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104: Theme 1 > Physiology of the Alimentary system > Flashcards

Physiology of the Alimentary system Flashcards

1
Q

What are the Accessory organs to the GI system?

A
  • Gall bladder
  • Liver
  • Pancreas
  • Parotid Salivary gland
  • Submandibular salivary gland
  • Sublingual salivary gland
  • Tongue and Tooth
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2
Q

Label the diagram

A

-

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3
Q

How does coordinated motility work in the majority of the GI tract?

A
  • The smooth muscle acts a functional syncytium using gap junctions to cause peristaltic waves of motion
  • Outer muscle bundles are longitudinal inner bundles are circular
  • causes involuntary movement
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4
Q

What is the ENS?

A

The Intrinsic Enteric Nervous System

  • this is the intrinsic control of GI motility and secretion
  • these are reflex contractions in response to local stimuli i.e stretch, hormones, irritation and nutrients
  • The Myenteric plexus in the muscularis layer is in control of motility
  • The Submucosal plexus in the submucosal layer is in control of secretion and local blood flow
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5
Q

Describe the external control of GI tract smooth muscle motility

A
  • CNS sends a signal via the extrinsic nervous pathway para and sympathetic
  • reaches the outer longitudinal muscle
  • goes to the myenteric ganglia through an Interneuron to an afferent sensory neuron through the circular muscle ( motility)

or

  • to the circular muscle through a motor neuron into the Submucosal ganglia via another motor neuron known as the secretomotor neuron ( secretion and blood flow)
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6
Q

What is the stimulus and effect of Chylocystokinin (CCK)?

A
  • its secretion is stimulated by fat, protein and acid
  • secreted in the I cells in the small intestine

Effect

  • stimulates pancreatic secretions ( hence stimulated by acids and fat)
  • stimulates gall bladder contraction and growth of exocrine pancreas
  • inhibits gastric emptying
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7
Q

What is the stimulus and effect of Motilin?

A
  • stimulated by fat, acid ad nerves
  • secret in the M cells of the duodenum and jejunum

Effects

  • stimulates gastric and intestinal motility
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8
Q

What mechanism causes contraction in the smooth cells of the GI tract?

A
  • a fluctuating negative electrical potential difference resulting in:

> Slow waves: gradually increasing until it passes threshold potential

> Spike potentials: generate smooth muscle contraction

  • receptors on the smooth muscle are stimulated by stretch, the hormone motilin and acetylcholine or parasympathetic stimulation
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9
Q

Describe the two types of contraction that occur in GI smooth muscle/

A

Segmentation

  • used for mixing circular contraction occurs back and forth in a pendular motion

Peristalsis

  • used for propulsion, requires functional mysenteric plexus
  • local distention causes a contraction behind the bolus and relaxation in front
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10
Q

Name and describe an ENS innervation dysfunction

A

Hirschsprung’s disease

  • rare congenital absence of the myenteric plexus,
  • usually in the distal colon
  • lacks peristalsis and undergoes continuous spasms
  • leads to functional obstruction and severe constipation
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11
Q

Describe the pharyngeal phase of deglutition

A
  • Bolus in the pharynx signals the swallowing centre in the medulla oblongata and pons in the brain stem
  • motor referents in trigeminal, glossopharyngeal and vagal nerves cause series of muscle contractions moving the bolus through the oropharynx into laryngopharynx into the oesophagus
  • soft palette elevates over posterior nares to close nasal pharynx
  • the epiglottis closes over the larynx opening –> respiration is inhibited
  • upper oesophageal sphincter relaxes
  • pharyngeal muscle contraction propels bolus into the oesophagus
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12
Q

Describe the Oesophageal phase

A
  • This is coordinated via the intrinsic myenteric and extrinsic vagal innervation
  • primary peristalsis moves bolus downwards
  • circular muscle contracts behind the bolus
  • longitudinal muscle contracts in front of it to shorten fibres and push the wall outwards
  • mucus lubricates and reduces friction
  • the lower oesophagus and the lower oesophageal sphincter relaxes
  • the stretching caused by the bolus stimulates the secondary peristalsis
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13
Q

LOS = Lower Oesphogeal

Name two Oesophageal motility dysfunctions

A

Achalasia

  • LOS fails to relax causing food to remain in the oesophagus
  • maybe caused by a vagal or myenteric defect
  • causes distention, inflammation, infection and ulceration

Gastro-oesophageal reflux

  • LOS tone lost leading to flow of acidic gastric content into the oesophagus
  • causing inflammation and ulceration
  • may be linked to hiatus hernia (a portion of the stomach protrudes through the diaphragm into thorax causing gastric reflux)
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14
Q

Describe the structure of the stomach and their roles in storage

A
  • Fundus: acts primarily as a reservoir for storage of stomach contents
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15
Q

Describe how mixing occurs in the stomach

A
  • Slow peristaltic waves are initiated in the body of the stomach moving stomach contents towards pyloric antrum.
  • Food is forced back for further mixing and digestion.
  • This process of propulsion and retropulsion occurs in cycles to produce chyme
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16
Q

Describe the process of emptying the stomach

A

•More powerful peristaltic contractions build to force chyme into the duodenum

How emptying is regulated

  • Excitatory regulation: ENS/ANS neuronal stimulation and hormones eg motilin
  • Inhibitory regulation: ANS regulation, duodenal enterogastric reflexes and hormones eg CCK, secretin

Regulation is extensive with primary inhibitory feedback signals originating from the SI

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17
Q

Explain how the CNS and the SI are involved in regulation of gastric emptying

A
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18
Q

Which hormones reduce gastric emptying? Explain the process which stimulates their release.

A
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19
Q

Name two gastric motility dysfunctions

A

Dumping Syndrome

  • Rapid emptying of gastric contents into the small intestine
  • Occurs following ingestion of large meal after gastrectomy characterized by nausea, pallor, sweating, cramps, vertigo, and sometimes fainting within minutes
  • May be caused by hypertonic duodenal contents causing rapid entrance of fluid

Gastroparesis

  • Stomach fails to empty
  • Prevents proper digestion
  • Causes bloating and nausea
  • May be caused by gastric cancer or peptic ulcers occasionally observed through impaired vagal stimulation to the stomach in severely diabetic patients who develop autonomic neuropathy
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20
Q

What are the two types of Motility in the small intestine? Explain them.

A

Segmentation

  • stretch receptors trigger myenteric stimulation of muscle contraction
  • no net movement

Propulsive peristalsis

  • controlled by stretch hormones and ENS
  • Excitatory control hormones: gastrin, CCK, insulin, motilin, serotonin
  • Inhibitory control hormones: secretin and glucagon
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21
Q

What is the function of the following reflexes?

  • Gastroenteric reflex
  • Gastroileal reflex
  • Migrating motor complex (MMC)
A

Gastroenteric reflex: gastric distention activates myenteric plexus to promote SI peristalsis

Gastroileal reflex: gastric distention promotes peristalsis in the ileum to force chyme through the ileocecal valve into the caecum

Migrating motor complex (MMC)

  • Series of peristaltic contractions, between meals, every 90 mins sweeps contents of the SI into the colon
  • Intrinsic enteric control, hormone motilin
  • Absence of the MMC can lead to bacterial overgrowth
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22
Q

Name three ways in which peristalsis can be disrupted in the SI

A
  • Peristaltic rush: mucosal irritation stimulates the ENS and ANS neural reflexes to rapidly seep contents of the SI into the colon
  • Paralytic ileus: loss of peristalsis following mechanical trauma i.e surgery
  • Vomiting: reverse peristalsis initiated in the distal small intestine (or the vom centre in the brain) to expel intestinal and gastric contents
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23
Q

What is the overall function of the Large Intestine?

A

Motility more sluggish to optimize:

  • Absorption of water and electrolytes (proximal)
  • Formation and storage of faeces (distal)
  • Commensal microbiome aids digestion, synthesises of B and K vitamins
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24
Q

Describe the structure of the large intestine and how it helps its function

A
  • the longitudinal muscle in the muscularis is thickened to form three bands - taeniae coli
  • the taeniae coil tonically contract to form haustral bulges, used later in mixing
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25
Q

What type of motility is there in the large intestine and how is motility controlled?

A
  • Mixing contractions: occurs via haustral churning

Peristalsis movements

  • mass movements 2-3x per day: force contents into sigmoid colon and rectum
  • gastro-colic and duodeno-colic reflexes: mass movements occur after meals caused by stretching via the ANS
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26
Q

What happens during a defecation reflex?

A
  • Mass movements push faecal matter into the normally empty rectum
  • Stretch receptors are stimulated and activate the ENS and parasympathetic ANS
  • Involuntary contraction of the longitudinal muscle in the rectum opens the internal anal sphincter
  • The constricted external anal sphincter is voluntarily relaxed to allow defecation
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27
Q

What are the major salivary glands and what are their secretions??

A

Parotid

  • serous, watery secretions containing amylase

Submandibular

  • serous and mucus

90% of saliva

Sublingular

  • thicker mucus predominantly secreted for lubrication
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28
Q

What are the components of saliva?

A
  • H2O
  • Electrolytes: buffer
  • alpha-amylase (ptyalin)
  • lysozyme: hydrolysis of peptidoglycans in the wall of gram -ve bacteria
  • lingual lipase: activated in the stomach and SI
  • lactoferrin: chelates iron to prevent microbial multiplication
  • Kallikrein: converts alpha-2-globulin into bradykinin
  • Secretory IgA: prevents microbial attachment to epithelium
  • Mucin: lubrication
  • organics urea and uric acid
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29
Q

Describe the formation of hypotonic saliva in acinar cells

A
  • primary secretion in the acinus is isotonic
  • made up of Cl-, Na+ H2O and HCO3-
  • NKCC1 transporter at the basolateral membrane used to transport Cl- into the acinus
  • in the Duct, Na+ is changed for K+
  • and Cl- is exchanged for HCO3-
  • hypotonic saliva ends up K+ and HCO3- rich and Na+ and Cl- poor
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30
Q

Describe the parasympathetic control of the salivary secretion rate

A
  • sight, thought, smell taste and tactile stimulation signal salivary nuclei in the medulla for secretion
  • sublingual and submandibular control occurs via Cranial Nerve VII
  • parotid control is via CN VIII
  • results in an increase in amylase and mucin containing watery saliva, also results in vasodilation
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31
Q

Describe the sympathetic stimulation of saliva secretion

A
  • control is via the superior cervical ganglion
  • results in vasoconstriction increased amylase secretion but overall reduced saliva production (dry mouth)
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32
Q

What is Sjögren’s syndrome?

A
  • salivary gland dysfunction
  • an autoimmune disease that destroys the exocrine glands
  • commonly affects tear and saliva production
  • dry eyes and dry mouth, known as sicca syndrome
33
Q

What is Xerostomia?

A
  • dry mouth
  • patients lack adequate saliva
  • dental caries and halitosis commonly due to bacterial overgrowth
  • difficulty speak or swallowing solid food due to inadequate lubrication
34
Q

What exocrine cell types form the Gastric (oxyntic) gland?

A
  • Parietal (oxyntic) cells: produce HCl and intrinsic factor
  • Mucous neck cells: produce thin mucus
  • CHief cells: produce pro-enzyme pepsinogen (renin in neonates) and gastric lipase

These cells secrete gastric juices

  • Gastric pits form into gastric glands
35
Q

What endocrine gland cells make up the Gastric (oxyntic) gland?

A
  • G cells: secrete the hormone gastrin
  • D cells: secrete the hormone somatostatin: D cells activated by H+ ions, somatostatin stimulate G cells
  • Enterochromaffin-like (ECL) cells: secrete histamine
36
Q

What is the action of gastrin?

A

Results in

  • Parietal cells –> secretion of HCl (H+ stimulates pepsinogen conversion to pepsin)
  • Chief cells –> secretion of pepsinogen
  • lower oesophageal sphincter contraction
  • Increases motility of the stomach: more mixing and peristalsis
  • relaces pyloric sphincter: allows movement of food into the duodenum
37
Q

What are the components of gastric juice?

A
  • water and electrolyte
  • Mucus
  • Pepsinogen (pro-enzyme): activated by H+ to form pepsin
  • Rennin only in neonates: coagulation of milk through casein proteolysis
  • Gastric lipase
  • HCl
  • Intrinsic factor: facilitates B12 absorption in the ileum ( needed for erythropoiesis in bone marrow, absence leads to pernicious anaemia)
38
Q

How does HCl secretion occur?

A
  • H2O –> H+ + OH-
  • H+K+ATPase proton pump: H+ being transported into the lumen of the stomach
  • K+ leaks back into stomach down cons. gradient
  • OH- + CO2 –( carbonic anhydrase CA)–> HCO3-
  • HCO3- Cl- exchange, Cl- moving into the parietal cell then the lumen of the stomach moving down cons. gradient
  • HCO3- causes venous blood to become alkaline postprandial (after a meal)
39
Q

How are parietal cells fit for function?

A
  • packed with tubulovesicles
  • fuse with the canalicular membrane as microvilli when stimulated
  • contain H+/K+ATPase and CA enzyme needed for production and secretion of H+
40
Q

What stimulates gastric acid secretion?

A
  • ACh
  • Gastrin from G cells (gastrin stimulates ECL cells)
  • Histamine from ECL cells ( enterochromaffin-like): histamine binds to H2 receptor
  • Gastrin –(2nd messenger activated inside the parietal cell)–> phospholipase C (PLC) –> IP3 –> Ca2+ –> H+ release
  • Histamin – (2nd messenger activated inside parietal cell) –> Adenylate cyclase (AC)–> cAMP –> H+ release
41
Q

What inhibits the secretion of gastric acids?

A
  • the hormone Somatostatin from D cells inhibit adenylate cyclase: therefore cAMP isn’t stimulated, blocking the Histamine pathway
  • Mucosal prostaglandin is an antagonist for H2 receptor
  • NSAIDs inhibit prostaglandin formation and increase gastric acid secretion
42
Q

What are pharmacological methods to inhibit gastric acid activity/ secretion?

A
  • Omeprazole: proton pump inhibitor inactivates H=/K+ATPase
  • Cimetidine: H2 receptor antagonist, inhibits stimulus for acid secretion (histamine action)
  • Atropine: ACh inhibitor, inhibits muscarinic receptors and vagal stimulation of acid secretion
43
Q

What is Gastritis?

A
  • inflammation of the gastric mucosa
  • most commonly caused by bacteria Helicobacter pylori: gram-negative, producing urease forming ammonia from ureas to neutralize acid and damage mucosal barrier
  • also caused by smoking, alcohol, NSAIDs, chronic stress
  • Restitution follows acute damage: this is rapid division of stem cells located in the neck of gastric glands
44
Q

Describe the process of atrophic gastritis

A
  • antibody-mediated destruction of parietal cells
  • causes hypochlorhydria (insufficient acid secretion)
  • and intrinsic factor deficiency: bit B12 malabsorption –> pernicious anaemia
45
Q

What are the three phases of gastric secretion?

A

Cephalic

Gastric

Intestinal

  • Excitatory: Chyme pH >3peptides that are present stimulate gastric secretions via vagus stimulation and gastrin
  • Inhibitory: Chyme: pH <2, leads to distention, increase in protein breakdown products, hypo-osmotic products inhibit gastric secretions via cholecystokinin, the hormone secretin is gastric inhibitory polypeptide?? overall slows the release of stomach content into the duodenum
46
Q

What are the primary secretions of the small intestine?

A
  • Intestinal juice: mucus/ HCO3- , in the duodenum
  • pancreatic juice: digestive enzymes
  • bile: from hepatocytes in the liver
47
Q

What are the key endocrine hormones in the small intestine and what do they all generally do?

A
  • Secretin
  • CCK
  • glucose-dependent insulinotropic peptide (CIP)
  • they regulate bile and pancreatic secretions
48
Q

What are secretory cells are found in the small intestine and what do they do?

A

These cells make up the villi found on the small intestine mucosa

  • microvilli: digests and absorbs nutrients
  • Goblet cells: secrets mucus
  • Enteroendocrine cells: secretes secretin, CCK or GIP
  • Paneth cells: secrets lysozymes and are capable of phagocytosis

Only in the Duodenum: Brunner’s glands secret mucus and HCO3-

49
Q

Where does the renewal of epithelial cells stem from, how long is turn over?

A
  • occurs in the crypt-villus junction
  • Stem cell cells found between Paneth cells and proliferative progenitors
  • turn over is 3-6 days
50
Q

Where is Secretin produced and what is its action?

A
  • produced in S cells: stimulate pancreatic and biliary bicarb secretions
51
Q

Where is CCK produced and what is its action?

A
  • produced in I cells
  • stimulate pancreatic and gallbladder secretion
52
Q

Where is GIP and what is its action?

( Glucose Dependent Insulinotropic Peptide or Gastric Inhibitory Peptide)

A
  • produced in K cells
  • may inhibit acid secretion or
  • stimulate insulin release
53
Q

What is the pancreas secretion structure?

A
  • consists of glandular epithelial clusters
  • 99% exocrine acinar clusters secreting pancreatic juices
  • 1% endocrine pancreatic islets: Islets of Langerhans
  • glucagon from alpha cells
  • insulin from beta cells
  • somatostatin from delta cells
  • pancreatic polypeptide from F cells
54
Q

Describe the structure of Acinar clusters starting from the acinus to the main duct

A
  • multiple acinar cells make up up an acinus which is linked by an intercalated duct
  • multiple acini form a lobule, the intercalated duct drains into the interlobular duct
  • the interlobular duct drains into the main pancreatic duct
55
Q

What is the difference between ductular and acinar secretions?

A
  • Ductular secretions have a higher conc. of NaHCO3-
  • Acinar secretions have a higher concentration of NaCl and enzymes
56
Q

What stimulates acinar enzyme production?

A
  • Acetylcholine released via parasympathetic vagus stimulation
  • CCK production is triggered by chyme containing fat and protein products
  • acinar cells produce a lower volume of pancreatic juices but they are enzyme-rich
57
Q

What stimulates ductal production of bicarbonate and water?

A
  • Secretin which is triggered by H+ in highly acidic chyme in the Duo
  • Ductal produce large volumes of HCO3- rich pancreatic juices that are enzyme-poor
58
Q

What are the five types of pancreatic enzymes?

A

- Proteolytic: released in the inactive form called zymogens

  • Amylase: hydrolyses starch, glycogen and other CHO
  • Lipases: hydrolyses fat into fatty acids and monoglycerides
  • Nucleases: digest RNA and DNA to nucleic acids
  • Trypsin inhibitor: prevents activation of trypsin to prevent pancreatic digestion
59
Q

Explain the activation of trypsin and the other proteolytic enzymes.

A
  • SI brush borders enterokinase cleaves hexapeptide from trypsinogen to form trypsin
  • trypsin cleaves and activates other proteolytic enzymes
  • this prevents autodigestion
60
Q

Explain duct secretion of NaHCO3

A
  • Na+ and HCO3- co-transported into pancreatic duct cell from the basolateral membrane (blood side)
  • HCO3- transported into the lumen via a Cl-/HCO3- exchange at the apical membrane of the cell
  • Cl- leaves through the CFTR under secretin stimulation via cAMP
  • pancreatic duct produces HCO3- through:

H2O + CO2 –(carbonic anhydrase)–> HCO3- + H+

  • H+ pumped out of the basolateral membrane through a Na+/H+ exchange
  • Na+ actively pumped out using Na/K-ATPase, K+ leaks out transcellular
  • Na+ and H2O move into lumen paracellular down osmotic and electrochemical gradient
61
Q

Explain the synthesis and secretion of bile in the liver

A
  • Bile is synthesised by hepatocytes lining sinusoidal blood vessels in the liver acinus
  • hepatocytes used oxygen from the portal triad to drive production of bile
  • bile produced drains into the blind-ended canaliculi and into the bile duct
  • in the gall bladder, the bile becomes more concentrated bile salts
62
Q

How is CCK secreted and what regulates the process?

A

CCK released in response to fat content causes:

  • gallbladder contraction
  • relaxation of the sphincter of Oddi, this drains into the duo

Secretin released in response to acidic chyme stimulates:

  • liver ductal secretion of HCO3-, H2O leading to more watery secretions

Vagal stimulation causes:

  • weak contraction of gallbladder
63
Q

What is Enterohepatic circulation of bile salts?

A
  • the continued recycling of bile salts via the portal vein used to drive bile synthesis in the liver
  • bile salts are actively reabsorbed from the ileum back into the liver
  • many hydrophobic drugs (acetaminophen (paracetamol)) can be deactivated by the liver and excreted into bile; slowing the elimination of the drug from the bodies system
64
Q

What are some causes of Gallstones>

A
  • excessive water and bile salt reabsorption from bile
  • excessive cholesterol in bile causing precipitation
  • inflammation of the epithelium (low-grade chronic infection)
65
Q

What 5 processes regulate the movement of water and electrolytes in GI tract?

A
  • Gut luminal
  • Enteric nervous system
  • Autonomic nervous system
  • Hormonal signals
  • Immunogenic signals
66
Q

What 2 routes of enterocyte transport are there?

A
  • transport can be paracellular, between tight junctions of cells down a conc. gradient
  • or transcellular, which may be against a conc. gradient requiring ATP
67
Q

What 3 types of enterocyte transport are there?

A
  • Passive
  • Solvent drag: tight junction transport, water moving to reach osmotic equilibrium, taking ions along with it
  • Active: Na/K ATPase
68
Q

What is the difference between villi and crypt enterocytes?

A

Brush border hydrolases

  • Villus: Abundant expression
  • Crypt: Minimal expression

Nutrient Transport

  • Villus: High
  • Crypt: Low

Net water/ ion transport

  • Villus: Absorption
  • Crypt: Secretion

Permeability

  • Villus: Low
  • Crypt: High
69
Q

What is the movement of water in the 3 sections of the SI?

A
  • Osmotic drag in the duodenum to reach osmotic equilibrium: this is to form isotonic chyme
  • Jejunum: reabsorbs, Na+, K+, Cl- and H2O
  • Ileum: secretes HCO3-
70
Q

What Na+ transport occurs in the small intestine and what is it’s impact?

A
  • Na+ transport drives the transport of other ions and organics
  • Transport is driven by the basolateral active transport of Na+ into the interstitial fluid via Na+/K+ ATPase, this creates an electrochemical gradient
  • secondary active transport occurs at apical carrier proteins
  • Na/glucose co-transporter
  • Na/ amino acid co-transport
  • Na/H antiport exchanger
  • Na/Cl symport co-transport

-

71
Q

What Cl- transport occurs in the SI?

A
  • there is a net positive charge in the paracelluar spaces because of Na+ transport absorption
  • provides an electrochemical gradient for Cl- absorption ( tight junction absorption)
  • apical symport co-transport with Na+ into the lumen then out through the basolateral membrane
  • in the distal ileum Cl- occurs passively through the apical membrane as there is antiport exchanger with HCO3-
72
Q

Explain NaCl absorption in the large intestine (Na+ and Cl- ions)

A
  • Driven by Na+/ K+ ATPase

Sodium entry by

  • Na+ channels facilitated diffusion
  • Na+/H+ antiport exchanger
  • Diffusion under Aldosterone control: increases Na channels at the expense of K+ ( secreted when lumen cons. is low)
  • Cl-/HCO3- a buffer for acid produced by bacteria: Cl- exchanged for HCO3- at the apical membrane
  • Na+ and Cl- movement creates an osmotic gradient for transcellular water movement
73
Q

What is Ouabain?

A
  • a plant-derived toxic substances
  • in low doses can treat hypotension
  • inhibits the sodium-potassium pump ( Na+/ K+ ATPase)
74
Q

How and where is water and NaCl secreted in the GI tract?

A
  • occurs via the crypt enterocytes ( maintains lumen liquid contents)
  • Na+/K+ ATPase forms a Na+ electrochemical gradient
  • this drives the movement of Na+, K+ and 2Cl- into crypt cells through the corresponding cotransporter
  • Cl- ions leave at the apical membrane into the intestinal lumen through Cl- channels such as CFTR
  • Cl- provides electronegativity in the intestinal lumen to draw Na+ via paracellular routes,
  • water moves down osmotic gradient following Na+
75
Q

What is Cystic Fibrosis and what is its result?

A
  • Congenital autosomal recessive disease
  • Deletion in the gene for the CFTR channel
  • CFTR is main Cl- channel in the apical membrane of the gut, pancreatic and airway epithelium
  • secretion of sticky mucus and high viscosity of luminal contents as Na+ and H2O movement into the lumen doesn’t occur
76
Q

How does Cystic fibrosis present in newborns?

A
  • presents with intestinal obstruction and meconium ileus in newborns
  • a thicker than moral meconium, causing a narrowing in the ileum resulting in intestinal obstruction
77
Q

What causes the Cholera toxin? What is the effect of this toxin?

A
  • released by gram-negative curved bacillus Vibrio Cholera
  • binds to cell receptor to irreversibly upregulate adenylate cyclase
  • this generates excess CAMP which stimulates Cl- secretion via CFTR Cl- channels

–> massive efflux of Cl-, Na+ and H2O into the crypts, especially in the jejunum

  • profuse watery diarrhoea; circulatory shock due to dehydration
78
Q

What is the treatment for the Cholera toxin?

A
  • Oral rehydration therapy
  • effects only reduced following enterocyte turnover as the binding is irreversible

104: Theme 1 (4 decks)

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