Liver, Biliary Tree and Pancreas Flashcards
1
Q
Into where does the stomach empty chyme?
A
The duodenum
2
Q
What are the key properties of chyme?
A
- Acidic
- Hypertonic
- Partly digested
3
Q
How is the acidic nature of chyme corrected?
A
By HCO3- secreted from the pancreas, liver, and duodenal mucosa
4
Q
When is HCO3- produced?
A
During the production of gastric acid
5
Q
How is the hypertonicity of chyme corrected?
A
Osmotic movement of water into the duodenum across its wall
6
Q
How is digestion of chyme completed?
A
- By enzymes from the pancreas and duodenal mucosa
- With bile acids from the liver
7
Q
What components is bile made up of?
A
- Bile acid dependant
- Bile acid independant
8
Q
What is the bile acid dependant component of bile secreted by?
A
Cells lining the canaliculi
9
Q
What does the bile acid dependant component of bile consist of?
A
- Bile acids (salts)
- Cholesterol
- Bile pigments
10
Q
Name the two primary bile salts
A
- Cholic acid
- Chenodeoxycholic acid
11
Q
What happens to bile salts in bile?
A
They are conjugated to amino acids and travel as micelles in the bile
12
Q
Where do bile salts play a major role?
A
In the digestion and absorption of fat
13
Q
What is the name of the majority bile pigment?
A
Bilirubin
14
Q
What secretes the bile acid independent component of bile?
A
Cells lining the intra-hepatic bile ducts
15
Q
What does the bile acid independant component of bile consist of?
A
Alkaline juice (HCO3-) like that form pancreatic duct cells
16
Q
Label this diagram
A
- A - Liver lobules
- B - Interlobular portal triads
- C - Central veins
- D - Hepatocytes
- E - Sinusoids
17
Q
What supports the livers function?
A
Its microscopic structure
18
Q
What is the basic functional unit of the liver?
A
A lobule surrounding a central vein
19
Q
What does the central vein of a liver lobule do?
A
Drains blood from the liver to the systemic veins
20
Q
Where does blood entering the liver lobule come from?
A
The hepatic portal vein and hepatic arteries
21
Q
Where does blood entering the lobule from the hepatic portal vein and the hepatic arteries enter the vessels?
A
At the periphery of the lobule
22
Q
How does blood entering the lobule via the hepatic portal vein and hepatic artery reach the central vein?
A
It flows through sinusoids
23
Q
What lines sinusoids?
A
Hepatocytes
24
Q
Where is bile formed?
A
Canaliculi
25
What happens to bile once it has been produced in canaliculi?
It flows towards the periphery into bile ducts
26
Label this diagram
* A - Deep lymphatic duct receiving lymph from perisinusoidal space
* B - Blood flowing in sinusoids from interlobular *(hepatic)* artery and *(portal)* vein
* C - Perisinusoidal spaces *(of Disse)*
* D - Peribiliary arterial plexus
* E - **Hepatocytes**
* F - **Central vein**
* G - Bile flowing from hepatocytes into bile canaliculi, to interlobular biliary ducts, and then to bile ducts in the extrahepatic portal triad
* H - **Bile canaliculi**
* I - **Interlobular portal triad**
* Ii - Hepatic portal vein
* Iii - Hepatic artery
* Iiii - Biliary duct
27
What are the main functions of hepatocytes?
* Produce bile
* Detoxify blood
28
What is the main function of the central vein?
Transports clean blood to hepatic vein
29
What does the duodenum do in response to gastric emptying?
Secretes cholecystokinin (CCK)
30
What effect does CCK have?
It stimulates the contraction of the gall bladder
31
What is the effect of the contraction of the gall bladder?
It ejects concentrated bile acids together with enzymes from the pancreas
32
What organs release alkali for digestion?
* Pancreas
* Liver
33
What is alkali released from the pancreas and liver in response to?
Secretin
34
What are bile acids released through?
The Ampulla of Vater
35
What is the role of bile acids?
Aid with the digestion and absorption of fats
36
Where do bile acids go once they have been released?
They continue to the terminal ileum
37
What happens to bile acids in the terminal ileum?
They are actively absorbed by the epithelium
38
What happens once bile acids have been absorbed by the ileum epithelium?
Venous return from the gut enters the **hepatic portal blood**
39
What happens when bile acids have reached the hepatic portal blood?
Hepatocytes actively take up bile acids, and re-secrete them into the Canaliculi
40
What is the ultimate fate of most bile acids?
* Most are recovered
* Some are unconjucated by the gut bacteria and lost
41
How is the loss of unconjugated bile acids dealt with?
Hepatocytes subsequently replace them
42
What happens to bile acids in between meals?
They return to the liver
43
When are bile acids secreted by canaliculi cell walls?
A long time before they are next needed
44
What happens to bile acids that are secreted before they are needed?
They are stored in the gall bladder
45
How is the volume of bile acids that needs to be stored reduced?
Bile acids are concentrated by the transport of salt and water across the gall bladder epithelium
46
What is the clinical importance of the concentration process of bile acids?
It increases the risk of precipitation, leading to **gall stones**
47
What are the consequences of gallstones?
**Often asymptomatic**, but can cause very painful **biliary colic**
48
What causes biliary colic?
The movement of gallstones into the neck of the gall bladder of biliary tree
49
What often follows biliary colic?
* Inflammation
* Infection of the gall bladder
50
What is inflammation of the gall bladder called?
Cholecystitis
51
When may pain from gallstones be worse?
After eating
52
Why may pain from gallstones be made worse after eating?
The secretion of CCK will cause the gall bladder to contract
53
What does the exocrine pancreas secrete?
* Alkaline juice *(HCO3-)*
* Enzymes
54
What enzymes does the exocrine pancreas secrete?
* Proteases
* Trypsin*(ogen)*
* Chymotrypsin
* Elastase
* Carboxypeptidase
* Amylases
* Lipases
55
What kind of organ is the exocrine pancreas?
A gland
56
What are the main components of the exocrine pancreas?
* Acini
* Ducts
57
What do the pancreatic acini do?
Secrete enzymes
58
In what form do the pancreatic acini secrete enzymes?
Mostly as inactive precursors
59
What happens to the enzymes being secreted from the pancreatic acini?
Packaged into condensing vacuoles, forming **zymogen granules**
60
What happens to zymogen granules?
They are secreted by exocytosis
61
Where are zymogen granules activated?
In the intestine
62
How are zymogen granules activated?
By enzymatic cleavage
63
What do the pancreatic ducts do?
Secrete alkaline juice
64
Why is HCO3- present in the blood at elevated concentrations?
Due to gastric acid secretion
65
How does the cellular mechanism of secretion of HCO3- in the pancreatic duct differ from in other cells?
It doesn't
ha ha trick question i got u
66
What is the mechanism of secretion of HCO3-?
* Na-K-ATPase sets up a Na+ concentration gradient
* Hydrogen ions are exported from the duct cell into ECF using the Na+ concentration gradient
* H+ ions combine with HCO3- to from H2O and CO2, which are taken up into the cell
* H2O and CO2 reform H+ and HCO3- inside the cell
* HCO3- is exported into the duct lumen
* H+ ion is recycled, 'going round in a circle' to carry more HCO3- from the ECF to the lumen
67
What is duct secretion of HCO3- stimulated by?
Secretin
68
What releases secretin?
Jejunal cells
69
What is secretin released from jejunal cells in response to?
Low pH
70
What facilitates secretin's action?
Cholecystokinin (CCK)
71
What are the two sources of pancreatic secretion?
1. Acinar
2. Duct
72
What is pancreatic acinar secretion stimulated by?
Cholecystokinin (CCK)
73
Where is CCK released from?
Duodenal APUD cells
74
What is CCK secretion and thus pancreatic acinar secretion stimulated by?
* Hypertonicity
* Fats
75
What stimulates pancreatic duct secretion?
Secretin
76
What is secretin release and thus pancreatic duct secretions stimulated in by?
Low pH
77
What is CCK secreted by the duodenum in reponse to?
Gastric emptying
78
What does CCK stimulate?
Contraction of the gall bladder muscle
79
What is the result of the contraction of the gall bladder muscle?
Biliary secretion
80
Are fats soluble in water?
No, *relatively insoluble*
81
What is the result of fats being relatively insoluble in water?
They tend to aggregate into large globules
82
What is the result of the aggregation of fats into large globules in water?
It prevents the effective action of digestive enzymes
83
What exacerbates the formation of large globules of fat in the stomach?
Acid
84
What do bile acids enable in the duodenum?
*With regards to fats*
Enable fats to be incorporated into small micelles
85
How big are the micelles formed with the aid of bile acids in the duodenum?
4-6nm
86
Describe the structure of the micelles that fats are incorporated into in the duodenum?
* Fats in the middle
* Polar components of the bile acids on the outside
87
What is the purpose of the bile acid-fat micelles?
* Generate a high surface area for the action of lipases
* Carry products into the 'unstirred layer'
88
What do lipases do to the bile acid-fat micelle?
Cleave the fatty acids from glycerol
89
Where is the 'unstirred layer' found?
Immediately next to the mucosa
90
What happens at the 'unstirred layer'?
Fatty acids can be released to slowly diffuse into the epithelial cells
91
What happens to fatty acids once inside the epithelial cells?
They are reconstituted into triacylglycerols, and re-expelled as chylomicrons
92
What are chylomicrons?
Structured small particles made up of lipids covered in phospholipids
93
What do chylomicrons do?
Facilitate the transport of fat in the lymphatic system from the gut to systemic veins
94
What is steatorrheoa?
Fatty faeces
95
What causes steatorrheoa?
Bile acids or pancreatic enzymes not being secreted in adequate amounts, resulting in fat in the faeces
96
What are the symptoms of steatorrheoa?
Faeces that-
* Pale
* Float
* Smell foul
97
What are bile pigments?
Excretory products
98
What is the most common bile pigment?
Bilirubin
99
When is bilirubin produced?
As a product of haemoglobin breakdown
100
What happens to bilirubin after production?
It is conjugated in the liver and secreted in the bile to be excreted in faeces
101
What happens if bilirubin cannot be excreted?
It accumulates in the blood, giving the condition known as **jaundice**
102
What is inevitable when ingesting food and water?
We also risk ingesting toxins
103
What toxins are we at risk of ingesting when eating and drinking?
* Chemical
* Bacteria
* Viruses
* Protozoa
* Nematodes
* Cestodes
* Trematodes
104
What are nematodes?
Roundworms
105
What are cestodes?
Tapeworms
106
What are trematodes?
Flukes
107
How can the defence mechanisms that the GI tract has to deal with toxins be subdivided?
* Innate
* Adaptive
108
What are the types of innate immunity?
* Physical
* Cellular
109
What physical innate defences are present in the GI tract to deal with toxins?
* Sight
* Smell
* Saliva
* Stomach acid
* Small intestine secretions
* Colonic mucus
* Anaerobic environment
* Peristalsis
* Segmentation
110
How does the sight and smell of food act as a defence?
If food looks or smells bad, you don't eat it
111
How does memory act as a defence?
If food tastes bad, you don't eat it next time
112
What pH is saliva?
7.0
113
What does saliva contain?
* Lysozyme
* Lactoperoxidase
* Complement
* IgA
* Polymorphs
114
How does saliva act as a defence?
It washes toxins down into the stomach
115
How does stomach acid act as a defence?
Low pH kills the majority of bacteria and viruses
116
What are the small intestine secretions?
* Bile
* Proteolytic enzymes
117
How do the small intestine secretions act as a defence?
* Means there is a lack of nutrients
* Cause the shredding of epithelial cells
118
What is the purpose of the colonic mucus?
Protects the colonic epithelium from it's contents
119
What areas in the GI tract have an anaerobic environment?
* Small bowel
* Colon
120
What is the normal intestinal transit time?
12-18hrs
121
What happens if peristalsis is slowed?
Gut infections are prolonged
122
Give an example of an infection that can be prolonged by slowed peristalsis?
Shigellosis
123
What cellular innate defences are present in the GI tract to deal with toxins?
* Neutrophils
* Macrophages
* Natural killer cells
* Tissue mast cells
* Eosinophils
124
What are macrophages called in the liver?
Kupffer cells
125
What do NK cells do?
Kill virus infected cells
126
When are eosinophils recruited?
In parasitic infections
127
Where does all venous blood from the GI tract pass before returning to the systemic circulation?
Through the liver - *the hepatic portal system*
128
What are Kupffer cells?
Specialised macrophages in the liver
129
Draw a diagram illustrating blood and bile flow through the hepatic portal system
130
What adaptive defences does the GI tract have to protect against toxins?
* B lymphocytes
* T lymphocytes
* Lymphatic tissues
131
What do B lymphocytes do?
Produce antibodies, *including IgA and IgE*
132
What are IgA and IgE particularly effective against?
Extracellular microbes
133
What are T lymphocytes directed against?
Intracellular organisms
134
What is Mucosal Associated Lymphoid Tissue (MALT) in the GI tract called?
Gut Associated Lymphoid Tissue (GALT)
135
How is GALT distributed?
* Diffusely distributed
* Nodular in three locations-
* Tonsils
* Peyer's patches
* Appendix
136
What do Peyer's patches look like?
137
What is reduced salivary flow known as?
Xerostomia
138
What can cause xerostomia?
* Severe illness
* Dehydration
139
What does xerostomia lead to?
Microbial overgrowth in the mouth and dental caries
140
What can microbial overgrowth in the mouth and dental caries lead to?
Parotitis
141
What is parotitis?
Salivary glands infections
142
What microbe causes parotitis?
Staphylococcus aureus
143
What is achlorhydria?
Absent or low gastric acid production
144
What can cause achlorhydria?
* Pernicious anaemia
* Drugs such as H2 antagonists
* PPIs
145
What are patients with achlorhydria more susceptible to?
Shigellosis, cholera, and salmonella infections
146
What is the clinical relevance of patients taking a protein pump inhibitor?
In a hospital environment, they are at increased risk of acquired Clostridium difficile
147
Give 3 examples of resistant organisms?
1. Mycobacterium tuberculosis
2. Some enteroviruses
3. Helicobacter Pylori
148
What is mycobacterium tuberculosis resistant to?
Gastric acid
149
What kind of bacterium is mycobacterium tuberculosis?
Acid and alcohol fast bacterium
150
Give 3 examples of enteroviruses that are resistant?
1. Hepatitis A
2. Polio
3. Coxsackle
151
What are some enteroviruses resistant to?
Gastric acid
152
Why is Helicobacter Pylori resistant?
It produces urease, which acts on urea to produce a protective cloud of ammonia
153
What do mast cell granules contain?
Histamine
154
Which gut infections recruit mast cells?
Those that activate complement
155
What does the recruitment of mast cells lead to?
The release of histamine
156
What does the release of histamine cause?
Vasodilation and increased capillary permeability, *which can give massive fluid loss*
157
How much fluid is lost per hour in cholera?
May get losses of 1litre/hr
158
What is the mortality of cholera if untreated?
60%
159
What is the clinical significace of GALT?
* Tonsillitis
* Ileocaecal lymphatic tissue
* Appendicitis
160
What conditions are related to ileocaecal lymphatic tissue?
* Mesenteric adenitis
* Typhoid fever
161
What is mesenteric adenitis a common cause of?
Right iliac fossa pain in children
162
What can mesenteric adenitis be easily mistaken for?
Appendicitis
163
What is mesenteric adenitis mostly caused by?
Adenovrius or coxsackie virus
164
What does typhoid fever cause?
## Footnote
*With respect to Peyer's patches*
Inflamed Peyer's patches in the terminal ileum
165
What is the potential outcome of inflamed Peyer's patches in typhoid fever?
They can perforate and kill patients
166
What do many causes of appendicitis arise from?
Lymphoid hyperplasia at the appendix base
167
Why can lymphoid hyperplasia at the appendix base lead to appendicitis?
It leads to obstructed outflow.
## Footnote
*Stasis leads to infection*
168
When is purulent appendictis more common?
During epidemics of chickenpox in children
169
How may the appendix be obstructed, *other than lymphoid hyperplasia*?
* By a faecolith
* By a worm
170
What is a faecolith?
Calcified faecal matter
171
How can faecoliths be visualised?
On an X-ray
172
What to the GI tract's defence mechanism require?
The GI tract itself to have an intract blood supply
173
What can intestinal or hepatic ischaemia be due to?
* Arterial disease
* Systemic hypertension
* Intestinal venous thrombosis
174
What can intestinal or hepatic ischamia lead to?
* Overwhelming sepsis
* Rapid death *(within hours)*
175
What does liver failure increase susceptibility to?
* Infections
* Toxins
* Drugs
* Hormones
176
What chemical will be present in increased amounts in the blood in liver failure?
Ammonia
177
Why is ammonia present in the blood in increased amounts in liver failure?
Due to failure of the urea cycle
178
What is ammonia produced by?
* Colonic bacteria
* Deamination of amino acids
179
What is the clinical significance of an increase blood level of ammonia?
Can cause hepatic encephalopathy
180
What are the causes of liver failure?
* Industrial solvents
* Drugs
* Viral hepatitis
* Mushroom poisioning
* Alcohol
181
What is the main cause of liver failure worldwide?
Viral hepatitis
182
What is the main cause of liver failure in the UK?
Alcohol
183
What is hepatic fibrosis also known as?
Cirrhosis
184
What does hepatic fibrosis lead to?
Portal venous hypertension
185
What does portal venous hypertension lead to?
Porosytemic shunting
186
What does portosystemic shunting lead to?
* Toxin shunting
* Oesophageal varices
* Haemorrhoids
* Caput medusa
187
What are bile pigments?
Excretory products
188
What is the most common bile pigment?
Bilirubin
189
What is bilirubin produced as a product of?
Haemoglobin breakdown
190
What happens to bilirubin after production?
It is conjugated in the liver and secreted in the bile to be excreted in faeces
191
What happens if bilirubin cannot be excreted?
It accumulates in the blood
192
What condition is caused by accumulation of bilirubin in the blood?
Jaundice
193
What hormone does the liver notably break down?
Insulin
194
What are the functions of the liver, in relation to blood proteins?
* Producing albumin
* Producing coagulation factors
* Producing thrombopoietin
* Amino acid synthesis
195
What is the most abudant plasma protein?
Albumin
196
What is albumin essential for?
Maintaining the oncotic pressure needed for proper distribution of body fluids
197
What coagulation factors are produced by the liver?
* I
* II
* V
* VII
* IX
* X
* XI
* Protein C
* Protein S
* Antithrombin
198
What is coagulation factor I also known as?
Fibrinogen
199
What is coagulation factor II also known as?
Prothrombin
200
What is thrombopoietin?
A glycoprotein hormone
201
What does thrombopoietin do?
Regulates the production of platelets by bone marrow
202
What aspect of amino acid synthesis is the liver responsible for?
Transamination
203
What are the tests for liver function?
* ALT/AST levels
* Bilirubin levels
* Alkaline phosphate levels
* Albumin levels
* Prothombin time *(clotting)*
204
What does the presence of ALT or AST in the blood indiciate?
Liver damage
205
Why is ALT and AST present in liver damage?
In hepatocellular damage, the ruptured membranes will allow aminotransferases into the blood stream
206
What do raised levels of bilirubin or alkaline phosphate indicate?
Cholestasis *(obstruction of the bile ducts)*
207
What happens to bilirubin in cholestasis?
Unable to excrete bilirubin, plasma concentration rises
208
What is alkaline phosphatase?
An enzyme in cells lining the liver's biliary ducts
209
What happens to alkaline phosphatase in cholestasis?
Plasma levels rise with obstruction
210
What happens to albumin in chronic liver disease?
Levels are reduced
211
What does prothrombin time measure?
The clotting tendency of blood
212
What kind of tests are those for albumin levels and prothrombin time?
Synthetic function
213
Why does liver damage cause jaundice?
Damaged hepatocytes have a reduced capacity to excrete bilirubin. This leads to bilirubin accumulating in the blood, giving jaundice
214
What is the name for the clinical condition describing increased levels of bilirubin?
Hyperbilirubinaemia
215
What are the symptoms of hyperbilirubinaemia?
Yellowish pigmentation of the skin, conjunctival membranes over the scleae and other mucus membranes
216
When is jaundice clinically detectable?
At levels \>40µmol/L *(normal range \<22µmol/L)*
217
What are the types of jaundice?
* Pre-hepatic
* Hepatic
* Post-hepatic
218
What is the underlying pathology of pre-hepatic jaundice?
Excessive bilirubin production, *and the liver is unable to cope with the excess bilirubin*
219
What usually causes excessive bilirubin production in pre-hepatic jaundice?
An increased breakdown of red blood cells *(haemolysis)*
220
What are the lab findings in pre-hepatic jaundice?
* Unconjugated hyperbilirubinaemia
* Reticulocytosis
* Anaemia
* Increased LDH
* Decreased haptoglobin
221
What are the main causes of pre-hepatic jaundice?
* Inherited
* Congential hyperbilirubinaemias
* Acquired
222
What are the inherited causes of pre-hepatic jaundice?
* Red cell membrane defects
* Haemoglobin abnormalities
* Metabolic defects
223
What are the congential hyperbilirubinaemias leading to pre-hepatic jaundice?
* Gilbert's syndrome
* Criger-Najjar syndrome
* Dublin-Johnson syndrome
224
How common is Gilbert's syndrome?
Present in 10% of the population
225
How common is Crigler-Najjar syndrome?
Rare
226
How common is Dublin-Johnson syndrome?
Rare
227
What are the acquired causes of pre-hepatic jaundice?
* Immune
* Mechanical
* Acquired membrane defects
* Infections
* Drugs
* Burns
228
Give an example of a mechanical cause of pre-hepatic jaundice?
RBC's running across metal heart valves
229
What is the main pathology of hepatic jaundice?
Reduced capacity of liver cells to secrete conjugated bilirubin into the blood
230
What are the lab findings in hepatic jaundice?
* Mixed unconjugated and conjugated hyperbilirubinaemia
* Increase in the liver enzymes ALT and AST
* Abnormal clotting
231
What are the main causes of hepatic jaundice?
* Congential
* Hepatic inflammation
* Drugs
* Cirrhosis
* Hepatic tumours
232
What are the congential causes of hepatic jaundice?
* Gilbert's syndrome
* Crigler-Najjar syndrome
233
What are the main causes of hepatic inflammation?
* Viral
* Autoimmune hepatitis
* Alcohol
* Haemochromotosis
* Wilson's disease
234
What are the viral causes of hepatic inflammation?
* Hepatitis A, B, C, and E
* Epstein Barr Virus (EBV)
235
What drugs can cause hepatic jaundice?
Paracetamol
236
What are the main causes of cirrhosis?
* Alcohol
* Chronic hepatitis
* Metabolic disorders
237
What are the main kinds of hepatic tumours?
* Hepatocellular carcinoma
* Metastases
238
What is the main pathology of post-hepatic jaundice?
Obstruction to the drainage of bile
239
What is the consequence of the obstruction to the drainage of bile?
Causes a back up of bile acids into the liver, and so the passage of conjugated bilirubin is blocked
240
What are the types of obstructions to the drainage of bile?
* Intrahepatic
* Extrahepatic
241
What are the lab findings in post-hepatic jaundice?
* Conjugated hyperbilirubinaemia
* Bilirubin in the urine *(makes urine dark)*
* Increased canalicular enzymes (ALP)
* Can be incresed liver enzymes (ALT/AST)
242
What are the main causes of intrahepatic post-hepatic jaundice?
* Hepatitis
* Drugs
* Cirrohosis
* Primary biliary colic
243
What are the extrahepatic causes of post-hepatic jaundice?
* Gallstones
* Biliary stricture
* Carcinoma
* Pancreatitis
* Sclerosig cholangitis
244
What carcinomas can cause post-hepatic jaundice?
* Head of pancreas
* Ampulla
* Bile duct
* Porta hepatis lymph nodes
* Liver metastases
245
Is there bilirubin in the faeces in post-hepatic jaundice?
No, *it is pale*
246
What is the pathology of alcoholic liver disease
1. Fatty liver
2. Alcoholic hepatitis
3. Cirrhosis
247
What is the pathogenesis of fatty liver?
* Alcohol metabolism generates NADH from NAD+. Increased NADH induces fatty acid synthesis, and decreased NAD+ results in a decrease in fatty acid oxidation
* There is an accumulation of fatty acids in the liver, with glycerol being converted to TAGs
* TAGs accumulate, giving fatty liver
248
What is alcoholic hepatitis?
Inflammation of hepatocytes
249
What happens in cirrhosis?
Liver cell necrosis followed by nodular regeneration and fibrosis
250
What is the result of liver cirrhosis?
* Increased resistance to blood flow
* Derenged liver function
251
What are the potential complications of alcoholic liver disease?
* Hepatocellular carcinoma
* Liver failure
* Wericke-Korsakoff syndrome
* Encephalopathy
* Dementia
* Epilepsy
252
What are the causes of liver cirrhosis?
* Alcohol
* Wilson's Disease
* Biliary cirrhosis
* Haemochromotosis
* Hepatitis B or C
* Autoimmune hepatitis
* α1-antitrypsin deficiency
253
What are the clinical features of liver cirrhosis?
* Liver dysfunction
* Jaundice
* Anaemia
* Bruising
* Palmar erythema
* Dupuytren's contracture
254
What are the results of investigations indicating liver cirrhosis?
* May be increase ALT/AST
* Increased ALP
* Increased bilirubin
* Decreased albumin
* Deranged clotting
255
What is involved in the management of cirrhosis?
* Stopping drinking
* Treating complications
* Transplantation
256
What is portal hypertension defined as?
Portal venous pressure \>20mmHg
257
What can portal hypertension be caused by?
* Obstruction of the portal vein
* Obstruction of flow within the liver
258
What are the main causes of obstruction of the portal vein?
* Congenital
* Thrombosis
* Extrinsic compression
259
What are the main causes of obstruction of flow within the liver?
* Cirrhosis
* Hepatoportal sclerosis
* Schistosomiasis
* Sarcoidosis
260
What may portal hypertension lead to?
* Ascites
* Splenomegaly
* Pathologies related to porto-systemic anastomoses
261
How does portal hypertension cause ascites?
The high pressure in the portal venous system means blood is backed up into the abdomen. The **increase in hydrostatic pressure** in the abdomen means **less fluid is reabsorbed** into blood vessels at the end of capillary beds
262
What may contribution to the development of ascites if the liver is damaged?
**Reduced oncotic pressure** inside the vessels, due to lack of plasma proteins
263
Why does portal hypertension cause splenomegaly?
Due to subsequent increase blood pressure in the spleen
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How do pathologies related to porto-systemic anatomoses arise with portal hypertension?
There are several anastomoses bewteen the hepatic portal and systemic veins. As such, when the pressure is increased in the portal venous system, blood is backed up through these anastomoses, increasing the blood pressure
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What does increased blood pressure in porto-systemic anatomoses cause?
* Vessels to dilate
* Vessels to protrude into lumen
* Rupturing
* Ulceration
* Haemorrhage
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What pathologies can arise due to increased pressure in porto-systemic anastomoses?
* Oesophageal varices
* Rectal varices
* Caput Medusae
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Label this diagram
## Footnote
*Include the porto-systemic anastomoses, running from portal to systemic.*
* A - Esophageal vein
* B - **Left gastric to Azygous/Oesphageal anastomoses**
* C - Stomach
* D - Left gastric vein
* E - Hepatic portal vein
* F - Splenic vein
* G - Inferior mesenteric vein *(IMV)*
* H - Retroperitoneal veins
* I - Colon
* J - **Colonic/Splenic/Portal to Retroperitoneal veins of the posterior abdominal wall or diaphragm anastomoses**
* K - Superior rectal vein
* L - Rectal veins
* M - Inferior rectal vein
* N - Anus
* O - **Superior rectal to inferior rectal anastomoses**
* P - Epigastric veins
* Q - Umbilicus
* R - **Paraumbilical to small epigastric of abdominal wall anastomoses**
* S - Paraumbilical vein
* T - Superior mesenteric vein *(SMV)*
* U - Liver
* V - Inferior vena cava *(IVC)*
* W - Azygous vein
*
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What does increased pressure in the left gastric to azygous/oesophageal anastomoses lead to?
Oesophageal Varices
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What does increased pressure in the superior rectal to inferior rectal anatomoses lead to?
Rectal varices
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What does increased pressure in the paraumbilical to small epigastric of abdominal wall anastomose cause?
Caput Medusae
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Where are the portal veins involved in the portal to retroperitoneal veins of posterior abdominal wall or diaphragm located?
On the posterior aspects *(bare areas)* of secondarily retroperitoneal viscera or the liver
272
What happens to bile acids in between meals?
They return to the liver
273
What secrete bile acids?
Canaliculi cell walls
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When are bile acids secreted?
Long before they are next needed
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Where are bile acids stored until they are needed?
In the gall bladder
276
How is the volume of bile acids that need to be stored reduced?
They are concentrated by the transport of salt and water across the gall bladder epithelium
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What is the problem with the process of concentration of bile acids?
It increases the risks of precipitation
278
What does precipitation of bile acids lead to?
Gall stones
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What are the symptoms of gallstones?
* Often asymptomatic
* Can cause painful biliary colic, or obstruction
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When do gallstones cause biliary colic?
When they move itno the neck of the gall bladder or biliary tree
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What is biliary colic often followed by?
* Inflammation of the gall bladder **(cholecystitis)**
* Infection of the gall bladder
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When may pain from gallstones be worse?
After eating
283
Why may pain from gallstones be worse after eating?
The secretion of cholecystokinin (CCK) will cause the gall bladder to contract
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Label this diagram
## Footnote
*Indicate the clinically relevant locations of gallstones, and what they cause*
* A - Hepatic ducts
* B - Common hepatic duct
* C - Hartmann's pouch
* D - Common bile duct
* E - Pancreatic duct
* F - Sphincter of Oddi
* G - Ampulla of Vater
* H - Duodennum
* I - Gall bladder
1. **Causing biliary obstruction**
2. **Stone causing gallstone pancreatitis**
3. **Asymptomatic gallstones**
4. **Impacted in cystic duct, causing acute cholecystitis**
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What is pancreatitis?
An inflammatory process
286
What causes pancreatitis?
Effects of enzymes released from pancreatic acini
287
What are the macroscopic features of chronic pancreatitis?
* Oedema
* Haemorrhage
* Necrosis
288
What are the symptoms of acute pancreatitis?
* Severe pain
* Vomiting
* Dehydration
289
What will be found in investigations indicating pancreatitis?
* Increased amylase
* Increase glycaemia
* Increasde ALP
* Increased bilirubin
* Decreased Ca2+
290
What are the macroscopic features of chronic pancreatitis?
* Fibrosis
* Calcification
291
What are the symptoms of chronic pancreatitis?
* Pain
* Malabsorption
* Jaundice
292
What does malabsorption caused by chronic pancreatitis cause?
* Steatorrheoa
* Decreased albumin
* Weight loss
293
What are the causes of pancreatitis?
* Gallstones
* Ethanol
* Trauma
* Steroids
* Mumps
* Autoimmune
* Scorpion bite
* Hyperlipidaemia
* ERCP / Iatrogenic
* Drugs
294
How can gallstones cause pancreatitis?
They block the pancreatic duct or Ampulla of Vater
295
How can ethanol cause pancreatitis?
Hyper-stimulation of pancreatic secretions
296
What % of pancreatic carcinomas do ductal adenocarciomas account for?
90%
297
What % of cancer deaths do pancreatic carcinomas account for?
~5%
298
What is the clinical presentation of pancreatic carcinomas?
* Initially symptomless
* Then lots of symptoms all at the same time
* Obstructive jaundice
* Pain
* Vomiting
* Malabsoprtion
* Diabetes
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