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liver + friends Flashcards

1
Q

tumour marker for pancreatic cancer

A

CA-19-9

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2
Q

hepatitis E brainstorm

A
  • RNA hepevirus
  • faecal-oral route
  • incubation period: 3-8 weeks
  • Central and South-East Asia, North and West Africa, and in Mexico
  • similar disease to hep A, but carries a significant MORTALITY (20%) during PREGNANCY
  • does not cause chronic disease or an increased risk of hepatocellular cancer
  • CONSIDER IF PX HAS SIGNIF TRANSAMITIS IN 1ST TRIM PREG
  • thrombocytopenia
  • undercooked pork
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3
Q

post splenectomy vaccines + prophylactic abx

A

Pneumococcal vaccination (with regular boosters every 5 years).
Seasonal influenza vaccination (yearly, typically every autumn).
Haemophilus influenza type B vaccination (one-off).
Meningitis C vaccination (one-off).

low-dose prophylactic antibiotics - phenoxymethylpenicillin

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4
Q

what are some common causes of hepatomegaly

A

Cirrhosis: if early disease, later liver decreases in size. Associated with a non-tender, firm liver

Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge

Right heart failure: firm, smooth, tender liver edge. May be pulsatile

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5
Q

presentation of hepatitis A

A

incubation period 2-4 weeks
flu-like prodrome
nausea, arthralgia
can progress to cause hepatosplenomegaly + jaundice

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6
Q

common sources of hep A infection

A

contaminated water or food
shellfish

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7
Q

how is hep A transmitted

A

faecal-oral route

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8
Q

how is hep B transmitted

A

direct contact w/ blood or bodily fluids
ie sex
needle sharing (UVDU/tattoos)
can also be passed by sharing toothbrushes, razors or contact w open cuts
can be passed from mum to baby during preg

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9
Q

how to screen for hep B

A

test for HBcAb (core antibodies implying past or current infection)

HBsAg (surface antigen implying current infection)

if +ve test

HBeAg (e antigen - a marker for viral replication + implies high infectivity)

viral load (HBV DNA)

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10
Q

presentation of viral hepatitis

A

may be asymptomatic or present with non-specific symptoms of:

Abdominal pain
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice

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11
Q

how is hep C spread

A

blood and body fluids

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12
Q

which viral hep are there vaccine’s for

A

A
B

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13
Q

how to cure hep C

A

direct-acting antiviral meds - sofobuvir

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14
Q

what type of virus is the diff viral heps

A

A = RNA
B = double stranded DNA
C = RNA
D = RNA
E = RNA

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15
Q

mx of hep C

A

direct-acting antivirals (DAAs) - sofobuvir

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16
Q

what is special about hep D

A

it can only survive in px who also have hep B

increases comps + severity of B

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17
Q

tx of hep D

A

pegylated interferon alpha over at least 48 weeks - not v effective + signif SEs

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18
Q

how is hepE transmitted

A

faecal-oral route

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19
Q

tx for hep E

A

usually v mild illness + no tx req

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20
Q

why might bilirubin be raised

A

obstruction of biliary tree

increased production

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21
Q

what might low albumin mean

A

oedema

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22
Q

what does a raised ALP mean

A

biliary obstruction
(or bone malignancy)

In patients with cholestasis (e.g., due to gallstones), ALT and AST can increase slightly, with a higher rise in ALP (“an obstructive picture”).
If ALT and AST are high compared with the ALP level, this is more indicative of a problem inside the liver with hepatocellular injury (“a hepatitic picture”).

other causes:
ALKPHOS pneumonic
Any fracture
Liver damage (post hepatic)
Kancer
Paget’s disease of bone and Pregnancy
Hyperparathyroidism
Osteomalacia
Surgery

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23
Q

what do raised ALT and AST mean

A

markers of hepatocellular injury

In patients with cholestasis (e.g., due to gallstones), ALT and AST can increase slightly, with a higher rise in ALP (“an obstructive picture”).
If ALT and AST are high compared with the ALP level, this is more indicative of a problem inside the liver with hepatocellular injury (“a hepatitic picture”).

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24
Q

mx of alcoholic hepatitis

A

steroids in acute eps

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25
Q

what are the causes of increased ferritin without iron overload

A

inflammation
alcohol excess
liver disease
CKD
malignancy

can see if iron overload is present using transferrin saturation

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26
Q

what are the causes of increased ferritin w iron overload

A

primary iron overload - hereditary haemochromatosis

secondary iron overload - following repeated transfusions

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27
Q

what is budd-chiari syndrome

A

blockage of the hepatic veins by a blood clot

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28
Q

budd-chiari syndrome presentation

A

The features are classically a triad of:

  • abdominal pain: sudden onset, severe
  • ascites → abdominal distension
  • tender hepatomegaly
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29
Q

initial ix for budd-chiari

A

ultrasound with Doppler flow studies

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30
Q

what is gilbert’s syndrome

A

an inherited (usually autosomal recessive) metabolic disorder

mild and intermittent elevation of unconjugated (indirect) bilirubin levels, due to defective conjugating enzymes in the liver

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31
Q

how to best assess acute liver failure

A

by looking at PROTHROMBIN time and albumin level
(prothrombin has shorter half-life so is best) Therefore INR is best

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32
Q

Type 1 autoimmune hepatitis antibodies and who gets it

A

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Affects both adults and children

Will have raised IgG levels

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33
Q

Type II autoimmune hepatitis antibodies and who gets it

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only

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34
Q

what is spontaneous bacterial peritonitis

A

form of peritonitis seen in patients with ascites secondary to liver cirrhosis

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35
Q

spontaneous bacterial peritonitis presentation

A

ascites
abdominal pain
fever

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36
Q

dx spontaneous bacterial peritonitis

A

paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli

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37
Q

tx spontaneous bacterial peritonitis

A

IV cefotaxime

abx prophylaxis after

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38
Q

what does cholecystokinin (CCK) do

A

Stimulates the gallbladder to contract + release stored bile upon detection of foods in stomach

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39
Q

what does bile contain

A

cholesterol
bile pigments - from broken down hb
phospholipids

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40
Q

causes of pre hepatic jaundice

A

excess haemolysis , increased unconjugated bilirubin

maleria
sickle cell anaemia
haemolytic disease of the newborn
gilberts syndrome

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41
Q

causes of hepatic jaundice

A

viral hepatitis
drugs
alcohol
cirrhosis

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42
Q

causes of post hepatic jaundice

A

obstruction of biliary system

gallstones
pancreatitis

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43
Q

risk factors for gallstones

A

F – Fat
F – Fair
F – Female
F – Forty

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44
Q

biliary colic

A

Severe, colicky epigastric or right upper quadrant pain
Often triggered by meals (particularly high fat meals)
Lasting between 30 minutes and 8 hours
May be associated with nausea and vomiting

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45
Q

first line ix for gallstones

A

transabdo USS

then MRCP to visualise biliary tree in more detail

46
Q

acute cholecystitis

A

gallbladder inflammation due to dysfunc of emptying (blockage of cystic duct)
RUQ pain
fever

47
Q

what sign on examination in cholecystitis

A

+ve murphy’s sign = severe pain on deep inhalation when examiners hand is pressed into RUQ

48
Q

mx acute cholecystitis

A

Nil by mouth
IV fluids
Antibiotics (as per local guidelines)

Endoscopic retrograde cholangio-pancreatography (ERCP) can be used to remove stones trapped in the common bile duct.

Cholecystectomy usually during the acute admission, within 72 hours. May be delayed for 6-8 weeks to allow the inflammation to settle.

49
Q

Gallbladder Empyema

A

infected tissue and pus collecting in the gallbladder

50
Q

Gallbladder Empyema tx

A

IV abx +
Cholecystectomy (to remove the gallbladder) OR
Cholecystostomy (inserting a drain into the gallbladder to allow the infected contents to drain)

51
Q

acute cholangitis

A

inflammation + infect of bile ducts
surgical emergency
due to
- Obstruction in the bile ducts stopping bile flow (i.e. gallstones in the common bile duct)
- Infection introduced during an ERCP procedure

52
Q

charcot’s triad

A

Acute cholangitis presents with this:
Right upper quadrant pain
Fever
Jaundice (raised bilirubin)

53
Q

mx acute cholangitis

A

Nil by mouth
IV fluids
Blood cultures
IV antibiotics (as per local guidelines)
Involvement of seniors and potentially HDU or ICU

ERCP
PTC if not suitable for above or above has failed

cholecystectomy

54
Q

what is PBC

A

autoimmune condition where the immune system attacks the small bile ducts in the liver, resulting in obstructive jaundice and liver disease

55
Q

PBC presentation

A

sx
white woman aged 40-60 years
Fatigue
Pruritus (itching)
Gastrointestinal symptoms and abdominal pain
Jaundice
Pale, greasy stools
Dark urine

signs
Xanthoma and xanthelasma (cholesterol deposits)
Excoriations (scratches on the skin due to itching)
Hepatomegaly
Signs of liver cirrhosis and portal hypertension in end-stage disease (e.g., splenomegaly and ascites)

56
Q

ix PBC

A

raised ALP (first one to be)
Anti-mitochondrial antibodies (AMA) - most spec to PBC
Anti-nuclear antibodies are present in about 35%
Raised immunoglobulin M (IgM) is a non-specific blood result finding
Liver biopsy may be used in diagnosing and staging the disease.

57
Q

mx PBC

A

Ursodeoxycholic acid
Cholestyramine for itching
Immunosupression in some
Liver transplant in end stage

58
Q

what is Primary sclerosing cholangitis (PSC)

A

condition where the intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct the flow of bile out of the liver and into the intestines

59
Q

RFs PSC

A

Male
Aged 30-40
Ulcerative colitis
Family history

60
Q

presentation PSC

A

Abdominal pain in the right upper quadrant
Pruritus (itching)
Fatigue
Jaundice
Hepatomegaly
Splenomegaly

61
Q

ix PSC

A

raised ALP

Autoantibodies not helpful

Magnetic resonance cholangiopancreatography (MRCP) is the diagnostic imaging investigation
= bile duct strictures

Colonoscopy for UC

62
Q

mx PSC

A

ERCP to treat dilate strictures
Liver transplant

Colestyramine for symptoms of pruritus
Replacement of fat-soluble vitamins
Monitoring for complications such as cholangiocarcinoma, cirrhosis and oesophageal varices

63
Q

comps of PSC

A

Cholangiocarcinoma develops in 10-20% of cases

64
Q

what are alpha cells for (in islets of langerhans)

A

glucagon production

65
Q

what are beta cells for (in islets of langerhans)

A

insulin production

66
Q

what are D cells for (in islets of langerhans)

A

somatostatin production

67
Q

what are PP cells for (in islets of langerhans)

A

pancreatic polypeptide production

68
Q

what are enterochrommaffin cells for (in islets of langerhans)

A

serotonin production

69
Q

causes of pancreatitis

A

I – Idiopathic

G – GALLSTONES
E – Ethanol (ALCOHOL consumption)
T – Trauma

S – Steroids
M – Mumps
A – Autoimmune
S – Scorpion sting
H – Hyperlipidaemia
E – ERCP
D – Drugs (azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

70
Q

pancreatitis sx

A

Severe epigastric pain
- radiating through to the back
- relieved by sitting forwards

N&V
Abdominal tenderness
Systemically unwell (e.g., low-grade fever and tachycardia)
Anorexia

71
Q

pancreatitis signs

A

cullens sign = bruising around periumbilical region
grey turners sign = bruising on flanks

72
Q

pancreatitis ix

A

Amylase is raised more than 3 times the upper limit of normal in ACUTE
Lipase is raised
Raised CRP
USS for gallstones
CT abdomen can assess for complications of pancreatitis

73
Q

Initial investigations are required as with any presentation of an acute abdomen

A

FBC (for white cell count)
U&E (for urea)
LFT (for transaminases and albumin)
Calcium
ABG (for PaO2 and blood glucose)

74
Q

glasgow score

A

used to assess the severity of pancreatitis
0 or 1 – mild pancreatitis
2 – moderate pancreatitis
3 or more – severe pancreatitis

75
Q

criteria for glasgow score

A

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

76
Q

mx pancreatitis

A

Moderate or severe cases should be considered for management on the high dependency unit (HDU) or intensive care unit (ICU).

Initial resuscitation (ABCDE approach)
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
Antibiotics if there is evidence of a specific infection (e.g., abscess or infected necrotic area)
Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

77
Q

what is chronic pancreatitis

A

chronic inflam of pancreas
presents with similar symptoms to acute pancreatitis, but generally less intense and longer-lasting

78
Q

most common cause of chronic pancreatitis

A

alcohol

79
Q

comps of chronic pancreatitis

A

Chronic epigastric pain
- boring through back
- worse after fatty food
- better leaning forward

Loss of exocrine function -> lack of pancreatic enzymes (particularly lipase)
- malabsorbtion: weight loss, steatorrhoea, defs, diarrhoea

Loss of endocrine function -> diabetes

Damage and strictures to the duct system -> obstruction in the excretion of pancreatic juice and bile

Formation of pseudocysts or abscesses

80
Q

majority of pancreatic cancers are

A

adenocacinomas
mostly in head of pancreas

dx late + poor prog

81
Q

pancreatic cancer presentation

A

painless obstructive jaundice - tumour at the head of the pancreas compresses the bile ducts, blocking the flow of bile out of the liver

Non-specific upper abdominal or back pain
Unintentional weight loss
Palpable mass in the epigastric region
Change in bowel habit
N&V
New-onset diabetes or worsening of type 2 diabetes

82
Q

when to refer for pancreatic cancer check

A

Over 40 with jaundice – referred on a 2 week wait referral

Over 60 with weight loss plus an additional symptom - referred for a direct access CT abdomen

additional sx:
Diarrhoea
Back pain
Abdominal pain
Nausea
Vomiting
Constipation
New-onset diabetes

83
Q

Trousseau’s sign of malignancy

A

migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma

84
Q

whipple

A

surgical operation to remove a tumour of the head of the pancreas that has not spread.

Involves the removal of the:
Head of the pancreas
Pylorus of the stomach
Duodenum
Gallbladder
Bile duct
Relevant lymph nodes

85
Q

what is cholangiocarcinoma

A

type of cancer that originates in the bile ducts (intra or extra hepatic) - majority are adenocarcinomas

86
Q

where is cholangiocarcinoma most common site

A

the perihilar region, where the right and left hepatic duct have joined to become the common hepatic duct

87
Q

cholangiocarcinoma sx

A

Obstructive jaundice
- Pale stools
- Dark urine
- Generalised itching

Unexplained weight loss
Right upper quadrant pain
Palpable gallbladder (swelling due to an obstruction in the duct distal to the gallbladder)
Hepatomegaly

88
Q

what is courvoisier’s law

A

states that a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is usually cholangiocarcinoma or pancreatic cancer.

89
Q

AST:ALT ratio for alcoholic hepatitis vs fatty liver

A

if the AST:ALT ratio is greater than 2, this suggests alcoholic hepatitis.

if the AST:ALT ratio is less than 1, this suggests non-alcoholic fatty liver disease.

90
Q

what organism typically causes ascending colangitis

A

e coli

91
Q

what is Fitz-Hugh-Curtis syndrome

A

complication of pelvic inflammatory disease in which the liver capsule becomes inflamed causing right upper quadrant pain -> scar tissue formation and peri-hepatic adhesions

usually occurs in women who have either chlamydia or gonorrhoea.

92
Q

RFs cholangiocarcinoma

A

PSC
Liver flukes (a parasitic infection)

93
Q

main type of primary liver cancer

A

hepatocellular carcinoma

94
Q

RFs hepatocellular carcinoma.

A

liver cirrhosis due to:

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Rarer causes (e.g., primary sclerosing cholangitis)

95
Q

what to screen px w liver cirrhosis for

A

offered screening for hepatocellular carcinoma every 6 months with:

Ultrasound
Alpha-fetoprotein

96
Q

presentation hepatocellular carcinoma (HCC

A

asx for long time, presents late so poor prog
Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Upper abdominal mass on palpation

97
Q

tumour marker for hepatocellular carcinoma

A

Alpha-fetoprotein

98
Q

first line imaging for hepatocellular carcinoma

A

Liver ultrasound

99
Q

marker for cholangiocarcinoma

A

CA19-9

100
Q

what is a haemangioma

A

common benign tumours of the liver
no probs

101
Q

what is Focal Nodular Hyperplasia

A

benign liver tumour made of fibrotic tissue
no probs

102
Q

complications of hep B

A

chronic hepatitis (5-10%). ‘Ground-glass’ hepatocytes may be seen on light microscopy
fulminant liver failure (1%)
hepatocellular carcinoma
glomerulonephritis
polyarteritis nodosa
cryoglobulinaemia

103
Q

Post splenectomy blood film features:

A

Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

104
Q

drugs that cause cholestasis

A

fluclox
co-amox
nitro
steroids
sulphonylureas

105
Q

who does type one AI hepatitis usually affect

A

women in their late forties or fifties

106
Q

presentation type one AI hepatitis

A

presents around or after menopause with fatigue and features of liver disease on examination

less acute than type 2.

107
Q

who does type two AI hepatitis usually affect

A

children or young people, more commonly girls

108
Q

presentation type two AI hepatitis

A

acute hepatitis with high transaminases and jaundice

109
Q

tx AI hepatitis

A

high-dose steroids (e.g., prednisolone)

110
Q

common factors indicating severe pancreatitis

A

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

finals (27 decks)

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