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Pathology - Respiratory Acidosis
Resulting from acute lung disease such as ARDS and airway obstruction, chronic lung disease like COPD, CNS depression caused by opioids, sedatives, and narcotics, or weakened respiratory muscles due to conditions like ALS, kyphoscoliosis, MS, and polio.
Primary issue: Elevated Pco2 levels (hypercapnia) due to reduced alveolar ventilation.
Compensatory response: HCO3 increases due to enhanced renal HCO3 reabsorption triggered by low pH and high Pco2.
Symptoms include hypoventilation, drowsiness, cognitive impairment, muscle jerks with hand flapping, and indications of elevated pressure within the skull (such as swollen optic nerves and a condition resembling a brain tumor).
Laboratory results: pH decreased, Pco2 increased, HCO3 increased.
Address the root cause of acute respiratory acidosis and consider using short-term mechanical ventilation to assist with breathing.
No intervention required for persistent respiratory acidosis.
Acute compensation occurs with a 1 mEq/L increase in bicarbonate for every 10 mm Hg increase in partial pressure of carbon dioxide.
Chronic compensation occurs with a 3.5 mEq/L rise in HCO3 for every 10-mm Hg increase in PCO2.
Resulting from acute lung disease such as ARDS and airway obstruction, chronic lung disease like COPD, CNS depression caused by opioids, sedatives, and narcotics, or weakened respiratory muscles due to conditions like ALS, kyphoscoliosis, MS, and polio.
Primary issue: Elevated Pco2 levels (hypercapnia) due to reduced alveolar ventilation.
Compensatory response: HCO3 increases due to enhanced renal HCO3 reabsorption triggered by low pH and high Pco2.
Symptoms include hypoventilation, drowsiness, cognitive impairment, muscle jerks with hand flapping, and indications of elevated pressure within the skull (such as swollen optic nerves and a condition resembling a brain tumor).
Laboratory results: pH decreased, Pco2 increased, HCO3 increased.
Address the root cause of acute respiratory acidosis and consider using short-term mechanical ventilation to assist with breathing.
No intervention required for persistent respiratory acidosis.
Acute compensation occurs with a 1 mEq/L increase in bicarbonate for every 10 mm Hg increase in partial pressure of carbon dioxide.
Chronic compensation occurs with a 3.5 mEq/L rise in HCO3 for every 10-mm Hg increase in PCO2.
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Pathology - Respiratory alkalosis
Acute respiratory alkalosis is triggered by hyperventilation and can also be caused by several conditions such as salicylate overdose, pneumonia, sepsis, pregnancy, pulmonary edema, pulmonary embolism, or cirrhosis.
Chronic respiratory alkalosis is induced by elevated altitudes or pregnancy.
Main issue: Reduction in Pco2 levels- Compensatory response: Reduction in bicarbonate levels due to heightened production of nitric acid in the kidneys.
Symptoms of acute respiratory alkalosis include reduced cerebral blood flow leading to light-headedness, anxiety, paresthesias, numbness around the mouth, tingling in the extremities, and hyperventilation. It may also result in cardiac arrhythmias.
Laboratory results show elevated pH, reduced Pco2, and decreased HCO3 levels.
Treat acute hyperventilation syndrome caused by worry by breathing into a paper bag to boost Pco2. Otherwise, address the underlying cause such as sepsis or pneumonia.
Acute compensation involves a reduction of 2 mEq/L of bicarbonate for every 10-mm Hg decrease in carbon dioxide pressure.
Chronic compensation occurs with a drop of 5 mEq/L in bicarbonate for every 10-mm Hg fall in Pco2.
Acute respiratory alkalosis is triggered by hyperventilation and can also be caused by several conditions such as salicylate overdose, pneumonia, sepsis, pregnancy, pulmonary edema, pulmonary embolism, or cirrhosis.
Chronic respiratory alkalosis is induced by elevated altitudes or pregnancy.
Main issue: Reduction in Pco2 levels- Compensatory response: Reduction in bicarbonate levels due to heightened production of nitric acid in the kidneys.
Symptoms of acute respiratory alkalosis include reduced cerebral blood flow leading to light-headedness, anxiety, paresthesias, numbness around the mouth, tingling in the extremities, and hyperventilation. It may also result in cardiac arrhythmias.
Laboratory results show elevated pH, reduced Pco2, and decreased HCO3 levels.
Treat acute hyperventilation syndrome caused by worry by breathing into a paper bag to boost Pco2. Otherwise, address the underlying cause such as sepsis or pneumonia.
Acute compensation involves a reduction of 2 mEq/L of bicarbonate for every 10-mm Hg decrease in carbon dioxide pressure.
Chronic compensation occurs with a drop of 5 mEq/L in bicarbonate for every 10-mm Hg fall in Pco2.
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Pathology - Rapidly Progressive (Crescentic) Glomerulonephritis
Type 1: Idiopathic or Goodpasture syndrome.
Type 2 (immune complex) glomerulonephritis can be caused by idiopathic factors, postinfectious conditions, systemic lupus erythematosus (SLE), IgA nephropathy, and Henoch-Schonlein purpura.
Category 3 (pauci-immune type): Conditions include idiopathic, Wegener granulomatosis, and microscopic polyangiitis.
Pathology
Light microscopy shows the formation of a crescent-moon shape between the Bowman capsule and glomerular tuft. This is caused by the deposition of fibrin in the Bowman space and the proliferation of parietal epithelial cells of the Bowman capsule.
Clinical Symptoms
Presence of nephritic syndrome characterized by hematuria, hypertension, and azotemia.
Signs and symptoms vary depending on the cause, such as hemoptysis and anti-GBM antibodies in Goodpasture syndrome.
Therapy
Administer diuretics and ACE inhibitors; consider immunosuppression with steroids or cytotoxic medicines based on the underlying reason; dialysis or transplant may be necessary.
Patients typically progress quickly to end-stage renal failure necessitating dialysis.
Rapidly progressive glomerulonephritis (RPGN) is a condition characterized by significant and advancing damage to the glomeruli. It includes various causes.
Type 1: Idiopathic or Goodpasture syndrome.
Type 2 (immune complex) glomerulonephritis can be caused by idiopathic factors, postinfectious conditions, systemic lupus erythematosus (SLE), IgA nephropathy, and Henoch-Schonlein purpura.
Category 3 (pauci-immune type): Conditions include idiopathic, Wegener granulomatosis, and microscopic polyangiitis.
Pathology
Light microscopy shows the formation of a crescent-moon shape between the Bowman capsule and glomerular tuft. This is caused by the deposition of fibrin in the Bowman space and the proliferation of parietal epithelial cells of the Bowman capsule.
Clinical Symptoms
Presence of nephritic syndrome characterized by hematuria, hypertension, and azotemia.
Signs and symptoms vary depending on the cause, such as hemoptysis and anti-GBM antibodies in Goodpasture syndrome.
Therapy
Administer diuretics and ACE inhibitors; consider immunosuppression with steroids or cytotoxic medicines based on the underlying reason; dialysis or transplant may be necessary.
Patients typically progress quickly to end-stage renal failure necessitating dialysis.
Rapidly progressive glomerulonephritis (RPGN) is a condition characterized by significant and advancing damage to the glomeruli. It includes various causes.
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Pathology - Alport Syndrome
X-linked dominant genetic condition characterized by a mutation in the alpha 5-chain of type IV collagen.
Pathology
Electron microscopy shows irregular areas of thickening or thinning in the glomerular basement membrane with longitudinal breaking of the lamina densa.
Clinical Symptoms and Signs
The combination of nephritis, nerve deafness, and eye problems such as cataracts, lens displacement, and corneal dystrophy may present initially with hematuria and erythrocyte casts.
Treatment: ACE inhibitors; kidney transplant may be considered for severe instances.
X-linked dominant genetic condition characterized by a mutation in the alpha 5-chain of type IV collagen.
Pathology
Electron microscopy shows irregular areas of thickening or thinning in the glomerular basement membrane with longitudinal breaking of the lamina densa.
Clinical Symptoms and Signs
The combination of nephritis, nerve deafness, and eye problems such as cataracts, lens displacement, and corneal dystrophy may present initially with hematuria and erythrocyte casts.
Treatment: ACE inhibitors; kidney transplant may be considered for severe instances.
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Pathology - Membranoproliferative Glomerulonephritis
Linked to hereditary lack of complement components.
Type I is observed in systemic lupus erythematosus, hepatitis B and C, and entails activation of both the conventional and alternative pathways.
Type II specifically entails the activation of the alternative route exclusively.
The majority of affected patients are under 30 years old.
Types I and II: Under light microscopy, the basement membrane shows reduplication (splitting) and the mesangial matrix expands into the capillary loops, creating a tram track appearance.
Type I: Electron microscopy reveals electron-dense deposits located beneath the endothelium.
Type II: Electron microscopy reveals a distinct dense deposit of uniform material within the glomerular basement membrane.
Clinical Symptoms
Type I typically manifests with nephrotic syndrome.
Type II typically manifests as nephritic syndrome characterized by hematuria and persistent renal failure.
Laboratory results: Reduced C3 levels, increased BUN and Cr, presence of RBCs and/or RBC casts in urine.
Treatment include corticosteroids and immunosuppression if deemed suitable for the root cause.
Prognosis involves gradual progression to renal failure with a high likelihood of recurrence post-transplant.
Notes
Linked to hereditary lack of complement components.
Type I is observed in systemic lupus erythematosus, hepatitis B and C, and entails activation of both the conventional and alternative pathways.
Type II specifically entails the activation of the alternative route exclusively.
The majority of affected patients are under 30 years old.
Types I and II: Under light microscopy, the basement membrane shows reduplication (splitting) and the mesangial matrix expands into the capillary loops, creating a tram track appearance.
Type I: Electron microscopy reveals electron-dense deposits located beneath the endothelium.
Type II: Electron microscopy reveals a distinct dense deposit of uniform material within the glomerular basement membrane.
Clinical Symptoms
Type I typically manifests with nephrotic syndrome.
Type II typically manifests as nephritic syndrome characterized by hematuria and persistent renal failure.
Laboratory results: Reduced C3 levels, increased BUN and Cr, presence of RBCs and/or RBC casts in urine.
Treatment include corticosteroids and immunosuppression if deemed suitable for the root cause.
Prognosis involves gradual progression to renal failure with a high likelihood of recurrence post-transplant.
Notes
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Pathology - IgA Nephropathy ( Berger Disease)
IgA deposition in the glomerular mesangium is the primary kidney illness that can occur following infections such as viral upper respiratory tract infection, gastrointestinal infection, or flu-like syndrome. It can also be a part of Henoch-Schonlein purpura.
Most frequently observed in children and young adults, with a higher prevalence in males than in females.
Pathology
Light microscopy reveals focal proliferative glomerulonephritis with diffuse mesangial expansion.
Electron microscopy reveals IgA mesangial deposits.
Exhibits recurring hematuria (red or cola-colored urine) 1-2 days following an upper respiratory or gastrointestinal infection.
Clinical Symptoms and Signs
High blood pressure, tiredness, and slight protein in the urine may be evident.
Laboratory results: Elevated serum IgA level in 50% of cases, normal serum complement levels, presence of red blood cells in urine.
Treatment include ACE inhibitors for proteinuria and steroids or immunosuppressants for specific instances.
20%-30% of people develop end-stage renal failure during a span of 20-30 years.
Berger disease is the predominant kind of acute glomerulonephritis in the United States and is widespread in Asia.
IgA deposition in the glomerular mesangium is the primary kidney illness that can occur following infections such as viral upper respiratory tract infection, gastrointestinal infection, or flu-like syndrome. It can also be a part of Henoch-Schonlein purpura.
Most frequently observed in children and young adults, with a higher prevalence in males than in females.
Pathology
Light microscopy reveals focal proliferative glomerulonephritis with diffuse mesangial expansion.
Electron microscopy reveals IgA mesangial deposits.
Exhibits recurring hematuria (red or cola-colored urine) 1-2 days following an upper respiratory or gastrointestinal infection.
Clinical Symptoms and Signs
High blood pressure, tiredness, and slight protein in the urine may be evident.
Laboratory results: Elevated serum IgA level in 50% of cases, normal serum complement levels, presence of red blood cells in urine.
Treatment include ACE inhibitors for proteinuria and steroids or immunosuppressants for specific instances.
20%-30% of people develop end-stage renal failure during a span of 20-30 years.
Berger disease is the predominant kind of acute glomerulonephritis in the United States and is widespread in Asia.
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Pathology - Acute and Chronic Pyelonephritis
Acute renal parenchymal infection is more common in women.
Chronic: Arises from persistent urinary tract blockage and repeated UTIs.
Study of diseases
Acute renal cortex involvement with neutrophilic infiltration and abscess formation in the interstitium, with potential rupture of abscesses leading to the presence of white blood cells in the tubular lumen, whereas glomeruli are unaffected.
Chronic kidney damage characterized by uneven scarring between the cortex and medulla, with tubules filled with protein-rich casts that give the kidneys a thyroid-like look. This condition progresses to tubular shrinkage and fibrosis in advanced stages.
Clinical presentation of acute pyelonephritis includes fever, flank pain with costovertebral angle tenderness, increased urination and painful urination, as well as symptoms of nausea, vomiting, and diarrhea.
Chronic episodes of acute pyelonephritis can cause renal hypertension and end-stage renal disease (ESRD).
Laboratory results indicate the presence of white blood cells and/or white blood cell casts in the urine.
Treatment for acute conditions includes antibiotics and intravenous fluids.
Chronic renal transplant is indicated for patients who have end-stage renal disease (ESRD).
Renal papillary necrosis is a consequence of acute pyelonephritis that occurs in individuals with diabetes or those who use phenacetin chronically. It is identified by ischemic necrosis at the tips of the renal papillae.
Diffuse cortical necrosis is a sudden widespread death of renal cortices, typically caused by a combination of disseminated intravascular coagulation (DIC) and end-organ vasospasm in connection with obstetric emergencies or septic shock. The medulla is normally unaffected.
Acute renal parenchymal infection is more common in women.
Chronic: Arises from persistent urinary tract blockage and repeated UTIs.
Study of diseases
Acute renal cortex involvement with neutrophilic infiltration and abscess formation in the interstitium, with potential rupture of abscesses leading to the presence of white blood cells in the tubular lumen, whereas glomeruli are unaffected.
Chronic kidney damage characterized by uneven scarring between the cortex and medulla, with tubules filled with protein-rich casts that give the kidneys a thyroid-like look. This condition progresses to tubular shrinkage and fibrosis in advanced stages.
Clinical presentation of acute pyelonephritis includes fever, flank pain with costovertebral angle tenderness, increased urination and painful urination, as well as symptoms of nausea, vomiting, and diarrhea.
Chronic episodes of acute pyelonephritis can cause renal hypertension and end-stage renal disease (ESRD).
Laboratory results indicate the presence of white blood cells and/or white blood cell casts in the urine.
Treatment for acute conditions includes antibiotics and intravenous fluids.
Chronic renal transplant is indicated for patients who have end-stage renal disease (ESRD).
Renal papillary necrosis is a consequence of acute pyelonephritis that occurs in individuals with diabetes or those who use phenacetin chronically. It is identified by ischemic necrosis at the tips of the renal papillae.
Diffuse cortical necrosis is a sudden widespread death of renal cortices, typically caused by a combination of disseminated intravascular coagulation (DIC) and end-organ vasospasm in connection with obstetric emergencies or septic shock. The medulla is normally unaffected.
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Pathology - Choledocholithiasis and Cholangitis
Choledocholithiasis is the occurrence of a gallstone in the common bile duct.
Cholangitis is inflammation and bacterial infection in the common bile duct caused by blockage, typically due to gallstones. Tumors might potentially be a cause. strictures or prior placement of biliary stents
Cholangitis Pathology: There are inflammatory alterations in the biliary wall with neutrophils present in the intra-luminal area.
Pathophysiology: Gallstones can go into the bile ducts outside the liver. Obstruction can allow bacteria, typically enteric gram-negative rods, to enter the biliary tree through the sphincter of Oddi, leading to infection and inflammation of the biliary tract.
Clinical Symptoms
Choledocholithiasis might be asymptomatic or manifest with biliary colic (pain in the right upper quadrant after eating) or jaundice.
Cholangitis manifests with Charcot triad, which includes severe colicky epigastric and right upper quadrant pain, nausea (especially after fatty meals), elevated body temperature, and jaundice. In extreme cases, it can progress to Reynolds pentad, which includes Charcot triad symptoms along with septic shock and altered mental status.
Possible complications are biliary cirrhosis, which can occur due to prolonged common bile duct obstruction, and septic shock, namely from cholangitis.
Laboratory results: High ALP and bilirubin levels, leukocytosis in chol patients. ERCP for stone removal, then cholecystectomy; antibiotics and supportive care for cholangitis.
Choledocholithiasis is the occurrence of a gallstone in the common bile duct.
Cholangitis is inflammation and bacterial infection in the common bile duct caused by blockage, typically due to gallstones. Tumors might potentially be a cause. strictures or prior placement of biliary stents
Cholangitis Pathology: There are inflammatory alterations in the biliary wall with neutrophils present in the intra-luminal area.
Pathophysiology: Gallstones can go into the bile ducts outside the liver. Obstruction can allow bacteria, typically enteric gram-negative rods, to enter the biliary tree through the sphincter of Oddi, leading to infection and inflammation of the biliary tract.
Clinical Symptoms
Choledocholithiasis might be asymptomatic or manifest with biliary colic (pain in the right upper quadrant after eating) or jaundice.
Cholangitis manifests with Charcot triad, which includes severe colicky epigastric and right upper quadrant pain, nausea (especially after fatty meals), elevated body temperature, and jaundice. In extreme cases, it can progress to Reynolds pentad, which includes Charcot triad symptoms along with septic shock and altered mental status.
Possible complications are biliary cirrhosis, which can occur due to prolonged common bile duct obstruction, and septic shock, namely from cholangitis.
Laboratory results: High ALP and bilirubin levels, leukocytosis in chol patients. ERCP for stone removal, then cholecystectomy; antibiotics and supportive care for cholangitis.
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Pathology - Gallbladder Tumor and Biliary Duct Tumor
Gallbladder adenocarcinoma (AGB): Linked to gallstones; the most prevalent primary tumor of the gallbladder; typically occurs in women over the age of 60.
Extrahepatic biliary ducts (EBD) and ampulla of Vater carcinoma: Uncommon: linked to Clonorchis sinensis infection and primary sclerosing cholangitis. Typically occurs in older males.
Terms and conditions: Gross examination reveals a growth pattern characterized by widespread thickening of the gallbladder wall. An exophytic pattern is observed, with irregular cauliflower-like masses growing into the lumen. Adenocarcinoma at a microscopic level showing varied levels of differentiation and commonly infiltrating the liver.
EBD: Appearance: tiny gray nodules located in the wall of the bile duct. Microscopic findings include adenocarcinoma with mucin-secreting cells, fibrous stroma, and epithelial proliferation.
AGB: Initial symptoms are gradual and similar to those of gallstones, including stomach pain, jaundice, loss of appetite, and nausea with vomiting.
The patient with EBD displays symptoms such as worsening obstructive jaundice, nausea, vomiting, weight loss, and an enlarged gallbladder that can be felt, which is not typical of gallstone disease.
Laboratory results for both types: High liver function tests and prolonged prothrombin time.
Treatment: Cholecystectomy, chemotherapy, radiation for AGB.
Ductal malignancies (EBD) cannot be removed with surgery and are managed with chemotherapy and/or radiotherapy, while ampullary cancers are typically surgically removed.
Gallbladder adenocarcinoma (AGB): Linked to gallstones; the most prevalent primary tumor of the gallbladder; typically occurs in women over the age of 60.
Extrahepatic biliary ducts (EBD) and ampulla of Vater carcinoma: Uncommon: linked to Clonorchis sinensis infection and primary sclerosing cholangitis. Typically occurs in older males.
Terms and conditions: Gross examination reveals a growth pattern characterized by widespread thickening of the gallbladder wall. An exophytic pattern is observed, with irregular cauliflower-like masses growing into the lumen. Adenocarcinoma at a microscopic level showing varied levels of differentiation and commonly infiltrating the liver.
EBD: Appearance: tiny gray nodules located in the wall of the bile duct. Microscopic findings include adenocarcinoma with mucin-secreting cells, fibrous stroma, and epithelial proliferation.
AGB: Initial symptoms are gradual and similar to those of gallstones, including stomach pain, jaundice, loss of appetite, and nausea with vomiting.
The patient with EBD displays symptoms such as worsening obstructive jaundice, nausea, vomiting, weight loss, and an enlarged gallbladder that can be felt, which is not typical of gallstone disease.
Laboratory results for both types: High liver function tests and prolonged prothrombin time.
Treatment: Cholecystectomy, chemotherapy, radiation for AGB.
Ductal malignancies (EBD) cannot be removed with surgery and are managed with chemotherapy and/or radiotherapy, while ampullary cancers are typically surgically removed.
Bile Duct Tumor
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Pathology - Acute and Chronic Pancreatitis
Acute pancreatitis is triggered by the activation of pancreatic enzymes leading to self-digestion of organs. It is linked to factors such as alcohol consumption, gallstones, high triglyceride levels, high calcium levels, certain medications (including thiazides and sulfonamides), mumps infection, and autoimmune disorders.
Chronic pancreatitis is a condition characterized by recurrent episodes of pancreatic inflammation, commonly linked to alcoholism and cystic fibrosis.
Pathology
Acute: Presence of hemorrhagic patches with regions of white fat necrosis. Microscopic findings include interstitial edema and inflammation, parenchymal necrosis with vascular injury, and calcium soap deposition.
Chronic condition characterized by fibrotic bands causing a lobular appearance, together with calcified concretions forming pseudocyst development. Microscopic findings show loss of acini with fibrous replacement, but the islets of Langerhans remain unaffected. mononuclear inflammatory infiltration
Symptoms and Signs
Acute: Intense pain in the upper abdomen and left upper quadrant that spreads to the back. Nausea, vomiting, and fever may develop with excessive alcohol consumption. Laboratory results: Leukocytosis, increased levels of serum lipase and amylase
Chronic: Repeated episodes of stomach and back discomfort; progression to pancreatic insufficiency resulting in malabsorption and diabetes. Laboratory results typically show normal levels of serum lipase and amylase.
Possible complications consist of disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), widespread fat necrosis, tetany, and acute kidney failure.
Treatment for acute condition includes supportive measures such as dietary restriction, intravenous fluids, Demerol for pain management, and the use of a nasogastric tube.
Treatment for chronic condition includes enzyme and insulin replacement therapy, as well as pain treatment.
Acute pancreatitis is triggered by the activation of pancreatic enzymes leading to self-digestion of organs. It is linked to factors such as alcohol consumption, gallstones, high triglyceride levels, high calcium levels, certain medications (including thiazides and sulfonamides), mumps infection, and autoimmune disorders.
Chronic pancreatitis is a condition characterized by recurrent episodes of pancreatic inflammation, commonly linked to alcoholism and cystic fibrosis.
Pathology
Acute: Presence of hemorrhagic patches with regions of white fat necrosis. Microscopic findings include interstitial edema and inflammation, parenchymal necrosis with vascular injury, and calcium soap deposition.
Chronic condition characterized by fibrotic bands causing a lobular appearance, together with calcified concretions forming pseudocyst development. Microscopic findings show loss of acini with fibrous replacement, but the islets of Langerhans remain unaffected. mononuclear inflammatory infiltration
Symptoms and Signs
Acute: Intense pain in the upper abdomen and left upper quadrant that spreads to the back. Nausea, vomiting, and fever may develop with excessive alcohol consumption. Laboratory results: Leukocytosis, increased levels of serum lipase and amylase
Chronic: Repeated episodes of stomach and back discomfort; progression to pancreatic insufficiency resulting in malabsorption and diabetes. Laboratory results typically show normal levels of serum lipase and amylase.
Possible complications consist of disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), widespread fat necrosis, tetany, and acute kidney failure.
Treatment for acute condition includes supportive measures such as dietary restriction, intravenous fluids, Demerol for pain management, and the use of a nasogastric tube.
Treatment for chronic condition includes enzyme and insulin replacement therapy, as well as pain treatment.
