HNS38 Common ENT Inflammatory Diseases: Anatomic And Physiologic Appraisal Flashcards
Rhinosinusitis
- Infectious (Clinical Practice)
- viral (rhino, para, adeno, influenza)
- bacterial (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis) - Allergic (Clinical Practice)
- seasonal / persistent - Occupational
- allergic / non-allergic - Drug-induced
- aspirin - Hormonal
- pregnancy have flare up of rhinitis - Other causes (food, emotional, atrophic, GORD)
- Idiopathic
Allergic rhinitis
Type 1 hypersensitivity involving IgE
Symptoms:
Early-phase symptom: Sneeze, Itch, Rhinorrhea, Mucosal oedema
Late-phase symptom: Chronic nasal obstruction (cellular infiltration)
Mediator: IgE (normal protective response against helminthic infection)
Effector: Mast cells:
- granules containing histamines, proteases, heparin, serotonin
- high affinity for Fc of IgE
- found in tissues exposed to environment (mucosal surface)
- Allergen bind to IgE on mast cell surface
- IgE receptor cross linking —> ↑ intracellular Ca —> Intracellular signaling pathway
- Mast cell degranulation
—> preformed granules: histamine, heparin, protease - Arachidonic acid enzymatic pathway activation
—> lipid mediators: prostaglandins, leukotriene, bradykinin - Transcriptional activation of cytokine genes
—> cytokine release (TNF, IL1, IL8)
Histamine: vasodilation, ↑ permeability, smooth muscle contraction, mucus secretion
Protease: tissue damage
Prostaglandin: vasodilation, smooth muscle contraction,
Leukotriene: smooth muscle contraction, ↑ permeability
Cytokine: induce inflammation, leukocyte recruitment (Eosinophil)
Physiological changes:
- Smooth muscle contraction —> bronchoconstriction
- Vasodilation and ↑ permeability —> angioedema, hives / flushing, itching
- Mucus secretion —> watery eyes, rhinitis
- Sensory neural stimulation —> coughing, sneezing
Th2 response: (Dendritic cell —> Th2 —> B cell IgE —> Mast cell)
Sensitisation phase: Dendritic cells prime Th2 development
—> Th2 cytokines (IL4) —> B cell producing IgE (specific to allergen)
—> IgE captured by mast cells with Fc receptor —> mast cells sensitised
Activation phase: re-exposure —> rapid degranulation —> type I reaction
Infective rhinitis
Usually virus first then bacteria
Bacterial:
- Haemophilus influenzae
- Streptococcus pneumoniae
- Staphylococcus aureus
- Moraxella catarrhalis
Symptoms:
Cloudy nasal discharge
Sinusitis
Sinus:
- Ciliated Pseudostratified columnar epithelium
- Organised pathways of mucociliary clearance (cilia beating uniformly towards one direction)
- Osteomeatal complex (opening of middle meatus)
Sinusitis:
- Obstruction due to Functional / Anatomical disturbance
- X-ray: Opacification of sinus, Air-fluid level
Complications:
- Eye / Orbit infection (Orbital cellulitis / abscess) (via lamina papyracea?)
- Brain infection (Cavernous sinus thrombosis)
Ear infections
- Otitis externa (most)
- Otitis media
- Inner ear (uncommon)
Otitis externa
Erysipelas, Furuncle, Otomycosis etc.
Bacteria: ***Staphylococcus aureus, Pseudomonas aeruginosa
Ear wax:
- Desquamated cell (dead cells from stratified squamous epithelium) + Cerumen (from ceruminous glands) + Sebum
- Water proof, ***Acidic —> inhibit growth of bacteria and fungi
- Pars tensa epithelium migrates outwards
Vicious cycle:
Introduction of bacteria
—> breed on moist dead skin, pus fills ear canal
—> **inflammatory reaction of ear canal skin
—> **swelling, **blockage, rapid cell turnover
—> **more dead skin produced
—> more bacteria bred
Otitis media
- Acute OM
- acute symptoms: pain, fever, hearing loss, discharge
- viral / bacterial
- usually originate from respiratory infection (from nose via Eustachian tube)
- Streptococcus pneumoniae / Haemophilus influenzae / Moraxella catarrhalis
- Complications:
—> Rupture of ear drum with pus discharge
—> pus goes in **Mastoid of temporal bone (Mastoiditis)
—> pus go to brain (CN palsies)
—> **Brain abscess - Chronic Suppurative OM
- infective process cause too much damage
—> **residual perforation of ear drum after AOM
- **Active (discharging) / Inactive (dry, can have no symptoms at all / normal)
Tonsils infection / Tonsillitis
Bacterial:
- Streptococci ***pyogenes, Staphylococci, Pneumococci, H. influenzae
Viral:
- Rhinovirus, Adenovirus, EBV
Other:
- Syphilis, Diphtheria, M. TB, Candida
Clinical features:
- Fever
- Sore throat
- ***Odynophagia (pain when swallowing)
- ***Trismus (locked jaw) —> Quinsy / Peritonsillar abscess
- ***Otalgia (ear pain, referred pain)
Bacterial:
- Swollen uvula
- ***Whitish spots (exudates)
- Red ***swollen tonsils
- Throat ***redness
- Gray furry tongue
Viral:
- Red swollen tonsils
- Throat redness
Pharyngitis
Attack of Pharyngeal mucosa (esp. posterior pharyngeal wall)
Larynx infection
- Supraglottis (airway, swallowing)
- Epiglottitis
—> Strawberry-like epiglottis
—> Thumb-sign of lateral neck X-ray - Glottis (voice)
- Subglottis
- Croup
Sialadenitis / Salivary gland infection
Causes:
- Viral
- ***Mumps —> Parotitis (sometimes bilateral, may lead to abscess formation)
- Coxsackievirus
- HIV
- Echovirus - Bacterial
- ***Staphylococcus
- TB, Syphilis - Noninfectious inflammatory (Autoimmune)
- ***Sjogren’s syndrome
Pathophysiology:
- Ascending duct infection related to dehydration / debilitation
- Secondary to ductal obstruction
- Stones
- Submandibular (Mixed) > Parotid (Serous), ∵ thicker mucous secretions and dependent position (located on floor)
Deep neck spaces infection (LN infections)
- Parapharyngeal
- complication of tonsillitis (e.g. Quinsy) / tonsillectomy, dental infection, petrous apex —> spread into LN
- fever, pain, **trismus, tonsil pushed **medially
- **Jugular vein thrombophlebitis (Lemierre syndrome), **Carotid artery erosion - Retropharyngeal
- children (more retropharyngeal LN)
- neck rigidity
- airway / dysphagia
- systemically unwell
- ***Mediastinitis - Submandibular / Sublingual (Ludwig’s angina)
Summary
- NOT all inflammatory conditions are infections
- Anatomy of head and neck
—> Clinical features
—> Complications - Pathophysiology
—> Risk factors
—> Treatment
