liver, biliary and pancreas problems

liver function

filters blood(processes meds, breaks down toxins) stores glygocen/vitamins/minerals, metabolizes fat/proteins/carbs, produces albimin and clotting factors, produces and excretes bile

hepatitis

liver inflammation caused by virus, ETOH, meds(tylenol)

viral hepatitis

virus attacks and kills hepatocytes, immune system tries to kill virus but kills hepatocytes too, inflammation and decreased liver function

prodromal hepatitis phase

infection in the blood flu like s/s, N/V, diarrhea, anorexia, fever, malaise, fatigue, joint and muscle pain

icteric hepatitis phase

liver damage, hepatomegaly(RUQ pain), jaundice, pruritis, dark tea color urine, clay color stool

convalescent hepatitis phase

s/s decrease over 2-4 months

hepatitis complications

chronic hepatitis - cirrhosis - liver cancer

liver failure - encephalopathy, bleeding, fluid retention(ascites)

chronic hepatitis

continual hepatocyte destruction and inflammation leading to irreversible scar tissue(cirrhosis) and chronic liver failure

hepatitis A(HAV)

transmitted: fecal oral

vaccine: yes, included in childhood vaccine schedule, HAV immunoglobulin within 2 weeks of exposure, acute phase only

diagnostics: HAV antibody, immunoglobulin IgM in active phase and IgG in recovery/immune

treatment” rest and support

hepatitis B(HBV)

transmitted: blood borne

vaccine: yes, included in childhood vaccine schedule, HBV immunoglobulin within 24 hrs of exposure, can be acute and chronic

diagnostics: HBV antigen= infection, HBV antibody= recovery/immune

treatment: acute phase = rest and support, chronic phase = antivirals, relapse common

hepatitis C(HCV)

transmitted: blood borne

vaccine: none, acute and chronic

diagnostics: HCV RNA test, HCV antibody 4 weeks into infection

treatment: acute = rest and support, chronic = antivirals, relapse common

hepatitis D(HDV)

transmitted: blood borne, only occurs in those with HBV

vaccine: HBV vaccine, acute and chronic

diagnostics: HDV antigen in early infection and HDV antibody for past and present

treatment: antivirals

hepatitis E(HEV)

transmission: fecal oral, dangerous to pregnant woman

vaccine: no, acute only

diagnostics: HEV antibody, IgG in active phase, IgG in recovery/immune

hepatitis labs

increased AST and ALT, bilirubin, ammonia, INR, PT and aPTT

cholelithiasis

gallstones, stones in gallbladder

cholecystitis

gallbladder inflammation usually associated with cholelithiasis

increased cholesterol and bile stasis leads to stones in gallbladder, stones move, stones get suck in ducts leading to obstruction, bile backup and cholecystitis

cholecystitis risk factors

female, family hx, increase cholesterol, fatty diet, forty plus, oral contraceptives, bile stasis, fertile, sedentary

cholecystitis clinical manifestations

stones in gallbladder = no s/s

stone moving/stuck = biliary colic with severe RUQ pain after fatty foods, can radiate to R shoulder/back, murphy’s sign(RUQ palpated leading to severe pain), N/V, indegestion

obstruction complications

obstruction leading to

bile obstruction = pale stool, fatty stool(steatorrhea), dark urine, jaundice, pruritis

cholecystitis = lithiasis s/s, fever

pancreatitis

cholecystitis diagnostics

abdominal ultrasound, endoscopic retrograde cholangiopancreatography(ERCP), increased WBC/bilirubin/ALT and AST

cholecystitis treatment

no s/s = no treatment

s/s = laparoscopic cholecystectomy, treatment of choice, right shoulder ain after, decreased fat diet for 4-5 weeks

transhepatic biliary catheter(T-tube)

decompresses obstructed bile ducts

indication - preop decrease liver function, postop open cholecystectomy

assess - output 1000 ml/day, bile leaking, patency

pancreatitis

pancreas inflamed and autodigestion

pancreas endocrine function

islets of Langerhans beta cells secrete hormones into blood stream, insulin decreases BS and glucagon increases BC

pancreas exocrine function

acinar cells release inactive digestive enzymes in pancreatic duct and activate once they are in the duodenum, protease(protein) lipase(fat) amylase(carbs)

acute pancreatitis patho

acinar cell injury - release of active pancreatic enzymes - ductal and pancreatic tissue autodigestion - inflammation and destruction

islet cell injury - impaired hormone secretion into blood stream

most cases are mild inflammation but can be severe life threatening necrotizing hemorrhagic pancreatitis with severity based on tissue damage and inflammation extent

chronic pancreatitis patho

repeated pancreatitis leading to chronic inflammation, fibrosis and chronic pancreatitis

pancreatitis risk factors

gallstones, ETOH, increased triglycerides, ERCP, drug reactions, cystic fibrosis

pancreatitis clinical manifestations

sudden epigastric or LUQ pain that radiates to the back, severe, worse with fat meals and when supine, better in fetal position, low grade fever, N/V

acute pancreatitis complications

inflammation - slow bile flow - increased bilirubin leading to jaundice

inflammation - leaky pancreatic blood vessels - pancreas edema - pseudocyst(infected, SBO, rupture leading to peritonitis)

acute pancreatitis complications cont.

increase blood sugar, hypocalcemia(autodigestion uses up Ca), necrosis(autodigestion kills tissue), hemorrhagic pancreatitis(eroded blood vessels)

systemic acute pancreatitis complications

systemic inflammatory response - altered coagulation(disseminated intravascular coagulation) - leaky systemic blood vessels - hypovolemia leading to shock and AKI - pleural effusion leading to ARDS

chronic pancreatitis s/s and complications

recurrent consistent abdominal pain

pancreas fibrosis - decreased endocrine function leading to decreased insulin and diabetes, decreased exocrine function leading to malabsorption of nutrients and weight loss, fatty stools and vitamin deficiency

pancreative cancer

pancreatitis diagnostics

increased lipase and amylase(not seen in chronic), increased WBC, triglycerides, glucose, bilirubin and decreased calcium

abdominal CT, can find pseudocyst and chronic fibrosis

pancreatitis acute treatment

supportive care, IV opioids and antispasmodics, NPO, IV fluids, antiemetics, electrolytes, monitor for complications, NG tube for suctioning

pancreatitis recovery and ongoing care

acute recovery: when food tolerated, small frequent increases in carbs and protein meals, decreasing fat, no ETOH or nicotine

chronic ongoing care: pain control, no ETOH or nicotine, nutritional supplements, diet of bland food with increased fat and carbs, DM management