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Foundations Of Medicine > 7.7 Adrenal Glands, Adrenaline & Cortisol > Flashcards

7.7 Adrenal Glands, Adrenaline & Cortisol Flashcards

1
Q

What TYPE of hormones does the adrenal cortex produce? What about the adrenal medulla?

A

Cortex: Steroid (Androgens, Glucocorticoids, Mineralocorticoids)

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2
Q

What are the three zones of the adrenal cortex, from the outside to the inside?

A
  • Zona Reticularis
  • Zona Fasciculus
  • Zona Glomerulosa
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3
Q

Where in the adrenal glands are catecholamines secreted from? Which catecholamines are secreted?

A
  • Secreted from adrenal medulla
  • Noradrenaline and andrenaline are secreted
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4
Q

What hormones are released from the adrenal medulla? What stimulates this? What is the result?

A
  1. Catecholamines (mainly adrenaline)
  2. Sympathetic stimulation
  3. Helps resist stress
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5
Q

What hormones are released from the zona reticularis? What stimulates this? What is the result?

A
  1. Androgens (mainly dehydroepiandrosterone)
  2. Adrenocorticotropic hormone
  3. Mostly male sex hormone
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6
Q

What hormones are released from the zona fasciculata? What stimulates this? What is the result?

A
  1. Glucocorticoids (cortisol)
  2. Adrenocorticotropic hormone
  3. Helps cope with stress; increases metabolic rate
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7
Q

What hormones are released from the zona glomerulosa? What stimulates this? What is the result?

A
  1. Mineralocorticoids (aldosterone)
  2. Angiotensin
  3. Regulates Na+, K+ and water concentration in blood
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8
Q

Which cells in the adrenal medulla release adrenaline and noradrenaline?

A

Chromaffin cells

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9
Q

In fundamental terms, what is the adrenal medulla? What does this make chromaffin cells?

A
  • Modified sympathetic ganglions
  • Therefore chromaffin cells are modified postganglionic neurons with no axons
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10
Q

How much adrenaline and noradrenaline is released from the adrenal medulla upon acetylcholine release from the preganglionic fibre?

A

Five times more adrenaline than noradrenaline

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11
Q

Why do neurons release noradrenaline, but NOT adrenaline?

A

Neurons lack the necessary enzyme to convert noradrenline to adrenaline; the adrenal medulla does not

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12
Q

Recall the five types of stress

A
  • Physical
  • Chemical
  • Psychological
  • Physiological
  • Social
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13
Q

Outline Hans Selye’s GAS

A
  • Alarm reaction
  • Resistance stage
  • Exhaustion (depletion of resources)
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14
Q

Outline the revised GAS

A
  • Alarm reaction (sympathetic response); varies depending on sex, and the stressor itself
  • Resistance stage: persist and adapt
  • Allostatic overload: Chronic problems arise due to stress mediators themselves
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15
Q

Describe the two main components of the alarm reaction of GAS

A
  • Noradrenaline release from sympathetic nerve terminals (some spillage into blood)
  • Release of adrenaline and nor-adrenaline from adrenal medulla
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16
Q

Describe the actions of catecholamines on the heart

A
  • Increased heart rate and contractility
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17
Q

Describe the actions of catecholamines on the lung

A

Bronchodilation

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18
Q

Describe the actions of catecholamines on the kidneys

A
  • Vasoconstriction
  • Increased renin release (leads to water retention)
19
Q

Describe the actions of catecholamines on skeletal muscle

A

Vasodilation

20
Q

Describe the actions of catecholamines on the liver

A
  • Increased gluconeogenesis
  • Glycogenolysis
21
Q

Describe the actions of catecholamines on adipose tissue?

A

Increased lipolysis

22
Q

Describe the actions of catecholamines on the pancreas

A
  • Increased glucagon, decreased insulin
23
Q

Draw the Feedback mechanism of cortisol from the hypothalamus to four target areas

24
Q

What is the relationship between cortisol and insulin? Why does this make sense? Therefore, what can be the long term effect of elevated stress?

A
  • Antagonistic
  • Makes sense; cortisol wants the body to show its cards, which involves release of glucose
  • Long term, this can lead to insulin resistance and therefore type 2 diabetes
25
In terms of cardiovascular function, which hormones is cortisol permissive to? What are the results of this?
- Adrenaline, Noradrenaline, Angiotensin II - Maintains contractility, vascular tone and blood pressure
26
HOW does cortisol maintain cardiovascular function?
- Increased beta receptors - Decreased nitric oxide - Increases catecholamine and Na/K pump synthesis
27
How does aldosterone increase sodium reabsorption? What effect does this have on one other ion? IGNORE THIS CARD
- Uses sodium potassium pumps - Therefore excretion of potassium also increases
28
Other than aldosterone production, what is a function of angiotension II?
Vasoconstrictor
29
Draw a diagram of the RAAS system, including the roles of renin and ACE. What area of the adrenal gland is acted on? Include the negative feedback mechanism.
30
Draw a diagram of the hormonal response to stress. Compare to 7.7.doxc. What is missing from that diagram?
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31
What is a pheochromocytoma?
Adrenal tumour: Pheo: Dusky Chromo: Colour Cytoma: Tumour
32
Describe the primary and secondary forms of Conn's syndrome
- Primary: aldosterone-secreting tumour in zona glomerulosa - Secondary: Hyperactivity of RAAS system due to low renal blood flow
33
What is the name for too-low levels of potassium? What can this cause?
- Hypokalaemia - Muscle weakness & cardiac toxicity
34
Why is sodium concentration not greatly impacted by conn's syndrome? What is the main issue, then?
- Cardiac muscle stretches, resulting in ANP secretion from the heart - Main problem is hypokalaemia
35
Cushing's Syndrome vs Cushing's disease + other secondary one
Syndrome: Primary, adenoma of adrenal cortex (20-25%) Disease: Secondary, Pituitary tumour increases ACTH release Other: ectopic secretion of ACTH (e.g. in lung cancer)
36
What is a common cause of cushing's syndrome/disease?
Large doses of glucocorticoids
37
What hormones are in excess during Cushing's disease?
- Cortisol - Dehydroepiandrosterone
38
Derive as many effects of cushing's disease as you can think of
- Gluconeogenesis (hyperglycemia -> adrenal diabetes) - Fat mobilisation into thorax, abdomen and face - Protein loss (weakness, osteoporosis) - Weakened immune system - Acne + facial hair (DHEA)
39
Draw the logical permutations of primary, secondary, and tertiary adrenal insufficiency
40
How can Addison's disease lead to hyperpigmentation?
- Overproduction of alpha melanocyte stimulating hormone in response to pituitary hyperstimulation
41
What is Addison's disease?
Primary adrenal insufficiency; autoimmune destruction of adrenal glands
42
How can secondary adrenal insufficiency arise?
Negative feedback suppression of HPA axis due to steroid medications
43
What are some consequences of cortisol deficiency?
- Decreased stress tolerance - Hypoglycaemia - Decreased gluconeogenesis - Decreased fuel mobilization - Hyperpigmentation
44
What are the consequences of aldosterone deficiency?
- Hyperkalemia - Acidosis - Hyponatremia - Decreased plasma volume and blood pressure - Tachycardia - Hypotension

Foundations Of Medicine (98 decks)

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