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N935 Pathophysiology > Hepatic Pathophysiology and Anesthesia Complications > Flashcards

Hepatic Pathophysiology and Anesthesia Complications Flashcards

1
Q

acute hepatitis is the result of (3)

A

viral infection
drug reaction
exposure to hepatotoxin ex) alcohol

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2
Q

acute fulminant hepatic failure pathophysiology (general)

A

rapid, massive necrosis of liver and a decrease in liver size

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3
Q

how is hepatitis A transmitted

A

oral fecal

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4
Q

how is hepatitis B and C transmitted

A

primarily percutaneously (needles/blood) and by contact with body fluids

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5
Q

hep a
severity
recovery

A

least severe

most recover in weeks to months

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6
Q

hep e
where it is found
transmission

A

found in 3rd world countries (similar to hep A)

transmission through fecal contamination

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7
Q

hep D
only occurs as (2 consideration)
transmission

A

only occurs as co infection with acute hep B or super infection with chronic hep B
transmission through fecal contamination/body fluids

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8
Q

HBsAg

A

surface antigen part of the hep B virus. a lipoprotein layer that the virus sheds that can be measured.
this lipoprotein antibody disappears with recovery

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9
Q

what can hep B lead to

A

fulminant hepatic necrosis or chronic hepatitis

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10
Q

hep C and diagnosis considerations

A

antibodies not present for long period, therefore difficult to diagnose.
produces asymptomatic carriers

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11
Q

hep C and possible progressive pathophysiology of the liver

A

rarely produces fulminant hepatic failure

significant number will develop cirrhosis or liver cancer

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12
Q

hep C vaccine

A

none available currently

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13
Q

acute hepatitis early clinical signs

A

often have prodromal illness for 1-2 weeks with fatigue, malaise, low grade fever, nausea and/or vomiting.
period may or may not be followed by jaundice for 2-12 weeks.

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14
Q

acute hepatitis recovery

A

usually takes 4 months, evidenced by normal serum transaminase

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15
Q

how to diagnose type of hepatitis

A

have to do serological testing or biopsy since s/sx overlap

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16
Q

chronic active viral hepatitis can be seen with

A

hep b and c

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17
Q

how to take precaution against infectious patients

A

avoid direct contact with blood and secretions
immunization highly effective against hep B
no vaccine for hep C and prior exposure does not create immunity
post exposure prophylaxis with hyperimmune globulin is effective for hep b but not c
do have ARV for hep C

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18
Q

drug induced acute hepatitis results from

A

direct dose dependent toxicity of a drug or metabolite
idiosyncratic drug reaction
combination of the two

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19
Q

most common cause of hepatitis

A

drug induced

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20
Q

chronic alcohol ingestion can result in fatty infiltration as a result of (3)

A

impaired fatty oxidation (beta oxidation)
increased uptake and esterification of fatty acids
diminished lipoprotein synthesis and secretion

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21
Q

toxic drug induced acute hepatitis offenders (4)

A

alcohol
acetaminophen
vinyl chloride (inhalation for a brief time)
carbon tetrachloride

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22
Q

idiosyncratic drug induced acute hepatitis offnders

A

volatile anesthetics

sulfonamides

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23
Q

toxic and idiosyncratic acute drug induced hepatitis

A

amiodarone

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24
Q

acute hepatitis preoperative considerations

A

postpone elective surgery until resolved as determined by LFT’s

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25
Q

alcohol withdrawal during surgery associated with mortality rate as high as

A

90%

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26
Q

patients with hepatitis are at risk for these 3 things during perioperative period

A

encephalopathy
coagulopathy
hepatorenal syndrome

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27
Q

preoperative labs to get if the patient has acute hepatitis includes

A 
BUN
creatitnine
bilirubin
electrolytes
glucose
transaminases
alk phos
albumin 
prothrombin time (INR)
platelet count
serum HBsAg
blood alcohol level if alcoholic
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28
Q

two electrolyte deficits you may see preoperatively during hepatitis

A

hypokalemia and metabolic alkalosis usually d/t vomiting. consider ABG
hypomagnesemia may exist in chronic alcoholics which predisposes to dysrhythmias

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29
Q

does elevated transaminase correlated with the degree of cellular necrosis

A

no, AST/ALT does not correlate well

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30
Q

best indicator of synthetic function of liver with hepatitis

A

PT.

prolongation >3-4 seconds (>1.5 INR) following administration of vitamin K indicative of severe liver dysfunction

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31
Q

preoperative evaluation of the emergent patient with acute hepatitis should include

A

cause and degree of impairment
exposure recording including alcohol intake, recreational drug use, recent transfusions, prior anesthetics
presence of n/v (RSI?)
correction of dehydration and electrolyte abnormalities
mental status changes suggest severe hepatic impairment
alcoholics: look for acute toxicity or withdrawal
vitamin K may be necessary to correct coagulopathy

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32
Q

goal of intraoperative management of hepatitis

A

preserve existing hepatic function

avoid factors that may be detrimental to the liver

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33
Q

acute viral hepatitis and anesthetics

A

may produce increased CNS sensitivity to anesthetics

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34
Q

alcoholic patients and intraoperative considerations

A

display cross tolerance to IV and volatile anesthetic agents
require CV monitoring due to: additive depressant effects of anesthetics and alcohol.
possible presence of cardiac myopathy (eccentric remodeling)

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35
Q

acute hepatitis and intraoperative considerations, IV or inhaled anesthetic?

A

inhalation agents are preferred to IV agents due to dependence on liver metabolism and alimentation. fewest number of anesthetic agents should be used

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36
Q

volatile agent of choice for hepatic issues

A

isoflurane, least effect on hepatic blood flow

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37
Q

induction doses of IV agents and hepatitis

A

can use standard induction doses generally as their action is terminated by redistribution versus metabolism. however, prolonged duration may occur if repeated doses of agents, particularly opioids, are administered

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38
Q

try to avoid these responses intraoperatively with hepatitis patients that decrease hepatic BF

A

hypotension
excessive SNS stimualtion
high mean airway pressures during controlled ventilation

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39
Q

regional anesthesia and liver abnormalities

A

can be used in the absence of coagulopathy

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40
Q

chronic hepatitis definition

A

defined as persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferase

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41
Q

classification of chronic hepatitis based on 3 distinct syndromes via liver biopsy

A

chronic persistent hepatitis
chronic lobular hepatitis
chronic active hepatitis

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42
Q

chronic persistent hepatitis

A

present with acute hepatitis (usually B or C)
eventually resolves
characterized by chronic inflammation of portal tracts (all tracts including ducts, veins, arteries, canniculi, etc) with preservation of the normal cellular architecture (which sets it apart)
usually does NOT progress to cirrhosis

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43
Q

chronic lobular hepatitis

A

present with cute hepatitis that resolves but followed by recurrent exacerbation
characterized by foci of inflammation and cellular necrosis in the lobiles
usually does not progress to cirrhosis

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44
Q

chronic active hepatitis

A

occurs most commonly as a sequela of hep b or c
characterized by chronic hepatic inflammation with destruction of cellular architecture- “more global”
evidence of cirrhosis present initially or eventually develops

45
Q

treatment of hep B

A

ARV + immune modulator drugs (interferon)

46
Q

treatment of hep C

A

ARV can cute more than 95% of these infected patients

47
Q

anesthetic management of patients with chronic persistent of chronic lobular hepatitis

A

treat like those with acute hepatitis

48
Q

anesthetic management of patients with chronic active hepatitis

A

assume cirrhosis, treat them as such

49
Q

most common causes of cirrhosis (4)

A

alcohol abuse
NAFLD
chronic active hep B and C
chronic biliary inflammation or obstruction

50
Q

result of cirrhosis

A

hepatocyte necrosis followed by fibrosis and nodular regeneration

51
Q

cirrhosis eventually results in

A

hepatic failure. is a progressive disease

52
Q

destruction of livers normal cellular and vascular architecture produces

A

obstruction of portal venous flow leading to portal HTN

impairment of normal synthetic and metabolic functions leading to multi system disease

53
Q

4 manifestations related to cirrhosis

A

spider angiomas
palmar erythema (due to volume distribution issue)
gynecomastia
splenomegaly

54
Q

3 major complications associated with cirrhosis

A

vatical hemorrhage from portal HTN (esophageal hemorrhages)
intractable fluid retention in the form of ascites
hepatic encephalopathy or coma

55
Q

child turcotte pugh score

A

severity of hepatic imparment and surgical risk estimated with this. considers 3 lab values (total bilirubin, serum albumin, INR) and 2 clinical evaluations (ascites, hepatic encephalopathy)
-then classes you A, B, or C which correlates with survival. C being the worst survival rate

56
Q

major cause of morbidity and mortality in cirrhotic patients

A

massive bleeding from esophageal varices

57
Q

medical treatment of variceal bleeding includes

A

replace blood loss with IV fluids and blood products
vasopressin, somatostatin, propranolol (slow HR, slow CO to liver) to reduce the rate of blood loss
balloon tamponade (hope they form a clot)
endoscopic sclerosis or ligation of the varicose
bleeding continues or recurs emergency surgery is indicated

58
Q

hematological considerations for a patient with cirrhosis

A

may present with anemia, thrombocytopenia/coagulopathy, leukopenia

59
Q

anemia related to cirrhosis associated with

A

blood loss
increased RBC destruction
bone marrow suppression
nutritional deficiencies

60
Q

thrombocytopenia/coagulopathy related to cirrhosis associated with

A

congestive splenomegaly due to portal HTN
decreased hepatic synthesis of clotting factors
enhanced fibrinolysis due to reduced elimination of factors that activate the fibrinolytic system

61
Q

leukopenia related to cirrhosis associated with

A

congestive splenomegaly due to portal HTN

62
Q

preoperative blood transfusion considerations related to cirrhosis

A

protein breakdown from excessive blood transfusions can precipitate encephalopathy (protein breakdowns causes nitrates/ammonia)
despite this risk coagulopathy should be corrected before surgery
should replete clotting factors with FFP and cryo
platelet transfusion should be considered immediately prior to surgery if platelet count <100,000

63
Q

cirrhosis preop considerations and circulatory manifestations

A

cirrhosis typically associated with hyper dynamic circulatory state
CO often increased and generalized peripheral vasodilation (looks like hypovolemia)
arteriovenous shunts can develop in the systemic and pulmonary circulation
superimposed alcoholic cardiomyopathy readily leads to CHF

64
Q

cirrhotic cardiomyopathy may be present due to

A

AV shunts or decreased blood viscosity

contribute to increased CO, above normal filling pressures, below normal SVR

65
Q

cirrhosis preop considerations and respiratory manifestations

A

hyperventilation common and results in primary respiratory alkalosis
hypoxemia frequent due to right to left shunts
shunting due to increased anomalous AV communication
also have VQ mismatch
decreased lung volumes (particularly FRC) due to ascites and diaphragm elevation
results in atelectasis

get CXR and ABG, maybe paracentesis

66
Q

cirrhosis preop considerations and renal manifestations and fluid balance

A

alterations in fluid and electrolyte balance are manifested as: ascites, edema, electrolyte abnormalities, hepatorenal syndrome
patients with cirrhosis and ascites have decreased renal perfusion, altered infrarenal hemodynamics, enhanced proximal and distal tubules Na+ reabsorption, impairment of free water clearance
dilutional hyponatremia is common
hypokalemia is common (secondary to hyperaldosteronism and diuretics)
abnormalities are most sever with onset of hepatorenal syndrome

67
Q

mechanisms believed to be related to ascites include

A 
portal HTN (increased hydrostatic pressure favors fluid transudation)
seepage of protein rich lymph fluid from the surface of the liver "sweating" (secondary to distortion and obstruction of lymphatic channels)
avid renal sodium (and often water) retention (hepatorenal syndrome)
68
Q

hepatorenal syndrome definition and causes

A

functional deficit in patients with cirrhosis that usually follows GI bleeding, aggressive diuresis, sepsis, major surgery. all can be iatrogenic

69
Q

hepatorenal syndrome is characterized by

A 
progressive oliguria (<400ml/day)
avid Na reabsorption
azotemia (alto of nitrogenous material in blood)
intractable ascites
very high mortality rate
70
Q

hepatorenal syndrome tx

A

supportive, often unsuccessful unless liver transplantation performed

71
Q

intraoperative fluid administration: colloids or crystalloids?

A

colloids

72
Q

diuresis of ascites and edema fluid should be done how?

A

accomplished over several days. loop directive should only be used after bed rest, sodium restriction, and spironolactone therapy have failed

73
Q

hepatic encephalopathy is characterized by

A

alterations in mental status
fluctutating neurological signs (asterixis, hyperreflexia)
EEG changes
some patients also have increased ICP

74
Q

toxin accumulation in GI tract that can be attributed to hepatic encephalopathy include

A

ammonia, methionine metabolites, short chain fatty acids, phenols (like cleaning agents)

75
Q

factors known to precipitate hepatic encephalopathy include

A

GI bleeding, increased dietary protein intake, hypokalemia alkalosis from vomiting or diuresis, infections, worsening liver function

76
Q

encephalopathy and sedatives

A

recommended to avoid, try to tx enceophalopathy preoperatively

77
Q

drug response to agents is unpredictable in cirrhosis due to changes in

A 
CNS sensitivity
Vd
protein binding
drug metabolism
drug elimination
TITRATE
78
Q

Vd of highly ionized NMBA’s is ________ in cirrhosis patents, therefore

A

increased

requires greater than normal loading doses

79
Q

hepatic elimination of NMBA’s is _________ in cirrhosis patients therefore

A

decreased

requires lower than normal maintenance doses

80
Q

cirrhosis and the anesthetic technique

A

cirrhotic liver is very dependent on hepatic arterial blood flow due to decreased portal blood flow. therefore, avoid anesthetic agents that reduce arterial blood flow
get an aline
regional anesthesia can be used without thrombocytopenia and coagulopathy, take great care fo avoid hypotension
propofol induction with isoflurane maintenance most commonly used
cisatracurium probably NMDA of choice
opioid supplementation reduces volatile agent requirement but have prolonged elimination time
usually RSI if have preop n/v/GIB/andominal distention

81
Q

CV unstable patients and those with active bleeding and intubation

A

should have awake intubation or RSI with cricoid pressure using ketamine or etomidate and succ

82
Q

cirrhosis and montioring

A

monitor 5 lead EKG esp due to coronary vasoconstriction in patients receiving vasopressin for esophageal varices
supplemental pulse ox with ABG to eval acid base status

83
Q

patient with right to left shunts and cirrhosis, intraoperative consideration

A

may not tolerate N2O, may require PEEP to treat VQ inequalities and subsequent hypoxemia

84
Q

most patients should have aline monitoring with cirrhosis as a result of these possibilities

A

excessive bleeding
rapid intercompartmental fluid shifts
surgical manipulations

85
Q

need these monitors for patients with cirrhosis

A 
cellsaver
blood warrmer
fluid
blood in room
CVC
many large bore IV's
aline
urinary catheter
86
Q

cirrhosis and fluid replacement

A

colloids intraop still take precedence over the Na restriction to manage intravascular fluid volume

87
Q

intraabdominal procedures in cirrhotic patients are often associated with

A 
increased bleeding (venous engorement from portal HTN, adhesions from previous surgery, coagulopathy(
fluid shifts (evacuation of ascites fluid, may need to give colloids. prolonged surgical procedure)
88
Q

citrate toxicity and blood transfusion in cirrhotic patients

A

citrate is normally metabolized by the liver
cirrhosis impairs citrate metabolism
citrate binds to serum Ca and leads to hypocalcemia
IV Ca is often necessary to reverse negative inotropic effects of decreased ionized Ca

89
Q

hepatobilitary disease characterized by

A

cholestasis, suppression of stoppage of bile flow

90
Q

most common cause of cholestasis

A

extrahepatic obstruction of biliary tract (obstructive jaundice) due to gallstones, stricture, tumor in common hepatic duct

91
Q

cholestasis can also be caused by intrahepatic obstruction due to

A

suppression or stoppage of bile flow at the level of the hepatocyte or bile canaliculus. most commonly results from vital hepatitis or idiosyncratic drug reaction

92
Q

treatment of extra hepatic obstruction

A

surgical

93
Q

treatment of intra hepatic cholestasis

A

medical

94
Q

extra hepatic obstruction and intrahepatic cholestasis two dx labs

A

predominately conjugated hyperbilirubinemia and marked elevation in alk phos

95
Q

cholangitis

A

concomitant chills or high fever from ascending bacterial infection of biliary systems

96
Q

how gallstones can cause acute pancreatitis

A

can obstruct pancreatic duct

97
Q

sx that presents with cholelithiasis

A

biliary colic secondary to obstruction of cystic duct

98
Q

hepatobiliary disease-preoperative considerations

A

most commonly present to OR for cholecystectomy
patients with acute cholecystitis should be treated medically
patients suffering from serious complications may require emergency cholecystectomy

99
Q

treatment for acute cholecystitis

A

nasogastric suction
IV fluids
abx
opioid analgesics

100
Q

patients with extra hepatic biliary obstruction from any cause develop this deficiency (and 2 considerations)

A

vitamin K deficiency
should be given vitamin K (requrires 24h for full response)
failure of PT to correct prior to surgery may necessitate FFP

101
Q

high levels of this lab may be associated with renal failure, esp in hepatobiliary disease patients

A

bilirubin levels

102
Q

long standing extra hepatic biliary obstruction is associated with

A

secondary biliary cirrhosis and portal hypertension

103
Q

hepatobiliary disease-intraoperative considerations

drugs that depend on biliary excretion

A

lap chole accelerates recovery
use of opioids can be problematic when intraoperative cholangiogram is to her performed
-opioid induced spasm of sphincter of Odd may theoretically result in false positive cholangiogram
some clinicians withheld opioids until after cholangiogram has been performed
in patients with biliary tract obstruction expect a prolonged DOA of drugs that are dependent on biliary excretion (ketamine, prop)
agents dependent on renal excretion are preferable
UOP with indwelling catheter preferable
maintenance of periop diuresis desirable

104
Q

sphincter of oddi spasm can be treated with

A

glucagon, naloxone

105
Q

common hepatic surgeries include

A

repair of lacterations
drainage of abcesses
resection of tumors

106
Q

how much liver can be resected

A

80-85%

107
Q

hepatic surgery general intraoperative considerations

A

administration of antifibrinolytics may reduce blood loss (aprotonin, aminocaproic acid, tranexamic acid)
hypoglycemia may occur following large liver resections
drainage of abcess may be complicated to peritoneal contamination (may repeatedly come back to OR for washout)

108
Q

postop complications of hepatic surgery include

A

bleeding, sepsis, hepatic dysfunction

postop mechanical ventilation may be necessary in patients undergoing extensive resection

N935 Pathophysiology (12 decks)

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