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PHM 604 GI > Cirrhosis > Flashcards

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
Q

Acute Variceal Bleeding Treatment: PRBCs

A
  • Only if Hgb <8g/dL
  • 1 unit = 1g/dL
26
Q

Acute Variceal Bleeding Treatment: Octreotide

A
  • IV bolus then infusion
  • Vasoconstricts dilated splantic vessels
  • Inhibits intestinal secretion
27
Q

Acute Variceal Bleeding Treatment: Endoscopic Variceal Ligation (EVL)

A
  • Banding of varix to kill it
28
Q

Acute Variceal Bleeding Treatment: Non-Selective BB

A
  • Admin only when bleed and vital signs stabilize
29
Q

SBP (Spontaneous Bacterial Peritonitis) Patho

A
  • 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
Q

SBP Diagnosis

A
  • Elevated WBC
  • Malaise, weakness
  • Abdominal pain
  • Fever
  • Paracentesis (takes 72hrs): PMN ≥ 250mm^3

PMN = WBC in ascitic fluid * %PMN

31
Q

SBP Active Treatments

A
  • 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
Q

SBP Prophylactic Treatment

A

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
Q

Hepatic Encephalopathy Pathphys

A

Decreased hepatic function and portosystemic shunting leads to a decrease in ammonia detoxification. The excess ammonia crosses the BBB and exhibits CNS effects.

34
Q

Hepatic Encephalopathy Presentation

A
  • Altered mental status (e.g slow responses, coma)
  • Elevated ammonia levels (but does not correlate with mental status)
35
Q

Hepatic Encephalopathy Treatments (Names)

A
  1. Remove precipitating factors
  2. Protein
  3. Lactulose
  4. Rifaximin
36
Q

Hepatic Encephalopathy Treatment: Remove Precipitating Factors

A
  • Psychotropic medications (e.g. benzos, anti-seizure meds, bipolar meds)
  • Treat UTI (?)
37
Q

Hepatic Encephalopathy Treatment: Protein

A
  • Patients need protein (in catabolic state)
  • Use dairy/vegetable sources w/ branched amino acids → less likely to cross BBB
38
Q

Hepatic Encephalopathy Treatment: Lactulose

A
  • 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
Q

Hepatic Encephalopathy Treatment: Rifaximin

A
  • 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
Q

Hepatorenal Syndrome Pathophys

A

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
Q

Hepatorenal Syndrome Diagnosis

A
  • 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
Q

Hepatorenal Syndrome Treatment

A
  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
Q

PKPD Changes in Cirrhosis: Decreased Liver Blood Flow

A
  • 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
Q

PKPD Changes in Cirrhosis: Loss of Hepatocyte Function

A
  • 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
Q

PKPD Changes in Cirrhosis: Decreased Albumin Production

A
  • Heavily protein bound drugs will have higher free concentrations (therefore higher therapeutic effect)
  1. Phenytoin: reduce dose if needed
46
Q

PKPD Changes in Cirrhosis: Reduced Renal Function Due to Increased SCr

A
  • Decreased renal perfusion possible
  • Hepatorenal syndrome possible
  • Monitor renal function
47
Q

PKPD Changes in Cirrhosis: Increased Therapeutic Response

A
  • 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

PHM 604 GI (4 decks)

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