Apex- Liver Flashcards
Which structure is responsible for eliminating bacteria from the liver?
A. Kupffer cell
B. Canaliculus
C. Sinusoid
D. Acinus
A. Kupffer Cell
(Acinus = Liver lobulue = functional unit of liver)
(Sinusoids are where the kuppfer cells are located)
(Bile canaliculi collect bile produced by the hepatocytes)
What is another name of rthe Acinus?
Liver lobule
*Functional unit of the liver
What is the functional unit of the liver
Liver lobule/Acinus
Where do lymph and proteins drain before emptying n=into the lymphatic duct?
space of Disse
What is the connective tissue covering that encapsulates the liver?
Glisson’s capsule
The liver receives SNS innervation from….
T3-T11
What % of lymph does the liver produce in the body?
~ 50%
What zone are the liver cells most susceptible to ischemic injury?
Zone 3 (Least oxygenated to begin with)
What zone has the highest concentration of CYP450 enzymes?
Zone 3
(also highest risk for ischemic injury)
(least oxygenated)
What drains blood from the intestine?
The portal vein
What produces bile and where is it stored?
Hepatocytes produce bile and it is stored in the GB
What zone is most oxygenated?
Zone 1
What cells drain bile into the bile duct?
Canaliculi
Label
The canniculi drain bile into the
1. Common hepatic duct
The 2. Cystic duct secretes bile and converges with the common hepatic duct to form the
3.. Common Bile duct
The 4.Pancreatic duct converges with the CBD to form the
5. Hepatopancreatic duct (Ampulla of vater)
& the 6. Sphincter of Oddi contracts to release bile into the dudodenum
What does the sphincter of Oddi do?
It controsl the flow of bile released from the common hepatic duct (CBD + pancreatic duct)
What is the ampulla of vater?
It’s where the CBD and pancreatic ducts converge
Another name for the apulla of vater
Hepatopancreatic duct
What do opioids do to the sphincter of oddi?
Contract it –> increases biliary pressure
What does bile even do? (3 things)
- Absorbs fat and fat soluble vitamins (DAKE)
- provides a pathway for excretion of bilirbuin and products of metabolism
(just think if you have a stone in your CBD, you cant drain bilirubin and thats why people get yellow)
- Alkalizes the duodenum
Cholecystokinin (CCK)
- where is it produced
- what increases it’s release?
- What does it’s release do?
It’s produced in the duodenum ;
Eating fat and protein increases CCK release
Increased CCK release stimulates GB contraction to increase the flow of bile into the duodeum
Where is the space of Disse and what is it?
It’s located between the hapatocyte and the sinusoid
-lymph and proteins drain here before emptying into hte lymphatic duct
What is this structue and label it
The liver lobule/Ascinus (functional unit of the liver)
- Central Vein (Big ol’ blue thing by it’s lonesome self)
- Hepatocytes (Pink)
- Bile cannulici (Green)
- Branch of the portal vein (Blue between green and red)
- Branch of the hepatic artery
- sinusoid (purple)
- Kuppfer cell (yellow)
8.
T/F: Sinusoids are capillaries
true
What most accurately describes hepatic perfusion?
A. hepatic artery provides 75% of liver blood flow
B. The portal vein provides 50% of liver blood flow
C. The hepatic artery provides 75% of the liver’s oxygen content
D. The portal vein provides 50% of the livers oxygen content
D. The portal vein provides 50% of the livers oxygen content
Hepatic artery supplies ____% liver blood flow and ___% O2 content
The portal vein supplies ____% liver blood flow and ___% O2 content
Hepatic artery - 25% blood flow + 50% o2 content (higher concentration of o2)
Portal vein- 75% liver blood flow + 50% o2 content
What serves as a blood reservoir incase of acute hemorrage?
The liver
-Receives 30% of cardiac output
First 3 branches coming off the descending aorta and what do they supply?
1. Celiac artery
- Liver (via hepatic artery) supplies 25% blood flow to liver/50% O2
- Spleen
- Stomach
2. Superior mesenteric artery (SMA)
- Pancreas
- Small intestine
- Large intestine/Colon
3. Inferior mesenteric artery (IMA)
- Large intestine/Colon
What drains blood from splanchic circulation
The portal vein
-supplies liver with 75% blood flow
50% o2
Normal portal vein pressure
7-10mmHg
Portal HTN = portal vein pressure > ____
20mmhg
Flow through the portal vein is autoregulated at what
Nothing, it’s not autoregulated.
So anything that increases splanchic vascular resistance, reduces portal vein flow (SNS stimulation, pain, hypoxia, hypercarbia)
How do varicies come about?
Bad liver > increase pressure through the portal vein
-portal HTN > back pressure on all the splanchic organs
>vessels become engorged in the esophagus, stomach and intestine.
What is acities from?
Portal HTN
increased pressure in the portal vein > fluid seeps out of the vasculature and into the abdominal cavity
What 2 major vessels supply blood to the liver?
Hepatic artery (
& Portal vein (drains sphlanchic circ)
The celiac artery provides blood flow to which 3 organs?
- Liver
- Spleen
- Stomach
The superior mesenteric artery supplies blood flow to what 3 organs?
- Pancreas
- Small intestine
- Large intestine/Colon
What organ receives blood flow from the inferior mesenteric artery?
The colon
4 things that increase splanchic vascular resistance
- hypoxia
- Pain
- SNS stimulation
- Propanolol
Hepatocytes produce: (Select 3):
- thrombopoietin
- alpha-1-acid glycoprotein
- immunoglobulins
- factor 3
- factor 7
- factor 8
thrombopoietin
Alpha-1-acid glycoprotein
factor 7
(factor 8 is produced by the sinusoids)
(factor 3 by the vascular endothelium)
What lab value is an early indicator of synthetic liver dysfunction and why?
PT
because factor 7 has the shortest half-life of all the procoagulant proteins
-whatever
The liver produces all the clotting factors except which 3?
3 (vascular endothelium)
4 (calcium from diet)
& von Willebrand (vascular endothelium)
T/F- the liver produces immunoglobulins
False- it produces all plasma proteins EXCEPT immunoglobulins
Vitamin K-depdent clotting factors and proteins
2, 7, 9, 10
C-S-Z
Why would someones ammonia level be high - where does ammonia come from
ammonia is a byproduct of protein metabolism.
-Protein gets broken down into ammonia > ammonia is cleared by liver
if liver not working, ammonia builds up > hepatic encephalopathy
Byproduct of protein metabolism
Ammonia
Byproduct of hemoglobin metabolism
Bilirubin
Where doe we get bilirubin
from the breakdown of hemoglobin
How is bilirubin removed from the body?
it’s conjugated with glucuronic acid in the liver, facilitating it’s elimination
-someone with liver failure cant do this and unconjugated bilirubin is neurotoxic (hepatic encephalopthy)
What coagulation protein stimulates platelet production
Thrombopoietin
Why are liver failure patients at risk for hypoglycemia?
Bc the liver clears insulin from systemic circulation
- increased insulin in systemic circulation = risk of hypoglycemia
2 physiologic functional categories of the liver
- Synthesis of proteins (coagulation and plasma proteins)
- metabolism (carbs, proteins, fats)
The liver converts ammonia to _______; which is elminated by the kidney
urea
Why might someone with liver dysfunction have a lower BUN
because the liver converts ammonia to urea , so low levels of urea (BUN) may be indicative of liver disfunction
life cycle of a RBC
120 days
What plasma proteins are synthesized in the liver?
All of them except immunoglobulins
Match each lab test with its underlying pathology:
- Transaminases:
- Prothrombin time:
- 5’-nucleotidase
- Bilirubin
- biliary obstruction, synthetic function, hepatocellular injury, hepatic clearance.
- Transaminases: hepatocellular injury
- Prothrombin time: synthetic function
- 5’-nucleotidase: biliary obstruction
- Bilirubin: hepatic clearance
What labs assess synthetic function of the liver (2)
PT and albumin
What labs assess hepatocellular injury (2)
AST, ALT
What lab assesses hepatic clearance?
Bilirubin
What 3 labs would be elevated in a biliary duct obstruction?
- Alkaline phosphatase
- Y-glutamyl transpeptidase
- 5’- nucleotidase
T/F - PT is very sensitive for acute hepatic injury
-why or why not
True
because factor 7 has a half-life of only 4-6 hours
Half life of albumin
21 days
(not sensitive for acute hepatic injury)
Most specific indicator of biliary duct obstruction
5’- Nucleotidase
What does marked elevation of AST and ALT suggest
hepatitis
An AST/ALT ratio > ____ suggests cirrhosis or alcoholic liver disease
>2
Normal PT
12-14 sec
Normal Albumin
3.5-5g/dL
(same as K)
Normal AST/ALT
AST 10-40
ALT 10-50
(think L = love = ALT loves a wider range)
What would indicate that a hematoma is starting to be reabsorbed? (lab)
increase in bilirubin
(as it’s reabsorbed, rbcs get broken down > bilirubin)
PT is shorterend or prolonged in viatmin K deficiency
prolonged
Normal bilirubin
0-11units/L
Why might someone with have an elevated alk phos but normal liver function
it’s also in bone, placenta, and tumors
-so maybe they pregnant? maybe they have a tumor?
Normal 5’- Nucleotidase
0-11
(same as bilirubin)
*indicates biliary duct obstruction
T/F- halothane hepatitis is an autoimmune response
True
What is the most common cause of chronic hepatitis?
Alcohol Abuse
What is the most common form of viral hepatitis?
Hep A
Which forms of hepatitis can cause cirrhosis
B & C
(Not A)
What is a co-infection that happens with hepatitis B
Hepatitis D
Which Hepatitis’s can be transmitted in a blood transfusion?
B & C
Which hepatitis’s are transmitted by the oral-fecal route?
A & E
(A&E channel broadcasts fecal-oral routes)
What is halothane metabolized into that can produce an immune-mediated response?
Trifluoacetic acid (TFA)
Most common cause of liver cancer
hepatitis
Drug-induced hepatitis can ber caused by what 3 drugs?
- Acetaminophen
- Halothane
- Alcohol
What is the antidote for acetaminophen OD?
Oral N-Acetylcystine
Most common cause of drug-induced hepatitis
Alcohol abuse
Whats another name of saying someone has liver inflammation
hepatitis
3 causes of hepatitis
- virus’s
- hepatotoxins (drugs)
- autoimmune responses
Most common cause of acute liver failure in the US
Acetaminophen OD
Max acetaminophen dose/day
4g/day
What is the toxic metabolite produced by acetaminophen? How is it elminated?
NAPQI
N-acetyl-p-benzoquinoneimine
it is conjugated with glutathione
What happens with tylenol OD
the liver congugates the toxic metabolite NAPQI + Glutathione
-when there is no more glutathione left, the concentration of toxic NAPQI rises > hepatocellular injury
Treatment of tylenol OD and what time frame must it be administered
oral N-acetylcystine within 8 hours of OD
Which volatile agents are metabolized into TFA
Halothane
Desflurane
Isoflurane
*but up to 20% of halothaine is metabolized, so much higher levesl of TFA comared to the others (0.02% des and 0.2% Iso)
Most common and second most common cause of chronic hepatitis
most common = alcoholism
2nd most common = hep c
6 risk factors for halothane hepatitis
- female
- over 40yo
- fat
- genetics
- more than 1 exposure
- CYP 2E1 induction (alchol, isoniazid, phenobarbital)
All of the following drugs should be avoided in the patient with acute hepatitis EXCEPT:
A. amiodarone
B. tetracycline
C. acetaminophen
D. Propanolol
D. Propanolol
(reduces portal pressure by reducing CO (b1) and splanchic vasoconstriction (b2)
How does propanolol reduce portal pressure (2 ways)
- Decerases cardiac output (b1) - less blood to go into portal circ
- Splanchic vasoconstriction (b2) - i dont understand
Ok to proceed to surgery if someone has acute hepatitis?
Not if it’s elective - postpone until sx resolve and LFTs normal
ok to proceed to elective surgery in someone with chronic hepatitis?
as long as the condition is stable
How are mac levels affected in someone whos not acutely intoxicated but is a chornic alcohol user
INCREASED MAC
You gotta anesthetize a drunk person; what are your first thoughts
Full stomach- RSI
Decreased MAC
Avoid Des (some literature says des reduces hepatic blood flow to a greater extent)
-No PEEP (increases resistance to hepatic drainage)
How quickly do s/s alcohol withdrawl present? When do they peak?
6-8 hrs after BAC returns to near normal
Peak 24-36 hours
Someone with heptitis, how is it going to affect your NMBs
prolong duration of sux 2nd to decreased pseudocholinesterase
-prolonged doa of roc bc of it’s biliary excretion (maybe use cist)
What receptors does alochol work at
it agonizes GABA (becomes downregulated with chonric use)
& antagonizes NMDA receptors /glutamate (becomes upregulated with chronic use)
-so when you have extra nmda receptors , and not many gaba receptors and stop drinking alcohol; you have extra stimulation of the nmda recpetors and less inhibitory receptors = the increase SNS response
vitamin B1 (thiamine) deficiency contributes to what syndrome
Wernike-Korsakoff syndrome
“Wernickes Aphasia” - due to loss of neurons in the cerebellum brought on by thiamine deficiency
You see a patient on Disulfiram - what is it and what are your concerns
-it’s a treatment for alocholics in recovery
-it inhibits dopa-beta hydroxylase (NE synthesis) -> Hypotension
Common physiologic changes in the patient with cirrhosis include all of the following EXCEPT:
A. Respiratory acidosis
B. Increased CO
C. Right to left shunt
D. Decreased GFR
A. Respiratory acidosis
P’ts with cirrhosis experience pulmonary vasodilation (lungs sense a decreased blood flow - bc its backing up in portal circulation - so they the pulm vasculature dilates to try to accept more blood)
right-to-left shunting - dont get
hypoxemia > they hyperventilate to offset the reduction in PaO2 creating a respiratory alkalosis
What is cirrhosis?
It’s when liver cells die and fibrotic tissues and nodules replace healthy tissue
-decerased # of functional hepatocytes
Most common cause of liver diseae
Non-alcoholic fatty liver disease
(fatty infiltration - obesity)
What genetic enzyme deficiency leads to cirrhosis
Alpha-1-antitrypsin deficiency (also leads to emphysema)
How does hemochoromatosis affect the liver?
Iron overload
*check coags
What is Wilson’s disease
a genetic cause of cirrhosis where copper accumulates in the tissue
(WIIIILLLSSSOONNNN - put copper pipes in his liver while stranded on an island with his volleyball)
Patient is at increased risk of perioperative morbidity and mortality if they have a child -Pugh score of ____ or a MELD score of ______.
Child-Pugh - C
MELD > 15
What 3 factors does the meld score look at?
- Bilrubin
- INR
- Creat
What does the MELD score predict?
90-day mortality in patients with ESLD.
What5 factors does the modified Child-Pugh score examine?
- Albumin
- PT
- bilirubin (MELD)
4 ascities
- encephalopathy
someone has splenomegaly, what do you want to check?
platelets
What might someones sodium look like if they have cirrhosis
Low
- decreased GFR activates RAAS > sodium and water retention > dilutional hyponatremia
What does TIPS procedure stand for?
Transjugular intrahepatic portosystemic shunt
What happens with a TIPS procedure?
a shunt is placed to shut blood from the portal vein (inflow vessel to the liver) to the hepatic vein (hepatic outflow vessel)
- it reduces portal pressure and backflow on splanchic organs
- decreased likelihood of esophgeal varices bleeding
- decreases volume of ascities
*temporary treatment for hepatorenal syndrome
Risk of TIPS procedure
hemorrhage
How are the kidneys affected with hepatorenal syndrome
the lack of blood flow to the liver (bc it’s diseased) - increaases cardiac output (volume going to the liver) but also leads to decreased SVR (hypotension) bc of the release of vasoactive substances
-kidneys become hypoperfused, RAAS activated, worsens issue
Match each phase of liver transplantation with its MOST likely complication:
- Pre-Anhapatic phase
- Anhepatic phase
- Neohepatic phase
-hyperkalemia, pulmonary aspiration of gastric contents, profound reduction of cardiac output
- Pre-Anhapatic phase + pulmonary aspiration of gastric contents
- Anhepatic phase + profound reduction in CO
- Neohepatic phase+ hyperkalemia
Most common indication for liver transplant +2 more
*HEP C*
- etoh liver diseae
- malignancy (interesting)
What starts and ends the pre-anahepatic phase?
what’s the goal
start - surgical incision
end - cross clamping of portal vein, hepatic artery, and IVC
goal is to mobilize the liver and vascular structures and isolate the CBD
What starts and ends the anhepatic phase of liver transplantation
goal
beings with removal of the native liver
ends with emplantation of donor liver
goal- remove and replace donor liver (allograft)
When does the neoheptaic phase of liver transplantation begin and end
begins with reperfusion of the donor liver
ends with biliary anastomosis (or transport to ICU)
-goal: perfuse the donor liver, anastomosis of hepatic artery and biliary structures
Pre-anahepatic phase goals:
hgb > ____
platelets > _____
fibrinogen > _____
MA(TEG) > ______
hgb > 7
platelets > 40
fibrinogen > 100
MA(TEG) > 45
What would you expect to happen to your blood pressure during the pre-anahepatic phase of liver transplant and why?
hypotension
-from draining ascities, compressing vascular structures, and ongoing blood loss
Where should your CVP be prior to clamping the IVC?
increase it to 10mmHg
What 3 things can result from large volume blood product administration
- lactic acidosis
- hyperkalemia
- hypocalcemia
why does large volume transfusion lead to hypocalemia?
bc of citrate toxicity
citrate binds calcium
concerns with crystalloid resusitation
can cause dilutional coagulopathy and thrombocytopenia and worsen your issue
What’s a bicaval clamp and your concerns
clamps are applied to IVC above and below the liver (full obstruction of IVC flow)
*significant preload reduction > hypotension, tachycardia
*aggressive fluid administration can lead to volume overload when clamps are released
What is the piggyback technique when isolating the liver
the IVC is side-clamped (IVC flow is partially obstructed)
- less preload reduction compared to bicaval clamp
- fewer blood products required
How is venovenous bypass used to isolate the liver for resection?
sites of cannulation
Site of cannulation leaving body and going to pump:
femoral vein - (systemic blood flow)
portal vein - (splanchic blood flow)
Site of cannulation leaving pump and returning to the body:
Axillary vein (blood returns to the IVC > heart)
3 potential complications of venovenous bypass for liver transplant
air embolism, thromboembolism, decannulation
Common problems with anhepatic phase of liver tranpsplant
worsening coagulopathy, blood loss, lactic acidosis, hypoglycemia (no glycogen storage)
*use sodium bicarb to combat acidosis
When does warm ischemic time begin and end and what is the time limit
begins when donor organ is removed from ice
ends when the donor liver is reperfused
<30-60 mins
How should you prepared for reperfusion of the donor liver
DECREASE POTASSIUM LEVEL beforehand bc it will rise!
- hyperventillate
- D50 + insulin
- Bicarb
- Albuterol
- Furosemide
First line tx for hyperkalemia (drugs) -2
calcium chloride (raide TP)
sodium bicairb
Should your CVP be elevated or reduced after the donor graft is being reperfused
REDUCED - if it’s high, it will cause congestion in the graft
How can you tell if the donor graft is taking well (3 things)
- return to normothermia (fastest check)
- stablization of glucose and acid-base balance
What is hte most important consideration during the neohepatic phase of liver transplantation.
How do you treat it?
Post-Reperfusion Syndrome
systemic hypotension > 30% below baseline for at least 1 mintue
(during the first 5 mins of reperfusion)
*It’s common! 10-60%
Treat: supportive - vasopressors, lyte correction (hyperkalemia, hypocalcemia), acid-base correction
2 signs of a poorly functioning graft (donor liver)
- contineud hemodynamic instablity
- lack of bile output
T/F- epidural anestheisia is a good method of pain control for liver transplant patients
false- coagulopathic! epiurals are contraindicated
-PCA
what would you anticipate your patient having once over in ICU (2 gtts)
PCA
Insulin (steroid-induced hyperglycemia)
What view should be avoided when performing a TEE in a patient with esophageal varices?
All transgastric views
All of the following drugs improve biliary hypertension EXCEPt:
A. Naloxone
B. Nitroglycerine
C. Glucagon
D. Octreotide
D. Octreotide
Why might the doc ask for a drug to relax the sphincter of oddi during cholangiogram?
because if it’s contracting it can lead to a false positive result
5 drugs you can use to relax the sphincter of Oddi and reduce biliary pressure (& Mneumonic)
NNAGG
Nitro
Naloxone
Atropine
Glyco
Glucagon
What happens when someone has obstructive biliary stones?
Bile cant flow into the small intestine; so it backs up into the liver and pancreas resulting in inflammation
T/F- glucagon increases risk of PONV
True!
What is Murphy’s sign
RUQ pain that is worse with inspiration
(GB disease)
- Cholecystitis:
- Cholelithiasis
- Choledocholithiasis:
What are they are what is the surgical treatment for each?
-
Cholecystitis:
- Inflammation of the GB (cholecystectomy)
-
Cholelithiasis
- Gallstones (cholecystecomy)
-
Choledocholithiasis:
- Stones in the CBD (ERCP)
Who gets an ERCP
someone with stones in their CBD
T/F- smoking is a risk factor for cholelithasis
False!
Bile is produced by ________ and stored in the ________
hepatocytes; gallbladder
why does the liver failure patient have hyperdynamic circulation with a low SVR and increase in CO?
because severe liver disease impairs the livers abilty to clear vasodilating substances from systemic ciruclation (SVR drops and CO picks up to try and compensate)
Propanolol reduces hepatic blood flow by causing:
A. Portal vein dilation
B. Portal vein constriction
C. Hepatic artery dilation
D. Hepatic artery constriction
D. Hepatic artery constriction
via beta 2 receptor blockade > vasoconstriction
When blood flow to the liver falls, what kicks in to preserve hepatic blood flow and how
The hepatic arterial buffer response
- if portal vein flow comprimised, the hepatic artery dilates
- if hepatic artery flow is compromised, the portal vein dilates
- severe liver disease impairs this buffer response.
What is the region most suseptible to hypoxic injury
Well i knew it was zone 3, but idk whats in there lol
- ok so zone 3 is near the central vein
- blood comes in from the terminal branches of the hepatic aretery and portal vein and enter the peipheray of the lobule (zone 1) - best oxygenated.
- zone 3 (near the central vein) recieves the least amount of o2, making it most susceptible to hypoxic injury. (+ of course has the highest conentration of CYP450 enzymes)
Most common form of viral hepatitis
A
- makes sense bc fecal-oral transmission is easier to aquire
- good thing hep A doesnt lead to chronic hepatitis, cirrhoisis, or cancer
