13-1: 1/30 - Absorption/malasborption

Front 1

The majority of fluids reabsorbed by the GI tract is __________.

Back 1

Endogenous secretions (saliva, bile, etc.)

Front 2

How much fluid is absorbed (per day) in the:
duodenum
jejunum
ileum
colon

Back 2

Duod/Jej: 5.5 L/day
Ileum: 2L/day
Colon/rectum: 1.3 L/day

Front 3

Crypts vs Villi:
Function
Hydrolytic Activity
Absorption/Secretion

Back 3

Villi: hydrolysis and absorption (breakdown nutrients for absorption)

Crypt: no hydrolytic activity, no absorption, mostly secretion

Front 4

_____ is passively absorbed.

Back 4

EtOH

Front 5

What do electrolyte carriers do? What are their limits?

Back 5

Electrolyte carriers follows [ ] grad, allow to absorb faster than by passive diffusion alone, but can be saturated, and won't work if there's no [ ] gradient`

Front 6

Provide examples of:
uniport
symport
antiport

Back 6

uniport: GLUT-2 (facilitates glucose absorption)

symport: Na+/glucose; Na/K/2Cl- co-transporter (all are absorbed)

Antiport: Cl/HCO3-; Na/H (one in, other out)

Front 7

How does most Na+ absorption occur? Where does it occur?

Back 7

OCCURS IN PROXIMAL BOWEL

Na+ absorbed mostly with Na/H pump:
On lamina propria side of cell, Na+ pumped out, K+ pumped in

On luminal side: Na+ pumped in (there is a drive since cell is pumping out Na+ on lamina side); H+ pumped out while Na+ pumped in from lumen

Water follows sodium.

Requires energy.

Front 8

Describe how most glucose is absorbed.

Back 8

Na/K/ATPase brings Na out of cell into lamina propria

Na+ comes in and glucose follows (cotransporter)

Glucose leaves into lamina propria via GLUT-2 carrier

Front 9

Where and how does electroneutral absorption occur?

Back 9

Ileum: electroneutral

Na/K/ATPase pump out Na+ on basolateral side of cell

Na+ pumped in while H+ pumped out of cell (and into lumen)

HCO3- pumped out into lumen, Cl- absorbed into cell

Allows for electroneutral absorption (Na+ and Cl- neutralize each other); this occurs in brush border in ileum and colon

Front 10

How does passive permeability differ throughout the GI tract?

How does this influence water absorption?

Back 10

Passive permeability decreases as progress more distally; dec'd flux in and out of lumen, need to be greedy and absorb H2O.

Front 11

Describe how Cl- secretion occurs in the intestine.

Back 11

Most secretion through Cl- pump, modified by cAMP

Lamina Propria:
2 Cl- in with 1 K+ and 1 Na+ (Na/K/2Cl- cotransporter)

K+ in, Na+ out via Na/K/ATP-ase

Lumen:
Cl- pumped out into lumen; controlled by cAMP levels. High cAMP-->high Cl- pumped out

Front 12

Via what cells does intestinal secretion occur?

Back 12

Crypt epithelial cells ; Cl- channels on apical membrane, which respond to hormones and NTs

Na+ and H2O follow Cl- passively

Front 13

Describe how HCO3- secretion occurs in the intestine.

Back 13

Lamina Propria:
Cl- OUT into lamina; HCO3- into cell (Na-dependent anion exchanger)

HCO3- INTO cell along with Na+ in (Na+HCO3- co-transporter)

Na+ INTO cell, H+ into lamina propria (Na/H exchanger)

Lumen:
Cl- INTO cell, HCO3- OUT of cell into lumen (exchange carrier)

Front 14

This hormone mediates sodium absorption in the colon.

Back 14

Aldosterone

Front 15

List the following for the three segments of the small bowel:
Secretions
Degree of digestion (High, Med, Low)
Degree of absorption (High, Med, Low)
Specific nutrients absorbed

Back 15

Duodenum:
Secretes CCK, Secretin, GIP, HCO3-

High degree of digestion

High degree of absorption--IRON, nutrients, water, ions

Jejunum:
No secretions
Med level of digestion
Med level of absorption; some ions, nutrients, water

Ileum:
Secretes PYY, HCO3-
Low digestion
Low absoprtion, but absorbs BILE ACIDS, B12, some ions, nutrients, water

Front 16

Antrum vs Duodenum:
Osmolality
pH

Back 16

Antrum: Hyperosmolic; pH ~5-6; emulsified triglycerides

Duodenum:
isoosmotic, pH~7, , micellar lipids

Front 17

Where are most carbohydrates absorbed?

Back 17

Duodenum, absorbed to a lesser extent in distal small bowel

Front 18

How does the luminal contents of the duodenum become isoosmotic?

Back 18

Duodenum is super permeable, fluid will be absorbed to the extent needed to have material in lumen be isoosmotic. PASSIVE PERMEABILITY.

Front 19

What is the role of intraluminal digestion?
Examples of relevant enzymes and products.

Back 19

Intraluminal digestion prepares meal for surface digestion and absorption

Pancreatic secretions:
Proteases (trypson, chymotrypsin, carboxypeptidases-->oligopeptides and aa's)

Amylase (-->maltose, dextrins)

Nucleases (DNAase, RNAase-->nucleotides)

Lipolytic Enzymes (Lipases, Cholesterol esterase, phospholipase A2-->2 monoglyceride and FAs; cholesterol and FAs; lysophospholipid & FAs)

Front 20

Describe the digestion of carbohydrates beginning in the intestinal lumen and ending at the brush order.

Back 20

At level of lumen:
Starch & Complex Carbs-->sucrose, glucose oligomers, lactose VIA salivary and pancreatic AMYLASE

At level of brush border:
Sucrose-->glucose, fructose VIA sucrase

Glucose oligomers-->glucose VIA glucoamylase

Lactose-->glucose, galactose VIA lactase

Front 21

Disaccharide digestion on brush border occurs prior to the absorption of ___________.

Back 21

Monosaccharides (Sucrose has to be broken down into glucose and fructose first)

Front 22

SGLT1:
Role

Back 22

Sodium Glucose Transporter; brings Na+/Glucose/Galactose into cell

Front 23

GLUT5:
Role

Back 23

Brings fructose into intestinal cell

Front 24

GLUT2:
Role

Back 24

Brings glucose, fructose, galactose FROM cell into bloodstream

Front 25

Where is most glucose absorbed?

Back 25

Mostly in duod, some in jejunum, very little in ileum (bc it's all mostly absorbed already)

Front 26

Effect of infectious enteritis on absorption of:
Glucose
Lactose
Sucrose

Back 26

Glucose: no effect; monosaccharide absorption doesn't require hydrolysis by brush border enzymes

Sucrase activity: mildly dec'd

Lactase: severely affected by infectious enteritis (enzymes die on brush border); takes a week or so to replenish after mucosal injury

Summary: not all absorptive functions equally susceptible to mucosal injury

Front 27

Lactose absorption:
Why does it vary between individuals?
How does absorption/secretion differ in someone with lactase deficiency?

Back 27

Genetic variation-->interpersonal variation of lactose absorption (lack lactase)

If lactase deficient, undigested lactose will remain in lumen (can't be absorbed without being broken down) and increases osmotic gradient,

thus, water will be secreted INTO the lumen.

Front 28

Why does lactose produce flatulence and diarrhea in the lactose intolerant?

Back 28

Although patient can't absorb lactose, bacteria in colon can digest it.

When bacteria digest it, they realease water, short chain fatty acids, and CO2 (also release H2, but that's absorbed and exhaled in breath). This is the cause of diarrhea and flatulence.

Note: SCFA production > > > absorption

Front 29

Breath H2 test:
Test
Associated disorder

Back 29

Breath H2 increases after lactose load in LACTASE DEFICIENCY

Front 30

In what situations might carbohydrate-induced diarrhea occur? Explain pathophys.

Back 30

Note: normally CHO in colon broken down into SCFA by bacteria; SCFA then are reabsorbed by colon.

1) Dec'd SCFA Salvage due to Abx (no bacteria available to breakdown CHO into SCFA)
2) CHO over-load! overwhelms bacteria's ability to breakdown CHO to SCFA.

Front 31

Cellulose:
What is it?
Benefits?

Back 31

Dietary fiber; not absorbed.

Increases stool weight and frequency. Nothing else.

Front 32

Effect of duodenal contents on gastric emptying? How?

Back 32

Duodenal contents delay gastric emptying and secretion via CCK, secretin, GIP.

Front 33

What is reactive hypoglycemia?
When is it seen?

Back 33

Gastric surgery sometimes results in removal of pylorus. No longer have precise control/emptying of gastric contents into duodenum.

With gastric surgery, get a large bolus of glucose into duodenum at once. Results in spike of insulin (hyperinsulinemia) followed by a plummeting glucose level (hypoglycemia).

AKA DUMPING SYNDROME

Front 34

Describe the digestion of protein beginning in the mouth and ending as amino acids.

Back 34

Proteins in lumen-->PEPSINS & PANC PROTEASES-->oligo and aa's

aa's-->absorbed

oligopeptides-->BRUSH BORDER PEPTIDASES-->dipeptides and tripeptides

dipeps and tripeps absorbed-->intracellular CYTOPLASMIC PEPTIDASES-->aa's

Front 35

Describe the transporters necessary to bring amino acids and dipeptides into cells.

Back 35

Na+/aa co-transported into cell

Dipep or Tripep/H+ co-transported into cell

H+/Na+ pump keeps H+ extracell to create gradient

Front 36

Where does most protein absorption occur?

Back 36

It occurs slowly throughout ALL of small intestine

Should be very little protein in feces.

Front 37

The majority of human pancreatic secretory proteins are _________.

Back 37

proteases

Front 38

What is cystinuria and how does it occur?
Effects?

Back 38

Basic aa's (L-arg) aren't absorbed properly (by kidney/intestines)
Can still absorb di/tripeptides which can contain arginine
but pts often get kidney stones, cystine in urine

Front 39

What is Hartnup disease and how does it occur?
Effects?

Back 39

Can't absorb neutral aa's (L-phen); asyx with adequate nutrition

but can be assocd w/dec'd synth 5HT, melatonin, niacin-->pellagra; ataxia, psychosis

Front 40

Briefly describe the digestion of fat beginning with the stomach and ending with mixed micelles.

Back 40

Stomach (some emulsion):
Oil-->GASTRIC LIPASE-->Monoglycerides, FFAs

Duodenum (after CCK release):
Oil-->BILE ACID + Co-lipase + Lipase (pancreatic)-->Emulsion-->Mixed Micelles (fatty inside, polar outside--SOLUBLE)

Note: lipase, phospholipase A2 and cholesterol esterase activities are enhanced by bile acids.

Front 41

Describe the transport of fat into the intestines and then into the bloodstream.

Back 41

2-monoglyceride and FFA's readily pass into cells, recombine to form TG, then chylomicrons (w/apolipoprotein)

Chylomicrons then enter LYMPHATICS.

No specific transporters necessary!

Front 42

Causes of steatorrhea.

Back 42

Pancreatic insufficiency
Hyperacidity o gastric-->duodenal contents
DEFICIENCY OF BILE SALTS (ileal resection)
Celiac disease (may have generalized malabsorption)
Dec'd chylomicron/apolipoprotein transport or synthesis (abetalipoproteinemia, lymphatic obstruction)

Front 43

D-Xylose:
Test
Diagnostic utility

Back 43

d-Xylose admin-->should find normal amounts the sugar in blood and urine (assess CHO absorption)

Helps distinguish between maldigestion and malabsorption

In maldigestion (pancreatic insuff):
Fecal fat will have high d-xylose; with normal d-xylose excretion and normal jejunal bx

In malabsorption (Celiac):
Fecal fat: inc'd d-xylose
d-xylose excretion dec'd
jejunal bx: abnl villi

Front 44

Haptocorrin:
Role

Back 44

Binds B12 in mouth (it's produced by salivary glands), protects and transports it to small bowel where it is given to IF.

Note: pancreatic proteases degrade haptocorrin to release B12 into the lumen.

Front 45

Describe iron absorption.

Back 45

Most dietary iron is ferric (Fe3+), which is insoluble

It's reduced to ferrous iron (Fe2+) by gastric acid and ferric reductase, located on absorptive surface.

Uptake regulated at enterocyte via DMT1 transporter. Leaves enterocyte via ferroportin. Bound by plasma transportin.

Front 46

Where does most iron absorption occur?

Back 46

Duodenum

Front 47

Describe how and where calcium absorption occurs.

Back 47

Mostly in duodenum, but occurs throughout gut.

Passive and paracellular transport across tight jns following electrochemical gradient.

Transported across cell by calbindin.

Extruded across basolateral membrane via Ca2+ APTase and Na/Ca exchanger.

REGULATED BY 1,25(OH)2 Vit-D

Front 48

Effects of jejunal resection.

Back 48

Slight dec in fat absorption, fluid/electrolyte absorption; MILD dec'd protein absorption

NORMAL sugar absorption

Front 49

Effects of ileal resection.

Back 49

MODEST decrease in fat abs, bile acid abs, B12 abs

Front 50

Effects of extensive small bowel resection.

Back 50

DRAMATIC dec in fat abs

Modest dec in protein abs, bile acid abs, B12 abs, fluid/electrolyte abs

Front 51

Effects of colon resection.

Back 51

Mild dec in fluid and electrolyte abs; normal otherwise

Front 52

Causes of weight loss with aging.

Back 52

-nutrient deficiencies
-biological senescence--inc'd body fat, reduced muscle mass
-dec'd energy requirements, reduced intake of protein; anorexia
-dec'd Ca2+ absorption w/age

Front 53

Effect of increased propulsive activity in intestines.

Back 53

Dec'd contact time of nutrients/fluid with villi-->DIARRHEA

Front 54

How does E. Coli cause diarrhea?

Back 54

E. Coli produces heat stable enterotoxin, stimulates guanylate cyclase-->inc cGMP-->inhibits neutral NaCl absorption and increases anion secretion

Front 55

Common causes of osmotic diarrhea.

Back 55

Poorly absorbed luminal osmols:
Lactose (lactase deficiency)
Sorbitol (chewing gum)
Na-Sulfate Lavage (Fleet phospho soda)
Mg Citrate

Front 56

Osmolar gap:
What is it?
Diagnostic utility?

Back 56

In osmotic diarrhea, diarrhea will be isosmolar, but Mg2+ (or whatever osmole is causing diarrhea) will displace Na+ and K+ (these will be dec'd)

Will result in osmolar gap! 2 x(Na+ + K+) will be less than normal osmolality.

in short, helps distinguish osmolar and secretory diarrhea

Front 57

How does a VIPoma result in diarrhea?

Back 57

Activates adenylalte cyclase linked to VIP receptor (via stimulatory G-protein)

Inc cAMP-->inc'd anion secretion (Cl-, H2O follows) into lumen
Dec'd neutral NaCl absorption

Front 58

How does cholera result in diarrhea?

Back 58

Cholera toxin binds membrane receptor, enters cell, activates adenylate cyclase

Inc'd cAMP-->inc'd anion secretion, dec'd neutral NaCl absorption

Front 59

How does bile acid diarrhea occur?

Back 59

Ileal resection (dec'd bile abs) or inc'd bile acids-->diarrhea

Front 60

C. difficile:
Toxin A vs Toxin B

Back 60

Toxin A directly increases epithelial permeability, stimulates net secretion

Toxin B: has greater inflammation induced cytotoxicity, but does not directly affect epithelium. Does not stimulate net secretion.

Front 61

How does inflammation induce diarrhea?

Back 61

Inc'd secretion, dec'd absorption

Stimulation of enteric nerves causing propulsive contractions, stimulated secretion

Mucosal destruction, inc'd perm

Nutrient malabs, maldigest

Front 62

What causes of diarrhea result in both secretory and osmotic diarrhea?

Back 62

Zollinger-Ellison

Celiac

Front 63

How does Zollinger-Ellison Syndrome cause diarrhea?

Back 63

Stimulated gastric acid increases fluid load

Acidified small bowel inactivates panc enzymes and injures epithelium

Inc'd panc NaHCO3- and fluid secretion

Maldigestion and malabsorption-->diarrhea and steatorrhea

Front 64

How does Celiac Sprue result in diarrhea?

Back 64

GLUTEN-->

1)Dec'd brush border hydrolase-->unabsorbed osmols

2)Villous atrophy (fluid, nutrient, electrolyte malabs)

3)Crypt hyperplasia (inc'd endogenous secretion)

4) inflammation induced secretion

Front 65

Osmotic vs Secretory Diarrhea:
Volume
Osmolar Gap
Sodium
pH (in children)

Back 65

Osm, Sec:
Vol: 200-500, >>500
Osm: (+) osm gap, (-) osm gap
Na+: <70 mEq/L, >70mEq/L
pH: <5, >6

Front 66

C. Difficile:
Tx

Back 66

Vanco or Metro

Front 67

Giardiasis:
Tx

Back 67

Metro

Front 68

VIPoma:
Tx

Back 68

Resection or octreotide

Front 69

Oral Replacement Solutions:
MOA

Back 69

Provide glucose, starch, sodium for absorption.

Secretion is unaffected, diarrhea may persist.