The Adrenal Glands Flashcards
Parts of the adrenal gland and what they secrete
Zona glomerulosa - mineralocorticoids
Zona fasiculata - glucocorticoids
Zona reticularis - glucocorticoids and small amount of androgens
Chromaffin cells - adrenaline, noradrenaline
Two types of androgens
Dehydroepiandrosterone
Androstenedione
How do corticosteroids exert their actions?
- Readily diffuse across plasma membrane
- Bind to glucocorticoid receptor
- Binding causes dissociation of chaperone proteins
- Receptor ligand complex translocates to nucleus
- Dimerisation with other receptors can occur
- Receptors bind to glucocorticoid response elements (GREs) or other transcription factors
Carrier protein of aldosterone
Serum albumin, and to a lesser extent transcortin
What does aldosterone play a central role in?
Regulation of plasma Na+, K+ and arterial blood pressure. Promotes expression of Na+/K+ pump, promoting reabsorption of Na+ and excretion of K+
The RAAS
Angiotensinogen > (renin) > Angiotensin I > (ACE) > Angiotensin II > ADH, Aldosterone, vasoconstriction
What effect does ADH have on water reabsorption?
Translocation of aquaporin channels aids reabsorption of water back into the blood
Primary hyperaldosteronism
Defect in adrenal cortex:
- Bilateral idiopathic adrenal hyperplasia
- Aldosterone secreting adrenal adenoma (Conn’s syndrome)
Secondary hyperaldosteronism
Due to over activity of the RAAS:
- Renin producing tumour e.g. juxtaglomerular tumour
- Renal artery stenosis
Best way to distinguish between primary and secondary hyperaldosteronism
Primary - low renin
Secondary - high renin
Signs of hyperaldosteronism
- High blood pressure
- Left ventricular hypertrophy
- Stroke
- Hypernatraemia
- Hypokalaemia
Treatment for hyperaldosteronism
- Aldosterone producing adenomas removed by surgery
- Spironolactone (mineralocorticoid receptor antagonist)
Carrier protein of cortisol
Transcortin
Actions of cortisol
- Increased protein breakdown in muscles
- Increased gluconeogenesis in liver
- Increased lipolysis in fat
- Resistance to stress (increased supply of glucose, raise blood pressure by making vessels more sensitive to vasoconstrictors)
- Anti inflammatory effects (inhibits macrophage activity and mast cell degranulation)
- Depression of immune response
Symptoms of Cushings
- Plethoric moon shaped face
- Buffalo hump
- Abdonimal obesity
- Purple striae
- Acute weight gain
- Hyperglycaemia
- Hypertension
Symptoms of Addison’s
- Postural hypotension
- Lethargy
- Weight loss
- Anorexia
- Increased skin pigmentation
- Hypoglycaemia
Most common cause of Addison’s
Destructive atrophy from autoimmune response
Hyperpigmentation in Addisons
Negative feedback on anterior pituitary reduced so more POMC to synthesise ACTH. ACTH itself activated melanocortin receptors on melanocytes. MSH stimulates melanin production
Addison’s crisis precipitated by:
- Severe stress
- Salt deprivation
- Infection
- Trauma
- Cold exposure
- Over exertion
- Abrupt steroid drug withdrawal
Addison’s symptoms
- Nausea
- Vomiting
- Pyrexia
- Hypotension
- Vascular collapse
Addison’s treatment
- Fluid replacement
- Cortisol
Which enzyme is needed to convert noradrenaline to adrenaline?
N-methyl transferase
G protein coupled receptor alpha 1 pathway
+ve Phospholipase C > Diacylglycerol and IP3 > PKC and Ca2+ release via IP3 receptor
G protein coupled receptor alpha 2 pathway
-ve Adenylyl cyclase > cAMP > Protein kinase A
G protein coupled receptor beta 1 and 2 pathway
+ve Adenylyl cyclase > cAMP > Protein kinase A
Phaeochromocytoma characteristics
- Severe hypertension
- Headaches
- Palpitations
- Diaphoresis
- Anxiety
- Weight loss
- Elevated blood glucose
Cortisol deficiency symptoms
- Weakness
- Tiredness
- Weight loss
- Hypoglycaemia
Mineralcorticoid deficiency symptoms
- Dizziness
- Low Na
- High K
Androgen deficiency symptoms
- Low libido
- Loss of body hair in women
