If Exam 5

Front 1

Paneth cells

Back 1

-bottom of intestinal crypts
-EXOCRINE (into duct)
-make defensins (antimicrobial peptides)
-eosinophilic, granules, lots rER (for protein pdcn)
-most in terminal ileum; not in colon
-granule fusion triggered by ACh or bacterial LPS (?)

Front 2

Parietal cells

Back 2

-stomach
-generate pH gradient via HCl secr (gastric acid)
-also secrete intrinsic factor (nec for vit B12 abs)
-BL: Cl/HCO3 xchgr
-Ap: K/H xchgr; K/Cl cotransp

Front 3

Stim/inhib of parietal cells

Back 3

+ histamine (strongest) [acts via cAMP]
+ gastrin [acts via Ca++]
+ vagus (ACh) (weak) [acts via Ca++]
- H+
- somatostatin [inhibs cAMP]
- secretin (both directly & D cell --> SS)

Front 4

ECL cells

Back 4

-secrete histamine
-EC-like cells: have hist instead of serotonin
+ by gastrin
- by somatostatin

Front 5

G cells

Back 5

-secrete gastrin
+ by stretch receptor
- by somatostatin

Front 6

D cells

Back 6

-secrete somatostatin (SS)
+ by high [H+] & secretin
SS then - on G, ECL & parietal cells

Front 7

S cells

Back 7

-pdc secretin
+ by high H+
--> act - on parietal cells
--> act + on D cells (which - on parietal)
--> act + on pancreatic duct cells (which pdc HCO3)

Front 8

secretin

Back 8

- made by S cells in duodenum
- triggered when duoden acidified
- travels from duod via circ to stomach --> inhib parietal cells
- travels from duod to panc --> incr HCO3 made
- "natures antacid"

Front 9

ulcers: Zollinger Ellison

Back 9

-breakdown of mucus barrier--> digestion of stom/duod wall
--gastrin-secreting tumor (panc) = excess acid;
- Dx = secretin inj (if response = incr gastrin, = tumor; if decr gastrin, know normal G cells are source of gastrin)

Front 10

ulcers: H. pylori

Back 10

-bacteria
-secretes NH4, buffers own microenviro so less acidic
- breaks urea into CO2 & NH4
-Dx: biopsy, antibod in blood, isotop urea, meas isotop CO2 exhaled (+ = urease enz of H.pylori present); if no labeled CO2 exhaled, excr renally

Front 11

ulcers: destructive factors

Back 11

-NSAIDs, aspirin
-inhib COX1 enz --> decr prostaglandins
-Pgds fcn: incr blood flow, HCO3 secr, mucin secr'n; decr acid & pepsin secr'n
-- lack of Pgds = + ulcer

Front 12

Anti-acid drugs

Back 12

- histamine-R blocker (Zantac, Pepcid AC) [*only for H2 receptor in stomach; won't get syst effects]
- proton pump inhib (PPI): prilosec, omeprazole, nexium; lowers H+ made
- pH buffer: HCO3 (Rolaid, TUMS); can get used up if lots of H+
*don't target ACh or SS b/c would have systemic effects

Front 13

Barrett's esophagus

Back 13

- devel in 10-20% of ppl w/ GERD
- premalig condn: esoph epithel changes from strat squam to simp columnar (like of stomach)
*strat squam = protective
simple columnar = absorptive
- if have BE, 40x more likely to devel esoph adenocarcinoma (v. lethal)

Front 14

GI tract Lamina Propria (LP)

Back 14

- rich in lymphocytes (immune cells)
- mostly antibody secreting B cells
- distal sm int has Peyer's patches

Front 15

Peyer's patches

Back 15

- dense immune cells in distal sm int
- help control what goes into blood stream
- microfold (M) cells; B & T lymphocytes, macrophages, dendritic cells

Front 16

Chief cells

Back 16

-stomach
-secrete pepsinogen
+ by ACh

Front 17

Pancreatic acinar cells

Back 17

-secrete pancreatic digestive enzymes
+ by ACh & CCK

Front 18

Pancreatic Duct Cell

Back 18

-secrete HCO3 into lumen
-neutralize acidic chyme from stom
+ by secretin (nature's antacid)

Front 19

interdigestive phase

Back 19

-low H+ secretion b/c no food there to digest
- GIP, GLP-1 act globally: inhib gastric emptying & gastric acid secr'n; also: facilitate insulin release, inhib appetite

Front 20

cephalic phase

Back 20

-smell/see meal, CNS signals via vagal nerve
-parietal, chief, panc, GB, salivary glands stim'd

Front 21

gastric phase

Back 21

food introduced
- increase [H+] via parietal cells
- increase vagal stim to chief (enz), panc, GB, & parietal
- stretch & chemoreceptors activ'd --> act on G cells to secr gastrin -> actvs ECL cells --> HISTAMINE +++ on parietal cells

Front 22

Early intestinal phase

Back 22

- acidic chyme passes pyloric sphincter to prox duodenum
- Chemoreceptor stims I cell to make CCK
- CCK --> + pancr, GB, pyl sphincter (to slow food passage so incr digest & abs)

Front 23

Late intestinal phase

Back 23

- chyme done in stom, so no need for high [H+] there
- goal: slow down food to max'z abs of nutrients from food
- H+ in duod stim S cells to make secretin
- secretin + on D cells -> SS made; - on parietal cells
- SS is - on G & ECL cells = less H+ made for stomach
*S cells make inhib peptides (GIP, GLP-1?)???

Front 24

Pancreatic cells

Back 24

- islet (endocrine peptides)
- acinar (secr enz & NaCl)
- centroacinar (secr H2O & NaHCO3)
- duct cells (secr H2O & NaHCO3)
~99% is exocrine; 1% islet endocrine

Front 25

Cl-channels

Back 25

- where Cl goes, H2O follows
- actv'd by incr in Ca++ or cAMP
- Ca: CCK or ACh can + on IP3 --> incr Ca++
- cAMP: + by secretin, - by SS; coord of Cl & Cl/HCO3 exchgr
*cAMP --> "acid tide" in blood b/c HCO3 pumped into lumen

Front 26

Acinar cells

Back 26

- "grape" like shape
- Na enters lumen via paracellular route

Front 27

acid tide

Back 27

- from pancreas cAMP activated Cl channel (Cl & Cl/HCO3 xchgr)
- pumps HCO3 into lumen, H+ into blood
- joins w/ HCO3 rich blood from stomach before reaches liver

Front 28

alkaline tide

Back 28

- from stomach parietal cells
- pump H+ into lumen, HCO3- into blood
- blood joins w/ H+ rich blood from panc before reaches liver = neutralized

Front 29

hepatocytes

Back 29

- sit at jcn btwn abs route (portal vein) & secretory route (bile duct)
- bathed in blood coming from GI tract (fenestrated sinusoid caps; slow velocity = lots of time)
- if don't want, put into bile canaliculi
- *respond to secretin just like panc duct cells: cAMP --> HCO3 into lumen (joins Na, Cl, bile)

Front 30

bile composition

Back 30

- 12% bile acids (synth from cholesterol in hepatocytes; esterified w/ Gly or taurine)
- amphipathic --> micelles
- strongly ionized at pH 6-8.5
- neg fdbk: if high cholic acid, enz sterol 7-OHase shut off (rate-lim enz)
- bile salts reclaimed by enterohepatic circ
-4% phospholipid (phosphatidylcholine)
- 1% cholesterol (inside of micelle)
-1% bile pigments
-xenobiotics (eg: drugs, pollutants, toxins)
-82% water

Front 31

enterohepatic circulation

Back 31

- fcn: reclaim/recycle bile
- sm amt loss in fecal matter
- active transport in distal ileum--> liver (via hepatic portal vein)
- anything spilled out of liver goes to kidney via hepatic vein, active transp

Front 32

bile pigments

Back 32

- from broken down RBCs
- bilirubin travels w/ albumin to hepatocyte
- conj in hepatocyte (w/ glucouronic acid) = more soluble, but not v soluble
- bilirub glucuronide on inside of bile micelle
- excreted via feces (too big to be excr by kidneys)

Front 33

gallstones

Back 33

- when too much H2O resorbed, bile crystallizes/aggregates
--due to insol components of bile (cholesterol, bile pigments)
- two types:
1) cholesterol stones (~75% in USA)
2) pigment stones (~25% in USA)
*common in overweight middle-aged women: wt = higher chol, age = decr GB motility, woman = more estrogen & Pg (insol, bring more Chol into micelle)

Front 34

gallstone symptoms

Back 34

-stone in hepatic duct: inflammation, pain, liver damage if prolonged obstruction (jaundice b/c accum bilirubin in blood)
- stone in common bile duct (further down; blocks both liver & panc): inflam, pain, liver damage/jaundice, pancreatitis (panc digests self)--> see panc enzymes (eg amylase) in blood, steatorrhea, inadequate insulin/glucagon pdc'n

Front 35

gallstone tx

Back 35

- endoscopic surg: cut sphincter to allow stone to pass; drag stone out of duct; mechanically crush stone
- cholecystectomy: remove GB
- ultrasound lithotripsy (break up stone w/ ultrasound)
- oral bile acid therapy: ursodeoxycholic acid (dissolves stone)

Front 36

major cells in: stomach, panc, intest
(enzymatic & ion transport)

Back 36

STOMACH:
enz = chief cell
ion = parietal (H+ to lumen, HCO3 to blood)
PANC
enz = acinar (panc dig enz)
ion = duct cells (HCO3 to lumen, H+ to blood)
INTESTINE
enz = abs columnar cell: brush border dig enz, nutrient transporters
ion = secretory columnar cell: Cl into lumen, H2O follows, Na paracellular

Front 37

general fcns of GI system sections

Back 37

stomach: digestion & mixing
intestines: dig, abs
villus: absorption
crypt: secretory

Front 38

intestinal epithelia: life cycle

Back 38

- born in the crypts
- migrate up the villi
- die at the villus tips
- shed into the lumen (digested to things that can be reabs)
*total life span: 3-5days (~20 for Paneth cells)
-one villus can have cells from multiple adjacent crypts

Front 39

GI stem cells: give rise to which 5 lineages

Back 39

1) Paneth
2) columnar cells (90%)
3) M cells (1%)
4) EC cells (1%)
5) goblet cells (6-10%)

Front 40

GI epithelial cell: fcns in crypt vs villus

Back 40

1) Paneth (same?)
2) columnar: crypt = secr, villus = abs
3) M cells:
4) EC cells: crypt = subst P, villus = secretin
5) goblet cells: crypt = neutral mucins; villus = acidic mucins

Front 41

GI epithelial cell: crypt columnar cell

Back 41

- Cl secretion
- Na/K/2Cl transporter brings Cl across BL side of membrane
- VIP activates adenyl cyclase --> incr cAMP--> PKA phosph'ls Cl channel (CFTR) on apical membr--> Cl into lumen

Front 42

GI epithelial cell: villus columnar cell

Back 42

- nutrient abs (apical --> BL mem)
- apical: sucrase: breaks disaccs to monosaccs (gluc)
- SGLT-1 Na/Gluc cotransp on apical side
- GLUT-2 allows glut to go down [grad] on BL side
- BL side: Na/K-ATPase

Front 43

GI epithelial cell: apical & brush border
- digestive enz
- transporters

Back 43

Digestive enz:
-aminopeptidases
-dipeptidases
-enterokinase
-maltase
-oligosaccharidase
-lactase
-sucrase
-alpha limit dextrinase
Transporters
-specific AA
-specific sugars (gluc, fruc)
-specific ion channels (Ca-activ'd Cl; cAMP-activ'd Cl)

Front 44

GI epithelial cell: basolateral membrane
-transporters

Back 44

[no dig enz]
Transporters:
-generic amino acids
- generic sugars
-Na/K ATPase
-Na/K/2Cl cotransporter

Front 45

Digestion hierarchy

Back 45

- crude digestion (pancreatic enz)
- refined digestion (brush border enz)
- active transp't (brush border transp)
- facilitated diffusion (BL transporters)
*active transport = have control over what comes into cell
once in cell, diffuse down [grad] across BL membr

Front 46

Carbohydrate digestion
-overview
-poly --> di
- di--> mono
- into cell (how?)
- across BL membr

Back 46

-overall: salivary amylase starts, stomach incr, insulin
- poly--> di (panc amylase)
- di--> mono (brush border enz)
- into cell:
--Fruc: GLUT5 (passive)
--Gluc & Galac: SGLT1 (Na coupled)
- GLUT2 across BL membr (passive)
(also on BL membr: Na/K-ATPase: Na out, K in)

Front 47

lactose intolerance (malabsorption syndrome)
- mechanism
- Sx
- Dx test

Back 47

- no/insufficient lactase enz--> lactose (disac) stays in lumen, can pull H2O into lumen (diarrhea)
- Sx: abd bloating, cramps, gas, nausea, vomiting,
- Dx: undigested lactose in gut broken down by bacterial fermentation --> H2 gas exhaled

Front 48

Carb digestion: GLP-1 fcn

Back 48

- secret'd by EC system
- signals panc to make insulin

Front 49

Protein digestion

Back 49

- panc proteases & peptidases
- brush border peptidases
- if not broken down to AAs in lumen, small proteins become AAs in cell, then cross BL membr
-- 7 indep apical AA transporters
-- 3 indep BL AA transpr

Front 50

Hartnup's disease

Back 50

- defect in apical AA transporter that carries neutral AAs
- won't see neutral AAs in blood if AA given as free, but will see if given as dipeptide (can enter cell via peptide transporter, then broken down inside cell to AA)

Front 51

Pancreatic & brush border enz collab

Back 51

- panc pcds trypsinogen
- trypsinogen --> trypsin (via enterokinase, from bb of sm int )
- trypsin: inhib diluted away in lumen of sm int --> trypsin activ's chymotrypsinogen--> chymotrypsin & procarboxypeptidase--> carboxypeptidase

Front 52

Fat digestion

Back 52

1) emulsified in stomach, droplets incr surf area
2) intestine: emuls fats incorp into bile salt micelles
3) bile salts attacked by panc lipases
4) fats removed from micelles by brushborder of jej & ileum
5) FAs diffuse across enterocytes, cross BL membr to circ
6) other fat dig pdts accum in sER, reassembled to lipids
7) sER & rER coalesce @ Golgi; rER apo-lipoprots & sER lipids assembled into chylomicrons
8) chylomicrons released by exocytosis on BL side
9) enter lacteals (too large for caps)
10) enter gen circ at thoracic duct
11) circ chylomicrons transport lipids to liver, adipose, muscle (assimilated via lipoprot lipase)

Front 53

Which aquaporin is expressed by intestinal epithelial cells?

Back 53

AQP8: allows passive diffusion of H2O

Front 54

flow of H2O along digestion: follows food & osmolarity

Back 54

- entering food broken down & electrolytes/enz secr'd (ACh/gastrin/histamine -->HCl, secretin--> NaHCO3, VIP-->NaCl) = high luminal Osm = H2O into lumen
- as nutrients abs, draw H2O into tissue
-