Patho Heptatics - Liver disease and normal liver function. PDF

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Liver disease and normal liver function. ...

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Liver Pathology Basic Liver Anatomy ● Largest visceral organ ● 3 lobes ● Should not be palpable ● Unique blood supply- 25% of CO ● Receives all venous blood from GI system called the portal vein and flow trough the liver 75% of blood ● Hepatic artery- 25% blood from the heart ● Veins from stomach, intestine, spleen, and pancreas all join to create the portal vein Liver Disease ● Portal hypertension ○ Elevation in pressure of portal circulation ○ When there is back up behind the liver, during disease, there is symptoms behind the liver ● Gastric varices and esophagus varices- bulging veins in the stomach and esophagus ○ Dilation of collateral vessels ○ Common clinical manifestation found by a scope ○ Huge bleeding risk- food can bump them and they can vomit blood or bloody stool ○ Varices are under pressure because of portal hypertension ● Nausea and vomiting ○ Congestion of vessels around the stomach ○ Stomach is irritated ○ PORTAL HYPERTENSION ● Splenomegaly ○ Congestive enlargement of the spleen- palpable ○ Backup of blood ○ Can trap platelets and lead to a low platelet count because they are all trapped ● Ascites ○ Fluid in the abdominal cavity ○ Elevated hydrostatic pressure in capillary beds and lead to fluid leaving the vessels and accumulates ○ >500mL= clinically detectable , normal is 150 ○ Weight gain ○ Abdominal distention ○ Paracentesis- puncture abdomen in order to remove fluid ○ Effect of all the fluid on the lungs and breathing b/c under the lungs ○ Can lead to a restrictive lung problem physical obstrcution ○ Distension is a slow progression ■ Be alert for fluid retention ■ Observe bilateral LE edema as a red flag that they also might have fluid in the abdomen ○ Fowler's position is usually more comfortable

○ No activity supine ○ Rest recommended Liver Functions and when it goes wrong ● Protein synthesis ○ Albumin- most abundant protein, responsible plasma oncotic pressure ■ Liver is responsible for maintaining plasma oncotic pressure→ peripheral edema ■ Higher than normal hydrostatic pressure and lower oncotic pressure in the capillaries ■ Reduced plasma oncotic pressure if failing ○ Clotting factors ■ Liver is responsible for making sure there is enough clotting factors ■ Fibrinogen too ■ Decreased ability to clot→ bleeding risk ■ Check hemoglobin and hematocrit levels. Expect hemoglobin to be low ■ Elevated prothrombin time ● Conjugation and secretion of bilirubin ○ Breakdown of RBC = bilirubin ○ Needs to be conjugation in order to be secreted from the liver through the urine and feces ○ Yellow in color, in large intestine turns brown ○ Less efficient at conjugating bilirubin so that unconjugated bilirubin goes throughout the body= yellow discoloration of skin, sclera, and mucous membrane. ○ jaundice / icterus ■ Merely a symptom of something else going wrong ○ Exercise reduced until resolved. Would not cancel therapy with jaundice ○ Refer all undiagnosed or untreated jaundice to MD ● Formation of Bile ○ Think of bile as urine of the liver ○ Deliver of end products. Produced by the liver, stored in the gallbladder ○ Impaired fat absorption and wont take in fat soluble vitamins ○ Cholestasis= Reduction or the stoppage of bile flow ■ pruritus - itchy skin. Bile acids accumulate and fuck with peripheral nerves. palms of the hands ■ Jaundice- decrease rate of bilirubin removal ● No bile= decrease rate of bilirubin removal ■ Pale stool- less brown bilirubin because less bile ■ Dark urine- can end up in the urine because it cannot end up in the feces ● Carbohydrate metabolism ○ Liver stores glycogen for us to hold on to ○ Gluconeogenesis - make new glucose ○ Worse at managing carb metabolism which will affect plasma glucose measures ○ Liver adds more glucose between meals

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Fasting hypoglycemia- when they are not eating they cannot maintain blood glucose levels. ● Blood Filter ○ “Detoxifier” ○ Important for metabolic waste ○ Blood from portal field through sinusoid to central vein ○ In the sinusoid there are resident macrophages and filter and eat things that are not supposed to be there. ○ Effect on hormones ■ estrogen - not metabolising estrogen. Effect period, and sterility. Low testosterone and high estrogen ■ Aldosterone- related to salt and water retention. ○ Immune Defense ■ Kupffer cells- in the vein ■ Abnormalities in immune function of the liver ● Urea Formation ○ Breakdown of amino acids- urea ○ First broken down into ammonia ○ Ammonia is toxic to us ○ Blood urea nitrogen (BUN)- amino acids get broken down in the liver and turned into urea in the liver. LOWER ○ Reduced amount of blood urea nitrogen ○ Liver converts ammonia into urea ● Hepatic encephalopathy ○ Loss of brain function. High amounts of ammonia ○ Not fully understood ○ Behavior abnormalities, confusion, sleep disturbance, confused,neurological signs: ■ Rigidity- resistant to movement ■ Hyperreflexia - reflexes are high ■ asterixis - wrist up and down, relaxation of flexion of the wrist ○ Brain function secondary to toxins Clinical Pathology ● Liver Enzymes / liver function tests ○ AST- aspartate aminotransferase ■ Involved in metabolic reactions ■ Should live inside hepatocytes but show up in the blood when there is loss of integrity of hepatocytes ■ Cell death ○ ALT- Alanine Aminotransferase ■ Metabolic reactions ■ Hepatocyte injury ■ Normally in the cell and show up outside the cell when something is wrong

■ Cell death ALP- Alkaline Phosphatase ■ Whenever biliary function is impaired you will release ALP in the blood ■ Cells of bile duct release these Other liver function tests ○ Bilirubin- elevated bilirubin b/c bilirubin cannot be conjugated and secreted ○ Albumin- reduced albumin b/c albumin is synthesized in the liver. Fluid leaking out of the vessels ○ Prothrombin time- INR- report finding as a ratio. Less good at making clotting factor so you would expect elevated time Liver Disease/ Hepatitis (inflammation of the liver) ○ Acute and chronic injury ○ Viral - A, B, C, effects of the virus are in the liver. ○ Bacterial ○ Auto-immune ○ Liver can be affected quite a bit before developing symptoms Liver disease by drug and toxin induced injury. LIVER DISEASE LECTURE 14:00 ○ Acetaminophen ○ Alcoholic liver disease ■ Hepatic steatosis- fatty liver- 90-100%. ■ Alcoholic hepatitis ■ Fibrosis and cirrhosis Hepatic Steatosis ○ Fat accumulate in liver cells ○ Metabolism of ethanol generate NADH which uses this to make lipids ○ Ethanol impairs synthesis lipoproteins. Worse at sending it to the blood ○ Lower blood lipids but more lipids in liver ○ Lipid synthesis mode ○ Can occur quickly ○ Clinically (can come and go): ■ Malaise ■ Anorexia ■ Upper abdominal discomfort ■ Tender hepatomegaly ■ Fever ■ Hyperbilirubinemia - high bilirubin in the blood ■ Elevated ALP- bile no the other enzymes b/c no cell death ■ Leukocytosis- moe WBC Alcoholic hepatitis ○ Unknown cause ○ Toxic injury maybe? Fibrosis and Cirrhosis ○ Ten years of heavy drinking ○ Looks like a viral origin ○

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Nonalcoholic fatty liver disease ○ NASH- nonalcoholic steatohepatitis ○ Increased mobilization of free fatty acids ○ Intracellular fat in the hepatocytes ○ Increased mobilization of FFA ○ Associated with: ■ Type 2 diabetes ■ Obesity ■ Dyslipidemia ■ Hypertension

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Cirrhosis ○ End stage liver disease ○ Progressive loss of normal tissue, replaced with fibrosis and nodular regeneration ○ Liver tries to regenerate at the same time as liver regeneration ○ Repeated injury either hepatitis or steatosis ○ Fibrosis pinching off hepatocytes creating blistery blood ○ Lead to portal HTN and obstructive bile/ biliary ○ Clinically ■ 40% asymptomatic ■ Anorexia ■ Weight loss ■ Weakness ■ 40% are asymptomatic until the most advanced stages

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Hepatic Failure ○ Non-reversible ○ Liver transplant is the best option PT Implications ○ Undiagnosed symptoms ○ Active, intense exercise should be avoided when liver is compromised ○ Medical treatment= rest ○ Exercise is risk of coagulopathy ■ Reduced clotting ability ■ Caution due to easy to bruising and bleeding ■ Extreme care with manual therapy and equipment Hepatic Referred pain ○ Right shoulder ○ Thoracic pain between scapula ○ Right upper trap ○ Right interscapular or subscapular area Alcohol Withdrawal Syndrome ○ 1. Anxiety (8 hrs) ○ 2. High blood pressure, increased body temp, unusual HR, confusion, nausea and vomiting (1-3 days) ○ 3. Hallucinations, fever, seizures, and agitation (1 week) Age related changes ○ Decreased liver mass ○ Decrease regeneration

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○ Decrease blood flow ○ Decrease hepatic enzymes Physiological impact of aging on liver ○ Worse at drug clearance ○ Reduced metabolic and detoxification ability ○ Impaired immune protection

● ● Summary 1. Portal Hypertension (varices, nusea, splenomegaly, ascites)

Increased pressure secondary to obstructed blood flow. Increased pressure causes increase capillary hydrostatic pressure causes fluid leakage

2. Peripheral edema

Drop in plasma oncotic pressure because of reduced albumin Further exaggerate the ascites b/c fluid leaks out. Will be pitting

3. Bleeding Risk

Decreased synthesis of clotting facotrs and fibrinogen Elevated prothrombin time (INR)

4. Jaundice

Decrease conjugated and secretion of bilirubin

5. Vitamin deficiency

Decreased fat absorption which carries fat soluble vitamins secondary to decreased bile

6. Cholestasis (pruritus, pale stool, jaundice, dark urine)

Decreased bile flow

7. Fasting Hypoglycemia

Impaired carb. Metabolism

8. Altered Sex Hormones

Reduced metabolism of estrogen in the lvier

9. Na and Water retention

Reduced metabolism of aldosterone in the liver

10. Decreased immune defense

Loss of immune function

11. Hepatic Encephalopathy (decreased BUN)

Decreased conversion to ammonia to urea Increased toxins to the brain...