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Flashcards in SPR L3 Adrenal Hormones (2) Deck (22):
1

Adrenal Hormones (2)

Hormones of the Adrenal Medulla

Learning Outcomes

  • Describe the consequences of primary adrenocortical insufficiency - Addison’s Disease
  • Describe the endocrine function of the adrenal medulla
  • Briefly describe the synthesis, secretion, transport and metabolism of catecholamines
  • List the different stimuli that can result in catecholamine secretion
  • Briefly describe the effects of catecholamines on the different adrenergic receptor types
  • Describe the main effects of excess catecholamine secretion

2

What do the following parts of the Adrenal Gland secrete?

Cortex

  1. Glomerulosa
  2. Fasiculata
  3. Reticularis 

4. Medulla 

  1. Aldosterone (Mineralocorticoids)
  2. Cortisol (Glucocorticoids)
  3. Adrenal Androgens 
  4. Catecholamines

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3

Where are the following secreted from?

  1. Aldosterone (Mineralocorticoids)
  2. Cortisol (Glucocorticoids)
  3. Adrenal Androgens 
  4. Catecholamines

Cortex

  1. Zona Glomerulosa
  2. Zona Fasiculata
  3. Zona Reticularis 

4. Medulla 

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4

What are some of the signs & symptoms of an adrenocortical tumour?

 

Cushing’s Syndrome

  • Increase in blood glucose, weight gain, increase in protein breadkdown, osteoporosis, diabetes, stretch marks

Conn’s Syndrome

  • Excess aldosterone – renal Na+ and H20 retention, renal K+ loss, renal H+ loss, high blood pressure, muscle cramps, excessive thirst, excessive urination

Adrenogenital Syndrome

  • Little effect in adults, precocious puberty in children

5

What are the following?

  1. Cushing's Syndrome
  2. Conn's Syndrome
  3. Adrenogenital Syndrome

  1. Increase in blood glucose, weight gain, increase in protein breadkdown, osteoporosis, diabetes, stretch marks
  2. Excess aldosterone – renal Na+ and H20 retention, renal K+ loss, renal H+ loss, high blood pressure, muscle cramps, excessive thirst, excessive urination
  3. Little effect in adults, precocious puberty in children

6

What are some of the signs and symptoms of adrenalcortical insufficiency?

 

Addison’s Disease = Primary adrenocortical insufficiency, destruction of both adrenal cortices

Lack of GLUCOCORTICOIDS- Loss of cortisol

 

  • hypoglycaemia, reduction in fat & protein metabolism, loss of weight, poor exercise tolerance, poor stress tolerance - DEATH

Lack of MINERALOCORTICOIDS

  • ↓ Na +; ↑ K+ and H+, ↓ Blood Volume, ↓ Cardiac Output (circulatory shock and death)

Lack of ADRENAL ANDROGENS

 

Secondary or tertiary adrenocortical insufficiency – due to a pituitary or hypothalamic abnormality results in insufficient ACTH

 

 

7

Which Adrenal Hormone isn't regulated through the hypothalamic pituitary pathway?

 

What is the main stimulus for it's production?

Aldosterone

 

Angiotensin II

8

What is a clinical sign associated with Addison's Disease?

 

Explain this.

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hyperpigmentation

Dark Palmar Creases

Brown Buccal Pigmentation

 

ACTH shares the same precursor molecule as melanocyte-stimulating hormone (MSH) i.e. pro-opiomelanocortin (POMC)

 

 

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9

Give an overview of the anatomy of the Adrenal Medulla

Adrenal medulla is stimulated in the same way as the sympathetic NS

 

Preganglionic Sympathetic Neuron from spinal cord to adrenal medulla, Ach released, communicates with Modified Postganglionic sympathetic neurone, epinephrine is released, enters blood vessels and circulates

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10

List the effects of SNS stimulation

 

 

Which neurotransmitters (NTs) are involved?

Dilates Pupil

Inhibits Salivation 

Accelerates heart 

 

For both ParaSymp and Symp, NT = Ach binding to nicotinic receptors binding to cell bodies on the PGN.

But in SYMP the POSTG NT = norepinephrine

 

 

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11

Catecholamine Secretion vs SNS activity

Outline

Adrenal Secretion 

Sympathetic Activation

Adrenal Secretion

  • Exerts its effects in all cells
  • Delay in the beginning
  • Prolonged effects (3-5 min)
  • Only generalised effects

Sympathetic Activation

  • Some organs/tissues have no innervation
  • Immediate effects
  • Rapid decay when activation ceases
  • Localised effects

12

What cells secrete Catecholamines?

Chromaffin Cells

13

  1. What cells secrete catecholamines?
  2. What proportions are Adrenaline and Noradrenaline?
  3. How are these transported in the blood?
  4. What is the stimulation for release?

  1. Chromaffin Cells
  2. 80% Adrenaline, 20% Noradrenaline
  3. They are water soluble - 50% are bound to plasma proteins

In the Chromaffine cells, they are packaged into chromaffin granules (if left in the cytoplasm they would be broken down by the enzymes there).

4. Ach from SNS

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14

Chromaffin cells secrete catecholamines

Outline the steps in Epinephrine production

Tyrosine (TH)

DOPA (AAD)

Dopamine (AbetaH)

Norepinephrine (PNMT)

(enzymes)

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15

Metabolism of Catecholamines

  1. How long does it take for inactivation?
  2. What is 90% of reuptake by?
  3. What are they metabolised by?
  4. What are they conjugated with and where?
  5. What are they excreted in?

  1. Catecholamines are inactivated rapidly
  2. 90% reuptake by extra neuronal sites
  3. metabolised by monoamine oxidase (MAO) or catechol-O-methytransferase (COMT)
  4. conjugation with glucuronide in liver
  5. excreted in urine and bile (Direct filtration into urine)

16

Mechanism of action of catecholamines

  1. Outline the mechanism
  2. To which receptor does Noradrenaline bind to with more affinity?
  3. To which receptor does Adrenaline bind to with more affinity?

  1. receptor mediated – adrenergic receptors

    peripheral effects depend upon type & ratio of receptors in target tissues

  2. Alpha

  3. Beta

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17

Differences between Adrenaline & Noradrenaline

  1. Which plays a bigger role in cardiac stimulation?
  2. Which plays a bigger role in constriction of blood vessels?
  3. Which plays a bigger role in increasing metabolism? (glycogenolysis in liver & skeletal muscle, gluconeogenesis, lipolysis, calorigenesis)

 

Comment on the following receptors

  1. A1
  2. A2
  3. B1
  4. B2
  5. B3

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  1. Adrenaline
  2. Noradrenaline
  3. Adrenaline

 

  1. Vascular, vasocontriction
  2. Presynaptic, target for antihypertensive drugs
  3. Heart, exclusively on heart
  4. Smooth Muscle 
  5. Fat (adipose tissue)

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18

Multiple Mechanisms of Adrengergic Receptor Signal Transduction

How do the following act?

  1. A1
  2. A2
  3. B1
  4. B2

  1. Acts through phospholipase C pathway to increase IP3
  2. Acts to decrease cAMP production
  3. Increases cAMP 
  4. Increases cAMP

(B - relaxation of smooth muscle, vasodilation, less Ca2+)

19

Some of the individual actions of catecholamines that contribute to the integrated sympathoadrenal
response to exercise

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20

Adrenomedullary dysfunction (very rare)

What is a Pheochromocytoma? 

Give some signs and symptoms.

a catecholamine-secreting tumour

  • hypertension
  • headache
  • sweating
  • palpitations
  • chest pain
  • anxiety
  • glucose intolerance
  • increased metabolic rate

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21

Give a summary of the adrenal stress response.

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22

Summary of the adrenal stress response.

  1. Which path gives rise to the short term response
  2. Which path gives rise to the long term response

  1. Sympathetic centres: sympathetic nerves (noradrenaline) and adrenal medulla (adrenaline/noradrenaline). Increased HR, BP, bronchioles dilate, increased blood glucose, decreased digestive activity => fight or flight response
  2. Release of CRH, Ant Pituitary, Secretion ACTH, Adrenal Cortex, Mineralocorticoids (salt and water retention, increased BV and BP) Glucocorticoids (increased blood glucose, increased catabolism of fat a protein, decreased inflammatory response and immune response)

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