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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
Q

Protein metabolism

A

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

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26
Q

Vit B12 digestion

A

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
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27
Q

Vit B12 absorption

A
  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
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28
Q

Vit B12 metabolism

A

Formation of blood and DNA (regenerates folate)
Delivered throughout body
Excess secreted by liver into bile, then recycled

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29
Q

Vit A digestion

A

micellar solubilization

Dietary retinal esters hydrolyzed to retinol in intestinal lumen before absorption

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30
Q

Vit A absorption

A

duodenal enterocytes take up retinol via passive and facilitated diffusion
Retinol incorported –> chylomicrons –> leaves mucosa into portal circulation

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31
Q

Vit A Metabolism

A

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

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32
Q

Vitamin D digestion

A

Mostly from endogenous synthesis in skin cells as a result of UV radiation

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33
Q

Vit D absorption

A

Passive diffusion into small intestinal mucosa (facilitated by pH)
absorbed into circulation unchanged in chylomicrons

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34
Q

Vit D metabolism

A

hydroxylated first in hepatocytes, and then in renal tissue to calcitriol
Promotes intestinal calcium and phosphate absorption
Termination of activity via CYP-450

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35
Q

Vitamin E digestion

A

esters may be hydrolyzed following micellar solubilization by pancreatic and duodenal esterases

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36
Q

Vit E absorption

A

passive diffusion across intestinal mucosa

incorporated into chylomicrons

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37
Q

Vit E metabolism

A

TG hydrolysis
Tocopherol remaining in remnant chylomicrons transported to liver
- resecreted as part of VLDL, or metabolized and excreted by liver

38
Q

Vit K digestion

A

K2 produced by intestinal bacteria

K1 dietary in vegetables and beef liver

39
Q

Vig K absorption

A

K1: carrier-mediated process, dependent on luminal bile salts
K2: entirely passive

40
Q

Vit K metabolism

A

essential for gamma-carboxylation of glutamate residues in coagulation factors

41
Q

Iron digestion

A

ingested mainly as myoglobin or hemoglobin

Mucosal ferrireductase reduces dietary Fe3+ –> 2+

42
Q

Iron absorption

A

mostly in proximal duodenum

bound to transferrin (made by liver) in circulation

43
Q

Iron metabolism

A

hepatocytes take up, secrete, and store iron via specific transferrin receptors
Utilized in intracellular enzymatic reactions
in cell, stored with ferritin (otherwise toxic)

44
Q

Magnesium absorption

A

active transport across ileal mucosa

passive diffusion across the rest

45
Q

Magnesium metabolism

A

enzyme cofactor
NT, muscular contractions
bone acts as a reservoir
renally excreted

46
Q

Phosphorus absorption

A

paracellular diffusion

Vitamin D-promoted transcellular

47
Q

Phosphorus metabolism

A

bone acts as reservoir
intracellular metabolism and growth
renally handled

48
Q

Celiac disease pathophys

A
  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
Q

Celiac disease S/S

A

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
Q

Chronic pancreatitis pathophys

A

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
Q

Chronic pancreatitis

A

chronic abd pain
normal/mildly elevated pancreatic enzyme levels
end stage: DM, steatorrhea

52
Q

Vit B12 deficiency pathophys

A 
pernicious anemia (megaloblastic, macrocytic anemia)
can also cause folate deficiency
53
Q

Vit B12 deficiency S/S

A

neuropathy due to demyelination

54
Q

Vit B1 deficiency pathophys

A

Wernicke’s encelopathy caused by decrease intake, increased requirement due to liver damage, decreased absorption

Most commonly associated with alcoholism

55
Q

Vit B1 deficiency S/S

A

ophthalmoplegia, nystagmus, ataxia, loss of recent memory, confusion

56
Q

Vit D deficiency pathophys

A 
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
Q

Vit D deficiency S/S

A

Rickets (bowing legs)

Osteomalacia: poorly mineralized skeletal matrix –> chronic muscleaches and pains

58
Q

Pellagra (B3 def) pathophys

A

Primary: inadequte niacin/tryptophan in diet
Secondary: adequate intake but other conditions

59
Q

Pellagra (B3 def) S/S

A

diarrhea
dementia
dermatitis
death

60
Q

Zn deficiency pathophys

A 
malabsorption
diarrhea
acrodermatitis
enteropathica
chronic liver disease
chronic renal disease
sickle cell
diabetes
malignanc
nutritional
61
Q

Zn deficiency S&S

A 
hair loss
skin lesions
diarrhea
wasting
acne
eyesight/taste/smell/memory malfunctions
congenital abnormalities
62
Q

Refeeding syndrome pathophys

A

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
Q

Refeeding syndrome mineral depletion sequelae

A

weakened cardiac muscles
weaked pulm muscles
hypokalemia –> cardiac arrest
hypophosphatemia –> impaired oxygen deliver, hypoxia

64
Q

Refeeding syndrome management

A

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
Q

Tests for fat malabsorption

A

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
Q

Tests for CH malabsorption

A

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
Q

Schilling test stage 1

A
  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
Q

Schilling test stage 1 abnormality

A

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
Q

Schilling test stage 2

A
  1. Ingest radioactive cobalamin bound to IF

2. Urine collection

70
Q

Schilling test stage 2 abnormality

A

Bacterial overgrowth

Loss of absorptive surface of the terminal ileum

71
Q

14C-glycocholic acid breath test

A
  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
Q

Selenium-75 labelled homotaurocholic acid test

A

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
Q

Trial of cholestyramine

A

binds bile salt, prevents diarrhea

3-day diagnostic test

74
Q

Definition of malnutrition

A

imbalance between supply and demand

75
Q

Usage of nutrients during starvation

A
  1. glucose from diet
  2. glycogen - 1 day
  3. gluconeogenesis
  4. Ketones
    depletion of fat supply –> muscle breakdown –> death
76
Q

Marasmus

A

protein and energy depletion

77
Q

Kwashiorkor

A

protein depletion
energy adequate
Edema

78
Q

Tests for pancreatic exocrine function

A

Direct: secretin/CCK
Indirect: PABA, pancrealauryl, dual-labelled Schilling test

79
Q

Secretin/CCK test

A
  1. iv infusion of secretin/CCK
  2. collect pancreatic secretions by a duodenal tube

usually bicarb quantified (easier)

80
Q

Indirect tests for pancreatic exocrine function

A
  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
Q

Parenteral nutrition indication

A

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
Q

TPN complications

A

infection
occlusions
hyperglycemia, hyperlipidemia
villous atrophy and bacterial translocation
hepatobiliary complications (cholestasis)
metabolic bone disease

83
Q

Enteral nutrition indication

A

when oral intake is insufficient/contraindicated
more cost effective
less risks

84
Q

Pancreatic stellate cell function

A

deposit ECM to facilitate tissue repair after wounding

hyperactive in chronic inflammatory/fibrotic states

85
Q

Prevention of autoactivation of trypsinogen

A

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
Q

Consequences of CFTR mutation

A

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
Q

CCK function

A

sphincter of Oddi relaxation
decreased acid secretion
decreased gastric emptying
increased pancreatic enzyme secretion

88
Q

Impaired fat solubilization clinical presentation

A

steatorrhea

fat-soluble vitamin deficiencies (ADEK)

89
Q

Brush border hydrolase deficiency consequences

A

Non-absorption of carbohydrates
Colonic digestion of carbs by bacteria –> gaseous distention/diarrhea

e.g. lactose deficiency

90
Q

Tests for celiac disease

A

endomysial/anti-tissue transglutaminase antibodies (Ab IgA)

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