Cirrhosis Flashcards

1
Q

What range of points are associated with each Child-Pugh grade?

A

Grade A = <7 points
Grade B = 7-9 points
Grade C = 10-15 points

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2
Q

What is the equation for the Mayo End-Stage Liver Disease (MELD) Score?

A

3.78[ln serum bilirubin (mg/dL)]
+ 11.29
[ln INR]
+ 9.57*[ln serum creatinine (mg/dL)]
+ 6.43

same equation; just if you prefer reading it this way
3.78[ln serum bilirubin (mg/dL)] + 11.29[ln INR] + 9.57*[ln serum creatinine (mg/dL)] + 6.43

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3
Q

What are MELD scores used for?

A

To determine your place on the liver transplant waitlist (higher score = higher priority/more pronounced disease)

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4
Q

Cirrhosis Complications

A
  • Ascites most common, 50% death rate w/in 5 years
  • Portal HTN
  • Variceal bleeding
  • Spontaneous bacterial peritonitis (SBP)
  • Hepatic encephalopathy
  • Hepatorenal syndrome common cause of death for a lot of patients
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5
Q

Cirrhosis Lab Values

A
  • Jaundice (high bilirubin)
  • LFTs/ALT and AST (can be increased or decreased due to acute and chronic alcoholism, respectively)
  • Low albumin
  • High PT/INR (poor clotting)
  • Low platelets
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6
Q

Cirrhosis Causes

A
  • Chronic alcohol use #1 cause
  • Hepatitis C
  • Fatty liver disease
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7
Q

Portal HTN/Ascites Pathophys

A

Hepatocytes scar and die off, resulting in a narrowed sinusoidal space. The narrowing of this space increases pressure and causes fluid backup (wants to avoid high-pressure space)

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8
Q

Ascites Physical Exam Characteristics

A
  • Full, dense abdomen
  • Bulging abdomen
  • Trouble breathing
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9
Q

Ascites Diagnosis

A
  • Abdominal ultrasound followed by paracentesis (drainage of ascitic fluid)
  • Serum ascites albumin gradient (SAAG): if serum albumin - ascitic albumin ≥ 1.1 then portal HTN is present
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10
Q

Ascites Treatments (Names)

A
  1. Na+ restriction
  2. Spironolactone
  3. Furosemide
  4. Midodrine
  5. Large volume paracentesis (LVP) conditional
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11
Q

Ascites Treatment: Na+ (Dose/Pearls)

A
  • Restrict to 2g/day
  • Do NOT fluid restrict
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12
Q

Ascites Treatment: Spironolactone

A
  • 50-100mg titrated prn up to 400mg/day
  • START BEFORE LOOP DIURETIC IF LOW BP
  • AEs: gynecomastia, hyperkalemia
  • Preferred over loop diuretics in cirrhotics (more diuresis for this patient population)
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13
Q

Ascites Treatment: Furosemide

A
  • 40mg/day titrated prn up to 160mg/day
  • Maintain 40:100 ratio of furosemide:spironolactone (dose optimization)
  • AE: hypokalemia
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14
Q

Ascites Treatment: Midodrine

A
  • Increases BP
  • Used in pt w/ hypoTN
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15
Q

Ascites Treatment: Large Volume Paracentesis (LVP)

A
  • Use when not responding to/tolerating diuretics and/or midodrine
  • Remove 4-8L of fluid q2weeks
  • Decreases BP and mortality
  • If taking out >5L, give 8g IV albumin per L removed
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16
Q

TIPS Procedure (Transjugular Intrahepatic Portosystemic Shunt)

A
  • Used when LVP cannot be tolerated AND failed diuretics
  • Used for refractory variceal bleeding
  • Restores blood flow from portal to hepatic vein via bypass stent placement
  • AE: hepatic encephalopathy (bypassing reduces ammonium metabolism)
  • Do NOT perform TIPS procedure if Hx of hepatic encephalopathy
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17
Q

Portal HTN/Variceal Bleeding Pathophys

A

More than appropriate blood flow leads to distention of GI vessels (which are not designed to hold high blood flow/BP)

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18
Q

Varices Diagnosis

A
  • Esophagogastroduodenoscopy (EGD)
  • Admission due to ascites
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19
Q

When to treat portal HTN?

A

When varices are present

20
Q

Portal HTN (+ varices) Treatment Drug Class

A

Non-selective beta blockers

21
Q

Portal HTN (+ varices) Treatment

A
  1. Propranolol 20-40mg BID
  2. Nadolol 20-40mg QD
  3. Carvedilol 3.125mg BID drops BP the most
  • Titrate until 60bpm
  • Hold BB if SBP <90mmHg, DBP <60mmHg, HR <60bpm
22
Q

Acute Variceal Bleeding Patho/Pearls

A
  • Blood vessel rupture (GI bleeding)
  • Causes 1/3 of cirrhosis-related deaths
  • Risk factor for SBP (peritoneal infection)
23
Q

Acute Variceal Bleeding Treatments (Names)

A
  1. IV isotonic solution (+O2 supp)
  2. PRBCs if necessary
  3. Octreotide
  4. Endoscopic Variceal Ligation (EVL)
  5. SBP Prophylaxis conditional
  6. Non-selective BB conditional
24
Q

Acute Variceal Bleeding Treatment: IV Isotonic Solution

A
  • NS or LR
  • Supplemental O2
25
Acute Variceal Bleeding Treatment: PRBCs
- Only if Hgb <8g/dL - 1 unit = 1g/dL
26
Acute Variceal Bleeding Treatment: Octreotide
- IV bolus then infusion - Vasoconstricts dilated splantic vessels - Inhibits intestinal secretion
27
Acute Variceal Bleeding Treatment: Endoscopic Variceal Ligation (EVL)
- Banding of varix to kill it
28
Acute Variceal Bleeding Treatment: Non-Selective BB
- Admin only when bleed and vital signs stabilize
29
SBP (Spontaneous Bacterial Peritonitis) Patho
- SBP = "spontaneous bacterial peritonitis" - Bacterial infection (enteric gram neg. and some pos.) in ascitic fluid - Bleeding in GI tract = higher risk of bacterial in peritoneal space and BP drops
30
SBP Diagnosis
- Elevated WBC - Malaise, weakness - Abdominal pain - Fever - Paracentesis (takes 72hrs): PMN ≥ 250mm^3 PMN = WBC in ascitic fluid * %PMN
31
SBP Active Treatments
- 1st line: 3rd gen cephalosporin → ceftriaxone 2g x5days - Ciprofloxacin x5 days if anaphylaxis to beta-lactams - IV albumin 1.5g/kg on day 1 then 1g/kg on day 3 (decreases mortality) - Repeat paracentesis 48hrs after ABX start to confirm efficacy/resistance - If PMN does not drop >25% then go with broad-spec ABX (e.g. carbapenems) x5 days
32
SBP Prophylactic Treatment
If acute variceal bleeding... - 1g ceftriaxone IV x7 days - Ciprofloxacin x7 days if allergic - Can de-escalate to PO when discharged If indefinite prophylaxis (Hx of SBP): - Ciprofloxacin 250-500mg QD for life - Bactrim DS (double strength) QD for life
33
Hepatic Encephalopathy Pathphys
Decreased hepatic function and portosystemic shunting leads to a decrease in ammonia detoxification. The excess ammonia crosses the BBB and exhibits CNS effects.
34
Hepatic Encephalopathy Presentation
- Altered mental status (e.g slow responses, coma) - Elevated ammonia levels (but does not correlate with mental status)
35
Hepatic Encephalopathy Treatments (Names)
1. Remove precipitating factors 2. Protein 3. Lactulose 4. Rifaximin
36
Hepatic Encephalopathy Treatment: Remove Precipitating Factors
- Psychotropic medications (e.g. benzos, anti-seizure meds, bipolar meds) - Treat UTI (?)
37
Hepatic Encephalopathy Treatment: Protein
- Patients need protein (in catabolic state) - Use dairy/vegetable sources w/ branched amino acids → less likely to cross BBB
38
Hepatic Encephalopathy Treatment: Lactulose
- Targets ammonia in GIT - Cathartic effects - Fermented/broken down by gut flora → prod. organic acids → lowers colonic pH → enhances movement of ammonia from blood into bowel → converted into ammonium and gets trapped in bowel → eliminated in stool Acute HE: - PO: 25mL q1-2h until ≥2 loose stools - Enema: 300mL retention enema for 1 hour q6-12h HE Prevention: - 15-60mL q6-12h - Titrate until 2-3 soft bowel movements qd
39
Hepatic Encephalopathy Treatment: Rifaximin
- Reduces bacteria that produces ammonia - *Add-on therapy to lactulose PRN* Acute HE: - 400mg PO q8h HE Prevention: - 550mg PO BID AEs: Well-tolerated
40
Hepatorenal Syndrome Pathophys
Splanchnic vasodilation due to portal HTN leads to reduced effective circulating volume. Decrease circulating volumes means less renal perfusion, which leads to AKI. *High mortality rate (95% w/in 30 days)
41
Hepatorenal Syndrome Diagnosis
- Cirrhosis w/ ascites and SCr ≥ 0.3mg/dL increase from baseline in 48hrs -OR- - ≥50% increase in baselines SCr in last 7 days w/ no improvement of SCr after 2 days of diuretic cessation and IV albumin use - If no improvement after 2 days → ESRD :(
42
Hepatorenal Syndrome Treatment
1. IV norepinephrine -AND- 2. IV albumin 1g/kg/day Measures of efficacy: - SCr decreases to 1.5mg/dL -OR- return within 0.3mg/dL of baseline over max 2 weeks - If after 4 days of therapy SCr remains the same or rises then d/c (lack of efficacy)
43
PKPD Changes in Cirrhosis: Decreased Liver Blood Flow
- Portal HTN shunts blood away from liver Impacts drugs w/ high first-pass (movement from GIT to liver) - Less first-pass and therefore higher systemic concentrations 1. Propranolol - titrate to effect 2. Morphine - titrate to effect or change to diff agent (e.g. Dilaudid/hydromorphone) 3. Carvedilol (Coreg) - titrate to effect - Decrease doses to compensate
44
PKPD Changes in Cirrhosis: Loss of Hepatocyte Function
- Decreased metabolic capacity - Phase I (CYP450) more affected than Phase II (glucuronidation and sulfation) - If drug is CYP-dependent → increased therapeutic effects/concentrations *Use agents metabolized by Phase II when possible* 1. Benzos: lorazepam (Phase II) > diazepam (CYP)
45
PKPD Changes in Cirrhosis: Decreased Albumin Production
- Heavily protein bound drugs will have higher free concentrations (therefore higher therapeutic effect) 1. Phenytoin: reduce dose if needed
46
PKPD Changes in Cirrhosis: Reduced Renal Function Due to Increased SCr
- Decreased renal perfusion possible - Hepatorenal syndrome possible - Monitor renal function
47
PKPD Changes in Cirrhosis: Increased Therapeutic Response
- Increased BBB permeability - Drugs acting on CNS can have greater therapeutic effects 1. Opioids 2. Benzos - Monitor effect and decrease doses prn - If pt is completely out of it after a dose, decrease the dose but only readmin AFTER their mental status returns to normal