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Medsci 312 > Lecture 20; Adrenal Gland Disease > Flashcards

Lecture 20; Adrenal Gland Disease Flashcards

1
Q

Can the adrenal glands be easily imaged?

A

No, very difficult

Two of them sit above the kidneys

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2
Q

How are the adrenal glands divided?

A

Into cortex and medulla regions

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3
Q

Describe what is produced where in the adrenal glands;

A

Cortex;

  • Zona Glomerulosa = Mineral corticoids i.e Aldosterone
  • Zona fasiculatis = Glucocorticois i.e cortisol
  • Zona retigulcaris = androgens (imp. in women)

Medulla
- Adrenalin and noradrenalin

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4
Q

What are the functions of cortisol?

A

Stress hormone, energy metabolism, glucose homoeostasis

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5
Q

What do all adrenal cortex hormones originate from?

A

Cholesterol back bone precursor

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6
Q

Describe the adrenal cortex hormone production circuit;

A

Co-ordinated enzymatic steps (one goes wrong can be very bad)

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7
Q

What is the most common enzyme defect in the adrenal cortex pathway and whats the effects of this?

A

21-OH dysfunction

Shunts hormone production to the development of testosterone
- Inc. 17-hydroxyprogesterone (measure this as indicator)

  • Decreased Aldosterone = Salt wasting and hyperkalemia
  • Decreased Cortisol = Impaired response to stress and illness
  • Increased testosterone = Virilization (in women)
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8
Q

Describe the HPA axis for cortisol production;

A

AVP and CRH in hypothalamus cause ACTH release from AP.

This results in cortisol release which negative feedbacks to hypothalamus and AP

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9
Q

What happens when there is excess secretion of glucocorticoids?

A

Cushings syndrome

  • Moon face
  • Obese
  • hypertension
  • mental abnormalities

Can be caused by;

  • Adenoma
  • Uncontrolled ACTH secretion
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10
Q

What happens in excess mineralcorticoid secretion?

A

Conn’s Syndrome

  • Na retention
  • Hypokalemia
  • Hypoklameic alkalosis
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11
Q

What may cause deficient adrenal gland hormone secretion?

A
  • Addinsons disease (hyperpigmentation, hypotension)
  • Secondary adrenal insufficiency (usual due to steroid medicaiton)
  • Adrenalectomy
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12
Q

Describe RAAS production of aldosterone;

A
  • Decreased BP, BV, and osmolarity cause renin release —-> ANG 2 release

ANG2 acts on adrenal gland with ACTH = Aldosterone production

Aldosterone = increased K excretion and increase Na absortion = Increased BV and BP

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13
Q

Whats key to know in NE and EP production?

A
  • Short lived in the circulation and are converted to stable metabolic products. (these can be measured for indirect values of EP and NE)
  • EP -> Metanephrine
  • NE -> Normetanephrine
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14
Q

What are the possible diseases when cortisol is in excess and insufficient?

A

Excess; Cushings syndrome

Insufficiency;

  • Primary Adrenal failure, Addison’s disease
  • Secondary Pituitary failure
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15
Q

What are the possible diseases when aldosterone is in excess and insufficient?

A

Excess; Primary hyperaldosteronism, hypertension and hypokalemia
Insufficiency; Adrenal failure, hypotension and ↑ sK+

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16
Q

What are the possible diseases when androgens are in excess and insufficient?

A

Excess; Virilization (women)

Insufficiency; No phenotype

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17
Q

What are the possible diseases when catecholamines are in excess and insufficient?

A

Excess; Pheochromocytoma, hypertension, paroxsymal symptoms

Insufficiency; No phenotype

18
Q

What is the assessment for excess cortisol;

A

Excess; 24 hr urinary free cortisol, 1mg overnight dexamethasone suppression test

19
Q

What is the assessment for insufficient cortisol;

A

Insufficiency

  • Primary 1µg short synacthen test, basal ACTH
  • Secondary 1µg short synacthen test
20
Q

What is the assessment for excess aldosterone;

A

Excess; Plasma aldosterone to renin ratio

21
Q

What is the assessment for insufficient aldosterone;

A

Insufficient; Renin (↑), aldosterone (↓), sK+ (↑)

22
Q

What is the assessment for excess androgens?

A

Excess; Plasma testosterone (women)

- Basal and ACTH-stimulated 17(OH) progesterone (CAH)

23
Q

What is the assessment for excess catecholamines?

A

Excess; Plasma metanephrines, 24 hr urinary metanephrines

24
Q

What are the signs and symptoms of primary adrenal insufficiency?

A
  • Fatigue, weakness
  • Pigmentation of the skin and mucous membranes
  • Bradycardia
  • Dehydration
  • Orthostatic hypotension
  • Weight loss
  • Loss of pubic hair
25
Q

What are some blood markers of primary adrenal insufficiency?

A

Decreased cortisol response to ACTH,
Hypoglycemia
↑ sK+, ↓ sNa+, ↑ s creat

Test; 1µg short synacthen test
basal ACTH

26
Q

What are the causes of primary adrenal insufficiency?

A

Autoimmune
Tuberculosis
Adrenoleukodystrohpy
Metastasis, hemorrhage

27
Q

What exactly becomes hyperpigmented in addinsons disease?

A

Palmar creases

Buccal mucosa

28
Q

How can primary and secondary adrenal insufficiency be differentiated?

A

Measuring plasma ACTH levels

  • Primary = High 200+ units
  • Secondary = normal, below 200

This is a compensatory mechanism in primary. Bi-product of high ACTH is MSH which causes the hyperpigmentation

29
Q

What is the Synacthen test?

A

Synthetic ACTH is given and cortisol levels are measured.

<550nmol/L indicates there is a problem (primary) or secondary

30
Q

What are some clinical clues as to the presense of primary aldosteronism?

A
  • Spontaneous hypokalemia
  • Diuretic induced hypoklamia
  • Refractory Hypertension
  • Family history
  • Hypertension in young adults
31
Q

What is another primary aldonesterism test?

A

Insulin tolerance test

32
Q

What are the possible treatment options for adrenal insufficiency?

A

Glucocorticoid

  • Hydrocortisone 15-25mg/day
  • Increase dose for duration of minor illness
  • HC 50-100mg tds for severe illness/major surgery

Mineralocorticoid (primary only)

  • Fludrocortisone 0.1-0.2mg od
  • Monitor renin and BP
  • No change for illness

Androgens for women

MedicAlert bracelet!!

33
Q

Describe the pathophysiolgy of primary hyperaldosteronism;

A
  • Increased aldosterone secretion b/c
    1) Aldosterone producing tumor (benign mostly)
    2) Bilateral adrenal hyperplasia

=
- Increased BV, BP and hypokalemia

RAAS pathway decreases a lot (feedbacl) but no effect

34
Q

What test can be done to detect primary hyperaldosteronism?

A

Screening plasma aldosterone to renin ratio (-ive feedback)

B/c high BP = Decreased Renin (glomerular feedback)

35
Q

What tests can be done to diagnose primary hyperaldosteroism?

A 
Potassium wasting (high in urine, low in serum)
Suppressed plasma Renin
Altered plasma renin;aldosterone ratio

Plasma aldosterone is on-supressible after salt loading

36
Q

What is pheochromacytoma?

A

Cancer of the adrenal gland that results in excess catecholamines

37
Q

How can pheochromacytoma be diagnosed?

A

Measure 24hr urine catecholamines (2-3x)

Urinary/serum fractioned metanephrines

CT/MRI

38
Q

Whats the incidence of Adrenal Incidentaloma?

A

1-2% of abdominal CT scans 2-10% at autopsy Prevalence ↑ with age
(1-7% of AI are carcinoma)
even if known malignancy, >50% are benign
10% associated with cortisol autonomy 3% pheochromocytoma
1% aldosteronoma

39
Q

How does a Adrenal Incidentaloma appear on the radiology?

A

Smooth, homogeneous favours adenoma

4cm

40
Q

What is a Adrenal Incidentaloma density?

A

High fat content favours adenoma
< 2 HU unenhanced CT scan = benign [33% of AI]
Loss of signal on “out of phase” MRI favours adenoma

Medsci 312 (28 decks)

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