Flashcards in The Liver Deck (37):
What is Cirrhorsis?
End stage of Liver disease in which the hepatocyte are progressively replaced with fibrous scartissue.
Are liver cells good at regeneration?
How is this affected in Cirrhosis
Yes, Liver cell reporduce well and the liver has a large fx reserve.
However, cirrhosis progressively replaces hepatocyte ares with scartcissue
What does a liver with cirrhosis look like
Etiologies of Cirrhosis
• Alcohol abuse (60-70% of cases) (This is a kind of toxic hepatitis)
• Hepatitis (10% ish)
• Drugs (e.g. methotrexate)
• Biliary disease (liver, bile ducts, gallbladder) (10% ish)
• Metb disorders (eg hemochromatosis)
o Inc Iron levels and deposition in liver
What is cryptogenic?
Same as idiopathic. Occasionally cirrhosis cause can be cryptogenic
Patho- Steps leading to portal HTN
• Hepatocytes destroyed -> cells regenerate -> fibrous scar tissue forms -> Vessel constriction -> portal HTN
What other issue will be present with vessel constriction in the liver?
Impeded perfusion to liver
Portal HTN will lead to what other major complications?
Fluid shift or ascites- (r/t inc pressure in peritoneal capillaries
Duct constriction -> bile flow impeded -> bile stasis
Reduction in Metabolic waste clearance- Normal or essential components in high levels can become toxic
Common MNFTS of Cirrhosis.
(Some vague, some specific)
Anorexia, weakness, wt loss
Hepatomegaly and jaundice (some forms do not present w/ jaundice)
How is the spleen potentially affected by Cirrhosis?
Portal HTN leads to increased hydrostatic pressure in splenic veins
Also r/t Anemia, leukopenia, thrombocytopenia (r/t bone marrow deficiencies from reduced components being provided by liver)
What is Varices?
Another potential MNFTS/Complication of Portal HTN
Refers to dilation of associated veins. (It is not localized like an aneurism )
What Gi issues is associated with Portal HTN
What is the Tx for Cirrhosis?
• Maximize regeneration (reduce workload)
o Diet modification
• small meals,
• high carb (high calorie)
• no fat (liver has to produce bile for breakdown)
o No alcohol
o Treat Compiications
Distinguish between Portal vein, Hepatic arteries and hepatic veins and hepatic duct?
(% of total fluid volume, source and output)
PORTAL- ~ 70% of total blood to liver. from GI tract to liver
HEPATIC A- ~30% of total blood to liver. From heart to Liver
HEPATIC V- Draining blood from liver emptying to inferior vena cava
Hepatic Duct- Bile- L+R lead to common hepatic -> common bile Duct-> sphincter of Oddi -> Duodenum
What is normal pressure for the portal vein system and how does this change in Portal HTN
Portal HTN is defined as: >12mmHg:
How do you describe the site of blockage causing Portal HTN?
Where are most?
Description could be pre, intra or post hepatic for blockages.
Most is Intra hepatic
What is portosystemic shunting?
Obstruction of venous blood flow through liver, leading the development of collateral channels between portal and venous system. Meaning some blood bypasses liver.
Hemerrhoidal and esophageal commonWhat
Describe the complications of portosystemic shunting
What are Esophogeal Varices?
Thin waled varicosities (twisted/collateral veins) that develop along esophageal mucosa and are subject to rupture. (i.e GI Hemorrhage)
Often MNFTS as Frank Blood
What is Frank Blood?
Frank blood is bleeding via rectum. Often associated with hemorrhage in the GI tract. (Beyond occult blood)
Why are toxin likely to develop in blood with portal HTN?
HTN leads to collateral connections (or channels) Passing of blood for Portal System to hemoroidal or other venous system, liver gets bypassed -> no metabolization or filtration in liver -> toxic compounds enter rest of venous system
What is Ascites
Excess fluid accumulation in peritoneal cavity
What might lead to Ascites?
• ET and Patho
o Cirrhosis and portal HTN
o Right sided heart failure
o Severe changes in HP or OP
o Water/Na retention
Two key MNFTS of Ascites
Dyspnea (Inc abdm cavity pressure oushing against lung expansion, reduces tidal volume)
Abd distension (fluid build up in abdominal cavity)
Tx of Ascites
o Small volume: use diuretics, Provide fluids and electrolytes
o Large volume: Paracentesis + volume expender (eg albumin)
What fx capacity of liver must be lost to lead to failure?
• l/o >80% fx capacity before failure
> 50% mortality (r/t late diagnosis)
Examples of Acute vs Chronic Liver failure?
o Fulminant hepatitis (ACUTE)
o Toxic liver damage – Alcohol (ACUTE)
o Cirrhosis (chronic)
VERY basic path and MNFTS of Liver failure
4 broad categories of complication involved in the failure?
Hepatic insuff and multi organ failure
4 major issues r/t hematology in Liver failure
o Impaired protein synthesis (Specific to hematology -clotting factors and fibrinogen)
• The liver also breaks down clots and this is impaired
o Depressed marrow function (r/t limited protein (aka resources) for the marrow to produce cells)
• Thrombocytopenia, leukopenia
o Inadequate clearance of activated clotting factors (Liver has major role in clot breakdown)
• DIC (Disseminated intravascular coagulation)
This refers many small clots develop across blood stream, this cause obstruction but also depletes resources for stopping actual bleeds
o GI bleeds (r/t to above)
Key Issues related to Metabolism complications in Liver failure
• inadequate bilirubin clearance
• Hypoalbuminemia (key colloid in Colloid osmotic pressure, less pull pressure in vessels- risk of hypervolemia)
o edema and ascites
• Defective urea cycle
o Hyperammonemia (ammonia is byproduct of protein metb)
• Reduced estrogen catabolism
Describe hepatorenal syndrome
• idiopathic renal failure (though reasons are discussed)
• severe reduction in renal perfusion
o link show liver improves so does kidney
• oliguria (limited urine leading to anuria…basically no urine) And azotemia (build up of nitrogenous waste products in blood)
Why is there a reduction in renal perfusion in liver failure
o Reduced perfusion r/t
• portal hypertension (stealing volume)
• fluid shifts
What is Hepatic encephalopathy?
Hepatic encephalopathy is:
• Neuro mnfts of liver failure
• Toxic compounds that can affect the brain are not detoxified
(Ex. ammonia, urea, nitrogenous compounds)
2 reasons toxins aren't processed properly in liver failure
o Liver impaired (hepatocytes impaired casuing reduced processing toxins)
o Porto systemic shunts (venous return skips the liver outright)
2 different ways changes in concentrations of toxic compounds could negatively affect the brain
(Eg. ammonia -> glutamate -> alter neurotransmission and osmolarity. Effecting action potentials with increasing concentration)
(Blood in brain vessels pulls out fluid and brain dehydration occurs)
Early MNFTS of hepatic encephalopathy
Asterixis (hand trembling) and hyperflexia (over active reflex)