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Clinical Conditions > 12. Head and Neck > Flashcards

12. Head and Neck Flashcards

1
Q

Where can infection of the superficial fascia spread?

A

Nowhere, simple cellulitis.

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2
Q

Where can infection of the retropharyngeal space spread?

A

Mediastinum.

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3
Q

Where can infection of the danger space (posterior to alar fascia) spread?

A

Diaphragm.

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4
Q

Where can infection of the parapharyngeal space spread?

A

T2/3, affecting carotid sheath structures.

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5
Q

Where can infection of the prevertebral fascial space spread?

A

T2/3.

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6
Q

What causes branchial cysts/fistulae?

A

Failure of pharyngeal clefts to recede.

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7
Q

What is the difference between branchial cysts and fistulae?

A

Cysts - fluid filled pockets, fistulae - openings between two epithelia.

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8
Q

Where are branchial cysts/fistulae seen?

A

Anterior border of SCM within the neck.

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9
Q

Why do atheromas form in the carotid sinus?

A

There is a bulge, leading to turbulent flow which damages epithelia.

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10
Q

What is the risk of carotid atheroma formation?

A

Embolism to brain causing stroke or TIA.

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11
Q

What is carotid sinus hypersensitivity?

A

Carotid sinus is very sensitive, small touch is detected as high pressure by CN IX so CN X efferent activates baroreceptors reflex to drop BP.

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12
Q

Why do scalp lacerations cause profuse bleeding?

A

Blood vessels are in deep connective tissue layer so can’t constrict. Lots of anastamoses. If epicranial aponeurosis involved, occipital and frontal bellies contract and pull wound open.

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13
Q

What is the danger triangle of the face?

A

Area bound by canthuses of the mouth and bridge of nose. Infection likely to track back here.

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14
Q

What are the general causes of enlarged lymph nodes?

A

Infection or malignancy.

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15
Q

How do enlarged lymph nodes present differently according to if the cause if malignant or infectious?

A

Malignant: hard, matted, non tender, immobile.
Infections: tender, firm, mobile.

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16
Q

What is tonsillitis?

A

Inflammation of the palatine tonsils.

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17
Q

What are the symptoms of tonsillitis?

A

Odynophagia and fever.

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18
Q

When are tonsillectomies performed?

A

In those prone to tonsillitis reinfections.

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19
Q

What is whiplash?

A

Acute and large force applied across C spine causing overstretching of tendons and ligaments of spine -> intense, sharp pain.

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20
Q

What is a Burst/Jefferson fracture?

A

Huge force to atlas causes bilateral fractures in posterior portion with avulsion of anterior arch.

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21
Q

Why do Burst/Jefferson fractures rarely cause spinal cord injury?

A

The fragments travel outwards.

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22
Q

What is a Hangman’s fracture?

A

Hyperextension of the neck -> bilateral fractures of pars interarticularis, damaged spinal cord, and death.

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23
Q

What is fracture pterion?

A

Fracture of the lateral side of the skull where sphenoid, temporal, parietal, and frontal bones fuse - thinnest portion of skull?

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24
Q

Explain the complication of a fractured pterion.

A

Middle meningeal artery lies deep to the pterion so fracture can rupture the artery -> extradural haematoma.

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25
Q

What is coning?

not sure this is in course

A

Increased ICP forces cerebellar tonsils through foramen magnum of occiput -> pressure on brainstem and death.

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26
Q

How is the skull of a neonate different to that of an adult, and why?

A

Suture lines aren’t fused at birth. This allows manoeuvrability when in birth canal and later growth of the brain.

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27
Q

What is the risk with calvaria in premature babies?

A

The bones are so far apart that they may not fuse -> brain damage.

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28
Q

What are the types of fractures of the skull?

A

Depressed fracture, linear fracture, comminuted fracture, coutercoup fracture, basilar fracture.

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29
Q

What is a depressed fracture of the skull?

A

Fracture caves in and can press on brain. Commonly at pterion.

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30
Q

What is a linear fracture of the skull?

A

Lines spread out from impact bone in several directions but bone doesn’t cave inwards.

31
Q

What is a comminuted fracture of the skull?

A

Skull splits into distinct pieces of bone, involves break in skin.

32
Q

What is a countercoup fracture of the skull?

A

Force travels round skull and occurs on opposite side to point of impact.

33
Q

What is a basilar fracture of the skull?

A

At back of head, basilar part of occipital bone.

34
Q

What are the types of mandibular fracture?

not sure if this is in course

A

Coronoid process fracture, congylar process fracture, angle of mandible fracture, body of mandible fracutre.

35
Q

What is a lateral cleft lip due to?

A

Failure of medial nasal prominence and maxillary prominence to fuse so split in mucosa up to nostril.

36
Q

What is a cleft palate due to?

A

Failure of palatal shelves to fuse in midline.

37
Q

What are the implications of cleft palate?

A

Difficulty suckling and with speech.

38
Q

What is foetal alcohol syndrome due to?

A

Alcohol intake in pregnancy causing neurodevelopmental delay.

39
Q

What are the physical features of foetal alcohol syndrome?

A

Short palpebral fissures (small eyes), no philtrum, small head, underdeveloped jaw, thin upper lip.

40
Q

What are the mental features of foetal alcohol syndrome?

A

Behavioural disorders, learning disorders, hearing and sight problems.

41
Q

What can cause olfactory nerve lesions?

A

Cribriform plate fractures, or meningitis.

42
Q

What is the result of olfactory nerve lesions?

A

Anosmia.

43
Q

What can cause optic nerve lesions?

A

Central retinal artery occlusion or compression by pituitary adenoma.

44
Q

What are the results of optic nerve lesions?

A

Loss of vision depending on site along nerve. Reduced visual acuity, visual fields and defective direct and consensual pupillary reflexes.

45
Q

What are the three sites of optic nerve damage?

A

Proximal to optic chiasm, at optic chiasm, at optic tract.

46
Q

What are the features of CN II lesions proximal to optic chiasm?

A

Carries all sensory from one eye so total loss in this eye. Reduced vision on lateral field of vision on same side.

47
Q

What are the features of CN II lesions at the optic chiasm?

A

Medial fibres supplying lateral fields of vision cross and are both damaged. Reduced peripheral vision - tunnel vision.

48
Q

What is the most common cause of CN II lesions at the optic chiasm?

A

Pituitary adenoma.

49
Q

What are the features of CN II lesions at the optic tract?

A

Fibres receiving information from other side’s field of vision damages, loss of vision in contralateral field of vision.

50
Q

What is a common cause of CN II lesions at the optic tract?

A

Parietal lobe tumour.

51
Q

What can cause oculomotor nerve lesions?

A

Cavernous sinus thrombosis most commonly, or raised ICP.

52
Q

What is the presentation of oculomotor nerve lesions?

A

Ptosis (loss of levator palpebrae superiosis) and down and out pupil (unopposed actions of superior oblique and lateral rectus). Loss of accommondation reflex and blown pupil if parasympathetic fibres involed (loss of constrictor pupillae).

53
Q

What is the cause of Horner’s syndrome?

A

Damage to sympathetic trunk.

54
Q

What can cause Horner’s syndrome?

A

Pancoast tumour.

55
Q

What is the presentation of Horner’s syndrome?

A

Ptosis (loss of superior tarsus), constricted pupil (myadrisis from loss of dilator pupillae) and anhydrosis (loss of sympathetically mediated sweating).

56
Q

What can cause a lesion of the trochlear nerve?

A

Cavernous sinus thrombosis.

57
Q

What is the presentation of trochlear nerve lesion?

A

Diplopia when looking down and in (superior oblique lost) - head tilt to compensate.

58
Q

What is the presentation of lesion to the trigeminal nerve?

A

V1 and V2 - sensory loss in distributions. V3 - loss of mastication muscle as well as sensory loss. Sympathetic fibres that hitch hike nerve damaged -> vasodilation and anhydrosis.

59
Q

What is Harlequin syndrome?

A

Damage to sympathetic fibres that hitch hike CN V at sympathetic trunk/thoracic cord.

60
Q

What is the presentation of Harlequin syndrome?

A

Vasodialtion and anhydrosis across entire half of face.

61
Q

What is trigeminal neuralgia?

A

Severe sharp pain within distribution of trigeminal nerve that lasts to seconds-minutes. From sudden movements or idiopathic.

62
Q

What is one of the first signs of increased ICP and why?

A

Can’t abduct eye as CN VI lesion.

63
Q

What is the presentation of abducens nerve palsy?

A

Paralysis of lateral rectus so diplopia on lateral gaze in affected eye.

64
Q

Where is the facial nerve at risk of lesion?

A

Parotid gland, facial canal, forceps delivery.

65
Q

What affects the facial nerve in the parotid gland and what are the effects?

A

Parotitis or malignancy, affects motor function.

66
Q

What affects the facial nerve in the facial canal and what are the effects?

A

Inflammation. Nerve to stapedius affected -> hyperacusis. Submandibular ganglion affect -> taste sensation, sublingual and submandiublar glands affected. Motor function also affected.

67
Q

What is the presentation of facial nerve palsy from forceps delivery?

A

Affects extracranial portion so only motor functions affected.

68
Q

What is Bell’s palsy?

A

Idiopathic damage to facial nerve affecting mostly motor functions.

69
Q

What is the presentation of Bell’s palsy?

A

Paralysis of facial muscles on the same side.

70
Q

What is the presentation of facial nerve lesion from stroke?

A

Unable to perform most facial actions apart from wrinkle forehead/raise eyebrows as frontalis is supplied by left and right facial motor nuclei.

71
Q

What are the consequences of vestibulocochlear nerve lesions?

A

Vestibular portion -> inability to balance => vertigo. Cochlear portion -> sensorineural hearing loss.

72
Q

What is a vestibular schwannoma?

A

Benign tumour of Schwann cells of vestibulocochlear nerve.

73
Q

What is the presentation of vestibular schwannoma?

A

Same as CN VIII lesions - vertigo and sensorineural hearing loss. If large enough, can impinge on CN VII in facial canal -> altered hearing, taste, and facial paralysis.

Clinical Conditions (13 decks)

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