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Nur 3010 exams > Liver, Biliary, and pancreatic disorders > Flashcards

Liver, Biliary, and pancreatic disorders Flashcards

1
Q

review of a&p: liver

A
  • largest gland of the body
  • located in the upper right abdomen
  • very vascular organ that receives blood from GI tract via portal vein and from the hepatic artery
  • inflammation: hepatomegaly
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2
Q

liver lobule cross section (2) + extra sinusoid

A
  • kupffer cells: phagocyte in the liver responsible for RBC breakdown (unconjugated bilirubin -> conjugated -> bile -> duodenum -> Large intestine -> small intestine -> rectum)
  • hepatocytes: major cell within liver, responsible for metabolic endocrine and secretory function (create bile, breakdown toxins, makes additional protein)

EXTRA
- sinusoid: carry blood into lobules adjacent to bile tract
- parasinusoidal space: show issues with cirrhosis
- inflammation liver -> activation of cells in parasinusoidal space are stimulated to create collagen -> fibrous -> increase resistance in sinusoid vessel -> increase pressure in portal vein -> ascites, portal vein HTN, esophageal varices

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3
Q

metabolic functions of the liver (8)

A
  • glucose metabolism
  • ammonia conversion -> blood urea nitrogen
  • protein metabolism -> ATP, NH3 (ammonia base) -> toxic to brain so liver converts (bad liver function increases ammonia)
  • fat metabolism (S/D into bile -> GI tract, cholesterol digestion)
  • vitamin and iron storage
  • bile formation
  • bilirubin excretion
  • drug metabolism (damage liver can’t metabolize certain drugs, dosing becomes toxic, alcohol metabolism)
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4
Q

liver function studies (7)

A
  • serum aminotransferase: AST, ALT, GGT
  • serum protein studies: total protein pre albumin + albumin (decrease liver fail, malnourish also contributes to low albumin)
  • direct/indirect serum bilirubin, urine bilirubin, urobilinogen (conjugated, unconjugated)
  • clotting factors: doesn’t measure directly, PT/INR, PTT
  • serum alkaline phosphatase
  • serum ammonia
  • lipids: increase cholesterol can indicate liver dysfunction
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5
Q

LFTS (4)

A

1) serum aminotransferase: indicators of injury to liver cells, detects hepatits
- alanine aminotransferease (ALT): levels increase primary in liver ds., used to monitor the course of hepatitis, cirrhosis, effects of treatments that may be toxic to the liver (increases w/ Tylenol faster)
- aspartate aminotransferase (AST): not specific to liver diseases, may be increased in cirrhosis, hepatitis, liver cancer
- gamma-glutamyl transferase (GGT): levels are associated with cholestatsis (bile stones -> bile duct -> increase bile), alcoholic liver disease

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6
Q

additional diagnostics of liver (5)

A
  • liver biopsy: allows for pathology of hepatocytes (diagnose cancer, alcoholic cirrhosis)
  • ultrasonography
  • CT
  • MRI
  • other: parencentesis
  • ultrasonography, CT, MRI show biliary roots
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7
Q

assessment of liver dysfunction (2)

A

1) healthy history
- previous exposure to hepatotoxic substances or infectious agents
- travel, alcohol, drug use
- lifestyle
2) physical assessment: increased role w/ cholesterol levels
- skin (s/sx jaundice)
- cognitive status (ammonia levels -> hepatic encephalopathy)
- palpation, percussion (hepatomegaly, dullness on percussion)

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8
Q

major causes of hepatic dysfunction (4)

A
  • liver failure associated with alcohol use
  • infection
  • fatty liver disease (nonalcoholic fatty liver disease(NAFLD), nonalcoholic steatohepatitis (NASH)
  • acute or chronic, cirrhosis of the liver: caused by hepatotoxicity (infection, Tylenol OD), biliary disease, alcoholism
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9
Q

what is nonalcoholic fatty liver disease (NAFLD)

A

fatty deposits without liver damage
- caused by diet high in processed foods

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10
Q

what is nonalcoholic steatohepatitis (NASH)

A

liver damage with fatty deposits

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11
Q

manifestations of hepatic disease (4)

A

(starts vague, RUQ pain, fatigue, etc.)
- jaundice
- portal vein HTN (ascites, varices)
- hepatic encephalopathy or coma
- nutritional deficiencies (don’t absorb fat soluble vitamins A,B,D,K)

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12
Q

jaundice (what, exceeds, types 4, most associated with liver disease)

A

yellow or greenish yellow sclera and skin cause dry increased serum bilirubin levels
- bilirubin level exceeds 2mg/dL (>5mg/dL -> need to do lab glucose)
- hemolytic (break down RBC faster than liver can conjugate, sickle cell disease/pregnancy), hepatocellular (liver can’t conjugate bilirubin), obstructive (liver conjugate but obstruction in bile duct), hereditary hyperbilirubiemia (RARE)
- hepatocellular and obstructive jaundice -> most associated with liver disease

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13
Q

hepatocellular jaundice sx (4)

A
  • mild or severely ill
  • lack of appetite, nausea or vomiting, weight loss
  • malaise, fatigue, weakness
  • headache, chills, fever, infection
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14
Q

obstructive jaundice sx (3)

A
  • dark orange-brown urine, clay colored stools
  • dyspepsia, intolerance of fats, impaired digestion (GI focus, perfuse greasy diarrhea)
  • pruritus (itching sensation)

TIP: no liver fail, only obstruction in bile duct -> bilirubin reabsorbed into blood -> excreted into urine, not GI -> clay bowels, dark orange-brown urine

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15
Q

portal vein HTN (2)

A
  • obstructed blood flor through the liver results in increased pressure throughout the portal venous system -> increased pressure
  • results in: ascites, esophageal varices
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16
Q

ascites (6) (what, exacerbated by)

A
  • portal HTN resulting in increased capillary pressure and obstruction of venous floor (forces blood out of vasculature -> peritoneal space)
  • vasodilation of splanchnic circulation (blood flow to major abdominal organs)
  • changes in ability to metabolize aldosterone, increasing fluid retention

exacerbated by
- decreased synthesis of albumin, decreasing serum osmotic pressure (third space)
- movement of albumin -> peritoneal cavity
- when drained, patient loses a lot of albumin -> albumin IV replacement needed

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17
Q

ascites assessment (4)

A
  • record abdominal girth and weight daily (baseline maintained)
  • patient may have striae, distended veins, umbilical hernia
  • assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave
  • monitor for potential fluid and electrolyte imbalance
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18
Q

ascites treatment (7)

A
  • low sodium diet
  • diuretics: spironolactone (first line) -> aldosterone antagonists
  • bed rest
  • paracentesis (U/S guided to drain abdominal cavity, reserved for symptomatic pt., can use respiratory deficiencies) -> monitor VS, abdominal circumference, s/sx bleeding d/t low clotting factor
  • administration of salt-poor albumin
  • transjugular intrahepatic portosystemic shunt (TIPS) - common
  • other methods: peritoneovenous

TIP: artificial shunt created in liver to allow reduction portal vein HTN -> Cath -> JV -> IVC -> liver -> bypass hepatocytes -> loses some filter capacity + implications for renal BF (liver failure + renal failure occur together)

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19
Q

esophageal varices (what, occurs, manifestations, extra)

A
  • engorgement of esophageal veins d/t portal HTN (increased pressure)
  • veins prone to bleeding
  • occurs in 30% patients with compensated (tolerated) cirrhosis and 60% patients with decompensated (hospitalized) cirrhosis
  • first bleeding episode has mortality rate 10% - 30% depending on severity
  • manifestations: hematemesis (teat in veins -> shock), melena, general deterioration, shock
  • pt. with cirrhosis should undergo screening endoscopy every 2-3 years
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20
Q

esophageal varices treatment (5) - pharamcology

A
  • treat for shock, administration oxygen
  • IV fluids, electrolytes, volume expanders, blood and blood products
  • vasopressin, somatostatin, ocetrotide: decrease bleeding (by vasodilating portal vein)
  • nitroglycerin in combination with vasopressin to reduce coronary vasconstriction
  • propranolol and nadolol to decrease portal pressure, used in combination with other treatment
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21
Q

esophageal varices treatment surgery (4)

A
  • balloon tamponade: balloon -> throat -> put pressure on esophageal wall to prevent further bleeding
  • endoscopic sclerotherapy: visualize bleeding
  • endoscopic vatical ligation: esophageal banding therapy
  • transjugular intrahepatic portosystemic shunt: doesn’t treat active bleed, decrease portal HTN
22
Q

esophageal varices nursing mgmt (4)

A
  • maintain safe environement: prevent injury, bleeding, infection
  • administer prescribed treatments and monitor for potential complications
  • encourage deep breathing and position changes
  • education and support of patient and family

TIP: can be exacerbated by lifestyle choices

23
Q

hepatic encephalopathy or coma (what, types, early signs)

A
  • life threatening complications: accumulation of ammonia (NH3) and other toxic metabolites in the blood
  • two major alterations underlie its development in acute and chronic liver disease:
    1) hepatic insufficiency: inability of the liver to detoxify toxic byproducts of metabolism
    2) portosystemic shunting: collateral vessels develop allowing elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter systemic circulation -> bypass liver -> no blood filter properly -> hepatic encephalopathy
  • early signs: mental changes, motor disturbances
24
Q

hepatic encephalopathy assessment (5)

A
  • EEG r/o CNS cause or seizures
  • changes in LOC
  • potential seizures (seizure precaution)
  • fetor hepaticus: accumulation of ammonia in blood manifested with stank breath
  • monitor fluid, electrolyte, ammonia levels (diagnostics)
25
Q

hepatic encephalopathy medical therapy (7)

A
  • eliminate precipitating cause (restore liver function)
  • lactulose PO to reduce serum ammonia levels (draw ammonia -> GI to excrete)
  • IV glucose to minimize protein catabolism
  • protein restriction
  • reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics (flagyl)
  • discontinue sedatives, analgesics, tranquilizers (eliminate potential other causes)
  • monitor or treat complications and infections
26
Q

hepatitis (hepta = liver, itis = inflammation) (types 2)

A

1) viral hepatitis: systemic viral infection that causes necrosis and inflammation of liver cells with characteristics symptoms and cellular and biochemical changes
- A/E: fecal oral route
- B/C: bloodborne
- D: only people with hepatitis B are at risk
- hepatitis G, GB virus C
2) nonverbal hepatitis: toxic and drug induced

27
Q

hepatitis A (transmission, manifestations, clear, vaccine)

A
  • spread by poor hand hygiene: fecal-oral
  • illness may last 4-8 weeks
  • mortality rate is 0.5% <40 years, 1-2% >40years
  • manifestations: mild flu like symptoms, low grade fever, anorexia, later jaundice, dark urine, indigestion, epigastric distress, enlargement of liver and spleen
  • cleared: 2 months
  • vaccine: (+), 2 vaccine course
28
Q

hepatitis A mgmt (3)

A

1) prevention
- good handwashing, safe water, and proper sewage disposal
- vaccine
- immunoglobulin (antibodies) for contacts to provide passive immunity
2) bedrest during acute stage
3) nutritional support: avoid hepatotoxins

TIP: incubation 2-6 weeks

29
Q

hepatitis B (transmitted, RF, manifestations, clear, vaccine)

A
  • transmitted: blood, saliva, semen, vaginal secretions; sexual transmitted, transmitted to infant at the time of birth
  • a major worldwide cause of cirrhosis and liver cancer
  • risk factors: healthcare exposure, blood product recipient in early 1980’s, unprotected sex, IV drug abuse (incarceration)
  • manifestations: incision and variable, similar to HAV, loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, weakness (sometimes not symptoms)
  • jaundice may or may not be evident
  • clear: YES
  • vaccine: (+)

TIP: long incubation period 1-6 months, DANGEROUS

30
Q

hepatitis C (transmitted, RF, clear, vaccine)

A

most common, NO VACCINE
- transmitted: blood, sexual contract including needle sticks, sharing of needles
- most common blood borne infection
- risk factors: similar to hep B
- cause of 1/3 cases liver cancer
- most common reason for liver transplant
- symptoms are usually mild (flu like sx)
- chronic carrier state frequently occurs
- clear: NO
- vaccine: (-)

TIP: incubation 15-60 days, mutates rapidly (NO VACCINE)

31
Q

hepatitis B mgmt (2)

A

1) medications for chronic hepatitis type B include alpha interferon and antiviral agents: entercavir (ETV) and tenofovir (TDF)
2) vaccine (best): for person at high risk, routine vaccination of infants
- passive immunization for those exposed
- standard precautions and infection control measures
- screening of blood and blood products

32
Q

hepatitis C mgmt (6)

A
  • antiviral medications (curable, expensive)
  • alcohol potentiates disease, meds that effect liver should be avoided
  • prevention: public health programs to decrease needle sharing among drug users
  • screening of blood supply
  • safety needs for health care workers
  • addiction is a disease as well
33
Q

hepatits D (transmitted, what, clear, vaccine)

A

only persons with HEP B are at risk
- transmitted: sexual contact transmission
- use of IV or injection drugs, patients undergoing hemodialysis, recipients of multiple blood transitions
- likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis
- interferon alfa is the only licensed drug available in the treatment for HDV infection

34
Q

hepatitis E (what, transmitted, prevention, vaccine)

A

similar to A, RARE
- transmitted: fecal oral route, contaminated water
- resembles hep A: self limiting, abrupt onset, not chronic
- prevention: good hygiene, handwashing

TIP: incubation 15-65 days

35
Q

other hepatitis (2)

A

similar to HPV, STREPT
- nonverbal hepatitis: toxic hepatitis, drug induced hepatitis (Tylenol OD)
- fulminant hepatic failure

36
Q

hepatic cirrhosis (types, manifestations, nursing interventions)

A

irreversible
1) types:
- alcoholic: scar tissue, characteristically surrounds the portal areas
- postnecrotic: broads bands of scar tissue
- biliary: scarring occurs in the liver around the bile ducts
2) manifestations: liver enlargement, portal obstruction, ascites, infection and peritonitis, varices, GI varices, edema, vitamin deficiency, anemia, mental deterioration
3) nursing interventions directed toward: managing sx.
- promoting rest
- improving nutritional status
- providing skin care
- reducing risk of injury
- monitoring and managing potential complications

37
Q

hepatic cirrhosis complications (major) (4)

A
  • bleeding and hemorrhage S/D clotting deficiency
  • hepatic encephalopathy (lactulose)
  • fluid volume excess (parencentesis, diuretic use)
  • increased portal vein pressure + decreased albumin = ascites, systemic edema
38
Q

liver cancer (3)

A

1) primary liver tumors (rare)
- associated with hep B/C
- hepatocellular carcinoma (HCC)
2) liver metastasis
- few cancers originate in the liver
- frequent site of metastatic cancer (vascular)
3) manifestations (vague)
- dull persistent pain, RUQ, back, or epigastrium
- weight loss, anemia, anorexia, weakness
- jaundice, bile ducts occluded, ascites, or obstructed portal vein (causing ascites)

39
Q

liver cancer nonsurgical management (6)

A
  • underlying cirrhosis, which is prevalent in patients with liver cancer, increases risk of surgery (hard to do surgery)
  • major effect of nonsurgical therapy may be palliative
  • radiation therapy
  • chemotherapy
  • percutaneous biliary drainage (under CT guidance)
  • other nonsurgical treatments
40
Q

liver cancer surgical management (3, including types)

A
  • treatment of choice for HCC if confined to one lobe and liver function is adequate
  • liver has regenerative capacity
  • types of surgery: lobectomy, cryosurgery (ablated process disease), liver transplant
41
Q

liver transplant (6) + extras

A

1) preoperative nursing interventions: support, education, encouragement are provided to help psychologically for the surgery
2) postoperative nuring interventions: monitor for infection, vascular complications, respiratory, and liver dysfunction, constant close monitoring
3) education about LT measures to promote health
4) adhere closely to therapeutic regimen, with special emphasis on administration, rationale, and side effects of immunosuppressive agents
5) education about signs/symptoms that indicate problems necessitating consultation with transplant team
6) emphasize importance of follow up laboratory tests and appointments with transplant team

extra:
- alcohol sober 16 months
- post transplant -> suppress immune system -> decrease infection -> lifelong anti reject meds + immunosuppression
- if liver failure post transplant -> body rejects liver or hepatitis -> fibrous of liver cells
- biopsy annually

42
Q

review A&P gall bladder, pancreas

A

gallbladder: stores and concentrates bile
pancreas:
- exocrine: amylase (carbs digest), trypsin (protein), lipase (fat digest), secretin (regulate GI tract)

43
Q

cholelithiasis - gall stones (types, RF, clinical manifestations)

A

1) 2 types: pigment stones, cholesterol stones
2) risk factors:
- cystic fibrosis
- diabetes
- changes in weight
- ill resection/disease
- estrogen therapy
- obesity
- females
- the “f’s”: fat, female, forty, fertile
3) clinical manifestations:
- often silent
- pain, biliary colic (bile -> obstructive bile duct), changes in urine and stool color, vitamin deficiency of fat solubles (A,D,E,K) -> bile helps absorb
- cholecystitis: inflammation of gallbladder -> infection (90% caused by gall stones)
- cholelithiasis: not caused by gall stones, sicker patients

44
Q

cholelithiasis medical mgmt (5)

A
  • ERCP common
  • dietary mangement (decrease processed fats, trans foods)
  • medications: ursodeoxycholic acid, chenodeoxycholic acid -> reduce side of stones, dissolves stones, prevents new stones
  • laparoscopic cholecystectomy
  • nonsurgical removal: instrument, intracorporeal/extracorporeal lithotripsy

TIP: meds take a long time, prophylaxis usage

45
Q

describe ERCP (4)

A
  • endoscopic is inserted through mouth -> duodenum
  • camera inserted throughout esophagus -> duodenum -> pancreatic duct
  • catheter reaches sphincter of vader to pull biliary stones out
  • dye is injected through a catheter into pancreatic or biliary ducts to identify location
46
Q

pancreatitis (acute, chronic)

A

(inflammation of liver can impair exocrine system/duct -> withhold alcohol)
1) acute: pancreatic duct becomes obstructed d/t gall stones, and enzymes back up, causing auto digestion and inflammation of the pancreas
- fever, jaundice, confusion, agitation, ecchymosis in the flank or umbilical area, and abdominal guarding
- elevations in lipase and amylase enzymes (auto digestion) (narcotic dilaudid, morphine)
2) chronic: progressive inflammatory disorder with destruction of the pancreas, cells are replaced by fibrous tissue, pressure within pancreas increases, obstructing pancreatic and common bile ducts (alcohol pancreatitis)
- severe upper abdominal and back pain accompanied by vomiting
- CT showing fibrotic changes, not as markedly elevated labs

47
Q

pancreatitis assessment (7)

A
  • patient history (gallstone, ETOH abuse)
  • knowledge and education needs
  • respiratory status and risk factors for postoperative respiratory complications
  • nutritional status
  • monitor for potential bleeding (concomitant with liver failure)
  • GI symtpms: after laparoscopic surgery, assess for loss of appetite, vomiting, pain, distention, fever - potential infection or disruption of GI tract (post surgery, within 24H -> no infection, r/t atelectasis (small collapse alveoli) -> cough, DB, IS, ambulate
48
Q

pancreatitis mgmt (5)

A
  • NPO (strict, stimulate peristalsis + external organs)
  • serial enzymes decreased
  • pain control
  • biliary drainage (if biliary obstruction)
  • when enzymes trend down, restart feeding slowly (ice chips): high carb, low fat/protein

TIP: cram feeding - chewing gum stimulates GI, assess pain + lipase (if yes, spit gum out)
- lipase causes auto digestion, no amylase (is increased)

49
Q

pancreatitis complications (5)

A
  • fluid and electrolyte disturbances d/t NPO
  • necrosis of the pancreas
  • shock
  • multiple organ dysfunction syndrome
  • DIC (disseminated intravascular coagulation)

clots throughout vascular system, platelets get consumed, coagulating inside vessel, doesn’t stop bleeding)

50
Q

interventions for patient undergoing surgery for gallbladder/pancreatic disease (post OP) (6)

A
  • low fowler position
  • NG or NPO until bowel sounds return; then a soft, low fat high carb diet (low intermittent suction)
  • care of biliary drainage system (home care education)
  • analgesics, pain management
  • turn, cough, deep breathing, splinting to reduce pain
  • ambulation: reduce risk atelectasis, reduce paralytic illeus, prevents muscular de-conditioning

Nur 3010 exams (13 decks)

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