Gastroenterology Flashcards

1
Q

Where and how is Vit b12 absorbed?

A
  1. in the terminal ileum
  2. Dietary vitamin B12 requires intrinsic factor, a glycoprotein secreted by the gastric parietal cells, for absorption in the terminal ileum. It is transported in the blood by haptocorrin and transcobalamin.
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2
Q

The presence of hematochezia (bright red blood) is generally associated what?

A

with colonic bleeding, although it may result from a brisk upper bleed.

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3
Q

The presence of melena—passage of black, tarry stools—generally results from what?

A

significant blood loss proximal to the ileocecal valve, including an upper gastrointestinal bleed. The color results from bacterial breakdown of the hemoglobin.

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4
Q

most likely cause of painless rectal bleeding in children >1 year?

A

meckels polyps

diagnose with

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5
Q

how does the addition of starch to ors help with water absorption?

A

fermentation to SCFA that can then be absorbed, yep its a thing. The addition of high-amylose maize starch (HAMS), a microbially-fermentable (or ‘resistant’) starch, to ORS results in delivery of non-absorbed carbohydrate to the colon where it is fermented to SCFA

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6
Q

how is dietary iron absorbed?

A

duodenum and proximal jejunim

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7
Q

where is calcium absorbed

A

predominantly absorbed in the duodenum and upper small intestine

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8
Q

genetic causes of acute pancreatitis?

A
  • Cationic trypsinogen gene (PRSS1)
  • Chymotrypsin C gene (CTRC)
  • Cystic fibrosis gene (CFTR)
  • Trypsin inhibitor gene (SPINK1)
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9
Q

what minimised trypsin activation in the pancreas?

A

the digestic proteases are stored in low calcium (6.3 pH secretory granules - zymogen), protease inhibitors in the cytoplasm also exist. this means they won’t get changed from pro-enzymes to super digesty enzymes.

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10
Q

How do H2 blockers work?

A

they act on the H2 (histamine) for gastric acide secretion in the parietal cells on the GI system (from the enterochromaffin life cells)

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11
Q

How do PPI’s work?

A

They do so by irreversibly inhibiting the stomach’s H⁺/K⁺ ATPase proton pump at the luminal membrane of the parietal cell in the GI tract

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12
Q

why do you check total igA in coeliac screening?

A

if total iGa is low, you can’t count on the EMA anti igA to mean anything, must use other means

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13
Q

what is the ddx for protein losing enteropathy and what would you look for?

A

IBD: symptoms
CHD: heart symptoms/signs
SLE: signs
coeliac: diarrhoea, weight loss, malabsoprtion, check igA and EMA IgA, iron deficiency and anaemia
CVID: check lymphocyte subsets and Ig
Primary intestinal telangectasia: liver function normal, loss of protein, ascites, chronic diarrhea, malabsorption

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14
Q

what are the categories of disorders of malbsorption?

A

A) mucosal

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15
Q

What lipid can be directly absorbed into the hepatic circulation?

A

medium chain fatty acids

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16
Q

what are the extra gastrointestinal manifestations of IBD?

A

Uveitis
Orofacial granulomatosis
Pyodermis gangrnosum, erythema nodosum
Liver: overlap into autoummne hepatitis and primary sclerosing cholangitis

17
Q

what is the gene most highly associated with Crohn disease?

A

NOD2 - stricturing disease

18
Q

What is ABCB4 associated with?

A

progressive familial intrahepatic cholestasis (PFIC or MDR deficiency - high GGT, jaundice, itch).

19
Q

What is a mutation in JAG1 associated with?

A

allagille syndrome & tetralogy of fallot

20
Q

What is a mutation in MYOSB associated with?

A

microvillous inclusion disease (congenital diarrhoea, TPN, IF, SB transplant

21
Q

what is the best way to measure vitamin D and why?

A

of 25-D is the standard method for determining a patient’s vitamin D status.

Vitamin D is transported bound to vitamin D–binding protein to the liver, where 25-hydroxlase converts vitamin D into 25-hydroxyvitamin D (25-D), the most abundant circulating form of vitamin D. Because there is little regulation of this liver hydroxylation step,

22
Q

how does sunlight catalyse vitamin d reaction?>

A

Cutaneous synthesis is normally the most important source of vitamin D and depends on the conversion of 7-dehydrochlesterol to vitamin D 3 (3-cholecalciferol) by ultraviolet B (UVB) radiation from the sun.