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FHB - GI/Metabolism - Exam 3 > Lecture 8 - 9 > Flashcards

Lecture 8 - 9 Flashcards

1
Q

What are the two paths of absorption?

A

Cellular path
- the substances enter the intestinal epithelial cells via the apical (luminal membrane) and are extruded via basolateral membrane to enter blood.

Paracellular path
-substances move across the tight junctions, through the lateral interspaces into blood.

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2
Q

What is the only substance that is absorbed through the intestinal epithelial cells?

A

Only monosaccharides are absorbed through the intestinal epithelial cells.

Monosaccharides are: glucose, fructose and galactose.

-Carbohydrates constitute ~50% of typical American diet.

Carbohydrates ingested are polysaccharides, disaccharides and very little amount of monosaccharides.

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3
Q

Starch is made up of both straight and branched chain polymers.

What are the:

  1. Straight chain
  2. Branched chain
A
  1. Straight –> AMYLOSE

2. Branched –> AMYLOPECTIN

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4
Q

What are the 3 disaccharides in food?

What are these disaccharides composed of?

A

The disaccharides in food are:

  1. trehalose
    - 2 glucose molecules
  2. sucrose
    - glucose + fructose
  3. lactose
    - glucose and galactose
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5
Q

Why is cellulose not digested?

What other molecule cannot be digested?

A

No enzymes to hydrolyze the beta 1,4 linkage of cellulose
- it is excreted

and branched chain of GLUCOSE
- contains alpha 1,6 linkage
alpha amylase does NOT break this down
(breaks down the straight chain)

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6
Q

What does alpha amylase hydrolyze, specifically?

A

hydrolysis of α 1,4 linkage only

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7
Q

What are the 3 products of glucose breakdown?

A

Breakdown of glucose produces:

  1. maltose
  2. Maltiotriose
  3. Alpha Limit Dextrins
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8
Q

Which amylase is most significant? Salivary alpha amylase or pancreatic?

What does it break down?

A

Pancreatic!

Pancreatic amylase (most significant) digests internal α-1,4-bonds in starch
 – yields a mixture of dissacharides, trissaccharides, and oligosacharides (alpha limit dextrin)
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9
Q

What are the following broken down into? Where???(test)

  1. α-limit dextrins
  2. maltOse
  3. maltotriose.
A

These disaccharides are further digested to monosaccharides by intestinal BRUSH BORDER enzymes:

  1. alpha-dextrinase
  2. Maltase
  3. Sucrase
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10
Q

Describe the breakdown from starch to glucose

A
  1. alpha amylase breaksdown starch into:
    - α-limit dextrins, maltose, maltotriose
  2. These contents are broken down at the brush border by the enzymes into:
    - α dextrinase
    - maltAse
    - Sucrase

(ose converted to ase)

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11
Q

What 3 disaccharides do not require amylase digestion?

A

trehalose, sucrose and lactose

Trehalose – digested by trehalase – two molecules of glucose.

Lactose - digested by lactase – glucose and galactose.

Sucrose - digested by sucrase – glucose and fructose.

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12
Q

What transporter transports glucose & galactose against their concentration gradients?
How?

How are these then transferred across the basolateral membrane?

A
  1. SGLT1
  2. coupled with Na

THE ONLY TRANSPORTER THAT RELIES ON SODIUM on the LUMINAL side cotransport

  1. facilitated diffusion via GLUT2
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13
Q

How is FRUCTOSE transported across apical & basolateral membranes?

A

Fructose - transported across apical & basolateral membranes by facilitated diffusion

GLUT5 (apical) - fructose specific
GLUT2 (basolateral).

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14
Q

What is the main issue with lactose intolerance?

What is the main problem?

How is this treated?

A
  1. lack/deficiency of LACTASE IN THE BRUSH BORDER
    - lactose is not digested to glucose & galactose
  2. lactose remains undigested and unabsorbed in the intestinal lumen and retains water causing OSMOTIC diarrhea
  3. Bacterially derived enzyme in tablet form to digest lactose
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15
Q

What is the more serious form of lactose intolerance?

Why?

How is this treated?

A

Congenital lactose intolerance (lack of jejunal lactase)– rare and very serious.

  • ESPECIALLY FOR NEWBORNS

–> energy deficiency and loss of water (dehydration)

Replace lactose with a sucrose or fructose diet to avoid diarrhea and its consequences

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16
Q

The following describes what?

Due to mutation of SGLT1 – very rare.

Can result in severe diarrhea and its consequences.

Fructose diet is recommended.

A

Glucose-Galactose mal-absorption

  • same symptoms as lactose intolerance
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17
Q

Where does protein digestion BEGIN?

Where is it completed?

A

Stomach, with the action of PEPSIN
(inactivated once the pH is too high –> intestine)

It is completed in the small intestine with pancreatic and brush-border proteases.

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18
Q

What is the difference in function of endopeptidases and exopeptidase?

A

Endopeptidases – hydrolyze the interior peptide bonds of proteins-
Example – pepsin, trypsin, chymotrypsin, elastase.

Exopeptidases – hydrolyze one amino acid at a time from the C-terminal ends of proteins and peptides - Example - carboxypeptidases A&B.

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19
Q

What is the key enzyme required for protein digestion?

A

ENTEROKINASE!!!

converts trypsinogen to trypsin

  • trypsin activates all other proenzymes
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20
Q

When is pepsinogen released?

When is it converted to pepsin?

When is pepsin inactivated?

Is this ESSENTIAL for protein digestion? Why or why not?

A
  1. meal in the stomach causes gastric CHIEF cells to secrete pepsinogen
  2. at low pH converted to PEPSIN
  3. Inactivated in DUODENUM due to higher pH (bicarbonate)
  4. NOT ESSENTIAL
    - since in people whose stomach has been removed or who do-not secrete gastric H+, have normal protein digestion and absorption.
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21
Q

What is the first step in INTESTINAL protein digestion?

A

Activation of trypsinogen into trypsin by ENTEROKINASE (brush border enzyme)

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22
Q

Which of the following are absorbable? Which are not?

  1. AAs
  2. Dipeptides
  3. Tripeptides
  4. Oligo-peptides
A

All are absorbable EXCEPT OLIGO-PEPTIDES

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23
Q

The activation of trypsin results in the activation of what 5 enzymes?

A 
trypsin
chymotrypsin
elastase
carboxypeptidase A
carboxypeptidase B
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24
Q

What do peptide transporters uptake?

What do they work in symport with?

How do all amino acids exit the cell?

A
  1. Uptake DRUGS
  2. H+
  3. Exit via facilitated diffusion
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25
Q

Define the main issue with the following:

  1. Single AA absorption
  2. Trypsinogen deficiency
  3. Cystinuria
A
  1. Single AA absorption
    - partially or completely compensated by absorption of di- and tri- peptides that will have their AAs hydrolyzed by enzymes in the cytoplasm of epithelial cells
    - OTHER TRANSPORTER to transport the amino acid if one is defective
  2. Trypsinogen deficiency
    - RARE + serious –> diet of partially hydrolyzed proteins
  3. Cystinuria
    - deficiency of cysteine transporters –> can lead to KIDNEY STONES
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26
Q

What are the major categories of lipids in the diet?

A

Triglycerides (major pool)**

Phospholipids
Cholesterol
Vitamins A, D, E and K (not lipids but fat soluble)

27
Q

How are lipids absorbed in the Gi tract if they are insoluble in water?

A

Emulsified and processed into chylomicrons

28
Q

What process increases the surface area for lipolytic enzymes?

A

Emulsification

29
Q

What are the emulsifying agents:

  1. In the stomach
  2. In the small intestine
A
  1. In the stomach
    - dietary proteins & INTENSE MOTILITY
  2. In the small intestine
    - BILE ACIDS
30
Q

What cells release GASTRIC LIPASE?

A

Gastric Chief Cells

  • hydrolyze 10% of dietary triglycerides
  • lipid digestion begins in the STOMACH
  • CCK slows down gastric emptying so that chyme can be slowly emptied and full lipid digestion occurs
31
Q

Where does most lipid digestion occur?

A

Small intestine (duh, gall bladder contracts)

Bile acids together with lysolecithin and products of lipid digestion surround and emulsify dietary lipids.

32
Q

What are the 3 important lipolytic enzymes that can work at a neutral pH?

A
  1. Pancreatic lipase
  2. Phospholipase A2
  3. Cholesterol Ester Hydrolase

LIPASE IS THE FIRST TO BE AFFECTED BY CHANGES IN pH
– see fatty stool & stetorrhea

33
Q

What is important for the re-activation of pancreatic lipase after bile acids inactivate pancreatic lipase?

PARADOXICAL action of Bile Acids is to inactive the pancreatic lipase by competing for a spot on the lipid

A

Cofactor Colipase
-Colipase binds to both bile acids and lipase
– anchors lipase to the fat droplet even in the presence of bile acids.

Pancreatic lipase
Hydrolyzes triglycerides to monoglycerides and fatty acids.

34
Q

What activates Phospholipase A2?

What is its function?

A
  1. Activated by TRYPSIN (secreted as proenzyme)

2. Hydrolyzes phospholipids into lysolecithin and fatty acids

35
Q

What is the function of Cholesterol Ester Hydrolase?

A

Cholesterol ester hydrolase
Hydrolyzes cholesterol ester to free cholesterol and fatty acids

  • also hydrolyzes ester linkages of triglycerides, producing glycerol.
36
Q

Define which molecule is responsible for the digestion of the following:

  1. Triglyceride
  2. Cholesterol Ester
  3. Phospholipid
A
  1. Triglyceride
    - Pancreatic Lipase
    - lingual lipase
    - gastric lipase (needs low pH)
  2. Cholesterol Ester
    - Cholesterol Ester Hydrolase
  3. Phospholipid
    - Phospholipase A2
37
Q

What are the 3 products of lipid digestion?

How are they solubilized in the intestinal lumen? (in what form?)

A
  1. Monoglycerides
    Fatty Acids
    Cholesterol
  2. form Mixed Micelles
38
Q

What is found in the CORE of the micelle?

In the exterior?

A

core = products of lipid digestion (hydrophobic)

outer = Ampiphatic (hydrophillic & hydrophobic) bile salts

39
Q

How do we absorb the products of lipid digestion?

A

MICELLES

  • hydrophobic inside = BILE ACIDS
  • hydrophilic outside = water soluble
40
Q

What happens to the micelles after the hydrophobic contents are absorbed?

A

Diffuse to the apical membrane of brush border epithelium

  • lipids released from micelles at apical membrane
  • micelles DO NOT ENTER THE CELL
  • Bile salts are left in intestinal lumen & reabsorbed in the ileum
41
Q

What happens to lipid digestion products INSIDE the cell?

What happens once they are packaged with APOPROTEINS?

A

Re-esterified with free fatty acids on smooth ER

  • form triglycerides, cholesterol ester, and phospholipids AGAIN
  1. form CHYLOMICRONS
    (triglyceride and cholesterol in the core, apoproteins outside)
42
Q

Describe the structure of the chylomicron.

How are they transported?

How are they returned to the bloodstream?

A

CHYLOMICRONS

triglyceride and cholesterol in the core, apoproteins outside

  1. since so large, transported via LYMPHATIC capillaries
  2. Thoracic duct that empties into the blood stream
43
Q

What are the 2 causes we discussed of Pancreatic Insufficiency?

What is the result?

A
  1. disease of exocrine pancreas = Chronic Pancreatitis (no LIPASE)

or Cystic Fibrosis

  1. Pancreatic enzyme secretion is deceptive and thus lipid digestion and absorption is affected

= STEATORRHEA (fatty stools)

44
Q

If the acidity of duodenal contents increases, what is the result? (which specifically)

What are 2 reasons that the acidity would increase?

A
  1. Pancreatic enzymes cannot function –> LIPASE will be affected
    & PEPSIN
  2. Gastric PARIETAL cells secrete excessive H+ (zollinger-ellison syndrome)
  3. Pancreas doesn’t secrete enough HCO3- to neutralize acidic chyme
45
Q

What occurs if there is a deficiency in BILE salts?

A

No micelle formation

  • lipid digestion/absorption is affected
    ex: ileal Resection –> enterohepatic circulation of bile is interrupted and thus lost in feces
46
Q

What is Abetalipoproteinemia?

A

Failure to synthesize Apo B

– chylomicrons are either not formed or are unable to be transported into lymph.

47
Q

Describe the mechanism of absorption of Lipids from the micelles to the chylomicrons (4)

A
  1. Micelles form with bile salts in intestinal lumen
  2. Diffusion of fatty acids, monoglycerides, and cholesterol into the cell
  3. Re-esterification in cell to triglycerides and phospholipids
  4. Chylomicrons form in the cell and are transferred to the lymph
48
Q

Where is the majority of fluid reabsorbed?

If absorption is disturbed, what is the result?

A
  1. Small intestine (7L)
    - minor in Colon (2L)
  2. Diarrhea

1-2L fluid/day comes from oral intake. Additional 8L is supplied by stomach, small intestine and the associated organs.

49
Q

What are the 2 routes of fluid & electrolyte reabsorption in the intestine?

Where are tight junctions most permeable/leaky?

Least?

A
  1. Paracellular
    - between TIGHT JUNCTIONS
  2. Transcellular
    - through the epithelial cells
  3. Leaky = SMALL INTESTINE (paracellular)
  4. Tight = COLON
    - no paracellular movement
50
Q

What is the major site of Na absorption in the small intestine?

  1. Duodenum
  2. Jejunum
  3. Ileum

What transporters are used on the apical side? (3)

A

JEJUNUM

  1. Na+ -monosaccharide cotransporters
  2. Na+ -amino acid cotransporter
  3. Na+ -H+ exchanger

H+ secreted (via Na-H)
and HCO3 - is reabsorbed into blood

51
Q

What additional transporter does the Ileum have, in addition to the ones located in the jejunum?

Na+ -monosaccharide cotransporters

Na+ -amino acid cotransporter

Na+ -H+ exchanger

A

Cl-HCO3 - exchanger! (apical)

  • both H+ and HCO3- are secreted on the APICAL side
52
Q

What is the net function in the ileum and in the jejunum (individually)

  1. Secretion
  2. Absorption

Of what?

A

Ileum:

Net absorption of NaCl

Jejunum:
NET absorption of NaHCO3-

53
Q

Describe the following for the intestine:

  1. Which epithelial cells secrete fluid & electrolytes? Which absorb
  2. Which unique channels are found on the basolateral side?

Are CFTR channels present?

A
  1. Intestinal CRYPTS
    - secrete fluid & electrolytes

Villi = absorb

  1. Na -K - 2Cl
    & NA-K ATPase

YES, chloride channels that allow chloride to diffuse into the LUMEN

54
Q

Because Cl- channels (CFTR) in the intestine are usually closed, what activates them?

What second messenger is released from the crypt cells?

A

Hormones:

  1. Ach & VIP
    - activate AC
  2. 2nd messenger = cAMP
    - cAMP opens the Cl- channels and causes Cl- secretion.
55
Q

Describe what is hyper-activated in CHOLERA.

A

Adenylyl Cyclase is highly activated

  • activates cAMP
  • opens CFTR Cl- channels to secrete Cl

(water and solutes follow)
= overwhelming diarrhea and thus DEHYDRATION

56
Q

What causes the following diarrhea:

  1. Osmotic
  2. Secretory

What are the major causes of both?

A
  1. Osmotic
    - presence of non-absorbable solutes (LACTASE deficiency)
  • lactose is not digested to glucose & galactose
  • undigested glucose is osmotically active thus absorbs water and causes osmotic diarrhea
  1. Secretory
    ex: Cholera
    - caused by excessive secretion of fluid by crypt cells (cl- channels overly active due to active A.C.)

Major cause = overgrowth of enterohepatic bacteria

Vibrio Cholerae or Escherichia Coli

57
Q

How is Na transport in the small intestine and colon different?

A

Colon: passive diffusion
(stimulated by aldosterone)

Small intestine: na-sugar cotransport, Na-AA cotransport, Na-H exchange

58
Q

What is needed to convert inactive for of calcium (D3) to the active form 1,25 - dihydroxycholecalciferol?

A

PTH!

59
Q

What does the active form of vitamin D produce?

What is the purpose of this protein?

What are two cases of inadequate calcium absorption?

A

calbindin D-28K

  • binds to calcium and maintains the electrochemical gradient necessary for calcium to passively diffuse into the cell

(low intracellular calcium)

  • pumped out via Ca-ATPase
  1. Rickets (children)
  2. Osteomalacia (adults)
60
Q

What protein is crucial for calcium absorption? What produces this protein?

A

calbindin D-28K

1,25-dihydroxycholecalciferol

61
Q

What cells are necessary to produce IF factor?

A

Parietal Cells!

secrete IF and H+

62
Q

What cells are lost in a Gastrectomy?

Thus, what is not released?

What clinical issue can this deficiency lead to?

A
  1. Parietal cells
  2. IF factor
    - no vitamin B12 absorption (COBALAMIN)
  3. Pernicious anemia
    * * need vitamin B12 injections to prevent this**
    - oral route will not work since there is no IF!!
63
Q

Where in the small intestine is vitamin B12 absorbed?

What is required?

A

Ileum

IF!!

  • vitamin B12 is released from food (by pepsin) and binds to R proteins
  • pancreatic proteases in the duodenum degrade R proteins and vitamin B 12 is transferred to IF (secreted by parietal cells)
  • the body needs vitamin B12 to make RBC’s You get this vitamin from eating foods such as meat, poultry, shellfish, eggs, and dairy products.

FHB - GI/Metabolism - Exam 3 (21 decks)

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