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MD4001 Physiology > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

Describe the structure of the adrenal/suprarenal glands

A

Comprised of two distinct tissues; Cortex which is glandular tissue derived from mesoderm and Medulla which is sympathetic nervous system derived from neural crest cells and secretes catecholamines

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2
Q

What are different sections of the cortex?

A
  • Zona glomerulosa which secretes mineralocorticoids such as aldosterone.
  • Zona fasciculata which secretes glucocorticoids such as cortisol, and corticosterone.
  • Zona reticularis which secretes gonadocorticoids, such as dehydroepiandrosterone and androstenedione
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3
Q

What is the blood supply of the adrenal glands?

A

Superior, middle and inferior adrenal arteries which anastomose under the capsule. Cortex recieves short cortical arterioles. Medulla recieves long cortical arterioles which pass via cortex

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4
Q

Explain the steroid hormone synthesis

A

Cholesterol is converted into pregnenolone in a rate limiting step. Pregnenolone is then converted to aldosterone, cortisol or androgens.

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5
Q

What is the long term stress response?

A

Mineralocorticoids released which causes retention of sodium ions and water by kidneys, increasing the blood volume and blood pressure.
Glucocorticoids released which causes proteins and fats broken down and converted to glucose leading to an increase in blood glucose. Immune system may be supressed.

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6
Q

What are the main effects of cortisol?

A
  • Gluconeogenesis in the liver,
  • Proteolysis which generates amino acids which are fed into gluconeogenesis so production of more glucose,
  • Lipolysis which generates glycerol which is fed into gluconeogenesis so production of more glucose!
  • Cortisol also causes reduction in lipogenesis and reduction in protein synthesis
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7
Q

What is the control of cortisol release?

A
  • Stimulated by stress (physical or mental),
  • Corticotropin releasing hormone targets anterior pituitary,
  • Adrenocorticotropic hormone released and targets zona fasciculata causing cortisol release
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8
Q

What can occur with excess glucocorticoid?

A

Cushing’s syndrome

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9
Q

What are the causes of Cushing’s syndrome?

A
  • ACTH-releasing pituitary tumour,
  • Abnormal function of hypothalamus, resulting in high levels of CRH,
  • Ectopic ACTH releasing tumour (normally in lungs/pancreas/kidney)
  • Adrenal cortex tumour,
  • Clinical administration of glucocorticoid drugs
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10
Q

What are the clinical features of Cushing’s syndrome?

A
  • Hyperglycaemia (gluconeogenesis and steroid diabetes),
  • Muscle wasting (proteolysis),
  • Increase in plasma free fatty acids (enhanced lipolysis),
  • Increased Insulin release which causes redistribution of fat to trunk and face.
  • Tissue oedema, hypokalaemia and hypertension.
  • GI tract ulceration due to excessive H+ secretion.
  • Decreased protein synthesis,
  • Increased neuronal excitability, lymph node lysis, inhibition of haematopoiesis,
  • Immunosupressive
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11
Q

What are the symptoms of Cushing’s syndrome?

A
  • Headaches, moon face and buffalo bump,
  • Muscular weakness,
  • Skin thinning, fragility, acne, hirsutism, striae.
  • Weight gain, slow healing of cuts, increased risk of infections, fatigue, glucose intolerance.
  • Depression, anxiety, irritability, loss of emotional control, cognitive difficulties, decreased libido.
  • Increased risk of fractures
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12
Q

What is the treatment for Cushing’s syndrome?

A
  • Surgical removal of tumour,

- Decreased glucocorticoid drug use.

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13
Q

What are the mechanisms controlling aldosterone secretion?

A
  • Release of ACTH,
  • Increase in plasma potassium concentration
  • Renin-angiotensin cascade
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14
Q

What is the action of aldosterone?

A
  • In kidney tubular cells, aldosterone binds the mineralocorticoid receptor and initiates gene expression,
  • Increases expression of apical epithelium sodium channels which causes reabsorption of sodium and water.
  • Increases activity of Na/K/ATPase,
  • Increase in blood volume and pressure
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15
Q

Explain the suppression of glucocorticoid activity in renal tubular cells

A

11 beta-HSD metabolizes cortisol so it has little affinity the mineralocorticoid and glucocorticoid receptor. Inhibition of this 11 beta-HSD prevents metabolisim of cortisol and so it preferentially occupies these receptors over aldosterone

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16
Q

What is Addison’s Disease and its causes?

A
  • Adrenal insufficiency which causes a lack of cortisol and aldosterone.
  • Can be caused by autoimmune adrenalitis (80% of cases), Tuberculosis/metastatic tumours, Impaired function of pituitary gland/decreased ACTH, HIV (decreased immunity and increased risk of viral/bacterial infections)
17
Q

What are the clinical features of Addison’s disease?

A
  • Loss of weight/appetite, muscle weakness, nausea and vomiting.
  • Low plasma glucose, especially after fasting due to lack of glucocorticoid actions.
  • Low plasma sodium and high plasma potassium due to lack of mineralocorticoids resulting in dehydration and hypotension.
  • Lethargy and dizziness on standing due to hypotension,
  • Severe cases present with skin pigmentation due to excess ACTH,
18
Q

What is the treatment of Addison’s Disease?

A
  • Glucocorticoid replacement therapy,

- Intravenous saline infusion if severely dehydrated and administration of fludrocortisone (mineralocorticoid agonist).

19
Q

What is the short term stress response?

A
  1. Glycogen breakdown to glucose,
  2. Increased BP,
  3. Increased breathing,
  4. Increased metabolic rate,
  5. Change in blood-flow patterns leading to alertness and decreased digestive and kidney activity
20
Q

Describe the synthesis of catecholamines

A

Occurs in chromaffin cells;

  • Tyrosine is converted to DOPA by TH (tyrosine hydroxylase), ACTH needed.
  • Dopa converted to dopamine by AADC (amino acid decarboxylase),
  • Dopamine to Noradrenaline by DBH,
  • Noradrenaline to Adrenaline by PNMT.
21
Q

What are the catecholamine effects when binding to alpha-adrenoceptors?

A
  • Reduction in cAMP,
  • Increase in calcium,
  • Increase in smooth muscle contraction (vascular, bladder and bowel),
  • No effect on bronchial smooth muscle or cardiac muscle,
  • Reduced insulin secretion,
  • Reduce parathyroid hormone secretion,
  • Reduced renin secretion
    (Noradrenaline mainly binds to alpha receptors)
22
Q

What are the catecholamine actions when binding to beta-adrenergic receptors?

A
  • Increase in cAMP,
  • Reduction in calcium,
  • Relaxation of smooth muscle.
  • Relaxation of bronchial smooth muscle, relaxation of intestinal smooth muscle, and increased contraction of cardiac muscle.
  • Increased glycogenolysis,
  • Increased lipolysis,
  • Increased erythropoiesis,
  • Increased insulin secretion,
  • Increased parathyroid hormone,
  • Increased renin secretion

MD4001 Physiology (18 decks)

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