TO DO LIVER & FRIENDS Flashcards
(98 cards)
1
Q
JAUNDICE
Why are liver patients vulnerable to infection?
A
- Impaired reticuloendothelial function
- Reduced opsonic activity
- Leucocyte function
- Permeable gut wall
2
Q
GALLSTONES
Give 3 causes of Gallstones
A
- Obesity and rapid weight loss
- DM
- Contraceptive pill
- Liver cirrhosis
3
Q
GALLSTONES
what are the clinical features of biliary colic from gallstones?
A
Most are asymptomatic
SYMPTOMS
- RUQ/epigastric pain (constant, >30 mins, worse after fatty foods, worse after meals)
- referred pain to right shoulder
- nausea + vomiting
SIGNS
- murphy’s sign negative (pain after eating but not on palpation)
4
Q
LIVER FAILURE
Give 5 causes of acute liver disease
A
- Viral hepatitis
- Drug induced hepatitis (e.g. paracetamol)
- Alcohol induced hepatitis
- Vascular - Budd-Chiari
- Obstruction
most common cause in UK is paracetamol overdose
5
Q
LIVER FAILURE
Give 5 causes of chronic liver disease
A
- Alcohol
- NAFLD
- Viral hepatitis (B,C,E)
- Autoimmune diseases
- Metabolic
- Vascular - Budd-Chairi
6
Q
LIVER FAILURE
what are the clinical features of chronic liver disease
A
SYMPTOMS
- fatigue
- anorexia
- jaundice
- bruising/bleeding
- confusion
SIGNS
- weight loss
- ascites
- caput medusae
- rectal haemorrhoids
- spider naevi
- gynaecomastia + hypogonadism
- hepatomegaly
7
Q
CIRRHOSIS
what are the clinical features of cirrhosis?
A
SYMPTOMS
- weight loss
- malaise
- fatigue
- easy bruising
SIGNS
- palmar erythema
- Dupuytren’s contracture
- leukonychia
- jaundice
- ascites
- spider naevi
- confusion + asterixis
- caput medusae
- haematemesis
8
Q
CIRRHOSIS
What investigations are done in someone with cirrhosis?
A
- FBC = anaemia + thrombocytopaenia
- U&Es = renal failure in acute
- LFTs = deranged, AST>ALT, raised GGT
- serum bilirubin = raised
- blood glucose = uncontrolled DM in NAFLD
- clotting = may be deranged
- hepatitis screen
- autoantibodies
- serum caeruloplasmin (screen for wilson’s)
- A1AT levels
- serum ferritin + transferrin (to screen for haemochromatosis)
- abdominal USS
- transient elastography
to consider
- AFP (to screen for HCC)
- liver biopsy (to grade + stage liver disease)
- UGI endoscopy (to assess for oesophageal varices)
9
Q
PORTAL HYPERTENSION
Give 3 causes of portal hypertension
A
- Pre-hepatic = blockage of hepatic portal vein before the liver (portal vein thrombosis)
- Hepatic = distortion of liver architecture (cirrhosis, schistosomiasis, Budd Chiari syndrome)
- Post-hepatic = venous blockage outside the liver (RHF, IVC obstruction)
10
Q
PORTAL HYPERTENSION
what is the clinical presentation of portal hypertension?
A
- often asymptomatic
- splenomegaly
- spider naevi
- GI bleeding
- ascites
- hepatic encephalopathy
11
Q
ASCITES
what are the causes of ascites with serum ascites albumin gradient (SAAG) >11g/L?
A
Indicates portal hypertension
LIVER (most common cause)
- cirrhosis/alcoholic liver disease
- acute liver failure
- liver mets
CARDIAC
- right HF
- constrictive pericarditis
OTHER
- budd-chiari syndrome
- portal vein thrombosis
- veno-occlusive disease
- myxoedema
12
Q
ASCITES
Describe the pathophysiology of ascites
A
- Increased intra-hepatic resistance leads to portal hypertension –> ascites
- Systemic vasodilation leads to secretion of RAAS, NAd and ADH –> fluid retention
- Low serum albumin also leads to ascites
Transudate = blockage of venous drainage
Exudate = inflammation
13
Q
ASCITES
Describe the treatment for ascites
A
- Restrict sodium and fluids
- Aldosterone antagonist (SPIRONOLACTONE) +/- loop diuretic (FUROSEMIDE)
- Paracentesis
- prophylactic antibiotics (CIPROFLOXACIN or NORFLOXACIN) to prevent spontaneous bacterial peritonitis
14
Q
HEPATITIS
Describe the natural history of HBV in 4 phases
A
- Immune tolerance phase: unimpeded viral replication –> high HBV DNA levels.
- Immune clearance phase: the immune system ‘wakes up’ = liver inflammation and high ALT
- Inactive HBV carrier phase: HBV DNA levels are low = ALT levels are normal, no liver inflammation
- Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver –> fibrosis
15
Q
HEPATITIS
what are the investigations for HBV?
A
- surface antigen (HBsAg) = active infection
- E antigen (HBeAg) = marker of viral replication + implies high infectivity
- core antibodies (HBcAb) = past or current infection
- surface antibody (HBsAb) = implies vaccination or past or current infection
- Hep B virus DNA (HBV DNA) = direct count of viral oea
16
Q
HEPATITIS
Give 3 side effects of alpha interferon treatment for HBV
A
- Myalgia
- Malaise
- Lethargy
- Thyroiditis
- Mental health problems
17
Q
HEPATITIS
Give 2 HBV specific symptoms
A
Arthralgia
Urticaria (hives)
18
Q
HEPATITIS
Describe the treatment for HCV
A
Direct acting antivirals (sofosbuvir or daclatasvir)
contact tracing
19
Q
HEPATITIS
Is HDV a RNA or DNA virus?
A
Incomplete RNA virus
Needs Hep B for assembly
20
Q
BUDD-CHIARI SYNDROME
What is Budd-Chiari syndrome?
A
Hepatic vein occlusion –> ischaemia and hepatocyte damage –> liver failure or insidious cirrhosis
21
Q
HAEMOCHROMATOSIS
90% of people with haemochromatosis have a mutation in which gene?
A
HFE - chromosome 6
22
Q
HAEMOCHROMATOSIS
Haemochromatosis is a genetic disorder, how is it inherited?
A
Autosomal recessive inheritance
23
Q
HAEMOCHROMATOSIS
Give 4 signs of haemochromatosis
A
- Fatigue, arthralgia, weakness
- Hypogonadism – eg erectile dysfunction
- SLATE-GREY SKIN (brownish/bronze)
- Chronic liver disease, heart failure, arrythmias
24
Q
HAEMOCHROMATOSIS
How might you diagnose someone with haemochromatosis?
A
- bloods - Raised ferritin, LFTs
- HFE genotyping - C282Y
- Liver biopsy - gold standard
25
HAEMOCHROMATOSIS
What is the treatment for haemochromatosis?
1. Iron removal - venesection
2. Monitor DM
3. Low iron diet
4. Screening for HFE
5. iron-chelating drugs (desferrioxamine)
26
HAEMOCHROMATOSIS
Give 2 complications of haemochromatosis?
Liver cirrhosis --> failure/cancer
| DM due to pancreatic depositions
27
A1AT
How is alpha 1 anti-trypsin deficiency inherited?
Autosomal recessive mutation in serine protease inhibitor gene
28
WILSONS DISEASE
What is Wilson's disease?
An autosomal recessive disorder of copper metabolism
| Excess deposition of copper in the liver
29
WILSONS DISEASE
How does Wilson's disease present?
Children = liver disease - hepatitis, cirrhosis, fulminant liver failure
Adults = CNS problems, mood changes, and Kayser-Fleischer rings
30
WILSONS DISEASE
What CNS changes are seen in a patient with Wilson's disease?
```
Tremor
Dysarthria
Dyskinesia
Ataxia
Parkinsonism
Dementia
Depression
```
31
WILSONS DISEASE
What is the treatment for Wilson's disease?
Lifetime treatment with penicillamine (chelating agent)
Low Cu diet - no liver, nuts, chocolate, mushrooms, shellfish
Liver transplant
32
AUTOIMMUNE HEPATITIS
How does autoimmune hepatitis present?
```
Fatigue, fever, malaise
Hepatitis
Hepatosplenomegaly
Amenorrhoea
Polyarthritis
Pleurisy
Lung infiltrates
Glomuleronephritis
```
33
AUTOIMMUNE HEPATITIS
What diseases are associated with autoimmune hepatitis?
Autoimmune thyroiditis
DM
Pernicious anaemia
PSCUC
34
PRIMARY BILIARY CHOLANGITIS
What is primary biliary cholangitis?
an autoimmune condition
characterised by granulomatous destruction of intrahepatic biliary ducts
this leads to cholestasis and subsequent leakage of bile into circulation
35
PRIMARY BILIARY CHOLANGITIS
what other conditions are associated with primary biliary cholangitis?
sjogrens syndrome
raynauds disease
autoimmune thyroid disease
rheumatoid arthritis
systemic sclerosis
36
PRIMARY BILIARY CHOLANGITIS
what are the clinical features of primary biliary cholangitis?
classic presentation = significant itching in middle-aged female
SYMPTOMS
- pruritus
- fatigue + weight loss
- dry mouth + eyes (sjogrens)
- obstructive jaundice (icteric, pale stool + dark urine)
SIGNS
- skin hyperpigmentation (increased melanin)
- clubbing
- mild hepatosplenomegaly
- xanthelsma + xanthomata
- scleral icterus
37
PRIMARY BILIARY CHOLANGITIS
What are the investigations?
- antimitochondrial antibodies (AMA)
- antinuclear antibodies (ANA)
- smooth muscle antibodies
- LFTs = obstructive jaundice (raised ALP, GGT + bilirubin, AST + ALT mildy deranged)
- coagulation profile = deranged in advanced disease
- serum immunoglobulin = raised IgM
- transabsominal USS (exclude other causes)
to consider:
- MRCP
- liver biopsy
38
PRIMARY BILIARY CHOLANGITIS
What is the treatment for primary biliary cholangitis?
1st line:
- ursodeoxycholic acid
- fat-soluble vitamin supplement (ADEK)
- cholestyramine (for symptomatic relief of pruritus)
2nd line
- liver transplantation (indicated in severe disease)
39
PRIMARY SCLEROSING CHOLANGITIS
what are the clinical features of primary sclerosing cholangitis?
SYMPTOMS
- pruritus
- fatigue
- abdominal pain (usually epigastric or RUQ)
- symptoms of underlying IBD (bloody stools, tenesmus, diarrhoea, steatorrhoea)
SIGNS
- jaundice
- signs of complications (Charcots triad, chronic liver disease)
40
PRIMARY SCLEROSING CHOLANGITIS
what are the investigations?
-LFTs = raised ALP + GGT, raised conjugated bilirubin, ALT/AST may or may not be elevated
- albumin = decreased in later disease
- viral hepatitis screen
- pANCA
- anti-mitochcondrial antibodies (AMA) (to rule out PBC)
- abdominal USS (to exclude other causes)
- MRCP = beaded appearance (due to multiple biliary strictures)
to consider
- ERCP (gold standard)
- liver biopsy
41
PRIMARY SCLEROSING CHOLANGITIS
What is the treatment for primary sclerosing cholangitis?
1st line
- observation + lifestyle optimisation (alcohol cessation, exercise)
- cholestyramine for pruritus (rifampicin = 2nd line)
- ADEK vitamin supplement
END STAGE LIVER DISEASE
- liver transplant
42
PRIMARY SCLEROSING CHOLANGITIS
What complications might occur due to primary sclerosing cholangitis?
- cholangitis
- biliary strictures
- choledocholithiasis
- metabolic bone disease
- end stage liver disease
- cholangiocarcinoma
- HCC
- colorectal tumour
43
ASCENDING CHOLANGITIS
what are the causes of ascending cholangitis?
- gallstones (most common)
- biliary strictures
- sclerosing cholangitis
- cholangiocarcinoma
- iatrogenic injury (e.g. ERCP)
44
ASCENDING CHOLANGITIS
What other symptoms can present with Charcot's triad with ascending cholangitis?
Reynolds pentad:
- Charcot's triad (fever, RUQ pain, jaundice)
- Hypotension
- Confusion/altered mental state
- dark urine and pale stool
45
ASCENDING CHOLANGITIS
What investigations might you do in someone who you suspect might have ascending cholangitis?
- trans-abdominal USS
- Blood tests - LFTS (ALP>ALT + raised bilirubin), CRP, FBC,
- MRCP = gold standard
46
ASCENDING CHOLANGITIS
Describe the management of ascending cholangitis
INITIAL
- IV broad spectrum antibiotics (cefotaxime + metronidazole)
- IV fluids
BILIARY DECOMPRESSION
- ERCP (first line)
- surgical drainage
ELECTIVE CHOLECYSTECTOMY
47
PERITONITIS
What are the investigations?
- FBC + CRP = raised inflammatory markers
- serum amylase (to rule out pancreatitis)
- ABG/VBG (to get serum lactate, see how unwell)
- paracentesis (ascitic tap)
to consider
- erect CXR (if perforation suspected)
- abdominal USS or CT (to identify abscess or obstruction)
- blood cultures
48
PERITONITIS
What is the management for peritonitis?
1st line:
- broad spectrum antibiotics (piperacillin-tazobactam or metronidazole with cetriaxone)
- fluid resuscitation via IV fluids
- analgesia (paracetamol + opioids)
- NG tube for feeding
2nd line
- surgery +/- peritoneal lavage
49
SPONTANEOUS BACTERIAL PERITONITIS
Name a bacteria that can cause spontaneous bacterial peritonitis
1. E. coli
2. S. pneumoniae
50
SPONTANEOUS BACTERIAL PERITONITIS
Describe the treatment for spontaneous bacterial peritonitis
Cefotaxime and metronidazole
51
ACUTE PANCREATITIS
Describe the pathophysiology of acute pancreatitis
Main two causes are alcohol and gallstones:–
Gallstones:
Blockage of bile duct = backup of pancreatic juices. This change in luminal concentration causes Ca2+ release inside pancreatic cells and cause them to activate trypsinogen early which digests the pancreas.
Alcohol:
Contracts the Ampulla of Vater obstructing the bile clearance and also messes with Ca2+homeostasis causing the same as above.
* Leaky and damaged pancreas an auto digest nearby structures causing haemorrhage and Grey
Turner’s sign abdominal skin discolouration from retroperitoneal bleeding.
* Deranges pancreatic function so can cause hyperglycemia from reduction of insulin production
52
ACUTE PANCREATITIS
What are the causes of acute pancreatitis?
I GET SMASHED – remember
I = Idiopathic
G = Gallstones (60%)
E = Ethanol = alcohol (30%)
T = Trauma
S = Steroids
M = Mumps
A = Autoimmune
S = Scorpion venom
H = Hyperlipidaemia/ hypothermia/ high Ca
E = ERCP (endoscopic retrograde cholangiopancreatography)
D = Drugs (furosemide, corticosteroid, NSAIDs, ACEi)
```
53
ACUTE PANCREATITIS
What investigations are done on someone you think has acute pancreatitis?
- serum amylase
- serum lipase
FOR SEVERITY SCORING
bloods - FBC, U&Es, LFTs
ABG
glucose
LDH
serum calcium
TO CONSIDER
- CXR
- AXR
- abdominal USS
54
CHRONIC PANCREATITIS
Name 3 causes of chronic pancreatitis
1. Excess alcohol - most common
2. CKD
3. Idiopathic
4. Recurrent acute pancreatitis
5. hereditary
6. CF - all have it from birth
7. autoimmune
8. tropical
55
CHRONIC PANCREATITIS
Describe how alcohol can cause chronic pancreatitis
Alcohol --> proteins precipitate in the ductal structure of the pancreas (obstruction) --> pancreatic fibrosis
56
CHRONIC PANCREATITIS
what is the clinical presentation of chronic pancreatitis?
SYMPTOMS
- epigastric pain (dull, radiating to back, improved by leaning forwards, occurs 15-30 mins after eating)
- steatorrhoea + diarrhoea (foul smelling + difficult to flush)
- N+V
- weight loss + fatigue
- features of diabetes (polydipsia + polyuria)
SIGNS
- epigastric tenderness
- signs of liver disease (jaundice + ascites)
- skin nodules
57
CHRONIC PANCREATITIS
What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?
IgG4
58
CHRONIC PANCREATITIS
What 2 enzymes, if raised, suggest pancreatitis?
LDH (lactate dehydrogenase) and AST>ALT
59
CHRONIC PANCREATITIS
Give 3 complications of chronic pancreatitis
- malabsorption
- duct obstruction
- pseudocysts
- DM
- pancreatic cancer
- metabolic bone disease (osteoporosis)
60
LIVER FAILURE
Name a drug that can cause drug induced liver injury
1. Co-amoxiclav
2. Flucloxacillin
3. Erythromycin
4. TB drugs
61
CHOLECYSTITIS
what is the management of cholecystitis?
1st line
- IV fluids + analgesia
- IV antibiotics (CERFUOXIME or METRONIDAZOLE)
- early laparoscopic cholecystectomy (within 1 week of diagnosis, often within 72hrs)
2nd line
- urgent cholecystectomy (if sepsis/gangrene/perforation suspected)
62
PRIMARY BILIARY CHOLANGITIS
what is the pathophysiology of primary biliary cholangitis?
* Due to prolonged bile duct blockage, bile isn’t ‘flushing’ out the tubes so bacteria can climb up from the GI tract and cause biliary tree infection and consolidation.
* This prevents bile entering the GI tract and causes jaundice.
* 5-10% mortality and infection can affect the pancreas too since it shares ducts with the gallbladder.
63
PORTAL HYPERTENSION
what are the pre-hepatic causes of portal hypertension?
portal vein thrombosis
64
PORTAL HYPERTENSION
what are the intrahepatic causes of portal hypertension?
- schistosomiasis
- cirrhosis
- budd-chiari syndrome
65
PORTAL HYPERTENSION
what are the post-hepatic causes of portal hypertension?
- RH failure
| - IVC obstruction
66
PORTAL HYPERTENSION
what is the pathophysiology of portal hypertension?
- Increased resistance to blood flow leads to portal hypertension causes splanchnic vasodilation
- This results in a drop in BP
- CO increases to compensate for BP resulting in salt and water retention
- Hyperdynamic circulation/increased portal flow leads to the formation of collaterals between portal and systemic systems
67
GI VARICES
what is the prevention of varices?
o Nonselective B blockade – propranolol – reduced resting pulse and decrease portal pressure
o Variceal banding repeated to obliterate varices
o TIPSS
o Liver transplant
68
A1AT
what is the pathophysiology of alpha-1-antitrypsin deficiency?
● A mutation in the alpha-1-antitrypsin gene on chromosome 14 leads to reduced hepatic production of alpha-1-antitrypsin which normally inhibits the proteolytic enzyme, neutrophil elastase
● Deficiency results in emphysema, liver cirrhosis and hepatocellular carcinoma
69
WILSONS DISEASE
what are the side-effects of chelating agents?
skin rash,
fall in WCC, HB and platelets,
haematuria,
renal damage
70
PERITONITIS
what are the causes of peritonitis?
bacterial = most common
- gram -ve coliforms - e.coli
- gram +ve staphylococcus
chemical - bile, old clotted blood
71
HEPATITIS
what is the clinical presentation of HAV?
nausea,
anorexia,
distaste for cigarettes
some become jaundiced - dark urine and pale stool
72
HEPATITIS
what are the test results for HBV?
● HBsAg is present 1-6 months after exposure
● HBsAg presence for more than 6 months implies carrier status
● Anti-HBs – antibodies
73
NON-ALCOHOLIC FATTY LIVER
which drugs increase the risk of developing non-alcoholic fatty liver disease?
Amiodarone, Tetracycline ,Methotrexate
74
NON-ALCOHOLIC FATTY LIVER
what are the investigations for non-alcoholic fatty liver disease?
- LFTs = raised ALT
- liver USS = confirm hepatic steatosis (seen as increased echogenicity)
- enhanced liver fibrosis (ELF) blood test = 1st line (>10.51= advanced fibrosis)
- NAFLD fibrosis score
- fibrosis-4 score
- fibroscan
- liver biopsy = gold standard
75
ALCOHOLIC LIVER DISEASE
what is the pathophysiology of alcoholic liver disease?
chronic excessive alcohol consumption leads to liver impairment
- alcohol is metabolised into acetaldehyde and then to acetate
- excessive NADH leads to greater fatty acid oxidation and subsequently fatty infiltration of the liver
- the production of free radicals results in increase in TNF-alpha causing hepatic inflammation
- chronic inflammation leads to liver fibrosis and eventually cirrhosis
76
ALCOHOLIC LIVER DISEASE
what are the investigations for alcoholic hepatitis?
LFTs - raised bilirubin, AST:ALT ratio>2, low albumin, raised GGT
FBC - macrocytic anaemia, thrombocytopaenia
Folate - may be deficient
Clotting - may be deranged (in advanced disease)
Exclude secondary causes - viral hep, autoimmune, HCC
to consider
- liver USS - hyperechoic + coarse echotexture
- fibroscan
- liver biopsy
77
ALCOHOLIC LIVER DISEASE
what is the management for alcoholic liver disease?
- alcohol abstinence
- weight loss
- smoking cessation
- immunisation (flu, pneumococcal, hep B)
- nutritional supplementation
- corticosteroids (prednisolone) if Maddrey's discriminant function score >32
- N-acetylcysteine for 5 days in advanced disease
- liver transplantation (requires 3 months abstinence before consideration)
78
HEPATITIS
what do the following serological markers indicate in HBV infection?
- HBsAg
- HBeAg
- HBV-DNA
- anti-HBs
- anti-HBc IgM
- anti HBc IgG
- anti HBe
- HBsAg = acute infection (persistence after >6months implies chronic infection)
- HBeAg = acute infection (persistence implies active viral replication) - can distinguish between active and inactive chronic infection
- HBV-DNA = implies viral replication (present in acute and chronic)
- anti-HBs = immunity to HBV from immunisation or previous cleared infection
- anti-HBc = implies previous or current infection
- anti-HBc IgM = recent infection within last 6 months
- anti-HBc IgG = persists long term
- anti-HBe = seroconversion and is present for life
79
BILE
what are the primary bile salts?
colic acid and chenodeoxycholic acid`
80
BILE
what are the secondary bile salts?
deoxycholic acid and lithocholic acid
81
BILE
how are primary bile salts turned into secondary bile salts?
Primary bile salts turn into secondary bile salts by dehydroxylation by bacteria in the gut
82
BILE
what is the process of lipid absorption?
Bile salts emulsify fats and pancreatic lipase hydrolyses fats into monoglycerides and fatty acids
Pancreatic lipase makes fatty acids form micelles which diffuse through epithelial cells
This forms chylomicrons which are absorbed into lymphatic system
83
CHRONIC PANCREATITIS
what are the investigations for chronic pancreatitis?
CT or MRI - pancreatic duct dilation, calcification, atrophy or pseudocysts
endoscopic ultrasound
fecal elastase test - decreased elastase
84
ACUTE PANCREATITIS
what are the risk factors?
- advancing age
- afro-caribbean ethnicity
- sex (female = gallstone related, male = alcohol related)
- high glycaemic diet
- obesity
- T2DM
- family history
85
ACUTE PANCREATITIS
what is the diagnostic criteria?
2/3 of following need to be met:
- clinical features consistent with pancreatitis
- elevation of serum amylase OR serum lipase
- radiological features consistent with pancreatitis
86
ACUTE PANCREATITIS
how is the severity calculated?
- modified Glasgow score
- PANCREAS
- P02 <8kpa
- Age >55
- Neutrophils >15x109/L
- Calcium <2mmol/L
- Renal function (urea >16mmol/L)
- Enzymes (AST>200U/L or LDH>600U/L)
- Albumin <32g/L
- Sugar (blood glucose>10mmol/L)
87
CHRONIC PANCREATITIS
what are the investigations?
- LFTs
- HbA1c
- transabdominal USS = first line imaging
- CT abdomen
to consider
- faecal elastase
- IgG4
- MRCP
- ERCP
88
PBC VS PSC
what are the differences between primary biliary cholangitis + primary sclerosing cholangitis
PRIMARY BILIARY CHOLANGITIS
- more common in middle aged women
- destruction of intrahepatic ducts only
- associated with autoimmune conditions
- often asymptomatic or fatigue, pruritus, jaundice + hepatomegaly
- raised ALP + GGT +/- conjugated bilirubin, anti mitochondrial antibodies (AMA)
- diagnosed via cholestatic LFTs, abdominal USS, history + exam
- treat with ursodeoxycholic acid, colestyramine + ADEK vita
PRIMARY SCLEROSING CHOLANGITIS
- more common in middle aged men
- inflammation of intrahepatic + extrahepatic ducts
- associated with ulcerative cholitis (UC)
- has symptoms of IBD + ascending cholangitis
- raised ALP + GGT +/- conjugated bilirubin, pANCA
- diagnosed via cholestatic LFTs, MRCP, history + exam
- treat with observation, colestyramine + ADEK vits
89
PERITONITIS
what are the risk factors?
- ascites
- low ascitic fluid protein concentration
- upper GI bleeding
- prior episode of SBP
90
PANCREATIC CANCER
what are the risk factors?
- increasing age (65-75yrs)
- male
- smoking
- diabetes
- chronic pancreatitis
- genetic (hereditary non-polyposis colorectal cancer, BRCA1 + 2
- multiple endocrine neoplasia
91
PANCREATIC CANCER
what are the clinical features?
SYMPTOMS
- painless jaundice
- epigastric or atypical back pain
- anorexia
- weight loss
- new onset diabetes (thirst, polyuria, nocturia)
- nausea + vomiting
- steatorrhoea
- pale stool + dark urine
SIGNS
- positive Courvoisier's sign (palpable gallbladder in the presence of painless jaundice)
- Trousseau sign of malignancy (migratory thrombophlebitis, blood vessels get inflamed with associated clot)
92
PANCREATIC CANCER
what are the investigations?
- LFTs = obstructive (raised ALP + GGT + bilirubin)
- coagulation profile (assess for liver mets)
- abdominal USS
- CT (or MRI) pancreas = double duct sign (simultaneous dilation of pancreatic + common bile ducts)
- CA 19-9
to consider:
- PET scan (for staging)
- endoscopic USS
- ERCP
93
PANCREATIC CANCER
when would you refer someone for 2ww?
- over 40 with jaundice = 2ww
- over 60 plus one of following (diarrhoea, back pain, abdo pain, N+V, constipation or new diabetes) = direct access CT abdomen
NOTE - pancreatic cancer is the only situation where a GP can do a direct access CT abdomen referral
94
PANCREATIC CANCER
where does it tend to spread to?
liver
peritoneum
lungs
bones
95
HEPATITIS
what is the management of HDV?
pegylated interferon alpha
96
NON-ALCOHOLIC FATTY LIVER
what are the different stages?
1. non-alcoholic fatty liver disease
2. non-alcoholic steatohepatitis (NASH)
3. fibrosis
4. cirrhosis
97
ASCITES
what are the causes of ascites that cause serum ascites albumin gradient (SAAG) <11g/L?
HYPOALBUMINAEMIA
- nephrotic syndrome
- severe malnutrition (e.g. kwashiorkor)
MALIGNANCY
- peritoneal carcinomatosis
INFECTION
- Tuberculous peritonitis
OTHER CAUSES
- pancreatitis
- bowel obstruction
- biliary ascites
- postoperative lymphatic leak
- serositis in connective tissue diseases
98
LIVER FAILURE
what is the management of chronic liver failure?
- lifestyle changes (weight loss, alcohol cessation)
- patient education
- surveillance (regular HCC screening)
- prevention of oesophageal varices (PROPRANOLOL)
- prevention of hepatic encephalopathy (RIFAXIMIN)
- manage ascites (SPIRONOLACTONE or FUROSEMIDE)
- liver transplantation
