26: Stomach Flashcards

1
Q

Parietal cell function: the players

A

HCL dissociate in to hydrogen and bicarb

  1. proton pump (hydrogen potassium)
  2. potassium and chloride channles
  3. carbonic anhydrase
  4. bicarb/chloride antiporter
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2
Q

Parietal cell function

A

hydrogen out, sodium in
potassium goes out and recycles continuously
so we get rid of H ions

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3
Q

Parietal cell function 2

A

Bicarb/cholride antiporter:
chloride comes in, and exits. like K
bicarb stays and diffuses into blood vessle

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4
Q

stomach is like a

A

washing machiene/grinder

to produce chyme and finish what mouth didn’t

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5
Q

mechanical digestion

A

gentle waves in stomach to mix bolus with juices
more vigours from body to stomach to pyloric region to move chyme
intense near pyloriys to opening of pyloric sphincter to squirt out teaspoons (1-2 per wave)

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6
Q

protein digestion

A

starts in stomach
HCl denatures protein molecs
HCl activates pesinogen to pepsin to break peptide bonds to A.As

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7
Q

Fat digestion

A

continues in stomach

gastric lipase splits triglycercides (but most effective at pH 5-6) (infant stomach)

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8
Q

HCl also

A

kills microbes

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9
Q

Mucous

A

keeps stomach walls from being digested

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10
Q

Things stomach absorbs

A

water
electrolytes
drugs (asprin)
fat (to slow passage of alcohol to intestine where it is quicker)
alcohol (more slowly if fat taken in too)

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11
Q

Cephalic Phase

A
anticipation 
prepare mouth and stomach 
sight, smell, memories, thoughts of food
salivation (facial and Glossopharyngeal)
gastic glands secrete gastric juices (Vagus)
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12
Q

Gastric Phase

A

breakdown of material

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13
Q

Intestinal Phase

A

controlled release of chyme

entry into duodenoum slows gastic activity, inc intestinal activity

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14
Q

Neural influence on Gastric Phase

A

strech receptors and chemoreceptors–> signal bolus entry
vigorous peristalsis and gastric gland secretions
chyme periodically released into duodenum

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15
Q

Endocrine influences on Gastric Phase

A

distention and pressure of food= G cells secrete gastrin

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16
Q

gastrin

A

inc gastric gland secretions and motillity

causes pyloric sphincter relaxation

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17
Q

Neural influence on Intesinal Phase

A

distension of duodenum and chem contents of chyme= activated symp nerves
this slows gastric activity

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18
Q

Endocrine influnce on Intesinal Phase

A

distension of duodenum and contents of chyme= hormonal release from dnteroendocrine cells here
secretin
cholecystokinin (CCK)

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19
Q

secretin

A

dec stomach secretions

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20
Q

CCK

A

dec stomach emptying

21
Q

gatric emptying

A

inc as bolus enters stomach

22
Q

distension of stomach and presence of food in it causes

A

secretion of gastric and vagaal nerve impulses

23
Q

secretion of gastric and vagaal nerve impulses stimulates

A

contraction of lower esophogeal spincter and stomach

relaxation of pylorc sphincter for emptying

24
Q

Enterogastric reflex regulates

A

regulate amount of chyme released into duodenum

CCK and secretin relases

25
CCK and secretic both
stim symp impulses and inhibit gastric emptying
26
Enterogastric reflex initiated by
distension of duodenum and contents of chyme | sensory impulses sent to medulla to inhibit parasymp stim of stomach
27
2 types of influence for intestinal and gastric phases
neural | endocrine
28
smooth muscle control
involuntary mostly ANS ACH and norepi membrane potential -50 to -60
29
smooth muscle types
single/unitary multiunit categorized by manner of excitation
30
unitary SM
walls of GI tract gall baldder walls walls of urinary bladder may not be in contact with motor neuron
31
Unitar SM is
autorythmic connect via gap junction: transmit APs from one fiber to another adhering to eachother=transmission of force slow synched graded contraction
32
conexons
entire unit and channels between cells
33
conexens
the individual cells that make up the unit
34
genotypes and phenotypes
want conexons that have same numbers so that channels work most efficiently
35
function syncytium
a group of cells that get one nervous system input. react as a group!
36
how smooth and skeletal muscle differ (smooth described)
SR poorly developed (SM) thick filaments of SM have actin grabbing heads entire lengthen thick and thin filaments arranged diagonally within cell for twisting motion
37
circular muscle
contracting at right angles to each other
38
smooth muscle varicosities
little bumps | release neurotransmitters into diffuse junctons of SM fiber
39
special features of SM (about contraction)
can sustain contraction for a long time without tiring at small NRG cost maintains low level of tone even w/o APs stress relaxation response
40
Stress relaxation in SM
stretch causes inc in tension tension decs w/in 1-2 minutes allows SM to change length but maintain ability to contract (important for storage organs) never goes down to zero!
41
Length-tension relationship
SM operate over wider range of resting lengths | generally broader length-tension relationships in SM compared to skeletal muscle
42
proton pump of parietal cell
pushes H out of cell | H+/K+ ATPase
43
antiporter
Cl-/HCO3-
44
why do we cross parietal cell?
to get into blood stream
45
where do CO2 and H2O come from
CO2: metabolism | H2O just in cell
46
carbonic anhydrase in parietal cell
major in disposing of cellular waste
47
Goal of parietal cell
to secrete HCl!
48
what makes CA?
H2O and CO2 make carbonic anhydrase
49
CA dissociates into
bicarb and H... we need to get rid of this