w10 liver Flashcards
what is portal hypertension?
- abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow
- caused by disorders that obstruct or impeded blood flow through any component of the hepatic portal system
what are causes of portal hypertension
-Vascular remodeling with intrahepatic shunts, thrombosis, inflammation, fibrosis (liver cirrhosis, hepatitis)
what happens if long-term portal hypertension persists?
varices, splenomegaly, hepatopulmonary syndrome, ascites, and hepatic encephalopathy
what is the normal liver under pressure?
12mmhG
problems r/t portal HTN-Varices: Distended, tortuous, collateral veins
Prolonged elevation of pressure in the hepatic portal vein causes collateral veins to open between the portal vein and systemic veins and their transformation into varices
- they are called caput medusae, hemorrhoidal varices
- rupture of varices can cause life-threatening hemorrhage
problems r/t portal HTN-splenomegaly
- Portal hypertension contributes to congestive splenomegaly caused by increased pressure in the splenic vein
- Thrombocytopenia from platelet sequestration is the most common symptom of congestive splenomegaly –> increased bleeding tendency
- also predictive of severity of esophageal varices
portal HTN and–> Hepatopulmonary syndrome (HPS)
-Respiratory complications of advanced liver disease and portal hypertension
HPS: Pulmonary vasodilation, increase pulmonary venous congestion, R-to-L shunting leading to hypoxemia
there is NO treatment for this
portal HTN and portopulmonary hypertension (PPH)
-Associated with vascular remodeling and pulmonary artery vasoconstriction. No specific clinical manifestations but may see dyspnea, cyanosis, digital clubbing
treatment–> target the pulmonary arterial vasculature to decrease pulmonary HTN W/ various medication options, and liver transplant
what is ascites?
accumulation of fluid in the peritoneal cavity
-traps body fluid in the peritoneal cavity -which decreases fluid available for normal physiologic functions
what causes ascites?
Cirrhosis, right heart failure, abdominal malignancies, nephrotic syndrome, and malnutrition
other contributing factors–> : Portal hypertension, decrease in albumin synthesis by liver, splanchnic arterial vasodilation, renal sodium and water retention
what is the overflow theory of ascites?
Capillary hydrostatic pressure–> capillary osmotic pressure =water to peritoneal cavity
what is the underfill theory of ascites?
increase in hepatic sinusoidal hydrostatic pressure and decrease in plasma oncotic pressure w/ weeping of lymph fluid from the surface of the liver and decreases plasma volume activity which activates ADH and RAAS volume overload
what is the forward theory r/t ascites?
Both. Circulating nitric oxide and carbon monoxide –> splanchnic vasodilation. decreases systemic vascular resistance overcomes compensatory cardiac output. Stimulation of baroreceptors activates renal sodium retention. Combined portal hypertension and splanchnic vasodilation –> fluid transudation and lymph formation –> ascites
clinical manifestations of ascites?
- Abdominal distention, increased abdominal girth, weight gain
- dyspnea
- increased RR, –> should assume a semi-flower’s position
- peripheral edema
- Dilutional hyponatremia
- Bacterial peritonitis –> fever, chills, abdominal pain, decreased bowel sounds, cloudy ascitic fluid
what is our treatment for ascites?
- dietary salt salt restriction and potassium-sparing diuretics, vasopressin receptor-2 antagonists are effective for dilutional hyponatremia
- Albumin may be given
- Monitor for hyponatremia and hypokalemia
- Paracentesis (but need to consider other risks)
- Treat bacterial peritonitis
- Peritoneovenous shunt and transjugular intrahepatic portosystemic shunt (TIPS) maybe offered
- Liver transplant
what is hepatic encephalopathy?
- Complex neurologic syndrome characterized by impaired behavioral, cognitive, and motor function
- May develop rapidly during acute fulminant hepatitis (type A); after portosystemic bypass or shunting (type B); or slowly during the course of cirrhosis, chronic liver disease, or portosystemic bypass (type C)
what are risk factors of hepatic encephalopathy?
-advanced liver disease, gastrointestinal bleeding, increased dietary protein, electrolyte imbalance, and hypoxia
what is the pathophysiology of hepatic encephalopathy?
- Results from a combination of biochemical alterations that affect neurotransmission
- Liver dysfunction and collateral vessels that shunt blood around the liver to the systemic circulation permit neurotoxins and other harmful substances absorbed from the gastrointestinal tract to accumulate and circulate freely to the brain
- Ammonia cannot be converted to urea by the diseased liver –> Reaches the brain –> Metabolized to glutamine, with osmotic disturbances and alterations in cerebral blood flow that interfere with neurotransmitters and cause astrocyte edema (cytotoxic edema) and oxidation
- increase BBB permeability (vasogenic edema)–> astrocytes swelling, brain edema, and intracranial hypertension
- excessive amount of gamma-miobutryic acid (GABA) and a decrease LOC
- Infection, hemorrhage, inflammation, electrolyte imbalance, sedatives, and analgesics also can precipitate stupor and coma in the presence of liver disease
manifestations, evaluation and treatment of hepatic encephalopathy
- Initial: Subtle changes in personality, memory loss, irritability, lethargy, and sleep disturbances
- In acute liver failure, symptom onset can be rapid: Confusion, disorientation to time and space, asterixis, slow speech, bradykinesia, stupor, convulsions, and coma
how do we diagnosis hepatic encephalopathy?
History of liver disease, clinical manifestations and psychometric testing; EEG, blood chemistry, liver function tests
how do we treat hepatic encephalopathy?
-Correction of fluid and electrolyte imbalances; manage cerebral edema with hypertonic saline, mannitol or hypothermia; dietary proteins; prevent ammonia absorption in the colon; reduce gut ammonia
what is jaundice? “icterus”
Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (total plasma bilirubin concentrations >2.5–3 mg/dL)
what causes jaundice?
-Extrahepatic obstruction to bile flow (gallstones)
-Intrahepatic obstruction (hepatocellular disease such as cirrhosis or hepatitis)
-Prehepatic obstruction: Excessive production of bilirubin (excessive hemolysis of red blood cells)
normal in newborns ONLY
what are the clinical manifestations of jaundice?
- Dark urine
- Clay-colored stools
- Yellow discoloration possibly occurring first in the sclera of the eye and then progressing to the skin
- Skin xanthomas (cholesterol deposits) and pruritus
- Anorexia, malaise, fatigue
what is the treatment of jaundice?
-Correct the cause: Jaundice is only a sign of an underlying disorder.
what is Hepatorenal syndrome (HRS)
Renal failure results from arterial vasodilation of the splanchnic vasculature, decreasing effective blood volume and renal vasoconstriction
-decrease in blood volume and decrease in BP–> causes renal perfusion and a decrease in GFR and oliguria (type 1)
intrarenal vasoconstriction as a key characteristic
what is the diagnosis of Hepatorenal syndrome (HRS)
: Exclude other causes; Blood work (potassium, creatinine), urine osmolality and specific gravity; investigate secondary problems
treatment of Hepatorenal syndrome (HRS)
-Systemic vasoconstrictors (α-adrenergic agonists and octreotide) and albumin, TIPS (as a bridge to liver transplant), liver and kidney transplantation
what is viral hepatitis
it is a common systemic disease affecting primary the liver
-various viral strains produce various forms of hepatitis