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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

A
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
Q

In terms of cardiovascular function, which hormones is cortisol permissive to? What are the results of this?

A
  • Adrenaline, Noradrenaline, Angiotensin II
  • Maintains contractility, vascular tone and blood pressure
26
Q

HOW does cortisol maintain cardiovascular function?

A
  • Increased beta receptors
  • Decreased nitric oxide
  • Increases catecholamine and Na/K pump synthesis
27
Q

How does aldosterone increase sodium reabsorption? What effect does this have on one other ion? IGNORE THIS CARD

A
  • Uses sodium potassium pumps
  • Therefore excretion of potassium also increases
28
Q

Other than aldosterone production, what is a function of angiotension II?

A

Vasoconstrictor

29
Q

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.

A
30
Q

Draw a diagram of the hormonal response to stress. Compare to 7.7.doxc. What is missing from that diagram?

A

`

31
Q

What is a pheochromocytoma?

A

Adrenal tumour:
Pheo: Dusky
Chromo: Colour
Cytoma: Tumour

32
Q

Describe the primary and secondary forms of Conn’s syndrome

A
  • Primary: aldosterone-secreting tumour in zona glomerulosa
  • Secondary: Hyperactivity of RAAS system due to low renal blood flow
33
Q

What is the name for too-low levels of potassium? What can this cause?

A
  • Hypokalaemia
  • Muscle weakness & cardiac toxicity
34
Q

Why is sodium concentration not greatly impacted by conn’s syndrome? What is the main issue, then?

A
  • Cardiac muscle stretches, resulting in ANP secretion from the heart
  • Main problem is hypokalaemia
35
Q

Cushing’s Syndrome vs Cushing’s disease + other secondary one

A

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
Q

What is a common cause of cushing’s syndrome/disease?

A

Large doses of glucocorticoids

37
Q

What hormones are in excess during Cushing’s disease?

A
  • Cortisol
  • Dehydroepiandrosterone
38
Q

Derive as many effects of cushing’s disease as you can think of

A
  • Gluconeogenesis (hyperglycemia -> adrenal diabetes)
  • Fat mobilisation into thorax, abdomen and face
  • Protein loss (weakness, osteoporosis)
  • Weakened immune system
  • Acne + facial hair (DHEA)
39
Q

Draw the logical permutations of primary, secondary, and tertiary adrenal insufficiency

A
40
Q

How can Addison’s disease lead to hyperpigmentation?

A
  • Overproduction of alpha melanocyte stimulating hormone in response to pituitary hyperstimulation
41
Q

What is Addison’s disease?

A

Primary adrenal insufficiency; autoimmune destruction of adrenal glands

42
Q

How can secondary adrenal insufficiency arise?

A

Negative feedback suppression of HPA axis due to steroid medications

43
Q

What are some consequences of cortisol deficiency?

A
  • Decreased stress tolerance
  • Hypoglycaemia
  • Decreased gluconeogenesis
  • Decreased fuel mobilization
  • Hyperpigmentation
44
Q

What are the consequences of aldosterone deficiency?

A
  • Hyperkalemia
  • Acidosis
  • Hyponatremia
  • Decreased plasma volume and blood pressure
  • Tachycardia
  • Hypotension

Foundations Of Medicine (98 decks)

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