Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Health Assessment > Hepatic > Flashcards

Hepatic Flashcards

1
Q

function of the liver

A

synthesizes glucose via gluconeogenesis
sotres excess glucose as glycogen
synthesizes cholesterol and proteins into hormones and vitamins
metabolizes fats, protiens, and carbs to generate energy
metabolizes drugs via CYP450 and other enzyme pathways
detoxifies blood
involved in the acute phase of immune support
processes HGB and stores iron
synthesizes coagulation factors
aids in volume control as a blood reservoir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what coagulation factors are not synthesized by the liver

A

Factor III, IV, VIII, vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T/F liver dysfunction can lead to multi-organ failure

A

true, nearly every organ is impacted by liver function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what seperates the right and left lobe of the liver

A

falciform ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how many segments are in the liver

A

8 based on blood supply and bile drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which vessels branch into each segment of the liver

A

portal vein and hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how many hepatic veins empty into IVC

A

3- right, middle, left hepatic veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where does the bile duct travel

A

along portal veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bile drains through the _____ ________ into ______ & _______

A

bile drains through the hepatic duct into gall bladder and common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

bile enters duodenum via

A

ampulla of vater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how much of the cardiac output goes to the liver

A

25%
1.25-1.5L/min

highes proprotionate CO of all organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where does the portal vein arise from

A

splenic vein and superior mesenteric vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

portal vein contains deoxygenated blood from which organs

A

GI organs (stomach, intestine), pancreas, spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

portal vein provides how much of hepatic blood flow (%)

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hepatic artery, which branches off the aorta, provides how much hepatic blood flow (%)

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

oxygen delivery sources to the liver

A

50% portal vein (deoxygenated)
50% hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hepatic arterial blood flow is inversely related to

A

portal venous blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

T/F hepatic blood is not autoregulated

A

false, hepatic artery dilates in response to low portal venous flow; keeping consistent HBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

portal venous pressure reflects what?

A

splanchnic arterial tone and intrahepatic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

normal hepatic venous pressure gradient

A

HVPG 1-5 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what hepatic venous pressure gradient is clincally significant for portal HTN, i.e chirroshis, esophageal varices

A

HVPG > 10 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

increasing portal venous pressure causes

A

blood to back up in systemic circulation
*esophagel and gastric varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what hepatic venous pressure gradient is associated with variceal rupture

A

HPVG > 12 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

risk factors for liver disease

A

family history
heavy ETOH
lifestyle
DM
obesity
illicit drug use
multiple partners
tattoss (basement tattoos)
blood transfusions (in the 80s)

rely heavily on “risk factors” for degree of suscpicion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when do liver symptoms begin to appear

A

late-stage liver disease

often asymptomatic until late-stage liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

physical exam findings of liver disease

A

pruritis
jaundice
ascites
asterixis (flapping tremor)
hepatomegaly
splenomegaly
spider nevi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hepato-biliary function tests

A

BMP, CBC
PT/INR
Aspartate aminotransferase (AST)
Alanine Aminotransferase (ALT)
bilirubin
alkaline phosphatase
ɣ-glutamyl-transferase (GGT)

*imaging includes: ultrasound, doppler US (portal blood flow), CT, MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

most liver-specific enzyme

A

alanine aminotransferase (ALT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which labs are elevated in late-stage liver disease

A

ɣ-glutamyl-transferase (GGT)
Alkaline phosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

labs suggesting hepatocellular injury

A

elevated AST/ALT (hepatocyte enzymes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

labs suggesting reduced synthetic function

A

decreased albumin
increased PT/INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

labs suggesting cholestasis

A

increased alkaline phosphatase
increrased GGT
increased bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

3 groups of hepatobiliary disease

A

hepatocellular injury
reduced synthetic function
cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

3 subclasses of hepatocellar injury and lab findings

A

Acute Liver Failure (ALF): hepatic enzymes may be elevated 25x

Alcoholic Liver Disease (ALD): AST:ALT ratio is usually 2:1

Non-Alcoholic Fatty Liver Disease (NALFD): AST:ALT ratio usually 1:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

bile pathway

A

hepatocytes secrete bile through bile ducts into common hepatic duct and go through gall bladder and common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

GallBladder stores bile to deliver during ________ , Common Bile Ducts secretes bile directly into _____

A

GB stores bile to deliver during meals, CBD secretes bile directly into duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

risk factors for cholelithiasis “gallstones”

A

obesity, increased cholesterol, DM, pregnancy, female, family Hx

80% asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

symptoms and treatment of cholelithiasis “gallstones”

A

S/S: RUQ referred to shoulders, N/V, indigestion, fever (acute, obstruction)

Tx: IVF, ABX, pain management
Lab Choleysectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is choledocolithiasis?
inital symptoms?
cholangitis?
treatment?

A

stone obstructing common bile duct > biliary colic
initial symptoms: N/V, cramping, RUQ pain
Cholangitis symptoms: fever, rigors, jaundice
Treatment: endoscopic removal of stone via ERCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how is Endoscopic Retrograde Cholangiopancreatography (ERCP) done

A

guidewire through Sphincter of Oddi into Ampulla of Vater to retrieve stone from pancreatic duct or common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

treatment for Spincter of Oddi Spasm

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

1.

what anesthetic is done with ERCP and what postion is the patient in

A

GA
patient prone with left tilt, head of patient to the right
Tape ETT to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is bilirubin

A

end product of heme- breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

unconjugated “indirect” vs “conjugated “direct” bilirubin

A

unconjugated bilirubin is protein bound to albumin, transported to the liver

conjugated bilirubin is water soluble, and excreted in the bile

42
Q

what is unconjugated hyperbilirubinemia and some causes?

A

caused by an imbalance between bilirubin synthesis and conjugation

43
Q

which hepatitises are most common
and which are more chronic

A

common: A,B,C,D,E
chronic: B,C

44
Q

what is conjugated hyperbilirubinemia and some causes?

A

causes by an obstruction, causing reflux of conjugated bilirubin into the circulation

45
Q

T/F VH is on the decline d/t vaccines and newer treatments

A

True!

46
Q

which type of viral hepatitis requires liver transplant in the US

A

Hep C Virus

47
Q

what newer tx has significantly reduced HCV in the US population

A

Tx b/o HCV genotype (75% type 1), HCV stage, +/- cirrhosis
12-week course Sofosbuvir/Velpatasvir
Provides 98-99% clearance of genotype 1A/1B

48
Q

characteristics of viral hepatitis

A
49
Q

what is most common cause of cirrohisis

A

alcoholic liver disease (ALD)
*top indication for liver transplants in the US
national prevalence of liver transplants for ALD is 2%

50
Q

treatment for alcoholic liver disease

A

centered around abstinence
manage symptoms of liver failure
platelet cound < 50K requires blood transfusion
liver transplant if criteria is met

51
Q

symptoms and labs of alcoholic liver disease

A

symptoms:
malnutrition, muscle wasting, parotid gland hypertrophy, jaundice, thrombocytopenia, ascites, hepatosplenomegaly, pedal edema
symptoms of ETOH withdrawal (DTs) may occur 24-72 hr after stopping
Labs:
increased mean corpuscular volume (MCV)
increased liver enzymes, ɣ-glutamyl-transferase (GGT), bilirubin
blood ethanol (acute intoxication)

52
Q

risk factors for non-alcoholic fatty liver disease

A

obesity, insulin resistance, DM2, metabolic syndome

53
Q

diagnosis of non-alcoholic fatty liver disease

A

hepatocytes contain > 5%
imaging and histology
*liver biopsy= gold standard in distinguishing NAFLD from other liver disease

54
Q

non-alcoholic fatty liver disease can progress to

A

non-alcoholic steatohepatitis, cirrhosis, hepatocellular carcinoma

55
Q

treatment of non-alcoholic fatty liver disease

A

diet, exercise
liver transplant for advanced fibrosis, cirrohiss, and related complications

56
Q

prevalence of non-alcoholic fatty liver disease

A
57
Q

non-alcoholic fatty liver disease (NAFLD) vs alcoholic fatty liver disease (AFLD)

A
58
Q

autoimmune hepatitis predominantly affects who

A

women

59
Q

autoimmune hepatitis

A

may be asymptomatic, acute, or chronic
+ autoantibodies and hypergammaglobuninemia
AST/ALT may be 10-20x normal in acute AIH
treatment: steroids, azathioprine
60-80% achieve remission, relapse is common
refractory disease requires immunosuppession
liver transplant when treatment fails or Acute liver failure ensues

60
Q

most common cause of drug induced liver injury

A

acetaminophen OD
*normally reversible after the drug is removed

61
Q

inborn errors of metabolism

A

groups of rare, genetically inheritied disorders that lead to a defect in the enzymes that breakdown and store protien, carbs, and fatty acid

occurs in 1: 2500 births
onset varies from birth to adolescence

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

62
Q

inborn errors of metabolism - 3 specific disorders

A

Wilson’s Disease
Alpha-1 Antitrypsin Deficiency
Hemochromatosis

63
Q

what is wilson’s 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

64
Q

symptoms, diagnosis, and treatment for wilsons disease

A

symptoms: range from asymptomatic to sudden-onset liver failure with neurologic and pyschiatric manifestations

Diagnosis: Lab tests serum ceruloplasmin,
aminotransferases,urine copper level
Possible liver biopsy for copper level

treatment: copper-chelation therapy & oral znic to bind copper in the GI tract

65
Q

what is alpha-1 antitryspin deficency

A

genetic disorder resulting in defective alpha-1 antitryspin protein.
alpha-1 antitryspin proteins protect the liver and lungs from neutrophil elastase
*neutrophil elastase is an enzyme that causes disruption of connective tissues leading to inflammation, cirrhosis, and hepatocellular carcinoma

66
Q

alpha-1 antitryspin
incidence
diagnosis
treatment

A

incidence 1:16K to 1:35K (likely to be underdiagnosed)
Diagnosis: confirmed with alpha-1 antitryspin phenotyping

treatment: pooled alpha-1 antitryspin is effective for pulmonary symptoms; however it doesnt help with liver disease
liver transplant is the only curative treatment

67
Q

hemochromatosis

A

excess iron in the body, leading to mutli-organ dysfunction

68
Q

causes of hemochromatosis

A

repetitive blood transfusion, high dose iron tranfusion
genetic - excessive intestinal absorption

69
Q

patient presentation of hemochromatosis

A

cirrohsis, heart failure, diabetes, adrenal insufficiency, or poly-arthopathy

excess iron accumulates in organs and causes damage to the tissues

70
Q

labs, diagnosis, treatment of hemochromatosis

A

Labs: elevated AST/ALT, transferrin saturation and ferritin

Diagnosis: genetic mutation test, ECHO and MRI to diagnose cardiomyopathies and liver abnormalities
-liver biopsy may quantify iron levesl in the liver and assess damage

treatment: weekly phlebotomy, iron-chelating drugs, liver transplant

71
Q

what is primary biliary cholangitis

previosuly known as biliary cirrhosis

A

autoimmune, progressive destruction of bile ducts with periportal inflammation and cholestasis
leads to liver scarring, firbosis, cirrhosis

72
Q

who is more at risk to develop primary biliary cholangitis

A

Females > males; diagnosed in middle ages
thought to be caused by exposure to environmental toxins in genetically susceptible individuals

73
Q

symptoms, Labs, imaging, and treatment for primary biliary cholangitis

A

symptoms: fatigue, jaundice, itching
Labs: increased Alk Phos, increased GGT, + antimitochrondrial antibodies
Imaging: CT/MRI/MRCP to rule out bile duct obtructions
Liver biopsy to reveal bile duct destruction and infiltration with lymphocytes
treatment: no cure, but exogenous bile acids slow progression

74
Q

what is Primary Sclerosing Cholangitis (PSC)

A

autoimmune, chronic inflammation of the larger bile ducts
intrahepatic and extrahepatic
fibrosis in biliary tree leading to strictures -> cirrhosis, ESLD

75
Q

Primary Sclerosing Cholangitis (PSC) affects men or women more? what age of onset

A

men, onset ~40s

76
Q

symptoms of Primary Sclerosing Cholangitis (PSC)

A

fatigue, itching, deficency of fat soluble vitamins (A,D,E,K), cirrhosis
↑alkaline phosphatase and ɣ-glutamyl-transferase, +auto-antibodies

77
Q

diagnosis and treatment of Primary Sclerosing Cholangitis (PSC)

A

diagnosis: MRCP/ERCP showing biliary strictures with dilated bile ducts
liver biopsy reinforces diagnosed (not always performed)

treatment:
no drug treatment proven to be effective
liver transplant - long term treatment
re-occurence is common after transplant due to to autoimmne nature

78
Q

acute liver failure

A

life threatening severe liver injury occuring with days to 6 months after insult
rapid increase in AST/ALT, AMS, coagulopathy
massive hepatocyte necrosis causes cellular swelling and membrane disruption

79
Q

causes of acute liver failure

A

50% of cases are drug-induced (majority acetaminophen)
viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP

80
Q

symptoms and treatment of acute liver failure

A

jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death

treatment: treat the cause, supportive care, liver transplant

81
Q

what is the final stage of liver disease

A

cirrhosis - normal liver parenchyma replaced with scar tissue

82
Q

symptoms/labs of cirrhosis

A

jaundice, ascites, varices, coagulopathy, encephalopathy
elevated AST/ALT, bilirubin, alkaline phosphatase, PT/INR, thrombocytopenia

83
Q

causes of cirrhosis

A

alcoholic fatty liver, NAFL, HCV, HBV
transplant is the only cure

84
Q

cirrhosis complications

A

portal HTN (HVPG > 5 mmHg)
ascites (most common complication)
spontaneous bacterial peritonitis (requires ABX)
varices
hepatic encephalopathy
hepatorenal syndrome
hepatopulmonary syndrome
portopulmonary HTN

85
Q

ascites

A

caused by portal HTN leading to increased blood volume and peritoneal accumulation of fluid
management: low salt diet, albumin replacement
transjugular intrahepatic portosystemic shunt (TIPS)
reduces portal HTN and ascites

86
Q

varices

A

present in ~50% of cirrhosis patients
hemorrhage is the most lethal complication
*beta blockers help reduce risk
*prophylactic endoscopic variceal banding and ligation
*refractory bleeding&raquo_space; balloon tamponande

87
Q

hepatic encephalopathy

A

build up of nitrogenous waste due to poor liver detoxification
neuropyschiatric symptoms (cognitive impairment to coma)
Tx: Lactulose, Rifaximin to decrease ammonia producing bacteria in the gut

88
Q

hepatorenal syndrome

A

excess endogenous vasodilators (NO, Prostacylin) decreasing systemic MAP and renal blood flow
tx: midodrine, octeoride, albumin

89
Q

hepatopulmonary syndrome

A

triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
platypnea (hypoxemia when upright) due to R to L intrapulmonary shunt

90
Q

portopulmonary HTN

A

Pulmonary HTN accompanied by portal HTN
systemic vasodilation triggers the production of pulmonary vasoconstrictors
treatment: PD-I, NO, prostacylcin analogs, and endothelin receptor antagonists
transplant is the only cure

91
Q

2 scoring systems to determine severity and prognosis of liver disease

A

CTP: points based on bilirubin, albumin, PT, enceophalopathy, ascites
MELD: score on bilirubin, INR, creatinine, sodium

92
Q

elective surgery is contraindicated in

A

acute hepatitis, severe chronic hepatitis, ALF

93
Q

anesthesia in liver disease- if the patient has cirrhosis what is the next step

A

Risk stratification with MELD or CTP score

94
Q

anesthetic considerations in liver disease

A
  • careful H&P
  • standard preop labs: CBC, BMP, PT/INR
  • low treshold for invasive monitoring
  • risk for aspiration, hypotension, hypoxemia
  • colloids > crystalloids
  • alcoholism increases MAC of VA
  • drugs may have slow onset/prolonged Duration of Action
  • bleeding/coagulation management
  • Succ and ciastracurium ideal
  • plasma cholinestase may be decreased in servere liver disease
95
Q

what NMBs are desired in pts with liver disease

A

Succinycholine and Ciastracurium
*plasma cholineserase may be decreased in servere liver disease

96
Q

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

A

used to manage portal HTN
stent between the hepatic vein and the portal vein
shunt portal flow to the systemic circualtion
reducing the portosystemic pressure gradient

97
Q

partial hepatectomy

A

resection to remove neoplasms, leaving adequate tissue for regernation
tolerable amount of resection d/o preexisting liver disease and function

98
Q

indications and contraindications to TIPS

A

Indications:
refractory variceal hemorrhage, refractory ascites
contraindications:
Heart failure, tricupsid regurgitation, severe pulmonary HTN

99
Q

anesthetic considerations for partial hepatectomy

A

anesthetic considerations
*invasive monitoring
blood products available
adequate vascular access for blood/pressors

surgeon may clamp the IVC or hepatic artery to control blood loss
maintain low CVP by fluid restriction prior to resection to reduce blood loss
Post op PCA
may cause posop coagulation disturbances

100
Q

liver transplant

A

definitive treatment for ESLD
alcoholic liver disease the most common indication > fatty liver, HCC
*living donor: surgies timed together for minimal ischemia time
brain dead donor: kept hempodynamically stable for organ perfusion

101
Q

intraop management for liver transplant

A

maintain hemodynamics (pressors/inotropes readily available)
ALine, CVC, PA CATH, TEE
control coagulation

102
Q

Liver transplant table of surgical and anesthetic considerations

A
103
Q

Anesthesia and liver disease - what MELD or CTP score should other alternatives be considered and work up for transplant

A

MELD> 16
Child Class C

104
Q

MELD score <10 or CTP A

A

Proceed to OR

105
Q

A patient with a MELD score 10-15 or CTP B. Should have what assessed next

A

Assess for Portal HTN
No: proceed to OR careful postop monitoring
Yes: consider preop TIPS procedure to optimize patient

Health Assessment (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions