Gastrointestinal 1 Flashcards

1
Q

Common symptoms of temporary conditions

A

o Nausea, vomiting, heartburn, gastritis, anorexia, gas pains, diarrhea, constipation, etc.

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2
Q

how are esophagus disorders diagnosied?

A

o endoscopy: allows us to view the inside of the GI.
o Gastroscopy: in the stomach and also allows to do small procedures without cutting open

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3
Q

role of esophagus

A

Is for transport and has very protective lining made with squamous epithelium.

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4
Q

what is achalasia and what causes it?

A
  • problem with the lower esophageal sphincter, where it meets with the stomach (doesn’t open/relax properly), so there is discomfort in swallowing (dysphagia)
  • Caused by neuronal degeneration (the loss of inhibitory neurons), causing problems in the opening of the sphincter.
  • Strategy is balloon dilation of the lower esophageal sphincter.
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5
Q

what are esophageal varices and what causes them?

A
  • veins are bulging out into the lumen of the esophagus, which are very fragile and can rupture, which would cause bleeding (high risk of hemorrhage)
  • Cause primarily with hepatic hypertension, where there are much more veins in the esophagus and rectal area (risk of hemorrhoids)
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6
Q

what causes esophagitis? which people are mostly affected?

A
  • infections: mainly fungi and viruses
  • in immunocompromised people and with motility disorder
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7
Q

normal physiology of swallowing

A

o Upper part is striated muscle and the lower part is smooth muscle – meaning that we choose to initiate swallowing reflex (oral phase), but once it gets into the pharynx (pharyngeal phase) and then the esophagus (esophageal phase), it is transported down to the stomach autonomously.

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8
Q

what is the role of the enteric nervous system? where does the input come from?

A
  • coordinate the GI processes.
  • For swallowing, the major control is through the myenteric plexus, which is found in the smooth muscle lining the esophagus.
  • Input: from periphery stimuli from oropharynx/larynx/esophagus, sensory neurons, swallowing sensor in brain
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9
Q

how often do we swallow?

A

1x/min (about 0.5ml)

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10
Q

how do the esophageal sphincters work in normal conditions?

A

o Pressure at rest is high at the sphincter, specifically the upper esophageal sphincter, so that nothing gets in by accident.
o When swallowing, it contracts from top to bottom, changing the pressure as it compresses the esophagus.

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11
Q

what are mechanisms preventing reflux and when are they altered?

A

o Lower esophageal sphincter is normally closed, and there is pressure on the outside keeping it closed.
o But increased intragastric pressure, obesity, and temporarily in pregnancy can cause problems.

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12
Q

what does GERD cause?

A
  • Causes heartburn, which is caused by contents in the stomach going back up.
  • Called since causes a burning sensation in the chest, including close to where the heart is found.
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13
Q

what is Hiatus hernia what can it cause?

A
  • a major problem that causes esophagitis.
  • loss mechanisms preventing reflux.
  • Upper part of the stomach slides to the hiatus, which is the opening of the diaphragm, and protrudes in the abdominal cavity.
  • This causes loss of some protective ability to keep acid out of the esophagus.
  • This pressure causes chest pain
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14
Q

what does reflux cause?

A

o Pain, hyperplasia (due to chronic injury), ulceration which can cause fibrosis, stricture (narrowing of the lumen), dysphagia, spasm (due to injury on innervation of esophagus), metaplasia.

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15
Q

risk factors for GERD

A
  • Obesity
  • Pregnancy due to the changes in pressure (but is reversible)
  • Hiatus hernia.
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16
Q

therapy/prevention for GERD

A
  • Lifestyle changes can decrease reflux: stop smoking, have better posture, don’t eat 2-3 hrs before bed, raise head of the bed, watch weight, limit caffein and fatty foods.
  • Can also take antacids.
  • For some circumstances, surgery is necessary.
17
Q

risk for developing esophageal carcinoma

A

alcohol and cigarette
(Things that can be prevented)

18
Q

parts/anatomy of the stomach

A
  • Main part is the body.
  • Fundus: the top
  • Antrum: lower part, close to the duodenum.
19
Q

what are the cells and their roles on their stomach

A

o Parietal cells: secrete HCl.
 Function is to kill the microorganism that is present in the food.
 Acid secretion by a proton pump (exchanging potassium and hydrogen), which is activated by acetylcholine, histamine, and gastrin.
 Populates major part of the stomach.
o Chief: pepsinogen (digestive enzyme)
o Enteroendocrine: hormones
o Mucous cells: mucous
 Protects surface of the stomach from the HCl, lines the surface of the stomach.

20
Q

what are the damaging and defensive forces in a normal stomach

A

o Damaging forces: gastric acidity and peptic enzymes
o Defensive forces: mucous and bicarbonate secretion, mucosal blood flow, apical surface membrane transport, epithelial regenerative capacity, prostaglandin synthesis.

21
Q

what can cause acute gastritis?

A

o classic cause is alcohol.
o But too much NSAIDs or other drugs and food poisoning can also cause this.

22
Q

how does smoking promote gastritis?

A

o Stimulate gastric acid secretion, stimulate bile salt reflux, cause alteration in mucosal blood flow, decrease mucous secretion, reduce prostaglandin synthesis, decrease pancreatic bicarbonate secretion.
o Also impairs healing.

23
Q

what causes peptic ulcers?

A
  • Imbalance: when injury overtakes the defence, so acid output wins against mucosal defence.
    o Parietal cells - HCl secretion
    o mucus cells - mucosal defense
24
Q

acute vs chronic peptic ulcers

A
  • Acute: gone down a certain distance, but eventually heals.
  • Chronic: damage has gone very deep due to continual damage, leading to high risk of perforation.
25
Q

locations of peptic ulcers and who is usually affected by these specific types

A

o gastric ulcers: usually occurs in the body of the stomach.
 Tend to occur in males.
o duodenal ulcers:
 have hemorrhage, perforation, and stricture (since duodenum is narrower, so continual healing and injury might result in a decrease in diameter of the lumen) as risks.
 Tend to occur in younger age range and in males.

26
Q

peptic ulcers cause risk of what?

A

o Hemorrhage: person can vomit blood or can go through the GI tract.
o Perforation: material can go into abdominal cavity.
o Carcinoma

27
Q

symptoms of peptic ulcers

A

o Pain, which is often relieved by eating.

28
Q

therapy for peptic ulcers

A

you want to block to acid output to allow the healing process to overcome the damaging stimulus.
o Antacids
o proton pump inhibitors
o H2 receptor blockers (histamine receptor)

29
Q

Properties permitting acid resistance and mucosal penetration of helicobacter pylori

A

o Flagella: bacterial motility and chemotaxis to colonize under mucosa
o Secretes enzymes: mucinase, protease, lipase (causes gastric mucosal injury)
o Urease: neutralize gastric acid to protect itself (by ammonia).
o Outer proteins: adhere to host cells.
o Type IV secretion system: allow to penetrate the wall of the wall and inject toxin.
o Effectors: IL-8 induction, host cell growth and apoptosis inhibition (promotes immune reaction)
o Secrete enzymes that promote lipid raft clusters and adhesion.

30
Q

mechanisms causing cell injury of helicobacter pylori

A

o HP-NAP: neutrophil activating protein
o Cag: cytotoxin-associated gene.
o VacA: pore-forming cytotoxin.
- Inflammatory and immune response: potent inducer of inflammation
o Neutrophils move in, macrophages are activating, causing the activation and release of factors.

31
Q

therapy for H. pylori

A
  • Ulcers cured with antacids plus antibiotics since it allows the neutralization of the acid and it kills H. pylori.
32
Q

what is acute gastric ulceration and what can cause it?

A
  • Severe physiological stress – occurring almost overnight.
  • Serious brain injury, severe burns, cardiovascular shock, major surgery
  • Rapid onset, and mainly stomach disruption of mucosal barrier.
  • Risk can rapidly escalate, leading to risk of hemorrhage and perforation.
33
Q

what can cause stomach cancer?

A
  • H. Pylori is a major cause of this
  • smoking causes 20% of cases
34
Q

what is pyloric stenosis? who is affected?

A
  • Problem is that the region where the stomach empties in the duodenum doesn’t open properly – causes babies to projectile vomit when drinking milk.
  • These children are born with this problem, but there is a small incision (allowing it to relax) that can be done to completely solve this issue for their whole life.
35
Q

physiology of the medullary vomiting center (input/paths)

A

o Central pathway: Chemoreceptor trigger zone that monitors blood and detects foreign compounds and causes vomiting.
o Vagal pathway: stimuli from GI tract, higher centers (smell, vision, etc.), and pharynx.
o Vestibular pathway (balance)
o These all converge on the vomiting center.

36
Q

common stimuli for vomiting

A

o Something that you eat that irritates the GI tract that triggers the …
o Food poisoning, binge eating, alcohol.
o Triggered by some drugs such as chemotherapy.

37
Q

Mechanics of vomiting

A

o Retching: the gagging, where the sphincter is closed and stomach is relaxed, but abdomen is contracting – initial event.
o there is some antiperistalsis movement and high intraabdominal pressure – it is the abdominal contraction that pushes everything out.
o Both esophageal sphincters have to open since the vomit has to come out.

38
Q

Role of neurotransmitters and agents to block nausea and vomiting:

A

o Serotonin is very important in vomiting – there are a lot of 5-HT receptors involved in the transmittance of signals to the vomiting center.
o Now we have drugs that block this pathway, leading to stop in nausea and vomiting.
 Used with chemotherapy.