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Cirrhosis TBL Flashcards

1
Q

What is cirrhosis?

A
  • a late stage of progressive liver disease in which there is distortion of hepatic architecture
  • Diffuse formation of regenerative nodules that lack normal organization
  • These nodules are surrounded by fibrous bands
  • Leads to inability of the liver to function properly (synthetically, hemodynamically)
  • In general, thought to be irreversible
  • Rarely, there can be regression of fibrosis- scar tissue can become thinner and eventually fragment
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2
Q

How long does it typically take to develop cirrhosis?

A

5-50 years

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3
Q

What occurs in cirrhosis?

A 
collagen deposition in space of Disse
activation of hepatic stellate cells
constriction of sinusoids
defenestration of sinusoids
Distorted sinusoidal architecture leads to increased resistance
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4
Q

What is portal hypertension?

A
  • A pathologic increase in the pressure of the portal system due to increased resistance to portal blood flow
  • Most commonly due to intrinsic liver disease but can be due to other causes
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5
Q

What are some causes of posthepatic portal hypertension?

A 
Budd-Chiari syndrome
Constrictive pericarditis
Inferior vena caval obstruction
Right-sided heart failure
Sever tricuspid regurg
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6
Q

What are some causes of intrahepatic portal hypertension?

A 
Primary biliary cirrhosis (intrahepatic)
Sarcoidosis (intrahepatic)
Schistosomiasis
Alcoholic cirrhosis (sinusoidal)
Alcoholic hepatitis (sinusoidal)
Cryptogenic cirrhosis
Postnecrotic cirrhosis
Sinusoidal obstruction syndrome (postsinusoidal)
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7
Q

What are some causes of prehaptic portal hypertension?

A

Portal vein thrombosis

Splenic vein thrombosis

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8
Q

What is the hepatic venous pressure gradient?

A

• We can measure the degree of portal hypertension by calculating the HVPG
• HVPG= Wedged HV Pressure- Free HV Pressure (mmHg)
– Normal= 3-5mmHg
– 5+ mmHg= Portal Hypertension
– 10+ mmHg= varices form
– 12+ mmHg= varices bleed

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9
Q

What are common complications of cirrhosis and portal hypertension?

A 
Encephalopathy
Ascites
Synthetic dysfunction (hypoalbuminemia, coagulopathy, hyperbilirubinemia, thrombocytopenia)
HCC
variceal bleed
hepatorenal syndrome
HPS
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10
Q

What is ascites?

A

• Ascites is defined as the pathologic
accumulation of fluid in the peritoneal cavity
• It is the most common complication of
cirrhosis
• Ascites is often the first clinical
decompensation to occur in cirrhotics
• Ascites is he most common complication of cirrhosis that leads to hospitalization

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11
Q

What is the pathophys of Ascites?

A
  1. Cirrhosis and Portal HTN
  2. Splanchnic and systemic vasodilation
  3. Decreased effective arterial volume
  4. Activation of neurohumeral systems
    - RAAS
    - SNS
  5. Sodium and water retention
  6. ”leaky” capillaries
    (alteration in pressures and permeability)
  7. Ascites
    Also caused by overwhelmed lymphatic system and altered Starling forces
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12
Q

What is the serum-ascites albumin gradient?

A

Serum albumin - ascitic albumin
Is considered high if 1.1+ g/dL
If high, then due to portal hypertension (cirrhosis, alcoholic hep, cardiac dz, massive liver mets, hepatic outflow obstruction, portal vein thrombosis)
If low, then NOT due to portal hypertension (peritoneal carcinoma, TB, pancreatic duct leak, biliary leak, nephrotic syndrome, serositis)

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13
Q

What are some complications of ascites?

A

Umbilical hernia
Tense ascites
Infection
Hepatic hydrothorax

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14
Q

What are the common causes of spontaneous bacteria peritonitis?

A

E. coli, Klebsiella, S. pneumo

PMN count 250+

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15
Q

How should ascites be managed?

A 
Salt restriction
Diuretics
Large volume paracentesis
Transjugular intrahepatic portosystemic shunt
Liver transplantation
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16
Q

What are varices?

A

Abnormal dilated veins seen in the setting of portal HTN
Prevalence correlates with severity liver disease
Variceal hemorrhage occurs 5- 10% yearly
Predictors of bleeding include size of varices, decompensated cirrhosis, presence of red wale signs
They often progressively increase in size

17
Q

How do you treat variceal bleeding?

A 
Hemodynamic
– Volume resuscitation (PRBCs)
– Correct coagulopathy
Pharmacologic
– Antibiotics
• High rate of infection
• Reduction in rebleeding
• Mortality benefit
– Octreotide (somatostatin analogue)
• Reduction in portal pressure
• Reduction in rebleeding rates
Endoscopic
– Esophageal band ligation
18
Q

How can you prevent a variceal rebleed?

A

– Repeat band ligation until eradication of varices
– Non-selective beta blocker
• i.e. Nadolol or Propanolol
• NSBBs reduce portal pressures through β-1 (decreased CO) and β-2 (splanchnic vasoconstriction) effects

19
Q

What is a transjugular intrahepatic portosystemic shunt?

A

like a cardiac stent
divert from high pressure portal vein system
bore hole through liver; portal vein is congested with blood, want blood out of the portal system

20
Q

What is hepatic encephalopathy?

A

• A reversible neuropsychiatric syndrome seen in patients with advanced liver disease
• Symptoms range from mild cognitive
impairment to coma
• Excess ammonia- key mediator

21
Q

Why do you see problems with ammonia in liver failure?

A 
• Liver
– Hepatocyte loss and porto-systemic
shunting (bypassing liver)
– Reduced capacity to detoxify ammonia
• Kidney
– Reduced ability of kidney to excrete
urea
– Increased ammonia production in
kidney
• Skeletal muscle
– increased breakdown of muscle and
increased production of glutamine
– Converted back to ammonia and
glutamate
• Gut
– Increased glutaminase activity (4-fold)
which results in shunting of glutamine
back to ammonia and glutamate
22
Q

What is the net effect of liver failure on ammonia metabolism?

A 
– Increased Production in gut from oral intake
– Impaired excretion by kidney
– Impaired breakdown by skeletal muscle
– Impaired breakdown by liver
• Excess ammonia taken up by brain astrocytes
– NH3+ glutamateàglutamine
– Osmotically activeàastrocyte swelling
– Alteration in neurotransmitters
23
Q

What can contribute to the precipitation of hepatic encephalopathy?

A 
Excess protein (?)
TIPS
Infection
GI bleed
Sedatives/hypnotics (hold on to them for much longer)
Diuretics
Zotemia
24
Q

How do you treat encephalopathy?

A

Lactulose

Rifaximin (antiboitic that combats bacteria responsible for ammonia production in the gut)

25
Q

Why does lactulose work on encephalopathy?

A
  • In the colon, lactulose is broken down into lactic acid and acetic acid, resulting in a lower colonic pH
  • Excess H+ Binds NH3 in gut and converts to NH4 which is not freely diffused back into blood stream
  • Ammonium ions NH4 are excreted
26
Q

What is hepatorenal syndrome?

A

• The rapid development of kidney failure inpatients with cirrhosis and portal
hypertension or in those with acute liver
failure
• Precipitated by a sudden insult such as aninfection, bleeding in the gastrointestinal
tract, or overuse of diuretic medications
• Extremely fatal

27
Q

What is the pathophys of hepatorenal syndrome?

A
  1. Splanchnic vasodilitation leads to reduced effective arterial volume
  2. Activation sympathetic NS and RAA system
  3. Impairment in compensatory increase in CO by cirrhotic cardiomyopathy
  4. Increased vasoactive mediators (NO, endothelin-1, leukotrienes, etc.)
  5. Net effect = splanchnic vasodilation and renal arterial vasocontriction
    NOTE: kidney is not the actual problem
28
Q

How is hepatorenal syndrome treated?

A 
Albumin 25%
• Volume expander
• 1g/kg day 1 followed by 20-40g/day
Octreotide
• Somatostatin analogue
• Inhibits endogenous vasodilator release
• 100-200 μg subcutaneously TID
Midodrine
• Selective alpha-1 adrenergic agonist
• Systemic vasoconstrictor
• 7.5-12.5 mg PO TID
29
Q

What is hepatopulmonary syndrome?

A

A syndrome of pathogenic intrapulmonary vasodilatation and impaired arterial
oxygenation. Seen in the setting of liver disease
• manifests as decreased arterial oxygenation
• Hypoxemia and increased A-a gradient
• Increase Nitric Oxide is thought to underlie the pathophysiology

30
Q

What is portopulmonary hypertension?

A

• elevated mean pulmonary artery pressure secondary to an increased pulmonary vascular resistance
• Occurs in the setting of portal hypertension
- Imbalance between vasodilating and
vasoconstricting molecules
- Systemic vasodilation but pulmonary
vasoconstriction

31
Q

What is the Child Turcotte Pugh Score?

A

Way to grade liver dz

Points for encephalopathy, ascites, bilirubin, albumin, PT

GI (3 decks)

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