Liver Systemic Effects & Diseases Flashcards

1
Q

What are the Cardiovascular Effects of Liver Dysfunction?

A

Hyperdynamic circulatory state.
-Unable to get rid of toxins, so they act as endogenous vasodilators (think sepsis)
-Inc CO, dec SVR, dec ABP
-Decreased blood viscosity
-Can lead to cardiomyopathy/CHF

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2
Q

How is Anemia caused by Liver Dysfunction?

A

Anemia is common in advanced hepatic disease.
-Hemolysis, folate deficiency, hemorrhage, or bone marrow suppression can occur.

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3
Q

How does Congestive Splenomegaly occur?

A

Obstruction of blood flow causes portal hypertension. Blood backs up to the spleen, causing congestive splenomegaly.
-Leads to platelet sequestration and thrombocytopenia
-Also causes Leukopenia

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4
Q

How is clotting affected with Liver Disease?

A

-Clotting factors are deficient
-Decreased clearance of fibrinolytic factors (increased fibrinolysis)

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5
Q

What are the Respiratory effects of Liver Dysfunction?

A

Restrictive Ventilatory Effects:
-Ascites prevents diaphragmatic descent, decreasing FRC
-Laying patient supine decreases FRC naturally
-Worse in COPD patients with alcoholism.

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6
Q

What is Hepatopulmonary Syndrome?

A

A triad of:
-Liver Disease
-Arterial Deoxygenation
-Widespread Pulmonary Vasodilation

Uncommon. Affects the lungs of people with advanced liver disease.
-Blood vessels in lungs dilate and increase in number, making it challenging for RBCs to absorb O2.
-V/Q mismatch. Lungs are unable to exchange, causing hypoxemia.
-Try to improve reversible pulmonary dysfunction if possible (thoracentesis or paracentesis)
-Be very careful with sedatives/opioids preop

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7
Q

What is Hepatic Hydrothorax?

A

Pleural effusion occurs due to fluid backing up.

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8
Q

What changes in fluid balance occur with Hepatic Disease?

A

-Relative intravascular hypovolemia due to paracenteses, diuretics, and AV shunting
-Increased hydrostatic pressure in hepatic venous system
-Decreased plasma oncotic pressure
-Leads to ASCITES and edema

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9
Q

What fluid and electrolyte disturbances are associated with Hepatic Disease?

A

Hypoalbuminemia
Sodium retention
Progressive decline in renal function
Decreased free water clearance
Dilutional hyponatremia
Hypokalemia

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10
Q

How does Liver Disease cause Renal Dysfunction?

A

Nothing is wrong with the kidneys themselves, but are experiencing renal hypoperfusion.
-Progressive decline in renal function.
-Can lead to Hepato-Renal Syndrome (HRS) and multi-system organ failure
-Supportive therapy
-Liver transplant

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11
Q

What is Hepatorenal Syndrome (HRS)?

A

Renal failure occurring with hepatic failure and portal hypertension.
-Impaired renal function without abnormality of the kidneys
-Due to decreased renal blood flow and decreased GFR
-95% mortality within weeks of onset
-Hepatic Transplant is only definitive treatment

Nagelhout:
-Need to increase RBF through renal vasodilation and vasoconstriction of splanchnic circulation

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12
Q

How does Liver dysfunction affect the CNS?

A

-Inability to clear neurotoxins from the GI tract leads to accumulation of nitrogenous wastes (Ammonia)
-Ammonia erodes the BBB, leads to brain edema.

Precipitating factors:
-GI bleed
-Electrolyte abnormalities
-Acid-Base Disorders
-Sepsis

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13
Q

What are the S/Sx of Hepatic Encephalopathy?

A

S/Sx:
-Asterixis (flapping of wrists)
-Hyperreflexia
-Mental Status Changes
-Eventually, Coma

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14
Q

What is the treatment for Hepatic Encephalopathy?

A

-Lactulose: alters pH of colon
-Neomycin: decreases colonic bacteria, preventing urea from being converted into ammonia. Decreases amount of ammonia being produced.
-Dietary protein restriction to decrease ammonia

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15
Q

What is Acute Hepatitis?

A

A mild inflammatory response to fulminant hepatic failure.
-1-2 week prodromal period
-S/Sx: Fever, malaise, N/V, jaundice
-Resolves in 2-12 weeks

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16
Q

What are the causes of Acute Hepatitis?

A

Viral:
-A, B, C, D & E
-Epstein-Barr virus
-Cytomegalovirus

Hepatotoxic substances

Adverse drug reactions

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17
Q

Which are the different routes of transmission of Hepatitis?

A

A & E: oral-fecal
B & C: body fluids and disrupted cutaneous barriers

Asymptomatic carriers: B & C

Chronic hepatitis:
B: 3-10%
C: 10-50%

18
Q

How is the Epstein-Barr Virus spread?

A

-Oral-oral contact
-Usually mild hepatitis
-Severe & fatal: RARE

19
Q

What is Cytomegalovirus?

A

-Herpes virus
-Mimics viral hepatitis
-Usually mild

20
Q

What is Drug-Induced Acute Hepatitis?

A

Drug-related injury to the liver results from an idiosyncratic reaction to a substance or an overdose resulting in toxicity.
-Resembles viral hepatitis
-Alcohol hepatitis is most common form of drug-induced hepatitis, results in fatty infiltration of the liver (causing hepatomegaly)

21
Q

What is Chronic Persistent Hepatitis?

A

-Limited to portal areas
-Relatively benign
-Hepatocyte function is preserved
-Progression to cirrhosis is rare

22
Q

What is Chronic Lobular Hepatitis?

A

-Recurrent exacerbations of acute inflammation
-Progression to cirrhosis is rare

23
Q

What is Chronic Active Hepatitis?

A

Progressive:
-Cellular destruction
-Cirrhosis
-Liver failure

Causes:
-Hep B or C
-Systemic Lupus Erythematosus
-Exposure to certain drugs (Methyldopa, Isoniazid, Nitrofurantoin)

24
Q

What is Cirrhosis?

A

Hepatocyte necrosis.
-Liver parenchyma (cells) are replaced by fibrous, nodular tissue that causes an interruption of portal venous blood flow.
-Liver function is now affected, get increased pressure in the portal system.

Nagelhout:
-Cirrhosis is defined as the histologic development of regenerative nodules surrounded by fibrous bands in response to chronic liver injury, which leads to portal hypertension and end-stage liver disease.

25
Q

What are the causes of Cirrhosis?

A

-Chronic hepatitis
-Chronic alcoholism
-Biliary obstruction
-Right sided heart failure

26
Q

What are the rare causes of Cirrhosis?

A

-NASH
-Alpha 1 antitrypsin deficiency
-Hemochromatosis
-Wilson’s Disease
-Budd-Chiari malformation

27
Q

What is Nonalcoholic Steatohepatitis (NASH)?

A

AKA Non-alcoholic fatty liver disease
-Broad spectrum of liver disorders r/t steatosis. Not due to alcohol use!!!!!
-Ranges from simple benign, to hepatitis.
-Inflammation of hepatocyte injury and may progress to cirrhosis and hepatocellular carcinoma.
-Associated with obesity, hyperlipidemia, and diabetes

28
Q

What is Alpha 1 Antitrypsin Deficiency?

A

Alpha 1 antitrypsin is produced in the liver to coat and protect the lungs (prevents breakdown of elastin).
-Neutrophils break down elastin by producing elastase.
-When we have an infection, the immune system sends WBCs (neutrophils) to attack bacteria, but they secrete elastase.
-Deficiency in A1A leads to the breakdown of elastin in lungs, leading to diffuse, damaged lung and eventual COPD.
-Diffuse damage to the lungs even if they’ve never smoked
-A1A accumulates in the liver, leading to hepatomegaly and eventual liver transplant being necessary

29
Q

What is Hemochromatosis?

A

An autosomal recessive disorder
-Iron deposits throughout the body
-Pancreas: DM
-Heart: CHF
-Hepatocellular carcinoma occurs in 15-20% of patients

30
Q

What is Wilson’s Disease?

A

An autosomal recessive disorder
-Defect in the gene needed for copper binding
-Leads to decreased serum ceruloplasmin (a protein that carries copper from the liver to the bloodstream and takes it where it is needed)
-Leads to copper accumulation throughout the body
-Will see distinct Kayser-Fleischer ring (copper ring) around the iris
-Neurologic and hepatic dysfunction due to copper being deposited around the body

31
Q

What is a Budd-Chiari Malformation?

A

The formation of hepatic vein thrombosis.

32
Q

What is Portal Hypertension?

A

Portal vein pressure > 20 mmHg
(normally 7-10 mmHg)
Backflow of blood leading to engorgement of key organs that feed the portal vein.

33
Q

What are Gastroesophageal Varices?

A

-Dilated mucosal veins due to reversal of portal venous (Splanchnic) blood
-May or may not bleed
-If they rupture, very problematic
-Hemodynamically significant
-Distal esophagus or proximal stomach
-The development of esophageal varices places the patient at risk for spontaneous, severe, upper GI hemorrhage.

34
Q

What is the treatment for Gastroesophageal varices?

A

-Banding (stops blood from leaking)
-Ligation
-Sclerotherapy (injecting a solution right into vein, causing it to scar and blood to reroute)
-TIPS procedure
-Octreotide

35
Q

What is the purpose of using Octreotide with esophageal varices?

A

Reduce portal and variceal pressures, as well as the splanchnic and systemic collateral blood flow. Decreasing venous return to the portal circulation.

36
Q

What is the cause and treatment of Ascites?

A

Causes:
-Portal HTN
-Hypoalbuminemia
-Na & H2O retention

Treatment:
-Diuresis
-LeVeen Shunt
-Paracentesis
-TIPS procedure

37
Q

What are the S/Sx of Spontaneous Bacterial Peritonitis?

A

A complication of cirrhosis.
-Fever (hyperdynamic state)
-Leukocytosis
-Abd pain
-Decreased bowel sounds
-Mortality is 50% after first episode

38
Q

What are the nutritional issues associated with Cirrhosis?

A

-Protein calorie malnutrition (low protein, no appetite, N/V is frequent)
-Megaloblastic anemia is common (folate is antagonized by alcohol)

39
Q

Why does Cirrhosis lead to hyperdynamic circulation?

A

Massive vasodilation of the splanchnic and periphery.
-Decreased blood viscosity secondary to anemia

40
Q

Why does arterial hypoxemia occur with Cirrhosis?

A

-PaO2 of 60-70 mmHg is normal in cirrhotic patients
-Blood vessels in lungs are dilating, difficult for RBCs to absorb the O2
-Diaphragm movement is impaired from ascites
-Lungs are unable to deliver adequate amounts of O2 to the body
-R to L pulmonary shunting occurs due to Portal HTN, smoking, COPD
-Possibly pneumonia

41
Q

Why does hypoglycemia occur with cirrhosis?

A

Malnutrition leads to decreased glycogen stores.
-Impaired gluconeogenesis: Liver is unable to convert Lactic acid into glucose

42
Q

Why is the immune system impaired with Cirrhosis?

A

Alcohol impairs immune system.
Pt at risk for:
-Viral infection
-Bacterial infection
-Cancer
-TB