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M2 GI > Advanced Liver Disease (Cirrhosis) > Flashcards

Advanced Liver Disease (Cirrhosis) Flashcards

1
Q

What arteries supplys the liver?

A

1) hepatic artery and vein
2) portal venous system (from small bowel)

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2
Q

What are the 2 major determinants of portal pressure?

A

portal venous flow and resistance

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3
Q

How does liver disease affect hepatic circulation?

What is the sequale of liver disease? (4)

A

∆ blood flow patterns through the inflow (portal vein) and the outflow (hepatic vein):

  • blood flow through alternate vessels within the splanchnic circulation (stomach, small/large intestines, pancreas, spleen, liver), resulting in varices
  • increased lymph production (due to increased hydrostatic, decreased oncotic pressures) that the liver and mesothelium can no longer resorb, resulting in ascites and 3rd spacing of fluid (edema of the legs, abdominal wall, and anasarca – all over the body)
  • increased hydrostatic pressure (due to vasoconstriction of renal arteries -> increased renal perfusion -> increased RAAS -> increased Na/H2O uptake -> increased hydrostatic pressure)
  • decreased vascular oncotic pressure (due to decreased albumin production) -> increased filtration -> edema/ascites
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4
Q

What is decompensated liver disease?

A

situation where the liver functions are increasingly disturbed to a degree that fluid accumulation or bleeding occurs

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5
Q

What is the definition of cirrhosis?

Prognosis?

A

severely scarred liver with regenerating liver cells surrounded by fibrous septa

irreversible with invariably poor prognosis

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6
Q

How is portal venous pressure measured?

A

because the portal vein cannot be easily accessed, it is measured:

directly – via abdominal vein catherization or portal/splenic vein puncture (rarely done)

indirectly - “wedged hepatic pressure recording” aka balloon catheter - used to assess the level of portal HTN caused by parenchymal liver disease

  • process: a balloon catheter is inserted into the HEPATIC VEIN and the pressure is measured when the balloon is inflated “wedged portal pressure” and when the balloon is deflated “free pressure”
  • wedged portal pressure – free pressure = wedged hepatic venous pressure gradient
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7
Q

What is the definition of portal HTN?

Pathophysiology?

Causes? (3)

A

increased pressure of PORTAL VENOUS system.

pathophys: increased resistance to portal venous flow and hh portal venous flow

  • cirrhotic liver disease - scar formation + liver regeneration
    • commonly caused by OH abuse, chronic hepB/C, schistosomiasis
  • non-cirrhotic liver disease (more of a vascular disease)
    • idiopathic portal HTN (common in India, Japan)nodular regenerative hyperplasia (NPH)
  • extrahepatic liver disease - problems with the inflow/outflow tract (thrombi, tumor, impaired flow)
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8
Q

Increased resistance to portal venous flow can be active or passive.

What causes each one?

A

can be due to passive or active resistance

Passive resistance

  • prehepatic – thrombosis, compression, or invasion by benign or malignant tumor
  • intrahepatic – parenchymal alterations
  • posthepatic – hepatic venous outflow obstruction

Active resistance

  • scars contain myofibroblasts with contractile elements that cause dynamic resistance to flow
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9
Q

How does splenic vein thrombosis affect portal venous flow?

A

causes PASSIVE resistance to portal venous flow.

results in opening of gastric/LUQ collaterals (ie pancreatitis = most common)

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10
Q

How does portal vein thrombosis affect portal venous flow?

What causes it?

A

causes hepatic ischemia

throbomsis in the portal vein is due to

  • hypercoagulopathy (due to decreased synthesis of anti-coagulants and hypoxic conditions in the portal vein)
  • decreased flow/stasis (due to upstream mechanical resistance)
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11
Q

How does alcohol or autoimmune processes affect portal venous flow?

A

PASSIVE resistance to portal venous flow.

causes sinusoidal parenchymal changes

chronic exposure results in parenchymal changes (ie collagen deposition, hepatocyte swelling, or infiltrating inflammatory cells) that cause obstruction or ∆flow

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12
Q

How does schistomiasis affect portal venous flow?

A

PASSIVE resistance to portal venous flow.

intrahepatic (presinusoidal) obstruction, resulting in parenchymal alterations

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13
Q

How does OH, toxins (bush tea, anti-cancer Tx, bone marrow transplant) affect portal venous flow?

A

PASSIVE resistance to portal venous flow.

causes post-sinusoidal parenchymal changes (affects the outflow tract/central vein)

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14
Q

What is Budd-Chiari?

How does it affect portal venous flow?

What does it result in?

A

thrombosis of hepatic vein

result in massive congestion, jaundice + ascites

causes passive resistance to portal venous flow

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15
Q

Why would the caudate lobe hypertrophy in the presence of a Budd-Chiari?

A

caudate lobe (typically) drains directly into the IVC and may hypertrophy to compensate for loss of portal vein (via budd chiari thrombosis)

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16
Q

Increased portal venous flow can be caused by these 3 major things.

A

parenchymal liver disease

arterioportal shunt (trauma, tumor erosion

splenomeagly

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17
Q

How does parenchymal liver disease after flow distribution? (4)

What results from this?

HIGH YIELD

A

parenchymal liver disease -> ∆ flow and pressure -> production of vasoactive substances (i.e. NO) that alter flow distribution:

  • increased resistance to flow to the liver
  • progressive vasodilation of the splanchnic circulation
  • peripheral vascular dilation
  • central vasoconstriction (ie renal/cerebral arteries)
    • vasoconstrictive effect on kidney arteries can be so severe that functional renal failure can develop (hepatorenal syndrome, HRS

Result

  • arterial hypotension
  • low peripheral resistance
  • high CO
  • hypervolemia

(first two is due to vasodilator effect, last two is due to vasoconstriction effect)

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18
Q

What is the hepatorenal syndrome caused by?

What is the sequelae of this?

A

parenchymal liver disease -> ∆ flow and pressure -> production of vasoactive substances (i.e. NO) that alter flow distribution. One of these effects is:

vasoconstrictive effect on kidney arteries, which can be so severe that functional renal failure can develop (hepatorenal syndrome, HRS)

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19
Q

What does it mean to have functional renal failure?

A

functional = no anatomical damage to the kidney, such that they can be transplanted into another person and still be functional

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20
Q

What causes splenomeagly? (4 covered)

How does it increase portal venous flow ?

A

cause: advanced liver disease results in increased pressure in the portal venous system prevents splenic outflow
* other causes: myelofibrosis, idiopathic (Banti’s syndrome), splenic vein thrombosis

portal venous flow: increased arterial inflow and subsequent increased venous outflow to the liver

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21
Q

How do varices develop in portal HTN?

What structures are at most risk of bleeding?

A

branches from all over the abdominal cavity merge to form the portal vein. Thus, whenever there is a blockage, collaterals may develop anywhere inside and outside of the abdominal cavity

increased portal HTN -> development of VARICES

those that occur in the GI submucosa are at risk of potential variceal hemorrhage

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22
Q

What are the sequelae of varices in cirrhotic patients (5).

Non-cirrhotic patients? (1)

A

cirrhotic patients with portal HTN are at increased risk of morbidity and mortality as a result of variceal hemorrhage due to:

  • severe underlying liver disease -> decompensate secondary to decreases in hepatic perfusion and tissue oxygenation
  • coagulation mechanisms are disturbed (decreased pro-thrombin, factor 5, 7 production -> prolonged PT time & decreased platelets if hypersplenism is present
  • fluid, electrolyte, and A/B imbalances; evident when ascites and edema are present
  • gut flora breaks down blood in the GI -> blood breakdown products are reabsorbed into the systemic circulation in excessive amounts
  • increased susceptibility to infections due to impaired immune system + bacterial leakage from the bowel into ascites or blood vessels

Non-cirrhotic patients with portal HTN (ie pre-hepatic portal or splenic vein obstruction)

  • do not have as many adverse complications with variceal bleeding compared to the cirrhotic patients
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23
Q

How do you treat bleeding varices? (3)

What is used in patients that are refractory to traditional treatments?

A
  • non-selective ß blockers (propranolol, nadolol, carvidolol)
  • endoscopic banding – process where esophageal varices are ablated (perform if ß blockers are contraindicated)
  • antibiotic prophylaxis – prevent infectionsTIPS (see above, in specific cases)splenectomy (rare)

Refractory cases: TIPS (transhepatic intrahepatic portosystemic shunt) – used to perform stent placements in patients with uncontrolled bleeding (usually after failure of endoscopy treatment)

24
Q

What is the Child-Pugh Score?

A

indicator of liver disease severity

25
Q

What are some methods of visualizing varices? (4)

A
  1. US, CT, MRI - visualize spleen, liver, vasculature
  2. Endoscopy – visualize varices and identify any potential upper GI bleeding sources; can perform interventional procedures to control bleeding sites
  3. barium swallow – rarely used for this purposes, but still mentioned
  4. Angiography - used in TIPS procedure
26
Q

What is TIPS?

A

TIPS (transhepatic intrahepatic portosystemic shunt) – used to perform stent placements in patients with uncontrolled bleeding (usually after failure of endoscopy treatment) or control refractory ascites

27
Q

What are some risk factors for variceal hemorrhage?

A
  • larger varices
  • endoscopic features (large, red whale markings or cherry red signs)
  • child-Pugh score of C (decompensated cirrhosis)
  • Wedged Hepatic Venous Pressure gradient >12
28
Q

What clinical presentation suggest varices?

A

low platelet count

splenomegaly and/or significant collateral circulation

29
Q

How do you screen for varices?

A

endoscopy

30
Q

What is ascites?

Why does it occur?

A

presence of free fluid in the peritoneal cavity (askos = bag)

occurs if the absorptive capacity of the lymphatic system is exceeded >5x capacity

31
Q

What is the pathophysiology behind ascites development?

(think back to cardiology…ugh)

A

∆ starling’s forces of oncotic pressure and hydrostatic pressure in the vascular and lymphatic circulations

32
Q

What causes ascites? (5 broad categories)

A

often a complication of cirrhosis, but can occur as a result of non-cirrhotic etiologies, such as

  • parenchymal damage
    • drug-induced liver disease
    • bush tea disease
    • chemotherapy
    • radiation
    • metz disease
  • liver outflow obstruction
  • budd-chiaris syndrome (hepatic vein occlusion)
  • heart failure
33
Q

Ascites associated w/ liver dz arises under the influence of these 4 factors.

A
  1. portal venous HTN
  2. hepatic sinusoidal HTN
  3. Hypoalbuminemia
  4. impaired renal excretion of Na/H2O
34
Q

How does portal venous HTN cause ascites?

A

causes movement of transudate fluid from vascular beds into the mesenteries and organs normally drained by the portal venous system. Results in overloading of the resorptive capacity of the capillaries and lymphatics g fluid leaks across the mesothelial surfaces and into the peritoneal cavity

  • contributes, but is not a primary cause of ascites seen in cirrhosis but does contribute to it
35
Q

How does hepatic sinusoidal HTN cause ascites?

A

parenchymal liver disease promotes fluid filtration from the hepatic sinusoids into the space of Disse. This excess lymph moves out of the space as liver lymph, but overwhelms the capacity of the lymphatic system and sweeps through the lymphatic walls into the peritoneal cavity “liver sweat”

think of it this way: in cirrhosis, there are focal areas of damage, such that the areas that are still functional have to process the extra lymph (which can overwhelm the lymphatic system, leading to ascites formation)

36
Q

What is liver sweat?

A

excess lymph flow overwhelms the capacity of the lymphatic system and sweeps through the lymphatic walls into the peritoneal cavity

37
Q

What is hypoalbuminemia caused by? (4)

How does it lead to ascites formation?

A
  • decreased production by cirrhotic liver
  • loss of albumin into peritoneal cavity
  • hemodilution due to fluid retention by the kidneys
  • malnutrition
38
Q

How does renal vasoconstriction play a KEY role in the genesis of ascites in cirrhosis?

A

Remember that there was fluid redistribution due to vasoactive substanes secreted by the liver in response to altered flow.

This results in 3rd spacing of fluid, which reduces ECV -> increased RAAS activation -> increased Na/H2O reabsorption -> increases hydrostatic pressure and therefore perpetuates ascites (Underfill theory)

39
Q

What are the 3 theories of ascites formation?

A

Underfill theory

Overfill theory

Vasodilation theory

40
Q

What is the underfill theory of ascites formation?

A

ascites with extravascular sequestration of fluids leads to decreased ECV

  • > decreased renal perfusiong RAAS activation
  • > increased Na/H2O reuptake
  • > increases hydrostatic pressure and therefore perpetuates ascites
41
Q

What is the overfill theory of ascites formation?

A

as cirrhosis progresses and albumin falls vascular oncotic pressure decreases, which results in excess fluid spilling out of the vascular space and into the interstitial space (ie overflows)

42
Q

What is the vasodilation theory of ascites formation?

A

peripheral arterial vasodilation with enhanced splanchnic flow + increased PVR due to shunts, pooling, and collaterals -> decreased ECV followed by renal Na/H2O retention -> ascites formation

43
Q

What is the typical history of a patient with ascites?

A
  • slowly progressing increasing abdominal girth, often with leg swelling
  • common accompanying symptoms include anorexia, weakness, fatigue
  • history of OH, Rx, biliary tract surgery, transfusion
44
Q

What is the typical physical exam of a patient with cirrohosis-induced ascites?

What about ascites in general?

A

Cirrhosis induced ascites *IMPT*

  • jaundice
  • spider angiomas
  • palmar erythema
  • gynecomastia

General signs of ascites:

  • fullness in the flanks with shifting dullness, fluid wave (indicates considerable ascetic fluid)
  • increased abdominal girth
  • respiratory compromise due to pleural effusions
  • peripheral edema
  • inguinal and umbilical hernias (due to increased abdominal pressure)
45
Q

How do you diagnose ascites?

A

US

paracentesis

46
Q

Paracentesis can be used to determine how to proceed in the treatment of a patient with ascites.

How?

A

SAAG (serum-ascites albumin gradient)

appearance of fluid

47
Q

If a patient has a SAAG >1.1, what additional tests do you want to order? (4)

SAAG (serum-ascites albumin gradient)

A

CBC (WBC + differential)

  • WBC = infection or malignancy (both can cause L shift)
  • increased RBC = malignancy or hepatic outflow obstruction

TP (total protein)

  • TP = infection, malignancy, hepatic outflow obstruction (rarely hypothyroidism)

Cytology (for malignancy)

Albumin

48
Q

The appearance of the ascites fluid determines what additional test to order.

cloudy

bloody

malignancy

milky

A

cloudy -> culture

bloody -> Hgb

malignancy -> cytology

milky -> TG, chyloµ levels (chylous ascites?)

49
Q

How do you treat ascites?

A
  1. treat underlying disease
  2. consider transplant due to poor prognosis
  3. Na restriction
  4. H2O restriction if serum sodium is <120mm/L
  5. Diuretics (spironolactone and/or amiloride)
50
Q

How do you treat for diuretic-resistant ascites?

A
  1. therapeutic paracentesis (of large volumes of ascites)
  2. TIPS
  3. extracorporeal ultrafiltration of ascetic fluid with reinfusion of protein concentrate
  4. liver transplant – increases 1-year survival from 25% g 75%
51
Q

What two drugs do you want to avoid in a patient with liver failure/ascites?

A

NSAIDs and Aminoglycosides

(due to potential for impaired renal function)

52
Q

What are the sequelae of ascites? (4)

A
  1. hepatic hydrothroax
  2. hernias (umbilical, inguinal)
  3. spontaneous bacterial peritonitis (SBP)
  4. hepatorenal syndrome
53
Q

What is hepatic hydrothroax?

How do you treat it?

A

Sequelae of ascites

pleural effusion – ascites fluid enters chest via diaphragmatic defects; mostly R-sided

trmt: similar to ascites

54
Q

How does ascites cause umbilical, inguinal hernias?

How do you treat it?

A

Sequelae of ascites

increased abdominal pressure causes pressure against weakened abdominal wall

trmt: ascites + elective surgical repair

55
Q

What is spontaneous bacterial peritonitis (SBP)?

What are some common pathogens? (3)

Symptoms indicative of SBP?

Diagnstic tests to confirm SBP?

Treatment?

Prognosis?

A

Sequelae of ascites - occurs when gut bacteria is translocated to mesenteric LN -> bacteremia -> bacterascites -> poor ascetic fluid opsonitic ativity -> SBP

common pathogens: E. coli, Klebsiella, pneumococcuscommon

sx: fever, abd. pain, mental status changes

diagnostic tests: ascites fluid cell count >500 WBC (>50% PMNs) + culture

Treatment: 3rd generation CEPHALOSPORIN (Cefotaxime)

Poor prognosis

56
Q

What is hepatorenal syndrome?

How does HRS result in ascites formation? (3)

Clinical manifestations of HRS? (5)

Purposes of treatmenT?

Prognosis?

A

Sequelae of ascites - functional renal failure caused by extreme mechanisms that ultimately result in ascites formation:

  • renal vasoconstriction + decreased GFR
  • maldistribution of intra-renal blood flow and cortical hypoperfusion
  • extreme Na/H2O retention due to excess RAAS activation

clinical manifestations:

  • severe liver disease with ascites
  • oliguria
  • normal urine sediment with decreased urine Na
  • variable progression (rapid in some, slow in others)
  • no recognizable pathological lesion in the kidneys

therapy: restore/maintain intravascular volumeuse of vasoactive substances to redistribute flow to enhance central vasodilation and peripheral and splanchnic vasoconstriction

**poor prognosis **

M2 GI (41 decks)

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