9 - Cirrhosis and Portal Hypertension Flashcards

(52 cards)

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
Esophageal Varices - Emergency
Hypotensive | Tachycardic
26
Esophageal Varices - Acute Treatment
Stabilize Hemodynamics (Give Volume) Decrease Portal Pressure (Octreotide Acutely - IV, Somatostatin) Locally stop bleeding (Banding) Prophylactic Antibiotics
27
Esophageal Varices - Chronic Treatment
``` Non-Selective Beta Blockers (Propanolol, Nadolol, Carvedilol) Banding Ablation TIPS Surgical Shunt Transplantation ```
28
TIPS
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
Surgical Shunts
Don't get used
30
Ascites DDX
``` Portal Hypertentsion Peritoneal Inflammation Ovarian Cancer Nephrogenic Ascites (Nephrotic Syndrome) Pancreatic Ascites Other ```
31
"Other" Ascites Etiologies
Schistosomiasis Non-Cirrhotic Portal Hypertension Polycystic Liver Disease
32
Portal Hypertension to Ascites - Pathway
``` 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
Ascites DUE TO PORTAL HTN - Characteristics
Serum - Ascites Gradient (SAG) > 1.1 g/dL | Transudate (Protein
34
Cirrhotic who develops ovarian cancer
SAG is STILL greater than 1.1!!
35
Ascites - Treatment
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
Hepatohydrothorax
Almost always on the R side Ascites in the chest Maybe because IVC perforates diaphragm? Ascites leaks through rents (
37
Hepatohydrothorax - Treatment
TIPS - for diuretic-refractory cases Liver Transplantation AVOID CHEST TUBES. Surgical repair usually not effective.
38
Spontaneous Bacterial Peritonitis
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
Spontaneous Bacterial Peritonitis - WBC
Ascites WBC > 500 or 250 with greater than 50% PMNs
40
Spontaneous Bacterial Peritonitis - Risk Factors
GI Bleeding/Hypotension Advanced Liver Disease Previous History
41
Spontaneous Bacterial Peritonitis - Organisms
E. Coli Klebsiella Pneumococcus Enterococcus
42
Spontaneous Bacterial Peritonitis - Treatment
Broad Spectrum Antibiotics Then narrow if culture results are known Re-tap after 48 hours to confirm response to therapy Volume expand (albumin)
43
Spontaneous Bacterial Peritonitis - Prevention
Early treatment of other infections Prophylactic Antibiotics to GI bleeders Oral Quinolones, TMP-Sulfa can prevent recurrence when given chronically
44
Spontaneous Bacterial Peritonitis - Presentation
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
If you've had Spontaneous Bacterial Peritonitis Once
You have to be on prophylaxis for the rest of your life!!
46
HepatoRenal Syndrome
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
Early Cirrhosis
Decrease in SVR is compensated by Increased HR, CO, Stimulation of RAAS, ADH
48
Late Cirrhosis
Splanchnic circulation is resistant to Angiotensin II & ADH Pressure must be maintained by local vasoconstriction Leads to HepatoRenal Syndrome
49
HepatoRenal Syndrome
Etiology is an exaggeration of mechanisms involved in ascites formation. Can happen in perfectly healthy kidneys!!
50
HepatoRenal Syndrome - Precipitants
GI Bleed Nephrotoxins (NSAIDS, Aminoglycosides, Sepsis) Iatrogenic (Diuresis, Paracentesis)
51
HepatoRenal Syndrome - Diagnosis
Euvolemic patient But look like a pre-renal patient Give fluid, but they STAY "pre-renal" appearing Urine Output
52
HepatoRenal Syndrome - Treatment
``` TIPS Glypressin Terlipressin Transplantation Midodrine (increasing vascular resistance) Octreotide (decreasing portal HTN) ```