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155 Cards in this Set

  • Front
  • Back
Hep A
- fecal oral (food or drinking water)
- In feces 2 or more weeks before onset of symptoms
- Can be in stool up to 1 week after jaundice starts
Chart of Hep A
- stool for 2 weeks first (incubation, no S/S)--> most contagious
-Anti HAV IgM in serum and stool becomes negative, signs and symptoms present (jaundice, increased ALT--> acute hepatitis within last 12 months)
- Anti HAV IgG shows immunity and is sign of past infection
* no chronic carrier state
Hep B
- bloodborne and body fluids
- can live on dry surface for 7 days
- kissing and sharing food items may spread via saliva
**more infectious than HIV
3 hep B antigens
Surface (HBsAg) (if have more than 6-12 months after infection = chronic hep B)
Core (HBcAg)
E (HBeAg)
Hep B chart
- Incubation period- no signs or proof of disease but still contagious (like 2 months)
- Antigens are highest before S/S show
- Antigens start going down when S/S show (jaundice, increased ALT)
- Anti HBc IgM- active hepatitis
-Anti HBe month later
- Anti HBs- IgG = immunity or past HBV infection
- HBc-IgG indicative of past infection
Chronic HBV
Antigen HBsAg for longer than 6-12 months = chronic carrier
- contagious, can transmit virus
- may have normal or elevated liver enzymes
Hep C
- used to be blood transfusion
- IV, sexual, body piercing, tattoos (additional data needed), hemodialysis, perinatal, occupational exposure
- some can't identify source
Patho of hepatitis
1) During acute infection, cytotoxic cytokines and natural killer cells cause liver damage
2) cause lysis of hepatocytes
3) cell necrosis
4) proliferation and enlargment of kupfer cells
5) inflammation of periportal areas --> interrupt bile flow
6) cholestasis (stagnant bile) --> cholecystitis
7) Widespread inflammation of the liver tissue
8) liver cells can regenerate over time if no comps occur
Systemic effects of antigen-antibody complex/compliment
- Rash
- Angioedema
- Arthritis
- Fever
- Malaise
- Cryoglobulineremia (proteins in blood)
- Glomerulonephritis
- Vasculitis
Acute hep manifestations
- last 1-4 months
- icteric or anicteric (symptoms or no symptoms)
- Incubation/acute:
-- malaise
-- Anorexia --> can even lose a lot of weight
-- Fatigue
-- Nausea
-- Occasional vomiting
-- Abdominal discomfort (RUQ)
-- HA
-- low grade fever
-- loss of smell
-- arthralgia
-- skin rashes
-- hepatomegally and tender
-- Splenomegally
-- lymphadenopathy
-- Jaundice (bilirubin in tissues) --> fever subsides when jaundice occurs
-- Dark urine (increased bilirubin)
-- light, clay stool
-- Bilirubin in blood
-- Pruritis (bile salts)
Convalescent phase
When jaundice goes away bu
- last for weeks to months (2-4 months)
- malaise
- fatigue
- hepatomegally stays for several weeks but splenomegally subsides
Hep A, B, C symptoms comparison
- A- almost all cases are resolves, absence of jaundice does not mean recover, acute, mild flu like symptoms
- B and C usually become chronic
C- usually asymptomatic, persistence, chronic
- most with acute recover with no problems
Anicteric hepatitis
Hep without jaundice, high percentage like this
Complications of Hep
- Fulminant hepatic failure (severe impairment and necrosis--> transplant/death)
- Chronic hep (surface antigen for longer than 6-12 months)
- Cirrhosis (fibrosis)
- Hepatocellular carcinoma
Alkaline phosphatase
Increased = impaired excretory function of liver
AST- aspartate aminotransferase, ALT Alanine, y-glutamyl transpeptidase (GGT)
show liver damage
Bed rest
Bed rest may be ordered while pt symptomatic, alternating periods of activity and rest are adequate
Treatment for acute viral hep
- no spcific tx
- Hep C- interferon
- adequate nutrition
- can usually be managed at home
- possible bed rest
- caution with hepatotoxic drugs
- antiemetics
- benadryl
Antiemetics for hep
- Dramamine, and Tigan
Hipnotic/sedative for hep
Treatment goals of Chronic Hep B
- focus is on:
--decreasing viral load
-- decreasing enzyme levels
-- decreasing rate of disease progression
-- decrease rate of drug resistant HBV
Long term goals for chronic Hep be treatment
- prevention of cirrhosis and hepatocellular cancer
- not all pts respond to current therapeutic regimens
a-interferon symptoms
- flulike symptoms
- depression
- hair thinning
- diarrhea
- insomnia
how to inject a-interferon
SUBCU! conventional- frequently (3x week) or long acting/pegylated (1x/week)
- Nucleoside analog
- taken for a yr for Hep B
- nucleoside analogs for Hep B
Treatment goals for Hep C
- eradicating virus
- reducing viral load
- Decreasing progression of disease (like liver carcinoma)
Meds for Hep C
- a-interferon and Ribavirin
3 nursing goals for hep
- relieve discomfort
- resume normal activities
- return normal liver function without complication
Hep A prevention
- wash hands*** (most important)
- Vaccine- over 12 months, IM deltoid (best protection)
- HAV and HBA given, 0, 1 month, and 6 months
Hep A booster
- 6-12 months after first injection
End stage renal failure should receive
Hep B vaccine before starting dialysis
Immune globulin
tricks body into thinking it has immunity, but you have to catch person at time of exposure

Hep B within 24 h
Successful vaccination of Hep B
10 mlU/mL or greater
Hep C prevention
- no vaccine
- no immuno globulin or antiviral for psot exposure rec
- screen of blood, organ, tissue donors
- infection control and precaution
- modify high risk behavior
Nursing Management after
- rest
- jaundice
- small, frequent meals
- dietary teaching (easier to eat in morning)
- carbonated beverages
- avoid hot and cold
- assessment for complications
** regular follow-ups for at least 1 year after dx to make sure they don't go in carrier state
Home education
- avoidance of alcohol
- medication education (a interferon subcu, side effects)
- give acetaminophen 30-60 min before a-interferon injection to control s/e
Ribavirin side effects
- anemia
- anorexia
- cough
- rash
- pruritis
- dyspnea
- taratogenic (careful with young women)
- insomnia

taken orally twice daily
Pegylated a-iterferon with ribavirin
- Rebetol and Copegrus- once a week
- Nonalcoholic Steatohepatitis
- accumulation of fat in liver (fatty changes in hepatocytes)
- not associated with alcohol, autoimmune disease, or hepatitis
- if progresses and scarring present than can get cirrhosis
NASH has increased risk for
- liver cs and hepatic failure
Risk factors for NASH
- obesity
- Insulin resistance syndromes
- DM
- Hypertriglycerides
- Recent rapid weight loss (fat released quickly into body)
- Meds
Meds associated with NASH
- cardizem
- Tamoxifen
- Amidoarone
- corticosteroids
labs for NASH
- increase bili
- increase ALT/AST (2-4xlarger)
- drop in albumin with progression
- elevated PT
Clinical management of NASH
- weight loss
- glucose control
- elimination of alcohol
- elimination of hepatotoxic meds
- Heart healthy diet
- twice as common in men
- insidious, prolonged course
Alcohol cirrhosis
"portal or nutritional" cirrhosis

Alcohol damage -->
1) fat accumulation in liver
2) scare formation --> can't expand but blood still going in --> back up --> portal hypertension --> verisces (esophageal, rectal)

- may have nutritional problems cause substituting alcohol for food
Postnecrotic cirrhosis
- complicationof viral, toxic, ideopathic hepatitis + alcohol
- bands of scare tissue form
- post hep B and hep C
Biliary cirrhosis
- associated with chronic biliary obstruction (stones)
- diffuse fibrosis of liver
- jaundice
Cardiac cirrhosis
- from long standing Right sided heart failure (backs up into portal vein)
Early Clinical Manifestations of Cirrhosis
- insidious
- anorexia
- dyspepsia
- flatulence
- N/V
- change in bowel habits or abdominal pain
- fever
- Lassitude (fatigue)
- weight loss
- enlarged liver or slpleen
Cirrhosis diet
- high in calories (3000 kcal/day)
- Increase carbs
- moderate to low fat
- protein restriction rarely justified (need protein at beginning esp, but may be restricted end stage cause of ammonia)
Late cirrhosis S/S causes
- hepatocellular failure
- portal HTN
late manifestations of cirrhosis
- jaundice
- peripheral edema
- ascites
- skin lesions
- hematologic disorders
- endocrine disturbances
- peripheral neuropathis
Jaundice results from
- liver can't conjugate or excrete it
- functional decline of liver cells
- compression of bile ducts
- usually present with end stage liver
- pruritis can develop
Skin lesions
- increased estrogen from liver inability to metabolize

- spiderangioma
- palmar erythema

- could get build up of steroidal hormones also
Endocrine disorders
Aldosterone increase from adrenal cortex and affects testes, ovaries --> fluid retention --> BP up

- alteration in hair distribution due to increased estrogen
- gynecomastia
- testicular atrophy
- Impotence
- Hyperaldosteronism (sodium retention, potassium loss)
Hematologic disorders
- thrombocytopenia
- leukopenia
- anemia
- splenomegally (back up of protal vein causes)
- bleeding tendencies
Peripheral neuropathy
- deficiences of thiamine, folic acid, and vitamin B12
Portal HTN
- unique to cirrhosis, can't expand anymore and blood back up
- esophageal to rectum varices
- increased resistance to blood flow in liver
caput medusae
ring of varices around umbilicus
most life threatening complication of cirrhosis
- bleeding varices
Hepatic encephalopathy
- elevation in ammonia levels (product of protein metabolism)
- asterixis
- suggestive of end stage
Characteristics of Portal hypertension
- Increased venous pressure in portal circulation
- Splenomegally
- Ascites
- large collateral veins (esp esophagus but can be anywhere)
- systemic HTN
- large % of cirrhosis pts have varices
Esophageal hemorrhage triggers
- alcohol
- poorly chewed food (sharp chips)
- acid reflux
- increased intraabdominal pressure (sneezing, vomiting, val salva)
- avoid aspirin, irritating foods that promote bleeding
- respiratory infection (don't want to cough or sneeze)
purple, back stools (bleeding above stomach)
hemorrhage- blood vomit
Supportive measure for acute bleeding
- fresh frozen plasma (with clotting factors)
- packed RBCs
- Vitamin K
- H2, proton pump (---prazole, prilosec)
- Neomycin (PO)
- Lactulose to prevent encephalopathy

- lactulose also causes diarrhea
Endoscopic ligation
- banding of varices
- few complications than sclerotherapy (inject varices to strengthen them)
Balloon tomponade
- put in by gastroenterologist
- controls hemorrhage by compression
- Sengstaken- Blakemore tube
- can develop necrosis of surrounding tissues
- airway issues also
Prevention of recurrent bleeding
- Beta blockers
- Inderol/ Propanolol if not asthma pt ***caution with this

- high risk of recurrent bleeding with higher mortality with each repeat
Balloon tompanade care
- label each lumen to avoid confusion
- deflate baloons for 5 minutes every 8-12 hours per institution policy to prevent necrosis
- saline lavage (iced)/ NG suction to remove blood
- monitor for complications
- scissors at bedside
- semi fowler postion
- oral/nasal care
- explanation of procedure
- check for patency
- positiong balloon verified y x-ray
Most common complication for balloon tompanade
aspiration pneumonia
Endoscopic scleropathy agent
- thromboses and obliteates distended veins
- for acute and chronic
Varices nursing management
- signs and symptoms of bleeding (H/H)
Shunting for varices
- used more after second major bleeding episode
- surgical v non-surgical
- associated with poor outcomes so it is last choice
TIPS (Transjugular intrahepatic portosystemic shunt)
- non-surgical procedure
- shunt between systemic and portal venous system
- redirect portal blood flow
- decreaess portal venous pressure and decomp varices
- increases risk for encephalopathy
decreased colloidal oncotic pressure from impared albumin synthesis

Increases portacaval pressure from portal HTN

- ankle and sacral
Ascites diet
- high carn, low Na (less than 2g)
- Diuretics
- Paracentesis
- I/O
- Daily weights
- Abdominal girth (kneeling if possible)
- extremities measurment
- void immediately beofre
- high fowlers or side of bed
- monitor for electrolyte imbalance
- dressin bleedagin and leakage
- done with abd pain or respiratory problems from ascites
Perioneovenous shunt
- reinfusion of ascitic fluid from abdomen to vena cava
- for ADVANCED liver disease
- not first line of therapy
Complications of Perioneovenous shunt
thrombosis, infection, fluid overload, DIC
get ammonia level!
- specific for encephalopathy
Goal for encephalopathy management
decrease ammonia formation

- sterilize with oral antibx (neomycin)
- lactulose traps NH2 in gut (traps ammonia in gut) and diarrhea helps it out
- cathartics/enemas
Hepatorenal syndrome
serious complication of cirrhosis

- functional renal failure with azotemia (hihg nitrogen, high BUN)
- oliguria
- intractable ascites
- no structual abnormalities of kidney
- decreased blood flow to kidney and can cause renal failure
Nursing Care of hepatic encephalopathy
- maintain safe environment
- assess carefully (responsiveness, sensory and monitor abnormalities, acid/base balance, effect of treatment measures)
- neurologic status q2h
- prevention of constipation (lactulose with solve this) and don't want them to strain
- limits physical activity
- control hypokalemia
- ensure proper nutrition
Pancreatitis most common in
- middle aged mend and women
- African American 3x more likely
Primary factors for pancreatitis
- biliary tract disease (gallbladder)
- alcoholism
Less common causes of acute pancreatitis
- trauma (post surgical, abd)
- viral (mups, HIV, coxsacki)
- penetrating duodenal ulcer
- cysts
- idopathic
- ancesses
- CF
- Kaposis's sarcoma
- metabolic disorders
-vascular disease
- post op GI
- meds (croticosteroids, thiazide, oral contraceptives, sulfa, NSAIDs)
Predominant symptoms of pancreas
- left upper quadrant pain
- medepigastrium
- commonly radiates to the back (its retroperitoneal)
- sudden
- severe, piercing, steady
- aggravated by eating
- not relieved by vomiting
Acute pancreatitis S/S
- flushing
- cyanosis
- Dyspnea
- Edema
- N/V
- bowel sounds decreased/absent --> have to listen for LONG time
- low grade fever (if sepsis could be higher)
- leukocytosis
- hypoTN (septic shock)
- tachycardia
- Jaundice
- Abdominal tenderness (pain!!)
- Abdominal distention
- Abnormal lung sounds, pleural effusions (crackles)
- Discoloration of abdominal wall (seepage of bloos stained exudate from pancreas in severe cases, full of infection)
- cavity continuous with surrounding pancreas
- filled with necrotic products and liquid
- may perforate or rupture into stomach
What lab is elevated in psuedocyst
- serum amylase VERY elevated

-lipase more specific
Pancreatic abscess s/s
upper abdominal pain
abdominal mass
high fever
requires surgical drainage (last thing what to do is take to OR!)
Pulmonary complication sof pancreatitis
- result from passage of pancreatic enzymes from peritoneum through transdiaphragmatic lymph
- pleural effusion
- atelectasis (don't want to cough and deep breath)
- Pneumonia
Cardiovascular complications of pancreatitis
Electrolyte problem of pancreatitis
tetany from hypocalcemia
- cause not understood
S/S of hypocalcemia
- everything uo
- CNS irritability
- enhanced reflexes
- laryngeal aspasm
tressou, chovsteks
Serum amylase
- elevated 24-72 hours
- not as specific, can go up with salivary or other hepatobilliary problems
Serum lipase
MOST specific for pancreatitis
Labs for pancreatitis
serum amylase
serum lipase
2 hour urinary amylase and renal amylase clearance
blood glucose
serum calcium (want ionizes and total calcium, if protein is low there will be more free calcium)
ERCP/ Endoscopic restrograde cholangeiopancreatopgraphy
gallbladder and pancreas
MRCP/ magentic resonance cholangiopancreatopgraphy
pancreas and hepatic system
Clinical goals of acute pancreatitis
- pain relief
- prevent or alleviate shock
- decrease pancreatic secretions (NPO, possible NG tube)
- F&E balance (calcium)
- Glucose regulation (beta cells, can get type 1 afterwards)
- nutritional support
- removal of precipitating cause (gallbaldder, stone, etc.)
* If secondary to alcoholism or pseudo cyst recovery is longer and harder
Conservative therapy for pancreatitis
Supportive care
- aggressive hydration
- pain management (IC morphine, antispasmadic agent)
- manage metabolic complications (have less insulin, giving them TPN at least 10% dextrose and they have glucose response, so higher glucose)
- minimizing pancreatic stimulation
Fluids for shock
Plasma or plasma volume expanders (dextrane or albumin)

- ongoing hypotention management
F& E imbalance fluid
Lactated ringer's solution
Suppression of pancreatic enzymes
- NG suction
Preventing Infection
- leading cause of mortality and morbidity
- monitor pt closely so antibx can be started asap if needed, preventive antibx are controversal
Treatment of ongoing hypotension
Dopamin (Intropin)
Peritoneal lavage or dialysis
- severe cases
- remove kinin and phospholipase A exudate
Surgical Intervention for pancreatitis
- if gallstones
- uncertain dx
- unresponsive to conservative therapy
- abscess, pseudocyst, severe peritonitis
Surgical progression tx
gallstones --> ERCP --> endoscopic sphinectomy --> laparoscopic cholecystectomy (wouldn't do if sepsis or have matter in belly, would want to have an OPEN surgery
- percutaneous drainage of pseudocyst
Drug therapy for acute pancreatitis
- IV morphine
- nitroglycerine- relaxes smooth muscles of biliary sphincters (spasm from extra enzymes)
- Antispasmatics (Bentul and Pro-Banthine)
- Carbonic anhydrase inhibitors (Diamox)
- Antacids
- H2 blockers or PP inhibitors
What does Diamox do
reduced bicarb concentration of pancreatic enzymes so pt doesn't get metabolic alckalosis from high bicarb thats in pancreatic enzymes
Nutritional supports
- NPO initially to reduce secretions (could be short to months long, depends on degree of illness)
- may require TPN
- IV lipids (if used)
- Supplemental ADEK (fat soluble vitamins) (decreasing K will cause increased PT/INR)
- monitor glucose
- small frequent meals
H2 receptor antagonist
Proton pump inhibitors
If giving IV lipids
- monitor triglycerides (they are already up before this!)
Diet for Acute pancreatitis
High carb
low fat
high protein

--> less likely to induce pancreatic enzyme production

- bland diet
- no caffeine or alcohol
Nursing care for acute pancreatitis
- monitor vitals
- I&O
- IV fluids
- Observe for side effects of medications
- Assess respiratory function (decreased breath sounds, pt saying short of breath, decreased pulse ox**)
- Pain assessment and management
- F&E balance
Positions for pain management
- side lying with HOB elevated 45 degrees
- knees up to abdomen
Nursing care for F&E balance of acute pancreatitis
- blood glucose monitoring
- monitoring for signs of hypocalcemia
--- tetany (jerking, irritability, twitching)
---numbess around lips/fingers
--- positive Chvostek (face) and Trousseau sign (hand)
***If don't have calcium level, ask for one, they can have seizures or resp arrest!
- monitor for hypomagnesemia --> cardiac arrythmias (PVCs)--> pt should be on telemetry
Nursing Implementation
- NG tube care
- frequent oral/nasal care
- observe for signs of infection
- wound care
- TPN protocol
- Central line care
- Observe for paralytic ileus, renal failure, mental changes (hypoxia, DTs)
fatty stools
- look frothy and are foul smelling
Chronic pancreatitis
continued inflammation and fibrosis, strictures and calcifications form (like liver cirrhosis)

- may follow acute pancreatitis
- may occur with no hx of acute condition

two types:
- chronic obstructive pancreatitis
- chronic calcifycing pancreatitis
Obstructive pancreatitis causes
- most common cause is inflammation of sphincter of oddi from cholelithiasis (gallstones)

- cancer of ampulla of vatar, duodenum, or pancreas
Chrocnic calcifying pancreatitis causes
- inflammation
- sclerosis- mainly in the head of the pancreas and around the pancreatic duct

- most common type of chronic pancreatitis
Clinical manifestations of chronic pancreatitis
- Abdominal pain (same areas as acute)
- heavy, gnawing feeling, burning and cramp-like
- abdominal tenderness
- malabsorption with weight loss
- constipation
- mild jaundice with dark urine
- steattorrhea (not making lipase so fatty stool, CF also has this)
- frothy urine/stool
- DM
Complications of Chronic pancreatitis
- pseudocyst formation
- bile duct or duodenal obstruction
- pancreatic ascites
- pleural effusion
- splenic vein thrombosis
- pseudoaneurysms
- pancreatic cancer
Diagnosing Chronic pancreatitis
- confirming may be difficult
- based on S/S, labs, and imaging
Lbs in chronic pancreatitis
- serum amylast/lipase may be elevated a little or not at all
- increases serum bilirubin
- increased alkaline phosphatase (bone cx also makes this go up)
Management of chronic pancreatitis
- prevention of attacks (during acute attacks follow acute therapy)
- relief of pain
- control of pancreatic exocrine and endocrine insufficiency
- Bland, low fat, high carb diet
- Bile salts for absorption of fat-soluble vitamins and preventing further fat loss
- control of diabetes/blood sugar
- no alcohol
- Pancreatic enzyme replacement
- acid neutralizing and acid-inhibiting drugs
Pancreatic enzyme replacement
- contain amylase, lipase, and trypsin
- enteric coated
- pancreatin (Viokase)
- pancrealipase (Cotazym)
Surgery for chronic pancreatitis
- indicated when billiary disease is present or if OBSTRUCTION or pseudocyst develops

- divert bile flow or relieve ductal obstruction
Focus of nursing care for chronic pancreatitis
care and health promotion

- dietary control (no alcohol)
- control diabetes
- taking pancreatic enzymes
- pt and family teaching
Metastasize areas for pancreatic cx
- liver, brain, bone
Increased risk for pancreatic cx
- DM
- Chronic pancreatitis
- Smoking
- Family hx
- Chemical exposure
- High fat diet
Clinical manifestations of pancreatic cancer
Similar to chronic pancreatitis
- rapid weight loss
- dull aching abdominal pain (upper back and epigastium)
- anorexia
- N/V
- Jaundice
Tumor marker Pancreatic cancer diagnosis

May be elevated in other biliary disease as well
Whipple procedure
- radical pancreaticoduodenectomy
Treatment for pancreatic cx
- radiation for pain management (palliative)
- Chemotherapy (may be used but poor response, may be palliative)
Nursing care for pancreatic cancer
- similar to care of pt with pacreatitis
- pain relief
- nutrition support
- attention to psych social issues (grief)
inflammation of the gallbladder
stone in gallbladder
Clinical manifestations of total bile flow obstruction
- obstructive jaundice (bile isn't flowing into duodenum)
- Dark amber urine, which foams when shaken
- No urobiligen in urine
- clay-colored stools
- pruritis
- intolerance for fatty foods (N, sensation of fullness, anorexia)
- bleeding tendencies (decreased K absorption)
- Steatorrhea (no bile salts in duodenum which prevents fat emulsion and digestion)
S/S of cholecystitis
- indigestion
- pain, tenderness in right upper quadrant--> may refer to right shoulder/scapula
- N/V with pain, restlessness, diaphoresis
- leukocytosis
- fever
biliary colic
spasms and pain caused from stone lodged in gallbladder ducts, usually a steady pain

- tachycardia, diaphoresis, prostration
- pain usually 3-6 hours after a high fat meal or when pt lies down
Gallbladder labs
AST, ALT, lipase, amylase (if pancreatic involvement), alkaline phosphatase, WBCs
Cholelithiasis interventions
- bile acids to dissolve stone
- don't normally treat gallstones with drugs cause removal is so successful
- ERCP- endo retrograde cholangeoppancreatography
- Endoscopic stone removal
- ESWL (extracorpeal shock wave litthotripsy)
Cholecystitis interventions
- pain control
- fluid balance
- prevention of infection with antibiotics
- NG if N/V, gastric decompression
-NSAIDs, anticholinergics to decrease secretion and counteract muscle spasms
What position helps after laproscopic cholecystectomy
- Sims position (left side, right knee flexed), helps get gas pocket away from abdomen
T tube care
protect skin if draining large amounts

- it is connected to a closed gravity drainage system
open cholescystectomy post op
- no heavy lifitng for 4-6 weeks
- sometimes told to remain on low fat diet for 4-6 weeks
- possible weight loss program
- most can tolerate regular diet, but should avoid excess fats