Malabsorption And Cronic Diarrhea Flashcards
MALABSORPTION
Malabsorption can result from a defect in the nutrient
digestion in the intestinal lumen or from defective
mucosal absorption. Maldigestion: Defective intraluminal hydrolysis of
nutrients. Impaired breakdown of nutrients - Carb → mono , di , oligosaccharides - Protein → amino acids , oligopeptides - Fat → fatty acids , monoglycerides Malabsorption: Defective mucosal uptake and
transport of digested nutrients , vit , minerals.
Causes
Carbohydrate malabsorption
Carbohydrate malabsorption Pancreatic insufficiency (amylase) Absence or reduction of the brush border disaccharidases . Transient reduction of these enzymes is common after an infection. Lack of sucrase and isomaltase. Congenital lactase deficiency A congenital deficiency in the glucose galactose transporter (SGLT-1) Small bowel bacterial overgrowth of normal flora
Fat malabsorption
Exocrine pancreatic insufficiency(Pancreatitis,
pancreatic cancer, pancreatic resection, cystic
fibrosis, Schwachman-Diamond syndrome, Johnson-
Blizzard syndrome, Impaired bile production or secretion Abetalipoproteinemia
Protein malabsorption
exocrine pancreatic enzyme deficiency, as occurs in
patients with cystic fibrosis.
congenital enterokinase deficiency is well-described
but rare.
Creatorrhea (ie, protein-losing enteropathy), is often
caused by the leakage of protein from the serum due
to inflammation of the mucosa, as in Crohn disease,
celiac disease, and protein sensitivity syndromes.
Congenital lymphangiectasia
Cp of malabsorption
Clinical Presentation Malabsorption may involve: – a broad range of nutrients i.e. panmalabsorption. – only a single nutrient or a class of nutrients i.e. specific malabsorption. Symptoms and signs of the disease depend on the deficiency of the nutrient(s) that is malabsorbed. -Steatorrhea: bulky, floating, malodorous stool-difficult to flush. - Weight loss. Diffuse abdominal pain. - Flatulence. Symptoms of anemia. - Weakness and fatigue. Bone aches. - Paresthesia. Abnormal bruising. - Tetany. Milk intolerance. - Night blindness. Amenorrhea & infertility. Symptoms
Signs of malabsorption
Signs
Pallor. Glossitis, stomatitis, cheilosis. Clubbing. Ecchymosis and purpura. Dermatitis. Dehydration and hypotension. Abdominal distention Edema. Peripheral neuropathy. Perianal excoriation
Malabsorption hx and PE
Approach and management
History GI tract symptoms: Stool characteristics: Diet history: Other symptoms:(Systemic symptoms:weakness, fatigue, and failure to
thrive, past medical history family history (especially for systemic and gastrointestinal conditions), medications , surgeries radiation exposure/treatments, caustic substance ingestion , allergies social history
Physical examination
Physical exam should include a full abdominal examination
hyper/hypoactive bowel sounds, abdominal distention, abdominal
tenderness
pallor muscle wasting,
abnormal deep tendon reflexes, skeletal deformities,
rashes, cardiac arrhythmia, Ecchymosis poor wound healing, , decreased visual acuity peripheral neuropathy , auditory disturbances, or cognitive impairment failure to thrive
Malnutrition delayed puberty.
Borborygmi, a significant increase in peristaltic activity
Dehydration
Malabsorption labs
Stool analysis reducing substances, pH , stool bile acids, quantitative stool fat, large serum proteins, ova and parasites, Testing for other chronic intestinal infections (Clostridium difficile, Cryptosporidium species)
Urinalysis: CBC Total serum protein and albumin levels fat-soluble vitamin levels levels of the low-density lipoprotein (LDL) cholesterol ESR& C-reactive protein level liver function tests &RFT +Electrolytes
Iron ,Magnesium , Zinc ,Phosphorous
Immunoglobulin G (IgG) and immunoglobulin A (IgA) antigliadin and IgA antiendomysial antibodies, or especially tissue transglutaminase antibodies
Imaging of malabsorption
Imaging
Computed tomography (CT): Pancreatitis Magnetic resonance cholangiopancreatography (MRCP):Exocrine pancreatic
insufficiency Magnetic resonance (MR) elastography: liver stiffness, liver fibrosis, hepatic
amyloidosis, and other conditions that increase liver stiffness. Endoscopic retrograde cholangiopancreatography (ERCP):Pancreatic insufficiency
- Crohn disease - visualized duodenal mucosa cobblestoning.
Endoscopy with biopsy (indicated for diagnoses that require both visualization
and biopsy): - Celiac disease - visualized reduced duodenal folds or mucosal scalloping.
Treatment & Management
Of malabsorption
Medical Care (antibiotics, cholestyramine(bile acid malabsorption) oral supplements( loss of pancreatic enzymes), Immunosuppressive medications, elimination diet) Surgery ? Diet Associated symptoms: Fever Vomiting Pain Distention Jaundice Concurrent problem: Joint pain and swelling skin rash dysphagia oral ulcer perianal fistula
Osmotic diarrhea
Osmotic diarrhea is caused by nonabsorbed nutrients in the intestinal
lumen as a result of one or more of the following mechanisms: (1)intestinal damage (e.g., enteric infection); (2) reduced absorptive surface area (e.g., active celiac disease); (3) defective digestive enzyme or nutrient carrier (e.g., lactase deficiency) (4) decreased intestinal transit time (e.g., functional diarrhea); (5) nutrient overload, exceeding the digestive capacity (e.g., overfeeding, sorbitol in fruit juice).
Etiology of chronic diarrhea
Infection o E-coli ◦ Giardia lamblia ◦ Entamoeba histolytica ◦ Cryptosporidium parvum Inflammatory ◦ Cow milk protein intolerance ◦ Food allergy ◦ IBD Malabsorption ◦ Celiac disease ◦ Cystic fibrosis ◦ Bacterial overgrowth ◦ Short bowel syndrome ◦ Defective sodium absorption ◦ Congenital chloride losing diarrhea ◦ Bile deficiency or chronic cholestasis Osmotic Lactase deficiency (Primary or Secondary post- infectious) Excessive fructose intake Laxative overuse Others Toddler diarrhea (functional diarrhea) Endocrinal e.g., thyrotoxicosis Immunodeficiency Neoplastic e.g., neuroblastoma
Hx of chronic diarrhea
◦ When did it start? Duration? ◦ What is the patient usual bowel habit? ◦ Consistency? Frequency? Volume of stool? ◦ Are the lose motion interspersed by normal ones? ◦ Content: Undigested food? Blood? Mucous? fatty? ◦ Foul smelling?
◦ previous similar attack? ◦ Contact with sick patient? ◦ Antibiotic use? ◦ Travelling? ◦ Oral intake? Weight loss? Activity? ◦ Urine output?
Continue
◦ Past medical history: Antenatal history in detail (prenatal U/S, NICU admission and course, neonatal screening).
recurrent infections
previous hospitalization ◦ Past surgical:
bowel resection
congenital GIT anomalies repaired ◦ Medications:
laxative or antibiotics ◦ Allergy: cow milk
Continue
o Nutritional history in detail (fructose, lactose, gluten,
carbonated drinks, water source) o Family history
Consanguinity
Similar case in the family
Immunodeficiency
Celiac disease
IBD
o Social history (any stress at home or school).
Complete physical examination
In chronic diarrhea
Complete physical examination
◦ General, start with GIT then other systems ◦ Examine stool
Cronic diarrhea examination
Hydration status
Weight and height should be measured and put on the appropriate
charts. • Weight loss is seen in many disorders like CF, Coeliac disease, IBD. weight and height are usually normal in toddlers diarrhoea.
• Pallor - CF, Coeliac disease.
• Fever- Infection, TB, CF and HIV.
• Clubbing- CF
Hyperpigmentation- Addison’s disease, Celiac
disease • Generalized lymphadenopathy- Lymphoma, HIV. • Stomatitis and Perianal fistula- Crohn’s disease. • Hepatomegaly -lymphomas, metastatic carcinoid,
IBD. • Ascites - TB and lymphoma Poor weight gain or weight loss. • Signs of systemic diseases like fever, rash and
arthritis.
Stepwise Diagnostic Approach to Children with Diarrhea
STEP 1 -Intestinal Microbiology -Stool cultures -Microscopy for parasites -Viruses -H2 breath test -Screening Test for Celiac Disease: -Serology according to age and level of IgA (including AGA(, antigliadin antibody) IgA/IgG,
EMA(endomysial antibody) IgA/IgG, tTG IgA) Non-invasive Tests for: -Intestinal function (including double sugar test, xylosemia, iron - absorption test) -Pancreatic function (amylase, lipase, fecal elastase) -Intestinal inflammation (fecal calprotectin, rectal nitric oxide) Tests for Food Allergy: -Prick/patch tests for foods Abdominal Ultrasounds (Scan of Last Ileal Loop)
STEP 2 Evaluation of Intestinal Morphology:
• Endoscopy and standard jejunal/colonic histology* • Electron microscopy • Imaging (upper or lower bowel series, capsule endoscopy)
STEP 3 Special Investigations: -Intestinal immunohistochemistry -Antienterocyte antibodies -Autoantibodies -Brush-border enzymatic activities -Motility and electrophysiologic studies
Tt of chronic diarrhea
Treatment
◦ Frist stabilize the patient (ABCs) ◦ Hydration ◦ Electrolytes replacement ◦ Proper diet ◦ Zinc supplementation is important in both prevention and
therapy of chronic diarrhea
◦ Special treatment according to the cause
cow’s milk intolerance.
An immunologic reaction to one or more milk
proteins . CMPA and lactose intolerance CMPA can develop in exclusively and partially
breast-fed infants. Diagnosis begins with a thorough history, including
a family history of atopy, and a complete physical
examination to rule out other causes, to identify any
comorbid conditions, and to classify the CMPA as
mild to moderate or as severe.
symptoms in -GIT as regurgitation, vomiting, and changes in the
pattern of bowel movements, -Skin symptoms including atopic dermatitis,
angioedema, and urticaria.
Symptoms of the respiratory tract are less common. Skin prick tests and radioallergosorbent testing Both tests neither prove nor disprove the diagnosis of
CMPA, so elimination diets and food challenges are
the best means of diagnosis. However, these serologic
markers can be helpful in predicting the course of the
illness.
Elimination diets and food challenges are the best
means of diagnosis and treatment.
Celiac disease
Also known as gluten sensitive enteropathy Genetic autoimmune disease due to sensitivity to gliadin
fraction of gluten (in wheat, rye and barely). Mode of inheritance Autosomal recessive and
multifactorial. Incidence is 0.5-2% in developed world. 50 times more common in children with down syndrome.
Celiac disease
Pathophysiology
Clinical picture
Pathophysiology
◦ Gluten sensitize mucosal lymphocytes lead to
autoimmune reaction that damage the surface
epithelium leading to villous atrophy. ◦ Later on, it cause generalized defects in mucosal
transport and malabsorption.
Clinical picture
◦ Present around 6 to 12 month of age with feeding gluten
diets. ◦ May appear at any age. ◦ Chronic diarrhea (steatorrhea) with large pale, bulky,
greasy, offensive stool. ◦ Abdominal distension & pain. ◦ Failure to thrive. ◦ Associations with celiac disease: IDDM, selective IgA
deficiency, intestinal lymphoma, autoimmune thyroiditis
and rheumatoid arthritis.
Tt of celiac dis
◦ Gluten free diet life long ◦ Nutritional support: supplemental calories, vitamins and
minerals.
Diagnosis of celiac
IgA anti-tissue transglutaminase antibodies and IgA anti-
endomysial antibodies with total serum lgA are the Gold
standard screening test. ◦ Two mandatory requirement for diagnosis are:
Small intestinal biopsy showing atrophied villi and hyperplastic
crypts with intraepithelial lymphocyte. Complete clinical remission with gluten free diet.
Crohn’s
Crohn’s: Chronic, inflammation of random segments of GI tract, and
move around – through the wall involvement Often develop enteric fistulas between loops of bowel &/or nearby
organs Subtle onset, crampy abd pain, diarrhea, fever, anorexia, wt loss,
malaise, joint pain, greatly increase rate of cancer, Anemia (common),
increase ESR, hypoalbuminemia 48
Ulcerative colitis
Ulcerative colitis -Chronic, recurrent disease of colon & rectal mucosa -Inflammation, ulceration, hemorrhage, edema – localized in a portion of the GI tract (may be removed) -Peak onset at 12 years of age -Diarrhea, lower abd pain with passage of stool and gas, blood & mucous in stool, anorexia, weight loss
Treatment same for both Crohn’s and UC
Treatment same for both Crohn’s and UC Antibiotics Anti-inflammatory Immunosuppressive Antidiarrheal
Nutrition counseling (high protein/carb with low fiber
diet)
Surgery
Hirschsprung’s Disease:
Hirschsprung’s Disease: “Hirschsprung disease is a developmental disorder characterized by the absence of ganglia in the distal colon, resulting in a functional obstruction. M>F, > with T-21 and congenital heart defects At birth, fail to pass meconium, anorexia, abdominal distension and emesis ribbon-like, foul-smelling stools; intestinal obstruction, abd discomfort/distension,
bloating, distention, constipation, FTT, anemia. (fever, GI bleeding & diarrhea =
enterocolitis, life-threatening) Diagnosed: - clinical hx, lower GI series, rectal biopsy Management: Fluids & electrolytes, monitoring, NG for suction pain meds, antibiotics, barium/air enema, rectal irrigation (bowel preperation), surgery
Gastroesophageal Reflux
Normally caused by an incompetent/poorly developed lower esophageal
(cardiac) sphincter – very common ~50% of all infants Peak at 1-4 months Infants – reduce vol of feeds, thickening formula (rice
cereal), keep infant upright after feeds, smoke exposure elimination . small,
frequent meals, limit contributing foods (acidic, caffeine, carbonated,
peppermint, fatty/greasy foods), no food just before bed Medications may be required intermittently or continuously
Gerd
Differentiate between hypertrophic pyloric
stenosis and gastroesophageal reflux
Gastroesophageal reflux disorders GERD
Gastroesophageal reflux disorders GERD
1:300 infants Poor wt. gain (FTT), respiratory problems, behavior problems, pain Diagnose with -Clinical history -Upper GI series and endoscopy - pH probe, - Allergy testing(milk) Tx Depends on severity -Mild will tx like GER and resolve by months -Severe may require medications and/or surgery (Nissen fundoplication)
