Here is a compilation of essays on ‘Hormonal Disorders’ for class 9, 10, 11 and 12. Find paragraphs, long and short essays on ‘Hormonal Disorders’ especially written for school and college students.
Contents
- Essay on Hormonal Disorders
- Essay # 1. Hormonal Disorders of Pancreas:
- Essay # 2. Hormonal Disorders of Thyroid:
- Essay # 3. Hormonal Disorders of Parathyroid:
- Essay # 4. Hormonal Disorders of Adrenal Cortical:
- Essay # 5. Hormonal Disorders of Gastro-Intestinal:
- Essay # 6. Hormonal Disorders of Pituitary Gland:
- Essay # 7. Hormonal Disorders of Sexual Development:
Essay on Hormonal Disorders
Essay Contents:
- Essay on the Hormonal Disorders of Pancreas
- Essay on the Hormonal Disorders of Thyroid
- Essay on the Hormonal Disorders of Parathyroid
- Essay on the Hormonal Disorders of Adrenal Cortical
- Essay on the Hormonal Disorders of Gastro-Intestine
- Essay on the Hormonal Disorders of Pituitary Gland
- Essay on the Hormonal Disorders of Sexual Development
Essay # 1. Hormonal Disorders of Pancreas:
The endocrine pancreas consisting of the Islets of Langerhans secretes two hormones namely, glucagon and insulin.
Glucagon increases blood glucose level due to:
(i) Glycogenolysis in the liver,
(ii) Inhibition of glycogen sysnthesis in the liver,
(iii) Gluconeogenesis in the liver,
(iv) Lipolysis in adipose tissue,
(v) Stimulation of insulin release from beta cells, and
(vi) Stimulation of catecholamine release.
Stress Causes Hyperglucagonemia:
The release of pancreatic glucagon is mediated by the sympathetic innervation to the islets, but the alpha cells are capable of responding directly to certain stresses, such as intense hypoxia. Glucagon secreting tumors of the pancreas (glucagonomas) also produce excess of glucagons.
The patients are mildly diabetic. α-cells are comparatively insensitive to glucose in diabetes mellitus. The plasma glucagons level is within the normal range even though the level of glucose is well above the normal level. The reduced sensitivity of the α□cells to glucose and the increased response to leucine are restored to normal by injecting small doses of insulin.
Effects of Insulin Deficiency:
Deficiency of insulin results in Diabetes mellitus. The severity is dependent on the extent of the deficiency in insulin release. Diabetes mellitus was first described about 1500 B.C. in Egypt. Mellitus in latin means honey, referring to the high sugar content of the urine in diabetics.
The word diabetes is derived from the Greek word, meaning siphon referring to the large volume of water excreted in this disease. In England, for centuries the disease is known as “pissing evil” indicating the large volume of urine passed by people suffering from diabetes.
Causes of Diabetes Mellitus:
Diabetes is generally considered due to the deficiency of insulin. However, there are many reasons for the occurrence of diabetes and the disease should be considered as a heterogenous group of diseases. The following table shows the different types of diabetes. In patients suffering from Insulin dependent Diabetes Mellitus, insulin-secreting β-cells in the islets of Langerhans decrease markedly due to the development of islet cell-surface antibodies.
Juvenile Onset Diabetes develops in youth. The symptoms appear suddenly and the disease requires replacement therapy. This type of diabetes may also be caused by a virus. Initially one virus is involved but later a number of infections such as mumps and rubella cause the damage.
Noninsulin dependent diabetes mellitus is the more common form of diabetes. The majority of people who suffer from Maturity Onset Diabetes have above normal levels of insulin, but their tissues do not respond to the hormone. This condition known as insulin resistance may be caused by a number of factors.
Based on the mechanism of action of insulin, resistance to insulin can be divided into three types:
(i) Pre-receptor,
(ii) Receptor and
(iii) Post-receptor insulin resistance.
Decrease in the number of receptors is the cause of type A insulin resistance. Circulating antibodies to some portion of the insulin receptors results in impaired binding of insulin to the receptors in the target cells, this type of resistance to insulin is Type B. In majority of cases, the resistance to insulin is post-receptor type due to the complexity of the intracellular pathways of insulin action.
Non-Insulin Dependent Diabetes Mellitus (NIDDM) occurs in middle aged and old persons. NIDDM patients in contrast to IDDM patients retain the ability to synthesize, store and release insulin to all insulin secretagogues except venous glucose. Insulin secretion by the β-cells is dependent upon the recognition of the gluose level in the extracellular fluid.
The high -Km glucose transporter GLUT2 and glucose phosphorylating enzyme, glucokinase are implicated in coupling insulin secretion to extracellular glucose levels. Mutations in the gene coding for this enzyme are a common cause of an autosomal dominant form of NIDDM that usually occurs in the childhood.
Patients who suffer from insulin resistance and normally functioning pancreatic islets have high levels of insulin in the circulating blood. Some patients treated with exogenous insulin develop antibodies to insulin, and these antibodies inhibit access of active insulin to the receptors of the hormone.
Insulin resistance can also develop in individuals who produce abnormal type of insulin that has reduced affinity to insulin receptors. In familial hyperproinsulinemia, patients possess high circulating levels of a partially cleaved proinsulin.
This abnormality is due to a mutation of arginine 32 at the cleavage site connecting the B chain to the connecting (C) peptide. Another defect involves a mutation at the cleavage site connecting the C peptide to A chain.
Islet Cell Tumors:
The neoplasms of the islets are three types:
i. Insulinoma,
ii. Glucagonoma and
iii. Somatostatinoma.
Malignancies of the pancreatic islets have profound effects on protein, carbohydrate and lipid metabolism. Benign and malignant tumors of insulin secreting type release insulin without any control leading to hypoglycemia. In severe conditions, it leads to convulsions and death, if the tumors are not surgically operated.
Symptoms of Diabetes:
a. Hyperglycemia:
This is a condition in which blood glucose level increases above the normal level of 120 mg per 100 ml blood. Above 180 mg. the renal threshold for glucose is exceeded and glucose is excreted in the urine. Continuous hyperglycemic condition occurs when peripheral tissues do not utilize glucose and liver releases excess of glucose. Decrease in the functioning of anterior pituitary, and adrenal cortex leads to hyperglycemia.
b. Glycosuria:
In glycosuria the blood sugar level exceeds the renal threshold of 180 mg/ 100 ml blood. In such a condition, the renal tubules fail to reabsorb the entire quantity of glucose filtered. Consequently some glucose that remains unabsorbed is excreted along with urine and therefore sugar appears in the urine.
The symptoms of diabetes are hyperglycemia, glycosuria, ketosis, acidosis, polyurea, polydispia (increased thirst), and weight loss in spite of polyphagia (increased hunger). Hyperglycemia may be regarded as the primary defect and results both from an increased production of glucose in the liver and failure of peripheral tissues, such as muscle and adipose tissue, to take up glucose although the extra cellular fluid is rich in glucose.
In the absence of insulin, the rate of glycogenolysis in the liver is enhanced and glycogenesis is inhibited. Gluconeogenesis is favored. The increased breakdown of fats leads to high levels of free fatty acids in the plasma, which further inhibit the uptake of glucose by skeletal muscle and are metabolized to ketone bodies such as acetone, β-hydroxybutyric acid and aceto-acetic acid in the liver.
The accumulation of these strong acids in the plasma leads to severe metabolic acidosis and the elimination of acetone in the lungs provides a useful diagnostic indication as it can readily be detected in the breath of ketotic diabetics.
In skeletal muscle net protein catabolism becomes pronounced and the amino acids produced provide further substrate for gluconeogenesis in the liver. The conversion of proteins through amino acids into glucose, which cannot be metabolized and excreted in the urine leads to wasting of muscles and loss of weight in the diabetic patient.
When the concentration of glucose in the plasma increases above the renal threshold of 180 mg/100 ml, the quantity of glucose filtered in the glomerulus exceeds the capacity of the renal tubules to reabsorb and glucose appears in the urine.
Glucose in the tubular fluid that is not absorbed exerts a powerful osmotic effect and a profuse diuresis (polyurea) and associated thirst and drinking (polydispia) are the most characteristic symptoms of diabetes.
Net loss of water and electrolytes in the kidney leads to pronounced dehydration and this is frequently exacerbated by further loss of fluid due to vomiting. Severe dehydration reduces blood volume leading to circulatory failure and renal vasoconstriction. In the last stages, anuria leads to uraemia, coma and death.
The above-mentioned symptoms are acute in the absence of insulin. The long-term effects of lack of insulin are less efficient wound healing and gangrene. Coronary, retinal, cerebral and renal arteries and arterioles are prone to atherosclerotic changes and the basement membranes of the capillaries of diabetics are thicker than in normal people.
Action of Insulin in Diabetes:
Administration of insulin reverses the changes produced due to the deficiency of insulin and the condition is restored to normal.
The changes which occur are:
(i) Liver glycogenesis is stimulated consequently.
(ii) The blood sugar level becomes normal,
(iii) Gluconeogenesis is regulated and excessive conversion of amino acids into glucose is inhibited,
(iv) Rate of protein synthesis is promoted and muscular wasting is checked,
(v) Increased conversion of glucose into fat takes place. So that the fatty acids are not metabolized,
(vi) Ketone bodies are not formed and ketosis is stopped, and
(vii) Glucose and ketone bodies are not excreted through urine. The level of potassium and phosphate in the blood is reduced.
Oral Anti-Diabetic Agents:
In place of insulin, a number of oral hypoglycemic drugs are recently used for the treatment of diabetes. These chemicals include sulfonamides, glybenzcyclamide, tolbutamide and chlorpropamide. Sulfonamides stimulate the secretion of insulin. Therefore, it is necessary that the pancreatic islets should contain functional β-cells.
These substances potentiate the activity, of externally administered insulin by inhibiting the activity of the enzyme insulinase, which breaks down insulin. α□ cells are destroyed by the administration of sufonylurea and biguanides so that the production of glucagon by these cells is inhibited.
Essay # 2. Hormonal Disorders
of Thyroid:
Causes of Thyroid Deficiency:
Thyroid hormones exert influence on a number of physiological processes and are required for the activity of numerous other hormones. Therefore, any abnormality in the functioning of the thyroid gland leads to gross alterations in the physiological functioning of an individual. Reduced production of thyroid hormones is referred to as hypothyroidism while overproduction of thyroid hormones is hyperthyroidism. These two abnormalities can occur at birth (Congenital) or later in life.
Hypothyroidism is the term used to describe the condition where insufficient thyroid hormone is secreted. Thyroid tissue may be totally absent in the infant. In adult it results if severe thyroid damage is caused surgically, by radioiodine or by X-ray therapy. Thyroid function can also be reduced by antithyroid drugs, auto-immune disease or chronic deficiency of iodine.
Any defect at the level of pituitary or hypothalamus can also result in hyper or hypothyroidism due to increased or decreased production of TSH. Such conditions are known as secondary and tertiary hyper or hypothyroidism.
Abnormalities in the functioning of the thyroid gland may be genetic (familial) and involve failure in growth or normal function of the thyroid gland. Genetic defects can also lead to synthesis of abnormal hormones resulting in defects in iodine trapping or organification, defective thyroglobin formation and secretion.
Causes of Excessive Thyroid Activity:
Abnormally high thyroid secretion is known as hyperthyroidism or thyrotoxicosis, which is caused due to primary thyroid over activity. Enlargement of the thyroid associated with hyperfunction (toxic goiter) produces a wide range of symptoms. Grave’s disease is the common disorder in which goiter is associated with thyrotoxicosis and exophthalmia. The following (table 2) shows the major physiological changes in hyper and hypothyroidism.
Symptoms of Hypothyroidism:
Hypothyroidism produces two types of disorders. In infants and young the disease is known as Cretenism and in adults reduced activity of the thyroid causes a disorder known as Myxoedema.
1. Cretenism:
Immediately after birth, symptoms of cretinism do not appear because the hormone is supplied by the mother and later upto six months, the infant obtains the hormone through the mother’s milk. The different stages of child development such as holding up of head by three months, closure of anterior fontanelle by five months, crawling, sitting and teeth development by six to seven months, standing, walking and talking by one to one and half year are all delayed.
a. Dentition and Skeleton:
Teeth are deformed, growth is stunted and fingers are short and club-like in appearance.
b. Skin and Vitamins:
Skin of cretins is characterized by the rough texture, thickness and formation of wrinkles. Hair is scarce. Skin becomes yellowish in color due to accumulation carotene.
c. Face and Appearance:
The facial features of a cretin are characterized by the idiotic look, bloated wide face with wide nostrils, broad nose and with depressed bridge. Lips are thick and parted. Tongue is large and protrudes out of mouth and saliva continuously oozes. Abdomen is characterized by swollen pot belly and the umbilicus protruding.
d. Digestive System and Metabolism:
Cretins have reduced appetite. Movements of the alimentary canal are reduced leading often to constipation. As compared to. normal children the Basal Metabolic Rate of cretins is reduced by 25 to 40%. Consequently, the body temperature is low. Fat is irregularly distributed over the clavicles.
e. Mental Growth:
Cretins are frequently deaf and dumb. Their mental faculties are not well developed and suffer from various degrees of mental retardation and idiocy.
f. Blood:
The blood sugar level of cretins is low but they have high sugar tolerance. The serum cholesterol level is high but iodine level is low.
g. Urine:
Due to reduced protein metabolism, excretion of creatinine in the urine is reduced from the normal value of 0.6 to 7.8 mg per day to 0 to 3.8 mg.
h. Immunity:
Immunity of children suffering from creatinism is much reduced. Such children suffer frequently from cold and infections. Their resistance to toxins is also very much reduced.
i. Reproductive System:
Cretins are sexually retarded. The sex glands, reproductive organs and secondary sexual characters are all underdeveloped.
Various congenital abnormalities of the hypothalamo-pituitary-thyroid axis that cause goiter can cause congenital hypothyroidism with cretinism. Thyroxin crosses the placenta, and unless the mother is hypothyroid, growth and development are normal until birth. However, treatment must be started soon after birth if mental retardation is to be prevented.
When the mother is also hypothyroid, as in the case of iodine deficiency, the mental deficiency is more severe, and less responsive to treatment after birth. Increased use of iodized salt has now reduced the incidence of maternal iodine deficiency. However, it is common in many parts of the world, and it has been estimated that about 20 million people in the world now have various degrees of brain damage caused by iodine deficiency in utero.
2. Myxoedema or Gulls’s Disease:
Hypothyroidism in the adult is referred to as myxoedema (Greek, myxa-mucus and oidema-swelling) because of the characteristic mucinous protein deposit in the cutaneous tissues. The disease is eight times more frequent in occurrence in females than in males.
a. Appearance:
Individuals suffering from this disorder have swollen face and puffy, bloated appearance in the body due to the accumulation of a muco-protein substance forming the myxomatous tissue. Other symptoms of the disease are loss of hair from the axillae, pubis, head and eyebrows. Cheeks look like parchment. Tongue and larynx are swollen causing a hoarse and slow-slurring speech, characteristic of this disease. Fat deposition over the body is irregular.
b. Metabolism and Digestive System:
The metabolic rate in persons suffering from this disease is lowered by 40% leading to low body temperature and intolerance to cold. Body weight increases and appetite is reduced. Movement of the digestive tract are reduced leading to constipation.
c. Blood Vascular System:
Iodine content of the blood and glucose level are reduced and tolerance to glucose level is increased. Cholesterol level is very high above 300 mg /100mg. Patients are anemic and plasma albumin level is high. Respiratory rate is reduced.
The heart rate decreases followed by stroke volume, the cardiac output and blood pressure. Circulation time is increased.
d. Urine:
Due to reduced metabolism of proteins, nitrogen excretion is reduced.
e. Behavior:
Mental faculties are reduced. The patient is lethargic, dull, apathetic md sleepy. Suffers’ from loss of memory. Reflexes are very slow.
f. Reproductive System:
Reproductive glands, organs and secondary sexual characters are all degenerated. Persons are impotent. Females suffer from amenorrhea.
Causes of Hyporthyroidism:
(1) Thyroid stimulating hormone is a glycoprotein hormone consisting of a common alpha and specific beta chains. The alpha chain is common to other glycoprotein hormones. Several clinical cases show congenital, isolated TSH deficiencies associated with cretinism, displaying severe mental and growth retardation with the failure to go through puberty. In these cases, the TSH has the alpha chain but the beta chain is lacking, therefore the TSH is nonfunctional resulting in deficiency symptoms.
(2) TSH controls the thyroid function by binding to its receptor at the basolateral membrane of the thyroid follicular cells. Mutations in the gene encoding the TSH receptor leads to hypothyroidism.
(3) In cretins non development of the thyroid gland is responsible for decreased thyroid function. This condition may be familial in origin and may also occur in maternal autoimmune thyroiditis.
(4) Congenital goiter may also be associated with thyroid dyshormonogenesis due to hereditary defects in hormone synthesis or metabolism.
(5) Genetic failure in the development of the thyroid hormone receptors in the target tissues results in hypothyroidism.
(6) Most or all the tissues of an individual may become resistant to the action of thyroid hormone leading to hypothyroidism.
(7) Failure of the conversion of T4 into T3 in peripheral tissues, which is the more active physiologically more relevant thyroid hormone, can lead to hypothyroidism.
(8) Defective synthesis of the thyroglobulin and secretion can lead to hypothyroidism.
Goiter:
Goiter is the enlargement or swelling of the thyroid gland. The enlargement or overgrowth of the gland is not due to inflammation or malignancy. In simple or compensatory type of goiter, the gland becomes enlarged to produce normal level of hormones due to deficiency of iodine.
Simple type of goiter can be differentiated into three types:
1. Colloid Goiter:
Colloid goiter is prevalent in areas where the drinking water is deficient in iodine. It is endemic in nature and benign. In order to produce normal levels of the hormone, the gland becomes hypertrophied. The alveoli are distended with colloid. Iodinated salt intake is the preventive measure for the incidence of this disease.
2. Diffuse Parenchymatous Goiter:
The columnar epithelial cells lining the follicles hypertrophy and multiply in number due to which the lumen of the follicles becomes obliterated.
3. Nodular Goiter:
This type is characterized by the appearance of nodular swelling in some part of the gland.
Causes:
(i) The main cause for goiter is the deficiency of iodine in the body,
(ii) Goiter can also be produced from the ingestion of chemicals, which interfere with thyroid function, such as antithyroid drugs, like methylthiouracil, propylthiouracil, and carbimazole.
(iii) The presence of goitrogenic substances in the food, such as cabbage and turnip, which contain a chemical substance known as goitrin.
(iv) Faecal contamination of drinking water,
(v) Trypanosome infection, and
(vi) Simple goiter may be due to the increased requirement of thyroid hormone during puberty, pregnancy and lactation. It may also develop as a result of congenital deficiencies of thyroid enzyme systems.
4. Toxic Goiter:
When swelling or enlargement of the thyroid gland results in excess secretion of thyroid hormones, the condition is known as toxic goiter. The follicular epithelial cells are hypertrophied and hyperplastic. Excessive hormone production leads to hyperthyroidism and Grave’s disease.
5. Hokkaido Goiter:
During the synthesis of thyroid hormones, inorganic iron is taken up from the blood and converted into organic form by reacting with the amino acid tyrosine. High concentration of iodine inhibits organification of iodine and causes hypothyroidism.
Hyperthyroidism:
Hyperthyroidism or thyrotoxicosis are terms used for the condition when the thyroid secretion is abnormally high due to primary thyroid overactivity. Enlargement of the thyroid gland together with its hyperfunction (toxic goiter) can produce a wide range of symptoms. Grave’s disease is the commonest in which goiter is associated with thyrotoxicosis and exophthalmos.
The eyeball is displaced by the growth of a small pad of fat in the tissue behind the eyeball. In this disease, thyroid hormone secretion is increased by 10 times above the normal level. Thyroid gland becomes enlarged leading to nodular or diffuse type of goiter. Thus the symptoms of Grave’s disease are hyperthyroidism, exophthalmos and goiter.
In hyperthyroid activity, the most important symptoms are weight loss, increased metabolic rate, tremors, sensitivity to adrenaline, and increased blood supply to the gland. Due to increased metabolic rate more heat is generated due to which the skin becomes hot and sweaty. Heartbeats are faster even in sleep. The person becomes tense, restless and sleepless. In thyrotoxicosis, due to mental stimulation, the patient becomes very nervous, irritable and restless.
Grave’s Disease:
In Grave’s disease the thyroid gland is diffusedly enlarged and there is a protrusion of the eyeball called exophthalmos due to swelling of the extraocular muscles and connective tissue within the rigid bony walls of the orbit. This pushes the eyeball forward.
Graves’s disease is an autoimmune disease in which circulating antibodies formed against TSH receptor activate the receptor, making the gland hyperactive. These antibolies are called as TSH-R (stim) Ab for TSH receptor stimulating antibolies.
Other symptoms of the disease include:
i. Body Weight:
Due to increased metabolic rate, most of the metabolites are used up and the body weight is drastically reduced.
ii. Skin:
Skin becomes soft and moist due to sweating. There is increased blood flow in the skin due to vasodilation to enable heat loss.
iii. Skeleton:
The patient suffers from osteoporosis due to increased loss of calcium and phosphate from bones.
iv. Mental Condition:
A person suffering from Grave’s disease is highly irritable, restless, tense and sleepless. He is sharp and emotional.
v. Blood Vascular System:
There is increase in the blood sugar level leading to glycosuria. Sugar tolerance is lowered. Serum cholesterol level increases considerably. There is a significant increase in the heart rate often reaching upto 140 per minute. This leads to increased cardiac output. Heart is easily irritable. Blood pressure is increased and there is fall in circulation time.
Immunoglobulins and Thyroid Stimulation:
Adams and Purves (1956) found that the blood of patients suffering from Grave’s disease contained normal levels of TSH. Hyperactivity of the thyroid was due to the presence of another factor with a much more protracted thyroid stimulating action.
This substance was called as Long Acting Thyroid Stimulator (LATS). LATS is one of a group of IgG immunoglobulins, which affect the thyroid termed Thyroid Stimulating Immunoglobulins (TSI) or Thyroid Stimulating Antibodies (TSAb).
These are produced in response to undefined stimuli by thymus dependent lymphocytes in certain individuals with a genetic predisposition and may act as antibodies against thyroid antigens. The actions of LATS on the thyroid are similar to those of TSH in that both increase adenyl cyclase activity. While the effects of TSH are rapid and transient, the actions of LATS are progressive and prolonged.
Thyroid hormones suppress TSH production by negative feedback at the pituitary level, but do not effect LATS production. Therefore, in toxic goiter, LATS is elevated while TSH levels are low. Antibodies can also be formed against thyroglobulin (TG Ab) and thyroid peroxidase (P Ab). TG Ab and P Ab cause damage to the thyroid gland which may be severe enough to cause hypothyroidism.
Antithyroid Drugs:
Drugs that inhibit thyroid function act either by interfering with the iodide trapping mechanism or by blocking the organic binding of iodine. The thiocarbamides are a group of substances related to thiourea, inhibit the iodination of monoiodotyrosine and block the coupling reaction.
The two clinically used drugs are propylthiouracil and methimazole. These two drugs may ameliorate thyrotoxicosis by suppressing the immune system and thereby depressing the formation of TSH-R block Ab.
They may also inhibit the biosynthesis or alter the structure of thyroglobulin. Thyrotoxicosis can also be treated by ablation of the hyperactive gland by surgery or radio-iodine. Surgery is more effective and rapid but it leads to hypothyroidism. Similar is the condition with radio-iodine therapy. Thyrotoxicosis can be treated with beta adrenergic blocking agent like propranolol before antithyroid drugs or surgery.
Essay # 3. Hormonal Disorders of Parathyroid:
i. Hypoparathyroidism:
Parathormone is essential for life. Removal of the parathyroid glands gradually leads to decrease in plasma calcium level, and if it is not checked, results in a progressive increase in neuromuscular excitability leading to tetany and death.
The acute consequences of removal of parathyroid hormone are most commonly found in patients following either accidental removal of the parathyroids or damage to the blood supply during operations on the neck, specially thyroidectomy. In such conditions tetany occurs within a few days after the operation and is sometimes associated with mental symptoms such as psychosis.
These patients are treated to restore blood calcium levels to the normal level by slow intravenous infusion of calcium gluconate. Later treatment involves the promotion of intestinal absorption of calcium by administration of vitamin D3 and by oral supplementation of calcium.
Hypoparathyroid patients, display hypocalcemia as their major clinical symptom. This hypocalcemia is caused partly by the deficience of dihydroxy chole calciferol (Vitamin D3). Restoration of normal calcium level can be attained by treatment with vitamin D3 or related metabolites.
Tetany is produced in man and animals by the removal of the parathyroid glands two or three days after the operation or hypoparathyroidism. Tetany is more severe in young persons than older persons. It is also more severe in pregnancy, lactation and with high protein diet.
The symptoms are as follows:
a. Increased Neuromuscular Irritability:
Peripheral nerves become hyperexcitable due to accumulation of fluid around the periferal nerves. Spinal cord also becomes hyperexcitable. Excitation of the midbrain where the respiratory center is located leads to spasm of the respiratory muscles and ultimately to asphixiation and death. Convulsions alternate with paralysis. In muscles creatine phosphate content is reduced and its resynthesis is slowed down.
b. Changes in blood and Heart:
Serum calcium level below 10 mg/100 ml and inorganic phosphate content increases above 5mg/ 100 ml reaching 8 mg or more. Blood clotting becomes slower and defective. Heart rate is increased.
c. Respiration:
Due to respiratory muscular spasms, respiration becomes rapid and noisy.
Other Symptoms:
There is increase in body temperature. The calcium and phosphate levels of urine become increased. Salivation is also increased.
i. Features of Tetany in Man:
Convulsions are the most serious complications of the hypoparathyroid condition. Latent tetany can be detected by the following signs.
ii. Trousseau’s Sign or Carpopedal Spasm:
This condition is due to the occlusion of arterial blood supply to the forearm.
iii. Chevostek’s Sign:
Tapping over the facial nerves near the styloid process results in contraction of the facial muscles.
ii. Hyperparathyroidism:
Oversecretion of parathormone results in abnormally high blood calcium levels associated with lowered blood phosphate levels. Renal calcium level is increased due to increased glomerular filtration of calcium and often results in the formation of kidney stones. Demineralization of bones of varying degrees of severity is often observed.
In man primary hyperparathyroidism is usually the result of the presence of a benign tumor (adenoma) of one or more of the parathyroid glands. Secondary hyperthyroidism often results from a peripheral defect of parathormone action.
The resulting hypocalcemia is the stimulus to enhanced parathyroid chief cell activity. Secondary hyperparathyroidism is a frequent consequence of chronic renal failure. Retention of phosphate depresses serum calcium levels and reduced synthesis of vitamin D3 by the kidney impairs intestinal calcium absorption. Excessive levels of parathormone are then secreted in response to lowered levels of calcium.
Symptoms:
General weakness in body, renal calculi, renal failure, formation of renal stones, loss of muscular tone, loss of appetite, nausea, vomiting, increased thirst, mental retardation, and polyurea due to the damage of the renal tubules are the general symptoms in hyperparathyroidism.
Blood calcium level is increased and phosphate level is reduced. Urine calcium level is increased. Demineralization of bones, especially mobilization of calcium and phosphorus leads to softening of the bones and cyst formation.
Essay # 4. Hormonal Disorders of Adrenal Cortical
:
Total loss of adrenal gland function occurs due to a congenital developmental defect or adrenal destruction during a particular disease state. The adrenal abnormality may be of primary origin and involve a failure of glucocorticoid or mineralocorticoid biosysnthesis due to a genetic defect related to an absence or faulty structure of a particular enzyme.
Overproduction of a particular corticosteroid may be due adrenocortical adenoma or carcinoma, resulting in excess Cortisol (Cushing’s syndrome) or in excess secretion of aldosterone (Conn’s syndrome). Hypo secretion of adrenal may be of secondary origin and involve a defect in mechanism in the control of Cortisol or aldosterone secretion.
Disorders of Cortisol Secretion:
a. Addison’s Disease:
The disease may be of primary origin and involve total destruction of the glands. Frequently it is due to bilateral tubercular destruction of the glands. Atrophy due to tuberculosis involves the cortex as well as the medulla. In idiopathic atrophy only the cortex is involved.
Clinical Features:
Persons suffering from this disease show muscular weakness due loss of sodium and chloride and defective glycogen formation. They are easily fatigued. In exposed areas of the skin, there is increased pigmentation due to melanin synthesis. Gastro-intestinal disturbances and vomiting occur. Blood pressure is lowered. Metabolic rate is reduced and persons show subnormal body temperature.
Potassium is retained, and sodium and chloride are excreted in large quantity leading to salt craving. Blood glucose level is low and persons suffer from weight loss. Due to loss of ions and water blood becomes concentrated. More water is lost from the capillaries and accumulates in the tissues leading to oedema. Patients show restlessness, lack of mental concentration and insomnia.
The increased integumental pigmentation, an important feature of the disease is due to the absence of Cortisol feedback to the hypothalamus. Excessive amounts of ACTH are secreted and ACTH is structurally similar to MSH.
Due to this ACTH acts on melanocytes and increases melanin production of the skin. In Addison’s disease of secondary and tertiary origin, the defect may reside at the level of pituitary or hypothalamus respectively.
b. Cushing’s Syndrome:
This disease was first described by Cushing in 1932. It refers to any clinical condition due to excessive and prolonged secretion and action of glucocorticoids. Primary Cushing’s syndrome is due to adrenocortical tumors. Cushing’s syndrome of secondary origin may derive from a pituitary tumor secreting an excess of ACTH or corticotroph hyperplasia.
Clinical Features:
Some of the symptoms of Cortisol excess are central obesity, hypertension, glucose intolerance, hirsutism (excessive hair growth), osteoporosis due to bone decalcification and loss of protein matrix, polyurea and polydipsia.
In addition to these symptoms in females masculinisation with development of male secondary sexual characters such as growth of beard, moustaches, under-development of mammary glands, musculature, etc., are often observed.
Wound healing is slow and poor. Minor injuries cause bruises. Wasting of muscles occurs in the limbs. In blood sodium level increases but potassium level decreases. Eosinopenia, lymphocytopenia and plycythaemia are noticed. Patients are mentally deranged. Males suffer from impotence, and atrophy of testes.
The hyperglycemia resulting from excess glucocorticoids leads to “steroid diabetes”, where prolonged elevated levels of glucose in time, may lead to pancreatic b-cell destruction and diabetes mellitus.
Central obesity is due to change in the fat distribution caused by the lipolytic action of ACTH and glucocorticoids on the normal fat depots. The redistribution of fat is not due to the direct actions of glucocorticoids but due to insulin that is secreted in response to increased hepatic glucose formation. Insulin exerts a lipogenic effect in other areas of the body, such as the face, upper back, and supraclavicular fat pads.
The catabolic actions of glucocorticoids on skeletal muscles cause thinning of the extremities. The resultant effects are the face becomes round or moon-face and back of the neck develops a buffalo hump. Fatty deposits are tender and painful. Skin shows purple striae over the abdomen and thighs due to the loss of protein matrix.
Loss of the protein matrix of bones causes osteoporosis, which may severely affect the spinal column. Polyurea and polydipsia are due to loss of large volume of water as a result of solvent drag during the process of excessive glucose excretion by the kidneys.
Disorders of Aldosterone Secretion:
i. Conn’s Syndrome:
Conn described this disease in 1955, which is caused due to hyper-secretion of aldosterone caused by adrenal adenoma, but in some cases due to adrenal carcinoma or hyperplasia. The main symptoms of this disease are hypertension, muscular weakness, retention of sodium and alkalosis. The over-secretion of aldosterone increases renal distal tubular excretion of potassium and hydrogen ions in exchange for reabsorbed sodium.
This leads to plasma hypernatremia and hypokalemia. Loss of hydrogen ions leads to metabolic alkalosis. The hypernatremia is usually associated with water retention, leading to severe hypertension. Muscle weakness is caused due to the depletion of potassium. Metabolic alkalosis decreases the level of calcium resulting in tetany. Secondary hyperaldosteronism is produced in congestive cardiac failure, cirrhosis of liver and other conditions.
The zona reticularis of the adrenal cortex produces sex hormones namely androgens. Overproduction of the androgens is associated with tumors in the adrenal cortex.
During fetal life, excessive production of androgens leads to pseudohermaphroditism or eunuchs. In such subjects both male and female sex characters are present but both are incompletely developed.
In childhood, excessive formation of sex hormones in females leads to precocious development of sexual characters. Menstruation starts early in life and breasts develop fully in size. Other changes include growth of hair on the pubis, axillae and voice. In male children, early puberty sets in resulting in the development of secondary sexual characters.
In adults, the main features are the reversal of sex characters. In females virilism or masculinity develops leading to change of female into male. Mammary glands reduce in size; moustaches and beard start to grow. The voice becomes husky and male like. The pubic hair grows in male pattern and clitoris enlarges to look like penis. Menstruation stops and uterus, vagina and ovaries degenerate.
Essay # 5. Hormonal Disorders of Gastro-Intestinal:
a. Pancreatic Cholera or Watery Diarrhea Syndrome:
This disorder is due to the development of tumors in the pancreas. Although these tumors secrete hormones that are normally produced in the pancreas, they also secrete Vasoactive Intestinal Peptide or gastrin. Vasoacitive Intestinal Peptide (VIP) stimulates intestinal water secretion, and tumors consisting of the VIP secreting cells are responsible for pancreatic cholera or the watery diarrhea syndrome.
b. Zollinger-Ellison Syndrome:
Patients with Zollinger-Ellison syndrome or Gastrinoma have high circulating gastrin levels (hypergastrinemia) of tumor origin. The over production of gastric acid results in severe duodenal ulcer formation. Zollinger-Ellison syndrome is of two types. Type I is due to hyperplasia of the antral G cells and Type II is due to gastrinoma of the pancreatic cells.
c. Achalasia:
Lower oesophageal sphincter prevents the regurgitation of stomach contents. The functioning of this structure is regulated by one or more gastrointestinal hormones. Gastrin and motilin control the contractions of the lower oesophageal sphincter, while vasoactive intestinal peptide inhibits the tone of the lower oesophageal sphincter.
Failure of the gastro-oesophageal junction to relax and open leads to obstruction of the passage of food into stomach and accumulation in the oesophagus. This condition is known as Achalasia. The smooth muscle of this junction is hypersensitive to normal circulating levels of gastrin, which is responsible for the prolonged contraction characteristic of this disorder. Gastro-oesophageal reflux is due to abnormal relaxation of the sphincter, and gastrin levels are low in some patients with this condition.
Therapeutic Uses of Gastro-Intestinal Hormones:
A number of gastrointestinal hormones are used in clinical practice. Gastrin is used for testing the potential for gastric acid secretion. Chlecystokinin is used for evaluation of gall bladder and exocrine pancreatic functions.
Secretin is used in the treatment of duodenal ulcer because it inhibits gastric acid secretion and stimulates pancreatic bicarbonate ion secretion. Secretin and glucagons stimulate tumor gastrin secretion and are used in the diagnosis of the Zollinger-Ellison syndrome.
Essay # 6. Hormonal Disorders of Pituitary Gland:
Adenohypophysis:
Dysfunction of the pituitary gland may involve undersecretion or oversecretion of one or more hormones. Hyposecretion of the pituitary gland may as a result of destruction of normal glandular cells within the pituitary by an expanding tumor, disruption of hypothalamo-hypophyseal vascular connections, or damage or disease of the hypothalamus.
Hypersecretion can be due to neoplasia or hypertrophy and hyperplasia, resulting from increased stimulation of the pituitary gland by hypothalamus. Lesions in the pituitary gland can effect the acidophil or basophils or chromophobes or the entire gland.
Tumors arising in a particular type of cell produce the signs of hyperactivity of not only those cells but also the signs of hyperactivity of adjacent cells due to irritation or symptoms of hypoactivity of the adjacent cells due to degeneration caused by pressure.
Any disorder produced in the anterior lobe of pituitary has adverse effects on other endocrine glands as this lobe produces tropic hormones which control the activities of all the other endocrine glands. Generally, hyperactivity leads to hypoactivity in due course of time due to exhaustion of the wells due to overactivity. The type of disorders produced due to the hypophyseal hormones are shown in Table 3.
Effects of Growth Hormone Excess:
Over-secretion of growth hormone occurs mostly as the result of acidophil tumors of the anterior pituitary. If excessive secretion of growth hormone occurs before the closure of the epiphyses, gigantism will result. In adults the disorder is acromegaly.
1. Gigantism:
This condition is rare. Excessive growth of normal pattern leads to extremely large individuals with normal bodily proportions. The growth period is prolonged due to delay in the closure of epiphyses. In gigantism skeleton is very tall between 6 to 8 feet.
2. Acromegaly:
Tumors of somatotrophs of the anterior pituitary secrete large amounts of growth hormone, leading to acromegaly in adults. Hypersecretion of growth hormone is accompanied by hyper-secretion of prolactin in 20% to 40% patients with acromegaly because they have tumors made up of somatomammotrophs. If growth hormone over-secretion occurs after the closure of epiphyses, the abnormal growth manifests itself at the extremities (acromegaly – large extremities).
The principal findings of acromegaly are enlargement of hands and feet to become spade like (acral parts) and protrusion of the lower jaw (Prognathism). Overgrowth of soft tissues leads to enlargement of organs such as spleen, pancreas, thyroid and kidneys, while other symptoms may be related to pressure exerted by the enlarged pituitary itself on the optic chiasma.
Overgrowth of malar, facial and frontal bones combines with prognathism to produce the coarse facial features called acromegalic facies. Body hair is increased in amount. The skeletal changes predispose to osteoarthritis. About 25% of patients have abnormal glucose tolerance tests, and 4% develop lactation without pregnancy.
Other important clinical features of acromegaly include bowing of the spinal cord, and increase in the antero-posterior length of the chest, presenting a Gorilla like appearance. The Tongue is enlarged. The subcutaneous tissues of the hands, feet, nose, lips and skin increase in amount and develop deep furrows. Metabolic rate is increased and patients tend to become diabetic.
Effects of Growth Hormone Deficiency:
Decreased secretion of growth hormone is most commonly noticed in cases of pituitary insufficiency or hypopituitarism and its effects are therefore difficult to separate from the associated failure of other pituitary hormones.
In childhood and adolescence deficiency of growth hormone produces profound impairment of growth.
Growth hormone plays only a small role in controlling growth in early childhood because pituitary dwarfs grow normally up to 2 to 4 years of age. Later until puberty growth hormone plays the main role in rate of growth of the long bones and hence increase in stature.
During this period persons deficient of growth hormone grow at less than half of the normal growth rate. Another reason for short stature can be growth hormone releasing hormone (GRH) deficiency.
Clinical Features:
In Lorain-Levy type of dwarfism, growth is stunted and the adult reaches a maximum size of 3 feet. Such dwarfs suffer from the non-development of sex organs and secondary sexual characters. Therefore an adult pituitary dwarf resembles a normal child. All the other features, including mental growth and metabolic rate are normal.
In Brissaud type of dwarfism, persons have short stature and stout due to excessive deposition of fat in the body. They have round and chubby face. However, they are lethargic and sleepy. Secondary sexual characters such as moustaches and beard do not grow and growth of hair over the body is also scarce.
In mixed type, the patients are short, fatty and hairless. They have large accessory nasal sinuses and prominent supraorbital ridges, and other features of acromegaly.
In another group of dwarf children, the plasma growth hormone concentration is normal or elevated but there are congenital abnormalities” of the growth hormone receptor as a result of gene deletions or point mutations. The resulting condition is known as growth hormone insensitivity or Laron dwarfism.
Plasma immunoglobin F-I level is reduced and in most cases, the plasma growth hormone-binding protein concentration is also reduced indicating genetic defects in the extracellular portion of the growth hormone receptor.
Short stature can result from abnormalities in GH metabolism other than deficient secretion. Thus growth hormone levels are normal in African pigmies; therefore their small stature is due to other factors, either a slightly abnormal and less efficient GH molecule, or a failure of peripheral response to GH or deficient somatomedin secretion.
Effects of Deficiency of Vasopressin:
Diabetes Incipidus:
Damage to the functioning of the neurohypophyseal system results in severe depression or suppression of vasopressin secretion. This condition produces in man the disorder diabetes incipidus. The characteristic feature of this disease is the production of large volumes of urine up to 10 liters per day of dilute urine (polyurea) with the secondary consequence of severe, thirst and excessive fluid intake (polydipsia). Diabetes incipidus can be controlled satisfactorily by administration of arginine vasopressin or similar substances.
Essay # 7. Hormonal Disorders of Sexual Development:
The reproductive system is very complex. Many events occur that result in abnormalities in sexual development. Most defects have a genetic basis and are produced due to failure of steroid hormone synthesis or failure of their action on target tissues.
a. Hermaphroditism:
Sex steroidal hormone imbalance in male or female fetus results in hermaphroditism. A true hermaphrodite is an individual with both male and female sex organs namely, ovaries and testes. This condition is rare. A male pseudohermaphrodite is one in which the testes are present but the genital ducts and external genital organs are that of female or of an incompletely differentiated male.
Similarly, female pseudohermaphrodites possess ovaries but the external genitalia and gonoducts are that of male. In female pseudohermaphrodites, the male type of external genitalia is due to the excessive production of androgens. The degree of masculinization depends upon the amount and period of exposure to androgens. Female pseudohermaphroditism in most patients is due to congenital adrenal hyperplasia resulting in failure of Cortisol production.
In the absence of Cortisol, there is no negative feedback inhibition to the hypothalamus, which results in increased ACTH secretion and increased synthesis of androgens by the adrenal cortex. The androgens in excess are responsible for virilization of the external genitalia and development of masculine secondary sexual characters.
Male pseudohermaphroditism is due to se chromosomal abnormalities, mutant genes or defective gonadogenesis due to teratological factors. Male pseudohermaphroditism in some cases may be due to a defect in the LH receptors of fetal Leydig cells in the testes. A number of inborn errors of testosterone production can also result in male pseudohermaphroditism.
b. Hypogonadism and Hypergonadism:
Defects in the normal development of secondary sexual characters at puberty may result from defects that reside at the level of the gonads (primary), at the level of pituitary (secondary), or at the level of the hypothalamus (tertiary) (Fig. 1A). Primary hypogonadism is due to the failure in production of gonadal steroids due to any one of a number of causes.
Failure in the negative feedback inhibition at the pituitary or hypothalamus by steroid hormones leads to increased gonadotropin secretion in the face of hypogonadism (hypergonadotropic hypogonadism Fig. 1 B). Secondary hypogonadism results from a defect of in pituitary gonadotropin secretion (hypogonadotropic hypogonadism (Fig. 1 C).
Hypergonadism involving overproduction of gonadal steroids is related to a primary defect (hypogonadotropic hypergonadism Fig. 1 D) at the level of gonads involving tumors of the steroid secreting Leydig cells in the male or follicular thecal cells in the female or to a secondary defect (hypergonadotropic hypergonadism Fig. 1 E) involving overproduction of pituitary gonadotropic hormones.
Hypogonadotropic hypogonadism due to deficiency of gonadotropin releasing hormone (GnRH) commonly occurs in female athletes. Severe physical exercise in these women alters the integrity of various neuroendocrine systems.
Exercise induced deficiency of hypothalamic secretion of GnRH produces the syndrome hypothalamic amenorrhea. GnRH treatment is used to induce puberty in children with constitutional delay of growth and puberty, and in children with hypogonadotropic hypogonadism.