Skin and Musculoskeletal Pathology Flashcards
What is the Epidemiology of Carcinoma Of The Oral Cavity?
- Squamous cell carcinoma- 90-94% of malig tumours of oral cavity
- Worldwide oral squamous cell carcinoma 6th most common cancer (>300,000 new cases diagnosed/yr)
- Globally 5% cancers for men & 2% for women
- Overall incidence & mortality attributed to oral squamous cell carcinoma is increasing
- Survival rates less than 50%
- Tumours can arise in any part of oral cavity- highest freq in floor of mouth, venterolateral tongue, retromolar region, lower lip, soft palate & gingiva
Pathogenesis
• Atypical= dysplastic cells= tumour (spectrum- starts gradually)
What is the Aetiology of Carcinoma Of The Oral Cavity?
Aetiology
• Tobacco use & alcohol abuse- dominant risk factors;
o Strongly synergistic
o 75% of disease burden or oral & oropharyngeal malignancies
o Oral smokeless tobacco- major cause in Indian subcontinent, parts of South-East Asia, China and Taiwan
o May be consumed in betel quids containing areca nut and calcium hydroxide
• HPV infec;
o Some strains HPV more oncogenic than others e.g. 16 & 18
o High oncogenic genotypes e.g. HPV16 & 18 also in a variable but small amount of oral and up to 50% oropharyngeal squamous cell carcinomas (especially involving the tonsils & tongue base)
o HPV infec from oral/genital contact may be important (oral genital contact)
o Interestingly these patients have a better overall survival than HPV negative patients
• Can cause benign
• Dietary factors;
o Fruit & veg high in vits A & C- protective against oral neoplasia, related to inherent anti-oxidant properties
o Meat & red chilli powder- risk factors
• Genetic factors;
o Fam history of head & neck cancer may be a risk factor for the disease and it is postulated that inherited genomic instability may increase susceptibility
What are Pre-cancerous Lesions & Conditions of Carcinoma Of The Oral Cavity??
- Submucous fibrosis
- Actinic keratosis- damage caused by sunlight (more prone to skin tumours, actin colitis in lips)
- Lichen planus
- Leukoplakia (white thickening of oral cavity) & erythroplakia
- Chronic hyperplastic candidosis- can be caused by candidia infecs (over time= cancer)
What is invasion in Carcinoma Of The Oral Cavity?
Lymphovascular invasion worsens prognosis, the mechanism of spread is always tumour embolism;
• Local metastases = cervical lymph nodes
• Distant = mediastinal lymph nodes, lung, liver, bone
What is Carcinoma Of The Larynx?
- Squamous cell carcinoma most common
- 12,000 men & women diagnosed with cancer of the larynx every year
- Age adjusted incidence 3.6 per 100,000
- Normally treated with total laryngectomy
Pathogenesis
• Hyperplasia= dysplasia= carcinoma in situ= invasive carcinoma
What is the Aetiology Carcinoma Of The Larynx?
- Tobacco & alcohol- major risk factors
- HPV (6 & 11) infec
- Diets; low in green leafy veg & high in salt, preserved meats & dietary fats
- Metal/plastic workers
- Exposure to paint, diesel & gasoline fumes, asbestos
- Radiation exposure
- Laryngopharyngeal reflux
- Genetic susceptibility
What is Lichen Planus?
Non-Malignant (Benign) Inflamm Conditions
• Muco-cutaneous condition
• Unknown pathogenesis but may be T cell mediated autoimmune response
• Cutaneous lesions= itchy, purple, papules forming plaques with Wickham’s striae (white striae)
• Oral lesions= reticular striations, plaque- like, erosive, ulcerative lesions, desquamatve gingivitis
• Small risk of malig transformation
What are Vocal Cord Nodules & Polyps?
Non-Malignant (Benign) Inflamm Conditions
• Histologically look the same but clinically look diff
• Reactive lesions
• Most often seen in heavy smokers or in individuals who impose great strain on their vocal cords (singers’ nodules)
• Adults and predominantly men affected
• Most commonly associated with a voice change e.g. hoarseness, change in voice quality, and increased effort in producing the voice
• Usually located on the true vocal cords
What are Nasal Polyps?
Non-Malignant (Benign) Inflamm Conditions
• Recurrent rhinitis attacks= eventually lead to focal protrusions of mucosa
• May reach 4cm (can block nasal passage- e.g. cause snoring)
• When large (-/+ multiple) can encroach the airway & impede sinus drainage
• Features point to an allergic aetiology, but most patients with nasal polyps are not atopic
• Histology: oedematous mucosa with loose stroma containing hyperplastic/cystic mucous glands and infiltrated with mixed inflammatory infiltrate rich in eosinophils
What is Sinusitis?
Non-Malignant (Benign) Inflamm Conditions
• Role in nasal polyps (sinusitis attacks)
• Acute sinusitis usually proceeded by acute or chronic rhinitis
• Maxillary sinusitis can arise from extension of a periapical infec from an upper tooth through the antral floor (oral flora, inflammatory reaction is non specific)
• Acute sinusitis may progress into chronic, especially if impairment of sinus drainage
o As a result of the inflammatory oedema of the mucosa
o May impound the suppurative exudate producing empyema of the sinus
• Obstruction most often affects the frontal and anterior ethmoid sinuses
• Causative microorganisms = mixed microbial flora usually inhabitants of the oral cavity, severe forms may be caused by fungi e.g. mucomycosis esp in diabetics
• Complications = potential of spread into the orbit or into the enclosing bone producing cranial osteomylitis, meningitis or cerebral abscess – very rare!
What is Acute & Chronic Otits Media?
Acute & Chronic Otits Media (often involves middle ear &mastoid)
• Mostly in infants & children
• (Diabetic patients can develop severe infecs)
• Often viral, associated with generalised upper resp tract symptoms
• Primary/ secondary bacterial infecs= acute otitis media
• Streptococcus pneumoniae, H.influenzae & Moraxella catarrhalis
• Chronic disease usually form recurrent +/- persistent episodes & failure of resolution of acute bacterial infecs
• Causative agents in chronic disease usually- Pseudomonas aeruginosa, Staphylococcus aureus or fungal
•
• Potential complications;
o Eardrum perforation
o Aural polyps, cholesteatoma
o Mastoiditis, temporal cerebritis/ abscess
o Destructive necrotising otitis consequence of otitis media in a diabetic person especially when P.aeruginosa is the causative organism (diabetics can develop severe infecs)
What is Cholestatoma?
• Associated with chronic otitis media
• Pathogenesis of the lesion unclear: chronic inflamm & perforation of eardrum with squamous epithelium ingrowth or metaplasia of secretory epithelial lining of middle ear
• Cystic lesions lined by keratinising squamous epithelium (makes keratin), & filled with debris & cholesterol clefts- cyst can rupture & contents can make inflamm response around it
• Precipitates surrounding inflammatory reaction which is enhanced if the cyst ruptures & may result in a foreign body giant cell reaction
• Treatment- can be removed surgically
• Potential complications:
o Progressive enlargement may lead to erosion of ossicles, the labyrinth (dizziness) and adjacent bone or the surrounding soft tissue
o Hearing loss
o Very rarely CNS complications: brain abscess and meningitis
What is Symptomatic Ototsclerosis?
- Abnormal bone deposition in the middle ear
- Usually bilateral
- Usually begins in early decades of life, most cases are familial
- Pathogenesis: Uncoupling of normal bone resorption and bone formation
- Initially fibrous ankylosis = bony overgrowth = anchorage of middle ear bones to oval window
- Degree of immobilisation governs the severity of hearing loss
- Process is slowly progressive eventually leading to marked hearing loss
What is Labyrinthitis?
- Inflamm disorder of inner ear (labyrinth)
- Disturbs balance & hearing (e.g. tinnitus, nausea, loass of balance)
- Bacteria/ viruses can cause acute labyrinth inflamm in conjunction with local/ systemic infecs
- Autimmune processes e.g. Wegner granulomatosis or polyarteritis nodosa
What are Carcinomas of the ear?
Carcinomas (mostly of external ear)
• External ear (pinna) - Basal cell and squamous cell carcinomas, tend to occur in elderly men and are associated with actinic radiation
• Ear canal - Squamous cell carcinoma, middle-aged to elderly women, not associated with sun exposure
• Actinic keratosis can proceed these tumours
What are Paragangliomas of the ear?
Paragangliomas (mostly in middle ear)
• Most common tumour of the middle ear, originating in the paraganglia
• Presenting symptoms - pulsatile tinnitus, hearing loss, aural pressure/fullness, dizziness, otalgia, and bloody otorrhea (ear discharge)
What is Sialadenitis?
- Gland inflamm
- Slaivary duct obstruct (stones)- bacterial infec
- Autoimmune (Sjogren’s syndrome)
- Get dry mouth
What are tumours of the Salivary Glands
- Benign or malignant
- Benign are more common but depends on site e.g. parotid & submandibular gland benign more common but in minor salivary glands (e.g. tongue) malig tumours incidence is higher
MALIGNANT TUMOURS • Mucoepidermoid • Acinic cell carcinoma • Polymorphous low grade carcinoma • Adenoid cystic carcinoma • Salivary duct carcinoma
What is Pleomorphic Adenoma?
Pleomorphic Adenoma (salivary gland tumour);
o 2/3 of all salivary tumours (80% in parotid)
o Variable histological; appearance (mixed tumour- as have diff components to it)
o Mixed epithelial & myoepithelial in chondromyxoid stroma
o May recur after surgery
o Malignant transformation (V small proportion)
o Treated by surgery but may recur if not treated properly
o Malig transformation (can transform into another malig form e.g. squamous cell carcinoma)
What is Warthin’s Tumour?
o Benign salivary tumour
o 5-10% of total salivary neoplasms
o Characteristic cyctic spaces lined by tall epithelial cells with dense lym[hoid stroma (adenolymphoma)
What is Inflammatory Skin Disease?
Inflammatory Skin Disease
• Infections
• Non-infectious inflammatory diseases
o Dermatitis/psoriasis
o Blistering
o Connective tissue diseases, eg Lupus Erythematosus/Dermatomyositis
o Skin lesions as sign of systemic disease
o Skin lesions caused by metabolic disorders
• Plus many rare types
What is Eczema/ Dermatitis?
- Many types (eczema Greek for ‘boil over’)
- Very common (5% children in UK)
- Varies from trivial to severe
- A reaction pattern rather than specific disease
What are the stages of Dermatitis?
Dermatitis (Eczema)
Clinically 3 stages;
1. Acute dermatitis - skin red, weeping serous exudate +/- small vesicles. (boiling over appearance)
2. Subacute dermatitis - skin is red, less exudate, itching ++, crusting.
3. Chronic dermatitis - skin thick & leathery 2ndry to scratching (not due to disease but reac from patient scratching)
What is the microscopy of Dermatitis?
- Spongiosis (intracellular oedema within epidermis)- fluid comes out of skin & weeps
- Chronic inflamm- predominantly superficial dermis
- Epidermal hyperplasia & hyperkeratosis- mild in acute dermatitis, marked in chronic dermatitis
What is Atopic Eczema?
- Usually starts in childhood, occasionally adults
- Often fam history
- Associated with asthma & hayfever
- Type 1 hypersensitivity reac to allergen
What is Contact Irritant Dermatitis?
- Contact irritant dermatitis - direct skin injury by irritant (irritant too long on hands= reac) e.g. acid, alkali, strong detergent etc
- Contact allergic dermatitis (need to develop reac)- nickel, dyes, rubber. Act as haptens which combine with epidermal protein to become immunogenic & cause reac (look at distrib in reac e.g. if on tummy could be from belt buckle, nickel in earrings if on ears)
What is Dermatitis of Unknown Aetiology?
Morphological subtypes:
• Seborrhoeic dermatitis - affect areas rich in sebaceous glands: scalp, forehead, upper chest (ehere sebciuos galnds sit)
• Nummular dermatitis - coin shaped lesions
What is Psoriasis?
- 1-2 % of population
- Well defined, red oval plaques on extensor surfaces - (knees, elbows, sacrum).
- Fine silvery scale (can be torn off- bleeding). Auspitz sign. Removal of scale causes small bleeding points.
- +/- pitting nails.
- +/- sero-negative arthritis (affecting small joints).
- Can affect extensor surface on back of head
Pathogenesis- clinical & microscopic features reflect massive cell turnover (too fast)
What is the microscopy of Psoriasis?
Psoriasiform hyperplasia” - distinct appearance:
• i) Regular elongated club shaped rete ridges
• ii)Thinning of epidermis over dermal papillae.
• iii)Parakeratotic (contain nuclei) scale.
• iv)Collections of neutrophils in scale (Munro microabscesses)
What is the aetiology of Psoriasis?
- Genetic factors. Some have fam history. Multiple loci [psoriasis Susceptibility/ PSORS genes] many in region of major histocompatibility complex on Chromosome 6p2 implicated. Same area involved in other autoimmune disorders eg IBD,MS
- Env trigger factors,[ie Acquired factors] infec, stress, trauma, drugs e.g. may come into hospital for something else then causes psoriosis
- Disregulation of immune system
