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CasePresentation

Cholelithiasis


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IntroductionCholelithiasis

Presence of one or more calculi (gallstones) in thegallbladder

common health problem, affecting about 1 out of every1,000 people and is the fifth leading cause of hospitalizationamong adults and accounts for 90% of all gallbladder andduct diseases.

prognosis is usually good with treatment unless infectionoccurs, in which case the prognosis depends on its severityand response to antibiotics.

Prevalence of cholelithiasis is affected by many factorsincluding;

Ethnicity


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Gallstones

tend to be asymptomatic

Diagnosis is usually by ultrasonography.

made of cholesterol, calcium bilirubinate, or a mixture ofcholesterol and bilirubin pigment

Migration of gallstones may lead to occlusion of the biliaryand pancreatic ducts, causing pain (biliary colic) andproducing acute complications, such as acute cholecystitis,ascending cholangitis, or acute pancreatitis.

Asymptomatic gallstones

In patients with asymptomatic gallstones discoveredincidentally, the likelihood of developing symptoms orcomplications is 1-2% per year

In most cases as m tomatic allstones do not re uire an


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Biliary colic

Pain termed biliary colic occurs when gallstones fortuitouslyimpact in the cystic duct during a gallbladder contraction,increasing gallbladder wall tension.

In most cases, the pain resolves over 30 to 90 minutes asthe gallbladder relaxes and the obstruction is relieved.

Episodes of biliary colic are sporadic and unpredictable.

The patient localizes the pain to the epigastrium or rightupper quadrant and may describe radiation to the rightscapular tip.

From onset, the pain increases steadily over about 10 to 20minutes and then gradually wanes.


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Predisposing factors

Age - elderly people are prone to gallstoneformation because of weakened immunesystem and deteriorating body organs.

Diabetic - are prone to gallstone formationbecause of impaired protein synthesis andfatty acid storage.

Genetic - family with a history of

cholelithiasis has a high risk of acquiring thedisease condition.

Precipitating factor


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Excess alcohol consumption

Oral contraceptives.

High fat, low fiber diet.

Rapid weight loss.

Women who have had many children.(multiparity)

Hemolytic disorders such as sickle cell anemia, hereditaryspherocytosis.

Liver cirrhosis.

Diabetes.

Female gender.

Inflammatory bowel disease such as crohns.

Signs and symptoms

Symptoms usually manifest after a stone, which is greater


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Cholangitis- If the common bile duct is blocked for aperiod of time, certain bacteria may grow in the

stagnant bile producing symptoms of cholangitis.

Jaundice- a yellow pigmentation of the sclerae, skin,and deeper tissues cause by excessive accumulation ofbile pigments in the blood. The accumulation is due to

the continuous blockage of bile to the intestines whereit is partly excreted as waste.

Pancreatitis- stones blocking the lower end of thecommon bile duct where it enters the duodenum mayobstruct secretion from the pancreas producing

pancreatitis.

Note: Often there are no symptoms.

Additional symptoms that may be associated withthis disease:


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heartburn- because of vomiting

gas/flatus, excessive - decrease in peristalsis because ofdecrease in water in the intestine.

abdominal indigestion- decrease ability to emulsify fats,intolerance to fatty foods leading to indigestion

abdominal fullness, gaseous-decrease in peristalsis

because of decrease in water in the intestine.


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Complications of gallbladder stones

Acute cholecystitisoccurs when persistent stone impaction in the cystic duct causesthe gallbladder to become distended and progressively inflamed.

Chronically, gallstones may cause progressive fibrosis of thegallbladder wall and loss of gallbladder function, termedchronic cholecystitis.

Gallbladder adenocarcinoma

an uncommon cancer that usually develops in the setting ofgallstones and chronic cholecystitis.

commonly invade the adjacent liver and common bile duct,producing jaundice.

Medical Intervention

Dissolution Agents (Cholesterol Stones)

Extracor oreal Shock Wave Lithotri s


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Personal Data

NAME: Mrs. Dimakasuka

ADDRESS: Bgy. Calaocan, Santiago City, Isabela

BIRTHDAY: January 11, 1968

BIRTHPLACE: Quezon City

AGE: 43 years old

NATIONALITY: Filipino

DIALECTS SPOKEN: Ilokano, Tagalog

RELIGION: Roman Catholic

EDUCATIONAL ATTAINMENT: High School Graduate

OCCUPATION: Vendor

DATEOF ADMISSION: June 02, 2011 CHIEF COMPLAINT: fever bod weakness severe abdominal ain


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History of Past Illness

She acquired chicken pox and measles when she was young and wasalready twice hospitalized for the delivery of both her children but aside fromthat she was never brought to hospital for conditions which are related to her

condition now.

However during the past 5 months (starting January 2011) the patienthas been experiencing pain on her right upper side part of the abdomen whichshe ignored. And she verbalized that it was a tolerable pain and was easilyrelieved by rest and sleep. Due to her work, Mrs. Dimakasuka was not able tohave a check up or medical examinations done. Two months before the

hospitalization, she experienced an intense abdominal pain accompanied bynausea and vomiting but instead of going to the hospital for checkup she justtook pain medications.

HISTORY of PRESENT ILLNESS

Two days prior to admission the patient again experienced severeabdominal pain while at work accompanied by fever (May 31). By 11 pm of June2, 2011 she was admitted at CVAH with chief complaints of fever, bodyweakness, severe abdominal pain, nausea and vomiting He was immediatelyattended by the nurses by taking his vital signs. Her consent was signed. Shewas immediately examined by Dr. JJ with orders made and carried out. The

patient was inserted with an IVF of D5LRS 1L x 30gtts/min inserted at her lefthand. She had undergone laboratory exams such as, CBC, Urinalysis, HBT


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LABORATORY AND DIAGNOSTIC EXAMS

HBTPancreas Ultrasound

Results:

Abnormally contracted gallbladder with a lithiasis atthe neck.

Intrahepatic and extrahepatic ducts are not dilated.

Unremarkable liver and pancreas.

(-) for ascites


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Analysis and Interpretation of

Results

Abnormally contracted gallbladderwith a lithiasis at the neck.


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Physical AssessmentJune 2, 2011 (upon admission, based on the patient's

chart)

Patient Is conscious, coherent but in distress with

steady severe aching pain in the right upperquadrant of the epigastrium radiating to the rightshoulder

Vital signs:

BP- 90/60

T- 38

P-80

R-28


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June 3,2011 (patient's chart)

Patient is conscious and coherent withIVF of 1L D5LRS regulated at 30

gtts/min still with (+) jaundice, tolerable

pain in the right upper quadrant of theepigastrium

Vital signs:

BP-100/70T-37.1

PR-87

RR-21


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Sclera: appears yellowish

Lips: pale:dry

Skin: yellowish in color

:warm to touchAbdomen: guarding behavior upon palpation


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Anatomy and

Physiology


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The gallbladder stores bile, which is released when foodcontaining fat enters the digestive tract, stimulating the

secretion of cholecystokinin (CCK). The bile emulsifies fatsand neutralizes acids in partly digested food. After beingstored in the gallbladder, the bile becomes moreconcentrated than when it left the liver, increasing itspotency and intensifying its effect on fats.

The liver's cells (hepatocytes) excrete bile into canaliculi,which are intercellular spaces between the liver cells. Thesedrain into the right and left hepatic ducts, after which biletravels via the common hepatic and cystic ducts to thegallbladder. The gallbladder, which has a capacity of 50

milliliters (about 5 tablespoons), concentrates the bile 10fold by removing water and stores it until a person eats. Atthis time, bile is discharged from the gallbladder via thecystic duct into the common bile duct and then into theduodenum (the first part of the small intestine), where itbegins to dissolve the fat in ingested food.


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The liver excretes approximately 500 to 1000 milliliters (50to 100 tablespoons) of bile each day. Most (95%) of the bile

that has entered the intestines is resorbed in the last part ofthe small intestine (known as the terminal ileum), andreturned to the liver for reuse.

Metabolic functions, such as the maintenance of glucose(blood sugar) levels

Synthetic functions, such as the synthesis of serum proteinssuch as albumin, blood clotting (coagulation) factors, andcomplement (a mediator of inflammatory responses)

Storage functions, such as the storage of sugar (glycogen),

fat (triglycerides), iron, copper, and fat soluble vitamins (A, D,E, and K)

Catabolic functions, such as the detoxification of drugs


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Pathophysiology


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Cholelithiasis

RUQ colickypain(January, 2011

June 2011,

Bile stasis become amedium for bacterial

growth

Inflammation

Endogenous

pyrogens

Release of chemicalmediatorsReset of

hypothalamus

Fever

obstruction

Conjugated bilirubin

Escape from liver intothe blood stream

Infection

Stimulates the gallbladderto produce more bile.

Stimulates the secretionof Cholecystokinin

Indigestion of fats

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