Motility and secretions of the liver, pancreas and intestines Flashcards

1
Q

Name three secretions released from the small intestine in response to the products of gastric digestion

A

Mucus: Brunner’s glands in the duodenal mucosa secrete alkaline mucus

Ions: Intestinal epithelium secretes Na-, Cl- and HCO3- into the lumen, water follows by osmosis. (Note - overall there is a net absorption of water from the small intestine)

Hormones: Secretin, CCK, Motilin, VIP, GIP

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2
Q

State the function of 5 enteric hormones released from the small intestine

A

Motilin: stimulates MMC via the enteric and ANS which functions between meals

VIP: increases blood flow to the GI tract

GIP: inhibits gastric secretion, stimulates insulin secretion

CCK: inhibits gastric motility and secretions. Stimulates GB contraction and enzyme secretion from the pancreas

Secretin: inhibits gastric motility and secretions. Stimulates bile production in the liver and HCO3- secretion from the pancreas

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3
Q

What are the main secretions of the exocrine pancreas?

A

Alkali: Isotonic solution rich in HCO3- secreted from duct cells. Neutralises duodenal contents

Digestive enzymes: Secreted by pancreatic acini.

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4
Q

Name 5 digestive enzyme secreted from the exocrine pancreas

A

Trypsin
Chymotrypsin
Carboxypeptidase
Pancreatic amylase
Lipases
Phopholipase
Ribonuclease

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5
Q

Explain how pancreatic enzymes are activated

A

Pancreatic enzymes are synthesized as zymogens, which are inactive precursors. This is because pancreatic enzymes are very powerful and if active would digest the cells that produce them. Once secreted a membrane bound enterokinase on the surface of epithelial cells of the small intestine cleaves the zymogen to produce the active enzyme.

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6
Q

Decribe the mechanism of HCO3- secretion from the pancreas

A

CO2 from the extracellular fluid is converted to HCO3- and H+ by carbonic anhydrase. The bicarbonate ions are pumped out into the pancreatic duct lumen by an anion exhanger (Cl- ions)

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7
Q

Describe the control of pancreatic secretions

A

Enzyme secretion: Stimulated by CCK (secreted by the duodenum) and ACh (released by parasympathetic, postganglionic neurones of the vagus nerve).

Alkali secretion: stimulated by secretin (released from the duodenum). Alkali secretion potentiated by CCK and ACh which increase the effects of secretin.

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8
Q

Describe the three phases of pancreatic secretion

A

Cephalic: thought, smell, taste of food and swallowing stimulates release of Ach and gastrin by vagal stimulation, which increases secretion of pancreatic enzymes.

Gastric: proteins and gastric digestion causes release of gastrin and ACh which increases pancreatic enzyme secretion

Intestinal: Products of digestion stimulate the release of secretin and CCk which act on the panceras to increase secretion of enzymes and bicarbonate ions

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9
Q

Describe the cycle of bile acid formation and secretion

A

Bile acids are water soluble derivatives of cholesterol. Bile acids are secreted and continuously reabsorbed by the terminal ileum into the portal circulation. There are then released back into the bile cannaniculi

Primary bile acids synthesised from cholesterol are complexed to taurine and released into the bile cannaniculi.

25% of reabsorbed bile acids are unconjugated due to digestion by intestinal bacteria. These are reconjugated and released. If the bile acids have been dehydroylated, they are conjugated to glycine (secondary bile acids) and secreted.

Some of the dehydroxylated bile acids will not be reconjugated and will be lost in the faeces.

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10
Q

What are the 6 major components of bile?

A

Bile salts

Phospholipids (lecithin)

Ions (bicarbonate, sodium, calcium)

Cholesterol

Bile pigments (e.g. bilirubin and metabolic end products)

Trace metals

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11
Q

State 4 functions of bile salts

A
  1. Emulsification of dietary lipids, making them accessible to pancreatic lipases
  2. Elimination of cholesterol
  3. Prevention of cholesterol precipitation in the gall bladder
  4. Facilitation of the absorption of fat-soluble vitamins.
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12
Q

Describe the digestion and absorption of fats

A

Fats (triglycerides) are emulsified by bile and phospholipids into emulsion droplets. This makes them more soluble and presents them to pancreatic lipase in the small intestine.

Pancreatic lipase digests fats into monoglycerides and fatty acids which are held in micelles (combined with bile salts and phospholipids) along with fat-soluble vitamins

The micelles are unstable and diffuse into an unstirred layer next to the surface of the epithelial cells.

The fatty acids and monoglycerides diffuse across the cell membrane and are reassembled into fats inside the cell

Triglyceride droplets are packaged into chylomicrons. These are exported across the basolateral membrane and leave the intestinal villi via lacteals to enter the lymphatic system.

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13
Q

Describe the digestion and absorption of carbohydrates and monosaccharides

A

Digestion of carbohydrates begins in the mouth though the action of salivary amylase.

In the duodenum, pancreatic amylase breaks down starch and other carbohydrates into disaccharides.

Enzymes within the microvilli of the intestinal cells breakdown disaccharides into monosaccarides.

Monosaccharides are transported across the intestinal epithelium via Na+/Glucose co-transporters on the apical surface and leave the cell via GLUT2 at the basolateral surface. Na+ is pumped back out of the cell via a Na/K-ATPase

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14
Q

Describe the digestion and absorption of proteins and amino acids

A

Proteins are initially digested in the stomach by pepsins and HCl.

In the small intestine, polypeptides fragements are digested by trypsin, chymotrypsin and carboxypeptidase enzymes into smaller peptide fragments.

Peptide fragments further digested to amino acids and transported into the blood by co-transporters. There are specific types of transporter depending on the nature of the amino acid.

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15
Q

Decribe how calcum is transported across the intestinal epithelium

A

Calcium transport is stimulated by vitamin D and PTH. Absorption is primarily in the duodenum and jejunum.

Enterocytes take up calcium by passive diffusion through a Ca2+ chaneel. Once inside the cell, Ca2+ is complexed with calbindin (CaBP). Calcium is transported across the basolateral surface by Ca-ATPase.

Some calcium is stored in vesicles released from the cell via exocytosis.

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16
Q

Describe how iron is transported across the intestinal epithelium

A

Only 10% of the iron that is ingested is absorbed. Most dietary iron is only absorbed in the form of heme.

Non-heme iron absorption depends on the oxidation state. Fe3+ is insoluble and cannot be absorbed and forms a precipitate if it isn’t chelated.

In the stomach Fe3+ is reduced to Fe2+ which is a more soluble form and absorbed by carrier proteins on the brush border membrane. Iron in heme is removed and joins the intracellular pool.

Iron is then either stored in the cytoplasm bound to ferritin or transported into the blood bound to transport proteins (transferrin).

Ferritin releases iron when levels are depleted

17
Q

How is Vitamin B-12 absorbed

A

In the stomach vitamin B-12 binds to R protein.

In the duodenum and jejunum it is releasd and bings to intrinsic factor,

In terminal ileum the vitamin B12-IF complex is absorbed by receptor-mediated endocytosis.

18
Q

State 3 functions of the large intestine

A

To extract Na+ and water from the luminal contents.

To make and store faeces.

To move faeces towards the rectum.

19
Q

What is the main secretion of the large intestine and what is its function?

A

The luminal epithelium of the large intestine secretes an alkaline mucus (from Goblet cells). This serves to:

protect the epithelium from acid, abrasion, and bacterial activity.

provide an adherent medium for holding faecal matter together.

20
Q

Describe how the transport of water varies between the large and small intestine

A

The Na/K-ATPase is a key transporter in driving the reabsorption of water in the intestine. As Na+ moves out of the cell, water follows by osmosis. The route water takes depends on the strength of tight junctions between the intestinal epithelial cells.

In the jejunum tight junctions are leaky:
As Na+ ions are pumped out of the cell they are absorbed into the blood, causing water to flow from the lumen to the blood through tight junctions (paracellular)

In the colon tight junctions are more rigid:
Na+ is transported into the cell from the lumen via electrogenic Na+ channels and pumped out into lateral spaces where they absorbed into the blood. Because tight junctions are rigin water moves transcellularly.

21
Q

Function of the ileocaecal valve

A

The ileocaecal valve is a one-way valve guarded by a sphincter. It separates the terminal end of the ileum from the caecum.

Function:
prevents back-flow of faecal contents from the colon.
controls the rate at which ileal chyme enters the colon.

Regulated by neural and hormonal mechanisms.

22
Q

Function of motility of the colon

A

facilitates the efficient absorption of water and salts (haustral contractions)

permits the orderly evacuation of faeces (mass movements)

23
Q

Haustral contractions

A

Combined contractions of longitudinal and circular muscle produces movement which mixes the contents of the proximal colon and facilitates water absorption.

Intestinal contens change from fluid to mush in the transverse colon and are solid by the time they reach the sigmoid colon

24
Q

Mass movements

A

A series of modified peristaltic events that produce perful contractions which propel the luminal contents from the beginning of the transverse colon to the sigmoid colon.

Occur 1-3 times a day.

25
Q

Gastrocolic reflex

A

Increase in colonic motility following a meal. (particularly 1st meal)

Mediated by gastrin and by the extrinsic autonomic nerves to initiate mass movements in the colon. This pushes the colonic contents into the rectum, triggering the defaecation reflex.

26
Q

Describe the valsalva manoeuvre

A

Process of voluntary defaecation

Full inspiration followed by forced expiration against a closed glottis causes the diaphragm to move downwards.

The abdominal and thoracic muscles are contracted.

Increased pressure in the abdomen forces faecal contents into the rectum.

The defaecation reflex is initiated.

27
Q

State 4 physiological functions of intestinal bacteria

A

provides immunity against common bacteria

converts bilirubin to urobilinogens and forms secondary bile acids

degrades digestive enzymes

digests mucus

synthesizes certain vitamins (e.g. vitamin K)

metabolizes undigested polysaccharides

28
Q

Why can oral antibiotics affect digestion and absorption

A

Oral antibiotics are non-specific and kill the commensal anaerobic bacteria as well as the pathogenic bacteria.

Intestinal bacteria play a role in digestion and absorption and therefore the antibiotics disrupt this balance leading to side effects.

29
Q

How does oral rehydration therapy work?

A

Glucose is co-transported into epithelial cells with Na+ which moves down its chemical and electrical gradient. Na+ is then pumped back out into the intestinal lumen by a Na/K-ATPase, which is also drives the reabsorption of water in the small intestine via osmosis.

In continous or heavy diarrhoea, large amounts of water and Na+ are lost due to malabsorption.

ORT contains glucose, water and electrolytes. Glucose promotes the reabsorption of Na+ ions into epithelial cells which also encourages the reabsorption of water.

30
Q

Explain the symptoms of lactose intolerane

A

Lactose intolerance results from low levels of the lactase enzyme at the brush border of the intestine which breaks fown lactose into gluose and galactose.

Lactose therefore passes through the small intestine until it reaches the large intestine where intestinal bacteria break it down. This produces gas as a by-product, causing flatus. The presence of glucose and galactose in the colon alter the osmotic gradient and cause water to be drawn into the large intestine, resulting in diarrohoea.

31
Q

Why does malabsorption occur?

A

Malabsoprtion occurs when the gastrointestinal tract fails to carry out its functions normally. This can arise either because the digestive process is incomplete or because absorption is impaired

Causes:
Lack of enzymes (pancreatitis, pernicious anaemia)
Damage to the bowel structure (Chrons, coeliacs)
Increased GI motility (IBD, infective diarrhoea, hyperthyroidism)
Length of bowel reduced (surgery)

32
Q

Describe the acid/base balance in the digestive process

A

The acid-base balance is controlled by secretiions of the stomach and the duodenum.

Parietal cells in the stomach extract CO2 and H2O from the blood which is converted to H+ and HCO3- by carbonic anhydrase. H+ and Cl- are secreted into the lumen of the stomach and HCO3- is secreted into the blood, therefore the blood leaving the stomach is slightly alkaline (alkaline tide)

Cells of the pancreas extract Na and HCO3- ions (produced by the reaction with carbonic anydrase) from the blood which is secreted into the duodenum to neutralise acidic chyme from the stomach. The H+ ions are secreted into the blood, making it more acidic (acid tide)

This means the net acid-base balance during digestion is constant.

33
Q

Describe the neurological control of the defaecation reflex

A

Activation of pressure/stretch receptors in rectum by faecal material excites afferent fibres which travel to the sacral spinal cord.

This leads to increased activity in parasympathetic pelvic splanchnic nerves resulting in increased peristalsis & relaxation of the internal anal sphincter

An initial reflex contraction of the external anal sphincter prevents defaecation occurring.

Sensory signals travel to the cortex so that the desire to defaecate is consciously perceived and a decision taken as to whether to proceed

If yes: the external anal sphincter and pelvic floor relax. Faeces are expelled. Valsalva manouvre aids process

If no: There is conscious further contraction of the external anal sphincter and faecal material is moved back into the rectum. The rectum accommodates this material and sensory afferent signals decrease. The urge to defaecate passes

34
Q

What is faecal incontinence?

A

Inability to control the process of defaecation

35
Q

Give five common causes of faecal incontinence

A
  1. Normal structure & function simply overwhelmed
    e. g. Severe diarrhoea
  2. Damage to puborectalis leading to a descending perineum & increased anorectal angle
    E.g. Post partum, obstetric injury
  3. Pudendal nerve injury leading to loss of conscious control of external anal sphincter
    E.g. Obstetric injury
  4. Visceral nerve injury leading to loss of sensation / coordination of reflex
    E.g. Diabetes mellitus, multiple sclerosis
  5. Anal sphincter injury meaning the patient is unable to generate sufficient anal tone to maintain continence
    E.g. 3rd/4th degree tear during parturition
  6. Anatomical abnormalities
    Congenital or acquired anatomical abnormality that means the normal continence mechanisms are bypassed
  7. Higher cortical dysfunction
36
Q

Describe how the acid-base balance of the body is disturbed by vomiting and diarrhoea

A

Vomiting: excessive vomiting leads to large losses of secreted acids from the body. The alkaline tide is then not neutralised which can result in metabolic alkalosis

Diarrhoea: excesses loss of fluid in the faeces leads to dehydration and a loss of NaHCO3, which results in metabolic acidosis due to the lack of bicarbonate ions.

37
Q

Hirschprung’s disease

A

Congenital disorder where there is localised absence of the enteric nervous system in the colon.

Causes constipation at birth. Requires surgical resection of the affected bowel.