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Phase 2 v2 > 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
  • 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.
(Now called “Reynold’s Pentad”.)

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4
Q

What is the main risk factor for ascending cholangitis?

A
  • Biliary obstruction (e.g. cholelithiasis, PSC etc.)
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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.
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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.
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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.

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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.
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9
Q

What is the most common bacterial cause of ascending cholangitis?

A
  • E. Coli (gram -ve bacilli).
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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.
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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.

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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).
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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)
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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.

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15
Q

What is the clinical presentation of acute liver failure?

A
  • Hepatic encephalopathy.
  • Jaundice.
  • Abdominal pain.
  • Nausea/vomiting.
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16
Q

What are the most common causes of ALF?

A
  • Paracetamol overdose (By far most common cause).
  • Acute hepatitis B.
  • Autoimmune hepatitis.
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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.

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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.
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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.
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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.

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21
Q

What are the common complications of acute liver failure?

A
  • Hypoglycaemia.
  • Encephalopathy/coma.
  • Bacterial hepatitis.
  • Renal failure.
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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.
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23
Q

What dosage is the threshold for paracetamol overdose?

A

75mg/kg/24hr.

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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).
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25
Q

What is the presentation of a suspected paracetamol overdose?

A

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).
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26
Q

What are the investigations indicated in paracetamol overdose?

A
  • 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).
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27
Q

What is the treatment for paracetamol overdose?

A

- Acetylcysteine (if over 150mg/kg/24hr has been ingested, give immediately).

  • Ondansetron (anti-emetic).
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28
Q

When do paracetamol overdose patients require specialist management?

A
  • 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).
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29
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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30
Q

What are the two different types of pancreatitis?

A
  • Acute
  • Chronic
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31
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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32
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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33
Q

What are the investigations used in acute pancreatitis?

A

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.
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34
Q

What is the treatment for acute pancreatitis?

What about if it is concurrent with cholecystitis due to cholelithiatic obstruction?

A
  • Supportive therapy (O2, analgesia, fluids PRN).

If patient has acute pancreatitis AND cholangitis caused by a gallstone:

EMERGENCY ERCP.

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35
Q

What are the potential complications of acute pancreatitis?

A
  • Renal failure (AKI) due to hypovolaemia.
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36
Q

What is chronic pancreatitis?

A

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

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37
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).
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38
Q

What is the main cause of chronic pancreatitis?

A
  • Poorly understood.
  • Main cause is chronic alcohol abuse (70-80% of cases).
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39
Q

What are the risk factors for chronic pancreatitis?

A
  • ALCOHOL IS THE MAIN RISK FACTOR.
  • FH
  • Coeliac disease.
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40
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.
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41
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.
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42
Q

What is the main potential complication of chronic pancreatitis?

A
  • Diabetes due to reduced insulin secretion (called type 3c diabetes).
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43
Q

What is alcoholic liver disease?

A

Chronic liver disease caused by chronic heavy alcohol consumption.

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44
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
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45
Q

What are the three main stages of alcoholic liver disease?

A
  • Alcoholic fatty liver (1st)
  • Alcoholic hepatitis (2nd)
  • Alcoholic liver cirrhosis (3rd)
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46
Q

What is the pathophysiology of alcoholic 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.

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47
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).
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48
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).
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49
Q

What is the most common cause of chronic liver disease?

A
  • Alcoholic liver disease.
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50
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.
  • *- 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.
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51
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).
52
Q

What is primary sclerosing cholangitis?

A
  • Chronic inflammation of the extra and/or intrahepatic ducts, leading to fibrosis and stricture.
53
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).
54
Q

What disease is heavily linked to primary sclerosing cholangitis?

A

Ulcerative collitis

55
Q

What is the pathophysiology of primary sclerosing cholangitis?

A
  • 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
Q

What are the investigations used for primary sclerosing cholangitis?

A
  • 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
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.

58
Q

What are the common complications of primary sclerosing cholangitis?

A
  • End-stage liver disease
  • Osteoporosis
  • Hepatocellular carcinoma/cholangiocarcinoma.
59
Q

How is secondary sclerosing cholangitis different to primary sclerosing cholangitis?

How is autoimmune hepatitis different?

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.
60
Q

What is cholecystitis? What is the usualy cause?

A
  • Acute inflammation of the gall bladder, usually caused by gallstones (90%).
61
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.

62
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).
63
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.
64
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.
65
Q

What is the treatment for cholecystitis?

A
  • 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
Q

How does ascending cholangitis present differently to cholecystitis?

A
  • Ascending cholangitis (or acute cholangitis). Will have Jaundice (charcot’s triad) which is absent in cholecystitis (no jaundice).
67
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.
68
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.
69
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.
70
Q

What are gall stones normally made from?

A
  • 90% of gallstones are made of cholesterol.
71
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.
72
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.
73
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).
74
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.
75
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.
76
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.

Many others too…

77
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).
78
Q

What is the pathophysiology of liver cirrhosis?

What are the potential complications of portal hypertension?

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
79
Q

What are the investigations used for liver cirrhosis?

What should be screened for in patients with 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.

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
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).
81
Q

What does a raised anti-microbial antibody (AMA) level indicate?

A
  • Primary biliary cirrhosis. (this is differend to primary sclerosing cholangitis).
82
Q

What is the formal name of liver cancer?

A

Hepatocellular carcinoma.

83
Q

What is the most common precursor to hepatocellular carcinoma?

A
  • Cirrhotic liver.
84
Q

What is the clinical presentation of liver cancer?

A
  • RUQ pain.
  • Jaundice.
  • Abdominal distension.
  • Typical cancer signs (weight loss, fatigue etc.)
85
Q

What is the investigation used in suspected hepatocellular carcinoma?

A
  • Raised AFP (Alpha-fetoprotein).
  • Liver USS.

BIOPSY IS NOT NORMALLY REQUIRED.

86
Q

What is the treatment for hepatocellular carcinoma?

A
  • Resection of the carcinoma.
  • If the liver is in end-stage liver disease, liver transplant.
  • Chemo if cancer to advanced to resect.
87
Q

What is the most common form of pancreatic cancer?

A
  • Primary pancreatic ductal adenocarcinoma.
88
Q

What is the clinical presentation of pancreatic cancer?

A
  • 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
Q

What is the investigation used in suspected pancreatic ductal adenocarcinoma?

A
  • CT abdomen.
90
Q

What is the treatment for pancreatic cancer?

A
  • Surgical resection of the tumour.
  • Pancreatin (enzyme replacement).
91
Q

What is peritonitis? What is the most common cause?

A
  • Inflammation of the peritoneum, commonly caused by bacteria.
92
Q

What is the clinical presentation of peritonitis?

A
  • Abdominal pain.
  • Fever.
  • Ascites.
93
Q

What is the investigation used for suspected peritonitis?

A
  • Paracentesis of ascitic fluid + culture.

Will appear cloudy, or bloody.

94
Q

What is the 1st line treatment for peritonitis?

A
  • Cefotaxime (cephalosporin).
95
Q

What is ascites?

A
  • Pathological collection of fluid in the peritoneal cavity.
96
Q

What is the most common cause of ascites?

A
  • Liver cirrhosis.
97
Q

What are the investigations used to diagnose ascites?

A
  • Physical examination/palpation (abdomen distension).
  • USS abdomen is definitive.
98
Q

What is an inguinal hernia?

A

Protrusion of the abdominal/pelvic contents either through the internal inguinal ring (indirect) or through the wall of the inguinal canal (direct).

99
Q

What is a direct inguinal hernia?

A
  • Protrusion of the abdominal contents directly through the wall of the inguinal canal.
100
Q

What is an indirect inguinal hernia?

A
  • Protrusion of the abdominal contents through the deep inguinal ring.
101
Q

Who is most commonly affected by inguinal hernias?

A
  • Middle aged men.
102
Q

What is the clinical presentation of an inguinal hernia?

A
  • Groin pain that comes on when the hernia bulges, and goes away when the hernia stops bulging.
  • Palpable mass in the groin.
103
Q

What is the treatment for an inguinal hernia?

A
  • Surgical repair.
104
Q

What is a1 antitrypsin deficiency?

A
  • 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
Q

What are the key presenting features of AAT deficiency?

A
  • Panacinar emphysema (involves entire alveolus).
  • Bronchiectasis.
  • Liver disease (hepatitis and jaundice).
106
Q

What are the investigations used in AAT deficiency?

A
  • Spirometry. Obstructive pattern.
  • AAT screening. Will show low AAT.
  • LFTs. Show liver disease.
107
Q

What causes both the respiratory and hepatic presentations of AAT deficiency?

A

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
Q

What investigations are used in AAT deficiency?

A
  • AAT screening. Shows low levels of AAT.
  • Spirometry (obstructive pattern)
  • LFTs. Show hepatocellular disease/inflammation.
109
Q

What is the management of AAT deficiency?

A
  • IV AAT therapy.
  • Stop smoking.
  • SABA
  • Liver transplant.
110
Q

What is a common treatment for ascites?

A
  • Diuretics. These reduce the fluid overload, hopefully reducing ECF volume.
111
Q

What are the 4 types of hepatitis?

A
  • A
  • B
  • C
  • Autoimmune
112
Q

What is the vaccination system for each type of hepatitis?

A
  • Hep A. Vaccine at request.
  • Hep B. Routine vaccination on the NHS.
  • Hep C. No vaccine available yet.
  • Autoimmune hep. No vaccine.
113
Q

What is the route of transmission for each hepatitis?

A
  • Hep A. Faecal/oral.
  • Hep B. Percutaneous/permucosal. (Unprotected sex/IV drug use).
  • Hep C. Infectious blood transmission. (IV drug use).
114
Q

Which is the most common hepatitis in the UK for drug users?

A
  • Hep C. This is via IV drug use, and not routinely vaccinated against like hep B is.
115
Q

What are the tests for each of the 4 types of hepatitis?

A

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
Q

What is the treatment for autoimmune hepatitis?

A
  • Azathioprine (DMARD) + prednisolone (corticosteroids).
117
Q

What is haemochromatosis?

A
  • Autosomal recessive disorder that leads to buildup of iron in the body.
118
Q

What is the clinical presentation of haemochromatosis?

A
  • Bronzing of skin.
  • Hepatomegaly.
  • Loss of libido.
  • Diabetes mellitus.
  • Pseudogout.
119
Q

What investigations are used for haemochromatosis?

A

1st line - Serum transferrin saturation. Raised.

Also - Serum ferratin. Raised.

120
Q

What is the treatment for haemochromatosis?

A

Initially monitor and keep dietary iron low.

Phlebotomy to remove iron from blood if disease gets more severe.

121
Q

What is Wilson’s disease?

A
  • Autosomal recessive disorder associated with buildup of copper in the body.
122
Q

How does Wilson’s disease relate to the liver?

A
  • Lots of the copper is stored in the liver. This causes hepatitis and eventually cirrhosis/liver failure.
123
Q

What is the presentation of Wilson’s disease?

A
  • Kayser - Fleischer rings (dark rings around the eyes).
  • Tremor/dysarthria (neuro symptoms).
  • Jaundice/hepatic tenderness (hepatic symptoms).
124
Q

What are the tests used for Wilson’s disease?

A
  • LFT’s. High AST/ALT and high bilirubin.
  • 24 Hour copper excretion test. Will be raised.
125
Q

What is the treatment for Wilson’s disease?

A
  • Zinc. This reduces Cu absorption in the gut.
126
Q

What is the first line treatment for alcohol withdrawal?

A
  • Chlordiazepoxide.

Phase 2 v2 (14 decks)

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