PHS 204 Adrenal Gland

Question 1

What is the anatomical location of the adrenal gland?

Answer 1

The adrenal glands are two pyramid-shaped glands,
•each located retroperitoneally, on top of the kidneys.
•Also called ‘suprarenal’ organs.

Question 2

Each adrenal gland is made up of

Answer 2

I.adrenal cortex and;
II.the adrenal medulla.

Question 3

Describe the relationship between the adrenal gland and kidneys

Answer 3

Has a paracrine interaction with the kidney, influencing the kidneys’ functions.
•aldosterone acts on kidney, which stimulates Na reabsorption and K excretion. H2O reabsorption follows Na reabsorption, resulting in an increase in effective circulating volume and therefore increase BP.

Question 4

Composition of adrenal cortices

Answer 4

The adrenal cortices comprise of
•Zona glomerulosa
•Zona fasciculata
•Zona reticularis
•The medulla zone has no scientific division.

Question 5

Hormonal function of the adrenal cortex

Answer 5

The adrenal cortex takes part in steroidogenesis (from cholesterol origin), producing glucocorticoids, mineralocorticoids, and androgen.

Question 6

Hormones of the adrenal cortex

Answer 6

Adrenal cortex
•Zona glomerulosa- mineralocorticoids eg aldosterone
•Zona fasciculata- glucorcorticoids eg cortisol (dominant in humans; stress hormone), corticosterone (dominant in animals) while cortisone is a synthetic form of cortisol*.

•Zona reticularis- DHEA -Dehydroepiandrosterone- (weak androgen)

Question 7

Hormones of the adrenal medulla

Answer 7

Adrenal medulla
•Catecholamines- Epinephrine, Norepinephrine, dopamine.

Question 8

Describe the transport form of aldosterone

Answer 8

Aldosterone
Combine loosely with plasma
protein
About 50% is in free form

Question 9

Inter relationship between free
& bound form
- TRANSCORTIN -

Answer 9

normal plasma conc.
3 mg%
Binding capacity - 20 pg / d1.
Synthesized in liver.
Increased by ostrogen
pregnancy.
liver cirrhosis, nephrosis &
multiple myeloma.

Question 10

Describe the Regulation of AGs: HPA AXIS

Answer 10

HYPOTHALAMO-PITUITARY-ADRENAL (HPA) AXIS
•Various stimuli initiate the negative feedback mechanism to the hypothalamus, which stimulates the release of corticotropic releasing hormone (CRH)/Arginine vasopressin (AVP)
•CRH/AVP acts on the anterior pituitary gland to release adenocorticotropin hormone (ACTH).
•ACTH acts on adrenal cortex to release its hormones.

Question 11

EFFECTS OF MINERALOCORTICOIDS (Aldosterone)

Answer 11

•The mineralocorticoids help to regulate Na+ and K+ balance and extracellular fluid volume.
•The mineralocorticoids help to maintain the body’s salt and water levels, which, in turn, regulates blood pressure ( intravascular pressure).
•The renin-angiotensin-aldosterone system (RAAS).

Question 12

EFFECTS OF CATECHOLAMINES

Answer 12

•Adrenaline and noradrenaline hormones are responsible for initiating the fight-or-flight response during dangerous or stressful situations.

Question 13

What is ADDISON’S DISEASE?
What are the symptoms

Answer 13

*This is caused by an inability of the adrenal cortices to produce adequate adrenocortical hormones

Low secretion of cortisol and aldosterone

Signs and symptoms
Pain in your lower back, abdomen or legs
severe vomiting and diarrhoea, leading to dehydration
Low blood pressure
loss of consciousness
high potassium (hyperkalemia)

Hypoglycemia
Fatigue
Hypotension

Treatment: Hormone replacement

Question 14

How is an addisonian crisis caused and treated?

Answer 14

Stress precipitates a collapse

Causes.
After adrenalectomy.
After abrupt withdrawal of therapeutically administered Glucocorticoids

Treatment
Mineralocorticoids & Glucocorticoids
administration daily

Question 15

Cushing’s disease

Answer 15

Hypersecretion of ACTH by the anterior pituitary causes increased release of both cortisol and androgenic hormones from adrenal gland

Question 16

Cushing’s syndrome

Answer 16

It is characterized by excess cortisol secretion from the adrenal cortex
resulting from too much ACTH by pituitary.
• More in women of 20- 40 yrs

Question 17

Signs of Cushing’s syndrome

Answer 17

Excess body and facial hair growth in women (from excess androgen secretion)
Mood swings and psychosis may occur as the effect of excess cortisol on cognitive function.
Truncal obesity: results from the mobilization of fat in the lower parts of the body to the trunk causing the abdomen to become protuberant as the extremities become thin and wasted.

Purple striae: appear on the abdomen as a result of the stretching of the abdominal skin.
They’re purple due to the collagen deficit in the tissues.
Round facial features: fat accumulation around the neck and cervical area is termed the buffalo hump.

Question 18

Causes of Cushing’s syndrome

Answer 18

Prolonged use of corticosteroid medicines
> Excess production of corticosteroid by adrenal cortex.- in adrenal tumor
Pituitary tumor- excess ACTH
> Ectopic production of ACTH by malignancies.- CUSHING DISEASES.

Question 19

Diagnosis of Cushing’s syndrome

Answer 19

A 24 hrs urine test - for Unbound cortisol
Dexamethazone test
Dexamethasone (1 mg) is administered orally at 11 pm, and a plasma cortisol level is obtained at 8 the next morning.
Suppression of cortisol to less than 5 mg/dL indicates that the hypothalamic-pituitary-adrenal axis is functioning properly.

Question 20

Management of Cushing’s syndrome

Answer 20

Management
- Radiation of the pituitary gland also has been successful, although it may take several months for control of
symptoms.
- Adrenalectomy is the treatment of choice in patients with primary adrenal hypertrophy.
- K supplement

Adrenal enzyme inhibitors (eg, metyrapone, aminoglutethimide,
mitotane, ketoconazole) may be used to reduce hyperadrenalism.
if the syndrome is caused by ectopic ACTH secretion by a tumor
* Surgical removal of pituitary gland
If due to steroid therapy - taper the dosage

Question 21

Action of StAR

Answer 21

Once cholesterol enters the cell, steroidogenic acute regulatory protein (StAR) regulates cholesterol transport from the outer mitochondrial membrane to the inner mitochondrial membrane.

In the inner mitochondrial membrane, the cholesterol can then be converted to pregnenolone via CYP11A1 (cholesterol desmolase/cholesterol side-chain cleavage, P450scc).

CYP11A1 catalyzes the rate-limiting step of steroid hormone production, and it is expressed in all three layers of the adrenal cortex.

Question 22

What conditions are glucocorticoids used to treat

Answer 22

Mainly because of their potent immunosuppressive and anti-inflammatory effects, glucocorticoids are used commonly in pharmacologic doses to treat diseases such as autoimmune disorders.

Question 23

Functions of glucocorticoids

Answer 23

Anti-inflammatory
Cardiovascular function
Decrease muscle mass
Increased blood glucose
Increased glomerular filtrate rate
Modulate emotions

Question 24

Clinical significance of transcortin

Answer 24

Transcortin levels in the third trimester of pregnancy are twice that in non-pregnant state. The increased total cortisol is, however, not associated with the symptoms of excess cortisol as the levels of (physiologically active) free form of cortisol are normal

Question 25

Characteristic features of type-I (IDDM)

Answer 25

It manifests before 40 years of age (usually between 12 and 15 years) and is also called juvenile onset diabetes.
It accounts for 10−20%.
Patients are usually lean.
Classical triad of presenting symptoms consisting of polyuria, polydipsia and polyphagia is associated with weight loss.
Ketosis and acidosis are common complications of this diabetes mellitus.
Plasma insulin levels are very low or undetectable.

Question 26

What is ketosis and its cause?

Answer 26

Since due to insulin deficiency the utilization of glucose is poor, the body turns to fats for obtaining energy by lipolysis. As a result of lipolysis, plasma levels of FFAs are increased. Excessive FFAs in plasma leads to:
Hypertriglyceridaemia and
Ketosis

Question 27

Consequences of ketosis

Answer 27

Cellular dehydration. Ketone bodies being hyperosmolar, remove water from the cells producing cellular dehydration.
Ketoacidosis. Ketone bodies being strong acids dissociated readily and release H+ ions. In the blood, these H+ions are buffered by bicarbonate ions (HCO3−) to form carbonic acid. Fall in bicarbonate level in the blood leads to acidosis called ketoacidosis.

Question 28

Features of ketoacidosis

Answer 28

Rapid, deep respiration (dyspnoea, Kussmaul breathing),
Acetone smell in patient’s breath and
Urine becomes highly acidic.
Electrolyte loss. The electrolyte and water loss further added to cellular dehydration.
Hypovolaemia and hypotension may ultimately result from water and electrolytic loss and cellular dehydration.
Coma and death. Depression of consciousness to the level of coma may eventually ensure owing to marked acidosis and dehydration which may finally lead to death.

Question 29

Effect of the fight or flight hormones

Answer 29

1. Breakdown of glycogen -> glucose (in liver and muscles), 2. this increases blood glucose concentration (to heart + skeletal muscles)_
2. Increases metabolic rate (1 energy release in tissue respiration)
3. 1 heartbeat rate; 1 blood pressure (faster transport of glucose + 0)
4. Constricts arteries in skin (pallor) -> more blood to muscles
5. 1 coagulation rate of blood
6. Relaxes bronchioles (1 air flow to lungs)
7. Pupil dilation (enhances vision)
8. Hair muscle contraction (“goose pimples”)