Lecture 9 Flashcards

1
Q

parts of the stomac

A

top: Fundus
mid: Body
low: Antrum

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2
Q

Gastritis & Peptic Ulcer Disease (PUD)

A

Ulcerations of gut mucosa that penetrate
the submucosa
– Gastric (typically near antrum)
– Duodenal (first few cm)

• Areas of breakdown continuously
exposed to gastric acid & pepsin
– Erosion
– Perforation

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3
Q

Etiology of Peptic Ulcer Disease

A

H.pylori
infection

H.pylori
infection

Stress &
Severe Illness

Gastritis

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4
Q

Etiology: Helicobacter pylori

A

• Gram negative bacteria residing under mucosal layer
– Present in ~90% adults; 10-15% develop symptomatic ulcerations
• Most common cause of gastritis and PUD
– Confirmed by endoscopy
• Mechanisms
– Damages mucosal cells and causes inflammation
• Also implicated in
– Gastric carcinoma
– Atrophic gastritis

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5
Q

Etiology: Medications / Substance Use

A
Substances
• Alcohol abuse
– Excessive ethanol can damage gastric
mucosa
• Ingestion of erosive substances
• Tobacco use
– Decreases bicarbonate secretion &
mucosal blood flow
– Exacerbates inflammation
• Poor diet
– Delayed wound / tissue healing
Medications
• NSAIDS and Aspirin
– Corrosive
– Inhibit prostaglandin synthesis
• Prostaglandins: essential for maintaining
mucous and bicarbonate barrier in the
stomach
• Corticosteroids
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6
Q

Symptomology

A

Chief complaint: Abdominal discomfort
– Dull, burning, transient pain; usually occurring on empty stomach
• Other symptoms:
– Bloating, burping, nausea, vomiting, anorexia
Can also be asymptomatic!

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7
Q

Nutritional Implications

A
• Impaired oral intake
– Pain, N/V, anorexia, malaise etc.
• Involuntary weight loss
• Nutrient imbalances / deficiencies
• Atrophic gastritis
– Risk B12 deficiency d/t lack intrinsic factor à impaired absorption
– Gastric acid enhances bioavailability à low acid states negatively influence
absorption, particularly Fe, Ca
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8
Q

Nutritional Diagnoses

• Some commonly associated with PUD

A
• Some commonly associated with PUD
– Inadequate food / oral beverage intake
– Altered GI function
– Involuntary weight loss
– Food and nutrition-related knowledge deficit
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9
Q

Management of PUD: Pharmacotherapy

A
• Antacids
– Neutralize acid, prevent formation of
pepsin
• Maalox, Tums, Gaviscon
• Proton pump inhibitors (PPI’s)
– Suppress acid production
• Omeprazole, esomeprazole, lansoprazole,
pantoprazole
• H2-receptor agonists
– Block histamine-stimulated gastric secretions
• Cimetidine, ranitidine
Prostaglandin analogs
– Reduce gastric acid and enhance
mucosal resistance to injury
• Misoprostol
• Mucosal barrier fortifiers
– Form a protective coating- bismuth - dark stool
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10
Q

H. pylori ”triple therapy”

A

7-14 day course 2 antibiotics + PPI
– Antibiotics
• Amoxicillin, tetracycline, metronidazole, clarithromycin
– Nelms Table 14.16
• 86-98% eradication rate
• Side effects: nausea, vomiting, abdominal pain
– May reduce compliance

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11
Q

Management of PUD: Nutrition

A

• Nutritional goals of care
– Support medical therapy & decrease symptoms
– Prevent weight loss & restore nutrient imbalances
• Nutrition therapy
– Trial restriction of foods that may increase acid secretion
• Black and red pepper, caffeine, coffee (inc. decaf), alcohol
– Avoid foods not tolerated (diet as tolerated or “DAT”)
• Meal considerations: timing & size
– Avoid lying down after eating
– Avoid larger meals close to bedt

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12
Q

Nutrition: Other Considerations

A

Historical dietary treatment: milk & cream
– Coat stomach
– Now know they increase gastrin and pepsin secretion
– Do NOT recommend
• pH of food prior to consumption has little effect after
consumption
– Restricting acidic juices/foods not warranted

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13
Q

Acute Symptomology

A
• Sharp, sudden, persistent, severe pain
• Melena
– Bloody/black stools
• Hematemesis
– Vomiting blood; “coffee ground emesis”
Serious complications
• Acute or chronic GI bleed
• Perforation
• Obstruction
• i.e. gastric outlet
obstruction
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14
Q

Surgical Treatment of PUD

A

• Surgical treatment significantly reduced post-1960
– Secondary to discovery of H. pylori
• Present day, indicated for:
– Severe cases, refractory to treatment
– Complications
• GI bleeds, perforation, obstruction of pyloric sphincter
• Types of surgery
– Vagotomy (with or w/o gastric resection)
– Gastroenterostomy

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15
Q

Vagotomy

A
• Interruption of the impulses
(cholinergic stimulation of
stomach) carried by the vagus
nerve to parietal cells
– ↓ acid production
– ↓ response to gastrin
• Truncal vagotomy with
– Pyloroplasty, or
– Antrectomy
• Highly selective vagotomy
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16
Q

Highly Selective Vagotomy

A
• Preferred choice to treating PUD
– Use depends on severity of
disease
• Proximal gastric vagotomy to
decrease acid secretion
• Preserves antral motility
• No pyloroplasty
• No rapid gastric emptying
17
Q

Truncal Vagotomy w/ Pyloroplasty

A
Vagus nerve cut at distal esophagus
– ↓ antral contraction
– Delayed emptying of solids
– ↓ pylorus relaxation
• Procedure to enhance pyloric drainage
required
• Pyloroplasty
– Surgical revision to widen pyloric canal
– Creates leaky pylorus to enhance
gastric emptying
• ↑ emptying of liquids and solids
18
Q

Gastric Surgeries (Gastrectomy)

A

• Resection of part of stomach (partial gastrectomy) and pylorus
– Alternative to pyloroplasty; gastric remnant anastomosed to small intestine
• Gastroduodenostomy (Billroth I)
– Removal of pylorus and/or antrum of stomach
– Anastomosis of proximal end of duodenum to distal end of remnant stomach
• Gastrojejunostomy (Billroth II)
– Removal of antrum
– Anastomosis of remnant stomach to side of jejunum à blind duodenal loop (stapled) to allow for bile and pancreatic secretions to flow into intestine (aid digestion and absorption)
• Roux-en-Y anastomosis
– Close to total gastrectomy
– Jejunum pulled up and anastamosed at distal end of esophagus or gastric remnant
– Duodenum then connected to small bowel to allow bile and pancreatic secretions to flow into
the intestine

19
Q

Gastric Surgeries (Gastrectomy)

A

Resection of part of stomach (partial gastrectomy) and pylorus
– Alternative to pyloroplasty; gastric remnant anastomosed to small intestine
• Gastroduodenostomy (Billroth I)
– Removal of pylorus and/or antrum of stomach
– Anastomosis of proximal end of duodenum to distal end of remnant stomach
• Gastrojejunostomy (Billroth II)
– Removal of antrum
– Anastomosis of remnant stomach to side of jejunum à blind duodenal loop (stapled) to allow for bile and pancreatic secretions to flow into intestine (aid digestion and absorption)
• Roux-en-Y anastomosis
– Close to total gastrectomy
– Jejunum pulled up and anastamosed at distal end of esophagus or gastric remnant
– Duodenum then connected to small bowel to allow bile and pancreatic secretions to flow into
the intestine

20
Q

• Gastroduodenostomy (Billroth I)

A

– Removal of pylorus and/or antrum of stomach

– Anastomosis of proximal end of duodenum to distal end of remnant stomach

21
Q

• Gastrojejunostomy (Billroth II)

A

Removal of antrum
– Anastomosis of remnant stomach to side of jejunum à blind duodenal loop (stapled) to allow for bile and pancreatic secretions to flow into intestine (aid digestion and absorption)

22
Q

• Roux-en-Y anastomosis

A

– Close to total gastrectomy
– Jejunum pulled up and anastamosed at distal end of esophagus or gastric remnant
– Duodenum then connected to small bowel to allow bile and pancreatic secretions to flow into
the intestine

23
Q

Vagotomy

A

Vagotomy Impaired motor function of the stomach

24
Q

Total gastric and truncal vagotomy

A

Gastric stasis and poor gastric emptying

25
Q

Subtotal gastrectomy with vagotomy

A

Early satiety
Delayed gastric emptying
Rapid emptying of hypertonic fluids

26
Q

Total gastrectomy

A
Early satiety, nausea, vomiting
Weight loss
Poor availability of bile acids and pancreatic enzymes b/c of
anastomotic changes
Malabsorption
PEM
Anemia
Dumping syndro
B12 deficiency
27
Q

Dumping Syndrome

A

Physiological response to presence of larger-than-normal amounts
of food and liquid in small intestine
– Healthy individual:
• Food partially digests in stomach 1-3h
• Enters duodenum slowly via pyloric sphincter; acidic chyme is neutralized by
pancreatic bicarbonate
• Secondary to loss of normal regulation of gastric emptying and
GI/systemic responses to a meal
– Accelerated gastric emptying à food “dumps” too quickly into small bowel
– Refined/simple sugars particularly problematic
• Rapidly absorb water from body

28
Q

Post-Gastrectomy Nutrition Goals of Care

A
• Adequate calories and nutrients
– Promote healing
– Attenuate weight loss
– Correct micronutrient deficiencies
• Symptom management
– Reflux
– Early satiety
– Dumping syndrome
29
Q

Nutrition Interventions Post-Gastrectomy

A
Dependent on GOals of care
reason for surgery
- pud with acute complication
gastric carcinoma; neojuvant treatment pre-op
bariatric surgery
Post-operative considerations
– EN (small bowel feeding tube)
• Pt’s post-op nutritional status
– PN
• Post-op complications; GIT not functioning, leaks etc.