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Patho > Q4 - GI > Flashcards

Q4 - GI Flashcards

1
Q

90% of water absorbed in?
Vit B12 + bile?
Most alcohol?
Acids bases and left over Na/K?

A

Small intestine (jejunum)
Ileum
Jejunum
Colon

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2
Q

Roles of the appendix

A

Monitor for foreign microbes that remain after the small intestine

Helps maturation Bcells and IgA antibodies early in life (MALT tissue)

Storehouse for healthy bacteria.

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3
Q

For people who are lactose intolerant, why do they have so much gas?

A

Lactose is 2 sugars bound together. Normally, an enzyme breaks them apart to be absorbed, but if this enzyme is not present, then the gut bacteria can feed on the unbroken lactose molecules and create gas.

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4
Q

How is Fructose intolerance linked to depression?

A

Fructose is broken down into tryptophan which is needed to make serotonin in the gut. Lack of serotonin can lead to depression.

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5
Q

What serologic test results indicate presence of celiac disease?

A

EMA and TTG

Emma has celiac disease… she drips poop :(

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6
Q

How does an atypical presentation of celiac disease differ from a classic presentation?

A

Classic: Diarrhea, abdominal discomfort, weight loss
Atypical: iron deficiency anemia, osteoporosis, elevated liver enzymes, weight loss, neurologic signs, dermatitis herpetiformis, and unexplained infertility

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7
Q

What is colonic diverticulosis associated with?

A

Diet low in fiber.

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8
Q

True diverticula include ______ layers of the bowel.

A

ALL

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9
Q

Criteria for Dx of functional constipation?

A

2 or more of following for at least 3 months:
Straining
Bristol 1-2 stools
Sensation of incomplete evacuation
Sensation of blockage
Manual maneuvers to assist
<3 BM/week
Loose stools rarely present

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10
Q

Primary causes of functional constipation?

A

Most common is Normal Transit + for abd px and bloating
Functional defication disorder
Slow Transit Constipation.

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11
Q

Main difference between functional constipation and IBS-C?

A

IBS-C = abd pain/discomfort
Functional C = bloating.

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12
Q

IBS is a dysregulation of _____ involving _____ and ______

A

The nervous system
Motor (motility - fast AND slow)
Sensory (HYPERsensitivity)

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13
Q

What is a hallmark sign of IBS?

A

Symptom free intervals.

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14
Q

Patient presents with mostly constipation and a few intermittent episodes of diarrhea. He has abdominal discomfort and bloating. Pain is crappy during the day but not at night. He also has HA and back pain. He does have times where he goes a few days or weeks without symptoms. Does he most likely have IBS or functional constipation?

A

IBS-C.
Functional constipation does not have loose stools, no abd discomfort (only bloating). Usually no other associated symptoms, and no symptoms free intervals.

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15
Q

What are alarm signs of Dyspepsia?

A

Weight loss, bleeding, anemia, vomiting, dysphagia and age >55

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16
Q

Difference between osmotic diarrhea, secretory and exudative diarrhea?

A

Osmotic - large amounts of poorly absorbed solutes cause water and Na to influx into the bowel lumen. Caused by MALABSORPTION. More common in chronic diarrheas
Secretory - large volume = enterotoxins produced by organisms
Small volume = IBD
Exudative - mucus, blood and protein from sites of active inflammation. Chrons and UC.

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17
Q

Most common organisms that cause infectious diarrhea?

A

Rotavirus, norovirus, ecoli, salmonella, c diff and giardia.

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18
Q

Gut contains MALT - mucosal associated lymphoid tissue.

A
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19
Q

What is the #1 type of good gut bacteria?

A

Bacteriodes.

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20
Q

When does the pain of a duodenal ulcer usually happen vs a gastric ulcer?

A

Duodenal ulcer pain is typically 2-3hrs after a meal and is relieved by eating more food.
Gastric ulcers have most pain on an empty stomach or soon after a meal.

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21
Q

T/F: Inflammatory diet is a risk factor for developing a peptic ulcer.

A

False
Biggest cause is H Pylori

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22
Q

How does HPylori survive in stomach pH?

A

Produces urease, which breaks down urea in gastric juice to produce ammonia which protects it from the stomach acidity.

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23
Q

Prostaglandins are _____ for the stomach. They do all these things________. _____ -inhibitors can cause a decrease in prostaglandins. This is how NSAIDS contribute to Peptic ulcer formation.

A

Protective
Increase mucous layer thickness
Decrease pH gradient,
Increase bicarb secretion
Increase mucosal blood flow
COX (COX pathway produces prostaglandins)

24
Q

Appendectomy may ____ the risk of getting UC. What is the MOST protective factor against developing UC? Most contributory factor to developing CD?

A

Reduce.
Smoking
smoking.

25
Q

Does CD or UC have more genetic contribution to disease development?

A

CD.

26
Q

CD or UC?
Transmural inflammation
Common Fistulas and strictures
Mouth to anus
Cobblestone ulceration pattern

A

CD

27
Q

CD or UC?
Limited to colon
Mucosal layer only
Seldom strictures and fistulas
Increased risk for colon Ca

A

UC

28
Q

Classify this level of severity for UC?
>=4 stools/day but minimal signs of toxicity

A

Moderate.
Mild is <4 stools/day, normal ESR and no s/s of Tox.

29
Q

Patho of UC

A

Decreased secretion of mucin which is an anti microbial and surface protectant of the colon. Without it, mucosa becomes more permeable and more passage of pathogens and antigens trigger the immune system reaction. T-cells become activated and produce cytokines/chemokines including TNF-alpha, IL-23 and IL12, oxygen free radicals and all potentiate the damage to the intestinal epithelium.
VASCULAR adhesion molecules (integrins) cause more lymphocytes to come into the gut and potentiate the inflammatory response.

30
Q

Patho of CD

A

Sometimes difficult to distinguish from UC pathologically other than the inflammation is transmural instead of only the mucosal layer like UC.
Immune response against intestinal bacteria, activation of integrins (adhesion molecules) and hyperactivity of T-Cells (IL12, 23 and 34) which activate cytotoxic enzymes that cause tissue damage.

31
Q

IBD vs IBS

A

IBD = chrons/UC
- inflammation on endoscopy
- abd pain, anemia, increased platelets, ESR and low albumin
- fever, bloody stools
- Fecal WBC and occult blood
IBS = syndrome (C, D or M)
- no tissue abnormality
- change in bowel habits
- no blood, no systemic lab issues, no fever, no WBC/occult blood.
- abd discomfort relieved with BM.

32
Q

What is cholecystokinin?

A

A hormone in mucosa of duodenum that stimulates contraction of the gallbladder.

33
Q

Why do gallstones urgently need to be removed?

A

Because the pressure of gallstones in the gallbladder or in the CBD can press up against the walls and decrease blood flow causing ischemia, necrosis and perforation.

34
Q

What is Suppurative Cholangitis

A

Surgical emergency because patients rapidly develop septic shock from their diseased bile ducts. Autoimmune attack (primary) or due to bile duct obstruction (secondary)

35
Q

Why do stones form in the gall bladder?

A

Issues with metabolism of cholesterol, bilirubin and BA and hypomotility of the gallbladder.

36
Q

What are the most common type of gallstones?
Other types?

A

Cholesterol,
Calcium
And pigmented

37
Q

When you have tenderness over the RUQ (Gallbladder) especially on deep inspiration what is that called?

A

Murphy’s sign.

38
Q

What would an elevated GGT or ALKphos indicate?

A

A duct blockage in the liver
These tests Hepatic excretory fxn

39
Q

What non invasive test can you do for elevated bilirubin before jaundice shows up?

A

Urine bili dipstick.

40
Q

What is jaundice?

A

An increase in the amount of UNconjugated bilirubin

41
Q

Some causes of Prehepatic jaundice?

A

Increased destruction of RBCs
SCD
Hemolytic anemia

42
Q

Causes of intra hepatic jaundice?

A

Decreased bili uptake by liver
Decreased conjugation of bili
Hepatocellular liver damage (hepatitis, cirrhosis, carcinoma)
Drug-induced cholestasis.

43
Q

Examples of posthepatic jaundice

A

Obstruction of bile flow
Gallstone
Tumor

44
Q

Decrease pumping ability of the ____ side of the heart can cause back up and portal HTN

A

Right side.

45
Q

What is usually the first clinical sign of portal HTN?

A

Ruptured esophageal varices.

46
Q

Ammonia is usually converted to ____ by the ______ and then excreted through urine. With a diseased liver, this is not possible, and the ammonia reaches the brain where it is converted into _______ which alters cerebral blood flow and interferes with NTs, causing edema and oxidation.

A

Urea
Liver
Glutamine

47
Q

How does fibrosis happen?

A

Inflammatory mediators activate stellate cells which trans differentiate into fibrogenic myofibroblasts and promote fibrotic processes. The fibrotic tissue is not able to participate in it’s normal function and can block things.

48
Q

What toxin is involved in alchoholic cirrhosis?

A

Acetaldehyde.

49
Q

What is the leading cause of acute obstructive pancreatitis?

A

Gallstones.

50
Q

What are some causes of acute pancreatitis other than obstruction?

A

Alcohol, viral infx or drugs

51
Q

What is the proposed primary mechanism of cell injury in acute pancreatitis? How does this damage the cells?

A

Calcium overload due to ethanol metabolites.
When intracellular Ca is too high, it causes inappropriate intracellular trypsin activation, impaired fluid and HCO3-secretion in ductal cells, and initiation of the nuclear factor pro-inflammatory pathway and cell necrosis. This then triggers inflammatory response.
Trypsin causes autodigestion

52
Q

What are HSPs and what do they do? How are they involved in pancreatitis?

A

Heat shock proteins
Cytoprotective by stabilizing protein folding, antioxidative and anti inflammatory. They downregulate Trypsinogen and nuclear factor pathway

BA and alcohol metabolites suppress HSP fxn and allowing the patho of acute pancreatitis.

53
Q

What enzymes are involved in pancreatitis?

A

Trypsinogen(Trypsin), chymotrypsin, lipase and elastase.

54
Q

T/F: in acute pancreatitis, you can have hypocalcemia or hypercalcemia.

A

True. Hypercalcemia results from Ethanol and BA metabolites
Hypocalcemia can also occur from autodigestion of mesenteric fat that release free fatty acids which form calcium salts (soaps). This can also lead to hypomagnesemia.

55
Q

Most common cause of chronic pancreatitis?

A

Alcoholism

56
Q

Chronic pancreatitis is more fibrotic.

A

Patho (18 decks)

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