ENT class_BMS250_February 12th.pptx

ENT class BMS250 Allergic Rhinitis and Complications Thiago Cavalcante, MD, ND Date: February 12th Learning Outcomes Describe the pathophysiology of allergic rhinitis, including the role of inflammation and immune system (IgE, mast cells), and relate to clinical features. Describe the risk factors a...

ENT class BMS250 Allergic Rhinitis and Complications Thiago Cavalcante, MD, ND Date: February 12th Learning Outcomes Describe the pathophysiology of allergic rhinitis, including the role of inflammation and immune system (IgE, mast cells), and relate to clinical features. Describe the risk factors and triggers for allergic rhinitis and chronic sinusitis, including the impact of intestinal bacterial, allergic diseases and intestinal permeability. Differentiate between allergic and non-allergic forms of rhinitis. Describe the complications of allergic rhinitis and its impact on patient's quality of life. Learning Outcomes Describe the pathophysiology and the etiology of chronic sinusitis and relate to clinical features. Describe the pathophysiology and etiology of nasal polyps, deviated septum and relate to their clinical features. Describe the pathophysiology and etiology of common disorders of the oral cavity, including pharyngitis, tonsillitis and aphthous ulcers and relate to their clinical features. Describe the pathophysiology and etiology of laryngitis, tracheitis and vocal cord disorders and relate to their clinical features, such as hoarseness and dysphagia. Pre-Assessment What is your understanding of the term "allergic rhinitis," and can you describe any elements pathophysiology that you are familiar with? of its In your own words, explain what you know about the risk factors and triggers associated with allergic rhinitis and chronic sinusitis. Are there any specific factors or connections you are aware of? Differentiate between allergic and non-allergic forms of rhinitis based on your current knowledge. What characteristics or features do you think distinguish these two conditions? Allergic Rhinitis Allergy is characterized by a heightened sensitivity to a foreign protein - referred to as an allergen - elicited through various modes of exposure, including ingestion, contact, or inhalation. Rhinitis is defined as an eosinophilic inflammation of the nasal mucosa and paranasal sinuses resulting from an IgE-mediated reaction. Allergic Rhinitis manifests as nasal congestion, obstructed airflow, increased mucous production, and drainage. These manifestations arise due to an unfavorable response to environmental or ingested stimuli. Allergic Rhinitis Pathophysiology: - The onset of allergic rhinitis in an atopic individual necessitates an initial phase of sensitization, succeeded by subsequent reexposure to a designated allergen. - Once happens sensitization, an antigen-presenting cell (such as dendritic cells, macrophages, or Langerhans cells assimilates a low-dose exposure of the antigen, subsequently presenting it to helper T lymphocytes. - Activated helper T lymphocytes produce cytokines, including IL4, IL-5 and IL-13, and engage with B lymphocytes, instigating the synthesis of allergen-specific IgE. - Upon subsequent exposure, the specific antigen binds to two distinct IgE antibodies affixed to the surface of mast cells, which are prevalent in the submucosa of respiratory and gastrointestinal tracts, the subconjunctiva of the eye, and the subcutaneous layer of the skin. - Subsequently, the allergen-specific IgE attaches to the high- Allergic Rhinitis Pathophysiology: - Following subsequent exposure, previously fixated IgE molecules identify allergens, triggering mast cell activation and the subsequent release of preexisting proinflammatory mediators, including histamine. - These released mediators initiate responses in blood vessels, nerves, and mucus glands, manifesting as the hallmark acute symptoms characteristic of allergic rhinitis, such as rhinorrhea, nasal congestion, nasal irritation, and sneezing. - Through crosslinking of allergen-specific IgE attached to mast cell surfaces by the respective allergen, mast cells undergo degranulation, releasing a spectrum of pre-formed and newly synthesized mediators, constituting the early phase response. - Histamine, a pivotal mediator in allergic rhinitis, stimulates the sensory nerve endings of the Vth nerve (trigeminal), eliciting sneezing. - Simultaneously, histamine, along with leukotrienes and prostaglandins, prompts mucous gland secretion (rhinorrhea), Allergic Rhinitis Pathophysiology: - Late phase response - 4-6 h after antigen stimulation. Prolongation of symptoms - sneezing, rhinorrhea, and mainly a sustained nasal congestion lasting for about 18-24 h. - Release of cytokines and leukotrienes leading to an influx of inflammatory cells (predominantly T lymphocytes, basophils and eosinophils) into the affected area (chemotaxis). - These cells release a variety of mediators such a leukotrienes, kinins, histamine contributing to symptom persistence and the progression of the late phase. - Mast cells production and release of cytokines like IL-4,IL-5, IL-13 are crucial to the orchestration of the late phase response. - The cytokines can upregulate the expression of 'adhesion molecules' like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. Allergic Rhinitis Allergic Rhinitis Etiology and Risk Factors: - AR is an inflammatory disease with complex physiopathology, which suggests that it is caused by a complex interaction between more than 100 genetic loci and a complex environment. - There are several well-known risk factors for allergic rhinitis, including atopy, asthma, eczema, and other allergies. - Parental history of allergic rhinitis, asthma, and pollen allergies is also a well-documented risk factor. - Food allergens such as milk, eggs, soy, and wheat, dust mites, and inhalant allergens such as pet dander most commonly cause allergic rhinitis in infancy and childhood along with comorbidities such as atopic dermatitis, otitis media, and asthma. - Pollen allergens become more significant in older children Allergic Rhinitis Etiology and Risk Factors - Gut microbioma: - Intestinal mucosa functions as a physiological functional unit that separates the gut from the inside environment of the body and provides protection, nutrition, and immune function. - There is evidence to suggest that gut microbiota may play a role in allergic disease pathogenesis. - Bacteria make up the gut microbiota, and the composition of the microbiota is highly dynamic and influenced by the host's diet. - There are four main classes of microbiomes: Bacteroidetes, Actinobacteria, Firmicutes, and Proteobacteria. - The formation, function, and regulation of the immune system are notably impacted by the ancient symbiotic relationship between humans and resident microorganisms, highlighting the pivotal role of the gut microbiota in allergic disorders. - An infant's diet, antibiotic use, habitat, and other environmental factors significantly alter the gut microbiome, leading to dysbiosis. Allergic Rhinitis Etiology and Risk Factors - Gut microbioma: - There has been increasing evidence that dysbiosis of gut microbiota is associated with atopy. - Additionally, the physiological features and immunological response crucial for the development of allergic disorders may be influenced by the gut microbiota in the human host. - As a consequence of various environmental and/or genetic factors causing gut dysfunction, Th1/Th2 homeostasis can be disrupted, affecting immunotolerance, disrupting allergen clearance, and increasing the risk of allergen rhinitis (AR). - It has been hypothesized that dysbiosis causes abnormal allergic reactions by shifting the immune response toward a Th2 response and the production of IgE in AR. - Probiotics may be one of the options clinicians may use to improve their patients' quality of life since treating AR is challenging. Allergic Rhinitis Allergic Rhinitis Etiology and Risk Factors - Gut microbioma: - Researchers found that in a fecal sample of 93 AR patients, the gut microbiome diversity had decreased, with an increased relative abundance of Bacteroidetes and decreased relative abundances of Actinobacterium, Proteobacterium, and Escherichia coli. - In addition, S. Shigella. E. coli, Parabacteroides, Lachnoclostridium, and Dialister were all identified as possible biomarkers for AR. - In AR patients, the Chao1 and Shannon diversity indices, nonparametric methods for estimating species diversity, were significantly lower. Bacteroidetes were particularly abundant in AR individuals, in contrast with Firmicutes. - In addition, Parabacteroides were increased in AR patients, while Oxalobacter and Clostridiales decreased. - According to another study, patients with AR had a greater variety of bacteria than healthy controls; phyla Firmicutes, Fusobacteria, Actinobacteria, Cyanobacteria, and Chloroflexi were significantly different. - Although bacterial diversity did not differ significantly between moderate and severe AR patients, nasal symptoms were associated with Butyrococcus and Eisenbergiella levels, suggesting that Allergic Rhinitis Clinical Features - Symptoms: Clear and watery nasal discharge, nasal congestion, postnasal drip, and itching of the nose, throat, and eyes. - Physical examination: o Mouth breathing, frequent sniffling and/or throat clearing, transverse supra-tip nasal crease, and dark circles under the eyes (allergic shiners). o Anterior rhinoscopy - swelling of the nasal mucosa and thin, clear secretions. The inferior turbinates may take on a bluish hue, and cobblestoning of the nasal mucosa may be present. o Palpation of sinuses may elicit tenderness in patients with chronic symptoms. o Pneumatic otoscopy is a valuable method for evaluating eustachian tube dysfunction. o It is essential to thoroughly examine these patients for indications of dermatitis or asthma and inquire about any Allergic Rhinitis Classification - Seasonal Allergic Rhinitis - symptoms can occur or increase as a result of pollination of certain plants to which patients are allergic. - Perennial Allergic Rhinitis - symptoms are usually constant, without seasonal variation. However, the intensity may vary. *Dust mites, animal dander, mold spores, and cockroaches (in inner cities) are common indoor allergens that cause perennial allergic rhinitis. *Perennial allergic rhinitis can also be triggered by food allergens, infection and nonspecific irritants. Symptoms can also be aggravated by other irritants, such as tobacco smoke, chemical fumes, and air pollution. - Other classifications may involve temporal incidence and the quality of life: Symptoms are classified as being intermittent (< 4 days/week or < 4 weeks’ duration) or persistent (> 4 days/week or > 4 weeks’ duration); and by the intensity of the symptoms, with either Allergic Rhinitis Complications - Adenoid hypertrophy - the immune parameters of the adenoids can also be altered by sensitization to allergens in AR. - Eustachian tube dysfunction It manifests as ear fullness, otalgia, and ear-popping. Chronic rhinosinusitis characterized by nasal inflammation with nasal congestion or discharge lasting longer than 3 months. Adenoid hypertrophy Allergic Rhinitis Nasal polyp Complications - Nasal polyps - the paranasal sinus mucosa may become inflamed, resulting in nasal polyps (nasal polyposis). - Obstruction of osteomeatal drainage predisposes patients with chronic rhinitis to bacterial sinus infections - Sleep disruption - rhinitis can cause significant sleep disruption due to sleepdisordered breathing, obstructive sleep apnea, and snoring. - Learning disturbances children with AR may have significant cognitive, fatigue, Obstruction of osteomeatal drainage Nonallergic Rhinitis The most common symptoms of nonallergic rhinitis are nasal obstruction and clear rhinorrhea. Sneezing and itchy, watery eyes are not common symptoms. It has been found that nonallergic rhinitis is more prevalent with advancing age. It is always advisable to ask patients with nonallergic rhinitis about over-the-counter nasal sprays, previous trauma, work exposure, or intranasal drug use. It is important to pay attention to epistaxis, pain, and unilateral symptoms as signs of a neoplasm. Nonallergic Rhinitis Viral Rhinitis - This common form of rhinitis can often be accompanied by other symptoms of viral illness, such as headaches, malaise, body aches, and coughing. - Viral rhinitis is typically characterized by nasal drainage that is either clear or white and can be associated with nasal congestion and sneezing. Occupational Rhinitis - The nose may be affected by a variety of indoor and outdoor pollutants. A few examples are dust, ozone, sulfur dioxide, cigarette smoke, and garden sprays. - Dry nasal passages, reduced airflow, rhinorrhea, and sneezing are typical symptoms of these agents. Nonallergic Rhinitis Occupational Rhinitis - Exposure to wood particles and chronic cigarette smoke has been associated with reduced ciliary movements in the nose. - These patients require strict environmental control. - A protective mask, avoidance, improving ventilation, and removing the causal agent will help limit exposure. Vasomotor Rhinitis - Vasomotor rhinitis (VMR) or idiopathic rhinitis is the most common form of NAR observed clinically. Nasal symptoms persist or intermittently occur in response to environmental conditions that normally do not affect normal individuals. - A parasympathetic, sympathetic, and nociceptive nerve dysregulation may be associated with the cause of vasomotor rhinitis, although the etiology is unclear. Nonallergic Rhinitis Vasomotor Rhinitis - As a result of an imbalance among mediators, the submucosal nasal glands produce more mucus and vascular permeability increases. - Mucous secretion is predominantly governed by the parasympathetic nervous system, while vascular tone is regulated by the sympathetic nervous system. - Mucus secretion and rhinorrhea neurotransmitter - acetylcholine. - parasympathetic - Management of the vascular tone of nasal mucosa vessels and modulating secretions initiated by the parasympathetic system - sympathetic neurotransmitters - norepinephrine and neuropeptide Y. - Furthermore, mast cell degranulation and the induction of the sneezing reflex are attributed to sensory neuropeptides and nociceptive type C fibers of the trigeminal nerve. Nonallergic Rhinitis Vasomotor Rhinitis - It is generally considered to be a perennial pathology. There is a risk of misdiagnosis of allergic rhinitis when seasonal changes in barometric pressure, temperature, or humidity exacerbate vasomotor rhinitis. - The environmental triggers for vasomotor rhinitis can include strong odors, cold air exposure, alcohol consumption, and spicy foods. - Even in the absence of identified triggers, patients can still experience persistent symptoms. - By examining the clinical history and excluding all other causes, VMR can be diagnosed. Nonallergic Rhinitis Nonallergic Rhinitis with Eosinophilia (NARES) - Recently described syndrome of nasal obstruction and congestion, accompanied by severe exacerbations such as sinusitis and polyposis. - They also have nasal smears with marked eosinophilia (> 25%) but are not allergic to inhalant allergens when tested topically or in vitro. - NARES remains unknown in its cause. Rhinitis Medicamentosa - Topical nasal decongestants such as oxymetazoline and phenylephrine are the most common cause of rhinitis medicamentosa. - When using topical agents chronically, rebound nasal congestion can result in severe obstruction as the effects diminish. Nonallergic Rhinitis Rhinitis During Pregnancy - Throughout pregnancy, estrogen concentrations increase in the body. In the nasal tissue, estrogen increases the amount of hyaluronic acid, leading to nasal congestion and edema. - A decrease in nasal cilia and an increase in mucous glands during pregnancy contribute to nasal congestion, decreasing mucus clearance. - During the second and third trimesters of pregnancy, rhinitis is usually at the height of its severity. - Similar symptoms can appear premenstrually on a cyclical basis in some patients. Nonallergic Rhinitis Vasculitides, Autoimmune, and Granulomatous Diseases - A thorough head and neck exam should be conducted on patients with rhinitis. - It is also important to determine if there is evidence of saddling or trauma on the nose, which may indicate a septal deficiency. - There are a variety of systemic disorders that can exhibit symptoms of chronic inflammation, vasculitis, and septal perforation, such as Wegener granulomatosis and cocaine abuse. - It is important to note the size and character of turbinates and rhinorrhea as well. - The patient needs also to be assessed for nasal polyposis or other intranasal masses. Chronic Rhinosinusitis The term rhinosinusitis refers to inflammation of the sinuses and nasal cavity caused by symptomatic nasal congestion. A chronic rhinosinusitis is defined as an inflammation of the nasal cavity and paranasal sinuses lasting more than 12 weeks. There is a wide range of severity and prevalence of the signs and symptoms of CRS. There is a high rate of nasal obstruction (81% to 95%), followed by facial congestion, pressure, and fullness (70% to 85%), discolored nasal discharge (51% to 83%), and hyposmia (61%–69%). It is common to have fatigue and myalgias, although high fevers are rarely seen. Chronic Rhinosinusitis Pathophysiology and Etiology - It is possible for chronic inflammation to block the nasal passage, inhibit drainage, and reduce oxygen tension in the bloodstream. As a result, bacteria can grow in these foci. - This can be further aggravated by ciliary dysfunction or structural abnormalities. - The nasal mucosa thickens in this condition due to persistent hyperemia, hyperplasia of mucous glands and lymphocyte and plasma cell infiltration. Chronic Rhinosinusitis Pathophysiology and Etiology It has been hypothesized that CRS is caused by a variety of factors, including: - Biofilms - Through the release of planktonic bacteria and/or toxins, bacteria in biofilms can still induce inflammation in the host environment. It has been shown that biofilms adversely affect postoperative outcomes in patients with CRS. - Bacterial superantingens - patients who have CRS with nasal polyps may develop such polyps because of the formation of superantigenic exotoxins produced by S. aureus. A superantigen can activate the immune system, release cytokines, and promote inflammation, according to this theory. Chronic Rhinosinusitis Pathophysiology and Etiology - Osteitis - According to studies, CRS may spread through the bone's Haversian system to include other sinuses. Chronic inflammation in the underlying bone may persist even after aggressive treatment of the underlying sinus mucosa, contributing to some recalcitrant CRS. - Allergy - In patients with CRS, allergies are more common, and when present, they can exacerbate symptoms. - Barrier and innate immune dysregulation - With CRS, mucociliary clearance is impaired and tight junctions are diminished, with CRSwNP having an epithelial barrier that is more porous. In addition, dysbiosis of the sinonasal microbiome is exacerbated by defects in Chronic Rhinosinusitis Pathophysiology and Etiology - General host factors - CRS is significantly increased by genetic factors and immune deficiencies. A number of systemic diseases can cause diffuse inflammation of the sinonasal mucosa, including granulomatosis with polyangiitis (formerly Wegener granulomatosis), aspirin-exacerbated respiratory disease (AERD, formerly known as Samter's triad), cystic fibrosis, immunodeficiency, and primary ciliary dyskinesia. A cascade of dysfunctional mucociliary clearance, mucus stasis, and subsequent bacterial overgrowth can be caused by this inflammation. Medical and surgical treatment for CRS is more likely to fail in patients with these conditions. Chronic Rhinosinusitis Clinical Features - Purulent drainage: green or yellow nasal discharge - Facial/dental pain: aching, fullness or pressure-like pain - Nasal obstruction: difficulty breathing from one or both nasal passages or cause mouth breathing - A chronic sinusitis may also cause hyposmia (insufficient sense of smell), headaches, ear pain, halitosis (bad breath), dental pain, or fatigue. - Despite having a 50% sensitivity, fever is an important indicator of sinusitis severity. - One or more of the following findings should be observed during nasal endoscopy or anterior rhinoscopy, according to The American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS): purulent drainage, polyps, polypoid changes in the mucosa, and edema or erythema. Nasal Polyps Nasal polyps develop from the sinonasal mucosa, and are benign inflammatory and hyperplastic growths. Usually arising from the lateral nasal wall or the ethmoid recess, these polyps appear in the nose or sinuses. Whether unilateral or bilateral, they can be single or multiple. They contain plasma cells, lymphocytes, eosinophils, and mucous glands within a loose mucoid stroma lined by respiratory epithelium. Nasal Polyps Nasal Polyps Etiology/Pathophysiology - The majority of nasal polyps are due to T-helper 2 (Th2) celldriven eosinophilia, immunoglobulin E (IgE) inflammation, with elevated interleukin-5 (IL-5), often related to an allergic environment or season. - The human body undergoes anatomical and functional changes with age, resulting in a buildup of thick mucus and impaired clearance of irritants and biologic offenders (viruses, bacteria, fungi), which can cause polyps to form. - Among these changes are decreased ciliary beat frequency, impaired mucociliary clearance, sinonasal mucosa atrophy with decreased vasculature, and decreased mucus secretion. - Each of these could lead to an increase in epithelial basement membrane permeability and a distortion in the normal osmotic regulation between cells. - A localized increase of cell and tissue size results from overall edema and chronic inflammation. Nasal Polyps Clinical Features In patients experiencing progressive nasal obstruction, nasal and/or facial congestion, decreased sense of smell and rhinorrhea (cardinal symptoms of CRS), nasal polyposis should be suspected. - It is important to conduct a physical examination that includes an anterior rhinoscopy, which can reveal polyps and other benign tumors. - The diagnosis of nasal polyposis can be made using anterior rhinoscopy or nasal endoscopy. Deviated septum A nasal septum is a 1 3 2 4 wall composed of osteocartilaginous tissue that separates two nasal cavities within the nose. In most cases, asymptomatic minor deviations of the septum are considered normal developmental variations. The degree of the deviation may affect nasal airflow in some patients, causing obstruction or impairing olfactory 5 Deviated septum Clinical presentations of nasal septal deviation include headaches, rhinosinusitis, high blood pressure, obstructive sleep apnea, and breathing sounds. For some patients, headache was explained by contact between the convex side and the mucosa of the peripheral nasal wall of the inferior or middle turbinates, or the lateral nasal wall of the nasal septum. In between them is the sensory nerve end, which will be affected and cause pain. As a result of nasal obstruction, septal deviations can lead to obstructive sleep apnea (OSA), which is a sleep disorder characterized by a cessation or significant decrease in airflow in the presence of effort to breathe. Pharyngotonsillitis There are an abundance of aerobic and anaerobic bacteria in the oropharynx and Waldeyer ring, including staphylococcus, nonhemolytic streptococci, lactobacilli, bacteroides, and actinomyces. The tonsillar and adenoid tissues can become infected with these organisms as well as other pathogenic bacteria, viruses, fungi, and parasites. Acute pharyngotonsilitis is typically caused by viruses (most common) or bacteria. Pharyngotonsillitis Clinical Features: Symptoms of acute pharyngotonsillitis include fever, malaise, odynophagia, dysphagia, and foul breath. - It is also possible to experience airway obstruction due to tonsillar enlargement caused by infection, which may result in symptoms such as mouth breathing, snoring, or sleep-disordered breathing. - A physical examination may reveal tonsillar enlargement, erythema, and exudates. Pharyngotonsillitis – Viral Infections - Viral infections are responsible for approximately 70 to 85% of acute pharyngotonsillitis cases. - Among the common viral pathogens are adenoviruses, rhinoviruses, Coronaviruses, Epstein-Barr viruses (EBVs), cytomegaloviruses (CMVs), Coxsackieviruses, herpes simplex viruses, HIVs, and influenza viruses. Pharyngotonsillitis – Viral Infections EBV - The virus is a member of the herpes family and causes acute pharyngitis as part of infectious mononucleosis. EBV has a preference for infecting and altering human B-lymphocytes. - EBV occurs after a 2- to 6-week incubation period, during which infected B cells proliferate. After this, "atypical" cytotoxic T lymphocytes appear in the blood as part of a cellular immune response. - EBV is transmitted by oral transmission, and symptoms include high fever, generalized malaise, lymphadenopathy, hepatosplenomegaly, and Pharyngotonsillitis – Viral Infections EBV - In many cases, the tonsils are severely enlarged to the point where the airways are compromised, and they are covered by an extensive grayishwhite exudate as a result. - Lymphoid hypertrophy is noted on the exam, especially in the posterior nodes, which is a hallmark of EBV. In younger people, symptoms of the virus are often milder. - There is also an association between EBV and Hodgkin and non-Hodgkin lymphomas, Burkitt lymphomas, nasopharyngeal carcinomas, and other Pharyngotonsillitis – Viral Infections HIV - Acute retroviral syndrome can also cause pharyngitis, which is a manifestation of HIV infection. - Symptoms of acute retroviral syndrome develop one to five weeks after an incubation period in which symptoms include fever, nonexudative pharyngitis, lymphadenopathy, and systemic symptoms such as arthralgia, myalgia, and lethargy. Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis - Group A beta-hemolytic streptococcus (GABHS) - In children, it is the main cause of acute bacterial pharyngotonsillitis. - There is a 2-to-5-day incubation period, and transmission occurs through droplet spread. - This condition is characterized by fever, sore throat, cervical lymphadenopathy, dysphagia, and odynophagia. Tonsillar and pharyngeal erythema with purulent exudate are typically found on physical Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis - Group A betahemolytic streptococcus (GABHS) Nonsuppurative Complications Scarlet fever - The condition occurs as a result of the bacteria producing endotoxins during acute streptococcal pharyngotonsillitis. - Symptoms include erythematous rash, fever, lymphadenopathy, dysphagia, and erythematous tonsils and pharynx covered with a yellow membrane. - The tongue may become red with desquamation of the papillae, which is commonly referred to as "strawberry tongue. Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis - Group A beta-hemolytic streptococcus (GABHS) Nonsuppurative Complications Acute rheumatic fever - It develops 1 to 4 weeks after an episode of pharyngotonsillitis caused by GABHS. - In response to streptococcal infection, cross-reactive antibodies are produced that affect heart muscle, causing endocarditis, myocarditis, or pericarditis. - There is little that can be done to reverse the effects of heart tissue damage once it has been caused. Poststreptococcal glomerulonephritis - Following pharyngotonsillar infection or skin infection with GABHS, the disease typically presents as acute nephrotic syndrome. - Deposition of immune complexes and circulating autoantibodies damage the glomerulus, which is the disease's pathogenic Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis - Group A beta-hemolytic streptococcus (GABHS) Nonsuppurative Complications Pediatric autoimmune neuropsychiatric disorder associated with group A streptococcal (PANDAS) infection - Following GABHS infection, children may experience abrupt onsets of obsessive-compulsive behaviors or tics. - A similar pathophysiology is thought to exist for Sydenham chorea, in which antineuronal antibodies cross-react with areas in the basal ganglia, resulting in behavioral and motor disturbances. Suppurative Complications Peritonsillar abscess A consequence of infection spreading from the superior pole of the tonsil into the potential space between the tonsillar capsule and the pharyngeal muscle bed. Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis Group A (GABHS) beta-hemolytic streptococcus Suppurative Complications Peritonsillar abscess - The most common pathogens are aerobics, like GABHS and Staph aureus, and Haemophilllus influenza as well as anaerobics, including Prevotella, Porphyromonas, Fusobacterium, and Streptococcus strains. - In most cases, peritonsillar abscesses occur unilaterally and present as severe pain, odynophagia, a muffled voice, and dysphagia. - An inflammation of the pterygoid muscles often leads to trismus. - During examination, the palate is unilaterally swollen with a medial displacement of the tonsil and significant Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis Group A beta-hemolytic streptococcus (GABHS) Suppurative Complications Parapharyngeal abscess - Infections caused by peritonsillar abscesses or tonsils can spread through the superior constrictor muscle into a potential space between the superior constrictor muscle and the deep cervical fascia, resulting in parapharyngeal space abscesses. - Tonsil and pharyngeal walls can be displaced medially due to this type of abscess. - The adjacent pterygoid muscle and paraspinal muscle are usually inflamed, resulting in trismus and decreased neck Pharyngotonsillitis – Bacterial Infections Acute Streptococcal Pharyngotonsillitis - Group A beta-hemolytic streptococcus (GABHS) Suppurative Complications - Retropharyngeal abscess an infection in the lymph nodes of the retropharyngeal space or from the spread of a peritonsillar abscess may cause this condition. This disease is more common in children and may cause fever, dysphagia, muffled speech, noisy breathing, stiff neck, and cervical lymphadenopathy. Pharyngotonsillitis – Bacterial Infections Non-Group A Streptococcal Pharyngitis - Group C and G streptococci commonly colonize the upper respiratory tract and can cause foodborne and waterborne pharyngitis outbreaks. - There is a similar presentation to group A streptococcal pharyngitis, though less severe symptoms are usually present. Pharyngeal diphtheria - It is caused by Corynebacterium diphtheria - As a result of childhood immunization, childhood diphtheria is now extremely rare, and it primarily affects unimmunized people. - Besides the usual symptoms of acute pharyngitis, this disease is characterized by a grayish, tightly adherent pseudomembrane covering the tonsils and Pharyngotonsillitis – Bacterial Infections Non-Group A Streptococcal Pharyngitis Pharyngeal diphtheria - After removing the pseudomembrane, bleeding is evident on the underlying surface. - A potential compromise to the airway may result from the disease spreading to the larynx and tracheobronchial tree. - There is the potential for cardiac toxicity and neurotoxicity with C. diphtheriae exotoxins. Exposure to sexually transmitted diseases - Neisseria gonorrhoeae and Treponema pallidum can cause tonsillar infections in patients. - Often, gonococcal pharyngitis. infections present as an exudative - Symptoms of primary oral syphilis include a painless chancre on the lips, buccal mucosa, or oropharynx. Secondary syphilis patients can suffer from oropharyngeal and tonsillar ulcers as well as bilateral tonsillar hypertrophy. Pharyngotonsillitis - Fungal Infections - Candida albicans overgrowth causes oropharyngeal candidiasis, also known as "thrush," and often occurs in patients who have undergone immunosuppression, radiation, or long-term broad-spectrum antibiotic treatment. - Upon examination, the pharyngeal mucosa is adorned with white cottage cheese-like plaques, which bleed when removed with a tongue depressor. Pharyngotonsillitis Recurrent Acute Tonsilitis - Several patients suffer from recurrent episodes of acute tonsillitis followed by complete recovery between episodes. - As a result of their location and the numerous crypts and crevices in them, tonsils tend to harbor bacteria. - Because of that, aggressive medical treatment for acute tonsillitis may not prevent additional infections. - The bacterial flora in children with recurrent tonsillitis is different from that in children with fewer infections and tends to be polymicrobial. - Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae are the bacteria most frequently isolated in recurrent tonsillitis. Pharyngotonsillitis Chronic Tonsilitis - In chronic tonsillitis, sore throat persists for at least three months and is accompanied by tonsillar inflammation, halitosis, and persistent tender cervical adenopathy. - In most cases of chronic tonsillitis, bacteria such as Staphylococcus aureus, Haemophilus influenza, and Bacteroides species are involved. Tonsilloliths - They are microbial biofilms that form within tonsillar crypts and have been linked to chronic cryptic tonsillitis and halitosis. - Often, patients complain of foreign body sensations in their throats and hard white masses in their tonsils. Aphthous Ulcers Human herpesvirus 6 is thought to be associated with their cause, although this remains uncertain. These ulcers usually appear as small round, painful ulcerations with yellow-gray fibrinoid centers surrounded by red halos on freely moving, nonkeratinized mucosa (eg, buccal and labial mucosa without attached gingiva and palate). A minor aphthous ulcer is smaller than 1 cm in diameter and heals in 10-14 days. Major aphthous ulcers exceed 1 cm in diameter and can cause significant disability because of the intense oral pain they are Aphthous Ulcers Aphthous ulcers appear to be predisposed to eruption by stress. According to a study, viral rhinitis frequency and bedtime after 11 PM are independent predictors of aphthous ulcers frequency and severity in college students. Various other conditions may present with large or persistent ulcerative stomatitis, such as erythema multiforme, drug allergies, acute herpes simplex, pemphigus, pemphigoid, epidermolysis bullosa acquisita, bullous lichen planus, Behçet disease or IBD. Sometimes, squamous cell carcinoma presents in this manner. In cases where the diagnosis is uncertain, an incisional biopsy is recommended. Supraglottitis (Epiglottitis) Children from 2 to 6 years of age are most likely to suffer from this disease, but it can affect adults as well. The most common pathogen is Haemophilus influenzae type B (HIB), and the HIB vaccine has significantly reduced (more than 90%) the incidence of supraglottitis. While supraglottitis is an infrequent infection, understanding the condition is crucial due to its elevated mortality rate when not diagnosed and treated promptly. Supraglottitis (Epiglottitis) Clinical Features - Symptoms include fever, difficulty breathing, and severe odynophagia, which results in drooling. - Children are usually irritable and leaning forward, and if they are able to speak, their voices are muffled. - Inspiratory stridor occurs late in the process when the airway is almost completely blocked. ***Further investigation should not be undertaken if supraglottitis is suspected because any procedure induced by anxiety in the patient, including intraoral examination and venipuncture, may result in Laryngitis Viral URIs are most commonly responsible for laryngeal and surrounding structures inflammation. Parainfluenza viruses can cause croup or laryngotracheobronchitis in children. Croup is characterized by a "barking" cough, although it can also result in laryngitis. Bacterial laryngitis may arise as a complication of viral laryngitis, typically manifesting around the seventh day of the illness. S pneumoniae, H influenzae, and M catarrhalis are the most common bacteria involved. Fungal laryngitis may be uncommon, but it should be taken into consideration for patients with immunosuppression or those who have recently undergone antibacterial treatment. Noninfectious causes - vocal trauma (e.g., due to yelling, screaming, or loud singing), inhalation injuries, allergies, gastroesophageal reflux disease (laryngopharyngeal reflux), asthma, and pollution. Those who smoke are at a higher risk for cancer and other Laryngitis Clinical Features - Symptoms include raspy, hoarse, or breathy voice, sometimes progressing to a complete loss of voice. - Patients with laryngitis are likely to experience a dry cough and anterior throat pain; they often feel the need to clear their throats. - A laryngitis patient's physical examination should focus on the head, neck, and lungs, but laryngitis is typically diagnosed on the basis of their history. - If it is essential to visualize the vocal cords, using indirect examination methods such as a mirror or flexible laryngoscopy typically reveals redness and swelling of the vocal cords and the adjacent structures. Bacterial Tracheitis It is believed to manifest as a secondary bacterial colonization subsequent to a viral respiratory tract infection. Occasionally, the subglottis and main bronchi are involved. In most cases, Staphylococcus aureus is isolated as the pathogen. Clinical Features - Acute exacerbation of airway obstruction with associated high fever and toxicity. - As with supraglottitis, the onset of symptoms is rapid, but drooling and dysphagia are not present. - There may be narrowing of the tracheal lumen on plain-film xrays of the neck, but endoscopy must be done in order to confirm the diagnosis. - It is characterized by a diffusely ulcerated tracheal mucosa and copious purulent secretions that partially obstruct the trachea lumen. References Shah S.B., & Emanuel I.A. (2020). Nonallergic and allergic rhinitis. Lalwani A.K.(Ed.), Current Diagnosis & Treatment Otolaryngology—Head and Neck Surgery, 4e. McGraw Hill. Strayer DS, Rubin E, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 7th ed. Lippincott Williams and Wilkins; 2014.Chapter 29: the Head and Neck. Li, J., Fang, F., Mei, M., & Wu, D. (2023). The gut microbiome and allergic rhinitis; refocusing on the role of probiotics as a treatment option. 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