Diarrhea Flashcards
Diarrhea: the basics
Diarrhea is a small bowel problem.
Absorption: movement from luminal side to blood and lymphatics.
Secretion: movement from mucosa to intraluminal space.
Net absorption = net ion flux = net difference absorption: secretion
Diarrhea the players
Receptors:
- Na+/H+ exchangers (NHEs)
- Na+/K+ pump
-Cl- and K+ channels
- organic solute carriers.
Water, ions (Na+, H+, Cl-, and K+) and solute transport (Na+ coupled glucose).
Salt absorption creates an osmotic gradient for water absorption (80% of water absorption occurs via paracellular pathway).
Osmotic vs Secretory Diarrhea
Osmotic Diarrhea
Osmotic Diarrhea
- Electrolytes: Na <70mEq/L
- Osmolarity: >(Na +K) x2
- pH <5
- Volume: <200 ml/day (10gm/kg/day)
Secretory Diarrhea
Secretory Diarrhea
- Electrolytes: Na >70 mEq/L
- Osmolarity = (Na +K) x2
- pH >6
- Volume: >200 ml/day (10gram/kg/day)
Toddler’s Diarrhea
- chronic diarrhea despite normal growth and exam.
- usually 6 months to 5 years.
- Diarrhea becomes more watery as the day progresses.
- Etiology is dietary: low fat diet leads to decreased intestinal transit time.
high carb diet, especially fructose and sorbitol leads to increased osmotic load.
Congenital Diarrhea
- Rare
- Vast majority are inherited
- Diarrhea starts within first few days of life.
- Disorders of selective nutrient/electrolyte assimilation versus
- Disorders of intestinal fialure: immune dysfunction/enterocyte cytoskeleton/brush border/ autoimmune.
Diagnosis of Congenital Diarrhea
Dietary challenges = key diagnostic test
-accurate assessment of stool volume, pH, reducing substances and electrolytes (during fasting and feeding states)
Secretory vs osmotic/malabsorptive.
If you stop feeding them and the diarrhea stops, it is an osmotic diarrhea.
If osmotic/malabsorptive: selective versus generalized (range of nutrients affected)
Upper GI SBFT to rule out malrotation with intermittent volvulus, and to also rule out congenital short bowel syndrome
Tufting Enteropathy
- Moderate to severe watery diarrhea in neonatal period (4 days to 4 weeks).
- Tufts of extruded epithelial cells, tear drop shaped, appear to shed into lumen.
- Total or partial villous atrophy and crypt hyperplasia.
Microvillous inclusion disease
100-500 ml/kg/day if taking PO
- High Na+ content of 100mmol/L
- light microscopy: villous atrophy without IELs, absence of marked crypt hypertrophy, Periodic acid-Schiff + material in upper crypt and villous epithelium.
- Diagnosis with transmission EM: intracellular inclusions and secretory granules. Microvilli depletion on apical epithelial surface. Microvilli present in intracellular inclusion bodies. Crypt epithelium shows secretory granules.
Evaluation of Congenital Diarrhea
Electrolytes, albumin, immunoglobulins, T and B cell subsets
Congenial Chloride Diarrhea
- Only diarrhea that leads to metabolic ALKALOSIS due to Cl/HCO3 exchange.
- Most common severe congenital secretory diarrhea
- Severe exacerbation of diarrhea a/w most febrile illnesses.
- Life long enteral KCL and NaCl supplementation, PPI, cholyestyramine.
-SLC26A3
Congenital Sodium Diarrhea
High volume, secretory diarrhea with high concentration of Na.
Tx: Lifelong use of PO fluids and slat supplements
Prebiotics
- Nondigestible food that promotes intestinal growth of beneficial bacterial
- Dietary oligosaccharides
- Risks: gas, GI upset, neonatal sepsis
Probiotics
- microorganisms introduced into the body for beneficial qualities
- possible risk of translocation in immune compromised patients
- possible indications: rotavirus, pouchitis
Pharmacology: absorbents and bulking agents
- Pectin, fiber, methylcellulose
- can affect absorption of other medications (MTX, warfarin)
Pharmacology “slowers”
- anti-cholinergics (belladonna alkaloids)
- opiates (loperamide)
Pharmacology: anti-inflammatories
Bismuth subsalicylate
Protein Losing Enteropathy
PLE is a syndrome and NOT a diagnosis.
Key: low albumin and lymphopenic.
Management: diuretics, high protein diet, low fat diet, MCT and fat soluble vitamin supplementation, and fix underlying problem.
PLE Mechanisms:
- Ulceration (IBD/peptic ulcer)
- Decreased capillary glycocalyx (sepsis, CDG Ib)
- Increased hydrostatic pressure (Fontan)
- Increased lymphatic pressure (lymphatic obstruction)
- Increased tight junction permeability (celiac disease, IBD)
- Disrupted epithelial glycosaminoglycans (GAG) CDGIb and Ic, IBD.
Autoimmune Enteropathy
Associated: thyroiditis, hematologic abnormalities (Coombs + anemia, neutropenia and thrombocytopenia), liver, kidney and pulmonary disease, splenomegaly.
Histology: villous atrophy. Massive mononuclear infiltrate in lamina propria (versus celiac disease which has intraepithelial lymphocytes).
Antienterocyte/anticolonocyte antibodies (Anti-75-AIE) are highly sensitive.
Supportive therapy: TPN, steroids, tacrolimus or sirolimus. Stem Cell Transplantation
IPEX Syndrome
- Immune dysregulation, polyendocrinopathy, enteropathy, X-linked.
- FOXP3 gene mutation results in compromised suppressor function of T regulatory cells.
- Clinical presentation: typical trial of AIE, autoimmune endocrinopathy, and eczema.
markedly increased IgE, peripheral eosinophilia, food allergies.
can have diabetes 2/2 islet cell destruction
severe secretory diarrhea
hypoalbuminemia and electrolyte disturbance requiring bowel rest and TPN
