MF3: GI Flashcards
Indication of cow’s milk formula allergy
Blood in the stool
Natal nutrition year 1
BIRTH TO 6 MONTHS:
> Supplemental vitamin D for breastfed infants (deficiency associated with rickets [bone])
> First complementary foods should be iron-rich (iron-stores from mom depleted)
6 TO 12 MONTHS:
> Gradually increase number of times that complementary foods offered
Measurement of growth neonates
> Weight, length, weight for height, and head circumference (HC)
> Decreased weight:
- Undernutrition: head and height not usually affected
- Underlying issue (ex. chronic renal issue): slowed head or height growth
> Head-sparing (nutrition) vs not head-sparing (genetic causes)
> Failure to thrive: inadequate growth or inability to maintain growth (growth charts)
- Biggest issue is problem with amount of calories offered
- Psychosocial: height and head growth failure before or at same time that weight slows down (opposite pattern of usual)
> Trends in growth patterns over time provide more valuable information than a single measurement
Genetics of cystic fibrosis
> Class 1: Defective production synthesis
Class 2: Defect on protein processing (ΔF508 70% of American White patients)
Class 3&4: dysfunctional/decreased function
Class 5: accelerated channel turnover
First milk after labor
- High in protein, sodium, immunoglobulins while being low in lactose
- Significant due to immune-boosting effects because of high immunoglobulins (“first immunization”) IgA, IgM, and IgG
- Vitamin E (anti-oxidant and increases lifespan of erythrocytes)
- Phosphorus and Ca to prevent tetany
- Microbiota like Bifidobacterium and
Lactobacillus along with oligosaccharides confer anti-bacterial activity to the gut - Lactoferrin increases iron absorption and prevents degrading the bacteria
Protein differences between breastmilk and formula
> Proteins in infant formulas are typically cow-milk based with a predominance of casein over whey (whey-casein ratio of 20:80 compared to breastmilk (55:45 in mature milk, 80:20 in colostrum)
Hydrolyzed protein formulas contain protein that has been broken down into simpler proteins and is better tolerated in infants with milk protein allergies
Presentation and Correcting meconium ileus
PRESENTATION
- Obstruction of bowels by mucus plug; nearly 10% of patients with CF are born with it
- X-ray and Histology: distended goblet cells in the intestinal mucosa.
- Abdominal distention (a swollen belly)
- Bilious (green) vomit
- No passage of meconium
CORRECTION
- Nasogastric decompression (hyperosmolar + N-acetylcystein enema)
- IV fluids and
- Antibiotics are administered
Clinical Presentation of cystic fibrosis
LUNGS
> Less water on airway surface (mucus obstructive and stagnant),
> Excess inflammation during infection further blocks airways
PANCREAS
> Pancreatitis → Fibrosis
> Less HCO3 → more acidic chyme → impair enzymes → poor digestion
> Can’t absorb fat soluble vitamins (A,D,E,K)
> Poor insulin secretion (block ducts) → diabetes
INTESTINES
> Mucus block ducts and impair cilia (malnutrition due to malabsorption)
> Gastroesophageal reflux
> Intestinal atresia (intestinal obstruction)
> Steatorrhea (fatty stools)
SWEAT GLANDS
> More salt in sweat glands (diagnostic)
LIVER
> Blocked ducts → stenosis → stones → cirrhosis
REPRODUCTIVE
> Females: delayed first period, thickened cervical mucus
> Males: absent vas deferens
Esophageal hiatus
> A small opening in the diaphragm which allows the esophagus to enter the abdomen (T10)
Hiatus hernia when a portion of the stomach pushes up through the diaphragm (if large can allow food and acid to back up in esophagus)
Constriction points of esophagus
- Cervical constriction: cricoid cartilage (C5/6)
- Thoracic constriction: aortic arch (T4/5)
- Abdominal constriction: esophageal hiatus where passes through diaphragm (T10/11)
Gastric acid control
CONTROL: acid production and release is tightly regulated through complex interplay involving
> Activators, such as, histamine (secreted by enterochromaffin-like cells), acetylcholine (released from enteric neurons), and gastrin (released from G cells in antrum in response to protein meal)
> Inhibitors including somatostatin, vasoactive intestinal peptide, secretin, and cholecystokinin
Stomach mucosa
> Physical barrier of viscous mucus
- Foveolar cells & mucus neck cells: secrete molecules that make mucosal barrier (water, electrolytes, phospholipids, mucin proteins, bicarb)
> Production of bicarbonate (HCO) to neutralize acid
> Prostaglandins, which activate mucous and bicarbonate secretion and inhibit acid production
Factors that disrupt gastroduodenal mucosal integrity
H. pylori
> Urease produces ammonia, creating an alkaline environment which helps H pylori survive in acidic mucosa.
> Colonizes mainly the antrum of the stomach, causes gastritis and peptic ulcers (usually duodenal)
> Can increase gastrin production and inhibit SST, increasing acidity in stomach
> Most common initial treatment is triple therapy: amoxicillin + clarithromycin + PPI (antibiotics cure pylori)
NSAIDS
> Inhibit prostaglandin production, part of mucosal protection and blood supply
Alcohol
Peptic ulcers and investigation
> Defect in the mucosa that extends to the muscularis mucosa.
Inner layers are susceptible to acidity.
Ability of mucosal cells to secrete bicarbonate is compromised
Complications include bleeding, perforation (→ peritonitis), penetration of the ulcer into a nearby organ, blockage that stops food from stomach to duodenum
INVESTIGATION
> Endoscopy
> Barium swallow
> Blood testing
> H pylori testing
Scleroderma
> Systemic sclerosis (SSc) is a multisystem autoimmune disorder characterized by immune activation, vasculopathy, and abnormal collagen deposition in the skin and various internal organs
GI tract is one of the most commonly affected internal organ systems (90% of patients) → dysmotility, malnutrition, GERD, decreased LES pressure
PPIs
> PPIs are the most potent suppressors of gastric acid secretion available and inhibit the daily production of acid (both basal and stimulated) by 80%-95%
Irreversibly inhibit H/K-ATPase in stomach parietal cells
PPIs are prodrugs that require activation in an acidic environment
Acid secretion resumes only after new proton pumps are synthesized and inserted into the luminal membrane of parietal cells (24- to 48-hour)
Used in peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome, component of H pylori infection, stress ulcer prophylaxis
Adverse effects: Gastrin increase with chronic PPI use, increased risk of C. difficile infection (spores), pneumonia, acute interstitial nephritis, VB12 malabsorption, decreased Mg/Ca absorption (osteoperosis)
Rigid sigmoidoscopy
Endoscopy from rectum to sigmoid colon
Where are things absorbed in the small intestine?
“Dude is just feeling ill bro”
d = Fe
j = folate (95% carbs + protein + fats)
i = B12, bile and water; Peyers Patches (organized lymphoid nodules), broader villi so less absorb
Celiac (path, presentation, diagnosis)
> Inadequate absorptive surface due to immunologic reaction to gluten, a protein found in wheat, barley, rye, and possibly oats
Tissue remodelling leads to loss of villi and function
Th1 response to gluten; a type IV hypersensitivity (delayed type) → B cells → IgA antibodies for tGT
> Diarrhea, weight loss, anemia, symptoms of vitamin/mineral deficiency, FTT, bloating, gas, iron deficiency
> Celiac panel: total/quantitative immunoglobulins, IgA anti-Tissue Transglutaminase, IgA Endomysial Abs
GI endoscopy with small bowel biopsy: usually duodenal mucosa
Small bowel meal: drinking barium (rule out DDx)
Quantitative fecal fat >7%
Epigastric pain DDx
pancreatitis, esophageal rupture, AAA, perforated ulcer can all cause epigastric pain
Pancreatic position
Stretch and weight
Acute pancreatitis pathophysiology
> Premature activation of enzymes in acinar cells (elevation in ductal pressures and problems with calcium homeostasis and pH) → recruiting neutrophils → inflammation → capillary permeability → edema, decreased TPR, possible MODS, fever, renal failure
Biliary obstruction, chronic alcoholism, hypertriglyceridemia
Acute pancreatitis vitals
> BP is low at 80/60 mmHg: leaky vessels → edema
> Tachycardic at 120 beats/minute: inflammatory response leads to edema → decreased TPR →baroreceptors activate to increase HR
> Oxygen saturation is 85% on room air: pulmonary edema and ARDS
Acute pancreatitis next steps
oxygen, IV fluids, ECG (monitor heart, could have hypoCa), vasoppressors for edema
