GI digestion and absorption Flashcards

1
Q

blood supply to intestinal villus

A

Each villus has n arteriole which divides into capillaries beneath epithelial cells. Each villus has a venule and a lacteal too

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2
Q

Where is protein digested

A

stomach, intestine, Brush border, intracellular peptidases

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3
Q

protein digestion in stomach

A

pepsin breaks down into small peptides.

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4
Q

protein digestion in small intestine

A

pancreatic proteases trypsin, chymotrypsin, carboxypeptidase, elastase break down into oligopeptides, di/tri peptides, amino acids.

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5
Q

protein digestion in brush border

A

•Peptidases break down oligopeptides into amino acids, dipeptides, tripeptides

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6
Q

protein digestion intracellularly

A

•Peptidases in the enterocyte can break down di/tri-peptides into amino acids

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7
Q

safeguard to control activation of proteases

A

Trypsinogen is activated by enterocyte bound enterokinase into trypsin > trypsin activates chymotrypsinogen into chymotrypsin > chymotrypsin activates proelastase into elastase > elastase activates procarboxypeptidase A into carboxypeptidase A > CPA activates procarboxypeptidase B into carboxypeptidase B

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8
Q

Protein absorption mechanisms

A
  1. Sodium dependent co-transporters that utilize the N+/K+ ATPase gradient are the major route for the different classes of amino acids. Water follows. 2. Sodium independent transporters of amino acids. 3. Specific carriers for small peptides (di- and tri-) linked to H+ uptake (co-transporter; example is PEP T1). 4. Pinocytosis of small peptides by enterocytes (infants)
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9
Q

Which lipids are essential fatty acids

A

Linoleic acid which is converted to arachidonic acid and alpha-linolenic acid (all are fatty acids)

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10
Q

Where are bile acids made

A

Primary bile acids are produced in the liver from cholesterol – cholic acid & chenodeoxycholic acid. Secondary bile acids are formed by bacteria in the intestines & colon

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11
Q

Bile recycline

A

•Bile is recycled during a meal by uptake in the distal ileum – enterohepatic circulation

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12
Q

How do bile salts facilitate absorption of fats

A

formation of micelles

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13
Q

summarize lipid digestion steps

A

lingual and gastric lipase > pancreatic lipase (triglycerides into free fatty acids) > bile salts solubilize fat into micelles > free fatty acids transported into enterocytes > triglycerides resynthesized and chylomicrons formed > released into lacteal

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14
Q

How are fat soluble vitamins absorbed

A

absorbed along the length of the small intestines and are carried in micelles and form chylomicrons similar to dietary lipids.

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15
Q

how are water soluble vitamins absorbed

A

•enter the enterocyte by simple diffusion (biotin, folic acid) or via specific transporters (e.g. Vit B12)

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16
Q

Compare absorption and secretion at the intestinal crypts vs villi

A

•There is a net fluid secretion from cells in the intestinal crypts and a net fluid absorption from enterocytes on the villi. Villi surface area > crypt surface area

17
Q

Describe absorption of water in intestines

A

follows movement of solutes- paracellular and/or transcellular. Colon has lowest paracellular permeability b/c water movement is linked to transcellular ion movement

18
Q

Where does the majority of secretion and absorption of fluids occur

A

secretion: stomach. Absorption: jejunum

19
Q

Where/how is sodium absorbed

A

•Absorbed all along the intestine, with most absorption in the jejunum (60-80%). Na/K ATPase gradient established. Mechanism via Na+/glucose & galactose or Na+/amino acid cotransport, NaCl cotransport, Na+/H+ exchange or passive diffusion via epithelial sodium channels (ENaC)

20
Q

Function of carbonic anhydrase

A

converts CO2 and water to H2CO3, which is then broken down to H ion and HCO3-

21
Q

Chloride absorption

A

Proximal intestines: passive due to loose TJs, offsets Na charge in intercellular space. Distal ileum and colon: Less leaky TJs, Cl/bicarb exchanger offsets acids produced by bacteria

22
Q

Potassium absorption

A

passive. Paracellular movement in jejunum, transcellular in colon. K is normally high in cells due to Na/K pump, but a gradient is established as luminal water decreases on approach to the colon, with passive flux of K into cells.

23
Q

Calcium and magnesium absorption

A

Ca++ and Mg++ compete for uptake by the cells. Ca++ enters enterocyte passively down its electrochemical gradient in proximal intestines. Ca ATPase pumps Ca out to the blood

24
Q

Vitamin D function

A

Synthesized in skin or absorbed by intestine. Stimulates uptake of Calcium by increasing Ca binding proteins and Ca ATPase molecules

25
Q

Iron absorption

A

regulated in proximal intestines. Transported as either heme or Fe. Two fates: binds to apoferritin to form ferritin that stays in the cell and is lost when the cell dies OR binds to transferrin (carrier protein), leaves the cell and goes into the blood

26
Q

Causes of diarrhea

A

motility disorders or osmotic diarrhea (celiac disease, lactose intolerance) or secretory diarrhea (ie. cholera)

27
Q

How does cholera cause secretory diarrhea

A

•Increases cAMP levels in cells and this in turn activates the CF chloride channel, (and thus water) on the luminal surface

28
Q

How does oral rehydration therapy work

A

•antibiotics plus KHCO3 to prevent hypokalemia and metabolic acidosis, glucose (or amino acids) with NaCl to facilitate the absorption of electrolytes and water

29
Q

chronic pancreatitis

A

deficiency of pancreatic enzymes

30
Q

Cysteinuria

A

genetic absence/defect of the Na+-amino acid transporters.

31
Q

Hartnup disease

A

genetic absence/defect of the neutral amino acid transporter

32
Q

steatorrhea

A

excessive loss of fat in stool due to fat malabsorption disorders such as liver disease (bile salt deficiency), pancreatic insufficiency, or weight loss meds

33
Q

pernicious anemia

A

impaired absorption of B12