NUR 152: Unit 7-Inflammation/hepatobiliary
Varices tx
*call HCP/RRT= Emergency 1. band ligation or sclerotx 2. ballon tamponade 3. Transjugular intrahepatic portosystemc shunt (TIPS) 4. B blockers, octreotide (somatostatin), vasopression *look for hematemesis or melena
Hepatitis: Dx test 1. ALT 2. AST 3. Alkaline phosphatase 4. serum proteins 5. Serum bilirubin 6. clotting test 7. fibro-sure 8. HCV antibody/HCV RNA 9. fibroscan 10. liver biopsy a) when is liver biopsy contraindicated?
1 & 2. Convert amino acids to proteins; when hepatocytes are damaged, these enzymes leak out causing the serum blood level to rise 3. function r/t liver and bone metabolism 4. albumin might be decreased bc liver isn't synthesizing them properly 5. Might be elevated bc liver isn't conjugating or secreting it into small intestine 6. might be prolonged because liver isnt making clotting proteins 7. biomarker; to assess for fibrosis 8. if HCV antibody is positive in the blood, then tested for chronic hepatitis (HCV RNA) 9. liver ultrasound to determine degree of fibrosis 10. mainly done for chronic hepatitis to determine degree of inflammation, fibrosis or cirrhosis; gold standard; requires consent; monitor for bleeding (liver very vascular) & lay on biopsied side for 30-60 min a) leukemia, poor clotting, anticoagulants or antiplatelets
1. Need __% of liver cells and lobules to function 2. Liver cells can regenerate up to __%
1. 10% 2. 75%
Tx for Hepatitis B 1. acute 2. chronic a) interferon b) Nucleotide/nucleoside analogs
1. Adequate nutrition, rest (decreases metabolic demand on liver), no alcohol; drug tx is reserved for severe HBV 2 a. antiviral, anti-proliferative, immune modulator; reduce viral load; SQ; flu-like s/s; screen for depression; assess CBC & liver fxn tests q 4-6 weeks 2 b. inhibit viral reproduction; mimic building blocks for DNA but are actually faulty so it halts DNA synthesis; long term tx; decrease viral load & serum liver enzymes, decreasing liver damage
Hep B.: symptoms
1. Anorexia 2. N/V 3. fever 4. fatigue 5. RUQ pain 6. Dark urine/light stools 7. joint pain 8. Jaundice
1. HBaAG 2. If HBV antibody is found, what does this mean for the pt?
1. Antigen 2. immunity through vaccine or previous infection
Acute pancreatitis: 1. Why? 2. Labs 3. TX (conservative)
1. Auto-digestion d/t GB disease or excessive alcohol 2. increased Amylase & lipase; hypocalcemia (calcium binds with fatty acids during dat necrosis), leukocytosis, hyperglycemia, hypertryglyceremia, liver fxn tests 3. NPO, may need NG or TPN (decrease pancreatic stimulation), pain meds, PPIs (decrease HCL & therefore pancreatic stimulation), IVF, comfort (flex trunk with knees up to abd or side-lying with HOB raised to 45), check breathing, monitor BG (may need insulin)
Complications of cirrhosis: Portal HTN: 1. Why does it occur 2. signs & symptoms 3. What occurs as compensation? 4. what complication can develop as a direct effect of the compensatory mechanism?
1. Bc with cirrhosis, structural changes occur that lead to obstruction of blood flow causing an increasing in venous pressure within the portal system; blood will back up 2. splenomegaly, large collateral veins, ascites, varices 3. Collateral circulation develops to try to decrease the pressure 4. Esophageal, gastric or hemorrhoidal varices; varicosities develop where collateral & systemic circulation meet
Explain the step of how Bilirubin is excreted
1. Bilirubin is an end-product of RBC destruction (Hgb catabolism) & bone marrow erythropoiesis 2. Bilirubin (unconjugated) binds to albumin to help it travel to the liver as it is fat soluble 3. unconjugated bilirubin is taken to liver where it is conjugated 4. Now conjugated bilirubin is excreted into small intestine (within bile); small amount is secreted into the bloodstream directly from the liver & another small portion may be reabsorbed into the circulation from the small intestine 5. In the intestine, bacterial deconjugation occurs & is converted into stercobilinogen, giving feces its brown color where it is excreted; the portions that make it back into the circulation are excreted (majority) via kidneys, giving urine its yellow color
Laxative (lactulose): 1. Action/use 2. Assessment 3. EO 4. NI 5. Evaluation/SE
1. Decreases pH in colon, inhibiting movement of ammonia into blood, decreasing ammonia levels; tx hepatic encephalopathy 2. assess abd distention, bowel sounds, bowel fxn (color, consistency, amount); Electrolytes & mental status before and during tx 3. decreased ammonia by 20-25%, improbed mental status; 2-3 soft Bm/day 4. Po 3-4x/day; Mix with fruit juice, water or flavored beverages; Give with full glass of water or juice; Increase bulk & fluid; Also can be given as enema 5. belching, abd pain, distention, flatulence, diarrhea; Hyperglycemia in DM pts
Clinical manifestation of cirrhosis: Neurologic (state cause) 1. Hepatic encephalopathy 2. peripheral neuropathy 3. asterixis
1. Due to ammonia buildup, abnormal neurotranmission, astrocyte swelling and inflammatory cytokines 2. due to diet deficiencies in thiamine, folic acid & B12; also due to toxin (ammonia) build up 3. ammonia buildup
True or False: 1. Infection is always the cause of inflammation.
1. False, infection always results in inflammation but inflammation doesn't only result from infection but also from mechanical, thermal, electrical, chemical or radiation injury
Manifestations of Hepatitis: 1. similarities 2. acute 3. chronic
1. Fatigue/malaise, jaundice, low-grade fever, myalgia/arthralgia, N/V, hepatomegaly 2. Anorexia, wt.loss, dark urine/light stools, decreased sense of taste or smell (foods), distaste of cigarettes, diarrhea or constipation, flu-like symptoms, lymphadenopathy, pruritus, RUQ tenderness, splenomegaly 3. elevated liver enzymes (for some they may be normal), anemia, ascites & lower extremity edema, asterixis, hepatic encephalopathy (confusion, agitation, difficulty concentrating), bleeding abnormalities, hyperbilirubinemia, palmar erythema, spider angiomas
Cholecystitis: 5 F's (risk factors) Other?
1. Female 2. Fat 3. Fertile (pregnancy) 4. Fair but also Native Americans 5. Forties/Fifties Others: estrogen therapy or PO contraceptives (affect cholesterol production & increase likelihood of gallbladder cholesterol saturation), familial tendencies
Hepatic encephalopathy: precipitating factors 1. GI hemorrhage 2. constipation 3. hypokalemia 4. hypovolemia 5. infection 6. cerebral depressants 7. metabolic alkalosis 8. paracentesis 9. dehydration 10. increased metabolism 11. uremia/renal failure 12. TIPS
1. GI hemorrhage-increases ammonia in GI bc blood is rich in proteins 2. constipation-increased ammonia bc food-products linger longer allowing for more deamination to occur 3. hypokalemia-K+ is needed by brain in order to be able to metabolize ammonia 4. hypovolemia-increases ammonia bc hepatic hypoxia; impairment of cerebral, hepatic, & renal fxn bc of decreased blood flow 5. infection-increases metabolic rate & sensitivity to toxins 6. cerebral depressants-decreased metabolism of drugs can lead to accumulation & produce cerebral depression 7. metabolic alkalosis-facilitation of ammonia across blood-brain barrier 8. paracentesis-loss of Na, K, and decreased blood volume 9. dehydration-potentiates (increased concentration) ammonia toxicity 10. increased metabolism-increase in workload on liver 11. uremia/renal failure-retention of nitrogenous metabolites 12. Transjugular intrahepatic portosystemic shunt (TIPS)-diverts blood flow around the liver (unable to process metabolites)
Cirrhosis: comfort measures 1. dyspnea- 2. encourage to 3. How should you weight someone with dyspnea
1. HOB at least 30 degrees 2. sit in chair 3. early in AM, standing up
Nutritional tx: cirrhosis w/o complications 1. Caloric needs 2. Protein restrictions? 3. Low in what is recommended? what foods to avoid? (a-I)
1. High calories 3000 cal/day with high carb & moderate to low fat 2. may or may not be appropriate, it is rarely justified bc malnutrition is more serious than hepatic encephalopathy 3. Low in Na+ if ascites & edema a) table salt, baking soda/powder b) canned/frozen food c) salted snacks/crackers d) smoked meats e) fish f) nuts g) olives, pickles h) ketchup I) beer
Types of inflammation: 1. Acute 2. chronic 3. local 4. systemic
1. Immediate response to tissue injury; short duration (minutes to days); To eradicate harmful stimuli & initiate repair; main cell neutrophils 2. Lasts weeks to years; Tissue repeatedly destroyed & repaired; is a consequence of disease or complication of inflammatory process; main cells are lymphocytes & macrophages 3. confined to an area 4. body wide
GI: Age-related considerations 1. Children 2. Older adults
1. Liver is last GI organ to mature; fully functional at age 12 & 50 kg; meds dosed 2. Decreased fxn & decreased response to injury; Lifetime ETOH use, obesity, co-morbidities, diet; delayed emptying and decreased UES opening & incompetent LES, decreased HCL & intrinsic factor, increased r.f constipation, enzyme changed in liver decreased ability to metabolize drugs and hormones; pancreas suffers fibrosis & fat deposition
Hepatitis: Acute 1. S/S? 2. Acute phase 3. Convalescent phase 4. most recover fully, t or f? 5. Relapse may occur after ___ mos? 6. T or F: disappearance of jaundice doesn't mean pt has totally recovered
1. Many have none 2. 1-6 mos; max infectivity; May have jaundice (yellow tone of tissues d/t alterations in normal bilirubin metabolism or disruption of flow) 3. Weeks-months; Malaise, hepatomegally remains for mos, splenomegally subsides 4. True 5. 2-3 mos 6. True
Clinical manifestation of cirrhosis: GI (state cause) 1. Anorexia 2. Dyspepsia (indigestion) 3. N/V 4. Change in bowel habits 5. dull abd pain 6. esophageal and gastric, hemorrhoidal varices 7. gastritis 8. Hematemesis
1. N/V, malabsorption, loss of appetite 2. ascites & n/v 3. build of toxins 4. enzymes not processed correctly 5. 6. varicosities develop where systemic and collateral circulation develop; these are fragile and bleed easily with increased pressure (portal HTN) 7. bile reflux 8. variceal bleed
Nursing care (conservative): cholecystitis 1. By mouth order? 2. Tubes? 3. Pain management, how? 4. meds 5. ______ management
1. NPO 2. NG 3. Pain management-MS (used cautiously-can make sphincter of oddi spasm & bile will be sent back) 4. Antispasmodics/anticholinergics (decrease spasms in gallbladder and biliary ducts, dry secretions); Antiemetics, Antibiotics 5. F & E management
Acute pancreatitis: nutritional support 1. initially 2. monitor 3. When allowed PO: 4. suspect intolerance if.. 5. may need to take what vitamins
1. NPO, may need NJ or parenteral 2. triglycerides if IV lipids 3. small, frequent feedings, high in carbs (stimulate pancreas less) 4. reports pain, increased girth & elevated pancreatic enzymes 5. ADEK
Anti-inflammation LS: 1. Nutrition 2. Vit. D, turmeric 3. Avoid... 4. _______ health. 5. sleep 6. Aerobic exercise 7. Stress management
1. Plant food, fish, avoid sat. fats, reduce sugar; high fluid intake 2. Anti-inflammatory but also anti-coagulants 3. enviro toxins 4. dental (can travel to heart or kidneys) 5. lack of sleep stimulates inflammatory responses (cortisol-stores fat & increases BG levels, both pro-inflammatory) 6. stimulates healthy immune fxn & anti-inflammation proteins 7. stress activates some immune cells when there is no trauma/infection to fight
Laparoscopic cholecystectomy: 1. benefits 2. who may not be a candidate 3. diet postop 4. postop care
1. Puncture wounds, minimal postop pain, short/no stay, 1 week down time 2. Those who have had multiple abd surgeries with a lot of scar tissue 3. Liquids for the rest of the day & light meals for a few days 4. Monitor for bleeding; Referred pain to shoulder & difficulty breathing from CO2, sims & ambulation helps
RANDI
1. Razor-electric only 2. Aspirin- none 3. Needles-smallest gauge 4. Decrease needle sticks 5. Injury-protect from
1. Name the cardinal signs of inflammation 2. Why do these signs occur? 3. systemic s/s
1. Redness, warmth, swelling, pain, altered function 2. Redness occurs from hyperemia from the vasodilation; Warmth occurs because of an increase in metabolism & hyperemia; Swelling occurs from fluid shift; Pain occurs from change in pH, fluid shift (pressure on nerve endings), prostaglandin release; Altered function occurs from pain & swelling 3. Increased WBC count with left shift, malaise, nausea, anorexia, tachycardia, tachypnea r/t complement activation & circulating inflammatory cytokines
1. T or F: Hep C can cause both acute or chronic 2. T or F: acute hep C has mild presentations
1. T 2. T
Hepatitis: Ambulatory care 1. T or F: most pt's are tx at home 2. Assess knowledge of? 3. Caution about? 4. Teach how important _______ is. How often? 5. Teach what 4 very important things? 6. Assess for what complications? 7. Teach to avoid?
1. T 2. nutrition 3. overexertion 4. follow up (at least 1/yr) 5. how to prevent transmission & what s/s to report; s/s of reoccurrence, cannot donate blood 6. bleeding, encephalopathy, increase in wt & abd girth, elevated liver enzymes 7. alcohol
Chole: Health promotion 1. Teach Native americans what? 2. if already has chronic cholecystitis may only report when s/s...
1. Teach the initial manifestations & to see HCP 2. When s.s of jaundice or obstruction
Functions of a blood clot
1. Traps bacteria/pathogen 2. framework for healing process
Acute Pancreatitis: Acute care 1. monitor 2. Assess for 3. observe for fever, why? 4. why is BG monitored?
1. VS (hemodynamic), F & E 2. Resp. fxn bc resp failure may occur (LS, O2 sat) 3. Resp. infections are common (turning, deep breathing, coughing, etc.) 4. to assess for B cells of langerhans fxn
Hepatitis: Nursing management 1. What is the number one prevention for HBV? 2. What are other prevention measures? 3. who especially should get the HBV vaccine? 4. Post exposure for HCV 5. Comfort measures/anorexia & nausea 6. fatigue measures
1. Vaccine 2. protected sex, needle sticks, infection precautions, no sharing razor or toothbrushes 3. at birth; older children who didn't get it as babies, at risk adults (ppl who live with infected person), if on HD, for post-exposure prophylaxis + immunoglobulins (within 24h) 4. Baseline tests for liver fxn test & anti-HCV, then follow up in 4-6 mos 5. quality food, small & frequent meals, no carbonated drinks, serve hot foods hot and cold foods cold 6. Let them rest/sleep
Cirrhosis: intervention 1. r/f sepsis, why? 2. Altered nutrition: diet should be 3. Fatigue: interventions regarding activity 4. Skin issues-ascites & other edema: interventions 5. Body image: need? 6. Tissue perfusion/Gas exchange 7. Changes in clotting factors & decreased Platelet
1. WBC get trapped in enlarged spleen, blood flow isn't as good, fluid in peritoneal cavity (bacteria from colon); decreased immune proteins 2. rich in CHO (easier to digest), some fat, proteins, vitamins & iron 3. modify activity 4. lotion (eucerin), oatmeal bath, meds for diuresing 5. emotional support 6. IVF, albumin, fresh frozen plasma (clotting factors), HOB elevated 7. safety precautions, FFP, give PLT, RANDI
Inflammation: Dx tests 1. blood tests 2. radiographic
1. WBC with differential (bacterial or viral; chronic or acute); CRP & ESR (inflammation presence) 2. CT, MRI-determine location & extent of inflammation
vascular function of the liver: 1. Breakdown of old 2. storage
1. WBCs, RBCs (bilirubin), bacteria 2. blood storage
Health promotion: cirrhosis 1. abstain from? 2. encourage?
1. alcohol 2. support groups (alcoholics anonymous)
Causes of liver disease/cirrhosis?
1. alcohol 2. viral hepatitis 3. autoimmune disease 4. Steatohepatitis (NASH) 5. drugs and toxins 6. biliary disease (back up) 7. metabolic or genetic causes 8. CVD (R HF)
Acute pancreatits: Ambulatory care 1. counseling abt 2. Diet 3. Teach 4. may require
1. alcohol & smoking 2. restriction of fats bc stimulate pancreas, avoid crash diets or binging 3. s/s of infection, DM, steatorrhea 4. enzyme supplementation
Common risk factors for cirrhosis: (6)
1. alcoholism 2. malnutrition 3. viral hepatitis 4. biliary obstruction 5. obesity 6. right sided HF
People at r/f HBV
1. asians & pacific islanders 2. HCPs 3. live with infected person
Hep C: 1. Most individuals are ______; damage occurs over... 2. Spread 3. who should get screened? 4. what is enough to make a dx
1. asymptomatic; over decades 2. sharing needles, blood or blood products, HD, organ transplant (prior to 1992), tattoos, intranasal cocaine, unprotected sex (MSM), perinatal 3. those who have a high risk sexual practice, injection drug users, baby boomers, blood before 1992 4. positive for antibody
Incisional chole: teaching post op
1. avoid heavy lifting for 4-6 weeks 2. sex may be resumed when the person feels ready 3. sometimes, a low fat diet for 4-6 weeks 4. if overwt., a diet to reduce wt is initiatied 5. Avoid excessive fats
Hepatorenal syndrome: 1. Type of renal failure with... 2. Explain why it occurs
1. azotemia, oliguria 2. d/t portal HTN and liver decompensation, liver will put out vasodilators (N.O.) & splanchnic & systemic vasodilation will occur. This leads to decreased arterial volume (hypotension), which will decrease blood flow to the kidneys. The kidneys respond by activating RASS (ascites) & renal vasoconstiction of efferent arteriole, renal failure follows
Hepatic encephalopathy: 1. explain how ammonia occurs in our body 2. T or F: ammonia crosses the blood-brain barrier 3. s/s
1. bacterial enzymatic deamination of amino acids in intestines results in ammonia, which is then taken to liver via portal circulation & converted to urea, which is then excreted through the kidneys 2. True, that's why it produces neurological s/s 3. altered LOC, inappropriate behavior; Sleep disturbances to trouble concentrating to coma; may occur gradually or suddenly; asterixis (flapping tremors in arms & hands); apraxia (impaired writing); hyperventilation, hypothermia, tongue fasciculations, grasping reflexes; fetor hepaticus (musty, seet smell bc of buildup of metabolic/digestive by products)
Secretory function of the liver: 1. ______ production 2. bilirubin
1. bile 2. conjugation and secretion of bilirubin
Clinical manifestation of cirrhosis: Skin (state cause) 1. Jaundice 2. spider angioma 3. purpura 4. petechiae
1. bilirubin accumulation due to inability to conjugate it and excrete it into small intestine 2. increased circulating estrogen 3. blotchy; due to bleeding under skin 4. point; due to bleeding under skin
Tx for shock:
1. blood 2. dextran or albumin 3. LR 4. Vasoactive drugs
1. Hepatic artery: 2. Portal vein:
1. brings in oxygen and nutrients to the liver; 25% 2. brings blood from the GI tract, including nutrients of digestion, drugs, toxins, bacteria; 75%
Fever: 1. Triggered by? 2. ____ Increase thermostatic set point 3. how is temp raised? 4. Benefits
1. by release of cytokines by initiating metabolic changed in hypothalamus 2. PGs 3. ANS increases muscle shivering & decreased sweating & decreased blood flow to periphery, epinephrine released which raises the metabolic rate 4. Increased killing of pathogens, increased phagocytosis & proliferation of T cells & interferon
Paracentesis: safety issues 1. Need... 2. What must be done first? 3. position 4. Fluid removal rate 5. monitor... 6. reliefs?
1. consent 2. void 3. sitting 4. slowly r.f shock/hypotension 5. F & E, BP & HR, bleeding 6. relieves pain, pressure & difficulty breathing
Acute care: cirrhosis 1. focus: 2. how to relieve pruritus 3. If jaundice, note 4. Note what from urine & stools 5. if edema/ascites: monitor 6. If on diuretics assess for?
1. conserving pt's strength while maintaining muscle strength & tone 2. baking soda, bath oils, antihistamines, lotions with calamine, soft or old linens; itch with knuckles 3. location, progression 4. color 5. I&O, daily wt, abd girth 6. hypokalemia, hyponatremia, renal fxn tests
Ambulatory care: cirrhosis 1. important for pt & caregiver to understand the importance of... 2. supportive care 3. Teach...
1. continual follow up 2. proper diet, rest, avoid hepatotoxic drugs, no alcohol, emotional support 3. adequate rest periods, early s/s of complications, skin care, drug SE, bleeding, protect from infection
Inflammation: 1. Primary prevention 2. Secondary 3. Collaborative a) which acronym? b) pharm
1. decrease r/f injury; hand hygiene; wounds clean & covered; using safety equipment; food & water safety 2. none 3a) RICE (rest, ice, compression, & elevation)- all decrease swelling; during first 24-48 hrs best; ice for 20 min q2-3 hr, elevation above heart level 3b) steroids, NSAIDs, monoclonal antibodies, antipyretics, analgesics, antimicrobials
Hepatitis: pathophysiology 1. Hepatocytes become targets of the virus by... 2. During acute hepatitis large # of hepatocytes are destroyed leading to liver related dysfunction... 3. Chronic hepatitis is? leads to 4. Systemic effects: In early phase antigen-antibody complexes form, activating complement, s/s?
1. direct action of virus or by cell mediated immune response 2. Bile production, coagulation, BG, Protein metabolism, detox & processing drugs, hormones, metabolites 3. insidious & silent. Leads to continual destruction of infected hepatocytes which leads to fibrosis then cirrhosis 4. Rash, angioedema, arthritis, fever, malaise, glomerulonephritis, abnormal circulating proteins
Clinical manifestation of cirrhosis: Metabolic (state cause) 1. Hypokalemia 2. Hyponatremia 3. hypoalbuminemia
1. due to hyperaldosteronism (liver unable to metabolize it) 2. water retention (hyperadosteronism & ^ ADH) 3. liver unable to synthesize plasma proteins
Cirrhosis: management 1. measure abd girth when? 2. what other labs? 3. type of diuretic recommended? 4. Skin care for edematous tissue:
1. early in AM 2. BUN & creatinine for hepatorenal syndrome 3. K sparring 4. air mattress & turning schedule, support abd with pillows; If taut, clean gently
Acalculous cholecystitis: 1. more frequent in? 2. associated with? 3. main cause? 4. other causes? 5. r/f? 6. inflammation pattern 7. during an acute attack, describe gallbladder
1. elders & critically ill 2. prolonged immobility, fasting, prolonged parenteral nutrition, DM 3. bile stasis-increased viscosity d/t fever, dehydration, decreased PO feed 4. adhesions, neoplasms, opioids/anesthetics 5. secondary infection from enteric pathogens & rupture 6. me be just in mucous lining or entire wall 7. gallbladder is edematous & hyperemic, distended or with pus; cystic duct may be involved
Chemical mediators: 1. complement 2. prostaglandins 3. Histamine
1. enzyme cascade that enhances phagocytosis, increases capillary permeability, chemotaxis & cell lysis 2. When cells are injured, arachidonic acid in cell membrane is converted to PGs; potent vasodilator, sensitizes pain receptors, pyrogenic 3. secreted from basophils, mast cells, platelets; Vasodilation & increases capillary permeability
Nursing assessment: Hepatitis 1. Past health hx: 2. Meds 3. Health perception 4. nutritional 5. elimination 6. activity 7. cognitive 8. roles 9. general 10. skin 11. GI
1. exposure to infected ppl, contaminated needles, recent travel, organ transplant, HD, blood transfusion before 1992, HIV 2. acetaminophen, new meds, OTC, herbs, supplements 3. IV drug use, chronic alcohol, malaise, distaste for ciggars, sexual behaviors 4. wt loss, anorexia, N.V 5. dark urine, light stools, constipation or diarrhea, rashes 6. fatigue, myalgias 7. RUQ pain, headache, pruitus 8. exposure as HCp, resident, jail, homeless 9. low grade fever, lethargy, lymphadenopathy 10. rash, jaundice, injection sites 11. hepato or splenomegaly
Cirrhosis: 1. define 2. Fibrosis leads to... 3. Compensated cirrhosis
1. extensive scarring of the liver, usually caused by a chronic irreversible reaction to hepatic inflammation and necrosis 2. cirrhosis; irregular lobes with impeded blood flow (hypoxia) 3. liver has significant scarring but performs essential functions w/o causing significant symptoms or complications
In early stages of compensation, signs of liver disease include: 1. 2. 3. 4. **
1. fatigue 2. change in wt. (bc n/v) 3. GI problems 4. abd pain & liver tenderness ** blood test may be normal
Cholecystitis s/s:
1. fever & leukocytosis (bc inflammation) 2. jaundice; dark urine, light stools 3. abd pain (RUQ or epigastric that may radiate to back, worse with deep breathing) 4. Fat indigestion; feeling of fullness; distention 5. N/V (bc not digesting food well)
Inflammation: Assessment 1. Hx 2. Exam findings a) wounds b) internal trauma
1. focus on determining trigger; physiological ability to respond to a trigger; s/s, duration & current tx methods 2a) red, warm, pain, swellings, drainage (infection) 2b) swelling, pain, fever, decreased function
Cirrhosis: Pt/caregiver teaching 1. chronic illness 2. complications to report 3. OTC drugs 4. No _______ 5. Effects of straining, coughing, sneezing, retching-what can happen?
1. follow up 2. blood in emesis, stool; change in LOC, asterixis; jaundice; worsening ascites 3. avoid NSAIDs, aspirin, all to be checked with HCP first 4. alcohol 5. increased r.f variceal hemorrhage
Clinical manifestation of cirrhosis: Cardiovascular (state cause) 1. fluid retention 2. peripheral edema 3. ascites a) S/S of ascites b) at r/f?
1. from an increase in circulating ADH & aldosterone (not metabolizing them), decreased renal perfusion (from hypovolemia d/t ascites) 2. from decreased albumin 3. -Decreased albumin (decreases oncotic pressure within circulation), -Portal HTN (causes proteins & fluid to shift from blood into lymph vessels, but when the lymph vessels can't carry anymore they leak into the peritoneal cavity. Now oncotic pressure within peritoneal cavity to pull additional fluids), -Hyperaldosteronism (poorly metabolized; increased sodium and water retention; bc there's less fluid in the vasculature, there is a decrease in renal perfusion, which will decrease the GFR [less filtration] & will stimulate the RASS & ADH) a) Abd distention, & wt gain, eversion of umbilicus, striae, dehydration, decreased urine OP, hypokalemia b) spontaneous bacterial peritonitis
Late manifestations of cirrhosis: 1. Jaundice 2. Hyperaldosteronism
1. from decreased ability to onjugate & excrete bilirubin into the small intestine; overgrowth of connective tissue in liver compresses bile ducts & leads to obstruction 2. from liver unable to metabolize it (retains Na & water and depletes K+
Cholecystitis: complications
1. gangrenous cholecystitis 2. subphrenic abscess 3. pancreatitis 4. biliary cirrhosis 5. ruptured gallbladder
Storage function of the liver: What does the liver store?
1. glucose 2. vitamins 3. minerals 4. fatty acids 5. albumin & beta globulins
Metabolic function of the liver: 1. Carb metabolims 2. protein " " 3. fat 4. detox
1. glycogenesis, glycogenolysis; gluconeogenesis 2. plasma proteins, clotting proteins, urea (from ammonia) 3. synthesis of lipoproteins, fatty acids; breakdown of triglycerides; synthesis and breakdown of cholesterol 4. kupffer cells phagocytize bacteria and toxins
RICE: Rationale behind each intervention 1. Rest 2. Ice (cold) or hot 3. compression/immobilization 4. Elevation
1. helps body use nutrients & O2 for healing; fibrin & collagen form across wound edges 2. Cold: best right away to promote vasoconstriction & decrease swelling & pain; Heat: best later; promotes healing by increasing circulation & removing debris 3. Compression: counter vasodilation & bleeding; Immobilization: promotes healing by decreasing metabolic needs 4. decrease edema by increasing venous return & lymph too (may be contraindication if arterial circulation is compromised)
Sengstaken-Blakemore tube: 1. Used for? 2. Placement where? Who? 3. Tissue perfusion precaution 4. Safety item 5. will pt be able to swallow? 6. watch for?
1. helps stop esophageal variceal bleeding by mechanical compression (20-40 mmHg) 2. gastric balloon to anchor and esophageal balloon; placed by HCP 3. deflate balloons q 8-12 hrs for 5 mins to prevent tissue necrosis 4. scissors at bed side, cut esophageal balloon 5. No 6. bleeding at insertion point, rupture or erosion of esophagus, aspiration (semi-fowlers; suction equipment), occlusion of airway
Complications of acute pancreatitis: (10)
1. hypovolemia/hemorrhage 2. acute renal failure (d/t inflammation spread) 3. Paralytic ileus (don't give anticholinergics bc decrease motility) 4. septic shock 5. pleural effusion, PE, resp. distress syndrome, pneumonia (from passage of enzymes through trans-diaphragmatic lymph vessels, causing inflammation of the diaphragm therefore atelectasis 6. Disseminated intravascular coagulation (DIC) 7. DM (bc increased BG) 8. tetany from hypoCa+ 9. ABD compartment syndrome (edema) 10. pancreatic pseudocyst & abscess (accumulation of fluid, enzymes, debris) (infected pseudocyst)
Nursing dx: Hepatitis 1. 2.
1. imbalanced nutrition: less than body requirements r/t anorexia, nausea 2. Activity intolerance r/t fatigue & weakness
Inflammation: Populations at risk 1. Young children 2. older adults 3. What other conditions predispose ppl for inflammation?
1. immature immune system may lead to a more severe inflammatory response bc immune is unable to control a minor pathogen 2. Less able to respond to foreign invaders 3. autoimmune diseases, allergies, DM, underinsured, smoking, immunosuppression, exposure to pathogens, genetics, poor sanitation, nutrition or living; pollution
Gerontologic Considerations: 1. incidence 2. Liver 3. capacity to respond to injury or regenerative 4. Vulnerability to drugs 5. HCV 6. what other things might contribute to cirrhosis? 7. why might variceal bleed be deadly? 8. Hepatic encephalopathy 9. liver transplant
1. increase incidence with increased age 2. decrease in size & altered metabolic breakdown 3. decreased 4. increased vulnerability for drug induced liver injury d/t many meds 5. growing in # in elderly; asymptomatic 6. chronic alcohol, obesity 7. bc of possible CVD, pulmonary diseases, anticoagulant tx 8. may be confused with dementia 9. poor candidate bc decreased ability to regenerate plus increased risks
Hepatic encephalopathy tx: Goal 1. Associated with? 2. symptoms 3. safety 4. problem increased by? 5. meds 6. diet
1. increased ammonia level 2. altered LOC, asterixis 3. measures to prevent constipation (fluids), falls 4. avoid GI bleed, hypokalemia, hypovolemia, infection, high protein 5. cephulac (Lactulose): traps ammonia in gut, neomycin & rifaximin (antibiotics: decrease flora in gut = decrease ammonia) 6. increase fluids to prevent constipation & dilute ammonia; avoid high protein (cautiously)
Chronic hepatitis (in general): 1. More likely to occur in? 2. what plays an important role in its development? 3. Which is more likely to become chronic, B or C? 4. Risk factors for progression to cirrhosis 5. manifestations
1. infants born to infected mothers or get it b4 age 5 2. altered cellular immunity 3. C, may develop chronic liver disease, cirrhosis, portal HTN & liver cancer 4. male, alcohol, fatty liver disease, excess Fe deposit in liver, metabolic syndrome, HIV 5. Anemia, coagulation problems, spider angiomas & palmar erythema, gynecomastia, spleno or hepatomegaly or cervical node lymph enlargement, hepatic encephalopathy, ascites
Cirrhosis: Dx tests (result & why) 1. Liver function tests (ALT, AST) 2. Liver biopsy 3. upper endoscopy 4. CT/MRI 5. Fibroscan 6. serum electrolytes 7. PTT 8. bilirubin 9. CBC 10. serum albumin
1. initially increased due to release from inflamed liver cells, but in end-stage liver disease they might be normal d/t the death and loss of hepatocytes 2. scarring from destruction of hepatocytes 3. varices 4. visualize liver (nodular) 5. ultrasound to see degree of fibrosis 6. hypokalemia, hyponatremia 7. prolonged (increased) bc clotting proteins aren't being synthesized 8. increased (liver unable to conjugate it or excrete it) 9. decreased bc splenomegaly 10. decreased bc liver unable to synthesize it
Acute inflammation: steps
1. injury to or death of tissue & release of chemical mediators 2. vasodilation & increased blood flow to area 3. swelling & partial separation of activated endothelial cells 4. Increased permeability & leakage of water, salts, fibrinogen, & other small plasma proteins 5. "walling off" area to delay spread of bacterium or toxin 6. Margination & migration of WBCs to area 7. Exudates fill spaces left by damaged, necrotic tissue 8. glucose & oxygen move to the area (support) 9. Release of nitric oxide & prostaglandin, endothelin, etc.
Pancreas: Functions 1. endocrine 2. exocrine
1. into blood stream (insulin/amylin, glucagon) 2. into duct (pancreatic enzymes)
Hepatitis: Acute care 1. Assess for ________ (Hint: hallmark sign) & where to assess for it 2. What size & frequency of meals is better and why? 3. What can help stimulate appetite 4. How much fluid is recommended? 5. What guides level of activity? 6. Emotional/psychological rest, promote?
1. jaundice: appear in sclera first, later in skin; hard palate & inner canthus of eye; urine may be dark 2. small, frequent meals bc easier to digest & not as exhausting; bigger breakfast is better bc anorexia is not as severe 3. mouth care, antiemetic, attractive meals, avoid very hot or very cold foods 4. 2.5-3 L/day 5. liver fxn tests & s/s 6. diversion activities, reading, hobbies
Vascular response to inflammation steps
1. local arterioles briefly vasoconstrict, after histamine is released they vasodilate 2. Chemical mediators increase capillary permeability 3. serous fluid, plasma proteins (oncotic pressure) leak into area 4. fibrinogen is activated to fibrin to strengthen clot 5. platelets release growth factors to start process of healing
Ascites tx 1. sodium 2. med 3. procedures 4. fluids 5. monitor
1. low sodium diet (2g/day) 2. diuretics, albumin 3. paracentesis, TIPS 4. 1-1.5 L/day; no fluid restriction unless severe 5. F & E
Inflammation: Acute care 1. s/s to monitor for in immunosuppressed 2. Fever a) what is it good for? b) most of the time, fever is reduced for? c) if an immunocompromised person gets a fever, what should they be started on? d) if temp is > 104.0 e) if > 105.8F f) T or f: older adults may have a blunted febrile response 3. T or F: people on NSAIDs may also have a blunted febrile response 4. Are sponge baths or cooling blankets recommended while febrile?
1. malaise, "not feeling well" 2a) important host defense mechanism; helps kill invaders more efficiently & halt their growth 2b) decrease anxiety, discomfort; or if very young or old or have significant medical problems 2c) antibiotics 2d) can damage cells, cause delirium & seizures 2e) hypothermic control center is damaged (including neurons) 2f) T 3. T 4. only if they are on antipyretics; if not on those meds, these cooling measures will only stimulate compensatory mechanisms and further increase temp
Abd assessment/ascites: 1. inspection 2. palpation
1. massive ascites (taut skin), umbilicus protrusion, caput medusae (dilated abd vein), jaundice 2. hepatomegaly
Tx for HCV 1. acute 2. chronic a) ___________ drugs
1. monitor or take direct acting antiviral drugs (DAAs) *interferon may also be used for HCV 2. DAAs-block proteins necessary for HCV replication; only a 12 week tx; cures chronic HCV (goal: eradicate virus)
Clinical manifestation of cirrhosis: Hematologic (state cause) 1. Anemia, Thrombocytopenia, leukopenia 2. coagulation disorders 3. Splenomegaly
1. overactivity of large spleen increases removal of RBCs, WBCs and platelets 2. decreased production of clotting proteins 3. occurs because of back up of blood from portal vein to spleen (portal HTN)
Acute pancreatitis: s/s (6)
1. pain in LUQ or mid-epigastric that commonly radiates to the back bc pancreas is retroperitoneal; sudden, severe, deep, piercing 2. abd tenderness, rigidity, guarding (d/t inflammation) 3. N/V (bc not digesting well), decreased bowel sounds (paralytic ileus may occur) 4. VS: hypotension & tachycardia & low grade fever from hemorrhage, shock, fluid shift, inflammation 5. Jaundice bc obstruction of bile duct, inflammation may spread to liver (decreased fxn) 6. Cullen's sign (bluish periumbilical discoloration) & Turner's sign (bluish flank discoloration)
Chole: Acute care 1. Management of 2. maintain _______ & ___ balance & ______ 3. for severe n/v 4. for less severe n.v 5. pruritus med 6. observe for s.s of obstruction: 7. observe for bleeding in... 8. Assess for infection:
1. pain, n/v, comfort, emotional support 2. F & E balance & nutrition 3. NPO, NG tube, nares care, oral hygiene, i & o 4. antiemetics 5. antihistamine 6. clay colored stools, dark urine (jaundice), steatorrhea, fever & increased WBCs 7. gums, mucous membranes, nose, injection sites; check PTT 8. fever, chills, VS
Open cholecystectomy: 1. when is this method preferred 2. diet 3. post-op care
1. peritonitis, cholangitis, gangrene or perforation, portal HTN 2. progress from liquids to regular after return of bowel sounds 3. prevent respiratory complication
Cholecystectomy: Routine postop. care 1. Care of T-bube: where is it placed? Skin care? drainage? 2. fluids related to this? 3. what are s.s of obstructed T tube or malfunctional T tube?
1. placed in common duct to keep it patent after surgery; skin needs to be cleansed daily with antiseptic & dry bc bile eats skin; drainage should be dark green & should keep flowing; connected to closed gravity system 2. encourage to replace fluids & electrolytes that are lost through the drainage 3. abd pain, nausea, fever, chills
Acute Liver failure: 1. ______ prognosis 2. Tx 3. s/s
1. poor 2. liver transplant 3. encephalopathy, DIC, GI bleed, renal s/s, hypoglycemia, edema & hypotension
Acute Pancreatitis: Health promotion 1. assess for 2. encouragement of early 3. eliminate
1. predisposing & etiologic factors 2. tx of these factors to prevent acute pancreatitis 3. alcohol
Esophageal & Gastric varices management: 1. Goal: 2. Avoid... 3. Meds: 4. For an active bleed... 5. All pt's with cirrhosis should have an... 6. What procedures can be done to prevent re-bleed? 7. What additional meds can be given during an active bleed (to prevent hepatic encephalopathy)? 8. Explain TIPS
1. prevent bleeding & variceal rupture by decreasing portal pressure 2. alcohol, aspirin & NSAIDs 3. Nonselective beta blockers (reduces r/f bleeding by decreasing portal HTN), somatostatin analog octreotide or vasopressin (produce vasoconstriction of the splanchnic arterial bed, decreasing portal blood flow and therefore lowering portal HTN) 4. first stabilize pt & manage airway, IV started, blood may be given, plasma, Vit K, protonix, antibiotics; RRT; balloon tamponade 5. upper endoscopy to assess for varices 6. band ligation & sclerotherapy 7. lactulose & rifaximin to prevent hepatic encephalopathy 8. considered after a 2nd major bleed; nonsurgical procedure in which a shunt is placed between the systemic & portal venous systems to redirect portal blood flow (transjugularly)
Milk thistle: 1. action 2. SE 3. effectiveness 4. duration
1. protects & promotes growth of hepatocytes & inhibits inflammation 2. hypoglycemia, interferes with liver enzymes 3. No real benefit (per research) 4. Can only take for a max of 6 yrs
Chronic inflammation: 1. Macrophage fxn 2. what other cell 3. Elevation in what lab values 4. Release of what? by the what?
1. releases thromboplastin for hemostasis & promote fibroblast activity; removes necrotic tissue & pathogen 2. lymphocyte 3. ESR & CRP 4. proteins (complement, clotting, protease inhibitors) by the liver
Cholestyramine (Questran): 1. uses 2. Nursing interventions 3. SE
1. relief pruritus by binding bile salts and excreting them through feces 2. Give with milk or juice; May bind to other drugs 3. N/V/D or constipation
Laparoscopic Teaching
1. remove bandages the day after surgery & may shower 2. Notify surgeon of redness, swelling, bile drainage or pus, severe abd pain, N/V, fever, chills 3. gradually resume normal activities (work-1 week) 4. may resume normal diet but a low fat diet is better for a couple of weeks
Cirrhosis: Conservative tx
1. rest 2. B- complex vitamins 3. no alcohol 4. no aspirin, acetaminophen, NSAIDs
Inflammatory process: 2 main functions plus an additional
1. restitution of normal functioning of cells following injury 2. Fibrous repair when functional cells cannot be restored Other: neutralizes and dilutes inflammatory agent (if any)
Acute pancreatitis: Nursing care 1. monitor for 2. what drug for pain? 3. What other med?
1. sepsis (can spread easy), hemodynamic stability, F & E (chvostek & trousseaus), resp distress, BG 2. MS 3. antibiotics
Acute pancreatitis: 1. define 2. causes 3. How do those causes cause pancreatitis?
1. serious & possible-life threatening inflammatory process of the pancreas 2. gallbladder disease, alcohol, viral infection, idiopathic, smoking, hypertriglyceridemia, trauma, cystic fibrosis, drugs 3. they injure pancreatic cells or activate pancreatic enzymes in the pancreas rather than in the intestines; may be d/t reflux of bile acids into pancreatic ducts (d/t stone/block)
When is TIPS contraindicated?
1. severe hepatic encephalopathy 2. hepatocellular carcinoma 3. severe hepatorenal syndrome 4. portal vein thrombosis
Cholecystitis: management 1. Diet 2. ERCP define & complications 3. Dissolution agents 4. lithotripsy 5. surgery * rapid wt loss??
1. small, frequent meals with some fat to promote gallbladder emptying; low salt; high fiber & calcium; fat soluble vitamins; bile salts to facilitate digestion & vitamin absorption 2. allows visualization of biliary system and dilation, placement of stents, & sphincterotomy can be done; pancreatitis, perforation, infection, bleeding 3. Bile salts (agent) dissolve stones 4. uses high energy waves to disintegrate gallstone, which then pass through; 1-2 hrs 5. laparoscopic cholecystectomy & open cholecystectomy * Avoid rapid wt loss as it promotes stone formation
Functions of the gallbladder:
1. storage of bile 2. concentration of bile 3. fat metabolism (bile)
Diagnostics: 1. Liver function test 2. WBC 3. ultrasound
1. to r/o liver disease; may be elevated if inflammation has spread 2. Increased WBCs 3. visualization of gallbladder; degree of inflammation
Examples: 1. Acute: local & systemic 2. Chronic: local & systemic
1. tonsilitis & anaphylaxis 2. IBS & Lupus
Hep B: Spread via
1. unprotected sex (small cuts on mucosal)-semen, vaginal secretions, saliva 2. needles (percutaneously) 3. blood products (GI bleed) 4. HD 5. Maternal-fetal route (perinatally)
Chole: ambulatory care 1. diet 2. Vitamins
1. usually low fat 2. ADEK
Nutrition tx 1. type (in general) 2. Adequate Kcal bc... 3. may need to decrease? 4. Vitamin supplements 5. May need what nutritional intervention
1. well balanced diet 2. often lose wt 3. fat, depends on how well it's tolerated (d/t decreased bile) 4. B complexes, Vitamin K, Folic acid & B12 5. Enteral or parenteral nutrition
endoscopic retrograde cholangiopancreatography (ERCP) 1. When is it done? 2. insertion? 3. Pre-procedure 4. post procedure 5. R.f?
1. when acute pancreatitis is suspected to be r/t gallstones 2. through mouth into duodenum 3. consent, allergies to iodine, shellfish 4. check gag reflex (NPO until return), VS, pain management 5. acute pancreatitis
Cholelithiasis: 1. develops when 2. T or F: stones cause pain as they pass through ducts & may cause obstruction 3. when the bile in gallbladder cannot escape, may lead to? 4. s/s of obstructed bile flow? 5. wether or not severe symptoms depend on? 6. when a stone is passing through, what is what causes the pain? 7. attacks commonly occur after?
1. when the balance that keeps cholesterol, bile, salts, & calcium is altered so that substances can precipitate into stones (ex. stasis of bile, infection) 2. T 3. cholecystitis 4. obstructive jaundice (no bile flow, bilirubin accumulation), dark urine, clay colored stools, pruritus, intolerance of fatty foods (n/v, fullness, anorexia), bleeding tendencies (decreased clotting proteins & decreased absorption of vit. K), steatorrhea 5. wether stones are stationary or mobile & whether there's an obstruction or not 6. spasms 7. a high-fat meal or when supine
Cellular response to inflammation: 1. neutrophils 2. monocytes 3. lymphocytes
1. within 6-12 hrs; phagocytize; short life span, soon you have an accumulation of dead neutrophils, digested bacteria & cellular debris forming pus 2. Within 3-7 days; Become macrophage; can multiply & fuse together to become a multi-nucleated giant cell "granuloma" 3. later; Humoral & cell immunity
Clinical manifestation of cirrhosis: Reproductive (state cause) 1. amenorrhea 2. testicular atrophy 3. Gynecomastia 4. impotence
2/3/4. because increased estrogen levels (in comparison to testosterone) due to liver not metabolizing it
What should pt report to HCP? What about OTC meds?
Bleeding, increased fatigue, nausea or anorexia. Check all OTC meds with HCP
describe how Amylase & lipase increase or decrease
Both rise within 2-12 hrs. In 3 days, Amylase returns to normal, but lipase stays elevated for up to 7-1o days
The liver breaks down _____ from old RBCs to _____ & ______. When released into the blood stream it binds to albumin and is referred to as_______. Once in the liver it is _____ then excreted into the intestines.
Hgb; bilirubin & biliverdin; unconjugated; conjugated
Describe location, lobes, and casing of the liver
Right epigastric region enclosed in peritoneum and has a right and left lobe; fibrous capsule enclosing it
T or F: all viral hepatitis medications decrease viral load
T
The liver performs more than 400 functions in 3 major categories: storage, protection, & metabolism. The liver stores many mineral and vitamins such as:
Vitamins ADEK, B1, B2 , B12 Folic acid Iron & copper
Inflammation: define
a normal and expected physiological response to cell injury. The response is protective in that it provides an opportunity for the body to heal and repair the injury
serum proteins made by the liver include ____
albumin, alpha and beta globulins (immune system proteins) and clotting factors
The liver synthesizes several plasma proteins such as ____ and clotting factors. The liver's role in carb metabolism involves storing and releasing ______, as the body's energy needs change.
albumin; glucose
The protective function of the liver involves the kupffer cells which carry out phagocytic activity, removing _____&____ from the blood
bacteria & toxins
Why does the r/f cholecystitis increase during pregnancy and post-pregnancy?
because hormonal factors delay emptying of gallbladder, leading to bile stasis = prone to gallstones
The gallbladder is a pear-shaped sac located ________. it functions to ______ & ______ about 45 ml of bile that comes from the liver. The presence of fat in the duodenum triggers bile release via the _____.
below liver; concentrate; store; common bile duct
The liver constantly forms and continually secretes ______ which is essential for the breakdown of _____.
bile; fat
The hepatic cells secrete _____ into small canals that merge to form larger _____________, that eventually unite to form the right and left _____________.
bile; interlobular ducts; hepatic ducts
Alkaline phosphatase (ALP)is a serum enzyme originating from ____ and ____ and serum levels rise when excretion is impaired bc of obstruction in the biliary tract.
bone; liver
WBCs are attracted to an area by...
chemotaxis
Why do Cullen's & Turner's sign appear?
from seepage of bloodstained exudate from pancreas; severe pancreatitis
what might stools appear like during cholecystitis/cholelithiasis?
greasy stools/diarrhea
The liver has rich blood supply. It receives its blood from the ____ & ______, resulting in about 1500 ml of flow through the liver q minute.
hepatic artery; portal vein
The common bile duct forms from the left and right ______ merging with the ______ from the gallbladder
hepatic ducts; cystic duct
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are serum liver enzymes that _____ in liver damage and inflammation
increase
Cholecystitis: define
inflammation of gallbladder; many times associated with cholelithiasis
The functional units of the liver are _____ & consisting of rows of hepatic cells or _________. Capillaries (_______) are in between these rows, where _____ cells phagocytize bacteria and toxins.
lobules; hepatocytes; sinusoids; Kupffer
The liver function in the metabolism of _____, considered essential for survival. It breaks down amino acids to remove ammonia, which is converted to ___ and excreted via kidneys.
proteins; urea
cytokines function
regulate immune response
How does the nurse properly measure abd girth?
supine or as tolerated, measure across fullest part of abd & mark two lines
Liver also participates in fat metabolism: breakdown of _____, synthesis of _____, _____ & ____ & synthesis and breakdown of _________
triglycerides lipoproteins, fatty acids, and ketones cholesterol
T or F: Hepatitis carriers can infect others even if they are w/o s/s
true
T or F: the liver is a blood reservoir
true
The liver inactivates drugs and sends them to be excreted. T or F
true
T or F: HBV majority resolves w/o any long term complications
true (although it can lead to chronic/cirrhosis)
