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Mar: Sem 2 - Health Assessment > Hepatobillary (bri's deck) > Flashcards

Hepatobillary (bri's deck) Flashcards

1
Q

What are the functions of the liver?

A
  • Synthesizes: glucose via gluconeogenesis and stores excess glucose as glycogen
  • Synthesizes: cholesterol & proteins into hormones and vitamins
  • Synthesizes: coagulation factors (all except factors III, IV, VIII, vWF)
  • Metabolizes: fats, proteins, carbs to generate energy
  • Metabolizes: drugs via CYP-540 and other enzyme pathways
  • Blood: Detoxifies
  • Blood: Processes Hgb and stores iron
  • Blood: Aids in volume control as a blood reservoir
  • Involved in the acute-phase of immune support

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2
Q

Nearly every organ is impacted by ____.

A

liver function- Liver dysfunction can lead to multi-organ failure

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3
Q

how many segments are in the liver?

A

8 segments
Based on blood supply & bile drainage

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4
Q

what are the R&L lobes separated by?

A

falciform ligament

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5
Q

____ vein and ____ artery branch into each segment

A
  • portal vein
  • hepatic artery

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6
Q

what 3 veins empty into IVC?

A

Right, Middle, Left hepatic veins

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7
Q
  • Bile ducts travel along ____.
  • Bile drains through the ____ into Gallbladder & Common Bile Duct
  • Bile enters duodenum via ____.
A
  • portal veins
  • hepatic duct
  • Ampulla of Vater

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8
Q

Liver recieves ____% of COP. which is about ____ L/min.

A
  • Receives 25% of COP
  • 1.25-1.5 liters per min
    highest proportionate COP of all organs

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9
Q

portal vein arises from ____ vein and ____ ____ vein

A
  • splenic vein
  • superior mesenteric vein

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10
Q

portal vein blood is deoxygenated from ?

A
  • GI organs
  • pancrease
  • spleen

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11
Q

portal vein provides ____% of HBF

A

75%

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12
Q

Which artery branches off the aorta?

A

hepatic artery

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13
Q

hepatic artery provides ____% of HBF

A

25%

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14
Q

how does the liver get O2?

A
  • 50% viaPortal vein (deoxygenated)
  • 50% via Hepatic artery

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15
Q

hepatic arterial blood flow is inversely related to

A

portal venous blood flow

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16
Q

how is hepatic blood flow autoregulated?

A

Hepatic art. dilates in response to low portal venous flow, keeping consistent HBF

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17
Q

Portal venous pressure reflects ____ tone and ____ pressure

A

splanchnic arterial tone and intrahepatic pressure

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18
Q

increased portal venous pressure causes

A

blood backsupinto to systemic circulation resulting in esophageal and gastric varices

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19
Q

hepatic venous pressure gradient is used to determine severity of?

A

portal hypertension

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20
Q

what is a normal Hepatic venous pressure gradient (HVPG)?

A

1-5 mmhg

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21
Q

this HVPG is clinically significant portal hypertension(cirrhosis, esophageal varicies)

A

> 10

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22
Q

this HVPG can see vriceal rupture

A

> 12

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23
Q

pts are often ____ until late-stage liver disease

A

asymptomatic

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24
Q

in later stages pts may only have??

A

vague s/s like disrupted sleep, and decreased appetite

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25
Q

liver function assessment relies heavily on

A

risk factors for degree of suspicion

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26
Q

Risk factors for impaired liver function (9)

A

Family hx
Heavy ETOH
Lifestyle
DM
Obesity
Illicit Drug use
Multiple partners
Tattoos
Transfusion

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27
Q

physical findings for impaired liver function (7)

A

Pruritis
Jaundice
Ascites
Asterixis (flapping tremor)
Hepatomegaly
Splenomegaly
Spider nevi

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28
Q

what labs are assessed for hepato-biliary function?

A
  • BMP, CBC
  • PT/INR
  • Aspartate aminotransferase (AST)
  • Alanine aminotransferase (ALT) most liver-specific enzymes
  • Bilirubin
  • Alkaline Phosphatase
  • ɣ-glutamyl-transferase (GGT)

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29
Q

what imaging is used for hepato-biliary function?

A
  • Ultrasound
  • Doppler U/S (Portal bld flow)
  • CT
  • MRI

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30
Q

what are the 3 groups of hepatobiliary disease per stoling?

A
  1. hepatocellular injury
  2. reduced synthetic function
  3. cholestasis

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31
Q

what do you see with hepatocellular injury?

A
  • ↑AST/ALT (hepatocyte enzymes)
  • Acute Liver Failure (ALF): may be elevated 25x
  • Alcoholic Liver Dz (ALD): AST:ALT ratio usually at least 2:1
  • NAFLD: ratio usually 1:1

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32
Q

what do you see with reduced synthetic function?

A
  • ↓Albumin
  • ↑PT/INR

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33
Q

what do you see with cholestasis?

A
  • ↑AlkPhosphatase
  • ↑GGT (gamma glutamyl transpeptidase)
  • ↑bilirubin

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34
Q

what do blood test look like for bilirubin overload (hemolysis)?
* amnotrasferase
* serum albumin
* prothrombin time
* bilirubin
* alkaline phhatase
* gamma gluamyl tranpeptidase
* blood urea nitrogen
* BSP/ICG (dye)

A
  • amnotrasferase: normal
  • serum albumin: normal
  • prothrombin time: normal
  • bilirubin: unconjugated
  • alkaline phhatase: normal
  • gamma gluamyl tranpeptidase: normal
  • blood urea nitrogen: normal
  • BSP/ICG (dye): normal

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35
Q

what do blood test look like for hepatocellular injury?
* amnotrasferase
* serum albumin
* prothrombin time
* bilirubin
* alkaline phhatase
* gamma gluamyl tranpeptidase
* blood urea nitrogen
* BSP/ICG (dye)

A
  • amnotrasferase: increased
  • serum albumin: decreased
  • prothrombin time: prolonged
  • bilirubin: conjugated
  • alkaline phhatase: normal
  • gamma gluamyl tranpeptidase: normal
  • blood urea nitrogen: normal
  • BSP/ICG (dye): retention of dye

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36
Q

what do blood test look like for cholestasis?
* amnotrasferase
* serum albumin
* prothrombin time
* bilirubin
* alkaline phhatase
* gamma gluamyl tranpeptidase
* blood urea nitrogen
* BSP/ICG (dye)

A
  • amnotrasferase: normal
  • serum albumin: normal
  • prothrombin time: normal
  • bilirubin: conjugated
  • alkaline phhatase: increased
  • gamma gluamyl tranpeptidase: increased
  • blood urea nitrogen: normal
  • BSP/ICG (dye): normal or retention of dye

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37
Q

haptocytes secrete bile through bile duct into ____ which goes to ____ and ____

A

CHD→ GB & CBD

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38
Q

____ stores bile to deliver during meals, and ____ secretes bile directly into duodenum

A
  • GB
  • CBD

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39
Q

risk facotrs for cholelithiasis? ____% are asymptomatic.

A
  • Obesity
  • ↑cholesterol
  • DM
  • pregnancy
  • female
  • family hx
    80% asymptomatic

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40
Q

s/s of cholelithiasis

A
  • RUQ pain, referred to shoulders
  • N/V, indigestion
  • fever (acute obstruction)

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41
Q

tx for cholelithiasis

A
  • IVF,
  • abx,
  • pain management
  • Lap Cholecystectomy

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42
Q

2 types of cholecystectomy

A
  • laparoscopic
  • open

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43
Q

Choledocolithiasis
* cause
* initial s/s
* cholangitis s/s:
* Tx:

A
  • Stone obstructing CBD→ biliary colic
  • Initial sx: N/V, cramping, RUQ pain
  • Cholangitis sx: fever, rigors, jaundice
  • Tx: Endoscopic removal of stone via ERCP
    Endoscopic Retrograde Cholangiopancreatography

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44
Q

how to perform endoscopic retrograde cholaniopancreatogrophy

A

Endoscopist threads guidewire through Sphincter of Oddi, into Ampulla of Vaterto retrieve stone from pancreatic duct or CBD

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45
Q

what position is ERCP normally positioned and what type of anesthesia do we use?

A
  • usually prone w/left tilt (tape ETT to left)
  • GA

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46
Q

what medication may be required to treat oddi spasm

A

glucogon

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47
Q

what is bilirubin

A

end product of heme-breakdown

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48
Q

what is hyperbilirubinemia

A

Unconjugated “indirect”bilirubin is protein bound to albumin, transported to liver, conjugated into to its H20-soluble “direct” state, excreted into bile

slide 17

verify this

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49
Q

what is unconjugated (indirect) hyperbilirubinemia

A

imbalance between bilirubin synthesis & conjugation

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50
Q

what is conjugated (direct) hyperbilirubinemia:

A

caused by anobstruction, causing reflux of conjugated bilirubin into the circulation

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51
Q

5 most common types of viral hepatitis

A
  • a
  • b
  • c
  • d
  • e

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52
Q

overal viral hepatitis is on the decline d/t vaccinees and newer treatment, however ____ and ____ are more chronic.

A
  • b and c

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53
Q

what is the most common VH requiring liver transplant in US

A

Hepatitis C Virus

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54
Q

what tx has reduced HCV in USA?

A
  • Treatment based on HCV genotype (75% type 1), HCV stage, +/- cirrhosis
  • 12 week course Sofosbuvir/Velpatasvir
  • Provides 98-99% clearance of genotype 1A/1B

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55
Q

charecterisitc features of viral hepatiis

A
  • B & C are bloodborne
  • B & C are chronic
  • C is the most chronic (75%)
  • Long incubation periods

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56
Q

Alcoholic liver disease (ALD) is ____ in America and the ____ cause of cirrhosis.

A
  • increasing
  • most common

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57
Q

what is the top indication for liver transplants US

A

ALD
national prevalence liver transplant for ALD is 2%

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58
Q

what is treatment for ALD?

A
  • Treatment centered around abstinence
  • Management symptomes of liver failure
  • Platelet count < 50,000 requires blood transfusion
  • Liver transfusion an option if criteria is met

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59
Q

s/s of ALD (8)

A
  • Malnutrition
  • Muscle wasting
  • Parotid gland hypertrophy
  • Jaundice
  • thrombocytopenia
  • Ascites
  • Hepatosplenomegaly
  • Pedal edema
    *Sx of ETOH withdrawal may occur 24-72h after stopping

John Makes Me Paranoid At Home Through Phonecalls

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60
Q

lab values for ALD

A
  • ↑Mean corpuscular volume (MCV)
  • ↑Liver enzymes
  • ↑ɣ-glutamyl-transferase (GGT)
  • ↑Bilirubin
  • Blood ethanol (acuteintox)

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61
Q

Non-alchoholic fatty liver disease is when hapatocytes contain ____% fat and is r/t what 4 things?

A
  • > 5% fat
  • Obesity, Insulin resistance, DM2, Metabolic syndrome

slide 23

62
Q

NAFLD progresses to

A

NASH (nonalcoholic steatohepatitis), cirrhosis, hepatocellular carcinoma
NAFLD & NASH have become additional leading causes of liver transplant in US

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63
Q

NAFLD:
* diagnose:
* Tx:

A

Dx: Imaging and histology
- Liver biopsy= gold standard in distinguishing NAFLD from other liver dx

Tx: Diet, exercise
- Liver transplant is indicated for advanced fibrosis, cirrhosis, related complications

slide 23

64
Q

autoimmune hepatitis predominantly effects ____ and may be ____, ____, or ____.

A
  • women
  • asymptomatic, acute, or chronic

slide 26

65
Q

pt with autoimmune hepatitis have _ & _

AST/ALT may be ____ in acute AIH

A
  • +autoantibodies & hypergammaglobulinemia
  • 10-20x more than normal

slide 26

66
Q

Autoimmune Hepatitis treatment

A

steroids, azathioprine

slide 26

67
Q

in AIH ____% achieve remission but relapse is common. Refactory disease requires ____. When is liver transplant indicated?

A
  • 60-80% achieve remission; relapse is common
  • Refractory disease requires immunosuppression
  • Liver transplant indicated when tx fails or acute liver failure ensues

slide 26

68
Q

Drug induced liver injury is most commonly caused by and is normally reversable after ____?

A
  • Most common cause:Acetaminophen OD
  • Normally reversable after drug is removed

slide 26

69
Q
  • what is inborn errors of metabolism
A
  • Group of rare, genetically inherited disorders that lead to a defect in the enzymes that breakdown and store protein, carbohydrates &fatty acids

slide 27

70
Q

inborn errors of metabolism occurs in

A

1: 2500 births

slide 27

71
Q

inborn errors of metabolism onset varies from birth to adolescenst but when do the most severe forms appear?

A

Most severe forms appear in the neonatal period and carry a high degree of mortality

slide 27

72
Q

what 3 specific disorders cause inborn errors of metabolism?

A
  • Wilsons Disease
  • Alpha-1 Antitrypsin Deficiency
  • Hemochromatosis

slide 27

73
Q

What is wilsons disease AKA hepatolenticular degeneration

A
  • Autosomal recessive disease characterized by impaired copper metabolism
  • Excessive copper buildup leads to oxidative stress in the liver,basal ganglia, and cornea

slide 28

74
Q

Wilsons disease:
* S/s:
* Dx:
* TX:

A
  • Sx: range from asymptomatic to sudden-onset liver failure along with neurologic & psychiatricmanifestations
  • Dx: Lab tests (serum ceruloplasmin, aminotransferases, urine copper level) Possible liver biopsy for copper level
  • Tx: Copper-chelation therapy & oral zinc to bind copper in the GI tract

slide 28

75
Q

what is alpha 1 antitrypsin deficiency?

A

Gentetic disorder resulting in a defectiveα-1 antitrypsin protein

slide 29

76
Q

α-1 antitrypsin proteins protect the liver & lungs from ____ which isan enzyme that causes disruption of connective tissues, leading to inflammation, cirrhosis, and HCC

A
  • neutrophil elastase: an enzyme that causes disruption of connective tissues, leading to inflammation, cirrhosis, and HCC

slide 29

77
Q

what is the incidence of alpha-1 antitrypsin deficiency?

A

Incidence1: 16,000 to1: 35,000, although it is likely underdiagnosed

slide 29

78
Q

what disorder is the number 1 genetic cause of liver transplant in childer

A

α-1 antitrypsin deficiency is the #1 genetic cause of liver transplant in children

slide 29

79
Q

alpha 1 antitrypsin deficiency:
* dx
* tx

A
  • Dx: confirmed w/α-1 antitrypsin phenotyping
  • Tx: pooledα-1 antitrypsin is effective for pulmonary symptoms; however, it doesn’t help with liver disease
    Liver transplant is the only curative treatment for liver disease inα-1 antitrypsin deficiency

slide 29

80
Q

what is hemochromatosis

A
  • Disorder assoc w/ excess iron in the body, leading to multi-organ dysfunction
  • May be genetic, causing excessive intestinal absorption of iron
  • May also be caused by repetitive blood transfusions or high-dose iron infusions
  • Excess iron accumulates in organs and causes damage to the tissues

slide 30

81
Q

pts with hemochromatosis may present with

A

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

slide 30

82
Q

what will labs show with hemochromatosis?

A

Labs reveal elevated AST/ALT, transferrin saturation, and ferritin

slide 30

83
Q

Hemochromatosis:
* dx:
* tx:

A
  • Dx: genetic mutation testing, Echocardiogram & MRI diagnose cardiomyopathies and liver abnormalities
  • Liver bx may quantify iron levels in the liver and assess the level of damage
  • Tx: weekly phlebotomy, iron-chelating drugs, liver transplant

slide 30

84
Q

What is primary biliary cholangitis (PBC), previously known as biliary cirrhosis

A
  • Autoimmune, progressive destruction of bile ducts withperiportal inflammation & cholestasis
  • Can lead to liver scarring, fibrosis, cirrhosis
  • Females > Males; often dx’d in middle-ages
  • Thought to be complicated by exposure to environmental toxins in genetically susceptible individuals

slide 31

85
Q

PBC:
* s/s
* labs
* imaging
* tx:

A
  • Sx: jaundice, fatigue,& itching
  • Labs: ↑Alk Phos,↑GGT, + Antimitochondrial antibodies
  • Imaging: CT,MRI, & MRCP to r/o bile duct obstructions
  • Liver biopsy reveals bile duct destruction andinfiltration w/lymphocytes
  • Tx: No cure, but exogenous bile acids slow progression

slide 31

86
Q

what is primary sclerosing cholangitis (PSC)

A
  • Autoimmune, chronic inflammation of the larger bile ducts
  • Intrahepatic and extrahepatic
  • Fibrosis in biliarytree→strictures (beads on string appearance)→ cirrhosis, ESLD
  • Males>Females, onset ̴40’s

slide 32

87
Q

PSC:
* s/s
* labs
* dx
* liver biopsy
* drug tx

A
  • Sx: Fatigue, itching, deficiency of fat-soluble vitamins (A,D,E,K), cirrhosis
  • Labs:↑alkaline phosphatase andɣ-glutamyl-transferase, +auto-antibodies
  • Dx: MRCP or ERCP showing biliary strictures w/ dilated bile ducts
  • Liver biopsy reinforces dx, but isn’t always performed
  • No drug treatments are proven to be effective
  • Liver transplant is only long term treatment
  • Re-occurrence is common after transplant d/t autoimmune nature

slide 32

88
Q

Easy way to differentiats between Primary Sclerosing and Primary Biliary Cholangitis

A
  • Primary Sclerosing: “beads on a string” from fibrosis, also Intra AND extrahepatic
  • Primary Biliary: intrahepatic ducts affected only
89
Q

this is a life-threatening severe liver injury occurring within days to 6 months after insult and has a rapid increase in AST/ALT, AMS, coagulopathy

A

acute liver failure

slide 34

90
Q

how many cases of acute liver failure are drug inced?

A

50% (majority tylenol)

slide 34

91
Q

other causes of acute liver failure (5)

A
  • Viral hepatitis,
  • autoimmune
  • hypoxia,
  • ALF of pregnancy,
  • HELLP (Hemolysis, Elevated Liver Enzymes and Low Platelets)

slide 34

92
Q

how does acute liver failure happen?

A

Massive hepatocyte necrosis→ cellular swelling &membranedisruption

slide 34

93
Q

acute liver failure:
- s/s
- tx:

A
  • Sx: Jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death
  • Tx: Treat the cause, supportive care, liver transplant

slide 34

94
Q

this is the final stage of liver disease where normal liver parenchyma is replaced with scar tissue, and is often asymtomatic in early stages

A

cirrhosis

slide 35

95
Q

s/s of cirrhosis

A
  • jaundice
  • ascites
  • varices
  • coagulopathy
  • encephalopathy

slide 35

96
Q

most common causes of cirrhosis

A

Alcoholic fatty liver, NAFL, HCV, HBV

slide 35

97
Q

Chirrhosis:
- labs
- tx:

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

slide 35

98
Q

complications of cirrhosis (8)

A
  • portal HTN
  • ascites
  • spontaneous bacterial peritonitis
  • varices
  • hepatic encephalopathy
  • hepatorenal syndrome
  • hepatopulmonary syndrome
  • portopulmonary HTN

slide 36-38

99
Q

this has HVPG >5 and ↑vascular resistance within the portal venous system

A

portal htn

slide 36

100
Q

this is the most common complication of cirrhosis, where portal-HTN leads to ↑blood volume & peritoneal accumulation of fluid. It is managed with ↓Salt diet, albumin replacement or Transjugular Intrahepatic Portosystemic Shunt (TIPS).

A

ascities
TIPS- Reduces P-HTN and ascites

slide 36

101
Q

this is the most common infection r/t cirrhosis and requires abx

A

Spontaneous Bacterial Peritonitis

slide 36

102
Q

this is present in ̴50% cirrhosis pts

A

varices

slide 37

103
Q

Hemorrhage is most lethal complication of cirrhosis, what can be done to help prevent this/treat it?

A
  • Beta blockers help reduce risk
  • Prophylactic endoscopic variceal banding & ligation
  • Refractory bleeding → balloon tamponade

slide 37

104
Q

this is a buildup of nitrogenous waste d/t poor liver detoxification. It has neuropsychiatric symptoms (cognitive impairment → coma).

A

hepatic encephalopathy

slide 37

105
Q

tx for hepatic encephalopathy

A
  • Lactulose, Rifaximin to ↓ammonia-producing bacteria in gut

slide 37

106
Q

what is hepatorenal syndrome and what is it tx?

A
  • Excess endogenous vasodilators (NO, PGs)→↓systemic MAP→↓RBF
  • Tx: Midodrine, Octreotide, Albumin

slide 38

107
Q

hepatopulmonary syndrome has a triad of chronic liver disease which is?

A
  • hypoxemia
  • intrapulmonary vascular dilation
  • platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt

slide 38

108
Q

what is portopulmonary HTN? what is its tx?

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

slide 38

109
Q

for anesthesia with liver disease pts when is elective surgery contraindicated?

A
  • acute hepatitis
  • severe chronic hepatitis
  • ALF

slide 39

110
Q

what are the 2 scoring systems to determine severity and prognosis of liver disese?

A
  • Child-Turcotte-Pugh (CTP):
  • Model for End Stage Liver Disease (MELD)

slide 39

111
Q

what is Child-Turcotte-Pugh (CTP)

A

points based on bilirubin, albumin, PT, encephalopathy, ascites

Ask Bill, Al, Pete, and Brian (Brain=brain/encephalopathy)

slide 39

112
Q

what is the Model for End Stage Liver Disease (MELD):

A

scorebased on bilirubin, INR, creatinine, sodium

double date for Bill, Iris, Craig and Sarah

slide 39

113
Q

here is aguide on whether or not to proceed or cancel surgery for pts with liver disease

A

slide 40

114
Q

what preop labs should be performed in pts with liver disease?

A
  • CBC
  • BMP
  • PT/INR

slide 41

115
Q

Liver disease has a ____ threshold for invasive moniotoring, and an increased risk for?

A
  • Low threshold
  • increased risk for aspiration, hypotension, hypoxemia

slide 41

116
Q

what is better for resuscitation for liver disease?

A

colloids > crystalloids

slide 41

117
Q

how does alcholism effect MAC?

A

increases MAC of volatile anesthetics

slide 41

118
Q

with liver disease what should be considered with medications? And what anesthesia meds are ideal?

A
  • drugs may have a slow onset or a prolonged duration of action
  • Succs and cisatricurium are ideal because they are not liver metabolized

slide 41

119
Q

what may be decreased in severe liver disease?

A

plasma cholineterase

slide 41

120
Q

what should be controlled in pts with liver disease

A

bleeding/coagulation

slide 41

121
Q

What is Transjugular Intrahepatic Portosystemic Shunt (TIPS_

A
  • procedure to manage portal HTN
  • Stent or graft placed btw hepatic vein and portal vein
  • Shunts portal flow to systemic circulation
  • Reduces the portosystemic pressure gradient

slide 41

122
Q

what are the indications for TIPS procdure?
contraindications?

A

Indications:
* Refractory variceal hemorrhage
* Refractory ascites

Contraindications:
* Heart Failure
* Tricuspid regurgitation
* Severe pulmonary HTN

slide 42

123
Q

This is a resection to remove neoplasms, leaving adequate tissue for regeneration. It has a tolerable amount of resection d/o preexisting liver disease and function, and up to 75% removal is tolerated in pts with normal liver function

A

partial hepatectomy

slide 43

124
Q

anesthesia considerations for a partial hepatectomy

A
  • Invasive monitoring
  • Blood products available
  • Adequate vascular access for blood/pressors

slide 43

125
Q

what may a surgeron due to control blood loss during a partial hepatectomy?

A
  • clamp IVC or hepatic artery

slide 43

126
Q

what is stardard practice for a partial hepatectomy to reduce blood loss?

A

Standard practice is to maintain low CVP by fluid restriction, prior to resection to reduce blood loss

slide 43

127
Q

what do pts often require in PACU after a partial hepatectomy?

A

PCA postoperatively

slide 43

128
Q

postop coagulation disturbances are caused by

A

liver resection

slide 43

129
Q

what is a definitive treatmeant for ESLD?

A

liver transplant

slide 44

130
Q

what is the most common indication for a liver transplant? what are other reasons for one?

A
  • alcoholic liver disease most common
  • fatty liver
  • Hepatocellular carcinoma (HCC)

slide 44

131
Q

why do we time living donor liver transplants at the same time?

A

minimal ischemia time

slide 44

132
Q

what is done with a liver that is harvested from brain dead donor

A

liver is kept hemodynamically stable for organ to perfuse

slide 44

133
Q

what is the intraoperative management for a liver transplant?

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

slide 44

134
Q

Surgical and anesthesia considerations for liver transplant: (this is mostly an FYI for practice)
* preoperative
* disection
* anhepatic
* reperfusion
* posttransplantation

A
  • Preoperative: Surgical - transplantation evaluation Anesthetic - preop eval, vascular access, blood availability
  • Dissection: Surgical - incision, mobilization of liver and vascular structures Anesthetic - hemodynamic compromise from fluid loss
  • Anhepatic: surgical - clamping of hepatic artery, portal vein, removal of diseased liver, anastomosis of IVC. Anesthetic - hemodynamic compromise from full or partial IVC clamping, metabolic acidosis from citrate intoxication
  • Reperfusion: Surgical - anastomosis of hepatic artery Anesthesia - hemodynamic instability, dysrhythmias, hyperkalemia, acidosis
  • Posttransplantation: surgical - hemostasis, eval graft, US. Anesthesia - ICU admission, early or late extubation, management of hemodynamics

slide 45

135
Q

t/f The liver is the largest internal organ in the body

A

True

kahoot

136
Q

What are the metabolic functions of the liver?

A

a. Carbohydrate metabolism
b. Protein metabolism
c. Fat metabolism
d. Rocuronium metabolism

kahoot

137
Q

What part of the liver cleans the blood as it passes through

A

Kupffer cells

kahoot

138
Q

The liver performs which of the following
a. Forms many compounds from carbohydrate intermediaries
b. Conversion of galactose and fructose to glucose
c. Glucogenesis
d. Storage of large amount of glycogen

A

all of them

kahoot

139
Q

The most common cause of cirrhosis is?

A

ETOH

kahoot

140
Q

t/f Cirrhosis results in splenomegaly, esophageal varices and left heart failure

A

False, its right heart failure

kahoot

141
Q

Cirrhotic patients should be resuscitated with

A

Colloids

kahoot

142
Q

vitamin k is used to treat an elevated PT which measures the ____ pathway

A

Extrinsic

kahoot

143
Q

A platelet count less than ____ requires preoperative replacement
a. 100K, 150K, 50K, 75K

A

all of them

kahoot

bri is confused by this

144
Q

t/f

Anesthetic drugs may cause postoperative liver dysfunction to be exaggerated

A

True

kahoot

145
Q

t/f Chronic alcoholism increases MAC for iso and this probably due to cross tolerance

A

True

kahoot

Marlea is confused by this - direct contradiction to Kane
Ashley is also confused by this…:(

146
Q

Plasma cholinesterase may be ____ in severe liver disease

A

Decreased

kahoot

147
Q

Manifestation of alcohol withdrrawl occur in ____ hours
after receiving no alcohol intake

A

24-72 hrs

kahoot

148
Q

T/F Hepatitis is the most commonly transmitted blood borne pathogen

A

False

kahoot

149
Q

Drugs that can cause hepatitis include

A
  • Analgesics
  • Anticonvulsants
  • VAA’s
  • Tranquilizers

kahoot

150
Q

What surgical procedure is associated with the highest mortality
a. Bka
b. Orif of the tibia
c. Laparotomy
d. Coronary angioplasty

A

C. laparotomy

kahoot

Mar: Sem 2 - Health Assessment (32 decks)

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