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62 Cards in this Set
- Front
- Back
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Which Hepatitis is associated with Liver Cancer
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Hep B 60% of all liver cancer
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Hep A treatment
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Supportive
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HIATAL HERNIA AND REFLUX
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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) |
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HIATAL HERNIA AND REFLUX CLINICAL MANIFESTATIONS
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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 |
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HIATAL HERNIA AND REFLUX MEDICATIONS
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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 |
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What is a HIATAL HERNIA
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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 |
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ASSESSMENT FOR HIATAL HERNIA
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Heartburn
Regurg Pain Dysphagia Belching Nutritional status Lungs for asthma from regurg History of cardiac problems Diagnosis |
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What is ACHALASIA
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Failure of a ring of muscle (as a sphincter) to relax (completely)
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What are the MAJOR FUNCTIONS OF THE PANCREAS
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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 |
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Pathophysiologic Processes in Acute Pancreatitis
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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 |
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Acute Pancreatitis CAUSES
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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 |
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Acute Pancreatitis SYMPTOMS
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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 |
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Acute Pancreatitis DIAGNOSIS
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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 |
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Acute Pancreatitis ASSESSMENT
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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) |
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Acute Pancreatitis TREATMENT
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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 |
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Complications of Acute Pancreatitis
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Hypovolemia
Hemorrhage Acute renal failure Paralytic ileus Hypovolemic or septic shock |
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Complications of Acute Pancreatitis CONTINUED
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Pleural effusion, respiratory distress syndrome, pneumonia
Multisystem organ failure Disseminated intravascular coagulation Diabetes mellitus |
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Acute Pancreatitis DRUG THERAPY
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Anticholinergics – Atropine
Glucogons Insulin Zantac Antibiotics |
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Acute Pancreatitis -- Nutrition less than Body Requirements
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Interventions
TPN When taking PO – small frequent meals, moderate to high CHO, increase protein, decreased fat, bland, no caffeine or alcohol, vitamin replacement, Ensure |
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Acute Pancreatitis
NURSING DIAGNOSIS |
Acute pain
Imbalanced nutrition Risk for fluid volume deficit Risk for infection Ineffective breathing pattern |
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Chronic Pancreatitis
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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 |
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INTERVENTIONS FOR CHRONIC PANCREATITIS
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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 |
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PEPTIC ULCER DISEASE WHAT IS IT ?
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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 |
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PEPTIC ULCER CLINICAL MANISFESTATIONS
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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 |
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PEPTIC ULCER NURSING DIAGNOSIS
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PAIN
RISK FOR FLUID VOLUME DEFICIT INEFFECTIVE INDIVIDUAL COPING ALTERED NUTRITION SLEEP PATTERN DISTURBANCES |
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DRUG THERAPY FOR PEPTIC ULCERS
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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 |
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PROTON PUMP INHIBITORS
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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 |
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DRUGS FOR H-PYLORI
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AMOXICILLIN
TETRACYCLINE BIAXIN FLAGYL PEPTO-BISMOL H2 AND PROTON PUMP INHIBITOR’S |
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PEPTIC ULCER COMPLICATIONS AND MANAGEMENT
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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 |
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PEPTIC ULCER ASSESSMENT
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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 |
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PEPTIC ULCER INTERVENTIONS
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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 |
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PEPTIC ULCER INTERVENTIONS (CONT)
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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 |
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PEPTIC ULCER PERFORATION
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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 |
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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 |
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GASTRODUODENOSTOMY
FOR PEPTIC ULCER |
STOMACH ANASTOMOSED TO DUODENUM
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BILLROTH I
FOR PEPTIC ULCER |
DISTAL PORTION OF STOMACH REMOVED AND THE REMAINDER IS ANASTOMOSED TO THE DUODENUM.
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GASTROJEJUNOSTOMY OR BILLROTH II
FOR PEPTIC ULCER |
THE LOWER PORTION OF THE
STOMACH IS REMOVED AND THE REMAINING IS ANASTOMOSED TO THE JEJUNUM |
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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 |
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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 |
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PYLOROPLASTY
FOR PEPTIC ULCER |
MAY DO WITH VAGATOMY
OPENS PYLORAS STOMACH EMPTIES BETTER HEINEKE-MIKULICZ-MOST COMMON PLYORIS STRICTURE ENLARGED |
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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 |
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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 |
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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 |
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DUMPING SYNDROME ?
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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 |
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DUMPING SYNDROME
EARLY SYMPTOMS |
VERTIGO
TACHYCARDIA SYNCOPE PALLOR PALPITATIONS |
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DUMPING SYNDROME
LATE SYMPTOMS |
DIZZINESS
PALPITATIONS TACHYCARDIA CONFUSION SWEATING |
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DIETARY MANAGEMENT OF DUMPING
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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 |
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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 |
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What is CHOLECYSTITIS
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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 |
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What happens with CHOLECYSTITIS
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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 |
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CHOLECYSTITIS
OTHER CAUSES ? |
OTHER CAUSES:
TRAMA INADEQUATE BLOOD SUPPLY LONG ANESTHESIA EDEMA TUMORS |
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CLINICAL MANIFESTATIONS OF CHOLECYSTITIS ARE?
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PAIN IN ABD RADIATING TO RIGHT SHOULDER
N/V ANOREXIA DYSPEPSIA ABD FULLNESS BELCHING FEVER JAUNDICE CLAY STOOLS STEATORRHEA REBOUND TENDERNESS |
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DIAGNOSIS OF CHOLECYSTITIS
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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 |
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INTERVENTIONS FOR CHOLECYSTITIS
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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 |
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POST_OP DISCHARGE INSTRUCTIONS CHOLECYSTECTOMY
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Usual activities in 1- 3 weeks
Pain control Diet and tolerance of food Wound care |
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CHOLELITHIASIS
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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 |
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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 |
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CHOLELITHIASIS Assessment
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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 |
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GALLSTONES Diagnosic tests
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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 |
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GALLSTONES TREATMENT
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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 |
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WHAT IS THE Liver?
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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 |
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What does the Liver Do?
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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 |
