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Digestion and absorption Flashcards

1
Q

Luminal phase

A

hydrolyzation and solubilization of fats, proteins and CHs by pancreatic and biliary secretions

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2
Q

Mucosal phase

A

terminal hydrolysis of carbohydrates and peptides

Processing and packaging of fats into chylomicrons for cellular export

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3
Q

Transport phase

A

transportation of nutrients across the intestinal mucosa into systemic body fluids

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4
Q

Essential fatty acids

A 
alpha-linolenic acid (omega-3)
linoleic acid (omega-6)
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5
Q

Acinar cells

A

secrete chloride-rich juice in resting state

secrete pancreatic enzymes when stimulated

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6
Q

centroacinar and duct cells

A

secrete water and electrolytes containing sodium, HCO3, K, Cl
Secrete large amounts of Na and HCO3- when stimulated

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7
Q

Innervation of exocrine pancreas

A

PNS: vagus
Sym: celiac and superior mesenteric ganglia

Above itneract with small intrinsic ganglia –> blood vessels, acini, duct cells, islet cells

NT: ACh, VIP stimulate secretion of pancreatic juice

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8
Q

Low rate of HCO3- secretion by duct cell

A

Mainly relies on CO2 diffusion into cell –> carbonic anhydrase
Acid exported via H-Na exchanger, driven by Na/K ATPase
Bicarb exported by HCO3-/Cl- exchanger
Cl- balanced by CFTR, driven by secretin/VIP stimulation

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9
Q

High rate of HCO3- secretion by duct cell

A

Import of HCO3- by HCO3/Na co-transporter, driven by Na/K ATPase
Export mainly through CFTR channel, driven by secretin/VIP stimulation

(Minor: HCO3/Cl- exchanger, HCO3- channel)

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10
Q

Acinar cell secretion

A

Enzymes stored in zymogen granules, then released upon stimulation

Hormones: secretin, CCK

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11
Q

Activation of trypsinogen

A

Enzyme inactive until it reaches the lumen of duodenum

Trypsinogen activated by brush border enzyme enteropeptidase (enterokinase), by removal of a trypsinogen activating peptide (TAP cleavage)

Trypsin can autocatalyze trypsinogen and also other zymogens

Pancreatic acinar cells produce pancreatic secretory trypsin inhibitor (PST1) proteolytic enzyme inhibitors to prevent autodigestion

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12
Q

Cephalic phase of pancreatic secretion

A

Sight of food –> activates neural pathways –> pancreas produces small volume of viscid secretion

Purpose: mobilize enzymes so they are within duct lumen, ready to be flushed out when secretion increases significantly

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13
Q

Gastric phase of pancreatic secretion

A

Distention of stomach –> activates vago-vagal pathway that induces some pancreatic secretion

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14
Q

Intestinal phase of pancreatic secretion

A

most significant

Chyme enters duodenum –> enzyme secretion at full potential
Regulated by secretin and CCK

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15
Q

Secretin during intestinal phase of pancreatic secretion

A

Stimulated by pH <4.5
Secreted by duodenum
Stimulates pancreatic duct cells to secrete mostly electrolyte rich fluid (HCO3-)

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16
Q

CCK during intestinal phase of pancreatic secretion

A

stimulated by broken down FAs, AAs
Secreted by duodenum
Stimulates vagal afferent fibres –> vagal efferent –> intrinsic pancreatic cholinergic neurons –> acinar cell secretion
(may also act through blood, also potentiates secretin-induced fluidsecretion)
To secrete pancreatic enzymes

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17
Q

Carb digestion

A
  1. Salivary amylase
  2. Pancreatic amylase - most responsible
  3. Brush border carbohydrases perform further hydrolysis (produce glucose, galactose, fructose)
  4. Colonic bacterial flora - metabolize oligosaccharides that reach colon (produce short-chain fatty acids)
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18
Q

Carb absorption

A

duodenum and upper jejunum mature villus cells = highest capacity for monosaccharide absorption (glucose, galactose, fructose)

Glucose/galactose via Na-dependent SGLT1
Fructose via Na-independent GLUT5
Monosaccharides transported to basolateral side via GLUT2

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19
Q

Carb metabolism

A
  1. Insulin –> GLUT4 translocated to cell surface
  2. Glucose –> G6p, converted to glycogen
  3. Glycogenolysis via glycogen phosphorylase –> G1P –> glycolysis
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20
Q

Fat digestion

A
  1. Gastric lipase from chief cells
  2. Gastric mixing, FAs, dietary proteins, lecithin, lysolethicin and bile salts promote emulsification
  3. Intestinal hydrolysis by pancreatic enzymes in prox. duodenum (lipase, cholisterolesterase, etc)
  4. Micellar solubilization via bile salts
  5. Micelles diffuse through “unstirred water layer” on enterocte surface, delivering lipolytic products only (bile salts recycled or excreted)
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21
Q

Fat absorption

A

Mostly in jejunum and proximal ileum
Short/med-chain FAs cross via FA binding proteins (without micelles), enter portal blood directly
Long-chain via micelles –> bind cytosolic FA binding proteins –> re-esterified in ER to triglycerides –> lymph
TGs, PLs, cholesterol and apolipoproteins –> chylomicrons –> exocytosis –> central lacteal –> lymph –> thoracic duct –> L. subclavian vein –> systemic circulation
Bile salts reform micelles or recycled

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22
Q

Fat metabolism

A

Lipoprotein lipase on endothelium hydrolyzes TGs in chylomicrons to FAs and glycerol
FAs enter adipocytes, muscles, hepatocytes
Adipocytes and mucles: esterify FAs –> TGs, or to PLs
Hepatocytes: FAs –> TGs
Glycerol –> gluconeogenesis (liver)
Adipocytes –> release stored lipids via hormone-sensitive lipase - hydrolyze TGs to FAs and glycerol
Hepatocytes: beta-oxidation

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23
Q

Protein digestion

A 
Gastric pepsins
Pancreatic enzymes (trypsin, chymotrypsin, elastin, carboxypeptidases A and B) in proximal duodenal lumen
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24
Q

Protein absorption

A

Di- and Tri-peptides cross via H+-dependent Pept1
Brush border hydrolases hydrolyze larger oligopeptides - cross via Na dependent/independent transporters
AA transporters on basolateral surface of enterocytes

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25
Protein metabolism
Proteins stored in all tissues for structure or function Excess AA: converted to TGs or glucose then glycogen Protein is constantly metabolized to accommodate demand
26
Vit B12 digestion
Released by mastication and gastric acid 1. R-proteins from saliva and parietal cells bind free cobalamin at low pH 2. Pancreatic enzymes in duodenum hydrolyze R-protein and allow IF to bind cobalamin
27
Vit B12 absorption
1. IF-cobalamin complex resists pancreatic proteolysis, taken up by specific ileal enterocyte receptors 2. Complex separated within enterocyte 3. B12 accumulates in mitochondria, transported out basolaterally 4. B12 immediately binds ileal pool of transcobalamin II, required for transportation in portal/systemic circulation 5. Transcobalamin-cobalamin complex endocyted by cells, then enzymatically released
28
Vit B12 metabolism
Formation of blood and DNA (regenerates folate) Delivered throughout body Excess secreted by liver into bile, then recycled
29
Vit A digestion
micellar solubilization | Dietary retinal esters hydrolyzed to retinol in intestinal lumen before absorption
30
Vit A absorption
duodenal enterocytes take up retinol via passive and facilitated diffusion Retinol incorported --> chylomicrons --> leaves mucosa into portal circulation
31
Vit A Metabolism
Hepatocytes hydolyze retinyl esters to release free retinol --> bind retinol-binding protein and prealbumin in sinusoids, OR stored ins tellate cells as RBP-bound retinol Retinol may undergo oxidation to retinal --> retinoic acid for phototransduction Secreted into bile
32
Vitamin D digestion
Mostly from endogenous synthesis in skin cells as a result of UV radiation
33
Vit D absorption
Passive diffusion into small intestinal mucosa (facilitated by pH) absorbed into circulation unchanged in chylomicrons
34
Vit D metabolism
hydroxylated first in hepatocytes, and then in renal tissue to calcitriol Promotes intestinal calcium and phosphate absorption Termination of activity via CYP-450
35
Vitamin E digestion
esters may be hydrolyzed following micellar solubilization by pancreatic and duodenal esterases
36
Vit E absorption
passive diffusion across intestinal mucosa | incorporated into chylomicrons
37
Vit E metabolism
TG hydrolysis Tocopherol remaining in remnant chylomicrons transported to liver - resecreted as part of VLDL, or metabolized and excreted by liver
38
Vit K digestion
K2 produced by intestinal bacteria | K1 dietary in vegetables and beef liver
39
Vig K absorption
K1: carrier-mediated process, dependent on luminal bile salts K2: entirely passive
40
Vit K metabolism
essential for gamma-carboxylation of glutamate residues in coagulation factors
41
Iron digestion
ingested mainly as myoglobin or hemoglobin | Mucosal ferrireductase reduces dietary Fe3+ --> 2+
42
Iron absorption
mostly in proximal duodenum | bound to transferrin (made by liver) in circulation
43
Iron metabolism
hepatocytes take up, secrete, and store iron via specific transferrin receptors Utilized in intracellular enzymatic reactions in cell, stored with ferritin (otherwise toxic)
44
Magnesium absorption
active transport across ileal mucosa | passive diffusion across the rest
45
Magnesium metabolism
enzyme cofactor NT, muscular contractions bone acts as a reservoir renally excreted
46
Phosphorus absorption
paracellular diffusion | Vitamin D-promoted transcellular
47
Phosphorus metabolism
bone acts as reservoir intracellular metabolism and growth renally handled
48
Celiac disease pathophys
1. Mucosa primed by previous trigger 2. Gliadin derived peptides processed by HLA class II molecules for presentation to helper T cells 3. Helper T cells activated, invasion of the surface by CD8 4. Direct gliadin toxicity --> release of transglutaminase, CLs with gliadin --> neoepitope target for gliadin
49
Celiac disease S/S
primarily affects the mucosal layer of the small intestine intermittent diarrhea, abd pain, bloating, but no "typical" signs and symptoms can also present with signs and symptoms of vitamin deficiency (also osteoporosis/malacia, peripheral neuropathy, dermatitis herpetiformis, follicular hyperkeratosis/dermatitis)
50
Chronic pancreatitis pathophys
Intraductal plugging/obs (alcohol, stones, tumors) Direct toxins: act on acinar cells to release cytokines --> stimulate the stellate cell to produce collagen and to establish fibrosis - also stimulates macrophages, neutrophils, lymphocytes Oxidative stress (idiopathic) Necrosis-fibrosis Ischemia (from obs and fibrosis) - exacerbation rather than initiation Autoimmune - association with Sjogren's, primary biliary cirrhosis, renal tubular acidosis
51
Chronic pancreatitis
chronic abd pain normal/mildly elevated pancreatic enzyme levels end stage: DM, steatorrhea
52
Vit B12 deficiency pathophys
``` pernicious anemia (megaloblastic, macrocytic anemia) can also cause folate deficiency ```
53
Vit B12 deficiency S/S
neuropathy due to demyelination
54
Vit B1 deficiency pathophys
Wernicke's encelopathy caused by decrease intake, increased requirement due to liver damage, decreased absorption Most commonly associated with alcoholism
55
Vit B1 deficiency S/S
ophthalmoplegia, nystagmus, ataxia, loss of recent memory, confusion
56
Vit D deficiency pathophys
``` inadequte exposure to sunlight malabsorption lack of vit D in breast milk medications elevated parathyroid hormone ``` Low Vit D --> decrease Ca absorption and enhances phosphorus absorption Vit D --> maturation of osteoclasts --> resorption of bone
57
Vit D deficiency S/S
Rickets (bowing legs) Osteomalacia: poorly mineralized skeletal matrix --> chronic muscleaches and pains
58
Pellagra (B3 def) pathophys
Primary: inadequte niacin/tryptophan in diet Secondary: adequate intake but other conditions
59
Pellagra (B3 def) S/S
diarrhea dementia dermatitis death
60
Zn deficiency pathophys
``` malabsorption diarrhea acrodermatitis enteropathica chronic liver disease chronic renal disease sickle cell diabetes malignanc nutritional ```
61
Zn deficiency S&S
``` hair loss skin lesions diarrhea wasting acne eyesight/taste/smell/memory malfunctions congenital abnormalities ```
62
Refeeding syndrome pathophys
Starvation --> depletion of intracellular minerals (phosphate, Mg, K) Serum concentration maintained due to intracellular compartment shrinkage 1. Glucose administration --> insulin released, glucagon decrease 2. Insulin-stimulated protein, glycogen, and fat synthesis - requires minerals and cofactors 3. Insulin stimulates K+ absorption into cells via Na/K symporter (to aid in glucose transport) 4. Mg/phos taken up into cell, water follows, expansion of intracellular fluid vol 5. Reduction in serum phosphate, Mg, and K - already depleted 6. Rapid decrease in renal excretion of Na and water due to glucose - expansion of ECFV, TBW 7. Fluid repletion to maintain urine output --> may lead to fluid overload, CHF, pulmonary edema and cardiac arrhythmias
63
Refeeding syndrome mineral depletion sequelae
weakened cardiac muscles weaked pulm muscles hypokalemia --> cardiac arrest hypophosphatemia --> impaired oxygen deliver, hypoxia
64
Refeeding syndrome management
Start low, go slow! Correct existing deficiencies Correct volume depletion, monitor renal function Supplement with thiamine prior to administration of glucose Monitor levels of phosphate, K, Mg Prophylactic K and P gradually increase caloric administration
65
Tests for fat malabsorption
Fecal fat excretion Sudan III stain - examination of undigested muscle fiber, as well as neutral and split fats; screening test for steatorrhea 14C-Triolein Breath Test - test for pancreatic function - triolein triglyceride releases CO2 when hydrolyzed - exhaled-radiolabelled 14CO2 measured after ingestion - low levels of 14CO2 --> lipase deficiency - could be confounded by pulmonary disease, age-related triolein metabolism changes and the presence of colon bacteria
66
Tests for CH malabsorption
Lactose/hydrogen breath test - Absence of lactase --> lactose goes undigested into colon --> bacterial fermentation to release hydrogen gas - false positives due to may be caused by small intestine bacterial overgrowth D-xylose test - measure of maximal intestinal absorption area - poorly metabolized aldopentose, absorbed in duodenum and jejunum - ingest D-xylose - 5-hour urine collection for xylose excretion; >4 is normal - abnormality due to: disorders affecting the mucosa of the proximal small intestine such as celiac disease/tropical sprue - poor sens, spec
67
Schilling test stage 1
1. Ingest radioactive cobalamin, with im injection of unlabelled cobalamin - saturate liver receptors so that all that is absorbed will be excreted 2. Collect urine over 24 hours
68
Schilling test stage 1 abnormality
Pernicious anemia - IF insufficiency Pancreatic insufficiency - inhibition of transfer of cobalamin from R factor --> IF Loss of absorptive surface of the terminal ileum Bacterial overgrowth (second stage would be abnormal as well)
69
Schilling test stage 2
1. Ingest radioactive cobalamin bound to IF | 2. Urine collection
70
Schilling test stage 2 abnormality
Bacterial overgrowth | Loss of absorptive surface of the terminal ileum
71
14C-glycocholic acid breath test
1. Radiolabelled bile acid | 2. If compound is not absorbed in small bowel and reach the colon - de-conjugated by colonic bacteria and release 14CO2
72
Selenium-75 labelled homotaurocholic acid test
Radioactive compound resistant to bacterial deconjugation Degree of retention of compound at 7 days following po intake provides an index of absorption retention - malabsorption
73
Trial of cholestyramine
binds bile salt, prevents diarrhea | 3-day diagnostic test
74
Definition of malnutrition
imbalance between supply and demand
75
Usage of nutrients during starvation
1. glucose from diet 2. glycogen - 1 day 3. gluconeogenesis 4. Ketones depletion of fat supply --> muscle breakdown --> death
76
Marasmus
protein and energy depletion
77
Kwashiorkor
protein depletion energy adequate Edema
78
Tests for pancreatic exocrine function
Direct: secretin/CCK Indirect: PABA, pancrealauryl, dual-labelled Schilling test
79
Secretin/CCK test
1. iv infusion of secretin/CCK 2. collect pancreatic secretions by a duodenal tube usually bicarb quantified (easier)
80
Indirect tests for pancreatic exocrine function
1. PABA test: indirect measure of chymotrypsin - PABA cleaved, measured in urine 2. Pancreolauryl test: fluoroscein dilaurate given orally hydrolyzed by pancreatic esterases to release fluoroscein --> excreted in urine 3. Dual-labelled Schilling test
81
Parenteral nutrition indication
Indicated for patients expected to have non-functioning GI for >7 days Patient needs to be able to tolerate large fluid volumes, and be hemodynamically and metabolically stable Stopped when patient meets 75-100% needs TPN (central) preferred
82
TPN complications
infection occlusions hyperglycemia, hyperlipidemia villous atrophy and bacterial translocation hepatobiliary complications (cholestasis) metabolic bone disease
83
Enteral nutrition indication
when oral intake is insufficient/contraindicated more cost effective less risks
84
Pancreatic stellate cell function
deposit ECM to facilitate tissue repair after wounding | hyperactive in chronic inflammatory/fibrotic states
85
Prevention of autoactivation of trypsinogen
Any accidentally activated trypsin bound by PST1, then degraded by chymotrypsin C Some hereditary mutations of cleavage sites for chymotrpsin C --> accumulation of activated trypsin in the pancreas --> pancreatitis
86
Consequences of CFTR mutation
Very thick pancreatic secretions --> obstructions, due to halted alkaline fluid production Zymogen autoactivation within the duct cells Leads to loss of acini, replacement by fibrous tissue
87
CCK function
sphincter of Oddi relaxation decreased acid secretion decreased gastric emptying increased pancreatic enzyme secretion
88
Impaired fat solubilization clinical presentation
steatorrhea | fat-soluble vitamin deficiencies (ADEK)
89
Brush border hydrolase deficiency consequences
Non-absorption of carbohydrates Colonic digestion of carbs by bacteria --> gaseous distention/diarrhea e.g. lactose deficiency
90
Tests for celiac disease
endomysial/anti-tissue transglutaminase antibodies (Ab IgA)

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