Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics II > Exam 5 > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Typical presentation of GERD

A

Heartburn
Acid regurgitation
Belching
Bloating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Atypical presentation of GERD

A 
Chest pain
Laryngitis/hoarseness
Asthma
Insomnia
Chronic cough
Aspiration pneumonia
Tooth decay
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Alarm S/S of GERD

A 
Needs to be evaluated:
Severe dysphagia
Odynophagia
Weight loss
Persistent vomiting
Bleeding
Hematemesis
Anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment goals for GERD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of mild/intermittent heartburn

A

Lifestyle changes
Antacids
OTC H2RAs
OTC PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of GERD

A

Lifestyle changes
Rx-strength H2RAs
Rx PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of erosive or moderate/severe symptoms

A

Lifestyle changes
Rx PPIs
High Dose PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

AE of H2RAs

A

HA, dizziness, diarrhea, constipation, fatigue

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

OTC PPIs

A

Omeprazole
Lansoprazole
Esomeprazole
Omeprazole-sodium bicarb

Dont use for more than 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Omeprazole

A

20mg QD for all indications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lansoprazole

A

15mg QD for mild heart burn and GERD

30mg QD for 8 weeks then 15mg QD for erosive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Esomeprazole

A

20mg QD for mild heartburn and GERD

20-40mg QD x8 weeks then 20mg QD for erosive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Rabeprazole

A

20mg QD for GERD and erosive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pantoprazole

A

40mg QD for GERD and erosive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Dexlansoprazole

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

PPI dosing

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Omeprazole-Sodium Bicarb (Zegerid)

A

IR

Doesnt need to be enteric coated because bicarb increases the stomach pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

PPI drug interactions

A

Iron, azoles (acidic environment needed)
Warfarin- omeprazole only
Clopidogrel- prevents metabolism of clopidogrel due to CYP2C19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

PPI AE

A 
HA
Dizziness
Possible vitamin/mineral deficiencies:
B-12
Iron
Magnesium
Calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

PPI Concerns

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Reasons for PPI failure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Maintenance PPI therapy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

GERD therapy adjustments

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Metoclopramide (Reglan)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Surgery for GERD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Special populations- Pediatrics and GERD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Special populations- Pregnancy and Lactation and GERD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Counseling Questions for GERD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the pathophysiology of GERD?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Drugs that worsen GERD

A

CCB
caffeine
nicotine
Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Hiatal hernia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Pathophysiology of reduced esophageal clearance

A 
Reduced peristalsis (achalasia)
Prolongs time refluxed food material is in contact with esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Pathophysiology of mucosal resistance

A

Esophageal mucosal layer doesnt produce mucus or respond to bicarbonate neutralization.
Happens frequently in the elderly due to decreased saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Pathophysiology of delayed gastric emptying

A

Increased gastric volume increases frequency of reflux as well as amount of refluxate
Common in diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Mucosal defense mechanisms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

H. pylori

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How do NSAIDs cause peptic ulcer disease?

A

The inhibition of COX1 results in reduced mucus and bicarbonate secretion and impaired platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

1st line N/V treatment in chemo

A

Serotonin receptor blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Types of diarrhea

A 
Osmotic
Inflammatory 
Secretory
Infectious 
Altered motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Osmotic diarrhea

A 
Poorly absorbed intestinal substances (carbs) retain water within the intestine. 
Carbohydrate malabsorption  (lactose intolerance), Mg-containing medications, lactulose, sorbitol
Fasting reduces stool volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Inflammatory diarrhea

A

Blood, protein, or mucus from an inflamed or ulcerated mucosa
-Ulcerative colitis and Crohns disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Lactose intolerance

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Secretory diarrhea

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Acute infectious diarrhea

A

Bacterial- C. diff, shigella, E.coli, campylobacter, salmonella
Viral- gastroenteritis
Parasitic- giardia, cryptosporidium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Altered motility

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Causes of secondary constipation

A

Hypercalcemia- gut atony
Hypothyroidism- slows digestive contraction
Parkinsons disease- lack of dopamine to stimulate peristalsis
Diabetes- gastroparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Secondary medication causes of constipation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

IBD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Pathophysiology of IBD

A 
Alteration of makeup of intestinal microbiota
Disruption of mucus layer
Dysregulated immune activity
Genetic factors
Environmental factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Gut microbiome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Intestinal immune system

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Intestinal epithelium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Immunopathophysiology in IBD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Biliary tree

A

In pancreatitis, anything that blocks a duct effects all organs in the biliary tree.
Gallbladder, pancreas, duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Endocrine pancreas

A

Insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Exocrine pancreas

A

Duct cells

Bicarb, amylase, lipase, protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Alcohol-induced pancreatitis

A

> 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Common causes of PUD

A

NSAIDS
H.pylori
Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

NSAID caused PUD

A 
Chronic condition
Gastric >Duodenal 
May be asymptomatic 
Deep ulcers
More severe GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

H. Pylori caused PUD

A 
Chronic condition
Duodenal > gastric
Epigastric symptoms
Superficial ulcers
Less severe bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Stress caused PUD

A 
Acute condition
Gastric > Duodenal 
Asymptomatic 
Most superficial ulcer depth
More severe GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Uncommon causes of chronic peptic ulcer

A 
Idiopathic
Hypersecretion of gastric acid
Viral infections
Radiation therapy
Chemo
Infiltrating disease (Crohn's disease)
Smoking
Psychological stress
Potentially alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

NSAIDs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Equal COX1 and COX2 effect

A

Meloxicam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

COX-2 inhibitors

A

Celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

COX-1 inhibition causes on GI mucosa

A

Peptic ulcers, GI bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

COX-1 and 2 inhibition causes on Kidney

A

Na and H20 retention
Hypertension
Hemodynamic acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

COX 1 and 2 inhibition causes on heart

A

Stroke
MI
COX 2> COX 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How do COX 1 inhibitors cause mucosal injury and bleeding?

A

Decreased mucosal blood flow
Reduced mucus and bicarb secretion
Impaired platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How do COX 2 inhibitors cause mucosal injury and bleeding?

A

Reduced angiogenesis
Impaired healing
Increased leukocyte adherence
Leukocyte activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Risk factors associated with NSAID induced ulcers

A 
Age >65
Previous peptic ulcer
high-dose NSAIDs
NSAID + aspirin, bisphosphonates, antiplatelet selective serotonin reuptake inhibitors
H.Pylori
Cigarette smoking
Alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

GI prophylaxis for patients on chronic NSAIDs and aspirin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Misoprostol

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the major method of toxicity for H. pylori?

A

Stimulates the inflammatory response (major)
Ammonia is toxic to epithelial cells
Increases pepsin which can degrade mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Complications of PUD

A

GI Bleeding
GI perforation
Low risk of gastric cancer secondary to H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Assessment of PUD

A 
Ask about NSAIDs
Review meds
Review medical history
Ask about smoking and alcohol
What relieves/worsens
S/S of GI bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Symptoms of PUD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

PUD Diagnostic testing

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are PUD alarm symptoms

A

Elderly, Family h/o GI malignancy, Weight loss, Dysphagia, Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

H. Pylori endoscopic testing
Histology
Culture
Urease

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q 
H. Pylori endoscopic testing
Blood antibodies (ELISA)
Blood antibodies (IgG)
Urea breath test 
Fecal antigen
A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Which H. Pylori test is recommended for post treatment eradication confirmation?

A

Fecal or breath test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the first treatment option for H.pylori induced PUD?

A

PPI- BID
Tetracycline- 500mg QID
Metronidazole- 500mg TID-QID
Bismuth- 262mg-524mg QID

Duration: 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the second treatment option for PUD?

A

PPI- BID
Clarithromycin- 500mg BID
Metronidazole- 500mg BID
Amoxicillin- 1000mg BID

Duration: 10-14 days (14 preferred)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What do you do with PPI after 14 days of tx for PUD?

A

May stop after 14 days or continue QD if bleeding ulcer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Pylera

A

Combination of bismuth subcitrate, metronidazole, and tetracycline.
Take 3 capsules QID for 10 days with PPI BID
Very expensive, but FDA approved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the recommended PUD therapy if no PCN allergy or MCL exposure?

A

Either

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the recommended PUD therapy is no PCN allergy but recent MCL exposure?

A

Bismuth quadruple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the recommended PUD therapy if a PCN allergy present?

A

Bismuth quadruple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the recommended PUD therapy if PCN allergy and recent MCL exposure?

A

Bismuth quadruple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Esomeprazole dosing for NSAID/ASA induced PUD

A

20mg QD for 4-8 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Lansoprazole dosing for NSAID/ASA induced PUD

A

15mg QD for 4 weeks (duodenal)

30mg QD for 8 weeks (gastric)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Omeprazole dosing for NSAID/ASA induced PUD

A

20mg QD for 4-8 weeks (duodenal)

40mg QD for 8 weeks (gastric)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Pantoprazole dosing for NSAID/ASA induced PUD

A

40mg QD for 4 weeks (duodenal)

40mg QD for 8 weeks (gastric)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Rabeprazole dosing for NSAID/ASA induced PUD

A

20mg QD for 4 weeks (duodenal)

20mg QD for 6-8 weeks (gastric)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Treatment for NSAID induced PUD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Treatment of ASA induced PUD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Sucralfate

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Stress ulcer prophylaxis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Why do ICU patients get stress ulcers?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Tx for upper GI bleed

A

Ensure hemodynamic stability
Volume resuscitation
Correct coagulopathy and/or thrombocytopenia
Endoscopic hemostasis
PPI- high dose bolus vs continuous infusion
Correct underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

S/S GI bleeding

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

GI bleeding Tx

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Etiologies of N/V

A

Gastrointestinal processes, infections, acute MI, migraine, vestibular disorders, metabolic disorders, psychiatric disorders, drug withdrawal, post-op, food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Types of N/V in cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Which patients receive prophylaxis for N/V before, during, and after chemo?

A

Low
Moderate
High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are fluid and electrolyte causes for N/V in cancer patients?

A

Hypercalcemia (Very common due to PTH secretion of tumors)

Dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are drug-induced causes of N/V in cancer patients?

A

Opioids

antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are tumor/metastases-related causes of N/V in cancer patients?

A 
GI obstruction
Brain melts (tumor spreads to brain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What are misc. related causes of N/V in cancer patients?

A

Infection

Radiation therapy

125
Q

Post-op N/V

A

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
Q

PONV risk factors

A

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
Q

Nonpharm treatment of PONV

A 
Dietary changes
Positioning (vestibular)
Relaxation
Biofeedback
Acupuncture
128
Q

N/V symptoms

A

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
Q

Treatment options for N/V

A 
Antacids
Antihistamines-anticholinergics
Phenothiazines
Dopamine antagonists
Serotonin (5HT3) receptor antagonists
Neurokinin receptor antagonists
Corticosteroids 
Benzodiazepines
Cannabinoids
130
Q

Antihistamines for N/V

A

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
Q

Phenothiazines for N/V

A

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
Q

Dopamine antagonists in N/V

A

Haloperidol
Olanzapine
Droperidol
Metoclopramide

133
Q

Haloperidol and Olanzapine in N/V

A 
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
Q

Droperidol

A

Excellent antiemetic but rarely used
BBW for torsades
Side effects similar to that of haloperidol, but also hypotension and tachycardia

135
Q

Metoclopramide

A

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
Q

5HT3 Receptor Antagonists for N/V

A

Dolasetron
Granisetron
Ondansetron
Palonosetron
All have a risk of QTc prolongation (dose dependent)
Ondansetron interacts with strong 3A4 inhibitors

137
Q

5HT3 Receptor antagonists drug information

A

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
Q

Neurokinin Receptor Antagonists for N/V

A

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
Q

Corticosteroids for N/V

A

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
Q

Benzodiazepines for N/V

A

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
Q

Cannabinoids for N/V

A

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
Q

Approaches to treatment in N/V patients

A

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
Q

Vertigo

A

Vomiting after head motion
Meclizine or hydroxyzine
Promethazine second line

144
Q

Motion sickness

A

Diphenhydramine, dimenhydrinate, or scopolamine

145
Q

Chemotherapy- induced N/V high risk regimen

A

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
Q

How do you reduce baseline risk in post op NV

A

Use regional anesthesia
Use IV anesthesia (propofol preferred)
Minimize intraoperative and postoperative opioids
Adequate hydration

147
Q

PONV prophylaxis

A

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
Q

PONV treatment

A

Initially 5HT3 antagonist
If failed prophylaxis choose 1 or 2 agents from a different class
Control pain
Give fluids

149
Q

N/V in pregnancy

A

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
Q

What are the types of acute diarrhea?

A 
Osmotic
Inflammatory
Infectious
Secretory
Altered motility
151
Q

Chronic diarrhea

A

Any of acute, PLUS
diabetes
IBD
Hyperthyroidism

152
Q

Presentation of diarrhea and potential cause

A

Typically self-limiting
Stool analysis
Fever? probably infectious
Blood? Pain? Either infectious or inflammatory
Severe dehydration/hemodynamic instability? May need to hospitalize.

153
Q

Supportive treatment of diarrhea

A 
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
Q

Treatment options for diarrhea

A

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
Q

Loperamide

A

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
Q

Diphenoxylate and Difenoxin

A 
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
Q

Ocreotide

A

Somatostatin analog
Blocks serotonin, inhibits intestinal secretion and stimulates intestinal absorption
Used for tumor related secretory diarrhea

158
Q

Treatment of infectious diarrhea

A

C.diff

  • stop offending agents if possible
  • Oral Vanc or fidaxomycin
  • Probiotics for prophylaxis
  • Fluids
  • Do NOT give antidiarrheals

Travelers diarrhea

159
Q

Diverticulosis and Diverticulitis

A

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
Q

Tx of acute diverticulitis

A

Abx recommended in complicated. May be reasonable in uncomplicated
If fever or signs of infections use abx
Clear, liquid diet
Pain control

161
Q

Celiac disease

A

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
Q

`Mucositis

A

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
Q

Constipation

A

Fewer than 3 bowel movements/week

164
Q

GI causes of constipation

A

IBS
Diverticulitis
Hemorrhoids
Obstruction (cancer)

165
Q

Metabolic/endocrine causes of constipation

A

Diabetes
hypothyroidism
Hypercalcemia

166
Q

Lifestyle causes of constipation

A

Pregnancy
Inadequate fluid
Low fiber
Sedentary lifestyle

167
Q

Neurogenic/Psychogenic causes of constipation

A

Stroke
Spinal cord/brain injury
Psychiatric diseases

168
Q

Drug induced constipation

A

Slow motility- opioids, anticholinergics (antihistamines/phenothiazines, CNS agents, urinary incontinence agents), CCVs, aluminum and calcium antacids, iron

169
Q

Alarm symptoms of constipation

A

Hematochezia, melena, family H/O colon cancer, IBD, anemia, weight loss, anorexia, N/V

Colonoscopy if any are present!

170
Q

Treatment of constipation non-pharm

A

Increase fluids and fiber

Increase activity

171
Q

Fiber

A

Fiber- bulk-forming, increases frequency of defecation by retaining water in intestine and increasing GI motility
Examples- psyllium, methylcellulose and polycarbophil

172
Q

Laxatives for constipation treatment

A

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

173
Q

Bulk-forming laxatives and onset

A

Fiber

1-3 days

174
Q

Softener laxatives and onset

A

Docusate
1-3 days
Used preventative

175
Q

Lubricant laxative and onset

A

Mineral oil
1-3 days
Not used often due to aspiration risk

176
Q

Osmotic laxatives and onset

A 
Lactulose, sorbitol- 1 day
PEG (miralax)- 1 day
Mag citrate- 1-6  hours
Sodium phosphate- 1-3 hours
PEG (GOLYTELY)- Rapid
177
Q

Stimulant laxatives and onset

A

Bisacodyl- 1-12 hours
Senna- 6-12 hours
Mag citrate- 1-6 hours
Glycerin suppository- 30 minutes

178
Q

Dosing:
Psyllium
Docusate
Mineral oil

A

Psyllium- 4-6g/day
Docusate- 100mg po BID
Mineral oil- 15-45ml po once

179
Q

Dosing:
Lactulose, sorbitol
PEG (Miralax)
Bisacodyl

A

Lactulose- 15-30mP QD, or 30 150mL once
PEG (miralax)- 17g QD
Bisacodyl- 10mg PO or PR QD

180
Q 
Dosing:
Senna
Mag citrate
Glycerin supp
PEG (GoLYTELY)
A

Senna- 1-2 tbs PO BID
Mag citrate- 150-300mL PO once
Glycerin supp- Suppository once
PEG(GoLYTELY)- 4000ml once

181
Q

Lubiprostone

A

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)

182
Q

Linaclotide and Plecanatide

A

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

183
Q

Opioid- induced constipation

A

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

184
Q

Methylnaltrexone

A 
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
185
Q

Naloxegol (Movantik)

A 
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
Q

Naldemedine (Symproic)

A 
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
Q

OIC treatment algorithm

A

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
Q

Post Operative Ileus

A

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
Q

Laxative abuse

A

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
Q

Irritable bowel

A

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
Q

Treatment of IBS with constipation predominant

A

Fiber
Do not use osmotic laxatives
Lubriprostone, Linaclotide, Tegaserod are last line
Tegaserod is emergency use only due to CV events

192
Q

Treatment of IBS with diarrhea predominant

A

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
Q

Symptom control in IBS

A

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
Q

Types of IBD

A

Ulcerative colitis and Crohns disease

195
Q

Complications of crohns disease

A

Inflammation
Stenosis
Fistula

196
Q

Ulcerative colitis depth and location

A

Depth- Mucosa and submucosa

Location- Rectum and colon

197
Q

Ulcerative colitis fistulas, strictures, bleeding

A

Fistulas- rare
Strictures- rare
Bleeding- common >90%

198
Q

Ulcerative colitis abdominal pain, distribution, diarrhea, characterization

A

Abdominal pain- Unusual
Distribution- Continuous
Diarrhea- 10-30%
Characterization- “Steady” disease

199
Q

Crohns disease depth and location

A

Depth- Transmural

Location- Terminal ileum, but can occur at any part of the GI tract

200
Q

Crohns disease fistulas, strictures, bleeding

A

Fistulas- common
Strictures- common
Bleeding- Common (<50%) but less severe than UC

201
Q

Crohns disease abdominal pain, distribution, diarrhea, characterization

A

Abdominal pain- common
Distribution- Discontinuous
Diarrhea- >70%
Characterization- Flares alternating with remission

202
Q

Local complications of UC

A

Toxic megacolon- ulceration extends below submucosa (perforation), high fever, elevated WBC, and tachycardia present
Significantly higher risk of colon cancer

203
Q

Local complications of crohns disease

A

Hemorrhage
Perforation
Obstruction
Cancer

204
Q

Systemic complications of both UC and CD

A

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

205
Q

Clinical presentation and work up of CD

A

Abdominal findings- cramping, pain, chronic diarrhea, nausea, vomiting, weight loss
Symptoms related to systemic manifestations- blurred vision, arthritis, skin findings
DC NSAIDS
Colonoscopy

206
Q

Clinical presentation and work up of UC

A

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

207
Q

Pharmacologic treatment for IBD

A 
Aminosalicylates (5-ASA) (first)
Corticosteroids
Antimicrobials
Immunomodulators
Biologics (last)
Supportive- enteral and parenteral nutrition in severe disease
208
Q

Sulfasalazine in IBD

A 
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
209
Q

Mesalamine derivatives in IBD

A

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
210
Q

Corticosteroids for IBD

A

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
Q

Steroid AE

A 
Hyperglycemia
Hypertension
Osteoporosis
Acne
Fluid retention
Weight gain
Psychosis
Increased susceptibility to infection
Cataracts, glaucoma
212
Q

Antibiotics in IBD

A

Not used as monotherapy
Metronidazole- 500mg PO Q8H
Interactions- warfarin, disulfiram-like with alcohol
AE- N, metallic taste, paresthesias

213
Q

Azathioprine/ 6-Mercapropurine in IBD

A

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

214
Q

Methotrexate for IBD

A

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
Q

Cyclosporine in IBD

A

IV infusion
Drug interactions- statins, macrolides, azoles, diltiazem, verapamil.
AE- nephrotoxicity, hyperlipidemia, HTN

216
Q

Biologics for IBD

A

Antibodies to TNF-alpha
Selective adhesion molecule inhibitors
IL12/IL23 inhibitor
JAK inhibitors

217
Q

Antibodies to TNF-a

A

Blocks binding to its receptors, decreasing immune response

Infliximab, adalimumab, certolizumab, golimumab

218
Q

Selective adhesion molecule inhibitors

A

Blocks adhesion of lymphocytes to epithelium

Natalizumab, vedolizumab

219
Q

IL12/IL23 inhibitor

A

Reduces the inflammatory response by blocking the secretion of IL-6, IL-17, and TNF-a
Ustekinumab (Stelara)

220
Q

JAK inhibitors

A

JAK signals IL12 and IL23

Tofacitinib

221
Q

Infiliximab

A

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
Q

Infliximab toxicities

A

Infusion reactions
Premedicate with APAP, diphenydramine, and possibly steroids
Autoimmune reactions- lupus, hemolytic anemia

223
Q

Adalimumab, certolizumab, and golimumab toxicities

A

SQ administration- injection site reactions

May worsen/cause HF

224
Q

Vedolizumab and natalizumab toxicities

A

May increase risk of infections and liver injuries

225
Q

Ustekinumab toxicities

A

Test for TB before initiating

May cause hypersensitivity reactions and increase risk for infections

226
Q

Tofacitinib toxicities

A

Test for TB before initiating

227
Q

Which biologics have a BBW for increasing lymphoma and infection risk?

A

Infliximab, adalimumab, certolizumab, golimumab

228
Q

Which biologic has the BBW of PML?

A

Natalizumab

229
Q

Which biologics have no BBW?

A

Vedolizumab, usetkinumab

230
Q

Which biologic has a BBW for increasing lymphoma, VTE, and infection risk?

A

Tofacitinib

231
Q

Treatment of active UC- mild-moderate diseases

A

Mild-moderate extensive disease- 5-ASA oral agents, corticosteroids (budesonide) if 5-ASA failed
Mild-moderate distal disease- 5-ASA topical agents

232
Q

Treatment of active UC- severe

A

Steroids, anti-TNF (refractory to steroids), cyclosporine if hospitalized

Use vedolizumab, tofacitinib, or golimumab as alternative to anti-TNF

233
Q

Do you use AZA/6MP or antibiotics in active UC?

A

No

234
Q

Prevention of relapse of UC

A

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
Q

Treatment of active CD

A

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
Q

Prevention of relapse CD

A

AZA/6MP in combo with anti-TNF

Natalizumab, vedolizumab, ustekinumab if worked acutely

237
Q

Treatment of toxic megacolon

A

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
Q

Indications for surgery

A 
Life threatening hemorrhage
Perforation
Cancer
Toxic megacolon
Failure of or intolerance to maximal medical therapy
Obstruction
Abscess not amenable to drainage
239
Q

IBD and pregnancy

A

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
Q

Acute pancreatitis

A

Rapid onset, generally no long term complications if patient survives acute attack
Severe abdominal pain
Acutely elevated pancreatic enzymes

241
Q

Chronic pancreatitis

A

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
Q

Causes of acute pancreatitis

A

Gallstones, alcohol, and hypertriglyceridemia (>1000) most common causes
can also be caused by infections, hypercalcemia, abdominal trauma, IBD, etc.

243
Q

Medication causes of acute pancreatitis

A 
Azathioprine
Estrogens
Furosemides
Steroids
Opiates
Sulfonamides
Propofol
Tetracycline
Statins
Valproic acid
Thiazides
ACE-Is
244
Q

How do ACE-Is cause acute pancreatitis?

A

Local angioedema

245
Q

How do estrogen/OC/HRT cause acute pancreatitis?

A

Microemboli

Hypertriglyceridemia

246
Q

How do statins cause acute pancreatitis?

A

Directly toxic

May be related to myalgias/rhabdo

247
Q

How do diuretics cause acute pancreatitis?

A

Loops- directly toxic

Thiazides- hypercalcemia, hypertriglyceridemia

248
Q

How does valproic acid cause acute pancreatitis?

A

Directly toxic

249
Q

How do azathioprine, sulfonamides, and tetracyclines cause acute pancreatitis?

A

Hypersensitivity reactions

These are the same drugs that cause AKI

250
Q

Clinical presentation of acute pancreatitis

A

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
Q

Laboratory findings in acute pancreatitis

A

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
Q

Amylase in pancreatitis

A

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
Q

Lipase in pacreatitis

A

<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
Q

What amylase or lipase values are diagnostic of pancreatitis?

A

> 3x ULN

Elevations do not correlate with etiology or severity of disease

255
Q

Prognostic criteria pancreatitis

A

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
Q

Management of acute pancreatitis

A

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
Q

G-tube vs J-tube

A

G-tube is in the stomach

J-tube is in the jejunum

258
Q

Fluid management for acute pancreatitis

A

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
Q

Pain and Nausea control for pancreatitis

A

Narcotics are mainstay
-Hydromorphone (Dilaudid) preferred
Morphine is also reasonable
PCA who need frequent narcotic dosing

Promethazine and serotonin antagonists (Zofran) for N

260
Q

Infections in pancreatitis

A

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
Q

Octreotide

A

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
Q

Complications of acute pancreatitis

A

Local- acute fluid collection, pancreatic necrosis and abscess, pseudocyst
Systemic- shock, hypotension, acute renal failure, acute respiratory distress syndrome, GI bleeding
Chronic pancreatitis

263
Q

Chronic pancreatitis cause

A

Irreversible damage
Alcohol (inflammation-> necrosis -> fibrosis)
Idiopathic
Gallstones are not associated with chronic pancreatitis

264
Q

Symptoms of chronic pancreatitis

A

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
Q

Treatment of chronic pancreatitis

A 
No alcohol! 
Control of pain
Give pancreatic enzymes
Insulin if diabetes
Smaller, more frequent low-fat meals
266
Q

Complications of chronic pancreatitis

A

Malabsorption
Chronic abdominal pain
DM
Pancreatic cancer

267
Q

Pancreatic enzymes

A

Treatment for chronic pancreatitis
Amylase, lipase, protease
Helps with malabsorption, steatorrhea, osmotic diarrhea, pain, slows progression

268
Q

Dose of pancreatic enzymes

A

Based on lipase content
25000-40000 units lipase per meal, half for snack
Not interchangeable

269
Q

Lipase in creon, zenpep, pancreaze

A

Creon- 3,000-24,000 units
Zenpep- 3,000-25,000 units
Pancreaze- 4,200-21,000 units

270
Q

Lipase in ultresa, viokace, pertzye

A

Ultreza- 13,900-23,000 units
Viokace- 10,440-20,880
Pertyze- 8000-16,000 units

271
Q

Pancreatic enzymes counseling points

A

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
Q

Treatment of abdominal pain in chronic pancreatitis

A 
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
Q

Pancreatic cancer

A

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
Q

Enteral nutrition

A

via the gastrointestinal tract

GI tract contains about 75% of its nutrition from the gut mucosa so preferred

275
Q

Parenteral nutrition

A

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
Q

TPN vs PPN

A

Total parenteral nutrition given through central line

Peripheral parenteral nutrition given through peripheral system

277
Q

Ileus

A

Decreased peristalsis resulting in decreased bowel sounds, painful distended abdomen, N, V

278
Q

-ostomy

A

New functional opening

279
Q

Gastric residual

A

Volume retrieved from the stomach upon aspiration of gastric contents through a gastronomy tube; generally, if >200mL you are intolerant of enteral nutrition

280
Q

Fistula

A

Abnormal communication between two epithelial cell lines

281
Q

Marasmus

A 
Chronic protein and calorie malnutrition 
Decreased energy intake vs. increased energy expenditure
Visceral protein (albumin, prealbumin) production preserved
282
Q

Kwashiorkor

A

Acute or chronic protein malnutrition; adequate calorie intake
Decreased synthesis vs decreased intake
Marked depletion of visceral proteins

283
Q

Why does malnutrition occur with critical illness?

A

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
Q

Rehabilitation

A

Loss of skeletal muscle mass; weakness

285
Q

What are the risks for malnutrition in the ICU?

A

Stressors- SIRS, infection, trauma
Previous history of malnourished (EtOH)
NPO

286
Q

Visceral proteins

A

Synthesized from the liver by dietary amino acids

Prealbumin has a half life of 3 days and is used in acute phase

287
Q

Weight considerations for nutrition

A

ABW= IBW + 0.25(ABW-IBW)

If ABW >130% of IBW use adjusted

288
Q

Nutritionally at-risk adults

A

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
Q

calorie vs Kcal

A

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
Q

How long can you live without food and water?

A

Food- 60 days

Water- 5-7

291
Q

Macronutrients

A

Carbohydrates (Dextrose)- 3.4Kcal/g
Protein (AA)- 4Kcal/g; 0.16g nitrogen
Lipid- 10Kcal

292
Q

Micronutrients

A

Vitamins
Minerals
Trace elements

293
Q

What is the basic composition of nutrition?

A

Macronutrients
Micronutrients
Electrolytes
Water

294
Q

Basal energy expenditure vs Resting energy expenditure

A

Estimate (calculation) based on demographics

REE- measure

295
Q

Empiric strategy for estimation of energy requirements

A

Maintenance- 20-25kcal/kg/day
Critically ill- 25-30kcal/kg/day
Trauma- 30-35kcal/kg/day
Burn- 35-50kcal/kg/day

296
Q

Empiric strategy for estimation of protein requirements

A

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
Q

What is a caloric recipe?

A

Dextrose 50-60% (max 7g/kg/day)
Protein 20-30% (max 2.5g/kg/day)
Lipids 10-20% (max 2.5g/kg/day)

298
Q

Daily fluid provisions

A

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
Q

Potassium

A

Major intracellular cation (130mEq/L
Normal serum 3.5-5
Require 0.5-1mEq/kg/day

Involved in action potentials, movement of glucose

300
Q

Magnesium

A

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
Q

Phosphorous

A 
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

302
Q

How do you determine if the gut is working?

A 
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

303
Q

When would you use a PPN?

A 
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
304
Q

Timing of nutrition

A

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
Q

Refeeding syndrome

A 
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

306
Q

Nutritional endpoints

A

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

307
Q

Approach for providing nutrition support

A 
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
308
Q

IV electrolyte replacement

A

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

309
Q

Infusion times for electrolytes

A

K- Central (20meq/L) and peropheral (10meq/L)
Mg- 1g/hr
Phos- 7.5mmol/hr

Therapeutics II (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions