Malabsorption And Cronic Diarrhea Flashcards

1
Q

MALABSORPTION

A

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.

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2
Q

Causes

 Carbohydrate malabsorption

A

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

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3
Q

Fat malabsorption

A

 Exocrine pancreatic insufficiency(Pancreatitis,
pancreatic cancer, pancreatic resection, cystic
fibrosis, Schwachman-Diamond syndrome, Johnson-
Blizzard syndrome,  Impaired bile production or secretion  Abetalipoproteinemia

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4
Q

Protein malabsorption

A

 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

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5
Q

Cp of malabsorption

A
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
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6
Q

Signs of malabsorption

A

Signs
 Pallor.  Glossitis, stomatitis, cheilosis.  Clubbing.  Ecchymosis and purpura.  Dermatitis.  Dehydration and hypotension.  Abdominal distention  Edema.  Peripheral neuropathy.  Perianal excoriation

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7
Q

Malabsorption hx and PE

A

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

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8
Q

Malabsorption labs

A

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

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9
Q

Imaging of malabsorption

A

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.

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10
Q

Treatment & Management

Of malabsorption

A
 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
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11
Q

Osmotic diarrhea

A

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).

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12
Q

Etiology of chronic diarrhea

A
 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
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13
Q

Hx of chronic diarrhea

A

◦ 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).

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14
Q

Complete physical examination

In chronic diarrhea

A

Complete physical examination

◦ General, start with GIT then other systems ◦ Examine stool

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15
Q

Cronic diarrhea examination

A

 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.

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16
Q

Stepwise Diagnostic Approach to Children with Diarrhea

A

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

17
Q

Tt of chronic diarrhea

A

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

18
Q

cow’s milk intolerance.

A

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.

19
Q

Celiac disease

A

 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.

20
Q

Celiac disease

Pathophysiology
Clinical picture

A

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.

21
Q

Tt of celiac dis

A

◦ Gluten free diet life long ◦ Nutritional support: supplemental calories, vitamins and
minerals.

22
Q

Diagnosis of celiac

A

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.

23
Q

Crohn’s

A

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

24
Q

Ulcerative colitis

A

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

25
Q

Treatment same for both Crohn’s and UC

A

Treatment same for both Crohn’s and UC Antibiotics Anti-inflammatory Immunosuppressive Antidiarrheal
Nutrition counseling (high protein/carb with low fiber
diet)
Surgery

26
Q

Hirschsprung’s Disease:

A

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

27
Q

Gastroesophageal Reflux

A

 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

28
Q

Gerd

A

Differentiate between hypertrophic pyloric

stenosis and gastroesophageal reflux

29
Q

Gastroesophageal reflux disorders GERD

A

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)