CHAPTER I

PRELIMINARY

1.1 Background
The Respiratory System Block is the thirteenth block in semester IV
of the Competency Based Curriculum (KBK) system of Medical
Education, Faculty of Medicine, Muhammadiyah University, Palembang
One of the learning strategies of the Competency Based Curriculum
(CBC) system is Problem Based Learning (PBL). Tutorial is an
implementation of the Problem Based Learning (PBL) method. In the
tutorial students are divided into small groups and each group is guided by
a tutor / lecturer as a facilitator to solve existing cases.

1.2 Purpose and objectives

The purpose and objectives of this case study tutorial report are:
1. As a tutorial group task report that is part of the KBK learning system
at the Faculty of Medicine, Muhammadiyah University, Palembang.
2. Can solve the case given in the scenario with the method of analysis
and learning group discussion.
3. The achievement of the objectives of the tutorial learning method.

1
 CHAPTER II
DISCUSSION

2.1 Tutorial Data

Tutor : dr. Sheila Yonaka Lindri, M.Kes
Moderator : Raga Tetra Putra
Desk secretary : Rima Putri
Board secretary : Tasya Salsabila
Time : Tuesday, 2 June 2020
At: 10.30 - WIB
Tutorial rules:
1. Turn off the cellphone or idle.
2. Raise your hand when asking relevant opinions and questions.
3. Permission when going out of the room.
4. Respect each other's opinions and remain calm and not noisy.

2
2.2 Case Scenario
“ Gesundheit ”
Mr. Fazli, a 25 years old cleaning service came to the doctor with a
chief complaint of sneezing excessively which has become worse since 2
days ago. Complaints have been felt since 2 years ago. Complaints arise
especially in the morning and at work, more than 4 times a week and are
felt to interfere with the activity of Mr. Fazli. Mr. Fazli also complained of
colds, itching of the eyes and nasal congestion. Mr. Fazli never took
medication and only took cold medicine bought at the street vendor. Mr.
Fazli grandfather has a history of asthma.

Physical Examination: General Appearance: looks mildly sick, compos

mentis
Vital sign: BP: 110/70mmHg, Pulse: 90x/minute reguler, contain and
resistance is normal, RR: 22x/m T: 37,00C
Head: Eyes: Allergic shiner (+)
ENT Status:
- Ear: tymphany membrane intact, light reflection +/+
- Nose: Narrow Cavum nasi, secrete (+/+) white colored, hypertrofi
concha, livide, mass (-) transverse nasal crease (+), allergic salute (+).
- Throat: Symetric Arcus faring, uvula in the middle, tonsil T1-T1 calm,
posterior faring normal, .

Laboratory Examination: Hb 14,0 g/dl, HT: 42 g/dl, leukosit 3500,

trombosit 200.000, eritrosit 4,6 x 1012, diff count 0/7/45/0/45/3

2.3 Clarification of Terms:

No. Clarification of terms Meaning
1 Sneeze Release spasmodically strong air through
the nose and mouth (Dorland, 2015).
2 Asthma Recurrent paroxysmal dyspnea attack, with

3
 wheezing due to spasmodic contraction of
the bronchi. this condition is usually caused
by manifestations of allergies (allergic or
extrisic. a) or secondary to chronic or
recurrent conditions (intrisic. a) (Dorland,
2015).

3 Nasal congestion Blockage due to inflammation of the nasal

lining (Dorland, 2015).
4 Composmentis Normal consciousness, fully aware, can
answer all questions about the
circumstances around him (Dorland, 2015).
5 Tymphanic Thin layer of tissue that covers the
membrane intac tymphani surface (Dorland, 2015).
6 Allergic shiner Allergy shiners are the collection of blood
or fluid under the eyes due to swelling of
tissues in the nasal cavity (Dorland, 2015).
7 Uvula A small fleshy object hanging from the soft
palate (Dorland, 2015).
8 Allergic salute Nose rubbing due to itching with palms in
upward motion (Dorland, 2015).
9 Cold Lower temperature when compared to
human body temperature (Dorland, 2015).
10 Itching of eyes s an irritating sensation that makes you want
to scratch your skin (Dorland, 2015).
11 Cavum nasi A hollow place or space or a potential space
on the nose (Dorland, 2015).
12 Secrete Compounds with certain substances
produced by glands (Dorland, 2015).
13 Hypertrofi concha Increased volume of concha (a thin bone
plate which is form the bottom of the lateral
wall nasal cavity and mucous membranes

4
 are lining the plate) (Dorland, 2015).

14 Livide Changes color as caused by contussion or

bruising (Dorland, 2015).

2.4 Identification of problems

1. Mr. Fazli, a 25 years old cleaning service came to the doctor with a
chief complaint of sneezing excessively which has become worse since
2 days ago. Complaints have been felt since 2 years ago. Complaints
arise especially in the morning and at work, more than 4 times a week
and are felt to interfere with the activity of Mr. Fazli.
2. Mr. Fazli also complained of colds, itching of the eyes and nasal
congestion.
3. Mr. Fazli never took medication and only took cold medicine bought at
the street vendor.
4. Mr. Fazli grandfather has a history of asthma.
5. Physical Examination: General Appearance: looks mildly sick, compos
mentis
Vital sign: BP: 110/70mmHg, Pulse: 90x/minute reguler, contain and
resistance is normal, RR: 22x/m T: 37,00C
Head: Eyes: Allergic shiner (+)
ENT Status:
Ear: tymphany membrane intact, light reflection +/+
Nose: Narrow Cavum nasi, secrete (+/+) white colored, hypertrofi
concha, livide, mass (-) transverse nasal crease (+), allergic salute (+).
Throat: Symetric Arcus faring, uvula in the middle, tonsil T1-T1 calm,
posterior faring normal .
6. Laboratory Examination: Hb 14,0 g/dl, HT: 42 g/dl, leukosit 3500,
trombosit 200.000, eritrosit 4,6 x 1012, diff count 0/7/45/0/45/3

5
2.5 Priority of problems
Problem identification number 1, because it can increase morbidity and
mortality. the sneezing excessively which has become worse since 2 days
ago is the main complain that brought mr. fazli to the doctor so we have to
cure it first and it wont make another unwanted complications.

2.6 Analysis of problems

1. Mr. Fazli, a 25 years old cleaning service came to the doctor with a chief
complaint of sneezing excessively which has become worse since 2 days
ago. Complaints have been felt since 2 years ago. Complaints arise
especially in the morning and at work, more than 4 times a week and are
felt to interfere with the activity of Mr. Fazli.
a. What is the histology,anatomy,and physiology of the case?
Answer:
Anatomy
Respiration system
The respiratory system includes the airway to the lungs, the lungs
themselves, and the thorax (chest) and abdominal breathing muscles
that play a role in producing air flow through the airways in and out of
the lungs. The airway is a tube or pipe that carries air between the
atmosphere and the air bag (alveoli), with the latter (alveoli) being the
only place of gas exchange between air and blood. If the respiratory
tract is stretched from end to end, it will extend to 1500 miles
(Sherwood, 2014).

6
 Figure 1. Outer Nose and Septum Nasi (Snell,2012).

The nose consists of the outer nose and the rice cavity. The nasi
cavity is divided by the rice septum into 2 parts right and left (Snell,
2012).
Outer Nose
The outer nose has two oval shaped holes called nares, which are
separated from each other by the nasi septum. Lateral edges, nasi-
style, are round and can be moved. The external nasal frame is formed
by the os nasale, the maxillary frontal processus, and the pars nasalis
ossis frontalis. Below, the nasal framework is formed by hyaline
cartilage plates (Snell, 2012).
1) Outer Nose Blood Supply
Outer nose skin gets blood from branches a. ophtalmica and a.
maxillaris. Nasi-style skin and the bottom of the septum get blood
from branches a. fascialis (Snell, 2012).
2) External Sensory Nerve Supply
N. infratrochlearis and flax nasales externae n. ophthalmicus (n.
cranialis V) and ramus infraorbitalis of the maxillary nerus (n.
cranialis V) take care of the external nose (Snell, 2012).

Cavum Nasi
7
 Figure 2. Cavum Nasi (Snell,2012).

The nasi cavity extends from the nares in front to the posterior
nasal apertures or the chonae in the back, where the nose empties into
the nasopharynx. Rice vestibulum is an area inside the rice cavity
located directly behind the nares. Rice Cavum is divided into 2 parts,
left and right by the rice septum. Rice septum is formed by cartilage
such as rice, vertical lamina osis ethmoidalis and vomer (Snell, 2012).
1) Cavum Nasi Wall
Each portion of the nasi cavity has a base, roof, lateral wall and
medial wall or septum wall (Snell, 2012).
a. Baseline: Formed by the proccessus palatinus os maxilla and
horizontal lamina ossis palatini.
b. Roof: The roof is narrow and formed anteriorly starting from the
bottom of the nasal trunk by os nasale and os frontale, in the middle
by the lamina cribrosa ossis ethmoidalis, located below the anterior
cranii fossa, and posteriorly by the lower part of the corpus ossis
sphenoidalis.
c. Lateral wall: The lateral wall has 3 bony protrusions called the
superior, medium and inferior nasal concha. The area under each
concha is called the meatus.

8
 a. Recessus sphenoethmoidalis is a small area located above the superior
nasal concha. In this area there is a sphenoid sinus estuary.
b. Superior rice meatus: Located under the superior nasal concha. Here is
the posterior ethmoid sinus estuary.
c. Meatus nasi media: Located under the nasal concha media. This
meatus has a rounded bulge, called the ethmoid bulla formed by sinus
ethmoidales medii which empties into its upper edge. A curved gap,
called the hiatus semilunaris, is located just below the bull. The
anterior end of the hiatus leading into a funnel-shaped channel is
called the infundibulum, which will be in contact with the frontal
sinus. The maxillary sinus empties into the media rice meatus through
the hiatus semilunaris.
d. Inferior rice meatus: Located under the inferior nasal concha and is
the place of the mouth of the lower end of the nasolacrimal duct,
which is protected by a fold of the mucosa membrane.
d. Medial wall: Formed by a rice septum. The upper part is formed by
lamina verticalis ossis ethmoidalis and os vomer. The anterior part is
formed by the septalis cartilage. This septum is rarely located in the
median plane, so that one portion of the rice cavity is larger than the
other side.
ii. Membran Mucosa Cavum Nasi
The vestibulum is coated with modified skin and has coarse hair. The
area above the superior nasal concha is covered by the olfactory
mucosa membrane and contains sensitive nerve endings of the
receptor receptors. The lower part of the nasi cavity is covered by a
respiratory mucosa membrane. In the respiratory area there is a large
woven vein in the submucosal connective tissue (Snell, 2012).
iii. Cavum Nasi Nerve Supply

9
 Figure 3. Nerve Cavum Rice Supply (Snell,2012).

N. olfactorius originating from the mucosa olfactorius membrane goes

up through the lamina cribrosa os ethmoidale to the olfactori bulb.
Nerves for general sensation are branches n. ophthalmicus (N. VI) and
n. maxillaris (N. V2) division n. trigeminus (Snell, 2012).
iv. Cavum Nasi Vascularisation

10
 Figure 4. Cavum Nasi Vascularisation (Snell,2012).

Cavum nasi vascularisation originates from branches a. maxillaris

which is one of the terminal branches a. carotis externa. The most
important branch is a. sphenopalatina. A. sphenopalatina anastomoses
with superior labial arterial septalis ramus which is a branch of a.
fascialis in the vestibulum region. Blood in the submucosa vein woven
flowed by veins that accompany the arteries (Snell, 2012).
v. Cavum Nasi Lymph Flow
Lymph vessels drain lymph from the vestibulum to the submandibular
nodi. Other parts of the cavum nasi flowed into the lymph nodes
cervicales profundi superiores (Snell, 2012).

Vasculature of nasal cavity

The nose has a very rich vascular supply – this allows it to effectively
change humidity and temperature of inspired air. The nose receives
blood from both the internal and external carotid arteries:
a. Internal carotid branches:
• Anterior ethmoidal artery
11
 • Posterior ethmoidal artery
The ethmoidal arteries are branch of the ophthalmic artery. They
descend into the nasal cavity through the cribriform plate (Jones,
2019).
b. External carotid branches:
• Sphenopalatine artery
• Greater palatine artery
• Superior labial artery
• Lateral nasal arteries
In addition to the rich blood supply, these arteries form
anastomoses with each other. This is particularly prevalent in the
anterior portion of the nose (Jones, 2019).
The veins of the nose tend to follow the arteries. They drain into
the pterygoid plexus, facial vein or cavernous sinus. In some
individuals, a few nasal veins join with the sagittal sinus (a dural
venous sinus). This represents a potential pathway by which infection
can spread from the nose into the cranial cavity (Jones, 2019).

Figure 5. Vasculature of nasal cavity (Netter, 2016).

Innervation of nasal cavity

The front and top of the nasal cavity are sensory from the anterior
netetoid, which is a branch of the nosociliary, which originates from
the nophthalmic nerve (N.V1). The other nasal cavity, mostly gets
12
sensory from the maxillary through the sphenopalatinum ganglion.
The sphenopalatinum ganglion in addition to providing sensory
innervation also provides vasomotor or autonomic innervation for
nasal mucosa. This ganglion receives sensory fibers from the
n.maxilla (N.V2), parasympathetic fibers from the n.petrosus
superficial mayor and sympathetic fibers from n.petrosus profundus.
The sphenopalatinum ganglion is located behind and slightly above
the posterior end of the concha media (Soetjipto, 2016).
The olfactory nerve descends from the lamina cribrosa from the
lower surface of the olfactory bulb and ends up in the receptor cells in
the olfactory mucosa in the upper third of the nose (Soetjipto, 2016).

Gambar ... Innervation of nasal cavity (Jones, 2019)

Physiology
The role of the nasal cavity is to humidify and warm the inspired
air. Also, as the air passes through, the nasal cavity removes minute
airborne particles and other debris before the air reaches the lower
airways. Columnar epithelium lines the nasal cavity. This type
of epithelial lining also secretes mucus that coats the lining and helps
with the mucociliary clearance of minute aerosolized particles that
become trapped in the nasal mucosa. The nasal cavity also functions

13
to facilitate drainage for the secretions from the adjacent paranasal
sinuses. It also captures the odor bearing particles and transmits them
to the olfactory recesses, that are in the superior portion of the nasal
cavity, just medial to the superior turbinates. Air containing mucosal
lined sinuses surround the nasal cavity, which includes the frontal,
paired maxillary, sphenoid, and ethmoid sinuses. These cavities
directly communicate with the nasal cavity. The secretions from these
sinuses drain into the nasal cavity via the thin-walled ostia. Like the
nasal cavity, the wall lining of the sinuses also secretes mucus. The
cilia on the surface sweep the mucus in a carpet like fashion and move
them towards the nasal ostia. The hard palate lines the floor of the
nasal cavity. The lateral walls are spiral shaped mucosal folds that
overlie the turbinates and sinus ducts draining into the ostia. The spiral
shape of the turbinates is designed to increase the surface area for the
inspired air (Sobiesk, 2019).
The nasal cavity functions to humidify, warm, filter, and act as a
conduit for inspired air, as well as protect the respiratory tract through
the use of the mucociliary system. The nasal cavity also houses the
receptors responsible for olfaction. If any of the functions of the nasal
cavity are compromised, the result is likely to manifest in signs and
symptoms of clinically significant disease processes. Understanding
the anatomy, physiology, and function of a properly functioning nasal
cavity is essential in diagnosing and treating the underlying pathology
(Sobiesk, 2019).
The airway starts from the nasal canal (nose). The nasal
passages open into the pharynx (Sherwood, 2014). When air flows
through the nose, there are three different functions that are carried
out by the nasal cavity, namely as follows (Guyton, 2017).
1) The air is warmed by the surface of a large concha and septum
with a total area of approximately 160 cm2.
2) The air is moistened until it is almost completely moist even
before the air leaves the nose.
14
3) Partially filtered air.
All of these functions are collectively called the function of the
upper airway humidifier. Usually the temperature of inspirational air
rises to 1̊F over body temperature and with 2-3% water vapor
saturation before air reaches the trachea (Guyton, 2017).
Feathers at the entrance of the nostrils are important for filtering
large particles. However, it is far more important to remove particles
through turbulent precipitation. That is, the air flowing through the
nasal passages hit many barrier walls such as konka, septum and
pharyngeal walls. Each time the air hits this barrier, it must change
the direction of its flow. Particles suspended in air have a momentum
and mass far greater than air, so they cannot change the direction of
their travel as fast as air. Therefore, these particles continue to
advance forward, hit the surface of these barriers, and then be snared
by the mucus coating and transported by cilia to the pharynx to be
swallowed (Guyton, 2017).

Histology

Figure 5. Histology of the Nasal Cavity

Source: Mescher (2017)

Most of the nasal cavity is covered by mucosa with ciliated

cylindrical multilevel epithelium. Ciliated cylindrical cells are cells
that have 250-300 cilia on their apical surface. Respiratory
epithelium is generally located above a thick basement membrane
(BM) with hundreds of long cilia (C), there are also mucus-

15
 producing goblet (G) cells. Its proprietary lamina contains many
blood vessels (V) (Mesecher, 2017).

b. What is the meaning Mr. Fazli, a 25 years old cleaning service came
to the doctor with a chief complaint of sneezing excessively which has
become worse since 2 days ago?
Answer:
The meaning is inflammatory response where when inflammation
occurs the body will issue inflammatory mediators such as histamine
and leukotrienes which can cause sneezing. This reaction is likely
caused by an allergy. For the meaning of getting worse since two days
ago this is the progression of the disease (Price, 2015).
Nasal reflexes have occurred. Nasal mucosa is a receptor associated
with breathing. irritation of the nasal mucosa will cause a sneezing
reflex. One of the physiology of the nose is to filter the air entering the
respiratory tract. Dust particles, viruses, bacteria and fungi that are
inhaled with air will be filtered in the nose by hair (vibrissae) in the
vestibulum of nasi, cilia and mucous palette. Dust and bacteria will be
attached to the mucous membrane and large particles will be removed
by a sneeze reflex (Irawati et al., 2016).

c. What is the etiology of sneezing?

Answer:
Based on the way of entry, allergens are divided into:
1. Inhalant allergens, which are allergens that enter along with the
air respiration, such as house dust, mites, epithelial flakes from
feathers animals, and also mushrooms.
2. Ingestant allergens, namely allergens that enter the
gastrointestinal tract, consist foods such as milk, eggs, chocolate,
fish and shrimp.
3. Injectant allergens, which are allergens that come in via injection
or puncture, for example penicillin or bee stings
16
 4. Contactant allergens, which enter through contact with skin or
tissue mucosa, for example cosmetics or jewelry. The most
common causes of rhinitis are inhalant allergens in adults and
ingestants in children, whereas in children often found to be a
problem others such as urticaria and digestive disorders
(Ilavarase, 2010).

Sneezing is a protective reflex response a sneeze (or sternutation) is

expulsion of air from the lungs through the nose and mouth, most
commonly caused by the irritation of the nasal mucosa. Sneezing can
further be triggered through sudden exposure to bright light, a
particularly full stomach and physical stimulants of the trigeminal
nerve, as a result of central nervous system pathologies such as
epilepsy, posterior inferior cerebellar artery syndrome or as a
symptom of psychogenic. The factors that play role in the etiology of
the sneeze reflex are listed below,
1. Rhinitis Photic sneeze reflex (ACHOO syndrome)
2. Physical stimulations of the trigeminal nerve
3. Central nervous system pathologies
4. Psychogenic (intractable) sneezing
5. Snatiation* reflex
6. Sexual ideation or orgasm (Songu, 2009)

d. What is the cause of complaints sneezing since 2 days ago?

Answer:
Hypersensitivity reactions are the basis of allergic rhinitis. This
disease is an inflammatory disease that begins with the stage of
sensitization and followed by the stage of provocation or allergic
reaction. In response to inflammation the body secretes inflammatory
mediators such as histamine which is the main mediator that plays a
role in the onset of symptoms. Histamine stimulates receptor III at the

17
 end of the vidianus nerve, causing itching in the nose and sneezing
(Nisa, 2017).
In the case of possible allergic rhinitis. The cause of sneezing in
allergic rhinitis is allergens both inhalant or ingestant allergens such as
dust, mites, cigarette smoke, odors, weather changes, and high
humidity (Rizqun, 2017).
Allergic Rhinitis, Based on by Irawati et al that allergic rhinitis
consists of 2 phases, first Immediate Phase Allergic Reaction (IPAR)
which lasts from contact with allergens for up to 1 hour thereafter and
Late Phase Allergic Reaction (LPAR) which lasts for 2-4 hours with a
peak of 6-8 hours (hyper-reactivity phase ) after exposure and can last
up to 24-48 hours (Irawati et al., 2016).
So we can conclude that its already Late Phase Allergic Reaction
(LPAR).

e. What are the trigger factors in complaints experienced by Mr. Fazli?

Answer:
Trigger factors in patient experienced,
- Exposure to pollen
- Fungi spores
- Dust when cleaning the house
- Animal (Sheikh et al., 2018).

f. What is the correlation between age, gender and job in the case?
Answer:
Age:
Based on epidemiological studies, prevalence rhinitis is questioned
10-20% and keep increasing in the final conclusion.Average age the
onset of allergic rhinitis is 8-11 years, and 80% of pregnancy rhinitis
develops with age 20 years. Generally, allergic rhinitis arises in age
young (teenagers and young adults) (Nurjannah, 2011).

18
 Onset of allergic rhinitis is common in childhood, adolescence, and
early adult years, with a mean age of onset 8-11 years, but allergic
rhinitis may occur in persons of any age. In 80% of cases, allergic
rhinitis develops by age 20 years. The prevalence of allergic rhinitis
has been reported to be as high as 40% in children, subsequently
decreasing with age. In the geriatric population, rhinitis is less
commonly allergic in nature (Sheikh et al., 2018).
Gender:
In a study in Medan, from 31 allergic rhinitis sufferers, found more
women than men at a ratio of 1.58: 1 and research in Palembang got
from 259 allergic rhinitis sufferers 122 male and 137 womenn
(Nurjannah, 2011). However, at Utama (2010) research gets the
incidence rate between men and women is 1: 1.
In childhood, allergic rhinitis is more common in boys than in girls,
but in adulthood, the prevalence is approximately equal between men
and women (Sheikh et al., 2018).
Job:
Cleaning service is one of the jobs that is often exposed to
allergens. The increased risk of the occurrence of rhinitis due to work
related to the length of work of a person in this case increases the
duration and intensity of allergen exposure to the individual.
However, other studies have shown that there is no significant
relationship between length of work and the incidence of allergic
rhinitis (Supit et al., 2019).

g. What is the pathophysiology of sneezing?

Answer:
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast cells/basophils
will bind to specific allergens → mastocyte and basophil
degranulation → the release of preformed mediators, especially
histamine, newly formed mediators such as Prostaglandin D2 (PD2),
19
 Leukotrien D4 (LTD4), Leukotrien C4 (LTC4), bradykinin, platelet
activating factor (PAF), cytokines (IL3, IL4, IL5, IL6) GM-CSF
(Granulocyte Macrophage Colony Stimulating Factor) and the release
of Intercellular Adhesion Molecule 1 (ICAM 1) → histamine
stimulates H1 receptors on the nerve endings of vidianus → afferent
nerve stimulation → sneezing

Infiltrate the nasal lining upon exposure to an inciting allergen (most

commonly airborne dust mite fecal particles, cockroach residues,
animal dander, moulds, and pollens) → Activate T cells (T helper
(Th0)) → release of epithelial cytokines (IL-1) → Th0 proliferate to
Th1 and Th2 → Th2 release cytokines (IL-3, IL-4, IL-5,1L-13) →
IL-4 and IL-13 bind with their receptors on the surface of B
lymphocyte cells → activate B lymphocyte cells → B lymphocyte
cells produce Immunoglobulin E (IgE) in blood circulation →
allergen-specific IgE antibodies attach to high-affinity receptors on the
surface of tissue-resident mast cells and circulating basophils → the
allergen binds to IgE on the surface of those cells and cross-links IgE
receptors → resulting in mast-cell and basophil activation and the
release of neuroactive and vasoactive mediators such as histamine and
the cysteinyl leukotrienes → histamine will activate H1 receptors at
the nerve end of the vidianus → cause itching on the nose and
sneezing (Irawati et al., 2016), (Wheatley, 2015) dan (Small, 2018).

h. What are the possible disease of sneezing?

Answer:
Possible diseases with frequent sneezing namely asthma, allergic
rhinitis, sinusitis (Kowalak et al., 2017).
Possible disease with sneezing symptons,
1. Allergic rhinitis
2. Infectious rhinitis
3. NARES (non-allergic rhinitis with eosinophilia syndrome)
20
 4. Vasomotor of rhinitis (Songu, 2009)

i. What is the meaning complaints have been felt since 2 years ago?
Answer:
The meaning is, maybe patient have experienced allergic rhinitis
perennial, and symptons arise intermiten and aren’t activated by
seasons but arise every year.
Shows that the grievances felt by Mr. Fazli is now a disease
progression (allergic rhinitis) that he experienced 2 years ago. This
can be expected because of inadequate treatment or only
treat/eliminate symptomatic symptoms without eliminating/addressing
the cause.
The meaning is probably the first exposure (two years ago it was
sensitized). Based on research, states that increasing the length of
work in this case increasing the duration and intensity of allergen
exposure to an individual who has been sensitized has an important
role in increasing the risk of the individual suffering from rhinitis. It
also illustrates the progression of the disease to moderate-severe
persistent allergic rhinitis (Supit et al., 2019).

j. What is the meaning complaints arise especially in the morning and at

work, more than 4 times a week and are felt to interfere with the
activity of Mr. Fazli?
Answer:
The meaning for symptoms more than 4 times / week is included in
the classification of persistent allergic rhinitis. The meaning to
interfece with the activity is included in the classification of moderate-
severe allergic rhinitis. So Mr.Fazli has persistent moderate-severe
allergic rhinitis (Klimek et al., 2019).

21
 k. What is the corellation sneezing that arise especially in the morning
and at work, more than 4 times a week and are felt to interfere with
the activity with perceived complaints?
Answer:
The correlation between sneezing that arise especially in the
morning and at work, more than 4 times a week and are felt to
interfere with the activity with perceived complaints is a classification
of allergic rhinitis. Show that Mr. Fazli has moderate-to-severe
persistent allergic rhinitis.

2. Mr. Fazli also complained of colds, itching of the eyes and nasal
congestion.
a. What is the meaning Mr. Fazli also complained of colds, itching of the
eyes and nasal congestion?
Answer:
The meaning of the symptoms experienced by Mr. Fazli is a
clinical manifestation of allergic rhinitis, while the clinical symptoms
of allergic rhinitis can be in the form of repeated sneezing attacks,
runny and numerous rhinorrhea, nasal congestion, itchy nose and eyes,
and sometimes accompanied by lacrimation.
Its meaning is a clinical manifestation of allergic rhinitis. The
clinical manifestation is sneezing which can be accompanied by other
symptoms like colds, noses stuffy eyes, nose and itching accompanied
by a lot of lacrimation (Rafi et al., 2015)

b. What is the etiology of colds, itching of the eyes and nasal

congestion?
Answer:
Cold
- heredity
- Genetic trait that has lung disease and weak respiratory organs.
- Environmental factor
22
 - like cold and humid air, dusty environments and cigarette smoke
can reduce oxygen supply to the lungs.
- Excessive mucus production
Problems with the arrangement of bones or muscles in the upper back
(Sudoyo et al., 2017)

c. What are the pathophysiology of colds, itching of the eyes and nasal
congestion?
Answer:
Cold
Infiltrate the nasal lining upon exposure to an inciting allergen (most
commonly airborne dust mite fecal particles, cockroach residues,
animal dander, moulds, and pollens) → Activate T cells (T helper
(Th0)) → release of epithelial cytokines (IL-1) → Th0 proliferate to
Th1 and Th2 → Th2 release cytokines (IL-3, IL-4, IL-5,1L-13) →
IL-4 and IL-13 bind with their receptors on the surface of B
lymphocyte cells → activate B lymphocyte cells → B lymphocyte
cells produce Immunoglobulin E (IgE) in blood circulation →
allergen-specific IgE antibodies attach to high-affinity receptors on the
surface of tissue-resident mast cells and circulating basophils → the
allergen binds to IgE on the surface of those cells and cross-links IgE
receptors → resulting in mast-cell and basophil activation and the
release of neuroactive and vasoactive mediators such as histamine and
the cysteinyl leukotrienes → histamine will cause mucosa glandular
and goblet cell hypersecretion and capillary permeability increases →
cold (Irawati et al., 2016), (Wheatley, 2015) dan (Small, 2018).

Itching of the eyes

Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast cells/basophils
will bind to specific allergens → mastocyte and basophil
degranulation → the release of preformed mediators, especially
23
 histamine, newly formed mediators such as Prostaglandin D2 (PD2),
Leukotrien D4 (LTD4), Leukotrien C4 (LTC4), bradykinin, platelet
activating factor (PAF), cytokines (IL3, IL4, IL5, IL6) GM-CSF
(Granulocyte Macrophage Colony Stimulating Factor) and the release
of Intercellular Adhesion Molecule 1 (ICAM 1) → release of
histamine by IgE on the surface of mast cells in the conjunctiva →
itching of the eyes.

Nasal congestion
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast cells/basophils
will bind to specific allergens → mastocyte and basophil
degranulation → the release of preformed mediators, especially
histamine, newly formed mediators such as Prostaglandin D2 (PD2),
Leukotrien D4 (LTD4), Leukotrien C4 (LTC4), bradykinin, platelet
activating factor (PAF), cytokines (IL3, IL4, IL5, IL6) GM-CSF
(Granulocyte Macrophage Colony Stimulating Factor) and the release
of Intercellular Adhesion Molecule 1 (ICAM 1) → histamine
stimulates the occurrence of sinusoidal vasodilation and concha →
nasal congestion

d. What are relation between additional complain and the chief

complain?
Answer:
Shows that Mr. Fazli has allergic rhinitis. WHO ARIA definition
(Allergic Rhinitis and its Impact on Asthma) is a disorder of the nose
with symptoms of sneezing, rhinorrhea, itching and congestion after
the nasal mucosa is exposed to allergens mediated by IgE (Irawati et
al, 2012). Allergic rhinitis (AR) is an atopic disease characterized by
symptoms of nasal congestion, clear rhinorrhea, sneezing, and nasal
pruritis (Akhouri et al, 2020).

24
3. Mr. Fazli never took medication and only took cold medicine bought at
the street vendor.
a. What is the meaning of Mr. Fazli never took medication?
Answer:
We want to rule out the differential diagnosis of medical rhinitis.

b. What is the meaning of Mr. Fazli only took cold medicine bought at
the street vendor?
Answer:
We want to shows the patient's efforts to treat or eliminate
symptomatic complaints rather than eliminate the cause.

c. What are the possibility of cold medicine that being consumed?

Answer:
Paracetamol, ibuprofen, decongestan (Pseudoephedrine,
phenylephrine, etc), antihistamin (fexofenadine, loratadine, cetrizine)

4. Mr. Fazli grandfather has a history of asthma.

a. What is the meaning Mr. Fazli grandfather has a history of asthma?
Answer:
The meaning is, this can be a risk factor for allergic rhinitis.
some things that can be risk factors for allergic rhinitis are age,
gender, history family and other atopy history with incidence of
allergic rhinitis. Family history has a role in decreased atopy in
children. Allergic rhinitis usually obtained in atopic families with a
history of allergic manifestations others such as asthma and urticaria
/ dermatitis atopy / eczema. Allergic rhinitis can occur in 75% of
people with asthma (Nurjannah, 2011).
Shows that Mr. Fazli has a history of atopy from his grandfather.
Asthma is one of the respiratory allergies. Asthma is a chronic
inflammatory disease of the bronchial mucosa that causes bronchial
hyperresponsiveness, airway constriction and variable and reversible
25
 air flow obstruction (Huether, 2017). Allergy is a disease in the form
of a reaction that is produced in a short time by the body's immune
due to the presence of a substance that is in the environment called
an allergen. Allergies can occur because the body produces excess
specific IgE (Immunoglobulin E) antibodies as the body's immune
response to allergen exposure. Allergens are generally harmless and
are abundant in the environment. Allergic reactions begin in the
body that is exposed to allergens and then cause a response to
produce IgE then IgE will stick to mastocyte cells that contain
mediators that can trigger allergic reactions. When the body is re-
exposed to the same allergen, the allergen will bind to IgE that
attaches to mastocyte cells. The bond that occurs between allergens
and IgE antibodies triggers mastocyte cells to become active then
break and release mediators such as histamine, leukotrin, and other
mediators that can cause inflammation in the form of clinical
symptoms of allergies (Kurnia et al, 2019).

b. What is the relationship his grandfather history and chief complain?

Answer:
A child who comes from a family with a history of allergic
disease will be at risk of experiencing allergic disease two to three
times higher than those who have no family history of allergic
disease. Respiratory allergies can arise due to genetic and
environmental factors. Genetic factors are obtained from a history of
parental atopy. Atopy is a genetic factor that is inherited in the
family in the form of IgE antibody control in response to low-dose
allergens. Parents who suffer from respiratory allergies tend to have
children who suffer from respiratory allergies too. In addition to
genetic factors, the environment also affects respiratory allergies.
Allergens in the environment can trigger respiratory allergies
(Johansson et al., 2006).

26
 Mr. Fazli experienced complaints that he felt now (allergic rhinitis)
due to a genetic history from his family. Family history of atopic
disease is one of the allergic rhinitis’s risk factor. Patients will often
have a family history of allergic rhinitis or asthma (Akhouri et al,
2020). Respiratory allergies can arise due to genetic and
environmental factors. Genetic factors are obtained from a history of
parental atopy. Atopy is a genetic factor that is inherited in the
family in the form of IgE antibody control in response to low-dose
allergens. Parents who suffer from respiratory allergies tend to have
children who suffer from respiratory allergies too (Kurnia et al,
2019).
Genetic factors can be proven by a family history of allergic
diseases. A child who comes from a family with a history of allergic
disease will be at risk of having an allergic disease two to three times
higher compared to that no family history of allergic disease.
Diseases such as atopic dermatitis, asthma, allergic rhinitis are
allergic symptoms in atopic individuals. Atopy is a personal and / or
familial tendency, usually in childhood or adolescence, to sensitize
and produce IgE in response to allergen exposure, usually protein.
The term atopy cannot be used before evidence of IgE sensitization
is indicated by a positive Radio Allergo Sorbent Testing (RAST) or
skin prick test (UTK). The emergence of symptoms at a certain age
that varies from each allergic disease is a natural course of a disease
called atopic march (Weninggalih et al, 2009).

5. Physical Examination: General Appearance: looks mildly sick, compos

mentis
Vital sign: BP: 110/70mmHg, Pulse: 90x/minute reguler, contain and
resistance is normal, RR: 22x/m T: 37,00C
Head: Eyes: Allergic shiner (+)
ENT Status:
- Ear: tymphany membrane intact, light reflection +/+
27
- Nose: Narrow Cavum nasi, secrete (+/+) white colored, hypertrofi
concha, livide, mass (-) transverse nasal crease (+), allergic salute (+).
- Throat: Symetric Arcus faring, uvula in the middle, tonsil T1-T1
calm, posterior faring normal, .
a. How is the interpretation of physical examination results?
Answer:
The interpretation of physical examination results are:
Physical examination
Physical
No. Normal In the case Interpretation
examination
Don’t look Looks mildly
Abnormal
General
1. sick sick
Appearance
Composmentis Normal

100-120/60- BP:
Normal
80 mmHg 110/70mmHg
Pulse:
Pulse: 60-
90x/minute Normal
100x/minutes
reguler
2. Vital sign
contain and resistance is
Normal
normal
16-
RR: 22x/m Normal
24x/minutes

36,5-37,5C T: 37,00C Normal

Head

3. Allergic Allergic
Eyes Abnormal
shiner (-) shiner (+)

ENT status

No. ENT status In the case Interpretation

28
 Tymphany
Normal
1. Ear membrane intact

Light reflection +/+ Normal

Narrow cavum nasi Abnormal

Secrete (+/+) white

Abnormal
colored

Hypertrofi concha Abnormal

Livide Abnormal
2. Nose

Mass (-) Normal

Transverse nasal
Abnormal
crease (+)

Allergic salute (+) Abnormal

Symetric Arcus
Normal
faring

Uvula in the
Normal
Throat middle
3.
Tonsil T1-T1 calm Normal

Posterior faring
Normal
normal

Interpretation of physical examination and ENT status: Allergic

rhinitis

b. How the abnormal mechanism of physical examination results?

Answer:
The abnormal mechanism of physical examination results are:
1) Allergic shiner

29
 Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → the release of preformed mediators,
especially histamine, newly formed mediators such as
Prostaglandin D2 (PD2), Leukotrien D4 (LTD4), Leukotrien C4
(LTC4), bradykinin, platelet activating factor (PAF), cytokines
(IL3, IL4, IL5, IL6) GM-CSF (Granulocyte Macrophage Colony
Stimulating Factor) and the release of Intercellular Adhesion
Molecule 1 (ICAM 1) → histamine stimulates the occurrence of
sinusoidal vasodilation and concha → nasal congestion (nasal
obstruction) → secondary venous stasis → dark shadow in the
area under the eyes → allergic shiner (+)
2) Narrow cavum nasi, hypertrofi concha, livide
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → the release of preformed mediators,
especially histamine, newly formed mediators such as
Prostaglandin D2 (PD2), Leukotrien D4 (LTD4), Leukotrien C4
(LTC4), bradykinin, platelet activating factor (PAF), cytokines
(IL3, IL4, IL5, IL6) GM-CSF (Granulocyte Macrophage Colony
Stimulating Factor) and the release of Intercellular Adhesion
Molecule 1 (ICAM 1) → histamine stimulates the occurrence of
sinusoidal vasodilation and concha → hypertrofi concha, livide
→ narrow cavum nasi
3) Secrete (+/+) white colored
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → the release of preformed mediators,
especially histamine, newly formed mediators such as
30
 Prostaglandin D2 (PD2), Leukotrien D4 (LTD4), Leukotrien C4
(LTC4), bradykinin, platelet activating factor (PAF), cytokines
(IL3, IL4, IL5, IL6) GM-CSF (Granulocyte Macrophage Colony
Stimulating Factor) and the release of Intercellular Adhesion
Molecule 1 (ICAM 1) → histamine stimulates hypersecretion of
mucosal glands and goblet cells and capillary permeability →
secrete (+/+) white colored
4) Transverse nasal crease (+)
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → the release of preformed mediators,
especially histamine, newly formed mediators such as
Prostaglandin D2 (PD2), Leukotrien D4 (LTD4), Leukotrien C4
(LTC4), bradykinin, platelet activating factor (PAF), cytokines
(IL3, IL4, IL5, IL6) GM-CSF (Granulocyte Macrophage Colony
Stimulating Factor) and the release of Intercellular Adhesion
Molecule 1 (ICAM 1) → histamine stimulates fine fibers C
which don’t have myelin → itchy nose → the behavior of
rubbing the nose with the back of the hand → if over time will
cause the emergence of transverse lines in the nasal dorsum of
the 1/3 bottom → transverse nasal crease/allergic crease
5) Allergic salute (+)
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → the release of preformed mediators,
especially histamine, newly formed mediators such as
Prostaglandin D2 (PD2), Leukotrien D4 (LTD4), Leukotrien C4
(LTC4), bradykinin, platelet activating factor (PAF), cytokines
(IL3, IL4, IL5, IL6) GM-CSF (Granulocyte Macrophage Colony
Stimulating Factor) and the release of Intercellular Adhesion
31
 Molecule 1 (ICAM 1) → histamine stimulates fine fibers C
which don’t have myelin → itchy nose → the behavior of
rubbing the nose with the back of the hand → allergic salute (+)

6. Laboratory Examination: Hb 14,0 g/dl, HT: 42 g/dl, leukosit 3500,

trombosit 200.000, eritrosit 4,6 x 1012, diff count 0/7/45/0/45/3
a. How is the interpretation of laboratory examination results?
Answer:
Laboratory In the
No. Normal Interpretation
examination case
M: 13,5-18,0
1. Hb gr/dl 14,0 g/dl Normal

FM: 12-16 gr/dl

2. HT 3xHb 42 g/dl Normal

3500- 3500
3. Leukosit Normal
3 3
10.500/mm /mm
150.000- 200.000
4. Trombosit Normal
400.000/mm3 /mm3
M: 4,6-6,2 x
1012 sel/L 4,6 x 1012
5. Eritrosit Normal
FM: 4,2-5,4 x sel/L
1012 sel/L
Basophil: 0-1
Eosinophil: 0-5
Banded N.: 0-3 Eosinophil ↑

Segmented N.: 0/7/45/0/4 Banded N. ↑

6. Diff count
40-60 5/3 Segmented N.

Limfocyte: 20- ↓

45
Monocyte:2-6
Interpretation: Eosinophil ↑, Banded N. ↑, Segmented N. ↓

32
 b. How is the abnormal mechanism of laboratory examination results?
Answer:
Sensitization stage → the same allergy enters and attaches to the
surface of the sensitized nasal mucosa → IgE in mast
cells/basophils will bind to specific allergens → mastocyte and
basophil degranulation → mast cells release chemotactic molecules
→ eosinophil and neutrophil cell accumulation in the target tissue
→ laboratory examination: Leukosit ↑ (Eosinophil ↑, Banded N. ↑,
Segmented N. ↓)

7. How to diagnose?
Answer:
To diagnose the disease in the case are:
a. Anamnesis
1) Patien’s identity : Mr. Fazli, a 25 years old cleaning service
2) Main complain : Sneezing excessively which has become
worse since 2 days ago.
3) Disease’s progress : Complaints have been felt since 2 years
ago. Complaints arise especially in the morning and at work,
more than 4 times a week and are felt to interfere with the
activity of Mr. Fazli.
4) Additional complain: Mr. Fazli also complained of colds,
itching of the eyes and nasal congestion.
5) Treatment history : Mr. Fazli never took medication and only
took cold medicine bought at the street vendor.
6) Family history : Mr. Fazli grandfather has a history of asthma.
b. Physical examination : Eyes: Allergic shiner (+)
c. ENT status : Narrow Cavum nasi, secrete (+/+) white colored,
hypertrofi concha, livide, transverse nasal crease (+), allergic salute
(+).

33
 d. Laboratory examination : Eosinophil ↑, Banded N. ↑, Segmented N.
↓

8. What is the differential diagnosis in the case?

Answer:
The differential diagnosis in the case are:
e. Allergic rhinitis
f. Vasomotor rhinitis
Allergic rhinitis Vasomotor rhinitis

An idiopathic state.
Allergic reactions in atopic
Several theories are
patients who have previously
suspected:
been sensitized with the same
Etiology allergen, the release of a a. autonomic system
chemical mediator when there dysfunction
is repeated exposure to the b. Neuropeptide
specific allergen c. High NO levels
d. Trauma
Thought to be due to an
a. The sensitization / first
imbalance of autonomic
contact with allergens is
nerve impulses in the
Pathophysiology initiated
nasal mucosa in the form
b. RAFC and RAFL allergic
of increased
reactions
parasympathetic activity

a. Typical: Repeated a. Dominant: Nasal

sneezing attacks congestion,
b. Runny snot (rhinorrhea) changing right and
Clinical
and many left depending on
manifestation
c. Nose feels itchy and position
blocked b. Mucoid or serous
d. Itchy eyes accompanied by rhinorrhea

34
 lacrimation c. Rarely accompanied
by eye symptoms
Anterior rhinoscopy
obtained:

a. Typical features of
mucosal edema,
a. Anterior rhinoscopy is
nose, dark red or
obtained: edematous mu-
dark red konka, but
cosa, wet, pale or livid
sometimes also pale
with dilute and numerous
b. Konka's surface can
secretions
Physical be slippery or
b. Allergic shinner
examination bumpy
c. Allergic salute
c. In the nasal cavity
d. Allergic crease
there are usually a
e. Facies adenoid
few mucoid
f. Cobblestone appearance
secretions. but in
g. Geographic tounge
the type of
rhinorrhea secret
serous and
numerous
Skin Test + -

Eosinophils do not
Nose discharge Increased eosinophils
increase

Blood
Increased Normal
eosinophils

Blood IgE Increased Do not increase

a. Main: avoid allergens a. Avoid stimulus /

Treatment causes trigger factors
b. Medical: b. Sympathomimetic:

35
 1) Antihistamine 1) Oral
(histamine H-1 decongestants
antagonist) 2) Nose wash
2) Sympathomimetics 3) Topical
(nasal decongestants) corticosteroid
3) Corticosteroid 4) Topical
preparations anticholinergics
4) Anticholinergic for severe
preparations rhinorrhea
5) New: anti leukotriene,
anti IgE
Neurectomy N.
Not helpful Helpful
Vidianus

9. What is the additional examination in the case?

Answer:
a. In vitro:
- Calculate eusinofil in peripheral blood, can be normal / increase.
- Total IgE
- Specific IgE with RAST, ELISA.
- Nasal cytology examination
b. In Vivo:
- Cukit skin test
- intracutaneous / intradermal test (Irawati et al, 2016).

10. What is the working diagnosis in the case?

Answer :
Moderate-severe persistent allergic rhinitis.
a. Definition
Answer:

36
 Allergic rhinitis (AR) is an atopic disease characterized by
symptoms of nasal congestion, clear rhinorrhea, sneezing, and nasal
pruritis. It can affect one in every six individuals and has
associations with significant morbidity, loss of productivity, and
health-care costs. Historically, the belief was that AR was a
condition of the nasal passages only, but the treatment of AR is now
as a systemic disease due to its close association with asthma and
atopic dermatitis. AR can classify as either seasonal
(intermittent) or perennial (chronic), with approximately 20% of
cases being seasonal, 40% perennial, and 40% with features of
both. Outside of nasal symptoms, patients suffering from untreated
AR can also have allergic conjunctivitis, post-nasal drip, non-
productive cough, Eustachian tube dysfunction, and chronic
sinusitis. Once diagnosed, AR is treatable with a variety of
modalities, with intra-nasal glucocorticoids being first-line therapy
(Akhouri, 2020).

b. Epidemiology
Answer:
Prevalence of allergic rhinitis based on physician diagnosis is
approximately 15%; however, the prevalence is estimated to be as
high as 30% based on patients with nasal symptoms. AR is known
to peak in the second to fourth decades of life and then gradually
decline. The incidence of AR in the pediatric population is also
quite high, making it one of the most common chronic pediatric
disorders. According to data from the International Study for
Asthma and Allergies in Childhood, 14.6% in the 13 to 14 year age
group and 8.5% in the 6 to 7 year age group display symptoms of
rhinoconjunctivitis linked to allergic rhinitis. Seasonal allergic
rhinitis seems to be more common in the pediatric age group,
whereas chronic rhinitis is more prevalent in adults (Akhouri,
2020).
37
 A systematic review from 2018 estimated that 3.6% of adults
had missed work and 36% had impaired work performance due to
allergic rhinitis. Economic evaluations have shown that indirect
costs associated with lost work productivity account for the majority
of the cost-burden for AR (Akhouri, 2020).
Prevalence of allergic rhinitis in Indonesia reaches 1.5-12.4%
and tends to be every increase the year. From WHO data regarding
the epidemiology of allergic rhinitis in North America and Western
Europe,an increase in the prevalence of rhinitisallergies from 13-
16% to 23-28% the past 10 years. Enhancement prevalence of
allergic rhinitis in age school children in Western Europe become
double. Prevalence of allergic rhinitis seasonal and perennial in the
USA increased to 14.2%, the highest at the age of 18-34 years and
35-49 year (Rafi et al., 2015).
Epidemiologically, AR Affects 10–30% of world population and
the prevalence is still increasing.2 According to the 2008 World
Allergy Report6, the prevalence of AR in the low and middle
income countries in Asia Pacific Region was estimated to be around
5–45%. Unfortunately, the prevalence rate among adults in
Indonesia is still unknown. Meanwhile, it is shown that 64.6% of
AR patients who visited the Department of Otolaryngology-Head &
Neck Surgery, Dr. Hasan Sadikin General Hospital Bandung were
between 10 to 29 years old, a relatively productive age group.
Besides, it is also found that, based on occupation, 45.1% of the
patients were students (Fauzi, 2015).

c. Etiology
Answer:
Environmental factors (tobacco smoke, pollution, infections,
diet) acting on a genetic background (family history) contribute to
the development of AR which may follow earlier atopic dermatitis
but also occurs as the initial manifestation of allergy. Sensitisation
38
 may take place via the nose. Local IgE production can occur
without evidence of systemic sensitization (Scadding, 2015).

d. Risk Factors
Answer:
1. Other atopic diseases (asthma and eczema)
2. Family history of atopy
3. Air pollution (vehicle smoke exposure)
4. Exposure to cigarette smoke and kitchen smoke
5. Take care of cats or dogs
6. Socio-economic conditions
7. Body mass index
8. Take paracetamol or aspirin (Wang, 2005).
Important risk factors of allergic rhinitis include elevated
exhaled nitric oxide, allergic sensitization to common household
allergens, parental rhinitis, being overweight and high total serum
IgE (Baumann et al., 2015).
Risk factors for developing AR include a family history of
atopy, male sex, a presence of allergen-specific IgE, a serum IgE
greater than 100 IU/mL before age 6, and/or higher socioeconomic
status. Studies in young children have shown a higher risk of AR in
those with early introduction of foods or formula and/or heavy
exposure to cigarette smoking in the first year of life. Although
many recent studies have evaluated the link between pollution and
development of AR, no significant correlation yet exists
definitively. Interestingly, there are several factors identified that
may have a protective effect on the development of AR (Akhouri,
2020).

e. Classification
Answer:

39
First allergic rhinitis can be divided into 2 types based on the nature
of the process, namely (Irawati et al, 2012):
1. Seasonal allergic rhinitis (seasonal, hay fever, polynosis). In
Indonesia there is no known seasonal allergic rhinitis, only in
countries that have 4 seasons. Allergens are specific causes,
namely pollen (pollen) and mold spores. Therefore the proper
name is pollinosis (Irawati et al, 2012).
2. Allergic rhinitis throughout the year (perennial). Symptoms in
this disease occur intermittently or continuously, without
seasonal variations, so they can be found throughout the year.
The most common causes are inhalant allergens, especially in
adults, and ingestant allergens. Main inhalant allergens are
allergens in the house (indoor) for example: mites and allergens
outside the home (outdoor). Ingestant allergies are often a cause
in children and are usually accompanied by other allergic
symptoms, such as urticaria, indigestion. Physiological disorders
in the perennial group are milder compared to the seasonal
group but because it is more persistent, complications are more
often found (Irawati et al, 2012).

Therefore, allergic rhinitis is now classified according to

symptom duration (intermittent or persistent) and severity (mild,
moderate or severe) The Allergic Rhinitis and its Impact on Asthma
(ARIA) guidelines have classified,
1. The “intermittent” allergic rhinitis as symptoms that are
present less than 4 days per week or for less than 4 consecutive
weeks
2. The “persistent” allergic rhinitis as symptoms that are present
more than 4 days/week and for more than 4 consecutive weeks.

Symptoms are classified,

40
 1. Symptoms are categorized as mild when patients have no
impairment in sleep and are able to perform normal activities
(including work or school)
2. Symptoms are categorized as moderate/severe if they
significantly affect sleep or activities of daily living, and/or if
they are considered bothersome. It is important to classify the
severity and duration of symptoms as this will guide the
management approach for individual patients (Small, 2018).

f. Patogenesis / Pathophysiology
Answer:
In allergic rhinitis, numerous inflammatory cells, including mast
cells, CD4-positive T cells, B cells, macrophages, and eosinophils,
infiltrate the nasal lining upon exposure to an inciting allergen
(most commonly airborne dust mite fecal particles, cockroach
residues, animal dander, moulds, and pollens). In allergic
individuals, the T cells infiltrating the nasal mucosa are
predominantly T helper 2 (Th2) in nature and release cytokines
(e.g., interleukin [IL]-3, IL-4, IL-5, and IL-13) that promote
immunoglobulin E (IgE) production by plasma cells. Crosslinking
of IgE bound to mast cells by allergens, in turn, triggers the release
of mediators, such as histamine and leukotrienes, that are
responsible for arteriolar dilation, increased vascular permeability,
itching, rhinorrhea, mucous secretion, and smooth muscle
contraction in the lung. The mediators and cytokines released
during the early phase of an immune response to an inciting allergen
trigger a further cellular inflammatory response over the next 4–8 h
(late-phase inflammatory response) which results in recurrent
symptoms (usually nasal congestion) that often persist (Small,
2018)

g. Clinical manifestation
41
 Answer:
Allergic rhinitis (AR) is an atopic disease characterized by
symptoms of nasal congestion, clear rhinorrhea, sneezing, and nasal
pruritis (Akhouri, 2020).
- Sneezing
- Rinore
- Nasal Congstion
- Itching of the eyes and nose
- Many lacrimation (Rafi et al., 2015).
The typical symptom of allergic rhinitis is the presence of repeated
sneezing attacks. Actually sneezing is a normal symptom, especially in
the morning or when there is contact with large amounts of dust. This is a
physiological mechanism, i.e self-cleaning process. Sneezing is primarily
a symptom in RAFC and sometimes in RAFL as a result of the release of
histamine. Other symptoms are runny (runny nose) runny and many,
nasal congestion, itchy nose and eyes, which are sometimes accompanied
by lots of tears coming out (lacrimation). Often the symptoms that arise
are incomplete, especially in children. Sometimes. nasal congestion is the
main complaint or the only symptom expressed by the patient (Irawati et
al., 2016).

11. How is the treatment in the case?

Answer:
To treatment the disease in the case are:
a. Promotive, preventive
The most ideal therapy for allergic rhinitis patients is to avoid
contact with the allergens. Because the patient is a cleaning service
(allergic to dust), education can be given to avoid contact with dust
such as working with masks (Irawati et al., 2016).
b. Curative
• Topical corticosteroid→ Beclomethasone dipropionate: Given
100 mcg (2 sprays) into each nostril twice a day or 50 mcg (1
42
 sprays) into each nostril 3-4x a day; a maximum total of 400
mcg (8 sprays) per day.
• Then evaluated after 2-4 weeks. If it improves, move down to
the previous stage and continue treatment for 1 month.
• If it fails, then evaluate the diagnosis, evaluate compliance and
look for infections or other causes.
a) Consider sedentary immunotherapy. The way this treatment
is carried out on inhalant allergies with severe symptoms and
has lasted a long time, as well as with other methods of
treatment do not give satisfactory results. The goal of
immunotherapy is the formation of igG blocking antibodies
and decreased IgE. There are 2 common methods of
immunotherapy, intradermal and sublingual.
b) Increased use of topical corticosteroids.
c) Rinorrhea → ipratropium bromide: to treat rhinorrhea that is
accompanied by rhinitis, a dose of 42 micrograms is given for
each nostril 2-3 times a day up to 84 micrograms for 4 days if
cold symptoms are present or for 3 weeks if allergic rhinitis is
accompanied.
d) Nasal itching/sneezing → topical corticosteroids +
Antihistamin
e) Fixed nasal obstruction → Decongestants (3-5 days):
Pseudoefedrin 4x 60 mg or oral corticosteroids (short term)
→ if failed: surgical referral
f) Conjunctivitis → antihistamin: Cetirizine 1x 5-10 mg
(Irawati et al., 2016).
c. Operative
Partial conjunctomy (partial inferior concha cutting),
concopiasti or multiple outfractured, inferior turbinoplasty need
to be considered if inferior concha hypertrophy is severe and
cannot be minimized by means of cauterization using 25%
AgNO3 or trichlor acetate (Irawati et al., 2016).
43
 Source: (Irawati et al., 2016).

12. What is the complication in the case?

Answer:
The complications of the disease are (Irawati et al., 2016):
1. Nasal polyps, some researchers have found that nasal allergy is
one of the factors causing nasal polyp formation and recurrence of
nasal polyps
2. Effusion otitis media which is often residif, especially in children
3. Rhinosinusitis

13. What is the prognosis in the case?

Answer:
Quo ad vitam :Dubia ad bonam
Quo ad fungsionam :Dubia ad bonam
Quo ad sanationam :Dubia ad bonam

14. What is the SKDU in the case?

Answer:

44
 Ability Level 4: diagnose, manage independently and completely.
4A. Competence achieved at the time of graduating doctor.
Competence achieved at the time of graduating doctor
Doctor graduates are able to make clinical diagnoses based on history
taking, physical examination and supporting examination results, as well
as proposing disease management or carrying out disease management
independently according to clinical tasks entrustable (entrustable
professional activity) during education and at ability assessment.

15. What is Islamic point of view?

Answer:

Meaning:
Islam is clean, then so be you guys are clean. Surely not enter paradise
except those who are clean (HR Bayhaqi).

Qs yunus 57

Meaning:
Hi people, you have come to teach you a lesson from your Lord and
healer for diseases in the chest and guidance and mercy for those who
believe.
2.7 Conclusion
Mr. Fazli, a 25 years old cleaning service complains sneezing
excessively, colds, itching of the eyes and nasal congestion because
of experiencing moderate-severe persistent allergic rhinitis.

2.8 Conceptual framework

45
 Atopy Factor from a Job: Cleaning Service
grandfather who has a
history of asthma Allergen exposure

Hipersensivity reaction type 1

Release of inflammatory
mediators

Release of histamine and

leukotrine

Allergic rhinitis

Sneezing excessively Colds (Rhinorrea) Itching of the eyes Nasal congestion

REFERENCES
46
Akhouri, S., Steven AH. 2020. Allergic Rhinitis. USA: StatPearls Publishing
LLC.
Baumann et al. 2015. Prevalence and Risk Factors For Allergic Rhinitis in Two
Resource Limited Settings in Peru with Disparate Degrees of
Urbanization. Clinical and Experimental Allergy. 45(1): 192-199.
Fauzi et al. 2015. Prevalence of Allergic Rhinitis based on World Health
Organization (ARIA-WHO) questionnaire among Batch 2010 Students
of the Faculty of Medicine Universitas Padjadjaran. Althea Medical
Jurnal 2(4): 620-624.
Guyton, AC. 2017. Buku Ajar Fisiologi Kedokteran. Edisi 12. Singapore:
Elsevier.
Huether, SE., Kathryn LM. 2017. Buku Ajar Patofisiologi. Edisi VI. Vol. 2.
Singapore: Elsevier.
Ilavarase, N. 2010. Prevalensi Gejala Rinitis Alergi di Kalangan Mahasiswa
Fakultas Kedokteran Universitas Sumatera Utara Angkatan 2007-
2009 : Cross Sectional Study. Medan: Fakultas Kedokteran
Universitas Sumatera Utara.
Irawati, N et al. 2016. Buku Ajar Ilmu Kesehatan Telinga Hidung Tenggorokan
Kepala dan Leher: Rinitis Alergi. Jakarta: Balai Penerbit FKUI. 128-
133.
Johansson, K et al. 2006. Otolaryngology Head and Neck Surgery: Allergic and
Nonallergic Rhinitis. Philadelphia: Lippincott Williams & Wilkins.
351-63.
Jones, Oliver . 2019. The Nasal Cavity. (Online)
https://teachmeanatomy.info/head/organs/the-nose/nasal-cavity/ [access
04 June 2020].
Klimek, L et al . 2019. ARIA Guideline 2019: Treatment of Allergic Rhinitis in the
German Health System. Allergo J Int 28: 255-276.
KKI (Konsil Kedokteran Indonesia). 2019. Standar Kompetensi Dokter Indonesia
Jakarta: Konsil Kedokteran Indonesia.
Kowalak et al. 2017. Pathophysiology Textbook. Jakarta: EGC.

47
Kurnia, FN et al. 2019. Faktor Pencetus Kejadian Alergi Pernapasan Pada
Pasien Dewasa di RSUPN Dr. Cipto Mangunkusumo. Jurnal
Sumberdaya Hayati. 5(2): 11-12.
Mescher, AL. 2017. Histologi Dasar Junqueira. Edisi 14. Jakarta: EGC.
Netter, FH. 2016. Atlas of Human Anatomy 25th Edition. Jakarta: EGC. 35-50.
Nisa, R. 2017. Kejadian Rinitis Alergi dengan Komplikasi Otitis Media Akut pada
Anak Usia 5 Tahun. Journal Medula Unila. 7(1): 55.
Nurjannah. 2011. Faktor Risiko Rinitis Alergi Pada Pasien Rawat Jalan Di
Poliklinik THT-KL Rumah Sakit Umum Daerah Zainoel Abidin
(RSUDZA) Banda Aceh Tahun 2011. Jurnal Kedokteran Syiah Kuala.
11(2): 60-65.
Price, SA., Lorraine, MW. 2015. Patofisiologi: Konsep Klinis Proses-proses
Penyakit. Jakarta: EGC.
Rafi, M et al. 2015. Gambaran Rinitis Alergi Pada Mahasiswa Fakultas
Kedokteran Universitas Riau Angkatan 2013-2014. Journal of Medical
FK Universitas Riau. 2(2): 1–11.
Rizqun. 2017. Kejadian Rhinitis Alergi dengan Komplikasi Otitis Media Akut
pada Anak Usia 5 Tahun. Journal Medula Unila. 7(1):54-55.
Scadding, GK. 2015. Optimal Management of Allergic Rhinitis. Archieve of
Disease in Childhood BMJ Journals. 100(6): 576-582.
Sheikh et al. 2018. Allergic Rhinitis Clinical Presentation. (Online)
https://emedicine.medscape.com [access 2 June 2020].
Sherwood, L. 2014. Fisiologi Manusia: dari Sel ke Sistem. Edisi 8. Jakarta: EGC.
Small, P et al. 2018. Allergic Rhinitis. Allergy, Asthma and Clinical Immunology.
14(2): 51.
Snell, RS. 2012. Anatomi Klinik untuk Mahasiswa Kedokteran. Jakarta: Penerbit
Buku Kedokteran EGC.
Sobiesk, JL., Sunil M. 2019. Anatomy, Head and Neck, Nasal Cavity. USA:
StatPearls Publishing LLC.
Soetjipto, D., Retno SW. 2016. Buku Ajar Ilmu Kesehatan Telinga Hidung
Tenggorokan Kepala dan Leher: Hidung. Jakarta: Balai Penerbit FKUI.
118-120.
48
Songu, M., Cemal C. 2009. Sneeze Reflex: Facts and Fiction. SAGE Journals.
3(3): 131-141.
Sudoyo, AW et al. 2017. Textbook of Internal Medicine Volume I edition VI.
Jakarta: Interna Publishing.
Supit, V et al. 2019. Hubungan Lama Kerja dengan Kejadian Rinitis Alergi pada
Pekerja Pabrik Roti di Manado. Jurnal Medik dan Rehabilitasi . 1(3): 1-
4.
Utama, DS. 2010. Hubungan Antara Jenis Aeroalergen Dengan Manifestasi
Klinis Rinitis Alergika. Semarang: Bagian Ilmu Kesehatan THT-KL FK
Undip.
Wang, DY. 2005. Risk Factors for Allergic, Genetic or Environmental Rhinitis.
Therapy and Clinical Risk Management. 115-123.
Wheatley, LM., Alkis T. 2015. Allergic Rhinitis. The New England Journal of
Medicine. 372(5): 456-463.

49