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Clinical Medicine 4 > Dr. Houston (GI)-Exam 1 > Flashcards

Dr. Houston (GI)-Exam 1 Flashcards

1
Q

Most of digestive tract follows a basic structural
plan with the digestive tract wall consisting of layers:
* What are the first two layers closest to the lumen+ what is contained in them?

A

Mucosa:
* Epithelum
* Lamina propria (connective tissue)
* Muscularis mucosae (smooth m. to give ridges for increase SA)

Submucosa: Have nerves and plexes here to regulate secretations

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2
Q

Most of digestive tract follows a basic structural
plan with the digestive tract wall consisting of layers:
* What is the third and forth layer closest to the lumen+ what is contained in them?

A

Muscularis externa (smooth muscle layers- 3RD ONE IN STOMACH WITH oblique muscle):
* Inner circular layer
* Outer longitudinal layer (propels and breaks down food)

Serosa:
* Areolar tissue: have reticular fiber + others fibers
* Mesothelium: slippery layer to decrease frictrion

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3
Q

What is the 2nd brain for GI?

A
  • Enteric nervous system: Myenteric plexus, submucosal plexus and parasympathetic ganglion of myenteric plexus
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4
Q
A
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5
Q

What is the mucus made up of?(3) What is its function?

A
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6
Q

why does the GI tract need to be highly vascularized?(2)

A
  • Delivers O2 and bicarbonate (need it to feed into the mucus)
  • Carries away acid that makes it into the LAMINA PROPRIA)

If we lose this then it will decrease the protective measures

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7
Q

Esophagus
* What epithelium is the mucosa made up of? What is it more susceptible to?

A
  • Startatified squamous epithelium
  • More susceptiable to acid damage because do not have muscal layer with muscus lining
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8
Q

Esophagus
* What does the LES allow?
* What is the resting pressure? Why
* What happens if there is decrease pressure?

A
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9
Q

Esophagus:
* What are the defense mechanisms

A
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10
Q

GERD
* Where does this occur?
* What is happening?
* how does this occur?

A

Where: Esophagus

What: Stomach acid refluxes back into esophagus

How: LES resting pressure 10-45 mmHg.
* If <10mmHg LES becomes looser, gastric acid reaches esophagus, pH damages tissue

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11
Q

What happens when reflux comes up?

A
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12
Q

BARRETT’S ESOPHAGUS
* Where does this happen?
* What does it cause?
* How does this occur?

A
  • Where: Esophagus
  • What: Abnormal change (metaplasia) in cells of lower portion of esophagus. Replacement of normal stratified squamous epithelium lining of esophagus by simple columnar epithelium
  • How: Repeat, chronic GERD
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13
Q

Barrett’s esophagus:
* Epithelium continuously what?
* Gradually replaced with what?
* Greater risk of what?

A
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14
Q

MALLORY-WEISS TEAR
* Where does this occur?
* What happens?
* How does this happen?

A
  • Where: Gastro-esophageal junction, near LES.
  • What: Gastro-esophageal laceration syndrome refers to bleeding from a laceration in the mucosa at the junction of the stomach and esophagus
  • How: It is most often caused by violent coughing or vomiting
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15
Q

Digestive enzymes and hydrochloric acid would get digested stomach and duodenal mucosa if not for what? (3)

A
  • the mucus coating the walls and bicarbonate ions secreted by the duodenum which neutralizes the acid.
  • the blood flowing to the stomach and duodenum brings in even more bicarbonate which helps neutralize the hydrochloric acid.
  • stomach and duodenum secrete small signalling molecules called prostaglandins. Prostaglandins **stimulate mucus **and bicarbonate secretion, vasodilate the nearby blood vessels allowing more blood to flow to the area, promote new epithelial cell growth, and also inhibit acid secretion.
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16
Q

Gastrin:
* stimulated what? (2)
* In the duodenum: what glands are there and what do they do?
* Stomach and duodenal mucosa would get digested if not for what?

A
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17
Q

Pepic ulcer disease:
* Where does this occur?
* What is happening?
* How does this happen?

A
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18
Q

H.pylori bacteria:
* Where does this occur?
* What is the gram stain?
* Colonizes where? What does it release?
* Starts where?

A
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19
Q

NSAIDS:
* Inhibits what?
* What does it cause?

A
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20
Q

H.pylori
* What are they? What do they release and why?

A

H. pylori are gram-negative bacteria that colonize the gastric mucosa and release adhesins that help them adhere to gastric foveolar cells as well as proteases that cause damage to mucosal cells.

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21
Q

H. pylori
* The majority of individuals with H. pylori don’t develop any problems, but sometimes it causes what?
* Over time, what happens?

A
  • The majority of individuals with H. pylori don’t develop any problems, but sometimes it causes a patchy pattern of damage that starts in the antrum, and then spreads to the rest of the stomach and eventually into the duodenum.
  • Over time the damage erodes deeper and deeper into the mucosa, eventually causing ulcers.
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22
Q

Another cause of gastric ulcers, and less so duodenal ulcers, are what?
* What do they inhibit?
* What do they reduce? What does that cause?

A
  • Another cause of gastric ulcers, and less so duodenal ulcers, are nonsteroidal anti-inflammatory drugs, like ibuprofen.
  • NSAIDs inhibit the enzyme cyclooxygenase which is involved in the synthesis of inflammatory prostaglandins.
  • Reducing the level of prostaglandins over a prolonged period of time, however, leaves the gastric mucosa susceptible to damage, and over time ulcers can begin to develop.
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23
Q
A
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24
Q

What are all the components of the liver

A

The image depicts the microscopic anatomy of a liver lobule, which is the functional unit of the liver. It shows how blood from the hepatic artery and portal vein flows through sinusoids (capillaries) in the liver, where it is filtered by hepatocytes (liver cells). The hepatocytes are arranged in plates and are responsible for metabolic functions and bile production. Bile produced by the hepatocytes is drained into bile canaliculi, which eventually lead to bile ducts. The diagram also highlights the perisinusoidal space (space of Disse), Kupffer cells (liver macrophages), and other structural components of the liver lobule.

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25
Q
  • Architectural arrangement of hepatocytes in the liver lobule enhances what?
  • How does bile move?
  • The sphincter of Oddi, located where? WHat does this do?
A
  • Architectural arrangement of hepatocytes in the liver lobule enhances the rapid exchange of material.
  • Bile originating in the bile canaliculus drains into a series of ducts that eventually join the pancreatic duct near where it enters the duodenum.
  • The sphincter of Oddi, located at the duodenal connection between the bile duct and the pancreatic duct, regulates drainage of bile and pancreatic juice into the duodenum.
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26
Q

HEPATITIS
* Where does this occur?
* What is happening?
* How is this happening?

A
  • Where: Liver hepatocytes
  • What: Liver inflammation – hepatocyte damage and death. As damage ↑ = ↑ serum [transaminases] in their blood will increase - ALT, AST. Jaundice. Hepatomegaly
  • How: Usually via a virus. Hepatocytes present abnormal proteins on their MHC class 1 = hepatocyte apoptosis by the cytotoxic T cells (Councilman Body).
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27
Q

What is happening with viral heptitis?

A
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28
Q

How does Hep a, b, c, d, e spread?

A
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29
Q

CIRRHOSIS
* Where does this occur?
* What is happening?

A

Where: Liver

What:
* Inflammation of the liver. scarred and damaged = fibrotic (cirrhosis) usually irreversible = “end-stage” or “late-stage” liver damage.
* Injured liver cells come together and form regenerative nodules = bumpy appearance.
* Also between nodules is fibrotic tissue and collagen.

30
Q

CIRRHOSIS
* Fibrosis process mediated by what? Where are they located? What is the normal and abonormal state?
* Hepatocytes injury causes what?

A
  • Fibrosis process mediated by stellate cells. Stellate cells sit in perisinusoidal space (between the sinusoid and hepatocyte). Normal state = would healing. Constant injury = constant fibrosis.
  • Hepatocytes injury causes secretion paracrine factors that “activates” and changes the stellate cells.
31
Q

Cirrhosis:
* When activated, the stellate cells lose what? What happens to them? What does that cause?
* As this fibrotic tissue builds up, it starts to what?

A
  • Hepatocytes injury causes secretion paracrine factors that “activates” and changes the stellate cells.
  • When activated, the stellate cells lose vitamin A, proliferate, and start secreting transforming growth factor beta1, or TGF-beta, which then causes them to produce collagen, which is the main ingredient in extracellular matrix, fibrosis, and scar tissue.
  • As this fibrotic tissue builds up, it starts to compress the central veins and sinusoids. Can lead to portal hypertension
32
Q

Pancreatic A+P
* What is the exocrine function? What cells?
* How does the pancrease protect itself?

A
33
Q

PANCREATIC A&P
* Normally, trypsinogen isn’t activated until when?
* But if trypsinogen and these zymogens become activated too early, then it can cause what?

A
  • Normally, trypsinogen isn’t activated until it is cleaved by protease enteropeptidase which is found in the duodenum.
  • But if trypsinogen and these zymogens become activated too early, then it can cause acute pancreatitis, and this might happen as a result of any injury to the acinar cells, or anything that prevents the normal secretion of the proenzymes into the duodenum.
34
Q
A
35
Q

Alcohol-induced Acute Pancreatitis
* Alcohol increases what? What does it decrease?
* What is the result of that?
* A blocked duct =
* At the cellular level, one consequence is what?

A
  • Alcohol increases zymogen secretion from acinar cells while decreasing fluid and bicarbonate production from the ductal epithelial cells.
  • As a result, the pancreatic juices becomes thick and viscous, potentially forming a plug that can block the duct.
  • A blocked duct = pancreatic juices start backing up, increasing the pressure, and leading to distention of the duct itself.
  • At the cellular level, one consequence is membrane trafficking becomes disrupted
36
Q

Alcohol-induced Acute Pancreatitis
* Zymogen granules might fuse with what? What does that cause?
* Trypsinogen might then be turned into what? What does that cause?
* Alcohol also contributes to pancreatitis in other ways like what?

A
  • Zymogen granules might fuse with lysosomes bringing trypsinogen into contact with lysosomal digestive enzymes.
  • Trypsinogen might then be turned into activated trypsin which begins the cascade of digestive enzyme activation and autodigestion of the pancreas — which is acute pancreatitis.
  • Alcohol also contributes to pancreatitis in other ways e.g. stimulating acinar cells to release inflammatory cytokines which attracts a strong immune reaction.
37
Q

Gall stone-induced Acute Pancreatitis
* What happens with the gallstone

A

With gallstones what happens is that they sometimes get lodged at the sphincter of Oddi which blocks the release of pancreatic juices, similar to the alcohol-induced protein plug.

38
Q

Chronic pancreatitis:
* When does this happen?
* What decreases?
* What does it lead to?

A
39
Q
A

Stellate

40
Q
A

Hepatitis

41
Q
A

Chronic pancreatitis

42
Q

What are the two subgroups of IBD? (where does this occur and why does it occur?)

A
43
Q

What is the difference in depth of UC and Crohn’s disease?

A
44
Q

CROHN(’S) DISEASE
* Where does this occur?
* What is happening?
* How is this happening?

A
  • Where: Anywhere along GI tract – most commonly ilium and colon
  • What: Type of IBD. Immune-related – triggered by a pathogen
  • How: Dysfunctional immune response – genetics predisposition
45
Q

UC
* Where is this happening?
* What is happening?

A
46
Q

UC
* It is what in origin? What is secondary?
* Combination of what?
* What is happening?
* Pattern for ulceration seems to be what?

A
47
Q

UC
* Affects what?
* What is the difference between flare and remission?
* What is the autoimmune aspect?

A
48
Q

Celiac disease/sprue
* Where?
* What is happening?

A

Where: Small intestine

What:
* immune system-mediated disorder where 33 amino acid peptide component of gluten called gliadin in food triggers the body’s immune cells to attack the cells in the small intestine.
* Gluten’s found in wheats and grains

49
Q

CELIAC DISEASE/SPRUE-HOW
* Gliadin in small intestine binds to what? What does that cause?
* Then phagocytosed by who and what happens?
* Finally, the helper T cells also recruit what?

A
  • Gliadin in small intestine binds to IgA in the mucosal membrane. gliadin-IgA complex, for some reason, binds to a transferrin receptor, TfR, (which is usually used to help absorb iron and seems to be over-expressed in patients with Celiac disease) and trancytosed across the intestinal lining.
  • Then phagocytosed by macrophages and presented to T helper cells which release inflammatory cytokines, molecules that initiate inflammation e.g. IFNγ, TNF. Furthermore, helper T cell stimulates B cells to produce more IgA antibodies against the gliadin.
  • Finally, the helper T cells also recruit killer CD8+ T cells, destroy intestinal lining epithelial cells.
50
Q

ACUTE MESSENTERIC ISCHEMIA (SMALL BOWEL INFARCTION)
* Where does this happen?
* What is happening?
* How is this happening/

A
  • Where: Small intestine
  • What: Ischemia leading to necrosis via thombus, tumor, twisted (occlusive) or via decrease blood flow (nonocclusive)
  • How: Ischemia-reperfusion injury
51
Q
A
52
Q

ACUTE MESSENTERIC ISCHEMIA (SMALL BOWEL INFARCTION)
* Upon reperfusion, what happens?
* Cytokines cause what?
* just mucosal layer =
* all layers=

A
53
Q

TOXIC MEGA COLON
* Where does this occur?
* What is happening?

A

Where: Large Intestine

What:
* Acute toxic colitis with dilatation of the colon (mega colon).
* Dilatation can be either total or segmental. Toxic colitis = patients develop toxicity without megacolon.
* From IBD or pathogenic infection.
* Colon is unable to remove gas or feces - large intestine may eventually rupture.

54
Q

TOXIC MEGA COLON
* What is the hallmark?
* Nitric oxide generated by inflammatory (neutrophils and macrophages) in the inflamed portions of the colon causes what?
* Neutrophils also invade and do what?

A
  • Hallmark is inflammation extending beyond the mucosa into the smooth-muscle layers and serosa, thus paralyzing the colonic smooth muscle and leading to dilatation.
  • Nitric oxide generated by inflammatory (neutrophils and macrophages) in the inflamed portions of the colon,inhibiting smooth-muscle tone and leading to colonic dilatation
  • Neutrophils also invade and damage muscle cells by the release of proteolytic enzymes, cytokines, and leukotriene B4.
55
Q

TOXIC MEGA COLON-HOW
* Systemic uptake of cytokines and other inflammatory mediators leads what?
* What does no contribute?
* What disease is a type of TMC?

A
  • Systemic uptake of cytokines and other inflammatory mediators leads to fever, tachcardia, hypotension, and other signs of systemic toxicity.
  • Myenteric plexus involvement likely does not contribute to colonic dilatation.
  • Hirschsprung disease is a type of TMC in which a ganglion, or cluster of nerves is missing from birth, which ultimately leads to a blocked colon, causing it to enlarge.
56
Q

IRRITABLE BOWEL SYNDROME (IBS)
* Where?
* What is happening?

A

Where: Anywhere along GI tract – most commonly ilium and colon

What:
* Functional disorder. Recurrent abdominal pain leading to abnormal bowel motility (constipation and/or diarrhea).
* Different from IBD – IBS shows no inflammation, ulcers, or other damage to bowel

57
Q

IRRITABLE BOWEL SYNDROME (IBS)- HOW
* Underlying pathophysiology not what?
* What can often trigger sxs?
* What do solutes do?
* Excess water can also cause what?
* Short-chain carbohydrates are often what?

A
  • Underlying pathophysiology not fully understood. Visceral hypersensitivity.
  • Short chain carbohydrates (e.g. fructose) often trigger symptoms.
  • Solutes draw water across the gastrointestinal wall and into the lumen.
  • Excess water can also cause smooth muscle lining the intestines to spasm, and create diarrhea if the excess water’s not reabsorbed back into the body.
  • Short-chain carbohydrates are often metabolized by gastrointestinal bacterial flora which produce gas that could trigger more bloating, spasm, or pain.
58
Q

APPENDICITIS
* What is going on?
* What are the causes?
* What are the sxs?

A
  • Inflamed appendix.
  • Causes: Fecalith, undigested seeds, pinworm infection, lymphoid hyperplasia
  • Sxs: Pain. McBurney’s point. Fever
59
Q

APPENDICITIS-HOW
* Appendix always secreting mucus and fluids from its mucosa to do what?
* increase size =
* Also, gut bacteria now trapped & free to multiply =

A
  • Appendix always secreting mucus and fluids from its mucosa to keep pathogens from entering the bloodstream and also to keep the tissue moist - even when it’s plugged
  • increase size = increased pressure in the appendix = physically pushes on the afferent visceral nerve fibers = abdominal pain.
  • Also, gut bacteria now trapped & free to multiply = immune system to recruit white blood cells and pus starts to accumulate in the appendix.
60
Q

APPENDICITIS-HOW
* If obstruction persists can cause what?
* As more cells die, the appendiceal walls become what?

A
  • If obstruction persists can compresses small blood vessels that supply the appendix cell wall = ischemic and cell death = decreased mucus & increased bacteria.
  • As more cells die, the appendiceal walls become weaker = appendix may rupture = can allow the bacteria to escape the appendix and get into the peritoneum = periappendiceal abscess.
61
Q
A
62
Q
A
63
Q
A
64
Q
A
65
Q

CONSTIPATION (costiveness or dyschezia)
* Refers to what?
* What are the primary and secondary causes?

A
  • Refers to bowel movements that are infrequent or hard to pass.
  • Primary causes are intrinsic problems of colonic or anorectal function, whereas secondary causes are related to organic disease, systemic disease or medications.
66
Q
A
67
Q
A

E. IBS

68
Q
A

Hep C

69
Q
A

Large intestine only; autoimmune; submucosa

70
Q
A

Inflammatory diarrhea

Clinical Medicine 4 (15 decks)

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