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Stage 4 > Liver disease > Flashcards

Liver disease Flashcards

1
Q

Discriminating features in liver disease:

  1. Abdo pain, fever, rigors
  2. Pruritis
  3. Arthritis
  4. Pigmentation
  5. Bloody diarrhoea
  6. Weight loss
  7. SOB/emphysema
  8. Dry eyes/mouth
A
  1. Biliary colic, cholangitis
  2. Cholestatic disease
  3. Haemochromatosis, autoimmune hepatitis, hep B
  4. PBC, haemochromatosis
  5. PSC (IBD patients)
  6. Malignancy/end stage cirrhosis
  7. Alpha1anti-trypsin deficiency
  8. PBC
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2
Q

Clotting studies and proteins

  1. PT/INR
  2. Albumin
A
  1. Increased PT time as liver makes factors 2 7 9 10 aka vitamin K factors
  2. Decreased albumin indicates severe
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3
Q

Autoantibodies and immunoglobulins

  1. Autoimmune hepatitis
  2. PBC (mitochondBILE)
  3. PSC
  4. AAAlcoholic liver disease or NAFLD
A
  1. ANA + anti-smooth muscle + IgG (smooth G)
  2. Anti mitochondrial AMA + IGM (MMMitochondBILE)
  3. pANCA
  4. IgA
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4
Q

Metabolic syndrome criteria

A

Any 3 of:

  1. Waist circumference
  2. Hypertriglyceridemia / active Rx for dyslipidemia
  3. Low HDL cholesterol
  4. HTN
  5. Fasting plasma glucose >5.6 / active Rx for T2DM
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5
Q

Tumour markers

  1. a-fetoprotein
  2. CA19-9
A
  1. HCC

2. Cholangiocarcinoma

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6
Q

Wilsons diagnosis

A

↓caeruloplasmin + 24 hr urine Cu, slit lamp eye exam- K-F rings

Hepatolenticular degeneration = small liver

Flapping

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7
Q

ERCP uses

A

Only used therapeutically now as MRCP is used to diagnose - removes stones. 2-4% get pancreatitis

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8
Q

Liver biopsy indications

A

NOT for acute - just chronic

Chronic liver disease - identify cause, severity and stage (ie cirrhosis due to ALD - fat deposits and inflam cells)

Focal lesions are guided

Post transplant to monitor rejection

Risk of significant bleeding

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9
Q

Ix to detect liver stiffness/fibrosis

A

Transient elastogrphy / fibroscan

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10
Q

Liver transplant indications

A

Treatment resistant ascites, encephalopathy

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11
Q

In a cholestasis picture

  1. Anaemia
  2. WCC
  3. Reticulocytes
A
  1. Malignancy
  2. Ascending cholangitis
  3. Prehepatic jaundice/hemolysis
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12
Q

What signs differentiate cholecystitis from ascending cholangitis

A

Rigors, septic shock, hypotension and confusion

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13
Q

Bleeding prophylaxis after variceal bleed

A

Propanolol

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14
Q

How to determine if alcohol is playing a role in liver disease

A

Measure MCV

Talk to friends/relatives

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15
Q

Liver cirrhosis pathophysiology

A

Hepatic stellate cells (normally store vit D) in space of Disse (between hepatocytes and endothelium) become activated, form myofibroblast complex and deposit collagen > fibrous scar tissue/ECM

Liver becomes small nobly mass with irregular edges

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16
Q

Compensated vs decompensated liver disease

A

Compensated: 50% 10y survival
Spider naevie, palmar erythema, gynacomast, xanthelasma, bruising, oedema, hepatosplenomeg, clubbing, Dupytren’s contracture

Decompensated: 50% 18m survival
Jaundice, ascites (shifting dullness), encephalopathy, reduced GCS/concentration, asterixis (flapping tremor), oesoph varices, Spontaneous bacterial peritonitis

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17
Q

Collaterals due to portal HTN mean that blood from GI bypasses liver =

A

Contain toxins = encephalopathy

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18
Q

Why low platelets in liver disease

A

Portal HTN > splenomegaly

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19
Q

Case mentioned: Increased echogenicity, coarse nodular parenchyma and an irregular liver edge on USS

what is Dx and what may be seen on CXR

A

Alcoholic liver disease

Pleural effusion + elevated diaphragm

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20
Q

Cirrhosis gold standard Dx

A

Biopsy

Unless clear signs of cirrhosis ie ascites, coagulopathy, shrunken/nodular US

(large liver in early LD, small in late cirrhosis

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21
Q

Complication of cirrhosis
Varices
Pathology
Acute bleed treatment + prophylaxis

A

Portal hypertension: Backflow pressure from liver shunts blood up portal veins to systemic veins (wrong way) causing buldging/collaterals and varices

Acute variceal bleed = resus, ABx, terlipressin (vasopressin/vasoconstrictor), endoscopy - banding/adrenaline

consider TIPS but monitor for ammonia encephalopathy + HF

1’ prophylaxis - propanolol

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22
Q

Complication of cirrhosis
Ascites
2 theories
Management

A

Water and salt IN > out
Underfill theory: Hepatic vein (ascending from liver) outflow obstruction > transudate ie pressure squeezes fluid out of circulation

Overflow theory: Liver fails to filter out metabolites > vasodilation in systemic circulation > reduced GFR > RAS = retain NaCl + H2O

(ALWAYS TAP ASCITES)

Exclude SBP (WCC>250)
Restrict salt + water intake
Diuretics - furesomide/spironolactone
Therpeutic paracentesis /TIPS if diuretics arent working (replace fluid you remove with IV human albumin solution HAS else hepatorenal syndrome may occur)

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23
Q

Analysis of ascitic fluid

A

Cytology - only positive in 7%

Serum:Ascites albumin gradient:
High gradient means that there is portal hypertension which forces water into the peritoneal cavity but keeps albumin in the vasculature. Seen in Cirrhosis, alcoholic hep, HF, Budd-chiari syndrome, nephrotic syndrome (AKA transudate)

Low gradient indicates that there is lots of albumin in the peritoneal area and thus a peritoneal cause as opposed to due to portal hypertension/liver, such as TB, pancreatitis, infections, serositis, peritoneal cancer

WCC >250 = SBP

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24
Q

Spontaneous bacterial peritonitis
Sx
Dx
Mx

A

May be asymptomatic
Fever, abdo pain, encephalopathy, abdo pain, diarrhea/ileus, shock/hypothermia

WCC >250 = diagnostic

Mx: Tazocin + lifelong prophylaxis with cipro

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25
Q

Hepatorenal syndrome
Def
Types
Mx

A

Development of renal failure in a patient with severe liver disease (acute or chronic) in absence of any identifiable cause of renal pathology ie kidneys work fine

May be precipitated by SBP - which causes vasodilation and reduced CO which in turn activates vasoconstrictors locally = Increased portal HTN + kidney (HRS), brain (enceph), adrenal glands (insufficiency)

Type1: ACUTE
Type2: CHRONIC - due to refractory ascites

LIVER TRANSPLANT +
volume expansion (Albumin HAS)
Splanchnic vasoconstriction (Terlipressin)
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26
Q

30% with bloody ascites have

A

HCC

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27
Q

Hepatic encephalopathy
Grading
Pathophysiology
Mx

A

1 (Reduced attention, lack of awareness) - 4 (coma)

Precipitated by: Infection, acidosis, low sodium, constipation - ultimately caused by ammonia, benzos, hyponatremia and cytokines which cause the brain astrocytes to swell and cause oxidative stress

Mx: Treat precipitating factor
Regular lactulose +/- phosphate enema
Rifaximin- Ab, thiamine/ vit B

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28
Q

Risk management during cirrhosis

  1. HCC
  2. Variceal haemorrhage
  3. Viral superinfection
  4. Osteoporosis
  5. Ascites & SBP
  6. vitamin deficiencies
A
  1. Screening ultrasound and AFP every 6 months
  2. OGD at diagnosis of cirrhosis and every 2 years - propanolol for bleeding prevention
  3. Immunise against Hep A and Hep B
  4. Screen and treat
  5. Monitor regularly
  6. vit B and thiamine
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29
Q

common causes of HCC

A
  1. Metastasis
  2. Hep C
  3. Hep B
  4. ↑ metabolic syndrome: alcohol & obesity > ↑NAFLD > HCC
  5. Haemochromatosis, PBC, alpha1a deficiency
30
Q

Cancerous liver appearance

A

Small, craggy, scarred (back pressure of blood)

31
Q

HCC prevention
1’
2’
screening

A

1Primary: Hep B immunisation - high risk areas in Asia v good results + avoid carcinogens ie alcohol

Secondary (already have LD, avoid progression to HCC): Education and risk avoidance on Hep B Hep C, weight, smoking, alcohol
Rx for underlying conditions ie venesection in iron overload + diet and exercise for NAFLD

Screening: At risk patients get AFP + ultrasound = 6 monthly

32
Q

HCC screening strategy

A

Usual AFP and US every 6 months to cirrhotic patients

If liver nodule detected then CT/MRI image + biopsy if inconclusive

If increased AFP then spiral CT

33
Q 
HCC
Presentation
Ix
Dx
Staging
Mx
A

Itching, splenomegaly, bleeding varices, WEIGHT LOSS, jaundice, confusion/encephalopathy, RUQ pain, abdo distension, palmar erythema, spider naevi, gyncomastia, dup contracture
Decompensated = ascites, asterixis , encephalopathy

Ix: LFTs, clotting, albumin, AFP + CXR (lung/mets)
Lesion <1cm = repeat US at 4m
Lesion >1cm = CT contrast (HCC will have arterial supply that shows up WHITE) +/- MRI contrast

If NO HCC hallmarks (AFP) then biopsy but beware spreading Ca cells

Dx: >2cm mass on US + High AFP = Diagnostic (further Ix only to stage) - if diagnosis in doubt FNA/biopsy but beware ‘seeding’

Mx: Treat complications first!

  1. Single <2cm nodule with no cirrhosis etc = tumour resection
  2. Single <5cm nodule / 3 <3cm nodules + NO extrahepatic disease + NO macroscopic vessel invasion (MRI- espec portal & hepatic veins) aka MILANCRITERIA = Transplant
  3. If Single <5cm nodule / 3 <3cm nodules but there is extrahepatic disease = Radiofrequency ablation
  4. If multinodular = • Chemoembolisation/TACE - Hepatic angiography- cut off/ block arterial supply to tumour ie with gelatin then deliver chemotx directly to tumour
  5. If advanced stage with portal invasion = sorafenib - first line in advanced non-operable HCC

No transplant in patients with BMI over 40

34
Q

Acute liver failure features encephalopathy due to build up of toxic metabolites in brain > cerebral oedema = asterixis + bleeding/coagulopathy = Increased PT + Ascites due to fluid redistribution and decreased albumin + jaundice but what else is essential for Dx

A

In absence of pre-existing liver disease

35
Q

formal diagnosis of acute liver failure

A
  1. an increase in PT by 4-6seconds (INR >1.5)
  2. development of hepatic encephalopathy
  3. No pre-existing cirrhosis + illness of less than 6months duration
36
Q

Paracetamol poisoning pathophysiology

A

NAPQI is metabolised by glutathione but eventually that runs out and so metabolite build up occurs - treat with NAC N-acetylcysteine

37
Q

Test paracetamol on admission and then if patient ‘normal’ at 4hours if level below 200 then no antidote! What would make patient high risk and thus lower threshold to 150 (intermediate risk) or high (100)

A 
Malnutrition
Enzyme induction
alcohol
Anti-epileptic drugs
Rifampicin
38
Q

Acute liver failure classification

A

From onset of jaundice until encephalopathy
0-7d = Hyperacute - best prognosis with least raised bilirubin + cerebral oedema

9-28d = Acute - poor prognosis + cerebral oedema

1-3m = Subacute - poor prognosis + PT normal + cerebral oedema rare

39
Q
  1. Ecchymosis
  2. Leukonychia
  3. Koilonychia
  4. Onycholysis
  5. Pitting
A
  1. Bruise
  2. Leukonychia - white bands - hypoalbuminemia
  3. Koilonychia - spoon shaped. Iron def
  4. Onycholysis - nail thickened and separated. Psoriasis
  5. Pitting - small holes. Psoriasis
40
Q

Is the patient a middle aged woman? Are they itching? Are they tired….?

Is the patient a man with ulcerative colitis?

Is the patient in pain? Are they jaundiced? Are they vomiting?

A

PBC
PSC
Gallstones

41
Q

You know its CONJUGATED bilirubin rise becaus eof

A

Dark urine and pale stools

42
Q

Acute hepatic picture

Chronic Hepatic Picture

Cholestatic picture

Alcoholic

A

Acute hepatitic picture – ALT in 1000’s, ALP mildly raised

Chronic Hepatitic Picture – ALT in 100’s, Low albumin

Cholestatic picture – ALP up to 1000, High bilirubin, High GGT

Alcoholic - High GGT

43
Q

How does hepatic encephalopathy cause bradycardia

A

Cerebral oedema > Increased ICP = Papilloedema + HTN + bradycardia

44
Q

Avoid biopsy if possible in what two conditions

A

Cancer + compromised coagulopathy

45
Q

Paracetamol OD resus

A

5% dextrose NOT FFP (UNPREDICTABLE) or IV vit K - DONT correct PT! (unless overt bleeding)

46
Q

Check every acute liver failure patients paracetamol levels!

What may predict which patients wil die from paracetamol OD?

A

Lactate

47
Q

Paracetamol transplant criteria

A

pH <7.25
Lactate >3.5
ALL of the following OR any 2 + life-threatening deterioration
1. Grade III-IV encephalopathy
2. Creatinine >300
3. Prothrombin time >100seconds / INR >6.5

48
Q

Non-paracetamol transplant criteria

A 
PT >100
INR >6.5
Wilsons or Budd-Chiari = Any coagulopathy + encephalopathy
ANY 3 from following 5:
1. Unfavourable aetiology (not hepatitis A or B)
2. Age > 40
3. Jaundice to encephalopathy > 7 days
4. PT > 50 (INR > 3.5)
5. Bilirubin > 300
49
Q

Hep E IgM positive, which test would you perform to confirm?

A

RNA

50
Q

ALT is more specific for?

AST is more specific for?

A

ALT more specific for viral/acute

AST more specific for alcohol/cirrhosis

51
Q

Before a liver biopsy what drug should be stoipped?

A

Anti-coagulants

52
Q

Are there any medications that need to be suspended for patients who are having a CT scan?

A

Metformin (risk of developing lactic acidosis), stop any reno-toxic drugs

53
Q

Where does AI hep attack, PBC and PSC?

A

AI hep = hepatocytes
PBC = intra hepatic bile ducts
PSC = intra and extra hepatic ducts

54
Q 
PBC
Memory
Sx
Ix
Mx
A

Middle aged Mum, AMA, IgM (has BooBs = pBc)

Sx: Fatigue, itch, dry eyes and dry mouth

Ix: Exclude drugs, viral and gallstones via USS
ALP, AMA, IgM
Biopsy for disease staging - florid duct lesions intrahepatically

Mx: Ursodeoxycholic acid, no response = transplant
Itch = cholestyramine
If cirrhotic = HCC screen (AFP+US), varices screen

55
Q 
Autoimmune Hepatitis 
Memory
Sx
Ix - BIOPSY TO CONFIRM
Mx
A

Smooth OG AUTOmatic gun (ASMA + limp + IgG)

Sx: Any age/sex, FH of autoimmune. Often asymptomatic but nausea/anorexia and JOINT PAIN

Ix: ASMA + IgG + ALT
Confirm DIAGNOSIS with BIOPSY + assess stage for Rx
Periportal infiltrate!
(+ ANA)

Mx: Immunosuppression (steroids, azathioprine) aiming for normal ALT and IgG
2. Transplant

56
Q 
Primary Sclerosing Cholangitis
Memory
Sx
Ix
Mx
A

mANCAncer (man = UC + cancer risk)

Sx: UC symptoms + male. Fatigue, itch, RUQ pain, weight loss

Ix: pANCA + ALP
USS = bile duct dilatation
CT not used
MRCP: Intra + extrahepatic duct involvement. 'Beading' of biliary tree (stricture/dilatation)
Biopsy: May see 'onion skin' fibrosis
ERCP if MRCP inconclusive

Mx: Look for IBD. Screen for cholangiocarcinoma (Ca19-9) + colorectal ca (colonoscopy)
No specific Rx, treat itch with cholestyramine + strictures with ERCP

57
Q 
AMA
ANA/ASMA
ANCA
IgA
IgM
IgG
A 
Primary Biliary Cirrhosis
Autoimmune Hepatitis
PSC
Alcohol, NAFLD
Primary Biliary Cirrhosis
Autoimmune Hepatitis
58
Q

IgG4 + steroid responsive + pancreas involvement

Biochemical and cholangiogram similar to PSC

Often extra-hepatic ducts

A

IgG4 disease

59
Q

Autoimmune hepatitis type 2 is more common in ? and has which autoantibodies?

A

Women

LKM-1 LC-1 Anti-Liver-Kidney-Microsomal-1

60
Q

Biopsy use in:
PBC
PSC
AI hep

A
  1. Biopsy may not be needed - intrahepatic medium-sized duct lesions
  2. MRCP for large duct - beading, biopsy for small - onion skin fibrosis
  3. Gold standard - periportal infiltrate
61
Q 
Viral hepatitis incubation periods
HAV
HBV
HCV
HEV
A 
HAV = short <30
HAB = long >50
HAC = any
HEV = mean 40
62
Q 
Hep A
Route
Incubation
Ix
Risk
A

Faecal-oral, associated with poor sanitation and overcrowding
Very short incubation
IgG +ve once you get it wont get it again
NO risk of chronic liver disease but sometimes fulminant

63
Q 
Hep E
Route
Incubation
Ix
Risk
A

Faecal-oral, waterborne associated with pgs, rodents, monkeys
40days
HEV in blood and stool - IgG remains high
High mortality in pregnant

64
Q 
Hep B
Route
Incubation
Mx
Risk
A

Blood borne, mother-to-baby, contaminated needles V infectious
Longest incubation period >50
PEG-interferon a, or Tenofovir / Entecavir

5-10% = chronic > 15-40% = complication relating to cirrhosis. Can > HCC (HAV accounts for 50% of HCC)

6monthly surveillance for complics of cirrhosis- oesoph varices, HCC ie LFTs, α fetoprotein, abdo USS

65
Q

Hep B serology

  1. Infected
  2. After 1month of infection
  3. Body fighting infection
  4. Long term immunity/past infection
  5. What alone implies vaccination
  6. Chronic infection
A

S.E.C

  1. HBsAg - Surface
  2. HBeAg - Enveloped
  3. IgM to HBcAg - Core
  4. IgG to HBcAg + anti-HBs/c
  5. Anti-HBs
  6. HBsAg persists >6m +/- HBeAg + IgG
66
Q 
Hep C
Route
Incubation
Ix
Mx
Risk
A

Faecal-oral route, IVDU - SCREEN at risk groups
Variable incubation but diagnosis often spotted much later after dormant period
HCV antibodies mean exposure to HCV but don’t distinguish between past/current infection > do RNA PCR
Biopsy or fibroscan to assess chronic/cirrhosis state
PEG-IFN + Ribavirin + Antivirals

20% spontaneous resolution = HCV RNA -ve after 6months
80% chronic > 20% cirrhosis > 1.3rd HCC
Alcohol progresses disease

67
Q

At risk groups for Hep B and Hep C screening

A

Any hx of injecting or intranasal drug use
Blood transfusion or solid organ transplant before 1991
Long term dialysis
Any elevation of ALT
HIV or HBV infection
Born in a highly endemic country

68
Q

Alcoholic liver disease LFTs

A

AST > ALT (severe/alcohol)

Raised ferritin + GGT + MCV

69
Q

Most likely histology in NAFLD

A

Hepatocyte ballooning

70
Q

What is the most likely histology in autoimmune hepatitis

A

Portal tract infiltration with plasma cells

Stage 4 (12 decks)

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