Chronic Liver Failure Flashcards

1
Q

What is cirrhosis?

A

Irreversible diffuse fibrosis of the liver w/ regenerative nodules

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2
Q

What are regenerative nodules?

A

non-neoplastic nodules without sinusoids or portal triads

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3
Q

What are the types of cirrhosis?

A

Macronodular cirrhosis

Micronodular cirrohsis

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4
Q

What is the size of nodule formed in micronodular cirrhosis?

A

nodule ~1 mm diameter; usually alcoholic cirrhosis

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5
Q

What is the size of nodule formed in macronodular cirrhosis?

A

nodules >1 mm diameter and varying sizes

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6
Q

What are the causes of cirrhosis?

A

Alcohol
Post necrotic cirrhosis
Autoimmune cirrhosis
Metabolic disorders

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7
Q

Hepatic failure is a complication of cirrhosis. How does hepatic failure manifest?

A

Coagulation defects
Hypoalbuminemia
Hepatic encephalopathy

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8
Q

Liver failure can manifest as ______________ (bleeding/hypercoagulable/both) disorders

A

both disorders

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9
Q

How does hypercoagulability occurs in liver failure?

A

decreased synthesis of protein C/S, causing the patient to be hypercoagulable

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10
Q

Hepatic encephalopathy is a ___________ (reversible/irreversible) metabolic disorder.

A

reversible

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11
Q

Why does hepatic encephalopathy occur?

A
  1. Increased aromatic amino acids

2. Increased ammonia

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12
Q

How does increase in aromatic aa.s lead to encephalopathy?

A

Increase in the blood of aromatic amino acids that are then converted into false neurotransmitters (e.g., γ-aminobutyric acid)

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13
Q

What are the methods for reducing ammonia in the colon?

A

Decreasing protein intake
Oral neomycin
Lactulose

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14
Q

What are the factors that precipitate encephalopathy?

A

increased protein
metabolic alkalosis
sedatives
portosystemic shunts

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15
Q

What are the clinical findings of CLF?

A

alterations in the mental status.
somnolence and disordered sleep rhythms.
asterixis
coma and death in late stages

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16
Q

How metabolic alkalosis precipitates the encephalopathy?

A

It keeps ammonia in the NH3 state (less H+ ions in alkalosis)

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17
Q

What are the complications of cirrhosis?

A
Hepatic failure
Portal HTN
Ascites
Hepatorenal syndrome
Hyperestrinism
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18
Q

Portal HTN is defined as PV pressure that is greater than ____ (5/10) mm Hg

A

10

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19
Q

Normal PV pressure is

A

5–10 mm Hg

20
Q

What are the complications of Portal HTN?

A

(1) ascites
(2) congestive splenomegaly
(3) esophageal varices
(4) hemorrhoids
(5) periumbilical venous collaterals
(6) encephalopathy

21
Q

What are the posthepatic causes of Portal HTN?

A
  • Vena cava obstruction
  • Hepatic vein thrombosis (Budd-Chiari syndrome)
  • Veno-occlusive disease
  • Heart failure
  • Constrictive pericarditis
22
Q

What are the prehepatic causes of Portal HTN?

A
  • Portal vein thrombosis
  • Increased splenic flow
  • Massive splenomegaly
23
Q

What are the intrahepatic causes of portal HTN?

A
  • Cirrhosis
  • Schistosomiasis
  • Sarcoidosis
  • Primary biliary cirrhosis
  • Massive fatty change
  • Nodular regenerative hyperplasia
24
Q

What is the treatment of portal HTN?

A

Shunts are used in treating portal hypertension to reduce pressure

25
Q

What is the pathogenesis of ascites?

A

hepatic sinusoidal hypertension
percolation of hepatic lymph in peritoneal cavity
Splanchnic vasodilation
Secondary hyperaldosteronism

26
Q

How does hepatic sinusoidal hypertension and percolation of lymph leads to ascites?

A

Fluid from sinusoids leaks into the space of Disse, increasing the lymphatic flow upto 20L per day, above the capacity of thoracic duct. If there is hypoalbuminemia then fluid moves more easily in space of disse

27
Q

What is the normal thoracic duct lymph flow?

A

800-1000 ml/day

28
Q

How does splanchnic vasodilation leads to ascites?

A

Arterial splanchnic vasodilation leads to increase blood flow in splanchnic veins but causes arterial blood pressure to decrease, leading to decreased cardiac output. Low CO triggers RAAS and ADH that causes increased sodium and fluid retention

29
Q

What is the complication of congestive splenomegaly?

A

Congestive splenomegaly causes hypersplenism, producing various cytopenias (anemia, neutropenia, thrombocytopenia

30
Q

Ascites usually become clinically detectable when atleast ______ (200/500) mL have accumulated

A

500 mL

31
Q

The fluid is generally serous, having less than ___ (1/3) gm/dL of protein (largely albumin)

A

3 gm/dL

32
Q

What is the serum to ascites albumin gradient?

A

≥1.1 gm/dL

33
Q

What can we say if we find cells in the fluid (ascites)

A

Neutrophils suggests infection

Blood cells suggests disseminated intra-abdominal cancer

34
Q

Long standing ascites can lead to ____________

A

hydrothorax (often on RIGHT side)

35
Q

What r the clinical findings in ascites?

A
abdominal distention
prominent fluid wave (good test)
bulging flanks
flank dullness to percussion
shifting dullness to percussion
36
Q

There is increased risk for developing spontaneous _________ (sterile/bacterial/viral) peritonitis in ascites.

A

bacterial

37
Q

A difference >1.1 g/dL is ascites of _______ (liver/peritoneal) origin

A

liver

38
Q

a difference <1.1 g/dL is ascites of _________ (liver/peritoneal) origin

A

peritoneal

39
Q

Ascites of liver origin is a_____ (exudate/transudate) hence the expected difference between serum albumin and ascitic albumin is increased

A

transudate

40
Q

Ascitic fluid from peritonitis is an _________ (exudate/transudate) hence, the difference between serum and ascitic fluid is much less

A

exudate

41
Q

What is hepatorenal syndrome?

A

Reversible renal failure without renal parenchymal disease associated w/ liver disease

42
Q

Creatinine clearance is

A

40

43
Q

Serum BUN and creatinine both are __________ (increased/decreased) in hepatorenal syndrome

A

increased

44
Q

How does hyperesterinism occurs in cirrhosis?

A

Diseased liver cannot degrade estrogen and 17-ketosteroids (androstenedione)
Androstenedione is then aromatized (converted by aromatase) into estrogen in adipose cells

45
Q

What are the clinical findings of hyperesterinism in males?

A

gynecomastia
spider telangiectasia
female distribution of hair (concave pubic hair)
impotence and erectile dysfunction

46
Q

Why does impotency and ED occurs in hyperesterinism?

A

High estrogen makes Sex hormone binding globulin SHBG binds FT → ↓FT → ↓libido
(FT = free testosterone)