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Medical School Finals > Core: Hepatobiliary > Flashcards

Core: Hepatobiliary Flashcards

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USMLE® Step 1 flashcards
1
Q

Liver failure Aetiology

A
  • Viruses; HAV, HBV, HCV, CMV, HSV, EBV
  • POD
  • Antibiotics, NSAID’s, statins.
  • Acute fatty liver of pregnancy
  • HELLP
  • Alpha 1 antitrypsin, Wilsons, HH
  • Alcohol (acute on chronic)
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2
Q

Liver failure Pathology

A
  • Histology = multi-acinar necrosis

- Cerebral oedema due to break down of gut proteins to ammonia.

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3
Q

Acute liver failure types (timings)

A

1) Hyper-acute = jaundice to encephalopathy within 7 days
2) Acute = 8-28 days
3) Sub-acute = >21days yet <26 weeks.

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4
Q

Acute liver failure definition

A
  • Acute liver injury + encephalopathy + deranged coagulation
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5
Q

Liver failure presentation

A
  • Jaundice
  • Small liver
  • Encephalopathic signs - alteration in mental state, drowsiness, confusion, coma
  • Fetor hepaticus
  • Asterixus
  • Raised ICP due to cerebral oedema.
  • Bleeding and coagulopathic Sx.
  • Oedema and ascites due to low albumin.
  • Secondary renal failure - Hepatorenal syn.
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6
Q

Liver failure Ix

A

1) Bloods - LFT, Clotting and albumin (better markers than LFT), viral serology, Paracetamol level.
2) Imaging; CT/MRI/USS
3) Liver biopsy
4) EEG

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7
Q

Liver failure Rx - criteria for transfer to specialist unit

A

1) INR >3
2) Encephalopathy
3) Hypotensive despite fluid resus
4) Metabolic acidosis
5) PT in secs > than number of hours following POD

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8
Q

Liver failure Rx

A

1) ABCDE
2) Supportive care for encephalopathy; bowel wash out + mannitol for raised ICP + Lactulose and rifampicin.
3) Correct metabolic and electrolyte issues (including potassium and BM)
4) Correct coagulopathy w/ vit K, blood products.
5) ABx prophylaxis
6) Liver Tx is definitive.

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9
Q

Patient - Middle aged man w/ bronzed skin, T2DM and hepatomegaly.

A
  • Hereditary hemochromatosis
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10
Q

HH Aetiology

A
  • All types are AR inherited except Type 4 which is AD
  • Type 1 = HFE gene
  • Type 2 = Juvenile HJV or HAMP
  • Type 3 = TfR2 gene
  • Type 4 = Ferroportin
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11
Q

HH Pathology

A
  • HFE interacts w/ transferrin receptor 1 which mediated intestinal iron absorption.
  • Iron is absorbed exceeding binding capacity of transferrin.
  • Hepcidin (made in the liver) is normally downregulated in overload, this is not the case in HH allowing for sustained overload
  • Excess iron is taken up by the liver and other organs (kidneys, pancreas, brain, heart)
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12
Q

HH Presentation

A
  • Triad = Bronze skin + DM + hepatomegaly
  • Hypogonadism due to pituitary involvement.
  • Heart failure and arrhythmia
  • Arthralgia of the hands
  • Cirrhosis
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13
Q

Reversible effects of HH

A
  • Cardiomyopathy

- Skin pigmentation

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14
Q

Irreversible effects of HH

A
  • Cirrhosis
  • DM
  • Hypogonadism
  • Arthropathy
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15
Q

HH Ix

A

1) Bloods; serum iron is raised w/ a reduction in TIBC and transferrin saturation.
2) Genetic testing
3) LFT
4) Liver biopsy - not Dx but can help assess extent of damage.
5) MRI - reduced magnetic effect of the liver and panc due to the paramagnetic effects of ferritin and haemosiderin.

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16
Q

HH Rx

A

1) Venesection - remove excess iron to prevent tissue damage. 500ML tiwce a week until iron is normal and then 4x per year.
2) Screen relatives.

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17
Q

Wilson’s disease Aetiology

A
  • AR inherited.
  • Copper transporting ATPase
  • chromosome 13
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18
Q

Wilson’s disease Pathology

A
  • Mutation causes a failure in copper being incorporated into caeruloplasmin.
  • Low serum caeruloplasmin.
  • Mechanism of copper deposition is UK.
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19
Q

Wilson’s disease Presentation

A
  • Often kids
  • Liver problems; acute hepatitis, chronic hepatitis, cirrhosis
  • Neurological defects (tremor, dysarthria, tics and dementia) personality changes
  • KF rings
  • Renal tubular acidosis (Fanconi syn)
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20
Q

Wilson’s disease Ix

A

1) Serum copper and caeruloplasmin - both low.
2) Urinary copper - increased
3) Liver biopsy; suggestive if high levels of copper but not diagnostic.
4) Genetic testing

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21
Q

Wilson’s disease Rx

A

1) Lifelong penicillamine 1-1.5g/day. Chelates copper.

- SE = rashes, leucopenia and renal damage

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22
Q

Patient - Kid presents w/ behavioural problems, deranged LFT suggesting hepatitis. You notice a tremor and unusual movement and that his speech is unusual.

A

Wilson’s disease

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23
Q

Patient - COPD + Liver disease

A

Alpha 1 antitrypsin.

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24
Q

Alpha 1 antitrypsin aetiology

A
  • Genetics
  • Gene located on chromo 14
  • A1AT is an acute phase reactant.
  • A1AT inhibits proteolytic enzyme neutrophil elastase.
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25
Q

A1AT pathology

A
  • UK
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26
Q

A1AT Presentation

A
  • Some present in childhood, often presents later.

- Liver disease (cirrhosis) + Pulmonary emphysema.

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27
Q

A1AT Ix

A

1) A1AT is low - deficiency

2) Liver biopsy - Periodic acid Schiff positive.

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28
Q

A1AT Rx

A

1) Nil

2) Manage Sx and complications.

29
Q

Alcoholic liver disease aetiology

A
  • alcohol consumption
  • Ethanol is metabolised in the liver via 2 pathways.
  • its metabolism results in an increase in the NAD/NADH ratio.
  • This altered redox potential results in increased fatty acid synthesis and accumulation in the liver.
  • ROS are released causing damage.
30
Q

ALD Pathology

A
  • Fatty liver - cells become enlarged with fat (steatosis) which resolves w/ cessation.
  • Fibrosis due to alcohol transforming stellate cells to myofibroblasts.
  • Alcoholic hepatitis - fatty changes + infiltration of inflammatory cells and hepatocyte necrosis.
  • Alcoholic cirrhosis
31
Q

ALD Presentation

A
  • Fatty liver = often asymptomatic, or age RUQ pressure and hepatomegaly.
  • Alcoholic hepatitis = Changes on biopsy and often asymptomatic
  • Can produce jaundice and deranged LFT
  • Or patient can become acutely unwell w/ ascites and fever due to liver necrosis
  • Alcoholic cirrhosis =
  • Final stage
  • Patients are often well
  • signs of chronic liver disease.
32
Q

ALD Ix

A

Fatty liver

1) Elevated MCV indicates heavy drinking
2) LFT - elevated ALT,AST, GGT
3) Fibroscan

Alcoholic hepatitis

1) High WCC
2) Deranged LFT
3) Low albumin
4) Liver biopsy

33
Q

ALD Rx

A

1) Alcohol cessation (manage effects)
2) Alcoholic hepatitis - steroids and vitamins
3) Liver Tx

34
Q

Primary biliary cirrhosis aetiology

A
  • UK
  • Autoimmune
  • Serum anti-mitochondrial antibodies are found.
  • Mitochondrial antigen M2.
  • Molecular mimicry of E.coli.
  • Associated w/ Sjogren’s, scleroderma, thyroid disease, coeliac, glomerulonephritis
  • Destruction of bile ducts leads to a build up of toxins in the liver.
35
Q

PBC presentation

A
  • Women 40-50yo
  • Often asymptomatic and found with raised ALP or hepatomegaly
  • Itching
  • Fatigue
  • Jaundice
  • Hepatomegaly
  • Xanthelasma
  • RUQ discomfort.
36
Q

PBC Ix

A

1) Mitochondrial M2 antibodies - via elisa.
2) LFT - high ALP
3) Raised serum cholesterol
4) Raised IgM
5) Liver biopsy - portal tract infiltration or lymphocytes and plasma cells.

37
Q

PBC Rx

A

1) Ursodeoxycholic acid 10-15mg - improves bilirubin and transferase levels
2) Steroids
3) Supplement fat soluble vitamins
4) Bisphosphonates
5) Colestyramine for the itching or rifampicin or naloxone.

38
Q

Primary sclerosis Cholangitis aetiology

A
  • Chronic liver disease caused by a progressive cholestasis leading to fibrosis of bile ducts.
  • Autoimmunity (ANCA)
  • Associated with UC
  • Risk of developing cholangiocarcinoma
39
Q

PSC presentation

A
  • Most patients are male 40yo
  • Fatigue
  • Itching
  • RUQ pain
  • Sx may remit and recur
  • Jaundice
40
Q

PSC Ix

A

1) LFT - deranged w/ increased ALP, Transferases and GGT
2) ERCP or MRCP
3) IBD Ix

41
Q

PSC Rx

A

1) Repeated endoscopic dilatation of strictures can help ease Sx by maintaining bile outflow.
2) Ursodeoxycholic acid
4) Similar to PBC

42
Q

Acute Cholecystitis Aetiology

A
  • Infection and inflammation of the GB
  • Often arising from an initial event where the GB is obstructed from emptying.
  • Underlying stone disease.
  • Ischaemia of the GB occurs when then GB distends.
  • Infection due to E.coli, klebsiella, enterococcus and pseudomonas.
43
Q

Acute cholecystitis Presentation

A
  • Similar to biliary colic.
  • Sudden onset and severe constant pain.
  • RUQ and epigastric pain.
  • N&V
  • Fever and rigors
  • Murphy’s sign
  • Guarding.
44
Q

Acute cholecystitis Ix

A

1) FBC - Raised WCC
2) Raised Inflammatory markers
3) Deranged LFT
4) USS for stones, thick GB wall and focal tenderness over the GB

45
Q

Acute cholecystitis Rx

A

1) Cholecystectomy

2) Conservative Rx = NBM, fluids, analgesia and Abx - ceftriaxone + metronidazole.

46
Q

Gallstones Aetiology

A

Cholesterol stones -

  • Common
  • Hyperlipidaemia
  • Super saturation of the bile; crystallises out.

Pigment stones -

  • Black = calcium bilirubinate; associated w/ haemolytic anaemia.
  • Brown = calcium salts and fatty acids. Found in bile stasis and infection.
47
Q

Gallstones Presentation

A
  • Asymptomatic
  • Seen incidentally
  • Biliary colic - sudden onset severe RUQ pain
  • Associated w/ fatty foods
  • Radiation of pain to subscapular region RHS.
48
Q

Gallstones Ix

A

1) Bloods.
2) Raised inflammatory markers
3) LFT issues
4) USS

49
Q

Gallstones Rx

A

1) Shock dissolution
2) Cholesterol reducing meds such as statins.
3) ERCP retrieval.

50
Q

Post cholecystectomy syndrome

A
  • RUQ pain months after removal of GB
  • Similar pain to biliary colic.
  • Due to small bowel spasms at hepatic flexure.
51
Q

Liver cirrhosis Aetiology

A
  • Diffusely abnormal liver architecture.
  • Interferes w/ hepatic blood flow.
  • Alcohol, viral hepatitis, NAFLD, PBC, PSC, metabolic liver disease.
  • Chronic injury
  • Stellate cells transform to myofibroblasts causing fibrosis.
  • Portal vein blood flow into the liver is impaired.
52
Q

Liver cirrhosis presentation

A
  • RUQ discomfort
  • weakness, anorexia, fatigue
  • Ascites
  • Haematemesis
  • Itching due to cholestasis and build up of bile salts in the blood.
  • Jaundice.
  • Pale stools and dark urine.

o/e

  • Palmar erythema
  • Xantholasmata
  • Jaundice
  • raised JVP
  • Spider naevi
  • HSM
53
Q

Liver cirrhosis Ix

A

1) LFT
2) Albumin and PT are best indicators of hepatic function.
- Thrombocytopenia is the most sensitive and specific lad finding indicating cirrhosis in those w/ liver disease.
3) Electrolyte issues - low sodium due to oedema.
4) Fibroscan
5) USS for HCC
6) Endoscopy for varices.

54
Q

Liver cirrhosis Rx

A

1) Manage complications of decompensated liver disease.
2) USS for HCC
3) Rx the underlying cause.

55
Q

Portal HTN Aetiology

A
  • Portal vein is formed at the union of the SMA and splenic vein.
  • Blood is fed to liver from the bowel and then back to the heart from the liver via the hepatic vein.

a) Pre-hepatic = portal vein thrombosis
b) Hepatic = Distortion of the liver architecture; schistosomiasis and cirrhosis
c) Post hepatic = venous blockage beyond the liver; HF or IVCO

  • As the pressure increases, other collateral vessels compensate.
  • Gastro-oesophageal junction (varices), left renal vein, diaphragm, rectum.
56
Q

Portal HTN presentation

A
  • Sign of chronic liver disease.
  • Haematemesis (varices)
  • Malaena (upper GI bleeding)
  • Ascites
  • Collateral formation; dilated abdominal wall vessels, Caput medusa, haemorrhoids.
57
Q

Portal HTN Ix

A

1) USS for portal HTN - doppler.
2) Endoscopy for Varices
3) Bloods and viral serology
4) CT/MRI

58
Q

Portal HTN Rx

A

1) Rx portal HTN w/ BB - propranolol.
2) Endoscopic rx before bleeding; banding to stop vessels.
3) Transjugular intrahepatic portosystmic shunt - connecting hepatic vein and portal vein.

Acute bleeding;

  • Banding
  • Sclerotherapy
  • Systemic vasoconstriction w/ terlipressin and somatostatin.
  • Balloon tamponade.
59
Q

Pancreatitis Aetiology

A
  • Acute or chronic
  • Acute - in a normal panc which returns to normal.
Gallstones 
Ethanol 
Trauma 
Steroids 
Mumps, malignancy 
Autoimmune
Scorpion stings 
Hypercalcaemia or cholesterol 
ERCP 
Drugs - AZA, oestrogens, valproate, furosemide, metronidazole.
60
Q

Pancreatitis Presentation

A
  • Upper abdominal pain
  • Epigastric
  • N&V
  • involvement of the retroperitoneum leads to back pain.

o/e

  • Upper abdo tenderness
  • Shock
  • Cullens sign (peri-umbilical bruising)
  • Grey-turner’s sign (flank bruising)
61
Q

Pancreatitis Ix

A

1) Serum amylase - 3x upper limit of normal
2) Urinary amylase
3) Serum lipase
4) CRP/ESR
5) Bloods; ABG
6) CXR to exclude perforation.
7) USS for stones
8) Contrast CT 72hours after attack to assess extent of damage
9) ERRCP/MRCP

62
Q

Pancreatitis Rx

A

1) APACHE 2 scoring
2) ABCDE
3) NG tube removal of vomit
4) Prophylactic ABx - imipenem.
5) Analgesia - tramadol.
6) TPN feeding
7) Thromboprophylaxis.

63
Q

Pancreatic Ca Aetiology

A
  • Adenocarcinoma
  • Smoking
  • Excess alcohol or coffee
  • DM
  • Chronic pancreatitis
  • Genetics - PRSS-1 mutation
64
Q

Pancreatic Ca Presentation

A
  • Most are at the head of the pancreas.
  • Pain + anorexia + weight loss.
  • Many present late and have a long Hx of low-grade Sx.
  • Painless jaundice - distal common bile duct being blocked.
  • Malabsoprtion and steatorrhoea.
65
Q

Pancreatic Ca Ix

A

1) Patients often present at a later stage w/ invasive Ca.
2) USS - mass at the head of the pancreas.
3) CT + contrast.
4) PET for mets.
5) CA19-9

66
Q

Pancreatic Ca Rx

A

1) Whipple’s procedure - pancreatoduodenectomy + adjuvant/neo-adjuvant chemo.
2) Often palliate and manage Sx.

67
Q

Alcoholic hepatitis Management

A
  • Often nil

- Prednisolone for severe cases - Maddrey discriminant function value.

68
Q

Autoimmune hepatitis

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. UK
    - associated w/ other autoimmune disorders.
  2. Chronic liver disease
    - Acute hepatitis - fever, jaundice
    - Amenorrhoea
  3. Liver biopsy
    - Antibody testing
  4. Steroids and immunosuppressants; AZA.
    - Liver Tx

Medical School Finals (24 decks)

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