Disorders of the Upper Gastrointestinal Tract

Question 1

dysphagia

Answer 1

• difficulty swallowing; initiating swallowing is a voluntary thing
• Any skeletal stuff or disruption of the integrity in the esophagus, the smooth muscle, etc can disrupt this complicated neuromuscular process
• Stroke – impair cranial nerves that deal with the musculoskeletal apparatus
• Strictures – narrowing the esophagus
• Connective tissue disease
• Abnormal esophageal tone

Question 2

esophageal diverticulum

Answer 2

• because it’s a hollow muscular tube, its subject to outpouching
• Outpouching of the esophageal wall – diverticuli – defect in muscular wall that allows a little balloon that creates a pouch – if you build up pressures in the pouch, it gets bigger and can become a problem
• Progressive condition
• Pathology is in the muscularis layer – this is NOT mucosal problem – lack of integrity of muscular wall that lines the tube

Question 3

Achalasia

Answer 3

• in order to swallow, you need coordinated muscle movements
• Loss of peristalsis in distal third;
• Loss of LES (lower esophageal sphincter) function (relaxation) - Can lead to reflux
• 10:100,000, M = F. congenitally
• Duration of symptoms 4.7 yr in one study

Question 4

dysphagia vs regurgitation

Answer 4

• Dysphagia (Solids (91%), Liquids (85%))
• Regurgitation (76-91%) – there is a difference between regurgitation and vomiting (Means you are bringing up something that hasn’t reached the stomach - Vomiting means you are expelling stomach contents, Difficulty belching (85%), Heartburn (40-60%)

Question 5

GERD presentation

Answer 5

• Presentation (Heartburn, Regurgitation)
• Atypical presentations: Cough, Asthma, Laryngitis, CP, Hiccups
• Often left sided but not always
• Feeling of fullness
• Feels like stuff gets stuck high up in the esophagus and this is called a globus sensation

Question 6

GERD prevalence

Answer 6

• 1 of 5 experience HB or regurge weekly
• 2 of 5 experience monthly
• Estimate: 1/3 Americans

Question 7

GERD

Answer 7

• Weak or incompetent lower esophageal sphincter – this is a physiologic sphincter, not an anatomical sphincter (This means that it is not built the way as a classic sphincter but it acts like one)
• Cause of damage is the acidic gastric fluid causing reflux esophagitis
• The mucosa of the esophagus is there to protect us from the sharp parts of food (Does not do well with exposure to acid, The stomach does things to protect itself but the esophagus doesn’t have that stuff)

Question 8

Barrett’s esophagus

Answer 8

• Squamous mucosa normally lining the stomach is replaced by columnar epithelium.
• Associated with increased risk of development of esophageal cancer.
• Causes metaplastic changes
• The cells are converted to cells that are found in the stomach – NOT GOOD – on the way to cancer

Question 9

cancer of esophagus

Answer 9

• Squamous cell carcinoma <50%
• Adenocarcinoma >50% (Cancer of the glandular tissues)
• Adenocarcinoma – disease of wealth – associated with diet, weight, etc. (Arise from Barrett’s esophagus, Located in distal esophagus)
• Squamous carcinoma – disease of poor (Associated with alcohol and tobacco use, Can sometimes be referred to as “throat cancer”, Disease of lower socioeconomic status where the rates of alcohol and tobacco use is higher)

Question 10

Gastritis

Answer 10

• when the lining of the stomach gets inflamed – if you take away the irritation, the problem should go away. If it doesn’t, then its not acute gastritis
• Acute Gastritis (Transient, Associated with irritants, Local inflammatory response - Edema, Hyperemia
• Self limiting – if you take the irritant away, gastritis should resolve

Question 11

chronic gastritis

Answer 11

• Atrophy of glandular epithelium – loss of the glandular cells
• Can transform to dysplasia and cancer (gastrocarcinoma)
• Associated with alcohol, tobacco and chronic use of NSAIDs - REDUCTION IN PROSTAGLANDINS!!! – it is prostaglandins that stimulate mucosal barrier formation, If you take NSAIDs, you stop the barrier from reforming
• There is an element of direct contact because if there wasn’t, you wouldn’t have to take it with food
• People get less symptoms if you take 1 600 tab rather than 3 200 tabs because there is less surface area of the pill so causes less irritation – breaks down more slowly and the exposure to the mucosa is less

Question 12

Types of chronic gastritis

Answer 12

• Autoimmune (Peptic ulcer, Pernicious anemia – autoimmune disease (when people get pernicious anemia bc of gastric bypass, its not actually pernicious anemia), Gastric carcinoma)
• H. Pylori (Gastric atrophy – lining atrophy that can lead to metaplasia, etc., Metaplasia, Gastric cancer)
• Chemical gastritis

Question 13

peptic ulcer

Answer 13

• Stomach and duodenum
• Exposure to acid, pepsin – of the mucosal layer (Normally you have mucus on the surface of the stomach that keeps the acid from gaining exposure to the mucosal cells, The disease comes when you have a breakdown in the barrier and the mucosal layer is exposed directly to the acid)
• NSAID and Aspirin
• Duodenal is 5X gastric
• Duodenal ulcer (5X gastric, Early adulthood, Men more than women)
• Gastric ulcer (Older adult 50-75, Men more than women)
• Layers affected (Mucosa, Submucosa – the vasculature is in this layer – if the ulcer bleeds, you know it has hit this layer, Smooth muscle, Serosa)
• Complication (Hemorrhage - Underlying blood vessels or granulation tissue, Perforation - Involvement of serosa – open to the abdominal cavity, Obstruction – bc its inflammatory - Edema, spasm or scar tissue – causes the small intestine to sort of stick to itself)

Question 14

zollinger ellison syndrome

Answer 14

• Gastrinoma (cancer) - Gastrin secreting tumor – present like the pt has GERD but their “GERD” is not helped with normal tx like proton pump inhibitor
• Pancreas, stomach or duodenum – doesn’t have to be in the stomach (i.e. you can have a gastrinoma in the pancreas)
• Increased gastric secretion
• Intractable ulcer – does not respond to the normal ulcer treatments

Question 15

stress ulcer

Answer 15

-Curling ulcer (Burns – severe physically stress, Hemorrhage – trauma patients, Surgery, ICU , Fundus of stomach – top , Ischemia – any disruption in the blood flow to the stomach can lead to these ulcers - Denying blood flow to stomach because of trauma, burns, etc.)

Question 16

cancer of stomach

Answer 16

-Risk factors (Genetic predisposition – doesn’t mean that you will for sure get it, N-nitroso compounds – every time you eat meat at a high temp, you create these compounds that are known to be carcinogenic, Autoimmune gastritis, Gastric adenoma (benign polyps))

Question 17

malignant ulcer

Answer 17

• blood outside of the vascular system is toxic to tissues and can cause a lot of damage
• Irregular margins – normal gastric ulcer is round and very clear borders
• Large size
• Inverted margins

Question 18

H. pylori - the MCC of peptic ulcers

Answer 18

• Most common cause of peptic ulcer (?)
• All persons with DU
• 70% of patients with GU
• Correlation vs causation?? – most of us with or without ulcers test positive for H pylori and it is very widespread! (Many of us have H pylori and never get ulcers, You can’t isolate H pylori in every patient with an ulcer, Clinically, H pylori is associated with ulcers – whether this is correlation or causation isn’t entirely clear)

Question 19

Koch’s postulates

Answer 19

• The suspected causative agent of a disease must be found in every case, and absent in healthy individuals. – this is the one that is a problem for determining H pylori’s relationship with peptic ulcer disease
• The agent must then be isolated and grown outside the host (i.e. cultivated in a laboratory environment).
• When a healthy, susceptible host is inoculated with the agent, the host must develop the same disease.
• That same agent must then be reisolated from the experimental host.
• Bonus question: Is H Pylori testing an effective means of screening for PUD? – HARD TO SAY (If you come in with gastritis and he tests for H pylori and you’re positive, that doesn’t really tell you much because you may have had H pylori before you had peptic ulcer symptoms, When you have a test like this for an agent that may or may not be a cause, is there a good reason to test?)