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Year 3 TCDs > Liver, Biliary and Pancreatic Disease > Flashcards

Liver, Biliary and Pancreatic Disease Flashcards

1
Q

Name 5 signs that strongly suggest liver cirrhosis

A
  1. Spider naevi
  2. Palmar erythema
  3. Hepatomegaly
  4. Splenomegaly or ascites
  5. Abnormal collateral veins in the abdomen (ie. caput medusa)
  6. Jaundice (scleral icterus)
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2
Q

What causes hepatic encephalopathy?

A

Both acute liver failure + decompensated liver cirrhosis

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3
Q

What might precipitate a decompensation in previously stable liver cirrhosis?

A
  1. Infection
  2. Alcoholic binge
  3. GI bleed
  4. Hypoglycaemia
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4
Q

What result would indicate portal hypertension (transudate)?

A

Serum albumin ascites gradient > 1.1g/dL

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5
Q

What result would indicate peritoneal disease (exudate)?

A

Serum albumin ascites gradient < 1.1g/dL

Rare!

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6
Q

What result would indicate spontaneous bacterial peritonitis?

A

Microscopy showing > 500 white cells/mm3

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7
Q

Alcohol detoxification treatment of chlordiazepoxide is prescribed as follows:

Day 1: 40mg 4x/day
Day 2: 30mg 4x/day
Day 3: 20mg 4x/day
Day 4: 10mg 4x/day
Capsule bottle labelled: “chlordiazepoxide 5mg capsules. Take as directed”

What is the total quantity of capsules that should be present in the bottle, presuming he has taken the doses as advised above?

A

Total = 8+24+16+8

= 56 capsules

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8
Q

Prescribe a regular dose of an osmotic laxative for a patient at risk of hepatic encephalopathy. The patient has no known drug allergies. The aim is for the patient to have 2-3 loose stools/day.

A

Lactulose
Dose: 30ml
Route: Oral

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9
Q

What is the pathophysiological cause of jaundice?

A

Increased bilirubin in the body (clinically > 50uM/L)

  1. Unconjugated = not from liver/biliary tree (prehepatic cause)
  2. Conjugated = caused by liver/biliary disorders (hepatic/post-hepatic cause)
  • Conjugated = more common; dark urine + pale stools + itch
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10
Q

What are 2 causes of conjugated hyperbilirubinemia?

A
  1. Obstructive jaundice = blockage of bile flow thru bile ducts or intrahepatic/extrahepatic ducts
  2. Hepatocellular jaundice = hepatocyte damage (I.e. cirrhosis, hepatitis)
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11
Q

Name at least 2 common + uncommon examples of obstructive jaundice

A

Common: Gallstones in common bile duct, carcinoma of head of pancreas
- In duct, in duct wall, outside biliary duct

Uncommon: Sclerosing cholangitis, cholangiocarcinoma

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12
Q

Name at least 2 common + uncommon examples of hepatocellular jaundice

A

Common: Alcohol, hepatitis, cirrhosis, viral hepatitis, drug-induced, non-alcoholic fatty liver disease

Uncommon: Autoimmune liver disease, Hemochromatosis, Wilson’s disease

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13
Q

Describe the abdominal pain known as biliary colic

A
  • RUQ pain

- If associated with jaundice + fever = cholangitis (I.e. sepsis in biliary ducts)

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14
Q

Describe the abdominal pain associated with pancreatitis

A
  • Severe epigastric pain radiating to back

- Inflammation of pancreas usually caused by alcohol excess/gallstones blocking common bile duct

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15
Q

What is the likely diagnosis of painless jaundice?

A

Liver/pancreatic cancer

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16
Q

Name 6 risk factors for liver disease

A
  1. Alcohol abuse
  2. Drug use
  3. Travel
  4. History of blood transfusions
  5. Tattoos
  6. Unprotected sex
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17
Q

What are 9 signs of liver disease on an abdo exam?

A
  1. Fever
  2. Cachexia
  3. Hepatic encephalopathy (flap)
  4. Signs of chronic liver disease (I.e. gynecomastia, palmar erythema)
  5. Scars of surgery (I.e. cholecystectomy)
  6. RUQ/epigastric pain
  7. Hepatomegaly
  8. Splenomegaly
  9. Ascites
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18
Q

Outline liver function tests

A
  1. LFTs -> useful to monitor degree of liver damage + prognosis
    - Clotting factors (PT, INR), albumin (decreased in liver disease)
  2. Liver enzymes -> most useful to aid diagnosis
    - Transaminases (AST, ALT) -> most useful
    - Alkaline phosphatase (ALP)
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19
Q

What are the LFTs like in hepatocellular damage?

A

Increased ALT, AST&raquo_space; ALP = hepatocellular damage

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20
Q

What are the LFTs like in obstructive damage?

A

Increased ALP&raquo_space; ALT, AST = obstructive damage

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21
Q

What are 5 red flags for cancer of the liver?

A
  1. Weight loss
  2. Hard lymphadenopathy (Troisier’s node = L supraclavicular node -> Virchow’s sign)
  3. Hard, craggy liver edge
  4. Predisposing risk factors
  5. Thenar wasting
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22
Q

If a patient over 40y presents with painless obstructive jaundice what are you looking for on imaging?

A

Carcinoma of the head of the pancreas

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23
Q

What cancer usually metastasizes from other primary cancers such as lung cancer?

A

Liver cancer

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24
Q

What cancer are patients at increased risk of developing with liver cirrhosis? What blood test would you check?

A

Primary hepatocellular cancer

Check a-fetoprotein levels

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25
Q

If the gallbladder is palpable what rare cancer are you suspecting?

A

Cholangiocarcinoma

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26
Q

What is delirium tremens?

A

Rapid onset of confusion usually caused by withdrawal from alcohol

Occurs 3 days into withdrawal symptoms + lasts for 2-3 days

Untreated = seizures + death

Patients advised to reduce drinking gradually which allows receptors in the brain to adapt/started on detox regimens

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27
Q

Name 2 main drugs used in the management of acute alcohol withdrawal

A
  1. Benzodiazepine/carbamazepine
  2. Clomethiazole

Offer ORAL lorazepam, PARENTERAL lorazepam or haloperidol for delirium tremens

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28
Q

What is bilirubin?

A

Breakdown product of hemoglobin which isn’t soluble in water and thus is conjugated in the liver

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29
Q

What makes stool brown and urine dark?

A

Stercobilinogen + urobilinogen

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30
Q

What is hepatitis?

A

Inflammation of the liver

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31
Q

What is cirrhosis?

A

Fibrosis of the liver + nodule formation

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32
Q

What is the difference between acute and chronic hepatitis?

A

Inflammation > 6mo = chronic

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33
Q

What are the potential progressions of an acute hepatitis episode?

A
  1. Recovery (no long-term damage)
  2. Chronic hepatitis -> increased fibrosis -> cirrhosis
  3. Fulminant hepatitis (acute liver failure) -> death/transplant
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34
Q

What are the symptoms of acute hepatitis?

A

Typically: Unwell, jaundice, RUQ pain (swelling of liver in capsule which stretches + causes pain)

Severe: Confusion (encephalopathy), bruising (coagulopathy)
- These are symptoms of fulminant hepatitis

Increased ALT/AST (>1000)
Increased bilirubin
Coagulopathy
Renal impairment

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35
Q

What is chronic hepatitis and what are its symptoms?

A

Low grade inflammation of the liver

Symptoms:

  • Often none
  • Fatigue
  • Abnormal LFTs (mild increase in ALT)
  • Detected with screening
  • Present with cirrhosis
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36
Q

What is fulminant hepatitis?

A

Acute liver disease (hepatitis) with liver failure

Encephalopathy within 28d of jaundice

Poor prognosis (need transplant)

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37
Q

What are the 2 main things that occur in liver cirrhosis?

A
  1. Loss of function
    - Jaundice (no breakdown of hemoglobin)
    - Coagulopathy (no clotting factors being made)
    - Decreased drug metabolism (opiates + benzodiazepines especially)
    - Decreased hormone metabolism (Increased estrogen = spider naevi, palmar erythema, decreased body hair, gynecomastia, shrinking of genitals)
    - Increased risk of sepsis (decreased immune system)
  2. Portal HTN
    - Varices (esophageal, caput medusa)
    - Piles (rectal)
    - Ascites (fluid retention in abdomen)
    - Encephalopathy (increased ammonia + toxins in abdo)
    - Renal failure (renal artery vasoconstriction - hepatorenal syndrome)

** These are independent of each other. Portal HTN is easier to treat**

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38
Q

Name 6 causes of liver cirrhosis

A
  1. Alcohol
  2. Hepatitis B + C
  3. Autoimmune liver disease (autoimmune hepatitis, primary biliary sclerosis)
  4. Hemochromatosis
  5. Wilson’s disease
  6. Chronic obstruction
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39
Q

What is the scientific name for a fatty liver?

A

Steatosis

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40
Q

When does steatosis or steatohepatitis turn into cirrhosis?

A

With continued exposure more inflammation and cell death ensues

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41
Q

What are 4 signs of decompensated liver cirrhosis?

A
  1. Jaundice
  2. Ascites
  3. Encephalopathy
  4. Variceal bleeding

50% 2-yr survival of liver failure
Corticosteroid treatment has been shown to improve survival in the short-term (1mo) but increases risk of infections in the first 3mo

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42
Q

What are the components that make up bile?

A

Bile pigments (haem breakdown) + bile salts (cholesterol)

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43
Q

Where is bile produced and when is it released? How much bile is produced/day?

A

Produced by hepatocytes in the liver and stored in the gallbladder

It is released in response to food via hormonal (CCK-PZ) and fatal nerve to contract gallbladder

500-1000ml/day is produced

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44
Q

Bilirubin + what enzyme allows it to become soluble and excreted in bile?

A

Glucoronic acid

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45
Q

What are 4 causes of prehepatic jaundice (hemolysis)?

A
  1. RBC abnormality (I.e. sickle cell)
  2. Incompatible blood transfusion
  3. Drug reaction
  4. Hypersplenism
46
Q

What is the pathophysiology of prehepatic jaundice?

A
  • Glucuronyl transferase is saturated
  • Liver function normal
  • Liver increases conjugated bilirubin output -> dark stools
  • Excess of unconjugated bile in plasma
  • Unconjugated bilirubin is not excreted in urine thus little/no bilirubin in urine (urobilinogen)
47
Q

What are the 2 main causes of hepatocellular jaundice?

A
  1. Congenital
  2. Acquired
    - Infection -> viral hepatitis
    - Cirrhosis secondary to alcohol
    - Cirrhosis secondary to steatohepatitis (NASH)
    - Damage by toxins/drugs
48
Q

What is the pathophysiology of hepatocellular jaundice?

A
  • Unconjugated bilirubin increases (hepatocytes can’t function to conjugate bilirubin)
  • Increased ALT (transaminases)
49
Q

Explain neonatal jaundice/hyperbilirubinemia

A

> 85uM/L of bilirubin = visual presentation of jaundice

Occurs in 2/3 of all infants

Enzyme activity of glucuronyl transferase not at its peak level

50
Q

What is biliary atresia?

A

Extrahepatic biliary tree fails to form

Pathological, potentially toxic

Unconjugated hyperbilirubinemia
-> can penetrate BBB = kernicterus (stains brain tissues) -> encephalopathy

51
Q

What is the treatment for neonatal jaundice?

A
  1. Hydration
  2. Phototherapy (breakdown bilirubin molecules)
  3. Exchange transfusion (removing abnormal blood components + circulating toxins whilst maintaining adequate circulating blood volume)
52
Q

What are the 4 main things one should ask about jaundice?

A
  1. If the jaundice is with or without pain
  2. Duration
  3. Itching
  4. Colour of urine/stools
53
Q

What are the 3 main causes of post-hepatic jaundice (obstruction)?

A

Obstruction of conjugated bilirubin from hepatocyte to intestine:

  1. Obstruction of bile duct by stone
  2. Obstruction of bile duct by tumour
  3. Intra-hepatic cholestasis
54
Q

What is the pathophysiology of post-hepatic jaundice?

A
  • Increased conjugated bilirubin (H2O soluble) = increased dark urine
  • No bilirubin re-absorbed into intestine = pale stools (no stercobilinogen)
55
Q

What investigations would you perform for someone with post-hepatic jaundice?

A
  1. Trans-abdominal ultrasound
    - looking for dilated bile ducts
  2. CT
    - IV contrast (in aorta = white) = arterial phase
    - 3-phase CT = arterial, venous, + non-contrast phase
  3. Endoscopic retrograde cholangiopancreatography
    - For obstruction with stone to retrieve stone via mouth
56
Q

Outline the pathophysiology of hepatitis A

A
  • Feco-oral spread
  • Common in childhood
  • Endemic in developing world
  • 12wk duration
  • Immunization possible -> travel + other liver disease
  • treatment not needed as self-limiting
57
Q

What is the prognosis for hepatitis A?

A

Recovery in 99%

Fulminant hepatitis in 1-2% (liver disease is a risk factor)

58
Q

What antibody is measured to determine whether the infection is acute or chronic?

A

IgM (increased in 1-2wks) = acute infection

IgG = previous exposure to hepatitis A (remember hepatitis A cannot become chronic!)

There is a 2-3wk incubation period (but HAV can be spread in the stool during this time)

59
Q

Explain the pathophysiology of hepatitis B

A

Spread:

  • Blood (medical, IV drug use)
  • Sex
  • Vertical transmission (during vaginal birth)
  • Immunization available
  • 1 billion exposed (world’s 2nd biggest carcinogen -> liver disease)
60
Q

What factors determine the progression to chronic hepatitis?

A
  1. Age (I.e. < 1yr - 90% chance of progression to chronic)
  2. Immunosuppressed
  3. Route of infection
  4. Genotypes of infection
61
Q

What determines Hepatitis B cirrhosis prognosis?

A
  1. Rate of fibrosis
  2. Viral load of Hep B
  3. Biopsies -> show fibrosis + inflammatory markers
62
Q

What are the antibodies to determine the type of hepatitis B infection (acute v chronic)?

A

Anti-core IgM = acute infection

HBsAg (surface antigen) = determines if you have chronic infection (disappears within 24wks)

HBsAg positive + IgM anti-HBc negative = chronic infection

63
Q

What antigens are present in a patient that is Hep B immunotolerant? Immunoreactive?

A

HbeAg (E antigen) positive = immunotolerant

  • Increased viral levels = infectious carriers
  • Normal LFTs
  • Few liver problems

HbeAb (E antibody) positive = immunoreactive

  • Decreased viral levels = less infectious
  • ALT increased
  • Fibrotic/cirrhotic liver
64
Q

What treatment is available for hepatitis B?

A

Acute = no treatment needed (self-limiting)

Chronic = treatment but not curable

  • Antiviral -> suppression (I.e. nucleotide analogues which are also used in HIV drugs); Entecavir, life-long treatment
  • 48wk course of interferon -> stimulates immune system to develop response
  • Given to E antigen positive patients to kick them into antigen negative status
65
Q

Describe the pathophysiology of hepatitis C

A

Transmission:

  • IV drug use
  • Blood born
  • Medical
  • 10-20% don’t have any risk factors
  • sex + vertical transmission = 2-3%
  • No Immunization possible
  • Can become reinfected with hep C
66
Q

What are the possible outcomes of an acute hepatitis C infection?

A
  1. Full recovery (25%)
  2. Chronic hepatitis (75%) -> fibrosis -> cirrhosis

Mostly asymptomatic and discovered thru screening:

  1. Donors
  2. IV drug users
  3. Abnormal LFTs
67
Q

What testing is done to determine if someone has hepatitis C?

A
  1. Antibodies (showing exposure)
  2. PCR (if antibodies are positive to check for RNA)
    - If positive, likely chronic infection
68
Q

What is the treatment for hepatitis C?

A
  1. Interferon -> Ribavirin (24-48wks)

2. Protease inhibitors (expensive)

69
Q

Describe the pathophysiology of hepatitis E

A
  • Virtually identical to Hepatitis A (IgM + IgG)

- May cause maternal death in 2nd trimester -> fulminant hepatitis

70
Q

Describe the pathophysiology of hepatitis D (delta)

A
  • Imperfect virus (cannot replicate itself)
  • Requires co-infection with hepatitis B to replicate
  • Coats itself in hepatitis B surface antigen + then infects cells
  • Alone = no symptoms but with hepatitis B, increased risk of hepatitis B

Treatment = interferon (similar to hep B treatment)

71
Q

Name 4 other causes of hepatitis

A
  1. Hereditary -> Wilson’s, Hemochromatosis
  2. Drugs -> azithromycin, flucloxacillin, paracetamol, alcohol
  3. Infection -> EBV, CMV
  4. Autoimmune liver disease -> Crohn’s, Sarcoidosis, Ulcerative colitis, Hashimoto thyroiditis, Myositis, Scleroderma, Sjögren’s Syndrome
72
Q

Name 7 possible differentials for RUQ pain

A
  1. Acute pancreatitis
  2. Perforated ulcer
  3. Cholangitis/biliary colic
  4. Pyelonephritis/renal colic
  5. Acute mesenteric ischemia (embolism/thrombus)
  6. Pneumonia
  7. MI
73
Q

What does post-hepatic jaundice with marginally abnormal liver functions + increased ALP with severe pain, fever, and increased WBC indicate?

A

Gallstones with or without biliary colic, with cholangitis

74
Q

What investigations would you request for someone with gallstones?

A
  1. Image biliary tree via US abdo
    - Stone in biliary duct
    - Ducts dilated (= long-term obstruction to the flow of bile)
    - State/health of surrounding organs
75
Q

What questions are important to ask when dealing with obstructive jaundice and looking at a US?

A
  1. Are the bile ducts dilated?
  2. At what level is the obstruction?
  3. Can we identify the cause: tumour, stone, structure, etc?
76
Q

What is cholangitis? Cholelithiasis? Cholecystitis?

A

Cholangitis: inflammation of the bile duct

Cholelithiasis: Formation of gallstones

Cholecystitis: Inflammation of gallbladder

77
Q

How does biliary obstruction due to gallstones present?

A

Repeated biliary colic/attacks of cholangitis

Presents with painful jaundice + minimal dilation of bile ducts (early presentation)

78
Q

How does a carcinoma of the head of pancreas/ampulla of Vater present?

A

Progressively worsening painless jaundice + marked dilation of the biliary tree

79
Q

What hormone is responsible for causing the gallbladder to contract and bile to be released?

A

Cholecystokinin (CCK)

80
Q

Name the ducts involved in the biliary tree

A
  1. Common hepatic duct
  2. Cystic duct
  3. Common bile duct (#1 + #2)
81
Q

What are the 2 main roles of the pancreas?

A
  1. Endocrine function -> produce hormones to regulate blood sugar (I.e. insulin)
  2. Exocrine function -> produce enzymes to help digest food (I.e. pancreatic amylase, proteases, lipases)
82
Q

What are the consequences of an unwell pancreas?

A
  1. Diarrhea
  2. Bloating
  3. Flatulence
  4. Oily/foul smelling stool
  5. Weight loss
  6. Malnutrition
  7. Poor blood sugar control
  8. Diabetes
83
Q

What are the risk factors for poor pancreas health?

A
  1. Alcohol
  2. Smoking
  3. Increased fat diets
  4. Obesity
  5. Genetics (I.e. CF)
84
Q

What is acute pancreatitis and what are 8 causes?

A

Enzymes to break down food become activated before leaving the pancreas
- Attack/digest pancreatic tissue (autodigestion)

GET SMASHED
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hyperlipidemia/hypercalcemia/hypothermia
ERCP
Drugs (thiazide, pioglitazone)
85
Q

What are the symptoms of acute pancreatitis?

A
  1. Epigastric pain radiating to the back
  2. Nausea + vomiting
  3. Fever
86
Q

What blood tests are used to check for acute pancreatitis?

A

Increased amylase + lipase

87
Q

How is acute pancreatitis diagnosed?

A
  1. CT/MRI
  2. Endoscopic ultrasound
  • 1 in 10 cases become more severe involving kidneys + lungs and requires surgery (cholecystectomy) -> could result in pancreatic insufficiency
88
Q

What is chronic pancreatitis and what are risk factors for its development?

A

Irreversible destruction of pancreatic tissue

  1. Smoking
  2. Alcohol
  3. Meds
  4. Increased cholesterol
  5. Auto-immune conditions
  6. Genetics (I.e. CF, hereditary pancreatitis)
  7. Idiopathic
89
Q

What are the symptoms of chronic pancreatitis?

A
  1. Weight loss
  2. Pain
  3. Vision loss
  4. Malabsorption
  5. Foul smelling stools
  6. Diabetes
  • Abdo pain may be intermittent/chronic + very severe
  • Intense stabbing pains in epigastric radiating to back
  • Triggered by eating (especially fatty foods)
90
Q

How is chronic pancreatitis diagnosed? Treated?

A

Pancreatic stimulation test -> using secretin

Blood tests are not useful

Pancreas enzyme replacement therapy (PERT) for treatment

91
Q

Outline the 8 steps to a medication history

A
  1. Allergies/intolerances
  2. List regular medications
  3. List when required medications
  4. List any acute medications
  5. Recent changes to medications
  6. Any additional remedies
  7. Adherence to medications
  8. Plan for medications on admission - starting/stopping + reasons for doing so
92
Q

When recording medications that the patient is taking what are the 9 things that are important to record?

A
  1. Name of drug
  2. Brand
  3. Dose
  4. Frequency
  5. Time taken
  6. Formulation
  7. Route
  8. Indication
  9. Duration of prescription
93
Q

What drug doses need to be confirmed with the Drug + Alcohol centre?

A

Methadone + benzodiazepines

94
Q

What 2 questions should you ask people who are on nebulisers?

A
  1. Are the patient’s on these at home?

2. Are they regularly taking nebulisers?

95
Q

What 2 questions should you ask someone taking steroids?

A
  1. Are they maintenance oral steroids?

2. Have they taken a course of steroids recently?

96
Q

What questions must you ask someone on warfarin?

A
  1. Indication INR range
  2. Usual dose
  3. Which clinic they get their INR checked at
  4. Do they have a yellow book?
97
Q

What questions must you ask someone on insulin?

A
  1. How many units?
  2. Type of device
  3. Frequency
  4. Brand of insulin
98
Q

What type of drugs are taken once/week?

A

Methotrexate + bisophosphonates

99
Q

Name 4 signs of portal hypertension

A
  1. Caput medusa
  2. Esophageal varices
  3. Ascites
  4. Splenomegaly
100
Q

What typical blood test result is reduced in liver disease

A

Platelets (as spleen function is affected)

101
Q

What are 3 signs of hepatic encephalopathy?

A
  1. confusion
  2. decreased consciousness
  3. Fits
  4. Liver flap (asterixis)
102
Q

List 6 risk factors for decompensated liver disease

A
  1. Alcoholic binge
  2. Drugs (opioid analgesia)
  3. GI hemorrhage (increased ammonia)
  4. Metabolic disturbances (renal failure, hypoglycaemia)
  5. Infections
  6. Constipation (increased ammonia)
103
Q

What are 3 causes of transudate?

A
  1. Liver cirrhosis with portal HTN
  2. Congestive heart failure
  3. Nephrotic syndrome
104
Q

What are 2 causes of exudate?

A
  1. Malignancy (liver/peritoneal metastases)

2. Peritoneal TB

105
Q

What is the cause of pruritis?

A
  • Primary biliary cirrhosis
  • Cholangitis
  • Common bile duct stones
106
Q

Name 5 risk factors for acute hepatitis

A
  1. Hepatitis A (foreign travel, contact with other jaundiced ppl)
  2. Hepatitis B (unprotected sex, contaminated needles, blood transfusions)
  3. Epstein-Barr Virus (glandular fever)
  4. Drugs (antibiotics such as co-amoxyclav/augmentin)
  5. Alcohol (in excess)
107
Q

Describe the LFTs for

  1. Pre-hepatic (non-liver disease)
  2. Hepatic (hepatocellular damage)
  3. Post-hepatic (obstruction)
A
  1. Very high unconjugated bilirubin; Normal conjugated bilirubin, ALT/AST, ALP
  2. Normal unconjugated bilirubin; Very high conjugated bilirubin + ALT/AST; high ALP
  3. Normal unconjugated bilirubin; High conjugated bilirubin + ALT/AST; Very high ALP
108
Q

Why is it necessary to take multiple blood tests to check LFT levels with suspected gallstones?

A

ALT + ALP may be changing in opposite directions. ALT is likely to continue increasing while ALP will decrease from a high initial value

109
Q

What is the treatment for paracetamol overdose?

A

N-acetyl cysteine

110
Q

Name 2 signs of end of life stage liver failure as a result of fulminant hepatitis?

A
  1. Increased INR (clotting factor problem with liver)

2. Hypoglycemia (liver no longer able to synthesize glucose)

111
Q

Name 1 cause of development of acute fulminant hepatitis (rapid necrosis of hepatocytes)

A

Paracetamol overdose

Year 3 TCDs (24 decks)

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