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GI step u world questions > GI > Flashcards

GI Flashcards

1
Q

HOW DOES LATASE DEFICIENCY AND THE OSMOTIC DIARRHEA EFFECT THE BOWEL MUCOSA?

A

IT WILL SHOW NORMAL MUCOSA

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2
Q

Congenital variant of primary lactase deficiency is what kind of heritability .. recessive or dominant

A

it is autosomal recessive presenting with diarrhea after birth

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3
Q

what is more common - inherited or acquired lactase deficiency ?

A

acquired

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4
Q

what are secondary lactase deficiencies?

A

this is due to injury of the GI mucosa .. such as in celiac and crohns … if there is lactase deficiency from these conditions it is usually seen in association with other features such as iron deficiency , vitamin D deficiency

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5
Q

when do you see diffuse inflammatory infiltrates with necrophilic micro abscesses in the crypt lumina ?

A

ulcerative colitis .. present with intermittent bloody diarrhea and abdominal pain

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6
Q

Whipple disease

A

rare systemic infection caused by the bacteria TRO-PHERYMA WHIPPEI which is a gram POSITIVE bacillus bacteria

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7
Q

what systems does the tropheryma whipplei bacteria effect?

A

GI, neuro, lymphatic

(visual - to remember the bacteria name imagine getting a trophy for doing the whip it dance )

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8
Q

what are the associated factors that might predispose someone getting Whipple disease from the bacteria too-pheryma whipplei ?

A

male gender, HLA-B27 haplotype .. farming and north America and europe

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9
Q

what is found in the lamina proprietor in Whipple disease?

A

macrophages are distended int eh intestinal lamina ropria .. along with malabsorption diarrhea, weight loss and joint pain

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10
Q

MALT lymphomas of the stomach are what ? and what bacteria is associated with it?

A

H pylori .. MALT stands for mucosa associated lymphoid tissue lymphoma

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11
Q

ultrasonography is the preferred initial imaging test for the diagnosis of acute cholecystitis .. but what is an alternative means when ultrasonography is inconclusive?

A

nuclear medicine hepatobiliary scanning .. cholescintigraphy .. a radio tracer si administered intravenously and is preferentially taken up by the hepatocytes and excreted into the bile .. images of the tracer as it moves through the hepatobiliary system and intestine are obtained for up to several hours after injection - those with a patent cystic dot the gallbladder will be seen as the radio tracer accumulates and concentrates .. but in acute or chronic cholecystitis the radio tracer will be taken up by the liver with progressive ex ration into the common bile duct and proximal small bowel but the gallbladder will not be visualized due the obstruction

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12
Q

what are signs of acute cholecystitis (gallbladder inflammation ) on teh ultrasonography

A

wall thickening , pericholecystic fluid )

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13
Q

what is melena

A

bloody stool

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14
Q

what are friable masses

A

tumors that are easy to move

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15
Q

Lynch syndrome is what

A

hereditary nonpolyposis colon cancer .. autosomal dominant disease caused by defective DNA mismatch repair

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16
Q

DNA mismatch repair system (fixing errors shortly after the daughter strand are syntesized ) involved several genes including MSH2 and MLH1 which code for the human what and what homologs ?

A

MutS and MutL

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17
Q

what hormone is produced by the G cells in teh gastric antrum

A

gastrin

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18
Q

what stimulates G cells in the gastric antrum to release gastrin ?

A

dietary protein intake , gastrin releasing peptide in response to vagal stimuli , and increased gastric ph .. (so protein , high ph in the stomach

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19
Q

how does gastrin induce acid production

A

by binding to parietal cells and indirection binding enterochromaffin like cells (ECL) and inducing histamine release

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20
Q

what are enterochromaffin like cells

A

type of neuroendocrine cells found in the gastric glands of the gastric mucosa (in the vicinity of the parietal cells ).

They synthesize and secrete histamine in response to stimulation from the G cell .. Both the histamine from the ECL cells and gastric from the G cells work synergistically as the most important stimulators of HCL

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21
Q

why do PPIs lead to more acid when you stop them abruptly

A

because proton pump inhibitors like omeprazole and lansoprazole inhibit the hydrogen potassium -ATPase pump and decrease the HCl .. THIS will decrease the gastric ph which ice a trigger for gastrin formation … gastric then stimulates the ECL and parietal cells inducing hypertrophy ! … So PPIs have to be tampered

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22
Q

what kind of gastritis will chronic helicobacter pylori cause?

A

atrophic gastrin which is the thinning of the stomach lining .. it is multifocal .. versus autoimmune gastritis is concentrated int eh corpus - fundus (not all throughout)

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23
Q

how do non steroidal anti-inflammatory drugs like ibuprofen increase the risk of gastritis and peptic ulcer formation ?

A

because NSAIDS will inhibit prostaglandin .. and prostaglandins decrease acid production by inhibiting the downstream message of histamine and increases the bicarbonate formation from the gastric epithelial cells

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24
Q

is hemochromatosis autosomal recessive or dominant

A

recessive

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25
Q

what issues arise with the end organ damage due to hemochromatosis

A

cirrhosis, diabetes mellitus, cardiomyopathy, arthropathy

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26
Q

what kind of mutation causes hereditary hemochromatosis

A

missense mutation

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27
Q

what gene is effected in hereditary hemochromatosis

A

HFE gene (C282Y)

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28
Q

what are enterocytes

in

A

cells of the intestinal lining ..

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29
Q

transferrin and iron togeather - bind to the transferrin receptor with the aid of what protein?

A

FHE

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30
Q

when the HFE protein helps iron and transferrin to bind to the transferrin receptor - what happens next?

A

endocytosis of the iron transferrin complex .. which is then degraded and the iron is released and added to the labile iron pool

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31
Q

in hemochromatosis - where the HFE protein is mutated (reducing the endocytosis of the transferrin and iron complex ) - how is iron accumulated in teh body - by what two mechanisms ?

A

enterocytes increase apical expression of DMT1 (DIVALENT METAL TRANSPORTER) so that more iron is absobed into the lumen

Then Hepatocytes will decrease hepcidin synthesis - which increases ferroportin expression on the basolateral surface of the enterocytes (portal for iron to go through the cell lining of the gut to the plasma )

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32
Q

what is the sole known molecular target of hepcidin ?

A

the protein ferroportin .. which is a transmembrane conduit for the transfer of cellular iron to plasma- Hepcidin BLOCKS ferroportin .. which mean that iron doesnt get into the blood stream from the intestines .. also since ferroportin is on macrophages ..so when hepcidin binds ot the ferroportin

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33
Q

what two places is ferroportin found ?

A

in the enterocytes and macrophages ..

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34
Q

role of hepcidin and ferroportin on macrophages

A

hepcidin blocks the ferroportin channel so that iron cant get out and be recycled reducing systemic iron

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35
Q

what liver peptide hormone controlls iron avilability

A

hepcidin

which acts on the receptor ferroportin .. transmembrain iron exporter pr

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36
Q

most iron (20-25mg/daily) is recycles by what?

A

macrophages .. and a limited amount id derived brom intestinal absorption

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37
Q

what is ferritin

A

cellular iron storage protein

38
Q

major iron transporter in the plasma

A

transferrin

39
Q

mutation of the HFE protein leads to reduced iron uptake which then causes what?

A

causes enterocytes and hepatocytes to sense falsely low iron levels .. the enterocytes compesate by increasing the expression of divalent metal transporter 1 (MDT1) to increase the intestinal iron absorption

-hepatocytes compensate by decreasing hepcidin synthesiss which normally blocks the ferroportin transmembrane iron channel

40
Q

secretion site of somatostatin

A

D cells (pancreatic islets // gut mucosa)

41
Q

what does somatostatin Do in the stomache ?

(GI hormone)

A

decreases the secretion of most GI hormones .. suppressor !** reduces gastrin **which decreases stomach acid -

reduces pepsinogen secretion.

Somatostatin profoundly inhibits pancreatic enzyme, fluid, and bicarbonate secretion and reduces bile flow.

42
Q

where is cholecystokinin produced

A

I cells (small intestines )

43
Q

what does cholecystokinin do?

A

increses pancreatic enzyme and HCO3 secretion
(aids in the digestion of fat and protein due to its effects on the pancreaus

44
Q

where is secretin produced?

A

S cells (small intestine)

45
Q

what does secretin do?

A

increases pancreatic HCO3 secretion and reduces gastric H secretion
(the bicarbonate rich fluid that it stimulates from teh pancreus will reduce the acidic environment , making it more condusive to the digestion of fats which needs a more nutrual Ph

46
Q

GIP where is it produced

A

K cells (small intestine)

47
Q

GIP what does this GI hormone do?

glucose -dependent insulinotropic polypeptide … also kmown as gastric

A

increases insulin .. decreases gastric H secretion to protect the small intestins from acid damage ..

main role is to stimulate insulin secretion … (K cells)

48
Q

motilin is produced where or secreted where ?

A

via M cells in the small intestine

49
Q

what does motilin do

A

increases teh GI motility

50
Q

secretin effects on exocrine pancreatic ductal cells

A

stimulates the pancreatic ductal cells to release high volume of bicarbonate rich and chloride poor fluid into the small bowel .. neutralizes the HCL

51
Q

where is mcburneys point

A

right lower quadrant

52
Q

appendicitis illicits what two types of pain?

A

visceral - vague ,non-localized , dull constant and cramping quality … nausea
(due to luminal dissension and stretching of the smooth muscle .. carried by the general visceral afferent fibers )

somatic - sharp well localized
(usually due to irritation of the parietal peritoneum )- more severe and worsened with inspiration or pushing not he abdominal wall

53
Q

what is the pathway of pain experienced in appendicitis

A

afferent pain fibers for the appendix , proximal colon and peritoneum cross through the superior mesenteric plexus and enter the spinal cord at T10 creating referred pain at the umbilicus .. then as the appendix becomes more inflamed it irritated the parietal peritoneum and the abdominal wall and causes somatic pain that shifts from teh umbilical region to the mc burners point .. at this point one can experience rebound tenderness with mental palpation or sudden release of pressure

54
Q

what is the connection between crohns disease and gallstones ?

A

Bile acids are reabsorbed in the terminal ileum via transport proteins …. typically the terminal ileum is a location of activity in Crohns.. when the mucosa of the terminal ileum is inflamed - the bile acids are lost in the feces because they are not transported .. leading to supersaturation of cholesterol

55
Q

the presence of fluid filled cavity in teh liver with fevers, chills and right upper abdominal pain is suggestive of what

A

hepatic abscess…

if developing countries the abscesses are often associated with parasitic infections like entamoeba histolytic or echinococcal …

in the US associated with bacterial infections in 80% of the cases

56
Q

how can pyogenic bacteria gain access to the liver?

A

biliary tract infection like ascending cholangitis ..

portal vein pyemia (bowel or perotoneal sources )

hepatic artery .. systemic hematogenous seeding

direct invasion from peritonitis or cholecystectomy

penetrating trauma or injury

57
Q

enteric bacteria that causes hepatic abscesses would be what?

A

Ecoli and klebsiella and enterococci

58
Q

what cells are involved in hepatic fibrosis

A

stellate cells - transforming into myofibroblasts.. which are capable of proliferation , promoting chemotaxis and producing large quantities of collagen

59
Q

how do collagen stain with Masson trichrome stain?

A

blue

60
Q

how is cirrhosis visualized histologically ?

A

thickened collagenous bands .. which stain blue with Masson trichrome stain ..

61
Q

fat infiltration with hepatic steatosis is seen in what two things

A

alcoholic fatty liver and non alcoholic fatty liver

62
Q

what is the most likely cause of postprandial epigastric pain in teh setting of generalized atherosclerosis?

A

chronic mesenteric ischemia

63
Q

chronic mesenteric ischemia manifests how?

A

painful within an hour after meals when blood flow is needd ..

64
Q

annular pancreas

A

abnormal migration of the ventral pancreatic bud ..

65
Q

annular pancreas patho

A

rare congenital anomaly where the pancreas completely surrounds the second part of the duodenum - can compress the duodenal lumen or obstruct pancreatic drainage

66
Q

what two oral antibiotics can treat clostridium difficile?

A

Fidaxomicin
(macroclyclic antibiotic that inhibits RNA polymerase )

or vancomycin

67
Q

what is fidaxomicin ?

A

macrocyclic antibiotic

68
Q

how do macrolide antibiotics work?

A

inhibiting RNA transcription ..

69
Q

what are other macrolidic antibiotics ?

A

erythromycin, clarithromycin, and azithromycin

70
Q

H2 blockers for decreasing stomach acid like “tidine”s - will do so via what mechanism ?

A

Cyclic cAMP

71
Q

FROM what dermal layer is the spleen derived ?

A

mesodermal

72
Q

ascending colon is on what side?

d

A

RIGHT

73
Q

what are the symptoms of right sided colon adenocarcinoma?

A

occult blood loss
(iron deficiency anemia ..)

plus anorexia and malaise ..

74
Q

What are the symptoms of left sided adenocarcinoma ?

A

left sided colon cancers tent to infiltrate in teh intestinal wall and encircle the lumen .. causisng change in lowel habits like constipation and abdominal pain // nausea and vomiting ..

75
Q

lifstyel factors that increase chance of colon cancer?

A

obesity/ cigs/ red or processed meat // low veggie intake

76
Q

grossly bloody stool. / abdominal discomfort and low grade feer is characterisitc of what?

A

ulcerative colitis …

77
Q

Dyssynergic defication occures when

A

most commonly when the puborectalis muscles fails to relax // or when the interanl or extermal anal sphincter are messed up

normally occures in the elderly but sometimes with neurological disorder

78
Q

Diltiazem

A

non-dihydropyridine calcium channel blocker

79
Q

what are two non dihydropyridine calcium channel blockers?

A

diltiazem/ verapamil

80
Q

side effects of non - dihydropyridine calcium channel blockers

A

constipation

81
Q

rectocele is what

A

when the rectum prolapses into the posterior vaginal wall .. normally develops in the elederly

82
Q

epigastric pain that is worse at night and relieved by eating … ulcer int eh first portion of the duodenum

A

duodenal peptic ulcer disease ..

83
Q

90 percent of duodenal ulcers are caused by whay/

A

H pylori … the others are caused by NSAIDS

84
Q

What are regimens to eradicate H pylori?

A

antibiotics like tetracycline and metronidazole … PPIs like omeprazole .. and bismuth subsalicylate (peptobismol )

85
Q

what are the effects of peptobismol?

A

antibactierial / antiacid / anti-inflammatory

86
Q

elevated conjugated bilirubin levels are suggestive of what?

A

hepatobiliary disease .. cirrhosis or hepattitis ..

becasue teh bilirubin conjugates will relux back inot the plasma when te

87
Q

what is the hepatic metabolism of bilirubin?

A

uptake from teh bloodstream/ storage within the hepatocyte/ conjugation with glucuronic acid / biliary excretion

88
Q

what is bilirubin conjugated with int he liver?

A

glucuronic acid

89
Q

what does unconjugated bilirubin levels indicate ?

A

increased bilirubin formation .. when much of it has been destroyed through hemolysis OR if there is a slowing of the conjugation such as in gilbert syndrome

90
Q

what is gilbert syndrome?

A

familial disorder of bilirubin glucuonidation in wheich the production of UDP glucuronyl transferases is reduced

GI step u world questions (1 decks)

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