Upper Gastrointestinal Disorders

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Last updated 4:17 AM on 3/25/26
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111 Terms

1
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What organs are found in the Right Upper Quadrant?

  • Liver (majority)

  • Right kidney

  • Colon

  • Small portion of the pancreas

  • Gallgaldder

  • Small intestine

2
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What organs are found in the Left Upper Quadrant?

  • Liver (small portion)

  • Spleen

  • Left kidney

  • Stomach

  • Colon

  • Majority of pancreas

  • Small intestines

3
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What organs are found in the Right Lower Quadrant?

  • Colon

  • Small intestines

  • Right ureter

  • Appendix

  • Right ovary

  • Right fallopian tube

4
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What organs are found in the Left Lower Quadrant?

  • Colon

  • Small intestines

  • Left ureter

  • Left ovary

  • Left fallopian tube

5
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What structures lie along the midline of the abdomen?

  • Bladder

  • Uterus

  • Prostate

6
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How long is the adult Gi tract from lips to anus?

About 5.5 meters (18 feet)

7
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When can infants begin solid foods and why?

Around 6-8 months, when they can sit independently and primary teeth begin erupting; salivation increases and the microbiome shifts significantly

8
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What GI changes occur with aging?

Reduced nutrition absorption, decreased gastric acid, decreased tissue elasticity, weakened muscular contractions, increased incidence of GERD and constipation

9
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What is the clinical purpose of palpating abdominal quadrants?

To assess organ enlargement, tenderness, masses and localized pathology based on quadrant specific anatomy

10
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What are the functions of the Upper GI?

  • Production of saliva

  • Hold GI microbiome (influences nutrient absorption and overall well being)

  • Transportation of food and liquids to the stomach

  • Absorption of nutrients (carbohydrates) and medications into the bloodstream (sublingual)

11
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What are the qualities of saliva that make it good for digestion?

  • Is able to start the breakdown of carbohydrates

  • Lubricates food for easier swallowing

  • It has Amylase in it starts starch digestion

  • It has Lipase in it starts lipid digestion

  • It has a PH of 7.4 (buffers acids and protects teeth)

12
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What immune components are found in saliva?

Antimicrobial proteins and secretory IgA

13
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What are the major layers of the stomach wall?

  • Serosa (Outer connective tissue layer)

  • Muscularis

  • Submucosa (Glands and ducts)

  • Mucosa (Mucous spithelium, laminate proprietor, and muscularis mucosae)

14
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What do surface mucous cells produce and why?

Thick mucus to protect the GI lining and lubricate

15
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What do parietal cells secrete?

Hydrochloric acid and intrinsic factor

16
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Where are parietal cells mostly located?

In the fundus of the stomach

17
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What do chief cells secrete?

Pepsinogen (converted to pepsin for protein breakdown) and lipase (fat breakdown)

18
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What system do cholinergic effects belong to?

Parasympathetic

19
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What GI effects do cholinergic actions cause?

  • Increased gastric acid

  • Increased secretions

  • Increased motility

20
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What side effects come from cholinergic medications?

  • Diarrhea

  • Nausea/vomitting

  • GI cramping

21
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What are cholinergic meds used for?

Improve cognition in Alzheimer’s or increase bowel movement

22
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What system do anticholinergic effects belong to?

Sympathetic

23
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What GI effects do anticholinergic actions cause?

  • Decreased gastric acid

  • Consitpation

  • Dry mouth

  • Decreased esophageal sphincter pressure

24
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What side effects come from anticholinergic medications?

  • Dryness

  • Constipation

  • Slowed motility

  • GERD

25
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What are anticholinergic meds used for?

  • Diarrhea

  • IBS

  • GI Spasms

26
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What are common manifestations of GI Disorders?

  • Anorexia (loss of appetite — could be physical or psychological)

  • Nausea (Conscious, unpleasant sensation that occurs before or along with vomiting)

  • Vomiting (Sudden, forceful expulsion of stomach contents that is to protect the body)

27
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What inputs activate the vomiting center?

  • Cerebral cortex

  • Vestibular apparatus

  • Chemoreceptor trigger zone

28
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What neurotransmitters are involved in nausea and vomitting?

  • Dopamine

  • Serotonin

  • Opioid receptors

  • Norepinephrine

  • Acetylcholine

29
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Where is the vomiting center located?

In the medulla oblongata

30
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What is the CTZ and why is it important?

A chemoreceptor trigger zone in the area postrema with a permeable blood brain barrier, allowing detection of circulating chemicals

31
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What types of stimuli can trigger vomiting?

  • Motion

  • Sensory input (visual, olfactory, emotional)

  • Gastric/duodenal irritation

  • Pharyngeal stimulation

  • Circulating chemicals (drugs, alcohol, endotoxins)

32
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What acid-base imbalance does vomiting cause?

Metabolic alkalosis

33
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Why does vomiting cause metabolic alkalosis?

Loss of gastric acid leads kidneys to retain Na and bicarbonate while excreting K and H

34
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What are the categories of Anti-Emetic (anti nausea/vomiting) meds do we need to know?

  • Central nervous system agents (work by blocking neurotransmitters in the brain areas that trigger N/V, especially CTZ)

    • Serotonin Antagonisists (Block serotonin receptors in the gut and brain to prevent activation of the vomiting reflex)

    • Dopamine antagonists (Block dopamine receptors in the CTZ)

    • Antihistamines (Block H1 receptors in the brain and reduce vestibular signaling to the vomiting center)

  • Gastrointestinal agents

    • Pro kinetic agents (Increase GI motility, help move stomach contents forward, and block dopamine receptors)

    • Anticholinergics (Block acetylcholine in the vestibular system, reduction motion related signaling to the vomiting center)

35
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What is Ondansetron (Zofran)?

A serotonin antagonist: Serotonin normally stimulates vasodilation, intestinal secretion, intestinal motility, and sensation in the gut, this blocks serotonin in the GI tract and brain to stop all this

36
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What are the adverse effects of Zofran?

  • Prolonged QT intervals (risk of Torsades de Pointes)

  • Constipation

  • Headache

  • Immediate hypersensitivity

  • Fatigue/Malaise

  • Increased liver enzymes

37
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What are the nursing considerations for Zofran?

Through an IV push it much be over greater than 30 seconds (preferably 2-5 minutes) to reduce cardiac risk

38
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What is Promethazine (Phanergan)?

A dopamine antagonist: Dopamine normally stimulates the vomiting center, this blocks dopamine in the brain’s nausea pathways, stopping this

39
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What are the adverse effects of Promethazine?

  • Anticholinergic effects (Dry mouth, constipation, urinary retention, blurred vision)

  • Aspiration pneumonia (sedation and decreased gag reflex)

  • Extrapyramidal effects (involuntary movements: because dopamine blockade affects motor pathway)

  • Neuroleptic malignant syndrome (a rare but life threatening reaction to dopamine blockade)

  • BBW: Respiratory depression (contraindicated for children less than 2 years old)

  • BBW: Severe tissue injury (including gangrene if extravasation occurs)

40
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What are the nursing considerations for Promethazine?

  • Monitor for respiratory depression (sedation can suppress breathing)

  • Monitor IV site closely (High risk for extravasation and can cause severe tissue injury)

41
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What is Dismenhydrinate (Dramamine)?

An antihistamine that blocks H1 and acetylcholine receptors in the brain which reduces vestibular signaling, nausea pathways, and motion triggered vomiting

42
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What are the adverse effects of Dramamine?

  • Anticholinergic effects (Dry mouth, constipation, urinary retention, blurred vision)

  • Drowsiness

  • Confusion (especially in elderly patients)

  • Hypotension (Due to CNS and vascular effects)

43
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What are the nursing considerations for Dramamine?

  • Take 30-60 minutes before travel (prevents motion sickness before it starts)

  • Take with food or milk (to help reduce GI upset)

  • Use carefully in children younger than 2

  • Use carefully in the elderly (higher risk of confusion, falls, and anticholinergic burden)

44
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What is Scopalamine (scop patch)?

An anticholinergic medication that works by blocking acetylcholine, especially in the brain and vestibular system which is the pathways responsible for motion triggered nausea. This reduces motion related signaling, inner ear input to the vomiting center, and N/V from movement or vestibular imbalance

45
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What are the adverse effects of Scopalamine?

  • Anticholinergic effects (Dry mouth, blurred vision, constipation, urinary retention)

  • Drowsiness

  • Confusion

  • Hallucinations (more common in older adults due to CNS sensitivity)

46
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What are the nursing considerations for Scopolamine?

  • Transdermal patch placed behind the ear

  • Apply greater than 4 hours before antiemetic effect is needed (it takes time to absorb and reach therapeutic levels)

  • Patch can stay on for up to 72 hours

  • Use caution in children

  • Use carefully in elderly (higher risk of confusion, hallucinations, and anticholinergic burden)

47
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What is gastroparesis?

A condition where the staunch empties slowly because the normal movement of food through the stomach is impaired

48
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What causes gastroparesis?

Diabetes (can damage the vagus nerve/special cells in the stomach walls, when the vagus nerves is damaged the stomach cannot contract properly, therefore emptying is delayed

49
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What are symptoms of gastroparesis?

  • Intractable nausea/vomiting

  • Abdominal pain

  • Early fullness

  • Bloating

50
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What is Metoclopramide (Reglan)?

A prokinetic agent that promotes stomach emptying and increases peristalsis

51
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What are the adverse effects of Metoclopramide?

  • Anticholinergic effects

  • Hypotension (because it affects autonomic tone, causes vasodilation, and can trigger sedation)

  • Entrapyramidal effects (because it blocks dopamine)

  • Dysgeusia (altered taste because it affects central neurotransmitters)

  • SVT (rare but possible because of autonomic imbalance)

  • Neuroleptic Malignant Syndrome (rare but lifethreatening reaction to dopamine blockade)

  • BBW: Tardive dyskinesia (a serious, potentially permanent movement disorder, especially with higher doses or when using longer than 12 weeks)

52
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What infusion related reaction can occur with rapid administration of Metoclopramide?

Anxiety that is then followed by drowsiness

53
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What are the nursing considerations for IV administration of Metoclopramide?

Make sure to give 10 mg or less as a 1-2 minute push and more than 10 mg as a mini bag over 15 minutes

54
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What is GERD?

Gastroesophageal reflux disease which happens when the lower esophageal sphincter doesn’t stay closed from relaxing or weakening and acid reflux goes into the esophagus

55
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What causes GERD?

  • Bad diet

  • Obesity

  • Unhealthy lifestyle

  • Medications

  • Eating closer to bedtime

  • Pregnancy

56
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What symptoms does GERD cause?

  • Burning chest pain (heartburn)

  • Food regurgitation

  • Bad taste in mouth

  • Chronic cough or sore throat

  • Bloating

  • Stomach pain

57
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What is the progression of untreated GERD?

Reflux —> esophagitis —> mucosal injury and inflammation —> vascular changes and metaplasia

58
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What increases the risk of GERD progression?

  • Age

  • Obesity

  • Hiatal hernia

  • Delayed gastric emptying

  • Medications

  • Nicotine

59
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What prevention strategies are recommended for GERD?

  • Avoid trigger foods

  • Eat small meals

  • Avoid alcohol

  • Don’t lie down after eating

  • Stop smoking

  • Lose weight

60
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What is gastritis?

Inflammation of the stomach lining

61
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What causes gastritis?

  • Alcohol (irritates and erodes the stomach lining, increases acid, causes inflammation)

  • Infection usually from H. Pylori (It burrows in the mucosa and weakens the protective mucus causing inflammation and ulcer risk)

  • Medications especially NSAIDs (Block prostaglandins and reduce mucus/bicarbonate so the stomach lining becomes vulnerable)

  • Unhealthy food such as high fat, spicy, acidic, or processed foods (can irritate the stomach and increase acid production)

62
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What are the symptoms of gastritis?

  • Loss of appetite (inflamed mucosa make eating uncomfortable)

  • Pain (usually epigastric burning or gnawing)

  • Bloating (inflammation slows gastric emptying causing gas and distention)

  • Nausea/Vomiting

  • Heartburn (acid irritation of the stomach and sometimes the lower esophagus)

  • Indigestion (General upper Gi discomfort like fullness, pressure, or upset stomach)

63
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What is Peptic ulcer disease?

A condition where the stomach or duodenal lining develops an open sore due to a breakdown of the mucosal barrier, allowing gastric acid and pepsin to cause deeper tissue injury

64
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What causes peptic ulcer disease?

  • H. Pylori (a bacteria that burrows in the mucosa and weakens the protective mucus, increasing inflammation and acid sensitivity)

  • NSAIDs (block prostaglandins and decrease mucus, bicarbonate, and mucosal blood flow leaving the stomach lining unprotected)

  • Histamine (stimulates parietal cells which increases acid production)

65
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What are the stages of ulcer formation?

  • Stage 1: Normal (mucosa intact, protective mucus/ bicarbonate/ blood flow all work normally)

  • Stage 2: Erosion (Damage limited to the mucosa causing shallow injury, but not yet a true ulcer)

  • Stage 3: Ulcer (Damage extends into the submucosa and it is now officially a peptic ulcer, pain increases because the nerves and vessels are exposed)

  • Stage 4: Perforated (ulcer penetrates through muscularis to serosa and creates a hole into the abdominal cavity, this is a surgical emergency)

66
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What are damaging factors to the stomach lining?

  • Gastric acid

  • Pepsin

  • H. Pylori

  • NSAIDs

  • Tobacco

  • Alcohol

  • Hyperacidity

  • Duodenal gastric reflux

  • Ischemia/shock

67
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What are the protective factors to the stomach?

  • Mucus

  • Bicarbonate

  • Good blood flow

  • Tight epithelial barrier

  • Rapid cell regeneration

  • Prostaglandins

68
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What is the general cause of peptic ulcers?

When damaging factors overpower protective factors

69
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What is the Pathophysiology of peptic ulcers disease?

  • Damaging factors overpower protective mucosal defenses

  • Mucosal injury occurs which triggered histamine release

  • Histamine increases gastric acid, pepsinogen to convert to pepsin, blood flow and capillary permeability

  • Decreased mucus, bicarbonate, and mucosal synthesis weaken the barrier

  • A break in the mucosal barrier allows acid to penetrate deeper layers

  • Inflammatory erosion develops causing plasma protein loss

  • Vessel destruction occurs causing GI bleeding

  • Continued injury can progress through the mucosal barrier to submucosa to muscularis to serosa

  • And in severe cases, this can lead to perforation

70
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What are the two main types of ulcers?

  • Gatric

  • Duodenal

71
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Which type of ulcer is most common?

Duodenal ulcers

72
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What are the primary causes of duodenal ulcers?

  • H/ Pylori

  • NSAIDs

73
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What are the primary causes of gastric ulcers?

  • Chronic gastritis

  • H/ Pylori

  • NSAIDs

74
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What is the pathogenesis of duodenal ulcers?

Increased acid or pepsin breaks through the mucosal barrier and damages tissue

75
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What is the pathogenesis of gastric ulcers?

Decreased mucosal protection allows hydrogen ions (acid) to penetrate deeper tissues and trigger inflammation

76
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What are complications of duodenal ulcers?

Deep ulcerations, bleeding, and potential metaplasia or cancerous changes

77
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What are complications of gastric ulcers?

GI bleeding, gastric edema, and loss of plasma proteins

78
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When does pain typically occur with duodenal ulcers?

A couple hours after eating

79
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When does pain typically occur with gastric ulcers?

Immediately after eating

80
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What is an upper GI bleed?

Bleeding that originates above the ligament of Treitz (esophagus, stomach, or duodenum)

81
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What are common causes of upper GI bleeding?

Esophageal varicose and ulcers

82
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What is hematemesis?

Vomiting blood

83
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What is coffee ground emesis?

Partially digested blood that looks dark and granular due to stomach acid exposure

84
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What is Melena?

Black, tarry stool caused by digested blood from an upper GI bleed

85
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Why does an upper Gi bleed cause nausea, vomiting, or diarrhea?

Because blood acts as a gastric irritant

86
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How does an upper GI bleed affect perfusion?

Blood loss leads to hypovolemia which causes low BP, low HR, dizziness, pallor, vision changes, and decreased urine output

87
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What abdominal complications can occur from poor perfusion?

Mesenteric insufficiency leading to abdominal pain or bowel infarction

88
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What liver complication can occur from severe hypoperfusion?

Liver ischemia or necrosis

89
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What vital organs are at risk during hypoperfusion?

The brain and the myocardia (heart)

90
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What is the final systemic consequence of severe upper GI bleeding?

Lactic acidosis and shock

91
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What stimulates parietal cells to produce acid?

Acetylcholine (vagus nerve), histamine (mast cells), and gastrin (circulation)

92
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What does acetylcholine do to the parietal cell?

It binds to muscarinic receptors and increases intracellular calcium, stimulating acid secretion

93
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What does histamine do to the parietal cell?

It binds to H2 receptors and increases cAMP, activating the proton pump

94
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What does gastrin do to the parietal cell?

It stimulates acid secretion directly and indirectly by promoting histamine release

95
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What is the H/K ATPase pump?

The proton pump that secretes hydrogen ions into the stomach lumen

96
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What medication blocks histamines effect on acid secretion?

H2 blockers

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What type of medication blocks the proton pump directly?

Proton pump inhibitors (PPIs)

98
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How do antacids work?

They neutralize stomach acid but they do not reduce acid synthesis or secretion

99
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Why are Anticholinergics no longer used for acid suppression?

Because H2 blockers, PPIs, and antacids are more effective and safer

100
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What is Pantoprazole (Protonix)?

A proton pump inhibitor what irreversibly binds to the H/K ATPase proton pump, stopping ATP dependent hydrogen ion secretion and reducing HCl production by greater than 90% for 24 hours

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