approach to patient with hepatic disorders
TRANSCRIPT
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Approach to Patient withApproach to Patient with
Hepatic DisordersHepatic Disorders
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Liver Structure and FunctionLiver Structure and Function
largest organ in the body;largest organ in the body;
weighs about 1-1.5kgweighs about 1-1.5kg
Located in the RUQ of the abdomenLocated in the RUQ of the abdomenunder the right lower rib age againstunder the right lower rib age against
the diaphragmthe diaphragm
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Blood SupplyBlood Supply
a.a. 20% from Hepatic Artery (oxygen-20% from Hepatic Artery (oxygen-
rich)rich)
b.b.80% from Portal Vein (nutrient-rich)80% from Portal Vein (nutrient-rich)
A mixture of venous and arterial bloodA mixture of venous and arterial blood
bathes the liver cellsbathes the liver cells
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HepaticArtery
Portal Vein
Liver
Common capillary bed/
sinusoids of liver
Central Veins
of each Lobule
Hepatic Vein
Inferior Vena Cava
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Liver CellsLiver Cells
Hepatocytes 2/3 of liver mass andHepatocytes 2/3 of liver mass and
does most of the liver functionsdoes most of the liver functions
Kupffer cells engulf particulateKupffer cells engulf particulate
matter (bacteria) that enter the livermatter (bacteria) that enter the liver
through portal bloodthrough portal blood
Ito cells fat-storing cellsIto cells fat-storing cells
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Functions of LiverFunctions of Liver
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Glucose MetabolismGlucose Metabolism
Meal Glucose absorption in
intestines
Portal Circulation Liver
Glucose converted
to glycogen
Stored in
hepatocytes
I.
II.
Exercise Protein/Fat
breakdown
Liver creates glucose
(gluconeogenesis)
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Ammonia ConversionAmmonia Conversion
Ammonia from: use of amino acids
from protein forgluconeogenesis
Ammonia from: production
of intestinal flora/ from diet
Portal Circulation
Liver: converts ammonia to urea
Systemic circulation
Excreted in the kidneys
(urine)
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Protein MetabolismProtein Metabolism
Synthesizes plasma proteinSynthesizes plasma protein
(albumin, alpha and beta globulin)(albumin, alpha and beta globulin)
Clotting factors (prothrombin)Clotting factors (prothrombin) -- liver needs Vit. K to synthesize prothrombinliver needs Vit. K to synthesize prothrombin
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Fat MetabolismFat Metabolism
Fatty acids are degraded into ketoneFatty acids are degraded into ketone
bodies for energy duringbodies for energy during
hypoglycemic state, starvation andhypoglycemic state, starvation and
uncontrolled DM.uncontrolled DM.
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Vitamin and Iron StorageVitamin and Iron Storage
Large amounts of Vit. A, B, and D andLarge amounts of Vit. A, B, and D and
several B-complex vitamins areseveral B-complex vitamins are
stored in the liverstored in the liver
Iron and copper are also stored in theIron and copper are also stored in the
liverliver
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Drug MetabolismDrug Metabolism
First-pass Effect
Oral meds pass the
G.I.T.
Portal
circulation
Liver (metabolized)
Decreased
bioavailability
Bioavailability fraction of drug that reaches the systemic
circulation
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Bile FormationBile Formation
Formed by the hepatocytesFormed by the hepatocytes
Primary bile acids are cholic acid andPrimary bile acids are cholic acid and
chenodeoxycholic acid (CDCA)chenodeoxycholic acid (CDCA)
Major components: water(82%), bileMajor components: water(82%), bile
acids(12%), lecithin &otheracids(12%), lecithin &other
phospholipids (4%) and unesterifiedphospholipids (4%) and unesterified
cholesterol (0.7%)cholesterol (0.7%)
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Bilirubin ExcretionBilirubin Excretion
Degradation ofSenescent RBCs in
the spleen
Release ofHemoglobin
Heme
moleculeCO & biliverdin
bilirubin
Heme oxygenase Biliverdin reductase
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Enterohepatic Circulation
Bile
(conjugated bilirubin)
Bile ducts
duodenum
Ileum and colon
(converted into urobilinogen)
Excreted in feces
(stercobilin)
Reabsorbed into
portal circulation
Systemic circulation
kidney
Excreted in urine
Liver:
reexcreted into bile
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Clinical HistoryClinical History
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Symptoms of Liver DiseaseSymptoms of Liver Disease
Nature of DiseaseNature of Disease
Pattern of OnsetPattern of OnsetDisease ProgressionDisease Progression
Potential Risk FactorsPotential Risk Factors
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Symptoms of Liver DiseaseSymptoms of Liver Disease
A.A. Fatigue - most commonFatigue - most commoncharacteristic ofcharacteristic of liverliverdiseasedisease
e.g. lethargy, weakness,e.g. lethargy, weakness,restlessnessrestlessness
B. Nausea/Vomiting provoked byB. Nausea/Vomiting provoked by
odor ofodor of food or fatty foodfood or fatty foodintakeintake
C. RUQ pain/discomfort arises fromC. RUQ pain/discomfort arises fromstretching/irritation ofstretching/irritation of
GlissonsGlissons capsule w/ccapsule w/c
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D. Pruritus/Itching related toD. Pruritus/Itching related to
accumulationaccumulation of bileof bile
salts in the dermissalts in the dermis
E. Jaundice hallmark of liver diseaseE. Jaundice hallmark of liver disease
andand most reliable markermost reliable marker
of severityof severity
- accompanied by acholic- accompanied by acholic
tools/tools/ tea-colored urine?tea-colored urine?
e.g.e.g. jaundice without dark urine indicatesjaundice without dark urine indicatesunconjugated hyperbilirubinuriaunconjugated hyperbilirubinuria
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Nature of DiseaseNature of Disease
Hepatocellular injury vs.Hepatocellular injury vs.Cholestatic injuryCholestatic injury
Hepatocellular: ALT/AST elevated outHepatocellular: ALT/AST elevated outof proportion to alkaline phosphataseof proportion to alkaline phosphatase
Cholestatic: Alkaline phosphatase outCholestatic: Alkaline phosphatase outof proportion to ALT/ASTof proportion to ALT/AST
Viral vs BacterialViral vs Bacterial( Viral Hepatitis/ Liver( Viral Hepatitis/ Liver
abscess)abscess)
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Pattern of Disease (Staging)Pattern of Disease (Staging)
Course of disease (acute vs. chronic)Course of disease (acute vs. chronic)
Early vs. lateEarly vs. late
Pre-cirrhotic, cirrhotic, end stagePre-cirrhotic, cirrhotic, end stage
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Disease ProgressionDisease Progression
(Grading)(Grading)Severity and activity of diseaseSeverity and activity of disease
Active vs. inactive; mild moderate,Active vs. inactive; mild moderate,
severesevere
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Potential Risk FactorsPotential Risk Factors
A.A. Alcohol consumptionAlcohol consumption
for women: 2 drinks(22-30g/day)for women: 2 drinks(22-30g/day)
for men: 3 drinks (33-45g/day)for men: 3 drinks (33-45g/day)
Assess presence ofAssess presence ofabuse orabuse or
dependencedependence
Alcoholism defined on behavioralAlcoholism defined on behavioral
patterns andpatterns and consequences of alcoholconsequences of alcohol
intake not on the basis fointake not on the basis fo amount ofamount of
consumption.consumption.
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Abuse repetitive pattern of drinking alcoholAbuse repetitive pattern of drinking alcohol
that has adverse effects on social, family,that has adverse effects on social, family,
occupational and health statusoccupational and health status
Dependence alcohol-seeking behavior despiteDependence alcohol-seeking behavior despiteits adverse effectsits adverse effects
Have you ever had a drink firstthing in the morning to steady yournerves and get rid of hangover?
Eye-opener
E
Have you ever felt Guilty or bad
about your drinking?G
Have people Annoyed you bycriticizing your drinking?
A
Have you ever felt you ought to Cutdown on drinking?C
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B. MedicationsB. Medications Currently taking meds? on maintenanceCurrently taking meds? on maintenance
drugs? Herbal medicines? Birth controldrugs? Herbal medicines? Birth control
pills? Self-medication? Illicit drug use?pills? Self-medication? Illicit drug use?
C.C.LifestyleLifestyle Personal habits/hygienePersonal habits/hygiene Eating habits/food preferenceEating habits/food preference Sexual activity/preferenceSexual activity/preference Recent travelRecent travel
Environment/sanitation/occupationEnvironment/sanitation/occupationTattoe, piercing, needle-stick injuryTattoe, piercing, needle-stick injury Exposure/contact with patients with liverExposure/contact with patients with liver
diseasedisease
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D. Past Medical HistoryD. Past Medical History Previous hospitalizationsPrevious hospitalizations
Previously acquired diseasesPreviously acquired diseases
Recent surgeryRecent surgery
Blood transfusionsBlood transfusions
E. Family HistoryE. Family History Related familial diseases of the liverRelated familial diseases of the liver
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Physical ExaminationPhysical Examination
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A. IcterusA. Icterus
Assess for these areas:Assess for these areas:
sclerae (under natural light)sclerae (under natural light)
skin ( for fair-skinned individuals)skin ( for fair-skinned individuals)
oral-mucosa ( for dark-skinnedoral-mucosa ( for dark-skinned
individuals)individuals)
Clinically evident when serum bilirubinClinically evident when serum bilirubin
exceeds 2.5mg/dLexceeds 2.5mg/dL
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Types of JaundiceTypes of Jaundice
A. HemolyticA. Hemolytic - increased destruction of red- increased destruction of redblood cellsblood cells
e.g. transfusion reactions, Hemophiliae.g. transfusion reactions, Hemophilia
B. HepatocellularB. Hepatocellular inability of damaged liver inability of damaged livercells to clear normal amounts of bilirubin from thecells to clear normal amounts of bilirubin from thebloodblood
e.g. viral hepatitis, cirrhosise.g. viral hepatitis, cirrhosis
C. ObstructiveC. Obstructive occlusion of bile duct by occlusion of bile duct bygallstone, inflammatory process, tumor orgallstone, inflammatory process, tumor orenlarged organ (extrahepatic)enlarged organ (extrahepatic)
- obstruction of small bile ducts within- obstruction of small bile ducts withinthe liver (intrahepatic)the liver (intrahepatic)
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D. Hepatomegaly/SplenomegalyD. Hepatomegaly/Splenomegaly
liver size varies; not a reliable signliver size varies; not a reliable sign
of liver diseaseof liver disease
Palpation: assess liver edge forPalpation: assess liver edge for
unusual firmness, irregularity andunusual firmness, irregularity and
nodules.nodules.
E. Hepatic TendernessE. Hepatic Tenderness
Most reliable P.E. findingMost reliable P.E. finding
Discomfort/pain on touching/pressingDiscomfort/pain on touching/pressing
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F. AscitesF. Ascites
accumulation of excess fluid withinaccumulation of excess fluid within
the peritoneal cavitythe peritoneal cavity
Percussion: shifting dullnessPercussion: shifting dullness
(+) abdominal fluid wave(+) abdominal fluid wave
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G. Hepatic EncephalopathyG. Hepatic Encephalopathy Accumulation of ammonia due to damagedAccumulation of ammonia due to damaged
liver cells fot to brain dysfunctionliver cells fot to brain dysfunction P.E. : a. changes in personality, sleepP.E. : a. changes in personality, sleep
patterns,patterns, irritability, mentalirritability, mentaldullnessdullness
(not due to meds, F&E imbalance,(not due to meds, F&E imbalance,etc.)etc.)
b. asterixis/flapping tremors of bodyb. asterixis/flapping tremors of bodyand tongueand tongue
c. Fetor hepaticus sweet ammonialc. Fetor hepaticus sweet ammonialodor, fruity-odor, fruity- odor ofodor ofbreathbreath
* Trail-making test N=15-30secs* Trail-making test N=15-30secs
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H. OthersH. Others
Umbilical Hernia due to ascitesUmbilical Hernia due to ascites
Caput Medusa collateral veins seenCaput Medusa collateral veins seen
radiating from umbilicusradiating from umbilicus
Hyperpigmentation/Xanthelasma- tendonHyperpigmentation/Xanthelasma- tendonxanthomata due to increased lipids andxanthomata due to increased lipids and
cholesterolcholesterol
Kayser-Fleischer rings- golden brownKayser-Fleischer rings- golden browncopper pigment deposited at periphery ofcopper pigment deposited at periphery of
corneacornea.. Hepatic Bruit sound produced in lungHepatic Bruit sound produced in lung
CA.CA.
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Diagnostic ProcedureDiagnostic Procedure
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i. Lab Tests/Liver Functioni. Lab Tests/Liver Function
TestsTests
a.a. Pigment studiesPigment studies
b.b. Protein StudiesProtein Studies
c.c. PTPTd.d. Serum AminotransferasesSerum Aminotransferases
e.e. GGT,LDHGGT,LDH
f.f. Cholesterol StudiesCholesterol Studies
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a. Pigment Studiesa. Pigment Studies
Measures the ability of the liverMeasures the ability of the liverto conjugate and excreteto conjugate and excretebilirubinbilirubin
Serum bilirubin (direct) 0-0.3mg/dLSerum bilirubin (direct) 0-0.3mg/dL
(total) 0-0.9mg/dL(total) 0-0.9mg/dL
Urine bilirubin 0(0)Urine bilirubin 0(0)
Urine urobilinogen 0.05-2.5mg/24hrUrine urobilinogen 0.05-2.5mg/24hr
Fecal urobilinogen 40-200mg/24hrFecal urobilinogen 40-200mg/24hr
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b. Protein Studiesb. Protein Studies
Albumin: cirrrhosisAlbumin: cirrrhosis
chronic hepatitischronic hepatitis
edema, ascitesedema, ascites
Globulin: cirrhosisGlobulin: cirrhosis
liver diseaseliver disease
chronic obstructive jaundicechronic obstructive jaundice
viral hepatitisviral hepatitis
A/G ratio is reversed in chronic liverA/G ratio is reversed in chronic liverdiseasedisease
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c. Prothrombinc. Prothrombin
Normal 100% or 12-16secsNormal 100% or 12-16secs
Prolonged in liver diseaseProlonged in liver disease
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d. Serum Aminotransferasesd. Serum Aminotransferases
A. ALT (SGOT) 10-40unitsA. ALT (SGOT) 10-40units
- to monitor coure of- to monitor coure ofhepatitis/cirrhosis and effects ofhepatitis/cirrhosis and effects of
treatments that may be toxic to livertreatments that may be toxic to liver- Increased : liver disorder- Increased : liver disorder
b. AST (SGPT) 5-35 unitsb. AST (SGPT) 5-35 units
- present n tissues high in- present n tissues high inmetabolic activity (heart, liver,metabolic activity (heart, liver,skeletal muscle)skeletal muscle)
- increase with damaged tissues- increase with damaged tissues
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e. GGT/ LDHe. GGT/ LDH
Elevated in alcohol abuseElevated in alcohol abuse
Marker for biliary cholestasisMarker for biliary cholestasis
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f. Cholesterol Studiesf. Cholesterol Studies
Elevated in damaged liverElevated in damaged liver
Normal values:Normal values:
HDL M: 35-70mg/dLHDL M: 35-70mg/dLF: 35-85mg/dLF: 35-85mg/dL
LDL
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ii. Diagnostic Imagingii. Diagnostic Imaging
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a. US/CT scana. US/CT scan
First option for suspected obstructiveFirst option for suspected obstructive
jaundicejaundice
Can also detect fatty liverCan also detect fatty liver
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b. ERCPb. ERCP
Both diagnostic (biliary treeBoth diagnostic (biliary tree
visualization) and therapeutic ( stonevisualization) and therapeutic ( stone
extraction, stents)extraction, stents)
Extrahepatic cholestasis: dilatedExtrahepatic cholestasis: dilated
ductsducts
Intrahepatic cholestasis: ducts notIntrahepatic cholestasis: ducts not
dilateddilated
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c. Doppler US/MRIc. Doppler US/MRI
Asses hepatic vasculature andAsses hepatic vasculature and
dynamicsdynamics
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iii. Liver Biopsyiii. Liver Biopsy
Gold standard in evaluation of liverGold standard in evaluation of liver
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Gold standard in evaluation of liverGold standard in evaluation of liver
diseasedisease
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AlcoholicAlcoholicLiverLiver
DiseaseDisease
d h i i
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due to chronic, excessivedue to chronic, excessive
alcoholalcohol ingestioningestion
a.a. Fatty liverFatty liver
b.b. Alcoholic hepatitisAlcoholic hepatitis
c.c.
CirrhosisCirrhosis
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Alcoholic Cirrhosis (Laennecs)Alcoholic Cirrhosis (Laennecs)
An irreversible chronic injury of theAn irreversible chronic injury of the
hepatic parenchyma and extensivehepatic parenchyma and extensive
fibrosis in association of regenerativefibrosis in association of regenerative
nodulesnodules
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ii. Clinical Manifestationsii. Clinical Manifestations
Anorexia, malnutrition, wt. lossAnorexia, malnutrition, wt. loss
Sx of hepatocellular dysfunction: jaundice, portalSx of hepatocellular dysfunction: jaundice, portal
hypertension, bleeding varices, ascites,hypertension, bleeding varices, ascites,
encephalopathyencephalopathy
Hormonal disturbances:Hormonal disturbances:
Men: gynecomastia, testicular atrophyMen: gynecomastia, testicular atrophy
Women: virilization, menstrual problemWomen: virilization, menstrual problem
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iii. Lab Findingsiii. Lab Findings
Anemia due to G.I. blood lossAnemia due to G.I. blood loss
- coexistent nutritional deficiency (folic &- coexistent nutritional deficiency (folic &
B12)B12)
Elevated transaminasesElevated transaminases
Prolonged PTT reduced synthesis of clottingProlonged PTT reduced synthesis of clotting
proteins;proteins; Vit. KVit. K
Decreased serum albumin impaired proteinDecreased serum albumin impaired protein
synthesissynthesis
Increased ammonia levels may lead toIncreased ammonia levels may lead to
encephalopathyencephalopathy
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iv. Prognosisiv. Prognosis
Abstinence to alcohol consumption decreasesAbstinence to alcohol consumption decreases
morbidity/mortality and delays/preventsmorbidity/mortality and delays/prevents
complicationscomplications
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Major ComplicationsMajor Complications
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a. Portal Hypertensiona. Portal Hypertension
Normal pressure in portal veinNormal pressure in portal vein
( 5-10mmHg); PH is > 10mmHg( 5-10mmHg); PH is > 10mmHg
Damaged liver structures leads toDamaged liver structures leads to
increased resistance to portal bloodincreased resistance to portal blood
flow (presinusoidal, postsinusoidal &flow (presinusoidal, postsinusoidal &
sinusoidal venous compartments)sinusoidal venous compartments)
In Cirrhosis, resistance is usually atIn Cirrhosis, resistance is usually at
sinusoidal areasinusoidal area
portal venous system has no valvesportal venous system has no valves
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portal venous system has no valvesportal venous system has no valves
facilitates retrograde blood flow from highfacilitates retrograde blood flow from highpressure portal venous system to a lowerpressure portal venous system to a lower
pressure systemic circulationpressure systemic circulation
Cardioesophageal
junction
Rectum Retroperitoneal
space
Falciform
ligament of liver
Esophagogastric
varices
hemorrhoids ascites Periumbilical/abdominal
wall collaterals
(caput medusa)
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b.b. EsophagealEsophagealVaricesVarices
i.i. Factors to Bleeding:Factors to Bleeding: Muscular exertion from lifting heavyMuscular exertion from lifting heavy
objects; straining at stool, sneezing,objects; straining at stool, sneezing,coughing or vomiting.coughing or vomiting.
EsophagitisEsophagitis Irritation of vessels by poorly chewedIrritation of vessels by poorly chewed
foods or irritating fluids; reflux offoods or irritating fluids; reflux of
stomach contentsstomach contents salicylatessalicylates
ii Treatment:ii Treatment:
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ii. Treatment:ii. Treatment: Life- threatening EMERGENCY!!!Life- threatening EMERGENCY!!!
- replacement of blood loss to maintain- replacement of blood loss to maintain
intravascular volume BEFORE Dx studiesintravascular volume BEFORE Dx studies
and interventions to stop bleedingand interventions to stop bleeding
(hemostasis)(hemostasis)
*** excessive fluid administration would*** excessive fluid administration wouldincrease portal pressure leading to furtherincrease portal pressure leading to further
bleedingbleeding
Close monitoring of CVP, urine output,Close monitoring of CVP, urine output,
mental statusmental status
Only when hemodynamically stable shouldOnly when hemodynamically stable should
we proceed to Dx procedure andwe proceed to Dx procedure and
hemostasishemostasis
iii Medical Management:iii Medical Management:
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iii. Medical Management:iii. Medical Management:
c.c. Vasoconstrictors:Vasoconstrictors: Vasopressin generalizedVasopressin generalized
vasoconstriction leading to decreasedvasoconstriction leading to decreased
blood flow to portal venous systemblood flow to portal venous system
Somatostatin/Octreotide directSomatostatin/Octreotide direct
splanchnic vasoconstrictionsplanchnic vasoconstriction
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b. Balloon Tamponadeb. Balloon Tamponade
- tube introduced to the- tube introduced to thestomach, gastric balloon inflated andstomach, gastric balloon inflated and
pulled back into the stomach cardia.pulled back into the stomach cardia.- done if bleeding is too- done if bleeding is too
vigorous and endoscopy is notvigorous and endoscopy is notavailableavailable
e.g. triple lumen (Sengstaken-e.g. triple lumen (Sengstaken-Blakemore)Blakemore)
c Endoscopic Interventionc Endoscopic Intervention
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c. Endoscopic Interventionc. Endoscopic Intervention
first line of treatment to controlfirst line of treatment to control
bleeding acutely.bleeding acutely.c.i.c.i. Endoscopic SclerosisEndoscopic Sclerosis varices varices
injected with sclerosing agents via ainjected with sclerosing agents via a
needle- tip catheter passed throughneedle- tip catheter passed throughthe endoscopethe endoscope
c.ii. Endoscopic Band Ligation c.ii. Endoscopic Band Ligation
varices are ligated withvarices are ligated withendoscopically placed small elasticendoscopically placed small elastic
O-ringsO-rings
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d. non-selective beta adrenergicd. non-selective beta adrenergic
blocker causes hypotension andblocker causes hypotension and
eventually causes hypovolemia.eventually causes hypovolemia.
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Cirrhosis
with portal
hypertension
Splanchnic
arterial
vasodilation
Decreased in
circulating arterial
blood volume
Activation ofrenin-
angiotensin and
SNS and ADH
Kidney retains
sodium and water
hypervolemia
Persistent activation of systems for
retention of sodium and water;
ascites and edema formation
Continued arterial
underfilling
Management:Management:
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Management:Management:
b.b. Dietary ModificationDietary Modification
-- low sodium diet (2g/d NaCl)low sodium diet (2g/d NaCl)- to create a (-) Na balance leading to- to create a (-) Na balance leading todiuresisdiuresis
e.e. DiureticsDiuretics Spironolactone (Aldactone) first line ofSpironolactone (Aldactone) first line of
treatment for ascites from cirrhosistreatment for ascites from cirrhosis Furosemide may produce hyponatremiaFurosemide may produce hyponatremia
with prolonged usewith prolonged use Ammonium Chloride/Acetazolamide Ammonium Chloride/Acetazolamide
contraindicated (precipitates hepaticcontraindicated (precipitates hepaticcoma)coma)
*** daily wt loss should not exceed:*** daily wt loss should not exceed:
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daily wt. loss should not exceed: daily wt. loss should not exceed:
1-2kg in patients with1-2kg in patients with
ascites/edemaascites/edema0.5-0.75kg in patients without0.5-0.75kg in patients withoutedemaedema
*** fluid restriction is not attempted*** fluid restriction is not attemptedunless Na isunless Na is very lowvery low
Complications:Complications: Fluid and electrolyte imbalanceFluid and electrolyte imbalance
Encephalopathy due toEncephalopathy due tohypovolemia and dehydrationhypovolemia and dehydration
Decrease potassium = increasedDecrease potassium = increased
ammonia in systemic circulationammonia in systemic circulation
c Bed Restc Bed Rest
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c. Bed Restc. Bed Rest
- upright posture promotes activation- upright posture promotes activation
of RAAS system leading to decreasedof RAAS system leading to decreasedGFR, Na excretion and decreasedGFR, Na excretion and decreased
response to loop diureticsresponse to loop diuretics
d. Paracentesisd. Paracentesis
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d. Hepatic Encephalopathyd. Hepatic Encephalopathy
A complex neuropsychiatricA complex neuropsychiatric
syndrome characterized by these 4syndrome characterized by these 4
major factors:major factors:
Hepatocellular disease/portal systemicHepatocellular disease/portal systemiccollateral shuntscollateral shunts
Disturbances of awareness and mentationDisturbances of awareness and mentation
Shifting combinations of neurologic signs:Shifting combinations of neurologic signs:asterixis,rigidity,hyperreflexiaasterixis,rigidity,hyperreflexia
A characteristic symmetric high voltageA characteristic symmetric high voltage
triphasic slow wave pattern on ECGtriphasic slow wave pattern on ECG
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Hepatocellular
dysfunction
Shunting ofportal
venous bood
into systemic
circulation
Liver is
bypassed
Toxic substances
not detoxified by
liver
Accumulation
in systemic
circulation
Metabolic
abnormalities in the
CNS
***Ammonia not converted to urea
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Common PrecipitantsCommon Precipitants
Increased NitrogenIncreased NitrogenLoadLoad
- GastrointestinalGastrointestinal
bleedingbleeding
- Excess dietary proteinExcess dietary protein
- AzotemiaAzotemia
- ConstipationConstipation
Electrolyte andElectrolyte andMetabolicMetabolic
imbalanceimbalance
-
HypokalemiaHypokalemia- AlkalosisAlkalosis
- HypoxiaHypoxia
- HyponatremiaHyponatremia
- hypovolemiahypovolemia
DrugsD
rugs MiscellaneousMiscellaneous
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DrugsDrugs
- NarcoticsNarcotics
-TranquilizersTranquilizers
- SedativesSedatives
- diureticsdiuretics
MiscellaneousMiscellaneous
- InfectionInfection
-SurgerySurgery
- SuperimposedSuperimposed
acute liver diseaseacute liver disease
- Progressive liverProgressive liver
diseasedisease
- Portal-systemicPortal-systemic
shuntsshunts
EEGAsterixiM t l St tSt
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Deltawaves
-Coma; initiallyresponsive to noxiousstimuli, later
IV
Triphasicwaves
+Marked confusion,incoherent speech,
sleeping butarousable
III
Triphasic
waves
+Lethargy, moderate
confusion
II
Triphasic
waves
+/-Euphoria or depression,
mild confusion, slurredspeech, disordered sleep
I
EEGAsterixis
Mental StatusStage
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Treatment:Treatment:
Elimination or treatment ofElimination or treatment ofprecipitating factorsprecipitating factors
Lowering of blood ammonia levels byLowering of blood ammonia levels by
decreasing the absorption of proteindecreasing the absorption of proteinand nitrogenous products from theand nitrogenous products from the
intestineintestine