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PHASE ONE > Stomach, Liver, Gall bladder and Pancreas > Flashcards

Stomach, Liver, Gall bladder and Pancreas Flashcards

1
Q

Functions of the stomach (nine)

A 
Store and mix food
Dissolve and continue digestion 
Regulate emptying into duodenum 
Kill microbes
Secrete proteases
Secrete intrinsic factor
Activate proteases
Lubrication 
Mucosal protection
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2
Q

Key cell types in stomach

A

Mucous cells
Parietal cells
Chief cells
Enteroendocrine cells

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3
Q

Which cells secrete stomach acid? What is this acid?

A

Parietal cells

HCl

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4
Q

Is secretion of HCl energy-dependent? Why?

A

Yes - H+ ions need to be pumped into the lumen of the stomach against a concentration gradient

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5
Q

Which nervous system controls this secretion?

A

Parasympathetic

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6
Q

Which cells produce HCl?

A

parietal cells of the stomach

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7
Q

Chemical reactions in parietal cells

A

To begin with, water and co2 combine with parietal cell cytoplasm to produce carbonic acid (H2CO3). Carbonic acid then spontaneously dissociates into a hydrogen ion and bicarbonate ion HCO3-.

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8
Q

What happens to the H+ ions produced?

A

The hydrogen ion that is formed is transported into the stomach lumen via the hydrogen-potassium ATPase ion pump. This pump uses ATP as an energy source to exchange potassium ions into the parietal cells of the stomach with hydrogen ions.

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9
Q

What happens to the bicarbonate ion produced? What is the overall result of the H+ and HCO3- ion movement?

A

The bicarbonate ion is transported out of the cell into the blood via a transporter protein called anion exchanger which transports the bicarbonate ion out of the cell in exchange for a chloride ion. This chloride ion is then transported into the stomach lumen via a chloride channel.
This results in both hydrogen and chloride ions being present within the stomach lumen. Their opposing charges leads to them associating with each other to form hydrochloric acid (HCl).

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10
Q

Gastric acid secretion regulation; turning it ON (cephalic phase)

A

Innervation comes from vagal efferent nerve fibres of the parasympathetic nervous system.
Sight, smell, taste of food and chewing stimulates release of acetylcholine. ACh acts directly on parietal cells and triggers the release of gastrin and histamine. The net effect is increased acid production.

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11
Q

Gastric acid secretion regulation; turning it ON (gastric phase)

A

Gastric distension, presence of peptides and amino acids leads to gastrin release. Gastrin acts directly on parietal cells and triggers the release of histamine which also acts directly on parietal cells. The net effect is increased acid production.

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12
Q

Gastric acid secretion regulation; turning it ON (protein in the stomach )

A

Proteins in the lumen are a direct stimulus for gastrin release. The proteins act as a buffer taking up hydrogen ions and causing pH to rise.
This leads to decreased secretion of somatostatin, which leads to more parietal cell activity because of a lack of inhibition.

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13
Q

Gastric acid secretion regulation; turning it OFF (gastric phase)

A

Low lumin pH due to high concentration of H+ ions directly inhibits gastrin secretion and indirectly inhibits histamine release as a result.
Somatostatin release is stimulated which inhibits parietal cell activity.

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14
Q

Gastric acid secretion regulation; turning it OFF (intestinal phase)

A

In the duodenum, duodenal distension, low luminal pH, hypertonic luminal contents and the presence of amino acids and fatty acids triggers the release of enterogastrones secretin and cholecystokinin.

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15
Q

Effect of secretin

A

Inhibits gastrin release

Promotes somatostain release

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16
Q

Nervous system in the gastrointestinal tract

A

Enteric nervous system

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17
Q

Ulcer definition

A

A breach in a mucosal surface

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18
Q

Causes of peptic ulcers

A

Heliobacter pylori infection
NSAIDs
Chemical irritants (alcohol, bile salts, dietary factors)
Gastrinoma

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19
Q

What is a gastrinoma?

A

A gastrinoma is a tumor derived from G cells in the duodenum, pancreas or less commonly the stomach, that secretes the protein gastrin. There is hypersecretion of HCl acid into the duodenum, which causes the ulcers.

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20
Q

Gastric mucosa defences

A
  • Secretion of alkaline mucus (containing bicarbonate) which helps to resist the action of hydrochloric acid
  • Tight junctions between epithelial cells to prevent the passage of HCl and proteases between the cells to digest the underlying tissue
  • A population of stem cells deep in the gastric pits which divide to replace damaged cells regularly
  • A number of feedback loops to control the production and activation of proteases and HCl etc.
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21
Q

What do helicobacter pylori secrete? What does the secreted substance do? Why does this cause ulcers?

A

urease
splits urea into co2 and ammonia
Ammonia forms ammonium when combined with hydrogen ions. Ammonium damages gastric epithelium and an inflammatory response can further damage epithelium, leading to reduced mucosal defence.

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22
Q

What does NSAID stand for? Why do NSAIDs cause ulcers?

A

Non-steroidal anti-inflammatory drug

NSAIDs inhibit cyclo-oxygenase 1, which is needed for prostaglandin synthesis. Prostaglandin stimulates mucus secretion. As a results when its production is inhibited, there is reduced mucosal defence.

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23
Q

NSAIDs ulcers: treatment

A
  • Reduce acid secretion with protein pump inhibitors or H2-receptor antagonists
    • Protein pump inhibitors:
      • Omeprazole
      • Lansoprazole
      • Esomeprazole
    • H2-receptor antagonists
      • Cimetidine (taken off the market right now)
      • Ranitidine
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24
Q

Which cells produce pepsinogen?

A

Chief cells

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25
Q

What is pepsinogen?

A

Inactive form of pepsin

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26
Q

What is the conversion of pepsinogen to pepsin is dependent on what?

A

pH

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27
Q

At which pH is the conversion of pepsinogen to pepsin most efficient?

A

<2

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28
Q

What does pepsin break down?

A

Collagen in meat

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29
Q

What activates parietal cells?

A

ACh
Gastrin
Histamine

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30
Q

What turns pepsinogen to pepsin?

A

HCl

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31
Q

Protecting chief cells

A

Produce inactive form of pepsin, as pepsin can digest the cell. Thick layer of mucosa on chief cells to prevent HCl breaking down the cell and activating pepsin.

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32
Q

Total % of protein digestion by pepsin

A

20%

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33
Q

Empty stomach

A

50ml

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34
Q

Filling up stomach

A

1.5L

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35
Q

Receptive relaxation

A

Passive increase in volume mediated by parasympathetic nervous system acting on enteric nerve plexuses.

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36
Q

Receptive relaxation; nervous system coordination

A

Afferent input via vagus nerve.

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37
Q

Receptive relaxation local factors

A

Nitric acid and serotonin released be enteric nerve mediated relaxation.

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38
Q

Where do peristaltic waves start?

A

The gastric body

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39
Q

What do peristaltic waves cause?

A

Churning

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40
Q

Which cells regulate peristalsis and act as ‘pacemaker’

A

interstitial cells of Cajal

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41
Q

Where is there more powerful contraction?

A

gastric antrum

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42
Q

What happens to the pylorus when a peristaltic wave reaches it?

A

Pylorus closes.

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43
Q

Which cells are in charge of basal electral rhythem?

A

interstitial cells of Cajal

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44
Q

Where are interstitial cells of Cajal?

A

Muscularis propria

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45
Q

Rate of persitaltic waves per min

A

3/min

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46
Q

Peristalsis - depolarisation etc.

A

Pacemaker cells undergo slow depolaration-repolarisation cycles. Depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells. Excitatory neurotransmitter ACh and hormones further depolarise membrane. Action potentials generated when threshold is reached and leads to smooth muscle contraction.

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47
Q

Strength of peristalsis increased by …

A

Gastrin hormone (turns on HCl secretion and pepsinogen production)

Gastric distension due to food

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48
Q

What mediates gastric distension?

A

Mechanoreceptors

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49
Q

What decreases the strength of peristalsis?

A

Duodenal distension. There is an increase in duodenal luminal fat and duodenal osmolarity (due to increased concentration of lipids and amino acids). The duodenal lumen pH decreases and sympathetic nervous system action increases causes peristalsis to turn off (fight or flight system). Parasympathetic nervous system action decreases leading to les ACh being produced.

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50
Q

What causes dumping syndrome?

A

When the duodenum is overfilled with a hypertonic solution.

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51
Q

Symptoms of dumping syndrome

A

Vomiting, bloating,c ramps, diarrhoea, dizziness, fatigue, weakness, sweating, tachycardia.

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52
Q

How does the body prevent overfilling in the duodenum?

A 
Stomach starting to empty -> acidity rises; pH ↓
Fat + AA content in lumen ↑
Hypertonicity + lumen distended
Triggers secretion of enterogastrones 
Turn off parietal cells + chief cells
& leads to ↓ action of peristalsis
Short nerve pathway ↓ parasympathetic stimulation via Vagus
Less ACh 
↑ Sympathetic NS - turn stomach off
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53
Q

Overview of reasons for delayed gastric emptying

A

Drugs

  • Gastrointestinal agents
  • Anticholinergic medication
  • Miscellaneous
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54
Q

Gastrointestinal agents (delayed gastric emptying)

A
  • Aluminium hydroxide antacids
  • H2 receptor antagonists
  • H+ pump inhibitors
  • Sucralfate
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55
Q

Anticholinergic medication (delayed gastric emptying)

A
  • Benadryl
  • Opioid analgesics eg morphine
  • Tricyclic antidepressants
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56
Q

Miscellaneous (delayed gastric emptying)

A
  • Beta-adrenergic receptor antagonists

- calcium channel blockers

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57
Q

Afferent liver blood supply

A

Portal vein

Hepatic artery

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58
Q

Efferent liver blood flow

A

Hepatic veins

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59
Q

% distribution of afferent supply

A

75% portal vein

25% hepatic artery

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60
Q

Portal circulation

A

Portal vein comes from GI tract and blood flows into the liver; rich in nutrients.

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61
Q

Which system does the bile flow out of, and where to?

A

Through the biliary system

To the gall bladder

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62
Q

What are the components of portal triads?

A

Hepatic artery
Portal vein
Bile duct

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63
Q

7 liver functions

A

1) Detoxification (filtering and cleaning blood of waste products)
2) Immune functions (fights infections and disease)
3) Synthesis of clotting factors, proteins, enzymes, glycogen and fats
4) production of bile and breakdown of bilirubin
5) energy store - glyocgen and fats
6) regulation of fat metabolism
7) can regenerate

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64
Q

Metabolic role of the liver

A

Maintains a continuous supply of energy to the body - controlling metabolism of carbohydrates and fats

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65
Q

When do the metabolic roles of the liver vary?

A

Fasting, absorption, digestion

Multiple pathways

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66
Q

What regulates metabolic roles of the liver?

A

The endocrine glands e.g. pancreas, adrenal, thyroid

Nerves

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67
Q

Definitions of lipids

A

Lipids are esters of fatty acids and glycerol or orther compounds (cholesterol)

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68
Q

Solubility of lipids

A

Insoluble in water

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69
Q

What is a triglyceride?

A

1 glycerol molecule

3 Fatty acids

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70
Q

Saturated and unsaturated fatty acids

A

Saturated: solid at room temperature
Unsaturated: less tightly packed and liquid at room temperature

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71
Q

Lipid functions

A

Energy reserve
Structural
Hormone metabolism

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72
Q

Lipid - structural functions

A

Cell membrane
Integral to form and functions of cells
Inflammatory cascade

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73
Q

Lipid - hormone metabolism

A

cholesterol is the backbone of adrenocorticoid and sex hormones
Vitamin D

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74
Q

Where is most energy provided from?

A

The oxidation of lipids and carbohydrates and proteins

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75
Q

kcal/g for lipids

A

9-10kcal/g

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76
Q

Energy reserves in the body

A

Blood glucose
Glycogen stores
Muscle (protein)
Lipid reserve

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77
Q

For which of the energy reserves is the liver the main storage place?

A

Glycogen

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78
Q

How are lipids transported?

A

By chylomicrons

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79
Q

Where are lipids transported to?

A

Adipocytes and hepatocytes

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80
Q

Inflow into liver is via … carrying …

A

portal vein, hepatic artery and lymphatic system

carrying lipids, toxins and carbohydrates

81
Q

When lipids are broken down, what form are they stored in the liver in?

A

Fatty acids

82
Q

What are lipids transported as?

A

Lipids transported as triglycerides/fatty acids bound to albumin or within lipoproteins

83
Q

Diffusion of triglycerides

A

Triglycerides cannot diffuse through cell membrane. Instead, fatty acids are released through lipases to facilitate transport into the cell. In the cell fatty acids are re-esterified to triglycerides.

84
Q

Fatty acid uptake

  • Can they diffuse?
  • What kind of transport?
  • Transporter systems?
A

Diffusion through lipid bilayer of cell
Facilitated transport, which increases if substrate increases supply or there is an increase receptor molecules?

Several transporter systems:

  • FA binding proteins (mitochondrial AST) - induction to increase expression = increased uptake of FA in hepatocytes
  • FAT (fatty acid translocase)
  • FATP (fatty acids transport polypeptide)
85
Q

FA from adipocyte to hepatocyte

A
  1. Lipoprotein lipase hydrolyses to free fatty acids, which are taken up into adipocyte.
  2. FFA re-esterified. If there is a demand, they are release out through hormone sensitive lipase.
  3. They are transported to liver with hepatic lipase and taken up into hepatocyte where they are oxidised or stored as triglyceride.
86
Q

Insulin action and lipid metabolism

A

Insulin stimulates lipoprotein lipase enzymes to breakdown triglycerides and release free fatty acids to be stored in the form of triglycerides in adipose. Insulin reduces the activity of hormone-sensitive lipase leading to reduction of fatty acid export from adipocyte.

87
Q

Insulin resistance

A

Increased lipolysis in adipocytes leads to an increase of triglycerides in circulation. An increase “offer” of fatty acids to hepatocytes leads to an increased uptake. Higher glucose levels mean there is less demands for lipids to be used as an energy source.

88
Q

What is lipogenesis

A

Formation of lipids in liver

89
Q

What is lipogenesis dependent on?

A

insulin concentration and sensitivity

90
Q

Rate limiting step of lipogenesis?

A

Acetyl-CoA => Malonyl-CoA catalysed by Acetyl-CoA carboxylase

91
Q

Rate related to FAS

A

COMPLETE?

92
Q

Components of lipoproteins

A

Core triglyceride
Cholesterol-ester
surface monolayer of phospholipids, cholesterol and protein

93
Q

What are lipoproteins defined by?

A 
Their densities:
chylomicrons
very light density lipoproteins (vLDL)
light density lipoproteins (LDL) 
high density lipoproteins (HDL)
94
Q

What happens in lipoproteins as density increases?

A

Protein content increases

95
Q

Function of chylomicrons?

A

Carry lipids from the gut to muscle and adipose tissue

96
Q

What are the remnants that chylomicrons do not transport taken up by

A

The liver via receptor mediated endocytosis

97
Q

Where is cholesterol esterified? By what?

A

Intracellularly Acyl-CoA:cholesterol acyltransferase catalyses the esterification of cholesterol in lipoproteins

98
Q

Where are cholesterols processed?

A

Majority in the liver

99
Q

Ratio of internally produced (endogenous) vs dietary cholesterol

A

90:10

100
Q

How is cholesterol excreted?

A

Through bile

101
Q

What circulation is cholesterol involved in? What carries TF + cholesterol through circulatory system?

A

Enterohepatic circulation

Lipoproteins

102
Q

Fatty acid export from liver

A

ApoB (rER) and lipid components (sER) are added together by microsomal TAG transfer protein. Transported in a vesicle to the Golgi apparatus where ApoB is glycosylated (the reaction in which a carbohydrate is attached to a hydroxyl or other functional group of another molecule). The glycosylated ApoB and lipid contents bud off the Golgi A and move to the sinusoidal membrane of hepatocyte cell. The vesicle fuses with membrane the VLDL is released.

103
Q

What is fatty acid oxidation proportional to?

A

Plasma levels of free fatty acids released from adipocytes.

104
Q

Simplified process of liver disease

A
  1. Fatty Liver - deposits of fat causes liver enlargement
  2. Liver fibrosis - scar tissue formed
  3. Cirrhosis - growth of connective tissue destroys liver cells
105
Q

What causes the development of fatty liver?

A

Increased plasma in fatty acids (mainly triglycerides)

  • excess dietary fat intake
  • excess dietary caloric intake overall

Increased flux of fatty acids

  • increased release of FA from adipocytes
  • increased fatty acid uptake in hepatocytes

Decreased fatty acid oxidation

Decreased demands for lipids in fuel leading to increase storage; results in BLAND STEATOSIS

106
Q

Why does NAFLD come about?

A

Overstorage of unmetabolised energy exceeding the energy combustion capability of PPARa mediated system

107
Q

What is hepatic steatosis?

A

fat content exceeding 5-10% of the weight of the liver

108
Q

What is steatohepatitis?

A

increase steatosis
Apoptosis (cell-programmed death) of fat-laden hepatocytes release triglycerides and toxic FAs, which induce systems that lead to generation of reactive oxgygen species (ROS), leading to oxidative stress.
Oxidative stress induses the release of proinflammatory cytokines and overall there is inflammation

109
Q

Why does alcohol cause fatty liver?

A
  • High caloric load ⇒ energy load
  • Metabolised in the liver; increased load leads to:
    • Impairment and inhibition of PPARa and SREBP
      • Decrease in PPARa = decrease in fat oxidation
      • Decrease in SREBP = increase in FAS - lipogenesis
  • Damage to cell organelles ⇒ mitochondria, ER - reduced fat oxidation
  • Apoptic hepatocytes release TG and very long chain FA - augment liver injury
  • Stellate cell activation - leading to increased fibrogenesis
110
Q

Where is bile secreted?

A

in the liver by hepatocytes

111
Q

What is bile used for?

A

emulsify fats

112
Q

What is another function of bile?

A

excretory pathway for most steroid hormones

113
Q

Where is it stored and concentrated? Why is it concentrated?

A
  • gall bladder

- some NaCl and water are absorbed into the blood

114
Q

Where does the gall bladder lie?

A

at the junction of the right midclavicular line and costal margin

115
Q

How is the liver connected with the GI tract?

A

The portal vein

116
Q

What does the portal vein collect blood from?

A

the superior mesenteric vein which in turn is effectively the venous drainage of both the small and large intestines

117
Q

What shape are the hepatic lobules in a cross section?

A

Hexagonal

118
Q

What is at each corner of the hepatic lobules?

A

Portal triad:

  • hepatic portal vein
  • hepatic artery
  • bile duct
119
Q

What runs up the centre of each lobule?

A

central vein

120
Q

What does the central vein eventually become?

A

hepatic vein

121
Q

Where do substances absorbed from the small intestine wind up in?

A

hepatic sinusoid

122
Q

What are hepatic sinusoids and what type of epithelium do they have

A

type of blood vessel

fenestrated, discontinuous epithelium

123
Q

What is found in hepatic sinusoids?

A

o2 rich blood from hepatic artery and nutrient rich blood from the portal vein

124
Q

How are hepatocytes separated from hepatic sinusoids?

A

the spaces of Disse

125
Q

Eventual drainage into …

A

vena cava via central vein

OR taken up by hepatocytes in which they can be modified

126
Q

Why is the liver unique in terms of vasculature?

A

The majority of its blood supply comes from a vein - the portal vein - which is responsible for 80% of the supply with the remaining 20% supplied by the hepatic artery

127
Q

What happens when the branches of artery and vein leave the portal triad?

A

they join and blood is mixed as it enters the sinusoids

128
Q

Direction of bile vs blood?

A

bile heads in opposite direction to the blood

129
Q

What are the sinusoids lined with?

A

A continuous layer of specialised endothelial cells interspersed with Kupffer cells (macrophage)

130
Q

What is on the undersurface of sinusoids?

A

stellate cells

131
Q

What are stellate cells responsible for?

A

producing the extracellular matrix in the space of disse

132
Q

What is found between adjacent hepatocytes?

A

bile canaliculi

133
Q

What are bile canaliculi?

A

grooves running along the side of the hepatocytes, bound together by tight junctions, gap junctions and desmosomes which cross both cell membranes

134
Q

What is found in areas around bile canaliculi and what is their purpose?

A
  • Actin filaments

- serve to pump the formed bile toward the bile ducts

135
Q

Bile pathway to the GI tract:

A
  1. The bile ducts in the hepatic lobules draw either into the left or right hepatic ducts which in turn join to form the common hepatic duct.
  2. The cystic duct joins the common hepatic duct, allowing bile to collect in the gall bladder.
  3. After the cystic duct has joined the common bile duct, the duct becomes the common bile ducts
  4. The pancreatic duct then joins the common bile duct at a point known as the ampulla of vater
  5. These two ducts then enter the duodenum at the major duodenal papilla (2nd part of duodenum)
  6. A spincter around the two ducts, to regulate the entry of bile into the duodenum is called the sphincter of Oddi
136
Q

What is bile composed of?

A
  • Bile salts
  • Lecithin (phospholipid)
  • HCO3- and other salts
  • Cholesterol
  • Bile pigments
  • Trace metals
137
Q

What manufactures bile salts?

A

hepatocytes

138
Q

Bile salts, cholesterol and lecithin are aggregated into mixed micelles and maintain this aggregation in the gall bladder even when concentrated. The main reason for this is that…

A

bile salts are powerful detergents which they need to be for their fat emulsification function (bile salts are anionic - negative). However they are also capable of damaging cell membranes and so they are separated in micelles to reduce damage until they are required.

139
Q

The components of bile salts are secreted by 2 different cell types

A

Hepatocytes

Epithelial cells lining the bile duct secrete

140
Q

What do hepatocytes secrete in the production of bile salts?

A

bile salts
cholesterol
lecithin
bile pigments

141
Q

What do Epithelial cells lining the bile duct secrete?

A

most of HCO3- rich solution

142
Q

What stimulates the secretion of HCO3- rich solution?

A

secretin in response to the presence of acid in the duodenum

143
Q

The gall bladder receives its bile from the …

A

common hepatic duct

144
Q

The hepatic bile enters the gall bladder via the — duct. What happens to the bile duct there?

A
  • via the cystic duct

- stored and concentrated here (hepatic bile is relatively dilute and then concentrated in the gall bladder)

145
Q

When does bile leave here?

A

When the gall bladder contracts under the action of CCK (cholecystokin) which is released due to amino acids + fatty acids in the duodenum

146
Q

What provides oxygenated blood to the gall bladder?

A

cystic artery

147
Q

Enterohepatic circulation

A
  • During the digestion of a fatty meal, most of the bile salts entering the intestinal tract via the bile are absorbed by specific Na+ coupled transported in the jejunum and terminal ileum - the largest amounts are absorbed here
  • The absorbed bile salts are returned via the portal vein to the liver, where there are once again secreted into the bile
  • Uptake of bile salts from the portal blood into hepatocytes is driven by secondary active transport coupled to Na+
148
Q

What happens to the bile salts which escape the enterohepatic circulation?

A

lost in faeces, but the bile salts from cholesterol to replace it

149
Q

What is bile synthesised FROM?

A

cholesterol (The liver also secretes cholesterol extracted from the blood into the bile)

150
Q

When is bile secretion greatest?

A

during and just after a meal (Although the liver is always secreting some bile)

151
Q

What surrounds the common bile duct at the ampulla of vater?

A

sphincter of Oddi → a ring of smooth muscle

152
Q

What happens when the sphincter of Oddi is closed?

A

the dilute bile secreted by the liver is shunted into the gallbladder to be concentrated

153
Q

What is the significance of the bile duct system being a low pressure system?

A

So when the gallbladder fills with bile it must exhibit adaptive relaxation - which is where the size increases but the pressure doesn’t (opposite of what happens when you blow a balloon)

154
Q

Shortly after the beginning of a fatty meal, what hormone is released in response to fat in which part of the GI tract?

A

Cholecystokinin (CCK) is released in response to the presence of fat in the duodenum

155
Q

What are bile pigments formed from?

A

the haem portion of haemoglobin when old/damaged erythrocytes are broken down in the spleen and liver and can also occur in Kupffer cells

156
Q

What is the predominant bile pigment?

A

bilirubin

157
Q

What is bilirubin extracted from the blood by?

A

hepatocytes and actively secreted into bile

158
Q

What colour is bilirubin

A

yellow

159
Q

What happens after the bile enters the duodenum?

A
  1. The conjugated bilirubin travels to the small intestine until it reaches the ileum or the beginning of the large intestine where under the action of intestinal bacteria it is reduced through a hydrolysis reaction (a glucuronic acid group is removed) forming UROBILINOGEN
  2. Urobilinogen is lipid soluble (around 10% is reabsorbed into the blood and bound to albumin and transported back to the liver where urobilinogen oxidised to UROBILIN)
  3. Here it is either recycled into bile or transported to the kidneys where it is excreted in urine
  4. The remaining 90% of urobilinogen is oxidised by a different type of intestinal bacteria to form STERCOBILIN which is then excreted into the faeces
160
Q

What is jaundice?

A

yellow discolouration of the skin caused by high serum bilirubin level

161
Q

When is jaundice detectable clinically?

A

above 50 micromol per L

162
Q

3 main types of jaundice

A

Pre-haptic
Hepatic/intra-hepatic
Post-hepatic/Obstructive

163
Q

Hepatic/Intra-hepatic jaundice (result of, what does it cause physiologically, what is the liver unable to do, signs, caused by …)

A

Result of hepatocellular swelling e.g. in parynchymal liver disease, or abnormalities at a cellular level of the result of infection

Results - impaired cellular uptake, defective conjugation or abnormal secretion of bilirubin by the hepatocytes

Damaged liver unable to metabolise the unconjugated bilirubin resulting in a build up in serum unconjugated bilirubin

Signs = decreased urobilinogen, dark urine, pale or normal stools, enlarged spleen, yellow skin

Caused by - viral hepatitis, drugs, alcohol hepatitis, cirrhosis, jaundice of the newborn

164
Q

Post-hepatic/obstructive jaundice (when does it occur, signs, causes)

A

Occurs when the biliary system is damaged, inflamed or obstructed

Signs = elevated serum CONJUGATED bilirubin, dark urine, pale stools, normal levels of unconjugated bilirubin, decreased urobilinogen, no enlargement of the spleen, yellow skin

Causes: gallstones, pancreatic cancer, gallbladder cancer, bile duct cancer, pancreatitis (acute or chronic)

165
Q

If a gall stone becomes lodged at a point that prevents both bile and pancreatic secretions from entering the intestine then this will result in…

A

failure to both neutralise acid and adequately digest most organic nutrients (not just fat) which can result in severe nutritional deficiencies

166
Q

Location of pancreas in abdomen?

A

completely retroperitoneal apart from TAIL, which is attached to the spleen and is intraperitoneal

167
Q

What is the head of the pancreas closely related to? What clinical relevance does this have

A

The common bile duct, meaning a carcinoma or inflammation of the head of the pancreas can block the bile duct, resulting in post-hepatic / obstructive jaundice

168
Q

The pancreas receives its main blood supply from the …

A

coeliac trunk

169
Q

coeliac trunk

A

The coeliac trunk arises directly from the aorta and divides at the coeliac axis to form the gastric arteries, the hepatic artery and the splenic artery

170
Q

How is venous drainage achieved?

A

mainly by the splenic vein which then joins the superior mesenteric vein to form the PORTAL vein

171
Q

The exocrine pancreas secretes …

A
  • HCO3- (bicarbonate)

- Digestive enzymes

172
Q

Secretions arise from which tissue of the pancreas?

A

acinar

173
Q

What are the secretions secreted into?

A

ducts which converge into the PANCREATIC DUCT which in turn joins the COMMON BILE DUCT just before it enters the duodenum at the ampulla of Vater

174
Q

What is the purpose of the sphincter of Oddi?

A

It is a separate bundle of circular muscle which regulates flow into the duodenum and may serve also to prevent mixing of bile and pancreatic juice within the pancreatic duct

175
Q

The reflux of — down the pancreatic duct will result in…?

A
  • bile

- acute inflammation, due to its detergent properties

176
Q

Which cells secrete bicarbonate?

A

Epithelial cells lining the ducts known as duct cells

177
Q

Why is bicarbonate secreted?

A
  • In order to protect the duodenal mucosa from gastric acid

- It also buffers the material entering the duodenum to a pH suitable for enzyme action

178
Q

How is bicarbonate secretion stimulated?

A
  • The release of SECRETIN hormone from the small intestine in response to the presence of acid in the duodenum stimulates the secretion of HCO3- from both the PANCREAS and LIVER and also potentiates the action of the hormone CCK
179
Q

What else does secretin do?

A

Inhibits acid secretion and gastric motility in the stomach

180
Q

How is HCO3- secreted into the duct lumen?

A

Pancreatic duct cells secrete HCO3- into the duct lumen via an apical membrane Cl-/HCO3- exchanger:

  • H+ is pumped out of the duct cell in exchange for Na+ and reacts with HCO3- in the blood resulting in the formation of carbonic acid H2CO3 which then rapidly dissociate to H2O and CO2
  • CO2 then enters the duct cell via diffusion where - catalysed by carbonic anhydrase - it reacts with H2O in the duct cell to produce carbonic acid again which then dissociates to form H+ and HCO3-
  • The H+ is pumped out again via the sodium-hydrogen exchanger and enters the pancreatic capillaries to eventually meet up in the portal vein blood with the HCO3- produced by the stomach during the generation of luminal H+
181
Q

The energy for secretion of HCO3- is provided by the…

A

Na+/H+ ATPase pumps on basolateral membrane

182
Q

What happens to Cl-?

A

Cl- normally does not accumulate within the cell because these ions are recycled into the lumen via the CTFR channel via a paracellular route (moving through spaces between cells e.g. tight junction) into the ducts due to the electrochemical gradient established by chloride movement through the CFTR

183
Q

What type of enzymes can the digestive enzymes secreted be?

A

Either active or precursors (inactive form : zymogens)

184
Q

Which cells secrete digestive enzymes?

A

gland cells at the pancreatic end of the duct system

185
Q

What stimulates the release of digestive enzymes?

A

The release of gastrointestinal hormone CCK (produced in the small intestine) in response to the presence of amino acids and fatty acids in the small intestine stimulates the secretion of digestive enzymes

186
Q

What other actions does CCK have?

A
  • potentiates the action of secretin

- stimulates the contraction of the gall bladder and relaxes the sphincter of Oddi

187
Q

The enzymes that the pancreas secretes digest…

A
  • triglycerides → fatty acids and monoglycerides
  • polysaccharides → sugar
  • proteins → amino acids
  • nuclei acids → nucleotides
188
Q

Active digestive enzymes

A
  • Alpha-amylase (Convers starch into maltose)

- Lipase (converts triglycerides → monoglycerides and FAs)

189
Q

What is the role of precursor digestive enzymes?

A

protect pancreatic cells from autodigestion

190
Q

A key step in the activation of precursor digestive enzymes is mediated by – which is embedded in the luminal plasma membranes of the intestinal epithelial cells

A

enterokinase

191
Q

What is enterokinase?

A

A proteolytic enzyme that splits off a peptide from pancreatic trypsinogen to form the active enzyme TRYPSIN

TRYPSIN

  • A proteolytic enzyme which goes onto activate other pancreatic precursor enzymes by splitting off peptide fragments
  • e.g.: chymotrypsinogen → chymotrypsin
192
Q

What inhibits pancreatic exocrine secretion? What is it produced by?

A

Somatostatin produced by the D cells in pancreatic islets (islets of Langerhans)

193
Q

2 phases of pancreatic secretion?

A

Cephalic phase

Gastric phase

194
Q

Cephalic phase

A

Initiated by the sensory experience of seeing and eating food
Primarily involves parasympathetic vagus nerve innervation of acinar cells to produce digestive enzymes

195
Q

Gastric phase

A

Initiated by the presence of food in the atomach. Primarily involves parasympathetic vagus nerve innervation of acinar cells to produce digestive enzymes

196
Q

By the end of the cephalic and gastric phases, the pancreatic ducts are filled with…

A

inactive digestive zymogens (precursors) ready for release into the intestinal lumen along with bicarbonate via the sphincter of Oddi

197
Q

The liver receives blood from 2 sources (+ %)

A
  • 25% hepatic artery

- 75% hepatic portal vein

198
Q

Within the liver, the terminal branches of the hepatic artery and portal vein empty together into…

A

sinusoids surrounding hepatic cells

199
Q

Blood leaves the liver via the — — which eventually drains into the — — —

A
  • Hepatic vein

- inferior vena cava

PHASE ONE (19 decks)

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