Management of acute pancreatitis involves initially assessing the patient based on history, physical exam, and laboratory/imaging tests to confirm the diagnosis. Key factors include serum amylase and lipase levels over 3 times normal, abdominal pain, and imaging showing pancreatic inflammation. The condition is caused by premature activation of digestive enzymes within the pancreas due to various genetic and environmental factors. Treatment focuses on pain management, monitoring for complications, and treating any underlying causes like gallstones. Prognosis can be assessed using scoring systems like Ranson's criteria or CT severity index which evaluate markers of severity in the first 48 hours.
A presentation on the pathology and current management (with Especial emphasis on surgical management) of Portal Hypertension; a common complication of liver cirrhosis among other liver diseases. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.
This document outlines the plan for a presentation on Budd-Chiari syndrome. It begins with a brief history of the syndrome dating back to 1842. It then covers the definition, etiology, pathogenesis, clinical presentation, diagnosis and imaging. Etiology sections discuss hypercoagulable causes like myeloproliferative disorders and acquired causes such as oral contraceptives and pregnancy. Clinical presentation varies from acute to chronic forms. Imaging plays an important role in diagnosis, with ultrasound Doppler being the first-line investigation to assess patency of hepatic veins and inferior vena cava. The document is organized into two parts, with part A covering background information and part B to focus on management.
The document defines various types of strokes and transient ischemic attacks. It discusses the epidemiology, risk factors, clinical features, investigations, and management of strokes. The main types are ischemic and hemorrhagic strokes. Investigations include brain imaging like CT scan and MRI to identify the type of stroke and underlying causes. Treatment focuses on minimizing brain damage, preventing complications, rehabilitation, and reducing the risk of recurrence.
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
This document discusses psoas abscess, which is a collection of pus in the iliopsoas compartment. Psoas abscess can be primary (from hematogenous spread) or secondary (from infection of adjacent organs). Common causes of secondary psoas abscess include gastrointestinal, genitourinary, musculoskeletal, and vascular infections. Clinical features can include fever, back pain, limp, and abdominal or groin pain. Diagnosis involves blood tests and imaging like CT or MRI. Treatment requires appropriate antibiotics and drainage of the abscess, either percutaneously or through open drainage.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
A presentation on the pathology and current management (with Especial emphasis on surgical management) of Portal Hypertension; a common complication of liver cirrhosis among other liver diseases. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.
This document outlines the plan for a presentation on Budd-Chiari syndrome. It begins with a brief history of the syndrome dating back to 1842. It then covers the definition, etiology, pathogenesis, clinical presentation, diagnosis and imaging. Etiology sections discuss hypercoagulable causes like myeloproliferative disorders and acquired causes such as oral contraceptives and pregnancy. Clinical presentation varies from acute to chronic forms. Imaging plays an important role in diagnosis, with ultrasound Doppler being the first-line investigation to assess patency of hepatic veins and inferior vena cava. The document is organized into two parts, with part A covering background information and part B to focus on management.
The document defines various types of strokes and transient ischemic attacks. It discusses the epidemiology, risk factors, clinical features, investigations, and management of strokes. The main types are ischemic and hemorrhagic strokes. Investigations include brain imaging like CT scan and MRI to identify the type of stroke and underlying causes. Treatment focuses on minimizing brain damage, preventing complications, rehabilitation, and reducing the risk of recurrence.
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
This document discusses psoas abscess, which is a collection of pus in the iliopsoas compartment. Psoas abscess can be primary (from hematogenous spread) or secondary (from infection of adjacent organs). Common causes of secondary psoas abscess include gastrointestinal, genitourinary, musculoskeletal, and vascular infections. Clinical features can include fever, back pain, limp, and abdominal or groin pain. Diagnosis involves blood tests and imaging like CT or MRI. Treatment requires appropriate antibiotics and drainage of the abscess, either percutaneously or through open drainage.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
The document discusses an integrated approach to diagnosing splenomegaly. It begins by defining splenomegaly and examining the spleen. A step-wise approach is then outlined involving taking a thorough history, conducting a physical exam, ordering lab and imaging tests, and performing specialized testing to investigate for possible etiologies of splenomegaly such as infection, infiltration, congestion, and hyperplasia. The goal is to determine the underlying cause and provide appropriate treatment.
1) PAD is associated with increased risk of myocardial infarction and ischemic stroke due to shared risk factors of atherosclerosis.
2) Clinical features of PAD range from asymptomatic to intermittent claudication to critical limb ischemia manifested by rest pain, ulcers or gangrene.
3) Diagnosis involves assessment of symptoms and risk factors as well as tests such as ankle-brachial index, duplex ultrasound and angiography. Treatment depends on severity and may include lifestyle modification, medication, angioplasty or bypass surgery.
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
History taking and physical examination for lower gastro intestinal bleedAbino David
This document provides guidance on taking a history and performing a physical examination for a patient presenting with lower gastrointestinal bleeding. Key aspects of the history include determining the onset, nature, and color of bleeding or stools. The physical examination aims to identify potential sources of bleeding based on symptoms like abdominal pain, tenesmus, or pain related to defecation. Differential diagnoses depend on the location and characteristics of bleeding, with colonic sources making up 95% of cases such as diverticulosis, ischemia, or anorectal diseases. A full examination can help narrow the potential causes but may not be diagnostic on its own.
This document contains information on various biliary diseases including gallstones, cholangiocarcinoma, pancreatic cancer, and biliary strictures. It discusses the clinical presentation, investigations, and management of biliary obstructions of different types including those caused by stones, tumors, strictures, and cysts. The diagnosis and treatment of choledochal cysts and sclerosing cholangitis are also covered.
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
1. Abdominal pain is a common presenting symptom that can be caused by many intra-abdominal and extra-abdominal processes.
2. A thorough history and physical exam is important to help determine the cause, including assessing location, character, and timing of pain.
3. Differential diagnosis depends on factors like location of pain and patient characteristics, and may include conditions like appendicitis, cholecystitis, pancreatitis, or diverticulitis. Laboratory tests, imaging, and other evaluations can help make the diagnosis.
A 64-year-old man presented with sudden onset of pain and loss of sensation in his right leg. Examination found absent pulses, decreased sensation, and an inability to move his toes, indicating acute limb ischemia. The document discusses the etiology, pathophysiology, clinical evaluation, investigations including Doppler ultrasound and angiography, and treatment approaches for acute limb ischemia including thrombolytics, surgery, and amputation. The goal of therapy is to restore blood flow, preserve the limb if possible, and prevent recurrence through anticoagulation.
Deep vein thrombosis (DVT), is the formation of a blood clot in a deep vein, most commonly the legs.[2][a] Symptoms may include pain, swelling, redness, or warmth of the affected area. About half of cases have no symptoms. Complications may include pulmonary embolism, as a result of detachment of a clot which travels to the lungs, and post-thrombotic syndrome.[2][3]
Risk factors include recent surgery, cancer, trauma, lack of movement, obesity, smoking, hormonal birth control, pregnancy and the period following birth, antiphospholipid syndrome, and certain genetic conditions. Genetic factors include deficiencies of antithrombin, protein C, and protein S, and factor V Leiden mutation. The underlying mechanism typically involves some combination of decreased blood flow rate, increased tendency to clot, and injury to the blood vessel wall.
Volvulus is a twisting of the intestine resulting in blood vessel compression and ischemia. There are three main types: midgut, cecal, and sigmoid volvulus. Risk factors include chronic constipation, abnormal intestinal contents, and congenital malrotation. Signs include abdominal distension, pain, vomiting, and rapid heart rate. Diagnostic tests include abdominal x-rays, blood work, barium enema, and CT scan. Treatment depends on the type but may include surgery, sigmoidoscopy, or monitoring for signs of ischemia. Complications can be dehydration, ischemic bowel disease, perforation, peritonitis, and sepsis.
Oliguria is a low urine output defined as less than 1 mL/kg/hr in infants, less than 0.5 mL/kg/hr in children, and less than 300 mL daily in adults. It indicates an underlying disorder and can lead to acute renal failure if left untreated. Anuria is even less urine output at less than 50 mL/day. Causes of oliguria and anuria include pre-renal (low blood volume), renal (kidney damage), and post-renal (urinary tract obstruction). Evaluation and management depends on determining the cause through history, physical exam, urinalysis, and blood tests to guide volume replacement or other interventions to prevent further kidney injury.
1) Anorectal fistulas are abnormal connections between the anal canal and perianal skin that usually form after an anorectal abscess bursts spontaneously.
2) Park's classification system categorizes fistulas as intersphincteric, transphincteric, suprasphincteric, or extrasphincteric based on their path through the anal sphincter muscles.
3) Treatment options include fistulotomy, seton placement, advancement flaps, fibrin plugs, and the LIFT procedure. The goal is to drain infection and eradicate the fistula tract while preserving sphincter function and avoiding recurrence.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Testicular torsion refers to twisting of the spermatic cord and loss of blood supply to the testicle. It is a urological emergency as early diagnosis and treatment are needed to save the testicle. Ultrasound with Doppler is the primary imaging method and shows absent or decreased blood flow in the affected testicle compared to the normal side. Prompt surgical detorsion and orchioplexy are the definitive treatments.
Edema is defined and its mechanism explained with reference to the Starling's forces. The causes of localized edema and anasarca discussed.
In history taking, the site and distribution of edema, its duration, association with pain, variability, systemic illness, drug intake, trauma, radiation discussed.
The local and systemic examination described. The approach to investigation including lab tests and imaging explained.
Finally, management is discussed in short.
This document discusses perforated peptic ulcers. It first covers the surgical anatomy and blood supply of the stomach and duodenum. It then discusses the epidemiology, pathophysiology, risk factors, presentation, diagnosis, and treatment of perforated peptic ulcers. Key points include that perforations are more common in duodenal versus gastric ulcers and have a higher mortality rate for gastric ulcers. Risk factors include H. pylori infection, NSAID use, smoking, and Zollinger-Ellison syndrome. Patients typically present with sudden severe abdominal pain. Diagnosis involves upright chest x-rays showing free air. Treatment is surgical repair of the perforation.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Acute pancreatitis is an inflammatory condition of the pancreas characterized by abdominal pain and elevated pancreatic enzymes. The most common causes are gallstones and alcohol. In severe cases, pancreatic enzymes activate prematurely and digest the pancreas. This can lead to systemic inflammatory response and organ failure. Diagnosis is based on abdominal symptoms and blood tests showing elevated pancreatic enzymes. Severity is assessed using criteria like Marshall score and need for ICU care. Treatment involves hydration, pain control, treating the underlying cause, preventing infection, and nutrition support. Surgery is usually not needed for sterile pancreatic necrosis but may be for infected necrosis after 4 weeks.
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.
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
The document discusses an integrated approach to diagnosing splenomegaly. It begins by defining splenomegaly and examining the spleen. A step-wise approach is then outlined involving taking a thorough history, conducting a physical exam, ordering lab and imaging tests, and performing specialized testing to investigate for possible etiologies of splenomegaly such as infection, infiltration, congestion, and hyperplasia. The goal is to determine the underlying cause and provide appropriate treatment.
1) PAD is associated with increased risk of myocardial infarction and ischemic stroke due to shared risk factors of atherosclerosis.
2) Clinical features of PAD range from asymptomatic to intermittent claudication to critical limb ischemia manifested by rest pain, ulcers or gangrene.
3) Diagnosis involves assessment of symptoms and risk factors as well as tests such as ankle-brachial index, duplex ultrasound and angiography. Treatment depends on severity and may include lifestyle modification, medication, angioplasty or bypass surgery.
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
History taking and physical examination for lower gastro intestinal bleedAbino David
This document provides guidance on taking a history and performing a physical examination for a patient presenting with lower gastrointestinal bleeding. Key aspects of the history include determining the onset, nature, and color of bleeding or stools. The physical examination aims to identify potential sources of bleeding based on symptoms like abdominal pain, tenesmus, or pain related to defecation. Differential diagnoses depend on the location and characteristics of bleeding, with colonic sources making up 95% of cases such as diverticulosis, ischemia, or anorectal diseases. A full examination can help narrow the potential causes but may not be diagnostic on its own.
This document contains information on various biliary diseases including gallstones, cholangiocarcinoma, pancreatic cancer, and biliary strictures. It discusses the clinical presentation, investigations, and management of biliary obstructions of different types including those caused by stones, tumors, strictures, and cysts. The diagnosis and treatment of choledochal cysts and sclerosing cholangitis are also covered.
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
1. Abdominal pain is a common presenting symptom that can be caused by many intra-abdominal and extra-abdominal processes.
2. A thorough history and physical exam is important to help determine the cause, including assessing location, character, and timing of pain.
3. Differential diagnosis depends on factors like location of pain and patient characteristics, and may include conditions like appendicitis, cholecystitis, pancreatitis, or diverticulitis. Laboratory tests, imaging, and other evaluations can help make the diagnosis.
A 64-year-old man presented with sudden onset of pain and loss of sensation in his right leg. Examination found absent pulses, decreased sensation, and an inability to move his toes, indicating acute limb ischemia. The document discusses the etiology, pathophysiology, clinical evaluation, investigations including Doppler ultrasound and angiography, and treatment approaches for acute limb ischemia including thrombolytics, surgery, and amputation. The goal of therapy is to restore blood flow, preserve the limb if possible, and prevent recurrence through anticoagulation.
Deep vein thrombosis (DVT), is the formation of a blood clot in a deep vein, most commonly the legs.[2][a] Symptoms may include pain, swelling, redness, or warmth of the affected area. About half of cases have no symptoms. Complications may include pulmonary embolism, as a result of detachment of a clot which travels to the lungs, and post-thrombotic syndrome.[2][3]
Risk factors include recent surgery, cancer, trauma, lack of movement, obesity, smoking, hormonal birth control, pregnancy and the period following birth, antiphospholipid syndrome, and certain genetic conditions. Genetic factors include deficiencies of antithrombin, protein C, and protein S, and factor V Leiden mutation. The underlying mechanism typically involves some combination of decreased blood flow rate, increased tendency to clot, and injury to the blood vessel wall.
Volvulus is a twisting of the intestine resulting in blood vessel compression and ischemia. There are three main types: midgut, cecal, and sigmoid volvulus. Risk factors include chronic constipation, abnormal intestinal contents, and congenital malrotation. Signs include abdominal distension, pain, vomiting, and rapid heart rate. Diagnostic tests include abdominal x-rays, blood work, barium enema, and CT scan. Treatment depends on the type but may include surgery, sigmoidoscopy, or monitoring for signs of ischemia. Complications can be dehydration, ischemic bowel disease, perforation, peritonitis, and sepsis.
Oliguria is a low urine output defined as less than 1 mL/kg/hr in infants, less than 0.5 mL/kg/hr in children, and less than 300 mL daily in adults. It indicates an underlying disorder and can lead to acute renal failure if left untreated. Anuria is even less urine output at less than 50 mL/day. Causes of oliguria and anuria include pre-renal (low blood volume), renal (kidney damage), and post-renal (urinary tract obstruction). Evaluation and management depends on determining the cause through history, physical exam, urinalysis, and blood tests to guide volume replacement or other interventions to prevent further kidney injury.
1) Anorectal fistulas are abnormal connections between the anal canal and perianal skin that usually form after an anorectal abscess bursts spontaneously.
2) Park's classification system categorizes fistulas as intersphincteric, transphincteric, suprasphincteric, or extrasphincteric based on their path through the anal sphincter muscles.
3) Treatment options include fistulotomy, seton placement, advancement flaps, fibrin plugs, and the LIFT procedure. The goal is to drain infection and eradicate the fistula tract while preserving sphincter function and avoiding recurrence.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Testicular torsion refers to twisting of the spermatic cord and loss of blood supply to the testicle. It is a urological emergency as early diagnosis and treatment are needed to save the testicle. Ultrasound with Doppler is the primary imaging method and shows absent or decreased blood flow in the affected testicle compared to the normal side. Prompt surgical detorsion and orchioplexy are the definitive treatments.
Edema is defined and its mechanism explained with reference to the Starling's forces. The causes of localized edema and anasarca discussed.
In history taking, the site and distribution of edema, its duration, association with pain, variability, systemic illness, drug intake, trauma, radiation discussed.
The local and systemic examination described. The approach to investigation including lab tests and imaging explained.
Finally, management is discussed in short.
This document discusses perforated peptic ulcers. It first covers the surgical anatomy and blood supply of the stomach and duodenum. It then discusses the epidemiology, pathophysiology, risk factors, presentation, diagnosis, and treatment of perforated peptic ulcers. Key points include that perforations are more common in duodenal versus gastric ulcers and have a higher mortality rate for gastric ulcers. Risk factors include H. pylori infection, NSAID use, smoking, and Zollinger-Ellison syndrome. Patients typically present with sudden severe abdominal pain. Diagnosis involves upright chest x-rays showing free air. Treatment is surgical repair of the perforation.
Chronic pancreatitis is a progressive inflammatory condition of the pancreas characterized by irreversible morphological changes and loss of function. It is most commonly caused by long term heavy alcohol use. Symptoms include recurrent abdominal pain, steatorrhea due to exocrine insufficiency, and diabetes mellitus due to endocrine insufficiency. Diagnosis involves functional tests like fecal elastase and imaging modalities like CT, MRI, ERCP and EUS which demonstrate findings of pancreatic duct abnormalities, parenchymal changes and calcifications.
Acute pancreatitis is an inflammatory condition of the pancreas characterized by abdominal pain and elevated pancreatic enzymes. The most common causes are gallstones and alcohol. In severe cases, pancreatic enzymes activate prematurely and digest the pancreas. This can lead to systemic inflammatory response and organ failure. Diagnosis is based on abdominal symptoms and blood tests showing elevated pancreatic enzymes. Severity is assessed using criteria like Marshall score and need for ICU care. Treatment involves hydration, pain control, treating the underlying cause, preventing infection, and nutrition support. Surgery is usually not needed for sterile pancreatic necrosis but may be for infected necrosis after 4 weeks.
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.
Acute pancreatitis is an inflammatory condition of the pancreas caused by the early activation of digestive enzymes within the pancreas. It can range from mild to severe, and in severe cases, it can lead to organ failure. The most common causes are gallstones, alcohol use, and viral infections. Symptoms include severe abdominal pain, nausea, vomiting, and fever. Laboratory tests show elevated levels of pancreatic enzymes in the blood. Severity is assessed using the Ranson score or APACHE II score. Treatment involves intravenous fluids, bowel rest, pain medications, and treating the underlying cause. Complications can include pancreatic pseudocysts, abscesses, and necrosis.
1. The document summarizes guidelines for the management of acute pancreatitis, including diagnosis, etiology, risk stratification, initial management, role of ERCP, antibiotics, nutrition, and surgery.
2. Key points include diagnosing based on abdominal pain and elevated serum amylase/lipase, identifying gallstones and alcohol as common causes, and aggressively hydrating patients while considering nutrition via enteral feeding in severe cases.
3. Surgery is only recommended for gallstone pancreatitis patients without ongoing inflammation or fluid collections in order to prevent recurrence.
Acute Pancreatitis (According to American College of Gastroenterology 2013 gu...Jibran Mohsin
This Presentation focuses on definition, new classification, different scoring systems for severity, rationale for radiological signs and new management recommendations as per 2013 American College of Gastroenterology guidelines
Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis is defined by abdominal pain, elevated pancreatic enzymes, and imaging findings. It can be caused by multisystem diseases, biliary stones, drugs, infections, metabolic disorders, or injuries. The initial insult activates pancreatic enzymes prematurely, causing autodigestion and inflammation. Mild cases involve abdominal pain and vomiting while severe cases include shock and organ failure. Chronic pancreatitis is usually due to genetic mutations or duct abnormalities and involves recurrent abdominal pain, malnutrition, diabetes, and other complications. Treatment focuses on pain relief, nutrition, antibiotics if infected, and sometimes surgery for anatomical issues.
This document provides information about pancreatitis, including:
1. It describes the anatomy, blood supply, and functions of the pancreas.
2. It discusses the different types of pancreatitis according to the Marseille classification including acute, acute relapsing, chronic relapsing, and chronic pancreatitis.
3. It outlines the causes, pathophysiology, clinical features, investigations, differential diagnosis, and treatment of acute pancreatitis, including conservative treatment and indications for surgery.
George, a 40-year-old male with a history of chronic alcoholism and gallstones, presented with severe abdominal pain after starting sulfasalazine for ulcerative colitis. Lab results showed elevated amylase, lipase, and white blood cell count. The physician's diagnosis was acute pancreatitis, likely caused by sulfasalazine triggering the condition. Due to the severity of symptoms and lab abnormalities, the patient should be admitted to the ICU and given IV fluids, analgesics, and monitored closely for complications of acute pancreatitis.
The pancreas has both exocrine and endocrine functions. Its exocrine role includes secreting digestive enzymes from the ductal cells that help break down carbohydrates, lipids, and proteins. Its endocrine role involves the islets of Langerhans secreting hormones like insulin and glucagon to regulate blood sugar. Pancreatitis refers to inflammation of the pancreas and can be acute, recurrent, or chronic depending on factors like gallstones, alcohol use, metabolic issues, or postoperative complications. Symptoms include abdominal pain, nausea, and high amylase/lipase levels. Treatment involves pain relief, suppressing secretions, antibiotics, and sometimes surgery for complications or underlying issues.
The document summarizes information about the pancreas and pancreatitis. It describes the pancreas' anatomy and functions as both an exocrine gland that produces digestive enzymes and an endocrine gland that produces hormones like insulin. It then discusses pancreatitis, defining it as either acute or chronic, and describing causes, pathophysiology, symptoms, diagnostic tests, and treatment approaches for acute pancreatitis which include supportive care, pain management, and addressing complications to prevent issues like pancreatic necrosis.
Acute pancreatitis is an inflammatory process of the pancreas that is usually painful and self-limited. The most common causes are gallstones and alcohol abuse. In mild cases, patients can resume oral intake after symptoms improve. In severe cases, supportive care including fluid resuscitation and nutritional support via enteral feeding is important. Enteral nutrition is preferred over total parenteral nutrition due to lower risks of infection and lower costs with similar or better outcomes. The development of pancreatic necrosis is a marker of severe disease and risk of complications.
This document provides information on acute pancreatitis including its definition, causes, pathogenesis, clinical presentation, diagnosis, severity scoring systems, treatment goals, and approaches to nutrition. The key points are:
1. Acute pancreatitis is an inflammatory process of the pancreas that is usually painful and self-limited, with pancreatic function and morphology returning to normal after attacks. Gallstones and alcohol abuse are the most common causes.
2. The pathogenesis involves premature activation of digestive enzymes within the pancreas, leading to autodigestion and systemic complications in severe cases. Scoring systems like Ranson criteria and CT severity index are used to predict severity and guide management.
3. Treatment goals are to limit systemic
This document provides information on acute pancreatitis including its definition, causes, pathogenesis, clinical presentation, diagnosis, severity scoring systems, treatment goals, and approaches to nutrition. The key points are:
1. Acute pancreatitis is an inflammatory process of the pancreas that is usually painful and self-limited, with pancreatic function and morphology returning to normal after attacks. Gallstones and alcohol abuse are the most common causes.
2. The pathogenesis involves premature activation of digestive enzymes within the pancreas, leading to autodigestion and systemic complications in severe cases. Scoring systems like Ranson criteria and CT severity index are used to predict severity and guide management.
3. Treatment goals are to limit systemic
Acute pancreatitis is an inflammatory process of the pancreas that can involve surrounding tissues or remote organ systems. The most common causes are gallstones and alcohol. The pathogenesis involves premature activation of digestive enzymes within the pancreas that cause autodigestion. Clinical presentation includes severe upper abdominal pain and elevated pancreatic enzymes. Diagnosis requires abdominal pain consistent with pancreatitis plus elevated pancreatic enzymes or radiologic findings. Complications can include pancreatic necrosis, pseudocyst formation, and systemic inflammatory response.
The pancreas is both an exocrine and endocrine organ. Its exocrine function involves secreting enzymes to aid digestion. Its endocrine function involves producing hormones like insulin and glucagon that regulate blood sugar levels. The document discusses pancreatic anatomy, functions, and diseases like pancreatitis and diabetes that can arise from pancreatic dysfunction. It provides details on the causes, symptoms, diagnosis, and treatment of these conditions.
1. The pancreas is an elongated organ located in the abdominal cavity behind the stomach. It has three parts - head, body, and tail.
2. The pancreas has both exocrine and endocrine functions. Exocrine functions include producing pancreatic juice containing enzymes that digest carbohydrates, proteins, and fats. Endocrine functions include production of insulin, glucagon, and somatostatin by islets of Langerhans cells.
3. Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis symptoms include severe abdominal pain and its causes include gallstones and alcohol use. Chronic pancreatitis involves long-term inflammation that destroys the pancreas over
Acute liver failure is characterized by initial non-specific symptoms that progress to hepatic encephalopathy. It is defined as evidence of coagulopathy and mental alteration occurring within 26 weeks in a patient without pre-existing liver disease. Initial management involves fluid/electrolyte maintenance, nutrition, treatment of the underlying cause, and consideration of liver transplantation if criteria are met. ICU admission is warranted for altered sensorium, respiratory distress, bleeding, or hemodynamic instability. The prognosis depends on the severity and etiology of the liver injury.
The pancreas is a retroperitoneal organ divided into a head, neck, body, and tail. It has both exocrine and endocrine functions. The exocrine part secretes pancreatic juice to aid digestion, while the endocrine part contains islets of Langerhans that secrete insulin and glucagon. Pancreatitis is inflammation of the pancreas that can be acute or chronic. Acute pancreatitis commonly results from gallstones or alcohol and causes abdominal pain. Chronic pancreatitis is characterized by irreversible pancreatic tissue damage that can lead to diabetes and malnutrition over time. Treatment involves pain management, nutritional support, and sometimes surgery.
The document discusses acute pancreatitis, including:
1. It provides an overview of the normal anatomy and physiology of the pancreas, as well as the exocrine and endocrine functions.
2. It examines the causes, pathogenesis, clinical presentation, diagnosis, and severity scoring systems used to evaluate acute pancreatitis such as Ranson criteria.
3. It outlines the goals and approaches to treatment for both mild and severe acute pancreatitis, including supportive care, nutritional support, role of ERCP, and antibiotics for infected necrosis.
1. The document discusses chronic pancreatitis, providing details on its history, anatomy, physiology, classification, types, risk factors, and symptoms.
2. Chronic pancreatitis is characterized by persistent inflammation and irreversible fibrosis of the pancreas that decreases quality of life and can cause pain and exocrine/endocrine insufficiency.
3. Heavy alcohol consumption is the most common cause, accounting for 70-80% of cases, while other risks include genetic mutations, duct obstructions, trauma, and tropical or autoimmune etiologies.
The document describes the anatomy, histology, embryology, congenital anomalies, and types of pancreatitis of the pancreas. It notes that the pancreas has exocrine and endocrine components. It also lists the main congenital anomalies as agenesis, pancreas divisum, annular pancreas, and ectopic pancreas. The document provides details on the pathogenesis, morphology, clinical features, diagnosis, and treatment of both acute and chronic pancreatitis.
1. Acute pancreatitis is inflammation of the pancreas that is usually caused by gallstones or alcohol use.
2. It involves premature activation of pancreatic enzymes, inhibition of secretion, and generation of pro-inflammatory mediators.
3. Diagnosis is based on abdominal pain and elevated pancreatic enzymes in blood and urine. Imaging can identify complications like fluid collections or necrosis.
This document discusses acute pancreatitis, including its anatomy, risk factors, pathogenesis, symptoms, diagnosis, complications, and treatment approaches. It notes that acute pancreatitis is an inflammatory process of the pancreas caused by autolysis from abnormal activation of pancreatic enzymes. Treatment involves conservative management with pain control, fluid resuscitation, and prevention of infection. Operative intervention may be needed if conservative treatment fails or complications like necrosis or infection arise.
This document summarizes information about autoimmune hepatitis (AIH), including:
- It is a T-cell mediated immune attack on the liver that causes progressive damage and can lead to cirrhosis.
- Two main types (type 1 and type 2) are distinguished by their associated autoantibodies.
- Women are affected more often than men. Treatment involves immunosuppression with glucocorticoids alone or in combination with azathioprine to induce remission. Response to treatment and long term outcomes depend on disease severity at presentation.
This document provides information on autoimmune hepatitis, including:
- It is a chronic hepatitis of unknown etiology that can progress to cirrhosis. It is characterized by the presence of autoimmune antibodies and evidence of hepatitis.
- The two main types are type 1, associated with ANA/SMA positivity, and type 2, associated with LKM1 positivity.
- Treatment involves immunosuppressive drugs like prednisone, either alone or in combination with azathioprine. The goal is to induce and maintain remission.
- Remission is defined as resolution of symptoms and normalization of liver tests and histology. Treatment is then tapered slowly to maintain remission.
This document discusses congenital heart disease in adults. It notes that 1 million adults in the US have congenital heart disease, with 20,000 more reaching adulthood each year due to increased survival of children with CHD. Common adult presentations of CHD include effort dyspnea, atrial fibrillation, and right heart failure. The document reviews the pathophysiology, clinical features, diagnostic evaluation, and management of various CHD lesions that may present in adulthood, such as atrial septal defects, ventricular septal defects, patent ductus arteriosus, tetralogy of Fallot, Ebstein's anomaly, and coarctation of the aorta. Surgical and percutaneous interventions are discussed
Arterial blood gas analysis in clinical practice (2)Mohit Aggarwal
This document provides information about arterial blood gases (ABGs), including what an ABG is, the components that are measured, normal ranges, reasons for ordering an ABG, how to interpret ABG results, and types of acid-base imbalances. An ABG is a blood test that measures pH, oxygen, and carbon dioxide levels to help diagnose respiratory and metabolic conditions. The document outlines the steps to interpret an ABG and explains various acid-base disorders like respiratory acidosis, metabolic alkalosis, and mixed disorders. Compensation mechanisms of the lungs and kidneys in response to acid-base imbalances are also discussed.
This document defines acute respiratory distress syndrome (ARDS) and discusses its pathophysiology, risk factors, diagnosis, management, and ventilator strategies. ARDS is defined as acute onset bilateral pulmonary infiltrates, hypoxemia, and no heart failure. It was initially defined in 1971 and revised definitions in 1988 and 1994 established clearer criteria. Common causes are pneumonia, aspiration, and sepsis. Management involves treating the underlying cause, supportive ICU care, and lung protective ventilation with low tidal volumes (6 ml/kg) and moderate PEEP levels. Adjuncts like conservative fluid management, prone positioning, and recruitment maneuvers may provide benefits.
1. The document discusses the approach to evaluating and categorizing different types of chest pain, including acute coronary syndrome.
2. Key factors in the initial evaluation of chest pain include obtaining a detailed history, performing a physical exam, 12-lead EKG, and cardiac biomarker testing to help determine if the chest pain is caused by life-threatening conditions like myocardial infarction.
3. Patients are categorized as having possible acute ischemia, probable acute ischemia, or myocardial infarction based on their history, symptoms, physical exam findings, EKG results, and cardiac enzyme levels in order to determine the urgency of further testing and treatment.
The document discusses various types and causes of diarrhea including secretory, osmotic, inflammatory, steatorrhea, factitial, dysmotile, and iatrogenic causes. It provides details on evaluating diarrhea based on characteristics like stool appearance and volume, presence of blood or mucus, abdominal pain location, and related symptoms. Key tests mentioned for diagnosing the cause of diarrhea include stool studies for occult blood, white blood cells, pH, fat content, cultures, and electrolytes.
This document discusses Myasthenia Gravis, an autoimmune disorder where antibodies are produced against acetylcholine receptors at the neuromuscular junction. This leads to loss of functional acetylcholine receptors and weakness of muscles. Symptoms include fatigue of muscles that worsens with use and improves with rest. Early symptoms often involve the eyes, face, and throat. Later the limbs may be involved. Treatment focuses on increasing acetylcholine activity and decreasing the immune attack on motor end plates using anticholinesterase medications, immunosuppressants, plasmapheresis, and sometimes thymectomy. Classification is based on symptoms and presence of crisis requiring ventilation.
The document discusses the anatomy, physiology, and pathologies of the pituitary gland. It begins by describing the normal anatomy of the pituitary, including its location and that it is divided into anterior and posterior lobes. It then discusses the hormones produced by the anterior pituitary and the epidemiology of pituitary adenomas. Various types of pituitary tumors and other sellar masses are outlined. The natural history, clinical presentations, evaluation, and treatment options for pituitary tumors are summarized, including pharmacotherapy, surgery, and radiation therapy. Specific details are provided about prolactinomas, acromegaly, and Cushing's disease.
This document discusses the approach to evaluating and diagnosing patients presenting with headache. It begins by distinguishing between primary and secondary headaches. Primary headaches include migraine, tension-type headache, and cluster headache, while secondary headaches are caused by underlying conditions like head trauma, vascular disorders, or infections. The document outlines diagnostic criteria for common headache types and recommends investigations and treatment approaches based on the presence of "red flags" or alarming symptoms.
Approach to a patient with vasculitis and itsMohit Aggarwal
Vasculitis refers to inflammation of blood vessels. It can be primary or secondary to other conditions like drugs, infections, collagen disorders or malignancies. It involves various sizes of blood vessels from large arteries to small vessels. Common symptoms include fever, fatigue, rashes, arthritis, and organ involvement depending on the vessel type. Diagnosis is based on clinical features, lab tests like ANCA, and biopsy. Treatment involves immunosuppression. Prognosis depends on type and organ involvement.
Approach to a patient with positive ana levels (2)Mohit Aggarwal
This document discusses the approach to evaluating a patient with a positive ANA test result. It provides background on ANA testing and discusses the significance of various ANA patterns and titers. The document emphasizes that a positive ANA alone does not indicate a specific disease and must be interpreted based on the clinical context. It then reviews how to approach and evaluate common conditions associated with ANA positivity like SLE, Scleroderma, RA, and Sjogren's Syndrome.
Approach to a patient with hyponatremia (2) (1)Mohit Aggarwal
The document discusses hyponatremia, which refers to a low serum sodium level. It begins by defining hyponatremia and providing normal sodium levels. It then covers the frequency, age and sex predispositions, physiology/pathophysiology, types and causes. The types include hypovolemic, euvolemic, hypervolemic, redistributive, and pseudohyponatremia. Common causes are discussed like SIADH, heart failure, cirrhosis. The clinical approach involves assessing volume status, labs like sodium, osmolality, urine sodium. Management depends on the type and involves restricting free water intake or using hypertonic saline in severe cases to slowly correct the
Approach and management of chronic kidney disease sandeepMohit Aggarwal
Chronic kidney disease is a spectrum of conditions associated with progressive kidney function decline and damage. It is increasingly prevalent due to rising rates of diabetes and hypertension. Management involves identifying the underlying cause, calculating GFR to stage severity, investigating for complications, and slowing progression. Treatment focuses on managing complications through diet, medication, and preparing patients for renal replacement therapies like dialysis and transplantation if kidney failure occurs. The goal is optimizing quality of life and outcomes through a coordinated multidisciplinary approach.
Aphasias are language disorders caused by brain damage that affect speech and communication. There are two main categories: fluent aphasias where speech is smooth but contains errors, and non-fluent aphasias where speech is halting. The most common types are Broca's aphasia (non-fluent speech with intact comprehension) caused by damage to Broca's area, and Wernicke's aphasia (fluent but meaningless speech) caused by damage to Wernicke's area. Aphasias are diagnosed through language tests and neuroimaging and treated with speech therapy and sometimes medications. Prognosis depends on factors like age, lesion size and early rehabilitation.
1. Aortic regurgitation can be caused by diseases of the aortic root or valve such as aortopathy, calcific aortic stenosis, or bicuspid aortic valve.
2. In chronic aortic regurgitation, the left ventricle undergoes eccentric hypertrophy and maintains preload reserve to initially compensate for the volume overload. Over time, increased afterload can lead to decompensation.
3. Acute severe aortic regurgitation into a non-hypertrophied left ventricle results in a marked rise in left ventricular pressures and pulmonary edema due to the inability to increase stroke volume.
Antithrombotic in difficul clinical condition umeshMohit Aggarwal
This document discusses antithrombotic therapy in difficult clinical conditions. It covers high ischemic burden, high bleeding risk, non-cardiac surgery post procedures, high INR levels, pregnancy with prosthetic valves, renal dysfunction, and atrial fibrillation. It provides guidance on treatment strategies for balancing thrombotic and bleeding risks in these complex patients, including medication choices, dosing, and timing of therapy.
This document discusses antibiotic choice in the ICU. It provides epidemiological data from studies on infections in ICU patients. The most common infections are pneumonia, bloodstream infections, and UTIs. The pathogens vary between different ICU profiles such as medical, surgical, and pediatric ICUs. Principles of antibiotic use include targeting the likely pathogen while minimizing toxicity. Empirical antibiotic choices are discussed for common ICU infections like pneumonia, bloodstream infections, and UTIs. Antimicrobial resistance is an increasing problem addressed as well.
This document defines and discusses andropause (also known as male menopause), including its definition, symptoms, epidemiology, pathophysiology, effects of testosterone deficiency, monitoring and risks/benefits of testosterone replacement therapy. Some key points are: andropause is characterized by declining testosterone levels and affects quality of life; symptoms include reduced energy, libido and erectile dysfunction; prevalence increases with age, with 20% of men over 60 and 50% of men over 75 having low testosterone; testosterone replacement can improve symptoms in men with very low levels if administered carefully under medical supervision due to risks like prostate issues.
The tibial nerve originates from the sciatic nerve and supplies muscles in the leg and foot. Tarsal tunnel syndrome occurs when the tibial nerve is compressed as it passes through the tarsal tunnel behind the inner ankle. Symptoms include pain, tingling, and numbness in the foot and ankle. Diagnosis involves nerve conduction studies to evaluate tibial nerve function. Treatment focuses on reducing inflammation and pressure on the nerve through rest, ice, braces, and in severe cases, surgery to decompress the nerve in the tarsal tunnel.
Leveraging Generative AI to Drive Nonprofit InnovationTechSoup
In this webinar, participants learned how to utilize Generative AI to streamline operations and elevate member engagement. Amazon Web Service experts provided a customer specific use cases and dived into low/no-code tools that are quick and easy to deploy through Amazon Web Service (AWS.)
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
2. Pancreas is both a digestive
organ as well as an endocrine
gland located
reteroperitoneally in
between 1st
and 3rd
part of
duodenum, subserving
following 3 important
functions:
◦ neutralize chyme
◦ digestive enzymes
◦ hormones
5. COMPARTMENTALIZATION - digestive enzymes are contained
within zymogen granules in acinar cells
REMOTE ACTIVATION - digestive enzymes are secreted as
inactive proenzymes within the pancreas
PROTEASE INHIBITORS – pancreatic secretory trypsin inhibitor
(PSTI or SPINK1) is secreted along with the proenzymes to
suppress any premature enzyme activation.
AUTO “SHUT-OFF” – trypsin destroys trypsin in high
concentrations
Production of non specific antiproteases like alpha 1
antitrypsin and alpha 2 macroglobulin
6. Acute pancreatitis is the acute inflammatory process of pancreas
with variable involvement of other regional tissues or remote organ
systems.
Clinically defined by 2 out of 3 criteria
1. Symptoms,such as epigastric pain, consistent with the disease.
2. Serum amylase or lipase greater than 3 times the normal upper limit.
3. Radiological imaging consistent with the diagnosis using CT or MRI.
in case of acute pancreatitis Pancreatic function and morphology
return to normal after (or between) attacks
7. Various theories suggesting pathogenesis of acute
pancreatitis are :
1. Colocalisation of lysosomal hydrolases e.g cathepsin B
with trypsinogen leading on to its conversion to active form.
2. pancreatic injury may lead to altered secretion of activated
proteases or their proenzymes through the basolateral
membranes of the acinar cells followed by their leakage
into the interstitium . Enhanced pancreatic ductal
permeability allows activated enzymes to leak from the
duct and initiate pancreatic autodigestion.
8. 3. oxygen radicals released secondary to pancreatic injury can
cause inactivation of circulating protease inhibitors, thereby
contributing to the accumulation of activated proteases in
pancreatic tissue.
4. Reflux of bile in to the pancreatic duct or increased pancreatic
pressure because of the obstruction at the ampulla caused by
gall stones may lead on to leakage of proteases .
5. Numerous genetic mutations causing premature activation of
pancreatic zymogens within the pancreas also have been
proposed as part of the pathogenetic mechanism for hereditary
pancreatitis. e.g. Mutations in the cystic fibrosis
transmembrane conductance regulator (CFTR) and PSTI or
SPINK1.
9. All the above proposed mechanisms ultimately lead on to activation
of Proteolytic enzymes in the pancreas rather than in the intestinal
lumen. These enzymes cause auto digestion of pancreatic tissue
leading to the activation of inflammatory cascade.
Activating factors for these proenzymes are:
Endotoxins, Exotoxins,Viral infections, Ischemia, Anoxia, Direct
trauma, Activated proenzyme (e.g trypsin).
10. INITIAL PHASE
◦ acinar cell injury due to intrapancreatic digestive
enzyme activation
◦ Zymogen activation mediated by lysosomal
hydrolases e.g. cathepsin B
SECOND PHASE
◦ Intrapancreatic inflammation reaction
◦ Due to activation, chemoattraction, and
sequestration of neutrophils in the pancreas
* This neutrophil sequestration can activate trypsinogen
13. Anti HIV medication: Lamivudine,
didanosine, nelfinavir
Anti microbials:
dapsone,isoniazid,rifampin,penta
midine,pentavalent
antimonials,tetracyclines,erythrom
ycin,metronidazole,
Antihypertensives: ace inhibitors,
losartan, Furosemide,
Hydrochlorothiazide,alphamethyld
opa
Analgesics:
Acetaminophen,sulindac
IBD:
mesalamine,5ASA,sulfasalazine
Anti cancer drugs: L-Asparaginase,
6-Mercaptopurine, Cytosine
arabinoside
Steroids: Dexamethasone,
hydrocortisone,estrogen
Neuropsychiatric drugs:
valproate,carbamazapine,topiram
ate,clozapine
Others: Carbimazole,
methimazole,
Pravastatin,simvastatin Procainam
ide
Azathioprine, interferon alpha
14. Pain : Major symptom
◦ Vary from mild to severe,
constant pain
◦ Steady and boring in character
◦ Located in epigastrium and
periumbilical radiating to the
back
◦ Chest, flank and lower
abdomen
◦ Pain more intense on supine,
relieved by sitting
15. Nausea, vomitting, abdominal distention
Low grade fever, tachycardia, hypotension
Shock, jaundice
Erythematous skin nodules
In 10-20% of patients- basilar rales, atelectasis, and
pleural effusion
Bowel sounds usually diminished or absent
Palpable enlarged pancreas, or a pseudocyst in the upper
abdomen
Cullen’s Sign; grey turner sign; fox sign
17. Grünwald sign (appearance of ecchymosis, large bruise,
around the umbilicus due to local toxic lesion of the
vessels)
Körte's sign (pain or resistance in the zone where the
head of pancreas is located (in epigastrium, 6–7 cm
above the umbilicus))
Kamenchik's sign (pain with pressure under the
xiphoid process)
18. Mayo-Robson's sign (pain while pressing at the top of the
angle lateral to the Erector spinae muscles and below the
left 12th rib (left costovertebral angle (CVA))[2]
Mayo-Robson's point - a point on border of inner 2/3 with
the external 1/3 of the line that represents the bisection
of the left upper abdominal quadrant, where tenderness
on pressure exists in disease of the pancreas. At this point
the tail of pancreas is projected on the abdominal wall.
20. 1. History and physical
examination
Showing features consistent
with the diagnosis of ac.
Pancreatitis as discussed
in previous slides
1. Laboratory tests
2. Imaging studies
21. Serum amylase
Elevates within HOURS and can remain elevated for 4-5
days
High specificity when using levels >3x normal
Many false positives (see next slide)
Most specific = pancreatic isoamylase (fractionated
amylase
Normal values of serum amylase are 30-110IU/L
23. Serum lipase
The preferred test for diagnosis
Begins to increase 4-8H after onset of symptoms and
peaks at 24H
Remains elevated for days
Sensitivity 86-100% and Specificity 60-99%
>3X normal S&S ~100%
Normal levels of serum lipase are 5-208 u/l
24. Trypsinogen 2
◦ Excreted into the urine
◦ Used as a screening test for acute pancreatitis
Trypsinogen activated peptide
◦ Small peptide
Advantage
◦ Appear very early during the disease
Disadvantage
◦ Limited "diagnostic window".
decrease very quickly irrespective of the course of the disease
◦ Not suitable for rapid simple analysis
25. • Elevated ALT > 3x normal (in a non-alcoholic) has a positive predictive value of
95% for GS pancreatitis
• newer diagnostic tests like Serum Neutrophil –elastase,IL-6, and alpha
macroglobulin , urinary trypsinogen activated peptide, polymorphonuclear
leucocyte esterase have also been used in diagnosing acute pancreatitis.
Other tests used to determine prognosis include wbc count(15,000-20,000
leukocytes/ microliter)
( Hct > 44%)
Plasma glucose
Serum calcium
CRP(normal values are 10-21 mg/dl)
LDH levels
Serum triglycerides
ECG: ST segment and T wave abnormalities due to changes in vagal nervous
system and visceral venous thrombosis
26. Plain xray abdomen shows
1. Air in duodenal c loop
2. Colon cut off sign which represents distention of the
colon up to the transverse colon with a paucity of gas
distal to the splenic flexure.
3. The sentinel loop sign, which represents a focal dilated
proximal jejunal loop in the left upper quadrant
USG abdomen : mainly helpful in diagnosing gall stones
and pseudopancreatic cyst. It can also be used for fine
needle aspiration of the fluid collection in pancreatitis
28. CT
◦ Excellent in pancreas imaging
◦ Recommended in all patients with persisting organ
failure, sepsis or deterioration in clinical status (6-10
days after admission)
◦ Necrosis will be present at least 4 days after onset of
symptoms; if CT is ordered too early it will
underestimate severity
◦ Follow-up months after presentation as clinically
warranted for CT severity index of >3
29. Transverse CT scan obtained with intravenous and oral contrast material reveals
a large, edematous, homogeneously attenuating (73-HU) pancreas (1) and
peripancreatic inflammatory changes (white arrows). Although the
attenuation values are low, there is no pancreatic necrosis. Calcified
gallstones are seen in gallbladder (black arrow). 2 = liver (140 HU
30. MRI/MRCP newest “fad”
◦ Decreased nephrotoxicity from gadolinium
◦ Better visualization of fluid collections
◦ MRCP allows visualization of bile ducts for stones
Does not allow stone extraction or stent insertion
EUS(endoscopic ultrasonography)
◦ EUS is equal to MRCP and ERCP but far more sensitive
than either abdominal ultrasonography or CT in detecting
common duct stones.
◦ It might be the best method of evaluating bile duct in a
patient with acute necrotising pancreatitis
31. Biliary pancreatitis
Amylase Usually > 1000
IU
AST, ALT Acute elevation
with rapid resolution
Alkaline phosphatase and
bilirubin Increased
Ultrasound Gallstones,
dilated common bile duct
CT scan Gallstones,
dilated common bile duct
Alcoholic pancreatitis
S. amylaseUsually < 500
IU
AST,ALT Minimal
elevation that does not
fluctuate
ALP Not usually elevated
USG shows Changes of
chronic pancreatitis
Pancreatic calcifi cation,
dilated pancreatic duct
with stones
32.
33. AT ADMISSION
1. Age > 55 years
2. WBC > 16,000
3. Glucose > 200
4. LDH > 350 IU/L
5. AST > 250 IU/L
WITHIN 48 HOURS
1. HCT drop > 10
2. BUN > 5
3. Arterial PO2 < 60 mm Hg
4. Base deficit > 4 mEq/L
5. Serum Ca < 8
6. Fluid sequestration > 6L
34. AT ADMISSION
1. Age > 70 years
2. WBC > 18,000
3. Glucose > 220
4. LDH > 400 IU/L
5. AST > 250 IU/L
WITHIN 48 HOURS
1. HCT drop > 10
2. BUN > 5 after iv fluid
rehydration
3. Arterial PO2 < 60 mm Hg
4. Base deficit > 5 mEq/L
5. Serum Ca < 8
6. Fluid sequestration > 4L
35. Though ransons criteria is an excellent prognostic tool, but
it has 2 disadvantages:
◦ It can not be used with in 24 hrs of admission
◦ It is cumbersome though less as compared to apache II
score
39. 1. WBC > 15,000
2. Glucose > 180
3. BUN > 16
4. Arterial PO2 < 60 mm Hg
5. Ca < 8
6. Albumin < 3.2
7. LDH > 600 U/L
8. AST or ALT > 200 U/L
40. SIRS: systemic inflammatory
response syndrome is said to
be present if 2 of the
following criteria are full
filled:
1. Heart rate > 90 beats/minute
2. Core temperature <36°C or
>38°C
3. White blood count <4000
or >12000/mm3
4. Respirations >20/min or
PCO2 <32 mm Hg
41. CT Grade (balthazar grade)
◦ Normal 0 points
◦ Focal or diffuse enlargement 1 point
◦ Intrinsic change or fat stranding 2 points
◦ Single ill-defined fluid collection 3 points
◦ Multiple collections of fluid or gas 4 points
Necrosis Score
◦ None 0 points
◦ 1/3 of pancreas 2 points
◦ 1/2 of pancreas 4 points
◦ > 1/2 of pancrease 6 points
Severe = Score > 6 (CT Grade + Necrosis)
42.
43. Mild acute pancreatitis
▸ No organ failure
▸ No local or systemic
complications
Moderately severe acute
pancreatitis
▸ Organ failure that
resolveswithin 48 h (transient
organfailure) and/or
▸Local or systemic complications
without persistent organ failure
Severe acute pancreatitis
▸ Persistent organ failure (>48 h)
–Single organ failure
–Multiple organ failure
44.
45. Local complications
Necrosis Sterile, Infected, Organized
Pancreatic fluid collections •Peripancreatic fluid collections
•Pancreatic Pseudocyst causing pain,
rupture, hemorrhage, infection,Obstruction
of GIT .
•Acute necrotic collection
•Walled off necrosis
Pancreatic ascites Disruption of main pancreatic duct
Leaking pseudocyst
Involvement of contiguous organs by
necrotizing pancreatitis
Massive intraperitoneal hemorrhage
Thrombosis of blood vessels
Bowel infarction
Obstructive jaundice
46. Necrotizing pancreatitis
◦ severe form of acute
pancreatitis,
◦ increasing abdominal pain,
fever,
◦ marked leukocytosis,
◦ and bacteremia
Shown in cect as area
Of non enhancement
It can get infected or remain
sterile
47. APFC(acute peripancreatic fluid collection): Peripancreatic
fluid associated with interstitial oedematous pancreatitis with no
associated peripancreatic necrosis. This term applies only to areas of
peripancreatic fluid seen within the first 4 weeks after onset of
interstitial oedematous pancreatitis and without the features of a
pseudocyst.
Pseudocyst: An encapsulated collection of fluid with a well defined
inflammatory wall usually outside the pancreas with minimal or no
necrosis. This entity usually occurs more than 4 weeks after onset of
interstitial oedematous pancreatitis to mature.
Acute necrotic collection: A collection containing variable
amounts of both fluid and necrosis associated with necrotising
pancreatitis; the necrosis can involve the pancreatic parenchyma
and/or the peripancreatic tissues.
48. Walled of necrosis: A mature, encapsulated collection of
pancreatic and/or peripancreatic necrosis that has developed a well
defined inflammatory wall. WON usually occurs >4 weeks after onset
of necrotising pancreatitis.
Pancreatic pseudocyst Walled of necrosis
49. Systemic
complications
Pulmonary Pleural effusion, Atelectasis, Mediastinal abscess, Pneumonitis,
ARDS
Cardiovascular Hypotension, Hypovolemia, Sudden death, Nonspecific ST-T
changes in ECG, pericardial effusion
Hematologic DIC
GI Hemorrhage PUD, Erosive gastritis, Hemorrhagic pancreatic necrosis with
erosion into major BV, Portal vein thrombosis, Variceal
hemorrhage
Renal Oliguria, Azotemia, Renal artery and/or vein thrombosis, Acute
tubular necrosis
Metabolic Hyperglycemia, Hypertriglyceridemia, Hypocalcemia,
Encephalopathy, Sudden blindness (Purtscher’s retinopathy
Central Nervous System Psychosis, Fat emboli
Fat necrosis Subcutaneous tissues, Bone
50. Pulmonary: ARDS
◦ damage to the pulmonary surfactant layer by circulating
phospholipase A and free fatty acids
Cardiovascular: Circulatory shock
◦ a combination of volume depletion and hyperdynamic
circulatory state with decreased peripheral vascular
resistance
• Renal: Acute renal failure
– caused by circulatory shock and a selective increase in renal
vascular resistance
51. • GI: Hemorrhage
– erosion of the splenic or gastroduodenal arteries.
– diffuse mucosal bleeding from the antrum and
duodenum
– perforation of peripancreatic inflammation into any
portion of the gastrointestinal tract from esophagus to
colon.
– Splenic involvement by direct extension of the
inflammatory process or, secondarily, by splenic vein
thrombosis, which leads to gastric fundic varices.
52.
53. 1. Conventional measures:
Analgesics- to reduce pain, opiates like morphine,
tramadol, meperadine can be given. phentanyl has also
been tried by s/c and i/v route.
Patient is to be kept nill per oral
I/V fluids : early rigorous intravenous hydration is
important in preventing complications. 3-4 litres fluid
daily the form of crystalloids like RL, DNS has been
recommended. Or maintain urine output at 40-50 ml/hr
Oxygen inhalation ideally should be given to all patients
with acute severe pancreatitis.
54. 2. Diet and nutrition:
Patient is to be kept on I/V fluids initially, but can be
considered for early refeeding if:
Resolution or decreased abdominal pain
Patient is hungry
No signs of any organ dysfunction
Enteral feeding is superior to total parentral nutrition.not
much difference has been found between NG and NJ
feeding.
Start early refeeding with low fat high carb liquid diet
55. 3. Antibiotics
These are usually not indicated in mild acute pancreatitis because
of the risk of super infectionand development of resistance.
Can be given for prophylaxis in severe necrotising pancreatitis
and in treatment of infective necrosis
Organisms implicated in acute pancreatitis are usually were gram-
negative aerobic or anaerobic species (E.coli, Pseudomonas
aeruginosa, Proteus species, K. pneumoniae), with occasional
gram positives S. faecalis, Staph aureus, S viridans,
Staphylococcus epidermidis) and rare fungi (Candida species)
56. Antibiotics contd.
The antibiotics found to have maximum penetration in the
necrotic pancreatic tissue as well as having maximum
activity against the causative organisms are imipenem,
fluoroquinolones (ofloxacin,pefloxacin and ciprofloxacin)
and metronidazole.these antibiotics can be used for a
period of 7-21 days.not much benefit has been obtained
by a shorter or a longer course of therapy.
57. Endoscopic and surgical interventions
1. Sphincterotomy for gall stone pancreatitis
2. Pancretic duct stent placement to prevent pacreatic fluid
leakage
3. Necrosectomy mainly for infected necrosis or in cases of
sterile necrosis not accepting orally
4. Early cholecystectomy for gall stone pancreatitis
5. Percutaneous catheter drainage of necrotic material
58. Other modalities of treatment
1. Protease inhibitors (aprotinin, gabexate, mesilate) have
shown some positive results in few clinical trials
2. Platlet activating factor inhibitor (lexipafant)
3. antisecretory agents (somatostatin, octreotide): not
of much benefit
4. Probiotics have rather shown negative results in
some of the trials
59. Early course-0-72 hrs
Is there organ failure
NO
•Admission to ward
•NPO
•Pain control
•I/V hydration
•Nasal oxygen
•Regular hct,electrolyte
YES
•Admission to icu
•Same orders as ward admission
•Assisted ventilation if needed
•Assess for bile duct obstruction
•For jaundice – urgent ercp
60. YES
Later course > 72 hrs
Evidence of severe dis. Or
organ failure
Early refeeding
Evaluate for etiology
If GS early cholecystectomy
NO
Observe for biliary sepsis-
urgent ercp
Enteral feeding(NJ or NG)
CT to evaluate for necrosis
Consider antibiotic if
infective necrosis suspected
61. Late course : 7-28 days
Patient improving?
yes
Consider oral
refeeding
If on antibiotics, consider
FNAC of pancreas for culture
and change of antibiotics
If not on antibiotics and fnac
negative than keep off
antibiotics
no
62. Beyond 28 days
Patient improving?
Consider refeeding
If patient can not
tolerate feeding consider
necrosectomy
yes
Consider necrosectomy
by
endoscopic,radiological
or surgical means
no
63. The mortality rate in cases of mild acute pancreatitis is
around 5% whereas for severe necrotising pancreatitis
it may be as high as 30-70%.this warrants for timely
diagnosing and efficiently managing acute pancreatitis
so as to prevent complications and decrease mortality.
Many newer techniques for management of acute
pancreatitis are emerging, but the most important way
of reducing morbidity and mortality by this painful
disease is to attain healthy life style and abstain from
alcohal(the 2 most common causes of ac. Pancreatitis.)