The Adrenal Glands Flashcards

1
Q

Describe the anatomical division of the adrenal gland

A

The adrenal gland are found in the upper kidney and lie against the diaphragm. It consists of two regions, outer region and inner medulla (produces adrenaline and noradrenaline). During embryonic development, cortex is derived from mesoderm and medulla is derived from neural crest cells.
The cortex has 3 zones which have different arrangements of secretory cells and associated network of capillaries and sinusoids:
- Zona Glomerulosa
- Zona Fasciculata
- Zona Reticularis

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

Name the hormones produced by the different layers of the cortex and their function

A

Zona Glomeulosa - The cells on the outermost zone secrete the mineralcorticoids (e.g., aldosterone) that regulate body Na+ and K+ levels
Zona Fasciculata - Cells in this zone produce the glucocorticoids (e.g., cortisol) that have a number of important functions including the regulation of carbohydrate metabolism
Zona Reticularis - Deepest cortical zone and the cells secrete glucocorticoids and small amounts of androgens (dehydroepiandrosterone).

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

Describe in general terms, the structure and function of the steroid hormone

A

The steroid hormones are synthesised from cholesterol in adrenal glands and gonads. They are lipid soluble hormones, that bind to receptors of the nucleus receptor family to modulate gene transcription. They include:
- Glucocorticoids
- Mineralcorticoids
- Androgens
- Oestrohens
- Progestins

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

Explain Hyperaldosteronism

A

Primary - defect in adrenal cortex
Bilateral idiopathic adrenal hyperplasia. Aldosterone secreting adrenal adenoma. Seen by low renin levels (high aldosterone:renin ratio)
Secondary - Due to over activity of the RAAs
Renin producing tumour. Renal artery stenosis. High renin levels (low aldosterone:renin ratio).
Signs include high blood pressure, left ventricular hypertrophy, stroke etc.

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

Explain how cortisol secretion is controlled by ACTH and CRH

A

Cortisol is the most abundant corticosteroid and account for around 95% of glucocorticoid activity.
Adrenocorticotropic hormone (ACTH), is secreted from the anterior pituitary and is main factor in cortisol release. It is secreted with a circadian rhythm with pulsatilla secretion superimposed.
Secretion of ACTH, under control of corticotropin releasing factor (CRF). CRF is secreted is response to physical, chemical and emotional stressors. There is also negative feedback by glucocorticoids on both the hypothalamus and pituitary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain how ACTH can lead to increased pigmentation in certain areas of the body

A

ACTH is a single chain polypeptide. Initial biological precursor is a large protein called pro-opiomelanocortin (POMC). Post translational proceeding of POMC produces a range of biblically active peptides including ACTH, alpha MSH melanocyte stimulating hormone).
The clinical consequences of over secretion of ACTH relate to the direct effects of ACTH on tissues (increased pigmentation due to partial MSH activity) and the effect of ACTH on the adrenal cortex.

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

Describe the main actions of cortisol

A

Cortisol is lipophilic and must be transported bound to plasma proteins. Major transport protein is transcortin. Cortisol can cross the plasma membrane of target cells and bind to cytoplasmic receptors. Hormone/receptor complex enters nucleus and interacts with specific regions of DNA. Interaction changes rate of transcription of specific genes. The metabolic actions of cortisol include:
- Decreased amino acid uptake
- Decreased protein synth is and increased in proteolysis in most tissues (not liver)
- Increased hepatic gluconeogenesis and glycogenolysis
- Increased lipolysis in adipose tissue
- Increased Lipogenesis in adipose tissue
- Decreased peripheral uptake of glucose

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

Describe the structure and functions of adrenaline

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain how adrenaline exerts its effects on cells

A

Adrenaline is released as part of the fight or flight response, and is secreted in response to stressful situations. It has effects on:
- Cardiovascular system (increased cardiac output, increased blood supply to muscle).
- Central nervous system (increased mental alertness)
- Carbohydrate metabolism (increased glycogenolysis in liver and muscle)
- Lipid metabolism (increased lipolysis in adipose tissue).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the components and overall function of the renin angiotensin aldosterone system

A

The RAA system is a system of hormones involved in the regulation of plasma sodium concentration and arterial blood pressure. If concentration of plasma Na+ falls, cells of kidney nephron release renin. Fall in blood pressure/blood volume also stimulates renin release

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

Explain the clinical effects of excess cortisol secretion

A

Hyperactivity of adrenal cortex leading to increasing secretion of cortisol causes Cushing’s syndrome.
Signs of symptoms include:
- Increased muscle proteolysis and hepatic gluconeogenesis that may lead to hyperglycaemia which assoiciated polyuria and polydipsia
- Increased muscle proteolysis leads to wasting of proximal muscles and producing thin arms and legs and muscle weakness
- Increased Lipogenesis in adipose tissue leading to deposition of fat in abdomen
- Purple striae on lower abdomen, upper arms, thighs

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

Explain Cushing’s syndrome

A

Cushing’s syndrome can either be caused by external causes or endogenous causes.
- External causes include prescribe glucocorticoids (most common causes
- Endogenous causes are rare. They include:
Benign pituitary adenoma secreting ACTH (Cushing’s disease)
Excess cortisol produced by adrenal tumour (Adrenal Cushing’s)
Non pituitary-adrenal tumours producing ACTH e.g., small cell lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the clinical effects of too little cotrisol secretion

A

Adrenal insufficiency can result from primary or secondary causes. Primary adrenal insufficiency (Addisons disease), results of failure of adrenal gland itself. Most commonly, its a result from other causes e.g., tuberculosis infection, malignancy.
Secondary adrenal insufficiency is caused by failure of the pituitary gland or hypothalamus. Can result from a pan hypopituitarism or from isolated failure of ACTH production. Can also result from steroid-induced hypoadrenalism.

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

Explain Addison’s disease

A

Primary adrenal insufficiency involves the loss of both cortisol and mineralocorticoids and produces a complex situation that may present as an acute emergency (Addisonian Crisis) or as a chronic debilitating disorder (Addison’s disease)
- Insidious onset with initial non-specific symptoms of tiredness, extreme muscular weakness, anorexia, vague abdominal pain, weight loss and dizziness
- Extreme muscular weakness and dehydration
- Increased skin pigmentation particularly on exposed areas of the body, points of friction
- Decreased blood pressure due to sodium and fluid depletion
- Postural hypotension due to fluid depletion
- Hypoglycaemic episodes especially on fasting due to lack of glucocorticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the tests of adrenal cortical function

A

Measurement of plasma cortisol and ACTH levels and the 24hr urinary excretion of cortisol and its breakdown products are important in investigations suspected adrenocortical disease. In addition, dynamic function tests may be sued in the differential diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain how cortisol can have weak mineralocorticoid and androgen effects

A

Steroid receptors form part of a family of nuclear DNA binding proteins that include the thyroid and vitamin D receptors. 3 main regions: Hydrophobic hormone binding region, DNA binding regain, variable region. Percentage homology of the hormone binding region of the glucocorticoid receptor with the mineralocorticoid, androgen, oestrogen and thyroid receptors is 64%, 62%, 31%, 24%. Thus cortisol will bind to the mineralocorticoid and androgen receptors with low affinity. Binding may become significant when high levels of the hormone are present.