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GI/Hepatic > Exam 1 > Flashcards

Exam 1 Flashcards

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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
PUD: Hormonal and neuronal regulation of pancreatic secretions (3)
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
26
What is Peptic Ulcer Disease (PUD)?
Benign lesion of gastric or duodenal mucosa occurring at a site where the epithelium is exposed to acid and pepsin
27
Causes of PUD
H. pylori infection, NSAIDs, acid hypersecretion (Zollinger-Ellison & Cushing's ulcers)
28
PUD: What is Zollinger-Ellison syndrome?
Gastrin-secreting tumor of non-beta cells in endocrine pancreas that increase acid secretion
29
What is Gastroesophageal Reflux Disease (GERD)?
Acid and pepsin from the stomach flow backwards up into the esophagus - Heartburn
30
NSAID-induced PUD results from _____ & _____ injury
Systemic & topical
31
H. pylori infection leading to PUD MoA
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
32
PUD: What are drugs that inhibit secretion of acid?
PPI, H2RA, prostaglandins, muscarinic antagonists
33
PUD: What are drugs that prevent contact with acid?
Sucralfate, prostaglandin analogs
34
PUD: What are drugs that neutralize acid?
Antacids
35
PUD: What is the class of drugs that work against H. pylori? Examples?
Antibiotics - Clarithromycin, amoxicillin, metronidazole, bismuth
36
Inhibition of Proton Pump in PUD MoA, examples of direct & indirect ways
Blocks both basal and stimulated acid secretion - Direct inhibition: PPI - Indirect: CCK2 of gastrin, H2 of histamine, M3 of ACh
37
PUD: PPI MoA steps
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
38
PUD: PPI ADME (Absorption, Metabolism)
- Food stimulates acid production -> 30 mins before meals - Rapidly absorbed, highly protein bound, extensively metabolized by CYP2C19 & CYP3A4 - Asians slow metabolizers (CYP2C19 polymorphism)
39
PUD: H2RA MoA
- Inhibit acid production by reversibly competing with histamine - Inhibit basal acid secretion
40
PUD: H2RA examples
Cimetidine, ranitidine, famotidine, nizatidine **“-idine”**
41
PUD: H2RA ADME (Absorption, Distribution, Excretion)
- Rapidly absorbed, quick peak concentration - Small fraction protein bound - Excreted by kidneys
42
PUD: MoA of prostaglandin analog
- Bind to EP3 - Decrease cAMP and decrease gastric acid secretion - Stimulate mucin and bicarb secretion & increase mucosal BF
43
PUD: Prostaglandin analog examples
Misoprostol
44
PUD: Prostaglandin analog ADME
- Rapidly absorbed, rapidly & extensively **de-esterified** to form misoprostol acid - Food and antacids decrease rate of absorption
45
PUD: Sucralfate MoA
- 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
46
PUD: Antacids MoA
- Weak bases that neutralize hydrochloric acid to form salts and water - Increase pH and inactivate pepsin
47
PUD: Antacids examples
Sodium bicarbonate, Calcium carbonate
48
PUD: M1 receptor antagonist MoA & example
- Suppress neural stimulation of acid production via M1 receptors - Pirenzepine
49
PUD: H. pylori infection treatment
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
50
Risk factors of PUD
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
51
Low-dose aspirin use and risk in PUD
- Risk is dose-related - Risk diminishes with long-term use: =< 30 days use has the highest risk
52
Combination use of low-dose aspirin and nsNSAIDS vs COX2 inhibitors in PUD
Combination therapy generally increases the risk - nsNSAIDs: 6.77% - COX2i: 7.49%
53
nsNSAIDs safety comparison in PUD: ibuprofen, diclofenac, naproxen
- Naproxen has the highest risk - Diclofenac is the safest
54
PUD: Esophagogastroduodenoscopy (EGD) classification and treatment
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
55
PUD: What are the three components of the endoscopic hemostatic therapy (EHT)?
1. Injection therapy (100% ethanol) 2. Heater probe (cauterization) 3. Hemoclip therapy
56
PUD: Risk factors for rebleed post-EHT
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
57
PUD: Long-term risk assessment - Low risk level management
- No risk factors - Less ulcerogenic NSAID at lowest effective dose (diclofenac) - Avoid combined RX & OTC NSAIDs (naproxen)
58
PUD: Long-term risk assessment - Moderate risk level management
- 1-2 RFs, including low-dose aspirin - Less ulcerogenic NSAID + PPI - Less ulcerogenic NSAID + high-dose H2RA - Less ulcerogenic NSAID + misoprostol
59
PUD: Long-term risk assessment - High risk level management
- >3 RFs - Concomitant full-dose aspirin, corticosteroid, warfarin - Celecoxib + misoprostol + PPI
60
PUD: Long-term risk assessment - Very high risk level management
- Prior hx of ulcer complication - Stop NSAID if possible - Celecoxib + misoprostol + PPI
61
PUD: PPIs AEs
- 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
62
PUD: PPIs DDI
- 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
63
PUD: H2RA treatment dose
- **Equally effective given BID or QD at bedtime** - Bedtime dose can be added to PPI to maximize control of nocturnal acid secretion
64
PUD: H2RA AEs
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**
65
PUD: H2RA DDI
- 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
66
PUD: Misoprostol AEs
- GI: dose-related diarrhea - Genitourinary: menstrual irregularities, postmenopausal vaginal bleeding, spontaneous abortion - **C/I in pregnancy**
67
PUD: Sucralfate DDI
- 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**
68
PUD: indications for H. pylori testing
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)
69
PUD: Who should **NOT** get tested for H. pylori?
Patients with GERD and NO ulcer hx should not be tested
70
PUD: what can cause false negative test results for H. pylori?
1. Active Upper GI Bleeding (UGIB) 2. Antibiotic or bismuth use within 4 weeks 3. PPI use within 1-2 weeks
71
PUD: Non-invasive H. pylori testing
1. **Urea breath test (UBT)** 2. Stool antigen test (SAT) 3. Serology - ONLY test not affected by prior use of antibiotics, bismuth, or PPIs
72
PUD: Questions to ask before starting H. pylori testing
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
73
PUD: H. pylori regimen - Bismuth Quadruple indication & 4 classes of drugs
- 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
74
PUD: H. pylori regimen - Clarithromycin Concomitant indication & 4 classes of drugs
- 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
75
PUD: Initial management of dyspepsia
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
76
Stimulatory prokinetic drug targets for GERD treatment
- ACh: M2/3 muscarinic receptor - Motilin receptor - Serotonin: 5HT4 receptor
77
Inhibitory prokinetic drug target for GERD treatment
Dopamine: D2 receptor
78
GERD: Prokinetic drugs works on what cell types?
Smooth muscle cell, dopaminergic neuron, cholinergic neuron
79
GERD: Which prokinetic drug has a dual actions (both agonist and antagonist)?
Metoclopramide
80
GERD: Bethanechol works as _____ by _____; its SEs are ____
- Muscarinic receptor agonist - increasing force of contraction SEs: - CV: HoTN, bradycardia - Urinary: incr void pressure, decr capacity - Exocrine glands: incr secretion - Eye: pupil constriction
81
GERD: Metoclopramide works as _____; its PK profile is ____; and its SEs are ____
- D2 receptor antagonist & 5HT4 agonist - Oral F, cross BBB SEs: - Sedation - Dystonic reactions - Tardive dyskinesia - Anxiety - Gynecomastia/galactorrhea
82
GERD: Domperidone works as ____; its PK profile is ___; and its SEs are ____
- D2 receptor antagonist - Low oral F, limited ability to cross BBB SEs: - Headaches, gynecomastia/galactorrhea
83
GERD: Cisapride works as ____; and its SEs are ___
- 5HT4 agonist SEs: - Serious CV: ventricular tachycardia/fibrillation, QT prolongation **REMS** - 80 deaths, pulled from US market
84
GERD: Motilin works as ____; is secreted by ____; and stimulates gastric emptying by _____
- Motilin receptor (GPCR) agonist - Endocrime M cells in small intestine - Stimulating contraction of upper GI smooth muscle
85
GERD: Erythromycin works as ___; has ____ activity; used in ____ patients with _____ to improve gastric emptying time
- Motilin non-peptide agonist - Antibacterial - Diabetic; gastroparesis
86
GERD: Classic symptoms
heartburn and acid regurgitation
87
GERD: Atypical symptoms
Epigastric bloating/pain, early satiety, dyspepsia
88
GERD: Alarm symptoms
Dysphagia, chronic sore throat, bleeding or anemia, unexplained weight loss
89
GERD: Extraesophageal symptoms
Chronic cough, laryngitis, erosion of tooth enamel, asthma (association not clear)
90
GERD: 4 phenotypes
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
91
GERD: Causes
- 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
92
GERD: Triggering factors
- **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**
93
GERD: First-line medical treatment
PPIs
94
GERD: Diagnosis & Treatment - Classic presentation (heartburn, acid regurgitation, no alarm symptoms
Empiric trial of PPI for 8 wks
95
GERD: pregnancy treatment
Antacids, alginates (Gaviscon), sucralfate
96
GERD: Diagnosis & Treatment - At least 1 alarm symptom or failed PPI trial
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
97
GERD: Lifestyle modifications
- Weight loss - No food/snacks within 3 hrs of bedtime - Avoid trigger foods, smoking, alcohol - Elevate head of bed for nighttime symptoms
98
GERD: PPI counseling points
- 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
99
GERD: H2RA dose, when to refer pt to PCP
- 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
100
GERD: Gaviscon MoA, indication, administration
- 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
101
GERD: Prokinetic agents indication, examples
- Limited use due to frequent AEs - Only indicated for pts with gastroparesis (decr gastric motility) - Agents: metoclopramide, bethanechol, cisapride
102
GERD: Metoclopramide - MoA, AEs
1. MoA: Dopamine antagonist, serotonin agonist 2. AEs: CNS (most common), extrapyramidal rxn, tardive dyskinesia, neuroleptic malignant syndrome, Parkinsonian, GI, hematologic, genitourinary
103
GERD: Bethanechol - MoA, AEs
1. MoA: Cholinergic agonist 2. AEs: ‘uncoordinated GI contractions’ (abdominal cramps, flushing, sweating, lacrimation, salivation, headache), bronchial constriction with asthma
104
GERD: Cisapride - MoA, AEs, and DDI
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
105
GERD: surgical management - Best candidates, AEs, long-term follow up
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
106
What does ABCD stand for in nutritional assessment (NA)?
- Anthropometrics - Biochemistry labs - Clinical assessment - Dietary assessment
107
NA: **A**: How do you measure body weight?
ABW, IBW, UBW, BMI
108
NA: **A**: How do you calculate UBW 1. Change in weight over time 2. Recent weight change
1. ABW/UBW*100=%UBW 2. (UBW - ABW) / UBW*100=% weight loss
109
NA: **B**: Albumin is used for _____ due to ____ half life. Its serum level ____ quickly following physiological stress; therefore, albumin is a ___ acute phase reactant.
Chronic trends; longer; decreases; negative
110
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.
Iron; poor liver production or excessive loss through the kidneys; increases; positive
111
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.
Short term assessment; shorter; nutrition support; decreases; negative
112
NA: **B**: Serum proteins are prognostic indicators and reflect inflammation. T/F
T
113
NA: **B**: Serum proteins do NOT... (5)
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
114
NA: Deficiency of thiamine (B1) leads to...
Wernicke's encephalopathy, lactic acidosis, Korsakoff's psychosis, peripheral neuropathy
115
NA: Deficiency of Pyridoxine (B6) leads to...
Distal limb numbness or paresthesia, microcytic anemia
116
NA: Deficiency of Folic acid leads to... & other comments
- Macrocytic anemia - Decrease with increased cellular/tissue turnover (pregnancy, malignancy, hemolytic anemia)
117
NA: Deficiency of Cyanocobalamin (B12) leads to... & other comments
- Pernicious anemia, peripheral neuropathy - Decreased absorption in the elderly, long-term gastric acid suppression
118
NA: Deficiency of Ascorbic acid (C) leads to... Excess intake of Vitamin C leads to...
- Scurvy - Kidney stones, excess iron absorption
119
NA: Excess intake of Vitamin A leads to...
- Liver toxicity - Vit A is teratogenic
120
NA: Deficiency of Vitamin D leads to...
Rickets, osteomalacia, osteoporosis, hypocalcemia
121
NA: Deficiency of Vitamin K leads to... & ____ can be affected
- Bleeding - Anticoagulant therapy
122
NA: Deficiency of Chromium leads to...
Impaired glucose/protein utilization
123
NA: Excess intake of Copper leads to...
Wilson's disease
124
NA: Deficiency of Iodine leads to ___ & Excess intake leads to ___
- Hypothyroid goiter - Thyrotoxicosis
125
NA: Deficiency of Iron leads to...
Microcytic, hypochromic anemia, fatigue weakness, pallor
126
NA: Deficiency of Zinc leads to...
Impaired wound healing, dermatitis, altered taste
127
NA: drug-nutrient interaction; antibiotics
Vitamin K deficiency
128
NA: drug-nutrient interaction; Cholestyramine, colestipol
Vitamins ADEK & beta-carotene malabsorption
129
NA: drug-nutrient interaction; H2RAs/PPIs
Vitamin B12 malabsorption
130
NA: drug-nutrient interaction; Isoniazid
Vitamin B6 deficiency
131
NA: drug-nutrient interaction; warfarin
Vitamin K inhibits effect
132
NA: what are 3 ways to measure energy expenditure?
1. Population estimates 2. Harris-Benedict equation 3. Indirect calorimetry
133
NA: Population based estimate of illness, metabolic stress (BMI <30 kg/m^2)
25 to 30 kcal ABW/kg/day
134
NA: What do you have to keep in mind when using the Harris-Benedict equation?
Results must be modified by a factor that adjusts for the patient's clinical condition
135
NA: Indirect calorimetry measures _____ and is used to measure ____ & also determines ____
O2 consumed and CO2 produced; resting expenditure; Respiratory Quotient (RQ) - Most accurate
136
NA: Respiratory Quotient (RQ) is used to determine if the patient is ____
Overfed ( Value >1)
137
NA: Nitrogen balance is a clinical assessment of ____
Protein intake
138
NA: What is Holliday-Segar method?
- 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
NA: Complications of refeeding syndrome
1. Introducing glucose leads to thiamine deficiency 2. Introducing insulin leads to intracellular electrolyte shift: hypokalemia, -phosphotemia, -magnesemia
140
NA: Ways to prevent refeeding syndrome
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
EN: Absolute C/I
Mechanical intestinal obstructions, necrotizing enterocolitis
142
EN: Relative C/I
GI surgery, severe pancreatitis, short bowel syndrome, severe inflammatory bowel disease, intractable diarrhea, hemodynamic instability,GI bleeding, obstruction/ileus
143
EN: Absence of bowel sounds **is or is not** a contraindication to enteral feeding
is not
144
EN: Nonsurgical routes of administration
- Nasogastric, orogastric - Nasoduodenal, nasojejunal
145
EN: Surgical routes of administration
- Gastrostomy, percutaneous endoscopic gastrostomy (PEG) - Jejunostomy
146
EN: Advantages and disadvantages of stomach feeding
- (+): large reservoir capacity, high osmotic load, larger tubes, easier to place/replace - (-): increased aspiration risk
147
EN: Advantages and disadvantages of small intestine feeding
- (+): decreased aspiration risk - (-): small reservoir capacity, can't tolerate high osmotic load, more difficult to place/replace tubes
148
EN: Indications of nasogastric, orogastric insertion & aspiration risk
- Short-term, normal gastric emptying - High
149
EN: Indications of nasoduodenal, nasojejunal insertion & aspiration risk
- Short-term, impaired gastric emptying, increased risk of aspiration - Low
150
EN: Indications of gastrostomy, PEG insertion & aspiration risk
- Long-term, normal gastric emptying - High
151
EN: Indications of jejunostomy insertion & aspiration risk
- Long-term, normal gastric emptying, increased risk of aspiration - Low
152
EN: Continuous administration method
- Most common - Preferred in critically-ill - Less abdominal distention, V/D, aspiration - Small intestine feeding
153
EN: Cyclic administration method
- EN held during the day, administered at night - Decreased time receiving EN - Increased mobility
154
EN: Cyclic- bolus
- 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
EN: Cyclic- intermittent
- Used if intolerant to bolus - Give same volume (240-500 mL) over 20-60 mins
156
EN: Carbohydrate provides ___% of the total calories. Most common CHO source is ___; where as ___ is not generally a CHO source
40-90%; maltodextrin; lactose
157
EN: Protein provides ___% of total calories. Standard protein content contains up to ___%
4-32%; 15%
158
EN: Lipids provide ____% of total calories. Polymeric formulas contain ____% fat
1.5-55%; 30-40%
159
EN: Standard formulas of fluids are ____% of _____
80-85%; free water
160
EN: high protein formula is indicated for patients ___
requiring >1.5 g/kg/day
161
EN: high caloric density is indicated for patients ___
with fluid/electrolytes restriction
162
EN: elemental formula is indicated for ___ bc it contains ____
- Malabsorptive disorders, low fat requirements - Low fat, high % free AA
163
EN: peptide-based formula contains ___ and may be of benefit in ____
- Dipeptides/tripeptides - Malabsorption
164
EN: Renal formula is high ____, varying ____, and low ____. It is indicated for ___
- Caloric density; protein; electrolyte - Dialysis pts
165
EN: Hepatic formula contains high ____ and low ______. *Only* indicated in ______
- Branched chain; aromatic AA - Refractory hepatic encephalopathy
166
EN: Diabetic formula contains high ___ and low ___
fat; CHO
167
EN: Pulmonary formula contains high ___, low ____. Indicated for ____
- Fat, CHO - Acute Respiratory Distress
168
EN: Trauma and Burn formula contains ____, ____ (building blocks for proteins), _____ &/or ____
- Glutamine, arginine, nucleotides - omega-3 FA
169
EN: Initiation and advancement - Critically ill vs refeeding syndrome
- 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
EN: How to prevent aspiration pneumonia
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
EN: What is widely used as indicator of intolerance/risk of aspiration?
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
EN: Medications with special considerations
- Phenytoin: hold feeds 1-2 hrs before/after - Fluroquinolones/ Tetracyclines: hold feeds 1 hr before/after
173
PN: Nutritional screening in peds
1. Head circumference (measured <3 yrs) 2. Length (<2 yrs), Height (>= 2 yrs)
174
PN: Indications for peds
- Prematurity - Severe GI impairment - Feeding intolerance - Hypermetabolism, inadequate intake - Anticipated prolonged starvation (5-7 days in older peds, 24 hrs in neonates)
175
PN: Peripheral indications, +/- in peds
- 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
PN: Central IV access indication, +/- in peds
- Indication: preferred route of administration - (+): maximize nutrition, no limit on osmolarity (dextrose >12.5%, calcium) - (-): technical challenges, complications in peds
177
PN: What is 2-in-1 system? Preferred in ____, caution
- CHO, protein, micronutrients, multivitamins, trace elements in one bag - Lipids in separate bag - Preferred in peds - Avoid antimicrobial growth
178
PN: What is 3-in-1 system? Advantage? Disadvantage?
- 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
PN: What is CHO caloric value?
3.4 kcal/g
180
PN: What is GIR?
Glucose Infusion Rate - Standard procedure to calculate amount of dextrose in all infants - Determine how quickly the pt receives dextrose
181
PN: Protein: primary form, use ____ as tolerance indicator, titration, ___ should be added separately to protein
- AA - Blood urea nitrogen (BUN) - Not needed; begin at goal on day 1 of therapy - Cysteine
182
PN: Protein caloric value
4 kcal/g
183
PN: Role of Cysteine and its dose in peds
- Decrease pH, increase calcium & phosphorus solubility - 40 mg for each g of AA
184
PN: Lipids: primary form, requirement to prevent FFA deficiency, titration, monitoring
- 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
PN: Lipids account for ___% of total calories
20-50%
186
PN: Lipids caloric value in peds (20% fat emulsion)
10 kcal/g
187
PN: Factors affecting Calcium-Phosphate solubility - Calcium salt used, pH of final solution, temperature, order of mixing
- Gluconate > Chloride - Lower pH increases solubility = why cysteine added! - Lower temp increases solubility - Phosphorus, then Calcium to minimize precipitation
188
PN: Why is Zinc important in pediatrics?
- Required for maintenance of normal cell growth - Increased requirements: renal failure, high volume stool loss, fistula/stoma output, premature infants
189
PN: Why is Copper important in pediatrics?
- Hypochromic anemia - Increased requirements: jejunostomy, external biliary drainage - Decrease by half: cholestasis or liver function impairment
190
PN: Why is Manganese important in peds?
- Component of several enzymes - Decreased/Withhold: cholestasis or liver function impairment
191
PN: Why are Selenium and chromium important in peds?
Antioxidant defense in the neonate
192
PN: Adult indications
1. Requiring total bowel rest = **nonfunctioning GI tract** 2. NPO >= 7 days 3. Appropriate venous access
193
PN: Adult indications - Nonfunctioning GI tract examples
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
PN: Protein accounts for ___% of total calories in adults. This is equal to ____ g/kg/day.
- 10-30% - 0.8-2 g/kg/day
195
PN: Lipids accounts for ____% of total calories in adults and provides at least ____% of total calories to prevent essential FA deficiency
- 20-30% - 4-10%
196
PN: Lipids 10% contains ___ kcal/mL, 20% contains ___ kcal/mL, and 30% contains ___ kcal/mL
- 1.1 kcal/mL - 2 - 3
197
PN: CHO accounts for ___% of total calories in adults
45-65%
198
PN: Trace elements that are excreted via liver vs renally
- Liver: Copper, Manganese - Renal: Chromium, Selenium
199
PN: Continuous administration in adults - How and for whom
- How: over 24 hrs - For: inpatients, unstable fluid balance or glucose control
200
PN: Cyclic administration for adults - How and for whom
- How: over 12-18 hrs - For: home administration, cholelithiasis, hunger/enteral feeding
201
PN: IV compatibility - Meds that **CAN** be added to TPN
Regular insulin (ONLY), H2RAs, morphine, heparin
202
PN: IV compatibility - Meds to **AVOID**
Acyclovir, amphotericin B, minocycline, phenytoin
203
PN: IV catheter issues
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
PN: Metabolic complications
1. Hyperglycemia/ Hypoglycemia 2. Electrolyte abnormalities 3. HyperTG/ Pancreatitis 4. Essential FA Deficiency (EFAD) - rare 5. Re-feeding syndrome
205
PN: macronutrient changes in RF - CHO, Pre-albumin, Lipids, Protein
- 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
PN: Fluid, electrolyte, acid-base alterations in RF
- Metabolic acidosis - Hyperkalemia/ -phosphatemia/ -magnesemia - Oliguric ARF (x urine): impaired excretion of sodium and water - Non-oliguric ARF: considerable sodium loss in urine
207
PN: Trace elements and vitamins alteration in RF
- **Accumulation of Zinc, chromium** - Reduction of Selenium concentrations - Vitamin D deficiency - Elevated vitamin A
208
PN: nutrition plan for ARF
- Initiate standard recommendations - Consider specialty formulations if electrolyte abnormalities - Adjustments for HD or Continuous Renal Replacement Therapy (CRRT)
209
PN: nutrition plan for CRF
- Fluid and electrolyte restriction - Protein restriction (0.6-0.75 g/kg/day) - Protein calorie malnutrition common - Requirements change with renal replacement therapy
210
PN: CHO and lipids alterations in Hepatic Failure (HeF)
- CHO: insulin resistance common, decreased hepatic/muscle glycogen, hypoglycemia - Lipids: Increased lipolysis, increased risk for essential FA deficiency, fat malabsorption
211
PN: Protein alterations in HeF - AAA vs BCAA
- 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
PN: Fluid and electrolyte alterations in HeF
- Ascites and peripheral edema common in severe cirrhosis - Hyponatremia: excess total body sodium and total body water - Hypokalemia/ -magnesemia/ -phosphophatemia
213
PN: Vitamins and trace elements alterations in HeF
- Poor intake and malabsorption - Increased needs of ADEK, folic acid, thiamine, zinc, selenium - Decreased need for Copper & Manganese due to bile excretion
214
PN: Considerations in HeF - Meds, use of BW for calculation
- Meds with electrolyte effects = Spironolactone, furosemide - Meds which induce diarrhea = Lactulose - Use dry or lean BW
215
PN: CHO alterations in Pulmonary Failure (PF) - RQ, risk for hyperglycemia is increased by use of ______
- Glucose-based nutrition can contribute to elevated PCO2 - CHO RQ = 1 (highest) > protein > fat - Concomitant steroids
216
PN: Fluids, electrolytes, vitamins alterations in PF
- Pulm edema decreases oxygenation - Hypokalemia: albuterol, diuretics - Hypophosphatemia - Chronic steroid users: Ca/Vit D supplementation
217
PN: Considerations for PF - avoid ___, formula
- Strict avoidance of overfeeding to avoid CO2 -> worsen respiratory acidosis - Higher lipid, lower CHO formulas
218
PN: Metabolic response to stress in critically ill patients (CIP)
Activation of immune system - Increased inflammatory mediators and cytokines - Increased production of counter-regulatory hormones
219
PN: Nutritional alterations in CIP
- 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
PN: Specialty nutrition products for CIP
- Use **high protein, high calorie** formulas - **Immune enhancing**: contain glutamine, arginine, omega 3 FA, anti-oxidents
221
IBD: Crohn's Disease location and symptoms
- L: transmural, any part of the GI tract, often near ileocecal valve, discontinuous - S: watery diarrhea
222
IBD: Ulcerative colitis location & symptoms
- L: mucosal, distal rectum, colon, continuous - S: bloody diarrhea
223
IBD: TH1 cell is more involved in CD/UC. TH2 cell is more involved in CD/UC
- TH1: CD - TH2: UC
224
IBD: Aminosalicylates MoA
- 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
IBD: Aminosalicylates metabolism and C/I
- Sulfasalazine metabolized to 5-ASA and sulfapyridine - Sulfa allergy
226
IBD: Corticosteroids MoA and indicated population
- MoA: anti-inflammation - Moderate to severe
227
IBD: Immuno-modulators MoA and indicated population
- MoA: inhibit DNA replication - Severe who are steroid-resistance or -dependent - Methotrexate **only** in CD
228
IBD: Immuno-modulators examples
- Purine analog: 6-mercaptopurine, azathiopurine (prodrug) - Folate acid analog: methotrexate
229
IBD: Biologics 3 classes
1. TNFa inhibition 2. Interleukin inhibition 3. A4 Integrin inhibition, Janus kKinase inhibitor
230
IBD: TNFa inhibitor agents examples
Infliximab, adalimumab, certolizumab pegol
231
IBD: Interleukin inhibitor agent
Ustekinumab
232
IBD: A4 Integrin inhibitor agent
Vedolizumab
233
IBD: Classic presentation of UC
Bloody diarrhea, tenesmus, rectal urgency
234
IBD: Low risk of UC
Proctitis or left-sided, mild disease based on colonoscopy
235
IBD: High risk of UC
Extensive, <40 yrs, deep ulceration based on colonoscopy, high ESR/CRP, steroid dependence, hx of hospitalization, C. diff/CMV infection
236
IBD: Classic presentation of CD
Watery diarrhea, persistent RLQ pain, low grade fever
237
IBD: CD severity criteria - Remission
- <150
238
IBD: CD severity criteria - Mildly active
150-219
239
IBD: CD severity criteria - Moderately active
220-450
240
IBD: CD severity criteria - Severe-Fulminant
>450
241
IBD: Low risk of CD
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
IBD: Moderate-High risk of CD
<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
IBD: Rectal 5-ASA (Mesalamine) AE
Leakage (enema), localized bloating/burning pain
244
IBD: Rectal 5-ASA examples
Rowasa enema, Canasa suppository
245
IBD: Oral 5-ASA use and AEs
- Use: must deliver directly to small/large intestine, slower to induce remission, more AE than rectal - AE: diarrhea
246
IBD: Oral 5-ASA examples
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
IBD: Sulfasalazine MoA
- 5-ASA azo-bonded sulfapyridine - Sulfapyridine absorbed systemically once 5-ASA is released
248
IBD: Sulfasalazine AEs
Non dose related: rash, fibrosing alveolitis, hepatitis, hemolytic anemia, decreased sperm count/motility, bone marrow suppression - d/c drug
249
IBD: Sulfasalazine DI
Antibiotics, decreased absorption of folic acid or ferrous sulfate, displacement of high protein-bound drugs
250
IBD: Corticosteroids AEs
Fluid retention, glucose intolerance, moon face, acne, hair growth, hyperlipidemia, cataracts, osteoporosis, avascular necrosis, muscle pain/weakness, increased risk of infection, adrenal suppression
251
IBD: corticosteroid preferred agent
Budesonide
252
IBD: Corticosteroids are effective at ___ remission but not for ____ remission
Inducing; maintaining
253
IBD: Corticosteroid dosing
Oral and Rectal both no more than **8 weeks** total
254
IBD: Immunomodulators usage (2)
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
IBD: Azathioprine, 6-mercaptopurine AEs
- Non dose related: **pancreatitis,** rash, arthralgias, N/V - Dose related: BM suppression, increased infection risk, hepatitis - Increased cancer risk
256
IBD: Thipourine S-methyltransferase (TPMT) testing is recommended in which patients?
All pts prior to starting tx with azathioprine or 6-MP
257
IBD: Methotrexate works ___ and has ___ cancer risk than azathioprine or 6-MP, but may ___
Faster; lower; lose efficacy over time
258
IBD: Methotrexate AEs
Hypersensitivity, leukopenia, **hepatic fibrosis**
259
IBD: anti-TNFa BBW
- 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
IBD: Infliximab is what kind of mAb? Administration?
- Chimeric mAb - IV
261
IBD: Infliximab AEs
- Acute/delayed infusion rxn - Rare: BM suppression, severe liver toxicity
262
IBD: Certolizumab pegol is what kind of mAb? Administration?
- Pegylated humanized mAb - SQ
263
IBD: Certolizumab pegol AEs
- Overall well-tolerated - Upper respiratory tract infection, acute bronchitis, nasopharyngitis, fever
264
IBD: Adalimumab (Humira) is what kind of mAb? Administration? AE?
- Human mAb - SQ - Infection
265
IBD: Golimumab is what kind of mAb? Administration?
- Human mAb - SQ
266
IBD: Integrin inhibitor natalizumab MoA
Humanized mAb that targets the integrin a4 subunit of a4b7 integrin (gut) and a4b1 integrin (brain) - Nonselective
267
IBD: Integrin inhibitor natalizumab indication
Moderately to severely active CD who have failed to respond or cannot tolerate first-line therapy
268
IBD: Integrin inhibitor natalizumab AEs
Progressive multifocal leukoencephalopathy (PML) - Risk higher in JC virus sero+ - REMS program
269
IBD: Integrin inhibitor vedolizumab MoA
Humanized mAb that selectively targets **a4b7 integrin (gut)**
270
IBD: Integrin inhibitor vedolizumab AEs
**No increased risk of PML & cancer**
271
IBD: Ustekinumab (Stelara) MoA
- Human anti-IL12 & -23 mAb - Inhibit NK cell activation and CD4 T cell activation/differentiation
272
IBD: Ustekinumab AEs
- Reactivation of latent TB - Increased cancer risk - Reversible posterior leukoencephalopathy syndrome
273
IBD: Risankizumab (Skyrizi) MoA & Indication
- 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
IBD: Selective Janus kinase inhibitors (JAKi) BBW
- 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
IBD: JAKi DI
CYP3A4 inhibitors/inducers
276
IBD: JAKi tofacitinib selectivity, indication
- More selective for JAK1/2/3 - Moderate to severe **UC** in adults who have failed at least 1 anti-TNFa - NOT first line
277
IBD: JAKi upadacitinib selectivity, indication
- More selective for JAK1 - Moderate to severe **CD** in adults who have failed at least 1 anti-TNFa
278
IBD: Tx of low-risk, mild-moderately active UC - Remission induction
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
IBD: Tx of low-risk, mild-moderately active UC - Maintenance
Rectal mesalamine QHS - If oral mesalamine was used, d/c rectal and continue oral mesalamine
280
IBD: Tx of high-risk, mild-moderately active UC - Remission induction
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
IBD: Tx of high-risk, mild-moderately active UC - Maintenance
- If oral mesalamine: d/c rectal and continue oral mesalamine at same dose - Steroid dependence: long-term maintenance with biologic
282
IBD: Tx of moderately to severely active UC - Remission induction
Anti-TNFa mAb + Azathioprine - Vedolizumab in elderly or cancer - Ustekinumab if unresponsive to azathioprine
283
IBD: Tx of moderately to severely active UC - Maintenance
- If anti-TNF + Aza: anti-TNF long-term - Vedo/Usteki: continue - JAKi: continue at the lowest effective dose
284
IBD: Tx of severe-fulminant UC - Remission induction
- Severe: budesonide - Fulminant: Methylprednisolone IV or hydrocortisone IV until stable then switch to oral
285
IBD: Tx of severe-fulminant UC - Maintenance
- Severe: Azathioprine, 6-MP, or anti-TNF - Fulminant: infliximab, vedolizumab, or oral cyclosporine + aza or 6-MP
286
IBD: Tx of mild CD with low risk - Limited to ileum and proximal colon
1. Remission induction: budesonide 2. Maintenance: no replapse on budesonide taper- monitor, relapse on taper- restart budesonide + immunomodulator
287
IBD: Tx of mild CD with low risk - Diffuse or distal colon
1. Remission induction: Prednisone 2. Maintenance: no relapse-monitor, relapse- restart budesonide + immunomodulator
288
IBD: Tx of moderate to severe CD with moderate-high risk 1. Perianal or intestinal fistula 2. No fistula
1. Perianal or intestinal fistula: anti-TNF mAb + Azathioprine (Vedolizumab monotherapy in elderly or cancer) 2. No fistula: anti-TNF + Azathioprine or Vedolizumab
289
IBD: Tx of hospitalized pts with severe to fulminant CD
IV methylprednisolone
290
IBD: Tx of perianal or fistulizing CD
1. Anti-TNF (infliximab) 2. **Metronidazole**

GI/Hepatic (2 decks)

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