Lecture 14: Hepatic, Pancreatic, and Biliary Systems Flashcards
1
Q
Liver Functions
A
- conversions and excretion of bilirubin
- sole source of albumin and other plasma proteins
- produces bile
- production of clotting factors
- storage of vitamins
- aid in eliminating toxins from the body
- filters all the blood from the GI system
- primary organ for metastasis of cancer
2
Q
Pancreas
A
-function in digestion, digestive enzyme secretion and pancreatic juices
3
Q
Gallbladder
A
- stores and concentrates bile
- bile aids in emulsification, absorption, and digestion of fat
4
Q
Signs and Symptoms of Hepatic Disease
A
- hepatic failure
- dark urine and light stools
- skin changes
- spider angiomas
- neurologic symptoms
- asterixis
- hepatic osteodystrophy
- portal hypertension, ascites, hepatic encephalopathy
5
Q
Asterixis
A
- flapping tumor elicited by attempted wrist extension while forearm fixed
- most common neurologic abnormality associated with liver failure
- tremor absent at rest, decreased by intentional movement-maximal on substained posture-usually bilateral
- inability to catalyze ammonia in urine
- goes to brain and reacts with glutamate which leads to decrease in nerve signaling transmission
6
Q
Aging and Hepatic System
A
- liver ↓’s in size and weight – results in diminished blood flow
- requires more time to process substances
7
Q
Healing in Hepatic System
A
- liver injury followed by complete parenchymal regeneration, formation of scars, or a combo of both
- chronic hepatic injury, such as chronic viral hepatitis destroys the extracellular matrix framework: this type of destruction results in a combo of regenerated nodules separated by bands of fibrous connective tissue, termed cirrhosis
8
Q
Jaundice
A
- aka icterus
- common symptomof many different diseases and disorders
- yellow discoloration of the skin, sclerae, mucous membranes, and excretions owing to ↑’d bilirubin production, liver disease, or obstruction of bile flow
- bilirubin – end product from the normal breakdown of Hb
- bilirubin binds with albumin and, along with glucuronic acid, forms a complex known as conjugated bilirubin
- conjugated bilirubin transforms bilirubin from a lipid-soluble substance to a water soluble one that can be excreted in the bile or converted to colorless urobilinogen, which is then converted to urobilin (a yellow pigment) that is subsequently excreted in urine, giving normal urine its characteristic color
- urine turns a darker color and stool is light in color
9
Q
SIFTT for Jaundice
A
- after 4-6 weeks, activity and exercise can be resumed or ↑’d per individual tolerance, depending on the overall medical condition
- return of normal stool and urine colors is a sign of resolution
10
Q
Cirrhosis
A
- chronic end-stage liver disease characterized by a progressive loss of normal tissue that is replaced with fibrosis and nodular regeneration
- many types of cirrhosis each with a different cause, but alcohol abuse and HCV are the most common causes in the US
- once it has developed, it is usually not reversible
- patho: widespread destruction of hepatic cells replaced by fibrous cells (fibrotic regeneration): fibrous scarring distorts the liver and causes it to shrink and biliary channels may be altered or obstructed, producing jaundice
- once 80-90% of the liver is replaced with scar tissue, there is significant loss of function
- with liver malfunction, blood clotting disorders develop (coagulopathies), jaundice, edema, and metabolic problems
- may lead to portal HTN
- ↑’d pressure may lead to esophageal varices
- CM: hepatomegaly; nausea and vomiting; dull, abdominal ache; edema; jaundice; fatigue; indigestion; ascites (massive fluid accumulation)
- dx: abdominal X-rays, CT scan, blood studies (bilirubin), urine studies
- tx: may require Sx (paracentesis), drug therapy, non-invasive procedures
11
Q
SIFTT for Cirrhosis
A
- common symptom associated with cirrhosis is ascites
- detection of blood loss in the form of hematemesis, tarry stools, bleeding gums, frequent and heavy nosebleeds, or excessive bruising must be reported
- prevent ↑’d intrabdominal pressure
- reduce metabolic demands (frequent rests and avoiding unnecessary fatigue)
12
Q
Portal Hypertension
A
- abnormally high BP in the portal venous system
- high pressure in the portal veins causes collateral vessels to enlarge b/w the portal veins and the systemic veins, where BP is considerably lower
- high pressure and ↑’d flow volume result in problems such as esophageal varices, splenomegaly, ascites, and hepatic encephalopathy
- varices are distended, tortuous, veins 2° to prolonged ↑ of pressure
- the vomiting of blood from bleeding esophageal varices is the most common clinical manifestation of portal HTN
- anemia may develop from the prolonged slow bleeding associated w/ varices or rupture
- distended collateral (paraumbilical) veins may radiate over the abdomen, giving rise to the description caput medusae
- splenomegaly is caused by ↑’d pressure in the splenic vein
- hepatic encephalopathy occurs when the blood is shunted through collateral vessels to the systemic veins bypassing the liver: presence of toxic substances (e.g., ammonia) in the blood reaching the brain results in hepatic encephalopathy
13
Q
SIFTT for Portal Hypertension
A
-teach individuals how to modify and reduce pressure…anything that ↑’s intrabdominal pressure (coughing, straining at stool, or improper lifting)
14
Q
Hepatic Encephalopathy
A
- loss of brain function that occurs when the liver is unable to remove toxins from the blood
- potentially reversible, ↓’d level of consciousness in people with severe liver disease
- liver’s inability to metabolize ammonia one of most serious to nerve tissue
- high protein meals can lead to encephalopathy
- liver is unable to process nitrogenous metabolites
- protein-and gut-derived toxins normally are detoxified by the liver
- when toxins are no longer removed from the blood by the liver, they pass directly to the brain, where they have harmful effects on the nervous system
- stage I: slight personality changes, depression, slight tremor
- stage II: drowsiness, sleep disorders, changes in behavior, asterixis, ataxia, slurred speech
- stage III: confusion and somnolence, clonus, muscular rigidity, hypoactive reflexes
- stage IV: comatose state, abnormal reflexes
- eliminate or reduce sources of protein
15
Q
SIFTT for Hepatic Encephalopathy
A
- protective measures must be taken against falls and seizures
- skin breakdown in a client who is malnourished from liver disease and is immobile, jaundice, and edematous can occur in less than 24 hours
- client should follow a low protein diet
