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GI Final > Digestion and Absorption in GI Tract > Flashcards

Digestion and Absorption in GI Tract Flashcards

1
Q

Where does digestion begin and end?

A

begin in stomach and mouth

complete in SI

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2
Q

Where does absorption take place?

Function?

A

SI

movement of nutrients, H2O, electrolytes from lumen of the intestine into the blood

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3
Q

Cellular pathway

A

lumen-> apical membrane-> intestinal epithelial cell-> basolateral membrane -> blood

  • transporter in membrane
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4
Q

Paracellular pathway

A

across a epithelium

intestinal epithelial cell-> lateral intercellular space-> intestinal epithelial cell

-tight junctions

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5
Q

Types of digestive activity

A
  1. cavital (luminal)

2. membrane (contact)

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6
Q

Cavital digestive activty

A

digestion resulting from the action of enzymes secreted by the salivary glands, stomach, and pancreas

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7
Q

Membrane digestive activity

A

hydrolysis by enzymes synthesized by epithelial cells

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8
Q

Folds of Kerckrin

A

longitudinal folds in SI

villi and microvilli increase surface area of the SI

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9
Q

Where are villis the longest and shortest?

A

long: duodenum
short: terminal ileum

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10
Q

Microvillar surface, Brush border

A

site of activity for a # of digestive enzymes

barrier that must be traversed by nutrients, water, and electrolytes

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11
Q

cell types in intestinal epithelium (3)

A
  1. Enterocytes
  2. goblet cells
  3. paneth cells
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12
Q

enterocytes

A

epithelial cells

digestion, absorption, secretion

turnover rate: cells are replaced 3-6 days

suspectible to irradiation and chemotherapy

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13
Q

Goblet cells

A

mucus-secreting cells

physical, chemical and immunological protection

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14
Q

paneth cells

A

part of mucosal defenses against infection

secrete agents that destruct bacteria or produce inflammatory responses

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15
Q

How does enterocyte membrane control flux of solute and fluid btw the blood and lumen?
-4

A
  1. Pinocytosis
    - at base of microvilli
    - major mechanism in uptake of protein
  2. passive diffusion
    - particles move through pores in cell membrane or through intercellular spaces
  3. Facilitated diffusion
  4. Active diffusion
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16
Q

What barriers does the solution have to move across the enterocytes - from lumen to blood? (7)

A
  • unstirred layer of fluid
  • glycocalyx
  • apical membrane
  • cytoplasm of cell
  • basolateral membrane
  • basement membrane
  • wall of blood capillary or wall of capillary of lymphatic vessel
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17
Q

Adaptations in digestion in absorption

  • key factors
  • exceptions
A

alteration in fxn to maintain homeostasis

depends on capacity of intestine

exm. small bowel resection or bypass
- if ileum is resection, b12 and bile absorption is abolished

-genetic abnormalities can lead to loss of adaption

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18
Q

End products of carbohydrate digestion

A
  • glucose
  • galactose
  • fructose

**only MONOsaccharides are absorbeed by enterocytes

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19
Q

Key transporters in absorption of carbohydrates

  • Lumen side (2)
  • basolateral side (2)
A

Lumen

  1. SGLT1 (x2) - Na/glucose or galactose symporter (in)
  2. GLUT 5- frutose in

Basolateral
1. Na/K atpase (k in)
2. Glut 2 (x3)
glucose or galactose or fructose out

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20
Q

Lactose intolerance

A

failure to digest carbohydrates

brush border lactose is deficient or absent

undigested lactose remains in lumen and holds H2O and causes osmotic diarrhea
-> fermented into methane and H gas -> excess gas

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21
Q

Protein absorption location

A

stomach and SI

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22
Q

Lactose

- enzyme breakdown

A

lactase to breakdown into glucose and galactose

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23
Q

Sucrose

- enzyme breakdown

A

sucrase to breakdown into glucose and fructose

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24
Q

Starch

-ezyme breakdown

A

amylase, maltose (maltase), maltotriose (sucrase) breakdown into glucose

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25
Q

Enzymes for protein digestion (3)

A
  1. Endopeptidases
    - trypsin
    - chymotrypsin
    - elastase
  2. Exopeptidases
    - carboxypeptidases A and B
  3. Pancreatic protease
  • all in SI

stomach is pepsinogen

26
Q

Trypsin

A

catalyzes hydrolysis of trypsinogen (autocatalysis)

27
Q

Pancreatic proteases

A

digest themselves and each other

Proteins-> AA, oligopeptides, dipeptides, tripeptides

28
Q

Tranporters for protein digestions

  • lumen side (3)
  • basolateral side ( 2)
A

Lumen

  1. Na/H+ antiporter (Na out of lumen)
  2. Na+/ AA cotransporter (in cell)
    - 4 separate cotransporter for neutral, acidic, basic, and imino aa
  3. H+/ di/tripeptide cotransporter (in cell)

Basolateral

  1. Na/K atpase (k in cell)
  2. facilitated diffusion for AA
    - 4 separate diffusion for neutral, acidic, basic, and imino aa
29
Q

Main cause of disorder of protein assimilation

A

deficiency of pancreatic enzymes or defects in transporters of intestinal epithelial cells

30
Q

Chronic pancreatitis and cystic fibrosis

A

deficiency of pancreatic enzymes

31
Q

Congenital Trypsin absence

A

no pancreatic enzymes

32
Q

Cystinuria

A

defect/absence in Na/AA cotransporter
- transporter for dibasic AA absent in SI and kidney

-genetic disorder

  • AA secreted in urine
    • cystine buildup in urine and form crystals and stones
33
Q

Hartnup Disease

  • describe
  • symptoms
A
  • no neutral AA absorption
  • genetic disorder (SLC6A19 gene)
  • pellagra (defiency of niacin)
symptoms:
diarrhea, mood change
- red scaly skin rash
-photosensitivy
- short stature
- uncoordinated movement
-urine secretion of neutral AA
34
Q

Cystic fibrosis

  • describe
  • target organ
A

CFTR: Cl- channel in apical surface of duct cell

-pancreas first organ to fail

  • loss of HCO3 secretion
  • lead to acute or chronic pancreatitis
35
Q

Lipid digestion location

A

stomach and SI

36
Q

Types of lipid digested

A

triglyceride, cholesterol ester, phospholipids

- will breakdown into monoglyceride, FA, cholesterol, or lysolecithin

37
Q

Complication of lipid digestion

A

insolubility of lipid

  • need MICELLES to transport to apical membrane of intestinal epithelial cell for absorption
38
Q

Enzymes for stomach and lipid digestion

A
  1. Lingual and gastric lipases
    - lipid breakdown to glycerol and FA (small droplets)
    - > emulsify in stomach
  2. CCK
    - secreted when dietary lipids appear in SI
    - slows rate of gastric emptying
39
Q

Enzymes for small intestine and lipid digestion

A

** most lipid digestion occurs in SI

  • Bile salts emulsify lipds
  1. pancreatic lipase (colipase)
    - inactive bile salt
  2. Colipase
    - inactive form (procolipase)
    - activated by trypsin
    - works w pancreatic lipase
  3. cholesterol ester hydrolase
    - catalyze cholesterol production
    - hydrolyze triglyceride to produce glycerol
  4. Phospholipase A2
    - proenzyme activated by trypsin
40
Q

pancreatic lipase optimum ph

A

6

41
Q

Mechanism for lipid processing/assimilation (8)

A
  1. pancreatic enzyme secretion
  2. bile acid secretion
  3. emulsification
  4. solubilization by micelles
    5 . diffusion of micellular content into intestinal epithelial cells
    6.. reesterification
  5. chylomicron formation
  6. exocytosis of chylomicrons into lymphs
42
Q

What happens in for APoB in epithelial cells of SI

A

abetalipoproteinemia

- no absorption of dietary lipids

43
Q

Any abnormalities in lipid assimilation

A

STEATORRHEA

44
Q

Abnormalities of pancreatic enzyme secretion

-diseases(3)

A

damages regulation of acidity in duodenum (bc responsible for HCO3- secretion)

  1. pancreatic insufficiency
    - failture to secrete enough pancreatic enzymes
  2. Zollinger Ellison Syndrome
    - gastrin-secreting tumor of pancrease
    - increase H secretion by gastric parietal cells
    - overload of acid in duodenum
  3. Pancreatitis
    - impaired HCO3 and enzyme secretion
45
Q

Defiency of bile salts

- causes (2)

A

-interferes with micelles formation

Causes

  1. ileal resection
    - interrupt enterohepatic circulation of bile salts
    - bile salt pool is reduced
  2. small intestin bacterial overgrowth
    - bacteria deconjugate bile salts
    - impair micelle formation and fat malabsorption
    - damage intestinal mucosa
    - increase gastric acid secrtion and SI motility
46
Q

Tropical Sprue

  • causes
  • symptoms
  • treatment
A

decrease # of intestinal epithelial cells-> less microvillar surface area= impaired lipid absorption
- due to infection

Steatorrhea
- B12 and folate deficiency

diarrhea, cramps, nausea, weight loss, gas

TX: tetracycline, folate

47
Q

Celiac sprue

  • describe
  • prevalence
  • symptoms
  • tx
A

autoimmune disorder

antibodies against gluten (Gliadin)
- lead to destruction of SI villi (atrophy) as well as hyperplasia of intestinal crypts

malabsorption related to deficiencies in folate, iron, calcium, vitA/B/D

mostly in causasian and europeans, women>men

symptoms:
abdominal pain, constipation, diarrhea, weight loss, vomit, nausea, steatorrhea, numbness, rash, fatigue, easy bruising

tX: gluten free diet

48
Q

defects in digestion and absorption

A
  • causes malabsorption
  1. less acid secretion and churning in stomach
  2. decrease enzyme secretion in duodenum
  3. less SA and transport in SI
    - lymphatic obstruction
49
Q

Vitamins in GI tract

A
  1. Fat-soluble vitamins (DEKA)
    - same mechanism of absorption as lipids
  2. Water soluble vitamins(B1/2/3/12, C, biotin, folic acid, nicotinic acid, pantothenic acid)
    - absorbed via Na dependent cotransport mechanism
    - Vit B 12 (cobalamin) form complexes with other proteins to be absorbed (R proteins, **IF, transcobalamin)
50
Q

Vitamin B12

A

Cobalamin
- metabolic fxn with H acceptor coenzyme

  • reducing ribonucleotide to deoxy a step necessary in gene replication
  • important in DNA synthesis in RBC cells and folate

disease

  • pernicious anemia caused by RBC maturation when B12 is defiency
  • > macrocytic and megablastic anemia
51
Q

Disruption in absorption of Vitamin B12

A
  1. Gastrectomy: loss of parietal cells (source of IF)

2. Gastric bypass: exclusion of the stomach, duodenum, and proximal jejenum after absorption of Vitamin B12

52
Q

Pernicious anemia

A

stomach does not produce enough IF

  • lowers vitamin B12
    1. atrophic gastritis
    2. Autoimmune metaplastic atropic gastritis
53
Q

Atrophic gastritis

A

chronic inflammation of the stomach mucosa that leads to loss of parietal cells

54
Q

Autoimmune metaplastic atrophic gastritis

A

immune system attacks IF protein and gastric parietal cells

55
Q

Vitamin D/Calcium absorption

A

calcium absorption depends on the presence of Vitamin D

  • absorbed into enterocytes, but also reabsorbed
  • SI: binding protein calbindin

calcitrol and PTH govern

56
Q

Vitamin D defiency

- disease

A

RIckets (child)

results from inadequate calcium reabsorption

57
Q

Iron Absorption

A

secrets apotranferrin into bile, enters duodenum

Apotransferrin binds with free iron and hemoglobin => form transferrin
-> transferin binds to membrane receptors of intestinal epithelial cells -> absorbed via pinocytosis and later release

58
Q

What is absorbed in duodenum?

A 
fat
sugar
AA 
iron
folate
calcium
water
 electrolytes
59
Q

What is absorbed in jejunum?

A 
sugar
aa
calcium
water 
sodium
60
Q

What is absorbed in ileum

A

b12
bile salt
water
electrolytes

61
Q

What is absorbed in colon

A 
water
electrolytes
calcium
AA
medium triglycerides

GI Final (15 decks)

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