Final FA review > 3/4 GI > Flashcards

3/4 GI Flashcards

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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
Pleomorphic adenoma (benign mixed tumor)
-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).
26
Warthin tumor
- benign salivary gland tumor - Papillary cystadenoma lymphomatosum. - Benign cystic tumor in lymphoid tissue (with germinal centers).
27
Mucoepidermoid carcinoma
- Most common malignant salivary gland tumor. - Mucinous and squamous components. - It typically presents as a painless, slow-growing mass. - facial n. often affected.
28
What does chalasia mean?
-chalasia = relaxation.
29
Achalasia | -inc. risk of which cancer?
esophageal SCC.
30
Esophageal strictures are associated w/ingestion of what?
- Lye & acid reflux. | - 70-80% due to GERD.
31
- esophagus venous drainage? | - Where do you find esophageal varices?
- 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.
32
Adult onset asthma | -associated w/what common esophageal problem?
GERD
33
Obesity | -risk factor for squamous or adeno carcinoma of esophagus?
-adeno
34
Classic locations of esophageal cancer: - squamous vs adenocarcinoma - also, which is more common in the US?
- Squamous cell—upper 2 ⁄ 3 . - Adenocarcinoma—lower 1 ⁄ 3 . *Worldwide, squamous cell is more common. *In the United States, adenocarcinoma is more common.
35
Esophageal web | -inc risk for squamous or adeno carcinoma of esophagus?
-squamous
36
Cushing ulcer:
- acute gastritis | - inc. ICP = inc. vagal stim = inc. H production
37
How does achlorhydria cause G-cell hyperplasia?
-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).
38
Type A chronic gastritis
- pernicious anemia | - type 4 HSR.
39
Ménétrier disease
- 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.
40
Sister Mary Joseph nodule
-subcutaneous periumbilical metastasis.
41
Ruptured gastric ulcer on the lesser curvature of the stomach. -which artery will bleed?
-Bleeding from left gastric artery.
42
Ruptured ulcer on the posterior wall of the duodenum. | -which artery will bleed?
-Bleeding from gastroduodenal artery.
43
``` Ulcer complications -ant or post -which one more likely to 1-hemorrhage 2-perforate ```
- posterior = hemorrhage | - anterior = perforate
44
Perforated duodenal ulcer | -what can you see? pain where?
May see free air under the diaphragm with referred pain to the shoulder.
45
Tropical sprue vs Celiac - response to Abx? - location affected?
- tropical sprue does respond to Abx | - tropical sprue affects jejunum and ileum rather than duodenum like celiac disease.
46
Is mucus release inc or decreased in inflammatory states?
-increased
47
Paneth cell
- pathocytic & secretory functions. - occur at base of intestinal crypts. - first line of immune defense against intestinal microbes. - secrete lysozyme and defensins.
48
Liver failure after surgery think what?
-halothane anesthetic is very hepatotoxic.
49
Liver failure after surgery think what?
- halothane anesthetic is very hepatotoxic. | - can not be histologically distinguished from acute viral hepatitis.
50
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?
-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.
51
How to Dx celiac sprue? | -test for which Abs?
-IgA anti-endomysial & anti-tissue transglutaminase Abs.
52
Pulsatile vs non-pulsatile bleeding
- non-pulsatile = from a vein | - pulsatile = from an artery
53
Carcinoid tumor | -whats it look like histologically?
-there is no variation in shape & size of tumor cells. They all look alike.
54
Carcinoid tumor | -whats it look like histologically?
- there is no variation in shape & size of tumor cells. They all look alike. - commonly found in appendix.
55
Is the spleen a foregut derivative?
- No, but it stills gets fed by the celiac trunk. | - it originates from the dorsal mesentery.
56
Are the kidneys a foregut derivative?
- No, they are derived from mesoderm. | * kidneys are not a GI structure.
57
How does alcohol lead to macrocytosis?
Direct toxicity of alcohol on the marrow.
58
Why can you get hyperglycemia in pancreatitis?
Pancreatic beta-cells can be destroyed = no insulin = hyperglycemia.
59
IFN-gamma | -which receptor/signaling pathway does it use?
-JAK-STAT
60
- Duodenal atresia due to: | - Jejunal/ileal/colonic atresia due to:
- failure of recanalization. | - vascular accident in utero.
61
Which vessel needs to be occluded in utero to get "apple peel atresia"?
-SMA
62
Urease: what does it convert to what?
urea => CO2 & ammonia
63
Can GERD cause dysphagia & odynophagia?
yes
64
Elongation of lamina propria papallie, inflammatory cells (ie. neutros/eosinophils/lymphocytes). All w/in squamous epithelium. -Seen in which GI disease?
GERD.
65
Bisphosphonate | -major side effect?
-Errosive esophagitis, osteonecrosis of jaw.
66
Whipple disease | -Sxs: mnemonic
Foamy whipped cream in a CAN. - Cardiac problems - Arthralgias - Neuro problems.
67
- diastate resistant granules. | - the gram + cell wall stains well w/PAS.
Tropheryma whipplei
68
Is whipple disease invasive?
Yes
69
Celiac sprue | -associated w/which HLA?
- HLA-DQ2, HLA-DQ8 | - Northern European descent.
70
Celiac sprue - which parts of GI most affected? - how do you Dx?
- Distal duodenum/proximal jejunum. | - tissue transglutaminase antibodie levels used for Dx.
71
Which abs found in serum in celiac sprue?
- anti-endomysial - anti-tissue transglutaminase - anti-gliadin antibodies
72
Celiac sprue associated w/ | -which cancer?
T cell lymphoma
73
Histological appearance of celiac sprue
Blunting of villi, crypt hyperplasia.
74
Lactose tolerance test: + for lactase deficiency if:
- Administration of lactose produces symptoms, and glucose rises < 20 mg/dL. * lactose broken up into glucose & galactose.
75
Abetalipoproteinemia - presentation: - what accumulates where?
- 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
Very low pasma TG & chol levels seen in which disease?
Abetalipoproteinemia
77
Cause of acanthocytes?
ADEK malabsorption, ie. in abetalipoproteinemia. - deficient vitamin E - deficient lipids to make RBC plasma membrane
78
How do you test for pancreatic insufficiency?
d-xylose absorption test
79
d-xylose absorption test:
-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
- RLQ pain = | - LLQ pain =
- Crohns (terminal ileum) | - UC (rectum)
81
String sign on barium swallow:
Crohns
82
Lead pipe bowels
UC | -loss of haustra
83
Pseudopolyps | -UC or Crohns?
UC
84
UC vs Crohns | -which one is Th1 mediated, which is Th2?
- Crohns = Th1 (w/granulomas) | - UC = Th2
85
Crypt abscess = key feature of which disease? | -what do you find in the crypts?
UC | -neutros in the crypts.
86
Complications in UC:
Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right-sided colitis or pancolitis).
87
adalimumab
mab against TNF-alpha | -like infliximab
88
Sulfasalazine (5-ASA) | -for UC or Crohns?
UC
89
1° sclerosing cholangitis | -UC or Crohns?
UC
90
Migratory polyarthritis & kidney stones | -UC or Crohns?
Crohns. | -calcium oxalate.
91
IBS - Sxs: - can it get worse w/stress?
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
Two causes of appendicitis:
Fecalith or lymphoid hyperplasia | -adenovirus & measles most common
93
2 most common viruses that may lead to appendicitis
adenovirus & measles
94
Which dermatome does appendicitis affect?
T10
95
Diverticulitis commonly causes pain where?
- LLQ | - "left sided appendicitis".
96
pneumaturia - whats it mean? - when do you see it?
- air in your urine | - colon fistula w/bladder, can be seen in diverticulitis, Crohns, etc.
97
Killian triangle - what happens here? - where is this triangle?
- Zenker diverticulum. | - between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor.
98
Meckel's diverticulum - pain in what quadrant? - how do you Dx?
- RLQ | - pertechnetate study for uptake by ectopic gastric mucosa.
99
pertechnetate study | -Dx what disease with this?
Meckel's diverticulum | -study for uptake by ectopic gastric mucosa.
100
Intussusception - presentation? - most common location?
- colicky abdominal pain, currant jelly stools. - frank blood and mucus in stool. - ileocecal valve.
101
- Midgut volvulus more common in.. | - Sigmoid volvulus more common in...
- midgut = children | - sigmoid = elderly
102
Hirschsprung disease associated - w/mutation in which gene? - w/which genetics disease?
- RET gene. | - Downs syndrome.
103
Which parts of GI tract are always involved in hirschsprungs?
Rectum & anus. | -Neural crest cells migrate downward. These = last two areas.
104
Down syndrome associated w/which GI problems?
-Duodenal atresia, hirschsprungs.
105
Most common cause of small bowel obstruction?
Adhesions
106
Where are angiodysplasias most commonly found?
-Most often found in cecum, terminal ileum, and | ascending colon.
107
Double Bubble sign seen in which disease?
Duodenal Atresia.
108
Ileus - associated w/what? - hypo or hyperkalemia?
-Associated with abdominal surgeries, opiates, hypokalemia, and sepsis.
109
Ischemic colitis - most common cause? - most common location? - when do you get pain?
- atheroschleorisis of SMA - splenic flexure - post-prandial pain b/c thats when ATP requirement = highest.
110
If you suspect malabsorption, whats the first step in management?
Stool sample - sudan 3 stain looks for fat. - used to screen for malabsorption.
111
Corkscrew esophagus | -think what?
Diffuse esophageal spasm.
112
Courvoisier sign - what is it? - whats it seen in?
- obstructive jaundice w/palpable non-tender gallbladder. | - pancreatic adenocarcinoma.
113
Branches of splenic artery?
- short gastrics - left gastroepiploic - pancreatic branches
114
Intususseption - Dx? - Tx?
Barium enema for Dx and can also be therapeutic.
115
Dry skin and night blindness | -think what?
- vitamin A deficiency | - could be due to bile obstruction => fal malabsorption => ADEK deficiency.
116
VIPoma causes what kind of diarrhea?
Secretory
117
Anti-oncogene | -aka?
Tumor suppressor gene | -ie. p53, Rb.
118
``` Pneumatosis intestinalis (air in intestines) in infant w/abdominal pain & bloody stools. -diagnostic for what? ```
Necrotizing enterocolitis
119
Ulcer found in distal duodenum or other atypical locations | -think what disease
Zollinger-Ellison. - usually ocated in the pancreas - 2/3 of them are malignant.
120
Schilling test | -used to work up what?
B12 deficiency | -can use it to Dx pernicious anemia.
121
Juvenile colonic polyp - most commonly found where? - inc risk of adenocarcinoma?
- rectum, 80% of the time. | - only if there are multiple = Juvenile polyposis syndrome.
122
Peutz-Jeghers syndrome - inheritance pattern? - inc. risk of CRC?
- auto dom. | - yes
123
FAP - inheritance pattern? - which chrom? - what type of gene?
- auto dom - 5q - tumor suppressor = 2 hit hypothesis. *always involves the rectum.
124
Gardner syndrome | -Sxs:
- FAP + osseous and soft tissue tumors, congenital gypertrophy of retinal pigment epithelium. - osteomas usually arise in the skull.
125
Turcot syndrome | -Sxs:
- FAP + malignant CNS tumor. | * Turcot = Turban.
126
HNPCC - inheritance pattern? - which gene? - which part of GI tract is always involved?
- auto dom. * tumor arises de novo - DNA mismatch repair genes. - proximal colon always involved.
127
CRC | -which parts of colon are more commonly affected?
Rectosigmoid > ascending > descending.
128
“Apple core” lesion seen on barium enema x-ray | -think what?
CRC | -most likely left sided
129
- microsatellite instability pathway -> left/right? | - adenoma carcinoma sequence pathway -> left/right?
- microsatellite -> right sided carcinoma (typically) | - adenoma carcinoma -> left sided carcinoma (typically)
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