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Health Assessment > Hepatic Biliary Systems exam 3 > Flashcards

Hepatic Biliary Systems exam 3 Flashcards

mordecai

1
Q

What is cholelithiasis?

A

Gall stones. Hepatocytes secrete bile through bile ducts, into common hepatic duct, into gall bladder and common bile duct

Risk factors: fat pregnant female

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2
Q

Liver functions

Liver synthesizes glucose via _____.

Stores excess glucose as _____.

Synthesizes cholesterol and proteins into ____ and ____.

A

glucogenesis

glycogen

hormones and vitamins

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3
Q

Liver functions

Liver metabolizes fats, proteins and carbs to gerenate _____

Liver metabolizes drugs via ____ and other enzyme pathways

Liver _____ blood

A

energy

CYP 450

detoxifies

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4
Q

Liver functions

Liver is involved in the acute phase of ____ _____

Liver processes Hgb and stores ____

A

immune support.

iron.

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5
Q

Liver synthesizes all coag factors except 4. What are they?

Liver aids in volume control as a ___ _____

A

3, 4, 8( vWF)

blood reservoir

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6
Q

Liver has 8 segments. R and L lobes are separated by ____ ligament.

Where do the 3 hepatic veins empty?

A

Falciform (R lobe is bigger)

Right, middle and left hepatic veins empty into IVC!

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7
Q

Bile duct travels along ____ _____

Where does bile drain into?

How does bile enter duodenum

A

portal veins.

  • Bile drains through the hepatic duct into gall bladder & common bile duct
  • Bile enters duodenum via Ampulla of Vater
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8
Q

Describe O2 delivery in liver

A
  • 50% via Portal vein (deoxygenated)
  • 50% via Hepatic artery
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9
Q

What does portal vein arise from? How much hepatic blood flow does it supply?

Portal vein blood is deoxygenated blood from what 3 structures

A

portal vein arises from the splenic vein and superior mesenteric vein;makes up 75% HBF
* Portal vein blood is deoxygenated from GI organs, pancreas & spleen

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10
Q

What are 3 groups of hepatobiliary disease?

A

-hepatocellular injury (high AST/ALT)
-reduced synthetic function (low albumin, high PT/INR)
-cholestasis: high Alk phosphatase, low GGT, high bilirubin

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11
Q

What is choledocolithiasis?

Symtpoms?

A

-stone obsructing common bile duct–> biliary colic

initial: N/V, cramps, RUQ pain. Cholangitis sx: fever, rigors, jaundice

Tx: stone removal via ercp

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12
Q

What is ERCP?

What complication may happen?

A

-Endoscopics threads guidewire through sphincter of Oddi, into ampulla of vater to retrieve stone from pancreatic duct or common bile duct.
Positioning: prone w L tilt.
*May require glucagon for Oddi spasm!

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13
Q

What is primary biliary cholangitis aka biliary cirrhosis?

Tx?

women>

A

Autoimmune destruction of bile ducts with periportal inflammation and cholestasis. Leads to liver scarring, fibrosis, cirrosis.

No cure but exogenous bile acids slow progression

intrahepatic ducts only

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14
Q

Labs for Primary Biliary Cholangitis?

Liver biopsy reveals what?

A

Elevated Alk Phos, GGT and + antimitochontrial antibodies

Liver biopsy reveals bile duct destruction and infiltrations w lymphocytes

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15
Q

What is Wilson’s disease?

S/S?

AKA hepatolenticular degradation

A

-Autosomal recessive disease–> impaired copper metabolism.
-Excessive copper leads to oxidative stress in live, basal ganglia and cornea

S/S asymptomatic to sudden onset liver failure along w neurologic and psych manifestations

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16
Q

How is Wilson’s Disease diagnosed

A

serum ceruloplasmin, aminotransferases, urine copper level, liver biopsy (for Cu level)

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17
Q

What is the treatment of Wilson’s Disease

A

Treatment: copper chelation therapy and oral zinc to bind copper in GI

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18
Q

What is alpha-1 antitrpsin deficiency?
How is it diagnosed?

A
  • Genetic disorder resulting in a defective α-1 antitrypsin protein
  • Dx: confirmed w/ α-1 antitrypsin phenotyping

#1 cause of liver transplant in children!

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19
Q

α-1 antitrypsin proteins protect the liver & lungs from what?

A

neutrophil elastase–>enzyme that causes disruption of connective tissues, leading to inflammation, cirrhosis, and hepatocellular CA

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20
Q

How is alpha 1 antitrypsin deficiency treated

A
  • Tx: pooled α-1 antitrypsin is effective for pulmonary symptoms; doesn’t help with liver disease
  • Liver transplant is the only curative treatment
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21
Q

What is hemochromatosis?
What is the treatment

A

-Excess iron accumulation in body! Leads to multiorgan failure
Is genetic (excessive iron absorption) or may be caused by lots of blood transfusions or high dose iron infusions

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22
Q

Hemochromatosis: patients may present with what 5 conditions?

A

cirrhosis, heart failure, diabetes, adrenal insufficiency, or polyarthropathy

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23
Q

What’s the treatment for hemochromatosis?

A

Tx: weekly phlebotomy, iron chelating drugs, liver transplant

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24
Q

How is hemochromatosis diagnosed?

What are the labs?

A

Dx: genetic mutation testing
echo and MRI diagnose cardiomyoapthy and liver abnormalities.
Liver biopsy! may quantify iron levels and assess damage

Labs–> elevated ast/alt, transferrin saturation and ferritin

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25
Q

PSC

What is primary sclerosing cholangitis?

Prevalent in men in their 40’s

A

Autoimmune chronic inflammation of large bile ducts.
- Fibrosis in biliary tree→strictures (beads on string appearance)→ cirrhosis, ESLD

intrahepatic AND extrahepatic

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26
Q

How is PSC diagnosed?

beads on string*

A

Dx: MRCP or ERCP showing biliary strictures w dilated bile ducts
liver biopsy! but not always performed

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27
Q

Treatment for PSC? (primary sclerosing cholantitis?

A

Liver transplant! No drug treatment is effective. Reoccurence is common after transplane d/t auroimmune nature :(

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28
Q

What is cirrhosis? What are the symptoms

A

final stage of liver disease. Scarred liver!
asymptomatic in early stages. Late symptoms are jaundice, ascites, varices, coagulopathy, encephalopathy.

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29
Q

What are common causes of cirrhosis (4)

A

caused by alcoholic fatty liver, NAFL, HCV, HBV

30
Q

What are the labs seen in cirrhosis?
How is it treated?

A
  • Elevated labs: AST/ALT, bilirubin, Alk phosphatase, PT/INR
  • Thrombocytopenia
    Transplant is the only cure
31
Q

What are complications of cirrhosis? (8)

A

-portal HTN (hepatic venous pressure gradient >5)
-ascites
-bacterial peritonitis
-varices
-hepatorenal syndrome
-hepatic encepalopathy
-hepatopulmonary syndrome
-portopulmonary HTN

32
Q

What is ascites?
How is it managed?

A

Most common complication of cirrhosis.
* Portal-HTN leads to ↑blood volume & peritoneal accumulation of fluid
* Management: ↓Salt diet, albumin replacement
TIPS-reduces pulmonary HTn and ascites

33
Q

What are treatment of varices?

Present in 50% cirrhosis patients

A

-BB help reduce risk
endoscopic banding and ligation
Balloon tamponade for bleeding

34
Q

What is hepatic encephalopathy?

What is the treatment?

A
  • Buildup of nitrogenous waste d/t poor liver detoxification
  • Neuropsychiatric symptoms (cognitive impairment → coma)

Tx: Laculose, rifaximim to decrease ammonia

35
Q

What is hepatorenal syndrome?

What is the treatment?

A

** Excess endogenous vasodilators (NO, PGs)→ decrease systemic MAP and lower RBF!

  • Tx: Midodrine, Octreotide, Albumin
36
Q

What is hepatopulmonary syndrome?

A
  • Triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
  • Platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt
37
Q

What is portopulmonary HTN ?
What is the treatment?

A
  • Pulmonary HTN accompanied by portal HTN
  • Systemic vasodilation triggers production of pulmonary vasoconstrictors
  • Tx: PD-I’s, NO, prostacyclin analogs, and endothelin receptor antagonists
  • Transplant is only cure
38
Q

What are the 2 scoring systems to determine severity and prognosis of liver disease?

A

* Child-Turcotte-Pugh (CTP): points based on bilirubin, albumin, PT, encephalopathy, ascites
* Model for End Stage Liver Disease (MELD): score based on bilirubin, INR, creatinine, sodium

39
Q

Elective surgery contradicted in what 3 diagnosis?

A

acute hepatitis, severe chronic hepatitis and acute liver failure

40
Q

What is TIPS

Transjugular intrahepatic portosystemic shunt

A

-A stent/ graft placed between hepatic vein and portal vein.
-shunts blood flow to systemic circulation and reduces portosystemic pressure gradient

41
Q

What are TIPS indications? (2)
Contraindications? (3)

A

Indications: variceal hemorrhage, regractory ascites
Cx: HF, tricuspid regurgiation and severe pulm HTN

42
Q

What is partial hepatectomy?

A
  • Resection to remove neoplasms, leaving adequate tissue for regerenation
    Up to 75% removal is tolerated in patients w normal lvier!
43
Q

What are anesthetic considerations in partial hepatectomy?

A
  • Invasive monitoring
  • Blood products available
  • Adequate vascular access
  • maintain low CVP by fluid restriction, prior to resection to reduce blood loss
    -Surgeon may clamp IVC or hepatic artery to minimize blood loss
    -Prepare for post op coag disturbances
    -post op PCA
44
Q

Intra op Managment of liver transplant ?

A
  • Maintain hemodynamics (Pressors/Inotropes readily available)
  • A-line, CVC, PA cath, TEE
  • Control coagulation
45
Q

Preop considerations in liver transplants?

A

Pre op evaluation, vascular access and blood product availability.

46
Q

Intraop anesthesia considerations of liver disease?

A

High risk aspiration, hypotension, hypoxemia!

Plasma cholinesteraase may be decreased and NMDR will be prolonged!

Bleeding and coag managment

47
Q

How does alcoholism affect MAC?

Which NMB are preffered?

Drugs onset and duration?

A

Alcoholism increases MAC of volatile anesthetics

Succs and cisatracurium are ideal

Drugs may have a slow onset and prolonged duration of action!

48
Q

What to use for volume resuscitation in liver disease?

A

Colloids> crystalloids bc they are low in albumin and have low SVR

49
Q

What to watch for during reperfusion of transplanted liver?

A

Watch for hemodynamic instability, dysrhythmias, hyperkalemia, acidosis, pulmonary emboli, and cardiac arrest

50
Q

What are inborn errors of metabilism?

What are the 3 disorders?

A

-Groups of genetical disorders that lead to a defect in the enzymes that breakdown and store protein, carbs and fatty acids

-wilsons, alpha-1 antitrypsin deficiency and hemochromatosis`

occurs in 1:2500 births

51
Q

How is non alcoholic fatty liver diasese diagnosed?

Tx?

How does it progress?

A

Liver biopsy; hepatocytes contain >5% fat

Tx: diet, exercise; Liver transplant indicated for advanced fibrosis and cirrhosis

Progreses to non alcoholic steatohepatitis-> cirrhosis->hepatocellular carcinoma

52
Q

What’s the breakdown of oxygen delivery to the liver?

A

50% from portal vein (deoxygenated from GI organs, pancreas and spleen)
50% from hepatic artery

53
Q

What is concerning about increased portal venous pressure?

A

blood backs up into systemic circ causing esophageal and gastric varices!

portal venous pressure reflects splanchnic arterial tone and intrahepatic pressure

54
Q

Hepatic arterial flow is inversly related to what?

Hepatic artery dilates in response to ___________

A

portal venous blood flow!

dilates in response to low portal venous flow, to keep consistent hepatic blood flow

55
Q

What is normal portal venous pressure?

A

1-5 mmHg

56
Q

What portal venous pressure is considered clinically significant portal HTN (leading to cirrhosis and esophageal varices)?

A

> 10 mmHg

57
Q

What are the most liver-specific labs?

What lab will be elevated in late stage liver damage?

A

AST + ALTs

gamma-glutamyl-transferase (GGT; end stage liver)

58
Q

How may the AST/ALT enzymes differ between the 3 types of hepatocellular injuries?

A
  • Acute Liver Failure: ALT/AST may be elevated 25x
  • Alcoholic Liver Dz (ALD): AST:ALT ratio usually at least 2:1
  • Non Alcoholic Fatty Liver Disease: ratio usually 1:1
59
Q

How will you position pt for a lap chole?

A

reverse trendelenburg w/ a left tilt

60
Q

How will you position pt for an ERCP?

A

prone with a left tilt, head to patient’s right, tape ETT to left

61
Q

What is unconjugated bilirubin?

A

Protein bound to albumin, transported into liver and conjugated into its H20 soluble “direct” state, then excreted into bile

bilirubin: end product of heme breakdown

62
Q

What’s the difference between unconjugated and conjugated hyperbilirubinemia?

A

unconjugated: imbalance between bilirubin synthesis and conjugation (think physiologic jaundice of newborns, hgb disorders, hemolysis, drug-induced, sepsis)

conjugated: caused by an obstruction that causes conjugated bili into circulation (think cholestasis, cirrhosis, congenital infections, obstructive jaundice)

63
Q

What is the most common viral hepatitis requiring liver transplant in the US?

A

Hep C

64
Q

Whats the treatment for hep C?

A

12 week course of sofosbuvir/velpatasvir

provides 98-99% clearance of genotype 1a/1b

65
Q

What plt count requires blood transfusion?

A

< 50K

66
Q

When do ETOH withdrawal symptoms start to occur after they stop drinking?

A

24-72 hours

67
Q

what are some s/s of alcoholic liver disease?

A

malnutrition, muscle wasting, parotid gland hypertrophy (CHIPMUNK CHEEKS!), jaundice, thrombocytopenia, ascites, hepatosplenomegaly, pedal edema

68
Q

What is the most common cause of drug-induced liver injury?

A

acetaminophen overdose

69
Q

How is alcoholic disease treated?

A

Managment of symptoms of liver failure! Transufsion <50,000 Plt count.
-liver transfusion if criteria is met (2% of liver tx are for ALD)

70
Q

What are the lab values for autoimmune hepatitis? Treatment??

A

+ autoantibodies and hypergammaglobulinemia
AST and ALT 10-20 times normal

Tx: steroids, azathioprine;
Immunosuppression for refractory disaease, Liver tx may be indicated

affects women; asymptomatic, acute or chronic

71
Q

What are s/s of cholelithiasis?

What’s the treatment

A

s/s: RUQ pain referred to shoulders, N/D, indigestion, feve

Tx: IVF, antiopiotics, lap chole (reverse T w L tilt )

Health Assessment (30 decks)

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