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FINALS REVISION > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

what is the pathophysiology of pancreatitis

A

autodigestion of pancreatic tissue by pancreatic enzymes leading to necrosis

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2
Q

what are the symptoms of pancreatitis

A

severe epigastric pain radiating to back
vomiting
on examination - tenderness, ileus, low grade fever

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3
Q

what signs of pancreatitis

A

cullen’s (periumbilical) and grey-turner’s (flank) discolouration

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4
Q

what investigations for pancreatitis

A 
serum amylase raised
serum lipase (more specific) - longer half-life
early ultrasound
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5
Q

why is early ultrasound important in acute pancreatitis?

A

determine cause - if gallstones, then surgical removal

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6
Q

what scoring systems for pancreatitis

A

Glasgow, Ranson, APACHE II

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7
Q

GET SMASHED for pancreatitis

A 
gallstones
ethanol
trauma
steroids
mumps
autoimmune
scorpion venom
hypothermia, hypercalcaemia
ERCP
drugs (azathioprine, mesalazine, diuretics)
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8
Q

how is acute pancreatitis treated

A

fluid resus 3-6L?
analgesia - IV opioids
enteral nutrition
surgical - remove gallstones via ERCP/cholecystectomy, debridement of necrotic pancreas

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9
Q

what mode of inheritance in wilsons disease and what gene

A

autosomal recessive

- atp7b copper binding protein

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10
Q

what symptoms in wilsons disease

A

excess copper deposition in liver and brain

  • liver - chronic hepatitis and cirrhosis
  • neuropsychiatric symptoms
  • kayser-fleischer rings - copper deposition in descemet membrane
  • blue nails
  • haemolytic anaemia
  • renal tubular acidosis
  • osteopaenia
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11
Q

what neuro symptoms in wilsons

A

neuro

  • dysarthria
  • dystonia
  • concentration and coordination problems
  • basal ganglia - parkinsonism, asymmetrical motor problems
  • asterixis
  • dementia
  • chorea
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12
Q

what psych symptoms in wilsons

A

psychiatric - depression to psychosis

dementia

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13
Q

what investigations for wilsons

A
  • low serum caeruloplasmin
  • low total serum copper
  • gold standard liver biopsy
  • increased 24hr urinary copper excretion
  • genetic analysis of ATP7B gene
  • slit lamp examination of keyser fleischer rings in eyes
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14
Q

what mgmt of wilsons

A

copper chelation with:
penicillamine
trientene

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15
Q

what is haemochromatosis and what mode of inheritance which genes

A

iron accumulation

autosomal recessive HFE gene on chromosome 6

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16
Q

how does haemochromatosis present

A

later in women due to menstruation

  • fatigue
  • arthritis
  • erectile dysfunction
  • bronze skin
  • liver symptoms - hepatomegaly, cirrhosis, asterixis
  • diabetes mellitus
  • hypogonadotrophic hypogonadism
  • cardiac failure (due to dilated cardiomyopathy)
  • cognitive: memory and mood disturbance
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17
Q

what are the reversible complications of hereditary haemochromatosis

A

skin pigmentation

cardiomyopathy

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18
Q

what are the irreversible complications of hereditary haemochromatosis

A
  • diabetes mellitus
  • cirrhosis
  • hypogonadotropic hypogonadism
  • arthropathy
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19
Q

what is biliary colic

A

gallstones obstructing flow of bile from gallbladder

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20
Q

what are the symptoms of biliary colic?

A
  • RUQ pain worse after eating, particularly fatty meals
  • colicky pain
  • associated with nausea and vomiting
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21
Q

what investigation for biliary colic

A

ultrasound scan

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22
Q

what RFs for biliary colic

A
  • 4 Fs
  • Diabetes
  • Rapid weight loss
  • Crohn’s
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23
Q

what complications of gallstones/biliary colic

A
  • acute cholecystitis
  • acute pancreatitis
  • obstructive jaundice
  • ascending cholangitis
  • gallstone ileus
  • gallbladder cancer
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24
Q

what treatment for biliary colic

A

elective lap cholecystectomy

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25
Q

what is acute cholecystitis

A

inflammation of gallbladder due to bile being unable to drain
usually because of gallstone in cystic duct

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26
Q

what are the symptoms of cholecystitis

A 
RUQ pain
nausea vomiting
fever
tachycardia tachypnoea
Murphy's sign
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27
Q

what sign is associated with acute cholecystitis

A

Murphy’s sign

- inspiratory attest on palpation of RUQ only (not on LUQ)

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28
Q

how are LFTs in cholecystitis

A

typically normal

just the cystic duct that’s blocked

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29
Q

what investigations would you do for cholecystitis

A

USS
FBC - raised WCC
CRP raised
MRCP if unable to visualise with USS

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30
Q

what would you see on USS for cholecystitis

A
  • thickened gallbladder wall
  • sludge/gallstones in gallbladder
  • fluid around the gallbladder
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31
Q

what mgmt of cholecystitis

A
  • admit
  • NBM, IV fluids
  • NG tube if vomiting severe
  • IV Abx according to local guidelines
  • ERCP to remove gallstones
  • cholecystectomy within 1 week of diagnosis
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32
Q

what are complications of acute cholecystitis

A

gallbladder perforation
gallbladder empyema
gangrenous gallbladder
sepsis

33
Q

what treatment of gallbladder empyema

A

IV Abx and either cholecystectomy or cholecystostomy

34
Q

what is mirizzi syndrome

A

stone in cystic duct or in hartmann’s pouch causes compression of hepatic duct/common bile duct leading to obstructive jaundice
- deranged LFTs, jaundice etc.

35
Q

what are the main causes of liver cirrhosis

A
  1. Alcoholic liver disease
  2. NAFLD
  3. Hep B and C
36
Q

what is the pathophys of liver cirrhosis

A

chronic inflammation of liver causes fibrosis and nodule formation in the liver

37
Q

what are the symptoms of liver cirrhosis

A
  1. ascites
  2. telangiectasia
  3. jaundice
  4. hepatic encephalopathy
  5. caput medusae
  6. oesophageal varices
  7. easy bruising
  8. hepatosplenomegaly
  9. asterixis
  10. palmar erythema
38
Q

what blood tests should be ordered for suspected cirrhosis?

A

thrombocytopaenia
Enhanced Liver Fibrosis (ELF), NAFLD blood test
1. LFTs
2. Albumin low, prothrombin time increased
3. U+E for hepatorenal syndrome, hyponatraemia indicates severe fluid retention
4. Viral markers, autoantibodies
5. AFP as a marker for hepatocellular carcinoma

39
Q

what investigations for cirrhosis

A
  1. Bloods
  2. liver ultrasound scan
  3. fibroscan - transient elastography
  4. liver biopsy
  5. endoscopy to diagnose/treat oesophageal varices
40
Q

what changes seen on USS of cirrhosis

A
  1. nodularity to surface of vessels
  2. splenomegaly
  3. corkscrew vessels
  4. ascites
  5. enlarged portal vein with reduced flow
41
Q

what screening investigation for people at risk of cirrhosis every 2 years

A

fibroscan (transient elastography)

42
Q

what investigation in a patient newly diagnosed with cirrhosis

A

endoscopy to check for oesophageal varices

43
Q

how should patients with cirrhosis be screened for HCC every 6 months

A

AFP and uss

44
Q

what are the elements of the childpugh score for cirrhosis

A 
ABCDE
Albumin
Bilirubin
Clotting (INR)
Distended abdomen (ascites)
Encephalopathy
  1. ascites
  2. bilirubin
  3. albumin
  4. INR
  5. hepatic encephalopathy
45
Q

what scoring systems can be used for cirrhosis

A

Child Pugh or MELD (helps guide referral for liver transplant)

46
Q

what is the general management for cirrhosis

A
  1. high protein, low sodium diet
  2. endoscopy every 3 years for varices
  3. MELD score every 6 months
  4. manage complications
  5. consider liver transplant
47
Q

what are the complications of cirrhosis

A
  1. ascites and SBP
  2. portal HTN, varices and variceal bleeding
  3. hepatorenal syndrome
  4. hepatic encephalopathy
  5. hepatocellular carcinoma
  6. malnutrition
48
Q

what is the mgmt of stable varcies

A
  1. propranolol
  2. endoscopic band ligation
  3. injection of sclerosant into varices
  4. TIPS (transjugular intrahepatic portosystemic shunt)
49
Q

what is the mgmt of bleeding varices

A
  1. A-E resuscitation
  2. correct clotting - Vit K, FFP
  3. terlipressin
  4. IV Abx prophylactic
  5. endoscopic variceal band ligation
  6. insertion of sengstaken-blakemore tube
  7. TIPS if all else fails
50
Q

what is a common complication of TIPS

A

exacerbation of hepatic encephalopathy

51
Q

what is the management of ascites in cirrhosis (transudative)

A
  1. spironolactone
  2. low sodium diet
  3. paracentesis
  4. ciprofloxacin as prophylaxis against SBP
  5. TIPS or transplant in refractory ascites
52
Q

how does sbp present

A
  1. fever
  2. abdominal pain
  3. raised WCC and CRP, creatinine, metabolic acidosis
  4. ileus
  5. hypotension
53
Q

what are the most common organisms in sbp

A
  1. e. coli (gram neg rods)
  2. klebsiella
  3. gram +ve cocci (staph or enterococcus)
54
Q

how is sbp diagnosed

A

paracentesis fluid microscopy culture sensitivity prior to administration of Abx

55
Q

how is sbp managed

A

IV cefotaxime

56
Q

what is hepatorenal syndrome

A

splanchnic vasodilation

  1. portal hypertension leads to renal hypotension and hypoperfusion
  2. this leads to RAAS activation and renal vasoconstriction
  3. vasoconstriction and reduced circulating volume = reduced renal perfusion = CKD
57
Q

what are the two types of hepatorenal syndrome

A

Type 1 - very poor prognosis, rapidly progressive

Type 2 - slightly better prognosis, slowly progressive

58
Q

what is the mgmt of hepatorenal syndrome

A

liver transplant

  1. terlipressin
  2. volume expansion with 20% albumin
  3. TIPS
59
Q

what is hepatic encephalopathy

A

build up of toxins such as ammonia in blood

ammonia able to cross BBB

60
Q

how is hepatic encephalopathy treated

A

lactulose
add rifaximin
embolisation of portosystemic shunts/liver transplant

61
Q

what are the 4 grades of hepatic encephalopathy

A
  1. irritability
  2. confusion, inappropriate behaviour
  3. incoherent, restless
  4. coma
62
Q

what can precipitate hepatic encephalopathy

A 
constipation
TIPS
infection (eg. SBP)
electrolyte disturbance
GI bleed
high protein diet
medications (sedatives, diuretics)
hypokalemia
renal failure
63
Q

how does hepatic encephalopathy

A

confusion, altered GCS
asterixis
constructional apraxia inability to draw 5 point star
EEG - triphasic slow waves

64
Q

name 4 causes of acute liver failure

A
  1. alcohol
  2. viral hepatitis (A or B)
  3. paracetamol overdose
  4. acute fatty liver of pregnancy
65
Q

how does acute liver failure present

A
  1. jaundice
  2. coagulopathy (raised PTT)
  3. hypoalbuminaemia
  4. renal dysfunction (hepatorenal syndrome)
  5. hepatic encephalopathy
66
Q

what is the spectrum of alcoholic liver disease

A
  1. alcoholic fatty liver disease
  2. alcoholic hepatitis
  3. cirrhosis
67
Q

how does alcoholic hepatitis present?

A 
abdo pain
fatigue
pruritus, jaundice
myalgia
nausea vomiting
68
Q

what investigations for alcoholic hepatitis

A

LFTs
raised GGT
AST:ALT ratio >2, >3 = acute alcoholic hepatitis

69
Q

what treatment of alcoholic hepatitis

A
  • glucocorticoids

- pentoxyphylline

70
Q

what is used to calculate chance of benefit with glucocorticoids in alcoholic hepatitis

A

maddreys discriminant function - bilirubin and prothrombin time

71
Q

how is ascites classified

A

SAAG >11g/L

SAAG <11g/L

72
Q

give some causes of SAAG >11g/L ascites

A
  • liver problems (cirrhosis, liver mets, acute liver failure)
  • cardiac problems (RHF)
  • Budd Chiari, portal vein thrombosis,
  • myxoedema
73
Q

give some causes of SAAG <11g/L ascites

A
  • hypoalbuminaemia (nephrotic syndrome, kwashiorkor)
  • pancreatitis
  • peritoneal carcinomatosis
74
Q

how is ascites managed

A
  • low dietary sodium
  • spironolactone
  • therapeutic paracentesis (give albumin cover)
  • ciprofloxacin
  • TIPSS
75
Q

what is a complication of large volume paracentesis and how can this be prevented

A

paracentesis-induced circulatory dysfunction

albumin cover

76
Q

what can be seen on blood film in hyposplenism

A

howell-jolly bodies

siderocytes

77
Q

how is hyposplenism managed

A
  1. vaccines - PCV, flu, meningitis, haemophilus influenzae

2. prophylactic antibiotics

78
Q

what are the causes of hyposplenism

A 
splenectomy
coeliac
sickle cell
SLE
graves
amyloid

FINALS REVISION (17 decks)

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