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

Lecture 2 (GI)-Exam 1 Flashcards

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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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A
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4
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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
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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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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
What is first line for H. pylori?
CAP therapy: * PPI * Clarithromycin * Amoxicillin
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Do not worry about dosing-> know drugs
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Bismuth subsalicylate: * What are the effects? (4)
* Topical antimicrobial effect * Stimulates absorption of fluid/electrolytes * Anti-inflammatory * Binds bacterial toxins
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Bismuth subsalicylate: * What are the SE? (2) * Not recommended for who? * Do not usee in who? * CL?(4)
* 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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Metronidazole and tetracyline: * What are the effects?
In vitro activity against H. pylori
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Metronidazole and tetracyline: * What is the MOA and SEs?
31
PPIs * What is the effects?
* Promotes healing * Enhances antimicrobial effects
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NSAIDs mechanism of action * What is always circulating * What does it produce and cause?
33
* Where is COX-2 induced? What does it mediate
COX-2 induced at sites of inflammation * Mediate inflammation, pain, and fever
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NSAID Mechanism of action * What is the MOA of NSAIDs? What are thier effects?
NSAIDs block COX-1 and COX-2 * Reduce prostaglandin, thromboxane, prostacyclin synthesis * Reduce inflammation, pain, and fever
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NSAIDS * What happens when COX-1 is inhibited?
* Decreased gastric blood flow * Decreased mucous production * Inhibition of platelet activation (TXA2)->Cardioprotective
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NSAIDS * What is the MOA of COX-2 cause if inhibited? What happens? * increased risk of what?
Inhibition of prostacyclin * Vasoconstriction * Platelet aggregation Unopposed COX-1activity * Vasoconstriction * Platelet aggregation INCREASED risk of cardiovascular events
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NSAID-induced PUD * Cause what? * Progresses to what? * Rarely causes what?
* 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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NSAID-induced PUD * Risk increased with what? * Dependent on what? * Greater propensity to do what?
* Risk increases with advancing age (> 65 years independent risk) * Dependent on dose, duration, type of NSAID * Greater propensity to inhibit COX 1 increases risk
39
NSAID-induced PUD * Explain how Greater propensity to inhibit COX 1 increases risk? (3)
* Salicylates = higher risk (aspirin) * Low dose ASA + NSAID increases risk * Low dose ASA + clopidogrel increases risk
40
NSAID induced ulcer treatment * What is recommended to stop? * What is first line and the alternative if that is stop?
NSAIDs held / discontinued (recommended): * First-line: PPI x 8-weeks – most effective * Alternative: H2RA or sucralfate alternative
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NSAID induced ulcer treatment * What is first line if NSAIDs are not held? * Treat what if present?
* 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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Prevention of NSAID-related ulcers * What is most effective?
COX-2 specific agent + PPI
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Prevention of NSAID-related ulcers * What are the alternative treatments?
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Prevention of NSAID-related ulcers * What needs to be considered?
Cardiovascular and gastrointestinal risks should be considered
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Prevention of NSAID-related ulcers
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PUD maintenance therapy (long term PPI use) * Limited to high-risk subgroups of patients including patients with the following: (5)
* Refractory peptic ulcer * H. pylori-negative, NSAID-negative ulcer disease * Giant (>2 cm) ulcer and age >50 years or multiple comorbidities * Failure of H. pylori eradication, including rescue therapies * Frequently recurrent peptic ulcers (>2 documented recurrences a year) * **Continued NSAID use**
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Long term PPI therapy * What is most effective for GERD * Studies suggest what? * Most are what? * High quality studies have only shown what?
* 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**
48
GI bleeding - GI emergency * What are the two types? * What is the MC nonvariceal? * PUD assoicated= * SRMD=
Variceal or nonvariceal * MC nonvariceal = chronic PUD and stress related mucosal damage (SRMD) * PUD associated = prehospital * SRMD = critically ill hospitalized patients
49
Gi emergency: SRMD = critically ill hospitalized patients * What are is the cause? * Where? * _ areas
* Mucosal ischemia from splanchnic hypoperfusion and reduced gastric blood flow * Proximal stomach * Numerous areas
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GI bleeding: treatment * What is the txt? (supportive and therapic)(4)
51
Stress ulcer prophylaxis * Indiction for who? (7)
52
75 to 100% of ICU patients develop what?
75 to 100% of ICU patients develop SRMB within 1 to 3 days
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Stress ulcer prophylaxis * What is the prevention (2)
* Adequate fluid resuscitation * Maintain gastric pH > 4
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Stress ulcer prophylaxis: * What are the SE of H2RAs? (3) * What is the SE of PPI?(2)
H2RAs * May cause mental status changes * Thrombocytopenia * Renal dose adjustment PPI * Increase risk of C. diff and pneumonias
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Zollinger-Ellison syndrome * What is the patho of it? * What are the sxs?
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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Zollinger-Ellison syndrome * What is the txt?(3)
* Tumor resection if possible * Chemotherapy * High dose PPIs * Twice daily doses up to 180 mg / day
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Delayed Gastric Emptying: * MCC is what? * What are the sxs? * What do you need to rule out of? * How do evaluate it?
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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Delayed Gastric Emptying * What is the treatment?
Avoid food and medications that slow gastric emptying * Foods high in fat * Anticholinergics, opiates, dopamine agonists Control diabetes Prokinetic medications
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Prokinetics: metoclopramide * What is the MOA?
* Inhibits D2, 5HT3 receptors * Stimulates 5HT4 receptors * Increases LES pressure and gastric contractions * Mild antiemetic
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Prokinetics: metoclopramide * What are the SE?(3)
* Asthenia (weakness) * HA * Somnolence * EPS
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Prokinetics: Macrolide antibiotics * What are the examples? * What is the MOA? * Tolerance?
* Erythromycin / azithromycin / clarithromycin * Stimulates motilin receptors * Motilin stimulation increases GI motility and gastric emptying * Tolerance may develop in some patients
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Prokinetics: Macrolide antibiotics * What are the interactions to avoid?
Avoid concomitant administration with magnesium or aluminum-containing antacids
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Prokinetics: macrolides * What are the SEs?(5)
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Acute Pancreatitis * Edematous: Usually what? What type of care? * Necrotizing: More severe disorder in which what?
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
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Know severity
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Acute Pancreatitis Diagnosis * In acute pancreatitis, what do you need in order to dx?
71
acute pancreatitis on CT scan * Why is it good? (3)
* Helpful if diagnosis is in question * Helpful in determining prognosis * Helpful in detecting complications
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What are the causes of pancreatitis?
* Gallstones 40% * ETOH 40% * Other 20%
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Acute pancreatitis treatment approach * Evaluate for what? * What do you need to replace? * What needs to correct? * Initial _
* Evaluate for SIRS * Fluid replacement * Electrolyte correction: Mg, Ca, K * Initial NPO
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Acute pancreatitis treatment approach * What do you need to give if hyperglycemic? * What do you need to control? * Remove what? * Do not forget what?
* Insulin – if hyperglycemic * Pain control * Remove causative agents * Don’t forget – ETOH withdrawal
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Acute pancreatitis treatment approach * What is first line for fluid replacement? * What is the dosing? * Less aggressive in who?
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
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Acute pancreatitis treatment approach: Pain control * What may be used for mild disase? * What is considered maystay? * Caution in who?
* Ketorolac may be appropriate for mild disease * Opioids considered mainstay (any) * Caution: renal or liver disease
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Acute pancreatitis treatment approach: Pain control * Historically what was the DOC for pain? * What can be used as adjuncts?
* 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
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Acute pancreatitis treatment approach * What is the nutrition process?
* 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
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Acute pancreatitis treatment approach: Electrolyte/organ dysfunction * What do need to correct? * What is common? Monitor what?
* Electrolytes commonly abnormal->Correct * Transient organ dysfunction common-> Monitor liver, kidneys, lungs
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Acute pancreatitis treatment approach: Antibiotics * What is not recommended? Why? (3) * Consider for patients with what?
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
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Chronic pancreatitis * What does persistent pancreatic inflammation lead to?
Irreversible changes to pancreatic structure * Acinar cell destruction * Ductal dilation * Fibrosis * Calcium deposits * Increased risk of pancreatic cancer
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Chronic pancreatitis * What are the sxs? * What are things that can develop? * What is important?
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Chronic pancreatitis * What is the pain management?(4)
* Smoking and ETOH cessation * NSAIDS * Opioids * Procedural therapies
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Chronic pancreatitis * What do you need to treat for? * Manage what?
Treat pancreatic insufficiency * Steatorrhea * Diabetes mellitus Manage complications
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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
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Pancrelipase * What is it? * Ingested with what?
* Exogenous digestive hormones and enzymes required for normal digestion * Ingested with meals and snacks to improve digestion and absorption; decrease abdominal pain
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Pancrelipase * What are the indications?
* Exocrine pancreatic insufficiency * Pancreatitis * Pancreatic surgery * Cystic fibrosis * Steatorrhea – post gastrectomy syndrome * Pancreatic cancer
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Pancrelipase * What does Lipase, amylase and proteases do since they all have this?
* Lipase – hydrolysis and degradation of fats * Amylase – hydrolysis and digestion of starches * Proteases – breakdown proteins and amino acids
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Pancrelipase * What is the site of action? * Minimal what? * What is the dose based off what?
* 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
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Pancrelipase * What are the SE? * What do you need monitor?(4)
Adverse effects – minimal Monitoring * Abdominal symptoms * Weight / growth * **Stool character** * Blood glucose
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General approach to anorectal disorders
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What does not help with consitipation?
Stool softners: Docusate (Na or Ca) * More preventive
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ANorectal disorder treatment: * What should be included in all regimens?
WASH-> FIRST LINE
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Anorectal disorder treatment * What is the txt options for anorectal abscess?
Incision and drainage ± antibiotics * Cipro+ metro or augmentin
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Anorectal disorder treatment * Anal fissure: what are the treatment options?
Topical nitroglycerin or **nifedipine (DOC)** * Increased healing * Less adverse reactions * Increase anal blood flow and sphincter tone
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Anal fisure * Where is the MC location? What is another location? * What is commerically available?
* MC location = posterior * Lateral = underlying dx * Topical nifedipine not commercially available
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Hemorrhoids: * What are the treatment options? * What do you need to do?
* Initial conservative therapies * Rubber band ligation – internal * Hemorrhoidectomy Internal vs external->Staging of internal
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What are the medications for treatment of symptomatic hemmorhoids? (General?
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What is the role and precaustion of anesthetics local?
103
What is the role and precaustion of astringent and protectants topical?
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What is the role and precaustion of corticosteroids?
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What is the role and precaustion of topical vasoactive agents?
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What are the drugs that cause constipation?
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Constipation * Defined as what? * Varies by who? * What are the two types? * What is common?
108
Constipation: nonpharm * increase what? How should you do this? * What can you add? * Increase intake of what?
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Constipation: Bulk laxatives * What is the MOA?
* 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
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What is the MOA of osmotic laxatives?
* Increases solute load in intestine * Pulls water in * Increases stool volume and stretches bowel water * Triggers defecation reflex
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Constipation * What is first line in terms of meds? list them(3)
First-line = bulk-forming * Psyllium, methylcellulose, polycarbophil
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What can you add to first line for constipation?
Second-line = osmotic * Add to bulk-forming if no significant benefit in 2 to 4 weeks * PEG products (Miralax / Golytely) * Lactulose
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Stimulants * Can be used when? * limited what?
* Can be used if no BM in 2 days * Limited use recommended
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Laxatives * What do they cause? (aka MOA)
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
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secretagogues * Who should be uses these? (3) * Safe for what?
* Prescription products reserved for patients with refractory, chronic constipation * Chronic idiopathic constipation with failed first-line agents * Opioid induced constipation * Safe for prolonged use
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Suppositories and enemas * usually produce what? * Work similar to what?
* Usually produce bowels movement within 30 to 60 minutes * Work similarly to oral laxatives
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Suppositories and enemas * What are all the different types?
* Glycerin – osmotic * Bisacodyl – stimulant * Sodium phosphates – osmotic * Soap suds – stimulant / irritant * Combination
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Inflammatory bowel disease * What is used for dx? * Which one is curable and controllable? * Which one gets better or worse with smoking?
Colonoscopy and upper endoscopy diagnostic UC curable and CD controllable Smoking association * UC – prevents or delays * Crohn’s - worsens
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pharmacotherapy * No agent is what? * Specific agents should be individualized based what? * All classes work through what?
No agent is curative Specific agents should be individualized based on disease severity and location of disease All classes work through decreasing inflammation
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pharmacotherapy IBD
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pharmacotherapy IBD
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5-aminosalicylates (5-ASA) * What is sulfasalazine? How does it work?
Sulfasalazine = prototypical ASA * Sulfonamide (sulfapyridine) + mesalamine (5-aminosalicylic acid) * Cleaved by gut bacteria into separate molecules
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5-aminosalicylates (5-ASA) * How does mesalamine work?
Mesalamine = active form * Remains in gut and exerts its effects locally
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What does both mesalamine and sulfasalazine do? (MOA) * What is the CI?
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
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Glucocorticoids / immunomodulators-IBD * Glucocorticoids is not for what? * What are the Systemic Glucocorticoids agents? * What are the topical Glucocorticoids agents?
Glucocorticoids * Not indicated for maintenance therapy Systemic agents * Prednisone * Methylprednisolone Topical agents * Budesonide
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Glucocorticoids / immunomodulators * What are immunomodulators not indicated for? * What are the examples? (4)
Not indicated for induction * Methotrexate * Azathioprine * Cyclosporine * Tacrolimus | MCAT
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IBd – biologic agents * What are Anti TNF agents?
## Footnote *is first line
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IBD biologic agents * What are the non-ANTI-TNF agents and the Anti IL-21/23
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IBD-Biologic agents * What are the general SE? (5)
* Infusion reactions / anaphylaxis * Injection site reactions * Infection: TB, hepatitis reactivation * Increase risk of certain cancers * Demyelination disorders
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What is considered mild, moderate, severe and fulminant UC?
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UC treatment approach: INDUCTION * What is first and second line for mild to moderate?
* First-line: 5-ASAs -> Sulfasalazine / mesalamine * Alternative: oral budesonide
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UC treatment approach: INDUCTION * What is first for moderate to severe disease?
* Same as mild to moderate * ± systemic corticosteroids: Prednisone 40 to 60 mg/day
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UC treatment approach: INDUCTION * What is first for fulminant disease?
First line: systemic IV corticosteroids * Methylprednisolone
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UC treatment approach: MAINTENANCE * No role for what? Should be what?
No role for corticosteroids * Should be weaned over 3 to 4 weeks (from the induction section)
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UC treatment approach: MAINTENANCE * What is the treatment for mild to moderate diease? * What is the treatment for severe to fulminant disease?
Mild to moderate disease * First-line: 5-ASAs -> Sulfasalazine / mesalamine * Alternative: oral budesonide Severe to fulminant disease * Biologics ± immunomodulators * Infliximab ± azathioprine often first-line
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Crohn's treatment approach: Induction * What is not effective at inducing remission? * What type of therapy for more severe disease?
* Immunomodulators not effective at inducing remission * Step-down therapy for more severe disease
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Crohn's treatment approach: Induction * What is the txt for mild disease? * What is the the txt for moderate to severe disease?
Mild disease * First-line: Sulfasalazine / mesalamine * Not as effective for CD * Best side effect profile Moderate to severe disease * First-line: systemic steroids * + biologics
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Irritable Bowel Syndrome (IBS) - Symptoms * Abdominal pain/discomfort with what? (3)
* Diarrhea Predominance * Constipation Predominance * Alternating Diarrhea with Constipation
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Irritable Bowel Syndrome (IBS) - Symptoms * What are the other sxs
* 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
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What are the IBS red flags?
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IBS: Consitpation predominant * Increase what? * First line? Second line? * Consider what? * What was pulled from the market? * What are two other treatments?
* 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
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Opioid induced constipation * MC where? May see where? * What is first line generally?
* MC in hospital setting * May see in patients on chronic opioids outpatient * First-line generally traditional laxatives
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Opioid induced constipation * What are the Specific GI opioid antagonists? What do they do?
Bind to µ receptor in GI tract; reverse GI effects but not analgesic effects * Alvimopan (Entereg) * **Methylnaltrexone** * Naloxegol * Naldemedine
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IBS: diarrhea predominant * Avoid what? * What can you give for meds?
Avoid triggering foods Avoid diarrhea inducing foods / drugs * Caffeine * ETOH * Artificial sweeteners Antidiarrheals / antispasmodics 5HT3 antagonist - alosetron
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What does the FOMAP diet stand for?
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Antidiarrheals: Liperamide * OTC or prescription? * Does not do what? * Not well what? * What can it worsen? Who is it not recommended for?
* 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
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Antidiarrheals: Diphenoxylate/atropine * OTC or prescription * Class? * Well what? * Crosses what? What does it cause? * May worsen what? not recommend for who?
* 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
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Alternative therapies: IBS
154
Antidepressants and IBS * Modulates what? * Manage concomitant what?
Modulate perception of visceral pain Manage concomitant psychiatric diagnoses * Anxiety * Depression
155
Antidepressants and ibs * What are the specific agents?
Specific agent based on predominate symptoms * Tricyclic antidepressants * SSRIs * SNRIs
156
Intussuception * What is it? * MC occurs where? * What are the sxs/
* 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
Intussusception * Most cases can be both diagnosed and treated with what? * Typically who gets this?
* 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
Ischemic Colitis * What is it? Common in who? * Thought to be caused by what? * BUT ischemic olitis is almost always what?
* 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) ## Footnote PAIN OUT OF PROPORTION TO PHYSICAL EXAM. No tenderness, no guarding.
159
Ischemic Colitis * What aee the sxs? * How do you dx it? * What is the txt?
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
Toxic megacolon * What it is? * What is the MCC? * What are the sxs? * What are the goals?
161
Toxic megacolon * What is the inital therapy? (it is a lot, I did not know to break it up)
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
Acute diverticulitis * What it is? * What are the sxs? * What does the CBC show? * How do you dx it?
* Inflammation of diverticulum * SXS – Fever and LLQ pain * CBC – elevated WBC count * DX – Clinical, CT Abd and Pelvis with contrast ## Footnote During the acute episode * NO COLONOSCOPY * NO BARIUM ENEMA
163
Acute Diverticulitis * What are the MC organisms?
* E. coli * Enterobacter * Klebsiella * Bacteroides * Enterococcus
164
Acute diverticulitis treatment * What is the outpt treatment? * How long?
165
Acute diverticulitis treatment * What is the inpt treatment? * How long?

Pharm III (14 decks)

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