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ENT > Plastic Surgery > Flashcards

Plastic Surgery Flashcards

1
Q

what are the features of rhinoplasty procedure?

A

o incisions are made to access bones + cartilage
o bone may be removed, or grafts/synthetic filler added
o after reshaping the skin is redraped over structure of nose
o stents may be used to support

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2
Q

what are the features of mentoplasty procedure?

A

o Reduction of addition of material to a patients chin
o Chin rounding = osteotomy
o Chin augmentation = implants (intraoral or submental, alloplastic implants)

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3
Q

what are the features of otoplasty procedure?

A

o Cartilage splitting – incisions + repositioning of cartilage
o Cartilage sparing – avoid full thickness attempting to create more effective angles + curls

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4
Q

what is botulin toxins use in plastic surgery?

A

injected into muscles under facial wrinkles

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5
Q

what are facial fillers?

A

hydoronic acid, synthetic, collagen – fill up lines + hollows

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6
Q

what is blepharoplasty?

A

upper lid (take ellipse of skin), lower lid (more complicated)

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7
Q

what is skin rejuvenation?

A

use fat from patient = on NHS acnes scarring, hyaluronic acid

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8
Q

what is a face lift?

A

removal of excess skin, tightening of underlying tissues

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9
Q

how are wounds reconstructed?

A

o Primary closure – clean, simple cut
o Healing by secondary intention = treat infection, clean, debride
o Skin grafts and skin flaps

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10
Q

what are is the cause of acute tonsillitis?

A

Majority viral

B lactamase producing bacteria

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11
Q

what are the viral causes of acute tonsiliitis?

A

EBV, also rhinovirus, influenza, parainfluenza, enterovirus, adenovirus

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12
Q

what are the bacterial causes of acute tonsillitis?

A

streptococcus pyognes, H influenza, S aureus, streptococcus pneumoniae

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13
Q

what is the histology of the tonsils?

A

specialised squamous, deep crypts, lymphoid follicles and posterior capsule

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14
Q

what is the pathophysiology of acute tonsillitis?

A
  • Local inflammatory pathways result in oropharyngeal swelling, oedema, erythema and pain
  • Rarely swelling may progress to the soft palate and uvula or inferiorly to supraglottitis
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15
Q

what are the types of acute tonsillitis?

A
  • Acute parenchymatous
  • Acute Follicular
  • Acute Catarrhal Tonsillitis
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16
Q

what are the features of Acute parenchymatous tonsillitis?

A

swelling and erythema and whole tonsil

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17
Q

what are the features of Acute follicular tonsillitis?

A

crypts filled with infected fibrin and often spotted appearance

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18
Q

what are the clinical features of viral tonsillitis?

A

malaise, sore throat, temperature, able to undertake normal activity, possible lymphadenopathy

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19
Q

what are the clinical features of bacterial tonsillitis?

A

systemic upset, fever, odynophagia, halitosis, unable to work/school, lymphadenopathy, tonsillar exudates

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20
Q

how is tonsillitis diagnosed?

A

Centor Criteria

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21
Q

what are the features of the centor criteria?

A

o 1 point for each – absence of cough, fever, tonsil exudates, anterior cervical adenopathy, age <15
o Subtract point for >44

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22
Q

how do centor scores determine

A

o 0 or 1 point = no antibiotic
o 2 or 3 points = should receive antibiotic if symptom progress
o 4 or 5 points = treat empirically with antibiotic

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23
Q

what is the management of tonsillitis?

A
  • Supportive – eat&drink, rest, ibuprofen +/- paracetamol analgesia
  • 1st Line – antibiotics
  • 2nd Line – steroids
  • Hospital – IV fluid, IV antibiotic, steroid
  • Surgery - adenotonsillectomy
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24
Q

what is the antibiotics given in tonsillitis?

A

penicillin 500mg qd for 10 days (clarithromycin if allergic)

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25
Q

what is the indications for surgery in tonsillitis?

A

o 7 episodes in a year, 5 in 2 years consecutively or 3 or more in 3 preceding years, symptoms have been occurring for at least a year, the episodes of sore throat are disabling and prevent normal functioning

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26
Q

what are the complications of tonsillitis?

A

Quinsy, Airway obstruction, otitis media, sinusitis, spread of infection to brain, parapharyngeal abscess, retrophargyngeal abscess, rheumatic fever, septic arthritis, post streptococcal glomerulonephritis

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27
Q

what is a peritonsillar abscess?

A

abscess (pus) forms in the peritonsillar space between capsule of the tonsils (superiorly) and superior constrictor muscle

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28
Q

what are the causes of peritonsillar abscesses?

A

complication of bacterial tonsillitis, streptococcal organisms

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29
Q

what are the clinical features of peritonsillar abscess?

A
  • unilateral sore throat, odynophagia, headache, ipsilateral otalgia
  • hot potato voice, drooling, trismus, peritonsillar swelling, downwards displacement of tonsil, bulging soft palate on one side, deviated uvula away from side, systemic unilateral cervical lymphadenopathy
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30
Q

what is the management of peritonsillar abscess?

A

hospital admission for drainage along with IV antibitoics (e.g.benzylpenicillin)

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31
Q

what is a parapharyngeal abscess?

A

spread of infection from the tonsil or quinsy through the superior constrictor muscle of the pharynx into the parapharyngeal space

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32
Q

what is the cause of a parapharyngeal abscess?

A

complication of tonsillitis, dental infection

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33
Q

what are the clinical features of a parapharyngeal abscess?

A
  • sore throat, trismus, fever and malaise
  • swelling lateral pharyngeal wal – cause displacement of tonsil
  • erythematous upper lateral neck overlying tender swelling
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34
Q

what is the management of a parapharyngeal abscess?

A

referral to secondary Care

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35
Q

what are the complications of a parapharyngeal abscess?

A

airway obstruction, mediastinum infection, haemorrhage or carotid artery

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36
Q

what is a retropharyngeal abscess?

A

abscess in retropharyngeal space

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37
Q

what is the retropharyngeal space?

A

o space is posterior to pharynx
o bound by fascia anteriorly, paravertebral fascia posteriorly, carotid sheaths laterally
o extends inferiorly to mediastinum superiorly to base

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38
Q

what are the clinical features of retropharyngeal abscess?

A
  • sore throat, adnophagia, dysphagia, neck stoffness, voice change, malaise and/or lump, unilateral lymphadenopathy, rigors
  • neck swelling may be present
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39
Q

what is the management of retropharyngeal abscess?

A

emergency admission, airway care, incision and drainage + antibiotics

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40
Q

what is cause of mumps?

A

paramyxoviruses

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41
Q

what is the spread of infection of mumps?

A

virus moves from respiratory tract to parotid gland, where it replicates
Can enter CSF

42
Q

what other organs are can be affected by mumps?

A

brain, pancreas, testicles and ovaries (ependymal cells)

43
Q

what are the clinical features of mumps?

A
  • Symptoms usually develop 14-25 days after infection
  • Bilateral parotitis
  • Associated orchitis
  • Parotid duct may appear swollen and red
  • Headache, joint pain, feeling sick, dry mouth abdo pain, feeling tired, anorexia, fever
44
Q

how is mumps diagnosed?

A

clinical examination, PCR of nasal or saliva samples, raised plasma amylase

45
Q

what is the management of mumos?

A
  • Supportive – bed rest, fluid, pain relief, cool/warm compress
  • Prevent infection
  • Vaccine
46
Q

what are the complications of mumps?

A
  • Orchitis
  • Spontaneous abortion
  • Meningitis or encephalitis
  • Ovarium inflame
  • Brain inflame
  • Hearing loss
47
Q

what is the cause of Diptheria?

A

Corynebacterium dihtheriae

48
Q

what is the pathophysiology of diptheria?

A
  • transmission through air

* diphtherian toxin is produced – inhibits synthesis of new proteins, neurotoxic and endotoxic

49
Q

what are the clinical symptoms of dipetheria?

A
  • severe sore throat (tonsillitis) + grey white membrane across the pharynx
  • pseudomembrane of pharynx may become large + obstruct
  • temperature
  • breathing difficulty
  • polyneuritis – cranial nerve palsy
  • Shock can occur through myocarditis or toxaemia
50
Q

how is diphtheria diagnosed?

A

swab material below grey membrane, PCR

51
Q

how is diphtheria managed?

A
  • Antitoxin and erythromycin

* supportive

52
Q

what is the age group most affected by glandular fever?

A

most commonly effects 15-24 year olds - “kissing disease”

53
Q

what is the cause of glandular fever?

A
  • Ebsetin-Bar – spread through salvia

* Others: cytomegaly, HIV, HPV

54
Q

what is the pathophysiology of glandular fever?

A
  • Virus first replicates within epithelial cells in the pharynx, then primarily with B cells
  • Circulating B cells spread infection through liver, spleen, lymphnodes
55
Q

what is the triad of symptoms in glandular fever?

A

pharyngitis, fever and cervical lymphadenopathy

56
Q

what is the symptoms of infective mono?

A

Triad of pharyngitis, fever and cervical lymphadenopathy plus lymphocytosis with atypical lymphocyte

57
Q

what are the other clinical features of glandular fever?

A
  • Malaise, lethargy
  • Bilateral enlarged tonsils covered in exudate
  • Other – rash, jaundice/hepatitis, splenomegaly, palatal petchiae, haemolytic anaemia (cold agglutins IgM)
58
Q

how is glandular fever diagnosed?

A
  • IgM positive (antibiotics) – Paul Bunnel or monospot

* IgG positive – blood count + film + LFTs

59
Q

what is the management of glandular fever?

A
  • Bed rest
  • Paracetamol
  • Avoid sport for 8 weeks to avoid splenic rupture
  • Antivirals not effective
60
Q

why is penicillin avoided in glandular fever?

A

a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

61
Q

what is the cause of hand, foot and mouth disease?

A

coxsackie viruses (enterovirises) – A16, EV-17

62
Q

what is the route of spread of coxsackie virus?

A
  • spread through close contact, coughing, faecal
  • viremia develops followed invasion of skin + mucus membrane
  • incubation period 5-7 days
63
Q

what are the clinical features of hand, foot and mouth disease?

A
  • commonly kids
  • fever (without flu like symptoms)
  • sore throat
  • loss of appetite
  • a few days later appearance of rash and papules on hand and feet and around mouth – vesicles + macerated ulcers
  • ache in limbs
64
Q

how is hand, foot and mouth disease diagnosed?

A
  • clinically

* PCR test of viral transport medium

65
Q

what is the treatment of hand, foot and mouth disease?

A
  • Good hygiene to prevent spread – take off school/work

* Supportive – fluids, soft foods, paracetamol

66
Q

what are the two types of herpes simplex virus?

A
  • Type 1 – acquired in childhood, most cause of mouth ulcers

* Type 2 – more likely to reactivate (sexual contact)

67
Q

how is herpes simplex spread?

A

through saliva contact

68
Q

what is the infection pathway of herpes simplex virus?

A
  • Invades cells by binding to transmembrane receptors via their glycoprotein
  • Travels to cell nucleus and via pore injects its DNA
  • Latency Period – after primary infection an inactive form is stored in the sensory nerve cells where it can be reactivated
69
Q

what is the cause of primary gingivostomatitis?

A

HSV1

70
Q

what age group is commonly affected by primary gingivostomatitis?

A

pre school children

71
Q

what are the clinical features of Primary Gingivostomatitis?

A

 Systemic upset
 Sudden onset
 Vesicles + ulcers n the lips, buccal mucosa, and hard palate
 Halitosis + refusal to eat/drink

72
Q

what is the management of Primary Gingivostomatitis?

A

take up to 3 weeks, acyclovir

73
Q

what is the cause of cold sores?

A

HSV1

74
Q

what is the pathophysiology of cold sores?

A

various stimuli causes reactivation from nerves to cause active infection (stress, illness)

75
Q

what are the clinical features of cold sores?

A

oral lesion

76
Q

what is the management of cold sores?

A

acyclovir treatment or suppression (won’t treat latency)

77
Q

what is the clinical features of herpetic whitlow?

A

lesion on finger or thumb

78
Q

what is the management of herpetic whitlow?

A

self limiting, acyclovir

79
Q

what is the pathophysiology of Herpes Simplex Encephalitis?

A

trigmeninal + ophthalmic nerve involvement

80
Q

what are the clinical features of Herpes Simplex Encephalitis?

A

altered level of consciousness

81
Q

what is a diagnostic feature of Herpes Simplex Encephalitis?

A

Increased white cell count in CSF

82
Q

what is sialolithiasis?

A

Formation of calcified masses within a salivary gland

83
Q

where does sialolithiasis occur?

A

Most common with submandibular (95%), parotid (5%)

84
Q

what is the pathophysiology of sialolithiasis?

A

Composed of inorganic calcium and sodium phosphate salts mixed with mucous and cellular debris = calculi

85
Q

what is the cause of sialolithiasis?

A
  • Alteration in calcium metabolism
  • Dehydration
  • Reduced salivary flow rate
  • Altered pH salivary
  • Food debris, foreign body, bacteria – stuck in salvia glands
86
Q

what are the clinical features of sialolithiasis?

A
  • Pain – intermittent (worse before mealtimes)
  • Swelling of gland
  • Tenderness of gland
  • Palpable hard lump
  • Lack of salvia
  • Erythema of floor of mouth
87
Q

how is sialolithiasis diagnosed?

A

sialography, xray (appear radio opaque)

88
Q

what is the management of sialolithiasis?

A
  • Non-invasive – hydration, moist heat therapy, NSAIDs, sour foods, massage, shock wave therapy
  • Small stones normally pass
  • Silendoscopy
  • Surgery
  • Antibiotics to prevent infection
89
Q

what is Wegeners Granulomatosis?

A

Granulomatosis with Polyangiitis

90
Q

what is the cause Wegeners Granulomatosis?

A
  • Unknown – autoimmune condition

* Microbes and genetics implicated in pathogenesis

91
Q

what is the pathophysiology Wegeners Granulomatosis?

A
  • Small vessel vasculitis limited to respiratory tract and kidneys
  • Inflammation and infiltration by immune cells forming granulomas
92
Q

what is the histology of Wegeners Granulomatosis?

A

o Looks like granuloma (blood vessel infiltrated with neutrophils)
o Palsy immune necrotizing vasculitis

93
Q

what is the characteristic antibody associated with Wegeners Granulomatosis?

A

ANCA - react with proteinase 3 – activate neutrophils, increase their adherence, induce degranulation

94
Q

how is wegeners diagnosed?

A

presence of ANCA, FBC, EVC, ESR, CRP, urine casts, Xray

95
Q

how is wegeners managed?

A

high dose corticosteroids, DMARDs – methotrexate, cyclophosphamide, plasma exchange

96
Q

what are the kidney clinical features of Wegeners?

A

progressive glomerulonephritis – chronic kidney disease

97
Q

what are the ENT clinical features of Wegeners?

A

o Nose – pain, stuffiness, nosebleed, rhinitis, crusting, saddle nose deformity (perforated septum), paranasal and sinusitis
o Ears – hearing loss, serous otits media
o Oral cavity – strawberry ginvitis, ulceration, tooth destruction

98
Q

what are the trachea clinical features of Wegeners?

A

subglottal stenosis

99
Q

what are the lungs clinical features of Wegeners?

A

pulmonary nodules, pneumonia, haemorrhage, pleuritis

100
Q

what are the eye clinical features of Wegeners?

A

conjunctivitis, proptosis

101
Q

what are the non-specific clinical features of Wegeners?

A

fever, cough, w/loss, arthritis

102
Q

what are the skin clinical features of Wegeners?

A

nodules, purpura

ENT (13 decks)

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