Pathophysiology Of Liver And Biliary Tract

Front 1

Largest organ in body that acts as a reservoir for blood?

Back 1

liver

Front 2

liver holds how much blood volume?

Back 2

10-15% of blood volume

Front 3

liver receives ___ of CO

Back 3

25%

Front 4

1.provides 75% blood to liver;
2.major oxygen source; 3.partially deoxygenated blood;
4.passive vascular bed

Back 4

Portal vein

Front 5

1.provides 25% blood to liver;
2.provides 50% of oxygen; 3.compensatory mechanism to decreased HBF but is limited

Back 5

Hepatic artery

Front 6

Hepatic veins drain into?

Back 6

IVC

Front 7

Categories of Liver Disease

Back 7

1.Parenchymal

Cholestasis

Front 8

parenchymal liver disease subcategories

Back 8

Acute and chronic hepatitis
Cirrhosis

Front 9

Cholestasis liver disease subcategories

Back 9

With or without obstruction of extrahepatic biliary pathway

Front 10

Classifications of Hepatic Dysfunction

Back 10

1.Prehepatic
2.Intrahepatic(hepatocellular) 3.Extrahepatic (cholestatic)

Front 11

Prehepatic hepatic dysfunction etiology

Back 11

hemolysis, hematoma resorption, bilirubin overload from whole blood

Front 12

Intrahepatic hepatic dysfunction other name & etiology

Back 12

aka (hepatocellular)

viral, drugs, sepsis, hypoxemia, cirrhosis

Front 13

Extrahepatic hepatic dysfunction other name & etiology

Back 13

aka (cholestatic)

stones, sepsis

Front 14

typical cause of acute hepatitis? and other causes?

Back 14

virus

toxins or drugs

Front 15

name 5 hepatitis viruses and their occurance rate

Back 15

Hepatitis A (HAV) – 30% of cases
Hepatitis B (HBV) – 50% of cases
Hepatitis C (HCV) – 20% of cases
Hepatitis D (HDV)
Hepatitis E

Front 16

name Other viruses that can cause liver problems

Back 16

Cytomegalovirus
Epstein-Barr virus

Front 17

Chronic infections may follow which hepatitis viruses?

Back 17

HBV, HCV, and HDV

Front 18

Viral Hepatitis s/s

Back 18

1.May be asymptomatic or non-specific flu-like symptoms
2.jaundice

Front 19

viral hepatitis Diagnostic labs

Back 19

may show markedly increased aminotransferase levels

Front 20

Specific etiology of hepatitis is determined by?

Back 20

serologic testing

Front 21

Hepatitis A
a.virus involved?
b.body secretions where present?
c.protection/vaccinations?
d.antibody activity?
e.contagious?

Back 21

a.Picornavirus similar to poliovirus and rhinovirus
b.serum and stool
c.immune globulin & Hepatitis A vaccine
d.achieve high titers during convalescence & persist indefinitely conferring immunity
e.Highly contagious

Front 22

Acute Hepatitis Hepatitis A
a.routed of transmission?
b.viral shed period before onset of ______ ?
c.period when no longer infectious ?

Back 22

a.via food contaminated by feces-soiled hands of infected persons, ingestion of sewage-contaminated shellfish, sexual transmission, IV drug abuse with shared needles
b.Virus shed in stool 14 – 21 days before onset of jaundice
c.No longer infectious 21 days after onset

Front 23

Acute Hepatitis Hepatitis B
a.route of transmission?
b.body secretions where present? when?
c.Common modes of transmission?

Back 23

a.primarily via percutaneous route with infected serum or blood products
b.serum and body secretions early in course of acute phase
c.oral and genital sexual contact with bleeding lesions in rectal mucosa; to fetus during pregnancy

Front 24

Acute Hepatitis
Hepatitis C
a.route of transmission?
b.occurance rate?
c.common mode of transmission?
d.rate of perinatal exposure?

Back 24

a.parenteral routes such as blood transfusions, occupational exposure, IV drug abuse
b.Most common chronic blood-borne infection in U.S.
c.Shared percutaneous exposure (shared toothbrushes, razors)
Rate of perinatal infection low
d.low

Front 25

Acute Hepatitis
Hepatitis C
a.organ transplantation?
b.frequency in U.S.?
c.progression?
d.liver transplant?

Back 25

a.Organ recipients from donors with HCV antibodies have high likelihood of developing HCV infection
b.Predominant liver disease in U.S.
c.Slow progression to cirrhosis & possibly hepatocelluar CA
d.End-stage liver disease d/t HCV associated cirrhosis is

Front 26

Acute Hepatitis
Hepatitis D
a.population effected?
b.route of transmission?
c.combo w/ HBV?

Back 26

a.patients infected with HBV
b.Transmitted via percutaneous route
c.Combined infection with HBV and HDV produce more severe acute hepatitis

Front 27

Acute Hepatitis Diagnosis

Back 27

Dependent on appearance of clinical S/S

1.Serum aminotransferase concentrations (AST, ALT)
2.Anemia
3.Lymphocytosis
4.Serum bilirubin (usually no > 20 mg/dl)
5.serum albumin (decreased)
6. PT (prolonged)

Front 28

Acute Hepatitis S/S
a.onset?
b.manifestations?
c.course?

Back 28

a.gradual or sudden
b.Manifests as dark urine, fatigue, anorexia, nausea, low-grade fever is common, may have RUQ abd pain but is less common than generalized abd discomfort, myalgias and arthralgias (esp. with HBV; hepatomegaly and splenomegaly

c.S/S tend to abate with onset of jaundice

Front 29

Acute Hepatitis severe forms may present as? with what manifestations?

Back 29

acute liver failure – confusion, asterixis, peripheral edema, ascites

Front 30

Acute Hepatitis dx:
Serum aminotransferase concentrations
a.what is it?
b.when do they increase & decrease?
c.rise relationship to severity of hepatitis?
d.concentrations for mild hepatitis?

Back 30

a.sensitive indicators of liver cell injury and seen with viral hepatitis
b.AST and ALT increase 7 – 14 days before appearance of jaundice then begin to decrease
c.Rise in AST and ALT does NOT parallel severity of hepatitis
d.Concentrations < 500 IU/L usually indicate mild hepatitis

Front 31

Diagnosis of HBV
a.antibody and it's appearance?
b.antigen?
c.marker when antigen no longer detectable?
d.if antigen is detectable what does this mean?

Back 31

a.anti-HBc is antibody to core antigen and appears promptly after infection and persists indefinitely;
b.HBsAg
c.high titers of IgM anti-HBc may be only marker for acute HBV infection if HBsAg is no longer detectable; d.detection of HBsAg indicates active replication and the blood is therefore highly contagious

Front 32

Acute Hepatitis Clinical course
a.s/s period?
b.what happens to s/s as jaundice appears?
c.will liver fxn return?

Back 32

a.S/S 7 – 14 days before onset of dark urine and jaudice
b.Appetite returns and malaise decreases as jaundice increases
c.yes. l iver fxn will return

Front 33

Acute Hepatitis Clinical course
a.full recover when?
b.rarely progresses to what 2 things?
c.can develop into? and common cause?
d.what can take decades to develop?

Back 33

a.Full recovery may take up to 12 months in the elderly and those infected with HBV and HCV
b.Rarely progresses to fulminant liver failure and death
c.Chronic hepatitis can develop (exception is HAV; Most common causes are HBV and HCV
HCV poses risk for development of cirrhosis and primary hepatocellular carcinoma which may take decades to occur
d.primary hepatocelluar cancer

Front 34

acute hepatitis life-threatening complications

Back 34

Acute Hepatitis
Aplastic anemia
Hemolytic anemia
Hypoglycemia
Polyarteritis

Front 35

Symptomatic Acute Hepatitis
Treatment

Back 35

1.N/V – replace IVF and electrolytes
2.abstain from ETOH
3.Liver transplant – when encephalopathy and coagulation abnormalities develop

Front 36

Acute Hepatitis
Prevention

Back 36

Avoid exposure
Passive immunization with gamma globulin
Active immunization with specific vaccines

Front 37

HAV exposure tx
a.what is it?
b.route of administration?
c.when given?
d.effectiveness?
e.protection length?

Back 37

a.Pooled gamma globulin
b.IM
c.ASAP after exposure to known HAV
d.dramatically decreases incidence of HAV infection
e.short-term

Front 38

HAV prevention vaccine
a.what is it?
b.protection length?
c.recommended to what populations?

Back 38

inactivated vaccine provides protection for 5 – 10 years; c.high risk groups such as travelers to endemic areas, NICU workers, food handlers, children in daycare centers, and military personnel

Front 39

HBV exposure tx

Back 39

hepatitis B immune globulin and hepatitis B vaccine within 24 hours of exposure

Front 40

HBV prevention vaccine
a.when do antibody titers begin to decline?
b.speed of response to booster?
c.effect in HBV carriers?

Back 40

a.in 5 years 20 – 30% of those immunized lack protection;
b.prompt;
c.no value but does not create adverse effects if administered

Front 41

3 examples of drugs and toxins that can lead to acute hepatitis besides the hepatitis viruses.

Back 41

1.Acetaminophen overdose
2.Volatile anesthetics (Halothane Hepatitis)
3.Immune-mediated hepatotoxicity

Front 42

Acute Hepatitis:
Differential Dx of Post-Op Hepatic Dysfunction (8)

Back 42

1.Evaluate serial liver function tests
2.Rule out extrahepatic causes (CHF, resp. failure, PE, RI); Intrahepatic cholestasis (a/w prolonged surgeries, hypotension, arterial hypoxemia, massive blood transfusions)
3.Review all administered drugs – (catecholamines/sympathomimetics can cause splanchnic vasoconstriction resulting in hepatocyte ischemia)
4.Sources of sepsis
5.Sources of exogenous bilirubin (blood transfusions)
6.Rule out occult hematomas – (reabsorption causes hyperbilirubinemia)
7.Rule out hemolysis – (decreases in Hct or increases in reticulocyte count)
8.Immune-mediated hepatotoxicity

Front 43

Halothane Hepatitis
Possible causes: (3)

Back 43

Hepatotoxic metabolites
Immune hypersensitivity
Genetic predisposition

Front 44

Halothane Hepatitis
Risk Factors:
(5)

Back 44

1.Middle age
2.Obesity
3.Female
4.Repeat exposure (esp. w/in 28 days)
5.Prepubertal children are more resistant to condition

Front 45

Chronic Hepatitis
Characteristics (3)

Back 45

1.Prolonged elevation of liver chemistries
2.hepatocyte inflammation on liver bx
3.lasting 6 months or >

Front 46

Chronic Hepatitis
a.Common causes
b.other causes

Back 46

a.autoimmune, chronic viral hepatitis (HBV/HCV)

b.drugs, Wilson’s dz, alpha-1-antitrypsin deficiency, primary biliary cirrhosis, primary sclerosing cholangitis

Front 47

Chronic Hepatitis
a.range of S/S?
b.most common s/s?
c.extrahepatic manifestations?

Back 47

a.Range from asymptomatic to mild increases in serum aminotransferases to hepatic failure

b.fatigue, malaise, mild abd pain; Hepatomegaly with or w/o splenomegaly

c.arthralgias, arthritis, glomerulonephritis, skin rashes, amenorrhea, and thyroiditis

Front 48

Chronic Hepatitis dx

Back 48

1.immunologic and serologic testing
2.Liver bx

Front 49

Chronic Hepatitis:
benefit of liver bx?

Back 49

dx certain dz (Wilson’s dz or alpha-1-antitrypsin)

Front 50

Chronic Hepatitis:
Autoimmune hepatitis Findings

Back 50

1.Hypergammaglobulinemia

2.Increased serum aminotransferases (3 – 10 x’s normal)

3.Anti-nuclear antibodies

Front 51

Chronic Hepatitis:
Autoimmune hepatitis tx (2)

Back 51

Corticosteriods
Immunosuppressants

Front 52

Chronic Hepatitis B
a.what's detected? length of detection?
b.characters of HBV carriers?
c.characters of chronic HBV?
d.major determinant of chronicity?
e.risk factor?
f.what population are predominantly carriers of HBsAg?
g.risk factor for what progressive liver dz?

Back 52

a.HBsAg detectable for >6 months
b.HBV carriers – presence of HBsAg, normal aminotransferases, asymptomatic
c.Chronic – dx when HBsAg present, increased aminotransferases, clinical s/s
d.Age at time of infection is major determinant of chronicity (younger leads to more chronic)
e.Risk factor is presence of intrinsic or iatrogenic immunosuppression
f.Men are predominantly carriers of HBsAg (women more likely to clear HBsAg)
g.Risk factor for hepatocellular carcinoma

Front 53

Chronic Hepatitis B
a.Tx Goal
b.currently tx can only do what?
c.Txs
d.disadvantage of liver transplant in pts with HBV?

Back 53

a.eradicate HBV, prevent cirrhosis and CA;
b.currently can only suppress viral replication
c.interferon, lamivudine, liver transplant if liver failure
d.HBV will infect new liver

Front 54

Chronic Hepatitis C
a.prevealence after HCV?
b.prevealence compared to HBV?
c.Dx?
d.progression pattern?

Back 54

a.Follows in 85% of pts with HCV
b.More prevalent than HBV
c.persistently elevated aminotransferases, presence of anti-HCV antibodies
d.Progresses slowly over decades; usually will develop cirrhosis after approx. 30 yrs

Front 55

Chronic Hepatitis C
Risk factors for progression

Back 55

1.>40 yrs of age at time of initial infection
2.Daily ETOH consumption exceeding 50g
3.Male gender

Front 56

Chronic Hepatitis C Tx

Back 56

1.interferon (suppresses viral replication); may be combined w/ other antivirals (ribavirin)
2.One of the most common indications for liver transplant (Can reinfect transplant graft)

Front 57

Drug-induced Chronic Hepatitis:
a.drug examples
b.tx

Back 57

a.methyldopa, trazodone, isoniazid, sulfonamides, acetaminophen, aspirin, phenytoin

b.D/C suspected drug

Front 58

Wilson’s dz induced Chronic Hepatitis:
a.what is wilson's dz?
b.dx?
c.tx?

Back 58

a.absence of associated neurological s/s;

b.dx’d with liver bx and hepatic copper content

c.penicillamine

Front 59

Alpha-1-antitrypsin deficiency induced Chronic Hepatitis:
a.progresses to?
b.dx?

Back 59

a.progresses to cirrhosis; b.decreased alpha-1 globulin and serum tests for alpha-1-antitrypsin

Front 60

Primary biliary cirrhosis induced chronic hepatitis
a.indistinguishable from what on bx?
b.what skin disorders?
c.what serum levels are elevated?

Back 60

indistinguishable from chronic viral hepatitis on bx;
b.hyperpigmentation, pruritus,
c.increase in serum alkaline phosphatase

Front 61

Cirrhosis
a.common causes?
b.what happens to liver tissue?
c.dx?

Back 61

a.Most often result of chronic excessive ETOH consumption, HBV, HCV
b.Scarring of liver, disrupts structure, regenerating nodules of parenchyma
c.liver bx,irregular liver surface,

Front 62

Cirrhosis
S/S (9)

Back 62

1.Most common are fatigue and malaise
2.Palmar erythema,
3.spider nevi,
4.gynecomastia,
5.testicular atrophy,
6.portal HTN (splenomegaly, ascites)
7.Decreased hepatic blood flow
8.Enlarged palpable liver
9.esophageal varices
10.Labs: Decreased serum albumin, Prolonged PT, Increased serum aminotransferases, and alkaline phosphatase

Front 63

why is hepatic BF decreased in cirrhosis? compensatory mechanism?

Back 63

d/t increased intrahepatic resistance via portal vein;

compensated by increases in blood flow via hepatic artery

Front 64

Forms of Cirrhosis

Back 64

1.Alcoholic cirrhosis
2.Postnecrotic cirrhosis
3.Primary Biliary Cirrhosis
4.Hemochromatosis cirrhosis
5.Wilson’s dz

Front 65

Alcoholic Cirrhosis
a.cause?
b.Dx?
c.tx?

Back 65

a.chronic excessive ingestion of ETOH; daily ETOH consumption > 50g (3 –4 drinks) for 10 – 15 yrs
b. difficult b/c pts conceal ETOH abuse
c.cessation of ETOH consumption; nutritional support

Front 66

Postnecrotic cirrhosis
a.what is it?
b.common causes?
c.predominant population?
d.lab evaluation shows?
e.how does it progress?
f.death usually do to what?
g.tx?

Back 66

a.shrunken liver w/ regenerating nodules;
b.chronic viral hepatitis and autoimmune hepatitis; can be unknown (cryptogenic hepatitis);
c.women;
d.increased serum gamma globulin;
e.insidiously;
f. GI bleeding or hepatic failure; can progress to CA
g.supportive and symptomatic

Front 67

Primary Biliary Cirrhosis
a.population?
b.causes?
c.S/S?

Back 67

a.Women 30 – 50 yrs age
b.serum autoantibodies; bile duct lesions; possible immune mechanism
c.fatigue, generalized pruritus; jaundice 5 – 10 yrs after onset of pruritus; osteoporosis; renal tubular acidosis, CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia), Sjogren’s syndrome

Front 68

Hemochromatosis cirrhosis
a.what is it?
b.S/S?
c.Tx?

Back 68

a.large amounts of iron deposited in hepatocytes; more common in men; deposits in pancreas and heart result in DM and CHF
b. bronze discolored skin, hepatosplenomegaly, portal HTN, progression to CA; increased serum iron and ferritin; increases in alkaline phosphatase and aminotransferases; jaundice is uncommon
c. remove excess iron by phlebotomy

Front 69

Wilson’s dz
a.what is it?
b.S/S?

Back 69

a.hepatolenticular degeneration; autosomal recessive disorder; defect in gene for copper binding; leads to accumulation of copper
b.neurological (tremors, gait disturbance, slurred speech); hepatic (fatigue, jaundice, ascites, splenomegaly, gastroesophageal varices; hemolytic anemia, *hallmark sign is Kayser-Fleischer ring (thin brown crescent at periphery of cornea)

Front 70

Cirrhosis complications (15)

Back 70

1.Portal HTN
2.Gastroesophageal varices
3.Ascites
4.Spontaneous bacterial peritonitis
5.Hepatorenal syndrome
6.Malnutrition
7.hyperdynamic circulation
8.cardiomyopathy
9.arterial hypoxemia
10.hypoglycemia
11.duodenal ulcer
12.gallstones
13.hepatic encephalopathy
14.primary hepatocellular carcinoma
15.anemia

Front 71

Portal HTN
a.cause?
b.associated with? (4)

Back 71

a.increased resistance to blood flow;
b.hypoalbuminemia, increased secretion of ADH, ascites, hepatomegaly

Front 72

Gastroesophageal varices
a.what are they?
b.tx?

Back 72

a.massive dilation of submucosal veins

b.intubation to prevent aspiration; vasopressin w/ NTG; somatostatin or octreotide; propanolol to reduce portal HTN

Front 73

Ascites
a.how does it manifest? (5)
b.tx? (5)

Back 73

a.fluid wave across abd, right side pleural effusion; increased incidence w/ portal HTN, decreased serum albumin, renal retention of sodium

b.Tx – aldosterone antagonists; do NOT exceed 1 L/day diuresis; LeVeen shunt; paracentesis; IV albumin

Front 74

Spontaneous bacterial peritonitis
a.manifestations?
b.how is it facilitated?

Back 74

a.fever, leukocytosis, abd pain, decreased bowel sounds;

b.facilitated by portal HTN rerouting blood flow through collateral circulation

Front 75

Hepatorenal syndrome
a.manifestations

Back 75

a.renal failure; usually fatal; deeply jaundiced; moribund; tense ascites; hypoalbuminemia; hypoprothrombinemia; d/t decreased renal blood flow and glomerular filtration

Front 76

Cirrhosis:
Malnutrition

Back 76

protein, salt and water retention

Front 77

cirrhosis:
hyperdynamic circulation (8)

Back 77

1.increased cardiac output r/t vasodilating substances (glucagon)
2.increased intravascular fluid volume,
3.decreased viscosity of blood r/t anemia, 4.arteriovenous communications (esp. lungs), 5.cardiomyopathy manifests as CHF,
6.megaloblastic anemia d/t antagonism of folate by ETOH,
7.thrombocytopenia, accumulation of fibrin degradation products, DIC, 8.decreased liver clearance of substances

Front 78

cirrhosis:
Arterial hypoxemia
a.what is it?
b.cause?
c.increased frequency of?
d.effect of ETOH on lungs &esophageal sphincter tone?

Back 78

a.PaO2 60 – 70 mmHg
b.impaired movement of diaphragm r/t ascites; right to left intrapulmonary shunts d/t portal HTN; c.increased frequency of pneumonia;
d.inhibits phagocytic activity in lungs; regurgitation of gastric contents d/t decreased lower esophageal sphincter tone

Front 79

Cirrhosis:
Hypoglycemia
a.common with what abusive habit?
b.how does ETOH play a part?
c.why does metabolic acidosis occur? what IV fluid should be avoided?

Back 79

a.common in ETOH abuse; b.reflects glycogen depletion d/t malnutrition; ETOH-induced glycogenolysis and interference with gluconeogenesis;
c.inability to clear and convert lactate to glucose leading to metabolic acidosis (avoid LR)

Front 80

cirrhosis:
Duodenal ulcers
a.bleeding contributes to what?
b.what byproduct is increased and what is it's effect?

Back 80

a.bleeding contributes to anemia,
b.increases ammonia leading to hepatic encephalopathy

Front 81

cirrhosis:
Gallstones
a.what does it reflect?
b.caused by?

Back 81

a.chronic increases in bilirubin load
b.persistent hemolytic anemia and splenomegaly

Front 82

cirrhosis:
Hepatic encephalopathy manifestations (4)

Back 82

mental obtundation, asterixis, fetor hepaticus, slowing of EEG waves

Front 83

Cirrhosis Anesthesia
Management:
Increased post-op morbidity d/t?

Back 83

co-existing dz and increased incidences of complications

Front 84

Cirrhosis Anesthesia
Management:
Pre-op preparation of
Prolonged PT

Back 84

parenteral vitamin K; failure to respond reflects severe hepatocellular dz; promptly reverse prothrombin deficiencies d/t biliary obstruction

Front 85

Cirrhosis Anesthesia
Management: Preop
Correct thrombocytopenia or coagulopaties

Back 85

plt and FFP

Front 86

Cirrhosis Anesthesia
Management:preop Hypoglycemia

Back 86

administer glucose solutions

Front 87

Cirrhosis Anesthesia
Management: preop
elevated Ammonia levels

Back 87

– protein restriction, lactulose, neomycin

Front 88

Cirrhosis Anesthesia
Management: preop
prevention of postop ARF and sepsis in pts with elevated serum bilirubin levels

Back 88

Serum bilirubin > 8mg/dl
(severely jaundiced)

diuresis pre-op with mannitol and initiate antibx therapy

Front 89

Cirrhosis Anesthesia
Management: intraop what are the 3 H's you want to avoid?

Back 89

REMEMBER – Avoid increasing hepatic oxygen requirements, hepatic hypoxia, and hypoperfusion

Front 90

Cirrhosis Anesthesia
Management: Post-op
a.monitor for?
b.rule out?
c.onset of EtOH withdrawal syndrome?

Back 90

a.Monitor for effects of decreased hepatic blood flow
b.R/O cholestasis, sepsis
c.ETOH withdrawal syndrome 48 – 72 hrs after cessation of ETOH

Front 91

Cirrhosis Anesthesia
Management: intraop alcholic intoxicationed pts
a.why aspiration risk?
b.why increased bleeding risk?

Back 91

a.slowed gastric emptying and decreased LES tone

b.interference w/ plt aggregation

Front 92

Cirrhosis Anesthesia
Management: best NMBA to use and why?

Back 92

1.atracurium b/c metabolized by hoffman eimination and nonspecific esterases

2.cisatricurium b/c metabolized by hoffman elimination

Front 93

Acute Liver Failure
a.2 hallmark signs?
b.Liver failure presents when?
c.causes?

Back 93

a.AMS (hepatic encephalopathy) & impaired coagulation (prolonged PT)
b.when hepatic encephalopathy develops w/in 8 wks of onset
c.Most cases are a result of viral hepatitis and drug-induced liver injury

Front 94

Acute Liver Failure
S/S (11)

Back 94

1.Malaise,
2.nausea,
3.jaundice,
4.rapid onset of AMS,
5.Rapid progression to coma w/in 2 – 10 days
6.Increased serum aminotransferase, hypoglycemia,
7.respiratory alkalosis
8.Cerebral edema
9.systemic HTN and bradycardia
10.Hepatorenal syndrome – hypotension, decreased SVR, oliguria
11.High risk for bacterial and fungal infections

Front 95

Acute fatty liver of pregnancy
a.what is it?
b.associated with?
c.onset?
d.manifestations?
e.tx?

Back 95

a.accumulation of microscopic fat in hepatocytes;
b.a/w PIH and HELLP syndrome;
c.onset 3rd trimester; d.manifests as N/V, RUQ pain, malaise, anorexia, followed by jaundice 7 – 14 days later; can progress to death;
e.prompt termination of pregnancy

Front 96

Acute Liver Failure
Tx (5)

Back 96

1.treat Underlying causes
2.glucose in presence of hypoglycemia
3.PA catheter for intravascular fluid volume management
4.Vasopressors to improve MAP but may increase ischemia
5.Liver transplant

Front 97

why is plasma cholinesterase unaffected in acute liver failure?

Back 97

Half-life of plasma cholinesterase is 14 days

Front 98

Blood administration intraop w/ acute renal failure:
a.why adm warmed blood slowly?
b.for what 2 reasons is whole blood beter?

Back 98

a.decreased metabolism of citrate;
b.whole blood optimizes delivery of coagulation factors and minimizes ammonia

Front 99

what electrolyte imbalances are acute liver failure pt vulnerable to?

Back 99

decreased potassium, calcium, and magnesium

Front 100

Diseases of the Biliary Tract
Risk Factors

Back 100

Age > 40 yrs
Female
Obesity
Rapid wt loss
pregnancy

Front 101

what are the 2 types Gallstones

Back 101

1.hydrophobic cholesterol molecules (90%)
2.calcium bilirubinate and (more common w/ cirrhosis or hemolytic anemia)

Front 102

Name the causes of acute liver failure (7)

Back 102

1.viral hepatitis
2.drug induced - acetaminophen, idiosyncratic rxns (volatile agents, esp halothane, isoniazid, phenytoin, sulfonamides, propylthiouracil, amiodarone)
3.toxins - carbon tetrachloride, mushrooms
4.vascular events - ischemia, veno-occlusive dz (Budd-Chiari syndrome)
5.acute fatty liver of pregnancy
6.wilson syndrome
7.reye syndrome

Front 103

Acute cholecystitis

Back 103

obstruction of cystic duct

Front 104

Acute cholecystitis – S/S (5)

Back 104

1.NV,
2.fever,
3.severe abd pain, RUQ tenderness
4.dark urine and scleral icterus
5.Jaundice

Front 105

cholelithiasis present in what % of Acute cholecystitis cases?

Back 105

95%

Front 106

Acute cholecystitis - nature of the pain
a.begining and ending location?
b.cause?
c.onset and duration?

Back 106

a.begins mid-epigastrum and radiates to right upper abd to back or between scapulae b.lodging of stone in biliary duct (aka biliary colic);
c.abrupt and gradually subsides

Front 107

Acute cholecystitis - what does jaundice reflect?

Back 107

obstruction of common bile duct

Front 108

Acute cholecystitis
a.Dx
b.differential dx

Back 108

a.ultrasonography; radionuclide scanning most accurate

b.acute pancreatitis, alcoholic hepatitis, penetrating duodenal ulcers, acute appendicitis, acute MI, pyelonephritis, right lower lobe pneumonia

Front 109

Acute cholecystitis
Tx – (5)

Back 109

1.IVF,
2.electrolyte correction, 3.opioids for pain management,
4.antibx for febrile pts, 5.surgery when stable

Front 110

considerations for open cholecystectomy

Back 110

1.inflammation obscures anatomy;
2.common bile duct stones removal w/ ERCP unsuccessful
3.septic shock,
4.peritonitis,
5.pancreatitis,
6.portal HTN,
7.clotting abnormalities

Front 111

Acute cholecystitis
Complications

Back 111

1.Severe inflammation and necrosis of gallbladder
2.Localized perforation
3.Abcess formation
4.Gallstone ileus

Front 112

name some complications of laparoscopic surgery.

Back 112

Subcutaneous emphysema, pneumomediastinum, pneumothorax, pneumoscrotum, inappropriate ADH secretion

Front 113

why are Opioids controversial during cholecystectomies?

Back 113

possible spasm of sphincter of Oddi

Front 114

Tx spasm of sphincter of Oddi

Back 114

1.IV naloxone
2.glucagon
3.NTG

Front 115

Chronic Cholecystitis
a.what is it?
b.cause?
c.s/s?
d.Dx (2)
e.Tx (2)

Back 115

a.Gallbladder wall thickened, fibrotic, rigid;
b.follows a series of acute cholecystitis attacks
c.S/S Flatulence, heartburn, postprandial distress
d.ultrasonography, ERCP
e.elective cholecystectomy; alternative tx includes oral dissolution therapy (ursodiol) and extracorporeal biliary lithotripsy

Front 116

Choledocholithiasis
a.what is it?
b.s/s?
c.what can it result in?

Back 116

a.Lodgement of stones in common bile duct; lodge at point of insertion into ampulla of Vater

b.Fever, shaking chills, jaundice, RUQ pain;
c.acute pancreatitis