MODUL 1

FEVER
GROUP 14
• MUNAWWARAH : 110 2015 0004
• INNAL HAMDA : 110 2015 0019
• ROSMIATI : 110 2015 0032
• DIAN YUSTIKARINI : 110 2015 0046
• ARIDAYANA : 110 2015 0063
• REZKY DARMAWAN ARIFIN : 110 2015 0067
• TARNI RESTAMI RUSTAM : 110 2015 0074
• SRI ARIATNA DEWI : 110 2015 0075
• PRATIWI YUNIAR : 110 2015 0086
• FUAD ALAMSYAH : 110 2015 0113
Scenario
Male, 41 years old, Signed into hospital emergency room
with fever since 5 days ago. Sudden fever, height and persistence.
burning feeling throughout the body and not decreasing with the
provision of febrifuge. Chills and skin and yellowing eyes since 3
days ago, the color of his urine turned into brownish yellow like
tea, body limp and pain all over his body since 2 days ago and did
not improve with rest. Vomiting blood since 6 hours ago
frequency 2 times
Keyword
• Male, 41 years old Signed into hospital emergency room with
fever since 5 days ago.
• Sudden fever, height and persistence.
• burning feeling throughout the body and not decreasing with
the provision of febrifuge
• Chills and skin and yellowing eyes since 3 days ago
• the color of his urine turned into brownish yellow like tea
• body limp and pain all over his body since 2 days ago and did
not improve with rest.
• Vomiting blood since 6 hours ago frequency 2 times
Question
1. What’s the definition of fever and explain about the
classification!
2. How’s the pathomechanism of fever?
3. How’s the pathomechanism of jaundice?
4. How’s the pathomechanism of brownish yellow urine?
5. How’s the pathomechanism of vomiting blood?
6. How’s the pathomechanism of chills?
7. Explain about tropical disease that causing fever!
8. Why the fever is not decreasing by using anti fever?
9. What are the differential diagnose?
10. Explain about the step of diagnose!
11. How to prevent the disease?
1.What's the
definition of fever
and classification?
• Fever is an increase in body temperature from the normal
daily temperature variations
which is associated with increasing the temperature point in
the hypothalamus
(Dinarello & Gelfand, 2005).
• Normal body temperature ranges from 36.5 to 37.2 ° C.
The degree of temperature that can be said to be fever is a
rectal temperature ≥38.0 ° C or oral temperature ≥37,5 ° C or
axillary temperature ≥37,2 ° C (Kaneshiro &
Zieve, 2010).
CLASSIFICATION
Hectic fever

Cyclical
Septic fever
Fever

Continuous Remiten
Fever fever

Intermittent
fever
2. How’s the
pathomecanism of
fever?
 exogenous pyrogens and endogenous pyrogens

will stimulate the hypothalamic endothelium to form prostaglandins

Prostaglandins that form later will improve the

thermostat benchmark in the hypothalamic
thermoregulatory center.

The hypothalamus will assume the

temperature is now lower than the new
benchmark temperature
 and an increase in heat production and a decrease in
heat will eventually cause the body temperature to rise to
this new benchmark
Fever has three phases: phase cold, fever phase, and redness phase.

1. Phase of the coldness: phase increase in body temperature with

vasoconstriction of blood vessels and increased muscle activity that
seeks to produce heat so that the body will feel cold and chills.
2. Phase of the fever: the balance phase between heat production and
heat loss at an already elevated temperature point
3. Phase of the redness: phase drop in temperature with vasodilation of
blood vessels and sweats that seek to remove heat so the body will be
reddish
3. How’s the
pathomechanism of
jaundice?
 • Causes of jaudience
Decreased excretion of bilirubin conjugated in bile due to
intrahepatic factors that are functional or mechanical obstruction

• Classification:
Prehepatic: hemolysis in increased due to an increase in the
number of hemoglobin in the blood due to ineffective
erythropoiesis and circumstances after blood transfusion
Intrahepatic: acute viral hepatitis, cirrhosis
Posthepatic: obstruction of the bile ducts that can be caused by
gallstones, and tumors
4. How’s the
pathomechanism of
brownish yellow
urine?
5.How the
pathomecanism of
vomiting blood?
 gastric Vomitus that
inflammation contains blood

increased
structural lesion of parasympathetic
GI nervous system
activity

bleeding from a
motility disorders source proximal to
of the small bowel the ligament of
Treitz
6. How the
pathomecanism of
chill?
 the release of cytokines
increases the set point
and prostaglandins as
inflammatory diseases for body temperature
part of the
in the hypothalamus
inflammatory response

increase body the patient's body

the body temperature
temperature to the produces heat during
to rise
new set point. muscle contraction

Chills until the new set

point is reached

References
Stan Tian (2015-04-30). "The Main Flu Symptoms Fever, Aches and Chills". Healthguidance.org. Retrieved 2016-05-12.
7. Explain about
tropical disease that
causing fever!
• Infectious diseases by bacteria :
TBC (Tuberculosis)
Diphtheria
Pertussis
Tetanus Neontorum
Typhoid Fever
Leprosy
Anthrax
Leptospirosis
• Infectious diseases by virus:
 DBD (Dengue Fever)
Chikungunya
Measles
Hepatitis
Rabies
HIV-AIDS
Chickenpox
Avian influenza
Polio
• Infectious diseases by parasite:
Malaria
Filariasis
8. Why the fever is
not decreasing by
using anti fever?
Fever not decrease
with anti fever
 The patient didn’t follow of the doctor instruction
 The drug only treat the symptoms
 Physical condition
 Pathological factor
 Genetic factor
 Tolerance factor
9. What are the
differential diagnose?
LEPTOSPIROSIS
Definition
• Leptospirosis is a zoonotic disease caused by a spiral and
active-moving microorganism called Leptospira. The disease is
known by various names such as Mud fever, Slime fever
(Shlamnfieber), Swam fever, Autumnal fever, Infectious
jaundice, Field fever, Cane cutter and others
• Leptospirosis or jaundice is an important disease in humans,
rats, dogs, pigs and cows. The disease is caused by spirochaeta
leptospira icterohaemorrhagiae that lives in the kidney and
urine of mice.
Etiology
The genus Leptospira, the treponemataceae family, a spirochaeta
microorganism
Typical convoluted, thin, flexible, 5-15 um long, very fine spiral, 0-
1-0,2 one end is swollen to form a bundle
Moving active rotation, no foundation flagella Microscope dark
field chain of small coccus
L. icterohaemorrhagica (rat reservoir)
L. canicola (dog reservoir)
L. ponoma (reservoir of cattle and pigs)
Epidemiology
• Spread throughout the world (mostly in the tropics)
• It is found in dog pets, pigs, cattle, horses, cats, guinea pigs,
rodents, rodents Squirrels, weasels, bats,
• Living in kidney / urine
• Seasonal, temperate climates of peak incidence in summer
and fall, tropical climates peak incidence in the rainy season
Transmission
• Contact with groundwater, or mud contaminated with the
urine of infected animals
• Infection occurs when there is wound / erosion of the skin
and mucous membranes
• The bite of an infected animal
• Contact with culture (laboratory)
• Long exposures to puddles contaminated with intact skin
Pathophysiology
• Infectionleptospires appear in the blood invade all
tissues and organs particularly affecting the liver and
kidneycleared from the body by the host's immune
response
• May also settle in the convoluted tubules of the
kidneysshed in the urine for a few weeks to several months
or longer
• Subsequently cleared from the kidneys and other organs (may
persist in the eyes for much longer)
• Produces endotoxinattach onto the endothelial
cellscapillary vasculitis (endothelial necrosis and
lymphocytic infiltration)
• Vasculitis and leakagepetechiae, intraparenchymal bleeding
and bleeding along serosa and mucosa
• Lost of fluids into the third spacehypovolaemic shock and
vascular collapse
• • Humans react to an infection by producing specific anti-
Leptospira antibodies
• • Seroconversion
• – as early as 5–7 days after the onset of disease
• – sometimes only after 10 days or longer
• – IgM appear somewhat earlier than IgG and generally remain
detectable for months or even years but at low titre.
• Humans react to an infection by producing specific anti-
Leptospira antibodies
• • Seroconversion
• – as early as 5–7 days after the onset of disease
• – sometimes only after 10 days or longer
• – IgM appear somewhat earlier than IgG and generally remain
detectable for months or even years but at low titre.
Clinical manifestation
Leptospirosis has two distinct phases
namely the leptospiremia phase and the immune phase.
Phase leptospiremia
- Headaches are usually on the frontal
-Severe muscle pain, especially thigh, calf, and waist with
tenderness
-Mialgia
-High fever
-Shivering
-Nausea, with or without vomiting
-Jaundice
-Rash is macular to the skin
Immune phase
-The fever reaches a temperature of 40 C
-Shivering
-Complete pain in the neck, stomach and muscles
-There is bleeding in the form of epitaxis
-Symptoms of damage to the kidneys and liver
-Uremia
-Jaundice
-Purpura
-Petechiae
Therapy
Mild leptospirosis
• Doksisiklin peroral 2x100mg
• Ampisilin 500-750mg 4 x a day
• Amoksisilin 500mg 4 x a day

Severe leptospitosis
• Penisilin G iv or
• Ampisilin 4x1 gram
• Amoksisilin 4x1gr
• Eritromisin 4x500 mg
• Kemoprofilaksis
• Doksisiklin 200mg/week
Prognosis
If there is no icterus, the disease is rarely fatal. In cases with
icterus, the mortality rate is 5% in under 30 years of age, and in
elderly people reaching 30-40%
HEPATITIS
DEFINITION
Hepatitis is a diffuse inflammatory process in liver cells.
Hepatitis A is hepatitis caused by infection Hepatitis A Virus
ETIOLOGY
Hepatitis A is caused by hepatitis A virus. This virus includes
viruses RNA, single fiber, with molecular weight 2.25-2.28 x 106
dalton, symmetry icosahedral, diameter 27-32 nm and has no
sheath. Have VPg terminal protein at its 5'end and poly (A) at its
3'end. Long HAV genome: 7500-8000 base pairs. Hepatitis A virus
can be classified in the picornavirus family and the hepatovirus
genus.
Transmission of Hepatitis
• The disease is fecally-oral-transmitted from food and drink
infected
• Can also be transmitted through sexual intercourse
• The incubation period of the disease is 14-50 days, with an
average of 28 days
EPIDEMIOLOGY
• An estimated 1.5 million clinical cases of hepatitis A occur
throughout the world every year
• Seroprevalence of hepatitis A virus varies from several countries in
Asia
• In countries with moderate endemicities such as Korea, Indonesia,
Thailand, Sri Lanka and Malaysia
• Hepatitis A is still a health problem in the country growing like
Indonesia
Pathogenesis of Hepatitis A
Virus
 CLINICAL SYMPTOMS
Symptoms of hepatitis acute divided into 4 stages:
Incubation phase. It is the time between the entry of the virus and
its incidence symptoms or jaundice. On hepatitis A incubation
phase can last for 14-50 days, on average 28-30 days.
Prodromal phase (pre-jaundice). Phase between the occurrence of
complaints first and onset of jaundice. The onset can be brief or
insidious characterized by general malaise, muscle pain, joint pain,
fatigue, symptoms upper respiratory tract and anorexia
 COUNTINOUS
• The Jaundice Phase. Jaundice appears after 5-10 days, but may also
appear along with the appearance of symptoms
• Convalescent phase (healing). Beginning with the disappearance
jaundice and other complaints, but hepatomegaly and
abnormalities of liver function remain there is. Circumstances acute
will usually improve within 2-3 weeks.

\
CLINICAL DIAGNOSIS
Anamnesis
• Jaundice • Stained feces
• The color of urine is like tea • Nausea and vomiting
• Fever • Muscle and joint pain
• Decreased appetite
• Headache
• Anoreksi
Physical Examination
Jaundice (skin and sclera yellowing), urine dark color
Supporting investigation
Urine laboratory test: urinary and bilirubin urobilinogen, total
and direct serum bilirubin, ALT and AST, ALP, prothrombin time
(PT), total protein, serum albumin, IgG, IgA, IgM, and Complete
blood cell count.
PREVENTION
• Diligent hand wash
• Passive immunization with normal immunoglobulin
• Active immunization with dead vaccine
MANAGEMENT
• supportive therapy
• high-calorie diet
• cessation of treatment at risk of hepatotoxic
• restriction of alcohol consumption
 Yellow Fever
Yellow fever is a viral disease transmitted to humans
by mosquitoes in certain parts of South America and
Africa. Symptoms of infection include sudden fever,
chills, sore muscles, backache, headache, nausea and
vomiting not until six days after the virus enters the
body. After three to four days most patients recover
and the symptoms disappear.
Epidemiology
• Yellow fever is found in
tropical forests of Africa
and southern American
Asia there has never been
a reported case of yellow
fever but it is still at risk
• because suitable primates
and mosquitoes as
vectors are found widely.
Transmission

• Humans and monkeys are the main animals infected by this

virus.
• Specific mosquito species known as Aedes aegypti need to
transmit this virus.
• It takes three to six days for this disease to begin after
someone is bitten by an infected mosquito.
• An infected person may transmit this infection to the
mosquito for up to 5 days after symptoms occur. This infection
is not transmitted directly from person to person or from
animal to human.
Clinical Features
• Yellow Fever classic is a biphasic disease, there are 3
stages namely: infection, remission and intoxication.
• After an incubation period of 3-6 days sudden onset
of fever and chills followed by headache, backache,
myalgia, nausea and vomiting
• After 3-4 days, the symptoms and fever disappear
for several hours to 1 or 2 days and only recur in
patients who develop into fulminant intoxication
• The type of fever is biphasic (dromedary). The first
febrile phase relates to the acute phase of the
disease and is accompanied by relative bradycardia.
Diagnose
• Yellow fever is difficult to determine in the early stages
because there are a number of infections that have similar
signs and symptoms. Diagnosis requires a blood test.
• Laboratory tests show leukopenia, thrombocytopenia may be
found to increase hematocrit, prolonged prothrombin time,
transaminase enzyme, alkaline phosphatase, gammaglulamy
transferase
• An immunoassay capture enzyme examination can check for
specific IgM titres. IgM began to be detected on 7-10 days of
infection
Treatment
• Supportive therapy is aimed directly at correcting fluid loss
and and maintaining hemodynamic stability. Handling and
prevention of hypoglycemia, administration of H antagonists,
or inhibitorpompaproton (PPI) may be performed. Vitamin K
and Fresh Frozen Plasma (FFP) are recommended for treating
coagulation disorders. If acute kidney failure occurs then
dialysis can be taken
Typhoid fever
Definition of typhoid fever
Typhoid fever disease is a disease caused by Salmonella
bacteria, especially its derivatives of Salmonella typhi which
attacks the digestive tract. During infection, the bacteria
multiply in mononuclear phagocytic cells and are continuously
released into the bloodstream.
Epidemiology of typhoid fever
The incidence rate of typhoid fever in endemic areas
ranges from 45 by 100,000 population per year to 1,000 by
100,000 population per year. Incidence rate of typhoid fever in
European countries 3 by 100,000 population, in Africa that is
50 by 100,000 population, and in Asia 274 by 100,000
population. Indisens rate in Indonesia is still high at 358 per
100,000 rural population and 810 per 100,000 urban
population per year with average cases per year 600,000 -
1,500,000 sufferers.
Etiology of typhoid fever
Typhoid fever is caused by Salmonella typhi bacteria or
Salmonella paratyphi of the Salmonella Genus. These bacteria
are rod-shaped, gram-negative, do not form spores, motile,
encapsulated and have flagella (move with hair shakes).
 Patomechanism
food and drink contaminated
with Salmonella typhi spread to other body parts
bacteria

Liver and
mouth spleen

stomach small intestine Plaque peyeri

Clinical Symptoms

 fever
 Disturbance of the gastrointestinal tract
 Disturbance of consciousness
Diagnosis of typhoid fever

 Examination of Blood Edges

 Bacteriological examination with isolation and bacterial
cultures
 Serological tests
 Examination of germs molecularly
Procedures
• Rest and treatment to prevent complications
• A soft diet and supportive therapy (antipiretic, antiemetic, and
adequate fluids)
• Antibiotics, with options including:
Chloramphenicol 4 x 500 mg / day oral / IV to 7 days free of
fever
Tiamfenikol 4 x 500 mg
Cotrimoxazole 2 x 960 mg for 2 weeks
Ampicillin and amoxicillin 50-150 mg / kgBB for 2 weeks
Ceftriaxone 3-4 grams in dextrose 100 c
• In pregnancy : ampicillin, amoxicillin, ceftriaxone
Complications of typhoid
fever
Intestinal Complications
• Intestinal Bleeding
• Intestinal perforation

Extraintestinal complications
• Haemolytic anemia
• Thrombosis
• Pneumonia
• Hepatitis
• Meningitis
• Delirium
 Definition of Malaria
Mal :Bad
Malaria
Area :Air

Intechous diases causely plasmodium (protozoa) and transmitted by

female anopheles mosquitoes.
Epidemiology
Malaria includes cosmopolitan diseases spread widely
throughout the world, both in the tropics, subtropics and
cold climates. Among the latitudes and longitudes, there
are areas that are free of malaria, namely the Central and
South Pacific (Hawaii, New Zealand).
This is because there is no vector in the malaria-free
place, so the parasitic life cycle can not take place. An area
is said to be malaria endemic if constantly malaria
incidence rates can be identified and transmission naturally
lasts throughout the year
Types of Parasites Malaria disease is caused by the Protozoa genus
Plasmodium.

• causes malaria falciparum or malaria malignant malaria

Plasmodium
falciparum
/ malaria tropica / malaria perniciousosa

Plasmodium • causes malignant vivax or benign tertiana malaria.

vivax

Plasmodium
• causes malaria ovale or malaria tertiana benign ovale.
ovale

Plasmodium
• causes malaria malariae or quartan malaria.
malariae
a young tropozite form of plasmodium The shape of the Plasmodium
falciparum falciparum schizon

Macrogametocyte forms Plasmodium Plasmodium falciparum

falciparum microgametocyte form
 • Peak stage fever Patients who initially felt the cold turned to very hot. The body temperature rises
to 41 ° C causing the patient to thirst. Face redness, dry and burning skin, headache getting
worse, nausea and vomiting, pulse pulsing hard. This stadium lasts 2 to 6 hours.
Fever

• The patient feels very cold cold, so it shivers. The pulse is fast but weak, the lips and fingers are
blue, the skin is dry and pale. Usually found in children seizures. This stage lasts 15 minutes to 1
hour.
cold

• Patients sweat a lot until wet, the temperature drops drastically even below normal threshold.
Patients usually can sleep soundly and when awake feeling weak but healthy. This stadium lasts 2
Sweating to 4 hours
 Classification of malaria epidemiology
using spleen rate parameters (spleen
rate) or parasite rate (parasitic
number), as follows:

Hipoendemic : spleen rate or parasite rate 0-10

Mesoendemic : spleen rate or parasite rate 10-50%

Hyperendemic: spleen rate or parasite rate 50-75%, adults are usually

higher

Holoendemic : spleen rate or parasite rate> 75%, adult is usually low. 2

 •
• Cerebral
Hemolytic
malaria
anemia

• Black
water • Algid
Complications fever malaria
Malaria Disease Malaria can lead to several
complications, including:
Malaria Therapy

Based on its activity, anti-malarial drugs can be divided into:

Gametosida: to kill the sexual form of plasmodium (eg

chloroquine, quinine and primaquine).

Sporontosides: to inhibit oocysts (eg primaquine,

chloroguanid).

Skozinticide: to eradicate the form of tissue and hypnozoite

schizon (eg primaquine and pyrimethamine).

Skizonticide of blood: to kill the schizon that is in the blood

(eg chloroquine, quinine, meflokuin, halofantrine,
pyrimethamine, sulfadoxine, sulfon and tetracycline)
Prevention is intended for people living in endemic areas or who want to go to endemic areas:
1. Vector control
• Can use larvasida to eradicate larvae.
• Insecticide spray to eradicate adult mosquitoes.
• Use of insect killers containing DEET (10-35%) or picaridin 7%.
2. Personal Protection / Personal Protection Is an action that can protect people against infections, such as:
• Avoiding mosquito bites at the peak of sucking mosquitoes (evening and sunset).
• Use of bed nets (bed nets) soaked in previous insecticides, mosquito wire, insect repellent.
• Wear suitable and closed clothes.
• Use of prophylactic drugs if they wish to travel to endemic areas.
3. Malaria vaccine The malaria parasite has a complex life cycle, so the vaccine varies for each stage, such as:
• Assoual eksoeritrositik stadium The way it works inhibits the occurrence of clinical symptoms and
transmission of disease in endemic areas.
• erythrocytic asexual stadium The way it works prevents the occurrence of parasitic infections of the
erythrocytes, eliminates parasites in erythrocytes and prevents the sequestering of parasites in the
capillaries of internal organs so as to prevent the occurrence of severe malaria.
• Sexual stadium The way it works inhibits or reduces the transmission of malaria in an area. If rapidly
treated then the prognosis may be better, but if slow treatment will cause increased mortality.
Prevention of Malaria
10. Explain about the
step of diagnose!How
to prevent the
disease?
Anamnesis
Dig the history of the illness now. Ask Ask about other accompanying
about the following: symptoms:
• Onset and duration of fever: sudden • anorexia, dysphagia, malaise,
appearance, when and how long has headache, arthralgia, myalgia,
fever. difficult open mouth
• The nature of fever: subfebris, high, • bleeding manifestations: petechiae,
continuous, intermittent, higher in ecchymoses, epistaxis,
the afternoon and evening, is attack hematemesis, melena
by a certain interval. • shivering
Physical Examination
• Check to assess the presence of anemia, jaundice, edema (see basic lab
skills diagnostic and therapeutic).
• Note the status of tifose: decreased consciousness, dry hair, lips dry / split
/ peeled, dirty tongue, pale.
• Check for spontaneous bleeding manifestations (petechiae, ecchymoses,
epistaxis, gum hemorrhage, hematemesis, and melena).
• Conduct toll test
• Note the presence or absence of skin effloresensi. If available, rate the
type and location skin effloresensi: macula, papules, vesicles, crusts,
polymorphs.
• Check your mouth and oral cavity: note the spot clarity, white gray
membrane on tonsils, redness in farings, or larings, gum bleeding,
trismus.
• Check for gag reflex: open the patient's mouth by using the spatula, when
a seizure occurs, then gag reflex declared positive.
Laboratorium Test
• Regular blood
• Blood
• Serology Test
• Culture of bacteria, fungi, viruses
Radiology
• Plain photo
• Ultrasound
• CT-Scan
• MRI
11. How to prevent
the disease?
prevention
 Clean water
 Sanitary food handling
 Good hygiene
 Control the vectors (spraying of insecticides in areas where
the vectors breed or gather, killing them before they become
parasite carriers
 Educating the at risk population
 Sleeping under a treated bed net
 Vaccination