement

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53
Q

What are the signs and symptoms of phaechromocytoma?

A

HTN
Episodes of headaches, palpitations, pallor, sweating
Tremor, anxiety, N&V, chest/adbo pain

Crisis last ~15 mins
Generally otherwise well

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54
Q

What are the causes of phaechromocytoma?

A

Genetics - 25%
Malignancy - 15-20%
Benign - 80-85%

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55
Q

What genetics are associated with phaechromocytoma?

A

MEN, VHL, SDHB & SDHD mutations,

Neurofibromatosis

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56
Q

Describe the pre-operative treatment of phaechromocytoma

A

Alpha blockers initially
(Phenoxybenzamine/doxazosin)
Aim for SBP <120mmHg

Beta blockers if tachycardic
Labetolol, bisopropol

Encourage salt intake (maintain fluid status)

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57
Q

Define adrenal insufficiency

A

Inadequate adrenocortical function

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58
Q

What are the clinical features of adrenal insufficiency?

A 
Anorexia, weight loss
Fatigue, lethargy
Dizziness, hypotension
Abdo pain, vomiting, diarrhoea
Skin pigmentation
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59
Q

What is the ‘suspicious biochemistry’ associated with adrenal insufficiency?

A

Low Na
High K
Hypoglycaemia

60
Q

What test can be used to assess whether a patient has adrenal insufficiency?

A

Short SynACTHen test
Measure plasma cortisol levels before and 30m after IV ACTH injection

Normal: baseline >250nmol/L, post ACTH >480nmol/L

61
Q

What ACTH, renin and aldosterone levels are associated with adrenal insufficiency?

A

High ACTH
High Renin
Low Aldosterone

62
Q

Give three functions of Ca

A 
Muscle contraction
Bone growth and remodelling
Second messenger signalling
Stabilising of membranes
Enzyme co-factor
Secretion of hormones (insulin)
63
Q

What is the normal total calcium range?

A

2.2-2.6mmol/L

64
Q

Describe the position of the parathyroid glands

A

Usually 4 glands on the posterior aspect of the thyroid gland
2 at superior poles; 2 at inferior poles
Supplied by the inferior thyroid artery
10% of people have ectopic parathyroid glands

65
Q

What effect does PTH have on blood calcium levels?

A

Increases

66
Q

What are the actions of PTH in the kidneys?

A

Reabsorption of calcium at DCT
Internalisation of Na/PO4- co-transporter at PCT (hypophosphataemia and hypercalcaemia)
Inhibits N/H exchanger –> bicarbonate wasting (mild acidosis)

67
Q

What are the actions of PTH on the bones?

A

Continuous PTH = increased number and activity of osteoclasts

Intermittent PTH = increased number of osteoblasts

68
Q

What are the actions of PTH in the gut?

A

Stimulates the synthesis of active form of VIT D in the kidney (1,25-dihydroxycholecalciferol) –> increases Ca absorption in gut

69
Q

Where is PTH stored?

A

Chief cells in parathyroid gland

70
Q

What controls the secretion of PTH?

A

Ca Sensing Receptors (CaSR)

71
Q

Where are CaSR located?

A

Parathyroid gland
Thyroid
Kidney

72
Q

Describe what happens when CaSR are activated in the parathyroid gland

A

Rising Ca –> activates CaSR
Inhibits translation of PTH gene
PTH secretion inhibited

(Rising Ca –> activates calcium sensing proteases –> degrade PTH)

73
Q

What familial condition is associated with loss of function of the CaSR?

A

Familial hypocalciruric hypercalcaemia

74
Q

Describe what happens when CaSR are activated in the kidney

A

Increases urinary Ca and Mg excretion

Increases Na, K, Cl excretion

75
Q

Describe what happens when CaSR are activated in the thyroid

A

Stimulates the release of calcitonin from C cells –> lowers serum Ca

76
Q

Describe the process by which Vit D is activated

A

Cholecalciferol (UV light) and Ergocalciferol (diet) are inactivated

Hydroxylated in liver to 25-hydroxycholecalciferol (storage form)

Hydroxylated in kidneys to 1,25-dihydroxycholecalciferol (active form)

77
Q

Give three actions of Vit D

A

Increases calcium and phosphate absorption from gut
Bone mineralisation and mobiles Ca stores
Immunomodulation
Increases bone strength
Reduces insulin resistance
Interaction with RAAS

78
Q

Give the assay results associated with 25-hydroxycholecalciferol

A 
<15nmol/l = severe deficiency
15-30nmol/l = deficiency
>50nmom/l = adequate
79
Q

What is the normal range for 1,25-dihydroxycholecalciferol?

A

50-125pmol/L

80
Q

If a patient has a raised serum Ca, what should always be measured?

A

PTH

81
Q

When do symptoms of hypercalcaemia generally arise?

A

Serum Ca >3mmol/L

82
Q

Give some symptoms associated with hypercalcaemia

A

Confusion, depression, fatigue, coma
Shortening of QTc, bradycardia, HTN
Polyuria, nephrogenic DI, stones, nephrocalcinosis
Anorexia, constipation, nausea, pancreatitis
Muscle weakness, bone pain, osteoporosis

83
Q

Give DDx if Calcium and PTH are both raised?

A

Parathyroid overactivity
Familial hypocalciuric hypercalcaemia
Lithium

84
Q

Give DDx if Calcium is raised and PTH is normal?

A

Parathyroid overactivity
Familial hypocalciuric hypercalcaemia
Lithium

85
Q

Give DDx if Calcium is raised and PTH is undetectable?

A

Malignancy
Drugs (thiazide, lithium, calcium supplements)
Granulomatous disease

86
Q

What investigations are needed if a patient has hypercalcaemia?

A 
Hx and examination
CXR (signs of malignancy, hilar lymphadenopathy - signs of sarcoidosis)
FBC, ESR
TFTs
Myeloma screen
Short SynACTHen test
Vit D
87
Q

What are the ways in which malignancies can cause hypercalcaemia?

A

Osteolytic metastases and myeloma
Tumour secretes PTHrP
Tumour produces 1,25-dihydroxycholecalciferol

88
Q

What tumours are most likely to secrete PTHrP?

A

Squamous cell lung cancer
Oesophageal cancer
Renal cell carcinoma
Breast cancer

89
Q

What type of tumour is most likely to produce 1,25-dihydroxycholecalciferol?

A

Lymphoma (activated macrophages)

90
Q

Give examples of conditions which can produce endogenous 1,25-dihydoxycholecalciferol

A

Lymphoma
Sarcoid
Wegner’s granulomatosis

(usually responds to steroids)

91
Q

Why does adrenal insufficiency cause hypercalcaemia?

A

Increases PCT Ca reabsorption

Increases bone resorption

92
Q

Describe Milk-Alkali syndrome

A

Hypercalcaemia
Metabolic acidosis
Renal insufficiency

(ingestion of calcium and antacids - rare with PPI)

93
Q

What is the management of PTH independent hypercalcaemia?

A

Stop offending/contributing medications

Rehydrate (3-4L normal saline in 24h)

±loop diuretics - promotes calciuria

Bisphosphonates (inhibits bone reabsorption)

Steroids (haematological malignancy, vit D intoxication, granulomatous disease)

94
Q

Who is most likely to have primary hyperparathyroidism?

A

Postmenopausal women

95
Q

What are the causes of primary hyperparathyroidism?

A

85% isolated parathyroid adenoma
14% parathyroid hyperplasia
<1% parathyroid carcinoma

96
Q

What end organ damage is associated with primary hyperparathyroidism?

A

Bone:
Osteoporosis
Bone cysts, subperiosteal resorption
Brown tumours (collections of osteoclasts, mineralised bone and fibrous tissue)

Kidney:
Renal calculi
Nephrocalcinosis - calcium deposits in kidney
Renal impairment

Pancreatitis

97
Q

What investigations should be arranged to confirm diagnosis of primary hyperparathyroidism?

A 
DHx
U&amp;Es
PTH
Urine calcium:creatinine ratio
Vit D
98
Q

What investigations should be arranged to assess end organ damage in primary hyperparathyroidism?

A

DEXA

Renal USS

99
Q

When should MEN-1/2 be considered as a potential cause of primary hyperparathyroidism?

A

<40yr

Hx of hyperparathyroidism in 1st degree relative

100
Q

What investigations are needed if surgery is indicated in the management of primary hyperparathyroidims?

A

Sestamibi - radio labelled isotope –> taken up by parathyroid gland
Neck USS

101
Q

What are the indications for parathyroidectomy?

A

Calcium >3mmol/L
Hypercalciuria
Osteoporosis
Renal stones

102
Q

What complications are associated with parathyroidectomy?

A

Vocal cord paresis, haematoma causing tracheal compression

Transient hypocalcaemia,

“Hungry bones”

103
Q

If someone has no-end organ damage or is unfit for surgery for management of their primary hyperparathyroidism, what surveillance should they have?

A

Annual bone profile, renal function and urinary calcium

DEXA and renal USS every 3y

104
Q

Describe the medical RRx for primary hyperparathyroidism

A

Only if not fit for surgery

Bisphosphonates - preserve bone mass but little effect on calcium

Calcium sensing agonists (cinacalcet)
Reduces serum calcium but doesn’t prevent end-organ damage

105
Q

Give three causes of vitamin D deficiency

A 
Poor sunlight exposure
Malabsorption
Gastrectomy
Enzyme inducing drugs - anticonvulsants
Renal disease
106
Q

Define osteomalacia

A

Failure to ossify bones in adulthood as a result of Vit D deficiency leading to hypo-mineralisation of trabecular and cortical bone

107
Q

How does osteomalacia present?

A

Bone pain
Proximal myopathy
Hypocalcaemia

108
Q

What biochemistry results are suggestive of osteomalacia?

A 
Low calcium
Low phosphate
High Alk Phos
Low Vit D 
Elevated PTH
109
Q

What radiological appearances are associated with osteomalacia?

A

Looser zone - pseudo-fractures commonly occur in femur/pelvis
Osteopenia - areas of low bone density

110
Q

How can Vit D deficiency be managed?

A

Cholecalciferol (D3) = restores body stored, corrects metabolic disturbances

Alfacalidol (active Vit D) - in renal impairment, heal bony abnormalities

111
Q

Define diabetes

A

A metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbance of carbohydrate, protein and fat metabolism resulting in defects in insulin secretion, insulin action or both

112
Q

Describe and explain the symptoms of diabetes

A

Glycosuria –> depletion of energy stores
(Tired, weak, weight loss, difficulty concentrating, irritability)

Glycosuria –> osmotic diuresis
(Polyuria, polydipsia, thirst, dry mucous membranes, reduced skin turgor, postural hypotension)

Glucose shifts –> swollen ocular lenses
(Blurred vision)

113
Q

Describe and explain the presentation of insulin deficiency

A 
Ketone production
(N&amp;V, abdo pain, heavy/rapid breathing, acetone breath, drowsiness, coma)

Depletion of energy stores
(Weakness, polyphagia, weight loss, growth retardation in young)

Complications (T2DM)
(Microvascular, macrovascular, neuropathy, infection)

114
Q

What are the diagnostic values for diabetes in a fasting glucose test?

A

Normal: <7.0

Diabetes >7.0

115
Q

What are the diagnostic values for diabetes in a OGTT?

A

Normal: <7.8
IGT: 7.8-11.0
Diabetes: >11.1

116
Q

What HbA1c value corresponds to diabetes?

A

6.5% (48mmol/L)

117
Q

Describe T1DM

A

Chronic, progressive metabolic disorder characterised by hyperglycaemia and the absence of insulin secretion due to autoimmune destruction of beta cells in the Islets of Langerhans

118
Q

Describe T2DM

A

Chronic, progressive metabolic disorder characterised by hyperglycaemia, insulin resistance and relative impairment of insulin deficiency

119
Q

How is MODY inherited?

A

Autosomal dominant

120
Q

How many genes cause MODY, and what is the most common?

A

6 genes

HNF1-alpha 70%

121
Q

What are the three main features of MODY?

A

Often <25y at onset
Runs in families - autosomal dominant
Managed by diet, OHAs, insulin

122
Q

Define gestational diabetes

A

Carbohydrate intolerance with onset, or diagnosis, during pregnancy

123
Q

What risk factors are associated with gestational diabetes?

A

High BMI
Previous macrosomic baby/gestational DM
FHx of diabetes

124
Q

Who should be tested for gestational diagnosis, when and what is the criteria?

A

Women with risk factors
OGTT at 24-28 weeks

Fasting venous plasma glucose >/= 5.1mmol/L OR
1 hour value >/= 10.0mmol/L OR
Two hours after >/= 8.5mmol/L

125
Q

Give potential causes of secondary DM

A

Disorders of exocrine pancreas (pancreatitis, carcinoma, CF, haemochromatosis)

Endocrinopathies (Acromegaly, Cushing’s, phaechromocytoma)

Drug therapies (Immunosuppressive agents, anti-psychotics)

126
Q

Under fasting conditions, what is the basal secretion of insulin per hour?

A

40ug/h

127
Q

Describe the release of insulin

A

1st phase: stored insulin is released immediately due to increased plasma glucose levels

2nd phase: blood insulin levels starts to fall, the pancreas produces more insulin

128
Q

Give an example of a short/rapid (bolus) insulin

A

Novorapid

129
Q

Give an example of intermediate/long (basal) insulin

A

Determir
Degludec
Glargine

130
Q

Give and example of a mixed insulin

A

Novomix 30

Humalog Mix 25/50

131
Q

What is Whipple’s triad in regard to hypoglycaemia?

A
  1. Symptom of low blood glucose
  2. Measure low plasma glucose
  3. Symptoms improve with glucose
132
Q

At what concentration of blood glucose are counter-regulatory hormones released? What hormones are they? What is the effect?

A

3.8mmol/L

Glucagon and adrenaline

Sweating, palpitations, shaking, nausea, anxiety

133
Q

What what blood glucose concentration is cognitive function impaired?

A

2.5-2.8mmol/L

134
Q

How is mild hypoglycaemia treated in hospital?

A

Give 15-20g of quick acting carbohydrate
Test blood glucose after 15mins
If <4mmol/L repeat up to 3x

135
Q

How is moderate hypoglycaemia treated in hospital?

A

If capable and cooperative, 15-20g of quick acting carbohydrate

If not, 1.5-2 tubes GlucoGel or 1mg Glucagon IM

Test blood glucose levels after 15mins
If <4mmol/L repeat up to 3 times

136
Q

How is severe hypoglycaemia treated in hospital?

A 
Check ABC
Stop IV insulin
Give IV glucose over 10 mins
Test blood glucose after 10 mins
If <4mmol/L repeat
137
Q

How often does a person with diabetes need to check their blood glucose levels whilst driving?

A

Every 2 hours

138
Q

What are the three aspects of DKA?

A
  1. Metabolic acidosis (pH <7.3)
  2. Plasma glucose (>13.9mmol/L)
  3. Urinary/plasma ketones (++ on urine/ >3mmol/L in plasma)
139
Q

What are some of the symptoms of DKA?

A 
Breathlessness - Kussmaul's breathing
Abdominal pain 
Leg cramps
N&amp;V
Confusion
140
Q

What are some of the precipitants of ketoacidosis?

A 
New onset DM
Insulin omission
Acute illness
Steroids
Infections
141
Q

What losses are associated with DKA?

A

Water: 6-8L (100ml/kg)
Sodium: 500-1000mmol/L
Chloride: 350mmol/L
Potassium: 300-1000ml/L

142
Q

Describe the management of DKA

A

Treat the precipitant
Fluids
Potassium replacement
Insulin - with glucose once the blood glucose levels starts to fall

143
Q

How high are the blood glucose levels in HHS?

A

> 30mmol/L

144
Q

What are precipitating factors of HHS?

A

Infection
Poor compliance
Drugs

145
Q

Describe the management of HHS

A

Treat the precipitant

Fluids
0.9% saline
Rate of Na fall should not exceed 10mmol/24hr

Insulin
Rate of fall no more than 5mmol/L/hr

Other
LMWH
Foot protection

MBChB (14 decks)

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