Exam 3 Liver Disorder Flashcards
The liver is
Largest solid internal organ 1600g (3.5 lbs)
Falciform ligament divides into
R and L lobes (abd. wall)
Round ligament is the
“ Ligamentim Teres” (umbilicus)
Coronary ligament
diaphragm
Liver receives
25% of C.O.
How much blood comes from the Hepatic artery?
400ml from Hepatic Artery
How much blood comes from the Hepatic Portal vein
1000ml from Hepatic Portal Vein
Liver is covered by the
Covered by “Glisson capsule” –painful when distended in disease/inflammation
Filters blood for infections
Kuppfer cells, NK cells)
Liver and toxins
Neutralizes toxins
Liver and Bilirubin
Metabolizes Bilirubin from heme
Liver metabolizes nutrients
(Protein deamin.NH3 to Urea)
Liver and clotting
Synthesizes Prothrombin& clotting factors 7,9,10
Liver and hormones
Synthesizes Hormones(angiotensinogen, thrombopoietin, IGF-1, hepcidin)
Liver and cholesterol
Synthesizes Cholesterol, lipids, lecithin
Liver and bile
Synthesizes bile
Liver Stores:
Glycogen
Fe
Cu
Vit.A, K, E, D, B12
**Acute Liver Failure
Leading cause
Severe impairment or necrosis of liver cells without preexisting liver disease or cirrhosis
Pathophysiology of Acute Liver Failure (HPN)
Hepatocyte edema
Patchy areas of necrosis and inflammatory cell infiltrates disrupt parenchyma.
Necrosis irreversible.
**Acute Liver Failure
Clinical/lab manifestations AVAPHC RAP
Anorexia Vomiting Abdominal pain Progressive jaundice Hypoalbuminemia Coagulopathy Renal dysfunction Altered Mental Status Prolonged Prothrombin Time
**Portal Hypertension
Abnormally high blood pressure in the portal venous system / Increase to at least 10 mmHg (normal = 3 mmHg)
**Signs and symptoms of portal HTN (HAC)
Hematemesis, Ascites, Caput medusae
**Portal Hypertension-Types Three Types:Pr
Prehepatic Intrahepatic Post-hepatic
**Portal Hypertension-Types
Three Types: Prehepatic
Portal vein thrombosis
**Portal Hypertension-Types
Three Types: Intrahepatic
Fibrosis: cirrhosis, hepatitis, schistosomiasis (CHS)
**Portal Hypertension-Types
Three Types: Posthepatic
Post-hepatic (Hepatic vein thrombosis or Right CHF)
**Portal Hypertension Consequences (HP-VAHS)
Hepatopulmonary Syndrome Portopulmonary Hypertension Varices (Lower esophagus, stomach, rectum •Life threatening if ruptured) Ascites Hepatic Encephalopathy Splenomegaly
***Portal Hypertension : What happens with splenomegaly
Splenomegaly ->Thrombocytopenia: (↓thrombopoietin from liver and) platelet sequestration in spleen = Increased risk for bleeding
***Hepatopulmonary Syndrome : liver has
Liver has ↑production, or ↓clearance of vasodilators
***Hepatopulmonary Syndrome Pathophysiology
Causes V/Q mismatch in lungs
RBCs pass too quickly through lungs to exchange O2 = Hypoxemia and SOB
Perfusion adjustment to changes in ventilation
Response to reduced ventilation
Decreased airflow Reduced PaO2 in blood vessels Vasoconstriction in pulmonary blood vessels Decreased blood flow Blood flow matches airflow
Perfusion adjustments to changes in ventilation
Response to increased ventilation
Increased airflow Elevated PaO2 in blood vessels Vasodilation in pulmonary blood vessels Increased blood flow Blood flow matches airflow
***Hepatopulmonary Syndrome
Clinical manifestations:
- dyspnea that worsens moving from recumbent to upright position (“platypnea”)
- Clubbing of the fingers
- Spider angiomata
***Portopulmonary Hypertension Portal HTN leads to
Pulmonary HTN
Right sided HF
***Portopulmonary Vasoconstrictors and cirrhosis
↑↑↑in cirrhosis (endothelin“ET-1”) Causes vasoconstriction in lungs
***Portopulmonary Serotonin normally metabolized
Serotonin normally metabolized in liver
bypasses diseased liver in Portal HTN –acts on lungs Causes vascular smooth muscle hypertrophy/hyperplasia
***Mean PA pressure and portopulmonary HTN
> 25mmHg (normal ~ 14mmHg) Mean PA >50 contraind. for surgery
***Portal Hypertension Treatment
No definite treatment
Beta-blockers help prevent variceal bleeding
Bleeding varices:
***Treatment for bleeding Varices–> PEF
Fluid Resuscitation
•prophylactic antibiotics
vasoactive drugs (nonselective β-blockers and terlipressin-reduces portal vein pressure and increases mean arterial pressure (MAP))
•Endoscopic variceal band ligation, compression of the varices with an inflatable tube or balloon, and injection of a sclerosing agent
**Ascites: what is it?
Accumulation of fluid in the peritoneal cavity
Most common cause of Ascites
Cirrhosis
Clinical manifestations of Ascites
Abdominal distention
Ascites Evaluation
Serum-ascites albumin gradient (SAAG):
Most specific diagnostic indicator
***•SAAG for Ascites
(serum albumin) -(albumin level of ascitic fluid)
•Normal SAAG
<1.7
•In cirrhosis, what happens to hydrostatic pressure?
hydrostatic press. ↑↑↑= more water pushed out of vasc. space into peritoneum. Albumin doesn’t cross easily, concentrating serum albumin.
•Results in Higher SAAG
Ascites on Respiratory
10 –20 L fluid displaces diaphragm Causes dyspnea& ↓lung capacity
Ascites on Renal
Affects renal function -leads to H2O retention and dilutional hyponatremia
K+ sparing diuretics used
Ascites Fluid removed?
1-2 L removed via paracentesis relieves respiratory distress
**Ascites -> Removing too much fluid too fast
relieves pressure on blood vessels = hypotension, shock, death
Overflow theory
Renal sodium retention is stimulated by portal hypertension
Causes intravascular hypervolemia, which
overflows or “weeps” into the peritoneal cavity
Underfill Theory
Hepatic sinusoidal hydrostatic pressure increases, and plasma oncotic pressure
decreases
Causes weeping of the lymph fluid from the surface of the liver
Peripheral Arterial Vasodilation theory or Forward Theory
PICI
Is the synthesis of the overflow and underfill theories
Is the most accepted theory
Portal hypertension and splanchnic vasodilation occurs
Causes fluid transudation and lymph formation, producing ascites
Ascites – Medical Treatment diet
Dietary salt restriction
Medication management for Ascites
Potassium-sparing diuretics
Strong diuretics, such as furosemide or ethacrynic acid
For dilutional hyponatremia
Vasopressin receptor 2 antagonists:
Other additional management for Ascites
Possible administration of albumin
Monitor serum electrolytes, especially sodium and
potassium
Ascites – Surgical Treatment
Transjugular intrahepatic portosystemic shunt OR
peritoneovenous shunt →For refractory ascites
Ascites: Best treatment option
Liver transplant
Hepatic Encephalopathy
Blood shunted around failing diseased Liver.
***What happens with hepatic encephalopathy
Neurotoxic NH3 from intestinal protein digestion, normally converted to urea by liver, circulates to Brain
disrupting neurotransmission and increases intracranial
hypertension.
***Clinical manifestations of Ascites
SAM PC
◘Personality changes ◘Confusion ◘Memory loss ◘Asterixis (flapping tremor) ◘Stupor, coma, death
Hepatic Encephalopathy Treatment
Correct fluid and electrolyte imbalances
Withdraw depressant drugs metabolized by liver
↓ dietary protein intake
↓ intestinal bacteria
Hepatic Encephalopathy and intestinal bacteria
• Neomycin (sterlizes bowel) • Rifaximin ( ↓ intestinal NH3 production/absorption) • Sodium benzoate & L-ornithineL-aspartate (detoxify NH3)
Medication to decrease intestinal bacteria: Neomycin action
Sterilizes bowel
Medication to decrease intestinal bacteria: Lactulose action
prevents NH3 absorption from colon
Medication to decrease intestinal bacteria: Rifaximin action
↓ intestinal NH3 production/absorption)
Medication that decrease intestinal bacteria by detoxifying NH3
Sodium benzoate and L-ornithineL-aspartate (detoxify NH3)
What is Jaundice
“icterus”Yellow (or greenish) pigmentation of the skin caused by hyperbilirubinemia
***Jaundice and bilirubin concentration
total plasma bilirubin concentrations >2.5 mg/dL)
**Jaundice Causes Extrahepatic
obstructed bile flow (gallstones - conjugated bilirubin back flows into liver, then into blood)
***Jaundice Causes Intrahepatic
Intrahepatic obstruction ( CIRRHOSIS or HEPATITIS - conjugated and unconjugated backflow into blood)
***Jaundice Prehepatic cause
Excessive bilirubin from hemolytic ds– unconjugated in blood, not H2O soluble, not excreted in urine)
**Jaundice: Clinical manifestations (DCYS)
◘Dark urine
◘Clay-colored stools
◘Yellow discoloration first in the sclera then skin
◘Skin xanthomas (cholesterol deposits) and pruritus
***Hepatorenal Syndrome Pathophysiology
◘ Liver ds. causes hypotension = ↓ renal perfusion,
↓GFR and oliguria. Kidney secretes more renin.
◘ Diseased liver fails to remove excess angiotensin &
vasopressin which travel to kidneys causing ↑↑↑vasoconstriction resulting in kidney failure. resulting in kidney failure.(positive feedback loop)
***Hepatorenal Syndrome Two types:
Type I and Type II
***Hepatorenal Syndrome Two types: Type I (ACRO Big)
Type I
◘ Acute renal decompensation
◘ Creatinine >2.5 mg/dL
◘ Often fatal
Hepatorenal Syndrome Two types: Type II (CCG)
◘ Chronic renal decomp.
◘ Creatinine >1.5 mg/dL
◘ GFR <40 ml/min.
Hepatorenal Syndrome: Renal failure demonstrating
oliguria, hypotension, and peripheral vasodilation as a result of advanced liver disease
Usually associated with alcoholic cirrhosis
Hepatorenal syndrome
***Treatment of Hepatorenal syndrome
MAL
Manage fluid & electrolytes, bleeding, infections, and encephalopathy Administer systemic vasoconstrictors (α-adrenergic agonistsand terlipressin) and albumin Liver transplantation (and kidney in some cases)
***What is hepatitis
Systemic viral disease primarily affects the liver
Hepatitis A B C D, E
What is autoimmune hepatitis
Autoimmune hepatitis is a disease in which the body’s own immune system attacks the liver and causes it to become inflamed.
Hepatitis can cause
Can cause liver necrosis, Kupffer cell hyperplasia, and
infiltration of liver tissue by mononuclear phagocytes
Hepatitis and bile flow
Obstruction of bile flow and impairment of hepatocyte function
**Viral Hepatitis
Chronic active hepatitis
◘Seen with Hep B & C
◘ predisposition for splenomegaly, cirrhosis & carcinoma
***Viral Hepatitis : Fulminant hepatitis
◘ complication of B & C
◘Causes widespread hepatic necrosis
◘Is often fatal
Viral Hepatitis Phases; Incubation phase
Depends on virus
Viral Hepatitis: Prodromal (preicteric) phase
and clinical manifestations.
FeMAHP
Begins ~2 weeks after exposure; ends with the appearance of jaundice
Clinical manifestations: Fever, malaise, anorexia,
hepatomegaly and pain
***Viral hepatitis Highly transmissible: what phase
Prodromal
***Viral hepatitis : Icteric phase (AJ)
◘Acute phase of illness
◘Jaundice, fatigue & abdominal pain
***Viral Hepatitis Recovery phase (BSC)
Begins with the resolution of jaundice
Symptoms resolve after several weeks
Chronic or chronic active hepatitis may develop
***Viral Hepatitis Recovery phase (BSC)
◘Begins with the resolution of jaundice
◘Symptoms resolve after several weeks
◘Chronic or chronic active hepatitis may develop
Viral Hepatitis Treatment activity
Rest / Restrict physical activity as needed
Viral hepatitis treatment DIET
Maintain a low-fat, high-carbohydrate diet if bile flow is obstructed
Viral hepatitis avoid
Avoid direct contact with blood/body fluids of individuals with hepatitis B or C
**Hepatitis A Transmission:
fecal-oral route
**Hepatitis A Risk factors: c
rowded, unsanitary conditions
Acute but self-limiting infection
Hepatitis A
No carrier or chronic state with this one
Hepatitis A
Vaccine Available for which hepatitis (s)
Hepatitis A, B
**Prevention of Hepatitis A
Handwashing
Immunoglobulin before exposure or early in incubation
***Hepatitis B Transmission:
blood, body fluids
Maternal transmission occurs if the mother is infected
during the third trimester
Hepatitis B carrier state
50% of cases asymptomatic but contagious due to
carrier state
**Hepatitis B Vaccine
◘Vaccine available
◘Immunoglobulin provides post-exposure prophylaxis
**Hepatitis C: is the (MI)
Most common type transmitted by blood transfusion
Is also implicated in infections in pts. w/ IVDA & HIV
***Hepatitis C co infection?
Co-infection with B is common
% of patients developing chronic liver disease
80% of cases develop chronic liver disease
No vaccine is available
Hepatitis C
**Hepatitis C management
Antiviral medications help control
***Hepatitis D
Dependent on hepatitis B for replication
Treatment: Pegylated interferon alpha
Hepatitis E Transmission
Fecal-oral transmission
Contaminated water or uncooked meat
Hepatitis Most common in Asian and African countries
Hepatitis E
Common in developing countries
Hepatitis E
Hepatitis E vaccine
Vaccine in China but not in other countries
Hepatitis - Autoimmune: Definition
Rare, chronic, and progressive T cell–mediated
inflammatory liver disease
Clinical manifestations of Hepatitis- Autoimmune
◘ Asymptomatic until icteric phase
◘ Jaundice, fatigue, loss of appetite, and amenorrhea
Treatment of Hepatitis- autoimmune
Drugs? What is common with tx withdrawal.
Immunosuppressive drug therapy (e.g., corticosteroids or in combination with azathioprine) with remission within 24 months
Relapses common with treatment withdrawal
What is cirrhosis
Irreversible inflammatory fibrotic disease
Disrupts liver function and liver structure.
Most common causes of Cirrhosis
alcohol abuse AND viral hepatitis.
*****Cirrhosis Pathophysiology (DBB)
Damaged tissue regenerates with nodules & fibrosis.
Biliary channels become obstructed = portal hypertension.
Blood shunted around liver = hypoxic necrosis.
***Alcoholic liver disease: what is it?
Oxidation of alcohol causes damage to hepatocytes
***Alcoholic fatty liver (steatosis) (FMR)
- ↑ fat deposition secondary to ↓ in fatty acid oxidation and ↑lipogenesis
- mildest form
- reversible if drinking stopped
Alcoholic hepatitis (steatohepatitis) (ID)
- Is characterized by inflammation
* Degeneration and necrosis of hepatocytes
Alcoholic cirrhosis (fibrosis)
Toxic effects of alcohol metabolism, immunologic alterations, oxidative stress from lipid peroxidation and malnutrition occur.
***Nonalcoholic fatty liver disease
Infiltration of hepatocytes with fat w/o alcohol intake
Associated with obesity
Biliary Cirrhosis begins where
Begins in bile canaliculi and ducts
Primary biliary cirrhosis (autoimmune)
T-cell and antibody-mediated destruction of small
intrahepatic bile ducts
Secondary biliary cirrhosis
Obstruction of common bile duct
Primary sclerosing cholangitis
Chronic inflammatory fibrotic disease of the medium- and large-sized bile ducts outside of the liver
Cirrhosis – Fe overload disease
Hemochromatosis (autosomal recessive)
Cirrhosis Fe overload symptoms occur in
Symptoms occur in 40’s
Cirrhosis Fe overload is an
Increased iron deposits in liver, joints, skin
What occurs with Fe overload
Bronzing of skin occurs (hemosiderin)
Treatment of Cirrhosis Fe Overload
Phlebotomy, Chelation, Dietary changes
Cirrhosis – Cu overload disease is
Wilson’s Disease (autosomal recessive)
Wilson’s disease Pathology
Cu excretion for bile production is defective
Cu builds up in liver
Clinical manifestations of Wilson’s disease
Hepatic dysfunction, fatigue, jaundice
Kayser-Fleischer ( Cu ring in eye)
Treatment of wilson’s disease
Treatment w/ chelation (penicillamine)
A person has alcoholic liver disease. What is
the sequence for the development of this
disease?
- Incubation, prodromal, icteric, and recovery
- Prehepatic, intrahepatic, and extrahepatic
* *3. Steatosis, steatohepatitis, and fibrosis - Overflow, underfill, and peripheral artery vasodilation
Cholecystitis
Inflammation of the gallbladder
Acute vs chronic
Cholecystitis Clinical manifestations
• RUQ pain, Fever, leukocytosis, rebound tenderness
Treatment of Cholecystitis FARP
Pain control
Replacement of fluids / electrolytes
Fasting
Antibiotic administration
Cholecystitis and emergent
Perforated gallbladder: Immediate cholecystectomy
Cholelithiasis and symptoms
Gallstone obstruction
Many individuals have them but are asymptomatic
***Risk factors for Cholelithiasis
Rapid wgt. loss Obesity Middle age, Female gender, Oral contraceptives Pancreatic ds.
***Cholelithiasis Two types of stones:
Cholesterol: From cholesterol supersaturated bile
Pigmented: Calcium bilirubinate polymer
***Clinical manifestations of Cholelithiasis (EJI )
Epigastric & RUQ pain
• Intolerance to fatty foods
• Jaundice: Stone in the common bile duct
***Cholelithiasis and Biliary colic
Lodging of stones in the cystic or common duct
• Abdominal tenderness and fever indicates
Cholecystitis
***In cholelithiasis, When pressure builds against the distended wall of the gallbladder
There is a decrease in blood flow. This can result in necrosis,ischemia, and gallbladder perforation.
***Treatment of cholelithiasisi
Preferred treatment
• Laparoscopic cholecystectomy:
Cholelithiasis Large stones: Treatment
Lithotripsy
Rapidly advancing Cholelithiasis tx
• Transluminal endoscopic surgery:
2 other treatments for cholelithiasis
• Endoscopic retrograde cholangiopancreatography and
sphincterotomy with stone retrieval
Cholelithiasis Alternative treatment: Drugs that dissolve smaller stones such as
Bile acid chenodeoxycholic acid (CDCA) and ursodeoxycholic acid
• Ursodiol
Liver Transplant
Three Phases in Liver Transplant surgery: DAN ILN
◘ Dissection Phase →Incision for access
◘ Anhepatic Phase→ Liver isolated from circulation
◘ Neohepatic Phase→ New liver reperfused
**Anhepatic Phase (THD)
◘ Trial clamping of IVC 30-60 seconds.
◘ Hypotension usually ensues as the vena cava is cross-clamped due to a 50-60% reductionin venous return. Determine pt’s ability to withstand drop in preload.
**Neohepatic Phase
Most hemodynamic instability in this phase secondary to reperfusion of the portal vein -
Causes DROP in the systemic vascular resistance
even greater than that seen with vena cava crossclamp.
During neohepatic phase what indicates graft function ?
Decrease in C.O. and increase in SVR indicates graft
is functioning correctly and new liver is beginning
to metabolize vasoactive substances that produce
the characteristic low SVR and high C.O. in pts with
end stage liver disease.
Liver Transplant Coags:
◘FFP to maint. INR <1.5
◘Platelets to maint. count >50k
◘Cryoprecipitate to maint. Fibrinogen >150mg/dl
Liver transplant: What is MELD?
Model for End stage Liver Disease
The MELD uses (CIBN)
Creatinine,
INR
Bilirubin and Na to predict risk of mortality in pt.s with end-stage liver disease.
MELD Score of 25 =
30 day mortality rate of 50% in pts. undergoing abd. Surgery
◘6 (mild illness) to 40 (severe illness
Anesthesia Considerations for liver pts undergoing general surgery→Pts with chronic alcohol ingestion usually have
increased anesthetic requirements (MAC) for isoflurane (due to cross-tolerance).
Anesthesia Considerations for liver pts undergoing general surgery
Hepatic clearance of muscle relaxants must be
considered in pts with cirrhosis. Succinylcholine or
mivacurium are acceptable – but their actions may be
prolonged in pts with severe liver ds.
Anesthesia Considerations for liver pts undergoing general surgery Glucose peri-op____
Avoid______
may be needed for hypoglycemia
Avoid esophageal instrumentation in pts with varices
Anesthesia Considerations for liver pts undergoing general surgery→ What may be sufficient to provide analgesia and amnesia in critically ill pts. with acute liver failure undergoing surgery to correct life-threatening problem?
Low dose volatile anesthetics or even nitrous oxide
alone
Anesthesia Considerations for liver pts undergoing general surgery→Administer
Blood slowly to minimize risk of citrate intoxication (if infused too quickly could result in ↓Ca++ and ↓Mg++)
Describe the 3 main paths of blood flow in liver.
Hepatic vein
Right and Left hepatic arteries
Portal vein
Treatment of Acute liver failure (NABL)
N-acetylcysteine:For acetaminophen poisoning
Antiviral therapy (↑ survival rate in cases of viral hepatitis)
↓ blood ammonia levels
Liver transplantation
Explain the importance of protein metabolism in the liver and the consequences it could have on the body if compromised.
The loss of hepatic regulation of protein metabolism is what leads to a rapid death in acute liver failure,4 and that changes in protein metabolism play a role in complications of chronic liver failure such as the development of HE, ascites and last but not least, PCM.
