CASE STUDY

ACUTE PANCREATITIS
SUBMITTED BY:

JENNIFER AGUILUZ

MRS. MARIA EVELYN LUMIO R.N.

INTRODUCTION:
ACUTE PANCREATITIS IS AN INFLAMMATORY CONDITION OF THE PANCREAS CHARACTERIZED CLINICALLY BY ABDOMINAL PAIN AND ELEVATED LEVELS OF PANCREATIC ENZYMES IN THE BLOOD . ABNORMAL EXOCRINE AND ENDOCRINE FUNCTION CAN OCCUR DURING AN ACUTE ATTACK . IN PATIENTS WITH INTERSTITIAL OR MILD ACUTE PANCREATITIS THE GLAND RETURNS TO HISTOLOGIC AND FUNCTIONAL NORMALCY AFTER RECOVERY. ENDOCRINE FUNCTION RETURNS TO NORMAL SOON AFTER THE ACUTE PHASE, WHILE EXOCRINE FUNCTION MAY TAKE UP TO ONE YEAR FOR FULL RECOVERY . PATIENTS WITH NECROTIZING PANCREATITIS, ALSO REFERRED TO AS SEVERE ACUTE PANCREATITIS, CAN DEVELOP PERMANENT EXOCRINE AND ENDOCRINE INSUFFICIENCY DEPENDING UPON EXTENT OF NECROSIS . IN ONE REPORT, FOR EXAMPLE, 25 PERCENT OF 65 PATIENTS WHO SURVIVED FOLLOWING NECROSECTOMY DEVELOPED EXOCRINE INSUFFICIENCY . IN ADDITION, 33 PERCENT DEVELOPED NEW ONSET DIABETES AFTER A MEDIAN FOLLOW-UP OF 29 MONTHS. IN ANOTHER REPORT, 76 PERCENT OF 42 PATIENTS WITH SEVERE ACUTE PANCREATITIS FOLLOWED FOR 24 TO 36 MONTHS HAD ONGOING SYMPTOMS DUE TO PANCREATIC DYSFUNCTION, 32 PERCENT HAD NEW ONSET DIABETES, AND 20 PERCENT WERE ON PANCREATIC ENZYMES FOR THE DIARRHEA . SCARRING OF THE PANCREATIC DUCTS CAN PERSIST INDEFINITELY IN SOME PATIENTS, MIMICKING THE DUCTAL CHANGES OF CHRONIC PANCREATITIS . HOWEVER, CHRONIC PANCREATITIS, SIGNIFICANT PANCREATIC NECROSIS, OR PANCREATIC DUCTAL OBSTRUCTION SHOULD BE SUSPECTED IF OVERT EXOCRINE OR ENDOCRINE DYSFUNCTION PERSISTS OR INCREASES AFTER AN ATTACK OF CLINICALLY ACUTE PANCREATITIS. THE PATHOGENESIS OF ACUTE PANCREATITIS IS NOT FULLY UNDERSTOOD. NEVERTHELESS, A NUMBER OF CONDITIONS ARE KNOWN TO INDUCE THIS DISORDER WITH VARYING DEGREES OF CERTAINTY, WITH GALLSTONES AND CHRONIC ALCOHOL ABUSE ACCOUNTING FOR 75 PERCENT OF CASES IN THE UNITED STATES

ETIOLOGY
THERE ARE MANY CAUSES OF ACUTE PANCREATITIS, WHICH CAN BE EASILY IDENTIFIED IN 75%-85% OF PATIENTS. IN DEVELOPED COUNTRIES, OBSTRUCTION OF THE COMMON BILE DUCT BY STONES (38%) AND ALCOHOL ABUSE (36%) ARE THE MOST FREQUENT CAUSES OF ACUTE PANCREATITIS[3,8]. GALLSTONE-INDUCED PANCREATITIS IS CAUSED BY DUCT OBSTRUCTION BY GALLSTONE MIGRATION. OBSTRUCTION IS LOCALIZED IN THE BILE DUCT AND PANCREATIC DUCT, OR BOTH. DUCT OBSTRUCTION PROMOTES PANCREATITIS BY INCREASING DUCT PRESSURE AND SUBSEQUENT UNREGULATED ACTIVATION OF DIGESTIVE ENZYMES[9]. ALCOHOL ABUSE IS THE SECOND MOST FREQUENT CAUSE OF ACUTE PANCREATITIS, BUT THE CORRELATION BETWEEN ALCOHOL AND PANCREATITIS IS NOT COMPLETELY UNDERSTOOD[10]. IN EXPERIMENTAL MODELS, GORELICK SHOWED THAT ETHANOL DIRECTLY SENSITIZES ACINAR CELLS TO CHOLECYSTOKININ STIMULATION. AS THE DEVELOPMENT OF PANCREATITIS MIGHT BE AFFECTED BY BOTH GENETIC AND ENVIRONMENTAL FACTORS,

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

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

PAIN; SHE WAS BROUGHT TO ER SHE WAS ADMITTED AND WAS TRANSFERRED HERE AT EAMMC FEMALE WARD . FAMILY HEALTH HISTORY ACCORDING TO THE PATIENT DL M,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. PERSONAL / SOCIAL HISTORY THE PATIENT IS THE 3TH AMONG 6 SIBLINGS. SHE IS LIVING WITH HER FAMILY BECAUSE SHE DOESNT HAVE HER OWN FAMILY. SHE IS STILL SINGLE. THEY ARE ONLY FINANCIALLY SUPPORTED BY HER NEPHEWS AND NIECE WHO ARE WORKING.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.

PHYSICAL ASSESTMENT
ACTUAL FINDINGS NORMAL FINDINGS INTERPRETA TION -NORMAL

 HEAD y SKULL

-NORMOCEPHALIC -NO LUMPS

y SCALP

-NO NITS, 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. -WHITISH -NO NITS, LICE AND DANDRUFF -NO BALDNESS

-NORMAL

y HAIR
-STRAIGHT, BLACK WITH WHITE HAIR, 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

-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; BILATERAL BLINKING -NO SCALING -NO SECRETIONS -NO ERYTHEMA -NO REDNESS -PINK, SHINY, 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; BILATERAL BLINKING -NO SECRETIONS -NO ERYTHEMA -NO REDNESS

-NORMAL

y EYELIDS

-NORMAL

y LID MARGINS

-NORMAL

y LOWER PALPEBRAL CONJUNCTIVA

-PINK, SHINY, WITH VISIBLE BLOOD VESSELS -NO DISCHARGES

-NORMAL

y SCLERA

-WHITE IN COLOR -CLEAR - NO REDNESS

-NORMAL -WHITE/YELLOWISH IN AMERICANS -CLEAR, NO CLOUDINESS -NO REDNESS -FLAT -BROWN -EVEN COLORATION -SYMMETRICAL -ROUND -TRANSPARENT/SHINY -PERRLA(PUPILS EQUALLY ROUND, REACTIVE TO LIGHT & BLACK

y IRIS

-FLAT -BROWN -ROUND -TRANSPARENT/SHINY

-NORMAL

-PERRLA

-NORMAL

y PUPILS

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
- 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, E.G,BLUISH HUE, IN MEDITERRANEAN GROUPS AND DARK-SKINNED CLIENTS) -SOFT, MOIST, SMOOTH TEXTURE -SYMMETRY OF CONTOUR -ABILITY TO PURSE LIPS -NO TENDERNESS -PINK, MOIST -NO SWELLING

-DECREASE OF OXYGEN SUPPLY

y GUMS

-PINK, MOIST -NO SWELLING -NO TENDERNESS -NO DISCHARGES

-NORMAL

y TEETH

-WHITE

-NO TENDERNESS -NO DISCHARGES -NO RETRACTION(LOWER UPPER) DORSAL

-NORMAL AND

y TONGUE

-PINK, EVEN, ROUGH SURFACE AND MOIST

-32 IN NUMBER -WHITE -UPPER TEETH OVER-RIDES LOWER TEETH

-NORMAL

y FRENULUM

-MIDLINE -PINKISH -WITH VISIBLE VEINS -PINK, MOIST, NO SWELLING/NO TENDERNESS

-PINK, EVEN, ROUGH SURFACE AND MOIST

DORSAL

-NORMAL

y SOFT PALATE

y HARD PALATE

-BONY, LIGHT PINK IN COLOR, MOIST

-MIDLINE -PINKISH -WITH VISIBLE VEINS -PINK, MOIST, NO SWELLING/NO TENDERNESS

-NORMAL

-NORMAL

y UVULA

-MIDLINE MOVES WHEN THE CLIENT SAYS |AAH} -BONY, LIGHT PINK IN COLOR, MOIST -NORMAL

y TONSILS
-PINKISH -NO DISCHARGE -NO INFLAMMATION -PINK, MOIST -MIDLINE MOVES WHEN THE CLIENT SAYS |AAH} -NORMAL

 NECK
-SAME AS THE SKIN COLOR -NO LYMPHS, NO MASS -PINKISH -NO DISCHARGE -NO INFLAMMATION -NORMAL

 UPPER EXTREMITIES y SKIN

-NO ABRASIONS OR OTHER LESIONS -WHEN PINCHED, SKIN SPRINGS BACK TO PREVIOUS STATE - WITH EDEMA

-ERECT & MIDLINE -SAME AS THE SKIN COLOR -NO TENDERNESS -NO LYMPHS, NO MASS -SYMMETRICAL -MUSCLES EQUAL IN SIZE; HEAD CENTERED -COORDINATED, SMOOTH MOVEMENTS WITH NO DISCOMFORT

ACCUMULATI ON OF EXCESS

FLUID -WITH DISCOLORATION -WITH BRUISES -VARIES FROM LIGHT TO DEEP BROWN; FROM RUDDY PINK TO LIGHT PINK; FROM YELLOW OVERTONES TO OLIVE -NO EDEMA -NO ABRASIONS OR OTHER LESIONS -FRECKLES, SOME BIRTHMARKS, SOME FLAT AND RAISED NEVI -WHEN PINCHED, SKIN SPRINGS BACK TO PREVIOUS STATE -CONVEX CURVATURE -SMOOTH TEXTURE -HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS; 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; 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, RHYTHMIC, AND EFFORTLESS RESPIRATIONS -FULL SYMMETRIC EXCURSION -BRONCHIAL AND TUBULAR BREATH SOUNDS IN THE TRACHEA -VESICULAR AND BRONCHOVESICULAR BREATH SOUNDS

-DIFFICULTY OF BREATHING

-NORMAL

 LOWER EXTREMITIES y SKIN

-BROWN IN COLOR - NO ABRASIONS LESIONS

OR

OTHER

-UNBLEMISHED SKIN -UNIFORM COLOR -SILVER-WHITE STRIAE OR SURGICAL SCARS -FLAT, ROUNDED(CONVEX),OR SCAPHOID (CONCAVE) - SYMMETRIC MOVEMENTS CAUSED BY RESPIRATION - AUDIBLE BOWEL SOUNDS - NO TENDERNESS - RELAXED ABDOMEN WITH SMOOTH, CONSISTENT TENSION

y NAILS

- CONCAVE CURVATURE -BROWN PIGMENTATION LONGITUDINAL STREAKS

IN

- VARIES FROM LIGHT TO DEEP BROWN; FROM RUDDY PINK TO LIGHT PINK; FROM YELLOW OVERTONES TO OLIVE - NO EDEMA - NO ABRASIONS OR OTHER LESIONS - FRECKLES, SOME BIRTHMARKS, SOME FLAT AND RAISED NEVI - WHEN PINCHED, SKIN SPRINGS BACK TO PREVIOUS STATE - CONCAVE CURVATURE - SMOOTH TEXTURE - HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS; DARKSKINNED CLIENTS MAY HAVE BROWN OR BLACK PIGMENTATION IN LONGITUDINAL STREAKS - INTACT EPIDERMIS - PROMPT RETURN OF PINK OR USUAL COLOR (GENERALLY LESS THAN 4 SECS.) - HAS UPRIGHT POSTURE AND STEADY GAIT WITH OPPOSING ARM SWING; WALKS UNAIDED, MAINTAINING BALANCE - MAY SWAY SLIGHTLY BUT IS ABLE TO MAINTAIN UPRIGHT POSTURE AND FOOT STANCE. - 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 - CAN READILY DETERMINE THE POSITION OF FINGERS AND TOES

-NORMAL

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

PATHOPHYSIOLOGY

ANATOMY AND PHYSIOLOGY

GALLBLADER- THE GALLBLADDER IS A SMALL PEAR-SHAPED ORGAN THAT STORES AND CONCENTRATES BILE. THE GALLBLADDER IS CONNECTED TO THE LIVER BY THE HEPATIC DUCT. IT IS APPROXIMATELY 3 TO 4 INCHES (7.6 TO 10.2 CM) LONG AND ABOUT 1 INCH (2.5 CM) WIDE. THE FUNCTION OF THE GALLBLADDER IS TO STORE BILE AND CONCENTRATE. BILE IS A DIGESTIVE LIQUID CONTINUALLY SECRETED BY THE LIVER. THE BILE EMULSIFIES FATS AND NEUTRALIZES ACIDS IN PARTLY DIGESTED FOOD. A MUSCULAR VALVE IN THE COMMON BILE DUCT OPENS, AND THE BILE FLOWS FROM THE GALLBLADDER INTO THE CYSTIC DUCT, ALONG THE COMMON BILE DUCT, AND INTO THE DUODENUM (PART OF THE SMALL INTESTINE).

PANCREAS- THE PANCREAS IS A GLANDULAR ORGAN THAT SECRETES DIGESTIVE ENZYMES (INTERNAL SECRETIONS) AND HORMONES (EXTERNAL SECRETIONS). IN HUMANS, THE PANCREAS IS A YELLOWISH ORGAN ABOUT 7 INCHES (17.8 CM) LONG AND 1.5 INCHES. (3.8 CM) WIDE. THE PANCREAS CONTAINS ENZYME PRODUCING CELLS THAT SECRETE TWO HORMONES. THE TWO HORMONES ARE INSULIN AND GLUCAGON. INSULIN AND GLUCAGON ARE SECRETED DIRECTLY INTO THE BLOODSTREAM, AND TOGETHER, THEY REGULATE THE LEVEL OF GLUCOSE IN THE BLOOD. INSULIN LOWERS THE BLOOD SUGAR LEVEL AND INCREASES THE AMOUNT OF GLUCAGON (STOREDCARBOHYDRATE) IN THE LIVER. GLUCAGON SLOWLY INCREASES THE BLOOD SUGAR LEVEL IF IT FALLS TOO LOW. THE PANCREAS PRODUCES

THE BODY'S MOST IMPORTANT ENZYMES. THE ENZYMES ARE DESIGNED TO DIGEST FOODS AND BREAK DOWN STARCHES.

THE PANCREAS ALSO HELPS NEUTRALIZE CHYME AND HELPS BREAK DOWN PROTEINS, FATS AND STARCH. CHYME IS A THICK SEMIFLUID MASS OF PARTLY DIGESTED FOOD THAT IS PASSED FROM THE STOMACH TO THE DUODENUM. IF THE PANCREAS IS NOT WORKING PROPERLY TO NEUTRALIZE CHYME AND BREAK DOWN PROTEINS, FATS AND STARCH, STARVATION MAY OCCUR. 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 . MAJOR DUODENAL PAPILLATHE COMMON BILE DUCT AND THE PANCREATIC DUCT TOGETHER PERFORATE THE MEDIAL SIDE OF THE SECOND PORTION OF THE DUODENUM OBLIQUELY, SOME 7 TO 10 CM BELOW THE PYLORUS, FORMING A STRUCTURE DUODENUM- THE DUODENUM IS THE FIRST SECTION OF THE SMALL INTESTINE IN MOST HIGHER VERTEBRATES, INCLUDING MAMMALS, REPTILES, AND BIRDS. IN FISH, THE DIVISIONS OF THE SMALL INTESTINE ARE NOT AS CLEAR AND THE TERMS ANTERIOR INTESTINE OR PROXIMAL INTESTINE MAY BE USED INSTEAD OF DUODENUM.[2] IN MAMMALS THE DUODENUM MAY BE THE PRINCIPAL SITE FOR IRON ABSORPTION.[3] THE DUODENUM PRECEDES THE JEJUNUM AND ILEUM AND IS THE SHORTEST PART OF THE SMALL INTESTINE, WHERE MOST CHEMICAL DIGESTION TAKES PLACE. THE NAME DUODENUM IS FROM THE LATIN DUODENUM DIGITORUM, OR TWELVE FINGERS' BREADTHS. IN HUMANS, THE DUODENUM IS A HOLLOW JOINTED TUBE ABOUT 1012 INCH LONG CONNECTING THE STOMACH TO THE JEJUNUM. IT BEGINS WITH THEDUODENAL BULB AND ENDS AT THE LIGAMENT OF TREITZ. MINOR DUODENUM OFTEN PAPILLA- THE MINOR DUODENAL PAPILLA IS THE OPENING OF OTHER NAMES OF MINOR DUODENAL PAPILLA

THE ACCESSORY PANCREATIC DUCT INTO THE DUODENUM. IT IS SOMETIMES ABSENT, AND NONFUNCTIONAL.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.IT USUALLY RETURNS TO NORMAL WITHIN ONE WEEK. THIS METHOD IS QUICK, EASILY OBTAINED, AND INEXPENSIVE.75-92% SENSITIVE, 20 TO 60% SPECIFIC. LIPASE LIPASE LEVELS INCREASE WITHIN 4 TO 8 HOURS OF THE ONSET OF CLINICAL

SYMPTOMS AND PEAK AT ABOUT 24 HOURS.LEVELS DECREASE WITHIN EIGHT TO 14 DAYS. 86-100% SENSITIVE, 50-99% SPECIFIC. 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.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.HOWEVER, THESE TESTS ARE NOT SUFFICIENTLY RELIABLE FOR DIAGNOSING ACUTE BILIARY PANCREATITIS OR DETERMINING ITS ETIOLOGY.

DRUG STUDY
NAME OF DRUG OMEPRAZOL E DOSAGE/ ROUTE CAPSULE, DELAYED RELEASE ORAL TABLET, 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), THE HEALING OF EROSIVE ESOPHA INDICATION FOR THE TREATMENT OF GASTROESO PHAGEAL REFLUX DISEASE. 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, 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. NURSING RESPONSIBILITY 1.ADMINISTER BEFORE MEALS 2.ADMINISTER ANTACIDS IF NEEDED 3.REPORT SEVERE HEADACHE, WORSENING OF SYMPTOMS,FEVE R AND CHILLS

GITIS, AND H. PYLORIE RADICAT ION TO REDUCE THE RISK OF DUODEN AL ULCER RECURRE NCE.

E BLOCKS THE FINAL STEP IN ACID PRODUCTION , THUS REDUCING GASTRIC ACIDITY.

NAME DRUG

OF

DOSAGE/RO UTE TABLET, 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. THE DECREASE IN INTRACEL LULAR

ADVERSE EFFECT UNUSUAL SLOW OR FAST HEARTBEAT,DI ZZYNES OR PAINTING,YEL LOWING OF THE SKIN,SWELLIN G OF LEGS OR ANKLES

CALCIBLOC

CALCIBLO C IS USED TO TREAT PRINZMET AL'S ANGINA, HYPERTEN SION, AND OTHER VASCULAR DISORDER S SUCH AS RAYNAUD' S PHENOMEN ON. BY BLOCKING THE CALCIUM CHANNELS , CALCIBLO C INHIBITS THE

NURSING RESPONSIBILI TY 1.MONITOR BP 2.OBSERVE FOR CHEST PAIN 3.MONITOR FOR POSSIBLE DRUG ADVERSE REACTION

SPASM OF THE CORONARY ARTERY AND DILATES THE SYSTEMIC ARTERIES, RESULTS IN A INCREASE OF MYOCARDI AL OXYGEN SUPPLY AND A DECREASE IN SYSTEMIC BLOOD PRESSURE.

CALCIUM INHIBITS THE CONTRACT ILE PROCESSE S OF SMOOTH MUSCLE CELLS, CAUSING DILATION OF THE CORONAR Y AND SYSTEMIC ARTERIES, INCREASE D OXYGEN DELIVERY TO THE MYOCARDI AL TISSUE, DECREASE D TOTAL PERIPHER AL RESISTAN CE, DECREASE D SYSTEMIC BLOOD PRESSURE, AND DECREASE D AFTERLOA D.

NURSING CARE PLAN

ASSESTMENT y y SUBJECTIV E: |MASAKI TANG TYAN KO,WALA AKONG GANA KUMAIN}, AS VERBALIZE D BY THE PATIENT OBJECTIVE: WITH o FACI AL o GRIM ACE RESTLESSN ESS IRRITABILIT Y T- 36.7 P- 70 R- 21 BP- 160/70 DIAGNOSIS ACUTE PAIN RELATED TO INFLAMMATI ON,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, BY AN OBSTRUCTIO N OF PANCREATI C SECRETORY TRANSPORT AND BY AN ACTIVATION OF PANCREATI C ENZYMES. IN BILIARY ACUTE PANCREATI TIS, 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. INTERVENTION INDEPENDENT: 1.DETERMINE CLIENTS ACCEPTABLE LEVEL OF PAIN ON 0-10 USING PAIN SCALE 2.ENCOURAGE VERVALIZATI ON ON FEELINGS QABOUT PAIN 3.PROVIDE QUITE ENVIRONMENT 4.PROVIDE COMFORT MEASURES LIKE USE OF HEAT AND COLD 5.ENCOURAGE DIVERTIONAL ACTIVITIES LIKE SOCIALIZATIO N WITH OTHERS DEPENDENT: 1.ADMINISTER ANALGESIC AS DOCTOR ORDERED. 2.NOTIFY PHYSICIAN IF REGIMEN IS IN ADEQUATE EVALUATION AFTER 3 HOURS OF THE NSG. INTERVATION THE CLIENT VERBALIZED DECREASED IN PAIN AND PROMOTE REST.

y y

y y y y y y y

DISRUPTION OF PANCREATI C DUCTULES, WITH SUBSEQUEN T LOSS OF EXTRACELL ULAR COMPARTME NTATION.

3.TO MEET PAIN CONTROL GOAL. 4.MAINTAINS BEDREST AS PRESCRIBED

DISCHARGE PLANNING
MEDICATIONS: OMEPRAZOLE ( OMEPRON) 40MG CALCIBLOC 5MG ECONOMIC STATUS: DL M IS SINGLE, SUPPORTED FINANCIALLY BY HER NIECE AND NEPHEWS WHO ARE WORKING,CANT AFFORD FOR TO PAY FOR HER MEDICATIONS, AND OTHER NECESSITIES BECAUSE THE SALARY OF HER NIECE IS NOT THAT BIG ENOUGH FOR THEM BECAUSE THEY ALSO HAVE THEIR OWN FAMILY. 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, DECREASE MUSCLE TENSION, AND REDUCE STRESS. TENSION AND STRESSCAN ALSO BE REDUCED THROUGH BIOFEEDBACK. BEING MASSAGED OR APPLYING BACKRUB ISVERY RELAXING AND HELPS REDUCE STRESS. HEALTH TEACHINGS: -ENCOURAGE TO TAKE A WELL BALANCED DIET. -ENCOURAGE A HEALTHY LIFESTYLE. -EDUCATE PATIENT IN PAIN MANAGEMENT. OPD VISITS: TEACH PATIENT THAT IF ACUTE ABDOMINAL PAIN OR BILIARY TRACT DISEASE (AS EVIDENCEDBY JAUNDICE, CLAY- COLORED STOOLS, AND DARKENED URINE) OCCURS, SHE SHOULD NOTIFY IT TOTHE PHYSICIAN. SHE MAY REPORT TO THE PHYSICIAN AFTER 7 TO 10 DAYS TO KNOW THEINDICTOR OF DISEASE OR RESPONSE PROGRESSION.

DIET:
THE CLIENT SHOULD BE INSTRUCTED TO AVOID ALCOHOL, SPICY FOODS, ANY CAFFEINECONTAINING FOODS, HEAVY MEALS, HIGH FATTY FOODS. SMALL, FREQUENT FEEDING OF BLAND DIET.

SPIRITUAL CARE:
ENCOURAGE CLIENT TO PRAY IN ACCORDANCE WITH THEIR BELIEFS. ASK FOR HELP TO GOD FOR COMPLETE RECOVERY.

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

- MEASURE BLOOD GLUCOSE LEVELS FOUR-HOURLY - INSULIN MAY NEED TO BE ADMINISTERED ON A SLIDING SCALE; - PSYCHOLOGICAL SUPPORT IS PARAMOUNT, AS THE PATIENT MAY BE IN PAIN, SCARED AND FEELING VERY ILL; - PROVIDE SUPPORT AND EXPLANATION DURING INVESTIGATIONS. THESE ARE SHOWN IN BOX 2; - EDUCATE THE PATIENT ON LIFESTYLE MEASURES; FOR EXAMPLE, 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.