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AGACNP > Gastrointestinal disorders > Flashcards

Gastrointestinal disorders Flashcards

1
Q

Peptic ulcer diease (PUD)

A
  • A GI ulcer is a loss of enteric surface epithelium that extends deep enough to penetrate the muscularis mucosae, usually over 5mm in diameter.
  • PUD referes to a chronic disorder where the pt has a lifelong underlying tendency to develop mucosal ulcers at sites that are exposed to peptic juice.
    Most commons locations are the stomach and duodenum.
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2
Q

Causes of PUD

A
  • H. Hylori is present in 90% of duodenal ulcers and 75% in gastric ulcers.
  • Medications such as NSAIDs, ASA, glucocoritcoids.
  • Most common in men.
  • Duodenal ulcers are usually in youngr adults ages 30-55
  • Gastric ulcers are usually in older adults age 55-65
  • More common in smokers
  • Alcohol and dietary factors do not appear to cause ulcer disease
  • Role of stress is uncertain, type A personalities?
  • Zollinger-Ellison syndrome (too much stomach acid due to pancreatic tumor).
  • Cytomegalovirus
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3
Q

S/S of PUD

A

Gnawing epigastric pain.
“Feelings like something is eating me from the inside out.”
* Relief worsens with eating (gastrics)
* Relief of pain with eating (duodenal)

Physical findings are often unremarkable, may note some mild epigastric tenderness.
GI bleeding indicates melena, hematemesis, coffee ground emesis.
Perforation (acute abdomen): Severe epigastric pain, board like abdomen, quiet bowel sounds, rigidity.

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4
Q

Lab/diagnositcs of PUD

A

Normal, may note anemia on the CBC.
Consider endoscopy after 8-12 weeks of treatment.
Consider H.pylori testing.

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5
Q

Acid antisecretory agents

A
  • PPIs- Suppress gastric acid secretion by inhibition of the hydrogen/potassium enzyme system at the secretory surface of the gastric parietal cells.
    -Omeprazole, Pantoprazole, lansoprazole, rabeprazole
    -Should be administered 30 minutes before meals.
    -Safe for short term use but long term use can cause decrease B12, iron and calcium absorption, enteric infections (c-diff), pna, kidney disease and black box warning of increased incidence of osteoporotic hip fractures.
    -If you suspect an ulcer regardless if it’s been diagnosed, start a PPI–mainstay of tx. PPI more effective at healing ulcers.
  • H2 Receptor Antagonists- Decrease gastric acid secretion by blocking histamine 2 receptors on parietal cells.
    -Famotidine, cimetidine, nizatidine
    -Works well with dyspepsia.
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6
Q

Mucosal Protective Agents

A
  • Sucralfate (carafate)- Forms a protective barrier against acid, bile, and pepsin.
    -Requires acidic environment so cannot be used with antacids, PPIs or H2 blockers.
    -May bind some medications so should be given 2 hours before and after other meds.
    -Can cause increase aluminum so dose adjustment for renal impairment.
    -Associated with decreased incidence of nosocomial pna.
    -May cause constipation
  • Bismuth subsalicylate (pepto-bismol)- Promotes prostaglandin production/stimulates gastric bicarbonate.
    -Has direct antibacterial action again H.pylori.
  • Antacids (mylanta, Maalox, MOM)- Helps neutralize stomach contents and provide immediate relief.
    -Low dose aluminum and magnesium containing antacids promote ulcer healing by stimulating gastric mucosal defenses, rather than neutralizing gastric acidity.
    -High doses are associated with diarrhea, hyermag, and hypophos.
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7
Q

H.pylori eradication therapy

A

Two antibiotics + PPI w/or w/out bismuth for 10-14 days.
* Pts not allergic to penicillin and who have not previously recieved a macrolide:
-ECA- Esomeprazole + clarithromycin + amoxicillin or
-EBMT- Esomeprazole + bismuth + metronidazole + tetracycline or
-ECAM- Esomeprazole + clarithromycin + amoxicillin + metronidazole

  • Pts who are allergic to penicillin and who have not previously recieved a macrolide or unable to tolerate bismuth:
    -ECM: Esomeprazole + clarithromycin + metronidazole
  • Pts who are allergic to penicillin and who have previously recieve a macrolide:
    -EBMT: Esomeprazole + bismuth + metronidazole + tetracycline

Antiulcer therapy is recommended following the previous regimens for 3-7 weeks to ensure symptoms relief.
-PPI continued for 7 additional weeks
-H2 blocker or sucralfate continued for 6-8 weeks

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8
Q

GERD

A

A chronic condition characterized by back flow of acidid gastric contents into the esophagus.
Can be due to anatomic factors such as an incompetent lower esophageal sphincter, hiatal hernia, delayed gastric empyting (gastroparesis)

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9
Q

S/S of GERD

A

Retrosternal burning
Bitter taste in mouth
Belching, hiccough, dysphagia (more commong in elderly)
Excessive salivation
Frequently occurs at night and/or in recumbant position
May be releived by sitting up, antacids, water or food.

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10
Q

Diagnostics for GERD

A

Consider referral for EGD to rule out cancer, barrets esophagus, PUD.

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11
Q

Management of GERD

A
  • Non-pharmacologic measures:
  • Elevate HOB, avoid alcohol/caffeine/ spices/peppermint, stop smoking, weight reduction if obese.
  • Antacids PRN
  • H2 blockers in high doses at night or divded twice a day.
  • PPI if H2 blockers are ineffective.
  • GI/surgical consult
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12
Q

Diverticulitis

A

Inflammation or localized perforation of one or more diverticula with abscess formation.
More common in women than men.
Caused is not clear but found in low dietary fiber and age.

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13
Q

S/S of diverticulitis

A
  • Mild to moderate LLQ pain and fever are main clinical feature.
  • Pts with free perforation present with more generalized pain and peritoneal signs.
  • Constipation or loose stools may be present.
  • N/V
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14
Q

Lab/diagnostics of diverticulitis

A
  • Mild to moderate leukocytosis
  • Elevated ESR, c-reactice protein and procalcitonin level
  • Positive stool heme in 25% of pts.
  • Sigmoidoscopy shows inflamed mucosa (avoid during acute phase)
  • Plain abdominal films are obtained on all pts to look for evidence of free air (pneumoperitoneum)
  • May consider CT scan to evaluate abscess
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15
Q

Management of diverticulitis

A

NPO dependent on condition
IV fluids to mantain hydration
If significant GI bleed present, treat as outline under PUD.
Surgical consult
Antibioitic therapy if needed with augmentin

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16
Q

Cholecystitis

A

Inflammation of the gallbladder, associated with gallstones in >90% of cases.
Gallstones become impacted within the cystic duct and inflammation occurs behind the impaction.

Acalculous cholecytitis-absence of stone, 5% of cases.

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17
Q

S/S of cholecystitis

A

Often precipitate a large and/or fatty meal.
A sudden appearance of steady, severe pain in epigastrium or right hypochondrium.
Vomiting in many pts provides relief.
Positive Murphy’s Sign: deep pain on inspiration while fingers are placed under the right rib cage.
RUG tenderness to palpation
Palpable gallbladder in 15% of cases.
Muscle guarding and rebound pain
Fever.

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18
Q

Acute cholangitis

A

Acute inflammation/infection of the biliary duct system as well as obstruction of biliary flow.
* Charcot’s triade: jaundice, fever, abdominal pain.

19
Q

Lab/diagnostics of cholecystitis

A
  • Mild leukocytosis (12,000-15,000)
  • Serum bilirubin elevated
  • Serum ALT, AST, LDH and alkaline phosphatase levels are increased.
  • Amylase may be elevated (if >500, pancreatitis should be suspected).
  • Ultrasound is the gold standard
  • HIDA scan to visualize cystic duct obstruction
  • ERCP is used to diagnose diseases o the gallbladder, bile system, pancreas and liver. Major complication is pancreatitis, perforation, hemorrhage, acute cholangitis.
20
Q

Management of choleystitis

A

Pain management
NGT for gastic decompression
Maintain NPO, or low fat, low volume meals.
Crystalloid solutions D51/2NS
Surgical consult.

21
Q

Acute pancreatitis

A

Inflammation of the pancrease due to escape of pancreatic enzymes into surrounding tissue resulting in an autodigestive state of the pancreas.
Caused by:
#1 gallbladder disease
#2 heavy alcohol use
Hypercalcemia
Hyperlipidemia
Trauma
Meds: FATSHEEP
* Furosemide
* Asathioprine
* Tetracycline
* Sulfonamides/statins
* Hydrochlorothizaides
* Estrogen
* Ethanol
* Pentamidine

22
Q

S/S of pancreatitis

A

Abrupt onset of steady, severe epigastric pain worsened by walking and lying supine.
Pain that is improved by sitting and leaning forward
Pain usually radiates to the back but may radiate elsewhere
N/V is usually present
Weakness, sweating, and anxiety in severe attacks.

23
Q

Physical findings of pancreatitis

A
  • Upper abdomen tender to palpation, usually w/o guarding, rigidity or rebound—tells you it’s not acute abdomen.
  • Distended abdomen, absent bowel sounds (usually from ileus)
  • Fever
  • Tachycardia, hypotension, pallor, cool skin (d/t decreased intravascular volume)
  • Mild jaundice is common
  • If hemorrhagic:
    -Grey turner’s sign: Flank discoloration
    -Cullen’s sign: Umbilical discoloration
24
Q

Lab/diagnostics of pancreatitis

A

WBC elevation, degree depends on severity.
Hyperglycemia
Serum LDH and AST elevation
Serum Amylase (50-180) and lipase (14-280) are elevated up to 3x
BUN and coagulation values may be elevated
Hypocalcemia, levels <7 are associated with tetany–watch for chvostek’s/trousseau’s sign
Elevated CRP suggest pancreatic necrosis
CT scan more useful than US.

25
Q

Management of pancreatitis

A

Fluid therapy
Bed rest
Maintain NPO
NG tube suction
Pain control
Once pt is pain free and how bowel sounds, may start clear diet

26
Q

Ranson’s criteria to evaluate prognosis

A

If you have 5-6 risk factors=40% mortality
>7 risk factors=100% mortality

Prognostic signs at admission:
George: Grater than 55 yrs
Washington: WBC >16,000
Got: Glucose >200
Lazy: LDH >350
After: AST >250

Prognostic signs during the first 48 hrs:
He: Hct drop of >10
Broke: BUN increase >5
C: Calcium: <8
A: Arterial O2 <60
B: Base deficit >4
E: Estimated fluid sequestration >6L

27
Q

Bowel obstruction

A

Blockage o the lumen of intestines that impedes passage of gas and contents through the bowel.
Caused by:
* Adhesions (most common)
* Hernia
* Volvulus (more common in children)
* Tumors
* Fecal impaction
* Ileus (functional obstruction)

28
Q

S/S of bowel obstruction

A
  • Cramping periumbilical pain initially, later becomes constant and diffuse.
  • Vomiting withint minutes of pain (proximal obstruction)
  • Vomiting within 2 hours of pain (distal)
  • Minimal or no fever
29
Q

Physical findings of bowel obstruction

A
  • Minimal abdominal distention indicated proximal obstruction.
  • Pronounced abdominal distention indicated distal obstruction.
  • Mild tenderness but no peritoneal findings
  • High pitched, tinkling bowel sounds
  • Unable to pass stool/gas
30
Q

Lab/diagnostics of bowel obstruction

A
  • Lab findings normal in initial stages.
  • Later may see elevated WBCs and values consistent with dehydration.
  • Plain films show dilated loops of bowel and air-fluid levels:
    -Horizontal pattern in SBO
    -Frame pattern in LBO
31
Q

Management of bowel obstruction

A
  • Fluid resuscitation
  • NGT suction
  • Surgical intervention in all cases of complete obstruction
  • In partial obstruction, treat medically
32
Q

Ulcerative colitis

A

An idiopathic inflammatory condition characterized by diffuse mucosal inflammation of the colon.

33
Q

S/S of ulcerative colitis and chrons disease

A
  • Bloody diarrhea is the hallmark sign, they will fill the toilet up with blood.
  • Fecal urgency, tenesmus and abdominal cramping
  • Weight loss, malnutrition, anemia, fever.
34
Q

Lab/diagnostics of ulcerative colitis and chron’s disease

A

Stool studies are negative
Sigmoidoscopy establishes diagnosis

35
Q

Crohn’s disease

A

Also an ulcerative disease anywhere can occur anywhere in GI tract
Characterized by thickening of the mucosal wall with cobblestoning.

36
Q

Management of ulcerative colitis and chron’s disease

A

GI referral
Mesalamine (canasa) suppositories or enemas for 3-12 weeks–antinflammatory agent
Hydrocortisone suppository or enema

37
Q

Mesenteric infarct

A

A syndrome as a result of inadequate blood flow through the mesenteric circulation, leading to ischemia and gangrene of the bowel.

Caused by aterial or venous embolus or thrombosis
Atherosclerosis
Smoking
Usually occurs in older adults
Coagulopathy such as that following recent surgery increases risk.

Management: emergent surgery

38
Q

S/S of mesenteric infarct

A

Sudden onset of cramping, colicky abdominal pain that is out of proportion to physical exam findings.
N/V
Fever
Abdominal guarding and tenderness
Hyperactive to absent bowel sounds
Peritoneal findings increase as state progress
Shock
Blood in rectum

39
Q

Lab/diagnostics of mesenteric infarct

A

Elevatd amylase
Leukocytosis
1.) abdominal film
2.) CT

40
Q

Appendicitis

A

Inflammation of the appendix.
If untreated, gangrene and perforation may develop within 36 hours.
Most common presentation is among men 18-30.

Caused by:
* Fecalith- undigested foot particles that get trapped.
* Foreign body
* Inflammation
* Neoplasm

41
Q

S/S of appendicitis

A

Begins with vague, colicky umbilical pain
After several hours, pain shifts to RLQ which is a late exam finding.
Nause with 1-2 episodes of vomiting, more vomiting episodes suggest another diagnosis.
Pain worsened and localized with coughing.

42
Q

Physical findings of appendicitis

A
  • RLQ guarding with rebound tenderness
  • McBurney’s point tenderness- refers to the pain in the RLQ 1/3 distance from anterioir superioir iliac spine to the umbilicus.
    • Psoas sign: Pain with right thigh extension
    • Obturator sign: Pain with internal rotation of flexed right thigh
    • Positive Rovsing’s sign: RLQ pain when pressure is applied to the LLQ.
  • Low grade fever, high fever is suggestive of another diagnosis.
43
Q

Lab/diagnostics of appendicitis

A

Leukocytosis
CT or ultrasound to diagnose

44
Q

Management of appendicitis

A

Surgery
Fluids
Pain management

AGACNP (25 decks)

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