case 1: peptic ulcer Flashcards

(43 cards)

1
Q

chief complaints

A

hematemesis

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2
Q

history

A
  • dyspepsia and epigastric pain
  • stress
  • Spicy food, coffee and fatty food elicit pain
    ** these are myth risk factors for peptic ulcers
  • ibuprofen (Advil, 400 mg q.i.d for 6 months)
    for rheumatoid arthritis
    ** NSAIDs is an aggressive factor of peptic ulcer disease
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3
Q

physical exam

A
  • pallor
  • reclining position BP – 110/70, pulse rate – 100; on standing position BP – 90/50, pulse rate – 130
  • heart: regular rhythm with tachycardia
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4
Q

Why and how might change of positions affect
his BP and pulse rate?

A

heart rate and blood pressure are higher in standing and sitting positions due to gravity?

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5
Q

clinical tests

A

CBC – hematocrit (38), WBC (9,800) and platelets (300,000) are all within normal range

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6
Q

how peptic ulcer was diagnosed

A

endoscopy

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7
Q

treatment at ER

A
  • insertion of nasogastric tube
  • IV infusion normal saline
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8
Q

hematocrit

A

– a.k.a. packed cell volume (PCV)
or erythrocyte volume fraction (EVF), is the volume percentage (%) of RBC in blood
– Normal value – (♂) 41-53%, (♀) 36-46
– Anemia vs. polycythemia (Males with hemoglobin values less than 13 g/dL were classified as anemic, and those with values greater than 16.5 g/dL or hematocrit greater than 49 percent were categorized as having polycythemia)

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9
Q

why was hematocrit normal?

A
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10
Q

endoscopy

A
  • A nonsurgical procedure used to
    examine a person’s digestive tract
    – Use an endoscope, a flexible
    tube with a light and camera attached to it
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11
Q

other method to diagnose peptic ulcer

A

Barium X-ray of upper GI tract
– Barium is an X-ray contrast medium
– To study the appearance and
function of the parts of the gastrointestinal tract

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12
Q

describe the general structure of the stomach

A
  • most distensible part of GI tract
    – Cardia, fundus, body, antrum, pylorus, pyloric sphincter
    – Mucosa, submucosa, muscle (circular & longitudinal), and serosa
    – Gastric glands – deeper in the mucosa
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13
Q

what is the function of gastric glands?

A

secrete gastric juice

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14
Q

what do the gastric glands contain?

A
  • mucus (goblet cells)
  • Parietal cells – HCl & intrinsic factor
    (exocrine)
  • Intrinsic factor – a polypeptide that
    promotes absorption of vit B12 in the
    small intestine (ileum) → helps
    prevent pernicious anemia; the only
    essential function in stomach
    – Chief cells – secrete pepsinogen
    – Enterochromaffin-like cells (ECL) –
    histamine & serotonin (paracrine)
    – G cells secrete gastrin (endocrine,
    hormone)
    – D cells – secrete somatostatin
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15
Q

what secretes HCl?

A

parietal cells, containing H+-K+-ATPase (proton
pump)

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16
Q

describe the pathway of food in the stomach to secrete HCl

A
  • Food in stomach →
    – Activation of parietal cell → increases
    insertion of H+-K+-ATPase in the apical membrane
    – Net effect – transporting H+ & Cl- into the gastric lumen; HCO3- into blood
  • CA – carbonic anhydrase
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17
Q

composition of luminal fluid

A

isotonic H+, Cl-, K+ & Na+ (hydrochloric acid, gastric acid)
Why is the secretion isotonic?
- similar concentration of dissolved particles as blood

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18
Q

Gastric Endocrine Secretion – Gastrin

A
  • The gastroenteropancreatic (GEP) endocrine cells – some GI epithelial cells secrete hormones (blood-borne & ductless)
  • Stomach G cells – gastrin-producing cells in gastric antrum, duodenum & pancreas → blood circulation → parietal cells in fundus
    – Peptide of 17 a.a.; secretion stimulated by food (esp. protein); secretion of gastrin is inhibited by a decline in pH in stomach (acidic chyme). Why?
  • sodium bicarbonate from the isotonic secretion?
19
Q

functions of gastrin

A
  • Gastrin – help process food in stomach & duodenum by:
    – Enhances parietal cell secretion of acid
    – ↑ Histamine secretion from ECL cells → ↑ acid secretion
    – GI trophic action – proliferation of mucosal epithelial cells. Why? to expand stomach when filled with food?
    – Control of GI motility – ↑ contraction of stomach ( major)
  • Also ↑ contraction duodenum, ileum & lower esophageal sphincter tone
  • Relaxation of ileocecal sphincter (why would that help process food?)
  • Induces mass movement in colon
    – ↑ Secretion of pancreatic enzymes
20
Q

regulation of HCl secretion

A
  • 3 Limbs regulation -> increase acid secretion
    – Neural – acetylcholine (parasympathetic NS)-M3 receptor
    – Hormonal – gastrin (G cells)-CCK2 receptor
    – Paracrine – histamine (ECL cells)-H2 receptor
  • Histamine from ECL cells is the most potent stimulus
    – Acetylcholine (parasympathetic NS) acts on G, ECL & parietal cells
    – Gastrin acts on ECL & parietal cells
21
Q

vagus nerve (acetylcholine)

22
Q

Gastric Mucosal Barrier

A
  • Mucosal barrier enables stomach to contain acid without injuring itself
  • Structural protection – luminal membrane (1) & tight junctions (2)
  • Chemical protection – alkaline mucus (3)
    – Mucus gel layer slows diffusion of H+
    – HCO3- neutralizes H+ before reaching epithelium
  • Cytological protection – surface epithelial cells replaced every 4-7 days, due to endogenous prostaglandins (PGE2), gastrin & growth factors
23
Q

Functions of The Stomach

A
  • Storage of food (HCl), minimizing growth of bacteria
    – Along with salivary lysozymes and pepsin, killing most of the microorganisms ingested with food
  • Denaturation and partial digestion of proteins
    – Activation of pepsinogen to active pepsin (positive feedback)
    – Providing acid medium optimal for pepsin activity
    – Aiding in breakdown of connective tissue, muscle fibers and other proteins for faster pancreatic enzymatic digestion
  • Regulation the rate of food emptying into the small intestine
    – Digestion occurs at much slower rate than consumption
    – Allowing maximal intestinal digestion and absorption
  • Secretion of intrinsic factor (the only essential function)
  • Question – What would happen if the production of HCl is
    reduced?
24
Q

define Hypochlorhydria

A

deficiency of hydrochloric acid production in
the stomach

25
risk factors of hypochlorhydria
– Age – people over the age of 65 have the highest risk – Medications – proton pump inhibitors, antacids or heart burn medications – Helicobacter pylori infection
26
hypochlorhydria symptoms
– Gastrointestinal infections, bloating, burping, gas, diarrhea – Undigested food in the stool – Nutrient deficiencies
27
erosion
mucosal layer is damaged
28
Ulceration
mucosal, submucosal and/or muscle layers are damaged
29
Perforation
all four layers are damaged → stomach contents leak into abdominal cavity →peritonitis
30
types of ulcers
gastric, duodenal, esophageal
31
Peptic Ulcer Disease (PUD)
* Imbalance between the aggressive and defensive factors in the gastroduodenal mucosa – Aggressive factors – gastric acid, pepsin, Helicobacter pylori infection & NSAIDs – Protective factors – mucin, HCO3-, prostaglandins (epithelial cell replenishment) – PUD patients → ↑ gastric emptying rate → ↑ duodenum acidification → gastric metaplasia → ↑ H. pylori colonization in duodenum
32
Some Facts about Peptic Ulcer
* Epidemiology – lifetime prevalence – 5-10% * Helicobactor pylori infection (~85%) – Only infects gastric mucosa – Found in 80-95% of duodenal ulcers, due to gastric metaplasia (change in duodenal mucosa to gastric mucosa → decreases HCO3- production → decreases acid neutralization – Found in 70-90% of gastric ulcer * Non-steroidal anti-inflammatory drug (NSAIDs) (10-15%) * Overproduction of gastrin (Zollinger-Ellison syndrome) – 0.1% * “Myth” risk factors (not an initiator) – Cigarette smoking, stress, personality & occupation – Diet (spicy food, neutral fats), alcohol consumption
33
Helicobacter pylori Infection
– Gram-negative, curved, with 4-6 flagella, rod – Resides in gastric-type epithelium within mucosal layer (protects the bacteria from acid) – Is the main cause of peptic ulcers (85%) – Can also cause gastritis and stomach cancer
34
The Finding of H. pylori Pathogenesis
* The causative role of H. pylori infection in PUD was first elucidated by Barry J. Marshall and J. Robin Warren in 1984. * To prove the causative role, Marshall ingested inoculum of H. pylori and confirmed the presence of its infection. * Marshall and Warren received Nobel Prize for Medicine and Physiology in 2005. * H. pylori is now classed by WHO as a class 1 carcinogen. * H. pylori uses its flagella to penetrate gastric mucus layer to reach gastric epithelial cells (more neutral pH)
35
Mechanisms for H. pylori-induced GI injury
* H. pylori harm gastric epithelium by: – Producing urease to convert urea into ammonia * (NH2)2CO + H2O → CO2 + 2 NH3 * NH3 + H+ → NH4+ – NH3 is toxic to gastric epithelium – Produce proteases and other chemicals disrupts tight junctions and causes apoptosis * Mode of transmission – Likely oral-oral/fecal-oral – Age of acquirement – childhood
36
NSAIDs
* Function of cyclooxygenase (COX) – COX-1 – constitutively active, catalyzes production of gastric prostaglandins * Support blood flow in stomach wall * Enhance mucus and HCO3- production * Mediate somatostatin (from gastric D cells) suppression of acid secretion – COX-2 – induced as part of an immune response, inflammatory prostaglandins contribute to pain, heat, swelling * NSAIDs (non-steroidal anti-inflammatory drugs) – most widely used classes of drugs, non-selective – Ibuprofen (Advil), naproxen (Alleve), sulindac (Clinoril), aspirin, indomethacin (Indocin) – Baby aspirin (81 mg daily) → decrease gastric mucosal PGE2 → gastric lesions
37
NSAIDs and Peptic Ulcer
* NSAIDs → decrease gastric prostaglandins secretion → decrease mucin secretion → weaken the mucosal barrier → acid can directly injure the mucosa → causes gastric ulcers * Risk of NSAID-induced ulceration – Age > 60; increasing duration & dose of therapy – Concurrent steroid or anticoagulant use * Symptoms (quite variable) – Asymptomatic – Vague abdominal discomfort – Classical symptom – dyspepsia * Pain centered in the upper abdomen * Discomfort in the form of fullness, bloating, distention or nausea * 1-3 hr post-meal or midnight; relieved by food or antacid
38
Stress Ulcers
* Severe physiologic stress → (fight or flight) → splanchnic hypoperfusion → ischemic → a cascade of inflammatory responses are the key causes – In this sense, stress does cause stress ulcers – Acid alone does not cause stress ulcers * Splanchnic circulation – the blood flow to abdominal GI organs ( stomach, liver, spleen, pancreas, small intestine & large intestine * Cushing ulcer – ↑ intracranial pressure → vagus nerve → ↑ parietal cells → increase acid secretion * Curling ulcer – severe burn (>35%) → decrease gastric ischemia
39
Zollinger-Ellison Syndrome
* Caused by tumors * Most often found in the head of the pancreas and the upper small intestine * Produce the hormone gastrin and are called gastrinomas * Stimulates the parietal cells to secrete gastrin * → HCl secretion to maximal activity * → Gastrointestinal mucosal ulceration
40
Peptic Ulcer – Diagnosis
* Immediate endoscopy, X-ray or CT scan * Noninvasive test for H. pylori – Serological testing for IgG, can remain “+” for 3 yr after therapy – Urea breath test – use C13 or C14 labeled urea * (NH2)2CO + H2O → HCO3- + 2 NH3 → CO2 + 2 NH3 * Detect level of CO2 – Stool H. pylori antigen test * Invasive test for H. pylori – Biopsy for H. pylori culture or histology – Rapid urease test
41
Peptic Ulcer – Treatment
1. * decrease HCl secretion by parietal cells – Proton pump inhibitors (PPI, most effective) * Drugs ending in "prazole“ – omeprazole, esomeprazole – Histamine (H2) blockers (very safe) * Competitive antagonists at H2 receptors, e.g. ranitidine, cimetidine * decrease Basal & meal-stimulated HCl * H1 antagonists – anti-allergy, anti- vomiting, motion sickness – Anticholinergic drugs * Eradicate H. pylori – antibiotics (clarithromycin, amoxicillin, or metronidazole) * Mucosal protectants such as sucralfate require acidic environment for activation. As such, does not work with H2 blockers or antacids (decrease acidity) 2. * Mucosal protectants (protect mucosa) – Sucralfate (disaccharide-SO3-Al) * The negatively charged sucrose sulfate binds to positively charged proteins in the base of ulcers or erosions * → form a cross-linking, viscous, paste-like material * → physical barrier that restricts further caustic damage – Bismuth subsalicylate – like sucralfate, bismuth coats ulcers and erosions, creating a protective layer against acid and pepsin – Side effects – constipation & black stool * Re-establish mucosal barrier – prostaglandins (PGE & PGI) * Acidity – buffering acid & decrease acid secretion – Antacids – aluminum or magnesium hydroxide * Al(OH)3 + 3 HCl <--> AlCl3 + 3 H2O
42
Acute Gastritis
* Acute gastritis – submucosa inflammation * Causes – Non-steroidal anti-inflammatory drugs (NSAIDs) – Mast cells tumor (most common skin tumor in dogs) → ↑ histamine production → ↑ H+ production from parietal cells – Helicobacter pylori – humans, rare in cats, not in dogs
43
Gastroesophageal Reflux Disease (GERD)
* Normally lower esophageal sphincter (LES) closes to prevent acidic chyme from reflux * Reflux occurs when the LES is weak or relaxes inappropriately → GERD (heart burn) * Treatment – Antacids (neutralize HCl), mucosal protectants, reducing HCl production Gastroesophageal Reflux Disease (GERD)