Hepatology: Cirrhosis Flashcards
(41 cards)
Which cells cause collagen formation in liver, when inflammation occurs? [1]
Stellate cells
Describe how acute liver damage presents in the liver [2]
Acute damage:
- Not enough time for fibrotic material to be deposited
- If significantly toxic insult: liver cells collapse and liver shrinks
State two haemodynamic conseqeunces of:
- Acute liver failure [2]
- Chronic liver failure [5]
Acute liver failure:
* Cerebral oedema;
* Renal failure
Chronic liver failure:
Portal HTN:
* i) Ascites
* ii) Splenomegaly
* iii) Varices
* iv) Hepatic encephalopathy
Describe the clinical features hepatocellular dysfunction that occurs in acute and chronic liver failure [4]
- Jaundice
- Increased risk of sepsis
- Encephalopathy
- Coagulopathy
Describe the pathophysiology of portal HTN [3]
- 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
Explain specific change in blood flow from portal hypertension contributes to hepatic encephalopathy [1]
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
What effect does portal HTN have on cell count? [1]
Why? [1]
Causes pancytopenia (red blood cells, white blood cells and platelets decreased) due to splenomegaly
How does portal hypertension lead to ascites? [5]
- 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
What are the two reasons that ammonia builds up in the blood in patients with cirrhosis? [2]
- liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products
- collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly
Which factors make hepatic encephalopathy worse? [5]
Constipation
Dehydration
Electrolyte disturbance
Infection
Gastrointestinal bleeding
High protein diet
Medications (particularly sedative medications)
Describe the colour of urine & stools in ptx with CLD [2]
Light stool
Dark urine
Because bilirubin does NOT enter the bowel
Describe the cholestatic symptoms of chronic liver disease [3]
- Jaundice
- Pruritus: due to buildup of bile salts in your blood.
- Dark urine, pale stools
Describe the systemic symptoms of CLD [3]
- Weight loss
- Muscle loss
- Fatigue
Define what is meant be decompensated cirrhosis [1]
State 4 symptoms of this [5]
an acute deterioration in liver function in a patient with cirrhosis
Characterised by:
- jaundice
- ascites & peripheral oedema
- hepatic encephalopathy
- hepatorenal syndrome
- variceal haemorrhage
- sepsis
What is important to note about CLD symptoms? [1]
Often asymptomatic until liver decompensates
State 5 triggers for decompensated cirrhosis
Explain different signs that occur in compensated cirrhosis? [8]
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)
Which beta blockers would you use as a prophylaxis for variceal bleeding? [1]
Cardeviliol
How do you diagnose ascites? [3]
-
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)
Treatment for ascites? [5]
- Low Na diet
- Spironolactone
- Furosemide
- Paracentesis (removal of ascitic fluid; replacement of albumin is required)
- TIPSS
- Liver transplant
How is spontaneous bacterial peritonitis diagnosed? [2]
Ascitic tap:
- WCC > 250 mm3 (neutrophils 80%)
- Gram -ve often
Tx of SBP? [2]
IV antibiotics: IV cefotaxime
Human albumin solution
The most common organism found on ascitic fluid culture is []
The most common organism found on ascitic fluid culture is E. coli
Define hepatorenal syndrome [1]
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
