Exam 5 Flashcards

1
Q

Pathophysiology of GERD

A
Reduced lower esophageal sphincter pressure
Direct esophageal irritation
Hiatal Hernia
Achalasia (lack of motility)
Mucosal Resistance
Delayed gastric emptying
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2
Q

Conditions that may worsen or cause GERD

A

Smoking- lowers LES pressure and has acid neutralizing effects of saliva, increases acid production
Obesity (BMI >30)
Physical activity (LES relaxation)
Alcohol- direct irritant

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3
Q

Zollinger- Ellison Syndrome

A

Very rare, most commonly seen in men aged 50-60
Gastrinomas in pancreas or duodenum secrete large amounts of gastrin , often resulting in peptic ulcers and symptoms of GERD.
Tx- surgery, chemotherapy, high-dose PPI therapy
Suspect if patient has recurrent or refractory PUD or GERD
Associated with frequent diarrhea and duodenal ulcers

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4
Q

GERD complications

A

Esophagitis (Erosive esophagitis with ulcers occurs when GERD goes untreated)
Barrett’s esophagitis- increases risk of esophageal cancer
Strictures
Anemia
Cancer
Can worsen asthma/precipitate an attack- need to check if patients with frequent asthma exacerbations have GERD (50% do)
Can cause laryngitis
Atypical chest pain

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5
Q

Barrett’s Esophagus

A

Columnar epithelium replaces squamous epithelial lining during reparative process
This increases the risk of stricture by 30-80%
Increases the risk of cancer by 30-60x
Need endoscopic surveillance

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6
Q

Evaluation of GERD

A

Take pt history and empiric treatment

  • Typically aggravated by meals
  • Typically aggravated by recumbent position
  • If responds to PPI, the patient likely has GERD

Chest pain needs further evaluation

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7
Q

Typical presentation of GERD

A

Heartburn
Acid regurgitation
Belching
Bloating

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8
Q

Atypical presentation of GERD

A
Chest pain
Laryngitis/hoarseness
Asthma
Insomnia
Chronic cough
Aspiration pneumonia
Tooth decay
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9
Q

Alarm S/S of GERD

A
Needs to be evaluated:
Severe dysphagia
Odynophagia
Weight loss
Persistent vomiting
Bleeding
Hematemesis
Anemia
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10
Q

Alternate diagnosis in GERD; Pt presents with chest pain, what could it be?

A
CAD
Gallstones
Gastric/esophageal cancer
Peptic ulcer disease
Esophageal motility disorders
Pill induced esophagitis
Eosinophilic esophagitis
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11
Q

Diagnostic testing in GERD

A

Not necessary if PPI resolves symptoms, but symptoms do not always predict the erosive nature of the disease
Consider testing if symptoms persist on PPI or “alarm” symptoms (Endoscopy (EGD))

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12
Q

Endoscopy (EDG)

A
Necessary to determine:
Erosions
Rings (Schatzki rings)- mucosal disorder causing esophageal narrowing, common symptom dysphagia
Stricutres
Barrett's
Cancer- need additional biopsy
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13
Q

Treatment goals for GERD

A

Alleviate or eliminate symptoms
Heal esophagitis
Manage or prevent complications
Maintain remission

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14
Q

Nonpharm treatment of GERD

A

Elevate head of the bed
Weight loss
Avoid foods that may decrease lower esophageal sphincter pressure (fats, chocolate, alcohol, peppermint, spearmint)
Avoid foods that are direct irritants (spicy foods, OJ, tomato juice, coffee)
Eat small meals and avoid eating prior to sleep
Smoking cessation

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15
Q

Treatment of mild/intermittent heartburn

A

Lifestyle changes
Antacids
OTC H2RAs
OTC PPIs

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16
Q

Treatment of GERD

A

Lifestyle changes
Rx-strength H2RAs
Rx PPIs

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17
Q

Treatment of erosive or moderate/severe symptoms

A

Lifestyle changes
Rx PPIs
High Dose PPIs

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18
Q

Antacids

A

Only appropriate for intermittent or mild heartburn
Self treat for 2 weeks then see MD
Avoid aluminum and magnesium in CKD patients
Aluminum- constipation
Magnesium- Diarrhea
Tums (calcium carbonate)
DDIs- iron, antibiotics (quinolones, tcn), azoles, separate chelators by 2 hours

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19
Q

Histamine-2 Receptor Antagonists (H2RAs)

A
Nizatidine, famotidine, ranitidine, cimetidine
Famotidine most common
Cimetidine many DDI
Ranitidine pulled off market 
May reduce absorption of iron and azoles
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20
Q

Famotidine dosing

A

Mild- 10-20mg/day
Moderate/Severe- 40-80mg/day BID

Renal dosing if CrCl <50mL/min (give 50% of dose)

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21
Q

AE of H2RAs

A

HA, dizziness, diarrhea, constipation, fatigue

Increased confusion in elderly (dont use it patients over 75)

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22
Q

Proton Pump Inhibitors

A

Superior to H2RAs and should be used for erosive diseases
- Reasonable to try first for typical symptoms
All PPIs are equally effective at equal doses and more effective in erosive and nonerosive diseases

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23
Q

OTC PPIs

A

Omeprazole
Lansoprazole
Esomeprazole
Omeprazole-sodium bicarb

Dont use for more than 14 days

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24
Q

Omeprazole

A

20mg QD for all indications

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25
Lansoprazole
15mg QD for mild heart burn and GERD | 30mg QD for 8 weeks then 15mg QD for erosive disease
26
Esomeprazole
20mg QD for mild heartburn and GERD | 20-40mg QD x8 weeks then 20mg QD for erosive disease
27
Rabeprazole
20mg QD for GERD and erosive disease
28
Pantoprazole
40mg QD for GERD and erosive disease
29
Dexlansoprazole
30mg QD for GERD 60mg QD x8 weeks then 30g QD for erosive disease Dual delayed-release- first release 1-2 hours after dose, next release 4-5 hours later . Take without regards to meals.
30
PPI dosing
Start QD, 30 minutes before a meal In symptoms are uncontrolled may increase to BID dosing (preferred), switch PPIs, or increase dose PRN dosing only considered after initial treatment course
31
Omeprazole-Sodium Bicarb (Zegerid)
IR | Doesnt need to be enteric coated because bicarb increases the stomach pH
32
PPI drug interactions
Iron, azoles (acidic environment needed) Warfarin- omeprazole only Clopidogrel- prevents metabolism of clopidogrel due to CYP2C19
33
PPI AE
``` HA Dizziness Possible vitamin/mineral deficiencies: B-12 Iron Magnesium Calcium ```
34
PPI Concerns
Osteoporosis- inhibition of osteoclast mediated bone resorption ("old bone" not replaced) and inhibition of calcium absorption Reduced acidity encourages gut microflora growth (C. diff and pneumonia) Dementia ( Unknown cause, but increased risk)
35
Reasons for PPI failure
failure- symptoms persist after at least 8 weeks of double dose PPI Reasons- non-compliance #1 reason Persistent esophageal acid exposure (hypersecretory state, large hiatal hernia) Acid-sensitive esophagus Wrong diagnosis- eosinophilic esophagitis 30-40% of patients will not have good symptoms control
36
Maintenance PPI therapy
Non-erosive disease- treat initially for a 4-8 week course. Can trial d/c but 2/3rds will relapse Erosive disease- 8 weeks to heal but typically continue long term Zollinger-Ellison and Barrett's- lifelong
37
GERD therapy adjustments
``` For nonerosive disease: Transition to PPI to H2RA ("step down") Transition from H2RA to PPI ("step up") Adjust PPI dose, frequency, or switch Transition from scheduled to PRN Add bedtime H2RA therapy to daytime PPI therapy for nocturnal symptoms ```
38
Metoclopramide (Reglan)
Prokinetic agent -Increases LES pressure and augments gastric emptying Only use in the presence of proven gastroparesis 5-10mg po TID and HS CNS AE- Sedation, depression, irritability, EPS, not tolerated in elderly pts
39
Surgery for GERD
Done if pt: Will not take medications Noncompliance to meds or AE Large hiatal hernia (Nissen fundoplication) Refractory to meds or worried about long term medication AE
40
Special populations- Pediatrics and GERD
GERD is fairly common in infants in the first 5 years of life This is due to developmental immaturity of LES Non-pharm- changing formula, smaller, more frequent feedings, postural management, parent reassurance Can safely use H2RAs and PPIs
41
Special populations- Pregnancy and Lactation and GERD
Pregnancy- have a defective LES and high estrogen and progesterone levels Tx- lifestyle, TUMS preffered (due to calcium carbonate), H2RA and PPI after TUMS Do not use omeprazole Lactation- Antacids and H2RAs safe Can use PPI but should wait after 6 months of lactation if possible
42
Counseling Questions for GERD
Duration/frequency of symptoms Quality and timing of symptoms Use of alcohol and tobacco Dietary choices Medications already tried to treat symptoms and duration of OTC tx Other disease states present and medications being used
43
What is the pathophysiology of GERD?
Defective LES pressure or function -Spontaneous relaxation of LES (more common in recumbent position) -Increased intra-abdominal pressure-straining, bending over, coughing Direct esophageal irritation (drugs)
44
Drugs that worsen GERD
CCB caffeine nicotine Aspirin
45
Hiatal hernia
When part of the stomach pushes through the diaphragm causing the esophageal sphincter to be permanently open. Food can get trapped in this part of the stomach. Requires surgical repair Consider if reflux is not responsive to medication
46
Pathophysiology of reduced esophageal clearance
``` Reduced peristalsis (achalasia) Prolongs time refluxed food material is in contact with esophagus ```
47
Pathophysiology of mucosal resistance
Esophageal mucosal layer doesnt produce mucus or respond to bicarbonate neutralization. Happens frequently in the elderly due to decreased saliva
48
Pathophysiology of delayed gastric emptying
Increased gastric volume increases frequency of reflux as well as amount of refluxate Common in diabetes
49
Mucosal defense mechanisms
Bicarbonate- chemical barrier on GI lining. Neutralizes stomach acid Mucus production- physical barrier Blood flow to mucosa for healing purposes Prostaglandins-increases mucus and bicarb production, increases blood flow, decreases gastric acid secretion, limits back diffusion of acid into epithelium
50
H. pylori
Gram negative bacteria found in most people with peptic ulcer disease. H. pylori produces ammonia/urease which is toxic to the mucosal barrier. H. pylori produces cytotoxins and mucolytic enzymes
51
How do NSAIDs cause peptic ulcer disease?
The inhibition of COX1 results in reduced mucus and bicarbonate secretion and impaired platelet aggregation
52
1st line N/V treatment in chemo
Serotonin receptor blockers
53
Types of diarrhea
``` Osmotic Inflammatory Secretory Infectious Altered motility ```
54
Osmotic diarrhea
``` Poorly absorbed intestinal substances (carbs) retain water within the intestine. Carbohydrate malabsorption (lactose intolerance), Mg-containing medications, lactulose, sorbitol Fasting reduces stool volume ```
55
Inflammatory diarrhea
Blood, protein, or mucus from an inflamed or ulcerated mucosa -Ulcerative colitis and Crohns disease
56
Lactose intolerance
Deficiency of the lactase enzyme -unabsorbed lactose has an osmotic effect by pulling water into the intestinal lumen -Can be inherited or acquired - 3 week trial of diet free of milk and milk products tx- Dietary changes, probiotics, lactase supplements
57
Secretory diarrhea
Stimulating substances either increase or decrease absorption of large amounts of water and electrolytes - Amount exceeds the colons absorptive capacity Could be due to fat malabsorption, bacterial toxins, pancreatic or intestinal tumors, laxatives, misoprostol, digoxin, colchicine Fasting does not alter stool volume
58
Acute infectious diarrhea
Bacterial- C. diff, shigella, E.coli, campylobacter, salmonella Viral- gastroenteritis Parasitic- giardia, cryptosporidium
59
Altered motility
Caused by reduction in contact time with small intestine and premature emptying of the colon - intestinal resection - Metoclopramide, erythromycin Caused by bacterial overgrowth where normal flora replaced (antibiotics, PPI, H2 blockers) More pathogens will grow due to the inability to digest carbs
60
Causes of secondary constipation
Hypercalcemia- gut atony Hypothyroidism- slows digestive contraction Parkinsons disease- lack of dopamine to stimulate peristalsis Diabetes- gastroparesis
61
Secondary medication causes of constipation
Opioids- agonize mu receptors in the GI tract reducing GI motility Anticholinergics- Inhibit acetylcholine, reducing GI motility CCBs- Gut smooth muscle relaxation, reduces GI motility Iron- pulls water into stomach (out of colon); hardens stool; alters motility
62
IBD
Characterized by inflammation Ulcerative colitis- confined to rectum and colon; mucosa and submucosa disease Crohns disease- any part of the GI tract; terminal lumen; transmural disease Share common etiologies but exact etiology unknown
63
Pathophysiology of IBD
``` Alteration of makeup of intestinal microbiota Disruption of mucus layer Dysregulated immune activity Genetic factors Environmental factors ```
64
Gut microbiome
1000-1500 different species of bacteria IBD patients have decreased clostridium and increased campylobacter, shigella, E. coli Normal intestinal microbiota regulates immune system function by producing substances that reduces TNF-alpha, NF, and LPS activity and promotes regulatory T cell activity
65
Intestinal immune system
Goblet cells- mucus, keeps bacteria away from intestinal epithelial cells A-defensins and IgA protect against luminal microbiota Dendritic cells present antigens to native CD4 T cells CD4 T cells differentiate into subgroups (T helper cells)
66
Intestinal epithelium
Provides physical (intercellular junctions and tight junctions) and biochemical barriers to intestinal microorganisms Produce mucus, maintain and repair barrier, control response to bacteria Coordinates with innate and adapt immune systems Intestinal epithelial cells are guided by pattern recognition receptors which detect commensal vs pathogenic microbes and activates immune system if needed
67
Immunopathophysiology in IBD
Infiltration of lamina by innate and adaptive immune cells (innate first because it regulates homeostasis) These cells increase levels of inflammatory cytokines (IFN and cytokines), increasing intestinal permeability Leukocyte infiltration into inflamed intestinal mucosa which contributes to persistent inflammation
68
Biliary tree
In pancreatitis, anything that blocks a duct effects all organs in the biliary tree. Gallbladder, pancreas, duodenum
69
Endocrine pancreas
Insulin and glucagon
70
Exocrine pancreas
Duct cells | Bicarb, amylase, lipase, protease
71
Alcohol-induced pancreatitis
>50g/day alcohol for at least 5 years (4 beers/day) 5% of alcoholics develop pancreatitis Alcohol increases enzyme production Alcohol damages acinar cells which can cause premature enzyme activation
72
Common causes of PUD
NSAIDS H.pylori Stress
73
NSAID caused PUD
``` Chronic condition Gastric >Duodenal May be asymptomatic Deep ulcers More severe GI bleeding ```
74
H. Pylori caused PUD
``` Chronic condition Duodenal > gastric Epigastric symptoms Superficial ulcers Less severe bleeding ```
75
Stress caused PUD
``` Acute condition Gastric > Duodenal Asymptomatic Most superficial ulcer depth More severe GI bleeding ```
76
Uncommon causes of chronic peptic ulcer
``` Idiopathic Hypersecretion of gastric acid Viral infections Radiation therapy Chemo Infiltrating disease (Crohn's disease) Smoking Psychological stress Potentially alcohol ```
77
NSAIDs
Ibuprofen and Naproxen Aspirin included Ulcers develop in about 25% of chronic NSAID users (2-4% bleed) Risk is highest in the first month and persists for the duration (GI mucosa less prepared) Elderly at highest risk due to age-related changes in gastric mucosal defense
78
Equal COX1 and COX2 effect
Meloxicam
79
COX-2 inhibitors
Celecoxib
80
COX-1 inhibition causes on GI mucosa
Peptic ulcers, GI bleed
81
COX-1 and 2 inhibition causes on Kidney
Na and H20 retention Hypertension Hemodynamic acute kidney injury
82
COX 1 and 2 inhibition causes on heart
Stroke MI COX 2> COX 1
83
How do COX 1 inhibitors cause mucosal injury and bleeding?
Decreased mucosal blood flow Reduced mucus and bicarb secretion Impaired platelet aggregation
84
How do COX 2 inhibitors cause mucosal injury and bleeding?
Reduced angiogenesis Impaired healing Increased leukocyte adherence Leukocyte activation
85
Risk factors associated with NSAID induced ulcers
``` Age >65 Previous peptic ulcer high-dose NSAIDs NSAID + aspirin, bisphosphonates, antiplatelet selective serotonin reuptake inhibitors H.Pylori Cigarette smoking Alcohol ```
86
GI prophylaxis for patients on chronic NSAIDs and aspirin
Add PPI or misoprostol COX-2 inhibitors are less toxic to GI vs NSAIDs, but they inhibit prostacyclin which increases CV risk Combining COX-2 with aspirin negates any GI benefits H2RAs not used Do not typically add PPI for prophylaxis but can in high risk pts
87
Misoprostol
``` PGe analog- reduces acid secretion Indicated for patients requiring NSAID therapy to prevent ulceration (secondary to PPIs) Only used in combo with NSAIDs Contraindicated in pregnancy Diarrhea 200mcg 3-4 times daily ```
88
What is the major method of toxicity for H. pylori?
Stimulates the inflammatory response (major) Ammonia is toxic to epithelial cells Increases pepsin which can degrade mucosa
89
Complications of PUD
GI Bleeding GI perforation Low risk of gastric cancer secondary to H. pylori
90
Assessment of PUD
``` Ask about NSAIDs Review meds Review medical history Ask about smoking and alcohol What relieves/worsens S/S of GI bleed ```
91
Symptoms of PUD
Pts may be asymptomatic If no ulcer= nonulcer dyspepsia Described as burning, fullness, cramping Can have belching, bloating N/V, anorexia more common with gastric vs. duodenal Gastric- food precipitates pain Duodenal- food relieves pain, but painful 1-3 hours after food
92
PUD Diagnostic testing
Labs not helpful unless bleeding (reduced hematocrit/hemoglobin and FOB) H.Pylori testing should be performed in all patients with active PUD Consider testing H.pylori in patients needing long term NSAID therapy even without PUD Endoscopy if alarm symptoms
93
What are PUD alarm symptoms
Elderly, Family h/o GI malignancy, Weight loss, Dysphagia, Bleeding
94
H. Pylori endoscopic testing Histology Culture Urease
Histology- >95% specificity and sensitivity Biopsy not recommended for initial diagnosis Culture is 100% specific Urease test is >90% sensitive and specific. Biopsy is most common for urease test for rapid results. No H2Ra or PPI for 1-2 weeks or ABX for 4 weeks prior to biopsy.
95
``` H. Pylori endoscopic testing Blood antibodies (ELISA) Blood antibodies (IgG) Urea breath test Fecal antigen ```
ELISA- less accurate than endoscopic tests, but more accurate than office tests. Antibody titers can stay positive for 6 months- 1 year after infection is treated and they are not affected by medications. IgG-Fingerstick, less accurate than ELISA. Antibody titers can stay positive for 6 months- 1 year after infection is treated and they are not affected by medications. Quick, 15 minutes Urea breath test- >95% sensitivity and specificity. Tests for ACTIVE infection; results take 2 days. No H2Ra or PPI for 1-2 weeks, no abx for 4 weeks. Fecal antigen- >95% sensitivity and specificity. Tests for ACTIVE infection; results take 2 days. No H2Ra or PPI for 1-2 weeks, no abx for 4 weeks (may cause false negative, but less important that breath test)
96
Which H. Pylori test is recommended for post treatment eradication confirmation?
Fecal or breath test
97
What is the first treatment option for H.pylori induced PUD?
PPI- BID Tetracycline- 500mg QID Metronidazole- 500mg TID-QID Bismuth- 262mg-524mg QID Duration: 14 days
98
What is the second treatment option for PUD?
PPI- BID Clarithromycin- 500mg BID Metronidazole- 500mg BID Amoxicillin- 1000mg BID Duration: 10-14 days (14 preferred)
99
What do you do with PPI after 14 days of tx for PUD?
May stop after 14 days or continue QD if bleeding ulcer.
100
Pylera
Combination of bismuth subcitrate, metronidazole, and tetracycline. Take 3 capsules QID for 10 days with PPI BID Very expensive, but FDA approved
101
What is the recommended PUD therapy if no PCN allergy or MCL exposure?
Either
102
What is the recommended PUD therapy is no PCN allergy but recent MCL exposure?
Bismuth quadruple
103
What is the recommended PUD therapy if a PCN allergy present?
Bismuth quadruple
104
What is the recommended PUD therapy if PCN allergy and recent MCL exposure?
Bismuth quadruple
105
Esomeprazole dosing for NSAID/ASA induced PUD
20mg QD for 4-8 weeks
106
Lansoprazole dosing for NSAID/ASA induced PUD
15mg QD for 4 weeks (duodenal) | 30mg QD for 8 weeks (gastric)
107
Omeprazole dosing for NSAID/ASA induced PUD
20mg QD for 4-8 weeks (duodenal) | 40mg QD for 8 weeks (gastric)
108
Pantoprazole dosing for NSAID/ASA induced PUD
40mg QD for 4 weeks (duodenal) | 40mg QD for 8 weeks (gastric)
109
Rabeprazole dosing for NSAID/ASA induced PUD
20mg QD for 4 weeks (duodenal) | 20mg QD for 6-8 weeks (gastric)
110
Treatment for NSAID induced PUD
Stop NSAID acutely while ulcer is being treated (8 weeks) If pt has a bleed on NSAID + PPI do not restart NSAID Long term tx: NSAID + PPI/misoprostol COX-2 inhibitor + PPI in high risk patients Non-NSAID therapy if possible
111
Treatment of ASA induced PUD
Typically hold ASA acutely (risk vs benefit if stent patients on DAT) Long term, if ASA has to be continued - Add PPI Do NOT switch to clopidogrel
112
Sucralfate
Can be added to PPI therapy "Coats" the ulcer to prevent further acid damage and the GI mucosa to prevent HCl back diffusion. 1g po AC and HS (given QID) Separate by 2 hours from all other medications AE: constipation, hypophosphatemia
113
Stress ulcer prophylaxis
Appropriate for ICU patients, but not general hospital patients Appropriate for some non-ICU with risk factors H2RA or PPI IV in ICU (pantoprazole, esomeprazole) Non-pharm- enteral nutrition
114
Why do ICU patients get stress ulcers?
Critical illness causes splanchnic hypoperfusion because the body shits down blood flow to organs other than heart and brain. This causes reduced HCO2 secretion, mucosal blood flow, GI motility, and a disruption of mucosal barrier. This leads to an acute stress ulcer.
115
Tx for upper GI bleed
Ensure hemodynamic stability Volume resuscitation Correct coagulopathy and/or thrombocytopenia Endoscopic hemostasis PPI- high dose bolus vs continuous infusion Correct underlying cause
116
S/S GI bleeding
Symptoms related to hypovolemia (orthostasis) Signs related to hypovolemia ( AKI, hypotension, tachycardia) Greatly elevated BUN:SCr ration Reduced hemoglobin and hematocrit Hematemesis Hematochezia (bright red blood in stool- lower GI bleed) Melena (dark blood in stool-- upper GI bleed) Fecal occult blood- either type of bleeding
117
GI bleeding Tx
``` Resuscitation- Blood and 0.9% NS Reverse INR if needed and hold meds NOACs- andexanet alpha, Idarcizumab Correct thrombocytopenia if needed PPI infusion- Esomeprazole or pantoprazole 80-mg bolus followed by 8mg/hr IV for 72 hours ```
118
Etiologies of N/V
Gastrointestinal processes, infections, acute MI, migraine, vestibular disorders, metabolic disorders, psychiatric disorders, drug withdrawal, post-op, food poisoning
119
Types of N/V in cancer
Acute- w/in 24 hours Delayed- begins after 24 hours and may last 120 hours Anticipatory- learned behavior from poorly controlled N/V Breakthrough- N/V that occurs despite prophylaxis; requires rescue Refractory- prophylactic and rescue therapy fails
120
Which patients receive prophylaxis for N/V before, during, and after chemo?
Low Moderate High
121
What are fluid and electrolyte causes for N/V in cancer patients?
Hypercalcemia (Very common due to PTH secretion of tumors) | Dehydration
122
What are drug-induced causes of N/V in cancer patients?
Opioids | antibiotics
123
What are tumor/metastases-related causes of N/V in cancer patients?
``` GI obstruction Brain melts (tumor spreads to brain) ```
124
What are misc. related causes of N/V in cancer patients?
Infection | Radiation therapy
125
Post-op N/V
Occurs within 24-48 hours after surgery #1 surgery complications Triggers- duration of surgery (risk increases by 60% for every 30 minutes) Anesthetics (inhaled)- use regional anesthetics or IV Anxiety
126
PONV risk factors
Female gender Nonsmoker (smoking induced CYP450 which allows for faster anesthetic metabolism0 H/O motion sickness or PONV Intraoperative and postoperative opioid use 1 RF= 20% Moderate risk= 40% High risk= 60-80%
127
Nonpharm treatment of PONV
``` Dietary changes Positioning (vestibular) Relaxation Biofeedback Acupuncture ```
128
N/V symptoms
Abdominal pain (pancreatitis, obstruction, PUD) Diarrhea, myalgias (viral) Headache, stiff neck, CNS findings (meningitis) Significant, unintentional weight loss (cancer) Abrupt symptoms (pancreatitis, appendicitis, gastroenteritis, food poisoning, medications) After a meal (gastroparesis)
129
Treatment options for N/V
``` Antacids Antihistamines-anticholinergics Phenothiazines Dopamine antagonists Serotonin (5HT3) receptor antagonists Neurokinin receptor antagonists Corticosteroids Benzodiazepines Cannabinoids ```
130
Antihistamines for N/V
Diphenhydramine Hydroxyzine 25-50mg PO TID-QID Meclizine 12.5-25mg PO TID-QID Scopolamine patch Adverse reactions: dry mouth, urinary retention, constipation, sedation, ataxia, confusion Drug interactions: additive anticholinergics and CNS agents
131
Phenothiazines for N/V
Promethazine (Phenergan) 6.25-25mg PO/SUPP Q6H 6.25-12.5mg IV/IM Q6H BBW for tissue necrosis in injectable route Prochlorperazine (Combazine) AE: Anticholinergic, extrapyramidal symptoms, QT prolongation, sedation (more with promethazine) Drug interactions: additive anticholinergics and CNS agents
132
Dopamine antagonists in N/V
Haloperidol Olanzapine Droperidol Metoclopramide
133
Haloperidol and Olanzapine in N/V
``` Do not use with metoclopramide Haloperidol- 1-2mg PO Q4H PRN (can be given IM or IV as well) Side effects- Confusion, drowsiness, dystonias, QTc prolongation (especially IV) Olanzapine- 10mg PO (can give IM or IV as well) Side effects- Somnolence, dystonias Better tolerated than haloperidol ```
134
Droperidol
Excellent antiemetic but rarely used BBW for torsades Side effects similar to that of haloperidol, but also hypotension and tachycardia
135
Metoclopramide
5-10mg AC and HS (gastroparesis); 10-40mg PO/IV Q6H PRN for chemotherapy Dosed as high as 1-2mg/kg before chemo Side effects- Dystonias (including tardive dyskinesia-long term), drowsiness, diarrhea Reduce dose by 50% for CrCl <40mL/min Can increase risk of seizures Should be given before meals
136
5HT3 Receptor Antagonists for N/V
Dolasetron Granisetron Ondansetron Palonosetron All have a risk of QTc prolongation (dose dependent) Ondansetron interacts with strong 3A4 inhibitors
137
5HT3 Receptor antagonists drug information
Palonosetron has a long half life (QD dosing) Dolasetron lost FDA approval for CINV due to risk of torsades Ondansetron carries the most DDI due to substrate for CYP 1A2, 2D6, and 3A4. Watch with amiodarone, quinolones, macrolides, antipsychotics, azoles, and many more
138
Neurokinin Receptor Antagonists for N/V
Aprepritant (PO), Fosprepitant (IV) Rolapitant, netuplitant, fosnetupitant- PO Indicated only for highly emetogenic regimens Drug interactions- Induces CYP2C9, reduces warfarin efficacy Inhibitor and substrate of CYP3A4 (use in caution with strong 3A4 substrates (statins, azoles, macrolides) AE- fatigue, hiccups, weakness
139
Corticosteroids for N/V
Dexamethasone most common Utilized in low, moderate, and highly emetogenic regimens Good for delayed N/V Avoid in immunotherapies and cellular therapies Utilizes in non-chemo N/V Typically used 3-4 days so limited AE, but hyperglycemia, mood disturbances, delayed wound healing, and dyspepsia may be present
140
Benzodiazepines for N/V
Lorazepam- 0.5-2mg IV/PO Q4-6 H AE: somnolence, impaired memory and cognition, gait disturbance, irritability Good for anticipatory N from chemo and anxiety-related N/V Watch with other CNS depressing drugs
141
Cannabinoids for N/V
Dronabinol (Marinol) MOA- opposes serotonin in CTZ AE- abnormal thinking, appetite stimulation, euphoria, paranoia, may lower seizure threshold, habit-forming Caution with other CNS depressants Often used chronically in cancer/AIDS for appetite and nausea
142
Approaches to treatment in N/V patients
Viral gastroenteritis and other self-limiting conditions - Identify and treat underlying cause - Hydration - PRN promethazine ``` Gastroparesis -Metoclopramide Erythromycin is secondary -Optimize diabetic control -D/C opioids and anticholinergics ```
143
Vertigo
Vomiting after head motion Meclizine or hydroxyzine Promethazine second line
144
Motion sickness
Diphenhydramine, dimenhydrinate, or scopolamine
145
Chemotherapy- induced N/V high risk regimen
Day 1 (before chemo)- NK-1RA, 5-HT3 RA, and dexamethasone Day 2- Aprepitant (only if used on day 1) and dexamethasone Day 3-Aprepitant (only if used on day 1) and dexamethasone Day 4- Dexamethasone Olanzapine can be added to each days treatment regimen
146
How do you reduce baseline risk in post op NV
Use regional anesthesia Use IV anesthesia (propofol preferred) Minimize intraoperative and postoperative opioids Adequate hydration
147
PONV prophylaxis
Dexamethasone, promethazine at beginning of surgery Dolasetron, granisetron, ondansetron, droperidol, haloperidol can all be given at end of surgery Scopalamine patch- prior evening or 4 hours before surgery Choose 2 of the above if moderate-high risk
148
PONV treatment
Initially 5HT3 antagonist If failed prophylaxis choose 1 or 2 agents from a different class Control pain Give fluids
149
N/V in pregnancy
Caused by elevated hCG and estrogen Hyperemesis gravidarum- requires hospitalization can cause hypokalemia, dehydration, weight loss more than 5%, ketonuria Treat with Vit B +doxylamine, OTC ginger, dimenhydrinate If not dehydrated add metoclopramide or ondansetron PO If dehydrated do IV
150
What are the types of acute diarrhea?
``` Osmotic Inflammatory Infectious Secretory Altered motility ```
151
Chronic diarrhea
Any of acute, PLUS diabetes IBD Hyperthyroidism
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Presentation of diarrhea and potential cause
Typically self-limiting Stool analysis Fever? probably infectious Blood? Pain? Either infectious or inflammatory Severe dehydration/hemodynamic instability? May need to hospitalize.
153
Supportive treatment of diarrhea
``` Treat underlying cause Fluids and electrolytes Oral vs IV fluids depending on severity Can have hypo or hypernatremia Hypokalemia common Bicarb loss with resultant metabolic acidosis ```
154
Treatment options for diarrhea
Adsorbents/bulk-forming agents first- pull water out of stool -polycarbophil, psyllium, methylcellulose, aluminum hydroxide, kaolin-pectin, cholestyramine Opiate-like agents if bulk forming do not work Delay onset of intraluminal contents Loperamide, diphenoxylate- atropine, difenoxin-atropine Antisecretory agents- bismuth subsalicylate Ocreotide
155
Loperamide
Imodium Agonizes intestinal opioid receptors to slow GI motility 4mg once then 2mg after each unformed stool (max 16mg/day) Well tolerated 1st line after bulk-forming agents
156
Diphenoxylate and Difenoxin
``` Diphenoxylate-atropine (Lomotil) Agonizes central and intestinal opioid receptors to slow GI motility Atropine is used to discourage abuse 5mg PO TID-QID DDI: Do not give with MAOIs, linezolid AE: drowsiness, dizziness, HA ``` Difenoxin-atropine (Motofen) Active metabolite of diphenoxylate Does not cross BBB, non CNS effects
157
Ocreotide
Somatostatin analog Blocks serotonin, inhibits intestinal secretion and stimulates intestinal absorption Used for tumor related secretory diarrhea
158
Treatment of infectious diarrhea
C.diff - stop offending agents if possible - Oral Vanc or fidaxomycin - Probiotics for prophylaxis - Fluids - Do NOT give antidiarrheals Travelers diarrhea
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Diverticulosis and Diverticulitis
Diverticulum- Outpouching of intestinal wall Diverticulosis- the presence of diverticula Diverticulitis- the inflamed diverticuli. Acute, left sided abdominal pain, diarrhea or constipation Bleeding is uncommon Diverticulitis classification Complicated- Abscess, obstruction, peritonitis Uncomplicated- colon wall thickening only
160
Tx of acute diverticulitis
Abx recommended in complicated. May be reasonable in uncomplicated If fever or signs of infections use abx Clear, liquid diet Pain control
161
Celiac disease
Inflammatory diarrhea that results in malabsorption Gluten insensitivity Evaluate iron, folic acid, B-12 and Vit D Steroids may be helpful for refractory patients
162
`Mucositis
Inflammation/ulceration of Gi tract from chemotherapy and/or radiation Prevent using H2Ra or PPI Can cause both constipation or diarrhea, but more commonly diarrhea Tx- Hydration, loperamide, octreotide if loperamide failed
163
Constipation
Fewer than 3 bowel movements/week
164
GI causes of constipation
IBS Diverticulitis Hemorrhoids Obstruction (cancer)
165
Metabolic/endocrine causes of constipation
Diabetes hypothyroidism Hypercalcemia
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Lifestyle causes of constipation
Pregnancy Inadequate fluid Low fiber Sedentary lifestyle
167
Neurogenic/Psychogenic causes of constipation
Stroke Spinal cord/brain injury Psychiatric diseases
168
Drug induced constipation
Slow motility- opioids, anticholinergics (antihistamines/phenothiazines, CNS agents, urinary incontinence agents), CCVs, aluminum and calcium antacids, iron
169
Alarm symptoms of constipation
Hematochezia, melena, family H/O colon cancer, IBD, anemia, weight loss, anorexia, N/V Colonoscopy if any are present!
170
Treatment of constipation non-pharm
Increase fluids and fiber | Increase activity
171
Fiber
Fiber- bulk-forming, increases frequency of defecation by retaining water in intestine and increasing GI motility Examples- psyllium, methylcellulose and polycarbophil
172
Laxatives for constipation treatment
Step-wise approach Bulk-forming (Fiber) Stool softeners- allows water and lipids to penetrate stool Osmotic- fluid accumulation/binding, stimulates peristalsis Stimulant laxatives- mucosal irritation that stimulates peristalsis
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Bulk-forming laxatives and onset
Fiber | 1-3 days
174
Softener laxatives and onset
Docusate 1-3 days Used preventative
175
Lubricant laxative and onset
Mineral oil 1-3 days Not used often due to aspiration risk
176
Osmotic laxatives and onset
``` Lactulose, sorbitol- 1 day PEG (miralax)- 1 day Mag citrate- 1-6 hours Sodium phosphate- 1-3 hours PEG (GOLYTELY)- Rapid ```
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Stimulant laxatives and onset
Bisacodyl- 1-12 hours Senna- 6-12 hours Mag citrate- 1-6 hours Glycerin suppository- 30 minutes
178
Dosing: Psyllium Docusate Mineral oil
Psyllium- 4-6g/day Docusate- 100mg po BID Mineral oil- 15-45ml po once
179
Dosing: Lactulose, sorbitol PEG (Miralax) Bisacodyl
Lactulose- 15-30mP QD, or 30 150mL once PEG (miralax)- 17g QD Bisacodyl- 10mg PO or PR QD
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``` Dosing: Senna Mag citrate Glycerin supp PEG (GoLYTELY) ```
Senna- 1-2 tbs PO BID Mag citrate- 150-300mL PO once Glycerin supp- Suppository once PEG(GoLYTELY)- 4000ml once
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Lubiprostone
Amitiza Chronic idiopathic constipation, IBD- constipation, or opioid induced constipation Activates Cl channels which increase intestinal fluid secretion. Softens stool, increases motility, promotes BM Not systemically absorbed Takes 24 hours to 1 week to work Do not give to patients with GI obstruction AE- N/D Dosing- 24mcg BUD (CIC) or 8mg BID (IBS-C)
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Linaclotide and Plecanatide
Linzess- liaglutide and Trulance- Plecanatide Chronic idiopathic constipation or irritable bowel constipation Increases cGMP which increases Cl and bicarb secretion into intestine which increases intestinal fluid and GI mobility DO not give to patients with GI obstruction ADE- Diarrhea BBBW- dehydration in pediatric patients
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Opioid- induced constipation
Opioids agonize mu receptors in gut smooth muscle, reducing GI mobility Tolerance to this adverse effect does not develop Use lowest possible opioid dose Scheduled, stimulant laxatives with routine opioids -Docusate and senna 2 tabs BID most common Stimulant must be part of both treatment and prevention regimen
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Methylnaltrexone
``` Relistor Opioid induced constipation Mu receptor antagonist Contraindicated in GI obstruction Oral and SubQ Needs to be renally dosed AE- abdominal pain, gas, N, diarrhea Treatment only, not prevention 450mg QD (PO) 12mg SQ QD ```
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Naloxegol (Movantik)
``` Naloxone conjugated with a PEG polymer so cant cross BBB Mu receptor antagonist Contraindicated in GI obstruction and strong 3A4 inhibitors Oral AE- abdominal pain Renal dosing Treatment only, not prevention 25mg QD ```
186
Naldemedine (Symproic)
``` Mu receptor antagonist Opioid induced constipation Treatment only not prevention Contraindicated in GI obstruction and strong 3A4 inhibitors Oral AE- abdominal pain Does NOT need renal dosing 0.2mg QD ```
187
OIC treatment algorithm
Prevent using stimulant +/- stool softener Tx- increase dose of stimulant and add stool softener if not on Opioid reduction Peripherally acting mu-receptor antagonist
188
Post Operative Ileus
Use Alvimopan (Entereg)- causes transient inhibition of GI motility after surgery Selective mu receptor antagonist BBW- only for short term (15 doses) Contraindicated in patients taking more than 7 days of opioids prior to alvimopan
189
Laxative abuse
Trying to maintain daily bowel movements (elderly) Trying to lose weight Taking routinely can cause dependence Can lead to serious health concerns Aluminum- osteomalacia Fluid and electrolyte abnormalities Cathartic colon
190
Irritable bowel
Affects young women most commonly S/S- chronic abdominal pain, bloating at least for 3 months Diarrhea, constipation, or both Depression and anxiety are common comorbidities Pain often relieved with defecation Food is common precipitant
191
Treatment of IBS with constipation predominant
Fiber Do not use osmotic laxatives Lubriprostone, Linaclotide, Tegaserod are last line Tegaserod is emergency use only due to CV events
192
Treatment of IBS with diarrhea predominant
Dietary changes Loperamide not helpful Alosetron- 5HT3 antagonist, indicated in women, restricted use due to severe AE Eluxadoline- mixed mu receptor agonist. Causes CNS depression, pancreatitis, hepatitis
193
Symptom control in IBS
Probiotics- helps bloating and flatulence Antispasmotics- dicyclomine (Bentyl)- 30mg PO QID, increase to 40mg QID after 1 week. Anticholinergic AE Peppermint oil has potential benefit Tricyclic antidepressants- Analgesic effect, not used often
194
Types of IBD
Ulcerative colitis and Crohns disease
195
Complications of crohns disease
Inflammation Stenosis Fistula
196
Ulcerative colitis depth and location
Depth- Mucosa and submucosa | Location- Rectum and colon
197
Ulcerative colitis fistulas, strictures, bleeding
Fistulas- rare Strictures- rare Bleeding- common >90%
198
Ulcerative colitis abdominal pain, distribution, diarrhea, characterization
Abdominal pain- Unusual Distribution- Continuous Diarrhea- 10-30% Characterization- "Steady" disease
199
Crohns disease depth and location
Depth- Transmural | Location- Terminal ileum, but can occur at any part of the GI tract
200
Crohns disease fistulas, strictures, bleeding
Fistulas- common Strictures- common Bleeding- Common (<50%) but less severe than UC
201
Crohns disease abdominal pain, distribution, diarrhea, characterization
Abdominal pain- common Distribution- Discontinuous Diarrhea- >70% Characterization- Flares alternating with remission
202
Local complications of UC
Toxic megacolon- ulceration extends below submucosa (perforation), high fever, elevated WBC, and tachycardia present Significantly higher risk of colon cancer
203
Local complications of crohns disease
Hemorrhage Perforation Obstruction Cancer
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Systemic complications of both UC and CD
Hematobiliary- fatty liver, hepatitis, cirrhosis, cholangiocarcinoma, gallstones Joints- arthritis (asymmetric) Ocular- Iritis and uveitis (blurred vision, eye pain, and photophobia) Dermatologic- erythema nodosum, pyoderma gangrenosum
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Clinical presentation and work up of CD
Abdominal findings- cramping, pain, chronic diarrhea, nausea, vomiting, weight loss Symptoms related to systemic manifestations- blurred vision, arthritis, skin findings DC NSAIDS Colonoscopy
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Clinical presentation and work up of UC
Abdominal findings- Pain, hematochezia (blood in stool), need to rule out C. Diff Symptoms related to systemic manifestations- blurred vision, arthritis, skin findings DC NSAIDS Colonoscopy
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Pharmacologic treatment for IBD
``` Aminosalicylates (5-ASA) (first) Corticosteroids Antimicrobials Immunomodulators Biologics (last) Supportive- enteral and parenteral nutrition in severe disease ```
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Sulfasalazine in IBD
``` Not as commonly used No benefit to sulfa group and contributes to AE Sulfa antibiotic + mesalamine Mesalamine is the active ingredient Avoid in sulfa and aspirin allergies AE- GI disturbances, HA, arthralgias Response correlates with dose Folic acid supplementation needed ```
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Mesalamine derivatives in IBD
Mesalamine - avoid in ASA allergy - Oral products- GI AE , HA - Rectal- flatulence, HA - If extended or DR, do not open crush or chew - Give with meals if GI AE Mesalamine derivatives - Olsalazine-diarrhea - Balsalazide- HA, GI
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Corticosteroids for IBD
Prednisone 40-60mg/day Rate of taper depends on dose and duration Use IV for acute flares (hydrocortisone, methylpresnisolone) Budesonide (Entocort)- works in terminal ileum. Limited systemic absorption due to extensive first pass metabolism
211
Steroid AE
``` Hyperglycemia Hypertension Osteoporosis Acne Fluid retention Weight gain Psychosis Increased susceptibility to infection Cataracts, glaucoma ```
212
Antibiotics in IBD
Not used as monotherapy Metronidazole- 500mg PO Q8H Interactions- warfarin, disulfiram-like with alcohol AE- N, metallic taste, paresthesias
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Azathioprine/ 6-Mercapropurine in IBD
Azathioprine is metabolized in 6-MP Drug interactions- allopurinol decreases elimination and can cause significant hematologic toxicity AE- N, fever, rash, arthralgia, infection, pancreatitis BBW- myelosuppression, neoplastic disease 6MP- hematologic toxicities, pancreatitis
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Methotrexate for IBD
Weekly IM Bone marrow suppression, folic acid deficiency BBW- hepatotoxicity, lymphoma, exfoliative dermatitis, diarrhea and ulcerative stomatitis, pulmonary toxicity, increased risk of opportunistic infections, drug clearance is reduced in ascites, renal impairment, and pleural effusions
215
Cyclosporine in IBD
IV infusion Drug interactions- statins, macrolides, azoles, diltiazem, verapamil. AE- nephrotoxicity, hyperlipidemia, HTN
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Biologics for IBD
Antibodies to TNF-alpha Selective adhesion molecule inhibitors IL12/IL23 inhibitor JAK inhibitors
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Antibodies to TNF-a
Blocks binding to its receptors, decreasing immune response | Infliximab, adalimumab, certolizumab, golimumab
218
Selective adhesion molecule inhibitors
Blocks adhesion of lymphocytes to epithelium | Natalizumab, vedolizumab
219
IL12/IL23 inhibitor
Reduces the inflammatory response by blocking the secretion of IL-6, IL-17, and TNF-a Ustekinumab (Stelara)
220
JAK inhibitors
JAK signals IL12 and IL23 | Tofacitinib
221
Infiliximab
5mg/kg weeks 0,2, and 6 (induction) then 5mg/kg every 8 weeks for maintenance. Only induction is infusion BBW- infections (TB, sepsis, fungal and other opportunistic infections), increased risk of lymphoma in adolescent or young adult males (also in receiving AZA or 6MP concomitantly) Must have TB test before initiating
222
Infliximab toxicities
Infusion reactions Premedicate with APAP, diphenydramine, and possibly steroids Autoimmune reactions- lupus, hemolytic anemia
223
Adalimumab, certolizumab, and golimumab toxicities
SQ administration- injection site reactions | May worsen/cause HF
224
Vedolizumab and natalizumab toxicities
May increase risk of infections and liver injuries
225
Ustekinumab toxicities
Test for TB before initiating | May cause hypersensitivity reactions and increase risk for infections
226
Tofacitinib toxicities
Test for TB before initiating
227
Which biologics have a BBW for increasing lymphoma and infection risk?
Infliximab, adalimumab, certolizumab, golimumab
228
Which biologic has the BBW of PML?
Natalizumab
229
Which biologics have no BBW?
Vedolizumab, usetkinumab
230
Which biologic has a BBW for increasing lymphoma, VTE, and infection risk?
Tofacitinib
231
Treatment of active UC- mild-moderate diseases
Mild-moderate extensive disease- 5-ASA oral agents, corticosteroids (budesonide) if 5-ASA failed Mild-moderate distal disease- 5-ASA topical agents
232
Treatment of active UC- severe
Steroids, anti-TNF (refractory to steroids), cyclosporine if hospitalized Use vedolizumab, tofacitinib, or golimumab as alternative to anti-TNF
233
Do you use AZA/6MP or antibiotics in active UC?
No
234
Prevention of relapse of UC
5-ASA agents-oral (dont use with anti TNF) 5-ASA agents- topical if distal disease in combo with oral AZA/6MP- Especially if anti-TNF was used in combo, effective if steroids were effective or cyclosporine was effective Can use infliximab, vedolizumab, golimumab, or tofaxitinib if responded to active treatment
235
Treatment of active CD
Steroids for all (parenteral agents in severe) Intramuscular MTX Anti-TNF in moderate to severe disease (including fistulizing), steroid-resistant disease Natalizumab or vedolizumab only if anti-TNF failed Ustekinumab- last line if everything as failed Metronidazole/Cipro if fistulizing
236
Prevention of relapse CD
AZA/6MP in combo with anti-TNF | Natalizumab, vedolizumab, ustekinumab if worked acutely
237
Treatment of toxic megacolon
Supportive measures -Fluids and electrolytes -D/C meds that slow motility (anticholinergics, opiates) Empiric Abx- broad spectrum, gram neg anaerobes High dose IV steroids Emergent and surgical intervention
238
Indications for surgery
``` Life threatening hemorrhage Perforation Cancer Toxic megacolon Failure of or intolerance to maximal medical therapy Obstruction Abscess not amenable to drainage ```
239
IBD and pregnancy
Mesalamine and sulfasalazine are acceptable -All category B (except Asacol, C) Folic acid should be given with sulfasalazine Do not use steroids, azathioprine, or mercaptopurine- D MTX- category X Infliximab, adalimumab, certolizumab, and golimumab are category B
240
Acute pancreatitis
Rapid onset, generally no long term complications if patient survives acute attack Severe abdominal pain Acutely elevated pancreatic enzymes
241
Chronic pancreatitis
Multiple attacks without correction of risk factors -Progressive inflammation and long-standing injury Anatomical and functional compromise- irreversible Chronic abdominal pain Pancreatic enzymes may not be elevated
242
Causes of acute pancreatitis
Gallstones, alcohol, and hypertriglyceridemia (>1000) most common causes can also be caused by infections, hypercalcemia, abdominal trauma, IBD, etc.
243
Medication causes of acute pancreatitis
``` Azathioprine Estrogens Furosemides Steroids Opiates Sulfonamides Propofol Tetracycline Statins Valproic acid Thiazides ACE-Is ```
244
How do ACE-Is cause acute pancreatitis?
Local angioedema
245
How do estrogen/OC/HRT cause acute pancreatitis?
Microemboli | Hypertriglyceridemia
246
How do statins cause acute pancreatitis?
Directly toxic | May be related to myalgias/rhabdo
247
How do diuretics cause acute pancreatitis?
Loops- directly toxic | Thiazides- hypercalcemia, hypertriglyceridemia
248
How does valproic acid cause acute pancreatitis?
Directly toxic
249
How do azathioprine, sulfonamides, and tetracyclines cause acute pancreatitis?
Hypersensitivity reactions | These are the same drugs that cause AKI
250
Clinical presentation of acute pancreatitis
Moderate to severe abdominal pain -Radiates to upper quadrants or back -Described as "knife-like", constant, severe -Aggravated by eating N/V Cullens and Grey-Tuners signs (rare)- blood accumulations More severe pancreatitis- hypotension, renal failure, fever, diminished bowel sounds, dyspnea and tachypnea
251
Laboratory findings in acute pancreatitis
Leukocytosis (inflammation vs infection) Hyperglycemia Hemoconcentration due to dehydration (Hematocrit, BUN, creatinine all elevated) Hypocalcemia and Hypoalbuminemia Elevated C-reactive protein (CRP) - Good marker for severity buy delayed (72h) Elevated pancreatic enzymes
252
Amylase in pancreatitis
60-180units/L Rise 4-8 hours after initial attack, peak at 24 hours, return to normal over 3-5 days Not specific to pancreas
253
Lipase in pacreatitis
<200units/L Specific to pancreas Longer half life than amylase so may remain elevated after amylase returns to normal Takes longer to rise than amylase
254
What amylase or lipase values are diagnostic of pancreatitis?
>3x ULN | Elevations do not correlate with etiology or severity of disease
255
Prognostic criteria pancreatitis
Ransons criteria- specific to pancreatitis, 11 variable assessed on admission and 48 hours later Apache II score- ICU prognosis predictor, 12 variables within 24 hours, best predictor of severity CT severity index- measures inflammation and necrosis Atlanta scoring system-combines all 3, research only
256
Management of acute pancreatitis
Remove cause or treat underlying condition Pancreas "rest: clear fluids and advance diet slowly when pain subsides (try to feed in 24 hours). Enteral or parenteral nutrition if npo >5 days Fluid management Pain and nausea control Treat infections Surgery (cholecystectomy)
257
G-tube vs J-tube
G-tube is in the stomach | J-tube is in the jejunum
258
Fluid management for acute pancreatitis
Volume depletion due to "third spacing" of intravascular fluid due to inflammation and increased capillary membrane permeability Reduction in intravascular volume can lead to reduced perfusion of key organs (acute renal failure, pancreatic necrosis, hemodynamic instability) Aggressive IV fluids (NS or LR) -Patients may need >5L fluid in first 12-24 hours Monitor vital signs, urine output, hematocrit, BUN
259
Pain and Nausea control for pancreatitis
Narcotics are mainstay -Hydromorphone (Dilaudid) preferred Morphine is also reasonable PCA who need frequent narcotic dosing Promethazine and serotonin antagonists (Zofran) for N
260
Infections in pancreatitis
Not common Prophylactic abx not recommended Indicated if infected necrosis found -sterile necrosis should not be treated unless patient deteriorates -Account for some of the mortality in acute pancreatitis -Avoid abx if possible.
261
Octreotide
Potent inhibitor of pancreatic enzyme secretion May reduce mortality Reserved for severe acute pancreatitis Doses studied- 0.1mg SQ Q8H, 0.5mcg/kg/hr by continuous infusion
262
Complications of acute pancreatitis
Local- acute fluid collection, pancreatic necrosis and abscess, pseudocyst Systemic- shock, hypotension, acute renal failure, acute respiratory distress syndrome, GI bleeding Chronic pancreatitis
263
Chronic pancreatitis cause
Irreversible damage Alcohol (inflammation-> necrosis -> fibrosis) Idiopathic Gallstones are not associated with chronic pancreatitis
264
Symptoms of chronic pancreatitis
Chronic low-level abdominal pain Fat malabsorption due to decreased production of enzymes (steatorrhea) Malnutrition Weight loss, nausea Diabetes (bc of lack of insulin production) Enzymes are typically not elevated
265
Treatment of chronic pancreatitis
``` No alcohol! Control of pain Give pancreatic enzymes Insulin if diabetes Smaller, more frequent low-fat meals ```
266
Complications of chronic pancreatitis
Malabsorption Chronic abdominal pain DM Pancreatic cancer
267
Pancreatic enzymes
Treatment for chronic pancreatitis Amylase, lipase, protease Helps with malabsorption, steatorrhea, osmotic diarrhea, pain, slows progression
268
Dose of pancreatic enzymes
Based on lipase content 25000-40000 units lipase per meal, half for snack Not interchangeable
269
Lipase in creon, zenpep, pancreaze
Creon- 3,000-24,000 units Zenpep- 3,000-25,000 units Pancreaze- 4,200-21,000 units
270
Lipase in ultresa, viokace, pertzye
Ultreza- 13,900-23,000 units Viokace- 10,440-20,880 Pertyze- 8000-16,000 units
271
Pancreatic enzymes counseling points
Avoid in pork allergy Take with meals or snacks Do not crush or chew enteric coated formulations Avoid taking with calcium or magnesium antacids AE- stomach upset, nausea, diarrhea, hyperuricemia, oral and perianal irritation
272
Treatment of abdominal pain in chronic pancreatitis
``` Non-narcotic choices given before meals -tylenol, NSAIDs, Tramadol Pancreatic enzymes -High doses of proteases (non-enteric coated so they work in duodenum) Many patient need narcotics ```
273
Pancreatic cancer
Very poor prognosis Often presents when inoperable or metastasized 5 year survival rate of 5% Risk factors- smoking, obesity, chronic pancreatitis Symptoms- abdominal pain, jaundice, weight loss, hyperglycemia
274
Enteral nutrition
via the gastrointestinal tract | GI tract contains about 75% of its nutrition from the gut mucosa so preferred
275
Parenteral nutrition
Via the vascular system, usually venous Limited to 900-1000mOsm/L For every 1% there are 50mOsm/L For every 1% AA there are 100mOsm/L
276
TPN vs PPN
Total parenteral nutrition given through central line | Peripheral parenteral nutrition given through peripheral system
277
Ileus
Decreased peristalsis resulting in decreased bowel sounds, painful distended abdomen, N, V
278
-ostomy
New functional opening
279
Gastric residual
Volume retrieved from the stomach upon aspiration of gastric contents through a gastronomy tube; generally, if >200mL you are intolerant of enteral nutrition
280
Fistula
Abnormal communication between two epithelial cell lines
281
Marasmus
``` Chronic protein and calorie malnutrition Decreased energy intake vs. increased energy expenditure Visceral protein (albumin, prealbumin) production preserved ```
282
Kwashiorkor
Acute or chronic protein malnutrition; adequate calorie intake Decreased synthesis vs decreased intake Marked depletion of visceral proteins
283
Why does malnutrition occur with critical illness?
Immune system activates SIRS (systemic inflammatory response syndrome) which causes increased oxygen energy demand, leading to catabolism causing malnutrition Also, the mobilization of fatty acids, proteins, and glucose causes catabolism leading to malnutrition
284
Rehabilitation
Loss of skeletal muscle mass; weakness
285
What are the risks for malnutrition in the ICU?
Stressors- SIRS, infection, trauma Previous history of malnourished (EtOH) NPO
286
Visceral proteins
Synthesized from the liver by dietary amino acids | Prealbumin has a half life of 3 days and is used in acute phase
287
Weight considerations for nutrition
ABW= IBW + 0.25(ABW-IBW) | If ABW >130% of IBW use adjusted
288
Nutritionally at-risk adults
Involuntary weight loss of 10% of usual body weight within 6 months or 5% within 1 month Involuntary loss of 10 pounds within 1 month BMI less than 18.5 Increased metabolic requirements Inadequate intake
289
calorie vs Kcal
calorie- amount of energy required to raise the temp of 1 mL of water by 1 C Kcal- amount of energy required to raise the temp of 1 L of water by 1 C
290
How long can you live without food and water?
Food- 60 days | Water- 5-7
291
Macronutrients
Carbohydrates (Dextrose)- 3.4Kcal/g Protein (AA)- 4Kcal/g; 0.16g nitrogen Lipid- 10Kcal
292
Micronutrients
Vitamins Minerals Trace elements
293
What is the basic composition of nutrition?
Macronutrients Micronutrients Electrolytes Water
294
Basal energy expenditure vs Resting energy expenditure
Estimate (calculation) based on demographics | REE- measure
295
Empiric strategy for estimation of energy requirements
Maintenance- 20-25kcal/kg/day Critically ill- 25-30kcal/kg/day Trauma- 30-35kcal/kg/day Burn- 35-50kcal/kg/day
296
Empiric strategy for estimation of protein requirements
Maintenance- 1-1.5g/kg/day Critically ill- 1.5-2g/kg/day Trauma- 2-2.5g/kg/day Burn- 2-2.5g/kg/day
297
What is a caloric recipe?
Dextrose 50-60% (max 7g/kg/day) Protein 20-30% (max 2.5g/kg/day) Lipids 10-20% (max 2.5g/kg/day)
298
Daily fluid provisions
Should provide 30-35 mL/kg/day unless contraindicated Watch for sensible and insensible water loss Monitor 24 hour in and outs and volume parameters
299
Potassium
Major intracellular cation (130mEq/L Normal serum 3.5-5 Require 0.5-1mEq/kg/day Involved in action potentials, movement of glucose
300
Magnesium
Fourth major cation (1500mEq total) Mainly found in bone Normal serum Mg 1.3-2.1mg/dL There is an innacurate reflection of intracellular cells, need ionized Mg but not common Require 20mEq/day (240mg/day) Involved in ATP-mediated actions, ion transport, calcium channel activity, nerve conduction
301
Phosphorous
``` Major intracellular anion (700g total) Predominantly found in bone Normal serum Phos 2.5-4.5mg/dL Poor reflection of total body stores Require 1000mg/day ``` Involved in cellular energy, resp function, myocardial contractility, glucose utilization
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How do you determine if the gut is working?
``` Succus entericus- 7L/day Oral-1500 Gastric-1500 Duodenal- 1000 Pancreas- 500 Ileum-3000 ``` Assess if pt is having pain or is having bowel movement
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When would you use a PPN?
``` Need nutrition and cant get TPN Acute or chronic bowel obstruction Severe ileus Prolonged inflammatory bowel disease Enteric fistula Severe shock Inability to tolerate enteral route ```
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Timing of nutrition
Earlier the better burns> trauma> surgery> medicine After 7 days for well nourished patients, within 24 hours for burns Within 3-5 days for nutritionally at risk patients Start at about 25-30% goal rate and titrate
305
Refeeding syndrome
``` Electrolyte and fluid abnormalities resulting from reintroduction of energy in the face of chronic or accelerated malnutrition; energy hyper-utilization Hypophosphatemia Hypomagnesemia Hypokalemia Gluconeogenesis (hyperglycemia) Fluid shifts ``` Prevent by aggressive supplementation of phos, k, mag before and during nutrition
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Nutritional endpoints
Weight- Nonspecific Visceral Proteins- Albumin (half life is too long to evaluate) Transferin- may be falsely elevated Prealbumin- preferred Retinol-binding protein- used due to short half life Nitrogen balance If Nin > Nout= anabolic
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Approach for providing nutrition support
``` Assess need and optimal route Estimate protein, caloric, and volume needs Choose enteral or parenteral formula Calculate goal rate and formula Assess risk for refeeding syndrome Initiate treatment ```
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IV electrolyte replacement
Identify cause (diuretics, oral calcium, refeeding syndrome) Know ICU/hospital policy Always replace Mg before or with K Watch renal function and give 50% dose of Mg, K, and phos if needed
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Infusion times for electrolytes
K- Central (20meq/L) and peropheral (10meq/L) Mg- 1g/hr Phos- 7.5mmol/hr