Lecture 14: Hepatic, Pancreatic, and Biliary Systems Flashcards
(31 cards)
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
16
Q
Ascites
A
- accumulation of serous fluid w/in the peritoneal cavity, the potential space b/w the lining of the liver and the lining of the abdominal cavity
- caused by cirrhosis in 85% of cases
- associated with aldosterone
- patho: high pressure in the liver and splanchnic vessels, excessive lymph is produced that leaks into the tissues and the abdominal cavity; becomes clinically detectable when more than 500 ml has accumulated; as ascites sequesters more and more bodily fluid, the kidneys respond by retaining Na+ and H2O, which expands plasma volume and thereby accelerates portal HTN and further formation of ascites
- CM: weight gain, abdominal distention, ↑’d abdominal girth, and peripheral edema, dyspnea with ↑’d respiratory rate occurs when fluid displaces diaphragm
- tx: restriction of Na+ intake and fluid and administration of diuretics
17
Q
SIFTT for Ascites
A
- monitor for the possible development of bacterial peritonitis
- fever, chills, abdominal pain, and tenderness should be reported
- review hydrostatics p. 6
18
Q
Viral Hepatitis
A
-common liver infection and can eventually regenerate with little or no permanent damage
-complications may arise d/t old age and serious underlying disorders
-long incubation period often occurs b/w acquisition of the infection and
development of the first symptoms
-virus causes hepatocyte injury and death either by directly killing the cells or by activating the inflammatory and immune reactions
-5 types recognized
-HBV is relatively stable in the environment and remains viable for at least 7 days on environmental surfaces at room temperature
-prodromal stage: fatigue, anorexia, malaise, depression, HA, weakness, arthralgia, myalgia, photophobia, nausea and vomiting; infection is highly transmissible
-clinical stage: begins 1-2 weeks after the prodromal stage; actual illness: itching, abdominal pain, indigestion, appetite loss, and jaundice (liver can’t remove bilirubin from blood)
-recovery stage: begins with resolution of jaundice and lasts 2-6 weeks
-prevention: vaccines for A and B; C none-screen the blood supply, encourage healthcare professionals to take precautions when handling blood and body fluids, educate people about high-risk behaviors
-dx: hepatitis profile; liver function studies; WBC count; liver biopsy
19
Q
HAV
A
- due to overcrowding and poor sanitation
- primary mode of transmission is the oral-fecal route
- improper handwashing and personal hygiene
- highly contagious – can last 4-8 weeks
- most predominant type
- incubation period is 15 to 50 days
- tx: symptomatic, rest for persons who are jaundiced
- prognosis: rarely fatal and does not lead to chronic hepatitis or cirrhosis; most people recover fully and become immune to HAV
20
Q
HBV
A
- transmitted parenterally through needles, sexual relations, post-transfusion, and perinatally from mother to child
- highly infectious: 100 times more infectious than HIV
- considered a sexually transmitted disease
- incubation period is 1 to 6 months – symptoms occur ~ 60 days
- tx: various drug treatments if active carrier
- prognosis: in adults with normal immune status, most (94-98%) recover completely from newly acquired HBV infections; immunity from future infection
21
Q
HCV
A
- 20% of all cases; most cases follow transfusion
- most commonly associated with injection-drug use
- often asymptomatic
- chronic hepatitis C varies greatly in its course, mild to severe
- tx: rapidly changing area of clinical practice
- prognosis: 20-30% develop cirrhosis
22
Q
HCD
A
-those exposed to blood and blood products; requires a
concomitant infection with hepatitis B to survive
23
Q
HEV
A
- fecal-oral transmission
- in people who visit endemic area
24
Q
SIFTT for Hepatitis
A
-wear personal protective equipment whenever appropriate
-client with undiagnosed hepatitis presenting with joint symptoms will not respond to therapy
Any time intervention fails to provide symptomatic relief or resolution of symptoms, the results must be reported to MD for further follow-up
-adequate rest to conserve energy is important
-individuals should gradually return to pre-illness levels of activity
-HBV and the Athlete…
-2 cases of HBV transmission through exposure to blood during sports participation have been documented
-American Academy of Pediatrics (AAP) made recommendations to minimize risk of bloodborne pathogen transmission in context of athletic events and has issued safety precautions
-no evidence has been reported that intense, highly competitive training is harmful for the asymptomatic HBV-infected person
25
Drug Related Hepatotoicity
- non-viral liver inflammation that occurs secondary to exposure to certain chemicals, drugs, and most recently, herbal preparations and other botanicals
- most common drug-induced liver failure is acetaminophen
- patho: apoptosis as a result of tumor necrosis factor; binding of drug to cellular proteins, which causes an immunologic response, leading to cell death; inhibiting metabolism of drugs; mitochondrial dysfunction with formation and accumulation of reactive oxidative species
- tx: once a substance has caused liver damage, this substance (as well as chemically similar compounds) must be avoided for life
26
Alcohol Related Liver Disease
- 40% of deaths from cirrhosis are alcohol-related
- 30% of HCC (hepatocellular carcinoma) cases are a result of alcohol-related liver disease
- men, 6-8 alcohol-containing beverages daily over a 5-year period can lead to liver disease; in women, only 3-4 drinks/day
- women are more vulnerable to the effects of alcohol-produce less alcohol dehydrogenase which decreases ethanol content in stomach so women absorb 75% more alcohol into bloodstream
- 90% of heavy drinkers develop fat accumulation in the liver
- may result in hepatomegaly and splenomegaly
- poor prognosis if the person continues to drink alcohol
- frequently, the disease will stabilize if the person stops drinking
27
Pancreatitis
- potentially serious inflammation of the pancreas that may result in autodigestion of the pancreas by its own enzymes
- most common causes are biliary tract disease and alcoholism
- patho: protein precipitates block the pancreas and harden; structural changes lead to fibrosis and atrophy of the glands; pseudocysts, containing pancreatic enzymes and debris, form; an abscess results if infected; irreversible changes in the pancreas 2° to chronic inflammation
- caused by long-standing alcohol abuse in more than 50% of adult cases
- acute pancreatitis: most common cause is gallstones followed by chronic alcohol consumption-edematous: causing fluid accumulation and swelling; necrotizing: causing cell death and tissue damage
- CM: steady epigastric pain, abdominal pain (may refer to back); diabetes may result 2° to damage to islets of Langerhans
- dx: ↑ serum amylase and lipase levels; blood and urine glucose tests; WBC count, CT scan and ultrasonography
- tx: maintain circulation and fluid volume; drug therapy; if acute, may subside spontaneously within several days
28
SIFTT for Pancreatitis
-for the client who is restricted from eating or drinking to rest the GI tract and ↓ pancreatic stimulation, even ice chips can stimulate enzymes and ↑ pain
29
Cholelithiasis (Gallstones)
-formation or presence of gallstones that remain in the lumen of the gallbladder or are ejected w/ bile into the cystic duct
-80% consist primarily of cholesterol
-20% are composed of bilirubin salts
-RF: older age, genetics, obesity, rapid weight loss, pregnancy
-CM: most gallstones are asymptomatic; 25% cause painful symptoms; most common obstruction site is the cystic duct-causes abdominal pain (biliary colic); painful symptoms are frequently related to meals; pain often radiates to right shoulder and upper back
-tx: no treatment is the usual recommendations for anyone w/ asymptomatic gallstones; laparoscopic cholecystectomy is the treatment of choice for
symptomatic gallbladder disease
-prognosis: with medical tx is usually good
30
SIFTT for Cholithiasis
- physical activity may play an important role in the prevention of symptomatic gallstone disease in up to a third of all cases
- usual post-op exercises (e.g., breathing, turning, coughing, wound splinting, compressive stockings, leg exercises) for any surgical procedure
31
Cholecystitis
-gallbladder inflammation
-calculi (gallstones) form from bile and become lodged in the cystic duct causing obstruction to bile flow and painful distention of the gallbladder
-patho: bile flow becomes blocked and the gallbladder becomes inflamed and distended (E. coli may contribute to inflammation) (study picture on p 12)
-CM: severe abdominal pain in the right upper quadrant and often into the back, between the shoulders or the front of the chest; colic; nausea and vomiting;
chills; low-grade fever; jaundice; belching; flatulence; indigestion
-dx: X-rays, ultrasonography, technetium-labeled scan shows cystic duct obstruction, blood studies (bilirubin)
-tx: lithotripsy (breaks up gallstones), diet modification; laparoscopic cholecystectomy (gallbladder resection) often is performed during the first hospitalization for acute cholecystitis
-SIFTT same as with cholelithiasis
