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Liver/pancreas Flashcards

(109 cards)

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1
Q

What is the substance that gallstones are most commonly formed by?

A

Cholesterol

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2
Q

What are the risk factors for gallstones?

A

Fat, fair, female, forty

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3
Q

What is the pain like that is associated with gallstones?

A

Severe, colickly epigastric or RUQ pain, triggered by meals (especially fatty meals), lasts between 30 minutes and 8 hours, can also radiate to shoulder

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4
Q

What LFTs are raised in a hepatic picture?

A

ALT and AST

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5
Q

What LFTs are raised in obstructive picture/biliary tree disease?

A

ALP, GGT and bilirubin (also get deranged clotting in obstruction)

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6
Q

What investigations can be done in someone presenting with RUQ pain?

A

1st line = USS abdomen
MRCP - sensitive and specific for biliary tract disease

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7
Q

When is a laparoscopic cholecystectomy indicated?

A

When the patient is symptomatic of gallstones or the gallstones are leading to complications

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8
Q

What pain relief can be given to patients with gallbladder pain whilst waiting for elective surgery?

A

If severe IM diclofenac
If mild/moderate - paracetamol plus NSAID

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9
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder which is caused by blockage of the cystic duct preventing the gallbladder from draining (most often gallstones)

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10
Q

What features are present in acute cholecystitis?

A

RUQ pain, fever, nausea, vomiting, tachycardia, RUQ tenderness, Murphy’s sign positive, raised inflammatory markers and WBC

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11
Q

What management is done for those with acute cholecystitis?

A

Nil by mouth, IV fluids, antibiotics, NG tube, ERCP can be used to remove trapped stones

Cholecystectomy can be performed during acute admission or be delayed for 6-8 weeks

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12
Q

What complications can occur due to acute cholecystitis?

A

Sepsis, gallbladder empyema, gangrenous gallbladder, perforation

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13
Q

What are the two main causes of acute cholangitis?

A

Obstruction in bile ducts stopping bile flow or infection introduced during ERCP procedure

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14
Q

What are the most common organisms that cause acute cholangitis?

A

E.coli, Klebsiella, enterococcus

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15
Q

What is charcot’s triad?

A

RUQ pain, fever, jaundice = acute cholangitis

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16
Q

What is the management of acute cholangitis?

A

IV fluids, nil by mouth, IV antibiotics, blood cultures, ERCP to remove stones

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17
Q

What is decompensated liver cirrhosis?

A

When the liver is damaged to the point that is cannot function adequately and clinical complications such as jaundice are present

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18
Q

What examination findings are present in someone with severe liver disease?

A

Cachexia, jaundice, hepatomegaly, small nodular liver, splenomegaly, spider naevi, palmar erythema, gynaecomastia, bruising, excoriations, ascites, caput medusae, leukonychia, asterixis

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19
Q

When is a non-invasive liver screen performed?

A

In a patient with abnormal LFTs without a clear cause

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20
Q

What blood tests will be deranged in someone with severe liver disease?

A

Low albumin (due to reduced synthetic function of the liver)
Increased PT (due to reduced clotting production)
Thrombocytopenia (advanced disease)
Hyponatraemia (due to fluid retention)

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21
Q

What is a Fibroscan/transient elastogrpahy scan used for?

A

Assesses the stiffness of the liver to determine the degree of fibrosis

Used in all patients at risk of cirrhosis

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22
Q

What scores can be used in someone with end stage liver disease?

A

MELD score or the Child-Pugh score - done every 6 months

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23
Q

Why do patients with cirrhosis develop malnutrition?

A

Loss of appetite, protein metabolism in the liver is affected and therefore muscle tissue is broken down to be used as fuel

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24
Q

Why does portal hypertension occur in those with liver cirrhosis?

A

Liver cirrhosis increases the resistance to blood flow in the liver which thereby increases pressure in portal system and results in splenomegaly

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25
Why do oesophageal varices form in liver cirrhosis?
Portal hypertension causes swollen and tortuous vessels at sites where collaterals form between portal and systemic venous systems = distal oesophagus This also causes caput medusae
26
What prophylaxis is given to patients with oesophageal varices to prevent bleeding?
1st line = non-selective beta blockers e.g. propranolol 2nd line = variceal band ligation
27
What is the management for bleeding oesophageal varices?
ABCDE and immediate senior help Activate major haemorrhage protocol Blood transfusions Terlipressin or somatostatin can cause vasoconstriction Prophylactic broad spectrum antibiotics Urgent endoscopy with variceal band ligation
28
What is the most common complication of cirrhosis?
Ascites
29
How does ascites form in those with liver cirrhosis?
Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and into the peritoneal cavity The drop in circulating volume then activates RAAS leading to fluid and sodium retention
30
What kind of ascites is caused by cirrhosis?
Transudative
31
What is the management of ascites?
Low sodium diet, aldosterone antagonists, ascitic tap/drain, prophylactic antibiotics, TIPS
32
What is spontaneous bacterial peritonitis?
Infection within the asicitc fluid and peritoneal lining without a clear source of infection - most commonly caused by E.coli and Klebsiella
33
What is the management for spontaneous bacterial peritonitis?
Sample for ascitic fluid, IV broad spectrum antibiotics
34
How does liver disease lead to kidney disease? (hepatorenal syndrome)
Portal hypertension causes portal vessels to release vasodilators which leads to reduced BP The kidneys therefore activate RAAS which leads to vasoconstriction of the renal vessels Renal vasoconstriction and low systemic pressure results in kidneys being starved of blood and reduced kidney function
35
What toxin is built up during hepatic encephalopathy?
Ammonia - liver cells unable to metabolise ammonia into harmless waste products
36
How does hepatic encephalopathy present?
Reduced consciousness and confusion
37
What is the management for hepatic encephalopathy?
Lactulose, antibiotics (rifaximim), nutritional support
38
What are the progressive stages of alcoholic liver disease?
Alcoholic fatty liver --> alcoholic hepatitis --> cirrhosis
39
What LFTs are consistent with alcoholic liver disease?
ALT and AST will be raised AST > ALT (2:1) GGT also raised with high alcohol consumption
40
What investigations can be done in someone with alcoholic liver disease?
Liver USS, FibroScan, endoscopy to assess for varices, CT/MRI, liver biopsy
41
What nutritional support is given to those with alcoholic liver disease?
High protein diet, thiamine replacement
42
What tools can be used to assess for alcohol dependence?
CAGE questions, AUDIT questionnaire
43
What symptoms are present 6-12 hours following alcohol withdrawal?
Tremor, sweating, headache, cravings, anxiety
44
What symptoms occur 12-24 hours and 24-48 hours following alcohol withdrawal
12-24 = hallucinations 24-48 = seizures
45
How long following alcohol withdrawal can delirium tremens develop?
24-72 hours
46
Which receptors in the brain are affected with chronic alcohol use and are they down/up regulated?
GABA becomes downregulated and glutamate becomes upregulated Both have relaxing effect of electrical activity of the brain
47
What symptoms are associated with delirium tremens?
Confusion, agitation, delusions, hallucinations, tremor, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias
48
What can be prescribed to prevent alcohol withdrawal?
Chlordiazepoxide - given orally as a reducing regime titrated to the required dose (given for 5-7 days)
49
What can be prescribed to prevent Wernicke-Korsakoff syndrome?
IM/IV Pabrinex (high dose vitamin B) followed by long term oral thiamine
50
What causes Wernicke-Korsakoff syndrome?
Alcohol excess leads to thiamine deficiency and thiamine is poorly absorbed in the presence of alcohol Wernicke-Korsakoff syndrome is a result of thiamine deficiency
51
What are the features of Wernicke encephalopathy?
Confusion, oculomotor disturbances, ataxia
52
What are the features of Korsakoff syndrome?
Memory impairment and behavioural changes
53
What are the progressive stages of NAFLD?
NAFLD --> non-alcoholic steatohepatitis (NASH) --> fibrosis --> cirrhosis
54
What are the risk factors for NAFLD?
Obesity, poor diet, low activity levels, T2DM, high cholesterol, high BP, smoking
55
What is found on the LFTs of someone with NAFLD?
AST and ALT raised ALT > AST
56
What is the first line investigation for assessing fibrosis in NAFLD?
Enhanced liver fibrosis blood test (>10.51 is advanced)
57
What is the gold standard for diaganosing NAFLD?
Liver biopsy
58
What is the management for NAFLD?
Weight loss, healthy diet, exercise, avoid alcohol, control any co-morbidities, refer to specialist if fibrosis
59
What are the main causes of pancreatitis?
Alcohol, gallstones, ERCP
60
What is the presentation of someone with pancreatitis?
Severe sudden onset epigastric pain radiating to the back, vomiting, abdominal tenderness, fever, tachycardia, eccyhmoses
61
What blood tests results are raised in pancreatitis? (used to diagnose)
Amylase and lipase Lipase is more sensitive and specific but amylase is used more often
62
What scoring system is used to assess severity and what are the components of it?
Glasgow score - PANCREAS PaO2 <8kpa Age >55 Neutrophils (WBC >15) Calcium <2 uRea >16 Enzymes - LDH >600 or AST/ALT >200 Albumin <32 Sugar (glucose >10)
63
How is pancreatitis managed?
IV fluids, analgesia, IV antibiotics if evidence of infection, ERCP to treat gallstones, nutritional support
64
What complications can occur due to acute pancreatitis?
Necrosis of pancreas, infection in a necrotic area, abscess formation, peripancreatic fluid collections, pseudocysts, chronic pancreatitis
65
What is the most common cause of chronic pancreatitis?
Alcohol
66
What complications can occur due to chronic pancreatitis?
Loss of exocrine function - lack of pancreatic enzymes (notably lipase) Loss of endocrine function - diabetes
67
How is chronic pancreatitis managed?
Abstinence from alcohol and smoking, analgesia, Creon (replacement pancreatic enzymes), insulin
68
What is the presentation of hepatitis?
Abdominal pain, fatigue, flu-like illness, itching, muscle and joint aches, N+V, jaundice
69
How is hepatitis A spread and how is it managed?
Transmitted in contaminated water (faecal-oral route), vaccination to prevent, management is supportive
70
How is hepatitis B spread and how is it managed?
Transmitted by direct contact with blood or bodily fluids and vertical transmission, supportive treatment and antivirals, vaccine is available
71
Which antigen shows active infection with hepatitis B?
HBsAg
72
Which viral marker shows vaccination with hepatitis B vaccine?
HbsAb
73
How is hepatitis C spread and how is it managed?
Spread by blood and bodily fluids, no vaccine is available but now curable with direct-acting antivirals, without treatment develops into chronic hepatitis C
74
When is someone likely to develop a hepatitis D infection?
Can only get hepatitis D infection when there is a concurrent hepatitis B infection, increases complication and severity of hepatitis B
75
How is hepatitis E spread and how is it managed?
Transmitted by faecal oral route, mild illness and no treatment is required, there is no vaccine
76
Which antibodies are associated with type 1 autoimmune hepatitis?
ANA, anti-actin, anti-SLA/LP
77
Which antibodies are associated with type 2 autoimmune hepatitis?
anti-LKM1, anti-LC1
78
What are the typical LFTs of someone with autoimmune hepatitis?
High AST/ALT with minimal change in ALP Raised IgG levels
79
What are the presenting features of haemochromatosis?
Chronic tiredness, joint pain, bronze pigmentation to skin, testicular atrophy, erectile dsyfunction, amenorrhoea, hepatomegaly
79
What is the treatment for autoimmune hepatitis?
High dose steroids or immunosuppressants, liver transplant
80
What results will be found on an iron study of someone with haemochromatosis?
Raised ferritin, high transferrin, low total iron binding capacity High transferrin differentiates it from other differentials of high ferritin
81
What is the management of haemochromatosis?
Venesection at regular intervals, monitoring
82
What is the pathophysiology of Wilson's disease?
Autosomal recessive condition resulting in excessive accumulation of copper in the body especially in the liver and CNS
83
What are the features of Wilson's disease?
Chronic hepatitis which can lead to cirrhosis, tremor, dysarthria, dystonia, Parkinsonism, Kayser-Fleischer rings in cornea
84
What is the initial screening test for suspected Wilson's disease?
Serum caeruloplasmin (will be reduced)
85
What is the management for Wilson's disease?
Copper chelation using penicilliamine or trientene
86
What are the features of alpha-1-antitrypsin deficiency?
COPD and bronchiectasis in the lungs Dsyfunction, fibrosis and cirrhosis of the liver
87
What investigations are performed in alpha-1-antitrypsin deficiency?
Serum alpha-1-antitrypsin levels, genetic testing, high resolution CT, liver biopsy
88
What is the management of alpha-1-antitrypsin deficiency?
Stop smoking, symptomatic management of COPD, liver/lung transplant, monitoring for complications
89
What are the symptoms of pancreatic cancer?
Painless obstructive jaundice, diarrhoea, N+V, abdo/back pain, new onset diabetes
90
What surgical procedure is done in early pancreatic cancer?
Whipple's resection is performed (done in head of pancreas tumours = most common)
91
What investigations are done in those with suspected pancreatic cancer?
CT = 1st line, biopsy for definitive diagnosis
92
What is the main risk factor for developing cholangiocarcinoma?
Primary sclerosing cholangitis
93
What are the features of cholangiocarcinoma?
Painless obstructive jaundice, persistent biliary colic symptoms, palpable mass in RUQ, weight loss
94
What investigations are done in someone with suspected cholangiocarcinoma?
USS upper abdo = 1st line, biopsy = definitive
95
What tumour marker is raised in cholangiocarcinoma?
CA19-9
96
What is the most common type of liver cancer?
Hepatocellular carcinoma
97
What are the risk factors for developing HCC?
Alcoholic liver disease, NAFLD, hepatitis B/C, liver cirrhosis
98
What tumour marker is used for HCC?
Alpha-fetoprotein
99
What symptoms are seen in liver cancer?
Enlarged liver, worsening liver function, jaundice, abdo pain, abdo mass
100
What investigations are done in liver cancer?
USS = 1st line, CT/MRI, biopsy = definitive
101
What medications can be used to manage severe alcoholic hepatitis?
Corticosteroids such as prednisolone to reduce mortality - used during acute episodes
102
What sign is seen on CT imaging in someone with pancreatic cancer?
Double duct sign
103
Bile acid malabsorption is a complication following cholecystectomy, what are the symptoms and how is it managed?
Watery green diarrhoea Treated with cholestyramine
104
What investigations are done in primary sclerosing cholangitis and what is found?
MRCP will show beaded appearance of bile duct
105
What are the features of primary biliary cholangitis?
Fatigue, pruritus, cholestatic jaundice, hyperpigmentation, xanthelasmas, hepatosplenomegaly (associated with autoimmune conditions)
106
How is primary biliary cholangitis diagnosed?
mitochondrial antibodies, abdo USS or MRCP done to exclude extra hepatic biliary obstruction
107
How is primary biliary cholangitis managed?
1st line - ursodeoxycholic acid, cholestyramine for itching
108

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