Upper Respiratory tract Flashcards
Upper Respiratory tract consists of?
- Nose
- Naso-pharynx
- Larynx
- Paranasal sinuses
- Eustachian tube
- Middle ear
DEFENCE MECHANISMS of
Filtration of 10 to 20,000 litres air per day
- Muco-ciliary transport system (“escalator”)
- Cough/sneeze/gag/swallow reflex
- Richly vascularised/erectile • MALT (Waldeyer’s ring)
- White blood cells and Ig A secretion
What diseases cause problems with the MUCO-CILARY TRANSPORT SYSTEM?
Primary ciliary dyskinesia(recessive condition - cilia fucked)
• Kartagener’s syndrome (type of primary ciliary dyskinesia - situs invertus occurs as well) - triad of bronchiectasis, chronic sinusitis, situs inversus totalis
- Infertitiliy due to
RHINITIS
What is the cause and effects of the acute
What happens in chronic rhinits?
Acute
- Aetiology – viruses, bacteria, allergens (seasonal and perennial vasomotor rhinitis), occasionally fungi
- Effects – inflammation – congested, oedematous, rhinorrhoea - watery or mucoid, or muco purulent Chronic
- Atrophy of mucous glands and surface epithelium, squamous metaplasia, fibrosis
- [type I & type III(antigen-antibody) hypersensitivity reactions]
SINUSITIS
What is the cause and what are the effects?
What happens in chronic cases?
Acute
• Aetiology – as for rhinitis. • [NB. maxillary antrum infections from teeth] • Effects – mucocoele or empyema; orbital cellulitis, osteomyelitis, meningitis, cerebral abscess
Chronic Nasal and naso-sinal polyps
PHARYNGITIS
What is the acute cause and effects of it?
What happens in chronic cases?
Acute
- Aetiology -viruses, bacteria e.g. Streptococcci, Haemophilus etc (Also diphtheria, tuberculosis, gonorrhoea, syphilis), fungi e.g. Candida sp
- Effects – tonsillitis, retropharyngeal abscess peritonsillar abscess (quinsy), cervical adenitis(lymph node infection), parapharyngeal abscess, Ludwig’s angina (severe diffuse cellulitis that presents an acute onset and spreads rapidly, bilaterally affecting the submandibular, sublingual and submental spaces resulting in a state of emergency)
Chronic
• Continuing irritation from another source
This person shows
Cardinal triad
- Giant cell transformation
- Arteritis/phlebitis
- Zonal (“geographical”) necrosis with karyorrhexis(destructive fragmentation of the nucleus of a dying cell whereby it’s chromatin is distributed irregularly through the cytoplasm) / leukocytoclasis
Granulomatosis with polyangiitis (GPA, Wegener’s granulomatosis)
A 50-year-old woman presents with a 3 month history of crusting and bleeding of the nose. On examination the mucosa of the septum and turbinates is thickened and ulcerated. X-rays and CT scan show destruction of the intranasal structures.
What does does this person have and what does it affect?
Who normally is affected by GPA?
Wha are the symptoms and signs?
What investigations would you do?
What are the complications and prognosis?
Nose and paranasal sinuses Lungs Kidneys (75%) Other organs (isolated or systemic)
Limited form - lungs only
Churg-Strauss(eosinophilic granulomatosis with polyangiitis)/PAN/MCD/CVD/microscopic polyarteritis & overlap syndrome
Normally affects• 30 – 50 years • M:F 1:1 • Usually Caucasian (80 – 90%) • Aetiology: unknown - ? autoimmune
• Symptoms numerous and varied – multi-system disease • Signs: Ulcers, sores crusting in and around nose, with destruction of nasal cartilage Rhinorrhoea, often bloody Subglottic stenosis (20%) causing hoarseness, stridor, dyspnoea or cough Chronic ear infections Haemoptysis Haematuria
Investigations
FBC, ESR U & Es Anti-neutrophil antibodies (C-ANCA(80%), PANCA(15%)) (90%) – low specificity Urinalysis – protein, blood, casts Nasal endoscopy Lung function tests CXR
Biopsy(gold standard diagnosis)
• Complications: Mechanical - nasal septum perforation/deformity - airway stenosis Functional - respiratory failure - renal failure
• Prognosis: Untreated - 50 % mortality at 5 years Treated - 90% will achieve long term remission Renal function determinant
What is the treatment for GPA?
Drugs eg steroids, cyclophosphamide
Also methotrexate, azothioprine, cyclosporin
Tumour Necrosis Factor (TNF) – trials Sometimes trimethoprim/sulphamethoxazole Surgery
What is this?
What cells causes this
Stewart’s granuloma – 10 cases 1933 Non-heating granuloma Midline granuloma Granuloma ganrenescens Lethal granuloma
NK T-cell non-Hodgkin’s lymphoma
You can see a lot of micropapollary
solid cystic underlying stroma intraepithelial
55 year old male with polypoidal mass uniltateral(bilateral is benign usually)
What does this person have?
Who are most likely to get these
INVERTED PAPILLOMA
Transitional papilloma
Ringertz tumour
“Schneiderian” papilloma – nose & paranasal sinuses derived embryologically from ectoderm but description encompasses inverted, cylindric cell (oncocytic) & exophytic (fungiform) histological patterns, which behave differently
M:F 5:1 • 40- 70 years • 19% all tumours of nose and paranasal sinuses • Aetiology unknown – ? smoking, chemical pollutants, allergens, chronic sinusitis, • HPV 6/11 (low risk)
INVERTED PAPILLOMA
What is the differential diagnosis for it?
What is samter’s triad?
Inflammatory (“allergic”) nasal polyp [NB. Samter’s triad – nasal polyposis, asthma, & aspirin hypersensitivity]
Fungiform /exophytic papilloma
Cylindric cell/oncocytic papilloma
Verruca vulgaris (“viral wart”)
Carcinoma (including ex-inverted papilloma)
What does this person have and what is the treatment and natural history?
Inverted papilloma
Natural history: Recurrence rate 40 - 66% Malignant change up to 53%….probably closer to 1.5 - 2% Multi-centric (“field change” phenomenon) Synchronous or metachronous Pre-malignant potential – dysplasia, SCC, adenocarcinoma, MEC etc
Treatment: Surgery - endoscopic versus en-bloc Continued long term surveillance
What does this person have?
SQUAMOUS CELL CARCINOMA
A 70-year-old man presents with a 4 month history of unilateral nasal obstruction and epistaxis.
On examination a large mass is seen in the right nose.
What does this person have?
What is the epidemeology?
What is the cause?
What are the signs and symptoms?
What investigations would you do?
How would you treat?
95 % Sino nasal Squamous cell carcinoma, many variants 3 % lymphoma, NHL or HD 2 % others, sarcoma, haematolymphoid, neuroendocrine, metastasis, rarities Beware pseudo-tumours/mimics
SCC • 70 years. Uncommon under 40 years • M : F 1.5 : 1 - 2 : 1 • 24% of all tumours of nose and paranasal sinuses (7% and 75% respectively) • Commoner in Japan and South Africa • Aetiology: unknown – smoking, chemical pollutants, snuff, various occupations [HPV, smoking, alcohol in oro-pharynx]
- Symptoms and signs: Blocked nose and sinuses Epistaxis Pain behind nose or upper teeth Swelling around the eyes Numbness cheek, upper lip upper teeth, side of nose Headache Speech change Diplopia/telecanthus(increased distance between corner of the eyelid but pupil distance same)
- Investigations: Xrays CT Scan MRI Scan Nasal endoscopy Biopsy(gold standard)
Treatment: Depends on site, stage, grade, general health etc Surgery (+/- reconstruction/prosthetics)(best treatment) Radiotherapy Occasionally chemotherapy GF receptor antagonists Cyclin kinase inhibitors Photodynamic therapy (PDT) Oncolytic viruses Vaccines
What is the diagnosis of this?
The person has a background of wood work wood workers, furniture makers (hard woods e.g. oak, beech etc), chromate exposure (leather workers, electroplaters etc)
Intestinalised pattern is indistinguishable morphologically & immunophenotypically from metastatic colo-rectal adenocarcinoma
• Artificial distinction between surface mucosal versus minor SG origin
ADENOCARCINOMA
What does this person have?
- Symptoms: Nasal obstruction Epistaxis Headaches Facial swelling Other
- Signs: Nasal mass Orbital mass Proptosis Other
male 7-19
Originate in close proximity to the posterior attachment of the middle tubinate near the superior border of the sphenopalatine foramen
Due to high hormone (testosterone) - hormone therapy useless
A 15-year-old boy presents with recurrent epistaxis. On examination there is a mass in the region of the nasopharynx.
what investigations would you do?
What is the treatment?
Juvenile nasal angiofibroma.
Investigation: Xrays CT Scan MRI Scan Angiography -> biopsy is hazardous
• Treatment: Surgery Pre-operative embolisation – coils, PVA, Onyx®, sclerosant
This is common in 50-60 year olds and younger age groups
More common in men 2:1
less in europe and NA. Morecommon in china, malaysia, indonesia and east africa
there is a risk factor with EBV and HLA A2
They have the following symptoms
Blocked nose Telecanthus Epistaxis Deafness Tinnitus Lymphadenopathy
The neoplasm blocks the Eustachian tube causing secretory otitis media or “glue ear” with conduction deafness
A 20-year-old woman presents with a 3 month history of unilateral conduction deafness and cervical lymphadenopathy.
what investigations would you do?
What treatment do you give?
Investigations: CXR CT Scan MRI Scan Bone Scan Nasal endoscopy
Biopsy look for EBV LMP-1, in-situ EBERs (shown in pic)EBV DNA/RNA quantification studies
Treatment: Depends on stage and grade Radiotherapy – external and internal Chemotherapy(this is the best treatment) Surgery(just to get biopsy for diagnosis)– lymph nodes in neck, recurrences
A 20-year-old woman returns from a holiday in Russia with a sore throat. On examination there is a dull grey membrane in the oropharynx
what does the person have?
What complications can happen?
Diphtheria • Aetiology: Corynebacterium diphtheria (Gram positive bacillus). Exotoxin formation
- Histopathology: “pseudomembrane” Coagulum of dead cells, fibrin, inflammatory cells and bacteria
- Complications: Death due to Asphyxia Renal or cardiac failure
Treatment: Antibiotics Antitoxin Vaccine – toxoid, DTP immunisation
A chinese figure shown at the bottom
A 30-year-old Asian man presents with a 2 month history of hoarseness and painful dysphagia.
On examination there is a lesion on the right vocal cord.
Necrotising granuloma seen
How would you investigate further?
What are the treatment?
tuberculous laryngitis
< 40 years Now older • M > F
- Aetiology: Mycobacterium tuberculosis (acid alcohol fast bacillus – ZN stain) • Laryngeal involvement in 37.5% autopsy cases of pulmonary tuberculosis (Auerbach 1946) Now uncommon
- Differential diagnosis: Other granulomatous conditions (equally rare) Carcinoma
Investigations: CXR Sputum - microscopy and culture (L-J medium) Laryngoscopy Biopsy – Z-N/fluorescent, PCR Tuberculin skin test (TST), PPD eg Mantoux/Heaf Interferon gamma release assays (IGRAs) eg QuantiFERON®- TB Gold In-Tube (QFT-G) test
Treatment: Antibiotics – anti-tuberculosis therapy regime (triple/quadruple) Resistant strains
A 40-year-old woman who is a teacher presents with a 2 month history of hoarseness. On examination two nodules are seen on the vocal cords.
Squamous metaplasia seen
what do they have?
What is the cause
What treatment
Benign vocal cord polypi/laryngeal nodules (singers’ nodes)
VOCAL CORD POLYP/ LARYNGEAL NODULE
- “Singer’s /teacher’s/preachers’/hawker’s/town crier’s/housewife’s/screamer’s” node or nodule • Other exudative conditions of Reinke’s space
- Age and sex dependent on aetiology
- Aetiology: vocal cord abuse, cigarette smoking, pharyngo-laryngeal reflux disease, other pollutants, nasal disease • Site, unilateral or bilateral • NB. hypothyroidism/myxoedema & Reinke’s diffuse oedema – identical histopathology
Reason you get - poor vascular to larynx - hard to drain - oedematous polyp happen
Treatment: Surgery or laser cordectomy – may recur “Contact (intubation) granuloma” or ulcer - voice abuse pharyngo-laryngeal reflux instrumentation
25 year old women with a 4 month history of hoarseness - multiple papillary lesion of vocal chord
What do they have and what are they at a risk of?
Squamous epithelial hyperplasia with viral laringeal papilamtosus - caused by hpv -> at risk of invasive carcinoma
Dysplasia - mild, moderate, severe • Dysplasia - low grade, high grade • WHO LIN/SIN – I, II, III • Ljubljana classification (risk stratification) • Carcinoma in situ, pTis • Viral respiratory/laryngeal papillomatosis & HPV infection
Pic shows moderately differentiated squamous cell carcinoma
Which gland is most likely to be benign and which is most likely to be malignant
Connective tissue tumours are: haemangiomas and lipomas
