This document discusses short bowel syndrome, which results from surgical resection or congenital defects that leave less than 200cm of small intestine. It causes an inability to maintain nutrition from a normal diet. Causes in adults include surgery, radiation, cancer, and diseases. In children, causes include birth defects affecting the intestines. Consequences include malnutrition, diarrhea, vitamin deficiencies, and electrolyte abnormalities. Management involves specialized diets, oral rehydration solutions, medication to slow transit or aid absorption, and in severe cases, intestinal transplantation. Surgical techniques can also increase surface area or slow transit to improve absorption.
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.
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.
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
Early management of SBS includes replacement of fluid and electrolytes.
Enteral feeding should begin once the patient stabilizes.
Continuous enteral feeding is preferred.
For enteral feedings, hypoallergenic protein hydrolysate formulas or breast milk are usually best tolerated
this is a detailed presentation on the principles of surgical nutrition. the presentation started with surgical metabolism and epidemiology of malnutrition in surgical patients. Furthermore, the aetiology of malnutrition was discussed in surgical patients. Finally, the various types of nutritional support, enteral and parenteral, was discussed under indications, types, access, advantages, disadvantages, complications and monitoring.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
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disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
- 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
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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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
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
2. INTRODUCTION:
A TYPE OF INTESTINAL FAILURE WHICH RESULTS FROM
EITHER
• SURGICAL RESECTION (USUALLY OCCUR WHEN TOTAL
BOWEL LENGTH IN SITU <200CM)
• CONGENITAL DEFECTS
• DISEASE ASSOCIATED LOSS OF ABSORPTION
CHARACTERIZED BY INABILITY TO MAINTAIN PROTEIN-
ENERGY, FLUID, ELECTROLYTE, OR MICRONUTRIENT
BALANCE WHEN ON A NORMAL DIET
4. Pathophysiologic Consequences of
Massive Resection
GENERAL
• Malnutrition and weight loss
• Diarrhea and steatorrhea
• Vitamin and mineral
deficiencies
• Fluid and electrolyte
abnormalities
SPECIFIC
• Gastric hypersecretion
• Cholelithiasis
• Liver disease
• Nephrolithiasis
6. Consequences of site specific resection
A. JEJUNAL RESECTION:
• LOSS OF DIGESTIVE ENZYMES- INITIAL AND
TEMPORARY REDUCTION IN NUTRIENT ABSORPTION
• LOSS OF PHYSIOLOGICAL GASTROINTESTINAL
FEEDBACK MECHANISM- RAPID GASTRIC EMPTYING
B.Duodenal resection
• PROTEIN , CHO, FAT MALDIGESTION
• CA, MG, IRON, FOLATE MALABSORPTION
• FAT SOLUBLE VIT DEFICIENCY
7. .
C.ILEAL RESECTION
• REABSORPTION OF SECRETED FLUID BY SMALL
INTESTINE LOST- NET SECRETORY RESPONSE
• LOSS OF B12 ABSORPTION
• LOSS OF ENTEROHEPATIC CIRCULATION- BILE
SALT DEFICIENCY AND FAT MALABSORPTION
• LOSS OF ILEAL-COLONIC BRAKE (PEPTIDE YY,
GLP-1, NEUROTENSIN)
8. .
D.LOSS OF ILEOCECAL VALVE:
SMALL INTESTINAL DILATTATION AND SLOWER
MOTILITY LEADING TO BACTERIAL
OVERGROWTH
BACTERIAL OVERGROWTRH IN TURN LEADS TO
MANY COMPLICATIONS SUCH AS:
Competition of nutrients, bacterial translocation,
endotoxemia, liver injury, D-lactic acidosis
9. .
E. LOSS OF COLON
• COLON IN CONTINUITY IS IMPORTANT AFTER A
MASSIVE SMALL BOWEL RESECTION AS COLON
ADAPTS FOR THE ABSORPTIVE FUNCTIONS OF
SMALL INTESTINE
• FERMENTATION OF MALABSORBED
CARBOHYDRATES TO SHORT CHAIN FATTY ACIDS
BY COLONIC FLORA
10. PROGNOSIS
• LENGTH OF BOWEL REMAINING
• PRESENCE OF COLON
• INTACT ILEOCECAL VALVE
• INTACT DUODENUM
• COMORBODITIES AND UNDERLYING CAUSE
(CROHNS DISEASE, RADIATION ENTERITIS,
PSEUDO-OBSTRUCTION)
ROLE OF CITRULLINE: <20uMOL/L indicative of
permanent intestinal failure
11. Phases Of SBS
• Acute Phase
Immediately after bowel resection and lasts for 1-3 months
Ostomy output greater than 5 liters per day
Life threatning dehydration and electrolyte imbalances
Extremely poor absorption of all nutrients
Development of hypergastrenemia and hyperbilirubinemia
12. Adaptation phase
Begins 12 – 24 hours after resection and last up to 1-2 years
90% adaptation occurs during this phase
Enterocyte, villus hyperplasia and increased crypt depth
ocurrs resulting in increased absorptive area
Luminal nutrition is essential for adaptation and should be
initiated as early as possible
Parenteral nutrition is essential through out this period
13. Maintenance phase
Absorptive capacity is maximum during this phase
Nutritional metabolic homeostasis can be achieved with
oral feeding
14. COMPLICATIONS OF SHORT BOWEL SYNDROME
EARLY:
• DEHYDRATION
• ELECTROLYTE
IMBALANCE- slow
replacement
• Hypergastrinemia
LATE:
A)METABOLIC COMPLICATIONS-
• Micronutrient deficiency
• B12, EFA deficiency
• Bacterial overgrowth
• High oxalate levels
B)TPN RELATED PROBLEMS:
• liver dysfunction
• Catheter related problems
15. MANAGEMENT
A.EARLY GOALS:
• Begin TPN within 24 hrs
• TPN requirements generally persists for the
next 7-10 days
• Measurement and replacement of fluid and
electrolyte losses every 2 hrs
• Monitoring of blood glucose levels
16. B.ENTERAL NUTRITION
• Started after initial stabilization of patient
• TRICKLE FEEEDING: continuous feeding stimulates
adaptation process
• Initial feeding should be 5% of the patients total calorie
requiremnt
• This is gradually increased every 3 to 7 days and weaning of
TPN done simultaneously
• Consider elemental diet if there is an underlying
inflammatory process
• Soluble fibers to slow down intestinal transit time if colon is
intact
• Successful weaning indicated by amount of enteral fluid loss
which reflects the degree of carbohydrate malabsorption
17. Diet and Fluid Suggestion
COLON PRESENT COLON ABSENT
Carbohydrate 50%-60% of caloric
intakeComplex carbohydrate
40%-50%
Fat 20%-30% caloric intake 30%-40%
Ensure adequate essential
fats MCT/LCT
LCT
Protein 20%-30% caloric intake
High biologic values
same
Fiber Soluble soluble
Fluids ORS and/or hypotonic ORS
Oxalate Restrict _______
18. C.ORS
• To decrease dehydration and to decrease TPN fluid requirements in
patients with residual jejunum ending in a jejunostomy
• Optimal Na concentration : at least 90 mmol/L, which is usual
concentration of small bowel effluent, adding glucose promote
further active salt absorption
• For patients with no jejunum, but have residual ileum, presence of
glucose in ORS is not critical because ileal water absorption is not
affected by presence of glucose
• Patients with SBS should be cautioned against consumption of plain
water and should be encouraged to drink ORS whenever they are
thirsty
19. D. PHARACOLOGICAL ADJUNCTS
• ANTIMOTILITY AGENTS: loperamide,
diphenoxlate, clonindine, codeine
• OCTREOTIDE : inhibits pancreatic secretion
and decreases intestinal transit time. Should
be only considered if >3litres of iv fluids
required
• CHOLESTYRAMINE for bile acid malsbsorption
• GLUTAMINE : helps in adaptation process
21. NONTRANSPLANT OPTIONS
A. TO SLOW INTESTINAL TRANSIT TIME
1.SEGMENTAL REVERSAL OF SMALL BOWEL:
• approx 10cms can be reversed as longer length tends
to obstruct
• The reversed segment placed distally
2.Interposition of colon in antiperistaltic or isoperistaltic
direction (8-24cms of colon can be used)
3.Intestinal valves
4.Retrogade Electrical pacing
22. ,B. TO INCREASE INTESTINAL AREA
1.LONGITUDINAL INTESTINAL LENGTHENING
AND TAILORING (LILT)
• Used mainly in children (dilated residual
intestine with dysmotility and bacterial
overgrowth)
• Intestine and its mesentric arterial blood
supply is divided longitudinally along its
mesentric border, creating a double lumen
which is reanastomosed.
• Increases the function but not the surface area
25. 2.SERIAL TRANSVERSE ENTEROPLASTY
• Series of
transverse
anastomosis to
increase intestinal
area
• One large tube is
converted into a
narrower zigzag
• Alters area to
volume ratio
27. B.INTESTINAL TRANSPLANT
CONSIDERED IN PATIENTS WITH
• life threatening complications of intestinal failure
• those destined for lifelong TPN
• where native intestine must be removed (tumor)
• Overt liver failure due to TPN
• Thrombosis of 2 or more central veins
• 2 or more episodes catheter related sepsis in a
year
• Single ep of line related fungemia, septic shock,
ards
28. B.INTESTINAL TRANSPLANT contd.
• Entire length of small intestine is usually
anastomosed side to side with ileostomy
• Can be combined with liver transplant
• Enteral feeding can be started after
establishment of postoperative intestinal
motility but supplemental iv fluids can be
required upto 1 year