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Pharm III > Lecture 2 (GI)-Exam 1 > Flashcards

Lecture 2 (GI)-Exam 1 Flashcards

1
Q

Child pugh
* What is it for?
* Used to recommend what?
* Not avaviable for what?

A
  • Scoring system used to assess and define the severity of cirrhosis
  • Used to recommend dose adjustments for patients with liver disease
  • Not available for all medications
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2
Q

Child-Pugh Grading
* What is the limitation?

A

Ascites grading and encephalopathy grading somewhat subjective

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3
Q
A
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4
Q

Child-pugh: Changes need to be made
* Grade A?
* Grade B?
* Grade C?

A
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5
Q

Gastritis:
* What is it?
* Imbalance between what?
* How do you dx it?
* What are the sxs? (3)

A

Inflammation of gastric mucosa
* Imbalance between mucosal defenses and acidic environment

Diagnosis: endoscopy

Symptoms: epigastric pain, nausea, vomiting

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6
Q

Gastritis: acute
* What is it?
* MCC?
* What are other causes?

Gastritis: chronic:
* MCC
* Other cause?

A

Acute gastritis
* Gastric erosions (not ulcers)
* MCC ETOH/NSAIDS
* Severe stress: sepsis, shock, trauma

Chronic gastritis
* MCC Helicobacter pylori
* Autoimmune

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7
Q

Gastritis treatments:
* What is the txt? (general)

A
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8
Q

Peptic ulcer disease
* Defect in what?
* The management based on what?

A
  • Defect in the gastric or duodenal wall that extends through the muscularis mucosa into the deeper layers of the wall.
  • The management based on the etiology, ulcer characteristics, and anticipated natural history
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9
Q

Peptic ulcer disease
* Chronic what?
* What are the two types?

A
  • Chronic lesions in areas exposed to excess gastric acid and peptic juices
  • Gastric ulcers and duodenal ulcers
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10
Q

Peptic ulcer disease
* What are the sxs

A
  • 70% asymptomatic
    * 43 to 87% present with GI bleeding
  • Epigastric pain ± radiation to back
  • Nausea / vomiting
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11
Q

Gastric ulcers
* decreased what?
* What is the MCC? What is another cause?
* May be associated with what?

A
  • Decreased mucosal protection against gastric acid
  • MCC H. pylori infection (70%) then NSAIDs
  • May be associated with gastric malignancies-> MALT lymphoma and adenocarcinoma
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12
Q

Gastric ulcers
* What are the sxs?
* What can erode?
* Potentional for what?

A
  • Symptoms worse 30 min after eating
  • Avoid meals – weight loss
  • Erode into left gastric artery
  • Potential for severe upper GI bleeding

  • “Gee, I’m not hungry”
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13
Q

Duodenal ulcers
* Decreased and increased what?
* MCC? What is another cause?
* What is the sxs?

A
  • Decreased mucosa protection and increased gastric acid secretion
  • MCC H. pylori (~90%)
  • Zollinger Ellingson syndrome
  • Symptoms improve with eating – weight gain

“Dude, give me food”

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14
Q
A
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15
Q

Helicobacter Pylori
* What is the morphology?
* What type of activity? What does that cause?

A

Spiral, microaerophilic, gram negative bacteria with flagella

Urease, catalase and oxidase activity
* Urease = converts urea to ammonia – creates alkaline microenvironment
* Catalase = survival of phagocyte oxidation – creates inflammation

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16
Q

Helicobacter Pylori
* Transmitted how?
* What can it develop into? (2)

A

Transmitted gastro-oral or fecal-oral routes
* 10 to 20% develop peptic ulcer disease
* 1% develop gastric CA

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17
Q

H. Pylori diagnosis
* What are the two ways?
* patients?
* What is an option?

A

Endoscopic vs non-endoscopic tests
* Patients < 60 years without alarms features
* Non-endoscopic testing is an option (conditional recommendation)

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18
Q

H. Pylori diagnosis
* What are the diagnostic test? (2)

A
  • Endoscopic – biopsy for rapid urease = test of choice
  • Non-endoscopic – Urea breath test, fecal antigen, antibody tests
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19
Q

H. Pylori diagnosis
* What are the dx for eradication?
* Delay confirmation testing until when? (2)

A

Tests for eradication
* Endoscopic – biopsy for rapid urease
* Non-endoscopic – urea breath test, fecal antigen

Delay confirmation testing until:
* Four weeks after bismuth or antibiotics complete and two weeks after PPI complete

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20
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21
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22
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23
Q

Treatment of H. Pylori positive ulcers- Eradication of infection
* What is there resistance aganist?
* What may be low?
* What is most effective? What type of meds?

A
  • Antimicrobial resistance increasing (clarithromycin)
  • Adherence may be low
  • Initial regimen most effective
  • PPIs more effective than H2RAs
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24
Q

Treatment of H. Pylori positive ulcers-Eradication of infection
* Why is PPIS more effective than H2RAs? (4)

A
  • Promote ulcer healing
  • Increase gastric pH
  • Decrease gastric volume
  • Twice daily dosing more effective than daily
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25
Q

What is first line for H. pylori?

A

CAP therapy:
* PPI
* Clarithromycin
* Amoxicillin

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26
Q
A

Do not worry about dosing-> know drugs

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27
Q

Bismuth subsalicylate:
* What are the effects? (4)

A
  • Topical antimicrobial effect
  • Stimulates absorption of fluid/electrolytes
  • Anti-inflammatory
  • Binds bacterial toxins
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28
Q

Bismuth subsalicylate:
* What are the SE? (2)
* Not recommended for who?
* Do not usee in who?
* CL?(4)

A
  • May blacken tongue / stool
  • Tinnitus
  • Not recommended for children < 12 years
  • Do not use in pregnancy
  • CI: allergy to salicylates, renal insufficiency, gout, GI bleed
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29
Q

Metronidazole and tetracyline:
* What are the effects?

A

In vitro activity against H. pylori

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30
Q

Metronidazole and tetracyline:
* What is the MOA and SEs?

A
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31
Q

PPIs
* What is the effects?

A
  • Promotes healing
  • Enhances antimicrobial effects
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32
Q

NSAIDs mechanism of action
* What is always circulating
* What does it produce and cause?

A
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33
Q
  • Where is COX-2 induced? What does it mediate
A

COX-2 induced at sites of inflammation
* Mediate inflammation, pain, and fever

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34
Q

NSAID Mechanism of action
* What is the MOA of NSAIDs? What are thier effects?

A

NSAIDs block COX-1 and COX-2
* Reduce prostaglandin, thromboxane, prostacyclin synthesis
* Reduce inflammation, pain, and fever

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35
Q

NSAIDS
* What happens when COX-1 is inhibited?

A
  • Decreased gastric blood flow
  • Decreased mucous production
  • Inhibition of platelet activation (TXA2)->Cardioprotective
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36
Q

NSAIDS
* What is the MOA of COX-2 cause if inhibited? What happens?
* increased risk of what?

A

Inhibition of prostacyclin
* Vasoconstriction
* Platelet aggregation

Unopposed COX-1activity
* Vasoconstriction
* Platelet aggregation

INCREASED risk of cardiovascular events

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37
Q

NSAID-induced PUD
* Cause what?
* Progresses to what?
* Rarely causes what?

A
  • Cause superficial mucosal damage shortly after ingestion
  • Progress to erosions but typically heal within a few days
  • Rarely causes ulcers or bleeding
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38
Q

NSAID-induced PUD
* Risk increased with what?
* Dependent on what?
* Greater propensity to do what?

A
  • Risk increases with advancing age (> 65 years independent risk)
  • Dependent on dose, duration, type of NSAID
  • Greater propensity to inhibit COX 1 increases risk
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39
Q

NSAID-induced PUD
* Explain how Greater propensity to inhibit COX 1 increases risk? (3)

A
  • Salicylates = higher risk (aspirin)
  • Low dose ASA + NSAID increases risk
  • Low dose ASA + clopidogrel increases risk
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40
Q

NSAID induced ulcer treatment
* What is recommended to stop?
* What is first line and the alternative if that is stop?

A

NSAIDs held / discontinued (recommended):
* First-line: PPI x 8-weeks – most effective
* Alternative: H2RA or sucralfate alternative

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41
Q

NSAID induced ulcer treatment
* What is first line if NSAIDs are not held?
* Treat what if present?

A
  • First-line: PPI x 12 weeks
  • Continue PPI prophylaxis
  • Consider alternative NSAID
    * Less COX-1 specific or COX-2
  • Treat H. pylori if also present
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42
Q

Prevention of NSAID-related ulcers
* What is most effective?

A

COX-2 specific agent + PPI

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43
Q

Prevention of NSAID-related ulcers
* What are the alternative treatments?

A
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44
Q

Prevention of NSAID-related ulcers
* What needs to be considered?

A

Cardiovascular and gastrointestinal risks should be considered

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45
Q

Prevention of NSAID-related ulcers

A
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46
Q

PUD maintenance therapy (long term PPI use)
* Limited to high-risk subgroups of patients including patients with the following: (5)

A
  • Refractory peptic ulcer
  • H. pylori-negative, NSAID-negative ulcer disease
  • Giant (>2 cm) ulcer and age >50 years or multiple comorbidities
  • Failure ofH. pylorieradication, including rescue therapies
  • Frequently recurrent peptic ulcers (>2 documented recurrences a year)
  • Continued NSAID use
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47
Q

Long term PPI therapy
* What is most effective for GERD
* Studies suggest what?
* Most are what?
* High quality studies have only shown what?

A
  • PPIs are the most effective treatment for GERD
  • Studies suggest have identified associations with long-term PPI therapy
  • Most are flawed and do not establish a cause-and-effect relationship
  • High quality studies have only shown a relationship between PPIs and intestinal infections
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48
Q

GI bleeding - GI emergency
* What are the two types?
* What is the MC nonvariceal?
* PUD assoicated=
* SRMD=

A

Variceal or nonvariceal
* MC nonvariceal = chronic PUD and stress related mucosal damage (SRMD)
* PUD associated = prehospital
* SRMD = critically ill hospitalized patients

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49
Q

Gi emergency: SRMD = critically ill hospitalized patients
* What are is the cause?
* Where?
* _ areas

A
  • Mucosal ischemia from splanchnic hypoperfusion and reduced gastric blood flow
  • Proximal stomach
  • Numerous areas
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50
Q

GI bleeding: treatment
* What is the txt? (supportive and therapic)(4)

A
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51
Q

Stress ulcer prophylaxis
* Indiction for who? (7)

A
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52
Q

75 to 100% of ICU patients develop what?

A

75 to 100% of ICU patients develop SRMB within 1 to 3 days

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53
Q
A
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54
Q

Stress ulcer prophylaxis
* What is the prevention (2)

A
  • Adequate fluid resuscitation
  • Maintain gastric pH > 4
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55
Q

Stress ulcer prophylaxis:
* What are the SE of H2RAs? (3)
* What is the SE of PPI?(2)

A

H2RAs
* May cause mental status changes
* Thrombocytopenia
* Renal dose adjustment

PPI
* Increase risk of C. diff and pneumonias

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56
Q
A
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57
Q
A
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58
Q

Zollinger-Ellison syndrome
* What is the patho of it?
* What are the sxs?

A

Hypersecretion of gastric acid
* Gastrin secretion from neuroendocrine tumor (gastrinoma) -> increased HCL production by parietal cells
* Severe, refractory PUD (txt is not working)
* Diarrhea (increase acid production and damage occurs)

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59
Q

Zollinger-Ellison syndrome
* What is the txt?(3)

A
  • Tumor resection if possible
  • Chemotherapy
  • High dose PPIs
  • Twice daily doses up to 180 mg / day
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60
Q

Delayed Gastric Emptying:
* MCC is what?
* What are the sxs?
* What do you need to rule out of?
* How do evaluate it?

A

MCC idiopathic (associated with multiple disease states)
* SXs – early satiety, bloating, gastric fullness, nausea. Symptoms are worsened by eating.
* DDX: Need to rule out gastric outlet obstruction
* Evaluation – Endoscopy may exclude a structural abnormality. UGI w/ small bowel follow through.

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61
Q

Delayed Gastric Emptying
* What is the treatment?

A

Avoid food and medications that slow gastric emptying
* Foods high in fat
* Anticholinergics, opiates, dopamine agonists

Control diabetes

Prokinetic medications

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62
Q

Prokinetics: metoclopramide
* What is the MOA?

A
  • Inhibits D2, 5HT3 receptors
  • Stimulates 5HT4 receptors
  • Increases LES pressure and gastric contractions
  • Mild antiemetic
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63
Q

Prokinetics: metoclopramide
* What are the SE?(3)

A
  • Asthenia (weakness)
  • HA
  • Somnolence
  • EPS
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64
Q
A
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65
Q

Prokinetics: Macrolide antibiotics
* What are the examples?
* What is the MOA?
* Tolerance?

A
  • Erythromycin / azithromycin / clarithromycin
  • Stimulates motilin receptors
  • Motilin stimulation increases GI motility and gastric emptying
  • Tolerance may develop in some patients
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66
Q

Prokinetics: Macrolide antibiotics
* What are the interactions to avoid?

A

Avoid concomitant administration with magnesium or aluminum-containing antacids

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67
Q

Prokinetics: macrolides
* What are the SEs?(5)

68
Q

Acute Pancreatitis
* Edematous: Usually what? What type of care?
* Necrotizing: More severe disorder in which what?

A

Edematous pancreatitis
* Usually mild & self-limited disorder
* Supportive care

Necrotizing pancreatitis
* More severe disorder in which degree of pancreatic necrosis correlates with severity of attack & systemic manifestations

69
Q

Know severity

70
Q

Acute Pancreatitis Diagnosis
* In acute pancreatitis, what do you need in order to dx?

71
Q

acute pancreatitis on CT scan
* Why is it good? (3)

A
  • Helpful if diagnosis is in question
  • Helpful in determining prognosis
  • Helpful in detecting complications
72
Q

What are the causes of pancreatitis?

A
  • Gallstones 40%
  • ETOH 40%
  • Other 20%
73
Q

Acute pancreatitis treatment approach
* Evaluate for what?
* What do you need to replace?
* What needs to correct?
* Initial _

A
  • Evaluate for SIRS
  • Fluid replacement
  • Electrolyte correction: Mg, Ca, K
  • Initial NPO
74
Q

Acute pancreatitis treatment approach
* What do you need to give if hyperglycemic?
* What do you need to control?
* Remove what?
* Do not forget what?

A
  • Insulin – if hyperglycemic
  • Pain control
  • Remove causative agents
  • Don’t forget – ETOH withdrawal
76
Q

Acute pancreatitis treatment approach
* What is first line for fluid replacement?
* What is the dosing?
* Less aggressive in who?

A

First-line lactated ringers
* 5 to 10 mL/kg/hr or 20 mL/kg bolus; followed by 3 mL/kg/hr
* First 24 to 48 hours

Less aggressive in patients with cardiac disease or renal dysfunction

77
Q

Acute pancreatitis treatment approach: Pain control
* What may be used for mild disase?
* What is considered maystay?
* Caution in who?

A
  • Ketorolac may be appropriate for mild disease
  • Opioids considered mainstay (any)
  • Caution: renal or liver disease
78
Q

Acute pancreatitis treatment approach: Pain control
* Historically what was the DOC for pain?
* What can be used as adjuncts?

A
  • Historically meperidine DOC (no more bc toxin metabolite that is renally elim.-> not good for ppl with decrease renal fxn)
  • Acetaminophen / NSAIDS may be used as adjuncts
79
Q

Acute pancreatitis treatment approach
* What is the nutrition process?

A
  • Oral feeding may resume when pain improved and labs normalizing
  • Patients with severe acute pancreatitis may require enteral feeding if unable tolerate oral diet by day 5
  • Parenteral nutrition rarely required
80
Q

Acute pancreatitis treatment approach: Electrolyte/organ dysfunction
* What do need to correct?
* What is common? Monitor what?

A
  • Electrolytes commonly abnormal->Correct
  • Transient organ dysfunction common-> Monitor liver, kidneys, lungs
81
Q

Acute pancreatitis treatment approach: Antibiotics
* What is not recommended? Why? (3)
* Consider for patients with what?

A

Empiric antibiotics not recommended
* No reduction in pancreatic necrosis
* No reduction in mortality
* Good antibiotic stewardship

Consider for patients with necrosis who deteriorate or fail to improve within 7 to 10 days

82
Q

Chronic pancreatitis
* What does persistent pancreatic inflammation lead to?

A

Irreversible changes to pancreatic structure
* Acinar cell destruction
* Ductal dilation
* Fibrosis
* Calcium deposits
* Increased risk of pancreatic cancer

83
Q

Chronic pancreatitis
* What are the sxs?
* What are things that can develop?
* What is important?

84
Q

Chronic pancreatitis
* What is the pain management?(4)

A
  • Smoking and ETOH cessation
  • NSAIDS
  • Opioids
  • Procedural therapies
85
Q

Chronic pancreatitis
* What do you need to treat for?
* Manage what?

A

Treat pancreatic insufficiency
* Steatorrhea
* Diabetes mellitus

Manage complications

87
Q

Malabsorption / steatorrhea
* What do you need to replace and why?
* What do you give?
* Reduction of what?
* What do you need to give to help with weight

89
Q

Pancrelipase
* What is it?
* Ingested with what?

A
  • Exogenous digestive hormones and enzymes required for normal digestion
  • Ingested with meals and snacks to improve digestion and absorption; decrease abdominal pain
90
Q

Pancrelipase
* What are the indications?

A
  • Exocrine pancreatic insufficiency
  • Pancreatitis
  • Pancreatic surgery
  • Cystic fibrosis
  • Steatorrhea – post gastrectomy syndrome
  • Pancreatic cancer
91
Q

Pancrelipase
* What does Lipase, amylase and proteases do since they all have this?

A
  • Lipase – hydrolysis and degradation of fats
  • Amylase – hydrolysis and digestion of starches
  • Proteases – breakdown proteins and amino acids
92
Q

Pancrelipase
* What is the site of action?
* Minimal what?
* What is the dose based off what?

A
  • Site of action: duodenum
  • Minimal systemic absorption
  • Dose: Based on lipase component
    * 500 to 2500 units/kg/dose with each meal (25, 000 to 50, 000 units/meal)
    * 50% dose per snack
93
Q

Pancrelipase
* What are the SE?
* What do you need monitor?(4)

A

Adverse effects – minimal

Monitoring
* Abdominal symptoms
* Weight / growth
* Stool character
* Blood glucose

94
Q

General approach to anorectal disorders

95
Q

What does not help with consitipation?

A

Stool softners: Docusate (Na or Ca)
* More preventive

96
Q

ANorectal disorder treatment:
* What should be included in all regimens?

A

WASH-> FIRST LINE

97
Q

Anorectal disorder treatment
* What is the txt options for anorectal abscess?

A

Incision and drainage
± antibiotics
* Cipro+ metro or augmentin

98
Q

Anorectal disorder treatment
* Anal fissure: what are the treatment options?

A

Topical nitroglycerin or nifedipine (DOC)
* Increased healing
* Less adverse reactions
* Increase anal blood flow and sphincter tone

99
Q

Anal fisure
* Where is the MC location? What is another location?
* What is commerically available?

A
  • MC location = posterior
  • Lateral = underlying dx
  • Topical nifedipine not commercially available
100
Q

Hemorrhoids:
* What are the treatment options?
* What do you need to do?

A
  • Initial conservative therapies
  • Rubber band ligation – internal
  • Hemorrhoidectomy

Internal vs external->Staging of internal

101
Q

What are the medications for treatment of symptomatic hemmorhoids? (General?

102
Q

What is the role and precaustion of anesthetics local?

103
Q

What is the role and precaustion of astringent and protectants topical?

104
Q

What is the role and precaustion of corticosteroids?

105
Q

What is the role and precaustion of topical vasoactive agents?

106
Q

What are the drugs that cause constipation?

107
Q

Constipation
* Defined as what?
* Varies by who?
* What are the two types?
* What is common?

108
Q

Constipation: nonpharm
* increase what? How should you do this?
* What can you add?
* Increase intake of what?

109
Q

Constipation: Bulk laxatives
* What is the MOA?

A
  • Insoluble methylcellulose fibers
  • Take up water in the large intestine forming a large mass
  • Intestinal wall distension
  • Stimulation of mechanoreceptors
  • Induce contraction and relaxation of intestinal smooth muscle
110
Q

What is the MOA of osmotic laxatives?

A
  • Increases solute load in intestine
  • Pulls water in
  • Increases stool volume and stretches bowel water
  • Triggers defecation reflex
111
Q

Constipation
* What is first line in terms of meds? list them(3)

A

First-line = bulk-forming
* Psyllium, methylcellulose, polycarbophil

112
Q

What can you add to first line for constipation?

A

Second-line = osmotic
* Add to bulk-forming if no significant benefit in 2 to 4 weeks
* PEG products (Miralax / Golytely)
* Lactulose

113
Q

Stimulants
* Can be used when?
* limited what?

A
  • Can be used if no BM in 2 days
  • Limited use recommended
114
Q

Laxatives
* What do they cause? (aka MOA)

A

Irritant and stimulant laxatives
* Prevent water reabsorption in the colon and / or
* Promote water secretion from the intestinal mucosa
* Irritate nerve fibers of the intestinal mucosa
* Stimulate defecation

115
Q

secretagogues
* Who should be uses these? (3)
* Safe for what?

A
  • Prescription products reserved for patients with refractory, chronic constipation
  • Chronic idiopathic constipation with failed first-line agents
  • Opioid induced constipation
  • Safe for prolonged use
116
Q

Suppositories and enemas
* usually produce what?
* Work similar to what?

A
  • Usually produce bowels movement within 30 to 60 minutes
  • Work similarly to oral laxatives
117
Q

Suppositories and enemas
* What are all the different types?

A
  • Glycerin – osmotic
  • Bisacodyl – stimulant
  • Sodium phosphates – osmotic
  • Soap suds – stimulant / irritant
  • Combination
118
Q

Inflammatory bowel disease
* What is used for dx?
* Which one is curable and controllable?
* Which one gets better or worse with smoking?

A

Colonoscopy and upper endoscopy diagnostic

UC curable and CD controllable

Smoking association
* UC – prevents or delays
* Crohn’s - worsens

119
Q

pharmacotherapy
* No agent is what?
* Specific agents should be individualized based what?
* All classes work through what?

A

No agent is curative

Specific agents should be individualized based on disease severity and location of disease

All classes work through decreasing inflammation

120
Q

pharmacotherapy IBD

121
Q

pharmacotherapy IBD

122
Q

5-aminosalicylates (5-ASA)
* What is sulfasalazine? How does it work?

A

Sulfasalazine = prototypical ASA
* Sulfonamide (sulfapyridine) + mesalamine (5-aminosalicylic acid)
* Cleaved by gut bacteria into separate molecules

123
Q

5-aminosalicylates (5-ASA)
* How does mesalamine work?

A

Mesalamine = active form
* Remains in gut and exerts its effects locally

124
Q

What does both mesalamine and sulfasalazine do? (MOA)
* What is the CI?

A

MOA:
* Interferes with arachidonic acid production by affecting thromboxane and lipoxygenase synthesis pathways
* Free radical scavenging
* Interfere with TNF and TGF activity
* Primarily used in UC

CI: sulfonamide or salicylate allergy

126
Q

Glucocorticoids / immunomodulators-IBD
* Glucocorticoids is not for what?
* What are the Systemic Glucocorticoids agents?
* What are the topical Glucocorticoids agents?

A

Glucocorticoids
* Not indicated for maintenance therapy

Systemic agents
* Prednisone
* Methylprednisolone

Topical agents
* Budesonide

127
Q

Glucocorticoids / immunomodulators
* What are immunomodulators not indicated for?
* What are the examples? (4)

A

Not indicated for induction
* Methotrexate
* Azathioprine
* Cyclosporine
* Tacrolimus

MCAT

131
Q

IBd – biologic agents
* What are Anti TNF agents?

A

*is first line

132
Q

IBD biologic agents
* What are the non-ANTI-TNF agents and the Anti IL-21/23

133
Q

IBD-Biologic agents
* What are the general SE? (5)

A
  • Infusion reactions / anaphylaxis
  • Injection site reactions
  • Infection: TB, hepatitis reactivation
  • Increase risk of certain cancers
  • Demyelination disorders
134
Q

What is considered mild, moderate, severe and fulminant UC?

135
Q

UC treatment approach: INDUCTION
* What is first and second line for mild to moderate?

A
  • First-line: 5-ASAs -> Sulfasalazine / mesalamine
  • Alternative: oral budesonide
136
Q

UC treatment approach: INDUCTION
* What is first for moderate to severe disease?

A
  • Same as mild to moderate
  • ± systemic corticosteroids: Prednisone 40 to 60 mg/day
137
Q

UC treatment approach: INDUCTION
* What is first for fulminant disease?

A

First line: systemic IV corticosteroids
* Methylprednisolone

138
Q

UC treatment approach: MAINTENANCE
* No role for what? Should be what?

A

No role for corticosteroids
* Should be weaned over 3 to 4 weeks (from the induction section)

139
Q

UC treatment approach: MAINTENANCE
* What is the treatment for mild to moderate diease?
* What is the treatment for severe to fulminant disease?

A

Mild to moderate disease
* First-line: 5-ASAs -> Sulfasalazine / mesalamine
* Alternative: oral budesonide

Severe to fulminant disease
* Biologics ± immunomodulators
* Infliximab ± azathioprine often first-line

140
Q

Crohn’s treatment approach: Induction
* What is not effective at inducing remission?
* What type of therapy for more severe disease?

A
  • Immunomodulators not effective at inducing remission
  • Step-down therapy for more severe disease
141
Q

Crohn’s treatment approach: Induction
* What is the txt for mild disease?
* What is the the txt for moderate to severe disease?

A

Mild disease
* First-line: Sulfasalazine / mesalamine
* Not as effective for CD
* Best side effect profile

Moderate to severe disease
* First-line: systemic steroids
* + biologics

142
Q

Irritable Bowel Syndrome (IBS) - Symptoms
* Abdominal pain/discomfort with what? (3)

A
  • Diarrhea Predominance
  • Constipation Predominance
  • Alternating Diarrhea with Constipation
143
Q

Irritable Bowel Syndrome (IBS) - Symptoms
* What are the other sxs

A
  • Abdominal Bloating
  • Mucous in the stool
  • Fecal Urgency
  • Feeling of incomplete stool evacuation
  • Associated GI symptoms – difficulty swallowing,
  • Other Symptoms – headache, insomnia, myalgias, TMJ disorder, back/pelvic pain
  • 50% of fibromyalgia patients have IBS
144
Q

What are the IBS red flags?

146
Q

IBS: Consitpation predominant
* Increase what?
* First line? Second line?
* Consider what?
* What was pulled from the market?
* What are two other treatments?

A
  • Increase dietary fiber and fluid intake
  • First-line laxatives: bulk laxatives
  • Second-line laxatives: osmotic
  • Consider antispasmodics
  • Secretagogues: Serotonin-4 agonist – pulled from US market July 2022
  • Psychotherapy
  • Antidepressants
147
Q

Opioid induced constipation
* MC where? May see where?
* What is first line generally?

A
  • MC in hospital setting
  • May see in patients on chronic opioids outpatient
  • First-line generally traditional laxatives
148
Q

Opioid induced constipation
* What are the Specific GI opioid antagonists? What do they do?

A

Bind to µ receptor in GI tract; reverse GI effects but not analgesic effects
* Alvimopan (Entereg)
* Methylnaltrexone
* Naloxegol
* Naldemedine

149
Q

IBS: diarrhea predominant
* Avoid what?
* What can you give for meds?

A

Avoid triggering foods

Avoid diarrhea inducing foods / drugs
* Caffeine
* ETOH
* Artificial sweeteners

Antidiarrheals / antispasmodics

5HT3 antagonist - alosetron

150
Q

What does the FOMAP diet stand for?

151
Q

Antidiarrheals: Liperamide
* OTC or prescription?
* Does not do what?
* Not well what?
* What can it worsen? Who is it not recommended for?

A
  • OTC
  • Does not cross the BBB
  • Not well absorbed
  • May worsen diarrhea in some causes (toxin: increase contact time-> more tissue damage)
  • Do not recommend if patient has fever or bloody stool
152
Q

Antidiarrheals: Diphenoxylate/atropine
* OTC or prescription
* Class?
* Well what?
* Crosses what? What does it cause?
* May worsen what? not recommend for who?

A
  • Prescription only
  • Class V controlled substance
  • Well absorbed
  • Crosses BBB
  • CNS depression
  • May worsen diarrhea in some causes (toxin: increase contact time-> more tissue damage)
  • Do not recommend if patient has fever or bloody stool
153
Q

Alternative therapies: IBS

154
Q

Antidepressants and IBS
* Modulates what?
* Manage concomitant what?

A

Modulate perception of visceral pain

Manage concomitant psychiatric diagnoses
* Anxiety
* Depression

155
Q

Antidepressants and ibs
* What are the specific agents?

A

Specific agent based on predominate symptoms
* Tricyclic antidepressants
* SSRIs
* SNRIs

156
Q

Intussuception
* What is it?
* MC occurs where?
* What are the sxs/

A
  • Telescoping or prolapse of one portion of the bowel into an immediately adjacent segment.
  • Most commonly occurs at the terminal ileum
  • SXS – abdominal pain, vomiting, “currant jelly” stools
157
Q

Intussusception
* Most cases can be both diagnosed and treated with what?
* Typically who gets this?

A
  • Most cases can be both diagnosed and treated with barium enema or air enema
  • Typically, a child with severe intermittent abdominal pain; will not say currant jelly; sausage like mass on palpation or imaging
158
Q

Ischemic Colitis
* What is it? Common in who?
* Thought to be caused by what?
* BUT ischemic olitis is almost always what?

A
  • Ischemia of the colon (GUT ANGINA) most often affects the elderly (90% of patients > 60 y/o ).
  • Thought to be caused by small vessel atherosclerosis
  • Ischemic colitis is almost always nonocclusive. (emboli are the most common cause of occlusive acute mesenteric ischemia)

PAIN OUT OF PROPORTION TO PHYSICAL EXAM. No tenderness, no guarding.

159
Q

Ischemic Colitis
* What aee the sxs?
* How do you dx it?
* What is the txt?

A

Symptoms – postprandial abdominal pain followed by rectal bleeding
* Lactic acid is elevated >2

Diagnosis – CTA Abdomen and Pelvis

Treatment – Supportive (bowel rest, IV fluids, pain control, ABX, ± anticoagulation) - surgery is rarely required.

160
Q

Toxic megacolon
* What it is?
* What is the MCC?
* What are the sxs?
* What are the goals?

161
Q

Toxic megacolon
* What is the inital therapy? (it is a lot, I did not know to break it up)

A

Supportive care and medical management – prevents surgery in 50%
* Fluids and electrolyte replacement
* NPO
* ± NG decompression (not rectal)
* Stop medications that decrease intestine motility
* ± total parenteral nutrition
* Broad-spectrum antibiotics (pip/taxo, carbopenem, vanco+metro)
* NO bowel prep, barium enema, colonoscopy
* Treat underlying cause if possible
* IBD associated TM – corticosteroids DOC
* C. difficile - antibiotics (Fidaxomicin or oral vanco)

162
Q

Acute diverticulitis
* What it is?
* What are the sxs?
* What does the CBC show?
* How do you dx it?

A
  • Inflammation of diverticulum
  • SXS – Fever and LLQ pain
  • CBC – elevated WBC count
  • DX – Clinical, CT Abd and Pelvis with contrast

During the acute episode
* NO COLONOSCOPY
* NO BARIUM ENEMA

163
Q

Acute Diverticulitis
* What are the MC organisms?

A
  • E. coli
  • Enterobacter
  • Klebsiella
  • Bacteroides
  • Enterococcus
164
Q

Acute diverticulitis treatment
* What is the outpt treatment?
* How long?

165
Q

Acute diverticulitis treatment
* What is the inpt treatment?
* How long?

Pharm III (14 decks)

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