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Insuficiencia Heptica

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					Insuficiencia Hepática e
  Hipertensión Portal




          Dr. Michel Baró A
                agudo    necrosis




Daño Hepático           regeneración   Insuficiencia hepática



                                       encefalopatía hepática
            crónico      cirrosis


                                          hipertensión portal

                                          hepatocarcinoma
  Funciones del hígado:
Digestión Síntesis de la bilis
 Detoxificación hormonas y compuestos extraños
 Biosíntesis Síntesis factores de coagulación, albúmina
 Energía del Metabolismo Metabolismo de glúcidos,
                                    proteínas, grasas

 Otras Funciones Filtración y almacenamiento de sangre
                             Almacenamiento de vitaminas y hierro
Tests de evaluación del hígado
    “Pruebas (daño) hepáticas”       Tests de función hepática

•   GOT/ASAT                     •   Albúmina
•   GPT/ALAT                     •   Protrombina
•   Bilirrubina total            •   Colesterol total
•   Bilirrubina directa          •   Amonemia
•   Fosfatasas
    alcalinas                    • Bromosulftaleína
•   GGT                          • Verde indocianina
•   LDH
                                         hipoglicemia


                                         hemorragia


                Disminución síntesis
                                          edema

Insuficiencia
hepática
                                           ictericia

                Disminución depuración
                                           encefalopatía

                                           hiperestrogenismo
Estimated prevalence of common causes of acute liver failure
worldwide
Principal causes of acute liver failure


      Table 7-2. Principal Causes of Acute-Liver Failure
      Drug-related hepatotoxicity
        Acetaminophen
        Idiosyncratic drug reactions
      Indeterminate etiology
      Viral hepatitis
        Acute hepatitis B
        Acute hepatitis A
        Others (hepatitis E, others rare)
      Autoimmune hepatitis
      Ischemic liver injury
        Cardiogenic "shock"
        Other (eg, cocaine, methamphetamines, ephedrine)
      Miscellaneous causes
        Wilson disease
        Budd-Chiari syndrome
        Acute fatty liver of pregnancy
        Malignancy
        Veno-occlusive disease

        Toxinas (micetismo)
Reactivation of inactive hepatitis B after chemotherapy (A)
Acetaminophen metabolic pathway




                        N-acetyl-p-benzoquinoneimine
Acetaminophen toxicity nomogram
Drugs implicated in idiosyncratic liver injury leading to
acute liver failure
                   Table 7-6. Drugs Implicated in Idiosyncratic Liver Injur y Leading to Acute Liver Failure
        Infrequent But Not                                                  Combination Agents with Enhanced
        Rare                       Rare                                     Toxicity


        Isoniazid                  Didanosine                               Ethanol-acetaminophen
        Sulfonamides               Sustiva (efavirenz)                      Trimethoprim-sulfamethoxazole
        Phenytoin                  Metformin                                Rifampin-isoniazid
        "Statins"                  Ofloxacin
        Propylthiouracil           Ketoconazole
        Halothane                  Meth yldopa
        Disulfiram                 Allopurinol
        Valproate                  Nefazodone
        Amiodarone                 Quetiapine
        Dapsone                    Isoflurane
                      *
        Bromfenac                  Lisinopril
                          *
        Troglitazone               Nicotinic acid
        Herbals †                  Imipramine
                                   Gemtuzumab
                                   Ecstasy
                                   (methylenedioxymethamphetamine)
                                   Labetalol
                                   Etoposide
                                   Flutamide
                                   Tolcapone



        *
        Removed from the market.

        †
            Usually combinations of various herbal agents.
Acute liver failure caused by Wilson disease




             Table 7-7. Acute Liver Failure Caused by Wilson Disease
 Most patients are younger than 30 y
 Non-immune hemolytic anemia is often present with high bilirubin levels (> 20 mg/dL)
 Kayser-Fleischer rings may be absent
 Alkaline phosphatase levels may be depressed
 Serum ceruloplasmin is typically decreased, but it may be normal in 15% of cases
 Serum uric acid is often very low secondary to a renal tubular defect
 Almost universally fatal without hepatic transplantation
 Female: male ratio, 2:1
Basic physical findings in acute liver failure
Cerebral edema on CT scanning in a patient with acute liver failure
(A)
Physical findings in patients with advanced hepatic
encephalopathy and cerebral edema
Oxygen delivery curve
Renal parameters in acute liver failure


     Table 7-13. Renal Parameters in Acute Liver Failure
     Hemodynamic changes
     Hypotension
     High cardiac output
     Low systemic vascular resistance
     Tachycardia
     Possible lactic acidosis
     Serum factors elevated
     Renin
     Aldosterone
     Tumor necrosis factor-α
     Prostaglandins
     Urine findings
                        *
     Low urine volume
     Low urinary sodium
     Increased potassium
     Increased urinary urobilinogen



     *
     Presence of high urinary volume suggests tubular necrosis.
Intraoperative photographs of related living-donor liver
transplantation (A)
Intraoperative photographs of related living-donor liver
transplantation (B)
Massive liver necrosis secondary to halothane anesthesia
Histologic findings in a selection of patients with acute
liver failure (A)
Histologic findings in a selection of patients with acute
liver failure (B). Acetoaminofeno
Histologic findings in a selection of patients with acute
liver failure (C): Halotano
Histologic findings in a selection of patients with acute
liver failure (D): Halotano
Histologic findings in a selection of patients with acute
liver failure (E): sindrome de Reye
Histologic findings in a selection of patients with acute
liver failure (F): Enfermedad de Wilson
Histologic findings in a selection of patients with acute
liver failure (G): Melanoma
Histologic findings in a selection of patients with acute
liver failure (H): Tuberculosis
Histologic findings in a selection of patients with acute
liver failure (I): Amiloidosis
Histologic findings in a selection of patients with acute
liver failure (J): Miocardiopatía
                 Encefalopatía hepática

 NEUROTOXINAS:                                ALTERACIÓN DE LA BHE
 •Amomio
     •Aumento transporte aa neutrales (BHE)
     •Aumento osmolalidad astrocitos
     •Alteración actividad electrica
 •Oxindole



ALTERACIÓN DE LA NEUROTRANSMISIÓN:
•GABA
•Glutamato                       ALTERACIÓN DEL METABOLISMO
•Catecolaminas                   ENERGÉTICO CEREBRAL
•Serotonina
•Histamina
•Melatonina           EDEMA CEREBRAL
                         HIPOPERFUSIÓN CEREBRAL
                         ATROFIA CORTICAL
                  Encefalopatía hepática

•Amonio, Producido en:

       •intestino
       •Enterocitos
       •flora comensal,
       •H. pylori

•Detoxificación

       •Hepática         Glutamina (interfiere fx mitocondrial del astrocito)
       •Muscular

•Aumenta por

       •Disminución del aclaramiento hepático
       •Shunting (TIPS)
                   Encefalopatía hepática

•Aumento transporte aa neutrales (BHE)

    •Aumento actividad transportador de L-aminoácidos
    •Aumento transporte de triptófano, tirosina y fenilalanina
    •Alteración síntesis dopamina, norepinefrina y serotonina

•Aumento osmolalidad astrocitos

    •Acumulación de glutamina en astrocitos
    •Efecto sólo en ratas con shunt
    •Vasodilatación cerebral vía NO

•Alteración actividad electrica

    •Inhibición de potenciales postsinápticos excitatorios e inhibitorios


•Oxindole: Metabolito tóxico del triptófano
                  Encefalopatía hepática

ALTERACIÓN DE LA NEUROTRANSMISIÓN:

•GABA:
         •Producido por flora comensal del intestino y detoxificado en el hígado
         •Complejo neurotransmisor GABA-benzodiacepina: inhibidor SNC
         •Animales expuestos al amonio o manganeso aumentan
          la expresión del gen del receptor de benzodiazepina del astrocito

•Glutamato

         •Disminución del glutamato cerebral total
         •Aumento del glutamato extracelular

•Catecolaminas

         •Disminución de la norepinefrina cerebral
Ammonia and glutamate metabolism in the brain
Hepatic encephalopathy: assessment of mental status
Asterixis
Blood ammonia concentration in hepatic encephalopathy
Laennec’s cirrhosis and encephalopathy (A)
Laennec’s cirrhosis and encephalopathy (B)
Factors precipitating acute episodes of encephalopathy




                                (diuréticos)
Precipitants of hepatic encephalopathy in cirrhotic patients

Drugs
Benzodiazepines
Narcotics
Alcohol
Increased ammonia production, absorption or entry into the brain
Excess dietary intake of protein
Gastrointestinal bleeding
Infection
Electrolyte disturbances such as hypokalemia
Constipation
Metabolic alkalosis
Dehydration
Vomiting
Diarrhea
Hemorrhage
Diuretics
Large volume paracentesis

Portosystemic shunting
Radiographic or surgically placed shunts
Spontaneous shunts
Vascular occlusion
Portal vein thrombosis
Hepatic vein thrombosis
Primary hepatocellular carcinoma

				
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posted:7/25/2011
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