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20005 > GI physiology and pathophysiology > Flashcards

GI physiology and pathophysiology Flashcards

1
Q

what is the GIT wall made of

A
  • mucous membrane
  • lamina propria
  • muscularis mucosae
  • submucosa
  • muscularis externa
  • serosa
  • submucosal plexus
  • myenteric plexus
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2
Q

what does the mucosa do

A

facilitates movement of food

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3
Q

what does the lamina propria and muscularis mucosae do

A

they are part of movement and motility

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4
Q

what does the submucosa do

A

its involved in secretion

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5
Q

what does the submucosal plexus do

A

its the first layer of the enteric nervous system and is involved in excretion

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6
Q

what does the myenteric plexus do

A

its part of motility

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7
Q

what are the stages of smooth muscle contraction

A
  1. intracellular Ca increases when Ca enters cell from extracellular fluid or sarcoplasmic reticulum
  2. Ca binds to calmodulin. it is a calcium binding messenger protein
  3. Ca calmodium complex activates myosin light chain kinase
  4. MLCK phosphorylates myosin light chains in myosin heads - increasing myosin ATPase activity
  5. phosphorylated myosin binds with acting forming cross bridges
  6. actin slide along myosin - contraction
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8
Q

what does the enteric nervous system do in the GIT

A

works independently of the CNS controlling local reflexes, changing motility or secretion

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9
Q

what do the sensory neurones of the ENS do

A
  • monitor changes in luminal activity eg distension
  • pH
  • osmolarity
  • levels of nutrients
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10
Q

what do efferent secretomotor neurons do in the ENS

A
  • stimulate or inhibit effector cells, smooth muscle cells, epithelial cells that secrete or absorb fluid, electrolytes, submucosal blood vessels and enteric endocrine cells
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11
Q

what does parasympathetic modulation of the ENS do

A

promotes motility and secretion

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12
Q

what does sympathetic modulation of the ENS do

A

inhibits motility and secretion by contracting sphincerts

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13
Q

what does the myenteric plexus do

A

mainly controls GI motility

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14
Q

what does the submucosal plexus do

A

mainly controls GI secretion

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15
Q

what is peristalsis

A

an intrinsic local reflex that helps move food through the GI tract towards the anus

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16
Q

how does peristalsis work

A

muscle contractions behind the food bolus

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17
Q

what do excitatory neurones do in peristalsis

A

excitatory neurones behind the food bolus allow contractions of circular muscles by releasing ACH

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18
Q

what do inhibitory neurones do in peristalsis

A

allow for circular muscles to relax which is facilitated by nitric oxide and vasoactive intestinal peptide

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19
Q

what is Hirschsprung disease

A
  • severe constipation with an absence of the ENS in the distal colon
  • has a segment of increased tone, narrow lumen and devoid of propulsive activity
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20
Q

what is achalasia

A
  • a failure of oesophageal peristalsis and relaxation of the lower oesophageal sphincter when swallowing
  • come from loss of VIP and NO inhibitory interneuron and the excitatory neural tone dominates
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21
Q

what is the slow wave motility mechanism

A
  • cyclical changes in membrane potential
  • generated by pacemaker cells
  • regulator of GIT motility
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22
Q

what is the role of segmentation and haustration in motility

A
  • mix the contents of small and large intestine
  • contracts circular muscle and pinches off different regions
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23
Q

what does the migration motor complexes do in motility mechanism

A
  • cycle of electrical activity triggering motor activity in the fasting state
  • clears the content of stomach before next meal
  • mediated by ghrelin, motilin and vagus nerve
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24
Q

what is the role of mass movement in the motility mechanism

A
  • enhanced rate of peristalsis
  • triggered by gastrocolic and duodenoscopic reflexes
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25
Q

what is the hormone ghrelin

A

stimulate you to want to eat again

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26
Q

what is the hormone motilin

A

stimulates the movement of things out of your stomach to prepare the next food to enter

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27
Q

what does the gastroileal reflex do

A

stomach promotes the opening of the ileoceacal sphincter

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28
Q

what does the colonoileal reflex do

A

inhibits ileal emptying when the colon is streatched

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29
Q

what does the gastrocolic/ duodenocolic reflexes do

A

where food entering the stomach or duodenum promotes the motility of the colon

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30
Q

what does the enterogastric reflex do

A

distension of the small and large intestine inhibits stomach motility and secretion

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31
Q

what does intestinointestinal reflex do

A

over distension of one part of the intestine leads to relaxation of the rest of the intestine

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32
Q

what is the gastric accommodation reflex

A

allows the stomach to relax and increase compliance to accommodate food volume

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33
Q

what is the innervation of the gastric accommodation reflex

A

vagovagal reflex pathway, activate the inhibitory motor neurones

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34
Q

what is the function of the gastric accommodation reflex

A
  • prevents pressure rising
  • provides time to allow efficient mixing and break down of food
  • allows stomach to be a temporary store
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35
Q

what are the stages of the gastric accommodation reflex

A
  1. food enters stomach
  2. sensory receptors detect distension and stretching of stomach walls
  3. volume and pressure information sent to brain stem via vagus nerve
  4. efferent vagal nerve signal to fundus and proximal stomach
  5. activation of inhibitory motor neurones and release of VIP and NO
  6. relaxation of smooth muscle cells in stomach wall
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36
Q

what is gastroparesis

A

delayed gastric emptying in the absence of stomach blockage. caused by vagal injury

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37
Q

what is emesis

A

the vomiting centre in the medulla oblongata from sensory and psychological inputs

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38
Q

what tiggers nausea and vomiting

A

chemoreceptor trigger zone in the area postrema allowing chemical changes in bloodstream to induce these feelings

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39
Q

what does the nucleus of the solitary tract do in vomiting

A

initiation and integration of reflexed
- also triggered by motion sickness

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40
Q

what are the stages of vomiting reflex

A
  1. stimuli from stomach/ pharynx
  2. visceral afferents
  3. chemoreceptor trigger zone
  4. vomiting centre
  5. vomiting reflex
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41
Q

how does the action of vomiting work

A
  1. wave of reverse peristalsis in the distal small intestine
  2. skeletal muscles contract to decrease thoracic pressure and increase abdominal pressure
  3. abdo wall and pyloric contraction, opens lower oesophageal sphincter
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42
Q

what is haematemesis

A
  • vomiting blood either red clots of coffee grounds
  • cause my upper GI bleed
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43
Q

what are the different types of small bowel obstructions

A
  • extrinsic compression
  • internal blockage of the lumen by abnormal material
  • mural disease encroaching on the lumen
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44
Q

what are the symptoms of small bowel obstruction

A
  • abdominal pain
  • bloating
  • severe constipation
  • vomiting
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45
Q

what factors regulate gastric motility and emptying

A
  • volume of chyme
  • degree of fluidity
  • presence of fat, acid, hypertonicity or distension
  • emotion
  • intense pain
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46
Q

how does volume of chyme affect gastric motility and emptying

A

increase volume stimulate motility and emptying

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47
Q

how does the degree of fluidity affect motility and emptying

A

increased fluidity allows more rapid emptying

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48
Q

how does fat, acid, hypertonicity or distension effect gastric motility and emptying

A

in the duodenum they inhibit further gastric motility and emptying until the duodenum has coped with factors already present

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49
Q

how does emotion and intense pain effect motility and emptying

A
  • emotion can stimulate or inhibit
  • intense pain will inhibit
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50
Q

what is the internal control of defication

A
  • enteric muscle
  • smooth muscle
  • involuntary control
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51
Q

what is the external control of defecation

A
  • skeletal muscle
  • voluntary control
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52
Q

what does stretching the rectum cause

A
  • increases peristalsis through the ENS
  • increase regional peristalsis via spinal activation of PNS
  • relax of internal anal sphincter
  • contraction of external anal sphincter
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53
Q

what is the role of gastrocolic/ duodenocolic reflexes in defecation

A
  • mass movement after meal
  • mediated by vagus nerve following distension of stomach and duodenum
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54
Q

what is the role of the intrinsic reflex in defecation

A
  • mediated by ENS in rectal wall
  • faeces enter > distension > afferent signal through myenteric plexus > peristaltic waves > faeces to anus > internal anal sphincter relaxed
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55
Q

what is the role of the parasympathetic spinal reflex in defecation

A

stimulation of nerve ending sin rectum > signal to spinal cord > reflex back via pelvic nerves > PNS signal intensity peristalsis and relax internal anal sphincter

56
Q

what are the stages of the defecation reflex

A
  1. stimulation of stretch receptors
  2. stimulation of parasympathetic motor neurones in sacral spinal cord
  3. stimulation of somatic motor neurones
  4. increase peristalsis throughout large intestine
  5. distension of rectum
  6. relaxation of internal anal sphincter
  7. contraction of external anal sphincter
57
Q

what is reflex bowel

A
  • spinal cord damage above T12
  • loss of bowel sensation
  • loss of descending control from brain
  • defecation reflex in tact
  • sphincters retain some tone
58
Q

what is flaccid bowel

A
  • spinal cord damage below T12
  • loss of bowel sensation
  • loss of descending control from brain
  • loss of defecation reflex
  • loss of reflex tone of sphincters
59
Q

what are the types of diarrhoes

A
  • it is impaired GI water absorption
  • osmotic diarrhoea
  • secretory diarrhoea
  • exudative diarrhoea
  • abnormal intestinal motility
60
Q

what causes osmotic diarrhoea

A
  • non-absorbable solute accumulate in small intestine
  • solute create osmotic pressure
61
Q

what causes secretory diarrhoea

A

reduced ion absorption or increase intestinal ion secretion

62
Q

what causes exudative diarrhoea

A

inflammatory damage to intestinal mucosal cells. inflammation obstructs the absorptive surfaces and leaves solutes that are normally absorbed

63
Q

what is melaena

A

foul smelling black tarry stool

64
Q

what causes melaena

A
  • upper gastrointestinal bleeding eg peptic ulceration
  • blood is degraded by HCL an intestinal enzymes
65
Q

what are the chemical and mechanical processes of digestion in the oral cavity

A
  • chewing
  • lubrication
  • salivary amylase and lipase
66
Q

what are the chemical and mechanical processes of digestion in the stomach

A
  • churning
  • pepsin
  • chymosin
  • gastric lipase
67
Q

what are the chemical processes of digestion in the pancreas

A
  • trypsin
  • chymotrypsin
  • elastase
  • carboxypeptidase
  • pancreatic amylase
  • pancreatic lipase
68
Q

what are the mechanical process of the small intestine smooth muscle

A

churning and propulsion

69
Q

what are the chemical processes of digestion in the gall bladder

A

bile saltes

70
Q

what are the chemical processes of digestion in the intestinal brush border

A
  • aminopeptidase
  • carboxypeptidase
  • dipeptidase
  • lactase
  • sucrase
  • maltase
71
Q

what are the chemical and mechanical processes of digestion in the large inestine

A

churning and bacterial fermantation

72
Q

what are the gastric secretory cells involved in digestion

A
  • mucous cells
  • chief cells
  • parietal cells
  • enterochromaffin-like cells
  • G cells
  • D cells
73
Q

what are the enzymes involved in digestion

A
  • amylase
  • pepsin
  • trypsin, chymotrypsin, carboxypeptidase
  • lipase
  • maltase, sucrase, lactase
  • peptidases
  • enterokinase
  • bile salts
74
Q

what are the hormones that regulate digestion

A
  • gastrin (gastric motility)
  • cholecystokinin
  • secretin (bile secretion and ejection of bile from gallbladder
  • motilin
  • somatostatin
  • gastrin releasing peptide
  • gastric inhibitory peptide
  • VIP (dilation of intestinal capillaries)
75
Q

what are the structures of the pancrease

A
  • main pancreatic ducts
  • bile duct
  • accessory pancreatic duct
  • minor duodenal papilla
  • major duodenal papilla
76
Q

what does the pancreas do in digestion

A
  • supplies digestive enzymes for the duodenum
  • bicarbonate-rich fluid to neutralize acidic chyme
77
Q

how does pancreatic fluid enter the duodenum

A

through the sphincter of Oddi into the hepatopancreatic ampulla

78
Q

which hormones control exocrine pancreatic secretion

A
  • secretin
  • cholecystokinin
79
Q

what does secretin do

A

controls pancreatic aqueous bicarbonate secretion

80
Q

what does cholecystokinin

A

control of pancreatic digestive enzyme secretion

81
Q

what are the stages of secretin activing

A
  1. acid in duodenum
  2. increases secretin release from duodenal mucosa
  3. stimulate pancreatic duct cells
  4. increases secretion of aqueous NAHCO3- solution in the duodenal lumen
  5. neutralizes the acid in duodenum
82
Q

what are the stages of cholecystokinin activity

A
  1. fat and protein products in duodenum
  2. increase CCK release from duodenal mucosa
  3. stimulates pancreatic acinar cells
  4. increase secretion of pancreatic digestive enzymes as zymogens in duodenal lumen
  5. causes digestion of fat and protein products
83
Q

what does bicarbonate solution do from the pancreases

A
  • neutralise acid
  • optimise pH for pancreatic enzymes
  • protects small intestine
84
Q

what does lipase do from pancreatic secretion

A
  • breaks down lipids
  • hydrolyses dietary triglycerides to monoglycerides and free fatty acids
  • secreted in active form
85
Q

what does amylase do from pancreatic secretion

A
  • breaks down carbohydrates
  • converts to polysaccharides to disaccharide, maltose
  • secreted in active form
86
Q

what does proteolytic enzymes do

A

-trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase
- hydrolyse proteins to amino acids
- secreted in inactive form

87
Q

what is the function of endopeptidase

A

converts trypsinogen to trypsin

88
Q

how is proenzyme activated

A
  1. trypsinogen activated by cleavage to trypsin by endopeptidase in duodenal boarder
  2. trypsin cleaves trypsinogen to activate more trypsin
  3. trypsin cleave other proenzymes activating them
89
Q

what is autodigestion

A
  • inappropriate/ premiture trypsin activation
  • the interior of the zymogen granule is acidic and contains protease inhibitors (SPINK1) to stop autodigestion
    loss of SPINK1 can lead to pancreatitis
90
Q

how is HCO3- secreted

A
  1. CO2 converted to HCO3 by carbonic anhydrase
  2. HCO3 transported into pancreatic ducts by anion exchanger
  3. source of luminal Cl is provided by the cystic fibrosis transmembrane conductance regulator
  4. accumulation of anions drives water and Na reabsorption paracellularly
  5. H+ accumulation is prevented by Na/H allowing further CO2-HCO3
91
Q

when in neural signalling used

A
  • fast onset
  • specific responses
  • energetically expensive
92
Q

when is endocrine signalling used

A
  • slow onset
  • coordinated responses
  • cheaper energetically
93
Q

when are both endocrine and neural signalling used in the GIT

A

when there a fast onset is needed but needs long term maintenance

94
Q

what are the 3 phase of GIT secretion

A
  • cephalic
  • Gastric
  • Intestinal
95
Q

what is the cephalic phase

A

initiation of GI secretion by sensory stimuli in anticipation of food

96
Q

what is the chemically happens in the cephalic phase

A
  • lubrication with saliva
  • acid is present in stomach
  • bicarbonate present to neutralise acidic chyme
  • active enzymes in place for food to arrive
97
Q

what is the neural regulation in the cephalic phase

A
  • PNS activation through sensory input and cerebral cortex
  • vagus nerve transmits signals to GIT
  • ACh stimulates secretion from parietal cells
98
Q

what is the hormonal regulation in the cephalic phase

A
  • sensory input stimulates gastrin releasing peptide
  • this stimulate release of gastrin -> stimulates gastric acid secretion
99
Q

what are the stages of the cephalic phase

A
  1. sensory stimuli to vagus nerve to ACh release
  2. ACG to muscarinic cholinergic receptor to parietal cells secrete acid
  3. gastrin released from G cells in antrum
  4. gastrin receptors on parietal cells -> acid secretion
  5. ECL cells -> histamine release -> parietal cells secrete acid
  6. inhibit the release of somatostatin from D cells
100
Q

what is the function of the gastric phase

A
  • enhance secretions started in cephalic phase
  • acidify chyme
  • initiated protein digestion
101
Q

what do stretch receptors do in gastric phase

A

match degree of secretion to predicted quantity of food ingested

102
Q

what do chemoreceptors do in gastric phase

A

matches degree of secretion to expected nutritional quality of food ingested

103
Q

what is the neural regulation of the gastric phase

A
  • presence of food triggers stretch receptors -> vagus nerve -> stomach activates ENS
  • ENS, local reflexes
  • enhanced gastric secretions, motility and muscle contractions
104
Q

what is the hormonal regulation in the gastric phase

A
  • regulated by gastrin
  • food cause gastrin release from G cells
  • stimulation: gastric acid and pepsinogen secretion
105
Q

stages of the gastric phase - distension

A
  1. distention of stomach by food
  2. stretch- sensitive neurones
  3. PNS mediated vagovagal reflex
106
Q

stages of the gastric phase - protein digestion

A
  1. peptides and amino acids released
  2. G cells secrete gastrin
  3. stimulates acid and acinar cell secretion
  4. stimulate chief cell to secrete pepsinogen
107
Q

what is the function of the intestinal phase

A
  • control rate of chyme entry to duodenum
  • maintain optimal condition for enzymatic digestion of food
108
Q

what is the neural regulation of the intestinal phase

A
  • chyme in duodenum activates stretch receptors and chemoreceptors
  • signals through ENS and vagus nerve
  • enterogastric reflex, inhibiting gastric motility and secretion
  • slows emptying of stomach
109
Q

what is the hormonal regulation of the intestinal phase

A
  • cholecystokin and secretin
  • CCK in presence of pat and protein
  • simulates bile and pancreatic enzymes for digestion
  • secretin for acidic chyme, secretes bicarbonate-rich pancreatic juice
110
Q

what are the stages of the intestinal phase

A
  1. acidic cyme entering the duodenum stimulate s cells
  2. s cells release secretin
  3. secretin stimulate HCO3 and constricts pyloric sphincter
  4. fatty acids and peptones stimulate vagovagal reflex
  5. stimulates acinar and duct cells
111
Q

what does gastrin do when secreted

A

stimulates acinar cell secretion

112
Q

what does fatty acids do when secreted

A

stimulate cholecystokinin secretion

113
Q

what does CCK stimulate when secreted

A

relaxation of sphincter of Oddi and gallbladder contractions

114
Q

what do bile salts do when secreted

A

emulsify lipid droplet, increasing surface area for digestion

115
Q

what is inflammatory bowel disease

A

chronic inflammation of the GIT affecting secretion and absorption

116
Q

what is gastroesophageal reflux disease

A

dysregulation of gastric acid secretion which flows back into the oesophagus

117
Q

what is exocrine pancreatic insufficiency

A

pancreases fails to secrete sufficient digestive enzymes impairing digestion and reabsorption

118
Q

what is peptic ulcers

A

sores that form on the lining of the stomach, duodenum or oesophagus

119
Q

what does the enteric nervous system do in digestion regulation

A
  • neurones in the GIT wall
  • is independent and regulates GIT function
  • location regulation
  • coordinating peristalsis
  • sensing and responding to contents
120
Q

what does the parasympathetic nervous system do in digestion regulation

A

rest and digest to increase blood flow, stimulate secretion and enhance motility

121
Q

what does the sympathetic nervous system do in digestion regulation

A

inhibition of digestion, reduces blood flow, slows down motility

122
Q

what is the gastrin feedback loop

A
  1. gastrin stimulates gastric acid
  2. stomach pH too acidic negative feedback mechanism reduces gastrin secretion
  3. gastric acid production decreased
123
Q

what is the secretin feedback loop

A
  1. secretin stimulate pancreas to secrete HCO3
  2. neutralise acidic chyme
  3. reduction in gastric motility and acid secretion
  4. pH in duodenum becomes less acidic from HCO3
  5. secretin is downregulated preventing over-neutralisation
124
Q

what is the CCK feedback loop

A
  1. CCK stimulates pancreas to secrete digestive enzymes
  2. gallbladder contracts
  3. inhibition of gastric motility and gastric acid secretion
  4. nutrients are absorbed
  5. CCK release reduced
125
Q

how are amino acids absorbed

A
  1. oligopeptides and short polypeptide chains
  2. hit brush boarder peptidase
  3. become amino acids
  4. absorbed through AA transporters (Na coupled)
126
Q

what happens when there is an amino acid transport mutation

A

either loss or mutation cause metabolic problems and growth and developmental defects

127
Q

how are monosaccharides absorbed

A
  1. disaccharides broken into monosaccharides
  2. glucose and galactose go to secondary active transport
  3. fructose through facilitated transports
  4. monosaccharides to blood through GLUT2
128
Q

how are fatty acids absorbed

A
  1. fats -> cholesterol -> central lipid portion of bile micelles
  2. core micelles contain lipid digestion product and exterior has amphipathic bile salts
  3. micelle diffuse to brush boarder membrane
  4. lipids released from micelle are absorbed
  5. epithelial cell products of lipid digestion are reesterified
129
Q

what are the results of impaired digestion

A

nutrients aren’t broken down and are too large to absorb

130
Q

what are the results of intestinal mucosal damage

A
  • reduced absorptive surface area
  • disruptive functioning of transport proteins
  • impaired integrity of intestinal barrier
131
Q

what are the results of altered GIT motilite

A

rapid transit time reduces time available for absorption

132
Q

what are the results of bacterial overgrowth in GIT

A
  • bacteria compete with host for nutrients or deconjugate bile acids
  • affects fat absorption
133
Q

what are the results of deficiencies in transporters of the GIT

A

they affect the expression or functionality of specific transporters that move nutrients across intestinal lining

134
Q

what are the results of malfunctioning bile production and secretion

A

liber or gallbladder conditions, these are needed to emulsify and absorb fats

135
Q

what does activated charcoal do

A
  • adsorbs noxious substance onto surface to prevent absorption form GIT

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