GI Disorders: Liver, Biliary, Pancreas Flashcards

1
Q

Liver Diseases

A
  • Hepatitis: inflamm of liver
  • Cirrhosis: constant inflamm leading to irreversible fibrosis & scarring
  • Liver CA
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2
Q

Primary liver CA vs. Secondary liver CA

A
  • Hepatocellular Carcinoma = primary liver CA
  • Secondary liver CA or Liver metastases = metastatic tumors in liver from a tumor outside the liver
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3
Q

Acute liver disease causes (top 3)

A
  • Hep A virus
  • Hep B virus new or reactivation
  • Drug-induced (mostly Acetaminophen)
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4
Q

Chronic liver disease causes (top 3)

A
  • Hep B and C virus
  • Alcohol
  • Non-Alcoholic Steatohepatitis (NASH)
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5
Q

Pruritis presentation

A
  • Excessive itching on body, mostly hands and feet
  • *Impacts quality of life, including mental health & sleep
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6
Q

Why does pruritus happen?

A

Caused by accumulation of bile salts under skin d/t liver can’t process bc hepatocytes not functioning properly

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7
Q

Pruritus treatment

A
  • Antihistamines (eg Benadryl) = INEFFECTIVE
  • *Cholestyramine removes bile salts
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8
Q

Jaundice presentation

A
  • Yellowing of skin, sclera
  • Gray clay-colored stools
  • Amber colored urine
  • Pruritus
  • Elevated serum bilirubin
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9
Q

Why does jaundice happen?

A

Elevated bilirubin
(Bilirubin usually byprod of RBC breakdown, stored in liver and secreted w bile)
(If liver can’t metabolize and secrete bilirubin, it builds up in plasma)

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10
Q

Obstructive jaundice - types of obstruction in biliary system

A
  • Inflamm/edema
  • Scarring
  • Fibrosis
  • Gallstones migrate into biliary system
  • Any obstruction interfering w normal bile flow (eg tumor)
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11
Q

Obstructive jaundice treatment

A
  • Endoscopic procedures w stenting
  • Surgery
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12
Q

Jaundice labs

A
  • High total bilirubin
  • High direct (conjugated) bilirubin level: greater than 0.3%
  • Low indirect (unconjugated) bilirubin level (high see in neonatal jaundice)
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13
Q

Direct (conjugated) bilirubin levels

A

0.1 - 0.3 mg/dl

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14
Q

Total bilirubin levels

A

0.3 - 1 mg/dl

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15
Q

Indirect (unconjugated) bilirubin levels
(due to RBC breakdown)

A

0.2 - 0.8

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16
Q

Hepatic encephalopathy presentation

A

*CNS disturbances
- Altered mental status
- Decreased LOC
- Changes in motor function
- Confusion, insomnia, somnolence
- Asterixis

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17
Q

Why does hepatic encephalopathy happen?

A
  • Liver can’t metabolize waste products d/t inflamm & hepatocyte malfunction
  • Liver scarring causes blood to bypass liver and miss being detoxified
  • Waste products, specifically ammonia, accumulate in blood, causing CNS disturbance
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18
Q

Hepatic encephalopathy treatment

A
  • Lactulose: promote excretion of ammonia in stool (can cause diarrhea)
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19
Q

Coagulopathies presentation

A
  • Thrombocytopenia (pltlt < 150,000)
  • Prolonged PT & INR
  • DIC: combo of clot & excessive bleed (GI tract, pulm, IV sites, wounds, puncture sites)
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20
Q

Portal HTN

A

Occurs in setting of cirrhosis

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21
Q

Effects of Portal HTN

A
  • Esophageal varices (melena, hematemesis)
  • Rectal varices (hemorrhoids, bleed)
  • *Ascites
  • Splenomegaly
  • *Dilated abd veins
  • Spider angiomas
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22
Q

Why does portal HTN happen?

A
  • Scarring in liver impede blood flow –> increase pressure in portal vein
  • Blood backs up, causing shunting of blood around liver –> increased pressure in surrounding vessels
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23
Q

Ascites

A

Abnormal accumulation of protein-rich fluid in peritoneal cavity

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24
Q

Ascites presentation

A
  • Abd distension
  • Edema in lower extremities
  • SOB
  • N/V
  • Pleural effusions d/t exchange of fluid across diaphragm into pleural space
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25
Q

Why does ascites happen?

A
  • Portal HTN –> high press –> accumulation of substances –> confused kidney so hold onto fluid
  • Contributing factor = decreased albumin
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26
Q

Ascites treatment

A
  • Sodium restriction (< 2g/day)
  • Diuretics (spironolactone & furosemide)
  • Paracentesis (removal of ascites via needle)
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27
Q

Hepatitis

A

Inflammation prevents normal liver function
- Limited ability to detoxify substances
- Decreased prod of proteins & clotting factors
- Inability to store vitamins, fat & carbs

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28
Q

Hepatitis risk factors

A
  • Hep virus (acute or chronic)
  • Alcohol (chronic)
  • Prescribed meds (acute): statins, phenytoin, isoniazid, anabolic steroids
  • OTC meds (acute): NSAIDs, Acetaminophen
  • Toxins (acute)
  • Autoimmune (acute)
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29
Q

Hep A Virus

A
  • Acute
  • Vaccine available
30
Q

Hep A transmission

A
  • Fecal
  • Oral
  • Contaminated food/water
  • Close contact w infected persons
31
Q

Hep B Virus

A
  • Acute/chronic
  • Vaccine available
32
Q

Hep B transmission

A
  • Blood
  • Bodily fluids
  • Vertical transmission
33
Q

Hep C virus

A
  • NO vaccine
  • Acute/chronic
34
Q

Hep C transmission

A
  • Blood
  • Bodily fluids
  • Vertical transmission
35
Q

Cirrhosis

A

Chronic disease of liver causes: cell destruction, fibrosis, scarring
Irreversible

36
Q

Cirrhosis top 3 causes

A
  • Chronic HBV/HCV infection
  • Alcohol
  • NASH
37
Q

Cirrhosis liver transplant

A
  • Hep C related cirrhosis is most common reason for transplant
  • Childs Pugh or MELD score
38
Q

Cirrhosis nursing assess

A
  • VS: infection, FVE, FVO
  • Resp: SOB d/t ascites or pleural effusions, pulse ox
  • Peripheral edema
  • Bleed: gums, ecchymosis, epistaxis, petechiae
  • Skin, sclera, urine, stool color
  • Mental status
  • I&O
  • *Acid-base disorders: resp alkalosis (tachypnea, high ammonia, hypoxia), met alkalosis (diarrhea, diuretics)
39
Q

Cirrhosis nursing intervention

A
  • Administer prescribed diuretics & electrolyte replacement: K d/t diuretics, MG d/t ETOH abuse and diarrhea, PHOs d/t diuretics & ETOH abuse
  • Restrict sodium and fluid intake
  • Restrict protein intake
  • HOB & leg elevation
  • Administer vitamin K, blood products, FFP, Cyropercipitate
  • Promote rest & skin integrity: bathe in tepid water, emollients
40
Q

Cirrhosis pt education

A
  • Disease process
  • Dietary & fluid restrict
  • No alc intake
  • Meds metabolized by liver or herbs & supplements
  • Diet and nutrition; adequate calories
  • Bleeding precautions
41
Q

Liver cancer transplant

A

Development of small localized HCC in cirrhotic liver –> move up pt in transplant list

42
Q

Liver CA surgical intervention

A
  • Partial hepatectomy
  • Reserved for 1-4 small liver metastases in setting of no other metastatic disease in body
43
Q

Liver CA nursing assess

A
  • Pain & advocate for pain control
  • Psychosocial issues: anxiety, fear, depression
  • Therapeutic side effects: neutropenia, skin alterations, N/V, etc.
44
Q

Liver CA pt teaching

A
  • Explain CA therapies
  • Potential side effects & complications
45
Q

Cholecystitis

A

Inflamm of gallbladder caused by obstructed bile flow
- Calculous cholecystitis: stones present
- Acalculous cholecystitis: NO stones

46
Q

Cholecystitis risk factors

A
  • Increased age
  • Female > male
  • European descent > African descent
  • Obesity
  • Rapid weight loss or weight loss surgery
  • Diet high in saturated fats
  • Pregnancy (elevated progesterone)
  • Meds: estrogen, octreotide, cholesterol-lowering meds
47
Q

Calculous cholecystitis

A
  • Vary in size (pea - softball), number (single - multiple)
  • Vary in composition: cholesterol (most common), pigmented (excess bilirubin), mixed (combo of both)
  • Most found blocking cystic duct or common bile duct = choledocholithiasis
48
Q

Acalculous cholecystitis

A

Biliary stasis (bile flow stops or is reduced) d/t:
- Decreased gallbladder contraction
- Sphincter of Oddi spasms

  • Possibly r/t sepsis, surgery, DM
  • D/t factors that stop release of cholecystokinin (hormone activated by eating that causes gallbladder to contract)
49
Q

Cholecystitis surgical treatment

A
  • Laparoscopic cholecystectomy
  • T-tube (biliary drainage tube)
50
Q

Laparoscopic cholecystectomy

A
  • General anesthesia
  • Several small incisions in abdomen
  • CO2 gas instilled in abd for visualization
  • Laparoscope (small thin telescope) and surgical instruments inserted thru incisions to remove gallbladder
51
Q

T-tube (biliary drainage tube)

A

If stones present in common bile duct, monitors bile drainage + connected to drainage bag to make a closed system

52
Q

Cholecystitis nursing assessment

A
  • VS: increased temp & decreased BP = inflamm & infection, tachypnea = pain & anxiety
  • Pain
  • Skin turgor: dehydration
  • Abd assessment: rebound tenderness, guarding, +Murphy’s sign, rigid abd muscles
  • Stool: clay-colored stools, do they float or are they oily (steatorrhea)
  • I&Os
  • LFTs high, BUN/Cr high, K low, WBC high
53
Q

Cholecystitis nursing intervention

A

Preoperative:
- Maintain NPO
- Administer IV fluids & meds (abx, pain meds, antiemetics)
- Semi-fowler position

Post-operative:
- Cough & deep breathing to prevent atelectasis
- Mobility, monitor incision sites for infection

T-tube care:
- Empty drainage bag as necessary
- Skin care

54
Q

Cholecystitis pt teaching

A
  • S&S of infection, jaundice
  • Pain med education
  • Constipation prevention, low-fat diet
  • Shower instead of bathing, timing to first shower
  • When to remove bandages
  • Activity level: no heavy lifting
  • No driving while on narcotic

T-tube:
- Care of insertion site, monitor bile color and amount, assess for jaundice

55
Q

Acute pancreatitis

A
  • Mild to severe
  • Severe cases of often present w life-threatening complications
  • Acute pancreatitis is reversible
  • Common causes: gallstones, alcohol, surgery
56
Q

Chronic pancreatitis

A
  • Chronic dz
  • Irreversible
  • Alteration of exocrine and endocrine function of pancreas
  • Incidence increases w age
  • Common causes: prolonged alcohol use, cystic fibrosis, hyperlipidemia/hypertrigylceridemia
57
Q

Acute pancreatitis

A

Inflamm of pancreas caused by release of pancreatic enzymes that “autodigest” pancreas and tissue

58
Q

Acute pancreatitis risk factors

A
  • Gallstones: women > men, gallstones obstruct bile duct and area where common bile duct pancreatic duct empty into dudoenum
  • Alc: men > women, 1/3 of all cases, usually after binge drink

Other causes:
- Trauma
- Surgery
- Bile duct abnormalities
- Medication reactions
- Infectious organisms

59
Q

Acute pancreatitis clinical manifestations

A
  • *Sudden severe epigastric pain in LUQ, mid-abd, radiation to back shoulder & blades
  • *Signs of severe acute pancreatitis Grey Turner’s sign: flank bruising d/t leaking exudate and blood
  • *Cullen’s sign: umbilicus bruising indicating hemorrhage, inflamm & tiss damage
60
Q

Acute pancreatitis nursing assess

A
  • VS: increased T, HR, tachypnea, low BP
  • Oxygen status: pleural effusion
  • Pain
  • Abd assess: rebound tenderness, guarding, rigid abd muscles
  • *Grey turner’s sign or Cullen’s sign
  • *Serum amylase high, serum glucose high, hypocalcemia
61
Q

Acute pancreatitis nursing intervention

A
  • Maintain NPO status
  • IV fluid administration
  • Provide enteral nutrition per orders
  • Administer ordered meds: analgesics, antiemetics, histamine blockers/PPIs, antispasmodics, sedatives
  • Encourage cough and deep breathing
62
Q

Acute pancreatitis pt education

A
  • *Dz symptoms, progression, diagnostic procedures, interventions
  • *Abstain from alc
  • Abstain from smoking
  • Nutritional counsel, low-fat diet, small freq meals, vitamin supplements
  • Med education
63
Q

Chronic pancreatitis risk factors

A

*Heavy alc consumption = #1 cause

Other risk factors:
- Age
- African American race
- Hereditary disorder of pancreas
- Cystic fibrosis
- Hypercalcemia, hyperlipidemia, hypertriglyceridemia

64
Q

Chronic pancreatitis

A

Inflamm cause release of pancreatic enzyme –> autodigestion of pancreas for prolonged time –> fibrosis, loss of normal pancreatic function

65
Q

Chronic pancreatitis clinical manifestations

A
  • Upper abd LUQ pain that radiates to back
  • Pain worsens after overeating or drinking (especially alc)
  • N/V
  • Weight loss despite regular eating pattern
  • Diarrhea
  • Pale/clay-colored stools
  • Steatorrhea or oily stools
66
Q

Chronic pancreatitis nursing assess

A
  • Vital signs + weight
  • Labs: blood gluc, amylase, lipase, LFTs
  • Pain & abd exam
  • Jaundice: skin, sclera, stool
67
Q

Chronic pancreatitis nursing interventions

A
  • Administer meds as ordered: pancreatic enzymes, GI prophylaxis
  • Pain relief measures
  • Nutritional eval + consult
68
Q

Chronic pancreatitis pt teaching

A
  • Avoid alc
  • Do not chew pancreatic enzymes (extended-release formulation)
  • Low fat diet
  • Avoid foods irritating gastric lining
  • Alc and smoking cessation programs
69
Q

Pancreatic CA

A
  • Ductal adenocarcinoma
  • Neuroendocrine tumors
  • Insulinomas
  • Glucagonomas
70
Q

Pancreatic CA risk factors

A

*Exact cause unknown

High associations:
- Cigarette smoking
- High-fat diet
- Consumption of meats, fried foods, refined sugars, nitrates
- Diabetes
- Chronic pancreatitis
- Family hx of pancreatic CA
- Ashkenazi Jewish descent
- African American race
- Age > 60 yrs
- Men > women

71
Q

Pancreatic CA medical/nursing management

A
  • Pain: opioids, nerve blocks
  • Exocrine/endocrine: insulin, pancreatic enzymes
  • Biliary obstruct: endoscopic stenting procedures to restore bile flow
  • Weight loss: high calorie diet, appetite stimulants
  • Palliative care
  • Psychosocial/spiritual support

Locally advanced unresectable dz:
- Palliative concomitant chemo + radiation therapy

Metastatic dz:
- Palliative systemic chemo + investigational chemo

72
Q

Pancreatic CA nursing management

A
  • Pain management (PCA) + assess
  • *NG tube to low suction: DO NOT MANIPULATE. Could disrupt anastomosis.