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DEMS Pt 1 > Cirrhosis and Liver Failure > Flashcards

Cirrhosis and Liver Failure Flashcards

1
Q

Cirrhosis

A

Late stage of progressive hepatic fibrosis

Characterized histologically by regenerative nodules surrounded by fibrous tissue

Generally irreversible

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2
Q

Two types of cirrhosis

A

Compensated (no complications)

Decompensated (complications)

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3
Q

Complications of Cirrhosis

A

Portal hypertension- leads to variceal hemorrhage, ascites, and encephalopathy

Liver insufficiency- encephalopathy, jaundice

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4
Q

Etiologies of Cirrhosis

A 
Viral
Alcoholic liver disease*
Autoimmune
Metabolic
Vascular
Non-alcoholic fatty liver disease
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5
Q

What lab values should make you suspicious for cirrhosis?

A 
Liver insufficiency:
Low albumin ( 1.3)
High bilirubin (> 1.5 mg/dL)

Portal hypertension:
Low platelet count (

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6
Q

What imaging findings are suspicious for cirrhosis?

A 
Imaging studies (CT/US/MRI):
Nodular liver
Caudate hypertrophy
Ascites
Splenomegaly
Venous collaterals
Hepatocellular carcinoma
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7
Q

Model for End-Stage Liver Disease (MELD) Score

A

Mathematical survival model created from data on patients undergoing TIPS

MELD score estimates risk of 3-month mortality

Uses 3 laboratory values

- Serum total bilirubin
- Serum creatinine
- INR

Highest MELD score priority for transplant

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8
Q

Calculating MELD Scores

A
  1. 4 + 9.8 x log (INR) +
  2. 2 x log (Cr) +
  3. 8 x log (Bilirubin)
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9
Q

Mechanisms of Portal Hypertension and which one is predominantly responsible for portal hypertension in cirrhosis?

A

Portal hypertension can result from:
increase in resistance to portal flow and/or
increase in portal venous inflow (Splanchnic vasodilation (increased nitric oxide))

Increased intrahepatic resistance is the initial mechanism leading to portal hypertension

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10
Q

What is the site of increased resistance in cirrhosis?

A

Sinusoidal

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11
Q

What are the two main things that lead to increased resistance in cirrhosis?

A

Increased intrahepatic resistance in cirrhosis is not only structural (sinusoidal fibrosis and regenerative nodules) but also functional (active vasoconstriction)

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12
Q

In Portal Hypertension, what causes Splanchnic Vasodilation?

A

Increase in NO

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13
Q

NO in cirrhosis

A

In Cirrhosis, Nitric Oxide (NO) Activity is Reduced and Vasoconstrictors (VC) are Increased

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14
Q

What is the safest and most reproducible method to measure portal pressure?

A

measurement of the hepatic venous pressure gradient (HVPG)

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15
Q

Hepatic venous pressure gradient (HVPG)

A

obtained by subtracting the free hepatic venous pressure (FHVP) from the wedged hepatic venous pressure (WHVP)

HVPG = WHVP - FHVP

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16
Q

HVPG findings

A

Normal HVPG is 3-5 mmHg
HVPG is Normal in Presinusoidal Portal Hypertension
HVPG is Increased in Sinusoidal Portal Hypertension
HVPG is Increased in Post-Sinusoidal Portal Hypertension
HVPG is Normal in Post-Hepatic Portal Hypertension

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17
Q

Predictors of vericeal hemorrhage

A

Variceal size (bigger more likely to bleed)
Red signs
Child B/C (measure of disease severity)

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18
Q

How to reduced the Risk of Variceal Rupture

A

Decrease portal pressure, decreases transmural pressure and decreases wall tension

19
Q

Treatment for variceal bleed

A

Endoscopic variceal band ligation:
Bleeding controlled in 90%
Rebleeding rate 30%

Compared with sclerotherapy:
Less rebleeding
Lower mortality
Fewer complications
Fewer treatment sessions
20
Q

Transjugular Intrahepatic Portosystemic Shunt

A

(TIPS)

Done by interventional radiologists
Creates new communication for blood to flow through, bypassing the liver
Reduces the pressure

Good for variceal bleeding that can’t be fixed endoscopically

Done to manage refractory ascites

If on transplant list and have coagulation can use this

Complications: portal-systemic encephalopathy and liver failure.

21
Q

What to do for a pt with a variceal bleed due to liver failure

A

Immediately give a vasoconstrictors (e.g., octreotide*)

and call GI for endoscopy

22
Q

Octreotide

A

A vasoconstrictor that decreases splanchnic flow, slightly increases intraheptaic resistance and decreases portal pressure

23
Q

What is the Most Common Cause of Ascites?

A

cirrhosis (80%)

24
Q

Mechanism of ascites development

A

Result from an Increase in Nitric Oxide, leading to vasodialtion, decreased systemic vascular resistance, activation of RAAS system, Na2+ and H2O retention and ascites

25
Q

Natural History of Ascites

A

Portal Hypertension- No Ascites

Uncomplicated Ascites

Refractory Ascites

Hepatorenal Syndrome

26
Q

What is the Most Sensitive Method to Detect Ascites?

A

Ultrasound

27
Q

Initial Workup of Ascites

A

Diagnostic Paracentesis:

PMN count
Culture
Protien/albumin

28
Q

Serum-Ascites Albumin Gradient (SAAG) calculation

A

serum albumin minus ascites albumin (should be drawn at the same time)

29
Q

SAAG

A

correlates with sinusoidal pressure
>1.1 SAAG

The cutoffs for SAAG and ascites protein levels are 1.1 g/dL and 2.5 g/dL respectively. Cirrhotic ascites is typically high SAAG and low protein; cardiac ascites is high SAAG and high protein; and ascites secondary to peritoneal malignancy is typically low SAAG and high protein.

30
Q

Therapies for ascites

A

Salt restriction and Diuretics
Large volume paracentesis

TIPS (if refractory and low MELD score)

31
Q

Refractory Ascites

A

Occurs in ~10% of cirrhotic patients

Diuretic-intractable ascites (80%): Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications

Diuretic-resistant ascites (20%): No response to maximal diuretic therapy (400 mg spironolactone + 160 mg furosemide/day)

32
Q

Hepatorenal Syndrome

A

Renal failure in patients with cirrhosis, advanced liver failure and severe sinusoidal portal hypertension

Absence of significant histological changes in the kidney (“functional” renal failure)

Marked arteriolar vasodilation in the extra-renal circulation

Marked renal vasoconstriction leading to reduced glomerular filtration rate

Besides renal failure, patients with HRS have sodium and water retention

Ascites is universal in patients with HRS.
If ascites is absent, renal failure is more likely due to other causes

Hyponatremia is almost universal in HRS.
If serum sodium is normal, diagnosis of HRS is unlikely

33
Q

Types of Hepatorenal Syndrome

A

Type 1
Rapidly progressive renal failure (2 weeks)
Doubling of creatinine to >2.5 or halving of creatinine clearance (CrCl) to 1.5 mg/dL or CrCl

34
Q

Major Criteria in the Diagnosis of Hepatorenal Syndrome

A

Advanced hepatic failure and portal hypertension

Creatinine > 1.5 mg/dL or creatinine clearance

35
Q

Management of Hepatorenal Syndrome

A

Proven efficacy:
Liver transplantation

Under investigation:
Vasoconstrictor + albumin
Transjugular intrahepatic portosystemic shunt (TIPS)
Vasoconstrictor (Terlipressin)
Extracorporeal albumin dialysis (ECAD)

Ineffective:
Renal vasodilators (prostaglandin, dopamine)
Hemodialysis

36
Q

Spontaneous bacterial peritonitis and hepatorenal syndrome

A

Spontaneous Bacterial Peritonitis (SBP) Complicates Ascites and Can Lead to Renal Dysfunction

37
Q

What is the Most Common Infection in Cirrhotic Patients? and what’s the mechanism?

A

Spontaneous Bacterial Peritonitis (SBP)

Bacterial translocation-migration of viable microorganisms from the intestinal lumen to mesenteric lymph nodes and other extraintestinal organs and sites

38
Q

Mechanisms of Bacterial Translocation

A
  1. Intestinal Bacterial Overgrowth- Dysmotility Delayed transit time
  2. Intestinal Permeability- Mucosal Hypoxia, Acidosis
    ATP depletion, NO, LPS, TNF
  3. Impaired Immunity- Impaired chemotaxis, migration, phagocytic function, complement deficiency, etc.
39
Q

Microorganisms in SBP and treatment

A

Gram negative bacilli (72%)

cephalosporins
NO aminoglycosides

40
Q

Recurrence of Spontaneous Bacterial Peritonitis

A

Common!!
70% chance of developing another episode within the first year
So prophylaxis

41
Q

Hepatic Encephalopathy

A

Neuropsychiatric complication of cirrhosis

Ammonia is the culprit

Results of both:
Portosystemic shunt (spontaneous, surgical or radiographic) and Chronic liver failure

Failure to metabolize neurotoxic substances
Hyperammonemia results in glutamine accumulation

Alterations of astrocyte morphology and function (Alzheimer type II astrocytosis)
Astrocytes only cells in brain that can metabolize ammonia

42
Q

How to diagnose hepatic encephalopathy

A

Clinical diagnosis

Clinical findings and history important
Ammonia levels are unreliable
Ammonia has poor correlation with diagnosis
Measurement of ammonia not necessary
Number connection test
Slow dominant rhythm on EEG
43
Q

Treatment for encephalopathy

A 
Identify and treat precipitating factor:
Infection
GI hemorrhage
Prerenal azotemia
Sedatives
Constipation

lactulose or antibiotics (kill bacteria that produce ammonia)
Adjustment in dietary protein (short-term if at all)

44
Q

Hepatic Encephalopathy Precipitants

A 
Excess protein
TIPS
Infections
Sedatives/hypnotics
Diuretics
GI bleeding

DEMS Pt 1 (35 decks)

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