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Endocrine > Adrenal glands > Flashcards

Adrenal glands Flashcards

1
Q

Where are the adrenal glands located?

A

Above the kidneys

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2
Q

What are the three major layers of the adrenal gland?

A

Capsule
Adrenal cortex
Adrenal medulla

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3
Q

What are the three zones of the adrenal cortex (list from out to in).

A

Zona glomerulosa
Zona fasciculata
Zona Reticularis

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4
Q

What does the zona glomerulosa produce?

A

Mineralocorticoids such as aldosterone

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5
Q

What does the zona fasciculata produce?

A

Glucocorticoids such as cortisol

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6
Q

What does the zona reticularis produce?

A

Adrenal androgens such as testosterone

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7
Q

What is the precursor for all products of the adrenal cortex?

A

Cholesterol

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8
Q

How does cholesterol proceed through the metabolism?

A

Straight down to aldosterone
Diverted off to cortisol precursors
Cortisol precursors to cortisol or androgen precursors
Androgen precursors to androgens

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9
Q

How is cortisol and androgen release regulated?

A

By ACTH release from the anterior pit

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10
Q

What is the negative feedback for cortisol release?

A

Cortisol inhibits hypothalamus and ant pit

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11
Q

What effects does cortisol have on circulation and renal efficiency?

A

Increase CO and BP

Increase renal blood flow and GFR

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12
Q

What effects does cortisol have on metabolism?

A

Increase blood sugar
Increase lipolysis and central redistribution
Increase proteolysis

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13
Q

What effects does cortisol have on the CNS?

A

Mood lability
Euphoria/psychosis
Decrease libido

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14
Q

What effects does cortisol have of bone and connective tissue?

A

Increase osteoporosis
Decrease serum Ca
Decrease collagen formation
Decrease wound healing

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15
Q

WHat effects does cortisol have on the immune system?

A

Decrease cap dilation
Decrease leukocyte migration
Decrease macrophage activity
Decrease inflammatory cytokine production

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16
Q

What are the clinical uses of cortisol?

A

Suppress inflammation
Suppress immune system
Replacement therapy

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17
Q

How much cortisol is used in replacement therapy?

A

Enough to restore normal levels

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18
Q

How much cortisol is used in suppression therapy?

A

> 10x dose used in replacement

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19
Q

How should you give steroids?

A

PO if well

IV/IM if unwell

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20
Q

How is aldosterone release regulated?

A

RAAS

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21
Q

Describe RAAS

A

Drop in BP stim renin release
Renin converts angiotensinogen to angiotensin I
ACE converts angiotensin I to angiotensin II
Angiotensin II stim aldosterone release

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22
Q

What effect does aldosterone have?

A

Increases Na retention in kidneys therefore increasing BP

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23
Q

What are the two broad categories of adrenal dysfunction?

A

Hypo and hyper production

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24
Q

What two areas of the adrenal gland are affected by adrenal insufficiencies?

A

Cortex and medulla

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25
Q

What are some common causes for primary adrenal insufficiencies?

A 
Infection- TB/HIV
Autoimmune
Tumours
Haemorrhage-  Waterhouse-Friderichsen syndrome
Genetic defects
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26
Q

What two forms of adrenal insufficiency affect the adrenal cortex?

A

Primary

Secondary

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27
Q

What is an adrenal insufficiency of the adrenal MC producing area of the adrenal gland called?

A

Addison’s disease

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28
Q

What is the most common cause of Addison’s disease?

A

Autoimmune destruction

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29
Q

What other autoimmune diseases is Addison’s disease linked with?

A

T1DM

Autoimmune thyroiditis

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30
Q

How does Addison’s disease present?

A 
Anorexia/weight loss
Fatigue
DIzziness
Low BP
Abdo pain
Vomiting 
Diarrhoea
Skin pigmentation (due to elevated ACTH levels)
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31
Q

How do you treat Addison’s disease?

A

Fludrocortisone- if suspect Addison’s treat as such until proven otherwise.

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32
Q

How does adrenal insufficiency tend to present?

A 
Anorexia/weight loss
Fatigue
DIzziness
Low BP
Abdo pain
Vomiting 
Diarrhoea
Skin pigmentation (due to elevated ACTH levels)
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33
Q

What blood chemistry would you see in Addison’s disease?

A 
Low Na
High K
Hypotension
Raised renin
Low aldosterone
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34
Q

What blood chemistry would you see in adrenal insufficiency?

A 
Low Na
High K
Hypotension
Hypoglycemia
Raised renin
Low aldosterone
Raised ACTH levels
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35
Q

How do you diagnose Addison’s disease/adrenal insufficiency?

A

Synacthen test

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36
Q

How do you do a synacthen test?

A

Give ACTH and check cortisol levels at: 0, 30, 60 and 90 mins. Baseline should be >250nmol/l. Should rise to >550nmol/l

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37
Q

Give a genetic cause of adrenal insufficiency

A

Congenital adrenal hyperplasia (CAH)

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38
Q

What are some causes of secondary causes of adrenal insufficiency?

A

Excessive exogenous steroid

Pit problems resulting in lack of ACTH

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39
Q

What is the most common cause of secondary adrenal insufficiency?

A

Exogenous steroids

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40
Q

How does secondary adrenal insufficiency present?

A 
Weight loss/ Anorexia
Fatigue
Dizziness
Abdo pain
Vomiting
Diarrhoea
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41
Q

How do you treat secondary adrenal insufficiency?

A

Treat underlying cause

Hydrocortisone

42
Q

How should you administer hydrocortisone?

A

Large does in morning
Small does at lunch
Nothing after as will cause sleep problems

43
Q

What is an excess of cortisol called?

A

Cushing’s syndrome

44
Q

What can cause Cushing’s syndrome?

A

Pit adenoma- Cushing’s disease (too much ACTH)
Ectopic ACTH/CRH production
Adrenal adenoma/carcinoma
Nodular hyperplasia
Iatrogenic- too much exogenous steroid atrophying adrenal glands.

45
Q

How can Cushing’s present?

A 
Interscapular fat pad
Thin skin/ bruising
Proximal muscle wasting/thin arms and legs
Central obesity
Moon face
Striae- dark colour/purple
46
Q

What signs can you get in Cushing’s?

A 
Hypertension
Osteoporosis- rare in obesity
Hyperglycemia
Poor wound healing
Infections
Eye problems
47
Q

How do you diagnose Cushing’s?

A

Overnight dexamethasone suppression test
Low dose dexamethasone suppression test
Urine free cortisol test

48
Q

How do you do an overnight dexamethasone suppression test?

A

1mg dexa at midnight and cortisol test at 8am

<50 is normal and >100 is abnormal

49
Q

What is the best test for diagnosis Cushing’s?

A

Low dose dexa suppression test

50
Q

How do you do a low dose dexa suppression test?

A

0.5mg dexa every 6 hours

<40 is normal

51
Q

What is a normal result in a urine free cortisol test?

A

<250

52
Q

How do you differentiate between primary and secondary Cushing’s?

A

Primary ACTH<1
Secondary pit origine <300
Secondary ectopic origine >300

53
Q

How do you treat Cushing’s?

A

Treat underlying cause
Metyrapone
Ketoconazole

54
Q

What is Cushing’s disease?

A

Pit adenoma producing too much ACTH leading to Cushing’s syndrome

55
Q

What two forms of hyperaldosteronism can you have?

A

Primary/Conn’s syndrome

Secondary

56
Q

What causes secondary hyperaldosteronism?

A

Decrease blood flow to the kidneys increasing aldosterone release.

57
Q

What causes primary hyperaldosteronism?

A

Adenoma or hyperplasia of adrenal glands.

Remember not all nodules are significant!!!

58
Q

What is primary hyperaldosteronism?

A

Autonomous production of aldosterone

59
Q

What is another term for primary hyperaldosteronism?

A

Conn’s syndrome

60
Q

How does primary hyperaldosteronism present?

A

Hypertension
Hyperkalemia
Alkalosis
Raised BP

61
Q

How do you diagnose hyperaldosteronism?

A

Confirm aldosterone excess by doing:

Ratio of plasma aldosterone and renin. If ratio raised diagnose subtype

62
Q

How do you diagnose the subtype of hyperaldosteronism?

A

CT imaging

Adrenal vein sampling (use cortisol as a control)

63
Q

How do you treat primary hyperaldosteronism?

A

Remove underlying cause (only in the young)

Spironolactone

64
Q

What causes Congenital Adrenal Hyperplasia?

A

The loss of an enzyme in the metabolism of cholesterol to steroids

65
Q

What is the most commonly lost enzyme in CAH?

A

12alpha hydroxylase

66
Q

What does the loss of 12alpha hydroxylase do?

A

Inability to produce aldosterone or cortisol so direct metabolites down testosterone route

67
Q

What are some symptoms of CAH?

A

Addison’s style symptoms
Early puberty in males
Ambiguous female genitalia
Poor weight gain

68
Q

How do you diagnose CAH?

A

Genetic testing

Synacthen test but look for 17-OH progesterone

69
Q

How do you treat CAH?

A

Give GC and MC replacement

Correct physical abnormalities

70
Q

Is the loss of the adrenal medulla much of a problem?

A

No as catecholamines (adrenaline etc) are made elsewhere too.

71
Q

What is a major cause of adrenal medulla overaction?

A

Phaeochromocytoma

72
Q

What is pheochromocytoma?

A

Tumour derived from chromaffin cells in the adrenal medulla

73
Q

What is another name for the pheochromocytoma?

A

10% tumour

74
Q

What is a common triad of symptoms in pheochromocytoma?

A

Hypertension- labile or postural
Paroxysmal (fast on/off) sweating
Headaches

75
Q

What are some of the symptoms of pheochromocytoma?

A 
Hypertension- labile or postural
Paroxysmal (fast on/off) sweating
Headaches
Pallor
Tachycardia
Hyperglycemia
Low K
Lactic acidosis
76
Q

How do you diagnose pheochromocytoma?

A

24h urine catecholamines

Plasma catecholamines at time of symptoms

77
Q

What do you have to do once you’ve diagnosed pheochromocytoma?

A

ID the source- MRI or MIBG (radio uptake) to do this

78
Q

How do you ID where a pheochromocytoma is?

A

MRI or MIBG (radio uptake)

79
Q

How do you treat pheochromocytoma?

A

Treat underlying cause
Alpha and beta blockers
Always give alpha first

80
Q

What is pheochromocytoma often associated with?

A

MEN2
VHL
Succinate dehydrogenase B and D mutations
Neurofibromatosis

81
Q

What is an extra adrenal gland source of excessive catecholamine production?

A

Extra adrenal paraganglioma

82
Q

Where can extra adrenal paragangliomas be found?

A

Anywhere in the sympathetic chain

83
Q

In panhypopituitarism what is the most important hormone to replace?

A

Cortisol

84
Q

Why does ACTH not tend to be measured directly?

A

Needs to be sent to lab on ice and processed ASAP

85
Q

What time of day and how often should cortisol replacement be given?

A

Large dose in morning
Smaller dose at lunch
Nothing in evening or won’t sleep

86
Q

What do you need to monitor when taking fludrocortisone and why?

A

Blood chemistry and BP to check not retaining too much salt

87
Q

What is an Addisonian crisis?

A

Symptomatic Addison’s- especially with low BP

88
Q

How do you treat an Addisonian crisis?

A

Fluid and hydrocortisone

89
Q

Why can you use hydrocortisone to treat and Addisonian crisis?

A

Because GC have a degree of efficacy at MCR.

90
Q

What should you do to their medication if a patient receiving cortisol replacement therapy is ill?

A

Minor illness- double dose and keep doubled for 24hrs after illness
Major illness- Double dose and wean off after

91
Q

How do you treat Conn’s disease?

A

Spironolactone

92
Q

What is Conn’s disease?

A

Primary hyperaldosteronism

93
Q

How does Conn’s disease present?

A

Raised BP and Na

Low K

94
Q

What does Metyrapone do?

A

Block GC production

95
Q

What two kind of steroids can the adrenal gland produce?

A

Glucocorticoids

Mineralocorticoids

96
Q

How do GCs work?

A

Bind to nuclear receptors which can then form a dimer with the help of +Glucocorticoid Recognition Element or bind to nGRE remain as a monomer

97
Q

Are GC monomers and dimers active?

A

Monomer inactive

Dimer active

98
Q

Are GCs restricted to acting on just their own receptors?

A

No, they can act on MCR too

99
Q

What negative effects can activation of the GCR have?

A

Increase feeding

Increase alcohol cravings

100
Q

What negative effects can actions of the GC on the MCR have?

A

Skin atrophy and poor wound healing

101
Q

How can you mitigate GCR effects on alcohol cravings?

A

By giving the morning after pill

102
Q

What does a solid mass in the adrenal gland suggest?

A

Metastasis- lung met most common

Endocrine (23 decks)

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