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Patho II > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

colorectal cancer is the __ deadliest cancer in US

A

2nd

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2
Q

Diarrhea is the __ leading cause of death worldwide

A

3rd

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3
Q

segments of the GI tract

A

mouth, pharynx, esophagus, stomach, small intestine, large intestine, sphincters between segments

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4
Q

GI tract accessory organs

A

salivary glands, liver, gallbladder, pancreas

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5
Q

layers of the GI tract (outside to inside)

A
  • serosa (outerlining)
  • longitudinal muscle
  • myenteric (Auerbach’s) nerve plexus
  • circular muscle
  • submucosa
  • submucosa (Meissner’s) nerve plexus
  • muscularis mucosae
  • mucosa
  • epithelial linging
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6
Q

major functions of the digestive system

A
  • motility
  • digestion
  • absorption
  • secretion
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7
Q

2 processes of digestion

A
  • mechanical (chewing/mastication)
  • chemical (action of enzymes)
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7
Q

absorption

A
  • mechanism of the nutrients being digested are then being absorbed from the GI lumen into the blood stream
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8
Q

___ helps with digestion and absorption

A

secretions

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9
Q

where does most absorption occur?

A

small intestine

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10
Q

once the nutrients are absorbed from the GI lumen, where do the nutrients in the blood stream go?

A

to the liver

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11
Q

motility

A

food keeps moving along the GI tract through this process, aided by contractions of the smooth muscle in the GI tract

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12
Q

HPV connects the __ as well as the __ to the liver, where the liver gets nutrients first

A

small intestine; colon

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13
Q

endocrines (hormones)

A

all GI hormones are peptides released into the blood to act on the distant target cells

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14
Q

GI hormones

A

-gastrin
-secretin
-cholecystokinin (CCK)
-glucose-dependent insulinotropic peptide (GLIP) or gastric inhibitory peptide (GIP)
-motilin

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15
Q

paracrines

A

some are peptides (somatostatin), and some are not (exp. histamine)

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16
Q

histamine

A
  • gastrin and ACh cause release from cells in stomach
  • stimulates acid secretion
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17
Q

what does a Histamine H2 receptor blocker do?

A
  • decreases acid secretion
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18
Q

exp. of histamine H2 blockers

A

Cimetidine (Tagamet), Ranitidine (Zantac)

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18
Q

Neurocrines (neurotransmitters)

A
  • some are peptides (VIP - vasoactive intestinal peptide), some are not (ACh, NE)
  • nerves release –> diffuse to target cells
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19
Q

site of production gastrin

A

antrum of stomach

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20
Q

site fo production CCK

A

small intestine

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21
Q

site of production secretin

A

small intestine

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22
Q

Gastrin does what to stomach 1.) acid secretion 2.) motility

A

stimulates, stimulates

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23
Q

CCK does what to stomach 1.) acid secretion 2.) motility

A

inhibits, inhibits

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24
Q

secretin does what to stomach 1.) acid secretion 2.) motility

A

inhibits, inhibits

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25
Q

intrinsic control

A

enteric nervous system

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26
Q

enteric nervous system (ENS)

A
  • myenteric (Auerbach’s) plexus
  • submucosal (Meissner’s) plexus
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27
Q

extrinsic control

A

autonomic nervous system
- PNS (rest & digest)
- SNS

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28
Q

what stimulates the PNS?

A

ACh

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29
Q

what stimulates the SNS?

A

mainly inhibits via NE

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30
Q

GI reflexes

A
  • local within (ENS)
  • long loop
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31
Q

local reflexes

A
  • afferent fibers from gut terminates in ENS
  • affects (+ or -) secretion, peristalsis, mixing movement
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32
Q

long loop reflex

A

gut –> afferent nerve –> prevertebral ganglia –> efferent nerve –> gut

reflexes: gastrocolic, enterogastric, colonoileal

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33
Q

Vagovaval reflexes

A

stomach/ duodenum –> aff. N. –> brain stem –> Eff. N. –> stomach/duodenum

controls gastric motor and secretory activity

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34
Q

defecation reflexes

A

colon/rectum –> aff. N. –> spinal cord –> Eff. N. –> colon/rectum

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35
Q

pain reflexes - overall

A

inhibition of GI tract

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36
Q

GI regulation of smooth muscle

A
  • unitary (single-unit) smooth muscle
  • slow waves
  • spike potentials
  • muscle contractions (helps with motility)
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37
Q

unitary (single unit) smooth muscle

A
  • functions as a syncytium
  • gap junctions
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38
Q

functions as a syncytium

A
  • nucleated mass of protoplasm produced by merging of cells
  • large areas of sm contract as a single unit
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39
Q

gap junctions

A
  • low resistance pathways for ion movement
  • between bundles of cells and layers of SM
  • signal propagation - AP spreads from cell to cell
  • within and between muscle layers
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40
Q

slow waves and spike potentials are caused by

A

rhythmical changes in membrane potential caused by variations in sodium conductance

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41
Q

slow waves

A
  • interstitial cells of Cajal - pacemaker cells
  • dictates maximum frequency of SM contraction
  • independent of nervous/hormonal stimuli
  • increase in amplitude leads to increase spike potential frequency which leads to increase in strength of contraction
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42
Q

Spike potentials (or APs)

A
  • occurs when slow waves reach threshold (-40 mV)
  • casuse SM contraction
  • Ca++ entry leads to contraction
  • affected by nervous/hormonal stimuli
  • increase in frequency leads to stonger contraction
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43
Q

what is required for peristalsis?

A

Myenteric plexus

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43
Q

gastrointesinal movements

A

peristalsis

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44
Q

T/F atropine (blcoks ACh receptors) which increases peristalsis

A

FALSE

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44
Q

segmentation contractions also called?

A

rhythmic segmentation (local)

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44
Q

where does segmentation contractions occur?

A

small and large intestines

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45
Q

blood flow proportional to local activity, what happens when you eat a meal?

A

increase in blood flow (2-3 fold) for 3-6 hours

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46
Q

causes of activity-induced blood flow?

A
  • vasodilator hormones: gastrin, secretin, CCK
  • vasodilator kinins
  • low oxygen (high adenosine)
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47
Q

what effects the nervous control of blood flow?

A
  • PNS increases gut activity which leads to increased blood flow
  • SNS directly decreases blood flow (Autoregulatory escape, exercise, shock)
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48
Q

voluntary

A

initiates swallowing process

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49
Q

3 stages of swallowing

A
  • voluntary
  • pharyngeal
  • esophageal
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50
Q

pharyngeal

A

passage of food through the pharynx into esohagus

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51
Q

esophageal

A

passage of food from pharynx to stomach

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52
Q

primary peristalsis

A

swallow-induced peristalsis

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53
Q

secondary peristalsis

A

elicited by esophageal distention

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54
Q

disorders that could effect swallowing

A
  • CVA (stroke)
  • cranial nerve damage
  • muscular dx (MG, polio, botulism)
  • anesthesia can have an effect
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55
Q

aspiration

A

UES and pharyngeal contrations are not coordinated
(effect is primary peristalsis)

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56
Q

GERD

A

backwash of acid, pepsin, and bile into esophagus

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57
Q

heartburn/acid indestion effects (_/10) people

A

1

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58
Q

GERD can lead to

A
  • stricture of esophagus (scar tissue)
  • aspiration
  • chronic sinus infection (reflex into throat)
  • barrett’s esophagus (lead to esophageal cancer)
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59
Q

what helps with regualtion of gastric emptying?

A

chyme

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60
Q

what is chyme

A
  • food bous mixed with acid
  • must enter duodenuma at a proper rate
  • pH must be optimal (7) for enzyme function
  • slow enough for nutrient absorption
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61
Q

Immediately after a meal

A

emptying does not occur before onset of gastric contractions

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62
Q

small intestinal motility contributes to digestion and absorption by

A
  • mixing chyme: with digestive enzymes and other secretions
  • circulation of chyme: to achieve optimal exposure to mucosa
  • propulsion of chyme: in an aboral direction
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63
Q

two types of movements in small intestine following a meal

A
  • peristalsis: a propulsive movement recall “Law of Gut”
  • segmentation: a mixing movement

(regulated by slow waves)

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64
Q

functions of large intestine SM

A
  • mixes chyme: enhances fluid/electrolyte absorption (haustral contractions)
  • propels fecal material: mass movements
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65
Q

Musculature of large intestine

A
  • longitudinal SM: 3 groups
  • circular SM - continuous to anus
  • internal anal sphincter - a thickening of circular SM
  • external anal sphincter - striated muscle, that surrounds internal anal sphincter
  • haustra (Haustrations) - not fixed, appear & disappear
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66
Q

lists of sphincters

A
  • UES (pharyngoesophageal)
  • LES (gastroesophageal)
  • pyloric sphincter (gastroduodenal)
  • Ileocecal valve/sphincter
  • internal anal sphincter
  • external anal sphincter
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66
Q

3 levels to control defecation

A
  • intrinsic reflex
  • spinal cord reflex
  • involvement of higher centers
67
Q

peristaltic reflex

A

stretch bowel, proximal of contraction, distal relaxation

68
Q

enterogastric reflex

A

from duodenum to regulate gastric emptying

69
Q

gastroileal reflex (gastroenteric)

A

gastric distention relaxes ileocecal sphincter

70
Q

intestino-intestinal reflex

A

over-distention or injury of the bowel segment causes entire bowel to relax

71
Q

gastro- duodenocolic reflex

A

distension of the stomach/duodenum initiates mass movements

72
Q

defecation reflex (rectospincteric)

A

rectal distention initiates defecation

73
Q

types of secretory glands

A

single cell: mucous or goblet cells
simple: indentations in the epithelium (crypts of lieberkühn)
Tubular: acid-secreting oxyntic gland
complex: salivary, pancreas

74
Q

control of secretions

A
  • local: tactile, distention, irritation
  • reflex: nervous input
  • hormonal: GI input
75
Q

mucus composition properties

A
  • thick secretion that is mainly water, electrolytes and glycoproteins
76
Q

mucus is essential for digestion because

A
  • adherent: sticks to food
  • body: coats well
  • low resistance (for slippage): lubrication
  • self-adherent: sticks together
77
Q

mucus is resistant to __ by the GI enzymes, buffering capacity (glycoproteins) to _____

A

digestion, neutralize acid

78
Q

2 types of saliva

A

serous - water secretion, contains alpha-amylase (ptyalin) –> carbohydrate digestion
mucous - contains mucin (lubrication)

79
Q

how much saliva is secreted a day

A

800-1500 mL/day

max rate of secretion is 4 mL/min

80
Q

salivary glands (4)

A

parotid (serous)
submandibular (mucous/serous)
sublingual (mucous/serous)
buccal (mucous)

81
Q

what 2 glands contribute to 90% of total saliva secreted?

A

parotid & submandibular

82
Q

ionic composition of saliva

A

K+ 7x the plasma
HCO-3 3x the plasma

83
Q

T/F saliva is hypotonic

A

true

84
Q

effect of loss of saliva?

A

cal lead to K+ depletion

85
Q

functions of saliva

A
  • lubrication and binding
  • solubilizes dry food
  • initiates starch digestion
86
Q

clinical correlation to saliva

A

oral hygiene, xerostomia (dry mouth), drooling

87
Q

functions of the stomach

A
  • short-term storage reservoir
  • secretion of intrinsic factor
  • chemical and enzymatic digestion is initiated, particularly of proteins
  • liquefication of food
  • slowly released into small intestine for further processing
88
Q

Gastric (oxytonic) gland cell types

A

mucous neck cells: mucus
peptic cells (chief cells): pepsinogen, renin
parietal cells: HCl, intrinsic factor
G-cells: release gastrin
Enterochromaffin-like (ECL) cells: release histamine

89
Q

what increases HCl production?

A

gastrin
histamine
ACh

90
Q

what decreases HCl production?

A

somatostatin

91
Q

the gastric mucosa has a ___ and an __ basis to prevent back-leak of hydrogen ions

A

physiological, anatomical

92
Q

what strengthens gastric mucosal barrier?

A

mucus, HCO3- secretion, gastrin, PGs, epidermal growth factor

93
Q

what weakens gastric mucosal barrier?

A

H. pylori, aspirin, ethanol, NSAIDs, bile salts

94
Q

peptic ulcers

A

occur when damaging effects of acid and pepsin overcome the ability of mucosa to protect itself

  1. high acid and peptic content
  2. irritation
  3. poor blood supply
  4. poor secretion of mucus
  5. infection of H. pylori
95
Q

gastic ulcers

A

main problem is decreased ability of mucosa to protect itself

96
Q

duodenal ulcers

A

main problem is exposure to increased amounts of acid and pepsin

97
Q

treatment of peptic ulcers

A

antacids; (H2 antagonists, PPIs)

98
Q

pancreas

A
  • as chyme floods into small intestine 2 things must happen
    1.) Acid must be neutralized to prevent damage to duodenal mucosa
    2.) Macromolecular nutrients - proteins, fats, and starch must be broken down much further so their constituents can be absorbed

BIG THINGS PANCREAS DOES
- digestive enzymes for all food types
- bicarb solution to neutralize acid chyme

99
Q

Where is bile stored?

A

gall bladder

100
Q

Where is bile made?

A

liver

101
Q

What is bile?

A

emulsification NOT breaking it down

102
Q

Pancreatic secretions

A
  • Trypsin, chymotrypsin, elastase
  • Carboxypeptidase
  • Lipase
  • Amylase
103
Q

Trypsin, chymotrypsin, elastase

what is there substate and action?

A

substrate: proteins
action: break peptide bonds in proteins to form peptide fragments

104
Q

Carboxypeptidase

what is the substate and action?

A

substrate: Proteins
action: splits off terminal amino acid from carboxyl end of protein

105
Q

Lipase

what is the substate and action?

A

substrate: fats
action: splits off 2 fatty acids from triglycerides, forming 3 fatty acids and monoglycerides

106
Q

Amylase

what is the substate and action?

A

substrate: polysaccharides
action: splits polysaccharides into glucose and maltose

107
Q

what helps activate the proteolytic enzymes and where are they located?

A

enterokinases, located on the intestinal mucosal cells

108
Q

control of pancreatic secretion

A
  • increase in acid from stomach
  • increase in secretin secretion from SI
  • increase in plasma secretin
  • increase in bicarb secretion from the pancreas
  • increase in flow of bicarb into SM
  • neutralization of intestinal acid in SI
109
Q

T/F Secretin is nature’s antacid

A

true

110
Q

liver & its major function

A

severs as a secretory organ, major function is to secrete bile

111
Q

other critical functions fo the liver

A
  • processes and stores nutrients
  • serves as a filter and functions in the removal of old RBCs which leads to Hgb processing and generation of bilirubin
  • responsible for the synthesis of plasma proteins (albumin, clotting proteins, angiotensinogen, steroid binding proteins)
112
Q

bile secretion and liver function flow

A
  • increase in CCK secretion from the fatty acids in the duodenum
  • increase in plasma CCK
  • 1.) leads to contraction of gall bladder –> increases bile flow into CBD
  • 2.) leads to relaxation of sphincter of oddi –> increase in bile flow into the duodenum
112
Q

causes of gallstones:

A
  1. too much absorption of water from bile
  2. too much absorption of bile acids from bile
  3. too much cholesterol in bile
  4. inflammation of epithelium
112
Q

effects of gallstones on the body

A
  • causes intense pain
  • inflammation issues
  • obstruction issues
  • make fat digestion a bigger problem b/c lack of bile flowing into the duodenum
113
Q

small intestine secretions

A

brunner’s glands: secrete an alkaline mucus
- compound mucus gland in duodenum
- protects the mucosa from acid chyme
- stimulated by local irritation - vagus (ACh)
- inhibited by sympathetic NE

Crypts of Lieberkühn: mostly secrete waterlike fluid

114
Q

Basis of digestion

A

involves the breakdown or hydrolysis (addition of water molecule) of nutrients to smaller molecules that can be absorbed in SI

114
Q

Large intestine secretions

A
  • contains Crypts of Lieberkühn but there are no villi or enzymes
  • crypts mainly secrete alkaline mucus
  • mucus secretion increase by PNS stimulation
115
Q

T/F pepsinogen only gets converted to pepsin in the presence of bicarb

A

False

presence of HCl

115
Q

4 mechanisms are critical for the transport of substances across the intestinal cell membrane

A
  1. active transport: primary and secondary
  2. passive diffusion
  3. facilitated diffusion: carrier mediated
  4. endocytosis: this allows large proteins (immunoglobulins) to be absorbed in babies. does NOT occur in adults
116
Q

a nutrient must cross how many barriers to be absorbed by blood or lymph?

A

8

117
Q

What gets absorbed in the stomach?

A

ethanol, NSAIDs, aspirin

118
Q

what gets absorbed in the duodenum and jejunum?

A

nutrients, vitamins, various ions, water and electrolytes

119
Q

what gets absorbed in the ileum?

A

bile salts and vitamin B12

120
Q

what gets absorbed in the colon?

A

water and electrolytes

121
Q

what gets absorbed in the rectum

A

drugs such as steroids and salicylates

122
Q

starch digestion

A
  • begins with alpha-amylase in saliva (5% digestion in mouth, up to 40% in stomach)
  • continues in SI with pancreatic amylase
  • final digestion occurs at brush border
123
Q

disaccharides

A

maltose
surcrose
lactose

124
Q

final products of carbohydrate digestion are all monosaccharides, mostly ___

A

glucose 80%

fructose 10%
galactose 10%

125
Q

glucose and galactose require what for absorption?

A

secondary active transport
compete fro membrane carriers (SGLUT-1)
energy from Na K APTase

125
Q

what could be a problem with carbohydrate digestion and absorption?

A

lactose intolerance

126
Q

fructose requires what for absorption?

A

facilitated diffusion by (GLUT-5)
does not require energy
requires concentration gradient

127
Q

digestion of proteins occurs in 3 locations

A

intestinal lumen - stomach (pepsin digests collagen) & SI (endopeptidases -trypsin/chymotrypsin, exopeptidase - carboxypeptidase)
brush border - oligopeptidases, dipeptidases
cytoplasm of mucosal cells - di- tri- peptidases

128
Q

enterokinase activates

A

trypsinogen

129
Q

proteolytic enzymes are __ and __ very rapidly

A

activated; destroyed

130
Q

trypsin is

A

autocatalytic and activates other proenzymes

131
Q

Proteolytic enzymes __ themselves

A

digest

132
Q

luminal digestion produces __ amino acids and __ small peptides

A

40%; 60%

133
Q

abnormalities of protein absorption?

A

pancreatic insufficiency
hartnup dx (malabsorption of tryptophan)

134
Q

digestion of triglycerides

A
  • triglyceride introduced in duodenum
  • fatty acid/ 2-monoglyceride by enterocyte
  • triglyceride is repackaged to form chylomicron
135
Q

3 main processes must occur for triglyceride to be absorbed into blood

A
  • emulsification: large aggregates of dietary triglyceride are broken down
  • enzymatic digestion: to yield monoglyceride and fatty acids. both can diffuse into enterocyte
  • reconstitution of triglyceride and chylomicron formation
136
Q

liver has __ densisty cholestrol

A

low

137
Q

statins traget

A

LDL, plaque formation form endogenous cholestrol

138
Q

chylomicrons life cycle

A
  • formed in enterocyte in SI and packaged by GA
  • secreted by exocytosis into interstitial space
  • enter central lacteal* of villi and transported to venous system via thoracic duct
  • lipoprotein lipase (on capillary endothelial cells) works with apolipoprotein C to degrade triglyceride to FFA and glycerol within chylomicron

1.) FFA and glycerol respired by cells or resynthesized to triglycerides for storage
2.) chylomicron remnant is phagocytized in hepatocytes(liver)

139
Q

cholesterol is an important precursor for all __ hormones

A

steroid

139
Q

familial lipoprotein lipase deficiency would lead to..

A

increase chylomicron, increase in triglyceride = triglycerideenemia

exp. propofol

140
Q

malaborption

A

as a general phenomenon is defined clinically in terms of fat malabsorption because fat can be measured easily ins tool, unlike carbohydrates and proteins

141
Q

motility disorders

A

moving through too rapidly

141
Q

digestion disorder

A

pancreatitis (not enough lipase)

142
Q

absorption disorders

A

sprue
resection of SI
steatorrhea

143
Q

when chyme is “hypotonic”

A

water is absorbed

144
Q

when chyme is “hypertonic”

A

water enters intestine

144
Q

chyme is usually

A

isotonic

145
Q

sodium absorption causes __ absorption

A

water

146
Q

sodium is absorbed by ___ of SI

A

epithelial cells (enterocytes)

147
Q

Sodium uptake creates ___ electrical potential in gut lumen, that provides gradient for ___ uptake

A

negative; chloride

148
Q

water follows Na and Cl in accordance with ..

A

osmotic forces

149
Q

what percentage of total body Na is absorbed each day by the intestine

A

15%

150
Q

___ absorption of Na can lead to rapid Na __ and death

A

decreased; depletion

151
Q

2 processes establish an osmotic gradient that pulls water into lumen of the intestine:

A

1.) increased osmotic pressure resulting form the digestion of foodstuffs
2.) Crypt cells actively secrete electrolytes, leading to water secretion

152
Q

water secretion by crypt cells is driven by

A

chloride secretion

153
Q

the apical (luminal) membrane contains a ___ chloride channel- “cystic fibrosis transmembrane conductance regulator” or CFTR

A

cyclic AMP-dependent

154
Q

when chloride exits cells through chloride channels

A

sodium and water follow

155
Q

mutations in gene for ion channel CFTR result in

A

cystic fibrosis

156
Q

innervation of the vomiting center

A

sensory signals:
- originate in the pharynx, esophagus, and upper small intestine
- afferent signals transmitted via vagal and sympathetic nerves

motor impulses:
- to upper GI tract via CN VII, IX, X, XII
- to lower GI tract via vagal and sympathetic nerves
- to diaphragm and abdominal muscles via spinal nerves

157
Q

antiperistalsis

A
  • can begin as low as the ileum
  • prelude to vomiting
  • pushes GI contents into the duodenum
  • this distention excites the vomiting act
158
Q

Vomiting act steps

A
  1. deep breath
  2. UES open
  3. glottic closes
  4. elevation of soft palate
  5. contraction of diaphragm (a downward motion) and muscles increases pressure in the stomach
  6. LES relaxes
  7. Gi contents force out mouth
159
Q

Obstruction at pylorus

A

acidic vomitus - can lead to metbaolic acidosis

160
Q

Obstruction below duodenum

A

neutral or basic vomitus, usually little change in whole body acid-base status

161
Q

obstruction at distal large intestine

A

severe constipation can cause vomiting when contents of SI accumulate

162
Q

causes of obstruction

A
  1. cancer
  2. ulcer
  3. spasm
  4. paralytic use
  5. adhesions
163
Q

low obstruction causes extreme __ with __ vomiting

A

constipation; less

164
Q

high obstruction causes extreme

A

vomiting

Patho II (5 decks)

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