Physiology: Gi

Front 1

where is the auerbach's (myenteric) plexus?

Back 1

between outer longitudinal and inner circular mm.

Front 2

what is the major neurotransmitter in the myenteric and submucosal plexus?

Back 2

Nitric Oxide

Front 3

what do vagal signals affect?

Back 3

stomach peristalsis, acid, panc acinar & HCO3 secretion, GB contraction,

minimal effect on small intestine

Front 4

what are the 3 major salivary glands?

Back 4

paratid, submandibular, sublingual

Front 5

what triggers saliva secretion?

Back 5

both symp (T1-T3 sup. cervical gang) and parasymp (facial, glossopharyngeal)

Front 6

what are the components of saliva?

Back 6

alpha-amylase (digest starch)
bicarb (neutralize bact acid)
mucin (glycoproteins, lubricate)

Front 7

where are parietal and chief cells found?

Back 7

Fundis of stomach

Front 8

name two GI hormone that belong to the same protein family

Back 8

gastrin, CCK (identical C term, active region can bind each other's R)

Front 9

what part of stomach is endocrine? exocrine?

Back 9

endo: lower 1/3
exo: upper 2/3 (pepsin, HCl, IF etc)

Front 10

where is gastric produced?

Back 10

G cells, antrum of stomach

Front 11

Is NO a secretalogue or abs stimulant?

Back 11

secretalogue

Front 12

Is ACh a secretalogue or abs stimulant?

Back 12

secretalogue

Front 13

Is NE/Epi a secretalogue or abs stimulant?

Back 13

stim. net abs

Front 14

what is the action of gastrin?

Back 14

in. H+ secretion, in. gastric mucosa

Front 15

what regulates gastric production?

Back 15

increased by:
stomach distention, aa (esp trp and phe), peptides, vagal stim,
decreased by:
H+ secretion, and stomach pH <1.5

Front 16

what makes CCK (cholecytokinin)?

Back 16

I cells of duodenum, jej.

Front 17

what does CCK do?

Back 17

1. in. panc. secretion
2. in. GB contraction
3. inhibits gastric emptying

Front 18

what triggers CCK production?

Back 18

lumenal fat (C18>C16>C8) and aa from gastric chyme in duo (decreased by secretin and stomach pH < 1.5)

Front 19

why in cholelithiasis, pain worsens after fatty food meal?

Back 19

production of CCK -> squeezes GB

Front 20

what makes secretin?

Back 20

S cells of duodenum?

Front 21

what does secretin do?

Back 21

in. panc HCO3, inhibits gastric acid secretion

Front 22

what triggers secretin production?

Back 22

acid, fatty acids in duo lumen

Front 23

what makes somatostatin?

Back 23

D cells in pancreatic islet; GI mucosa

Front 24

what does somatostatin do?

Back 24

increases Na reabs

inhibits:
1. acid and pepsinogen secretion
2. panc. and small intestine fluid secretion
3. GB contraction
4. release of insulin/glucagon
5. de. gastrin, CCK, secretin, VIP, GIP

Front 25

what regulates somatostatin?

Back 25

increased by acid;
inhibited by vagus

Front 26

what are octreotide, lanreotide?

Back 26

long-lasting somatostatin mimic, for carcinoid syndrome (e.g. VIPoma)

Front 27

what makes GIP (gastric inhibitory peptide)?

Back 27

K cells in duo and jej

Front 28

function of GIP?

Back 28

exocrine: decrease H+ secretion and peristalsis
endocine: increase insulin release

Front 29

what do parietal cells secret?

Back 29

intrinsic factor, gastric acid

Front 30

what do chief cells secret?

Back 30

pepsinogen, gastric lipase,

Front 31

what happens when there's autoimmune destruction of parietal cells?

Back 31

de. IF -> anemia

Front 32

what triggers stomach acid production?

Back 32

increase:
histamine, ACh, gastrin
decrease:
somatostatin, GIP, PGs

Front 33

what's the optimal pH for pepsin?

Back 33

1-3 (pepsin digest 15% of total protein)

Front 34

what secrets bicarbonate in the gut?

Back 34

musocal cells (together with mucus) in stomach and duodenum;
stimulated by secretin

Front 35

What is the pathophys of cholera?

Back 35

cholera toxin -> ADP-ribosylation of alpha-s subunit of GM1-ganglioside receptor of enterocyte luminal membrane (Gprotein R) -> const. active -> in. cAMP -> + anion secretion, - Na reabs -> diarrhea
(same for E.Coli heat-liable toxin)

Front 36

What is the pathophys of pertussis toxin

Back 36

ADP ribosylate alpha-i subunit -> INACTIVATION of G-protein R -> cAMP+++ -> + anion secretion, - Na reabs -> diarrhea

Front 37

What is guanylin? what bacterial toxin is implicated?

Back 37

gut hormone, binds guanylin R on gut epithelium -> receptor guanylate cyclase -> GTP to cGMP -> + anion secretion, - Na reabs -> diarrhea
(same with E.Coli heat stable enterotoxin (STa)
(NO stim. soluble GC)

Front 38

what is an effective treatment for bacterial diarrhea?

Back 38

treat with nutrient (e.g. glucose, aa) + electrolyte + H2O
nut-coupled Na transport not dependent on cAMP or cGMP, not affected by cholera, pertussis or E.Coli toxins.

Front 39

what is the major transporter for acidic a.a. (glu, gln, asp)

Back 39

none, used in energy metab as fuel for small intestine

Front 40

what is the relationship between cholera and cystic fibrosis?

Back 40

CF may give immunity to cholera & add + selection, cos CF has defective Cl- channels (targetted by cholera toxins)

Front 41

how are peptides/aa taken up in jejunum?

Back 41

as di/tri-peptides, cotransport with H+

Front 42

how are peptides/aa taken up in ileum?

Back 42

as single aa by membrane transporters, some Na-dep, some thru facilitated diffusion

Front 43

how common is celiac disease?

Back 43

~1 in 200 (atrophy of villi in prox. sm. bowel in rxn to gluten -> gliadin -> immune rxn)

Front 44

what are the two sphincters for the esophagus?

Back 44

1. cricopharyngeal sphincter
2. LES (lower eso sphnicter)

Front 45

muscle distribution in esophagus?

Back 45

upper 1/3: striated
middle 1/3: mixed
lower 1/3: smooth

Front 46

What happens when LES is too tight?
too loose?

Back 46

too tight: achalasia
too loose: reflux esophagitis

Front 47

what is the action of NO on the gut?

Back 47

sm. mm. relaxation, e.g. relaxes LES

Front 48

what two factors relaxes LES?

Back 48

NO, VIP

Front 49

what is receptive relaxation? what mediates it?

Back 49

upper 1/3 of stomach (reservoir), on reception of food, relaxes, reg. by vagal n.

Front 50

what is antral systole?

Back 50

when food passes stomach antrum, increase pyloric sphincter tone (rigid but partially open) so that small food can pass, big food reflux back for further churning

Front 51

where is iron reabsorbed in the gut?

Back 51

in proximal duodenum

Front 52

where is folate reabsorbed in the gut?

Back 52

distal duodenum

Front 53

where is B12 and bile salts reabsorbed in the gut?

Back 53

distal ileum

Front 54

where is short-chain fatty acids reabs in the gut?

Back 54

cecum

Front 55

(T/F) gut sm mm. myosin light chain needs phosphorylation to interact with actin to cause contraction

Back 55

TRUE

Front 56

what activates phosphorylation of myosin light chain in gut sm mm.?

Back 56

Ca/Calmodulin -> activates MLC kinase -> P myosin light chain

Front 57

what factors inhibit gastric emptying/acid secretion?

Back 57

CCK, GIP, fat, secretin, VIP

Front 58

what is the action of VIP and where is it secreted?

Back 58

secreted by sm mm. and nerves of intestines;
relaxes intestinal sm mm, cause pancreatic HCO3 secretion and inhibits gastric H+, relaxes LES, cause vasodilation (secretalogue)

Front 59

what is the effect of parasympathetics (ACh)

Back 59

inc. saliva, gastric H+, panc enz and HC03, simulates enteric nervous system to create intestinal peristalsis and relaxes sphincters.

Front 60

what is the effect of sympathetics (NE)

Back 60

inc. saliva, dec. splanchnic blood flow, motility, constricts sphincters

Front 61

what is migrating motor complex (MMC)?

Back 61

during fasting and b/w meals, ~90 min intervals, gut peristalsis to clear for the next meal (phase I: no spike; II: irreg spikes; III: reg spikes)

Front 62

t/f. the MMC is regulated by vagus`

Back 62

FALSE. it's autonomic

Front 63

what is basic electrical rhythm?

Back 63

pacemaker, not affected by hormones, baseline determining max freq of contractions, but does not determine actual contraction freq

Front 64

t/f. basic electrical rhythm decreases from proximal to distal in small intestine, and inc. from prox to distal in colon

Back 64

true

Front 65

what stimulates MMC?

Back 65

motilin, opioid, somatostatin

Front 66

what inhibits MMC?

Back 66

meal (gastrin, CCK)

Front 67

what is spike potential?

Back 67

on top of BER, affected by hormones and neurotransmitters, determines actual contraction of gut sm mm.

Front 68

t/f. Symp (Epi/NE) stimulates spike potential; parasym (ACh) inhibits spike potential.

Back 68

FALSE. reverse is true.

Front 69

t/f. small bowel is leakier

Back 69

true (prox to distal dec. in permeability)

Front 70

what parasym plexus innervates the gut? symp?

Back 70

parasymp: vagal and pelvic (distal colon and rectum)
symp:celiac, SM, IM

Front 71

what happens when LES is too loose? too tight?

Back 71

reflux esophagitis; achalasia

Front 72

what happens when antral systole is too loose? too tight?

Back 72

dumping syndrome (vaso-vagal discharge with hypertension);
gastroparesis (usu. diabetic w/ neuropathy, impaired/no gastric motility and delayed emptying)

Front 73

describe the three phases of gastric digestion

Back 73

cephalic phase, 30-40%, chewing etc -> vagus -> gastrin and H+
gastric phase, 50%, distension, luminal peptides/aa -> vagus -> gastrin/H+
intestinal phase: 10%, gastric chyme distention and aa -> acid

Front 74

describe the 3 phases of pancreatic exocrine digestion

Back 74

1. cephalic: 50%, smell etc -> vagal -> ductular + acinar
2. gastric: distention, aa -> vagal -> gastrin -> acinar
3. intestinal: lum. fat (C18>12>8), gastric chyme -> CCK, secretin -> vagal -> acinar + ductular

Front 75

t/f. CCK acts via vagal stimulations

Back 75

true

Front 76

what't the major inhibitor of gastric acid secretion?

Back 76

somatostatin

Front 77

gastric luminal fat triggers production of what factors?

Back 77

GIP, somatostatin, VIP

Front 78

t/f. proton pumps in parietal cells are always present on apical side

Back 78

false. they're stored in tubulovesicles at rest, and fuse with luminal membrane when stimulated

Front 79

describe acid secretion in parietal cells

Back 79

apical side:
H/K ATPase: H out, K in;
K recycled out through: K/Cl channel
H+ comes from H2CO3, which also gives HCO3-, which goes out through:
basolateral side:
HCO3-/Cl- antiporter

Front 80

what is omeprazole?

Back 80

proton pump inhibitor
(subsituted benzimidazole: acid changes to sulfonamide (rxn w/ cysteine thiol groups) -> bind luminal domains of alpha unit of pump to inhibit ATPase)

Front 81

what receptors stimulate gastric acid secretion on basolateral side and give some antagonists.

Back 81

histamine (cAMP): ranitidine, cimetidine, famotidine
ACh (PIP2): anticholinergics
gastrin (PIP2): no clinically useful inhibitor
prostaglandin: misoprostol (PGI2, PGE2 stimulates receptor)

Front 82

what are some remedies for stomach ulcer?

Back 82

proton pump inhibitors
anti histamines
anti cholinergics
PG receptor antagonist (misoprostol)
antacids and coating agents (sucralfate, CBS)

Front 83

what are the different cell types of gastric (oxyntic) gland?

Back 83

surface/neck mucus cells (mucus, HCO3)
endocrine cells
cheif cells (pepsinogen, gastric lipase)
histamine mast cells (regulate pepsin and acid)
pareital cells (HCl and IF)

Front 84

what factors stimulate chief cell pepsinogen release (pepsinogen granules on apical surface)

Back 84

thru PIP2:
gastrin, CCK, GIP
thru AC:
secretin, VIP, PG(E), beta-agonist

Front 85

group the following:
trypsin, chymotrypsin, elastase, carboxypeptidase

with:
endopeptidase, exopeptidase, basic aa, aromatic aa, alipathic aa, C-term bonds

Back 85

endopep:
trypsin - basic
chymo - aromatic
elastase - alipathic

exopep:
carboxypeptidase - C-terminal bonds

Front 86

what different cell types are there in intestinal cells?

Back 86

villus:
columlar polarized epi
mucus/goblet cells
crypt:
mucosal endocrine
Paneth cells -> defensin (anti microb)

3-5 days turnover from crypt to apoptosis at tip

Front 87

choose:
intestinal villus cells:
BB hydrolase: high/low
nut. trans.: high/low
net absorption/secretion
permeability: high/low

do the same for crypt cells

Back 87

villus:
BB hydrolase: high
nut. trans.: high
net absorption
permeability: low

crypt:
BB hydrolase: low
nut. trans.: low
net secretion
permeability: high

Front 88

what increase aggressive factors for stomach ulcer?

Back 88

(aggressive factors: acid, pepsin)
nicotin, gastric acid, NSAIDs, H pylori (cause inflammation, stimulate acid secretion)

* H pylori survives stomach acid through urease H + NH3 -> NH4, buffer acidity

Front 89

what decrease protective factors for stomach ulcer?

Back 89

(protective factors: mucus, bicarb)
NSAIDs (inhibits arachidonate, which inhibits mucus, HCO3, cos PGE&F stimulate mucus release),
H pylori
bile acids

Front 90

what are the different pancreatic enzymes?

Back 90

alpha amylase
lipase, phospholipase A, colipase
proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)

Front 91

what converts trypsinogen to active trypsin?

Back 91

enterokinase/enteropeptidase, a duodenal BB enzyme.

Front 92

what activates zymogens of chymotrypsin, carboxypeptidases etc?

Back 92

trypsin (trypsin also activates more trypsinogen)

Front 93

wot common digestive problem do CF patients have?

Back 93

panc insufficiency (thick mucus -> self digestion of panc by panc enzymes); malabsorption, steatorrhea (fatty stool), poor intake of fat-soluble vitamins

Front 94

dorsal and ventral pancreas (development): which part is which?

Back 94

body, tail, part head/uncinate: dorsum
part head/uncinate, bile duct: ventral (main conduit)

Front 95

what triggers zymogen granule release in acinar cells in pancreas?

Back 95

thru IP3 -> NO -> cGMP -> PKs:
ACh (major), CCK, bombesin, substance P

thru AC/cAMP-> PKs:
secretin, VIP

Front 96

> how many grams of stool a day is considered diarrhea?

Back 96

200g

Front 97

sucrase and what is 1 gene, cleaved post-translationally?

Back 97

isomaltase; cleaved by trypsin, but still non-covalently connected on BB membrane.

Front 98

what glucose linkages do amylose and amylopectin have?

Back 98

amylose: alpha 1-4 only
amylopectin: alpha 1-4 and 1-6

Front 99

amylase digest what glucose linkage?

Back 99

alpha 1-4, to give maltose, maltotriose, alpha-limit dextran (amylopectin)

Front 100

in neonates, panc. amylase not well developed. what's important for digesting sugars?

Back 100

salivary amylase

Front 101

pancreatic amylase digests starch to what?

Back 101

oligosaccharides, maltose, maltoriose
(only monosaccharides are absorbed)

Front 102

t/f. lactase drops to 10% neonatal amount by 5-10 years

Back 102

true

Front 103

oligosaccharide hydrolases are present where? include what?

Back 103

at BB of intestine (rate-limiting step in carb digestion)
sucrase, lactase, trehalase (digest trehalose in mushrooms)

Front 104

how do the following enzymes break alpha-limit dextrans?
glucoamylase, isomaltase, sucrase

Back 104

glucoamylase: alpha 1-4
isomaltase: alpha 1-6
sucrase: maltose and maltosetriose to glucose

Front 105

jaundice results from what?

Back 105

elevated bilirubin levels

Front 106

what is bilirubin?

Back 106

product of heme metabolism

Front 107

match:
GLUT5, SGLT1, GLUT2

apical, basolateral, fructose, glucose, galactose, a.a.

Back 107

GLUT5: fructose, apical
SGLT1: glucose/Na+ symport, apical

GLUT2: basolateral: fructose, galactose, glucose

a.a. have their own Na-coupled transporter on apical side, and transporter on basolateral side.

(3Na/2K ATPase on basolateral side to create gradient)

Front 108

what is kernicterus?

Back 108

mother-fetus blood mismatch -> inc. hemolysis, inc. bilirubin -> jaundice

Front 109

what is breast-milk jaundice?

Back 109

in fetus, beta-glucoronidase deconj bili -> reabs for clearance by placenta. breast milk has glucoronidase

Front 110

give the heme degradation pathway

Back 110

in spleen:
heme -> (heme oxygenase) biliverdin -> (biliverdin reductase) bilirubin

in liver (bound to cytosolic ligandin and Z-proteins after facilitated diffusion uptake)
bilirubin conjugated to glucoronide (bilirubin UDP glucoronosyl-transferase) -> excreted into bile -> colon bact conversion to urobilinogen -> feces, or small fraction enterohepatic circulation or UB

Front 111

what happens to urobilinogen after enterohepatic circulation?

Back 111

some re-excreted in bile, some renal excretion
urobilinogen -> (oxidation) urobilin (yellow colour in urine/stool)

Front 112

what are the properties of conj. vs unconj. bilirubin?

Back 112

conj:
soluble, non-toxic, cannot be reabs in GI

unconj:
insoluble, reabs in GI, toxic, can cross BBB (esp in neonates where BBB is think) -> inhibits RNA syn and carb metab (neonatal kernicterus)

Front 113

with bile duct obstruction, can u detect urobilinogen in urine? in stool?

Back 113

none in both.
(none in urine cos need to go through enterohepatic circulation (bilirubin converted to UB only in gut). bili in bile cannot flow to gut -> no UB made)

Front 114

with cholestasis, what becomes major site of clearnace for conjugated bilirubin? how?

Back 114

kidneys.
unconj. bilirubin bound avidly to albumin, cannot be filtered out in kidneys.
but some conj. bilirubin are not bound to albumin, and glom. filterated, but may form bilirubin gallstones.

Front 115

what causes conj. hyperbilirubinaemia? name two disorders

Back 115

defect in cannicular transport
dublin johnson (pigment in hepatic lysosome)
rotor's (no pigment)

Front 116

what causes unconj. hyperbilirubinemia?

Back 116

inc. rbc hemolysis (mom-fetal incompatible); defective conjugation (e.g. def. bilirubin UDP glucoronyl transferase)

gilbert (partial UDPGT activity, benign until fasting/stressed)
crigler-najjar syndrome:
type I: complete loss -> death
II: partial loss

Front 117

what are some therapeutic strategies for unconj. hyperbilirubinemia?

Back 117

1. phenobartital -> inc. UDPGT
2. freq feeding (dec. enterohepatic circulation)
3. phototheraphy (inc. solubility of unconj. bili -> inc. excretion in urine) (esp in neonates cos small mass:surface ratio)
4. exchange fusion
5. bili binders (e.g. agar)

Front 118

what's phase I detoxification?

Back 118

redox and hydrolysis:
make polar and soluble
can make toxic intermediate
P450-dep monooxygenase

Front 119

what is phase II detox?

Back 119

conjugation:
inc. solubility:
1. glucoronide
2. sulfation
dec. solubility:
3. methylation

Front 120

describe acetaminophen detox pathway

Back 120

most: conj. to sulfate and glucoronate;
5-15%: P450-dep -> NAPQI -> conj to GSH -> mercapturic acid -> eliminate in kidneys
NAPQI electrophilic, can rxt with sulfhydryl gps (covalent) -> necrosis (happens when GSH is depleted)

Front 121

why are alcoholics more susceptible to acetaminophen toxicity?

Back 121

alcoholics:
1. induction of P450 (makes more NAPQI)
2. depletion of GSH (cannot conj NAPQI to make mercapturic acid for elim in kidneys)

Front 122

how do you treat acetaminophen toxicity?

Back 122

treat with N-acetyl-cystein, which is a precursor for GSH -> inc. conj. of NAPQI.

Front 123

how do you treat patients with mutated MTTP (microsomal triglycerides transport protein)?

Back 123

no MTTP: cannot take up fatty acids on basolateral side.
can give medium-chain TG (hydrolysed by lipase more rapidly and more soluble, diffuse directly across lumenal cells into portal blood)

Front 124

how are long-chain triglycerides digested and absorbed?

Back 124

lumen:
emulsify -> lipolysis (lipases) -> solubilize -> diffuse
musocal:
1. uptake (binding proteins for free f.a. and 2-monoglycerides)
2. transport to smooth ER
3. TG resynthesis from f.a.
4. package into chylomicrons (MTTP-dep)
5. export chylo to lymphatics on basolateral side (MTTP-dep)

*MTTP = microsomal TG transport protein

Front 125

what protein do you test for general liver function?

Back 125

albumin (55-60% of all plasma protein), made by liver, hydrophilic, bind and transport hydrophobic proteins

Front 126

how is liver portal venous pressure measured?

Back 126

indirectly by wedged hepatic VP;
hep. VP gradient = WHVP - free HVP (or IVC pressure)

normal should be low since hep. portal venous blood flow is very low and constant

Front 127

what are the values of HVPG and PVP for portal hypertension

Back 127

normal hep. venous pressure gradient (=WHVP - free HVP/IVC P) should be very low (since blood flow in portal system is low and constant)

portal HT: > 5 mmHg HVPG or > 12 mmHg portal venous pressure (measured by wedged hep. VP)

Front 128

t/f. inc. portal vascular resistance or inc. inflow -> portal hypertension

Back 128

true

Front 129

what are the different types of portal hypertension?

Back 129

prehepatic (e.g. portal vein thrombosis)
intrahepatic (e.g. cirrhosis)
post hepatic (e.g. IVC obstruction)

Front 130

what happens to blood vessels in the portal system when there is portal hypertension?

Back 130

portosystemic collaterals form (eso, abd, stomach, periumbillical area, rectum) -> variceal bleeding

Front 131

what are the complications of portal HT?

Back 131

1. splenomegaly and hypersplenism -> sequestration of rbc, wbc and platelets -> low platelet count
2. variceal bleeding
3. heptaic encephalopathy (cos build up ammonia -> CSF glutamine, also trp metab and GABA-like stuff)
4. ascites (liver and intestinal lymph), favored by hypoalbuminemia (often in cirrhosis)

Front 132

what are the characteristics of liver cirrhosis?

Back 132

1. collagen deposition
2. inc. cell dize
3. regenerative nodules
4. contraction of myofibroblasts

Front 133

where is ammonia metabolized? what is it metabolized to? why is it toxic?

Back 133

in liver, to urea (mainly from glutamate).
NH3 can cross BBB, esp toxic to glial cells

Front 134

t/f liver uses mainly carbs as fuel

Back 134

false: prefers fatty acids.

Front 135

what is the pathology of CF? what are the related symptoms?

Back 135

defective Cl- channel, thick mucus, high Cl- in sweat, intestinal obstruction, panc duct blocked, acinar cells atrophy/self-destruction, poor digestion, lung infections

Front 136

what is diabetic diarrhea?

Back 136

adrenergic neuropathy due to reduced blood flow -> inc. anion secretion and reduced Na reabsorption

Front 137

how do u treat diabetic diarrhea?

Back 137

treat with alpha2 adrenergic R agonist (e.g. clonidine) or Octreotide (somatostatin analog, stim. net absorption)

Front 138

what is celiac disease?

Back 138

autoimmune rxn to gliadin (short peptide undigestable from gluten_ -> villi atrophy -> dec. CCK, gastrin, secretin

Front 139

what is increased urine amylase diagnostic of?

Back 139

pancreatitis

Front 140

mix and match:
hartnup's disease, cystinuria, lysinuric proterin intolerance.

dibasic a.a., cationic a.a. ,
neutral a.a.,(basolateral or lumenal?)

Back 140

hartnup's: neutral a.a. on lumenal
cystinuria: dibasic a.a. on lumenal (Cys, Ornithine, Lys, Arg (COLA)
lysinuric PI: cationic a.a. on basolateral (OLA)

Front 141

excess cystein from cystinuria can result in what? treat with what?

Back 141

kidney stones. treat with acetazolamide to alkalize urine

Front 142

what is more severe? cystinuria, hartnup's or lysinuric prot. intolerence?

Back 142

lysinuric protein intolerance (def transport for cationic aa (lys, arg, orn) at basolateral side. (for the other two, def. lumenal transporters,but di/tri-peptides can be taken up and broken down intracellularly and transported through basolateral transporters, mutated in LPI)

Front 143

what are the effects of increased short-chain fatty acids (diet carb digested by colon flora and bact)

Back 143

inc. NHE
preferred fuel for colonocytes
inc. mucosal proliferation
inc. Na abs

Front 144

t/f
inc aldosterone leads to:
prox colon: inc. Na pump/ PD-dep Na channel
distal colon: inc. NHE

Back 144

false, reverse

Front 145

what is the compensatory mech for small bowel resection or disease?

Back 145

inc. villi width and height, inc. Na abs by inc. NHE

Front 146

diff. bile acid-dep flow vs b.a.-indep flow (both -> canalicular)

Back 146

b.a.-dep: active trans of b.a., electrolytes follow;
indep: active trans of electrolytes

--> canalicular, rate limiting

Front 147

what are the components of bile acid secretion?

Back 147

bile acid-dep flow, bile acid-indep flow -> canalicular;
ductular secretion (stim. by secretin via cAMP):
1. inc. Cl-/HCO3- -> lumen neg and alkaline -> Na and H20 outflow
2. Cl- channel open to fill lumen with Cl-

Front 148

give examples of bile acids metabolism disorders (reasons for inadequate b.a. for digestion of fat)

Back 148

1. cholestasis (bile flow failure)
2. ileal resection
3. bact outgrowth (decong. -> readily reabs b.a. -> dec. in gut -> malabs and toxi decong. b.a.)

Front 149

t/f
f.a. absorption: rate limiting = diffusion of micelles thru "unstirred H20 layer"

Back 149

true. (lower pH near plasma membrane -> f.a. protonated -> more soluble)

Front 150

what converts cholecterol to bile salts?

Back 150

7alpha hydroxylase (rate limiting, bile salts feedback inhibit both 7a and HMG CoA reductase)

Front 151

dietary fat absorption is ?% efficient?

Back 151

95% !!!

Front 152

bile acids conjugated to __ and __ to make them charged to increase solubility?

Back 152

taurine and glycine

Front 153

liver lobule vs hepatic acinus

Back 153

lobule: central vein in center, triad at corner (hep artery, portal vein, bile duct)

acinus: triad at center, zone 1-3, 1 most regen and resistant to hypoxia

Front 154

what's the main function of gall bladder?

Back 154

store and concentrate bile (by extracting water)

Front 155

what is primary vs secondary bile salts?

Back 155

primary: cholate and chenodeoxycholate
secondary: after bacterial deconj. (-> primary via reabs, reconj. in liver)
-> tertiary ursodeoxycholate (more soluble, used as med to inc. bile flow for ppl with small stone)

Front 156

where and how is bile reabs?

Back 156

>90% reabs via apical Na-dep bile transporter (ASBT) in ielum

Front 157

what are the 3 different types of lipases?

Back 157

sepcific for TG
1. gastric (hydrolyse f.a. at 3 position)
2. panc (hydrolyse at 1 and 3 position)

also for acylglycerols, chol esters, vit esters, phospholipids:
3. bile-salt activated, made by panc (e.g. phospholipase A2, chol esterase)

Front 158

t/f
gastric lipase requires co-lipase but panc lipases do not

Back 158

false. panc lipase requires co-lipase, which binds and displace bile salts coating surface of oil droplets, which inhibit binding of panc lipase

Front 159

t/f
panc lipase is at large excess, >90% must be lost before u see fatty stool

Back 159

true