oral med and pathology p262 (275) Flashcards

1
Q

acquired diseases classification

A

VIITAMIIN

V ascular

I nfective

I nnflammatory

T rauma

A uto-immune

M etabolic

I diopathic

I atrogenic

N eoplastic

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2
Q

Vacular diseases of

A

circulatory origin

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3
Q

Infective diseases are

A

caused by the entrance into the body of organisms (bacteria, protozoans, fungi or viruses)

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4
Q

Inflammatory disorders

A

result in the immune system attacking the body’s own cells or tissues may cause abnormal inflammation, which results in chronic pain, redness, swelling, stiffness and damage to normal tissues

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5
Q

Trauma

A

physical injury, sometimes chronic and low stress or singular and dynamic

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6
Q

Auto-immune diseases are

A

caused by antibodies or lymphocytes produced against substances naturally present in the body

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7
Q

Metabolic diseases

A

disrupt the processes of energy conversion and utilisation on a cellular level

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8
Q

Idiopathic disease are

A

any diseases with an unknown cause or mechanism of apparently spntaneous origin

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9
Q

Iatrogenic disease

A

due to activity of a physician or medication effects

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10
Q

neoplastic diseases are

A

conditions that cause tumour growth - both benign and malignants

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11
Q

neoplasm

A

abnorma growth of cells (tumour)

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12
Q

congentital diseases

A

diseases, defects or deformities dating from birth but not necessarily hereditary

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13
Q

symptoms

A

something a pt feels or observes which they regard as abnormal e.g. pain, weakness of limb

discovered when taking hx

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14
Q

sign

A

functional abnormality demonstrated by a physical exam of pt

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15
Q

syndrome

A

combination of symptoms and/or signs which commonly occur together e.g. TMJD syndrome

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16
Q

how to present a case

A

name

age

occupation

residence

how long ago since presentation

presentation itself and duration of

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17
Q

macule

A

flat, non palpable lesions <10mm in diameter usally pigmented

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18
Q

papules

A

elevated, palpable lesions <10mm

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19
Q

plaques

A

either elevated/depressed compared to skin surface

>10mm diameter

may be flat topped or rounded

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20
Q

nodules

A

firm papules or lesions that extend into dermis or subcutanoues tissue

e.g. cysts, lipoma, fibromas

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21
Q

vesicles

A

small, clear, fluid filled blisters <10mm in diameter

vesicles are characteristic of herpes infections, acute allergic contact dermamtitis and some autoimmune blistering disorders

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22
Q

bullae

A

clear fluid-filled blisters >10mm in diameter

may be caused by burns, bites, irritant or allergic contact dermaitits and drug reactions

classic autoimmune bullous diseases inc pemphigus vulgaris and bullous pemphigoid

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23
Q

pustules

A

vesicles contain pus

common bacterial infections and folliculiltiis and can be seen in some inflammatory disorders

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24
Q

urticaries (wheals or hives)

A

characterized by elevated lesions caused by localized edema.

Wheals are pruritic and red.

are a common manifestation of hypersensitivity to drugs, stings or bites, autoimmunity, and, less commonly, physical stimuli including temperature, pressure, and sunlight.

typical wheal lasts < 24 h.

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25
scale
heaped-up accumulations of horny epithelium that occur in disorders such as psoriasis, seborrheic dermatitis, and fungal infections. Pityriasis rosea and chronic dermatitis of any type may be scaly.
26
crusts/scabs
dried serum, blood, or pus. Crusting can occur in inflammatory or infectious skin diseases (eg, impetigo)
27
erosions
open areas of skin that result from loss of part or all of the epidermis. can be traumatic or can occur with various inflammatory or infectious skin diseases. An excoriation is a linear erosion caused by scratching, rubbing, or picking.
28
ulcers
result from loss of the epidermis and at least part of the dermis. Causes include venous stasis dermatitis, physical trauma with or without vascular compromise (eg, caused by decubitus ulcers or peripheral arterial disease), infections, and vasculitis
29
petechiae
nonblanchable punctate foci of hemorrhage. Causes include platelet abnormalities (eg, thrombocytopenia, platelet dysfunction), vasculitis, and infections (eg, meningococcemia, Rocky Mountain spotted fever, other rickettsioses)
30
purpura
larger area of hemorrhage that may be palpable. Palpable purpura is considered the hallmark of leukocytoclastic vasculitis. Purpura may indicate a coagulopathy. Large areas of purpura may be called ecchymoses or, colloquially, bruises
31
atrophy
thinning of the skin, which may appear dry and wrinkled, resembling cigarette paper. may be caused by chronic sun exposure, aging, and some inflammatory and neoplastic skin diseases, including cutaneous T-cell lymphoma and lupus erythematosus. also may result from long-term use of potent topical corticosteroids.
32
scars
areas of fibrosis that replace normal skin after injury. some scars become hypertrophic or thickened and raised. Keloids are hypertrophic scars that extend beyond the original wound margin
33
telanglectases
foci of small, permanently dilated blood vessels that may occur in areas of sun damage, rosacea, systemic diseases (especially systemic sclerosis), or inherited diseases (eg, ataxia-telangiectasia, hereditary hemorrhagic telangiectasia) or after long-term therapy with topical fluorinated corticosteroids.
34
erosion vs ulceration
Erosion - partial epithelial thickness loss, but can still clinically see epithelium Ulceration - full loss of epithelium with possible yellow fibrin deposits
35
linear lesions
straight line and are suggestive of some forms of contact dermatitis, linear epidermal nevi, and lichen striatus. Traumatically induced lesions, including excoriations caused by the patient's fingernails, are typically linear.
36
annular lesions
rings with central clearing. Examples include granuloma annulare, some drug eruptions, some dermatophyte infections (eg, ringworm), and secondary syphilis
37
nummular lesions
circular or coin-shaped; an example is nummular eczema.
38
target lesions *bull's eye/iris*
appear as rings with central duskiness are classic for erythema multiforme
39
serpigingous lesions
linear, branched, and curving elements. Examples include some fungal and parasitic infections (eg, cutaneous larva migrans).
40
reticulated lesions
lacy or networked pattern. Examples include cutis marmorata and livedo reticularis.
41
herpetiform lesions
grouped papules or vesicles arranged like those of a herpes simplex infection.
42
zosteriform lesions
lesions clustered in a dermatomal distribution similar to those of herpes zoster.
43
verrucous lesions
irregular, pebbly, or rough surface. Examples include warts and seborrheic keratoses.
44
lichenification
thickening of the skin with accentuation of normal skin markings; it results from repeated scratching or rubbing.
45
induration
deep thickening of the skin, can result from edema, inflammation, or infiltration, including by cancer. Indurated skin has a hard, resistant feeling. Induration is characteristic of panniculitis, some skin infections, and cutaneous metastatic cancers
46
umbillicated lesions
have a central indentation and are usually viral. Examples include molluscum contagiosum and herpes simplex.
47
red lesion called
erythema result from many different inflammatory or infectious diseases. Cutaneous tumors are often pink or red. Superficial vascular lesions such as port-wine stains may appear red.
48
yellow skin due to
jaundice, xanthelasmas and xanthomas, and pseudoxanthoma elasticum.
49
violet skin due to
result from cutaneous hemorrhage or vasculitis. Vascular lesions or tumors, such as Kaposi sarcoma and hemangiomas, can appear purple. A lilac color of the eyelids or heliotrope eruption is characteristic of dermatomyositis.
50
shades of blue, silver or gray in oral tissues due to
result from deposition of drugs or metals in the skin, including minocycline, amiodarone, and silver (argyria). Ischemic skin appears purple to gray in color. Deep dermal nevi appear blue.
51
black skin lesions due to
melanocytic, including nevi and melanoma. Black eschars are collections of dead skin that can arise from infarction, which may be caused by infection (eg, anthrax, angioinvasive fungi including Rhizopus,meningococcemia), calciphylaxis, arterial insufficiency, or vasculitis
52
Nikolsky sign
epidermal shearing that occurs with gentle lateral pressure on seemingly uninvolved skin in patients with toxic epidermal necrolysis and some autoimmune bullous diseases.
53
9 points for describing a mucosal swelling
Site ➡Trauma Area? ➡Gingiva? Size ➡Static? ➡ Increasing/Decreasing Surface ➡Normal Mucosa? ➡Granulation tissue? ➡Smooth? ➡Tessellated? ➡Ulceration? Colour Consistency ➡Soft/Friable? ➡Firm? ➡Hard/Bony? Shape Base ➡Pedunculated? (stalk) ➡Sessile? (immobile) Bleeding ➡Spontaneous? ➡Trauma induced? Fnctional Limitation
54
ulceration key questions | 8
where size and shape blister or ulcer how long for - more than 2 weeks recurrent - same or different sites painful margins - flat, raised, rolled base - soft, firm, hard
55
parotid gland secretion type
serous
56
submandibular gland secretion type
mixed - mainly serous (90%)
57
sublingual gland secretion type
mixed - mainly mucous
58
direct salivary gland problems | 6
aplasia duct atresia sarcoidoisis HIV gland infiltration cystic fibrosis
59
aplasia of salivary gland
congenital absence of one or more salivary glands ectodermal dysplasia - abnormal development of anatomy of ectodermal origin e.g. skin, hair, teeth, sweat glands
60
duct atresia of salivary gland
failure of duct to canalise can result in formation fo salivary retention cysts
61
sarcoidosis of salivary glands
presence of collection of glanulomas can occur in any organ but often affect salivary glands causing large massess and facial palsy
62
HIV and salivary glands
partoid enlargement occurs in up to 10% of pts
63
2 types of salivary gland infiltration
amlyoidosis haemachromatosis
64
amyloidosis of salivary gland
build up of protein fibrils lymphoepithelial cysts
65
haemachromatosis of salivary glands
causes xerostomia
66
cystic fibrosis and salivary glands
causes plugging of acinar ducts with precipitated secretions essentially microscoptic sialoliths
67
radiotherapy effect on saliva glands
salivary tissues are particularly sensitive to radiotherapy * highly differentiated and specilised state * reduction of quality and quantity of saliva (not because of their high mitotic figures like other radiosensitive tissues)
68
radiotherapy effect on quality of saliva
usually reproduced 4-8weeeks after finishing tx thick, viscous and bad tasting fibrosis of salivary tissue can occur due to enderarteritis
69
Graft vs Host disease and salivary glands
experienced mainly in haematopoetic stem cell pts results in sjorgren's syndrome
70
anti-neoplastic drugs and saliva glands (chemo)
reduced secretion early apoptosis of salivary glands cells ## Footnote w
71
radioiodine effect on salivary glands
reduction in gland function inc lymphocytic infiltrate
72
anti-muscarininc cholinergic drugs e.g.
tricylic antidepressants - amitryptiline antipsychotics - clozapine, risperidone antihistamines - chlorphenenamine atropine diuretics - furosemide, bendroglumethiazide cytotoxic - azathioprine, cyclosporin
73
drugs which can cause dry mouth
anti-muscarininc cholinergic drugs
74
indirect salivary problems classess
chronic medical issues acute medical problems
75
chronic medical issues which can cause dry mouth | 6
dehydration diabetes (mellitus and insipidus) renal disease stroke addison's disease persistent vomitting
76
acute medical problems which can cause dry mouth | 4
acute oral diseases burns vesiculobulous disease haemorrhage
77
modified european criteria for sjorgren's syndrome dx
dry eyes/mouth need 4 or more for dx * subjective or objective findings * autoanitbody findings * imaging findings * radionucleotide findings * histopahtology findnsg
78
eye symptoms for sjogrens
presistent troublesome dry eyes for >3months recurrent sensation of sand/gravel in the eyes tear subsitutes used >3times day
79
oral symptoms for sjogrens
daily feeling of a dry mouth for >3months recurrent swelling of salivary glands as an adult frequently drink liquid to aid swallowing fo dry foods
80
3 types of sjorgren's
sicca syndrome primary secondary
81
sicca sjogrens syndrome
partial sjogren's findings
82
primary sjogren's syndrome
no connective disease but meets criteria otherwise
83
secondary sjogren's syndrome
CT disease SLE, rheumatoid arthritis, scleroderma
84
dry mouth management
prevent oral disease caries * fluoride * OHI * tx plan candida/staphlyococci * angular cheilits * sore tongue reduce symptoms * salivary substitutes * water/chewing gum
85
hypersalivation is
Constant stimulation of salivary centre of brain located in the superior salivary nucleus of the facial nerve can have true (rare) or perceived (common)
86
true hypersalivation causes
stroke degenerative CNS condistions - CJD, MS, Alzheimers drugs
87
perceieved hypersalivation causes
dysphagia
88
viral salivary gland infections
paramyxovirus unilateral or second attacks possible
89
bacerial salivary gland infections
ALWAYS an underlying cause dehydration and flow reduction flow obstruction diabetes immune suppression abnormal anatomy
90
salivary gland obstruction 3 possible
recurrent parotiditis chronic obstructive saliadentitis sialolithiasis
91
recurrent parotiditits effect
HIV bacterial infection causes duct sclerosis
92
chronic obstructive sialadentitis effect
usually caused by sialothiasis can be post-op
93
sialothiasis effect
usually submandibular 2x as much calcium in this gland Vs parotid also alkaline and mucous due to saliva flow at sight of food pain is often peri-prandial possible link w gout
94
secretion retention can cause | 2
mucocele duct obstruction
95
mucocels can be | 3
extravasation mucocele - trauma of excretory duct and escape of mucous into surrounding tissues retention mucocele (mucous retention cyst) - intermittent duct obstruction in elderly pts superficial mucocele
96
salivary gland hyperplasia can occur in | 2
sialosis sjorgrens
97
sialosis
chronic, bilateral, diffuse, non-inflammatory, non-neoplastic swelling of the major salivary glands that primarilyaffects the parotid glands, but occasionally involves the submandibular glands and rarely the minor salivary glands This can be painless or in some instances tender.
98
most common salivary tumour
Pleomorphic adenoma - has dual origin in glandular and myoepithelial components
99
dental pain characterisitcs
short sharp pain introduced by pressure, thermal and chemical inductions gets worse with time
100
neuropathic pain characterisitcs
Constant burning/aching pain Fixed location Often a fixed intensity Chronic Regional Pain Syndrome (CRPS) * Autonomic nerve version of neuropathic pain Usually a history of ‘injury’
101
possible 'injuries' that can cause neuropathic pain
trauma extractions routine tx without complications herpes zoster (shingles) episode destructive tx for pain
102
systemic meds for neuropathic pain
pregablin gabapetin tricyclic antidepressants (amitryptiline)
103
topical medication for neuropathic pain
capasaicin EMLA benzdamine
104
atypical odontalgia
Dental pain without detected pathology Distinct pattern of pain * Pain free or mild between episodes * Intense unbearable pain ➡ 2-3 weeks duration ➡ Settles spontaneously
105
persistent idiopathic facial pain
pain which poorly fits into chronic pain syndromes often high disability levels often other systemic features - musculo-skeletal pain syndromes often responds poorly to tx
106
trigeminal neuralgia
a trigeminal autonomic cephalgia (TACs) acute spasms of sharp, shooting pain trigger point may be identified * brought on by: movement, eating, talking, worse with cold weather remissions and relapses
107
trigemial neuralgia tx
carbamazepine (modified release) oxcarbazepine lamotrigine | MRI scan
108
surgical options for trigemial neuralgia
Peripheral neurectomies trigeminal Nerve Balloon Compression Microvascular decompression (MVD) Radiosurgery – Gamma knife | after MRI scan
109
red flags for TN
Younger patient (>40yrs) Sensory deficit in facial region - hearing loss – acoustic neuroma Other Cranial nerve lesions ALWAYS test cranial nerves (identify sensory deficit) systematic examination ALL patients now get MRI
110
cluster headaches
‘Trigeminal Autonomic Cephalgias (TAC’s)’ Symptoms Intense pain ➡generalised or localised headache ➡usually/evening night vasomotor changes ➡lacrimation ➡nasal congestion ➡swelling over painful site ➡pupillary and conjunctival changes variable
111
dyseasethesia
Abnormal sensory PERCEPTION in ABSENCE OF ABNORMAL STIMULUS ALL modes of oral sensation involved * thermal * taste * touch * moistness burning mouth
112
TMD pain history
almost any chronic face/head/neck pain (inc wisdom teeth pai) symptoms show periodicity morning/evening exacerbation parafunctional clenching
113
TMD exam
Focal muscle tenderness ➡ Masticatory muscles ➡ sternomastoid ➡ Trapezius tenderness over TMJ itself limitation of opening locking (dispalcement with reduction) Joint noise ➡ crepitus - degenerative OA changes ➡ click - related to disc dysfunction (dispalcement with reduction) Deviation on opening ➡ common finding with muscle dysfunction Dental occlusion upset
114
management of TMD
Physical therapy exercises education - supportive yawning etc stress management (CBT, mediatation) Soft diet analgesia Bite splint (over all occlusal surfaces - soft or hard or hybrid) Biochemical manipulation ➡ Tricyclic (not SSRI) ➡ other anxiolytic medication
115
non keratinised oral mucosa
lining mucosa oral surface of lips, FOM, ventral tongue
116
keratinised oral mucosa
masticatory mucosa (hard and part of soft palate, gingiva)
117
orthokeratinised
nuclei free keratin layer least common form of epithelium hard palate and gingiva
118
parakeratinised
immature form of orthokeratinised same layers but more indistict, not as many finger like projections as ortho speciliased lingual papilla, partially nucleated
119
oral epithelium structure type
stratified squamous epithelium
120
characterisitcs of stratified squamous epithelium
has a cuboidal basal layer flattened surface layer ultimately they will shed as anucleate ‘squames’ cell division occurs in basal cell layers and suprabasal (ground up) prickle cell layer formed from desmosomes joining
121
basement membrane in strat squam epith
basal lamina ➡lamina lucida (epithelium side) ➡lamina densa (lamina propria side) reticular connective tissue (Type III collagen)
122
lamina propria characteristics
loose areolar connective tissue Feeder vessels elastic fibres lymphatic vessels
123
submucosa
may or may not be present contains adipose salivary gland tissue A variable number of Fordyce spots or granules are scattered throughout the nonkeratinized tissue. These are a normal variant, visible as small, yellowish bumps on the surface of the mucosa. They correspond to deposits of sebum from misplaced sebaceous glands in the submucosa that are usually associated with hair follicles
124
9 types of epithelium reactive lesions
keratosis acanthosis elongated rete ridges atrophy erosion ulceration oedema blister dysplasia
125
acanthosis
hyperplasia of stratum spinosum
126
elongated rete ridges
hyperplasia of basal cells
127
atrophy
reduction in number of viable layers
128
erosion
partial epithelial thickness loss but can still see epithelium
129
ulceration
full thickness loss with fibrin on surface (yello)
130
reactive oedema types | 2
➡ Intracellular - also known as cloudy swelling, most common form of cellular injury ➡ Intercellular (Spongiosis)
131
blister
Vesicle - circumscribed, elevated lesion < 5mm in diameter containing clear serous fluid Bulla - a vesicle with a diameter > 5mm Contents * Superficial epithelium (serous) * Deep epithelium (blood filled) n.b feeder vessels
132
dysplasia
disordered maturation (growth) in a tissue epithelial dysplaisa (cellular atypia) can only be dx histopathologically (not clinical)
133
predictors of malignancy | 2
architectural changes - abnormal maturation and stratification cytological abnormalities - cellular atypia
134
cellular atypia | 3 key features
pleomorphism hyperchromatism basal cell hyperplasia
135
WHO 2005 epithelial dysplasia grading
hyperplasia dysplasia ➡ Mild ➡ Moderate ➡ Severe carcinoma in situ
136
basal hyperplasia | WHO 2005
Increased cell numbers Architecture ➡regular stratification ➡basal compartment is larger than normal No cellular atypia
137
mild dysplasia | WHO 2005
Architecture - changes in lower 1/3 Cytology - mild atypia ➡ Pleomorphism ➡ Hyperchromatism ➡ Basal Cell hyperplasia
138
moderate dysplasia | WHO 2005
Architecture - change into the middle 1/3 Cytology moderate - atypia
139
severe dysplasia | WHO 2005
Architecture - changes in the upper 1/3 Cytology - severe atypia and numerous mitoses, abnormality high
140
carcinoma in situ | WHO 2005
theoretic concept of MALIGNANT CELLS IN THE LAMINA PROPRIA malignant but not invasive abnormal architecture ➡full thickness (or almost full) of viable cell layers pronounced cytological atypia ➡mitotic abnormalities