Liver and friends Flashcards
(126 cards)
1
Q
What are the 2 main types of cholangitis?
A
- Ascending cholangitis (Otherwise known as acute cholangitis).
- Primary sclerosing cholangitis.
- NOTE: there can be overlap between them.
2
Q
What is ascending cholangitis?
A
- Acute infection of the biliary tree usually due to an obstruction.
- Strongly associated with Charcot’s triad.
3
Q
What are the symptoms of ascending cholangitis?
A
Charcot’s triad:
- RUQ pain
- Jaundice
- Fever
If severe:
- Changed mental status.
- Hypotension.
(Now called “Reynold’s Pentad”.)
4
Q
What is the main risk factor for ascending cholangitis?
A
- Biliary obstruction (e.g. cholelithiasis, PSC etc.)
5
Q
What is the pathophysiology of ascending cholangitis?
A
- Obstruction of the CBD.
- Causes cultivation of a bacterial infection (normally E. coli) that spreads up the biliary tree.
6
Q
What are the investigations used for ascending cholangitis?
A
- LFTs. Hyperbilirubinaemia. Raised ALP and raised GGT.
- Blood culture: Positive (usually E. coli).
- First line imaging: Abdominal USS.
- ERCP gold standard.
7
Q
What is the treatment for ascending cholangitis?
A
- Cefuroxime (cephalosporin) + metronidazole (antimicrobial) as broad spectrum choice until cultures return.
- IV fluids.
- Analgesia (e.g. paracetamol/morphine).
- ERCP.
IF SEPTIC, SEPSIS 6.
8
Q
How is presentation of cholecystitis different to presentation of ascending cholangitis?
How is presentation of primary sclerosing cholangitis different to ascending cholangitis?
A
- Cholecystitis. Will have a +ve murphys sign (pain in RUQ on palpation during inspiration). Will also NOT have jaundice.
- Primary sclerosing cholangitis. More insidious onset, and strong association with UC.
9
Q
What is the most common bacterial cause of ascending cholangitis?
A
- E. Coli (gram -ve bacilli).
10
Q
How can ascending cholangitis cause pancreatitis?
A
- Pancreatitis.
- If common bile duct obstruction is very distal, the pancreatic duct is also obstructed, which causes acute pancreatitis.
11
Q
What is the treatment for sclerosing cholangitis?
A
MANAGE THE SYMPTOMS OF DECREASED LIVER FUNCTION:
- Rifampicin to reduce itching (pruritus).
- ERCP + balloon dilatation.
When end stage liver disease, transplant.
12
Q
What are the components of a LFT and what do they mean?
A
- ALT and AST high in hepatocellular injury.
- ALP high in both biliary obstruction and bone disease.
- GGT high in biliary obstruction. May also be raised due to alcohol/drugs.
- If ALP is raised and GGT is normal, suggests bone disease (e.g. vit D deficiency/osteomalacia).
- AST>ALT indicates cirrhosis (>1) and acute alcoholic hepatitis (>2).
13
Q
How can urine and stool presentation be used to determine the potential causes of jaundice?
A
- Normal urine (unconjugated bilirubinaemia) and stool suggests pre-hepatic jaundice (e.g. haemolytic anaemia).
- Dark urine (conjugated bilirubinaemia) and normal stool suggests hepatic jaundice (e.g. hepatitis).
- Dark urine (conjugated bilirubinaemia) and steatorrhoea suggests post-hepatic jaundice (e.g. biliary tree obstruction)
14
Q
What is acute liver failure?
A
Rapid decline in hepatic function characterised by:
- Jaundice
- Encephalopathy
- INR>1.5 (extrinsic pathway).
AND NO PRIOR HISTORY OF LIVER DISEASE.
15
Q
What is the clinical presentation of acute liver failure?
A
- Hepatic encephalopathy.
- Jaundice.
- Abdominal pain.
- Nausea/vomiting.
16
Q
What are the most common causes of ALF?
A
- Paracetamol overdose (By far most common cause).
- Acute hepatitis B.
- Autoimmune hepatitis.
17
Q
What is the generalised pathophysiology of acute liver failure?
A
Generally, it is the massive and acute necrosis of hepatocytes, leading to liver failure.
18
Q
How is ALF further categorised?
A
By the time lapsed between onest of jaundice and onset of encephalopathy:
- Hyperacute. 7 days or less.
- Acute. 8-28 days.
- Subacute. 29 days to 12 weeks.
19
Q
What are some of the key investigations performed following a diagnosis of ALF? What are the expected findings?
What additional investigation is done in suspected paracetamol overdose?
A
- PT/INR (extrinsic pathway). Will be >1.5.
- LFTs. Raised AST/ALT and hyperbilirubinaemia.
- Creatinine/urea. Raised if kidney failure is present (common complication of ALF).
- ABG. Metabolic acidosis w/ raised lactate.
- Blood glucose levels. Hypoglycaemia due to reduced gluconeogenesis.
FOR SUSPECTED PARACETAMOL OVERDOSE:
- Measure serum paracetamol concentration. MUST BE DONE AT LEAST 4 HOURS AFTER CONSUMPTION FOR RESULT TO BE VALID.
20
Q
What is the generalised management for acute liver failure when encephalopathy has developed?
A
As soon as encephalopathy develops:
- ICU admission.
- Bed 30 degrees (for ICP management) and intubate (to secure the airway).
- Use propofol/fentanyl for analgesia (short half life).
- Give fluids (carefully monitor BP). Can be given containing glucose if patient is hypoglycaemic.
CONSIDER ALL ACUTE LIVER FAILURE PATIENTS FOR TRANSPLANT.
21
Q
What are the common complications of acute liver failure?
A
- Hypoglycaemia.
- Encephalopathy/coma.
- Bacterial hepatitis.
- Renal failure.
22
Q
What is the pathophysiology of paracetamol overdose liver failure?
A
For paracetamol overdose:
- Normally, paracetamol is metabolised by CYP450 enzymes into NAPQ1.
- NAPQ1 is toxic, and so is then conjugated by glutathione (an antioxidant) to deem it safe.
- In paracetamol overdose, glutathione stores are depleted, leading to NAPQ1 not being conjugated. This causes hepatocellular injury and acute liver failure.
23
Q
What dosage is the threshold for paracetamol overdose?
A
75mg/kg/24hr.
24
Q
What are the investigations for a suspected paracetamol overdose?
A
FOR PARACETAMOL OVERDOSE:
- Paracetamol levels in blood AFTER 4 HOURS SINCE OVERDOSE.
- Creatinine/urea. Check for renal failure.
- Glucose levels. Check for hypoglycaemia.
- LFTs. Check for acute liver failure.
- ABG (check for metabolic acidosis/ lactic acidosis).
25
What is the presentation of a suspected paracetamol overdose?
May be asymptomatic.
Common presentation includes:
- Nausea and vomiting.
- Abdominal pain.
- Metabolic acidosis.
- Jaundice, hepatomegaly, hepatic encephalopathy - POTENTIALLY COMA (Acute liver failure).
- Haematuria/proteinuria (AKI - rare).
26
What are the investigations indicated in paracetamol overdose?
- Serum paracetamol concentration.
MUST BE DONE AT LEAST 4 HOURS AFTER INGESTION TO BE VALID.
- LFTs. Raised ALT, raised INR\>1.3 = Acute liver injury.
- Urea, creatinine. Raised = AKI.
- ABG. Metabolic acidosis (due to liver failure). Raised lactate (lactic acidosis).
27
What is the treatment for paracetamol overdose?
**- Acetylcysteine** (if over 150mg/kg/24hr has been ingested, give immediately).
- Ondansetron (anti-emetic).
28
When do paracetamol overdose patients require specialist management?
- Signs of liver injury (jaudince, encephalopathy/coma, asterixis, INR\>1.3 etc.)
- Hypoglycaemia.
- Signs of AKI (high creatinine/urea).
- Lactic acidosis (raised lactate on ABG).
29
What is acute pancreatitis?
What is the diagnostic criteria?
- Inflammation of the pancreas with acinar cell injury.
Diagnostic criteria - must have at least 2/3 of the following:
- Severe epigastric/ lower back pain.
- Raised amylase or lipase.
- Suggestive findings on imaging.
30
What are the two different types of pancreatitis?
- Acute
- Chronic
31
What is the clinical presentation of acute pancreatitis?
- Epigastric/ upper GI pain that radiates through to the back. (Sudden onset).
- Nausea/vomiting.
- Potentially hypovolaemia.
32
What are the risk factors for/ causes of acute pancreatitis?
Remember this as I GET SMASHED:
- Idiopathic
- Gallstones
- Ethanol (alcohol)
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion stings
- Hyperlipidaemia/hypercalcaemia
- ERCP
- Drugs
33
What are the investigations used in acute pancreatitis?
Diagnostic investigations:
- Lipase (1st line) and amylase (2nd line) - raised.
- Immediate imaging not normally needed for diagnosis.
- However, RUQ USS should be done anyways to check for cholelithiasis.
34
What is the treatment for acute pancreatitis?
What about if it is concurrent with cholecystitis due to cholelithiatic obstruction?
- Supportive therapy (O2, analgesia, fluids PRN).
If patient has acute pancreatitis AND cholangitis caused by a gallstone:
EMERGENCY ERCP.
35
What are the potential complications of acute pancreatitis?
- Renal failure (AKI) due to hypovolaemia.
36
What is chronic pancreatitis?
Progressive injury to the pancreas, resulting in scarring and permanent loss of function.
37
What is the clinical presentation of chronic pancreatits?
- Dull epigastric pain, radiating to the back. Pain gets better with leaning forwards. Can be classified using the Ammann classification:
- Type A. Short, remitting episodes of pain.
- Type B. Longer, constant episodes of pain.
- Steatorrhoea.
- Weight loss (due to pain on eating).
38
What is the main cause of chronic pancreatitis?
- Poorly understood.
- Main cause is chronic alcohol abuse (70-80% of cases).
39
What are the risk factors for chronic pancreatitis?
- ALCOHOL IS THE MAIN RISK FACTOR.
- FH
- Coeliac disease.
40
What are the investigations used to diagnose chronic pancreatitis?
- CT or MRI abdomen is 1st line. Look for signs such as enlarged pancreas, calcifications etc.
- Gold standard. Pancreatic biopsy + histology. Look for acinar damage, fibrosis, increased connective tissue etc. (generally only used in high risk patients where imaging was inconclusive).
- Consider use of genetic testing in younger patients.
41
What is the treatment for chronic pancreatitis?
- Stop alcohol intake and stop smoking (1st line)
- Analgesia. Paracetamol or NSAIDs (1st line)
- Pancreatic enzyme replacement therapy - pancreatin (1st line) + omeprazole (PPI) so the enzymes can function better.
- ERCP drainage if there is biliary involvement.
42
What is the main potential complication of chronic pancreatitis?
- Diabetes due to reduced insulin secretion (called type 3c diabetes).
43
What is alcoholic liver disease?
Chronic liver disease caused by chronic heavy alcohol consumption.
44
What is the clinical presentation of alcoholic liver disease?
- PROLONGED HIGH ALCOHOL CONSUMPTION.
- RUQ pain.
- Hepatomegaly.
When more severe:
- Asterixis/confusion (hepatic encephalopathy).
- Jaundice
- Splenomegaly
45
What are the three main stages of alcoholic liver disease?
- Alcoholic fatty liver (1st)
- Alcoholic hepatitis (2nd)
- Alcoholic liver cirrhosis (3rd)
46
What is the pathophysiology of alcoholic liver disease?
Alcohol is normally metabolised through two main enzymes:
- CYP450
- Alcohol dehydrogenase
If the there is sustained high alcohol intake, strain is put on these pathways leading to:
- Increased free radicals in the liver.
- Increased fatty infiltration of hepatocytes.
Also, high alcohol intake leads to recruitment of hepatic macrophages, which secrete TNF-a and further amplify inflammatory processes.
All of these pathological processes result in cirrhosis, inflammation and hepatocyte necrosis in the liver.
47
What characteristic cells are found histologically in people suffering with alcoholic liver disease?
- Mallory bodies. Especially seen in the later stages (alcoholic hepatits, alcoholic liver cirrhosis).
48
What are the risk factors for alcoholic liver disease?
- Excessive, prolonged alcohol consumption MAIN ONE.
- Hep C - makes ALD more severe/progressive.
- Female (easier to get as a female, yet more prevalent in men).
49
What is the most common cause of chronic liver disease?
- Alcoholic liver disease.
50
What investigations are conducted to diagnose alcoholic liver disease?
CAGE/AUDIT questionnaire:
- Used to assess alcohol intake/dependancy.
LFTs (liver function tests):
- AST and ALT both rise, but AST more so.
* *- High GGT**
- Low albumin
- Raised bilirubin (both conjugated and unconjugated).
- In very severe alcoholic liver disease (cirrhosis) AST and ALT may be normal due to extreme levels of necrosis.
Hepatic USS - GS AND FIRST LINE.
- Look for hepatomegaly and cirrhosis.
- Should be carried out every 6-12 months for those with liver cirrhosis to screen for hepatocellular carcinoma.
51
What is the treatment for alcoholic liver disease?
- Alcohol abstinence and smoking cessation.
- Weight loss.
- Corticosteroids (prednisolone) to control inflammation if there is no renal failure.
- Consider loop diuretics (furesomide) for ascites.
- LIVER TRANSPLANT IN THE CASE OF ADVANCED ALCOHOLIC LIVER DISEASE (CIRRHOSIS).
52
What is primary sclerosing cholangitis?
- Chronic inflammation of the extra and/or intrahepatic ducts, leading to fibrosis and stricture.
53
What is the clinical presentation of primary sclerosing cholangitis?
Usually asymptomatic in early stages.
Can cause:
- Pruritus
- Jaundice
- RUQ pain
- NO FEVER (unless infection occurring too).
54
What disease is heavily linked to primary sclerosing cholangitis?
Ulcerative collitis
55
What is the pathophysiology of primary sclerosing cholangitis?
- Chronic inflammation of/ injury to the biliary ducts leads to fibrosis and stricture.
- Will eventually spread to intrahepatic ducts and cause liver disease too.
56
What are the investigations used for primary sclerosing cholangitis?
- MRCP (1st line) and ERCP (2nd line). Look for strictures.
- LFTs. Extremely high ALP and GTT. Slightly/moderately raised AST/ALT (pattern indicative of cholestatic disease). Hyperbilirubinaemia is sustained in more advanced disease.
57
What is the treatment given for primary sclerosing cholangitis?
If asymptomatic:
- Monitor and wait.
- Lifestyle advice (stop drinking and increase exercise).
If symptomatic:
- ERCP + balloon dilatation.
58
What are the common complications of primary sclerosing cholangitis?
- End-stage liver disease
- Osteoporosis
- Hepatocellular carcinoma/cholangiocarcinoma.
59
How is secondary sclerosing cholangitis different to primary sclerosing cholangitis?
How is autoimmune hepatitis different?
- Secondary sclerosing cholangitis. Will have an identifiable primary cause (e.g. recurrent pancreatitis).
- Autoimmune hepatitis. Will have a hepatic LFT pattern (Very high AST/ALT, slightly high ALP/GGT) and potentially raised IgG and ANA.
60
What is cholecystitis? What is the usualy cause?
- Acute inflammation of the gall bladder, usually caused by gallstones (90%).
61
What is the clinical presentation of cholecystitis?
- RUQ pain
* *- +ve murphy's sign**
- Fever
- Potentially a palpable gall bladder.
USUALLY NO JAUNDICE - DISEASE OF GALLBLADDER NOT LIVER.
62
What are the risk factors for cholecystitis?
- Gall stones.
- Diabetes.
- Nil by mouth (fasting or IV nutrition, as this will decrease gall bladder motility).
63
What is the pathophysiology of cholecystitits?
- Blockage of the cystic duct/neck of the gallbladder leads to cholestasis.
- Bile builds up in the gallbladder, increasing pressure and causing irritation.
- Triggers release of prostaglandins, which mediate inflammation in the gallbladder wall.
- In extreme cases, this can cause perforation/necrosis of the gallbladder.
64
What are the investigations used for cholecystitis?
- USS abdomen. Will show thickened gallbladder wall.
- If septic: CT/MRI to find the source of the infection. Blood culture to assess antibiotic sensitivity.
65
What is the treatment for cholecystitis?
- Analgesia (paracetamol or morphine as appropriate).
- IV fluids until can tolerate oral intake.
**- Laproscopic cholecystectomy EARLY AS POSSIBLE (with prophylactic antibiotics to reduce risk of infection).**
66
How does ascending cholangitis present differently to cholecystitis?
- Ascending cholangitis (or acute cholangitis). Will have Jaundice (charcot's triad) which is absent in cholecystitis (no jaundice).
67
What is cholelithiasis?
- Gall stones. Usually made of cholesterol, and can be in the gall bladder, cystic duct, common bile duct or pancreatic duct.
68
What are the clinical symptoms of cholelithiasis?
Usually asymptomatic until obstruction occurs. Then:
* *- Biliary colic pain**
- Often associated with eating (cholecystic movement).
- If CBD obstruction present, may cause jaundice.
69
What are the risk factors for cholelithiasis?
- Age (peak at 70)
- Female (3:1)
- Nil by mouth (fasting/IV nutrition) as this causes gallbladder hypomobility.
- Diabetes/obesity (these cause increased cholesterol).
- FH.
70
What are gall stones normally made from?
- 90% of gallstones are made of cholesterol.
71
What is the pathophysiology Mirizzi syndrome?
- Gall stones become trapped in the gallbladder neck/cystic duct and put pressure through the wall onto the CBD/CHD. This causes jaundice too.
72
What is the pathophysiology of Bouveret syndrone?
- Gallstone erodes the wall of the gallbladder, which forms a fistula with the duodenum.
- Gallstone passes into the duodenum, and blocks it.
73
What are the investigations used for cholelithiasis?
- USS abdomen. If no stones shown, but blockage of the CBD (choledocholithiasis) still suspected, use MRCP (2nd line).
- LFTs. If uncomplicated (contained in gall bladder/cystic duct) LFTs normal. If obstructing the CBD, biliary pattern (Very high ALP, GTT, hyperbilirubinaemia).
74
What are the treatments for cholelithiasis?
- Analgesia as appropriate (paracetamol, diclofenac, buprenorphine etc.)
**- For uncomplicated gall stones: Laparoscopic cholecystectomy.**
- For choledocholithiasis: Initial ERCP to achieve biliary drainage THEN laparoscopic cholecystectomy.
75
What is liver cirrhosis?
- Liver cirrhosis is characterised by fibrosis and conversion of normal liver architecture into structurally abnormal nodules known as regenerative nodules.
76
What is the clinical presentation of liver cirrhosis?
- Abdominal distension.
- Jaundice.
- Hepatomegaly.
- Pruritus.
- Haematomesis (due to gastric varices).
- Melaena (due to GI bleeding caused by portal hypertension).
- Spider naevi.
Many others too...
77
What are the risk factors of liver cirrhosis?
- Alcohol abuse (alcoholic liver cirrhosis).
- IV drug use/unprotected sex (Hep B/C).
- Obesity/diabetes (non-alcoholic fatty liver disease).
78
What is the pathophysiology of liver cirrhosis?
What are the potential complications of portal hypertension?
Liver cirrhosis activates the hepatic stellate cells. This causes:
- Collagen (I and III) deposition in the parenchyma.
- Stellate cells become contractile.
Both of these effects increase hepatic resistance, contributing to portal hypertension.
Portal hypertension can cause:
- Gastric varices.
- Ascites
79
What are the investigations used for liver cirrhosis?
What should be screened for in patients with liver cirrhosis?
LFTs.
- Generally, there will be raised AST and ALT, with AST:ALT being greater than one.
- Hyperbilirubinaemia.
- Hypoalbuminaemia.
Prolonged INR/PT time.
USS liver.
GI endoscopy - Used to assess for gastric varices, and should be done every 1-3 years to screen for gastric varices for all with liver cirrhosis.
80
What is the treatment for liver cirrhosis?
- AVOID NSAIDS AND PARACETAMOL.
- Spironolactone (potassium-sparring diuretic) to treat ascites.
- Liver transplant (if permanently decompensated function).
- Propranolol (to treat gastric varices).
81
What does a raised anti-microbial antibody (AMA) level indicate?
- Primary biliary cirrhosis. (this is differend to primary sclerosing cholangitis).
82
What is the formal name of liver cancer?
Hepatocellular carcinoma.
83
What is the most common precursor to hepatocellular carcinoma?
- Cirrhotic liver.
84
What is the clinical presentation of liver cancer?
- RUQ pain.
- Jaundice.
- Abdominal distension.
- Typical cancer signs (weight loss, fatigue etc.)
85
What is the investigation used in suspected hepatocellular carcinoma?
- Raised AFP (Alpha-fetoprotein).
- Liver USS.
BIOPSY IS NOT NORMALLY REQUIRED.
86
What is the treatment for hepatocellular carcinoma?
- Resection of the carcinoma.
- If the liver is in end-stage liver disease, liver transplant.
- Chemo if cancer to advanced to resect.
87
What is the most common form of pancreatic cancer?
- Primary pancreatic ductal adenocarcinoma.
88
What is the clinical presentation of pancreatic cancer?
- Unexplained epigastric pain.
- Painless obstructive jaundice (if a tumour in the head of the pancreas spreads to the CBD).
- Typical cancer symptoms (weight loss, fatigue etc.)
89
What is the investigation used in suspected pancreatic ductal adenocarcinoma?
- CT abdomen.
90
What is the treatment for pancreatic cancer?
- Surgical resection of the tumour.
- Pancreatin (enzyme replacement).
91
What is peritonitis? What is the most common cause?
- Inflammation of the peritoneum, commonly caused by bacteria.
92
What is the clinical presentation of peritonitis?
- Abdominal pain.
- Fever.
- Ascites.
93
What is the investigation used for suspected peritonitis?
- Paracentesis of ascitic fluid + culture.
Will appear cloudy, or bloody.
94
What is the 1st line treatment for peritonitis?
- Cefotaxime (cephalosporin).
95
What is ascites?
- Pathological collection of fluid in the peritoneal cavity.
96
What is the most common cause of ascites?
- Liver cirrhosis.
97
What are the investigations used to diagnose ascites?
- Physical examination/palpation (abdomen distension).
- USS abdomen is definitive.
98
What is an inguinal hernia?
Protrusion of the abdominal/pelvic contents either through the internal inguinal ring (indirect) or through the wall of the inguinal canal (direct).
99
What is a direct inguinal hernia?
- Protrusion of the abdominal contents directly through the wall of the inguinal canal.
100
What is an indirect inguinal hernia?
- Protrusion of the abdominal contents through the deep inguinal ring.
101
Who is most commonly affected by inguinal hernias?
- Middle aged men.
102
What is the clinical presentation of an inguinal hernia?
- Groin pain that comes on when the hernia bulges, and goes away when the hernia stops bulging.
- Palpable mass in the groin.
103
What is the treatment for an inguinal hernia?
- Surgical repair.
104
What is a1 antitrypsin deficiency?
- Autosomal codominant genetic disorder that results in the production of dysfunctional alpha-1 antitrypsin proteins.
- This causes AAT deficiency/build-up in the liver, causing both respiratory and hepatic pathology.
105
What are the key presenting features of AAT deficiency?
- Panacinar emphysema (involves entire alveolus).
- Bronchiectasis.
- Liver disease (hepatitis and jaundice).
106
What are the investigations used in AAT deficiency?
- Spirometry. Obstructive pattern.
- AAT screening. Will show low AAT.
- LFTs. Show liver disease.
107
What causes both the respiratory and hepatic presentations of AAT deficiency?
Respiratory presentation - Deficiency of AAT leads to inadequate neutralisation of neutrophil elastase in the lungs. Causes symptoms similar to those seen in COPD.
Hepatic disease - Some of the mutant AAT polymerises in the liver. This polymer is hepatotoxic and causes liver inflammation/damage.
108
What investigations are used in AAT deficiency?
- AAT screening. Shows low levels of AAT.
- Spirometry (obstructive pattern)
- LFTs. Show hepatocellular disease/inflammation.
109
What is the management of AAT deficiency?
- IV AAT therapy.
- Stop smoking.
- SABA
- Liver transplant.
110
What is a common treatment for ascites?
- Diuretics. These reduce the fluid overload, hopefully reducing ECF volume.
111
What are the 4 types of hepatitis?
- A
- B
- C
- Autoimmune
112
What is the vaccination system for each type of hepatitis?
- Hep A. Vaccine at request.
- Hep B. Routine vaccination on the NHS.
- Hep C. No vaccine available yet.
- Autoimmune hep. No vaccine.
113
What is the route of transmission for each hepatitis?
- Hep A. Faecal/oral.
- Hep B. Percutaneous/permucosal. (Unprotected sex/IV drug use).
- Hep C. Infectious blood transmission. (IV drug use).
114
Which is the most common hepatitis in the UK for drug users?
- Hep C. This is via IV drug use, and not routinely vaccinated against like hep B is.
115
What are the tests for each of the 4 types of hepatitis?
A - IgM anti-hepatitis A virus testing (IgM anti-HAV).
B - HBsAg +ve indicates infection. IgG +ve is acute, IgG -ve is chronic.
C - HCV antibody testing.
Autoimmune - LFTs (raised AST/ALT), presence of ANA (anti-nuclear antibodies), and presence of ASMAs (anti-smooth muscle antibodies).
116
What is the treatment for autoimmune hepatitis?
- Azathioprine (DMARD) + prednisolone (corticosteroids).
117
What is haemochromatosis?
- Autosomal recessive disorder that leads to buildup of iron in the body.
118
What is the clinical presentation of haemochromatosis?
- Bronzing of skin.
- Hepatomegaly.
- Loss of libido.
- Diabetes mellitus.
- Pseudogout.
119
What investigations are used for haemochromatosis?
1st line - Serum transferrin saturation. Raised.
Also - Serum ferratin. Raised.
120
What is the treatment for haemochromatosis?
Initially monitor and keep dietary iron low.
Phlebotomy to remove iron from blood if disease gets more severe.
121
What is Wilson's disease?
- Autosomal recessive disorder associated with buildup of copper in the body.
122
How does Wilson's disease relate to the liver?
- Lots of the copper is stored in the liver. This causes hepatitis and eventually cirrhosis/liver failure.
123
What is the presentation of Wilson's disease?
- Kayser - Fleischer rings (dark rings around the eyes).
- Tremor/dysarthria (neuro symptoms).
- Jaundice/hepatic tenderness (hepatic symptoms).
124
What are the tests used for Wilson's disease?
- LFT's. High AST/ALT and high bilirubin.
- 24 Hour copper excretion test. Will be raised.
125
What is the treatment for Wilson's disease?
- Zinc. This reduces Cu absorption in the gut.
126
What is the first line treatment for alcohol withdrawal?
- Chlordiazepoxide.
