Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

exam 6 physiology > exam 6 > Flashcards

exam 6 Flashcards

1
Q

4 layers of GI tract wall

A

mucosa
submucosa
muscularis externa
serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

-bottom layer of it is muscularis mucosa (movement of villi)
-made of simple columnar epithelium

A

mucosa layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CT layer
-blood and lymph vessels
-submucosal plexus at bottom of it

A

submucosa layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. circular muscle
  2. myenteric plexus
  3. longitudinal muscle
A

muscularis externa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

CT covering and support GI tract in abdominal cavity

A

serosa layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

submucosal and myenteric plexus “little brain”

A

enteric NS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. circular folds
  2. villi
  3. microvilli (brush border)
    areeee
A

tremendous surface area available for absorption of materials from lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

lacteals (lymph vessels) and capillary network

A

inside villus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

control systems regulate conditions in (ECF/lumen of tract)
volume and composition
(stimuli all come from where in GI tract)

A

lumen of tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ECL cells
(paracrine)

A

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

D cells
(paracrine)

A

somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

the brain in the gut

A

Enteric nervous system
ENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ENS-
parasympathetics:
sympathetics:

A

P: Ach and preganglionic (major regulator)
S: NE and postganglionic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

different neurontransmitters than can be released:

A

ach
amines
NO
many peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

long reflex loop:

A

stimulus is going all the way to the CNS and change autonomic to change GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

short reflex loop:

A

stimulus goes directly to the ENS and you have immediate corrections in the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

-linear chain of neurons that extend the entire length of GI tract
-control muscle of muscularis externa

A

myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

responsible for coordinated functions along GI tract
1. increase tone of gut wall
2. increase intensity of rhythmic contractions
3. slight increase in rate of rhythmic contractions
4. increase conduction velocity of eletrical waves along gut wall
5. inhibition of sphincter contraction

A

myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

focused on each individual local area
-intestinal secretions
-absorption
-contraction of mucosal muscle

A

submucosal plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

contraction narrows lumen:

contraction shortens tube:

this is part of

A

circular

longitudinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

these sensory neurons monitoring the gut are activated by change in GI lumen or wall

A

vago-vagal reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mouth
oropharynx
upper esophageal sphincter
upper 1/3 of esophagus
external anal sphincter

A

skeletal (voluntary)
controlled by somatic MN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

lower 2/3 of esophagus
stomach
small intestine
large intestine
gallbladder
biliary and pancreatic ducts

A

smooth (involuntary)
autonomic NS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

usually inhibitory

A

sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

stimulatory or inhibitory
depending on final neurotransmitter released

A

parasympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

collects all venous outflow from most GI organs

A

portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

all portal outflow goes to what before entering vena cava

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

type of saliva that contains ptyalin (a amylase)
-watery secretion

A

serous
-parotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

thick secretions containing mucin
-lubrication and protection of surfaces

what type of saliva

A

mucous
-buccal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

pyramidal in shape
secrete isosmotic serous saliva(Cl, bicarb, K)

A

acinar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

columnar in shape
-organized in tubules
-secrete mucous

A

mucous cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

move saliva out of acini
-prevent backflow of saliva into acini!

A

intercalated duct cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

columnar epithelial cells
tight junctions
modify saliva

A

striated ducts (interlobular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

around serous acini
-contract to move saliva into and through ducts

A

myoepithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

predominate regulator of saliva production

-critical for initiation and sustaining high levels of saliva secretion

A

parasympathetic NS (Ach/muscarinic receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

as flow rate of saliva increases:

A

-less time for ductal modication
-saliva more closely resembles plasma
-becomes more basic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

reflex activations of parasympathetic that stimulates saliva production:

A

taste (sour)
smell of food
ingestion of irritating food
nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

role of sympathetic NS (NE/adrenergic receptors)

A

minor role and helps parasymapthetic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is saliva production inhibited by

A

fear sleep fatigue dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is saliva production

A

automomic
thinking/seel/smellling food
conditioned saliva
chewing
nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

unstimulated saliva most from:

stimulate saliva most from:

A

submand

parotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

initiate reflexes to prepare digestive tract for incoming food:

A

cephalic phase of GI control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

three stages of deglutition (swallowing)

A
  1. voluntary stage
  2. pharyngeal stage
  3. esophageal stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q
  1. pharyngeal stage of swallowing
A

-involuntary reflex
- soft palate pulled upward and closes off naopharynx
-epiglottis closes off trachea <2 sec
-Upper Esophagus Sphincter relaxes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Esophageal function:
sphincters and peristalsis
1
2
3

A
  1. transport of solids and liquids from pharynx to stomach
  2. prevent air intake-UES
  3. prevents reflux (stomach to esophagus) -LES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

two types of peristalis:

A

primary and secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

continuation of peristaltic wave initiated during pharyngeal phase of swallowing (8-10 secs)

A

primary peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

activated by esophageal distension from retained food in esophagus (stuff left behind)
(distension or low pH)

A

secondary peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

first 1/3 of esophagus (UES)

A

somatic motor neuron (voluntary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

lower 2/3 of esophagus (LES)

A

autonomic motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

area in the brain that controls GI function (swallowing center)

A

dorsal vagal complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

in primary peristalsis
wave of ______ in front of bolus

A

relaxation
caudad

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

in primary peristalsis
wave of _____ behind bolus

A

contraction
orad

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

vago-vagal reflex

released
orad of bolus:
caudad of bolus:

A

orad of bolus: Ach -> cause contraction
caudad of bolus: NO -> cause relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

between swallows, UES and LES remain

A

closed
-both have tonic contractile properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

when do UES and LES relax

A

UES- during swallowing
LES- as peristaltic wave approaches (pressure allows it to relax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

reflux of gastric contents into esophagus

A

GERD
gastro-esophageal reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

3 main functions of gastric (stomach)

A
  1. temp storage of ingested material
  2. production of chyme
  3. meter delivery of chyme to duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

gastric motility patterns
1
2
3
4

A
  1. receptive relaxation
  2. perstalsis (trituration/homogenization)
  3. emptying (pyloric sphincter)
  4. migrating motility complex (MMC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q
  1. relaxes to accommodate the volume of the meal
  2. reduce pressure increases preventing gastric reflux and premature gastric emptying
A

receptive relaxation of gastric motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q
  1. chyme production
  2. trituration: mix ingested nutrients with gastric secretions, breakdown large particles and increase SA for digestion
A
  1. peristalsis (trituration/homogenization) of gastric motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q
  1. ~200 kcal/hr released into small intestine
  2. important not to overload small intestine
A
  1. emptying (pyloric sphincter)
    of gastric motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q
  1. sweep ingested solids that cannot be digested out of stomach and through intestinal tract
  2. occurs during fasting
  3. takes about 90 mins to go from stomach to colon
A
  1. migrating motility complex (MMC) of gastric motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is the 1. gastric receptive relaxation initiated by:

A

-stretch of gastric or duodenal wall
-protein or fat in duodenum( will releases CCK to produce long reflex to relax stomach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

which is short and which is long

ENS reflex
vago-vegal reflex

A

ENS short
vago-vegal long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q
  1. gastric receptive relaxation is caused by
A

inhibitory signals (NO, VIP) from ENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

accommodates increased volume of food and slows emptying

A
  1. gastric receptive relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q
  1. gastric peristalsis/trituration is generated bywhat cells
A

pacemaker cells (interstitial cells of Cajal) (spontaneously generate electrical signals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

in 2. gastric peristalsis, smooth muscle cells undergo spontaneous phases of depolarization and repolarizations=

A

Basic Electrical Rhythm (BER)

3 waves every minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

acts to mix and break down (triturate) gastric contents (retropulsion)
-gastric emptying

A
  1. gastric peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

-peristaltic wave forces ___ through this
-causes _____ sphincter to contract to reduce volume released to Small Intestine

A

chyme

pyloric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

which will empty faster?
means high in glucose, high in protein, solid meals

A

meal high in glucose will empty faster>protein> solid meal (fat takes the longest to digest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

total emptying of the stomach takes about:

small intestine:

A

4 to 5 hours

small intestine: 3 to 5 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

factors that increase force of antral contractions:

such as:

A

increase gastric emptying

such as
gastrin (gastric hormone)
distension of stomach(contents of stomach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

factors that decrease force of antral contractions

A

decrease gastric emptying

such as
contents of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

hormones secreted by duodenum in response to nutrients and acid in chyme:
(to reduce gastric emptying in stomach)

1
2
3

A

enterogastrones
1. CCK (fat, protein)
2. secretin (Acid)
3. GIP (carbohydrates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

thought to initiate the migrating motility complex MMC

A

motilin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

occurs every 90 mins until meal is ingested

A

MMC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

gastric secretions:
Two processes in GI secretion
1
2

A
  1. exocrine (into lumen of duct)
  2. endocrine (into blood)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

exocrine cells.
name their product and function
parietal cell (oxyntic):
chief cell:
surface mucous cells:

A

parietal cell: HCL and intrinsic factor- activate pepsinogen and sterilize meals

chief cell: pepsinogen- protein digestion

surface mucous cells: mucus, HCO3-, trefoil factors - gastroprotection (protect lining of stomach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

paracrine cells.
name product and function
ECL cells:
D cells:

A

ECL cells: histamine- regulation of gastric secretion
D cells: somatostatin- regulation of gastric secretion

82
Q

endocrine cells.
name product and function.
G cells:
Gr cells:

A

G cells: gastrin- regulation of gastric secretion
Gr cells: Ghrelin- stimulate hunger

83
Q

NS cell.
name product and function.
nerves:

A

nerves: gastrin-releasing peptide and ach- regulation of gastric secretion

84
Q

oxyntic gland (corpus) is abudant in

A

parietal and chief cells

85
Q

pyloris gland (antral) is abundant in

A

-mucus-secreting cells
-hormones that regulate gastric function

86
Q

mechanism of acid secretion by parietal cells (HCl secretion in lumen):

we then also secret/absorb base into the blood and that can cause a rise in the pH of blood known as

A

apical K+/H+ primary active transporter

alkaline tide

87
Q

oxyntic cells are activated by:

inhibited by:

A

activated:
histamine, Ach, gastrin
(also stretch of stomach aka distension of stomach, AA, and peptides)

inhibited by:
somatostatin
(CCK; it decreases it)

88
Q

combination of factors creates a greater level of acid secretion that just additive=

which basically means

A

synergism

ach, histamine, and gastrin together produce greater acid secretion that would separately

89
Q

what stimulates D cells to secrete somatostatin to inhibit parietal cells

A

a drop in pH
(d cells controls amount of HCl amount)

90
Q

3 phases of GI activation:

A
  1. cephalic phase
  2. gastric phase
  3. intestinal phase
91
Q

stimulants of cephalic phase of acid secretion:

and is mediated by:

A

sight, smell, taste, or thoughts of food
(comes from outside of GI tract)

mediated by parasympathetics

92
Q

gastric phase of acid secretion is mediated by signals that arise from ______(so it occurs when you have FOOD in our stomach!) and initiates:

A

gastric lumen

initiates short and long reflex loops

93
Q

during gastric phase of acid secretion, the food in the stomach is going to ____ acid which increase the pH to prevent what:

A

buffer acid

prevents stimulation of somatostatin secretion (so can put more acid in stomach)

94
Q

intestinal phase stimuli:

these will then stimuli the release of what:

A

-increased H+
-distension
-osmolarity
-fats in duodenum

stimulate the release of:
enterogastrones (CCK, secretin, GLP-1, GIP)

95
Q

the release of enterogastrones from intestinal phase of acid secetion inhibit:

A

parasympathetic function-> which will inhibit function of parietal cells -> end result to reduce acid secretion

96
Q

Interdigestive Period.

  1. acid is secreted at what levels?
  2. lack of buffer(food) causes
  3. possible function for this:
A
  1. low
  2. low pH
  3. this is a fasting period which means so food in GI tract so possibly to sterilize gastric lumen
97
Q

Why acid?
acid facilitates digestion of _____, protects against _____, and increases absorption of _____,___,____

A

proteins

pathogens

B12, Fe, Ca

98
Q

PPis- the purple pill

A

proton pump inhibitor
-binds to and inhibits H+ - K+ pump

99
Q

is a glycoprotein that is screted by oxyntic cells

A

intrinsic factor

100
Q

what is required for B12 absorption

A

intrinsic factor

101
Q

secretes pepsinogen to initiate digestion of protein

A

chief cells

102
Q

pepsinogen activated to pepsin by

A

low pH (inactivated by pH>5)

103
Q

chief cells main activation through local and vagal reflexes that

A

release Ach

104
Q

only known appetite stimulant

A

Ghrelin (comes from GR cells)

105
Q

gastric mucosal barrier:

A

2 hydrophilic layers separated by hydrophobic barrier and protects epithelial layer from acidic lumen

106
Q

if the acid gets access to the lining of the stomach or the acid fails to be neutralized in the small intestine, what happens

A

ulcers

107
Q

where in small intestine are CCK, secretin, Gip, and HCO3- secreted

A

duodenum

108
Q

where does most of the nutrients we digest and absorb occur

A

most in duodenum and then decreases throughout rest of small intestine (jujunum and illeum)

109
Q

where are each Fe, bile acids, and B12 absorbed in small intestines?

A

Fe: duodenum
bile acids and B12: ileum

110
Q

what is occurring during motility in the duodenum

A

MMC, segmentation, peristalsis

111
Q

stimuli that controls the small intestinal motility:

A

-distention of duodenum
-nutrient content of chyme
-gastroenteric reflex (short feedback loop from stomach to small intestine)
-hormones

112
Q

hormones that stimulate and inhibit control of small intestinal motility:

A

stimulate: CCK, gastrin, insulin, serotonin

inhibit: secretin and glucagon

113
Q

2 patterns of motility of small intestine:

A
  1. segmentation
  2. peristalsis
114
Q
  1. segmentation pattern of motility mixing is important for:
A

mixing:
1. chyme with digestive enzymes
2. emulsifying fats
3. adjusting pH to be more basic
3. exposing mucosa to chyme

(basically is mixing things together to break them apart)

115
Q
  1. peristalsis pattern of motility is important for:
A

moving chyme thru small intestine

116
Q

the duration of feeding pattern for the small intestine depends on

A

caloric content of meal and nutrient composition of meal

117
Q

what is the order of digestion for proteins, carbs, fats?

A

fats>proteins>carbs

(fats take the longest to digest)

118
Q

Net rate of movement of any substance across the intestinal epithelium is influenced by:

A

surface area and motility

119
Q

North-South vector influenced by

A

motility -> transit time

(faster->less time for absorp.->more stuff we lose in our feces)

(slower->more time for absorp-> less stuff we lose in our feces)

120
Q

East-West influences by

A

surface area

121
Q

what substances in the small intestine require digestion? (need to be broken down into “building blocks” to be absorbed into the body)

A

carbohydrate, protein, fat

122
Q

substances presented for digestion and/or absorption in the intestines:

A

-macronutrients (need to be broken down)
-electrolytes (na, k, ca, mg, fe, ci, po4)
-water
-bile salts
-vitamins- fat soluble, water soluble
-drugs

123
Q

what factors do we need to influence digestion in the intestines

A

motility, large SA, neutral pH, hydrolytic enzymes (carbohydrate, protein, fat), emulsifying fat

124
Q

what factors do we need to influence absorption in the intestines

A

large SA, specialized cells, specific transport mechs, energy, blood/lymph flow

125
Q

what has a very high reserve capacity where most substances are completely digested/absorbed in proximal (25%)

A

small intestine

126
Q

what are the consequences of the small intestine having a very high reserve capacity

A

increase intake produces increase absorption, may produce increase in storage and obesity

127
Q

digestive enzymes in small intestine require what to function?
and from where

A

neutral pH

mainly from pancreatic HCO3- but also HCO3- from bile from liver

-stomach has H+ so need to neutralize it for enzymes to work in SI

128
Q

what are the two sites for digestion of protein and carbohydrate in the small intestine

A
  1. intraluminal (stage I-pancreatic hydrolases)
  2. mucosal surface (stage II- brush border hydrolases)
129
Q

at the mucosal surface site for digestion of protein and carbohydrate, what are the end products of the brush border hydrolysis?

A

AA, di and tripeptides, glucose, galactose, fructose

130
Q

where is fat digestion completed

A

in the lumen of the small intestine at the intraluminal site

so ONLY have stage I digestion for fats

131
Q

this cannot be digested and is lost in feces

A

fiber (cellulose)

132
Q

the carbohydrates ->polysaccharides and disaccharides need to be broken down into bulding blocks (monosaccharides) before they can be absorbed. what are the 3 monosaccharides they are broken down into

A

glucose
fructose
galactose

133
Q

when does the digestion of carbohydrates begin

A

when food is exposed to salivary amylase

134
Q

how are glucose and galactose absorbed across the cell?

how is fructose?

A

glucose/galactose: across apical in secondary active transport coupled to Na+ (SGLT transporters doing absorption)

then by faciliated diffusion through basolateral membrane (GLUT transporters doing secretion)

fructose: absorbed passively across apical and basolateral membranes by faciliated diffusion (GLUT transporters)

135
Q

protein is added to the lumen of SI in form of

A

mucus and enzymes

136
Q

protein digestion begins in the stomach by:
and is inactivated by BASIC pH in small intestine

and is important for:

A

pepsin (active form of pepsinogen that is secreted by chief cells)

important for collagen digestion

137
Q

what are absorbed across the intestinal epithelium which are produced by trypsin, chymotrypsin, carboxypolypeptideases, and elastase (interluminal site stage I of intestines)?

brush border peptidases produce _____

A

amino acids and small peptides

amino acids

138
Q

intestinal cells have a transporter that is extremely broad and can be used for drug delivery

A

peptide transporter 1 (PEPT1)

139
Q

the digestion of fat REQUIRES:

(segmentation)
which requires what (two things) to prevent fat globules from reassembling?

(this is just basically increasing the surface area available for digestion)

A

emulsification

requires bile salts and lecithin (phospholipid)

140
Q

bile sats/acids are produced from

A

cholesterol

141
Q

90% of fat digestion occurs

A

in the small intestine (10% lingual lipase of saliva from taste buds)

142
Q

fat digestion only uses (pancreatic lipase/brush border) in the small intestine.

enormous quantities of this secreted

A

pancreatic lipase for digestion (colipase)

143
Q

digestion products are solubilized in this which help to remove TG digestion products from fat globs so the fat digestion can continue. then transports TG digestion products to brush border membrane so that they can be absorbed

A

micelles

144
Q

what is the one nutrient that is not absorbed into the blood? where does it go instead?

A

fats

(chylomicrons) goes into lymphatic system which will then deliver it to the circulatory system

145
Q

fatty acids and monoglycerides cross the apical membrane via

A

simple diffusion

146
Q

TG and other hydrophobic substances packaged into _____ and secreted across the basolateral membrane via exocytosis in fat absorption of intestine.

These then enter ______ vessels via lacteals and transported to systemic veins to enter circulation

A

chylomicrons

lymphatic

147
Q

chylomicrons are required for fat (excretion/absorption)

A

absorption

148
Q

responsible for chemical digestion of fat?

responsible for emulsification of fat?

A

lipase

bile acids/salts

149
Q

what cells…

absorb Na, Cl, H2O:

secrete Na Cl, H2O:

in the small intestine (villus and crypts anatomy)

A

absorb: surface cells (mature cells)
secrete: crypt cells (immature stem cells)

150
Q

If there is not enough secretion (of Na, Cl, and H2O) from crypt cells to lumen, this can cause:

If there is too much secretion, this can cause:

(we want a normal flow/balance between surface and crypt cells!)

A

not enough: cystic fibrosis

too much: infectious diarrhea

151
Q

SURFACE CELLS
1.during the prandial state (when you have food in the digestive tract), it is (electroneutral/electrogenic).

  1. what moves transcellularly?
    paracellularly?
  2. transport mechanism for apical and basolateral membrane?
A
  1. electrogenic
  2. trancellularly: Na+
    paracellularly: H2O and Cl- (since water follows passively)
  3. apical: Na+/glucose via secondary active symporter
    basolateral: glucose via facilitated diffusion and Na+ via Na,K-ATPase
152
Q

SURFACE CELLS
1. during the post-prandial state (fasting), it is (electroneutral/electrogenic).

  1. what moves transcellularly?
    paracellularly?
A
  1. electroneutral
  2. transcellularly: Cl and Na
    paracellularly: H2O
153
Q

the Na, Cl, and H2O secretion process in crypt cells is (eletrogenic/elctroneutral)

A

electrogenic

154
Q

CRYPT CELLS
1. what moves transcellularly and via what channel?
paracellularly?

A

transcellularly: Cl via CFTR channel

paracellular: Na and H2O

155
Q

having more ____ inside crypt cell will modify the CFTR channel causing an increase in cl movement through the channel

A

cAMP

156
Q

in cholera and E.coli infections, massive diarrhea occurs because of

A

enterotoxins that INCREASE cAMP-> increases Cl secretion via CFTR into gut lumen

157
Q

B12 ABSORPTION PROCESS
in stomach:
in duodenum:
in illeum:
inside cells:

A

stomach: binds to R-binding protein and B12 at low pH

duodenum: proteases digest R-binding protein and B12 binds to intrinsic factor

ileum: intrinsic factor/B12 binds to IFCR and taken into cells

cells: intrinsic factor degraded and B12 binds to TCII-> BL via exocytosis

158
Q

the absorption of water soluble vitamins (Thiamin, riboflavin, niacin, pyridoxin, pantothenate, biotin, ascorbic acid) is done by

A

cotransport with Na and completed in upper small intestine

159
Q

examples of maldigestion:

malabsorption:

A

maldigestion:
pancreatic insufficiency
liver disease
biliary obstruction
(steatorrhea occurs early)

malabsorption:
achlorhydria
short bowel
mucosal disease
lactose intolerance

160
Q

poor motillity of the colon causes greater _____ and hard feces in transverse colon causes _____

A

absorption (of Na, Cl, and H2O)

constipation

161
Q

if you have excess motility in the colon, this causes less ______ which results in______

A

absorption
results in diarrhea or loose feces

162
Q

where does the absorption of H2O and electrolytes from chyme to solid feces take place in the colon (compaction)

A

proximal 1/2
(absorbing colon)

163
Q

where does the storage of fecal matter until it can be expelled taken place in the colon

A

distal 1/3 (storage colon)

164
Q

happens from enhanced bowel salvage maneuver (increasing thoracic pressure against closed colon glottis to push feces out)

A

diverticula (diverticulitis)

165
Q

movement of material from cecum through ascending colon

fecal matter gradually exposed to mucosal surface

A

haustrations (mixing movements) of colon motility

166
Q

movement of material from transverse to sigmoid

forces feces into rectum
(1-3x day)

A

mass movements (propulsive movements)

167
Q

when is the defecation relex initiated

A

when feces enters rectum

168
Q

excessive mass movemends would cause (diarrhea/constipation)

A

diarrhea

169
Q

in duct cell secretion of the pancreas, when SECRETIN binds to its receptors on duct cells it

A
  1. induces cAMP
  2. phosphorylation of CFTR
  3. increases Cl conductance
  4. increases HCO3- secretion

(need CFTR for bicarb to be secreted into lumen to neutralize pH)

170
Q

when is secretin released into the duodenum?

when is secretin release max in segment of duodenum

A

when acid from stomach increases to a pH below 4.5

pH<4.5

max when pH=3

171
Q

compare secretin and CCK if the following were given.

HCL:
Soap:
Peptone:

A

HCl: stimulates duct cells to release secretin to release bicarb and H2O to neutralize pH

soap: stimulate both secretin and CCK-RP secretion (which will lead to CCK secretion)

Peptone: stimulates acinar cells to stimulates CCK-RP and monitor peptide to indirectly stimulate release of CCK to release enzymes

high pancreatic secretion of enzymes which stimulated acinar cells to secrete CCK
(low H2O and bicarb)

172
Q

both phases of pancreatic secretion are mediated by vagovegal reflex:

A

cephalic (20%) and gastric (5-10%) (contents in stomach)

low volume, high enzyme secretion (Ach/GRP)

173
Q

fats/proteins do no directly stimulate CCK, they stimulate it through

A

CCK-RP

174
Q

in the intestinal phase of pancreatic secetion…

acid-> _____->______
fat/protein->______->______

A

acid->secretin->bicarbonate
fat/protein->(CCK-RP)CCK->enzymes

175
Q

the secretion rate on ionic composition of pancreatic juice is directly related to

A

the amount of secretin, Ach, and CCK we have

176
Q

as the flow of pancreatic juice composition goes up (high secreiton rates), what occurs:

A

Na and K stay constent

HCO3- goes up
Cl- goes down (because have less time for exchange between bicarb and Cl)

177
Q

when pancreatic juice has low concen rates:

A

na and k same
HCO low
Cl high

178
Q

-disorder of exocrine pancreatic function where trypsin activation causes pain, inflammation
-consequences reflect decreased digestive enzyme production

A

pancreatitis (acute or chronic)

179
Q

functional unit of liver

A

liver lobule

180
Q

what are the many functions of hepatic

A
  1. cleansing and storage of blood
  2. metabolism of nutrients
  3. synthesis of proteins
  4. metabolism of hormones, chemicals
  5. storage of energy, vitamins, iron
  6. excretion of lipid- soluble waste products
181
Q

what has high blood and lymph flow

A

liver

182
Q

the resistance of vessels to blood flow is very (high/low) in the liver

A

low

182
Q

what increases resistance in the liver which can cause a type of edema (portal hypertension)

A

cirrhosis

183
Q

bile salts (acids) and lecithin are required for _______ and _____ of dietary fat

A

(emulsification) digestion
absorption (micelles)

184
Q

____ of lipophilic metabolites (bilirubin), excess cholesterol, other waste products, drugs, and toxins is another role of bile

A

excretion

185
Q

what secretes bile salts, cholesterol, lecithin, bilirubin, and may other lipophilic substances into the bile duct

A

hepatocytes

186
Q

these cells modify primary secretion and add HCO3 to bile duct

A

duct epithelial cells

187
Q

the bile can move into the ____where it can be stored and concentrated or it can move directly in to the _____to be recirculated in what is called the ____ where it can be reabsorbed

A

gallbladder

small intestine
enterohepatic circulation

188
Q

these secrete organic component of bile into bile duct

bile duct cells secretes:

can either go : for:

A

hepatocytes

na, h2o, and hco3

gallbladder for storage or small intestine for fat digestion

189
Q

gall bladder cells are (electroneutral/electrogenic)

A

electroneutral

190
Q

gall stones formed so had this procedure and have no problems with fat digestion and bile flows directly into duodenum

A

cholecystectomy

191
Q

what substances in the bile decrease when it is stored in gall bladder?

increase?

A

decrease:
water
HCO3
Na
Cl

increase:
bile salts, bilirubin, cholesterol, FA, lecithin, Ca and K

192
Q

this via blood stream causes:
1. gallbladder contraction
2. relaxation of sphincter of Oddi

A

CCK

193
Q

FA found in duodeum,
what are the steps?

A

via CCK-RP, CCK secretion increases,
gallbladder contracts-> increase bile flow into common bile duct

sphincter of oddi relaxes-> increase bile flow into duodenum

194
Q

functions to conserves bile salts

ALLOWS SECRETION TO BE MUCH MUCH GREATER THAN SYNTHESIS (So liver doesn’t have to produce as much bc it can recirculate!!)

A

enterohepatic circulation

195
Q

the transport process here in the ilium that will allow these bile salts to be reabsorbed is a apical __________________

A

sodium-dependent bile salt transporter (ASBT)

196
Q

drugs that inhibit Bile Recycling and are used to lower LDL levels in blood (to lower blood cholesterol levels)

which will allow more what to be lost in the feces?

A

BARI (bile acid reabsorption inhibitors)

allows more bile salts to be lost in the feces

197
Q

two types of BARI’s:

A
  1. bile acid sequestrants
  2. ASBT inhibitors
198
Q

this BARI binds to bile salts in intestinal lumen and block transport.

what are the benefits of this?

A

bile acid sequestrants

benefits: drug works in intestinal lumen (doesn’t need to be absorbed) and reduce harmful side effects

199
Q

this BARI reduces cholesterol levels in ECF and increases excretion rate of bile salts

A

ASBT inhibitors

200
Q

(disorders of biliary secretion) if you have disfunction of hepatocytes, it is going to impair:

A

bilirubin and bile salt secretion

201
Q

hepatocyte dysfunction occurs from

A

drugs such as acetaminophen, viral hepatitis, toxins
and
fibrosis, cirrhosis

exam 6 physiology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions