Physiology Flashcards
(120 cards)
1
Q
secretin
A
GI peptide hormone
AC, cAMP
location: duodenum, jejunum
stimuli: ACID (duodenal pH below 4.5), (fat)
inhibited by: ?
Actions
stimulates: pancreatic and bile BICARB secretion, pancreatic growth
inhibits: acid secretion
2
Q
gastrin
A
GI peptide hormone: CCK-2 receptors
location: antrum/pylorus, duodenum
G cell
stimuli: protein, distention, vagal vagal
inhibited by: acid (antrum pH below 3.5)
Actions
stimulates: acid secretion, mucosal growth
3
Q
cholecystokinin (CCK)
A
GI peptide hormone: CCK-1 receptors
location: duodenum, jejunum, ileum
stimuli: protein, fat, (acid)
inhibited by: pancreatic enzymes inactivate releasing factors
Actions
stimulates: pancreatic bicarb and ENZYME secretion, gallbladder contraction, pancreatic growth
inhibits: gastric emptying
4
Q
gastric inhibitory peptide (GIP)
A
GI peptide hormone
location: duodenum, jejunum
stimuli: protein, fat, carbs
inhibited by: ?
Actions
stimulates: insulin release
inhibits: acid secretion
5
Q
motilin
A
GI peptide hormone (cyclic release every 90 min)
location: duodenum, jejunum
stimuli: vagal vagal, (fat), (acid)
inhibited by: atropine, mixed meal
Actions
stimulates: gastric and intestinal motility
6
Q
Location of GI hormones
- antrum
- duodenum
- jejunum
- ileum
A
- gastrin
- gastrin (less), CCK, secretin, GIP, motilin
- CCK, secretin, GIP, motilin
- CCK (less)
7
Q
What GI hormones are released by protein digestion products?
A
gastrin, CCK, GIP
8
Q
What GI hormones are released by fat digestion products?
A
CCK, GIP
secondary: secretin, motilin
9
Q
What GI hormones are released by carbohydrate digestion products?
A
GIP
10
Q
What GI hormones are released by acid?
Inhibited?
A
secretin
secondary: CCK, motilin
inhibited: gastrin
11
Q
What GI hormones are released by stomach distention?
A
gastrin
12
Q
What GI hormones are released by vagal vagal stimulation?
A
gastrin, motilin
13
Q
What GI hormones stimulate/inhibit acid secretion?
A
stimulate: gastrin
inhibit: secretin, GIP
14
Q
What GI hormones stimulate the pancreas (bicarb, enzymes, growth)?
A
all 3: CCK
all but enzymes: secretin
15
Q
What GI hormones stimulate the gallbladder (bile bicarb, contraction)?
A
bicarb: secretin
contraction: CCK
16
Q
What GI hormones stimulate gastric emptying?
A
CCK
17
Q
What GI hormones stimulate insulin release?
A
GIP
18
Q
What GI hormones stimulate mucosal growth?
A
gastrin
19
Q
What GI hormones stimulate gastric and intestinal motility?
A
motilin
20
Q
vasoactive intestinal peptide (VIP)
A
GI neurocrine: nitric oxide action
location: mucoase and sm. muscle of GI tract
Actions
relax: sphincters, gut circular muscle
stimulate: intestinal and pancreatic secretion
21
Q
GRP (Bombesin)
A
GI neurocrine: vagal vagal
location: gastric mucosa
Actions
stimulate: gastrin release
22
Q
Enkephalins
A
GI neurocrine: stimulate opiod receptors
location: mucosa and sm. muscle of GI tract
Actions
stimulate: sm. muscle contraction
inhibit: intestinal secretion
23
Q
somatostatin
A
Paracrine
location: GI mucosa, pancreatic islets
stimuli: acid
inhibited by: vagus
Actions
inhibits: gastrin and other peptide hormone release
24
Q
histamine
A
Paracrine
location: oxyntic gland mucosa ECL-cell
stimuli: gastrin
Actions
stimulates: acid secretion
25
Zollinger-Ellison syndrome
Gastrinoma
over production of gastrin: lots of acid
Sx: duodenal ulcer, diarrhea, steatorrhea
26
Werner-Morison Syndrome
Pancreatic cholera
over production of VIP
Sx: diarrhea, metabolic acidosis, dehydration, hypokalemia
high rates of intestinal secretion
27
1. Which 2 hormones share the same 5 C-terminal amino acids?
2. What do you need for these two molecules to have activity?
3. What is the role of sulfate in these?
4. What allows these to pass through the liver without being activated?
gastrin: 4 C terminal a.a.; can have sulfate group on Tyr 6 (not required for activation)
CCK: 7 C-terminal a.a.; MUST have sulfate at Tyr 7 for activity
NH2 at C terminal a.a.: protect from inactivation in liver
28
When do gastrin/CCK family have
1. gastrin activity: receptor?
2. CCK activity: receptor?
1. sulfated/unsulfated tyrosine at position 6 from C terminal or un-sulfated tyrosine at position 7 or fragments from 4-6 a.a. long: CCK-2 receptor
2. sulfated tyrosine at position 7: CCK-1 receptor
29
Secretin family of peptides: what is required for activity
1. secretin
2. VIP
3. GIP
4. glucagon
1. ALL 27 a.a. (so it can form helix)
2. ?
3. ?
4. ALL 29 a.a.
30
Will GI hormones be released in response to whole proteins, fats, and carbs?
NO
| they must be partially digested
31
How does gastrin stimulate gastric acid secretion?
1. release of histamine from ECL cells
| 2. direct action on parietal cells
32
What potentiates
1. secretin
2. gastrin
3. ACh/CCK?
1. CCK and Phe (more bicarb)
2. histamine
3. secretin?
33
extrinsic nervous system
autonomic nervous system of gut divided into parasympathetic and sympathetic
34
nerves of parasympathetic nervous system for GI
vagus n. (mouth to transverse colon)
| pelvic n. (rest of colon)
35
vagovagal reflex
afferent signal travels to brain and then back through vagal efferents (in the same nerve)
36
nerves of sympathetic nervous system for GI
spinal cord nerves
37
enteric (intrinsic) nervous system
Auerbach's, submucosal nerve plexus
receives info from: PNS, SNS, mucosa, epithelial cells, sm. muscle cells
directly innervate target cells, connect sensory receptors
38
What do these enteric nervous system nerves use for actions
1. efferent fibers
2. sympathetic
3. interneurons (which are inhibitory/excitatory?)
1. Ach
2. NE
3. Ach, serotonin, VIP, NO, somatostatin
excitatory: Ach, substance P
inhibitory: VIP, NO
39
nexus
connections between sm. muscle cells that allow them to contract as one
40
phasic contraction
last few sec. to a minute then relaxes
41
tonic contraction
sphincters
myogenic: product of sm. muscle cells themselves
last for hours until stimulis causes them to relax
42
chewing
```
voluntary and reflexive
jaw drops and causes reflexive action to close
1. reduce particle size
2. mix food with saliva
3. increase SA for enzymes
```
43
swallowing
1. tongue presses against palate
2. triggers reflex of upper constrictor
3. peristalsis begins and pushes bolus back of pharynx
4. epiglottis blocks off trachea
5. upper esophageal sphincter relaxes
44
atm pressure in the esophagus
1. above diaphragm
2. below diaphragm
1. neg. because in thorax
| 2. pos.
45
```
UES pressure
1. as swallowing
2. not swallowing
LES
1. as food reaches diaphragm
```
1. low
2. high
1. relax
46
primary peristalsis
initiated by swallowing
47
secondary peristalsis
when something becomes stuck in esophagus
48
cells in
1. orad (body and funds)
2. pyloric region
1. parietal cells
| 2. gastrin cells
49
functions of stomach
1. STORAGE
2. reduce particle size
3. regulate gastric emptying
50
accommodation
oral part of stomach relaxes when the LES relaxes
allows a large amount of food without increasing pressure too much
VAGOVAGAL reflex
51
slow wave frequency
1. gastric motility from orad to body to funds to caudal to pylorus
2. intestines
1. weak or absent in the orad
contractions increase in strength and freq.
2. high then decrease as move distally
52
Cells of Cajal
pacemaker cells of peristalsis in stomach and sm. intestines
53
spiking of slow waves
1. stomach
2. small intestine
1. not req. for contraction but does cause stronger, longer contractions
2. req. for contraction (depends on food eaten)
54
slow waves
1. frequency
2. amplitude in stomach
3. amplitude in sm. bowel
occur all the time
set max. frequency of contraction
1. does not change
2. changes to change number of contraction
3. does not change (spikes are what matters)
55
gastric emptying
1. liquid
2. fatty meal
3. osmotic solutions
1. increase
2. inhibits (CCK is released)
3. slows
56
vagotomy
impairs gastric emptying
57
segmentation
movement of sm. bowel that mixes food
58
law of the intestine
contraction that moves part of the material through the gut?
59
migrating motor complex
MOTILIN triggers
| every 90 min get intense contractions at one site of sm. bowel for several seconds in FASTING gut
60
ileocecal valve
regulates amount from ileum into cecum
tonically contracted: myogenic
intrinsically regulated (all in gut)
reflex from the gut regulated by CCK
61
colon innervation
1. proximal and transverse
2. distal
PNS
1. vagus
2. pelvic n.
62
mass movement
colon contractions are weak
1. 1-2x a day hausfrau disappear and move contents down
2. happens again: go to rectum
3. internal anal sphincter relaxes: urge to defecate
63
rectophincteric reflex
causes defecation in people with spinal problems
1. can contract external sphincter (pudendal n.): causes feces to move back
2. later rectum will become full and cause a stronger urge to defecate
64
saliva functions
1. lubricant
2. speech
3. digestion: amylase, lipase
4. taste food
5. protection: dental caries, thermal, noxious stimuli, vomit
6. kill bacteria: lactoferrin (take up iron), lysozyme, IgA binding protein
65
pH optimum of
1. lipase
2. amylase
1. pH 4
| 2. pH 7
66
What innervates salivary glands?
1. PNS
2. SNS
```
1. CN VII and IX
ACh: IP3, Ca: secretion, vasodilation, myoepithelial cell contraction metabolism, growth
2. T1-3 (superior cervical ganglion)
NE: cAMP
inhibitory
```
67
acinar cells
original saliva secretion
68
duct cells
modify saliva
69
electrolytes
1. high rate of saliva secretion
2. low rate
hypotonic at all rates (at very high it approaches isotonic)
K remains the same
1. increases: Na, Cl, HCO3
2. low Na Cl
70
electrolyte movement from acinus to duct
1. acinus: secrete K, Cl, Na, HCO3 into lumen
2. secrete K and HCO3 into lumen
3. Na/Cl move out of duct lumen
impermeable to water
more Na/Cl leave than K/HCO3 enter: hypotonic
71
stimulation of saliva secretion
1. PNS
2. ACh
3. secretion of saliva and increased blood flow
4. cellular metabolism: kallikrein: plasma protein: bradykinin: increased blood flow
72
salivary nucleus of the medulla
1. stimulate
2. inhibit
1. conditioned reflexes, smell, taste, pressure, nausea
| 2. fatigue, sleep, fear, dehydration
73
H+ ion
location: stomach: oxyntic gland mucosa: parietal cell
Action:
activates pepsinogen to pepsin
kills bacteria
digests protein
74
pepsinogen
location: stomach: chief cell
must be activated: by acid
stimulation: Ach (vagus and secretin cause Ach)
Action: digests protein by cleaving interior peptide bonds (NOT essential)
75
function of stomach products
1. mucus
2. water
1. lubricates food, protects lining of stomach (neck cells)
| 2. dissolves and dilutes ingested material
76
intrinsic factor (IF)
location: stomach: parietal cell
Action: absorption of Vit. B12
77
products of gastric gland cells
1. epithelial
2. neck cells
3. chief
4. parietal
1. mucus
2. mucus and stem cells
3. pepsinogen
4. HCl, IF
78
H/K ATPase
H into lumen, K into cell
maintenance
1. water becomes H (supplies H/K ATPase) and OH in cell
2. OH combines with CO2: bicarb
3. bicarb leaves cell (basolateral) and Cl comes in
4. Cl leaves passively (lumen)
5. Na/K ATPase: Na out (basolateral) and K into cell (supplies K for H/K ATPase; K also back leaks)
79
carbonic anhydrase
catalyzes OH and CO2 to bicarb
80
tubulovesicles
parietal
| contain H+ so it doesn't leave cell
81
canaliculus
parietal cell
| interconnected with lumen of gastric gland on apical membrane cell
82
How do parietal cells release acid?
tubulovesicles that contain acid fuse with canaliculua to increase apical membrane SA and release H+
lots of mitochondria
83
What accounts for the potential difference across the oxytinic gland mucosa?
Cl secretion
84
What allows parietal cells to release acid (5)?
1. H/K ATPase
2. mitochondira
3. tubulovesicles and canaliculus
4. barrier, potential difference
5. Cl secretion
85
What can disrupt cell membrane and cause separation of charges across mucosa to decrease potential difference (approaches 0)?
aspirin
| ETOH
86
Concentrations of ions in gastric juice
1. high rate of secretion
2. low rate of secretion
all rates: high Cl; isosmotic
1. H, Cl, K
2. Na, Cl, K
87
electrolyte composition of fluid in stomach
1. pure oxyntic fluid (parietal)
2. non-oxyntic fluid
1. HCl, K
| 2. NaCl, bicarb, little K (always produced at low rates and is overwhelmed when parietal cells are stimulated)
88
What happens in chronic vomiting?
metabolic acidosis
| hypokalemia
89
3 major stimulators of acid secretion
1. gastrin (G cell): stimulate secretion of histamine and acid
2. histamine (ECL (eneterchrommafin cell)): potentiates effect of gastrin on parietal cell acid secretion
3. ACh (neural): stimulates acid secretion
90
histamine receptor pathway
AC/cAMP
91
gastrin receptor pathway
PL-C/IP3/Ca
92
basal acid secretion
peaks at midnight, no food in stomach
| NOT due to gastrin (don't know what causes it)
93
sham feeding on acid secretion
1. bland food
2. regular food
3. self selected food
1. low secretion
2. mid
3. high secretion
94
In the absence of gastrin (remove duodenum/antrum) what stimulate acid secretion?
vagus n. directly stimulates parietal cells (gastrin cells too)
95
cephalic phase: stimulation of acid secretion
stimulus: chewing, swallowing, smell, taste
vagus:
1. Ach
2. GRP, G cell, gastrin
stimulation at parietal cell: Ach, Gastrin
96
gastric phase: stimulation of acid secretion
stimulus: distention
vagus:
1. Ach
2. GRP, G cell, gastrin
local reflexes: Ach
stimulus: digested protein
G cell: gastrin
stimulation at parietal cell: Ach, gastrin
97
intestinal phase: stimulation of acid secretion
stimulus: digested protein
intestinal G cell: gastrin
stimulation at parietal cell: circulating amino acids, gastrin
98
all phases: stimulation of acid secretion
gastrin and Ach: ECL cells: histamine
99
What inhibits gastrin release and acid release from parietal cells?
somatostatin (released at pH below 3)
100
oxyntic gland area and antrum: inhibition of acid secretion
stimulus: pH below 3
SOMATOSTATIN: inhibits gastrin and acid release
101
duodenum: inhibition of acid secretion
stimulus: acid
SECRETIN: inhibits gastrin and acid release
Nervous reflex: inhibits acid secretion
stimulus: hyper-osmotic solutions
unidentified enterogasterone: inhibits acid secretion
stimulus: FA
GIP: inhibits gastrin and acid secretion
unidentified enterogasterone: inhibits acid secretion
102
jejunum: inhibition of acid secretion
stimulus: FAGIP: inhibits gastrin and acid secretion
| unidentified enterogasterone: inhibits acid secretion
103
acid secretion in response to meal
1. empty stomach
2. food in stomach
3. as food volume decreases
4. 304 hours after acid release
1. pH less than 2: acid and gastrin inhibited
2. neutralizes acid: acid released
3. pH decreases: decreases acid secretion
4. back to inhibition of acid
104
pancreas: aqueous secretion
NaHCO3
ductule and centroacinar cells: high volume
neutralizes acids in the duodenum
regulation: secretin
105
pancreas: enzymatic secretion
enzymes
acinar cell: low volume
stimulus: Ach, CCK
106
zymogen granules
location of enzymes until stimulus arrives
107
mechanism of pancreatic secretion
1. bicarb secreted into lumen of duodenum in exchange for Cl into cell (maintained by back leak into lumen)
2. CO2 from blood enters cell and combines with OH to make bicarb
3. acid leftover returns to blood via H/Na transport (H into blood, Na into cell)
4. Na concentration maintained by Na/K ATPase
108
ions in pancreatic secretion at
1. low rate
2. high rate
Na always high
K always same
1. low bicarb, high Cl
2. low Cl, high bicarb
109
concentrations of Cl and Na in secretions of
1. gastic acid
2. pancreatic secretion
1. high Cl at all rates
| 2. high Na at all rates
110
pancreatic enzyme secretion
1. synthesis on rough ER
2. hydrophobic leader seq. so that it can pass through the cisterna (membrane) of RER
3. budded off into transitional elements
4. in golgi: incorporated into vacuoles that concentrate enzymes until mature zymogen granule
5. zymogen granule moves to the apical membrane and waits for a stimulus
6. Ca is 2nd messenger that causes release
all steps are ongoing except 6
steps 3-5 require ATP
111
pancreatic secretion
1. cephalic phase (sham feeding)
2. intestinal
1. increase in enzymes but not much aqueous secretion
2. major phase
decrease in pH: secretin: release bicarb
digestion products (FA and AA): I cells: CCK: vagovagal: enzyme secretion and bicarb secretion
112
How is bile made and what happens with a meal?
1. Liver: CHOLESTEROL plus water, Ca, K, Cl, Na
2. from liver to gallbladder: secretin adds bicarb, Na, H2)
3. gallbladder: CONCENTRATE (Na, Cl, HCO3, water leave)
4. eat a meal: CCK and ACh cause bile to leave gallbladder and enter duodenum
113
7 hydroxylase
rate limiting step of bile syn.
114
cholic acid
primary bile acid
115
chenodeoxycholic acid
primary bile acid
116
secondary bile acid
bacteria cause formation
conjugate with a.a. (GLYCINE or TAURINE) to make water soluble
in gut: go from water soluble bile salts to bile acids
117
deoxycholic acid
secondary bile salt
| conjugates with glycine to make water soluble bile salt
118
lithocholic acid
secondary bile salt
| conjugates with taurine to make water soluble bile salt
119
micelle
amphipathic
| bile salts surround fat and hold them apart giving SA for lipase to break down fat
120
What makes it easier for liver to extract things from blood?
counter current flow of bile and blood makes a concentration gradient
