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GI Exam 3 (Liver)
Terms in this set (132)
What is the name for the parenchymal cells of the liver that are responsible for most of the synthetic/metabolic functions?
T/F: None of the cells of the liver can regenerate if there is damage.
false! they can regenerate! that's actually what causes half the diseases of the liver tbh.
Which cell type lines the sinusoids of the liver and allow for exchange to occur?
T/F: Endothelial cells are permeable to all substances, including formed elements of the blood.
FALSE! they are permeable to all substances EXCEPT the formed elements
What is the name of the phagocytic cells of the liver?
Which cell type is the primary target of injury in many liver disorders?
(these ones can get inflamed and cause obstruction of bile ducts)
What is the function of Ito cells in the liver?
(aka "stellate cells")
in lipid droplets!
also if injured, these cells transform into cells that produce collagen, resulting in
What is the function of Albumin?
-MAINTAIN ONCOTIC PRESSURE!!! (plasma volume)
-carrier for poorly soluble substances
T/F: Albumin levels respond rapidly to changes in synthesis due to it's short half life.
Albumin levels respond SLOWLY. it has a longgg half life of
(which isn't that long if you ask me but whatever)
Which clotting factor produced in the liver has a half life of 6 hours and is very quick to respond to changes in synthesis?
D. plasma thromboplastin
E. Stuart factor
(this is factor VII)
How do you measure levels of Factor VII in the blood?
A. order serum factor VII levels
C. PT! (prothrombin time)
(different from PTT which is the partial thromboplastin time)
Which protein produced by the liver is a protease inhibitor that inactivates harmful enzymes?
What is one of the important enzymes that Alpha 1-antitrypsin inhibits?
(elastase breaks down elastin which leads to connective tissue disease in the lung and liver)
Which of the following is NOT a protein produced by the liver?
B. Factor VII
C. Alpha 1-antitrypsin
the liver produces VLDL's, but they convert to LDL in the blood somewhere.
T/F: Ceruloplasmin is a iron containing protein produced by the liver.
T/F: Acute phase reactants such as CRP are specific to the liver.
False! they are not specific to the liver. they just indicate inflammation, but not where.
Glycogenesis occurs when there is (high/low) glucose in the bloodstream.
liver takes in excess glucose and stores it as glycogen
Glycogenolysis occurs when there is (high/low) glucose in the bloodstream.
liver breaks down glycogen to release glucose into blood
Which metabolic process takes place in the liver when glycogen stores have been exhausted?
(creating new glucose from stuff like amino acids and certain carbs to try and maintain glucose homeostasis)
Under conditions of (high/low) glucose, the liver synthesizes Fatty Acids from glucose and ______ to store energy in the form of fat.
= Fatty Acids
(makes sense if you think about the words "fatty acids")
Jill has been locked in a closet for 4 days and has not eaten a thing. What is her liver converting fatty acids into to supply her body with energy?
Cholesterol can be combined with ________ to form triglycerides.
cholesterol + Fatty Acids = triglycerides
How does the liver eliminate cholesterol from the body?
in the form of BILE and BILE SALTS!
Deamination of amino acids in the liver produces _________, which is a
(ammonia is converted to Urea by liver, which is now water soluble and can be peed out)
Jaundice is caused by the accumulation of which substance?
A. unconjugated bilirubin
B. conjugated bilirubin
C. both A and B
D. none of the above
C. both A and B
Which form of bilirubin is a lipophilic toxin?
What 2 general processes can cause unconjugated hyperbilirubinemia?
-Hemolysis (excess breakdown of RBCs=excess production of unconjucated bilirubin=liver can't keep up)
-insufficient conjugation (liver can't conjugate at a normal rate/at all)
Physiologic jaundice of the newborn involves low levels of _______, the molecule that conjugates bilirubin.
(this jaundice is transient and can be treated w phototherapy bc sunlight makes bilirubin water soluble hehe)
T/F: It takes longer for pre-term infants to produce a normal amount of glucuronate.
What 2 genetic conditions can cause insufficient conjugation of bilirubin?
T/F: Gilbert's Syndrome is a genetic condition that causes a complete inability to conjugate bilirubin.
Gilbert's- decreased ability to conjugate (not too severe)
Crigler-Najjar- INABILITY to conjugate
T/F: Most of circulating bilirubin is conjugated bilirubin.
FALSE! (which is the opposite of what i expected)
most of circulating bilirubin is unconjugated bc as soon as it becomes conjugated in the liver, the liver excretes it. it doesn't go back into the blood stream
Which form of bilirubin is water soluble and non-toxic?
You see a patient in the ER freaking out bc their skin is yellow. They tell you their urine has been darker lately, almost like the color of tea. Which form of bilirubin do you expect to be causing this jaundice?
unconjugated is not water soluble and doesn't get excreted in the urine. (of course in real life you would have to rule out other stuff but you get my point) this tea-colored urine is not a problem! it just looks funny.
What is the most common cause of Conjugated hyperbilirubinemia?
What is the name of the rare, benign genetic condition that can cause Conjugated Hyperbilirubinemia?
(i remember this bc it looks like Dublin and irish people are good and conjugated bilirubin is the good kind)
T/F: Jaundice caused by conjugated hyperbilirubinemia needs to be urgently treated.
you don't need to treat jaundice from Conjugated, you just need to find out the underlying cause and treat that! conj bili is non-toxic so who cares if they look a little funky?
Which category of liver enzymes rise quickest and highest when biliary ducts are obstructed?
Canalicular Enzymes! (Alk Phos and GGT)
Which liver enzymes rise highest and fastest when there is cell lysis ?
Intracellular Enzymes! (AST, ALT, LDH)
T/F: Alkaline Phosphatase is specific for the liver.
False!!!!! you need to order "total alk phos with isoenzymes"
Which isoenzyme of Alkaline Phosphatase is primarily from the liver?
What is the most common cause of elevation of GGT levels?
Active liver disease
Which liver enzyme can also be used as an indicator of alcohol consumption?
Both ALT and AST require _________ as a cofactor, so deficiency of this will cause lower ALT/AST levels.
T/F: Since AST is found in large amounts in the kidneys, heart and skeletal muscle, you should order isoenzymes to make the test more specific to the liver.
FALSE!!! everything was true in that statement, but there are NO isoenzymes for ALT or AST!
Which Transaminase is more specific to the liver?
ALT! (bc it is present in other organs, but in low levels)
Which disease very commonly causes very high elevations of the transaminases?
HEPATITIS! (both viral and toxic)
Which of the following enzymes is the most specific to the liver?
A. Alkaline Phosphatase
C. SGPT (ALT)
LDH is prolly the least specific bc it is found in all tissues
Which organs contain the highest concentration of LDH?
Heart, Kidneys, Skeletal Muscle (the same 3 that have large amounts of AST if that helps)
Which isoenzymes of LDH are most specific to the liver?
LD4 and LD5 (but still not totally liver-specific)
T/F: Alcoholic Hepatitis causes high elevation of SGOT/SGPT.
False! Alcoholic hepatitis follows a unique pattern. it can have normal or mildly elevated transaminase levels, whereas viral and toxic hepatitis cause high elevations.
Which product of bilirubin metabolism gives color to stool?
Urobilinogen! (lack of urobilinogen causes clay-colored stools)
Which of the following is not included in "LFTs"?
A. serum bilirubin
B. serum albumin
E. serum ammonia
C. PTT (i tried to be tricky here hehe)
remember we wanna test for decreased factor VII so we wanna do a PT not a PTT! (but the PT is included in LFTs, just so ya know.)
When you order serum bilirubin levels, which types can you DIRECTLY measure?
TOTAL and CONJUGATED (direct) bilirubin!
Which Liver Function Test is great for following progression of chronic liver disease?
(remember albumin levels don't decrease with acute liver problems)
BUN levels will (increase/decrease) with severe liver disease.
DECREASE bc the liver is losing its ability to synthesize urea from ammonia
-also, BUN changes with HYDRATION and all sorts of other things so it's not very specific to liver.
Increased levels of _________ can cause CNS depression and altered mental status in a patient with liver disease.
Which diagnostic test assesses the texture of the liver?
B. liver biopsy
D. Liver-Spleen Scan
T/F: Alcoholic Hepatitis is irreversible.
it is completely reversible if the patient stops drinking!
What is the most common precursor to cirrhosis?
Alcoholic Hepatitis (once cirrhotic changes occur, it is no longer reversible)
Frank Gallagher comes into the ER complaining of nausea and right upper abdominal pain. He has a temp of 102.6, his skin appears slightly yellowed, and his liver is palpable and tender on PE. He tells you he just got back from spending a week in Vegas for his best friend's bachelor party and that he "drank so much he stole Mike Tyson's tiger". Also, he is a full blown degenerate alcoholic who is destroying his family. What do you expect his diagnosis to be?
What do you expect each of the following lab results to be in a patient with Alcoholic Hepatitis?
Liver Enzyme Panel:
-CBC: elevated WBC (bc infections are v common w this), macrocytic anemia
-Liver Enzymes: mild elevations in ALT, AST, Alk Phos; HIGH GGT
What serum bilirubin level and prothrombin time indicate SEVERE disease? What percent mortality is associated with this?
-Serum Bilirubin >10 mg/dL
-PT >6 seconds above control
How do you treat Alcoholic Hepatitis?
-STOP DRINKING BEFORE YOU DIE
Daily steroids for 1 month
-vitamins (folate and thiamine) if needed
-TNF inhibitors (pentoxifylline)- v pricey
T/F: Fatty liver is irreversible.
it is reversible if you treat the underlying cause!
What are the 2 most common causes of Fatty Liver?
-Alcohol consumption (Alcoholic Fatty Liver Disease or AFLD if you will)
-Metabolic Syndrome (Nonalcoholic Fatty Liver Disease NAFLD)
When does "Fatty Liver of Pregnancy" occur, and what does it do to the mom/baby?
-it can legit kill mom and baby bc of rapid onset of liver failure
Patient comes to your office kinda feeling like crap. He is quite fat and has a PMH of diabeetus and HTN. He tells you he feels abnormally tired, nauseated, has lost his massive appetite, and has some pain in his right upper belly. On PE you find that his liver is enlarged and tender! AHA a clue! What test must be done to definitively diagnose him?
-symptoms are very nonspecific, but he has NAFLD! (big clues were the metabolic syndrome, and tender hepatomegaly! v common finding w this!)
-Definitive Dx: LIVER BIOPSY!
How do we treat a patient with Fatty Liver?
-AFLD: stop fcking drinking or you'll get cirrhosis
-NAFLD: lose some fcking weight and hit the gym
T/F: Subfulminant Acute Liver Failure is sudden liver failure without pre-existing liver disease with development of hepatic encephalopathy within 8 weeks.
this is the correct definition of FULMINANT!
(important- WITHOUT pre-existing disease, WITHIN 8 weeks!)
-Subfulminant- hep enceph onset 8 weeks- 6mths later
What is the most common cause of Acute liver failure?
-teenagers rlly need to stop trying to "kill themselves" by ODing on tylenol....idiots.
What is the 2nd most common cause of Acute liver failure? (hint: it's kinda similar to the #1 most common cause)
Idiosyncratic Drug Reactions (unpredictable!)
-anti-TB drugs, antiepileptics, antibiotics
Which hepatitis can cause acute liver failure?
Viral Hepatitis, but mostly Hep B
What are some sign/symptoms you will see in a patient with cerebral edema due to Acute Liver Failure?
main culprit of this: Ammonia!
-Mild: confusion, memory lapse, loss of diurnal rhythm, behavioral changes
-Severe: seizure, asterixis, coma
Why do you limit protein in patients with hepatic encephalopathy?
because protein metabolism produces Ammonia, which just so happens to be the big bad wolf that causes this encephalopathy. So restricting protein intake reduces the production of ammonia! Ta-Da!
What drug can be given to draw ammonia from the bloodstream into the GI tract to be eliminated? What is the major side effect of this drug?
Lactulose! gives ya some real nasty diarrhea
How do you treat severe hepatic encephalopathy?
-mannitol for cerebral edema
What electrolyte abnormality is most commonly seen with acute liver failure?
low Na, high K
Part of your million-dollar workup for suspected Acute liver failure is a serum glucose test. What result is commonly seen?
Name 5 tests done as part of the ridiculously long workup for suspected Acute Liver Failure.
(my answer is 5 that I think are most important)
-LFTs (levels don't correlate well w severity)
-Serum Ammonia (should be v low if normal!)
-serum Acetaminophen level
The treatment for Acute Liver Failure is long af. What is it lmao
-Coag Defects: IV vit K, platelet transfusion
-Fluid/Elec Imbalance: Fluids at 2ml/kg/hr
-Prophylactic Abx (everyone!)
-H2RA/PPI to prevent stress gastritis (everyone!)
-Hepatitis: IV Acyclovir
Acetylcysteine within 24 hrs
for acetaminophen toxicity
-Mushroom poisoning: Penicillin G
-Severe cerebral edema:
, elevate HOB!
T/F: Emergency liver transplant may be performed if someone has Acute liver failure due to acetaminophen toxicity.
you can do the transplant for anyone else, but NOT apap etiology!
What is Cirrhosis of the liver?
the end result of hepatocellular injury, causing nodular regeneration and fibrosis of the liver.
What are the 2 main causes of Cirrhosis?
-HEP C (ppl won't know they have it, then all of a sudden they have cirrhosis lol)
-can have both of these combined!!!!
Which type of Cirrhosis is common in alcoholism?
MICROnodular (nodules <1mm, liver is sandpapery)
Which type of Cirrhosis is common in viral hepatitis?
MACROnodular (big nodules...obviously)
Which type of Cirrhosis has a higher incidence of hepatocellular carcinoma?
What is the name of the strange contractions of the hands seen commonly in patients with Cirrhosis?
Jack Dawson comes to the ER because he is throwing up blood. Ruptured esophageal varices are seen on endoscopy and treated appropriately. You're smart so you suspect some sort of liver problem, but he does not drink. He really hasn't been feeling right lately. On PE you note a palpable enlarged liver, red palms, and Dupuytren contractures of the hands. He has dilated veins on his abdomen. What is the most likely diagnosis?
Decompensated Cirrhosis! because he isn't a drinker, I'm thinking probable Hepatitis as a cause
Why would you see Cheilosis and glossitis in a patient with Micronodular Cirrhosis?
micronodular- common w alcoholics
alcoholics are poorly nourished and cheilosis/glossitis are caused by vitamin deficiencies
Anemias are a common finding in patients with cirrhosis. What type of anemia is most common?
MICROcytic! (anemia of chronic disease)
What workup results do you expect to see in a patient with compensated cirrhosis?
trick question, compensated cirrhosis will likely have normal-ish lab tests! (bc their body is controlling it right now)
Why would a man with cirrhosis complain of erectile dysfunction and loss of libido?
Estrogen is not being degraded by the liver anymore, so these guys have increased estrogen levels in their blood!
Why might someone with Cirrhosis have palmar erythema?
it has to do with altered hormone metabolism
T/F: Unconjugated hyperbilirubinemia is what causes jaundice in a patient with early Cirrhosis.
it's CONJUGATED!!! bc the liver holds on to the ability to conjugate bilirubin for dear life.
What is the diagnostic essential for Cirrhosis?
LIVER BIOPSY!!! tells us the type of cirrhosis and if pt has progressed to cancer or not
How would you treat/educate a patient with Cirrhosis?
-no more booze!
-Encephalopathy- limit protein intake!
-Vaccinations (hep A/B, pneumo, flu)
A cirrhotic patient has a microcytic anemia. How do you treat this? How do you treat a macrocytic anemia?
-Microcytic= iron deficiency. give Ferrous Sulfate
-Macrocytic-give Folic Acid
What are the contraindications for a liver transplant?
cancer, sepsis, advanced cardiopulmonary disease, HIV +
What is the first drug used to treat ascites if sodium and fluid restriction has been unsuccessful?
Patients with Cirrhosis commonly have ascites. How do you treat ascites? (this is true for anyone w ascites btw)
1. Sodium and fluid restriction
3. Furosemide (added to spironolactone)
What are some considerations to keep in mind if you are going to perform a paracentesis on a patient with ascites?
-the quicker you pull fluid out, the quicker it will reaccumulate!
-you can't remove more than 6L at a time!
IV albumin 10g/L of fluid removed!
What does the TIPS procedure do that relieves ascites?
-it's a stent from the portal vein to the hepatic vein. it lets some circulation bypass the liver
-complication: hepatic encephalopathy (put them on lactulose hehe)
Name 2 complications of Cirrhosis. (there are a ton)
-upper GI bleeding
What does the MELD score predict?
mortality in patients with cirrhosis
What MELD score do you need before you will be considered for the transplant list?
14 or higher!
What is the main cause of Portal Hypertension?
What are the main sites for collateral bloodflow with Portal Hypertension?
GE Junction (Varices)
T/F: Symptoms of Portal Hypertension include hepatomegaly and acute liver failure.
there are noooooo symptoms of portal HTN! but you will see sx of the underlying disease that is causing it :)
What class of drugs is used to prevent future bleeds in patients with portal hypertension and ruptured esophageal varices?
NONSELECTIVE BETA BLOCKERS!!! (propanolol)
-dose determined by 25% decrease in HR (but can't go below 55bpm)
T/F: Hemochromatosis is copper deposits in the liver and pancreas.
it's IRON deposits!!!!!!!
What is the most common genetically transmitted disease in the white population?
T/F: Hemochromatosis is inherited in an autosomal dominant pattern.
Describe the classic patient with hemochromatosis, ie; what does the patient look like, what gender, what age?
-Caucasian men over 50
What is the classic triad of Hemochromatosis?
bronze skin, hepatomegaly, Diabetes!
What is the diagnostic essential for Hemochromatosis?
-Serum iron studies (iron & ferritin levels)
-Liver Biopsy (tells us iron content, if progressed to cirrhosis or not)
What is the first line treatment for hemochromatosis?
-weekly blood draws of
for 2-3 yrs
What is the name of the chelation agent give to chelate iron in a patient with hemochromatosis?
What is Wilson's Disease?
Autosomal Recessive inborn error of copper metabolism that causes BOTH excess absorption and decreased excretion of copper, resulting in copper buildup in liver and brain (basal ganglia).
What condition is associated with Kayser-Fleischer rings?
these are the copper rings in the cornea!
Wilson's disease presents between ages 6 and 40. What are some differences in how children present vs young adults?
Children: HEPATIC problems (hepatomegaly, jaundice, RUQ pain)
Young Adults: NEURO problems (tremor, dysarthria, involuntary movements)
What are the diagnostic essentials for Wilson's Disease?
Serum Copper studies (serum copper, serum ceruloplasmin, urinary copper)
You suspect Wilson's disease in a patient. Their copper studies results just came back. What do you expect to see if this patient has Wilson's?
Serum Copper LOW
Serum Ceruloplasmin REDUCED/NORMAL
Urinary Copper INCREASED
Why is ceruloplasmin likely low in patients with Wilson's Disease?
because the liver is damaged and is not producing as much ceruloplasmin
Besides the diagnostic essentials, what imaging should you obtain on a patient with suspected Wilson's disease?
Cranial CT scan! to see if there are copper deposits in the brain
How do you treat Wilson's Disease?
-Zinc Salt (Galzin): blocks absorption of Cu
-Dietary Restriction of Cu: shellfish, mushrooms, chocolate
-Penicillamine: CHELATES Cu! (can't take if PCN allergic, also causes kidney damage so watch BUN/Cr!!!!!)
-Neuro damage is permanent :(
What are the 3 most common predisposing factors for hepatocellular carcinoma?
HEP B, HEP C, CIRRHOSIS!
Jack Mehoff was diagnosed with cirrhosis 6 years ago. He has never had an episode of decompensation, and his cirrhosis has been stable since diagnosis. He comes to the ER vomiting blood and has bad ascites and signs of encephalopathy. What should you suspect until proven otherwise?
(big hint was the stable cirrhosis that deteriorated)
What is the initial test of choice for hepatocellular carcinoma?
CT scan- will show a poorly defined mass
What serum test is highly indicative of Liver Cancer?
SERUM ALPHA-FETO PROTEIN!
-rarely seen in pts over age 3. only seen in HCC, germ cell tumors, or liver mets
What test gives you a definitive diagnosis of HCC?
Liver biopsy of course!
What is the only curative treatment option for liver cancer?
surgery! (if you catch it early enough)
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