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LMP301 > LMP301 Lecture 9: Adrenal Disease > Flashcards

LMP301 Lecture 9: Adrenal Disease Flashcards

Adrenal Diseases

1
Q

Where are the adrenal glands?

A

On top of the kidneys

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2
Q

What happens to the adrenal gland during stressful situations?

A

enlarge

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3
Q

Adrenal gland is divided into…

A
  • cortex

- medulla

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4
Q

The cortex of the adrenal gland is divided into…

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
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5
Q

The adrenal medulla is a part of the…

A

SNS

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6
Q

Zona glomerulosa secretes….

A

aldosterone

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7
Q

zona fasciculata secretes…

A
  • cortisol

- adrenal androgens & estrogens

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8
Q

zona reticularis secretes…

A
  • cortisol

- adrenal androgens & estrogens

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9
Q

The adrenal medulla secretes…

A
  • E
  • NE
  • Dopamine
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10
Q

What is the first enzyme to act on cholesterol during the biosynthesis of steroid hormones?

A

Cholesterol side chain cleavage hormone

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11
Q

What are the steroid hormones?

A
  • aldosterone
  • cortisol
  • testosterone
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12
Q

ACTH

A

Signal needed for biosynthesis of steroid hormones

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13
Q

Enzyme cascade for aldosterone synthesis

A
  1. Cholesterol side chain cleavage hormone
  2. 3B-hydroxysteroid dehydrogenase
  3. 21 OH’ase
  4. 11 OH’ase
  5. 18 OH’ase
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14
Q

Enzyme cascade for cortisol synthesis

A
  1. Cholesterol side chain cleavage hormone
  2. 17 OH’ase
  3. 3B-hydroxysteroid dehydrogenase
  4. 21 OH’ase
  5. 11 OH’ase
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15
Q

Enzyme cascade for testosterone synthesis

A
  1. Cholesterol side chain cleavage hormone
  2. 17 OH’ase
  3. 17,20 OH’ase
  4. 3B-hydroxysteroid dehydrogenase
  5. 21 OH’ase
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16
Q

Which enzyme is unique to aldosterone synthesis?

A

18 OH’ase

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17
Q

Pathway of aldosterone synthesis

A
  1. Cholesterol
  2. Pregnenolone
  3. Progesterone
  4. Deoxycorticosterone
  5. Corticosterone
  6. Aldosterone
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18
Q

Pathway of cortisol synthesis

A
  1. Cholesterol
  2. Pregnenolone
  3. 17-OH pregnenolone
  4. 17-OH progesterone
  5. 11-deoxycortisol
  6. Cortisol
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19
Q

Pathway of testosterone synthesis

A
  1. Cholesterol
  2. Pregnenolone
  3. 17-OH pregnenolone
  4. DHEA
  5. Androstenedione
  6. Testosterone
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20
Q

Cortisol can affect…

A

metabolism of carbs, proteins, and fat

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21
Q

Effect of cortisol on carb metabolism

A

Raise blood glucose

  • gluconeogenesis in liver
  • reduce glucose used and stored
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22
Q

Effect of cortisol on protein metabolism

A

Break down muscle

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23
Q

Effect of cortisol on fat metabolism

A

Break down fat

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24
Q

What happens when glucocorticoids are present in excess?

A

cause central distribution of fat -> goes to face, neck, trunk

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25
Q

How do cortisol travel in the body?

A

90 - 98% is bound to proteins

  • albumin
  • cortisol binding globulin (CBG)
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26
Q

When can an increase of CBG be found?

A
  • Pregnancy

- Estrogen treatment

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27
Q

How is cortisol metabolized in the body?

A
  1. Liver

2. Excreted in urine

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28
Q

Axis that controls cortisol secretion

A

Hypothalamic-pituitary-adrenaocortical axis

  1. Hypothalamus -> CRH
  2. a. pituitary -> ACTH
  3. adrenal cortex -> cortisol
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29
Q

Feedback of cortisol

A

Cortisol inhibits ACTH and CRH

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30
Q

What stimulates production of CRH?

A

Stress

Sleep/wake

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31
Q

What is too much cortisol called?

A

Cushing’s syndrome

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32
Q

Possible causes of Cushing’s syndrome

A
  • tumour at pituitary (ACTH overproduction)
  • ectopic ACTH
  • adrenal gland tumour (excess cortisol)
  • exogenous glucocorticoids
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33
Q

Ectopic ACTH

A

ACTH produced by cells other than the pituitary

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34
Q

What cells may produce ACTH, other than pituitary?

A

small cell carcinoma in the lung

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35
Q

some sources of exogenous glucocorticoids

A
  • oral
  • inhaled
  • topical creams
36
Q

Clinical features of Cushing’s Syndrome

A
  • Acne
  • Moon face
  • Osteoporosis
  • abdominal fat
  • stripes on abdomen
  • high BP
  • buffalo hump
37
Q

At what time during the day is cortisol levels the highest?

A

Morning

38
Q

What is used to screen for Cushing’s?

A

24h urine test:

  • High cortisol in the urine
  • Can also be caused by stress & obesity
39
Q

What tests are used to diagnose Cushing’s?

A
  • plasma cortisol
  • low dose dexamethasone test
  • high dose dexamethasone test
  • plasma ACTH
40
Q

dexamethasone is…

A

a cortisol analogue

41
Q

When is plasma cortisol measured?

A

8AM

10 PM

42
Q

What is looked for in a plasma cortisol test?

A

Cortisol will not vary with time of day in patients with Cushing’s

43
Q

What is looked for in a low dose dexamethasone test?

A
  • normal: slow cortisol production by 50%

- Cushing’s: can’t slow cortisol production

44
Q

What is looked for in a high dose dexamethasone test?

A
  • Cushing’s disease: slow cortisol productivity by 50%

- Other causes: will not slow cortisol productivity

45
Q

Why is high dose dexamethasone test used?

A

Which of the Cushing’s syndrome causes it was

46
Q

Difference between Cushing’s disease and syndrome

A

Disease: cause is specifically a pituitary tumour producing too much ACTH

Syndrome: tissues being exposed to too much cholesterol for too long

47
Q

What is looked for in plasma ACTH?

A
  • high ACTH = ectopic ACTH tumors

- low ACTH = adrenal tumours

48
Q

What order are tests used to diagnose Cushing’s?

A
  1. Screening: plasma cortisol
  2. Confirmation: low dose dexamethasone
  3. Differential diagnosis of cause: high dose dexamethasone; plasma ACTH
49
Q

Cortisol is the counter hormone of…

A

insulin

50
Q

Aldosterone is only produced in the zona glomerulosa because…

A
  • doesn’t have 17 OH’ase
  • have 18 OH’ase
  • have 18 hydroxysteroid dehydrogenase
51
Q

What regulates aldosterone production and secretion?

A
  • Renin-ANG II system (major)
  • ACTH
  • Potassium
52
Q

Biological effect of aldosterone

A

Raise BP:

  • Na and H2O retention
  • K and H secretion
53
Q

Why is hypertension seen in patients with Cushing’s?

A

all cortisol precursors and cortisol have some kind of mineralocorticoid effects (SAME EFFECT AS ALDOSTERONE)

54
Q

Renin is released in response to…

A
  • Low tubular Na+
  • Low BP at renal arteries
  • SNS stimulation
55
Q

Increased K+ has what effect on aldosterone?

A

Stimulates secretion/production

56
Q

ACTH has what effect on aldosterone?

A

Very little effect, especially in normal situations

57
Q

Function of renin

A

angiotensinogen -> ANG I

58
Q

Function of ACE

A

ANG I -> ANG II

59
Q

Clinical features of excess aldosterone

A
  • high BP
  • neuromuscular weakness due to lack of K+
  • polydipsia & polyuria
60
Q

Why is a symptom of excess aldosterone polydipsia & polyuria?

A
  • hypokalemia causes ADH resistance = more water secreted
61
Q

nephrotic diabetes insipidus is caused by…

A

ADH resistance

62
Q

High aldosterone is…

A

Conn’s syndrome

Low-renin hyperaldosteronism

63
Q

High aldosterone is usually due to…

A

adrenal tumours

64
Q

Conn’s syndrome is ___ hyperaldosteronism

A

primary

65
Q

Secondary hyperaldosteronism = high ___

A

renin

66
Q

Secondary hyperaldosteronism is usually associated with…

A

renal, heart, liver disease

67
Q

Secondary hyperaldosteronism is also known as…

A

renal artery stenosis

68
Q

Which type of hyperaldosteronism is more common?

A

secondary

69
Q

Primary hyperaldosteronism: sequence of events

A
  1. adrenal gland secretes a lot of aldosterone
  2. aldosterone causes increased Na+ retention & increase K+ loss
  3. High Na+ causes decreased renin
  4. causes decreased ANG II
70
Q

Secondary hyperaldosteronism: sequence of events

A
  1. Decreased blood flow at renal artery
  2. Increased renin
  3. Increased ANG II
  4. Increased aldosterone
  5. Increased Na+ retention
  6. Increased K+ loss (also caused by high aldosterone)
71
Q

Diagnosis of hyperaldosteronism

A
  • low K+ (a lot excreted)
  • High aldosterone
  • renin low (primary)
  • renin high (secondary)
72
Q

Acid-base status in patients with hyperaldosteronism?

A

Metabolic alkalosis (H+ secreted because Na+ is retained)

73
Q

Low aldosterone is ___ disease

A

Addison’s

74
Q

Addison’s disease (and what is it due to?)

A

Low aldosterone

- Due to autoimmune destruction of the cortex

75
Q

Causes of hypoadrenalism

A
  • Autoimmune destruction of cortex
  • Gland destruction caused by tuberculosis, infections, cancer
  • Secondary / tertiary hypoadrenalism caused by ACTH deficiency (pituitary / hypothalamus problem)
  • Long-term corticosteroid therapy: breaks the HPA axis
76
Q

Difference between primary and secondary and tertiary hypoadrenalism

A
  • primary: problem at adrenal gland (ACTH high)
  • secondary: problem at a. pituitary (ACTH low)
  • tertiary: problem at hypothalamus (CRH low)
77
Q

Clinical features of hypoadrenalism

A
  • lethargy
  • anorexia
  • weight loss
  • increased pigment in hand and mouth (Addison’s)
  • abdominal pain
78
Q

Why is there increased pigment for Addison’s?

A

melanocyte-stimulating hormone is secreted along with ACTH (which is secreted in high amounts)

79
Q

Acute crisis for hypoadrenalism

A
  • dehydration
  • hypotension
  • nausea
  • vomiting
80
Q

Biochemical features of hypoadrenalism

A
  • low NA+
  • high K+
  • mild metabolic acidosis
  • hyperuremia
  • hypoglycemia
  • high ACTH (primary)
81
Q

Diagnosis of hypoadrenalism

A

Short Synacthen test

82
Q

Problem with testing serum aldosterone

A

Have to have normal to compare to (the normal must be from the same person)

83
Q

Synacthen is a ____ analogue

A

1-24 ACTH

84
Q

Short Synacthen test is also called…

A

ACTH stimulation test

85
Q

Short Synacthen test

A
  1. measure serum cortisol
  2. give synacthen
  3. measure cortisol 30 min later
86
Q

Interpreting short Synacthen test

A

Normal: cortisol rise rapidly
Addison’s: no change
Adrenal atropy: slight rise

87
Q

Anti-hypertensive agents used (RAAS)

A
  • ACE inhibitor
  • ANG II receptor blocker
  • Block aldosterone receptor
  • Block renin receptor

LMP301 (18 decks)

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