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Physiology Flashcards

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

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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

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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

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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

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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

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6
Q

Location of GI hormones

  1. antrum
  2. duodenum
  3. jejunum
  4. ileum
A
  1. gastrin
  2. gastrin (less), CCK, secretin, GIP, motilin
  3. CCK, secretin, GIP, motilin
  4. CCK (less)
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7
Q

What GI hormones are released by protein digestion products?

A

gastrin, CCK, GIP

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8
Q

What GI hormones are released by fat digestion products?

A

CCK, GIP

secondary: secretin, motilin

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9
Q

What GI hormones are released by carbohydrate digestion products?

A

GIP

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10
Q

What GI hormones are released by acid?

Inhibited?

A

secretin

secondary: CCK, motilin
inhibited: gastrin

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11
Q

What GI hormones are released by stomach distention?

A

gastrin

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12
Q

What GI hormones are released by vagal vagal stimulation?

A

gastrin, motilin

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13
Q

What GI hormones stimulate/inhibit acid secretion?

A

stimulate: gastrin
inhibit: secretin, GIP

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14
Q

What GI hormones stimulate the pancreas (bicarb, enzymes, growth)?

A

all 3: CCK

all but enzymes: secretin

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15
Q

What GI hormones stimulate the gallbladder (bile bicarb, contraction)?

A

bicarb: secretin
contraction: CCK

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16
Q

What GI hormones stimulate gastric emptying?

A

CCK

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17
Q

What GI hormones stimulate insulin release?

A

GIP

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18
Q

What GI hormones stimulate mucosal growth?

A

gastrin

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19
Q

What GI hormones stimulate gastric and intestinal motility?

A

motilin

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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

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21
Q

GRP (Bombesin)

A

GI neurocrine: vagal vagal

location: gastric mucosa

Actions
stimulate: gastrin release

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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

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23
Q

somatostatin

A

Paracrine

location: GI mucosa, pancreatic islets
stimuli: acid

inhibited by: vagus

Actions
inhibits: gastrin and other peptide hormone release

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24
Q

histamine

A

Paracrine

location: oxyntic gland mucosa ECL-cell
stimuli: gastrin

Actions
stimulates: acid secretion

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25
Q

Zollinger-Ellison syndrome

A

Gastrinoma

over production of gastrin: lots of acid

Sx: duodenal ulcer, diarrhea, steatorrhea

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26
Q

Werner-Morison Syndrome

A

Pancreatic cholera

over production of VIP

Sx: diarrhea, metabolic acidosis, dehydration, hypokalemia

high rates of intestinal secretion

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27
Q
  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?
A

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

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28
Q

When do gastrin/CCK family have

  1. gastrin activity: receptor?
  2. CCK activity: receptor?
A
  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
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29
Q

Secretin family of peptides: what is required for activity

  1. secretin
  2. VIP
  3. GIP
  4. glucagon
A
  1. ALL 27 a.a. (so it can form helix)
  2. ?
  3. ?
  4. ALL 29 a.a.
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30
Q

Will GI hormones be released in response to whole proteins, fats, and carbs?

A

NO

they must be partially digested

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31
Q

How does gastrin stimulate gastric acid secretion?

A
  1. release of histamine from ECL cells

2. direct action on parietal cells

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32
Q

What potentiates

  1. secretin
  2. gastrin
  3. ACh/CCK?
A
  1. CCK and Phe (more bicarb)
  2. histamine
  3. secretin?
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33
Q

extrinsic nervous system

A

autonomic nervous system of gut divided into parasympathetic and sympathetic

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34
Q

nerves of parasympathetic nervous system for GI

A

vagus n. (mouth to transverse colon)

pelvic n. (rest of colon)

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35
Q

vagovagal reflex

A

afferent signal travels to brain and then back through vagal efferents (in the same nerve)

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36
Q

nerves of sympathetic nervous system for GI

A

spinal cord nerves

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37
Q

enteric (intrinsic) nervous system

A

Auerbach’s, submucosal nerve plexus
receives info from: PNS, SNS, mucosa, epithelial cells, sm. muscle cells
directly innervate target cells, connect sensory receptors

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38
Q

What do these enteric nervous system nerves use for actions

  1. efferent fibers
  2. sympathetic
  3. interneurons (which are inhibitory/excitatory?)
A
  1. Ach
  2. NE
  3. Ach, serotonin, VIP, NO, somatostatin
    excitatory: Ach, substance P
    inhibitory: VIP, NO
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39
Q

nexus

A

connections between sm. muscle cells that allow them to contract as one

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40
Q

phasic contraction

A

last few sec. to a minute then relaxes

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41
Q

tonic contraction

A

sphincters
myogenic: product of sm. muscle cells themselves
last for hours until stimulis causes them to relax

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42
Q

chewing

A 
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
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43
Q

swallowing

A
  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
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44
Q

atm pressure in the esophagus

  1. above diaphragm
  2. below diaphragm
A
  1. neg. because in thorax

2. pos.

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45
Q 
UES pressure
1. as swallowing
2. not swallowing
LES
1. as food reaches diaphragm
A
  1. low
  2. high
  3. relax
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46
Q

primary peristalsis

A

initiated by swallowing

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47
Q

secondary peristalsis

A

when something becomes stuck in esophagus

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48
Q

cells in

  1. orad (body and funds)
  2. pyloric region
A
  1. parietal cells

2. gastrin cells

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49
Q

functions of stomach

A
  1. STORAGE
  2. reduce particle size
  3. regulate gastric emptying
50
Q

accommodation

A

oral part of stomach relaxes when the LES relaxes
allows a large amount of food without increasing pressure too much
VAGOVAGAL reflex

51
Q

slow wave frequency

  1. gastric motility from orad to body to funds to caudal to pylorus
  2. intestines
A
  1. weak or absent in the orad
    contractions increase in strength and freq.
  2. high then decrease as move distally
52
Q

Cells of Cajal

A

pacemaker cells of peristalsis in stomach and sm. intestines

53
Q

spiking of slow waves

  1. stomach
  2. small intestine
A
  1. not req. for contraction but does cause stronger, longer contractions
  2. req. for contraction (depends on food eaten)
54
Q

slow waves

  1. frequency
  2. amplitude in stomach
  3. amplitude in sm. bowel
A

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
Q

gastric emptying

  1. liquid
  2. fatty meal
  3. osmotic solutions
A
  1. increase
  2. inhibits (CCK is released)
  3. slows
56
Q

vagotomy

A

impairs gastric emptying

57
Q

segmentation

A

movement of sm. bowel that mixes food

58
Q

law of the intestine

A

contraction that moves part of the material through the gut?

59
Q

migrating motor complex

A

MOTILIN triggers

every 90 min get intense contractions at one site of sm. bowel for several seconds in FASTING gut

60
Q

ileocecal valve

A

regulates amount from ileum into cecum
tonically contracted: myogenic
intrinsically regulated (all in gut)
reflex from the gut regulated by CCK

61
Q

colon innervation

  1. proximal and transverse
  2. distal
A

PNS

  1. vagus
  2. pelvic n.
62
Q

mass movement

A

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
Q

rectophincteric reflex

A

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
Q

saliva functions

A
  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
Q

pH optimum of

  1. lipase
  2. amylase
A
  1. pH 4

2. pH 7

66
Q

What innervates salivary glands?

  1. PNS
  2. SNS
A 
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
Q

acinar cells

A

original saliva secretion

68
Q

duct cells

A

modify saliva

69
Q

electrolytes

  1. high rate of saliva secretion
  2. low rate
A

hypotonic at all rates (at very high it approaches isotonic)
K remains the same
1. increases: Na, Cl, HCO3
2. low Na Cl

70
Q

electrolyte movement from acinus to duct

A
  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
Q

stimulation of saliva secretion

A
  1. PNS
  2. ACh
  3. secretion of saliva and increased blood flow
  4. cellular metabolism: kallikrein: plasma protein: bradykinin: increased blood flow
72
Q

salivary nucleus of the medulla

  1. stimulate
  2. inhibit
A
  1. conditioned reflexes, smell, taste, pressure, nausea

2. fatigue, sleep, fear, dehydration

73
Q

H+ ion

A

location: stomach: oxyntic gland mucosa: parietal cell

Action:
activates pepsinogen to pepsin
kills bacteria
digests protein

74
Q

pepsinogen

A

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
Q

function of stomach products

  1. mucus
  2. water
A
  1. lubricates food, protects lining of stomach (neck cells)

2. dissolves and dilutes ingested material

76
Q

intrinsic factor (IF)

A

location: stomach: parietal cell

Action: absorption of Vit. B12

77
Q

products of gastric gland cells

  1. epithelial
  2. neck cells
  3. chief
  4. parietal
A
  1. mucus
  2. mucus and stem cells
  3. pepsinogen
  4. HCl, IF
78
Q

H/K ATPase

A

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
Q

carbonic anhydrase

A

catalyzes OH and CO2 to bicarb

80
Q

tubulovesicles

A

parietal

contain H+ so it doesn’t leave cell

81
Q

canaliculus

A

parietal cell

interconnected with lumen of gastric gland on apical membrane cell

82
Q

How do parietal cells release acid?

A

tubulovesicles that contain acid fuse with canaliculua to increase apical membrane SA and release H+
lots of mitochondria

83
Q

What accounts for the potential difference across the oxytinic gland mucosa?

A

Cl secretion

84
Q

What allows parietal cells to release acid (5)?

A
  1. H/K ATPase
  2. mitochondira
  3. tubulovesicles and canaliculus
  4. barrier, potential difference
  5. Cl secretion
85
Q

What can disrupt cell membrane and cause separation of charges across mucosa to decrease potential difference (approaches 0)?

A

aspirin

ETOH

86
Q

Concentrations of ions in gastric juice

  1. high rate of secretion
  2. low rate of secretion
A

all rates: high Cl; isosmotic

  1. H, Cl, K
  2. Na, Cl, K
87
Q

electrolyte composition of fluid in stomach

  1. pure oxyntic fluid (parietal)
  2. non-oxyntic fluid
A
  1. HCl, K

2. NaCl, bicarb, little K (always produced at low rates and is overwhelmed when parietal cells are stimulated)

88
Q

What happens in chronic vomiting?

A

metabolic acidosis

hypokalemia

89
Q

3 major stimulators of acid secretion

A
  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
Q

histamine receptor pathway

91
Q

gastrin receptor pathway

A

PL-C/IP3/Ca

92
Q

basal acid secretion

A

peaks at midnight, no food in stomach

NOT due to gastrin (don’t know what causes it)

93
Q

sham feeding on acid secretion

  1. bland food
  2. regular food
  3. self selected food
A
  1. low secretion
  2. mid
  3. high secretion
94
Q

In the absence of gastrin (remove duodenum/antrum) what stimulate acid secretion?

A

vagus n. directly stimulates parietal cells (gastrin cells too)

95
Q

cephalic phase: stimulation of acid secretion

A

stimulus: chewing, swallowing, smell, taste
vagus:
1. Ach
2. GRP, G cell, gastrin

stimulation at parietal cell: Ach, Gastrin

96
Q

gastric phase: stimulation of acid secretion

A

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
Q

intestinal phase: stimulation of acid secretion

A

stimulus: digested protein
intestinal G cell: gastrin

stimulation at parietal cell: circulating amino acids, gastrin

98
Q

all phases: stimulation of acid secretion

A

gastrin and Ach: ECL cells: histamine

99
Q

What inhibits gastrin release and acid release from parietal cells?

A

somatostatin (released at pH below 3)

100
Q

oxyntic gland area and antrum: inhibition of acid secretion

A

stimulus: pH below 3
SOMATOSTATIN: inhibits gastrin and acid release

101
Q

duodenum: inhibition of acid secretion

A

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
Q

jejunum: inhibition of acid secretion

A

stimulus: FAGIP: inhibits gastrin and acid secretion

unidentified enterogasterone: inhibits acid secretion

103
Q

acid secretion in response to meal

  1. empty stomach
  2. food in stomach
  3. as food volume decreases
  4. 304 hours after acid release
A
  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
Q

pancreas: aqueous secretion

A

NaHCO3

ductule and centroacinar cells: high volume

neutralizes acids in the duodenum

regulation: secretin

105
Q

pancreas: enzymatic secretion

A

enzymes

acinar cell: low volume

stimulus: Ach, CCK

106
Q

zymogen granules

A

location of enzymes until stimulus arrives

107
Q

mechanism of pancreatic secretion

A
  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
Q

ions in pancreatic secretion at

  1. low rate
  2. high rate
A

Na always high
K always same
1. low bicarb, high Cl
2. low Cl, high bicarb

109
Q

concentrations of Cl and Na in secretions of

  1. gastic acid
  2. pancreatic secretion
A
  1. high Cl at all rates

2. high Na at all rates

110
Q

pancreatic enzyme secretion

A
  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
Q

pancreatic secretion

  1. cephalic phase (sham feeding)
  2. intestinal
A
  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
Q

How is bile made and what happens with a meal?

A
  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
Q

7 hydroxylase

A

rate limiting step of bile syn.

114
Q

cholic acid

A

primary bile acid

115
Q

chenodeoxycholic acid

A

primary bile acid

116
Q

secondary bile acid

A

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
Q

deoxycholic acid

A

secondary bile salt

conjugates with glycine to make water soluble bile salt

118
Q

lithocholic acid

A

secondary bile salt

conjugates with taurine to make water soluble bile salt

119
Q

micelle

A

amphipathic

bile salts surround fat and hold them apart giving SA for lipase to break down fat

120
Q

What makes it easier for liver to extract things from blood?

A

counter current flow of bile and blood makes a concentration gradient

GI (12 decks)

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