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Hannah GI 2 > digestion and absorption > Flashcards

digestion and absorption Flashcards

1
Q

sources of amylase

A

saliva, and pancreas

  • all other come from intestinal mucosa
  • carb digestion
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2
Q

where do chymotrypsin, carboxypeptidase, and elastase come from? enterokinase, dipeptidase, and amino-oliogopeptidase ? pepsin?

A
  1. pancrease
  2. intestinal mucosa
  3. stomach
    * protein digestion
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3
Q

where does lingual lipase come from? gastric lipase? all other lipid digestive proteins?

A
  1. saliva
  2. stomach
  3. pancreas
    * *no lipid enzymes come from intestine
    * * don’t forget bile helps lipid digestion in SI
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4
Q

what are the two types of digestive activity?

A
  1. cavital (luminal)
    - digestion by enzymes secreted from salivary glands, stomach, and pancreas
  2. membrane (contact)
    - hydrolysis from enzymes released by epithelial cells of microvili surface of enterocytes in intestinal mucosa
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5
Q

what are the large longitudinal folds of the SI that aid absorption

A

folds of kerckring

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6
Q

where are microvilli the longest

A

duodenum,

shortest in terminal ileum

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7
Q

function of enterocytes in intestinal epithelium? goblet cells? paneth cells?

A
  1. epithelial cells
    - digestion, absorption, secretion,
    - turnover: 3-6 days
    - sensitive to chemotherapy
  2. goblet = mucus secreting cells for protection
  3. paneth = immune cells that destroy bacteria or cause inflammatory response
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8
Q

what is pinocytosis

A
  • main mechanism of protein uptake into blood from SI

- occurs at base of microvilli

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9
Q

describe the path of a solute moving across the microvilli into the blood or lymph for absorption

A

unstirred luminal space–> glycocalyx –> apical membrane–> intracellular cytoplasmic space–> basolateral membrane–> basement membrane–> lymph/blood capillary wall

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10
Q

T/F

lactase deficiency genetic abnormality can lead to a loss of digestive/absoprtive adaptation of the GI tract

A

true

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11
Q

what form of carbs are absorbed by enterocytes

A

monosacchrides only
-glucose, galactose, and fructose

starch –> maltose –> 2 glucose
lactose–> glucose + galactose
sucrose –> fructose + glucose

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12
Q

describe the carb transporters on the apical and basolateral side of the enterocyte

A

luminal side

  • SGLT1 (for glucose and galactose) moves Na+ and carb into cell
  • GLUT5 (for fructose) moves carb into cell

basolateral side

  • GLUT2 moves all type of carbs into blood
  • Na/K ATPase
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13
Q

what are the side effects of impaired lactose digestion

A

lactase deficiency cause lactose in SI which can’t be absorbed

  • pulls water and causes OSMOTIC DIARRHEA
  • ferments and causes EXCESS GAS
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14
Q

is pepsin an exo or endopeptidase

A

endopeptidase converted from pepsinogen by low pH in the stomach

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15
Q

what converts trypsinogen to trypsin at the brush border of SI

A

enterokinase

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16
Q

what converts trypsinogen to trypsin, chymotrypsinogen to chymotrypsin, proelastase to elastase, and all other protein zymogens

A

trypsin cleaves them to active form

  • trypsin, chymotrypsin, and elastase are endopeptiadases
  • carboxypeptidases are exopeptidases
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17
Q

describe the protein transporters on the apical and basolateral side of the enterocyte

A

luminal

  • Na/H exchanger (brings Na into cell)
  • Na/amino acid symporter (4 different types for all charges of amino acids)
  • H+/di-tri-peptide symporter

peptidase converts di-tri-peptides to aminoacide in the cell

basolateral

  • Na/K ATPase
  • amino acid transporter by facilitated diffusion (4 types for 4 different charges [basic, acidic, neutral, imino] )
18
Q

what does chronic pancreatitis and cystic fibrosis cause in terms of GI absorption

A

*failure of pancreas

causes deficiency of pancreatic enzymes and will impair protein digestion/ absorption

19
Q

what pathology is caused by a genetic disorder that causes a defect or absent dibasic (COAL) Na+/ amino acid symporter on the luminal membrane of enterocytes

A

cystinuria

  • dibasic (COAL) amino acids are secreted in urine
  • cystine is in urine
  • cystine build up in urine can cause crystals or stones to form therefore can cause kidney stones
20
Q

describe the pathology behind Hartnup disease

A
  • recessive genetic disorder
  • mutation in SLC6A19 gene
  • causes malabsorption or neutral amino acids
  • resembles pellagra symptoms (niacin def)
    symptms: diarrhea, CNS probs, UV rash, photosensitivity, short
    dx: tryptophan and serotonin found in urine in high levels
21
Q

what is associated with loss of HCO3- secretion from duct cells of pancreas, causing loss of ability to secrete pancreatic enzymes from duct and eventual pancreatitis

A

cystic fibrosis

-CFTR regulated Cl- channel defect on apical surface of pancreatic duct cells

22
Q

describe lipid digestion in stomach

A
  1. gastric and lingual lipase begin breakdown of triglycerides into glycerol and fatty acids
  2. lipids become small fatty droplets
  3. small droplets are emulsified in stomach by dietary proteins (NOT BILE)
  4. CCK ensures time for lipid breakdown by slowing gastric emptying. released when lipids first enter SI
23
Q

how does lipid digestion in the SI differ from stomach

A
  • most lipid digestion occurs here
    1. bile emulsifies fat
    2. pancreatic enzymes are secreted into SI for digestion
  • pancreatic lipase is secreted in active form but inhibited by bile salts. pro-colipase is converted to colipase in the SI by trypsin and removes bile from pancreatic lipase. cholesterol hydrolase breaks cholesterol and TAGs, and phospholipase A (activated by trypsin) breaks down phospholipids
24
Q

what is the optimum pH for pancreatic lipase

A

6

TAG–> 2 FA + monoglyceride

25
Q

T/F

lipids are solubilized into micelles for absorption with the help of bile and phospholipids

A

true

26
Q

describe the movement of lipids across the brush-border (apical) and basolateral membrane

A
  1. micelles package half-digested lipids
  2. micelles diffuse across apical membrane (brush border)
  3. lipids are re-esterified into original lipid form
  4. lipids packaged in chylomicron form surrounded by phospholipids
  5. chylomicron is exocytosed into lymph (thoracic duct)
27
Q

what enzyme signal is on chylomicrons that is of critical importance for absorption of dietary lipids

A

ApoB
- leads to abetalipoproteinemia
(leads to fat soluble vitamin deficiency A,C,D,E, K)
-causes steatorrhea (any lipid assimilation disorder causes this )

28
Q

what is the failure to secrete adequate amounts of pancreatic enzymes

A

pancreatic insufficiency

29
Q

what causes impaired HCO3 and enzyme secretion by the pancreas

A

pancreatitis

30
Q

how does Zollinger-Ellison syndrome affect pancreatic enzyme secretion

A

the gastrinoma increases parietal cell release of acid which will reach the duodenum in higher than normal amounts. regulation of duodenum pH by HCO3 for neutralization is key for integrity of pancreatic enzyme function. the low pH of the duodenum in ZES causes impaired pancreatic enzymes, so it will affect digestion of lipids, as well as absorption of proteins and carbs

31
Q

what occurs as a result of bile salt deficiency, what can cause this?

A

interferes with fat emulsification and micelle formation leading to fat malabsorption

  1. ileal resection (disrupts bile recycling)
  2. SIBO (small intestinal bacterial overgrowth)
    - bacteria deconjugates bile impairing micelle formation
    - bacteria disrupts mucosa
32
Q

what causes SIBO to occur

A
  1. decreased gastric acid secretion

2. small intestine dysmotility

33
Q

what is tropical sprue

A
  • a malabsorption disease found in tropical regions thought to be caused by intestinal infection
  • decreases # of intestinal cells and surface area
  • decreased lipid absorption bc decreased SA
  • causes nutritional deficiencies particularly folate and B12
  • symptoms: steatorrhea, diarrhea, wt losss, indigestion
  • tx: tetracycline (antibitoic) and folate for 6 months
34
Q

what is celiac sprue

A
  • autoimmune disorder that causes Ab formation against gliadin component of gluten
  • causes destruction of microvilli and hyperplasia of intesitinal crypts
  • leads to malabsorption of nutrients (folate, iron, calcium, A, B D)
  • symp: ab pain, constipation, diarrhea, wt loss, steatorrhea, tingling hands and feet, itchy skin, fatigue
  • tx: gluten free diet
35
Q

describe absorption of fat soluble vitamins, water soluble vitamins, and vitamin B12

A
  1. fat soluble = same as lipid absorption
  2. water soluble = via Na dependent cotransport in SI
  3. B12 = complexes with R proteins in stomach, pancreatic proteases cleave R protein and then it complexes with IF, crosses apical membrane and binds to transcobalamin II in mucosa and then absorbed to blood in distal ileum
36
Q

important functions of B12

A
  • nerve myelination
  • folate recycling
  • gene replication (reduces DNA/RNA)
  • DNA synthesis in RBCs for maturation
  • def = pernicious anemia (immature RBC), and macrocytic/ megaloblastic anemia
37
Q

disruptions of vitamin B12 absorption

A
  1. gastrectomy (loss of parietal cells)
  2. gastric bypass (bypass to distal jejunum)
  3. ileal resection (loss of ileum)
  4. atrophic gastritis (destroys stomach mucosa and parietal cells)
  5. autoimmune metaplastic gastritis (attacks IF protein and gastric parietal cells)
38
Q

describe absorption of Vitamin D and conversion to active form

A
  1. cholecalciferol (from sun or diet) becomes main circulating (inactive) form 25,OH,cholecalciferol in liver
  2. in kidney renal proximal tubule- 1-alpha-hydoxylase (CYP1a) converts to active 1,25 OH cholecalciferol
    * active Vit D allows calcium absorption
39
Q

describe iron absorption in intestine

A
  • apotransferrin from bile binds free iron and Hg and is absorbed via pinocytosis in intestine
    1. Fe3+ changed to Fe2+
    2. enter cell by transporter or DMT
    3. if attached to heme it will be cleaved off by heme oxygenase
    3. Fe2+ leaves cell by ferroportin
    4. hephaestin will turn it back to Fe3+ to bind to transferrin for plasma transport
40
Q

where is calcium absorbed

A

-mainly in proximal SI with folate and iron, but some in middle SI

41
Q

where are MCTs absorbed

A

colon

Hannah GI 2 (11 decks)

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