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62 Cards in this Set

  • Front
  • Back
Which Hepatitis is associated with Liver Cancer
Hep B 60% of all liver cancer
Hep A treatment
Supportive
HIATAL HERNIA AND REFLUX
GERD (gastro intestinal reflux disease)
Digestive disorder which effects the LES (lower esophageal sphincter)
Occurs more in overweight and pregnancy
More occurs in clients with hiatal hernia (gastric acid pH iis 1.5-2.0 and esophagus is 6.0-7.0)
Most common in > age 45
Dietary choices may play a role (coffee, chocolate, fatty foods, etc.
Medications may cause reflux (calcium channel blockers, nitrates, and anticholinergics)
HIATAL HERNIA AND REFLUX CLINICAL MANIFESTATIONS
Heartburn/acid indigestion/dyspepsia
Cough/wheezes at night
H2O brash –fluid in throat
Dysphagia –How much, when , constant or intermittant
Odynophagia-painful swallowing
Chest pain
Beltching
Bloating
Gas
HIATAL HERNIA AND REFLUX MEDICATIONS
antacids- neutralize acids by increasing the pH , use for short time, long term use may cause diarrhes, altered calcium levels, and increase of magnesium. Must watch for drug interactions-(Coumadin, Theophyllin, Dilantin, Inderal, and Procardia. If needed more than 3 wks should contact doctor
chronic reflux and heartburn-may prescribe H2 blockers (Pepcid,Zantac, Tagamet, or proton pump inhibitors-Prilosec, Previdid, Aciphex, and Protonix
Prokenetic drugs-Reglan, side effects-increased gastric emptying, may neutrolize neurologic and phycotropic drugs. Urecholine, side effects include: cramping, diarrhea,increase saliva, and urinary urgency
What is a HIATAL HERNIA
Protrusion of stomach through esophageal hiatus into the thorax
Asymptomatic or S/S similar to GERD
Sliding hernia
Most common
Esophageal reflux and complications
Rolling hernia
Slow bleeding resulting from venous obstruction
Iron deficiency anemia
ASSESSMENT FOR HIATAL HERNIA
Heartburn
Regurg
Pain
Dysphagia
Belching
Nutritional status
Lungs for asthma from regurg
History of cardiac problems
Diagnosis
What is ACHALASIA
Failure of a ring of muscle (as a sphincter) to relax (completely)
What are the MAJOR FUNCTIONS OF THE PANCREAS
Secretes fluid containing digestive enzymes into the duodenum
Secretes the hormones, insulin and glucogon
Secretes sodium bicarbonate into the duodenum which neutralizes acid coming from the stomach
Pathophysiologic Processes in Acute Pancreatitis
Lipolysis – lipase causes fat necrosis
Fatty acids are released and binds with calcium which forms a soap like substance
This leads to decrease in serum calcium and parathyroid levels
Proteolysis – auto-digestion which involves trypsin which can lead to clot formation and gangrene
Necrosis of blood vessels – elastase Is activated by trypsin and causes the elastic fibers of the blood vessels to dissolve, which results in bleeding
Inflammation – leukocytes rush to the necrosis and hemorrhage occurs, which may lead to bacterial infection
Acute Pancreatitis CAUSES
Gallstones ( 45%)
Alcoholism
Drugs ( Lasix, steriods, opiates )
Mumps
Increased levels of lipids, increased calcium, hyperparathyroidism
Damage to the pancreas from blunt or penatrating trauma (ERCP, renal failure, transplant)
Cancer of the pancreas
Reduced blood supply to pancreas
Acute Pancreatitis SYMPTOMS
Usually sudden, severe abdominal pain
Coughing and vigorous movement may make it worse
N/V
Tachycardia, orthostatic hypotension
Jaundice
Cullen’s sign (gray-blue discoloration of the abdomen and perium-bilical area)
Turner’s sign (gray-blue discloration of the flanks
If severe may be in shock
Acute Pancreatitis DIAGNOSIS
Amylase and Lipase ( amylase 3 X normal but then returns back to normal after 3-7 days, and Lipase and urine amylase ^ in 2 weeks )
Bilirubin, alkaline phosphatate, ALT which may indicate and obstruction
Abdominal x-rays may show dilated bowel
Ultrasound may show gallstones and swelling
CT scan will show the size of the pancreas
ERCP is done only when a gallstone is the suspected cause
Acute Pancreatitis ASSESSMENT
Observe for all of the symptoms in the previous slide
Decreased bowel sounds, abd distention and tenderness
Lungs – atelectasis, pleural effussion, dyspnea, orthopnea
Look for neurological changes (alcohol withdrawal or sepsis)
Acute Pancreatitis TREATMENT
Most are hospitalized ( some in ICU )
NPO, possible NG tube for up to 6 weeks
IV
O2, possible ventilator
Relieve pain – PCA pump with Demerol which has less spasms in smooth muscles
Oral hygiene
Urine output
Complications of Acute Pancreatitis
Hypovolemia
Hemorrhage
Acute renal failure
Paralytic ileus
Hypovolemic or septic shock
Complications of Acute Pancreatitis CONTINUED
Pleural effusion, respiratory distress syndrome, pneumonia
Multisystem organ failure
Disseminated intravascular coagulation
Diabetes mellitus
Acute Pancreatitis DRUG THERAPY
Anticholinergics – Atropine
Glucogons
Insulin
Zantac
Antibiotics
Acute Pancreatitis -- Nutrition less than Body Requirements
Interventions
TPN
When taking PO – small frequent meals, moderate to high CHO, increase protein, decreased fat, bland, no caffeine or alcohol, vitamin replacement, Ensure
Acute Pancreatitis
NURSING DIAGNOSIS
Acute pain
Imbalanced nutrition
Risk for fluid volume deficit
Risk for infection
Ineffective breathing pattern
Chronic Pancreatitis
Progressive destructive disease of the pancreas, characterized by remissions and exacerbations
Loss of exocrine function
Presenting S/S differ from acute
Abd pain is the major sign which is a continous burning and gnawing
May have dyspnea, weight loss, jaundice, dark urine, polyuria, polydipsia, and polyphagia
Labs - ^ amylase and lipase, bilirubin, alk phos, ^ BS
INTERVENTIONS FOR CHRONIC PANCREATITIS
Pain Rx – may become dependent
Enzyme replacement – are essential for dietary management
Pancreatin and pancrelipase : come in caps, powder of tabs and should not be given with foods containing protein
Insulin therapy – may be on TPN and may have unstable BS, must closely monitor
H2 blockers and Proton pump inhibitors
Diet – TPN, long term, 4000-6000 calories/day, with reduction of fat
PEPTIC ULCER DISEASE WHAT IS IT ?
Ulcer- lesion which occurs in the lining of the stomach or duodenum, where pepsin and acid are present.
20 million/ year develop one ulcer during their lifetime
40,000 have surgery and 6,00 die from complications of ulcers
95% in duodenum and 95-100% are due to H-pylori
can develop at any age/rare in teenagers
duodenal ulcers- adults 30-50 years old
gastric-over 60 years old
PEPTIC ULCER CLINICAL MANISFESTATIONS
1st symptom is pain
epigastric tenderness
with perforation
rigid board like abdomen
rebound tenderness
hyperactive bowel sounds, that diminish
Dyspepsia (most common)
Melena
Gastric ulcer pain/vomiting
S/S fluid volume deficit-orthostatic hypotension
Less common s/s - n/v, loss of appetite, and weight loss
PEPTIC ULCER NURSING DIAGNOSIS
PAIN
RISK FOR FLUID VOLUME DEFICIT
INEFFECTIVE INDIVIDUAL COPING
ALTERED NUTRITION
SLEEP PATTERN DISTURBANCES
DRUG THERAPY FOR PEPTIC ULCERS
GOAL –
RELIEVE PAIN
HEAL ULCER
GET RID OF H-PYLORI
TYPES
ANTACIDS
H2 BLOCKERS
PROSTAGLANDIN ANOLOGS – protect the stomach from NSAID’S
MUCOSAL BARRIER FORTIFERS
PROTON PUMP INHIBITORS
PROTON PUMP INHIBITORS
GASTRIC ACID INHIBITORS DELAYED RELEASE, EFFECTS THE ACID LEVEL IN THE STOMACH SO MAY INTERFERE WITH OTHER DRUG ABSORPTION, SHOULD ONLY BE USED FOR 4-8 WEEKS, ADVERSE EFFECTS – NAUSEA, DIARRHEA, AND HEADACHE
PRILOSEC – USED TO TREAT ULCERS AND GERD
PREVACID – TAKE AT HS
PROTONEX – TAKE WITH FOOD, IS PO OR IV
DRUGS FOR H-PYLORI
AMOXICILLIN
TETRACYCLINE
BIAXIN
FLAGYL
PEPTO-BISMOL
H2 AND PROTON PUMP INHIBITOR’S
PEPTIC ULCER COMPLICATIONS AND MANAGEMENT
HEMORRHAGE:15-20 %MOST SERIOUS COMPLICATION
MOST COMMON IN OLDER ADULTS WITH GASTRIC ULCERS CAUSES: GASTRIC OR DUODENAL ULCERS ESOPHAGEAL CANCER
ESOPHAGEAL VARACIES
GASTRITIS
GASTRIC CANCER
PEPTIC ULCER ASSESSMENT
NURSE MONITERS AND DOCUMENTS
FOR BRIGHT RED BLOOD COFFEE GROUND EMESIS,
BLACK TARRY STOOLS HEMOGLOBIN AND HEMATOCRIT CLOTTING FACTORS [PT, PTT, BLEEDING TIME]
VITAL SIGNS WEAKNESS, PERSPIRATION WITH SHOCK= HYPOTENSION, CHILLS, PALPATATIONS, WEAK PULSES, DIAPHORESIS
PEPTIC ULCER INTERVENTIONS
NOTIFY PHYSICIAN OF MAJOR BLEEDING
MAY REQUIRE BLOOD TRANSFUSION
MAY NEED ENDOSCOPIC THERAPY= MORE AFFECTIVE IF ACTIVE BLEED
USE HEATER PROBE TO ELECTROCOAGULATE
MAY INJECT EPINEPHRINE OR ALCOHOL INTO BLEEDING SITE
ALSO MAY USE LASER
PEPTIC ULCER INTERVENTIONS (CONT)
MAY NEED NASOGRASTIC TUBE TO DECOMPRESS THE STOMACH
PURPOSE-
CHECK FOR BLOOD
ASSESS AMOUNT OF BLEEDING
DECOMPRESS THE STOMACH
ADMINISTER SALINE LAVAGE
WHEN IN PLACE CONFIRM PLACEMENT WITH X-RAY
IRRIGATE TO MAINTAIN PATENCY
SALINE LAVAGE
USED TO IRRIGATE UNTIL RETURNS LIGHT PINK
CAN BE PERFORMED WITH ASEPTO UNTIL PINK
ALSO CAN BE DONE WITH BAG OF NS ATTACHED TO NG
MAY USE H2 BLOCKERS AND ANTACIDS TO DECREASE ACID LEVELS
INSTRUCT PATIENT AND FAMILY TO AVOID NSAIDS
PEPTIC ULCER PERFORATION
2-3% OCCURANCE
6-7 % MORTALITY
STOMACH WALL BREAKS AND CONTENTS ENTER THE PRITONAL CAVITY
S/S
SUDDEN SHARP PAIN OVER ABDOMEN
ABDOMIN BECOMES HARD, RIGID AND TENDER
PATIENT MAY ASSUME KNEE CHEST POSITION
MAY LEAD TO BACTERIAL SEPTICEMIA, HYPOVOLEMIC SHOCK
NURSING RESPONSIBILITIES=
IMMEDIATE RESPONSE
FLUID REPLACEMENT
ANTIBIOTICS
NPO
NG TO DRAIN STOMACH OF CONTENTS
V/S
MONITER FOR SEPTIC SHOCK
PROCEDURE
GASTROENTERSTOMY
BODY OF STOMACH CONNECTED TO SMALL BOWELL, USUALLY THE JEJUNUM
BYPASSES DUODENAL CONTENTS
REDUCES PLYORIDUODENAL ACTIVITY
DIVERTS ACID FROM THE ULCERATED AREA
DONE WITH VAGOTOMY BECAUSE DOES NOT CHANGE THE SECRETION OF PARIETAL CELLS
GASTRODUODENOSTOMY
FOR PEPTIC ULCER
STOMACH ANASTOMOSED TO DUODENUM
BILLROTH I
FOR PEPTIC ULCER
DISTAL PORTION OF STOMACH REMOVED AND THE REMAINDER IS ANASTOMOSED TO THE DUODENUM.
GASTROJEJUNOSTOMY OR BILLROTH II
FOR PEPTIC ULCER
THE LOWER PORTION OF THE
STOMACH IS REMOVED AND THE REMAINING IS ANASTOMOSED TO THE JEJUNUM
TOTAL GASTRECTOMY
FOR PEPTIC ULCER
REMOVES THE ENTIRE STOMACH FROM THE LES TO THE DUODENUM AND CONNECTS THESE 2 ENDS TOGETHER (ANASTOMOSIS)
LOSES FUNCTION OF GASTRIC MUCOSA
DUMPING SYMDROME AND ANEMIA MAY OCCUR
VIT B 12 IS LOST
VAGATOMY
FOR PEPTIC ULCER
ELIMINATES THE ACID SECRETING STIMULAS TO GASTRIC CELLS AND DECREASES THE RESPONSE OF THE PARIETAL CELLS
3 TYPES:
1.TRUNCAL-VAGAL TRUNKS ARE REMOVED & ANTURM REMOVED REMAINING AREA OF STOMACH IS ANASTOMOSED TO PROXIMAL DUEODENUM [BILROTH I], OR TO JEJUNUM [ BILROTH II]
2. SELECTIVE-ONLY BRANCHES ARE TRANSECTED
BETTER RESPONSE WITH FEWER ULCER RETURN
3. PROXIMAL GASTRIC VAGATOMY
NERVE SUPPLY TO THE ACID SECRETING CELLS CUT
PYLOROPLASTY
FOR PEPTIC ULCER
MAY DO WITH VAGATOMY

OPENS PYLORAS

STOMACH EMPTIES BETTER

HEINEKE-MIKULICZ-MOST COMMON

PLYORIS STRICTURE ENLARGED
FOR PEPTIC ULCER
POST-OP CARE
NG TUBE [ NO IRRIGATION UNLESS ORDERED]

WATCH FOR ABD DISTENTION WHICH MAY CAUSE STRAIN ON SUTURES

ALSO TACHYCARDIA, FEELS FULL, HYPOTENSION
WATCH FOR BLEEDING
POST-OP ASSESSMENT
FOR PEPTIC ULCER
D R A P E S
D = DRESSING
R = RESPIRATORY
A = ABDOMINAL ASSESSMENT / AMBULATE
P = PAIN MEDICINE / PATENCY OF TUBE
E = ELIMINATION
S = SPLINT
FOR PEPTIC ULCER
POST-OP
COMPLICATIONS
DUMPING SYNDROME
REFLUX GASTROPATHY/BILE REFLUX GASTROPATHY : IN SURGERIES WHICH THE PYLORUS IS REMOVED OR BYPASSED.
S/S :
BILE IN STOMACH
SATIETY
ABD DISCOMFORT
VOMITING
DUMPING SYNDROME ?
Rapid emptying of gastric contents into small intestines
Fluid shift into gut
Abdominal distension
Early symptoms occur within 30 minutes of eating
Late dumping syndrome 90 minutes to 3 hours after eating
Managed by dietary measures
DUMPING SYNDROME
EARLY SYMPTOMS
VERTIGO

TACHYCARDIA

SYNCOPE

PALLOR

PALPITATIONS
DUMPING SYNDROME
LATE SYMPTOMS
DIZZINESS

PALPITATIONS

TACHYCARDIA

CONFUSION

SWEATING
DIETARY MANAGEMENT OF DUMPING
HIGH PROTEIN, HIGH FAT, LOW CARBS
SMALL MEAL
NO LIQUID WITH MEALS
PECTIN POWDER
LOW ROUGHAGE
NO MILK, SUGARS, OR SWEETS
LIE DOWN AFTER MEALS FOR 20-30 MIN
COMPLICATIONS, CONT.
FOR PEPTIC ULCER
DELAYED GASTRIC EMPTYING
CAN BE CAUSED BY
EDEMA AT THE SUTURE LINE
ADHESIONS
HYPOKALEMIA
HYPONATREMIA
HYPOPROTEINEMIA
AFFERENT LOOP SYNDROME
MAY OCCUR WHEN THE DUODENAL LOOP IS OBSTRUCTED
MAY OCCUR AFTER A BILLROTH II
S/S :
BLOATING
PAINFUL CONTRACTIONS
N/V
RECURRENT ULCERATIONS OCCUR IN 5 % OF THE PATIENTS
What is CHOLECYSTITIS
Acute inflammation of the wall of the gallbladder
Acute usually R/T cholelthiasis and cholecystitis
Usually obstructed by a calculus, which leads to ischemia tissue death and sloughing
Rupture may occur, then an abscess and pertonitis
Pain Is R/T spasams
A calculus is believed to be R/T a bacterial infection
E-coli
Strep-D
Staph
Salmonella
What happens with CHOLECYSTITIS
CHRONIC - REPEATED ATTACKS
WALL BECOMES DISEASED AND STONES DEVELOP AND WALL FIBROSES
COMPLICATIONS:
PANCREATITIS AND CHOLANGITIS ( BILE DUCT )
LEADS TO JAUNDICE ( SEE IN EYES AND SKIN )
BILIRUBIN > 2.5/MG/DL, SKIN ITCHES
CLAY COLORED STOOLS
URINE BECOMES DARK AND FOAMY D/T EXCESS BILE
CHOLECYSTITIS
OTHER CAUSES ?
OTHER CAUSES:
TRAMA
INADEQUATE BLOOD SUPPLY
LONG ANESTHESIA
EDEMA
TUMORS
CLINICAL MANIFESTATIONS OF CHOLECYSTITIS ARE?
PAIN IN ABD RADIATING TO RIGHT SHOULDER
N/V
ANOREXIA
DYSPEPSIA
ABD FULLNESS
BELCHING
FEVER
JAUNDICE
CLAY STOOLS
STEATORRHEA
REBOUND TENDERNESS
DIAGNOSIS OF CHOLECYSTITIS
NO SPECIFIC LABS BUT
LDH, AST, ALK PHOS WILL BE ELEVATED
BILLIRUBIN UP IF OBSTRUCTION
INCREASE WBC
INCREASE SERUM AMYLACE
ULTRASOUND OF RUQ
GI SERIES TO R/O OTHER PROBLEMS
CHOLECYSTAGRAM
HEPATOBILIARY SCAN : USES RADIOACTIVE ISOTOPE TO LOOK AT DUCT
INTERVENTIONS FOR CHOLECYSTITIS
Non- surgical
Drugs
Demeral
no morphine which causes spasms at the spincter of Oddi
Antispasmotic/anticholergenics (Bentyl)
Tigan for N/V
Diet
Low fat
Low volume
Avoid fried, rich pastries, chocolate, onions, broccli
May need NG tube if N/V
Small frequent meals
POST_OP DISCHARGE INSTRUCTIONS CHOLECYSTECTOMY
Usual activities in 1- 3 weeks
Pain control
Diet and tolerance of food
Wound care
CHOLELITHIASIS
Define: hard solid matter formed from bile (cholesterol and bilirubin) precipitate out of solution and form crystals.
Usually the cause of cholecystitis
May lie dormant or move to other parts of the bilary tree
Causes
a familiar tendency
diet related
sedentary lifestyles
anything that increases the cholesterol in the bile may be causative factor
many people have a combination of factors
CHOLELITHIASIS
Frequency
women over 20 (especially pregnant) and people over 60 yrs of age
overweight
crash diets
medications-birth control and cholesterol lowering agents
diabetics
native Americans and Mexican Americans
CHOLELITHIASIS Assessment
severe steady pain in upper abdomen most typical-may be intermittent, pain may be between shoulder blades, severity depends upon the movement of stone, if blocking cystic duct will cause spasms
vomiting
diaphoresis
jaundice
tachycardia
GALLSTONES Diagnosic tests
most impt is physical exam and description of pain
liver enzymes-alk phos, LDH, bilirubin
oral cholecystogram- patients swallows pills
ultra sound
ERCP best test if stones are in CBD
percutaneous transhepatic cholangiography
GALLSTONES TREATMENT
Goal is to rest the gallbladder by diet
If symptomatic may require cholecystectomy
Drugs include pain meds no Morphine due to it may cause biliary colic, Demoral is choice
antispasmotics-Bentyl,
antiemetics
Chenodiol ( bile acid) used to dissolve the stones in clients who are poor surgical candidates or elderly---is expensive and takes long time
Ursodiol used in clients with stones r/t rapid weight loss
Questran helps relieve purities r/t excessive bile salts in skin
Lithotripsy-dissolves stones with sound waves under water.done under conscious sedation
Percutaneous transhepatic biliary catheter may be inserted to relieve congestion
WHAT IS THE Liver?
Largest organ in body next to skin
Beneath diaphragm, most on right side of body
500 functions
Reservoir 500-1000cc blood
Filters & detoxifies blood, kupffer cells
What does the Liver Do?
Stores nutrients
Fat soluble vitamins:
A, D, E, K, B12, B1, B2, Fe, phospholipid, cholesterol
Synthesizes:
bile, serum albumin, globulins, prothrombin, fibrogen, blood coagulation factors V, VII, VIII, IX, XI, XII, urea
Converts bilirubin to bile & stores extra Fe as ferritin