cholecystitis + pancreatitis (SG 2) Flashcards
gallbladder function
collects, concentrates, and stores bile that comes from the liver, which is then released to the duodenum (SI) via the common bile duct (CBD)
bile
made up of cholesterol, bilirubin, and bile salts
a digestive fluid made by the liver to help break down fat + remove waste
cholecystitis
inflammation of the gallbladder as a result of obstruction
ACUTE: isolated episodes lasting days to weeks; does not cause permanent damage
CHRONIC: continuous and recurrent information; can cause permanent damage
calculous v. acalculous
CALCULOUS: cholelithiasis (gallstones) cause obstruction; this form is more common
ACALCULOUS: no cholelithiasis causing inflammation
risk for cholecystitis
prior family hx / genetic predisposition
DM 2* (changes the bile concentration + slows down gallbladder motility)
gastric bypass surgery
crohn’s dz (dec. absorption of bile salts)
rapid weight loss (inc. cholesterol release)
sickle cell dz (break down of rbc, inc. bilirubin)
calculous cholecystitis
most often occurs to any change in concentration of bile components: cholesterol, bilirubin, bile salts, which leads to formation of cholelithiasis that clog the CBD resulting in inflammation
four f’s of cholecystitis
1.) female hormones
estrogen slows down GB emptying/motility
2.) forty +
3.) fat
4.) fertile
inc. progesterone, which slows GB motility
tx of cholecystitis
COLLAB:
acute / persistent pain management, weight loss
MEDS:
opioids (morphine / dilaudid), NSAID (ketorolac)
*SE: diarrhea, NV, dizziness, rashes, SJ syndrome, anaphylaxis
PREVENT OBESITY:
low fat / cholesterol foods, regular exercise
recognizing signs of ACUTE cholecystitis
ASSESS:
diet + lifestyle, pain in abdomen (RUQ) + scapula / shoulder; may present with murphy’s sign
LABS:
increased WBC, alkaline phosphate + AST / aspartate transferase (liver involvement), LDH / lactate dehydrogenase (tissue damage), serum bilirubin
DIAGNOSITC:
x-rays, ultrasounds, ERCP / MRCP
recognizing signs of CHRONIC cholecystitis
S+S
jaundice, icterus, pruritus (bile salt accumulation on skin), NV, tachycardia, steatorrhea
drug interactions w/ cholecystitis
NSAID: aspirin
antihypertensives
diuretics
penicillins
cephalosporins
carbapenems
pancreas function (2)
important for regulation of metabolism
EXOCRINE: secretes enzymes for digestion of fat, carbs, and proteins
LIPASE for fat, AMYLASE for carbs, PROTEASE / TRYPSIN for proteins
ENDOCRINE: contains islets of langerhans; alpha (glucagon for inc. blood sugar / energy) and beta (insulin to regulate / dec. blood sugar)
pancreatitis
inflammation of the pancreas
r/t pancreatic digestive enzymes (lipase, amylase, protease / trypsin) activated prematurely (autodigestion); enzymes begin to eat the pancreas itself
acute + chronic
acute pancreatitis
short term (days to weeks), early tx prevents long term damage to pancreas
*R/T ALCOHOLISM; prevalent during celebrations / holidays
risk for pancreatitis
biliary tract disease (possible obstruction since GS can travel)
trauma
ALCOHOLISM (acinar cells in pancrease metabolizes alcohol to ethanol, which triggers autodigestion / destroys tissue)
hypertryglicermia
viral infections (hep b)
medications (antiepileptic drugs, vaporic acid, ACE inhibitors)
smoking
recognizing signs of ACUTE pancreatitis
ASSESS:
severe abdominal (LUQ, mid-epigastric) pain, jaundice, cullen’s sign (ecchymosis w.in periumbilical area), bleeding, hypoactive BS, inc. HR + temp, dec. BP (signs of shock / hemorrhage), tender abdomen, edema / swelling
LABS:
amylase and lipase, serum bilirubin and alkaline phosphatase and ALT (liver), WBC, ESR (inflammation), magnesium and calcium
DIAGNOSTIC:
ultrasound, CT scan, x-ray
tx of ACUTE pancreatitis
typically stronger meds for abdominal pain (PCA / fentanyl patches)
NPO
low calcium may lead to tetany (inc. cramps, twitching, and numbness)
decrease in gastric acid r/t use of PPIs
chronic pancreatitis
progressive dz with remissions and exacerbations that may lead to pancreatic insufficiency / atrophy
ethanol from alcohol consumption may lead to the creation of protein plugs, which clog pancreatic ducts
recognizing signs of CHRONIC pancreatitis
abdominal pain (burning)
ascites
respiratory compromise
steattorhea
weight loss
jaundice
dark urine
DIABETES (polyuria, polydipsia, polyphagia)
tx of CHRONIC pancreatitis
NSAIDS (opioids)
PERT (pancreatic enzyme replacement therapy)
use of PPIs (dec. acid secretions)
TPN / enteral feedings / vitamins
NO ALCOHOL
low carb, high protein diet
