Peptic Ulcers Flashcards

1
Q

Peptic Ulcer

A

A peptic ulcer is a break in the protective mucosal lining of the lower esophagus, stomach, or duodenum
*These breaks expose the Submucosa to gastric secretions and cause autodigestion of deeper layers of the GI tract wall

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2
Q

Where are peptic ulcers found? (3 with explanation)

A
  1. Lower esophagus – Gastric acid from the stomach can reflux into the lower esophagus and cause problems
  2. Antrum of stomach (lower portion) – Cells that produce hydrochloric acid are found primarily here
  3. Duodenum
    - -Most common place to find them
    - -Unlike the stomach, the duodenum doesn’t have a thick alkaline mucous covering its membrane, but it does receive acidic contents from the stomach
    - -Particularly vulnerable to ulceration
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3
Q

Erosion Ulcer (4)

A
  1. A type of superficial ulcer = an erosion
  2. Where the mucosal lining is thinned or truly broken
  3. The underlying blood vessels and muscle layers are completely intact and unaffected
  4. Largely asymptomatic because gastric acid isn’t interacting with nervous tissue
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4
Q

Acute Ulcer (2)

A
  1. Ulceration penetrates through submucousal layer and into muscle layer
  2. This is when ulcers become painful because gastric acid starts to interact with the nerves within the wall of the GI track
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5
Q

Perforating Ulcer

A

When an ulcer perforates (penetrates through all the layers of the GI tract) can be very dangerous because it exposes the body cavity to the contents of the tract

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6
Q

Risks for Peptic Ulcer Disease (6)

A
  1. Smoking
  2. H.Pylori infection
  3. Habitual use of non-steriodal anti-inflammatory drugs (NSAIDs)
  4. Habitual use of alcohol
  5. High psychological stress.
  6. Some chronic diseases are associated with the development of peptic ulcers: Emphysema, rheumatoid arthritis, and liver cirrhosis

*Risk factors increase chance of developing peptic ulcer either by increasing gastric acid production or by increasing inflammation, or both

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7
Q

H.Pylori (5)

A
  1. Found in the stomach of 50% of all humans
  2. In most people there are no symptoms, but the bacterium can trigger ulcers in 10-15% of those infected
  3. The bacteria is thought to cause more than 90% of duodenal ulcers and 80% of gastric ulcers
  4. Thought to trigger ulcers by stimulating acid production in the stomach and/or by triggering local immune (inflammatory) responses.
  5. Contributes to stress or potential injury to the mucosal lining and if you have one of the other risks factors in addition to presence of H.Pylori then you get enough damage to the lining that an ulcer develops
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8
Q

What occurs with presence of H.Pylori? (3)

A
  1. Increases gastric acid production
    - May be due to release of bacterial toxins or irritation of mucosal lining
  2. If detected by the immune system, it can trigger a local inflammatory response
    - Inflammation increases damage to mucosal lining
  3. Bacterial toxin released by H.Pylori can irritate mucosal lining
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9
Q

Duodenal Ulcers

A

Duodenum is particularly vulnerable to the acid coming from the stomach and doesn’t have alkaline mucous covering; often heal spontaneously but reoccur within months

*It is the most frequently seen type of ulcer

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10
Q

Factors that contribute to Duodenal Ulcers (5)

A
  1. Hypersection of gastric acid and pepsin
    - The more gastric acid and pepsin produced by the stomach, the more that the duodenum needs protection
    - Smoking, H. Pylori infection, excess parietal cells, etc
  2. Elevated plasma Gastrin levels
    - Excess production of gastrin leads to excess production of gastric acid and pepsin
  3. Inadequate secretion of pancreatic sodium bicarbonate
  4. Excessively rapid gastric emptying
    - If stomach empties very quickly, it doesn’t give duodenum enough time to neutralize the acid coming in
  5. Immune reaction to H. Pylori infection
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11
Q

Characteristic Manifestation of Duodenal Ulcers

A

Chronic intermittent pain in the epigastric region
-The pain occurs and causes discomfort for a while then spontaneously heals then comes back

(Very different from gastric ulcers, which tend to be very acute and don’t spontaneously heal)

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12
Q

Food-pain relief pattern: Duodenal Ulcers

A

You consume a meal and then about an hour after the meal, when the food has moved out of the duodenum, you start to feel pain from the acid hitting the duodenum

*If you consume more food, then 20-30 min after you consume it the pain is relieved as food enters duodenum, but then as the food moves out you feel pain again 1 hour after eating

RELIEF = 20-30 min after eating 
PAIN = 1 hour after eating
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13
Q

Food-pain relief pattern: Gastric Ulcers

A

You eat a meal and the food immediately enters the stomach so you don’t immediately feel pain because the food is between the acid and the ulcer, but 20-30 min after the meal when the food moves out of the stomach, the acid hits the ulcer and gives you pain
*If you consume more food, the food immediately relieves the pain, but then the cycle starts over 20-30 min later

RELIEF= immediately after eating 
PAIN= 20-30 minutes after eating
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14
Q

Duodenal and Gastric Ulcer Treatments (4)

A
  1. Use of antacids (including histamine blockers)
    - Histamine being blocked in the stomach, because histamine in the stomach stimulates acid production
  2. Proton pump inhibitors (ex. Omeprazole)
  3. Antibiotic to treat the H Pylori infection
  4. Anti-cholinergic drugs to inhibit secretion, suppress gastric motility, delay gastric emptying
    - More relevant for duodenal ulcers
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15
Q

PPIs

A

The pumps move hydrogen ions out of the parietal cells and into the stomach, and in the stomach it binds with chloride to make hydrochloric acid, so this is getting blocked by PPIs

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16
Q

CCK and Secretion (4 steps)

A

1st: The food that moves from the stomach into the duodenum triggers the duodenal mucosal cells to release CCK and secretin
2nd: CCK and secretin act on liver and pancrease to stimulate release of bile and digestive juices into duodenum
3rd: Secretin acts on the exocrine portion of the pancreas and binds to duct cells to stimulate release of sodium bicarbonate (alkaline) solution
4th: The alkaline solution is released from pancreas and enters duodenum to neutralize the acid coming from the stomach
* Protective measure

17
Q

Stress Ulcers (4)

A
  1. An acute form of peptic ulcers that tend to accompany sever illness, systemic trauma, or neural injury
  2. Usually involves multiple sites distributed throughout the stomach and duodenum
  3. Stress ulcers are essentially ischemic ulcers
  4. Triggering of stress response that acutely changes level of perfusion to the GI tract, leading to the development of the ulcer
18
Q

Steps leading to stress ulcer (6 steps)

A

1st: SNS stimulation
2nd: Decreased mucosal blood flow
3rd: Mucosal metabolism declines
4th: Decreases mucous production
5th: Exposes mucosa to gastric acid
6th: Autodigestion and ulcer formation

19
Q

Cushing’s Ulcer (3)

A

A type of stress ulcer that is particularly severe…

  1. It involves some sort of trauma and activation of stress response, but the trauma is to part of the brain where the vagal nerves originate
  2. When we get trauma to this part of the pain can lead to a stress response and intense activation of the vagus nerves stimulating gastric acid production
  3. So there is decreased blood flow and mucous production PLUS strong vagal stimulation of gastric acid, making the ulcers more numerous and more severe
20
Q

Maldigiestion

A

an abnormality interfering with digestion of food

21
Q

Malabsorption

A

an abnormality interfering with absorption

  • anything that causes maldigestion will cause malabsorption
  • there are some primary malabsorption conditions, usually when they involves the absorptive surface area of the small intestine
22
Q

Maldigestion and Malabsorption Disorders

A

Interference with nutrient digestion or absorption in the small intestine

Malabsorptive and Maldigestive disorders often occur together

23
Q

Pancreatic Insufficiency

A
  1. A deficient production of the pacreatic enzymes (Lipase, amylase, trypsin, chymotripsin)
  2. Affects both exocrine and endocrine portion of pancreas
  3. Caused usually by pancreatic disease like pancreatitis, pancreatic carcinoma
24
Q

What occurs if you don’t have pancreatic enzymes? (4)

A
  1. Losing the pancreatic enzymes can be very devastating to the exocrine pancreas
  2. The pancreatic enzymes are necessary for digesting every type of food: Pancreatic lipase to digest fat, amylase digests carbs, etc
  3. Most important for breaking down fat because lipase comes only from pancreas
    * Will be especially affected and can cause devastating effects
  4. People with pancreatic insufficiency will have body wasting and trouble maintaining their weight
25
Q

Signs of Pancreatic Insufficiency

A
  1. large amount of fat in the stool (steatorrhea) and weight loss
    * Steatorrhea: stool will have very fowl odor and be oily, float, etc. – >Clear sign of not digesting fat
  2. Body wasting/ trouble maintaining weight
26
Q

Bile Salt Insufficiency (4)

A
  1. Interferes significantly with fat digestion
  2. when present alone it won’t affect fat digestion to the same degree as pancreatic deficiency (won’t see steatorrhea, but will see abnormal stool)
  3. Stool will appear gray or clay colored because the bilirubin in the bile is what colors feces brown, so in the absence of excreted bile and bilirubin, the stool will no longer be brown
  4. Certain conditions decrease production of bile by the liver: Advanced liver disease (cirrhosis), obstructions of the bile ducts
27
Q

Clinical Manifestations of Bile Salt Insufficiency (pathophys and then 4 explanations)

A

related to poor intestinal absorption of fat and fat-soluble vitamins (A, D, E, K)
*Most affects fat soluble vitamins because without bile salt, we can digest some fat, but the fat soluble vitamins get trapped in the large lobules of fat and we can’t access them

  1. Vitamin A: associated with night blindness
  2. Vitamin D: associated with decreased calcium absorption with bone demineralization (osteoporosis), bone pain, and fractures
  3. Vitamin K: associated with prolonged Prothrombin time, leads to bleeding and spontaneous bruising
  4. Vitamin E: may cause neurological effects in children
28
Q

Lactase (2)

A
  1. An enzyme found bound to the plasma membrane of mucosal cells in the small intestine; the membrane bound enzyme that breaks down lactose in the small intestine
  2. Bound to the brush border membrane are disaacharadisases enzymes
29
Q

Lactose Intolerance

A
  1. Ability to continue to produce lactase beyond weaning (breast feeding) is a recessive trait in mammals
  2. The dominant trait is to have a progressive decline in our ability to produce lactase beyond childhood and adulthood because we are no longer consuming mother’s milk
  3. However the human race has evolved to have this recessive trait commonly (producing lactase into adulthood)
  4. There are many individuals (many African Americans, Middle Eastern) who have the dominant trait and don’t have lactase in adulthood
30
Q

Lactose Intolerance Pathophys (4)

A

In the individuals who have the dominant trait and don’t produce lactase in adulthood….

1st: With these individuals, as lactose moves through the small intestine it enters the large intestine undigested and then gets consumed by intestinal bacteria of the colon
2nd: These bacteria that consume it undergo fermentation process; the byproduct of fermentation is gas
3rd: Result is gas cramping, flatulence, and elevated osmolarity of feces in the colon → osmotic diarrhea
4th: People with this lactase deficiency have an easier time with cultured dairy (cheese, yogurt) because the milk has been incorporated with non-harmful bacteria that have broken down some of the lactose in the milk

31
Q

Clinical Manifestations of Lactose Intolerance (3)

A

painful cramping, flatulence, and diarrhea