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GIT physiology > Endocrine Role of Adrenal Glands > Flashcards

Endocrine Role of Adrenal Glands Flashcards

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1
Q

Where are adrenal glands found

What are they morphologically

A

Superior poles of kidneys

2 glands in 1

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2
Q

What is found in the outer cortex (80%)

A

Many steroid hormones

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3
Q

What is found in the inner medulla (20%)

A

Secretes adrenaline, nor-adrenaline

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4
Q

Pathway of formation of adrenaline

A
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5
Q

How much does adrenaline account for (in terms of secretion)

A

80%

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6
Q

How much does noradrenaline account for (in terms of secretion)

A

20%

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7
Q

Blood concentration of adrenaline

A

10-10 M

Can increase to 10-7 M in stress

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8
Q

Effects of adrenal medulla hormones on CVS

A
  • INCREASED CO
  • Increased HR
  • Increased SV
  • Increased BP
  • INCREASED BLOOD RE-DISTRIBUTION
  • Increased BF to coronary muscle
  • Decreased BF to GIT
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9
Q

Effects of adrenal medulla hormones on GIT

A

Decreased motility

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10
Q

Effects of adrenal medulla hormones on skin

A

Increased sweating

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11
Q

Effects of adrenal medulla hormones on skeletal muscle

A

Increased tension generated

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12
Q

Effects of adrenal medulla hormones on nervous tissue

A

Increased brain arousal, reflex speed, aggression, anxiety

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13
Q

Metabolic effects of adrenal medulla hormones

A
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14
Q

What is Pheochromocytoma

What does it arise from

A
  • Rare catecholamine producing tumour
  • Arises from chromaffin cells of adrenal medulla or from sympathetic ganglia
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15
Q

Symptoms of pheochromocytoma

A

5 Ps

  1. Pressure - sudden major increase in BP
  2. Pain - abrupt throbbing headache, chest, abdominal pain
  3. Perspiration - generalised diffuse diaphoresis
  4. Palpitations usually with true tachycardia often with feelings of panic or anxiety
  5. Pallor of skin from vasoconstriction
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16
Q

What does the adrenal cortex produce

A

Steroid hormones

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17
Q
  1. What are mineralocorticoids derived from
  2. Are they stored
  3. When are they synthesised
A
  1. Derived from cholesterol
  2. Not stored
  3. Synthesised on demand

ALDOSTERONE - NB

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18
Q

What are glucocorticoids bound to

A

Plasma

e.g. cortisol - pregnancy and childbirth

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19
Q

What are weak androgens/sex steroids

What do they do

A

Intra cellular receptors - cytoplasmic or nuclear

Alter gene activity

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20
Q

Structure of adrenal gland

A

Hormones produced in each layer are different

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21
Q

Formation of hormones from cholesterol

A
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22
Q
  • What parts of adrenal gland are glucocorticoids secreted by
  • Name 3 examples
  • What is cortisol blood conc
A
  • Secreted by zona fasiculata and reticularis (smaller amounts)
  • Cortisol, corticosterone, cortisone
  • **** 5-25 ug/100ml
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23
Q

What is cortisol release controlled by

A

HPA axis

Dexamethasone suppression test

Based on -ve feedback

Test cause of hypercortisolemia

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24
Q

What is the pattern of cortisol secretion

A
25
Q
  1. Where is Adrenocorticotrophin produced
  2. What sort of hormone is it
  3. What is its precursor
A
  1. Anterior pituitary
  2. Peptide hormone => prepro -> pro
  3. Precursor Pro-Opio-Melano-Corticotrophin (POMC)
26
Q

What are beta endorphins

A

Natural pain killers

27
Q

Clinical manifestation of lack of cortisol

A

Pigmentation of skin

28
Q

What is over-produced when we’re not producing cortisol

A

MSH

Melanocyte-Stimulating Hormone

29
Q

Pathway for production of cortisol

A

CRH

|

ACTH

|

CORTISOL (free)

30
Q

What is cortisol carried by

Where is it made

Examples

A

Cortisol binding globulin TRANSCORTIN

Made by the liver

31
Q

Effect of an increase in oestrogen on cortisol

A

Increases cortisol

32
Q

Effect of increase in free cortisol on CRH and ACTH

A

Inhibits CRH and ACTH

Liver makes more transcortin to bind more cortisol

33
Q

How is cortisol transported

A

Bound in plasma by cortisol binding globulin transcortin, which is synthesised by the liver

34
Q

What is the metabolic effect of cortisol

A

Spares glucose and promotes breakdown of protein and fat

Overall catabolic and diabetogenic

35
Q

What are the anti-inflammatory and immunosuppressive effects of cortisol

A
  • Inhibit early and late phases of inflammation
  • Inhibit edema formation, fibrin deposition, leukocyte migration, phagocytic activity, collagen deposition and capillary and fibroblast proliferation
  • Inhibit enzyme phospholipase A2 and COX-2
  • Inhibit release of TNF-alpha, IL-2 and platelet activating factor
  • Inhibits release of histamine and serotonin
36
Q

Overall anti-inflammatory effects

A
  • Reduction in inflammation
  • Reduction in autoimmune rxns
  • Decreased healing
  • Decreased immune protection
37
Q

What are synthetic glucocorticoids used to treat

A

Inflammatory disorders

  • Eczema
  • Asthma
  • Prevent transplant rejection
38
Q

CV effects of cortisol

A

Potentiates effects of adrenaline

=> increased beta-adrenergic sensitivity

39
Q

effect of cortisol on bone

A

Inhibition of bone formation

  • Decreased osteoblast production
  • Decreased Ca2+ production
40
Q

Effect of cortisol on tissue repair

A
  • Increased AA uptake by liver
  • Increased plasma hepatic proteins

NOTE: Breaks down protein everywhere else => peripheral muscle wastage

41
Q

Mineralocorticoid like effects of cortisol

A
  • Only significant at prolonged high levels
  • Increased sodium and water re-absorption
  • Increased K+ excretion

=> maintain blood vol in dehydration, hemorrhagic stress

42
Q

What is excreted in urine with high levels of cortisol

A

Glucose

43
Q

What would happen in complete absence of cortisol

A

Never learn what a stressor is

44
Q

CORTISOL - metabolic effect

A

increased energy substrates

45
Q

CORTISOL - mineralocorticoid effect

A

Dehydration

Hemorrhagic stress

46
Q

CORTISOL - CV effect

A

Increased cardiac potential

47
Q

CORTISOL - hepatic effect

A

Hepatic AA for tissue repair

48
Q

CORTISOL - immune effect

A

Prevents over stimulation of immune system

Increases platelet production by stimulation of factors 7 and 8 in clotting rxn

49
Q

CORTISOL - RBC effect

A

Increased O2 carriage

50
Q

CORTISOL - Platelet effect

A

Prevents blood loss

51
Q

What is Cushing’s syndrome caused by

A

Excess endogenous or exogenous glucocorticoids

primarily at adrenal level

Stretch marks => breakdown of fats

52
Q

What is Cushing’s disease caused by

A

Overproduction of ACTH and cortisol

53
Q

7 consequences of Cushing’s syndrome

A
  • HYPERGLYCEMIA
  • increased blood glucose => increased gluconeogenesis
  • insulin resistant diabetes
  • LIPOLYSIS
  • Increased plasma FFA
  • Specific distribution of fat
  • Moon face, buffalo torso
  • INCREASED PROTEIN CATABOLISM
  • muscle weakness
  • IMMUNE SYSTEM SUPPRESSED
  • Poor wound healing
  • HYPERTENSION
  • Due to weak mineralocorticoid activity
  • FLUSHED APPEARANCE
  • Increased RBC
  • DEPRESSED MOOD
54
Q

Treatment of Cushing’s Syndrome

A

Ketoconazole or metyrapone

  • block steroid biosynthesis

IF SEVERE

  • Bilateral adrenalectomy
55
Q

Addison’s disease

A
  • Primary adrenocortical insufficiency
  • Adrenal cortex is destroyed
  • Usually result of infection - TB, autoimmune disease
  • Insufficient production of cortisol, often accompanied by aldosterone and adrenal androgen deficiency
  • Inability to maintain blood glucose between meals
  • Inability to deal with stress
  • Susceptibility to inflammation and allergies
  • Pigmentation - increased ACTH, POMC, MSH
56
Q

** Know consequences of taking out enzymes in this rxn

A
57
Q

21 beta hydroxylase deficiency

A

CONGENITAL ABNORMALITY

  • Adrenogenital syndrome or congenital adrenal hyperplasia
  • Unable to produce mineralocorticoids or glucocorticoids
  • Produce adrenal androgens - virilisation/masculinisation of females
  • In utero - cause masculinisation of external genitalia
  • In children - increase growth, suppression of gonadal fct
58
Q

17 alpha hydroxylase deficiency

A

Less common

  • No glucocorticoids or adrenal androgens
  • Overproduction of corticosterone but inhibits aldosterone levels - inhibitory feedback

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