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Y2 Endocrine > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is acromegaly caused by

A

Excess growth hormone

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2
Q

Describe the process of releasing growth hormones and its negative feedback mechanism

A

1) GHRH (growth hormone releasing hormone) released from the hypothalamus into anterior pituitary gland
2) This stimulates the somatotropes in anterior pituitary gland to secrete GH (growth hormone) into the blood
3) GH stimulates the release of IGF-1 from the liver

The release of IGF-1 and GH inhibits the release of GHRH and stimulates the release of somatostatin
Somatostatin is a negative regulator of GH as well

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3
Q

Role of somatostatin in growth hormone production

A

Inhibits release of growth hormone

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4
Q

What is IGF-1

A

Insulin-like growth factor released by the liver which stimulates systemic body growth and has anabolic effects

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5
Q

What is gigantism

A

Excess growth hormone during childhood causing unusually tall stature and rapid growth

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6
Q

Which cells secrete GH in the anterior pituitary gland

A

Somatotropes

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7
Q

Most common cause of acromegaly

A

Pituitary adenoma

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8
Q

Acromegaly can be caused by malignancy in which cells of the pituitary gland

A

Somatotropes

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9
Q

Causes of acromegaly

A

Pituitary adenoma
Ectopic release of GH
Ectopic release of GHRH
Hypothalamic tumours

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10
Q

Which cancers can cause ectopic release of GHRH

A

Carcinoid (neuroendocrine tumour)
Small cell lung cancer

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11
Q

Symptoms of acromegaly

A

Large hands and feet
Frontal bossing
Bulging out of lower jaw (prognathism)
Macroglossia
Obstructive sleep apnea
Enlarged nose
Visual loss
Headaches
Joint pain

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12
Q

What can cause visual loss

A

Pituitary adenomas compressing the optic chiasm

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13
Q

What is usually seen due to tumours compressing the optic chiasm

A

Bitemporal hemianopia

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14
Q

What is bitemporal hemianopia

A

partial blindness where vision is missing in the outer half of both the right and left visual field

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15
Q

Which conditions are at increased risk due to acromegaly

A

Hypertension
CVD
Colon cancer
Insulin resistance
Osteoporosis

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16
Q

Why may acromegaly cause obstructive sleep apnea

A

Due to enlarged nasopharynx; acromegaly causes thickened soft tissues

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17
Q

Why may hypopituitarism occur in acromegaly

A

Due to large pituitary adenoma causing infarction of pituitary tissue hence impairing function of the rest of the pituitary gland

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18
Q

What lab tests can be done to diagnose acromegaly

A

IGF-1 level
Oral glucose tolerance test

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19
Q

Why is IGF-1 level measured instead of GH

A

Because GH level is highly variable whereas IGF-1 is relatively constant hence more reliable

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20
Q

When should you do glucose tolerance test for acromegaly

A

If IGF-1 is raised or uncertain to confirm the diagnosis

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21
Q

What would the lab test results be for acromegaly (IGF-1 levels and glucose tolerance test)

A

Raised IGF-1 level
GH level not suppressed after administration of glucose

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22
Q

Why would the GH level be suppressed after administration of glucose in normal healthy people

A

Because GH acts like glucagon which would be suppressed due to high levels of insulin

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23
Q

Why may growth decrease if you eat lots of refined sugars and carbs during childhood

A

Because these food raises insulin level the most which would inhibit GH secretion

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24
Q

Except IGF-1 level and glucose tolerance test, what other tests may be done for acromegaly if patients present certain symptoms

A

MRI / CT / PET scan
Visual field test
Test for deficiencies in other pituitary hormones

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25
Q

Management of acromegaly

A

Surgery is first line
Drugs second
Radiotherapy third

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26
Q

What drugs may be used for acromegaly

A

Somatostatin analogues
GH antagonists (but not really used)

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27
Q

Examples of somatostatin analogues

A

Lanreotide
Octreotide
Sandostatin LAR

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28
Q

Effects of somatostatin analogues

A

Reduces GH (remember somatostatin is a negative regulator for GH)
Shrinks tumour
Relieves headache

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29
Q

Side effects of somatostatin analogues

A

Local stinging
Flatulence
Diarrhea
Abdominal pain
Gallstones

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30
Q

Why is GH antagonist last line for drug therapy

A

It doesn’t shrink tumour size
Decreases IGF-1 but serum GH concentration may increase

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31
Q

When is radiotherapy used to treat acromegaly

A

For those where surgery and drug therapy failed

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32
Q

Why is radiotherapy avoided in those of reproductive age

A

It can cause hypopituitarism and it is associated with thyroid cancer

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33
Q

Describe the structure of the adrenal gland

A

Outer layer - cortex, made of 3 layers
Center- medulla

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34
Q

What are the 3 layers of the cortex

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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35
Q

Function of adrenal gland

A

Synthesis and release of steroid hormones and catecholamines

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36
Q

Which steroid is synthesised and released by zone glomerulosa

A

Mineralcorticoids

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37
Q

Which layer of the adrenal cortex secretes glucocorticoids

A

Zona fasciculata

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38
Q

Which hormones are secreted by zone reticularis

A

Adrenal androgens

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39
Q

What does the medulla of adrenal gland secrete

A

Catecholamines

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40
Q

Main glucocorticoid secreted by the adrenal gland

A

Cortisol

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41
Q

Main mineralocorticoid secreted by the adrenal gland

A

Aldosterone

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42
Q

What are the catecholamines secreted by the adrenal medulla

A

Epinephrine (adrenaline)
Norepinephrine (noradrenaline)
Dopamine

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43
Q

Which cells make up the most of medulla

A

Chromaffin cells

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44
Q

What is the starting material for the synthesis of all steroids

A

Cholesterol

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45
Q

Aldosterone is regulated by which systems

A

Renin-angiotensin system

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46
Q

Cortisol and androgens are regulated by which system

A

Hypothalamis-pituitary- adrenal axis (HPA)

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47
Q

What factors can trigger the production of CRH from hypothalamus

A

Stress
Time of day
Illness

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48
Q

Describe the HPA axis

A

Hypothalamus secretes CRH in response to stress/illness/time of day -> CRH stimulates the release of ACTH from anterior pituitary gland -> ACTH travels through blood to the adrenal cortex to stimulate the synthesis and secretion of cortisol

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49
Q

Describe how dose cortisol level vary throughout the day

A

Highest during the day
Lowest in the night

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50
Q

Describe the renin-angiotensin system

A

1) trigger factors stimulating release of renin from kidneys
2) Renin cleaves angiotensin into angiotensin I
3) ACE cleaves angiotensin I into angiotensin II
4) Angiotensin II exerts its effects and stimulates release of aldosterone and ADH

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51
Q

Function of RAAS

A

to regulate blood pressure and fluid balance

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52
Q

What are the triggers for RAAS

A

Decrease in blood pressure (renal hypotension)
Sympathetic stimulation
Reduced sodium

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53
Q

Where is ACE found

A

Vascular endothelium of the lungs

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54
Q

How does angiotensin II increase blood pressure

A

Stimulate release of aldosterone
Stimulate release of ADH
Stimulate vasoconstriction
Increases sodium reabsorption at proximal tubule (hence water)

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55
Q

How does aldosterone increase blood pressure

A

Increases sodium retention by increasing sodium potassium channels in epithelial sodium channels in distal tubule
= increases sodium reabsorption and potassium excretion

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56
Q

How does ADH increase blood pressure

A

Insert aquaporin channels to increase permeability of the collecting duct to water

Increase sodium reabsorption at ascending limb of loop of hence (hence water)

= more water retained instead of excreted into urine

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57
Q

Why does high level of aldosterone lead to lower levels of potassium

A

Because aldosterone increases the activity of sodium potassium pump which pumps sodium in and potassium out.

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58
Q

How do steroids exert an action

A

Bind to intracellular receptors to affect transcription of certain genes

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59
Q

Cortisol (glucocorticoids) actions on circulation

A

Increase cardiac output
Increase in blood pressure
Increase in renal blood flow and filtration rate

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60
Q

Cortisol actions on metabolism

A

Increases blood sugar
Increases lipolysis
Increases proteolysis
Increases osteoclast activity

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61
Q

Effect on bones due to long term steroid use

A

Accelerated osteoporosis

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62
Q

Immunological effects of the cortisol

A

Decrease in capillary diltatation
Decrease in macrophage activity
Decrease in leukocyte migration
Dcrease in inflammatory cytokine production

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63
Q

Use of steroids

A

Suppress inflammation
Suppress immune system

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64
Q

Examples of when is steroid used

A

Asthma
RA
Ulcerative colitis, Crohn’s disease (IBD)

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65
Q

Effects of aldosterone through binding to mineralocorticoid receptor

A

Regulates blood pressure
Sodium/Potassium balance
Regulation of extracellular volume

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66
Q

What is Addison’s disease

A

= primary adrenal insufficiency (including all the primary causes)

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67
Q

Most common primary cause of adrenal insufficiency

A

Autoimmune destruction

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68
Q

Primary causes of adrenal insufficiency (Addison’s)

A

Autoimmune destruction
Surgery
Trauma
Infections
Haemorrhage (Waterhouse Friderichsen Syndrome)
Sarcoidosis / neoplasm

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69
Q

Which infection is associated with Addison’s

A

TB

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70
Q

Most common secondary cause of adrenal insufficiency

A

Chronic exogenous steroid

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71
Q

How may excess exogenous steroid lead to adrenal insufficiency

A
  1. steroids exert negative feedback on ACTH production hence ACTH may be suppressed for a long term -> Unable to produce enough ACTH during metabolic stress when they stop taking steroids -> adrenal insufficiency
  2. atrophic adrenal glands unable to respond to ACTH
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72
Q

Secondary causes of adrenal insufficiency

A

Excess exogenous steroid
Panhypopituitarism
CRH deficiency

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73
Q

Addison’s disease is associated with which other autoimmune diseases

A

T1 diabetes
Autoimmune thyroiditis (Hashimoto’s / grave’s)
Pernicious anemia

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74
Q

Clinical features of adrenal insufficiency

A

Unexplained weight loss / anorexia
Skin hyperpigmentation
Fatigue
Hypotension
Hypoglycaemia
Abdominal pain
Vomiting
Loss of pubic hair / axillary hair

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75
Q

Mneumonic for symptoms of adrenal insufficiency (W STEROID)

A

Sugar and sodium low
Tired
Electrolyte imbalance (hyperkalaemia and hyponatraemia)
Reproductive changes (loss of pubic hair / axillary hair)
O lOw blood pressure
Increased skin pigmentation
Diarrhea and vomiting

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76
Q

What causes skin hyperpigmentation in Addison’s disease

A

Due to high ACTH level stimulates melanocytes to produce melanin

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77
Q

Why would there be high ACTH levels in Addison’s disease

A

Due to low level of steroids -> less negative feedback -> ACTH and CRH not inhibited

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78
Q

Lab tests for adrenal insufficiency

A

Blood tests - Na+, K+ levels, glucose level
ACTH levels
SYNACTHEN test
Renin/aldosterone level
21 hydroxylaze autoantibodies
CT scan / MRI

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79
Q

What is synacthen test for adrenal insufficiency

A

Injection of synthetic ACTH and measure cortisol level before and 30 minutes after injection

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80
Q

Synacthen test that suggests adrenal insufficiency

A

low cortisol level 30 minutes after injection

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81
Q

Renin Aldosterone level that suggests adrenal insufficiency

A

High renin
Low aldosterone

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82
Q

What Na+ and K+ levels can suggest adrenal insufficiency

A

Hyponatraemia
Hyperkalaemia

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83
Q

What is the characteristic trio of lab results suggesting adrenal insufficiency

A

Hypoglycaemia
Hyponatraemia
Hyperkalaemia

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84
Q

Management of Adrenal insufficiency

A

Hydrocortisone
+ Fludrocortisone if aldosterone is insufficient
(usually both are used)
Sick day rules and education

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85
Q

Hydrocortisone is the synthetic replacement for which steroid

A

Cortisol

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86
Q

What are the sick day rules for adrenal insufficiency

A

Double the dose during moderate intercurrent illness
Self inject IV hydrocortisone during severe intercurrent illness
Cannot miss a dose of steroids, they need steroids for life

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87
Q

What is Addisonian (adrenal) crisis

A

Exacerbation of adrenal insufficiency where the absence of steroid hormones can lead to life-threatening situations

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88
Q

Symptoms of Addisonian (adrenal) crisis

A

Hypotension
Reduced consciousness
hypoglycaemia
Hyponatraemia
Hyperkalaemia
Very unwell

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89
Q

Management of Addisonian crisis

A

Do not delay treatment, treat ASAP
IV hydrocortisone
IV fluid resuscitation
Treat underlying cause
Monitor electrolytes, blood pressure continuously

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90
Q

What can trigger Addisonian crisis

A

Acute illness
Trauma
Infection
Withdrawal / forgot to take steroids

these causes stress which increases demand for cortisol

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91
Q

What happens to the adrenal gland in absence of ACTH / CRH

A

Atrophy due to long term failure to be exposed to and stimulated by ACTH / CRH

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92
Q

What are some differences in clinical features between primary and secondary adrenal insufficiencies

A

Primary adrenal insufficiency causes skin hyperpigmentation but secondary adrenal insufficiency will not due to no increase in ACTH

Aldosterone will not be affected because it is regulated by renin-aldosterone system instead of by ACTH / CRH

Secondary does not have hyperkalaemia

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93
Q

What may be excluded in the management of secondary adrenal insufficiency

A

The use of fludrocortisone because aldosterone is not deficient

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94
Q

Pathogenesis of osteoporosis

A

Activity of osteoclasts > activity of osteoblasts leading to decrease in bone density (bone loss)

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95
Q

When do people achieve their peak bone mass

A

Usually in their 20s

96
Q

What are the regulating factors for peak bone mass

A

Genetics (70-80 %)
Body Weight
Sex hormones
Diet
Exercise

97
Q

Is a higher peak bone mass beneficial

A

Yes, it is more protective against osteoporosis

98
Q

Common fracture sites due to osteoporosis

A

Neck of femur
Humeral neck
Vertebral body
Distal radius

99
Q

What can a fracture in the vertebral body lead to

A

Loss in height
Kyphosis due to vertebral bodies compressing into each other

100
Q

What happens to the ribcage in severe kyphosis

A

Rests on the pelvis and causes discomfort

101
Q

Risk factors of osteoporosis

A

Female
Age
Post-menopausal women
Oestrogen deficiency
Long term use of steroids
Alcohol, smoking
Malabsorption
Vit D / calcium deficiency
Endocrine disorders
Rheumatoid arthritis
Chronic liver disease

102
Q

Why are post menopausal women at risk of osteoporosis

A

Due to reduced oestrogen level

103
Q

Why does steroid use increases risk of osteoporosis

A

Increases osteoclast activity

104
Q

What GI conditions can cause malabsorption hence increase risk for osteoporosis

A

IBD
Coeliac

105
Q

What endocrine disorders increases risk of osteoporosis

A

Acromegaly
Hyperparathyroidism
Cushings
Diabetes

106
Q

Investigations for osteoporosis

A

Tests to exclude non-osteoporotic low impact fractures
Fragility Fracture risk assessment ( may be skipped under certain circumstances)
DXA scan
Deficiencies in vitamin D / Calcium

107
Q

Which online assessment tools are used to calculate the fragility fracture risk score

A

QFracture (preferred)
FRAX

108
Q

When should 10-year fragility fracture risk score be calculated

A

Before DEXA scan except certain circumstances

109
Q

Under what circumstances allow patients to be sent for DXA scan directly instead of calculating their fragility fracture risk first

A

> 50 female that has previous fragility fractures

<40 with major risk factors for fragility fractures

110
Q

Why is QFracture preferred over FRAX

A

Because FRAX underestimates certain factors

111
Q

What factors does FRAX underestimate

A

Long term use of steroids
History of multiple fragility fractures
Heavy drinking and smoking

112
Q

What should be done to those with a intermediate risk of fragility fracture close to recommended threshold + with associated risk factors

A

Send for DXA

Even though they did not reach the threshold, it is still important to send them for DXA because they present with risk factors and also because the online assessment tools may underestimate risk of certain factors

113
Q

What does T score in DXA scan represent

A

The number of standard deviations a patient’s bone density is from the average for a healthy young adult of the same gender

114
Q

Interpret the T scores from DXA

A

Normal = T > -1
Osteopenia = -2.5 < T < -1
Osteoporosis = T </ -2.5

115
Q

Management for those with T score > -2.5

A

Advise on changing habits that are risk factors for osteoporosis
Treat the conditions that are risk factors for osteoporosis
Repeat DXA within 2 years

116
Q

Management for those with T score </ -2.5

A

Begin drug treatment
Advise on lifestyle changes

117
Q

What drugs are used to treat osteoporosis

A

Bisphosphonates
Denosumab
Teriparatide
HRT (hormone replacement therapy)

118
Q

Examples of bisphosphonates used for osteoporosis

A

Alendronate
Zoledronic acid

119
Q

What are bisphosphonates and what are their effects

A

Analogues of pyrophosphate which is absorbed onto the bone and taken up by osteoclasts. This induces death of osteoclasts

120
Q

Side effects of bisphosphonate

A

GI disturbance
Headache
Oesophagitis
Osteonecrosis (rare)
Atypical femoral fracture (rare

121
Q

What can be used for a osteoporotic patient who cannot tolerate oral preparations

A

Yearly injection of zoledronic acid

122
Q

First line drug used for osteoporosis

A

Bisphosphonate (aledronate)

123
Q

What are the alternatives for bisphosphonate

A

Denosumab
Teriparatide
Romosozumab

124
Q

What is denosumab and its actions

A

It is a mAB. It binds to RANKL to inhibit this receptor which inhibits the activity of osteoclasts

125
Q

Who should be considered to be given HRT

A

early menopausal women
Young post-menopausal women

126
Q

Side effects of HRT

A

Breast tenderness
Leg cramps
Changes in mood
Increases risk of blood clots, breast cancer and endometrial cancer

127
Q

What lifestyle advices should be given to all patients with osteoporosis

A

Smoking cessation
Reduce alcohol consumption
Regular weight bearing exercises

128
Q

What differentials should be taken into account when a patient presents with low impact fractures

A

Pathological fracture due to metastases / primary bone cancer?

Any secondary causes such as endocrine diseases / chronic liver or kidney diseases

129
Q

What is Cushing’s syndrome

A

A condition caused by excess cortisol

130
Q

Types of causes of Cushing’s syndrome

A

ACTH dependent
ACTH independent
Exogenous cause

131
Q

ACTH dependent causes of Cushing’s syndrome

A

Pituitary adenoma (Cushing’s disease)
Ectopic ACTH poduction
Ectopic CRH production

132
Q

What conditions can cause ectopic ACTH production

A

Carcinoid / carcinoma
Small cell lung cancer

133
Q

Which lung cancer can cause ectopic ACTH production

A

Small cell lung cancer

134
Q

ACTH independent causes of Cushing’s

A

Nodular hyperplasia
Adrenal adenoma
Adrenal carcinoma

135
Q

What is the most common endogenous cause of Cushing’s

A

Pituitary adenoma

136
Q

What is the most common cause of Cushing’s

A

Excess / long term use of glucocorticoids (steroids)
= iatrogenic

137
Q

What conditions may require long term use of steroids

A

Asthma
Rheumatoid arthritis
IBD
Organ transplants

138
Q

How does long term steroid use lead to adrenal cortex atrophy

A

Long term steroid use causes chronic suppression of ACTH. This eventually leads to atrophy of the adrenal gland due to long term failure to be exposed and respond to ACTH

139
Q

Clinical features of Cushing’s

A

Easy bruising due to thinning of skin
Facial swelling and redness
Proximal myopathy
Buffalo hump
Increased abdominal fat
Striae
Hyperpigmentation in ACTH dependent causes of Cushing’s

140
Q

Cushing’s syndrome can increase the risk of which conditions

A

Hypertension
Osteoporosis
Diabetes
Obesity

141
Q

What is buffalo hump

A

collection of fat accumulated on the back of the neck

142
Q

Sequence of investigations for Cushing’s

A

1) do tests to establish that there is excess cortisol
2) do tests to find the underlying cause

143
Q

What investigations can be done to establish that there is excess cortisol

A

24 hour urinary free cortisol
Low dose dexamethasone suppression test
Late night salivary cortisol measurement

144
Q

Describe the low dose dexamethasone suppression test

A

Dexamethasone is a strong glucocorticoid
Low dose dexamethasone should be able to suppress ACTH level in normal people (negative feedback). In patients with excess ACTH, low dose will not be able to suppress it.
Excess ACTH suggests excess cortisol due to ACTH dependent causes

145
Q

What feature of cortisol will be absent in patients with Cushing’s syndrome when we test them with late night salivary cortisol measurement

A

Diurnal variation of cortisol

146
Q

Investigations for identifying the cause of Cushing’s syndrome

A

Plasma ACTH
High dose dexamethasone suppression test
MRI/ CT / PET scan
Petrosal sinus sampling

147
Q

Why is plasma ACTH level tested first in order to find the underlying cause of Cushing’s

A

To see whether the excess cortisol is due to ACTH independent / dependent causes

148
Q

What is the high dose dexamethasone suppression test used for

A

To differentiate between pituitary adenoma and ectopic ACTH prodcution that is causing Cushing’s

149
Q

Describe the result of high dose dexamethasone in patients with pituitary adenoma

A

High dose dexamethasone will be able to suppress ACTH level if the patient has pituitary adenoma. This is because the pituitary adenoma is less responsive towards normal negative feedback but it is more responsive towards high dose glucocorticoids

150
Q

Describe the result of high dose dexamethasone in patients with ectopic ACTH production

A

ACTH level not suppressed

151
Q

When is petrosal sinus sampling used for Cushings

A

Invasive sampling that is used if imaging / other investigations have been insufficient to reach a diagnosis

152
Q

Describe the petrosal sinus sampling

A

Invasive procedure sampling ACTH level from the veins draining pituitary gland

153
Q

If suspecting a patient with Cushing’s who is on long term steroid therapy, what investigations should you suggest

A

Low and high dose dexamethasone will not be useful.
Advise to lower steroid use

154
Q

Management of Cushing’s syndrome

A

GRADUALLY stop steroids if Cushing’s was due to long term steroid use
Surgery
Drugs

155
Q

Why should you gradually stop steroids instead of abruptly to treat a patient with Cushing’s

A

Abruptly stopping it can cause Addisonian crisis because the patients are likely to have developed suppression of their normal endogenous steroid production

= abruptly stopping it will lead to supply of steroid < demand = exacerbation of adrenal insufficiency

156
Q

What drugs can be used to treat Cushing’s

A

Ketoconazole
Metyrapone
Mitotane

157
Q

When are drugs used in the management of Cushing’s

A

In preparation for surgery to temporarily reduce glucocorticoid level

Long term in patients who are unfit for surgery

158
Q

What is pseudo-Cushing’s

A

When patients present with symptoms like Cushing’s but does not have Cushing’s

159
Q

What is the difference between pseudo-Cushing’s and Cushing’s

A

Psuedo-Cushing’s still has diurnal variation for cortisol but Cushing’s does not

160
Q

What can cause pseudo-Cushing’s

A

Chronic alcoholism

161
Q

What is primary aldosteronism

A

Excess of aldosterone independent of the renin-angiotensin-aldosterone system

162
Q

Causes of primary aldosteronism

A

Bilateral idiopathic hyperplasia
Aldosterone producing adenoma (Conn’s adenoma)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

163
Q

What is the most common cause of primary aldosteronism

A

Bilateral idiopathic hyperplasia

164
Q

Hallmark features of primary aldosteronism

A

Hypertension
Hypokalaemia

165
Q

Does hypokalaemia occur in all patients with primary aldosteronism

A

No, only 30% of patients will have hypokalaemia.

166
Q

Who should you suspect that may have primary aldosteronism

A

Those with moderate - severe hypertension
Those with resistant hypertension
Those with hypertension + sleep apnea
Those with hypertension + adrenal mass
Those with hypertension + family history of primary aldosteronism / family history of early onset stroke

167
Q

Sequence of investigations for primary aldosteronism

A

1) establish that there is excess aldosterone
2) confirm diagnosis of PA
3) Find underlying cause of PA

168
Q

What investigations can be done to establish that there is excess aldosterone

A

Measure aldosterone:renin ratio

Raised = excess aldosterone

169
Q

What investigations can be done to confirm the diagnosis of primary aldosteronism

A

Saline suppression test

If saline does not suppress aldosterone = primary aldosteronism

170
Q

What investigations can be done to find the underlying cause of primary aldosteronism

A

CT of adrenal gland

Adrenal vein sampling

171
Q

When should adrenal vein sampling be used

A

To differentiate between bilateral and unilateral hyperplasia

To see whether the excess aldosterone was due to an adrenal adenoma or not

172
Q

What does the management of primary aldosteronism depend on

A

Whether it is unilateral / bilateral

173
Q

Management of primary aldosteronism (unilateral)

A

Unilateral adrenalectomy
Mineralocorticoid receptor antagonist

174
Q

When is mineralocorticoid receptor antagonist used in the management of primary aldosteronism

A

Used to temporarily reduce aldosterone level to prepare patients for surgery

To be used as a long term treatment if the patient is unfit for surgery

175
Q

Management of primary aldosteronism (bilateral)

A

Mineralocorticoid receptor antagonists

176
Q

Examples of mineralocorticoid receptor antagonists

A

Spironolactone
Eplerenone

177
Q

What is a side effect of spironolactone but not eplerenone

A

Gynaecomastia

178
Q

What drugs can be used if mineralocorticoid receptor antagonists are not tolerated

A

ENaC inhibitors

179
Q

What causes congenital adrenal hyperplasia (CAH)

A

21 hydroxylase deficiency

180
Q

What is the function of 21 hydroxylase

A

It is an enzyme in adrenal gland required for conversion of progesterone into aldosterone and cortisol

181
Q

How does 21 hydroxylase deficiency affect the steroid level

A

Because 21 hydroxylase is not there to convert progesterone into aldosterone and cortisol, there will be extra progesterone around.
The extra progesterone is diverted to produce more testosterone

182
Q

Classic steroid levels seen in congenital adrenal hyperplasia

A

Low aldosterone
Low cortisol
High testosterone

183
Q

Types of congenital adrenal hyperplasia

A

Typical: more severe form normally presented at birth / before birth

Non-typical: milder form normally presented at childhood /early adulthood

184
Q

Clinical features of CAH

A

Adrenal insufficiency symptoms
(poor weight gain, fatigue, skin hyperpigmentation)
Adrenal crisis
Excess androgen symptoms
Genital ambiguity
Irregular periods

185
Q

What are the excess androgen symptoms

A

Facial hair
Short
Early puberty
Deep voice
Rapid growth during childhood but final height is still shorter than average

186
Q

What symptoms may not be presented in non-classic CAH

A

Aldosterone insufficiency (e.g. hypotension)

187
Q

Investigations for CAH

A

Check serum concentrations of progesterone, testosterone and androgen precursors

188
Q

Management for CAH

A

Cortisol replacement (hydrocortisone)
Aldosterone replacement in some
Surgical correction
-e.g. for those with genital ambiguity
Avoid overusing steroid treatment

189
Q

What is hypercalcaemia

A

When the serum calcium concentration is greater than 2.6 mmol

190
Q

Normal level of serum calcium

A

2.2 - 2.6 mol

191
Q

Where can calcium be found

A

Mostly in bones
1% in intracellular and extracellular compartments

192
Q

What is the function of calcium in intracellular compartments

A

For intracellular signalling

193
Q

What is the function of calcium in extracellular compartments

A

Mostly free or bound to albumin

194
Q

What is corrected level of calcium

A

Serum calcium level taking into account the calcium bound to albumin as well

195
Q

Which factors regulate extracellular concentration of calcium

A

Calcitonin
PTH
Vitamin D

196
Q

Which cells produce calcitonin

A

Parafollicular cells in thyroid gland

197
Q

How is a decrease in calcium level regulated

A

1) Decrease in calcium level detected by CaSR in parathyroid glands
2) This stimulates the release of PTH from parathyroid glands
3) PTH stimulates
- the release of calcium from large calcium stores in bones
- increase in reabsorption of calcium in renal tubule
- activation of vitamin D

198
Q

What happens when vitamin D is activated

A

Increases absorption of calcium in enterocytes from food

199
Q

Causes of hypercalcaemia

A

Primary hyperparathyroidism
Tertiary hyperparathyroidism
Malignancy
Thyrotoxicity
Thiazides, lithium
Vitamin D toxicity
Familial hypocalciuric hypercalcaemia
Granulomatous diseases (TB, sarcoidosis)

200
Q

What can cause vitamin D toxicity

A

Ingestion of excess vitamin D
Sarcoidosis
Lymphoma

201
Q

What is primary hyperparathyroidism

A

Excessive release of PTH causing hypercalcaemia

202
Q

How do malignancies cause hypercalcaemia

A

Some tumours can secrete PTHrP which mimics the actions of PTH

Some tumours can increase osteoclastic activity -> break down of bones -> release calcium stored

203
Q

How do thiazides cause hypercalcaemia

A

increasing calcium reabsorption into the distal convoluted tubule in exchange for sodium.

Thiazide function: reduces sodium and water reabsorption to decrease blood pressure

204
Q

What is primary hyperparathyroidism

A

excess production of PTH by parathyroid gland

205
Q

Causes of primary hyperparathyroidism

A

Parathyroid hyperplasia
Parathyroid gland adenoma
Parathyroid carcinoma

206
Q

What is the most common cause of primary hyperparathyroidism

A

Parathyroid adenoma

207
Q

What is tertiary hyperparathyroidism

A

When the glands become autonomous after a period of prolonged secondary hyperparathyroidism, producing excessive PTH even after the cause of hypocalcaemia has been corrected

208
Q

Most common cause of tertiary hyperparathyroidism

A

Chronic kidney disease

209
Q

What is secondary hyperparathyroidism

A

increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease

210
Q

Causes of secondary hyperparathyroidism

A

Vitamin D deficiency
Conditions that lead to loss of extracellular Ca2+
Calcium malabsorption / inadequate Ca2+ intake
Conditions causing abnormal PTH activity

211
Q

What conditions can lead to loss of extracellular Ca2+

A

Pancreatitis
Rhabdomolysis

212
Q

Presentation of rhabdomyolysis

A

Pain in proximal muscle
Myalgia

213
Q

Causes of rhabdomyolysis

A

Severe hypothyroidism
Statins

214
Q

Investigations for rhabdomyolysis

A

Creatinine Kinase (high)

215
Q

What conditions can cause abnormal PTH activity

A

Kidney disease
Pseudohypoparathyroidism

216
Q

What is pseudohypoparathyroidism

A

PTH resistance - cells unable to respond to PTH so low calcium. Low calcium triggers more PTH secretion hence high PTH

217
Q

Does secondary hyperparathyroidism lead to hypercalcaemia

A

No, it mostly leads to low or normal calcium levels.

218
Q

Effect of PTH on Ca2+ and phosphate leves

A

Increases calcium reabsopriton
Decreases phosphate reabsorption

219
Q

Describe the lab results indicating primary hyperparathyroidism

A

High calcium
High / normal PTH
Decreased PO4 3-
Increased ALP

220
Q

Describe the lab results indicating secondary hyperparathyroidism

A

Low / normal Calcium
High PTH
High PO4 3- in kidney disease
but low PO4 3- in vitamin D deficiency

221
Q

Describe the lab results indicating tertiary hyperparathyroidism

A

High calcium
High PTH
High PO4 3- (since tertiary is usually due to chronic kidney disease)

222
Q

What is familial hypocalciuric hypercalcaemia

A

Inherited condition causing hypercalcaemia due to mutation in CaSR

223
Q

CaSR function in the kidneys

A

Increase excretion of Ca2+ in urine when serum Ca levels are high

224
Q

Difference between familial hypocalciuric hypercalcaemia and primary hyperparathyroidism

A

Hypocalciuric in FHH but not in PH

225
Q

Clinical features of hypercalcaemia

A

Stones - renal calculi
Thrones - polyuria, constipation
Abdominal Groans- pancreatitis, abdominal pain
Moans- depression, psychosis
Bones- fragility fracture, bone pain
Hypertension
Dehydration
Thirst

226
Q

How does chronic hypercalcaemia cause hypertension

A

Causes calcium deposits in the vessels leading to increased rate of hypertension and CVD

227
Q

Investigations for hypercalcaemia

A

Serum Calcium
Serum PTH
LFT
Bone profile
24 hour Urinary calcium
Bone scan
X ray / US

228
Q

What test results do you need confirm the diagnosis of primary hyperparathyroidism

A

Raised Ca
Raised PTH
Urine calcium level not elevated

229
Q

What test is done to exclude familial hypocalciuric hypercalcaemia

A

24 hour urinary calcium - urinary calcium will be low in FHH whereas it will be normal in Primary hyperparathyroidism

230
Q

Management of hypercalcaemia

A

IV fluids resuscitate
Bisphosphonates
Surgery
Cinacalet
Steroids

231
Q

What is the treatment for granulomatous disease e.g. sarcoidosis and TB

A

steroids

232
Q

When do patients with hypercalcaemia need to be admitted and resuscitated using IV fluids

A

If the patient has acute kidney injury / dehydrated

233
Q

First line treatment for primary hyperparathyroidism

A

Surgery

234
Q

What if patients with primary hyperparathyroidism doesn’t want surgery

A

Cinacalet first
then Bisphosphonate

235
Q

Why is bisphosphonate therapy third line for hypercalcaemia caused by primary hyperparathyroidism

A

Because it increases bone density but it does not prevent more renal stones

236
Q

PTH effect on phosphate

A

increase in PTH decrease phosphate
because phosphate forms insoluble salts with calcium which reduces plasma calcium level and since PTH wants to increase calcium, phosphate level needs to decrease

Y2 Endocrine (6 decks)

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