GI absorption: Nutrients/Water/Electrolytes Flashcards

1
Q

What are the factors that influence the rate of fluid absorption?

Where does the most/least fluid absoprtion occur?

A

Luminal Osmolality

Rate of active solute transport

Bowel segment (Most fluid absorption - duodenum + proximal small intestine- jejunum; least fluid absorption - colon)

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2
Q

If you ingest hypotonic food, fluid is __ to make things isotonic. Fluid is added to __ food to make things isotonic. All this happens in the __ prior to entering the small intestine.

A

Fluid is removed to make hypotonic food isotonic

Fluid is added to hypertonic food to make things isotonic

Happens in the duodenum

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3
Q

With increasing distance down the GI tract, what is the permeability of water?

A

The farther down the GI tract you go, the lower the permeability to water.

Most permeable: duodenum and jejunum

Least permeable: rectum

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4
Q

Describe the process of neutral sodium absorption in the gut. During which phase in what part if the gut is this type of transport most important?

T/F: This is a major route of salt reabsorption in the colon.

Describe the effect of cAMP on this type of transport

A

Uses apical NCC, NHE3, and AE1 to drive salt inside the cell

True

Increased cAMP transport blocks these channels

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5
Q

Describe how linked transport leads to Na reabsorption

A

Coupled transport of sodium with other things (either SGLT2 or other things like AAs, peptides, fat soluble vitamins etc)

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6
Q

Describe how linked transport is used to treat cholera

A

Na+/Glucose therapy: lots of glucose/little salt >> SGLT2 >> causes solvent drag (water passively follows absorption of solute) >> rehydrate cholera pts

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7
Q

How is calcium absorbed in the gut (hint: there’s 2 ways)? What is the primary absorption site of calcium?

What is the role of VitD in calcium reasborption?

A

calcium enters thru whatever calcium channel>> calbindin traps calcium inside cell (regulates intracellular calcium levels) >> release of Ca2+ to efflux channels

Also absorbed paracellularly

Duodenum = primary absorption site of calcium

Vit D regulates the expression of Ca2+ channels

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8
Q

What is the primary site of absorption for Iron? Describe the process of iron absorption at this site.

What are the roles of ferritin, ferroportin, hepcidin, hephaestin and transferrin? What are the two iron channels involved and what do they do?

How do we get rid of excess iron?

A

Primary site of absorption of iron = proximal small instestine

Ferritin: binds intracellular iron; bound iron is for storage

Ferroportin: Transports iron out of the cell to send it to the bloodstream (via hephaestin ; changes Fe2+ back to Fe3+)

Transferrin: binds Fe3+ and transports it in the bloodstream

Hepcidin: blocks ferroportin which decreases iron reabsorption (prevents iron release)

DMT1 and Heme transporter; DMT1 transports non heme iron/Heme transporter transports heme iron

Shedding of epithelial cells (which will have iron bound to ferritin in them)

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9
Q

What is the body’s response to iron deficiency/iron overload (i.e. of the iron transporters/proteins discussed, which one is upregulated/downregulated and how does that affect iron retention/excretion)

A

Iron deficiency: increased iron uptake (increased transferrin), less iron lost in shedding epithelial cells

Iron overload: decreased uptake (decreased transferrin), more iron lost in shedding epithelial cells

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10
Q

Describe the process of chloride absorption and secretion in the gut.

What is the significance of the CFTR channel? How is it regulated by cAMP levels?

A

Absorption: apical AE1 and NCC involved in chloride reaborption

Secretion: Apical CFTR kicks Cl- out. Increased cAMP levels overstimulate CFTR channel

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11
Q

Describe the changes in chloride absorption in Cystic Fibrosis. How is meconium ileus demonstrative of CF?

A

CFTR channel defect

Loss of cAMP dependent chloride transport

Decreased chloride secretion (water secretion) >> surface membrane drier

Meconium = much drier, which forms pebbles that cause bowel obstruction

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12
Q

What is the mechanism by which Cholera toxin causes secretory diarrhea?

How do you treat cholera?

A

Cholera Tx increases Cl- secretion and inhibits sodium reabsorption

Cholera tx >> increased cAMP levels >> upregulated CFTR >> increased Cl- secretion (water follows) = secretory diarrhea

Treatment: anti-biotics or salt/sugar solution (utilizes SGLT2 mechanism)

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13
Q

What are the differences between the small bowel and the colon with regards to the following?:

permeability gradient

presence of nutrient transporters

effect of aldosterone

glucocorticoids

A

Permeability gradient: small bowel has permability gradient throughout; colon has low permeability throughout

Nutrient transporters: yes in small instestine; not in colon

Aldosterone: no effect in small intestine; increases Na+ absorption via ENaC channels in colon

Glucocorticoids: increase Na uptake in both

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14
Q

Describe the differences in ion absorption in proximal and distal colon

What is the role of amiloride in regulating Na absorption?

What’s the difference between secretory and osmotic diarrhea?

A

Proximal colon: Na+ reabsorption also coupled to short chain fatty acid transport

Distal colon: aldosterone increases # ENaC channels >. increases Na+ reabsorption

Amiloride - diuretic; blocks Na+ absorption via ENaC

Secretory diarrhea: happens when there’s increased ion secretion; Osmotic diarrhea: happens when there’s malabsorption of solutes, which creates high osmotic pressure

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15
Q

Explain the general process of intraluminal digestion. What is the role of the PepT protein?

A

Pancreatic proteases breakdown proteins into di/tri peptides >> transported via PepT into cell >> intracellular di/tri peptidases break down di/tripeptides into amino acids >> aa’s absorbed into portal blood

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16
Q

Explain the general process of luminal digestion

A

(begins in the stomach)

Protein broken down by pepsin >> oligopeptide >> broken down by various enzymes (trypsin/chymotrypsin/carboxypeptidases A,B/elastase)

17
Q

Intraluminal digestion of carbohydrates begins in the mouth via the __ enzyme and continues in the ___. T/F: The process also happens in the stomach.

The a-1-4 linkages in amylose are cleaved by __, turning amylose

into __, and __

A

Salivary amylase

Proximal duodenum

Falsehood. The stomach doesn’t have salivary amylase.

Amylase, maltotriose and maltose

18
Q

Amylopectin is broken down into __, __ and __ by amylase. __ is formed b/c amylose can’t break down a-1-6 bonds. Isomaltase further breaks it down to __ and __.

Describe the process of brush border digestion of carbs

A

Maltotriose, maltose, alpha-limit dextran

Maltose and sucrose

Brush border digestion:

Maltose broken down into 2x glucose

Sucrose broken down into glucose and fructose

Lactose broken down into glucose and galactose

19
Q

Draw and describe the transport of glucose and fructose across an enterocyte (name the transporters and what side they’re on)

A

Apical SGLT1/2: Na+/Glucose or galactose

Apical GLUT5: Fructose

Basolateral: Glucose

20
Q

Explain how insulin regulates the activity of GLUT2

What happens with GLUT2 in between meals vs when glucose conc is high

A

Insulin stops GLUT2 from translocating to the basolateral membrane >> stops glucose absorption into bloodstream

In between meals: GLUT2 translocates to BLM per usual

High glucose conc: GLUT2 translocates to both apical and basolateral membranes to increases glucose uptake

21
Q

Describe the functions of the following lipid enzymes:

Lipase-colipase complex

Phospholipase 2

Cholesterol esterase

A

Lipase-colipase complex: triglycerides >> FAs and monoglycerides

PhosphoLipase 2: lecithin >> FAs and Lysolecithin

Cholesterol esterase: Cholesterol ester >> FAs and Free cholesterol

22
Q

Describe the role of colipase in facilitating lipid break down

A

Colipase frees up the active site of lipase, which can be inhibited by bile acids

23
Q

What is the role of chylomicrons in fat digestion (i.e. what two things make it different from micelles)?

A

Chylomicrons are composed of proteins and fats, so they can package both. They also package and transport things to be transported in lymph vessels, not in the blood stream

24
Q

Fill in the table below the role of colonic bacteria in carbohydrate digestion

A
25
Q

What is the significance of butyrate to colonocytes and cancer prevention?

A

Butyrate is used as a nutrient by colonocytes and also an anti-colon cancer agent

26
Q

Why are deconjugated bile acids potentially harmful?

A

Deconjugated bile acids release taurine, which generates hydrogen sulfide, which is harmful to cells?

27
Q

What are the rate limiting steps for carbohydrate and protein digestion?

What is the rate limiting step for lipid digestion?

A

Rate limiting steps for carb/protein digestion: product transport into cells

Rate limiting steps for lipid digestion: moving products closer to cell membranes via micelles

28
Q

Briefly describe the hydrogen breath test. Give an example disease that this can be used to test for (hint: Susie has this). What causes the symptoms experienced with this disease?

A

Bacterial overgrowth/malabsorption of sugars >> H2 and CH4 gases released >> absorbed into bloodstream and get to lungs >> gases in expired air and measured

Lactose intolerance

The gas released by bacterial digestion of lactose causes symptoms of discomfort

29
Q

What are the sources of colonic gas and of these, which is the most common?

A

Swallowed air

CO2 from carbonic anhydrase

Nitrogen

Bacterial fermentation (produces CH4, CO2 and H2)

Gas diffusion from blood to lumen