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DIARRHEA Final Group 8
DIARRHEA Final Group 8
DIARRHEA Final Group 8
REPORTERS
Cobankiat, Clarine
Come, Christian Kenneth
Concepcion, Kevin Chuck
MEMBERS
Collado, Janssen
Colobong, Carlomar
Contreras, Rio
reatment and OBJECTIVES
• Discuss diarrhea and the various metabolic
changes observed with it.
• Evaluate the nutritional status of the
patient presented on each case.
• Determine the adequacy of the patients’
diet before and during diarrhea.
• Explain the corresponding treatments for
each case.
WHAT IS DIARRHEA ?
DIARRHEA
1. DURATION
1. Acute Diarrhea
2. Chronic Diarrhea
2. CAUSE
3. Infectious
4. Non-infectious
3. MECHANISM
5. Osmotic
6. Secretory
CLASSIFICATION OF DIARRHEA
• DURATION
CLASSIFICATION OF DIARRHEA
DURATION: ACUTE DIARRHEA
Reduced Reduced
grams/litre mmol/litre
osmolarity ORS osmolarity ORS
Sodium chloride 2.6 Sodium 75
Glucose, anhydrous 13.5 Chloride 65
Glucose,
Potassium chloride 1.5 75
anhydrous
Trisodium citrate,
2.9 Potassium 20
dihydrate
Citrate 10
Total Osmolarity 245
DIARRHEA CASE A
• A mother brought her 10-months old, 8-kg
daughter to a health center because of diarrhea of
one day duration which occurred 4 times. There
was no accompanying vomiting. She has been
breastfed since birth. At 5 months old, Lugaw with
fish and vegetables were started. At the onset of
diarrhea, the mother stopped breastfeeding and
giving solid foods and instead shifted to giving
“am” with sugar. The child is alert, with good skin
turgor and adequate urine output.
Carbohydrates the patient takes
( a quick summary)
• 3 major sources of carbohydrates in the
diet
– Sucrose (disaccharide) – glucose + fructose
– Lactose (disaccharide ) – glucose + galactose
– Starch ( polysaccharide ) – amylase +
amylopectin
• starch – homopolymer of glucose forming an -
glucosidic chain called glucosan
Digestion of Carbohydrates
• Mouth: enzyme ptyalin (-amylase)
• S. Intestine: Pancreatic amylase
– Intestinal epithelial cells: Brush border enzymes or
Disaccharidases
Disaccharidases
– Function: splits disaccharides into their respective
monosaccharides.
– Location: enterocytes in the brush border
– Lactase Lactose Glucose + Galactose
– Sucrase
– Maltase
– -Dextrinase
Absorption of Carbohydrates
– Glucose & Galactose
• Na-dependent process
• Via SGLT-1
• Exits intestinal cells and absorbed by the capillaries via
GLUT2 transporter
Lactase (Disaccharidase) Defficiency
• 2 Types
– Congenital Lactase Defficiency
• Autosomal recessive disorder
• Mutation in the gene encoding for Lactase
• Symptoms abate by termination of milk or milk containing products
• Results in removal of unabsorbed lactose in the lumen to the large
intestines
• Flora in the L.intestine ferments Lactose and convert Lactose Lactate
• Result: Diarrhea and abdominal discomfort
• Irritation of mucosa
– Acquired Lactase Deficiency
• Down regulation of Lactase gene expression
• Presents after childhood
– Effects of Diarrhea in Motility, Fluid volume, Acid-
Base balance and Composition
• Motility: Greatly increased
• Fluid Volume: Increased secretion of Intestinal cells
• Acid-Base balance: Chlorine, Potassium, Sodium
Evaluation of the nutritional status
and hydration state of the patient
Assessment Chart of Hydration
Ideal weight for age of the patient using
Gomez Classification
• Data:
– Actual body weight: 8 kg.
– Ideal body weight: 19.4 lbs or 8kg (19.4 divided by
0.4536)
– Ideal weight for age = Actual / Ideal x 100
• 8 / 8 x 100 = 100% (with in normal range)
Adequacy of Px Diet
• BIRTH TO 6 MONTHS OF AGE – breast
milk/formulated milk
• 6 TO 8 MONTHS OF AGE – breast milk/formulated
milk and baby cereals
• 8 TO 12 MONTHS OF AGE – breast milk/formulated
milk, baby cereals with a few servings of finely
chopped meat
– The diet of the patient was inadequate. The early
termination of milk ingestion of the patient lead to the
manifestation of Congenital Lactase Deficiency which
resulted to diarrhea.
Treatment
• Oral rehydration salts
• Switching to bland, starchy foods like strained
bananas, applesauce, and rice cereal until the
diarrhea stops.
• Switching the diet of the infant by avoiding the
following until diarrhea diminshes:
– Greasy foods
– Too much fiber in the diet
– Milk products
Biochemical Significance of “AM”
• “AM” is naturally made from rice which contains fiber
• Fiber – a non digestible part of rice that helps promote
regular bowel movement
– Fermented by the colonic microflora with the production of short
chain fatty acids (SCFA), hydrogen, carbon dioxide and biomass.
– Hydrolysed by membranous or extra-cellular enzymes secreted by
bacteria via Embden-Meyerhoff pathway which leads to the
production of pyruvate.
– Pyruvate is immediately converted to acetate, propionate and
butyrate, and gases: carbon dioxide (CO2), hydrogen (H2), and
methane (CH4).
• Fiber helps in diarrhea by increasing fecal bulk but a low fiber
diet (10g) is preferred because too much bulk may aggravate
diarrhea.
DIARRHEA CASE B
Clinical History:
Vital signs:
• Weight: 11 kg.
• Temperature: 37 C.
• CR: 100 bpm
• RR: 20 cpm
SIGNS AND SYMPTOMS
• Sunken eyeballs.
• Dry mouth and tongue.
• Poor skin turgor.
• Decreased urine output.
• Slight distended with hypoactive bowel sound
in the abdomen.
• Serum Electrolytes: Na – Normal;
• K – decreased.
ASSESSMENT
Nutritional Status
• Breastfed for 2 months,
then shifted to Bonna 1:2
dilution.
• Started solid food at 4
months old.
• Given “lugaw” since the
onset of diarrhea
Electrolyte status
• Serum Electrolytes: Na – Normal
• K – decreased(hypokalemia)
Normal values:
• Sodium = 135-145 meq/L
• Potassium = 3.5-5 meq/L
Sequence of diarrhea
• Diarrhea is mainly caused by abnormal fluid and
electrolyte transport by decreased absorption or increased
secretion.
1 • Human colon is capable of absorbing 3-5 L per 24 hrs