Endocrine Role of Adrenal Glands Flashcards

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

25
1. Where is Adrenocorticotrophin produced 2. What sort of hormone is it 3. What is its precursor
1. Anterior pituitary 2. Peptide hormone =\> prepro -\> pro 3. Precursor Pro-Opio-Melano-Corticotrophin (POMC)
26
What are beta endorphins
Natural pain killers
27
Clinical manifestation of lack of cortisol
Pigmentation of skin
28
What is over-produced when we're not producing cortisol
MSH Melanocyte-Stimulating Hormone
29
Pathway for production of cortisol
CRH | ACTH | CORTISOL (free)
30
What is cortisol carried by Where is it made Examples
Cortisol binding globulin TRANSCORTIN Made by the liver
31
Effect of an increase in oestrogen on cortisol
Increases cortisol
32
Effect of increase in free cortisol on CRH and ACTH
Inhibits CRH and ACTH Liver makes more transcortin to bind more cortisol
33
How is cortisol transported
Bound in plasma by cortisol binding globulin transcortin, which is synthesised by the liver
34
What is the metabolic effect of cortisol
Spares glucose and promotes breakdown of protein and fat Overall catabolic and diabetogenic
35
What are the anti-inflammatory and immunosuppressive effects of cortisol
* 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
Overall anti-inflammatory effects
* Reduction in inflammation * Reduction in autoimmune rxns * Decreased healing * Decreased immune protection
37
What are synthetic glucocorticoids used to treat
Inflammatory disorders * Eczema * Asthma * Prevent transplant rejection
38
CV effects of cortisol
Potentiates effects of adrenaline =\> increased beta-adrenergic sensitivity
39
effect of cortisol on bone
Inhibition of bone formation * Decreased osteoblast production * Decreased Ca2+ production
40
Effect of cortisol on tissue repair
* Increased AA uptake by liver * Increased plasma hepatic proteins NOTE: Breaks down protein everywhere else =\> peripheral muscle wastage
41
Mineralocorticoid like effects of cortisol
* Only significant at prolonged high levels * Increased sodium and water re-absorption * Increased K+ excretion =\> maintain blood vol in dehydration, hemorrhagic stress
42
What is excreted in urine with high levels of cortisol
Glucose
43
What would happen in complete absence of cortisol
Never learn what a stressor is
44
CORTISOL - metabolic effect
increased energy substrates
45
CORTISOL - mineralocorticoid effect
Dehydration Hemorrhagic stress
46
CORTISOL - CV effect
Increased cardiac potential
47
CORTISOL - hepatic effect
Hepatic AA for tissue repair
48
CORTISOL - immune effect
Prevents over stimulation of immune system Increases platelet production by stimulation of factors 7 and 8 in clotting rxn
49
CORTISOL - RBC effect
Increased O2 carriage
50
CORTISOL - Platelet effect
Prevents blood loss
51
What is Cushing's syndrome caused by
Excess endogenous or exogenous glucocorticoids primarily at adrenal level Stretch marks =\> breakdown of fats
52
What is Cushing's disease caused by
Overproduction of ACTH and cortisol
53
7 consequences of Cushing's syndrome
* 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
Treatment of Cushing's Syndrome
Ketoconazole or metyrapone - block steroid biosynthesis IF SEVERE - Bilateral adrenalectomy
55
Addison's disease
* 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
\*\* Know consequences of taking out enzymes in this rxn
57
21 beta hydroxylase deficiency
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
17 alpha hydroxylase deficiency
Less common * No glucocorticoids or adrenal androgens * Overproduction of corticosterone but inhibits aldosterone levels - inhibitory feedback