This document presents the case of a 56-year-old woman with longstanding diarrhea. Testing revealed elevated fasting serum gastrin levels over 1,200 pg/ml, indicating Zollinger-Ellison syndrome caused by a gastrinoma tumor. Imaging found thickened gastric folds and a slightly prominent pancreatic head. Biopsy of a duodenal nodule showed gastric metaplasia. The patient's basal acid output was greatly elevated at 57.4 mmol/hr, confirming the diagnosis of Zollinger-Ellison syndrome. Due to her obesity and risks from surgery, she was treated medically with ranitidine and propantheline, which controlled her symptoms and acid levels despite ongoing hypergastrine
This document provides information about non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). It discusses the pathogenesis of NAFLD/NASH involving insulin resistance and a two-hit model. It provides details on risk factors, clinical presentation, diagnosis, staging of disease, and treatment recommendations focusing on lifestyle changes like diet and exercise.
This document discusses endocrine tumors of the pancreas, focusing on insulinomas. It describes the investigations and treatment for insulinomas, which are the most common functional pancreatic endocrine tumor. Insulinomas originate from beta cells in the pancreas and cause hypoglycemia. Diagnosis involves demonstrating hypoglycemia along with high levels of insulin and C-peptide. Treatment is surgical resection, which is curative for benign insulinomas. For malignant insulinomas, the median survival time is 5 years.
Pancreatic neuroendocrine tumors (pNETs) are the most common endocrine tumors of the abdomen. Insulinomas are a functional type of pNET that secretes excess insulin, causing hypoglycemia. Insulinomas are typically benign and solitary tumors located within the pancreas that are challenging to localize due to their small size. Diagnosis involves demonstrating hypoglycemia along with inappropriately elevated insulin and C-peptide levels during fasting. Localization methods include CT, MRI, EUS, and arterial calcium stimulation with selective catheterization and venous sampling, with EUS and arterial calcium stimulation being the most sensitive. Complete surgical resection remains the primary treatment for insulinomas.
This document provides an overview of nonalcoholic fatty liver disease (NAFLD). It defines NAFLD and discusses its prevalence, risk factors, pathogenesis involving insulin resistance and lipid peroxidation, natural history including progression to nonalcoholic steatohepatitis (NASH) and fibrosis, clinical features such as elevated liver enzymes and asymptomatic presentation, diagnosis using imaging and biopsy, and treatment options focusing on weight loss through diet and exercise. The pathogenesis involves fat accumulation due to insulin resistance followed by lipid peroxidation and inflammation. Sustained weight loss through lifestyle changes is the primary treatment recommendation.
TCELL - Case Presentation-2 - Copy.pptxDrAijazTalani
This document describes the case of a 5-year-old female child admitted with abdominal distension and increased appetite. Examination found hepatomegaly and distension. Tests showed elevated liver enzymes and lipids. She was diagnosed with glycogen storage disease (GSD), likely type 1a based on symptoms and tests. GSD results from a deficiency in glycogen breakdown enzymes in the liver. Type 1 is the most common type, caused by glucose-6-phosphatase deficiency leading to hypoglycemia and hepatomegaly. Management involves frequent feedings and cornstarch to maintain blood glucose levels.
This document discusses acute pancreatitis, including:
- The pathophysiology of acute pancreatitis involving autodigestion of the pancreas from digestive enzymes.
- Common causes like gallstones, alcohol use, and hypertriglyceridemia.
- Diagnosis using clinical signs/symptoms confirmed with blood tests like serum amylase and lipase and imaging like CT scans.
- Determining severity using criteria like Ranson score, APACHE II score, and evidence of organ failure or complications on CT scan.
- Treatment focuses on pain control, IV fluids, nutritional support like enteral feeding, and antibiotics only for infected pancreatic necrosis.
This document provides an overview of acute pancreatitis including:
- The pathophysiology of premature activation of digestive enzymes within the pancreas leading to autodigestion.
- Common etiologies like gallstones, alcohol use, and hypertriglyceridemia.
- Diagnosis through clinical signs/symptoms confirmed with lab tests like serum amylase and lipase levels or imaging like CT.
- Determining severity using criteria like Ranson score, APACHE II score, or evidence of organ failure/necrosis on CT.
- Goals of treatment include halting disease progression, preventing organ failure through aggressive hydration and nutritional support, adequate pain control, and ERCP for severe gall
This document provides information about non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). It discusses the pathogenesis of NAFLD/NASH involving insulin resistance and a two-hit model. It provides details on risk factors, clinical presentation, diagnosis, staging of disease, and treatment recommendations focusing on lifestyle changes like diet and exercise.
This document discusses endocrine tumors of the pancreas, focusing on insulinomas. It describes the investigations and treatment for insulinomas, which are the most common functional pancreatic endocrine tumor. Insulinomas originate from beta cells in the pancreas and cause hypoglycemia. Diagnosis involves demonstrating hypoglycemia along with high levels of insulin and C-peptide. Treatment is surgical resection, which is curative for benign insulinomas. For malignant insulinomas, the median survival time is 5 years.
Pancreatic neuroendocrine tumors (pNETs) are the most common endocrine tumors of the abdomen. Insulinomas are a functional type of pNET that secretes excess insulin, causing hypoglycemia. Insulinomas are typically benign and solitary tumors located within the pancreas that are challenging to localize due to their small size. Diagnosis involves demonstrating hypoglycemia along with inappropriately elevated insulin and C-peptide levels during fasting. Localization methods include CT, MRI, EUS, and arterial calcium stimulation with selective catheterization and venous sampling, with EUS and arterial calcium stimulation being the most sensitive. Complete surgical resection remains the primary treatment for insulinomas.
This document provides an overview of nonalcoholic fatty liver disease (NAFLD). It defines NAFLD and discusses its prevalence, risk factors, pathogenesis involving insulin resistance and lipid peroxidation, natural history including progression to nonalcoholic steatohepatitis (NASH) and fibrosis, clinical features such as elevated liver enzymes and asymptomatic presentation, diagnosis using imaging and biopsy, and treatment options focusing on weight loss through diet and exercise. The pathogenesis involves fat accumulation due to insulin resistance followed by lipid peroxidation and inflammation. Sustained weight loss through lifestyle changes is the primary treatment recommendation.
TCELL - Case Presentation-2 - Copy.pptxDrAijazTalani
This document describes the case of a 5-year-old female child admitted with abdominal distension and increased appetite. Examination found hepatomegaly and distension. Tests showed elevated liver enzymes and lipids. She was diagnosed with glycogen storage disease (GSD), likely type 1a based on symptoms and tests. GSD results from a deficiency in glycogen breakdown enzymes in the liver. Type 1 is the most common type, caused by glucose-6-phosphatase deficiency leading to hypoglycemia and hepatomegaly. Management involves frequent feedings and cornstarch to maintain blood glucose levels.
This document discusses acute pancreatitis, including:
- The pathophysiology of acute pancreatitis involving autodigestion of the pancreas from digestive enzymes.
- Common causes like gallstones, alcohol use, and hypertriglyceridemia.
- Diagnosis using clinical signs/symptoms confirmed with blood tests like serum amylase and lipase and imaging like CT scans.
- Determining severity using criteria like Ranson score, APACHE II score, and evidence of organ failure or complications on CT scan.
- Treatment focuses on pain control, IV fluids, nutritional support like enteral feeding, and antibiotics only for infected pancreatic necrosis.
This document provides an overview of acute pancreatitis including:
- The pathophysiology of premature activation of digestive enzymes within the pancreas leading to autodigestion.
- Common etiologies like gallstones, alcohol use, and hypertriglyceridemia.
- Diagnosis through clinical signs/symptoms confirmed with lab tests like serum amylase and lipase levels or imaging like CT.
- Determining severity using criteria like Ranson score, APACHE II score, or evidence of organ failure/necrosis on CT.
- Goals of treatment include halting disease progression, preventing organ failure through aggressive hydration and nutritional support, adequate pain control, and ERCP for severe gall
Masterclass Liver Care - Vitafoods 2016Koen Jacobs
The liver performs many essential functions including detoxification, protein synthesis, production of biochemicals for digestion, storing glycogen, and decomposing red blood cells. Liver disease can result from alcohol use, viruses, autoimmune conditions, genetic disorders, or non-alcoholic fatty liver disease (NAFLD). NAFLD occurs when excess fat accumulates in the liver and is increasing worldwide due to the rise in obesity and metabolic syndrome. Poor diet and lifestyle factors contribute to NAFLD progression. Choline plays an important role in liver health by supporting phospholipid membranes, lipoprotein synthesis, and methylation reactions, and higher intakes may be needed to prevent NAFLD.
The document discusses diseases of the pancreas, including congenital anomalies, endocrine and exocrine pancreatic diseases, acute and chronic pancreatitis, and pancreatic tumors. It provides details on the causes, pathophysiology, clinical presentation, diagnosis, and treatment of each condition. Key points include the role of gallstones and alcohol as common causes of acute pancreatitis, the use of CT and lab tests to diagnose and determine severity, and supportive care along with surgical or endoscopic interventions for severe cases.
This document summarizes multiple endocrine neoplasia type 1 (MEN1), a rare hereditary cancer syndrome characterized by tumors of the parathyroid glands, pancreas, and pituitary gland. MEN1 is caused by mutations in the MEN1 gene and is inherited in an autosomal dominant pattern. Diagnosis involves identifying biochemical abnormalities and tumors associated with MEN1. Management focuses on surgery to remove tumors, with the goal of preventing complications from hormone hypersecretion. Lifelong screening is required due to the high risk of recurrent and multiple tumors developing over time.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be due to an ACTH-secreting pituitary adenoma (Cushing's disease), an ectopic ACTH-secreting tumor, or an adrenal tumor. Diagnostic tests include midnight salivary cortisol levels, dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, radiation therapy, or medication to suppress cortisol levels. Even after successful treatment, patients remain at higher risk for cardiovascular disease.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be pituitary-dependent (Cushing's disease), adrenal-dependent (adenoma or carcinoma), or caused by an ectopic ACTH-secreting tumor. Diagnostic tests include urine and salivary cortisol levels, low and high dose dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, adrenalectomy, or medication to suppress cortisol production while managing comorbidities. The prognosis has improved with effective treatments but risks remain high without treatment.
This document summarizes neuroendocrine tumors of the gastrointestinal tract. It discusses that these tumors arise from neuroendocrine cells and can secrete markers like synaptophysin. They can be functional, secreting hormones, or non-functional. Imaging studies help in surgical planning and staging. Multiple endocrine neoplasia type 1 can cause pancreatic and gastric neuroendocrine tumors. Specific types of neuroendocrine tumors are discussed like gastrinomas, insulinomas, glucagonomas and VIPomas. Treatment involves surgery, medical management, and screening based on tumor type and location.
This document discusses polycystic ovary syndrome (PCOS) and its implications. It begins with the diagnostic criteria for PCOS including hyperandrogenism, oligo/amenorrhea, and polycystic ovaries. It then covers the diagnostic workup involving physical exams, laboratory tests, ultrasound, and optional tests. The document discusses the implications of PCOS for health including metabolic syndrome and future cardiovascular risks. It covers the implications for infertility such as treatments including lifestyle changes, clomiphene citrate, gonadotropins, laparoscopic ovarian drilling, metformin, and assisted reproduction. The implications for pregnancy with PCOS including gestational diabetes, pregnancy induced hypertension, preterm birth, birth weight,
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS has a multifactorial origin involving both genetic and environmental factors like diet and exercise. Key aspects of PCOS include irregular periods, high androgen levels, polycystic ovaries, insulin resistance and its associated health risks. Treatment focuses on lifestyle changes, medication like metformin to reduce insulin resistance, and hormone therapy depending on a patient's goals.
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS is associated with insulin resistance and an increased risk of conditions like diabetes and heart disease. Lifestyle changes including diet and exercise are recommended as first-line treatment, especially for overweight patients. Medications like metformin can also help address insulin resistance and related issues.
An inflammatory condition of the pancreas
Acute pancreatitis is a reversible process,
whereas Chronic pancreatitis (CP) is irreversible
Acinar Cell Injury
This document discusses polycystic ovary syndrome (PCOS), including its definition, diagnostic criteria, pathophysiology, clinical features, evaluation, and management. PCOS is the most common endocrine disorder in women of reproductive age, affecting 5-10% of women. It is characterized by ovarian dysfunction, hyperandrogenism, and polycystic ovaries. Treatment focuses on managing symptoms and preventing long-term complications through lifestyle modifications, medications, and fertility treatments.
1. The boy has been experiencing recurrent episodes of intense nausea and vomiting for over 3 years, with stereotypical cyclical pattern consistent with cyclic vomiting syndrome.
2. Diagnostic workup found no underlying cause and the boy is otherwise healthy between episodes. Management includes lifestyle modifications and abortive/prophylactic medications like ondansetron and amitriptyline which have reduced severity and frequency of episodes.
3. Cyclic vomiting syndrome is an important consideration for children presenting with stereotypical episodes of vomiting, and further workup is only needed if alarm symptoms are present that suggest an alternative underlying cause.
Gastroparesis is a syndrome of objectively delayed gastric emptying in the absence of a mechanical obstruction and cardinal symptoms of nausea, vomiting, early satiety, bloating, and/or upper abdominal pain
Neuroendocrine tumors of the pancreas (PNETs) are a diverse group of neoplasms that can be functional or non-functional. Functional PNETs secrete hormones that cause distinct syndromes, while non-functional PNETs do not secrete hormones or their secretion does not cause symptoms. The most common functional PNETs are insulinomas, gastrinomas, vipomas, and glucagonomas. Treatment involves surgical resection with the goal of cure for localized disease. For advanced or metastatic disease, palliative treatments are used to control hormone secretion and tumor growth.
A 38-year-old woman presents with upper abdominal pain worse after meals but no other symptoms. Her H. pylori test is positive. The doctor treats her empirically with Prevpac. A year later, she reports frequent heartburn. Lifestyle modifications and PPI treatment are recommended. She does not need an endoscopy unless symptoms fail to improve.
This document summarizes non-alcoholic fatty liver disease (NAFLD) from an endocrinology perspective. It defines NAFLD and related terms, discusses the pathophysiology involving insulin resistance and lipotoxicity, epidemiology as a growing global problem, challenges in diagnosis and evaluation, and currently available treatment options focusing on lifestyle modification and insulin sensitizers. Key points covered include the need for accurate definitions to classify disease subtypes, the role of the adipose tissue-liver axis in disease progression, and limitations of non-invasive testing underscoring the continued need for liver biopsy in certain cases.
Iodine deficiency disorder and metabolic syndromeGunJee Gj
Iodine deficiency can cause goiter and impaired brain development. Symptoms include enlargement of the thyroid gland, neurological deficits, and delayed sexual maturation. It is assessed by palpation, ultrasound, and urinary iodine levels. Daily iodine requirements range from 50 μg for infants to 150 μg for those over 12 years old. The metabolic syndrome is defined as abdominal obesity plus two other risk factors and increases the risk of cardiovascular disease and diabetes. It involves central obesity, high triglycerides, low HDL, high blood pressure, and elevated fasting glucose. Lifestyle modifications including diet, exercise, and weight loss are first-line treatment approaches.
Masterclass Liver Care - Vitafoods 2016Koen Jacobs
The liver performs many essential functions including detoxification, protein synthesis, production of biochemicals for digestion, storing glycogen, and decomposing red blood cells. Liver disease can result from alcohol use, viruses, autoimmune conditions, genetic disorders, or non-alcoholic fatty liver disease (NAFLD). NAFLD occurs when excess fat accumulates in the liver and is increasing worldwide due to the rise in obesity and metabolic syndrome. Poor diet and lifestyle factors contribute to NAFLD progression. Choline plays an important role in liver health by supporting phospholipid membranes, lipoprotein synthesis, and methylation reactions, and higher intakes may be needed to prevent NAFLD.
The document discusses diseases of the pancreas, including congenital anomalies, endocrine and exocrine pancreatic diseases, acute and chronic pancreatitis, and pancreatic tumors. It provides details on the causes, pathophysiology, clinical presentation, diagnosis, and treatment of each condition. Key points include the role of gallstones and alcohol as common causes of acute pancreatitis, the use of CT and lab tests to diagnose and determine severity, and supportive care along with surgical or endoscopic interventions for severe cases.
This document summarizes multiple endocrine neoplasia type 1 (MEN1), a rare hereditary cancer syndrome characterized by tumors of the parathyroid glands, pancreas, and pituitary gland. MEN1 is caused by mutations in the MEN1 gene and is inherited in an autosomal dominant pattern. Diagnosis involves identifying biochemical abnormalities and tumors associated with MEN1. Management focuses on surgery to remove tumors, with the goal of preventing complications from hormone hypersecretion. Lifelong screening is required due to the high risk of recurrent and multiple tumors developing over time.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be due to an ACTH-secreting pituitary adenoma (Cushing's disease), an ectopic ACTH-secreting tumor, or an adrenal tumor. Diagnostic tests include midnight salivary cortisol levels, dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, radiation therapy, or medication to suppress cortisol levels. Even after successful treatment, patients remain at higher risk for cardiovascular disease.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be pituitary-dependent (Cushing's disease), adrenal-dependent (adenoma or carcinoma), or caused by an ectopic ACTH-secreting tumor. Diagnostic tests include urine and salivary cortisol levels, low and high dose dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, adrenalectomy, or medication to suppress cortisol production while managing comorbidities. The prognosis has improved with effective treatments but risks remain high without treatment.
This document summarizes neuroendocrine tumors of the gastrointestinal tract. It discusses that these tumors arise from neuroendocrine cells and can secrete markers like synaptophysin. They can be functional, secreting hormones, or non-functional. Imaging studies help in surgical planning and staging. Multiple endocrine neoplasia type 1 can cause pancreatic and gastric neuroendocrine tumors. Specific types of neuroendocrine tumors are discussed like gastrinomas, insulinomas, glucagonomas and VIPomas. Treatment involves surgery, medical management, and screening based on tumor type and location.
This document discusses polycystic ovary syndrome (PCOS) and its implications. It begins with the diagnostic criteria for PCOS including hyperandrogenism, oligo/amenorrhea, and polycystic ovaries. It then covers the diagnostic workup involving physical exams, laboratory tests, ultrasound, and optional tests. The document discusses the implications of PCOS for health including metabolic syndrome and future cardiovascular risks. It covers the implications for infertility such as treatments including lifestyle changes, clomiphene citrate, gonadotropins, laparoscopic ovarian drilling, metformin, and assisted reproduction. The implications for pregnancy with PCOS including gestational diabetes, pregnancy induced hypertension, preterm birth, birth weight,
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS has a multifactorial origin involving both genetic and environmental factors like diet and exercise. Key aspects of PCOS include irregular periods, high androgen levels, polycystic ovaries, insulin resistance and its associated health risks. Treatment focuses on lifestyle changes, medication like metformin to reduce insulin resistance, and hormone therapy depending on a patient's goals.
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS is associated with insulin resistance and an increased risk of conditions like diabetes and heart disease. Lifestyle changes including diet and exercise are recommended as first-line treatment, especially for overweight patients. Medications like metformin can also help address insulin resistance and related issues.
An inflammatory condition of the pancreas
Acute pancreatitis is a reversible process,
whereas Chronic pancreatitis (CP) is irreversible
Acinar Cell Injury
This document discusses polycystic ovary syndrome (PCOS), including its definition, diagnostic criteria, pathophysiology, clinical features, evaluation, and management. PCOS is the most common endocrine disorder in women of reproductive age, affecting 5-10% of women. It is characterized by ovarian dysfunction, hyperandrogenism, and polycystic ovaries. Treatment focuses on managing symptoms and preventing long-term complications through lifestyle modifications, medications, and fertility treatments.
1. The boy has been experiencing recurrent episodes of intense nausea and vomiting for over 3 years, with stereotypical cyclical pattern consistent with cyclic vomiting syndrome.
2. Diagnostic workup found no underlying cause and the boy is otherwise healthy between episodes. Management includes lifestyle modifications and abortive/prophylactic medications like ondansetron and amitriptyline which have reduced severity and frequency of episodes.
3. Cyclic vomiting syndrome is an important consideration for children presenting with stereotypical episodes of vomiting, and further workup is only needed if alarm symptoms are present that suggest an alternative underlying cause.
Gastroparesis is a syndrome of objectively delayed gastric emptying in the absence of a mechanical obstruction and cardinal symptoms of nausea, vomiting, early satiety, bloating, and/or upper abdominal pain
Neuroendocrine tumors of the pancreas (PNETs) are a diverse group of neoplasms that can be functional or non-functional. Functional PNETs secrete hormones that cause distinct syndromes, while non-functional PNETs do not secrete hormones or their secretion does not cause symptoms. The most common functional PNETs are insulinomas, gastrinomas, vipomas, and glucagonomas. Treatment involves surgical resection with the goal of cure for localized disease. For advanced or metastatic disease, palliative treatments are used to control hormone secretion and tumor growth.
A 38-year-old woman presents with upper abdominal pain worse after meals but no other symptoms. Her H. pylori test is positive. The doctor treats her empirically with Prevpac. A year later, she reports frequent heartburn. Lifestyle modifications and PPI treatment are recommended. She does not need an endoscopy unless symptoms fail to improve.
This document summarizes non-alcoholic fatty liver disease (NAFLD) from an endocrinology perspective. It defines NAFLD and related terms, discusses the pathophysiology involving insulin resistance and lipotoxicity, epidemiology as a growing global problem, challenges in diagnosis and evaluation, and currently available treatment options focusing on lifestyle modification and insulin sensitizers. Key points covered include the need for accurate definitions to classify disease subtypes, the role of the adipose tissue-liver axis in disease progression, and limitations of non-invasive testing underscoring the continued need for liver biopsy in certain cases.
Iodine deficiency disorder and metabolic syndromeGunJee Gj
Iodine deficiency can cause goiter and impaired brain development. Symptoms include enlargement of the thyroid gland, neurological deficits, and delayed sexual maturation. It is assessed by palpation, ultrasound, and urinary iodine levels. Daily iodine requirements range from 50 μg for infants to 150 μg for those over 12 years old. The metabolic syndrome is defined as abdominal obesity plus two other risk factors and increases the risk of cardiovascular disease and diabetes. It involves central obesity, high triglycerides, low HDL, high blood pressure, and elevated fasting glucose. Lifestyle modifications including diet, exercise, and weight loss are first-line treatment approaches.
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
2. Case Presentation
A 56 year old woman has had diarrhea for
8 years, initially intermittent and now daily
for 3 years. She stated “there’s not a
bathroom in the state that I have not
visited”. Diarrhea did not respond to OTC
medications.
3. 56 y.o. with diarrhea, continued
Past medical/surgical history:
– morbid obesity (BMI 42 kg/m2)
– status post TAH with BSO
• Family history:
– Mother: COPD, ulcers, kidney stones
– Father: MI
• Social history: negative
• ROS: negative
• Physical exam: morbid obesity.
• CBC and chem 14: all normal except for ALT 54.
• Stool microbiology studies negative.
• Sigmoidoscopy were normal.
4. Case: Imaging
• Upper GI/SBFT : thickening of folds of stomach
and proximal small intestine
• Abdominal CT scan: thick gastric folds; slight
prominence of the pancreatic head without a
distinct mass; single gallstone; diffuse fatty
infiltration of the liver.
• EGD: prominent gastric folds; excessive gastric
secretions (400 ml); no esophagitis or ulcers; 4
mm duodenal nodule biopsy: gastric
metaplasia
5. Biochemical tests
• Fasting serum gastrin 1,200 pg/ml
(normal, < 100)
• Basal acid output after referral and on
medication:
– 57.4 mmol per hr (normal, < 5 mmol/hr)
• Diagnosis: Zollinger-Ellison syndrome
6. GI Endocrine System vs.
Other Endocrine Tissues
Non-GI GI
Distribution of cells Discrete Glands Scattered cells or islands of
cells (islets) in GI tract/panc.
Regulation by
Hypothalamus/Pituitary
Common Minimal to non-existent
Hormonal assays
readily available
Yes No
Knowledge about physiology High Variable
Functional tumors* Common Uncommon
* Non-GI and GI tumors may coexist in the MEN-1 and MEN-2b syndromes
10. GI Peptides That Act
Principally as Neuropeptides
• Calcitonin gene-related peptide (CGRP)
• Dynorphin and related gene products
• Enkephalin and related gene products
• Galanin
• Gastrin-releasing peptide (GRP)
• Neuromedin U
• Neuropeptide Y
• Peptide histidine isoleucine (PHI) or peptide histidine methionine
(PHM)
• Pituitary adenylate cyclase–activating peptide (PACAP)
• Substance P and other tachykinins (neurokinin A, neurokinin B)
• Thyrotropin-releasing hormone (TRH)
• VIP
11. Paracrine inhibition of G cell release by
somatostatin (STS) from adjacent D cells
Gastric antral mucosa
12. GI/Panreatic Peptides That May
Function as Hormones, Neuropeptides,
or Paracrine Agents
• Somatostatin
• Cholecystokinin (CCK)
• Corticotropin-releasing factor (CRF)
• Endothelin
• Neurotensin
18. Zollinger-Ellison Syndrome
• “Islet cell” tumor of the pancreas [or of the
duodenum]
• Hypergastrinemia
• Gastric acid hypersecretion
• Consequences of acid hypersecretion :
– PUD, GERD [ with or without complications]
– Diarrhea, malabsorption
19. Epidemiology of
Z-E syndrome
• Any age group ( mean age 50 years)
• Male : Female 3:2
• Annual incidence 0.5 - 1.0 per million
• MEN-1 in approximately 25% of cases
30. Symptoms in patients with the
Zollinger-Ellison syndrome
• Pain and diarrhea 50-60%
• Pain without diarrhea 25%
• Diarrhea without pain 20%
• Heartburn ± dysphagia 30%
• MEN-1 features 20-25%
31. Locations of peptic ulcers
in ZE syndrome
• Duodenal bulb
• Post-bulbar
duodenum
• Jejunum
• Esophagus
• Stomach
• Marginal (stomal)
32. Clinical features suspicious for
Zollinger-Ellison syndrome (ZES)
• History of PUD and
nephrolithiasis
• Family history of PUD, kidney
stones
• PUD in the absence of
Helicobacter pylori or
NSAID usage
• PUD in association with
chronic diarrhea
• Post-bulbar duodenal ulcer
• Multiple duodenal and/or
jejunal ulcers
•PUD refractory to standard
medical therapy
33. Diagnosis of ZE Syndrome
• Begins with clinical suspicion
(pretest probability)
• Fasting serum gastrin measurement
– high sensitivity (> 95%)
– poor specificity, even at high levels
– modest positive predictive value
– excellent negative predictive value
35. Diagnosis of ZE Syndrome
• Fasting serum gastrin measurement
– high sensitivity (> 95%)
– low specificity and modest positive predictive
value can be enhanced with provocative
testing with secretin (2 IU/kg or 0.4 ug/kg i.v.)
or calcium infusion (4 mg/kg calcium
gluconate per hour for 3 hours), where
likelihood ratios increase 10-15 fold with a +
test result and decrease 10-fold with a - test
result
36. Management of ZE syndrome:
• Acid control takes precedence over tumor
search
• Tumor search is designed to find tumor
and to stage its/their extent
• Tumor search and possible resection for
cure is only prudent for patients who are
surgical candidates
44. MEN syndromes
• MEN-1:
• MEN 2a:
• MEN 2b:
• Parathyroid tumor(s)
• Pancreatic tumor
– gastrin, insulin, VIP
• Pituitary tumor
– prolactin, ACTH
• Medullary thyroid Ca or
hyperplasia
• Pheochromocytoma
• Parathyroid disease
• 2b , without parathyroid
• 2b, with gangioneuromatosis,
Marfanoid habitus
45. Genetics of MEN-1
• Germ cell mutation at 11q13 in 90% of
MEN-1, with loss of heterozygosity
implicated in endocrine tumorigenesis
• Chromosome 11q13 product is menin
• Function of menin ?
• Mutations in 11q13 also occur in several
cases of “sporadic” islet cell tumors such
as gastrinomas
51. Case, continued
• She was felt to be a poor surgical
candidate.
• In 1985 ranitidine was increased to 300
mg q6h and propantheline 7.5 mg q6h
added, with basal acid output < 5 mmol
per hr and relief of all symptoms.
• She was switched to a PPI in 1989 and
has remained asymptomatic despite
fasting serum gastrins > 1,000 pg/ml.
52. Clinical Course
• CT scans show variable changes in the
head of the pancreas and a few tiny low-
density hepatic lesions, cysts vs mets vs
focal fat.
• Current meds: glyburide, risedronate,
atorvastatin, and lansoprazole.
• Her basal acid output 24 hours after
lansoprazole (trough) was 0.
53.
54. What about her serum calcium?
1985: Ca 10.3, 9.4, 10.0, 10.1
PTH: 47 (0-50) ; 127 (50-150)
1989: Ca 9.7
1993: Ca 10.4
1994: Ca 9.7
2003: Ca 10.4 at PHD
PTH (intact): 76 (0-54)
Diagnosis: MEN-1 with ZE and hyperparathyroidism
55. Influence of liver metastases on
survival in gastrinoma patients
undergoing surgery
56. Prognostic factors in various
PETs for decreased survival
• Female gender
• Absence of MEN1 syndrome
• Presence of liver metastases
• Extent of liver metastases
• Presence of lymph node
metastases
• Growth of liver metastases
• Presence of bone metastases
• Incomplete tumor resection
• Nonfunctional tumor (worse
than functional) (p <0.01)
• Development of ectopic
Cushing’s syndrome
(gastrinomas)
• Increased depth of tumor
invasion
• Primary tumor size (>3 cm)
• Various histologic features
• Flow cytometric features (i.e.,
aneuploidy)
• Increased chromogranin A in
some studies
• Increased gastrin level (p
<0.001) (gastrinomas)
• Lack of progesterone
receptors
• Ha-Ras oncogene or p53
overexpression
• High HER2/neu gene
expression (gastrinomas)
• High 1q loss of heterozygosity
(gastrinomas)
• Increased EGF or IGF receptor
expression (gastrinomas)
• Loss of 1p, 3p, 3q, 6q; gain of
7q, 17, 17p, 20q