Module 7: Complication of Cirrhosis Flashcards

Dr. Covert EXAM VI

1
Q

Which factors are used to classify the stage of liver disease when using Child-Pugh?

A

-determines the severity of liver disease
-used for considerations in drug dosing

-Tbili, PT (prothrombin time), Albumin, Ascites, Encephalopathy

A: 5-6 points
B: 7-9 points
C: 10-15 points (severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Model of End-stage Liver disease (MELD)

A

-assess the 1-year mortality and
-assess the position on the transplant list

score
10-19: 6% mortality
20-29: 19.6%
30-39: 52.6%
>40: 71:3%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Maddrey Discriminate Function

(just know what it is for)

A

-help to decide if steroids are needed in EtOH-related liver disease

asses PT and Tbili
-if >32 -> poor prognosis, use steroids
-Prednisolone 40 mg PO daily x 4 weeks, then 2-week taper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes fluid accumulation in the peritoneal cavity?

A

-activated RAAS system:
sodium and fluid retention (in the blood vessels)

-reduction in albumin
decreased oncotic pressure in the blood vessel -> fluid shifts to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a Paracentesis?

A

-catheter instilled into the abdomen and the fluid is drained off

-some patients may have it acutely or chronically (depending on how quickly the fluid backs up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In patients who undergo Paracentesis, what should be administered to them?

A

if a large volume of removal (>5L paracentesis)
6-8g of 25% (25g/100ml) albumin /L removed

if more than 10L paracentesis ->
60-80g of 25% albumin / L removed

-there are also 5% (5g/100ml) products -> but 25% is better bc we want more albumin to restore the oncotic pressure and 5% would need more volume which they have more than enough!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which diuretics are used in Ascites management?

A

-Spironoalctone and furosemide
(ratio of 100 mg spironolactone: 40 mg furosemide)

-goal is to facilitate Na excretion, and maintain eukalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain the ratio between Spironolactone and furosemide

A

in ascites: spironolactone is ued as the diurtetic
whereas in HF patients it is used to mitigate the RAAS system

is furosemide not the stronger diuretic???

in patients with hyperkalemia use a higher dose of furosemide than spironolactone (since K sparing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which electrolytes should be restricted to cirrhosis patients with Ascites?

A

-Sodium (Na+) restricted: <2g/day
-fluid restricted: <1L/day, only if severe hyponatremia (<125 mmol/L)

Vaptans (tolvaptan, conivaptan) improve Na but not outcomes
ADR: hepatotoxicity -> so not often used
short-term (<30 day) use only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are Vaptans often not used in patients with Ascites?

A

-they are often hypotonic hypervolemic hyponatremia -> sodium and fluid restriction works best

-Vaptans provide aquaresis -> excretion of water without electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes Encephalopathy in patients with cirrhosis?

A

-accumulation of nitrogenous substances
-Hyperammonemia (bc the liver can’t eliminate it)
-cause CNS toxicity (altered mental status)

-treat only symptomatic patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who should be treated with Hepatic Encephalopathy prophylaxis?

A

-high-risk patients
-patients with a history of encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is hepatic Encephalopathy treated?

A

-Lactulose:
*MOA: traps ammonia from the blood to the gut (converts it to ammonium, charged), kills bacteria, and osmotically removes ammonia from the body with the stool

*titrate to 2-3 loose bowel movements per day, not to a dose

-Rifaximin
*adjunctive to Lactulose, avoid monotherapy
it has only 1 MOA, whereas Lactulose has 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Esophageal varices

A

-varices are small blood vessels around the esophagus (where it connects to the stomach)

-they develop to to reduce pressure in severe portal hypertension -> blood flows through this vessels to relieve pressure

-these vessels are fragile and may burst (upper GI bleeding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Who is indicated to receive therapy for Esophageal varices?

A

-varices > 5 mm - need endoscopy to assess
treat with medication or endoscopic variceal ligation (EVL)

-varices < 5mm + increased risk of bleeding
Child pugh B or C

-acute hemorrhage (variceal bleed)
patients vomit blood, hemodynamically unstable, anemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are Primary prevention therapy options in Esophageal varices?

A

Non-selective BB: Propanolol, Nadolol, Carvedilol

-if they can’t tolerate BB or other reasons to not start BB (severe COPD?) -> endoscopic variceal ligation (EVL) every 2-8 weeks
-> esophagogastroduodenoscopy (EDG) 3-6 months after EVL, then every 6-12 months

17
Q

What is the goal BP when treating patients with BB in esophageal varices?

A

SBP >90 mmHg
HR: 55-60 bpm

18
Q

Endoscopic Variceal Ligation (EVL) vs Sclerotherapy

A

-EVL: putting a band over the varices

-Sclerotherapy: injecting a sclerosing agent into variceal lumen

19
Q

Treatment options in variceal hemorrhage?

A

variceal is bleeding (different from varices that are identified but do not bleed)

-Blood transfusion/ volume resuscitation
-Control acute bleeding and prevent re-bleed (drugs or endoscopy)
-Prophylaxis for spontaneous bacterial peritonitis (SBP)

20
Q

Drugs used to stop variceal bleeding

A

-after volume resuscitation and giving blood
-prevent worsening of the bleed

-Octreotide: selective vasoconstriction of varices
50 mcg IV bolus
50 mcg/h continuous infusion for 2-5 days

also Vasopressin, Somatostatin, Terlipressin

21
Q

Other treatment options in variceal bleeds

A

-Transjugular Intrahepatic Portosystemic Shunt
(TIPS)
*a placed stent between portal and hepatic vein, no pharmacologic need for secondary treatment

-Balloon Occluded Retrograde Transvenous Obliteration (BRTO)
balloon applies pressure to the bleeding varices

22
Q

What are the treatment options for secondary prevention?

A

for life-time

-Propanolol: twice a day
20-40 mg PO BID
max (no ascites): 320 mg PO daily
max (w/ ascites): 160 mg PO daily

-Nadolol
20-40 mg PO daily
max (no ascites): 160 mg PO daily
max (ascites): 60 mg PO daily

-EVL: every 1-4 weeks until variceal eradication

-Prophylaxis for spontaneous bacterial peritonitis (SBP) X 7 days

23
Q

Which organism may cause Spontaneous bacterial peritonitis (SBP)

A

-Infection of ascitic fluid:
Klebsiella pneumonia, E. coli, S. pneumo

-develops in 10-20% of patients with ascites

24
Q

How is SBP diagnosed?

A

-assess polymorphonuclear leukocytes (PMNs, immature white blood cells) after Paracentesis in ascitic fluid -> treat if > 250

-treat when SBP s/sx are seen: fever, abdominal pain, high WBC, AKI, acidosis, encephalopathy

25
Q

When to use SBP prophylaxis (prevention)?

A

-prophylaxis (prevention), not treatment

-in patients with Variceal bleed
Ceftriaxone 1g IV daily X 7 days
Ciprofloxacin 750 mg PO daily or 400 mg IV BID X 7 days

-in survivors of SBP (life-long prophylaxis, high risk of reinfection)
Ciprofloxacin 500 mg PO daily
Bactrim 1 DS tab PO daily

26
Q

Treatment of SBP

A

cover Klebsiella pneumo, E. coli, Strep pneumo

-Cefotaxime (or Ceftriaxone) 2 g IV Q 8h, Ceftriaxone 2 g IV daily X 7 days

-consider covering MRSA and Pseudomonas if the patient with healthcare-associated SBP

-25% albumin: greater benefit in patients with AKI and jaundice
1.5g/kg on day 1
1g/kg on day 3

27
Q

When does albumin have a great benefit when treating SBP?

A

patients with AKI and jaundice

28
Q

Pathophysiology of Hepatorenal Syndrome

A

-Portal HTN -> splanchnic (organs of the abdomen) vasodilation -> lowering circulation volume, causing hypotension

-due to hypotension -> activation of the RAAS system

RAAS causes sodium retention (Ascites)
RAAS causes vasoconstriction (Hepatorenal syndrome)

29
Q

How is Hepatorenal Syndrome diagnosed?

A

-Cirrhosis + ascites
-increase in SCr >/= 0.3 from baseline with 48h or more than 50% increase in 7 days

-no response after 2 days of diuretics (due to ascites) being stopped and albumin (1g/kg) infusion

-no shock
-no nephrotoxic meds
-no structural kidney disease

30
Q

Hepatorenal Syndrome Treatment

EXAM

A

-ultimately liver transplant (mortality w/o a transplant is 50-70%)

  1. Albumin + diuretic withdrawal
    -Albumin 25%: 1 g/kg/day (max of 100 g/ day) on day 1, then 40-50 g/day while on vasoconstrictor
    if no response add Vasoconstrictor

-Vasoconstrictors: treats splanchnic vasodilation -> increase circulating volume -> (-) RAAS
Terlipressin (Newly FDA-approved)
Norepinephrine
Octreotide + Midodrine (less effective)

If no response after 7 days, may discontinue therapy
If response, continue for up to 14 days