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Second Year > Head and Neck Pathology > Flashcards

Head and Neck Pathology Flashcards

1
Q

What are common head and neck symptoms?

A

Sore throat, dysphagia, dysphonia, odynophagia, ulcers, neck lumps, sore throat, earache (referred otalgia?), discharge, cough, snoring, stretor, hoarseness, drooling.

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2
Q

What investigations can you use to investigate head and neck symptoms?

A

Endoscopy, indirect laryngoscopy, fibre optic nasolaryngoscopy, auscultation for carotid/thyroid bruites, FNAC (for non-pulsatile lumps), cytology, CT, MRI, PET, USS, XRay, contrast swallow.

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3
Q

What are the 7 S’s you use to describe neck lumps?

A

Site (level I-V), size, shape, sore, skin, stuck, soft?

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4
Q

What are the causes of neck lumps?

A

Reactive lymph nodes, thyroglossal cysts, cystic hygroma, solitary thyroid nodules, parathyroid disease, thyroid cancer, diffuse thyroid enlargement, multinodular goitre, branchial cyst.

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5
Q

What are reactive lymph nodes? What do they appear like?

A

Normal, swollen nodes in response to acute infection.

They are oval, round, soft, smooth, mobile and non-tender.

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6
Q

What is a thyroglossal cyst?
What imaging is useful for this?
How would you treat this?

A

Dilatation of thyroglossal duct remnant, may become infected and start discharging if ruptures through skin. If it ruptures it may become a sinus. It appears as a lump over thyroid that moves on tongue protrusion and grows with age.

USS prior to removal to ensure functional thyroid tissue elsewhere.

Antibiotics, cyst drainage, must remove hyoid bone to reduce chances of recurrence.

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7
Q

What is a cystic hygroma?
What imaging is useful for this?
How would you treat this?

A

It is a collection of fluid filled sacs (cysts) that result from lymphatic malformation. Appears as soft, painless lump, may be translucent.

USS, MRI.

Surgical excision.

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8
Q

What can be the cause of a solitary thyroid nodule?

A

Cyst (due to haemorrhage), adenoma (benign follicular tissue), carcinoma, lymphoma, prominent nodule in multinodular goitre.

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9
Q

How should you investigate a solitary thyroid nodule?

A

USS. If fine reassure and discharge, if not FNAC and cytology (can’t distinguish between follicular adenoma and follicular carcinoma (must do tissue biopsy and histology - graded 1-5; 1 - didn’t get enough tissue, 2 - normal, 3 - dysplastic 4 - mostly likely cancer, 5 - carcinoma).

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10
Q

What are the red flag symptoms associated with a solitary thyroid nodule?

A

Pain going to ear, weight loss, hoarseness, haematemesis.

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11
Q

How are solitary thyroid nodules generally treated?

A

Thyroid lobectomy.

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12
Q

What are the four types of thyroid cancer and how do they differ?

A

Papillary - lymphatic metastasis common.
Follicular - haematogenous metastasis common.
Medullary - familial aggression, arises from parafollicular C cells.
Anaplastic - aggressive, local spread, very poor have poor prognosis.

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13
Q

How is thyroid cancer treated?

A

Removal of neoplasm with thyroid gland and lymph nodes.

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14
Q

What are the causes of diffuse thyroid enlargement?

A

Colloid goitre, Grave’s disease, thyroiditis.

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15
Q

What is goitre?

A

Swelling in the neck caused by an enlarged thyroid gland.

NB - can cause compressive neck symptoms (dysphagia, stridor, compression of trachea).

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16
Q

What are the causes of colloid goitre?

A

Gland hyperplasia, iodine deficiency, puberty, pregnancy, lactation.

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17
Q

What sign indicates retrosternal goitre?

A

Pemberton’s sign: if choking when raising arms.

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18
Q

What is the aetiology of Grave’s disease?

A

Auto-antibodies directed against thyroid stimulating hormone. Results in hyperparathyroidism.

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19
Q

In which gender and age group is Grave’s disease most common?

A

Females, middle age.

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20
Q

What symptoms are associated with Grave’s disease?

A

thyroid eye disease (exophthalmos), fatigue, acropachy, clubbing, pre-tibial myxoedema, weight loss.

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21
Q

How is Grave’s disease treated?

A

anti-thyroids, beta-blockade (as patients are tachycardic), radio-iodine, surgery.

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22
Q

What is thyroiditis? What can cause it?

A

General term for swelling of the thyroid gland.

Causes: post-partum thyroiditis, infection, autoantibodies against thyroid gland, drugs/chemical damage.

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23
Q

What are the indications for thyroidectomy?

A

Airway obstruction, (suspected) malignancy, thyrotoxicosis, cosmesis, retrosternal extension.

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24
Q

What are the complications of a thyroidectomy?

A

Bleeding (primary/secondary), voice hoarseness, thyroid storm (life-threatening: produce too many hormones, leading to increased HR, BP and temperature), infection, hypoparathyroidism, hypothyroidism, keloid/hypertrophic scar.

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25
Q

What are the causes of thyrotoxicosis?

A

Hyperparathyroidism, inflammation of the thyroid gland, meds (e.g. amoidarone, lithium as these encourage excess hormone production).

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26
Q

What symptoms are associated with thyrotoxicosis?

A

Diarrhoea, weight loss, tremor, sweating, palpitations, agitation, increased HR, thinning of hair.

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27
Q

How is thyrotoxicosis treated?

A

Anti-thyroids, beta-blockers, radio-iodine, surgical excision.

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28
Q

What is thyrotoxicosis? How does it differ from hyperthyroidism?

A

Thyrotoxicosis is the presence of too much thyroid hormone in the body and hyperthyroidism is when thyrotoxicosis is due to overproduction of thyroid hormone by the thyroid gland.

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29
Q

What is the difference between hyperthyroidism and hypothyroidism?

A 
Hyperthyroidism = producing too many hormones. 
Hypothyroidism = producing too little hormones.
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30
Q

What are the symptoms associated with hyperthyroidism?

A

Anxiety, irritability, difficulty sleeping, fatigue/tiredness, sensitivity to heat, enlarged thyroid, palpitations, tremor, weight loss.

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31
Q

What are the symptoms associated with hypothyroidism?

A

Fatigue, weight gain, depression, sensitivity to cold, dry skin/hair, muscle ache.

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32
Q

How do you treat hyperthyroidism?

A

Anti-thyroids, beta-blockade, radio-iodine, surgery.

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33
Q

How do you treat hypothyroidism?

A

Daily hormone replacement (levothyroxine).

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34
Q

What are the causes of hyperthyroidism?

A

Grave’s disease, hyper-functioning thyroid nodules, thyroiditis, meds (iodine), pregnancy, thyroid cancer.

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35
Q

What are the causes of hypothyroidism?

A

Some autoimmune dx, damage from thyroid cancer/hyperthyroidism Rx.

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36
Q

How would you investigate thyroid disease?

A

TFTs (TSH, T3, T4), low TSH and high T3/4 indicates hyperthyroidism.

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37
Q

What are two causes of multi-nodular goitre?

A

Toxic goitre, Grave’s.

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38
Q

Who is toxic goitre seen in? What investigations should you use? And what signs will you see?

A

Mostly seen in elderly. Do TFTs, FNAC, CXR. No eye signs, AF and hyperthyroidism.

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39
Q

What kind of parathyroid disease is most common? What investigations would be useful in investigating parathyroid disease?

A

Hyperparathyroidism most common.

U&Es, creatinine, Ca, phosphate, parathyroid hormone, bicarbonate, vit D, USS, CT, MRIs (identify ectopic glands), isotope scanning (detect diseased glands).

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40
Q

What symptoms are associated with parathyroid disease?

A

Painful stones - renal calculi, polyuria, renal failure.

Aching bones - pathological fractures, osteoporosis, bone pain.

Psychic moans - anxiety, depression, confusion, paranoia.

Abdominal groans - abdominal pain, constipation, peptic ulcers, pancreatitis, weight loss.

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41
Q

What surgery do you do for hypoparathyroidism?

A

You ONLY do surgery for hyperparathyroidism.

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42
Q

What are the causes of hyperparathyroidism? How is this investigated and treated?

A

Adenoma(s), hyperplasia, secondary hyperparathyroidism (due to dx lowering Ca, body compensates too much, so normal Ca, but high phosphate, e.g. in renal failure).

Overproduction of PTH leads to increased serum Ca. This is because PTH normally regulate Ca, phosphorus and vit D.

Supplements and dietary change.

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43
Q

What is stridor?

A

Clinical sign of airway obstruction.

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44
Q

What are the different types of stridor and what sort of obstruction are they caused by?

A

Inspiratory - laryngeal
Expiratory - tracheobronchial
Biphasic - glottis/subglottis

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45
Q

How would you treat stridor?

A

Nebulised oxygen and adrenaline, IV dexamethasone (heliox), (definitive) airway management.

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46
Q

What is a branchial cyst?

A

Congenital remnant of fusion failure of branchial arches which has become infected and enlarged and lymph node degeneration.

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47
Q

What are the signs of a branchial cyst?

A

Transilluminates, smooth, soft, non-tender lump anterior to the SCM at junction between upper and middle thirds.

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48
Q

How are branchial cysts managed?

A

Excision to prevent further infection.

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49
Q

Categorise the neck lumps into

  1. non-thyroid related
  2. parathyroid related
  3. solitary thyroid nodule
  4. Diffuse thyroid enlargement
A
  1. reactive lymph node, thyroglossal duct, cystic hygroma, branchial cyst.
  2. hyperparathyroidism, hypoparathyroidism.
  3. carcinoma (follicular, papillary, medullary, anaplastic), cyst, adenoma, lymphoma.
  4. colloid goitre, Grave’s disease, thyroiditis.
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50
Q

What is a pharyngeal pouch?

A

Herniation of pharyngeal mucosa between the thyropharyngeus and cricopharyngeus of inferior constrictor of pharynx.

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51
Q

How can you investigate a pharyngeal pouch?

A

With barium swallow (will see apple core).

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52
Q

What symptoms are associated with a pharyngeal pouch?

A

Hoarseness, dysphagia, aspiration pneumonia, regurgitation, weight loss.

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53
Q

How is pharyngeal pouch treated?

A

Excision (endoscopic/open), dilate.

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54
Q

What is a cleft lip or palate?

A

Gap in the upper lip/palate present from birth.

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55
Q

What causes of cleft lip or palate?

A

Happens due to baby’s face not joining together correctly. Related to folic acid intake during pregnancy.

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56
Q

What complications are associated with a cleft lip/palate?

A

Difficulties and malnutrition is not treated properly. Ear infections, speech problems, breathing problems can also result.

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57
Q

How is cleft lip/palate managed?

A

Surgery.

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58
Q

Give examples of salivary gland disease.

A

Tumour of the salivary glands, e.g. pleomorphic adenoma, inflammation of the salivary glands, e.g. parotiditis, duct calculi (blocks flow of saliva, v. painful but simple to remove, see swelling all over affected gland).

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59
Q

What do you want to ask in your history about a patient presenting with hoarseness?

A

Duration, persistent/intermittent? Pain? Choking? Coughing? Swallowing? Voice user (singer/teacher)? Asthma? Rhinosinusitis? Reflux? Smoker? Meds? H&N symptoms?

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60
Q

What can cause hoarseness?

A

Nodules (screamer’s/singer’s nodes), (haemorrhagic) cyst, vocal abuse, laryngitis, infection, smoking, reflux, laryngeal cancer (laryngeal stoma), chronic laryngitis (these patients are chronically hoarse).

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61
Q

What can cause vocal cord paralysis?

Remember - can paralysis one or both cords depending on cause.

A

Nothing visibly wrong with cords due to interruption of nerve supply (recurrent laryngeal nerves). On left side recurrent laryngeal nerve lies close to hilum (if lung cancer spreads to hilar lymph nodes can cause nerve compression).

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62
Q

What are the three different categories of things that can cause dysphagia?

A
  1. something in the lumen (e.g. foreign body)
  2. problem with the wall (stricture, tumour, pouch etc.)
  3. something compressing the lumen (e.g. thyroid, heart, mediastinal mass).
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63
Q

What are the key things to ask in a history of a patient with dysphagia?

A

What is difficult (eating or drinking or both)? - drinking suggests NM cause, eating suggests narrowing of tube. Persistent or intermittent? Pain? Where? Well localised in the neck? Poorly localised further down?

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64
Q

What is FOSIT/globus pharyngeus?

A

Persistent feeling of a lump in the throat where there is actually nothing there. Can swallow normally so not true case of dysphagia. NOT a red flag symptom.

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65
Q

What can cause FOSIT?

A

Silent acid reflux (larynpharyngeal reflux), stress/anxiety, circopharyngeal spasm.

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66
Q

How do you treat head and neck cancer?

A

Curative or palliative?
Surgery, chemotherapy, radiotherapy.
Surgery involves neck dissection, removal of tumour (and surrounding lymph nodes) and flap reconstruction.

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67
Q

How do malignant nodes differ from normal nodes?

A

They are round, firm, irregular, fixed and non-tender.

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68
Q

What are causes of airway obstruction?

A

Foreign body, infection (e.g. epiglottitis, tonsillitis, croup, bronchitis), neck swelling, tumour, vocal cord paralysis, laryngomalacia (commonest paed cause).

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69
Q

What are the signs of airway obstruction?

A

Stridor (high pitched, wheezing noise made by disrupted airflow.

Inspiratory airflow indicates an issue with tissue above vocal cords. Expiratory stridor indicates a blockage in the trachea. Biphasic stridor indicates vocal cord obstruction or just below.

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70
Q

How would you manage airway obstruction?

A

ABC, secure airway (intubate, cricothyroidectomy (through cricothyroid membrane), tracheostomy, humidified oxygen, steroids, adrenaline nebulised.

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71
Q

What is tonsillitis?

A

Inflammation of the tonsils.

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72
Q

What are the causes of tonsillitis?

A

Viruses (most common - these include EBV), bacteria (these include B-haem, strep B).

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73
Q

What are the differences between viral and bacterial tonsillitis?

A

Bacterial tonsillitis - patients have white pus spots on tonsils, swollen neck nodes, fever, no cough.

Viral tonsillitis - patients have red, swollen tonsils and a red throat.

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74
Q

What symptoms are associated with tonsillitis?

A

Sore throat, dysphagia, hoarseness, fever, headache, cough, nausea.

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75
Q

What are the complications associated with tonsillitis?

A

Risk of glomerulonephritis, rheumatic fever, quinsy.

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76
Q

How is tonsillitis treated?

A

Penicillin V +/- anaerobic cover if acute, analgesia, anti-septic gargle (difflam), tonsillectomy, airway obstruction management. AVOID amoxicillin/ampicillin.

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77
Q

What is quinsy?

A

A.k.a. peritonsillar abscess. Rare, potentially serious complication of tonsillitis.

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78
Q

What causes quinsy?

A

Bacteria from tonsils spreading to surrounding areas and forming a collection of pus (abscess) between the wall of the mouth and tonsils.

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79
Q

What are the indications for tonsillectomy?

A 
If any of:
- >1 quinsy/6-7 attacks in 1y
-5 per year over 2y
3 per year over 3y
-daily activities disrupted
-obstructive sleep apnoea
-malignancy (lymphoma, rhabdomyosarcoma)
tonsillectomy indicated.
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80
Q

What is laryngomalacia?

A

Congenital softening of tissues of larynx above the vocal cords. Common cause of noisy breathing in children.

Laryngeal structure is floppy and malformed.

(self-limiting)

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81
Q

What is the most common nasal deformity?

A

Nasal septal deviation (can be congenital or acquired (trauma)).

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82
Q

What is a saddle deformity?

A

A marked depression/collapse along the mid portion of the nasal bridge.

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83
Q

What can cause a saddle deformity?

A

Septal perforation, surgery, trauma.

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84
Q

What are the complications associated with a saddle deformity?

A

Blockage of the nose, predisposing to rhino sinusitis, issues with Eustachian tube, nasal haematoma.

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85
Q

How is saddle deformity treated?

A

Post-traumatic rhinoplasty.

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86
Q

What is a nasal septal perforation?

A

Hole in the cartilage of nasal septum.

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87
Q

What can cause a nasal septal perforation?

A

Trauma, previous septoplasty, cocaine use.

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88
Q

What signs are associated nasal septal perforation?

A

Whistling when breathing in and out (smaller holes make more whistling).

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89
Q

What complications can arise from nasal septal perforation?

A

Can lead to collapse of the nose.

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90
Q

What happens in the nasal septum haematoma?

A

Anterior part of nasal septum composed of cartilaginous plate with closely adherent perichondrium and mucosa. Submucosal BVs are torn as buckling forces pull the perichondrium from the cartilage. Blood collects between the perichondrium and septal cartilage.

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91
Q

What complications are associated with nasal septal haematoma?

A

Progressive obstruction, deformity.

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92
Q

How is nasal septal haematoma treated?

A

Drain quickly, if left for a long time can become septic.

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93
Q

What is rhinosinusitis?

A

Concurrent inflammatory and infective processes affecting the nasal passage and continuous paranasal sinuses.
Can be chronic (allergic/non-allergic), with or without polyps (benign), or acute (bacterial, tends to last less than 12wks).

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94
Q

How can you investigate rhinosinusitis?

A

Sinus radiographs (poor visulisation of the osteomeatal complex and the anterior ethmoid sinuses, high rate of false positives (incl. air-fluid levels, mucosal thickening and sinus opacification).

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95
Q

What bacteria can cause rhinosinusitis?

A

S. pneumonia, H. influenza, both, M. catarrhalis, S. aureus, S. progenies, gram negatives.

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96
Q

How is adult rhinosinusitis classified?

A

Acute - acute onset of symptoms, duration <12 wks, symptoms usually resolve.

Recurrent acute - >1 to <4 episodes of acute rhinosinusitis per year, complete recovery between episodes, symptom free for >8wks between acute attacks in absence of Rx.

Chronic - duration of symptoms >12wks, persistent inflammatory changes on imaging >4wks after starting appropriate Rx.

Acute Exacerbations of Chronic - worsening of existing symptoms or appearance of new symptoms. Complete resolution of acute (but not chronic) symptoms between episodes.

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97
Q

What symptoms will patients experience with rhinosinusitis?

A

Major factors: facial pain/pressure, hyposmia/anosmia, nasal congestion/obstruction, purulent postnasal drain, olfactory disturbance, cough not due to asthma (children only).

Minor factors: headache, fever, fatigue, halitosis, dental pain, cough (adults).

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98
Q

What complications are associated with rhinosinusitis?

A

Infection can spread from sinuses and cause meningitis, intracranial abscesses and orbital sepsis.

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99
Q

How is rhinosinusitis treated?

A

B-lactams (penicillin, cephalosporins), macrocodes (erythromycin, clarithromycin).

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100
Q

What risks are associated with sinus surgery?

A

CSF leak, orbital complications, worse case scenario: blindness.

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101
Q

What complications are associated with acute periorbital swelling?

A

Optic neuritis, blindness (have a low threshold for admitting these patients as an emergency to get ophthalmologist opinion, urges CT, IV antibx and emergency surgery).

102
Q

How do you treat periorbital swelling?

A

If tiny bit red can give antibx and send home. If abscess, drain the pus.

103
Q

What is Pott’s Puffy Tumour?

A

It refers to a non-neoplastic complication of frontal sinusitis. it is a subperiosteal abscess associated with osteomyelitis. This results in a swelling of the forehead and requires an emergency referral.

104
Q

How do you treat a Pott’s Puffy tumour?

A

Frontal sinus surgery (drain frontal sinus) or endoscopic sinus surgery (ESS).

105
Q

What is ethmoidal mucocele and what does it result from?

A

No drainage or blockage of air cells leads to cyst formation which puts pressure on the orbit and can cause double vision/

106
Q

What symptoms are associated with ethmoidal mucocele?

A

Double vision.

107
Q

How is ethmoidal mucocele treated?

A

Endoscopic sinus surgery.

108
Q

Where does epistaxis most commonly result from?

A

Little’s area (right behind the middle of the nose, very anterior - it is an anastomosis of all the BVs supplying the nose).

Sphenopalatine is the most common vessel to bleed.

109
Q

How can you investigate epistaxis?

A

Anterior or endoscopic rhinoscopy, lab exam.

110
Q

What are the causes of epistaxis?

A

Trauma (aka. nose picking), anti-coagulants, iatrogenic (surgery), idiopathic, hypertension, allergy, atrophic rhinitis, tumour, congenital or acquired nasal defects.

111
Q

How is epistaxis managed?

A

Appropriate first aid (pinching of nose), antibiotic ointments (base-tin, bactrian), cautery (silver nitrate under LA, diathermy under GA), nasal packing (anterior or posterior nasal packs), check vital signs - need IV?

Surgery for serious epistaxis - endoscopic sphenopalatine artery ligation, transmaxillary IMA ligation, intraoral IMA ligation, ant/post ethmoidal ligation, ECA ligation, septodermaplasty/laser ablation, embolisation.

112
Q

What is hereditary haemorrhagic telangiectasia?

A

Abnormal blood vessel formation in the skin, mucous membranes, leads to many nose bleeds. It is a rare autosomal dominant genetic disorder.

113
Q

What are the complications of hereditary haemorrhagic telangiectasia?

A

Anaemia.

114
Q

How is HHT treated?

A

Laser coagulation, young’s procedure, septodermoplasty.

115
Q

What are angiofibromas?

A

Very vascular tumours that arise in patients with very rare conditions. Only seen in men (late teens-20s).

DO NOT biopsy these patients as they can bleed to death.

116
Q

How are angiofibromas managed?

A

Perioperative embolisation and surgery.

117
Q

Who does nasal carcinoma tend to affect?

A

V. rare, tends to affect men in 50s.

118
Q

What symptoms will someone with nasal carcinoma experience?

A

Unilateral hearing loss with epistaxis is a red flag. Tumour obstruction of Eustachian tube blocks drainage of middle ear, this is why you get hearing loss.

119
Q

How are nasal carcinomas treated?

A

Radiotherapy, surgery, combined therapy.

120
Q

What are the causes of olfactory dysfunction?

A

Rhinosinusitis, post-viral infections and trauma.

121
Q

How do you diagnose acute otitis media?

A

Otoscopy.

Remember - it is common in 3-18 month olds.

122
Q

What microbiology is involved in acute otitis media?

A

H. influenza, strep. pneumonia, M. catarrhalis.

123
Q

What signs and symptoms will a patient with acute otitis media present with?

A

Vague signs, child unwell, rubbing ear, high fever.

Increasing pain, systemic upset, sleep disturbance, ear discharge.

124
Q

What are the complication associated with otitis media?

A

Tympanic membrane perforation, acute mastoiditis, mastoid abscess (requires mastoidectomy), facial nerve palsy, ossicular/cochlear damage, labrynthitis, chronic perforation (COM), febrile convulsion, brain abscess, meningitis, sub/extradural empyema.

125
Q

What is the treatment of acute otitis media?

A

Wait a few days before giving antibx. Analgesia (call, ibuprofen), antibx (amoxicillin, or co-amoxiclav, erythromycin/clarithromycin 2nd line - 5-7 days only), long course (4-6wks - recurrent AOM episodes, low dose).

Recurrent or complicated AOM may require grommet insertion +/- adenoidectomy.

126
Q

What is otitis media with effusion?

A

Sterile fluid underneath ear drum, classically due to failure of Eustachian tube (can’t equalise pressure, lining of middle ear absorbs air continually, pressure in middle ear drops to create a vacuum, lining of middle ear secretes fluid to fill this).

127
Q

What causes otitis media with effusion?

A

Eustachian tube failure, adenoidal hypertrophy or resolving AOM in children, tumour blocking Eustachian tube in adults - must refer to ENT.

128
Q

What are the risk factors for otitis media with effusion?

A

Day care, older siblings, parental smoking, cleft palate, Down’s syndrome.

129
Q

What are the signs of otitis media with effusion?

A

Dull TM, fluid levels, bubbles.

130
Q

What symptoms are associated with otitis media with effusion?

A

Hearing loss, speech delay, behavioural problems, academic decline, imbalance.

131
Q

What complications are associated with otitis media with effusion?

A

Can lead to tympanic membrane perforation, small hole with lead to hearing loss, big hole will lead to greater hearing los.

132
Q

How do you treat otitis media with effusion?

A

Grommet insertion. In children wait for a few months as most don’t need it. Only insert grommet if persistent (few months) or affects education. Can also use auto inflation (auto vent balloon in those 4+) or hearing aids (BAHA - electrodes on bones in cochlea for those with conductive hearing loss).

133
Q

What are grommets?

A

Plastic tubes that can sit in the ear drum and bypass the Eustachian tube and equalise the pressure. Grommets make their way out of the ear, eardrum pushes it out and it heals itself.

134
Q

What damage can occur to the ossicles?

A

E.g. eroded incus can result from chronic infection.

Malleus gets its blood supply from the tympanic membrane, stapes from the proventary, incus gets whats left in the middle, so if there is vasculitis, can lead to erosion.

In middle ear can also get fibrosis between bony walls and ossicles (inhibits movements and therefore function - conductive hearing loss).

135
Q

What is otosclerosis? What is mostly affected by this?

A

Stapes affected by this.

Bony deposition in the annular ligament (fixes stapes so sound doesn’t go through the oval window well). Prevents sound conduction in cochlea leading to conductive hearing loss.

136
Q

What are the signs and symptoms of otosclerosis?

A

Signs - normal tympanic membrane, ossicles become knitted together into an immobile mass.

Symptoms - conductive hearing loss.

137
Q

What is a cholesteatoma?

A

NOTHING to do with cholesterol.

Skin (keratinised squamous epithelium) in middle ear, where it shouldn’t be. Can be congenital or acquired. Normally skin migrates out of the ear.

138
Q

What are the symptoms associated with cholesteatoma?

A

Gradual hearing loss in affected ear, watery, smelly discharge from ear.

139
Q

What complications are associated with cholesteatoma?

A

Cause problems as they grow and are destructive. Skin in the wrong place can erode bone and spread backwards into the mastoid bone. If very unlucky can erode into facial nerve/brain and cause brain abscess.

140
Q

How is cholesteatoma treated?

A

Removal with surgery under GA. If spreads to mastoid - mastoidectomy.

141
Q

What is involved in clinical assessment of hearing?

A 
Clinical testing
Tuning fork tests
Audiometry 
Objective testing
Otoscopy
Whispered voice test (whisper at 60, mask over ear by rubbing tragus, no lip reading).
142
Q

What are some ear symptoms?

A 
Hearing loss
Tinnitus - ringing in ear
Vertigo - sensation of movement
Otalgia - pain in ear
Otorrhoea - discharge from ear
Facial Weakness
143
Q

How are ear problems generally picked up in children?

A

Often picked up by teachers, who notice problems with speech development, school performance or behavioural problems.

144
Q

How would you assess if a child had hearing loss?

A

Place child on parent’s lap and use otoscope for the ear.

145
Q

What are the risk factors for hearing loss in children?

A

Maternal perinatal infections, delivery issues (prematurity, anoxia), neonatal infections, drugs, jaundice, growth, immunisations, passive smoking, breast vs bottle feeding.

At risk group (SNHL) - special baby care unit, FH, meningitis, perinatal sepsis (ToRCH - toxoplasmosis, rubella, CMV, herpes).

146
Q

Describe the two tuning fork tests.

A

Weber - test of lateralisation. Normal hearing leads to central test, if sensorineural hearing loss will lateralise to unaffected side, if conductive hearing loss will lateralise to the affected side (as no background noise).

Rinne - test that compares perceived loudness of air conduction to bone conduction in one ear at a time. In normal ear air>bone (positive), sensorineural hearing loss air>bone (positive, conductive hearing loss air

147
Q

What tuning fork do you use for the tuning fork tests?

A

512Hz.

148
Q

What are the different types of audiometry?

A 
Pure tone audiometry 
Distraction test
Visual reinforcement audiometry 
Play audiometry 
Tympanometry
149
Q

What are the different types of objective testing?

A

Otoacoustic emissions

Auditory brainstem response

150
Q

What age group is pure tone audiometry done in?

A

4+ yrs.

151
Q

What age group are distraction tests done in?

A

6-18 months.

152
Q

What age group is visual reinforcement audiometry done in?

A

12 months - 3 years.

153
Q

What age group is play audiometry done in?

A

3-5 years.

154
Q

What is pure tone audiometry?

A

Classic hearing test.
Trying to find lowest sound a person can hear in different pitches at different volumes. The lowest volume at the lowest pitch is known as the threshold of hearing.

Earphones worn to block out noise, and get information from both ears.

Can do it for bone and air conduction.

Hearing is a logarithmic scale (0= quietest noise humans can hear). Yellow is frequencies of normal speech. Audiograms focus on normal speech frequencies.

155
Q

What is a distraction test?

A

Child’s attention is kept in front and monitor response to noises either side of them.

156
Q

What is play audiometry?

A

Keep child occupied and monitor response to noises.

157
Q

What is tympanometry? What does it help detect? What sort of graphs are created from this?

A

Assists in detection of fluid in middle ear, perforation of ear drum, a stiff ear, an eardrum that moves too much and wax blocking the EAC.

Tympanometry pushes air pressure into the ear canal, making the ear drum move back and forth. This assesses the middle ear pressure (should be 0 (atmo)). It also measures the mobility of the tympanic membrane. Graphs created are called tympanographs.

158
Q

What different types of tympanographs can you get?

A

Type A - normal.
Type B - tympanic membrane immobile, hole in eardrum, eardrum full of fluid.
Type C - middle ear pressure low.

159
Q

What are otoacoustic emissions?

A

Sounds given off by the inner ear when the cochlea is stimulated by a sound (given off by the outer hair cells vibrating). Vibration produces nearly inaudible sound that echoes into the middle ear.

This sound can be measured with a small probe in the ear canal. If normal hearing sound produce emissions.

In hearing loss greater than 25-30dB do not produce these emissions.

160
Q

What can an otoacoustic emissions test detect?

A

Blockage in the outer ear canal, presence of middle ear fluid, damage to the outer hair cells in the cochlea.

161
Q

What is the auditory brainstem response?

A

Measures response of auditory brainstem and cochlear nerve, responses taken up by electrode and interpreted by the machine.

162
Q

Which frequencies tend to be lost first in hearing loss? What is a big exception?

A

Hearing first loss from high frequency areas, this is because these frequencies are picked up closest to the outer ear.
Note that menieres disease causes damage to low frequency areas.

163
Q

What is presbyacusis?

A

Age related hearing loss. High frequencies lost first. Starts over 30s.

164
Q

What will you see on the audiograph of someone with noise induced hearing loss?

A

Dip and rise in audiograph.

165
Q

What can noise cause hearing loss?

A

Noise can damage the hair cells in the cochlea.

166
Q

What substances are ototoxic?

A

Medications, e.g. Gentamicin (damages inner ear and causes high frequency hearing loss).

167
Q

What other things can sometimes cause hearing loss?

A

Head injury or viral infections can also cause cochlea or cochlear nerve damage.

168
Q

What is menieres disease?

A

Raised pressure in the ear leading to low frequency, unilateral sensorineural hearing loss, spontaneous vertigo, tinnitus, aural fullness which can last for a few hours and can happen every few days, weeks or months and causes fluctuating progressive unilateral hearing loss.

169
Q

How is menieres disease managed?

A

Betahistine (improve blood supply to ear), bendofluazide (reduce pressure in endolymphatic component), intratympanic dexamethasone (injected), intratympanic gentamicin (kill off nerve cells).

May need vestibular rehabilitation.

170
Q

What is a vestibular schwannoma?

A

Aka. acoustic neuroma

A benign tumour of the schwann cells of the vestibulocochlear nerve that won’t metastasise.

171
Q

If someone presents with SN hearing loss in one ear what must they be referred for?

A

An MRI.

172
Q

What symptoms are associated with vestibular schwannoma?

A

SN hearing loss in one ear, tinnitus, vertigo. If v. large can get persistent headaches, double vision, numbnss/weakness of the face, ataxia.

173
Q

How are vestibular schwannomas managed?

A

Monitoring of tumour, excision, stereotactic radiotherapy (precise beams).

174
Q

What are the two types of hearing loss and how do they differ?

A

Sensorineural - issue with cochlea or cochlear nerve.

Conductive - issue with outer or middle ear. note - can see air bone gap on audiographs.

175
Q

What is trachoma?

A

An infectious disease caused by chylamdia trachomatis. Malnutrition predisposes to this.

176
Q

What signs/symptoms are associated with trachoma?

A

Granulation of inner eyelid, eyelids turn inward and scratch cornea.

177
Q

How is trachoma managed?

A

SAFE (surgery, antibiotics face washing, environmental).

178
Q

What is onchocerciasis?

A

Aka river blindness.
Transmitted by blackfly and caused by a parasitic worm onchocerca volvulus. People at increased risk if near riverside areas.

179
Q

What symptoms are associated with onchocerciasis?

A

Blackfly larvae cause eye lesions, inflammation and scarring.

180
Q

How is onchocerciasis managed?

A

Annual ivermectine and vector control.

181
Q

How is avoidable blindness avoided?

A

Hygiene, sanitation, clean water, improved access to eye care, improved nutrition, awareness and education.

182
Q

What are causes of avoidable blindness?

A

Industrial (lesions), vit A deficiency, corneal scars (measles, traditional eye remedies, infections, rubella, cataracts). Higher incidence of eye trauma in developing countries.

183
Q

How do auricular haematomas form?

A

Can result from direct injury or trauma. Shearing forces to the anterior auricle can lead to separation of the anterior auricular cartilage and the perichondrium. This leads to tearing of the BVs and haematoma formation.

184
Q

How do you treat an auricular haematoma?

A

Must drain before it turns into an abscess and damages cartilage.

185
Q

What is otitis externa?

A

Inflammation of the outer ear canal skin.

186
Q

What causes otitis externa?

A

Can be associated with foreign body (producing very extensive inflammatory reaction around it, can result in closure of EAC and collection of secretions), can be fungal, bacterial (secondary to eczema), allergic.

187
Q

What symptoms are associated with otitis externa?

A

Itching, pain, discharge, hearing loss.

188
Q

How is otitis externa treated?

A

Topical ear drops (antibx and steroids to settle inflammation and get rid of microbes). If ear full of debris may need to get it sucked out first (aural microsuction), water precautions essential).

189
Q

What is malignant otitis externa?

A

NOT cancerous. Osteomyelitis of the temporal bone. Often seen in elderly and diabetics. Without treatment, this can be fatal.

190
Q

What are the signs and symptoms associated with malignant otitis externa?

A

Severe ear pain, headaches, exposed visible bone in the ear canal, can often see granulation in ear canal too.

191
Q

How is malignant otitis externa treated?

A

Systemic antibiotics (sometimes for months).

192
Q

What is tinnitus? What can cause it?

A

Perception of noise, can be buzzing, grinding, whistling, humming, hissing…

Causes - hearing loss, stress.

193
Q

If tinnitus if unilateral or pulsatile what does this mean?

A

More likely to be a vascular problem.

194
Q

How can tinnitus be managed?

A

Sound enrichment, stress management.

195
Q

What can cause vertigo?

A

Benign positional vertigo, menieres, vestibular neuritis/labyrinthitis.

196
Q

What is important to establish if a patient presents with vertigo?

A

Duration, frequency, associated symptoms, precipitating factors.

197
Q

What is the aetiology of benign positional vertigo?

A

Otoconia (calcium carbonate particles) in semi-circular canals, floating around, vertigo is not spontaneous.

198
Q

How do you test for benign positional vertigo?

A

Dix-Hallpike test.

199
Q

What symptoms are associated with benign positional vertigo?

A

Vertigo precipitated by specific changes in head position (classic is turning over in bed, particles take a few seconds to move through gravity, when they stop they feel dizzy for a few seconds as the fluid stops moving. Lasts for a few seconds, happens several times a day but no associated symptoms.

200
Q

How is benign positional vertigo cured?

A

The epley manovure.

201
Q

What is vestibular neuritis?

A

Inflammation of the vestibular nerve.

202
Q

What is labyrinthitis?

A

Inflammation of the inner ear.

203
Q

What can cause vestibular neuritis/labyrinthitis?

A

Reactivation of latent HSV infection of vestibular ganglion. May have started after a cold or flu.

204
Q

What symptoms are associated with vestibular neuritis/labyrinthitis?

A

Spontaneous vertigo, no associated symptoms in vestibular neuritis. Associated with unilateral hearing loss in labyrinthitis. Will last a few days and patients only experience a few episodes of decreasing severity.
Residual motion provoked vertigo (after acute phase, patients moves their head and it can cause dizziness again).

205
Q

What treatment is given for vestibular neuritis/labyrinthitis?

A

Acute - vestibular sedatives (properazine only for a few days (central compensation - must promote adaptation of brain to new signals)), chronic - vestibular rehabilitation (exercises to promote compensation and recovery from spontaneous vertigo).

206
Q

What can cause facial palsy?

A

Can be to do with intratemporal pathology (e.g. cholesteatoma) or extratemporal pathology (e.g. a parotid gland tumour). May be idiopathic e.g. in Bell’s palsy but must still refer to ENT to ensure it is actually idiopathic.

207
Q

How is Bell’s palsy treated?

A

Steroids.

208
Q

What is the pathophysiology of allergy?

A

Type 1 hypersensitivity reaction. During sensatisation, plasma (T and B) cells produce IgE which binds to specific IgE receptors on mast cells and basophils. Re-exposure leads to mast cell degranulation (release of histamines, leukotrienes, prostaglandins and chromatomic factors). The products of mast cell degranulation cause vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction.

209
Q

What is allergy?

A

Patients with allergies have high levels of IgE specific to allergens - this causes them to have an exaggerated immune response to seemingly harmless antigens. These reactions are ACQUIRED.

210
Q

What happens in the acute phase of an allergic reaction?

A

Exposure of antigen, Ag+ specific IgE, degranulation of mast cells with release of histamine, cytokines, interleukins, leukotrienes, prostaglandins from their granules causing systemic vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction.

211
Q

What happens in the late phase of an allergic reaction (2-4h)?

A

Due to migration of leukocytes (e.g. neutrophils, lymphocytes, eosinophils and macrophages) to their initial site (cellular immunity).

212
Q

What can be used to investigate allergy?

A

Diagnosis often by history.
Skin tests (responses to known allergens - high NVP, up to 15% false positives, if react to saline test invalid).
RAST (presence and levels of allergen specific IgE).
Total serum IgE, nasal allergen challenge and nasal cytology can also be done.

213
Q

What are common allergies?

A

Eczema, hayfever, allergic rhinitis, asthma, food allergies (e.g. peanuts, milk, soy, eggs, wheat, fish…).

214
Q

What are the risk factors associated with allergy?

A

Hereditary, race, alterations in exposure to infection in early childhood, environmental pollution, allergen levels, dietary changes, occupation (flour, dust, latex = occupational rhinitis).

215
Q

What symptoms can people with allergies experience?

A

Utricaria (hives), angioedema, flushing, rashes, burning, itching, rhinitis, asthma, anaphylaxis (nauses, vomiting, abdominal cramps, diarrhoea, difficulty breathing, swelling/tenderness of mouth).

216
Q

How are allergies managed?

A

Allergen avoidance.
Topical nasal steroids, systemic steroids, antihistamines, sodium cromoglycate, allergen immunotherapy, anti-IgE, epinephrine, theophylline, antileukotrienes, glucocorticoids.

Need drugs to prevent activation of cells/degranulation. Immunotherapy better for allergic rhinitis, asthma, allergic conjunctivitis etc, not great for food allergy, atopic dermatitis etc. Patients given progressively larger doses, increasing IgG antibody production blocking IgE production due to chronic exposure.

217
Q

What is allergic rhinitis?

A

Allergic inflammation of nasal airways. It is caused when a sensitised individual inhales an allergen.

218
Q

What are the risk factors for allergic rhinitis?

A

Atopy, FH, alterations in exposure to infectious dx in childhood, environmental pollution, allergen levels, dietary changes, association with asthma and atopic dermatitis.

219
Q

What are the two types of allergic rhinitis and give examples of allergens in each.

A

Seasonal - e.g. hayfever

Perennial - e.g. HDM, cat, mould spores etc.

220
Q

What symptoms are associated with allergic rhinitis?

A

Sneezing, itching, nasal blockage, rhinorrhoea.
Chronic obstruction, hyposmia (air unable to reach olfactory area), hyperreactivity, bleeds (vasodilation as a result of oedema, leukotrienes and histamines can cause further oedema and blockage).

221
Q

How is allergic rhinitis managed?

A

If mild - anti-histamines and regular saline rinsing of nasal passages.
If severe - topical steroid sprays or turbinate reduction surgery/fix nasal deformities to allow better application of medication.

222
Q

What are causes of non-allergic rhinitis?

A

Infection, over-sensitive blood vessels in the nose, over use of decongestion causing a blocked/running nose, irritation in/around nose, sneezing, anosmia.

223
Q

How is non-allergic rhinitis treated?

A

Nasal douching, anti-histamines, nasal steroids.

224
Q

When do the maxillary and ethmoid sinuses form?

A

0-4 months.

225
Q

When doe the sphenoid sinus form?

A

3-7 years.

226
Q

When does the frontal sinus form?

A

8+ years.

227
Q

How many URTIs are normal children?

A

8 episodes a year for up to 15 days.

228
Q

How would you investigate a child with a blocked/runny nose?

A

Nasal speculum, otoscope (auriscope), spatula test (blockage), nasal endoscopy (difficult may need EUA), digital nasal otoscopy in older children.

229
Q

What can cause a blocked/runny nose in children?

A

Rhinitis, large adenoids (sleep apnoea?), sinusitis, polyps (associated with CF), foreign body.

230
Q

What symptoms/signs may a child with a blocked/runny nose present with?

A

Nasal discharge, pain, sneezing, loss of function.

Babies may have stopped feeding.

231
Q

What complications might a child with a runny/blocked nose experience?

A

Snoring may affect quality of sleep, periorbital cellulitis, proptosis, vision affected, bone structure v. thin and pus and infection can spread into eye space, choanal atresia (bilateral manifests as unable to breath and Rx involves surgery to remove membrane and putting up a stent).

232
Q

What is choanal atresia?

A

It is a congenital disorder where the back of the nasal passage (choana) is blocked, usually by abnormally bony or soft tissue (membranous) due to failed recanalization of the nasal fosse during foetal development.

233
Q

How do children with airway problems usually present?

A

Usually an emergency, Hx of foreign body, recent illness, feeding problem, stridor (inspiratory).

234
Q

What can cause airway issues in children?

A

Large tonsils, epiglottitis, short neck (subglottis is narrowest), foreign body, laryngomalacia.

235
Q

What commonly do rhinology patients present with?

A

Nasal obstruction (permanent vs intermittent), nasal discharge, sneezing, epistaxis, facial pain, nasal deformity (post-traumatic?), anosmia, dysomnia.

236
Q

What is Samter’s triad?

A

Asthma
Aspirin sensitivity
Polyps

237
Q

What kind of workers are at increased risk of rhinology problems?

A

Woodworkers

238
Q

What drug can cause septal perforation?

A

Cocaine

239
Q

What are the three pathways you can look at the nose through?

A
  1. straight on to the Eustachian tube
  2. middle meatus
  3. superior meatus and olfactory region
240
Q

What rhinology investigations are available?

A

Allergy tests (skin prick, RAST), FBC, ANCA, ESR, ACE (for Wegner’s/sarcoid), CTS, Xray (facial trauma), MRI, rhinomanometry.

241
Q

What sort of discharge does infective rhinosinusitis cause?

A

Runny, pink discharge.

242
Q

What sort of discharge does allergic rhinitis?

A

Clear, runny discharge.

243
Q

What is ANCA?

A

Antineutrophil cytoplasmic antibodies are autoantibodies produced by a person’s immune system that mistakenly target and attack proteins within a person’s neutrophils. ANCA testing detects and measures the amount of these antibodies in the blood.

244
Q

What is ESR?

A

Erythrocyte sedimentation rate is the rate at which RBCs sediment in a period of one hour. It is a non-specific marker of inflammation.

245
Q

What is craniocynotosis?

A

The baby’s sutures fuse prematurely. May need surgery if it is severe.

246
Q

What is (chronic suppurative otitis media) perforated tympanic membrane?

A

Chronic inflammation of the middle ear and mastoid process with a discharge from the middle ear through a perforated tympanic membrane for at least 6 weeks.

247
Q

What can cause (chronic suppurative otitis media) perforated tympanic membrane?

A

Occurs following an URTI that has lead to acute otitis media.

248
Q

What symptoms will someone with (chronic suppurative otitis media) perforated tympanic membrane experience?

A

Hearing loss, repeated ear infections, can be asymptomatic.

249
Q

How is (chronic suppurative otitis media) perforated tympanic membrane treated?

A

Surgery (only if symptomatic or patient wants to go swimming).

250
Q

What is tympanosclerosis? What can cause it?

A

Calcium deposits in the tympanic membrane. Occurs due to grommet insertion or acute otitis media with perforation.

Second Year (9 decks)

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