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Phase 2a diseases > Liver and friends > Flashcards

Liver and friends Flashcards

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.
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2
Q

What is ascending cholangitis?

A
  • Otherwise known as acute cholangitis.
  • Acute infection of the biliary tree usually due to an obstruction.
  • Strongly associated with Charcot’s triad.
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3
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad:

  • RUQ pain
  • Jaundice
  • Fever

If severe:

  • Changed mental status.
  • Hypotension.
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4
Q

What are the risk factors for ascending cholangitis?

A
  • > 50 YO
  • Cholelithiasis.
  • Benign/malignant stricture in CBD.
  • Sclerosing cholangitis.
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5
Q

What is the pathophysiology of ascending cholangitis?

A
  • Obstruction of the CBD.
  • Bacterial seeding of the biliary tree.
  • When acute infection occurs (usually E. coli), this can result in ascending cholangitis.
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6
Q

What is the pathophysiology of SEPTIC ascending cholangitis?

A
  • As the CBD blockage progresses, the pressure in the CBD increases.
  • This can lead to extravasation of the bacteria, causing sepsis.
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7
Q

What are the investigations used for ascending cholangitis?

A
  • LFTs. Hyperbilirubinaemia. Raised ALP and usually raised GGT.
  • CRP. Raised (acute inflammation).
  • FBC. Raised WCC.
  • Blood culture: Positive (usually E. coli).

IF SEVERE DISEASE:

  • ABG. Metabolic acidosis and raised lactate.
  • Creatinine/urea. Raised due to renal disease.
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8
Q

What is the treatment for ascending cholangitis?

A
  • ERCP. Reduces biliary pressure.
  • Cerufoxime (cephalosporin) + metronidazole (antimicrobial).
  • Strong analgesia (morphine + paracetamol).

IF SEPTIC, SEPSIS 6.

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9
Q

What are the differentials for 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. NOT FINISHED YET.
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10
Q

What is the most common bacterial cause of ascending cholangitis?

A
  • E. Coli (gram -ve bacteria).
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11
Q

What is the main complication of ascending cholangitis?

A
  • Pancreatitis.
  • If common bile duct obstruction is very distal, the pancreatic duct is also obstructed, which causes acute pancreatitis.
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12
Q

What is the treatment for ascending cholangitis?

A

1st line:

  • Fluid resuscitation.
  • Potentially oxygen required.
  • Antibiotic therapy (to clear the infection) Give IV until adequate biliary drainage has been achieved.
  • Clear the obstruction (e.g. the gall stone) using ERCP.
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13
Q

What is the treatment for sclerosing cholangitis?

A

MANAGE THE SYMPTOMS OF DECREASED LIVER FUNCTION:

  • Rifampicin to reduce itching (puritis).
  • Ca2+ and Vit. D supplementation for osteopenia.
  • Immunosuppression if autoimmune hepatitis.
  • ERCP can be used to dilate the strictures.

WHEN END-STAGE LIVER DISEASE/LIVER FAILURE REACHED:

  • Liver transplant.
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14
Q

What are the potential complications of ascending cholangitis?

A
  • Sepsis is the main potential complication, due to the infection progressing.
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15
Q

What are the components of a LFT and what do they mean?

A
  • ALT is found in high concentrations in the hepatocytes, and enters the blood following HEPATOCELLULAR INJURY.
  • ALP synthesis is increased following CHOLESTASIS (inability of bile to flow into the duodenum) AND BONE BREAKDOWN.
  • GGT is also raised in response to BILE FLOW OBSTRUCTION OR HEAVY ALCOHOL USE.
  • If ALP is raised and GGT is normal, suggests non-hepatobiliary pathology (e.g. vitamin D defficiency or bone fractures)
  • Hyperbilirubinaemia doesn’t always cause jaundice. The stool and urine help identify the cause:
  • Normal urine + normal stool = pre-hepatic cause
  • Dark urine + normal stool = hepatic cause
  • Dark urine + pale stool = post-hepatic cause.
  • AST>ALT indicates cirrhosis and acute alcoholic hepatitis.
  • ALT>AST indicates chronic liver disease.
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16
Q

What is acute liver failure?

A

Rapid decline in hepatic function characterised by jaundice, encephalopathy and INR>1.5.

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17
Q

What is the clinical presentation of acute liver failure?

A
  • Hepatic encephalopathy.
  • Jaundice.
  • Abdominal pain.
  • Nausea/vomiting.
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18
Q

What are the risk factors for acute liver failure?

A
  • Female
  • > 40 YO
  • Chronic alcohol abuse
  • Hep B
  • Use of hepatotoxic drugs
  • Overdose of paracetamol.
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19
Q

What is the generalised pathophysiology of acute liver failure?

A

Generally, it is the massive necrosis of hepatocytes, leading to liver failure.

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20
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.
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21
Q

How is acute liver failure investigated and what are the results?

A
  • Assess for encephalopathy (Babinski reflex, asterixis, general awareness assessment etc.).
  • INR measurement > 1.5 (indicative of extrinsic coagulopathy).
  • LFT’s. Hyperbilirubinemia, VERY high AST/ALT, SLIGHTLY high ALP.
  • Amylase/lipase - check for pancreatitis (a common complication of acute liver disease).

FOR PARACETAMOL OVERDOSE:

  • Creatinine/urea. Check for renal failure.
  • Paracetamol levels in blood.
  • ABG (check for metabolic acidosis).
  • Lactate.
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22
Q

What is the treatment for acute liver failure?

What is the specific treatment for acute liver failure due to paracetamol overdose?

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.

FOR PARACETAMOL OVERDOSE:
- Acetylcysteine.

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23
Q

What is acute pancreatitis?

What is the diagnostic criteria?

A
  • 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.
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24
Q

What are the two different types of pancreatitis?

A
  • Acute

- Chronic

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25
Q

What is the clinical presentation of acute pancreatitis?

A
  • Epigastric/ upper GI pain that radiates through to the back. (Sudden onset).
  • Nausea/vomiting.
  • Potentially hypovolaemia.
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26
Q

What is the pathophysiology of acute pancreatitis?

A
  • Mechanism poorly understood.
  • Intracellular Ca2+ accumulates.
  • Direct insult to acinar cells.
  • Intrapancreatic enzyme activation.
  • Generalised inflammation.
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27
Q

What are the risk factors for/ causes of acute pancreatitis?

A

Remember this as I GET SMASHED:

  • Idiopathic
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion stings
  • Hyperlipidaemia/hypercalcaemia
  • ERCP
  • Drugs
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28
Q

What are the investigations used in acute pancreatitis?

A

Diagnostic investigations:

  • Lipase (1st line) and amylase (2nd line) - raised.
  • Imaging not normally needed.

OTHER:

  • CRP raised.
  • Raised haematocrit/urea/creatinine is indicative of hypovolaemia.
  • After diagnosis, RUQ USS should be done to check for biliary pathology.
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29
Q

What is the treatment for acute pancreatitis?

A
  • Hartmann’s solution.
  • Analgesia PRN (Ibuprofen, codeine, morphine).
  • Ondansetron (anti-emetic).

If the patient has gall stones but no cholangitis:
- Cholecystectomy.

If patient has gall stones AND cholangitis:
- Emergency ERCP.

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30
Q

What are the potential complications of acute pancreatitis?

A
  • Renal failure (AKI) due to hypovolaemia.
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31
Q

What is chronic pancreatitis?

A

Progressive injury to the pancreas, resulting in scarring and permanent loss of function.

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32
Q

What is the clinical presentation of chronic pancreatits?

A
  • 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).
33
Q

What is the pathophysiology of chronic pancreatitis?

A
  • Poorly understood.

- Main cause is chronic alcohol abuse (70-80% of cases).

34
Q

What are the risk factors for chronic pancreatitis?

A
  • ALCOHOL IS THE MAIN RISK FACTOR.
  • FH
  • Coeliac disease.
35
Q

What are the investigations used to diagnose chronic pancreatitis?

A
  • 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.
36
Q

What is the treatment for chronic pancreatitis?

A
  • 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.
37
Q

What is the main potential complication of chronic pancreatitis?

A
  • Diabetes due to reduced insulin secretion (called type 3c diabetes).
38
Q

What is alcoholic liver disease?

A

Chronic liver disease caused by chronic heavy alcohol consumption.

39
Q

What is the clinical presentation of alcoholic liver disease?

A
  • PROLONGED HIGH ALCOHOL CONSUMPTION.
  • RUQ pain.
  • Hepatomegaly.

When more severe:

  • Asterixis/confusion (hepatic encephalopathy).
  • Jaundice
  • Splenomegaly
40
Q

What are the three main stages of alcoholic liver disease?

A
  • Alcoholic fatty liver.
  • Alcoholic hepatitis.
  • Alcoholic liver cirrhosis.
41
Q

What is the pathophysiology of alcoholic fatty liver disease?

A

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.

42
Q

What characteristic cells are found histologically in people suffering with alcoholic liver disease?

A
  • Mallory bodies. Especially seen in the later stages (alcoholic hepatits, alcoholic liver cirrhosis).
43
Q

What are the risk factors for alcoholic liver disease?

A
  • 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).
44
Q

What is the pathophysiology of alcoholic liver disease?

A
45
Q

What is the epidemiology of alcoholic liver disease?

A
  • Most common cause of chronic liver disease.

- Usually presents in men

46
Q

What investigations are conducted to diagnose alcoholic liver disease?

A

CAGE/AUDIT questionnaire:
- Used to assess alcohol intake/dependancy.

LFTs (liver function tests):

  • AST and ALT both rise, but AST more so.
  • 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.
47
Q

What is the treatment for alcoholic liver disease?

A
  • 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).
48
Q

What is primary sclerosing cholangitis?

A
  • Chronic inflammation of the extra and/or intrahepatic ducts, leading to fibrosis and stricture.
49
Q

What is the clinical presentation of primary sclerosing cholangitis?

A

Usually asymptomatic in early stages.

Can cause:

  • Pruritus
  • Jaundice
  • RUQ pain
  • NO FEVER (unless infection occurring too).
50
Q

What are the risk factors for primary sclerosing cholangitis?

A
  • Male (2:1)
  • History of IBD (especially UC).
  • FH (first degree relative).
51
Q

What is the pathophysiology of primary sclerosing cholangitis?

A
  • Chronic inflammation of/ injury to the biliary ducts leads to fibrosis and stricture.
  • This causes cholestasis in the ducts, which increases the risk of cholelithiasis and infection.
  • If prolonged, can cause liver cirrhosis and parenchymal damage, causing end-stage liver disease.
52
Q

What are the investigations used for primary sclerosing cholangitis?

A
  • LFTs. Extremely high ALP and GTT. Slightly/moderately raised AST/ALT (pattern indicative of cholestatic disease). Hyperbilirubinaemia is sustained in more advanced disease.
  • MRCP (1st line) and ERCP (2nd line). Look for strictures.
53
Q

What is the treatment given for primary sclerosing cholangitis?

A

If asymptomatic:

  • Monitor and wait.
  • Lifestyle advice (stop drinking and increase exercise).

If symptomatic:
- ERCP + balloon dilatation. Give ciprofloxacin prophylactically due to high infection risk.

When end-stage liver disease:
- Liver transplant (if possible).

54
Q

What are the common complications of primary sclerosing cholangitis?

A
  • End-stage liver disease
  • Osteoporosis
  • Hepatocellular carcinoma/cholangiocarcinoma.
55
Q

What are the potential differentials for primary sclerosing cholangitis?

A
  • 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.
56
Q

What is cholecystitis?

A
  • Acute inflammation of the gall bladder, usually caused by gallstones (90%).
57
Q

What is the clinical presentation of cholecystitis?

A
  • RUQ pain
  • +ve murphy’s sign
  • Fever
  • Potentially a palpable gall bladder.

USUALLY NO JAUNDICE - DISEASE OF GALLBLADDER NOT LIVER.

58
Q

What are the risk factors for cholecystitis?

A
  • Gall stones.
  • Diabetes.
  • Nil by mouth (fasting or IV nutrition, as this will decrease gall bladder motility).
59
Q

What is the pathophysiology of cholecystitits?

A
  • 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.
60
Q

What are the investigations used for cholecystitis?

A
  • USS abdomen. Will show thickened gallbladder wall.

- If septic: CT/MRI to find the source of the infection. Blood culture to assess antibiotic sensitivity.

61
Q

What is the treatment for cholecystitis?

A
  • Analgesia (paracetamol or morphine as appropriate).
  • IV fluids until can tolerate oral intake.
  • Laproscopic cystectomy EARLY AS POSSIBLE (with prophylactic antibiotics to reduce risk of infection).
62
Q

What are the differentials for cholecystisis?

A
  • Peptic ulcers. Usually pain will be more epigastric and associated with food intake.
  • Ascending cholangitis (or acute cholangitis). Will have Jaundice (charcot’s triad) which is absent in cholecystitis.
63
Q

What are the main complications of cholecystitis?

A
  • Gall bladder perforation.

- Surgical damage to the cystic duct during laproscopic cholecystectomy.

64
Q

What is cholelithiasis?

A
  • Gall stones. Usually made of cholesterol, and can be in the gall bladder, cystic duct, common bile duct or pancreatic duct.
65
Q

What are the clinical symptoms of cholelithiasis?

A

Usually asymptomatic until obstruction occurs. Then:

  • Biliary colic pain
  • Often associated with eating (cholecystic movement).
  • If CBD obstruction present, may cause jaundice.
66
Q

What are the risk factors for cholelithiasis?

A
  • 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.
67
Q

What is the pathophysiology of cholelithiasis?

A
  • 90% of gallstones are made of cholesterol.

- Asymptomatic until they cause obstruction.

68
Q

What is the pathophysiology Mirizzi syndrome?

A
  • Gall stones become trapped in the gallbladder neck/cystic duct and put pressure through the wall onto the CBD/CHD. This causes jaundice too.
69
Q

What is the pathophysiology of Bouveret syndrone?

A
  • Gallstone erodes the wall of the gallbladder, which forms a fistula with the duodenum.
  • Gallstone passes into the duodenum, and blocks it.
70
Q

What are the investigations used for cholelithiasis?

A
  • 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).
71
Q

What are the treatments for cholelithiasis?

A
  • Analgesia as appropriate (paracetamol, diclofenac, buprenorphine etc.)
  • For uncomplicated gall stones: Laparoscopic cholecystectomy.
  • For choledocholithiasis: Initial ERCP to achieve biliary drainage THEN laparoscopic cholecystectomy.
72
Q

What is liver cirrhosis?

A
  • Liver cirrhosis is characterised by fibrosis and conversion of normal liver architecture into structurally abnormal nodules known as regenerative nodules.
73
Q

What is the clinical presentation of liver cirrhosis?

A
  • Abdominal distension.
  • Jaundice.
  • Hepatomegaly.
  • Pruritus.
  • Haematomesis (due to gastric varices).
  • Melaena (due to GI bleeding caused by portal hypertension).
  • Spider naevi.
  • Hepatomegaly.
    Many others too…
74
Q

What are the risk factors of liver cirrhosis?

A
  • Alcohol abuse (alcoholic liver cirrhosis).
  • IV drug use/unprotected sex (Hep B/C).
  • Obesity/diabetes (non-alcoholic fatty liver disease).
75
Q

What is the pathophysiology of liver cirrhosis?

A

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

Liver cirrhosis is reversible to a point. However, beyond that point it becomes irreversible - this is believed to be due to the deposition of elastin, which is resistant to remodelling.

76
Q

What are the potential complications of liver cirrhosis?

A
  • Portal hypertension.
  • Gastric varices.
  • Ascites.
  • Hepatocellular carcinoma.
77
Q

What are the investigations used for liver cirrhosis?

A

LFTs.

  • Generally, there will be raised AST and ALT, with AST:ALT being greater than one.
  • Hyperbilirubinaemia.
  • Hypoalbuminaemia.

Prolonged INR/PT time.

Hyponatraemia.

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.

78
Q

What is the treatment for liver cirrhosis?

A
  • AVOID NSAIDS AND PARACETAMOL.
  • Spironolactone (potassium-sparring diuretic) to treat ascites.
  • Liver transplant (if permanently decompensated function).
  • Propranolol (to treat gastric varices).

Phase 2a diseases (18 decks)

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