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PNP #2 > Disorders of the Liver and Pancreas Heptobilary > Flashcards

Disorders of the Liver and Pancreas Heptobilary Flashcards

1
Q

Liver

A

“Metabolic factory” of the body

  • Largest internal organ in the body; essential for life
  • Functions in the manufacture, storage, transformation, and excretion of many substances involved in metabolism, production of plasma proteins and clotting factors, Breakdown of old and damaged erythrocytes, Bile production

-Receives blood from hepatic portal vein
Transport of nutrients from intestine to liver
-Hepatocytes store nutrients
Play role in carbohydrate, protein, fat metabolism

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2
Q

Pancreas

A

Exocrine (contributes to digestion) and endocrine functions (insulin, glycagon, somatostatin, and pancreatic polypeptide)

Secretes digestive enzymes, electrolytes
Trypsin
Chymotrypsin
Carboxypeptidase
Ribonuclease 
Pancreatic amylase
Bicarbonate ions

Pancreatic duct joins bile duct to enter duodenum

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3
Q

slide 6 has manifesations of liver disease

A

.

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4
Q

Prehepatic jaundice

A

Result of excessive destruction of red blood cells

Characteristic of hemolytic anemias or transfusion reactions

Unconjugated bilirubin level elevated

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5
Q

Intrahepatic jaundice

A

Occurs with disease or damage to hepatocytes

Hepatitis or cirrhosis

Both unconjugated and conjugated bilirubin levels may be elevated.

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6
Q

Posthepatic jaundice

A

Caused by obstruction of bile flow into gallbladder or duodenum

Tumor, cholelithiasis

Increased conjugated bilirubin level
Light-colored stool caused by absence of bile

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7
Q

Bilirubin Measurement in Jaundice

A

Direct or conjugated bilirubin can be measured in the blood.

Total bilirubin is measured in blood.

Indirect or unconjugated bilirubin = total bilirubin minus direct bilirubin

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8
Q

Cirrhosis

A

Progressive destruction of the liver – leads to cellular death when 80 – 90% f the liver has been destroyed

Damaged liver regenerate as fibrotic areas instead of functional cells, causing lymph damage and alterations in live restructure, function and blood circulation

Extensive diffuse fibrosis
Interferes with blood supply
Bile may back up.

Loss of lobular organization

Degenerative changes may be asymptomatic until disease is well advanced.

Liver biopsy and serologic test to determine cause and extent of damage

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9
Q

Causes of cirrhosis

A

-Alcoholic liver disease (15%)
-Biliary cirrhosis
Associated with immune disorders
-Postnecrotic cirrhosis
Linked with chronic hepatitis (26% Hep C, 15% Hep B) or long-term exposure to toxic materials
-Metabolic
Usually caused by genetic metabolic storage disorders
-

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10
Q

Functional Losses with Cirrhosis

A

 Decreased removal and conjugation of bilirubin
 Decreased production of bile
 Impaired digestion and absorption of nutrients
 Decreased production of blood-clotting factors (Prothrombin/Fibrogen) & plasma Proteins (albumin)
 Impaired glucose and glycogen metabolism
 Impaired conversion of ammonia to urea
 Inadequate storage of iron and vitamin B12
 Congestion in intestinal walls and stomach
 Impairing digestion and absorption
 Development of esophageal varices **next slide
 Hemorrhage
 Development of ascites, an accumulation of fluid in the peritoneal cavity **following 2 slides
 Causes abdominal distention and pressure

 Decreased inactivation of hormones and drugs- Drug dosages must be carefully monitored to avoid toxicity.
 Decreased removal of toxic substances (ammonia & drugs)
 Reduction of bile entering the intestine- Impairs digestion and absorption
 Backup of bile in the liver- Leads to obstructive jaundice
 Blockage of blood flow through the liver- Leads to portal hypertension
 Congestion in the spleen- Increases hemolysis

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11
Q

Cirrhosis: Subjective Data

A
  • Personality changes, forgetfulness, disorientation
  • Fatigue, drowsiness, mild tremors, or flue-like sx
  • Gynecomastia, ab distention & measure abd girth
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12
Q

Initial manifestations often mild and vague

of cirrhosis

A

Fatigue, anorexia, weight loss, anemia, diarrhea

Dull aching pain may be present in upper right abdominal quadrant.

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13
Q

Advanced cirrhosis

A

Ascites and peripheral edema
Increased bruising
Esophageal varices (May rupture, leading to hemorrhage, circulatory shock)
Jaundice, encephalopathy

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14
Q

Cirrhosis: Treatment

A

 Avoidance of alcohol or specific cause
 Avoid fatigue
 Avoid exposure to infection
 Supportive or symptomatic treatment
 Dietary restrictions (high carbohydrate intake and vitamin supplements, restrict protein, fat, & Na++)
 Balancing serum electrolytes (possibly diuretics)
 Paracentesis
 Antibiotics to reduce intestinal flora (neomycin)

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15
Q

Cirrhosis: Treatment

A

-Esophageal and gastric varice:
Long-term management
Shunting procedures
Monitor for hypovolemia & bleeding

  • Drug therapy Vitamin K blood clotting
  • Emergency treatment if esophageal varices rupture
  • Liver transplantation (suitable living donor = liver tissue is able to grow in both donner and recipient providing a complete functional liver for both)
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16
Q

Hepatitis

A

Inflammation of the liver results in degeneration and necrosis.

Mild inflammation impairs hepatocyte function.

More severe inflammation and necrosis may lead to obstruction of blood & bile flow

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17
Q

?

A 
Alcoholic (Fatty liver)
Idiopathic (Fatty liver)
Viral hepatitis (Local infection)
Infection elsewhere in body(infectious mononucleosis or amebiasis) 
Chemical or drug toxicity
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18
Q

Viral Hepatitis

A

Cell injury results in inflammation and necrosis in the liver.
-Degrees of inflammation and damage vary.

Liver is edematous and tender.

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19
Q

Causative viruses

A 
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
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20
Q

*Hepatitis A (HAV)

know mainly abc and how they are transmitted

A

o Small RNA virus
o Infectious hepatitis
o Transmitted by fecal-oral route in areas of inadequate sanitation or hygiene
–Often from contaminated water or shellfish
o Sexual transmission has occurred during anal intercourse.
o Acute but self-limiting infection
o No carrier or chronic state
o Fecal shedding of virus before onset of signs
o Vaccine available for travelers, food care workers, and health care workers

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21
Q

*Hepatitis B (HBV)

A

o Partially double-stranded DNA virus
o Over 50% of HIV-positive patients are positive for HBV.
o 50% of patients are asymptomatic but contagious because of carrier state.
o Chronic inflammation can occur.
o Transmission primarily by infected blood
o Sexual transmission has been noted.
o Tattooing and body piercing may transmit the virus.
o Vaccine available, routinely given to children

22
Q

*Hepatitis C (HCV)

A

 Single-stranded RNA virus
 Most common type transmitted by blood transfusion
 May exist in a carrier state
 About 50% of patients enter the chronic state.
 Increases risk of hepatocellular carcinoma
 Treated with interferon injections

23
Q

Hepatitis D (HDV)

A

o Also called delta virus
o Incomplete RNA virus
 Requires HBV to replicate and produce active infection
o HDV infection increases severity of HBV infection

Transmitted by blood

24
Q

Hepatitis E (HEV)

A

 Single-stranded RNA virus
 Transmitted by oral-fecal route
 No chronic or carrier state

25
Q

FIRST STAGE
Viral Hepatitis: Manifestations
Preicteric stage

A 
Fatigue and malaise
Anorexia and nausea
General muscle aching
Sometimes fever, H/A, mild URQ discomfort
LFT elevated (AST & ALT)
26
Q

SECOND STAGE
Viral Hepatitis: Manifestations
Icteric stage *longest for Hep B

A

Onset of jaundice
Stools light in color, urine becomes darker, skin puritic
Liver tender and enlarged (hepatomegaly) = mild aching pain
Severe cases blood clotting times prolonged

27
Q

THIRD STAGE
Viral Hepatitis: Manifestations
Posticteric stage—recovery stage

A

Reductions in signs
Weakness persists for weeks
Hep A 8-10w; Hep B 16w

28
Q

Viral Hepatitis: Treatment

A

• No method of destroying hepatitis viruses in the body
• Only body defense is formation of antibodies via vaccination
• Supportive measures (Rest, diet high in protein, carbohydrate, and vitamins)
• Chronic hepatitis can be treated with INTERFERON.
o Decreases viral replication
o Effective in only 30% to 40% of individuals
o Drug combination (slow-acting interferon plus antiviral drug) more effective

29
Q

Gallbladder Disorders

A

• Cholelithiasis
o Formation of gallstones
o Solid material (calculi) that form in bile
• Cholecystitis
o Inflammation of gallbladder and cystic duct
• Cholangitis
o Inflammation usually related to infection of bile ducts
• Choledocholithiasis
o Obstruction of the biliary tract by gallstones

30
Q

Gallbladder Disorders (Cont.)

A
  • Gallstones vary in size and shape.
  • Form in bile ducts, gallbladder, or cystic duct

• May consist of:
o Cholesterol or bile pigment
o Mixed content with calcium salts

• Small stones
o May be silent and excreted in bile

• Larger stones
o Obstruct flow of bile in cystic or common bile ducts; cause severe pain, which is often referred to subscapular area

31
Q

Risk factors for gallstones

A 
Women twice as likely to develop stones
High cholesterol in bile
High cholesterol intake 
Obesity 
Multiparity
Use of oral contraceptives or estrogen supplements
Hemolytic anemia
Alcoholic cirrhosis
Biliary tract infection
32
Q

4F’s of gallbladder=

A

Fat, Fertile, Female, Forty

33
Q

Obstruction of a duct by a large calculi

A

o Sudden severe waves of pain
 Radiating pain right shoulder/neck

o Nausea and vomiting usually present

o Pain continues, and jaundice develops.
 Bile backs up into the liver and blood.
 Risk of ruptured gallbladder if obstruction persists
 Pain decreases if stone moves into duodenum

o Surgical intervention may be necessary.
 May be removed using laparoscopic surgery
 Low-fat diet necessary following surgery

34
Q

Inflammation of the pancreas

A

Results in autodigestion of the tissue

Premature activation of pancreatic proenzymes (trypsin, amylase and lipase) which digests the pancreatic tissues = massive inflammation, bleeding & necrosis

35
Q

May be acute or chronic

Acute Pancreatitis

A

Acute form considered a medical emergency

36
Q

Pancreas lacks a fibrous capsule…

Acute Pancreatitis

A

Destruction may progress into tissue surrounding the pancreas

Substances released by necrotic tissue lead to widespread inflammation
–Hypovolemia and circulatory collapse may follow.

37
Q

Chemical peritonitis results in bacterial peritonitis.

Acute Pancreatitis

A

Septicemia may result.

Adult respiratory distress syndrome and acute renal failure are possible complications.

38
Q

Causes

Acute Pancreatitis

A

Gallstones
Alcohol abuse
Sudden onset may follow intake of large meal or large amount of alcohol

39
Q

Acute Pancreatitis: Manifesations

A
  • -Severe epigastric or abdominal pain radiating to the back (primary symptoms) Pain increases in supine position
  • -Signs of shock (Caused by hypovolemia d/t inflammation and hemorrhage – low PB, palor, diaphoresis, rapid & weak pulse)
  • -Low-grade fever until infection develops (then temperature may then rise significantly)
  • -Abdominal distention and decreased bowel sounds (Decreased peristalsis and paralytic ileus)
40
Q

Diagnostic tests

Acute Pancreatitis

A

Serum amylase levels—first rise, then fall after 48 hours
Serum lipid levels are elevated.
Hypocalcemia
Leukocytosis

41
Q

Treatment

Acute Pancreatitis

A

Oral intake is stopped.
Treatment of shock and electrolyte imbalances
Analgesics for pain relief – NOT MORPHINE – (causes spasm of the sphincter of Oddi)

42
Q

LIVER PROBLEM PEOPLE

A

dont have vit k so they bruise easly
there is so much extra uric acid that its fucks with neuro
jaundice - because the liver is not breaking down billirubin
encephalopathy

splenomegaly
portal hypertension
anemia- because liver cant store WBCs and the bofy can use b12 and iron which wont create WBCS
leukopenia- low blood sells that puts them in a risk of infection
gynemomastia -big titties
pruritus
first place you will see jaundice will be in the eyes

43
Q

every time you see high levels of bilirubin

A

think of liver

44
Q

females should always have hemoglobin levels

A

between 120-160

45
Q

hepititis is

A

really inflammation of the liver

46
Q

when the liver starts to degenerate

A

it because fibirous and it wont function as well

47
Q

for ascities

A

the diuretics will draw the fluid the from the peri cavity into the vascular system so that they can remove the fluid because thats how diuretics work

48
Q

hep difference between crhrosis

A

altered taste ad smakk
fever
malaisa
headache

49
Q

galbladder mani

A
  • sudden severe waves of pain
  • nausea and vomiting
  • if pain continues, and jundice develops
  • +surgical intervention may be mecessarn
50
Q

clincal manis caused by bile flow (chart)

A
  • jaundice
  • dark urine
  • cramping
  • steatorrhea

PNP #2 (10 decks)

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