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Nursing - Bloomberg > 💊370: GI Disorders + Pharm > Flashcards

💊370: GI Disorders + Pharm Flashcards

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1
Q

Gastro-Esophageal Reflux (GER)

A
  1. Backflow of Acid from stomach into esophagus
  2. Usually short lived. And seldom causes more serious problems
  3. Usually heartburn after eating
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2
Q

Gastric-Esophageal Reflux Disease (GERD)

A

Associated wit weak or incomplete lower esophageal sphincter (LES)

Reflux esophagitis involves mucosal injury to esophagus, hyperaemia, and inflammation.

May also produce resp symptoms such as wheezing, chronic cough, hoarseness

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3
Q

What are risk factors for GERD?

A
  1. Decreased LES tone (alcohol, smoking, fatty/spicy/fried foods, caffeine, chocolate)
  2. Increased intraabdominal/gastric pressure (pregnancy, obesity, lying down after meals)
  3. Physiological abnormalities (hiatal hernia)
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4
Q

What medications are associated with decreased LES tone?

A
  1. Calcium channel blockers
  2. Bets-Blockers
  3. Anticholinergics
  4. Benzodiazepines
  5. Theophylline
  6. Nitrates
  7. Barbiturates
  8. Narcotics
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5
Q

What medications are associated with injury to the esophageal mucosa?

A
  1. NSAIDs
  2. Biphosphonates
  3. Potassium supplements
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6
Q

What are complications of GERD?

A
  1. Esophagitis
  2. Esophageal strictures
  3. Barrett’s Esophagus = squamous mucosa gradually replaces by columnar epithelium resembling stomach and intestines = ⬆️ risk esophageal cancer ♋️
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7
Q

What are diagnostic tests for GERD?

A
  1. Hx of reflux
  2. ECG to exclude cardiac origin
  3. Barrium swallow
  4. Esophagoscopy
  5. pH Monitoring (24hr ambulatory through NG) (decreases with incompetent LES)
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8
Q

Nissen Fundoplication for GERD

A
  1. When symptoms continue despite medication and lifestyle changes
  2. Upper part of stomach (fundas) is wrapped around LES and sutured to strengthen the sphincter
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9
Q

Peptic Ulcer Disease (PUD)

A

Break in continuity of lower esophageal, gastric, or duodenal mucosa (any part that comes in contact with gastric juices - acid + pepsin)

Acute or chronic, superficial or deep

Duodenum most common site. Antrum of stomach second.

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10
Q

What are defensive factors of the stomach and duodenum to avoid self-digestion?

A
  1. Mucus = secreted by mucosa cells
  2. Bicarbonate = neutralizes H+ ions (Acid)
  3. Blood flow = maintains mucosal integrity
  4. Prostaglandins = stim secretion of mucus + bicarb, promotes vasodilation, suppresses gastric acid
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11
Q

Helicobacter Pylori

A

Gram Negative Bacteria that releases toxin that destroys gastric + duodenal mucosa, reducing the epithelium’s resistance to ACID-PEPSIN.

Secretes urease which produces ammonia to buffer acidity of its environment.

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12
Q

What are possible causes of PUD?

A
  1. H. Pylori
  2. Chronic drug use
  3. NSAIDs, Aspirin
  4. Corticosteroids
  5. Alcohol
  6. Acute trauma, major illness, or infection (stress ulcers)
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13
Q

What are diagnostic tests for PUD?

A
  1. Clinical manifestations
  2. Lab tests: CBC, stool occult blood
  3. Barrium Swallow/radiological imaging
  4. Endoscopy
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14
Q

What are diagnostic tests for Helicobacter Pylori?

A
  1. Urea breath test
  2. Serologic rest for antibodies
  3. Endoscopic biopsy
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15
Q

What is the treatment for Helicobacter Pylori?

A

2 or more antibiotics + proton pump inhibitor (PPI)

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16
Q

What are management strategies for an active GI bleed?

A
  1. NG tuve inserted for gastric decompression
  2. Rest
  3. Iced saline lavage (May contain Norepinephrine)
  4. Gastos copy and coagulation by laser or cautery
  5. Surgery maybe necessary
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17
Q

What are complications of PUD?

A
  1. Obstruction = edema, scar tissue, muscle spasm
  2. Perforation
  3. Peritonitis
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18
Q

What are signs and symptoms of Peritonitis?

A
  1. Severe, acute abdominal pain radiating throughout abdomen + shoulder
  2. Rigid, board-like abdomen
  3. Absent bowel sounds
  4. Symptoms of shock
19
Q

Vagotomy

A

Cutting the cavalier nerve fibres selectively to eliminate the acid-secreting stimulus to gastric cells

20
Q

Pyloroplasty

A

Often performed with Vagotomy, involves widening of the existing exit of the stomach at the pylorus.

Enhances gastric emptying.

21
Q

Subtotal Gastrectomy

A

Billroth 1 = gastroduodenostomy (Antrum of stomach joined to duodenum)

Billroth 2 = gastrojejunostomy (Antrum of stomach joined to jejunum)

Both require antrectomy

22
Q

What is the pathophysiology of Ulcerative Colitis?

A
  1. Inflammatory process involves only mucosa + submucosa
  2. Usually starts in rectum + sigmoid colon, spreading to entire colon
  3. Inflamed and swelling lesions become mucosal hemorrhages
  4. Abscesses result and coalesce into ulcers (hemorrhage, edema, and purluent drainage)
  5. Become necrotic + sloughing of bowel mucosa (ulcerative + exudative inflammation)
  6. Heals as scarring and fibrosis
  7. Atrophy, narrowing, thickening and shortening of colon
  8. Malabsorption + increased risk of infection
23
Q

What are clinical manifestations of Ulcerative Colitis?

A
  1. Insidious onset
  2. Recurrent exacerbation + remission
  3. Frequent bloody diarrhea (+ pus and mucus)
  4. Crampy abdominal pain
  5. LEFT abdominal tenderness
  6. Rectal bleeding
  7. TENESMUS (incomplete defecation)
  8. Dehydration
  9. Weight loss
  10. Anemia
  11. Low grade FEVER
  12. Weakness
24
Q

Crohn’s Disease

A

Aka REGIONAL ENTERITIS

Inflammation of any segment of GI Tract, extending through all layers of GIT. May involve regional LYMPH nodes and the MESENTERY.

25
Q

What is the pathophysiology of Crohn’s Disease?

A
  1. Granulomatous (nodular) type of inflammation spreads slowly and gradually
  2. Shallow ulceration of mucosa + submucosa development
  3. Lymph nodes enlarge + lymph flowin submucosa blocked
  4. Causes edema, mucosal ulceration, fissures, abscesses
  5. Ulcers + fissures involve entire thickness of bowel wall (TRANSMURAL)
  6. Chronic inflammation, fibrosis, thicken bowl wall, scarring narrows Lumen
  7. Lead to local obstruction, abscess formation, fistula formation
26
Q

What are clinical manifestations of Crohn’s Disease?

A
  1. Chronic relapsing + slowly progressive
  2. Intermittent, usually less bloody diarrhea +/- steatorrhea
  3. Generalized abdominal pain or in RLQ
  4. Weight loss
  5. N/v
  6. Low grade FEVER
  7. Malaise
27
Q

What is included on a routine blood and stool test for IBD?

A
  1. CRP
  2. ESR
  3. CBC
  4. Electrolytes(Na, K, Cl)
  5. Liver enzymes
  6. Vitamin B12
  7. Vitamin D
  8. Calprotectin (stool protein)
  9. Lacto Ferris (stool protein)
  10. Stool culture
28
Q

What are specialized blood tests for IBD?

A
  1. pANCA (perinuclear anti-neutrophil antibody) = UC from CD
  2. ASCA (anti-Saccharomyces cervisiae antibody) = CD from UC
  3. CBir1 (anti-flagellin antibody) = CD
  4. OmpC (anti-OmpC antibody) = CD
  5. TPMT (thiopurine methyltransferase)
29
Q

What are classes of anti-ulcer drugs?

A
  1. Anti secretory agents
  2. Mucosal protectants
  3. Antacids
  4. Antibiotics
30
Q

What is the mechanism of action for Histamine2 Receptor Antagonists (H2RAs)?

A

Selective, competitive blockade of H2 receptors on parietal cells:
⬇️ H+K+ATPase activity
⬇️ basal and stimulate gastric acid secretion

Effective for PUD/duodenal ulcers and GERD

31
Q

What is a prototype of Histamine2 Receptor Antagonists (H2RAs)?

A

Ranitidine (Zantac)

32
Q

What are side effects of Histamine2 Receptor Antagonists (H2RAs)?

A
  1. Headache
  2. Diarrhea
  3. N/v
  4. May inhibit CYP450
33
Q

What is the mechanism of action for Proton Pump Inhibitors (PPIs)?

A

Potent, irreversible inhibitors of H+K+ATPase:
⬇️ basal and stimulates gastric acid release
⬇️ acid secretion

Effects persist until new enzyme is synthesized (3-5 days)

34
Q

What are common uses of Proton Pump Inhibitors (PPIs)?

A
  1. PUD/duodenal ulcers
  2. GI bleeds
  3. GERD unresponsive to H2RAs
  4. H. Pylori (with antibiotics)
35
Q

What are common side effects of Proton Pump Inhibitors (PPIs)?

A
  1. Rarely headache
  2. diarrhea
  3. N/v
  4. Pneumonia
  5. Fracture risk - dec Ca absorption
  6. Risk of C. Diff.
36
Q

What is an example of Proton Pump Inhibitors (PPIs)?

A

Omeprazole (Losec)

37
Q

What antibiotics are usually used for H. Pylori?

A
  1. Clarithromycin
  2. Amoxicillin or metronidazole

+ PPI

38
Q

What is the mechanism of action for Misoprostol (Cytotec)?

A

Prostaglandins analog creates GI protective effects.

Used to PREVENT NSAID-indices PUD

39
Q

What are side effect of Misoprostol (Cytotec)?

A
  1. Diarrhea
  2. Abdominal pain
  3. Dysmenorrhea
  4. Abortefacient (contraindicated in pregnancy)
40
Q

What is the mechanism of action for Anracids?

A

Neutralizes gastric acid to decrease gut walk injury.
⬇️ Pepsin activity (if pH above 5)
Stimulated prostaglandins production

Used for PUD + GERD symptomatic relief

41
Q

What are side effects of Antacids?

A
  1. Constipation or diarrhea depending on scent

2. Some contain sodium = worsen HTN or CHF

42
Q

What are examples of an antacid?

A
  1. Magnesium hydroxide (milk of magnesia)
    +++diarrhea, accumulation in renal impairment can lead to CNS depression
  2. Calcium carbonate (Tums)
    = constipation, belching, flatulence, acid rebound, hypercalcemia.
43
Q

Which drugs are useful for GERD?

A
  1. Antacids (mild cases only)
  2. H2RAs
  3. PPIs (most effective)
  4. Prokinetic agents (ex. Metoclopramide) (symptom relief only)

Nursing - Bloomberg (52 decks)

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