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Clinical 2 (Part B) > 19 - Cirrhosis > Flashcards

19 - Cirrhosis Flashcards

1
Q

What does cirrhosis mean?

A

tawny, yellow/orange colour of diseased liver

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2
Q

Top 2 causes in western world

A
  • chronic alcohol abuse

- chronic hepatitis C

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3
Q

Less common causes of cirrhosis

A
  • nonalcoholic steatohepatitis (NASH)
  • chronic hepatitis B
  • medications (isoniazid, amiodarone, methotrexate)
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4
Q

Where does liver receive blood from?

A

hepatic artery and portal vein

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5
Q

Chronic liver disease can lead to liver scarring and cause ?

A

hepatic fibrosis

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6
Q

Cirrhosis causes blood flow to be _____

A

altered

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7
Q

Complications from cirrhosis

A
  • portal hypertension
  • esophageal and gastric varies with risk of variceal bleeding
  • ascites
  • spontaneous bacterial peritonitis (SBP)
  • hepatic encephalopathy
  • other: includes hepatorenal syndrome, hepatopulmonary syndrome
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8
Q

What is portal hypertension?

A
  • increased blood pressure in the portal venous system

- hepatic venous pressure gradient (HVPG) > 5 mmgHg

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9
Q

What are 2 reasons why portal hypertension develops?

A

1) Scarring of liver causes mechanical obstruction of blood flow from portal vein to liver
2) Splanchnic (GI) arterial vasodilation and decreased response to vasoconstrictors increases blood flow to portal vein

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10
Q

What are varices?

A
  • Portal hypertension with HVPG > 10 mmHG lead to esophageal and gastric varies
  • Small veins in the lower esophagus and stomach become distended as blood is redirected
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11
Q

What is ascites?

A
  • Portal hypertension can lead to a cascade of events resulting in ascites - accumulation of fluid in the peritoneal cavity
  • Sodium retention, low serum albumin (decreased oncotic pressure), fluid leaks into peritoneal cavity
  • Within 10 years, about half of all patients with cirrhosis develop ascites, and half of those patients die within 2 years
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12
Q

What is spontaneous bacterial peritonitis? (SBP)

A
  • infection of ascitic fluid without an obvious surgically treatable source
  • bacteria from GI tract end up in ascitic fluid
  • exact mechanism has not been definitely elucidated (bacterial translocation? hematogenous transmission?)
  • E. Coli, K. Pneumoniae, and pneumococci are most commonly isolated
  • High mortality rate (<50% survival 1 year after 1st episode)
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13
Q

What is hepatic encephalopathy?

A
  • Decreased liver function causes neurotoxins to accumulate, affects brain function
  • Most commonly implicated: ammonia - increased levels in arterial blood due to decreased liver function, shunting of blood around liver
  • Ammonia believed to play key role as attempting to lower levels improves HE, y et blood levels do not correlate with mental status
  • Glutamine and endogenous benzodiazepines are among other substances that may play a role
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14
Q

____ is the most accurate way to confirm cirrhosis, but usually not necessary.

A

Biopsy

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15
Q

Biopsy is not necessary, can usually diagnose from ??

A

1) signs and symptoms

2) lab values/abnormal endoscopy/abnormal radiographic tests

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16
Q

Symptoms of cirrhosis?

A
  • weight loss
  • fatigue
  • anorexia
  • jaundice
  • impotence/decreased libido in men
  • abdominal distension
  • confusion/mental status changes
  • pruritis
  • GI bleeding
  • dark coloured urine (due to increased levels of bilirubin)
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17
Q

What signs on a physical exam would you see?

A
  • Hepatomegaly
  • Splenomegaly
  • Spider angiomata
  • Caput medusa
  • Digital clubbing
  • Gynecomastia and testicular atrophy in men
  • Jaundice
  • Asterixis
  • Ascites
  • Fetor hepaticas
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18
Q

What are some lab value abnormalities in cirrhosis?

A
  • Moderately elevated aminotransferases (AST:ALT - 2:1 common in alcohol liver disease)
  • Elevated alkaline phosphatase (2-3 times normal) with concomitant GGT rise
  • Decreased serum albumin (test of liver function)
  • Prolonged prothrombin time and elevated INR (test of liver function)
  • Hyperbilirubinemia
  • Thrombocytopenia, leukopenia, anemia
  • Increased serum creatinine
  • Hyponatremia
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19
Q

What are some abnormal radiographic tests ?

A
  • Ultrasonography - can detect hepatic nodules and irregularities, ascites
  • CT or MRI - can detect hepatic nodules, ascites, varices
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20
Q

What are the two tools for grading severity of liver disease?

A

1) Cild-Pugh Classification:
- used for recommending drug dosage adjustments in liver failure
- considered bilirubin, albumin, degree of ascites, degree of encephalopathy, degree of prolongation of PT

2) Model for End-Stage Liver Disease Score (MELD Score):
- Used in the allocation of liver transplants
- Considers creatinine, bilirubin, and INR
- Predicts 3 month mortality
* how you decide if someone is eligible for liver transplant

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21
Q

Treatment?

A
  • Slow rate of progression, modify causative factors such as alcohol
  • Treat complications
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22
Q

What are complications that may arise?

A

1) Varices
2) Ascites
3) Spontaneous Bacterial Peritonitis
4) Hepatic Encephalopathy

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23
Q

What are the 2 aspects to treating varices caused by portal hypertension ?

A

i) Primary prophylaxis of varices
ii) Treatment of acute variceal bleeding
iii) Secondary prophylaxis of varies

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24
Q

Describe primary prophylaxis of varices:

-No varices?

A

No treatment

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25
Q

Describe primary prophylaxis of varices:

-Small varices with no risk factors?

A

No treatment

26
Q

Describe primary prophylaxis of varices:

-Small varices with risk factors for variceal hemorrhage (red wales, child-pugh score C) ?

A

Treat patient with nonselective beta-blocker

27
Q

Describe primary prophylaxis of varices:

-Medium to large varices with no bleeding?

A

Treat patients with nonselective beta blocker

OR

endoscopic variceal ligation

28
Q

What are some non-selective beta blockers?

A
  • Propranolol - start at 20 mg PO BID
  • Nadolol - start at 20 mg PO daily
  • Carvedilol - start at 6.25 mg PO BID

-Titrate as tolerated - q3days to heart rate 55-60 ppm continue indefinitely except in ESLD

29
Q

Mechanism of non-selective beta blockers ?

A

decrease portal venous inflow by decreasing cardiac output (beta-1) and by decreasing splanchnic blood flow (beta-2)

which decreases build up of blood into the varices

30
Q

Describe treatment of acute variceal bleeding.

A
  • Medical emergency (15-20% mortality)
  • Need to maintain blood pressure with fluids, control/correct bleeding (RBCs, platelets as needed)
  • Octreotide
  • EVL in conjunction (band varices and then they fall off)
  • Prophylaxis for SBP - up to 7 days ciprofloxacin or ceftriaxone
  • If still bleeding with Octreotide and EVL, transjugular intrahepatic portosystemic shunt (TIPS)
31
Q

Dosing and MOA of Octreotide

A

ASAP - 50 mcg IV x 1, then 50 mcg/hr IV continuous infusion x 3-5 days (inhibits vasodilatory glucagon and has local splanchnic vasoconstrive effect)

32
Q

Why do we do secondary prophylaxis of varices ?

A

Why? More than half of patient re-bleed (even higher mortality rate with re-bleeding).

33
Q

What is Tx for secondary prophylaxis of varices ?

A

nonselective beta-blocker (propranolol or nadolol) + chronic EVL

34
Q

Secondary prophylaxis of varices:

If patient previously had ____, then possible liver transplant candidate.

A

TIPS

35
Q

Treatment of ascites:

With new onset ascites, need a ____

A

diagnosis

36
Q

Treatment of ascites:

What is diagnostic paracentesis?

A

measure cell count with differential, ascitic fluid total protein, ascitic fluid cultures

37
Q

Treatment of ascites:

What is SAAG ?

A

serum-ascites albumin gradient

SAAG = [serum albumin] - [ascitic fluid albumin] (measure both on same day)

38
Q

Treatment of ascites:

What level of SAAG is accurate for diagnosing ascites from portal hypertension?

A

SAAG > 11g/L is 97% accurate for diagnosing ascites from portal hypertension

39
Q

Treatment of ascites:

What is the medication Tx?

A
  • diuresis
  • sodium restriction to 2g/day

(fluid restriction usually not necessary unless sodium < 120 mmol/L)

40
Q

Treatment of ascites:

What diuretics do you use?
What ratio?

A

Furosemide (loop diuretic)
+
Spironolactone (K+ sparing diuretic)

in a 40mg:100mg ratio to maintain normokalemia

41
Q

Treatment of ascites:

How do you titrate the diuretics (furosemide + spironolactone)?

Max dose ?

A

Titrate diuretics up every 3-5 days for goal of 0.5 kg weight loss daily (max dose 160 mg furosemide: 400mg spironolactone)

42
Q

Treatment of ascites:

What do we monitor for with diuretics?

A

electrolytes (K+) and sCr

43
Q

Treatment of ascites:

How do we treat ascites refractor to diuretics?

A

therapeutic paracentesis (can sometimes drain well over 5 L)

44
Q

Treatment of ascites:

What medications should you avoid?

A

avoid NSAIDs, generally avoid ACEi/ARBs

  • NSAIDs can cause fluid retention
  • ACEi/ARB associated with increased mortality in cirrhosis
45
Q

Treatment of ascites:

Can also use ____ _____ for varies, weight risk to benefit in refractory ascites

A

beta blockers

46
Q

Presentation of SBP (spontaneous bacterial peritonitis)

A

-may be asymptomatic, but often presents with one or more of fever, abdominal pain, encephalopathy, confusion, renal failure

47
Q

How is SBP (spontaneous bacterial peritonitis) diagnosed?

A

polymorphonuclear leukocyte (PMN) > 250 cells/mm^3 and positive ascitic fluid bacterial cultures

48
Q

When do we treat SBP (spontaneous bacterial peritonitis) empirically?

A

if PMNs > 250 or if signs/symptoms of infection

49
Q

What do we use to treat SBP (spontaneous bacterial peritonitis)?

A
  • Broad spectrum antibiotics to cover E. coli, K. pneumoniae, and pneumococci
  • 3rd gen cephalosporin preferred (cefotaxime 2g IV q8h)
  • quinolone is second line (ciprofloxacin)
50
Q

How long do we treat SBP (spontaneous bacterial peritonitis) ?

A

5 day Tx course (10 days usually not necessary)

51
Q

Following episode of SBP, give long-term prophylaxis with ?

A

-quinolone
OR
-sulfa-trim

(lower dose than standard dose)
-can be once daily, 5 days/week, or weekly dosing

52
Q

How can hepatic encephalopathy present?

A
  • acutely (episodic)
  • continually (persistent)
  • recurring (more than 1 episode < 6 months apart)
53
Q

What are precipitating factors for hepatic encephalopathy?

A
  • electrolyte abnormalities (dehydration, diuretic overuse)
  • infection
  • GI bleeding
  • constipation
54
Q

What is the mainstay of therapy in treating hepatic encephalopathy?

A

reduce ammonia levels

55
Q

List 3 treatments for hepatic encephalopathy

A
  • Lactulose
  • Rifaximin
  • Neomycin/metronidazole
56
Q

Describe Lactulose route of administration for treating hepatic encephalopathy

A
  • can give orally (typically 15-30mL/dose), nasogastrically, or rectally
  • prefer PO/NG (PR inconvenient - 300mL lactulose qs to 1L with H20, retain 1hr)
57
Q

Describe lactulose metabolism and MOA for treating hepatic encephalopathy

A
  • metabolized to acetic acid and lactic acid
  • lowers ammonia by more than one mechanism, including: laxative effect = less time for systemic ammonia absorption from gut, decreased pH leaves NH4+ cations “trapped” in acidified colon
58
Q

How do you give lactulose to treat hepatic encephalopathy?

A

Acutely can give q1h to initiate laxative effect, then titrate for approx 3 soft stools daily.

Monitor for improved mental status

59
Q

Describe Rifaxamin for treating hepatic encephalopathy

A
  • poorly absorbed synthetic antibiotic
  • believed to reduce ammonia-producing bacteria in the gut
  • Rifaximin 550 mg PO BID
  • Part 3 EDS in Manitoba ($1000+ monthly in 2018) - use in conjunction with lactulose in overt recurrent HE not responding to maximum tolerated doses of lactulose alone
60
Q

Describe neomycin/metronidazole for treatment of hepatic encephalopathy

A

not commonly used anymore, higher risk of side effects (neomycin - ototoxicity, nephrotoxicity; metronidazole - neurotoxicity)

Clinical 2 (Part B) (30 decks)

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