Malabs

Question 0

maldigestion

Answer 0

failure to breakdown (hydroxylse) complex nutrients

Question 1

malabsorption

Answer 1

failure to transport simple nutrients and products of digestion

Question 2

where are carbs absorped

Answer 2

jejunum>distal SB>duo

none in colon

Question 3

4 steps to carb abs

Answer 3

1) physical denaturation (larger polys–>smaller polys via mastication to increase SA)
2) amylase (polys–>oligos + disach) *need netral PH
3) BB digestion: oligos –>monos (lactose, glucose, fructose)
4) CHO absorption

Question 4

rate limiting step carbs

Answer 4

absorption not digestion except lactose in lactose intolerance

Question 5

lactose absorbed by

Answer 5

lactase

Question 6

glucose

Answer 6

cleaved one at a time from alpha dextrins via binfunctional enxymes

Question 7

fructose

Answer 7

sucrase breaks sucrose into glucose + fructose (2 glucoses)

Question 8

2 apical membrane transporters

Answer 8

GLUT5- fructose facilitated diffusion

SGLT1- glucose/galactose- active co transport with Na driven by Na/KaTPase on other side

Question 9

GLUT2

Answer 9

facilitated diffusion on basolateral

Question 10

during starvation

Answer 10

decrease energy therefore decrease Na/K ATPase so Na accumulate in cell whiel glucose still goes through GLUT2

Question 11

colonic savage

Answer 11

2-20% of starch undigestable therefore bacteria ferment to small chain fatty acids, H20< Co2, H+ and methane and enterocytes abs small chain fatty acids for energy and caloric supllement

but if you increase ingestion or decrease fermentation (antibotics)–> less abs–>diarrhea

Question 12

protein digestion

Answer 12

1) metabolic breakdown (proteins–>oligopeptides + amino acids)
2) gatric hydrolysis- low ph activates pepsin from ppsinogen–>digests 10-15% of dietary protein (not essential)
3) typrsin and luminal digestion
panc realeases trypsinogen–>enterokinases and trypsin turn tyrpsinogen to trypsin–>activates 4 other peptides–>autodigestion to turn off
4)absorption

Question 13

3 ways of protein absorption

Answer 13

apical AA transporters
di,tri, tetra varrier molecules
paracellular **food allergies

Question 14

disease of single aa transporter

Answer 14

asymptomatic

Question 15

hartnup

Answer 15

AR neutral amino acid disease that leads to pellagra, ataxia, psychosis

Question 16

cystinuria

Answer 16

AR dibasic aa disorder–>cystine ppts in kidney tubules

Question 17

6 steps of fat digestion

Answer 17

1) emulsification- cooking, mastification, antral grinding
2)gastric hydrolysis (chief cells release gastrin–>gastric lipase–>TAGs to DAGs) –neglicible effect
2)completion of hydrolysis
FA stimulate CCK, GIP–>increase panc and biliary secretions–>pancreatic lipases (TAG–>MAG + 2 FA)
4)micelle formation
5) chylomicron formation
6)post processing dietary fat

Question 18

why is gastric lipase ideal for stomach

Answer 18

active at low ph

Question 19

what does pancreatic lipase need to be active

Answer 19

alkaline ph (<2.5 perm inactive)
bile salts (emulsify fat and increase sA)
pancreatic co-lipase-- prevents lipase frm going away from oil, h20 interface

Question 20

micelle formation

Answer 20

MAG/FA, phospholipids + bile salts (micelle)–>transport to BB–>FA/MAG diffuse through, micelle goes back for more FA and MAG

Question 21

chylomicron formation

Answer 21

once isnside entero..
2MAG + FA=TAG–>ER and golgi coat TAG with apo and hydrophilic proteins–>chylo diffuses to lacteals, lymphatics, peripheral tissue

**bypasses liver

Question 22

post processing dietary fat

Answer 22

in periphehral tissue LPL breaks TAG down to FA + glycerol –>TAG again and remaining chylo shell (VLDL and HDL) which goes to liver

Question 23

celiac disease

Answer 23

TTG deamninates glutamine in fliadin–>gives it high affinity for HLADQ2 or DQ8–>present to CD4+ cells–>antigliadin ab and auto abs to ttg