1. Apa perbedaan penelitian ini dengan sebelumnya?

Penelitian sebelumnya menggunakan tikus sebagai subjeknya

2. Apa komplikasi dari rhinitis alergi?
Common allergic rhinitis complications
A. Nasal polyps with marked pathognomonis: mucous glands are inspired, cellulose is more
expensive (more eosinophils and lymphocytes T CD4 +), epithelial hyperplasia, hyperplasia
trophies, and squamous metaplasia.
B. Otitis media is often residif, especially in children.
C. Paranasal sinusitis is the inflammation of one or more nasal nasal sinuses. Occurs due to
edema of sinus ostia by allergic processes in the mucosa causing blockage of ostia resulting
in decreased oxygenation and air pressure of the sinus cavity. This will nourish the growth of
bacteria in anaerobic bacteria and will cause damage to the function of the epithelial barrier,
among others, due to mucosal decomposition by the alkaline protein mediators released by
eosinophil (MBP) cells with the consequences of sinusitis will be more severe
3. Mekanisme rhinitis alergi
Allergic rhinitis is an inflammatory disease that begins with the stage of sensitization and is
followed by an allergic reaction. Allergic reactions consist of two phases: fast phase allergic
reaction (FPAR) which lasts from contact with allergen up to 1 hour later and late phase
allergic reaction (LPAR) lasting 2-4 hours with peak 6-8 hours (hyperreactivity phase) after
exposure and may take 24-48 hours.

In the first contact with allergens or sensitization stages, macrophages or monocytes acting
as a presenting cell (antigen presenting cell / APC) will capture allergens attached to the
surface of the nasal mucosa. Once processed, the antigen forms a short fragment of peptide
and combines with a class II HLA molecule to form a peptide complex of MHC class II (Major
Histocompatibility Complex) which is then presented on helper T cells (Th0). Then the
presenting cell will release a cytokine like interleukin 1 (IL-1) which will activate Th0 to
proliferate into Th1 and Th2. Th2 will produce various cytokines such as IL-3, IL-4, IL-5, and
IL-13, IL-4 and IL-13 may be bound by their receptors on the surface of B lymphocytes, so
 that B lymphocytes become active and will produce immunoglobulins E (IgE). IgE in the
blood circulation will enter the tissue and bound by IgE receptors on the surface of
mastocytes or basophils (mediator cells) so that both of these cells become active. This
process is called sensitization that produces sensitized mediator cells. When sensitized
mucosa is exposed to the same allergen, the two IgE chains will bind to specific allergens and
degranulation of the mastocytes and basophils with the result of the release of a Performed
Mediator, especially histamine. In addition to histamine was also issued Newly Formed
mediators including prostaglandin D2 (PGD2), Leukotrienes D4 (LT D4), Leukotrienes C4 (LT
C4), bradykinin, platelet activating factor (PAF), cytokines (IL-3, IL-4, IL -5, IL-6, GM-CSF
(Granulocyte Macrophage Colony Stimulating Factor) etc. These are called Fast Radiation
Allergy Reactions (FRARs).
Histamine will stimulate H1 receptors on the tip of the vidian nerve, causing itchy nose and
sneezing. Histamine will also cause the mucosal glands and goblet cells to experience
hypersecretion and increased capillary permeability resulting in rinorrhea. Another symptom
is nasal congestion due to sinusoid vasodilatation. In addition to histamine stimulate
Vidianus nerve endings, also causes stimulation of the nasal mucosa resulting in the
expenditure of Inter Cellular Adhesion Molecule 1 (ICAM1). In FRARs, mastocyte cells will
also release chemotactic molecules that cause the accumulation of eosinophils and
neutrophils in the target tissue. This response does not stop here, but the symptoms will
continue and reach the top 6-8 hours after exposure. In LRARs is characterized by the
addition of species and the number of inflammatory cells such as eosinophils, lymphocytes,
neutrophils, basophils and mast cells in the nasal mucosa as well as an increase in cytokines
such as IL-3, IL-4, IL-5 and Granulocyte Macrophag Colony Stimulating Factor (GM-CSF) And
ICAM1 on nasal secretions. The onset of symptoms of hyperactivity or hyperresponsiveness
nose is due to the role of inflammatory mediators from eosinophils with granulnya as
Eosinophilic Cationic Protein (ECP), Eosiniphilic Derived Protein (EDP), Major Basic Protein
(MBP), and Eosinophilic Peroxidase (EPO). In this phase, in addition to the specific factors
(allergens), non-specific irritant factors can aggravate symptoms such as cigarette smoke,
odors that stimulate, changes in weather and high humidity (Irawati, Kasakayan, Rusmono,
2008).
Microscopically there is a dilation of vessels (vascular bad) with goblet cell enlargement and
mucus-forming cells. There is also an enlargement of the intercellular space and thickening
of the basement membrane, as well as the infiltration of eosinophil cells in the nasal
mucosal and submucous tissues. The description found is at the time of the attack. Beyond
the state of attack, the mucosa returns to normal. However, the attack can be continuous
(persistent) throughout the year, so that over time the changes were irreversible, ie a
proliferation of connective tissue and mucosal hyperplasia, so it appears thickened nasal
mucosa.
4. Bagaimana cara kerja aromaterapi melalui inhalasi?
That when the essential oil is inhaled, the odor molecule contained in the essential oil of
sandalwood is received by the olfactory ephitelium. Once received in olfactory ephitelium,
the odor molecule is transmitted as a message to the inhalation center located at the back
of the nose. In this place, various neuron cells change the odor and deliver it to the central
nervous system (CNS) which is then brought to the limbic system of the brain. The limbic
system of the brain is a place of memory storage, mood, happy emotions, anger, personality,
 sexual orientation, and his behavior. In the limbic system, the odor molecule will be
transmitted to the hypothalamus for translation. In the hypothalamus, all the elements in
essential oil stimulate the hypothalamus to produce corticotropin release factor (CRF). The
CRF process further stimulates the pituitary gland to increase the production of
Proopioidmelanocortin (POMC) so that the enkephalin production by the adrenal medulla
increases. The pituitary gland also produces endorphins as neurotransmitters that affect the
mood to relax.
5. Apa efek samping stroid topikal pada anak-anak?
SIDE EFFECTS
Side effects, both local and systemic, are more common in infants and children, long-term
topical corticostroid use, strong potency, and extensive application of lesions.
Local Side Effects
The use of long-term topical corticostroid or strong potential to induce skin atrophy, striae,
telangiectasia, purpura, hypopigmentation, acneiformis, perioral dermatitis, hypertrichosis,
and moonface. In uncontrolled and uncommon topical use of uncontrolled topical
corticostroid is a topical corticostroid addiction. Some examples of topical corticosteroid
addiction, ie facial erythematous lesions after peeling, thin and red scrotum skin, vulvodynia,
perianal atrophy, and recalcitrant atopic dermatitis. The use of long-term topical kortikostal
on the face can cause topical corticosteroid-induced rosacea-like dermatitis (TCIRD) or
topical steroid-dependent face (TSDF).
Systemic Side Effects
Kortikostroid potent topical and strong to be absorbed and cause systemic effects, including
Cushing's syndrome, the emphasis of the hypothalamic-pituitary gland-adrenal gland,
metabolic disorders such as hyperglycemia, abnormal renal / electrolyte, such as
hypertension, edema, edema Cryptococcus. In general these side effects are reversible,
improving after the drug stops, except the atria striae which is more difficult to overcome
due to damage to the skin barrier.