CASE STUDY

´ACUTE PANCREATITISµ
SUBMITTED BY:

JENNIFER AGUILUZ

MRS. MARIA EVELYN LUMIO R.N.

.

. ALCOHOL ABUSE IS THE SECOND MOST FREQUENT CAUSE OF ACUTE PANCREATITIS. OR PANCREATIC DUCTAL OBSTRUCTION SHOULD BE SUSPECTED IF OVERT EXOCRINE OR ENDOCRINE DYSFUNCTION PERSISTS OR INCREASES AFTER AN ATTACK OF CLINICALLY ACUTE PANCREATITIS. GALLSTONE-INDUCED PANCREATITIS IS CAUSED BY DUCT OBSTRUCTION BY GALLSTONE MIGRATION. IN PATIENTS WITH INTERSTITIAL OR MILD ACUTE PANCREATITIS THE GLAND RETURNS TO HISTOLOGIC AND FUNCTIONAL NORMALCY AFTER RECOVERY. ALSO REFERRED TO AS SEVERE ACUTE PANCREATITIS. 33 PERCENT DEVELOPED NEW ONSET DIABETES AFTER A MEDIAN FOLLOW-UP OF 29 MONTHS. GORELICK SHOWED THAT ETHANOL DIRECTLY SENSITIZES ACINAR CELLS TO CHOLECYSTOKININ STIMULATION. IN ADDITION. NEVERTHELESS. OR BOTH. AS THE DEVELOPMENT OF PANCREATITIS MIGHT BE AFFECTED BY BOTH GENETIC AND ENVIRONMENTAL FACTORS. WHICH CAN BE EASILY IDENTIFIED IN 75%-85% OF PATIENTS. FOR EXAMPLE. CHRONIC PANCREATITIS.INTRODUCTION: ACUTE PANCREATITIS IS AN INFLAMMATORY CONDITION OF THE PANCREAS CHARACTERIZED CLINICALLY BY ABDOMINAL PAIN AND ELEVATED LEVELS OF PANCREATIC ENZYMES IN THE BLOOD . THE PATHOGENESIS OF ACUTE PANCREATITIS IS NOT FULLY UNDERSTOOD. SIGNIFICANT PANCREATIC NECROSIS. PATIENTS WITH NECROTIZING PANCREATITIS. 25 PERCENT OF 65 PATIENTS WHO SURVIVED FOLLOWING NECROSECTOMY DEVELOPED EXOCRINE INSUFFICIENCY . CAN DEVELOP PERMANENT EXOCRINE AND ENDOCRINE INSUFFICIENCY DEPENDING UPON EXTENT OF NECROSIS . AND 20 PERCENT WERE ON PANCREATIC ENZYMES FOR THE DIARRHEA . IN ANOTHER REPORT. OBSTRUCTION OF THE COMMON BILE DUCT BY STONES (38%) AND ALCOHOL ABUSE (36%) ARE THE MOST FREQUENT CAUSES OF ACUTE PANCREATITIS[3. DUCT OBSTRUCTION PROMOTES PANCREATITIS BY INCREASING DUCT PRESSURE AND SUBSEQUENT UNREGULATED ACTIVATION OF DIGESTIVE ENZYMES[9]. A NUMBER OF CONDITIONS ARE KNOWN TO INDUCE THIS DISORDER WITH VARYING DEGREES OF CERTAINTY. WHILE EXOCRINE FUNCTION MAY TAKE UP TO ONE YEAR FOR FULL RECOVERY . 76 PERCENT OF 42 PATIENTS WITH SEVERE ACUTE PANCREATITIS FOLLOWED FOR 24 TO 36 MONTHS HAD ONGOING SYMPTOMS DUE TO PANCREATIC DYSFUNCTION. ABNORMAL EXOCRINE AND ENDOCRINE FUNCTION CAN OCCUR DURING AN ACUTE ATTACK . MIMICKING THE DUCTAL CHANGES OF CHRONIC PANCREATITIS . BUT THE CORRELATION BETWEEN ALCOHOL AND PANCREATITIS IS NOT COMPLETELY UNDERSTOOD[10]. SCARRING OF THE PANCREATIC DUCTS CAN PERSIST INDEFINITELY IN SOME PATIENTS. ENDOCRINE FUNCTION RETURNS TO NORMAL SOON AFTER THE ACUTE PHASE.8]. HOWEVER. IN EXPERIMENTAL MODELS. OBSTRUCTION IS LOCALIZED IN THE BILE DUCT AND PANCREATIC DUCT. IN DEVELOPED COUNTRIES. IN ONE REPORT. WITH GALLSTONES AND CHRONIC ALCOHOL ABUSE ACCOUNTING FOR 75 PERCENT OF CASES IN THE UNITED STATES ETIOLOGY THERE ARE MANY CAUSES OF ACUTE PANCREATITIS. 32 PERCENT HAD NEW ONSET DIABETES.

TRIGGERS AND EXACERBATE ACUTE PANCREATITIS. IN FACT. HOWEVER. BUT THE PATHOGENETIC THEORIES ARE CONTROVERSIAL. THE EXACT MECHANISM UNDERLYING ALCOHOLIC ACUTE PANCTEATITIS HAS NOT BEEN EXTENSIVELY ELUCIDATED. LITTLE IS KNOWN ABOUT THE OTHER CAUSES OF ACUTE PANCREATITIS. THESE THEORIES ARE CONTROVERSIAL. IT IS NOT SUFFICIENT TO CAUSE THE MORPHOLOGICAL CHANGES OF ACUTE PANCREATITIS[34]. TRYPSIN ACTIVATION AND PANCREATIC AUTODIGESTION[32]. ENZYME ACTIVATION WITHIN THE PANCREAS LEADS TO AUTO-DIGESTION OF THE GLAND AND LOCAL INFLAMMATION. THERE ARE VARIOUS CAUSES WHICH MAY CAUSE ACUTE PANCREATITIS AND LEAD TO PANCREATIC DUCT OBSTRUCTION AND BLOCKAGE OF PANCREATIC JUICE OUTFLOW UNDER CERTAIN CIRCUMSTANCES. IN THE PRESENCE OF EXOCRINE PANCREATIC HYPERSTIMULATION. AND UNREGULATED ACTIVATION OF TRYPSIN WITHIN PANCREATIC CANARD CELLS WOULD INCREASE. WE SPECULATE THAT THE MAIN PRECONDITIONS THAT TRIGGER ACUTE BILIARY PANCREATITIS ARE PANCREATIC HYPERSTIMULATION AND BILE-PANCREATIC DUCT OBSTRUCTION. THERE IS NO EVIDENCE THAT SUPPORTS IT[35]. ALTHOUGH ACINAR HYPERSTIMULATION HAS OFTEN BEEN IMPLICATED IN ACUTE PANCREATITIS PATHOGENESIS. ACUTE PANCREATITIS OCCURS WHEN INTRACELLULAR PROTECTIVE MECHANISMS TO PREVENT TRYPSINOGEN ACTIVATION OR REDUCE TRYPSIN ACTIVITY ARE OVERWHELMED[33]. WHICH INCREASE PANCREATIC DUCT PRESSURE. INDICATING THAT OTHER EVENTS MUST OCCUR IF THE CHANGES INDUCED BY PANCREATIC DUCT OBSTRUCTION LEAD TO ACUTE PANCREATITIS. THE PREDOMINANT THEORIES OF ACUTE BILIARY PANCREATITIS ARE COMMON PATHWAY THEORY AND GALLSTONE MIGRATION THEORY. AND UNREGULATED ACTIVATION OF TRYPSIN WITHIN PANCREATIC ACINAR CELLS. HOWEVER. WHEN INTRACELLULAR PROTECTIVE MECHANISMS TO PREVENT TRYPSINOGEN ACTIVATION OR REDUCE TRYPSIN ACTIVITY ARE OVERWHELMED. ALTHOUGH PANCREATIC DUCT OBSTRUCTION MAY PLAY AN IMPORTANT ROLE IN THE PATHOGENESIS OF GALLSTONE PANCREATITIS. BILE REFLUX. IN OUR HYPOTHESIS. PANCREATIC DUCT PRESSURE. THE ETIOLOGY AND PATHOGENESIS OF ACUTE PANCREATITIS HAVE BEEN INTENSIVELY INVESTIGATED[2]. ACTIVE TRYPSIN REFLUX. WE HYPOTHESIZE THAT THERE IS A COMMON PATHOGENIC PATHWAY THAT TRIGGERS VARIOUS FORMS OF ACUTE PANCREATITIS: ACUTE BILIARY PANCREATITIS AND OTHER FORMS OF ACUTE PANCREATITIS.FAILURE TO INHIBIT TRYPSIN ACTIVITY OR TO WASH ACTIVE TRYPSIN INTO PANCREATIC DUCTS MIGHT PROMOTE ALCOHOLIC PANCREATITIS[11]. ACUTE PANCREATITIS OCCURS. ACTIVE TRYPSIN REFLUX. WE HYPOTHESIZE THAT PANCREATIC ACINAR HYPERSTIMULATION. IN THE PRESENCE OF DUCT OBSTRUCTION. WHICH INCREASES PANCREATIC DUCT PRESSURE. WHICH CONSENT THAT THE KEY FACTOR FOR ACUTE BILIARY PANCREATITIS IS BILE-PANCREATIC DUCT OBSTRUCTION. .

I WILL BE ABLE TO: TDEFINE WHAT IS ACUTE PANCREATITIS TTRACE THE PATHOPHYSIOLOGY OF ACUTE PANCREATITIS TENUMERATE THE DIFFERENT SIGN AND SYMPTOMS OF ACUTE PANCREATITIS TIDENTIFY AND UNDERSTAND DIFFERENT TYPES OF MEDICAL TREATMENT NECESSARY FOR THE TREATMENT OF ACUTE PANCREATITIS DEMOGRAPHIC DATA NAME: D. HOW IT IS ACQUIRED AND PREVENTED. NO MEDS TAKEN OR CONSULTATION MADE.SO FINAL DIAGNOSIS: ACUTE PANCREATITIS PAST MEDICAL HISTORY ACCORDING TO THE PATIENT DL M. CAUSES OF ACUTE PANCREATITIS. I WILL BE ABLE TO KNOW WHAT ACUTE PANCREATITIS IS.ITS OCCURRENCE. 2 DAYS PTA THE PATIENT STILL HAVE THE SAME ABDOMINAL PAIN. OBJECTIVES GENERAL: AFTER THIS CASE STUDY. M. SHE HAD COMPLETED HER CHILDHOODIMMUNIZATION. SHE HAS HYPERTENSION AND TAKES AMILODIPINE AND METROPOLOL TO MANAGE HER ILLNESS. SHE HAD NO ALLERGY TO FOODS OR MEDICATIONS.I. CHART. HISTORY OF PRESENT ILLNESS ACCORDING TO THE PATIENTS SO. DIFFUSE. ADDRESS: QUEZON CITY AGE: 58 YEARS OLD SEX: FEMALE NATIONALITY: FILIPINO RELIGION: ROMAN CATHOLIC DATE & TIME OF ADMISSION: DEC. 3 DAYS PRIOR TO ADMISSION THE PATIENT EXPERIENCED SUDDEN ONSET OF ABDOMINAL PAIN. THIS TIME IT WAS MORE SEVERE AND BASE ON THE ASSESTMENT THE PATIENT IS NEGATIVE TO BLADDER CHANGE.L. ITS TREATMENTS AND PREVENTION. THE PATIENT COULD NOT ANY MORE TOLERATE THE . FEW HOURS PTA. SPECIFIC: AFTER THE COMPLETION OF THIS STUDY.20 .2010 9:15AM MODE OF ARRIVAL: WALK IN CHIEF COMPLAINT: SEVERE ABDOMINAL PAIN SOURCE OF INFORMATION: PATIENT.

DOESNT KNOW ANYONE OF HER RELATIVES WHO WAS DIAGNOSED WITH THE SAME DISEASE AND ADMITTED THAT HYPERTENSION IS MOSTLY ON THEIR GENES BUT NOT THIS TYPE OF DISEASE. LICE AND DANDRUFF -NO BALDNESS -NORMOCEPHALIC -SMOOTH -NO LUMPS -ABSENCE OF MODULES OR MASSES -NO AREA OF TENDERNESS -SYMMETRICAL WITH PROTRUSIONS ON THE LATERAL PART OF PARIETAL FOREHEAD AND OCCIPITAL BONE. OILY HAIR -NORMAL -BLACK OR BROWN IN COLOR -HAIR IS EVENLY DISTRIBUTED -NO AREA OF BALDNESS -THICK -FINE -CURLY/KINKY/STRAIGHT -DRY/OILY/SHINY HAIR -NORMAL y FACE -SYMMETRICAL WITH MOVEMENT . PHYSICAL ASSESTMENT ACTUAL FINDINGS NORMAL FINDINGS INTERPRETA TION -NORMAL  HEAD y SKULL -NORMOCEPHALIC -NO LUMPS y SCALP -NO NITS.ACCORDING TO THE PATIENT SHE REALLY DOESNT KNOW WHERE SHE GET THIS KIND OF DISEASE BECAUSE THE PATIENT IS KNOWN TO BE A HEALTH CONSCIOUS PERSON AND DOESNT EAT TOO MUCH FATTY AND SALTY FOODS. SHE WAS BROUGHT TO ER SHE WAS ADMITTED AND WAS TRANSFERRED HERE AT EAMMC FEMALE WARD . SHE IS LIVING WITH HER FAMILY BECAUSE SHE DOESNT HAVE HER OWN FAMILY. THEY ARE ONLY FINANCIALLY SUPPORTED BY HER NEPHEWS AND NIECE WHO ARE WORKING. -WHITISH -NO NITS. LICE AND DANDRUFF -NO BALDNESS -NORMAL y HAIR -STRAIGHT. BLACK WITH WHITE HAIR. PERSONAL / SOCIAL HISTORY THE PATIENT IS THE 3TH AMONG 6 SIBLINGS. FAMILY HEALTH HISTORY ACCORDING TO THE PATIENT DL M.PAIN. SHE IS STILL SINGLE.

-EXPRESSIONS APPROPRIATE TO SITUATIONS y EYES -SYMMETRICAL -NO CLOUDINESS -NO LACRIMATION -SYMMETRICAL WITH MOVEMENT -EXPRESSIONS APPROPRIATE TO SITUATIONS -SYMMETRICAL -NO PROTRUSIONS -DEAR OR NO CLOUDINESS -NO EXCESSIVE LACRIMATION -MOVES SYMMETRICALLY -HAIR EVENLY DISTRIBUTED -SKIN INTACT -EQUALLY DISTRIBUTED -CURVED SLIGHTLY OUTWARD -SKIN INTACT -NO DISCHARGE -NO DISCOLORATION -LIDS CLOSE SYMMETRICALLY -APPROXIMATELY 15-20 INVOLUNTARY BLINKS PER MINUTE. REACTIVE TO LIGHT & BLACK y IRIS -FLAT -BROWN -ROUND -TRANSPARENT/SHINY -NORMAL -PERRLA -NORMAL y PUPILS .NO REDNESS -NORMAL -WHITE/YELLOWISH IN AMERICANS -CLEAR. SHINY. NO CLOUDINESS -NO REDNESS -FLAT -BROWN -EVEN COLORATION -SYMMETRICAL -ROUND -TRANSPARENT/SHINY -PERRLA(PUPILS EQUALLY ROUND. BILATERAL BLINKING -NO SCALING -NO SECRETIONS -NO ERYTHEMA -NO REDNESS -PINK. WITH VISIBLE BLOOD VESSELS -NO DISCHARGES -NORMAL y EYEBROWS -SYMMETRICAL -NORMAL y EYELASHES -EQUALLY DISTRIBUTED -CURVED SLIGHTLY OUTWARD -SKIN INTACT -NO DISCHARGE -NO DISCOLORATION -LIDS CLOSE SYMMETRICALLY -APPROXIMATELY 15-20 INVOLUNTARY BLINKS PER MINUTE. SHINY. BILATERAL BLINKING -NO SECRETIONS -NO ERYTHEMA -NO REDNESS -NORMAL y EYELIDS -NORMAL y LID MARGINS -NORMAL y LOWER PALPEBRAL CONJUNCTIVA -PINK. WITH VISIBLE BLOOD VESSELS -NO DISCHARGES -NORMAL y SCLERA -WHITE IN COLOR -CLEAR .

BLUISH HUE. MOIST. SMOOTH TEXTURE -SYMMETRY OF CONTOUR -ABILITY TO PURSE LIPS -NO TENDERNESS -PINK. MOIST -NO SWELLING -DECREASE OF OXYGEN SUPPLY y GUMS -PINK. IN MEDITERRANEAN GROUPS AND DARK-SKINNED CLIENTS) -SOFT. E. MOIST -NO SWELLING -NO TENDERNESS -NO DISCHARGES -NORMAL .WAXY CERUMEN -PRESENCE OF CILIA -NORMAL y HEARING ACUITY -WITH GOOD HEARING ACUITY IN BOTH EARS -NORMAL y NOSE -NO LESIONS -PRESENCE OF CILIA -WITH GOOD HEARING ACUITY IN BOTH EARS -NORMAL y LIPS -DARKER LIPS -ABILITY TO PURSE LIPS -SYMMETRIC AND STRAIGHT -NO DISCHARGE OR FLARING -UNIFORM COLOR -NO TENDERNESS -NO LESIONS -PRESENCE OF CILIA -UNIFORM PINK COLOR(DARKER.ACCOMMODATION y EYE MOVEMENT -MOVES IN UNISON -COORDINATED -MOVES IN UNISON -COORDINATED -NORMAL y FIELD OF VISION *VISUAL ACUITY -GOOD PERIPHERAL VISION -20/20 IN BOTH EYES -NORMAL y EAR -SAME AS THE COLOR OF THE FACE -NO SWELLING -SHELL SHAPE -NORMAL -PARALLEL WITH OUTER CANTHUS OF THE EYES -SAME AS THE COLOR OF THE FACE -NO SWELLING -NO TENDERNESS -SHELL SHAPE -FIRM CARTILAGE -YELLOWISH -DRY/WAXY CERUMEN -PRESENCE OF CILIA -NO FOREIGN BODY y EAR CANAL .G.

EVEN. NO MASS -SYMMETRICAL -MUSCLES EQUAL IN SIZE. SKIN SPRINGS BACK TO PREVIOUS STATE . MOIST -MIDLINE -PINKISH -WITH VISIBLE VEINS -PINK. MOIST -NORMAL y TONSILS -PINKISH -NO DISCHARGE -NO INFLAMMATION -PINK. HEAD CENTERED -COORDINATED. MOIST -MIDLINE MOVES WHEN THE CLIENT SAYS |AAH} -NORMAL  NECK -SAME AS THE SKIN COLOR -NO LYMPHS.WITH EDEMA -ERECT & MIDLINE -SAME AS THE SKIN COLOR -NO TENDERNESS -NO LYMPHS. ROUGH SURFACE AND MOIST -32 IN NUMBER -WHITE -UPPER TEETH OVER-RIDES LOWER TEETH -NORMAL y FRENULUM -MIDLINE -PINKISH -WITH VISIBLE VEINS -PINK. MOIST. SMOOTH MOVEMENTS WITH NO DISCOMFORT ACCUMULATI ON OF EXCESS . EVEN. LIGHT PINK IN COLOR. NO MASS -PINKISH -NO DISCHARGE -NO INFLAMMATION -NORMAL  UPPER EXTREMITIES y SKIN -NO ABRASIONS OR OTHER LESIONS -WHEN PINCHED. MOIST. LIGHT PINK IN COLOR. ROUGH SURFACE AND MOIST DORSAL -NORMAL y SOFT PALATE y HARD PALATE -BONY. NO SWELLING/NO TENDERNESS -PINK. NO SWELLING/NO TENDERNESS -NORMAL -NORMAL y UVULA -MIDLINE MOVES WHEN THE CLIENT SAYS |AAH} -BONY.y TEETH -WHITE -NO TENDERNESS -NO DISCHARGES -NO RETRACTION(LOWER UPPER) DORSAL -NORMAL AND y TONGUE -PINK.

FLUID -WITH DISCOLORATION -WITH BRUISES -VARIES FROM LIGHT TO DEEP BROWN. SKIN SPRINGS BACK TO PREVIOUS STATE -CONVEX CURVATURE -SMOOTH TEXTURE -HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS. AND EFFORTLESS RESPIRATIONS -FULL SYMMETRIC EXCURSION -BRONCHIAL AND TUBULAR BREATH SOUNDS IN THE TRACHEA -VESICULAR AND BRONCHOVESICULAR BREATH SOUNDS -DIFFICULTY OF BREATHING -NORMAL . SOME BIRTHMARKS. FROM YELLOW OVERTONES TO OLIVE -NO EDEMA -NO ABRASIONS OR OTHER LESIONS -FRECKLES. UNIFORM TEMPERATURE -CHEST WALL INTACT -NO TENDERNESS -NO MASSES -FULL AND SYMMETRIC CHEST EXPANSION -VESICULAR AND BRONCHOVESICULAR SOUNDS y ANTERIOR THORAX -UNBLEMISHED SKIN -UNIFORM COLOR  ABDOMEN -WITH PAIN -QUIET. SOME FLAT AND RAISED NEVI -WHEN PINCHED. RHYTHMIC. DARKSKINNED CLIENTS MAY HAVE BROWN OR BLACK PIGMENTATION IN LONGITUDINAL STREAKS -INTACT EPIDERMIS -PROMPT RETURN OF PINK OR USUAL COLOR(GENERALLY LESS THAN 4 SECONDS) -DECREASE O2 SUPPLY y NAILS -NO TENDERNESS -NO MASSES  CHEST AND BACK y POSTERIOR THORAX -FULL EXPANSION -TACHYPNEA -NORMAL -CHEST SYMMETRIC -SKIN INTACT. FROM RUDDY PINK TO LIGHT PINK.

. MAINTAINING BALANCE .HAS UPRIGHT POSTURE AND STEADY GAIT WITH OPPOSING ARM SWING. ROUNDED(CONVEX). CONSISTENT TENSION y NAILS . SOME BIRTHMARKS.NO EDEMA .MAINTAIN STANCE FOR AT LEAST 5 SECS ACCUMULATI ON OF EXCESS FLUID -NORMAL  MOTOR FUNCTIONS: -REPEATEDLY AND RHYTHMICALLY TOUCHES THE NOSE .RAPIDLY TOUCHES EACH FINGER TO THUMB WITH EACH HAND . SOME FLAT AND RAISED NEVI .CONCAVE CURVATURE .VARIES FROM LIGHT TO DEEP BROWN. WALKS UNAIDED.RELAXED ABDOMEN WITH SMOOTH.SYMMETRIC MOVEMENTS CAUSED BY RESPIRATION .PROMPT RETURN OF PINK OR USUAL COLOR (GENERALLY LESS THAN 4 SECS.NO ABRASIONS OR OTHER LESIONS .NO ABRASIONS LESIONS OR OTHER -UNBLEMISHED SKIN -UNIFORM COLOR -SILVER-WHITE STRIAE OR SURGICAL SCARS -FLAT.INTACT EPIDERMIS .WHEN PINCHED.OR SCAPHOID (CONCAVE) .SMOOTH TEXTURE .) . FROM RUDDY PINK TO LIGHT PINK. FROM YELLOW OVERTONES TO OLIVE .AUDIBLE BOWEL SOUNDS . SKIN SPRINGS BACK TO PREVIOUS STATE . DARKSKINNED CLIENTS MAY HAVE BROWN OR BLACK PIGMENTATION IN LONGITUDINAL STREAKS .CONCAVE CURVATURE -BROWN PIGMENTATION LONGITUDINAL STREAKS IN .CAN READILY DETERMINE THE POSITION OF FINGERS AND TOES -NORMAL .FRECKLES.HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS.MAY SWAY SLIGHTLY BUT IS ABLE TO MAINTAIN UPRIGHT POSTURE AND FOOT STANCE.NO TENDERNESS . LOWER EXTREMITIES y SKIN -BROWN IN COLOR .

CAN READILY DETERMINE THE POSITION OF FINGERS AND TOES .RAPIDLY TOUCHES EACH FINGER TO THUMB WITH EACH HAND ..MAINTAINS HEEL-TOE WALKING ALONG STRAIGHT LINE REPEATEDLY AND RHYTHMICALLY TOUCHES THE NOSE .

PATHOPHYSIOLOGY .

PANCREAS. THE PANCREAS CONTAINS ENZYME PRODUCING CELLS THAT SECRETE TWO HORMONES. AND INTO THE DUODENUM (PART OF THE SMALL INTESTINE). AND THE BILE FLOWS FROM THE GALLBLADDER INTO THE CYSTIC DUCT.THE GALLBLADDER IS A SMALL PEAR-SHAPED ORGAN THAT STORES AND CONCENTRATES BILE. BILE IS A DIGESTIVE LIQUID CONTINUALLY SECRETED BY THE LIVER.8 CM) WIDE.ANATOMY AND PHYSIOLOGY GALLBLADER. THE FUNCTION OF THE GALLBLADDER IS TO STORE BILE AND CONCENTRATE.8 CM) LONG AND 1. IN HUMANS. THE PANCREAS PRODUCES . THE BILE EMULSIFIES FATS AND NEUTRALIZES ACIDS IN PARTLY DIGESTED FOOD.6 TO 10. AND TOGETHER. GLUCAGON SLOWLY INCREASES THE BLOOD SUGAR LEVEL IF IT FALLS TOO LOW. THEY REGULATE THE LEVEL OF GLUCOSE IN THE BLOOD. THE TWO HORMONES ARE INSULIN AND GLUCAGON. A MUSCULAR VALVE IN THE COMMON BILE DUCT OPENS. INSULIN AND GLUCAGON ARE SECRETED DIRECTLY INTO THE BLOODSTREAM. THE GALLBLADDER IS CONNECTED TO THE LIVER BY THE HEPATIC DUCT. (3. IT IS APPROXIMATELY 3 TO 4 INCHES (7.2 CM) LONG AND ABOUT 1 INCH (2.5 CM) WIDE.THE PANCREAS IS A GLANDULAR ORGAN THAT SECRETES DIGESTIVE ENZYMES (INTERNAL SECRETIONS) AND HORMONES (EXTERNAL SECRETIONS). INSULIN LOWERS THE BLOOD SUGAR LEVEL AND INCREASES THE AMOUNT OF GLUCAGON (STOREDCARBOHYDRATE) IN THE LIVER. ALONG THE COMMON BILE DUCT.5 INCHES. THE PANCREAS IS A YELLOWISH ORGAN ABOUT 7 INCHES (17.

THE ENZYMES ARE DESIGNED TO DIGEST FOODS AND BREAK DOWN STARCHES.THE MINOR DUODENAL PAPILLA IS THE OPENING OF OTHER NAMES OF MINOR DUODENAL PAPILLA THE ACCESSORY PANCREATIC DUCT INTO THE DUODENUM.[2] IN MAMMALS THE DUODENUM MAY BE THE PRINCIPAL SITE FOR IRON ABSORPTION. AND INEXPENSIVE. IF THE PANCREAS IS NOT WORKING PROPERLY TO NEUTRALIZE CHYME AND BREAK DOWN PROTEINS. SOME 7 TO 10 CM BELOW THE PYLORUS. OR TWELVE FINGERS' BREADTHS.75-92% SENSITIVE.[3] THE DUODENUM PRECEDES THE JEJUNUM AND ILEUM AND IS THE SHORTEST PART OF THE SMALL INTESTINE.THE BODY'S MOST IMPORTANT ENZYMES. INCLUDING MAMMALS. IN FISH.THE DUODENUM IS THE FIRST SECTION OF THE SMALL INTESTINE IN MOST HIGHER VERTEBRATES. THE DIVISIONS OF THE SMALL INTESTINE ARE NOT AS CLEAR AND THE TERMS ANTERIOR INTESTINE OR PROXIMAL INTESTINE MAY BE USED INSTEAD OF DUODENUM. IT IS SOMETIMES ABSENT. THE DUODENUM IS A HOLLOW JOINTED TUBE ABOUT 10­12 INCH LONG CONNECTING THE STOMACH TO THE JEJUNUM.IT USUALLY RETURNS TO NORMAL WITHIN ONE WEEK. AND NONFUNCTIONAL. EASILY OBTAINED. FATS AND STARCH. ACCESSORY PANCREATIC DUCT-A DUCT OF THE PANCREAS THAT BRANCHES FROM THE CHIEF PANCREATICDUCT AND OPENS IN TO THE DUODENUM ABOVE IT CALLED ALSO DUCT OFSANTORINI . FORMING A STRUCTURE DUODENUM. IT BEGINS WITH THEDUODENAL BULB AND ENDS AT THE LIGAMENT OF TREITZ. 20 TO 60% SPECIFIC. AND BIRDS. MINOR DUODENUM OFTEN PAPILLA. THE NAME DUODENUM IS FROM THE LATIN DUODENUM DIGITORUM. CHYME IS A THICK SEMIFLUID MASS OF PARTLY DIGESTED FOOD THAT IS PASSED FROM THE STOMACH TO THE DUODENUM. IN HUMANS. FATS AND STARCH.THE IS SANTORINI'S MINOR CARUNCLE. LABORATORY AMYLASE SERUM AMYLASE LEVELS START INCREASING FROM 2 TO 12 HOURS AFTER THE ONSET OF SYMPTOMS AND PEAKS AT 12 TO 72 HOURS. THE PANCREAS ALSO HELPS NEUTRALIZE CHYME AND HELPS BREAK DOWN PROTEINS. LIPASE LIPASE LEVELS INCREASE WITHIN 4 TO 8 HOURS OF THE ONSET OF CLINICAL . REPTILES. THIS METHOD IS QUICK. STARVATION MAY OCCUR. MAJOR DUODENAL PAPILLATHE COMMON BILE DUCT AND THE PANCREATIC DUCT TOGETHER PERFORATE THE MEDIAL SIDE OF THE SECOND PORTION OF THE DUODENUM OBLIQUELY. WHERE MOST CHEMICAL DIGESTION TAKES PLACE.

THE HEALING OF EROSIVE ESOPHA INDICATION FOR THE TREATMENT OF GASTROESO PHAGEAL REFLUX DISEASE. DELAYED RELEASE ORAL TABLET. 86-100% SENSITIVE.FEVE R AND CHILLS . 50-99% SPECIFIC.SYMPTOMS AND PEAK AT ABOUT 24 HOURS.REPORT SEVERE HEADACHE.LEVELS DECREASE WITHIN EIGHT TO 14 DAYS. THESE TESTS ARE NOT SUFFICIENTLY RELIABLE FOR DIAGNOSING ACUTE BILIARY PANCREATITIS OR DETERMINING ITS ETIOLOGY.ADMINISTER ANTACIDS IF NEEDED 3. MECHANISM PROTON PUMP INHIBITOR THAT SUPPRESSES GASTRIC ACID SECRETION BY SPECIFIC INHIBITION OF THE H+/K+ATPASE IN THE GASTRIC PARIETAL CELL. BY ACTING SPECIFICALL Y ON THE PROTON PUMP.ADMINISTER BEFORE MEALS 2.HOWEVER. DRUG STUDY NAME OF DRUG OMEPRAZOL E DOSAGE/ ROUTE CAPSULE.SERUM TRYPSIN ASSAY IS NOT WIDELY AVAILABLE AND THEREFORE IS NOT ROUTINELY USED. HEPATIC FUNCTION STUDIES HEPATIC TRANSAMINASE LEVELS MAY BE ELEVATED IN PATIENTS WITH PANCREATITIS CAUSED BY ALCOHOL ABUSE OR CHOLELITHIASIS WITH OBSTRUCTION. OMEPRAZOL ADVERSE EFFECT OMEPRA ZOLE DELAYED RELEASE CAPSULE S ARE CONTRAI NDICATE D IN PATIENT S WITH KNOWN HYPERSE NSITIVIT Y TO ANY COMPONE NT OF THE FORMULA TION. DELAYED RELEASE ORAL CAPSULE ORAL ACTION COMPOUN D THAT INHIBITS GASTRIC ACID SECRETI ON AND IS INDICATE D IN THE TREATM ENT OF GASTRO ESOPHA GEAL REFLUX DISEASE (GERD). WORSENING OF SYMPTOMS. NURSING RESPONSIBILITY 1. TRYPSIN/ELASTASE ELEVATED TRYPSIN LEVEL HAS A BETTER LIKELIHOOD RATIO FOR DETECTING PANCREATITIS THAN THE AMYLASE LEVEL AND IS PROBABLY THE MOST ACCURATE SERUM INDICATOR FOR ACUTE PANCREATITIS.

MONITOR BP 2. THE DECREASE IN INTRACEL LULAR ADVERSE EFFECT UNUSUAL SLOW OR FAST HEARTBEAT. CALCIBLO C INHIBITS THE NURSING RESPONSIBILI TY 1. AND H. PYLORIE RADICAT ION TO REDUCE THE RISK OF DUODEN AL ULCER RECURRE NCE. BY BLOCKING THE CALCIUM CHANNELS . HYPERTEN SION. THUS REDUCING GASTRIC ACIDITY.MONITOR FOR POSSIBLE DRUG ADVERSE REACTION .DI ZZYNES OR PAINTING. EXTENDED RELEASE ORAL TABLET ORAL CAPSULE ORAL ACTION INDICATIO N TREATME NT OF HIGH BLOOD PRESSUR E MECHANIS M CALCIBLO C INHIBITS THE INFLUX OF EXTRACEL LULAR CALCIUM THROUGH MYOCARDI AL AND VASCULAR MEMBRAN E PORES BY PHYSICAL LY PLUGGING THE CHANNEL.YEL LOWING OF THE SKIN. NAME DRUG OF DOSAGE/RO UTE TABLET. AND OTHER VASCULAR DISORDER S SUCH AS RAYNAUD' S PHENOMEN ON.OBSERVE FOR CHEST PAIN 3.SWELLIN G OF LEGS OR ANKLES CALCIBLOC CALCIBLO C IS USED TO TREAT PRINZMET AL'S ANGINA. E BLOCKS THE FINAL STEP IN ACID PRODUCTION .GITIS.

RESULTS IN A INCREASE OF MYOCARDI AL OXYGEN SUPPLY AND A DECREASE IN SYSTEMIC BLOOD PRESSURE.SPASM OF THE CORONARY ARTERY AND DILATES THE SYSTEMIC ARTERIES. CALCIUM INHIBITS THE CONTRACT ILE PROCESSE S OF SMOOTH MUSCLE CELLS. DECREASE D SYSTEMIC BLOOD PRESSURE. AND DECREASE D AFTERLOA D. INCREASE D OXYGEN DELIVERY TO THE MYOCARDI AL TISSUE. CAUSING DILATION OF THE CORONAR Y AND SYSTEMIC ARTERIES. . DECREASE D TOTAL PERIPHER AL RESISTAN CE.

36.WALA AKONG GANA KUMAIN}. y y y y y y y y y .70 R. INTERVENTION INDEPENDENT: 1.ADMINISTER ANALGESIC AS DOCTOR ORDERED.7 P. INTERVATION THE CLIENT VERBALIZED DECREASED IN PAIN AND PROMOTE REST. BY AN OBSTRUCTIO N OF PANCREATI C SECRETORY TRANSPORT AND BY AN ACTIVATION OF PANCREATI C ENZYMES. 2. AS VERBALIZE D BY THE PATIENT OBJECTIVE: WITH o FACI AL o GRIM ACE RESTLESSN ESS IRRITABILIT Y T.ENCOURAGE DIVERTIONAL ACTIVITIES LIKE SOCIALIZATIO N WITH OTHERS DEPENDENT: 1.160/70 DIAGNOSIS ACUTE PAIN RELATED TO INFLAMMATI ON.DETERMINE CLIENTS ACCEPTABLE LEVEL OF PAIN ON 0-10 USING PAIN SCALE 2.21 BP.PROVIDE COMFORT MEASURES LIKE USE OF HEAT AND COLD 5.NURSING CARE PLAN ASSESTMENT y y SUBJECTIV E: |MASAKI TANG TYAN KO.EDEMA DISTENTION OF THE PANCREAS AND TO PERITONEAL IRRITATION INFERENCE ACUTE PANCREATI TIS IS CHARACTER IZED BY A LOSS OF INTRACELLU LAR AND EXTRACELL ULAR COMPARTME NTATION. OUTFLOW OBSTRUCTIO N WITH PANCREATI C DUCT HYPERTENSI ON AND A TOXIC EFFECT OF BILE SALTS CONTRIBUTE TO PLANNING AFTER 3 HOURS OF NURSING INTERVEN TION THE CLIENT WILL BE ABLE TO VERBALI ZE RELIEF ON PAIN AND CONTROLL ED.ENCOURAGE VERVALIZATI ON ON FEELINGS QABOUT PAIN 3. IN BILIARY ACUTE PANCREATI TIS.NOTIFY PHYSICIAN IF REGIMEN IS IN ADEQUATE EVALUATION AFTER 3 HOURS OF THE NSG.PROVIDE QUITE ENVIRONMENT 4.

SUPPORTED FINANCIALLY BY HER NIECE AND NEPHEWS WHO ARE WORKING. OPD VISITS: TEACH PATIENT THAT IF ACUTE ABDOMINAL PAIN OR BILIARY TRACT DISEASE (AS EVIDENCEDBY JAUNDICE. -EDUCATE PATIENT IN PAIN MANAGEMENT. AND DARKENED URINE) OCCURS. TREATMENT: THE CLIENT SHOULD BE ENCOURAGED TO LEARN AND USE OF RELAXATION TECHNIQUESINCLUDING GUIDED IMAGERY AND MUSIC THERAPY ARE USED TO SHIFT THE FOCUS OF THE BRAINAWAY FROM THE PAIN. -ENCOURAGE A HEALTHY LIFESTYLE. SHE SHOULD NOTIFY IT TOTHE PHYSICIAN. HEALTH TEACHINGS: -ENCOURAGE TO TAKE A WELL BALANCED DIET. . WITH SUBSEQUEN T LOSS OF EXTRACELL ULAR COMPARTME NTATION.DISRUPTION OF PANCREATI C DUCTULES. AND OTHER NECESSITIES BECAUSE THE SALARY OF HER NIECE IS NOT THAT BIG ENOUGH FOR THEM BECAUSE THEY ALSO HAVE THEIR OWN FAMILY.TO MEET PAIN CONTROL GOAL. CLAY. TENSION AND STRESSCAN ALSO BE REDUCED THROUGH BIOFEEDBACK.MAINTAINS BEDREST AS PRESCRIBED DISCHARGE PLANNING MEDICATIONS: OMEPRAZOLE ( OMEPRON) 40MG CALCIBLOC 5MG ECONOMIC STATUS: DL M IS SINGLE. 4. BEING MASSAGED OR APPLYING BACKRUB ISVERY RELAXING AND HELPS REDUCE STRESS. SHE MAY REPORT TO THE PHYSICIAN AFTER 7 TO 10 DAYS TO KNOW THEINDICTOR OF DISEASE OR RESPONSE PROGRESSION. AND REDUCE STRESS. DECREASE MUSCLE TENSION.COLORED STOOLS. 3.CANT AFFORD FOR TO PAY FOR HER MEDICATIONS.

THIS WILL INVOLVE CARE OF NASOGASTRIC TUBE ASPIRATION AND PSYCHOLOGICAL SUPPORT. ASK FOR HELP TO GOD FOR COMPLETE RECOVERY. ACCURATE FLUID BALANCE IS ESSENTIAL . SPICY FOODS. FREQUENT FEEDING OF BLAND DIET. . HEAVY MEALS. TEMPERATURE AND RESPIRATION MEASUREMENTS AT LEAST HOURLY.ADMINISTER THE PRESCRIBED ANTIBIOTICS AND ENSURE UNIVERSAL INFECTION CONTROL MEASURES ARE PRACTISED TO PROTECT THE PATIENT. HIGH FATTY FOODS. . FOR EXAMPLE.UNDERTAKE REGULAR OBSERVATIONS.GIVE ORAL CARE TO NIL-BY-MOUTH PATIENTS AND MONITOR FOR PARALYTIC ILEUS. . SUCH AS REGULAR HYGIENE. SMALL. AND ENCOURAGE DEEP BREATHING EXERCISES TO HELP PREVENT ATELECTASIS AND PROMOTE REMOVAL OF SECRETIONS. PULSE. . ANTI-EMETICS MAY BE NEEDED TO CONTROL NAUSEA AND VOMITING. ANY CAFFEINECONTAINING FOODS. THE NURSE SHOULD ACT ON THE RESULTS ACCORDINGLY.PATIENTS GENERALLY REQUIRE HOURLY URINE MEASUREMENT WHILE THEY ARE IN THE ACUTE STAGE. SPIRITUAL CARE: ENCOURAGE CLIENT TO PRAY IN ACCORDANCE WITH THEIR BELIEFS. . . ENSURE THE CORRECT SIZE TED STOCKINGS ARE WORN. PASSIVE EXERCISE MAY BE APPROPRIATE IN SOME CASES. .GIVE CORE NURSING CARE. IF THE PATIENT IS LETHARGIC.REGULARLY TURN THE PATIENT TO HELP PROTECT THE SKIN. CONTINUOUS ELECTROCARDIOGRAM AND OXYGEN SATURATION MONITORING SHOULD ALSO BE UNDERTAKEN.DIET: THE CLIENT SHOULD BE INSTRUCTED TO AVOID ALCOHOL. IN THE ACUTE STAGE IT MAY BE NECESSARY TO TAKE PATIENTS' BLOOD PRESSURE. AND PROMOTE EXERCISE.TAKE MEASURES TO PROTECT THE PATIENT FROM THROMBOEMBOLISM. AND KEEP THE PATIENT WELL HYDRATED. WHO MAY BE SEPTIC FROM OTHER INFECTIONS.GIVE PRESCRIBED INTRAVENOUS FLUIDS AND OTHER PRODUCTS TO CORRECT HYPOVOLAEMIA. . IN ADDITION. LOW MOLECULAR WEIGHT HEPARIN MAY BE PRESCRIBED FOR SOME PATIENTS. AS THE PATIENT MAY SWEAT CONSIDERABLY. NURSING MANAGEMENT: OFFER REGULAR ANALGESIA TO PROMOTE COMFORT.

. .EDUCATE THE PATIENT ON LIFESTYLE MEASURES. SCARED AND FEELING VERY ILL. ADVISE KEEPING TO A LOW FAT DIET TO HELP PREVENT GALLSTONES AND/OR TO REDUCE ALCOHOL CONSUMPTION IF THIS IS APPROPRIATE FOR THE PARTICULAR PATIENT. . THESE ARE SHOWN IN BOX 2.INSULIN MAY NEED TO BE ADMINISTERED ON A SLIDING SCALE. . FOR EXAMPLE..PSYCHOLOGICAL SUPPORT IS PARAMOUNT.MEASURE BLOOD GLUCOSE LEVELS FOUR-HOURLY . AS THE PATIENT MAY BE IN PAIN.PROVIDE SUPPORT AND EXPLANATION DURING INVESTIGATIONS.

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