Pathophysiology III

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son850
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143352
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Pathophysiology III
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2012-03-26 14:42:42
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Quiz III Review
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  1. The largest and most metabolically complex organ. Has a remarkable capacity for regeneration in response to injury of this organ.
    Liver
  2. The liver consists of many microscopic functional units
    Lobules
  3. These make up the bulk of the liver
    Hepatocytes (parenchymal (functional part) cells)
  4. What are the important function of hepatocytes?
    • 1. Regulation of carbohydrate homeostasis
    • 2. Excretion of Bile
    • 3. Clotting factors
    • 4. Serum Albumin
    • 5. Formation of Urea
    • 6. Detoxification of Drugs
  5. Increased bilirubin production
    Decreased liver uptake / conjugation
    Decreased biliary excretion
    Are found in what condtion?
    Hyperbilirubinemia - increased bilirubin levels are indicative of liver disorder
  6. What compounds are tested for in cases of liver conditions?
    • ALP (alkaline phasphatase - found in liver, bone, placenta) - this compound is detected when there is an impairment of bile formation
    • GGT (gamma-glutamyl transpeptidase) - the compound is detected when there is an obstruction of the common ducts
    • AST (aspartate transaminase) - indicates liver injury (rises in cases of MI, heart failure, muscle injury, CNS disease)
    • ALT (alanine aminotransferase) - found in liver cells indicating liver disease
    • Serum Albumin - decreased in chronic liver disease Serum Ig - rises in cases of chronic liver disease
    • αFP (alpha fetoprotein) - increase indicates primary hepatcellular carcinoma
  7. Excessive accumulation of lipid in hepatocytes. The most common response of the liver to injury. The most common cause of macrovascular type of this condition
    • Fatty Liver
    • Pathogenesis: triglycerides accumulate in the liver because of increased input through synthesis from FFA (free fatty acids) or decreased export as VLDL from the hepatocytes. Increased triglyceride synthesis may result from increased delivery or availability of FFA or from decreased oxidation of FFA in the liver
    • Due to:
    • 1. Alcoholism
    • 2. Obesity
    • 3. Diabetes
    • Pathology: Triglycerides accumulate as large droplets displacing nuclei making cells look "fat"
  8. A spectrum of clinical syndromes and pathologic changes in the liver caused by alcohol (ethanol). This condition is #1 associated with Fatty Liver Disease.
    • Alcoholic Liver Disease
    • Pathogenesis: major factor is the quantity of alcohol consumed, patients nutritional status, genetic, and metabolic traits
    • If consumed in large quantities & regularly for years will produce liver injury; Women - 20g, Men- 60g
    • Greater susceptibility in females
    • Over 90% of Alcohol is metabolized by the liver
    • Alcohol eventually metabolizes into Acetaldehyde (which can cause lipid metabolism problem)
    • Pathology: simple accumulation of neutral fat in hepatocytes to cirrhosis and hepatocellular carcinoma
    • Sign / Symptoms: Patient with a fatty liver are usually asymptomatic
    • Tests show an increase in GGT (detects obstruction of common duct)
    • AST & ALT are elevated too, but AST > ALT in elevation
  9. Diffuse disorganization of normal hepatic structure by regenerative nodules that are surrounded by fibrotic tissue.
    • Cirrhosis - due to chronic alcohol abuse (Asia & Africa get cirrhosis due to HBV leading to death)
    • Pathology:
    • 1. Involve entire liver
    • 2. Fibrosis (irreversible), even with regenerating nodules
    • 3. Usually irreversible damage
    • Pathogenesis: Cirrhosis is end stage of many forms of liver injury, fibrosis & regenerating nodules (no chance of recovery)
    • "Bridges" connect hepatic artery and portal vein to hepatic venules, restoring intrahepatic circulation; increased portal vein pressure leads to portal hypertension
    • Signs / Symptoms: portal hypertension with variceal bleeding, ascites, or liver failure;
    • Many patients with cirrhosis are typically asymptomatic
    • Other: weakness, anorexia, malaise, weight loss
    • Dramatic presentation: massive GI bleeding from esophageal varices (second to portal hypertension)
    • Firm liver with blunt edge is typical, splenomegaly, palmar erythma (due to vasodilation of skin), testicular atrophy
    • Complications: Splenomegaly, jaundice, ascites, hepatocellular carcinoma
    • Diagnosis:
    • Decreased Serum Albumin and prolonged PT (clotting)
    • , modest elevation of ALT, hypersplenism also can lead to leukopenia and thrombocytopenia
    • Ultrasound may reveal textual abnormalities
  10. An inflammation of the liver characterized by diffuse or patchy necrosis affecting all acini (berry-shaped cell clusters)
    • Hepatitis - major causes hepatic viruses, alcohol, and drugs
    • Pathology: hepatocellular necrosis, mononuclear inflammatory infiltrate
    • Signs / Symptoms:
    • 1. Nausea & vomiting / anorexia
    • 2. Fever
    • 3. Jaundice
    • Lab finding: Increased levels of Bilirubin, ALT, AST
    • Prognosis: Usually resolves 4-6 weeks (acute state)
  11. Diffuse liver inflammation caused by specific hepatotropic viruses
    • Acute Viral Hepatitis
    • General Manifestations: fever, diarrhea, anorexia, and abdominal pain, juandice (liver-specific symptoms)
    • Elevated Ig, ALT, AST, Bilirubin levels
  12. A single-stranded RNA virus.
    Viral antigen found in Serum, Stool, and Liver (fecal-oral transmisssion)
    Incubation period: 15-60 days
    No Chronic State associated with this strain
    Most common in children and yound adults
    IgM antibodies appear in the acute stage but diminish within several weeks, followed by the development of protective IgG antibodies appear in the late / chronic state of disease, which persist usually for life.
    • Hepatitis A virus (HAV)
    • Diagnosis: IgM antibody detection
  13. A double-stranded DNA virus
    Associated with infective Dane particle
    Transmission: Blood and Body Fluid
    Incubation period: 45-180 days
    Has a Chronic State associated with this strain
    • Hepatitis B virus (HBV) - chronicity is more prevalent than in HCV strain
    • Diagnosis: HBsAg in serum
  14. Associated with Hepatitis B
    Associated with a viral surface coat on Dane particles
    Presence in serum is usually first evidence of Acute HBV and implies infectivity of blood.
    Incubation period: 1-6 weeks
    It's antibody counterpart appears weeks to months later
    It's detection indicates past HBV infection and relative immunity.
    • HBsAg (Hepatitis B surface Antigen)
  15. Associated with Hepatitis B
    Associated with a viral core on in Dane particles
    Found in infected liver cells but undetectable in serum / blood; biopsy is best route
    Acute infection - IgM predominates
    Chronic infection - IgG predominates
    • HBcAg (Hepatitis B core Antigen)
  16. Associated with Hepatitis B
    1. Found only in HBsAg-positive serum
    2. Reflects more viral replication, greater infectivity of the blood and a greater likelihood of progression to chronic liver disease
    3. Antibodies against this points to relatively lower infectivity and usually indicates a benign outcome (better prognosis).
    • HBeAg (Hepatitis B e Antigen)
  17. A single-stranded RNA virus
    Transmission: Blood and Body Fluid
    Incubation period: 14-160 days
    Has a Chronic State associated with this strain
    Highest likeliness of Chronic States (75+%)
    Can be obtained through medical procedures (i.e. transfusions (80%), surgery)
    • Hepatitis C virus (HCV)
    • Diagnosis: anti-HCV serum antibody
  18. A single-stranded defective-RNA virus
    Transmission: Blood and Body Fluids
    Incubation period: 30-180 days
    Has a Chronic State associated with this strain
    Must have HBV to get this strain
    Hepatitis D virus (HDV)
  19. A single-stranded RNA virus
    Transmission: Waterborne (Fecal-Oral route)
    Incubation period: 15-60 days
    Severe forms possible in pregnant women (which can lead to death)
    No Chronic State associated with this strain
    Typically found in developing countries
    Must have HAV to get this strain
    Hepatitis E virus (HEV)
  20. What is the most common type of primary liver cancer?
    • Hepatocellular Carcinoma
    • Causes:
    • HBV is largely responsible
    • Fungal Aflatoxins has a factor
    • Chronic HCV has a factor
    • Diagnosis:
    • α-FP in serum
    • Ultrasound, CT, MRI
    • Liver biopsy
    • Prognosis and Treatment: Surgical Resection is best but only in some cases. Death often occurs in a few months
    • Radioactivity / Chemotherapy usually unsucessful
  21. Metastatic cancer is the most common hepatic malignancy (from elsewhere: lung, breast, colon, pancreas, stomach)
    Liver Metastases
  22. Formation or presence of calculi (gallstones) in the gallbladder. Cholesterol is the major contributing factor to this condition (bile can not compensate for the excess cholesterol leading to formation of these)
    • Cholelithiasis
    • Factors include:
    • 1. Female sex
    • 2. Obesity
    • 3. Increased age (over 40-50 years)
    • 4. Western Diet (high protein, low fiber)
    • 5. Family History
    • Signs / Symptoms:
    • mostly asymptomatic
    • Stones may traverse the cystic duct with or without symptoms of obstruction (persistent obstruction leads to inflammation
    • Roller coaster ride of pain (pain increasing and decreasing for several hours)
    • Nausea & Vomiting
    • Pain in epigastrium / Right upper quandrant (liver region) radiating to the right lower scapula
    • Diagnosis: Ultrasound
  23. A chronic systemic autoimmune disease that primarily involves the joints
    • Rheumatiod Arthritis (nodules develop in ~30% of patient with this RA)
    • Peripheral Joints (i.e. wrists, metacarpophalangeal joints) are symmetrically inflamed (synovial fluid (10K-50K WBCs/μLis turbid, yellow and sterile), leading to progressive destruction of articular structures (leading to degeneration) usually accompanied by systemic symptoms
    • Precise cause is unknown; a genetic predisposition has been identified, environmental factors / geographic location may play a role
    • Immune complexes (Type III Sensitivity) produced by synovial lining cells and in inflamed blood vessel. Plasma cells produce antibodies (rheumatiod factor (RF)) that contribute to these complexes
    • Elevated ESR (erythrocyte sedimentation rate) and C-reactive protein indicate inflammations
    • Sign / Symptoms - Insidious onset, often beginning with systemic joint symptoms (primarily affecting small joints such as in the hands and feet - can affect large joints but rare; general fatigue; morning stiffness lasting over 60 mins; low-grade fever (whole body)
    • Diagnosis - Serum RF / anti-cyclic citrullinated peptide antibody (anti-CCP antibody - 70% of RA patients have antibodies to human y-globulin however, SLE patients will test positive for this as well), X-rays
  24. How to diagnose a patient with RA?
    • Must have at least 4 of the following and must be present for at least 6 weeks
    • Arthritis of 3+ joints
    • Arthritis of hand joints
    • Morning stiffness for over an 1+ hours
    • Rheumatoid nodules
    • Systemic Arthritis
    • Imaging changes (i.e. X-ray)
    • Serum RF (positive in <5% of cases)
  25. What disorders can simulate RA?
    • Crystal-induced arthritis (Gout)
    • Osteoarthritis
    • SLE (Systemic Lupus Erythematosus)
  26. This releases inflammatory mediators, which erode cartilage, subchondral bone, articular capsule, and ligaments?
    • Hyperplastic synovial tissue / pannus
  27. There are several common forms of fixed deformities in RA. Please identify?
  28. The most common joint disorder, often becomes symptomatic in the 40s-50s and is nearly universal by age 80.
    A chronic arthropathy characterized by disruption and potential loss of joint cartilage along with other joint changes, including some hypertrophy (osteophyte formation). Symptoms include gradually developing pain aggravated or triggered by activity, stiffness < 30 mins of awakening and after inactivity.
    • Osteoarthritis (OA) / Degenerative Joint Disease (affecting older people)
    • Pathophysiology - microfractures plus tissue growth leads to osteophytes / bone spurs entering the articular surface
    • Subchondral bone stiffens, then undergoes infarction, and develops subchondral cysts. Attempts to repair causes subchondral sclerosis and osteophytes at joint margins
    • Sign / Symptoms - Beginning with one or a few joints desribed as a deep ache. Pain worse on weight bearing, but eventually will become constant. Stiffness follows awakening or inactivity but lasts < 30 mins and lessens with movement.
    • Lab Findings
    • Not triggered through inflammation
    • WBC count low / normal
    • Blood work
    • RA - negative
    • RF - negative
    • ESR Normal
    • Anti-CCP - negative
    • Imaging - X-ray may not detect; may show articular destruction; density of bone by bone spur location
  29. There are two kinds of OA, what are they and what are differences?
    • Primary (Idiopathic) OA - Localized in certain joints
    • Secondary OA - trauma, congential joint abnormalities, metabolic defects, endocrine and neuropathic diseases

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