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Final FA review > 3/4 GI > Flashcards

3/4 GI Flashcards

1
Q

Where is gastrin made and where is it sent?

A
  • made by G cells in gastric antrum.

- sent to blood, its a hormone.

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2
Q

Who does gastrin act on?

A
  • gastrin stimulates ECL cells to make histamine.
  • histamine acts on parietal cells to make acid.

*gastrin also directly stimulates parietal cells as well. But majority of its effect on parietal cells is indirectly thru histamine.

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3
Q

What are parietal cells stimulated by?

A

-gastrin, histamine, ACh.

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4
Q

Whats the most important mechanism for stimulating parietal cells?

A

-ECL cells & histamine

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5
Q

Where is the highest pH you’ll find in a healthy body?

A
  • veins leaving stomach b/c of all the bicarb that gets pumped into there for all the acid thats pumped into lumen.
  • you make up for it by all the bicarb secretions that are pumped into intestines later.
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6
Q

Which receptors do the stimulatory factors for parietal cells act on?

  • gastrin =
  • ACh =
  • histamine =
A
  • gastrin = CCKb = Gq
  • ACh = M3 = Gq
  • histamine = H2 = Gs

*they all inc. cAMP which inc. activity of H/K ATPase.

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7
Q

Hypertrophy of brunners glands

  • seen in what disease?
  • seen where?
A
  • Peptic ulcer disease

- duodenal submucosa

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8
Q

Pancreatic secretions

  • Isotonic fluid;
  • low flow =
  • high flow =
A
  • low flow= high Cl-
  • high flow=high HCO3-
  • -think of the CFTR channel that pumps Cl (& Na & H2O) into secretions.
  • the lower the flow, the more time it has to pump this in.
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9
Q

What are the monosaccs?

A

-glucose, galactose, fructose.

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10
Q
  • enterocytes take up glucose via?

- pump it into blood via?

A
  • SGLT1 (Na+ dependent).
  • thats why gatorade has sugar and sodium in it.
  • Transported to blood by GLUT-2.
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11
Q

enterocytes take up galactose via?

-pump it into blood via?

A

SGLT1 (Na+ dependent)

-Transported to blood by GLUT-2.

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12
Q

enterocytes take up fructose via?

-pump it into blood via?

A
  • GLUT-5 (facilitated diffusion, doesn’t need Na).

- Transported to blood by GLUT-2.

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13
Q

D-xylose absorption test:

A
  • distinguishes GI mucosal damage from other causes of malabsorption.
  • D-xylose = monosacc that can be absorbed directly w/o action of any enzymes (salivary, pancreatic, etc.) b/c its already a monosacc.
  • -Its absorption requires an intact mucosa only.
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14
Q

Peyers patches

  • encapsulated?
  • where is it found?
  • which layers?
  • what are its specialized cells called?
  • which bug invades through here?
A
  • Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum.
  • M cells.
  • shigella.
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15
Q

How do you turn bile acids into bile salts?

-what do you use to conjugate it?

A

-bile acids conjugated to glycine or taurine, making them water soluble.

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16
Q

Whats the rate limiting enzyme in bile synthesis?

A

Cholesterol 7α-hydroxylase.

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17
Q

How is bilirubin removed from blood?

A

Bilirubin is removed from blood by liver, conjugated with

glucuronate, and excreted in bile.

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18
Q
  • hepatocyte uptake of unconj. bili = active or passive?

- hepatocyte secretion of conj. bili = active or passive?

A
  • hepatocyte uptake of unconj. bili = passive process

- hepatocyte secretion of conj. bili = active process.

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19
Q

Direct & indirect bilirubin

-are they water soluble?

A
  • Direct bilirubin—conjugated with glucuronic acid; water soluble.
  • Indirect bilirubin—unconjugated; water insoluble.
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20
Q
  • Can indirect bilirubin be peed out?

- what gives pee its yellow color?

A

-No, its not water soluble. Its not filtered by glomerulus.
-Excreted in urine as urobilin, which gives yellow color of
urine.

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21
Q
  • What enzyme conjugates bilirubin?

- Where is it found?

A
  • UDP-glucuronosyl-transferase

- hepatocytes

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22
Q

What happens to conjugated bilirubin once its in the gut?

A
  • Gut bacteria convert it to urobilinogen.
  • 80% is oxidized to stercobilin & pooped out.
  • 20% is divided:
  • -90% recycled in terminal ileum.
  • -10% excreted in urine as urobilin.
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23
Q

What gives urine yellow color?

A

-Urobilinogen is colorless. Once it hits the air in the kidneys, turns into urobilin which is yellow.

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24
Q

biphasic tumor

A

-any tumor involving both stromal and epithelial

tissue.

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25
Q

Pleomorphic adenoma (benign mixed tumor)

A

-most common salivary gland tumor.
-Presents as a painless, mobile mass.
-Composed of chondromyxoid stroma and epithelium
and recurs if incompletely excised.
*has irregular borders, hard to excise completely.

-if you get signs of facial nerve damage, the tumor has
transformed into a carcinoma (malignant).

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26
Q

Warthin tumor

A
  • benign salivary gland tumor
  • Papillary cystadenoma lymphomatosum.
  • Benign cystic tumor in lymphoid tissue (with germinal centers).
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27
Q

Mucoepidermoid carcinoma

A
  • Most common malignant salivary gland tumor.
  • Mucinous and squamous components.
  • It typically presents as a painless, slow-growing mass.
  • facial n. often affected.
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28
Q

What does chalasia mean?

A

-chalasia = relaxation.

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29
Q

Achalasia

-inc. risk of which cancer?

A

esophageal SCC.

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30
Q

Esophageal strictures are associated w/ingestion of what?

A
  • Lye & acid reflux.

- 70-80% due to GERD.

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31
Q
  • esophagus venous drainage?

- Where do you find esophageal varices?

A
  • Most drained via esophageal veins to azygos to SVC.
  • Some drained from left gastric vein to the portal vein. In portal HTN there will be backup.

-Varices found in lower 1/3 of esophagus.

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32
Q

Adult onset asthma

-associated w/what common esophageal problem?

A

GERD

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33
Q

Obesity

-risk factor for squamous or adeno carcinoma of esophagus?

A

-adeno

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34
Q

Classic locations of esophageal cancer:

  • squamous vs adenocarcinoma
  • also, which is more common in the US?
A
  • Squamous cell—upper 2 ⁄ 3 .
  • Adenocarcinoma—lower 1 ⁄ 3 .

*Worldwide, squamous cell is more common.
*In the United States, adenocarcinoma is more
common.

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35
Q

Esophageal web

-inc risk for squamous or adeno carcinoma of esophagus?

A

-squamous

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36
Q

Cushing ulcer:

A
  • acute gastritis

- inc. ICP = inc. vagal stim = inc. H production

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37
Q

How does achlorhydria cause G-cell hyperplasia?

A

-low levels of gastric acid in the stomach. Will result in increased gastrin b/c you’ve lost the negative feedback. (leads to G-cell hyperplasia).

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38
Q

Type A chronic gastritis

A
  • pernicious anemia

- type 4 HSR.

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39
Q

Ménétrier disease

A
  • Gastric hypertrophy with protein loss, parietal cell atrophy, and inc. mucous cells.
  • Precancerous.
  • Rugae of stomach are so hypertrophied that they look like brain gyri.
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40
Q

Sister Mary Joseph nodule

A

-subcutaneous periumbilical metastasis.

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41
Q

Ruptured gastric ulcer on the lesser curvature of the stomach.
-which artery will bleed?

A

-Bleeding from left gastric artery.

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42
Q

Ruptured ulcer on the posterior wall of the duodenum.

-which artery will bleed?

A

-Bleeding from gastroduodenal artery.

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43
Q 
Ulcer complications
-ant or post
-which one more likely to 
1-hemorrhage
2-perforate
A
  • posterior = hemorrhage

- anterior = perforate

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44
Q

Perforated duodenal ulcer

-what can you see? pain where?

A

May see free air under the diaphragm with referred pain to the shoulder.

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45
Q

Tropical sprue vs Celiac

  • response to Abx?
  • location affected?
A
  • tropical sprue does respond to Abx

- tropical sprue affects jejunum and ileum rather than duodenum like celiac disease.

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46
Q

Is mucus release inc or decreased in inflammatory states?

A

-increased

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47
Q

Paneth cell

A
  • pathocytic & secretory functions.
  • occur at base of intestinal crypts.
  • first line of immune defense against intestinal microbes.
  • secrete lysozyme and defensins.
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48
Q

Liver failure after surgery think what?

A

-halothane anesthetic is very hepatotoxic.

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49
Q

Liver failure after surgery think what?

A
  • halothane anesthetic is very hepatotoxic.

- can not be histologically distinguished from acute viral hepatitis.

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50
Q

If you have acute liver failure, why do you get inc. PT time but your albumin level is fine? If liver cell is failing to make coag factors isn’t it also failing to make albumin?

A

-yes it is but albumin has a long half life (20 days), compared with some coag factors. Factor 7 has a half life of 3-6 hours.

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51
Q

How to Dx celiac sprue?

-test for which Abs?

A

-IgA anti-endomysial & anti-tissue transglutaminase Abs.

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52
Q

Pulsatile vs non-pulsatile bleeding

A
  • non-pulsatile = from a vein

- pulsatile = from an artery

53
Q

Carcinoid tumor

-whats it look like histologically?

A

-there is no variation in shape & size of tumor cells. They all look alike.

54
Q

Carcinoid tumor

-whats it look like histologically?

A
  • there is no variation in shape & size of tumor cells. They all look alike.
  • commonly found in appendix.
55
Q

Is the spleen a foregut derivative?

A
  • No, but it stills gets fed by the celiac trunk.

- it originates from the dorsal mesentery.

56
Q

Are the kidneys a foregut derivative?

A
  • No, they are derived from mesoderm.

* kidneys are not a GI structure.

57
Q

How does alcohol lead to macrocytosis?

A

Direct toxicity of alcohol on the marrow.

58
Q

Why can you get hyperglycemia in pancreatitis?

A

Pancreatic beta-cells can be destroyed = no insulin = hyperglycemia.

59
Q

IFN-gamma

-which receptor/signaling pathway does it use?

A

-JAK-STAT

60
Q
  • Duodenal atresia due to:

- Jejunal/ileal/colonic atresia due to:

A
  • failure of recanalization.

- vascular accident in utero.

61
Q

Which vessel needs to be occluded in utero to get “apple peel atresia”?

A

-SMA

62
Q

Urease: what does it convert to what?

A

urea => CO2 & ammonia

63
Q

Can GERD cause dysphagia & odynophagia?

A

yes

64
Q

Elongation of lamina propria papallie, inflammatory cells (ie. neutros/eosinophils/lymphocytes). All w/in squamous epithelium.
-Seen in which GI disease?

A

GERD.

65
Q

Bisphosphonate

-major side effect?

A

-Errosive esophagitis, osteonecrosis of jaw.

66
Q

Whipple disease

-Sxs: mnemonic

A

Foamy whipped cream in a CAN.

  • Cardiac problems
  • Arthralgias
  • Neuro problems.
67
Q
  • diastate resistant granules.

- the gram + cell wall stains well w/PAS.

A

Tropheryma whipplei

68
Q

Is whipple disease invasive?

A

Yes

69
Q

Celiac sprue

-associated w/which HLA?

A
  • HLA-DQ2, HLA-DQ8

- Northern European descent.

70
Q

Celiac sprue

  • which parts of GI most affected?
  • how do you Dx?
A
  • Distal duodenum/proximal jejunum.

- tissue transglutaminase antibodie levels used for Dx.

71
Q

Which abs found in serum in celiac sprue?

A
  • anti-endomysial
  • anti-tissue transglutaminase
  • anti-gliadin antibodies
72
Q

Celiac sprue associated w/

-which cancer?

A

T cell lymphoma

73
Q

Histological appearance of celiac sprue

A

Blunting of villi, crypt hyperplasia.

74
Q

Lactose tolerance test: + for lactase deficiency if:

A
  • Administration of lactose produces symptoms, and glucose rises < 20 mg/dL.
  • lactose broken up into glucose & galactose.
75
Q

Abetalipoproteinemia

  • presentation:
  • what accumulates where?
A
  • Presents in early childhood with failure to thrive, steatorrhea, acanthocytosis, ataxia, night blindness.
  • fat accumulates in enterocytes b/c you cant make chylomicrons and you also cant make VLDL.
76
Q

Very low pasma TG & chol levels seen in which disease?

A

Abetalipoproteinemia

77
Q

Cause of acanthocytes?

A

ADEK malabsorption, ie. in abetalipoproteinemia.

  • deficient vitamin E
  • deficient lipids to make RBC plasma membrane
78
Q

How do you test for pancreatic insufficiency?

A

d-xylose absorption test

79
Q

d-xylose absorption test:

A

-testing for pancreatic insufficiency.
-normal urinary excretion in pancreatic insufficiency;  dec. excretion with intestinal mucosa defects or bacterial
overgrowth.
-basically all d-xylose needs to be absorbed is an intact mucosa.

80
Q
  • RLQ pain =

- LLQ pain =

A
  • Crohns (terminal ileum)

- UC (rectum)

81
Q

String sign on barium swallow:

A

Crohns

82
Q

Lead pipe bowels

A

UC

-loss of haustra

83
Q

Pseudopolyps

-UC or Crohns?

A

UC

84
Q

UC vs Crohns

-which one is Th1 mediated, which is Th2?

A
  • Crohns = Th1 (w/granulomas)

- UC = Th2

85
Q

Crypt abscess = key feature of which disease?

-what do you find in the crypts?

A

UC

-neutros in the crypts.

86
Q

Complications in UC:

A

Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right-sided colitis or pancolitis).

87
Q

adalimumab

A

mab against TNF-alpha

-like infliximab

88
Q

Sulfasalazine (5-ASA)

-for UC or Crohns?

A

UC

89
Q

1° sclerosing cholangitis

-UC or Crohns?

A

UC

90
Q

Migratory polyarthritis & kidney stones

-UC or Crohns?

A

Crohns.

-calcium oxalate.

91
Q

IBS

  • Sxs:
  • can it get worse w/stress?
A

Must have 2 out of 3:

  • Pain improves with defecation
  • Change in stool frequency
  • Change in appearance of stool

*can get worse w/stress.

92
Q

Two causes of appendicitis:

A

Fecalith or lymphoid hyperplasia

-adenovirus & measles most common

93
Q

2 most common viruses that may lead to appendicitis

A

adenovirus & measles

94
Q

Which dermatome does appendicitis affect?

A

T10

95
Q

Diverticulitis commonly causes pain where?

A
  • LLQ

- “left sided appendicitis”.

96
Q

pneumaturia

  • whats it mean?
  • when do you see it?
A
  • air in your urine

- colon fistula w/bladder, can be seen in diverticulitis, Crohns, etc.

97
Q

Killian triangle

  • what happens here?
  • where is this triangle?
A
  • Zenker diverticulum.

- between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor.

98
Q

Meckel’s diverticulum

  • pain in what quadrant?
  • how do you Dx?
A
  • RLQ

- pertechnetate study for uptake by ectopic gastric mucosa.

99
Q

pertechnetate study

-Dx what disease with this?

A

Meckel’s diverticulum

-study for uptake by ectopic gastric mucosa.

100
Q

Intussusception

  • presentation?
  • most common location?
A
  • colicky abdominal pain, currant jelly stools.
  • frank blood and mucus in stool.
  • ileocecal valve.
101
Q
  • Midgut volvulus more common in..

- Sigmoid volvulus more common in…

A
  • midgut = children

- sigmoid = elderly

102
Q

Hirschsprung disease associated

  • w/mutation in which gene?
  • w/which genetics disease?
A
  • RET gene.

- Downs syndrome.

103
Q

Which parts of GI tract are always involved in hirschsprungs?

A

Rectum & anus.

-Neural crest cells migrate downward. These = last two areas.

104
Q

Down syndrome associated w/which GI problems?

A

-Duodenal atresia, hirschsprungs.

105
Q

Most common cause of small bowel obstruction?

A

Adhesions

106
Q

Where are angiodysplasias most commonly found?

A

-Most often found in cecum, terminal ileum, and

ascending colon.

107
Q

Double Bubble sign seen in which disease?

A

Duodenal Atresia.

108
Q

Ileus

  • associated w/what?
  • hypo or hyperkalemia?
A

-Associated with abdominal surgeries, opiates, hypokalemia, and sepsis.

109
Q

Ischemic colitis

  • most common cause?
  • most common location?
  • when do you get pain?
A
  • atheroschleorisis of SMA
  • splenic flexure
  • post-prandial pain b/c thats when ATP requirement = highest.
110
Q

If you suspect malabsorption, whats the first step in management?

A

Stool sample

  • sudan 3 stain looks for fat.
  • used to screen for malabsorption.
111
Q

Corkscrew esophagus

-think what?

A

Diffuse esophageal spasm.

112
Q

Courvoisier sign

  • what is it?
  • whats it seen in?
A
  • obstructive jaundice w/palpable non-tender gallbladder.

- pancreatic adenocarcinoma.

113
Q

Branches of splenic artery?

A
  • short gastrics
  • left gastroepiploic
  • pancreatic branches
114
Q

Intususseption

  • Dx?
  • Tx?
A

Barium enema for Dx and can also be therapeutic.

115
Q

Dry skin and night blindness

-think what?

A
  • vitamin A deficiency

- could be due to bile obstruction => fal malabsorption => ADEK deficiency.

116
Q

VIPoma causes what kind of diarrhea?

A

Secretory

117
Q

Anti-oncogene

-aka?

A

Tumor suppressor gene

-ie. p53, Rb.

118
Q 
Pneumatosis intestinalis (air in intestines) in infant w/abdominal pain & bloody stools.
-diagnostic for what?
A

Necrotizing enterocolitis

119
Q

Ulcer found in distal duodenum or other atypical locations

-think what disease

A

Zollinger-Ellison.

  • usually ocated in the pancreas
  • 2/3 of them are malignant.
120
Q

Schilling test

-used to work up what?

A

B12 deficiency

-can use it to Dx pernicious anemia.

121
Q

Juvenile colonic polyp

  • most commonly found where?
  • inc risk of adenocarcinoma?
A
  • rectum, 80% of the time.

- only if there are multiple = Juvenile polyposis syndrome.

122
Q

Peutz-Jeghers syndrome

  • inheritance pattern?
  • inc. risk of CRC?
A
  • auto dom.

- yes

123
Q

FAP

  • inheritance pattern?
  • which chrom?
  • what type of gene?
A
  • auto dom
  • 5q
  • tumor suppressor = 2 hit hypothesis.

*always involves the rectum.

124
Q

Gardner syndrome

-Sxs:

A
  • FAP + osseous and soft tissue tumors, congenital gypertrophy of retinal pigment epithelium.
  • osteomas usually arise in the skull.
125
Q

Turcot syndrome

-Sxs:

A
  • FAP + malignant CNS tumor.

* Turcot = Turban.

126
Q

HNPCC

  • inheritance pattern?
  • which gene?
  • which part of GI tract is always involved?
A
  • auto dom.
  • tumor arises de novo
  • DNA mismatch repair genes.
  • proximal colon always involved.
127
Q

CRC

-which parts of colon are more commonly affected?

A

Rectosigmoid > ascending > descending.

128
Q

“Apple core” lesion seen on barium enema x-ray

-think what?

A

CRC

-most likely left sided

129
Q
  • microsatellite instability pathway -> left/right?

- adenoma carcinoma sequence pathway -> left/right?

A
  • microsatellite -> right sided carcinoma (typically)

- adenoma carcinoma -> left sided carcinoma (typically)

Final FA review (52 decks)

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