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1. GER vs. GERD?
2. Conservative therapy for GERD in infants? (4)
3. Conservative therapy for GERD in adults? (6)
1. GER = gastroesophageal reflux and GERD (disease). GER = passage/reflux of gastric contents into the esophagus - every child has it. GERD occurs when there are symptoms/complications that cause discomfort or danger.
2. Normalize feeding volume/frequency, use thickened formula, non-prone sleeping position, consider trial use hypoallergenic formula
3. Avoid large meals, don't lie down right after eating, sleep with left side down, lose weight, avoid caffeine/chocolate/acidic foods, eliminate exposure to tobacco smoke, NSAIDS, OCPs, limit stress
1. What are pharmacologic therapies for GERD? (4)
2. What are some problems with PPI (5)
1. Antacids - neutralize gastric acid (MgOH, AlOH) - but infants with high Al levels --> osteopenia, microcytic anemia, neurotoxicity, problems with bone homeostasis)
2. H2 receptor antagonists
- 3. PPIs - irreversible inhibitors of H+/K+ ATPase which brings H+ into gastric lumen.
- Chronic PPI use --> decreased Ca absorption in gut --> decreased osteoclast activity/bone resorption (greater risk of hip fractures in men)
4. Sucralfate - coats mucosal lining to prevent further damage from GERD
2. Fractures, nutritional deficiencies (Fe, B12), enteric infections, benign gastric polyps, carcinomas
1. What is esophagitis?
2. What are symptoms? (5)
3. What are causes? (4)
1. Irritation/inflammation of the esophagus, usually caused by GERD
2. Heartburn, indigestion, epigastric abdominal pain, chest pain, difficulty sleeping after eating, regurgitation/vomiting, etc
3. (1) Infection (rare) - candida, herpes, can use PPI/antifungals/antivirals
(2) GER - eosinophilic esophagitis (most common) caused by GER, often caused by food allergy. Treatment - allergy testing/elimination diet, PPI, (example Barrett's esophagus - disorder that changes epithelium of esophagus) and Carcinoma (GERD + esophagitis --> mucosal damage --> epithelial changes)
(3) Caustic Ingestion - symptoms (dysphagia, drooling, abdominal pain), diagnosed by endoscopy. Caused by alkali (worse)/acid that delays gastric emptying--> long-term complications (carcinoma, dysmotility, esophageal strictures
(4) Congenital/Anatomical - fistulas, hiatal hernia, esophageal astresia
1. Describe symptoms of cow's milk protein allergy (CMPA) (4)
2. When does it present?
4. What is the protein and carb makeup of breast milk vs. cow's milk?
1. GER, blood in stool, irritability with feeds, eczema
2/ First few weeks of life, but generalyl resolves within a year
3. If BFeeding, should start elimination diet of milk, soy, beef (can use alternate milks). Transition to cow's milk at 1 year of life. IF NOT BREASTFEEDING, substitute with protein hydrosylate, soy protein, or amino acids.
4. Breast milk is 40:60 casein:whey , while cow's milk is 80:20 WHEY IS BETTER. Carbs - both lactose. Fat - human milk fat vs. butter fat.
1. What is gastritis?
2. Symptoms? (4)
3. Causes? (5)
4. Treatment? (3)
- 1. Gastritis is inflammation of the stomach lining
- 2. Symptoms: nausea, vomiting hemorrhage, abdominal pain, malase/anorexia/headache
- 3. Alcohol, corrosive substrates, drugs (NSAIDS), trauma/stress, H. Pylori, post-viral, tobacco
4. (1) Avoiding NSAIDS and aggravating/acidic foods (2) Treatment with acid suppressants for 6-12 weeks (usually PPI instead of HwRA) (3) If symptoms persist, then endoscopy with biopsy to check for H pylori and ulcers
1. What is H Pylori?
2. What does it lead to? (3)
3. Mechanism of action? (6)
4. Risk factors for H pylori> (4)
5. Who should be screened? (3)
6. Test? (2)
1. Cancer-producing gram-negative bacteria that transmits via fecal/gastric/oral-oral mechanisms (humans = primary reservoir)
2. Gastritis, gastric ulcer disease (~60% of ulcers in adults) or Gastric MALT lymphoma (mucosa-associated lymphoma tissue)
3. (1) H Pylori releases urease
--> (2) protects bacteria from human gastric acid and (3) forms ammonia damaging gastric epithelium leading to (4) host inflammatory response increasing neutrophils --> (5) mucosal damage/injury (6)(also increases gastric acid secretion
4. Developing country, low SES, african american/hispanic, exposure at daycare/foster homes, etc. More common with increasing age
5. Children with iron-def anemia, persistent diarrhea, those with family history of gastric cancer.
- 6. Noninvasive - urea breath test/stool antigen
- Invasive - biopsy (gold standard)
1. What is dumping syndrome?
2. Symptoms? (5)
3. What's it most associated with
4. What else do people suffer from? Why? What else is it called?
1. Ingested foods bypass stomach too rapidly and enter SI largely undigested. Rapid loading of the small intestine with hypertonic stomach contents leads to rapid entry of water into intestinal lumen and acute intestinal distension
2. Nausea, dizziness, cramping, vomiting bloating, fatigue, dizziness, diarrhea
3. RYGB surgery
4. Hypoglycemia bc rapid dumping triggers excessive amounts of insulin into bloodstream from pancreas (ALIMENTARY HYPOGLYCEMIA)
1. What is celiac disease?
2. Symptoms? (5)
3. What is it associated with (def wise)
4. Sole treatment? Maintenance?
5. Environmental factors? (3)
- 1. Permanent intolerance to gluten. Exposure to gluten triggers inflammatory/autoimmune response in small intestine
- 2. Malabsorption, nutritional deficiencies (Fe, Zn, B1, B6,9,12, ADEK, magnesium, phosphate albumin, calcium/vit D, prolonged prothrombin time, etc), abdominal pain, dairrhea, weight loss, lack of essential FAs --> brain myelinization.
- 3. IgA deficiency
- 4. Gluten-free diet, checking vitamin levels (ADEK, B1,2,6,9,12, zn, fe)
5. Infant feeding practices, microbiome influence on intestinal permeability (c-section abbies), rotavirus infections
1. Define ulcerative colitis and crohn's disease
2. How do they differ?(5)
3. What is the treatment for them?
4. how do they vary for cancer risk?
5. Are probiotics effective for treating these?
- 1. UC = diffuse mucosal inflammation limited to colon, affects rectum.
- Crohn's - occurs anywhere from mouth to anus, inflammation
2. UC has a lot more rectal bleeding
and severe diarrhea
, while CD is associated with more abdominal pain, severe weight loss, and >40% have growth problems
3. Well-balanced diet, small frequent meals, liquid supplement, surgical intervention, etc.
4. Both have cancer risks that increases with duration of disease. Colonoscopies are recommended.
5. Proably but data is limited - very few placebo-controlled trials, mostly animal studies, reduced frequency of pain but not severity.
0. What is IBS/funcitonal ab pain characterized by?
1. What are the symptoms of irritable bowel syndrome/functional abdominal pain?
1.5 Who does it occur more in? When? What might precede the diagnosis?
2. What things commonly exacerbate this condition?
3. What treatments are available? (3)
0. Disordered brain-gut communication due to autonomic nerve system dsyfunction
1. Chronic abdominal pain and altered bowel habits at least once a week for two months. Associated with 2 or more of the following at least 25% of the time (improves after pooping, associated with change in stool frequency/form)
1.5 women, common in late adolescence. Preceded by long history of constipation/viral gastroenteritis
2. Physical (constipation, lactose intolerance, H pylori, celiac disease, drug therapy)/psychological stressors, physiologic phenomena (GER, gastric emptying, gas, etc), fiber/H2O, milk, fat 4 Ps (prunes, plums, peaches, pear), gum, xylitol, sorbitol, wheat, lactose
3. Counseling (id'ing triggers, strategies, peppermint oil which block Ca2+ channels), CBT, biofeedback, hypnosis, self-relaxation pharmaceutical (SSRIs, antidepressants, dietary fiber, mineral oil)
Dietary modifications - low-fat meals, small/frequent meals, avoid fructose, sorbitol/aspartame/gum chewing, high-fiber diet, lactose-free diet, probitoics
1. Describe normal evacuation of stool (6)
2. What is constipation? For men vs. women?
3. What causes it? (4)
4. Again, what type of diet causes constipation?
5. What are 3 phases of treatment for constipation?
1. Maintained by resting tonicity in internal anal sphincter, enhanced by contraction puborectalis muscle. (1) When 15 cc of stool enters rectum --> (2) stretch receptors
are activated --> (3) relaxation of internal anal sphincter --> (4)stool passes to external anal sphincter --> (5) relax sphincter -->(6) evacuation
Enter, activate, relax, pass, relax, pass
2. Constipation = small/infrequent stool. less than 3x for women, less than 5x for men
(low exercise, stress, dehydration), diet
(High fe, Al, Ca or low fiber diet)
4. diet (High fe, Al, Ca or low fiber diet)
5. Phase I - evacuation
(enema/mineral oil, laxatives)
- Phase II - Maintain evacuation (goal: 1 formed, soft stool/day)
- - Infants--> give oatmeal, prune juice, laxatives, corn syrup and avoid fiber, enemas, mineral oil.
Phase III - weaning off medications
- reduce laxatives/softening agents gradually, increase fiber intake (don't exceed 20 g/day). Don't add fiber at beginning bc it can cause stool to be compacted
1. How does intestinal flora compare in breastfed vs. formula fed infants?
2. What is more important after delivery?
3. What do low BW infants that have been hospitalized in NICU have? (4)
1. Breastfed - have bifidobacterium species (lactobacilli and staph), while formula fed have bifidobacteria, bacteriodes - E coli, staph, clostridia
2. Environmental factors - Csection babiesh ave low bacteroides species.
3. Prolonged antibiotic, parental nutrition, delayed oral feedings, intuution --> lower levels of lactobillus and bifidobacteria.
1. What is small intestinal/bowel bacterial overgrowth (SIBO)
2. What causes it? (6)
3. Complications of SIBO (5)
4. Treatment (2)
1. Disorder of excessive bacterial growth in small intestine NOT BOWEL
2. (1) decreased acid secretion (2) intestinal dysmotility (3) mechanical obstruction (4) immunodeficiency (5) fistulas (6) antibiotic use (7) malabsorption - rapidly digested food nourishes bad bacteria/yeast rather than feeding lactobacillus/bifidobacterium fiber.
Can also be caused by chronic diarrhea, crohn's, celiac disease, short gut diease
3. C. difficile infection, mucosal injury (decreased protien absorption), deconjugated bile acids (fat malabsorption, fat-sol vit def), vitamin B12 def
Diet - high protein, low in plant foods to promote growth of bacteriodes species. OR lacto-vegetarian diet to promote growth of lactobacillus/bifidobacterium
Medication - probiotics, soluble fiber, etc.
1. NAFLD vs. NASH?
2. Disease progression?
3. Treatment (4)
1. Non-alcohol fatty liver disease (macrovesicular steatosis >5% of hepatocytes) vs. Non-alcoholic steatohepatitis (macro and microvesicular steatosis with inflammation and cellular injury)
2. Healthy liver + fatty infiltration + obesity/insulin resistance --> NAFL ---(oxidative stress)---> NASH --> Cirrhosis
3. Reduce liver fat by insulin-sensitizing agents, vitamin E antioxidants, fish oils, probiotics.