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A Sacrifice toBecome A
Doctor
Group 2
Thursday, September 16th,2010
Medical Faculty
Tarumanagara University
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A Sacrifice To Become A DoctorAn 18 years-old young man, came to private
practice doctor, with chief complaint: fever and headachefor about 6 days. The fever occurs only during afternoonand night time, and become deteriorated every day. Healso felt nausea, bellyful and puffed up. He hadn’t paststools for 3 days.
His past history: he came to Jakarta to become adoctor, studies in private university since 2 months ago. Livesand eats in the surroundings street vendors of his boardinghouse.
Physical exam: vital signs: temperature 38,5°C, BP100/70 mmHg, HR 66x/min, RR 16x/min. There was a coated
tongue. Abdomen: bowel sound hyperactive, mildepigastric tenderness, liver normal, spleen size Schuffner 1.Laboratory: Hb 11g/dL, leukocyte 3900/mm3,
erythrocyte 4.500.0000/mm3, thrombocyte 145.000/mm3.
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Constipation
Decrease in stool frequency :
< 3stools per week / > 3days without stools andincomplete passing stool (hard stool)
Decreased fluidity of bowel movement
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Etiology of Constipation Lifestyle : Low fibre diet, low intake of water, less workout , expirience
irregularity bowel habits Drugs : Antikolinergik, ca-blocker, aluminium hidroxyde, fe suplement,
calsium, opiat
Structural defects :
Tumor, strictur, hemorhoid, perineum abses, megacolon Metabolic/endocrine disorder : Cystic fibrosis
Increases Ca
Decreased k
Uremia
hypothyroidism
Idiopatic slow colon transit
Irritable bowel syndrome type constipation
Functional : Lack of privacy
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Functional Constipation (Rome III)
1. Must include two or more of the following: Straining during at least 25% of defecation Lumpy or hard stools in at least 25% of defecation Sensation of incomplete evacuation for at least 25% of
defecation
Sensation of anorectal obstruction/blockage for at least25% of defecation
Manual maneuver to facilitate at least 25% of defecation Fewer than three defecations per week
2. Loose stools are rarely present without the useof laxative
3. Insufficient criteria for irritable bowel syndrome
(criteria fulfilled for the last 3months with symptom onset at least6months prior to diagnosis )
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Definition of Typhoid Fever
Acute enteric infectious disease
caused by Salmonella typhi (S.Typhi).
prolonged fever, Relative bradycardia, apatheticfacial expressions, roseola, splenomegaly,
hepatomegaly, leukopenia.
intestinal perforation, intestinalhemorrhage
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Structure and Physiology
Gram-negative, non – spore-forming bacilli.Ferment glucose, maltose, and mannitol
but not lactose or sucrose. (TSIA test: -/+)Reduce nitrates and do not produce
cytochrome oxidase.Does not produce gas (Almost all
salmonellae produce gas withfermentation).
Motile by means of peritrichous flagellaResistant to sodium deoxycholate, brilliant
green, sodium tetrathionate (all canreduce other enteric bacteria growth)
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Antigen
Salmonella typhi has 3 kind of antigen: Flagella antigen (H): survive up to 60⁰C, to
alcohol and acid. IgG is the antibody againstthis antigen
Somatic antigen (O): located in outermembrane, survive up to 100⁰C, to alcoholand acid. IgM is the antibody against thisantigen
Vi antigen: located on O antigen, preventphagocytosis, survive up to 60⁰C, not resistantto alcohol and acid
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A schematic diagram of a single Salmonella typhi cell
showing the locations of the H (flagellar), 0 (somatic), and Vi
(K envelope) antigens.
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Pathophysiology
Salmonella Typhi
survives the acidity of the stomach
invades the Peyer’s Patches of the intestinal wall
macrophages (Peyer’s Patches)
the bacteria is within the macrophages and survives
bacteria spreads via the lymphatics while inside themacrophages
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Pathophysiology
access to Reticuloendothelial system, liver, spleen, gallbladderand bone marrow
First week: elevation of the body temperature
Second week: abdominal pain, spleen enlargement and rose spots
Third week: necrosis of the Peyer’s Patches
leads to perforation, bleeding
and, if left untreated, death is imminent
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Pathogenesis
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S.Typhi.
stomach
Lower
ileum
peyer's patches &
mesenteric lymph nodes
thoracic
duct
1st bacteremia
(Incubation stage)
10-14d
(mononuclearphagocytes )
2nd bacteremia
liver 、spleen、gall、
BM ,ect
early stage&acme stage
(1-3W)
LN Proliferate,swell
necrosis
defervescence stage
3-4w
Bac. In gall
Bac. In
feces
S.Typhi eliminated
convalvescence stage
(4-5w)
Enterorrhagia,i
ntestinal
perforation
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Sign and Symptoms
Fever Malaise Diffuse abdominal pain Anorexia Nausea Vomiting Diarrhea Constipation Delirium Intestinal hemorrhage Bowel perforation
Death Coated tongue Hepatomegaly Splenomegaly
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Incidence and Timing of Various Manifestations ofUntreated Typhoid Fever
Incubation Week 1 Week2
Week 3 Week 4 Post
Systemic Recoveryphase ordeath
(15% ofuntreatedcases)
10%-20%relapse; 3%-4% chronic
carriers;long-termneurologicsequelae(extremelyrare);gallbladder
cancer(RR=167;carriers)
Stepladder
fever patternor insidiousonset fever
Very
common
Very common
Acute highfever
Very rare
Chills Almost all
Rigors Uncommon
Anorexia Almost all
Diaphoresis Very common
Incubation Week 1 Week 2 Week 3 Week 4 Post
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Incubation Week 1 Week 2 Week 3 Week 4 Post
Neurologic
Malaise Almost all Almost all Typhoidstate
(common)Insomnia Very
commonConfusion/delirium
Common Verycommon
Psychosis Very rare Common
Catatonia Very rare
Frontalheadache(usuallymild)
Verycommon
Meningeal
signs
Rare Rare
Parkinsonism
Very rare
Ear, nose, and throat
Coatedtongue
Verycommon
Sore throatf
Incubation Week 1 Week 2 Week 3 Week 4 Post
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Incubation Week 1 Week 2 Week 3 Week 4 Post
Pulmonary
Mild cough Common
Bronchiticcough
Common
Rales Common
Pneumonia Rare
(lobar)
Rare Common
(basal)
Cardiovascular
Dicroticpulse
Rare Common
Myocarditis Rare
Pericarditis Extremelyrareg
Thrombophlebitis Very rare
Incubation Week 1 Week 2 Week 3 Week 4 Post
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Incubation Week 1 Week 2 Week 3 Week 4 Post
Gastrointestinal
Constipation Verycommon
Common
Diarrhea Rare Common (pea soup)
Bloating withtympany
Verycommon
(84%)
Diffuse mildabdominalpain
Verycommon
Sharp rightlowerquadrant pain
Rare
Gastrointestinalhemorrhage
Very rare;usually trace
Very common
intestinalperforation
Rare
Hepatosplenomegaly
Common
Jaundice Common
Gallbladderpain
Very rare
Incubation Week 1 Week 2 Week 3 Week 4 Post
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Incubation Week 1 Week 2 Week 3 Week 4 Post
Urogenital
Urinaryretention
Common
Hematuria Rare
Renal pain Rare
Musculoskeletal
Myalgias Very rare
Arthralgias Very rare
Rheumatologic
Arthritis (large joint)
Extremely rare
Dermatologic
Rose spots Rare
Miscellaneous
Abscess(anywhere) Extremelyrare Extremelyrare Extremely rare
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Laboratory Examination
1. Routine examination
Complete Perifer Blood test
mostly leucopenia (possibly normal
leukocytes or leukocytosis)
Mild anemia and trombositopenia
Leukocytes count : aneosinofilia and
limfopeniaLED : increased
SGOT,SGPT : increased
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2. Widal test used to determine theexistency of aglutinin in the patient’s serum - Aglutinin O (from bacteria’s body) - Aglutinin H ( bacteria’s flagela )- Aglutinin Vi (simpai kuman )
Factors that affect Widal test:- Premature treatment of antibiotic- Disability of develop antibodies and
corticosteroid treatment- Time of blood taking
- History of vaccination- Anamnestic reaction ( caused by past typhoid
infection)- Examination tecnic of the laboratorium
To diagnose
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3. Blood culture
Positif (+) result typhoid fever +
Negative (-) result possibility of typhoid fever,because of :
- Early antibiotic treatmentinhibits growth of bacteria.
- Lackness of blood volume (± 5cc of blood)
- Vaccination history
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Laboratory StudiesCulture The criterion standard for diagnosis of typhoid fever has
long been culture isolation of the organism. Cultures arewidely considered 100% specific.
Culture of bone marrow aspirate is 90% sensitive until at least5 days after commencement of antibiotics
Blood, intestinal secretions (vomitus or duodenal aspirate),and stool culture results are positive for S typhi inapproximately 85%-90% of patients with typhoid fever whopresent within the first week of onset
Multiple blood cultures (>3) yield a sensitivity of 73%-97%
Stool culture alone yields a sensitivity of less than 50%, andurine culture alone is even less sensitive
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Incubation Week1
Week2
Week3
Week4
Bone marrowaspirate (0.5-1 mL)
90% (may decrease after 5 d ofantibiotics)
Blood (10-30 mL),stool, or duodenalaspirate culture
40%-80% ~20% Variable (20%-60%)
Urine 25%-30%, timing unpredictable
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Specific serologic tests Assays that identify Salmonella antibodies or antigens support the
diagnosis of typhoid fever, but these results should be confirmed
with cultures or DNA evidence. The Widal test was the mainstay of typhoid fever diagnosis for
decades. It is used to measure agglutinating antibodies against Hand O antigens of S typhi
Indirect hemagglutination, indirect fluorescent Vi antibody, andindirect enzyme-linked immunosorbent assay (ELISA) for
immunoglobulin M (IgM) and IgG antibodies to S typhi polysaccharide, as well as monoclonal antibodies against S typhi flagellin,37 are promising, but the success rates of these assays varygreatly in the literature.
Other nonspecific laboratory studies erythrocyte sedimentation rate (ESR), thrombocytopenia, and
relative lymphopenia elevated prothrombin time (PT) and activated partial
thromboplastin time (aPTT) and decreased fibrinogen levels
Mild hyponatremia and hypokalemia are common
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Imaging Studies
Radiography: Radiography of the kidneys,ureters, and bladder (KUB) is useful if bowelperforation (symptomatic or asymptomatic) issuspected.
CT scanning and MRI: These studies may bewarranted to investigate for abscesses in the liveror bones, among other sites.
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Histologic Findings Infiltration of tissues by macrophages (typhoid cells) that
contain bacteria, erythrocytes, and degeneratedlymphocytes
In the mesenteric lymph nodes, the sinusoids are enlargedand distended by large collections of macrophages andreticuloendothelial cells
The spleen is enlarged, red, soft, and congested; its serosalsurface may have a fibrinous exudate. Microscopically, thered pulp is congested and contains typhoid nodules
The gallbladder is hyperemic and may show evidence ofcholecystitis
Liver biopsy specimens from patients with typhoid feveroften show cloudy swelling, balloon degeneration withvacuolation of hepatocytes, moderate fatty change, andfocal typhoid nodules
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Preventions Hand washing with soap and water before eating and especially
after handling any raw foods such as eggs, meat, or produce. Avoid foods and beverages from street vendors. It is difficult for
food to be kept clean on the street, and many travelers get sickfrom food bought from street vendors.
If you drink water, buy it bottled or bring it to a rolling boil for 1minute before you drink it. Bottled carbonated water is safer than
uncarbonated water. Ask for drinks without ice unless the ice is made from bottled orboiled water. Avoid popsicles and flavored ices that may havebeen made with contaminated water.
Eat foods that have been thoroughly cooked and that are still hotand steaming.
Avoid raw vegetables and fruits that cannot be peeled.Vegetables like lettuce are easily contaminated and are veryhard to wash well.
When you eat raw fruit or vegetables that can be peeled, peelthem yourself. (Wash your hands with soap first.) Do not eat thepeelings.
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Vaccination
Ty21a is an oral vaccine that requires four dosesadministered two weeks before travel. TheTy21a immunization requires a booster everyfive years with the minimum vaccination age of
6 years. ViCPS vaccine is injected once and requires
only one dose administered one week beforetravel. ViCPS requires a booster every two years
with a minimum vaccination age of 2 years.
Table 1: Typhoid Vaccines Available in the United States
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Table 1: Typhoid Vaccines Available in the United States
VaccineName
HowGiven
Number ofDoses
Necessary
TimeBetween
Doses
Total TimeNeeded toSet Aside
ForVaccination
MinimumAge For
Vaccination
BoosterNeeded
Every...
Ty21a(Vivotif
Berna,SwissSerumandVaccineInstitute)
1capsulebymouth
4 2 days 2 weeks 6 years 5 years
ViCPS(TyphimVi,Pasteur
Merieux)
Injection 1 N/A 2 weeks 2 years 2 years
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Tips to Reduce Your Risk of
Salmonella from Eggs Keep eggs refrigerated at ≤ 45° F (≤7° C) at all times.
Discard cracked or dirty eggs.
Wash hands, cooking utensils, and food preparation surfaceswith soap and water after contact with raw eggs.
Eggs should be cooked until both the white and the yolk are firm
and eaten promptly after cooking.
Do not keep eggs warm or at room temperature for more than 2hours.
Refrigerate unused or leftover egg-containing foods promptly.
Avoid eating raw eggs.
Avoid restaurant dishes made with raw or undercooked,
unpasteurized eggs. Restaurants should use pasteurized eggs inany recipe (such as Hollandaise sauce or Caesar salad dressing)that calls for raw eggs.
Consumption of raw or undercooked eggs should be avoided,especially by young children, elderly persons, and persons withweakened immune systems or debilitating illness.
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Treatment Bedrest and treatment to prevent complication and speed
healing Diet and supportive therapy restore a sense of comfort and
optimal patient health Medication (antimicrobial) stop and prevent the spread
microbial.
Chloramfenicol Tiamfenicol Chotrimoxazol Amphicilin and Amoxcillin Sefalosporin 3rd generation Fluorokuinolon group :
Norfloxacin Cifrofloxacin Ofloxacin Pefloxacin Fleroxacin
Corticosteroid
Antibiotic Recommendations b Origin and Se erit
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Antibiotic Recommendations by Origin and Severity
Location Severity First-Line Antibiotics Second-Line
Antibiotics
South Asia, East
Asia 4548, 40
Uncomplicated Cefixime PO Azithromycin PO
Complicated Ceftriaxone IV or Cefotaxime IV
Aztreonam IV or Imipenem IV
Eastern Europe,Middle East, sub-Saharan Africa,South America 46, 49
Uncomplicated Ciprofloxacin PO or Ofloxacin PO
Cefixime PO or Amoxicillin PO or TMP-SMZ POor Azithromycin PO
Complicated Ciprofloxacin IV or Ofloxacin IV
Ceftriaxone IV or Cefotaxime IV or Ampicillin IVor TMP-SMZ IV
Unknowngeographic origin orSoutheast Asia 50, 45
48, 40, 46, 49
Uncomplicated Cefixime PO plus Ciprofloxacin PO or Ofloxacin PO
Azithromycin PO*
Complicated Ceftriaxone IV or Cefotaxime IV, plus Ciprofloxacin IV or Ofloxacin IV
Aztreonam IV or Imipenem IV, plus Ciprofloxacin IVor
Ofloxacin IV
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Intestine Complication
Intestine Bleeding
Bowel Perforation
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Complication Neuropsychiatric manifestations (In the past 2 decades,
reports from disease-endemic areas have documenteda wide spectrum of neuropsychiatric manifestations oftyphoid fever.) A toxic confusional state, characterized by disorientation,
delirium, and restlessness, is characteristic of late-stagetyphoid fever
Facial twitching or convulsions may be the presentingfeature. Frank meningitis is rare. Encephalomyelitis maydevelop, and the underlying pathology may be that ofdemyelinating leukoencephalopathy. In rare cases,transverse myelitis, polyneuropathy, or cranialmononeuropathy develops.
Stupor, obtundation, or coma indicates severe disease. Focal intracranial infections are uncommon, but multiple
brain abscesses have been reported. Other less-common neuropsychiatric manifestations events
have included spastic paraplegia, peripheral or cranialneuritis, Guillain-Barré syndrome, schizophrenialike illness,mania, and depression.
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Complication Kidney : glomerulonefritis, pielonefritis,perinefritis.
Lung : pneumonia, empiema, pleuritis. Respiratory
Cough
Ulceration of posterior pharynx
Occasional presentation as acute lobar pneumonia
(pneumotyphoid) Cardiovascular : gagal sirkulasi perifer,miokarditis,
tromboflebitis Nonspecific electrocardiographic changes occur in 10%-
15% of patients with typhoid fever.
Toxic myocarditis occurs in 1%-5% of persons with typhoidfever and is a significant cause of death in endemiccountries.
Pericarditis is rare, but peripheral vascular collapse withoutother cardiac findings is increasingly described.
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Complication
Hepatobiliary : hepatitis,kolesistitis. Mild elevation of transaminases without symptoms
Jaundice may occur in persons with typhoid fever and maybe due to hepatitis, cholangitis, cholecystitis, or hemolysis.
Pancreatitis and accompanying acute renal failure and
hepatitis with hepatomegaly have been reported.59
Intestinal manifestations
The 2 most common intestinal hemorrhage (12% in oneBritish series) and perforation (3%-4.6% of hospitalizedpatients).
Approximately 75% of patients have guarding, reboundtenderness, and rigidity, particularly in the right lowerquadrant.
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Complication
Genitourinary manifestations Excrete S typhi in their urine at some point during their illness. Immune complex glomerulitis60 and proteinuria have been
reported, and IgM, C3 antigen, and S typhi antigen can bedemonstrated in the glomerular capillary wall
Nephritic syndrome may complicate chronic S typhi bacteremia associated with urinary schitomiasis
Nephrotic syndrome may occur transiently in patients withG6PD deficiency
Cystitis: Typhoid cystitis is very rare. Retention of urine in thetyphoid state may facilitate infection with coliforms or othercontaminants.
Hematologic manifestations : anemia hemolitik,
trombositopenia, KID,trombosis. Subclinical disseminated intravascular coagulation (DIC) is
common in persons with typhoid fever Hemolytic-uremic syndrome is rare Hemolysis may also be associated with G6PD deficiency
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Complication
Musculoskeletal and joint manifestations : osteomielitis,periostitis, spondilitis, artritis. Skeletal muscle characteristically shows Zenker
degeneration, particularly affecting the abdominal walland thigh muscles.
Clinically evident polymyositis may occur
Athritis is very rare and most often affects the hip, knee, orankle.
Late sequelae (rare in untreated patients andexceedingly rare in treated patients) Neurologic - Polyneuritis, paranoid psychosis, or catatonia Cardiovascular - Thrombophlebitis of lower-extremity veins Genitourinary -Orchitis Musculoskeletal Periostitis, often abscesses of the tibia and ribs Spinal abscess (typhoid spine; very rare)
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Differential Diagnose Abdominal Abscess Malaria
Amebic Hepatic Abscesses
Rickettsial diseases
Appendicitis
Toxoplasmosis
Brucellosis
Tuberculosis
Dengue Fever
Tularemia Influenza
Leishmaniasis
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Suggestions
Bed rest Take a proper medicine
Better sanitation such as well-cooked food,hygiene water, etc
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