coughing and shortness of breath in children.docx

7/27/2019 COUGHING AND SHORTNESS OF BREATH IN CHILDREN.docx

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RESPIRATORY SYSTEM

PBL MODULE 2

COUGHING AND SHORTNESS OF BREATH IN CHILDREN

REPORT

BY GROUP B1

NAME:

MOHD ALIFF HALIMIE BIN MUSA C11108771

NAZIRUL MUNIR BIN ABU HASSAN C11108795

MUHAMMAD HAFIY BIN MOHD RUSLI C11108808

THIAGARAJAN A/L KANDAPAN C11108763

ELDIE RAHIM PRADANA C11108217

IIN BANISWARA C11108193

NEERMALADEVI PARAMASIVAM C11108755

NUR ADILAH BINTI SHAHARUDDIN C11108779

ZALIKHA BINTI MOHD NASIR C11108787

NURAYSHA BINTI NURULLAH C11108803

MEDICAL FACULTY

UNIVERSITAS HASANUDDIN

MAKASSAR 2010


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COUGHING AND SHORTNESS OF BREATH IN CHILDREN

Scenario

A 3 years old boy is taken to the hospital by his mother due to severe fever, the boy has not had

enough sleep since last night and getting very irritable. According to the mother, she has

frequently taken her boy to several doctors within the last 3 months for coughing and

unstoppable runny nose, sometimes even with difficulty in breathing. His last month recorded

body weight from POSYANDU was 10kgs. He is the third boy, the other two older brothers are

also experiencing similar problems, but as bad as this one.

Keyword

3 years old boy Severe fever Not had enough sleep and getting very irritable Coughing, unstoppable runny nose and difficulty in breathing for last 3 month Last month body weight is 10kgs Family history; elder brothers with similar symptoms

Clarification of Difficult Word

1. Irritable - Capable of reacting to stimulus/prone to excessive anger2. POSYANDU - Pos Layanan Terpadu3. Runny nose (Rhinorrhea) - Is any mucus-like material that comes out of the nose

Question

1. What is the appropriate weight for 3 years old boy?2. Why the boy getting very irritable?3. Classification of fever.4. What causes the unstoppable runny nose?5.

How comes only sometimes difficulty in breathing present?

6. How this case related with the brothers?7. What is the pathomechanism for all the symptoms?8. What is the relation between runny nose and difficulty in breathing?


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Differential Diagnosis

1. Allergic Rhinitis2. Common Cold3. Lung Tuberculosis4. Bronchitis

Answers

1. What is the appropriate weight for 3 years old boy?

According to WHO Child Growth Standards, the weight for 3 years old boy is between 12

- 16kg with mean weight of 14.343kg.


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2. Why this boy getting very irritable?

Irritable is a state of being overly sensitive to stimulation. The term irritable is used for

infants and young children. Children, who are irritable may, for example cry easily.

Irritability can be a very early sign of serious problems. Although irritability is not asymptom of any specific disease, it should arouse suspicion in the parent that something

might be wrong with the child, even though there not appear others symptoms yet.

The cause of irritability is hard to figure out in very young children who cannot talk.

Being overtired, hungry, teething, having soiled diapers and the need for attention may

cause mild irritable. Irritable may also as a response to pain, fright or discomfort. In

some cases, serious medical condition can cause irritability such as infection in any part

of body.

3. Classification of fever.

Normal body temperature: 36-37C Fever/ febrile : >37C Subfebrile : 37-38C Febris continue : >38C & fluctuate 38C & fluctuate >1C Febris intermittent : >38C & fluctuate >1C, tempt


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germ-fighting fluids will often be pushed into the nose - triggering the same kind of

mucus production that occurs during a cold. In many cases, however, parents can

identify the presence of a sinus infection by the length of time that mucus is being

produced in the child's nose. If the nasal discharge has been present for two weeks

without improvement, no matter what the color, the leakage could be the result of a

sinus infection a condition that may require a health care provider's attention and acourse of antibiotic treatment. A runny nose accompanied by severe sinus or facial

pressure or high fever also may signal a sinus infection.

Another major cause of runny nose in kids is allergic reaction, or "allergic rhinitis," in

which nasal tissues excrete mucus as an immunological response to antigenic particles

from plants, dust, pollen or other substances such as cat dander. Commonly known as

"hay fever," allergic rhinitis affects more than 15 percent of U.S. children. An allergy-

caused runny nose occurs in two basic modes: "seasonal" and "perennial." Seasonal

allergic rhinitis may attack a child's nasal passages during a particular season, usually

spring, summer or fall, in response to pollen or reproductive spores released by

vegetation. But some children are affected by allergic rhinitis regardless of the time of

year. For these victims of "perennial allergic rhinitis," the reason for the nasal discharge

may be household dust mites, mold or animal dander (dead skin and/or hair shed by

pets). In some cases, household irritants such as tobacco smoke or chemical-based

products may be responsible for a child's runny nose, and these substances should be

eliminated whenever possible.

5. How comes only sometimes difficulty in breathing present?

The episodes of difficulty of breathing or dyspneu happen because during the onset of

the inflammation process, for example in an allergic reaction, asthma or infection

attack, the airways become inflamed and narrower as the muscles surrounding them

constrict. The flow of air is blocked partially or completely as mucus produced by the

inflammation fills a narrower passageway. This mechanism is severe only at the onset of

inflammation reaction and has the restriction affect on the airway. That way this child

only has recurrent episodes of difficulty in breathing.

Increasing of nasal drips also can lead to obstruction of the airway. These happen whenthe mucus has move backflow to the pharynx or opening of larynx and then

accumulated there. This also will narrow the airway and cause difficulty in breathing or

dyspneu.


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6. How this case related with the brothers?

In disease that has suffered in the members of family, there are two possible etiologies

for that disease. Ether is because of infection or it related to the genetic factors.

In this case, the only possible factor is infection. This is because the infection of therespiratory track is very easy to transmit usually through air as droplet. So, the

possibility of one of family member to spread the disease to other members is very high.

According to the scenario, the patient is a youngest brother and affected most severely

compared with the others two older brothers. This is because in immunity defense

system of this boy is not yet well develops.

Besides that, the possibility for this child and two others brother suffered this disease

because of genetic factor is very low. This can be explaining by the mechanism of

recessive and dominant inheritance.

In recessive inheritance, both parents carry a normal gene (N), and a faulty,recessive gene (n). The parents, although carries are unaffected by the faultygene. Their offspring are affected, not affected or just carriers.

In dominant inheritance, one parent has a single, faulty dominant gene (D),which overpowers its normal counterpart (d), affecting that affecting that

parent. When the affected parent mates with an unaffected and non-carrier

mate (dd), the offspring are either affected or not affected, without the carriers.


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7. What is the pathomechanism for all the symptoms?

Dyspnea

Pathophysiology of Dyspnea

Dyspnea is the experience of shortness of breath. It may or may not be

associated with suffering. A runner in a race may be severely dyspneic and yet be

enjoying life. A dyspneic patient dying with lung cancer with very similar

physiologic parameters may be suffering greatly, as the meaning and context of

the dyspnea are entirely different.

Respiration as a bodily function is virtually unique in the degree to which it is

under both reflexive and volitional control. The survival advantage of such a

control is obvious. We continue to breath when deeply asleep (or in a coma),and yet we can hold our breath, if need be, to escape through smoke or water.

Perhaps because of this, the linkage between psychological states and breathing

is tighter and more complex than it is for other physical symptoms. Dyspnea is

often associated with panic and anxiety; panic may present as dyspnea, and

dyspnea may induce panic.

My education about dyspnea, brief as it was in medical school, stressed the

importance of blood gases. I learned that CO2 build-up and oxygen deprivation

were the critical factors that result in dyspnea. Although undoubtedly important

in keeping the body alive, their importance in the experience of dyspnea has

been exaggerated. If an oxygen saturation monitor is attached to a dyspneic

runner at the end of a race, it will register normal. This reveals an important

clinical pearl: oxygen saturation is insensitive in identifying patients with

dyspnea. That is, one cannot rely on the oxygen saturation to tell who is

dyspneic. Patients can be very dyspneic with normal saturations. Of course,

patients with low oxygen saturations (below 90%) are far more likely to be

dyspneic than are patients with normal saturations. However, oxygen saturation

also lacks specificity as a predictor of dyspnea; many patients with low oxygen

saturations (for example, patients with chronic lung disease or those who live at

high altitude) will not be dyspneic, especially at rest. Studies have suggested that

hypoxia correlates best with exertional dyspnea and poor exercise tolerance.Conversely, oxygen therapy has been shown to be a most helpful method to

relieve exertional dyspnea and improve exercise tolerance. Studies have been

mixed in testing the relief of rest dyspnea associated with hypoxia with oxygen

therapy.Oxygen levels are excellent indicators of changing pulmonary

physiology. The implications of the lack of sensitivity and specificity of oxygen

saturation in identifying dyspnea are profound. As with pain, we lack a "scanner"


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for dyspnea that can reliably identify who is short of breath. We have no choice

but to ask if dyspnea is present, or at least look for signs of distress that might

suggest dyspnea, such as rapid respirations or a look of panic. In fact, the oxygen

saturation meter can cause dyspnea by inducing panic and fear in patients,

family, and clinicians as the saturation number falls (often accompanied by an

ominously lower-pitched beeping tone).

Palliative Care Note

Oxygen saturation cannot be depended upon to identify dyspnea. Patient report

or signs of agitation or anxiety are the best means of identifying dyspnea.

Elevations in carbon dioxide levels appear to stimulate dyspnea more than do

low oxygen levels. Elevated partial pressure of arterial carbon dioxide (PaCO2)

levels have been found to be an independent stimulus of dyspnea.However,

increased respiratory drive does not necessarily result in dyspnea if it occurs

unimpeded. Patients with certain forms of increased respiratory drive, such as

diabetic ketoacidosis and pregnancy, may not experience dyspnea. What does

cause dyspnea is an imbalance between the perceived need to breathe and the

perceived ability to breathe. Elevated PaCO2 levels may be one among a number

of factors that contribute to the brain's perception of a need to breathe.

Palliative Care Note

Dyspnea results when there is an imbalance between the perceived need to

breathe and the perceived ability to breathe.

Recent studies have suggested that the body's ability to determine whether

breathing is occurring normally relies on considerably more than high CO2 levels

or low oxygen levels.64

Nerves in the nose sense the passage of air. Stretch

receptors in and about the lungs signal expansion and contraction of the lungs.

Thoracic muscles and ribs signal that they are moving, a good sign breathing is

occurring normally. These nerves tell the brain "all is well" and allow respirations

to continue automatically and largely unconsciously in the nondyspneic person.

The brain senses no imbalance between the ability to breathe and the need to

breathe. If there is a sudden cessation of airflow or respiratory muscle

movement, as measured by these nerves, the brain quickly goes into alarm

mode - before any measurable change in blood gases occurs.


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Imagine you are being held one foot below water. Go ahead - hold your breath.

Note how quickly there is a desire to breathe. You can suppress this need for a

while, although it will build rapidly. (Your oxygen saturation may fall slightly and

your CO2 saturation may rise slightly by the time you must breathe, contributing

a bit to the need to breathe.) If you were truly underwater, you would panic

almost immediately. This psychological state would result in a severe imbalancebetween the perceived need to breathe and the perceived ability to breathe.

You would desperately struggle to get to the surface. When you finally breathe

again, notice how quickly your dyspnea is relieved. Do you really believe it was

because your blood gases were so quickly normalized?

Patients more commonly are dyspneic while breathing. What is happening here?

The perception of respiratory fatigue is a key component. Although our

understanding of both peripheral and central receptor involvement in fatigue is

poor, it is clear that the brain is able to sense fatigue, much as you can sense any

overworked muscle. However, unlike wobbly leg muscles that signal you to stop

running, tired thoracic muscles must continue to work in an attempt to meet a

perceived need to breathe. The brain senses a mismatch: the need to breathe

continues, but the ability of the body to meet that need with tired muscles is in

doubt. Dyspnea is a wake-up call to this mismatch.

Short of altering lung physiology, how can this mismatch be addressed?

Decreasing the perceived need through energy conservation can help. Patients

with emphysema, who have minimal thoracic expansion, may ventilate

adequately but receive a signal from the thoracic muscles that they are not

moving enough, much as in the underwater example above. A number of studies

have demonstrated that fooling these muscles by activating vibrating devicesduring inspiration can lessen dyspnea.

65-67The perception that the body is not

able to meet this need can also be addressed by inhibiting the perception of

muscular fatigue with opioids and other drugs (see below).

As should have been apparent in the breath-holding experiment, perceived need

is also intimately connected to the psyche. Perceived need and perceived

inability to meet that need can quickly result in panic. Panic, in turn, can

stimulate increased ventilatory effort, which can result in more fatigue and

increased panic - a vicious cycle. Panic, fear, and anxiety are common affective

components of dyspnea. Beyond shear panic, dyspneic patients think about what

their dyspnea means. Does dyspnea reflect a good run, as it might to a jogger, or

impending death? If dyspnea occurs with increasingly mild exertion, the patient

is reminded of growing dependence on others. As with other symptoms, patients

monitor the trend of their dyspnea - is it getting better or worse? One reason the

runner does not suffer from dyspnea is that he or she knows it will end when the

running ends. The patient dying of COPD or lung cancer projects into a future

wherein dyspnea worsens. These cognitive processes commonly trigger affective


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responses. In addition to panic, fear, and anxiety, patients may become

depressed and angry.

Fever

Pathogenesis of Fever

Pyrogens

The term pyrogen is used to describe any substance that causes fever.

Exogenous pyrogens are derived from outside the patient; most are microbial

products, microbial toxins, or whole microorganisms. The classic example of an

exogenous pyrogen is the lipopolysaccharide (endotoxin) produced by all gram-

negative bacteria. Pyrogenic products of gram-positive organisms include the

enterotoxins of Staphylococcus aureus and the group A and B streptococcal

toxins, also called superantigens.

Pyrogenic Cytokines

Cytokines is a small proteins that regulate immune, inflammatory, and

hematopoietic processes. For example, the elevated leukocytosis seen in severalinfections with an absolute neutrophilia is the result of the cytokines interleukin

(IL) 1 and IL-6. Some cytokines also cause fever; formerly referred to as

endogenous pyrogens, they are now called pyrogenic cytokines. The pyrogenic

cytokines include IL-1, IL-6, tumor necrosis factor (TNF), ciliary neurotropic factor

(CNTF), and interferon (IFN). (IL-18, a member of the IL-1 family, does not appear

to be a pyrogenic cytokine.) Other pyrogenic cytokines probably exist

A wide spectrum of bacterial and fungal products induces the synthesis and

release of pyrogenic cytokines, as do viruses. However, fever can be a

manifestation of disease in the absence of microbial infection. For example,

inflammatory processes, trauma, tissue necrosis, or antigen-antibody complexes

can induce the production of IL-1, TNF, and/or IL-6, whichindividually or in

combinationtrigger the hypothalamus to raise the set point to febrile levels.


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Elevation of the Hypothalamic Set Point by Cytokines

During fever, levels of prostaglandin E2 (PGE2) are elevated in hypothalamic

tissue and the third cerebral ventricle. The concentrations of PGE2 are highest

near the circumventricular vascular organs (organum vasculosum of lamina

terminalis)networks of enlarged capillaries surrounding the hypothalamic

regulatory centers. Destruction of these organs reduces the ability of pyrogens

to produce fever. Thus, it appears that both exogenous and endogenous

pyrogens interact with the endothelium of these capillaries and that this

interaction is the first step in initiating feveri.e., in raising the set point to

febrile levels.

Pyrogenic cytokines such as IL-1, IL-6, and TNF are released from the cells and

enter the systemic circulation. Although the systemic effects of these circulating

cytokines lead to fever by inducing the synthesis of PGE2, they also induce PGE2

in peripheral tissues. The increase in PGE2 in the periphery accounts for the

nonspecific myalgias and arthralgias that often accompany fever. It is thought

that some systemic PGE2 escapes destruction by the lung and gains access to the

hypothalamus via the internal carotid. However, it is the elevation of PGE2 in the

brain that starts the process of raising the hypothalamic set point for core

temperature.

There are four receptors for PGE2, and each signals the cell in different ways. Ofthe four receptors, the third (EP-3) is essential for fever: when the gene for this

receptor is deleted in mice, no fever follows the injection of IL-1 or endotoxin.

Deletion of the other PGE2 receptor genes leaves the fever mechanism intact.

Although PGE2 is essential for fever, it is not a neurotransmitter. Rather, the

release of PGE2 from the brain side of the hypothalamic endothelium triggers the

PGE2 receptor on glial cells, and this stimulation results in the rapid release of

cyclic adenosine 5'-monophosphate (cyclic AMP), which is a neurotransmitter


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Cough

A cough is a sudden and often repetitively occurring reflex which helps to clear

the large breathing passages from secretions, irritants, foreign particles and

microbes. The cough reflex consists of three phases: an inhalation, a forced

exhalation against a closed glottis, and a violent release of air from the lungs

following opening of the glottis, usually accompanied by a distinctive sound.

Coughing can happen voluntarily as well as involuntarily.

Frequent coughing usually indicates the presence of a disease. Many viruses and

bacteria benefit evolutionarily by causing the host to cough, which helps to

spread the disease to new hosts. Most of the time, coughing is caused by a

respiratory tract infection but can be triggered by choking, smoking, air pollution

asthma, gastroesophageal reflux disease, post-nasal drip, chronic bronchitis,

heart failure and medications such as ACE inhibitors.

Treatment should target the cause by for example smoking cessation or

discontinuing ACE inhibitors. Some people may be worried about serious

illnesses, and reassurance may suffice. Cough suppressants such as codeine or

dextromethorphan are frequently prescribed, but have been demonstrated to

have little effect. Other treatment options may target airway inflammation or

may promote mucus expectoration. As it is a natural protective reflex,

suppressing the cough reflex might have deleterious effects, especially if the

cough is productive.

Mechanism of productive cough

Cough is an important defence mechanism of the body. It serves to clear the

airway of excessive secretions and foreign matter. It can be either voluntary or

involuntary. As a reflex, it is activated when:

There is either inhaled particulate matter or irritant gases in the airway(certain gases such as ammonia, nitric acid and sulfuric acid and nitrogen

dioxide can irritate the airway)

There is a large amount of mucus in the airway (either because ofexcessive secretion or impaired clearance)

There is a large amount of edema or pus in the airway Thermal stimuli (very hot or very cold air can sometimes trigger the

cough reflex but, usually, this only occurs in people who already have

some pathology in the lungs)


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The cough reflex includes transmission of impulses via afferent (sensory)

neurons from specialized receptors located in respiratory tissue to a central

cough center, then transmission of nerve impulse from the central cough center

via efferent (motor) neurons back out to respiratory muscles. Cough receptors

are located within the epithelial layer of respiratory tissue. There are both

mechanical receptors and chemical receptors. The mechanical receptors aresensitive to touch and displacement and are located primarily in the larynx,

trachea, and carina. Chemical receptors are sensitive mostly to noxious gases

and fumes. These receptors are located more in the larynx and bronchi.

Receptors are found in respiratory bronchioles. but extend no further down the

respiratory tree then this. Cough receptors tend to become less sensitive when

continuously stimulated.

Cough receptors send their impulses to a central cough center via the vagus

nerve, the glossophayrngeal, trigeminal and phrenic nerves. The vagus may also

send messages to the cough center from higher centers of the brain. These

additional vagal afferents may be able to suppress the cough center. So, in one

respect, vagal afferents (directly from the receptors in respiratory tissue)

stimulate the cough center; in another respect, other vagal afferents (originating

from a higher center in the brain) can suppress the cough center.

There is much debate about where the central cough center in the brain is

located. Most likely it is not one single center, but rather is distributed

throughout the brain in a few locations spread out through the medulla

oblongata of the brainstem . The efferent nerves that carry impulses from the

cough center to the muscles that will result in a cough include the phrenic nerve

and the efferent branches of the vagal nerve.

An effective cough depends on an interaction between the volume of gas that is

inhaled and the properties of the mucus lining the airways. To begin with there is

an initial inspiration of air (ranging from 50% of tidal volume to 50% of vital

capacity). This volume of air stretches the expiratory muscles (like a rubber band

getting ready to snap back). When the muscles start to snap back (beginning of

expiratory phase), the glottis closes very briefly (this increases pressure in the

lungs even more so, so that when the glottis opens the air is expelled with a

greater force), then the glottis opens and the air is expelled (cough). The purpose

of the cough is to remove mucus, so the properties of the mucus also contribute

to the effectiveness of the cough. Mucus is most effectively dispersed in the

expelled volume of air if it contains a large amount of water.


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8. What is the relation between runny nose and difficulty in breathing?

Runny nose is a condition where there is mucus secretion from the nasal cavity. This

condition is usually caused by infections. Hence, if postnasal drip occurs, whereby the

mucus from the nasal cavity drops back into the posterior of the throat, there are great

chances of inflammation of the upper airways due to the blockade caused by the

mucus. Hence, this will cause the obstruction of the airway and further causes

disturbance in gaseous exchange. As a result, dyspnea might occur.

Differential Diagnosis

Allergic Rhinitis Primary TB Common ColdBoy

3 years old Severe fever and

worsening at night XCough for 3

months XRunny nose for 3

months X XDifficulty in

breathing XUnderweight Inherited /Contagious Inherited Contagious Contagious


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Allergic Rhinitis

Introduction

Allergic rhinitis is an allergic reaction that happens when your immune system overreact

to substances that you have inhaled, such as pollen. The two types of allergic rhinitis are

seasonal allergic rhinitis (hay fever) and perennial allergic rhinitis, which occurs year-

round. Hay fever is caused by outdoor allergens. Perennial allergic rhinitis is caused by

indoor allergens such as dust mites, pet dander, and mold.

Symptoms of allergic rhinitis resemble a cold, but they are not caused by a virus the way

a cold is. When patient breathe in an allergen, their immune system springs into action.

It releases substances known as IgEs into nasal passages, along with inflammatory

chemicals such as histamines. The nose, sinuses, or eyes may become itchy andcongested. Scientists aren't sure what causes your immune system to overreact to an

allergen.

Allergic rhinitis is common, affecting about 1 in 5 Americans. Symptoms can be mild or

severe. Many people who have allergic rhinitis also have asthma.

Signs and Symptoms

Allergic rhinitis can cause many symptoms, including the following:

Stuffy, runny nose Red, itchy, and watery eyes

tears from the lacrimal sac into the nasal cavity. Excess tears flow through

nasolacrimal duct which drains into the inferior nasal meatus. This is the

reason the nose starts to run when a person is crying or has watery eyes

from an allergy, and why one can sometimes taste eye drops

Post-nasal drip Swollen eyelids Itchy mouth, throat, ears, and face Sore throat Dry cough Headaches, facial pain or pressure Partial loss of hearing, smell, and taste
http://en.wikipedia.org/wiki/Tearshttp://en.wikipedia.org/wiki/Tearshttp://en.wikipedia.org/wiki/Lacrimal_sachttp://en.wikipedia.org/wiki/Nasal_cavityhttp://en.wikipedia.org/wiki/Inferior_nasal_meatushttp://en.wikipedia.org/wiki/Inferior_nasal_meatushttp://en.wikipedia.org/wiki/Nasal_cavityhttp://en.wikipedia.org/wiki/Lacrimal_sachttp://en.wikipedia.org/wiki/Tears


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Fatigue Dark circles under the eyes

Causes

The body's immune system is designed to fight harmful substances like bacteria and

viruses. But in allergic rhinitis, the immune system overresponds to harmless substances

-- like pollen, mold, and pet dander -- and launches an assault. This attack is called an

allergic reaction.

Seasonal allergic rhinitis is caused by an allergic reaction to pollens and spores

(depending on the season and area) as they are carried on the wind. Sources include:

Ragweed -- the most common seasonal allergen (fall) Grass pollen (late spring and summer) Tree pollen (spring) Fungus (mold growing on dead leaves, common in summer)

Year-round allergic rhinitis is caused by an allergic reaction to airborne particles from

the following:

Pet dander Dust and household mites Cockroaches Molds growing on wall paper, house plants, carpeting, and upholstery

Risk Factors

Family history of allergies Having other allergies, such as food allergies or eczema Exposure to secondhand cigarette smoke Male gender

Diagnosis

In anamnesis, the question that should be asked are:

Do symptoms change depending on the time of day or the season?


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Do you have a pet? Have you made changes to your diet? Are you taking any medications?

We will perform a physical exam and may also recommend a skin test to find out what

patient is allergic to. In a scratch test, for example, small amounts of suspected allergensare applied to the skin with a needle prick or scratch. If there is an allergy, a hive

(swollen reddened area) forms within about 20 minutes. Sometimes a blood test may be

used to find out which allergens they react to.

With young children, it can help to watch what they do. For example, a child with

allergic rhinitis may wiggle his nose and push it upward with the palm of the hand.

Prevention

Preventing them exposure to allergens is the best way to control symptoms. These steps

may help

If patient have hay fever, during days or seasons when airborne allergens are high:

Stay indoors, and if possible, close the windows. Use an air conditioner. Avoid using fans that draw in air from outdoors. Don't hang laundry outside to dry. Bath or shower and change the clothes after being outside. Use a HEPA air filter in the bedroom.

If patient have perennial allergic rhinitis:

Cover the pillows and mattress with dust mite covers. Remove carpet; install tile or hardwood floors. Use area rugs and wash them

often in very hot water.

Keep pets out of the bedroom.

Use a HEPA filter on the vacuum. Use an air purifier. Wash bedding and toys such as stuffed animals in very hot water once a week.


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Treatment

The best way to reduce symptoms is to prevent exposure to allergens.

Drugs (such as antihistamines, decongestants, and nasal corticosteroid sprays) may help

control allergy symptoms. Some complementary and alternative therapies may also beused to treat the symptoms of allergic rhinitis.

Patient may recommend immunotherapy ("allergy shots"). This treatment includes

regular injections of an allergen, with each dose being slightly larger than the previous

dose. The immune system should gradually get used to the allergen so that it no longer

reacts to it.

In addition, certain lifestyle and dietary changes may help prevent or improve symptoms

of allergic rhinitis.

Medications

Depending on the type of allergic rhinitis patient have. If they have perennial allergic

rhinitis, we may need to take medication daily. If they have seasonal allergic rhinitis (hay

fever) we may start medications a few weeks before the pollen season begins.

Nasal corticosteroids

These prescription sprays reduce inflammation of the nose and help relieve sneezing,

itching, and runny nose. They are most effective at reducing symptoms, although we

may not see improvement for a few days to a week after patient start using them.

Beclomethasone (Beconase) Fluticasone (Flonase) Mometasone (Nasonex) Triacinolone (Nasacort)

Antihistamines

Antihistamines are available in both oral and nasal spray forms, and as prescription

drugs and over-the-counter remedies. Over-the-counter antihistamines are short-acting

and can relieve mild-to-moderate symptoms. All work by blocking the release of

histamine in the body.

Over-the-counter antihistamines -- Include diphenhydramine (Benadryl),chlorpheniramine (Chlor-Trimeton), clemastine (Tavist). These older

antihistamines can cause sleepiness. Loratadine (Claritin) and cetrizine (Zyrtec)

do not cause as much drowsiness as older antihistamines.


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Prescription antihistamines -- These medications are longer-acting than over-the-counter antihistamines and are usually taken once a day. They include

fexofenadine (Allegra).

Decongestants

Many over-the-counter and prescription decongestants are available in tablet or nasal

spray form. They are often used with antihistamines.

Oral and nasal decongestants -- Include Sudafed, Actifed, Afrin, Neo-Synephrin.Some decongestants may contain pseudoephedrine, which can raise blood

pressure. People with high blood pressure or enlarged prostate should not take

drugs containing pseudoephedrine. Nasal decongestants can cause "rebound

congestion," where the nasal passages swell. Avoid using nasal decongestants

for more than 3 days in a row and do not use them if patient have emphysema

or chronic bronchitis.

Leukotreine modifiers

These prescription drugs block the production of leukotreines, which are inflammatory

chemicals produced by the body. They are taken once a day and do not cause

sleepiness, and are also used to treat allergic asthma. Leukotreine modifiers include

montelukast (Singulair) and zafirlukast (Accolate).

Cromolyn sodium (NasalCrom)

This over-the-counter nasal spray prevents the release of histamine and helps relieve

swelling and runny nose. It is most effective when taken before symptoms start and may

needed to be used several times a day.

Nasal atropine

Ipratropium bromide (Atrovent) is a prescription nasal spray that can help relieve a very

runny nose. People with glaucoma or an enlarged prostate should not use Atrovent.

Eye drops

Antihistamine eye drops -- relieve both nasal and eye symptoms; examplesinclude azelastine, olopatadine, ketotifen, and levocabastine

Decongestant eye drops -- such as phenylephrine and naphazolineEye drops may cause stinging or even headache.


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Other Treatments

Allergy shots (immunotherapy) are often recommended to anyone 7 years and older

who has severe allergy symptoms or who also has asthma. Immunotherapy accustoms

the immune system to allergens through regular injections of small doses of an allergen

over a long period of time.

Nasal irrigation or nasal lavage can help reduce symptoms of allergic rhinitis, studies

show. The technique uses a neti pot, bulb syringe, or squeeze bottle to flush out nasal

passages with saline solution (salt water).

Prognosis and Complications

Chances are your symptoms of allergic rhinitis can be treated, but they will appear eachtime you are exposed to an allergen.

Although perennial allergic rhinitis is not a serious condition, it can interfere with many

important aspects of life. Depending on how severe your symptoms are, allergic rhinitis

can lead you to miss school or work. Medication may cause drowsiness and other side

effects. Your allergies could also trigger other conditions, such as eczema, asthma,

sinusitis, and ear infection (called otitis media). Seasonal allergies may improve as you

get older.

Immunotherapy (allergy shots) may cause uncomfortable side effects (such as hives and

rash) and may have dangerous side effects such as anaphylaxis. It often requires years oftreatment and is effective in about two-thirds of cases.


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Common Cold

Introduction

The common cold (viral upper respiratory tract infection (VURI), acute viralrhinopharyngitis, acute coryza, or cold) is a contagious, viral infectious disease of the

upper respiratory system, caused primarily by rhinoviruses and coronaviruses.[1]

Common symptoms include a sore throat, runny nose, and fever. There is no cure;

however, symptoms usually resolve spontaneously in 7 to 10 days, with some symptoms

possibly lasting for up to three weeks.

Signs and symptoms

Symptoms are cough, sore throat, runny nose, and nasal congestion; sometimes thismay be accompanied by conjunctivitis (pink eye ), muscle aches, fatigue, headaches,

shivering, and loss of appetite. Fever is often present thus creating a symptom picture

which overlaps with influenza. The symptoms of influenza however are usually more

severe. The common cold usually resolves spontaneously in 7 to 10 days, but some

symptoms can last for up to three weeks. In children the coughs lasts for more than 10

days in 35-40% and continue for more than 25 days in 10%.

Those suffering from colds often report a sensation of chilliness even though the cold is

not generally accompanied by fever, and although chills are generally associated with

fever, the sensation may not always be caused by actual fever. In one study, 60% ofthose suffering from a sore throat and upper respiratory tract infection reported

headaches,often due to nasal congestion.

Complications

The common cold can lead to symptoms of acute bronchitis, bronchiolitis, croup,

pneumonia, sinusitis, otitis media, or strep throat. People with chronic lung diseases

such as asthma and COPD are especially vulnerable. Colds may cause acute

exacerbations of asthma, emphysema or chronic bronchitis.
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Causes

Viruses

The common cold is due to a viral infection of the upper respiratory tract. The most

commonly implicated virus is a rhinovirus (30-50%), a type of picornavirus with 99known serotypes. Others include: coronavirus (10-15%), influenza (5-15%)

[4], human

parainfluenza viruses.

Risk factors

Spending time in an enclosed area with an infected person or in close contact withan infected person. Common colds are droplet-borne infections, which means that

they are primarily transmitted through breathing in tiny particles that the infectedperson emits when he coughs, sneezes, or exhales.

Frequently touching eyes, nose, or mouth with contaminated fingers. A history of smoking extends the duration of illness by about three days. Getting fewer than seven hours of sleep per night has been associated with a risk

three times higher of developing an infection when exposed to a rhinovirus.

Low blood vitamin D levels are associated with an increased the risk of getting acommon cold. Whether this relation is causal has yet to be determined.

Common colds are seasonal, occurring more frequently during winter outside oftropical zones. This is believed to be partly due to a change in behaviors such as

increased time spent indoors, which puts infected people in close proximity to other

people, rather than to exposure to cold temperatures.

Low humidity increases viral transmission rates

Pathophysiology
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The common cold is a disease of the upper respiratory tract

The common cold virus is transmitted mainly from contact with the saliva or nasalsecretions of an infected person, either directly, when a healthy person breathes in the

virus-laden aerosol generated when an infected person coughs or sneezes, or by

touching a contaminated surface and then touching the nose or eyes.

Symptoms are not necessary for viral shedding or transmission, as a percentage of

asymptomatic subjects exhibit viruses in nasal swabs. It is generally not possible to

identify the virus type through symptoms, although influenza can be distinguished by its

sudden onset, fever, and cough.

The major entry point for the virus is normally the nose, but can also be the eyes (in this

case drainage into the nasopharynx would occur through the nasolacrimal duct). From

there, it is transported to the back of the nose and the adenoid area. The virus then

attaches to a receptor, ICAM-1, which is located on the surface of cells of the lining of

the nasopharynx. The receptor fits into a docking port on the surface of the virus. Large

amounts of virus receptor are present on cells of the adenoid. After attachment to the

receptor, virus is taken into the cell, where it starts an infection. Rhinovirus colds do not

generally cause damage to the nasal epithelium. Macrophages trigger the production of

cytokines, which in combination with mediators cause the symptoms. Cytokines cause

the systemic effects. The mediator bradykinin plays a major role in causing the local

symptoms such as sore throat and nasal irritation.[4]

The common cold is self-limiting, and the host's immune system effectively deals with

the infection. Within a few days, the body's humoral immune response begins

producing specific antibodies that can prevent the virus from infecting cells.

Additionally, as part of the cell-mediated immune response, leukocytes destroy the virus

through phagocytosis and destroy infected cells to prevent further viral replication. In

healthy, immunocompetent individuals, the common cold resolves in seven days on

average.

Prevention

The best prevention is staying away from people who are infected, because the

overwhelming majority of infections are acquired by inhaling virus-laden air that an

infected person has coughed, sneezed, or breathed out.
http://c/Users/user/Desktop/Common_cold.html%23cite_note-Eccles2005-3http://c/Users/user/Desktop/Common_cold.html%23cite_note-Eccles2005-3http://c/Users/user/Desktop/Common_cold.html%23cite_note-Eccles2005-3http://en.wikipedia.org/wiki/Humoralhttp://en.wikipedia.org/wiki/Antibodieshttp://en.wikipedia.org/wiki/Leukocyteshttp://en.wikipedia.org/wiki/Leukocyteshttp://en.wikipedia.org/wiki/Antibodieshttp://en.wikipedia.org/wiki/Humoralhttp://c/Users/user/Desktop/Common_cold.html%23cite_note-Eccles2005-3


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Management

There are currently no medications or herbal remedies which have been conclusively

demonstrated to shorten the duration of illness. Treatment comprises symptomatic

support usually via analgesics for fever, headache, sore muscles, and sore throat.

Conservative

Treatments that help alleviate symptoms include simple analgesics and antipyretics such

as ibuprofen and acetaminophen / paracetamol. Evidence does not show that cold

medicines are any more effective than simple analgesic. and are not recommended for

use in children due to no evidence supporting their effectiveness and the potential of

harm.

Getting plenty of rest, drinking fluids to maintain hydration, and gargling with warm salt

water, are reasonable conservative measures. Evidence for encouraging the active

intake of fluids in acute respiratory infections is lacking as is the use of heated

humidified air. Saline nasal drops may help alleviate nasal congestion.

Antibiotics and antivirals

Antibiotics are not effective against the viruses that cause the common cold and due to

their side effects cause overall harm. There are no approved antiviral drugs for the

common cold even though some preliminary research has shown benefit.

Alternative treatments

Main article: Alternative treatments used for the common cold

Many alternative treatments are used to treat the common cold. However, there is

insufficient scientific evidence to support the use of any alternative medicine

treatments. Honey may be an effective treatment of cough and improved sleep

difficulty in children more than no treatment or dextromethorphan.

Prognosis

The common cold is generally mild and self-limiting.
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Epidemiology

Upper respiratory tract infections are the most common infectious diseases among

adults, who have two to four respiratory infections annually. Children may have six to

ten colds a year (and up to 12 colds a year for school children). In the United States, the

incidence of colds is higher in the fall (autumn) and winter, with most infectionsoccurring between September and April. The seasonality may be due to the start of the

school year, or due to people spending more time indoors (thus in closer proximity with

each other) increasing the chance of transmission of the virus.

Lung Tuberculosis

Introduction

Tuberculosis (TB) is another example of a lower respiratory tract infection. It is caused

by the microorganism Mycobacterium tuberculosis, which usually infects by inhalation

of droplets, person to person, and colonizes the respiratory bronchioles or alveoli. It can

also enter the body through the gastrointestinal tract, by means of ingestion of

contaminated unpasteurized milk, or, occasionally, through a skin lesion.

After nearly 30 years of decline, starting in the mid-1980s, the number of cases of

tuberculosis diagnosed in the United States began to climb. Reasons for this includedincreasing numbers of immigrants from areas where tuberculosis is endemic, increased

poverty and homelessness in this country, and the advent of HIV/AIDS and a surge of

immunocompromised persons. Although this increase has begun to taper off, the U.S.

Center for Disease Control and Prevention noted that despite a low TB rate reported in

2004 (4.9 cases per 100,000 population), the rate of decline for 2003 and 2004 were the

smallest since 1993.

If a significant amount of the mycobacterium bypasses the defense mechanisms of the

respiratory system and successfully implants in the lower respiratory tract, the host

mounts a vigorous immune and inflammatory response. Because of this vigorousresponse, which is primarily T-cell mediated, only approximately 5% of people exposed

to the bacillus develop active tuberculosis. Only those individuals who develop an active

tuberculin infection are contagious to others and only during the time of active

infection.


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Racial and Ethnic Implications

TB rates greater than the U.S. average were observed in certain racial/ethnic

populations in 2004: Hispanics, blacks, and Asians living in the U.S. have 7.5, 8.3, and

20.0 times higher frequency of infection than whites, respectively. In 2004, TB was

reported more frequently among Hispanics (an increase of 1.2% from 2003 to 2004)than among any other racial/ethnic population in the U.S. Slightly more than half

(53.7%) of U.S. cases were in foreign-born persons. To address the high rate of TB

among foreign-born persons living in the U.S., custom and immigration efforts are

directed to improve overseas screening of immigrants and refugees, strengthen the

current notification system about the arrival of those suspected of having TB, ensure

completion of treatment among TB patients who cross the border, test recent arrivals

from high-incidence countries for latent infection, and treat to completion. March 24 of

each year is being celebrated as World TB Day.

Risk Factors for Tuberculosis Exposure and Infection

Those most at risk of exposure to the bacillus are those living in close quarters with

someone who has an active infection. This includes homeless individuals living in

shelters where tuberculosis is present, as well as family members of infected individuals.

Children may be especially susceptible. Immigrants to this country from developing

nations frequently arrive with active or latent infection.

Also at risk of exposure to and development of tuberculosis are health care workers

caring for the infected, and those individuals using the same health care clinics or

hospital units as people who have active infection. Of those exposed to the bacillus,

individuals who have inadequate immune systems, including the undernourished, the

elderly and the young, individuals receiving immunosuppressant drugs, and those

infected with the human immunodeficiency virus (HIV), are most likely to become

infected. The virulence of the strain also affects transmission, with certain highly

infective strains identified. TB control is hindered by the emergence of multi-drug

resistance and the synergistic effect of HIV/AIDS. A significant number of TB cases in

Africa have been linked to HIV infection.

Immune Response to Tuberculosis

Because the tuberculosis bacillus is difficult to destroy once colonization of the lower

respiratory tract occurs, the goal of the immune response is to surround and seal off the

bacilli, rather than to kill them. The cell-mediated response involves T cells as well as

macrophages. Macrophages encircle the bacilli, after which T cells and fibrous tissue

wall off the bacilli and macrophage complex. This complex of bacilli, macrophages, T


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cells, and scar tissue is called a tubercle. The tubercle eventually becomes calcified and

is called Ghon's complex, which can be seen on chest radiograph. Before engulfment of

the bacteria is complete, the material liquefies. At this time, viable microorganisms can

gain access to the tracheobronchial system and spread airborne to infect others. Even

when adequately walled off, the bacillus may survive within the tubercle. It is believed

that because of this viability, approximately 5 to 10% of individuals who do not initiallydevelop tuberculosis may have a clinical demonstration of the disease at some other

time in their lives, perhaps when they have become immunocompromised by age, other

infection, or the need for anti-inflammatory medications. In fact, many if not most cases

of active tuberculosis occur in individuals whose primary infection occurred decades

earlier.

Among those infected, damage to the lung is caused by the bacilli as well as by a

vigorous immune and inflammatory reaction. Interstitial edema and permanent scarring

of the alveoli increase the distance for diffusion of oxygen and carbon dioxide,

decreasing gas exchange. Also, the deposition of scar tissue and production of tubercles

decrease surface area available for gas diffusion, decreasing diffusion capacity. If the

disease is extensive, abnormalities in the ventilation:perfusion ratio occur that can lead

to hypoxic vasoconstriction of pulmonary arterioles and pulmonary hypertension.

Decreased lung compliance occurs with scar tissue.

Multi-Drugs Resistant Tuberculosis

A recent worldwide and serious complication of tuberculosis is the development of

tuberculin bacilli resistant to many drug combinations. Resistance develops when

individuals do not complete the course of their therapy, and mutations of the bacillus

make it non-responsive to the antibiotics that were used for a short time. The tuberculin

bacillus mutates rapidly and often. Drug-resistant tuberculosis can also occur if an

individual cannot mount an effective immune response, for instance, as seen in AIDS

patients or in the malnourished. In these cases, antibiotic therapy is only partially

effective. Health care workers or others who are exposed to these strains of bacillus also

may develop drug-resistant tuberculosis, which can result in years of morbidity and

frequently even in death. Those who have multi-drug-resistant tuberculosis will need to

undergo more toxic and expensive treatments that are more likely to fail.

Clinical Manifestations

Clinical indications of tuberculosis may be absent with initial infection and may never be

present if active infection does not occur. If active tuberculosis develops, an individual

usually demonstrates the following:


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Fevers, especially in the afternoon. Malaise. Night sweats. Loss of appetite and weight loss. A productive, purulent cough accompanied by chest pain is common with active

infection.

Diagnostic Tools

A positive skin test for tuberculosis demonstrates cell-mediated immunity and isevidence only of previous exposure of the lower respiratory tract to the bacillus. It is

not evidence that active tuberculosis ever developed.

Active tuberculosis is diagnosed by collection of a sputum sample followed bymicroscopic examination for the presence of acid-fast bacilli or culturing of the cells

followed by identification and drug susceptibility testing of the isolates. Microscopysuffers from low sensitivity, especially in extrapulmonary tuberculosis and conditions

of low bacillus count, which are common among HIV-infected individuals. Sputum

culture of an actively infected individual will reveal the bacillus but takes a

significantly longer time to complete.

Drug-resistance testing is traditionally performed using conventional methods ineither solid or liquid media. More recently, molecular techniques based on PCR in

conjunction with electrophoresis, sequencing, or hybridization are being used to

detect gene mutations associated with the development of drug resistance. These

molecular techniques have been used to complement smear results and clinical

diagnosis.

Chest radiograph demonstrates current or previous tubercle formation.

Complications

Severe disease may lead to overwhelming sepsis, respiratory failure, and death. Multi-drug-resistant TB may develop. Passage to others of the drug-resistant strain

may occur.

Treatment

Treatment of individuals who have active tuberculosis is lengthy because the bacillusis resistant to most antibiotics and rapidly mutates when exposed to antibiotics to

which it is sensitive. Currently, treatment of individuals who have an active infection

includes a combination of four drugs and lasts at least 9 months or longer. If the

person does not respond to those drugs, other drugs will be tried and different

protocols will be followed.


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Individuals who develop a positive tuberculosis skin test after having beenpreviously negative, even if they show no symptoms of active disease, are usually

put on a 6- to 9-month antibiotic regimen to support their immune response and to

increase the likelihood that the bacillus will be eradicated completely.

If drug-resistant tuberculosis develops, more toxic drugs will be administered. Thepatient may be kept in the hospital or under some type of forced quarantine ifcompliance with the medical therapy is unlikely or impossible.

Bronchitis

Introduction

Bronchitis is an acute inflammation of the air passages within the lungs. It occurs when

the trachea (windpipe) and the large and small bronchi (airways) within the lungs

become inflamed because ofinfection or other causes.

The thin mucous lining of these airways can become irritated and swollen. The cells that make up this lining may leak fluids in response to the inflammation. Coughing is a reflex that works to clear secretions from the lungs. Often the

discomfort of a severe cough leads you to seek medical treatment.

Both adults and children can get bronchitis. Symptoms are similar for both. Infants usually get bronchiolitis, which involves the smaller airways and causessymptoms similar to asthma

Causes

Several viruses cause bronchitis, including influenza A and B, commonly referred to as

"the flu." A number ofbacteria are also known to cause bronchitis, such as Mycoplasma

pneumoniae, which causes so-called walking pneumonia. Bronchitis also can occur

when you inhale irritating fumes or dusts. Chemical solvents and smoke, including

tobacco smoke, have been linked to acute bronchitis. People at increased risk both of

getting bronchitis and of having more severe symptoms include the elderly, those withweakened immune systems, smokers, and anyone with repeated exposure to lung

irritants.
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Symptoms

Acute bronchitis most commonly occurs after an upper respiratory infection such as the

common cold or a sinus infection. You may see symptoms such as fever with chills,muscle aches, nasal congestion, and sore throat. Cough is a common symptom of

bronchitis. The cough may be dry or may produce phlegm. Significant phlegm

production suggests that the lower respiratory tract and the lung itself may be infected,

and you may have pneumonia. The cough may last for more than two weeks. Continued

forceful coughing may make your chest and abdominal muscles sore. Coughing can be

severe enough at times to injure the chest wall or even cause you to pass out. Wheezing

may occur because of the inflammation of the airways. This may leave you short of

breath.

Exams & Tests

Doctors diagnose bronchitis generally on the basis of symptoms and a physical

examination.

Usually no blood tests are necessary. If the doctor suspects the patient has pneumonia, a chest x-ray may be ordered. Doctors may measure the patient's oxygen saturation (how well oxygen is

reaching blood cells) using a sensor placed on a finger.

Sometimes a doctor may order an examination and/or culture of a sample ofphlegm coughed up to look for bacteria.

Treatment

By far, the majority of cases of bronchitis stem from viral infections. This means that

most cases of bronchitis are short-term and require nothing more than treatment of

symptoms to relieve discomfort.

Antibiotics will not cure a viral illness.o Experts in in the field of infectious disease have been warning for years that

overuse of antibiotics is allowing many bacteria to become resistant to the

antibiotics available.o Doctors often prescribe antibiotics because they feel pressured by people's

expectations to receive them. This expectation has been fueled by both

misinformation in the media and marketing by drug companies. Don't expect

to receive a prescription for an antibiotic if your infection is caused by a virus.

Acetaminophen (Feverall, Panadol, Tylenol), aspirin, or ibuprofen (Motrin, Nuprin,Advil) will help with fever and muscle aches.
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Drinking fluids is very important because fever causes the body to lose fluid faster.Lung secretions will be thinner and easier to clear when the patient is well

hydrated.

A cool mist vaporizer or humidifier can help decrease bronchial irritation. An over-the-counter cough suppressant may be helpful. Preparations with

guaifenesin (Robitussin, Breonesin, Mucinex) will loosen secretions;dextromethorphan-the "DM" in most over the counter medications (Benylin,

Pertussin, Trocal, Vicks 44) suppresses cough.
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coughing and shortness of breath in children.docx

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