GI

Question 1

What are some clinical manifestations of GI illnesses?

Answer 1

• anorexia- decrease in appetite
• nausea
• vomiting (emesis)
  
  • comes from part of brain called vomition center
  • this area coordinates everything responsible for emesis reflex
  • many things trigger vomition center
    
    • ​chemoreceptor trigger zone- by ventricle and has access to CSF and blood
    • cerebral cortex also attached to vomition center- certain situations can cause vomiting
• hematemeis- bloody vomit
• melena- blood in stool
  
  • tarry
  • occult= hidden

Question 2

What is diarrhea?

Answer 2

• passage of more than 200g per day of feces
• depends on origin
• osmotic vs secretory
  
  • osmotic- caused by things in stool that hangs onto water
  • secretory- cholera
• inflammatory vs noninflammatory
  
  • inflammatory- associated with WBC
  • noninflammatory- IBS

Question 3

What is constipation?

Answer 3

• infrequent passage of stool
• could be a primary problem or as a problem associated with another disease condition
• causes
  
  • failure to respond to urge to defecate
  • inadequate dietary fiber
  • inadequate fluid intake
  • weakness of abdominal muscles
  • inactivity

Question 4

Why do we need the lower esophageal sphincter?

What makes up the lower esophageal sphincter?

Answer 4

• Regulates the flow of food from the esophagus into the stomach
• Intragastric pressure is higher in stomach (5mmHg) than the esophages (0 mmHg)
  
  • so, contents will want to go into esophagus
• different cell types in stomach vs esophagus
• gastric distention and high fat meals increase relaxation
• vagus n innervates LES, GI tract up to a point, but we don’t know the exact NT involved (it’s not Ach)

what makes the lower esophageal sphincter?

• muscles within wall of esophagus
  
  • internal-circular muscles of the distal esophagus
• stricture of the diaphragm also keeps esophageal sphincter closed
  
  • external- portion of the diaphragm
• oblique muscles of the stomach

Question 5

What is purpose of upper esophageal sphincter?

Answer 5

prevent air from going into stomach

Question 6

What does manogram of esophagus look like?

Answer 6

• wavelike constriction down tube of esophagus
• when at sphincters, completely different
  
  • upper- constricted at baseline
    
    • when swallowing, sphincter relaxes (all the way to 0), allows food to pass and then closes
  • lower- constricted at baseline
    
    • relaxes when swallowing
• pressure in stomach around 5, which is why we need the spincter

Question 7

How does the lower esophageal sphincter work? relax?

Answer 7

• LES normal state is constricted (tonically constricted)
  
  • nervous innervation tells it to relax when swallowing
    
    • we don’t know exactly what causes this relaxation (unsure if NT involved)
      
      • we know it’s not Ach, NE or Epi
      • some intermediary NT that is involved that we don’t know about

Question 8

How does upper esophageal sphincter work?

Answer 8

• made up of horshoe shaped muscles
  
  • several muscles
• cricopharyngeal muscle<– need to know this one
  
  • muscle is constricted at baseline via innervation to the muscle
    
    • when constricted, pushes esophagus against trachea, and smush esophagus so nothing can get through
  • when it’s time to swallow, innervation stops, constriction stops, muscle relaxes, opens up, and allows food to pass
  • Whitney said this muscle is “tonically relaxed” in class, could mean that WITHOUT innervation to the muscle, the muscle is relaxed normally. There is constant innervation to the cricopharyngeal muscle causing constriction

Question 9

How are LES and UES different?

Answer 9

UES opposite from LES. (only in regards to the INNERVATION and what the innervation makes the muscle do! both are always constricted at baseline)

• LES is tonically constricted. Innervation makes LES relax.
• The UES is tonically relaxed, innervation tells it to constrict, once innervation stops, then it opens up (relaxes again) and allows food to pass.

Question 10

What is dysphagia?

Answer 10

difficulty swallowing

2 causes:

• oropharyngeal dysphagia- pain in mouth/throat when swallowing
  
  • or, maybe with Whitney’s change in definition, from goolge- difficulty initiating a swallowing reflex
• esophageal dysphagia- variety of causes including ulcers, reflux, cancers, pathogens can cause esophagus to be inflamted
  
  • google:
    
    • Esophageal dysphagia is a form of dysphagia where the underlying cause arises from the body of the esophagus, lower esophageal sphincter, or cardia of the stomach, usually due to mechanical causes or motility problems

Question 11

What is odnyphagia?

Answer 11

• painful swallowing

Question 12

What is pyrosis?

Answer 12

heartburn

Question 13

What is prominent cricopharyngeus?

Answer 13

• the cricopharyngeal muscle never wants to relax, always constricted
• this causes food to back up, eventually causing a dilation of the esophagus

Question 14

What is achalasia?

Answer 14

• Altered peristalsis- not wave, all constricting together
• LES fails to open up during swallowing
• resting LES highly constricted at baseline

eventaully, the food will continuously get stuck and dilation can occur (megaesophagus)

Question 15

What is treatment for achalasia?

Answer 15

give muscle relaxant

sx can also cut LES and allow it to be open

Question 16

What are some causes of GERD?

Answer 16

• Incompetent LES
• Delayed gastric emptying
• acid hypersecretion
• decreased salivation
  
  • salivation normally washes reflux out of esophagus and back into staomch
  • less saliva= less washout= more irritation

Question 17

What are some reasons for an incompetent LES?

Answer 17

physiological

• Weak basal LES pressure
• Inadequate LES response to increased abomdinal pressure
  
  • LES should constrict with increased abd pressure (coughing, defecation, situps, all increase abd pressure)
• inadequate LES response to gastric constractions
• transient relaxation of the LES
  
  • most common reason
  • this transient relaxation has nothing to do with swallowing
• anatomical*
• hiatal hernia

Question 18

What is pathophys behind dysfunctional anti-reflux barrier?

Answer 18

Question 19

What are GERD symptoms?

Answer 19

• reflux involves mucosal injury to the esophagus, hyperemia, and inflmmation
  
  • chronic inflammation can lead to cancer
• heartburn
  
  • 30-60 min after eating
  • made worse by bending at the waist
  • most often occurs at night
    
    • hormones may play a role
• belching and chest pain
• respiratory symptoms- wheezing, chronic cough, and hoarseness
  
  • refluex comes up esophagus and goes into larynx/tranchea cause wheezing/cough

Question 20

What is chronic GERD?

Answer 20

• Persisten reflux- cycle of mucosal damage that causes hyperemia, edema, and erosion of the luminal surface
• strictures
• barrett’s esophagus
  
  • normal squamous mucosa-metaplastic columnar mucosa
    
    • more suited for evironment of erosion, but increased r/f cancer
• increased risk for cancer

Question 21

Treatment for GERD?

Answer 21

• Conservative measures first
• avoidance of positions and conditions that increase GERD
  
  • avoid large meals and foods that reduce LES tone
    
    • caffeine, fats, choclate
  • smoking and alcohol
  • meals eatne sitting up
  • avoid bending for long periods of time
  • weight loss
• aggressive treatment
  
  • block gastric acid secretion
  • drugs that increase motility

Question 22

What is the gastric mucosal barrier?

Answer 22

• most of the times diseases that affect stomach will affect gastric mucosal barrier
• acids are important for the indiscriminate digestion of food
• mucosa- water repellent hydrophobic layer
• bicarb- trapped in the mucus gell
• restitution- how quickly cell turnover
  
  • ​turnovers every couple of days in stomach
• High gastric blood flow
  
  • ​if any acid gets through mucosa, gets rid of the acid as soon as possible

Question 23

What is gastritis?

Answer 23

• damage to the gatric mucosa with acute inflammation, necrosis and hemorrhage
  
  • damaging factors overwhelm the protective factors of the stomach
  • any injury (h pylori, nsaids, tobacco, alcohol, gastric hyperacidity, duodenal-gastric reflex, ischemia, shock) can overwhlem protective and then we get ulcerations and autodigestion of walls of stomach
• acute gastritis
• chronic gastritis
  
  • autoimmune gastritis
  • multifocal atrophic gastritis
  • chemical gastropathy
  • helicobacter pylori gastritis

Question 24

How do NSAIDs cause damage to stomach?

Answer 24

• decrease prostaglandin, (normally prostaglandin initiates pain response and allows vasodilation)
• block prostaglandin, stop vasodilation, and pain
• stop high gastric blood flow to walls, so we loose high gastric blood flow, acid gets into stomach through mucosal layer
• acid getting through mucosal layer but there’s no high gastric blood flow washing acid away. decreased defenses so therefore more prone to ulcerations

Question 25

What is H pylori gastritis?

Answer 25

• H. pyrlori was culture and characterized in 1983
• has flagella- allows the basteria to be mobile in mucus
• has urease- generates ammonia from urea (elevates pH)
  
  • affects protective barriers
• adhesins- enhance bacterial adherence to foveolar cells
  
  • special proteins on surface that allows bacteria to adhere directly to wall and not be washed away
• toxins- may be involed in disease progression (CagA)

Question 26

What is peptic ulcer disease?

Answer 26

• Group of ulcerative d/o that occur in the upper GI tract
  
  • caused by combo of acid and pepcin. both cause damage individually, but these two combine will greatly increase amount of damage
  • when they breakdown the mucosa, we get ulceration, bleeding, very painful
• exposes submucosal layer ot gastric contents
  
  • autodigestion
    
    • exposes acid to cells underneath mucosal layer
• most common
  
  • h. pylori
  • increased acid
    
    • most people whotake a lot of nsaids or have h pylori also have increase in amount of acid that they release or decrease in bicarb they release, causing further damage
  • decreased bicarb

Question 27

What are duodenal ulcer?

Answer 27

• seen in a wide variety of patients, pain between meals and in the early morning
  
  • anyone, less likely to be elderly (elderly more likely to be gastric)
  • more common
• most often occurs in the bulb
• Hpylori infection (#1 cause)
  
  • toxins and enzymes that promote inflammation and ulceration
• hypersecretion of stomach acid and pepsin
• use of NSAIDS (#2 cause)
  
  • ​PGs: mucosal blood flow/secretion HCO3
• High gastrin levels
• acid production by cigarette smoking

Question 28

What are gastric ulcers?

Answer 28

• Tend to develop in the antral region, adjacent to the acid-secreting mucosa of the body
• seen most in the elderly, pain not associated with eating
• clinical manifesations
  
  • like duodenal except pain can be immeidately after eating
  • tend to be chronic
  • increase anorexia, vomiting and weight loss

Question 29

What are stress ulcers?

Answer 29

• An acute peptic ulcer related to severe illness, neural injury, or systemic trauma (not due to stress)
• multiple sites
• ischemic ulcers
  
  • within hours of event (hemorrhag,e heart failure, severe burns- curling ulcer)
• Cushing ulcers
  
  • develop as a result of head trauma/brain surgery
  • decreased mucosal blood flow
  • overstimulation of vagal nuclei (hypersecretion of acid)
    
    • overwhelms protective areas

Question 30

Cancer of the stomach?

Answer 30

• relatively uncommon tumor, accounts for 3% malignancies
• most common fatal cancer in US
• Genetic predisposition
• more common in men and Type A blood
• Carcinogenic factors (N-nitroso compounds and benzoprene)
  
  • ash and burn particles
• infection with H pylori appears to serve as a co-factor
• usually asymptommatic until late in their course
• symptoms are vague- indigestion, anorexia, weight loss, vague pain, and vomiting

Question 31

What is point of small intestine?

What is absorbed in duodenum, jejunum, and ileum?

Answer 31

absorption

enormous surface are which assist in efficient absorption

Duodenum

• iron
• calcium
• folic acid

Jejunum

• carbs
• proteins
• fats

Ileum

• bile salts
• B12

Question 32

What is irritable bowel syndrome?

Answer 32

• Functional gastrointestinal disorder characterized by abdominal pain and constipation with or without mucous discharge and episodic diarrha
• believed to be the result from dysregulation of intestinal motor and sensory function modulated by CNS
  
  • Cause increase and decrease in motility depending on day/moment
• increased motility and abnormal intestinal contraction in response to psychological and physiologic stress
• disease of exclusion
  
  • ​non inflammtory- no WBC found in feces!

Question 33

Clinical featurse of irritable bowel synrome

Answer 33

• Abdominal pain relieved by defecation
• altered frequency of bowel movement
• sensation of incomplete evacuation
• passage of mucus upon defecation
• abnormal myoelectric and motor activities in the GI tract

Treatment

• antidepressants

Question 34

What is inflamamtory bowel disease?

Answer 34

• either crohn’s disease or ulcerative colities
• commonalities
• inflammation of the bowel- on endoscopy
• lack of confirming evidence of a proven causative agent
• pattern of familial occurrence
• accompanied by systemic manifestation

Question 35

Causes of inflammatory bowel disease?

Answer 35

• hereditary predispositon
• epithelial defects
  
  • defects in intestinal epithelial tight junciton barrier
• microbiota
• theory of environmental trigger- take something in that causes us to make antibodies
• ​or ​get virus- antibody looks a lot like own cell, start attacking self

Question 36

Systemic manifestation of inflammatory bowel disease?

Answer 36

• arthritis (spine, SI joint, large joints of arms/legs)
• inflammatory condition of the eye
  
  • blood shot eyes
• skin lesions- erythema nodosum
  
  • bruises associated with inflammation within wall of blood vessel
• hypercoagulability of the blood
• stomatitis- kanker sores
• autoimmune anemia

Question 37

What is crohn’s disease?

Answer 37

• can affect any area from mouth to the anus
• recurrent granulomatous type of inflammatory response
• progressive, relentless and disabling
• hallmark-sharply demarcated granulomatous lesions that are surrounded by normal appearing mucosal tissue
• skip lesions- patches of inflammation
• all layer of bowel involved (submucosal most involved)
• ulcerations can produce longitudinal and transverse inflammatory fissures that extend into lymphatics
  
  • can lead to small amount of blood in feces

Question 38

Clinical course of crohn’s disease?

Answer 38

• Often variable: periods of exacerbaiton and remission
• symptoms are often related to the location of the lesions (nutritional deficiencies)
• diarrhea (small amounts of blood)
• colicky pain
• weight loss
• fluid and electrolyte disorder
• malaise

Question 39

What is ulcerative colitis?

Answer 39

• Nonspecific inflammatory condition confined to the rectum and colon
• affects primarily the mucosal layer (unlike crohn’s)
• affected site tends to be continuous
• leads to the formation of pinpoint mucosal hemorrhages, which can become necrotic and ulcerate
• as a result of the inflammatory process, the mucosal layer develops tongue-like projections that resemble polyps

Question 40

Symptoms of ulcerative colities?

Answer 40

• Diarrhea
  
  • because mucosal layer is involved, the stool typically contain blood and mucus
  • lots of blood and diarrhea
• mild abdominal cramping
• anorexia
• weakenss

Question 41

Treatment ulcerative colities?

Answer 41

immunosuppressant

steroids

broad spectrum antibiotics

surgery

Question 42

Differences in crohn’s vs ulcerative colities?

Answer 42

Question 43

What is appendicitis?

Answer 43

• Appendix becomes inflammaed, swollen and gangrenous, and it eventually perforates if not treated
• thought to be related to intraluminal obstruciton with a fecalith (hard piece of stool) or twisting
• occlusion of lumen–> continued mucosal secreiton–> increased intraluminal pressure–> limit venous blood flow–> hypoxia–> mucosa ulcerates–> bacteria invation–> futher increase in intraluminal pressure–> artieral ciruclation become thrombosed–> gangrene and perforation
• appendix
  
  • long thin tube coming off of cecum

Question 44

What is diverticular disease?

Answer 44

• herniations/outpouchings of mucosa thorugh the muscle layers of the colon wall, especially the sigmoid colon

Question 45

What is diverticulum?

Answer 45

presence of one or more herniations

Question 46

What is diverticulosis?

Answer 46

presence of multiple diverticulum

• neither diverticulosis or diverticulum means that you will have any symptoms
• common to have either when olrder
  
  • ​have clinical implications when one of herniations perforate and then you get symptoms and called diverticulitis

Question 47

Diverticulitis?

Answer 47

clinical symptoms of diverticulosis

Question 48

What is diverticulum disease?

Answer 48

problems with diverticulitis

Question 49

Patho of diverticulosis?

Answer 49

• with age, within areas of sigmoid colon, pressure increases in lumen
• walls and circular muscle gets thinner with age
• part of mucosa can herniate into pockets b/w muscle
• dangerous because where herniation is, wall will be very thing, blood vessel close to wall
  
  • easy for vessel to break through wall, get bleeding
  • leak chyme into peritoneum. infection big problem

Question 50

Prevalence of diverticulum disease?

Answer 50

• common in western society
• almost non-existent in many african nations and underdeveloped countries
• suggest dietary factors
• decrease in physical activity
• effects of aging

Question 51

Why is diverticulum disease more common in the sigmoid colon?

Answer 51

• Because it has the narrowest lumen, intraluminal pressure is the highest there
  
  • (law of laplace T= P xR)

Question 52

What is diverticulitis?

Answer 52

complication of diverticulosis

inflammation and gross or microscopic perforation of the diverticulum

usually caused by a fecalith (piece of stool getting stuck)

Question 53

What is malabsorption syndrome?

Answer 53

• contesllation of symptoms arising from multiple causes
• persons with conditions that diffusely affect he small intestine and reduce its absorptive functions share certain common features
• celiac sprue, crohn’s and bowel resection

Question 54

What are symptoms of malabsortpion syndrome?

Answer 54

• diarrhea
• steatorrha
• flatulence- bacteria in tract producing CO2. if not absorbing the products, they stay in GI tract longer and bacteria have more fuel to make more gas
• bloating
• abdominal pain, cramp and abdominal distention
• weakenss, muscle wasting, weight loss
• easy bruising and bleeding- not absorbing iron/vit K that we need
• bone pain- from inability to absorb Ca

Question 55

What is celiac sprue?

Answer 55

• Rare chronic disease in which there is a characteristic mucosal lesion of the small intestine
• imapris nutrient absorption
• improves when gluten is removed from the diet
• believed to be immunologic response to gluten
• loss of absorptive villi
  
  • lose SA and absorptive properties in small intestine

Question 56

What is gluten and how is it normally digested in the body?

Answer 56

• Gluten is a protein in husk of wheat
• When we absorb gluten, we breka it down into gliadin
• Gliadin is able to be absorbed. When it gets into epithelial cells and mucosa, patients with celiac disease react to gliadin
• Any cell with gliadin will be recognized as foreign, and antibodies start to attack
• Not a real autoimmune disease- just autoimmune like since it’s something generally present at high levels in the body
• Difference between other disease is that the microvilli can be regrown as long as patient avoids celiac.

Question 57

How does exocrine portion of pancreas work?

Answer 57

• Digestive enzymes ( chymotrypsin, pancreatic amylase, lipases, carboxypolypetidase, ribonuclease etc) are relased as enzymes
  
  • activated by trypsin in duodenum
• typsin inhibitors released from acinar cells to make sure nothign is activated while inside the pancreas

Question 58

What is acute pancreatitis?

Answer 58

• Escape of activated pancreatic enzymes into the pancreas and surrounding tissues
• two main causes
  
  • gall stones
  • alcohol
• both activate trypsin within acinar cells
• symptoms: pain, nausea, vomting
• can be very painful, present with extreme abdominal pain with n/v

Question 59

How does alcohol cause chronic pancreatiits?

Answer 59

• more pancretic enzymes, less inhibitors, causing autodigestion
  
  • also can cause protein plugs which cause duct obstruction

Question 60

What is chronic pancreatiits?

Answer 60

• usually manifests itself in episodes that are similar to those of acute pancreatitis
• persistent recurring episodes of pain
• often precepitated by alcohol abuse or overeating
• anorexia, nausea, vomiting, constipation, and flatulence are common
  
  • not brekaing down food, food remains solid and not absorbed
  • larger pieces of food are not associated with a lot of water and lead to constipation
• as the disease progresses- diabetes mellitus and malabsorption
  
  • start to lead to endocrine dysfunction