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ESA2 - Metabolism, Endocrinology and Haematology > The Adrenal Glands > Flashcards

The Adrenal Glands Flashcards

(73 cards)

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1
Q

True or False:

The adrenal glands are outside of the renal fascia

A

False

Encapsulated within renal fascia

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2
Q

How many layers does the adrenal cortex have?

A

3

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3
Q

What are the layers of the adrenal cortex?

A

Zona glomerulosa, zona fasiculata, zona reticularis

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4
Q

What is produced in the zona glomerulosa of the adrenal cortex?

A

Mineralocorticoids (eg aldosterone)

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5
Q

What is produced in the zona fasiculata of the adrenal cortex?

A

Glucocorticoids (eg cortisol)

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6
Q

What is produced in the zona reticularis of the adrenal cortex?

A

Glucocorticoids + small amounts of androgens

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7
Q

What is produced in the adrenal medulla?

A

Adrenalne and noradrenaline

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8
Q

What are chromaffin cells?

A

They are neuroendocrine cells found mostly in the medulla of the adrenal glands

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9
Q

What are corticosteroids?

A

Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex

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10
Q

What is an example of a mineralocorticoid?

A

Aldosterone

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11
Q

What is an example of a glucocorticoid?

A

Cortisol

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12
Q

What are steroid hormones synthesised from?

A

Cholesterol

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13
Q

What is the adrenal cortex derived from in embryonic development?

A

Mesoderm

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14
Q

What is the adrenal medulla derived from in embryonic development?

A

Neural crest cells

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15
Q

How do corticosteroids exert their actions?

A

By regulating gene transcription

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16
Q

Outline how corticosteroids regulate gene transcription

A

1) Diffuse across plasma membrane
2) Bind to glucocorticoid receptors
3) Chaperone proteins on receptors dissociate
4) Receptor-ligand complex translocates to nucleus
5) Dimerisation with other receptors can occur
6) Receptors bind to glucocorticoid response elements (GREs) or other transcription factors

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17
Q

What is a hormone response element?

A

A hormone response element (HRE) is a short sequence of DNA within the promoter of a gene that is able to bind a specific hormone receptor complex and therefore regulate transcription

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18
Q

Where is aldosterone synthesised and released by?

A

Zona glomerulosa of adrenal cortex

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19
Q

What carrier proteins bind to aldosterone?

A

Serum albumin and transcortin

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20
Q

What is the role of aldosterone?

A

RAAS
In distal tubules and collecting ducts - promotes expression of Na+/K+ pump to promote reabsorption of Na+ and excretion of K+, influencing water retention, blood volume and thus blood pressure

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21
Q

Outline the RAAS

A

1) Renin released from kidney cleaves angiotensinogen (released from liver) into angiotensin I
2) ACE in lungs cleaves angiotensin I into angiotensin II
3) Angiotensin II stimulates aldosterone release from adrenal cortex, vasoconstriction of arterioles and ADH release from the posterior pituitary
4) ADH release -> translocation of aquaporin channels in nephron aids reabsorption of water back into blood
4) Aldosterone increases expression of Na+/K+ pump in collecting ducts - increased reabsorption of Na+

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22
Q

How is the RAAS initiated?

A

Input eg hypotension, hypovolaemia

Decrease in renal perfusion, drop in blood pressure, increased sympathetic tone from baroreceptor activation leads to more renin release from kidney

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23
Q

What is primary hyperaldosteronism due to?

A

Defect in adrenal cortex

eg bilateral idiopathic adrenal hyperplasia, conn’s syndrome, aldosterone secreting adenoma

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24
Q

Describe the renin and aldosterone levels in primary hyperaldosteronism

A

Low renin - high aldosterone

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25
What is secondary hyperaldosteronism due to?
Over activity of the RAAS eg renin producing tumour, renal artery stenosis
26
Describe the renin and aldosterone ratio in secondary hyperaldosteronism
High renin levels Low aldosterone:renin ratio
27
What are some signs of hyperaldosteronism?
High BP, LV hypertrophy, stroke, hypernatraemia, hypokalaemia
28
How can hyperaldosteronism be treated?
Surgery, spironolactone (mineralocorticoid receptor antagonist)
29
What is cortisol synthesised and released by?
Zona fasiculata
30
What is cortisol synthesised and released in response to?
CRH (corticotropin-releasing hormone) released from hypothalamus -> ACTH (Adrenocorticotropic hormone) released from anterior pituitary -> cortisol released from adrenal cortex
31
What is cortisol's carrier protein in plasma?
Transcortin
32
What are the catabolic effects of cortisol?
Increased protein breakdown in muscle Increased gluconeogenesis in liver Increased lipolysis in fat
33
Aside from catabolic effects, what are the other actions of cortisol?
Resistance to stress, anti-inflammatory effects (inhibits macrophage activity+mast cell degranulation), depression of immune response
34
Why is cortisol perscribed to organ transplant patients?
It depresses the immune respnse
35
Outline the HPA axis
Stressor (eg pain, fever, hypoglycaemia, low BP): 1) Hypothalamus releases CRH to anterior pituitary 2) Anterior pituitary releases ACTH to adrenal cortex 3) Adrenal cortex releases cortisol to target tissues
36
What are the net effects of glucocorticoid actions on metabolism?
Increased glucose production, breakdown of protein, redistribution of fat
37
Why does cortisol release lead to increased glycogen storage?
Increases glucose -> increased insulin so liver glycogen stores increase
38
What are the effects of cortisol on muscle?
Increased protein degradation Decreased protein synthesis Decreased glucose utilisation Decreased sensitivity to insulin (Cortisol inhibits insulin-induced GLUT4 translocation in muscle so has glucose sparing effect)
39
What are the effects of cortisol on fat?
Redistribution of fat especially in abdomen, supraclavicular fat pads, dorso-verical fat pad and face (Buffalo hump and moon face) Decreases glucose utilisation Decreases sensitivity to insulin Increases lipolysis
40
What is Cushing's syndrome?
Chronic excessive exposure to cortisol
41
What is the most common cause of Cushing's syndrome?
Prescribed glucocorticoids
42
What are some endogenous causes of Cushing's syndrome?
1) Pituitary adenoma secreting ACTH (Cushing's DISEASE) 2) Excess cortisol produced by adrenal tumour (Adrenal Cushing's) 3) Non pituitary-adrenal tumours producing ACTH+/CRH eg small cell lung cancer
43
What is Cushing's disease?
An excess of cortisol in the blood level CAUSED BY a pituitary tumour secreting adrenocorticotropic hormone
44
What are the signs and symptoms of Cushing's syndrome?
``` Moon-shaped face Buffalo hump Abdominal obesity Purple striae (proteolysis - skin weaker) Acute weight gain Hyperglycaemia Hypertension ```
45
What are some examples of steroid drugs?
Prednisolone, dexamethasone
46
What are steroid drugs often used to treat?
Inflammatory diseases, allergies, organ transplant, auto-immune conditions
47
What is an important point about stopping steroid medication?
Steroid dosage should be reduced gradually and not stopped suddenly
48
What is Addison's disease?
Chronic adrenal insufficiency
49
What is the most common cause of Addison's disease?
Destructive atrophy from autoimmune response
50
What are the signs and symptoms of Addison's disease?
Postural hypotension, lethargy, weight loss, anorexia, increased skin pigmentation, hypoglycaemia
51
Why does Addison's disease lead to increased skin pigmentation?
Decreased cortisol -> negative feedback on anterior pituitary reduced -> more POMC required to synthesise ACTH -> more a-MSH produced -> melanin synthesis
52
What are the symptoms of an Addisonian crisis?
Nausea, vomiting, pyrexia, hypotension, vascular collapse
53
What is an addisonian crisis?
A life threatening emergency due to adrenal insufficiency
54
What is an addisonian crisis often precipitated by?
Stress, salt depravation, infection, trauma, cold exposure, over exertion, abrupt steroid drug withdrawal
55
How is an addisonian crisis treated?
Fluid replacement, cortisol
56
What are some examples of androgens excreted by the zona reticularis?
DHEA and androstenedione
57
True or False: The adrenal medulla is a modified sympathetic ganglion of the autonomic nervous system
True
58
How is noradrenaline converted to adrenaline?
N-methyl transferase
59
Why do 20% of chromaffin cells secrete noradrenaline as opposed to adrenaline (like the other 80%)?
20% lack the N-methyl transferase enzyme to convert NA into adrenaline
60
What type of receptors are adrenergic receptors?
GPCRs
61
What adrenergic receptors in the heart increase HR and contractility?
B1
62
What adrenergic receptors in the lungs cause bronchodilation?
B2
63
What adrenergic receptors in the blood vessels cause vasoconstriction?
a1
64
What adrenergic receptors in the blood vessels cause vasodilation?
B2
65
What adrenergic receptors in the kidney causes increased renin secretion?
B1, B2
66
What adrenergic receptors in the muscle cause increased glycolysis and glygogenolysis?
a1, B2
67
What adrenergic receptors in the pancreas increase glucagon secretion?
a2
68
What adrenergic receptors in the pancrease decrease insulin secretion?
a2, B2
69
What adrenergic receptors in adipose tissue increases liplysis?
B2
70
How does adrenaline increase HR?
1) B1 adrenergic receptor - G-alpha S subunit 2) GDP for GTP exchange, dissociation of alpha subunit 3) Stimulates adenylyl cyclase - cAMP 4) cAMP can directly activate HCN chanels - funny current 5) cAMP activates PKA - phosphorylation of HCN channels, phosphorylation of L-type Ca2+ channels - potentiates opening, creasing the slope of the upstroke of the AP
71
What is pheochromocytoma?
Chromaffin cell tumour | Catecholamine-secreting (mainly NA) tumour that may precipitate life-threatening hypertension
72
What are some characteristics of pheochromocytoma?
Severe hypertension, headaches, palpitations, diaphoresis, anxiety, weight loss, hyperglycaemia
73
What are catecholamines derived from?
Tyrosine

ESA2 - Metabolism, Endocrinology and Haematology (19 decks)

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