Renal, Hormones- Test 3

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diagnostic tests for liver, bilary and pancreatic functions

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potential symptoms anticipated in pt experiencing problems w/ accessory digestive organs

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differeniate pathophy associated with clinical manif - cirrohosis and hepatitis

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care plan for pt experiencing problems w/ acc digestive organs

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nursing implications r/t medications to treat liver, bilary, pancreatic disorders

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id teaching needs of pt with chronic acc digestive organ dysfunction

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*gallbladder purpose AND dysfunction symptoms

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purpose - storage and dehydration of bile (produced in liver). producing bile concentrate ready to respond in presence of dietary fat

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path fats travel in regards to gallbladder/bile

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fats enter duodenum

release of choleystokinin (prod in pancreas)

stimulates GB

allows release of bile from GB

bile flows thru cystic duct --- to common bile duct --- into duodenum to begin breakdown of dietary fat

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3 main pancreatic enzymes involved in digestion

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amylase - carbs

lipase - fats

trypsinogen/trypsin - proteins

----------------- others
enterokinase
chyme
choleycysokinin (stim gb to release bile)

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what stimulates GB to release bile

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cholecystokinin

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pancreatic normal activity consist of...(2)

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1) secretion of bicarb - cause juices to become alkaline (ph=8) which neutralizes gastic acid

regulated by secretin

2) secretion of insulin
which allows for storage of excess glucose amounts

moves glucose from blood stream into cell

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**what activity can a patient with pancreatitis NOT do

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smoke

decreased secretin production - more acid in gut

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< secretin = ________

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secretion of bicarb -- which makes pancretitic juices alkaline

< secretin = more acid in gut

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liver function - metabolism of nutrients

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detoxification, protein synthesis, aids in digestion.

metabolism of nutrients
---protein bd aa to ammonia
---carb
---fats

****bd nutrients - metabolism
bd aa - NH3

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liver function - storage of?

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fat sol vitamins ADEK
minerals IRON
glycogen - storage form of glucose - glyconeogenesis in liver -

bile prod & excretion via heaptic ducts

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albumin serum level of ___ is incompatible with life

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under 2.2

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liver also snythesizes ___

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albumin - blood protein, truck driver of blood stream - transports substances thru out body
-drugs
-vitamins
-hormones
-immunoglobins

also essential in maintain osmolarity

TANG in blood
body calls on extravascular to come intravascular - dilute

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decreased albumin can cause

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3rd spacing
fluid in to body tissues

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liver also detox what substances and is responsible for?

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drugs, blood, hormones, and is responsible for conversion of ammonia to urea -- then is excreted by kidney

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liver also cogulates blood by

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producing clotting factors
-prothrombin and fibrinogen-

vitamin k - critical component of clotting (fat soluable)

problem with bleeding -- indiciates LIVER ds

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problem with bleeding can indicate...

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liver disease

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LO1 - dx tests

total protein
albumin

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total protein nv 5.5-9.0

albumin nv 3.5-5.5

decrease in these values indicate a pt with malnutrition and could indicate liver damage

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which labs can show pt is malnurouished?

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dec albumin
dec total protein

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***patients with liver diease should NOT eat what kind of diet?

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high protein - cannot break it down
which increase NH3 levels

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LO1 dx test

bilirubin
ammonia
prothrombin time

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total bilirub nv 0.2 - 1.0
direct bilirub nv 0.1 -0.3

ammonia nv 15-45
**liver disorder if increased*

prothr time nv 10-13 sec

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normal ammonia level is?
what indicates liver disease regarding ammonia levels?

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15-45

increased levels indicate liver ds

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other dx studies for liver/pancreas/...

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ct - detects abn
mri - detects abn
us - detect thickening strutural walls, struc abn

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what dx study is a clear indicator of GB disease?

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ultrasound

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***what is percutaneous cholangiogram?

when done?
purpose?

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injection of dye into biliary system

dye can trace route that bile takes from liver to duodenum

done post GB - look for strictures, stones that doc didnt know about

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what is ERCP?

endoscopic retrograde cholangiopancreatography

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endoscopy - direct visulation of dig tract down to and including duodenum

often done in conjunction with cholangiogram - dye traces route of bile to duodenm**

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LO4 plan of care - digest organs

nursing dx for
any client with accessory digestive organ disorder

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altered nutrition: less body requirements r/t to acc organ dysfunction

-assess ht & wt
-assess protein (album & prealbum)
-dietary restrictions
-assess need for supplements

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decreased albumin tracks ___ term malnutrition

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long term maln -- 6 weeks protein intake

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decreased pre albumin tracks ____ term malnutrtion

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short term maln
(7-10 day protein intake)

trend up with TPN

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cholelithiasis - pathophy,
risk factors, symptoms, treatments

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lith=stone
asis= condition of

GB stones, calculi
cause by bilary sludge due to altered cholesterol or bile metabolism

gb bile concentrated - gets hard - causes stone

risk factors - female, obesity, >40 yrs age

FEMALE-FAT-FORTY
no symptoms

treat -

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cholecystitis

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inflam of GB wall caused by gallstones which have obstructed flow of bile via cystic duct

inflam caused by over stimulation trying to get around stone

GB wall thickens

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LO2 symptoms - acc dig organs

acute cholecytitis

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timing, characteristics,accompanied by?

acute---timing after eatin (esp fatty foods), freq at night
epigastric, RUQ, radiation to right scapula or back, severe dull and constant

accompanied by -- n/v, fever, increased pain w/ breathing, belching

nausea - not bd food, stomach irritated
increased pain - diaphragm on phrenic nerve
belching - trouble bd fat, producing gas

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LO2 - sympt acc dig organs

chronic choleycytitis

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timing, characteristics, accompanied by

after repeated acute episodes

protection --- thickening GB wall

GB shrinkage - inability to perform function of concentrating storing and releasing bile

absence of urobililinogen to color stools and excess of circulating bilirubin

-clay colored stools
-dark amber urine
- increased serum levels bilirubin

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chronic cholecystitis caused ___ stools, ____ urine and ___ levels bilirubin

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clay colored stools, dark amber urine, increased levels bilirubin

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complications of cholecystitis

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blocked common bile duct - blocks all bile - impairs fat metabolism

risk for jaundice or pancreatitis

obstruction jaundice
normal flow blocked, allowing excess circulating bile

bile salts accum on skin
-discoloartion
-itching - difficult to control w/ medication
-sclera yellow

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common bile duct obstructed - what substances are blocked

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bile

pancreatitic enzymes

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goal of gallbladder patient
r/t
acute pain
alter gas exchange
alter bowel func

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relieve and control pain, to allows ambulation, deep breathing (pre and post op)


prevent ateclatisis and pneumonia - lung sounds, pulse ox, ics, oxygen, ambulation, hug me support

prevent ileus, restore normal function - bowel sounds bm, flatus?
restritc use narcs asap - ambulation

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pain btw shoulders in post op gallbladder pt indicates

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gas entrapment

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interventsions for post op gallbladder

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small freq meals, low fat, replace fat sol vitamins

analgesics, anti spasmodics/anticholinergics, BENTYL (spasm pain)

spams can causes ileus

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jp drain is watchdog for

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internal bleeding

serosang is expected first 24-48 hrs

p 24 hrs drainage will progresss from serosang to bile colored

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T tube is used for ___
allows for ____
normal drainage, how long, NEVER _____

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convienent access for monitoring post op biliary complications

clamp 1-2 hrs before and after meals === looking for GB symptoms

normal drainage 400 cc
maintained 7-10 post op
NEVER irrigate

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*****teach post op gallbladder/cholecystectomy patients what?

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avoid high cholesterol foods
avoid foods high in fat
avoid gassy foods

small more freq meals
maintain restriction on fat content post op (gives body time to adjust to fact there is no GB and concentrated bile)
fat soluable vitamins replacement

signs of infections

no heavy lifting 4-6 wks lap
8 wks open

drain care, expected volumes

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acute pancreatitis is -- poss causes?

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autodigestion process - premature activation of enzymes results in pancreatic cell destruction

not digesting CHO, proteins, Fats -- digesting itself

- incompentent sphincter of oddi
- panc duct obstruction

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precusor to pancreatitis

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alcohol

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chronic pancreatitis is

2 types

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LT auto digestion

progressive destruction of pancr with fibrotic tissue replacement (Scar)

chronicobstructive- biliary ds and inflam sphincter of oddi

chronic calicifying pancr -- MOST COMMON - d/t chronic alchol abuse

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2 causes pathophy of chronic pancreatitis

1. proteolysis
2. blood vessel necrosis

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protein degradation

trypsin responsible for autodigestion of pancrea -- involved in formation of

EDEMA, HEMORRHAGE, NECROSIS of pancreas

2, bv necrosis
elastase dissolves elastic fibers of bv and ducts causing bleeding - hemmorrhage

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pathophys chronic pancreatitis cause hemorrhage and edema

which protiens are degraded to begin this process

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tryspin - autodigestion edema, hem, necrosis

elastase - hemmorrhage

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chronic pancreatitis --

lipolysis

inflammation

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lipase caused fat necrosis and release of fatty acids that combine with calicum which result in HYPOCALEMIA
--cal out of blood to combine with fatty acids) blood serum calicum LOW

2. leukocytes collect in areas of panc bleeding and necrosis can lead to pseudocyst and abscesses

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what electrolyte imbalance is common with chronic pancreatitis??

why??

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hypocalemia

calicum is drawn out of blood to combine w/ fatty acids produced from fat necrosis (lipase)

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cullen's sign

turners sign

mean what?

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cullens - bluish discoloration periumbilicus - results from severe hem from chronic panc

turners - bluish discoloration left flank area - peritontitis

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murphys sign??

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elicited when client reacts to pain and stops breathing

commmon in clients with cholecystitis

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steathorra is associated with acute or chronic pancreatitis?

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chronic

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amylase 25-130

if elevated always indicates what?

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pancreatitis

if lipase is also elevated it rules out any other cause

lipase 10-40

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enzyme replacement given to pancreatitis patients... important things to know with adminstration

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pancrease -

must take BEFORE ORAL INTAKE

MIX WITH WATER OR JUICE WITHOUT PROTEIN COMPONENT

MOUTH CARE A MUST - RINSE

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pancreas acid production

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secretin secreted in pancreas which turns off gastric acid production in stomach

bicarb produced in pancreas

deficient secretin + deficient bicarb = increased gastric acid

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pancreas secretes insulin -- deficient levels create

treatments

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unstable blood glucose

insulin drip
insulin coverage schedules
careful monitoring of levels

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pancreas pharmacologic treatments

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insulin drip, insulin coverage schedules, BENTYL (antispasmodic/anticholinergic)
-anticipate reduction in bowel function
-requires freq bowel assessments to prevent secondary paralytic ileus or bowel obstruction

TPN - malnutrition

NPO - cannot break down food
pre-albumin - malnutrition

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should a pancretitis patient be on bedrest or ambulatory?

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bedrest until under control. bedrest allows for lower metabolic needs, which can divert more energy to healing

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which patient is not permitted to drink alcohol or ingest caffeine

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pancreatitis

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acute pancreatitis pt will be NPO until

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abd pain reduces - reduction in panc stimulation

foods are re-introduced:
1. liquids
2.small more freq meals HIGH CHO
LOW FAT
LOW PROTEIN

NO ALCOHOL, CAFFEINE OR SMOKING

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decreased pancreas output interrupts bicarb production and _____ secretion

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secretin secretion - which stops gastric acid secretion in stomach

dec secretin + dec bicarb = more gastric acid

tx - antacids

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the damage healing damage healing process of pancreatitis leads to

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pan cancer

****A SILENT KILLER******

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pancreatitis teachin points about re-occurence
4 points

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1. abd pain / distention
2. steatorrhea
3. hyperglycemia
4. weight loss

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common first symptom of pancreatic cancer

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jaundice

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lab/dx studies that indiciate pancreatic cancer

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elevated CEA (tumor maker for abd cancer)

ca19-9
ca242

CT scan - shows tumor

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survival of pancreatic cancer is ____ why?

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low
b/c of need for pancreas for digestive properties, often dx late as the symptoms are vague and go unnoticed

poor prognosis

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what is cirrhosis

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scar tissue which forms on the liver and prevents efficient liver function

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liver function tests (LFTs)

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elevation = liver damage or stress


AST - SGPT 8-35

ALT - SGOT 4-26

alkaline phosphatase 30-126 (measure of enzyme produced in liver)

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ammonia comes from

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protein

bacteria in gut - metabolism of that bacteria is ammonia

ammonia crosses BBB -- brain swells hepatic enceph

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increased blood ammonia levels leads to ____ what are some symptoms

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hepatic enceph, brain swells, (Nh3 increased 67)

pt will be nutsy, thinking werid

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prothrombin time is ____ in liver ds

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elevated
nv - 10-13 seconds

inc ammonia
inc pt

clotting, fat soluble vitamins, potassium altered

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pathophys of cirrhosis

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chronic progressive ds, degeneration & destruction

regeneration causes fibrosis -- scar tissue, not flexible, disrupts normal blood and bile flow

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hepatocellular necrosis is r/t what condition - what is it

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cirrhosis

not enough blood, dec circulation, cell death

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types of cirrhosis

most common

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laennecs -- alcoholic -- most common (Scar tissue & fat from around portal areas)

postnecrotic - complication of hepatitis (scar tissue r/t episodes of viral hep)

bilary - complication GB issue + bile duct (scar tissure forms around bile ducts)

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compensated stage of cirrhosis

s/s

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compensated -

flatulence - not bd fat correctly
- abd pain, fever, edema (ankles - dec albumin)

hepatomegaly **first symptom** palp and percus show evidence of dullness over liver

fector hepaticus -- fruity musty breath odor

skin lesions - spider angioma, palmar erthythema

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decompensated stage of cirrhosis

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jaundice - fibrosis prevents outflow - comes out in skin

weakness and muscle wasting - imp nutrition

weight loss - imp nutrition

mild fever, continous - necrosis

anemia, purpura - blood clotting issues

sparse body hair

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late stages of cirrhosis

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endocrine disturbances - sexual hormone -- gyneomastia, testicular atrophy, ammenorrhea

esophageal varices r/t portal hypertension - clotting abn, gi bleed

neuro deficits - cog changes, peripheral neuropathies, ASTERIXIS(liver flap)

hepato enceph! ammonia abover 67

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complications of cirrhosis

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bleeding tendencies - inc PT

hepatorenal syndrome - liver renal syndrome (filter blood -- if liver isnt filtering more stress on kidneys)

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liver cirrhosis leads to prolonged ____

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prothrombin time

altered coagulation due to DECREASED VITAMIN K STORES

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EARLY CIRRHOSIS treatment....

LATE CIRRHOSIS treatment

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EARLY - osm diuretic

LATE - paracentesis

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hepatorenal syndrome occurs when?

s/s

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after EV/GI bleeding, diuretic therapy for ascites, or onset encephalopathy

azotemia - retention of waste products that are normally excreted

oliguira - urine output <400ml/day

intractable ascites

monitor renal status

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ascites is

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fluid trapped in peritoneal cavity , decreased albumin (osmotic event) TANG

osm pressure --- out
portal HTN --- out

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these drugs are to be used with extreme caution in cirrhosis patients

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1. indocin (indomethacin)
2. aspirin
3. tylenol

all are metab by liver = stress to liver

cannot detoxify = then to kidneys -------> renal issues

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portal hypertension

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high pressure and high volume as result from obstructive process in liver

NEW collateral circulation develops

around obstruction

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portal hypertension develops ______ common sites for this occurs where

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esopophagus, abd wall (caput medusae) peritoneal cavity (ascites) rectum (hemorrhoids)

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increased volume in vascular space - compensates by

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looking for collateral circulation

systemic circulation

bleeding in esp varices - due to prolonged vomiting, increased prothrombin time

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hepatic encephalopathy -- ammonia -- explain

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results from elevated levels of ammonia

ammonia results from bacteria breakdown of protein in gut
--inability of liver to properly metabolize ammonia and convert to urea

ammonia is neurotoxin

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treatment for hepatic encephalopathy

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lactulose - controlled diarrhea
titrated to ammonia levels

if pt is dehydrated -- in ARF delay lactulose b/c of 3rd spacing --- ascites -----lasix

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albumin in bloods leads to

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muscle wasting -