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116 Cards in this Set

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Largest organ in body that acts as a reservoir for blood?
liver
liver holds how much blood volume?
10-15% of blood volume
liver receives ___ of CO
25%
1.provides 75% blood to liver;
2.major oxygen source; 3.partially deoxygenated blood;
4.passive vascular bed
Portal vein
1.provides 25% blood to liver;
2.provides 50% of oxygen; 3.compensatory mechanism to decreased HBF but is limited
Hepatic artery
Hepatic veins drain into?
IVC
Categories of Liver Disease
1.Parenchymal

Cholestasis
parenchymal liver disease subcategories
Acute and chronic hepatitis
Cirrhosis
Cholestasis liver disease subcategories
With or without obstruction of extrahepatic biliary pathway
Classifications of Hepatic Dysfunction
1.Prehepatic
2.Intrahepatic(hepatocellular) 3.Extrahepatic (cholestatic)
Prehepatic hepatic dysfunction etiology
hemolysis, hematoma resorption, bilirubin overload from whole blood
Intrahepatic hepatic dysfunction other name & etiology
aka (hepatocellular)

viral, drugs, sepsis, hypoxemia, cirrhosis
Extrahepatic hepatic dysfunction other name & etiology
aka (cholestatic)

stones, sepsis
typical cause of acute hepatitis? and other causes?
virus

toxins or drugs
name 5 hepatitis viruses and their occurance rate
Hepatitis A (HAV) – 30% of cases
Hepatitis B (HBV) – 50% of cases
Hepatitis C (HCV) – 20% of cases
Hepatitis D (HDV)
Hepatitis E
name Other viruses that can cause liver problems
Cytomegalovirus
Epstein-Barr virus
Chronic infections may follow which hepatitis viruses?
HBV, HCV, and HDV
Viral Hepatitis s/s
1.May be asymptomatic or non-specific flu-like symptoms
2.jaundice
viral hepatitis Diagnostic labs
may show markedly increased aminotransferase levels
Specific etiology of hepatitis is determined by?
serologic testing
Hepatitis A
a.virus involved?
b.body secretions where present?
c.protection/vaccinations?
d.antibody activity?
e.contagious?
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
Acute Hepatitis Hepatitis A
a.routed of transmission?
b.viral shed period before onset of ______ ?
c.period when no longer infectious ?
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
Acute Hepatitis Hepatitis B
a.route of transmission?
b.body secretions where present? when?
c.Common modes of transmission?
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
Acute Hepatitis
Hepatitis C
a.route of transmission?
b.occurance rate?
c.common mode of transmission?
d.rate of perinatal exposure?
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
Acute Hepatitis
Hepatitis C
a.organ transplantation?
b.frequency in U.S.?
c.progression?
d.liver transplant?
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
Acute Hepatitis
Hepatitis D
a.population effected?
b.route of transmission?
c.combo w/ HBV?
a.patients infected with HBV
b.Transmitted via percutaneous route
c.Combined infection with HBV and HDV produce more severe acute hepatitis
Acute Hepatitis Diagnosis
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)
Acute Hepatitis S/S
a.onset?
b.manifestations?
c.course?
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
Acute Hepatitis severe forms may present as? with what manifestations?
acute liver failure – confusion, asterixis, peripheral edema, ascites
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?
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
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?
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
Acute Hepatitis Clinical course
a.s/s period?
b.what happens to s/s as jaundice appears?
c.will liver fxn return?
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
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?
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
acute hepatitis life-threatening complications
Acute Hepatitis
Aplastic anemia
Hemolytic anemia
Hypoglycemia
Polyarteritis
Symptomatic Acute Hepatitis
Treatment
1.N/V – replace IVF and electrolytes
2.abstain from ETOH
3.Liver transplant – when encephalopathy and coagulation abnormalities develop
Acute Hepatitis
Prevention
Avoid exposure
Passive immunization with gamma globulin
Active immunization with specific vaccines
HAV exposure tx
a.what is it?
b.route of administration?
c.when given?
d.effectiveness?
e.protection length?
a.Pooled gamma globulin
b.IM
c.ASAP after exposure to known HAV
d.dramatically decreases incidence of HAV infection
e.short-term
HAV prevention vaccine
a.what is it?
b.protection length?
c.recommended to what populations?
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
HBV exposure tx
hepatitis B immune globulin and hepatitis B vaccine within 24 hours of exposure
HBV prevention vaccine
a.when do antibody titers begin to decline?
b.speed of response to booster?
c.effect in HBV carriers?
a.in 5 years 20 – 30% of those immunized lack protection;
b.prompt;
c.no value but does not create adverse effects if administered
3 examples of drugs and toxins that can lead to acute hepatitis besides the hepatitis viruses.
1.Acetaminophen overdose
2.Volatile anesthetics (Halothane Hepatitis)
3.Immune-mediated hepatotoxicity
Acute Hepatitis:
Differential Dx of Post-Op Hepatic Dysfunction (8)
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
Halothane Hepatitis
Possible causes: (3)
Hepatotoxic metabolites
Immune hypersensitivity
Genetic predisposition
Halothane Hepatitis
Risk Factors:
(5)
1.Middle age
2.Obesity
3.Female
4.Repeat exposure (esp. w/in 28 days)
5.Prepubertal children are more resistant to condition
Chronic Hepatitis
Characteristics (3)
1.Prolonged elevation of liver chemistries
2.hepatocyte inflammation on liver bx
3.lasting 6 months or >
Chronic Hepatitis
a.Common causes
b.other causes
a.autoimmune, chronic viral hepatitis (HBV/HCV)

b.drugs, Wilson’s dz, alpha-1-antitrypsin deficiency, primary biliary cirrhosis, primary sclerosing cholangitis
Chronic Hepatitis
a.range of S/S?
b.most common s/s?
c.extrahepatic manifestations?
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
Chronic Hepatitis dx
1.immunologic and serologic testing
2.Liver bx
Chronic Hepatitis:
benefit of liver bx?
dx certain dz (Wilson’s dz or alpha-1-antitrypsin)
Chronic Hepatitis:
Autoimmune hepatitis Findings
1.Hypergammaglobulinemia

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

3.Anti-nuclear antibodies
Chronic Hepatitis:
Autoimmune hepatitis tx (2)
Corticosteriods
Immunosuppressants
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?
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
Chronic Hepatitis B
a.Tx Goal
b.currently tx can only do what?
c.Txs
d.disadvantage of liver transplant in pts with HBV?
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
Chronic Hepatitis C
a.prevealence after HCV?
b.prevealence compared to HBV?
c.Dx?
d.progression pattern?
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
Chronic Hepatitis C
Risk factors for progression
1.>40 yrs of age at time of initial infection
2.Daily ETOH consumption exceeding 50g
3.Male gender
Chronic Hepatitis C Tx
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)
Drug-induced Chronic Hepatitis:
a.drug examples
b.tx
a.methyldopa, trazodone, isoniazid, sulfonamides, acetaminophen, aspirin, phenytoin

b.D/C suspected drug
Wilson’s dz induced Chronic Hepatitis:
a.what is wilson's dz?
b.dx?
c.tx?
a.absence of associated neurological s/s;

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

c.penicillamine
Alpha-1-antitrypsin deficiency induced Chronic Hepatitis:
a.progresses to?
b.dx?
a.progresses to cirrhosis; b.decreased alpha-1 globulin and serum tests for alpha-1-antitrypsin
Primary biliary cirrhosis induced chronic hepatitis
a.indistinguishable from what on bx?
b.what skin disorders?
c.what serum levels are elevated?
indistinguishable from chronic viral hepatitis on bx;
b.hyperpigmentation, pruritus,
c.increase in serum alkaline phosphatase
Cirrhosis
a.common causes?
b.what happens to liver tissue?
c.dx?
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,
Cirrhosis
S/S (9)
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
why is hepatic BF decreased in cirrhosis? compensatory mechanism?
d/t increased intrahepatic resistance via portal vein;

compensated by increases in blood flow via hepatic artery
Forms of Cirrhosis
1.Alcoholic cirrhosis
2.Postnecrotic cirrhosis
3.Primary Biliary Cirrhosis
4.Hemochromatosis cirrhosis
5.Wilson’s dz
Alcoholic Cirrhosis
a.cause?
b.Dx?
c.tx?
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
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?
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
Primary Biliary Cirrhosis
a.population?
b.causes?
c.S/S?
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
Hemochromatosis cirrhosis
a.what is it?
b.S/S?
c.Tx?
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
Wilson’s dz
a.what is it?
b.S/S?
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)
Cirrhosis complications (15)
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
Portal HTN
a.cause?
b.associated with? (4)
a.increased resistance to blood flow;
b.hypoalbuminemia, increased secretion of ADH, ascites, hepatomegaly
Gastroesophageal varices
a.what are they?
b.tx?
a.massive dilation of submucosal veins

b.intubation to prevent aspiration; vasopressin w/ NTG; somatostatin or octreotide; propanolol to reduce portal HTN
Ascites
a.how does it manifest? (5)
b.tx? (5)
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
Spontaneous bacterial peritonitis
a.manifestations?
b.how is it facilitated?
a.fever, leukocytosis, abd pain, decreased bowel sounds;

b.facilitated by portal HTN rerouting blood flow through collateral circulation
Hepatorenal syndrome
a.manifestations
a.renal failure; usually fatal; deeply jaundiced; moribund; tense ascites; hypoalbuminemia; hypoprothrombinemia; d/t decreased renal blood flow and glomerular filtration
Cirrhosis:
Malnutrition
protein, salt and water retention
cirrhosis:
hyperdynamic circulation (8)
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
cirrhosis:
Arterial hypoxemia
a.what is it?
b.cause?
c.increased frequency of?
d.effect of ETOH on lungs &esophageal sphincter tone?
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
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?
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)
cirrhosis:
Duodenal ulcers
a.bleeding contributes to what?
b.what byproduct is increased and what is it's effect?
a.bleeding contributes to anemia,
b.increases ammonia leading to hepatic encephalopathy
cirrhosis:
Gallstones
a.what does it reflect?
b.caused by?
a.chronic increases in bilirubin load
b.persistent hemolytic anemia and splenomegaly
cirrhosis:
Hepatic encephalopathy manifestations (4)
mental obtundation, asterixis, fetor hepaticus, slowing of EEG waves
Cirrhosis Anesthesia
Management:
Increased post-op morbidity d/t?
co-existing dz and increased incidences of complications
Cirrhosis Anesthesia
Management:
Pre-op preparation of
Prolonged PT
parenteral vitamin K; failure to respond reflects severe hepatocellular dz; promptly reverse prothrombin deficiencies d/t biliary obstruction
Cirrhosis Anesthesia
Management: Preop
Correct thrombocytopenia or coagulopaties
plt and FFP
Cirrhosis Anesthesia
Management:preop Hypoglycemia
administer glucose solutions
Cirrhosis Anesthesia
Management: preop
elevated Ammonia levels
– protein restriction, lactulose, neomycin
Cirrhosis Anesthesia
Management: preop
prevention of postop ARF and sepsis in pts with elevated serum bilirubin levels
Serum bilirubin > 8mg/dl
(severely jaundiced)

diuresis pre-op with mannitol and initiate antibx therapy
Cirrhosis Anesthesia
Management: intraop what are the 3 H's you want to avoid?
REMEMBER – Avoid increasing hepatic oxygen requirements, hepatic hypoxia, and hypoperfusion
Cirrhosis Anesthesia
Management: Post-op
a.monitor for?
b.rule out?
c.onset of EtOH withdrawal syndrome?
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
Cirrhosis Anesthesia
Management: intraop alcholic intoxicationed pts
a.why aspiration risk?
b.why increased bleeding risk?
a.slowed gastric emptying and decreased LES tone

b.interference w/ plt aggregation
Cirrhosis Anesthesia
Management: best NMBA to use and why?
1.atracurium b/c metabolized by hoffman eimination and nonspecific esterases

2.cisatricurium b/c metabolized by hoffman elimination
Acute Liver Failure
a.2 hallmark signs?
b.Liver failure presents when?
c.causes?
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
Acute Liver Failure
S/S (11)
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
Acute fatty liver of pregnancy
a.what is it?
b.associated with?
c.onset?
d.manifestations?
e.tx?
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
Acute Liver Failure
Tx (5)
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
why is plasma cholinesterase unaffected in acute liver failure?
Half-life of plasma cholinesterase is 14 days
Blood administration intraop w/ acute renal failure:
a.why adm warmed blood slowly?
b.for what 2 reasons is whole blood beter?
a.decreased metabolism of citrate;
b.whole blood optimizes delivery of coagulation factors and minimizes ammonia
what electrolyte imbalances are acute liver failure pt vulnerable to?
decreased potassium, calcium, and magnesium
Diseases of the Biliary Tract
Risk Factors
Age > 40 yrs
Female
Obesity
Rapid wt loss
pregnancy
what are the 2 types Gallstones
1.hydrophobic cholesterol molecules (90%)
2.calcium bilirubinate and (more common w/ cirrhosis or hemolytic anemia)
Name the causes of acute liver failure (7)
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
Acute cholecystitis
obstruction of cystic duct
Acute cholecystitis – S/S (5)
1.NV,
2.fever,
3.severe abd pain, RUQ tenderness
4.dark urine and scleral icterus
5.Jaundice
cholelithiasis present in what % of Acute cholecystitis cases?
95%
Acute cholecystitis - nature of the pain
a.begining and ending location?
b.cause?
c.onset and duration?
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
Acute cholecystitis - what does jaundice reflect?
obstruction of common bile duct
Acute cholecystitis
a.Dx
b.differential dx
a.ultrasonography; radionuclide scanning most accurate

b.acute pancreatitis, alcoholic hepatitis, penetrating duodenal ulcers, acute appendicitis, acute MI, pyelonephritis, right lower lobe pneumonia
Acute cholecystitis
Tx – (5)
1.IVF,
2.electrolyte correction, 3.opioids for pain management,
4.antibx for febrile pts, 5.surgery when stable
considerations for open cholecystectomy
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
Acute cholecystitis
Complications
1.Severe inflammation and necrosis of gallbladder
2.Localized perforation
3.Abcess formation
4.Gallstone ileus
name some complications of laparoscopic surgery.
Subcutaneous emphysema, pneumomediastinum, pneumothorax, pneumoscrotum, inappropriate ADH secretion
why are Opioids controversial during cholecystectomies?
possible spasm of sphincter of Oddi
Tx spasm of sphincter of Oddi
1.IV naloxone
2.glucagon
3.NTG
Chronic Cholecystitis
a.what is it?
b.cause?
c.s/s?
d.Dx (2)
e.Tx (2)
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
Choledocholithiasis
a.what is it?
b.s/s?
c.what can it result in?
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