Paediatrics Gastrointestinal PDF

Paediatrics Updated: Feb 2023 GASTROENTEROLOGY – PHYSIOLOGICAL PECULIARITIES IN CHILDREN MOUTH SYSTEM OF MILK TEETH 1. Internal mucus membrane of lips is thin and mob...

Paediatrics Updated: Feb 2023 GASTROENTEROLOGY – PHYSIOLOGICAL PECULIARITIES IN CHILDREN MOUTH SYSTEM OF MILK TEETH 1. Internal mucus membrane of lips is thin and mobile. I, II– incisors 2. Gingival humps are prominent and during sucking they are III– canines filled with blood and become hard. IV, V– primary molars 3. Developed cheek muscles. 6– permanent molars 4. Tongue is relatively big, thick and rigid and able to move from (grow in the 6th year of the distal to the proximal oral cavity. life) 5. Mandible is relatively small and moves distally (physiological retroganthia). 6. Articular joints of the mandible are not yet fully developed OESOPHAGUS STOMACH 1. Relatively short oesophagus, The pillars of the diaphragm are not closed enough in children (they close in 2. Child’s oesophagus does not have pronounced five the 12th-13th year of life); deflections. The cardia of the stomach is not muscular and not strongly developed. 3. The food from the root of a child’s tongue quickly and easily The oesophagus pulls the cardia of the stomach up falls into the stomach. The pyloric sphincter is well-developed. 4. Oesophageal mucosa is quite thin and very well vascularized, The stomach stays in a vertical position - the so called “open bottle” but the muscles are weak. phenomenon. Stomach capacity = 30 ml + 30 ml × month of life (this is especially important until age of 6-8 months.)  Paediatrics Updated: Feb 2023 SMALL INTESTINE SIGMOID COLON 1. The length is two times less than in adult. 1. It is longer 2. The membrane is thin and well vascularized. 2. It is mobile 3. The intestinal glands are bigger than in adult. 3. Increasing in size during life 4. The villi of SI are not well developed 4. The localization of sigmoid colon is upper in children who are younger 5 5. The area where SI binds to LI is not well developed (valve of years than in schoolchildren (in schoolchildren it is in the pelvic cecum) cavity). LARGE INTESTINE RECTUM 1. The large intestine is not completely developed. 1. In schoolchildren the rectum is in the small pelvis. 2. The length of the large intestine is the same as the body 2. It is longer. length (in any age of a 3. It is mobile child), 4. The ampulla of rectum is absent in newborn and it formed by the 1st Only by the age of 4 LI is in the length of adults haustra year appears after 6 months of life. 5. Rectum finds its anatomical place by the age of 2y 3. Muscular tissue of appendix is weaker than adults  Paediatrics Updated: Feb 2023 PANCREAS LIVER 1. The weight of the pancreas in newborns is small: it weighs 2-3 grams. 1. Before the birth the liver is the largest organ of the body. 2. The weight of the pancreas increases when a child grows; it is 4 times (occupies 1/3-1/2 of the abdominal cavity) bigger at the end of the first year of life and even 30 times bigger in 2. It is in the upper quadrant of the abdomen and one part of the adults. right epigastrium. 3. The lobe pancreatic system in young children is weakly developed, so the 3. The left lobe is very large before the birth pancreas is uniform and homogeneous. 4. It grown fairly quickly, but the height and weight of the child 4. The number of insulin-producing islets of Langerhans is predominant in grow faster. the infant’s pancreatic structure and is rapidly increasing until the third year of life, but since the fourth year of life, the intensive growth stops. 5. The activity and number of pancreatic enzymes, the amount of FUNCTIONS. bicarbonate begin to increase with proper nutrition of a child. 1. Excretion and bile production 6. Exocrine pancreatic activity is stabilized in the 2nd-3rd year, but it still 2. Metabolism remains insufficient and highly dependent on a child’s diet. 3. Detoxification 4. The production of factors of blood clotting and participation in FUNCTIONS. the production of blood vessels 1. Endocrine: Insulin production 2. Exocrine function: Protein (Trypsin), Carbohydrate (Amylase) and Fat (Lipase) breakdown  Paediatrics Updated: Feb 2023 GERD Symptoms occurring due to gastric contents reflux into oesophagus or oropharynx ETIOPATHOGENESIS SYMPTOMS DIAGNOSIS TREATMENT Primary: Clinic Non Pharmacological LES defect à Acid reflux of gastric Infants Children/ Esophogastro- Position contents into oesophagus Adolescence duodenoscopy Lie baby/child on left side with the àDisruption of distal mucosa. Repetitive Repetitive +biopsy head raised at 300 vomiting vomiting Oesophageal pH Avoid lying down for 3 hours after Secondary: Sitting up in 1st Heartburn analysis eating. Stimulation of vomiting centre yr. of life Dysphagia LES examination After feeding baby: keep upright (Intestinal infections and Refusal to eat Sore throat (Oesophageal for 15-20mins and let them burp obstruction, food allergy, Poor weight Chronic manometry) Diet metabolic diseases, tumours) gain cough/ Night X-ray with contrast Babies: Thick, warm, grated food. Apnoea coughing for ddx Feed often and slowly, with enough Predisposing factors in babies: attacks/ Hoarseness liquids between meals. 1. Lie on their backs Bradycardia (in the Older: Avoid greasy, fried food, 2. Liquid meals Dyspnoea morning) citrus, chocolate etc. 3. Not good enough peristalsis seizures Hematemesis 4. Food – stomach – esophagus Pharmacological volume proportion Complications Antacids 5. Anatomical differences in Erosive esophagitis H2 blockers (Ranitidine) 5- digestive tract in infant (Angle Oesophageal stricture 10mg/kg/d of His is less acute à more PPI (Omeprazole) 1-2mg/kg/d (Only Barret’s oesophagus vertical lie of stomach) used in acute vomiting due to cardiotoxic effect/ Increased risk of GI infections)  Paediatrics Updated: Feb 2023 GASTRITIS ETIOPATHOGENESIS DIAGNOSIS TREATMENT ACUTE 1. Acute GI infection: Helicobacter Diagnosis is made from Non Pharmacological pylori, various viral (rotavirus) and medical history and Position bacterial (staphylococci, salmonella) symptoms: Lie baby/child on left side with the head raised at 300 2. Food poisoning Fever Avoid lying down for 3 hours after eating. 3. Food allergens; Acute non expanding After feeding baby: keep upright for 15-20mins and let pain In upper abdomen them burp 4. Medication: NSAIDS, (but palpation yields pain Glucocorticoids, Cytostatic, Iron Diet in entire abdomen) supplements, Dyspepsia Babies: Thick, warm, grated food. Feed often and slowly, 5. Stress: mental and physical (severe Vomiting with enough liquids between meals. illness, trauma, major surgery) Diarrhoea with liquid Older: Avoid greasy, fried food, citrus, chocolate etc. 6. Ionizing radiation, especially in the feces/ mucus abdominal area. Pharmacological Antacids H2 blockers (Ranitidine) 5-10mg/kg/d PPI (Omeprazole) 1-2mg/kg/d (Only used in acute vomiting due to cardiotoxic effect/ Increased risk of GI infections) CHRONIC H. Pylori infection (most common) Symptoms: Diet: à Inflammation of gastric mucosa Moderate pain in upper avoid spicy, greasy, roasted food (mononuclear cell infiltration) à abdomen Gastritis à Mucosal atrophy à Early satiety Acid-reducing medicines: Intestinal metaplasia. Abdominal distention o Proton pump inhibitors (Omeprazole) Food allergens. Nausea o H2 blockers (Ranitidine) Bile reflux. Non-productive vomiting For H.Pylori: Medicines: NSAIDS, Glucocorticoids, Triple therapy for 2 weeks (Omeprazole 40mg+ Clarithromycin Cytostatics. Diagnosis: 500mg+ Amoxicillin 1g) OR Autoimmune diseases. Endoscopy + Biopsy Quadruple (add on bismuth 120mg 4x/d) Rapid urase test Urea breath test  Paediatrics Updated: Feb 2023 PEPTIC ULCERS ETIOPATHOGENESIS SYMPTOMS DIAGNOSIS TREATMENT PRIMARY ULCER Pain in upper abdomen Endoscopy + Diet: More frequent in duodenum. avoid spicy, greasy, roasted food o Stomach Ulcer à Pain 1-2hrs H. Pylori infection (most common) à Increased after meal. (food aggravates production of HCL and pepsin & Decreased PPI+ H.pylori eradication: pain) mucus production in duodenumà Triple therapy 2x/day for 2 weeks: Inflammation of mucosa à Mucosal atrophy à o Duodenal Ulcer à Pain 2-4hrs 1. Omeprazole 40mg+ Ulcer after meal, lasts 0.5-2hrs. 2. Clarithromycin 500mg+ (Disbalance btw. harmful and protective factors) Radiates to back and right 3. Amoxicillin 1g Biopsy + Genetics pectoral area. (food relieves Urase test pain) SECONDARY ULCER Early satiety More frequent in stomach Abdominal distention Medicines: NSAIDS, Glucocorticoids, Cytostatics. Alcohol, smoking Nausea Stress Vomiting (more in gastric ulcer) Severe conditions (shock, sepsis, burns) Weight loss  Paediatrics Updated: Feb 2023 FUNCTIONAL DISORDERS CLINICAL FEATURES DIAGNOSIS TREATMENT Infant colic Recurrent and prolonged periods of crying (>3hours), An infant who is < 5 Change milk formula if milk allergy fussing or irritability without obvious cause month when the suspected. (Functional During colic: Abdomen swells, legs are attracted to symptoms start and stop During colic: Belly massage, swinging, abdominal abdomen, gas is emitted. No evidence of failure to convenient posture Pain) thrive, fever, or illness Probiotics: Lactobacillus reuteri Monitor using a diary IBS ≥2 months abdominal pain associated with one of the Same as symptoms (criteria) Treatment based on type of IBS. following (on ≥4 days per month): + o Constipation predominant à Soluble o Related to defecation (disappears after) Lab (CBC, ESR, CRP, fiber diet + Laxatives (Duphalc) o Change in frequency of stool Celiac Ab) o Diarrhea predominant à Soluble fiber o Change in form (appearance) of stool Instrumental tests (US, diet + Antidiarrheals (Loperamide) o In children with constipation, the pain does not resolve Endoscopy, abdominal x- o Variable stool patter type à with the resolution of the constipation (resolution of ray) Spasmolytics pain indicates functional constipation) Stool analysis o (Spasmomenum) (C.difficine/blood) to exclude pathology Functional At least 2 months with ≥1 of the following bothersome Same as symptoms (criteria) Episodically, depending on the prevailing dyspepsia symptoms on ≥4 days per month: + symptoms. o Postprandial fullness (unpleasant sensation of prolonged Lab (CBC, ESR, amylase, persistence of food in stomach) liver enzymes, Celiac Ab) o Increase physical activity o Early satiety Instrumental tests (US, o Regulate diet o Epigastric pain or burning not associated with defecation Endoscopy, abdominal x- o H2 blockers - Ranitidin, ray) o Proton pump inhibitors (Omeprazole) SUBTYPES: Urine & stool analysis to exclude pathology o Digestive enhancers (enzymes - Kreon, Post prandial distress syndrome: postprandial fullness or Pangrol) early satiety that prevents finishing a regular meal o Abdominal suppressants (Espumisan) o Spasmolytic (Spasmomen, Duspatalin) Epigastric pain syndrome: o Prokinetic agents (Domperidon) bothersome epigastric pain or burning not relieved by defecation  Paediatrics Updated: Feb 2023 CHRONIC NON INFECTIOUS DIARRHEA Chronic- lasnng >2 weeks Diarrhoea- Increase in stool frequency (>3x/day) OR Decreased stool consistency (loose, liquid, watery) AETIOLOGY & PATHOGENESIS 1. Increase in intestinal motor activity 2. Decrease in absorption 3. Increase in intraluminal 4. Inflammation (IBD) (abnormal intestinal transit): (Osmotic diarrhea) secretion and exudation o IBS, o Lactose intolerance o IBD o Toddlers diarrhea (Chronic non-specific diarrhea) o Celiac disease o VIPoma’s à due to excessive fluid intake with a diet o Cystic fibrosis o Toxins (Cholera) consisting of low-fat and high carbs OR excessive o Cholestasis fructose/sorbitol intake MALABSORPTION SYNDROME (OSMOTIC CHRONIC DIARRHEA) Any disorder affecnng the absorp_on or luminal processing of ingested nutrients causes the clinical syndrome of malabsorpnon. CAUSES SYMPTOMS Weight loss (or not gaining) Digestion phase Disease Chronic diarrhea Abnormal cavital Cystic fibrosis Abdominal distension (gas production in colon (intraluminal) digestion Chronic pancreatitis because of non or abnormal resorption in Cholestatic liver disease intestines) Small bowel syndrome Recurrent Abnormal intercellular Cow’s milk protein intolerance abdominal pain (Mucosal) digestion Food allergy Poor appetite Celiac disease Mixed GI disorder Diabetes Hypoparathyroidism Scleroderma  Paediatrics Updated: Feb 2023 CELIAC DISEASE ETIOPATHOGENESIS SYMPTOMS DIAGNOSIS TREATMENT Genetic disorder (HLA-DQ2 & Symptoms become apparent when gluten o Total IgA, if deficit à IgA Dietary DQ2) ingestion begins: antiendomysial antibody (EMA) (lifelong): Diarrhea gluten-free diet Gluten in the diet Constipation o Tissue transglutaminase antibody ↓ Vomiting (tTG) à Avoid rye, Cellular immunity stimulated Abdominal pain barley, wheat ↓ Failure to thrive- loss of appetite, failure to o Genetics: HLA DQ2/8 Immune inflammation gain weight, irritability. ↓ Anorexia o Intestinal biopsy à severe Mucosal microvilli atrophy Abdominal distention- secondary to mucosal damage of proximal SI. Intraepithelial lymphocyte intestinal gas and fluid accumulation. Mucosal microvilli atrophy proliferation Anemia Intraepithelial lymphocyte Crypt hypertrophy Vitamin deficiency proliferation Crypt hypertrophy. Short stature, delayed puberty  Paediatrics Updated: Feb 2023 INFLAMMATORY BOWEL DISEASE CHRONS UC Deep transmural mucosal inflammation Inflammation of the large intestinal mucosa, which is always proximal. throughout the gastrointestinal tract The inflammation is found only in the mucous membrane and in the from mouth to rectum and anus. sub-mucus, Typical morphological trait: is the Typical morphological trait: crypt abscesses formation of granulomas. Complications: Toxic megacolon Complications: Stenosis, fistulas, frequent exacerbations and faster remission. abscesses, anal disorders (acute tares, longitudinal fistulas, and abscesses). Constant active inflammation is common SYMPTOMS DIAGNOSIS Intestinal Extra-intestinal 1. History and Physical exam Stomach ache Joint damage- arthritis 2. Growth chart Chronic diarrhoea (+/- blood) Eyes- uveitis, episcleritis in eyes 3. CBC- ↑CRP, ↑ESR, anemia, ↑platelet count Weight loss Skin- Erythema nodosum and pyoderma 4. Imaging: Fever gangrenosum 5. Upper GI series with small bowel follow-through or Chron’s- more systemic Primary sclerosing cholangitis symptoms Autoimmune hepatitis and pancreatitis. CTà to detect small bowel involvement. 6. Upper endoscopy- more sensitive than contrast studies in identifying proximal CD involvement. 7. Colonoscopy- with biopsy and visual features can be diagnostic. 8. Stool occult blood 9. Stool culture- must exclude infection. 10. Clostridium difficile toxin assay 11. Ova and parasites studies