Liver Advanced Patho

Question Answer
When the motility is disturbed at the esophageal sphincter, we get problems with acidity> GERD
When the motility is disturbed in the intestines, we get diarrhea, or decreased= constipation
When diarrhea and constipation are associated with abdominal discomfort, but colon looks healthy= IBS
Zollinger–Ellison syndrome only disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.
the gallbladder is the storage site for bile which is produced by the liver cells
3 components to bile are bile acids (digestive fx/detergent), cholesterol and bilirubin
Bile passes into the bile ducts> right hepatic and left hepatic into the common hepatic duct into the> common bile duct into the duodenum to pour bile> stored in the gallbladder
When does the gallbladder release bile? when you eat fatty food, the presence of fat stimulates cholecystokinin hormone release bile through cystic duct> common bile duct> duodenum where it joins pancreatic lipase to emulsify fat
What if the gallbladder had a stone in it? it would hurt> when they eat fat
Small gallbladder stone and obstructive jaundice would require surgery because it would pass into the cyctic duct and then the common bile duct> impacted and would affect bilirubin going from liver to the intestine= obstructive jaundice
Arterial blood supply to the liver comes from the hepatic artery from abdominal aorta 30%
2/3 of the blood that comes to the liver comes from where? the portal vein from the gut- deoxygenated- because the liver detoxifies and metabolizes everything
The portal vein drains the stomach, the s. intestines, the colon, pancreas, spleen, peritoneal cavity- which is carried to the liver then to the hepatic vein and out the inferior vena cava to the heart and general circulation
The pressure in the portal vein is low, so when it’s high it’s called portal htn, normally it’s 5-10 mm mercury and in your arteries, it’s 90mm mercury
The portal vein can be blocked or obstructed by thrombosis> the blood is too thick and there is a blood clot forming, the blood cannot pass and will accumulate causing Ascites> water accumulating backwards
What increases the pressure in the portal vein? Cirrhosis/ fibrous tissue- most important cause of portal HTN
The end stage of any chronic live dz is? Liver cirrhosis
With liver cirrhosis we get… back up pressure in the portal vein and the structures drained by the portal vein> the abdominal structures> ascites, splenomegaly, and varices
Inside the liver, the blood coming from the portal vein and the hepatic artery mix inside the liver in wide capillaries called sinusoids> macrophages seen there because this is where the detox process takes place
Liver factory responsible for synthesis/metabolism and detoxification
Liver detoxification 2 major toxins ammonia from proteins and converts to urea excreted by kidneys. If not, affects LOC (encephalopathy). Also, bilirubin from RBC broken vby spleen= heme into biliverdin into bilirubin
Bilirubin at 1st is water insoluble and needs… to pass through the liver to make it water soluble and detoxify, get rid of it
Liver synthesis of 2 proteins albumin and clotting factors
Liver synthesis of albumin/major plasma protein oncotic pressure> keeps water in blood vessels> causes hypovolemia, vBP and edema- also drugs bind to albumin, so having less= more free drugs in system> give less meds
Liver synthesis of all clotting factors except factor VIII and Von Wilebrand (out of 13), when you get a cut you need plts and a stable fibrin clot (13 different proteins/clotting cascade) or= prolonged bleeding ^INR
LFT ALT, AST, Albumin and PT- has to do with liver (cells) itself
ALT has higher specificity for the liver- viral- intracellular- injured liver cells do not tell you about liver fx- just injury
AST has more to do with drug/etoh induction- do not tell you about liver fx- just injury
The day you die of liver failure liver enzymes will be normal- smoke from the fire will be extinguished- you don’t have any more liver cells- higher in acute liver dz
Albumin if the liver fx is impaired, the liver will not be able to make albumin so low albumin= bad liver fx. Also tells you if the issue is chronic b/c ? life is 20 days. 5 ? lifes= steady state. If below normal, it’s been 100 days
What lab is helpful with acute liver issues? ALT and AST
What lab is helpful with chronic liver problems? albumin
PT/INR is a key clotting factor, and liver produces most, and any slight liver dysfx, whether acute or chronic will affect this, so INR is the MOST SENSITIVE TEST- the best one
Biliary obstruction from liver cells right/left hepatic duct> common hepatic duct> cystic duct from gallbladder> common bile duct> duodenum> hepatitis and cirrhosis- liver cells are swollen= intra hepatic biliary obstruction
Other causes of biliary obstruction- extra hepatic biliary obstruction small gallbladder stone that became impacted in the common bile duct bile cannot flow from the liver to the intestine
another causes of biliary obstruction- extra hepatic biliary obstruction the pancreatic head- tumor compressing the common bile duct
Cholestatic liver fx tests related to bile obstruction> total and direct bilirubin, alkaline phosphatase, and GGT
tests for biliary obstruction bile acids, cholesterol, and ^ serum bilirubin (most important), also alkaline phosphatase and gamma glutamyl transferase (GGT)
alkaline phosphatase ^ during biliary obstruction- less specific- can be + in a prego- + in any pt in bone with bone d/o (pagets dz)
gamma glutamyl transferase (GGT) ^ during biliary obstruction- more specific
story of Bili unconjugated and single he’s indirect (cannot measure directly), cannot get rid of him (insoluble)> the liver takes care of Bili, gets married with glucuronic acid> now direct (measured in the plasma), conjugated now easy to get rid of b/c water soluble
total bilirubin 1mg (50/50) the sum of indirect (0.5mg) and direct bilirubin (0.5mg) you get 3 readings
hyperbilirubinemia when you >1mg total bilirubin- both are increased
when bilirubin is >3 starts to show in the sclera and mucous membranes- jaundiced- clinical dx- no labs needed
let’s say the total bilirubin is 10 and 7 out of 10 are indirect and 3 is direct indirect is from the blood- destroying RBC- hemolytic jaundice. The opposite would be a liver issue> intra/extra hepatic bile obstruction> obstructive jaundice
normally when the liver manufactures direct bilirubin, we can get rid of it, how intestines worked on by intestinal flora/bacteria forming a compound called urobilinogen> stercobilinogen and stercobilin (brown)
urobilinogen, stercobilinogen and stercobilin some urobilinogen goes back to liver by the portal vein and kidney to pee out (normal yellow color).
Cannot get rid of indirect bilirubin unless liver processes it and changes it to it’s conjugated form
How do we get rid of direct bilirubin? we pee it out as urobilinogen or poop it out as stercobilin
Stone became impacted in common bile duct and has obstructive jaundice bilirubin accumulates, direct bilirubin ^, not making, urobilinogen, stercobilinogen and stercobilin, stool is clay colored, skin is yellow, and urine is brown- also itchy skin d/t bile acids
When it’s hepatitis or cirrhosis both direct and indirect goes up, but an obstruction causes the direct to go up more
Acute liver d/o, inflammation acute viral hepatitis> same s/s prodromal, poor appetite, fatigued, abdominal pain, jaundice, bloating> A (feco/oral), B (sex/blood/body fluids/S.E. Asia- fatal in prego), C (blood/body fluids), E (feco/oral)
Hepatitis C usually chronic- rare to have it as acute- can cause cirrhosis- most important
Hep B can be acute and if chronic can= cancer/hepatoma- more than cirrhosis
Hep B serologic test (DNA/RNA) DNA core antigen and core Ab, surface antigen and surface Ab- surface Ab- 4 measurements- having the surface Ag ^ in system >6 months= chronic hep B
Hepatitis A trivial- can be like a cold but can be severe in adults
ALT increases in viral
Acute liver dz and alcoholism and hepatotoxic drugs flagyl and Tylenol potentiates hepatic injury ^ AST
Ischemic injury severe hemorrhage and v in BP depriving liver of blood supply, liver enzymes high
Chronic liver d/o end result of any liver dz (chronic hepatitis C)
In all chronic liver dz enzymes not as high- liver fx will be greatly disturbed-PT/INR^/albuminv/bilirubin ^ impaired
Alcoholic liver dz 1) fatty liver (returns to normal) u/s shiny 2) alc. fatty (steato) hepatitis 3) alc. liver cirrhosis
Alcoholic liver cirrhosis dx of exclusion
Steato hepatis in a non-etoh pt NASH syndrome- lots of fat but no etoh- pt is obese
Auto immune liver cells are attacked= chronic inflammation/fibrosis= cirrhosis> MIDDLE AGED JAUNDICED FEMALE> detect anti smooth Ab
Hemochromatosis, congenital- abnormal metabolism of iron – in duodenum, receptors saturated easily, sky high deposited in SQ tissue, bronze color> to liver, ^ ferritin/vTIBC, cirrhosis, to pancreas, bronze diabetes, heart arrhythmias
Wilson’s Dz, congenital, copper metabolism ^ damages liver/cirrhosis, Kayser- Fleischer rings in the eyes/low ceruloplasmin- send to opthomologist, weak, jaundiced, itching- dancing, psychosis> copper in basal ganglia> chorea-like
?1-antitrypsin deficiency substance is beneficial because trypsin destroys proteins and can cause COPD even if they never smoked> you see a liver and lung problem> first presents w/COPD
Cholestatic liver dz bile is not moving, it’s static
Gallbladder stone impacted in the common bile duct dx by ERCP and U/C
Primary biliary cirrhosis and primary sclerosing cholangitis causes of cholestatic liver dz
Primary biliary cirrhosis autoimmune biliary obstruction of ducts- middle aged jaundiced, itching, female> +AMA anti-mitochondria Ab
primary sclerosing cholangitis inflammation of the bile ducts (intra/etra)- d/t ulcerative colitis/crohns- inflammatory- chemicals like cytokines and interleukin will flow through portal vein to the liver to bile duct= sclerosis= beaded string, increases direct bilirubin (liver)
Liver cirrhosis is the end stage of any chronic dz irreversible, pathologic stage, inflammatory, fibrosis
Cirrhosis meaning stone- turning liver into a useless stone
2 problems with liver cirrhosis liver is functionless (stone) and portal hypertension
Liver loss of function detox> ammonia (proteins)/bilirubin and synthesis of albumin (edema, hypovolemia) and clotting factors (^INR)- going to bleed-
2 things will combat bleeding when you cut a vessel 1st) plt plug, transient, superficial and minor, 2nd) fibrin clot- significant and can kill you-internal ^INR
Loss of liver function when not synthesizing albumin can cause (David) prerenal failure/hypovolemia- hepatorenal syndrome- need transplants of both simultaneously
Hepatic encephalopathy presentation when gradual…1st manifestation is inversion of sleep rhythm- sleepy in am b/c they don’t sleep at night- when chronic- also agitated and irritable
Acute encephalopathy bleeding into the gut or vomit into gut passes into intestines- the flora digests it, produces ammonia and 2 days later= coma
Portal Hypertension causes fibrosis and obstruction- back-up pressure- in the peritoneal cavity veins- hydrostatic pressure pushing water- Ascites, splenomegaly, and varices–
Ascites portal hypertension is the cause- can have this with normal albumin? too much hydrostatic pressure is the cause> memorize/know the slide
Capillary permeability only open/impaired in 2 conditions infection and inflammation—or cancer
Other types of ascites (ovarian cancer) the pts fluid is rich in albumin because the capillaries are open
Splenomegaly d/t portal htn the spleen enlarges and gets aggressive- destroys plts- hypersplenism- low plt count- 1st thing to stop bleeding- superficial- peticia, pinpoint
Esophageal varices d/t portal htn blood comes from the gut> portal vein but when there’s obstruction, the blood goes to small veins at the end of esophagus> porto systemic anastomosis – ruptured- bleeding-vomiting- ammonia-encephalopathy/comma
A patient who has generalized edema loss of fx
Ascites portal htn
A pt who needs less dose of a drug (albumin) loss of function
A pt who has reversal of sleep rhythm encephalopathy- detox fx- ammonia- loss
Prolonged bleeding time platelets/splenomegaly- thrombocytopenia- portal htn
Pt with elevated INR Loss of function