Absorption And Digestion - Dr. Rogers Flashcards
Lactose Intolerance
X digest Dairy Carbohydrates
X lactase enzyme in the brush border (makes it Glucose+Galactose)
Lactose in SI ——> SCFAs and H2 = acetate, butyrate, propionate
= holds H2O in lumen with it
= Osmotic Diarrhea and ferments into methane and H+ gas
Primary Sugars
Sucrose
Lactose
Starch
Secondary sugars
Amylase, Glycogen, EtOH, Lactic Acid, Pyruvic Acid, Pectins, Dextrins
Where does carb metabolism start
Oral cavity, amylase attacks starch
Where is lactose and sucrose attacked in the GI
In the SI most in duodenum (Lactase, Sucrase)
Pancreatic Amylase = starch continues
Most absorption of carbs happens and reason for it
Villi folds called FOLDs of KERCKRING (longitudinal folds) and increase SA
Where are the enzymes found
In the brush border of the villi
Maltose
Trehalose
Lactose
Sucrose
Glucose + Glucose
Glucose + Glucose
Glucose + Galactose
Glucose + Fructose
STARCH breaks down to
- Starch —AMYLASE—> Maltose——> 2Glucose
How is Glucose absorbed
SGLT1 = absorbs glucose and galactose from lumen GLUT5 = fructose absorption from lumen GLUT2 = absorbs glucose + galactose + fructose into blood
SGLT1 inhibitors
Can be used in Diabetes to slow glucose absorption
Which is the fastest sugar transporter
SGLT1 since it used Na+
X GLUT2
Glycogen gets stored in high amounts
How to test for carbohydrate digestion problems
- Breath Tests : methane, CO2 labeled isotope, Lacotse, sucrose
- Ingest D-xylose and see how much is able to get absorbed and present in urine (general statement for carbohydrate digestion problem)
In lactose intolerance what can you find in the tests run
Normal D-xylose
Positive Lactose breath test (H+ and methane sensed)
Protein digestion problems is
X pancreatic enzymes or X transporter of the SI epithelial cells
Chronic Pancreatitis
X pancreatic enzymes - proteases like trypsinogen get activated in pancreas and eats up pancreas and no enzymes are produced
Also no neutralization of stomach
Congenital Trypsin Absence
X trypsin
= no pancreatic enzymes activated
Cystinuria
X SLC3A1 transporter or SLC7A9 (absorb Cysteine, Lys, Arg, Ornithine in proximal tubule of kidney)
= AA secreted in feces and urine
Hartnup Disease
X absorb neutral AA
Pellagra (niacin deficiency)
Mutation in SLC6A19 gene (neutral AA transporter)
Sx: D, mood changes, neuro problems, red scaly skin, photosensitive, NEUTRAL AA in URINE = TRYPTOPHAN + SEROTONIN by products
Cystic Fibrosis
X CFTR transport = cl- channel pumped into cell for HCO-3 facilitated diffusion into stomach and SI to neutralize stomach
= cant move enzymes into GI form ducts
= can lead to pancreatitis
= disrupt gastric and duodenal mucosa
= X protease + X neutralization of stomach
Where does protein get digested initially
STOMACH
Pepsinogen—» Pepsin
10%-20%
Where does most of protein digestion happen
SI from pancreatic enzymes zymogen
Trypsin, chymotrypsin, carboxypeptidase, elastase
——> di and tri peptides
ROLE of carboxypepidase
Cleaves AA at carbonyl ends into individual AAs
So they can be absorbed by enterocytes and other cells
How are protein enzymes activated
By enterokinase = trypsinogen
By trypsin
In Cystic Fibrosis congenital trypsin absence - NO Trypsin
Epithelial cell of SI transporters on lumen side
AA cotransporter with Na+ to get into the cell
Of di and try with H+
Transporters on the epithelial cells of the blood side
Facilitated diffusion for each type of AA
Steatorrhea
Fat and lipid in the stools
Recurrent greasy, pale, foul smelling D
Wright loss, ABD pain,
Worsened when she started eating bread
SI bowel biopsy’s
CELIAC DISEASE
Celiac Disease
Ab against gluten compounents = tTG + IgA and DGP and IgG
=destruction of SI mucosa and villi
= malabsorption (Iron, VIT, ca, folate deficiency)
= D, C, ABD pain, N, V, steatorrhea
More common in F and Caucasian
Tropical Sprue
From infection of mucosa from traveling usually
Reduced microvilli and lipid absorption- steatorrhea
Folate and VIT 12 deficiency, D, N, cramps
Tx: tetracycline Ab and folate for 6mos
How are lipids digested
Bile salts and lecithin emulsify lipids into micelles from the liver
Where are lipids digested
Mouth = lingual lipase
Stomach = Gastric Lipase -> TAGs (10%)
CCK ——> inhibits gastric emptying for more mixing + activated gallbladder for bile release
SI = most of it
Where are most of lipids digested
SI
Has BILE SALTS
Has PANCREATIC enzymes =
1. Pancreatic Lipase : inactive when bound to bile salts, is active when secreated, colipase is activated by trypsin, colipase activated inactivated pancreatic lipase
2. Cholesterol ester hydroplane : active when secreted free cholesterol and TAGs—> glycerol made
3. Phospholipase A2 : proenzyme when secreted, activated by trypsin (act on phospholipids)
steps tp break down fats
- Micelles solubilize
- Diffusion of micelle contents (FAs + its backbones) across apical membrane
- Re-esterification (put FAs back on the backbone)
- Chylomicron forms by ApoB (X ApoB = no exocytosis of chylomicrons into lymph
- Exocytosis of chylomicrons into lymph ——> LIVER
5.
Problems with lipid digestion anywhere causes
Steatorrhea
Pancreatitis
Trypsin a pancreatic enzyme gets activated in the pancreas and eat it up
=X HCO-3 and enzymes released into duodenum
Pancreatic insufficiency
Can secrete right amount of pancreatic enzymes
Zollinger-Ellison Syndrome
GASTRIN secreting tumor in pancreas
Increase H+ by parietal cells in gastric mucosa
- high acidity in duodenum
Reasons for insufficient bile salt secretion
Ileal resection = X bile salt enterohepatic recirculation
Liver Disease
Gallbladder Disease
*micelles cant be formed in SI
What happen in Small Intestine Bacterial Overgrowth (SIBO)
Too little gastric secretion + dysmobility can cause this
Changes in pH can happen which effects enzyme effect
Dx: Breath test = methane and H+
Bacterial Deconjugate Bile Salts—> no micelles forming
=Steatorrhea
What do you see is testing celiac disease e
Lipid absorption dysfunction
Serological test = + for t-TG-IgA
Urea breath test- = no peptic ulcer
H+ breath test - = no lactose intolerance
D-Xylose test normal = no carb absorption problems
Water solvable VIT
B and C
Most absorbed with Na+ cotransport
VIT B12 (cobalamin) forms complex with proteins (IF, R-protein in saliva, Transcobalamin2) to get absorbed
Fat soluble vits
Absorbed as other lipids
Importance VIT B12
RNA and DNA = to make RBS
Nerve myelination, and cofactor for folate coenzyme recycling
How VIT B 12 is absorbed in the GI
VIT b12 +binding protein ——> stomach
R-protein made in stomach and binds to vitB12 in stomach
*in stomach Pepsin cleaves binding protein off
VITB12 + R-Protein ——> Duodenum
IF secreted by parietal cells go to duodenum
*in duodenum trypsin cleaves r-Protein off and IF binds
VITB12+ IF——> ILEUM
VIT B 12 deficiency
Pernicious Anemia + weakness in nerve conduction
X RBC maturation
Macrocytic and megoblastic anemias
Pernicious Anemia in the Stomach effects
NO IF made
- Atrophic Gastritis = chronic inflammation of stomach - X parietal cells
- Autoimmune Metaplastic Atrophic Gastritis = immune cells attack IF protein or Parietal cells
What surgeries can cause problems with VIT b12 absorption
- Gasterectomy = no parietal cells
- Gastric Bypass = pass stomach, esophagus—-> distal Jejunum
- Crohns Diease = Ileum is removed
X VIT D
helps with Ca + absorption
Rickets - childhood
Osteomalacia - adults
Ca+2 absorption
Across enterocytes with VITD
Reabsorption at Kidney with PTH
Calcitonin ——I reabsorption
IRON absorption
With VIT C
Liver secretes apotransferrin into bile
Apotransferrin ——> duodenum and bind to free Fe(Fe+2) +Hb = transferrin
Transferrin ——> SI epithelial cell receptors (absorbed and released)
Role of VIT C in iron absorption
Iron is readily absorbed as Fe+2 (animal)
Plants have Fe+3 ———VITC———> Fe+2
Ferritin and Ferroportin
Ferritin = stores iron in the cells Ferroportin = releases iron into blood to get stored else where
Electrolyte absorption
SI : Na, Cl, HCO, K, H2O ABSORBED
Crypts of SI ——> SECRETE
H2O and volume absorbed in proportion isosmotic
Jejunum electrolytes
Ileum electrolytes
Colon electrolytes
NA+ ABSORBED a lot (for carbs and AA)
NA+ absorbed and HCO secreted (with bile and VitB12)
NA+ absorption and K secretion (modulated by aldosterone)
Cholera toxin and electrolytes
Massive Cl- secretion
Cholera increases cAMP = increased Cl secreation
= Na and H2O secretion a lot also
= MASSIVE D
Secretory D
Absorptive D
Cholera
Lactose Intolerance
