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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) |
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Hep B chart
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- 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 |
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Chronic HBV
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Antigen HBsAg for longer than 6-12 months = chronic carrier
- contagious, can transmit virus - may have normal or elevated liver enzymes |
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Hep C
|
- used to be blood transfusion
- IV, sexual, body piercing, tattoos (additional data needed), hemodialysis, perinatal, occupational exposure - some can't identify source - |
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Patho of hepatitis
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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 |
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Systemic effects of antigen-antibody complex/compliment
|
- Rash
- Angioedema - Arthritis - Fever - Malaise - Cryoglobulineremia (proteins in blood) - Glomerulonephritis - Vasculitis |
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Acute hep manifestations
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- 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) |
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Convalescent phase
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When jaundice goes away bu
- last for weeks to months (2-4 months) - malaise - fatigue - hepatomegally stays for several weeks but splenomegally subsides |
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Hep A, B, C symptoms comparison
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- 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 |
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Anicteric hepatitis
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Hep without jaundice, high percentage like this
|
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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 |
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Alkaline phosphatase
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Increased = impaired excretory function of liver
|
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AST- aspartate aminotransferase, ALT Alanine, y-glutamyl transpeptidase (GGT)
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show liver damage
|
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Bed rest
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Bed rest may be ordered while pt symptomatic, alternating periods of activity and rest are adequate
|
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Treatment for acute viral hep
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- no spcific tx
- Hep C- interferon - adequate nutrition - can usually be managed at home - possible bed rest - caution with hepatotoxic drugs - antiemetics - benadryl |
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Antiemetics for hep
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- Dramamine, and Tigan
|
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Hipnotic/sedative for hep
|
benadryl
|
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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 |
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Long term goals for chronic Hep be treatment
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- prevention of cirrhosis and hepatocellular cancer
- not all pts respond to current therapeutic regimens |
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a-interferon symptoms
|
- flulike symptoms
- depression - hair thinning - diarrhea - insomnia |
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how to inject a-interferon
|
SUBCU! conventional- frequently (3x week) or long acting/pegylated (1x/week)
|
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Epivir
|
- Nucleoside analog
- taken for a yr for Hep B |
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Hepsera
|
- nucleoside analogs for Hep B
|
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Treatment goals for Hep C
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- eradicating virus
- reducing viral load - Decreasing progression of disease (like liver carcinoma) |
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Meds for Hep C
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- a-interferon and Ribavirin
|
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3 nursing goals for hep
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- relieve discomfort
- resume normal activities - return normal liver function without complication |
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Hep A prevention
|
- wash hands*** (most important)
- Vaccine- over 12 months, IM deltoid (best protection) |
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Twinrix
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- HAV and HBA given, 0, 1 month, and 6 months
|
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Hep A booster
|
- 6-12 months after first injection
|
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End stage renal failure should receive
|
Hep B vaccine before starting dialysis
|
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Immune globulin
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tricks body into thinking it has immunity, but you have to catch person at time of exposure
Hep B within 24 h |
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Successful vaccination of Hep B
|
10 mlU/mL or greater
|
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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 |
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Nursing Management after
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- 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 |
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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 |
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Ribavirin side effects
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- anemia
- anorexia - cough - rash - pruritis - dyspnea - taratogenic (careful with young women) - insomnia taken orally twice daily |
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Pegylated a-iterferon with ribavirin
|
- Rebetol and Copegrus- once a week
|
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NASH
|
- 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 |
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NASH has increased risk for
|
- liver cs and hepatic failure
|
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Risk factors for NASH
|
- obesity
- Insulin resistance syndromes - DM - Hypertriglycerides - Recent rapid weight loss (fat released quickly into body) - Meds |
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Meds associated with NASH
|
- cardizem
- Tamoxifen - Amidoarone - corticosteroids |
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labs for NASH
|
- increase bili
- increase ALT/AST (2-4xlarger) - drop in albumin with progression - elevated PT |
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Clinical management of NASH
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- weight loss
- glucose control - elimination of alcohol - elimination of hepatotoxic meds - Heart healthy diet |
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Cirrhosis
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- twice as common in men
- insidious, prolonged course |
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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 |
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Postnecrotic cirrhosis
|
- complicationof viral, toxic, ideopathic hepatitis + alcohol
- bands of scare tissue form - post hep B and hep C |
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Biliary cirrhosis
|
- associated with chronic biliary obstruction (stones)
- diffuse fibrosis of liver - jaundice |
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Cardiac cirrhosis
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- from long standing Right sided heart failure (backs up into portal vein)
|
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Early Clinical Manifestations of Cirrhosis
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- insidious
- anorexia - dyspepsia - flatulence - N/V - change in bowel habits or abdominal pain - fever - Lassitude (fatigue) - weight loss - enlarged liver or slpleen |
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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) |
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Late cirrhosis S/S causes
|
- hepatocellular failure
- portal HTN |
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late manifestations of cirrhosis
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- jaundice
- peripheral edema - ascites - skin lesions - hematologic disorders - endocrine disturbances - peripheral neuropathis |
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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 |
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Skin lesions
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- increased estrogen from liver inability to metabolize
- spiderangioma - palmar erythema - could get build up of steroidal hormones also |
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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) |
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Hematologic disorders
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- thrombocytopenia
- leukopenia - anemia - splenomegally (back up of protal vein causes) - bleeding tendencies |
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Peripheral neuropathy
|
- deficiences of thiamine, folic acid, and vitamin B12
|
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Portal HTN
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- unique to cirrhosis, can't expand anymore and blood back up
- esophageal to rectum varices - increased resistance to blood flow in liver |
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caput medusae
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ring of varices around umbilicus
|
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most life threatening complication of cirrhosis
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- bleeding varices
|
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Hepatic encephalopathy
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- elevation in ammonia levels (product of protein metabolism)
- asterixis - suggestive of end stage |
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Characteristics of Portal hypertension
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- 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 |
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Esophageal hemorrhage triggers
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- 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) |
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Melena
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purple, back stools (bleeding above stomach)
|
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Hematemesis
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hemorrhage- blood vomit
|
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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 |
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Endoscopic ligation
|
- banding of varices
- few complications than sclerotherapy (inject varices to strengthen them) |
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Balloon tomponade
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- put in by gastroenterologist
- controls hemorrhage by compression - Sengstaken- Blakemore tube - can develop necrosis of surrounding tissues - airway issues also |
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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 |
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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 |
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Most common complication for balloon tompanade
|
aspiration pneumonia
|
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Endoscopic scleropathy agent
|
Scleromate
- thromboses and obliteates distended veins - for acute and chronic |
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Varices nursing management
|
- signs and symptoms of bleeding (H/H)
|
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Shunting for varices
|
- used more after second major bleeding episode
- surgical v non-surgical - associated with poor outcomes so it is last choice |
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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 |
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Edema
|
decreased colloidal oncotic pressure from impared albumin synthesis
Increases portacaval pressure from portal HTN - ankle and sacral |
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Ascites diet
|
- high carn, low Na (less than 2g)
- Diuretics - Paracentesis - I/O - Daily weights - Abdominal girth (kneeling if possible) - extremities measurment |
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Paracentesis
|
- 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 |
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Perioneovenous shunt
|
- reinfusion of ascitic fluid from abdomen to vena cava
- for ADVANCED liver disease - not first line of therapy |
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Complications of Perioneovenous shunt
|
thrombosis, infection, fluid overload, DIC
|
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Asterixis
|
get ammonia level!
- specific for encephalopathy |
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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 |
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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 |
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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 |
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Pancreatitis most common in
|
- middle aged mend and women
- African American 3x more likely |
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Primary factors for pancreatitis
|
- biliary tract disease (gallbladder)
- alcoholism |
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Less common causes of acute pancreatitis
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- 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) |
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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 |
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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) |
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Pseudocyst
|
- cavity continuous with surrounding pancreas
- filled with necrotic products and liquid - may perforate or rupture into stomach |
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What lab is elevated in psuedocyst
|
- serum amylase VERY elevated
-lipase more specific |
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Pancreatic abscess s/s
|
upper abdominal pain
abdominal mass high fever leukocytosis requires surgical drainage (last thing what to do is take to OR!) |
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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 |
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Cardiovascular complications of pancreatitis
|
hypotension
|
|
Electrolyte problem of pancreatitis
|
tetany from hypocalcemia
- cause not understood |
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S/S of hypocalcemia
|
- everything uo
- CNS irritability - enhanced reflexes - laryngeal aspasm tressou, chovsteks |
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Serum amylase
|
- elevated 24-72 hours
- not as specific, can go up with salivary or other hepatobilliary problems |
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Serum lipase
|
MOST specific for pancreatitis
|
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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) Triglycerides |
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ERCP/ Endoscopic restrograde cholangeiopancreatopgraphy
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gallbladder and pancreas
|
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MRCP/ magentic resonance cholangiopancreatopgraphy
|
pancreas and hepatic system
|
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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 |
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Fluids for shock
|
Plasma or plasma volume expanders (dextrane or albumin)
- ongoing hypotention management |
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F& E imbalance fluid
|
Lactated ringer's solution
|
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Suppression of pancreatic enzymes
|
- NPO
- NG suction |
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Preventing Infection
|
- leading cause of mortality and morbidity
- monitor pt closely so antibx can be started asap if needed, preventive antibx are controversal |
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Treatment of ongoing hypotension
|
Dopamin (Intropin)
|
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Peritoneal lavage or dialysis
|
- severe cases
- remove kinin and phospholipase A exudate |
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Surgical Intervention for pancreatitis
|
- if gallstones
- uncertain dx - unresponsive to conservative therapy - abscess, pseudocyst, severe peritonitis |
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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
|
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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
|
Zantac
|
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Proton pump inhibitors
|
Prilosec
|
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If giving IV lipids
|
- monitor triglycerides (they are already up before this!)
|
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Diet for Acute pancreatitis
|
High carb
low fat high protein --> less likely to induce pancreatic enzyme production - bland diet - no caffeine or alcohol |
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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) |
|
steatorrhea
|
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
|
CA19-9
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) |
|
Cholecystitis
|
inflammation of the gallbladder
|
|
Choleilithiasis
|
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 |