CAM Exam #3

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DrJBlack
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214141
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CAM Exam #3
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2013-04-19 00:43:46
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Nutrition Osteomy Obesity
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Nutrition, Osteomy, Obesity
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  1. marasmus
    • chronic condition leading to total intake deficiency
    • decrease protein and calories
    • waste somatic/skeletal protein & adipose
    • spares visceral protein production
    • severe involvement affects cell-mediated immunity
  2. kwashiorkor
    • adequate calorie intake but protein deficiency
    • depeletion of visceral & somatic protein
    • spares adipose
    • catabolic pts; secondary to trauma, burns, infection
    • impaired immune function
  3. mixed marasumus-kwashiorkor
    • severe protein-calorie malnutrition in chronically ill, starved pts undergoing hypermetabolic stress
    • reduced visceral protein synthesis superimposed on wasting somatic protein and energy (adipose tissue) stores
    • immunocompotence lowered leading to increased infection and poor wound healing
  4. albumin
    • synthesized from liver
    • normal range:  3.5-5 g/dL
    • affected by volume, liver/renal failure, trauma, burns, sepsis, age
    • Marker of illness, NOT infection
  5. starvation process
    glycogen from liver depleted ~48 hrs, muscle depleted ~12 hours -> catabolism of skeletal muscle -> AA into glucose -> prolonged starvation -> fat stores used and decerease proteolysis
  6. starvation
    • normal suppression of proteolysis seen with prolonged fasting doesn't occur in sepsis
    • still breakdown protein
    • high cortisol concentrations --> persistent hyperglycemia --> inhibits lipolysis
    • septic pts can have enormous untapped fat stores and still catabolize muscle
    • primary source for GLU in early starvation (1wk) comes from skeletal muscle proteins
  7. starvation:  what happens to growth hormone, thyroid stimulating hormone, insulin or other factors?
    • ↑ GH → CHO & fat breakdown; protein buildup
    • ↓ TSH → ↓ TH → ↓ basal metabolic rate and energy
    • ↓ insulin → ↑ glucagon → hyperglycemia & protein breakdown
    • ↑ catecholamines
    • ↑ ketone bodies → ↑ energy & ↓ protein breakdown
  8. 0-10-20
    • 0-10 kg     → 100 kcal/kg
    • 10-20 kg   →   50 kcal/kg + 1000 kg
    • >20 kg     →   20 kal/kg + 1500 kg
  9. Enteral (PO)
    • natural, safe, cheap
    • Always use this route if possible; easiest way to gut
    • nutrients absorbed into portal system and pass through liver → more efficient nutrient use
    • Indicated for:  functioning GI tract and able to eat enough to sustain life
  10. Parenteral
    • greater flexibility
    • Indicated for:  GI tract not functioning & unable to receive enteral nutrition > 5-7 days
  11. Reasons for Nutrition Support
    • limit catabolism
    • substrate for healing
    • increase survival
  12. Goals of Stress Response
    • maintain GLU (energy) & O2
    • minimize injury
  13. Energy Substrates:  Carbs
    • GLU parallels degree of injury
    • increase hepatic production of 3 - C precursors (fats/AA)
    • breakdown liver glycogen
  14. Energy Substrates:  AA
    • skeletal muscle breakdown skewed (alanine and glutamine)
    • muscle N transferred to liver
  15. Energy Substrates:  Fats
    • catecholamine regulates lipolysis
    • provides 3 carbon fragments to liver
    • major provider of energy substrates in early sepsis and trauma (regulated through leptin?)
    • omega-6 FA:  pro-inflammatory; essential fat comes from soy beans
    • omega-3 FA:  non-essentail fat comes from fish oils
    • overload on protein, it will turn into fat
  16. T/F:  The Harris-Benedict and Ireton Jones equation applies to parenteral nutrition.
    FALSE - it does not apply to PN
  17. Problems with Nutritional Parameters
    • UUN will be invalid if Clcr < 50 mL/min
    • UUN & prealbumin are not helpful if pt hasn't received goal volumes of feeding consistently for 3-4 days prior to test
    • 6.25 g of protein = 1 g N
  18. Nutrients
    • Fat = 9 kcal/g
    • Protein = 4 kcal/g (not to be included in calorie estimates and no glutamine in TPN due to instability)
    • Carbohydrateinfused = 3.4 kcal/g
    • Carbohydrateenodgenous/eaten = 4 kcal/g (molecule of water sits on carb making it less dense)
    • Trace minerals:  Cr3+, Zn2+, Se3+, Fe3+, Mn2+ (toxicity reversible in adults not kids, both due to renal fxn)
    • Vitamins:  thiamine
  19. What are the branched chain AA?
    isoleucine, leucine, valine
  20. Why do we give EN?
    • preserves villi
    • gets tings to the stomach the best
    • we can give glutamine which is a major enterocyte fuel source, major N transfer agent to viscera, essential AA in catabolic stress
  21. When is post-pyloric the best to use?
    • gastric ileus
    • recent surgery
    • needs frequent procedures and have to stop and go with feedings
  22. Refeeding Syndrome
    • severely malnourished and develops severe electrolyte abnormalities (phosphorus, potassium, magnesium)
    • muscle mass, cell mass, ATP repleted → low values → cardiac arrest
  23. What is normal osmolarity?
    280-290 mOsm/kg
  24. ADH
    • depends on urinary concentration
    • secreted in response to increased osmolality and to decreased volume
    • acts on distal CT/CD to reabsorb water
    • acts via V2 receptors and aquaporion 2
    • acts only on water
  25. Colloids
    • blood
    • plasma/albumin
    • synthetics
  26. Crystalloids
    • N/S - shift things back and forth of intravascular volume to ICF
    • dextrose - (NOT good for resucitation) has an automatic shift out of intravascular fluid
    • N/S + dextrose
    • 154 mEq/L of saline in water (NS)
  27. Rules of Fluid Replacement
    • replace blood with blood
    • replace plasma w/ colloid
    • resuscitate w/ coloid
    • replace ECF depletion with saline
    • rehydrate w/ dextrose
  28. Tx for hypovolemia
    • Sxs: seizures if too fast of drop or rise (levels), lethargy, weakness, anorexia, muscle cramps, emesis
    • Acute:  LR via large bore IV then blood
    • LR resembles blood and can use for burns when there's blood loss
    • Subacuteisotonic/hypotonic:  NS or 1/2 NS or LR (vomiting use NS; diarrhea use LR)
    • Subactuehypertonic: D5W
  29. Tx for hypervolemia (cardiac/renal failure)
    • water restriction
    • diuretics
    • ↓ albumin
    • ↓ Na+ (Na+ is more of a refection of water)

    Need urine output before starting IV K+
  30. Sodium
    • main EXTRACELLULAR cation
    • responsible for tonicity
    • Normal:  135-145 mEq/L
    • reflection of total body water, not sodium itself
  31. Potassium
    • main INTRACELLULAR cation
    • Normal:  3.5-5 mEq/L
    • serum levels don't reflect body stores
    • affected by drugs, blood pH, decrease Mg2+
    • evaluating K+, you must consider pH before adjustments
    • HCO3-, insulin, GLU will cause K+ to go inside the cell
  32. Magnesium
    • 2nd most abundant intracellular cation
    • predominant cofactor
    • Normal:  1.4-2.6 mg/dL
    • located 1/2 in soft tissue, 1/2 in bone, less than 1% in blood
    • hypermagnesia → flappy muscles due to less contration (relaxation)
    • hypomagnesia → seizures
  33. Calcium
    • important cation in cell metabolism, coagulation, bone growth
    • Normal:  8-10.5 mg/dL
    • Correction for albumin = [(4 - serum albumin) x 0.8] + serum Ca2+
    • acidosis ↓ Ca2+ binding to albumin and promotes Ca2+ excretion
    • hyperventilation ↑ Ca2+ binding
    • mild hypomagnesia → ↑PTH → ↑Ca2+
    • severe hypomagnesia → ↓PTH → ↓Ca2+
    • acute hypophostemia → ↓Ca2+
    • thiazide spares Ca2+ while furosemide decreases Ca2+
  34. Phosphate
    • sixth most abundant element in body
    • principle ion in bone mineral
  35. Bicarb
    • principle EXTRACELLULAR buffer
    • Normal:  18-27 mEq/L
    • ↑K+ → ↓HCO3- reabsorption
    • phosphate depletion → ↓HCO3- reabsorption
    • you only give half of what you calculate
  36. Vitamin A
    • Functions:  VISION, cell development and halth, immunity
    • Food Sources:  liver, milk, egg yolks; beta carotene is in yello-orange fruits & vegetables
    • Deficiency:  eyes (night blindness), skin (hyperkeratosis), and other epithelial tissues
    • Toxicity can be fatal
    • Polar bear has the most [vit A] in their liver
    • carotenoids = antioxidants + source of vitamin A
  37. Vitamin D
    • made in skin from cholesterol and activated in liver and kidney
    • regulates blood Ca2+ levels, need active kidney to have vit D
    • food sources:  milk & cereals
    • Deficiency:  rickets in kids; osteomalacia and osteoporosis in adults
    • Active vitamin D = 1,25(OH)2D
  38. Vitamin E
    • antioxidant → protecting cell membranes from free radicals
    • deficiency:  erythrocyte hemolysis
    • toxicity is rare
    • prolonged deficiency:  nueromuscular dysfunction (not a cure for muscular dystrophy)
    • plant oils have vitamin E
  39. Vitamin K
    • K = Koagulation
    • blood clotting and bone formation
    • deficiency:  increased hemorrhage risk
    • excess can interfere with anticoagulation meds
  40. What do all fat soluble vitamins have in common?
    • absorbed by small intestine
    • no bile, no absorption
  41. What do all water soluble vitamins have in common?
    • generally renally excreted, not stored
    • coenzymes
    • energy (CHO) metabolism
  42. Thiamin
    • helps synthesize NT
    • deficiency:  BERIBERI (nerve degeneration, edema, enlarged heart, heart failure)
  43. riboflavin
    • supports antioxidants (vit A & E)
    • deficiency:  cracks at the corner of the mouth (angular chelitis) and inflammation of mouth and tongue
    • patients at risk:  alcoholics, non-dairy diet, long term pheobarbital
    • milk is a good source
  44. niacin
    • supports fatty acid synthesis (cholesterol)
    • deficiency:  pellagra → decrease appetite and weight → (3Ds) diarrhea, dementia, dermatitis → death
    • Toxicity:  at high doses → used for treating high cholesterol (SE:  skin flushing, liver damage)
    • chicken is a good source
  45. patothenic acid
    • coenzyme A component
    • AA metabolism
    • DNA synthesis
    • mushrooms are good source
  46. biotin
    • AA metabolism
    • FA synthesis
    • DNA synthesis
  47. vitamin B6
    • coenzyme in protein & AA metabolism
    • supports immune system
    • deficiency:  microcytic hypochromic anemia
    • permanent nerve damage w/ high doses (>200 mg/d)
    • bananas are a good source
  48. folate
    • coenzyme in DNA synthesis and cell division
    • needed for normal RBC synthesis
    • Deficiency:  megaloblastic anemia (can contribute to neural tube defects; women childearing age needs 400 mcg/d)
    • cereals, grains, legumes, vegetables
    • can decrease breast cancer risk by 50%
  49. vitamin B12
    • needed for normal folate fxn (DNA & RBC synthesis)
    • maintains myelin sheath around nerves
    • Deficiency:  pernicious anemia (megaloblastic anemia + nerve damage)
    • no intrinsic factor in gut, you can't absorb it
    • fish, meats, liver, eggs, milk
  50. vitamin C
    • antioxidant - donates and accepts H+ atoms readily
    • collagen and steroid synthesis
    • deficiency:  scurvy causes fatigue, pinpoint hemorrhages, bleeding gums, joint pain
    • toxicity:  may cause GI distress in high doses
    • protects cell membranes from damage by free radicals
    • needs are higher for smokers
    • don't stop vitamin C abruptly 
  51. carnitine "L-carnitine"
    • AA that helps metabolize fat in mitochondria and protein buildup of fat deposits in heart
    • give long term valproate → carnitine deficency
  52. Celiac disease
    • immune-mediated enteropathy cause by a permanent sensitivity to gluten in genetically susceptible individuals
    • DQ2 and/or DQ8 positive HLA halotype is necessary, but NOT sufficient for development
    • unique b/c the environmental trigger (gluten) and autoantigen (tissue Transglutmainase) are known
    • eliminate gluten will resolve disease
    • one of the most common genetially based diseases
  53. Types of Celiac Disease
    • Classical
    • Silent
    • Latent
  54. Classical Celiac Disease
    • GI malabsoption
    • Dx established by sertological testing, biopsy evidence of villous atrophy
    • improves sxs w/ GF diet
  55. Silent Celiac Disease
    • asymptomatic but have a positive serological testing and villous atrophy on biopsy
    • detected by screening/endoscopy
  56. Latent Celiac Disease
    • (+) serology but no villous atrophy on biopsy
    • asymptomatic but later may develop sxs and/or histological changes
  57. Tissue Transglutaminase (TTG)
    • normal gut enzyme released during injury and stabilizes cross-linking of proteins in granulation tissue
    • autoantibody against TTG → active celiac disease
    • always screen for IgA deficiency
  58. Diagnosis of Celiac Disease
    • can happen at any age
    • women > men
    • adults > kids
    • clincial suspicion
    • + serology
    • biopsy confirmation
  59. Dental SE of celiac disease
    • vertical linear defects in secondary teeth (severe)
    • cavities in unusual spots
  60. Biopsy Confirmation for Celiac Dz
    • obtainted at descending duodenum at ampulla of vater
    • degrees of villous atrophy w/ hyperplasia of crypts and increased intraepithelial lymphocyte count
  61. Challenge with Celiac Disease
    not confirming disease, but identify individuals who may have Cd then selecting the appropriate test to screen them
  62. Tx Celiac Dz
    • only tx = strict adherence to GFD
    • decreases intestinal damage and autoimmune dz
    • decreases cancer risk and health care cost
    • improves QOL and life expectancy
  63. Zonulin
    regulates intestinal permeabilty and found in BBB
  64. Regulators of appetite
    • psychological & cultural
    • neural affarents
    • gut peptides (leptin helps ↓ appetite)
    • metabolites
    • hormones (cortisol, leptin, insulin)
  65. How is appetite regulated with obesity?
    ↑ adipose → ↑ leptin → ↑ POMC → ↓ food intake ↑ expenditure
  66. Limitations to BMI calculation
    • edema
    • extreme muscularity
    • muscle wasting
  67. Risk Factors Obesity (CHIDDS)
    • Coronary heart disease
    • HTN
    • Increased waist size
    • Diabetes
    • Dyslipidemia
    • Sleep apnea
  68. Determinants of Obesity (piic)
    • intrapersonal
    • interpersonal
    • community
    • public policy
  69. Determinants of Obesity:  Intrapersonal (KMoPS)
    • knowledge
    • motivation
    • preferences
    • socioeconomic limitations
  70. Determinants of Obesity:  Interpersonal (CuSST)
    • culture
    • screen time
    • social support
    • time constraints
  71. Determinants of Obesity:  Community
    • built environment
    • food availability at stores
    • workplace food environment
  72. Determinants of Obesity:  Public Policy (faz)
    • food pricing
    • advertisments
    • zoning regulations
  73. BMI
    kg/m2

    • Underweight → < 18.5
    • Normal → 18.5 - 24. 9
    • Overweight → 25 - 29.9
    • Obese I → 30 - 34.9
    • Obese II → 35 - 39.9
    • Obese III → ≥ 40
  74. Assessment Strategy for Obesity
    • identify BMI ≥ 25
    • assess motivation to lose weight
    • assess for secondary obesity (medical referral)
    • assess risk factors
  75. Risk Factors with Obesity
    • coronary heart disease
    • T2DM
    • dyslipidemia
    • HTN
    • increased waist circumference (women < 35 in; men < 40 in)
    • sleep apnea
  76. Stages of Change
    • pre-contemplation
    • contemplation
    • preparation
    • action
    • maintenance
  77. pre-contemplation
    • has no intention of taking action within the next 6 mos
    • Strategy:  Awareness
  78. contemplation
    • intends to take action in next 6 mos
    • Strategy:  Motivation
  79. preparation
    • intends to take action within the next 30 days and has taken some behavoiral steps in this direction
    • Strategy:  Goal setting
  80. action
    • has changed behavoir for less than 6 mos
    • Strategy:  Problem solving
  81. maintenance
    • has changed behavoir for more than 6 mos
    • Strategy:  Avoiding relapses
  82. Tx Strategy:  Weight Maintenance
    BMI ≥ 25 to < 30 with ≤ 1 risk factor
  83. Obesity Tx:  Lifestyle Modifications
    • BMI ≥ 25 to < 27 with ≥ 2 risk factors
    • low calorie diet , but not very low 
    • increased exercise - 30 min of mod excercise on most days of the week; 1 hr/d of mod exercise may be required to lose weight; start slow and gradually increase intensity; perform med exam before starting program
    • behavoir modifciation through self monitoring (journaling, food/exercise log), stress mgmt, stimulus control (using smaller plate, not eating in front of tv)
    • Goals:  wt loss 5-10% of initial wt over 6 mos (1-2 lbs/wk), SMART goals
  84. Obesity Tx:  Drug Therapy
    • BMI ≥ 27 to < 30 with ≥ 2 risk factors
    • BMI ≥ 30 to < 35
    • BMI ≥ 35 to < 40 with ≤ 1 risk factors
    • Short Term:  phentermine, diethylpropion, benzphetamine, phendimetrazine
    • Long Term:  orlistat (lipase inhibitor), locaserin (5-HT2c agonist), phentermine/topiramate (sympathomimetic/anticonvulsant)
    • Monitor by dcumenting pt progress 1-2 times/mos for 1-2 mos, then monthly thereafter
    • d/c meds after 3-4 mos if wt loss or maintenance of prior wt loss is not apparent
  85. phentermine
    • CIV
    • MOA:  increases Norepi in hypothalamus
    • take early in the day to avoid insomnia
    • ADE:  increased BP, palpitations, arrhythmias, insomnia
    • Avoid in HTN and insomnia pts
    • CI: hypothyroidism, agitated states, hx of substance abuse, glaucoma
    • inexpensive, but can only use for 12 wks
  86. Similar to phentermine
    • benzphetamine CIII
    • diethypropion CIV
    • methamphetamine CII (can't be Rx for wt loss in OH)
    • phendimetrazine CIII
  87. Orlistat
    • MOA:  decrease dietary fat absorption through selective inhibition of the GI lipase
    • Take within 1hr of consming food containing fat
    • ADE:  soft stools, ab pain, flatulence, fecal urgency, incontinence (limit dietary fat prior to initiation of orlistat)
    • severe diarrhea may decrease absorption of oral medications
    • consider multivitamin, backup contraception, separate orlistat from other meds
    • OTC but severe GISE
  88. Lorcaserin
    • MOA:  activate 5HT2c stimulating POMC nuerons in hypothalamus
    • Evaulate response at 12 wks; if pts has not lost ≥ 5% of baseline body wt, d/c therapy
    • ADE:  HA, URI, nausea, dizziness, fatigue
    • CI Clcr < 30 mL/min and caution in severe hepatic impairment
    • alternative to phenteramine; not a lot of wt loss evidence and expensive
  89. phentermine/topiramate ER
    • CIV
    • MOAphentermine:  sympathomimetic amine
    • MOAtopiramate:  appetite suppression and satiety enhancement
    • take w/ or w/o food in AM
    • ADE:  dry mouth, paresthesia, insomnia, dizziness, dysgeusia
    • REMS requiring prescriber educated and limited dispensing to certified mail order pharmacies
    • childbearing potential women must be on aproved contraception; pregnancy testing recommended before and monthly during therapy
    • graudally wean off to avoid seizures
    • more wt loss potential; have to titrate, only available through special mail order, brand name expensive
  90. Obesity Tx:  Surgery
    • BMI ≥ 35 to < 40 with ≥ 2 risk factors
    • BMI ≥ 40
    • most effective, but most risky
    • restrict/reduce food intake by reducing stomach volume
    • malabsorption by reducing the absorptive surface of alimentary tract
    • nutrient and drug absorption altered
  91. IBS-D & C Therapeutic Goals
    • focus on pt primary complaint
    • dietary & drug therapy
    • CNS sxs depression
  92. Tx Approach for IBS-D & C
    • Non-pharm = primary role (psychotherapy, cognitive behavoiral tx, relaxation tx, hypnotherapy, demonstrated to decrease IBS sxs)
    • Mild, less frequent episodes → dietary restrictions/changes
    • Persistent → PRN antispasmodics, antidiarrheal agents
    • Severe → neurohormonal targets (5HT4 partial agonist, 5HT3 antagonist)
  93. Tx IBS pain
    • antispasmodics (dicyclomine & hyoscyamine) = 1st line
    • block PNS of Ach and decrease colon contractions
    • take before meals if post prandial sxs dominate
  94. IBS-D and IBS-C similarities
    • overall enhanced sensitivity/perception of pain (hypersensitivity)
    • non GI sxs (MUST screen pts to make sure anxiety & depression are controlled)
  95. IBS-C
    • decreased contrations and longer transit time
    • higher threshold for sensation → takes more for pt to sense movement or time to reduced sensitivity for distension

    Dx → symptomatic tx including stress mgmt and patient education → ↑ dietary fiber & fluid intake → consider bulk forming and/or antispasmodic → add 5-HTpartial agonist → add psychosocial behavoiral modifications (consider antidpressant for pain)
  96. Dietary Fiber
    • Bran, pysillium (soluble preferred)
    • increase BM, but DOES NOT HELP PAIN
    • require higher doses → tolerance issues
    • stimulants NOT recommended
    • Goal:  bulkier, softer, easier to pass stools
  97. Osmotic Laxatives
    • Lactulose & Sorbital
    •   disaccharide sugars → galactose & fructose
    •   not digested → draws water → ↑ motility ↓transient time

      wicked cramping (esp in elderly) → start w/ lower dose

    • PEG 3350
    •   draws water into lumen & ↑ GI motility & ↓transient time

      effect seen in ~2 wks → indicated for short-term use, safe & effective for 6 wks, used in patients with chronic constipation
  98. Tegaserod
    5-HT4 partial agonist in GI tract → ↑ motility ↓ visceral pain sensation

    • CI < 55 yoa
    • Monitor:  rectal bleeding, bloody diarrhea, ab pain
    • can cause cardiac SE and significant diarrhea → hypovolemia, hypotension, syncope
  99. Zelnorm
    • approved for emergency only & require hospitalization
    • not for women > 55 yoa w/ IBS-C
  100. Lubipristone
    • Cl (Cl2) channel activator - bicyclic FA
    • enhances intestinal fluid & electrolyte conc. in intestine & lacks systemic absorption - local effect
    • take w/ food & water (immediately after/during meal)
    • indicated for chronic idiopathic constipation & IBS-C in women ≥ 18 yoa
    • can cause severe nausea
    • Short term use:  4 wks
    • Long term use:  6-12 mos
  101. Linaclotide
    • guanyl cyclase (GC-C) agonist → ↑ Cl and HCO3- secretion
    • ↑ intestinal transit time
    • ↓ visceral hypersensitivity
    • 2 wk adminstration → improve outcomes
    • can be use in men
    • ≥ 18 yoa & take 30 min before breakfast
  102. IBS-D
    ↑ contractions and shorter GI transits

    • lower threshold for sensation → takes less stool present in bowel to feel like you have to go
    • rectal spasms/contractions w/ distension

    s/s:  lower ab pain, bloating, distension rectal, > 3 stools/d, extreme urgency, mucus passage (sign)

    Dx → symptomatic tx including stress mgmt and patient education → lactose free/caffeine free diet; counsel on trigger foods → add loperamide/other antispasmodic → add 5-HT3 antagonist → add psychosocial behavoiral modifications (consider antidpressant for pain)
  103. loperamide
    • episodic/continuous
    • ↑ intestinal transit
    • ↓ electrolyte/water reabsoption
    • strengthen renal sphincter tone
  104. diphenoxylate w/ atropine
    • CV - opiod agonist
    • slows intestinal contractions and peristalsis
    • allows water to be reabsorbed
    • no response in 48 hr → benefit unlikely
  105. cholestyramine
    bile acid sequestrant and binds fluid in stool
  106. aloesteron
    • 5-HT3 antagonist
    • acts on 5HT receptors in GI tract
    • ↓ motility and ↓ visceral sensation

    • indicated for women w/ severe IBS sxs who fail conventional therapy
    • indicated for severe IBS sxs, who fail conventional therapy
    • can cause serious constipation, ischemic colitis, death
  107. antidepressants
    • just for PAIN
    • TCA  → moderate-severe ab pain tx by modulating pain perception and altering GI transit time
    • paroxetine → stool passage "well being" - no cange in ab pain
  108. Ulcerative Colitis (UC) Pathophysiology
    • rectum + colon +/- terminal ileum
    • primary lesions occurs in crypts of mucosa
    • ulcers surround unaffected tissue (pseudopolyps)
    • collar-button ulcer
    • Dx:  clinical suspicioin, bx, sigmoidoscopy, colonoscopy, extracolonic manifestations
  109. Minor (Local) Complications of UC
    • hemorrhoids
    • anal fissures
    • perirectal abscesses
  110. Major (Local) Complications of UC
    massive colonic hemorrhage, colonic perforation, colonic strictures, colon cancer
  111. Toxic megacolon (UC)
    • colonic distension and acute colitis w/ systemic toxicity
    • ulcer extends below submucosa and reaches serosa
    • vasculitis
    • thrombosis of small arteries
    • bowel perforation
  112. Systemic Complications of UC (DONT HJ)
    • dermatolgoical & mucosal complications
    • ocular 
    • nutritional deficiencies
    • thromboembolic disease
    • hepatobillary
    • joint (ankylosing spondylitis, arthritis)
  113. UC Therapeutic Goals
    • Resolve acute inflammation & complications
    • maintain remission
  114. Tx Mild-Mod UC:  distal colitis
    • sulfasalazine/mesalamine (enema/supp), or CS enema
    • meslamine (enema/supp) > topical CS/oral aminosalicylates 
    • improvement ~4wks
  115. Tx Mild-Mod UC:  colitis
    • PO sulfasalzine/meslamine
    • Olsalazine option for remission and indicated for intolerance to sulfsalazine
  116. Tx Mild-Mod UC:  remission
    • Proctitis:  meslamine supp
    • Distal colitis:  meslamine enemas 
    • Colitis:  reduce meslamine/sulfasalzine PO
  117. Tx Initial Mod-Severe UC
    aminosalicylates + prednisone
  118. Tx Remission Mod-Severe UC
    prednisone tape then ↓ aminosalicylate dose
  119. Tx No Remission Mod-Severe UC
    • add immunosuppressants (azathiprine/mercaptopurine)
    • consider infliximab if no response
  120. Tx Initial Severe-Fulminant/Intractable UC
    • Patients are hospitalized, NPO, bowel rest
    • Hydrocortisone IV
  121. Tx Remission Severe-Fulminant/Intractable UC
    • Patients are hospitalized, NPO, bowel rest
    • Convert prednisone, add aminosalicylates (1-2 mos), then attempt steroid withdrawl
  122. Tx No Remission Severe-Fulminant/Intractable UC
    no response w/ hydrocortisone (5-7 d), add cyclosporine IV
  123. Crohn's Disease Pathology
    • terminal ileum most common site → Entire GI tract/discontinuous
    • deep, elongated, intestinal lumen narrowed → cobblestone
    • acute exacerbations & remission
    • diarrhea & ab pain
    • hematochezia (bright red blood in stools) w/ perirectal, perianal lesions
    • small-bowel involvement & strictures →
    • Crohn's Disease
  124. Compared to UC, Crohn's disease has...
    • greater fistula & bleeding
    • more challenging tx
    • greater reliance on drugs and higher recurrence rate
    • EQUAL cancer risk with UC
  125. Crohn's Disease Tx Goal
    remission and reduction of sxs
  126. Mild-Mod Crohn's Disease:  ilecolonic/colonic
    aminosalicylates PO
  127. Mild-Mod Crohn's Disease:  perianal
    aminosalicylates PO and/or metronidazole
  128. Mild-Mod Crohn's Disease:  small bowel
    • meslamine/metronidazole
    • Add budesonide for terminal ileal/ascending colonic disease
  129. Mod-Severe Crohn's Disease:  ilecolonic/colonic, perianal, small bowel
    • Same for Mild-Mod tx + prednisone
    • add infliximab if fistulizing
  130. Mod-Severe Crohn's Disease:  Remission (Response)
    taper prednisone after 2-3 wks
  131. Mod-Severe Crohn's Disease:  No remission (no response)
    add immunosuppressants (azathioprine/mercaptopurine) or methotrexate, infliximab, or switch to adalimumab
  132. Severe-Fulminant Crohn's Disease
    • same as UC
    • hydrocortisone IV
    • if no response w/i 7 days, start cyclosporine IV
  133. H. pylori-induced PUD
    • chronic condition
    • duodenum > stomach
    • more pH dependent
    • epigastric pain
    • superficial ulcer
    • less severe GI bleeding, single vessel
  134. NSAID induced PUD
    • chronic condition
    • stomach > duodenum
    • less pH dependent
    • often asymptomatic
    • deep ulcer
    • more severe GI bleeding
  135. Risk Factors for PUD
    • age > 60
    • concomittant corticosteroid therapy/anticoagulant use
    • duration of NSAID use
    • cigarette smoking
    • alcohol consumption
    • previous upper GI bleed/peptic ulcer
  136. Pain in gastric ulcers vs. peptic ulcers
    • duodenal ulcer pain occurs 1-3 hours postprandial and usually relieved w/ food
    • food may precipitate/accentuate gastric ulcer pain
    • antacids usually provide immediate pain relief in most ulcers
  137. H. pylori tests:  endoscopic
    • expensive
    • uncomfortable
    • muscosal bx
    • histology, culture, biopsy (rapid) urease
  138. H. pylori tests:  nonendoscopic
    • more convienient 
    • less expensive
    • Aby detection, urea breath test (used post-tx to confirm eradication >4wks), stool antigen
  139. Tx H. pylori
    • Triple Eradication Regimen is TOC - BID dosing
    • Drug 1:  PPI
    • Drug 2:  clarithromycin
    • Drug 3:  amoxicillin/metronidazole (if PCN/macrolide allergic)

    • Quadruple Eradication Therapy - QID dosing
    • Drug 1:  PPI or H2RA (for 4-6 wks)
    • Drug 2:  bismuth subsalicylate
    • Drug 3:  metronidazole
    • Drug 4:  tetracycline/amoxicillin/clarithromycin
  140. Counseling Points for H. pylori tx
    • PPI should be taken 15-30 minutes before meal
    • amoxicillin shouldn't be used in PCN-allergic
    • metronidazole should be avoided with alcohol
    • bismuth salts may cause blackened tonuge, black stools, and/or constipation
  141. Tx NSAID-induced PUD
    • determine HP status
    • discontinue NSAID:  PPIs, H2RAs, or sucralfate
    • continue NSAID:  PPIs preferred
  142. Zollinger-Ellison syndrome
    one/more tumors (gastrinomas) form in pancreas/duodenum → secrete gastrin → bind to CCK on PC → ↑ Ca2+ → proton pump to be translocate → ↑ HCl

    • causes ulcers in unusual places
    • locate the tumor → surgical removal
    • PPIs are DOC

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