Acute Pancreatitis

CASE STUDY  ´ACUTE PANCREATITISµ

 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 PATIENTS 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,DOESNT 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 DOESNT 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 DOESNT KNOW WHERE SHE GET THIS KIND OF DISEASE BECAUSE    THE PATIENT IS KNOWN TO BE A HEALTH CONSCIOUS PERSON AND DOESNT EAT TOO MUCH FATTY AND SALTY FOODS.

PHYSICAL ASSESTMENT 



HEAD  SKULL  y

y

y

y

 SCALP

ACTUAL FINDINGS

NORMAL FINDINGS

-NORMOCEPHALIC -NO LUMPS

-NORMOCEPHALIC -NORMAL  -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. -NORMAL 

-NO NITS, LICE AND DANDRUFF  -NO BALDNESS

INTERPRETA  TION

HAIR 

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

-NORMAL 

FACE 

-STRAIGHT, BLACK WITH WHITE  HAIR, OILY HAIR  -BLACK OR BROWN IN COLOR  -HAIR IS EVENLY DISTRIBUTED -NO AREA OF BALDNESS -THICK  -FINE  -CURLY/KINKY/STRAIGHT  -DRY/OILY/SHINY HAIR  -SYMMETRICAL WITH MOVEMENT 

-NORMAL 

-EXPRESSIONS APPROPRIATE TO  SITUATIONS y

y

y

y

y

y

y

y

EYES

EYEBROWS

EYELASHES

EYELIDS

LID MARGINS

-SYMMETRICAL  -NO CLOUDINESS -NO LACRIMATION

-SYMMETRICAL 

-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

LOWER  PALPEBRAL  CONJUNCTIVA

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

 SCLERA

-WHITE IN COLOR  -CLEAR  - NO REDNESS

IRIS

-FLAT  -BROWN -ROUND -TRANSPARENT/SHINY 

-PERRLA y

-SYMMETRICAL WITH MOVEMENT  -EXPRESSIONS APPROPRIATE TO  SITUATIONS

-NORMAL 

-SYMMETRICAL  -NO PROTRUSIONS -DEAR OR NO CLOUDINESS -NO EXCESSIVE LACRIMATION

-NORMAL 

-MOVES SYMMETRICALLY  -HAIR EVENLY DISTRIBUTED -SKIN INTACT 

-NORMAL 

-EQUALLY DISTRIBUTED -CURVED SLIGHTLY OUTWARD

-NORMAL 

-SKIN INTACT  -NO DISCHARGE  -NO DISCOLORATION -LIDS CLOSE SYMMETRICALLY  -APPROXIMATELY 15-20 INVOLUNTARY BLINKS PER   MINUTE; BILATERAL BLINKING -NORMAL  -NO SCALING -NO SECRETIONS -NO ERYTHEMA -NO REDNESS

-NORMAL 

-PINK, SHINY, WITH VISIBLE BLOOD  VESSELS -NO DISCHARGES -NORMAL  -WHITE/YELLOWISH IN AMERICANS -CLEAR, NO CLOUDINESS -NO REDNESS

BLACK 

-FLAT  -BROWN -EVEN COLORATION -SYMMETRICAL  -ROUND -TRANSPARENT/SHINY 

PUPILS -PERRLA(PUPILS EQUALLY ROUND, REACTIVE TO LIGHT &

-NORMAL 

-NORMAL 

ACCOMMODATION y

EYE MOVEMENT 

-MOVES IN UNISON -COORDINATED

-NORMAL  -MOVES IN UNISON -COORDINATED

FIELD OF VISION *VISUAL ACUITY 

-NORMAL 

y

-GOOD PERIPHERAL VISION -20/20 IN BOTH EYES y

EAR 

y

EAR CANAL 

y

y

y

y

HEARING ACUITY 

 NOSE 

LIPS

GUMS

-SAME AS THE COLOR OF THE  -NORMAL  FACE  -NO SWELLING -PARALLEL WITH OUTER CANTHUS -SHELL SHAPE  OF THE EYES -SAME AS THE COLOR OF THE  FACE  -NO SWELLING -NO TENDERNESS -SHELL SHAPE  - WAXY CERUMEN -FIRM CARTILAGE  -NORMAL  -PRESENCE OF CILIA -YELLOWISH -DRY/WAXY CERUMEN -PRESENCE OF CILIA -WITH GOOD HEARING ACUITY IN -NO FOREIGN BODY  -NORMAL  BOTH EARS

-NO LESIONS -PRESENCE OF CILIA

-DARKER LIPS -ABILITY TO PURSE LIPS

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

-WITH GOOD HEARING ACUITY IN BOTH EARS

-SYMMETRIC AND STRAIGHT  -NO DISCHARGE OR FLARING -UNIFORM COLOR  -NO TENDERNESS -NO LESIONS -PRESENCE OF CILIA

-NORMAL 

-DECREASE  OF OXYGEN  SUPPLY 

-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 -NORMAL  -NO TENDERNESS -PINK, MOIST  -NO SWELLING

y

y

y

y

y

y

y

 TEETH

-WHITE 

 TONGUE 

-PINK, EVEN, ROUGH  SURFACE AND MOIST 

FRENULUM

-MIDLINE  -PINKISH -WITH VISIBLE VEINS

 SOFT PALATE 

HARD PALATE 

UVULA

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

-NORMAL  AND

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

-PINK, EVEN, ROUGH  SURFACE AND MOIST 

DORSAL  -NORMAL 

-PINK, MOIST, NO SWELLING/NO  TENDERNESS

-BONY, LIGHT PINK IN COLOR,  MOIST 

-MIDLINE  -PINKISH -WITH VISIBLE VEINS

-NORMAL 

-PINK, MOIST, NO SWELLING/NO  TENDERNESS

-NORMAL 

-BONY, LIGHT PINK IN COLOR,  MOIST 

-NORMAL 

-MIDLINE MOVES WHEN THE CLIENT   SAYS |AAH}

 TONSILS -PINKISH -NO DISCHARGE  -NO INFLAMMATION

-PINK, MOIST  -MIDLINE MOVES WHEN THE CLIENT  -NORMAL   SAYS |AAH}

  NECK 

-SAME AS THE SKIN COLOR  -NO LYMPHS, NO MASS



UPPER EXTREMITIES  SKIN y

-PINKISH -NO DISCHARGE  -NO INFLAMMATION

-ERECT & MIDLINE  -SAME AS THE SKIN COLOR  -NO TENDERNESS -NO LYMPHS, NO MASS -SYMMETRICAL  -MUSCLES EQUAL IN SIZE; HEAD -NO ABRASIONS OR OTHER  CENTERED LESIONS -COORDINATED, SMOOTH -WHEN PINCHED, SKIN SPRINGS  MOVEMENTS WITH NO DISCOMFORT  BACK TO PREVIOUS STATE  - WITH EDEMA

-NORMAL 

ACCUMULATI ON OF  EXCESS

FLUID -WITH DISCOLORATION -WITH BRUISES

y

 NAILS

-NO TENDERNESS -NO MASSES

-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  -DECREASE  O2 SUPPLY 



CHEST AND BACK  POSTERIOR   THORAX y

-FULL EXPANSION -TACHYPNEA

-CONVEX CURVATURE  -SMOOTH TEXTURE  -HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS; DARK  SKINNED CLIENTS MAY HAVE  BROWN OR BLACK PIGMENTATION IN LONGITUDINAL STREAKS -INTACT EPIDERMIS -PROMPT RETURN OF PINK OR  USUAL COLOR(GENERALLY LESS  THAN 4 SECONDS)

-NORMAL 

y



ANTERIOR   THORAX

ABDOMEN

-UNBLEMISHED SKIN -UNIFORM COLOR 

-WITH PAIN

-CHEST SYMMETRIC -SKIN INTACT; UNIFORM  TEMPERATURE  -CHEST WALL INTACT  -NO TENDERNESS -NO MASSES -FULL AND SYMMETRIC CHEST  EXPANSION -VESICULAR AND BRONCHOVESICULAR SOUNDS

-DIFFICULTY  OF  BREATHING

-QUIET, RHYTHMIC, AND EFFORTLESS RESPIRATIONS -FULL SYMMETRIC EXCURSION -BRONCHIAL AND TUBULAR  BREATH SOUNDS IN THE TRACHEA -VESICULAR AND BRONCHOVESICULAR BREATH  SOUNDS -NORMAL 



LOWER  EXTREMITIES y

y

 SKIN

 NAILS

  MOTOR 

FUNCTIONS:

-BROWN IN COLOR  - NO ABRASIONS LESIONS

OR

- CONCAVE CURVATURE  -BROWN PIGMENTATION LONGITUDINAL STREAKS

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

ACCUMULATI - VARIES FROM LIGHT TO DEEP ON OF  BROWN; FROM RUDDY PINK TO EXCESS LIGHT PINK; FROM YELLOW  FLUID IN 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 

-REPEATEDLY AND RHYTHMICALLY TOUCHES THE   NOSE  - RAPIDLY TOUCHES EACH FINGER   TO THUMB WITH EACH HAND - CAN READILY DETERMINE THE  POSITION OF FINGERS AND TOES

- CONCAVE CURVATURE  - SMOOTH TEXTURE  -NORMAL  - HIGHLY VASCULAR AND PINK IN LIGHT-SKINNED CLIENTS; DARK  SKINNED 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 -NORMAL  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

- 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 1012 INCH LONG CONNECTING THE  STOMACH TO THE  JEJUNUM. IT BEGINS WITH THE DUODENAL BULB AND ENDS AT THE LIGAMENT OF TREITZ.   MINOR

DUODENUM

PAPILLA-

THE MINOR

DUODENAL

PAPILLA IS

THE

OPENING

OF 

 THE ACCESSORY PANCREATIC DUCT INTO THE DUODENUM. IT IS SOMETIMES ABSENT, AND OFTEN

NONFUNCTIONAL.THE

OTHER

NAMES

OF

MINOR

DUODENAL

PAPILLA

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 DRUG OMEPRAZOL  E 

OF  DOSAGE/  ROUTE  CAPSULE, DELAYED RELEASE  ORAL   TABLET, DELAYED RELEASE  ORAL  CAPSULE  ORAL 

ACTION

INDICATION

MECHANISM

ADVERSE   NURSING EFFECT  RESPONSIBILITY  COMPOUN FOR THE  PROTON OMEPRA 1.ADMINISTER  D THAT   TREATMENT  PUMP ZOLE  BEFORE MEALS INHIBITS OF  INHIBITOR  DELAYED GASTRIC GASTROESO  THAT  2.ADMINISTER  ACID PHAGEAL   SUPPRESSES RELEASE  ANTACIDS IF   SECRETI REFLUX GASTRIC CAPSULE   NEEDED ON AND DISEASE. ACID   S ARE  IS  SECRETION CONTRAI 3.REPORT  INDICATE  BY SPECIFIC  NDICATE   SEVERE  D IN THE  INHIBITION D IN HEADACHE,  TREATM OF THE  PATIENT    WORSENING OF  + + ENT OF  H /K   S WITH  SYMPTOMS,FEVE  GASTRO ATPASE IN KNOWN R AND CHILLS ESOPHA  THE  HYPERSE  GEAL  GASTRIC  NSITIVIT  REFLUX PARIETAL   Y TO ANY  DISEASE  CELL. BY  COMPONE  (GERD), ACTING   NT OF   THE   SPECIFICALL   THE  HEALING   Y ON THE FORMULA OF  PROTON  TION. EROSIVE  PUMP, ESOPHA OMEPRAZOL 

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

  NAME DRUG CALCIBLOC

OF DOSAGE/RO UTE  TABLET, EXTENDED RELEASE  ORAL   TABLET  ORAL  CAPSULE  ORAL 

ACTION

INDICATIO  N

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

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

 MECHANIS  M

ADVERSE  EFFECT 

CALCIBLO OF  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 

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

 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

y y

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 

y y y y y

 T- 36.7 P- 70 R- 21 BP- 160/70

DIAGNOSIS

INFERENCE

PLANNING

INTERVENTION

ACUTE PAIN RELATED TO INFLAMMATI ON,EDEMA DISTENTION OF THE  PANCREAS AND TO PERITONEAL  IRRITATION

ACUTE  AFTER 3 INDEPENDENT: PANCREATI HOURS OF  1.DETERMINE    TIS  NURSING IS CLIENTS CHARACTER  INTERVEN ACCEPTABLE  IZED BY A   TION THE  LEVEL OF  LOSS OF  CLIENT  PAIN ON 0-10 INTRACELLU   WILL BE USING PAIN LAR AND ABLE TO  SCALE  EXTRACELL   VERBALI 2.ENCOURAGE  ULAR  ZE   VERVALIZATI COMPARTME  RELIEF  ON ON  NTATION, BY  ON PAIN FEELINGS AN AND QABOUT PAIN OBSTRUCTIO CONTROLL  3.PROVIDE    N ED. OF  QUITE  PANCREATI ENVIRONMENT  C 4.PROVIDE   SECRETORY  COMFORT   TRANSPORT   MEASURES AND BY AN LIKE USE OF  ACTIVATION HEAT AND OF  COLD PANCREATI 5.ENCOURAGE  C ENZYMES. DIVERTIONAL  IN BILIARY  ACTIVITIES ACUTE  LIKE  PANCREATI  SOCIALIZATIO  TIS,   N OUTFLOW  OTHERS OBSTRUCTIO   N WITH DEPENDENT: PANCREATI C DUCT  1.ADMINISTER  HYPERTENSI ANALGESIC ON AND A AS DOCTOR   TOXIC ORDERED. EFFECT OF  2.NOTIFY  BILE SALTS PHYSICIAN IF  CONTRIBUTE  REGIMEN IS IN  TO ADEQUATE 

EVALUATION AFTER 3 HOURS OF THE   NSG. INTERVATION   THE CLIENT   VERBALIZED DECREASED IN PAIN AND PROMOTE  REST.

WITH

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,CANT 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.