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Cardio > Biochemistry Pituitary and Adrenal > Flashcards

Biochemistry Pituitary and Adrenal Flashcards

1
Q

Conditions with Increased ACTH (low cortisol/ increase primary production) also present with:

A
  1. Beta endorphins
  2. Melanocyte hormone (increased pigmentation)

Cleaved from: pro-opiocortin

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2
Q

From Cholesterol produces:

A
  1. Aldosterone
  2. Cortisol
  3. Testosterone (25%)
  4. Oestradiol
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3
Q

cortisol Epi production rate

A

Most important glucocorticoid

Production rate c. 25mg/day

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4
Q

Cortisol forms

A

90% protein bound (CBG and Albumin)

Free Fraction physiologically active

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5
Q

Cortisol Effects

A 
Carbohydrate metabolism
•	Insulin antagonist
•	Gluconeogenesis
Protein Catabolism
Immunosuppression (can be done therapeutic)
“Permissive action”
•	Catecholamines
•	Free water clearance – w/o cortisol inappropriate ADH production there H2O retention - hyponatraemia
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6
Q

Test for Cortisol

A

Total Cortisol level e.g. bound and free

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7
Q

Pathology of Cortisol

A

Significant abnormalities in proteins such as loss of proteins or an increase in proteins (pregnancy)

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8
Q

Increase production of Cortisol

A

Increase in total and increase in free fraction as binding proteins saturated.

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9
Q

Cortisol control

A
  • Negative feedback
  • Diurnal (lowest at midnight, rise am, decreases in day)
  • Stress (exercise, emotion)
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10
Q

Primary Causes of Cortisol suppression:

A
  • Congenital adrenal hyperplasia
  • Enzyme defect
  • Selective or total destruction via a variety of causes
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11
Q

Selective destruction of cortex causes

A

Autoantibodies

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12
Q

Total adrenal destruction cause

A

Bacterial and fungal infections
TB
Metastatic carcinoma
Amyloidosis

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13
Q

Secondary Adrenal Insufficiency causes

A

Steroids – ACTH deficiency due to hypothalamic or pituitary disease

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14
Q

Adrenal Insufficiency Consequences:

A
  1. Hypoglycaemia
  2. Hypo-natraemia
  3. Hyperkalaemia
  4. Hypotension
  5. Pigmentation
  6. Non-Specific
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15
Q
  1. Hypoglycaemia
A

Uncommon seen in neonates/cause adrenal crisis

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16
Q
  1. Hypo-natraemia
A

Destruction leads to aldosterone loss and so Sodium loss and…

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17
Q
  1. Hyperkalaemia
A

Potassium retention from aldosterone

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18
Q
  1. Hypotension
A

Primary Cause (lack of negative feedback = ADH inappropriate control

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19
Q
  1. Pigmentation
A

Primary Causes – due to cleavage to form ACTH and so melanocyte hormone produced

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20
Q

Addison’s Disease symptoms:

A
  • Lethargy
  • Anorexia
  • Pigmentation of hands and mouth – look at non sun-exposed areas.
  • Abdominal pain
  • Weight loss
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21
Q

Acute Adrenal Crisis:

A
  • Vomiting
  • Nausea
  • Dehydration
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22
Q

Laboratory Investigations available →

A

Serum Cortisol
Dynamic synacthen (synthetic ACTH) stimulation test
ACTH

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23
Q

Serum Cortisol

A

Problems as

  1. A strong diurnal rhythm
  2. If the patient is stressed false raised
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24
Q

Dynamic synacthen (synthetic ACTH) stimulation test

A 
Short: 250 ug given IM
Looking for: Rise on cortisol
Normal’s:
•	Incremental rise >200 nmol/L
•	Absolute rise >600 nmol/L
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25
Q

ACTH

A

Differentiates 1o/20

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26
Q

Synacthen stimulation test:

A
  1. Normal rise (+200) and exceeds 600
  2. Flat basal, no increase aove +600 – abnormal
  3. Baseline normal, response abnormal – poor increase
  4. V. high – severe stress
  5. V. high – Iatrogenic (hydrocortisone)
27
Q

Causes of poor increase

A

a. Early stages w/ reserved adrenal function

b. Patient on steroids recently

28
Q

• Primary adrenal failure

A

lack aldosterone (cortisol) >Na loss and K secretion

29
Q

Electrolytes failure

A

• >Hyponatraemia >low plasma osmolality >reduced ADH (not completey reduced) – as cortisol permissive

  • Loss of water to correct hyponatraemia
  • Salt loss continuous and therefore water loss will be as well
  • IV V becomes depleted ADH will eventually be secreted and some reabsorption
30
Q

Electrolytes in adrenal failure

A

• Hyponatraemia, hyperkalaemia, volume depletion

31
Q

21-hydroxylase enzyme action

A
  1. Aldosterone (progesterone to Deoxycorticosterone)
  2. Cortisol (17-OH progesterone to Deoxycortisol)
    Gland still stimulated therefore overproduction of androgens.
32
Q

21-hydroxylase Deficiency

A

Reduced aldosterone an reduced Cortisol

33
Q

CAH Presentation

A

Ambiguous external genitalia

34
Q

CAH Epi

A

> 90% of cases of CAH

35
Q

CAH Marker

A

Increased 17 alpha OH progesterone

36
Q

CAH Classical Form

A

Incidence 1:5,000-1:20,000
Simple virilising
Salt wasting
Late onset

37
Q

CAH Clinical Manifestations New Born

A

Ambiguous external genitalia
Pigmented scrotum
Salt wasting
Sudden unexplained death (males)

38
Q

CAH Clinical Manifestations Adult

A

Hirsutism (females) – most common in PCOS
Menstrual cycle disorder
Subfertility

39
Q

CAH Investigations

A

Blood
Urine
Karyotype

40
Q

CAH Blood investigations

A
  • 17 alpha hydroxyl progesterone (also following synactin as baseline not good but response is diagnostic)
  • Electrolytes (hypo Na+, hyper K+)
  • Glucose - neonates
  • Increased Androstenedione
  • Increased Testosterone
  • Renin – mineral-corticoid treatment monitor
  • 17-OHP profiles (shows under/over treatment monitoring)
41
Q

CAH Renin results

A

Over: Renin reduced volume expands
Under: Renin increased volume depleted

42
Q

CAH Urine

A

Electrolytes

Steroid profile

43
Q

CAH Karyotype

A

For determining the sex

44
Q

Hypercortisolism (Cushing’s) → 2 types

A

ACTH High

ACTH low

45
Q

Hypercortisolism (Cushing’s) → ACTH high causes

A

Pituitary Cushing’s Disease

Ectopic (lung)

46
Q

Hypercortisolism (Cushing’s) → ACTH low

A

Adenoma’s – adrenal feedback
Carcinoma – adrenal feedback
Iatrogenic - overtreatment

47
Q

Clinical features of Cushing’s

A
  1. Mental disturbances
  2. Fat redistribution, truncal obesity striae
  3. Protein Catabolism
  4. Osteoporosis
  5. Poor wound healing
  6. Bruising
  7. Hyperandrogenism
  8. Hirsutism
  9. Acne
  10. Amenerrhoea
  11. Insulin resistance
  12. Glucose intolerance
  13. Salt retention
  14. Hypertension
  15. Immunosuppression
48
Q

Initial Investigation – define excess cortisol production 7 ways

A
  1. Serum Cortisol
  2. Salivary Cortisol
  3. Urine Free cortisol
  4. Dexa suppression
  5. Yanovski
  6. CRH testing
  7. High dose dexa
49
Q

➢ Serum cortisol

A

Midnight/ 08:00 am
• Limited value
• Increased in stress
• False negative values in Cushing’s patients

50
Q

➢ Salivary cortisolNB increased in stress illness and obesity
Problems in urine collection
Many assays not specific for cortisol

A

Midnight/09:00
• Demonstrate loss of diurnal rhythm
• Easy to collect at home, stress free environment
➢ D

51
Q

➢ Urine free cortisol

A

NB increased in stress illness and obesity
Problems in urine collection
Many assays not specific for cortisol

52
Q

➢ Dexamethasone Suppression

A

1 mg over night test (to exclude Cushing’s) – 09:00 am cortisol should be <50 nmol/L

53
Q

Dexamethasone problem

A

High false positive rate
• Absorption dexamethasone
• Failure to take tablet
• Increased metabolism

54
Q

Dexamethasone false negative

A

Cyclical Cushing’s (wax/waning)

55
Q

Low dose dexamethasone

A

0.5 mg 6 hourly for 48 hours
→ Normal suppress
→ Cushing’s – no suppression

56
Q

➢ Yanovski

A

Define excess cortisol production: looking at CRH following dexamethasome

57
Q

Yanovski test

A

Cushing’s syndrome = massive cortisol increase after 15 mins

Normal = Cortisol low

58
Q

Serum Cortisol (09:00) =

A

523 nmol/L 9150-700)

59
Q

UFC =

A

445/L/ 24 hrs (<120)

60
Q

Post dexamethasone cortisol:

A

Serum Cortisol (09:00) = 531 nmol/L

61
Q

➢ Ectopic V Pituitary ACTH production

A
  • Bilateral Inferior Petrosal Sinus Sampling (BIPSS) – to differentiate
  • Cushing’s disease – Increase ACTH in blood post pituitary
  • Central – peripheral gradient +3
62
Q

➢ High Dose Dexamethasone

A

2 mg 6 hourly for 48-72 hours
• Pituitary dependant (Cushing’s disease) suppress – w/ enough dexa
• Adrenal and Ectopic ACTH no suppression

63
Q

Ectopic sources of ACTH response to CRH

A

Don’t respond

64
Q

Cushing’s disease response to CRH

A

Exaggerated ACTH production

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