ENDOCRINOLOGY.pptx
- 1. ENDOCRINOLOGY PREPARED BY: EUNICE KARIMA
- 2. Module Outcomes • Use the nursing process to manage patients with; Pituitary disorders Thyroid disorders Parathyroid disorders Adrenal disorders Diabetes
- 3. Pituitary disorders • Syndrome of inappropriate Antidiuretic hormone. SIADH • Acromegaly • Growth failure • Simmonds's disease Thyroid disorders • Hyperthyroidism (graves disease) • Hypothyroidism (myxedema) • Goiter • Cancer of the thyroid, neoplasm
- 4. Parathyroid hormone disorders • Hyperparathyroidism • Hypoparathyroidism Adrenal disorders • Cushing’s disease • Addison’s disease • Conn’s disease • Congenital adrenal hyperplasia • Pheochromocytoma
- 5. Diabetes mellitus • Risk factors • Classification • Pathophysiology • Assessment and diagnostic findings • Management (nutrition, pharmacologic, heath education, exercise, monitoring sugar levels) • Complication; long term complications, Acute complications
- 6. Introduction To Endocrinology Endocrine glands •Pituitary, •Thyroid •Parathyroid •Adrenals •Pancreatic islets •Ovaries •Testes
- 8. • Endocrine glands secrete their products directly into the blood stream. • The endocrine glands secrete chemical substances called hormones. • Together with the nervous system, hormones help to regulate organ function. • The endocrine glands are composed of secretory cells arranged in minute clusters known as acini. • The glands have a rich blood supply so that the hormones they produce enter the bloodstream rapidly. • Hormones are chemical messengers produced by glands-directly diffused into the blood stream and carried from the glands to specific target tissues or organs.
- 9. • The hormone levels are maintained at a constant level. In a normal physiological process, this is enabled by the negative feedback. i.e. increase in hormone concentration- the production of that hormone is inhibited. Decrease in a hormone level concentration- production of such hormone is increased. • Hormones are important in the regulation of the internal environment of the body and affect every aspect of life. • A hormone can alter the function of the target tissue by interacting with the chemical receptors; Either On the cell membrane Or outside the cell membrane
- 10. The Pituitary Gland • Also called; hypophysis • The pituitary gland is a master gland:- it secretes hormones that control the secretion of other hormones in other endocrine glands. Location •In the hypophyseal fossa of the spheolenoid bone.(In the inferior aspect of the brain- below the hypothalamus. Size • size of a pea, weighs 500mg.
- 12. •The pituitary gland and hypothalamus act as a unit to regulate the activities of most of the other endocrine glands. •The two organs are connected by a pituitary stalk also called an infindibulum. •The pituitary gland has 3 lobes. The two main lobes originate from different types of cells.
- 13. Lobes of the Pituitary Gland Anterior pituitary gland/lobe-(Adenohypophysis)- an up growth of glandular epithelium. Intermediate Lobe- A thin strip of tissue whose function in human is not known. Posterior pituitary gland-(Neurohypophysis).- a down growth of nerve tissues from the brain.
- 15. Blood supply • Arterial blood supply Internal carotid artery. • The anterior lobe- is indirectly supplied by blood that has passed through the capillary bed of the hypothalamus. This blood connection is called the pituitary portal system. • The posterior lobe- is supplied directly by the internal carotid artery. Venous drainage short portal veins
- 16. Anterior Pituitary Gland •The anterior pituitary gland is supplied by blood that has already passed through the hypothalamus. •There is a mesh of capillaries/network of blood vessels from the hypothalamus that supply blood with: Nutrients and Oxygen Releasing and stimulating hormones to the Anterior pituitary gland The blood connection between the hypothalamus and the Anterior pituitary gland is called the pituitary portal system.
- 17. The Hypothalamus A brain structure that coordinates body process to help achieve homeostasis. It directly influences the autonomic nervous system (controls the involuntary physiological processes e.g. BP, digestion, sexual arousal) and by indirectly controlling the hormonal system. • The hypothalamus secretes and releases: Releasing and inhibiting hormones for the hormones produced in the Anterior pituitary lobe.
- 18. Hypothalamus Anterior pituitary gland Growth hormone releasing hormone GhRh Growth hormone Gonadotropin Realising Hormone Follicle stimulating hormone and Luteinizing hormone Thyrotropin releasing hormone Thyroid stimulating hormone Corticotrophin realising hormone Adrenocorticotropic hormones Prolactin releasing and inhibiting hormone Prolactin hormone
- 19. Hormones of the Anterior pituitary Gland • Hormones secreted in the anterior pituitary gland either act on specific organs/tissues directly or influence/stimulate the release of hormones in the target organs • The anterior pituitary hormones whose function is to stimulate release of hormones in other endocrine glands include: • FSH and LH-ovaries and testes. • Adrenocorticotropic ACTH- adrenal glands to produce adrenocorticosteroid hormones. • Thyroid stimulating hormone- thyroid gland- thyroid hormones.
- 20. •Pituitary hormones that act directly on specific organs include:: growth hormone, prolactin hormone. •Prolactin hormone- acts on the breast to stimulate milk production. •Growth Hormones Actions of the growth hormone are essential for normal growth. These actions include; Stimulating growth of bones and muscles. increase protein synthesis. increase breakdown of fatty acids on fat metabolism. The growth hormones is largely restricted in organs such as ; liver
- 21. •Adrenocorticotropic hormone (ACTH) Stimulates synthesis and secretion of adrenal cortical hormones. E.g. glucocorticoids(cortisol), adrenal androgens(sex hormones) , epinephrine and norepinephrine. •Thyroid stimulating hormones. Stimulates synthesis and secretion of thyroid hormone in the thyroid glands. •Follicle stimulating Hormone Synthesis and secretion of testosterone, estrogen and progesterone
- 22. Posterior Pituitary Gland/ Neurohypophysis • Formed by a downward growth of nerve cells. • The neurons of these nerve cells have their cell bodies in the hypothalamus. (Supraoptic nuclei and para ventricular nuclei). • The axons of these neurons form the hypothalamohypophyseal tract. • Which is the connection between the hypothalamus and posterior pituitary glands.
- 24. Hormones of the Posterior pituitary gland •The hormones are synthesized in the hypothalamus and travel to the posterior pituitary gland for storage. Anti diuretic hormone ADH Control the excretion of water by the kidneys. Causes smooth muscle contraction. Oxytocin Facilitates milk ejection during lactation. increase the force of uterine contractions during labour and delivery.
- 27. Pituitary Disorders • Syndrome of inappropriate Antidiuretic hormone. SIADH • Acromegaly • Growth failure • Simmonds's disease
- 28. THYROID GLAND • A butterfly shaped organ in the neck. • Has two lobes which are roughly cone shaped and connected by an isthmus. Location • In the neck. • In front of the larynx and trachea. • At the level of the 5th , 6th, 7th cervical vertebrae and 1st thoracic vertebrae.
- 31. Blood supply • Arterial blood supply Superior thyroid artery –a branch of external carotid artery. Inferior thyroid artery- branch of the subclavian artery. Venous return Thyroid veins that drains into internal jugular veins.
- 32. • The gland is composed of; Cuboidal epithelium- forms spherical follicles that produce/ secrete colloid. • Colloid is a thick sticky protein material that contains large precursor molecules of thyroid hormone called, thyroglobulin-contains tyrosine residue. Parra follicular cells- also called the C- cells. They are located between the follicles and they produce calcitonin. Hormones secreted by the thyroid gland T3(tri-iodothyronine) and T4 (tetra-iodothyronine/ thyroxine)- these two make up the thyroid hormone. The number on the T represents the number of iodine atoms present in the hormone. calcitonin
- 34. Role of Iodine • Iodine is majorly used by the thyroid gland in the body for the synthesis of its hormones. It is essential in the formation of the thyroid hormones. • Normally, iodine is ingested in diet and absorbed in the blood stream in the GIT. • The thyroid gland then selectively takes up the iodine from the bloodstream in a process called iodine tapping. • The iodine is then concentrated in the thyroid cells where iodide ions are converted into iodine molecules that react with tyrosine to form thyroid hormone.
- 35. Secretion of the Thyroid Hormone • The hypothalamus is triggered by exercise, stress, malnutrition, low plasma levels of T3 and T4, elevated temperature. • The hypothalamus stimulates the release of thyrotropin release hormone which stimulates the release of thyroid stimulating hormone by the anterior pituitary gland. • Thyroid stimulating hormones stimulates the release into blood stream.
- 37. Functions of Thyroid Hormone Affects most body cells by; Increasing their basal metabolic rate and heat production Regulating the metabolism of fats, carbohydrate and protein. Essential for normal growth and development especially the skeletal and nervous system by regulating a number of key growth factors. It also indirectly stimulates the release of Growth hormone. Enhances the effects of other hormones like the adrenaline and noradrenaline. Metabolic effects of the thyroid hormone are similar to those of the stimulation of adrenaline and noradrenaline receptors.
- 38. Calcitonin • Produced by parafollicular/ C-cells in the thyroid gland. Functions Acts on the bone cells and kidneys to reduce the blood calcium levels when they are raised. Promotes storage of calcium in the bones Inhibits reabsorption of the calcium in the kidneys, intestines. The effects of calcitonin are opposite those of the parathyroid hormone
- 39. Disorders • Hyperthyroidism • Hypothyroidism • Goitre • Neoplasms
- 42. Parathyroid Glands • They are 4 glands embedded in the posterior aspect(behind) the thyroid glands. 2 glands in each thyroid lobe. • The hormone produced in this glad is called parathormone / parathyroid hormone • Functions of parathormone Regulate calcium and phosphorous metabolism. Helps to raise calcium levels and lower phosphorous levels. The secretion of parathormone is regulated by serum calcium levels.
- 43. How the Parathormone Works • Increased secretion of parathormone causes increased calcium absorption in the kidneys, intestines and bones. • It increases the release of calcium into the blood by causing less new bone to be formed and more old bone to be broken down. • This raises the blood calcium levels and helps in maintaining blood calcium within normal limits (8.5- 10.5 mg/dL) (2.1-2.6mmol/L). • The diseases associated with the parathyroid hormone include; hyperparathyroidism and hypoparathyroidism.
- 44. CALCIUM • Calcium in the body is found in the skeletal system-99% (bones and teeth) and in the blood (1%). • The small amount of calcium located outside the bone circulates in the serum in 3 forms; Ionized calcium-50% partly bound to protein-albumin Complexed-Bound to non-protein inions like carbonate , phosphate and citrate. The normal total serum calcium level is 8.5 to 10.5 mg/dL (2.1–2.6 mmol/L). • Role of calcium Transmitting nerve impulses. Helps to regulate muscle contraction and relaxation, including cardiac muscle. Calcium is instrumental in activating enzymes that stimulate many essential chemical reactions in the body. Plays a role in blood coagulation.
- 45. Hyperparathyroidism • Excess production of the parathormone leading to increased Reabsorption of calcium from kidneys, bones and intestines. This increases the levels of calcium in the blood. • The disease is characterized by decalcification of bones and renal calculi (kidney stones due precipitation and development of excess calcium in the blood).
- 46. Clinical Manifestation • Fatigue • Muscle weakness • Nausea and vomiting • Hypertension • Cardiac dyarrthmias- increased calcium causes a decrease in the excitation potential of nerves and muscle tissue. • Renal calculi- resulting from the precipitation of excess calcium causing obstruction, pyelonephritis, renal failure. • Decalcification and demineralization of bones causes musculoskeletal e.g skeletal pain, bone deformities, pain on bearing weight. • Bone tumors composed of benign giant cells resulting from an overgrowth of osteoclasts.
- 47. Assessment and diagnostic findings • Persistent levels of elevated serum calcium levels and parathormone. • Bone changes visible on the X-rays and bone scans. Tests done include; • PTH immunoassay- test that measures the level of PTH in the blood. • Double antibody parathyroid hormone test.
- 48. Management • Recommended treatment is; parathyroidectomy-surgical removal of abnormal parathyroid tissue in patients with extremely elevated calcium levels. • Hydration therapy-prevent renal calculi formation. • Mobility-encourage mobility because bones subjected to normal stress produce less calcium compared to patients on bed rest. • Dietary restriction- of calcium. • Diuretics- promote renal excretion of excess calcium. • Calcitonin-promote calcium deposit into the bones and reduce absorption of calcium in the kidneys, intestines. • Dialysis
- 49. Complications Hypercalcemic crisis • Occurs with extreme elevation of serum calcium levels above 3.7 mmol/L or 15mg/Dl • May results in neurologic, cardiovascular and renal symptoms that are life threatening.
- 50. HYPOPARATHYROIDISM • There is less production of the parathormone. • Reduced levels of parathyroid hormone causes decrease absorption of calcium in intestines, decreased resorption of calcium from bones and decreased reabsorption of calcium from kidney. • This causes; decrease in calcium levels, increase in phosphorous levels.
- 51. Causes of Hypoparathyroidism • Inadequate secretion of parathyroid hormone may occur after; Interruption of blood supply Surgical removal of parathyroid gland tissue during thyroidectomy Parathyroidectomy Radical neck dissection
- 52. CLINICAL MANIFESTATION • Chief symptom is hypocalcemia- causes irritability of the neuromuscular system causing Tetany. • Uncoordinated tremors ad contraction • Numbness , tingling, cramps in the extremities. • Photophobia • Seizures • Anxiety • Irritability
- 53. Management • Goal of management; raise calcium serum levels and eliminate symptoms of hypocalcemia. • IV parathormone. • Diet high in calcium and low in phosphorus • Sedative agents e.g. phenobarbital • Hypocalcemia and tetany occurring after thyroidectomy should be treated by administering calcium gluconate to decrease neuromuscular irritability and seizure activities.
- 54. Adrenal Glands • Are called supra-renal glands. Location • Upper pole of each lobe. • Enclosed within the renal fascia. Blood supply • Arterial: branches of abdominal aorta and renal arteries. • Venous return: suprarenal veins Right gland: drains into inferior vena cava Left gland: left renal veins
- 55. Parts of the Adrenal Glands • Outer part: adrenal cortex -Glucocorticoids- Hydrocortisone- affects glucose metabolism -Mineralocorticoids- Aldosterone- affects electrolyte metabolism -Androgens- Sex hormones. • Inner part: adrenal medulla Catecholamine -epinephrine -norepinephrine
- 56. Release of Adrenal Hormones • Hypothalamus secretes corticotrophin releasing hormone which stimulates anterior pituitary gland to release ACTH adrenocorticotrophic hormone stimulates adrenal cortex to secrete glucocorticoids, mineralocorticoids, androgens. • Hormones of the adrenal glands help in management of stress to the body.
- 57. Adrenal Hormones • Hormones of the adrenal glands help to manage stressors that threaten homeostasis. E.g. exercise, temperature, fasting, infection, diseases, emotional situations, fright, etc.. • They manage the stressors through; Short term responses (fight and flight)- adrenal medulla. long term responses- adrenal cortex.
- 58. ADRENAL CORTEX Adrenal cortical hormones include; - Glucocorticoids- Hydrocortisone- affects glucose metabolism -Mineralocorticoids- Aldosterone- affects electrolyte metabolism -Androgens- Sex hormones. • These hormones produce a long term response to stress.
- 59. Androgens • Exerts similar effects to those of the male sex hormones. • Androgens have less effects when secreted in normal amounts. • When secreted in large amounts/ in excess , it causes masculinization. • The adrenal gland may also secret small mounts of estrogen (female sex hormones)
- 60. GLUCOCORTICOIDS • Main glucocorticoid: hydrocortisone (Cortisol) • Other glucocorticoid hormones secreted in small amounts: corticosterone and cortisone • Secretion of glucocorticoids is stimulated by: ACTH in the pituitary glands and stress. • The stimulation occurs between 4 AM- 8AM ( highest) and from midnight-3AM (lowest). • Secretion of glucocorticoids follows the circadian cycle. Changes in sleeping and waking pattern changes the ACTH/cortisol secretion.
- 61. Functions of Hydrocortisone • Breakdown (catabolism) of protein and fat that makes glucose and other substances available for use. Gluconeogenesis- formation of new sugars. Lipolysis- breakdown of triglycerides into fatty acids and glycerol for energy production. Stimulate breakdown of proteins releasing amino acids that are used for synthesis of protein (e.g. enzymes) and for energy production. Therefore, increased hydrocortisone results in elevated blood glucose levels. • Promoting absorption of sodium and water from renal tubules- weak mineralocorticoid effect.
- 62. Glucocorticoids and Glucose Metabolism • Increased hydrocortisone results in elevated blood glucose levels. • Administration of glucocorticoids causes: Diabetes mellitus- due to increased glucose level in the body. Increased protein breakdown leading to muscle wasting and poor wound healing. Redistribution of body fat. Large amounts of glucocorticoids administration can cause atrophy of adrenal glands. Osteoporosis and peptic ulcers.
- 63. Other effect of Glucocorticoids(steroids) • Promote absorption of sodium and water from he renal tubules – weak mineralocorticoid effect. • Anti-inflammatory actions. • Suppression of immune responses. Glucocorticoids in form of corticosteroids are administered to inhibit inflammatory response to tissue injury and suppress allergic manifestation
- 64. Mineralocorticoids • Aldosterone is the main mineralocorticoid. Functions Maintenance of water and electrolyte balance in the body. - Stimulates the reabsorption of sodium ions (Na+) by renal tubules and excretion of potassium (K+) in the urine. Sodium reabsorption is accompanied by: retention of water and therefore, aldosterone is involved in the regulation of blood volume and blood pressure.
- 65. • The release of aldosterone is stimulated; 1. Blood potassium levels • When blood potassium levels are elevated leads to secretion of more aldosterone and vice versa. High potassium levels means low sodium levels. 2. Angiotensin When reduced blood flow to the kidneys/increased potassium level/ decreased sodium levels. the kidney produces renin enzyme the renin enzyme converts Angiotensinogen (produced in the liver) into Angiotensin I. Angiotensin converting enzyme (secreted in the lungs and proximal kidney tubules) converts Angiotensin I to Angiotensin II the Angiotensin II stimulates secretion of Aldosterone.
- 66. Adrenal Medulla • Functions as part of the autonomic nervous system. • It develops from the nervous system in the embryo and is part of the sympathetic division of the autonomic nervous system. • Hormones secreted in the adrenal medulla include; Adrenaline/ epinephrine- greater effects on the heart and metabolic processes. Noradrenaline/ norepinephrine- more influence on blood vessels. • These two hormones are structurally similar producing similar effects. • They produce a short term response to stress.
- 67. Release of hormones in the adrenal medulla • Any imbalance in homeostasis/ stress. causes stimulation of preganglionic sympathetic nerve fibers that travel directly to the cells of the adrenal medulla. which causes release of catecholamine's.
- 68. Function of Catecholamine • They potentiate the fight and flight responses by; Increasing the heart rate Increasing blood pressure. Diverting blood to essential organs (heart, brain and skeletal muscles) by dilating their blood vessels and constricting the blood vessels of the less essential organs like skin. Dilating the pupils.
- 69. Response to Stress • When the body is under stress, homeostasis is disturbed. • To restore it and in some cases to maintain life, there is an immediate and if necessary, long-term responses. • Stressors include; exercise, fasting, infection, fright, temperature changes, infection, disease and emotional situations. • Immediate response: is described as fight and flight. It is mediated by the sympathetic part of the autonomic nervous system. • Long-term response: ACTH from the anterior pituitary gland stimulates the release of glucocorticoids and mineralocorticoids from the adrenal cortex and more prolonged response to stress occurs.
- 70. PANCEATIC ISLETS/ ISLETS OF LANGERHANS • The cells that make up the pancreatic islets; Are Found in clusters Are irregularly distributed throughout the pancreas. Do not have ducts but secrete their hormones directly into the blood stream. • There are 3 main types of cells in the pancreatic islets; Alpha cells- secrete glucagon Beta cells-most numerous and secrete insulin Delta cells-secrete somatostatin (GHRIH)
- 71. Blood Glucose Levels • Normal levels; 3.5-8 mmol/L (63-144 mg/100ml). • The blood glucose levels are controlled mainly by the opposing actions of insulin and glucagon. • Glucagon increases blood glucose levels • insulin reduces blood glucose levels INSULIN • Is a polypeptide consisting of 50 amino acids whose main function is to lower raised blood nutrient levels.( glucose, amino acids and fatty acids)
- 72. • Insulin has an anabolic effect- it promotes the storage of nutrients. • When these nutrients especially glucose are in excess, insulin promotes their storage by: Increasing conversion of glucose to glucagon by the liver and skeletal muscles. Accelerate the uptake of amino acids by cells and synthesis of protein. Acting on cell membranes and stimulating uptake and use of glucose by muscles and connective tissue. Promote synthesis of fatty acids and storage of fat in adipose tissue. Decreasing glycogenolysis- breakdown of glycogen into glucose. Prevent breakdown of fat and protein and formation of new sugars (gluconeogenesis)
- 73. • The secretion of insulin is stimulated by: Increased blood glucose levels Parasympathetic stimulation Raised blood amino acids and fatty acids levels Gastrointestinal hormones e.g. gastrin, secretin and cholecystokinin. • The secretion is inhibited by; Sympathetic stimulation Glucagon Adrenaline Cortisol somatostatin
- 74. GLUCAGON • It increases blood glucose levels by stimulating; Conversion of glycogen to glucose in the liver and skeletal muscles (glycogenolysis) Formation of new sugars (gluconeogenesis) • The secretion of glucagon is stimulated by a low blood glucose level and exercise. • It is decreased by somatostatin and insulin. Somatostatin (GHRIH) • This hormone is also secreted by the hypothalamus. • Its effect is to inhibit the secretion of both insulin and glucagon in addition to inhibiting the secretion of growth hormone from the anterior pituitary gland.
- 75. DIABETES MELLITUS • Is a group of metabolic disease characterized by elevated levels of glucose in blood (hyperglycemia) resulting from defects in insulin secretion (in the pancreas), insulin action (cells stopped responding to insulin) or both. Types of diabetes mellitus • Type 1 DM- insulin dependent diabetes • Type 2 DM- non-insulin dependent diabetes • Diabetes associated with other conditions • Gestational diabetes
- 76. Physiology and Pathophysiology of Diabetes • Insulin is secreted by the beta cells in the islets of langerhans. It is an anabolic or storage hormone. • When someone eats a meal, insulin secretion increases and moves glucose from the blood into the muscles and fat cells. • In those cells, insulin; • Transports and metabolizes glucose for energy. • Stimulates storage of glucose in the liver and muscle in form of glycogen. • Signals the liver to stop the release of glucose. • Enhances storage of dietary fat in adipose tissue. • Accelerate transport of amino acids from dietary proteins into cells • Inhibits the breakdown of stored glucose, protein and fat.
- 77. • During fasting period(between meals and overnight), the beta cells continously releases small amounts if insulin; another pancreatic hormone called glucagon is released when blood glucose levels decrease and stimulates the liver to release stored glucose. • The insulin and glucagon together maintain a constant level of glucose in the body by stimulating or inhibiting the release of glucose from the liver. • Initially, the liver produce glucose through the breakdown of glycogen (glycogenolysis). • After 8-12 hours without food, the liver forms glucose from the breakdown of non-carbohydrate substances including amino acids (gluconeogenesis).
- 78. Type I Diabetes • Also known as insulin dependent diabetes.( patients were classified according to the treatment of the diabetes). • It is characterized by the destruction of the pancreatic beta cells. • The destruction can be caused by; Genetic factors- people inheriting the genetic predisposition to type 1 diabetes. Immunological factors- autoimmune response against islets cells and endogenous (internal) insulin. Environmental factors- viruses or toxins tat may initiate the destruction of beta cells.
- 79. • The destruction of the beta cells leads to: Decreased insulin production Unchecked glucose production by the liver. Fasting hyperglycemia- Post-prandial hyperglycemia- the glucose derived from the food cannot be stored in the liver but instead remains in the bloodstream and contribute to post- prandial hyperglycemia. Glycosuria- excessive loss of glucose in urine that is usually accompanied by excessive loss of fluids and electrolytes. • If the concentration of glucose in the blood exceeds the renal threshold , the kidneys may not reabsorb all the filtered glucose, the glucose then appears in urine. • In people with insulin deficiency, glycogenolysis and gluconeogenesis occur in an unrestrained fashion and contribute to further hyperglycemia. • Fat breakdown occurs resulting to increased production of ketone bodies.
- 80. Type 2 Diabetes Mellitus • The two main problem related to inulin in type 2 diabetes are; Insulin resistance Impaired insulin secretion Insulin resistance • Refers to decreased tissue sensitivity to insulin. • Normally: insulin binds to special receptors on cell surfaces and initiates a series of reaction involved in glucose metabolism. • In Type 2 Diabetes: the intracellular reactions are diminished and so insulin is rendered less effective at stimulating glucose reuptake by the tissue and regulating glucose release by the liver.
- 81. • To overcome the insulin resistance and to prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level t a normal or slightly elevated level. • However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rise and type 2 diabetes develops. • Despite the impaired insulin secretion in type 2 diabetes, there is enough insulin present to prevent breakdown of fat and the accompanying production of ketones. • Therefore, DKA does not typically occur in type 2 diabetes. • Uncontrolled type 2 diabetes however caused HHNK (hyperglycemic hyperosmolar non-ketotic syndrome) • Insulin resistance is usually associated with obesity making exercise and weight loss the primary treatment of type 2 diabetes.
- 82. Gestational Diabetes • It is any degree of glucose intolerance with its onset on pregnancy. • Hyperglycemia in pregnancy is because of the secretion of placental hormones which causes insulin resistance. • Selective screening for gestational diabetes is done for mothers who; Are age 25 years or older Age 25 or younger and obese Family history of diabetes in first degree relatives Member of ethnical/racial group with a high prevalence of diabetes e.g native America, Hispanic America
- 83. Gestational Diabetes • Gestational diabetes increases the risk of getting hypertensive disorders during pregnancy. • Initial management of gestational diabetes is dietary modification and blood glucose monitoring. • If hyperglycemia persists, insulin is prescribed. Oral antidiabetic medication should not be used during pregnancy.
- 84. CLINICAL MANIFESTATIONS • Clinical manifestations of all types of diabetes include; Polyuria- increased urination Polydipsia- increased thirst occurs as a result of the excess loss of fluid associated with osmotic diuresis Polyphagia- increased appetite resulting from catabolic state induced by insulin deficiency and breakdown of proteins an fats. • Other symptoms include; Fatigue and weakness Sudden vision changes Tingling or numbness in hands and feet Dry skin Skin lesions and wounds that are slow to heal. Recurrent infection • The onset of type 1 diabetes is associated with sudden weight loss or nausea, vomiting or abdominal pains if DKA has developed.
- 85. Criteria for the Diagnosis of DM 1. Symptoms of diabetes plus casual or plasma glucose concentration (RBS)equal to or greater than 200mg/Dl (11.1 mmol/L). • Casual is defined as any time of the day without regard to time sice last meal. • The classic symptoms of DM include; polyuria, polydipsia, polyphagia and unexplained weight loss. 2. Fasting plasma glucose concentration greater than or equal to 126mg/dL (7.0 mmol/L). • Fasting is defined as no caloric intake for at least 8 hours.
- 86. 3. 2-hour post load glucose equal to or greater than 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test. • The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. • However, this third criteria is not recommended for routine clinical use.
- 87. Diabetes Management • The goal of diabetes management is to; • Normalize insulin activity. • Normalize the blood glucose levels(euglycemia) without hypoglycemia and without seriously disrupting the patients usual lifestyle and activity. • Reduce the development of vascular and neuropathic complication. • There are 5 components of diabetes management; 1. Nutritional management 2. Exercise 3. Monitoring of sugar level and ketone 4. Pharmacologic therapy 5. Education
- 88. Nutritional management • Diet and weight control. • Patient is to control total caloric intake to attain a reasonable body weight and control of blood glucose levels. • Nutritional management of the diabetic patient includes the following goals; Providing all the essential food constituents (e.g. vitamins, minerals) necessary foe optimal nutrition. Meeting energy needs. Achieving and maintaining a reasonable weight. Preventing wide daily fluctuations in blood glucose levels, with blood glucose levels as close to normal as is safe and practical to prevent or reduce the risk for complications. Decreasing serum lipids levels, if elevated, reduce the risk for macrovascular disease.
- 89. Exercise • It lowers blood glucose levels and reduces cardiovascular risk factors • Exercise lowers blood glucose levels by; increasing uptake of glucose by muscles, improve insulin utilization and improve circulation and muscle tone. • Exercise also alters the blood lipid levels, increasing levels of high density lipoproteins and decreasing total cholesterol and triglyceride levels.
- 90. Monitoring Glucose levels and ketones • Blood glucose monitoring allows for the detection and prevention of hypoglycemia and hyperglycemia. • Self-monitoring of blood glucose may involve obtaining a drop of blood from the fingertip, applying the blood on a regent strip and allowing the blood to stay on the strip unto the meter gives a digital read out of the blood glucose value. • Urine test for glucose was used to monitor diabetes on s daily basis • Testing for ketone bodies in urine to help monitor type 1 diabetes using the urine dipstick.
- 91. Pharmacologic therapy • In the absence of adequate internal insulin, pharmacological insulin therapy is essential. • Exogenous insulin is administered for life in type 1 diabetic patients. • In type 2 diabetes, insulin may be necessary for long-term basis to control glucose levels if diet and oral agents fail. • Insulin injection are administered two or more times daily depending on the level of glucose in the blood, accurate monitoring of blood glucose level is therefore essential. • Insulin preparations vary according to 3 main characteristics; time course of action, species(source) and manufacturer.
- 92. Time course of action • Insulins are grouped into several categories depending on the onset, peak and duration of action Rapid acting insulin • Are blood glucose lowering agents that produce a more rapid effect that is of shorter duration that regular insulin. • Example; lispro and aspart. • Are indicated to be used in rapid reduction of glucose level, to treat postprandial hyperglycemia and to prevent nocturnal hypoglycemia. Short acting insulin or regular insulin • Regular insulin is a clear solution and is usually administered 20-30 minutes before a meal, either alone or with a long acting insulin. • Examples; regular insulin(humalog R, Novolin R )
- 93. Intermediate-acting insulins • Examples include; NPH (neutral protamine Hagedorn), Lente insulin. • Have an onset of 3-4 hours. • They appear white and cloudy. Long acting insulins • Examples; ultralente insulin. • Are referred to as peak less insulin because they tend to have a long, slow, sustained action rather than sharp, definite peak actions. • Are mostly given once a day, coz the insulin is absorbed slowly over 24 hours. • It is not mixed with other insulin because of it nature of being a suspension with a pH of 4.
- 94. 2. Species (source) • Insulin used to be obtained from beef(cow) and pork (pig) pancreas. • However, human insulin are now available. They are produced by recombinant DNA technology and have largely replaced insulin rom anima source. 3. Manufacturers The insulins made by different companies are usually used interchangeably provided the concentration, species and type of insulin are the same.3
- 95. Complications of Insulin Therapy Local allergic reactions • A local allergic reaction (redness, swelling, tenderness and induration or a 1-4 cm wheal) may appear at the injection site 1 to 2 hours after he insulin. • The reactions usually occur during the beginning stages of therapy and disappear with continue use of insulin. • Antihistamine is usually prescribed to be taken 1 hour before the insulin injection.
- 96. Systemic allergic reaction • These are rare complications of insulin therapy. • There is an immediate local skin reaction that gradually spreads into generalized Urticaria (hives) that are occasionally associated with generalized edema or anaphylaxis. • Treatment is desensitization, with small doses of insulin administered in gradually increasing the amounts using a desensitization kit. Insulin lipodystrophy • Refers to a localized reaction in the form of either lipoatrophy or lipohypertrophy, occurring at the site at insulin injections. • Lipoatrophy is loss of subcutaneous fat and appears as light dimpling or more serious pitting of subcutaneous fat.
- 97. • Lipohypertrophy is the development of fibro fatty masses at the injection site that is caused by the repeated use of an injection site. • If insulin is injected into scarred areas, absorption may be delayed. • Insulin is one reason that rotation of injection sites is so important. Insulin resistance • Insulin resistance has been defined as daily insulin requirement of 200 units or more. • It occurs mostly due to obesity.
- 98. Morning hyperglycemia • An elevated blood glucose level upon rising in the morning cause by insufficient amount of insulin. • It is caused by; • The dawn phenomenon • The somogyi effect • Insulin waning
- 99. Pineal Gland • Size: a small body about 10 mm long • Location: Attached to the roof of the third ventricle and id connected to it by a short stalk containing nerves that terminate in the hypothalamus. • Appearance: reddish brown in colour and is surrounded by a capsule. • The pineal glands tends to atrophy after puberty and may calcify later in life. • The main hormone secreted by the pineal gland is melatonin
- 100. Melatonin • Its secretion is controlled by daylight and levels fluctuate during each 24-hour period- it is highest at night and lowest around midday. • Secretion is also influenced by the number of daylight hours. Ie. Seasonal variation. Functions • It is associated with the coordination of the circadian and diurnal rhythms of many tissues, possibly influencing the hypothalamus. • Inhibition of growth and development of the sex organ before puberty, possibly by preventing synthesis of release of gonadotrophins.
- 101. Thymus Gland Thymosin • Is the hormone produced by the thymus gland. • It is involved in the development of T-lymphocytes for the cell- mediated immunity