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GI/Hepatic > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

PUD: Two main secretory glands in GI

A

Oxyntic glands and pyloric glands

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2
Q

PUD: 3 main cells in the oxyntic gland

A
  1. Parietal cells
  2. Chief cells
  3. Enteroendocrine cells
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3
Q

PUD: What does parietal cells secrete?

A

Acid

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4
Q

PUD: What does chief cells secrete?

A

Pepsinogen

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5
Q

PUD: What does enteroendocrine cells secrete?

A

Histamine

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6
Q

PUD: 2 main cells in the pyloric gland

A
  1. G cells
  2. D cells
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7
Q

PUD: What does G cells secrete?

A

Gastrin

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8
Q

PUD: What does D cells secrete?

A

Somatostatin

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9
Q

PUD: Histamine is produced by ____ cells, _____ gastric acid secretion, and is a ____ mediator that works on _____ receptor

A
  • Enteroendocrine/Chromaffin-like (ECL)
  • Induces
  • Paracrine
  • H2
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10
Q

PUD: Gastrin is produced by ____ cells, is the _____ of gastric acid secretion, and is a _____ mediator

A
  • Antral G
  • Most potent inducer
  • Endocrine
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11
Q

PUD: Somatostatin is produced by ____ cells, ______ gastric acid secretion

A
  • Antral D
  • Inhibits
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12
Q

PUD: Histamine receptor

A

H2

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13
Q

PUD: ACh receptor

A

M3

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14
Q

PUD: Gastrin receptor

A

CCK2

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15
Q

PUD: Prostaglandin receptor

A

EP3

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16
Q

PUD: Proton pumps in parietal cells are activated by 2 pathways:

A

Ca2+-dependent pathway, cAMP-dependent pathway

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17
Q

PUD: H+, K+/ATPase pump generates the largest ____

A

ion gradient

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18
Q

PUD: Receptors involved in the stimulatory pathway of acid secretion

A

M3, CCK2, H2 receptors

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19
Q

PUD: Receptors involved in the inhibitory pathway of acid secretion

A

EP3

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20
Q

PUD: Protective mechanism in the superficial epithelial cell

A

EP3, M1 stimulatory pathway secrete mucus and bicarbonate for acid neutralization

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21
Q

PUD: Defense against acid in the lower esophageal sphincter

A

Prevents reflux of acid gastric contents

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22
Q

PUD: Defense against acid in the stomach

A

Secretion of a mucus layer by trapping secreted bicarbonate at the cell surface

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23
Q

PUD: Prostaglandins enhance mucosal resistance by _____(2)

A
  1. Reducing basal and stimulated gastric acid secretion
  2. Enhancing epithelial cell bicarbonate secretion, mucus production, cell turnover, and local BF
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24
Q

PUD: Defense against acid in duodenum

A

Bicarbonate neutralizes acid

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25
Q

PUD: Hormonal and neuronal regulation of pancreatic secretions (3)

A
  1. Parasympathetic stimulation
  2. Secretin causes secretion of fluid & bicarbonate
  3. Cholecystokinin (CCK) causes secretion of digestive enzymes from pancreas and contraction of gallbladder and release of bile into duodenum
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26
Q

What is Peptic Ulcer Disease (PUD)?

A

Benign lesion of gastric or duodenal mucosa occurring at a site where the epithelium is exposed to acid and pepsin

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27
Q

Causes of PUD

A

H. pylori infection, NSAIDs, acid hypersecretion (Zollinger-Ellison & Cushing’s ulcers)

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28
Q

PUD: What is Zollinger-Ellison syndrome?

A

Gastrin-secreting tumor of non-beta cells in endocrine pancreas that increase acid secretion

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29
Q

What is Gastroesophageal Reflux Disease (GERD)?

A

Acid and pepsin from the stomach flow backwards up into the esophagus

  • Heartburn
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30
Q

NSAID-induced PUD results from _____ & _____ injury

A

Systemic & topical

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31
Q

H. pylori infection leading to PUD MoA

A
  1. Suppression of somatostatin by inflammatory mediators causes disinhibition (induction) of gastrin release from G cells
  2. Ammonium hydroxide produced by H. pylori derived urease increases gastric pH & stimulates gastrin secretion
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32
Q

PUD: What are drugs that inhibit secretion of acid?

A

PPI, H2RA, prostaglandins, muscarinic antagonists

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33
Q

PUD: What are drugs that prevent contact with acid?

A

Sucralfate, prostaglandin analogs

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34
Q

PUD: What are drugs that neutralize acid?

A

Antacids

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35
Q

PUD: What is the class of drugs that work against H. pylori? Examples?

A

Antibiotics
- Clarithromycin, amoxicillin, metronidazole, bismuth

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36
Q

Inhibition of Proton Pump in PUD MoA, examples of direct & indirect ways

A

Blocks both basal and stimulated acid secretion
- Direct inhibition: PPI
- Indirect: CCK2 of gastrin, H2 of histamine, M3 of ACh

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37
Q

PUD: PPI MoA steps

A
  1. Prodrugs that require activation in acid environment
  2. Conformational change into tetracyclic active sulfenamide
  3. Rapidly reacts to form a covalent disulfide bond with the PP
  4. Irreversible inactivation of the pump
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38
Q

PUD: PPI ADME (Absorption, Metabolism)

A
  • Food stimulates acid production -> 30 mins before meals
  • Rapidly absorbed, highly protein bound, extensively metabolized by CYP2C19 & CYP3A4
  • Asians slow metabolizers (CYP2C19 polymorphism)
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39
Q

PUD: H2RA MoA

A
  • Inhibit acid production by reversibly competing with histamine
  • Inhibit basal acid secretion
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40
Q

PUD: H2RA examples

A

Cimetidine, ranitidine, famotidine, nizatidine

“-idine”

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41
Q

PUD: H2RA ADME (Absorption, Distribution, Excretion)

A
  • Rapidly absorbed, quick peak concentration
  • Small fraction protein bound
  • Excreted by kidneys
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42
Q

PUD: MoA of prostaglandin analog

A
  • Bind to EP3
  • Decrease cAMP and decrease gastric acid secretion
  • Stimulate mucin and bicarb secretion & increase mucosal BF
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43
Q

PUD: Prostaglandin analog examples

A

Misoprostol

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44
Q

PUD: Prostaglandin analog ADME

A
  • Rapidly absorbed, rapidly & extensively de-esterified to form misoprostol acid
  • Food and antacids decrease rate of absorption
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45
Q

PUD: Sucralfate MoA

A
  • Cross-linking produces a viscous, sticky polymer that adheres to epithelial cells and ulcer craters
  • Inhibit hydrolysis of mucosal proteins by pepsin
  • Stimulate local production of prostaglandins and epidermal growth factor
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46
Q

PUD: Antacids MoA

A
  • Weak bases that neutralize hydrochloric acid to form salts and water
  • Increase pH and inactivate pepsin
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47
Q

PUD: Antacids examples

A

Sodium bicarbonate, Calcium carbonate

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48
Q

PUD: M1 receptor antagonist MoA & example

A
  • Suppress neural stimulation of acid production via M1 receptors
  • Pirenzepine
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49
Q

PUD: H. pylori infection treatment

A

Combination of triple therapies
1. Anti-infectives: Amoxicillin (cell wall synthesis), Clarithromycin (protein synthesis), Metronidazole
2. Bismuth subsalicylate: coating agent, disrupt cell wall of H. pylori
3. PPI

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50
Q

Risk factors of PUD

A
  1. > 65 yrs
  2. Past hx of ulcer or complication
  3. High dose or multiple NSAIDs
  4. NSAID-related dyspepsia
  5. Concomitant aspirin (including low dose), corticosteroid, antiplatelet agent, anticoagulant, oral bisphosphonate, SSRI
  6. Chronic comorbidity (CVD, rheumatoid arthritis)
  7. H. pylori infection
  8. Alcohol
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51
Q

Low-dose aspirin use and risk in PUD

A
  • Risk is dose-related
  • Risk diminishes with long-term use: =< 30 days use has the highest risk
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52
Q

Combination use of low-dose aspirin and nsNSAIDS vs COX2 inhibitors in PUD

A

Combination therapy generally increases the risk
- nsNSAIDs: 6.77%
- COX2i: 7.49%

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53
Q

nsNSAIDs safety comparison in PUD: ibuprofen, diclofenac, naproxen

A
  • Naproxen has the highest risk
  • Diclofenac is the safest
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54
Q

PUD: Esophagogastroduodenoscopy (EGD) classification and treatment

A

Ia (spurting blood): IV PPI + EHT
Ib (oozing blood): IV PPI + EHT
IIa (visible non-bleeding vessel): IV PPI + EHT
IIb (adherent clot): Oral PPI
IIc (flat pigmented spot: Oral PPI
III (clean ulcer base): Oral PPI

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55
Q

PUD: What are the three components of the endoscopic hemostatic therapy (EHT)?

A
  1. Injection therapy (100% ethanol)
  2. Heater probe (cauterization)
  3. Hemoclip therapy
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56
Q

PUD: Risk factors for rebleed post-EHT

A
  1. Hemodynamic instability
  2. Large ulcer > 2cm
  3. Failure to start PPI post-EHT
  4. Use of heparin post-EHT
  5. Endoscopy-proven active bleed
  6. Moderate-severe liver disease
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57
Q

PUD: Long-term risk assessment
- Low risk level management

A
  • No risk factors
  • Less ulcerogenic NSAID at lowest effective dose (diclofenac)
  • Avoid combined RX & OTC NSAIDs (naproxen)
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58
Q

PUD: Long-term risk assessment
- Moderate risk level management

A
  • 1-2 RFs, including low-dose aspirin
  • Less ulcerogenic NSAID + PPI
  • Less ulcerogenic NSAID + high-dose H2RA
  • Less ulcerogenic NSAID + misoprostol
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59
Q

PUD: Long-term risk assessment
- High risk level management

A
  • > 3 RFs
  • Concomitant full-dose aspirin, corticosteroid, warfarin
  • Celecoxib + misoprostol + PPI
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60
Q

PUD: Long-term risk assessment
- Very high risk level management

A
  • Prior hx of ulcer complication
  • Stop NSAID if possible
  • Celecoxib + misoprostol + PPI
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61
Q

PUD: PPIs AEs

A
  • GI: increased risk of C. difficile diarrhea, benign gastric fundic polyps, ECL hyperplasia
  • Respiratory: CAP
  • Musculoskeletal: osteoporosis, hip/wrist/spine fracture (RF: high dose, multiple daily dose, prolonged use >5-7 days)
  • Hypomagnesemia (use >1 yr)
  • Hematologic (more common in critically ill): bone marrow suppression
  • Dose-dependent decrease in Vit B12
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62
Q

PUD: PPIs DDI

A
  • Inhibition or induction of CYP enzymes: Omeprazole highest risk vs Lansoprazole/ rabeprazole minimal, Rifampin & St. John’s wort decreased omeprazole level
  • Decreased F of ketoconazole, ampicillin, iron, digoxin, atazanavir
  • May increase risk of digoxin-associated cardiotoxicity secondary to hypomagnesemia
  • Sucralfate delays absorption & decreases F
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63
Q

PUD: H2RA treatment dose

A
  • Equally effective given BID or QD at bedtime
  • Bedtime dose can be added to PPI to maximize control of nocturnal acid secretion
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64
Q

PUD: H2RA AEs

A

Cimetidine > famotidine or nizatidine
- CNS: fever (inhibition of H2 in the hypothalamus)
- Ocular: exacerbation of chronic glaucoma pain/blurred vision
- CV (rapid IV): HoTN, sinus bradycardia, AV block only Cimetidine
- Nosocomial pneumonia
- CAP: most common during first 30 days of use
- Mild bilateral gynecomastia cimetidine

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65
Q

PUD: H2RA DDI

A
  • Cimetidine: inhibition of hepatic CYP enzymes (nizatidine & famotidine do not), decreased hepatic BF, additive myelosuppression, decr oral F of Al/Mg antacids
  • All H2RAs: Decr oral F of ketoconazole & renal tubular secretion
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66
Q

PUD: Misoprostol AEs

A
  • GI: dose-related diarrhea
  • Genitourinary: menstrual irregularities, postmenopausal vaginal bleeding, spontaneous abortion
  • C/I in pregnancy
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67
Q

PUD: Sucralfate DDI

A
  • Decr oral F of cimetidine, digoxin, ketoconazole, phenytoin, ranitidine, tetracycline, theophylline, warfarin, ciprofloxacin, norfloxacin
  • Antacids, H2RAs, PPIs can decrease the activation of sucralfate
  • Take sucralfate first then take antacids, H2RAs, PPIs at least 2 hrs later
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68
Q

PUD: indications for H. pylori testing

A
  1. Active or healed ulcer
  2. Low-grade gastric MALT lymphoma
  3. Hx of endoscopic resection of early-stage gastric cancer
  4. <60 yrs with uninvestigated dyspepsia and no alarm symptoms
  5. Chronic low-dose aspirin use
  6. Chronic NSAID use
  7. Unexplained Fe deficiency anemia
  8. Adults with immune thrombocytopenic purpura (ITP)
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69
Q

PUD: Who should NOT get tested for H. pylori?

A

Patients with GERD and NO ulcer hx should not be tested

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70
Q

PUD: what can cause false negative test results for H. pylori?

A
  1. Active Upper GI Bleeding (UGIB)
  2. Antibiotic or bismuth use within 4 weeks
  3. PPI use within 1-2 weeks
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71
Q

PUD: Non-invasive H. pylori testing

A
  1. Urea breath test (UBT)
  2. Stool antigen test (SAT)
  3. Serology
    - ONLY test not affected by prior use of antibiotics, bismuth, or PPIs
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72
Q

PUD: Questions to ask before starting H. pylori testing

A
  1. Has the patient ever taken a macrolide for any reason?
  2. Is the patient allergic to PCN?
  3. What is the local resistance rate to Clarithromycin?
    - US: resistance, so lower efficacy
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73
Q

PUD: H. pylori regimen
- Bismuth Quadruple indication & 4 classes of drugs

A
  • PCN allergy, hx of Clarithromycin (macrolide) use
  • 14 days
    1. Bismuth subsalicylate QID with food, HS
    2. Metronidazole QID with food, HS
    3. Tetracycline QID with food, HS
    4. PPI QD or BID empty stomach/ 30 min before meal
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74
Q

PUD: H. pylori regimen
- Clarithromycin Concomitant indication & 4 classes of drugs

A
  • NO: PCN allergy, hx macrolide, macrolide resistance
  • 14 days
    1. Clarithromycin BID with food
    2. Amoxicillin BID with food
    3. Metronidazole BID with food
    4. PPI BID empty stomach/ 30 min before meal
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75
Q

PUD: Initial management of dyspepsia

A
  1. Empiric PPI (4 wks) or H2RA (8 wks)
  2. Empiric antibiotic tx for HPI for 14 days
  3. Endoscopy first, then directed therapy: >= 50 yrs or any alarm symptom
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76
Q

Stimulatory prokinetic drug targets for GERD treatment

A
  • ACh: M2/3 muscarinic receptor
  • Motilin receptor
  • Serotonin: 5HT4 receptor
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77
Q

Inhibitory prokinetic drug target for GERD treatment

A

Dopamine: D2 receptor

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78
Q

GERD: Prokinetic drugs works on what cell types?

A

Smooth muscle cell, dopaminergic neuron, cholinergic neuron

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79
Q

GERD: Which prokinetic drug has a dual actions (both agonist and antagonist)?

A

Metoclopramide

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80
Q

GERD: Bethanechol works as _____ by _____; its SEs are ____

A
  • Muscarinic receptor agonist
  • increasing force of contraction
    SEs:
  • CV: HoTN, bradycardia
  • Urinary: incr void pressure, decr capacity
  • Exocrine glands: incr secretion
  • Eye: pupil constriction
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81
Q

GERD: Metoclopramide works as _____; its PK profile is ____; and its SEs are ____

A
  • D2 receptor antagonist & 5HT4 agonist
  • Oral F, cross BBB
    SEs:
  • Sedation
  • Dystonic reactions
  • Tardive dyskinesia
  • Anxiety
  • Gynecomastia/galactorrhea
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82
Q

GERD: Domperidone works as ____; its PK profile is ___; and its SEs are ____

A
  • D2 receptor antagonist
  • Low oral F, limited ability to cross BBB
    SEs:
  • Headaches, gynecomastia/galactorrhea
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83
Q

GERD: Cisapride works as ____; and its SEs are ___

A
  • 5HT4 agonist
    SEs:
  • Serious CV: ventricular tachycardia/fibrillation, QT prolongation REMS
  • 80 deaths, pulled from US market
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84
Q

GERD: Motilin works as ____; is secreted by ____; and stimulates gastric emptying by _____

A
  • Motilin receptor (GPCR) agonist
  • Endocrime M cells in small intestine
  • Stimulating contraction of upper GI smooth muscle
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85
Q

GERD: Erythromycin works as ___; has ____ activity; used in ____ patients with _____ to improve gastric emptying time

A
  • Motilin non-peptide agonist
  • Antibacterial
  • Diabetic; gastroparesis
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86
Q

GERD: Classic symptoms

A

heartburn and acid regurgitation

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87
Q

GERD: Atypical symptoms

A

Epigastric bloating/pain, early satiety, dyspepsia

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88
Q

GERD: Alarm symptoms

A

Dysphagia, chronic sore throat, bleeding or anemia, unexplained weight loss

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89
Q

GERD: Extraesophageal symptoms

A

Chronic cough, laryngitis, erosion of tooth enamel, asthma (association not clear)

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90
Q

GERD: 4 phenotypes

A
  1. Non-erosive reflux disease (NERD): more common in females, 30% less likely to respond to PPIs
  2. Erosive esophagitis (EE): more likely to be male, Caucasian, obese
  3. Eosinophilic esophagitis (EoE): allergic rxn to food or environmental allergen
  4. Barrett’s esophagus: predisposes to esophageal cancer
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91
Q

GERD: Causes

A
  • Transient lower esophageal sphincter relaxations (TLESRs)
  • Hiatal hernia: decreases LES contraction, traps gastric acid
  • Decreased esophageal motility: delayed refluxate clearance
  • Delayed gastric emptying: increased gastric volume
  • Non-acid reflux (bile acid, gas)
  • Reflux hypersensitivity; functional heartburn
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92
Q

GERD: Triggering factors

A
  • Obesity
  • Alcohol or tobacco use
  • Fatty/spicy food, chocolate, mint, caffeine, carbonated beverage
  • Drugs: anticholinergics, beta agonist, alpha antagonist, narcotics, oral contraceptives, xanthine derivative (caffeine), Ca channel blocker
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93
Q

GERD: First-line medical treatment

A

PPIs

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94
Q

GERD: Diagnosis & Treatment
- Classic presentation (heartburn, acid regurgitation, no alarm symptoms

A

Empiric trial of PPI for 8 wks

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95
Q

GERD: pregnancy treatment

A

Antacids, alginates (Gaviscon), sucralfate

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96
Q

GERD: Diagnosis & Treatment
- At least 1 alarm symptom or failed PPI trial

A
  1. Multiple biopsies to rule out EoE
  2. Endoscopy (+) for EE or Barrett’s esophagus: PPI therapy with long-term maintenance tx (follow-up endoscopy to confirm healing)
  3. Endoscopy normal: High-resolution esophageal manometry, 24hr-pH or impedance-pH monitoring
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97
Q

GERD: Lifestyle modifications

A
  • Weight loss
  • No food/snacks within 3 hrs of bedtime
  • Avoid trigger foods, smoking, alcohol
  • Elevate head of bed for nighttime symptoms
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98
Q

GERD: PPI counseling points

A
  • Swallow capsule whole (do not chew/crush)
  • If difficulty swallowing, open capsule and mix the contents with applesauce or juice (except grapefruit)
  • Take all your med for 4 -8 wks, even if you feel better
  • AEs: stomach pain, diarrhea, constipation, headache
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99
Q

GERD: H2RA dose, when to refer pt to PCP

A
  • Start with 8 - 12 wks of BID
  • Reassess at 2- 8 wks: titrate, add prokinetic, or change to PPI if indicated (better when used in combo of H2RA+prokinetic than alone, less effective than PPI)
  • CanNOT be dosed qhs as monotherapy to treat GERD
  • Can be added to PPI for nighttime acid suppression
  • If no improvement for >2 wks, refer to PCP
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100
Q

GERD: Gaviscon MoA, indication, administration

A
  • Alginate reacts with bicarbonate in saliva to form a “raft” that floats on gastric contents
  • May be used prn for short-term relief
  • Must take each dose with full glass of water, then avoid recumbency for at least 1 hr
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101
Q

GERD: Prokinetic agents indication, examples

A
  • Limited use due to frequent AEs
  • Only indicated for pts with gastroparesis (decr gastric motility)
  • Agents: metoclopramide, bethanechol, cisapride
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102
Q

GERD: Metoclopramide
- MoA, AEs

A
  1. MoA: Dopamine antagonist, serotonin agonist
  2. AEs: CNS (most common), extrapyramidal rxn, tardive dyskinesia, neuroleptic malignant syndrome, Parkinsonian, GI, hematologic, genitourinary
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103
Q

GERD: Bethanechol
- MoA, AEs

A
  1. MoA: Cholinergic agonist
  2. AEs: ‘uncoordinated GI contractions’ (abdominal cramps, flushing, sweating, lacrimation, salivation, headache), bronchial constriction with asthma
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104
Q

GERD: Cisapride
- MoA, AEs, and DDI

A
  1. MoA: 5HT4 agonist
    - Only available through REMS
  2. AEs: GI (most common), CV (ventricular tachy, V fib, torsades de pointes, QT prolongation)
  3. DDI: CYP3A4 inhibitor, grapefruit juice, hx heart disease or electrolyte disorder
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105
Q

GERD: surgical management
- Best candidates, AEs, long-term follow up

A
  1. Best candidate: asymptomatic on PPI, positive symptom index on pH monitoring, normal esophageal motility
  2. AEs: dysphagia, gas bloating (cannot belch)
  3. Restart PPIs, 2nd surgery
    - Does not reduce cancer risk in pts with Barrett’s esophagus
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106
Q

What does ABCD stand for in nutritional assessment (NA)?

A
  • Anthropometrics
  • Biochemistry labs
  • Clinical assessment
  • Dietary assessment
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107
Q

NA: A: How do you measure body weight?

A

ABW, IBW, UBW, BMI

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108
Q

NA: A: How do you calculate UBW
1. Change in weight over time
2. Recent weight change

A
  1. ABW/UBW*100=%UBW
  2. (UBW - ABW) / UBW*100=% weight loss
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109
Q

NA: B: Albumin is used for _____ due to ____ half life. Its serum level ____ quickly following physiological stress; therefore, albumin is a ___ acute phase reactant.

A

Chronic trends; longer; decreases; negative

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110
Q

NA: B: Transferrin is affected by ___ stores. Low level of transferrin is due to ____ or ____. Its serum level ____ quickly following physiological stress; therefore, albumin is a ___ acute phase reactant.

A

Iron; poor liver production or excessive loss through the kidneys; increases; positive

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111
Q

NA: B: Prealbumin is used for _____ due to ____ half life. It has acute effects of _____. Its serum level ____ quickly following physiological stress; therefore, albumin is a ___ acute phase reactant.

A

Short term assessment; shorter; nutrition support; decreases; negative

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112
Q

NA: B: Serum proteins are prognostic indicators and reflect inflammation. T/F

A

T

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113
Q

NA: B: Serum proteins do NOT… (5)

A
  1. Reflect body stores of protein
  2. Define malnutrition
  3. Measure response to nutrition intervention
  4. Assess nutritional satus
  5. Indicate how much protein to give
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114
Q

NA: Deficiency of thiamine (B1) leads to…

A

Wernicke’s encephalopathy, lactic acidosis, Korsakoff’s psychosis, peripheral neuropathy

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115
Q

NA: Deficiency of Pyridoxine (B6) leads to…

A

Distal limb numbness or paresthesia, microcytic anemia

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116
Q

NA: Deficiency of Folic acid leads to… & other comments

A
  • Macrocytic anemia
  • Decrease with increased cellular/tissue turnover (pregnancy, malignancy, hemolytic anemia)
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117
Q

NA: Deficiency of Cyanocobalamin (B12) leads to… & other comments

A
  • Pernicious anemia, peripheral neuropathy
  • Decreased absorption in the elderly, long-term gastric acid suppression
118
Q

NA: Deficiency of Ascorbic acid (C) leads to… Excess intake of Vitamin C leads to…

A
  • Scurvy
  • Kidney stones, excess iron absorption
119
Q

NA: Excess intake of Vitamin A leads to…

A
  • Liver toxicity
  • Vit A is teratogenic
120
Q

NA: Deficiency of Vitamin D leads to…

A

Rickets, osteomalacia, osteoporosis, hypocalcemia

121
Q

NA: Deficiency of Vitamin K leads to… & ____ can be affected

A
  • Bleeding
  • Anticoagulant therapy
122
Q

NA: Deficiency of Chromium leads to…

A

Impaired glucose/protein utilization

123
Q

NA: Excess intake of Copper leads to…

A

Wilson’s disease

124
Q

NA: Deficiency of Iodine leads to ___ & Excess intake leads to ___

A
  • Hypothyroid goiter
  • Thyrotoxicosis
125
Q

NA: Deficiency of Iron leads to…

A

Microcytic, hypochromic anemia, fatigue weakness, pallor

126
Q

NA: Deficiency of Zinc leads to…

A

Impaired wound healing, dermatitis, altered taste

127
Q

NA: drug-nutrient interaction; antibiotics

A

Vitamin K deficiency

128
Q

NA: drug-nutrient interaction; Cholestyramine, colestipol

A

Vitamins ADEK & beta-carotene malabsorption

129
Q

NA: drug-nutrient interaction; H2RAs/PPIs

A

Vitamin B12 malabsorption

130
Q

NA: drug-nutrient interaction; Isoniazid

A

Vitamin B6 deficiency

131
Q

NA: drug-nutrient interaction; warfarin

A

Vitamin K inhibits effect

132
Q

NA: what are 3 ways to measure energy expenditure?

A
  1. Population estimates
  2. Harris-Benedict equation
  3. Indirect calorimetry
133
Q

NA: Population based estimate of illness, metabolic stress (BMI <30 kg/m^2)

A

25 to 30 kcal ABW/kg/day

134
Q

NA: What do you have to keep in mind when using the Harris-Benedict equation?

A

Results must be modified by a factor that adjusts for the patient’s clinical condition

135
Q

NA: Indirect calorimetry measures _____ and is used to measure ____ & also determines ____

A

O2 consumed and CO2 produced; resting expenditure; Respiratory Quotient (RQ)
- Most accurate

136
Q

NA: Respiratory Quotient (RQ) is used to determine if the patient is ____

A

Overfed ( Value >1)

137
Q

NA: Nitrogen balance is a clinical assessment of ____

A

Protein intake

138
Q

NA: What is Holliday-Segar method?

A
  • Estimates fluid needs
  • First 10 kg: 100 mL/kg (4mL/kg/hr)
  • Second 10 kg: 50 mL/kg (2mL/kg/hr)
  • Each additional kg: 20 mL/kg (1mL/kg/hr)
139
Q

NA: Complications of refeeding syndrome

A
  1. Introducing glucose leads to thiamine deficiency
  2. Introducing insulin leads to intracellular electrolyte shift: hypokalemia, -phosphotemia, -magnesemia
140
Q

NA: Ways to prevent refeeding syndrome

A
  1. Provide <50% of goal calories in first 24 hrs
  2. Slowly titrate to goal over 4-7 days
  3. Replete vitamins and trace element deficiencies (thiamine)
  4. Hold feedings if significant hypophosphatemia, -kalemia, -magnesemia
141
Q

EN: Absolute C/I

A

Mechanical intestinal obstructions, necrotizing enterocolitis

142
Q

EN: Relative C/I

A

GI surgery, severe pancreatitis, short bowel syndrome, severe inflammatory bowel disease, intractable diarrhea, hemodynamic instability,GI bleeding, obstruction/ileus

143
Q

EN: Absence of bowel sounds is or is not a contraindication to enteral feeding

A

is not

144
Q

EN: Nonsurgical routes of administration

A
  • Nasogastric, orogastric
  • Nasoduodenal, nasojejunal
145
Q

EN: Surgical routes of administration

A
  • Gastrostomy, percutaneous endoscopic gastrostomy (PEG)
  • Jejunostomy
146
Q

EN: Advantages and disadvantages of stomach feeding

A
  • (+): large reservoir capacity, high osmotic load, larger tubes, easier to place/replace
  • (-): increased aspiration risk
147
Q

EN: Advantages and disadvantages of small intestine feeding

A
  • (+): decreased aspiration risk
  • (-): small reservoir capacity, can’t tolerate high osmotic load, more difficult to place/replace tubes
148
Q

EN: Indications of nasogastric, orogastric insertion & aspiration risk

A
  • Short-term, normal gastric emptying
  • High
149
Q

EN: Indications of nasoduodenal, nasojejunal insertion & aspiration risk

A
  • Short-term, impaired gastric emptying, increased risk of aspiration
  • Low
150
Q

EN: Indications of gastrostomy, PEG insertion & aspiration risk

A
  • Long-term, normal gastric emptying
  • High
151
Q

EN: Indications of jejunostomy insertion & aspiration risk

A
  • Long-term, normal gastric emptying, increased risk of aspiration
  • Low
152
Q

EN: Continuous administration method

A
  • Most common
  • Preferred in critically-ill
  • Less abdominal distention, V/D, aspiration
  • Small intestine feeding
153
Q

EN: Cyclic administration method

A
  • EN held during the day, administered at night
  • Decreased time receiving EN
  • Increased mobility
154
Q

EN: Cyclic- bolus

A
  • Most common in long-term care setting
  • 240-500 mL of formula administered over 5-10 mins Q 4-6 H
  • Often well-tolerated, but may result in cramping, N/V/D, aspiration
155
Q

EN: Cyclic- intermittent

A
  • Used if intolerant to bolus
  • Give same volume (240-500 mL) over 20-60 mins
156
Q

EN: Carbohydrate provides ___% of the total calories. Most common CHO source is ___; where as ___ is not generally a CHO source

A

40-90%; maltodextrin; lactose

157
Q

EN: Protein provides ___% of total calories. Standard protein content contains up to ___%

A

4-32%; 15%

158
Q

EN: Lipids provide ____% of total calories. Polymeric formulas contain ____% fat

A

1.5-55%; 30-40%

159
Q

EN: Standard formulas of fluids are ____% of _____

A

80-85%; free water

160
Q

EN: high protein formula is indicated for patients ___

A

requiring >1.5 g/kg/day

161
Q

EN: high caloric density is indicated for patients ___

A

with fluid/electrolytes restriction

162
Q

EN: elemental formula is indicated for ___ bc it contains ____

A
  • Malabsorptive disorders, low fat requirements
  • Low fat, high % free AA
163
Q

EN: peptide-based formula contains ___ and may be of benefit in ____

A
  • Dipeptides/tripeptides
  • Malabsorption
164
Q

EN: Renal formula is high ____, varying ____, and low ____. It is indicated for ___

A
  • Caloric density; protein; electrolyte
  • Dialysis pts
165
Q

EN: Hepatic formula contains high ____ and low ______. Only indicated in ______

A
  • Branched chain; aromatic AA
  • Refractory hepatic encephalopathy
166
Q

EN: Diabetic formula contains high ___ and low ___

A

fat; CHO

167
Q

EN: Pulmonary formula contains high ___, low ____. Indicated for ____

A
  • Fat, CHO
  • Acute Respiratory Distress
168
Q

EN: Trauma and Burn formula contains ____, ____ (building blocks for proteins), _____ &/or ____

A
  • Glutamine, arginine, nucleotides
  • omega-3 FA
169
Q

EN: Initiation and advancement
- Critically ill vs refeeding syndrome

A
  • Initiate at 20-50 mL/hr and titrate up by 10-25 mL/hr Q 4-8 H based on tolerance
  • Critically ill: titrate to goal in 48-72 hrs (ASAP)
  • Refeeding syndrome: titrate to goal over 3-4 days or slower
170
Q

EN: How to prevent aspiration pneumonia

A
  1. X bolus
  2. Start low, go slow
  3. X lay flat, head 30 degrees up
  4. Mouth hygiene
  5. if intolerance to stomach feeds, change to small intestine feeds
171
Q

EN: What is widely used as indicator of intolerance/risk of aspiration?

A

Gastric residuals
- Hold EN for >500mL residuals
- Commonly checked Q 4-8 hrs
- Monitor trend in residuals rather than a single point in time

172
Q

EN: Medications with special considerations

A
  • Phenytoin: hold feeds 1-2 hrs before/after
  • Fluroquinolones/ Tetracyclines: hold feeds 1 hr before/after
173
Q

PN: Nutritional screening in peds

A
  1. Head circumference (measured <3 yrs)
  2. Length (<2 yrs), Height (>= 2 yrs)
174
Q

PN: Indications for peds

A
  • Prematurity
  • Severe GI impairment
  • Feeding intolerance
  • Hypermetabolism, inadequate intake
  • Anticipated prolonged starvation (5-7 days in older peds, 24 hrs in neonates)
175
Q

PN: Peripheral indications, +/- in peds

A
  • Indications: bridge while waiting for central catheter to be placed, partial nutritional supplementation
  • (+): easier, quicker
  • (-): max osmolarity 900-1000 mOsm/L, limited amount of dextrose (<12.5%), limited amount of micronutrients (Ca)
176
Q

PN: Central IV access indication, +/- in peds

A
  • Indication: preferred route of administration
  • (+): maximize nutrition, no limit on osmolarity (dextrose >12.5%, calcium)
  • (-): technical challenges, complications in peds
177
Q

PN: What is 2-in-1 system? Preferred in ____, caution

A
  • CHO, protein, micronutrients, multivitamins, trace elements in one bag
  • Lipids in separate bag
  • Preferred in peds
  • Avoid antimicrobial growth
178
Q

PN: What is 3-in-1 system? Advantage? Disadvantage?

A
  • All ingredients combined into one bag
  • (+): Less risk of contamination and bacterial growth
  • (-): Formulation more sensitive to destabilization with certain electrolyte [ ] & low dextrose/AA, incompatible meds
179
Q

PN: What is CHO caloric value?

A

3.4 kcal/g

180
Q

PN: What is GIR?

A

Glucose Infusion Rate
- Standard procedure to calculate amount of dextrose in all infants
- Determine how quickly the pt receives dextrose

181
Q

PN: Protein: primary form, use ____ as tolerance indicator, titration, ___ should be added separately to protein

A
  • AA
  • Blood urea nitrogen (BUN)
  • Not needed; begin at goal on day 1 of therapy
  • Cysteine
182
Q

PN: Protein caloric value

A

4 kcal/g

183
Q

PN: Role of Cysteine and its dose in peds

A
  • Decrease pH, increase calcium & phosphorus solubility
  • 40 mg for each g of AA
184
Q

PN: Lipids: primary form, requirement to prevent FFA deficiency, titration, monitoring

A
  • 20% fat emulsion
  • 0.5 to 1 g/kg/day
  • Start low and titrate daily as tolerated
  • Monitor TG and decrease lipids of TG > 250
185
Q

PN: Lipids account for ___% of total calories

A

20-50%

186
Q

PN: Lipids caloric value in peds (20% fat emulsion)

A

10 kcal/g

187
Q

PN: Factors affecting Calcium-Phosphate solubility
- Calcium salt used, pH of final solution, temperature, order of mixing

A
  • Gluconate > Chloride
  • Lower pH increases solubility = why cysteine added!
  • Lower temp increases solubility
  • Phosphorus, then Calcium to minimize precipitation
188
Q

PN: Why is Zinc important in pediatrics?

A
  • Required for maintenance of normal cell growth
  • Increased requirements: renal failure, high volume stool loss, fistula/stoma output, premature infants
189
Q

PN: Why is Copper important in pediatrics?

A
  • Hypochromic anemia
  • Increased requirements: jejunostomy, external biliary drainage
  • Decrease by half: cholestasis or liver function impairment
190
Q

PN: Why is Manganese important in peds?

A
  • Component of several enzymes
  • Decreased/Withhold: cholestasis or liver function impairment
191
Q

PN: Why are Selenium and chromium important in peds?

A

Antioxidant defense in the neonate

192
Q

PN: Adult indications

A
  1. Requiring total bowel rest = nonfunctioning GI tract
  2. NPO >= 7 days
  3. Appropriate venous access
193
Q

PN: Adult indications
- Nonfunctioning GI tract examples

A

Major burns/trauma, short bowel syndrome, post-GI surgery, severe inflammatory disease of the bowel, intractable diarrhea, high vasopressor requirements, obstruction/ileus, GI bleed, severe pancreatitis

194
Q

PN: Protein accounts for ___% of total calories in adults. This is equal to ____ g/kg/day.

A
  • 10-30%
  • 0.8-2 g/kg/day
195
Q

PN: Lipids accounts for ____% of total calories in adults and provides at least ____% of total calories to prevent essential FA deficiency

A
  • 20-30%
  • 4-10%
196
Q

PN: Lipids 10% contains ___ kcal/mL, 20% contains ___ kcal/mL, and 30% contains ___ kcal/mL

A
  • 1.1 kcal/mL
  • 2
  • 3
197
Q

PN: CHO accounts for ___% of total calories in adults

A

45-65%

198
Q

PN: Trace elements that are excreted via liver vs renally

A
  • Liver: Copper, Manganese
  • Renal: Chromium, Selenium
199
Q

PN: Continuous administration in adults
- How and for whom

A
  • How: over 24 hrs
  • For: inpatients, unstable fluid balance or glucose control
200
Q

PN: Cyclic administration for adults
- How and for whom

A
  • How: over 12-18 hrs
  • For: home administration, cholelithiasis, hunger/enteral feeding
201
Q

PN: IV compatibility
- Meds that CAN be added to TPN

A

Regular insulin (ONLY), H2RAs, morphine, heparin

202
Q

PN: IV compatibility
- Meds to AVOID

A

Acyclovir, amphotericin B, minocycline, phenytoin

203
Q

PN: IV catheter issues

A
  1. Phlebitis
  2. Thrombosis (clot)
  3. Pneumothorax (more common in central due to accidental puncture of the lung)
  4. Infiltration (non-irritating fluid)/Extravasation (Vesicant or irritating fluid)
  5. Arrythmias
204
Q

PN: Metabolic complications

A
  1. Hyperglycemia/ Hypoglycemia
  2. Electrolyte abnormalities
  3. HyperTG/ Pancreatitis
  4. Essential FA Deficiency (EFAD) - rare
  5. Re-feeding syndrome
205
Q

PN: macronutrient changes in RF
- CHO, Pre-albumin, Lipids, Protein

A
  • CHO: hyperglycemia, peripheral insulin resistance, impaired metabolism
  • Pre-albumin: excreted renally; falsely elevated in ARF & CKD
  • Lipids: Decreased catabolism of TG, increased TG synthesis from FFA
  • Protein: significant protein catabolism and urea accumulation, removed by dialysis
206
Q

PN: Fluid, electrolyte, acid-base alterations in RF

A
  • Metabolic acidosis
  • Hyperkalemia/ -phosphatemia/ -magnesemia
  • Oliguric ARF (x urine): impaired excretion of sodium and water
  • Non-oliguric ARF: considerable sodium loss in urine
207
Q

PN: Trace elements and vitamins alteration in RF

A
  • Accumulation of Zinc, chromium
  • Reduction of Selenium concentrations
  • Vitamin D deficiency
  • Elevated vitamin A
208
Q

PN: nutrition plan for ARF

A
  • Initiate standard recommendations
  • Consider specialty formulations if electrolyte abnormalities
  • Adjustments for HD or Continuous Renal Replacement Therapy (CRRT)
209
Q

PN: nutrition plan for CRF

A
  • Fluid and electrolyte restriction
  • Protein restriction (0.6-0.75 g/kg/day)
  • Protein calorie malnutrition common
  • Requirements change with renal replacement therapy
210
Q

PN: CHO and lipids alterations in Hepatic Failure (HeF)

A
  • CHO: insulin resistance common, decreased hepatic/muscle glycogen, hypoglycemia
  • Lipids: Increased lipolysis, increased risk for essential FA deficiency, fat malabsorption
211
Q

PN: Protein alterations in HeF
- AAA vs BCAA

A
  • Plasma [ ] of Aromatic AA (AAA), methionine, glutamine increase in cirrhosis -> AAA may cross BBB –> hepatic encephalopathy
  • Plasma [ ] of Branched chain AA (BCAA) often depressed
212
Q

PN: Fluid and electrolyte alterations in HeF

A
  • Ascites and peripheral edema common in severe cirrhosis
  • Hyponatremia: excess total body sodium and total body water
  • Hypokalemia/ -magnesemia/ -phosphophatemia
213
Q

PN: Vitamins and trace elements alterations in HeF

A
  • Poor intake and malabsorption
  • Increased needs of ADEK, folic acid, thiamine, zinc, selenium
  • Decreased need for Copper & Manganese due to bile excretion
214
Q

PN: Considerations in HeF
- Meds, use of BW for calculation

A
  • Meds with electrolyte effects = Spironolactone, furosemide
  • Meds which induce diarrhea = Lactulose
  • Use dry or lean BW
215
Q

PN: CHO alterations in Pulmonary Failure (PF)
- RQ, risk for hyperglycemia is increased by use of ______

A
  • Glucose-based nutrition can contribute to elevated PCO2
  • CHO RQ = 1 (highest) > protein > fat
  • Concomitant steroids
216
Q

PN: Fluids, electrolytes, vitamins alterations in PF

A
  • Pulm edema decreases oxygenation
  • Hypokalemia: albuterol, diuretics
  • Hypophosphatemia
  • Chronic steroid users: Ca/Vit D supplementation
217
Q

PN: Considerations for PF
- avoid ___, formula

A
  • Strict avoidance of overfeeding to avoid CO2 -> worsen respiratory acidosis
  • Higher lipid, lower CHO formulas
218
Q

PN: Metabolic response to stress in critically ill patients (CIP)

A

Activation of immune system
- Increased inflammatory mediators and cytokines
- Increased production of counter-regulatory hormones

219
Q

PN: Nutritional alterations in CIP

A
  • Hyper-metabolism (burn pts)
  • Hyperglycemia due to insulin resistance
  • Accelerated lipolysis
  • Loss of muscle mass and protein degradation in vital organs
  • Cytokine release -> reprioritize protein synthesis
  • Significant fluid and electrolyte disturbances
220
Q

PN: Specialty nutrition products for CIP

A
  • Use high protein, high calorie formulas
  • Immune enhancing: contain glutamine, arginine, omega 3 FA, anti-oxidents
221
Q

IBD: Crohn’s Disease location and symptoms

A
  • L: transmural, any part of the GI tract, often near ileocecal valve, discontinuous
  • S: watery diarrhea
222
Q

IBD: Ulcerative colitis location & symptoms

A
  • L: mucosal, distal rectum, colon, continuous
  • S: bloody diarrhea
223
Q

IBD: TH1 cell is more involved in CD/UC. TH2 cell is more involved in CD/UC

A
  • TH1: CD
  • TH2: UC
224
Q

IBD: Aminosalicylates MoA

A
  • Metabolized in the distal gut, Azo bond links to bacterial
  • 5-aminosalicylate (5-ASA) = responsible for anti-inflammation
  • Exact MoA UKN, but not due to COX inhibition
225
Q

IBD: Aminosalicylates metabolism and C/I

A
  • Sulfasalazine metabolized to 5-ASA and sulfapyridine
  • Sulfa allergy
226
Q

IBD: Corticosteroids MoA and indicated population

A
  • MoA: anti-inflammation
  • Moderate to severe
227
Q

IBD: Immuno-modulators MoA and indicated population

A
  • MoA: inhibit DNA replication
  • Severe who are steroid-resistance or -dependent
  • Methotrexate only in CD
228
Q

IBD: Immuno-modulators examples

A
  • Purine analog: 6-mercaptopurine, azathiopurine (prodrug)
  • Folate acid analog: methotrexate
229
Q

IBD: Biologics 3 classes

A
  1. TNFa inhibition
  2. Interleukin inhibition
  3. A4 Integrin inhibition, Janus kKinase inhibitor
230
Q

IBD: TNFa inhibitor agents examples

A

Infliximab, adalimumab, certolizumab pegol

231
Q

IBD: Interleukin inhibitor agent

A

Ustekinumab

232
Q

IBD: A4 Integrin inhibitor agent

A

Vedolizumab

233
Q

IBD: Classic presentation of UC

A

Bloody diarrhea, tenesmus, rectal urgency

234
Q

IBD: Low risk of UC

A

Proctitis or left-sided, mild disease based on colonoscopy

235
Q

IBD: High risk of UC

A

Extensive, <40 yrs, deep ulceration based on colonoscopy, high ESR/CRP, steroid dependence, hx of hospitalization, C. diff/CMV infection

236
Q

IBD: Classic presentation of CD

A

Watery diarrhea, persistent RLQ pain, low grade fever

237
Q

IBD: CD severity criteria
- Remission

A
  • <150
238
Q

IBD: CD severity criteria
- Mildly active

A

150-219

239
Q

IBD: CD severity criteria
- Moderately active

A

220-450

240
Q

IBD: CD severity criteria
- Severe-Fulminant

A

> 450

241
Q

IBD: Low risk of CD

A

No/mild symptoms, normal/minimal elevation in CRP/fecal calprotectin levels, >30 yrs, limited distribution of bowel inflammation, superficial/no ulceration on colonoscopy, lack of perianal complications, no prior intestinal resections, no strictures/fistulas

242
Q

IBD: Moderate-High risk of CD

A

<30 yrs, smoking, elevated CRP/fecal calprotectin levels, deep ulcers on colonoscopy, long segments of small/large bowel involvement, perianal disease, extra-intestinal manifestations, hx of bowel resection surgery

243
Q

IBD: Rectal 5-ASA (Mesalamine) AE

A

Leakage (enema), localized bloating/burning pain

244
Q

IBD: Rectal 5-ASA examples

A

Rowasa enema, Canasa suppository

245
Q

IBD: Oral 5-ASA use and AEs

A
  • Use: must deliver directly to small/large intestine, slower to induce remission, more AE than rectal
  • AE: diarrhea
246
Q

IBD: Oral 5-ASA examples

A
  1. Azo-bonded prodrugs: olsalazine (2 azo-bonded molecules), balsalazide (inert carrier 1 azo bond molecule)
  2. Delayed-release 5-ASA: Asacol enteric-coated tablets targets terminal ileum, colon, Pentasa soft gel capsules target duodenum, jejunum, ileum, colon, Lialda enteric coated, double matrix targets terminal ileum, colon
247
Q

IBD: Sulfasalazine MoA

A
  • 5-ASA azo-bonded sulfapyridine
  • Sulfapyridine absorbed systemically once 5-ASA is released
248
Q

IBD: Sulfasalazine AEs

A

Non dose related: rash, fibrosing alveolitis, hepatitis, hemolytic anemia, decreased sperm count/motility, bone marrow suppression
- d/c drug

249
Q

IBD: Sulfasalazine DI

A

Antibiotics, decreased absorption of folic acid or ferrous sulfate, displacement of high protein-bound drugs

250
Q

IBD: Corticosteroids AEs

A

Fluid retention, glucose intolerance, moon face, acne, hair growth, hyperlipidemia, cataracts, osteoporosis, avascular necrosis, muscle pain/weakness, increased risk of infection, adrenal suppression

251
Q

IBD: corticosteroid preferred agent

A

Budesonide

252
Q

IBD: Corticosteroids are effective at ___ remission but not for ____ remission

A

Inducing; maintaining

253
Q

IBD: Corticosteroid dosing

A

Oral and Rectal both no more than 8 weeks total

254
Q

IBD: Immunomodulators usage (2)

A
  1. Steroid-sparing (can maintain remission during corticosteroid wean in steroid-dependent pts): Require 3-6 months of chronic dosing to become effective
  2. Decrease antibody formation to anti-TNFa agents (infliximab)
255
Q

IBD: Azathioprine, 6-mercaptopurine AEs

A
  • Non dose related: pancreatitis, rash, arthralgias, N/V
  • Dose related: BM suppression, increased infection risk, hepatitis
  • Increased cancer risk
256
Q

IBD: Thipourine S-methyltransferase (TPMT) testing is recommended in which patients?

A

All pts prior to starting tx with azathioprine or 6-MP

257
Q

IBD: Methotrexate works ___ and has ___ cancer risk than azathioprine or 6-MP, but may ___

A

Faster; lower; lose efficacy over time

258
Q

IBD: Methotrexate AEs

A

Hypersensitivity, leukopenia, hepatic fibrosis

259
Q

IBD: anti-TNFa BBW

A
  • Increased risk/delayed diagnosis of TB, invasive fungal infections, sepsis, cancer (non-Hodgkin’s lymphomas)
  • Lupus-like syndrome
  • New onset or exacerbation of demyelinating CNS disease/CHF
  • Reactivation of chronic Hep B
260
Q

IBD: Infliximab is what kind of mAb? Administration?

A
  • Chimeric mAb
  • IV
261
Q

IBD: Infliximab AEs

A
  • Acute/delayed infusion rxn
  • Rare: BM suppression, severe liver toxicity
262
Q

IBD: Certolizumab pegol is what kind of mAb? Administration?

A
  • Pegylated humanized mAb
  • SQ
263
Q

IBD: Certolizumab pegol AEs

A
  • Overall well-tolerated
  • Upper respiratory tract infection, acute bronchitis, nasopharyngitis, fever
264
Q

IBD: Adalimumab (Humira) is what kind of mAb? Administration? AE?

A
  • Human mAb
  • SQ
  • Infection
265
Q

IBD: Golimumab is what kind of mAb? Administration?

A
  • Human mAb
  • SQ
266
Q

IBD: Integrin inhibitor natalizumab MoA

A

Humanized mAb that targets the integrin a4 subunit of a4b7 integrin (gut) and a4b1 integrin (brain)
- Nonselective

267
Q

IBD: Integrin inhibitor natalizumab indication

A

Moderately to severely active CD who have failed to respond or cannot tolerate first-line therapy

268
Q

IBD: Integrin inhibitor natalizumab AEs

A

Progressive multifocal leukoencephalopathy (PML)
- Risk higher in JC virus sero+
- REMS program

269
Q

IBD: Integrin inhibitor vedolizumab MoA

A

Humanized mAb that selectively targets a4b7 integrin (gut)

270
Q

IBD: Integrin inhibitor vedolizumab AEs

A

No increased risk of PML & cancer

271
Q

IBD: Ustekinumab (Stelara) MoA

A
  • Human anti-IL12 & -23 mAb
  • Inhibit NK cell activation and CD4 T cell activation/differentiation
272
Q

IBD: Ustekinumab AEs

A
  • Reactivation of latent TB
  • Increased cancer risk
  • Reversible posterior leukoencephalopathy syndrome
273
Q

IBD: Risankizumab (Skyrizi) MoA & Indication

A
  • Human selective anti-IL-23 mAb
  • Inhibits NK cell activation and CD4 T cell activation/differentiation
  • ONLY for moderate to severe CD (not for UC)
274
Q

IBD: Selective Janus kinase inhibitors (JAKi) BBW

A
  • Serious infections: TB, invasive fungal, opportunistic
  • Lymphoma, malignant solid tumors
  • Increased risk of CV death, MI, stroke, DVT, PE, arterial embolism with at least 1 RF
275
Q

IBD: JAKi DI

A

CYP3A4 inhibitors/inducers

276
Q

IBD: JAKi tofacitinib selectivity, indication

A
  • More selective for JAK1/2/3
  • Moderate to severe UC in adults who have failed at least 1 anti-TNFa
  • NOT first line
277
Q

IBD: JAKi upadacitinib selectivity, indication

A
  • More selective for JAK1
  • Moderate to severe CD in adults who have failed at least 1 anti-TNFa
278
Q

IBD: Tx of low-risk, mild-moderately active UC
- Remission induction

A
  1. Rectal mesalamine daily QHS (suppositories for proctitis, enema for left-sided)
  2. No improvement (NI) at 2 wks: increase rectal mesalamine BID
  3. NI at 2 wks: add hydrocortisone suppositories QD and reduce mesalamine back to QHS
  4. NI at 2-4 wks: add oral mesalamine
  5. NI at 2-4 wks: add oral budesonide
279
Q

IBD: Tx of low-risk, mild-moderately active UC
- Maintenance

A

Rectal mesalamine QHS
- If oral mesalamine was used, d/c rectal and continue oral mesalamine

280
Q

IBD: Tx of high-risk, mild-moderately active UC
- Remission induction

A
  1. Oral mesalamine + Rectal mesalamine (Sulfasalazine for arthritis)
  2. NI at 2-4 wks: oral mesalamine + rectal corticosteroid QD
  3. NI at 2-4 wks: add budesonide
  4. NI at 2-4 wks: replace budesonide with oral prednisone
281
Q

IBD: Tx of high-risk, mild-moderately active UC
- Maintenance

A
  • If oral mesalamine: d/c rectal and continue oral mesalamine at same dose
  • Steroid dependence: long-term maintenance with biologic
282
Q

IBD: Tx of moderately to severely active UC
- Remission induction

A

Anti-TNFa mAb + Azathioprine
- Vedolizumab in elderly or cancer
- Ustekinumab if unresponsive to azathioprine

283
Q

IBD: Tx of moderately to severely active UC
- Maintenance

A
  • If anti-TNF + Aza: anti-TNF long-term
  • Vedo/Usteki: continue
  • JAKi: continue at the lowest effective dose
284
Q

IBD: Tx of severe-fulminant UC
- Remission induction

A
  • Severe: budesonide
  • Fulminant: Methylprednisolone IV or hydrocortisone IV until stable then switch to oral
285
Q

IBD: Tx of severe-fulminant UC
- Maintenance

A
  • Severe: Azathioprine, 6-MP, or anti-TNF
  • Fulminant: infliximab, vedolizumab, or oral cyclosporine + aza or 6-MP
286
Q

IBD: Tx of mild CD with low risk
- Limited to ileum and proximal colon

A
  1. Remission induction: budesonide
  2. Maintenance: no replapse on budesonide taper- monitor, relapse on taper- restart budesonide + immunomodulator
287
Q

IBD: Tx of mild CD with low risk
- Diffuse or distal colon

A
  1. Remission induction: Prednisone
  2. Maintenance: no relapse-monitor, relapse- restart budesonide + immunomodulator
288
Q

IBD: Tx of moderate to severe CD with moderate-high risk
1. Perianal or intestinal fistula
2. No fistula

A
  1. Perianal or intestinal fistula: anti-TNF mAb + Azathioprine (Vedolizumab monotherapy in elderly or cancer)
  2. No fistula: anti-TNF + Azathioprine or Vedolizumab
289
Q

IBD: Tx of hospitalized pts with severe to fulminant CD

A

IV methylprednisolone

290
Q

IBD: Tx of perianal or fistulizing CD

A
  1. Anti-TNF (infliximab)
  2. Metronidazole

GI/Hepatic (2 decks)

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