Oral cavity Flashcards
1
Q
The pharynx is covered by a complete ring of lymphoid tissue called
A
Waldeyers’s ring
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
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
4
Q
Unlike the palatine tonsil, the adenoid has no
A
capsule
5
Q
Adenoid response to adverse conditions
A
Hyperplasia and obstruction
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
7
Q
The lateral surface of each palatine tonsil is covered by
A
pharyngeal fascia
8
Q
lateral surface of each palatine tonsil is attached to
A
the superior pharyngeal constrictor muscle
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
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
11
Q
Adenoid hyperplasia
A
Enlarged pharyngeal lymphoid tissue
12
Q
the primary cause of sleep-disordered breathing in children
A
Adenoid hyperplasia
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
14
Q
Treatment of Adenoid hyperplasia
A
Adenoidectomy
15
Q
Tonsillar hyperplasia can contribute to
A
obstructive sleep apnoea syndrome (OSAS)
16
Q
obstructive sleep apnoea syndrome (OSAS) OSAS is characterised by
A
reduction (hypopnoea) or cessation (apnoea) of oronasal airflow despite respiratory effort
17
Q
Untreated OSAS can cause
A
failure to thrive,
aspiration,
chest infections,
and cor pulmonale
18
Q
Treatment of Tonsillar hyperplasia
A
Treatment is surgical — tonsillectomy or intracapsular tonsillar resection (tonsillotomy)
19
Q
OSAS is common in children with
A
developmental delay, neurological impairment and craniofacial dysmorphism
20
Q
What is the gold standard for an objective correlation of ventilatory abnormalities.
A
Polysomnography
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
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
23
Q
Treatment of Herpes simplex stomatitis
A
Systemic antiviral therapy
including anaesthetics or topical antiviral agents (acyclovir, penciclovir
24
Q
Clinical features of Candidal stomatitis
A
Burning in the mouth and tongue with superficial white foci, and exudates on the mucosa.
25
Candidal stomatitis aetiology
Candida albicans
26
Who is most at risk of infection with Candidal stomatitis
severely immunosuppressed hosts. Candidiasis affects individuals with diabetes mellitus, reduced resistance, and after prolonged administration of antibiotics, chemotherapy, steroids, oral contraceptives, and after radiotherapy
27
Treatment and prognosis of Candidal stomatitis
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
28
What is Allergic stomatitis
Hypersensitivity reactions on the oral mucosa and the lips, with varying severity, with or without angioneurotic oedema
29
Causes of Allergic stomatitis
almost all drugs, dental material, mouthwashes, toothpaste, cosmetics, chewing gum, and also to some foods, e.g. fruit, fish, protein, and milk.
30
Herpes zoster definition
resulting from reactivation of the varicella-zoster virus
31
Morphology of clinical features of Herpes Zoster
Unilateral rapidly progressive vesicles are quickly followed by fibrinous superficial epithelial defects
32
Nerve distribution of Zoater on face
Affects the segments of the face innervated by the second and third divisions of the trigeminal nerve
33
Tx of Herpes zoster
high-dose regimens of systemic antiviral agents (acyclovir, valacyclovir, famciclovir) within 48 h
34
Bnefits of prompt Herpes zoster tx commencement
shown to reduce the duration and severity of the acute disease and somewhat reduce the risk of postherpetic neuralgia
35
Ludwig angina Definition and aetiology
rapidly expanding diffuse inflammation of the floor of mouth, submandibular and sublingual spaces often caused by dental infections.
36
Clinical features of Ludwig angina
The patient's floor of mouth is swollen, the tongue might be swollen or elevated. A CT sacan is most useful.
37
Treatment of ludwig angina
Airway control is the first priority of treatment, followed by i.v. antibiotics and timely surgical drainage
38
Early otorhinolaryngologic symptoms of HIV/AIDS
angular cheilitis and Kaposi sarcoma
39
Chronic aphthae (recurrent aphthous stomatitis)
recurrent oral ulcerations, generally small with an erythematous base
40
Chronic aphthae (recurrent aphthous stomatitis) anatomical locations
buccal mucosa, the tongue, the palate, and the gingiva
41
Accimpanying features of Chronic aphthae (recurrent aphthous stomatitis)
regional lymph nodes may be swollen
, and concomitant stomatitis
42
Aphthae can be triggered by
infections, hormonal factors such as menstruation, and certain foods
43
Symptomatic treatment of aphthous stomatitis
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
Hyperkeratosis
velvety or nodular epithelial lesion
45
Leukoplakia
Flat epithelial plaque or white thickening that cannot be wiped off
46
Hyperkeratosis and leukoplakia causes
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
Prognosis of leukoplakia depends on
Degree of dysplasia and can lead to CA
48
Treatment and dx in leukoplakia
Diagnosis is made by biopsy and histological examination. Treatment consists of surgical removal and avoidance of possible causative agents
49
Bowen’s disease (erythroplakia) definition
clinical diagnosis and means “red patch”
premalignant lesion or carcinoma in situ
50
Aetiopthogenesis of Bowen’s disease (erythroplakia
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
Bowen’s disease (erythroplakia) treatment
The lesion must be biopsied and, as a treatment option, excised with an adequate margin
52
Acute tonsillitis
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
Clinical presentation of acute tonsillitis
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
Clinical features of lymphoepithelial organs in acute tonsillitis
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
How acute tonsillitis progresses to follicular tonsillitis
Yellow spots corresponding to the lymphatic follicles form on the tonsils
56
What type of tonsillitis occurs when yellow spots occur over the openings of the crypts,
lacunar tonsillitis
57
describe membrane that forms in pneumococcal tonsillitis
seldom confluent and rarely spreads beyond the tonsil.
58
Most episodes of acute pharyngitis and acute tonsillitis are caused by the following viruses
herpes simplex virus, Epstein–Barr virus (EBV), cytomegalovirus, adenovirus, and measles virus.
59
The most common bacteria causing tonsillitis
β-haemolytic streptococci
60
DX of Acute tonsillitis
ESR
CRP
FBC
Paul Bunnell or infectious mononucleosis testing and urinalysis
61
Differential diagnosis Acute tonsillitis
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
Differential blood count IN ACUTE TONSILLITIS EXCLUDES
mononucleosis and leukaemia.
63
Other forms and types of acute tonsillitis
Nasopharyngitis
Lingual tonsillitis
Infection of the lateral bands
64
The standard treatment in patients with streptococcal tonsillitis is
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
Infectious mononucleosis (glandular fever)
This is an infection caused by the Epstein–Barr virus, which chiefly affects children and adolescents
66
Clinical presentation of Infectious mononucleosis (glandular fever)
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
The blood picture of Infectious mononucleosis
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
Approximately 30% of IM develops secondary bacterial infections with
β haemolytic Streptococcus
69
Diagnosis of infectious mononucleosis
This is made from the clinical findings, the characteristic blood picture, and the Paul Bunnell test (demonstration of heterophile antibodies in the serum).
70
Treatment in IM
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
Chronic tonsillitis
History and features
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
The systemic effect of chronic tonsilitis may become evident through
reduced resistance, fatigue, unexplained high temperature, and loss of appetite
73
Pathogenesis of chronic tonsillitis
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
Chronic tonsillitis diagnosis
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
Chronic pharyngitis
This is a comprehensive term for several chronic irritative or inflammatory conditions of the pharyngeal mucosa
76
Classification of Chronic pharyngitis
Simple
Atrophic
Chronic Hyperplastic
77
Chronic pharyngitis simple
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
Chronic hyperplastic Chronic pharyngitis
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
Chronic atrophic Chronic pharyngitis
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
Chronic pharyngitis pathogenesis
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
Chronic pharyngitis differential diagnosis
Sjögren syndrome, Plummer–Vinson (Paterson–Brown– Kelly) syndrome, and malignancy of any part of the pharynx or oesophagus.
82
Treatment of Chronic pharyngitis
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
Peritonsillar abscess
This is usually a complication of acute tonsillitis caused by accumulation of purulent exsudate (pus) in the peritonsillar space
84
Peritonsillar abscess clinical features
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
In Peritonsillar abscess inflammation spreads from the tonsillar parenchyma to the surrounding tissue; an abscess forms between
between the capsule of the tonsil and the tonsillar fossa (inferior constrictor muscle) within a few days
86
Diagnosis of peritonsillar abscess
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
Peritonsillar abscess Differential diagnosis
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
Treatment of perotonsillar abscess
t. High doses of antibiotics, analgesics and diet modification. Surgical evacuation of purulent exsudate
89
Prognosis of peritonsillar abscess
Regression of the inflammation and prevention of an abscess are possible with timely administration of antibiotics
90
Septicaemia during or after tonsillitis (tonsillogenic sepsis)
It starts with...
mild tonsillar infection and ends with life-threatening thrombophlebitis of the internal jugular vein
91
More severe complication of Septicaemia during or after tonsillitis (tonsillogenic sepsis)
potential septic embolisation and metastatic abscesses in the lungs, liver or brain or septic arthritis osteomyelitis
92
Clinical features. Tonsillogenic sepsis
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
Pathogenesis of Tonsillogenic sepsis
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
Diagnosis of Tonsillogenic sepsis
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
Septicaemia during or after tonsillitis (tonsillogenic sepsis) treatment
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
Retropharyngeal abscess in children Aetiology
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
Retropharyngeal abscess in children clinical features
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
Differential diagnosis Retropharyngeal abscess in children
Benign and malignant prevertebral tumours must be considered
99
Treatment of Retropharyngeal abscess in children
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
Juvenile angiofibroma epidemiology
exclusively in young males, beginning about the age of 10 years. It tends to resolve spontaneously after the age of 20–25 years
101
Clinical features of Juvenile angiofibroma
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
Rhinoscopy in Juvenile angiofibroma shows...
occlusion of the nasopharynx by a smooth, greyish-red tumour with visible surface vessels
103
Diagnosis of Juvenile angiofibroma
This is made by endoscopy and CT or MRI. Angiography of the carotid artery is indicated for an extensive tumour
104
Superselective angiography of the branches of the carotid is performed to allow
therapeutic embolisation
105
The differential diagnosis of Juvenile angiofibroma should include
hypertrophied adenoids, choanal polyp (which is soft and does not bleed), lymphoma, chordoma, and teratoma
106
Treatment of Juvenile angiofibroma
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
