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MBBS 3: Internal Medicine > Acute and Chronic Liver Disease > Flashcards

Acute and Chronic Liver Disease Flashcards

1
Q

Functions of the liver?

A
  1. production of bile
    - for fat digestion
  2. reception and metabolization of absorbed products from digestion
  3. detoxification of toxic substances received from digestion
  4. storage and release of carbohydrates
  5. production of proteins - primarily plasma proteins
    e.g. albumin, clotting factors
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2
Q

What is acute liver injury?

A

hepatocellular dysfunction causing coagulopathy (INR >1.5) and encephalopathy in someone without known liver disease

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3
Q

Causes of acute liver injury?

A
  1. Acute viral hepatitis
  2. Drug-induced liver injury: acetaminophen (Panadol), idiosyncratic drug reactions
  3. Alcohol hepatitis
  4. Wilson disease
  5. Autoimmune hepatitis
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4
Q

What is acute liver failure?

A
  1. ALT, AST more than 10 times ULN in person without previous chronic liver disease
    PLUS
  2. Hepatic encephalopathy OR prolonged prothrombin time (raised INR >1.5)
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5
Q

Management of acute liver failure?

A
  1. Address cause if possible
  2. More frequent monitoring of LFTs, urea, electrolytes, glucose, INR in intensive care
  3. Supportive management of volume status (i.e., give fluids gently)
  4. Watch for adrenal insufficiency (similar to septic shock) and consider trial of hydrocortisone
  5. NAC (N-acetylcysteine) if acetaminophen OD
  6. Controversial: antibiotic ppx, fresh frozen plasma, blood and urine cultures
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6
Q

Distinguishing between acute and chronic liver disease?

A
  1. Remember cirrhosis is a manifestation of CLD (not acute)
  2. Look for physical exam findings that there are chronic issues
  3. Imaging can help
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7
Q

What is cirrhosis?

A

Diffuse destruction of hepatic parenchyma which is replaced by scar tissue and regenerating nodules

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8
Q

Describe the liver progression to cirrhosis?

A

healthy liver > fatty liver > liver fibrosis > cirrhosis of liver

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9
Q

Symptoms of cirrhosis?

A
  1. Anorexia
  2. Weight loss
  3. Fatigue
  4. Yellow eyes
  5. Pruritus
  6. GI bleeding
  7. Increasing abdominal girth
  8. Impotence and loss of sexual drive
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10
Q

Chronic liver disease physical findings?

A
  1. palmar erythema
  2. terry nails
  3. Dupuytren contracture
  4. spider angiomata
  5. encephalopathy - confusion
  6. sparse body hair
  7. muscle wasting
  8. hobnail fibrotic liver
  9. dilated vessels
  10. ascites
  11. jaundice - yellow, itchy skin
  12. low blood pressure
  13. in men - gynecomastia and testicular atrophy
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11
Q

Describe the lab findings in cirrhosis?

A
  1. Elevated bilirubin
  2. Moderately elevated liver injury markers (ALT, etc.) –> however, in some cases the ALT can be normal
  3. Increased INR
  4. Reduced albumin
  5. Hyponatremia due to inability to excrete free water (due to antidiuretic hormone secretion)
  6. Thrombocytopenia – due to portal hypertension and congestive splenomegaly
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12
Q

Diagnosis of cirrhosis?

A
  1. Easy when multiple physical examination findings are present
  2. Ascites plus low platelets are helpful findings
  3. Imaging: ultrasound shows small liver with irregular edges, ascites, nodules in the liver tissue
  4. Non-invasive serological tests: AST-platelet ratio (APRI), FIB-4
  5. Non-invasive imaging tests: transient elastography
  6. Liver biopsy: gold standard test, with limitations
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13
Q

Complications of cirrhosis?

A
  1. Hepatocellular carcinoma (liver cancer)
  2. Decompensation: Ascites, Spontaneous bacterial peritonitis, Portosytemic encephalopathy
  3. Hepatorenal syndrome – acute renal failure
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14
Q

Most common causes of cirrhosis?

A
  1. Viral hepatitis C and B
  2. Alcoholic hepatitis
  3. Non-alcoholic steatohepatitis (NASH)
  4. Hemochromatosis
  5. Less common causes: many, including autoimmune hepatitis and Wilson disease
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15
Q

Hepatitis A and E and liver disease?

A

hepatitis A and E cause acute hepatitis but not chronic forms

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16
Q

Hepatitis B?
Diagnosis? Risk factors?

A
  1. diagnosis: Hepatitis B is diagnosed with HBsAg
  2. risk factors: HBV more common in people born prior to vaccine and in people with family history (i.e., mother-to-child transmission)
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17
Q

Hepatitis C?
Diagnosis? Risk factors?

A

diagnosis: diagnosed with 2 stage approach: HCV antibody and then confirmed with HCV RNA (viral load)
risk factors: HCV common in people who inject drugs, have multiple transfusions

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18
Q

What is alcoholic cirrhosis? Causes?

A
  • History of significant alcohol consumption for many years (probably at least 5 years).
  • One definition of significant is >210 grams per week in men and >140 grams per week in women
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19
Q

Alcohol units?

A

units = strength (ABV) x volume (ml)/1000
- One Carlsberg (330 ml) has ~15 grams of alcohol
- Chibuku super (1.25 Liters) has ~40 grams of alcohol

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20
Q

What is found on physical examination and lab findings in alcoholic cirrhosis?

A
  • physical exam is typical for cirrhosis
  • there is no specific test for alcohol cirrhosis: except possibly AST:ALT ratio >2
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21
Q

Nutritional issues in patients with alcoholic cirrhosis?

A
  1. Malnutrition in 20-60% of patients
  2. Heavy alcohol use can reduce dietary calorie intake, esp. when alcohol comprises >50% of calories/day.
  3. Reduced calories impairs nutrient digestion and absorption, decrease protein synthesis, increase catabolism of gut proteins.
  4. Acute alcohol use also causes gut mucosal erosions
  5. Heavy drinkers are thin
  6. Protein deficiencies are common
  7. Vitamin/mineral deficiencies also common: thiamine, folate, iron, and vitamin B6
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22
Q

Treatment of alcoholic cirrhosis?

A
  1. Treatment is usually supportive
  2. Referral to substance use treatment is critical
  3. Avoid other hepatotoxic medications
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23
Q

What is non-alcoholic steatohepatitis (NASH)?

A

Liver fat accumulation (called Non-alcohol Fatty Liver) that leads to inflammation and progressive chronic liver disease (NASH is when inflammation is present)

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24
Q

Epidemiology of NASH?

A

NAFL common now in upper-income countries: up to 40% have liver fat

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25
Q

Risk factors of NASH?

A

central obesity, type 2 DM, dyslipidemia, and metabolic syndrome

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26
Q

Symptoms of NASH?

A

NAFL and NASH are often asymptomatic and discovered incidentally (elevated ALT, fat on imaging) or once cirrhosis has occurred

27
Q

Diagnosis of cirrhosis due to NASH?

A
  1. Imaging (ultrasound or CT) shows hepatic steatosis
  2. Exclusion of significant alcohol use
  3. Absence of coexisting causes of chronic liver disease
  4. Liver biopsy (assess whether its NAFL or NASH)
28
Q

Treatment of NASH?

A
  1. Diet and exercise
  2. Weight loss: target 7-10% of body weight at a rate of 0.5-1 kg per week
  3. Reassess ALT after weight loss to see if it is reducing
  4. If diabetic, improve control, regimen should include metformin
  5. If non-diabetic, high dose vitamin E (800 IU daily) can be tried (research on this excluded diabetics); risk of bleeding due to inhibition of platelet aggregation
  6. Other pharmacotherapies are unproven and there is large research focus on NASH treatments
29
Q

Hemochromatosis?

A

Iron overload: deposits in any organ but liver is first because or portal blood flow
- can be caused by multiple transfusions like in sickle cell disease

30
Q

Describe hereditary hemochromatosis?

A

Genetic disorder (mutation in HFE gene) in which the intestinal mucosa absorbs excess amount of dietary iron which accumulates and deposits in the liver, pancreas, heart, synovium, thyroid, pituitary and adrenal glands.
- Presents at age 40+ in men; post-menopause in women

31
Q

Describe iron overload due to home-brewed beer?

A
  • Preparing beer in iron pots or drums (iron can leach out from steel containers) can create beer that has 46-82 mg/L of iron (versus 0.5 mg/L in commercial beer)
  • This had been described as major cause of liver cirrhosis in Southern Africa; less now with commercial brewing
32
Q

Clinical features of hemochromatosis?

A
  1. Weakness, lethargy, weight loss
  2. Abdominal pain – splenomegaly
  3. Arthralgias, arthritis through iron deposition in the synovium
  4. Loss of libido and impotence – from pituitary hypogonadism
  5. Arrhythmias and heart failure
  6. Increased skin pigmentation – bronze skin
  7. DM
  8. Elevated transaminases
  9. Other endocrine disorders – hypogonadism, hypothyroidism etc
33
Q

Diagnosis of hemochromatosis?

A
  1. Elevated serum transferrin, ferritin and iron
  2. Liver biopsy
  3. HFE gene testing
  4. Imaging – MRI may suggest existence of iron overload
34
Q

Treatment of hemochromatosis?

A
  1. Phlebotomy – usually weekly at first (each 500ml of whole blood has 200 – 250mg of iron) aiming at serum transferrin levels <50% and ferritin <50ng/ml
    - Thereafter phlebotomy can be done every 2 – 4 months
  2. Avoid iron supplements and foods with excess Vit C (vitamin C promotes iron absorption)
  3. If patient is transfusion-dependent (like some with sickle cell disease) chelation should be considered with Desferoxamine / deferasirox / deferiprone
35
Q

Wilson disease (hepatolenticular degeneration)?

A

An autosomal recessive disorder of copper metabolism
The copper transporter ATP7B has reduced function leading to accumulation of copper that affects the liver, brain, eyes, heart, kidneys, and hematopoetic cells
Chronic copper deposits in liver causes cirrhosis
Diagnosis usually made at age 5-35 years old
Affects 1 out of 30,000 individuals

36
Q

Clinical manifestations of Wilsons disease?

A

Liver - Asymptomatic liver disease to fulminant liver cirrhosis
Neuro - Incordination, tremor, dysathria, excessive salivation, & dysphagia
Psych - Mood disturbances, hysteria, schizophrenia, bipolar mood disorder
Eyes - Kaiser-Fleischer rings and sunflower cataracts in the eyes
Heamatology - Coombs negative hemolytic anemia
Kidneys - Fanconni syndrome, renal tubular acidosis, kidney stones, microscopic hematuria & proteinuria
Cardiac - Rarely cardiomyopathy

37
Q

Diagnosis of Wilsons disease?

A

Physical examination
Liver biopsy and
Kaiser-Fleicher rings in the eyes
Blood tests: elevated serum Copper and low serum ceruloplasmin (<20mg/dl; this protein made in liver carries copper around the body)

38
Q

Treatment of Wilsons disease?

A

Treatment is liver transplantation
Reduce dietary copper (esp. organ meats, chocolate, nuts, shellfish)
Copper chelation with D-penicillamine: this agent binds to copper in the body and promotes excretion in the urine
Oral zinc supplementation (blocks copper absorption)

39
Q

Primary biliary cirrhosis?

A

Cause is unknown but may be autoimmune: the T cells attach intralobular bile ducts leading to bile duct destruction.
Associated with other autoimmune conditions – autoimmune thyroiditis, Type 1 DM, IgA deficiency, scleroderma - CREST(calcinosis, Raynaud, esophageal dysmotility and telangiectasia)
Bile duct damage –> cholestatic picture, with eventual cirrhotic liver disease.
Affects primarily women, ages 30-60 years

40
Q

Clinical features of primary biliary cirrhosis?

A

Most are asyptomatic or insidious fatigue, could be discovered incidentally because of elevated LFTs
90% are women age 35 to 60
Pruritus is usually the first symptom – can be localized to the palms and soles or generalized
After many years jaundice and gradual darkening of exposed areas
Steatorrhoea and malabsorption of lipid-soluble vitamins
Xanthelasmas (deposits of lipids) around the eyes, Xanthomas (around tendons and joints)
Signs of liver failure and portal hypertension after 5 to 10 years
Signs of other autoimmune diseases – Type 1 DM, RA, CREST, Vit D deficiency etc

41
Q

Diagnosis of primary biliary cirrhosis?

A

Demographics: Middle aged women
Elevated ALP (2 to 20 times normal)
Positive AMA (antimitochondrial antibodies) in serum is hallmark

42
Q

Other conditions associated primary biliary cirrhosis?

A

Hypercholesterolemia (85%)
Osteopenia (35 to 50%)
Renal Tubular Acidosis (50%)
Gall stones (40%)
Fat soluble vitamin deficiencies
Steatorrhea with malabsorption and weight loss

43
Q

Treatment of primary biliary cirrhosis?

A

No curative medical treatment
Ursodiol (13 to 15mg/kg/day)– can delay progression of disease. It improves biochemical and histological features. The drug replaces hydrophobic bile acids with hydrophilic and relatively non-toxic bile acids
Cholestyramine (12 to 16g/day) to manage the pruritus
Low fat diet to reduce steatorrhoea
Supplement fat soluble vitamins A, D, E and K
Zinc supplementation to manage eye complications
Manage osteoporosis and osteomalacia with Vit D, Calcium and bisphosphonates
Liver transplantation

44
Q

Complications of liver cirrhosis?

A

Esophageal and other varices (major cause of death)
Ascites
Spontaneous bacterial peritonitis (SBP)
Hepatorenal syndrome (HRS)
Portosystemic encephalopathy
Hypersplenism
Hepatocellular Carcinoma

45
Q
A
46
Q

What is ascites? Causes?

A

Accumulation of fluid in the peritoneum (normal = 150ml)
Occurs due to portal hypertension and abnormalities in certain pathways including the renin-angiotensin-aldosterone (RAA) system, leading to increased renal retention of sodium and water, increased splanchnic volume and decreased lymphatic drainage by the peritoneum

47
Q

Clinical features of ascites?

A

Patients may present with increased abdominal girth, umbilical herniation, scrotal edema and peripheral edema

48
Q

Complications of ascites?

A
  1. Spontaneous Bacterial Peritonitis (SBP) – infection of the peritoneal fluid with gut or other bacteria
  2. Anorexia
  3. Esophageal reflux
  4. Dyspnoea from pressure on the diaphragm
  5. Hepatorenal syndrome
49
Q

Recommended puncture sites for ascitic tap?

A
50
Q

Reasons for ascitic tap?

A
51
Q

What is ascitic fluid analysis?

A

Cell count (WBC plus differential)
Culture (aerobic and anerobic in blood culture bottles)
Chemistries – protein and albumin – compare with serum albumin, (in some cases measuring amylase, triglygcerides, glucose, and pH may be useful)
Cytology – look for cancer cells

52
Q

What is SAAG?

A

Measure the SAAG- serum albumin ascites gradient
SAAG >1.1 means there ascites is from portal hypertension with its many differential causes

53
Q

Management of ascites?

A
  1. Reduce alcohol use, restrict dietary sodium and water intake
  2. Diuretics Furosemide and spironolactone (works on the aldosterone part of the RAA system)
    - Ratio of furosemide to spironolactone should be 40:100mg per day
  3. Repeated large volume (>4 liters) paracentesis with albumin replacement
  4. Shunt operations such as TIPS (Transjugular Intrahepatic Portosystemic Shunt) and other portosystemic shunt operations
  5. Liver transplantation
54
Q

Spontaneous bacterial peritonitis?

A

Infection in ascites without a clear cause, translocation of bacteria from the gut
May present with fever or hypothermia, abdominal discomfort and delirium

55
Q

Diagnosis of spontaneous bacterial peritonitis?

A

Ascites have >250 neutrophils on cell count

56
Q

Organisms that cause spontaneous bacterial peritonitis?

A

Common bacteria – E.coli, Klebsiella and less Streptococcus and Staph
When multiple organisms – consider secondary peritonitis eg perforation of gut

57
Q

Treatment of SBP?

A

Broad spectrum antibiotics – 3rd generation cephalosporins.
If more than 1 episode, consider SBP prophylaxis daily oral antibiotics (such as quinolones or trimethoprim-sulfamethoxazole).
1 and 2 year mortality remain high – 70 and 80% respectively

58
Q

Hepatorenal syndrome?

A

Progressive functional renal failure (not affecting the renal structure) accompanying severe decompensated liver disease (usually associated with cirrhosis and tense ascites)
Results from splanchnic vasodilation and vasoconstriction of renal cortical arterioles
Suspect this when a patient with chronic liver disease / cirrhosis develops renal failure over day/weeks without other known cause
Very bad prognosis; typically >90% of patients with HRS will die

59
Q

Portsystemic encephalopathy?

A

Acute mental status with behavioural changes, asterixis (flapping hands), fetor hepaticus (feculent-fruity odor to breath)
Due to accumulation of systemic toxins in the brain and other potential mechanisms (CNS blood flow)
In person with cirrhosis, this can be precipitated by a GI bleed, dehydration, electrolyte abnormalities, or new medication

60
Q

Clinical features of portsystemic encephalopathy?

A

In most cases (90%), there is increased ammonia levels; but levels don’t correlate with degree of PSE.

61
Q

4 stages of PSE?

A
  1. inappropriate behavior, altered sleep pattern, asterixis
  2. confusion, disorientation, asterixis
  3. stupor, somnolent, hyperreflexia, rigidity, clonus
  4. deep coma with no response to stimuli, flaccid limbs
62
Q

Treatment of PSE?

A
  1. lactulose
  2. antibiotics
63
Q

Lactulose as treatment for PSE?

A

helps convert ammonia to ammonium in the gut; helps reduce ammonia levels in blood.
- You titrate the dose until 2-3 bowel movements per day are achieved

64
Q

Antibiotics as treatment of PSE?

A

focus on reducing bacterial levels in the gut
1. Rifaximin is a nonabsorbable antibiotic with broad spectrum
2. Neomycin (oral Aminoglycoside) has been used historically but has side effects (renal and hearing)
3. Metronidazole is good option

MBBS 3: Internal Medicine (72 decks)

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