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Physiology GI > Physiology 1.30.13 Intestinal Absorption > Flashcards

Physiology 1.30.13 Intestinal Absorption Flashcards

1
Q

What part of GI tract is food absobed?

A

Small Intestine

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2
Q

what is Celiac Spprue :

A

problems with absoprtion of nutrients with patients

Sensitive to gluten –> increase destructino of SA

Susspetivele to destuction of cell divison
normall

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3
Q

How often is epithelium changed

A

changed every 5-7 days

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4
Q

What happened to man that was poisoned with Polonium?

A

Destroyed/damaged epithelial cell–> died

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5
Q

What is the stored form of animal carbs called? What are its branches like?

A

Glycogen

alpha1,4, and alpha 1,6

Higlhly branched

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6
Q

What is vegetable form of stored carbs?

A

Starch! 45-60% of dietery CHO

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7
Q

What are types of vegetbal carbe

A

Amylose (alpha 1,4) linear

Amylopectin alpha 1.4 and alpha 1.6

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8
Q

How are sugars linked in Amylose

A

Linear

Alpha 1,4

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9
Q

How is Amylopectin linked

A

Alpha 1,4; alpha 1.6

Not as much alpha 1,6 linkages as glycogen

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10
Q

What two sugars make up Sucrose

A

Glucose and Fructose

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11
Q

What two sugars make up Lactose

A

Glucose and galactose

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12
Q

Where can fructose be found?

A

In Fruit

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13
Q

What is role of amylase? What organs secrete amylase

A

Amylase is secreted as an active enzyme

It is released from Mouth, and released during hewing to break down carbs (Salivary Amylase)- secretion from exocrine pancreatic acinar cells

It is also secreted by PANCREASE (pancreatic amylase) and is stimulated by CCK

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14
Q

What hormone stimulates the release of pancreatic amylase

A

CCK

Secretion from exocrine pancreatic acinar cell

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15
Q

What can alpha amylase cut??? is it an exoenzyme or endoenzyme

A

It is an ENDOENZYME!! –> MONOSACCHARIDES ARE NOT generated

Glucose is never the product of amylase activity

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16
Q

Can alpha amyloase break terminal alpha 1,4 linkages?

A

NO!

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17
Q

Can alpha amylase reak down adjacent 1,4 linkages

A

NO!

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18
Q

Can alpha amylase break down brnaching 1.6 linakges

A

NO!

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19
Q

Can alpha-amylase breakdown terminal alpha-1,4 linkages?

A

NO!

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20
Q

What is cellulose

A

Major polysachaide in plants

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21
Q

What is the linkage of Cellulose

A

Beta-1,4 linkages

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22
Q

Can amylose breakdown beta 1,4 linakes? why or why not?

A

NO! B/c amylase can’t break down beta linakges

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23
Q

How is CHO digestion completed?

A

by membrane bound enzymes

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24
Q

Lactase

A

breaks down lactose –> glucose + Galactose

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25
Q

Maltase

A

Can break down TERMINAL alpha-1,4 linakges

Breaks down alpha-dextrins –> Glucose
Will generate single glucose molecule

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26
Q

Sucrase

A

Sucrase

Breaks down Sucrose –> Glucose + Fructose

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27
Q

Isomaltase

A

Breaks down alpha-dextrins –> Glucose (

Only enzyme to breakdown alpha 1,6 linkagesW

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28
Q

what is the only enzyme that breaks down alpha-1,6 enzymes

A

Isomaltase

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29
Q

Lactose Intolerance

A

Nearly all infants and children are able to digest lactose

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30
Q

When does lactase activity decrease

A

after weaning (time course dependent on hereditary factors)

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31
Q

What causes lactase deficiency

A

it is autosomal recessive (3% Danes are LI
97% Thais are LI)

therefore thais probably have less milk in diet

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32
Q

What happens when lactose is ingested bu there is no lactase activity (or activity is deficinet)

A

Lactase-deficient individuals hyrolyze less lactose to glucose

bacteria product form lactsoe breakdown –> Hydorgen

Lactase goes into Large Intestine, not absorbed by SI

Colonic bacteria metabolize lactose to yield H2

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33
Q

What sugars does SGLT1 bring in?

A

Sodium Dependent glucose/galactose transporter 1

SGLT1 brings in Glucose and Galactose

34
Q

What sugar does GLUT2 transport?

A

GLUT2 transports glucose

it has low affinity
and high capacitance

(means that concentration of glucose needs to be very high for it tow work)

35
Q

what channel transports fructose

A

GLUT 5

36
Q

Describe Model #1

A
  1. Na/K ATPase generates DF for transport process (Na is pumped out)
  2. SGLT1 brings in Glucose and agalacatorse
  3. GLUT2 goes to membrane when glucose is present (increase affinithy, hgh ccapacitance)
  4. GLUT 5 brings in Fructose
37
Q

Describe the concept of MOdel 2 of sugar transprort

A
  1. Na/K ATPase creates DF
  2. SGLT brings in Na, Galactose, Glucose
  3. GLUT 5 brings in fructose

Fructose also enters interstitial space thrugh Glut 2

38
Q

What is Congenital Glucose-Galactose Malabsorption

A

no SGLT transproter!

  1. not using Na
  2. Leads to HYPOGLYCEMIA, unless something done quickly, person can die
39
Q

What is the Tx of congenital Glucose-Galactose Malabsorption

A

1 High Fructose Diet b/c still absorbing Fructose normally though GLUT 5

40
Q

What is the disease caleld when no GLUT2

A

Fanconi-Bickel Syndrome

41
Q

What is Fanconi- Bickel Syndrome

A

No Glut 2 moleucels

Hypoglycemic, but nto b/c can’t absorb glucose (Normal intestinal glucose absoprtion) -Hypoglycemia b/c cannot scavenge glucose from kidneyy

  • Glucose absorption in intestine is fine
  • Is GLUT2 important? NOt sure
42
Q

What is Cholear?

A

problem with fluid transprot

Need a lot of fluid and electorlyes

Need to wait to replace etpithelium

43
Q

How logn does it take for epithelium to to change

A

7-10 days

44
Q

What is oral rehydration therapy

A

Gatorade

Pedialyte

45
Q

What are the primary lipids in diet

A

Triglycerides (90%)

3FA +glycerol backbone

46
Q

What other lipids are in die

A

smalelr amts of sterols, sterol esters, PL

47
Q

At body temp, lipids are ….

A

liquid drpets

48
Q

What is the body’s only soure of essential FA

A

Dietary fat

49
Q

Where are unesterified cholesterol derived form

A

animal cell membranes

50
Q

Where are esterified cholesterol usually found

A

only in liver and food made from blood products

51
Q

What enzymes break down lipid (3)

A
  1. Salivary Lipases
  2. Gastric lipase (acid pH)
  3. Pancreatic Lipase (alkaline pH0
52
Q

What kind of cells secrete Gastric Lipase? Functin of Gastric lipase

A

Chief Cells!!! breakdown fats!

53
Q

What doe parietal cells secrete?

A

HCl

54
Q

What do Chef Cells (body of stomach) release

A

Gastric lipase and Pepsinogen (activated into pepsin by basic enivornment ??

55
Q

Are lipases H-phobic of H-philic

A

Lipases are H-philic

56
Q

What doe Bile acids + Lecithin do?

A

emulsify fats

57
Q

What stimulates the release of CCK?

A

Presence of FA in duodenum stimulates release of CCK

Causes gall bladder to release bile acids

58
Q

What is the function of CCK?

A

causes gall-bladder to release bild acids

59
Q

Do bile salts inhibit or activiate lipase activity

A

INHIBIT!

b/cit is in micelle

60
Q

Wher are short chain FA, medium chain FA, glycerol (<12 C ) tranported

A

Can move as unesterified FA directily inot portal cirulation Exported to capillary –> Hepatic Portal System

61
Q

What were >12 C..how are they transproted

A

They are reesterified to triglycerisdes (cholesterol is esterified to cholesterol estes)

These resynthesized lipids accumulate in vesicles of SER to form pre-chylomicorns of about 100nm in diameter

Prechylomicrons are coated with PL and beta-lipoprotein to fomr chylomicrons which exit the cell
ER –> Golcig –> Chyomicron –> too big for portal hepatic cystem

Go into lympahtics

Liver never sees it

62
Q

What is the Zollinger-Ellison Syndrome

A

Occurs when Gastrin-Secreting tumor of pancreas causes increased H secretion

H secretion continues unbated b/c gastrin secreted by pancreatic tumor cells is not subject to negative feedback inchibition by H+

No negative feedback inhbition by H+!! Gastrin continually secreted

63
Q

What kind of medication can you when you have Zollinger-Ellison Syndrome

A
  1. Omeprazole- H+/K+ ATPase inhibitor

2. Cimetadine- H2 Antagonist

64
Q

What happens with Chronic Pancreatitis and Cystic Fibrosis. How does it cause Steattorhea

A

Decreased Lipase Secretion

Digestive

65
Q

How does Gastrinoma and Zollinger-Ellison lead to Steattorhea

A

Decreased lipase function (b/c lipase doesn’t work under acidic conditions)

66
Q

How does Celiac Sprue lead to Steattorhea

A

Mucosal dysfunction (lacks absorption)

67
Q

How does Orlistat (Xenical-Alli) lead to Steattorhea

A

Pancreatic Lipase Inhibition

68
Q

How does Cholestyramine and Colestepol lead to Steattorhea?

A

Bile acid sequestration

Digestive

69
Q

How can you test/diagnose Celiac Disease/ malabsorption syndromes

A

D-xylose tests

70
Q

Can intestines absorb disaccharides?

A

NO! Only monosacchardies!

71
Q

What are the enzyme boudn to the surface of intestinal celsl

A

Brush border enzymes
Lactase
Glucoamylase (maltase)
Sucrase-somatlase

72
Q

where is activity of brush border enzymes the highest

A

In jejunum

73
Q

is GTUT 2 necessary for intestinal glucose absorption? Or does it play a major role in intestinal glucose uptake?

A

NO! If it did then GLUT 2 shoudl compensate for a lack of SGLT1 in Congential glucose galactose malabsoprtion patients

They are severely malabsoprtive phenotype!

74
Q

What is the Fanconi-Bickel Syndome ?

Phenotype of Fanconi-Bickel Syndrome

A

Mutations in GLUT2

Phenotype including Hypoglyceamia and glycosuria

-Due to absensce of GLUT2 form other tissues sucha s kidney, rather thana fiatulreu to absorb intestinal glucose

75
Q

What is Congential Glucose-Galactorse Malabsorption (CGM)

A

mutationsin SGLT1 leads to an inability to absorb glucose or galactose across across the intestinal epithelium.

Failture ot thrie, weak ,lethargic, and have watery diarrhea

Fed on Fructose wll thrive and dvelop normally

76
Q

What is Congentical Sucrase-Isomaltase Deficienty (CSID)

A

disease phenotype iwth multipe causes

Autosomal recessive human intestinal disorder that is characterized by fermentative diarrhea, abdominal pain and cramps upon ingestino of sugar

77
Q

What happens to glucose once it reaches heptaic

A

passes immediately into circualtiont o be used by body

78
Q

what happens to frucose

A

immedialtely cleared by liver and phosphorylated by fructokinase before entering glycoslysis or being convereted to glycogena dn stored or released into circulation as glucose

79
Q

What happens to galactose

A

almost immediately cleared by liver and convertedto glycogen for storage or rleased into ciruclation as glucose

80
Q

What is not found in blood

A

Therefore, ess. no galactose or fructose is found in teh blo

81
Q

where does most of the lipid absorption take place?

A

in duodenum and jejunum

82
Q

where does most of the lipid absorption take place?

A

in duodenum and jejunum

Physiology GI (4 decks)

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