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
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
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.
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
Pathogenesis
A.Replication of cells
(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
(3.) Diffuse enlargement of the liver can also be brought about by lymphohistiocytic cell
An increase in the volume of sinusoidal cells and hepatocytes due to an enlargement of their cellular
(1.) Endothelia and Kupffer cells can be stimulated to considerable proliferation, so that in clinical
(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
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
(2.) An enhanced formation of lymph or reduced lymph drainage can cause enlargement of the liver.
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
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.
http://www.textbookofbacteriology.net/salmonella.html
meragikan glukosa, manosa dan manitol untuk menghasilkan asam dan gas,
selama 15 menit. Salmonella tetap dapat hidup pada suhu ruang dan suhu
yang rendah selama beberapa hari dan dapat bertahan hidup selama
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.
(patch of payer) terjadi hiperplasi, nekrosis dan ulkus. Sistemik timbul gejala
panas, instabilitas vaskuler, inisiasi sistem beku darah, depresi sumsum tulang dll
(Darmowandowo, 2006)
IgM dan IgG untuk memudahkan fagositosis Salmonella oleh makrofag. Seluler
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.