Clinical Biochemistry part I
Blood glucose and Diabetes Mellitus, Lipid metabolism disorders, Water and electrolytes disorders and therapeutic drug monitoring TDM
This document discusses nutrition in surgery and provides an overview of key topics including nutritional assessment, requirements, interventions, and complications. Nutritional assessment involves taking a history, physical exam including anthropometric measures, and lab tests to evaluate a patient's nutritional status. Enteral and parenteral nutrition routes are described. Enteral nutrition is preferred when possible as it supports gut health while parenteral nutrition is for cases of total gut failure. Complications of both enteral and parenteral nutrition are outlined. The goal of nutritional intervention is to identify and support patients at risk of malnutrition.
The document discusses gastric outlet obstruction (GOO), which refers to any mechanical impediment to gastric emptying. It can be caused by benign or malignant conditions. Common benign causes include peptic ulcer disease and gastric polyps, while pancreatic cancer is a frequent malignant cause. Symptoms include vomiting, weight loss, and dehydration. Diagnosis involves imaging like barium studies and endoscopy. Treatment of GOO focuses on rehydration, nutritional support, and correcting electrolyte imbalances. Surgical intervention may be needed for persistent or malignant obstructions.
This document discusses nutrition in the ICU. It begins by introducing malnutrition as a common problem in hospital patients that is linked to increased mortality and complications. It then covers nutritional requirements, noting formulas to estimate energy needs and increased requirements due to stress factors like fever and sepsis. Assessment of nutritional status is also reviewed, along with the main routes of nutrition support - oral, enteral via tubes, and parenteral. Potential complications of nutritional support are outlined, including refeeding syndrome, overfeeding, and hyperglycemia. The document provides an overview of the key considerations and challenges regarding nutrition for critically ill patients in the ICU.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
Appropriate and safe assessment and administration of fuid therapy and nutritional support is of key importance in good surgical practice. It is imperative that the preoperative nutritional state of the patient and the impact of any surgical intervention are taken into account when considering nutritional requirements and the mode of nutrient delivery.
Clinical Biochemistry part I
Blood glucose and Diabetes Mellitus, Lipid metabolism disorders, Water and electrolytes disorders and therapeutic drug monitoring TDM
This document discusses nutrition in surgery and provides an overview of key topics including nutritional assessment, requirements, interventions, and complications. Nutritional assessment involves taking a history, physical exam including anthropometric measures, and lab tests to evaluate a patient's nutritional status. Enteral and parenteral nutrition routes are described. Enteral nutrition is preferred when possible as it supports gut health while parenteral nutrition is for cases of total gut failure. Complications of both enteral and parenteral nutrition are outlined. The goal of nutritional intervention is to identify and support patients at risk of malnutrition.
The document discusses gastric outlet obstruction (GOO), which refers to any mechanical impediment to gastric emptying. It can be caused by benign or malignant conditions. Common benign causes include peptic ulcer disease and gastric polyps, while pancreatic cancer is a frequent malignant cause. Symptoms include vomiting, weight loss, and dehydration. Diagnosis involves imaging like barium studies and endoscopy. Treatment of GOO focuses on rehydration, nutritional support, and correcting electrolyte imbalances. Surgical intervention may be needed for persistent or malignant obstructions.
This document discusses nutrition in the ICU. It begins by introducing malnutrition as a common problem in hospital patients that is linked to increased mortality and complications. It then covers nutritional requirements, noting formulas to estimate energy needs and increased requirements due to stress factors like fever and sepsis. Assessment of nutritional status is also reviewed, along with the main routes of nutrition support - oral, enteral via tubes, and parenteral. Potential complications of nutritional support are outlined, including refeeding syndrome, overfeeding, and hyperglycemia. The document provides an overview of the key considerations and challenges regarding nutrition for critically ill patients in the ICU.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
Appropriate and safe assessment and administration of fuid therapy and nutritional support is of key importance in good surgical practice. It is imperative that the preoperative nutritional state of the patient and the impact of any surgical intervention are taken into account when considering nutritional requirements and the mode of nutrient delivery.
This document discusses nutrition and nutritional support for patients. It notes that malnutrition is common in hospitalized patients, especially those with gastrointestinal diseases or postoperative complications, and that malnourished patients have higher risks of complications and death. The aim of nutritional support is to identify at-risk patients and meet their nutritional needs through the most appropriate route to minimize complications. Methods of assessment and artificial nutritional support through enteral or parenteral means are described, along with their potential complications.
Malabsorption refers to disorders that disrupt digestion and nutrient absorption in the small intestine. This can lead to malnutrition and various anemias from deficiencies. Diagnosis involves tests like fecal fat analysis, D-xylose absorption tests, and vitamin B12 absorption (Schilling) tests. Treatment focuses on correcting nutritional deficiencies through supplements and treating any underlying diseases through measures like gluten-free diets for celiac disease or antibiotics for bacterial overgrowth.
Clinical features and diagnosis of malabsorptionFarshad Mirzavi
The document provides an overview of malabsorption, including its causes, mechanisms, diagnosis, and laboratory tests used for evaluation. It discusses the three key steps required for normal nutrient absorption and lists factors that may damage the intestine and cause malabsorption. Common tests described include stool tests to measure fat, blood tests of vitamin/mineral levels, breath tests for lactose intolerance, imaging to detect structural abnormalities, and biopsy for abnormal cells. Carbohydrate and fat malabsorption are evaluated using tests like D-xylose absorption, lactose tolerance, breath hydrogen, and fecal fat determination. Specific disorders are investigated using antibodies for celiac disease and the Schilling test for pernicious anemia.
Nutrition is essential for surgery patients as surgical procedures and fasting can quickly lead to malnutrition. Patients with severe protein depletion are more likely to experience postoperative complications like pneumonia and infection. Nutritional status should be assessed through history, diet assessment, physical exam, and lab tests. Malnutrition is caused by reduced food intake, malabsorption, altered metabolism, and more. Nutritional requirements vary but are generally 25-30 calories/kg/day and 1.5-2 grams of protein/kg/day. Nutrition can be provided enterally through tubes or parenterally through IVs. Enteral nutrition is preferred over parenteral when possible.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
Nutritional assessment in chronic liver diseaseShaimaa Elkholy
Protein Energy Malnutrition (PEM) is highly prevalent among patients with chronic liver disease. One of the problems is how to assess these patients nutritionally. yet no standard golden rule for their nutritional assessment.
This document discusses nutrition for various liver conditions. It recommends for hepatitis patients a high protein, moderate fat and carbohydrate diet along with plenty of fluids. For cirrhosis, it suggests a similar diet with moderate sodium and soft foods if needed, as well as vitamin and mineral supplements. The goals are to aid liver regeneration and recovery through optimal nutrition while avoiding further strain on liver function.
This document discusses peptic ulcer disease (PUD), including its definition, epidemiology, etiology, symptoms, investigation, and treatment. PUD is caused by acid and pepsin digestion of the stomach or duodenal lining. Key contributing factors include Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use. Common symptoms are abdominal pain and vomiting. Diagnosis involves endoscopy with biopsy and testing. Treatment aims to relieve symptoms, promote healing, and eradicate H. pylori if present through medications like PPIs, H2 blockers, and antibiotic combinations.
The document provides an overview of pancreatitis, including:
1) It defines acute pancreatitis as an inflammatory disorder of the pancreas characterized by severe abdominal pain and elevated pancreatic enzymes. Common causes include gallstones, alcohol abuse, and medications.
2) It describes chronic pancreatitis as a progressive disease caused by long-standing pancreatic inflammation leading to loss of exocrine and endocrine function. Common causes are alcohol consumption and genetic factors.
3) Symptoms of acute pancreatitis include severe abdominal pain while chronic pancreatitis causes deep abdominal or back pain often associated with meals along with steatorrhea and weight loss.
This document provides an overview of chronic diarrhea and malabsorption syndrome. It discusses the pathophysiology of chronic diarrhea including osmotic, secretory, inflammatory, and motility disorders. Common causes are then outlined for both infectious and non-infectious etiologies. Management involves fluid/electrolyte replacement, treating the underlying cause, and symptomatic relief. Malabsorption syndrome and its causes relating to the pancreas, liver, intestine, and motility are also reviewed. Specific conditions like celiac disease and Whipple's disease are described.
This document discusses the evaluation and management of chronic diarrhea and malabsorption syndrome. It begins with an introduction to chronic diarrhea and outlines the pathophysiology, including osmotic, secretory, inflammatory, and motility disorders. Common causes are then reviewed including infections, malignancies, celiac disease, tropical sprue, and short bowel syndrome. Management involves fluid/electrolyte replacement, treating the underlying cause, and symptomatic relief. Malabsorption syndrome and its specific etiologies like celiac disease, Whipple's disease, and tropical sprue are also summarized. The document stresses the importance of a thorough clinical evaluation to identify the cause and guide appropriate investigations and therapy.
This document discusses the evaluation and management of chronic diarrhea and malabsorption syndrome. It begins with an introduction to chronic diarrhea and outlines the pathophysiology, including osmotic, secretory, inflammatory, and motility disorders. Common causes are then described, such as infections, inflammatory bowel diseases, malabsorption syndromes, and functional disorders. The document also discusses specific conditions like HIV enteropathy, celiac disease, tropical sprue, and short bowel syndrome. It emphasizes that a thorough clinical evaluation is needed to identify the cause and guide treatment, which may include fluid/electrolyte replacement, antimicrobials, or treating the underlying condition. Chronic diarrhea poses diagnostic challenges but addressing the cause is important for managing
NUTRITION CARE IN PATIENT ESOPHAGEAL CARCINOMA WITH RYLE'S TUBE FEEDINGnurfarahin87
Patient is a 63-year-old woman diagnosed with esophageal carcinoma who is receiving Ryle's tube feeding. Her nutrition assessment found weight loss, low hemoglobin and electrolyte levels, and inadequate calorie and protein intake from her current feeding regimen. Her nutrition diagnosis is inadequate enteral nutrition intake. The intervention aims to gradually increase her feeding volume and frequency if tolerated. Monitoring will include biochemical markers and feeding tolerance. Management of tube feeding complications like vomiting aims to minimize risks and maintain adequate nutrition support for her cancer treatment.
GASBARRINI A. Nutrizione Clinica e Gastroenterologia. ASMaD 2017Gianfranco Tammaro
PROF. ANTONIO GASBARRINI - Convegno "Il Presente ed il Futuro della Nutrizione Clinica" - 24/03/2017 - Sala Rita Levi Montalcini - Ospedale S.Eugenio - ROMA
Sito ASMaD: http://www.asmad.net
Canale Youtube: https://youtu.be/FYlsQzE8xfk
This document discusses nutritional support for critically ill patients. It notes that these patients are hypermetabolic and have increased nutritional needs. Malnutrition can develop rapidly in critically ill patients and exert deleterious effects. Nutritional assessment in critically ill patients is difficult but includes anthropometric measurements, biochemical tools, and clinical and dietary assessments. The timing and route of providing nutrition is complex, and enteral nutrition via a feeding tube is generally preferred over parenteral nutrition when possible. Ongoing monitoring is important for patients receiving nutritional support.
Drug-induced diarrhea is caused by around 700 drugs and accounts for 7% of all adverse drug effects. Common causes include antibiotics, laxatives, anticancer drugs, and NSAIDs. Antibiotics can lead to overgrowth of Clostridium difficile bacteria and cause pseudomembranous colitis. Risk factors for antibiotic-associated diarrhea (AAD) include prolonged or repeated antibiotic use, advanced age, underlying illnesses, hospitalization, and immunosuppression. Treatment involves rehydration, replacing the causative antibiotic, and antibiotics like metronidazole or vancomycin for C. difficile infections. Probiotics may help restore the intestinal bacterial balance.
Clinical Biochemistry part III
Tumors and tumor markers, Toxicology, TDM, pregnancy, Paediatric clinical chemistry, screening of newborns for diseases, inborn errors of metabolism, geriatric Clinical chemistry, Nutritional assessment
This document discusses nutrition and nutritional support for patients. It notes that malnutrition is common in hospitalized patients, especially those with gastrointestinal diseases or postoperative complications, and that malnourished patients have higher risks of complications and death. The aim of nutritional support is to identify at-risk patients and meet their nutritional needs through the most appropriate route to minimize complications. Methods of assessment and artificial nutritional support through enteral or parenteral means are described, along with their potential complications.
Malabsorption refers to disorders that disrupt digestion and nutrient absorption in the small intestine. This can lead to malnutrition and various anemias from deficiencies. Diagnosis involves tests like fecal fat analysis, D-xylose absorption tests, and vitamin B12 absorption (Schilling) tests. Treatment focuses on correcting nutritional deficiencies through supplements and treating any underlying diseases through measures like gluten-free diets for celiac disease or antibiotics for bacterial overgrowth.
Clinical features and diagnosis of malabsorptionFarshad Mirzavi
The document provides an overview of malabsorption, including its causes, mechanisms, diagnosis, and laboratory tests used for evaluation. It discusses the three key steps required for normal nutrient absorption and lists factors that may damage the intestine and cause malabsorption. Common tests described include stool tests to measure fat, blood tests of vitamin/mineral levels, breath tests for lactose intolerance, imaging to detect structural abnormalities, and biopsy for abnormal cells. Carbohydrate and fat malabsorption are evaluated using tests like D-xylose absorption, lactose tolerance, breath hydrogen, and fecal fat determination. Specific disorders are investigated using antibodies for celiac disease and the Schilling test for pernicious anemia.
Nutrition is essential for surgery patients as surgical procedures and fasting can quickly lead to malnutrition. Patients with severe protein depletion are more likely to experience postoperative complications like pneumonia and infection. Nutritional status should be assessed through history, diet assessment, physical exam, and lab tests. Malnutrition is caused by reduced food intake, malabsorption, altered metabolism, and more. Nutritional requirements vary but are generally 25-30 calories/kg/day and 1.5-2 grams of protein/kg/day. Nutrition can be provided enterally through tubes or parenterally through IVs. Enteral nutrition is preferred over parenteral when possible.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
Nutritional assessment in chronic liver diseaseShaimaa Elkholy
Protein Energy Malnutrition (PEM) is highly prevalent among patients with chronic liver disease. One of the problems is how to assess these patients nutritionally. yet no standard golden rule for their nutritional assessment.
This document discusses nutrition for various liver conditions. It recommends for hepatitis patients a high protein, moderate fat and carbohydrate diet along with plenty of fluids. For cirrhosis, it suggests a similar diet with moderate sodium and soft foods if needed, as well as vitamin and mineral supplements. The goals are to aid liver regeneration and recovery through optimal nutrition while avoiding further strain on liver function.
This document discusses peptic ulcer disease (PUD), including its definition, epidemiology, etiology, symptoms, investigation, and treatment. PUD is caused by acid and pepsin digestion of the stomach or duodenal lining. Key contributing factors include Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use. Common symptoms are abdominal pain and vomiting. Diagnosis involves endoscopy with biopsy and testing. Treatment aims to relieve symptoms, promote healing, and eradicate H. pylori if present through medications like PPIs, H2 blockers, and antibiotic combinations.
The document provides an overview of pancreatitis, including:
1) It defines acute pancreatitis as an inflammatory disorder of the pancreas characterized by severe abdominal pain and elevated pancreatic enzymes. Common causes include gallstones, alcohol abuse, and medications.
2) It describes chronic pancreatitis as a progressive disease caused by long-standing pancreatic inflammation leading to loss of exocrine and endocrine function. Common causes are alcohol consumption and genetic factors.
3) Symptoms of acute pancreatitis include severe abdominal pain while chronic pancreatitis causes deep abdominal or back pain often associated with meals along with steatorrhea and weight loss.
This document provides an overview of chronic diarrhea and malabsorption syndrome. It discusses the pathophysiology of chronic diarrhea including osmotic, secretory, inflammatory, and motility disorders. Common causes are then outlined for both infectious and non-infectious etiologies. Management involves fluid/electrolyte replacement, treating the underlying cause, and symptomatic relief. Malabsorption syndrome and its causes relating to the pancreas, liver, intestine, and motility are also reviewed. Specific conditions like celiac disease and Whipple's disease are described.
This document discusses the evaluation and management of chronic diarrhea and malabsorption syndrome. It begins with an introduction to chronic diarrhea and outlines the pathophysiology, including osmotic, secretory, inflammatory, and motility disorders. Common causes are then reviewed including infections, malignancies, celiac disease, tropical sprue, and short bowel syndrome. Management involves fluid/electrolyte replacement, treating the underlying cause, and symptomatic relief. Malabsorption syndrome and its specific etiologies like celiac disease, Whipple's disease, and tropical sprue are also summarized. The document stresses the importance of a thorough clinical evaluation to identify the cause and guide appropriate investigations and therapy.
This document discusses the evaluation and management of chronic diarrhea and malabsorption syndrome. It begins with an introduction to chronic diarrhea and outlines the pathophysiology, including osmotic, secretory, inflammatory, and motility disorders. Common causes are then described, such as infections, inflammatory bowel diseases, malabsorption syndromes, and functional disorders. The document also discusses specific conditions like HIV enteropathy, celiac disease, tropical sprue, and short bowel syndrome. It emphasizes that a thorough clinical evaluation is needed to identify the cause and guide treatment, which may include fluid/electrolyte replacement, antimicrobials, or treating the underlying condition. Chronic diarrhea poses diagnostic challenges but addressing the cause is important for managing
NUTRITION CARE IN PATIENT ESOPHAGEAL CARCINOMA WITH RYLE'S TUBE FEEDINGnurfarahin87
Patient is a 63-year-old woman diagnosed with esophageal carcinoma who is receiving Ryle's tube feeding. Her nutrition assessment found weight loss, low hemoglobin and electrolyte levels, and inadequate calorie and protein intake from her current feeding regimen. Her nutrition diagnosis is inadequate enteral nutrition intake. The intervention aims to gradually increase her feeding volume and frequency if tolerated. Monitoring will include biochemical markers and feeding tolerance. Management of tube feeding complications like vomiting aims to minimize risks and maintain adequate nutrition support for her cancer treatment.
GASBARRINI A. Nutrizione Clinica e Gastroenterologia. ASMaD 2017Gianfranco Tammaro
PROF. ANTONIO GASBARRINI - Convegno "Il Presente ed il Futuro della Nutrizione Clinica" - 24/03/2017 - Sala Rita Levi Montalcini - Ospedale S.Eugenio - ROMA
Sito ASMaD: http://www.asmad.net
Canale Youtube: https://youtu.be/FYlsQzE8xfk
This document discusses nutritional support for critically ill patients. It notes that these patients are hypermetabolic and have increased nutritional needs. Malnutrition can develop rapidly in critically ill patients and exert deleterious effects. Nutritional assessment in critically ill patients is difficult but includes anthropometric measurements, biochemical tools, and clinical and dietary assessments. The timing and route of providing nutrition is complex, and enteral nutrition via a feeding tube is generally preferred over parenteral nutrition when possible. Ongoing monitoring is important for patients receiving nutritional support.
Drug-induced diarrhea is caused by around 700 drugs and accounts for 7% of all adverse drug effects. Common causes include antibiotics, laxatives, anticancer drugs, and NSAIDs. Antibiotics can lead to overgrowth of Clostridium difficile bacteria and cause pseudomembranous colitis. Risk factors for antibiotic-associated diarrhea (AAD) include prolonged or repeated antibiotic use, advanced age, underlying illnesses, hospitalization, and immunosuppression. Treatment involves rehydration, replacing the causative antibiotic, and antibiotics like metronidazole or vancomycin for C. difficile infections. Probiotics may help restore the intestinal bacterial balance.
Clinical Biochemistry part III
Tumors and tumor markers, Toxicology, TDM, pregnancy, Paediatric clinical chemistry, screening of newborns for diseases, inborn errors of metabolism, geriatric Clinical chemistry, Nutritional assessment
This document provides an overview of hormones and their biochemistry. It begins with definitions of hormones and the endocrine system. It then discusses the general functions of hormones and classifications of hormones based on their chemical composition and mechanisms of action. The document explores the mechanisms of action of different hormone groups, including those that act through intracellular receptors and cell surface receptors using various second messengers like cAMP, cGMP, calcium, and phospholipids. It also examines hormones with unknown second messengers that can act through pathways like tyrosine kinase, JAK/STAT, protein tyrosine phosphatases, and NF-kB. Insulin is highlighted as a major hormone with no known second messenger.
This document provides an overview of molecular biology presented by Aaser Abdelazim. It discusses topics such as nucleic acid structures and functions, DNA replication, transcription, translation, mutations and repair. It also describes gene expression regulation and applications of molecular biology. Additionally, it covers molecular organization of the cell, what is molecular biology, gene concepts, DNA and RNA structures, DNA replication, transcription and translation processes. The document is intended as teaching material for molecular biology.
1. The document discusses biological oxidation and carbohydrate metabolism. It provides objectives and details on the digestion and absorption of carbohydrates, as well as the pathways of glycolysis and oxidation of NADH outside mitochondria.
2. Key points include that biological oxidation occurs gradually through enzymes and produces ATP, while non-biological oxidation can be explosive. Carbohydrates are digested to monosaccharides then absorbed by active or passive transport.
3. Glycolysis converts glucose to pyruvate or lactate, and shuttles like the glycerophosphate and malate-aspartate shuttles oxidize extramitochondrial NADH.
This document provides an overview of body fluids and electrolyte balance. It begins with the objectives of describing body fluid compartments and distribution, water and electrolyte balance mechanisms, and relating fluid disorders to clinical aspects. Key points include that total body water is 60% of body weight, with two-thirds being intracellular fluid and one-third extracellular fluid including plasma and interstitial fluid. Electrolytes such as sodium, potassium, and chloride are also discussed. Mechanisms for regulating fluid and electrolyte balance like the renin-angiotensin-aldosterone system and antidiuretic hormone are covered. Conditions involving fluid imbalance like dehydration and overhydration are explained.
The document discusses acid-base balance and blood buffers. It describes the sources of protons and alkalis in blood, including carbonic acid, sulfuric acid, and sodium bicarbonate. It also discusses the buffer systems in plasma, including the respiratory and carbonic anhydrase systems. Disturbances in acid-base balance can be respiratory or metabolic in origin. The mechanisms of the intrinsic and extrinsic pathways of blood coagulation are summarized.
This document provides an overview of immunology and the immune system. It begins with definitions of immunology and a brief history of the field. It then describes the development of the immune system in bone marrow and thymus. Subsequent sections cover the spleen, lymph nodes, primary and secondary lymphoid organs, immune cells, innate and adaptive immunity, cellular and humoral immunity, immunoglobulins, and antigens. The document is presented as lecture notes on immunology.
The document discusses various biochemical tests used to identify microorganisms (M.Os). It describes tests such as decarboxylase tests to detect amino acid decarboxylation; carbohydrate fermentation tests to detect sugar utilization; starch hydrolysis and citrate utilization tests; gelatin liquefaction; coagulase production; and phenylalanine deamination. It also discusses triple sugar iron agar tests, casein digestion, urease production, methyl red/Voges-Proskauer tests, and other assays. The purpose is to biochemically characterize M.Os and diagnose bacteria based on their metabolic properties and enzyme production.
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).
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
3. 8/15/23 Aaser Abdelazim Clinical Biochemistry 3
1. Clinical biochemical tests comprise over of all
hospital laboratory investigations
2. Most biochemical tests are now performed at the site of
clinic especially during major operations like transplantation
not only in clinical biochemistry labs.
3. Most laboratories are now computerized and use:
1.The par-coding for specimens
2.Automated methods in analysis
This leads to:
A.High degrees of productivity .
B.Improves the quality of service.
C.Allow direct access to the results by clinicians.
4. 8/15/23 Aaser Abdelazim Clinical Biochemistry 4
History
Clinical examination
Diagnostic services
Imaging Physiological tests
ECG, EEG, lung functions
Lab services
Hematology Histopathology Immunology Microbiology
Clinical biochemistry
Core tests Emergency tests
Specialized tests
Place of clinical biochemistry in medicine
5. 8/15/23 Aaser Abdelazim Clinical Biochemistry 5
Core tests commonly
requested by physician
e.g., U, LFTs and Es
(Urea, liver function tests
electrolytes )
Core tests
1. Not all labs introduce
the service but it
restricted only to
some reference
centers
2. Needed to diagnose
rare diseases
Specialized tests
1. Done immediately
2. Results taken on call
3. Need to work out of
normal hours of lab.
4. All labs should
perform theses tests.
Emergency tests
Core biochemical tests
Sodium, potassium, chloride, bicarbonates
Urea, creatinine
Calcium, phosphates
Total proteins, albumins
Bilirubin, alkaline phosphatase
ALT, AST
T4, TSH
ɣ-GT, CK
Blood gases
Amylase
Specialized tests Emergency tests
Hormones Urea and electrolytes
Special proteins Blood glucose
Trace elements Blood gases
Vitamins Paracetamol
Drugs Salicylates
Lipids and lipoproteins Calcium
DNA analysis Amylase
6. 8/15/23 Aaser Abdelazim Clinical Biochemistry 6
Nutritional assessments and
diagnosis of digestive disorders
AASER ABDELAZIM
Professor of Medical Biochemistry
Zagazig University, Egypt
University of Bisha, KSA
aaserabdelazim@yahoo.com
7. 8/15/23 Aaser Abdelazim Clinical Biochemistry 7
Mal nutrition:
Definition:
qIts is a common problems among peoples in developed countries
qIt may means starvation but it had a much wider meaning (both inadequacy in
any nutrient in the diet as well as excess food intake).
qMal nutrition can be resulted from exposing the body to injuries or in major
surgical operations
•Decrease
intake
•Loss of
nutrients
Decrease
the
nutrient
store
Specific
metabolic
and
biochemical
effects
Clinical
signs and
symptoms
Consequence of mal nutrition:
8. 8/15/23 Aaser Abdelazim Clinical Biochemistry 8
Assessment of mal nutrition:
HISTORY EXAMNATION BIOCHEMICAL INVESTIGATIONS
qChange in weight
qPoor wound healing
qExposed to heavy
infections
qHistory of food and
water intake over past 7
days.
qAsking about appetite
qTypes of food intake
Examine:
qHeight
qWeight
qArm circumference
qSkin-fold thickness
qBody mass index(BMI)
BMI =
Weight (Kg)
(Height)2 meters
qProteins : but affected by
other factors e.g. liver
qBlood glucose: low and
ketosis in starvation
qLipids: fasting plasma TGs
qVitamins:
qMinerals: trace and major
elements
BMI Nutritional state
< 18.5 Underweight
18.5-24.9 Normal weight
25-29.9 Overweight
> 29.9 Obese
9. 8/15/23 Aaser Abdelazim Clinical Biochemistry 9
Lab assessment of vitamins deficiency:
Vitamin Deficiency state Lab assessments
Water soluble
Ascorbate Scurvy Plasma level
Thiamine (B1) Beri-Beri Plasma level /Transketolase activity
Riboflavin (B2) Rare single deficiency Plasma level /GRD activity
Pyridoxine (B6) Dermatitis/anemia Plasma level/AST activity
Cobalamine (B12) Pernicious anemia Serum B12/full blood count
Folate Megaloblastic anemia Serum/blood folate/ CBC
Niacin Pellagra Urinary niacin metabolites
Fat soluble
Vitamin A Blindness Serum vitamin A
Vitamin D Osteomalcia /rickets Serum 25-hydroxychalciferol
Vitamin E Anemia/ neuropathy Serum vitamin E
Vitamin K Defective clotting Prothrombin time PT
10. 8/15/23 Aaser Abdelazim Clinical Biochemistry 10
It may ranges from simple dietary supplements to total parenteral nutrition (TPN)
Spectrum of nutritional support:
11. 8/15/23 Aaser Abdelazim Clinical Biochemistry 11
Patients requirements of nutrients:
(1) ENERGY:
Harris-Benedict equation
for energy need calculation
Principle Sources Of Energy:
qCARBOHYDRATES: (4 Kcal/g)
qLIPIDS: (9 Kcal/g)
qAMINO ACIDS: (4 Kcal/g)
(2) NITROGEN:
qAmino acids provide nitrogen
and also yield energy.
qProteins should be 10-15 % of
total calories requirements
(3) VITAMINS AND TRACE ELEMENTS:
qThey called micronutrients
because they needed by minute
amount.
qRecommended Dietary
allowances (RDAs) postulate these
requirements
12. 8/15/23 Aaser Abdelazim Clinical Biochemistry 12
Average daily requirements of vitamins Average daily requirements of essential
trace elements
Average daily requirements of vitamins and essential trace elements/day:
13. 8/15/23 Aaser Abdelazim Clinical Biochemistry 13
Digestive system:
qIs a tube runs through the body.
qIts function is to prepare nutrients to be
absorbed in to blood then transported to
all tissues.
qNutrients will be digested in oral cavity,
stomach and intestine.
qSalivary, pancreatic and intestinal
secretions aid in the digestive sate.
15. 8/15/23 Aaser Abdelazim Clinical Biochemistry 15
MALABSORPTION
Definition: Impairment of absorptive mechanism; it can be occurred at any
stage of life form many causes. Resulting in weight loss in adults and
growth failure in children.
Causes and consequences of malabsorption:
16. 8/15/23 Aaser Abdelazim Clinical Biochemistry 16
Biochemical investigations of malabsorption
Tests identify malabsorption Tests identify pancreatic functions
1. Fecal fats test
2. Fecal microscopy
3. butterfat test
4. C14 triglycerides test
5. Xylose absorption test
1. Lundh test
2. Secretin test
3. pancreolauryl test
17. 8/15/23 Aaser Abdelazim Clinical Biochemistry 17
Tests identify malabsorption:
1) Fecal fats: presence of fatty stool; measurement of total fats in five days
collected stool.
2) Fecal microscopy: presence of fat globules
3) Butterfat test: presence of CM in patient blood after fat load indicates normal
absorption
4) C14 triglycerides test: oral load of radio-labelled C14 triolein is absorbed
and metabolized and C14 CO2 is measured in breath If present indicates
normal digestion and absorption
5) Xylose absorption test: serum measure of xylose after oral load indicates
normal absorption of monosaccharides.
18. 8/15/23 Aaser Abdelazim Clinical Biochemistry 18
Tests identify pancreatic functions:
1) Lundh test: collection of duodenal contents after meal and the activities of
pancreatic trypsin and amylase were measured.
2) Secretin test: I/V injection of secretin lead to stimulation of pancreatic
secretions which is assessed by measurement of pancreatic amylase and
trypsin in duodenal contents.
3) Pancreolauryl test: flourescein dilaurate is hydrolyzed by cholesterol
esterase in pancreatic secretions then the water soluble flourescein is
absorbed and excreted in urine while its fluorescent color indicates
• Normal absorption.
• Normal pancreatic functions
19. 8/15/23 Aaser Abdelazim Clinical Biochemistry 19
Other biochemical tests investigate malabsorption and GIT
diseases
Test Purpose
1. Urea breath test Used to identify patients with helicobacter pylori
which is strongly associated with peptic ulcer
2. Hydrogen breath test Assesses bacterial overgrowth in intestine
3. Lactose /sucrose
tolerance test
Measure functions defects in disaccharidases like
lactase and sucrase.
4. Fecal chymotrypsin/
elastase
Used to measure of pancreatic functions mainly in
cystic fibrosis.
5. Intestinal
permeability
Biologically inert polymers are used to assess
mucosal permeability by measuring their
excretion in urine after oral load.
6. Schilling test Assess vitamin B12 absorption
20. 8/15/23 Aaser Abdelazim Clinical Biochemistry 20
Gastrointestinal disease Description
(1) Inadequate digestion Seen in chronic pancreatitis due lack of pancreatic
enzymes.
(2) Inadequate intestinal mucosal
surface
Seen in coeliac disease (an autoimmune disorder of
the small intestine that occurs in genetically
predisposed people of all ages from middle
infancy onward. Symptoms include pain and
discomfort in the digestive tract, chronic
constipation and diarrhoea, failure to thrive (in
children), anaemia and fatigue, but these may
be absent.
(3) Infections of bowel Affecting the mucosa and sub mucosa or entire
bowel
(4) Abnormal bowel anatomy
(5) Insufficient bowel Occurs after removal of bowel in bowel infarction or
repeat surgery for chronic bowel disorders
(6) Malignant diseases Usually not associated except in cases associated
of abnormal bowel motility or tumors secretes
VIP
Generalized malabsorption occurs due to a lot of gastrointestinal diseases include:
GASTROINTESTINAL DISEASE
21. 8/15/23 Aaser Abdelazim Clinical Biochemistry 21
Condition Effect
Inadequate bile
salt secretion
q Occurs in many types of liver diseases and give rise to fat
malabsorption.
q Associated with Osteomalcia or rickets due to failure of
vitamin D absorption.
Vitamin B12
malabsorption
Condition associated with pernicious anemia due failure to
secrete the intrinsic factor in gastric mucosal atrophy.
Inherited
deficiencies
of intestinal
saccharidases
Due to deficiency of some enzymes that digest disaccharides
like lactase& sucrase (lactose/sucrose intolerance).
Other conditions associated with specific malabsorption
23. 8/15/23 Aaser Abdelazim Clinical Biochemistry 23
Aaser M. Abdelazim
Professor of Biochemistry
Zagazig University, Egypt
University of Bisha, KSA
aaserabdelazim@yahoo.com
LIVER FUNCTION TESTS
24. 8/15/23 Aaser Abdelazim Clinical Biochemistry 24
Liver Functions Tests
1.Functions of human liver.
2.Major tests used in diagnosis of liver
disorders.
3.Major changes in plasma enzymes and their
indication in liver diseases.
4.Major pathological changes in liver.
5.Hepatic coma.
6.Jaundice.
25. Functions of liver:
1.Metabolism (Lipid, Proteins,
Carbohydrates)
2.Storage (Glycogen, Vitamins, Vitamin
B12)
3.Excretory function (Bilirubin,
Cholesterol).
4.Detoxification (Phenbarbiton,
Amonia, Steroid Hormones, Benzoic)
5.Hematological function (Blood
formation, Blood volume, Blood
coagulation).
CAH: chronic active hepatitis
8/15/23 25
Aaser Abdelazim Clinical Biochemistry
Liver is the master organ in the body, it serve all other organs
27. 8/15/23 Aaser Abdelazim Clinical Biochemistry 27
Major tests used to diagnose liver
functions
•ALT
•AST
•GGT
•ALP
•LDH
•5` nucleosidase
1. Albumin (cirrhosis)
2. (α, ᵦ, ɣ) globulins
(Cholestasis)
3. Immunoglobulins(IGs)
- IgG: chronic active
hepatitis
- IgA: portal cirrhosis
- IgM: biliray cirrhosis, viral
hepatitis
1. Anti mitochondrial .
Ab.(CAH, Biliray
cirrhosis
2. Anti nuclear:
autoimmune
hepatitis
3. Anti smooth
muscle: CAH
Plasma enzymes Plasma proteins Serology
CAH: Chronic active hepatitis
28. (1) Serum ALT (sGPT)(N= up to 35 U/ml)
It presents in high concentration In:
1. Liver
2. Skeletal muscles
3. Kidneys
4. Heart
Marked increase(10- 100
times)
1.Viral hepatitis
2.Toxic liver hepatitis
3.Circulatory failure
Moderate increase
1.Liver cirrhosis
2.Cholestatic jaundice
3.Liver congestion
4.Secondary to cardiac failure
5.Extensive trauma
8/15/23 28
Aaser Abdelazim Clinical Biochemistry
Major changes in plasma enzymes and its indication in
liver diseases
Causes of ALT increase
29. It present in high concentration In:
1.Heart
2.Liver
3.Muscle
4.Kidenys
Physiological increase
In newborn its increase
= 1.5 of normal level
Marked increase (10-
100 times )
1.Myocardial infraction
2.Viral hepatitis
3.Toxic liver cirrhosis
4.Circulatory failure due
to
-Shock
-Hypoxia
Artefacual increase
Due to hemolysis of
blood in lab.
Led to its release
8/15/23 29
Aaser Abdelazim Clinical Biochemistry
Moderate increase
1.Liver cirrhosis
2.Cholestatic jaundice
3.Liver infiltration
4.Skeletal muscle
disease
5.After trauma or surgery
(2) Serum AST (sGOT)(N= up to 40 U/ ml)
Causes of AST increase
30. Presents in high concentration In:
1.Bone
2.Liver
3.Kidneys
4.Lactating mammary glands
5.Intestinal wall
6.Placenta
Physiological
1.Children until
puberty 2.5 times of
adult level
2.Pregnancy
Bone diseases
1.Osteomalcia
2.Rickets
3.Bone carcinoma
4.Healing stage of bone
fractures
Liver diseases
1.Cholestatic jaundice*
2.Hepatitis
3.Cirrhosis
4.Tumors * *
5.Infiltration * *
8/15/23 30
Aaser Abdelazim Clinical Biochemistry
(3) Serum Alkaline Phosphatase (ALP) N= (50-190 U/L)
Causes of ALP increase
34. Major pathological changes in liver
Liver cell damage Cholestasis Infiltration of liver
Impaired the secretion of bile
Then accumulated in the
plasma
1. Secondary to a disease
2. Abscess
3. Parasitic emboli
As bilhariziasis cause
destruction of cells
Destruction of cell
Acute: as viral infection Chronic : Loss of function
8/15/23 34
Aaser Abdelazim Clinical Biochemistry
35. (1) Liver cell damage
Causes:
•Viral infection
•Toxins (alcohol, paracetamol, acetaminophen)
•Hypoxia and congestion in chronic heart failure (CHF).
•Secondary to biliray obstruction.
Biochemical effect:
1. Release of intracellular constituents into blood.
2. High sGOT (AST) and sGPT(ALT).
- Massive destruction: sudden fall after high elevation
- Chronic destruction: high level for long time
ALT than AST Means liver viral hepatitis
AST than ALT
Means excess damage,
cirrhosis, hypoxia and tumors
8/15/23 35
Aaser Abdelazim Clinical Biochemistry
36. 8/15/23 Aaser Abdelazim Clinical Biochemistry 36
Liver diseases and AST-to-ALT ratio
Disease Ratio
EtOH 1.5
Drugs 2.0
Cirrhosis 1.4-2.0
Hepatocellular carcinoma (HCC) > 1.5
Intra hepatic cholestasis > 1.5
Extra hepatic cholestasis 0.7-0.8
Acute viral hepatitis < 0.65
Acute myocardial infraction (MI) > 3.0
37. With jaundice (Cholestatic jaundice) With out jaundice
1. Gall stones
2. Carcinoma (obstruction
of bile duct)
1. Some forms of Viral hepatitis
2. Biliary cirrhosis
3. Drugs : phenothiazine.
1. Plasma Bilirubin increased to be 50 mg/dl
2. ALP increases
3. ALT, AST increases
4. Increase GGT
5. Increase 5` nucleotidase
1. Obstruction to only part of biliary
system
2. Cholengitis
3. Primary biliary cirrhosis
Biochemical
changes
8/15/23 37
Aaser Abdelazim Clinical Biochemistry
(2) Cholestasis
Intra hepatic
Extra hepatic
38. Biochemical changes:
Abscess
(1)
Amyloidosis
(2)
Tuberculosis
(3)
1. Increase synthesis in
sinusoids
2. Regarded to circulation
3. But it highest in Cholestasis
8/15/23 38
Aaser Abdelazim Clinical Biochemistry
High serum ALP
High serum GGT
Normal bilirubin
ALT and AST normal or slight raised
Why?
(3) Liver infiltration
(5) Carcinoma from lung or stomach
Parasitism
(4)
CAUSES
39. 8/15/23 39
Aaser Abdelazim Clinical Biochemistry
17.1 µmol/l bilirubin=1 mg/dl
Case study (1):
0.41 mg/dl
41. 8/15/23 Aaser Abdelazim Clinical Biochemistry 41
1. Liver function tests indicate mild cell damage; this appeared from
normal levels of AST and Bilirubin and slight increase of ALT (38/N =
<35).
2. High serum ALP indicates one of the following:
a) Bone metastasis tumor; and this not excluded by normal level
of Ca as ALP is very high (bone scan is very important here)
b) Metastatic breast carcinoma
c) Hepatic metastatic carcinoma from breast
3. Further investigations are required
a) Bone scan
b) Tumor markers
c) Histopathological examinations
Comments on case 1
Aaser
42. 8/15/23 Aaser Abdelazim Clinical Biochemistry 42
Hepatic coma
Definition: is the occurrence of confusion, altered level of consciousness as a
result of liver failure.
Biochemical findings
High blood ammonia
qSerum ammonia levels are
elevated in 90% of patients.
qNot all hyperammonemia
(high ammonia levels) is
associated with coma.
Abnormal liver function tests
indicating liver failure
43. 8/15/23 Aaser Abdelazim Clinical Biochemistry 43
Causes: other causes with hepatic faliure may predispose coma like:
Type Cause
Excessive
nitrogen
load
1. Consumption of large amounts of protein
2. Gastrointestinal bleeding e.g. from esophageal varices (blood is high in protein, which
is reabsorbed from the bowel),
3. Renal failure (inability to excrete nitrogen-containing waste products such as urea),
4. Constipation
Electrolyte
or
metabolic
disturbance
1. Hyponatraemia (low sodium level in the blood) and hypokalaemia (low potassium
levels)—these are both common in those taking diuretics, often used for the treatment of
ascites
2. Alkalosis (decreased acid level),
3. Hypoxia (insufficient oxygen levels),
4. Dehydration
Drugs and
medications
1. Sedatives: such as benzodiazepines (often used to suppress alcohol withdrawal or
anxiety disorder),
2. Narcotics: (used as painkillers or drugs of abuse) and sedative antipsychotics, alcohol
intoxication
Infection Pneumonia, urinary tract infection, spontaneous bacterial peritonitis, other infections
Others
Surgery, progression of the liver disease, additional cause for liver damage (e.g. alcoholic
hepatitis, hepatitis A)
Unknown In 20–30% of cases, no clear cause for an attack can be found
44. 8/15/23 Aaser Abdelazim Clinical Biochemistry 44
Hepatic failure
The energy to brain cells is decreased
Due to depletion of α-ketoglutarate
(NH3)
Crosses the blood-brain barrier
(NH3)
Glutamate Glutamine
Excess Glutamine lead to
increase the osmotic pressure
in brain cells (become swollen)
Increase the activity of GABA in brain due to
conversion of α-ketoglutarate in to glutamate
(inhibitory neurotransmitter)
Brain edema (cytotoxic type)
Ammonia (NH3) accumulates in
the systemic circulation
45. 8/15/23 45
Aaser Abdelazim Clinical Biochemistry
1. Definition of jaundice
2. Bilirubin metabolism
3. Causes of jaundice
4. Differential diagnosis of jaundice
46. 8/15/23 Aaser Abdelazim Clinical Biochemistry 46
1) Is a yellow discoloration of skin or/and sclera due to high
concentration of plasma Bilirubin over 40 µmol/l
2) Normal plasma total bilirubin is less than 22 µmol/l (3-15
µmol/l OR 0.3 -1 mg/dl )
3) Normal conjugated = 0.1 mg/dl
1. See bilirubin metabolism figure (3)
2. Main causes of high bilirubin are three
figure (4)
• Hemolysis
• Failure of conjugation mechanism in
liver
• Obstruction in biliary system
17.1 µmol/l bilirubin=1 mg/dl
Jaundice
qIndicates an elevated level of
serum bilirubin .
qIn neonates it is important to
determine the concentration of
Unconjugated bilirubin in order to
decide the treatment required
qIn adults most common type is
due obstruction.
47. 8/15/23 Aaser Abdelazim Clinical Biochemistry 47
Figure (2) Bilirubin metabolism
Water soluble
•Non water soluble (not secreted
from kidneys)
•It is neurotoxic
•Can cause permanent brain
damage in neonates
•Brown coloration of feces
•If not present lead to pale
colored feces
Bacteria
Orange color of urine on
long standing
49. 8/15/23 Aaser Abdelazim Clinical Biochemistry 49
Hemolysis
Plasma
Unconjugated
bilirubin
Main in neonates
>> 200 µmol/l (12
mg/dl); need
phototherapy
>> 300 µmol/l(17
mg/dl); need
exchange transfusion
Extra hepatic obstruction
Both Plasma
bilirubin and
ALP
Little or no
urobilinogen in
urine
Pale stool
Partial
Complete
ALP with
bilirubin within
reference range
Level of ALP
indicate the
degree of
obstruction
Hepatocellular damage
Both Plasma
bilirubin and
ALP with ALT
and AST
Obstruction occurs
here secondary to
hepatic cell
damage by toxins
or infection
conjugated
Indicates
damage of
liver cells
Little or no
Stercobilinogen
in intestine
50. 8/15/23 Aaser Abdelazim Clinical Biochemistry 50
Laboratory differential diagnosis of jaundice
Feature Hemolytic Cholestatic Hepatocellular
Serum Bilirubin
>75 µmol/l (4.38 mg/dl)
(Unconjugated)
(Indirect)
Over 3 times than in
hemolytic
(Conjugated) (Direct)
>75 µmol/l but later
(Unconjugated/conjugated)
Conjugated increased when
obstruction occurs later on
Bilirubin in urine
Not present
(Unconjugated is not water
soluble and bound to albumin
and not filtered )
Present Present
(high level of conjugated bilirubin)
Urine
Urobilinogen
Increased Decreased /absent Decreased/absent
Stool Normal
Clay/pale in color
(no bilirubin reaches the
intestine)
Normal
Reticulocytosis + - -
Hemoglobin
/Haptoglobin Decrease Normal Normal
Plasma enzymes LDH may increased
1. ALP over 3 times the
reference range it act
as a mirror for the
degree of obstruction.
2. High AST, ALT, GGT
and LDH
High ALP but appear later
High ALT and AST
Due to hepatocytes damage
51. 8/15/23 Aaser Abdelazim Clinical Biochemistry 51
Neonatal jaundice
Causes:
1.Inability of immature liver of neonates to produce UDPG- transferase
2.Higher turnover of neonatal erythrocytes shortly after birth to replace fetal HbF
with normal HbA
Neonatal jaundice
Transient
Physiological jaundice of the
newborn (PJN)
Sustained
1. Hemolytic diseases
2. Biliray artesia (post
hepatic type)
3. Idiopathic neonatal
hepatitis (rare) (hepatic
jaundice)
1. Blood groups
incompatibility
between mother and
fetus (+ direct anti-
globulin)
2. Absorption of large
hematoma.
52. 8/15/23 Aaser Abdelazim Clinical Biochemistry 52
Blood cells of mother Blood cells of fetus
Both come in contact
1. Through transfusion
2. Or during pregnancy
Immune system of
mother recognized
them as foreigners
Produce antibodies
against them
RBCs destruction
This usually not
affects the 1st
child but affects
the second one
Mechanism of neonatal jaundice
Aaser
Group (O) or
RH-
Group (A/B) or
Rh+
1. High amounts of IgM (anti-A, anti-B)
2. Small amounts of IgG (anti-A, anti-B)
53. 8/15/23 Aaser Abdelazim Clinical Biochemistry 53
Consequence of neonatal jaundice
Treatment
Phototherapy if the level exceed 10 mg/dl
Source of light emitted light of 450 nm
Unconjugated
bilirubin
(insoluble)
Soluble bilirubin
Kernicterus
Brain cell nuclei stained yellow
Damaged due to high
bilirubin can cross blood
brain barrier (not occurs in adults
why?! Here type of bilirubin is unconjugated
which is water insoluble).
Usually brain is damaged if
the level reaches > 20
mg/dl
cerebral palsy, deafness,
mental retradation
54. 8/15/23 Aaser Abdelazim Clinical Biochemistry 54
Physiological jaundice of the newborn (PJN)
Transient condition/ phenomena in which
bilirubin subsides within few weeks
Other factors affecting neonatal hyperbilirubinemia
1.Decrease binding of Unconjugated bilirubin to albumin
2.reabsorption of intestinal meconium
3.constituents in mother’s milk. Progesterone and other hormones in
breast milk as well as beta-glucuronidase may suppress neonatal
conjugation of bilirubin
1. Increase total and Unconjugated bilirubin
2. Near-normal conjugated bilirubin
3. Normal hepatic enzymes if there is no iflammation
Physiological jaundice of the newborn (PJN)
58. 8/15/23 Aaser Abdelazim Clinical Biochemistry 58
Aaser M. Abdelazim
Professor of Biochemistry
Zagazig University, Egypt
University of Bisha, KSA
aaserabdelazim@yahoo.com
KIDNEY FUNCTION TESTS
59. 8/15/23 59
Aaser Abdelazim Clinical Biochemistry
1. Anatomical view of the kidneys and
nephrons.
2. Functions of kidneys
3. Renal functions tests
4. Glomerular function tests
5. Tubular function tests
6. Renal disorders
7. Renal failure
RENAL function tests
60. 8/15/23 Aaser Abdelazim Clinical Biochemistry 60
Fig (1): Kidney anatomy
Anatomical view of human kidney
64. Renal function tests
Glomerular function Tubular function
(1) Urine examination (see the practical part)
(2) BUN
(3) Serum Creatinine
(4) Creatinine clearance
(5) Urea clearance
8/15/23 64
Aaser Abdelazim Clinical Biochemistry
Urine concentration test
Vasopressin test
Urine dilution test
Plasma electrolytes
Maximal tubular reabsorption of glucose and
secretion of Para Amino Hippuric acid (PAH )
65. Blood urea nitrogen (BUN)
8/15/23 65
Aaser Abdelazim Clinical Biochemistry
Proteins
Liver
Urine
Urea MW= 60.06
60 gm urea contains 28 gm N
BUN= UNx28/60
Blood
Ammonia
(Toxic)
Urea
Urea
Amino acids
•Urea mainly come from metabolism of proteins
•It is a save product of ammonia (urea cycle)
•Secreted in urine (N= 20-40 gm /day)
•Normal plasma level= 20-40 mg/dl
68. Normal serum = men: 0.8-1.3 mg/dl , women: 0.6-1.0
mg/dl or (60-120 µmol/l)
Creatinine is best used to urea for assessment of
renal functions:
• Not affected by diet
• Non-threshold i.e. Completely execrated in urine not reabsorbed from
tubules
• Mainly of endogenous origin
• Creatinine is mainly excreted from kidneys while 75% only from urea are
excreted in kidneys and 25% in colon.
8/15/23 68
Aaser Abdelazim Clinical Biochemistry
Creatinine MW= 113.12 g/mol
Serum creatinine
70. 8/15/23 Aaser Abdelazim Clinical Biochemistry 70
Increased in :
• Renal failure
• Decrease renal perfusion due to (CHF)
• Renal obstruction
• Acute tubular necrosis
• Glomerulonephritis
• Hypothyroidism
• Skeletal muscle trauma
• Ketonemia (diabetic ketoacidosis)
• Diabetic nephropathy
• Rhabdomyolosis
• Eclampsia and pre-eclampsia
• Creatine supplement
• Dehydration
• Drugs
Hydantion: tranqulizer, Cephalosporins
,Aminoglycosides, Diuretics, methyldopa:
parkinsonism Cemetidine , trimethoprim
Decreased in:
•Amputations
•Low muscle mass
•Muscular dystrophy
•Myasthenia gravis
•Pregnancy
Abnormalities of Serum Creatinine
One mg/dl of creatinine is 88.4 μmol/l.
71. 8/15/23 Aaser Abdelazim Clinical Biochemistry 71
CKD according to creatinine levels
kidney disease is divided into five stages according to creatinine level.
CKD stage
1 2 3 4 5
Cr level
(mg/dl)
<1.6 1.6-2 2.1-5 5.1-7.9 >8
A. Peoples with creatinine levels >2 mg/dl should take their treatments as soon as
possible.
B. Usually stage 1 indicate mild impairment of kidney functions and need only
some changes in routine
1. Change the diet routine (take egg white-lean meat-fruits)
2. Increase the exercise
3. Depend on the natural food and plants to lower the creatinine.
72. Creatinine coefficient
•The amount of Creatinine excreted in
urine/ kg BWt/ day
•N= 1.5 gm /day in male and 1.0
gm/day for female
•Depends on:-
1.Body muscle mass
2.Body conditions
8/15/23 72
Aaser Abdelazim Clinical Biochemistry
73. 8/15/23 Aaser Abdelazim Clinical Biochemistry 73
Creatinine clearance
Biochemical indications:
• Assess renal glomerular function
• Drug monitoring
• Advanced stages of renal failure
Amount of Creatinine filtered = the amount of Creatinine excreted
GFR x Cr conc. In Plasma = Cr conc. In urine x urine Volume
GFR (C) x P = U x V
U x V
P
C (Cr clearance) =
mg/dl x ml/ min /mg/dl = ml / min
Comments the Normal levels =107-139 in male and 87-107 in females.
Levels less 90ml/min indicate bad.
74. 8/15/23 Aaser Abdelazim Clinical Biochemistry 74
Creatinine clearance test
It is two part test ; 24-hour urine collection and blood samples are measured
78. 8/15/23 Aaser Abdelazim Clinical Biochemistry 78
Mw of Creatinine = 113.12 g/mol
To convert from µmol/l to mg/dl divide on 88.4
Urine volume/ minute (V) =
Urine /day
24x60
=
2160
1440
= 1.5 ml/minute
P= 150 µmole of Creatinine in plasma = 1.33 mg/dl
U= 7.5 mmole of Creatinine in urine = 66.3 mg/dl
Creatinine clearance =
UxV
P
66.3 x1.5
1.33
= 74.7 ml/minute !
=
This level indicates low flow rate its normal is (107-139 ml/minute)
Case study (1)
After correction of that urine is collected after 17 hours only the Cr Cl
become 105 ml / minute this indicate normal flow rate
Aaser
79. (2) Tubular functions tests:
Test:
1.Allow patient to take water after 6 pm but no food.
2.Come to lab at 7am,
3.Take urine samples at 7(zero time), 8, 9 am
Results
Any of these samples its Sp Gr should be more 1026 indicates good renal function
With in 1020 minor renal failure
1010-1015 : severe renal damage
8/15/23 79
Aaser Abdelazim Clinical Biochemistry
Contra indication:
1)High blood urea
2)Patients with clinical signs of RF
Uses:
Used for testing the renal concentration ability in response to water deprivation
Can assess :
ØNormal ADH
ØNormal response of DCT to ADH.
(1) Urine concentration test (water deprivation test):
80. (2) Vasopressin test:
Test
1.At 8 pm patient take 5 units of vasopressin tanate.S/C
2.Collect urine at 7, 8, 9 am
3.Sp gr should be more 1020 : good renal function
(3) Urine dilution test (water load test):
1. Water not allowed to patient over night
2. Come at mooring to lab
3. Take 1000 ml water to drink completely
4. Collect 4 urine samples one hour interval after drinking
Results :
q Normal urine led down in 4 hrs is 700 ml at least
q Sp gr. Of one of the 4 at least = 1004
q Severe damaged kidneys secrets urine with sp gr not less than 1010
and volume not mor than 400 ml
Contra indications of water load test
•Odema
•Hyponatremia
•Renal failure with water intoxication
8/15/23 80
Aaser Abdelazim Clinical Biochemistry
81. 8/15/23 81
Aaser Abdelazim Clinical Biochemistry
(4) Tubular maximum of glucose reabsorption and
PAH secretion
TmG =GFR x Pg – Ug x V
Amount of glucose reabsorbed = amount of glucose filtered – amount
of glucose secreted
TmPAH = UPAH x V – GFR x PPAH
Para amino hippuric acid (PAH) actively excreted = PAH filtered- PAH
absorbed
N = 350±75 minutes
84. 8/15/23 Aaser Abdelazim Clinical Biochemistry 84
Notes on the report
1.High Na level =150 mmol/l (N= 136-145 mmol/l).
2.High BUN = 91.6 mg/dl (N= 20-40 mg/dl)
3.Normal creatinine level= 0.71 mg/dl (N= 0.6-1.2 mg/dl)
4.Normal blood glucose = 97.2 mg/dl (N=120-130 mg/dl)
Comments on Case study (2)
MW of Urea = 60.06 g/mol
Water deprivation test in this case is dangerous!!
It is contra indicted in patients with high BUN and Na levels
History and high urine volume with normal blood glucose indicate
diabetes insipidus
So no need for further tests except ADH level mointoring and radiology like
CT or MRI for confirmation
The main cause of thirst, is her hyppernatremia and high water loss (polyurea)
Aaser
86. 8/15/23 Aaser Abdelazim Clinical Biochemistry 86
1. Causes of glomerular dysfunctions
2. Biochemical changes in glomerular dysfunctions
3. Causes of tubular dysfunctions
4. Biochemical changes in tubular dysfunctions
5. Picture of acute renal failure
6. Picture of chronic renal failure
Biochemical changes in renal diseases
87. 8/15/23 Aaser Abdelazim Clinical Biochemistry 87
The end results of renal diseases is the disturbance in nephron functions
Glomerular dysfunctions Tubular dysfunctions
1. Congestive heart failure
2. Acute/chronic glomerulonephritis
3. Acute renal fauilure
4. Low systemic blood
pressure(hemorrahge/dehydration
/shock)
5. Any disease in glomerulus
6. Renal circulatory shortage
1. Acute tubular necrosis
2. Prolonged renal circulatory
shortage
3. Progressive tubular damage due
to:
• High blood calcium
• Hyperuricemia
• Hyperkalemia
• Galactosemia
• Poisons as heavy metals toxicity
88. 8/15/23 Aaser Abdelazim Clinical Biochemistry 88
Biochemical changes in Glomerular dysfunctions
In plasma
Uremia
Hypocalcemia
Hyperkalemia Acidosis
Hyperphosphatemia
1. Increase plasma
urea/creatinine
2. Reduced the k
secretion
Low blood Na due
to high blood K
Na
K
H
H
Due to failure of
vitamin D activation
Acidosis
1
4
3
2
5
1. Decrease GFR
2. Acidosis
Due to failure of
vitamin D activation
89. 8/15/23 Aaser Abdelazim Clinical Biochemistry 89
In urine
Low urine
led down
(Oligurea)
Low urea/creatinine
Low uric acid/K
As a logic picture of plasma
Biochemical changes in Glomerular dysfunctions
90. 8/15/23 Aaser Abdelazim Clinical Biochemistry 90
Biochemical changes in tubular dysfunctions
• Reduction of water
reabsorbtion
• Failure to secret H
and reabsorb HCO3
Large volume of
dilute urine
/acidosis
• Impaired Na/K
reabsorption
Potassium
depletion(hypo K)
Hypo P/ normal
urea
• Generalized
amino acid urea
• Low blood uric
acid/P
Acquired fanconi
syndrome
1. Low specific gravity
2. Polyurea
3. Low urea
4. High Na Urine
98. 8/15/23 Aaser Abdelazim Clinical Biochemistry 98
(A man aged 40 years old presenting with lion pain has a serum
creatinine of 2.5 mg/dl, 24-houred collected urine equals 2160 ml
and found to have urine creatinine level equals 66.4 mg/dl, serum
urea 80 mg/dl, serum sodium 140 mmol/l, urine sodium 700mmol/l
and serum glucose 130 mg/dl).
1. Calculate creatinine clearance (CrCl).
2. Comment on your calculated CrCl and mention the TWO conditions
that lead to this case?
3. Calculate fractional excretion of sodium (FENa) and serum
osmolality and interpret the results.
4. If an error in timed collected urine was subsequently reported, and
the actual collection time was 12 hours only. How does this affect
the results?
Case study (3)
99. 8/15/23 Aaser Abdelazim Clinical Biochemistry 99
Biochemical changes in chronic renal failure
Glomerular dysfunctions Tubular dysfunctions
Generalized disease of nephrone
1. Chronic glomerulonephritis
2. Polycystic kidney
Similar to
100. 8/15/23 Aaser Abdelazim Clinical Biochemistry 100
Biochemical finding in chronic renal failure
Osmotic polyurea marked at night
Metabolic acidosis(retention of PO4, SO4 and
organic acids)/ failure of kidneys to secrete H
Impaired glucose tolerance
High blood urea/ creatinine/ marked fall in
creatinine clearance
High plasma amylase?
Hypocalcemia /hyperkalemia if there is oligurea
due to excess loss of Na and Cl
Low concentration power of kidneys
Protein urea (not more than 5 gm/day)
1
4
3
2
8
7
6
5
102. 8/15/23 Aaser Abdelazim Clinical Biochemistry 102
The biochemical course of a typical patient with CRF before/after hemdialysis
103. 8/15/23 Aaser Abdelazim Clinical Biochemistry 103
How hypocalcaemia and secondary hyperparathyroidism develop in renal disease
104. 8/15/23 Aaser Abdelazim Clinical Biochemistry 104
Biochemical finding in acute glomerulonephritis
Oligurea
Hematurea (smoky urine due to acute inflammation/
high blood vessels damage)
Proteinurea (5-10 gm/day)
Odema (Na& water retention)/ capillary damage
and increase permeability
Low creatinine clearance
Low plasma proteins due to hemedulition
1
4
3
2
6
5
105. 8/15/23 Aaser Abdelazim Clinical Biochemistry 105
Hepatorenal syndrome
oAcute renal failure with advanced liver disease this may be due to
•Liver cirrhosis
•Metastatic tumors
•Alcoholism (inducing sever hepatitis).
oThe condition characterized by:
•Oliguria.
•Benign urine sediment.
•Low sodium excretion.
•Progressive rise in plasma creatinine.
•Reduction in GFR usually masked.
PROGNOSIS: bad unless improves the liver functions.
115. 8/15/23 Aaser Abdelazim Clinical Biochemistry 115
Diagnosis of heart
disorders
Aaser M. Abdelazim,
Professor of Biochemistry
Zagazig University, Egypt
University of Bisha, KSA
aaserabdelazim@yahoo.com
116. 8/15/23 Aaser Abdelazim Clinical Biochemistry 116
MYOCARDIAL INFARCTION (MI)
Definition: also known coronary thrombosis, most common of mortality and
morbidity in adults, diagnosed from chest pain and elevated heart enzymes.
It occurs due to narrowing of arteries supply cardiac muscles, inducing chest
pain (angina pectoris).
117. 8/15/23 Aaser Abdelazim Clinical Biochemistry 117
DIAGNOSIS OF HEART DISORDERS:
1. History: Chest pain
2. ECG: Changes indicates the severity and the site of infraction
3. Biochemical tests:
q Testing the heart enzymes CK, LDH, AST
q Other biochemical indicators: Myoglobin, Troponin I& T and lipid profile.
(a) (b) (c)
(a) Normal ECG (b) 2 hrs after the
onset of chest pain
elevated ST
segment
(c) 24 hrs after the
onset of chest pain
further episode of
chest pain
118. 8/15/23 Aaser Abdelazim Clinical Biochemistry 118
HEART ENZYMES:
Enzymes Characteristics
(1) Total CK
qTotal CK: is released from all types of damaged muscle cells
including the cardiac muscles.
qIs the 2nd enzyme released and reaches its peak within 24-48 hrs
from the onset the heart attack.
(2) CK-MB
qIt is a strong marker for early confirmation of heart infraction.
qIt is the 1st enzyme raised (6 hrs after the incident)
qUsed in post-operative patients for suspected myocardial
infraction, as it only increased in myocardial infraction.
qIt is indicated in the second infraction within few days of the 1st
one.
(3) AST and ALT
qThese enzymes are not highly specific for heart
qThey also elevated in liver, lung, muscles disorders
qAST is more present in heart than any other tissues.
qAST reaches its peak after 48 hours.
(4) LDH
qTotal LDH is nonspecific for heart.
qIt elevated in other liver, RBCs disorders.
qIsoenzymes LDH1, 2 are specific for heart.
qThey reach the peak within 4 days from the heart attack.
119. 8/15/23 Aaser Abdelazim Clinical Biochemistry 119
Enzyme
Start of rise
(hrs)
Peak
(hrs)
Duration of rise
(hrs)
CK-MB 3-8 12-24 1.5-3
CK total 4-8 24-48 3-6
AST 6-8 24-48 3-6
LDH1,2 12-24 48-72 6-12
Pattern of cardiac enzymes in the episode of myocardial
infraction:
Note that:
1) All enzymes may be appeared normal in patient plasma until 4 hrs after the
infraction.
2) The level of the enzymes in plasma correlates with the infraction size.
3) Very high levels may indicate myocardial necrosis.
120. 8/15/23 Aaser Abdelazim Clinical Biochemistry 120
2 4 6 8
0x
5x
2x
4x
1x
3x
6x
7x
LDH
AST
CK
ALT
On admission all the
results within the
reference range
Fold
increase
above
the
upper
limit
of
reference
range
Enzymes in plasma after uncomplicated MI
Duration in days
121. 8/15/23 Aaser Abdelazim Clinical Biochemistry 121
Indicator Characteristics
(1) Myoglobin
qIs the absolute first marker for MI
qStarted to be elevated in patients serum after 1-3 hrs from
the onset of chest pain.
qIt is very useful for the early detection of MI in patients in
emergency department.
Troponin I & T
It forms Troponin complex with
troponin C
qAre specific markers for acute MI.
qThey released form damaged cardiac muscles within 3-8
hrs from infraction, but they remain elevated for much longer.
q Troponin T takes about 2 weeks to return to normal level;
while Troponin I takes 5-10 days only.
q Normal level of Troponin T = 0-0.1 µg/L; Troponin I =(1-
3µg/L)
Other Biochemical inductors for MI:
Conditions predispose MI are; Diabetes Mellitus, Smoking, Hyperlipidemia, Hypertension
122. 8/15/23 Aaser Abdelazim Clinical Biochemistry 122
Parameters Characteristics
(1)Plasma appearance
qGive indication about the level of TAGs in blood.
qClear plasma indicates TAGs lower than 200 mg/dl.
qTurbid plasma indicates TAGs levels with in 300 mg/dl.
qCloudy to opaque plasma indicates TAGs over 600 mg/dl.
qCreamy layer appeared on the surface of the plasma within
4 hours indicates the presence of CM.
(2) Serum total cholesterol
qNormal serum levels equal (130-220 mg/dl).
qUsed to monitor chronic heart disease.
(3) Serum HDL-cholesterol
qNormal serum levels equal (30-75 mg/dl).
qLevels over 60 mg/dl are good indicator about negative
heart disorders.
qEvery 1 mg/dl decrease in HDL increases the risk of CHD
by 2-3%.
(4) Serum LDL-cholesterol
qNormal serum levels equal (65-175 mg/dl).
qHigh levels are bad indicator for CHD.
(5) Serum
Triacylglycerides
qNormal serum levels equal (40-160 mg/dl).
qTGs are not strong predictors for atherosclerosis and CHD
(6) Risk factor for CHD
qEquals the total cholesterol/ HDL-cholesterol
qLow risk (3.3-4.4).
qAverage risk (4.4-7.1).
qModerate risk (7.1-11).
qHigh risk (over 11).
Lipid profile:
127. 8/15/23 Aaser Abdelazim Clinical Biochemistry 127
Bone disorders not imply hypocalcaemia or hyperclacemia, conversely sever
bone diseases can occur whilst blood calcium is quite normal.
Bone metabolism:
Osteocyte
Bone trabecula
Osteoblast
Osteoclast
qBone is continuously broken and reformed this called
(bone remodeling).
qOsteoclast cells are responsible for bone resorption .
Hydroxproline is a good markers for collagen
breakdown and so for bone resoption.
qOsteoblast cells are responsible for bone formation.
qOsteoblasts have high activity of ALP
qOsteocalcin is a good marker for bone ossification
and osteoblast activity.
Common bone diseases are:
qOsteoporosis
qOsteomalcia and rickets
qPaget’s disease: irregular bone resorption and formation
128. 8/15/23 Aaser Abdelazim Clinical Biochemistry 128
Disorders Biochemical markers
(1) Bone metastasis qCalcium not indicative (high, low or normal).
qPhosphate also not indicative.
qPTH low
qALP high/normal
(2) Osteomalcia, rickets qLow calcium
qHigh PTH
q25-hydroxycholecalciferol low
(3) Paget’s disease qCalcium is normal
qALP is grossly elevated
qHydroxy proline is high
(4) Osteoporosis qBiochemistry not indicative
qCalcium level unaffected
qALP is high
(5) Renal Osteodystrophy qLow calcium
qVery high PTH
(6) Ostitis fibrosa cystica
(primary
hyperparathyrodism)
qHigh calcium
qLow / normal phosphate
qHigh PTH
Diagnosis of bone disorders:
130. 8/15/23 Aaser Abdelazim Clinical Biochemistry 130
Normal ALP= 50-190 U/L
Case study comments
131. 8/15/23 Aaser Abdelazim Clinical Biochemistry 131
CENTRAL NERVOUS SYSTEM
Neurology laboratory tests
132. 8/15/23 Aaser Abdelazim Clinical Biochemistry 132
qThe central nervous system consists of the brain, spinal cord, and neuron
processes.
qThe central nervous system is surrounded by membranes of the meninges.
qThe outer covering is a thick membrane consisting mostly of collagen.
qThe ventricles or chambers produce the cerebrospinal fluid, which circulates to
the subarachnoid space where it cushions and feeds the brain.
qThis clear fluid, with a volume of approximately 100 ml, exchanges chemicals
with blood to feed the cells of the nervous system and carry away waste products.
CENTRAL NERVOUS SYSTEM
Metabolic view of brain:
1) The brain directs most metabolic processes in the body.
2) Brain cells are not energy producers, but have a constant need for energy.
3) Under normal conditions, the brain uses glucose as its sole source of energy.
When glucose levels are low, the brain can use some ketones as energy
sources.
Chemical analysis of CSF
qChemical analysis of cerebrospinal fluid provides information about trauma,
infection, and demyelinating diseases.
qMost commonly, glucose and total protein are measured in spinal fluid. However,
laboratory tests for lactate, immunoglobulin proteins, and other biochemicals are
available (see the following table).
133. 8/15/23 Aaser Abdelazim Clinical Biochemistry 133
Test Normal value Description
CSF cell count < 5 cells/mm3 qGood indicator for acute inflammatory conditions for CNS
qAbout 70% of WBCs in CNS are Lymphocytes
qMonocytes represent 30%
qDuring pleocytosis ; WBCs significantly increased.
CSF Chloride 700-750 mg/dL Decrease the value is an indicator for meningitis
CSF Glucose 50-75 mg/dL qIncreased in hyperglycemia
qDecreased in:
Bacterial infection, CNS inflammations, chemical meningitis,
hypoglycemia, subarachnoid hemorrhage.
Blood glucose more reduced in bacterial than viral meningitis.
CSF color Clear qRed color: indicates bleeding
qCloudy: in high WBCs count, high proteins and melanoma
qYellow: hyperbilirubinemia
CSF Glutamine 6-15 mg/dL Increase in hepatic coma, hepatic encephalopathy, liver failure,
Reye syndrome.
This test will be done for patients if there is a coma with
unknown origin.
CSF IgG index
IgG Index
IgG(CSF)/IgG(Serum)
0.29-0.59 High level of IgG in CSF indicates damage of blood-CNS barrier
Increase in chronic CNS infection, systemic lupus
erythematosus (SLE), multiple sclerosis, neurosyphilis, viral
infection.
CSF LDH < 40 U/L High level indicates; bacterial meningitis, CNS leukemia, stroke.
Neurology laboratory tests
134. 8/15/23 Aaser Abdelazim Clinical Biochemistry 134
Test (continue ) Normal Description
CSF Lactic acid 10-25 mg/dL qThe test examine the degree of oxygen deprivation in brain
tissue.
qHigh levels indicate; bacterial meningitis , fungal meningitis or
any states increase anaerobic brain metabolism.
Opening pressure 70-200 mmH2O qNormal CSF pressure should be less than 200 mmH2O.
qHigh CSF pressure indicates also high ICP.
qThe pressure should be measured before obtain the samples.
qHigh pressure indicates; bacterial infection, fungal infection,
T.B, tumors, hemorrhage.
CSF Total Proteins 15-45 mg/dL qHigh levels are a good indicator for brain damage.
qIncreased in; intra cranial hemorrhage, malignancies,
infections, multiple sclerosis.
CSF Pyruvate 0.5-1.5 mg/dL Low pyruvate indicates; chronic hemolytic anemia, metabolic
liver diseases, myelodysplastic syndromes, PK deficiency,
sidropastic anemia.
WBCs CSF < 5 WBCs/ mm3 qBacterial infection (>1000 cells)
qFungal infection (variable)
qViral infection (< 100 cells)
sBPP CSF (soluble
Beta proteins
precursors).
> 450 U/L qUsed mainly to detects Alzheimer disease
qLow levels indicates Alzheimer
VDRL CSF Non reactive qThis test is specific test for neurosyphilis.
qFalse positive results can obtained if there is a blood, protein,
autoimmune disorders,
135. 8/15/23 Aaser Abdelazim Clinical Biochemistry 135
Assessment of
Respiratory Disorders
Aaser M. Abdelazim
Professor of Medical Biochemistry
Zagazig University, Egypt
University of Bisha, KSA
aaserabdelazim@yahoo.com
136. 8/15/23 Aaser Abdelazim Clinical Biochemistry 136
INTRODUCTION
RESPIRATION
(1) Pulmonary ventilation
(2) External respiration
(3) Respiratory gas transport
(4) Internal respiration
Breathing: means
movement of air In and
Out of the body
Oxygen loading and
carbon dioxide loading
Transportation of gases
by blood stream
Exchange between
capillary and body cells.
137. 8/15/23 Aaser Abdelazim Clinical Biochemistry 137
(1) BREATHING (PULMONARY VENTILATION)
(A) Inspiration: Diaphragm flattens creates a vacuum pulling air into the lungs
(B) Expiration: Muscles relax and push air out of the lungs
138. 8/15/23 Aaser Abdelazim Clinical Biochemistry 138
RESPIRATORY VOLUMES AND CAPACITIES
Volume Definition
Tidal Volume (TV) Volume of air moved into and out of the lungs each
breath
Inspiratory reserve
volume (IRV)
Amount of air you can forcibly be taken in
Expiratory reserve
volume (ERV)
Amount of air that can be forcibly expelled
Residual Volume Air that cannot be expelled from the lungs
Vital capacity (VC) Total amount of exchangeable air TV + IRV + ERV
Dead Space volume The amount of air that doesn’t make it to the lungs in
a breath.
139. 8/15/23 Aaser Abdelazim Clinical Biochemistry 139
(2) EXTERNAL RESPIRATION
qGas exchange at the lungs
qOxygen into blood and CO2 removed from blood
140. 8/15/23 Aaser Abdelazim Clinical Biochemistry 140
(3) GAS TRANSPORT IN THE BLOOD
q Oxygen forms oxyhemoglobin with
hemoglobin molecules.
q CO2 in transported via bicarbonate in
plasma.
141. 8/15/23 Aaser Abdelazim Clinical Biochemistry 141
(4) INTERNAL RESPIRATION
qExchange of gases between blood
and tissue cells.
qOxygen unloaded and CO2 loaded.
142. 8/15/23 Aaser Abdelazim Clinical Biochemistry 142
Terms Description
Hypoxia qInadequate supply of oxygen to the body tissues
qCauses skin to become cyanotic
Carbon Monoxide
Poisoning
CO binds to the binding site that oxygen binds to on hemoglobin
preventing gas transport of oxygen
Hyperventilation Body’s reaction to increased levels of carbon dioxide or acids in
blood.
Respiratory terms qEupnea: normal respiratory rate.
qHyperpnea: Increased respiratory rate (exercising)
qApnea: stopped breathing.
qDyspnea: difficult breathing.
SOME TERMS:
143. 8/15/23 Aaser Abdelazim Clinical Biochemistry 143
Arterial blood gases (ABGs):
Collection and handling of arterial blood gases:
1) The specimen for blood gases and pH should be arterial or arterialized
capillary blood
2) All air bubbles should be removed.
3) Air contamination will reduce the CO2 and increases the O2 in the sample due
to the difference in the PO2 and PCO2 tension of these gases in the
atmosphere.
4) Use the correct amount of heparin (0.05 mg heparin/ml blood).
5) The specimen must be placed in ice water until analysis or examined
immediately.
144. 8/15/23 Aaser Abdelazim Clinical Biochemistry 144
Calculations in blood gas analysis:
pH = 6.1 + log HCO3 /(PCO2 x 0.0301)
Given arterial pH and PCO2, the formula to solve for bicarbonate is derived as follows:
For example, calculate HCO3 given pH 7.50 and PCO2 of 30 mm Hg.
7.50 = 6.1 + log [HCO3 /(30 x 0.0301)]
7.50 = 6.1 + log (HCO3/0.9)
1.4 = log (HCO3 /0.9)
inv. log 1.4 = (HCO3 /0.9)
25 = (HCO3 /0.9)
25 X 0.9 = HCO3 = 23 mmol/L
145. 8/15/23 Aaser Abdelazim Clinical Biochemistry 145
Venous Versus Arterial Samples:
There are five main evaluations we need to consider in interpreting ABGs in the
clinical setting:
1)Acid-base status
2)Alveolar ventilation
3)Oxygenation status
4)O2 transport
5)Carboxyhemoglobin
146. 8/15/23 Aaser Abdelazim Clinical Biochemistry 146
ACID-BASE STATUS
(1) Metabolic Acid-Base Disturbances:
Metabolic acidosis Metabolic alkalosis
qDiabetic ketoacidosis qVomiting
qUremia qGastric suction
qRenal tubular acidosis qLow potassium or chloride level
qLactic acidosis qLiver cirrhosis with ascites
qGIT loss of HCO3 , fluids and
potassium
qCorticoid excess (Mineralocorticoids)
qToxins qMassive blood transfusion
qHypertension due to dehydration qHigh doses of alkalis in acidosis
148. 8/15/23 Aaser Abdelazim Clinical Biochemistry 148
APPROACH TO INTERPRETING ACID-BASE DISTURBANCE:
In order to interpret acid-base disturbances, the following five factors are considered:
1. pH
2. HCO3–
3. PCO2
4. Anion gap
5. Assessment for compensation
qVentilation and PCO2 relationship
oVentilation is inversely proportional to the resulting PCO2.
oVentilation increases in response to a drop in plasma and cerebrospinal fluid
(CSF) pH detected by the respiratory center in the medulla.
oLikewise, the kidneys compensate for a primary respiratory defect. The respiratory
system can never completely compensate for a metabolic defect, but renal
compensation can almost be complete.
149. 8/15/23 Aaser Abdelazim Clinical Biochemistry 149
qSteps for determination of acid base disturbances:
Steps Interoperation
1) Determine if the patient is acidemic or
alkalemic, based on pH.
Normal pH 7.4±0.03
2) The primary disorder is determined by
evaluating HCO3– and PCO2
1. If HCO3– is elevated and pH is elevated, there
is metabolic alkalosis.
2. If both are decreased, there is metabolic
acidosis.
3. If HCO3– is within the normal reference range
and PCO2 is elevated but the patient is
acidotic, the condition is respiratory acidosis.
4. If bicarbonate is within the normal reference
range and PCO2 is decreased but the patient
is alkalotic, the condition is respiratory
alkalosis.
3) Determine the anion gap from the formula
Anion gap= (Na+K)-(Cl+HCO3) or (Na)-(Cl+HCO3)
So anion gap is the difference between cations and
anions in the blood Normal = 10-20 mmol/L and
without K = 6-15 mmol/L
In metabolic acidosis and mixed acid-base
disorders, the anion gap is significantly elevated.
4) pH, HCO3–, and PCO2 are considered to
determine if compensation is as expected based
on the typical ratio of 20:1 for bicarbonate to
carbonic acid.
1. both decreased HCO3– and PCO2 should
produce a slightly decreased or nearly normal
pH if they are in metabolic acidosis
compensation.
150. 8/15/23 Aaser Abdelazim Clinical Biochemistry 150
Steps Interoperation
4) pH, HCO3–, and PCO2 are considered to
determine if compensation is as expected based
on the typical ratio of 20:1 for bicarbonate to
carbonic acid. ...........(Continued)
2. To determine the actual ratio of bicarbonate to
carbonic acid, PCO2 is converted to H2CO3
using the relationship PCO2 X0.03 =H2CO3
3. Metabolic acidosis with a normal anion gap
is associated with:
A. renal diseases such as proximal or distal
renal tubular acidosis,
B. Renal insufficiency with HCO3– loss,
C. Hypoaldosteronism with potassium-sparing
diuretics.
D. Other causes include loss of alkali due to
diarrhea or ureterosigmoidostomy or ingestion
of carbonic anhydrase inhibitors, such as the
medications used to treat glaucoma.
4. Metabolic acidosis with a high anion gap is
generally due to:
A. Addition of acid from ketoacidosis;
B. Lactic acidosis from hypoperfusion or
decreased circulation
C. Toxic ingestions of aspirin, ethylene glycol, or
methanol.
D. Renal insufficiency.
Compensation for metabolic acidosis or alkalosis is achieved initially by the
respiratory system. How?!
151. 8/15/23 Aaser Abdelazim Clinical Biochemistry 151
RESPIRATORY DISORDERS
Disorders Diagnosis
Chronic bronchitis These patients have chronic hypoxia, as indicated
by low SO2 and PO2, and CO2 retention, as
indicated by increased bicarbonate and PCO2.
Fetal Lung Maturity 1. Immature fetal lung resulted from the decrease
in the lung surfactant (phosphatidyl choline,).
2. It occurs to premature babies (< 37 weeks) or
weight < 2500 g.
3. causing decreased oxygenation of the
collapsed alveoli and cyanosis and respiratory
distress in the neonate
Respiratory Distress Syndrome (RDS) The arterial blood gases initially indicate
1.Very low PO2,
2.Normal or low PCO2, and
3.Elevated pH causing respiratory alkalosis.
152. 8/15/23 Aaser Abdelazim Clinical Biochemistry 152
ALCOHOL
Aaser M. Abdelazim
Professor of Medical Biochemistry
153. 8/15/23 Aaser Abdelazim Clinical Biochemistry 153
ALCOHOL
qAlcohol is a drug with no receptors.
qIts effect on the cells and organs is not understood.
qFor clinical purposes alcohol is calculated in units (One unit = 200-300 mmol of ethanol).
qThe legal limit for driving in countries like UK is (80 mg/dl/17.4 mmol/L) and there is a
pressure to be (50 mg/dl / 10.9 mmol/L.)
qEthanol (EthOH) contents of some drinks shown in figure (1).
154. 8/15/23 Aaser Abdelazim Clinical Biochemistry 154
Effect of Ethanol on organs system
Organ Condition Effect
CNS Acute Disorientation and coma
Chronic Memory loss and pschycoses
Withdrawal Seizures, delirium tremens
Cardiovascular Chronic Cardiomayopathy
Skeletal muscles Chronic Myopathies
Gastric mucosa Acute Irritation and gastritis
Chronic Ulcerations
Liver Chronic Fatty liver, cirrhosis,
deceased tolerance to
xenobiotics
Kidney Acute Diuresis
Blood Chronic Anemia, thrombocytopenia
Testes Chronic Impotence
155. 8/15/23 Aaser Abdelazim Clinical Biochemistry 155
ALCOHOL METABOLISM
Alcohol (EthOH) is metabolized into acetaldehyde by two main pathways:
1.Alcoholic dehydrogenase produce acetaldehyde when the level (1-5 mmol/L).
2.Microsomal P450 oxygenase produce also acetaldehyde at levels above 5 mmol/L.
H2O
Alcohol
(1) Alcohol dehydrogenase
NAD+ NADH+H
Acetaldehyde
O2
(2) Microsomal P450 oxygenase
NADPH+H NADP+
H2O2
Catalase
156. 8/15/23 Aaser Abdelazim Clinical Biochemistry 156
ACUTE ALCOHOL POISONING
Acute alcohol poisoning carried in to two categories:
1) Alcoholic coma
§ It is difficult to distinguish alcoholic coma from the coma due to head injuries or coma due
to other drugs.
§ Blood ethanol level is a good guide for these conditions also blood osmolality and osmolal
gap is useful.
1) Continual alcohol metabolism due to continual high concentrations.
Recovery from acute alcohol poisoning
qThe recovery is rapid in absence of renal and hepatic disorders
qThe elimination is increased if there is a high hepatic blood flow and high oxygenation.
qUsually alcohol induce hypoglycemia (6-36 hours) after ingestion due to inhibition of
gluconeogenesis especially when there is malnutrition or fasting.
qKetoacidosis may be developed in some drinkers with malnutrition.
157. 8/15/23 157
Dr/ Aaser Abdelazim ---- lecturer of Medical
Biochemistry and Molecular Biology
EthOH Acetaldehyde
ADH
Acetate
Acetaldehyde dehydrogenase (ALDH)
NAD NADH+H
Pyruvate
Lactate
NAD NADH+H
Oxaloacetate
Malate
LDH
MDH
Both are sources for gluconeogenesis
MECHANISMS OF HYPOGLYCEMIA INDUCED BY
ALCOHOL TOXICITY
ACIDOSIS
HYPOGLYCEMIA
Aaser Abdelazim Clinical Biochemistry
159. 8/15/23 Aaser Abdelazim Clinical Biochemistry 159
CHRONIC ALCOHOL ABUSE
Chronic alcohol abuse effect due to
qAcetaldehyde toxicity
qFailure of one or more of haemostatic and synthetic mechanisms in liver
Effects of chronic alcohol abuse:
(1) HEPATOMEGALY: due to high TAGs (as it excessively synthesized in liver from
carbohydrates) and low protein concentration.
(2) IMPAIRED GLUCOSE TOLERENCE AND DIABETES MELLITUS.
(3) HYPERTRIGLYCERIDEMIA
(4) LIVER CIRRHOSIS
(5) PORTAL HYPERTENSION (lead to esophageal varices).
(6) COAGULATION DEFECTS
(7) CARDIOMYOPATHY
(8) PERIPHERAL NEUROPATHY
160. 8/15/23 Aaser Abdelazim Clinical Biochemistry 160
DIAGNOSIS OF CHRONIC ALCOHOLIC ABUSE
qIt is difficult to diagnose chronic alcohol abuse and usually determined by history.
qThere is no specific markers for ethanol abuse.
qHowever some blood components may be useful in the diagnosis of chronic alcohol abuse.
Blood components Comments
Uric acid Some patients show hyperuricemia
GGT 80% of alcohol abusers show high blood GGT BUT
qit induced by other drugs like phenytion & phenobarbitone.
qNot specific (induced by all liver disorders)
qUsed to monitor alcohol abuse.
TAGs High triglycerides (high synthesis from carbohydrates in liver)
Transferrin High in 90% of alcohol abusers