This document discusses peptic ulcer disease and its main cause, Helicobacter pylori bacteria. It notes that H. pylori infection is present in about half of the world's population and increases the risk of gastric cancer and peptic ulcers. At least 95% of duodenal ulcer patients are infected with H. pylori. The document discusses various tests used to diagnose H. pylori infection, including urea breath tests and biopsy tests. Eradication of H. pylori through treatment is recommended for patients with peptic ulcers who test positive for the infection.
The tricarboxylic acid (TCA) cycle occurs in the mitochondria and involves the oxidation of acetyl-CoA derived from pyruvate to carbon dioxide, generating reduced coenzymes (NADH and FADH2) that donate electrons to the electron transport chain. The TCA cycle consists of 8 steps where citrate synthase catalyzes the first reaction combining acetyl-CoA with oxaloacetate, and malate dehydrogenase catalyzes the last step regenerating oxaloacetate. One turn of the TCA cycle generates 3 NADH, 1 FADH2, and 1 ATP via
Biosynthesis and degradation of porphyrin and hemesountharya Sen s
This document summarizes the biosynthesis and degradation of porphyrin and heme. It discusses how glycine and succinyl CoA are condensed to form δ-aminolevulinate, the starting material for porphyrin synthesis. Four molecules of porphobilinogen then condense to form the porphyrin ring. A series of reactions incorporates iron to form heme. Heme is degraded through heme oxygenase to form biliverdin and bilirubin, which is transported to the liver bound to albumin.
Fatty liver, or steatosis, is defined as an excessive accumulation of lipids in the liver replacing liver cells. This can progress to liver cirrhosis. Causes include overfeeding of fats or carbohydrates, increased fatty acid mobilization to the liver from fat depots, decreased fatty acid oxidation, and decreased export of fats from the liver. Lipotropic factors help transport triglycerides from the liver by facilitating phospholipid and protein biosynthesis, such as essential fatty acids, inositol, choline, methionine, and proteins. Antilipotropic factors inhibit this process through interfering with phospholipid and protein biosynthesis, like overfeeding of cholesterol or substances like carbon tetrachloride.
This document discusses iron metabolism in the human body. It covers:
1) Molecules involved in iron transport including DMT1, ferroportin, transferrin receptors, hephaestin, transferrin, ferritin, and hepcidin.
2) Steps of iron absorption in the gut and transport through the body.
3) Utilization of iron in erythropoiesis to produce hemoglobin.
4) Disorders of iron metabolism like iron deficiency anemia, hemochromatosis, and atransferrinemia.
This document summarizes the metabolism of branched chain amino acids (BCAAs) - valine, isoleucine, and leucine. It discusses that the initial reactions in BCAA catabolism are common, involving transamination, oxidative decarboxylation, and dehydrogenation to form acyl-CoA derivatives. It then explains that the subsequent catabolism of each BCAA differs and leads to the formation of acetyl-CoA and succinyl-CoA. One key point is that defects in BCAA catabolism can cause metabolic disorders like maple syrup urine disease, where the branch chain keto acid dehydrogenase enzyme is deficient.
Gluconeogenesis is the pathway by which organisms synthesize glucose from non-carbohydrate precursors like lactate, pyruvate, glycerol, and certain amino acids. This occurs mainly in the liver and to a lesser extent in the kidneys. While some steps are reversible versions of glycolysis, three irreversible steps of glycolysis are bypassed. Specifically, pyruvate is converted to oxaloacetate then phosphoenolpyruvate through carboxylation and decarboxylation reactions requiring ATP and GTP. This generates free glucose which is an important control point, as glucose-6-phosphate is typically further processed rather than released as free glucose except in a few tissues.
The tricarboxylic acid (TCA) cycle occurs in the mitochondria and involves the oxidation of acetyl-CoA derived from pyruvate to carbon dioxide, generating reduced coenzymes (NADH and FADH2) that donate electrons to the electron transport chain. The TCA cycle consists of 8 steps where citrate synthase catalyzes the first reaction combining acetyl-CoA with oxaloacetate, and malate dehydrogenase catalyzes the last step regenerating oxaloacetate. One turn of the TCA cycle generates 3 NADH, 1 FADH2, and 1 ATP via
Biosynthesis and degradation of porphyrin and hemesountharya Sen s
This document summarizes the biosynthesis and degradation of porphyrin and heme. It discusses how glycine and succinyl CoA are condensed to form δ-aminolevulinate, the starting material for porphyrin synthesis. Four molecules of porphobilinogen then condense to form the porphyrin ring. A series of reactions incorporates iron to form heme. Heme is degraded through heme oxygenase to form biliverdin and bilirubin, which is transported to the liver bound to albumin.
Fatty liver, or steatosis, is defined as an excessive accumulation of lipids in the liver replacing liver cells. This can progress to liver cirrhosis. Causes include overfeeding of fats or carbohydrates, increased fatty acid mobilization to the liver from fat depots, decreased fatty acid oxidation, and decreased export of fats from the liver. Lipotropic factors help transport triglycerides from the liver by facilitating phospholipid and protein biosynthesis, such as essential fatty acids, inositol, choline, methionine, and proteins. Antilipotropic factors inhibit this process through interfering with phospholipid and protein biosynthesis, like overfeeding of cholesterol or substances like carbon tetrachloride.
This document discusses iron metabolism in the human body. It covers:
1) Molecules involved in iron transport including DMT1, ferroportin, transferrin receptors, hephaestin, transferrin, ferritin, and hepcidin.
2) Steps of iron absorption in the gut and transport through the body.
3) Utilization of iron in erythropoiesis to produce hemoglobin.
4) Disorders of iron metabolism like iron deficiency anemia, hemochromatosis, and atransferrinemia.
This document summarizes the metabolism of branched chain amino acids (BCAAs) - valine, isoleucine, and leucine. It discusses that the initial reactions in BCAA catabolism are common, involving transamination, oxidative decarboxylation, and dehydrogenation to form acyl-CoA derivatives. It then explains that the subsequent catabolism of each BCAA differs and leads to the formation of acetyl-CoA and succinyl-CoA. One key point is that defects in BCAA catabolism can cause metabolic disorders like maple syrup urine disease, where the branch chain keto acid dehydrogenase enzyme is deficient.
Gluconeogenesis is the pathway by which organisms synthesize glucose from non-carbohydrate precursors like lactate, pyruvate, glycerol, and certain amino acids. This occurs mainly in the liver and to a lesser extent in the kidneys. While some steps are reversible versions of glycolysis, three irreversible steps of glycolysis are bypassed. Specifically, pyruvate is converted to oxaloacetate then phosphoenolpyruvate through carboxylation and decarboxylation reactions requiring ATP and GTP. This generates free glucose which is an important control point, as glucose-6-phosphate is typically further processed rather than released as free glucose except in a few tissues.
Methionine, cysteine and branched chain amino acidsKAVIN6369950450
This document summarizes key information about sulfur-containing amino acids methionine and cysteine. Methionine is an essential amino acid that can be converted to cysteine. Both amino acids play important roles in transmethylation reactions and glutathione synthesis. Cysteine forms disulfide bonds and is involved in taurine synthesis. Genetic disorders involving these amino acids like cystinuria, cystinosis, and homocystinurias are also discussed.
Lipoproteins are complexes of lipids and proteins that transport lipids through the bloodstream. There are four main types of plasma lipoproteins - chylomicrons, VLDL, LDL, and HDL - which differ in size, density, and lipid/protein composition. Chylomicrons carry dietary lipids from the intestine to other tissues, VLDL transports endogenous lipids from the liver, LDL carries cholesterol, and HDL transports cholesterol from tissues to the liver for processing or excretion. The metabolism and interactions between these lipoproteins, such as the transfer of lipids between them, are tightly regulated and essential for maintaining lipid homeostasis.
The document discusses carbohydrate metabolism, specifically glucose metabolism and the pathways involved in glucose oxidation and storage. It covers the following key points:
1) Glycolysis and the citric acid cycle are the two major pathways for glucose oxidation and energy production. Glycolysis occurs in the cytoplasm and citric acid cycle in the mitochondria.
2) Glycolysis converts glucose to pyruvate, producing a small amount of energy. Pyruvate can then enter the citric acid cycle or be converted to lactate.
3) The citric acid cycle further oxidizes acetyl groups from pyruvate, producing more energy through the electron transport chain.
The document discusses lipid metabolism and β-oxidation of fatty acids. It notes that triacylglycerols are broken down into free fatty acids and glycerol in the gut. Fatty acids are transported via lipoproteins or albumin and undergo β-oxidation in the mitochondria to generate acetyl-CoA. β-Oxidation involves four steps per fatty acid: dehydrogenation, hydration, second dehydrogenation, and thiolysis. This shortens the fatty acid by two carbons, producing acetyl-CoA and reducing equivalents.
The document summarizes the metabolism of various amino acids. It notes that some amino acids are glucogenic, producing pyruvate or TCA cycle intermediates, while others are ketogenic, producing acetyl-CoA or acetoacetate. Key points include:
- Alanine can be readily formed from pyruvate via transamination and is important for gluconeogenesis.
- Arginine produces ornithine and urea and is the precursor for nitric oxide and creatine synthesis.
- Serine can be converted to glycine and provides one-carbon units via tetrahydrofolate. Its carbon skeleton feeds into other amino acids.
- Glutamate is central to amino acid
The document discusses the electron transport chain (ETC) in mitochondria. It describes the ETC as a series of electron carriers embedded in the inner mitochondrial membrane that transfers electrons from NADH and FADH2 to oxygen. These carriers include nicotinamide nucleotides, flavoproteins, iron-sulfur proteins, coenzyme Q, and cytochromes. The passage of electrons through this chain is coupled to the pumping of protons across the membrane and generation of ATP by ATP synthase. The document also lists some inhibitors that block electron transport at specific sites in the chain such as rotenone, antimycin A, and cyanide.
This document summarizes iron metabolism. It discusses:
- The functions of iron as part of hemoglobin, myoglobin, cytochromes and iron-containing enzymes.
- How iron is absorbed in the small intestine and transported to tissues by transferrin. Iron is stored in ferritin and hemosiderin.
- Disorders of iron metabolism include iron deficiency, which can cause anemia, and iron overload disorders like hemochromatosis.
1) Porphyrins are biomarkers that can identify toxicity to the heme biosynthesis pathway. Disturbances can cause accumulations of porphyrin intermediates in urine.
2) Testing porphyrin levels can identify biochemical damage from toxic exposures like mercury and monitor chelation therapy. Abnormal levels also correlate with conditions like chemical sensitivities and neurological disorders.
3) Case studies show porphyrin testing identified arsenic exposure from an elevated ratio and confirmed mercury toxicity in an autistic child with challenges excreting heavy metals.
This document summarizes the metabolism of the branched chain amino acids valine, leucine, and isoleucine. It describes how they are first transaminated to their corresponding keto acids, then undergo oxidative decarboxylation by alpha-keto acid dehydrogenase to form acyl-CoA thioesters. These are further dehydrogenated and enter different pathways, with valine being converted to propionyl-CoA and being glycogenic, leucine producing acetyl-CoA and acetoacetate and being ketogenic, and isoleucine undergoing both glycogenic and ketogenic fates. Defects in these pathways can cause diseases like maple syrup urine disease.
The document summarizes key aspects of sulfur-containing amino acid metabolism. It discusses how methionine is converted to cysteine and cystine and its role in transmethylation reactions through the intermediate S-adenosylmethionine (SAM). SAM transfers methyl groups to various acceptors and is converted to S-adenosylhomocysteine. Homocysteine can then be remethylated to regenerate methionine or condensed with serine to form cystathionine for cysteine synthesis. Transmethylation reactions are important for activating many compounds and regulating protein turnover through methylation. Causes of hypermethioninemia include impaired utilization, excessive remethylation, and hepatic dysfunction.
Formation and fate of Ammonia
Transdeamination, oxidative and non oxidative deamination, Ammonia transport, Ammonia intoxication, Ammonia detoxification
This document summarizes key information about the metabolism of the branched chain amino acids valine, leucine, and isoleucine. It discusses that they are essential amino acids whose metabolism begins in muscle tissue. The first three reactions - transamination, oxidative decarboxylation, and dehydrogenation - are common to all three amino acids. Conditions like maple syrup urine disease and isovaleric acidemia occur due to defects in later steps of this metabolic pathway.
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARSYESANNA
- Lactose in milk is broken down by lactase into glucose and galactose. Galactose is metabolized mainly in the liver.
- Galactose is converted to glucose through a series of reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies in enzymes involved in galactose metabolism can cause galactosemia, a serious genetic disorder if galactose is not restricted from the diet.
The document discusses nucleotide metabolism, specifically purine and pyrimidine nucleotide biosynthesis. It describes how purine nucleotides like IMP are synthesized through multi-step pathways requiring various precursors. IMP then branches into AMP and GMP synthesis pathways. Purine synthesis is regulated by controlling levels of PRPP and at the first two rate-limiting steps. The synthesis of pyrimidine nucleotides also utilizes PRPP and multi-step pathways to synthesize nucleotides from precursors.
This document summarizes the metabolism of fructose and galactose. It explains that fructose is metabolized differently in the liver versus muscle, and outlines the key steps in each tissue. It also discusses hereditary defects that can occur in fructose metabolism, including essential fructosuria and hereditary fructose intolerance. The document then summarizes galactose metabolism, noting it is converted to glucose-1-phosphate in the liver through a series of enzymatic steps before entering glycolysis. Finally, it briefly discusses galactosemias which can occur due to inherited defects in galactose metabolism.
This document discusses plasma proteins and their measurement. It begins by explaining the main components of blood and plasma. It then discusses the different plasma proteins including albumin, globulins, and coagulation factors. The document explains how to separate serum from blood and measure total proteins, albumin, and globulins. It provides the normal ranges for these values and discusses causes of hypo- and hyperproteinemia. Overall, the document provides a comprehensive overview of plasma proteins and their clinical assessment.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
Hemoglobin is a protein in red blood cells that carries oxygen throughout the body. It is composed of four polypeptide chains, two alpha chains and two beta chains, as well as an iron-containing heme group. Abnormalities in the hemoglobin protein chains or levels can result in hemoglobinopathies. Common hemoglobinopathies include sickle cell disease, where a mutation in the beta chain causes red blood cells to take on a sickle shape, and thalassemias, where reduced production of the alpha or beta chains causes anemia. Other clinically significant hemoglobin variants involve single amino acid substitutions that can alter oxygen affinity and cause issues like decreased oxygen delivery or increased red blood cell destruction.
The document summarizes the organization of the mitochondrial electron transport chain. It describes the five complexes of the electron transport chain (Complexes I-V), including their components, functions, and electron transfer processes. Specifically, it details how Complexes I, III, and IV transfer electrons from donors like NADH to final acceptors like oxygen. This generates a proton gradient across the inner mitochondrial membrane, which Complex V then uses to synthesize ATP through oxidative phosphorylation.
Glycogen is the major storage carbohydrate in animals and is stored primarily in the liver and skeletal muscle. Glycogenesis is the process of glycogen synthesis from glucose, which takes place in the cytoplasm of liver and muscle cells. Glycogenolysis is the breakdown of glycogen into glucose-1-phosphate, and is regulated by hormones like glucagon and insulin to control blood glucose levels. Deficiencies in enzymes involved in glycogen metabolism can cause glycogen storage diseases.
The document discusses peptic ulcer disease, specifically focusing on the role of Helicobacter pylori infection as the main cause of gastric and duodenal ulcers. It details how H. pylori infection increases the risk of gastric cancer and peptic ulcers. The document then discusses various diagnostic tests for H. pylori infection and peptic ulcer disease, including biopsy, urea breath tests, and stool antigen tests. It also discusses the recommended treatment of peptic ulcer disease when patients are infected with H. pylori.
This document provides information on the causes, diagnosis, and management of peptic ulcer disease and gastric outlet obstruction. It discusses that peptic ulcers are caused by an imbalance between aggressive factors like acid secretion and defensive factors. Infection with H. pylori is a key cause. Diagnosis involves endoscopy with biopsy. Management focuses on treating H. pylori infection and using antisecretory drugs. Surgery is reserved for complications or refractory cases. Gastric outlet obstruction is usually due to peptic ulcer disease but can also be caused by malignancy, inflammation, or other conditions.
Methionine, cysteine and branched chain amino acidsKAVIN6369950450
This document summarizes key information about sulfur-containing amino acids methionine and cysteine. Methionine is an essential amino acid that can be converted to cysteine. Both amino acids play important roles in transmethylation reactions and glutathione synthesis. Cysteine forms disulfide bonds and is involved in taurine synthesis. Genetic disorders involving these amino acids like cystinuria, cystinosis, and homocystinurias are also discussed.
Lipoproteins are complexes of lipids and proteins that transport lipids through the bloodstream. There are four main types of plasma lipoproteins - chylomicrons, VLDL, LDL, and HDL - which differ in size, density, and lipid/protein composition. Chylomicrons carry dietary lipids from the intestine to other tissues, VLDL transports endogenous lipids from the liver, LDL carries cholesterol, and HDL transports cholesterol from tissues to the liver for processing or excretion. The metabolism and interactions between these lipoproteins, such as the transfer of lipids between them, are tightly regulated and essential for maintaining lipid homeostasis.
The document discusses carbohydrate metabolism, specifically glucose metabolism and the pathways involved in glucose oxidation and storage. It covers the following key points:
1) Glycolysis and the citric acid cycle are the two major pathways for glucose oxidation and energy production. Glycolysis occurs in the cytoplasm and citric acid cycle in the mitochondria.
2) Glycolysis converts glucose to pyruvate, producing a small amount of energy. Pyruvate can then enter the citric acid cycle or be converted to lactate.
3) The citric acid cycle further oxidizes acetyl groups from pyruvate, producing more energy through the electron transport chain.
The document discusses lipid metabolism and β-oxidation of fatty acids. It notes that triacylglycerols are broken down into free fatty acids and glycerol in the gut. Fatty acids are transported via lipoproteins or albumin and undergo β-oxidation in the mitochondria to generate acetyl-CoA. β-Oxidation involves four steps per fatty acid: dehydrogenation, hydration, second dehydrogenation, and thiolysis. This shortens the fatty acid by two carbons, producing acetyl-CoA and reducing equivalents.
The document summarizes the metabolism of various amino acids. It notes that some amino acids are glucogenic, producing pyruvate or TCA cycle intermediates, while others are ketogenic, producing acetyl-CoA or acetoacetate. Key points include:
- Alanine can be readily formed from pyruvate via transamination and is important for gluconeogenesis.
- Arginine produces ornithine and urea and is the precursor for nitric oxide and creatine synthesis.
- Serine can be converted to glycine and provides one-carbon units via tetrahydrofolate. Its carbon skeleton feeds into other amino acids.
- Glutamate is central to amino acid
The document discusses the electron transport chain (ETC) in mitochondria. It describes the ETC as a series of electron carriers embedded in the inner mitochondrial membrane that transfers electrons from NADH and FADH2 to oxygen. These carriers include nicotinamide nucleotides, flavoproteins, iron-sulfur proteins, coenzyme Q, and cytochromes. The passage of electrons through this chain is coupled to the pumping of protons across the membrane and generation of ATP by ATP synthase. The document also lists some inhibitors that block electron transport at specific sites in the chain such as rotenone, antimycin A, and cyanide.
This document summarizes iron metabolism. It discusses:
- The functions of iron as part of hemoglobin, myoglobin, cytochromes and iron-containing enzymes.
- How iron is absorbed in the small intestine and transported to tissues by transferrin. Iron is stored in ferritin and hemosiderin.
- Disorders of iron metabolism include iron deficiency, which can cause anemia, and iron overload disorders like hemochromatosis.
1) Porphyrins are biomarkers that can identify toxicity to the heme biosynthesis pathway. Disturbances can cause accumulations of porphyrin intermediates in urine.
2) Testing porphyrin levels can identify biochemical damage from toxic exposures like mercury and monitor chelation therapy. Abnormal levels also correlate with conditions like chemical sensitivities and neurological disorders.
3) Case studies show porphyrin testing identified arsenic exposure from an elevated ratio and confirmed mercury toxicity in an autistic child with challenges excreting heavy metals.
This document summarizes the metabolism of the branched chain amino acids valine, leucine, and isoleucine. It describes how they are first transaminated to their corresponding keto acids, then undergo oxidative decarboxylation by alpha-keto acid dehydrogenase to form acyl-CoA thioesters. These are further dehydrogenated and enter different pathways, with valine being converted to propionyl-CoA and being glycogenic, leucine producing acetyl-CoA and acetoacetate and being ketogenic, and isoleucine undergoing both glycogenic and ketogenic fates. Defects in these pathways can cause diseases like maple syrup urine disease.
The document summarizes key aspects of sulfur-containing amino acid metabolism. It discusses how methionine is converted to cysteine and cystine and its role in transmethylation reactions through the intermediate S-adenosylmethionine (SAM). SAM transfers methyl groups to various acceptors and is converted to S-adenosylhomocysteine. Homocysteine can then be remethylated to regenerate methionine or condensed with serine to form cystathionine for cysteine synthesis. Transmethylation reactions are important for activating many compounds and regulating protein turnover through methylation. Causes of hypermethioninemia include impaired utilization, excessive remethylation, and hepatic dysfunction.
Formation and fate of Ammonia
Transdeamination, oxidative and non oxidative deamination, Ammonia transport, Ammonia intoxication, Ammonia detoxification
This document summarizes key information about the metabolism of the branched chain amino acids valine, leucine, and isoleucine. It discusses that they are essential amino acids whose metabolism begins in muscle tissue. The first three reactions - transamination, oxidative decarboxylation, and dehydrogenation - are common to all three amino acids. Conditions like maple syrup urine disease and isovaleric acidemia occur due to defects in later steps of this metabolic pathway.
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARSYESANNA
- Lactose in milk is broken down by lactase into glucose and galactose. Galactose is metabolized mainly in the liver.
- Galactose is converted to glucose through a series of reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies in enzymes involved in galactose metabolism can cause galactosemia, a serious genetic disorder if galactose is not restricted from the diet.
The document discusses nucleotide metabolism, specifically purine and pyrimidine nucleotide biosynthesis. It describes how purine nucleotides like IMP are synthesized through multi-step pathways requiring various precursors. IMP then branches into AMP and GMP synthesis pathways. Purine synthesis is regulated by controlling levels of PRPP and at the first two rate-limiting steps. The synthesis of pyrimidine nucleotides also utilizes PRPP and multi-step pathways to synthesize nucleotides from precursors.
This document summarizes the metabolism of fructose and galactose. It explains that fructose is metabolized differently in the liver versus muscle, and outlines the key steps in each tissue. It also discusses hereditary defects that can occur in fructose metabolism, including essential fructosuria and hereditary fructose intolerance. The document then summarizes galactose metabolism, noting it is converted to glucose-1-phosphate in the liver through a series of enzymatic steps before entering glycolysis. Finally, it briefly discusses galactosemias which can occur due to inherited defects in galactose metabolism.
This document discusses plasma proteins and their measurement. It begins by explaining the main components of blood and plasma. It then discusses the different plasma proteins including albumin, globulins, and coagulation factors. The document explains how to separate serum from blood and measure total proteins, albumin, and globulins. It provides the normal ranges for these values and discusses causes of hypo- and hyperproteinemia. Overall, the document provides a comprehensive overview of plasma proteins and their clinical assessment.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
Hemoglobin is a protein in red blood cells that carries oxygen throughout the body. It is composed of four polypeptide chains, two alpha chains and two beta chains, as well as an iron-containing heme group. Abnormalities in the hemoglobin protein chains or levels can result in hemoglobinopathies. Common hemoglobinopathies include sickle cell disease, where a mutation in the beta chain causes red blood cells to take on a sickle shape, and thalassemias, where reduced production of the alpha or beta chains causes anemia. Other clinically significant hemoglobin variants involve single amino acid substitutions that can alter oxygen affinity and cause issues like decreased oxygen delivery or increased red blood cell destruction.
The document summarizes the organization of the mitochondrial electron transport chain. It describes the five complexes of the electron transport chain (Complexes I-V), including their components, functions, and electron transfer processes. Specifically, it details how Complexes I, III, and IV transfer electrons from donors like NADH to final acceptors like oxygen. This generates a proton gradient across the inner mitochondrial membrane, which Complex V then uses to synthesize ATP through oxidative phosphorylation.
Glycogen is the major storage carbohydrate in animals and is stored primarily in the liver and skeletal muscle. Glycogenesis is the process of glycogen synthesis from glucose, which takes place in the cytoplasm of liver and muscle cells. Glycogenolysis is the breakdown of glycogen into glucose-1-phosphate, and is regulated by hormones like glucagon and insulin to control blood glucose levels. Deficiencies in enzymes involved in glycogen metabolism can cause glycogen storage diseases.
The document discusses peptic ulcer disease, specifically focusing on the role of Helicobacter pylori infection as the main cause of gastric and duodenal ulcers. It details how H. pylori infection increases the risk of gastric cancer and peptic ulcers. The document then discusses various diagnostic tests for H. pylori infection and peptic ulcer disease, including biopsy, urea breath tests, and stool antigen tests. It also discusses the recommended treatment of peptic ulcer disease when patients are infected with H. pylori.
This document provides information on the causes, diagnosis, and management of peptic ulcer disease and gastric outlet obstruction. It discusses that peptic ulcers are caused by an imbalance between aggressive factors like acid secretion and defensive factors. Infection with H. pylori is a key cause. Diagnosis involves endoscopy with biopsy. Management focuses on treating H. pylori infection and using antisecretory drugs. Surgery is reserved for complications or refractory cases. Gastric outlet obstruction is usually due to peptic ulcer disease but can also be caused by malignancy, inflammation, or other conditions.
Cholera is a bacterial disease caused by Vibrio cholerae that causes severe watery diarrhea and dehydration. It occurs in outbreaks related to contaminated water supplies in areas with poor sanitation. Clinical presentation includes sudden onset of painless, copious watery diarrhea and vomiting leading to severe dehydration and death if untreated. Diagnosis is confirmed by identifying the bacteria in a stool sample. Treatment focuses on oral rehydration and intravenous fluids to replace fluid and electrolyte losses. Antibiotics are given to shorten the duration of illness and reduce spread.
1. Malabsorption syndromes can involve defects in digestion or absorption of nutrients and present with symptoms of nutrient deficiencies.
2. Celiac disease is an immune-mediated disorder triggered by ingestion of gluten that results in damage to the small intestine and malabsorption. It is diagnosed through small bowel biopsy and treatment is a lifelong gluten-free diet.
3. Tropical sprue is a malabsorption syndrome of the small intestine seen in tropical regions, whose cause is thought to be an infectious agent. It resembles celiac disease and improves with antibiotic treatment.
This document discusses the pathophysiology, evaluation, and management of chronic diarrhea in children. It begins by defining chronic, persistent, and protracted diarrhea. Worldwide, chronic diarrhea is a major cause of childhood death, with rotavirus, cryptosporidium, and giardia being common causes in developing countries. The document outlines the steps to evaluate chronic diarrhea, including stool tests, intestinal microbiology, screening for celiac disease, tests of intestinal function, and imaging/endoscopy if needed. Common causes discussed include cow's milk protein allergy, tropical sprue, celiac disease, and intestinal lymphangiectasia. Management involves nutritional rehabilitation, identifying and avoiding food triggers, antibiotics for infections,
Celiac disease is an autoimmune disorder triggered by ingesting gluten, which damages the small intestine's lining. It affects about 1 in 100 people worldwide. The disease is caused by an interaction between gluten and the small intestine in genetically predisposed individuals. There is no cure, but following a strict gluten-free diet can help manage symptoms and prevent complications like osteoporosis and intestinal cancer. A biopsy of the small intestine is required for diagnosis to confirm the characteristic damage to intestinal villi.
Celiac disease is an autoimmune disorder triggered by gluten in genetically susceptible individuals. It was first described by a Greek physician around 2000 years ago. The disease causes damage to the small intestine and can present with a wide range of symptoms. It is diagnosed through blood tests, genetic testing, and biopsy of the small intestine. The only treatment is a lifelong gluten-free diet, which allows the intestines to heal. Strict adherence to the diet is required to avoid complications.
Necrotizing enterocolitis (NEC) is a life-threatening condition that affects the intestines of premature infants. It results from necrosis of the intestinal tissue and can range from mild to severe. Risk factors include prematurity, formula feeding, and bacterial or viral infections. Symptoms may include abdominal distension, bloody stools, and temperature instability. Diagnosis involves x-rays showing pneumatosis intestinalis or portal venous gas. Treatment focuses on gut rest, broad-spectrum antibiotics, surgery for perforation or failure to improve, and careful feeding advancement after recovery. Outcomes depend on severity but may include strictures, adhesions, or short bowel syndrome.
Necrotizing enterocolitis (NEC) is a life-threatening condition that affects the intestines of premature infants. It results from necrosis of the intestinal tissue and can range from mild to severe. Risk factors include prematurity, formula feeding, and bacterial or viral infections. Symptoms may include abdominal distension, vomiting, and bloody stools. Diagnosis is confirmed through x-ray evidence of pneumatosis intestinalis or portal venous gas. Treatment involves gut rest, antibiotics, surgery for perforation or failure to improve. Despite advances, NEC remains a major cause of death in preterm neonates.
This document provides information on gastroesophageal reflux disease (GERD) and acute gastroenteritis in children. It discusses the definition, epidemiology, risk factors, types, mechanisms, etiology and treatment of these conditions. For GERD, it describes the difference between physiologic and pathologic reflux. It also outlines diagnostic tests and treatment approaches including lifestyle changes, medications and surgery. For acute gastroenteritis, it defines the condition and discusses causative agents such as viruses, bacteria and parasites. It compares secretory and osmotic diarrhea and describes the pathogenesis of infectious diarrhea.
Inflammatory bowel disease (IBD) refers to chronic inflammation conditions like Crohn's disease and ulcerative colitis that damage the gastrointestinal tract. Common symptoms include persistent diarrhea, abdominal pain, bloody stools, weight loss and fatigue. The exact causes are unknown but involve a genetic predisposition and exaggerated immune response to environmental triggers. Complications can include colon cancer, malnutrition, and in severe cases perforation or toxic swelling of the colon. Diagnosis involves lab tests, endoscopy, and imaging. Treatment focuses on anti-inflammatory drugs, immune suppressors, antibiotics, nutrition and sometimes surgery to remove diseased sections of bowel.
Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It is caused by mutations in the CFTR gene that result in abnormal ion transport in epithelial cells. This leads to thick, sticky mucus production in organs like the lungs and pancreas. Key gastrointestinal manifestations of cystic fibrosis include meconium ileus in infants, distal intestinal obstruction syndrome, exocrine pancreatic insufficiency treated with pancreatic enzyme replacement therapy, and an increased risk of gastrointestinal cancers. Cystic fibrosis also increases the risk of liver disease and cystic fibrosis-related diabetes. Overall, cystic fibrosis is a multi-system genetic disease that significantly impacts the lungs and gastrointestinal system through defects in ion transport.
Inflammatory bowel disease (IBD) refers to chronic inflammatory conditions of the intestines, including Crohn's disease and ulcerative colitis. The exact causes are unknown but may involve genetic and environmental factors that trigger an immune response in the gastrointestinal tract. Crohn's disease causes transmural inflammation throughout the digestive tract and can involve any part from mouth to anus, while ulcerative colitis only affects the large intestine and causes ulcers, sores and bleeding within the colon. Both involve periods of active disease and remission.
1- Understand the pathophysiologic mechanisms involved in chronic diarrhea.
2. Classification the causes of chronic diarrhea in resource-rich and resource-limited countries
3- Know how to evaluate a child who has chronic diarrhea
4. Know the therapies for the many causes of chronic diarrhea
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.
This document discusses benign and malignant lesions of the intestines. It begins by providing background on the intestines and burden of colorectal cancer worldwide. It then describes the histology and patterns of abnormality seen in small intestinal biopsies for various conditions like celiac disease, tropical sprue, stasis syndromes, and Whipple's disease. It also discusses the histologic patterns seen in colonic inflammation and different types of active colitis.
This document discusses peptic ulcers and their treatment. It begins by defining a peptic ulcer as a disruption of the stomach or duodenal mucosa caused by acid and pepsin exposure. Risk factors include H. pylori infection, NSAID use, smoking, stress, and excess acid secretion. Symptoms can include epigastric pain, nausea, vomiting, weight loss, and bleeding. Treatment aims to eradicate H. pylori, relieve symptoms, heal ulcers, and prevent recurrence. The standard first-line treatment is a proton pump inhibitor combined with two antibiotics for 14 days.
This document discusses chronic diarrhea and its causes and management. It defines persistent diarrhea as acute diarrhea lasting over 2 weeks, while chronic diarrhea has a more insidious onset and is usually due to non-infectious causes lasting over 2 weeks. Common causes of persistent diarrhea include malnutrition, infections, and food allergies. Chronic diarrhea requires further evaluation to identify underlying inflammatory, malabsorptive, intestinal, metabolic, or other conditions as the cause. Management of both involves rehydration, controlling diarrhea, identifying the cause, and rehabilitation.
Acute diarrhea lasts less than two weeks and is usually caused by viral or bacterial infections. Chronic diarrhea lasts longer than two weeks and can be caused by inflammatory bowel disease, malabsorption issues, parasitic infections, or irritable bowel syndrome. Risk factors for acute diarrhea include exposure to infectious agents. Diagnosis involves stool testing and potentially endoscopy, while treatment focuses on rehydration for acute cases and identifying the underlying cause for chronic cases.
This document discusses the mechanism and regulation of hydrochloric acid secretion in the stomach. It contains the following key points:
1) Hydrochloric acid is secreted by parietal cells in the stomach through an energy-requiring process that transports protons against a concentration gradient. This involves the K+-ATPase pump and generation of hydrogen ions from carbonic acid.
2) Gastrin and histamine are the main stimulators of acid secretion. Gastrin secretion is inhibited by acidic pH in a feedback loop.
3) Tests of gastric function include analysis of resting gastric contents, pentagastrin testing to measure maximal acid output, and insulin-induced hypoglycemia testing.
Spectrophotometry and colorimetry are analytical techniques that use light to determine properties of substances. Spectrophotometry measures how much light is absorbed by a solution and can be used to determine concentration. It works by passing light through a sample and measuring the absorption at specific wavelengths. Many factors can affect the measurements, including concentration, path length, and calibration. Spectrophotometry has wide applications in fields like chemistry, medicine, food science and more.
This document discusses the principles and applications of nephelometry and turbidimetry. Both methods measure the scattering of light by particles in solution, but differ in how the scattered light is measured. Nephelometry measures scattered light at an angle, usually 90 degrees, to the incident light beam. Turbidimetry measures light transmitted through the solution in the direction of the incident beam. Factors that affect scattering include particle concentration, size, shape, wavelength of light, and refractive indices of particles and solvent. Applications include determining concentrations of substances like proteins, sulfate, and ammonia in biochemical and environmental analysis.
The document discusses hemoglobin synthesis, which consists of two parts: globin synthesis and heme synthesis. Globin is synthesized through transcription and translation of genes on chromosomes 16 and 11. Heme is synthesized through the Shemin cycle, where glycine and succinyl-CoA are condensed to form delta-aminolevulinic acid, which undergoes further modifications to ultimately form protoporphyrin IX. Protoporphyrin then binds iron to form heme. Heme synthesis is regulated by feedback inhibition of delta-aminolevulinic acid synthase, and both heme and globin are required for the formation of functional hemoglobin.
This document discusses the structure and function of haemoglobin and the transport of gases in the blood. It provides a history of discoveries about haemoglobin dating back to the 17th century. Key points covered include the tetrameric structure of haemoglobin, with each subunit binding one heme group and iron atom. Haemoglobin is able to efficiently transport oxygen and carbon dioxide via changes in its quaternary structure and binding of effectors like hydrogen ions, carbon dioxide and 2,3-BPG. The sigmoidal oxygen dissociation curve illustrates haemoglobin's ability to load and unload oxygen in the lungs and tissues respectively. Factors like pH, temperature and organic phosphates influence the curve.
This document discusses pilot studies and pretesting of surveys. It defines a pilot study as a small-scale trial of the research process to assess feasibility, while pretesting specifically refers to testing survey questions to ensure they are clear and understood by respondents. The key objectives of pilot studies and pretesting are to validate research tools and methods, identify any issues, and improve the quality and rigor of the full research project. Sample sizes of 10-30% of the planned study are typically used for pilot testing.
This document provides an overview of proteins and amino acids. It discusses the 20 standard amino acids that make up proteins, how they are joined by peptide bonds, and how amino acids are classified. It also outlines several important roles of proteins in biological processes, including enzymatic catalysis, transport, mechanical support, and growth regulation.
This document discusses carbohydrates, including their classification, roles, and functions. Carbohydrates can be classified as monosaccharides, disaccharides, oligosaccharides, or polysaccharides based on the number of sugar units present. Examples of monosaccharides are glucose and galactose. Important polysaccharides include glycogen, starch, and cellulose. Carbohydrates serve important structural and metabolic roles, such as providing energy, storing energy as glycogen, detoxifying the body, and being components of genetic material and cellular structures.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
2. DIORDERS OF THE STOMACH
10/12/2020 GIT Disorders Dr E.W.Ojong 2
3. PEPTIC ULCER DISEASE
Helicobacter pylori is now accepted to be the main cause of gastric
and duodenal ulcers; other causes include NSAIDs and, very rarely,
the Zollinger–Ellison syndrome.
The bacterium is present in the mucous layer of the stomach in half
of the population of the world.
Carriers of the organism are at increased risk of gastric cancer
(twofold to tenfold) and peptic ulcer (threefold to tenfold).
About 90% of gastric cancer patients are infected with H. pylori,
compared with 40% to 60% of age-matched controls and there is a
significant correlation between infection rates and gastric cancer
incidence and mortality.
10/12/2020 GIT Disorders Dr E.W.Ojong 3
4. PEPTIC ULCER DISEASE
At least 95% of patients with duodenal ulcer disease are
infected with H. pylori, and eradication of H. pylori is the
recommended treatment for patients with duodenal or
gastric ulcer who are H. pylori-positive.
The reason for a gastric mucosal infection causing
duodenal ulceration is complex but involves a number of
pathways leading to increased acid production.
Infection always causes a chronic inflammation even
when endoscopic investigation appears normal.
10/12/2020 GIT Disorders Dr E.W.Ojong 4
5. DIAGNOSIS OF PEPTIC ULCER
DISEASE
Biopsy tests may give false negative results because colonisation
may be patchy, and hence multiple sites are sampled.
Basal and post-prandial gastrin levels are higher in those with
infection, and returns to normal when the infection is treated.
H. pylori produces urease, and hydrolysis of endogenous urea to
bicarbonate and ammonia may create a more hospitable
microenvironment for its survival in the stomach. The ability of the
organism to rapidly hydrolyse urea is the basis of the urea breath
tests and of the direct urease tests on gastric biopsy samples.
Mammalian cells do not produce urease.
10/12/2020 GIT Disorders Dr E.W.Ojong 5
6. DIAGNOSIS OF PEPTIC ULCER
DISEASE
Urea breath tests are simple to perform, with sensitivity and
specificity both greater than 95%. Urea labelled with either 13C or
14C is given orally as a drink or a capsule to swallow with water;
urease from gastric H. pylori rapidly hydrolyses the ingested urea
to produce labelled bicarbonate, which is absorbed into the blood
and exhaled as 14CO2 or 13CO2.
While serological tests are used to identify patients who have
been infected with the organism, they are less helpful in
confirming its eradication because of the slow reduction in
antibody titres.
In the stool test, specific H. pylori antigens are detected in
microtiter plates coated with polyclonal antibodies.
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7. DIORDERS OF THE INTESTINE
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8. COELIAC DISEASE (GLUTEN
SENSITIVE ENTEROPATHY)
This is a T-cell mediated response to gluten – one of the
major proteins in wheat, but also present to a lesser
extent in oats, barley and rye.
Coeliac disease has a genetic component with a higher
(1%) prevalence in populations that have evolved on a
wheat and barley based diet such as Caucasians.
It is much rarer in other populations such as Africans
and Asians.
10/12/2020 GIT Disorders Dr E.W.Ojong 8
9. COELIAC DISEASE (GLUTEN SENSITIVE ENTEROPATHY)
In susceptible individuals, transglutaminases (enzymes
released from intestinal cells when injured) attempt to
cross-link glutamine residues on absorbed gluten
peptides but because this protein resists degradation an
antigenic complex then forms between glutaminase and
gluten.
This complex triggers a T-cell mediated response in the
small intestinal mucosa with resultant inflammation
whenever gluten is ingested.
Repeated inflammation damages the small intestinal
mucosa causing small nutrient malabsorption and
episodes of osmotic diarrhoea.
10/12/2020 GIT Disorders Dr E.W.Ojong 9
10. COELIAC DISEASE (GLUTEN SENSITIVE ENTEROPATHY)
Severe cases of coeliac disease typically present at <2 years of age
with failure to thrive, abdominal distension and diarrhoea but with
the advent of more sensitive tests more patients are diagnosed
who have mild intestinal symptoms, iron deficiency anaemia,
vitamin D deficiency and frequently another auto-immune disease,
e.g. diabetes mellitus type 1 and thyroid involvement.
Circulating antibodies to tissue transglutaminase (tTG) are found in
patients with coeliac disease and testing for anti-tTG IgA is the first
line investigation of choice. Anti-tTG IgA has a high sensitivity and
specificity for coeliac disease and is useful both in screening and in
monitoring the response to treatment.
A small intestinal (Jejunal) biopsy for histology is the gold standard -
the mucosa becomes flattened, with villous atrophy, and infiltrated
with lymphocytes.
10/12/2020 GIT Disorders Dr E.W.Ojong 10
12. LACTOSE INTOLERANCE
Lactose is a disaccharide which reduces
Benedict’s reagent.
Lactose can be distinguished from glucose
by the use of glucose oxidase method which
gives a negative result with lactose.
It is found mainly in milk and diary products
10/12/2020 GIT Disorders Dr E.W.Ojong 12
13. LACTOSE INTOLERANCE
Lactose in humans is synthesized only in the
mammary glands.
During intestinal digestion, it is broken
down into glucose and galactose by the
intestinal enzyme lactase.
There are two known forms of lactase
deficiency, one in infants and young children,
and the other in adults.
10/12/2020 GIT Disorders Dr E.W.Ojong 13
15. LACTOSE INTOLERANCE
Lactose intolerance may be genetic or
acquired.
Because lactose intolerance subjects have
lactase deficiency, lactose digestion and
absorption will not occur.
The gut is flooded with undigested lactose
load which osmotically retain fluid, causing
diarrhoea.
10/12/2020 GIT Disorders Dr E.W.Ojong 15
16. LACTOSE INTOLERANCE
Bacterial fermentation of sugar in the colon leads to
gaseous acidic stool.
Stools typically have a low pH and are positive for
reducing substances (in this case glucose from bacterial
action on undigested lactose).
Since lactase is located in the brush border of the
mucosal cells, secondary deficiency may occur in diseases
associated with morphological changes of the jejunal
mucosal e.g. coeliac disease, tropical sprue, parasitic
infections (particularly Giardia lamblia and Strongyloides
stercoralis).
10/12/2020 GIT Disorders Dr E.W.Ojong 16
17. LACTOSE INTOLERANCE
This deficiency is usually reversible following
recovery from the above mentioned
disorders.
In Africa, childhood lactase deficiency is
usually secondary to kwashiorkor and acute
viral gastroenteritis in which there is
widespread damage to mucosal cells.
Acquired lactase deficiency is very common
in adult Africans.
10/12/2020 GIT Disorders Dr E.W.Ojong 17
18. SYMPTOMS OF LACTOSE INTOLERANCE
Abdominal symptoms occur as soon as milk
and milk products (milk, ice-cream or
yoghurt)which contain lactose are
consumed,
Abdominal bloating
Abdominal cramp
Flatus
Diarrhoea
10/12/2020 GIT Disorders Dr E.W.Ojong 18
19. SMALL BOWEL BACTERIA OVERGROWTH
The small intestine is usually sterile.
However, in some conditions, anaerobic bacteria
colonise the intestine.
This often causes fat malabsorption, due at least partly
to excessive deconjugation of bile acid conjugates by
the bacteria and the premature passive reabsorption of
the resulting unconjugated bile acids.
Fat malabsorption and fat-soluble vitamin (A, D, E and
K) deficiency.
10/12/2020 GIT Disorders Dr E.W.Ojong 19
20. SMALL BOWEL BACTERIA OVERGROWTH
This leads to a relative deficiency of bile salts in the
intestinal lumen and decreased micelle formation.
Vitamin B12 deficiency may also develop due to its
consumption by the bacteria.
The clinical symptoms of bacterial overgrowth are
abdominal pain, diarrhoea, and steatorrhea.
10/12/2020 GIT Disorders Dr E.W.Ojong 20
21. ABNORMALITIES OF THE SMALL INTESTINE
ASSOCIATED WITH BACTERIAL OVERGROWTH
Overgrowth may occur where there is stagnation of bowel contents such as in:
Impaired bowel motility (advanced age, denervation as in diabetes mellitus, infiltrations as
in amyloidosis, and strictures);
Fistula between small and large bowel;
Gastric hypochlorhydria
Blind loops (small bowel diverticula, surgical loops).
Impaired systemic immune mechanisms
Use of oral antibiotics
Use of proton pump inhibitors
intrinsic small bowel disease (e.g. jejunal diverticulosis, coeliac disease, small bowel
Crohn’s disease)
Autonomic neuropathy
Systemic sclerosis
Post-gastrectomy
10/12/2020 GIT Disorders Dr E.W.Ojong 21
22. DIAGNOSIS OF SMALL BOWEL BACTERIA OVERGROWTH
The gold standard investigation is jejunal aspiration and
demonstrating an elevated bacterial count of >l07
organisms/mL and >l04 anaerobes/mL .
Hydrogen breath tests following lactulose (a sugar laxative
only broken down by bacterial action) or glucose
administration can also be used.
10/12/2020 GIT Disorders Dr E.W.Ojong 22
23. PROTEIN LOSING ENTEROPATHY
In health, most of the protein in faeces
represents sloughed enterocytes and proteins in
secretions.
Albumin loss is < 1% of the serum pool.
Losses of serum proteins can increase 10-100 fold
into the bowel lumen and their passage in the
faeces.
10/12/2020 GIT Disorders Dr E.W.Ojong 23
24. PROTEIN LOSING ENTEROPATHY
Protein loss through the GIT can be caused by a wide range of
disorders, e.g. inflammation or ulceration of a segment of the
small or large bowel as in Crohn’s disease and ulcerative colitis) or
stomach, diseases in which the intestinal lymphatics are
obstructed, conditions where there is increased lymphatic
pressure (e.g., lymphoma and Whipple disease), and disorders
associated with altered immune status (such as systemic lupus
erythematosus and some food allergies).
10/12/2020 GIT Disorders Dr E.W.Ojong 24
25. DIAGNOSIS OF PROTEIN LOSING ENTEROPATHY
The diagnosis of protein-losing enteropathy is considered in patients with
hypoalbuminaemia in whom renal loss, liver disease, and malnutrition have
been excluded.
Faecal clearance of alpha -l-antitrypsin (AT), after measurement in serum and a
weighed timed stool sample is used as a marker of GI protein loss.
AT in faeces and serum is measured most conveniently by radial
immunodiffusion.
Faeces should be collected quantitatively, preferably for 3 days, in pre-weighed
containers and kept refrigerated.
The AT is extracted into saline before analysis.
AT clearance (mL/d) is calculated as [(faecal weight x faecal AT
concentration)/serum AT], where faecal weight is expressed in g/day, faecal AT
in mg/kg faeces, and serum AT in mg/L.
10/12/2020 GIT Disorders Dr E.W.Ojong 25
27. ACUTE PANCREATITIS
An acute episode of enzymatic destruction of the
pancreas due to the escape of active pancreatic enzymes
into the pancreatic tissue.
The probable common mechanism is premature
activation of proteases within the pancreas.
There is leakage of activated pancreatic enzymes into the
pancreas and surrounding tissues with acute
inflammation and haemorrhage.
Acute pancreatitis is a medical emergency with acute
severe abdominal pain with rapid progression to shock.
10/12/2020 GIT Disorders Dr E.W.Ojong 27
28. CAUSES AETIOLOGY OF ACUTE PANCREATITIS
Gallstones
Alcohol (usually following heavy binge type ingestion –
typical presentation is a male patient presenting with
acute abdominal pain on a Monday or Tuesday morning
after a heavy weekend of drinking)
Infections (e.g. mumps)
Hypertriglyceridaemia
Trauma
Hypercalcaemia.
Iatrogenic (e.g. post surgical)
Idiopathic
Miscellaneous: cardiac surgery, scorpion bite
10/12/2020 GIT Disorders Dr E.W.Ojong 28
29. BIOCHEMICAL FEATURES OF ACUTE PANCREATITIS
Hyperglycaemia due to transient β-cell dysfunction
Hypocalcaemia that occurs as a result of deposition of insoluble
calcium soaps that form as a result of lipase digestion of fat in the
retroperitoneum.
Obstructive jaundice with elevated conjugated bilirubin, ALP and
GGT may indicate an obstructed common bile duct due to gall
stones, a pancreas head carcinoma or ascaris worms.
Lipaemic serum may indicate that hypertriglyceridaemia, may be
the predisposing cause of the acute pancreatitis.
Elevated procalcitonin (PCT) – a marker of gram –ve sepsis may also
be increased in acute pancreatitis.
10/12/2020 GIT Disorders Dr E.W.Ojong 29
30. DIAGNOSIS OF ACUTE PANCREATITIS
Serum amylase is the most widely used, but returns to
normal relatively rapidly (+72 hours) because of renal
clearance.
Amylase is not entirely specific - increases (usually
smaller) are seen in other acute upper GIT pathology e.g.
perforating duodenal ulcer or bowel infarction.
Other useful tests include urine amylase,
amylase/creatinine clearance ratio (increased in acute
pancreatitis).
Serum lipase is recommended as it suffers from very few
of these drawbacks; however, it is a lot more more
expensive.
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31. CHRONIC PANCREATITIS
An inflammatory disease characterized by
persistent and progressive destruction of the
pancreas leading to destruction of both
endocrine and exocrine function.
The destroyed pancreatic parenchyma is
replaced by fibrous tissue and cysts.
Presents with malabsorption (particularly of
fat), and sometimes with secondary diabetes.
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32. CHRONIC PANCREATITIS
In Western countries, the most common
cause is alcohol (60% to 90% of all cases of
chronic pancreatitis), although as only 5% to
15% of heavy drinkers develop the disease.
There are clearly other predisposing factors
(e.g., smoking and diets high in fat and
protein).
10/12/2020 GIT Disorders Dr E.W.Ojong 32
33. CAUSES AETIOLOGY OF CHRONIC PANCREATITIS
Alcohol
Tropical (Nutritional)
Hereditary (Trypsinogen and inhibitory protein
defects, cystic fibrosis, trans-membrane regulator
CFTR defects
Idiopathic
Trauma
Hypercalcaemia
10/12/2020 GIT Disorders Dr E.W.Ojong 33
35. GASTRINOMA AND THE ZOLLINGER-ELLISON
SYNDROME
The G cells located in the distal part of the stomach (antrum)
normally secrete gastrin, a hormone.
In normal physiological conditions, an alkaline medium created by
food or antacids stimulates the secretion of gastrin.
The gastrin in turn stimulates the parietal cells of the stomach to
produce gastric acid.
This leads to the reduction of the pH to acidic levels in the stomach.
By negative feedback, the low pH medium created by the gastric
acid suppresses further production of gastrin by the G cells of the
antrum of the stomach.
10/12/2020 GIT Disorders Dr E.W.Ojong 35
36. GASTRINOMA AND THE ZOLLINGER-ELLISON
SYNDROME
A tumour involving the delta cells of the islet of langerhans is called
the delta cell adenoma (may either be benign or malignant).
This tumour causes the condition known as Zollinger-Ellison
syndrome.
In this syndrome, the delta cells secrete excessive amounts of
gastrin.
This then stimulates the parietal cells of the stomach to produce an
increased volume of gastric juice.
The enormous output of hydrochloric acid and pepsin leads to
severe peptic ulcer sometimes accompanied by excessive diarrhoea.
10/12/2020 GIT Disorders Dr E.W.Ojong 36
37. GASTRINOMA AND THE ZOLLINGER-ELLISON
SYNDROME
Ulcer maybe single or multiple in the oesophagus, second, third and
fourth portion of the duodenum and in the jejunum, in addition to
the stomach and duodenal bulb.
The diagnosis of gastrin-secreting pancreas should be suspected if
the plasma fasting gastrin concentration is over 400pg per
ml(normal level is less than 200 pg per ml).
A confirmatory test is demonstration of a 400 pg per ml or more rise
of serum gastrin concentration from the fasting level on infusion of
15 mg of calcium gluconate per kg body weight over four hours.
10/12/2020 GIT Disorders Dr E.W.Ojong 37
38. GASTRINOMA AND THE ZOLLINGER-ELLISON SYNDROME
A comparable test can be carried out with a secretin preparation.
Intravenous injection of secretin- about 1 unit per kg body weight –
produces a high increase in serum gastrin concentration in patients
with gastrinoma. This is not seen in patients with ordinary duodenal
ulcer.
Zollinger-Ellison syndrome may also be due to:
Hyperplasia or tumour of the gastric G cells
Familial gastrinoma
Parathyroid adenomas
Adenoma or carcinoma of pituitary gland, thyroid gland, adrenal medulla
(phaechromocytoma)
Pernicious anaemia
Atrophic gastritis
10/12/2020 GIT Disorders Dr E.W.Ojong 38
39. THE WATERY DIARRHOEA HYPOKALAEMIA
ACHLORHYDIA SYNDROME (VIPOMA)
A vipoma is a non-beta pancreatic islet cell tumour secreting
vasoactive intestinal peptide (VIP), resulting in a syndrome of
watery diarrhoea, hypokalaemia, and achlorhydria (WDHA
syndrome).
They are rare but potentially fatal if unattended to urgently.
The severity of the diarrhoea is comparable to that seen in
cholera with excretions in excess of 2 L/24 h.
The diagnostic feature of the diarrhoea is that it continues
despite prolonged fasting.
Plasma VIP concentrations are elevated 4–5-fold;
10/12/2020 GIT Disorders Dr E.W.Ojong 39
40. THE WATERY DIARRHOEA HYPOKALAEMIA
ACHLORHYDIA SYNDROME (VIPOMA)
VIPomas have the same propensity as glucagonomas for
malignancy and the same imaging techniques are used to localize
the tumour as in glucagonomas.
Diagnosis is by serum VIP levels. Tumour is localized with CT and
endoscopic ultrasound.
While surgery is usually considered, their medical management
remains important with rehydration and correction of electrolyte
disturbances in severe cases, and use of antidiarrhoeals (e.g.
loperamide, codeine phosphate and somatostatin analogues).
10/12/2020 GIT Disorders Dr E.W.Ojong 40
42. MALABSORPTION
A condition that prevents absorption of
nutrients through the small intestine.
Malabsorption may be caused by infection,
medication, small intestine surgery and
disorders such as coeliac disease.
Symptoms include weight loss, bloating and
sometimes diarrhoea. Eventually, the brain,
nervous system, bones, liver and other
organs can be affected.
10/12/2020 GIT Disorders Dr E.W.Ojong 42
43. CAUSES OF MALABSORPTION
The main causes of malabsorption are
Gastric: Zollinger-Ellison syndrome, gastrectomy
Pancreatic: cystic fibrosis, chronic pancreatitis, pancreatic
cancer.
Bile acid deficiency: small bowel bacterial overgrowth,
terminal ileal disease or resection.
Reduction in absorptive surface: coeliac disease, tropical
sprue, inflammatory bowel disease
Specific disorders: hypolactasia, vitamin B12 deficiency
10/12/2020 GIT Disorders Dr E.W.Ojong 43
44. BIOCHEMICAL EVIDENCE OF MALABSORPTION
Iron, Haemoglobin and MCV – Iron, Folate and B12
Malabsorption.
Albumin – protein malabsorption
Cholesterol, Vitamins A and D and prothrombin time (Vit
K) – fat malabsorption.
Plasma Calcium, Magnesium, Phosphate and Zinc –
electrolyte and small molecule malabsorption
10/12/2020 GIT Disorders Dr E.W.Ojong 44
45. DIAGNOSIS OF MALABSORPTION
Gastroscopy (with duodenal biopsy for histology)
Faecal elastase for pancreatic function
TTG antibodies for coeliac disease
Stool reducing substances and osmolar gap (to identify
carbohydrate malabsorption)
Faecal fat and faecal steatocrit (a measurement of the
percentage of fat in faeces) –(fat malabsorption)
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46. ASSIGNMENT
1. Discuss the biochemical changes associated with
diarrhoea.
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