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GIGU Exam 1 > Absorption And Digestion - Dr. Rogers > Flashcards

Absorption And Digestion - Dr. Rogers Flashcards

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
Q

How are protein enzymes activated

A

By enterokinase = trypsinogen
By trypsin
In Cystic Fibrosis congenital trypsin absence - NO Trypsin

26
Q

Epithelial cell of SI transporters on lumen side

A

AA cotransporter with Na+ to get into the cell

Of di and try with H+

27
Q

Transporters on the epithelial cells of the blood side

A

Facilitated diffusion for each type of AA

28
Q

Steatorrhea

A

Fat and lipid in the stools

29
Q

Recurrent greasy, pale, foul smelling D
Wright loss, ABD pain,
Worsened when she started eating bread
SI bowel biopsy’s

A

CELIAC DISEASE

30
Q

Celiac Disease

A

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
Q

Tropical Sprue

A

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
Q

How are lipids digested

A

Bile salts and lecithin emulsify lipids into micelles from the liver

33
Q

Where are lipids digested

A

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
Q

Where are most of lipids digested

A

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
Q

steps tp break down fats

A
  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
Q

Problems with lipid digestion anywhere causes

A

Steatorrhea

37
Q

Pancreatitis

A

Trypsin a pancreatic enzyme gets activated in the pancreas and eat it up
=X HCO-3 and enzymes released into duodenum

38
Q

Pancreatic insufficiency

A

Can secrete right amount of pancreatic enzymes

39
Q

Zollinger-Ellison Syndrome

A

GASTRIN secreting tumor in pancreas
Increase H+ by parietal cells in gastric mucosa
- high acidity in duodenum

40
Q

Reasons for insufficient bile salt secretion

A

Ileal resection = X bile salt enterohepatic recirculation
Liver Disease
Gallbladder Disease
*micelles cant be formed in SI

41
Q

What happen in Small Intestine Bacterial Overgrowth (SIBO)

A

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
Q

What do you see is testing celiac disease e

A

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
Q

Water solvable VIT

A

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
Q

Fat soluble vits

A

Absorbed as other lipids

45
Q

Importance VIT B12

A

RNA and DNA = to make RBS

Nerve myelination, and cofactor for folate coenzyme recycling

46
Q

How VIT B 12 is absorbed in the GI

A

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
Q

VIT B 12 deficiency

A

Pernicious Anemia + weakness in nerve conduction
X RBC maturation
Macrocytic and megoblastic anemias

48
Q

Pernicious Anemia in the Stomach effects

A

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
Q

What surgeries can cause problems with VIT b12 absorption

A
  1. Gasterectomy = no parietal cells
  2. Gastric Bypass = pass stomach, esophagus—-> distal Jejunum
  3. Crohns Diease = Ileum is removed
50
Q

X VIT D

A

helps with Ca + absorption
Rickets - childhood
Osteomalacia - adults

51
Q

Ca+2 absorption

A

Across enterocytes with VITD
Reabsorption at Kidney with PTH
Calcitonin ——I reabsorption

52
Q

IRON absorption

A

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
Q

Role of VIT C in iron absorption

A

Iron is readily absorbed as Fe+2 (animal)

Plants have Fe+3 ———VITC———> Fe+2

54
Q

Ferritin and Ferroportin

A 
Ferritin = stores iron in the cells 
Ferroportin = releases iron into blood to get stored else where
55
Q

Electrolyte absorption

A

SI : Na, Cl, HCO, K, H2O ABSORBED
Crypts of SI ——> SECRETE
H2O and volume absorbed in proportion isosmotic

56
Q

Jejunum electrolytes
Ileum electrolytes
Colon electrolytes

A

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
Q

Cholera toxin and electrolytes

A

Massive Cl- secretion
Cholera increases cAMP = increased Cl secreation
= Na and H2O secretion a lot also
= MASSIVE D

58
Q

Secretory D

Absorptive D

A

Cholera

Lactose Intolerance

GIGU Exam 1 (19 decks)

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