Adrenal gland


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  • Cellular mechanism of aldosterone action
  • In 2nd monthly test
  • In 2nd monthly test
  • In 2nd monthly test
  • In 2nd monthly test
  • Adrenal gland

    2. 2. INTRODUCTION • The body has two adrenal ( supra renal) glands, each located on the superior pole of each kidney. Each adrenal gland is structurally and functionally differentiated into two regions or zones: 1. Adrenal cortex: This is the outer or peripheral zone of the adrenal gland, which makes up the bulk of gland. 2. Adrenal medulla: This is the inner zone of the adrenal gland.
    3. 3. ADRENAL CORTEX • The adrenal cortex is divided into three zones. Each zone has a different cellular arrangement and secretes different groups of steroid hormones. • The layers/zones of the adrenal cortex. Formula for remembering layers. (GFR) 1. Zona-Glomerulosa: This is the outer most zone of the adrenal cortex which secretes mineralocorticoids.
    4. 4. ADRENAL CORTEX 2. Zona-Fasciculata: This is the middle zone of the adrenal cortex which secretes glucocorticoids and adrenal androgens. 3. Zona-Reticularis: This is the inner most zone of the adrenal cortex which secretes glucocorticoids and adrenal androgen, but in a small quantities.
    5. 5. HORMONES OF THE ADRENAL CORTEX • The adrenocortical hormones and their functions in the body are classified into: 1. Mineralocorticoids 2. Glucocorticoids 3. Adrenal androgens
    6. 6. 1. MINERALOCORTICOIDS • These hormones help to control the water and electrolyte homeostasis, particularly the concentration of Na+ and K+ ions. Mineralocorticoids include the following hormones: a) Aldosterone ( principal hormone). b) Deoxy corticsterone. c) Corticosterone. d) 9-alpha-Fluorocortisol. e) Cortisol. f) Cortisone.
    7. 7. 2. GLUCOCORTICOIDS • The glucocorticoids are group of hormones concerned with normal organic metabolism and resistance to stress. Glucocorticoids include the following hormones: a) Cortisol. b) Corticosterone. c) Cortisone. d) Prednisone. e) Mythyl prednisone.
    8. 8. 3. ADRENAL ANDROGENS • These are steroids which exhibit actions similar to testosterone. Biosynthesis of adrenocortical hormones: Acetate | Cholesterol | Pregnenolone 17-OH-pregnenolone | / Progesterone Cortisol Androgen | Aldosterone
    9. 9. 1.ALDOSTERONE • INTRODUCTION: This is a hormone of the adrenal cortex, secreted by the outermost layer called the zone glomerulosa. Daily secretion = 150 ug/day. Normal plasma level : 6 ng/100 ml.
    10. 10. MCQ • The secretion of aldosterone is caused by? • a) angiotensin II • b) ACTH • c) epinephrine • d) insulin
    11. 11. MCQ • Aldosterone secretion is regulated by the following except? • a) ACTH • b) calcium • c) blood volume • d) potassium
    12. 12. • HALF-LIFE: The half-life of aldosterone is short, about 20 minutes. • TRANSPORT: Most of the secreted aldosterone is bound to albumin, with a lesser amount bound to corticosteroid binding globulin (CBG). The transport is as follows: I. 60% bound with plasmaproteins (mostly albumin). II. 40% transported in free form.
    13. 13. • METABOLISM: Most aldosterone is converted in the liver to a tetra hydroglucronide derivative, but some is changed in the liver and kidneys to an 18 glucronide. The glucronide which is unlike the breakdown products of other steroids. It is converted to free aldosterone by hydrolysis at a pH of 1.0 and is therefore referred to as the “ acid-labile conjugate”.
    14. 14. • METABOLISM: Less than 1% of the secreted aldosterone appears in the urine in free form. 5% is in the form of “acid labile conjugate” and upto 40% is in the form of the tetrahydroglucronide.
    15. 15. • REGULATION OF ALDOSTERONE SECRETION: A. Factors increasing aldosterone secretion: a) Increased K+ ions. b) Decreased Na+ ions. c) Undefined pituitary factors. d) ACTH. e) Hypovolemia. f) Hypotension. g) Increased renin angiotensin. h) Stress. i) Adrenal adenoma (Conn’s Syndrome) j) Idiopathic adrenal hyperplasia.
    16. 16. Factors stimulating aldosterone release from the adrenal cortex: Angiotensin II is the most important trophic factor for the zona glomerulosa and one of the two most important stimulators of aldosterone release. Even a 0.5 mM increase in plasma [K] stimulates aldosterone release. In turn, aldosterone regulates plasma [K] by promoting K secretion in the collecting ducts. Angiotensin III has 100% aldosterone releasing activity but only 40% of the pressor activity of aldosterone. ACTH as well as a decrease in plasma [Na] stimulate aldosterone release but the stimulatory effects of acute administration of pharmacologic doses of ACTH on aldosterone release are transient if at all.
    17. 17. ALDOSTERONE ESCAPE • When excess aldosterone is administered, it causes excess Na+ and water absorption increasing ECF volume, in turn increasing blood volume. Increased blood volume causes increased cardiac output and blood pressure. Pressure diuresis and pressure natriuresis cause a secondary loss of Na+ and water. This process is called aldosterone escape.
    18. 18. EFFECTS OF ALDOSTERONE • A. Effects on renal tubules: The main action of aldosterone is to maintain balance of the electrolyte contents of the body fluid. The sites of action are the ascending limb, loop of Henle, and distal and collecting tubules. i) Aldosterone causes increased tubular reabsorption of Na+ in exchange for K+ and H+ ions. The lack of aldosterone causes an excess loss of Na+ in urine.
    19. 19. ii) Aldosterone increases K+ secretion into the distal and collecting tubules of the kidneys. This may be due to ionic exchange with Na+ reabsorption. Excess aldosterone causes hypokalemia and muscle paralysis. iii) Aldosterone causes water absorption due to the concentration gradient created by Na+ absorption, increasing EFC volume.
    20. 20. B. General effects on: i. Circulation: increases blood volume and cardiac output. ii. Blood pressure: increases blood pressure due to increased cardiac output, blood volume and venous return.
    21. 21. iii. Sweat glands and salivary glands: aldosterone causes increases Na+ and Cl- reabsorption. And at the same time, it increases K+ secretion. iv. GIT: causes increased Na+ and Cl- absorption from the intestine, simultaneously increasing water reabsorption from GIT.
    22. 22. CORTISOL • INTRODUCTION: Cortisol is also known as hydrocortisone. This hormone is most abundunt and essential for life. It is responsible for about 90% of glucocorticoid activity. • Site of formation: Cortisol is secreted by the zona fasiculata and zona reticularis layers of the adrenal cortex of the adrenal gland
    23. 23. • Bio-synthesis: This hormone is a 21 carbon atom steroid which is synthesized from acetyl-CoA cholesterol. Daily secretion rate = 15 mg/day Half-life = 90 – 100 minutes Normal plasma level = 94% bound with cortisol binding protein, 6% in free form.
    24. 24. • Regulation of cortisol: The secretion of glucocorticoids is regulated by hormone of anterior pituitary gland called adrenocortcotropic hormone (ACTH). The control of glucocorticoid secretion is under a typical negative feedback mechanism. The two principle stimuli are stress and low blood level of glucocorticoids.
    25. 25. • Regulation of cortisol: Both conditions stimulate the hypothalamus to secrete a regulating hormone called corticotropin releasing hormone(CRH). This secretion initiates the release of ACTH from the anterior pituitary gland. ACTH is carried through blood to the adrenal cortex where it stimulates glucocorticoid secretion.
    26. 26. • Effects of cortisol: A. Metabolic effects: 1. Carbohydrate metabolism: a) Cortisol stimulates gluconeogenesis in the liver by mobilizing amino acids from extra hepatic tissues (muscles) and by increasing the enzymes of gluconeogenesis.
    27. 27. b) It decreases the utilization of glucose by cells by decreasing oxidation of NADH2, which is needed for glycolysis, and by decreasing glucose transport into the cells. c) It increases blood glucose levels due to increased gluconeogenesis and decreases glucose utilization. This condition is called adrenal diabetes.
    28. 28. 2. Protein metabolism: a) The principle effects of cortisol on the metabolic systems of the body is reduction of protein stores in all body cells except those of the liver. This is caused by both decreased protein synthesis and increases catabolism of protein in the cells. b) It inhibits amino acid entry into all cells except the liver. c) It increases amino acid concentration in blood. d) It increases urea level in blood.
    29. 29. 3. Fat metabolism: a) It mobilizes fatty acids from adipose tissues. b) It increases free fatty acid concentrations in blood. c) It increases utilization of free fatty acids for energy. d) It causes ketosis due to increased conversion of free fatty acids into acetyls-CoA.
    30. 30. 4. Electrolyte metabolism: a) It promotes Na+ and Cl- retention from the renal tubules. b) It increases excretion of K+ by kidneys. 5. Water metabolism: It causes diuresis by suppressing ADH secretion or by increasing destruction of ADH by the liver cells.
    31. 31. B. General effects: 1.On C.V.S. a) Cortisol increases blood pressure because of increased production of angiotensionogen. b) Increased sensibility of vascular smooth muscle to nor-adrenaline and adrenaline.
    32. 32. 2. On blood cells: a) Increases the platelet count. b) Decreases blood clotting time. c) Increases total WBCs. d) Decreases lymphocytes, eosinophils and basophils. e) Increases neutrophils, monocytes and RBC count.
    33. 33. 3. On C.N.S. : a) Low cortisol levels cause restlessness, insomnia, and inability to concentrate. b) Causes excitation of the CNS. 4. On GIT: a) Increases gastric acidity and may cause a peptic ulcer.
    34. 34. 5. On bone: a) Excess cortisol may cause a defect in the synthesis of protein matrix. b) It decreases the deposition of calcium. c) It increases the loss of calcium in urine. d) It decreases absorption of calcium from the GIT.
    35. 35. 6. On infection, inflammation, and trauma: a) Large doses of cortisol decrease the formation of antibodies due to its destructive effect on lymphoid tissues. b) It decreases tissue response to bacteria. c) It is anti- inflammatory. d) It is anti- allergic. e) It delays wound healing.
    36. 36. COMMON THERAPUTIC USES OF GLUCOCORTICOIDS • Bronchial asthma. • Chronic bronchitis. • Emphysema. • Sarcoidosis. • Ulcerative colitis. • Crohn’s disease. • SLE, cerebral edema. • Skin diseases. • Hodgkin’s disease.
    37. 37. SUMMARY OF ADVERSE EFFECTS OF GLUCOCORTCOIDS • Hypertension. • Peptic ulcer, pancreatitis. • Nocturia, polyurea. • Insomnia, depression and psychosis. • Amenorrhea. • Hyperglycemia. • Osteoporosis. • Pathological fractures. • Cataract.
    38. 38. PATHOLOGY OF ADRENAL CORTEX • ADDISON’S DISEASE: This disease results from failure of adrenal cortex to produce adrenocortical hormones. Causes: 1. Atrophy of the adrenal cortex. 2. Tuberculosis. 3. Surgical removal of adrenal gland. 4. Tumor. 5. Deficiency of enzymes (responsible for the formation of aldosterone). 6. Hemorrhage and infarction. 7. Meningococal septicaemia. 8. Amyloidosis. 9. Schilder’s disease.
    39. 39. Clinical features of Addison's disease: a) Symptoms: Weight loss, anorexia, malaise, fever, depression, impotence, abdominal pain, nausea, vomiting, diarrhoea, syncope, constipation etc. b) Signs: General wasting, loss of weight, loss of body hair, buccal pigmentation, postural hypotension, dehydration, vitiligo etc.
    40. 40. Investigations: • Blood cortisol level. • The short ACTH stimulation test. • Plasma ACTH level. • Electrolytes and urea ( classically shows hyponatremia, hyperkalemia and high urea levels). • Blood glucose levels may be low.
    41. 41. Investigations: • Adrenal antibodies are present. • Chest X-rays may show evidence of tuberculosis. • Serum aldosterone level is increased. • Hypercalcemia. Treatment: Long term treatment is replacement with glucocorticoids and mineralcorticoids.
    42. 42. MCQ • In Addison’s disease, the following is seen? • a) hyperkalemia • b) increase in ECF volume • c) hyperglycemia • d) high blood pressure
    43. 43. CUSHING’S SYNDROME • Introduction: This syndrome is characterized by a clinical state of increased free circulating glucocortcoid. • Causes:  Adrenal cortex tumor that secretes excess cortisol. (20%)  Anterior pituitary gland tumor that secretes excess ACTH.(80%)
    44. 44. • Causes:  Abdominal tumor that secretes excess ectopic ACTH.(0.5%)  ACTH administration.  Adrenal carcinoma.  Cortisol administration.  Alcohol induced pseudo Cushing’s syndrome.
    45. 45. • Clinical features of Cushing’s syndrome: A. Symptoms:  Central obesity.  Fat accumulates the face, neck and trunk.  Depression, insomnia, psychosis.  Amenorrhea, oligomenorrhoea.  Decreased libido.  Thin skin, easy bruising.  Hair growth on face, acne.  Muscular weakness.  Back pain.  Polyurea and polydipsia.
    46. 46. B. Signs :  Acne, thin skin, bruising, hirsutism, striae (purple), pigmentation.  Moon face, buffalo hump, central obesity (pendulous abdomen, tomato head, potato body and four match stick limbs).  Kyphosis, rib fractures.  Poor wound healing.  Hypertension, glucosuria.  Proximal muscle wasting, proximal myopathy.  Edema.
    47. 47. • Diagnosis: ( diagnosis of Cushing’s syndrome is based on the following investigations).  Clinical features = buffalo hump, moon face, masculinizing effect.  Blood glucose level increases.  Blood cortisol level increases.  Urinary secretion of the 17 hydroxysteroids increases.
    48. 48. • Diagnosis:  Over night dexamethasone suppression test +Ve.  Low dose dexamethasone test.  Insulin tolerance test.  Corticotropic releasing hormone test.  Adrenal CT- scan.  Chest x-ray.
    49. 49. • Treatment:  Removal of adrenal tumors.  Suppression of ACTH secretion.  Bilateral adrenalectomy.
    50. 50. MCQ • All are seen in Cushing’s syndrome except? • a) truncal obesity • b) hypertension • c) hypoglycemia • d) hirsutism
    51. 51. THE END
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