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MBChB - year 2 > Week 1 GI lectures > Flashcards

Week 1 GI lectures Flashcards

1
Q

What is enteropathy?

A

Damage to the small bowel

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2
Q

With what condition in young women should coeliac disease be checked for?

A

Iron deficiency

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3
Q

What is TTG?

A

Tissue Transglutaminase

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4
Q

What grains contain gluten?

A

Wheat, rye, barley and oats

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5
Q

What is necessary but not sufficient for coeliac disease?

A

DQ2/8

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6
Q

If you don’t have DQ2/8 can you have coeliac disease?

A

no

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7
Q

Are people with coeliac disease born with it?

A

No - there is a genetic disposition but to develop the disease you must be exposed to gluten (needs a trigger)

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8
Q

What are the GI symptoms of coeliac disease?

A

Diarrhea, indigestion, constipation, vomiting, chronic abdo pain, weight loss, anorexia, inadequate growth in children

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9
Q

What other symptoms (non-GI) does coeliac disease cause?

A
  • bone symptoms
  • iron deficiency
  • hepatitis
  • neuro symptoms (anxiety, depression, cerebellar ataxia, chronic fatigue, epilepsy and seizures)
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10
Q

What should be done when it is suspected that a patient has coeliac disease?

A

A duodenal biopsy

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11
Q

What are the muscular layers of the digestive tract wall?

A

Outer longitudinal and inner circular

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12
Q

How is the function of the smooth muscle in the digestive tract wall controlled?

A

The interstitial cells of Cajal

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13
Q

How do the interstitial cells of Cajal control the smooth muscle in the digestive tract?

A

They set the basal electrical rhythm (BER) - create action potential Ca2+ influx K+ efflux

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14
Q

What is the function of the intrinsic - myenteric/submucosal nerve plexus?

A

Controls all facets of the GI tract

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15
Q

What nerve supplies fibres to the myenteric/submucosal nerve plexus?

A

Sympathetic and parasympathetic fibres of the vagus nerve

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16
Q

What is the function of the extrinsic nerve plexus?

A

Modifies the intrinsic pathways

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17
Q

What situation does parasympathetic innervation predominate in?

A

Relaxed situations

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18
Q

What substance promotes excitation (contraction) in the digestive tract wall?

A

Acetyl choline

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19
Q

What substances promote relaxation in the digestive tract wall?

A

VIP and nitric oxide

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20
Q

Are the muscles of mastication under voluntary or involuntary control?

A

Voluntary (skeletal muscle)

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21
Q

What secretions occur in the mouth?

A

Saliva

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22
Q

What is the function of saliva?

A
  • Lubrication for swallowing (and speech)
  • Antibacterial - lysozyme, thiocyanate
  • Amylase (carbohydrate digestion)
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23
Q

What digestion begins in the mouth?

A

Complex carbohydrate digestion (starch - plants, and glycogen - animals)

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24
Q

How does the digestion of complex carbohydrates begin in the mouth?

A

Amylase breaks alpha1,4 linkage - hydrolyses into a mixture of maltose and glucose

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25
Q

Why can’t cellulose be broken down in humans?

A

We lack cellulase to break the beta1,4 linkage

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26
Q

What contribution does the mouth have in absorption?

A

None

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27
Q

What are the two salivary reflexes?

A
  • Simple / unconditioned salivary reflex

- Acquired/ conditioned salivary reflex

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28
Q

What is the simple/ unconditioned salivary reflex?

A

Chemo and pressure receptors in the oral cavity –> afferent nerve fibres to the salivary centre in the medulla

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29
Q

What is the acquired/ conditioned salivary reflex?

A

When saliva production is increased due to thinking about food

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30
Q

What type of saliva is produced due to the low level constant parasympathetic stimulation?

A

Continuous flow of watery saliva

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31
Q

What type of saliva does sympathetic stimulation produce?

A

Low volume thick saliva rich in mucus

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32
Q

What is the function of the oesophagus?

A

Acts as a conduit to propel bolus from the pharynx to the stomach

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33
Q

Is swallowing voluntary or involuntary?

A

It is initiated voluntarily (pharyngeal phase = 1 second) and then completed involuntarily (oesophageal phase 5-9 seconds)

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34
Q

What nerve provides the innervation for the primary peristaltic wave?

A

The vagus nerve, controlled by the swallowing centre in the medulla

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35
Q

What is the secondary peristaltic wave?

A

If food gets stuck pressure receptors in the oesophagus trigger more forceful contractions

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36
Q

What is secreted in the oesophagus?

A

Mucus for lubrication and protection

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37
Q

What digestion occurs in the oesophagus?

A

None

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38
Q

What absorption occurs in the oesophagus?

A

None

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39
Q

How is food stored in the stomach?

A

Receptive relaxation - BER

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40
Q

How are food and gastric secretions mixed in the stomach?

A

Strong antral peristalsis propels chyme against the closed pyloric sphincter

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41
Q

What factors control gastric emptying?

A

Factors in the stomach:
- Volume of chyme
- Degree of fluidity of the chyme (positive effect)
Factors in the duodenum:
- Enterogastrones, secretin and cholecystokinin (inhibitory and more powerful effect)

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42
Q

What is secreted in the stomach?

A

Gastrin, HCl, histamine, pepsinogen, somatostatin

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43
Q

What is the function of Gastrin?

A
  • Along with vagal stimulation it causes the release of HCl
  • along with vagal stimulation it promotes the secretion of pepsinogen
  • acts on ECL cells causing them to secrete histamine
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44
Q

Where and what causes gastrin to be secreted?

A

Gastrin is released by G-cells in the pyloric gland area in response to vagal stimulation and the presence of protein in the stomach

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45
Q

What cells secrete HCl and why?

A

Parietal cells secrete HCl when stimulated by gastrin and vagal stimulation

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46
Q

What cells secrete Histamine and why?

A

ECL cells (Enterochromaffin like cells) secrete histamine when stimulated by gastrin and vagal stimulation

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47
Q

What cells secrete pepsinogen and why?

A

Chief cells secrete pepsinogen when stimulated by gastrin and vagal stimulation

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48
Q

How does pepsinogen turn into pepsin?

A

In the presence of acid (autocatalysis)

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49
Q

What cells secrete somatostatin and why?

A

D cells secrete somatostatin in response to increased acid

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50
Q

What is the function of somatostatin?

A

Inhibits gastrin

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51
Q

What are the functions of HCl?

A
  • Pepsinogen to pepsin
  • Connective tissue and muscle fibre breakdown
  • denatures proteins
  • provides barrier immunity
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52
Q

What (except for HCl) do parietal cells secrete?

A

Intrinsic factor

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53
Q

What does intrinsic factor do?

A

Combines with b12 to facilitate absorption in the terminal ileum

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54
Q

What is absorbed in the stomach?

A

Alcohol and aspirin

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55
Q

What are the two phases of stimulation of gastric secretion?

A

Cephalic and gastric

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56
Q

What is the cephalic phase?

A

smelling, tasting chewing food = increased Ach release Vagus Nerve

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57
Q

What is the gastric phase?

A

Presence of proteins in stomach, distention, certain food types (caffeine alcohol)

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58
Q

What inhibits gastric secretions?

A
  • removal of proteins as the stomach empties
  • accumulation of acid
  • intestinal phase
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59
Q

Why does the accumulation of acid inhibit gastric secretions?

A

It causes D cells to release somatostatin which inhibits parietal, G and ECL cells

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60
Q

What is the intestinal phase?

A

The enterogastric reflex - enterogastrones released (CCK and secretin) which inhibit parietal cells and chief cells as well as smooth muscle contractions

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61
Q

What are the two types of motility that occur in the small intestines?

A

segmentation and migrating motility complex

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62
Q

What is segmentation?

A

Chyme is mixed with digestive enzymes and is slowly propelled through the digestive tract.

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63
Q

What type of contractions occur in segmentation?

A

Oscillating, ring like contractions of circular smooth muscle.

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64
Q

What is segmentation controlled by?

A

Controlled by BER and influenced by gastrin and the extrinsic nervous system

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65
Q

What is the Migrating Motility complex?

A

Following absorption there are between-meal short peristaltic contractions that sweep up the remnants of the meal aswell as mucosal debris and bacteria, moving towards the colon - it takes roughly 100-150 minutes to migrate from the stomach

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66
Q

What is the Migrating Motility complex regulated by?

A

The hormone motilin

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67
Q

What is secreted by the small intestines?

A

1.5L of aqueous salt and mucus.

No digestive enzymes (these come from the pancreas and liver)

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68
Q

What are the functions of the exocrine pancreas?

A
  • Production of bicarbonate

- Production of pancreatic enzymes

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69
Q

What is the function of the bicarbonate that is produced by the exocrine pancreas?

A

Neutralizes the pH of the chyme from the stomach

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70
Q

How does the exocrine pancreas know to release bicarbonate?

A

Acidity in duodenum releases Secretin from S Cells – travels in bloodstream to pancreas causing stimulate of bicarbonate from Pancreatic Duct Cells.

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71
Q

What triggers the release of pancreatic enzymes?

A

Fat>Protein products in duodenum causes release of Cholecystokinin (CCK) –travels in bloodstream stimulating release of pancreatic enzymes from Pancreatic Acinar cells

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72
Q

How do the pancreatic enzymes aid digestion?

A
  • Proteins - pancreatic proteolytic enzymes break proteins into small peptide chains and amino acids
  • Fats - Pancreatic lipase hydrolyses dietary triglycerides into monoglycerides and free fatty acids
  • carbohydrates - pancreatic amylase breaks polysaccharides into disaccharides
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73
Q

What is the liver responsible for the metabolism and detoxification of?

A
  • Alcohol
  • Drugs
  • Steroidal hormones
  • Non-steroidal hormones
  • Insulin
  • Growth hormones
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74
Q

What does the liver produce and regulate?

A
  • Triglycerides
  • Phospholipids
  • Lipoproteins
  • Cholesterol
  • Acetyl-CoA
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75
Q

What vitamins does the liver store?

A 
A
D
E
K
B12
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76
Q

What happens if triglycerides aggregate together?

A

They form large fat droplets in the chyme and can avoid the action of pancreatic lipase

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77
Q

Where is bile secreted?

A

The liver

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78
Q

Where is bile stored?

A

The gallbladder

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79
Q

What do the bile salts do to the large fat droplets in the chyme?

A

Convert them into lipid emulsion. The smaller fat droplets now repel each other

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80
Q

What does lecithin support the production of?

A

Water soluble micelles which allows fats to be transported to the small intestine mucosa for absorption

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81
Q

What is bile secretion controlled by?

A
  • chemicals
  • hormones
  • neural
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82
Q

How do chemicals influence bile secretion?

A

Bile salts are choleretic. After they participate in fat digestion and absorption, they are reabsorbed into enterohepatic circulation and stimulate more bile secretion

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83
Q

What does choleretic mean?

A

Choleretics are substances that increase the volume of secretion of bile from the liver as well as the amount of solids secreted.

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84
Q

What hormones are involved in the control of bile secretion?

A

Secretin

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85
Q

How is neural control involved in the control of bile secretion?

A

The vagal nerve (cephalic phase)

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86
Q

What happens in the small intestine in relation to FAT digestion?

A

They are now absorbable monoglycerides and free fatty acids

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87
Q

What happens in the small intestine in relation to CARBOHYDRATE digestion?

A

They are reduced to disaccharides (and some monosaccharides)

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88
Q

What happens in the small intestine in relation to PROTEIN digestion?

A

They have been reduced to small peptide fragments and amino acids but this is still NOT COMPLETE

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89
Q

What is the brush border?

A

Actin stiffened hair like projections on the epithelial surface of the intestinal mucosa

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90
Q

What are disaccharidases?

A

Maltase, sucrase, lactase - they complete carbohydrate digestion by hydrolysing disaccharides into monosaccharides

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91
Q

What are examples of monosaccharides?

A

Glucose
Galactose
Fructose

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92
Q

What is the function of aminopeptidases?

A

They change the remaining peptide fragments into their amino acid constituents

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93
Q

How is the small intestine adapted for absorption?

A

The small intestine is highly adapted for absorption (the duodenum and jejunum perform most absorption)
There is multiple folds to increase surface area, villi and microvilli also increase surface area

94
Q

What two substances absorption is regulated?

A

Calcium and iron

95
Q

What is found at the bottom of the villi?

A

Crypts of Lieberkühn

96
Q

How much of carbs fats and proteins ingested are absorbed?

A

All ingested are absorbed, nothing is wasted

97
Q

How are fats absorbed?

A
  • Monoglycerides and free fatty acids are brought to the intestinal mucosa by micelle
  • these then cross the lipid bilayer by active diffusion
  • Triglycerides aggregate and coated with lipoprotein to form Chylomicrons
  • Chylomicrons cannot cross basement membrane of blood capillaries so enter circulation via lymphatic vessels (central lacteals)
98
Q

How are carbohydrates absorbed?

A
  • Now in monosaccharide form, glucose and galactose are absorbed into epithelial cell by means of Na2+ and energy dependent active transport (Sodium and Glucose co-transporter – SGLT)
  • Fructose enters blood by passive facilitated diffusion via GLUT-5
  • Monosaccharides enter interstitial fluid via protein facilitated glucose transporter GLUT-2
  • Then all enter blood by simple diffusion
99
Q

How are proteins absorbed?

A
  • Now in simplest form, amino acids are absorbed in similar way to glucose and galactose via amino acid symporters. They enter epithelial cell by means of Na2+ and energy dependent active transport
  • Glucose, galactose and amino acids all get a “free ride” on energy expended for Sodium transport
  • Many amino acids have specific symporters
  • Remaining small peptides enter cell via Na/H symporter and are broken down by intracellular peptidases
  • Amino acids directly enter blood stream by facilitated diffusion
100
Q

How are water soluble vitamins absorbed?

A

Absorbed with water

101
Q

How are fat soluble vitamins absorbed?

A

Carried in micelles and absorbed with end products of fat digestion

102
Q

How is vitamin B12 absorbed?

A

It binds with intrinsic factor to form a complex which is resistant to breakdown by gastric secretion. It is absorbed in the terminal ileum by pinocytosis

103
Q

What is pinocytosis?

A

the ingestion of liquid into a cell by the budding of small vesicles from the cell membrane

104
Q

How is iron absorbed?

A

By duodenal enterocytes. Iron is absorbed in its ferrous form and its absorption is improved by vitamin C

105
Q

How is iron stored in the body?

A

Some is used immediately, bound to transferrin for transport in the blood and the remaining iron is stored in cells as ferritin

106
Q

How is calcium absorbed?

A

2/3 absorbed by activated vitamin D stimulated active transport after activated by PTH

107
Q

What happens to calcium that is not absorbed?

A

Passes out in faeces

108
Q

What is the function of motility in the large intestines?

A

Primarily for storage and drying. Haustral contractions cause slow shuffle chyme residue forward (once every 30 minutes)

109
Q

What causes the haustral contractions in the large intestines?

A

Autonomous rhythmicity of colonic mucosal cells

110
Q

What is secreted in the large intestine?

A

Alkaline mucous solution

111
Q

What is the function of the alkaline secretions of the large intestine?

A

They have an entirely protective function

112
Q

What digestion takes place in the large intestine?

A

NONE

113
Q

What absorption takes place in the large intestine?

A

Some salt and water absorption but not as much as in the small intestion

114
Q

What type of absorption is sodium absorbed by?

A

Active absorption

115
Q

How is chloride absorbed?

A

Chloride follows sodium passively down an electrical gradient

116
Q

Where does the common bile duct pass?

A

Behind the duodenum

Through the head of the pancreas

117
Q

Where does the common bile duct join into?

A

The main pancreatic duct

118
Q

Where does the main pancreatic duct open into?

A

The 2nd part of the duodenum (the ampulla of vater)

119
Q

How is the flow of bile regulated?

A

By the sphincter of Oddi (smooth muscle)

120
Q

How much bile can the gallbladder store?

A

30-50ml

121
Q

What happens to bile in the gallbladder?

A

It gets concentrated (H20 and salts are reabsorbed)

122
Q

Where is the gallbladder located?

A

It lies in the GB fossa on the inferior surface of the right lobe of the liver

123
Q

Where is it possible to palpate the fundus of the gallbladder?

A

Between the lateral border of recuts abdominus and the costal margin (9th costal cartilage)

124
Q

What are the components of bile?

A 
Conjugated bilirubin
Bile acids
cholesterol 
water
electrolytes
phospholipids
125
Q

What is bilirubin?

A

A product of the breakdown of old red blood cells.

126
Q

Is unconjugated bilirubin soluble or insoluble?

A

Insoluble in water

127
Q

How is unconjugated bilirubin transported in the blood?

A

Bound to albumin as it is insoluble in water

128
Q

What is the haem from haemoglobin broken down into?

A

Biliverdin

129
Q

Is conjugated bilirubin soluble or insoluble?

A

Soluble in water

130
Q

How are primary bile acids made?

A

Cholesterol derivatives are conjugated with the amino acids glycine and taurine

131
Q

How are primary bile acids converted to secondary bile acids?

A

By bacterial action in the gut

132
Q

What does amphipathic mean?

A

They have both hydrophilic and hydrophobic (lipophilic) properties

133
Q

What does vagal stimulation do to the gallbladder?

A

It promotes gallbladder contraction

134
Q

Where is CCK released from?

A

The duodenum in response to presence of luminal fat

135
Q

What effect does CCK have on the gallbladder?

A

Contraction of the gallbladder and relaxation of the sphincter of Oddi which results in the release of the contents of the gallbladder into the duodenum

136
Q

What mediates the closure of the sphincter of Oddi and the relaxation of the gallbladder?

A

Sympathetic nerves and the gut hormones VIP and somatostatin

137
Q

What does VIP stand for?

A

Vasoactive intestinal polypeptide

138
Q

Where do 95% of bile acids go?

A

They recirculate via enterohepatic circulation meaning they go round and round this circuit

139
Q

What is the synthesis of new bile acids in the liver compensating for?

A

Faecal loss

140
Q

What happens if the bile acids aren’t absorbed in the terminal ileum?

A

Then they can reach the large intestine and cause “bile salt diarrhoea”`

141
Q

What causes bile salt diarrhoea?

A

If the bile acids aren’t reabsorbed in the terminal ileum and they reach the large intestine (/colon)

142
Q

What are the 5Fs that put someone at risk for getting gallstones?

A
  • Female
  • Fair
  • Fertile
  • Forty
  • Fat
143
Q

What risk factors are there for gallstones?

A
  • 5Fs
  • Increasing age
  • Family history
  • Caucasian race
  • Low fibre diet
  • IBD
144
Q

What are the three main types of gallstone?

A

Cholesterol stone
Bile pigment stone
Mixed stones

145
Q

How can cholesterol stones be identified?

A

Usually solitary, oval and large (up to 3cm)

146
Q

How can bile pigment stones be identified?

A

Multiple irregular stones, hard.

associated with chronic haemolysis (e.g. sickle cell)

147
Q

How can mixed stones be identified?

A

They are the most common stone type (80%) of stones. There will be multiple, multi-faceted stones with a laminated structure with layers of cholesterol, bile pigment and calcium salts

148
Q

What are the three main events that lead to gallstones?

A
  • Cholesterol supersaturation
  • Biliary stasis
  • increased secretion of bilirubin
149
Q

What is cholesterol supersaturation?

A

High levels of cholesterol that lead to supersaturation. This typically occurs when oestrogen levels are high or when bile acid levels are low

150
Q

When could oestrogen levels be high?

A

Obesity, pregnancy, OCP, liver disease

151
Q

When can bile acid levels be low?

A

Following small bowel resection or in active Crohns disease when enterohepatic circulation is ineffective

152
Q

When can biliary stasis occur?

A

During periods of fasting or starvation - can be observed during prolonged total parenteral nutrition

153
Q

When can the secretion of bilirubin be increased?

A

When there is increased breakdown of RBCs or when there is failure of hepatic conjugation

154
Q

When does biliary colic occur?

A

When a stone is impacted in the gallbladder - usually the neck or Hartmann’s pouch

155
Q

What are the symptoms of biliary colic?

A

Pain in the epigastrium/RUQ/ through to back which is usually provoked by eating (due to contraction of the gallbladder).
Vomiting is common

156
Q

Does biliary colic cause jaundice?

A

NO

157
Q

What do the LFTs look like in biliary colic?

A

Often normal

158
Q

What is the treatment for recurring biliary colic?

A

Cholecystectomy

159
Q

What is acute cholecystitis?

A

When an impacted stone in the gallbladder leads to oedema/inflammation and development of infection within the gallbladder wall

160
Q

What are the symptoms of acute cholecystitis?

A

Pain, nausea, vomiting, fever and abdominal tenderness

161
Q

What is Murphy’s sign?

A

Extreme tenderness over the fundus of the gallbladder which is elicited by palpating the fingers up towards the costal margin as the patient takes a deep inhalation

162
Q

What are the test results of acute cholecystitis?

A

Raised inflammatory markers
sometimes abnormal LFTS
+/- jaundice

163
Q

How is acute cholecystitis treated?

A

Antibiotics
analgesia
cholecystectomy

164
Q

What is empyema?

A

A severe infection

165
Q

What is AST/ALT?

A

The hepatocyte enzymes (AST is also found in cardiac muscle cells)

166
Q

What is ALP/GGP?

A

Alkaline phosphatase/ GGP are enzymes associated with bile duct cells, but there is an isoenzyme of ALP produced in bones

167
Q

If all of the results from a LFT are raised what does this suggest?

A

obstructive/cholestatic pathology

168
Q

If all LFT results are raised but normal ALP and GGT what does this suggest?

A

Hepatic pathology

169
Q

What are the signs/symptoms of obstructive jaundice?

A
  • Pale stools
  • Dark urine
  • Yellow sclerae
  • Pruritis - itchy skin
  • hepatomegaly
  • abdominal tenderness/palpable gallbladder
170
Q

why in obstructive jaundice would a patient have pale stools and dark urine?

A
  • Pale stools – fat isn’t getting absorbed as the bile isn’t getting to the right place
  • Dark urine – bilirubin getting peed out
171
Q

What are the three ways in which biliary obstruction can occur?

A
  • extrinsic compression
  • intramural obstruction
  • intraluminar obstruction
172
Q

What is the main way of imaging for biliary obstruction?

A

Transabdominal ultrasounds

173
Q

What is extrinsic compression?

A

Something on the outside squeezing in

174
Q

What is intramural obstruction?

A

something in the tube causing the lumen to be smaller

175
Q

What is intraluminar obstruction?

A

something in the lumen blocking it

176
Q

What is MRCP?

A

Magnetic resonance cholangiopancreaticogram

177
Q

What is MRCP good for?

A

it is good for showing the biliary tree and pancreatic ducts

178
Q

What can cause extrinsic compression?

A

Tumours, inflammation, mirizzi syndrome

179
Q

What are intramural causes of biliary obstruction?

A

Tumours, inflammation, scarring/fibrosis

180
Q

What are intraluminar causes of biliary obstruction?

A

stones or sludge

181
Q

What causes a duodenal ulcer?

A

Acid that came out of the stomach and eroded the surface of the duodenum

182
Q

What are risk factors for a duodenal ulcer?

A

Male
Smokers
Stress considered to increase risk
Associated with increased acid secretion in the stomach

183
Q

Where does the vagus nerve run to innervate the stomach?

A

Down either side of the oesophagus

184
Q

What stimulates parietal cells to produce acid during the cephalic phase?

A

Vagal stimulation

185
Q

How is acid regulated in the gastric phase?

A

Negative feedback - when there is too much acid the G cells stop producing gastrin

186
Q

What is the aim of treatment for duodenal ulcers?

A

Reducing acid production

187
Q

How are duodenal ulcers treated medically?

A

H2 antagonists

PPIs

188
Q

How are duodenal ulcers treated surgically?

A

Vagotomy
subtotal gastrectomy
antrectomy

189
Q

What is a vagotomy?

A

The vagal nerves innervating the stomach are cut so they can’t stimulate acid production

190
Q

What is a subtotal gastrectomy?

A

Parts of the stomach where the G cells are is removed

191
Q

What is H.pylori?

A

It is a bacteria with an unusually high urease level allowing it to break down urea, releasing ammonia and CO2 meaning when it releases this neutralises the acid surrounding it allowing it to survive in the acidic environment of the stomach

192
Q

Why does H. Pylori infection cause duodenal ulcers?

A

When H. pylori breaks down urea and affects the pH of the acid in the stomach this causes the G cells to produce more gastrin which then causes excess acid to be secreted

193
Q

What is the first line of treatment of H. pylori infection?

A

Omeprazole, metronidazole and amoxycillin

194
Q

What is the second line of treatment of H. pylori infection?

A

Omeprazole, clarithromycin and amoxycillin

195
Q

How do you treat H. Pylori infection if a patient is allergic to penicillin?

A

Omeprazole, metronidazole and clarithromycin

196
Q

What does gastric cancer present with?

A

anorexia
weight loss
anaemia

197
Q

What cells can be found in intestinal metaplasia that aren’t usually there?

A

Goblet cells

198
Q

Is there an association between H. pylori and acid reflux?

A

NO

199
Q

What are the parietal and chief cell densities like in patients with H. Pylori infection?

A

There is reduced densities of parietal and chief cells

200
Q

Why is there reduced densities of parietal and chief cells in H. Pylori infections?

A

H. pylori gastritis produces atrophy of gastric mucosa

201
Q

What supplies oxygenated blood to the liver? (30-40%)

A

The hepatic artery

202
Q

What supplies the remaining 60-70% of the blood to the liver?(deoxygenated)

A

The portal vein

203
Q

Where does the portal vein enter the liver?

A

The porta hepatis

204
Q

What makes up the portal triad?

A

A branch of the portal vein, a branch of the hepatic artery and a bile duct

205
Q

What takes all of the blood out of the liver?

A

The hepatic vein

206
Q

What is the blood in the portal vein rich in?

A

Food products from the gut and broken down RBCs from the spleen

207
Q

What is the structure of the portal vein like?

A

It is wide and thin walled

208
Q

How are hepatocytes arranged?

A

They lie in plates and cords so that blood can pass through them

209
Q

Where is material exchanged with blood in hepatocytes?

A

At the sinusoidal surface

210
Q

What are the three types of surface in hepatocytes?

A

Sinusoidal
Intercellular
canalicular

211
Q

When would AST/ALT be raised?

A

In hepatocyte damage

212
Q

When would bilirubin be increased?

A

In cholestasis

213
Q

When would Alk Phos be raised?

A

In cholestasis

214
Q

When would albumin levels be lowered?

A

In long term impaired synthesis

215
Q

When would PTT be lowered?

A

In short term impaired synthesis

216
Q

What is cholestasis?

A

Bile stasis caused by impaired bile synthesis or secretion or obstruction to flow

217
Q

What is PTT?

A

Prothrombin time

218
Q

What is cirrhosis?

A

A diffuse process with fibrosis and nodule formation

219
Q

What does cirrhosis indicate?

A

End stage liver disease

220
Q

What is cirrhosis the result of?

A

Chronic inflammation over many years

221
Q

What causes the chronic inflammation that causes cirrhosis?

A

Persistence over many years of an injury causing agent.
The body’s natural response to this is fibrous scarring and hepatocyte regeneration. This is eventually irreversible and cirrhosis develops
(up to a point it may be reversible)

222
Q

What happens if you take away 40-60% of the liver?

A

It would regenerate in 6-8 weeks

223
Q

What are causes of cirrhosis?

A

Alcohol
Hepatitis
biliary disease
haemochromatosis

224
Q

What are causes of hepatitis (and therefore cirrhosis)

A 
Alcohol
metabolic disease
viral infections
auto-immune disease
biliary disease
drugs/toxins
cryptogenic
225
Q

What are complications of cirrhosis?

A

Portal hypertension
liver failure
Hepatocellular (liver) cancer

226
Q

what is portal hypertension?

A

Cirrhosis leads to increased resistance to blood flow through the liver –> increased pressure in portal circulation

227
Q

What does portal hypertension lead to?

A
  • Portal-systemic shunts and varices
  • Ascites
  • Splenomegaly
228
Q

What are some effects of liver disease?

A
  • Altered intermediary metabolism e.g. impaired synthesis of urea and glycogen
  • Reduced albumin & other transport proteins
  • Coagulation disorders
  • Reduced complement so prone to infection
  • Jaundice
  • Altered xenobiotic metabolism e.g. drugs
  • Circulatory and endocrine disturbances
229
Q

What secretory proteins can have their production impaired due to liver disease?

A
  • Albumin
  • Transport proteins
  • coagulation and fibrinolysis proteins
  • complement
  • protease inhibitors
230
Q

What are the LFTs like in prehepatic jaundice?

A
  • Total bil = Slightly raised
  • Conj. bil = normal
  • Unconj bil = Slightly raised
  • Urobilinogen = normal / slightly raised
  • Urine colour = normal
  • Stool colour = Normal
  • Alk Phos = normal
  • ALT and AST = normal
231
Q

What are the LFTs like in hepatic jaundice?

A
  • Total bil = Slightly raised
  • Conj. bil = Slightly raised
  • Unconj bil = Slightly raised
  • Urobilinogen = Slightly raised
  • Urine colour = dark
  • Stool colour = normal
  • Alk Phos = Slightly raised
  • ALT and AST = High
232
Q

What are the LFTs like in post - hepatic jaundice?

A
  • Total bil = high
  • Conj. bil = high
  • Unconj bil = normal
  • Urobilinogen = slightly lowered
  • Urine colour = Dark
  • Stool colour = Pale
  • Alk Phos = High
  • ALT and AST = Slightly raised

MBChB - year 2 (25 decks)

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