Session 5 Flashcards

(72 cards)

1
Q

Chyme properties

A

Enters duodenum from stomach
Hypertonic (more solute:solvent than plasma) - increases as digestion takes place
Acidic
Only partially digested

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2
Q

Mechanism to solve hypertonicity of chyme

A

Add more solvent- water from ECF/circulation

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3
Q

Mechanism to solve acidity and partial digestion of chyme

A

Secretions from pancreas- enzymes and bicarbonate ions

Liver secretions - bicarbonate ions and bile

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4
Q

Chyme is hypertonic because

A

Food produces a lot of solutes that are dissolved in gastric juice

Stomach wall is largely impermeable to water

Water cannot dilute solute in chyme (toxicity)

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5
Q

How does movement of water from circulation/ECF into duodenum occur

A

Relatively permeable to water

Brunners glands

Chyme release must be controlled as too much can overwhelm duodenum (liver/pancreas secretions)

Chyme is isotonic when it leaves duodenum (generally)

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6
Q

Pancreas exocrine basics

A

Exocrine portion approx 90% of pancreas
Ductal system secretes products

Digestive enzymes and other secretions go through Sphincter of Oddi when it is relaxed

Acinus cells produce enzymes, centroacinar cells produce more of aqueous component, ductal system modifies aqueous secretion

Converge and comes out of major pancreatic duct

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7
Q

Pancreas innervated by

A

Sympathetic- inhibits (reduced blood supply)

Parasympathetic/vagus = stimulates, hormones

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8
Q

How does acinus produce enzymes

A

Stimulated by vagus and cholecystokinin (CKK), as hypertonicity/small peptides/fats detected in duodenum

Produces enzymes: amylase/lipases (active), proteases (inactive)

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9
Q

Proteases

A

Inactive

trypsin, chymotrypsin, elastase, carboxypeptidase

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10
Q

Formation of enzymes cellular level

A

Formed on Rough endoplasmic reticulum
Moved to Golgi complex
Condensing vacuoles
Concentrated in zymogen granules
Released with appropriate stimulus (parasympathetic or CKK)

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11
Q

Features of zymogen granules

A

Membrane bound
Contains zymogen- inactive pre cursor of an enzyme, e.g. trypsinogen converted to trypsin in intestinal lumen

Avoids digesting pancreas

If pancreatic enzymes (amylase/lipase) appear in blood- signifies pancreatic damage/pancreatitis

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12
Q

At higher flow rates

A

Increased secretion of HCO3

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13
Q

Features of liver

A

Largest single organ
energy metabolism
Detoxification
Plasma protein production

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14
Q

Features of hepatocytes

A

Chief functional cell of liver

Comprise approx of 80% of mass of liver

Very active at producing proteins/lipids for export

Contain lots of ER, Golgi membranes and glycogen

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15
Q

Features of zones of acinus

A

Toxins coming into liver impact zone 1 more (nearer blood)

Ischeamia is more likely to damage zone 3 (further away from blood supply)

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16
Q

Liver drains into

A

Portal vein - not as deoxygenated as normal vein, liver can extract some oxygen

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17
Q

Venous structure of liver

A

Blood flowing in: venous portal blood, arterial blood (hepatic arteries)- flowing towards central vein which drains into hepatic veins (vena cava)

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18
Q

Bile flow out of liver

A

Along canaliculi

Bile ducts to duodeum

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19
Q

Most of bile composes of

A

Bile salts

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20
Q

Fibre role

A

Binds components of bile to cholesterol and allows us to secrete it in faeces

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21
Q

2 major components of bile

A

Bile acid dependant
- secreted into canaliculi by hepatocytes
- Contains bile acids and pigments

Bile acid independent
- secreted by duct cells
- similar alkaline solution to pancreatic duct cells
- stimulated by secretin

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22
Q

What are the 2 primary bile acids

A

Colic acid
Chenodeoxycholic acid

(Further bile acids formed in gut)

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23
Q

What are bile salts

A

Bile acids that are conjugated with the amino acids
(Glycine/taurine)

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24
Q

Why can’t bile acids be released into the gut without bile salt

A

Not always soluble at duodenal pHs (bile salts generally are)

Amphipathic structure - (hydrophilic end is water soluble and hydrophobic end is lipid soluble), act at oil/water interface,crucial for emulsification of dietary lipids

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25
Role of bile acids in Digestion of fats
Lipids tend to form large globules by the time they reach duodenum Low surface area for enzymes to act Bile acids emulsify fat into smaller units and help disperse droplets Increases surface area for lipases to act
26
What are micelles
Vehicle to carry hydrophobic molecules through an aqueous medium Products of lipid digestion- cholesterol, monoglycerides, free fatty acids Diffuse with products to brush border of epithelial cells
27
What happens to lipids at epithelial cells
Lipids diffuse down concentration gradient into intestinal epithelial cell Re-sterilised back to triglycerides, phospholipids, cholesterol Reformed lipids are packaged with apoproteins (chylomicrons)
28
What happens once reformed lipids are packaged with apoproteins (chylomicrons)
Exocytosis from basolateral membrane, too large to enter capillaries, enter lymph capillaries Chylomicrons travel through lymphatic system to find thoracic duct which eventually drains into left subclavian/left IJV
29
What happens to bile salts when lipids enter gut epithelial cells
Remain in gut lumen, reabsorbed in terminal ileum, return to liver in portal blood, liver extracts bile salts and reuses them Liver does not have to synthesis total bile acid requirements Good fibrous diet combines with bile salts and a bit of cholesterol to take them out of the body and lower overall cholesterol
30
What does the gallbladder do
Sits on inferior surface of liver In transpyloric plane (L1) Storage facility for bile, concentrates bile by removing water and ions (can lead to gallstones), combined with water when released again CCK released from duodenum stimulates gallbladder contraction (relaxed sphincter of Oddi)
31
What is Steatorrhoea
If bile acids/salt or pancreatic lipases are not secreted in adequate amounts: - fat in faeces - pale - floating - foul smelling
32
Other important excretory product
Billirubin- breakdown product of haemoglobin, conjugated in liver to make soluble and secreted into bile Excreted in faeces, accumulates in blood if cannot be excreted and cause jaundice
33
Important points about carbohydrate digestion
Only monosaccharides can be absorbed Glucose is only absorbed with sodium Carbohydrates of plant origin cannot be digested in the SI, pass into LI (utilised and partially digested by bacteria in colon), provides vital nutrients for gut bacteria
34
End products of carbohydrate metabolism
Glucose, galactose, fructose
35
Common dietary carbohydrate- starch
Amylose (alpha 1,4) = breaks down to maltose by amylase, breaks down into glucose , Amylopectin (alpha 1,4 and 1,6) = breaks down to dextrin by isomaltase, breaks down into amylose and then glucose by amylase
36
Common dietary sugar lactose
Disaccharide, lactose broken down by lactase (brush border enzymes) to glucose and galactose
37
Common dietary sugar sucrose
sucrose converts to glucose and fructose
38
Products of common dietary carbohydrates
Glucose, galactose and fructose = monosaccharides
39
Features of enterocytes
Columnar cells in SI that absorb nutrients Na K+ ATPase on basolateral side = sodium can be moved into cell Apical = SGLT 1 Co-transporter for glucose or galactose and sodium GLUT 5 brings fructose from lumen of gut into cytosol
40
How are glucose, galactose and fructose moved from the cytosol of the enterocyte
Through transporter in basolateral membrane called GLUT 2, then moved to venous drainage of small intestine which goes through portal system and into liver
41
Protein digestion
1- stomach 2- intestinal lumen 3- brush border 4- cytosolic peptidases
42
Protein digestion in stomach
1- stomach (chief cells reside in gastric glands, release inactive protease called pepsinogen which is converted to pepsin in lumen of stomach due to acidic conditions) Shorter chains of protein and some amino acids formed and enter duodenum
43
How are proteins digested in intestinal lumen
Enter into duodenum, pancreas releases zymogens (proteases), activated in lumen, trypsinogen converted to trypsin by enteropeptidase (brush border enzyme) Trypsin goes on to activate other pro-enzymes including more trypsinogen
44
Action of trypsin
Trypsinogen- trypsin Chymotrypsinogen- Chymotrypsin Proelastase - elastase Procarboxypeptidase A- carboxypeptidase A Procarboxypeptidase B- carboxypeptidase B
45
Major proteases groups
Endopeptidases- produce shorter polypeptide chains as break down bonds in middle (trypsin, chymotrypsin and elastase) Exopeptidases- break off bonds towards end of chain so can cleave of dipeptides or amino acids (carboxypeptidase A and B)
46
How many major proteases
5
47
What do brush border proteases do
Enterocytes express peptidases to digest amino acids and shorter peptides Enterocytes are able to absorb dipeptides and tripeptides using a PepT1 transporter (takes short peptides into cytosol of enterocyte), amino acids are co-transported in with sodium
48
Cytosolic peptidase role in protein digestion
In cytosol of enterocyte Small peptides are broken down into amino acids by cytosolic peptidases (Certain di and tri peptides can be absorbed into blood along with amino acids)
49
how does water move across small intestinal epithelia
Inter-cellular spaces between enterocyte and tight junctions Water can move out or into lumen, trans-cellularly (related to movement of sodium due to Na+ K+ ATPase) or para-cellularly (driven by sodium accumulation and hyperosmotic solution in intracellular spaces)
50
What are oral rehydration solutions
Water with Na+ and Glu Presence of this drives uptake of water
51
Sodium drives
Water absorption
52
Chloride drives
Water secretion
53
Features of water secretion
Chloride moves into cell through basolateral membrane in Na+ Cl- K+ channel If cAMP levels rise, Cl- is secreted through cystic fibrosis transmembrane conductance regulator protein (CFTR) Chloride secreted through CFTR, sodium drawn through tight junctions, resulting NaCL in lumen of gut causes water to move in
54
Vitamin B12 deficiency symptoms and causes
Neurological problems and megaloblastic anaemia Caused by lack of intrinsic factor (parietal cells), hypochlorhydria (not enough stomach acid, e.g. gastric atrophy, PPI), not enough B12 in food, inflammation of terminal ileum (crohn’s disease)
55
Features of lactose intolerance
Deficiency of enzyme, lactose, diminishes after age 2 Disaccharide remains in gut lumen creating high osmotic pressure, draws water into lumen, results in diarrhoea When lactose reaches colon it is fermented in gut which causes flatus and bloating
56
Features of IBS
Diagnosed in absence of documented abnormalities 10-15% of adults Abdominal pain, bloating, flatulance, diarrhoea, constipation, rectal urgency 2:1 female to male 20s-40s more impacted Associated with psychological disorders
57
Features of coeliac disease
Immunological response to gluten (found in wheat, rye and barley) Damages mucosa = flattening of villi, hypertrophy of crypts, lymphocytes in epithelium/LP Leads to impaired digestion and malabsorption causes- genetic factor, under diagnosed
58
Symptoms of coeliac disease
Malabsorption Diarrhoea Weight loss Flatulence and distension= pain Anaemia (less iron absorption) Neurological symptoms due to less Ca+
59
Investigations and treatment for coeliac disease
Blood tests- IgA to smooth muscle endomysium and tissue Upper GI endoscopy = duodenal biopsy, mucosal pathology (reduced or absent villi) Treatment = gluten free diet, improvements usually quick
60
How much bile does the liver produce each day
Approx 250-1000mls/day of bile (bile acids, bile pigments and alkaline juice)
61
Structural and functional unit of liver
Structural- lobule Functional- acinus
62
Micelles allow
Lipids to move through an aqueous environment
63
How is large sa created for absorption in SI
Permanent intestinal folds (plica circulares), villi and microvilli
64
How are dipeptides/tripeptides absorbed
Via peptides transporter (co transport with H+)
65
Active absorption of calcium in the intestines requires
Vitamins D
66
Vitamin B12 is absorbed in the
Terminal ileum bound to intrinsic factor
67
Blood supply to midgut
superior mesenteric artery
68
blood supply to hindgut
Inferior mesenteric artery
69
Details of superior mesenteric artery supplying midgut
Starts at L1 Gives off marginal artery, middle colic artery, right colic artery and ileo-colic artery to large intestinw
70
What happens at L12
Abdominal aorta gives off Coeliac trunk to foregut
71
Hindgut blood supply details
Inferior mesenteric artery around L2/L3 Gives off left colic artery and sigmoid arteries Becomes superior rectal artery
72
What is the watershed area
Area in the large Instestine around T12 to L2 on the left that has the weakest blood supply Vulnerable to ischeamia during BP drops