9 - Cirrhosis and Portal Hypertension Flashcards

1
Q

What is cirrhosis?

A

End stage of chronic liver disease
Regenerative nodules surrounded by fibrous septa
Disruption of architecture of liver

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2
Q

Common etiologies of Cirrhosis

A

Alcohol
Viral Hepatitis
NAFLD
Genetic/Metabolic Diseases

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3
Q

Pathway to Cirrhosis

A

Injury
Inflammation –> Fibrosis
Resolution OR Cirrhosis —> HCC

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4
Q

Forms of Injury Leading to Cirrhosis

A
Viral Hepatitis
Alcohol
Steatohepatitis
PBC
???????
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5
Q

Cirrhosis Pathogenesis

A

Stellate cells sit in space of disse and store Vita A
During cirrhosis, they transform into myofibroblasts and make and deposit collagen

Stimulated by inflammation, cytokines and toxins

Collagen I & III are deposited in all portions of the lobule

Ultimately architecture and vasculature of hepatocytes are disrupted.

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6
Q

Complications of Cirrhosis

A

Portal Hypertension

Varices
Ascites
Hepatohydrothorax
Spontaneous Bacterial Peritonitis
Hepato-Renal Syndrome
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7
Q

Anatomy - 2 sources of blood flow to liver

A

Hepatic Artery

Portal Vein

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8
Q

Pre-Hepatic Hyptertension

A

Portal Vein Thrombosis

Splenic Vein Thrombosis

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9
Q

Intra-Hepatic Portal Hypertension

A

Pre-Sinusoidal (Schistosomiasis)
Sinusoidal (Cirrhosis)
Post-Sinusoidal (Veno-occlusive disease) - Bush Tea or medications

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10
Q

Post-Hepatic Portal Hypertension

A

Budd - Chiari:

Obstruction of vena cava or hepatic vein

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11
Q

Liver Blood Flow - High Flow

A

Mesenteric Vessels feeding the portal vein

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12
Q

Liver Blood Flow - Low Pressure

A

Sinusoidal network

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13
Q

Effects of Cirrhosis

A

Fixed scarring of liver
Sinusoidal blood vessels - Increased resistance
This causes increased pressure in portal vein
However, portal vein FLOW actually increases as well

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14
Q

Why does portal vein flow increase in response to cirrhosis, even though the pressure is increased due to resistance?

A

Cytokines (like TNF) are released in response to the increased sinusoidal resistance and mildly increased portal vein pressure.
This leads to nitrous oxide release
NO release leads to splanchnic bed dilatation
This leads to increased splanchnic flow

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15
Q

Systemic effects of cirrhosis

A

High cardiac output

Low SVR

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16
Q

Catheter in Hepatic Vein - Deflated Ballooon

Measures what?

A

Free HV Pressure

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17
Q

Catheter in Hepatic Vein - Inflated Ballooon

Measures what?

A

Portal Vein Pressure

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18
Q

Normal PV - HV pressure gradient

A

Less than 7

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19
Q

Significant PV - HV pressure gradient for Portal Hypertension

A

Greater than 10

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20
Q

Cirrhosis - Effects on Blood Flow - Portal Hypertension

A

Fibrosis restricts blood flow, increases portal vein pressure
Collaterals acquire increased pressure, affecting spleen, esophagus, stomach (varices), gastropathy
Ascites due to fluid shift into the peritoneum
Shunting of blood from liver decreases metabolism of “toxins”
Portal bacteremia not cleared induces peritonitis

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21
Q

Physical Exam Findings of Cirrhosis

A

Telangiectasias

Varices

22
Q

Esophageal Varices

A

Sequellae of Portal Hypertension
Risk of bleeding proportional to size and degree of portal hypertension
Graded in increasing size I, II or III
Even with optimal therapy, risk of death from an esophageal bleed is greater than 20%

23
Q

Gastric Varices

A

Also from portal hypertension

Near Gastro-Esophageal Junctures

24
Q

Portal Gastropathy

A

Gastropathy from portal hypertension
Oozing capillaries
Leads to anemia in some cirrhotic patients

25
Q

Esophageal Varices - Emergency

A

Hypotensive

Tachycardic

26
Q

Esophageal Varices - Acute Treatment

A

Stabilize Hemodynamics (Give Volume)
Decrease Portal Pressure (Octreotide Acutely - IV, Somatostatin)
Locally stop bleeding (Banding)
Prophylactic Antibiotics

27
Q

Esophageal Varices - Chronic Treatment

A
Non-Selective Beta Blockers (Propanolol, Nadolol, Carvedilol)
Banding Ablation
TIPS
Surgical Shunt
Transplantation
28
Q

TIPS

A

Transjugular Intrahepatic Porto-Systemic Shunt
From Portal Vein to IVC
A good portion of the portal venous flow bypasses liver entirely!

Complication: 20% develop hepatic encephalopathy

29
Q

Surgical Shunts

A

Don’t get used

30
Q

Ascites DDX

A
Portal Hypertentsion
Peritoneal Inflammation
Ovarian Cancer
Nephrogenic Ascites (Nephrotic Syndrome)
Pancreatic Ascites
Other
31
Q

“Other” Ascites Etiologies

A

Schistosomiasis
Non-Cirrhotic Portal Hypertension
Polycystic Liver Disease

32
Q

Portal Hypertension to Ascites - Pathway

A
Cirrhosis
Splanchnic Arterial Vasodilation
Arterial Underfilling
Systemic Vasoconstriction
Renal Vasoconstriction

Also decreased blood albumin.
This leads to increased hydrostatic pressure and decreased oncotic pressure (all in vessels)
Increases lymph pressure
Lymph and the rest spills out into peritoneum
Initially resorbed by peritoneal surface of diaphragm (communicates with supradiaphragmatic lymphatics
Ascites formation exceeds reabsorption when HVPG > 10 mm HG

33
Q

Ascites DUE TO PORTAL HTN - Characteristics

A

Serum - Ascites Gradient (SAG) > 1.1 g/dL

Transudate (Protein

34
Q

Cirrhotic who develops ovarian cancer

A

SAG is STILL greater than 1.1!!

35
Q

Ascites - Treatment

A

Treat underlying condition
Bedrest
Sodium & Fluid Restriction
Diuretics (Spironolactone, Furosemide, Amiloride, HCTZ, Metolazone, Zaroxyln)
Large-Volume Paracentesis
TIPS
Surgery (Leveen or Denver Shunt, Liver Transplantation)

36
Q

Hepatohydrothorax

A

Almost always on the R side
Ascites in the chest
Maybe because IVC perforates diaphragm?
Ascites leaks through rents (

37
Q

Hepatohydrothorax - Treatment

A

TIPS - for diuretic-refractory cases
Liver Transplantation
AVOID CHEST TUBES. Surgical repair usually not effective.

38
Q

Spontaneous Bacterial Peritonitis

A

Infection of ascitic fluid
Independent of another intra-abdominal source
Monomicrobial
Enteric flora enters portal circulation, not cleared
OR
Translocation of bacteria from the gut

39
Q

Spontaneous Bacterial Peritonitis - WBC

A

Ascites WBC > 500 or 250 with greater than 50% PMNs

40
Q

Spontaneous Bacterial Peritonitis - Risk Factors

A

GI Bleeding/Hypotension
Advanced Liver Disease
Previous History

41
Q

Spontaneous Bacterial Peritonitis - Organisms

A

E. Coli
Klebsiella
Pneumococcus
Enterococcus

42
Q

Spontaneous Bacterial Peritonitis - Treatment

A

Broad Spectrum Antibiotics
Then narrow if culture results are known
Re-tap after 48 hours to confirm response to therapy
Volume expand (albumin)

43
Q

Spontaneous Bacterial Peritonitis - Prevention

A

Early treatment of other infections
Prophylactic Antibiotics to GI bleeders
Oral Quinolones, TMP-Sulfa can prevent recurrence when given chronically

44
Q

Spontaneous Bacterial Peritonitis - Presentation

A

Not typical! Not usually abdominal pain. They come in with something else!

If a cirrhotic is admitted to the hospital, you should perform a paracentesis, or you might miss it!!

45
Q

If you’ve had Spontaneous Bacterial Peritonitis Once

A

You have to be on prophylaxis for the rest of your life!!

46
Q

HepatoRenal Syndrome

A

Late stage cirrhosis

The compensatory local vasodilators protecting your kidneys in the early stages are starting to not work as well!

Decreased vasodilators
Increased vasoconstrictors

47
Q

Early Cirrhosis

A

Decrease in SVR is compensated by Increased HR, CO, Stimulation of RAAS, ADH

48
Q

Late Cirrhosis

A

Splanchnic circulation is resistant to Angiotensin II & ADH
Pressure must be maintained by local vasoconstriction

Leads to HepatoRenal Syndrome

49
Q

HepatoRenal Syndrome

A

Etiology is an exaggeration of mechanisms involved in ascites formation.
Can happen in perfectly healthy kidneys!!

50
Q

HepatoRenal Syndrome - Precipitants

A

GI Bleed
Nephrotoxins (NSAIDS, Aminoglycosides, Sepsis)
Iatrogenic (Diuresis, Paracentesis)

51
Q

HepatoRenal Syndrome - Diagnosis

A

Euvolemic patient
But look like a pre-renal patient
Give fluid, but they STAY “pre-renal” appearing
Urine Output

52
Q

HepatoRenal Syndrome - Treatment

A
TIPS
Glypressin
Terlipressin
Transplantation
Midodrine (increasing vascular resistance)
Octreotide (decreasing portal HTN)