adult health 2 FINAL

true/false: the pancreas has both endocrine AND exocrine functions

TRUE

cholecystitis

inflammation of the gallbladder

acute cholecystitis can be broken down into which groups?

calculous and acalculous

acute calculous cholecystitis

-made of calcium, cholesterol, phosphorus, and protein

-most common

-inflammation caused by gallstones (irritates the inside of gallbladder)

-cause inflammation, impaired circulation, edema (inflames until PERFORATION, contents flow into abdomen)

acute acalculous cholecystitis

-inflammation WITHOUT stones

-cannot fill/empty; poor BF, twisted duct

chronic cholecystitis

-will see jaundice

-repeated episodes of duct obstruction causing chronic inflammation

-calculi almost always present

-permanent changes (necrosis, atrophy)

-can be d/t low fat diets= high risk for CHRONIC

incidence and prevalence for cholecystitis

-usually occurs in affluent countries (diet, lifestyle)

-more common in women than men (d/t estrogen increasing cholesterol and bile)

etiology and genetic risk for cholecystitis

-familial or genetic tendency (don’t know if it’s ALL genetic)

-family nutrition habits (families eat the same)

other risk factors for cholecystitis

-T2DM

-gastric bypass surgery

-chron’s disease

-rapid weight loss

-sickle cell disease

history for cholecystitis

-diet HIGH in fat, calories, carbs, and LOW in fiber

-low fat diet = reduces demand for bile release

-body isn’t used to digesting fat, struggle to break it down

-fatty foods make gallbladder contract

-sedentary = BILE STASIS

-ask about HRT

lab assessments for cholecystitis

-WBC (high d/t inflammation)

-alkaline phosphatase (ALP), AST, LDH (all high if there is an obstruction from gallbladder is affecting liver function)

-bilirubin (liver can’t hand off to gallbladder)

-amylase and lipase (pancreatic enzymes d/t blockage)

diagnostic assessment for cholecystitis

-RUQ ultrasound (BEST INITIAL TEST, shows inflammation and outline of stones)

-HIDA scan (follows normal flow of bile)

-ERCP (looks at bile and pancreatic ducts)

-XRAYS ONLY SHOW CALCIFIED STONES

ERCP

-endoscopic retrograde cholangiopancreatography

-similar to EGD/endoscopy

MRCP

MRI with contrast

acute symptoms of cholecystitis

-pain (RUQ radiating to the right shoulder, persistent/acute, rebound tenderness, doctor will palpate)

-indigestion

-fever (d/t inflammation)

-N/V

-GI symptoms with certain foods

-olds and DM PT’s present differently

chronic symptoms for cholecystitis

-d/t prolonged symptoms

-jaundice & clay-colored stools (bilirubin NOT where it’s supposed to be)

-dark urine (bilirubin backs up into circulation)

-icterus (sclera of eyes turns yellow)

-steatorrhea (improper fat absorption)

-fever/tachycardia (brings PT to hospital→ perforation)

-fat intolerance (eat fatty foods)

nutrition for managing acute gallbladder pain

-avoid fatty foods

-NPO if N/V (gallbladder attack)

drug therapy for managing acute gallbladder pain

-IVF (if NPO, avoid electrolyte imbalances)

-opioid for acute pain (morphine/hydromorphone)

-ketorolac for mild/moderate pain (IV NSAID, monitor for GI bleeds)

-antiemetics

-ursodiol to dissolve or stabilize gallstones (long-term tx ONLY, prevent gallstones from growing)

percutaneous drain placement (cholecystitis)

-opens the blocked duct to allow bile to flow

-can be internal, external, or both

-educate PT’s about how to maintain their drains/bags

internal percutaneous drain

connect liver to duodenum (out of circulation)

external percutaneous drain

goes from liver OUT of the body (gravity)

internal/external percutaneous drain

-mix of both, bile ALWAYS has a place to go

laparoscopic cholecystectomy

-crush stones, aspirate bile, remove gallbladder

OPEN PROCEDURE ONLY FOR PERFORATION

post-op care for lap. cholecystectomy

-pain control (oral opioid/NSAID)

-antiemetics

-activity (help get rid of excess air from surgery)

-diet (clear liquids, SLOWLY include fatty foods)

-monitor sites for swelling!

open cholecystectomy

-if gallbladder is ruptured or abscessed

-JP drain (in gallbladder bed)

OUTPUT: serousanguinous with bile

-JP drains come out after 24hrs

-hospitalized 1-2 days (need opioid meds, splint, TCDB)

nutrition for post-cholecystectomy

-low fat/high fiber diet

-avoid gas producing foods

-small frequent meals (BEST OPTION)

foods to avoid for cholecystitis

fast food, fried food, butter

education regarding pain relief (cholecystitis)

start with acetaminophen, careful with NSAIDS

education on post-cholecystectomy syndrome

-PT will still have same symptoms even after gallbladder is removed

-d/t OTHER UNDERLYING ISSUE:

-pseudocyst (benign)

-leak from bile duct

-missed stone

-pancreas/liver mass

acute pancreatitis

-inflammation of the pancreas

-can be life-threatening

-autodigestion and fibrosis of pancreas (d/t pancreas releasing premature enzymes, damages tissue)

complications of acute pancreatitis

-jaundice (obstructed flow to liver)

-pancreatic pseudocyst (leak of fluid causes a cyst)

-DM (destruction of pancreas, endocrine)

-pleural effusion (leaking of contents, can cause pneumonia)

-MODS (NHP: multiple organ dysfunction)

-ARDS (NHP)

-coagulation deficits (severity leads to death, NHP)

-sepsis (NHP)

-hypovolemic shock (NHP)

incidence and prevalence of acute pancreatitis

-"attacks” common during holidays and vacation when alcohol consumption is high

-common following cholithiasis and biliary tract problems (postpartum)

etiology and genetic risk for acute pancreatitis

-alcohol use and gallstones (two most common causes)

-trauma (GSW, etc)

-ERCP (d/t contrast)

history for acute pancreatitis

-collect hx after pain is controlled

-ask about alcohol usage and medical problems

dx: clinical picture and symptoms

physical assessment for acute pancreatitis

-severe abdominal pain (often mid-epigastric or LUQ, radiating to shoulder)

-jaundice

-gray-blue discoloration of abdomen, umbilicus, flanks

-vital signs

other symptoms for acute pancreatitis

-leakage of pancreatic enzymes into subQ tissue

-paralytic ileus

-peritonitis

-rigid abdomen

-PAIN GOES AWAY IN FETAL/TRIPOD POSITION

psych assessment for acute pancreatitis

ALCOHOL CESSATION

etiology for acute pancreatitis

-amylase (elevates first for 2-3 days, most specific)

-lipase (5-7 days after attack, also more specific)

-WBC, ESR (inflammation)

-ALT (bile duct is involved)

-serum bilirubin, alkaline phosphatase (same as ALT)

-BUN and glucose (SEVERE chronic pancreatitis)

other dx assessments for acute pancreatitis

-abdominal ultrasound (shows CAUSE)

-contrast enhanced CT (most reliable, tells us that the pancreas is inflamed, GOOD FOR DX)

managing acute pain (acute pancreatitis)

-as well as inflammation and treat symptoms

-PCA (continuous, immense pain)

-transdermal fentanyl (patch)

-epidural analgesia (severe cases)

-H2 blockers and PPI’s (help with gastric acid secretion)

-side lying position or fetal (helps with pain)

-NPO/NGT (can be painful, monitor skin and hydration)

-ERCP (physically remove stones/open ducts→ LAST RESORT)

promoting nutrition (acute pancreatitis)

-initially NPO in early stages (lower production of enzymes)

-antiemetics

-enteral feeding (NJT)

-bland, non-GI irritating foods

-mod-to-high carb, high protein, low fat

-supplements PRN

MGMT for acute pancreatitis

-no alcohol

-what to watch out for

-how to prevent it from happening again

-psych, AA, etc

chronic pancreatitis

-progressive destructive disease of pancreas characterized by remissions and exacerbations

-inflammation and fibrosis of tissue contribute to pancreatic insufficiency

chronic calcifying pancreatitis (CCP)

-alcohol is the MAJOR contributor

-most common type, men > women

chronic obstructive pancreatitis (COP)

-inflammation, spasm, and obstruction of sphincter of Oddi (isn’t open)

autoimmune pancreatis

-chronic inflammatory process

-pancreas attacking itself, Ig’s invading pancreas

-common to also have autoimmune in lungs and liver

-high risk for pancreatic cancer

idiopathy and hereditary pancreatitis

-gene mutations

-endo: PT will have DM

-exo: can’t digest food

chronic calcific pancreatitis

-axial unenhanced CT image

-demonstrates multiple pancreatic calcifications (common finding in chronic pancreatitis)

-the pancreatic duct is also dilated, although that is generally better delineated on post-contrast images

symptoms for chronic pancreatitis

-abdominal pain (continuous, burning pain)

-ascites (liver complications)

-respiratory compromise (leakage into thoracic cavity)

-steatorrhea (fat excretion in stools)

-muscle wasting

-weight loss

-jaundice

-dark urine

-polyuria, polydipsia, polyphagia (PT is a new-onset diabetic)

labs/imaging for chronic pancreatitis

-ERCP, CT scans, ABD US

-amylase and lipase (not SUPER elevated, body is compensating)

-bilirubin and alkaline phosphatase (blockage between pancreas and liver)

managing acute and persistent pain (chronic pancreatitis)

-drug therapy:

-opioids (be careful)

-non-opioid

surgical MGMT for chronic pancreatitis

ONLY FOR COMPLICATIONS OR UNCONTROLLED PAIN

drugs for chronic pancreatitis

-H2 blocker or PPI

-nutritional interventions same as acute pancreatitis

-TEN/TPN as needed (if we HAVE TO)

-avoid high fat food

-4000-6000 calorie diet (impaired absorption)

-avoid alcohol

pancreatic enzyme replacement therapy (chronic pancreatitis)

-standard care to prevent malnutrition, malabsorption, excessive weight loss (if PT can tolerate it)

-contain amylase, lipase, and protease

-take with all meals and snacks

-don’t chew, crush, etc

-should immediately see improvement

care coordination and transition MGMT for chronic pancreatitis

-easily accessible toilet facilities (frequent BM’s)

-collaborate with case MGMT for assistance

-education (preventing exacerbations)

-skin care (moisture barrier for BM’s)

-MGMT of DM (diabetes educator, endocrinologist, AA)

liver facts

>400 functions

-older you get = decreased liver (less drug absorbance)

-ALWAYS ask about alcohol use

-liver failure = increased ALT/AST

cirrhosis

-characterized by widespread fibrotic (scarred) bands of connective tissue that are both NECROTIC AND IRREVERSIBLE

-caused by chronic inflammation

-tissue become nodular

-nodules block blood and lymph flow

-liver shrinks in size and hardens

types of cirrhosis

-post necrotic

-laennec’s (alcoholic)

-biliary

post-necrotic cirrhosis

caused by Hep. C, drugs, toxins

laennec’s (alcoholic) cirrhosis

chronic alcoholism

biliary cirrhosis

chronic obstruction, autoimmune disease

portal HTN

-persistent increase in portal vein pressure (d/t increased resistance or obstruction of BF through PV)

-dilation of vessels in stomach, esophagus, intestines, rectum

-causes splenomegaly

ascites

-excessive abdominal fluid d/t portal HTN

-causes “third spacing”, edema and hypovolemia

esophageal varices

-distended veins in the esophagus

-blood backs up, causing distention

-thin/fragile vessels

-CAN BE LIFE-THREATENING

biliary obstruction

-high risk for bleeding/bruising, jaundice

-bile decreased, prevents absorption of fat-soluble vitamins (vit. K)

complications of cirrhosis are d/t…

-depends on amount of damage done to liver

-metabolic abnormalities

more about portal HTN

-blood backs up into alternate routes

-causes thrombocytopenia

-causes splenomegaly

-ascites, esophageal varices, prominent abdominal veins

hepatic encephalopathy

-if caught early, it’s reversible

- “portal system encephalopathy”

-sleep/cognitive/speech problems→ early presentation

-persistent increase in complex cognitive syndrome

-ammonia will be INCREASED, PT can’t detoxify protein/byproducts d/t cirrhosis

-worsened by high protein, infection, hypovolemia, constipation, drugs, hypokalemia, GI bleeding (high protein)

other complications of hepatic encephalopathy

-hepatorenal syndrome

-spontaneous bacterial peritonitis

-hepatopulmonary syndrome

hepatorenal syndrome

poor prognosis, low kidney function, high BUN/Cr, can’t get electrolytes out

spontaneous bacterial peritonitis

ascitic fluid contaminated by bowel bacteria (dx by paracentesis)

hepatopulmonary syndrome

increased pressure makes it hard to breathe

incidence and prevalence for cirrhosis

-chronic liver disease and cirrhosis are major causes of death

-from viral hepatitis (C), alcohol use, bile disease

hepatitis C

leading cause of cirrhosis and liver cancer in the US

hepatitis B and D

most common causes of cirrhosis worldwide

NAFLD

associated with obesity, DM2, metabolic syndrome

history for cirrhosis

-social history (alc/drug intake, toxic chemicals

-family hx, biliary issues, HF, blood transfusions

psychosocial assessment for cirrhosis

-subtle and obvious changes

-basic changes→ DRASTIC decreased LOC

alcohol withdrawal

-heavy/prolonged use

MONITOR FOR:

-tremors (6-8hrs after alc exposure)

-agitation

-confusion

-delusions

-hallucinations

-tachycardia, HTN, diaphoresis, seizure risk

physical assessment for cirrhosis

-many early symptoms are vague (fatigue, wt changes, anorexia, N/V, pain/tenderness)

LATE STAGE:

-jaundice and icteric sclera (yellowing)

-pruritis (dry/itchy)

-petechia (easy bruising, CF’s/platelets)

-ascites, peripheral edema

-hepatomegaly

-splenomegaly

-increased abdominal girth

-fetor hepaticus (fruity breath)
-impaired neuro fxn (progress to COMA)

-asterixis (tremor, hand-flapping)

lab assessments for cirrhosis

-liver enzymes (HIGH, most specific = AST)

-alkaline phosphatase (HIGH)

-gamma-glutamyl transferase (HIGH, measure if damage to liver/bile ducts = biliary obstruction)

-bilirubin (serum HIGH, uro-: HIGH, not excreting)

-albumin (LOW)

-PT/INR (HIGH, less prothrombin)

-platelets (LOW, less thrombopoetin)

-ammonia (HIGH, byproduct)

-sodium (LOW, diluted d/t ascites)

-anemia d/t blood loss

imaging assessments for cirrhosis

abdominal x-rays (liver is SWOLLEN, CT/MRI→ masses, benign/malignant)

other dx assessments for cirrhosis

-liver US (most broad test)

-doppler US (portal vein thrombosis)

-US transient elastography (non-invasive test for LIVER STIFFNESS)

-arteriography (look @ portal veins from inside)

-EGD (varices, etc)

BIOPSIES ARE HIGH-RISK

managing fluid volume for cirrhosis

-diuretics (loop and potassium-sparing, I/O and electrolytes)

-IV ABX (S/S of spontaneous bacterial peritonitis)

-vitamin supplements (thiamine, folate, multivitamin, ESLD and liver can’t store these)

-paracentesis

-respiratory support (dyspnea, crackles, pneumonia)

-fluid and electrolyte imbalance (accumulation, prevent progression)

ASCITES PT’s: low sodium diet (1-2g), avoid high fluid volume, NO TABLE SALT

paracentesis

-may be done at bedside or in procedure area (US guidance, relieve S/S, dx, LARGE NEEDLE)

-may be therapeutic or diagnostic

-specimens sent to lab

-potential for large fluid volume shift (remove >5L of fluid, body tries to refill and pull from vessels→ circulatory collapse, hypovolemia)

PRE-OP: PT education, consent, orders

POST-OP: wt, output (3 C’s), VS

-fluid bolus of albumin

drug therapy to reduce portal pressure

-beta blockers (propranolol): lower HR and PVP

-vasoactive drugs (octreotide): low BF by vasoconstricting portal area

-IV ABX (GI bleeds)

endoscopy for cirrhosis

-all PT’s screened for varices

-endoscopic variceal ligation (rubber bands cut off circulation)

-endoscopic sclerotherapy (chemicals injected, causes clotting and collapse vessels)

emergency treatment for esophageal varices and excessive bleeding

3 openings of the tube:

-gastric aspiration- blood

-inflating the esophageal balloon

-inflating the gastric balloon

esophageal balloon is inflated to a pressure of 20-40mm Hg

esophageal balloon compresses the esophageal veins

gastric balloon is inflated with 250cc of air, applies pressure to the fundal veins when slight traction is applied

transjugular intrahepatic portal-systemic shunt (TIPS)

-unresponsive to other ascites/bleeding tx’s

-done in interventional radiology lab

-jugular vein access

-shunt through liver to reduce portal vein pressure and varices and alleviate ascites

-blood bypasses liver filtration (not causing backup, but includes toxins that the liver would have filtered normally)

sheathe→needle→balloon→shunt

planning and implementation for preventing/managing confusion

-monitor ammonia levels or neuro status

-high carb, moderate fat, high protein diet (moderate protein diet if ammonia is elevated, want it to heal but still filter)

drug therapy for ammonia MGMT

-lactulose: promotes ammonia secretion, titrate to 2-4 soft stools/day (losing ammonia, monitor electrolytes)

-rifaximin or neomycin sulfate: monitor for changes in LOC, asterixis, fetor hepaticus (destroy normal GI flora, no opioids, barbs, benzo’s, NEPHROTOXIC AND ONLY SHORT-TERM USE)

managing pruritis

-avoid being too warm

-avoid irritants

-corticosteroid creams (cool compresses, moisturizers)

-drug therapy if other tx not effective (SSRI’s help with itching)

home care MGMT for cirrhosis

setup, diuretics/lactulose, comfort (HF, elevate feet)

self MGMT for cirrhosis

-nutrition, no drugs, drains/bags (no more than 2L)

-multivitamins/supplements

-bleeding

healthcare resources for cirrhosis

-HH nurse

-AA

-support groups

-palliative/hospice care (ESLD)