Types of Tonsillitis: An Overview of Causes and Treatments
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Published: Wed, 30 May 2018
There are 2 main types of tonsillitis: acute and chronic. Acute tonsillitis can either be bacterial or viral in origin. Subacute tonsillitis is caused by the bacterium Actinomyces. Chronic tonsillitis can last for long periods of time if not treated, and is mostly caused by bacterial infection.
Symptoms of tonsillitis include a severe sore throat, (which may be experienced as referred pain to the ears), painful/difficult swallowing, coughing, headache, myalgia (muscle aches), fever and chills. Tonsillitis is characterized by signs of red, swollen tonsils which may have a purulent exudative coating of white patches (i.e. pus). Swelling of the eyes, face, and neck may occur.
In some cases, symptoms of tonsillitis may be confused with symptoms for EBV infectious mononucleosis, known colloquially as mono(US) or Glandular Fever (elsewhere). Common symptoms of Glandular Fever include fatigue, loss of appetite, an enlarged spleen, enlarged lymph nodes, and a severe sore throat, sometimes accompanied by exudative patches of pus.
It is also important to understand that symptoms will be experienced differently for each person. Cases that are caused by bacteria are often followed by skin rash and a flushed face. Tonsillitis that is caused by a virus will develop symptoms that are flu-like such as runny nose or aches and pains throughout the body. Even though the infection will not cure immediately, tonsillitis symptoms usually improve 2 or 3 days after treatment starts.
Acute tonsillitis is caused by both bacteria and viruses and will be accompanied by symptoms of ear pain when swallowing, bad breath, and drooling along with sore throat and fever. In this case, the surface of the tonsil may be bright red or have a grayish-white coating, while the lymph nodes in the neck may be swollen. The most common form of acute tonsillitis is strep throat, which can be followed by symptoms of skin rash, pneumonia, and ear infection. This particular strand of tonsillitis can lead to damage to the heart valves and kidneys if not treated. Extreme tiredness and malaise are also experienced with this condition with the enlargement of the lymph nodes and adenoids.
Chronic tonsillitis is a persistent infection in the tonsils. Since this infection is repetitive, crypts or pockets can form in the tonsils where bacteria can store. Frequently, small, foul smelling stones (tonsilloliths) are found within these crypts that are made of high quantities of sulfur. These stones cause a symptom of a full throat or a throat that has something caught in the back. A foul breath that is characterized by the smell of rotten eggs (because of the sulfur) is also a symptom of this condition. Other symptoms that can be caused by tonsillitis that are not normally associated with it include snoring and disturbed sleep patterns. These conditions develop as the tonsils enlarge and begin to obstruct other areas of the throat. A person’s voice is generally affected by this type of illness and changes in the tone of voice a person normally has. While a person may only become hoarse, it is possible for laryngitis to develop if the throat is used too much while the tonsils are swollen or inflamed. Other uncommon symptoms that can be experienced with tonsillitis include vomiting, constipation, a tongue that feels furry or fuzzy, difficulty opening the mouth, headaches and a feeling of dry or cotton mouth.
Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils. The tonsils work by surrounding them with white blood cells which causes the body to develop a fever that can become extremely high in children. Should the infection become serious, the tonsils will inflame and become painful. The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.  This is the area in the back of the throat that lies between the voice box and the tonsils.
Tonsillitis may be caused by Group A streptococcal bacteria, resulting in strep throat. Viral tonsillitis may be caused by numerous viruses such as the Epstein-Barr virus (the cause of infectious mononucleosis) or adenovirus.
Sometimes, tonsillitis is caused by a infection of spirochaeta and treponema, in this case called Vincent’s angina or Plaut-Vincent angina.
Although tonsillitis is associated with infection, it is currently unknown whether the swelling and other symptoms are caused by the infectious agents themselves, or by the host immune response to these agents. Tonsillitis may be a result of aberrant immune responses to the normal bacterial flora of the nasopharynx.
The viruses that cause tonsillitis are often the ones that frequently affect the respiratory system or breathing. Most cases are caused by a virus and will only require treatment of sore throat remedies that can be bought over the counter. Bacteria-caused tonsillitis, however, is treated with prescribed antibiotic medication to reduce the risk for further complications. Tonsillitis most often affects children whose tonsils are responsible for fighting infections. This is also true because as we age, our tonsils become less active. Rare cases have been diagnosed with fungi or parasites being the cause. This generally takes place in persons with weakened immune systems.
There is no research to state that smoking cigarettes causes tonsillitis, however it is widely accepted that smoking weakens the immune system. Also, children and adults who live in a smoke-prone environment may be exposed to factors that could result in a tonsillectomy.
Treatments of tonsillitis consist of pain management medications and lozenges. If the tonsillitis is caused by bacteria, then antibiotics are prescribed, with penicillin being most commonly used. Erythromycin and Clarithromycin are used for patients allergic to penicillin.
In many cases of tonsillitis, the pain caused by the inflamed tonsils warrants the prescription of topical anesthetics for temporary relief. Viscous lidocaine solutions are often prescribed for this purpose, and anaesthetic throat lozenges containing benzocaine, lignocaine, benzydamine and flubiprofen are widely avaliable without prescription.
Ibuprofen or other analgesics such as aspirin or paracetamol can help to decrease the edema and inflammation, which will ease the pain and allow the patient to swallow liquids sooner.
When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, some rare infections may last for up to two weeks.
Chronic cases may indicate tonsillectomy (surgical removal of tonsils) as a choice for treatment.
Additionally, gargling with a solution of warm water and salt may reduce pain and swelling. If you are suffering from tonsilloliths (Tonsil stones) try to avoid dairy products like milk, ice cream, yogurt etc.
An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy). Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre’s syndrome).
In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years), or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are certainly still protected from infection by the rest of their immune system.
Bacteria feeding on mucus which accumulates in pits (referred to as “crypts”) in the tonsils may produce whitish-yellow deposits known as tonsilloliths. These may emit an odour due to the presence of volatile sulfur compounds.
Hypertrophy of the tonsils can result in snoring, mouth breathing, disturbed sleep, and obstructive sleep apnea, during which the patient stops breathing and experiences a drop in the oxygen content in the bloodstream. A tonsillectomy can be curative.
In very rare cases, diseases like rheumatic fever or glomerulonephritis can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations
Bronchitis is an obstructive respiratory disease that may occur in both acute and chronic forms.
Acute bronchitis: Inflammation of the bronchial passages most commonly caused by infection with bacteria or viruses. Acute bronchitis is generally a self-limiting condition in healthy individuals but can have much more severe consequences in individuals who are weakened with other illness or who are immunocompromised. Symptoms of acute bronchitis often include productive cough, dyspnea and possible fever.
Chronic bronchitis: Chronic bronchitis is a chronic obstructive pulmonary disease that is most frequently associated with cigarette smoking (approximately 90% of cases). Chronic bronchitis may also be caused by prolonged exposure to inhaled particulates such as coal dust or other pollutants. The disease is characterized by excess mucus production in the lower respiratory tract. This mucus accumulation can impair function of the ciliated epithelium and lining of the respiratory tract and prevent the clearing of debris and organisms. As a result, patients with chronic bronchitis often suffer repeated bouts of respiratory infection. Chronic bronchitis sufferers are often referred to as “blue bloaters” as a result of the cyanosis and peripheral edema that is often present.
Manifestations of chronic bronchitis
- Productive, chronic cough
- Production of purulent sputum
- Frequent respiratory infections
- Hypoxia, cyanosis
- Symptoms of cor pulmonale
- Fluid accumulation in later stages
Treatment of chronic bronchitis
- Cessation of smoking or exposure to irritants
- Bronchodilators to open airway passages
- Expectorants to loosen mucus
- Anti-inflammatories to relieve airway inflammation and reduce mucus secretion
- Prophylactic antibiotics for respiratory infections
- Oxygen therapy
Asthma is a condition characterized by reversible bronchospasm and chronic inflammation of airway passages. The incidence of asthma has been steadily increasing in recent years. Although the exact etiology is still uncertain, there appears to be a definite genetic predisposition to the development of asthma.
A key component of asthma appears to be airway “hyper reactivity” in affected individuals. Exposure to certain “triggers” can induce marked bronchospasm and airway inflammation in susceptible patients. Individuals with asthma appear to produce large amounts of the antibody IgE that attach to the mast cells present in many tissues. Exposure to a trigger such as pollen will result in the allergen-binding mast cell-bound IgE, which in turn causes the release of inflammatory mediators such as histamine, leukotrienes and eosinophilic chemotactic factor.
Some Potential Asthma Triggers
Allergens – Pollen, pet dander, fungi, dust mites
- Cold air
- Cigarette smoke
- Strong emotions
- Respiratory tract infections
Clinical Classification of Asthma
- Mild intermittent – Attacks occur 2 times per week or less
- Mild persistent – Attacks occur more than 2 times per week
- Moderate persistent – Attacks occur daily or almost daily and are severe enough to affect activity
- Severe persistent – Attacks are very frequent and persist for a long period of time; attacks severely limit activity
The response of a patient with asthma to these triggers can be divided into an “early phase” and a “late phase.”
Early phase of asthma: The early phase of asthma is characterized by marked constriction of bronchial airways and bronchospasm that is accompanied by edema of the airways and the production of excess mucus. The bronchospasm that occurs may be the result of the increased release of certain inflammatory mediators such as histamine, prostaglandins and bradykinin that, in the early stages of asthmatic response, promote bronchoconstriction rather than inflammation.
Late phase of asthma: The late phase of asthma can occur several hours after the initial onset of symptoms and manifests mainly as an inflammatory response. The primary mediators of inflammation during the asthmatic response are the white blood cells eosinophils that stimulate mast cell degranulation and release substances that attract other white cells to the area. Subsequent infiltration of the airway tissues with white blood cells such as neutrophils and lymphocytes also contributes to the overall inflammatory response of the late phase of asthma.
Manifestations of asthma
Rapid, shallow breathing
Increased respiratory rate
Excess mucus production
Barrel chest due to trapping of air in the lungs
Staging of the Severity of an Acute Asthma Attack
Stage I (mild)
Adequate air exchange
Stage II (moderate)
Respiratory distress at rest
Stage III (severe)
Marked respiratory distress
Marked wheezing or absence of breath sounds
Stage IV (respiratory failure)
Severe respiratory distress, lethargy, confusion, prominent pulsus paradoxus
Complications of asthma
Possible complications of asthma can include the occurrence of status asthmaticus, which is a life-threatening condition of prolonged bronchospasm that is often not responsive to drug therapy.
Pneumothorax is also a possible consequence as a result of lung pressure increases that can result from the extreme difficulty involved in expiration during a prolonged asthma attack. Marked hypoxemia and acidosis might also occur and can result in overall respiratory failure.
Treatment of asthma
The appropriate drug treatment regimen for asthma is based on the frequency and severity of the asthma attacks and may include the following:
Avoidance of triggers, and allergens.
Improved ventilation of the living spaces, use of air conditioning.
(Examples: albuterol, terbutaline) – Short acting Î’-adrenergic receptor activators. May be administered as needed in the form of a nebulizer solution using a metered dispenser or may be given subcutaneously. These drugs block bronchoconstriction but do not prevent the inflammatory response.
3. Xanthine drugs
(Example: theophylline) – Cause bronchodilation but may also inhibit the late phase of asthma. These drugs are often used orally as second-line agents in combination with other asthma therapies such as steroids. Drug like theophylline can have significant central nervous system, cardiovascular and gastrointestinal side effects that limit their overall usefulness.
4. Anti-inflammatory drugs
(Corticosteroids) – Used orally or by inhalation to blunt the inflammatory response of asthma. The most significant unwanted effects occur with long-term oral use of corticosteroids and may include immunosuppression, increased susceptibility to infection, osteoporosis and effects on other hormones such as the glucocorticoids.
5. Cromolyn sodium
Anti-inflammatory agent that blocks both the early and late phase of asthma. The mechanism of action is unclear but may involve mast cell function or responsiveness to allergens.
6. Leukotriene modifiers
(Example: Zafirlukast) – New class of agents that blocks the synthesis of the key inflammatory mediators, leukotrienes.
Emphysema is a respiratory disease that is characterized by destruction and permanent enlargement of terminal bronchioles and alveolar air sacs. Well over 95% of all patients with emphysema were chronic cigarette smokers. Although the exact etiology of emphysema is still uncertain, it appears that chronic exposure to cigarette smoke causes chronic inflammation of the alveolar airways, which results in infiltration by lymphocytes and macrophages. Excess release of protease enzymes such as trypsin from lung tissues and leukocytes can digest and destroy the elastic walls of the alveoli.
Alveolar air sacs become enlarged and distended as their structure is affected and their elasticity lost. Levels of a protective enzyme Î±-1-antitrypsin have been shown to be lacking in certain individuals who are chronic cigarette smokers. This enzyme inactivates destructive protease enzymes in lung tissue. In fact, a rare form of emphysema occurs in individuals who are not cigarette smokers but who have a genetic lack of Î±-1-antitrypsin.
Manifestations of emphysema: The major physiologic changes seen in emphysema are a loss of alveolar (lung) elasticity and a decrease in the overall surface area for gas exchange within the lungs.
Manifestations include the following:
Tachypnea (increased respiratory rate): Because the increased respiratory rate in these individuals is effective in maintaining arterial blood gases, one does not usually see hypoxia or cyanosis until the end stages of the disease. Patients with emphysema are often referred to as “pink puffers” because of their high respiratory rates and lack of obvious cyanosis.
Barrel chest from prolonged expiration
Lack of purulent sputum
Possible long-term consequences, including cor pulmonale, respiratory failure
Dyspnea that may be severe
Dry or no cough
Respiratory infection common
Onset usually after 40 years of age
Onset usually after 50 years of age
History of cigarette smoking
History of cigarette smoking
Cor pulmonale common
Cor pulmonale in terminal stages
Types of Emphysema
The bronchi and trachea are so sensitive to light touch that very slight amount of foreign matter or other causes of irritation initiate the cough reflex. The larynx and carina (the point where the trachea divides into the bronchi) are especially sensitive, and the terminal bronchioles and even the alveoli are sensitive to corrosive chemical stimuli such as sulphur dioxide gas or chlorine gas. Afferent nerve impulses pass from the respiratory passages mainly through the vagus nerves to the medulla of the brain. There, an automatic sequence of events is triggered by the neuronal circuits of the medulla, causing the following effect.
First, up to 2.5 liters of air are rapidly inspired. Second, the epiglottis closes, and the vocal cords shut tightly to entrap the air within the lungs. Third, the abdominal muscles contract forcefully, pushing against the diaphragm while other expiratory muscles, such as the internal intercostals, also contract forcefully. Consequently, the pressure in the lungs rises rapidly to as much as 100 mm Hg or more. Fourth, the vocal cords and the epiglottis suddenly open widely, so that air under this high pressure in the lungs explodes outward. Indeed, sometimes this air is expelled at velocities ranging from 75 to 100 miles per hour. Importantly, the strong compression of the lungs collapses the bronchi and trachea by causing their non-cartilaginous parts to invaginate inward, so that the exploding air actually passes through bronchial and tracheal slits. The rapidly moving air usually carries with it any foreign matter that is present in the bronchi or trachea.
Carbon monoxide (CO) is a colorless, odorless gas that is produced during the combustion of fuels such as gasoline, coal, oil, and wood. As you know, CO is a poison that may cause death if inhaled in more than very small quantities or for more than a short period of time. The reason CO is so toxic is that it forms a very strong and stable bond with the hemoglobin in RBCs (carboxyhemoglobin). Hemoglobin with CO bonded to it cannot bond to and transport oxygen. The effect of CO, therefore, is to drastically decrease the amount of oxygen carried in the blood. As little as 0.1% CO in inhaled air can saturate half the total hemoglobin with CO.
Lack of oxygen is often apparent in people with light skin as cyanosis, a bluish cast to the skin, lips, and nail beds. This is because hemoglobin is dark red unless something (usually oxygen) is bonded to it. When hemoglobin bonds to CO, however, it becomes a bright, cherry red. This color may be seen in light skin and may be very misleading; the person with CO poisoning is in a severely hypoxic state.
Although CO is found in cigarette smoke, it is present in such minute quantities that it is not lethal. Heavy smokers, however, may be in a mild but chronic hypoxic state because much of their hemoglobin is firmly bonded to CO. As compensation, RBC production may increase, and a heavy smoker may have a hematocrit over 50%.
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