Hepatology: Cirrhosis Flashcards

1
Q

Which cells cause collagen formation in liver, when inflammation occurs? [1]

A

Stellate cells

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2
Q

Describe how acute liver damage presents in the liver [2]

A

Acute damage:
- Not enough time for fibrotic material to be deposited
- If significantly toxic insult: liver cells collapse and liver shrinks

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3
Q

State two haemodynamic conseqeunces of:

  • Acute liver failure [2]
  • Chronic liver failure [5]
A

Acute liver failure:
* Cerebral oedema;
* Renal failure

Chronic liver failure:
Portal HTN:
* i) Ascites
* ii) Splenomegaly
* iii) Varices
* iv) Hepatic encephalopathy

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4
Q

Describe the clinical features hepatocellular dysfunction that occurs in acute and chronic liver failure [4]

A
  • Jaundice
  • Increased risk of sepsis
  • Encephalopathy
  • Coagulopathy
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5
Q

Describe the pathophysiology of portal HTN [3]

A
  • Chronic inflammation and damage to liver cells causes fibrotic scar tissue to occur in nodules and space of Disse.
  • Hepatic stellate cells become contractile
  • Fibrotic tisue increases resistance in the liver, perturbing blood flow and creating portal hypertension
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6
Q

Explain specific change in blood flow from portal hypertension contributes to hepatic encephalopathy [1]

A

Collaterals between splenic and renal veins: spleno-renal shunts: allow blood from bowel to bypass the liver and leak into systemic circulation, ammonia included (instead of being converted to urea and excreted). Goes to brain

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7
Q

What effect does portal HTN have on cell count? [1]
Why? [1]

A

Causes pancytopenia (red blood cells, white blood cells and platelets decreased) due to splenomegaly

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8
Q

How does portal hypertension lead to ascites? [5]

A
  • Increased pressure in portal system causes fluid to leak out of the capillaries in the liver and into peritoneal cavity. Increase in pressure also causes release of splachnic vasodilators.
  • Drop in circulating volume due to vasodilators on splachnic vessels and fluid forced out causes reduced pressure in kidneys
  • Renin is released
  • Aldosterone is secreted via RAAS
  • Increased aldosterone increase Na+ and therefore fluid reabsorption
  • Cirrhosis is causes low albumin levels, which decreases oncotic pressure
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9
Q

What are the two reasons that ammonia builds up in the blood in patients with cirrhosis? [2]

A
  1. liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products
  2. collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly
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10
Q

Which factors make hepatic encephalopathy worse? [5]

A

Constipation
Dehydration
Electrolyte disturbance
Infection
Gastrointestinal bleeding
High protein diet
Medications (particularly sedative medications)

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11
Q

Describe the colour of urine & stools in ptx with CLD [2]

A

Light stool
Dark urine
Because bilirubin does NOT enter the bowel

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12
Q

Describe the cholestatic symptoms of chronic liver disease [3]

A
  • Jaundice
  • Pruritus: due to buildup of bile salts in your blood.
  • Dark urine, pale stools
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13
Q

Describe the systemic symptoms of CLD [3]

A
  • Weight loss
  • Muscle loss
  • Fatigue
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14
Q

Define what is meant be decompensated cirrhosis [1]
State 4 symptoms of this [5]

A

an acute deterioration in liver function in a patient with cirrhosis

Characterised by:
- jaundice
- ascites & peripheral oedema
- hepatic encephalopathy
- hepatorenal syndrome
- variceal haemorrhage
- sepsis

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15
Q

What is important to note about CLD symptoms? [1]

A

Often asymptomatic until liver decompensates

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16
Q

State 5 triggers for decompensated cirrhosis

A
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17
Q

Explain different signs that occur in compensated cirrhosis? [8]

A

Palmar erythema:
- caused by elevated oestrogen levels

Gynaecomastia and testicular atrophy:
- due to endocrine dysfunction

Jaundice:
- by raised bilirubin

Hepatomegaly (enlargement of the liver)

Bruising:
- due to abnormal clotting

Leukonychia (white fingernails)
- associated with hypoalbuminaemia

Ascites (fluid in the peritoneal cavity)

Excoriations (scratches on the skin due to itching)

Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)

Clubbing & dupuytrens contracture

Xanthomas (raised, waxy-appearing, frequently yellowish-colored skin lesions)

18
Q

Which beta blockers would you use as a prophylaxis for variceal bleeding? [1]

A

Cardeviliol

19
Q

How do you diagnose ascites? [3]

A
  • Clinical exam:
    i) peripheral oedema
  • Ascitic tap: test WCC & cytology for spontaneous bacterial peritonitis or malignancy caused ascites
  • A high gradient (SAAG >11) indicates portal hypertension and suggests a nonperitoneal cause of ascites
  • Liver ultrasound: confirms flow in portal system (normally is anti-grade, but once scarred it reverses into retrograde flow)
20
Q

Treatment for ascites? [5]

A
  • Low Na diet
  • Spironolactone
  • Furosemide
  • Paracentesis (removal of ascitic fluid; replacement of albumin is required)
  • TIPSS
  • Liver transplant
21
Q

How is spontaneous bacterial peritonitis diagnosed? [2]

A

Ascitic tap:
- WCC > 250 mm3 (neutrophils 80%)
- Gram -ve often

22
Q

Tx of SBP? [2]

A

IV antibiotics: IV cefotaxime
Human albumin solution

23
Q

The most common organism found on ascitic fluid culture is []

A

The most common organism found on ascitic fluid culture is E. coli

24
Q

Define hepatorenal syndrome [1]

A

HRS: renal failure in setting of cirrhosis
- Functional circulatory changes in the kidneys that overpower physiologic compensatory mechanisms and lead to reduced glomerular filtration rate

  • Urinary Na excretion less than 10
25
Q

What is the difference between HRS type 1 and type 2? [2]

A

HRS type 1: rapid renal failure after acute trigger (SBP)

HRS type 2: progressive renal failure

26
Q

Tx for HRS? [3]

A
  • Terlipressin (alsos selective vasodilation of renal vessels)
  • Human albumin solution (HAS)
  • Liver transplantation
27
Q

Describe the different grades of hepatic encephalopathy? [4]

A

Grade I: inattention, confusion, altered sleep pattern

Grade II: lethargy, asterixis, slight personality disorder, slurred speech

Grade III: aggression, rigor, clonus, somnolent

Grade IV: coma

28
Q

State 5 triggers of hepatic encephalopathy [6]

A
  • Constipation
  • Sepsis
  • GI Bleeding
  • Drugs: opiods, benzodiazepines, diuretics
  • Dehydration
  • Portal vein thrombosis
29
Q

Which drug classes can induce H.E? [3]

A

opiods, benzodiazepines, diuretics

30
Q

Describe the treatment for hepatic encephalopathy [3]

A

Lactulose: laxative that reduces NH3 production in bowel

Phosphate enema (relieve constipation)

Rifaximin: modulates the gut flora resulting in decreased ammonia production

31
Q

State the cause of jaundice

A
32
Q
A
33
Q
A
34
Q

What is the name for the package of care that should be provided for suspected cirrhotic patients? [1]

A

Cirrhosis Care Bundle: plan for tx

35
Q

Why may patients with cirrhosis be prescribed vitamin K? [1]

A

Patients with cirrhosis may have vitamin K deficiency, due to the malabsorption due to cholestatic liver disease; restores blood clotting ability

36
Q

Abnormal liver function tests without a clear cause require a non-invasive liver screen, which includes testing for which pathologies? [7]

A

Ultrasound liver: diagnose fatty liver

Hepatitis B and C serology

Autoantibodies: autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis

Immunoglobulins: autoimmune hepatitis and primary biliary cirrhosis

Caeruloplasmin: Wilsons disease

Alpha-1 antitrypsin levels (alpha-1 antitrypsin deficiency)

Ferritin and transferrin saturation (hereditary haemochromatosis)

37
Q

Which autoantibodies are relevant to liver disease include [4]

A

Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)

Antimitochondrial antibodies (AMA)

Antibodies to liver kidney microsome type-1 (LKM-1)

38
Q

The [] blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease.

What is key about this? [1]

A

The enhanced liver fibrosis (ELF) blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease.

It is NOT used in patients with other causes of liver disease.

The enhanced liver fibrosis (ELF) test is a blood test that measures three molecules involved in liver matrix metabolism to give a score reflecting the severity of liver fibrosis.

39
Q

What ELF scores indicate advanced fibrosis? [1]

What ELF score indicates that is unlikely advanced fibrosis? [1]

A

10.51 or above – advanced fibrosis

Under 10.51 – unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)

40
Q

What imaging modality is first line for cirrhosis caused by non-alcoholic fatty liver disease? [1]

A

Ultrasound

41
Q

Upon ultrasound imaging of non-alcoholic fatty liver disease, how would fatty changes appear? [1]

A

increased echogenicity.