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Metabolism, Endocrinology & Haematology > The Adrenal Glands/ Adrenal Disorders > Flashcards

The Adrenal Glands/ Adrenal Disorders Flashcards

1
Q

The adrenal gland is made up of what two distinct areas?

A

The cortex and the medulla

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2
Q

What are the three layers of the cortex called?

What are each responsible for?

A

Zona glomerulosa - mineralcorticoids

Zona fasiculata -glucocorticoids

Zona reticularis- androgens

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3
Q

The adrenal medulla is a modified what?

It is made up of what kind of cells?

A

Sympathetic ganglion

Chromaffin cells

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4
Q

Steroid hormones are synthesised from what?

A

Cholesterol

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5
Q

Are steroid hormones lipid or water soluble?

A

Lipid soluble

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6
Q

Steroid hormones bind to what kind of receptors?

How do they exert their affect?

A

Nuclear (intracellular) receptors

They modulate gene transcription

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7
Q

How do corticosteroids exert their actions by regulating gene transcription?

A

They diffuse across the PM, bind to glucocorticoid receptors which leads to dissociation of chaperone proteins

Receptor ligand complex translocates to the nucleus

Receptors bind to GREs or other TFs

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8
Q

Which is the most abundant mineralcorticoid?

A

Aldosterone

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9
Q

Where is aldosterone synthesised and released?

A

Zona glomerulosa of the adrenal cortex

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10
Q

What is the carrier protein commonly used by steroid hormones?

A

Albumin protein

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11
Q

Aldosterone plays a key role in what process?

A

Regulation of plasma Na+ and K+ (blood volume)

Regulation of arterial BP

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12
Q

Where does the main action of aldosterone occur?

What does it do here?

A

In distal tubules and collecting ducts of the nephron
It promotes expression of Na/K pump (promoting the reabsorption of Na and excretion of K)
=water retention

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13
Q

In the RAAS, what molecule cleaves angiotensinogen to angiotensin I?
Where is this produced and in response to what?

A

Renin

Kidney in response to hypotension and hypovolaemia

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14
Q

What is responsible for the conversion of Angiotensin I to Angiotensin II?
Where does it have its effects?

A

Angiotensin converting enzyme (ACE)

In lung endothelial cells

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15
Q

Angiotensin II acts on what 3 things to produce its affects?
What are these affects?

A

Arterioles- vasoconstriction
Adrenal cortex- release aldosterone to increase expression of Na/K pump
Posterior pituitary- produce ADH to translocate aquaporin channels and aid reabsorption

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16
Q

What is hyperaldosternism?

What are the two types? How are they defined?

A

Over production of aldosterone
Primary - defect in adrenal cortex
Secondary - over activity of RAAS

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17
Q

What is the most common cause of hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia

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18
Q

What is the best way to distinguish between primary and secondary hyperaldosteronism?

A

The alsoterone:renin ratio
Primary- high (low renin)
Secondary- low (high renin)

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19
Q

What is an example of secondary hyperaldosteronism?

A

Renal artery stenois

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20
Q

What are the signs of hyperaldosteronism?

A 
High blood pressure
LV hypertrophy 
Stroke 
Hypernataemia 
Hypokalaemia
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21
Q

What is the treatment for hyperaldosteronism?

A

Surgery- if from tumour

Spironolactone (mineralcoricoid antagonist)

22
Q

Which is the most abundant corticosteroid?

A

Cortisol

23
Q

Where is cortisol synthesised and released?

In response to what?

A

From the Zona fasiculata of the adrenal cortex

In response to ACTH

24
Q

How does negative feedback control the release of cortisol?

A

Cortisol feeds back to the hypothalamus and anterior pituitary to inhibit CRH and ACTH

25
Q

What is the carrier protein that is used to transport cortisol?

A

Transcortin

26
Q

What are the actions of cortisol?

A 
Catabolic effects: 
-proteolysis 
-lipolysis 
-gluconeogenesis + (inhibits GLUT4- glucose sparing effect)
Resistance to stress 
Anti-inflammatory 
Depression of immune system
27
Q

What is Cushing’s syndrome?

A

A condition caused by chronic excessive exposure to cortisol

28
Q

What are the endogenous and exogenous causes of Cushing’s syndrome?

A

Endogenous:

  • Bengin pituitary tumour (Cushing’s disease)
  • Excess cortisol production by adrenal tumour (Adrenal Cushing’s)
  • Small cell lung cancer (V rare)- secretes ACTH

Exogenous:
-Prescribed glucocorticoids

29
Q

What are the signs and symptoms of Cushing’s syndrome?

A 
Plethoric moon-shaped face 
Dorsocervical fat pad "buffalo hump" 
Abdominal obesity 
Purple striae 
Acute weight gain 
Hyperglycaemia 
Hypertension
30
Q

Apart from Cushing’s syndrome, what are steroid drugs such as Prednisolone and Dexamethasone used to treat?

A 
Asthma
IBD
RA
Other auto-immune conditions 
Suppression of immune rejection
31
Q

What is Addision’s disease?

What is it now most commonly caused by?

A

Chronic adrenal insufficiency

Destructive atrophy from autoimmune response

32
Q

What are the signs and symptoms of Addison’s disease?

A 
Postural hypotension 
Lethargy 
Weight loss
Anorexia 
Increased skin pigmentation 
Hypoglycaemia
33
Q

How does Addison’s cause hyperpigmentation?

A
  1. More POMC is produced through reduced negative feedback on anterior pituitary which produces melanin
  2. ACTH activates melanocortin receptors
34
Q

What is “Addisonian Crisis”

A

A life threatening emergency due to adrenal insufficiency

35
Q

What factors can precipitate an Addisonian crisis?

A 
Severe stress
Salt deprevation 
Infection 
Trauma 
Cold exposure 
Abrupt steroid withdrawl
36
Q

What are the symptoms of Addisonian crisis?

A 
Nausea 
Vomiting 
Pyrexia 
Hypotension 
Vascular collapse
37
Q

What is the treatment for someone in an Addisonian crisis?

A

IV fluid replacement

IV cortisol

38
Q

The innermost layer of the adrenal cortex secretes what?

A

Androgens

39
Q

The chromaffin cells of the adrenal medulla lack what feature?

A

Axons

40
Q

What do the chromaffin cells of the medulla release upon stimulation by the sympathetic nervous system?

A

Adrenaline (about 80%)

Noradrenaline (about 20%)

41
Q

Adrenaline and Noradrenaline are both derivatives of which amino acid?

A

Tyrosine

42
Q

What do the chromaffin cells of the adrenal medulla only secrete around 20% noradrenaline?

A

20% of the cells lack N-methyl transferase which is an enzyme needed to convert noradrenaline into adrenaline

43
Q

What are the actions of adrenaline on the heart?

What receptors are activated?

A

Increased heart rate
Increased contractility
Beta1 receptors: GalphaS –>activation of adenylyl cyclase–> cAMP–> PKA –> Target Proteins

44
Q

What receptors are activated by adrenaline in the lungs?
What affect does this have on them?
How?

A

Activation of beta2 receptors
Causes bronchodilation
Through GalphaS–>Adenylyl cyclase activation–>cAMP–>PKA–>Target proteins

45
Q

What affect does adrenaline have on blood vessels?
Which GPCR subunit is involved?
What are the downstream pathways of receptor activation ?

A

Vasoconstriction (if alpha1-skin,gut): GalphaQ–>Activates phospholipase C–> DAG IP3—>PKC and Ca2+ release via IP3 receptor–>Target proteins

Vasodilation (if beta2-skeletal muscle):Galphai–>Inhibits Adenylyl cyclase–> decreased cAMP, PKA

46
Q

How does adrenaline increase the heart rate?

A

PKA activation leads to phosphorylation of HCn channels and L-type Ca2+ channels with potentials opening
Increasing the SLOPE of the upstroke of the action potential

47
Q

What is Phaeochromocytoma?

A

A chromaffin cell tumour that secretes catecholamines (mainly noradrenaline)

48
Q

What are the characteristics of Phaeochromocytoma?

A 
Severe hypertension /hypotension 
Headaches 
Palpitations 
Anxiety 
Weight loss 
Elevated blood glucose 
Collapse
49
Q

Why it is VITAL to decrease long-term use of steroids gradually over time and not just stop abruptly?

A

The steroids suppress the individuals HPA axis and therefore lose the negative feedback that is required to damped cortisol production leadings to excess secretion and potentially sudden death- addisonian crisis

50
Q

How do you test for adrenocortical function?

A
  • Plasma cortisol (bear in mind time of day)
  • ACTH levels
  • 24 hours excretion of cortisol and its breakdown products
  • dynamic function tests: dexamethasone suppression tests and ACTH stimulation tests
51
Q

A normal response on a Synacthen test would usually exclude what?
Why?

A

Addison’s disease

No response to the administered ACTH as the tumour/ectopic ACTH secretion does not respond ????

Metabolism, Endocrinology & Haematology (13 decks)

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