medicine-hepatic disorders Flashcards
function of liver in relation to metb what is nec for the proper processes to take place
Takes glucose from portal vein and converts it to glycogen which is stored for later use. Can synthesize additional glucose (gluconeogenesis) from amino acids or protein breakdown or lactate from exercising muscles. When this gluconeogenesis uses protein it has ammonia as byproduct (also produced by bact in intestines). liver converts this ammonia to urea
protein metb-syntheizes all plasma proteins but gamma globulins. Vit K nec for synthesis of prothrombin and some clotting factors
fat-makes bile in hepatocytes and the bile salts help breaks down fatty acids for prod of energy and ketone bodies when strving or uncontrolled DM. Synthesizes cholesterol, lecithin and other lipoproteins
drugs and hormones metb by liver
what does the liver produce
what storage functions does liver have
what excretory functions does liver have
Synthesizing plasma proteins, nonessential amino acids, Vit A and essential nutrients such as iron, Vit D, B12, bile
STORES vit A, B, D and B complex, iron, copper
also glycogen etc
bilirubin (made from hgb) gets conjugate by hepatocytes and becomes bile excreted in stool and can be excreted by urine
where is bile made, stored and conc? when is the bile signalled to release
wat quadrant is this in?
what does biliary sludge possibly lead to
Bile is made in liver & stored & conc in gal bladder. When we eat fatty foods it signals bile duct to open &emulsify fats
liver and gallbladder in R upper quadrant
biliary sludge-tiny stones, sludgy bile that can block the bile duct. With this erosion etc it canleak out into sterile cavityautodigestion that can lead to sepsis
how is liver fx measured
can you rely just on these tests? why?
• Fx measured in terms of serum enzyme activity (serum aminotransferases, alkaline phosphatase, lactate dehydrogenase) and serum concentrations of proteins (albumin and globulins), bilirubin, ammonia, clotting factors and lipids
cant just rely on the tests because other disorders can affect test results
pigment studies: eg bilirubin, urine bilirubin, fecal urobilinogen what do they meas and when would they be abnormal (in gen)
meas ability of liver to conjugate and excrete bilirubin
abn in liver and biliary tract disease and assoc w jaundice clinically
protein studies eg serum albumin, serum globulin
what affects either albumin or globulin
the normal ratio of albumin to globulin is A1.5:G1 or A2.5:G1 how is this affected in chronic liver disease
proteins made by liver
albumins are affected by cirrhosis, chronic hep, edema, ascites
globulins affected by cirrhosis, liver disease, chronic obstr jaundice and viral hep
in chronic liver disease the globulin ratio is higher and albumin dec
how would prothrombin time be affected by liver disease
PTT may be prolonged w liver disease
are serum aminotransferases better for detecting acute or chroni liver disease
which serum aminotransferase is elevated in acohol abuse
when does ALT elevate and what can it be used for
is it specific to liver
acute
alcohol abuse elevates GGT
• ALT inc primarily in liver disorders, might help monitor course of hepatitis or cirrhosis or effects of tx that may be toxic to liver
yes mostly for liver
wwhen does AST elevate and what can it be used for
is it specific to liver
• AST- present in the tissues that have high metabolic activity, so inc if death of tissues of organs such as heart, liver, skeletal muscle and kidneys.
o Although not specific to liver disease, may be high in cirrhosis, hepatitis, and liver cancer
which serum aminotransferase indicates cholestasis and what else is it used for
• GGT- high levels are associated with cholestasis and can also be due to alcoholic liver disease. min value in liver disease is confirming hepatic origin of elevated alkaline phosphatase level
when would cholesterol levels be inc and dec
cholesterol inc in biliary obstr and dec in parenchymal liver disease
what are the major complications of liver biopsy and what must be done and treated before biopy
when would biopsy not be preferred method
how is the biopsy done
• Bleeding and bile peritonitis after liver biopsy are major complications so coagulation studies done before. so do coag studies and treat before the biospy
if there is ascites or coag abn might do other method
can use needle biospy, percutaneous with U/S or transvenously, or laparoscopically
specific nursin considerations for percutaneous needle biopsy
coag studies and blood standing by
have pt breathe deeply a few times and then hold breath at end of expiration. quick iopsy is done
other diagnostics for liver
US, MRI, CT and radioisotpe liver scan, laparoscpoy
liver disease more common in men or women?
most common cause of parenchymal damage?
acute or chronic liver issue more common?
- men 2x more
- Most common cause is from malnutrition, especially r/t alcoholism
- May be acute or chronic. Moreso chronic
most common and significant mnfts of liver disease
why do nutritional def arise
• Most common mnfts: jaundice, portal htn, ascites and varcites, nutritional def, and hepatic encephalopathy
nutritional def, due to inabiity of damamged liver cells to metb certain vitamins
how do parenchymal cells respond to most noxious agents
• Parenchyma cells respond to most noxious agents by replacing glycogen w lipids, producing fatty infiltration w or without cell death or necrosis. Commonly associated w inflammatory cell infiltration and growth of fibrous tissue
why can jaundice occur
what are the types
what is the risk of severe jaundice
- Results from impairment of heptic intake, conjugation of bilirubin, or excretion of bilirubin into the biliary system
- Types of jaundice: hemolytic, hepatocellular and obstr jaundice, and jaundice d/t hereditary hyperbilirubinemia
prolonged jaundice can lead to pigment stones in gallbladder and vv bad jaundice eg 10x normal i risk for brainstem damage
where and why is bilirubin conjugated
in hemolytic jaundice is the bilirubin conjugated or unconjugated. what about fecal and urine biliinogen
are there major mnfts or complic
hepatocytes remove bilirubin from bllod and chemically conjugate it to glucuronic acid that makes it more soluble in aqueous soln then gets carried in bile into duodenum
its mostly unconjugated. • Fecal and urine urobilinogen levels are inc but no bilirubin in urine
not gen major mnfts or complic
hepatocellular jaundice
would serum aminotransferases be affected
does the jaundice cause mnfts? what if its prolonged?
• AST and ALT inc- indicating cellular necrosis
- In prolonged jaundice, cell damage develops so both ypes of jaundice (obstr and hepatocellular) appear together
- May be mildy or severely ill, w lack of appetite, nausea, malaise, fatigue, weakness, and possibly wt loss
- Pt may report- headache, chills, fever
what can cause obstr jaundice
• Maybe caused by the occlusion of the bile duct from a gallstone, an inflm process, a tumor, or pressure from an enlarged organ (liver, gallstone)
• May also involve small bile ducts within the liver
• Intraheptiacobstr from stasis and thickening of bile within the canliculi may occur after ingestion of certain medications (cholestatic agents)
o agents include phenothiazines, antithyroid meds, tricyclic antidepressant agents, androgens and estrogens
what happens in obstr jaundice
how are AST, ALT, GGT Affected?
• bile cannot flow normally into the intestine and become backed up into the lvier substance, it is then reabsorbed into the blood and stains the skin, mucous membranes and sclerae. (whether it is intrahepatic or extrahepatic)
o AST, ALT< and GGt levels rise only moderately but alkaline phosphate and bilirubin are elevated
mnfts of obstructive jaundice
o it is excreted in the urine which becomes deep orange and foamy. Bc of dec amount of bile in the intestinal tract, stools become light or clay coloured
o skin may itch intensely- baths help
o dyspepsia and intolerance to fatty foods may develop bc of impaired fat digestion in the absence of intestinal bile
hereditary hyperbilirubinemia
when does this happen physiologiclly?
names of the syndromes?
benign’ cholestatis jaundice of preg w retention of conjugated bili, prob secondary to unusual sensitivity to hormones of preg
also beign recurrent intrahepatic cholestasis
• Gilberts syndrome is familial disorder char by inc level of unconjugated bilirubin that causes jaundice
Serum bili is inc but everything r/t liver is normal and no hemolysis
.
caused by inborn errors of biliary metb=
• Dubin-johnson syndrome (chronic idiopathic jaundice w pigment in the lvier)
• Rotors syndrome (chronic familiar conjugated hyperbilirubinema without pigment in the liver)
2 major conseuqences of portal HTN
• two major consequnces: ascites and varices
why is ascites cyclical
– means it leads to
cirhosis w portal HTN–splanchnic arterial vasodilation–dec in circ blood vol–activation of RAA and SNS and ADH–kindey retains Na and H20–hypervolemia–persistent activation of systems for retention of Na and H20; ascites and edema formation–continued arterial underfilling and the cycle repeats
inc in cap p and obstr of venous blood flow through the damaged liver and vasodilation that occurs in the splanchnic circulation (arterial supply and venous drainage og GI system from distal esophagus to the midrectum including liver n spleen)
• liver cant metb aldosterone so inc sodium and h2o retention- inc intravascular vol, inc lymph flow and dec synthesis of albumin by damaged liver contribute to movement of fluid into peritonral space
• process becomes self-perpetuating- loss of fluis into spaces causes further sodium and water retention by kidney to maintain vascular vol
what does the liver fail to metb that contributes to dev of ascites
aldosterone leads to inc sodium and water retention
how much fluid can be in abd in ascites. is it just water in the peritoneal caivty? what else and how does this affect osmotic P
- large amounts of albumin rich fluid, 15 L or more, may accumulate in peritoneal cavity as ascites
- osmotic p decreases and with inc portal pressure more movement of fluid into peritoneal cavity
mnfts of ascites
what would you see if percusion or if pt was supine
what can you do daily to assess inc of ascites?
- inc abdominal girth and rapid weight gain
- Pt may be short of breath
- striae& distended veins may be visible,
- Umbilical hernias also occur,
- Fluid and electrolyte imbalance
- Percussion of abd- for shifting dullness or by detecting fluid wave fluid wave is likely to be found if large amounts of fluid)
- Flanks bulge in supine
- Daily measurement
medical mgmt of ascites (headings)
Dietary modification: diuretics bed rest paracentesis transjugular intrahepatic portosystemic shunts
- spironolactone an aldosterone blocking agent is most often first line therapy. it is K sparing
- oral diuretics such as furosemide may be added but be cautious bc long term- hyponatremia could occur
diet considerations of ascites
if this fails what is next line of tx
• Negative sodium balance to reduce fluid retention
• Might be reduced to 500mg if accumulation is not controlled.
diuretics if not controlled by Na restriction
which diuretic is first line Tx of ascites and why? what might be used in conjunction and what lyte is a concern with this
what is max daily wt loss if pt has ascites
complic and why
- spironolactone an aldosterone blocking agent is most often first line therapy. it is K sparing
- oral diuretics such as furosemide may be added but be cautious bc long term- hyponatremia could occur
- daily wt loss should not exceed 1-2kg w asicites and peripheral edema or .5-.75 kg wout edema
- possibly complications: fluid and lyteimb and encephalopathy (enceph d/t dehydration nd hypovolemia. when K is depleted ammonia inc)
with bedrest is upright pos better for pt with ascites
- upright position is associated with activation of the R-A-A system and SNS
- causes reduced renal glomerular filtration and sodium excretion and dec response to loop diuretics
paracentesis as Tx of ascites
is it commonly done
how much can you take out
what must it be in combo with and why?
now mostly done for diagnostic exam
• Large vol (5-6L) have been shown to be a safe method for treating patients w severe ascites
• This technique in combo w IV infusion of salt poor albumin or other colloid is standard mgmt. the albumin helps correct dec in effective arterial blood vol that leads to NA retention and makes pt more hemodynamically stable after Tx and prevents reaccum of fluid
Transjugular intrahepatic portosystemic shunt (TIPS)
as tx for ascites
why?
- To reduce portal htn, stent inserted to serve as an intrahepatic shunt between the portal circulation and hepatic vein
- Treatment of choice for refractive ascites
- works well to Dec Na retention, improves renal response to diuretic therapy, and preventing reccurence of fluid accum
nursing mgmt of ascites
- Assessment and documentation of I and outs, abd girth, daily weight
- Monitors serum ammonia and e- levels
what is the major risk for pt during paracentesis and therefore what should be meas very frequently
hypovolemia
meas BP
what is the most sginificant source of bleed in cirrhosis
esophageal varices
how do varices dev
what other liver complication might they inc risk of
- Develop in majority of patients w cirrhosis
- Varicosities that develop from elevated p in the veins that drain into the portal system
- Prone to rupture and are often the source of massive hemorrhages from the upper Gi tract and the rectum
- Once they form, they inc in size and eventually bleed
the inc bleeding mightinc nitrogen load and ammonia leading to hepatic encephalopathy
what puts pt at risk of hemm from varices
• Factors that contribute to hemorrhage- muscular exertion from lifting heavy objects, straining at stool sneezing, coughing, vomiting, esophagitis irritation of vessels by poorly chewed food, reflux of stomach contents, meds that erode esophageal mucosa or interfere with cell replication
mnfts of varices
if pt is suspected of bleeding from eophageal varix is it gen true
- Hematemesis, melena, or general deterioriation in mental or physical status and often have a hz of alcohol abuse
- S&S of shock
30% of pts are actually bleeding form other source
diagnostics for esophageal varices
• Endoscopy used to identify the bleeding site, along with barium swallow, ultrasonography, CT and angiography
consideration with endoscopy and giving fluids
gag refex must return beore can be done safely
when might portal HTN be suspected
if dilated abd veins and hemorrhoids detected
splenomegaly ad ascites may be present
