9. Abdomen & Digestive System (TT) Flashcards

Question

What happens to the pH of the salivary secretions as flow rate increases?

Answer 1

* At rest, the pH is more acidic * When the flow rate increases, it becomes more basic, since HCO₃^-secretionis stimulated by agonists that stimulate primary secretion

Answer 2

* Enzymes: α-amylase, Lingual lipase * Mucins * Kallikrein * Antimicrobial proteins: Lysozymes, lactoferrin, lactoperoxidase, proline-rich proteins, IgA

Answer 3

* α-amylase * Lingual lipase

Answer 4

Digests starch to maltose.

Answer 5

Starts fat digestion

Answer 6

* Glycoproteins * Provide the barrier and binding functions of the mucous secretions

Answer 7

* A protein that cleaves proteins to produce vasodilator peptides (e.g. bradykinin) * It is found in the mucous secretions of the salivary glands

Answer 8

* Lysozymes * Lactoferrin * Lactoperoxidase * Proline-rich proteins * IgA

Answer 9

* By the autonomic nervous system, with the parasympathetic nervous system playing the most important role -\> PNS causes the production of large volumes of saliva. * Substance P and VIP also cause increase production of saliva.

Answer 10

Parasympathetic nervous system causes increased rate of saliva production by stimulating primary secretion and inhibiting secondary secretion, which produces lots of dilute saliva: * ACh acts of M3 receptors that increase IP₃ and therefore Ca²⁺ in the cytoplasm * Ca²⁺stimulates protein kinases that phosphorylate channels on the apical and basolateral membranes * As a result, the permeability of the apical membrane to Cl^- and the basolateral membrane to K⁺ is increased * Phosphorylation of the cytoskeletal elements induces exocytosis of vesicles containing proteins such as amylases Substance P and VIP also increase intracellular Ca²⁺, so they also initiate secretion.

Answer 11

Sympathetic stimulation increases salivary secretion, producing a viscous saliva: * Noradrenaline binding to α receptors increases IP₃, which increases intracellular Ca²⁺ * Ca²⁺ stimulates protein kinases that phosphorylate channels on the apical and basolateral membranes * As a result, the permeability of the apical membrane to Cl^-and the basolateral membrane to K⁺ is increased * Phosphorylation of the cytoskeletal elements induces exocytosis of vesicles containing proteins such as amylases * Binding to β receptors raises cAMP, which activates protein kinase A and stimulates amylase secretion from vesicles

Answer 12

* Both increase the secretion of saliva, which is an exception to the normal rule * Sympathetic stimulation results particularly in the increase of amylase secretion and vasoconstriction of blood vessels that supply the glands -\> Leads to production a more serous, less dilute saliva.

Answer 13

Parasympathetic

Answer 14

Salivary nucleus of the medulla: * Stimulated by: Conditioned reflexes, Smell, Taste, Pressure, Nausea * Inhibited by: Fatigue, Sleep, Dehydration, Fear

Answer 15

Cranial nerves IX (glossopharyngeal) and X (vagus)

Answer 16

T1 to T3 nerve roots, which synapse at the superior cervical ganglion.

Answer 17

Unites with the common bile duct to drain into the duodenum.

Answer 18

It is alkaline, so it can neutralise the acidity of the stomach acid.

Answer 19

The primary secretion and secondary modification is similar to that in the salivary glands.

Answer 20

It hydrates digestive proteins released from the acinar cells.

Answer 21

Yes, but it can be increased up to 10-fold by receptor activation.

Answer 22

It is basically the same as in the salivary gland. Acinar cells essentially secrete isotonic NaCl: * Na⁺/K⁺-ATPase on the basolateral membrane creates a sodium gradient for the NKCC * Basolateral NKCC (Na⁺-K⁺-2Cl^- co-transporter) accumulates Cl^- ions inside the cell * Cl^- ions diffuse across the apical membrane through channels * K⁺ diffuses out through basolateral channels * Na⁺ ions can also diffuse between cells into the lumen through tight junctions, along the electrical gradient established by Cl^- movement * H₂O follows by osmosis

Answer 23

* It is the CFTR (cytsic fibrosis transmembrane conductance regulator) * It is mutated in cystic fibrosis, so secretion is mutated in these individuals

Answer 24

Duct cells modify primary secretion. The process is very similar to in the salivary glands: * **Cl^-** is reabsorbed on the apical membrane through Cl^-/HCO₃^- exchangers (AE), BUT then it exits the cell through Cl^- channels on the APICAL membrane * **HCO₃^-** secreted in exchange for Cl- by the Cl^-/HCO₃^-exchanger -\> HCO₃^- is formed from CO₂ and H₂O in the cell * **H⁺** from bicarbonate production is lost by the basolateral Na⁺/H⁺ exchanger (NHE1) * **Na⁺**and **K⁺** diffuse between cells down the electrochemical gradient * **H₂O** permeability is low

Answer 25

No, some of them are precursors that are later activated.

Answer 26

In the small intestine.

Answer 27

* Proteases -\> Trypsinogens, chymotrypsinogens, proproteases, procarboxypeptidases * Amylases * Lipases * Nucleases

Answer 28

* Trypsinogens * Chymotrypsinogens * Proproteases * Procarboxypeptidases These are all zymogens that will be activated in the small intestine lumen.

Answer 29

It prevents autodigestion of the cells that secrete them.

Answer 30

* Presence of protease inhibitors in the secretory vesicles with the zymogens * Presence of nondigestive proteases to degrade active enzymes

Answer 31

* Cephalic phase * Sight, smell and taste of food * Mediated by: ACh * Gastric phase * Distension of the stomach * Mediated by: ACh, Gastrin * Intestinal phase * Feedback phase, caused by the pH, distension, amino acids and fatty acids in the duodenum * Mediated by: ACh, Secretin, CCK (Cholecystokinin)

Answer 32

* Sight, smell and taste of food * Mediated by: ACh

Answer 33

* Distension of the stomach * Mediated by: ACh, Gastrin

Answer 34

* Feedback phase, caused by the pH, distension, amino acids and fatty acids in the duodenum * Mediated by: ACh, Secretin, CCK (Cholecystokinin)

Answer 35

* ACh and CCK -\> On acinar and duct cells * Gastrin and secretin -\> Only on duct cells

Answer 36

* Released from vagal impulses * Triggered by: * Higher command (medulla) * Vagovagal reflex triggered by amino acids, fatty acids in duodenum (feedback loop from duodenum)

Answer 37

* Released from G cells in the antrum of stomach * Triggered by: * Vagal stimulation of GRP-containing neurons in response to distension of stomach GRP = Gastrin-releasing peptide

Answer 38

* Released from S cells in the duodenal epithelium * Triggered by: * H⁺ in duodenum

Answer 39

* Released by I cells in the duodenal epithelium * Triggered by: * Amino acids and fatty acids in the duodenum

Answer 40

* Vagovagal reflex (ACh feedback) * S cells in duodenal epithelium cause secretin release -\> Stimulated by H⁺ in duodenum * I cells in duodenal epithelium cause CCK release -\> Stimulated by amino acids and fatty acids in the duodenum

Answer 41

* Chloride * Bicarbonate (Add flashcards on this?)

Answer 42

* Secretes -\> H⁺, pepsinogen, mucus, HCO₃^-, intrinsic factor (IF) * Mixes by muscular contraction * Releases humoral factors -\> Gastrin, somatostatin, histamine

Answer 43

It is cleaved into pepsin in the stomach for the digestion of proteins.

Answer 44

They form a protective layer that prevents the stomach itself from being digested.

Answer 45

It is used downstream in the small intestine to promote vitamin B12 absorption.

Answer 46

Stimulates gastric acid secretion.

Answer 47

Inhibits acid secretion.

Answer 48

Acts locally to stimulate gastrin acid secretion.

Answer 49

Stimulate gastric secretion: * Gastrin (hormone) * Histamine (paracrine factor) Inhibit gastric secretion: * Somatostatin (hormone)

Answer 50

* Antiseptic role * Initiate digestion by denaturing proteins * Promote truncation of pepsinogen to pepsin (and creates the right pH for its function)

Answer 51

* Fundus -\> Receives food * Body -\> Secretes acid, pepsinogen, IF * Antrum -\> Releases gastrin, somatostatin and holds food

Answer 52

Oxyntic glands

Answer 53

Pyloric sphincter

Answer 54

It is characterised by the gastric glands (a.k.a. oxyntic glands), which are invaginations of the epithelium that increase surface area.

Answer 55

Glands comprise pits, which open into a neck, which leads to a base. Below all this is a gastric muscalaris mucosa.

Answer 56

In the pit: * Superficial epithelial cells In the neck: * Mucous cells In the neck and base: * Parietal (oxyntic) cells * Chief (peptic) cells In the base: * Endocrine cells

Answer 57

* Superficial epithelial cells -\> Secrete mucus and HCO₃^- * Mucous cells -\> Secrete mucus * Parietal (oxyntic) cells -\> Secrete B12 and HCl * Chief (peptic) cells -\> Secrete pepsinogen * Endocrine cells -\> Secrete regulators such as gastrin, somatostatin (via the bloodstream)

Answer 58

* At the top of the pit and in the surface lining of the stomach * Secrete mucus and HCO₃^-

Answer 59

* In the base and neck of the pit * Secrete HCl and intrinsic factor (for vitamin B12 absorption in the ileum)

Answer 60

* In the base and neck of the pit * Secrete pepsinogen

Answer 61

* In the neck of the pit * Secrete mucous

Answer 62

* At the base * Secrete regulators such as gastrin, somatostatin via the bloodstream -\> These regulate gastrin acid secretion

Answer 63

* In an unstimulated stomach, the basal secretion originates from surface epithelial cells * This juice is rich in Na⁺ and Cl^- * In the stimulated stomach, this is replaced by juice secreted by parietal cells * This juice is concentrated HCl It is worth noting how much the Na⁺ concentration falls when the stomach is stimulated.

Answer 64

* Surface epithelial cells * The juice is high in Na⁺ and Cl⁺, as well as some bicarbonate to neutralise the stomach acid

Answer 65

* Parietal (oxyntic) cells * The juice is high in concentrated HCl

Answer 66

H⁺/K⁺-ATPase

Answer 67

* Secretory canaliculus (when stimulated) * This is an invagination of the apical membrane into the cell * Provide a larger surface area for secretion * Tubulovesicles (when unstimulated) * Found in the cytoplasm just under the apical membrane * Contain H⁺/K⁺-ATPases that are involved in secretion of HCl into the stomach Note: The diagram is drawn with the basolateral membrane behind the page and the apical membrane in front of the page.

Answer 68

Parietal (oxyntic) cell

Answer 69

* They contain the H⁺/K⁺-ATPases * When the stomach is stimulated, the vesicles fuse with the membrane, inserting the ATPases into the membrane for acid secretion

Answer 70

They increase the surface area of the apical membrane for acid secretion.

Answer 71

* Vesicle is arranged so that ATPase is 'inside out' * Even though there is ATP in the cytoplasm, the ATPase cannot funcition because the K⁺ cannot recycle back into the tubulovesicles * Low K⁺ availability within the vesicle 'brakes' the activity of the ATPase

Answer 72

As low as pH 1.

Answer 73

* Cells: Parietal cells The process is very similar to that in type A intercalated cells of the collecting duct: * Carbonic anhydrase catalyses hydration of CO₂ in the cytosol to yield H⁺ and HCO₃^- * H⁺ions are pumped into the lumen by the H⁺/K⁺-ATPase on the apical membrane in exchange for K⁺ -\> The ATPases are inserted into the membrane from vesicles when the stomach is stimulated * K⁺ recycles out of the cell through apical K⁺ channels * HCO₃^- exits across basolateral membrane by a Cl^-/HCO₃^- exchanger to the interstitial fluid, then the blood * Cl^-ions diffuse through channels on the apical membrane to join H⁺ ions in the lumen * Water follows by osmosis Net result: Secretion of HCl

Answer 74

It becomes more alkaline ('alkaline tide').

Answer 75

* Omeprazole ('Losec') * It prevents acid secretion into the lumen of the stomach

Answer 76

Membrane recycling

Answer 77

The movement of tubulovesicles containing H⁺/K⁺-ATPases into the membrane in parietal cells of gastric glands in the stomach.

Answer 78

* Vagal stimulation (neurocrine) * Gastrin (endocrine) * Histamine (paracrine)

Answer 79

* Acetylcholine from the vagus nerve binds to M3 muscarinic receptors * This triggers an IP₃ cascade * PLC is activated, causing release of calcium from the ER * This calcium upregulates the fusion of tubulovesicles with the membrane, inserting H⁺/K⁺-ATPases into the membrane * This causes gastric acid secretion to be increased

Answer 80

* G cells * Triggered by stimulation of GRP-containing nerves by vagus or protein digestion products in the stomach lumen

Answer 81

* Gastrin is released from G cells in response to stimulation of GRP-containing nerves by vagus or protein digestion products in lumen. * Binds to CCK_B receptors * This triggers an IP₃ cascade * PLC is activated, causing release of calcium from the ER * This calcium upregulates the fusion of tubulovesicles with the membrane, inserting H⁺/K⁺-ATPases into the membrane * This causes gastric acid secretion to be increased

Answer 82

Enterochromaffin-like cells

Answer 83

* Gastrin is released from enterochromaffin-like cells * Binds to H₂ receptors * This triggers an adenylate cyclase cascade * cAMP is increased, which stimulates PKA * PKA upregulates the fusion of tubulovesicles with the membrane, inserting H⁺/K⁺-ATPases into the membrane * This causes gastric acid secretion to be increased

Answer 84

* Ranitidine ('Zantac') * It causes decreased gastric acid secretion

Answer 85

* There are 3 main ways of stimulating gastric acid secretion endogenously -\> ACh, gastrin and histidine * Antagonists of histidine receptors (e.g. ranitidine) produce a much more singificant decrease in acid secretion than would be expected * This resulted in the common mediator theory: * Not only do ACh and gastrin act directly on the parietal cells that secrete the acid, but they also act on the enterochromaffin-like (ECL) cells that release histamine, and their binding stimulates the histidine release * This indirect pathway is responsible for a large fraction of gastric acid secretion stimulation * As a result, when histidine antagonists are used, they stop a large amount of gastric acid secretion

Answer 86

* Inhibits adenylyl cyclase and reduces gastric acid secretion from parietal cells of the gastric glands. * It essentially has the opposite action to histamine.

Answer 87

* Stimulated by: Low luminal pH * Inhibited by: ACh

Answer 88

S cells in the duodenum

Answer 89

* Release is stimulated by acid in the duodenum * Inhibits gastrin release * Stimulates somatostatin release Together, this inhibits the gastric acid secretion.

Answer 90

* Can cause gastric ulcers * This occurs by the inhibition of somatostatin (which usually inhbits gastric acid secretion)

Answer 91

* Cephalic phase * Sight, smell and taste of food * Mediated by: ACh, GRP (gastrin-releasing peptide) * Gastric phase * Distension of the stomach -\> Initiates vagovagal reflex * Protein digestion products -\> Stimulate gastrin release from G cells * Intestinal phase * Presence of protein digestion products in the intestine * Stimulates gastrin release from G cells in the duodenum

Answer 92

* Cephalic = 30% * Gastric = 60% * Intestinal = 10%

Answer 93

* Truncation of the N-terminal end to yield pepsin * This is a spontaneous event that occurs in acidic environments * Once active, a pepsin molecule can activate other pepsinogen molecules

Answer 94

About 1/5th.

Answer 95

It is secreted from secretory granules that fuse with the apical membrane of chief (peptic) cells.

Answer 96

It is stimulated by: * **ACh** -\> Binding to M3 receptors and triggering an IP₃ cascade that leads to Ca²⁺ signalling * **Gastrin + CCK** -\> Binding to CCK_B receptors and triggering an IP₃ cascade that leads to Ca²⁺ signalling * **Secretin** -\> Binding to receptors that are coupled to adenylate cyclase that leads to cAMP signalling

Answer 97

* Mucin (a glycoprotein secreted from mucous cells) that combines with water, salt and phospholipids * The result is a gel that is up to 200 micrometers thick

Answer 98

The gel is a barrier to H⁺ ion diffusion.

Answer 99

HCO₃^- acts to neutralise any H⁺ ions that get into the protective mucous layer of the stomach.

Answer 100

Secretion is stimulated by ACh acting on M3 receptors that induces an IP₃ cascade and therefore Ca²⁺ signalling.

Answer 101

* The acid 'bores' through the mucus without any lateral spread * This stream of H⁺is termed a 'viscous finger'

Answer 102

* Aspirin, alcohol and antiinflammatory drugs * These can result in gastric ulcers

Answer 103

* Na⁺ * K⁺ * Cl^- * HCO₃^- * Fe²⁺ * Ca²⁺

Answer 104

* 9L (2L ingested and 7L secreted) * Only 100ml is excreted in the stool each day

Answer 105

In total, about 8.9L of water are absorbed per day: * Small intestine -\> About 8.5L of water is reabsorbed here * Colon -\> About 400ml of water

Answer 106

No, it only reabsorbs about 400ml of fluid per day, which is about 10% of its capacity.

Answer 107

Hypertonic, because water is reabsorbed in the colon, which is a tight epithelium, leaving the faeces hypertonic.

Answer 108

* Can replace that lost from urination, perspiration and respiration * Can be used for subsequent secretions

Answer 109

* Small intestine * **Leaky** epithelium * Lots of **paracellular** transport * **Bulk** absorptive role -\> Absorbs about 8.5L of fluid per day * Colon/rectum * **Tight** epithelium * Mostly **transcellular** transport * Absorbs about 400ml of fluid per day, which is only 10% of its absorptive capacity

Answer 110

* Colon/rectum * Because it is a tight epithelium

Answer 111

No, there is also: * HCO₃^- secretion in the duodenum * NaCl secretion (net) from immature cells at the ends of villi

Answer 112

* Na⁺/K⁺-ATPase on the basolateral membrane creates a hypertonic interstitial fluid * Co-transported molecules and ions such as chloride help with this * This creates an osmotic gradient for the movement of water from the lumen to the interstitial fluid * Water can move via: * Transcellular route -\> Through aquaporins * Paracellular route -\> Through tight junctions * Water moves from the interstitial fluid to the blood due to Starling forces

Answer 113

No, the disticntion is not very pronounced.

Answer 114

* Basolateral Na⁺/K⁺-ATPase creates a sodium gradient across the epithelial cells * This gradient is utilised by sodium co-transporters and exchangers on the apical membrane that can be used to reabsorb other solutes into the cell * These other solutes are then moved acorss the basolateral membrane into the interstitial fluid (and then blood)

Answer 115

* Diffusion through channels * **ENaC** (sodium) * **CFTR** (chloride) * Na⁺/H⁺ exchange * **NHE** (sodium-hydrogen exchanger) * Na⁺-glucose co-transport * **SGLT** (sodium-glucose) * Na⁺-amino acid co-transport * **System B** * Na⁺-chloride co-transport * Direct NaCl co-transport (**NCC**) * Indirect co-transport via Cl^-/HCO₃^-(**AE**, driven by the aforementioned NHE)

Answer 116

* Epithelial sodium channel * Allows absorption of sodium into intestinal epithelial cells by diffusion

Answer 117

* Cystic fibrosis transmembrane conductance regulator * It is a channels in the apical membrane of intestinal epithelial cells that allows chloride diffusion (out of the cell usually)

Answer 118

* Sodium-hydrogen exchanger * It is on the apical membrane of epithelial cells in the intestine and moves sodium into the cell while moving hydrogen out of the cell

Answer 119

* Sodium-glucose linked transporter * Co-transporter on the apical membrane of epithelial cells that is used to move sodium and glucose into epithelial cells together

Answer 120

* Sodium-chloride co-transporter * It is on the apical membrane of epithelial cells in the intestine, moving sodium and chloride into the cell

Answer 121

* Anion exchanger * It is usually on the apical membrane of epithelial cells in the intestines and moves chloride into the cell while moving bicarbonate out

Answer 122

No, different processes play the dominant role in the duodenum, jejunum, ileum, colon and rectum.

Answer 123

* Duodenum * SGLT + AA co-transporters -\> Glucose absorption and amino acid absorption * NHE * Jejunum + Ileum * SGLT + AA co-transporters -\> Glucose absorption and amino acid absorption * NHE with AE -\> Chloride absorption * NCC -\> Chloride absorption * Colon * NHE with AE -\> Chloride absorption * Some NCC -\> Chloride absorption * Rectum * ENaC Note that these divisions are not so clear-cut. It is worth considering the general changes that occur along the GI tract. In the whole small intestine there is amino acid and glucose absorption, with chloride absorbed paracellularly. In the jejunum and ileum, there is also chloride reabsorption through the cell. In the colon, chloride absorption continues, but is is not so much of a sodium-dependent process. Finally, by the rectum there is just sodium reabsorption.

Answer 124

* Na⁺/K⁺ ATPase in transports Na⁺ into interstitial fluid * Other solutes exit the cell through channels and carriers

Answer 125

Aldosterone

Answer 126

Na⁺/K⁺-ATPase and associated K⁺-channel on the basolateral membrane

Answer 127

Whether that solute is moving up or down a concentration gradient.

Answer 128

All is driven by the basolateral Na⁺/K⁺-ATPase on the basolateral membrane. Absorptive: * **Amino acids** -\> Via co-transporter on apical membrane and carrier on basolateral membrane * **Glucose** -\> Via SGLT1 on apical membrane and GLUT2 on basolateral membrane * **Sodium** -\> Via NHE3 on apical membrane and basolateral Na⁺/K⁺-ATPase * **Chloride** -\> Via paracellular route due to sodium in the interstitial fluid * **Potassium** -\> Via paracellular route Secretory (in order to neutralise stomach acid): * **Bicarbonate** * NHE1 on basolateral membrane moves hydrogen out of the cell * This moves the carbonic anhydrase reaction equilibirum to the right, accumulating bicarbonate inside the cell * This is added to by the NBC1 (sodium-bicarbonate co-transporter) on the basolateral membrane, which moves more bicarbonate into the cell * The bicarbonate moves out of the cell by an AE (bicarbonate-chloride exchanger) * The chloride moves back out into the lumen via a CFTR, which allows this secretion to continue

Answer 129

All is driven by the basolateral Na⁺/K⁺-ATPase on the basolateral membrane. Absorptive: * **Amino acids** -\> Via co-transporter on apical membrane and carrier on basolateral membrane * **Glucose** -\> Via SGLT1 on apical membrane and GLUT2 on basolateral membrane * **Sodium** -\> Via NHE3 on apical membrane and basolateral Na⁺/K⁺-ATPase * **Chloride** * Via paracellular route due to sodium in the interstitial fluid * ALSO by AE (Cl^-/HCO₃^- exchanger) and NCC an the apical membrane, then exiting via the KCC1 on the basolateral membrane -\> This is the main difference between this and the duodenum * **Potassium** -\> Via paracellular route No secretory function, unlike duodenum.

Answer 130

* SGLT1 on apical membrane * GLUT2 on basolateral membrane

Answer 131

All is driven by the basolateral Na⁺/K⁺-ATPase on the basolateral membrane. Paracellular transport is less important because it is a tight epithelium. Absorptive: * **Sodium** -\> Via ENaC on apical membrane and basolateral Na⁺/K⁺-ATPase * **Chloride** * Via AE (Cl^-/HCO₃^- exchanger) then exiting via the ClC-2 channel on the basolateral membrane * This is driven by removal of H⁺ by the NHE1 on the basolateral membrane, which shifts the carbonic anhydrase reaction towards producing H⁺ and HCO₃^-, which is used by the AE * **Potassium** -\> MAY be absorbed via H⁺/K⁺exchanger on the apical membrane, then via the K⁺/Cl^-co-transporter on the basolateral membrane Secretory: * **Potassium** -\> MAY be secreted via potassium channels on the apical membrane, driven by the Na⁺/K⁺-ATPase on the basolateral membrane

Answer 132

* It becomes less reliant on the paracellular route and less reliant on sodium in the lumen for co-transport * Instead, there is an Na⁺/H⁺exchanger on the basolateral membrane that drives the AE on the basolateral membrane

Answer 133

It depends on where.

Answer 134

* Duodenum, jejunumm and ileum * Passive reabsorption via the paracellular route * Colon and rectum * Active absorption by the apical H⁺/K⁺exchanger and basolateral K⁺/Cl^- symporter * Active secretion via the basolateral Na⁺/K⁺-ATPase and then apical K⁺ channels in colon * Passive secretion via the paracellular route (assuming there is the electrochemical gradient) The relative importance of these pathways depends on K+ balance and is hormonally controlled.

Answer 135

Colon and rectum

Answer 136

* Aldosterone stimulates the Na⁺/K⁺-ATPase on the basolateral membrane -\> Increases potassium secretion * Hypokalaemia stimulates absorption

Answer 137

NOTE: A small amount of passive secretion can also happen via the paracellular route.

Answer 138

NOTE: A small amount of passive absorption can also occur via the paracellular route.

Answer 139

* Secretion from cells in crypts of Lieberkuhn * These are immature cells found at the base of the villi in the small and large intestines

Answer 140

The mechanism is identical to the mechanism of primary secretion in the acinar cells of the pancreas: * Na⁺/K⁺-ATPase on the basolateral membrane creates a sodium gradient for the NKCC * Basolateral NKCC (Na⁺-K⁺-2Cl^- co-transporter) accumulates Cl^- ions inside the cell * Cl^- ions diffuse across the apical membrane through channels * K⁺ diffuses out through basolateral channels * Na⁺ ions can also diffuse between cells into the lumen through tight junctions, along the electrical gradient established by Cl^- movement * H₂O follows by osmosis The net result is essentially the secretion of a dilute saline.

Answer 141

Secretion can be upregulated by (for example) cholera toxin: * Cholera toxin uncouples a G-protein * This activates cAMP production * cAMP stimulates chloride channels on the apical membrane and potassium channels on the basolateral membrane * Excessive secretion ensues * This leads to diarrhoea Toxins that increase intracellular calcium have the same effect.

Answer 142

* Dietary intake = 1g/day * Intestinal secretions = 0.15g/day * Intestinal absorption = 0.35g/day * Renal excretion = 0.2g/day

Answer 143

* Upper duodenum * Against a concentration gradient

Answer 144

* Ca²⁺ crosses apical membrane via ECaC (epithelial calcium channels) * Ca²⁺ binds in the cytosol to calbindin, which transports it across the cytosol to the basolateral membrane * Ca²⁺ exits into the interstitial fluid via a Ca²⁺-ATPase and NCE (sodium-calcium exchanger) * Ca²⁺ can also be internalised in vesicles, which travel across the cytosol and fuse with the basolateral membrane

Answer 145

ECaC (Epithelial calcium channels)

Answer 146

* Ca²⁺-ATPase * NCE (Sodium-calcium exchanger)

Answer 147

The vitamin D-derived protein calcitriol stimulates ECaC (epithelial calcium channel) and calbindin (chaperone protein across the cytosol) synthesis.

Answer 148

Involved in: * O₂ transport * DNA synthesis * Electron transport * Binding to proteins in order to prevent damage from free radicals

Answer 149

* Fe²⁺crosses the apical membrane by the bivalent cation transporter DCT1, which is dependent on the H⁺ gradient generated by the acidity of the duodenum lumen * Any Fe³⁺ in the lumen is reduced to Fe²⁺ by iron reductase on the apical membrane, so it can be taken up by DCT1 * Heme can also be taken up by a haem transporter on the apical membrane, after which it is converted to Fe²⁺ by haem oxidase * The Fe²⁺in the cell is converted to Fe³⁺ by ferroxidase * Fe³⁺can now enter one of two pathways: * Absorptive pathway * Fe³⁺ binds to iron-binding proteins, which take it to the basolateral membrane * A complex of two proteins (hephaestin and IREG1) transports the Fe³⁺ into the blood * In the blood, the Fe³⁺ is bound to transferrin for transport * Storage pathway * Fe³⁺ binds to ferritin in the cytoplasm, where it is stored * When needed, the Fe³⁺ can be mobilised and taken to the hephasetin/IREG1 complex for transport into the blood

Answer 150

* Fe²⁺ * Haem

Answer 151

Iron reductase

Answer 152

Divalent cation transporter DCT1 -\> This is a co-transporter that requires a H⁺gradient generated by the acidity of the duodenum lumen

Answer 153

Cu²⁺ and Zn²⁺

Answer 154

Haem transporter

Answer 155

Haem oxidase

Answer 156

Ferroxidase

Answer 157

Iron-binding protein

Answer 158

Hephaestin/IREG1 complex

Answer 159

Transferrin

Answer 160

Epithelial cells of the duodenum

Answer 161

* Iron can be stored in the "storage pathway" in these cells, bound to ferritin protein * If iron in the body drops, it can be transported into the blood via the hephaestin/IREG1 complex * If iron in the body rises, then it remains stored in the storage pathway until the epithelial cells are shed every 5 days

Answer 162

Small intestine

Answer 163

* Have folds of mucosa * On these folds, there are villi * On the villi, the epithelial cells have a ruffled apical ('brush border') membranes

Answer 164

Enterocytes

Answer 165

Every 3-7 days

Answer 166

* None * Glucose * Digestion in the lumen, then absorption across the cell * Proteins to amino acids * Digestion on the apical membrane, then absorption across the cell * Disaccharides, such as sucrose * Absorption into the cell, then hydrolysis intracellularly * Di- and tripeptides * Digestion in the lumen, then resynthesis intracellularly after absorption * Triglycerides

Answer 167

* Starch * Sugars -\> e.g. lactose

Answer 168

α-1,4 and α-1,6 glycosidic bonds

Answer 169

* Salivary amylase initiates starch digestion, which is completed by pancreatic amylase * This yields maltose, maltotriose and α-limit dextrins * Brush border enzymes on the epithelial cells hydrolyse these products and sucrose and lactose * This releases glucose, fructose and galactose, which can be absorbed

Answer 170

Because it can only hydrolyse α-1,4 internal bonds, not the α-1,6 bonds.

Answer 171

* α-dextrins * Maltotriose * Maltose

Answer 172

* Glucoamylase * Sucrase * Isomaltase * Trehalase * Lactase

Answer 173

* Glucoamylase * Sucrase (Only α-1,4 dextrins) * Isomaltase

Answer 174

* Glucoamylase * Sucrase * Isomaltase

Answer 175

* Glucoamylase * Sucrase * Isomaltase

Answer 176

* Trehalase

Answer 177

* Glucoamylase, sucrase and isomaltase are all involved in the digestion of α-dextrins, maltotriose and maltose * Lactose is digested by lactase * Sucrose is digested by sucrase * Trehalose is digested by trehalase

Answer 178

The hydrolysis of lactose to glucose and galactose.

Answer 179

* The hydrolysis of maltose to 2 glucose monomers * The hydrolysis of maltotriose to 3 glucose monomers

Answer 180

It is a two enzyme complex. Sucrase: * Hydrolysis of sucrose to glucose and fructose * Hydrolysis of maltose to glucose monomers * Hydrolysis of maltotriose to glucose monomers Isomaltase: * Hydrolysis of α-limit dextrins, maltose and maltotriose to glucose monomers

Answer 181

Glucose and galactose: * Absorbed through SGLT1 (a sodium-dependent carrier) * If the glucose concentration in the lumen increases, GLUT2 can also be inserted into the apical membrane Fructose: * Absorbed through GLUT5 facilitated diffusion proteins

Answer 182

Through GLUT2 transporters.

Answer 183

Mid-jejunum

Answer 184

A deficiency in the lactase enzyme.

Answer 185

It results in glucose and galactose malabsorption.

Answer 186

* SGLT1 -\> In the small intestine, proximal tubule (S3 segment), RBC, heart * SGLT2 -\> In the proximal tubule (S1 segment), liver and brain

Answer 187

No, because there are also SGLT2 transporters in the proximal tubule.

Answer 188

* Fructose usually moves across the apical membrane down its concentration gradient via GLUT5 proteins * When this needs to happen against a concentration gradient, the GLUT5 can act as an exchanger by using the glucose that has accumulated inside the cell (by the SGLT1 protein) to energise the uptake of fructose

Answer 189

* When luminal glucose concentration is high, glucose can move down its concentration gradient across the apical membrane * This requires GLUT2 proteins (as oppose to the SGLT1 co-transporter), meaning that they must be inserted into the apical membrane * This is a calcium-dependent process

Answer 190

* Pepsin in the stomach breaks down proteins into smaller polypeptides * These are further broken down by pancreatic endopeptidases (e.g. trypsin) and exopeptidases (e.g. carboxypeptidases) -\> This produces oligopeptides (2-6 amino acids) and amino acids * The oligopeptides can be further broken down by brush border enzymes on the enterocytes of the small intestine to yield dipeptides and tripeptides * The amino acids, dipeptides and tripeptides can now be absorbed into the enterocytes

Answer 191

Pepsin -\> It is involved in the breakdown of proteins to polypeptides.

Answer 192

* Endopeptidases * Exopeptidases

Answer 193

* Trypsin * Chymotrypsin * Elastase

Answer 194

Carboxypeptidases

Answer 195

* Cross apical membrane via sodium-dependent co-transporters or sodium-independent facilitated diffusion proteins * There are carriers for the different classes of amino acids (neutral, cationic, basic) * Cross basolateral membrane through passive facilitated diffusion proteins

Answer 196

* Cross the apical membrane via PepT-1 (a hydrogen-dependent co-transporter) * Cytosolic peptidases convert the peptides to amino acids * Now these can cross the basolateral membrane through passive facilitated diffusion proteins

Answer 197

* PepT-1 * They are driven by the acidity of the lumen of the GI tract

Answer 198

By the end of the jejunum

Answer 199

* No, they can also be absorbed using facilitated diffusion proteins * These are sodium independent * They can function using exchange mechanisms too * The accumulation of one amino acid in the enterocyte can be used to energise the uptake of a different amino acid by exchange via the facilitated diffusion protein

Answer 200

Sodium-dependent co-transporters: * B -\> Neutral amino acids * B⁰⁺-\> Neutral and cationic amino acids * X_AG- -\> Anionic amino acids Sodium-independent facilitated diffusion proteins: * b⁰⁺ -\> Neutral and cationic amino acids * y+ -\> Cationic NOTE: The sodium-independent facilitated diffusion proteins can be driven by the exchange of amino acid (that has been accumulated inside the enterocyte) back into the intestinal lumen.

Answer 201

Sodium-indepedent facilitated diffusion proteins: * asc = Neutral amino acids * L = Neutral amino acids * y+ = Cationic amino acids

Answer 202

* Mutation in system B (sodium-dependent co-transporter for the absorption of neutral amino acids into enterocytes) * This means that L-phenylalanine and other neutral amino acids cannot be reabsorbed from the renal tubule, so they are excreted in the urine * In the GI tract, this is not a problem because PepT-1 is functioning in parallel, allowing uptake of these amino acids as dipeptides and tripeptides

Answer 203

* Mutation in system B⁰⁺ and system b⁰⁺(sodium-dependent co-transporter or sodium-independent facilitated diffusion protein for the absorption of neutral and cationic amino acids into enterocytes) * This means that L-arginine and other neutral/cationic amino acids cannot be reabsorbed from the renal tubule, so they are excreted in the urine * In the GI tract, this is not a problem because PepT-1 is functioning in parallel, allowing uptake of these amino acids as dipeptides and tripeptides

Answer 204

They hydrolyse the dipeptides and tripeptides that are taken up into enterocytes, so that amino acids are produced that can cross the basolateral membrane and enter the blood.

Answer 205

Dipeptides, because of the PepT-1 carrier that increases the rate of absorption.

Answer 206

* They depolarise the membrane and acidify the cell * This is because the PepT-1 protein is a co-transporter with H⁺, so intracellular H⁺ is increased

Answer 207

* Muscular movements of stomach emulsify TAGs (transformation into emulsion of oil droplets in water), which is aided by lingual lipases * In the small intestine, bile salts break down large lipid droplets into smaller lipid droplets, increasing the surface area for lipase activity * Pancreatic lipase digests triglycerides to monoglycerides and free fatty acids * Colipase (from the pancreas) coordinates binding of lipase to emulsion * The products form mixed micelles * Micelles diffuse to an unstirred acidic layer near the apical membrane and dissociate at the cell surface

Answer 208

* Lingual lipases * Pancreatic lipases

Answer 209

* A protein co-enzyme required for optimal enzyme activity of pancreatic lipase * It is secreted from the pancreas

Answer 210

* Bile salts are detergents that decrease surface tension to make smaller oil droplets * i.e. They break large lipid droplets into smaller ones

Answer 211

There is an unstirred layer of acid at the apical membrane of enterocytes. This causes the micelles to dissociate.

Answer 212

* Glycerol and short-chain fatty acids * They can move to the apical membrane and diffuse through it, then do the same at the basolateral membrane

Answer 213

* Cholesterol * Lysophospholipids * Long-chain fatty acids * Monoglycerides

Answer 214

* The triglycerides are reassembled in the SER * Apoproteins are produced in the RER * The triglycerides and apoproteins combine to form chylomicrons Note: The components that are not included in micelles (short-chain fatty acids and glycerol) pass straight across the cell and diffuse across the basolateral membrane into the blood.

Answer 215

* They are exported by the Golgi apparatus, pass into lymphatic capillaries * The lymph drains back into left subclavian vein via thoracic duct

Answer 216

Via the Golgi apparatus.

Answer 217

Smaller, very low density lipoproteins (VLDLs) are secreted into the lymphatic system instead.

Answer 218

* Thiamine B1 * Riboflavin B2 * B12 * Vitamin C * Folic acid

Answer 219

Vitamins A, D, E, K

Answer 220

* Passive diffusion via the paracellular route * Transcellularly, via specific Na⁺-coupled co-transporter proteins * Binding to specific apical receptors (B12)

Answer 221

Another name for vitamin B12 is cobalamin: * Cobalamin is bound to proteins in food * Gastric secretions include IF (intrinsic factor) * A cobalamin-IF complex forms * The complex can then interact with a receptor on the apical membrane of enterocytes * The receptor and the bound complex can then be endocytosed into the cell * These can then be processed by a lysosome to degrade the receptor and IF * The cobalamin is then packaged with transcobalamin II (a chaperone protein) for exocytosis into the blood

Answer 222

* They are presented for absorption dissolved in bile micelles * They diffuse across the apical membrane * In most cases, they are incorporated back into chylomicrons for export out of the cell

Answer 223

* Compartments under low pressure to allow storage of waste * Sphincters closed to prevent outflow

Answer 224

* Increase in pressure of storage compartment so as to drive outflow * Sphincters open to allow outflow

Answer 225

* Sensory systems to inform about filling * Reflex pathways to generate voiding * Higher control centres to enable voluntary voiding * Appropriate muscles

Answer 226

Movement of faeces into the rectum .

Answer 227

Expandable organ for the temporary storage of faeces.

Answer 228

* Internal anal sphincter * Smooth muscle * Controlled by ANS * External anal sphincter * Striated muscle * Under voluntary control

Answer 229

The anal canal is the final part of the rectum.

Answer 230

* Longitudinal folds called anal (or rectal) columns * These are joined at their distal ends by transverse folds

Answer 231

They mark the point of transition between columnar epithelial epithelium (inside) and the stratified squamous epithelium (outside).

Answer 232

The anal canal features a network of veins. During defecation, strain can increase the pressure, causing distension of the veins and increasing the likelihood of haemorrhoids.

Answer 233

* Meissner's plexus -\> Submucosal * Auerbach's plexus -\> Myenteric

Answer 234

A system of afferent sensory neurons, interneurons and motor neurons.

Answer 235

* It can, but it can also be stimulated by sympathetic and parasympathetic fibres. * There are also afferent fibres that feed back information to control centres in the brain.

Answer 236

* Parasympathetic -\> Near the organ * Symapthetic -\> Proximal ganglia near the spinal cord

Answer 237

* Parasympathetic nervous system stimulates smooth muscle * Sympathetic nervous system inhibits smooth muscle Except for the sphincter of the anorectum!

Answer 238

* Parasympathetic * Pelvic splanchnic nerves (S1-S4) * Promotes defecation: stimulation of rectal motility and relaxation of internal sphincter. * Sympathetic * Nerve roots L1-L3, passing through the mesenteric and pelvic plexuses * Promotes continence: inhibition of rectal smooth muscle and contraction of internal sphincter. * Somatic * Pudendal nerve (S2-S4) * Controls the external anal sphincter

Answer 239

* Pelvic splanchnic nerves * S1-S4

Answer 240

* Pudendal nerve * S2-S4

Answer 241

* No, the rectum is empty most of the time but faeces are moved into the rectum from the sigmoid colon by peristaltic contractions. * Distension of the rectal walls triggers the defecation reflex.

Answer 242

Distension of the rectum by faeces triggers two reflex loops: * Short reflex loop: * Activation of the myenteric plexus of the enteric nervous system of the sigmoid colon and rectum * This increases local peristalsis * As a result, more faeces is moved into the rectum, ready for defecation * Long reflex loop: * Stimulation of parasympathetic motor nerves in sacral region, including the pelvic splanchnic nerves -\> This leads to increased peristalsis of the large intestine so there is more faecal material pushed into the rectum and also causes relaxation of the internal anal sphincter * Stimulation of somatic motor neurons, including the pudendal nerve -\> This leads to contraction of the external anal sphincter

Answer 243

* Taking a deep breath * Closure of the glottis * Contraction of abdominal wall muscles to push faecal content of the colon downwards

Answer 244

Anorectal sampling of the contents.

Answer 245

Enables discrimination between gas, liquid and solid -\> This allows fine-tuning of the defecation reflex accordingly.

Answer 246

* Peristaltic contraction diminishes until additional expansion of the rectum restimulates the defecation reflex. * Rectal content may return back to the colon.

Answer 247

Around 15mmHg.

Answer 248

* Above around 55 mmHg, the external anal sphincter is forced to relax * Occurs in infants and in adults with severe spinal cord injury

Answer 249

* Consistency of stool * Delivery of colonic content to the rectum * Rectal capacity and compliance * Anorectal sensation * Function of the anal sphincter mechanism * Muscles and nerves of the pelvic floor

Answer 250

* Diarrhoea * Spinal cord pathologies * Hirschprung's syndrome

Answer 251

* An increase in stool liquidity and weight (200 g/day) * Caused by: * Increased fluid secretion by the small or large intestine * Decreased water reabsorption by intestines * These can be due to bacterial or viral infection of the colon or small intestine * Liquids are more difficult to contain and the chemical stimulus to defecate is high

Answer 252

* Spinal cord injury * Multiple sclerosis

Answer 253

* Congenital polygenic disorder * Caused by arrest of the caudal migration of the neural cell crest (precursors of ganglion cells) * Characterised by congenital agenesis of the Auerbach’s plexus in the rectum and upwards -\> Results in an “aganglionic” rectum that fails to relax in response to faeces * Main problem is constipation

Answer 254

* Noradrenaline causes relaxation of the smooth muscle -\> Administering NA to a sample of rectum muscle caused contraction to stop * Acetylcholine stimulates contraction of the smooth muscle -\> Administering carbachol (a cholinomimetic drug) to a sample of rectal muscle caused contraction to happen

Answer 255

* There is a sample of smooth muscle that has a baseline amount of contraction * Noradrenaline causes contraction of the smooth muscle -\> Administering NA to a sample of rectum muscle caused contraction to increase * Acetylcholine stimulates relaxation of the smooth muscle -\> Administering carbachol (a cholinomimetic drug) to a sample of rectal muscle caused decreased contraction

Answer 256

* A sample of the IAS showed a baseline amount of contraction * When electrically stimulated, the muscle relaxed * In the presence of atropine or guanethidine, this relaxation still happened -\> Therefore the relaxation is not mediated by ACh or NA * In the presence of TTX, this relaxation did not happen -\> Therefore the relaxation is mediated by nerves (but not resulting in ACh or NA) * Thus, another mediator must be present: * When L-NOARG (an inhibitor of nitric oxide synthase) is present, relaxation does not occur -\> Therefore NO is involved in the relaxation

Answer 257

* The dots show points where electrical stimulation of the internal anal sphincter occurs, causing relaxation of the sphincter * L-NOARG is an inhibitor of nitric oxide synthase -\> When added, it causes the inhibition of the relaxation * L-arginine inhibits the effects of L-NOARG since it is a substrate for the NOS pathway -\> When added, it causes relaxation to resume * Thus, we can see that NO is important in internal anal sphincter relaxation

Answer 258

It causes release of NO from a nitrergic nerve terminal, which then acts to relax the smooth muscle.

Answer 259

* Topical NO donors * Topical sildenafil (phosphodiesterase 5 inhibitor) -\> PDE is involved in degradation of cGMP (involved in NO synthesis) * Ca²⁺ channels blockers -\> Calcium is involved in smooth muscle contraction * Topical bethanechol (muscarinic receptors agonist) * Adrenoreceptor modulators (e.g. indoramin, α₁-adrenoreceptor blocker)

Answer 260

* α₁-adrenoreceptor agonist (e.g. phenylephrine)

Answer 261

* Decrease contraction -\> To treat anal fissures * Increase contraction -\> To treat incontinence

Answer 262

Phenylephrine (α₁ agonist)

Answer 263

Indoramin (α₁ blocker)

Answer 264

* Local enteric plexus * A control centre in the central nervous system that communicates with the plexus

Answer 265

* The reflux of gastric contents, especially acid, into the oesophagus. * It often produces a characteristic burning sensation in the midline of the chest, known to older generations as "heartburn". * It seems to happen because the cardiac "sphincter" of the stomach is relatively easily overcome by high pressure in the stomach. * So, reflux is common after large fatty meals, common in obese people.

Answer 266

An area of necrosed lining of the stomach, proximal duodenum or oesophagus caused by gastric secretions (especially the acid component).

Answer 267

* Can be asymptomatic * Range of pain from vague discomfort to significant pain. * They can also bleed if the acid erodes beyond the epithelium into the underlying tissues -\> Symptoms relate to the bleeding rather than to the ulcer itself: * Iron-deficiency anaemia * Melaena -\> Black stool, stained by digested haemoglobin (more serious anaemia) * Occasionally an ulcer may present as an acute GI bleed, if an artery or arteriole in the base of the ulcer crater has been eroded by the acid * Less commonly, perforation can occur where the whole thickness of the intestinal wall is eroded, leading to inflammation of the peritoneum (called peritonitis) that lines the peritoneal cavity

Answer 268

You reduce the effects of the stomach acid by: * Direct antacids * Histamine antagonists * Blockers of H⁺-K⁺ ATPase

Answer 269

* Aluminium hydroxide [IMPORTANT] * Magnesium hydroxide ('Milk of magnesium') * Magnesium trisilicate

Answer 270

Advantages: * Rapid relief of symptoms Disadvantages: * Relief is short-term and mild * Does not address the underlying problem * Associated with side effects

Answer 271

* Examples: Sucralfate (physical barrier), misoprostol (prostaglandin PG-E1 analogue) Advantages: * Rapid relief of symptoms without antacid side-effects. * Slightly longer duration of relief than antacids. Disadvantages: * Weak protective effect * Relief still short-lived

Answer 272

Antacids do not provide relief for a long enough period for the ulcers to heal -\> Long-term suppression of acid secretion allows time for this to happen.

Answer 273

* Histamine antagonists (e.g. ranitidine) * Inhibitors of H⁺/K⁺-ATPase (e.g. omeprazole) * Muscarinic antagonists (e.g. pirenzepine) [EXTRA]

Answer 274

* Omeprazole * They inhibit the H⁺/K⁺-ATPase, which is the primary source of acid secretion in the stomach * Therefore, they are the most potent suppressors of acid secretion, and the most commonly used in the UK to treat peptic ulcers

Answer 275

* Ranitidine * Block the amplifying effect of the mast (ECL) cells on parietal cell stimulation, and so substantially reduce acid secretion without completely blocking it * They are used to treat peptic ulcers

Answer 276

* Pirenzepine * Act on both the mast (ECL) cell and the parietal cell to inhibit acid secretion * Have widespread systemic parasympathetic side-effects, and so are relatively little used now

Answer 277

* Yes, and several hypotheses have been put forward to explain the link between H. pylori and ulcers: at present there is no agreement on the mechanism. * A paradox is that H. pylori is present in stomach and intestine of many people who do not develop ulcers, but eradication of the bacterium from a patient with established ulcers substantially lowers the risk of recurrence (from 35% to 2% in 12 months).

Answer 278

Antibiotics are combined with drugs to suppress the symptoms of the ulcer: * Amoxicillin/clarithromycin and metronidazole -\> Antibiotics * Omeprazole -\> H⁺/K⁺-ATPase inhibitor

Answer 279

* Steroids and NSAIDs (non-steroidal anti-inflammatory drugs) These cause peptic ulcers because: * Secretion of gastric mucus (that usually has a protective role for the stomach) is stimulated by local prostaglandins * Steroids and NSAIDs reduce prostaglandin formation and therefore increase the risk of peptic ulcer formation.

Answer 280

* Aspirin [IMPORTANT] * Ibuprofen and naproxen * Glucocorticoids (corticosteroids)

Answer 281

* "Enteric coated" aspirin -\> Aspirin coated with a substance that does not dissolve in the stomach but does dissolve in the duodenum. So, although the aspirin will still reduce the formation of gastric prostagladins, it will not have the direct damaging effect on the gastric mucosa. * Misoprostol -\> Synthetic prostaglandin

Answer 282

* Myogenic regulation * Regional regulation by the enteric nervous system and GI hormones * Migrating motility complex (MMC) [EXTRA] * Intestinal reflexes

Answer 283

* The smooth muscle of the GI tract responding to stretch, such as occurs when a bolus of food passes * Neurally controlled (by the enteric plexus) over very short distances * Dilation in front of bolus, constriction behind

Answer 284

* The enteric plexus receives input from sensors within the intestinal wall and can also control motility over short distances, long segments, or the whole length of the intestine. * This control can be in response to: * The chemical constituency of the food * The physical consistency of the food (e.g. how digested) * The presence of toxins or substrates that trigger activity of the enteric immune system * All of these plexus-regulated motility patterns are subject to modulation by local gastrointestinal hormones.

Answer 285

A wave of activation spreading caudally from the stomach, regulated by a gastric pacemaker. It is not typically part of the motility pattern seen during digestion of a meal, but occurs: * during long gaps between meals * in anticipation of a meal * frequently during a period of fasting or hunger This motility pattern appears to have a kind of "housekeeping" function, preventing stagnation of intestinal contents and therefore helping to maintain a healthy gut flora.

Answer 286

* Regional and local reflexes exist within the intestine to control movement of food and the emptying of the gut. * For example, the rate of gastric emptying may be influenced not only by the contents of the stomach but also by the contents of the duodenum – for example, whether the duodenum still contains food from the previous wave of gastric emptying, and whether the luminal pH has returned to alkaline levels. * Again, some of these "reflexes" are actually mediated by local hormones, but many are functions of the enteric plexus.

Answer 287

* Regional segmentation * Localized + Longer peristalsis * Localized reverse peristalsis (even in normal digestion) * Reverse peristalsis, especially in the proximal small intestine, as part of the vomiting reflex.

Answer 288

It largely undergoes regulation by the enteric plexus and GI hormones that influence the plexus: * Different rates of emptying according to the contents of the meal (fatty meals stay in the stomach for much longer than mainly-protein meals) * Co-ordination of gastric motility with the opening of the pyloric sphincter (fatty meals produce long periods of churning against a closed sphincter) * Pyloric sphincter is opened in the vomiting reflex when there is reverse peristalsis in the small intestine Local and regional reflexes (also mediated by the enteric plexus) play a role: * Emptying can be influenced by the contents of the duodenum (e.g. whether the duodenum still contains food from the previous wave of gastric emptying and whether the luminal pH has returned to alkaline levels)

Answer 289

* Segmentation * Pendular activity

Answer 290

The partially-digested food mass in the stomach.

Answer 291

* To ensure that the body receives enough nutrients from its food, the small intestine mixes the chyme using smooth muscle contractions called segmentations. * Segmentation involves the mixing of chyme about 7 to 12 times per minute within a short segment of the small intestine so that chyme in the middle of the intestine is moved outward to the intestinal wall and contacts the mucosa. * In the duodenum, segmentations help to mix chyme with bile and pancreatic juice to complete the chemical digestion of the chyme into its component nutrients.

Answer 292

The way in which waves of constriction sweep up and down the small intestine, like a pendulum.

Answer 293

* Peristalsis * It is triggered by distension and mediated by the enteric nervous system

Answer 294

* Anti-emetics * Laxatives * Anti-diarrhoeal drugs * Parasympathomimetics * Opiates

Answer 295

They inhibit motility, leading to constipation.

Answer 296

* They inhibit motility, leading to constipation. * This is because they reduce neural activity.

Answer 297

* Diet low in fibre * Dehydration * Lack of exercise -\> Connection between poor abdominal muscle tone and prolonged intestinal transit time * Anticholinergic drugs * Opiates

Answer 298

* Haemorrhoids ("piles") * Diverticular disease (small herniations in the wall of the colon, apparently caused by high pressures in a constipated gut) * May be associated with colon cancer

Answer 299

* Improving diet: * Increasing fibre content * Increasing fluid intake * More exercise

Answer 300

* Lubricants (e.g. paraffin) * Ease the passage of the faeces * Bulk formers (e.g. sterculia (Normacol)) * Increase the fibre content of the faeces and also help to retain water, so softening the stool * Osmotic laxatives (e.g. magnesium salts) * Retain water in the colon and so soften the stool * Motility stimulants (e.g. bisacodyl) * Usually cholinergic agonists, often with some direct effect on smooth muscle.

Answer 301

* It's not appropriate to use anti-diarrhoeal drugs if there is an infection in the gut -\> The diarrhoea is part of the normal physiological mechanism for expelling the infection. * Most commonly used as part of the treatment of non-infectious inflammatory processes in the gut, such as inflammatory bowel disease (Crohn's disease and ulcerative colitis).

Answer 302

* Adsorbent agents * Absorb water and ions and result in a more solid stool, which is less irritating to the gut wall * e.g. Kaolin * Anti-cholinergic agents * Inhibit gut motility and secretion and can act as antispasmodics in irritable bowel disease and inflammatory bowel disease * e.g. Hyoscyamine * Opiates * Strongly inhibit gut motility * e.g. Loperamide

Answer 303

One that is useful against vomiting and nausea.

Answer 304

* Toxins or infections in the gut or in the blood * Anti-emetic drugs not useful * Drugs that induce nausea and/or vomiting as a side-effect of their action (e.g. opiates and cytotoxic drugs used in treatment of cancer) * Anti-emetics useful * Disturbances of balance (e.g. travel sickness and infections of the labyrinth and vestibule of the inner ear) * Anti-emetics useful

Answer 305

Because vomiting is often a helpful way to remove the infection from the gut.

Answer 306

* Cholinergic muscarinic antagonists (in general, less potent than the next two) * Dopamine (mainly D2) antagonists * Serotonin 5HT-3 antagonists And the fourth category is mainly restricted to use in disturbances of the inner ear (including travel sickness): * Histamine H1 antagonists In other words, most anti-emetic drugs work on the CNS and gut motility also.

Answer 307

Enterokinase

Answer 308

Isosmotic salt/glucose solution

Answer 309

* Taste * Gastric acid * Mucus * Mucosal immune system