liver Flashcards
major functions of liver
Metabolism &/or storage of: Fat, CHO, PRO, vitamins and minerals
Blood volume reservoir: Distends/compresses to alter circulating blood volume
Blood filter: Helps purify blood
Blood clotting factors: Including prothrombin & fibrinogen
Drug metabolism and detoxification
Is the liver the largest organ in the body?
YES, it weighs lbs.
where does the liver lie?
the right epigastric region
where is most of the liver enclosed?
in the peritoneum
what type of capsule divides the liver into a left & right low?
fibrous capsule
what the the functional parts of the liver
the lobules
fill in the blank: each lobule has rows of hepatic cells (_) arranged around a central vein
hepatocytes
fill in the blank: The _ (capillaries) are in between the hepatocytes and are lined with Kupffer cells
sinusoids
Fill in the blank: _ _ remove bacteria and toxins from
the blood
Kupffer cells
portal circulation
The portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas
The blood enters the liver through the portal vein.
The absorbed products of digestion come directly to the liver, and are sent to the lobules.
This is the “first pass effect”
The functions of the liver are numerous and
can be summarized into 4 main categories:
digestive
endocrine
hematologic
excretory
digestive function
Bile secretion (helps with fat digestion).
Processing and storage of fats, carbs, proteins, and minerals.
endocrine funtion
Metabolism of glucocorticoids, mineralcorticoids, and sex hormones.
Regulation of carb, fat, and protein metabolism.
hematologic function
Temporary storage of blood.
Removal of bilirubin (broken down hgb) from bloodstream.
Synthesis of blood clotting factors.
excretory function
Excretion of bile pigment & cholesterol.
Synthesis of urea
Detoxification of drugs and other foreign substances
typically when talking about LFTs we are talking about which labs?
ALT, AST, & Alk Phos.
thinking of all liver tests which increase and which decrease when the liver is not working?
ALT, AST, & Alk Phos = increase.
bilirubin= increase
serum ammonia= increase
serum protein= decrease
serum albumin= decrease
prothrombin time = increase.
jaundice [icterus]: what is it and whats the cause?
Yellowish discoloration of skin and deep tissues.
Caused by increased level of bilirubin in the bloodstream.
Usually causes problems and is noticeable with total bilirubin is greater than 2-2.5mg/dl.
Look at conjugated versus unconjugated to determine possible cause.
3 classifications of jaundice
Hemolytic: increased breakdown of RBCs
Hepatocellular: liver unable to take up bilirubin from blood or unable to conjugate it
Obstructive: decreased or obstructed flow of bile
bilirubin
By product of heme breakdown, mainly hemoglobin
Elevations of INDIRECT (unconjugated) bilirubin =
bilirubin overproduction OR impaired liver functioning
overproduction ex: hemolysis, ineffective erythropoiesis.
Elevations of DIRECT (conjugated) bilirubin =
liver working, but can’t get the bilirubin out
EX. bile duct obstruction, gall stones.
Jaundice: Clinical Manifestations
Urine = darker
Liver enzymes = elevated
Stools = Normal or clay colored, d/t liver infection that reduces bile production or flow.
Pruritis d/t bilirubin build up; specifically on palms of hands & soles of feet or generalized.
define viral hepatits
Inflammation of the liver.
systemic virus that affects the liver.
what are the different types of hepatitis?
HAV, HBV, HCV
Other viruses that cause hepatitis: Epstein-Barr, cytomegalovirus.
can hepatitis occur from other causes?
yes, from Alcohol abuse, drugs, chemicals, and bacteria.
which Hepatitis is most dangerous in pregnancy?
Hep E
patho of viral hepatitis
1.Viral infection
2.Immune response: inflammatory mediators
3.Lysis of infected cells
4.Edema and swelling of tissue
5.Tissue hypoxia
6.Hepatocyte death!
describe the prodromal phase
2 weeks after exposure.
s/s: Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low-grade fever.
HIGHLY transmissible
describe the icteric phase
Begins with jaundice, usually occurs 1-2 weeks after prodromal stage & lasts 2-6 weeks.
s/s: Jaundice, dark urine, clay-colored stools.
Liver enlarged and may be painful to palpation
Fatigue, abdominal pain persists or increases in severity.
can develop to chronic hep B or C.
describe the recovery phase
Resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender
LFT & enzymes return to normal 2-12 weeks after onset of jaundice.
can happen with hep A, B or C.
Viral Hepatitis: Complications
Chronic hepatitis
Liver cirrhosis
Liver cancer
Fulminant viral hepatitis – acute liver failure
Hepatitis A
considered food borne illness r/t unclean sanitation practices.
Transmission: fecal-oral, parental, sexual.
Acute onset with fever.
Usually mild severity
Does NOT lead to chronic hepatitis.
Usually affects children and adult.
prevention: Hand hygiene, Hep A vaccine.
Hepatitis B
Transmission: parental, sexual
Insidious onset: has a long incubation period.
Severe disease, may be prolonged course or develop into chronic.
Any age group affected
Prevention: HBV vaccine (children & HCW) and safe sex and hygiene
Hepatitis C
Transmission: parental, sexual
Insidious onset, Mild to severe symptoms.
Can develop into chronic hepatitis (80%)
Any age is affected
prevention: Screening blood, hygiene; NO vaccine.
Leads to hepatocellular carcinoma, liver transplant.
Hep A vaccine
2 doses 6 months apart
Recommendations: All children beginning at age 12 months, Special “high risk” populations.
Hep B vaccine
3 doses at least 4 months apart
Recommendation: All infants beginning as newborns
Hep C
NO VACCINE.
Pharm for HBV: Two classes of drugs are used for chronic HBV….
Interferons
Nucleoside analogs
Pharm for HBV:
Disadvantages of treatment:
Prolonged therapy
Costs and adverse effects
High relapse
Pharm for HBV:
Treatment is only for high-risk patients:
↑ AST levels
Hepatic inflammation
Advanced fibrosis
Pharm for HCV
Treatment is only recommended for patients with chronic disease
However this thought process is changing with the introduction of newer, very effective drugs
Now easily treatable and eliminated in most all patients
Treated with direct-acting antiviral therapy and interferon-based regiments
Some require treatment along with a nucleoside analogue medication as well
DEFINE Cirrhosis
Irreversible, inflammatory, fibrotic liver disease.
Structural changes from injury (alcohol/viruses) & fibrosis.
Chaotic fibrosis leads to obstructive biliary channels and blood flow that cause jaundice and portal hypertension.
Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure.
Cirrhosis Common Causes
Hepatitis B&C
Excessive alcohol intake
Idiopathic
Non-alcoholic fatty liver disease [NASH, NAFLD]
name the 1st stage of alcoholic liver disease
Alcoholic fatty liver: Mildest, asymptomatic
name the 2nd stage of alcoholic liver disease
Alcoholic steatohepatitis: Precursor to cirrhosis
increase hepatic fat storage, Inflammation, degeneration of hepatocytes w/ infiltration of WBC that leads to inflammation.
stimulating irreversible fibrosis.
S/S: anorexia, Nausea, Jaundice, edema
very concerning phase.
name the 3rd stage of alcoholic liver disease
Alcoholic cirrhosis: Fibrosis and scarring alter liver structure.
Cirrhosis: patho
1.Liver cells destroyed
2.Cells try to regenerate
3.Disorganized process
4.Abnormal growth
5.Poor blood flow and scar tissue
5.Hypoxia
6.Liver failure
Cirrhosis: Early Manifestations
GI disturbances: N/V, Anorexia, Flatulence, Change in bowel habits.
Fever, weight loss
Palpable liver
Cirrhosis: Late Manifestations
Jaundice
Peripheral edema
Decreased albumin & PT
Ascites
Skin lesions
Hematologic problems (anemia, bleeding)
Endocrine problems
Esophageal & anorectal varices
Encephalopathy
portal hypertension
Resistant portal blood flow leads to varices & ascites
portal hypertension causes
Causes: systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output = ascites
portal hypertension complications
asymptomatic until the complications occur.
Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
portal hypertension treatment
prevent/treat complications.
liver transplant
Hepatic Encephalopathy
30-45% of cirrhosis patients.
LOC is the primary driver of diagnosis.
Correlate with liver labs: mainly ammonia which is primary chemical driver of LOC changes
goes from changes in behaviors to confusion to coma
Acute liver failure:
Separate liver failure NOT caused by cirrhosis or other type of liver disease.
Can occur 6-8 weeks after a viral hepatitis or metabolic liver disease.
5 days to 8 weeks after an acetaminophen overdose.
Acute liver failure patho:
edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue.
Acute liver failure: signs & treatment
Signs are similar to cirrhosis symptoms.
Treatment: not much, liver transplant
Acute liver failure: most common cause
acetaminophen overdose
acetaminophen antidote
acetylcysteine
lactulose
Class: Hyperosmotic laxative
Indication: reduction of ammonia absorption in hepatic encephalopathy
MOA: reduces blood ammonia levels by converting ammonia to ammonium
Given PO, enema/rectal
Can be given to titrate by # of stools or by ammonia levels.
Not just given for high ammonia levels though– must have signs/symptoms of encephalopathy
Make sure that patient is NOT hypokalemic
rifaximin
MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)
SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
indication: Second line if lactulose isn’t working.
sometimes given preventive, depends on HCP
Given PO
associated with an increased risk of C diff.
