End stage liver disease/Cirrhosis

Question 1

Give me an overview of Cirrhosis and its causes

Answer 1

Late stage of progressive hepatic fibrosis with distortion of hepatic architecture and formation of regenerative nodules.

It is caused by alcoholism, viral hepatitis B and C, Metabolic liver disease, Hemochromatosis, Immune diseases (autoimmune hepatitis, primary billiary cirrhosis), Vascular disease (budd-chiari), DILI

Question 2

Cirrhotic liver traits

Answer 2

Chronic, Irreversible, extensive fibrosis, regenerative nodules, Scarring

Question 3

What are the signs and symptoms of cirrhosis?

Answer 3

Non specific Sx: anorexia, weight loss, weakness, fatigue

S/Sx of hepatic decompensation: Jaundice, Pruritis, upper GI bleeding, Ab. distention (Ascites), Confusion (Hepatic encephalopathy)

Question 4

What physical examinations show the findings of cirrhosis?

Answer 4

Question 5

What are some cirrhosis diagnostics?

Answer 5

Question 6

What is a Fibroscan/Transient Elastography/FIB-4

Answer 6

Non invasive ultrasound methods that measure the amount of liver fibrosis

Question 7

Describe the child pugh classification

Answer 7

Grades diseases severity, predicts long term risk of mortality and quality of life. Combination of physical and laboratory findings

Question 8

Describe the Child Pugh Classification chart and what it means.

Answer 8

One- and two-year survival rate:
-A: 100 and 85%
-B 80 and 60%
-C 45 and 35%

Question 9

Model for end stage liver disease score (MELD score)

Answer 9

Assess survival in patients with liver disease and prioritize organ allocation of cadaveric livers for transplantation

Uses serum, creatinine, bilirubin, INR, dialysis status, omitting ascities and encephalopathy

6 (less ill) to 40 (supa sick)

Question 10

Compensated VS Decompensated Cirrhosis

Answer 10

Compensated:
-Asymptomatic
-Non specific Sx, fatigue, loss of appetite, weight loss
-May have elevated HVPG and varices, but not experience complication of variceal bleeding, ascites, SBP, or encephalopathy

Decompensated:
-Symptomatic
-Ascites (abdominal distention)
-HE (confusion, lethargy)
-Muscle wasting, palmar erythema

Median survival is shorten <1.6 years once patient develops a decompensating event

Question 11

What is the overview of cirrhosis complications?

Answer 11

-PORTAL HYPERTENSION (hallmark)
-Increased vascular resistance
-Portosystemic collaterals

Question 12

What causes portal hypertension complications?

Answer 12

Build of blood in scar tissue causes portal hypertension

Question 13

Give me the overview of Portal HTN

Answer 13

Hepatic Venous Pressure gradient (HVPG) > 5 mmHg between portal & CNS = Portal Hypertension. This is associated with acute variceal bleeding

Clinical significant portal hypertension (CSPH), If HVPG >/= 10mmHg it increases risk of esophageal and gastric varices and bleeding (increase chance of decompensation)

Question 14

What is the main goal of portal HTN and variceal bleeding treatment

Answer 14

Prevention of Bleeding and re-bleeding

Question 15

What is the primary prophylaxis for variceal bleeding?

Answer 15

Screen for varices at the time of cirrhosis diagnosis

Non selective beta adrenergic blocking (NSBB): Main stay of treatment: Propranolol, nadolol, Carvedilol

Endoscopic variceal ligation (EVL): Endoscopic therapy by pacing rubber bands around varices: Alternative for patients who cannot take NSBBs (asthma or hypoglycemic)

Question 16

Tell me the pearls of NSBBs

Answer 16

Not indicated for patients without varices

Medium to large varices that have not bled can recieve NSBB or EVL

NSBBs dose reduced or DC’d if persistent low SBP < 90 or severe adverse effects
-if low arterial pressure you can switch from carvedilol to propranolol or nadolol

Question 17

Tell me what an NSBB does

Answer 17

Decreases cardiac output (B1 blockage)

Decrease portal flow by splanchnic arterial vasoconstriction (B2 blockage)

Decrease resistance by intrahepatic vasodilation (a1 blockage) - carvedilol only

Question 18

What is the result of beta blocker treatment and what is the first line preferred?

Answer 18

Beta blockers have lower decompensation/death rate

Carvedilol achieves higher hemodynamic response and lower rebleeding than propranolol

Question 19

Tell me everything you know about carvedilol in regards to portal hypertension.

Answer 19

Carvedilol causes intrahepatic vasodilation via nitric oxide release further decreasing portal pressure (a1 blockage)

-Significant decrease in HVPG compared to traditional NSBBs
-Not required titration
-More likely to cause systemic hypotension
-Preferred management for PH

Carvedilol 3.125 mg BID, titrate to max 6.25 BID
-titrate not guided by HR, only maintain SBP above 90 mmH
-greater HVPG reduction but higher potential to cause systemic hypotension

Question 20

What should I monitor for betablockers? And the contraindications.

Answer 20

B blockers continue indefinitely, monitor renal impairment, hypotension, bradycardia, bronchospasm, hypoglycemia

Absolute contraindications:
Asthma, 2nd 3rd degree atrioventricular block (w/o pace maker), sick sinus syndrome, extreme bradycardia (<50 bpm)

Relative contraindications:
-Psoriasis, peripheral arterial disease, chronic obstructive pulmonary disease, pulmonary artery hypertension, insulin-dependent diabetes mellitus, Raynaud syndrome

Question 21

Give me a summary of NSBBs used in PH

Answer 21

Question 22

Tell me about acute variceal bleeding

Answer 22

Question 23

How do you manage acute variceal bleeding?

Answer 23

Question 24

Tell me about octreotide and what is it for

Answer 24

First line

Synthetic somatostatin analog, potent splanchnic vasoconstriction, decrease portal and collateral blood flow

Dose: Bolus 50 mcg IV then 50 mcg/hr infusion x 2-5 days
Side Effects: Hyperglycemia, Vomiting, bradycardia, hypertension, arrhythmia, diarrhea, and abd. pain

More effective in controlling acute bleeding

Question 25

Tell me about vasopressin

Answer 25

Natural occurring hormone, non-specific vasoconstrictor Dose: 0.2-0.4 units/min, increased every hour by 0.2 units/min to max dose 0.8 units/min x 24 hrs max Side Effects: abdominal cramping, nausea, tremor, worsening hypertension, angina, monitor closely for signs/symptoms of ischemia (myocardial, peripheral, bowel necrosis) -Non-FDA, guideline dosing, reserving for treatment failures

Question 26

Tell me about Terlipressin

Answer 26

Synthetic analog of vasopressin Dose: 2 mg IV Q4-6h x 24-48h then 1 mg IV Q4-6h x 2-5 days Side effects: Abd. pain, dyspnea, ischemia, respiratory failure Black box warning: May cause serious or fatal respiratory failure, do not start in patients with hypoxia Off label use for variceal bleeding

Question 27

Tell me about acute variceal bleeding infections prophylaxis

Answer 27

Variceal hemorrhage, increase risk for severe bacterial infection, and increase mortality so a short term antibiotic is recommended. You initiate antibiotics after emergent endoscopy within 12 hours admission Antibiotics to prevent SBP: Ceftriaxone 1g IV q24 x 7 days preferred Oral ciprofloxacin bactrim can be considered

Question 28

What is ascites? What is the goal of therapy?

Answer 28

Ascites is the 1st common sign of decompensation It is the accumulation of excessive fluid within abdomen, bulging of abdominal with shifting flank dullness, it is an indication of adv. liver disease The goal of therapy is to minimize ascitic fluid and decrease peripheral edema

Question 29

What is the physiological process of ascites? What are the classification of ascites?

Answer 29

Grade 1 - Mild Ascites: only detected by ultrasound Grade 2 - Moderate ascites: Moderate symmetric distension of abdomen Grade 3 - Marked distension of the abdomen

Question 30

Give me the response to treatment for the different types of ascites

Answer 30

Ascitic fluid culture is obtained if infection is suspected

Question 31

What is SAAG and what does it mean if its >/= 1.1?

Answer 31

Portal hypertension by liver disease

Question 32

What happens if ascitic fluid protein > 2.5?

Answer 32

Cardiac source ascites

Question 33

Describe the flowchart for Ascites

Answer 33

Question 34

Give me some methods to manage ascites

Answer 34

Alcohol abstinence Sodium restriction to 2 g Diuretics - sprinolactone and furosemide (mainstay treatment) Monitor serum K, renal function, and daily weight If tense ascites is present, paracentesis should be performed Avoid Medications: ACEIs, ARBs, NSAIDs, beta blockers, nephrotoxic drugs

Question 35

What is the flow chart for initial therapy of patient's with cirrhosis and ascites?

Answer 35

Question 36

Tell me about Spironolactone and furosemide

Answer 36

Spironolactone 100 mg and furosemide 40 mg QD, titrate every 3 to 5 days -maintain ratio 100:40 -max dose spironolactone 400mg, furosemide 160mg

Question 37

Tell me about Amiloride

Answer 37

Amiloride 10 mg BID, titrate every 4 days in increments of 10 mg to a max 30 mg BID or 10-40 mg QD per AASLD guidelines -alternative to people who cannot take spironolactone (they got gyno or som)

Question 38

What do I monitor for diuretic complication management?

Answer 38

Diuretic Therapy for Management of Ascites Diuretic complication management * Monitor electrolyte and acid-base disturbance: hyponatremia, hyperkalemia, metabolic alkalosis * Monitor renal function, pre-renal azotemia due to over diuresis * Sign of hypovolemic, dizziness, orthostatic hypotension, ↑ HR Patient counseling * Weight monitoring daily * Without peripheral edema: weight loss up to 0.5 kg/day (0.5 liter/day) * With edema: weight loss up to 1 kg/day (1 liter/day)

Question 39

How do I manage refractory ascites?

Answer 39

Alternate options Transjugular intrahepatic portosystemic shunt (TIPS): stent is inserted via catheter to portal vein to divert blood flow and reduce portal hypertension Peritoneovenous shunt: surgical implanted valve connect to vein that empties ascitic fluid directly into superior vena cava * complications or worsening hepatic function * considered in refractory patients who are not candidate for paracentesis, transplant, or TIPS

Question 40

What does albumin do in treating ascites?

Answer 40

fyi in large volume paracentesis give 6-8g/liter if removed

Question 41

What is Spontaneous bacterial peritonitis?

Answer 41

Question 42

How do you manage SBP at the start?

Answer 42

Question 43

Recall the empiric antibiotic treatment vs the short term prophylaxis treatment for SBP

Answer 43

Empiric Antibiotic Treatment for SBP * Recommend 3rd generation cephalosporin * Cefotaxime 2g IV q8h * Ceftriaxone 2g IV q24h (AASLD) * Empiric treatment should not be delayed while waiting for culture result * Antibiotic course of 5-7 days Short-term Antibiotic Prophylaxis for SBP * Short-term prophylaxis x 7 days with acute GI bleeding * Ceftriaxone 1 g IV QD; change to oral antibiotic when bleeding is controlled and oral intake is resumed, total duration 7 days (including oral agents) * Ciprofloxacin 500 mg PO BID * Bactrim DS (double-strength) 1 tablet PO BID * Norfloxacin 400 mg PO BID (no longer available in US)

Question 44

Recall the long term SBP prophylaxis

Answer 44