Adrenal Glands Flashcards

1
Q

What are the three parts of the adrenal gland?

A
  • capsule
  • cortex
  • medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the different parts of the adrenal gland responsible for?

A
  • cortex = steroidogenisis

- medulla = catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three different parts of the adrenal cortex?

A
  • zona glomerulosa (mineralocorticoids) - aldosterone
  • zona fasiculata (glucocorticoids) - cortisol
  • zona reticularis (androgen precursors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are corticosteroids?

A

mineralocorticoids and glucocorticoid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the precursor for lipid derived hormones?

A

cholesterol

  • hormones are synthesised on demand
  • via conserved biosynthetic pathways
  • enzymes found in mitochondria/ER
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the rate listing step when synthesising lipid hormones?

A

cholesterol to prognenolone via prenenolone synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is the enzyme pregnenolone synthase regulated?

A

by the Adrenocorticotropic Hormone (ACTH)
- CRH secreted by the hypothalamus
- causes ACTH secretion from the anterior pituitary
- ACTH induces the enzyme
therefore ACTH induces steriodogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the main role of glucocorticoids?

A
  • metabolic effects
  • anti-inflammatory
  • immunosuppressive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the main role of mineralocorticoids?

A
  • water and electrolyte balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are corticosteroids transported in the blood?

A

TRANSCORTIN - Corticosteroid Binding Globulin

  • binds 90% of cortisol
  • binds 60% of aldosterone

will NOT bind to synthetic steroids - these bind to albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do steroids generally have longer-term actions?

A

because they induce changes in transcription and translation of genes, their effects are to induce synthesis of specific proteins - receptors are intracellular

aldosterone CAN have more immediate effects as some cells have receptors on the surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are glucocorticoids released?

A

hypothalamus detects stress/excitement/anticipation

  • secretes CRH
  • acts on the anterior pituitary to release ACTH
  • ACTH acts on the adrenal glands, and induces PS
  • cholesterol - prognenolone
  • synthesis of cortisol begins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What effects does cortisol have on the body?

A

raises blood glucose:

  • lipolysis
  • protein catabolism
  • glucogenesis

raises blood pressure:
- sensitises blood vessels to adrenaline

suppresses the immune system
- reduces inflammation

induces osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is involved in the negative feedback process?

A

cortisol acts back on the

  • hypothalamus to stop the secretion of CRH
  • anterior pituitary to stop the secretion of ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the mechanism of action of mineralcorticoids?

A

binding of aldosterone to MC receptors causes:

  • Na uptake
  • Water reabsorption
  • Increasing blood pressure

aldosterone release is triggered by

  • angiotensin II
  • low salt levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of action of spironolactone?

A

competitively inhibits the MC receptors

17
Q

What can chemical modifications to the steroid backbone of corticosteroids cause?

A
  • can vary the duration of action

- can vary the selectivity for MC/GC receptors

18
Q

What are examples of the three different durations of actions of corticosteroids?

A

Short - 8 - 12 hours

  • hydrocortisone
  • fludrocortisone

Intermediate - 12 - 36 hours
- prednisolone

Long - 36 - 72 hours

  • dexamethasone
  • betamethasone
19
Q

What are examples of the three different selectivities of corticosteroids?

A

Mixed GC/MC
- prednisolone

Pure GC

  • dexamethasone
  • betamethasone
  • beclomethasone

Mainly MC
- fludrocortisone

20
Q

What are the residues of the steroid backbone that are essential for corticosteroid activity?

A

3, 4, 5 C residues on the A ring

21
Q

What do modifications of the 1, 2 C residues on the A ring of the steroid backbone cause?

A

increase the influence of the molecule on GC receptors over MC receptors
- increases GC activity (GC/MC ratio)

22
Q

What residue is essential for GC activity?

A

11 C residue on the C ring

23
Q

What reside is essential for MC activity?

A

21 C residue on the D ring

24
Q

What does modifications to the 17 C residue on the D ring of the steroid backbone cause?

A

produces molecules with maximum GC potency

25
Q

What are the three different uses of steroids?

A
  • replacement therapy
  • restoring endocrine control
  • anti-inflammatory/immunosuppressant
26
Q

What is Addison’s disease?

A

hypo function of the adrenal glands

  • Appetite Loss, Unintentional Weight Loss
  • Discolouration of the Skin
  • Dehydration
  • Increased Thirst & Need to Urinate Frequently
  • Salt, Soy Sauce, Liquorice cravings
  • Oligomenorrhoea
  • No Energy/Motivation
  • Sore Muscles and Joints
27
Q

What is the treatment for Addison’s disease?

A

Hydrocortisone (GC) with/without

Fludrocortisone (MC)

28
Q

What is congenital adrenal hyperplasia?

A
fault in the steroidogenesis pathway
- loss of enzymes in the pathways 
- unable to produce GCs/MCs 
= unable to produce cortisol 
- no negative feedback 
- ACTH output raised
- over-production of androgens 

features of males in newborn girls, and male features having an earlier onset in males

29
Q

What is the treatment for congenital adrenal hyperplasia?

A

exogenous cortisol (dexamethasone/betamethasone)

  • replaces the lack of cortisol
  • restores endocrine control by restoring the negative feedback loops
30
Q

When and how would corticosteroids be used as anti-inflammatory, immunosurpressing agents?

A

work by reducing the mediators of inflammation and immune responses

  • asthma
  • eczema
  • arthritis
  • psoriasis
  • allergic rashes
  • itching
31
Q

What steroid agents would work as anti-inflammatory, immunosurpressing agents?

A
  • hydrocortisone
  • prednisolone
  • beclamethasone
  • dexamethasone
  • budesonide
32
Q

What are the side effects and issues of steroid treatments?

A
  • drug induced Cushing’s Syndrome (lipolysis)
  • osteoporosis (induced osteoclasts)
  • increased risk of infection (anti-inflammatories) - oral thrush
33
Q

What is aminoglutethimide used for?

A

to inhibit steroid synthesis, by blocking enzymes in the pathway, including PS

  • Cushing’ Syndrome
  • Postmenopausal Breast Cancer
  • Prostate Cancer
34
Q

What is metyrapone used for?

A

selective inhibition of steroid synthesis, blocking the final enzymes further down the pathway of GC and MCs

  • Cushing’s syndrome
  • Hyperaldosteronism

side effects:
- Hirsutism in women because of excess androgens

35
Q

How is metyrapone used as a test for anterior pituitary function?

A

remove the negative feedback by inhibiting cortisol production

the anterior pituitary SHOULD then produce MORE ACTH in response to this

36
Q

What is tetracosatide/synacthen used for?

A

they are ACTH mimetic to test for adrenal insufficiency

they stimulate the synthesis and release of adrenal hormones