GI week 2

5-ASA MOA

Topical anti-inflammatory effect on diseased GI mucosa

5-ASA uses

Ulcerative colitis, mild Crohn’s (colonic)

5-ASA adverse effects

Sulfasalazine: GI upset, headache, arthralgia, bone marrow suppression, folate deficiency

Sulfasalazine unique fact

Requires folate supplementation

Pentasa release site

TIme released microngranules throughout small intestine(Only Asa that doesnt do the colon>pentagon is important like small intestine)

Asacol/Apriso release site

ASA; pH sensitive released into Distal ileum & colon

Lialda release site

ASA; pH sensitive release into Colon

Glucocorticoid MOA

Suppress inflammatory cytokines (TNF‑α, IL‑1), chemokines, COX‑2, PLA2, NF‑κB

Glucocorticoid uses

Moderate–severe IBD flares

Glucocorticoid adverse effects

Cushingoid features, hyperglycemia, osteoporosis, infections, adrenal suppression

CUSHINGOID: cataracts, ulcers, skin, hump/hypertention, infection, necreosis, growth slowing, osteoporosis, icn ICP, diabetes

Budesonide MOA

Topical steroid with high first‑pass metabolism

Budesonide uses

Mild–moderate Crohn’s (ileum/proximal colon), UC (Uceris)

Budesonide adverse effects

Increased toxicity with CYP3A4 inhibitors

Azathioprine/6‑MP MOA

Purine antimetabolites → inhibit DNA/RNA synthesis → suppress T‑cells

Azathioprine/6‑MP uses

Crohn’s, UC, autoimmune hepatitis, transplant, rheum diseases

Tofacitinib MOA

JAK inhibitor → blocks JAK‑STAT cytokine signaling; dec inflammation

Tofacitinib uses

Moderate–severe UC

Tofacitinib adverse effects

Infections, TB reactivation, shingles, ↑ cardiac events, DVT, cancer (You dont know Fact Jak)

Ozanimod MOA

S1P receptor modulator → prevents lymphocyte egress from lymph nodes> reduced immune response

Ozanimod uses

Moderate–severe UC, multiple sclerosis

Ozanimod adverse effects

Cardiac conduction issues, liver injury, skin cancers, infections, PML

Ozanimod contraindications

Cardiac disease, untreated sleep apnea, MAOIs

Etrasimod MOA

S1P receptor modulator → decreases circulating lymphocytes>dec inflammatory response (Mod think modulator)

Etrasimod uses

Moderate–severe UC

Etrasimod adverse effects

Cardiac issues, liver injury, skin cancers, infections, PML

Anti‑TNF MOA

Bind TNF‑α → block pro‑inflammatory signaling

Anti‑TNF drugs

Infliximab*, adalimumab, certolizumab, golimumab

Anti‑TNF (infliximab) uses

Moderate–severe Crohn’s & UC

Anti‑TNF (Inflixamab) adverse effects

TB reactivation, Hep B reactivation, infections, infusion reactions, skin cancers, lymphoma

Vedolizumab MOA

Blocks α4β7 integrin → prevents WBC migration into GI tissue>less inflammation (a4b7»no WBC into GI tissue so they get VEDOed)

Vedolizumab uses

Moderate–severe Crohn’s & UC (2nd line)

Vedolizumab adverse effects

Infections, arthralgia, neutralizing antibodies

Ustekinumab MOA

Blocks IL‑12 & IL‑23 → inhibits cell‑mediated inflammation (Tom Brady (12) and MJ (23) are kin goats)

Ustekinumab uses

Moderate–severe Crohn’s & UC

Ustekinumab adverse effects

Infections, headache, allergic reactions, slight ↑ cancer risk

Guselkumab(Tremfya) and Risankizumab(Skyrizi); MOA, Uses, ADE

Block IL‑23 p19 → reduce pro‑inflammatory cytokines. Used for Moderate–severe Crohn’s & UC. ADE: Infections, hypersensitivity, headache, liver injury (The goats as well IL23>)

Bulk‑forming laxatives MOA + Ex

Psyllium; Hydrophilic colloids → increase stool bulk → stimulate peristalsis

Osmotic laxatives

Mg salts, sorbitol, lactulose, PEG

Stimulant laxatives MOA

Senna, bisacodyl; Direct enteric nerve stimulation → increased motility

Lubiprostone MOA +uses

Activates type‑2 chloride channels → ↑ fluid secretion; Chronic constipation, IBS‑C (Lube up with Cl)

Linaclotide MOA + Uses

Activates guanylate cyclase‑C → ↑ Cl⁻, HCO₃⁻, water secretion. Used for Chronic constipation, IBS‑C

Dicyclomine/Hyoscyamine MOA

M1 anticholinergic → ↓ GI motility & spasm (Clo like cholinergic; DIe cholinergic=anti)

Alosetron MOA

5‑HT3 antagonist → ↓ visceral pain, ↓ colonic motility. Used for Severe IBS‑D in women

Peppermint oil MOA

Blocks kappa‑opioid, 5‑HT3, and Ca²⁺ channels; Used for IBS-D

Loperamide MOA

Peripheral μ‑opioid agonist → slows motility. Used for Diarrhea. ADES: QT prolongation, QRS widening, torsades

Amitriptyline MOA + Use

Inhibits 5‑HT & NE reuptake; Used for IBS‑D, neuropathic pain, migraine prophylaxis

Albendazole/Mebendazole MOA + Use

Inhibit microtubules → block glucose uptake in parasites. Used for worms (Worms are tubes>inbhibit microtubules youre good)

Thiabendazole use

Cutaneous larva migrans, strongyloides, trichinosis

Ivermectin MOA + Use

Opens glutamate‑gated Cl⁻ channels → paralysis of parasite. Strongyloides, scabies

Nitazoxanide MOA

Inhibits pyruvate:ferredoxin oxidoreductase. Used for Cryptosporidiosis, giardiasis

TMP‑SMX MOA + Use

Blocks folate synthesis. Used UTI, MRSA, PCP, Listeria (if pen‑allergic), Stenotrophomonas, Cyclospora

Phenylketonuria dietary treatment

Restrict phenylalanine

Maple syrup urine disease dietary treatment

Restrict branched‑chain amino acids

Glycogen storage disease dietary treatment

Provide nocturnal cornstarch

Hereditary fructose intolerance dietary treatment

Avoid fructose and sucrose

Galactosemia dietary treatment

Eliminate milk and dairy products

Sitosterolemia dietary treatment

Restrict plant sterols

Adrenoleukodystrophy dietary treatment

Restrict very‑long‑chain fatty acids

Abetalipoproteinemia dietary treatment

Low‑fat diet, high MCT intake, high‑dose vitamins A and E

Abetalipoproteinemia clinical features

Neonatal diarrhea, steatorrhea, Failure to thrive, hemolytic anemia, retinal degeneration, neurologic decline

Abetalipoproteinemia biochemical defect

Absent chylomicrons, VLDL, LDL due to MTP mutation»cannot get fat into body

Why abetalipoproteinemia causes vitamin deficiency

Cannot absorb fat‑soluble vitamins (A, D, E, K) A and E particularly because D and K get small endogenous synthesis

Why MCTs help in abetalipoproteinemia

MCTs are absorbed directly into portal blood without chylomicrons

Long‑chain fatty acid absorption

Requires chylomicrons and lymphatic transport

Medium‑chain fatty acid absorption

Directly absorbed into portal circulation

Post‑gastrectomy dietary needs

Increase iron and vitamin B12

Post‑gastrectomy(removal of stomach) clinical features

Early satiety, dumping syndrome, diarrhea, vomiting, iron deficiency, B12 deficiency

Why gastrectomy causes iron deficiency

Loss of gastric acid prevents Fe³⁺ → Fe²⁺ conversion needed for absorption

Why gastrectomy causes B12 deficiency

Loss of intrinsic factor from parietal cells prevents ileal absorption

Vitamin B12 absorption step 1

B12 binds haptocorrin in stomach, then intrinsic factor in duodenum

Vitamin B12 absorption step 2

B12‑IF complex absorbed in terminal ileum via Cubam receptor

Causes of B12 malabsorption

Atrophic gastritis, autoimmune gastritis, gastrectomy, gastric bypass, chronic PPI use

Post‑gastrectomy treatment

Small frequent meals, moderate fat restriction, oral iron, parenteral B12

Diet therapy for kidney stones

Reduce oxalate, increase calcium

Enteric hyperoxaluria mechanism

Fat malabsorption → calcium preferentially binds fatty acids → free oxalate absorbed → kidney stones

Foods high in oxalate

Root vegetables, tea, cocoa, peanuts, bran, rhubarb

Treatment of enteric hyperoxaluria

Increase calcium intake, high fluids, low‑oxalate diet, moderate fat restriction

Key components of nutrition assessment

Diet history, weight history, symptoms, physical exam, body composition, nutrient stores, daily requirements

Elements of diet history

Specific diet patterns, allergies, intolerances, fast food frequency, 24‑hour recall, food diaries, supplements

GI conditions affecting nutrition

Dysphagia, gastroparesis, PUD, chronic nausea, diarrhea, celiac disease, Crohn disease

Surgical history affecting nutrition

Gastric bypass, ulcer surgery, bowel resections, cholecystectomy

Chronic illnesses affecting nutrition

DM, CHF, CKD, cirrhosis, cancer, AIDS, TB, SLE

Symptoms of nutrient deficiencies

Pica (iron), anemia (iron/folate/B12), bruising (vit K/C), night blindness (vit A), sore tongue (B vitamins), rash (niacin/zinc), neuropathy (B1/B12)

Symptoms of fat malabsorption

Steatorrhea, ADEK deficiency, essential fatty acid deficiency

Weight history components

Current weight, ideal weight, % ideal weight, max lifetime weight, desired weight, recent weight change

Significant weight loss thresholds

5% in 1 month or >10% in 6 months

Central vs peripheral obesity

Central obesity(intraabdominal) linked to metabolic syndrome and higher cardiometabolic risk

Physical signs of malnutrition

Temporal wasting, glossitis, cheilosis, peripheral edema, ecchymoses

Protein requirement rule‑of‑thumb

Normal 0.8–1 g/kg/day

BMI Parameters

<15 manourished;15-25 Normal; 25-30=overweight; 30-35 Obesity 1; 35-40 Obestity 2; 40-45 Obesity 3

Caloric value of carbohydrates

4 kcal per gram

Caloric value of protein

4 kcal per gram

Caloric value of fat

9 kcal per gram

Caloric value of alcohol

7 kcal per gram

Prolonged fast energy state

Ketone production increases

Components of total energy expenditure

Resting energy expenditure (REE), thermic effect of food (TEF), activity energy expenditure (AEE)

Factors increasing Resting Energy Expenditure

Growth, pregnancy, lactation, fever, sepsis, hyperthyroidism

Factors decreasing Resting Energy Expenditure

Aging, fasting, hypothermia, hypothyroidism

High‑protein diet effect on Thermic Effect of Food

Increases energy expenditure due to higher digestion cost