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Pathophysiology > mod 11 digestive > Flashcards

mod 11 digestive Flashcards

1
Q
  1. Define anorexia:
  2. Define nausea:
  3. Define vomiting:
  4. Define retching:
  5. Define projectile vomiting:
  6. Name the 3 types of abdominal pain and briefly describe each:
  7. What are the 3 types of GI bleeding and describe each:
A
  1. A lack of a desire to eat despite physiologic stimuli that would normally produce hunger
  2. A subjective experience that is associated with a number of conditions
  3. The forceful emptying of the stomach and
    intestinal contents through the mouth
  4. Nonproductive vomiting
  5. Spontaneous vomiting
  6. Visceral: hard to localize or characterize

Parietal: localized pinpointed pain from

Referred: pain perceived distant from affected site

  1. upper GI: (above tritz ligament) vomiting, dark blood in stool, coffee grounds
    lower Gi: no vomiting - just in stool dark or light, mucous
    Occult: not visible. Detected by fecal test or anemia
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2
Q
  1. Define constipation:
  2. If constipation is primary, what causes it?
  3. If constipation is secondary what causes it?
  4. Diarrhea is marked by…
  5. What are the 3 major mechanisms of diarrhea?
  6. What are the systemic effects of diarrhea? What is it associated with?
A
  1. infrequent or difficult defecation. <3 times per week
  2. slow transit or a pelvic floor or outlet dysfunction
  3. many different factors such as diet, medications, various disorders, aging
  4. Presence of loose, watery stools. Can be large or small volume
  5. osmotic, secretory, and motility
  6. Dehydration, Electrolyte imbalance, and Weight loss. Malabsorption syndromes
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3
Q
  1. What is GERD?
  2. What can GERD develop into?
  3. What are the symptoms (typical, atypical, and associated)?
  4. What triggers GERD?
  5. What are risk factors?
  6. When does it typically occur, what worsens and improves it?
A
  1. Gastroesophageal Reflux Disease. Reflux of acid into esophagus due to low resting tone of lower esophageal sphincter.
  2. reflux esophagitis, Barrett Syndrome, and esophageal adenocarcinoma
  3. Typical: heartburn and acid regurgitation.

Atypical: Chest pain Hoarseness/laryngitis
Chronic cough
Asthma, and Globus (sensation of something in the back of their throat)

Associated: Dysphagia, and Dyspepsia (indigestion)

  1. Nicotine, Alcohol, Caffeine, Peppermint, Chocolate, Anticholinergic, Calcium channel blockers, Nitrates
  2. Obesity, Hiatal hernia, Medications: calcium channel blockers, Pregnancy, Heliobacter pylori
  3. Occurs 30 – 90 minutes after a meal, Worsens with reclining, Improves with antacids, sitting, or standing
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4
Q
  1. How do we diagnose GERD?

2. How do we treat GERD?

A
  1. Clinical diagnosis/history, Barium esophagram, Upper endoscopy, 24-hour pH testing, Esophageal manometry
  2. weight loss, elevate head, no meals 2-3 hrs before bedtime, eliminate trigger foods, proton pump inhibitors, H-2 antagonists, and antacids
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5
Q
  1. What peptic ulcer disease?
  2. Describe the pathogenesis:
  3. What causes the vasoconstriction?
  4. What causes the eating away at the mucosal layer?
A
  1. when there is damage to the mucosal barrier
  2. inadequate blood supply interferes with epithelial regeneration. Mucous layer breaks down making an ulcer in the underlying layers
  3. stress, smoking, shock, circulatory impairment, scar tissue, anemia.
  4. Aspirin, NSAIDs, alcohol and chronic gastritis, excessive glucocorticoid secretion or ingestion
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6
Q
  1. How do NSAIDs lead to ulcers?
  2. How does H-pylori cause ulcers?
  3. What are 3 complications that can arise from a peptic ulcer?
A
  1. decreased prostaglandin leads to less HCO3- and minimized mucosal secretion, and less blood flow.
  2. produces ammonia that decreases acid production which allows bacteria to burrow into mucosa which produces auto antibodies
  3. Hemorrhage (common), perforation (ulcer can errode through wall allowing chyme to enter into peritoneal cavity), and obstruction from scar tissue development
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7
Q
  1. What are the signs of a peptic ulcer?
  2. What are the diagnostic tests?
  3. How do we treat peptic ulcers?
A
  1. Epigastric burning or localized pain,
    usually following stomach emptying
  2. Fiberoptic endoscopy, Barium x-ray, Endoscopicbiopsy
  3. determine cause and reduce exacerbative factors, antibiotics and proton pump inhibitor
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8
Q
  1. What is the most common type of peptic ulcer?
  2. What causes them?
  3. What symptoms differentiate duodenal ulcers from other types?
  4. Where do gastric ulcers typically develop, and why?
  5. Contrary to duodenal ulcers, are gastric ulcers relieved or exacerbated by food intake? What about relief from antacids?
A
  1. duodenal ulcer
  2. H-pylori and use of NSAIDs
  3. pain at night, pain 2-3 hours after eating, relieved by eating and by antacids
  4. In the antral region of the stomach because of too much acid
  5. exacerbated, antacids minimal relief.
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9
Q
  1. What are the 2 inflammatory bowel diseases?
  2. How can these be described?
  3. What causes them (4)?
A
  1. Ulcerative colitis and Crohn disease
  2. Chronic, relapsing inflammatory bowel disorders
  3. Genetics, Environmental factors, Alterations of epithelial barrier functions, Altered immune reactions to intestinal flora
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10
Q
  1. ………. ……… is a Chronic inflammatory disease that causes ulceration of the colonic mucosa.
  2. Which parts of the colon are affected?
  3. What are the symptoms of ulcerative colitis?
  4. How do we treat?
A
  1. ulcerative colitis
  2. sigmoid colon and rectum (strating from rectum and working its way up)
  3. Diarrhea (10 to 20/day), Urgency, Bloody stools, Cramping
  4. 5- aminosalicyclate therapy followed by steroids for mild disease

Thioprine and immunomodulatory agents or vedolizumab are used for serious disease

surgery for severe disease

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11
Q
  1. Name the inflammatory bowel disease that causes Granulomatous colitis, ileocolitis, or regional enteritis
  2. Is this disease idiopathic? What part of the digestive tract does it affect?
  3. Crohn disease cause what kind of leisions? Can it affect only one side of the intestinal wall? What can come as a result of the ulcerations?
  4. Crohn causes problems with digestion and absorption of which substances?
  5. Does surgery help?
  6. How can we treat?
A
  1. Crohn Disease
  2. Yes. any part of the digestive tract, from mouth to anus
  3. skip leisions, yes, adhesions, fissures and/or fistulas
  4. proteins, nutrients, and B12 and folic acid, steatorrhea (can’t digest fats)
  5. no
  6. team approach, anti-inflammatory drugs, steroids, antimotility drugs, antimicrobials, supplements, immunotherapeutic agents
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12
Q
  1. Colorectal cancer is sporadic, appearing after age 50, but can also be caused by what?
  2. What do the symptoms depend upon?
  3. What are the 2 stool based screening tests that can be done? Non-stool tests?
  4. Where can tumor markers be identified?
  5. If a patient has a family history, when do we begin screening?
A
  1. genetics - adenomatous polyposis (by age 40)
  2. location, size, and shape of the lesion and are silent in the early stages
  3. Guacic Test and Fecal immunochemical test (tests for globin - more specific). Colonoscopy and CT
  4. In the blood (carcinoembryonic antigen and CA-19-9) and in tumor tissue (K-RAS and BRAF)
  5. at 40
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13
Q
  1. Name the 3 types of jaundice:

2. What causes the yellow color?

A
  1. Prehepatic (hemolytic), Hepatic (cirrhosis, cancer etc.), and Posthepatic (obstructive- gallstones or scar tissue).
  2. Hyperbilirubinemia
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14
Q
  1. What is ascites and its most common cause?
  2. What is ascites associated with (4)?
  3. What is the mortality rate if ascites is associated with cirrhosis?
  4. How do we treat?
A
  1. Accumulation of fluid in the peritoneal cavity. Most commonly caused by cirrhosis.
  2. Portal hypertension, Decreased synthesis of albumin by the liver, Splanchnic vasodilation, Renal sodium and water retention
  3. 25% in 1 year
  4. paracentesis
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15
Q
  1. What is hepatic encephalopathy?
  2. What are the early symptoms?
  3. What are the late symptoms?
A
  1. Cells in the nervous system are vulnerable to neurotoxins absorbed from the GI tract that, because of liver dysfunction, circulate to the brain
  2. Subtle changes in personality, memory loss, irritability, disinhibition, lethargy, and sleep disturbances
  3. Confusion, disorientation to time and space, flapping tremor of the hands (asterixis), slow speech, bradykinesia, stupor, convulsions, and coma (due to build up of ammomia)
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16
Q
  1. What is hepatorenal syndrome?

2. What are the symptoms?

A
  1. kidney failure as a result of advanced liver disease (Robbie)
  2. oliguria and complications of advanced liver disease
17
Q
  1. What is cirrhosis?
  2. What are the different types of cirrhosis?
  3. The severity and rate of progression depend on what?
A
  1. Irreversible inflammatory, fibrotic liver disease in which Biliary channels become obstructed and cause
    portal hypertension
  2. Alcoholism, Billiary (immune disorder), Postnecrotic (from chronic hepatitis or toxins), and Metabolic (genetic metabolic storage disorders)
  3. what caused it
18
Q
      1. Describe the 3 stages of alcoholic cirrhosis:

4. How do we treat cirrhosis?

A
  1. Initial stage - fatty liver: Enlargement of the liver. Asymptomatic and reversible with reduced alcohol intake
  2. Second stage - alcoholic hepatitis: Inflammation and cell necrosis. Fibrous tissue formation—irreversible change
  3. Third stage - end stage: Fibrotic tissue replaces normal tissue. Little normal function remains
  4. No alcohol, supportive care, dietary restrictions, balance electrolytes, paracentesis, antibiotics to reduce flora, liver transplant
19
Q
      1. Name and define the 4 types of gallbladder disease:
A
  1. Cholecystitis: inflammation of the
    gallbladder from obstruction of the cystic duct
  2. Cholelithiasis – gallstones
  3. Choledocholithiasis – gallstone obstructing the biliary tract, i.e., the common bile duct
  4. Cholangitis – bacterial infection superimposed on an obstruction of the biliary tree
20
Q
  1. What causes gallstones?
  2. What two types are there?
  3. What are the risks to getting gallstones?
  4. What are the symptoms?
  5. How to treat?
A
  1. Impaired metabolism of cholesterol, bilirubin, and bile acids
  2. Cholesterol: bile that is supersaturated w/ cholesterol (most common)

Pigmented or Bilirubinate: brown = infected bile, or black = stasis - chronic liver disease or hemolytic

  1. Obesity, Middle age, Female, Oral contraceptives, Rapid weight loss, Native American, Gallbladder, pancreas, or ileal disease
  2. R upper gastric, or epigastric pain, intolerance to fatty foods
  3. surgery
21
Q
  1. What is always the cause of cholecystitis?

2. What are the symptoms?

A
  1. gallstone lodged in the cystic duct

2. pain similar to gallstones, fever, leukocytosis, rebound tenderness, abdominal muscle guarding

22
Q
  1. Describe pancreatitis:
  2. What could happen as a result of pancreatitis?
  3. Describe what happens in obstruction:
  4. Is pancreatitis acute or chronic? Which is a medical emergency?
  5. What causes acute pancreatitis most commonly?
  6. Where is pain located for acute pancreatitis?
A
  1. Inflammation resulting in autodigestion of the tissue
  2. Substances released by necrotic tissue lead to widespread inflammation. Hypovolemia and circulatory collapse may follow.
  3. Obstruction to the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction
  4. can be either. Acute is an emergency
  5. gallstones and alcohol abuse
  6. epigastric pain radiating to back
23
Q
  1. What tests are done to confirm acute pancreatitis?

2. How do we treat?

A
  1. Serum amylase and serum lipase
  2. Oral intake is stopped. Treatment of shock and electrolyte imbalances,
    Analgesics
24
Q
  1. What is transit time?
  2. Doesn’t matter the age, sex, race, or anything, is it safe to assume that chest pain is GI?
  3. What is another name for C. diff?
  4. How does C.diff work?
A
  1. time it takes bolus from entering the mouth and exiting the anus
  2. No. always rule out MI first
  3. pseudomembranous colitis
  4. its toxins causes mucosal damage

Pathophysiology (11 decks)

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