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Gastroenterology > 09: Cirrhosis & Portal Hypertension > Flashcards

09: Cirrhosis & Portal Hypertension Flashcards

1
Q

What is cirrhosis?

A
  • End-stage chronic liver disease
  • Characterized by regenerative nodules surrounded by fibrous septa, disruption of architecture
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2
Q

What are common etiologies of cirrhosis?

A
  • Alcohol
  • Viral hepatitis
  • Non-alcoholic fatty liver disease
  • Genetic/metabolic

NB: All these etiologies have same cirrhotic presentation.

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3
Q

Trace the pathway to cirrhosis.

A
  1. Injury
  2. Inflammation
  3. Fibrosis
    1. Resolution (if intervene at stage 0-3 fibrosis)
  4. Cirrhosis –> HCC

NB: Average time from injury to cirrhosis = 20yrs.

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4
Q

Describe the pathogenesis of cirrhosis.

A
  • Inflammation, cytokines and/or toxins stimulate stellate (ito) cells
  • Stellate cell transforms into myofibroblast and deposits **type I & II collagen **in all portions of lobule
  • Architecture and vasculature disrupted; diffusion of solutes impaired
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5
Q

What are the complications of cirrhosis?

A
  • Portal hypertension
    • Varices
    • Ascites
    • Hepato-renal syndrome
  • Loss of synthetic function
    • Hepatic encephalopathy
    • Protein loss
      • Coagulopathy
      • Decreased muscle mass
      • Infection (2/2 loss of complement)
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6
Q

List the causes of portal hypertension.

A
  • Pre-hepatic:
    • Portal vein thrombosis
    • Splenic vein thrombosis
  • Intra-hepatic:
    • Pre-sinusoidal: schistosomiasis
    • Sinusoidal: cirrhosis
    • Post-sinusoidal: veno-occlusive disease
  • Post-hepatic:
    • Budd-Chiari syndrome (occlusion of vena cava of hepatic vein)
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7
Q

Describe blood flow through the liver.

A
  • High flow (mesenteric vessels)
  • Low pressure (vast network of sinusoids)
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8
Q

What are the efffects on blood flow of portal hypertension?

A
  • Fibrosis restricts blood flow –> ↑portal vein pressure
  • Collaterals acquire ↑pressure –> varices of spleen, esophagus & stomach; gastropathy (mucosal friability)
  • Ascites due to fluid shift into peritoneum
  • ↓toxin metabolism due to shunting –> peritonitis
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9
Q

What pressure defines portal hypertension?

A
  • Measure the portal vein-hepatic vein pressure gradient
  • **Free HV pressure **= catheter w/ deflated balloon in hepatic vein
  • **Wedged PV pressure **= inflated ballon in hepatic vein
  • PV-HV pressure > 10 mmHg = significant pHTN (nl = <7 mmHg)
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10
Q

Describe the pathophysiology of portal hypertension.

A
  • ↑resistance to inflow/outlow due to fixed scarring of liver
  • ↑flow to portal system
    • ↑splanchnic flow (vasodilation/NO), due to:
      • ↑eNOS activity in splachnic bed
      • shear stress releasing VEGF & TNF –> ↑NO production
      • ↑heme oxygenase activity & CO production
    • ↑cardiac output
      • low SVR
    • ↑blood volume
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11
Q
A
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12
Q

What are esophageal varices and how are they treated?

A
  • Extremely dilated sub-mucosal veins in the lower third of the esophagus
  • Risk of bleeding; death from bleed >20%
  • Acute therapy:
    • Stabilize hemodynamics
    • Decrease portal pressure (**octreotide **or somatostatin)
    • Endoscopy (banding)
    • Transjugular Intrahepatic Porto-Systemic Shunt (TIPS)
      • ​Produces connection between portal and hepatic veins
    • Surgical shunt; limited indications:
      • Cirrhosis of children
      • Budd-Chiari syndrome
      • Non-cirrhotic pHTN
  • Chronic therapy: beta-blockers (propranalol or nadolol) or banding ablation
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13
Q

What are ascites?

A

Accumulation of fluid in the abdomen

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14
Q

What can cause ascites?

A
  • Portal hypertension
    • Cirrhosis
    • Hepatic (or portal vein) occlusion
    • Heart failure
  • Peritoneal inflammation
    • TB peritonitis
    • Carcinomatosis
  • Ovarian cancer
  • Nephrogenic ascites
  • Pancreatic ascites
  • Other (schistosomiasis, non–cirhotic portal HTN, polycystic liver disease)
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15
Q

Trace the pathway of ascites in portal HTN.

A
  1. Cirrhosis –> portal hypertension
  2. Splanchnic arterial vasodilation –> ↓systemic vascular resistance
  3. Arterial underfilling –> sensed “hypovolemic” state
  4. Stimulation of systemic vasoconstrictors
  5. Renal vasoconstriction (to retain Na & H2O)
  6. Early stages of cirrhosis
    1. ↑systemic & local vasodilators
    2. preserved renal perfusion
  7. Late stages of cirrhosis
    1. ↓local vasodilators, ↑local vasoconstrictors
    2. Hepatorenal syndrome
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16
Q

Describe the pathophysiology of ascites.

A
  • ↓albumin due to hepatic synthetic dysfunction –> ↓oncotic pressure –> fluid leaking out of vascular space
  • ↑sinusoidal hydrostatic pressure –> ↑fluid movement from sinusoids to space of Disse –> ↑hepatic, thoracic duct lymph flow
    • ↑lymph production exceeds capacity of lymphatics to return it to circulation –> XS lymph spills into peritoneal cavity
    • initially reabsorbed by peritoneal surface of diaphragm (communicates with supradiaphragmatic lymphatics)
    • when ascites formation > reabsorption, clinically evident ascites occurs
  • Hypovolemia activates RAAS pathway & sympathetic nerve activity –> renal Na & H2O retention
  • ADH secretion increases w/ more profound vasodilation –> water retention & hyponatremia
17
Q

How is ascites due to portal hypertension diagnosed?

A
  • Serum-ascites albumin gradient (SAG) > 1.1 g/dL
  • WBC < 50 cc/mm; mostly mononuclear
  • Normal ascitic fluid amylase
18
Q

What is the treatment for ascites?

A
  • Bedrest
    • Na+ restriction (1.5-2 g/day)
    • Fluid restriction (1.5L if Na+ <120)
  • Diuretics (maximum dose)
    • **Spironolactone **(aldosterone inhibitor)
    • **Furosemide **(loop diuretic)
    • Amiloride, HCTZ, Metolazone, Zaroxyln
  • Large-volume paracentesis
  • TIPS (for refractory ascites)
  • Surgery (Leveen/Denver shunt; transplantation)
19
Q

What is a hepatic hydrothorax and how is it treated?

A
  • Ascites leak through rents (<1cm holes in diaphragm)
  • Dx by fluid characterstics (similar to ascites)
  • TIPS is treatment of choice if refractory
  • Liver transplant may be necessary
  • Avoid chest tubes; surgical repair not usually effective
20
Q

What is spontaneous bacterial peritonitis?

A

Infection of ascitic fluid independent of another intra-abdominal source (e.g., perforation); monomicrobial; source: a) enteric flora enters portal circulation, not cleared or b) translocation of bacteria from gut

21
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Ascites WBC > 500 or 250 w/ greater than 50% PMNs

22
Q

What risks contribute to spontaneous bacterial peritonitis?

A
  • GI bleeding/hypotension
  • Advanced liver disease
  • Previous history of SBP
23
Q

How is spontaneous bacterial peritonitis prevented?

A
  • Early treatment of other infections
  • Prophylactic antibiotics to GI bleeders
  • Oral quinolones, bactrim can prevent recurrence when given chronically
24
Q

What are the most common organisms in spontaneous bacterial peritonitis, and how is it treated?

A
  • E. coli, Klebsiella, Pneumococcus, Enterococcus
  • Broad spectrum abx and then narrow spectrum abx if culture results known
  • Re-tap after 48 hours to confirm therapy response
  • Volume expand with albumin (reduce hepato-renal syndrome)

NB: SBP does not have same presentation as acute peritonitis (no abdominal pain or fever; pts often p/w hepatic encephalopathy and/or fatigue).

25
Q

What are the differences between early and late stage cirrhosis?

A
  • Early: ↓SVR compensated by ↑HR, CO; stimulation of RA and SNS, ADH
  • Late: splanchnic circulation resistant to AngII, vasopressin; pressure maintained by local vasoconstriction –> HRS (↓kidney perfusion, ↑creatinine levels)
26
Q

What is the etiology of hepato-renal syndrome?

A

Exaggeration of mechanisms involved in ascites formation; precipitated by GI bleed, nephrotoxins (NSAIDs, aminoglycosides, sepsis), or iatrogenic (diuresis, paracentesis).

27
Q

How is hepato-renal syndrome diagnosed?

A
  • Euvolemic patient
  • Urine output < 800 cc/day (nl = 800-2K cc/day)
  • Urine sodium < 10 mEq/L (nl > 20 mEq/L)
  • Clean urine sediment
28
Q

What is the treatment for hepato-renal syndrome?

A
  • TIPS
  • Glypressin/Terlipressin
  • Transplantation
  • Midodrine 5-15mg PO TID
  • Octreotide 100-200mcg SQ TID

Gastroenterology (10 decks)

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