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GI & Nutrition > End stage liver disease/Cirrhosis > Flashcards

End stage liver disease/Cirrhosis Flashcards

1
Q

Give me an overview of Cirrhosis and its causes

A

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

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2
Q

Cirrhotic liver traits

A

Chronic, Irreversible, extensive fibrosis, regenerative nodules, Scarring

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3
Q

What are the signs and symptoms of cirrhosis?

A

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

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

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4
Q

What physical examinations show the findings of cirrhosis?

A
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5
Q

What are some cirrhosis diagnostics?

A
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6
Q

What is a Fibroscan/Transient Elastography/FIB-4

A

Non invasive ultrasound methods that measure the amount of liver fibrosis

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7
Q

Describe the child pugh classification

A

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

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8
Q

Describe the Child Pugh Classification chart and what it means.

A

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

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9
Q

Model for end stage liver disease score (MELD score)

A

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)

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10
Q

Compensated VS Decompensated Cirrhosis

A

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

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11
Q

What is the overview of cirrhosis complications?

A

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

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12
Q

What causes portal hypertension complications?

A

Build of blood in scar tissue causes portal hypertension

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13
Q

Give me the overview of Portal HTN

A

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)

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14
Q

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

A

Prevention of Bleeding and re-bleeding

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15
Q

What is the primary prophylaxis for variceal bleeding?

A

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)

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16
Q

Tell me the pearls of NSBBs

A

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

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17
Q

Tell me what an NSBB does

A

Decreases cardiac output (B1 blockage)

Decrease portal flow by splanchnic arterial vasoconstriction (B2 blockage)

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

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18
Q

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

A

Beta blockers have lower decompensation/death rate

Carvedilol achieves higher hemodynamic response and lower rebleeding than propranolol

19
Q

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

A

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

20
Q

What should I monitor for betablockers? And the contraindications.

A

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

21
Q

Give me a summary of NSBBs used in PH

A
22
Q

Tell me about acute variceal bleeding

A
23
Q

How do you manage acute variceal bleeding?

A
24
Q

Tell me about octreotide and what is it for

A

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

25
Q

Tell me about vasopressin

A

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

26
Q

Tell me about Terlipressin

A

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

27
Q

Tell me about acute variceal bleeding infections prophylaxis

A

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

28
Q

What is ascites? What is the goal of therapy?

A

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

29
Q

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

A

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

30
Q

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

A

Ascitic fluid culture is obtained if infection is suspected

31
Q

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

A

Portal hypertension by liver disease

32
Q

What happens if ascitic fluid protein > 2.5?

A

Cardiac source ascites

33
Q

Describe the flowchart for Ascites

A
34
Q

Give me some methods to manage ascites

A

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

35
Q

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

A
36
Q

Tell me about Spironolactone and furosemide

A

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

37
Q

Tell me about Amiloride

A

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)

38
Q

What do I monitor for diuretic complication management?

A

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)

39
Q

How do I manage refractory ascites?

A

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

40
Q

What does albumin do in treating ascites?

A

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

41
Q

What is Spontaneous bacterial peritonitis?

A
42
Q

How do you manage SBP at the start?

A
43
Q

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

A

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)

44
Q

Recall the long term SBP prophylaxis

A

GI & Nutrition (2 decks)

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