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Adrenal gland notes to study, Study notes of Physiology

Central Baptist College (CBC)Physiology

Adrenal gland notes to study , simple notes , effective notes

Typology: Study notes

2019/2020

Uploaded on 02/16/2020

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1. A 33 year old woman complained of weight gain, round face, thinning of her limbs, and
increased bruising of skin with discoloration on her prominent abdomen. Answer the following
questions based on your knowledge in physiology: ( 1+ 4+ 5)
What is the probable endocrinological disorder?
Cushing’s syndrome due to cortisol excess
Explain the metabolic actions of the hormone involved
Metabolic actions of cortisol
EFFECT ON PROTEIN METABOLISM
1. Protein break down / proteolysis in skeletal muscle and protein matrix of bone causes increase in plasma
amino acids (catabolic effect)
2. Muscle protein is mobilized for gluconeogenesis
EFFECT ON CARBOHYDRATE METABOLISM
1. Increased glucose formation in liver / hepatic gluconeogenesis
2. Increased secretion of glucagon, epinephrine (glycogenolytic hormones)
3. Decreased peripheral utilization of glucose
Glucocorticoids thus, exert an anti – insulin effect which leads to hyperglycaemia.
When blood glucose increases by 50% or more above normal, the condition is called adrenal diabetes.
EFFECT ON FAT METABOLISM
1. Lipolytic effect of epinephrine & GH – causes fatty acid mobilization from adipose tissue
increasing free fatty acids in plasma
2. Lipogenic effect – varies in different regions of the body In states of cortisol excess,
redistribution of fats in the body occurs (truncal obesity and buffalo hump in Cushing’s
syndrome) and fat deposition reflects increased food intake rather than change in rate of lipid
metabolism
EFFECT ON WATER AND MINERAL METABOLISM
1. Retention of Na+ and water
Mild mineralocorticoid activity causes retention of Na+& excretion of K+
Increases aldosterone secretion by increasing synthesis of angiotensinogen in liver leading to Na+retention
2. Promotes diuresis by increasing inactivation of ADH in liver and antagonizing action of ADH at the level
of distal tubules of kidney
Mention the major manifestations and their physiological basis
Truncal or centripetal obesity – occurs due to redistribution of body fat from extremities ( which is in the
abdominal wall,back, and face ) producing following clinical features:
Buffalo hump due to collection of fat at upper back
Moon face due to fat collection on the face
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  1. A 33 year old woman complained of weight gain, round face, thinning of her limbs, and increased bruising of skin with discoloration on her prominent abdomen. Answer the following questions based on your knowledge in physiology: ( 1+ 4+ 5)  What is the probable endocrinological disorder? Cushing’s syndrome due to cortisol excess  Explain the metabolic actions of the hormone involved Metabolic actions of cortisol EFFECT ON PROTEIN METABOLISM
  2. Protein break down / proteolysis in skeletal muscle and protein matrix of bone causes increase in plasma amino acids (catabolic effect)
  3. Muscle protein is mobilized for gluconeogenesis EFFECT ON CARBOHYDRATE METABOLISM
  4. Increased glucose formation in liver / hepatic gluconeogenesis
  5. Increased secretion of glucagon, epinephrine (glycogenolytic hormones)
  6. Decreased peripheral utilization of glucose Glucocorticoids thus, exert an anti – insulin effect which leads to hyperglycaemia. When blood glucose increases by 50% or more above normal, the condition is called adrenal diabetes. EFFECT ON FAT METABOLISM
    1. Lipolytic effect of epinephrine & GH – causes fatty acid mobilization from adipose tissue increasing free fatty acids in plasma
    2. Lipogenic effect – varies in different regions of the body In states of cortisol excess, redistribution of fats in the body occurs (truncal obesity and buffalo hump in Cushing’s syndrome) and fat deposition reflects increased food intake rather than change in rate of lipid metabolism EFFECT ON WATER AND MINERAL METABOLISM
    3. Retention of Na+^ and water Mild mineralocorticoid activity causes retention of Na+& excretion of K+ Increases aldosterone secretion by increasing synthesis of angiotensinogen in liver leading to Na+retention
    4. Promotes diuresis by increasing inactivation of ADH in liver and antagonizing action of ADH at the level of distal tubules of kidney  Mention the major manifestations and their physiological basis Truncal or centripetal obesity – occurs due to redistribution of body fat from extremities ( which is in the abdominal wall,back, and face ) producing following clinical features: Buffalo hump due to collection of fat at upper back Moon face due to fat collection on the face

Purple striae or cutaneous abdominal striae or stretch marks – skin and subcutaneous tissue becomes thin due to protein catabolism. The stretching of abdominal skin due t excessive subcutaneous fat deposition causes rupture of subdermal tissues producing reddish purple striae. Muscle weakness and backache due to protein catabolism Sodium and water retention may cause weighjt gain, oedema, and hypertension Hyperglycemia occurs due to gluconeogenesis and inhibition of peripheral utilization of glucose. It may lead to glycosuria and adrenal diabetes. Hirsutism and menstrual irregularity may occur due to adrenal androgens Susceptibility to osteoporosis and bone fracture is increased due to protein depletion and bone resorption Susceptibility to infection is increased due to immunosuppression Psychological and personality changes may occur due to CNS effects of glucocorticoids Blackening of skin may occur due to pigmentation caused by MSH like effects of excessive ACTH 2.Describe the regulation of secretion of cortisol and its physiological role. ( 5 marks) Regulation of cortisol secretion Circadian rhythm of glucocorticoid secretion The secretory rates of Corticotropin releasing factor (CRF), Adrenocorticotropic hormone (ACTH) and cortisol are high in the early morning but low in the late evening. This results from a 24 hour cyclic alteration in signals from the hypothalamus. When a person changes daily sleeping habits, the cycle changes correspondingly. Fig 91-10 Guyton Secretion of cortisol is controlled almost entirely by ACTH secreted by anterior pituitary gland. ACTH secretion is further controlled by corticotrophin releasing factor (CRF) from the hypothalamus. Fig 91-9 Guyton Stress stimuli , the most potent stimuli, activate the hypothalamo-pituitary-adrenal axis to cause rapid release of cortisol. Cortisol then initiates a series of metabolic effects directed towards relieving the damaging nature of the stressful state. Other stimuli such as circadian rhythm and emotions also stimulate the hypothalamo-pituitary-adrenal axis. The hypothalamo-pituitary-adrenal axis regulates glucocorticoid secretion by exerting its effect through  CRF  ACTH  Negative feedback of glucocorticoid (cortisol) secretion Control of CRF secretion

  1. Stressful stimuli act on hypothalamus to increase CRH secretion which ultimately increases cortisol secretion.
  2. Circadian rhythm
  3. ACTH acts on hypothalamus by short loop negative feedback mechanism to reduce secretion of CRH.
  4. Glucocorticoids exert a long loop negative feedback effect on CRF secretion Control of ACTH secretion
  5. Hypothalamic control on ACTH secretion is by

Glucocorticoids thus, exert an anti – insulin effect which leads to hyperglycaemia. When blood glucose increases by 50% or more above normal, the condition is called adrenal diabetes. EFFECT ON FAT METABOLISM

  1. Lipolytic effect of epinephrine & GH – causes fatty acid mobilization from adipose tissue increasing free fatty acids in plasma
  2. Lipogenic effect – varies in different regions of the body In states of cortisol excess, redistribution of fats in the body occurs (truncal obesity and buffalo hump in Cushing’s syndrome) and fat deposition reflects increased food intake rather than change in rate of lipid metabolism EFFECT ON WATER AND MINERAL METABOLISM
  3. Retention of Na+^ and water Mild mineralocorticoid activity causes retention of Na+& excretion of K+ Increases aldosterone secretion by increasing synthesis of angiotensinogen in liver leading to Na+retention
  4. Promotes diuresis by increasing inactivation of ADH in liver and antagonizing action of ADH at the level of distal tubules of kidney II Physiological action on various organs & systems EFFECT ON MUSCLE  Increases contractility & work performance EFFECT ON CONNECTIVE TISSUE  Decreased collagen synthesis leads to thinning of skin, thinning of wall of capillaries EFFECT ON BONE  Increased bone resorption  Demineralization of bone  Decreases collagen synthesis  Decreases calcium absorption from GIT EFFECT ON VASCULATURE Cortisol is essential for maintaining normal blood pressure by
  5. Sustaining myocardial performance
  6. Enhancing the vasopressor effect
  7. Decreasing production of vasodilator prostaglandin
  8. Maintaining normal blood volume EFFECT ON KIDNEY

 Increases GFR by increasing glomerular plasma flow  Rapid excretion of water load  Increase in calcium and phosphate excretion EFFECT ON GASTROINTESTINAL TRACT  Increases gastric acid secretion and decreases proliferation of gastric mucosal cells. EFFECT ON CNS In absence of cortisol

  1. Mood changes in the form of irritability, apprehension and inability to concentrate In excess of cortisol
  2. Increased brain excitability and insomnia
  3. Decreased memory function III Anti-inflammatory, Anti-allergic effect & Anti-immunity effect Cortisol blocks the early stages of inflammation and if it has already begun, cortisol causes rapid resolution of inflammation and increased rapidity of healing. Cortisol exerts its anti-allergic effect by reducing the number of circulating basophils and by protecting against release of secretory products of granulocytes, mast cells and macrophages such as serotonin, histamine and hydrolases. Cortisol inhibits both cellular and humoural immunity by decreasing proliferation of T cells and B cells. EFFECT ON BLOOD CELLS  Eosinopenia, Lymphopenia, Basopenia  Neutrophilia  Polycythemia IV Role of glucocorticoids in fetal life  Maturation of CNS, retina, and skin  Maturation of lungs
  4. Describe the mechanism of action and regulation of aldosterone secretion. ( 5 marks) Aldosterone is a mineralocorticoid hormone Mechanism of action of aldosterone The cellular sequence of events that leads to increased sodium reabsorption is as follows. Genomic actions of aldosterone Aldosterone diffuses readily to the interior of the tubular epithelial cells because of lipid solubility in the cellular membranes ↓ In the cytoplasm of tubular cells, Aldosterone combines with a highly specific cytoplasmic mineralocorticoid receptor (MR)

4.Adrenogenital syndrome (3 marks)

When androgen precursors are secreted in large amounts for example, in tumour of zona reticularis of adrenal cortex, certain abnormal features are produced. These constitute adrenogenital syndrome. Adrenal androgens exert masculinizing effect, which become prominent when secreted in excess amounts. Adrenal androgens are converted to oestrogen in peripheral tissues and serve as the source of oestrogen in males and postmenopausal females. Characteristic features of adrenogential syndrome are:

  1. In prepubertal males, excessive androgens produce precocious pseudopuberty (develop secondary sexual characteristics early).
  2. In adult males, oestrogen producing cells may produce female like secondary sexual characters such as enlargement of breasts (gynaecomastia), atrophy of testes, loss of libido and feminine body.
  3. In females, development of male secondary sexual characteristics such as beard, muscular body, breaking of voice, male pattern of hair growth, enlargement of clitoris and amenorrhoea.

Diagnosis – Excretion of 17 – ketosteroids (metabolic end product of androgens) in the urine is 10- times normal Treatment –Treatment with relatively small doses of cortisone is effective in suppressing the excessive secretion of adrenal androgen without causing abnormal metabolic or toxic effects. Genital reconstructive surgery

5.Physiological basis of pigmentation in Addison’s disease (2 marks)

Adrenocorticotrophic hormone (ACTH) and Melanocyte Stimulating Hormone (MSH) are derived from

the same precursor molecule, pro-opiomelanocortin (POMC). MSH normally stimulates melanocytes to produce melanin. In Addison’s disease, deficiency of cortisol leads to increased secretion of ACTH by negative feedback. Stimulant effect of excess ACTH and binding of ACTH to melanin receptors on the melanocytes (MSH like activity) to produce melanin leads to hyperpigmentation 6.physiological basis of permissive action of glucocorticoids ( 2 marks) Glucocorticoids are essential for some physiological actions of other hormones to take place. This is called as permissive action of cortisol ( as cortisol allows the specific actions of these hormones to occur , though it does not produce these effects by itself). They are Vaso pressor and broncho dilator effects of catecholamines Calorigenic effects of glucagon and catecholamines Lipolytic effects of catecholamines