This document provides an overview of the approach to diagnosing malabsorption syndromes. It begins with an introduction to maldigestion and malabsorption. It then describes the three phases of digestion and absorption - luminal, mucosal, and post-absorptive. Common defects in each phase are discussed along with the clinical features, examination findings, and tests used to diagnose specific nutrient malabsorptions of fat, carbohydrates, proteins, vitamins, and minerals. A variety of imaging, endoscopic, histologic, and other diagnostic tests are described. The document concludes with typical etiologies found for malabsorption syndromes.
• Coeliac disease is a genetically-determined chronic inflammatory intestinal disease induced by an environmental precipitant, gluten.
• Patients with the disease might have mainly non-gastrointestinal symptoms, and as a result patients present to various medical practitioners.
• Epidemiological studies have shown that coeliac disease is very common and affects about one in 250 people.
• The disease is associated with an increased rate of osteoporosis, autoimmune diseases, and malignant disease, especially lymphomas.
• The mechanism of the intestinal immune-mediated response is not completely clear, but involves an HLA-DQ2 or HLA-DQ8 restricted T-cell immune reaction in the lamina propria as well as an immune reaction in the intestinal epithelium.
To know basic etiology of this disease and difference between duodenal ulcer and peptic ulcer as well as how we can approach if children having peptic ulcer disease. By conservative and surgical means
• Coeliac disease is a genetically-determined chronic inflammatory intestinal disease induced by an environmental precipitant, gluten.
• Patients with the disease might have mainly non-gastrointestinal symptoms, and as a result patients present to various medical practitioners.
• Epidemiological studies have shown that coeliac disease is very common and affects about one in 250 people.
• The disease is associated with an increased rate of osteoporosis, autoimmune diseases, and malignant disease, especially lymphomas.
• The mechanism of the intestinal immune-mediated response is not completely clear, but involves an HLA-DQ2 or HLA-DQ8 restricted T-cell immune reaction in the lamina propria as well as an immune reaction in the intestinal epithelium.
To know basic etiology of this disease and difference between duodenal ulcer and peptic ulcer as well as how we can approach if children having peptic ulcer disease. By conservative and surgical means
INTRODUCTION
Dislocation of the hip is a common injury to the hip joint. Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis. This may happen to a varying degree. A dislocated hip, much more common in females than in males, is a condition that can either be congenital or acquired
Definition
• A dislocation is an injury in which a bone is displaced from its proper position
CLASSIFICATION
The relationship of the femoral head to the acetabulum is used to classify the dislocation. The three main patterns are posterior, anterior, and central.
POSTERIOR HIP DISLOCATION
Posterior dislocations account of more than 90% of dislocations and occur when the knee and hip are flexed and a posterior force is applied at the knee.
Posterior hip dislocations occur typically during MVAs, especially head-on collisions, when the knees of the front-seat occupant strike the dashboard. Energy is transmitted along the femoral shaft to the hip joint. If the leg is struck while in an adducted position, a posterior dislocation may result. If the leg is in neutral or an abducted position when struck, an anterior dislocation or fracture/dislocation may occur. In the latter case, the posterior wall of the acetabulum is fractured, making subsequent reduction less stable.
Several classification systems are used to describe posterior hip dislocations.
• The Thompson-Epstein classification is based on radiographic findings.
o Type 1 – With or without minor fracture
o Type 2 – With large, single fracture of posterior acetabular rim
o Type 3 – With comminution of rim of acetabulum, with or without major fragments
o Type 4 – With fracture of the acetabular floor
o Type 5 – With fracture of the femoral head
• The Steward and Milford classification is based on functional hip stability.
o Type 1 – No fracture or insignificant fracture
o Type 2 – Associated with a single or comminuted posterior wall fragment, but the hip remains stable through a functional range of motion
o Type 3 – Associated with gross instability of the hip joint secondary to loss of structural support
o Type 4 – Associated with femoral head fracture
Indigestion — also called dyspepsia or an upset stomach — is discomfort in your upper abdomen. Indigestion describes certain symptoms, such as belly pain and a feeling of fullness soon after you start eating, rather than a specific disease.
Fat, protien, lipids, carbohydrate Malabsorption and Chronic PancreatitisRebilHeiru2
Malabsorption is discussed among with chronic pancreatitis. This was a seminar presented at Gasteroenterology Unit at Adama Hospital Medical college. Fat, lipid, carbohydrate, minerals and vitamins absorption physiology and Pathologies with their approach to diagnosis and Mangement.
Short bowel syndrome (SBS) is a devastating condition in which small intestinal length is inadequate and characterized clinically by inability to absorb adequate enteral nutrition to sustain normal growth and development.
- 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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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).
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
2. INTRODUCTION
• Maldigestion: Defective intraluminal hydrolysis of nutrients. There is
impaired breakdown of nutrients (carbohydrates, protein, fat) to
absorbable split-products (mono-, di-, or oligosaccharides;
aminoacids; oligopeptides; fatty acids; monoglycerides)
• Malabsorption: Defective mucosal uptake and transport of
adequately digested nutrients including vitamins and trace elements.
3. The integrated processes of digestion and absorption
can be described in three phases:
Luminal Phase
Mucosal phase
Postabsorbtive /Removal phase
Disturbances of the absorptive process can take place in any of these
three phases or defect in one or more than one can coexist
4. Normal physiology
• 3 major phases:
– Luminal phase
• dietary fats, proteins, and carbohydrates are hydrolyzed and solubilized depending largely on
pancreatic and biliary secretions.
– Mucosal phase
• During the mucosal phase, final hydrolysis and uptake of saccharides and peptides takes place
from lumen into cells and lipids taken up by epithelial cells are processed and packaged for
cellular export.
– Post-absorptive phase
• transported via lymphatics and portal circulation from epithelial cells to other parts of the
body.
5. Defects in luminal phase
A. Impaired nutrient hydrolysis
Digestive enzyme deficiency Chronic Pancreatitis, pancreatic cancer
Inactivation of digestive enzymes ZollingerEllison Syndrome
Inadequate mixing of nutrients, bile, and
pancreatic enzymes
rapid intestinal transit
Gastrojejunostomy
total and partial gastrectomy
Failure to convert a proenzyme to active
form
Enterokinase
trypsinogen deficiencies
B. Impaired micelle formation
bile salt synthesis Cirrhosis
Impaired bile secretion Chronic cholestasis
bile salt loss (impaired enterohepatic bile
circulation)
Ileal disease/resection
Bile salt de-conjugation Bacterial Overgrowth
C. Impaired luminal availability and processing
Bacterial consumption of nutrients Small intestinal bacterial overgrowth
intrinsic factor Pernicious anemia –B12Def
6.
7. Understanding of the normal absorptive process helps a great
deal to understand causes and consequences of malabsorption
and thus guide us in designing an appropriate differential
diagnostic strategy.
10. Within villus absorptive cells
• FA + MAG= TG
• Triglycerides, cholesterol esters, phospholipid, and apoproteins =
chylomicron
• Transported to the intestinal lymphatics
14. • Absorption- active transport (glucose and galactose) or passive transport
(fructose)
• Carbohydrates that are not digested and absorbed
• bacterial degradation in the colon
• formation of short-chain fatty acids (butyrate, propionate, acetate, lactate)
• additional energy source
• preferred energy source for colonic epithelial cells
• Production of hydrogen and methane
• basis of noninvasive breath tests
• to look for malabsorption of particular carbohydrates
17. Uptake into enterocytes of amino acids, di and tripeptides
takes place by secondary active transport intracytoplasmic
breakdown into amino acids then absorption of amino
acids across the brush border by facilitated diffusion.
18. VITAMIN, MINERAL, AND TRACE ELEMENT
ABSORPTION
• Fat-soluble vitamins (A, D, E, and K)
• require solubilization in a mixed micellar phase
• Most vitamins and minerals
• proximal half of the small intestine
• except vitamin B12 & magnesium
• Magnesium
• distal intestine (including the colon)
• Bariatric Sx - Roux-en-Y gastric bypass
• deficiency of Vitamin B12, iron, calcium, and vitamin D
19. CLINICAL FEATURES
• Global malabsorption
• Example -celiac disease
• Impaired absorption of almost all nutrients
• Diarrhea with pale, greasy, voluminous, foul-smelling stools and weight loss
despite adequate food intake
• Partial or isolated malabsorption
• Specific nutrient
• Symptoms attributable to the particular nutrient
20. History
• Diarrhea:
– Most common
– watery, reflecting the osmotic load received by the intestine.
– Bacterial action
• hydroxy fatty acids from undigested fat
• increase net fluid secretion
• furhter worsening the diarrhea.
21. • Steatorrhea :
– fat malabsorption
– pale, bulky, and malodorous stools
– float on top of the toilet water and are difficult to flush
– floating oil droplets in the toilet following defecation.
22. • Weight loss and fatigue:
– Weight loss common
– patients may compensate by increasing their caloric consumption, masking
weight loss
– Higher chances
• diffuse diseases
• such as celiac disease and Whipple disease.
23. • Flatulence and abdominal distention:
– Bacterial fermentation of unabsorbed food
– gaseous products
• Hydrogen
• methane
– flatulence
– abdominal distention and cramps.
24. • Edema :
– Hypoalbuminemia
• chronic protein malabsorption or loss of protein into the intestinal lumen
• peripheral edema.
– Extensive obstruction of the lymphatic system
• intestinal lymphangiectasia
• protein loss.
• severe protein depletion
– ascites
26. • Bleeding disorders :
– vitamin K malabsorption
– subsequent hypoprothrombinemia
– Ecchymosis usually is the manifesting symptom
– melena
– hematuria
27. • Metabolic defects of bones:
– Vitamin D deficiency
• osteopenia
• Osteomalacia
• Bone pain
• pathologic fractures
• Malabsorption of calcium
– secondary hyperparathyroidism.
28. • Neurologic manifestations :
– Electrolyte disturbances
• hypocalcemia and hypomagnesemia
• Tetany
• Trousseau sign and the Chvostek sign.
– Generalized motor weakness
• pantothenic acid
• vitamin D
– Peripheral neuropathy
• Thiamine
– Loss for vibration and position
• Cobalamin
– Night blindness
• vitamin A
– Seizures
• biotin
29. Examination
• General Physical Examination
orthostatic hypotension
weight loss,muscle wasting, or both
loss of subcutaneous fat
cheilosis, glossitis, or aphthous ulcers of the mouth
peripheral edema
30. • Abdominal examination:
– may be distended
– bowel sounds may be hyperactive
– Ascites
• severe hypoproteinemia.
35. DIAGNOSIS
• Malabsorption of fat
• Most commonly used indicator of global malabsorption
• Most complex absorption process among macronutrients
• Hence, most sensitive to interference from disease processes
• Most calorically dense macronutrient
• critical factor in the weight loss
36. TESTS FOR FAT MALABSORPTION
• Fecal fat determination
• In healthy people, daily fecal fat excretion is <6 g/d
• 72 hour sample is ideal because it reduces errors and variability
• 70 to 120 g/day of dietary fat
• Avoid nonabsorbable fat substitutes, such as olestra
• Sudan III stain
• Qualitative test
37. • Near infrared reflectance analysis
• Equally accurate but less time-consuming than a 72-hour fecal fat
• Simultaneous measurement of fecal fat, nitrogen, and carbohydrates in a
single sample
• Acid steatocrit
• Gravimetric assay
• Performed on a spot stool sample
38. TESTS FOR CARBOHYDRATE MALABSORPTION
• As a general rule, tests for carbohydrate malabsorption rely upon the
fermentation of undigested carbohydrates
• D-xylose test
• Measures the absorptive capacity of the proximal small intestine
• Pentose monosaccharide
• Active sodium transporter and by passive diffusion
• Measure of the permeability of the proximal small intestine, rather than a specific
defect in D-xylose absorption
• Overnight fast
• Ingests a 25 g dose of D-xylose
• Urine is collected for the next five hours
• Normal excretion of D-xylose is 6.0 +/- 1.5 g
• Serum D-xylose concentration less than 20 mg/dL suggests abnormal absorption
39.
40. • False positive:
• delayed gastric emptying
• impaired glomerular filtration
• Small intestinal bacterialovergrowth
• course of antibiotic (rifamixin) will improve d-xylose absorption
• Negative test: normal in pancreatic enzyme deficiency, Crohn disease
(due to involvement of distalsmall intestine), lactose intolerance
• Because no involvment of proximal intestine
41. • Lactose tolerance test
• Oral administration of a 50 g test dose
• Blood glucose levels are monitored at 0, 60, and 120 minutes
• Increase in blood glucose by <20 mg/dL + the development of symptoms is
Diagnostic
• Measurement of breath hydrogen following lactose challenge
• Increase in breath hydrogen by more than 20 ppm is diagnostic
42. TESTS FOR PROTEIN MALABSORPTION
• Generally not performed
• Technically difficult
• Plasma citrulline and arginine concentrations are highly correlated to
small bowel length
43. ADDITIONAL TESTS
• SeHCAT(Selenium homocholic acid taurine) test
• Bile acid malabsorption e.g terminal ileal disease, resection, primary bile salt
malabsorption.
• Primary bile salt malabsorption may reflect impaired fibroblast growth factor
19 feedback inhibition causing excessive bile acid synthesis
• Administration of a selenium75 labeled synthetic bile acid
• Followed by measurement of retention of the bile acid by whole body scan or
gamma camera at seven days (abnormal is less than 5 percent)
44. •Tests for bacterial overgrowth
• Direct quantitative measurement of bacterial counts from aspirated intestinal
fluid.
• Normal counts < 10(4)/mL in the jejunum and 10(5)/mL in the ileum
• Requires intubation of the intestine
• Hydrogen breath tests with lactulose
45. • Schilling test
• Identifies the cause of vitamin B12 malabsorption
• Rarely performed
• availability of serum B12 and methylmalonic acid to diagnose B12 deficiency
• easy use of oral crystalline or parenteral injection of B12.
• Nevertheless, there may be occasional patients in whom it can be
informative.
46. Stage 1
• Administer a small oral dose 1ug of radiolabeled vitamin B12
• within one or two hours, a large intramuscular flushing dose of nonradiolabeled
vitamin B12
• Unlabeled B12 saturates vitamin B12 carriers
• radioactive vitamin B12 absorbed by the intestine is excreted in the urine
• If less than 7% to 10% of the administered dose is recovered in urine within
24 hours
• vitamin B12 malabsorption is confirmed
47. Stage 2
• oral administration of intrinsic factor done.
• pernicious anemia
• normalize after oral administration of intrinsic factor
Stage 3- In small bowel bacterial overgrowth(SIBO
improve after antibiotic therapy
Stage 4-Patients with pancreatic exocrine insufficiency
normalize with addition of pancreatic enzymes
48. • Tests for pancreatic insufficiency
• Direct tests
• administration of a meal or hormonal secretagogues
• stimulation of the pancreas
• duodenal fluid is collected and analyzed
• quantify normal pancreatic secretory content (ie, enzymes, and bicarbonate).
• A normal person should release a large volume of bicarbonate-rich
pancreatic fluid in response to the intravenous injection of secretin.
• Indirect tests measure the consequences of pancreatic insufficiency
and are more widely available
• declined by more than 90 percent
• insensitive to early pancreatic insufficiency
49.
50. • Serology :
– Serum anti-TTG, Serum antigliadin ,antiendomysial antibodies
– many pts with biopsy confirmed celiac have negative IgA antibodies screen due to
concurrent selective IgA deficiency which is common in celiac disease
– If IgA serology is negative and suspicion is high
– Serum IgA -IgA deficiency.
– Determination of fecal elastase and chymotrypsin
• 2 proteases produced by the pancreas
• distinguish between pancreatic causes and intestinal causes of malabsorption.
51. • Small bowel barium studies:
• mucosa pattern associated with celiac disease
• obliterated or coarsened.
• Small bowel dilatation and diverticulosis
– scleroderma.
• Regional enteritis of the small intestine
– Stricture
– Ulceration
– fistula formation.
• Other anatomic abnormalities, such as surgical changes or enterocolonic fistula.
52. • Plain abdominal x-ray film:
– Pancreatic calcifications are indicative of chronic pancreatitis.
53. • CT scan of the abdomen:
– evidence of chronic pancreatitis, such as pancreatic calcification or atrophy
– Enlarged lymph nodes
• Whipple disease
• lymphoma.
54. • Endoscopic retrograde cholangiopancreatogram (ERCP):
– pancreatic or biliary-related disorders
Severe pancreatic duct
changes with dilation of
the main pancreatic duct
and of the primary and
secondary branches.
55. • Upper endoscopy with small bowel mucosal biopsy :
– Examples of conditions that can be diagnosed this way include
• celiac sprue, giardiasis, Crohn disease, Whipple disease, amyloidosis,
abetalipoproteinemia, and lymphoma.
Scalloped duodenal folds
seen on endoscopy in a
patient with celiac disease.
57. • Histologic Findings:
– Depending on the cause
– A frequently encountered histologic finding
• villous atrophy
– celiac disease,
– tropical sprue,
– viral gastroenteritis,
– bacterial overgrowth,
– inflammatory bowel disease,
– immunodeficiency syndromes,
– lymphoma, and
– radiation enteritis.
58. ASPIRATION
• Fluid aspirated- Descending part of duodenum/jejunum.
• Examined microscopically for Giardia
• Cultured to detect SIBO- Gold standard for diagnosis. Normal counts
rarely exceed 10(4)/mL in the jejunum and 10(5)/mL in the ileum.
59. Video capsule endoscopy(VCE)
• Used to diagnose a wider range of disease such as crohn’s ds, celiac
disease and other malabsorptive disease.
• In refractory celiac disease, VCE can detect changes such as
ulcerations and strictures that suggest T- cell lymphoma.
60. Balloon Enteroscopy
• In some case of malabsorption, balloon enteroscopy with biopsies of the jejunum
and ileum can be helpful to establish the diagnosis.
• Comparison of VCE and BE
• Advantage-biopsy from altered mucosa area
• Disadvantage- time consuming and uncomfortable for the patients
61. • Tropical sprue (37%)
• CD (19%)
• Small intestinal bacterial overgrowth (10%)
• AIDS (5.4%)
• Giardiasis (5%)
• Hypogammaglobulinemia (4%)
• Intestinal tuberculosis (2.5%)
• Strongyloidiasis (2%)
• Immunoproliferative small intestinal disease (2%)
• Crohn’s disease 6 (2%), amyloidosis (1.5%)
• Intestinal lymphangiectasia (1%)
• Unknown (8%)
• Spectrum of malabsorption syndrome among adults & factors differentiating celiac disease &
tropical malabsorption Uday C. Ghoshal, Mansi Mehrotra, Sunil Kumar, Ujjala Ghoshal*, Narendra
Krishnani**,Asha Misra, Rakesh Aggarwal & Gourdas Choudhuri:Indian J Med Res 136, September
2012, pp 451-459
62. • Tropical sprue (29%)
• Celiac and Crohn's disease (15.3% each)
• Parasitic infestations (9.7%)
• Immune deficiency disorders (5.6%)
• Intestinal tuberculosis ( 2.4%)
• Spectrum of malabsorption in India--tropical sprue is still the leader.Dutta AK , Balekuduru A,
Chacko A. J Assoc Physicians India. 2011 Jul;59:420-2.
63. Management
• Two basic principles
– correction of nutritional deficiencies
– treatment of causative diseases.
64. • Nutritional support :
– Supplementing various minerals, such as calcium, magnesium, iron, and
vitamins, which may be deficient in malabsorption, is important.
– Caloric and protein replacement also is essential.
– Medium-chain triglycerides can be used as fat substitutes because they do not
require micelle formation for absorption and their route of transport is portal
rather than lymphatic.
– In severe intestinal disease, such as massive resection and extensive regional
enteritis, parenteral nutrition may become necessary.
65. • Treatment of causative diseases :
– lactose-free diet helps correct lactose intolerance; supplementing the first
bite of milk-containing food products with Lactaid also helps.
– Protease and lipase supplements are the therapy for pancreatic insufficiency.
– Antibiotics are the therapy for bacterial overgrowth.
– Corticosteroids, anti-inflammatory agents, such as mesalamine, and other
therapies are used to treat regional enteritis
66. Treatment of tropical sprue
• Treat deficiencies of Ca, Mg,K,vitamins A ,B, D.
• Parenteral vitamin B12, oral folate and iron replacement result in prompt
resolution of symptoms of anaemia, glossitis and anorexia, and result in weight
gain even before improvement in intestinal absorption.
• Folate supplementation improves villous atrophy.
• Antimicrobial agents :Tetracycline 250 mg four times daily (or doxycycline 100
mg once daily) for 3–6 months.
• Complete recovery is the rule in the returned traveller.
• In endemic sprue, relapses are common, occurring in 50% of affected people.
67. Management of celiac sprue
• Gluten-free diet helps treat celiac disease
Eliminate wheat, oats, rye, and barley from the diet
Beer, whiskey, and most vodkas are derived from wheat
WINE IS OKAY
• Pneumococcal vaccination as celiac ds is associated with hyposplenism
• Treatment with sulfones (dapsone) for dermatitis herpetiformis
• Screening of family members
• Steroids
• Refractory sprue
• Acute celiac crisis/ Celiac shock after gluten challenge
• Associated autoimmune hepatitis
68. Conclusion
• Etiology of malabsorption in tropical areas differs from that in
temperate countries
• Tropical sprue ,tuberculosis - a common cause of malabsorption in
India
• Celiac disease and inflammatory bowel disorders are emerging as
important causes
• Detailed history ,physical examination is mandatory
• The order of testing and choice of a particular test should be
individualized while considering the availability and expertise needed
for specialized testing.
• Emphasis should be put on defining an underlying disease entity
which then provides the basis for appropriate treatment.