Unit 4 - liver, gall bladder, and pancreas Flashcards
hepatomegaly
from inflammation and swelling within the hepatic parenchymal tissue
- palpate inferior hepatic margin
Elevated Liver Enzymes-Liver Profile
Aspartate aminotransferase (AST) (Liver parenchyma) Alanine aminotransferase (ALT) (Liver parenchyma) Lactic Dehydrogenase (LDH) (Liver parenchyma) Alkaline phosphatase (APT) Biliary ducts) Gamma glutamyl-transferase (GGT) (Biliary ducts)
Portal hypertension and splenomegaly
due to occlusion of the venous drainage from the liver via the hepatic veins into the inferior vena cava
- causes passive congestion in the hepatic portal and splenic veins, resulting in fluid back up and swelling in the organs
caval obstruction with pedal edema
due to occlusion of the venous drainage from the liver via hepatic veins into inferior vena cava, causing passive congestion in the lower extremities
depression of the clotting mechanism (prothrombin time)
- conversion of vitamin K to prothrombin is impaired
- prothrombin time normal is 11-15 sec; reduced w liver disease
- test is INR
Circulating Plasma Protein is Decreased - serum total protein in blood is __
7.0gms/dl, which is 7% of body weight
Anasarca
- generalized edema
- Hypoproteinemia & Hypoalbumenemia
Jaundice
Elevated Plasma Bilirubin
Ascites
due to hepatic portal enlargement
- Hepatic Portal Vein occlusion with passive congestion
Abdominal organs “weep” fluid (plasma)
- Compression of Hepatic Lymphatic Vessels-“weep” fluid (lymph)
- Hypoalbuminemia (decreased plasma proteins)
- Sodium/H2O retention due to decreased renal circulation
other signs of liver disease/summary
- pruritus
- gynecomastia (breast enlargement)
- hepatomegaly, splenomegaly
- red palms and spider nevi
- hemorrhagic tendency
- ascites, anasarca
End stage liver
Liver has lost all its ability to function
Model for End-Stage Liver Disease-MELD
scoring system for stages of liver failure 40 or more — 71.3% mortality 30–39 — 52.6% mortality 20–29 — 19.6% mortality 10–19 — 6.0% mortality ≤9 — 1.9% mortality
common causes of liver disease
infections: bacteria, viruses, fungi
toxic damage
neoplasia
autoimmune - hepatitis
Hepatitis A virus
Oral-fecal route mode of entry 28 day incubation 4-6 week course (self-limiting) Serological Blood Marker-Anti HAV IgM antibodies Vaccine-1992 Inactivated HAV
s/s of hep A
Constitutional Nausea & Diarrhea Jaundice with Pruritus Hepatomegaly Elevated liver enzymes (AST, ALT, LDH) Aversion to food
Hepatitis B
DNA Virus Transmission and entry Inoculation Oral-fecal route STD Dental or Medical Procedures Childbirth 120 day incubation Variable course (usually self-limiting)
components and blood markers of Hep B
Diagram shows that HBV has an incomplete ring of circular DNA within a core particle (HBcAg).
Surrounded by an intermediate protein coat (HBeAg) and a surface protein coat (HBsAg).
Anti-HBV antibodies
HBV Surface Antigen (HBsAG)
Australian Antigen
Hepatitis Associated Antigen (HAA)
s/s Hep B
Constitutional Nausea & Diarrhea Jaundice with Pruritus Hepatomegaly Elevated liver enzymes (AST, ALT, etc.) Aversion to food
recovery of Hep B
vaccine 90%-complete recovery -2%-HBV carriers 10%-chronic, progressive hepatitis and hepatic cirrhosis May develop 1° Hepatocellular Cancer
Hepatitis C
RNA Virus Incubation Period: 50-60 Days transmission/entry: Initially Blood Transfusion Related Injecting Drug Use Dental or Medical Procedures Childbirth Tattoos STD
hep C blood markers and outcomes
Serologic Blood Marker: Anti-HCV Antibodies
No current vaccine
1-6% may be HCV Carriers
50% Develop Chronic Hepatitis
20% Develop Cirrhosis and/or Hepatocellular carcinoma
Hep C s/s
Constitutional Nausea & Diarrhea Jaundice with Pruritus Hepatomegaly Elevated liver enzymes (AST, ALT) Aversion to food
Hepatitis D
RNA Virus
In combination with hepatitis B virus-highest overall mortality rate of all the acute viral hepatitis infections-at 20%.
Hep D blood markers
Serologic Blood marker
HDV total antibodies- indicates acute or chronic HDV infection.
Hepatitis E
RNA Virus-1955 Oral Fecal Transmission Route Incubation period: 3-8 weeks Has a preventive vaccine Comparable to HAV-symptoms/severity Self-limiting, 2% mortality rate 20% mortality rate in pregnancy Fulminant liver failure-3rd Trimester
Cirrhosis
Replacement of Normal Liver tissue with non-functional fat and connective (scar) tissue
Most cirrhosis is alcohol related (Laennec’s Cirrhosis)
Non-Alcoholic Fatty Liver Disease (NAFLD)
> 10% Liver Fat-May develop Cirrhosis
Diabetes mellitus
Elevated Cholesterol and Triglycerides
Obesity
Post-necrotic Cirrhosis
Toxins, Drugs
- tylenol
Biliary Cirrhosis
(Post Hepatic Obstructive)
Sclerosing cholangitis-autoimmune
Cirrhosis Progression
Development of a Fatty Liver
Replacement with nodular scar tissue
End stage liver disease (ESLD)
Hepatocellular failure
Hepatocellular Failure
End Stage Liver Disease (ESLD)
Mortality 100%-Uniformly Fatal
Liver Transplant
Contributing events to Morbidity & Mortality
Hemorrhage/Internal Bleeding
Depression of the Clotting Mechanism Easy Bleeding
Prothrombin time, INR
Low levels of Cytokine Thrombopoietin
Failure to detoxify ammonia (NH3) into Urea NH3 is converted to NH4+ (Ammonium Ion) Metabolic Acidosis (pH)
ammonia
Ammonia combines with water to form the Ammonium ion
Ammonium ionizes (disassociates) to ammonia and free hydrogen
As hydrogen ion concentration rises:
H+ increases-pH falls
Blood/Body Fluid becomes acidic
Thus, Metabolic Acidosis (pH <7.35)
Hepatic encephalopathy stages
Stage 1 - Personality changes Stage 2 - Muscle involvement Fasciculations, Asterixis Stage 3 - Violence Stage 4 - Hepatic Coma Hepatic fetor-mercaptans (sulfur compounds) & dimethyl sulfide from Cysteine “Breath of the Dead”
Glasgow Coma scale
Rates consciousness scale 3-15
Rates eye, verbal, motor responses
3=deep unconscious state, unresponsive
15=fully awake
Acute pancreatitis
Inflammation of pancreatic tissue and ducts Swelling and Pain (intense) Overuse of Alcohol Gall Stones Severe pain-often refers to the back 95% resolution in a few days-few weeks
Prolonged cases result in auto-digestion of the pancreas
Chronic pancreatitis
Chronic, ongoing pancreatic inflammation
May develop from acute pancreatitis or chronic alcohol abuse
In children-Cystic Fibrosis
Gradual replacement of functional tissue with scar tissue
Pancreatic Neoplasia
Benign Cysts and Tumors
Malignant Tumors (5 year survival < 5%) Occur most often in African-American males Risk factors: Smoking Diabetes mellitus Aging African American Male
Cholelithiasis (Gall Stones)
Females > Males
Disease of older individuals (>65 years)
Often seen in females 40-50 years of age
6 F’s of gall stones
“Fair, Fat, Female, Fertile, Flatulent, Forty”
etiology of gall stones
Precipitation of cholesterol and bile pigments
Stasis of bile
Biliary Tract Bacterial infection
s/s gall stones
Pain-upper right quadrant
May radiate to the mid upper back & shoulder
Relief-pain food pattern
