GI Module

Review the academy and ASPEN recommendations to identify adult malnutrition and general diagnosis

2 of the following Insufficient energy intake Weight loss Loss of muscle mass Loss of subcutaneous fat Localized or generalized fluid accumulation that may sometimes mask weight loss Diminished functional status as measured by hand-grip strength

Calculate mL/kg/day and kcal/kg/day given a patient's current enteral feeding regimen. Calculate infant ml/kg/day food and kcal/kg/day

JT is a 45 day old ex-26 week GA preterm infant (now corrected to 32 wk GA). He weighs 2.1kg. He is still fed via NG tube due to the inability to suck and swallow yet. His current feeding regimen includes Breastmilk 24 40mL every 3 hours (fortified to 24kcal/oz with human milk fortifier

What are the six basic processes of the digestive system?

1. Ingestion (taking in food) 2. Secretion (release of water, acid, buffers, and enzymes into lumen) 3. Mixing and propulsion (churning and movement through GI tract) 4. Digestion (mechanical and chemical breakdown of food 5. Absorption (passage of digested products from GI tract into blood and lymph) 6.Defacation (elimination of feces from GI tract)

What are the four pathophysiologic methods of diarrhea and the four classifications?

1. A change in active ion transport by either decreased sodium absorption or increased chloride secretion 2. Change in intestinal motility = 3. Increase in luminal osmolarity 4. Increase in tissue hydrostatic pressure ------------------------------ •Secretary diarrhea •Secretory diarrhea occurs when a stimulating substance either increases secretion or decreases absorption of large amounts of water and electrolytes •Clinically, secretory diarrhea is recognized by large stool volumes (>1 L/day) with normal ionic contents and osmolality approximately equal to plasma. •Fasting does not alter the stool volume in these patients. •Osmotic diarrhea •Osmotic diarrhea occurs when poorly absorbed substances retain intestinal fluids •This process occurs with malabsorption syndromes, lactose intolerance, administration of divalent ions or consumption of poorly soluble carbohydrate •As a poorly soluble solute is transported, the gut adjusts the osmolality to that of plasma; in so doing, water and electrolytes flux into the lumen. •Clinically, osmotic diarrhea is distinguishable from other types, as it ceases if the patient resorts to a fasting state. •Exudative diarrhea •Exudative diarrhea occurs due to inflammatory diseases of the gastrointestinal tract which discharge mucus, serum proteins, and blood into the gut • Altered intestinal transit (motor diarrhea) •Altered intestinal motility produces diarrhea by three mechanisms: reduction of contact time in the small intestine, premature emptying of the colon, and bacterial overgrowth •Intestinal resection or bypass surgery and drugs (such as metoclopramide) cause this type of diarrhea ----------------------------------- Treatment: Prevention Antiobiotics and bismuth subsalicylate are advocated to prevent traveler's diarrhea, in conjunction with treatment of drinking water and caution with consumption of fresh vegetables --------------------------- Desired outcome if prevention is unsuccessful, goals are: 1. Manage the diet 2. Prevent excessive water, electrolyte, and acid-base disturbances 3. Provide symptomatic relief 4. Treat curable causes; 5. Manage secondary disorders causing diarrhea

Gallbladder

A pear shaped sac located on posterior surface of liver. Stores and concentrates the bile produced by the liver, until needed

Immunosuppressant therapy for IBS

Agents that target the excessive immune response or cytokines involved in IBD -Steroid sparing effects Slow onset of action: 3-12 months Cyclosporine IV onset (7 days) -All agents have serious side effects Meds: Azathioprine (1.5-2.5mg/kg/day) 6-mercaptopurine 0.75mg-1.5mg/kg/day Cyclosporine 4mg/kg/day IV cont infusion MOA: Azathioprine ---GST--> 6-Mercaptopurine (inhibited by xanthine oxidase) ----HGPRT-> 6-thio-IMP (intermediary mercaptopurine) Inhibits: de novo purine synthesis, dna replication, and cellular reproduction (inactivated by TPMT) Thus: Suppresses cytotoxic T cell proliferation and function -Inhibits NK cell activity ***IMportant: test TMPT deficiency because will end in toxicity if patient if taking an azathioprine ------ Also: If on allopurinol (gout medication) it is xanthine oxidase inhibitor. Thus, it would lead to increased prsence of 6-MP in patients taking azathioprine ------------------------------ Meds: Methotrexate MOA: folate antimetabolite -in Crohn's the MOA is not clearly known, but is suspected to modulate immune response and have anti-inflammatory effects -Off label use, but recommended in Crohn's clinical practice guidelines -Used in steroid dependent and steroid-refractory Warning: Teratogenic ------------------------- Cyclosporine (CSA) MOA: calcineurin inhibitor; blocks T-cell intracellular signaling pathways to lead to lowered expression of IL-2 and IFN-gamma 0Preferential for Cell mediated T-cell proliferation ------------------------ ALl drugs: Side effects: Azathioprine / 6- Mercaptopurine= N/V, bone marrow suppression (10%), pancreatitis (5%), hypersensitivity (5%), rash, fever, hepatitis Cyclosporine (CSA)= Nephrotoxicity, seizures, hypertension, hepatitis, infection, hypertrichosis, gingival hyperplasia - Many significant drug - drug interactions Methotrexate (MTX)= Increased liver enzymes and hepatic fibrosis, GI effects (N/V/D), bone marrow suppression, hypersensitivity pneumonitis ------------------------------- Azathioprine induced prancreatitis: Dose dependent and acquired less than 4 weeks into initiation -Primarily with Crohn's disease -Unknown mechanism Acute, persistent, severe, epi9gastric pain often radiating to the back -CT, elevated lipase/amylase ------------------------------ All drugs, monitoring: Azathioprine / 6- Mercaptopurine - May take >4 months at target dose for max effect - Avoid prolonged sun exposure - Baseline LFTs, weekly CBC Cyclosporine (CSA) - Renal function (SCr, BUN) - BP - 4th dose trough levels (goal: 200 - 300 ng/mL) Methotrexate (MTX) - Periodic CBC - LFTs (liver enzymes, albumin) ±liver biopsy - Baseline CXR - Replace folic acid ---------------------------- Role in therapy: AZA/6-MP: -Long term maintenance of remission -Reduced need for corticosteroids CSA -Acute treatment of severe/fulminant or refractory UC (not rec for CD) MTW -Reserved for steroid dependent and steroid-refractory crohns disease -Caution/avoid if high hepatotoxic risk

Select the appropriate administration method of enteral nutrition given specific patient data`

Appropriate administration method of EN Method of delivery depends: On location of tip of feeding tube Stomach vs. intestine On clinical condition and intestinal function of patient Does stomach work (i.e., no impairment in gastric emptying) On environment in which patient resides No electricity so must have gravity feeds (i.e., bolus) On patient's tolerance to tube feeding Can only tolerate small volumes of feeds at a time ---------------------------------- Bolus: Deliver over 5 to 10 mins Feeds into stomach Avoid in patients with delayed gastric emptying and those at high risk of aspiration Intermittent Good for infants/children. 20-60 minute delivery

Small intestine Describe how the small intestine uses surface area using folds and villi, the three regions, the types of cells, brush border (and enzyme), absorption, segmentations, and the migrating motlity complex

Begins at the pyloric sphincter of the stomach, coils through the central and inferior part of the abdomen and opens into the large intestine. (most digestion and absorption of nutrients occurs in this small intestine) Divided into three regions: 1. Duodenum (the shortest region, starts at the pyloric sphincter) 2. Jejunum (empty which is how it is found at death) 3. Ileum (joins the large intestine at the ileocecal valve) Histology: 1. Absorptive cells of the epithelium release enzymes that digest food (known as brush border enzymes). In addition, intestine contains microvilli that absorb nutrients in chyme 2. Goblet cells: secrete mucus 3. Intestinal glands/ crypts of Lieberkuhn: form the cells lining the deep crevices of small intestine. They contain enteroendocrine cells: -S cells: secretin (released by stimulation of acidic chyme in the duodenum and stimulates the release of bicarbonate rich solution from pancrease inhibiting stomach motility, and pepsinogen release -CCK cells: cholecystokinin. Release is stimulated by lipids in the chyme. Stimulates pancreatic lipase and causes gallbladder to contract (releases bile into dudoenom to emulsify fats) also decreases stomach motility -K cells: glucose dependent insulinotropic peptide (GIP) 4. Paneth cells: secrete lysozyme -a bacterial enzyme, capable of phagocytosis, regulates the microbial population in the small intestine 5. Lamina propia: areolar connective tissue and an abundance of Mucosa-associated lymphoid tissue (MALT) 6. Duodenal cells: present in the submucosa and secrete alkaline mucus that hepls neutralize gastric acid in chyme 7. Circular folds, villi, and micro,villli: Used to enhance surface area and slow motility Circular folds: cause cyme to spiral and increases SA Villi: increases SA. Each is supplied by a arteriole, venule, blood capillary network, and lacteal lymphatic capillary. Nutriets absorbed by passing through the wall of a capillary. (absorptive) Microvilli: form fuzzy line called brush border (too small to be seen indvidually) ---------------- Juices of the small intestine: Intestinal juice: comprised ofwater, mucus, sodium bicarb. Along with pancreatic juice, provides a liquid medium that aids the absorption of substances from chyme in the small intestine Two types of movement in the small intestines (govered by the myenteric plexus) 1. Segmentations: localized mixing contracts that mix chyme with digestive juices to bring the particles of food into contact with the mucosa for absorption (doesnt push intestinal contents) 2. Migrating motility complexes: Peristalsis that occurs in a small intestine once most of the meal has been absorbed. Pushes chyme forward alng a short stretch of small intestines Chemical digestion: chyme enters the small intestine contains partially digested proteins (pepsin), carbohydrates (salivary amylase), and lipids (lingual and gastric lipases) -Complete digestion is a collective effort of pancreatic juice, bile, and intestinal juice in the small intestine -Carbohydrates: a-destinase, sucrase, lactase, maltase -Proteins: peptidases in the brush border: aminopeptidiase and dipeptidase Lipids: emulsified by bile salts and broken down by pancreatic lipase

Identify patients who would benefit from brief alcohol intervention and those appropriate for alcoholic hepatitis treatment

FRAMES: Feedback Responsbility Advice Menu Empathetic interviewing Self-efficacy

Prenteral additives

Heparin is only used in NICU (neonatal intesnive care unit) Reduced thrombophlebitis Enhanced lipid clearance Regular insulin Not for acute setting and for patients on stable PN H2 blockers stress ulcer prophylaxis PPIS are incompatibile Albumin should not be added. Increases microbial growth and infection risk Iron dextran, no native iron source in PN. Should not be added in 3 in 1, can interefere with ILE

Discriminate different modes of transmission for hepatitis A, B and C

Hepatitis A is spread through fecal oral route Hepatitis B is spread through parenteral, sexual route Hepatitis C is spread through parenteral route

Calculate maintenance fluid requirements based on patient-specific information

Holliday-Segar method (mL/day) Or 4-2-1 rule Page 2 of study guide -----_ Fluid deficit: 5 point assessment Volume deficit, osmolar disturbance (sodium), acid-base disturbance, potassium, renal function Page 2 of Study guide 1 = severity of dehydration effects

Anti-diarrheal agents: opiates

OPIATES •Opiates and opioid derivatives •(a) delay the transit of intraluminal contents or •(b) increase gut capacity, prolonging contact and absorption. •Enkephalins, which are endogenous opioid substances, regulate fluid movement across the mucosa by stimulating absorptive processes. •Limitations to the use of opiates include an addiction potential and worsening of infectious diarrhea •Loperamide (Diamode; Imodium®) •It acts only peripherally and does not have any CNS action - no analgesic or euphoric properties •It is antisecretory and it inhibits the calcium-binding protein calmodulin, controlling chloride secretion •Dosage forms - 2 mg capsules or 1 mg/5 ml solution - both are OTC •Diphenoxylate (Lomotil®; Lonox®) •It is combined with atropine to discourage abuse - excess dose - anticholinerigic effects - dry mouth •Dosage forms - 2.5 mg tablet and 2.5 mg/5 ml solution •Opiates should not be used in patients at risk of bacterial enteritis with E. coli, Shigella, or Salmonella. •Paregoric, tincture of opium, (2 mg/5 mL solution) is not widely prescribed today because of its abuse

Describe the anatomy of the mouth What are the present glands Describe the neural control of salivation What is amylase?

Oral ,or buccal cavity -Salivary glands: releases saliva into the oral cavity uses 3 glands: 1. Parotid gland (one on each side of face in cheek and has duct opening to mouth 2. Submandiublar gland (under the jaw) opens to the mouth of the floor 3. Sublingual gland (lies beneath tongue) Salivation is controlled by neural influences -Parasympathetic branch of ANS plays prominant role while sympathetic gland drys mouth Saliva helps: digestion of polysaccharides, to lubricate food, protect the oral cavity from bacteria, and combat invading microbes, while keeping mouth and teeth clean and at a pH of 7 Salivary amylase: breaksdown complex sugars and starches Lingual lipase gets activated in the acidic environment of the stomach and breaks down dietary triglycerides into fatty acids and diglycerides

Name some common GI diseases

Page 1 Image in notes

Biologic medications in IBS

TNF blockers: -All injectable preparations Extremely costly Serious AE Advantages -> quick onset (2 weeks) FDA black box warnings: -fatal infections -Malignancy - lymphomas -Tuberculosis evaluation ATTACH trial-> -Increased HF related hospitalizations and death Jain and Singh -> failed to detect an increased risk EXCEPT FOR THE ELDERLY AHA: for infliximab, avoid use in patients with moderate to severe HF; do not administer doses exceeding 5mg/kg Prior to intiating therapy: TST (tuberculin skin test) Hepatitis B screening Immunizations: up to date with all immunizations before initiating therapy -Infliximab (remicade) -Murine-human IgG antibody Route: IV only Dose: 5mg/kg IV infusion over 2 hours Time to response = 2 weeks ==== Adalimumab -SQ injections (every 2 weeks from start) Common adrs: headache, nausea, rash -SQ injection avoid infusion risk of infliximab (certolizumab can be used; combined with PEG to extend duration) ==== Ustekinumab (stelara) MOA: human IgG monoclonal antibody blocks IL-12 and IL-23 receptors on T cells Use: moderate to severe CD when: -Failed or intolerant to immunomodulatory or corticosteroid therapy but never failed anti-TNF therapy -Or, failed/intolerant to anti-TNF therapy ADR: headadche fatigue, dizziness Natalizumab -Monoclonal Ab against alpha-4 subunit of integrin molecule -Prevents leukocyte adhesion and migration across endothelium USE: restricted patients who failed other therapies Black box warning: progressive multifocal leukoencephalopathy -Limit use to patients who are not seropositive for anti-jC virus antibody CD-touch program - enroll and renew q 6 months -=== Vedolizumab -Human monoclonal antibody with blocks A4B7 integrin to selectively block gut lymphocyte trafficking Use in active CD and UC - failed previous therapy Dosing: 300mg IV at 0,2,6, weeks then every 8 weeks -Discontinue therapy by week 14 if there is no evidence of therapeutic benefit -Infuse over 30 minutes ADEs: headache, arthralgia, nasopharyngitis, fatigue, antibody development =========== Tofacitinib (Xeljanz®) • MOA: inhibitor of Janus kinases to block signaling of IL- 2, 4, 7, 9, 15, and 21. • NEWLY FDA- approved for moderate to severe ulcerative colitis • Dosing: 10mg BID for at least 8 weeks • ADRs: see anti- TNFs; neutropenia, ↑LDL • Advantage: ORAL dosage form

Describe the peritoneum

The Peritoneum is the MEMBRANE. Largest serous membrane in the body and divided into: -Parietal peritoneum (lines the wall of abdomen cavity) -Periotoneal Cavity (slim space containing lubricating serous fluid between the parietal and visceral portions. Can be distended by the accumulation of fluid (ascities) -Visceral Peritoneum: covers some of the organs in the cavity and is their serosa (tissue which lines certain internal cavities of the body forming a smooth, transparant, two layerered membrane lubricated by fluid from the serum

What are the two additives in infant formula and what do they do

These additives are associated with IMPROVED NEUROLOGICAL AND RETINAL DEVELOPMENT DHA = docosahexanoic acid synthesized from ALA -Important for neurological development -Highest concentration found in photoreceptor membrane ARA = arachidonic acid Required to achieve optimal growth

Describe HBV

Transmission Infectious blood or body fluids (e.g., semen, saliva) Sex with an infected partner Injection drug use that involves sharing needles, syringes, or drug-preparation equipment Birth to an infected mother (i.e. perinatal) Contact with blood or open sores of an infected person Needle sticks or sharp instrument exposures Sharing items such as razors or toothbrushes with an infected person Cannot be transmitted through casual contact --------------------------- HBV Viral replication 1. Replication begins upon attachment to hepatocyte 2. Particles transported to nucleus 3. DNA converted into close circular DNA and serves as template 4. Viral RNA transcribed and transported back to cytoplasm 5. Serves as reservoir for future viral templates --------------- pathophysiology 1. Acute infection 2. Chronic infection leads to 3a. Hepatocellular carcinoma 3b. Cirrhosis 3c. Decompensated cirrhosis All leads to: 4. Liver transplantation 5. Death ---------------------- Presentation: Symptoms of acute infection (30-50% individuals ≥5 years) Fever Fatigue Loss of appetite or abdominal pain Nausea/vomiting Dark urine Clay-colored bowel movements Joint pain Jaundice Chronic infection May be asymptomatic with no evidence of liver disease Liver disease may range from chronic hepatitis to cirrhosis or hepatocellular carcinoma (HCC) Goals and benefits of treatment: Prevention of long-term negative clinical outcomes (e.g. cirrhosis, liver transplantation, HCC, death) by durable suppression of HBV DNA Goal: sustained decrease in serum HBV DNA level to undetectable-suppression Secondary endpoints: decrease/normalize serum ALT Improve liver histology Induce HbeAg loss or seroconversion in HBeAg-positive disease Induce HBsAg loss or seroconversion Treatment often longterm/lifelong, particularly in HBeAg-negative patients ---------------------------- Treatment options: First line: Immune Modulating Therapy Pegylated interferon- α2a (Pegasys®) Nucleos(t)ide analogues Tenofovir alfenamide (Velmidy®) Tenofovir disoproxil fumarate(Viread®) hepatitis B immunoglobulin -provides passive immunity for post-exposure prophylaxis -Prepared from plasma of donors with HBsAb FOr unimmunized adults after exposure: 0.06ml/kg IM (within 24 hours of needle stick/14 days of sexual exposure) Infants born to HBsAG (+) mothers: 0.5mL IM within 12 hours of delivery -------------------------- Counseling for patients with HBV General counseling: Limit alcohol intake Get hepatitis A vaccine Limit acetaminophen to 2000mg/day Avoid herbal supplements PREVENT TRANSMISSION === Recommendations for HBV Vaccination All infants at birth Unvaccinated children <19 years Unvaccinated adults at risk or seeking vaccination History of STDs or multiple sex partners (>1 partner/6 months) Men who have sex with men Current/recent persons who inject drugs Household contacts & sex partners of persons with cHBV Healthcare workers with exposure to blood Clients & staff of institutions for developmentally disabled Travelers to regions with HBsAg prevalence ≥2% Recipients of clotting factors concentrates Correctional facilities inmates Chronic dialysis Chronic liver disease Pediatric —3 doses First dose: birth (w/n 12 hours if mother HBsAg (+); otherwise prior to discharge Second dose: 1 - 2 months Third dose: 6 - 18 months Adult (if not previously vaccinated) Recombivax HB & Engerix-B® — 3 doses: 0, 1, 6 months Hepislav-B® —2 doses: 0, 1 month Twinrix® accelerated schedule—4 doses: 0, 7 days, 21-30 days, +12 months ======

Alcoholic Liver Disease

Whats considered excessive? Women >= 4 drinks/occassion Men >= 5 drinks/occasion Women >=8 drinks/week Men >=15 drinks/week Standard drink = 12oz of beer 8-9 of malt liquor 5 fl oz of table wine 1.5 oz shot of distilled spirits Questionnaires for detecting alcoholism CAGE AUDIT AUDIT-C Normal metabolism progresses: alcohol---Oxidation---> acetaaldehyde -----ALDH---> acetate Abnormal pathogenesis due to alcohol Alcohol leads to fatty acid uptake and decreased fatty acid oxidation; thus, triglycerides accujmulate ALSO through acetaldehyde: 1. protein-acetaldehyde adducts arise from acetaldehyde. 2. Interfere with hepatic enzyme activities 3. Kuppfer cells are activated 4. Profibrogenic cytokines 5. Increased collagen and extracellular matrix 6. Leads to regenerative nodules (scarring) -------------------------------- Clinical features: Non specific symptoms: vague upper right quadrant abdominal pain, fever, nausea, diarrhea, anorexia -Can also cause jaundice Specific complications of chronic liver disease: ascites, edema, upper GI hemorrhage, encephalopathy Physical exame: -Enlarged liver/spleen Scleral icterus, palmar erythema, spider angiomas, parotid gland enlargement, digital clubbing, edema/ascites Lab findings: -Can be normal in early compensated alcoholic cirrhosis -Platelet count decreased even in early disease, and may fluctuate (reflective of portal hypertension with hyperspleenism) -Anemic (decreased HgB) -Total bilirubin: normal to elevated with advanced disease -Prothrombin times./INR increases -Sodium decreased in presence of ascites ALT & AST typically elevated AST>>>ALT ~2:1 -------------------- Diagnosis: -Continued alcohol use/abuse + clinical features -Liver biopsy considered (abstinent >=6 months to determine nonreversible disease) -Cirrhosis + continue to drink leads to <50% 5 year survival ----------------------- Treatment: Discriminant function (calculation) must be over 32 or MELD must be over 21 with alcohol abstinence and nutrition support (with absence of co-morbidity) Preferred treatment = prednisolone 32mg po daily for 4 weeks, then taper for 4 weeks Alternative = pentoxifylline 400mg TID for 4 weeks

Discuss issues related to optimal nutrition provision in adults and children with cancer, aids,critical illness, trauma, burn injury, inflammatory bowel, cystic fibrosis, pregnancy, and failure to thrive Describe important physiological impacts of AIDS wasting and treatment options

cancer: Important to maintain nutritional status -> enhanced survival and improvement in treatment tolerance In particular situations, may have to initiate specialized nutrition Occurs against a background of persistent hypermetabolism and chronic immune activation ------------------------ ****IMPORTANT: Aids wasting syndrome -> primarily characterized by involuntary weight loss consisting of both lean body and fat mass Lipodystrophy -> syndrome characterized by subcutaneous fat loss (in absence of lean body mass loss) with or without visceral abdominal fat accumulation; frequently accompanied by insulin resistance and dyslipidemia ------------------------ AIDS Treatment: FDA treatment for AIDS wasting syndrome: Appetite stimulants: -Megestrol acetate -Dronabinol (marinol) Growth hormone Anabolic-androgenic steroids -Oxandrolone ------------------------------------- TREATMENT OF LIPODYSTROPHY IN AIDS wasting Lipodystrophy = syndrome of peripheral subcutaneous fat loss with sparing of visceral fat (although accumulation of visceral fat may also occur) -Involves hypertriglyceridemia and insulin resistance Time dependent factors 1. Age >40yrs 2. HIV infection >7 yrs >=2 yrs since progression to diagnosis of AIDS >=3 yrs from nadir CD4 count (~200cells/mm^3) Drug dependent factors 1. Thymine analog use > 6months 2. Protease inhibitor use > 22 months Treatment: Egrifta (tesamorelin) Use: reduction of excess abdominal fat in HIV-infected patients with lipodystrophy MOA: binds to pituitary growth hormone-releasing factor (GRF) receptors and stimulates secretion of endogenous growth hormone which has anabolic and lipolytic properties Dose: 2mg SubQ daily AE: ISR and arthraliga ----------------------------- Critical illness-sepsis/trauma/burn Associated with changes in metabolic response: -Increases in energy expenditure -Protein catabolism -Oxidation of stored lipids -Significant alterations in body's ability to metabolize carbohydrates Leading to net loss of protein and lean body mass Can lead to malnutrition in 5-7 days in well-nourished patients, or 3-5 days in malnourished patients CAUTION FOR OVERFEEDING ------------------------------ Cystic fibrosis: growth retardation and failure-to-thrive Treatment = Calorie boosters SCANDICAL = 35kcals/tablespoon ---------------------------------- Pregnancy: Need an extra 300kcal/day during second and third trimesters Recommended weight gain = BMI <18.5 = 28-40lbs BMI 18.5-24.9 = 24-35 lbs BM between 25-29.5 = 15-24 lbs Twins = 44 lbs _______________________________________________ Failure to thrive Weight for age <5th percentile Weight for height <5th percentile decreased growth velocity -> weight falls by 2 major percentile lines in 6 month period

Presentation of constipation

• It is important to ascertain whether the patient perceives the problem as infrequent bowel movements, stools of insufficient size, a feeling of fullness, or difficulty and pain on passing stool. Laboratory tests • A series of examinations, including proctoscopy, sigmoidoscopy, colonoscopy, and barium enema, may be necessary to determine the presence of colorectal pathology. • Thyroid function studies may be performed to determine the presence of metabolic and endocrine disorders

Anti-diarrheal agents ADSORBENTS

•Adsorbents are used for symptomatic relief. •These products, many not requiring a prescription, are nontoxic, but their effectiveness remains unproven. •Adsorbents are nonspecific in their action; they adsorb nutrients, toxins, drugs, and digestive juices. •Polycarbophil absorbs 60 times its weight in water and can be used to treat both diarrhea and constipation. •Polycarbophil (Equalactin®; Fiber-Lax®; Fiber-Tabs™) •Dosage form: 500 mg chewable tablet - 4 times a daily - upto 6 g/day

Identify key counseling tips to help maximize the tolerability of bowel preparations

-Citrus flavors work best to mask salty taste DO NOT USE RED OR PURPLE FLAVORING AGENTS -Reconstitute with lukewarm water but refrigerate prior to use -Drink quickly -Use a straw to help bypass taste buds -Utilize split-dosing whenever possible

What are the four layers of the GI tract?

1. Mucosa: the layer of epithelium in direct contact with contents of GI tract (protection, secretion, absorption) *also contains Lamina Propia (connective tissue containing blood and lymph vessels & The Mucosa associated lymphatic tissue (MALT) *Also contains muscularis mucosae (many small folds which increases the SA for digestion/absorption. 2. Submucosa: many blood and lymph vessels that receive absorbed food molecules 3. Muscularis: voluntary skeletal muscle located in the mouth, pharynx, parts of the esophagus, and external anal sphincter to help with swallowing and defecation. Is composed of involuntary smooth muscles. Contractions breakdown food, mixing with secretions and moving along tract 4. Serosa/adventitia: superficial portion. Visceral peritoneum 4. Serosa

Recommend appropriate treatment for common fluid and electrolyte abnormalities

1. Oral replacement For mild-moderate dehydration failure rate of only 3.5% Underused by prescribers Contraindications: -Shock -severe dehydration -tractable vomiting -greater than 10ml/kg/hr stool losses -coma -acute abdomen -severe gastric distension Parental rehydration: Required for failure of PO therapy and all contradindications for PO ------------------ Medications that may cause hypokalemia: Loop and thiazide diuretics insulins amphoteracin B Hyperkalemia: diuetics Heparin ACE-I ARBs potassium Penicillin Bactrim Potassium function: determines resting membrane potential ------------------ Magnesium: Function: Cofactor for many enzyme systems for transfer reactions Muscle contractility Nerve conduction Hypermag: renal failure - paralysis, hypotension, AV block Hypomag: GI, renal losses, DRUGS: AMPHOTERACIN B. TACROLIMUS: - N, dizziness, weakness, convulsions -------------------- Calcium Neuromuscular activity Regulation of endocrine secretory activities Blood coagulation BONE METABOLISM -leads to osteoporosis CV issues Neuromuscular (cramps, seizures) ------------------ Phosphorus Bone and ell membrane composition, pH, forming ATP Hyper: renal dysnfuction Hypo: starvation, burns Causes: refeeding syndrome ---------------------------- Calcium supplementation: PO: 500-1500mg IV: 1-2g calcium Phosphorus: IV: 15-18mMole

Describe the most common components of a PN formulation

12 components make up PN: 1. Water 2. AA (4kcal/g) 3. Dextrose (3.4kcal/g) 4. Lipid injectable emulsions 5. Sodium 6. Potassium 7. Phosphorus 8. Chloride 9. Acetate 10. Calcium 11. Magnesium 12. Vitamins/trace elements Macronutrients provide energy and structural substrates 1. Water 2. AA 3. Dextrose 4. Lipid injectable emulsions Micronutrients support variety of metabolic activities necessary for cellular hemeostasis, such as enxzymatic reactions, fluid balance, and regulation of electrophysiologic processes 5. Sodium 6. Potassium 7. Phosphorus 8. Chloride 9. Acetate 10. Calcium 11. Magnesium 12. Vitamins/trace elements ------------------------- 2. AA = used primarily for protein synthesis. Infant amino acid products: Products: Trophamine Aminosyn Premasol More acidic pH than adult products Contains: little Na/Cl, but a lot of acetate Often add L-cystein at 40mg per gram(lowers pH) When administered in conjunction with cysteine, results in normalization of plasma amino acid concentrations to profile consistent with that of a breast-fed infant Pattern: AA requirements decrease as age increases ----------------- 3. Dextrose Primary source of energy for PN (50-70% of calories) Found as dextrose monohydrate PROVIDES 3.4KCAL/G Dextrose maximums= Peripheral = Pediatric: 12.5% Adult patients: 10% Central= ~35% ---------------------- 4. Fats (injectable lipid emulsions) -Source of condensed calories and essential fatty acids (linoleic acid, linolenic acid) ILE = -Aqueous emulsion of soybean oils -Long train triglycerides (linolenic and linoleic) -Egg yolk phospholipid included as emulsifier -Glycerol (contributes additiona energy-> 10kcal/g for ILE) 10% ILE provides 1.1 kcal/mL 20% ILE provides 2 kcal/mL 30% ILE provides 3kcal/mL Max of 3g/kg/day or 30-35% of total calories Minimum is 2% for total nutrient admixture (TNA, 3in1) Adjust based on triglyceride values #Examples: Nutrilipid 20% Soybean oil SMOFLipid 20% (only approved for adults) Soybean, MCT, olive oil, fish oil -------------------------------- Micronutrients - Electrolytes *salt form is preferred ---------------------------- Vitamins Pediatric and adult formulations available Water soluble = B Vitamins - 1, 2, 3, 5, 6, 12 Biotin Folate Ascorbic Acid Fat soluble = A, D, E, K Vitamin K not available in all adult formulations ----------------- Water Affected by total volume of PN ordered Not ordered by prescriber Added as sterile water for injection (SWI) QS to volume ordered for PN

Identify the pharmacologic mechanism of common agents for bowel preps

5 classes of agents: 1. Isoosmotic = PEG solutions (colyte, gavilyte-C, glytely). Inert polymer of ethylene oxide (passes through b owel without absorption or secretion. Advantages: osmotically balanced -> no fluid or electrolyte shifts Considered safe for use in patients with existing electrolyte abnormalities and those who cannot tolerate significant sodium load Disadvantages: requires patient to drink 4L of fluid Poor taste due to sulfate component and high salt concentration Higher risk of causing abdominal cramping or nausea/vomiting Least tolerable agent overall ALTERNATIVE: Sulfate-free polyethylene glycol electrolyte solutions -Decreased potassium, increased chloride Improved smell and taste of product efficacy and safety is comparable to PEG ALTERNATIVE: Moviprep (low volume PEG solution) -Formulate with ascorbic acid for flavor and cathartic action Cotraindicated in: glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia. Potential adverse effects of isosmotic agents: N/V, abdominal pain/cramping, pulmonary aspiration risk (stop intake 2 hours prior to procedure), mallory-weiss tear (tear in mucosa at junction of stomach and esophagus for major bleed), pill malabsorption, exacerbation of SIADH, Increased thirst ---------------------------------- Hyperosmotic agents -Sports drink or water + OTC PEG +/- bisacodyl -Commonly used, but not FDA approved Unclear efficacy and safety data (higher risk of hyponatremia compared to balanced solutions. -AVOID IN PATIENTS WITH ELECTROLYTE ABNORMALITIES Oral sulfate solution: Suprep -Hypertonic, but does not cause fluid or electrolyte shifts in practice. -Expensive ALTERNATIVE: OTC magnesium citrate -Saline solution that promotes bowel cleansing by: -Osmotic action drawing fluid into colo -Stimulates the release of cholecystokinin NOT FDA APPROVED and NOT RECOMMENDED Concern for magnesium toxicity: eliminates renally, AVOID USE IN CKD AND ELDERLY -Can cause bradycardia, hypotension, nausea, and drowsiness Palatability can be improved by chilling befroe use ALTERNATIVE: Sodium phosphate = osmoprep (combines tablets of sodium phosphate with glasses of water) USE IS NOT RECOMMENDED DUE TO LARGE FLUID AND ELECTROLYTE SHIFTS BBW: phosphate nephropathy, especially in the following patiets: elderly, renally impaired, meds that affect renal perfusion ---------------------------- Combination agents: Sodium Picosulfate/Magnesium Oxide/Citric Acid = Prepopik®, Clenpiq® Two mechanisms of action: Sodium picosulfate = stimulant laxative Magnesium/citrate = osmotic laxatives DATA SHOWS THIS AGENT MIGHT NOT BE AS EFFECTIVE AS OTHER BOWEL PREPS. ----------------------------------- Adjunctive agents: Stimulant laxatives -Bisacodyl (dulcolax) -Diphenylmethane derivative that stimulates colonic peristalsis -does not improve imaging when used with other 1st line agents -ADEs = include abdominal cramping and rare ischemic colitis Sennosides (senna) -Stimulant laxative similar to bisacodyl (no differences found between the stimulant options) -Relatively neutral effect on visualization, but may allow for decreased total voume MIISC adjunctive agents: Metoclopramide (reglan) -Mechanism enhances motility and accelerates gastric emptying -Has not been shown to improve tolerability of GI preparation -Risk of serious ADEs include EPS side effects, worsening in Parkinsons Simethicone: promotes clearance of excessive gas in the GI tract to reduce bloating and abdominal discomfort/pain -Not shown to improve quality of bowel prep but may reduce bubbles -> enhanced visualization

For each of the following complications: portal hypertension, esophageal varices, ascites, spontaneous bacterial peritonitis (SBP): A. Identify potential targets of pharmacological therapy B. For selected pharmacologic agents, describe the relevant mechanism(s) of action and expected outcomes C. Compare and contrast available non-pharmacologic and pharmacologic treatment options, in order to recommend a specific treatment regimen D. Create treatment goals for an individual patient E. Apply recommendations from evidence based guidelines

A. Cirrhosis -> portal HTN-> splanchnic dilation ->arterial underfilling->activation of vasconstrictor and antinatriuretic factors-> 1. Sodium and water retention (expansion of plasma volume) 2. Impaired free-water excretion 3. Renal vasoconstriction (hepatorenal syndrome) ALL CAUSE ASCITES Diagnosis: Physical examination (wave motion and dullness on percussioN) Ultrasound BNP (<200 = ascites) Abdominal paracentesis with fluid evaluation ---------------------- Abdominal paracentesis: Left lower quadrant on abdomen is preferred site -Minimum of 25mL must be collected -Collec count and differential -Chemical analyst Serum-ascites Albumin Gradient (SAAG) -If >1.1 the patient has portal hypertension Total protein: <2.5 = ascites from cirrhosis >2.5 = cardiac cause of ascites ---------------------------- B. Pharmacologic therapy Diuretic therapy: Loop diuretics: ●Effective - must use cautiously ●Can cause intravascular depletion ●Monitor electrolytes and renal function Aldosterone Antagonist ●Addresses pathophysiologic mechanism ●Best matches equilibration ●Monitor potassium and renal function Combination therapy recommended: Spironolactone + furosemide ALSO: Large volume paracentesis Pros: can remove large volume of ascites -need to replace albumin(8-10 gm albumin per liter fluid removed) -Reduces pressure on the diaphragm CONS: -bleeding from needle entry -perforation of bowel -infection -Re-accumulation of ascites ===== Medications to avoid: ●Angiotensin Converting Enzyme - Inhibitors ●Angiotensin Receptor Blockers ●Propranolol in refractory ascites ●NSAIDs/Aspirin -------------------------- C.Treatment plan: 1. Sodium restriction 2. Diuretic therapy 3. Medications to avoid D. Goals of treatment: 1. Treat underlying disorder/control ascites ●Less than 2 grams of sodium allowed per day ●Increase the daily urinary excretion of sodium ●Fluid restriction is not necessary unless the serum sodium concentration is less than 120 mmol/L or mental status changes attributed to hyponatremia develop 2. Prevent or relieve ascites-related symptoms -Dyspnea, abdominal pain, abdominal distension 3. Prevent life-threatening complications -Spontaneous bacterial peritonitis and hepato-renal syndrome

What is the duration of persistent/acute/chronic diarrhea?

Acute diarrhea <14 days Persistant >14 days Chronic >30 days

Compare and contrast the dextrose-amino acids (2in1) system for PN versus the total nutrient admixture (TNA)system in terms of convenience stability, and compatibility and potential to support microbial growth if contaminated

Admixture types 2-in-1 Dextrose + amino acids + micronutrients Lipid injectable emulsion separately infused 3-in-1 Dextrose + amino acids + micronutrients + lipid injectable emulsion Often referred to as TNA (total nutrient admixture) Advantages: Fat clearance better More cost effective Disadvantages of TNAs= -Larger particle size of admixed IVFE cannot be used in 0.22micron (bacteria eliminatingg filter) and requires larger pore size filter of 1.2microns -Admixed IVFE less stable -Formulations are more sensitive to destabilization with certain electrolyte concentrations -Formulation more sensitive to destabilization with certain electrolyte concentrations -Lower pH amino acid formulations may destabilize IVFE portion of admixture Formulation may be unstable when final concentration of IVFE is low Certain medications are incompatible with IVFE porton of admixter -Catheter occlusion more common with daily IVFE -------------------------- In the real world: Most pediatric hospitals use 2-in-1: May not have enough ILE for stable emulsion and can crack because of lower pH (demulsify) -Increased calcium-phosphorus needs so increased potential for precipitation -Morel ikely to have limited access and thus more likely to have compatbility issues -Worried about infection risk (should only hang ILE over 12hrs if draw up into new container from original containers) -Adult hospitals may use both methods Infection ILE > TNA > 2in1 PN formulations

Calculate amounts of fluid, calories, protein, carbohydrate (in mg/kg/min) fats, electrolytes, osmolarity provided by a given parenteral nutrition regimen

Amino acids = 1.5g/kg/day Using 10% amino acid solution Dextrose = 300 g/day Using 70% dextrose solution ILE = 1g/kg/day Using 20% ILE solution For our purposes, assume 150ml for electrolytes/vitamins/trace elements -------------------- You're calculating M1V1 = m2v2 with each part of TPN and then added together to find necessary ml of water. ------------------------- Calculating kcal = AA =4kcal/g Dextrose = 3.4kcal/g ILE = 10kcal/g ----------------------- Calculating GIR Will be given formula (g of dextrose * 1000) / (weight in Kg * 1440) 1440 = mins per day -------------- Osmolarity = find percentage of macronutrient in entire bag then multiply by 100 to find mOsm Example: 65g of AA/ 2400mL * (100) = percentage AA = 100mOsm per % Dex = 50mOsm per % --- 1 mMol of sodium phosphate contains 1.33 mEq of sodium 1 mMol of potassium phosphate contains 1.47 mEq of potassium mEq/day / total L = mEq/L This can then be plugged into chart

Given the desired amount of protein and dextrose in the parenteral nutrition formula, calculate the volumes of dextrose, crystalline amino acids, and water required to compound a PN solution

Amino acids = 1.5g/kg/day Using 10% amino acid solution Dextrose = 300 g/day Using 70% dextrose solution ILE = 1g/kg/day Using 20% ILE solution For our purposes, assume 150ml for electrolytes/vitamins/trace elements -------------------- You're calculating M1V1 = m2v2 with each part of TPN and then added together to find necessary ml of water. ------------------------- Calculating kcal = AA =4kcal/g Dextrose = 3.4kcal/g ILE = 10kcal/g ----------------------- Calculating GIR Will be given formula (g of dextrose * 1000) / (weight in Kg * 1440) 1440 = mins per day -------------- Osmolarity = find percentage of macronutrient in entire bag then multiply by 100 to find mOsm Example: 65g of AA/ 2400mL * (100) = percentage AA = 100mOsm per % Dex = 50mOsm per % --- 1 mMol of sodium phosphate contains 1.33 mEq of sodium 1 mMol of potassium phosphate contains 1.47 mEq of potassium mEq/day / total L = mEq/L This can then be plugged into chart

What are the drugs that causes constipation

Analgesics • Inhibitors of prostaglandin synthesis • Opiates Anticholinergics • Antihistamines • Anti-Parkinsonian agents (e.g., benztropine or trihexyphenidyl) • Phenothiazines • Tricyclic antidepressants Antacids containing calcium carbonate or aluminum hydroxide Calcium channel blockers Clonidine Diuretics (non-potassium-sparing) Nonsteroidal antiinflammatory agents

Corticosteroid therapy for IBS

Anti-inflammatory effects -Variable, nonspecific effects Blunt responses of Leukocytes/MPs to antigens T lymphocytes IL-1, IL-2, IL-6 Prdouction of prostaglandins and leukotrienes Response: 700-80% partial or full response 5 days will have 40% full responsive Used only short term Administration: Can be local or systemic ------------------- Hydrocortisone = topically applied Budesonide: Undergoes first pass metabolism, thus has lower bioavailability and lower side effects. Entocort = delivered primarily to the Illeum (only useful in CD) Uceris = delivered to colon (much more effective for UC) ----------------- Additional monitoring -Annual ophthalmic exams -Consider dual energy X ray absorpitiometry (DEXA) in high risk patients Place in therapy = short term use for active flares -NO Role in long term maintenance

Explain the differences in visceral proteins used for assessment of lean body mass

Asses LBM using three serum visceral proteins: -Albumin 2. Transferrin 3. Prealbumin Greatest value in assessing uncomplicated semi-starvation and recovery. -=----- Albumin -Half life 18-20 days -Function = Maintains plasma oncotic pressure; transports small molecules -Factors resulting in increased values: dehydration, anabolic steroids, insulin, infection -Factors resulting in decrease values: Overhydration, edema, kidney dysfunction, nephrotic syndrome, poor dietary intake, impaired digestion, burns, CHF, cirrhosis, thyroid/adrenal/pituitary hormones, trauma, sepsis ------------- Transferrin -Half life 8-9 -Function = Binds Fe in plasma; transports Fe to bone -Factors resulting in increased values: Fe deficiency, pregnancy, hypoxia, chronic blood loss, estrogens -Factors resulting in decrease values: Chronic infection,cirrhosis, burns, enteropathies, nephrotic syndrome, cortisone, testosterone ----------------------- PreAlbumin -Half life 2-3days -Function = Binds T3 and to a lesser extent T4 -Factors resulting in increased values: kidney dysfunction -Factors resulting in decrease values: Cirrhosis, hepatitis, stress, surgery, inflammation, hyperthyroidism, CF, kidney dysfunction, zinc deficiency *prealbumin is usually the one that is monitored

Determine the energy requirement of an individual based on various estimation/calculation methods

Assessment of nutrient requirements: -Clinical condition -Need for continued maintenance -Need for repletion -Physical activity level -Normal growth/development in children Energy requirements: -Population estimates based on weight (kcal/kg) -Equations that estimate individual's energy expenditure -Indirect calorimetry ------------- Kcal/kg method -Assumes standard values with additional requirements for repletion -Does not take into consideration age or gender differences -Which weight to use? Healthy, normal nutrition status = 20-25 kcal/kg/day Malnourished or metabolically stressed = 25-30 kcal/kg/day Major burn injury ( > 50% total BSA) = 30-40 kcal/kg/day In pediatrics = as age increases kcal/kg/day decreases (requirements can increase by 50% if metabolically stressed) ---------------------------- Caloric requirements -Increased metabolic rate Fever Sepsis Major surgery Trauma/burns chronic conditions Decreased metabolic rate: Obesity Neurological impairment Protein requirements increase by 50% or more if metabolically stressed --------------------------- Harris-Benedict equation to determine BEE (Use actual body weight in all patients) Considered most accurate in ICU patients ****Find out if equation is given to us? ---------------------------- Penn State equations to calculate REE The equation that ends in 6212 is used in critically ill ventilated patients The equation that ends in 3085 is used for older and obese patients ------------------------------- Indirect calorimetry Most accurate method Determines MREE (measured resting energy expenditure) Measures oxygen consumed and carbon dioxide produced Data can be used to also determine RQ (respiratory quotient) RQ reflects substrate oxidation, characterizes substrate use, and is calculated as VCo2/Vo2 If RQ > 1 represents lipogenesis (considered overfeeding) or hyperventilation RQ <0.7 may indicate ketogenic diet, fat gluconeogenesis, or ethanol oxidation Limitations: setting must be constant. Patient should be at complete rest for 1hr, must not receive bolus feedings iether by feeding tube or orally for 4 hrs. Should not have changes in substrate delivery in past 12hrs ------------------------------- PROTEIN REQIUREMENTS: Typical range = 0.8-1.5 g/kg/day Increased with critical illness/trauma/burns = -critical illness/trauma/burn = 1.5-2g/kg/day -CRRT = 2-2.5 g/kg/day -Severe burns with large surface area may require up to 3-4 g/kg/day

Antisecretory agents of diarrhea

Bismuth subsalicylate (Pepto-Bismol®) •It has antisecretory, antiinflammatory, and antibacterial effects •Available OTC for indigestion, relieving abdominal cramps, and controlling diarrhea, including traveler's diarrhea •Toxic if given excessively to prevent or treat diarrhea •Salicylate, which may interact with anticoagulants or may produce salicylism (tinnitus, nausea, and vomiting). •Bismuth subsalicylate suspension has been evaluated in the treatment of secretory diarrhea of infectious etiology as well. •In a dose of 30 mL every 30 minutes for 8 doses, unformed stools decrease in the first 24 hours. •Dosage forms: 262-mg chewable tablet, 262 mg/5 mL liquid, and 524 mg/15 mL liquid. •Dose: The usual adult dose is 2 tablets or 30 mL every 30 minutes to 1 hour up to 8 doses per day Probiotics •Lactobacillus preparations are considered probiotics agents that contain bacteria or yeast. •Lactic acid bacteria are dietary supplements that have been used for many years in hopes of replacing colonic microflora. •This supposedly restores normal intestinal function and suppresses the growth of pathogenic microorganisms. •Lactobacillus acidophilus; Lactobacillus bifidus; Lactobacillus bulgaricus •LactinexTM, Bacid®; Culturelle®; Dofus; Flora-Q™ - OTC •Dosage forms - granules, capsules, tablets •Yogurt - Activia! Octreotide (Sandostatin®) •Octreotide is a synthetic octapeptide analog of endogenous somatostatin •Octreotide blocks the release of serotonin and many other active peptides, and has been effective in controlling diarrhea and flushing. •It is reported to have direct inhibitory effects on intestinal secretion and stimulatory effects on intestinal absorption •Metastatic intestinal carcinoid tumors secrete excessive amounts of vasoactive substances, including histamine, bradykinin, serotonin, and prostaglandins. •Primary carcinoid tumors occur throughout the gastrointestinal tract, with most in the ileum. •Some patients have a violent, watery diarrhea with abdominal cramping •Octreotide has more recently been considered first-line therapy. •It does not appear to have an advantage over various opiate derivatives in the treatment of chronic idiopathic diarrhea, and has the disadvantage of being administered by injection •Because octreotide inhibits many other gastrointestinal hormones, it has a variety of intestinal side effects. •Dosage forms: SubQ, I.V, I.M. depot injection •Dose: I.V.: Initial: 50-100 mcg every 8 hours; increase by 100 mcg/dose at 48-hour intervals; maximum dose: 500 mcg every 8 hours

Describe chronic diarrhea and treatment

Caused by IBS (ulcerative colitis and crohns disease) -Malabsorption syndromes -As well as chronic infections Treatment: Antidiarrheal agents - Opioids • Loperamide • Diphenoxylate/Atropine • Eluxadoline - Crofelemer

Explain the pathophysiology of cirrhosis and portal hypertension.

Causes: -Alcohol consumption -Hepatitis B, C -Drugs and herbals Cholestatic liver diseases (primary/secondary biliary cirrhosis, primary sclerosing cholangitis -Metabolic liver diseases Pathophys: CIRRHOSIS -Chronic injury and inflammation leading ot collagen secretions during wound healing -Progressive replacement of normal hepatic cells with fibrous scar tissue (cirrhosis) -Diffuse, fibrotic disease -Normal liver architecture replaced by nodules -Develop sinusoidal congestion and portal hypertension IRREVERSIBLE PORTAL HYPERTENSION -Normal portal vein pressure = 5-10 mmHg and flows at 1-1.5 L/min Portal hypertension diagnosed >10-12mmHg -Result of sinusoidal damage/restructuring -Altered vasodilator/vasoconstriction secretion -Lower hepatic blood flow -Lower metabolism and synthesis -Lower first pass metabolism

Compare and contrast the Child-Pugh and Model for End-Stage Liver Disease (MELD) scoring systems for assessing severity of ESLD.

Child-Pugh has a lot of variability. Ascites and encephalopathy require judgement calls, thus may not be correctly adjusted for the scale. Very subjective MELD score was developed: calculates risk of death in 3 months. If patient scores over 20% on their MELD score, it means the patient is eligible for transplant. LESS SUBJECTIVE

Describe factors that influence fluid movement between the intracellular and extracellular fluid compartments

Compartments: 2/3 INtracellular 3% transcellular 1/3 extra celullar 1/4 of ECF = Intravascular 3/4 of ECF = Interstitial Age: Total body water decreases, while total body fat increases Also, as age increases intracellular fluid increases in body weight while extracellular decreases --------------- Changes compartments via osmosis Sodium = dominant extracellular osmole Potassium = primary intracellular osmole ------------------ Starling forces Governed by plasma oncotic and hydrostatic pressure, referred to as starling forces ---------------- Disruptions can lead to THIRD SPACING = accumulation of excess fluid in interstitium (edema) or potential fluid spaces (effusion)

List the potential complications of cirrhosis and explain their relationship to portal hypertension.

Complications of ESLD: Portal hypertension Esophagealvarices Hepatic encephalopathy Ascites Hepato-renal syndrome

Explain the rationale for the gradual increase in providing nutrition to prevent refeeding syndrome in the severely malnourished

Concerns with refeeding if previously severely malnourished - -Resulting severe hypophosphatemia (<.2mg/dL) - HF, edema, coma 1. In starvation: carbohydrate intake is reduced; thus, insulin secretion is reduced. 2. Fat/protein catabolized for energy 3. Intracellular loss of electrolytes But then when rapidly fed: 1. Shift from fat to carbohydrate metabolism rapidly boosts insulin secretions 2. This drives phos/K/Mg intracellularly to replace loss stores 3. Leads to respiratory failure, cardiac failure, hypotension, arrhythmias, seizures, coma, sudden death

Definition of constipation

Definition - several difficult-to-quantify variables: bowel movement frequency, stool size or consistency, and such symptoms as the sensation of incomplete defecation. •Normal people pass at least 3 stools per week. •Some of the definitions of constipation used in clinical studies include: •(a) less than 3 stools per week for women and 5 stools per week for men despite a high-residue diet, or a period of more than 3 days without a bowel movement; •(b) straining at stool greater than 25% of the time and/or 2 or fewer stools per week; or •(c) straining at defecation and less than 1 stool daily with minimal effort.

Describe pharmacologic treatment options for patients with acute or chronic symptoms of UC or Crohn's disease, including counselling points, monitoring paramaters, and side effects

Diagnosis: Endoscopy= -determine distribution of disease, looking for pattern and depth of inflammation Stool cultures = mostly to rule out other etiologies -------------- Treatment: Acute Goal = induce remission -Allevation of symptoms and suppression of inflammation during acute episodes Long-term goal: Maintenance of remission/prevention of relapse -Improve quality of life -Prevention of hospitalization or surgical intervention -Management of extraintestinal manifestations -Prevention of malnutrition -Reduce exposure to corticosteroids -Prevention of treatment-associated adverse effects Treatment considerations: -Achieving sustained remission is inpacted by response to treatment and is vital for adequate treatment of IBD. Patients who remain in remission for 1 year have 80% chance to stay in remission next year --------------------------- Pharmacological therapy: Plan (for acute disease) -Continue therapy until symptom remission -Improvement begins at 2-4 weeks Maximal improvement occurs within 12-16 weeks -Maintain response/remission -If patient responds to induction therapy

Nonpharmacologic management of diarrhea

Dietary management is first priority 1. Rehydration and maintanence of water and electrolytes are primary treatment goals 2. If the patient is volume depleted, replete 3. Rehydration of infants with acute diarrhea using rice-based solutions is effective

Nonpharm therapy of constipation

Dietary modification to increase the amount of fiber consumed Fiber, is not digested in the human GI tract, thus increases stool bulk and retention of water, increasing rate of transit of stool through the intestine. Patients are advised for 10g of crude fiber in daily diet Fruits, vegetables, and cereals have significant fiber content Bran, by product of milling wheat, is often added to foods to increase fiber content and contains a high amount of soluble fiber, which may be constipating Raw bran is generally 40% fiber Psyllium is nonpharm option and is safe and rich in polysaccharides

Recognize the signs and symptoms of IBD, including major differences between ulcerative colitis (UC) and crohn's disease

Differences: Crohn's = -Any part of GI tract, discontinuous -rare rectal involvment -very common ileal involvment -fistulas -rare crypt absesses Grunolmas -Cobblestone appearance Ulcerative colitis = -Colon only -Common rectal involvment -Very common crypt abcesses -No other presentations --------------------- Clinical presentation of IBD: Unexpected and variable occurences -Can be acute and go to remission with or without recurrences -Difficult to distinguish between ulcerative colitis and Crohn's Disease ------------------------ Signs and symptoms of ulcerative colitis vs crohns UC: -Blood diarrhea -Rectal Cramping -Rectal Urgency CD: -Chronic/nocturnal diarrhea --- Physical exam UC: Rectal disease Diarrhea (bleeding is common) abdominal pain erythema Ulceration; may develop pseudopolyps Mucosal lesions Continuous disease CD: Enter GI affected Diarrhea (less blood) abdominal tenderness/cramping Fistulae and perforations Cobblestone appearance of bowel wall Transmural lesions Non contiguous, with skip areas --- Histopathology: Ulcerative colitis has crypt abcesses (with neutrophil infiltration) Crohns disease = Granulomas that develop into fistulae ---------------------------- Physical signs: Ocular issues Dermatologic involvment = erythema, pyroderma gangrenosum, aphthous ulcers -------------------------------- Lab tests: UC: CBC -Increased WBC -Decreased Hgb/Hct -Increased ESR or CRP -Hypoalbuminemia -(+) perinuclear antineutrophil cytoplasmic antibodies ****** Crohn's Disease CBC: -Increased WBC -Increased ESR or CRP (+)anti-saccharomyces cerevisiase antibodies -Fecal markers? --------------------------

Emollient laxatives in constipation

Emollient Laxatives •Emollient laxatives are surfactant agents, docusate in its various salts, which work by facilitating mixing of aqueous and fatty materials within the intestinal tract. •They may increase water and electrolyte secretion in the small and large bowel. •These products result in a softening of stools within 1 to 3 days of therapy. •Emollient laxatives are ineffective in treating constipation, but are used mainly to prevent this condition. •They may be helpful in situations in which straining at stool should be avoided, such as after recovery from myocardial infarction, with acute perianal disease, or after rectal surgery. •It is unlikely that these agents would be effective in preventing constipation if major causative factors (e.g., heavy opiate use, uncorrected pathology, or inadequate dietary fiber) are not concurrently addressed. •Although docusates are generally safe, a few adverse effects have been noted. They may increase the intestinal absorption of agents administered concurrently and alter toxic potential.

Compare and contrast the enteral access options, including the gastric and small bowel routes for both short-term and long-term use

Enteral access options: Nasogastric or orogastric Indications: Short term 1. Intake gag reflex 2. Normal gastric emptying Tube placement options: manually at bedside Advantage: Ease of placement Allows for all methods of administration Disadvantages Potential tube displacement Potential increased aspiration risk ============================== Nasoduodenal or nasojejunal Indications: Short term High risk of GER or aspiration Impaired gastric motility or emptying Tube placement options: manually at bedside, fluroscopically, or endoscopically Advantages Potential reduced aspiration risk Allows for early post-injury or post-op feeding Multiple commercially available tubes and sizes Disadvantages Manual transpyloric passage requires greater skill Potential tube displacement or clogging Bolus or intermittent feeding not tolerated ============================= Gastrostomy Indications: Long-term Normal gastric emptyin Tube placement options: surgically, endoscopically, radiologically, or laproscopically Advantages Allows for all methods of administration Large-bore tubes less likely to clog Multiple commercially available tubes and sizes Low-profile buttons available Disadvantages Possible risks associated with each type of procedure Potential increased aspiration risk Requires stoma site care ====================== Jejunostomy Indications: Long-term Impaired gastric motility or emptying High risk of GER or aspiration Tube placement options: surgically, endoscopically, radiologically, or laproscopically Advantages Allows for early post-injury or post-op feeding Potential reduced aspiration risk Multiple commercially available tubes and sizes Disadvantages Possible risks associated with each type of procedure BOLUS OR INTERMITTENT FEEDING NOT TOLERATED Requires stoma site care

For each of the following complications: portal hypertension, esophageal varices, : A. Identify potential targets of pharmacological therapy B. For selected pharmacologic agents, describe the relevant mechanism(s) of action and expected outcomes C. Compare and contrast available non-pharmacologic and pharmacologic treatment options, in order to recommend a specific treatment regimen D. Create treatment goals for an individual patient E. Apply recommendations from evidence based guidelines

Esophageal varices: A: Caused by: -Portal Hypertension (increased portal pressure leads to varices due to increased dilation Varices lead to increased risk of GI bleeding Varices are overdilated veins from the liver that are extended to their limit. Target Prevention: -1/3 of patients with varices develop hemorrhage from site (usually GE junction or Fundus) Major cause of mortality and morbidity D. Treatment goals for primary prophylaxis of Esophageal varices: ============================ -Non-selective beta-blockers • Propranolol: 20 mg twice daily • Nadolol: 20-40 mg once daily • Reduce risk of 1st bleeding by 25-50% • Survival advantage questionable Titrating to efficacy: (Start low and go slow) • ↓ resting HR by 25% • goal HR 55-60 beats per minute • Length of treatment: • Lifelong therapy • Side effects: • Bronchoconstriction • May exacerbate HF • CNS effects ======================== -Carvedilol -Nitrates -Endoscopic band ligation (this is an endoscopy where surgeon puts a band and tightens a vein) -=---------------------------- Active bleeding esophageal varices: Treatment Goals: -Fluid resuscitation -Airway management -Control bleeding -Manage thrombocytopenia and coagulopathy -Prevention of infection -Prevent re-bleeding -Preservation of liver funciton Inital management: -Airway management -NG tube placement -Resuscitation to support perfusion (colloids for initial volume expansion) -PRBCs, platelets, FFP to correct coagulopathy (Hgb >8g/dL) -Initiate therapy for UGIB with PPI infusion -Antibiotics to prevent SBP Pharmacologic reduction of bleeding: Goal: reduce blood flow into portal system by inducing splanchic vasoconstriction -Reduce collateral blood flow -Initiate upon presentation Reduce active bleeding during procedure -Vasopressin is the most potent vasoconstrictor (use is limited by its large number of systemic ADEs) Octreotide is preferred vasoconstrictor (MOA: inhibits vasodilatory GI peptides (glucagon, vasoactive intestinal peptide (VIP), substance P -Vasoconstrictor effects limited to splanchnic circulation Meds: Octreotide: I.V. bolus: 35-50 mcg followed by continuous IV infusion of 25-50 mcg/hour (administered for up to 5 days to avoid early-rebleeding) -Half life of 1.5 hours (needs continuous infusion) Side effects: hyperglycemia

Compare and contrast colorectal cancer screening options

FYI and info Endoscopy: semirigid gastroscope (LED at the tip with electronic video images, also allows for washing, suctioning, and passage of instruments Types: 1. EGD = upper endoscopay mouth->esophagus->stomach->duodenum Best method for examining/diagnosing: upper gastrointestinal mucosa, gastric ulcers, barrets esophagus (flat mucosal lesions) 2. Colonoscopy: passing flexible colonoscope through anal cavity: rectum -> colon Able to visualize the entire colon . Gold standard for visualizing colonic mucosa Requires conscious sedation 3. Flexible sigmoidoscopy: similar to colonoscopy, but visualizes only rectum and sigmoid colon Primary uses: evaluation of diarrhea and rectal outlet bleeding 4. Small bowel endoscopy: typically performed to evaluate blood loss anemia without a located source Three methods: -Capsule endoscopy (diagnostic only, risk of capsule becoming stuck) -Push enteroscopy -device-assisted enteroscopy Endoscopic retrograde cholangiopancreatography (ERCP): uses side-viewing endoscope. Passed to duodenum to the ampulla of Vater. Use to: -retrieve bile stones from biliary ducts -Biopsy biliary or pancreatic tissues -Dilate or stent strictures ------------------------------------ Meat and potatoes Fecal occult blood test (FOBT): Pros: No cleansing, collected at home, low cost, minimal risk Cons: Lower sensitivity and specificity, still need colonoscopy if positive Stool DNA test Pros:No cleansing, no dietary restrictions, collect at home, minimal risk Cons: higher cost than occult blood tests, lower sensitivity for adenomas, still need colonoscopy if positive Sigmoidoscopy Pros: idscomfort is minimal, can perform biopsy or polypectomy, less extensive cleansing Cons:Does not visualize upper colon, BOWEL PREP NEEDED, meds and diet changes, invasive Colonscopy Pros:Most sensitive, visualizes rectum and entire colon, can perform biopsy or polypectomy Cons: BOWEL PREP NEEDED, meds and diet changes, sedation is commonly used, risk of complications Virtual colonoscopy Pros: Minimally invasive, no sedation required Cons: BOWEL PREP NEEDED, can miss small polyps, radiation exposure, limited coverage

describe the intiation of foods in the pediatric patient

Food should be introduced when the infant can: sit with support and has good neuromuscular control of head and neck -INdicate desire for food by opening mouth and leaning forward Age of introducing supplemental food depends on: development stage -growth rate -activity level Breast milk or iron-contiaining formula only recommended source of nutrition for 4-6 months Start single ingredient foods one at a time to identify food allergy Iron-fortified single grain infant cerals mixed with milk at 4-6 months of age and when can swallow non liquid foods Usually rice cereal 1st as it is unlikely allergen Pureed fruits and veges are initiated at 6=8 months of age and pureed meats and soft table food at 8 months Fruit juice- -Introduced when can drink from cup -Should not replacem ilk or infant formula Whole cow's milk: should: shouldnt be started before 12 months because doesn't provide optimal nutrition for infants during 1st year Contains low Vit E, Vit C, and iron Contains excessive protein, sodium, and potassim Non-fat and reduced -fat milk not recommended before 2 years of age due to low caloric density and need for fat for neurodevelopment Most children should feed 4-6 times a day Intake may be variable but total daily intake should remain constant Foods to avoid if <1: -Cows milk -Choking hazards -Honey Avoid all potential choking hazards til age 3

Describe various techniques to assess nutritional status Goals, Parts of the comprehensive assessment

Four major goals of nutritional status assessment: 1. Identify factors associated with increased risk of developing malnutrition (undernutrition, obesity, impaired metabolism) 2. Determine risk of malnutrition-associated complications 3. Establish estimated nutrition needs 4. Establish baseline parameters against which to measure nutrition therapy outcomes --------------------------------- Comprehensive assessment includes: 1. Medical/surgical/dietary history 2. Physical examination (anthropometrics, biochemical assessment; labs) 3. Subjective global assessment ------------------------ 1. Dietary history = weight change, appetite, nausea/vomiting, diet history, dietary restrictions, medications, level of activity/exercise, ability to secure and prepare food 2. Anthropometric measurements = -Gross measurements of body cell mass - Evaluate lean body mass (LBM) and fat stores ABW < 69% = IBW Severe malnutrition ABW 70-79% IBW = Moderate malnutrition ABW 80-89% IBW = Mild malnutrition -Failure to thrive = defined as one of the following: weight for age <5th percentile Weight for height <5th percentile Decrease growth velocity -> weight falls by at least 2 major percentile lines in 6 month period What reference to use to measure growth in children: WHO growth chart for ages 0-2 CDC growth charge for children > 2 Appropriate measurements: Height/length measurements = Until 3 years old Head circumference = until 3 years old IBW = 50 + 2.3(per inch over 5ft) 45.5 + 2.3 (per inch over 5 ft) BMI = weight in kg/ (height in meters)^2 Skinfold thickness = estimate of subcutaneous fat, reflecting changes in total body fat Midarm muscle circumference = estimate of skeletal muscle mass Abdominal fat (related to obesity complicattions -At risk if male >40 inches, at risk female >35 inches -Excludes patients <5ft tall or with BMI >35kg/m^2 Waist-to-hip ratio = "at risk" if >=1, "not at risk" of <1 in men and less than <0.8 in women Biochemical impedence LBM = higher electrical conductivity (less resistance in lean muscle) Fat = lower electrical conductivity (poor conductor because greater fluid and electrolyte content in fat) -Very small current is applied to appendage and then measure the impedance to flow of current. Assesses LBM, TBW, and compartmental distribution of water -Not as accurate in patients with edema, electrolyte imbalances, and obese ------------------------ 3. Subjective goal assessment Weight changes in previous 6 months For weight loss: <5% of usual body weight = "small" loss 5-10% = potentially significant loss >10% = definitely significant loss Dietary intake changes Normal vs. abnormal timeframe GI symptoms: -Anorexia N/V/D on a daily basis for >2 weeks Functional capacity -Patient's energy level Presence of disease states that may impact metabolic demands (i.e. no low, moderate, or high stress) Physical examination findings rated as normal, mild, moderate, or severe -Loss of subcutaneous fat (triceps and chest) -Muscle wasting (quadricepts and deltoids) -Edema (ankle and sacral) -Ascites Final result of subjective global assessment: Use to rank patients nutrition status as -adequately nourished -Moderately nourished -Severely malnourished

Evaluation of therapeutic outcomes in relation to diarrhea

General Outcomes Measures •Therapeutic outcomes are directed toward key symptoms, signs, and laboratory studies. •Constitutional symptoms usually improve within 24 to 72 hours. •Monitoring for changes in the frequency and character of bowel movements on a daily basis in conjunction with vital signs and improvement in appetite are of utmost importance. • Also, the clinician needs to monitor body weight, serum osmolality, serum electrolytes, complete blood cell counts, urinalysis, and culture results (if appropriate). Acute Diarrhea •Most patients with acute diarrhea experience mild to moderate distress. •In the absence of moderate to severe dehydration, high fever, and blood or mucus in the stool, this illness is usually self-limiting within 3 to 7 days. •Mild to moderate acute diarrhea is usually managed on an outpatient basis with oral rehydration, symptomatic treatment, and diet. •Chronic diarrhea •In the urgent/emergent situation, restoration of the patient's volume status is the most important outcome. •Toxic patients (fever, dehydration, or hypotension) require hospitalization, intravenous fluids and electrolyte administration, and empiric antibiotic therapy while awaiting culture and sensitivity results

Outline a monitoring plan for a patient receiving PN

Glucose, BUN, creatinine, and elecetroytes are usually monitored daily until a couple weeks in, then moved to 2-3 times a week. LFT, albumin and triglycerides should be down weekly Everything else as indicated FOR NEONATES Often start starter PN without labs First set of electrolytes at 24hours of life unless critically ill Try to minimize labs (not enough blood)

Interpret hepatitis B serologic markers

Hepatitis B serology: Anti-HBc core: only tells that you were exposed to the virus Anti-HBs: tells you whether you're immune IgM anti-HBc is useful if you know someone has an HBc infection, but you want to see if it is acute HBsAG becomes anti-HB as it is seroconverted

Work through workup for constipation

History Stool frequency Stool consistency Difficulty of defecation Possible causes Diet deficient in high-fiber items and consisting mainly of highly refined foods GI disorders Metabolic and endocrine disorders Pregnancy Neurogenic Psychogenic Drug induced Laxative abusers Symptoms seen with chronic constipation Fluid and electrolyte imbalances (hypokalemia) Protein-losing gastroenteropathy with hypoalbuminemia Syndromes resembling colitis Select appropriate diagnostic studies Proctoscopy Sigmoidoscopy Colonoscopy Barium enema Diagnosis 1. Treat specific cause 2. No diagnosis, symptomatic therapy A. Bulk-forming agents B. Dietary modification C. Alter lifestyle (exercise) D. Increase fluid intake E. Discontinue potential drug inducer Treatment

Compare and contrast human milk with different infant formulas

Human Milk (premature) = lower in protein, calcium, phosphorus, and sodium in comparison to increased needs of premature infant. -Can add human milk fortifiers or mix with premature infant formulas -Low birthweight infants may need gavage (bolus/intermittent feeds) because it is too weak to suck Human milk & standard formula = 20kcal/ounce -------------- Cost comparisons between infant formulas: Read to use formula is more expensive, but more convenient. Cheaper to buy the powdered formula Type of formula based on cheapest to priciest: Cow's milk based < semi-elemental < elemental ------------------------ Premature infant formula For infants <37 weeks GA Contains improved infant nutrition: 1. Increased caloric density (usually 22-24 kcal/oz) 2. Increased calcium 3. Increased phosphorus 4. Increased proteins 5. Increased MCT (improved digestion) Preemie infant formulas: Enfamil/ premature Similac Special Care with Iron INterim/ex-premature infant formulas: Given to premature infants upon discharge from NICU -Provides 22kcal/oz Examples: enfamil Neuropro Enfacare & Similic NEOSURE ============================= Term infant formulas: 4 main categories based on major caloric source for particular formula -Cow's milk based -Lactose-free products -Soy based (milk-free, lactose-free) -Protein hydrolysate/semi-elemental Can use infant formulas to reduce spit-up: Enfamil AR: (added rice to thicken formula with GERD, doesn't thicken til it hits the stomach) Can use lactose-free/reduced lactose infant formulas -Used for infants with lactose intolerance -Still contains milk proteins Examples: Enfamil Gentlease Gerber goodstart sooth Similac sensitive Can use SOY-based infant formulas: milk free/lactose free for milk allergy NOT RECOMMENDED FOR PREMATURE INFANTS. Can be used for vegetarian families DO NOT USE IN CONSTAPATION Protein hydrolysate/semi elemental infant formulas (for infants with milk and soy allergies) Examples: nutramigen, pregestimil, similac Alimentum ---------------- Formulas for infants-childrens 9-36 months in age: marketed as nutritious alternative to whole cow milk to promote toddler development. Contains at least same or more Ca, Vit D, contains increased amounts of vit C, Vit E, and iron than whole cow's milk. Enfagrow PREMIUM Toddler Transitions -Gerber goodstart gentle 2 -Go & Grow by similac -------------- Infant formulas for special medical conditions: Enfaport = chylothorax Ketocal = itnractable epilepsy, pyruvate dehydrogenase deficiency, glucose transport type-1 deficiency Similac PM 60/40 = Infants with renal dysfunction or cardiovascular disease (reduced potassium, calcium, phosphorus) ----------------------------- Dietary supplements for mother (OTC) Enfamil expecta prenatal dietary supplement Similac prenatal vitamin

Characterize the pathophysiologic mechanisms underlying inflammatory bowel disease

IBD = Crohn's disease (CD) + Ulcerative colitis (UC) -Charactertized by inflammation of the GI tract Crohn's disease = affects any portion of the GI tract -Focal asymmetric, transmural inflammation Ulcerative Colitis = mostly limited to colon and rectum (95) -Diffuse mucosal inflammation -Symmetrical, circumferential, uninterrupted pattern ------ Pathophysiologic mechanisms = TGF-B, IL-1, IL-6 -> Th17 Interferon-y, IL-12 -> Th1 Interleukin-4 -> Th2 ---------------------------- Described as locationally: =Crohn's disease is right sided disease, while ulcerative colitis is a left sided disease (ulcerative colitis typically does not extend past the splenic flexure) ----------------------- Pathophysiology of UC: -Always confined to rectum, extends proximally to colon -rectum only = proctitis -rectum and sigmoid colon = proctosigmoiditisi -entire colon = pancolitis Inflammatory response mediated by Th2 and Th17 cells -Only affects superficial layers of mucosa (so no severe obstructions) -Extensive mucosal damage leads to diarrhea and bleeding local complications: hemorrhoids, anal fissures, abscesses -Toxic megacolon = destension and acute colitis (leads to systemic toxicity) Colon cancer risk much higher in UC --------------------------- Crohn's disease: -Most often affects small intestine (typically terminal ileum and cecum) -~30% have isolated colonic involvment -Inflammatory response mediated by Th1 and Th17 cells -Antigens: -Primary = endogenous bacteria -Dietary sources = margarine, refined sugars (sucrose) Bowel wall injury is extensive (transmural): -Lumen tends to be narrowed -Ulcers tend to be deep and elongated and extend along longitudinal axis of bowels Complications= -small bowel sctricture and obstruction -Fistula and abscess formation

How would you analyze how a catheter occlusion occured/

If blood draws through the line and CVL is not heparinized then it is thrombolytic and requires antithrombotic agent -- If PN related could be: Calcium-phosphate = use acidic agent (HCL 0.1N to 0.2N) or cysteine HCL (50-100mg) Or could be lipid deposit = ethanol -- Drug related Identify drug and drug solubility = use acidic agent (HCL 0.1N to 0.2N) or cysteine HCL (50-100mg) or sodium bicarbonate if base soluble

Determine appropriate indications for parenteral nutrition

In adults, PN is not a emergent intervention and should only begin once patient is hemodynamically stable ***Usually candidate after 7-14 days NPO and unable to feed enterally Inability to absorb nutrients via GI tract Massive small bowel resection Intractable vomiting Severe diarrhea Bowel obstruction High-output GI fistula Pancreatitis Cancer Moderately-severely malnourished patients unable to receive enteral nutrition Pancreatitis (severe cases) Critical care Perioperative Minimum of 7-14 days prior to operation required to be effective Minimum 7-10 days post-op NPO status Hyperemesis gravidarum (severe cases) Eating disorders (severe cases) -------------------------------- Indications for PN - Pediatrics Recommended within the first 24hrs of life for infants weighing < 1500 grams (approximately 3 pounds 5 oz) If critically ill Within 2-3 days for term infants Within 3-5 days for children If unable to eat enterally within 5-7 days for other pediatric patients Indications for PN: 1. Enteral nutrition unlikely to provide adequate nutrition (premature infant within 24-48 hours. Other pediatric patients within 5-7 days) 2. When GI tract is not functional 3. Infants and children requiring extracorporeal membrane oxygenation 4. Organ failure (liver, renal, pulmonary, pancreas) when enteral nutrition is contraindicated and the child is catabolic

What are the two sets of nerves that innervate the GI tract What are the specifc plexus/NS functions?

Intrinsic: Enteric Nervous System (ENS) = extends from esophagus to the anus. and arranged into two plexus: 1. Myenteric plexus: Motor neurons supply the longitudinal and circular smooth muscle layers of the muscularis (controls motility) 2. Submucosal plexus: motor neurons supply secretory cells of the mucosal epithelium (controls secretions) Extrinsic: autonomic nervous system = sympathetic & parasympathetic fibers that supply GI tract form neural connections wit hthe ENS. 1. Stimulation of parasympathetic fibers innervate GI secretions and motility by increasing the activity of ENS neurons (rest & digest 2. Sympathetic nerves supply the GI tract cause a decrease in GI secretions and motility by inhibiting neurons of ENS (Fight or flight)

Identify risk factors for malnutrition

Involuntary weight loss >10% of UBW within 6 months OR >5% of usual body weight within 1 month Weight <20% of IBW Presence of chronic disease Increased metabolic requirements Altered diets or diet schedules, recent surgery, illness inadequate nutrition intake for >7 days Pediatric Idntification of malnutrition Z-score 1 is mild 2 moderate 3 severe ------------------------ FOR THE EXAM Inflammation can identify adult malnutrition sources: No inflammation = Starvation related Mild to moderate inflammation = Chronic disease Yes, Marked inflammation = Acute dises or Injury (like burns)

Describe the anatomy and glands of the Stomach Describe the process of the stomach, The Gastric Juice that composes the interior of the stomach, and chyme

J-shaped enlargement of the GI tract -begins in stomach, digestion of starch and triglycerides continues, digestion of proteins begin, the semisolid bolus is converted to liquid and certain sustances are absorbed Epithelial cells in the mucosa extend ddown into the lamina propia to form columns of secretory cells called gastric glands. Three types of glands: 1. Mucuous neck cells (secrete mucus) 2. Chief cells (secrete pepsinogen and gastric lipase) 3. Parietal cells (produce intrinsic factor (required for vitamin B12 absorption; more importantly, secretes hydrochloric acid) ALSo, contains enteroendocrine cells (G-cells) which affect stomach through hormones -After food reaches stomach, waves of peristalsis pass over the stomach every 15-25 seconds -Gastric content is mixed with gastric juices becoming the soupy liquid known as chyme -Food stored in the fundus is digested by salivary amylase; Once chyme is mixed with gastric juices, salivary amylase is deactivated and lingual lipase becomes activated Parietal cells: secrete H+ and Cl- seperately into the stomach lumen, producing HCl -Proton pumps powered by H=-K+ ATPases transport H+ into lumen while bringing K+ into the cell -HCl secretion by parietal cells can eb stimulated by: -ACh released by parasymphatetic neurons -Gastrin secreted by G cells -Histamine released by mast cells in the lamina propia HCl is used to kill many microbes in food, and partially denatures proteins and stimulates the secretion of hormones that promote the flow of bile and pancreatic juice -The stomach epithelial cells are protected from gastric juices by a thick layer of alkaline mucus secreted by the mucous neck cells The chief cells secrete pepsin, a proteolytic enzyme -Pepsin is inactive form; requires transformation to pepsinogen upon contact with HCl (most effective way to acidify environment of stomach) -Gastric lipase splits triglycerides into fat molecules into fatty acids and monoglycerides Mucous cells of stomach absorb some water, short chain fatty acids, drugs, and alcohol -Food from stomach is emptied into the duodenum

Compare and contrast marsmus and kwashiorkor

Marasmus= -Energy deficient -Muscular wasting and absence of subcutaneous fat -Visceral protein preserved Kwashiorkor = Protein-deficient with adequate calorie intake -Depletion of visceral protein -> hypoalbuminemia and edema -Appears sometimes during weaning and post-weaning phases for babies (called sugar babies) It is however, possible to have a mixed-marasmus-kwashiorkor -Prolonged protein malnutrition, when loss of subcutaneous tissue, muscle mass, and adipose stores are also prominent -Edema of kwashiorkor and cachexia of marsmus ------------------------- Comparisons: Marasmus= Clinical setting: Reduced energy intake Time course to develop: Months or years Clinical features: Starved appearance, weight <80% of standard for height, Triceps skinfold <3mm, mid-arm muscle circumference <15cm Laboratory findings: Creatinine-height index <60% standard Clinical course: Reasonable preserved responsiveness to short-term stress Mortality: Low unless unrelated to underlying disease Diagnostic criteria: Triceps skinfold <3mm, Mid-arm muscle circumference <15cm Kwashiorkor= Clinical setting: Reduced protein intake during stress state Time course to develop: Weeks Clinical features:Well-nourished appearance, easy hair pluckability, edema Laboratory findings: serum albumin <2.8g/dL, total iron-binding capacity <200mcg/dL, Lymphocytes <1500/mcL, Anergy Clinical course: Infections, poor wound healing, decubitus ulcers, skin breakdown Mortality: High Diagnostic criteria: Serum albumin <2.8g/dL, Edema At least one of the following: -Poor wound healing -Decubitus ulcers -Skin breakdown -easy hair pluckability

What are aminosalicylates and what are they for

Medications used in treating IBS that deliver 5-aminosalicylate (5-ASA mesalamine ) to inflamed GI tract Effectiveness is PRIMARY IN UC. Not effective for CD MOA = unknown...anti inflammatory -Decreases prostaglandin and leukotriene production -Inhibits bacteria-induced chemotaxis (lower TNF, IL-1) -Free radical scavenger -Inhibits nuclear factor Kb ------------- Pentasa= all of small intestine and colon Asacol, Liasa = affects Ileum and colon Sulfa salazine/balsalazide = all colon 5-asa enema (rowasa) = affects just rectum and distal colon 5-ASAs suppository (Canasa) = rectum =========================== Sulfasalazine (Azulfidine, sulfazine) Dosage = 500mg tabs Site of action: Colon -How? Bacterial degradation of diazo-bond delivers mesalamine and sulfapyridine -Where? Mesalamine works locally --Sulfapyridine is absorbed and excreted renally, and is responsible for the majority of side effects CA: G6PD deficiency AE: -HA, dypepsia, nausea, vomiting, fatigue Bone marrow suppression, crsytalluria risk (counsel on food intake) IMPORTANT (impairs folate absorption): -Supplement folate (1mg/day) ALLERGIES: All sulfonamides are not created equal (can be allergic to only some) -Steven johnson syndrome (rash/fever) -toxic epidermal necrolysis (TEN) =========================== Mesalamine CA: G6PD deficiency AE: lower incidence (no sulfa allergies) ONest: 2-4 weeks Important notes: -Large number of doses per day -Expensive brand names Balsalazide (colazal, Giazo) -Mesalamine linked to inert carrier by diazo bond -750mg DR capsule Site of Action = colon Olsalazine 2 mesalamine molecules linked by diazo bond 250mg DR capsule SOA: colon

Describe acute diarrhea and treatment

Often travelers diarrhea (TD) 3-7 days post arrival, resolves within 5 days ****Can be decreased by up to 60% risk if taking two tablets (524 mg) four times daily with meals and bedtime of bismuth subsalicylate Treatment: Supportive care Oral rehydration and electolyte management Avoid antimotility agents in pts w/ febrile, bloody diarrhea or associated colitis

Pathophysiology and likely causes of constipation

PATHOPHYSIOLOGY •Constipation is not a disease, but a symptom of an underlying disease or problem. •Approaches to the treatment of constipation should begin with attempts to determine its cause. •Constipation commonly results from a diet low in fiber or from use of constipating drugs such as opiates. •Finally, constipation may sometimes be psychogenic in origin. Possible Causes of Constipation •GI disorders: Irritable bowel syndrome, hemorrhoids, tumors, hernia, Hirschsprung's disease •Metabolic and endocrine disorders: Diabetes mellitus with neuropathy, hypothyroidism, pheochromocytoma •Pregnancy: Decreased physical activity, dietary changes, inadequate fluid intake, low dietary fiber, iron salts •Neurogenic causes: Brain trauma, spinal cord injury, CNS tumors, Parkinson's disease •Psychogenic causes: •Ignoring or postponing the urge to defecate, psychiatric diseases

Describe anatomy of Pancreas Describe the pancreatic duct, hepatopancreatic ampulla, Acini, pancreatic islets, and pancreatice juice

Pancreas lies posterior to the greater curvature of the stomach and is connected to the duodenum by two ducts: 1. Pancreatic duct: larger of the two, it joins the common bile duct from the liver and gallbladder and enters dudoenum as a dilated common duct known as the hepatopancreatic ampulla. Pancreatic juice and bile is regulated the sphincter of Oddi 2. Accessory duct: leads from pancreas and empties into duodenum superior to hepatopancreatic ampulla Pancreas is made of small clusters of glandular epithelial cells. 99% of these clusters are comprised of the exocrine portion of the organ (secrete a mixture of luid and digestive enzymes called pancreatic juice) 1% of the clusters comprise the pancreatic islets (islets of Langerhans) from the endocrine portion. Secretes insulin, somatostatin, and glucagon Pancreatic juice: water, sodium bicarbonate, and enzymes -Sodium bicarbonate gives pancreatic juice a slightly alkaline pH: helps in buffering the acidic gastric juice in chyme, stops the action of pepsin, and creates the proper pH for the action of the digestive enztmes in the small intestine. Digestive enzymes include: pancreatic amylase (digests starch, pancreatic lipase (digest triglycerides, Trypsin, chymotrypsin, carboxypeptidase, and elastase: digest protein into peptides, ribonuclease and deoxyribonucleases: digest RNA and DNA into nucleotides.

Discuss the similarities and differencies between various classes of enteral feeding formulations for infant, pediatric, and adult populations

Pediatric formulas (ages 1-12) Indications: 1. Children with special medical conditions requiring increased caloric intake which cannot be maintained on typical oral diet 2. Children with various GI dysfunctions 3. Children with metabolic disorders All are lactose-free and most are ~1kcal/mL ------------------ Adult enteral feeding formulation classification system: Standard polymeric = designed to meet needs of majority of patients with functional GI tracts. Not suitable for oral use Also can have feedings for disease specific patients: -Diabetic = high fat, low carb Renal = caloric dense, protein content varies, low electrolyte content -Pulmonary = high fat, low carb -Immunomodulation = supplemented with glutamine,arginine, nucleotides, and/or omega-3 fatty acids

Differentiate the key characteristics of various paripheral and central venous access devices

Peripheral venous access Access into peripheral vein Limited usage because require: Decreased dextrose concentration Decreased osmolarity Plenty of fluid Only recommended for short-term (≤ 10-14 days) ------------------- Central venous access Defined as catheter whose distal tip lies in distal vena cava or right atrium Most common sites of venipuncture for central access include subclavian, jugular, femoral, cephalic, and basilic veins Allow for: Increased dextrose concentration Increased osmolarity Blood aspiration/laboratory monitoring Extended periods of venous access (i.e., > 14 days) Infusions with very acidic or basic pH Large volume infusions Central venous access devices (CVADs) Grouped into 1 of 3 categories: Nontunneled: Economical, easily removable catheter that can be replaced over guidewire, and is useful in actue care and short duration therapies Disadvantages: catheter breakage not repairable, requires sutures to prevent dislodgement, high risk for infection Tunneled: good for long-term usage, dressing and sutures can be removed after 1 month, selfcare is easy and repair kit available. Disadvantages: operating room or specialized room for placement, requires small procedure for removal Implanted: Used for long-term tehrapies, site care only when accessed, monthly heparin flush, body image intact, no external segment for breakage ***PICC: peripherally inserted central catheter (nontunnled) Used in acute and home care for several weeks to months, low risk of placement complications, placement occurs anywhere from radiology suite to patient bedside Disadvantages: blood sampling not always feasible, self care may be difficult with anticubital placement, repair kits may not be available Peripheral catheters: -Advantage: least expensive, least risk for infection, no special placement room, clinicians easily trained in plcament -Disadvantages: Require site rotation every 48-72 hours, not appropriate to infuse solutions 400-600 mOsm/L, concentrated antibiotics, or vesicants. Midline catheters (peripheral) use for therapies lasting 2-4 weeks Midclavicular catheters (peripheral): used for t herapies 2-3 months.

Recognize patients who are candidates for treatment of chronic hepatitis B

Phases of Hepatitis B Review slide 73 of Hep Lecture Determine treatment candidacy for Chronic Hepatitis B: guidelines Slide 75

Describe the effects of malnutrition on organ and cellular function What is the correct order of physiological response to starvation?

Physiological response to starvation: 1. 1st few days = Glycogen for energy/Skeletal muscle for amino acids to make glucose When glycogen depleted = 2. Skeletal muscle for amino acids/ 3. Adipose tissue for fatty acids 4. Decrease in insulin secretion > 5 days = Ketone production from free fatty acid oxygen (protein sparing) Decreased basal metabolic rate and synthetic capacity of liver -> if severe deficiencies, decrease insulin secretion and increase glucagon + epinephrine Outcome = inappropriate reduction in LBM & altered function of every organ. Can impair immune system and wound healing ------------------------ Immune response to malnutrition - cell mediated response Impacts would healing: Protein energy malnutrition = decrease rate of would healing, increased incidence of wound infection -Vitamin C deficiency = failure of collagen synthesis -Zinc deficiency = Impaired DNA and protein synthesis

Describe hepatitis A

RNA Virus (Hepatovirus of Picornaviridae Family) Spread by fecal-oral route: person-to-person transmission uncooked HAV contaiminated foods lead to outbreaks Waterborne outbreaks infrequent in developed countries Stable in the environment for at least a month Inactivation requires: heating foods to a minimum of 85*C for 1 minutes OR 1:100 dilution bleach/water ----------------------------\ HAV Pathophysiology Oral Ingestion of HAV absorption by stomach entry into circulation uptake by liver replication within hepatocytes & GI epithelial cells released into the blood & secreted into bile by the liver reabsorbed to continue cycle OR excreted in stool --------------------------------Clinical presentation of HAV 1. Incubation period: viral replication within hepatocytes for 28 days 2. Prodromal period: Abrupt onset of nonspecific flu-like symptoms lasting 2 months (anorexia, N/V, malaise, HA 3. Icteric period: GI symptoms last 7-30 days ----------------------------- Diagnosis: Clinical description: 1. Discrete onset of symptoms (nausea, anorexia, fever, malaise, abdominal pain) 2. Jaundice or elevated serum aminotransferase levels Physical examination: 1. Icteric sclera, skin, secretions 2. 4-10 lb weight loss 3. Hepatomegaly Lab findings: Increased bilirubin, ALT, AST Confirmation: =Clinical case + positive hepatitis A immunoglobulin M antibody -Clinical case + link with person who has lab-confirmed hep A ----------------------------- Treatment Fluid replacement Antiemetics Anti-pyretics Rest Household contact precautions Post-exposure immunoglobulin or vaccine within 2 weeks if possible Prevention = key Good hand hygiene Active immunity through vaccination ----------------------------- Patients indicated to receive HAV vaccine: All children at age 1 year (i.e., 12-23 months) Children ages 2-18 who live in states/ communities where routine HAV vaccination implemented d/t high incidence Persons traveling to countries with high - intermediate HAV rates Men who have sex with men Users of illegal injection and noninjection drugs Persons who have occupational risk for infection Persons who have chronic liver disease Persons who have clotting-factor disorders Household member/ close contacts of adopted children newly arriving from countries with high to intermediate HAV endemicity ------------------------- Therapy: GammaSTAN S/D IM injection Concentrated antibodies from pooled human plasma Screened for HBsAg, HIV, and HCV RNA Virus inactivation step during manufacturing Provides passive immunity Temporary protection Pre-exposure prophylaxis: 0.02 mL/kg IM protects <3 months 0.06 mL/kg IM protects 3-5 months Post-exposure prophylaxis: 0.02 mL/kg IM within 14 days of exposure 80-90% effective in preventing HAV infection if administered within 2 weeks after exposure RNA virus that causes acute self-limiting infection Transmission Fecal-to-oral Incubation: ~28 days Prevention Vaccination for children ≥12 months and all at-risk individuals Good hand hygiene and disinfection with bleach dilution During international travel: avoid food & beverages likely contaminated Treatment Supportive care Post-exposure prophylaxis with vaccine or immunoglobulin

Describe how to manage anticoagulants for a patient undergoing colonoscopy

Recommendation depends on bleeding risk of procedure: Low risk = colonoscopy or EGD with or without biopsy, ERCP High risk = colonoscopy or EGD with dilation, polypectomy, ERCP with drainage Warfarin Low = Continue Ensure INR is not supratherapeutic High = Discontinue for ~5 days INR should be ≤ 1.5; consider bridging DOACs Low = Continue or hold morning dose High = Discontinue 2-4 days prior Bridging not recommended Aspirin Any risk = Continue Low dose ASA does not increase risk P2Y12 Inhibitors Low = Continue High = Discontinue (unless recent stent) Specific agents have specific discontinuation times Heparin Low = Continue High = Stop 4-6 hrs before procedure Skip 1 dose if using LMWH

Recognize factors contributing to an optimal bowel preparation

Risk factors of failed colonoscopy: 1. Failure to adequately follow bowel prep directions 2. Previous adequate bowel prep 3. Later start time 4. Indication = constipation 5. Tricyclic antidepressant use 6. Cirrhosis 7. Stroke 8. Dementia Can result in: cancelled procedures Increased procedure time -> increased cost Missed lesions Recommend repeat colonscopy within 1 year if inadequate Efficacy preferred over tolerability ------------------------- Preparation for a colonoscopy: 1. Clear liquid diet (1 day prior) 2. Low residue diet (3 days prior) Both show identical outcomes, low reside is better tolerated however. May take clear liquids up to 2 hours prior to procedure Bowel prep regimen: Split dosing (night before and day of procedure) results in better efficacy and tolerability than 1 single dose night prior Dietary restrictions: -No RED or purple substances (can be mistaken for blood) Food/drinks allowing in the clear lqiudi diet include: water, coffee/tea without milk or cream, sports drinks, clear broth Foods/drinks in low reside: white bread, white rice, potato, skinless chicken, fish, fruits without seeds

Identify signs, symptoms, and laboratory abnormalities that result from cirrhosis and explain their pathophysiology.

Signs and symptoms: -Asymptomatic -Pruritus -Edema, pleural effusions, respiratory difficulty -Malaise, anorexia, reduced libido, weight loss -Altered mental status -------------------- Assessment: Must diagnose cause of liver failure (acute vs chronic) and potential to reverse damage Assess hepatic reserve: -Liver has amazing capacity to support patient up to the end -Potential for supportive care to improve outcome -Presence of hepatorenal syndrome -Potential for liver transplantation (contraindicated for: active drinking or abstinence for <6 months/cancer) ---------------------- Diagnosis: History: • Presence of end stage issues • Identify onset of liver disease • Identify known causes ----------------- Lab Tests: LFT Protein synthesis: Albumin, PT/INR Excretion into bile ducts: Gilirubin, alkaline phosphatase, GGTP Hepatocellular injury: transaminases (AST, ALT) Detoxification: Ammonia ------------------------- Diagnosis Procedures Ultrasound - preferred method Biopsy: dangerous procedure -Causes bleeding (pt has limited clotting factors) Procedures: -percuss liver position -Needle over top of rib -Quick jab into liver -Pressure on area for 15-30 minutes ------------------------------ Severity assessment: Child-Pugh score, or MELD

HCV Etiology

Single-stranded RNA virus of Flavivirdae family -Lacks proofreading polymerase > frequent viral mutations Presentation: Often asymptomatic before development to cirrhosis Complications **Hepatic Cirrhosis End-stage liver disease Hepatocellular carcinoma #1 indication for liver transplantation in U.S. Extrahepatic Cryoglobulins: immune complexes Vasculitis Glomerulonephritis Dermatologic disordersSjögren's syndrome Arthritis Impaired glucose tolerance Fatigue Pain How to test HCV antibody screen If negative -> o exposure If positive -> screen for HCV RNA If it is <6months = acute >6months = chronic Assessment: Fibrosis determination: -Liver biopsy -Gold standard but most invasive Transient elastography Noninvasive, correlates liver stiffness to fibrosis cut off of 12.5 or > suggest fibrotic liver disease for HCV treatment APRI or FIB-4 calculators Uses standard blood tests to calculate -Less sensitive and specific GOAL OF TREATMENT: Sustained Virologic response (SVR): undectable HCV RNA in serum >=12 weeks post treatment using PCR assay -------------------------- Selecting a therapy regimen Key considerations: Genotype Cirrhosis status Treatment history Additional considerations Cost-effectiveness Length of therapy Pill burden renal function Severity of cirrhosis Drug interactions Comobidities ------------------------- Patient counseling avoid alcohol avoid sharing personal items Medication adherence Health diet + exercise

Identify appropriate indications and contraindications for the use of enteral nutrition

Slide 9 and 10 on enteral nutrition slide: Summary: Enteral for when GI tract works Short term: nasogastric, nasoduodenal, nasojejunal, Long term: gastrostomy jejunostomy Indications: 1. Must have functional GI tract 2. If the patient has a poor appetitie 3. If the patient has impaired swallowing function caused by neurological disease or oropharyngeal dysfunction 4. If patient is suffering from major trauma, burns, wounds, and/or critical illness who many not be able to meet metabolic demands of illness 5. Severely malnourished preoperative patients who ahve functioning GI tract ---------------------- Contraindications: 1. Non-operative mechanical GI obstruction 2. Intractable vomiting/diarrhea refractory to medical managment 3. Severe short-bowel syndrome (<100 cm of small bowel remaining) 4. Paralytic ileus 5. Distal high-output fistulas (too distal to bypass with feeding tube) 6. Severe GI bleed 7. Severe malabsorption 8. INability ot gain access to GI tract 9. Need is expected for <5-7 days for malnourished patients or 7-9 days if adequately nourished 10. Aggressive intervention is not warranted or not desired

For each of the following complications: spontaneous bacterial peritonitis (SBP): A. Identify potential targets of pharmacological therapy B. For selected pharmacologic agents, describe the relevant mechanism(s) of action and expected outcomes C. Compare and contrast available non-pharmacologic and pharmacologic treatment options, in order to recommend a specific treatment regimen D. Create treatment goals for an individual patient E. Apply recommendations from evidence based guidelines

Spontaneous Bacterial Peritonitis (SBP) Acute infection of ascites ●In patients with variceal hemorrhage, the frequency of SBP is significantly increased ○Prophylaxis against SBP is recommended when a patient presents with upper GI bleeding A. Causes: Ascitic fluid = good culture medium, so bacteria translocate from intestinal lumen to third space Gram - bacteria = e. coli, enterobacter, glebsiella Gram + bacteria - Strep Pneumoniae, staph, and enterococcus SBP Primary prophylaxis -May be an option if the ascitic fluid is low in protein concentration (<1.5g/dL) PLUS: Impaired renal function (sCr >1.5) or Liver failure (Child-pugh score of 9 or greater) Ciprofloxacin 500mg daily Bactrim DS once daily Levofloxacin 250mg once daily === Signs and symptoms: fever Altered mental status (encephalopathy) abdominal pain Renal failure Increased white blood cell count Empiric Therapy: antibiotic t herapy immediately upon inspection AFTER paracentesis and cultures drawn Antibiotic choice based on resistance patterns and patient specific factors -3rd generation cephalosporin (ceftriaxone/sefotaxime) -Fluoroquinolones (ofloxacin/ciprofloxacin) Supplement albumin Therapy should last 5-10 days Empiric Albumin: ascitic fluid PMN counts >250 cells/mL and clinical suscipicon of SBP who also have: SCr > 1mg/dL BUN >30mg/dL Total Bilirubin >4mg/dL Should receive 1.5 g albumin/kg body weight within 6 hours of detection and 1g/kg on day 3 A decrease in mortality from 29% to 10% was reported for those treated with cefotaxime + albumin

Describe the factors that influence the stability of PN formulatiosn and this effects compounding on PN formulations

Stability vs compatibility Degradation of nutrition components that changes original characteristics. Ability to add PN additivies, to maintain their chemical integrity and pharm activity. Compatibility = involves formation of precipitates -Can be solid (crystalline) or liquid (phase seprataion of oil and water in TNA) ------------------------- Osmolarity of PN Important because determines when solution is too concentrated for peripheral vein > 900 mOsm/L = central PN Pede patients can tolerate slightly higher amount. Y-site ILE with peripheral PN to help prevent phlebitis

Understand administrative guidelines for PN administration (e.g. storage, filtration, hang-time, infection control, continuous versus cyclic administration, and compatiblity with other medications/fluids)

Storage: USP 797 beyond risk classifies storage at medium risk: Room temperature = 30 hours Refrigeration = 9 days High rik: 48/14 Low risk: 24/3 --- Hangtime: 24 hours for all solutions EXECPT ILE drawn into separate container is good for 12 hours --- Multi-chamber bags: promote extended stability and separates ILE from rest of PN. At time of administration, seal/clamp is opened to mix contents. MVI and trace elements added prior to infusion Advantages - Lower risk for infections, less compounding time Disadvantages - preset concentration limits customization At time of administration, a seal allows contents to mix. --- Compounding order example: 1st combine AA and dextrose 2nd add electrolytes (1st should be phsophorus salt, last should be Calcium gluconate) 3rd add vitamins and trace elements Inspect for particulate matter;precipitation Add ILE (if TNA) QS to final volume with sterile water for injection --- Filtration = Use 0.22-micron filter with 2in1 PN formulation 1.2 must be used with TNA or separate ILE infusion --- Infection control AA and dextrose are poor grwowth media because of acidic pH and hypertonic, but can still happen Bacteria are caught by the 0.22micron filter Fungus is caught by the 1.2micron filter higher infection risk with ILEs (rare pathogen associated with ILE= malassezia furfur) INfection risk = ILE > TNA > 2in1 PN formulations Change tubing every 72-96 hrs for 2in1 24 hours for ILE and TNAs --------- Initially administration should be for 24 hours (continuous) Eventually may be able to cycle PN range form 8-22 hours of ycled PN -------------------- Polar and nonpoalr regions on same fat droplet align with polar and nonpolar regions Oil ends up separating from the water phase and first appears as subtle changes which may progress to yellow oil streaks. known as cracking (unsafe for infusion) DANGER: calcium phsophrous is major compatibility concern with PN formulations. Prescribers must be familiar with limitations for addition fo calckum and phosphate -------------------- Medications Precipitate sfrom medication incompatibilities or emulsion disruption from medicaiton additives Compatibility by Y-site infusion is not synonymous with admixture into PN formulation because time of exposrure between medication and PN is greatly increased with admixture

Identify appropriate non-pharmacologic treatments for patients with IBD

Surgery Nutrition Avoiding medications Surgery = resection of affected areas of the intestines and colon -Complete bowel resection (colectomy) is curative for culerative colitis (obviously, not true of CD) -Dranage of abscesses -Correction of fistulas Nutrition = -important due to risk of malnourishment -Eliminate foods that exacerbate symptoms = milk, high fiber foods -Vitamin supplementation -Enteral or parenteral nutrition in severe cases Medications to avoid -NSAIDS Anti-diarrheal medications -Loperamide (can precipitate to cause toxic megacolon) -Anticholinergic medications Narcotic analgesics

Describe constipation symptoms, nonpharm treatment, and pharm therapy

Symptoms: - Infrequent evacuation - Hard small feces - Difficult / painful evacuation of large-diameter stools - Excessive, unsuccessful time spent on toilet - Fecal incontinence • Non-pharmacologic treatment - Adequate fluid intake - Avoid caffeine/alcohol - Increase physical activity - Increased fiber - Regular bowel hygiene - Privacy - Appropriate foot support Constipation treatment Fiber • Bulk forming laxatives • Stool softeners • Stimulant laxatives • Osmotic agents • Lubricant laxatives • Guanylate cyclase-C agonist • Chloride channel agent • Peripheral opioid antagonist

How to you classify Ulcerative Colitis and Crohns Disease

TH1 affects Crohns TH2 affects UC Ulcerative Colitis Mild ● <4 stools/ day ● no systemic involvement ● normal ESR Moderate ● 4- 6 stools/ day ● minimal systemic involvement Severe ● >6 stools/ day with blood ● significant systemic involvement (fever, tachycardia, anemia) ● elevated ESR Fulminant >10 stools/ day with continuous bleeding ● toxic symptoms ● abdominal tenderness ● anemia requiring transfusion ● colonic dilation (toxic megacolon) ----------------------------------- Crohn's disease Mild to Moderate = ● ambulatory ● tolerating po intake ● well- hydrated ● no systemic involvement ● <10% weight loss Moderate to Severe = ● systemic involvement (including fever, significant weight loss) ● abdominal tenderness ● nausea/ vomiting ● anemia Severe to Fulminant = ● persistent symptoms despite steroids or biologics ● high fevers ● persistent vomiting ● intestinal obstruction ● peritoneal signs of involuntary guarding or rebound tenderness ● cachexia ● abscess

Describe the anatomy of the large intestine The 4 major regions, absorptive and goblet cells, haustral churning (haustra), action of bacteria (fermentation, production of which vitamins), and the defacation reflex

Terminal portion of GI tract, it completes absorption, produces certain vitamins, and forms and expluses feces from the body Divided into 4 regions: The ileocecal sphincter guards the opening into the large intestine from the small intestine -Cecum lies inferior to the ileocecal valve (the appendix is attached to the cecum as well). The open end of the cecum merges with a long tube called the colon, which is divided into ascending, transverse, descending, and sigmoid portions. -Sigmoid portion terminates (the rectum) -The opening of the anal canal is guarded by internal and external anal sphincters -Epithelium of the large intestine contains mostly absorptive and goblet cells: -Absorptive cells function primarily in water absorption -Goblet cells secrete mucus that lubricates the passage of the colonic contents There are no structural adaptations that increase SA. (small intestine is the focus of absorption) Mechanical digestion in large intestine: after a meal, gastrileal reflex intensifies peristalsis in the ileum and forces any chyme into the cecum. When the cecum is distended the contraction of the ileocecal sphincter intensifies. As food passes through the ileocecal sphincter, it fills the cecum and accumulates in the ascending colon -Haustral churning: the large intestine is divided into a series of pouches called haustra. Haustra remain relaxed and become distended while they fill up. When the distnesion reaches a certain point, the walls contract and squeeze the contents into the next haustrum ------ Chemical digestion: Final stage of digestion through activity of bacteria: 1. Chyme is prepared for elimination through bacterial action 2. Bacteria ferment any remaining carbohydrates and release H, CO2, and methane 3. Bacteria also convert any remaining proteins to AA 4. Bacterial products that are absorbed inthe colon include B vitamins and vitamin K ---- Chyme remains in large intestine for 3-10 hours and becomes solid due to water absorption now called feces -90% of water absorption occurs in small intestine, but large intestine is important enough to maintaing body water balance Defactaion reflex: -Peristaltic movements push fecal material from sigmoid colon to rectum

What are the two types of organs that make up the digestion tract

The gastrointestinal tract - the continues tube that runs from the mouth to the anus (mouth, pharynx, stomach, small intestine, large intestine) And the accessory digestive organs which aid in swallowing, secreting, of enzymes leading to chemical breakdown (teeth, tongue, salivary glands, liver, gall bladder, pancreas)

Liver Describe Lobes & falciform ligament, hepatocytes, Bile (ducts), Hepatic blood flow, and the portal triad Also the emulsification process and metabolism & storage

The heaviest gland of the body: 3lbs in the average adult It is devided into two principle lobes: -Large right lobe -Smaller left lobe -Lobes are separated by the falciform ligament Liver is composed of: 1. Hepatocytes (major functional cells of the liver that perform metabolic, secretory, and endocrine functions) and secretes bile 2. Bile canaliculi: small ducts between hepatocytes that collect bile. Bile passes from bile canaliculi -> bile ductules -> bile ducts. Biles merget o form the right and left hepatic ducts, this forms the common hepatic duct that joins the cystic duct from the gallbladder to carry bile to the duodenum 3. Hepatic sinusoids: highly permeable blood cappilaries between rows of hepatocytes. It receives oxygenated blood from the hepatic artery and the nutrient rich deoxygenated blood from the branches of the hepatic portal vein. Hepatic portal vein brings venous blood from the GI organs and spleen into the liver (blood contains nutrients, drugs, microbes, and toxins from GI tract) It is the site of uptake for oxygen, nutrients, and toxic substances for hepatocytes Term: Portal triad (a bile duct, branch of hepatic artery, and a branch of the hepatic vein) Bile: consists of water, bile salts, cholesterol, lecithin, and ions -Primary bile pigment: bilirubin. (phagocytoses aged RBC that release iron, globin, and bilirubin (derived from heme). Bilirubin is secreted into the bile and eventually broken down in the intestine (stercobilin, a breakdown product of bilirubin, gives feces brown color) Bile salts: breaksdown large liquid globules into smaller lipid globules (provides a large surface area for pancreatic lipase to rapidly digest triglycerides Besides bile, Liver metabolizes: 1. Carbohydrates 2. Lipids (stores triglycerides, synthesizes cholesterol, and uses cholesterol for bile salts 3. Proteins (deaminates amino acids so that the resulting amino acids can be used for ATP production. NH3 (ammonia) is converted to less toxic urea and excreted Liver and processes drugs and hormones: -detoxifies alcohol, excretes penicilllins and sulfonamides into the bile and chemically alters or excretes thyroid hormones. Also stores: glycogen, vitamins (A, B12, D, E, and K)

List potential complications associated with PN and how to prevent these complications

Three complications: Metabolic Electrolyte imbalance (i.e., Na, K, Phos, Mg, etc.) Deficiencies (i.e., vitamin, mineral, trace element) Acid-base balance Adjust chloride to acetate ratio in PN Glucose metabolism Hyperglycemia Hypoglycemia Liver impairment (IFALD) Metabolic bone disease Strategies to manage IF-associated (intestinal failure) liver complications Rule out non-PN factors Sepsis Biliary obstruction Herbal supplements Hepatotoxic medications Consider PN modifications Decrease dextrose Decrease soybean ILE (< 1 g/kg/day) Cycle PN -- Strategies to manage IF-associated liver complications Maximize enteral intake Prevent/treat bacterial overgrowth Pharmacotherapy Intestinal transplantation -- Infection Systemic Catheter/exit site Catheter/pump (mechanical) Air embolism Blood in catheter Cracking/tearing of catheter Catheter clot Phlebitis inflammation of vein

List potential complications of enteral access devices and use of enteral nutrition

Three types of potential complications: 1. Metabolic = If enteric feeding is done properly this is a rare complication; often results from improper nutrition delivery or underlying disease state Example: refeeding syndrome. May deplete phosphorus stores leading to death 2. GI N/V Abdominal distension/cramping (use metoclopramide, erythromycin) Aspiration (most serious, potentially life threatening) aspiration: risk factors Do not use blue foo coloring, may indicate improper position of feeding tube Diarrhea = Defined as >3-5 liquid stools/day or >250-500ml/day stool output for at least 2 consecutive days Constipation (difficult to define because of difference in normal stool pattern (four stools/day to one stool every 4-5 days) ----------------------- 3. Mechanical complications -Tube occlusion: Bore size of tube too small, frequent flushing of tube -Tube malfunction: breaking, cracking, or kinking -Tube dislodgement: Occurs in 25-41% of cases. can try to prevent with nasal bridle (for NGT placements) or balloon devices (for gastric or jejunal tubes) -Nasopulmonary intubation: most dreaded procedure-related complication with initial misplacement of nasoenteric tube into bronchopulmonary tree. Results in pneumothorax 50% of the time. Radiography is the gold standard for ensuring correct placement of fedding tube -Perforation of GI tract -Infection at site of insertion

What are some extra intestinal manifestations of Ulceratice colitis and crohns disease?

Ulcerative Colitis ● Hepatic ○ Fatty liver, chronic hepatitis, gallstones, primary sclerosing cholangitis, cirrhosis ● Musculoskeletal- arthritis ○ large joints (asymmetric) ○ knees>hips>ankles>wrists>elbows ○ ankylosing spondylitis ● Ocular ○ Inflammation of the eye, up to 10% of patients ● Dermatologic ○ Lesions, in 5- 10 % of patients ○ pyoderma gangrenosum Crohn's Disease ● Similar to UC, with the addition of: ● Nutritional deficiencies (common) ○ Weight loss ○ Growth failure ○ Vitamins, minerals, electrolyte deficiencies

Develop an approach to assess and evaluate drug-induced liver injury

What is hepatitis = inflammation of the liver Diagnosing DILI Conditions that require exclusion: Viral Hepatitis: A,B,C, E Alcholic liver injury autoimmmune liver disease Cancer involving liver Conventional durg injury Shock, ischemia, hypoxia Biliary tract disease Metabolic, inherited disorders HDS implicated Diagnostic hindrances: adulterants, unlabeled ingredients, contaminants ----- Assessment of liver enzyme injury Hepatocellular changes = >300% normal AST, ALT, LDH Cholestatic = Alk Phos 5NC GGT All over >300% Mixed injury = all lab values will be raised Monitoring every 90-180 days-------------------- ----- Assessment of Histologic changes -Centrolobular necrosis = Damage spreads outward from the middle of a lob in the liver Cause by acetaminophen -Nonalcoholic steatohepatitis (NASH) -Fatty infiltrates seen on imaging or biopsy -Tetracycline, valproate acid linked to NASH -Phospholipidosis = Accumulation of phospholipids Linked to amiodraone Generalized hepatocellular necrosis -Mimics changes seen with viral hepatitis -Isoniazid, ketoconazole Toxic cirrhosis or fibrosis -Scarring of liver from hepatitis -Methotrexate Liver vascular disorders -Focal lesions in hepatic venules, sinusoids, and portal veins -cytotoxic chemo, pyrrolizidine alkaloids, sex hormoes --------------------- Assessment of Severity of Liver Damage Markers of liver Function: -Albumin -Transferrin -Prothrombin time (PTT) (international normalized ratio (INR)) -Platelets --------------------- Hepatotoxic drug considerations in Chronic Liver Disease -If abnormalities in liver test seen, rule out other potential medications Monitor: AST,ALT ALK Phos -Start low and titrate drugs hepatically cleared Monitor: synthetic liver function, platelets, INR, albumin, Bilirubin Acetaminophen safe dose is <=2000mg/day Statis may be protective

Describe the anatomy of the esophagus

it is a collapsible muscular tube that lies posterior to the trachea -Begins at inferior end of laryngopharynx and ends at the superior portion of stomach Upper esophageal sphincter = skeletal muscle that regulates movement of food from pharynx to esophagus Lower esophageal sphincter = smooth muscle that regulates movement from esophagus to stomach Esophagus secrets mucus and transports food to the stomach

Select the most appropriate bowel regimen for a given patient scenario

symptomatic w/o risk factors • Screening beginning at 50 years old • FOBT annually • Sigmoidoscopy every 5 years + FOBT every 3 years • Colonoscopy every 10 years • Screening over the age of 75 is patient specific • Risk factors • Patient preference ---------------------- Family history of colorectal cancer • Colonoscopy recommended • 1st degree relative diagnosed ≥ 60 yo • Start at 50 years old • Test every 10 years • 1st degree relative diagnosed < 60 yo or two 1st degree relatives • Start at 40 years old or 10 years younger than relative at diagnosis • Test every 5 years -------------------------- Relative Contraindications to Colonoscopy Pregnancy Increased risk of complications during colonoscopy Recommend postponing colonoscopy until the post-partum period Known or suspected colonic perforation Recent myocardial infarction Toxic megacolon Fulminant colitis or severe inflammatory bowel disease with ulceration -------------------------- Meat and potatoes Algorithm: Contraindicated to procedure ->Yes: consider alternatives ->No: is patient at risk of electrolyte/fluid imbalance? ->Yes: PEG-ELS only ->No: is patient concerned about volume ->yes: low volume PEG solution or alternative ->No: 4-L PEG-ELS First line is PEG-ELS in all special populations but elderly (Low volume PEG-ELS) ------------- Special populations: CHF, Cirrhosis, kidney disease: -Sodium phosphate -Sodium picosulfate -Sulfate solutions -OTC PEG -Magnesium citrate IBS: Avoid sodium phosphate Lower GI bleeding: Avoid OTC PEG Pregnacny: Sodium phosphate Avoid colonoscopy in general

Describe Bulk forming laxatives of constipation

• Medications - Psyllium husk (Metamucil®) -fermentable - Methylcellulose (Citrucel®) - Polycarbophil (FiberCon®) • MOA - Absorbs water in intestine to form viscous liquid which promotes peristalsis and ↓ transit time • Use: Constipation (long term use OK) • Up to 3 days to work