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DEMAM SORE HARI_LBM 1 SGD 20

STEP 1

STEP 2
1. Mengapa demam di sore dan malam hari?
2. Mengapa lidah kotor di tengah, tepi dan ujungnya merah dan ada
tremor?
3. Mengapa di beri anti biotic dan turun panas tidak sembuh?
4. Mengapa ada pembesaran hati?
5. Mengapa suhu naik?
6. Mengapa mengalami kelainan di gastrointestinal(mual, muntah,
kembung, diare)?
7. Mengapa ada perasaan pucat serta gelisah?

STEP 3

1. Mengapa demam di sore dan malam hari?


Karena bakterinya gram negative seperti salmonella typhi,menginvasi
makrofag(IL1, TNF)merangsang hipotalamus PGE2menyebabkan
sel poin meningkatsuhu naik.pembuluh darah vasodilatasisuhu
menguapkeluar keringat.salmonella typhi penularannya melalui fecal
oral.

2. Mengapa lidah kotor di tengah, tepi dan ujungnya merah dan ada
tremor?
Menunjukkan bahwa bakteri itu melewati fecal oral. Karaktaeristik dari
bakteri.cenderung menyukai makanan asam atau pedas.
- Apa dia punya pigmen hitam?
- Kenapa merahnya di ujung?karena pembuluh darah
- Tremor :
3. Mengapa di beri antibiotic dan turun panas tidak sembuh?
Karena bakteri tersebut di vesica fellea(kripta)sehingga obat masuknya
kurang dalam.mungkin karena resistensi(mutasi genetic)secara alami
dan bisa di dapat.
Kemungkinan karena simtomatik.
4. Mengapa ada pembesaran hati?
Karena berkembang di hati dg baik,hepatomegali mendesak lambung
jg nervus2 di lambung sehingga mual muntah.

- hematogen
SalmonellaKelenjar getah bening mesentericaductus
thoracikusangulushepatomegali
- Mekanisme dg atau tanpa salmonella
- Peran salmonella dg hepatomegali
5. Mengapa mengalami kelainan di gastrointestinal(mual, muntah,
kembung, diare)?
-Kelainan gastrointestinal(aktivasi nerus vagus)bisa juga
Hepatomegalimendesak gastermual muntah kembuang
-Meningkatkan CAMPKe lumen ususmukosa usus rusak(epitel
villi)absorbsi air terganggudiare
6. Mengapa ada pucat serta perasaan gelisah?
Karena diare(kurang cairan)komposisi plasma
kurang(intestitial)viskositas naikaliran darah lambat jadi pucat
Panas dingingelisah
7. Apakah hipotalamus memiliki ambang batas?
8. Perlu di beri antipiretik atau tidak?
9. Beda gram negative dan positif?
10. Morfologi bakteri

SEMUA LI!!!!!!!!!!!!!!

STEP 4

STEP 7

1. Mengapa demam di sore dan malam hari?


Pyrogens (e.g., bacterial matter) elevate probably through mediation
by prostaglandins (p. 196) and interleukin 1 the set point of the
hypothalamic temperature controller.The body responds by
restricting heat loss (cutaneous vasoconstriction chills) and by
elevating heat production (shivering), in order to adjust to the new set
point (fever). Antipyretics such as acetaminophen and ASA (p. 198)
return the set point to its normal level and thus bring about a
defervescence.
Fever. Exogenous (e.g., bacteria) and endogenous pyrogens(various
interleukins and other cytokines from macrophages) can cause the
set-point temperature to rise above normal. This is triggered by
prostaglandin PGE2 in the hypothalamus. In the initial phase of fever,
the core temperature (although at its normal level) is too low
compared to the elevated set-point.This results in shivering to raise
the core temperature.As the fever decreases, i.e. the set-point
returns toward the normal temperature, the core temperature is now
too warm compared to the normalized set-point, resulting in
vasodilatation and sweating to lower the core temperature again.
Despopoulos, Color Atlas of Physiology 2003 Thieme
Specialized APCs (M cells in the intestinal wall or pulmonary macrophages in the lung) take
up antigens in mucosa and present them in the Peyers patches or local lymph nodes. This
probably enhances T cell-dependent activation of IgA-producing B cells, which are
preferentially recruited to the mucosal regions(homing) via local adhesion molecules and
antigen depots, resulting in a type of geographic specificity within the immune response .

Kayser - Color Atlas of Medical Microbiology (Thieme 2005)

2. .Mengapa lidah kotor di tengah, tepi dan ujungnya merah dan ada
tremor?
Apa dia punya pigmen hitam?

Niacin, also called nicotinic acid, functions in the body as coenzymes in the form of
nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide
phosphate (NADP). These coenzymes are hydrogen acceptors; they combine with
hydrogen atoms as they are removed from food substrates by many types of
dehydrogenases. The typical operation of both these coenzymes is presented in
Chapter 67. When a deficiency of niacin exists, the normal rate of dehydrogenation
cannot be maintained; therefore, oxidative delivery of energy from the foodstuffs to
the functioning elements of all cells cannot occur at normal rates. In the early
stages of niacin deficiency, simple physiologic changes such as muscle weakness
and poor glandular.
secretion may occur, but in severe niacin deficiency, actual tissue death ensues.
Pathological lesions appear in many parts of the central nervous system, and
permanent dementia or many types of psychoses may result. Also, the skin
develops a cracked,pigmented scaliness in areas that are exposed to mechanical
irritation or sun irradiation; thus, it appears that in persons with niacin deficiency,
the skin is unable to repair irritative damage.
Niacin deficiency causes intense irritation and inflammation of the mucous
membranes of the mouth and other portions of the gastrointestinal tract, resulting
in many digestive abnormalities that can lead to widespread gastrointestinal
hemorrhage in severe cases.It is possible that this results from generalized
depression of metabolism in the gastrointestinal epithelium and failure of
appropriate epithelial repair.The clinical entity called pellagra and the caninedisease
called black tongue are caused mainly by niacin deficiency. Pellagra is greatly
exacerbated in people on a corn diet, because corn is deficient in the amino acid
tryptophan, which can be converted in limited quantities to niacin in the body.

GUYTON PHYSIOLOGY,11TH EDITION.

Kenapa merahnya di ujung?


Tremor :
3. Mengapa di beri antibiotic dan turun panas tidak sembuh?

1.PG
Nociceptors. PG increase sensitivity of sensory nerve fibers towards
ordinary pain stimuli, i.e., at a given stimulus strength there is an
increased rate of evoked action potentials.
Thermoregulation. PG raise the set point of hypothalamic (preoptic)
thermoregulatory neurons; body temperature increases (fever).
Vascular smooth muscle. PGE2 and PGI2 produce arteriolar
vasodilation;PGF2, venoconstriction.
Gastric secretion. PG promote the production of gastric mucus and
reduce the formation of gastric acid Bronchial muscle. PGE2 and
PGI2 induce bronchodilation; PGF2 causes constriction.
Renal blood flow. When renal blood flow is lowered, vasodilating PG
are released that act to restore blood flow.
2.Acetaminophen (paracetamol) has good analgesic efficacy in toothaches and
headaches, but is of little use in inflammatory and visceral pain. Its mechanism
of action remains unclear. It can be administered orally or in the form of
rectal suppositories (single dose,0.51.0 g). The effect develops after about 30 min
and lasts for approx. 3 h.Acetaminophen undergoes conjugation to glucuronic acid
or sulfate at the phenolic hydroxyl group, with subsequent renal elimination of the
conjugate. At therapeutic dosage, a small fraction is oxidized to the highly
reactive N-acetylp-benzoquinonimine, which is detoxified by coupling to
glutathione. After ingestion of high doses (approx. 10 g), the glutathione reserves
of the liver are depleted and the quinonimine reacts with constituents of liver
cells. As a result,the cells are destroyed: liver necrosis.Liver damage can be
avoided if the thiol group donor, N-acetylcysteine, is given intravenously within 68
h after ingestion of an excessive dose of acetaminophen.Whether chronic regular
intake of acetaminophen leads to impaired renalfunction remains a matter of
debate.
3.Acetylsalicylic acid (ASA) exerts an antiinflammatory effect, in addition to
its analgesic and antipyretic actions.These can be attributed to inhibition of
cyclooxygenase ASA can be given in tablet form, as effervescent powder,
or injected systemically as lysinate(analgesic or antipyretic single dose,O.51.0 g).
ASA undergoes rapid ester hydrolysis, first in the gut and subsequently in the
blood. The effect outlasts the presence of ASA in plasma (t1/2 ~20 min), because
cyclooxygenases are irreversibly inhibited due to covalent binding of the acetyl
residue. Hence, the duration of the effect depends on the rate of enzyme
resynthesis. Furthermore,salicylate may contribute to the effect. ASA irritates
the gastric mucosa (direct acid effect and inhibition of cytoprotective PG
synthesis, and can precipitate bronchoconstriction(aspirin asthma, pseudoallergy)
due to inhibition of PGE2 synthesis and overproduction of leukotrienes. Because
ASA inhibits platelet aggregation and prolongs bleeding time (p. 150), it should not
be used in patients with impaired blood coagulability. Caution is also needed in
children and juveniles because of Reyes syndrome .
1. .Mekanisme hepatomegali
Compensatory Hyperplasia

Metabolic
Metabolic overload,
overload,
stress,
stress, cytokines,
cytokines,
etc.
etc.

Expression Hormones
Hormones
Expression of
of (norepinephrine,
protooncogenes
protooncogenes (norepinephrine,
(c-fos, insulin,
insulin, glucagon)
glucagon)
(c-fos, c-myk)
c-myk)

Growth
Growth factors
factors Renewed
Renewed cell
cell
(TGF,
(TGF, HGF,
HGF, etc.)
etc.) division
division

Color Atlas of Hematology - Practical and Clinical Diagnosis (Thieme 2004)

Pathogenesis
A.Replication of cells

A diffuse enlargement of the liver can be caused by cell replication.

(1.) Replication of hepatocytes in the form of excessive hyperplasia can occur occasionally after

extensive parenchymal necrosis or partial liver resection. However,this does not generally cause a

clinical discernible form of hepatomegaly.

(2.) In systemic haematological diseases, the liver is usually involved in extramedullary

haematopoiesis. This can result in hepatomegaly.

(3.) Diffuse enlargement of the liver can also be brought about by lymphohistiocytic cell

infiltrations. This generally involves inflammatory reactions to viral or bacterial diseases.


(4.) Diffuse hepatomegaly is also expected to occur as a result of malignant cell growth.

B.Enlargement of cellular structures

An increase in the volume of sinusoidal cells and hepatocytes due to an enlargement of their cellular

structures can be caused actively by proliferation or passively by storage processes.

(1.) Endothelia and Kupffer cells can be stimulated to considerable proliferation, so that in clinical

terms hepatomegaly occasionally results.

(2.) Proliferation of the smooth endoplasmic reticulum due to the prolonged induction of the

biotransformatory system localized at this site as a result of toxins,noxae or chemicals can bring

about clinically and sonographically detectable hepatomegaly.

(3.) Hepatocellular storage of abnormal quantities of cholesterol, fat, glycogen, proteins,

mucopolysaccharides,copper, iron, etc. occasionally leads to pronounced hepatomegaly. Hydropic

swelling of the hepatocytes is also included in this category.

C.Augmentation of the extracellular space

Diffuse enlargement of the liver can also arise from augmentation of the extracellular space.

(1.) An increase in blood both in the sinusoids and in Disses spaces culminates in hepatomegaly. This

can be witnessed particularly in cases of right heart failure, constrictive pericarditis, veno-

occlusive disease and the Budd-Chiari syndrome. Inflammation-related hyperaemia also occurs in

acute viral hepatitis.

(2.) An enhanced formation of lymph or reduced lymph drainage can cause enlargement of the liver.

Here fluid filled cysts can also be regarded as a cause of hepatomegaly.

(3.) A disorder of the bile flow, particularly in infants,leads to extensive hepatomegaly.

(4.) An increase in the extracellular matrix due to collagens,elastin, proteoglycans, glycoproteins,

etc. Also produces various degrees of hepatomegaly.


HEPATOLOGY PRINCIPLES AND PRACTICE,2ND EDITION.

Mekanisme dg atau tanpa salmonella.

After ingestion(uses CFTR to enter the gastrointestinal submucosa), infection with salmonellae is
characterized by attachment of the bacteria by fimbriae or pili to cells lining the intestinal lumen.
Salmonellae selectively attach to specialized epithelial cells (M cells) of the Peyer patches. The
bacteria are then internalized by receptor-mediated endocytosis and transported within
phagosomes to the lamina propria, where they are released. Once there, salmonellae induce an
influx of macrophages (typhoidal strains) or neutrophils (nontyphoidal strains).
The Vi antigen of S typhi is important in preventing antibody-mediated opsonization and
complement-mediated lysis. Through the induction of cytokine release and via mononuclear cell
migration, S typhi organisms spread through the reticuloendothelial system, mainly to the liver,
spleen, and bone marrow. Within 14 days, the bacteria appear in the bloodstream, facilitating
secondary metastatic foci (eg, splenic abscess, endocarditis). In some patients, gallbladder
infection leads to long-term carriage of S typhi or S paratyphi in bile and secretion to the stool.[17]
As a rule, infection with nontyphoidal salmonellae generally precipitates a localized response,
while S typhi and other especially virulent strains invade deeper tissues via lymphatics and
capillaries and elicit a major immune response.

Virulence factors of salmonellae are complex and encoded both on the organism's chromosome
and on large (34-120 kd) plasmids. Some areas of active investigation include the means by
which salmonellae attach to and invade the intestine, survive within phagosomes, effect a
massive efflux of electrolytes and water into the intestinal lumen, and develop drug resistance.
Several Salmonella pathogenicity islands have been identified that mediate uptake of the bacteria
into epithelial cells (type III secretion system [TTSS]), nonphagocytic cell invasion (Salmonella
pathogenicity-island 1 [SPI-1]), and survival and replication within macrophages (Salmonella
pathogenicity-island 2 [SPI-2], phoP/phoQ).

http://www.textbookofbacteriology.net/salmonella.html

Peran salmonella dg hepatomegali


2. Mengapa mengalami kelainan di gastrointestinal(mual, muntah,
kembung, diare)?

ENDOTOXIN The lipid A portion of gram-negative LPS has potent biologic activities that cause
many of the clinical manifestations of gramnegative bacterial sepsis, including fever, muscle
proteolysis, uncontrolled intravascular coagulation, and shock. The effects of lipid A appear to
be mediated by the production of potent cytokines due to LPS binding to CD14 and signal
transduction via TLRs, particularly TLR4. Cytokines exhibit potent hypothermic activity through
effects on the hypothalamus; they also increase vascular permeability, alter the activity of
endothelial cells, and induce endothelial-cell procoagulant activity. Numerous therapeutic
strategies aimed at neutralizing the effects of endotoxin are under investigation, but so far the
results have been disappointing.
Bacteria most often avoid these defenses through their cell surface polysaccharides either capsular
polysaccharides
or long O-side-chain antigens characteristic of the smooth LPS of gram-negative bacteria. These
molecules can prevent the activation and/or deposition of complement opsonins or limit the access of
phagocytic cells with receptors for complement opsonins to these molecules when they are deposited
on the bacterial surface below the capsular layer.
HARRISONS PRINCIPLES OF INTERNAL MEDICINE,16th EDITION
3. Mengapa ada pucat serta perasaan gelisah?
The limbic system(!A) and other areas of the brain influence hypothalamic
function. The limbic system controls inborn and acquired behavior (program
selection) and is the seat of instinctive behavior, emotions and motivation
(inner world). It controls the expression of emotions conveying important
signals to the environment (e.g., fear, anger, wrath, discomfort,joy,
happiness). Inversely, signals from the environment (e.g., odors) are closely
associated to behavior.
The limbic system has cortical components(hippocampus, parahippocampal
gyrus, cingulate gyrus, parts of olfactory brain) and subcortical components
(amygdaloid body, septal nuclei, anterior thalamic nucleus). It has reciprocal
connections to the lateral hypothalamus (chiefly used for recall of
programs) and to the temporal and frontal cortex.

Different programs exist for different behavioral reactions for example:


1. Defensive behavior (fight or flight). This program has somatic (repulsive facial
expression and posture, flight or fight behavior), hormonal (epinephrine, cortisol)
and autonomic (sympathetic nervous system) components. Its activation results in
the release of energy-rich free fatty acids, the inhibition of insulin release, and a
decrease in blood flow to the gastrointestinal tract as well as to rises in cardiac
output, respiratory rate, and blood flow to the skeletal muscles.
2.Physical exercise. The components of this program are similar to those of
defensive behavior.
3. Nutritive behavior, the purpose of which is to ensure an adequate supply,
digestion and intake of foods and liquids. This includes searching for food, e.g. in
the refrigerator, activation of the parasympathetic system with increased
gastrointestinal secretion and motility in response to food intake, postprandial
reduction of skeletal muscle activity and similar activities .
Despopoulos, Color Atlas of Physiology 2003 Thieme
1. Apakah hipotalamus memiliki ambang batas?

2. Perlu di beri antipiretik atau tidak?


In the intestinal tract,inhibition of PG synthesis would similarly be expected
to lead to damage of the blood mucosa barrier and enteropathy.In
predisposed patients, asthma attacks may occur, probably because of a lack
of bronchodilating PG and increased production of leukotrienes. Because this
response is not immune mediated,such pseudoallergic reactions are
potential hazard with all NSAIDs.PG also regulate renal blood flow as
functional antagonists of angiotensin II and norepinephrine. If release of
the latter two is increased (e.g., in hypovolemia),inhibition of PG production
may result in reduced renal blood flow and renal impairment. Other unwanted
effects are edema and a rise in blood pressure.
Resistensi??
When bacterial growth remains unaffected by an antibacterial drug, bacterial
resistance is present. This may occur because of certain metabolic characteristics
that confer a natural insensitivity to the drug on a particular strain of bacteria
(natural resistance). Depending on whether a drug affects only a few or numerous
types of bacteria, the terms narrow-spectrum (e.g., penicillin G) or broad
spectrum (e.g., tetracyclines)antibiotic are applied. Naturally susceptible bacterial
strains can be transformed under the influence of antibacterial drugs into
resistant ones (acquired resistance), when a random genetic alteration (mutation)
gives rise to a resistant bacterium. Under the influence of the drug, the
susceptible bacteria die off, whereas the mutant multiplies unimpeded.The more
frequently a given drug is applied, the more probable the emergence of resistant
strains (e.g., hospital strains with multiple resistance).Resistance can also be
acquired when DNA responsible for nonsusceptibility (so-called resistance plasmid)
is passed on from other resistant bacteria by conjugation or transduction.

Lllmann, Color Atlas of Pharmacology 2000 Thieme


Medical Microbiology And Infection At A Glance (Blackwell Science 2000)

3. Beda bakteri gram negative dan positif?


4. Morfologi bakteri
Bakteri adalah prokariot yang tidak memiliki inti sel dan retikulum
endoplasma.Bakteri memiliki dinding sel yg terdiri atas 2 membran
lapis-ganda fosfolipid yang dipisahkan oleh lapisan
peptidoglikan(gram negatif)atau suatu membran dalam yg
dikelilingi oleh lapisan peptidoglikan(gram positif).
ROBIN,KUMAR AND COTRAN.BUKU AJAR PATOLOGI EDISI
7.2007.EGC:JAKARTA
Salmonella is a Gram-negative facultative rod-shaped bacterium in the

same proteobacterial family as Escherichia coli, the family

Enterobacteriaceae, trivially known as "enteric" bacteria.

http://www.textbookofbacteriology.net/salmonella.html

Salmonella merupakan bakteri batang gram negatif yang bersifat motil,

tidak membentuk spora, dan tidak berkapsul. Kebanyakkan strain

meragikan glukosa, manosa dan manitol untuk menghasilkan asam dan gas,

tetapi tidak meragikan laktosa dan sukrosa. Organisme salmonella tumbuh

secara aerob dan mampu tumbuh secara anaerob fakultatif. Kebanyakan

spesies resistent terhadap agen fisik namun dapat dibunuh dengan

pemanasan sampai 54,4 C (130 F) selama 1 jam atau 60 C (140 F)

selama 15 menit. Salmonella tetap dapat hidup pada suhu ruang dan suhu

yang rendah selama beberapa hari dan dapat bertahan hidup selama

berminggu-minggu dalam sampah, bahan makannan kering, agfen

farmakeutika an bahan tinja. (Ashkenazi et al, 2002)

o Salmonella memiliki antigen somatik O dan antigen flagella HH. Antigen

O adlah komponen lipopolisakarida dinding sel yang stabil terhadap


panas sedangkan antigen H adalah protein labil panas. (Ashkenazi et al,

2002)

Patogenesis

S. typhi masuk ketubuh manusia melalui makanan dan air yang tercemar. Sebagian

kuman dimusnahkan oleh asam lambung dan sebagian lagi masuk ke usus halus.

(mansjoer, 2000) Setelah mencapai usus, Salmonella typhosa menembus ileum

ditangkap oleh sel mononuklear, disusul bakteriemi I. Setelah berkembang biak di

RES, terjadilah bakteriemi II (Darmowandowo, 2006).

Interaksi Salmonella dengan makrofag memunculkan mediator-mediator. Lokal

(patch of payer) terjadi hiperplasi, nekrosis dan ulkus. Sistemik timbul gejala

panas, instabilitas vaskuler, inisiasi sistem beku darah, depresi sumsum tulang dll

(Darmowandowo, 2006)

Imunulogi. Humoral lokal, di usus diproduksi IgA sekretorik yang berfungsi

mencegah melekatnya salmonella pada mukosa usus. Humoral sistemik, diproduksi

IgM dan IgG untuk memudahkan fagositosis Salmonella oleh makrofag. Seluler

berfungsi untuk membunuh Salmonalla intraseluler (Darmowandowo, 2006)



Medical Microbiology And Infection At A Glance (Blackwell Science 2000)

5. Morfologi bakteri
Enterobacteriaceae are Gram-negative, usually motile, facultatively
anaerobic rod bacteria. The species are subdivided into epidemiologically
significant serovars based on O, H, and K antigens. The most important
pathogenicity factors of Enterobacteriaceae are colonizing factors, invasins,
endotoxin,and various exotoxins. Enterobacteriaceae are the most
significant contributors to intestinal infections, which are among the most
frequent diseases of all among the developing world populace. Their natural
habitat is the intestinal tract of humans and animals. Some species cause
characteristic diseases. While others are facultatively pathogenic, they are
still among the bacteria most frequently isolated as pathogens (e.g., E. coli).
Morphology and culture. Enterobacteriaceae are short Gram-negative rods
with rounded ends, 0.51.5 lm thick, and 24 lm long (Fig. 4.17a).

Many have peritrichous flagellation. Species with many flagella (e.g., Proteus
species)show motility on the agar surface, which phenomenon is known as
swarming. Some Enterobacteriaceae possess a capsule.All bacteria in this family
can readily be cultured on simple nutrient mediums.They are rapidly growing
facultative anaerobes. Their mean generation time in vitro is 2030 minutes. They
showresistance to various chemicals(bile salts, crystal violet), which fact is made
use of in selective culturing. Endoagar is an important selective indicator medium;
it allows only Gram-negative rod bacteria to grow and indicates lactose breakdown.

Antigen structure. The most important antigens of the Enterobacteriaceae


are:
1.O antigens. Specific polysaccharide chains in the lipopolysaccharide complex
of the outer membrane (p. 156).
2. H antigens. Flagellar antigens consisting of protein.
3.K antigens. Linear polymers of the outer membrane built up of a repeated
series of carbohydrate units (sometimes proteins as well). They can cover the
cell densely and render them O inagglutinable (p. 155).
4.F antigens. Antigens of protein attachment fimbriae

Typhoid salmonelloses are caused by the serovars typhi and paratyphi A, B,


and C. The salmonellae are taken up orally and the invasion pathway is
through the intestinal tract, from where they enter lymphatic tissue, first
spreading lymphogenously, then hematogenously. A generalized septic clinical
picture results. Human carriers are the only source of infection. Transmission
is either direct by smear infection or indirect via food and drinkingwater.
Anti-infective agents are required for therapy (ampicillin, cotrimoxazole,
4-quinolones). An active vaccine is available to protect against typhoid fever
Typhoid salmonelloses. Attachment of typhoid salmonellae to cells of
the jejunum (M cells). Invasion by means of endocytosis, transfer, and exocytosis.
Phagocytosis in the subserosa by macrophages and translocation into
the mesenteric lymph nodes. Proliferation occurs. Lymphogenous and hematogenous
dissemination. Secondary foci in the spleen, liver, bone marrow, bile
ducts, skin (roseola), Peyers patches.
Kayser - Color Atlas of Medical Microbiology (Thieme 2005)