Absorption And Digestion - Dr. Rogers Flashcards

(58 cards)

1
Q

Lactose Intolerance

A

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

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2
Q

Primary Sugars

A

Sucrose
Lactose
Starch

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3
Q

Secondary sugars

A

Amylase, Glycogen, EtOH, Lactic Acid, Pyruvic Acid, Pectins, Dextrins

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4
Q

Where does carb metabolism start

A

Oral cavity, amylase attacks starch

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5
Q

Where is lactose and sucrose attacked in the GI

A

In the SI most in duodenum (Lactase, Sucrase)

Pancreatic Amylase = starch continues

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6
Q

Most absorption of carbs happens and reason for it

A

Villi folds called FOLDs of KERCKRING (longitudinal folds) and increase SA

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7
Q

Where are the enzymes found

A

In the brush border of the villi

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8
Q

Maltose
Trehalose
Lactose
Sucrose

A

Glucose + Glucose
Glucose + Glucose
Glucose + Galactose
Glucose + Fructose

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9
Q

STARCH breaks down to

A
  1. Starch —AMYLASE—> Maltose——> 2Glucose
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10
Q

How is Glucose absorbed

A
SGLT1 = absorbs glucose and galactose from lumen 
GLUT5 = fructose absorption from lumen
GLUT2 = absorbs glucose + galactose + fructose into blood
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11
Q

SGLT1 inhibitors

A

Can be used in Diabetes to slow glucose absorption

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12
Q

Which is the fastest sugar transporter

A

SGLT1 since it used Na+

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13
Q

X GLUT2

A

Glycogen gets stored in high amounts

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14
Q

How to test for carbohydrate digestion problems

A
  1. Breath Tests : methane, CO2 labeled isotope, Lacotse, sucrose
  2. Ingest D-xylose and see how much is able to get absorbed and present in urine (general statement for carbohydrate digestion problem)
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15
Q

In lactose intolerance what can you find in the tests run

A

Normal D-xylose

Positive Lactose breath test (H+ and methane sensed)

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16
Q

Protein digestion problems is

A

X pancreatic enzymes or X transporter of the SI epithelial cells

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17
Q

Chronic Pancreatitis

A

X pancreatic enzymes - proteases like trypsinogen get activated in pancreas and eats up pancreas and no enzymes are produced
Also no neutralization of stomach

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18
Q

Congenital Trypsin Absence

A

X trypsin

= no pancreatic enzymes activated

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19
Q

Cystinuria

A

X SLC3A1 transporter or SLC7A9 (absorb Cysteine, Lys, Arg, Ornithine in proximal tubule of kidney)
= AA secreted in feces and urine

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20
Q

Hartnup Disease

A

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

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21
Q

Cystic Fibrosis

A

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

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22
Q

Where does protein get digested initially

A

STOMACH
Pepsinogen—» Pepsin
10%-20%

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23
Q

Where does most of protein digestion happen

A

SI from pancreatic enzymes zymogen
Trypsin, chymotrypsin, carboxypeptidase, elastase
——> di and tri peptides

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24
Q

ROLE of carboxypepidase

A

Cleaves AA at carbonyl ends into individual AAs

So they can be absorbed by enterocytes and other cells

25
How are protein enzymes activated
By enterokinase = trypsinogen By trypsin In Cystic Fibrosis congenital trypsin absence - NO Trypsin
26
Epithelial cell of SI transporters on lumen side
AA cotransporter with Na+ to get into the cell | Of di and try with H+
27
Transporters on the epithelial cells of the blood side
Facilitated diffusion for each type of AA
28
Steatorrhea
Fat and lipid in the stools
29
Recurrent greasy, pale, foul smelling D Wright loss, ABD pain, Worsened when she started eating bread SI bowel biopsy’s
CELIAC DISEASE
30
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
31
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
32
How are lipids digested
Bile salts and lecithin emulsify lipids into micelles from the liver
33
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
34
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)
35
steps tp break down fats
1. Micelles solubilize 2. Diffusion of micelle contents (FAs + its backbones) across apical membrane 3. Re-esterification (put FAs back on the backbone) 4. Chylomicron forms by ApoB (X ApoB = no exocytosis of chylomicrons into lymph 5. Exocytosis of chylomicrons into lymph ——> LIVER 5.
36
Problems with lipid digestion anywhere causes
Steatorrhea
37
Pancreatitis
Trypsin a pancreatic enzyme gets activated in the pancreas and eat it up =X HCO-3 and enzymes released into duodenum
38
Pancreatic insufficiency
Can secrete right amount of pancreatic enzymes
39
Zollinger-Ellison Syndrome
GASTRIN secreting tumor in pancreas Increase H+ by parietal cells in gastric mucosa - high acidity in duodenum
40
Reasons for insufficient bile salt secretion
Ileal resection = X bile salt enterohepatic recirculation Liver Disease Gallbladder Disease *micelles cant be formed in SI
41
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
42
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
43
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
44
Fat soluble vits
Absorbed as other lipids
45
Importance VIT B12
RNA and DNA = to make RBS | Nerve myelination, and cofactor for folate coenzyme recycling
46
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
47
VIT B 12 deficiency
Pernicious Anemia + weakness in nerve conduction X RBC maturation Macrocytic and megoblastic anemias
48
Pernicious Anemia in the Stomach effects
NO IF made 1. Atrophic Gastritis = chronic inflammation of stomach - X parietal cells 2. Autoimmune Metaplastic Atrophic Gastritis = immune cells attack IF protein or Parietal cells
49
What surgeries can cause problems with VIT b12 absorption
1. Gasterectomy = no parietal cells 2. Gastric Bypass = pass stomach, esophagus—-> distal Jejunum 3. Crohns Diease = Ileum is removed
50
X VIT D
helps with Ca + absorption Rickets - childhood Osteomalacia - adults
51
Ca+2 absorption
Across enterocytes with VITD Reabsorption at Kidney with PTH Calcitonin ——I reabsorption
52
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)
53
Role of VIT C in iron absorption
Iron is readily absorbed as Fe+2 (animal) | Plants have Fe+3 ———VITC———> Fe+2
54
Ferritin and Ferroportin
``` Ferritin = stores iron in the cells Ferroportin = releases iron into blood to get stored else where ```
55
Electrolyte absorption
SI : Na, Cl, HCO, K, H2O ABSORBED Crypts of SI ——> SECRETE H2O and volume absorbed in proportion isosmotic
56
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)
57
Cholera toxin and electrolytes
Massive Cl- secretion Cholera increases cAMP = increased Cl secreation = Na and H2O secretion a lot also = MASSIVE D
58
Secretory D | Absorptive D
Cholera | Lactose Intolerance