This document summarizes the structure and functions of the adrenal cortex. It is divided into three zones: the zona glomerulosa secretes aldosterone and regulates sodium retention; the zona fasciculata secretes cortisol and regulates carbohydrate, fat, and protein metabolism; the zona reticularis secretes sex hormones like androgens. Conn's syndrome and Cushing's syndrome are also summarized, outlining their causes, clinical features, investigations, and treatments. Addison's disease, a condition of chronic adrenal failure, is briefly mentioned at the end.
This document discusses adrenal gland disorders. It describes the anatomy and functions of the adrenal cortex and medulla. It then covers various adrenal disorders including adrenal hypofunction (such as Addison's disease), hyperfunction (Cushing's syndrome and hyperaldosteronism), congenital adrenal hyperplasia, and adrenal crisis. It provides details on the causes, clinical presentations, investigations, and management of these various adrenal disorders.
This document summarizes diseases of the parathyroid and adrenal glands. It describes the anatomy and functions of the parathyroid glands, including calcium regulation and causes of hyperparathyroidism. It also details the zones of the adrenal cortex and their hormone productions, including cortisol, aldosterone, and androgens. Specific diseases are outlined such as Cushing's syndrome, Conn's syndrome, Addison's disease, and pheochromocytoma. Surgical indications and treatments are provided.
This document discusses renal function tests and their importance in assessing kidney function. It covers urine analysis including physical, chemical and microscopic examination. It also discusses various blood tests like serum creatinine, blood urea, uric acid and electrolytes to evaluate glomerular function. Tests of tubular function examined include urine concentration, vasopressin and water load tests. The significance of renal function tests in acute kidney injury is also highlighted. An addendum discusses cystatin C as a novel marker for non-invasive estimation of glomerular filtration rate and early renal impairment.
This document discusses hypercalcemia in malignancy. It begins with an introduction defining hypercalcemia and its prevalence in certain cancers. It then covers normal calcium metabolism regulation involving bone, plasma, vitamin D, and the RANK/RANKL pathway. Etiologies of hypercalcemia in malignancy include PTHrP-mediated humoral hypercalcemia, local osteolytic hypercalcemia, 1,25-dihydroxyvitamin D mediated, and hyperparathyroidism. Clinical presentation involves neurologic, gastrointestinal, cardiovascular, and renal symptoms. Diagnostic evaluation includes calcium levels and approaches based on etiology. Management involves increasing urinary calcium excretion, inhibiting bone resorption with bisphosphonates or den
The document discusses disorders of the adrenal gland, including hyperactivity and hypoactivity of the adrenal cortex. Regarding hyperactivity, it describes Cushing's syndrome, Conn's syndrome, and adrenogenital syndrome. It provides details on the causes, characteristic features, and tests used to diagnose Cushing's syndrome. For hypoactivity, it discusses primary and secondary adrenal insufficiency, including Addison's disease, its causes, features, and tests. It also briefly mentions congenital adrenal hyperplasia.
Addison's disease is a rare disorder of the adrenal glands that affects the production of cortisol and aldosterone hormones. It is characterized by progressive anemia, low blood pressure, great weakness, and bronze skin discoloration. Common causes include an autoimmune response, infection of the adrenal glands, or inadequate hormone secretion. Left untreated, it can lead to death. Symptoms include fatigue, weakness, pain, nausea, and hyperpigmentation. Diagnosis involves testing cortisol and aldosterone levels along with monitoring electrolytes. Treatment consists of medications to replace hormones and educate patients on managing stress and monitoring for crises. Nursing focuses on monitoring blood pressure, glucose, electrolytes, and signs of
The document discusses adrenal gland disorders including Addison's disease. It describes the anatomy and functions of the adrenal cortex and medulla. Addison's disease is caused by insufficient production of cortisol and aldosterone due to damage to the adrenal cortex. Signs include dehydration, hypotension, hyperpigmentation, and hypoglycemia. It is diagnosed through blood tests and stimulation tests and treated with corticosteroid and mineralocorticoid hormone replacement therapy. Untreated, adrenal crisis can occur during periods of stress and requires emergency treatment.
Management of oncology emergencies, Mohh'd sharshirMoh'd sharshir
This document summarizes the management of oncologic emergencies, focusing on tumor lysis syndrome (TLS). TLS is caused by massive lysis of tumor cells, releasing potassium, phosphate and uric acid. It is classified based on laboratory and clinical criteria. Risk is highest in Burkitt lymphoma, ALL and other high-grade lymphomas. Prevention focuses on IV hydration and hypouricemic agents like rasburicase or allopurinol. Electrolyte abnormalities are managed based on their severity. High-risk patients receive aggressive prevention while intermediate-risk patients generally receive allopurinol prevention.
This document discusses adrenal gland disorders. It describes the anatomy and functions of the adrenal cortex and medulla. It then covers various adrenal disorders including adrenal hypofunction (such as Addison's disease), hyperfunction (Cushing's syndrome and hyperaldosteronism), congenital adrenal hyperplasia, and adrenal crisis. It provides details on the causes, clinical presentations, investigations, and management of these various adrenal disorders.
This document summarizes diseases of the parathyroid and adrenal glands. It describes the anatomy and functions of the parathyroid glands, including calcium regulation and causes of hyperparathyroidism. It also details the zones of the adrenal cortex and their hormone productions, including cortisol, aldosterone, and androgens. Specific diseases are outlined such as Cushing's syndrome, Conn's syndrome, Addison's disease, and pheochromocytoma. Surgical indications and treatments are provided.
This document discusses renal function tests and their importance in assessing kidney function. It covers urine analysis including physical, chemical and microscopic examination. It also discusses various blood tests like serum creatinine, blood urea, uric acid and electrolytes to evaluate glomerular function. Tests of tubular function examined include urine concentration, vasopressin and water load tests. The significance of renal function tests in acute kidney injury is also highlighted. An addendum discusses cystatin C as a novel marker for non-invasive estimation of glomerular filtration rate and early renal impairment.
This document discusses hypercalcemia in malignancy. It begins with an introduction defining hypercalcemia and its prevalence in certain cancers. It then covers normal calcium metabolism regulation involving bone, plasma, vitamin D, and the RANK/RANKL pathway. Etiologies of hypercalcemia in malignancy include PTHrP-mediated humoral hypercalcemia, local osteolytic hypercalcemia, 1,25-dihydroxyvitamin D mediated, and hyperparathyroidism. Clinical presentation involves neurologic, gastrointestinal, cardiovascular, and renal symptoms. Diagnostic evaluation includes calcium levels and approaches based on etiology. Management involves increasing urinary calcium excretion, inhibiting bone resorption with bisphosphonates or den
The document discusses disorders of the adrenal gland, including hyperactivity and hypoactivity of the adrenal cortex. Regarding hyperactivity, it describes Cushing's syndrome, Conn's syndrome, and adrenogenital syndrome. It provides details on the causes, characteristic features, and tests used to diagnose Cushing's syndrome. For hypoactivity, it discusses primary and secondary adrenal insufficiency, including Addison's disease, its causes, features, and tests. It also briefly mentions congenital adrenal hyperplasia.
Addison's disease is a rare disorder of the adrenal glands that affects the production of cortisol and aldosterone hormones. It is characterized by progressive anemia, low blood pressure, great weakness, and bronze skin discoloration. Common causes include an autoimmune response, infection of the adrenal glands, or inadequate hormone secretion. Left untreated, it can lead to death. Symptoms include fatigue, weakness, pain, nausea, and hyperpigmentation. Diagnosis involves testing cortisol and aldosterone levels along with monitoring electrolytes. Treatment consists of medications to replace hormones and educate patients on managing stress and monitoring for crises. Nursing focuses on monitoring blood pressure, glucose, electrolytes, and signs of
The document discusses adrenal gland disorders including Addison's disease. It describes the anatomy and functions of the adrenal cortex and medulla. Addison's disease is caused by insufficient production of cortisol and aldosterone due to damage to the adrenal cortex. Signs include dehydration, hypotension, hyperpigmentation, and hypoglycemia. It is diagnosed through blood tests and stimulation tests and treated with corticosteroid and mineralocorticoid hormone replacement therapy. Untreated, adrenal crisis can occur during periods of stress and requires emergency treatment.
Management of oncology emergencies, Mohh'd sharshirMoh'd sharshir
This document summarizes the management of oncologic emergencies, focusing on tumor lysis syndrome (TLS). TLS is caused by massive lysis of tumor cells, releasing potassium, phosphate and uric acid. It is classified based on laboratory and clinical criteria. Risk is highest in Burkitt lymphoma, ALL and other high-grade lymphomas. Prevention focuses on IV hydration and hypouricemic agents like rasburicase or allopurinol. Electrolyte abnormalities are managed based on their severity. High-risk patients receive aggressive prevention while intermediate-risk patients generally receive allopurinol prevention.
Haematological disorders PACES - Station 5 Mamdouh Dorrah
This document discusses the evaluation and management of hematological disorders like anemia. It covers taking a thorough history including symptoms, risk factors, medications and lifestyle. The physical exam focuses on signs of anemia. Initial investigations for anemia types include blood counts, iron, B12 and folate levels. Depending on the results, further testing may include endoscopies, biopsy or bone marrow examination to determine the underlying cause such as nutritional deficiencies, infections, cancers or autoimmune disorders. Pernicious anemia specifically requires serology to guide long term treatment.
1. Oncological emergencies refer to urgent clinical situations in cancer patients caused by cancer or its treatment.
2. Some examples discussed are hypercalcemia, tumor lysis syndrome, lactic acidosis, hypoglycemia, syndrome of inappropriate antidiuretic hormone secretion, superior vena cava syndrome, spinal cord compression, severe cystitis, bladder hemorrhage, disseminated intravascular coagulation, and cardiac tamponade.
3. The document provides details on symptoms, signs, and treatment approaches for each of these conditions.
This patient has a history of lysinuric protein intolerance (LPI) since age 3 and later developed lupus nephritis. LPI is caused by a defect in the SLC7A7 gene which impairs transport of cationic amino acids. This led to immunological issues and kidney involvement over time. A renal biopsy at age 4.5 showed proliferative glomerulonephritis consistent with lupus nephritis stage IV. Managing both conditions together has been challenging with various treatments over the years.
This document discusses disorders of the adrenal glands, including hyperactivity and hypoactivity. Hyperactivity disorders include Cushing's syndrome, hyperaldosteronism, and adrenogenital syndrome. Cushing's syndrome can be caused by excessive cortisol secretion from the pituitary gland (Cushing's disease) or the adrenal glands (Cushing's syndrome). Symptoms include obesity, muscle weakness, osteoporosis, hyperglycemia, and hypertension. Hypoactivity disorders include chronic and acute adrenal insufficiency (Addison's disease and Addisonian crisis), which can be caused by adrenal gland failure or damage. Signs of Addison's disease include pigmentation, muscular weakness, hypotension,
The document discusses renal function tests (RFTs). It provides information on:
- The functions of the kidney including homeostasis, excretion, and hormonal functions.
- Common RFTs including urine analysis, serum creatinine, BUN, eGFR, and cystatin C. These tests are used to evaluate glomerular filtration rate and detect kidney problems.
- Additional details are given on clearance tests using inulin, creatinine and urea to estimate GFR. Urine analysis and tests of tubular function are also summarized.
This document discusses disorders of the adrenal cortex related to mineralocorticoid excess and deficiency. It begins by covering the anatomy and physiology of the adrenal cortex and its role in synthesizing mineralocorticoids like aldosterone. It then examines the causes, clinical features, diagnostic evaluation and management of conditions involving mineralocorticoid excess, including primary and secondary hyperaldosteronism, as well as pseudo-hyperaldosteronism. It also reviews primary and secondary adrenal insufficiency related to deficiencies in mineralocorticoids and glucocorticoids. Flowcharts are provided outlining algorithms for evaluating patients with suspected mineralocorticoid excess or adrenal deficiency.
This document provides an overview of endocrine system revision covering the anatomy and physiology of the hypothalamus, pituitary gland, thyroid gland, adrenal glands, and pancreas. It discusses the hormonal regulation and feedback mechanisms of the HPA axis and describes various endocrine disorders like acromegaly, hypothyroidism, Cushing's syndrome, Addison's disease, and diabetes. The learning objectives, endocrine functions, and key hormones released by each endocrine organ are summarized.
This document provides an overview of renal involvement in systemic conditions like diabetes mellitus and systemic lupus erythematosus. It discusses the anatomy of the kidneys and nephron, stages of diabetic nephropathy, risk factors, morphological changes, and treatment focusing on glycemic and blood pressure control. It also covers lupus nephritis, defining it as renal involvement in systemic lupus erythematosus, occurring in 40-70% of patients, with features like proteinuria, hematuria, and reduced renal function. Morphological changes in diabetic nephropathy include glomerular and tubular hypertrophy, thickening of the glomerular and tubular basement membranes
The document discusses Addison's disease and Cushing's syndrome. It begins by describing the adrenal glands and their role in producing steroid hormones. It then covers the zones of the adrenal cortex and their hormone productions. Next, it explains Addison's disease as resulting from hypoadrenalism and describes its symptoms and treatment. It also outlines Cushing's syndrome as caused by hypersecretion of hormones and notes its physiological effects and treatment options.
This document discusses endocrine disorders of the adrenal gland. It covers conditions such as Cushing's syndrome, congenital adrenal hyperplasia, hyperaldosteronism, and adrenal insufficiency. Cushing's syndrome is caused by excess cortisol and can be ACTH-dependent or -independent. It presents with central obesity, moon facies, buffalo hump, and purple striae. Tests include urine cortisol and low-dose dexamethasone suppression. Treatment depends on the cause but may include surgery or medication. Primary adrenal insufficiency involves deficiencies of both glucocorticoids and mineralocorticoids.
This document discusses various fluid and electrolyte imbalances in the human body. It covers topics like:
- Types of fluid compartments and their normal volumes and electrolyte contents
- Causes, features, and treatment of dehydration, hypovolaemia, hypervolemia, and fluid overload
- Causes, features, and management of various electrolyte imbalances including hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia
- Importance of slow correction and monitoring in treating electrolyte abnormalities to avoid complications
It provides a comprehensive overview of fluid and electrolyte physiology and disturbances.
This document discusses disorders of the adrenal cortex. It begins by outlining the learning objectives, which are to understand the etiology, pathophysiology, clinical manifestations, diagnostics, treatment, nursing care, and complications of adrenal cortex disorders. It then provides an overview of adrenal gland disorders in general before focusing specifically on the adrenal cortex and its hormones. Key points covered include the causes, symptoms, diagnostic tests, and treatment of adrenal hypofunction conditions like Addison's disease and adrenal hyperfunction conditions.
The document discusses the anatomy and functions of the adrenal glands. It describes that the adrenal glands are composed of an outer cortex that produces cortisol and other hormones, and an inner medulla that produces epinephrine. Conditions like Cushing's syndrome can result from excess cortisol production and cause symptoms like high blood pressure, weight gain, and bone loss. Other disorders addressed include Conn's syndrome, adrenal insufficiency, and adrenocortical tumors.
The document discusses various known and unknown uremic toxins that accumulate in patients with chronic kidney disease. It describes small water-soluble compounds like urea, guanidines, oxalate, phosphorus, and metabolic acids. It also covers protein-bound compounds such as p-cresol, homocysteine, and discusses how their removal during dialysis is hampered due to strong protein binding. The document provides details on the effects of these uremic toxins and potential strategies to enhance their removal or reduce their levels.
Hyperaldosteronism, also known as Conn syndrome, is the most common cause of secondary hypertension, accounting for 5-13% of cases. It is characterized by hypokalemia in around half of patients with aldosterone-producing adenomas and 17% of patients with bilateral hyperplasia. Diagnosis involves measuring plasma renin activity and plasma aldosterone concentration along with confirmation tests such as saline loading, saline infusion, or fludrocortisone suppression. Adrenal vein sampling may be used if surgical treatment is an option to determine if hyperaldosteronism is unilateral or bilateral.
The document summarizes the embryology, histology, anatomy, functions and pathologies of the adrenal cortex and medulla. It discusses topics like Cushing syndrome, hypercorticism, hyperaldosteronism, and adrenogenital syndrome. Tests for adrenal cortical function include measuring plasma and urinary hormone levels, and stimulation/suppression tests to localize tumors. Imaging modalities like CT, MRI, and nuclear scans are used for diagnosis.
The parathyroid glands regulate calcium levels in the blood and are usually located near the thyroid gland. Hyperparathyroidism occurs when the parathyroid glands overproduce parathyroid hormone, leading to high calcium levels. It can be primary due to adenomas or hyperplasia, secondary due to kidney disease, or tertiary after kidney transplantation. Symptoms include bones issues like fractures, kidney stones, abdominal pain, and fatigue. Diagnosis involves blood tests showing elevated calcium and parathyroid hormone levels. Treatment is parathyroidectomy to remove the overactive gland(s), with autotransplantation of normal glands as an option.
This document discusses a case of polycythemia (high hematocrit) in a twin baby born at term. At 14 hours of life, the baby's hematocrit was 74% and was diagnosed with polycythemia. A partial exchange transfusion was done at 46 hours to lower the hematocrit. The document then provides background on polycythemia including definitions, causes, effects, screening recommendations, and technical aspects of partial exchange transfusions. Polycythemia can cause complications due to increased blood viscosity and is typically treated in symptomatic infants to prevent harm.
Hypercalcemia of malignancy novel management therapyVishal Ramteke
This document discusses the case of a 56-year-old woman with metastatic breast cancer and hypercalcemia that was refractory to treatment with zoledronic acid and calcitonin. She was started on cinacalcet and dexamethasone, and then administered denosumab injections to further lower her calcium levels. Denosumab binds to RANK ligand to inhibit bone resorption and reduce calcium levels. After receiving denosumab injections on days 1, 8, 15, 29 and 60, the patient's total calcium levels decreased from 13.9 to 7.7 mg/dl. The document discusses how denosumab has been used off-label for persistent hypercalcemia of malignancy.
The document discusses urinary incontinence, including its definition, types, causes, assessment, and treatment options. The main types of incontinence covered are stress, urge, mixed, overflow, and extra-urethral incontinence. Assessment involves history, physical exam including stress tests and pelvic floor strength tests, and investigations like urine tests, pad tests, uroflowmetry, and urodynamics. Treatment depends on the type but may include pelvic floor exercises, medications, bulking agents, slings, artificial sphincters, injections, and surgeries.
Haematological disorders PACES - Station 5 Mamdouh Dorrah
This document discusses the evaluation and management of hematological disorders like anemia. It covers taking a thorough history including symptoms, risk factors, medications and lifestyle. The physical exam focuses on signs of anemia. Initial investigations for anemia types include blood counts, iron, B12 and folate levels. Depending on the results, further testing may include endoscopies, biopsy or bone marrow examination to determine the underlying cause such as nutritional deficiencies, infections, cancers or autoimmune disorders. Pernicious anemia specifically requires serology to guide long term treatment.
1. Oncological emergencies refer to urgent clinical situations in cancer patients caused by cancer or its treatment.
2. Some examples discussed are hypercalcemia, tumor lysis syndrome, lactic acidosis, hypoglycemia, syndrome of inappropriate antidiuretic hormone secretion, superior vena cava syndrome, spinal cord compression, severe cystitis, bladder hemorrhage, disseminated intravascular coagulation, and cardiac tamponade.
3. The document provides details on symptoms, signs, and treatment approaches for each of these conditions.
This patient has a history of lysinuric protein intolerance (LPI) since age 3 and later developed lupus nephritis. LPI is caused by a defect in the SLC7A7 gene which impairs transport of cationic amino acids. This led to immunological issues and kidney involvement over time. A renal biopsy at age 4.5 showed proliferative glomerulonephritis consistent with lupus nephritis stage IV. Managing both conditions together has been challenging with various treatments over the years.
This document discusses disorders of the adrenal glands, including hyperactivity and hypoactivity. Hyperactivity disorders include Cushing's syndrome, hyperaldosteronism, and adrenogenital syndrome. Cushing's syndrome can be caused by excessive cortisol secretion from the pituitary gland (Cushing's disease) or the adrenal glands (Cushing's syndrome). Symptoms include obesity, muscle weakness, osteoporosis, hyperglycemia, and hypertension. Hypoactivity disorders include chronic and acute adrenal insufficiency (Addison's disease and Addisonian crisis), which can be caused by adrenal gland failure or damage. Signs of Addison's disease include pigmentation, muscular weakness, hypotension,
The document discusses renal function tests (RFTs). It provides information on:
- The functions of the kidney including homeostasis, excretion, and hormonal functions.
- Common RFTs including urine analysis, serum creatinine, BUN, eGFR, and cystatin C. These tests are used to evaluate glomerular filtration rate and detect kidney problems.
- Additional details are given on clearance tests using inulin, creatinine and urea to estimate GFR. Urine analysis and tests of tubular function are also summarized.
This document discusses disorders of the adrenal cortex related to mineralocorticoid excess and deficiency. It begins by covering the anatomy and physiology of the adrenal cortex and its role in synthesizing mineralocorticoids like aldosterone. It then examines the causes, clinical features, diagnostic evaluation and management of conditions involving mineralocorticoid excess, including primary and secondary hyperaldosteronism, as well as pseudo-hyperaldosteronism. It also reviews primary and secondary adrenal insufficiency related to deficiencies in mineralocorticoids and glucocorticoids. Flowcharts are provided outlining algorithms for evaluating patients with suspected mineralocorticoid excess or adrenal deficiency.
This document provides an overview of endocrine system revision covering the anatomy and physiology of the hypothalamus, pituitary gland, thyroid gland, adrenal glands, and pancreas. It discusses the hormonal regulation and feedback mechanisms of the HPA axis and describes various endocrine disorders like acromegaly, hypothyroidism, Cushing's syndrome, Addison's disease, and diabetes. The learning objectives, endocrine functions, and key hormones released by each endocrine organ are summarized.
This document provides an overview of renal involvement in systemic conditions like diabetes mellitus and systemic lupus erythematosus. It discusses the anatomy of the kidneys and nephron, stages of diabetic nephropathy, risk factors, morphological changes, and treatment focusing on glycemic and blood pressure control. It also covers lupus nephritis, defining it as renal involvement in systemic lupus erythematosus, occurring in 40-70% of patients, with features like proteinuria, hematuria, and reduced renal function. Morphological changes in diabetic nephropathy include glomerular and tubular hypertrophy, thickening of the glomerular and tubular basement membranes
The document discusses Addison's disease and Cushing's syndrome. It begins by describing the adrenal glands and their role in producing steroid hormones. It then covers the zones of the adrenal cortex and their hormone productions. Next, it explains Addison's disease as resulting from hypoadrenalism and describes its symptoms and treatment. It also outlines Cushing's syndrome as caused by hypersecretion of hormones and notes its physiological effects and treatment options.
This document discusses endocrine disorders of the adrenal gland. It covers conditions such as Cushing's syndrome, congenital adrenal hyperplasia, hyperaldosteronism, and adrenal insufficiency. Cushing's syndrome is caused by excess cortisol and can be ACTH-dependent or -independent. It presents with central obesity, moon facies, buffalo hump, and purple striae. Tests include urine cortisol and low-dose dexamethasone suppression. Treatment depends on the cause but may include surgery or medication. Primary adrenal insufficiency involves deficiencies of both glucocorticoids and mineralocorticoids.
This document discusses various fluid and electrolyte imbalances in the human body. It covers topics like:
- Types of fluid compartments and their normal volumes and electrolyte contents
- Causes, features, and treatment of dehydration, hypovolaemia, hypervolemia, and fluid overload
- Causes, features, and management of various electrolyte imbalances including hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia
- Importance of slow correction and monitoring in treating electrolyte abnormalities to avoid complications
It provides a comprehensive overview of fluid and electrolyte physiology and disturbances.
This document discusses disorders of the adrenal cortex. It begins by outlining the learning objectives, which are to understand the etiology, pathophysiology, clinical manifestations, diagnostics, treatment, nursing care, and complications of adrenal cortex disorders. It then provides an overview of adrenal gland disorders in general before focusing specifically on the adrenal cortex and its hormones. Key points covered include the causes, symptoms, diagnostic tests, and treatment of adrenal hypofunction conditions like Addison's disease and adrenal hyperfunction conditions.
The document discusses the anatomy and functions of the adrenal glands. It describes that the adrenal glands are composed of an outer cortex that produces cortisol and other hormones, and an inner medulla that produces epinephrine. Conditions like Cushing's syndrome can result from excess cortisol production and cause symptoms like high blood pressure, weight gain, and bone loss. Other disorders addressed include Conn's syndrome, adrenal insufficiency, and adrenocortical tumors.
The document discusses various known and unknown uremic toxins that accumulate in patients with chronic kidney disease. It describes small water-soluble compounds like urea, guanidines, oxalate, phosphorus, and metabolic acids. It also covers protein-bound compounds such as p-cresol, homocysteine, and discusses how their removal during dialysis is hampered due to strong protein binding. The document provides details on the effects of these uremic toxins and potential strategies to enhance their removal or reduce their levels.
Hyperaldosteronism, also known as Conn syndrome, is the most common cause of secondary hypertension, accounting for 5-13% of cases. It is characterized by hypokalemia in around half of patients with aldosterone-producing adenomas and 17% of patients with bilateral hyperplasia. Diagnosis involves measuring plasma renin activity and plasma aldosterone concentration along with confirmation tests such as saline loading, saline infusion, or fludrocortisone suppression. Adrenal vein sampling may be used if surgical treatment is an option to determine if hyperaldosteronism is unilateral or bilateral.
The document summarizes the embryology, histology, anatomy, functions and pathologies of the adrenal cortex and medulla. It discusses topics like Cushing syndrome, hypercorticism, hyperaldosteronism, and adrenogenital syndrome. Tests for adrenal cortical function include measuring plasma and urinary hormone levels, and stimulation/suppression tests to localize tumors. Imaging modalities like CT, MRI, and nuclear scans are used for diagnosis.
The parathyroid glands regulate calcium levels in the blood and are usually located near the thyroid gland. Hyperparathyroidism occurs when the parathyroid glands overproduce parathyroid hormone, leading to high calcium levels. It can be primary due to adenomas or hyperplasia, secondary due to kidney disease, or tertiary after kidney transplantation. Symptoms include bones issues like fractures, kidney stones, abdominal pain, and fatigue. Diagnosis involves blood tests showing elevated calcium and parathyroid hormone levels. Treatment is parathyroidectomy to remove the overactive gland(s), with autotransplantation of normal glands as an option.
This document discusses a case of polycythemia (high hematocrit) in a twin baby born at term. At 14 hours of life, the baby's hematocrit was 74% and was diagnosed with polycythemia. A partial exchange transfusion was done at 46 hours to lower the hematocrit. The document then provides background on polycythemia including definitions, causes, effects, screening recommendations, and technical aspects of partial exchange transfusions. Polycythemia can cause complications due to increased blood viscosity and is typically treated in symptomatic infants to prevent harm.
Hypercalcemia of malignancy novel management therapyVishal Ramteke
This document discusses the case of a 56-year-old woman with metastatic breast cancer and hypercalcemia that was refractory to treatment with zoledronic acid and calcitonin. She was started on cinacalcet and dexamethasone, and then administered denosumab injections to further lower her calcium levels. Denosumab binds to RANK ligand to inhibit bone resorption and reduce calcium levels. After receiving denosumab injections on days 1, 8, 15, 29 and 60, the patient's total calcium levels decreased from 13.9 to 7.7 mg/dl. The document discusses how denosumab has been used off-label for persistent hypercalcemia of malignancy.
The document discusses urinary incontinence, including its definition, types, causes, assessment, and treatment options. The main types of incontinence covered are stress, urge, mixed, overflow, and extra-urethral incontinence. Assessment involves history, physical exam including stress tests and pelvic floor strength tests, and investigations like urine tests, pad tests, uroflowmetry, and urodynamics. Treatment depends on the type but may include pelvic floor exercises, medications, bulking agents, slings, artificial sphincters, injections, and surgeries.
This document discusses the normal anatomy of the male and female urethra and various pathologies that can affect the urethra, as seen on medical imaging. For the male urethra, it describes the anatomy in detail and covers acquired inflammatory diseases like gonorrhea and nonspecific urethritis. It also discusses strictures, calculi, condyloma, and other conditions. For the female urethra, it briefly outlines the anatomy and mentions acquired urethral diverticula. Various imaging techniques for evaluating the urethra are also reviewed, including retrograde urethrography, ultrasonography, and others.
This document provides information about various bone tumors. It begins by describing the structure of long bones and bone cells. It then classifies bone tumors as either benign or malignant, and lists examples of tumors from bone, cartilage, fibrous tissue and other origins. For each tumor type, it provides details on characteristics such as typical age, location, symptoms, radiological features, pathology and treatment options. Some of the specific bone tumors covered include osteoma, osteoid osteoma, osteoblastoma, osteochondroma, chondroma, chondroblastoma and giant cell tumor.
1. Acute renal failure (ARF) is an acute, potentially reversible condition where the kidneys fail to maintain homeostasis. Causes include prerenal factors like shock, congestive heart failure, or intrarenal injury from toxins. Symptoms range from nonspecific like fever to specific kidney issues like electrolyte imbalances. Treatment focuses on fluid management, electrolyte replacement, and potentially dialysis.
2. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It is usually caused by congenital anomalies or acquired glomerular diseases. Symptoms emerge late and include fatigue, nausea, and cardiac/bone issues. Treatment manages complications and slows progression with a low protein
This document discusses urinary incontinence in females. It defines stress incontinence as the involuntary loss of urine during activities that increase abdominal pressure like coughing or sneezing. It notes that stress incontinence and detrusor instability are the most common causes. For stress incontinence, conservative treatments include pelvic floor exercises while surgical options aim to elevate and support the bladder neck. For detrusor instability, behavioral changes and medications are usually first-line management.
The document discusses the anatomy and functions of the prostate gland. It is located below the bladder and in front of the rectum. The prostate secretes fluid that nourishes sperm. Common prostate problems include enlarged prostate (BPH), prostate cancer, and prostatitis. BPH causes urinary symptoms due to pressure on the urethra. Prostate cancer develops from gland cells and can spread to other organs if not detected early. Diagnosis involves exams, tests like PSA, and biopsies. Treatment depends on the condition but may include medications, surgery, radiation, or watchful waiting.
This document provides an overview of benign prostatic hyperplasia (BPH) presented by Prof. Dr. Sherine Ragy. It discusses the gross anatomy of the prostate, zonal anatomy, vascular supply, pathophysiology including the role of androgens. It also covers the natural history, definitions, complications and diagnosis of BPH including history, IPSS scoring, examination, PSA, and additional investigations. Non-surgical and medical therapy options are summarized including watchful waiting, alpha-blockers, 5-alpha reductase inhibitors and plant extracts. Common alpha-blockers and their dosing are listed.
The document discusses various surgical approaches and techniques in urology. It describes approaches to the kidney such as flank, anterior transperitoneal, and thoraco-abdominal approaches. It also discusses approaches to the ureter, bladder, prostate, penis, inguinoscrotal structures, and endoscopic techniques such as flexible urethroscopy, rigid and flexible ureteroscopy, percutaneous nephrolithotomy, and laparoscopy. Diagrams illustrate the various incision sites and instrumentation used.
This document provides information on inguinal-scrotal lumps including:
[1] It discusses various pathologies that can present as inguinal-scrotal lumps such as hernias, cysts, tumors and lymphadenopathy. [2] It reviews the anatomy of the inguinal region including the inguinal canal, spermatic cord and testes. [3] It provides guidance on assessing patients with inguinal-scrotal lumps including taking a history, performing an examination and deciding when imaging or biopsy may be needed.
This document provides information on pediatric malignant solid tumors, including Wilms tumor (nephroblastoma), neuroblastoma, and rhabdomyosarcoma. It discusses the epidemiology, histology, clinical presentation, risk classification, diagnostic workup, and standard treatment approaches for each of these tumor types. Pediatric cancer is the second leading cause of death in children, though survival rates have improved to over 70% with modern multimodal therapy.
This document provides an overview of common pediatric solid tumors, including definitions, epidemiology, etiology, types, symptoms and signs, staging, diagnosis, treatment, and prognosis for each tumor type. The tumors discussed include lymphomas, nephroblastoma (Wilms tumor), neuroblastoma, hepatoblastoma, and hemangioma. For each tumor type, the summary defines the tumor, discusses prevalence and risk factors, describes common subtypes, and outlines the standard diagnostic and treatment approaches.
Congenital abnormalities by Erum KhowajaErum khowaja
Congenital abnormalities can affect many body systems and organs. They have various causes including chromosomal abnormalities, single gene defects, mitochondrial disorders, and environmental factors. Some examples of congenital abnormalities discussed in the document are gastroschisis, an abdominal wall defect where intestines protrude through the umbilicus, and exomphalos where abdominal contents protrude through a weakness in the abdominal wall near the umbilical cord. Atresias are congenital obstructions that can occur in different parts of the GI tract. Hirschsprung's disease is a blockage of the large intestine due to improper muscle movement. Malrotation and meconium ileus are examples of congenital abnormalities of the intestines.
This document provides an overview of common congenital anomalies of the genitourinary system. It discusses abnormalities of the kidneys, ureters, bladder, urethra, and genitals. For each anomaly, it describes the presentation, evaluation, and typical treatment approaches. Common anomalies covered include horseshoe kidney, pelviureteric junction obstruction, vesicoureteric reflux, duplication of the urinary system, ectopic ureter, uretrocele, undescended testis, hypospadias, epispadias, bladder extrophy, and posterior urethral valves.
Hematuria for undergraduates
this is a presentation i prepared for medical students about hematuria, hope u like it
for more urology resources visit:
www.uronotes2012.blogspot.com
This document discusses diseases of the adrenal cortex, including hyperadrenalism and hypoadrenalism. It describes three hyperadrenal clinical syndromes caused by excess production of cortisol, mineralocorticoids, or androgens. Cushing syndrome is discussed in depth, outlining its causes such as Cushing disease and ectopic ACTH secretion. Hyperaldosteronism and adrenogenital syndromes are also summarized. Hypoadrenalism includes primary and secondary causes, with Addison disease and acute adrenal crisis covered as examples of primary hypoadrenalism.
This patient has hypokalemia with metabolic alkalosis. The combination of hypokalemia and hypertension suggests hyperaldosteronism, likely primary hyperaldosteronism (Conn syndrome). Aldosterone causes increased sodium reabsorption and potassium secretion in the distal tubule of the kidney, resulting in hypokalemia and metabolic alkalosis. Further workup would include plasma aldosterone and renin levels.
Cushing's syndrome is caused by excessive cortisol levels due to hyperfunction of the adrenal glands or pituitary gland. It results in central obesity, mood changes, high blood pressure, and other signs and symptoms. The dexamethasone suppression test is used to diagnose Cushing's syndrome by showing that cortisol levels are not suppressed as expected. Addison's disease is caused by primary adrenal insufficiency leading to cortisol and aldosterone deficiencies. Patients present with weakness, low blood pressure, and hyperpigmentation. The short Synacthen test shows no increase in cortisol levels in response to synthetic ACTH stimulation. Both conditions require lifelong hormone replacement therapy and treatment of underlying causes.
This document provides information on Cushing's syndrome, including its definition, epidemiology, causes, clinical features, investigations, treatment, and follow-up. Cushing's syndrome results from excess cortisol secretion and can be fatal if left untreated. It is rare, affecting about 2 per million people annually. The causes include pituitary adenomas (68% of cases), ectopic ACTH secretion (12%), and adrenal tumors (18%). Clinical features include weight gain, high blood pressure, and mood disturbances. Investigations involve tests to evaluate cortisol levels and distinguish ACTH-dependent from independent causes. Treatment options are surgery, radiation, medication, and adrenalectomy. Follow-up aims to detect recurrence through monitoring cortisol
Tumor lysis syndrome occurs when cancer cells release their contents into the bloodstream, causing electrolyte imbalances like hyperkalemia, hyperuricemia, and hyperphosphatemia that can damage organs. It is diagnosed when a patient develops acute kidney injury, arrhythmias, or seizures from their electrolyte changes. Treatment involves rapid hydration, uric acid-lowering drugs like allopurinol or rasburicase, and dialysis for severe electrolyte abnormalities or kidney injury. With advances in prevention and management, the prognosis for tumor lysis syndrome has improved in recent years.
The document discusses various diagnostic tests and procedures. It begins by outlining the phases of diagnostic testing as pre-test, intra-test, and post-test phases. It then describes specific tests like the complete blood count, which measures components of blood, and serum electrolyte testing, which evaluates electrolyte levels important for various body functions. The document provides details on normal ranges and clinical implications of results for these common lab investigations.
A 36-year-old male patient with HIV and alcoholism is brought to the emergency department in a comatose condition by his neighbour. Initial labs show signs of rhabdomyolysis including elevated creatine kinase, hypokalemia, hypophosphatemia, and reddish-brown urine. The patient is at risk for rhabdomyolysis due to alcoholism, cocaine and heroin use, hypokalemia, and hypophosphatemia. Creatine kinase is the most appropriate serum test to evaluate for rhabdomyolysis in this patient.
Cushing's syndrome is also called Hypercortisolism. Cushing's syndrome occurs due to high cortisol levels for a prolonged duration in the human body. However, the two terms namely Cushing's syndrome and Cushing's disease are not similar.
Cushing's disease is one cause of Cushing's syndrome characterized by increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland. Causes various physiological alterations in human systems. Affects an estimated 10-15 million people per year. Cushing’s syndrome most commonly affects adults aged 20-50 years and is more prevalent in females than males. Treatment of Cushing’s syndrome depends on the underlying cause of excess cortisol, the use of cortisol-inhibiting drugs but may include surgery, radiation, and chemotherapy.
Rhabdomyolysis is the destruction or disintegration of striated muscle resulting in the leakage of intracellular contents into circulation. It has many causes including trauma, compression injuries, exertion, drugs, infections, and metabolic disorders. The pathophysiology involves an influx of extracellular sodium, water and calcium into muscle cells and an efflux of intracellular potassium and myoglobin. Diagnosis is based on markedly elevated creatine kinase and presence of myoglobin in urine. Treatment focuses on aggressive fluid resuscitation, urine alkalinization, and renal replacement therapy if acute kidney injury develops to prevent complications.
Oncologic Emergencies and Symptom Managementflasco_org
1) Oncologic emergencies include conditions like hypercalcemia, tumor lysis syndrome, SIADH, hyperviscosity states, and increased intracranial pressure that require immediate medical intervention.
2) Tumor lysis syndrome occurs when cancer cells die off rapidly, releasing electrolytes and metabolites that can overwhelm the kidneys, potentially causing renal failure, arrhythmias or seizures. It is treated by managing individual electrolyte abnormalities and renal failure.
3) Increased intracranial pressure in cancer patients can be caused by vasogenic edema, hemorrhage, or obstruction of cerebrospinal fluid flow. Symptoms include headache, vomiting and altered mental status. Treatment involves steroids
Cushing's syndrome is defined as a state of chronic glucocorticoid excess leading to symptoms and signs of hypercortisolism regardless of the cause. The most common cause is Cushing's disease, which is due to excessive ACTH secretion from a pituitary tumor. Other causes include ectopic ACTH syndrome from a non-pituitary tumor and adrenal tumors such as adenomas. Clinical features include central obesity, hypertension, skin changes like striae, psychiatric symptoms, and metabolic derangements. Diagnosis involves biochemical testing for hypercortisolism and imaging tests to determine the underlying cause. Treatment depends on the specific cause but may include pituitary surgery, radiotherapy, or medical therapy with drugs. Prognosis
The adrenal glands are located above the kidneys and produce several important hormones. The adrenal cortex produces cortisol, aldosterone, and androgens. Cortisol aids metabolism and reduces inflammation. Aldosterone regulates sodium and potassium levels. Androgens influence sex drive. The adrenal medulla produces epinephrine and norepinephrine which help the body respond to stress. Diseases can occur if the adrenal glands produce too much or too little of these hormones.
Cushing syndrome is characterized by excess cortisol secretion caused by too much ACTH from the pituitary gland or excess cortisol from adrenal tumors. It presents with weight gain, thin extremities, moon face, skin changes, and metabolic complications. Diagnosis involves urine and blood tests to measure cortisol levels. Treatment depends on the underlying cause but may include surgery to remove tumors, radiation therapy, or medications to reduce cortisol levels. Nursing care focuses on preventing infections, injuries, skin breakdown and improving nutrition, fluid balance and body image.
Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. It is most often caused by gallstones or heavy alcohol use. A patient presents with acute upper abdominal pain that may radiate to the back. Laboratory tests show elevated pancreatic enzymes and imaging can identify gallstones or complications. Severity is assessed by the presence of organ failure or local complications like necrosis. Treatment involves fluid resuscitation and management of complications. The Ranson criteria uses factors at admission and within 48 hours to predict severe acute pancreatitis.
This document provides an overview of hematologic disorders and summarizes several types of anemias and myeloproliferative disorders. It describes the components of blood and the process of hematopoiesis. Key points about iron deficiency anemia include its microcytic, hypochromic appearance and common causes like blood loss or dietary deficiencies. Pernicious anemia results from vitamin B12 deficiency due to lack of intrinsic factor. Folic acid deficiency can also cause megaloblastic anemia. Aplastic anemia is a bone marrow failure disorder causing pancytopenia. Polycythemia vera involves overproduction of all blood cell lines. Leukemias are malignant disorders involving accumulation of immature blood cells with
The document discusses disorders of the adrenal gland, including glucocorticoid excess (Cushing's syndrome), mineralocorticoid excess (Conn's syndrome), and adrenal insufficiency (Addison's disease). It covers the anatomy and function of the adrenal cortex and medulla, signs and symptoms, diagnosis, and anesthetic considerations for surgeries involving the adrenal gland.
The document discusses the anatomy and clinical features of the anal canal and hemorrhoids. Key points include:
- The anal canal is 4 cm long and is lined by different types of epithelium above and below the pectinate line.
- Hemorrhoids are varicosities of the superior rectal veins that can be internal or external. They cause symptoms like bleeding with defecation and prolapse.
- Treatment depends on the grade of hemorrhoids and may include conservative measures, injections, banding, or surgery for more severe cases.
This document summarizes surgical treatments for several pleural diseases:
1) Pneumothorax is treated with observation for small cases or tube thoracostomy for large/symptomatic cases. Surgery like VATS is used for recurrent cases.
2) Empyema is diagnosed by pleural fluid analysis and treated initially with tube thoracostomy and fibrinolytics. Thoracoscopy or decortication surgery is used for later stages with loculations.
3) Mesothelioma is associated with asbestos exposure and difficult to diagnose, often requiring biopsy. Treatment options provide limited success.
The document provides guidance on performing an abdominal examination. It describes general rules for both the examiner and patient. Inspection begins with observing the contour of the abdomen and proceeds down the midline, noting features like the subcostal angle, epigastric pulsation, and umbilicus. Palpation techniques including light superficial palpation and deeper palpation are outlined. The spleen can be palpated using various methods like bimanual examination in both the supine and right lateral positions. Nature of any palpable spleen should be commented on.
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4. 2. Zona fasciculata : secretes glucocorticoids,
mainly cortisol (hydrocortisone ).
Metabolic effects of cortisol
• On fat (in excess) mobilization & deposition in
abnormal sites.
• On proteins catabolic, (in excess) muscle
wasting & osteoporosis.
• On carbohydrates : ↑ gluconeogenesis & ↓
glucose uptake by the muscle cells, (in excess)
hyperglycaemia.
• On H2O & electrolytes Na & H2O retention & K
excretion. o On blood (bone marrow) ↑RBCs & ↓
eosinophils & lymphocytes.
• Androgenic.
• Anti-allergic (tend to – Ag - Ab reaction).
• Anti - inflammatory (& in excess - fibrous tissue
formation & destroys elastic fibers ).
5. N.B.:
• Zona fasciculata is under the control of
ACTH.
• ACTH is derived from a large precursor
molecule which also gives rise to melanocyte
stimulating hormone, lipotropin & endorphins
(POMCpro-opio-melano-cortin).
3. Zona reticularis :
• Secretes sex hormones, mainly androgens &
small amount of oestrogen & progesterone.
• The main androgen is dehydro-
epiandrosterone which enhances protein
anabolism & promotes the development of
male 2ry sexual characters "& sexual hair in
♀.
• The end products of androgens are 17
ketosteroids ( which are excreted in urine).
• It is under the control of A.C.T.H.
N.B.
• Sources of androgens:
• In ♂ (adrenal, testes).
• In ♀ (adrenal).
7. Clinical picture:
1. Hypertension : may be severe, due to
Na retention.
2. Hypokalaemia : leading to :
• Apathy, Paraesthesia.
• Arrhythmias as extrasystoles.
• Atony of intestine constipation &
even paralytic ileus.
• Muscle weakness & even episodic
paralysis (& if the respiratory
musclesare affected dyspnea).
• Impaired glucose tolerance (in 50%)
because K has a direct effect on
insulin release from B cells & may
influence insulin action.
8. 3. Alkalosis "metabolic": Due to
heavy loss of H+ in urine tetany.
4. Absence of oedema : due to
K diuresis polyuria.
Impaired tubular reabsorption of
water (renal concentration defect)
polyuria "due to prolonged
Hypokalaemia".
10. N.B.
• Plasma renin level is high in cases of 2ry
hyperaldosteronism.
– You must stop ttt of HPN before
measurement of renin
• Aldosterone : high despite high Na load
(N=3 - 15ng/dl)
N.B.
• In 2ry hyperaldosteronism, aldosterone level can
be ↓by Na load.
• 4. U/S& adrenal CT.
11. Differential diagnosis :
a. From hypertensive conditions
associated with Hypokalaemia :
• Hypertension "malignant or renal" with
2ry hyperaldosteronism.
• Diuretics causing Hypokalaemia in
hypertensive patient.
• Cushing syndrome, CAH & rarely
Juxtaglomerular hyperplasia.
• Intake of exogenous
mineralocorticoids.
• K-losing nephropathies causing or
associated with HPN e.g. bartter's
syndrome, Liddle's syndrome.
b. From other causes of
Hypokalaemia & familial periodic
12. Treatment:
Surgical removal of the adenoma
(after correction of the electrolyte
imbalance).
Medical ttt:
• In bilateral adrenal hyperplasia.
• Amiloride (40mg/day) is preferable
to spironolactone (which leads to
gynaecomastia & impotence on
chronic use ).
13. CUSHING'S
SYNDROME
Causes:
Endogenous Cashing syndrome "
rare, yearly incidence of one/million".
Pituitary cushing syndrome
(cushing disease ).
• The most common cause of
endogenous Cushing (75 %).
• 80 % are caused by pituitary basophil
micro-adenoma secreting excessive of
ACTH " the remaining cases may be of
hypothalamic origin".
• it is commoner in ♀ than ♂.
14. Adrenal Gushing syndrome : (20
%)
• Caused by autonomous cortisol
production from adenoma, carcinoma
or hyperplasia of adrenals.
Ectopic Gushing syndrome :
( autonomous ACTH production ) e.g.
• Bronchogenic carcinoma, pulmonary
carcinoid.
• Thymoma, ovarian or pancreatic
carcinoma.
16. Clinical picture:
Abnormal deposition of fat in
certain sites :
• In the face becomes rounded
with bloated cheeks ( Moon face).
• In the interscapular region
(Buffalo hump).
• In the breasts & abdomen
(Trunkal obesity), but the buttocks
are hollow with thin limbs (lemon
on match sticks).
17.
18. Disturbances in protein
metabolism :
• ↑protein catabolism muscle
wasting & weakness (even proximol
myopathy).
• Osteoporosis :
• Kyphosis, shortening
• Pathological fractures.
• Bruises & purpura (due to ↓support of
blood vessels).
• Delayed healing of wounds.
• Stria rubra:
• Due to rupture of weakened s.c. collagen
fibers (together with fat mobilization)
purplish lines in the skin around the
19.
20. Disturbances in carbohydrate
metabolism :
• Hyperglycaemia & may end in
D.M. (in 15% of cases) which is
somewhat insulin resistant
(steroid diabetes)
Disturbances in fluid &
electrolytes balance :
• Na retention hypertension.
• Hypokalaemia polyuria,
alkalosis.
21. Sexual manifestations :
• In females
• Amenorrhea.
• Acne.
• Hirsutism.
• In males
↓sexual desire,
Impotence ↑estrogen.
22. General manifestations
• Plethoric face due to
polycythaemia.
• Psychiatric disturbances:
common, usually in the form of
depression.
• Obesity & stunted growth may
be the main presenting feature
in childhood.
23. Features suggesting the
aetiology :
• Evidence of virilizatation (Is most
common in) adrenal carcinoma.
• Hypokalaemic alkalosis, myopathy &
hyperpigmentation (occur most often
in) Ectopic Cushing syndrome ( the
distinguishing clinical features of
hypercortisolism are often absent).
• Age & sex :
• Children (more common in) adrenal
carcinoma.
• Adult ♂ Ectopic Cushing.
• ♀ in childbearing age " pituitary
Cushing.
26. Investigations which confirm
cushing syndrome.
• Plasma cortisol level :(N=5-20ug/dl) " at
8 AM "
The earliest indication of increase
cortisol secretion is loss of the diurnal
variation (circadian rhythm) " normally,
plasma cortisol level at 4 p. m. is <
50% of that at 8 a.m
N.B.
• Then, there is persistent elevation.
• Recently diurnal variation can be
detected by salivary cortisol.
27. • Urinary steroid excretion :
Hydroxy corticosteroids (17 oH Cs).
Urinary free cortisol excretion (the
most reliable index of
hypercortisolism).
• Overnight dexamethasone
suppression test:
Dexamethasone 1 mg is given orally
at night ( 11 pm ) & plasma is
obtained at 8 am the following
morning cortisol level <7ug/<dL
exclude hypercortisolism.
28. Investigations to differentiate
between the 3 forms of cushing
syndrome:
• Plasma ACTH:
Very high in Ectopic Gushing.
High in pituitary Cushing.
Low or absent in adrenal Cushing.
• CRH stimulation test: (1ug/kg I.V.)
ACTH & cortisol levels in pituitary
Cushing.
No effect —> in Ectopic or adrenal.
29. • High dose dexamethasone suppression test:
2 mg / 6 hours for 2 days is given orally.
In pituitary Cushing 50 % ↓of 24 hours
excretion of 17 OHCs or the plasma cortisol.
In adrenal or Ectopic Cushing no effect.
N.B. BIPSS
• Localization procedures :
Abdominal U/S & C.T. of adrenals for
adrenal tumours.
Sellar X-ray detects 10 - 15 % of pituitary
tumours & C.T. detects 85% of
microadenomas ( MRI is better ).
Chest x-ray -. for bronchial carcinoma.
30. Differential
diagnosis:• Exogenous obesity, essential HPN &
D.M. occurring separately or
combined :In such cases :
• Obesity is generalized.
• Plasma cortisol & urinary end products
normal.
• Other causes of obesity : e.g.
Myxoedema, Frohlich's syndrome, ..etc
• Other causes of Hirsutism.
• Other causes of osteoporosis.
31. • Women on oral oestrogen - containing
C.C.P.s may become overweight & may
have higher levels of plasma cortisol
(due to↑cortisol binding globulin).
• Patients suffering from LCF may
develop Cashing - like manifestations
due to impaired cortisol metabolism. In
such cases, plasma cortisol level is
raised but, manifestations of LCF are
prominent.
32. N.B.
• Pseudo - Cushing syndrome :
Chronic alcoholism, acute
severe illness, obesity &
depression may be associated
with mild ↑in cortisol levels &
absent diurnal variation.
33. Treatment:
Pituitary Cushing :
Surgery :
• Trans-sphenoidal hypophysectomy.
• Remission (85%).
• Complications...
Irradiation : e.g. Proton beams, alpha particles.
After ttt Cortisone for life.
Medical:
• Drugs that inhibit ACTH release e.g
CYPROHEPTADINE,VALPROATE;
BROMOCRIPTINE .
• Drugs that inhibit steroidogenesis e.g
KETOCNAZOL.
34. Adrenal Cushing :
Adrenal adenoma: removal.
N.B.
• Post-operative glucocorticoids replacement is
necessary for several months until function
returns in contralateral previously suppressed
gland.
Adrenal carcinoma removal.
• Preoperative ttt.: with enzyme inhibitor "
Metyrapone"
11 deoxycortisol cortisol
• Post-operative : Give mitotane " for residual
disease.
35. Ectopic Cushing :
• Surgical removal of the
tumour. Or
• Metyrapone ± Mitotane.
36. ADDISON'S DISEASE
Chronic adrenal failure = adrencortrical
insufficiency
= adrenal hypocorticism
Causes :
• 1. Auto-immune adrenalitis : ( most common cause,
70%)
N.B.
This may occur alone or in combination with other auto-
immune endocrine insufficiency including IDDM,
hypothyroidism (& sometimes hypogonadism,
Hypoparathyroidism or pernicious anaemia ) " Schmidt
syndrome " .
• 2. T.B. of the adrenal glands (10-20%).
• 3. Following bilateral adrenalectomy & congenital
enzymatic defects.
• 4. Sarcoidosis, secondaries, amyloidosis or
haemochromatosis (rare causes ).
37. Clinical picture:
Onset is usually insidious, mostly in the adult
life & the course is slowly progressive.
• Asthenia :
Weakness of muscles; Weight loss.
Due to : * Lack of cortisol.
* Hyperkalaemia.
* Hypoglycaemia.
+ muscles cramps due to hyponatraemia.
38. • Hypotension
Systolic blood pressure > 110
mmHg excludes Addison's
disease.
Postural hypotension
common due to hypovalaemia &
dehydration.
• Hypoglycaemia: leading to:
Drowsiness, hunger pain & even
coma.
39. • Hyperpigmentation: of skin & m.m.
Sites :
• Face, neck, groins, axillae, nipples,
friction areas, scars as umbilicus, areas
exposed to sunlight.
• m.m. of mouth, tongue, rectum (state
coloured patches).
Causes :
• Hypocorticism ACTH ↑melanocyte
stimulating hormone (& lipotropin) ↑
pigmentation.
• Destruction of the adrenal medulla :
diversion of tyrosine to form melanin
instead of adrenaline & noradrenaline.
40. N.B.
• Leucoderma may occur as a
part of autoimmune
disturbance.
• Hyperpigmentation isn't a
feature of Simmond's ,
disease.
41.
42. • Loss of adrenal androgen :
• ↓axillary & pubic hair in ♀(but in ♂, testicular
androgen is preserved).
• Infertility & amenorrhea in females.
• GIT disturbances :
• Nausia, vomiting, diarrhea (& even steatorrhea).
• Polyuria : due to Na diuresis .
• There may be tenderness in the renal angle in
T.B. of adrenals.
N.B.
The patients may present with Addisonian
crisis ( see later ).
43. Investigations:
• ↓plasma cortisol level.
• ↓24 hour urinary cortisol, 17 oHCs
or 17 Ks ( ketosteroids ).
• ACTH stimulation test " synacthen
test" ( 0.25 mgI.M. or I.V.)
• Normal response plasma cortisol ↑by
6 ug / dl above the basal value.
• In 1ry adrenal insufficiency no
response.
• In 2ry adrenal insufficiency normal
response
45. • Investigation to find the
cause :
• Adrenal antibodies - in
autoimmune Addison.
• X-ray:
- adrenal calcification in T.B. cases.
- evidence of pulmonary T.B.
46.
47. Differential
diagnosis:
• D.D. from 2ry hypo – adrenalism
• Other causes of pigmentation e.g.
racial, haemochromatosis, porphyria &
ancanthosis nigricans,
neurofibromatosis.
• Asthenia & pigmentation may occur
also in : e.g. pellagra, CML (especially,
in patients on busulfan therapy), CRF,
chronic arsenic poisoning,
thyrotoxicosis, advanced malignancy,
Malabsorption syndrome.
48. Treatment:
Replacement therapy :
• Glucocorticoids prednisolone 5 mg
in the morning & 2.5 mg in the
evening.
• Mineralocorticoids fludrocortisone
0.1 mg every other day.
N.B.
• Active T.B. cases should receive
anti-T.B. therapy.
49.
50. Acute Adrenal
Failure
Addisonian Crisis• Causes :
•In addison's disease :
• Previously undiagnosed patients may
present in crisis either spontaneously or
ppted by intercurrent illness.
• Patients already on ttt, on facing severe
intercurrent illness without increasing the
replacement dose.
•In sheehan syndrome if
ttt is initiated with thyroxin alone
without cortisone.
• After bilateral adrenalectomy (
or pituitary surgery ).
51. • After sudden corticosteroid
withdrawal.
• Acute meningococcal septicaemia
(waterhouse friderichsen syndrome).
Hge may occur in the adrenal gland
acute adrenal failure.
• Medical ttt for adrenal carcinoma
( e.g. with metyrapone, mitotane ).
• Massive thrombosis of adrenal
veins ( during pregnancy, puerperium &
burns).
52. Clinical Picture:
• Sudden onset of severe
weakness, mental confusion,
abdominal pain, anorexia;
nausia, vomiting, diarrhea.
• Dehydration shock.
• If not treated coma & death
within 24 hours.
54. Treatment of
addisonian crisis :
• Correction of volume depletion &
electrolyte status by I.V. saline &
glucose" 10 %".
• Hydrocortisone ( Solucortif) 100 mg
I.V. then 100 mg as I.V. infusion / 8 hours
(in 5 % glucose) then gradual tapering (
until the maintenance dose is reached
within 5 days ).
• Fludrocortisone: 0.1mg/day (added-
when the daily dose of hydrocortisone
has reached 100 mg/day).
• Proper ttt of infections & precipitating
factor.
56. CONGENITAL ADRENAL
HYPERPLASIA
" Adrenogenital Syndrome
"
• Definition :
Group of condition caused by
inherited enzymatic defects in the
enzymes necessary for the synthesis
of cortisol ↓cortisol ↑ ACTH
adrenal hyperplasia & ↑synthesis of
the hormone proximal to the block.
• Causes :
57. Enzyme
↓
Hormonal
changes
Clinical
features
17 oH ase ↓"
extremely
rare"
↓ glucocorticoids &
sex hormones.
↑mineralocorticoids.
HPN & Hypokalaemia.
In females sexual
infantilism.
In males
♂pseudohermaphroditism
21 oH ase ↓, "
it is the
commonest
form "
↓ glucocorticoids
&
mineralocorticoi
ds.
↑sex steroids
Salt losing syndrome :
Due to aldosterone ↓:
Hypotension.
Hyperkalaemia
-
♀ pseudohermaphroditism
-♂ precocious puberty
11 B oH ase
↓"accounts for
↑11deoxycorticosterone,
deoxycortisol &
androgens.
↓cortisol
Hypertension.
Virilization ♀
pseudohermaphroditism ♂
58. N.B.
• Pseudohermaphroditism :
(phenotypic sex disturbance ).
• True hermaphroditism :
(chromosomal sex disturbance).
[Differentiated by doing sex
chromatin pattern].
59. Treatment:
1. Replacement therapy :
• Prednisolone ( 7.5 mg / day ).
• To replace the deficient cortisol in
glucocorticoids deficient forms.
• --ACTH:
↓blood pressure in hypertensive
forms.
↓androgen in virilizing forms.
• Fludrocortisone (0.1mg/day) in
mineralocorticoid deficient forms.
60. Surgical correction :
• For ♀pseudohermaphroditism .
N.B.
In ♂ pseudohermaphroditism
male functioning is impossible
& so female sex assignment is
advisable surgical correction
of genitalia & gonadectomy are
required plus oestrogen
administration relatively
normal but infertile ♀.