Physiology Flashcards
1
Q
What is oral to arboral
A
Tube running from mouth to anus
2
Q
Where does carbohydrate digestion start
A
Mouth
3
Q
Where does protein digestion start
A
Stomach
4
Q
Parts of small intestine
A
Duodenum, Jejunum and Ileum
5
Q
Accessory structures of digestive tract
A
Salivary gland, pancreas, liver and gall bladder
6
Q
General structure of digestive tract wall
A
Mucosa
Submucosa
Muscularis externa
Serosa
7
Q
What does contraction of circular muscle cause
A
Narrow and long lumen
8
Q
What are adjacent smooth muscle cells joined by
A
Gap junctions to allow spread of electrical signal
9
Q
What drives slow wave electrical activity in the heart
A
Interstitial cells of Cajal
10
Q
Where are Interstitial Cells of Cajal located (ICC)
A
Between circular and longitudinal muscle layer and submucosa
11
Q
Relation between force and action potential
A
Force is related to number of action potentials discharg
12
Q
What does slow wave amplitude reaching threshold depend on
A
Neuronal, hormonal and mechanical stimuli
13
Q
What determines basic electrical rhythm (BER)
A
Slow wave activity
14
Q
Basic electrical rhythm (BER) in stomach
A
3 slow waves per minutes
15
Q
Basic electrical rhythm in small intestine
A
12 and 8 waves/min in duodenum and ileum respective
16
Q
Basic electrical rhythm in large intestine
A
8 and 16 waves/min proximal and distal colon
17
Q
Where does the basic electrical rhythm tend to push small intestinal contents towards
A
Aboral direction
18
Q
Where does the basic electrical rhythm tend to push large intestinal contents towards
A
Oral direction
19
Q
Where do sympathetic fibres synapse in GI tract
A
Preganglionic fibres (ACh) synapse in prevertebral ganglia (release NA). Postganglionic fibres (NA) innervate enteric neurones but also other structures
20
Q
Effect of sympathetic on GI tract
A
Decrease motility, secretion, blood flow and absorption. Increase sphincter tone
21
Q
Where do parasympathetic fibres synapse
A
Preganglionic fibres (ACh) synapse with enteric neurones within ENS
22
Q
Effect of parasympathetic on GI tract
A
Increase motility, secretion, blood flow and absorption
Decrease sphincter tone
23
Q
Where do the pelvic nerves supply to
A
Distal third of large intestine
24
Q
Two plexus found in ENS
A
Myenteric plexus - Regulate motility and sphincters
Submucous plexus - Modulate epithelia and blood flow
25
Another name for Myenteric and Submucous plexus
Auerbach's and Meissner's plexus
26
What can sensory neurones in ENS sense
Chemo, thermo or mechanoceptors
27
Example of local reflex
Peristalsis
28
Example of short reflex
Intestino-intestinal reflex
29
Examples of long reflex
Gastroileal reflex - Wanting to use toilet after breakfast
30
How does peristalsis come about in the GI tract
Bolus is pushed from oral to aboral.
Circular muscles relax aborally (release of NO and VIP from inhibitory interneuron/descending motorneurone)
Circular muscle contacts orally (release of ACh and substance P from excitatory/ascending motorneurone)
Longitudinal muscles are exact opposite
31
Major factors influencing obesity
Genetics, environment: energy dense food diet, cars, lack of exercise, less overall energy expenditure How
32
Consequences of obesity
Stroke, respiratory disease (sleep apnea), heart disease, osteoarthritis, cancer, dementia, NAFLD
33
How does long term obesity reprogramme the brain
The brain views the extra fat as normal and dieting as a threat to survival
34
Neural centre responsible for energy balance and body weight
Hypothalamus, lesioning ventromedial hypothalamus causes obesity and lateral causes leanness
35
What is satiation
Feeling of fullness between meals
36
What is satiety
Period of time between meals
37
How are meal sized limited
Satiation signals increase during meal to limit size
38
Name some satiation signals
Cholecystokinin, Peptide YY, Glucagon like peptide 1, Oxyntomodulin, Obestatin
39
Cholecystokinin (CKK)
Secreted from enteroendocrine cells in duodenum and jejunum. Released in proportion to lipids and proteins, signals via sensory nerves to hindbrain (nucleus of solitary tract) and stimulates this
40
Peptide YY
Secrete from endocrine mucosal L-cells of GI tract, levels increase postprandially. Inhibit gastric motility, slow emptying and reduce food intake
41
Glucagon like peptide 1 (GLP-1)
Secrete from L-cells of GI tract in response to food ingestion, inhibit gastric emptying and reduce intake
42
Oxyntomodulin (OXM)
Secreted by Oxyntic cells of small intestine postprandially. Suppresses apetite.
43
Satiation signals product of pro-glucagon gene
Glucagon-like protein 1 (GLP-1) and Oxyntomodulin OXN
44
Obestatin
Released from cells lining stomach/small intestine, peptide produced from gene encoding ghrelin. Actions unclear
45
What is a hunger signal
Ghrelin
46
What secretes Ghrelin
Oxyntic or Parietal cells in stomach
47
When do Ghrelin levels increase
Preprandial - Before meals, fasting and hypoglycaemia
48
What hormones report fat status to brain
Leptin ( From fat cells) and Insulin (Pancreatic cells)
49
Where are high levels of Insulin/Leptin receptors found
Hypothalamus
50
What does deletion of leptin/insulin receptor lead to
Obesity and maybe hyperglycemic/ insulinemic
51
Therapy for obesity
Leptin therapy, daily sc injections @ 10% predicted serum concentration. Given for 48 months.
52
Over the counter medication for obesity
Orlistat or Alli in UK - Inhibit pancreatic lipase thereby reducing triglyceride absorption and reducing calorie intake. Side effects of cramping + diarrhoea. Need vitamin supplement and not effective long term
53
Therapy for obesity with substantial weight loss
Bariatric surgery: gastric band, removal of portion of stomach or re-route small intestine to small stomach pouch. Reverse insulin resistance in most cases
54
Where is brown adipose tissue found
Neck, clavicle and spinal cord
55
Key function of uncoupling protein 1 (UCP-1)
Fatty acid activated protein, short circuits proton gradient in mitochondria and accelerates fuel oxidation, producing heat
56
Example of motility patterns in GI tract
Segmentation
Colonic mass movement
Migrating Motor Complex
Tonic contractions
57
Where do high pressure tonic contractions occur
Sphincters, low pressure in stomach (storage function)
58
Sphincters of GI tract
Upper/Lower Oesophageal Sphincter, Pyloric Sphincter, Illeocecal valve, Internal and external sphincter
59
Which part of the stomach is responsible for grinding
Antrum - Grinding, Body - Storage
60
What stimulation cause relaxation as food enter stomach
Vagal stimulation
61
Direction of mixing in stomach
Peristaltic contractions move retropulsively, from pylorus to fundus during mixing. Opposite way during emptying.
62
What is chyme
Food + gastric secretions to produce semi-liquid
63
What factors determine stomach emptying
Gastric and duodenal factors
64
How do gastric factors determine emptying
Rate of emptying proportional to volume of chyme in stomach. Distension increases motility. Emptying facilitated by thick liquid chyme.
65
Duodenal factors and stomach emptying
Neuronal - Decrease antral activity by signals from intrinsic nerve plexuses and ANS
Hormonal - Release of enterogastrones (Secretin and CCK) inhibits stomach contraction
66
What stimuli can drive duodenal factors
Fat - Delay gastric emptying
Acid - Neutralization of gastric acid by bicarbonate secreted from pancreas so pancreatic enzymes function
Hypertonicity - Products of carbohydrate and protein digestion osmotically active and draw water into small intestine, reduced plasma volume
Distension
67
Secretions of oxyntic mucosa (fundus and body) in stomach
Parietal cells - HCl, Intrinsic factor, Gastroferrin
Enterochromaffin like cell - Histamine
Chief cell - Pepsinogen
68
Secretions of pyloric gland area (antrum) in stomach
D cells - Somatostatin
| G cell - Gastrin
69
Function of HCl secreted from oxyntic mucosa
Activates pepsinogen to pepsin
Denatures protein
Kills microbes taken in with food
70
Function of Pepsinogen secreted from oxyntic mucosa
Inactive precursor of pepsin. Formed pepsin activates more pepsinogen (autocatalytic)
71
Function of intrinsic factor, Gastroferrin oxyntic mucosa
Bind vitamin B12 and Fe2+ respectively, help absorb
72
Function of Histamine secreted from oxyntic mucosa
Stimulate HCl secretion
73
Function of mucus secreted from oxyntic mucosa
Protective
74
Function of gastrin secreted pyloric gland area
Stimulate HCl secretion
75
Function of Somatostatin secreted pyloric gland area
Inhibit HCl secretion
76
Function mucous secretion from pyloric gland area
Protective
77
How is HCl secretion form gastric parietal cells regulated
Direct and Indirect pathway
Direct - ACh, Gastrin and Histamine stimulate Parietal cells triggering secretion of H+ into the lumen
Indirect - ACh and Gastrin stimulate Enterochromaffin-like Cells (ECL cells) to secrete Histamine which acts on parietal cells causing H+ entry into lumen
78
What stimuli acts on the PLC-IP3 signalling pathway
Gastrin and ACh
79
What stimuli acts on the cAMP-PKA signalling pathway
Histamine (Secretory) and Somatostatin and Prostaglandin (Inhibitory)
80
Resting vs activated state of Parietal cells
In resting state of parietal cells, H+/K+ ATPase is within cytoplasmic tubulovescicles. Stimulated state of parietal cells, H+/K+ ATPase traffics to apical membrane (Canaliculus) taking residence in extended microvilli
81
3 phases of gastric acid secretion
Cephalic phase - Before food reaches stomach, driven by CNS and Vagus nerve
Gastric phase - Food is in stomach, physical and chemical mechanism
Intestinal phase - Food has left stomach
Neuronal and hormonal mechanisms
82
What can cause vagal activation to initiate gastric phase
Sight, smell, taste of food, chewing and swallowing
83
Eventual effect of enteric neurone stimulation by vagus nerve
ACh direct release activating Parietal cells
Release of GRP causing release of Gastrin from G cells into systemic circulation - Activates Parietal cell
Release of Histamine from Enterochromaffic-like cells (ECL) that activate local parietal cells
Inhibit Somatostatin decretion by D cells
84
3 phases of gastric acid inhibition
Cephalic phase - Cessation of eating and emptying of stomach leads to vagal activity cessation
Gastric phase - Food exiting stomach leads to a fall in Antrum pH.. This stimulates release of Somatostatin from D cells, inhibiting G cells Gastrin release. Prostaglandin E2 acts locally to reduce Histamine and Gastrin mediated HCl secretion
Intestinal phase - Neuronal and hormonal factors reducing gastric motility reduce gastric secretions
85
How is the mucosa protected from HCl and Pepsin
Locally produced prostaglandins -
Reduce acid secretion
Increase mucus and bicarbonate secretion
Increase mucosal blood flow
86
Pathogen causing infection in gastric antrum, ulcer form
Helicobacter pylori
87
How does Helicobacter pylori cause ulcers
It's present in the mucus layer. It secretes agents that cause persistent inflammation weakening mucosal barrier until it eventually breaks down. This leaves the submucosa subject to attack by HCl and Pepsin
88
How do Non-Steroidal Anti-Inflammatory Drugs cause peptic ulcers
NSAID inhibit cyclo-oxygenase, reducing prostaglandin formation. This eventually leads to the breakdown of the mucus membrane, exposing the mucosa to HCl and Pepsin. This triggers gastric ulcers and cause bleeding
89
What can acid-reducing drugs be used for
Peptic ulcers, gastro-oesophageal reflux disease (GORD), acid hypersecretion and Cushings ulcers
90
What is Zollinger-Ellison syndrome
Gastrin-producing tumour or hyperplasia of Islet cells of Pancreas. Leads to peptic ulcers
91
What are Cushing's ulcers
Peptic ulcers due to raised intracranial pressure which increases vagal tone.
92
How do proton-pump inhibitors work
Inhibit H+/K+-dependant ATPase (proton pump)
93
Where are proton-pump inhibitors activated
In strong acidic environment such as the Canaliculus
94
Proton-pump inhibitor with longest plasma half life
Tenatoprazole
95
Which HCl secretion receptor antagonists are not used clinically
Muscarinic ACh receptors antagonists (obsolete) and Gastrin Receptor Antagonists (used in experiments)
96
What is used in combination with antibiotics and Histamine H2 antagonist (Ranitidine) to promote eradication of H.pylori and ulcer healing
Bismuth chelate, called Bismuth therapy
97
How is Bismuth Chelate orally administered
In combination with Ranitidine
98
What is succus entericus
Intestinal juice, clear to pale yellow in colour
99
How is surface area increased in the small intestine
Circular folds (valves of Kerckring), villi and microvilli
100
Secretions from small intestine
Gastrin - G cells of gastric antrum and duodenum
Cholecystokinin (CCK) - I cells of duodenum, jejunum
Secretin - S cells of duodenum
Motilin - M cells of duodenum, jejunum
Glucagon-like insulinotropic peptide (GIP) or Gastric Inhibitory Peptide - Incretin form K cells of duodenum and jejunum
Glucagon-like Peptide-1 (GLP1) - Incretin from L cells gut
Ghrelin - Gr cells of gastric antrum, SI and elsewhere
101
What receptors do secretion from small intestine work
G-Protein Coupled Receptors
102
What are Incretins
Incretins act upon Beta- cells of pancreas in feed-forward mechanism to stimulate release of Insulin
103
What does the succus entericus contain
Mucus (protection/lubrication from goblet cells), aqueous salt (for enzymatic digestion, crypts of Lieberkuhn)
104
Does the succus entericus have digestive juice
No
105
Does fasting increase or decrease succus entericus
Decrease
106
How does Na and Cl get into the lumen
Na/K/2Cl co transporter moves Cl into the cell along with Na and K. This Cl moves into the lumen via Cystic Fibrosis Transmembrane Conductance Regular (CFTR) which is a Ca channel. Na moves paracellularly along with water
107
How does aboral movement in the small intestine occur
Duodenum has frequent segmentation contractions (12/min), Ileum has fewer (9/min). Net movement aboral
108
What is segmentation in small intestine
Alternating contraction and relaxation of segments of circular muscle causing chopping of chyme back and forth. Initiated by small intestine pacemaker causing the basal electric rhythm
109
What is the migrating motor complex
Distinct pattern of electrochemical activity 90-120 mins between meals which helps clear debris and mucus
110
What triggers migrating motor complex
Motilin triggers this, Gastrin and CCK suppresses
111
Exocrine pancreatic secretions
Digestive enzymes (Acinar cells), aqueous NaHCO3- solution (Duct cells) into pancreatic duct
112
Function of Bicarbonate in the duodenum
Neutralize acidic chyme entering the duodenum
113
Why do patients with cystic fibrosis have reduced pancreatic fluid secretion
Pancreatic duct cells use a Cystic FIbrosis Transmembrane Conductance Receptor (CFTR) to channel Cl into the lumen. This Cl comes back into the cell via Cl/HCO3- antiport. In cystic fibrosis, CFTR doesn't function properly leading to less HCO3- production
114
Why are acinar cell proteases stored in zymogen granule
These would digest digest cells in the pancreas if released before the duodenum. Thus, they are released in response to elevated Ca2+
115
What activates pancreatic proteases
Enterokinase (Mucosal cells) in duodenum
116
3 phases of intestinal secretion
Cephalic - Vagal stimulation of Acinar cells
Gastric - Gastric distention evokes a vasovagal reflex resulting in parasympathetic stimulation of acinar and duct cells
Intestinal - Neutralizes and digests
117
Steps in neutralizing part of Intestinal control of pancreatic secretion
Acid in duodenal lumen
Increase Secretin release from S cells
Stimulation of pancreatic duct cells
Increase secretion of aqueous NaHCO3
118
Steps in digesting part of Intestinal control of pancreatic secretion
Fat and protein in duodenal lumen
Increase Cholecystokinein from I cells
Stimulation of pancreatic acinar cells
Increase secretion of digestive enzymes
119
Luminal vs membrane digestion
Luminal - Mediated by pancreatic enzymes secreted into the duodenum
Membrane - Enzymes situated at brush border of epithelial cells
120
What is assimilation in GI tract
Process of digestion + absorption
121
Amylose vs Amylopectin vs Glycogen
Amylose - alpha-1,4 linkage; branched chain
Amylopectin - alpha-1.4 and a-1,6 linkage; branched chain
Glycogen - Same as amylopectin but more branched
122
What forms are carbohydrates absorbed
As monosaccharides; glucose, galactose and fructose
123
What helps covert starch to oligosaccharides
Alpha-Amylase (From pancreas and salivary gland) in the lumen (intraluminal hydrolysis)
124
What converts oligosaccharides to monosaccharides
4 oligosaccharidases - Lactase, maltase, sucrase-isomaltase at brush border (membrane digestion)
125
alpha-Amylase can break a-1,4 linkages. Why can't it produce glucose then?
a-Amylase can break internal a-1,4 linkages, not terminal ones. It also can't cleave a-1,6 linkage at branch points or a-1,4 linkage adjacent to branch point
126
Why is loss of lactase significant
Lactose - Glucose + Galactose can only be mediated by Lactase. Loss of lactase makes you lactose intolerant
127
What can cleave terminal a-1,4 glycosidic bonds
Oligosaccharides and not a-Amylase
128
What is sucrase responsible for
Sucrose - Glucose + Fructose
129
Max length of monomers Maltase can degrade in oligomers
Maltase can degrade a-1,4 linkages in straight chain oligomers upto nine monomers in length
130
Only enzyme split branching a-1,6 linkage in a-dextrins
Isomaltase
131
Rate limiting for oligosaccharides
Lactase - Rate of hydrolysis is rate limiting in assimilation
For maltase, sucrase and isomaltase it is subsequent transport of released monomer
132
What causes lactose intolerance
Lactase insufficiency, can't digest lactose
133
What can cause lactose intolerance
Primary lactase deficiency - Lack of lactase persistence (LP) allele, most common cause
Congenital lactase deficiency - Rare autosomal recessive disease, can't digest lactose from birth
Secondary lactase deficiency - Acquired due to damage/infection of proximal small intestine
134
Where do final products of carbohydrate digestion enter and exit enterocytes
Apical and basolateral membrane respectively
135
What helps absorb glucose and galactose
Secondary active transport mediated by SGLT 1
136
What helps absorb fructose
Facilitated diffusion by GLUT5
137
How do monosaccharides exit the enterocyte
Facilitated diffusion by GLUT2
138
How does SGLT - sodium glucose co-transporter work
2Na+ bind to the SGLT1. This increases affinity for glucose. Glucose binds; this along with Na+ translocate from extracellular to intracellular. 2Na+ dissociate and affinity for glucose falls, causing its dissociation
139
How are proteins digested
Proteins - Oligopeptides - Amino acids
140
Protein digestion in stomach
HCl starts to denature proteins. Pepsin cleaves proteins to peptides. It is an endopeptidase - preference for bonds between aromatic and larger neutral amino acids.
141
Is pepsin essential for protein digestion?
No
142
5 pancreatic proteases (proenzymes)
Trypsin, chymotrypsin, elastase, procarboxypeptidase A and procarboxypeptidase B
143
Which enzymes have oligopeptides as end product
Trypsin, chymotrypsin and elastase (Endopeptidase)
144
Which enzymes have single amino acid end products
Procarboxypeptidase A and B (Exopeptidase)
145
Where are additional peptidases present
Brush border and cytoplasm of enterocytes
146
How are amino acids absorbed
Brush border cells - 7 mechanisms, 5 are Na+ dependant co-transporters, 2 are Na+ independant
Basolateral membrane - 5 mechanisms, 3 mediates efflux of amino acids and 2 mediate influx
147
How are bi, tri and tetrapeptides absorbed
H+-dependant mechanisms at brush border (co-transport). These are further hydrolysed to amino acids within enterocytes.
148
Exit of amino acids via basolateral membrane is via Na+ independent transporters
True
149
What is leptin
Satiety hormone released by fat cells, sends signals to the brain that tell us when to stop eating
150
How doe excess fat impede satiety signals
Amount of leptin in the body depends on the number of fat cells. Higher the number of fat cells, more leptin in the body. However, the brain stops responding to these hormones causing them to overeat
151
What waist circumference puts you at risk of heart disease and type 2 diabetes
Men > 40 inches and women > 35 inches
152
Longitudinal smooth muscle layer in caecum and colon is divided into three strands called
Taeniae coli
153
What type of muscles surround the internal anal sphincter
Internal anal sphincter is smooth muscles, surrounded by skeletal muscles of external anal sphincter
154
Sac like bulges in the large intestine are called
Haustra
155
Function of caecum and appendix
None in humans but cellulose metabolism in others
156
What permits entry into the caecum
Ileocaecal valve via gastroileal reflex
157
How does the gastroileal reflex work
Ileocaecal valve has a positive resting pressure. It relaxes in response to distention in duodenum. It contracts in response to distention of ascending colon
158
What has potential to cause appendicitis
Faecalith - Hard stony mass of faeces in intestinal tract, may block appendiceal orifice
159
Primary functions of colon
Absorption - Na, Cl and water to condense ileocaecal material
Absorption - Carbohydrates not absorbed by small intestine are broken into fatty acids by colonic flora. This farry acids are absorbed
Resovoir - Storage of colonic contents
Periodic elimination of faeces
160
Does the colon absorb macronutrients
Nil except short chain fatty acids formed by colonic flora conversion of carbohydrates not absorbed in small intestine
161
Does colon mucosa have villi
No but it has colonic folds, crypts and microvilli that increase surface area
162
What helps with electrolyte absorption in colon
Colonocytes which are surface epithelial cells in colon
163
How does water get absorbed into colon
Absorption of electrolytes drives absorption of water via osmosis
164
What colonic cells mediate ion secretion
Crypt cells
165
Function of goblet cells in colon
Secrete mucus containing glycosaminoglycans and trefoil proteins involved in host defence, stabilizing mucus layer and healing epithelium
166
What is secretory diarrhoea
Diarrhoea when electrolyte absorption is impaired
167
Significant loss of K in faeces may be due to
Secretory diarrhoea
168
What causes haustration
Alternating contractions of circular muscles with low frequency contributing to long transit time
169
What direction of movement does haustration cause
Orad - Towards the mouth
170
Significance of haustration
Mixes contents and allows time for fluid and electrolyte reabsorption
171
What patterns of motiity exist in large intestine
Haustration, peristaltic propulsive movement, defaecation
172
What is mass movement in the colon
Simultaneous contractions of large sections circular muscles in ascending and transverse colon that drives faeces into distal regions
173
What triggers mass movement or peristaltic propulsive movement
Gastrocolic response typically involving gastrin and extrinsic nerve plexus
174
Does mass or peristaltic propulsive movement occur in the distal colon
Yes to propel faeces into the rectum and trigger the defaecation reflex in response to stretch
175
Explain the defaecation reflex
If the passive distention of the rectum is large enough, it triggers an active contraction of rectal smooth muscles. This passive rectal distention also triggers the smooth internal anal sphincter muscles to relax (rectosphincteric reflex). If defaecatio isn't desired, skeletal muscles of external anal sphincter contract involuntarily
176
Main nerve of perineum that carries motor supply to external anal sphincter
Pudendal nerve
177
Contraction of smooth muscle in sigmoid colon and rectum does what to internal anal sphincter
Relaxes it
178
How is defaecation assisted
Straightening of anorectal angle, abdominal skeletal muscle contract and expiration against closed glottis
179
What is defective in Hirschsprung disease
Rectosphincteric reflex
180
What is the rectosphincteric reflex
Passive rectal distention if large enough can trigger smooth muscles of internal anal sphincter to relax
181
Function of colonic flora
Increase intestinal immunity by competing with pathogens, promote motility, maintain mucosal integrity, synthesize vitamin K2 and free fatty acids (from carbohydrates), activate some drugs
182
What is flatus
Intestinal gas
183
What is a burp or belch known as
Eructation
184
Causes of constipation
Ignoring or suppressing urge to defaecate, decreased colonic motility (age, improper diet, drugs), obstruction of faecal movement (cancer), paralytic ileus following abdominal surgery, impariment of motility/defaecation reflex (Hirschprung disease, absence of section of enteric nervous system)
185
Symptoms of constipation
Headache, abdominal discomfort, loss of appetite, general malasie
186
What causes feeling of malaise in constipation
Prolonged distention of large intestine not toxins absorbed from retained fecal matter
187
What drives water absorption
Passive process driven by transport of solues (Na+)
188
Where is the following transporter found -
Na+/glucose co-transport
Na+/amino acid co-transport
Throughout small intestine and most important in postprandial period
Found in colon in neonates
189
Where are the following transported found -
| Na+/H+ exchange
Duodenum and jejunum, stimulated by luminal HCO3-
190
Where are the following transported found -
| Parallel Na+/H+ and Cl-/HCO3- exchange
Ileum and colon most important in interdigestive period
191
Where are the following transporters found -
| Epithelial Na+ channels
Colon (distal particularly) and regulated by aldosterone
192
Which Na channel is hormonal regulated
Epithelial Na+ channels found in distal colon, by Aldosterone
193
Mechanism of Na+/glucose and Na+/amino acid co-transport
Secondary active transport, 2 Na+ move into the cell along with 1 glucose or 1 amino acid
194
What generates a transepithelial potential (Vte)
Overall transport of Na in which lumen is negative. This drives parallel absorption of Cl-
195
Where are NHE1 present
In basolateral membranes of entercoctyes whereas NHE2 and NHE3 are found at the apical surface of the enterocyte membrane
196
What exchangers is known as cellular pH housekeeper
NHE1 at basolateral membrane of enterocytes
197
What stimulates Na exchange at apical membrane in jejunum
Alkaline environment of lumen due to bicarbonate from pancreas
198
What does cAMP, cGMP and Ca2+ regulate in Na absorption
Reduce NaCl absorption by Na/H and Cl/HCO3 exchange in parallel, causing diarrhoea
199
How does Aldosterone regulate Na absorption
Opens Epithelial Na+ channels (ENaC), inserts more ENaC into membrane from intracellular vesicle pool and increase synthesis of ENaC and Na/K ATPase
200
Passive Cl- absorption
Electrogenic movement of Na creates a negative potential in the lumen which allows passive movement of Na+ trans or paracellularly
201
Non-electrogenic methods of Cl- absorption
Cl-HCO3 exchanger (Ileum and colon) and parallel Na/H and Cl/HCO3 exchange (Ileum and proximal colon)
202
Cellular mechanism of Cl- secretion
Low intracellualr Na drives inward movement of Na/Cl and K via Na/K/2Cl cotransporter. Intracellular Cl increases providing an electrochemical gradient for Cl to exit cell via CFTR on apical membrane
203
What activates CFTR mediated secretion of Cl
Bacterial exotoxins
Hormones and neurotransmitters
Immune cell products
Laxatives
204
Secondary messengers that activate CFTR
cAMP, cGMP and Ca2+
205
What can secretion of Cl-via apical CFTR cause
Secretory diarrhoea
206
How can diarrhoea cause metabolic acidosis
Due to HCO3- loss
207
Causes of diarrhoea
Impaired absorption - Congenital, inflammation, infection, excess bile in colon
Excessive secretion
Non-absorbale or poorly absorbale solute in intestinal luman - Lactase deficiency
Hypermotility- Not enough time to absorb water
208
How can Cholera cause diarrhoea
Cholera toxin enters enterocyte and inhibits GTPase activity. This increases activity of adenylate cyclase. Increased concentration of cAMP stimulates CFTR. CFTR promotes secretion of Cl- with Na and water follows causing diarrhoea
209
Why do sorbitol sweets cause diarrhoea
Sorbitol isnt well absorbed and hence causes diarrheoa
210
How do oral rehydration salts work
Oral rehydration salts have glucose and sodium. When 2 sodium bind to SGLT1, affinity for glucose increases. These are transported intracellulary. 2Na dissociate and affinity for glucose decreases causing its dissociation. Water follows Na into the cell
211
Action of opiods on alimentary tract
Inhibition of enteric neurones
Decrease peristalsis, increase segmentation
Increase fluid absorption
Constriction of pyloric, ileocaecal and anal sphincters
Increase tone of large intestine
212
Major opiods in diarrhoea
Codeine - Converted to low dose morphine in liver
Diphenoxylate - Low CNS penetration, low solubility in water (decrease abuse potential)
Loperamide - Low CNS penetration, low solubility, undergoes enterohepatic cycling
