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ENT > Oral cavity > Flashcards

Oral cavity Flashcards

1
Q

The pharynx is covered by a complete ring of lymphoid tissue called

A

Waldeyers’s ring

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2
Q

What is found found on the superior and posterior walls of the nasopharynx

A

The adenoid or pharyngeal tonsil that is a lobulated mass of lymphoid tissue

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3
Q

Waldeyers’s ring is comprised of

A

the adenoids (pharyngeal tonsils)

the palatine tonsils,

the lingual tonsil

and lateral pharyngeal bands,

scattered lymphoid follicles

and nodules near the Eustachian tube

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4
Q

Unlike the palatine tonsil, the adenoid has no

A

capsule

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5
Q

Adenoid response to adverse conditions

A

Hyperplasia and obstruction

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6
Q

The palatine tonsil is a large mass of lymphoid tissue located in the lateral part of the fauces, between

A

the glossopalatine and pharyngopalatine arches

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7
Q

The lateral surface of each palatine tonsil is covered by

A

pharyngeal fascia

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8
Q

lateral surface of each palatine tonsil is attached to

A

the superior pharyngeal constrictor muscle

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9
Q

The free surface of the tonsil is covered by

A

a closely adherent stratified squamous epithelium that extends into blind pouches or crypts

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10
Q

The mucosa of the dorsum of the tongue, posterior to the foramen caecum and the sulcus terminalis, is rough and freely mobile over the nearby parts. It has numerous lymph follicles which form the

A

It has numerous lymph follicles which form the l

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11
Q

Adenoid hyperplasia

A

Enlarged pharyngeal lymphoid tissue

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12
Q

the primary cause of sleep-disordered breathing in children

A

Adenoid hyperplasia

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13
Q

Clinical features of Adenoid hyperplasia

A

Nocturnal symptoms include snoring, mouth breathing, sleep pauses or breath holding, gasping, enuresis, and restless sleep. During the day, the children present with behavioural problems, morning headaches, dry mouth, halitosis, audible breathing, open-mouth posture, hyponasal speech, chronic nasal obstruction with or without rhinorrhoea and middle ear effusion

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14
Q

Treatment of Adenoid hyperplasia

A

Adenoidectomy

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15
Q

Tonsillar hyperplasia can contribute to

A

obstructive sleep apnoea syndrome (OSAS)

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16
Q

obstructive sleep apnoea syndrome (OSAS) OSAS is characterised by

A

reduction (hypopnoea) or cessation (apnoea) of oronasal airflow despite respiratory effort

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17
Q

Untreated OSAS can cause

A

failure to thrive,

aspiration,

chest infections,

and cor pulmonale

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18
Q

Treatment of Tonsillar hyperplasia

A

Treatment is surgical — tonsillectomy or intracapsular tonsillar resection (tonsillotomy)

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19
Q

OSAS is common in children with

A

developmental delay, neurological impairment and craniofacial dysmorphism

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20
Q

What is the gold standard for an objective correlation of ventilatory abnormalities.

A

Polysomnography

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21
Q

Features of Herpes simplex stomatitis

A

Burning sensation in the mouth, difficulty in eating, a feeling of being unwell, fever in the early stages, and clear vesicles in the mouth

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22
Q

Progression of vesicles in Herpes simplex stomatitis

A

h. The vesicles may progress to superficial circular or oval ulcers with a red centre

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23
Q

Treatment of Herpes simplex stomatitis

A

Systemic antiviral therapy

including anaesthetics or topical antiviral agents (acyclovir, penciclovir

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24
Q

Clinical features of Candidal stomatitis

A

Burning in the mouth and tongue with superficial white foci, and exudates on the mucosa.

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25
Q

Candidal stomatitis aetiology

A

Candida albicans

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26
Q

Who is most at risk of infection with Candidal stomatitis

A

severely immunosuppressed hosts. Candidiasis affects individuals with diabetes mellitus, reduced resistance, and after prolonged administration of antibiotics, chemotherapy, steroids, oral contraceptives, and after radiotherapy

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27
Q

Treatment and prognosis of Candidal stomatitis

A

Antimycotics are administered, and good oral hygiene is also crucial. The prognosis is good if the patient is relatively healthy. In immunosuppressed individuals, there is a risk of systemic spread if treatment is not adequate

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28
Q

What is Allergic stomatitis

A

Hypersensitivity reactions on the oral mucosa and the lips, with varying severity, with or without angioneurotic oedema

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29
Q

Causes of Allergic stomatitis

A

almost all drugs, dental material, mouthwashes, toothpaste, cosmetics, chewing gum, and also to some foods, e.g. fruit, fish, protein, and milk.

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30
Q

Herpes zoster definition

A

resulting from reactivation of the varicella-zoster virus

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31
Q

Morphology of clinical features of Herpes Zoster

A

Unilateral rapidly progressive vesicles are quickly followed by fibrinous superficial epithelial defects

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32
Q

Nerve distribution of Zoater on face

A

Affects the segments of the face innervated by the second and third divisions of the trigeminal nerve

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33
Q

Tx of Herpes zoster

A

high-dose regimens of systemic antiviral agents (acyclovir, valacyclovir, famciclovir) within 48 h

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34
Q

Bnefits of prompt Herpes zoster tx commencement

A

shown to reduce the duration and severity of the acute disease and somewhat reduce the risk of postherpetic neuralgia

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35
Q

Ludwig angina Definition and aetiology

A

rapidly expanding diffuse inflammation of the floor of mouth, submandibular and sublingual spaces often caused by dental infections.

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36
Q

Clinical features of Ludwig angina

A

The patient’s floor of mouth is swollen, the tongue might be swollen or elevated. A CT sacan is most useful.

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37
Q

Treatment of ludwig angina

A

Airway control is the first priority of treatment, followed by i.v. antibiotics and timely surgical drainage

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38
Q

Early otorhinolaryngologic symptoms of HIV/AIDS

A

angular cheilitis and Kaposi sarcoma

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39
Q

Chronic aphthae (recurrent aphthous stomatitis)

A

recurrent oral ulcerations, generally small with an erythematous base

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40
Q

Chronic aphthae (recurrent aphthous stomatitis) anatomical locations

A

buccal mucosa, the tongue, the palate, and the gingiva

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41
Q

Accimpanying features of Chronic aphthae (recurrent aphthous stomatitis)

A

regional lymph nodes may be swollen

, and concomitant stomatitis

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42
Q

Aphthae can be triggered by

A

infections, hormonal factors such as menstruation, and certain foods

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43
Q

Symptomatic treatment of aphthous stomatitis

A

borax solution, chlorhexidine, and topical corticosteroids. The lesions heal without scarring in 1–3 weeks. The course may extend over decades, and familial occurrences are known

44
Q

Hyperkeratosis

A

velvety or nodular epithelial lesion

45
Q

Leukoplakia

A

Flat epithelial plaque or white thickening that cannot be wiped off

46
Q

Hyperkeratosis and leukoplakia causes

A

chronic mechanical irritation by the irregular edge of teeth, irritation from a ill fiting denture, smoking, excess alcohol consumption, lichen planus, syphilis, and lupus erythematosus

47
Q

Prognosis of leukoplakia depends on

A

Degree of dysplasia and can lead to CA

48
Q

Treatment and dx in leukoplakia

A

Diagnosis is made by biopsy and histological examination. Treatment consists of surgical removal and avoidance of possible causative agents

49
Q

Bowen’s disease (erythroplakia) definition

A

clinical diagnosis and means “red patch”

premalignant lesion or carcinoma in situ

50
Q

Aetiopthogenesis of Bowen’s disease (erythroplakia

A

This is an intraepithelial squamous cell carcinoma with an intact basal membrane; the tumour has not yet invaded the subepithelial layer. It occurs on the skin or mucosa. Progression to true squamous cell carcinoma is possible at any time and is very common

51
Q

Bowen’s disease (erythroplakia) treatment

A

The lesion must be biopsied and, as a treatment option, excised with an adequate margin

52
Q

Acute tonsillitis

A

Tonsillitis is inflammation of the pharyngeal tonsils. The inflammation usually extends to other parts of the pharynx; therefore, the terms pharyngitis, tonsillopharyngitis and adenotonsillitis may also be used

53
Q

Clinical presentation of acute tonsillitis

A

igh temperature and possibly chills, especially in children. The patient complains of a burning sensation in the throat, persistent pain in the oropharynx, pain on swallowing (odynophagia), and pain radiating to the ear on swallowing. Opening the mouth is often difficult and painful, the tongue is coated, and there is halitosis. The patient also complains of headaches, thick speech, a marked feeling of malaise, and swelling and tenderness of the regional lymph nodes

54
Q

Clinical features of lymphoepithelial organs in acute tonsillitis

A

Both tonsils and the surrounding area, including the posterior pharyngeal wall, are deep red and swollen. In catarrhal tonsillitis there is no exudate on the tonsil. Later, yellow spots corresponding to the lymphatic follicles form on the tonsils

55
Q

How acute tonsillitis progresses to follicular tonsillitis

A

Yellow spots corresponding to the lymphatic follicles form on the tonsils

56
Q

What type of tonsillitis occurs when yellow spots occur over the openings of the crypts,

A

lacunar tonsillitis

57
Q

describe membrane that forms in pneumococcal tonsillitis

A

seldom confluent and rarely spreads beyond the tonsil.

58
Q

Most episodes of acute pharyngitis and acute tonsillitis are caused by the following viruses

A

herpes simplex virus, Epstein–Barr virus (EBV), cytomegalovirus, adenovirus, and measles virus.

59
Q

The most common bacteria causing tonsillitis

A

β-haemolytic streptococci

60
Q

DX of Acute tonsillitis

A

ESR

CRP

FBC

Paul Bunnell or infectious mononucleosis testing and urinalysis

61
Q

Differential diagnosis Acute tonsillitis

A

scarlet fever, diphtheria, infectious mononucleosis, agranulocytosis, leukaemia, hyperkeratosis of the tonsils, stage 2 syphilis, and, in unilateral disease, ulceromembranous tonsillitis, peritonsillar cellulitis or abscess, tuberculosis, and tonsillar tumours

62
Q

Differential blood count IN ACUTE TONSILLITIS EXCLUDES

A

mononucleosis and leukaemia.

63
Q

Other forms and types of acute tonsillitis

A

Nasopharyngitis

Lingual tonsillitis

Infection of the lateral bands

64
Q

The standard treatment in patients with streptococcal tonsillitis is

A

penicillin V for 10–14days.

Oral cephalosporins or macrolides can be used in patients allergic to penicillin.

As acute tonsillitis is a systemic, rather than local, disease, treatment should include bed rest, analgesics, a bland liquid diet, and ice packs.

The patient should be observed for complications. Local care should include oral and dental hygiene.

65
Q

Infectious mononucleosis (glandular fever)

A

This is an infection caused by the Epstein–Barr virus, which chiefly affects children and adolescents

66
Q

Clinical presentation of Infectious mononucleosis (glandular fever)

A

Patients often present with fever in the range of 38–39°C

and marked lymphadenopathy of the jugulodigastric group and the deep cervical chain, later becoming generalised.

The tonsil is very swollen and is covered with a fibrinous exudate or membrane.

The patient has rhinopharyngitis,

hepatosplenomegaly,

pain in the neck on swallowing,

and a marked feeling of being unwell

67
Q

The blood picture of Infectious mononucleosis

A

initially shows leukopenia, and then leukocytosis with a white blood cell count of 20,000–30,000 or more, 80– 90% of which are mononuclear cells and atypical lymphocytes

68
Q

Approximately 30% of IM develops secondary bacterial infections with

A

β haemolytic Streptococcus

69
Q

Diagnosis of infectious mononucleosis

A

This is made from the clinical findings, the characteristic blood picture, and the Paul Bunnell test (demonstration of heterophile antibodies in the serum).

70
Q

Treatment in IM

A

t. Symptomatic treatment includes oral hygiene and measures to reduce fever. Antibiotics may be given in secondary bacterial infection. An allergy-like rash may occur in response to ampicillin

71
Q

Chronic tonsillitis

History and features

A

The history is likely to reveal recurrent attacks of tonsillitis.

There is often little pain in the neck and little or no difficulty in swallowing.

There is halitosis and a bad taste in the mouth.

The cervical lymph nodes are often enlarged

72
Q

The systemic effect of chronic tonsilitis may become evident through

A

reduced resistance, fatigue, unexplained high temperature, and loss of appetite

73
Q

Pathogenesis of chronic tonsillitis

A

Impaired drainage of the tonsillar crypts leads to retention of cell debris, which forms a good culture medium for bacteria.

From crypt abscesses of this type, the infection extends via epithelial defects in the reticular epithelium into the tonsillar parenchyma to produce a cryptic parenchymatous tonsillitis.

In the long term, the tonsillar parenchyma undergoes fibrosis and atrophy

74
Q

Chronic tonsillitis diagnosis

A

The tonsils are more or less fixed to their base, and the surface is fissured or scarred. Watery exudate and greyishyellow material can be pressed out of the opening of the crypts by a tongue depressor. Erythema of the anterior faucial pillar is present

75
Q

Chronic pharyngitis

A

This is a comprehensive term for several chronic irritative or inflammatory conditions of the pharyngeal mucosa

76
Q

Classification of Chronic pharyngitis

A

Simple

Atrophic

Chronic Hyperplastic

77
Q

Chronic pharyngitis simple

A

a globus sensation,

constant throat clearing,

bouts of coughing,

a feeling of dryness or phlegm in the throat,

pain of varying degrees in the neck and on swallowing,

and tenacious secretions. The course is intermittent, and there is no generalised upset and no fever

78
Q

Chronic hyperplastic Chronic pharyngitis

A

The mucosa of the posterior pharyngeal wall is thickened and granular, with prominent solitary follicles. It is smooth red to greyish-red in colour, possibly with venous telangiectasis and secretion of stringy, colourless mucus. There is usually a very disturbing, strange sensation in the pharynx with compulsive throat clearing and swallowing, gagging, and even vomiting

79
Q

Chronic atrophic Chronic pharyngitis

A

The posterior pharyngeal wall is dry and glazed, often with dry, tough crusts of secretion. The mucosa is smooth, pink, often very tender and transparent, but may also be red and thickened. At night, there is a feeling of choking and disturbance of sleep. Older people are more often affected

80
Q

Chronic pharyngitis pathogenesis

A

The disease may be due to chronic exogenous damage from dust, chemicals, and heat. Common contributing factors are marked temperature changes, voice abuse, working in a smoky environment, working in a dry or improperly air-conditioned atmosphere, heavy smoking and drinking, oral breathing, chronic nasal airway obstruction, abuse of nose drops and sprays, chronic sinusitis, and hypertrophic adenoids. Other causes include endocrine disorders (e.g. menopause, hypothyroidism) or avitaminosis A

81
Q

Chronic pharyngitis differential diagnosis

A

Sjögren syndrome, Plummer–Vinson (Paterson–Brown– Kelly) syndrome, and malignancy of any part of the pharynx or oesophagus.

82
Q

Treatment of Chronic pharyngitis

A

Symptomatic treatment includes moisturising the pharyngeal mucosa with steam inhalations. A change of climate is advised. Patients may even have to change their job or place of residence

83
Q

Peritonsillar abscess

A

This is usually a complication of acute tonsillitis caused by accumulation of purulent exsudate (pus) in the peritonsillar space

84
Q

Peritonsillar abscess clinical features

A

The pain usually radiates to the ear, and opening of the mouth is difficult due to trismus. The speech is thick and indistinct. The pain is so severe that the patient often refuses to eat, the head is held over to the diseased side, and rapid head movements are avoided. The patient has sialorrhoea and oral foetor, swelling of the regional lymph nodes, increased fever with high temperatures of 39–40°C, and the general condition deteriorates rapidly. Patients also have an intolerable feeling of pressure in the neck, obstruction of the laryngeal inlet, and increasing respiratory obstruction. However, the symptoms may sometimes only be mild

85
Q

In Peritonsillar abscess inflammation spreads from the tonsillar parenchyma to the surrounding tissue; an abscess forms between

A

between the capsule of the tonsil and the tonsillar fossa (inferior constrictor muscle) within a few days

86
Q

Diagnosis of peritonsillar abscess

A

clinical picture of swelling, redness, and protrusion of the tonsil, faucial arch, palate, and uvula

The uvula is pushed towards the healthy side, and there is marked tenderness of the tonsillar area. Inspection of the pharynx may be difficult due to severe trismus. The blood count, CRP and ESR are typical of an acute infection

87
Q

Peritonsillar abscess Differential diagnosis

A

peritonsillar cellulitis, tonsillogenic sepsis, allergic swelling of the pharynx without fever (angioneurotic oedema), malignant diphtheria, agranulocytosis, specific tonsillar infections (tuberculosis and syphilis), and nonulcerating tumours of the tonsil or neighbouring tissues (malignant lymphoma, lymphoepithelial tumour, anaplastic carcinoma, or leukaemia)

88
Q

Treatment of perotonsillar abscess

A

t. High doses of antibiotics, analgesics and diet modification. Surgical evacuation of purulent exsudate

89
Q

Prognosis of peritonsillar abscess

A

Regression of the inflammation and prevention of an abscess are possible with timely administration of antibiotics

90
Q

Septicaemia during or after tonsillitis (tonsillogenic sepsis)

It starts with…

A

mild tonsillar infection and ends with life-threatening thrombophlebitis of the internal jugular vein

91
Q

More severe complication of Septicaemia during or after tonsillitis (tonsillogenic sepsis)

A

potential septic embolisation and metastatic abscesses in the lungs, liver or brain or septic arthritis osteomyelitis

92
Q

Clinical features. Tonsillogenic sepsis

A

septic temperature chart, strong pain in the neck, tenderness along the internal jugular vein, which appears as a tender, firm cord under the anterior edge of the sternocleidomastoid muscle, or tenderness of the jugulodigastric lymph nodes. There is often simultaneous reddening of the tonsillar area, but this is not essential. The patient has a severe constitutional upset, a left shift in the blood count with leukocytosis, splenomegaly, possible spread to the lung

93
Q

Pathogenesis of Tonsillogenic sepsis

A

Bacteria enter the bloodstream from the tonsil, or from a neighbouring focus of pus. Haematogenous, lymphogenous or direct spread of the abscess is possible

94
Q

Diagnosis of Tonsillogenic sepsis

A

This is based on the picture of chills and symptoms of septicaemia due to continuous or intermittent bacteraemia. There is a history of tonsillitis and symptoms of chronic tonsillitis

ESR increases rapidly, and there is rapidly rising leukocytosis. A defensive spasm of the cervical soft tissues occurs, with a relieving posture in the head and neck.

95
Q

Septicaemia during or after tonsillitis (tonsillogenic sepsis) treatment

A

If severe sepsis is suspected, high-dose penicillin or broad-spectrum antibiotics are started immediately to protect the body from infective metastases. Ligature of the internal jugular vein inferior to the thrombus and resection of the diseased segment, if the internal jugular vein is involved and tonsillectomy to eliminate the focus, need to be done. Abscess of the cervical soft tissues needs to be wide open and drained.

96
Q

Retropharyngeal abscess in children Aetiology

A

An abscess can form due to breakdown of lymphadenitis of the retropharyngeal lymph nodes following pharyngeal infection in children, especially during the first 2 years of life

97
Q

Retropharyngeal abscess in children clinical features

A

are swelling of the posterior pharyngeal wall, difficulty in swallowing, thick speech, difficulty in eating, elevated temperature, a relieving posture of the neck (differential diagnosis: torticollis), leakage of food through the nose, possibly nasal obstruction, croup, and laryngeal oedema

98
Q

Differential diagnosis Retropharyngeal abscess in children

A

Benign and malignant prevertebral tumours must be considered

99
Q

Treatment of Retropharyngeal abscess in children

A

This is by paramedian incision and drainage under general anaesthesia, with the head hanging to prevent aspiration of pus. The airway must be protected from aspiration by an endotracheal tube, and antibiotic cover is given

100
Q

Juvenile angiofibroma epidemiology

A

exclusively in young males, beginning about the age of 10 years. It tends to resolve spontaneously after the age of 20–25 years

101
Q

Clinical features of Juvenile angiofibroma

A

The tumour presents with increasing nasal obstruction, purulent rhinosinusitis due to obstruction of the nasopharynx, severe epistaxis, rhinolalia clausa, headaches, obstruction of the ostium of the Eustachian tube (causing conductive deafness), middle ear catarrh, and purulent otitis media

102
Q

Rhinoscopy in Juvenile angiofibroma shows…

A

occlusion of the nasopharynx by a smooth, greyish-red tumour with visible surface vessels

103
Q

Diagnosis of Juvenile angiofibroma

A

This is made by endoscopy and CT or MRI. Angiography of the carotid artery is indicated for an extensive tumour

104
Q

Superselective angiography of the branches of the carotid is performed to allow

A

therapeutic embolisation

105
Q

The differential diagnosis of Juvenile angiofibroma should include

A

hypertrophied adenoids, choanal polyp (which is soft and does not bleed), lymphoma, chordoma, and teratoma

106
Q

Treatment of Juvenile angiofibroma

A

The ideal method of treatment is surgery. Different approaches are available: midfacial degloving, transmaxillary access, or transpalatal access. Extensive tumours may need a craniotomy and mandibular osteotomy. For smaller tumours, the endoscopic endonasal techniques are useful. Preoperative embolisation of the feeding vessels is helpful in preventing or reducing of bleeding. Embolisation should ideally be done within 48 hours of surgery. Radiotherapy is an effective means of treatment, with a success rate of up to 80%

107
Q
A

ENT (11 decks)

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