The Adrenal Glands/ Adrenal Disorders Flashcards

(51 cards)

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?

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
What is the carrier protein that is used to transport cortisol?
Transcortin
26
What are the actions of cortisol?
``` Catabolic effects: -proteolysis -lipolysis -gluconeogenesis + (inhibits GLUT4- glucose sparing effect) Resistance to stress Anti-inflammatory Depression of immune system ```
27
What is Cushing's syndrome?
A condition caused by chronic excessive exposure to cortisol
28
What are the endogenous and exogenous causes of Cushing's syndrome?
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
What are the signs and symptoms of Cushing's syndrome?
``` Plethoric moon-shaped face Dorsocervical fat pad "buffalo hump" Abdominal obesity Purple striae Acute weight gain Hyperglycaemia Hypertension ```
30
Apart from Cushing's syndrome, what are steroid drugs such as Prednisolone and Dexamethasone used to treat?
``` Asthma IBD RA Other auto-immune conditions Suppression of immune rejection ```
31
What is Addision's disease? | What is it now most commonly caused by?
Chronic adrenal insufficiency | Destructive atrophy from autoimmune response
32
What are the signs and symptoms of Addison's disease?
``` Postural hypotension Lethargy Weight loss Anorexia Increased skin pigmentation Hypoglycaemia ```
33
How does Addison's cause hyperpigmentation?
1. More POMC is produced through reduced negative feedback on anterior pituitary which produces melanin 2. ACTH activates melanocortin receptors
34
What is "Addisonian Crisis"
A life threatening emergency due to adrenal insufficiency
35
What factors can precipitate an Addisonian crisis?
``` Severe stress Salt deprevation Infection Trauma Cold exposure Abrupt steroid withdrawl ```
36
What are the symptoms of Addisonian crisis?
``` Nausea Vomiting Pyrexia Hypotension Vascular collapse ```
37
What is the treatment for someone in an Addisonian crisis?
IV fluid replacement | IV cortisol
38
The innermost layer of the adrenal cortex secretes what?
Androgens
39
The chromaffin cells of the adrenal medulla lack what feature?
Axons
40
What do the chromaffin cells of the medulla release upon stimulation by the sympathetic nervous system?
Adrenaline (about 80%) | Noradrenaline (about 20%)
41
Adrenaline and Noradrenaline are both derivatives of which amino acid?
Tyrosine
42
What do the chromaffin cells of the adrenal medulla only secrete around 20% noradrenaline?
20% of the cells lack N-methyl transferase which is an enzyme needed to convert noradrenaline into adrenaline
43
What are the actions of adrenaline on the heart? | What receptors are activated?
Increased heart rate Increased contractility Beta1 receptors: GalphaS -->activation of adenylyl cyclase--> cAMP--> PKA --> Target Proteins
44
What receptors are activated by adrenaline in the lungs? What affect does this have on them? How?
Activation of beta2 receptors Causes bronchodilation Through GalphaS-->Adenylyl cyclase activation-->cAMP-->PKA-->Target proteins
45
What affect does adrenaline have on blood vessels? Which GPCR subunit is involved? What are the downstream pathways of receptor activation ?
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
How does adrenaline increase the heart rate?
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
What is Phaeochromocytoma?
A chromaffin cell tumour that secretes catecholamines (mainly noradrenaline)
48
What are the characteristics of Phaeochromocytoma?
``` Severe hypertension /hypotension Headaches Palpitations Anxiety Weight loss Elevated blood glucose Collapse ```
49
Why it is VITAL to decrease long-term use of steroids gradually over time and not just stop abruptly?
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
How do you test for adrenocortical function?
- 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
A normal response on a Synacthen test would usually exclude what? Why?
Addison's disease | No response to the administered ACTH as the tumour/ectopic ACTH secretion does not respond ????