GI/ LIVER Flashcards
1
Q
What is GORD?
A
Gastro-oesophageal reflux disease–> Where acid from the stomach refluxes through the lower oesophageal sphincter, irritating the lining of the oesophagus.
2
Q
What epithelium lines the oesophagus?
A
Squamous epithelium, making it more sensitive to the effects of stomach acid.
3
Q
What epithelium does the stomach have?
A
Columnar epithelium, protecting it against stomach acid.
4
Q
What is dyspepsia?
A
Indigestion–> Feeling of burning, pain or discomfort in the digestive tract
5
Q
What are the symptoms of GORD?
A
Dyspepsia: Heart burn Acid regurgitation Retrosternal/ epigastric pain Bloating Nocturnal cough Hoarse voice
6
Q
What is endoscopy used for and when might it be used in GORD?
A
Patients with evidence of GI bleed or other concerning features would be reffered.
Assesses for peptic ulcers and oesophageal or gastric malignancies.
7
Q
What are the key red flags that would make you suspicious of cancer and therefore need a 2 week endoscopy referral?
A
Dysphagia Over 55 Weight loss Upper abdominal pain/ reflux Treatment resistant dyspepsia Nausea/ vomiting Low haemoglobin/ raised platelets
8
Q
What lifestyle advice would be given to patients with GORD?
A
Reduce tea, coffee and alcohol Weight loss Avoid smoking Smaller, lighter meals Avoid heavy meals before bed Stay upright after meals
9
Q
What medication can be given to manage GORD?
A
Acid neutralising medicine-> Gaviscon/ Rennie
Proton pump inhibitors (reduce acid secretion)–> Omeprazole/ Lansoprazole
Ranitidine
10
Q
What is Ranitidine and its action?
A
Medicine used as an alternative to PPIs to treat GORD. H2 receptor antagonist which reduces stomach acid.
11
Q
What is the surgery that can be used to treat GORD called?
A
Laparoscopic fundoplication–> Ties the fundus of the stomach around the lower oesophagus to lower the sphincter.
12
Q
What stomach bacteria test is offered to anyone with dyspepsia and what kind of bacteria is it?
A
Helicobacter pylori
Gram negative aerobic bacteria
13
Q
How does H. pylori avoid the acidic environment in the stomach?
A
Forces its way into the gastric mucosa
14
Q
How does H. pylori cause damage?
A
Causes breaks in the mucosa, exposing the epithelial cells underneath to acid and causing gastritis, ulcers and increased risk of stomach cancer.
15
Q
What does H. pylori produce to neutralise stomach acid and how does this cause damage?
A
Ammonia which directly damages epithelial cells.
16
Q
What tests can be used to look for H. pylori?
A
Urea breath test
Stool antigen test
Rapid urease test
17
Q
What is a rapid urease test?
A
Small biopsy taken of the stomach mucosa during endoscopy. Urea is added to the sample and if H. pylori is present, they produce enzymes that convert the urea to ammonia.
18
Q
How is H. pylori eradicated?
A
Triple therapy: Proton pump inhibitor + 2 antibiotics for 7 days
19
Q
What is Barretts oesophagus?
A
When the oesophagus epithelium changes from squamous to columnar due to constant acid reflux. (metaplasia).
20
Q
Why do patients with Barrets oesophagus have to be monitored with regular endoscopy?
A
It is premalignant and increases the risk of adenocarcinoma development.
21
Q
How can Barretts oesophagus be treated?
A
Proton pump inhibitors, ablation treatment during endoscopy.
22
Q
Where do peptic ulcers most commonly form?
A
Duodenum (and stomach)
23
Q
Why do ulcers form?
A
When there is a breakdown in the protective layer of the stomach or duodenum and an increase in stomach acid.
24
Q
What makes up the protective layer of the stomach and how can it be broken down?
A
Mucus and bicarbonate
Can be broken down by medications (Steroids or NSAIDs) or H. Pylori
25
What can cause an increase in stomach acid?
```
Stress
Alcohol
Caffeine
Smoking
Spicy foods
```
26
What are the key presentations of a peptic ulcer?
```
Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding--> causes haematemesis, 'coffee gound' vomiting and melaena
Iron deficiency anaemia
```
27
How might you tell the difference between a gastric and duodenal ulcer in terms of their presentation?
Eating worsens pain of gastric ulcers and improves pain of duodenal ulcers.
28
What is haematemesis?
Vomiting blood
29
How are peptic ulcers diagnosed?
Endoscopy
(Rapid urease/ CLO test can be performed to check for H. Pylori)
*Biopsy should be considered to exclude malignancy.
30
How are peptic ulcers treated?
Same as GORD--> usually with high dose proton pump inhibitors.
31
What complications can peptic ulcers cause?
- Bleeding from ulcer (common and potentially life threatening)
- Perforation resulting in acute abdomen and peritonitis.
- Scarring and strictures of the muscle and mucosa, leading to pyloric stenosis.
32
What is pyloric stenosis and how does it present?
Narrowing of the pylorus (stomach exit), leading to difficulty in emptying stomach contents. Presents with upper abdominal pain, distention, nausea and vomiting.
33
What are the causes of an upper GI bleed?
- Oesophageal varices (enlarged veins)
- Mallory-Weiss tear (tear of mucous membrane)
- Peptic ulcers
- Stomach/ duodenal cancers
34
How do upper GI bleeds present?
- Haematemesis
- 'Coffee ground' vomit
- Melaena
- Haemodynamic instability causes large blood loss, causing low blood pressure, tachycardia and other signs of shock
- Symptoms of underlying pathology--> e.g. epigastric pain/ dyspepsia in peptic uclers
35
What causes 'coffee ground' vomit?
Vomiting digested blood that looks like coffee grounds
36
What is melaena?
Tar like, black greasy stool caused by digested blood.
37
What is the Glasgow-Blatchford score?
Scoring system in suspected upper GI bleed that scores patients based on their clinical presentation. >0 indicates high risk for upper GI bleed
38
What features are taken into account in the Glasgow-Blatchford score that indicate an upper GI bleed?
- Drop in Hb
- Rise in urea
- Blood pressure
- Heart rate
- Melaena
- Syncopy
39
Why do urea levels rise in upper GI bleeds?
Blood in the GI tract gets broken down by the acid and digestive enzymes, releasing urea which is then absorbed in the intestines.
40
What is the Rockall score?
Used for patients that have had an endoscopy to calculate their risk of rebleeding and overall mortality.
41
How is an upper GI bleed managed?
```
ABATED:
ABCDE approach to immediate resuscitation
Bloods
Access (cannula)
Transfuse
Endoscopy
Drugs (stop anticoagulants and NSAIDs)
```
42
What is looked for in the bloods taken for a suspected GI bleed?
```
Haemoglobin (FBC)
Urea (U&E's)
Coagulation (INR. FBC for platelets)
Liver diease (LFTs)
Crossmatch
```
43
What are the two main types of inflammatory bowel disease?
Ulcerative colitis and Crohn's disease
44
What are common of both crohn's and ulcerative colitis?
Both involve inflammation of the walls of the GI tract and have periods of remission and exacerbation
45
What makes Crohn's different to Ulcerative colitis? (NESTS)
No blood or mucus
Entire GI tract
Skip lesions (patchy inflammation)
Terminal ileum most affected and Transmural (full thickness) inflammation
Smoking is a risk factor
Also associated with weight loss, strictures and fistulas
46
What makes Ulcerative Colitis different to Crohn's?
```
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates to treat
Primary sclerosing cholangitis
```
47
What are the main presentations of inflammatory bowel disease?
Diarrhoea
Abdominal pain
Passing blood
Weight loss
48
How is inflammatory bowel disease tested for?
- Endsocopy with biopsy--> Diagnostic.
- Routine bloods for anaemia, infection, thryoid, kidney and liver function
- CRP indicates inflammation and active disease
- Faecal calprotectin
- Imaging to look to complications
49
What is Faecal calprotectin ?
Useful screening test for IBD---> Protein released by intestines when they are inflamed
50
What is the first line treatment for inducing remission in Crohn's? What can be added if these don't work alone
Steroids (e.g. oral prednisolone or IV hydrocortisone)
| Can add immunosuppressant
51
What are the first line medications offered to Crohn's patients to maintain remission?
Azathioprine
| Mercaptopurine
52
When can surgery be offered to those with Crohn's?
When the disease only affects the distal ileum, it is possible to surgically resect it and prevent further flares.
Can be used to treat secondary strictures and fistulas.
53
How is mild-moderate Ulcerative colitis treated to induce remission?
First line: Aminosalicylate
| Second line: Corticosteroids
54
How is severe ulcerative colitis treated to induce remission?
First line: IV corticosteroids
| Second line: IV ciclosporin
55
How can the disease be removed in ulcerative colitis?
Panproctocolectomy--> Removing colon and rectum will remove the disease.
56
What are the two outcomes of surgery used to treat ulcerative colitis?
Permanent ileostomy or ileo-anal anastomosis (J-pouch)
57
What is a J-pouch?
When the colon and rectum are removed and the ileum is folded back in itself and fashioned into a larger pouch that functions like a rectum. It is attached to the anus and collects stools.
58
What is Colostomy Surgery?
Part of the colon is removed, and a stoma is created- stoma is when part of the intestine is pulled through the abdominal wall to create an opening through which stool leaves the body.
59
What is IBS?
Functional bowel disorder- no identifiable organic disease underlying the gut symptoms.
60
How much of the population has IBS and who are more affectesd?
Up to 20% of population.
| More common in women and young people.
61
What are the main symptoms of IBS?
```
Diarrhoea
Constipation
Fluctuating bowel habits
Abdominal pain
Bloating
(Worse after eating, improved by opening bowels)
```
62
What is the criteria for diagnosis of IBS?
Diagnosis of exclusion:
- Normal FBC, EST, CRP blood tests
- Negative faecal calprotectin
- Negative coeliac disease serology
- Cancer excluded/ not suspected
- Symptoms that suggest IBS
63
What is the firstline management of IBS?
Lifestyle advice:
- Adequate fluid intake
- Regular small meals
- Limit processed foods, caffeine and alcohol
- Low FODMAP diet
- Trial of probiotic
- CBT
64
What is are the medication treatment options for IBS?
```
First line:
-Loperamide for diarrheoa
-Laxatives for constipation
-Antispasmodics for cramps
Second line:
- Tricyclic antidepressants
Third line:
-SSRIs antidepressants
```
65
What is coeliac disease?
Autoimmune condition where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel.
66
When does coeliac disease usually develop?
In early childhood (but can at any age)
67
What are the two auto-antibodies involved in coeliac disease?
- Anti-tissue transglutaminase (anti-TTG)
| - Anti-endomysial (anti-EMA)
68
What happens on exposure to gluten in coeliac disease?
Auto-antibodies are created that target the epithelial cells of the intestine and lead to inflammation.
69
Where does inflammation caused by coeliac disease particularly affect and what does it cause?
Affects small bowel- especially jejunum
| Causes atrophy of intestinal villi which causes malabsorption of nutrients and the symptoms of disease
70
How does coeliac disease present?
Often asymptomatic
- Failure to thrive in children
- Diarrhoea
- Fatigue
- Weight loss
- Mouth ulcers
- Anaemia (secondary to iron, B12 or folate deficiency)
- Dermatitis herpetiformis (Skin rash)
- Occasional neurological symptoms
71
What are the genetic associations with coeliac disease?
HLA-DQ2 (90%)
| HLA-DQ8 gene
72
How is coeliac disease tested?
* Investigations must be carried out whilst the patient is on a diet the contains gluten.
- Check IgA levels to exclude IgA deficiency.
- Antibody tests: Raised anti-TGG and anti endomysial antibodies
- Endoscopy and intestinal biopsy--> Show crypt hypertrophy and villous atrophy.
73
What other conditions is coeliac disease associated with?
```
Type 1 diabetes
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
```
74
What are the complications of untreated coeliac disease?
```
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma of intestine
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
```
75
What is the treatment of coeliac disease?
Lifelong gluten-free diet
76
What is a Mallory-Weiss tear and what usually causes it?
Linear mucosal tear at the oesophagastric junction that causes an upper GI bleed. Caused by a sudden increase in intra-abdominal pressure (e.g. coughing, retching, dry-heaves)
77
What cells does the mucose of the upper two thirds of the stomach contain?
Parietal cells
Chief cells
Enterochromaffin-like cells (ECL)
78
What do parietal cells secrete?
HCl
79
What do Chief cells secrete and what does this initiate?
Pepsinogen which initiates proteolysis
80
What do ECL cells release and what does this stimulate?
Histamine- stimulates acid release
81
What cells does the antral contain and what do they secrete?
Mucus secreting cells--> Release mucin and bicarbonate
G cells--> Secrete gastrin (stimulate acid release)
D cells--> Secrete somatostatin (suppresses acid secretion)
82
What is achalasia?
Failure of the LES to relax/ open during swallowing.
83
How does achalasia present?
Intermittent dysphagia (of both solids and liquids)
Regurgitation of food
Substernal cramps
84
What is scleroderma?
Systemic sclerosis--> a chronic autoimmune disease that causes hardening of connective tissue.
85
How does scleroderma affect the GI tract?
Diminished peristalsis and oesophageal clearance due to replacement of smooth muscle by fibrous tissue.
Causes GORD.
86
What is the definition of diarrhoea?
Loose/ liquid stools more than 3 times daily
87
What is acute diarrhoea?
Diarrhoea lasting < 14 days
88
What is persistent diarrhoea?
Diarrhoea lasting 14-30 days
89
What is chronic diarrhoea?
Diarrhoea lasting >14 days
90
What are the main non-infective causes of diarrhoea?
```
Cancer
IBD
IBS
Hormonal
Radiation
Chemical (antibiotics)
Anatomical
```
91
What are the main infective causes of diarrhoea?
Viral
Bacteria
Parasites
92
What antibiotics can give rise to diarrhoea?
Climpamycin, Ciprofloxacin, Co-amoxiclav, Cephalosporins can all give rise to C.Diff
93
What are the main viral causes of diarrhoea?
Rotavirus, Norovirus
94
What are the main bacterial causes of diarrhoea?
Campylobacter, Shigellla, Salmonella, S.aureus, B.cereus, E.coli, C.Diff, Cholera
95
What are the main parasitic causes of diarrhoea?
Giardia, crypto.
96
What causes watery diarrhoea?
Non-inflammatory causes (enterotoxins or superficial adherence/ invasion)
97
What causes bloody/ mucoid diarrhoea?
Inflammatory causes (invasion/ cytotoxins)
98
What is gastroenteritis?
Inflammation all the way from the stomach to the intestines that presents with nausea, vomiting and diarrhoea
99
What is dysentery?
Infectious gastroenteritis with bloody diarrhoea
100
What is norovirus and how long does it last?
Single-stranded RNA virus. Lasts 24-72 hours.
101
What is rotavirus and how long does it last?
Double stranded RNA virus. Lasts 3-8 days.
102
What is E.coli and what does it produce that causes diarrhoea?
Gram -ve bacteria that produces Shiga toxin.
103
What does Shiga toxin do?
Causes abdominal cramps, bloody diarrhoea and vomiting. Also destroys blood cells which leads to haemolytic uraemic syndrome.
104
What is campylobacter and what causes it?
Gram negative bacteria- main cause of travellers diarrhoea. Caused by raw/ improperly cooked poultry, untreated water and unpasteurised milk.
105
What is shigella and how is it spread?
Bacteria spread by faeces contaminated water, pools and food.
106
What is salmonella and how is it spread?
Bacteria spread by raw eggs, poultry or food contaminated with infected faeces of small animals.
107
What is Bacillus Cereus and how is it spread?
Gram positive bacteria spread through inappropriately cooked foods. Common on food not refrigerated immediately (e.g. rice)
108
After how long does Bacillus Cereus cause symptoms and how long does it last?
Cramping and vomiting within 5 hours of ingestion.
Watery diarrhoea after 8 hours when it reaches the intestines.
Resolves within 24 hours.
109
What is Yersinia Enterocolitica and how is it spread?
Gram -ve bacillus spread by raw/ undercooked pork, and contamintation with the urine/ faeces of other mammals/
110
How long is Yersinia Enterocolitica incubation and how long does it last?
incubation is 4-7 days.
| Can last 3 weeks or more.
111
How does Staph. Aureus cause infection?
Produces enterotoxins when growing on food. that cause enteritis.
112
What is giardia lamblia and how does it spread?
Microscopic parasite that lives in intestines of mammales and releases cysts in their stools. These can then contaminate food or water.
113
What does the pancreas consist of?
Exocrine (98%) and Endocrine cells
114
What is the function of the exocrine pancreas?
Secretion of digestive enzymes, ions and water into the duodenum.
115
What is the functional unit of the exocrine pancreas?
Acinus and its draining ductule
116
Where does the pancreatic duct enter the duodenum?
Joins to the common bile duct to enter at the ampulla of Vater.
117
What digestive enzymes do acinar cells produce?
Amylase, lipase, colipase, phospholipase, proteases
118
What is the action of the endocrine pancreas?
Release hormones into blood to control blood glucose levels
119
What cells does the endocrine pancreas contain and what do they secrete?
```
Alpha cells- glucagon
Beta cells - insulin
Delta cells- somatostatin
Pancreatic polypeptide cells
Enterochrommaffin cells - serotonin.
```
120
What is acute pancreatitis?
Rapid onset of pancreatic inflammation and symptoms
121
What is chronic pancreatitis?
Longer-term inflammation and symptoms with progressive and permanent deterioration in pancreatic function.
122
What are the three main causes of pancreatitis?
Gallstones
Alcohol
Post-ERCP
123
What is ERCP?
Procedure that uses an endoscope and X-rays to look at your bile duct and your pancreatic duct.
124
What is gallstone pancreatitis?
When gallstones get trapped at the ampulla of Vater, blocking the flow of bile and pancreatic juice into the duodenum and resulting in inflammation of the pancreas.
125
Why does alcohol cause pancreatitis?
Alcohol is directly toxic to pancreatic cells, resulting in inflammation.
126
What are the causes of pancreatitis?
```
I GET SMASHED:
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs
```
127
What are the main presentations of acute pancreatitis?
```
Severe epigastric pain
Pain that radiates to the back
Vomiting
Abdominal tenderness
Systemically unwell (fever, tachycardia)
```
128
What are the initial investigations of pancreatitis?
```
Glasgow score
Amylase--> Raised to >3X normal
C-reactive protein- monitors inflammation
Ultrasound (assesses for gallstones)
CT abdomen (assesses for complications)
```
129
What is the Glasgow score and what is the criteria needed to work it out?
```
Used to assess severity of pancreatitis.
(0-1= mild
2= moderate
3 or more= severe)
PANCREAS pneumonicL
Pa02<60
Age >55
Neutrophils (WBC>15)
Calcium <2
uRea >16
Enzymes
Albumin
Sugar (glucose>10)
```
130
How is acute pancreatitis managed?
```
Resuscitation (ABCDE)
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones if needed
Antibiotics if needed
Treatment of complications
```
131
What are the main complications of acute pancreatitis?
```
Necrosis
Infection
Abscess formation
Acute peripancreatic fluid collections
Pseudocysts
Chronic pancreatitis
```
132
What does chronic pancreatitis cause?
Fibrosis and reduced pancreatic function
133
What is the most common cause of chronic pancreatitis?
Alcohol
134
What are the key complications of chronic pancreatitis?
Chronic epigastric pain
Exocrine function loss causing lack of pancreatic enzymes
Endocrine function loss leading to diabetes
Damafe and strictures to duct system causing obstruction in excretion of pancreatic juice and bie
Formation of pseudocysts and abscesses
135
How is chronic pancreatitis managed?
Abstain form alcohol/ smoking
Analgesia
Replacement of pancreatic enzymes
Subcutaneous insulin regimes if diabetes develops
ERCP with stenting to treat strictures and obstruction.
Surgery may be required.
136
What are the main functions of the liver?
- Glucose and fat metabolism
- Detoxification and excretion--> Bilirubin, ammonia, drugs, hormones
- Protein synthesis--> Albumin, clotting factors
- Defence against infection
137
What are the main causes of acute liver injury?
```
Viral (A,B,EBV)
Drugs
Alcohol
Vascular
Obstruction
Congestion
```
138
What are the main causes of chronic liver injury?
Alcohol
Viral (B,C)
Autoimmune
Metabolic (iron, copper)
139
What is the alternative outcome to recovery in acute liver injury?
Liver failure
140
What is the alternative to recovery in chronic liver injury?
Cirrhosis leading to liver failure (Varices of hepatoma)
141
What are the common symptoms of acute liver injury?
Malaise, nausea, anorexia, occasionally jaundice
142
What are the common symptoms of chronic liver injury?
Ascites (fluid in peritoneal cavity)
| Oedema, Haematemesis, mailaise, anorexia, wasting, easy bruising, itching, hepatomegaly, abnormal LFTs
143
What are LFTs and what do they look for?
Serum Liver function tests:
| Serum albumin, bilirubin, prothrombin time
144
What is serum albumin a good marker for?
Synthetic function (ability of liver to synthesise proteins)
145
What serum measurements are good indications of synthetic function?
Prothrombin time (PT)/
International normalised ratio (INR)
Platelet count and albumin levels
146
What is prothrombin time?
Blood test that measures how long it takes blood to clot- Results given as INR (International normalised ratio)
147
What are aminotransferases and what happens to them during liver cell damage?
```
Enzymes contained in hepatocytes that leak into the blood during liver cell damage.
Aspartate aminotranferase (AST)
Alanine aminotransferase (ALT)
```
148
What are bile pigments?
Substances formed from the haem portion of haemoglobin when erythrocyes are broken down in the spleen and liver.
149
What is the predominant bile pigment and what colour is it?
Bilirubin- yellow.
150
Where are erythrocytes broken down?
By macrophages in the spleen and bone marrow and by kupffer cells in the liver.
151
What are erythrocytes broken down into?
Haem and globin
152
What is globin broken down into and what happens to it?
Amino acids which are used to generate new erythrocytes in the bone marrow
153
What is haem broken down into?
Biliverdin, Fe2+ and CO
154
What happens to the Fe2+ from the breakdown of haem?
It is transported to bone marrow to be implemented into new erythrocytes.
155
What happens to biliverdin?
It is reduced into unconjugated bilirubin which is toxic.
156
Where does unconjugated bilirubin go?
It is toxic and must be secreted. It is lipid soluble so must be transported to the liver bound to albumin.
157
What happens to unconjugated bilirubin in the liver?
It undergoes glucuronidation to make its soluble to be excreted and becomes conjugated bilirubin
158
Where does conjugated bilirubin travel to once it leaves the liver and what happens to it there?
The small intestine until it reaches the ileum where it is reduced to form urobilinogen
159
What happens to urobilinogen?
10% is reabsorbed into the blood bound to albumin and transported back to the liver where it is recycled into bile or transported to the kidneys and excreted in urine.
90% is oxidised into stercobilin which is excreted into the faeces
160
What is jaundice and what causes it?
Yellow discolouration of the skin due to raised serum bilirubin
161
What are the three steps in the progression of alcoholic liver disease?
1. Alcohol related fatty liver
2. Alcoholic hepatitis
3. Cirrhosis
162
What is alcohol related fatty liver?
When drinking leads to a build-up of fat in the liver. Process can be reversed in around 2 weeks
163
What is alcoholic hepatitis?
When drinking alcohol over a long period or binge drinking causes inflammation of the liver
164
What is liver cirrhosis?
When the liver is made up of scar tissue rather than healthy liver tissue. Irreversible
165
What is the recommended drinking limit?
14 units per week. (over 3 or more days)
166
What are the complications of excessive alcohol consumption?
```
Alcoholic liver disease
Cirrhosis
Alcohol dependance/ withdrawal
Wenicke-Korsakoff syndrome (WKS)
Pancreatitis
Alcoholic cardiomyopathy
```
167
What are the main signs of liver disease?
```
Jaundice
Hepatomegaly
Spider naevi
Palmar erythema (red palms)
Gynaecomastia (males developing breast tissue)
Bruising (due to abnormal clotting)
Acites
Caput medusae (distended epigastric veins)
Asterixis (hand tremor)
```
168
What investigations are done to look for alcoholic liver disease?
```
Bloods
Ultrasound
Endoscopy
CT/ MRI scans
Liver biopsy
```
169
What bloods are done to look for alcoholic liver disease and what do they show?
FBC- Raised MCV
LFTs- Elevated ALT and AST (Transaminases). Raised gamma-GT and ALP. Low albumin. Raised bilirubin in cirrhosis
Clotting- Elevated prothrombin time
U&Es- may be deranged. in hepatorenal syndrome
170
What can an ultrasound of the liver show?
```
Fatty changes (increased echogenicity).
Changes related to cirrhosis
```
171
What is the general management of alcoholic liver disease?
```
Stop drinking alcohol permanently.
Detox regime
Nutritional support (vitamins and high protein)
Treat complications of cirrhosis
Steroids in severe cases
Referral for liver transplant.
```
172
What are the different stages of alcohol withdrawal and their timings?
6-12 hours: tremor, sweating, headache, craving, anxiety
12-24 hours: Hallucinations
24-48 hours: seizures
24-72 hours: Delerium tremens
173
What is delerium tremens?
Medical emergency associated with alcohol withdrawal that has a mortality of 35% if untreated.
174
What causes delirium tremens?
Alcohol stimulates GABA receptors in the brain (which have a relaxing effect) and inhibits glutamate (NMDA) receptors, having a further inhibitory effect on the brains electrical activity.
Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system become up-regulated to balance the effects of alcohol. When alcohol is removed, GABA under-functions and glutamate over-functions causing extreme excitability with excess adrenergic activity.
175
What are the presentations of delirium tremens?
```
Acute confusion
Sever agitation
Delusions/ hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia
Arrhythmias
```
176
How is alcohol withdrawal managed?
CIWA-Ar assessment tool used to score the patient.
Chlordiazepoxide is a type of sedative used to combat the effects.
IV high-dose B vitamins followed by low dose thiamine
177
What is Wernicke-Korsakoff Syndrome (WKS)?
A disease that begins with Wernicke's encephalopathy followed by Korsakoff's syndrome. Caused by alcohol excess leading to thiamine (Vit B1) deficiency due to poor absorption in the presence of alcohol and poor diets of alcoholics.
178
What are the key features of Wernicke's encephalopathy?
Confusion
Oculomotor disturbances
Ataxia
179
What is ataxia?
Difficulties with coordinated movements
180
What are the key features of Korsakoff's syndrome?
Memory impairment and behavioural changes
181
What causes liver cirrhosis?
Chronic inflammation causes damaged liver cells to be replaces with scar tissue (fibrosis) and nodules of scar tissue form within the liver
182
What are the most common causes of liver cirrhosis?
Alcoholic liver disease
Non alcoholic fatty liver disease
Hep B
Hep C
183
What are less common causes of liver cirrhosis?
```
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochomatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs
```
184
What are the key signs of cirrhosis?
```
Jaundice
Hepatomegaly
Splenomegaly (caused by portal hypertension)
Spider naevi
Palmar erythema
Gynaecomastia and testicular atrophy
Bruising
Ascites
Caput medusae
Asterixis
```
185
What are spider naevi?
When widened venules cause threadlike red lines or patterns on the skin
186
What is palmar erythema and what causes?
Red palms caused by increased dilatation of surface capillaries in the hand due to hyperdynamic circulation.
187
What is gynaecomastia and what causes it?
Condition by which males develop breast tissue due to an imbalanced ratio of oestrogen and androgen activity.
188
What investigations can be done to check for liver fibrosis?
```
Bloods (ELF)
Ultrasound
Fibroscan
Endoscopy
CT/ MRI scan
Liver biopsy
```
189
What bloods indicate liver cirrhosis?
- ALT, AST, ALP and Bilirubin become deranged in decompensated cirrhosis
- Albumin and PT time indicate synthetic function
- Hyponatraemia indicates fluid retention in severe cases
- Urea and createnine become derganged in hepatorenal syndrome.
- Enhanced liver fibrosis (ELF) blood test is first line in non-alcoholic fatty liver disease
190
What may a cirrhosis ultrasound show?
```
Nodules on liver surface
Corkscrew appearance to arteries with increased flow (to compensate for reduced portal flow)
Enlarged portal vein
Ascites
Splenomegaly
```
191
What is a FibroScan
Test used to check the elasticity of the liver by sending high frequency sound waves into it to assess the degree of fibrosis.
192
What is the general management of cirrhosis?
```
Ultrasound/alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years
High protein, low sodium diet
MELD score every 6 months
Possible liver transplant
Manage complications
```
193
What is the 5 year survival once cirrhosis has developed?
50%
194
What are the main complications of cirrhosis?
Malnutrition
Portal hypertension-->varices and variceal bleeding
Ascites and spontaneous bacterial peritonitis
Hepato-renal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma
195
Why does cirrhosis lead to malnutrition?
It leads to increased use of muscle tissue as fuel and reduces the protein available for muscle growth by affecting the metabolism of proteins in the liver. It also disrupts the livers ability to store glucose as glycogen and release it when required, resulting in the body using muscle tissue as fuel.
196
How is malnutrition caused by cirrhosis managed?
Regular meals
Low sodium (to minimise fluid retention)
High protein and high calorie
Avoid alcohol
197
What are the sources of the portal vein?
Superior mesenteric vein and splenic vein
198
What is the action of the portal vein?
Brings venous blood from the spleen, pancreas, and small intestine so that the liver can process the nutrients and byproducts of food digestion
199
Why does cirrhosis cause portal hypertension?
Increases the resistance of blood flow in the liver, causing increased back-pressure into the portal system.
200
What does portal hypertension result in and where?
Varices at the sites where the portal system anastomoses with the systemic venous system:
- Gastro oesophageal junction
- Ileocaecal junction
- Rectum
- Anterior abdominal wall via the umbilical vein
201
What the varices?
enlarged/ swollen veins.
202
When do varices cause symptoms?
When the high blood flow causes bleeding.
203
How are stable varices treated?
Propanolol (beta blocker) reduces portal hypertension
Elastic band litigation
Injection of sclerosant
Transjugular intra-hepatic portosystemic shunt (TIPS)
204
How are bleeding oesophageal varices treated?
Vasopressin analogues--> cause vasoconstriction and slow bleeding.
Correct any coagulopathy with vit. K and fresh frozen plasma
Urgent endoscopy--> Injection os sclerosant or elastic band ligation.
Sengstaken-Blakemore tube-inflatable tube inserted to tamponade the bleeding varices
205
What is ascites?
Fluid in the peritoneal cavity
206
Why does cirrhosis cause ascites?
Increased pressure in the portal system causes fluid to leak out of the liver and bowel capillaries and into the peritoneal cavit.
207
What is transudative ascites?
Low protein content ascites
208
What does the fluid loss into the peritoneal space in ascites cause?
Drop in circulating volume, leading to reduction in blood pressure entering the kidneys. They sense this lower pressure and release renin, which leads to increased aldosterone secretion and reabsoprtion of fluid and sodium in the kidneys.
209
How is ascites managed?
Low sodium diet
Anti-aldosterone diuretics
Paracentesis (ascitic drain)
Prophylactic antibiotics against SBP
210
What is spontaneous bacterial peritonitis (SBP)?
When an infection develops in the ascitic fluid and peritoneal lining. (occurs in 10% of patients with ascites secondary to cirrhosis)
211
What are the key presentations of spontaneous bacterial peritonitis?
```
Asymptomatic
Fever
Abdominal pain
Deranged bloods
Ileus
Hypotension
```
212
What is Hepatorenal syndrome?
When portal hypertension leads to loss of blood volume in other areas of the circulation, including the kidneys. This leads to hypotension in the kidney and therefore the activation of the RAAS system, causing renal vasoconstriction. This combined with low circulating volume leads to starvation of blood to the kidney, causing rapid deterioration of kidney function. Fatal within a week unless there is a liver transplant
213
What is hepatic encephalopathy?
When a build of toxins (e.g. ammonia) affects the brain
214
Why does ammonia build up in the blood in patients with cirrhosis?
Functional impairment of the liver cells prevents them from metabolising it.
Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver altogether and enters the systemic system directly.
215
What is the acute presentation of hepatic encephalopathy?
Reduced consciousnnes and confusion.
216
What are the precipitating factors of hepatic encephalopathy?
```
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications
```
217
How is hepatic encephalopathy managed?
Laxatives--> Encourage excretion of ammonia
Antibiotics --> Reduce number of intestinal bacteria producing ammonia
Nutritional support
218
What is alcoholic fatty liver disease and what percentage of adults have it?
When fat is deposited in liver cells, intefering with their function.
30 % of adults
219
What are the 4 stages of NAFLD?
1. NAFLD
2. NASH (Non-alcoholic steatohepatitis)
2. Fibrosis
4. Cirrhosis
220
Wha are the risk factors for NAFLD?
```
Obesity
Poor diet
Sedentary lifestyle
T2 diabetes
High cholesterol
Advancing age
Smoking
High BP
```
221
What are the common liver function tests?
```
Alanine transaminase (ALT).
Aspartate transaminase (AST).
Alkaline phosphatase (ALP).
Albumin and total protein.
Bilirubin.
Gamma-glutamyltransferase (GGT).
L-lactate dehydrogenase (LD).
Prothrombin time (PT).
```
222
What is the next step when someone presents with abnormal liver function tests without clear cause and what does this include?
Non-invasive liver screen:
- Liver ultrasound
- Hep B/ C serology
- Autoantibody tests
- Immunglobulins
- Ceruloplasmin
- Alpha 1 Anti-trypsin levels
- Ferritin and transferrin saturation
- ELF (enhanced liver fibrosis) blood test
223
What autoantibodies are tested for in a non-invasive liver screen?
```
Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondiral antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)
```
224
How is non-alcoholic fatty liver disease managed?
```
Weight loss
Exercise
Stop smoking
Control of diabetes, BP and cholesterol
Avoid alcohol
```
225
What are the causes of hepatitis?
```
Alcoholic hepatitis
Non alcoholic liver disease
Viral
Autoimmune
Drug induced (paracetamol overdose)
```
226
What are the symptoms of hepatitis?
- Asymptomatic or non-specific
- Abdominal pain
- Fatigue
- Pruritis (itching)
- Muscle and joint aches
- Nausea and comiting
- Jaundice
- Fever
227
What are the typical biochemical findings in hepatitis (hepatic picture)?
Liver function tests become deranged with high transaminases (AST/ALT) and proportionally less rise of ALP.
228
What are transaminases?
Liver enzymes released into the blood as a result of inflammation of the liver cells.
229
What is the most common viral hepatitis worldwide?
Hep. A
230
What is Hep. A and how is it transmitted?
An RNA virus transmitted via the faecal-oral route (usually contaminated water or food)
231
How does Hep. A present?
Nausea, vomiting, anorexia and jaundice.
| Can cause cholestasis.
232
What is cholestasis and what does it cause?
Slowing of bile through the biliary system that presents with dark urine and pale stools.
233
How quickly does Hep A resolve and what is its management?
Resolves in 1-3 months with no treatment.
| Management is with basic analgesia
234
What is Hep B and how is it transmitted?
DNA virus transmitted by direct contact with blood or bodily fluids (e.g. sex or IV drug users, sharing toothbrushes, contact between minor cuts)
Can also be passed from mother to child during birth (Vertical transmission)
235
How quickly does Hep B resolve?
Within 2 months - however 10% become chronic Hep B carriers
236
What are the different types of viral markers for Hep B?
```
Surface antigens
E antigen
Core antibodies
Surface antibodies
Hep B virus DNA
```
237
What is the abbreviation for surface antigens and what do they indicate?
HBsAg
| If present, indicate active infection
238
What is the abbreviation for E antigens and what do they indicate?
HBeAg
| Marker of viral replication and implies high infectivity
239
What is the abbreviation for core antibodies and what do they indicate?
HBcAb
| Implies past or current infection
240
What is the abbreviation for surface antibodies and what do they indicate?
HBsAb
| Implies vaccination or past or current infection
241
What is the abbreviation for Hep B virus DNA and what does its presence indicate?
HBV DNA
| Direct count of viral load.
242
What is tested for when screening for Hep B?
HBcAb (for previous infection)
HBsAg (for active infection)
If positive, test for HBeAg and viral load.
243
How can you differentiate between acute, chronic and past Hep B infections?
Measure IgM and IgG versions of the HBcAb (core antibody). IgM implies active infection (high titre with acute infection, low titre with chronic infection), IgG indicates past infection.
244
What does a high level of HBeAg indicate?
The patient is in the acute phase of infection when the virus is actively replicating, meaning they are highly infectious.
245
How is Hep B managed?
```
Low threshold for screening in those at risk.
Refer for specialist management.
Notify public health
Stop smoking/ alcohol
Education about reducing transmission
Test for complications
Antiviral medication
```
246
What are symptoms of Hep B and when do they develop?
Most people do not get symptoms.
If symptoms do develop, they tend to happen 2 or 3 months after exposure to the hepatitis B virus:
Flu-like symptoms--> tiredness, fever, and general aches and pains
Loss of appetite
Nausea/ vomiting/ diarrhoea
Jaundice
These symptoms will usually pass within 1 to 3 months (acute hepatitis B), although occasionally the infection can last for 6 months or more (chronic hepatitis B).
247
Who is hep B vaccine routinely offered to?
Vaccine is offered to all babies born in the UK (need 3 top ups)
Also those at high risk:
-Babies born to hepatitis B-infected mothers
-Close family and sexual partners of someone with hepatitis B
-People travelling to a part of the world where hepatitis B is widespread
-Families adopting or fostering children from high-risk countries
-People who inject drugs or have a sexual partner who injects drugs
-People who change their sexual partner frequently
men who have sex with men
male and female sex workers
-People who work somewhere that places them at risk of contact with blood or body fluids, such as nurses, prison staff, doctors, dentists and laboratory staff
-People with chronic liver or kidney disease
248
What is Hep C and how is it transmitted?
RNA virus spread by blood and bodily fluids.
249
What is the disease course of hep C?
1 in 4 makes full recovery
| 3 in 4 become chronic --> Complications include liver cirrhosis and hepatocellular carcinoma
250
How is Hep C tested for?
Hep C antibody screening test
| Hep C RNA testing used to confirm diagnosis, calculate viral load and assess for individual genotype
251
How is Hep C managed?
Same as hep B but direct acting antivirals can also be used to cure infection in 90% of patients
252
What is hep D and which patients can get it?
RNA virus that can only survive in patients who also have Hep B. Attaches to HBsAg and can't survive without it so there are very low rates in the UK.
253
Are all forms of viral hepatitis notifiable diseases?
Yes
254
What is Hep E and how is it transmitted?
RNA virus transmitted by the faecal oral route. Very rare in UK
255
What is autoimmune hepatitis (what are the two types)?
Rare cause of chronic hepatitis with unknown cause- linked to genetic predisposition and triggered by environmental factors.
Type 1: occurs in adults
Type 2: occurs in children
256
How is autoimmune hepatitis treated?
With high dose steroids (prednisolone) that are tapered over time as other immunosuppressants are introduced.
257
What is haemochromatosis?
Iron storage disorder that results in excessive total body iron and deposition of iron in tissues
258
What causes haemochromatosis?
Autosomal recessive mutations in the HFE (human haemochromatosis protein) gene on chromosome 6.
259
What are the symptoms of haemochromatosis?
- Chronic tiredness
- Joint pain
- Pigmentation
- Hair loss
- Erectile dysfunction
- Amenorrhoea
- Cognitive symptoms
260
How is haemochromatosis diagnosed?
Serum ferritin levels
Transferrin saturation--> Allows distinction between high ferritin levels caused by iron overload or by other causes (inflammation or NAFLD)
Genetic testing to confirm
Liver biopsy with Perl's stain---> Establishes iron concentration in parenchymal cells
CT abdomen
MRI
261
What are the complications of haemochromatosis?
T1 diabetes (Iron in pancreas)
Liver cirrhosis
Endocrine/ sexual problems -->hypogonadism, impotence, amenorrhea, infertility (caused by iron deposits in pituitary and gonads)
Cardiomyopathy (iron deposits in heart)
Hepatocellular carcinoma
Hypothyroidism (iron deposits in thyroid)
Chrondocalcinosis/ pseudogout (calcium deposits in joints causing arthritis)
262
How is haemochromatosis managed?
Venesection (weekly to decrease total iron)
Monitor serum ferritin
Avoid alcohol
Monitor/ treat complications
263
What are the most common metabolic liver diseases?
Haemochromatosis
Alpha-I antitrypsin deficiency (AATD)
Wilson Disease
264
What is metabolic liver disease?
Disorders in which abnormal chemical reactions in the body disrupt the body's metabolism.
265
What is Wilson disease?
Excessive accumulation of copper in the body and tissues
266
What causes Wilson disease?
Autosomal recessive mutation in the Wilson disease protein (ATP7B copper-binding protein) on chromosome 13.
267
What is the function of the Wilson disease gene?
Responsible for various functions including the removal of excess copper in the liver.
268
What are the key features of Wilson disease?
Copper deposition leading to :
Hepatic problems (40%)
Neurological problems (50%)
Psychiatric problems (10%)
Kayser-Fleischer rings in cornea (brownish circles around iris)
Haemolytic anaemia
Renal tubular acidosis (caused by renal tubular damage meaning acids aren't excreted)
Osteopenia (loss of bone mineral density)
269
What does excess copper to to the liver?
Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis.
270
What neurological and psychiatric symptoms can Wilson disease cause?
```
Concentration and coordination issues
Dysarthria (speech difficulties)
Dystonia (abnormal muscle tone)
Deposition in ganglia leads to Parkinsonism (tremor, bradykinesia and rigidity)
Depression
Psychosis
```
271
How is Wilson disease diagnosed?
Low serum caeruloplasmin (copper transport protein)
Liver biopsy for liver copper content.
Elevated 24 hour urine copper assay
272
How is Wilson disease treated?
Copper chelation agents:
Penicillamine
Trientene
273
What is alpha-1-antitrypsin and where is it mainly produced?
Protease (enzymes that catalyse proteolysis) inhibitor produced in the liver.
274
What is elastase (action + where is is secreted from)?
An enzyme secreted by neutrophils that digests connective tissues.
275
What is the action of A1AT?
Binds to neurophil elastase, protecting tissues against digestion.
276
What is alpha-1-antitrypsin deficiency?
Autosomal recessive defect in the gene for A1AT on chromosome 14 causing a deficiency.
277
What 2 organs are mainly affected by alpha-1-antitrypsin deficiency and what does it do to them?
Liver--> Liver cirrhosis
| Lungs--> Bronchiectasis and emphysema
278
How does alpha-1-antitrypsin deficiency cause liver damage?
The mutant version of the protein is produced in the liver and gets trapped. It builds up and causes liver damage which progresses to cirrhosis over time.
279
How does alpha-1-antitrypsin deficiency cause lung damage?
The lack of functioning alpha-1-antitrypsin protein leads to an excess of protease enzymes that attack the connective tissue in the lungs, leading to bronchiectasis and emphysema over time.
280
How is alpha-1-antitrypsin deficiency diagnosed?
Low serum alpha-1-antitrypsin.
Liver biopsy--> Cirrhosis and acid-Schiff-positive staining globules
Genetic testing for A1AT gene
CT thorax
281
How is alpha-1-antitrypsin deficiency managed?
Stop smoking
Symptomatic management
Organ transplant if necessary
282
Where is bile produced and where is it stored? Where does it go once released
Produced in the liver and stored in the gallbladder. Released into the duodenum when needed
283
What does bile consist of?
```
95% water with things dissolved:
Bile salts
Bilirubin phospholipid
Cholesterol
Amino acids
Steroids
Enzymes
Porphyrins
Citamins
Heavy metals
Exogenous drugs
Xenobiotics
Environmental toxins
```
284
Where is bile initially secreted from and how does it get to the gallbladder?
Initially secreted from hepatocytes. Drains from both lobes of the liver via canaliculi, intralobular ducts and collecting ducts into the left and right hepatic ducts. These ducts amalgamate to form the common hepatic duct, which descends and joins the cystic duct- which allows bile to flow in and out of the gallbladder for storage and release. At this point, the common hepatic duct and cystic duct combine to form the common bile duct.
285
What is primary biliary cirrhosis?
Condition where the immune system attacks the small bile ducts of the liver.
286
What are the first areas to be affected in primary biliary cirrhosis and what does this cause?
Intralobar ducts (Canals of Hering) which causes obstruction of the outflow of bile (cholestasis)
287
What is cholestasis?
Obstruction of the outflow of bile
288
Why does primary biliary cirrhosis lead to liver failure?
The back-pressure of bile obstruction caused by autoimmune destruction of small bile ducts leads to fibrosis, cirrhosis and ultimately liver failure.
289
What key chemicals are usually excreted through the bile ducts into the intestines and what happens when they are not?
Bile acids, bilirubin and cholesterol
| Build up in the blood
290
What does excess serum bile acids cause?
Itching
291
What does excess serum bilirubin cause?
Jaundice
292
What does raised serum cholesterol cause?
Xanthelasma (Cholesterol deposits in skin and blood vessles)--> Increases risk of heart disease.
293
What are bile acids responsible for in the gut and what does a lack of them cause?
Help the gut digest fats. Therefore a lack causes GI disturbance, malabsorption of fats and greasy stools.
294
What does a lack of bilirubin in the stools cause?
Pale stools (bilirubin responsible for the dark colour)
295
What are the key presentations of primary biliary cirrhosis?
Fatigue
Pruritus (itching)
GI disturbance/ pain
Jaundice
Pale stools
Xanthoma/ Xanthelasma (cholesterol deposits in skin/ blood vessels)
Signs of cirrhosis and liver failure (ascites, splenomegaly, spider naevi)
296
How is primary biliary cirrhosis diagnosed?
```
Liver function tests
Autoantibodies
Raised ESR
Raised IgM
Liver biopsy
```
297
What is the first liver enzyme to be raised in obstructive pathology?
Alkaline phosophatase (ALP)
298
How is alkaline phosophatase treated?
Ursodeoxycholic acid--> Reduces intestinal absorption of cholesterol
Colestyramine--> Binds to bile acids to prevent absorption in the gut
Liver transplant for end stage liver disease
Immunosuppression
299
What is steatorrhoea?
Greasy stools due to lack bile salts to digest fats
300
What is primary sclerosing cholangitis?
Condition where the intra/extrahepatic ducts become strictured (abnormally narrowed) and fibrotic, causing obstruction of flow of bile out of the liver.
301
What is cholangitis?
Inflammation of the bile duct system
302
What are the associated causes of primary sclerosing cholangitis?
Causes unclear but linked to genetic, autoimmune, microbiome and environmental factors.
70% of cases linked to ULCERATIVE COLITIS
303
What are the risk factors for primary sclerosing cholangitis?
Male
30-40 y/o
Ulcerative colitis
Family history
304
What are the key presentations of primary sclerosing cholangitis?
```
Jaundice
Chronic right upper quadrant pain
Pruritis
Fatigue
Hepatomegaly
```
305
What do liver function tests show in primary sclerosing cholangitis?
Cholestatic picture: deranged ALP (alkaline phosphatase)
| May be rise in bilirubin as strictures become more severe, preventing it from being excreted.
306
How is primary sclerosing cholangitis diagnosed?
MCRP--> Magneic resonance cholangiopancreatography (MRI scan of the liver, bile ducts and pancreas which may show lesions or strictures)
LFTs
Autoantibodies
307
What are the complications of primary sclerosing cholangitis?
```
Cholangiocarcinoma (10-20% cases)
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble deficiencies
```
308
How is primary sclerosing cholangitis managed?
```
Liver transplant (Can be curative but can also bring other problems)
ERCP to stent strictures
Ursodeoxycholic acid
Colestyramine
Monitor/ treat complications
```
309
What is ERCP?
Endoscopic Retrogade Cholangio-Pancreatography--> Inserting a camera through GI tract to ampulla of Vater where it enters the bile duct. Uses X-rays and injecting contrast to identify any strictures which can then be dilated and stented.
310
What is primary liver cancer and what are the two main types?
Cancer that originates in the liver:
Hepatocellular carcinoma (80%)
Cholangiocarcinoma (20%)
311
What is secondary liver cancer?
Metastasis to the liver that can occur from almost any cancer.
312
What is the first stage in treating secondary liver cancer?
Look for the primary cancer (full body CT, thorough history, skin and breast exam)
313
What is the main risk factors for hepatocellular carcinoma (HCC)?
Liver cirrhosis due to:
- Viral hepatitis (B/C)
- Alcohol
- NAFLD
- Other chronic liver disease
314
What condition is cholangiocarcinoma associated with?
Primary sclerosing cholangitis (10% cases)
315
How does liver cancer present?
```
Asymptomatic for long period and presents late.
Non specific:
-Weight loss
-Abdominal pain
-Anorexia
-Nausea/vomiting
-Jaundice
-Pruritis
```
316
What investigations can be done for liver cancer?
- Alpha-feoprotein= tumour marker for hepatocellular carcinoma
- CA19-9= tumour marker for cholangiocarcinoma
- Liver ultrasounds
- CT/ MRI scans
- ERCP to take biopsies
317
What is the prognosis of primary liver cancer?
Very poor unless diagnosed early
318
How is hepatocellular carcinoma treated?
-Resection of early disease
- Liver transplant if isolated to liver
- Kinase inhibitors (inhibit proliferation of cancer cells)
(resistant to chemo and radiotherapy)
319
How is cholangiocarcinoma treated?
- Surgical resection of early disease
| - ERCP to place stent in bile duct where cancer is compressing duct.
320
What are Haemangiomas?
Common benign tumours of the liver often found incidentally
321
What is focal nodular hyperplasia?
Benign liver tumour made of fibrotic tissue often found incidentally and often related to oestrogen
322
What is an orthotopic transplant?
When an entire liver is transplanted straight from a deceased patient to a recipient.
323
What is a living donor transplant?
When a portion of liver is taken from a living donor and transplanted into a patient. The liver can then regenerate in both patients.
324
What are the main indications for liver transplant?
Acute liver failure--> Most commonly acute viral hepatitis and paracetamol overdose
Chronic liver failure--> May take around 5 months for liver to become available
325
When would a liver transplant be unsuitable?
- Significant co-morbidities
- Excessive weight loss and malnutritioin
- Active infection
- End-stage HIV
- Active alcohol use (6 months abstinence required)
326
What are the 3 types of jaundice?
Pre-hepatic
Hepatocellular
Post-hepatic
327
What is pre-hepatic jaundice?
When excessive red cell breakdown overwhelms the body's ability to conjugate bilirubin, causing excess unconjugated bilirubin in the blood.
328
What causes pre-hepatic jaundice?
Gilberts syndrome
| Haemolytic anaemia
329
What is hepatocellular jaundice?
When dysfunction of hepatic cells means the liver loses its ability to conjugate bilirubin
330
What causes hepatocellular jaundice?
```
Hepatitis (Viral, autoimmune)
Alcoholic liver disease
Haemochromatosis
Primary biliary cirrhosis/ sclerosing cholangitis
Hepatocellular carcinoma
Latrogenic (medication)
```
331
What is post-hepatic jaundice?
Obstruction of biliary drainage, leading to lack of conjugated bilirubin excretion
332
What causes post-hepatic jaundice?
```
Intra-luminal causes (gallstones)
Mural causes (Cholangiocarcinoma, strictures)
Extra-mural causes (Pancreatic cancer, abdominal masses)
```
333
What type of jaundice is it likely to be if there is no dark urine, stools are normal colour and there is no itching?
Pre-hepatic
334
What is biliary colic?
The pain associated with the temporary obstruction of the cystic or common bile duct due to a stone migrating from the gallbladder
335
What is cholecystitis?
Gallbladder inflammation
336
What is a reducible hernia?
Hernia what can be pushed back into the abdominal cavity
337
What is an irreducable hernia?
Hernia that cannot be pushed back into place
338
What are the three main complications of hernias?
Incarceration
Obstruction
Strangulation
339
What is incarceration?
When a hernia cannot be reduced back into its proper position and gets trapped in the herniated position
340
What is hernia obstruction?
Where a hernia causes a blockage in the passage of faeces through the bowel .
341
What is hernia strangulation?
Where a hernia is non-reducible and the base of the hernia becomes so tight it cuts off the blood supply.
342
What does the inguinal canal run between?
Deep inguinal ring (connects to the peritoneal cavity) to the superficial inguinal ring (where it connects to the scrotum)
343
What is the purpose of the inguinal canal in men?
Allows the spermatic cord and its contents to travel from the peritoneal cavity to the scrotum.
344
What passes through the inguinal canal in women?
Round ligament (passes from uterus to labia majora)
345
What is the processus vaginalis?
Pouch of peritoneum that extends from the abdominal cavity through the inguinal canal during fetal development, allowing the testes to descend through the inguinal canal into the scrotum.
346
What is a direct inguinal hernia?
When the deep inguinal ring remains patent and the processus vaginalis remains intact, allowing the bowel to herniate through the inguinal canal.
347
How do you differentiate a direct and indirect inguinal hernia?
When pressure is applied to the deep inguinal ring, an indirect inguinal hernia will remain reduced.
