Unit One Flashcards
What vessels supply the liver?
Hepatic A-20% o2 blood
Portal V-80% nutrient rich (from GI tract)
What does the liver regulate?
Glucose metabolism Protein metabolism Ammonia conversion Fat metab Vit/iron storage Bile formation (produce/secrete) Bilirubin excretion Drug metab
From what specific vessels do the liver receive and send blood? What would occur if there were a blockage at either of these points?
Sends to IVC (to heart) via central vein-liver enlargement
Receives from GI tract (Hep A, Port V)-cause GI enlargement (painful)
Define the following parts of the liver: Lobule Hepatic cell Sinusoids Canaliculus Kupffer cell
Lobule:functional unit of the cell
Hepatic cell:hepatocytes that pick up chems from blood and make into chems
Sinusoids-thin walled vessels allowing flow in and waste out (saturated in incoming blood)
Canaliculus-transport bile out to bile duct
Kupffer cell-macrophage of the liver, cleans dirty GI blood and break down hemoglobin.
What 3 things makes up the bile, what are their functions?
Where does this go? When?
Bile is green/yellow and made by the hepatocytes, then passed thru the canaliculi.
1. Bile salts: formed hepatocites from cholesterol, break down fat in intestine, allowing digestion/absorption of fat sol vits, recycled (18x) by portal blood to liver and excreted again (enterohepatic circulation)
2.bilirubin-derived from Kupffer cells breaking down hemoglobin.after liver conjugates bilirubin (water sol) it can be sent to canaliculi then duodenum then converting to urobilogen, then feces…some reabsorbed and process reoccurs. Some into systemic circ and excrete by kidney.
3.cholesterol-fats
Goes to GB in between meals, directly to duodenum during ingestion.
Describe the 3 big roles of carb (glucose) metabolism.
- Glycogenesis-when excess glucose in blood, liver stores as glycogen for later use.
- Glycogenolysis-when decreased glucose in blood, glycogen activated in liver and exported as glucose to blood.
- Gluconeogenesis-restoration of depleted glycogen stores by amino acids creating ammonia byproduct.
What does the liver use carbs, protein, and lipids for?
Carbs are converted to fat (triglycerides)-clogs A
Protein is synthesized from aa; ammonia converted to urea. (Albumin and others made for osmotic pressures and blood coags)
Trig are oxidized for energy, syn, packaged into lipoproteins to shuttle fatty acids. (When glucose not avail)
Bile is needed to absorb what vitamins?
What are some of these conversions needed for?
What does the liver store?
ADEK
K-required by metabolic process to form clot factors (prothrombin, fibrinogen, factor VIII).
D-converted in active (dihydroxy-)
Stores Iron (ferritin), B12
Diff indirect vs direct bilirubin.
Indirect: pre hepatic, unconjugated-fat sol bili
Direct: conjugated-water sol bili
What portion of the liver makes the lymph? What does it impact?
Disse spaces
Kupffer cells in sinusoids (porous) and disse space between endothelial lining of sinusoid and hepatocytes. Impacts fluid/ascites.
In the physical assessment for liver dysfunction, what will venous hums, Bruits, and frictions rub indicate?
Venous hum-collateral circulation
Bruit-rapid blood flow (liver ca)
Friction rub-inflamed peritoneum.
List the liver function tests (blood) and why they are useful, note any values.
Serum enzymes: ALT (liver specific 5-35) and AST: inc in liver damage, cell wall break and releases out)
Protein: dec w/ liver dz (not able to syn prot from aa)
Bilirubin:total 0.1-1.2-
Indirect:0.1-1:fat sol (inc when liver not able to convert)
Direct:0.1-0.3:wat sol (post liver conversion)
Ammonia:inc w/ liver dz (liver not converting to urea, risk for encephalopathy)
Lipids
Clot factors: inc time due to dec clot factors
Glucose
GGT-bile and/or obstruction d/o (ducts) and alcohol abuse
Alkaline phosphatase-obstructive biliary d/o (can be GB prob, GGT used to confirm liver dx)
What are the 4 types of jaundice?
- Hemolytic-RBC destruction (liver not processing excess bilirubin) INC:bili, total urobilogen
- Hepato cellular-damaged hepatocytes (not cleaning out normal bilirubin-not conjugating) infection/meds/dz/alcohol. INC: bili, urobil, AST/ALT
- obstructive-blockage/occlusion: extra hepatic-outer liver intrahepatic-inner liver (can’t flow out, bile too thick, stasis) tumor, stones. Dark urine, light stool, INC: bile salt (skin itch), dyspepsia, ALT/AST/GGT/bili/alk phos.
- Hereditary hyperbilirubinemia-inherited excess bilirubin w/ dec. conjugation.
Diff direct vs indirect hepatic dysfunction.
Direct:liver dz
Indirect:flow problem
Can be acute or chronic.
What are the 3 types of cirrhosis?
- Alcoholic:fatty deposits, scarring surrounding portal areas.
- Post necrotic:destruction caused by virus, toxicity.
- Biliary:obstruction of bile flow, infection, scarring at bile duct.
What occurs in the liver w/ cirrhosis?
Inflammation compresses lobules and replacement tissue is diffuse fibrotic interrupting structure/function. Dec expansion, and vascularity of blood,all back up (port HTN), bile (jaundice), and lymph (ascites).
In the assessment for cirrhosis what are the findings for both compensated and the more severe uncompensated categories?
Comp:inter fever, vascular spiders, palmar erythema, epistaxis, ankle edema, am indigestion/flatulent dyspepsia, abd pain, enlarged liver and splenomegaly (V back up-can have thrombocytopenia:bleed/leukopenia:infection as result).
Uncomp: ascites (3rd spacing can cause hypovol), jaundice, weakness, muscle wasting, fever, clubbing, purpura/bruising (dec platelet count), epistaxis, hypoten, sparse body hair, white nails (dec ferritin), gonadotrphy (hormones affected).
What are some treatments for the cirrhosis patient?
Antacids-gastric distress
Vits/nut supps-malnourished/unable to absorb
Diuretics K sparing (spironlactone-edema (Aldos over produced)
Antifibrotic (colchicine)-liver movement
Neomycin-SBP (spontaneous bacterial peritonitis)
Dec sodium-water retention
Iron/folic acid-anemia due to lack of ferritin stores
Lactulose-removes ammonia
Protein-lack of syn
Carbs-easy energy source prevent prot usage
No hepatotoxic meds, smaller meals, no alcohol
How is portal HTN caused, what does it affect, and what are the major consequences?
Inc pressure in portal system due to obstruction through liver. Above 22mmHg (norm 5-10). Collateral circulation causing:
Splenomegaly, most important:ascites and varices.
VEIN DISTENTION:esophageal, gastric, hemmorhoidal (prone to rupture, risk for bleed)
What is encephalopathy and how is it caused? What are some contributing factors?
CNS d/o caused by liver failure (ammonia build up entering brain).
Azotemia (inc BUN/creat and other waste),
constipation (not elim),
blood in GI (blood has protein-liver not converting ammonia to urea), dietary protein,
drug use.
Diff the stages of clinical manifestations in encephalopathy.
Stage 1:offset sleep pattern, lethargy. Asterixis, normal EEG.
Stage 2:disorientation, mood swings. Asterixis, fetor hepaticus (bad breath), EEG w/general slowing.
Stage 3:stuporous, incoherent, asterixis, deep ten ref, rigidity, Abnormal EEG.
Stage 4: coma, flaccidity, Major abnormal EEG.
How is Hep A transmitted? Common areas? Symptoms?
Oral fecal route (water, food, shellfish).
Underdeveloped areas.
Immune after resolved.
N/V, malaise.
Immunizations, bedrest, comfort, hygiene.
Incub 15-50 days.
Acute version.
How is Hep B transmitted? Long lasting results? TX?
Blood and body fluids. Remains in serum longer. incubation 28-160days.
Acute, but can become carrier state with recurrent infections leading to cirrhosis and/or carcinoma.
Immunizations: active-vaccine passive-globulin
Tx: Alfa interferon (helps SE), bedrest, nutrition.
How is Hep C transmitted? What can occur, is this tx or preventable, diag testing?
Blood born/sexual
Unstable RNA virus w/ mutation
Liver ca, cirrhosis, chronic infection. No cure, not tx.
Incub. 15-160 days.
Use of antiviral agent:peg interferon and ribavirin help, protease inhibs.
Testing: Alt (inc), ELISA, HCA RNA, liver bx.
