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Liver Flashcards

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1
Q

What is hepatic failure?

A

A condition where the liver fails to perform its normal functions, leading to a buildup of toxins in the body.

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2
Q

What is the portal vein composed of?

A

The portal vein is formed by the splenic vein and the superior mesenteric vein.

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3
Q

What percentage of hepatic blood flow (HBF) does the portal vein supply?

A

75% of HBF.

(But only 50% of the oxygen requirement)

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4
Q

What is the significance of the hepatic artery in relation to the portal vein?

A

The hepatic artery supplies oxygen to the liver parenchyma and joins the portal vein in the sinusoids.

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5
Q

What clinical signs indicate portal hypertension?

A

Ascites, splenomegaly, and caput medusae, and dilated periumbilical veins

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6
Q

What does asterixis refer to?

A

A movement disorder characterized by jerky motion of hands with wrist extension.

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7
Q

What are some metabolic causes of altered mental status in patients with ESLD?

A
  • Hyponatremia
  • Hypoglycemia
  • Hypothermia
  • Hepatic encephalopathy (HE)
  • Delirium tremens (DTs)
  • Postictal state
  • Wernicke’s encephalopathy
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8
Q

What diagnostic steps should be taken for a postictal ESLD patient with altered mental status?

A

Check Na+/Glucose levels, treat with thiamine and glucose, and conduct routine lab exams.

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9
Q

What are some nonspecific therapeutic steps for a postictal ESLD patient?

A

If not associated with ETOH withdrawal then:

  • Anticonvulsants without major CNS sedative properties
  • Phenytoin
  • Levetiracetam
  • Topiramate
  • Valproic Acid
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10
Q

What is the definition of portal hypertension?

A

An elevated portal venous perfusion pressure (PVPP) > 5 Torr.

PVPP=PVP-HVP >10 torr is “significant”

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11
Q

What are the primary causes of portal hypertension?

A

Increased portal venous resistance from these three sources!

  • Prehepatic (portal or splenic vein thrombosis)
  • Intrahepatic (cirrhosis)
  • Posthepatic (Budd-Chiari syndrome)
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12
Q

How does portal hypertension cause ascites?

A

Through splanchnic arteriolar vasodilation and activation of the RAAS system.

HRS- think renal vasoconstriction and hypoalbuminemia

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13
Q

What is the common mechanism for acute pharmacologic treatment of portal hypertension?

A

Decrease portal venous flow (PVF) via increased splanchnic arteriolar resistance.

Ie. Vasopressin and octreotide (mimics somatostatin)

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14
Q

What are the major clinical sequelae of portal hypertension?

A
  • Esophageal varices
  • Hepatic encephalopathy
  • Splenomegaly
  • Ascites
  • Hepatorenal syndrome (HRS)
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15
Q

What is the common mechanism for chronic pharmacologic treatment of portal hypertension?

A

Decrease PVF via increased splanchnic arteriolar resistance using nonselective beta-blockers.
-propranolol and carvedilol

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16
Q

What does a serum-to-ascites albumin concentration difference > 1.1 g/dL imply?

A

It is likely indicative of portal hypertension.

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17
Q

What findings on a non-contrast head CT are indicative of severe hepatic encephalopathy?

A

Diffuse cortical edema and poor differentiation of white and gray matter.

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18
Q

What is the role of vasopressin and octreotide in the treatment of portal hypertension?

A

They increase splanchnic vasoconstriction acutely.

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19
Q

What is the significance of a paracentesis result showing clear pink fluid with low WBC?

A

Spontaneous bacterial peritonitis (SBP) is unlikely.

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20
Q

What is the expected change in bicarbonate for acute respiratory acidosis?

A

(0.1)* change in PaCO2

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21
Q

What does the presence of ascites indicate in a patient with ESLD?

A

Fluid retention due to splanchnic vasodilation and activation of the RAAS system.

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22
Q

What is splanchnic vasodilation associated with in the context of renal artery vasoconstriction?

A

Hypoalbuminemia

This process leads to prerenal azotemia.

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23
Q

What are the CV-Pulmonary manifestations of ESLD?

A
  • Dilated Cardiomyopathy (ETOH related)
  • High Output Cardiac Failure
  • Portopulmonary Hypertension
  • Hepatopulmonary Syndrome
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24
Q

Define high output cardiac failure (HOHF).

A

Failure of the heart to meet body’s metabolic demands with resting cardiac index > 4.0 L/min/m²

Characterized by low systemic vascular resistance (SVR) or increased metabolic demand.

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25
What are the characteristics of low SVR in high output heart failure?
* Arteriolar vasodilation * Decreased systemic vascular resistance * Increased cardiac output
26
What are the consequences of decreased systemic vascular resistance?
* Decreased renal perfusion pressure * Chronic RAAS activation * Cardiac remodeling and hypertrophy
27
What conditions are included in the differential diagnosis of high output heart failure due to low systemic vascular resistance?
* AV Fistulae . * Mechanical causes * Liver Failure * Pregnancy * Paget’s Disease * Sepsis * Thiamine Deficiency (Beriberi) * Carcinoid Syndrome
28
What conditions are included in the differential diagnosis of high output heart failure due to increased metabolic demand?
* Severe anemia * Thyrotoxicosis * Myeloproliferative Disorders * Sepsis with fever
29
What is Portopulmonary Hypertension (PPH)?
Pulmonary hypertension (mean pulmonary artery pressure > 20 mm Hg) due to ESLD ## Footnote It results in hypoxemia and right heart failure.
30
What is the pathogenesis of Portopulmonary Hypertension?
Vascular remodeling due to smooth muscle proliferation after recurrent microthrombi in pulmonary arteries
31
What is the importance of distinguishing elevated pulmonary artery pressure due to high cardiac output versus elevated pulmonary vascular resistance?
It is crucial for liver transplantation eligibility ## Footnote Elevated pulmonary artery pressure > 45-50 Torr is a relative exclusion criterion.
32
What are the consequences of Portopulmonary Hypertension?
* Hypoxemia due to V/Q mismatch * Right heart failure
33
What characterizes Hepatopulmonary Syndrome (HPS)?
Intrapulmonary AV shunting via dilated pulmonary capillaries at lung bases leading to hypoxemia ## Footnote It is associated with elevated Aa gradient on arterial blood gas analysis.
34
How is Hepatopulmonary Syndrome diagnosed?
Often diagnosis of exclusion* Increased Aa gradient > 15 mm Hg with evidence of pulmonary vascular shunting on contrast echocardiography
35
What is the typical symptom complex associated with Hepatopulmonary Syndrome?
Platypnea and orthodeoxia ## Footnote Symptoms improve when lying down.
36
What is a common precipitating cause of Hepatic Encephalopathy (HE)?
* Increased nitrogen loads (GI bleed, dietary changes) - Narcotics (lengthen bowel transit) -Sepsis (SBP) - Diuresis *diuresis *TIPs
37
How does ammonia (NH3) metabolism relate to Hepatic Encephalopathy?
In liver failure, NH3 is not converted to glutamine, leading to increased systemic circulation and CNS effects. -astrocytes then convert it to glutamine in CNS leading to cerebral edema
38
What is the proper management of Hepatic Encephalopathy?
* Supportive care * Treat underlying cause * Lactulose * Oral non-absorbable antibiotics (Neomycin or Rifaximin)
39
What are the rules for correcting hyponatremia?
* Use 3% saline for symptomatic patients * Use 0.9% saline for asymptomatic patients * Correct at a rate of < 8 mmol/L/day for chronic cases
40
How do you calculate the sodium deficit for correcting hyponatremia?
Sodium deficit = [desired Na - current Na] x total body water (TBW) ## Footnote TBW is calculated as 0.6 times the weight in kg.
41
What should be the IV rate of infusion for correcting sodium deficit?
Volume (ml) of solution / Time (hours) ## Footnote This is determined by the desired rate of sodium correction.
42
What are the risks associated with too rapid correction of hyponatremia?
Osmotic demyelination syndrome (ODS) ## Footnote Risks are higher in patients with chronic alcoholism and malnutrition.
43
What is a common symptom of Hepatopulmonary Syndrome?
Shortness of breath when sitting up (platypnea) ## Footnote Symptoms improve when the patient is supine.
44
What is the significance of cerebral edema in the management of hyponatremia?
It may necessitate the use of hypertonic saline (3%) for correction.
45
What is the differential diagnosis of altered mental status in patients with ESLD?
* Metabolic * Hyponatremia * Hypoglycemia * Hypothermia * Hepatic Encephalopathy (HE) * Delirium Tremens (DTs) * Postictal State * Wernicke’s Encephalopathy * Drugs * Infection * Structural – CNS Injury (including Hypoxemia)
46
How do you manage a postictal patient with altered mental status?
* Check Na+/Glucose (FSG) * Treat with thiamine 100 mg IV, then glucose 1 amp of D50 * Perform exam and routine lab (CBC, BMP, CXR) * CT (non-contrast) if focal neuro finding; consider LP * If not associated with ETOH withdrawal, use anticonvulsant without major CNS sedative properties
47
What is the treatment for spontaneous bacterial peritonitis (SBP)?
Cefotaxime: 2g loading dose; adjust maintenance dose for renal failure
48
What is the significance of a serum-to-ascites albumin concentration difference greater than 1.1 g/dL?
It suggests portal hypertension
49
What is the incidence of Hepatorenal Syndrome (HRS)?
AKI in the setting of cirrhosis; constitutes < 25% cases of AKI with end-stage liver disease
50
What are the criteria for diagnosing HRS?
* Should NOT be made with evidence of structural kidney issues * Made only after adequate volume resuscitation with albumin * FE Na << 1 * Minimal or no proteinuria * Normal urinary sediment
51
What is the prevention strategy for HRS?
Treat SBP early with IV albumin at the time of diagnosis
52
What is the recommended treatment for critically ill patients with HRS?
* Norepinephrine or vasopressin * Terlipressin (vasopressin analogue) + albumin
53
What are the implications of a 12-hour urine output of 17 cc?
Indicates possible acute kidney injury and need for further evaluation
54
What is the significance of elevated ammonia levels in the context of liver disease?
Indicates hepatic dysfunction and potential for hepatic encephalopathy
55
What is the recommended fluid management for a patient with prerenal azotemia?
* Use IV fluids (colloid > crystalloid) * Monitor urine output
56
What should be considered if increasing respiratory distress is related to tense ascites?
Consider therapeutic paracentesis but plan on replacing lost volume with IV fluid
57
What is the initial treatment for a patient with suspected SBP?
Initiate antibiotic therapy with Cefotaxime
58
What complication can arise from therapeutic paracentesis in a patient with tense ascites?
Exacerbation of intravascular hypovolemia
59
What is the significance of a serum sodium level of 108 mEq/L?
It indicates severe hyponatremia, which can lead to neurological complications ## Footnote Severe hyponatremia requires urgent evaluation and treatment to prevent complications like seizures or coma.
60
What is the calculated osmolality formula?
2 [Na] + BUN/2.8 + glucose/18 ## Footnote This formula is used to estimate the serum osmolality based on sodium, BUN, and glucose levels.
61
What is the osmolar gap if the measured serum osmolality is 234 mOsm/kg and calculated osmolality is 225 mOsm/kg?
9 mOsm/kg ## Footnote An osmolar gap greater than 10 mOsm/kg may indicate the presence of unmeasured osmoles.
62
What is the management for a patient with CNS issues post-surgery?
Airway protection and treatment of hyponatremia ## Footnote Immediate management is critical to prevent complications from severe hyponatremia.
63
What therapy can correct chronic hyponatremia in liver failure patients?
Vasopressin 2 receptor antagonists like tolvaptan ## Footnote These medications help in managing hyponatremia by promoting free water excretion.
64
What is the formula to calculate sodium deficit?
TBW = .6 [weight in kg]; Na deficit = [desired Na – current Na] mmol/L x TBW ## Footnote This calculation helps in determining the amount of sodium needed to correct hyponatremia.
65
What should be used to correct acute hyponatremia in hypervolemic patients?
IV conivaptan ## Footnote Conivaptan is preferred for acute symptomatic hyponatremia, especially in cases of liver failure.
66
What does a serum-to-ascites albumin concentration difference greater than 1.1 indicate?
Likely portal hypertension ## Footnote This calculation helps differentiate between transudative and exudative ascites.
67
What is the clinical presentation of Delirium Tremens (DTs)?
Altered mental status, autonomic hyperactivity, hallucinations, seizures ## Footnote DTs occurs 2-10 days after the cessation of alcohol intake and is a medical emergency.
68
What is the treatment for Delirium Tremens?
Benzodiazepines and supportive therapy ## Footnote Benzodiazepines are the first-line treatment, and haloperidol may be added if necessary.
69
What characterizes Hepatorenal Syndrome (HRS)?
Decreased renal blood flow due to splanchnic vasodilation and renal vasoconstriction ## Footnote HRS presents with oliguric acute kidney injury in patients with end-stage liver disease.
70
What is the prevention strategy for Hepatorenal Syndrome?
Early aggressive treatment of underlying causes and albumin infusions ## Footnote Treating conditions like spontaneous bacterial peritonitis can help prevent HRS.
71
What is the significance of a urine sodium level of 45 mEq/L in the context of hyponatremia?
Indicates possible euvolemic or hypervolemic state ## Footnote Elevated urine sodium suggests that the kidneys are excreting sodium in response to volume overload.
72
Differential diagnosis for AMS in patient with ESLD
Metabolic Drugs Infection Structural- CNS injury (hypoxemia)
73
Differential for AMS in ESLD and Delayed anesthetic wake-up are similar What is added with delayed awakening from anesthesia?
NMBDs
74
Common neurological finding in hepatic encephalopathy work up
Diffuse cortical edema on CT -absence of sulcal markings -poor differentiation of white/gray matter
75
What is the serum ascites albumin concentration difference?
(Serum albumin)-(ascities albumin) >1.1g/dL portal hypertension likely <1.1 g/dL portal hypertension unlikely 97% predictive value
76
How do you measure Portal venous pressure?
Hepatic vein occlusion pressure
77
Ohms law in portal hypertension
V=IR PVP=PVF*PVR PVF=portal venous flow PVR=Portal venous resistance
78
Secondary cause of portal hypertension
increased PVF resulting from increased CO due to dilation of splanchnic arterioles with RAAS activation -think local increase of NO -this is target of pharmacological treatment of PH
79
HPS
Hepatopulmonary syndrome Basilar pulmonary AV fistula associated with ESLD causing hypoxemia related to V/Q mismatch (shunt)
80
81
Pathognomonic
Symptom specifically characteristic or indicative of a certain disease or condition
82
Why do we avoid mannitol in cerebral edema associated with hyponatremia?
Exacerbates hyponatremia
83
When can you not make the diagnosis of HRS?
Evidence of structural kidney issues- as manifest by proteinuria or hematuria -made after albumin resuscitation -normal sediment
84
Splanchnic
Organs of the abdominal cavity
85
Left shift of WBCs
Increase in immature white cells= infection
86

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