This document outlines various endocrinology topics including causes of conditions like Cushing syndrome, diabetes, stunted growth, hypercalcemia, hypoglycemia, hirsutism, and others. It also provides details on topics like diabetic management and complications, thyroid disorders, adrenal disorders, growth disorders, puberty disorders, obesity, and pituitary disorders. Treatment options and diagnostic criteria are discussed for many of these conditions.
The adrenal glands secrete hormones that regulate metabolism, electrolyte balance, and stress response. The medulla secretes epinephrine and norepinephrine, while the cortex secretes steroids such as cortisol and aldosterone. Cortisol secretion follows a diurnal rhythm controlled by the HPA axis. Primary adrenal insufficiency results from failure of the adrenal glands, while secondary is a failure of the HPA axis. Presentation includes fatigue, weight loss, hypotension, and hyperpigmentation. Diagnosis involves short corticotropin stimulation tests. Treatment is with glucocorticoid replacement such as hydrocortisone.
A 22-year-old male presented with jaundice, fatigue, and muscle pain for 6 months. Liver tests showed elevated bilirubin, AST, and prolonged PT/INR, suggesting a chronic liver disease. A 19-year-old female with history of chicken pox 8 months ago developed jaundice. Liver tests showed direct hyperbilirubinemia, elevated AST and markedly elevated ALP, indicating a cholestatic picture with ongoing activity. A 32-year-old alcoholic male with known cirrhosis showed mild elevation of AST and direct hyperbilirubinemia, with AST/ALT ratio of 3:1, consistent with alcoholic liver disease with ongoing activity.
A 19-year-old man presented with red urine, periorbital and pretibial edema. He was diagnosed with tonsillitis 3 weeks prior. Examination found hypertension and crackles in both lung bases. Urine analysis showed proteinuria and dysmorphic red blood cells. The most likely diagnosis is poststreptococcal glomerulonephritis resulting from the recent streptococcal infection. Treatment involves controlling hypertension, edema and complications through diuretics and sodium restriction. Renal biopsy showed diffuse proliferative glomerulonephritis with neutrophils and immune deposits consistent with poststreptococcal glomerulonephritis.
- A 55-year-old male presented with 3 weeks of weakness, fatigue, and weight loss. Physical exam found him to be thin and lean with oral pigmentation.
- Labs found leukopenia, a positive PPD test, low cortisol, increased ACTH, and a normal chest x-ray.
- The final diagnosis was tuberculosis adrenalitis, which had caused primary adrenal insufficiency.
This document provides an overview of approaches to evaluating and treating a patient presenting with jaundice. There are three main types of jaundice discussed: hemolytic, hepatic, and obstructive. For each type, the document outlines relevant clinical findings, laboratory investigations, and potential etiologies. Treatment options are also reviewed for obstructive jaundice, the most common cause being choledocholithiasis, which can be addressed through open or laparoscopic exploration/stone extraction or endoscopic papillotomy. Periampullary carcinoma is another potential etiology that may require curative surgery like the Whipple procedure or palliative interventions.
The fluid deprivation test is an important diagnostic tool used to distinguish between central diabetes insipidus and other causes of polyuria such as primary polydipsia. It involves withholding fluids from a patient for a period of time while closely monitoring urine output, osmolality, and electrolyte levels to check for an appropriate response to ADH.
Hyperparathyroidism is caused by overproduction of parathyroid hormone (PTH) resulting in abnormal calcium homeostasis. Primary hyperparathyroidism is caused by uncontrolled PTH production from a parathyroid adenoma in 85% of cases. Symptoms include bone and kidney problems, abdominal pain, weakness and mood changes. It is diagnosed based on high PTH and calcium levels. Treatment involves surgical removal of the affected parathyroid gland(s). Secondary and tertiary hyperparathyroidism are caused by prolonged hypocalcemia from kidney disease or malnutrition, and are treated medically or with parathyroidectomy if medications fail.
The adrenal glands secrete hormones that regulate metabolism, electrolyte balance, and stress response. The medulla secretes epinephrine and norepinephrine, while the cortex secretes steroids such as cortisol and aldosterone. Cortisol secretion follows a diurnal rhythm controlled by the HPA axis. Primary adrenal insufficiency results from failure of the adrenal glands, while secondary is a failure of the HPA axis. Presentation includes fatigue, weight loss, hypotension, and hyperpigmentation. Diagnosis involves short corticotropin stimulation tests. Treatment is with glucocorticoid replacement such as hydrocortisone.
A 22-year-old male presented with jaundice, fatigue, and muscle pain for 6 months. Liver tests showed elevated bilirubin, AST, and prolonged PT/INR, suggesting a chronic liver disease. A 19-year-old female with history of chicken pox 8 months ago developed jaundice. Liver tests showed direct hyperbilirubinemia, elevated AST and markedly elevated ALP, indicating a cholestatic picture with ongoing activity. A 32-year-old alcoholic male with known cirrhosis showed mild elevation of AST and direct hyperbilirubinemia, with AST/ALT ratio of 3:1, consistent with alcoholic liver disease with ongoing activity.
A 19-year-old man presented with red urine, periorbital and pretibial edema. He was diagnosed with tonsillitis 3 weeks prior. Examination found hypertension and crackles in both lung bases. Urine analysis showed proteinuria and dysmorphic red blood cells. The most likely diagnosis is poststreptococcal glomerulonephritis resulting from the recent streptococcal infection. Treatment involves controlling hypertension, edema and complications through diuretics and sodium restriction. Renal biopsy showed diffuse proliferative glomerulonephritis with neutrophils and immune deposits consistent with poststreptococcal glomerulonephritis.
- A 55-year-old male presented with 3 weeks of weakness, fatigue, and weight loss. Physical exam found him to be thin and lean with oral pigmentation.
- Labs found leukopenia, a positive PPD test, low cortisol, increased ACTH, and a normal chest x-ray.
- The final diagnosis was tuberculosis adrenalitis, which had caused primary adrenal insufficiency.
This document provides an overview of approaches to evaluating and treating a patient presenting with jaundice. There are three main types of jaundice discussed: hemolytic, hepatic, and obstructive. For each type, the document outlines relevant clinical findings, laboratory investigations, and potential etiologies. Treatment options are also reviewed for obstructive jaundice, the most common cause being choledocholithiasis, which can be addressed through open or laparoscopic exploration/stone extraction or endoscopic papillotomy. Periampullary carcinoma is another potential etiology that may require curative surgery like the Whipple procedure or palliative interventions.
The fluid deprivation test is an important diagnostic tool used to distinguish between central diabetes insipidus and other causes of polyuria such as primary polydipsia. It involves withholding fluids from a patient for a period of time while closely monitoring urine output, osmolality, and electrolyte levels to check for an appropriate response to ADH.
Hyperparathyroidism is caused by overproduction of parathyroid hormone (PTH) resulting in abnormal calcium homeostasis. Primary hyperparathyroidism is caused by uncontrolled PTH production from a parathyroid adenoma in 85% of cases. Symptoms include bone and kidney problems, abdominal pain, weakness and mood changes. It is diagnosed based on high PTH and calcium levels. Treatment involves surgical removal of the affected parathyroid gland(s). Secondary and tertiary hyperparathyroidism are caused by prolonged hypocalcemia from kidney disease or malnutrition, and are treated medically or with parathyroidectomy if medications fail.
This document provides information on the approach to a patient presenting with jaundice. It discusses the definitions, biochemistry, pathophysiology, history taking, physical examination, and investigations.
For a case example, it describes a 24-year-old female who presents with 4 days of fever, nausea, vomiting and anorexia. Her lab results show elevated bilirubin, ALT, and AST, with HAV IgM being positive on viral screening. Her examination and ultrasound are not suggestive of biliary obstruction. She is diagnosed with viral hepatitis A.
This document provides an overview of approaches to evaluating and diagnosing jaundice. It discusses the production and metabolism of bilirubin, measurement of bilirubin levels, clinical history and examination of patients, and laboratory and imaging tests used to classify jaundice as pre-hepatic, hepatocellular, or cholestatic. Common etiologies of each type are outlined, including inherited and acquired conditions.
Pseudohypoparathyroidism is characterized by peripheral resistance to parathyroid hormone rather than a deficiency, causing hypocalcemia and hyperphosphataemia. There are three main types - 1a, 1b, and 2 - which are all heterozygous genetic conditions involving haploinsufficiency of the GNAS1 gene. Type 1a is associated with short stature, round face, soft tissue calcification, and developmental delays. The molecular defect is in the GNAS1 gene which encodes the Gsa protein involved in several hormone signaling pathways. Types 1b and 2 also involve GNAS1 defects but have different clinical presentations and endocrinological effects.
This document discusses the evaluation and causes of chronic diarrhea. It begins by defining chronic diarrhea and outlining the normal stool production process. It then describes the main mechanisms that can cause diarrhea - osmotic, secretory, inflammatory, and dysmotility. Specific causes are discussed under each mechanism, including diseases, medications, toxins, and dietary factors. The document outlines the evaluation of a patient with chronic diarrhea, including history, physical exam, stool tests, imaging, and other lab tests. It provides guidance on testing for malabsorption and evaluating postsurgical causes of chronic diarrhea.
This patient is a 54-year-old female with type 2 diabetes presenting with worsening gastrointestinal symptoms of early satiety, heartburn and nausea despite dietary modifications. Investigations including EGD revealed mild antral erythema and food residue in her stomach, with a hiatal hernia present but no esophagitis or Barrett's esophagus. H. pylori testing was negative. The primary diagnosis is likely gastroparesis, and recommended treatment includes a proton pump inhibitor along with modifying her diabetes medications.
This document discusses jaundice and approaches to evaluating its underlying causes. It defines jaundice as yellowish discoloration from bilirubin deposition. Liver enzymes, imaging like ultrasound and CT, and procedures like ERCP can help differentiate causes like viral hepatitis, alcoholic liver disease, autoimmune conditions, and obstructive jaundice. A careful history, exam, and pattern of lab and imaging abnormalities can often reveal the etiology of jaundice. A liver biopsy may be needed in some unclear cases to establish a diagnosis.
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
This document discusses aplastic anemia, a condition characterized by pancytopenia and bone marrow hypocellularity. It defines aplastic anemia, discusses its causes (acquired from things like radiation, drugs, viruses, immune diseases, or inherited genetic syndromes), epidemiology, pathophysiology, clinical features including symptoms and examination findings, diagnostic testing including blood tests and bone marrow biopsy, and treatment options including hematopoietic stem cell transplantation, immunosuppression, supportive care, and prognosis.
HEPATOBILIARY PATHOLOGY QUESTIONS & ANSWERS
LIVER
BILEDUCT PATHOLOGY
CASE STUDY AND
IMAGE BASED QUESTIONS WITH
PROPER ELABORATED ANSWERS
REF:- ROBBINS PATHOLOGIC BASIS OF DISEASES (TEXT BOOK)
OTHER REFS:- HARSH MOHAN'S TEXT BOOK OF PATHOLOGY
ATLAS OF PATHOLOGY
INTERNET SOURCES
BEFORE GOING TO START THE QUESTIONS JUST GIVE A LOOK ON THE "LIVER PATHOLOGY" SLIDES FROM THE GIVEN LINK BELOW
https://www.slideshare.net/SurajDhara2/liver-pathology-107731001
HAVE A NICE DAY
This document provides an overview of hypocalcemia, including:
- Causes of hypocalcemia such as hypoparathyroidism, vitamin D deficiency, renal failure, sepsis
- Symptoms of hypocalcemia including neurological symptoms, muscle spasms, cardiac issues
- Diagnosis and treatment of hypocalcemia including IV calcium supplementation and monitoring calcium levels
- Etiologies of hypocalcemia like hungry bone syndrome, acute pancreatitis, medications that can cause hypocalcemia
- Overview of calcium regulation in the kidney and genes involved
Anemia And Its Classification By Dr Bashir Ahmed Dar Chinkipora Sopore KashmirProf Dr Bashir Ahmed Dar
Anaemia due to iron deficiency is the characteristic finding with a cancer of the colon (large bowel), stomach or gullet. Often the anaemia is the only clue to the presence of a bleeding source somewhere. Any person who develops iron deficiency anaemia with no obvious cause should be investigated for the presence of a bleeding point within the digestive system. Fortunately not all bleeding sources turn out to be cancers
A 45-year-old female patient was admitted to the hospital for 5 days with complaints of loose stools, vomiting, abdominal pain, and decreased hemoglobin, PCV, and WBC levels. She was diagnosed with acute gastroenteritis and hyperthyroidism. She was treated with ondansetron, metronidazole, pantoprazole, ceftriaxone, carbimazole, and propranolol. She was advised to follow a proper diet, maintain hygiene, and take medications regularly to manage her conditions.
The document discusses liver cirrhosis, including its causes, classification, complications, and pathophysiology. It notes that cirrhosis can result from viral infections like hepatitis, alcohol use, metabolic disorders like obesity and diabetes, immune disorders, vascular abnormalities, and genetic disorders. Complications of cirrhosis include portal hypertension, ascites, and hepatic encephalopathy. The pathophysiology of alcoholic liver disease is also examined, with ethanol metabolism damaging the liver through direct toxicity, oxidative stress, and inflammation, potentially culminating in fatty liver, alcoholic hepatitis, and alcoholic cirrhosis over time.
A 35-year-old male auto driver was admitted with decreased urine output for 3 days and abdominal pain and fever for 10 days. Examination found pallor and abdominal tenderness. Tests showed acute kidney injury and a urine culture grew gram-negative bacilli. He was diagnosed with acute pyelonephritis likely caused by E. coli infection. He received IV and oral antibiotics and underwent hemodialysis. His kidney function and other lab values gradually improved with treatment.
A 33-year old man with polyuria and polydipsiaUsama Ragab
Clinical case uncovered (CCU) series
Endocrinology and diabetes
Case number 11: A 33-year old man with polyuria and polydipsia
Medical case presentation of polyuria
Hypoparathyroidism is a condition characterized by decreased function of the parathyroid glands and low levels of parathyroid hormone, resulting in low calcium and high phosphorus levels in the blood. Symptoms range from tingling in the extremities to seizures and altered mental state. The condition is diagnosed based on low calcium and parathyroid hormone levels in the blood. Treatment involves calcium and vitamin D supplements to manage calcium levels, with some patients also requiring parathyroid gland transplants.
The document discusses diseases of the parathyroid glands, including hyperparathyroidism and hypoparathyroidism. It covers the physiology and functions of the parathyroid glands and parathyroid hormone. It describes the etiology, pathogenesis, and classification of primary, secondary, and tertiary hyperparathyroidism. The clinical features of hyperparathyroidism are also outlined.
The document discusses the causes, evaluation, and differentiation of conjugated and unconjugated hyperbilirubinemia. Key causes of unconjugated hyperbilirubinemia include hemolysis and ineffective erythropoiesis. Causes of conjugated hyperbilirubinemia include genetic disorders like Dubin-Johnson syndrome and Rotor syndrome, as well as viral hepatitis, alcohol, drugs, toxins, and autoimmune conditions. Evaluation involves liver function tests and distinguishing between intrahepatic and extrahepatic cholestasis. A case example is presented with elevated direct bilirubin and aminotransferases suggestive of hepatitis.
This document provides guidance on evaluating a patient presenting with jaundice. It outlines a systematic approach including focused history, examination, differential diagnosis, and appropriate lab tests and imaging. Liver function tests can indicate hepatitic or cholestatic patterns. Case examples demonstrate applying this approach, such as using imaging and endoscopy to diagnose an ampullary tumor, managing a variceal bleed in cirrhosis, and identifying acute hepatitis B. Key considerations include complications of liver disease and importance of screening high-risk populations.
This document discusses inflammatory bowel disease (IBD), specifically Crohn's disease and ulcerative colitis. It defines IBD as a group of conditions that cause inflammation of the digestive tract, and notes the two major types are Crohn's disease and ulcerative colitis. Crohn's disease can impact any part of the digestive tract and often spreads deep into tissues, while ulcerative colitis exclusively impacts the innermost lining of the large intestine and rectum. Symptoms for both include abdominal pain, diarrhea, weight loss and more. While causes are unknown, it is believed to involve defects in the immune system. Diagnosis involves blood tests, stool samples, imaging and endoscopy. Treatment depends on the severity but may include
This document provides a historical overview of diabetes. Some key points include:
- The earliest known record of diabetes is from an Egyptian papyrus from around 1500 BC. The term "diabetes" comes from the Greek word for "siphon" and was coined in the 3rd century BC.
- In the 16th century, diabetes was identified as a severe disorder affecting the whole body. The pancreas's role in diabetes was discovered in the 1870s but its function remained unknown.
- In 1921-1923, Banting, Best, and Macleod discovered insulin and its role in controlling blood sugar levels, representing a major breakthrough in diabetes treatment.
DIABETIC KETOACIDOSIS PRESENTATION BY ROOMA KHALIDRooma Khalid
This document discusses diabetic ketoacidosis (DKA). It defines DKA and its signs and symptoms. DKA occurs more often in type 1 diabetes and is characterized by blood glucose over 250 mg/dl, blood pH below 7.3, and ketones in serum over 5 mEq/L. Proper treatment of DKA involves fluid replacement, insulin administration, and monitoring of blood glucose, electrolytes, and pH to correct dehydration, hyperglycemia, and acidosis. Failure to treat the patient's DKA led to worsening of her condition.
This document provides information on the approach to a patient presenting with jaundice. It discusses the definitions, biochemistry, pathophysiology, history taking, physical examination, and investigations.
For a case example, it describes a 24-year-old female who presents with 4 days of fever, nausea, vomiting and anorexia. Her lab results show elevated bilirubin, ALT, and AST, with HAV IgM being positive on viral screening. Her examination and ultrasound are not suggestive of biliary obstruction. She is diagnosed with viral hepatitis A.
This document provides an overview of approaches to evaluating and diagnosing jaundice. It discusses the production and metabolism of bilirubin, measurement of bilirubin levels, clinical history and examination of patients, and laboratory and imaging tests used to classify jaundice as pre-hepatic, hepatocellular, or cholestatic. Common etiologies of each type are outlined, including inherited and acquired conditions.
Pseudohypoparathyroidism is characterized by peripheral resistance to parathyroid hormone rather than a deficiency, causing hypocalcemia and hyperphosphataemia. There are three main types - 1a, 1b, and 2 - which are all heterozygous genetic conditions involving haploinsufficiency of the GNAS1 gene. Type 1a is associated with short stature, round face, soft tissue calcification, and developmental delays. The molecular defect is in the GNAS1 gene which encodes the Gsa protein involved in several hormone signaling pathways. Types 1b and 2 also involve GNAS1 defects but have different clinical presentations and endocrinological effects.
This document discusses the evaluation and causes of chronic diarrhea. It begins by defining chronic diarrhea and outlining the normal stool production process. It then describes the main mechanisms that can cause diarrhea - osmotic, secretory, inflammatory, and dysmotility. Specific causes are discussed under each mechanism, including diseases, medications, toxins, and dietary factors. The document outlines the evaluation of a patient with chronic diarrhea, including history, physical exam, stool tests, imaging, and other lab tests. It provides guidance on testing for malabsorption and evaluating postsurgical causes of chronic diarrhea.
This patient is a 54-year-old female with type 2 diabetes presenting with worsening gastrointestinal symptoms of early satiety, heartburn and nausea despite dietary modifications. Investigations including EGD revealed mild antral erythema and food residue in her stomach, with a hiatal hernia present but no esophagitis or Barrett's esophagus. H. pylori testing was negative. The primary diagnosis is likely gastroparesis, and recommended treatment includes a proton pump inhibitor along with modifying her diabetes medications.
This document discusses jaundice and approaches to evaluating its underlying causes. It defines jaundice as yellowish discoloration from bilirubin deposition. Liver enzymes, imaging like ultrasound and CT, and procedures like ERCP can help differentiate causes like viral hepatitis, alcoholic liver disease, autoimmune conditions, and obstructive jaundice. A careful history, exam, and pattern of lab and imaging abnormalities can often reveal the etiology of jaundice. A liver biopsy may be needed in some unclear cases to establish a diagnosis.
CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC EN...Akhil Joseph
A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.
This document discusses aplastic anemia, a condition characterized by pancytopenia and bone marrow hypocellularity. It defines aplastic anemia, discusses its causes (acquired from things like radiation, drugs, viruses, immune diseases, or inherited genetic syndromes), epidemiology, pathophysiology, clinical features including symptoms and examination findings, diagnostic testing including blood tests and bone marrow biopsy, and treatment options including hematopoietic stem cell transplantation, immunosuppression, supportive care, and prognosis.
HEPATOBILIARY PATHOLOGY QUESTIONS & ANSWERS
LIVER
BILEDUCT PATHOLOGY
CASE STUDY AND
IMAGE BASED QUESTIONS WITH
PROPER ELABORATED ANSWERS
REF:- ROBBINS PATHOLOGIC BASIS OF DISEASES (TEXT BOOK)
OTHER REFS:- HARSH MOHAN'S TEXT BOOK OF PATHOLOGY
ATLAS OF PATHOLOGY
INTERNET SOURCES
BEFORE GOING TO START THE QUESTIONS JUST GIVE A LOOK ON THE "LIVER PATHOLOGY" SLIDES FROM THE GIVEN LINK BELOW
https://www.slideshare.net/SurajDhara2/liver-pathology-107731001
HAVE A NICE DAY
This document provides an overview of hypocalcemia, including:
- Causes of hypocalcemia such as hypoparathyroidism, vitamin D deficiency, renal failure, sepsis
- Symptoms of hypocalcemia including neurological symptoms, muscle spasms, cardiac issues
- Diagnosis and treatment of hypocalcemia including IV calcium supplementation and monitoring calcium levels
- Etiologies of hypocalcemia like hungry bone syndrome, acute pancreatitis, medications that can cause hypocalcemia
- Overview of calcium regulation in the kidney and genes involved
Anemia And Its Classification By Dr Bashir Ahmed Dar Chinkipora Sopore KashmirProf Dr Bashir Ahmed Dar
Anaemia due to iron deficiency is the characteristic finding with a cancer of the colon (large bowel), stomach or gullet. Often the anaemia is the only clue to the presence of a bleeding source somewhere. Any person who develops iron deficiency anaemia with no obvious cause should be investigated for the presence of a bleeding point within the digestive system. Fortunately not all bleeding sources turn out to be cancers
A 45-year-old female patient was admitted to the hospital for 5 days with complaints of loose stools, vomiting, abdominal pain, and decreased hemoglobin, PCV, and WBC levels. She was diagnosed with acute gastroenteritis and hyperthyroidism. She was treated with ondansetron, metronidazole, pantoprazole, ceftriaxone, carbimazole, and propranolol. She was advised to follow a proper diet, maintain hygiene, and take medications regularly to manage her conditions.
The document discusses liver cirrhosis, including its causes, classification, complications, and pathophysiology. It notes that cirrhosis can result from viral infections like hepatitis, alcohol use, metabolic disorders like obesity and diabetes, immune disorders, vascular abnormalities, and genetic disorders. Complications of cirrhosis include portal hypertension, ascites, and hepatic encephalopathy. The pathophysiology of alcoholic liver disease is also examined, with ethanol metabolism damaging the liver through direct toxicity, oxidative stress, and inflammation, potentially culminating in fatty liver, alcoholic hepatitis, and alcoholic cirrhosis over time.
A 35-year-old male auto driver was admitted with decreased urine output for 3 days and abdominal pain and fever for 10 days. Examination found pallor and abdominal tenderness. Tests showed acute kidney injury and a urine culture grew gram-negative bacilli. He was diagnosed with acute pyelonephritis likely caused by E. coli infection. He received IV and oral antibiotics and underwent hemodialysis. His kidney function and other lab values gradually improved with treatment.
A 33-year old man with polyuria and polydipsiaUsama Ragab
Clinical case uncovered (CCU) series
Endocrinology and diabetes
Case number 11: A 33-year old man with polyuria and polydipsia
Medical case presentation of polyuria
Hypoparathyroidism is a condition characterized by decreased function of the parathyroid glands and low levels of parathyroid hormone, resulting in low calcium and high phosphorus levels in the blood. Symptoms range from tingling in the extremities to seizures and altered mental state. The condition is diagnosed based on low calcium and parathyroid hormone levels in the blood. Treatment involves calcium and vitamin D supplements to manage calcium levels, with some patients also requiring parathyroid gland transplants.
The document discusses diseases of the parathyroid glands, including hyperparathyroidism and hypoparathyroidism. It covers the physiology and functions of the parathyroid glands and parathyroid hormone. It describes the etiology, pathogenesis, and classification of primary, secondary, and tertiary hyperparathyroidism. The clinical features of hyperparathyroidism are also outlined.
The document discusses the causes, evaluation, and differentiation of conjugated and unconjugated hyperbilirubinemia. Key causes of unconjugated hyperbilirubinemia include hemolysis and ineffective erythropoiesis. Causes of conjugated hyperbilirubinemia include genetic disorders like Dubin-Johnson syndrome and Rotor syndrome, as well as viral hepatitis, alcohol, drugs, toxins, and autoimmune conditions. Evaluation involves liver function tests and distinguishing between intrahepatic and extrahepatic cholestasis. A case example is presented with elevated direct bilirubin and aminotransferases suggestive of hepatitis.
This document provides guidance on evaluating a patient presenting with jaundice. It outlines a systematic approach including focused history, examination, differential diagnosis, and appropriate lab tests and imaging. Liver function tests can indicate hepatitic or cholestatic patterns. Case examples demonstrate applying this approach, such as using imaging and endoscopy to diagnose an ampullary tumor, managing a variceal bleed in cirrhosis, and identifying acute hepatitis B. Key considerations include complications of liver disease and importance of screening high-risk populations.
This document discusses inflammatory bowel disease (IBD), specifically Crohn's disease and ulcerative colitis. It defines IBD as a group of conditions that cause inflammation of the digestive tract, and notes the two major types are Crohn's disease and ulcerative colitis. Crohn's disease can impact any part of the digestive tract and often spreads deep into tissues, while ulcerative colitis exclusively impacts the innermost lining of the large intestine and rectum. Symptoms for both include abdominal pain, diarrhea, weight loss and more. While causes are unknown, it is believed to involve defects in the immune system. Diagnosis involves blood tests, stool samples, imaging and endoscopy. Treatment depends on the severity but may include
This document provides a historical overview of diabetes. Some key points include:
- The earliest known record of diabetes is from an Egyptian papyrus from around 1500 BC. The term "diabetes" comes from the Greek word for "siphon" and was coined in the 3rd century BC.
- In the 16th century, diabetes was identified as a severe disorder affecting the whole body. The pancreas's role in diabetes was discovered in the 1870s but its function remained unknown.
- In 1921-1923, Banting, Best, and Macleod discovered insulin and its role in controlling blood sugar levels, representing a major breakthrough in diabetes treatment.
DIABETIC KETOACIDOSIS PRESENTATION BY ROOMA KHALIDRooma Khalid
This document discusses diabetic ketoacidosis (DKA). It defines DKA and its signs and symptoms. DKA occurs more often in type 1 diabetes and is characterized by blood glucose over 250 mg/dl, blood pH below 7.3, and ketones in serum over 5 mEq/L. Proper treatment of DKA involves fluid replacement, insulin administration, and monitoring of blood glucose, electrolytes, and pH to correct dehydration, hyperglycemia, and acidosis. Failure to treat the patient's DKA led to worsening of her condition.
This document discusses the management of hyperosmolar hyperglycemic state (HHS), a metabolic emergency seen in uncontrolled type 2 diabetes. It defines HHS as severe hyperglycemia with plasma glucose over 33 mmol/L, altered mental status, and serum osmolarity over 320 mosm/L. Precipitating factors include newly diagnosed diabetes, consumption of sugary drinks, discontinuing medications, surgery, steroids or diuretics. Treatment involves rehydration, insulin to lower blood glucose, electrolyte replacement, and treating any underlying causes. Insulin doses are lower than in diabetic ketoacidosis but doubled if glucose does not fall adequately.
This document provides an overview of diabetes including:
- Definitions of diabetes and different types such as type 1, type 2, and gestational diabetes.
- Epidemiology and pathophysiology of diabetes.
- Clinical presentation including signs, symptoms, and diagnostic tests.
- Pharmacological and non-pharmacological treatment options including medications, diet, patient counseling.
- A case study is presented of a 40-year-old female patient with type 2 diabetes, hypertension, and endometrial issues who was admitted to the hospital with fever and bleeding.
This document provides an overview of endocrine disorders and their management. It discusses the major glands of the endocrine system including the hypothalamus, pituitary gland, thyroid, parathyroids, adrenals, pancreas, ovaries/testes, and kidneys. For each gland, it describes the hormones produced and their functions. The document also covers assessment and diagnostic evaluation of endocrine disorders. Specific disorders discussed in detail include diabetes insipidus, diabetes mellitus, diabetic ketoacidosis, and hyperglycemic hyperosmolar non-ketotic syndrome. Treatment, nursing management, and complications of these conditions are summarized.
Nephrotic syndrome, Characterized by heavy proteinuria>3.5g/m/day in adults,>...FarsanaM
Nephrotic syndrome, in paediatric patients(children), mainly Minimal change nephrotic syndrome (MCNS),Characterized by heavy proteinuria>3.5g/m/day in adults,>1g/m/day in children, hypoalbuminemia <2.5g/dL, oedema, hyperlipidemia 200mg/dL, Pathogenesis of MMCNS injury to the glomerular visceral epithelial cell( Podocyte) foot processes
This document provides a summary of diabetes mellitus (DM), including its definition, presentation, classifications, complications, investigations, and management. DM results from lack of or diminished insulin effectiveness and is characterized by hyperglycemia. There are two main types: type 1 DM is insulin-dependent while type 2 DM is non-insulin dependent initially but may eventually require insulin. Complications can include infections, neuropathy, retinopathy, and vascular diseases. Management involves lifestyle changes like diet and exercise as well as medications and insulin to manage blood glucose levels and prevent complications.
Diabetic ketoacidosis by Dr.Taniful.pptxTaniful Haque
A 37-year-old female with a history of type 1 diabetes was admitted to the ICU unconscious for 12 hours with respiratory distress and abdominal pain. Laboratory tests found ketones in her urine and blood glucose of 20.7 mmol/L, indicating diabetic ketoacidosis. She was treated with intravenous fluids, insulin therapy, and potassium supplementation to correct dehydration, hyperglycemia, and electrolyte imbalances. Diabetic ketoacidosis is a life-threatening complication of diabetes that occurs when there is not enough insulin to control blood glucose levels, leading to the breakdown of fat as an alternative energy source and producing ketone bodies that accumulate and cause metabolic acidosis.
Type 1 diabetes results from autoimmune destruction of pancreatic beta cells leading to insulin deficiency. It is the most common form of diabetes in children and adolescents. Type 2 diabetes is increasing in youth and is associated with obesity, family history, and insulin resistance. Both can cause long-term complications if not well-controlled. Diabetic ketoacidosis is a life-threatening complication of diabetes characterized by hyperglycemia, ketosis, and acidosis usually precipitated by infection or non-compliance with insulin therapy. Treatment involves fluid resuscitation, insulin therapy, and electrolyte replacement to resolve the metabolic abnormalities.
Hypoglycemia is defined as abnormally low blood glucose levels that expose individuals to potential harm. It is caused by underproduction or overutilization of glucose. In diabetes patients, hypoglycemia is commonly caused by excessive insulin doses, missed or delayed meals, increased exercise, or other factors. Symptoms range from mild neurogenic symptoms like sweating to more severe neuroglycopenic symptoms like seizures. Treatment involves oral carbohydrate intake or intravenous dextrose for more severe cases. Regular screening, education to prevent recurrence, and glucagon prescription are recommended to prevent hypoglycemia-related complications.
This case involves a 30-year old woman presenting with a wide range of symptoms over 12 months including fatigue, arthritis, rashes, oral ulcers, hair loss, and kidney problems. Physical exam and lab tests confirmed she meets enough criteria for a diagnosis of systemic lupus erythematosus (SLE) with class IV lupus nephritis. Her treatment plan includes cyclophosphamide, steroids, ACE inhibitors, and later azathioprine to control her SLE and protect her kidneys. Her response is being monitored through disease markers and renal function.
This document discusses adrenal insufficiency and its causes, presentation, diagnosis, and management. It can be primary or secondary. Primary adrenal insufficiency, also known as Addison's disease, is caused by destruction of the adrenal cortex leading to deficiencies in glucocorticoids, mineralocorticoids, and sex steroids. Its hallmark symptoms include fatigue, gastrointestinal issues, hyperpigmentation, and electrolyte abnormalities. Secondary adrenal insufficiency spares mineralocorticoid function and can result from pituitary or hypothalamic disease. Diagnosis involves ACTH and cortisol testing, and treatment is glucocorticoid and mineralocorticoid replacement.
Dr. Stacy Arvinna presented on various endocrine emergencies including:
1. Diabetic ketoacidosis is characterized by hyperglycemia, ketosis and acidemia due to insulin deficiency. It requires fluid resuscitation and insulin therapy.
2. Thyroid storm is a severe exacerbation of hyperthyroidism with multi-organ involvement. It has a high mortality and requires beta blockade, antithyroid drugs, iodine and corticosteroids.
3. Myxedema coma is the severe manifestation of hypothyroidism leading to decreased mental status and hypothermia. It requires gradual rewarming and high dose thyroid hormone replacement.
Cushing's syndrome is caused by excessive cortisol levels and can be due to exogenous glucocorticoid use or endogenous overproduction. It is characterized by central obesity, moon face, buffalo hump, skin changes, hypertension and diabetes. The diagnosis involves tests to check for cortisol suppression and circadian rhythm disturbances. Further tests are then used to determine the underlying cause as pituitary, adrenal or ectopic tumor. Treatment depends on the specific cause but may include surgery, medication or radiation. Pheochromocytomas are rare catecholamine-secreting tumors that cause hypertension and panic attacks. Diagnosis involves urine or plasma tests for metabolites and imaging to locate the tumor. Preparation with alpha-blockers is usually
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
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2. Mowafy medical symphony Revision
Endocrionology revision
Enumerate :
1. Causes of Cushing syndrome.
2. Causes of secondary diabetes.
3. Causes of stunted growth ( Dwarfism, short stature ). P14
4. Endocrinal causes of short stature. P 14
5. Causes of hypercalcemia.
6. Identify the TWO most common causes of hypercalcemia
o Primary hyperparathyroidism 55%
o Malignancy 30%
7. Causes of hypocalcemia.
o Chronic renal failure.
o Vitamine D deficiency.
o Hypoparathyroidism.
o Hyperphosphatemia.
o Acute pancreatitis.
8. Causes of fasting hypoglycemia
9. Causes of hirsutism.
10. Causes of gynaecomastia.
11. Causes of tetany.
12. Causes of hypoadrenalism.
13. Causes of hypothyroidism.
14. Causes of obesity.
3. Mowafy medical symphony Revision
15. Causes of loss of weight inspite of good appetite. P 95
16. Causes of nephrogenic DI.
17. Causes of hyperprolactinemia.
18. Acquired causes of hyperlipidemia
o Hypothyroidism
o DM
o Obesity/metabolic syndrome
o Primary biliary cirrhosis
o Nephrotic syndrome
o Diet high in saturated fat
o Drugs : anabolic steroids , beta blockers , thiazides …
19.Criteria for good diabetic control. P86
20.Endocrinal causes of hypertension.
21. Laboratory tests for hyperthyroidism.
22. Side effect of metformin.
23.Endocrinal causes of abdominal pain.
24. Plain X-ray skull in a case of acromegaly.
o Widening of sella turcica and erosion of posterior clenoids.
o Widening of nasal sinuses.
o Prominent supraorbital ridges & occipital protuberance.
o Prognathism with wide separation of teeth.
25. Define Impaired glucose tolerance :
Patients with levels between 140 and 199 mg/dL , 2h postprandial or random
blood glucose.
4. Mowafy medical symphony Revision
26.Genetic syndromes associated with diabetes
o Down’s syndrome.
o Turner’s syndrome.
o Feridreich’s ataxia
o Myotonia dystrophy.
27. Criteria for diagnosis of diabetes mellitus
o Classic symptoms of hyperglycemia PLUS random glucose of > 200
mg/dL
o Fasting plasma glucose of 126mg/dL or greater on TWO separate
occasions.
o 2 hours postprandial glucose of 200 mg/dL or greater confirm the
presence of diabetes.
28.Acute diabetic complications :
o Hypoglycemia
o DKA
o HHNK state
o Lactic acidosis.
29.Clinical stages of diabetic nephropathy
30. Skin complications of DM
31. Cardiovascular , neurological , urogenital complications of DM.
32. Endocrinopathies ,that may be associated with hyperglycemia.
o Acromegaly
o Cushing’s syndrome
o Pheochromocytoma
o Thyrotoxicosis.
o Somatostatinoma , glucagonoma.
5. Mowafy medical symphony Revision
33- Causes of precocious puberty.
In boys : puberty before age of 9 is considered precocious.
In girls : Breast development or pubic hair with onset < 7 years.
I. Isosexual precocity :
a) Central : ( Gonadotropin - dependent precocious puberty ) :
- It is caused by premature activation of GnRH
- Causes :
Idiopathic ( constitutional ).
Hypothalamic hamartoma : produces pulsatile gonadotropin-
releasing hormone (GnRH).
Damage to the inhibitory system of the brain : due to infection,
trauma, or irradiation.
b) Peripheral : ( Gonadotropin - independent precocious puberty )
- Androgen from testis or adrenal gland is increased but gonadotropin is low.
- Causes :
Congenital adrenal hyperplasia.
Gonadal tumors (such as arrhenoblastoma)
Adrenal tumors.
Germ cell tumor.
McCune–Albright syndrome : is a genetic disorder of bones, skin
pigmentation and hormonal problems along with premature puberty.
Exogenous sex steroid administration.
II. Heterosexual : Refers to the premature development of estrogenic features
in boys, such as breast development.
6. Mowafy medical symphony Revision
Diagnostic criteria of precocious puberty :
Breast development in boys before appearance of pubic hair or
testicular enlargement.
Pubic hair or genital enlargement (gonadarche) in boys with onset
before 9 years.
Pubic hair (pubarche) before 8 or breast development (thelarche) in
girls with onset before 7 years.
Menstruation (menarche) in girls before 10 years.
34- Criteria & causes of delayed puberty.
In girls :
- No breast development by 13 years, or
- No menarche by 3 years after breast development (or by 16).
In boys :
- No testicular enlargement by 14 years,
- Lack of pubic hair by age of 15, or
- More than 5 years to complete genital enlargement.
Causes :
a) Constitutional delay : it runs in families. ( The most common )
b) Systemic disease, e.g. chronic renal failure, thalassemia major.
c) Undernutrition e.g. anorexia nervosa, zinc deficiency.
d) Hypothalamic defects e.g. Kallmann syndrome, craniopharyngioma
e) Pituitary defects e.g. hypopituitarism.
f) Gonadal defects e.g. Turner syndrome, Klinefelter syndrome, Testicular
failure due to mumps orchitis.
g) Endocrine disorders e.g. hypothyroidism, Cushing's syndrome.
7. Mowafy medical symphony Revision
Give a short account on
1. Management of DKA
2. Clinical picture & treatment of hypoglycemic coma.
3. Different types of insulin.
4. Indications , adverse effects of insulin.
5. Diabetic nephropathy.
6. Diabetic neuropathy
7. Microvascular complications of DM
- Retinopathy - nephropathy - neuropathy
8. Oral hypoglycemic drugs
9. Management of type II diabetes ( drug details needed )
10.Diagnosis , treatment of hyperthyroidism.
11. Diagnosis & treatment of hypothyroidism.
12. Thyroid emergencies
o Thyrotoxic crisis ( thyroid storm )
o Myxedema coma
13. Clinical picture , investigations & treatment of primary hyperparathyroidism.
14. Management of Cushing’s syndrome.
15. Causes , Clinical picture , Investigations & treatment of chronic adrenal
failure.
16. Acute adrenal failure
17. Hazards of obesity.
18. Diagnosis , treatment of acromegaly.
8. Mowafy medical symphony Revision
19. Pituitary apoplexy.
o Def : sudden enlargement of the pituitary by hemorrhage into the
tumor
o C/P :
Pressure manifestations : Headache , vomiting , visual defect .
Panhypopituitarism : ……
o Investigations :
Lab : evaluate pituitary hormones , electrolytes , glucose.
Imaging : CT , MRI ( MRI is the most sensitive )
o TTT : Replacement therapy , Transsphenoidal surgical decompression
of the tumor. See panhypopituitarism
20. Management of tetany.
21. DD of polyuria.
22. DD of short stature.
23. DD of hypercalcemia.
24. DD of skin pigmentation.
9. Mowafy medical symphony Revision
Other new therapy for diabetes : *
Pramlintide :
o Is synthetic amylin analogue.
o Used in type 1 or insulin requiring type 2 DM.
o Given with current diabetic regimen.
o Mode of action : Pramlintide injected SC just before a meal slows gastric
emptying & suppresses glucagon but doesn’t alter insulin levels.
o S/E : nausea , vomiting , frequent dosing injection ( 3 times daily )
Oral hypoglycemic agents :
1- Sulfonylureas :
2- Biguanides ( Metformin )
3- Alpha glucosidase inhibitors : Acarbose ( glucobay )
o Prevent breakdown of CHO in intestine glucose absorption.
o Disadvantage : Contraindicated in hepatic patient , abdominal pain.
4- Glinides : Repaglinide , Nateglinide.
o Stimulate secretion of insulin from beta cells.
o Rapid onset & short duration , acts on post prandial hyperglycemia.
5- Thiazolidinediones : ( Rosigitazone )
o Increases insulin sensitivity
o Can be combined with sulfonylurea , metformin or insulin.
o Advantage : improve diabetic dyslipidemia.
o Disadvantage :
Contraindicated in mild liver impairment.
Given cautiously to patient with heart failure , renal impairment.
Weight gain , mild edema.
NB : all oral hypoglycemic drugs are given cautiously to patient with hepatic ,renal &
heart failure.
10. Mowafy medical symphony Revision
Endocrine doses
1- DM :
- Dose of insulin : P 80
- DKA : P 75 don’t forget the doses of the following :
i- Short acting insulin : 5 – 10 U / hour infusion
When blood glucose < 250 mg/dl : reduce insulin to 2 – 4 U / hour.
ii- Fluid therapy : 6 – 8 L is usually required.
At first saline is given , then change to glucose 5 % when blood glucose < 250
mg/dl.
iii- K therapy : add 20 – 40 m.eq to each 1 L of fluid.
2- SRG :
Caushing : Suppression test : by dexamethazone
- Small dose : 0.5 mg / 6h for 2 days
- Large dose : 2 mg / 6h for 2 days
Addison :
- Cortisone : 7.5 mg / d - Flurocortisone : 0.1 – 0.2 mg/d
Addisonian crisis : Hydrocortisone : 50 mg / 6h
NB : Dexamethasone 2mg IV is indicated before or during ACTH test because it
will not interfere with plasma cortisol assay.
3- Thyroid :
- Antithyroid drugs :
● Methyl thyouracil : 200 mg tds then reduce after 2 months to 100 mg tds for 2y
● Propyl thyouracil : 100 mg tds then reduce after 2 months to 50 mg tds for 2 y
● Carbimazole : 20 mg tds then reduce after 2 months to 10 mg tds for 2 years
Thyrotoxic crisis :
◊ Propyl thyouracil : 200 mg / 4 h orally , rectally or nasogastric.
◊ Propranolol : in full dose ( 1mg/ 5 min IV then 100 mg / 6h orally )
Hypothyroidism :
L thyroxin : start with 50 μg/d & gradually up to 100 – 200 μg /d orally
Myxedema coma : Thyroxine 250 μg IV
11. Mowafy medical symphony Revision
Cases
1- Male patient of 42 years old, presented with parasthesia in his hands & feet of
6 months duration. During this period he was admitted to the emergency hospital
with disturbed level of consciousness and left sided body weakness. He was fully
investigated and received medical treatment and discharged well after one week.
He advised to be kept on special diet regimen and specific drug ( injection ) used
daily. He gave history of palpitation & fainting attacks on standing. Clinical
examination revealed cachexia, white patches over the tongue. Pulse 98b/m, BP
standing 140/85 and recumbent 180/105 mmHg. Heart accentuated S2 with
ejection systolic murmur over the mitral area, Liver was enlarged 2 fingers with
rounded border but not tender. Neurological examination revealed superficial &
deep sensory affection.
a) What is the provisional diagnosis ?
b) Give an explanation to symptoms & signs in this patient.
c) If there are other complications to the primary disease ?
d) What is the pathogenesis of these complications ?
e) What are the investigations suggested for diagnosis ?
a) This is a case of complicated DM and hypertension.
b)
Peripheral neuropathy : parathesia of hands & feet
Autonomic neuropathy : fainting & postural hypotension & tachycardia.
Monilial infection : white patches over the tongue.
Accentuated S2 is due to hypertension
Ejection systolic murmur is due to functional AS
c) complications of DM see endocrinology book
d) pathogenesis of DM & its complications
Metabolic
Recurrent infections.
Vascular : micro & macro angiopathies
Biochemical : accumulation of sorbitol neuropathy.
e) Investigations : see endocrinology book
12. Mowafy medical symphony Revision
2- Female patient aged 32 years presented with backaches and fatigability with
polyuria. She was overweight. BP 140/100 mmHg. Fasting blood glucose 200mg%
a) Mention 4 signs that help the diagnosis.
b) What is the possible diagnosis and differential diagnosis ?
c) How would you treat such case ?
a)
Plethoric face.
Hirsutism and acne may be apparent in female
Pigmentation & purpura.
Trunkal obesity with stria rubra.
Moon face : rounded face , bloated cheeks.
Muscle wasting & weakness.
b)
Possible diagnosis : Cushing’s syndrome
DD :
Obese hypertensive diabetic patients.
Female taking oral contraceptive pills.
Chronic alcoholism.
Frolich’s syndrome : trunk obesity , hypogonadism , polyphagia.
Differentiate between 1ry & 2ry Cushing. ( ….. )
c) Treatment of Cushing : see endocrinology book p 53
13. Mowafy medical symphony Revision
3- A 40-year-old man is seen because of headaches, muscle aches, and chronic
low back and joint pain. As he enters the office, you notice his coarse facial
features, frontal bossing, and large jaw. When you shake his hand, you find he has
large, doughy, sweaty palms and, when he smiles, you note his teeth are widely
spaced. He has not seen a physician in 10 years and is taking no medications. His
back and joint pain have been worsening for 6 years, but his headaches started 6
months ago. His physical examination findings are significant for a BP of 150/100
mm Hg, pulse of 60 per minute, and respiratory rate of 12 per minute.
He returns in 2 weeks with old photographs that confirm a change in his physical
appearance over time, and the laboratory test results confirm your clinical
impression.
a) What is your initial diagnosis in this patient?
b) Besides the back and joint pain and the headaches, what other symptoms
would you look for to confirm or refute your diagnosis?
c) Besides the physical features you observe initially, what other abnormalities
would you look for on physical examination?
d) What laboratory tests should be performed initially?
e) What additional testing should be performed once the initial laboratory
results are known?
f) What is the preferred treatment in this patient?
a) What is your initial diagnosis in this patient?
Acromegaly should be your initial diagnosis.
b) Besides the back and joint pain and the headaches, what other
symptoms would you look for to confirm or refute your diagnosis?
Other symptoms to look for in this patient include a change in glove, ring, and
shoe sizes, spaces between the teeth, decreased libido and impotence, sweating,
new snoring, polyuria, polydipsia, and a change in vision.
14. Mowafy medical symphony Revision
c) Besides the physical features you observe initially, what other
abnormalities would you look for on physical examination?
Other physical features to look for in this patient include thick coarse skin,
enlarged extremities and organs, entrapment neuropathies, visual field
abnormalities, and decreased body hair and testicular size. Old pictures would
confirm the clinical suspicion.
d) What laboratory tests should be performed initially?
Initial laboratory tests in this patient would consist of the measurement of
IGF-1 (somatomedin C) and fasting GH levels. If the levels are elevated it
would suggest the diagnosis of acromegaly, which would be confirmed if
the GH levels did not suppress to less than 2 ng/mL in response to a
glucose load ( suppression test )
e) What additional testing should be performed once the initial laboratory
results are known?
If the initial laboratory results indicate acromegaly, a fasting blood sugar test
should be performed to rule out diabetes. Pituitary tests should include
measurement of the prolactin, FSH, LH. An MRI scan can show the extent of
the tumor, and formal visual field testing should be performed.
f) What is the preferred treatment in this patient?
The preferred initial treatment is surgical removal of the tumor. Bromocriptine
or a somatostatin (octreotide) analog may be useful as medical adjuncts.
Radiation therapy may be indicated for the destruction of residual tumor if
reoperation or surgical cure is not feasible. Postoperative hormonal testing is
indicated to reassess pituitary function. Echocardiography and colonoscopy
should be performed to evaluate for cardiomegaly and colon polyps.
15. Mowafy medical symphony Revision
4- A known diabetic patient was brought to the hospital in coma.
a) Enumerate the probable causes.
b) How would you differentiate between the 2 most common causes of
coma in diabetic patient aged 20 years ?
Answer : b) DKA & hypoglycemic coma : see endocrine book
5- A woman aged 55 years old, her weight is 95 kg & her height is 160 cm. She
was discovered by chance to be diabetic.
a) What are the laboratory criteria for diagnosis of DM?
b) Discuss oral anti-diabetic drugs ?
c) Describe one method by which you can know if she is obese.
d) Enumerate the hazards of obesity.
The answer : Needless to say that she is type 2 DM
c)
Diagnosis of obesity :
1- Body Mass Index ( BMI ) :
2- Skin fold thickness e.g. over triceps ( N : 20 mm in ♂ , 30 mm in ♀ ).
3- Estimation of body fat : ( Waist / hip ratio )
a. Central obesity : more fat in the upper body
( Apple shaped ) , associated with more morbidity .
b. Peripheral obesity : more fat in lower body ( pear
shaped ) , associated with less morbidity .
BMI Classification
18.5 – 25 normal weight
25 – 30 overweight
30 – 35 class I obesity
35 – 40 class II obesity
Over 40 class III obesity
16. Mowafy medical symphony Revision
6- A male diabetic patient 30 years old who received his usual insulin therapy in
the morning, but he neglected to take his breakfast, short time later he got blurring
of vision, irritability , excessive sweating, then he passed into coma.
a) What is the diagnosis ?
b) How can you prove your diagnosis ?
c) How can you treat this patient ?
d) What are the possible other causes of such diagnosis ?
7- A 25 year old pregnant female developed severe post-partum hemorrhage
which was successfully controlled. The baby was artificially fed as his mother’s
breast failed to secrete milk. The mother began to feel weak and she noticed
atrophy of her breasts.
a) What is the most probable diagnosis ?
b) What is the expected BP of the patient ?
c) How to prove your diagnosis by investigations ?
Three drugs were prescribed after the results of investigations were known, but the
patient started only by one of them, in order not to distress her stomach. Next day
the patient complained of severe abdominal colic, vomiting and diarrhea. Her BP
was dropping rapidly and she became irritable and confused.
d) What is your diagnosis ?
e) How to manage the case ?
The answer :
a) Sheehan syndrome.
d) Acute adrenal failure.
17. Mowafy medical symphony Revision
MCQ
1- Insulin is contraindicated in :
a) Type 1 DM
b) Complicated type 2 DM
c) DM with pregnancy.
d) Hypoglycemic coma.
2- Hypoglycemia is characterized by all the following EXCEPT
a) Blurring of vision.
b) Headache.
c) Dry skin
d) Pupillary dilatation.
3- Gynecomastia may be seen in all the following EXCEPT
a) Newborn infants
b) Klinefelter's syndrome
c) Hypopituitarism.
d) Turner’s syndrome
4- Secretion of which of the following hormones does not primarily occur
at night
a) Insulin
b) Growth hormone
c) Melatonin
d) Prolactin
5- Earliest changes observed by ophthalmoscope in background
retinopathy in diabetes
a) Venous dilatation
b) Microaneurysms
c) Increased capillary permeability
d) Arterio-venous shunts
18. Mowafy medical symphony Revision
6- Which is NOT a part of metabolic syndrome X
a) Hyperlipidemia
b) Obesity
c) Ischemic heart disease
d) Hypertension
7- Thiazolidinedione group of antidiabetic is
a) Voglibose
b) Nateglinide
c) Rosiglitazone
d) Glimepiride
8- All are features of diabetic ketoacidosis EXCEPT
a) Hyperthermia
b) Drowsiness
c) Dehydration
d) Air hunger
9- Commonest cause of coma in a diabetic is
a) DKA
b) Lactic acidosis
c) Hyperosmolar hyperglycemic non ketotic coma
d) Hypoglycemia
10- A patient of impaired fasting glucose ranges blood glucose value in
between
a) 96 - 106 mg/dL
b) 106 - 116 mg/dL
c) 100 - 125 mg/dL
d) 116 - 130 mg/dL
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11- Microalbuminuria is urinary albumin excretion ratio between
a) 10 - 20 μg/min
b) 20 - 200 μg/min
c) 30 - 300 μg/min
d) 40 - 400 μg/min
12- Myxedema coma is characterized by
a) Hypertension
b) Tachycardia
c) Euthermia
d) Hypoventilation
13- Upper segment > lower segment of body is found in all ( in dwarfism )
EXCEPT
a) Pituitary dwarf
b) Cretinism
c) Achondroplasia
d) Juvenile myxedema
14- Which cranial nerve is not involved in acromegaly
a) VIII
b) III, IV, VI
c) V
d) II
15- Pseudo-Cushing’s syndrome may be found in all EXCEPT
a) Myxedema
b) Chronic alcoholism
c) Obesity
d) Depression
20. Mowafy medical symphony Revision
16- Gynaecomastia may be produced after treatment with all EXCEPT
a) Spironolactone
b) Digitalis
c) Cimetidine
d) Rifampicin
17- Pheochromocytoma is not associated with
a) Weight gain
b) Fear of death
c) Paroxysmal hypertension
d) Constipation
18- Most common type of carcinoma of the thyroid gland is
a) Follicular
b) Anaplastic
c) Papillary
d) Mixed ( follicular & papillary )
19- Froehlich’s syndrome is characterized by all EXCEPT
a) Infantilism
b) Truncal obesity
c) Diabetes mellitus
d) Mental retardation
20 - Which is not a part of multiple endocrine neoplasia type 1
a) Pheochromocytoma
b) Tumor of pituitary
c) Tumor of pancreas
d) Hyperparathyroidism
21- Tertiary hyperparathyroidism is commonly found in
a) Rickets
b) Pseudohypoparathyroidism
c) Chronic renal failure
d) Malabsorption syndrome
21. Mowafy medical symphony Revision
22- Commonest cause of thyrotoxicosis is
a) Multinodular goiter
b) Hashimoto’s thyroiditis
c) Grave’s disease
d) Well differentiated carcinoma
23- Osmoreceptors are present in
a) Atria
b) Kidney
c) Anterior hypothalamus
d) Adrenal cortex
24- In Somogyi phenomenon commonly associated with type 2 DM, the dose
of insulin should be
a) Increased
b) Stopped
c) Decreased
d) Needs no change
25- Orlistat is used to treat
a) Diabetic nephropathy
b) Gout
c) Obesity
d) Anorexia nervosa.
26- Commonest cause of unilateral exophthalomos is :
a) Cavernous sinus thrombosis.
b) Retrobulbar tumor.
c) Chloroma.
d) Thyrotoxicosis.
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27- Sleeping pulse rate is NOT increased in
a) Anxiety neurosis.
b) Rheumatic carditis.
c) TB
d) Atropinised patient.
28- Cardiovascular finding of thyrotoxicosis do not include
a) Loud S1
b) Means-Lerman scratch.
c) Water hammer pulse.
d) Ejection click.
29- Myxedema is characterized by all EXCEPT
a) Butterfly rash in face.
b) Sinus bradycardia.
c) Solid edema.
d) Madarosis.
30- Acromegaly is associated with all of the following EXCEPT
a) Acanthosis nigricans
b) Fibromata mollusca
c) Micrognathia.
d) Cardiomegaly.
31- Klinefelter's syndrome is characterized by :
a) Small, soft testes.
b) Chromosomal pattern 46, XO
c) Upper segment > lower segment of body.
d) Gynecomastia.
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32- Tall stature is NOT characteristic of
a) Klinefelter's syndrome.
b) Marfan's syndrome.
c) Homocysteinuria.
d) Turner's syndrome.
33- All of the following are featured by skin pigmentation EXCEPT
a) Conn's syndrome.
b) Bronchogenic carcinoma.
c) Addison's disease.
d) Hemochromatosis.
34- Medical adrenalectomy is done by all EXCEPT
a) Aminoglutethimide.
b) Mitotane.
c) Mexiletine.
d) Metyrapone.
35- Sheehan's syndrome presents with
a) Cardiac failure.
b) Persistent lactation.
c) Fever
d) Cachexia.
36- Hypocalcemia is produced by all EXCEPT
a) Hysterical hypoventilation.
b) Acute pancreatitis.
c) Chronic renal failure.
d) Osteomalacia.
24. Mowafy medical symphony Revision
37- Thyrotoxicosis may be featured by all EXCEPT
a) Myopathy
b) Pretibial myxedema.
c) Hypernatremia.
d) Atrial fibrillation.
38- Hyperparathyroidism is NOT featured by
a) Acute pancreatitis.
b) Nephrocalcinosis.
c) Palpable neck swelling.
d) Pseudogout.
39- Malignant hypercalcemia is treated by all EXCEPT
a) Pamidronate.
b) Calcitonin
c) Calcitriol
d) Glucocorticoids.
40- Commonest cause of Addison's disease is
a) Granuloma
b) Idiopathic atrophy
c) Inflammatory necrosis.
d) Malignancy
41- Features of Addison's disease do not include
a) Diarrhea
b) Dizziness
c) Dermatitis
d) Dehydration.
42- Karyotype 47, XYY is
a) True hermaphroditism
b) Supermale
c) Klinefelter's syndrome.
d) Gonadal dysgenesis.
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The answers
1) D
2) C
3) D
4) A
5) B
6) C
7) C
8) A
9) D
10) C
11) B
12) D
13) A
14) C
15) A
16) D
17) A
18) D
19) C
20) A
21) C
22) C
23) C
24) C
25) C
26) D
27) A
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28) D
Means-Lerman scratch is an uncommon type of heart murmur which occurs in
patients with hyperthyroidism. It is a mid-systolic scratching sound best heard
over the upper part of the sternum or second left intercostal space at the end of
expiration. The murmur results from the rubbing of the pericardium against the
pleura in the context of hyperdynamic circulation and tachycardia, and may
mimic the sound of a pericardial rub.
29) A
Madarosis : hair loss of the eyebrows (superciliary madarosis) or loss of
eyelashes (ciliary madarosis).
30) C
31) D
32) D
33) A
34) C
Aminoglutethimide : antisteroid drug.
Mitotane : anti-neoplastic drug used in the treatment of adrenocortical
carcinoma.
Mexiletine : Class IB anti-arrhythmic.
Metyrapone : it blocks cortisol synthesis by inhibiting steroid 11β-hydroxylase.
35) D
36) A
37) C
38) C
39) C , Calcitriol : active vit D, also called 1,25-dihydroxycholecalciferol.
40) B
41) C
42) B
Supermale : 47, XYY
Klinefelter : 47, XXY