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GI > Digestion/Absorption Lecture (what I think is important) > Flashcards

Digestion/Absorption Lecture (what I think is important) Flashcards

1
Q

What is steatorrhea?

A

the excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine.

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2
Q

What is dumping syndrome?

A

Dummping too soon and too much of cyme into the small intestine. Can happen if lose control of the pyloric sphincter. Overwhelm the capacity of the small intestine. Too much osmotically activate particles in small intestine.

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3
Q

Important difference between crypt cells and all other intestinal cells

A

secretion mainly occurs (not absorption); mainly Na+ and Cl- are secreted

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4
Q

Ion transport in the colon

A
  • aldosterone can act on the colon to stimulate Na+ absorption
  • do not have SGLT transporters
  • presence of aquaporins
  • tight junctions are tighter
  • colon primarily for ion reabsorption
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5
Q

Ion transport in the ileum

A
  • presene of SGLT1 and Glut
  • ion transporters (Na+/H+ exchange, Cl-/HCO3- exchange)
  • aquaporins
  • tighter junctions
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6
Q

Ion transport in the jejunum

A

(only difference between jejunum and ileum - tightness of the tight junction)

  • presene of SGLT1 and Glut
  • ion transporters (Na+/H+ exchange, Cl-/HCO3- exchange)
  • aquaporins
  • not so tight junctions
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7
Q

Ion transport in the duodenum

A

(there is no difference between the duodenum and jejunum)

  • presene of SGLT1 and Glut
  • ion transporters (Na+/H+ exchange, Cl-/HCO3- exchange)
  • aquaporins
  • not so tight junctions
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8
Q

How is water reabsorbed?

A

(1) osmotic forces
(2) aquaporins
(3) paracellular junctions

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9
Q

Describe the properties of tight junctions in the intestines

A

Dudenum: high permeabilty, no resistance
Jejunum: high permeability, low resistane
Ileum: moderate permeability, moderate resistance
Colon: low permeability, high resistance

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10
Q

Where does the fluid in the GI tract come from?

A

diet, saliva, pancreatic juice and bile, small intestine, gastric juice

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11
Q

Who absorbs the fluid?

A

Small intestine, colon, excreted in feces

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12
Q

How does 1,25-(OH)2-D3 aid calcium absorption?

A

1,25-(OH)2-D3 aids calcium absorption by signaling epithelial cells to produce more transporter and binding proteins

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13
Q

Fun fact

A

Heme metabolism can occur in the duodenum as well. Remember, non-heme iron (Fe3+) and heme are reabsorbed in the duodenum. Heme is broken down in to bilirubin and the Fe3+ byproduct is stored.

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14
Q

What is zollinger-ellison syndrome?

A

a condition in which a gastrin-secreting tumor or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers.

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15
Q

How does too much acid affect lipid absorption?

A

Too much acidity in the stomach inactivated pancreatic enzymes (specifically pancratic lipases)

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16
Q

How do Tropical sprue and Ulcerative colitis/Crohn’s disease affect lipid digestion and absorption?

A

Loss of surface area

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17
Q

How does coeliac disease affect lipid absorption?

A

in people with coeliac disease the immune system reacts abnormally to gluten (a protein found in wheat, rye, barley and oats), causing small bowel damage. The tiny, finger-like projections which line the bowel (villi) become inflamed and flattened. This is referred to as villous atrophy.

18
Q

Bile Acid/Salt effect of fat absorption

A

When you have enough bile, fat is absorbed passively in the duodenum and jejunum. Bile acid is absorbed actively in the distal ileum/passively in the colon. When bile acid concentration is above or below the critical micelle concentration, site of fat absorption changes.

** Realize how critical secreting the right concentration of bile is **

19
Q

Describe bile acid absorption

A

(1) absorption of conjugated bile acid occurs in the ileum and requires a Na+ cotransporter
(2) absorption of unconjugated bile (more lipophilic) acid occurs passively (diffusion) in the colon

20
Q

Cellular processing of lipids

A
  • Lipids have to be resynthesized back into triglycerides, cholesterol ester, phosphatidylcholine (occurs in the smooth ER)
  • Exit cell in chylomicron via exocytosis into lacteal (not the blood stream)
21
Q

What two ways can lipids enter cell:

A

(1) Passive diffusion - must be broken down - FFAs and glycerol
(2) Micelle - enter via endocytosis - contains large monoglycerides (FA bound to glycerol), vitamin A, D, E, K and long-chain free fatty acids

22
Q

What is a colipase?

A

Colipase is a protein co-enzyme required for optimal enzyme activity of pancreatic lipase. It is secreted by the pancreas in an inactive form, procolipase, which is activated in the intestinal lumen by trypsin.

23
Q

Steps to digestion and absorption of lipids

A

Emulsification -> Hydrolysis by gastric lipases -> Further hydrolysis by pancreatic lipases (emulsification/solubilizaion by bile salt micelles) -> uptake of lipids (passive or micelle) -> resynthesis of lipids in the SER (chylomicrons) -> exocytosis, enter the lymph

24
Q

Consequences of gastric bypass (Roux -en-Y) surgery?

A

(1) malnutrition (bypass the duodenum)

(2) inability to produce intrinsic factor

25
Q

Absorption of vitamin B12?

A

Cobalamin/intrinsic factor bind to cubulin receptor in ileum, endocytosed

26
Q

Results of vit. B12 deficiency?

A

Deficiency results in pernicious anemia

27
Q

What causes R protein to unbind to vit. B12 ?

A

Proteolytic degradation of R protein (pancreatic insufficiency can lead to pernicious anemia)

28
Q

Where does Cobalamin/intrinsic factor absorption occur?

A

In the ileum

29
Q

Describe digestion and absorption of nucleoprotein

A

Digestion: pancreatic DNase and RNase, polynucleotides hydrolyzed by brush border phosphodiesterases and nucleotidases
Absorption: nucleoside transporters

30
Q

Abnormalities in lipid digestion and absorption

A
  1. Genetic (Chylomicron metabolism defects)
  2. Bile deficiency
  3. Pancreatic insufficiency
  4. Other (secondary)
    a. tropical sprue
    b. ulcerative coliti/crohn’s disease
    c. zollinger-ellison syndrome
    d. coeliac disease
31
Q

Abnormalities in proteindigestion and absorption

A
  1. Genetic
    a. enteropeptidase deletion
    b. trypsinogen deletion
    c. amino acidurias - cystinuria, prolinuria
    d. Hartnup’s disease -Trp transporter
  2. Pancreatic insufficiency
  3. Other
    decreased surface area, surgery, parasitic infection
32
Q

Describe protein absorption

A
  • Proteins are not absorbed as efficiently as carbohydrates; still quite a lot of protein absorbed in ileum which is absorbed
  • Di- & tri- peptides and free amino acids use carriers to enter intestinal cell (di- & tri- peptides and free amino acids are the products when large peptides interact with peptidases)
33
Q

What are the enzymes that digest protein?

A

Pepsin and pancreatic proteases

34
Q

Proteins in the diet

A

(1) animal and plant sources

(2) endogenous protein - from the epithelial cells that are shed off

35
Q

Abnormalities in carbohydrate digestion and absorption ?

A
  1. Genetic
    a. lactose intolerance
    b. glucose-galactose malabsorption(SGLT1)
  2. Pancreatic insufficiency
  3. Non-genetic (secondary)
    a. decreased surface area
    b. parasitic infections
36
Q

Purpose of bacterial fermentation of carbohydrates?

A 
- produces short chain fatty acids
Benefits: 
1. "salvages" calories 
2. lessens water loss in feces 
3. fight intestinal inflammation
37
Q

Where does most of carbohydrate reabsorption occur?

A

In the jejunum

38
Q

What is the difference between our amylases?

A

First, we have three amylases - salivary, pancreatic, membrane digestion
Second, the different amylases cause different levels of digestions (salivary amylase breaks down starch to partial converted starch, pancreatic amylase breaks down partially converted starch into different disacharide, membrane amylases break down disacharrides into glucose, galactose and/or fructose)

39
Q

How are our different nutrients absorbed

A

(1) Fats -> micelle, FFAs, TAGs (transport across the membrane)
(2) Proteins -> free AAs, di- and tripeptides (carrier transporter)
(3) Carbs. -> glucose, galactose, fructose (GLUT-S, SGLT-1)

40
Q

Where does digestion occur?

A

Intraluminal and membrane

GI (27 decks)

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