This document discusses diarrhea and provides details about its normal physiology and defining features. It covers three main sections: 1) Importance, normal function, and defining diarrhea, 2) The various implications of diarrhea including pathophysiology, classification, differential diagnosis, and treatment, 3) A case discussion on diarrhea to answer relevant questions. Key points include definitions of acute vs chronic diarrhea, classifications of chronic diarrhea into secretory, osmotic, steatorrheal, inflammatory, and other causes, and discussions of the normal motility, absorption and secretion in the gastrointestinal tract.
Diarrhea is loose, watery stools. Having
diarrhea means passing loose stools three or more times a day. Acute diarrhea
is a common problem that usually lasts 1 or 2 days and goes away on its own.
Diarrhea lasting more than 2 days may be a
sign of a more serious problem. Chronic diarrhea—diarrhea that lasts at least 4
weeks—may be a symptom of a chronic disease. Chronic diarrhea symptoms may be
continual or they may come and go.
Diarrhea of any duration may cause
dehydration, which means the body lacks enough fluid and electrolytes—chemicals
in salts, including sodium, potassium, and chloride—to function properly. Loose
stools contain more fluid and electrolytes and weigh more than solid stools.
People of all ages can get diarrhea. In the
United States, adults average one bout of acute diarrhea each year, and young
children have an average of two episodes of acute diarrhea each year.
This presentation is about Malnutrition in Pediatrics; Epidemiology, Risk factors, etiology, Clinical Evaluation, plotting on Growth charts and Management are Covered.
Diarrhea is loose, watery stools. Having
diarrhea means passing loose stools three or more times a day. Acute diarrhea
is a common problem that usually lasts 1 or 2 days and goes away on its own.
Diarrhea lasting more than 2 days may be a
sign of a more serious problem. Chronic diarrhea—diarrhea that lasts at least 4
weeks—may be a symptom of a chronic disease. Chronic diarrhea symptoms may be
continual or they may come and go.
Diarrhea of any duration may cause
dehydration, which means the body lacks enough fluid and electrolytes—chemicals
in salts, including sodium, potassium, and chloride—to function properly. Loose
stools contain more fluid and electrolytes and weigh more than solid stools.
People of all ages can get diarrhea. In the
United States, adults average one bout of acute diarrhea each year, and young
children have an average of two episodes of acute diarrhea each year.
This presentation is about Malnutrition in Pediatrics; Epidemiology, Risk factors, etiology, Clinical Evaluation, plotting on Growth charts and Management are Covered.
osmotic and secretory diarrhea. acute and chronic diarrhea. small bowel and large bowel diarrhea. amoebic and bacillary dysentery. investigation. treatment.
Dr. Adam Moeser - Gut Physiology from a Pathogens Point of ViewJohn Blue
Gut Physiology from a Pathogens Point of View - Dr. Adam Moeser, North Carolina State University, from the 2014 Boehringer Ingelheim North Carolina Swine Health Seminar, August 15, 2014, Wrightsville Beach, North Carolina, USA.
More presentations at http://www.swinecast.com/2014-boehringer-ingelheim-carolina-swine-health-seminar
Diarrhea & Constipation by dr Mohammed Hussien.
Ass. Lecturer of Gastroenterology & Hepatology
Kafrelsheik University
Membership at American Collage of Gastroenterology (ACG)
Membership at Egyptian association for Research and training in Hepatogastroentrology
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
- 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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
2. Plan
Section (1):
Importance, normal function, and defining the
subject
Section (2):
The subject and its various implication
(pathophysiology, classification, differential,
treatment… etc.)
Section (3):
Case discussion on the subject, and attempting to
answer the relevant questions
4. Importance
• Very common
• 1 billion suffer from an episode of acute
diarrhea worldwide each year
• 250,000 require hospitalization
• 5000 die (mostly elderly)
• Economic burden may exceed $20 billion
– Infectious and acute – most common
– Mostly developing countries, contrary to
constipation, mostly developed counteries.
5. Importance - 2
• Can be a mere nuisance symptopms at one
extreme
• On another, they can be life-threating.
– Mild symptoms can signal serious underlying illness
• Colorectal cancer
• Thyroid disease
• Imperative for clinicians to appreciate the
pathyophysiology, etiologic classification, and
diagnostic strategies, as well as principles of
management
6. Normal Physiology
• Small intestines digest and assimilate food
– Colon + Intestine do also:
• secretion + absorption of water & electrolyte
• Storage & transport of intraluminal contents aborally
• Salvage of nutrients after bacterial metabolism that are not
absorbed in small intestines.
– Alterations in fluid and electrolyte handling contribute
significantly to diarrhea.
– Alterations in motor + sensory functions of colon
result in highly prevalent syndromes such as IBS,
chronic diarrhea, and chronic constipation.
7. Functional level at different sites
• Stomach and small bowel:
– Synchronized MMC in fasting
– Accommodation, trituration, mixing, transit
• Stomach ¬ 3h
• Small Bowel 3 h
– Illeal Reservoir empties boluses
• Colon: irregular mixing, fermentation, absorption,
transit
– Ascending + transverse: resvervoirs
– Descending: Conduit
– Sigmoid/rectum: volitional reservoir
8. Neural control
• Intrinsic innervation (Enteric nervous system):
– Myenteric, submucosal, and mucosal neuronal layers
• They modulate the action of neurostransmiters (eg., Ach,
VIP, Opoids, NE, SE, ATP, and NO)
• Myenteric – smooth muscle
• Submucosal plexus – absorption + secretion
• Mucosal - blood flow
• Extrinsic: ANS: Vagus Small intestine+ proximal
colon; pelvic parasympathetic (S2-4) distal
colon; major substance: Ach, and Substance P.
– Sympathetic = excite sphincter + inhibit nonsphinteric
muscles
9. Its normal function
• Visceral afferents convey sensation from the gut
to CNS:
– Course along sympathetic fibres
– Go to cell bodies in DRG (in spinal cord)
– Go to dorsal horn of spinal cord
– Conveyed to brain along the lateral spinothalamic
tract + nocireceptive dorsal column pathway
– Projected after thalamus to insula + cerebral cortex to
be perceived.
• Others are just afferent synapses in prevertebral ganglia and
reflexly modulate intestinal motility
10. Intestinal Fluid Absorbtion and
Secretion
• Daily average 9 L of fluid in GI tract
– 1 L reaches colon as residual
• Stool excretion of fluid is about 0.2 L/d
• Colon has large capacitance and functional reserve
• Can recover four times its usual volume of 0.8 L/d
– Very helpful in intestinal absorptive or secretory disorders
– Sodium absorption in colon, ‘’electrogenic’’ @ apical
membrane.
• Neural plus non neural mediators affect the colon, such as
cholinergic, adrenergic and serotonergic mediators
• Can be affected by angiotensin + aldostrone secretion
– Due to Renal tubules have similar embryologic origin of distal
colon
11. Motility of Small Intestine
• cyclical event migrating motor complex MMC
– serves as a housekeeper to clear nondigestiable
residues
– Occurs while fasting
– On average 4 mins of propagation and contraction
– Occurs every 60-90 minutes.
• If you eat: small intestine produce irregular
mixing contraction of low amplitude
– Except at distal illium where powerful intermittent
contraction occur to empty illeum by bolus transfers
12. Ileocolonic Storage and Salvage
• Distal ileum acts as a reservoir and emptying place for bolus movements
intermittently
– Allows time to salvage of fluid + nutritents + electorlytes
• Segmentation by haustra in colon
– Compartmentalises food + facilitate mixing
– Rentention of residue + forms stools
• Resident bacteria in colon
– Digest unabsorbed carbohydrates
• Provides nutrients to mucosa
• Diarrhea happens due to alteration of
– its reservoir function @ proximal site
– Or Propulsive function @ left colon
• Contstipation happen as a result of disturbance of
– Rectal or segmoidal resoirvoir
– Dysfunction of pelvic floor
– Coordination of defecation
13. Defining it: Diarrhea
• Loosely defined as:
– Passage of abnormally liquid or unformed stools
– @ increased frequency
– For weight > 200 g/d
– Acute < 2 weeks, persistant 2-4 weeks
– Chronic > 4 weeks in duration
• < 200 g/d stool weight
1) Pseudodiarrhea – frequent urgency of passage of small volumes of
stool ( IBS or Proctits)
2) Fecal incontinence, involuntary discharge of rectal contents –
caused, often, by neuromascular or antorectal problems
– They should be always investigated in patients complaining of
‘’diarrhea’’
• Overflow Diarrhea due to fecal impaction happens in nursury
homes mostly
14. Acute Diarrhea
• 90% infectious agents
– Accompanied by:
• Fever Vomitting Abdominal pain
• Remaining 10%:
– Medication Toxins Ischemia Others
• Infectious agents: Fecal-oral transmission
– Infected food or contaminated water
– Disturbed flora by Antibiotics (C.dif.)
– Bypassing immune + non-immune defense mechanism
– Five high-risk group in US: Travelers, Food consumers,
Immunodeficient, daycare attendee and their family members, and
institutionalised patients.
– Clincial features: Profuse watery diarrhea secondary to intestinal
secretion.
– Treatment: Fluid and electrolyte replacement, ‘’ maybe’’ Antibiotics
15. The subject and its various
implication (pathophysiology,
classification, differential,
treatment… etc.)
17. Secretory causes
• Exogenous Stimulant Laxatives
• Chronic Ethanol Ingestions
• Other drugs and toxins
• Endogenous laxatives (dihydroxy bile acids)
• Idiopathic secretory diarrhea
• Certain bacterial infection
• Bowel resection
• Hormone producing tumors (VIPOMA, carcinoid, medullary
cancer of thyroid, mastocytosis, gastrinoma, colorectal
villous adenoma)
• Addison’s disease
• Congenital Electolyte absorption defect
18. Secretory causes
• Due to derangements in fluid and electrolyte
transport across the enterocolonic mucosa
– Characterised clinically by:
• Watery, large volume fecal utputs
• Typically painless and persist with fasting
• Thereis no malabsorbed solute
– Stool osmolality is accounted for by normal
endogenous electrolite with no fecal osmotic gap.
19. Medication
• Side effects from ingestion of drugs and toxins
– Most common secretory cause
• Over the counter medications
• Habitual use of stiumulant laxitives[e.g., senna, cascara]
• Chronic Ethanol consumption Enterocyte injury
– Impaired sodium and water absorption
• Inadvertant ingestion of certain toxins (e.g., arsenic)
• Bacterial infections occassionally persist and cause it
20. Bowel Resection, Mucosal Disease, or
Entercolic Fistula
• Inadquate surface for reabsorption of secreted fluids +
electrolyte
– Unlike other subsets:
• They tend to be worse while eating
• With disease states e.g., Chron’s ileitis or resection of <100 cm of
terminal illium
– Dihydroxy bile acids may escape absorption and stimulate colonic secretion
(Cholorrheic diarrhea)
» Called ‘’Idiopathic secretory diarrhea’’
• Idiopathic bile acid malabsorption 40% of unexplained chronic
diarrhea
• Fibroblast growth factor (FGF) 19 produced by eneterocyte results
in synthesis of excessive bile acids too much to be reabsorbed by
ileal function.
• It causes bile acids diarrhea
• Partial bowel obstruction, ostomy striction, or fecal impaction
– Can lead to paradoxically increased fecal output due to fluid hyper secretion
21. Hormones
• Uncommon, yet classic example for secretory.
– Metastatic Carcinoid tumors
• Produce watery diarrhea alone or as part of carcinoid sx
– Episodic flushing, Wheezing, Dysnea, Rt sided vavular heart dx
– Intestinal secretagogues (SE, Hista., PGC)
• Pellagra-like skin lesion, rarely happen due to serotonin with niacin depletion
– Gastrinoma (neuroendocrine tumor)
• Refractory peptic ulcer and diarrhea due to fat mal-abs.
– Watery diarrhea hypokalemia achlorhydria syndrome (Pancreatic cholera)
• Due to non-B cell pancreatic adenoma or VIPOMA
– Secretion of VIP and a host of other peptides.
• Often massive stool volume >3 L/d; daily, up to 20 L can be.
• Life threatening complications: dehydration, neuromascular dysfunction from electrolyte imbalance. Flushing, and
hyperglycemia may accompany VIPOMA
– Medullary carcinoma of thyroid
• Watery diarrhea due to calcitonin
– Systemic mastocytosis
• Associated with skin lesion, urticaria pigementosa
• Cause diarrhea that is secretory by histamine due to intestinal infiltration of mast cells
– Large colorectal villous adenoma
• Rarely associated with secretory diarrhea
• May cause hypokalemia, and can be inhibited by NSAID, and mediated by PGC
22. Congenital Defects in Ion Absorption
• Rarely, can cause diarrhea from birth.
– Include:
• Defective CL/HCO3 exchange (congenital chloridorrhea)
– With alkalosis (results from a mutated DRA [down regulated
adenoma] gene)
• Defective Na/H exchange (congenital sodium diarrhea)
– Results from a mutation in NHE3 (sodium hydrogen exchanger
gene
» Results in acidosis
• Adrenocortical insufficiency (addison’s disease)
– Can be accompanied with skin hyperpigmentation
23. Osmotic Cause
• Osmotic Diarrhea occurs when ingested, poorly
absorbably, osmotically active solutes draw enough fluid
into lumen to exceed the re-absorptive capacity of the
colon. Fecal water output increases in propotion to such
solute load. Ceases with fasting or with stopping
causative agents
• Examples:
– Osmotic laxatives (Mg, PO4, SO4)
– Lactase and other disacchride defeciency
– Nonabsorbable carbohydrates (sorbitol, lactulose,
polyethylene glycol)
24. Osmotic laxatives
• Ingestion of magnesium contaning antacid
– Typified by as tool of osmotic gap >50 mosmol/L
Serum Osmolarity (typically, 290 mosmol/kg) – [2 x(fecal
sodium + potassium concentration)]
Measurement of fecal somolarity is no longer
recommended
cause even when measured immediately after
evacuation
maybe erroneous because carbohydrates are
metabolized by clonic bacteria causing increase in
osmolarity
25. Carbohydrate malabsorption
• Acquired or congenital defects
– @ Brush border disaccharides
– Other enzymes
• Leading to osmotic diarrhea with low pH
– Common cause:
• Lactase deficiency
– Learn to avoid milk (3/4 of non-whites worldwide affected)
• Sugars: sorbitol, lactulose, or fructose Freq. mal-abs
• Ingestion of medications, gum, or candies sweetened
26. Steatorrheal causes
• Fat malabsorption may lead to:
– Greasy, foul smelling, difficult to flush diarrhea
– Associated with: Weight loss + nutritional loss
• Increased fecal output due to osmotic effect of fatty
acids. Quantitatively, steatorrhea is:
– Stool fat exceeding the normal 7 g/d
– Daily fecal fat averages 15-25 g with small intestine, and >
35 with pancreatic exocrine dysfunction. Its types:
1. Intraluminal maldigestion (pancreatic exocrine insufficiency,
bacterial overgrowth, bariatric surgery, liver disease)
2. Mucosal malabsorption (celiac sprue, Whipple's disease,
infections, abetalipoproteinemia, ischemia)
3. Postmucosal obstruction (1° or 2° lymphatic obstruction)
27. Intraluminal Maldigestion
• Pancreatic exocrine insufficiency >90% of pancreatic
function is lost.
– Chronic pancreatitis
• Sequel to ethanol abuse
– Cystic Fibrosis
– Pancreatic duct obstruction
– Rarely, somatostatinoma
• Bacterial overgrowth deconjucating bile aciss and alter
micelle formation
• Cirhossis or billiary obstruction leading to mild
steatorrhea due to deficient intraluminal bile acid
concentration
28. Mucosal Malabsorption
• Commonly, Coeliac Disease:
– Gluten sensitive enteropathy affects all ages
• Characteristic: villous atropy + crypt hyperplasia in proximal small bower
– Can present with fatty diarrhea associated with nutritional deficiency of varying severity
– Frequently without steatorrhea, can mimic IBS
• Tropical Sprue – similar histology + clinical
– Occur in residents or travellers to tropical climates
• Whipple’s disease
– Bacillus Tropheryma whipplei and histiocytic infiltration of small bowel mucosa
• Less common, and mostly young or middle aged men.
• Arthalgia, fever, lympadenopathy, and extreme fatigue
• Can affect CNS and endocardium
• Mycobacterium Avium intracellular infection in AIDS
• Abetalipoproteinemia
– Rare defect of chylomicron formation and fat malabsorption in children
– Association: acanthocytic erthrocyte, ataxia, and retinitis pigementosa
• Giardia: potozoal infection
• Medications (e.g., colchicine, cholestryamine, neomycin
• Amyloidosis
• Chronic Ischemia
29. Postmucosal Lymphatic Obstruction
• Rare: congenital intestinal lymphangiectasia
• Acquired: lymphatic obstruction
– Secondary to trauma, tumor, cardiac disease, or
infection
– Leads to unique constellation of fat malabsorption
with enteric losses of protein
– Lymphocytopenia
30. Inflammatory causes
• Generally accompanied by pain, fever, bleeding or
other inflammatory manifestation
– Mechanism depends on the lesion site which can be:
• Fat malabsorption
• Distrupted fluid/electrolyte absorption
• Hypersecretion or hyper motility from cytokines release
– Unifying features on stool analysis
• Presence of leukocytes or leukocyte derived proteins such as
‘’calprotectin’’
• With severe inflammation: exudative protein loss can lead to
anasarca
32. Idiopathic Inflamatory bowel disease
• Include: Chron’s disaese + Ulcerative colitis
– Range from mild to fulminant and life threatening
– Associated: uveitis, polyarthralgias, cholestatic liver
disease (primary sclerosing cholangitis), and skin esions
(erythema nodosum, pyoderma gangrenosum)
• Microscopic colitis: lymphocytic + collagenous collitis
– Chronic cause of watery diarrhea, esp. middle aged
women and NSAID, statins, PPI, SSRI people
– Biopsy of normal appearing colon is required for diagnosis
• Can exist with IBS or celiac sprue
• Responds wel to anti-infallmatory drugs e.g., bismuth, to opoid
agonist loperamide, or to budesonide
33. Others
• Primary or secondary Immunodeficiency
– Prolonged infectious diarrhea
• Selective IgA deficency
• Variable hypogammaglobulinemia
– Often prevalent and result of Giardiasis, bacterial overgrowth, or sprue
• Eosinophillic Gastroenteritis
– Eosinophil infilteration of mucosa, muscularis, or serosa causing diarrhea,
pain, vomitting, or ascitis
• Charcot leyden crystals due to extruded eosinophil contents on microscopic inspection of
stool
• Peripheral eosinophilia present 50-70% of patients
– Hypersensitivity to certain food can be present, but true allergy is rare
• Chronic inflammatory diarrhea:
– Radiation entercolitis
– Chrnic graft versus host disease
– Becht syndrome
– Cronkhite canada syndrome
34. Dysmotlity
• Rapid transit may accompany many diarrheas as a secondary or
contributing phenmnon.
– Primary dysmotility is unusual etiology of true diarrhea
• Stool features suggestion secretory diarrhea but mild steatorrhea of up to 14 g
of fat per day
• Hyperthyroidism, carcinoid syndrome and certain drugs (PGC, prokinetic
agents)
– Can produce hypermotility with resultant diarrhea
– Diabetic diarrhea, accompanied by peropheral and generalised
autonomic neuropathies.
– IBS is characterised by disturbed intestinal and colonic motor and
sensory responses to various stimuli.
• Smptomps of stool frequency typically cease at nigh
• Alternate with periods of constipation
• Accompanied by abdominal pain relieved by defecation
• Rarely, result in weight loss
35. Factitial causes
• Accounts 15% of unexplained diarrhea referred to
tertirary care centres, can be:
– Munchausen syndrome
– Eating disorders
– Self-adminstration of laxitatives or combination of
other medication (e.g., diuretics)
– Hypotension and hypokalemia are common co-presenting
features.
– History of psychiatric illness
– Disproportionately from careers in health care
36. Approach to The Patient: Chronic
Diarrhea
• Extensive workup, can be costly and invasive
• Direct it to History and physical examination first
• Hx + Px + Blood tests should attempt to characterize the
mechanism of diarrhea
– Through identifying diagnostically helpfful association
– Assess patients fluid/electrolte and nutrtional status
• Questions to be asked: Onset; duration; pattern;
aggrevating, and relieving factors; also, stool
characterization of their diarrhea.
• Presence of fecal incontinence, fever, weight loss, pain,
certain exposre (travel, medications, contacts with
diarrhea), and common extraintestinal manifestional (skin
changes, arthalgia, oral apthous ulcer)
37. • Therapeutic trial = appropriate + effective + definitive…
if we suspect a specific diagnosis
– Eg, chronic watery diarrhea that ceases with fasting in a
young adult
• DO LACTOSE RESTRICTED DIET
– Bloating and diarrhea persisting since a mountain
backpacking trip
• GIVE THEM METRNIDAZOLE for GIARDIASIS
– Post prandial diarrhea persisting following resction of
terminal ileum
• Maybe due to bile acid malabsorption
– GIVE THEM CHOLESTYRAMINE OR COLESEVELAM
– Yet persistant symptomops mean addition investigations
38. Additional investigation
• Suspect IBS:
– Evaluate with flexible sigmoidoscopy with colo-rectal
biopsy
• Normal findings = reassurance and treat empirically
– Antispasmodics, antidiarrhea, bulk agents, anxiolytic and
antidepressants.
• Chronic Diarrhea and hematochezia
– Evaluate with stool microbiologic studies and
colonscopy
39. We still we do not know..
• Quantitative stool collection
– Analayses yeild impottant objuctive data
• If stool > 200 g/d
– Do electrolyte concentration, pH, occult blood testing
– Leukocyte inspection (or leukocyte protein assay)
– Fat quantitation
– Laxative screens
• Secretory diarrhea (watery, normal osmotic gap)
– Possible medication related side effects (lax?)
– Microbiology for protozoas and parasites, Giardia antigen assay
– Small bowel aspirates to exclude bacterial overgrowth# with
quantitative cultures, glucose, or lactulose breath test
– Upper endoscopy and colonscopy with biopsies
– Small bowel x-ray with barium swallow
40. • Further evaluation of osmotic diarrhea
– Include tests for lactose intolerance + mg ingestion
– Low fecal pH suggests carbohydrate malabsorption
– Lactose malabsorption by lactose breath testing
• Fatty diarrhea
– Endoscopy with small bowel biopsy (aspirate for Giradia)
– Small bowel radiograph
– Pancreatic direct tests (secretin cholecystokinin stimulation test)
• Indirect tests such as assay of fecal elastase or chymotrypsin
• Bentiromide test because it has fallen out of favor because of sensitivity and specificity
• Chronic inflammatory-type diarrheas
– Presence of blood or leukocyte in stool
– Inspection for ova and parasites
– C. Difficile toxin assay
– Colonscopy with biopsy
– Small bowel contrast studies
41.
42.
43. Treatment: Chronic Diarrhea
• Depends on specific etiology
– Three modalities of treatment: Curative, suppressive or
empiracal
• Eradicated cause = Curative treamt eg., resection of a colonrectal
cancer or Antibiotics for Whipple’s disease
• Suppression of underlying condition eg., elimination of dietary
lactose for lactase deficiency or gluten for celiarc sprue, or use
steriods for idiopathic IBD; absorptive agens for illeal bile acid
malabsorption (cholestryramine) PPI (omeprazole) for gastric
hypersecretion of gastrinoma
• Empirical therapy beneficial for an evasive diagnosis
– Mild opiates for moderate diarrhea diphenoxylate or lopermide
– Codeine or tincture of opium for severe diarrhea
• Avoid antimotility in severe IBD to avoid toxic megacolon
• Clonidine, a2 adrengic agonist allow control for diabetic diarrhea
• Remember, it is always fluid and electrolyte replacement first.
• Fatty diarrhea, also replace them with fat soluble vitamins.
44. Case discussion on the subject, and
attempting to answer the relevant
questions
45. Case
• Abeer 23 year old female, Nurse
• Watery diarrhea 5x a day for a year
• Wake up at night – abdominal cramps
• Feeling need to empty her bowel (Tenismus)
• No relief or aggrevating symptomps ( Fasting =
less frequent)
• Past 6 months, she noticed weight loss of 5 kg
despite eating more
• No blood or mucos in stool
• No nausea, vomiting or fever
46. Px
• Pale, mildly dehydrated, and underweight (46 kg), height
162 cm
• BMI 17.5
• Blood Pressure = 110/58 mm Hg
• Pulse = 98 bpm
• RR = 18 bpm
• No clubbing, thyromegally, or lymphadenopathy
• Abdominal pain shows soft and non-tender abdomen with
no detectable ascites or organomegally
• Breast cardiovascular, chest, and neurological exam =
unremarkable
• There was mild lower limb edema
48. Questions - 1
1. What are the active problems in this patient?
– The active problems are Chronic Diarrhea, abdominal pain,
urgency, chronic weight loss
2. What other information in the history and physical examination
you need to know to reach the correct diagnosis?
3. What is the definition of diarrhea? When you label patient to
have acute vs chronic diarrhea?
4. How can you categorize chronic diarrhea?
49. Questions - 2
5. What laboratory tests you need to order (blood and stool) to
reach the diagnosis?
6. What do you think this young patient has? (Our DDx)
IBS
IBD
Pancreatice insufficiency
7. What further test you need to do to confirm the diagnosis?
8. Name the complications of chronic diarrhea.
9. How to assess nutrition in patient with chronic diarrhea?