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Oral Pathology > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

clinical

A

how the lesion looks to the eye; the descriptive appearances. if the appearance is unique the diagnosis can be made without further tests

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2
Q

radiographic

A

the appearance on the radiograph determines the diagnosis i.e periapical pathology (PAP)

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3
Q

historical

A

what patient reports of the personal history, family history, past and present medical and dental histories, histories, history of drug ingestion and history of the presenting disease or lesion

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4
Q

laboratory tests

A

including blood chemistries and urinalysis can yield a diagnosis

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5
Q

microscopic diagnosis

A

a lab test of sorts but is separate because evaluation of the specimen taken from the lesion gives very specific information. biopsy is often the main component of a definitive diagnosis

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6
Q

surgical diagnosis

A

surgical intervention shows if there is a traumatic bone cyst or a lingual bone concavity. diagnostic category of surgical diagnosis tells conclusively when the lesion is opened and an empty void is found that the diagnosis is a traumatic or a simple bone cyst. it give conclusive evidence

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7
Q

Therapeutic diagnosis

A

Nutritional deficiencies are diagnosed by therapeutic means e.g. angular chelitis may be associated with a B complex deficiency and ANUG response to hydrogen peroxide rinses

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8
Q

Differential diagnosis

A

The point in the diagnoses when the practitioner decides which test or procedure is required to rule out the conditions are originally and establish a definitive or final diagnosis

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9
Q

Clinical appearance of Fordyce’s granules

A

Appear as yellow lobules in clusters and are usually distributed over the buckle mucosa or Vermilion border of that involved lips

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10
Q

Clinical appearance of Torus Palatinus

A

May have various sizes and shapes, maybe lobulated and is covered by normal soft tissue

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11
Q

Clinical appearance of Mandibular tori

A

Are often lobulated or nodular and can appear fused together

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12
Q

Melanin pigmentation

A

The oral mucosa or gingival is commonly seen in dark skinned individuals

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13
Q

Retrocuspid papilla

A

A sessile nodule on the gingival margin of the lingual aspect of the mandibular canine’s

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14
Q

Lingual varicosities

A

Red to purple enlarge vessels or clusters of the vessels usually on the ventral and lateral surfaces of the tongue

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15
Q

Linea alba

A

A white line that extends anterioposteriorly and on the buccal mucosa along the occlusal plane

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16
Q

Leukoedemia

A

Refers to generalized opalescence on the buckle mucosa. Seen as a gray – white film on the buckle mucosa that when stretched becomes less prominent

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17
Q

Lingual thyroid nodule

A

Occurs when the thyroid tissue is either does not descend or remnants become trapped in the tissue the make up the tongue

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18
Q

Median rhomboid glossitis

A

Seen clinically as a flat or slightly raised oval or rectangle or erythrmatous area in the midline of the dorsal surface of the tongue. Maybe associated with a candida infection

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19
Q

Geographic tongue

A

Seen as a diffuse area devoid of filiform papilla on the dorsal and lateral borders of the tongue. Seen as erythrmatous patches that are surrounded by a white or yellow perimeter

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20
Q

Ectopic geographic tongue

A

Use describe the condition when it is found on the mucosal surfaces other than the tongue

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21
Q

Fissured tongue

A

Seen clinically when the dorsal surface of the tongue appears to have deep fissures or grooves that can become irritated if food collects in them

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22
Q

Hairy tongue

A

A condition in which the patient has an increased accumulation of keratin on the filiform papilla. The filiform papilla become elongated and can appear white, yellow, brown or black. The color of black hairy tongue is due to chromogenic bacteria, White from tobacco chemicals, alcohol and food. Anabiotic’s, corticosteroids, radiation, or Candida albicans can yield hairy tongue

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23
Q

Injury

A

Tissue damage caused by trauma or an alteration in the environment

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24
Q

Repair

A

The restoration of damaged or diseased tissue

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25
Inflammatory
A nonspecific response to injury and occurs in the same manner, regardless of the nature of the injury. Inflammation of a specific tissue is denoted with the suffix -itis. Can be acute or chronic
26
Immunity
The ability of an organism to resist or not be susceptible to injury or infection
27
Five classic signs of localized inflammation are:
Redness, heat, swelling, pain, loss of normal tissue function
28
Three systemic signs of inflammation are:
increase in body temperature (fever), increase in number of white blood cells (leukocytosis), enlargement of the lymph nodes (lymphadenopathy)
29
List and describe the microscopic events of the inflammatory process
A. Injury to tissue. B. Constriction of the microcirculation. C. Dilation of the microcirculation. D. Increase in permeability of the microcirculation. E. Exudate leaves the microcirculation, causes swelling. F. Increased blood viscosity. G. Decreased blood flow through the microcirculation. H. Migration and pavementing of white blood cells
30
Neutrophils/polymorphonuclear leukocytes (PMNs)
The first cells to immigrate to the site of injury and are the primary cells involved in acute inflammation. These cells phagocytize substances such as pathogenic microorganisms and tissue debris, injured tissue produces chemotactic factors that cause the PMNs to use the lysomal enzymes in their vacuoles to destroy the substances the PMNs have engulfed
31
Monocytes
The second cell to enter injured tissue where they become macrophages. Macrophages respond to chemotactic factors. The macrophage is capable of phagocytosis, is mobile, and has lysosomal enzymes in its cytoplasm that assist in the destruction of foreign substances. Besides phagocytosis, the macrophage acts as a helper during the immune response
32
Lymphocytes
Involved in chronic inflammation and immune response
33
Plasma cells
Involved in chronic inflammation and the immune response
34
Eosinophils and mast cells
Participate in both inflammatory and immune responses
35
Acute inflammation
If the injury is minimal and brief at sources removed from the tissue
36
Chronic inflammation
Chronic injury occurs of injury to the tissue continues. Sometimes acute and chronic inflammatory responses are superimposed on each other
37
What are the main white blood cells in acute inflammation
Mostly PMNs
38
White blood cells in chronic inflammation
Macro phages, lymphocytes and plasma cells are common
39
What can also start in chronic inflammation?
And chronic inflammation also start to see fibroblasts formed
40
Granulomatous inflammation
A distinctive form of chronic inflammation. Characterized by the formation of granulomas which are microscopic groupings of macrophages surrounded by lymphocytes and occasional plasma cells. The large macrophages can have multiple nuclei and are multinicleated giant cells. Certain infections tend to stimulate the formation of granulomas e.g. tuberculosis
41
Hyperplasia
And enlargement of tissue or organ resulting from an increase in the number abnormal cells. Pathological hyperplasia occurs in oral tissues. In the oral cavity an increase in the number of epithelial cells and the increased thickness of the epithelium commonly occur in response to chronic irritation or abrasion. As surface epithelial cells are lost, there is increased deviation of basil epithelial cells to replace the lost cells. The production of new cells is in excess of the original number of cells, so the epithelium becomes thick and in the tissue appear paler or whiter
42
Hyper trophy
And enlargement of a tissue or organ resulting from an increase in size but not in number of cells
43
Why is the repair process different in mucosa then and skin
Mucosal surfaces are wet and a scab does not form
44
Day of injury
A clot forms. As blood flows into injured tissue, the clot of a meshwork of fibrin is produced in the area of injury as a result of activation of the clotting mechanism. The clot consists of locally produced fibrin, clumped red blood cells and platelets (thrombocytes)
45
One day after injury
Acute inflammation taking place in the area of repair. Neutrophils emigrate from the microcirculation into injured tissue and phagocytosis of foreign substances and the chronic tissue occurs as part of the inflammatory response
46
Two days after injury
Monocytes immigrate from the microcirculation into the injured area as macrophages. Neutrophils are reduced in number as a chronic inflammatory process proceeds and fibroblasts increase in number within the injured connective tissue. They begin to produce new collagen fibers using the fibrin meshwork as a scaffold. The initial tissue formed in the connective tissue is called granulation tissue which is immature with more capillaries and fibroblasts than normal. This can get excessive or exuberant and appear vivid red. If surface epithelium is broken, epithelial cells reproduce and become mobile so they can immigrate and form a new surface at the end of the two days. Lymphocytes and plasma cells begin to emigrate from surrounding blood vessels into injured areas as chronic inflammation and an immune response begin
47
Seven days after injury
Fibrin is digested by tissue enzymes and sloughs off and the initial repair of the tissue is completed. The new tissue is thin and vascular
48
Two weeks after injury
The initial granulation tissue and its fibers have been remodeled giving the tissue it's full strength. This new tissue is scar tissue and appears whiter or paler because of the increased number of collagen fibers and decreased vascularity
49
Healing of primary intention
Refers to healing in which there is little loss of tissue such as in surgical incision. There is clean apposition of tissue. There is less scar tissue and a higher retention abnormal tissue
50
Healing by secondary intention
Involves an injury in which there is loss of tissue, so the edges of the tissue cannot be joined during healing. This produces more granulation tissue which leads to more scar tissue and loss of normal tissue function. Sometimes the excessive tissue need surgical correction. Also, if the excessive scarring is in the skin, it is called a keloid
51
Tertiary intention
Waiting to perform surgical tissue repair
52
Attrition
Wearing away of tooth structure during mastication. It is normal and occurs as we age. Notice it first with disappearance of memelons on incisor teeth and flattening of the occlusal cusps. It is influenced by diet, bruxism, tobacco chewing and work that involves abrasive dust
53
Abrasion
A pathologic wearing away of tooth structure that results from a repented of mechanical habit. It is most commonly seen in exposed roots services because cementum and dentin are not as hard as enamel; however, it is seen in enamel. It can be caused by toothbrushing, abrasive toothpaste, playing wind instruments, smoking a pipe
54
Erosion
Loss of tooth structure from chemical action. It is seen in people in acid using industries. It is generally seen on the facial and lingual surfaces of teeth. The pattern of a erosion seen in bulimia is on the lingual surfaces of the teeth caused by frequent vomiting
55
Bruxism
Grinding and clenching teeth for non-functional purpose. Attrition is accelerated by bruxism. Bruxism is managed by eliminating occlusal interference and protecting the teeth and supporting tissues from further destruction with acrylic splint. Bruxism is excessive attrition and can be made worse by abrasion that has sawed The teeth with a toothbrush or by bio mechanical force that has fatigued, flexed, fractured or deform the tooth structure. The weakened tooth structure is more susceptible to abrasion particularly toothbrush abrasion
56
Clinical features of placing aspirin on the soft tissue near tooth for pain
Tissue necrotic and white tissue may Slough and ulcerate
57
Treatment of placing aspirin on soft tissue near tooth for pain
Spontaneous and 7 to 21 days. Orabase to relieve symptoms. Start Endo?
58
Clinical feature of using phenol as a cavity sterilizing agent and cauterizing agent
Tissue gets white, sloughs and ulcerated
59
Treatment of using phenol as a cavity sterilizing agent and cauterizing agent
Time of healing depends on extent of destruction
60
Clinical feature of a child eating an electric cord
Wide tissue damage including tooth buds, scarring and disfigurement
61
Treatment of a child to eating an electric cord
May need plastic and oral surgery and orthodontics
62
Clinical features of a dramatic ulcer such as biting cheek, lips or tongue; denture or sharp food or dental procedure
Ulcerated tissue that if persistent leads to a raised lesion called a traumatic granuloma
63
Treatment of a dramatic ulcer such as biting cheek, lip or tongue; denture or sharp food and dental procedure
Will heal in 7 to 14 days. Otherwise it may need biopsy and or surgery
64
Clinical features of frictional keratosis such as chronic cheer tongue or edentulous ridge chewing
Opaque, white appearance from thickened keratin surface
65
Treatment of frictional keratosis such as chronic cheer tongue or edentulous ridge chewing
Eliminate cause or friction and time
66
Clinical feature of linea Alba
White raised line that forms most commonly on the buckle mucosa at the occlusal plane. It is epithelial hyperplasia
67
Treatment of linea Alba
Time; relieve symptoms if hurts. Cortisone ointment
68
Clinical feature of nicotine stomatitis (smoking)
At first erythematous from heat then opacification from keratinization. The red raised dots appear from blocking ducks of minor salivary ducts. These get inflamed. Drinking hot liquids can give a similar appearance
69
Mucocele
Involves a minor salivary gland and he ranula comes from an obstruction of the sub lingual salivary duct
70
Sialolithiasis
A pathologic condition in which one or more calculi or stone form in a salivary gland or duct. The difference between acute and chronic sialolithiasis is onset. Both are from obstruction and infection and the type of infiltrate
71
Chemical agents can start or amplify what?
The inflammatory response
72
What are the three systems that maybe activated during inflammation
1. The Kinin system. 2. Clotting.? 3. Complement system
73
Kinin system
Mediates information by causing increased dilation of the blood vessels at the injury site and increases the permeability of local blood vessels. The system is activated by substances in the blood and injured tissues. Components of the system induce PAIN
74
Clotting
Also mediate inflammation, since certain of its products that are activated when tissue is injured cause local vascular dilation impermeability by activating the Kinin system
75
Complement system
Involves the production of a sequential cascade plasma proteins that are present in the blood. In an inactive form, many of the plasma proteins function in both inflammatory and immunity components of the complement system cause mast cells to release the granules in their cytoplasm that contain histamine. Histamine increases vascular permeability and vasculodilation. Other components of the complement system cause cell death by creating holes in the cells membrane
76
Prostaglandins in the inflammatory response
Cause an increase in vascular dilation and permeability, tissue pain and redness and changed in connective tissues
77
Lysosomal enzymes in the inflammatory response
Come from granules of white blood cells and can damage connected tissue and the clot
78
Endotoxins and lysosomal enzymes in the inflammatory response
Come from pathogenic MO's and act as chemical mediators
79
Local factors that impair healing are:
Bacterial infections, tissue destruction in necrosis, hematoma, excessive movement of the injured tissue, and poor blood supply
80
Systemic factors are:
Malnutrition especially protein, calcium, zinc and vitamin C, immunosuppression from steroids or chemotherapy, genetic connective tissue disorders, metabolic disorders been age, renal failure or diabetes and smoking
81
Clinical features of periapical abscesses
pain, swelling, fistula, slight extrusion of the tooth
82
Radiographic appearance of a periapical abscess
None, thickening of the PDL space or radiolucency
83
Histological appearance of periapical abscess
Acute inflammatory infiltrate
84
Clinical features of periapical granuloma
Asymptomatic tooth sensitivity to percussion. Slight extrusion of tooth
85
Radiographic appearance of periapical granuloma
Slight thickening of the PDL space, periodontal radiolucency
86
Histological appearance of periodontal granuloma
Chronic inflammatory infiltrate
87
Clinical features of Radicular or periapical cyst
Asymptomatic
88
Radiographic appearance of radicular or periapical cyst
Radiolucency. Associated with root of a non-vital tooth
89
Histological appearance of radicular or periapical cyst
Space line by epithelium and surrounded by an infiltrate of chronic inflammatory cells
90
Clinical features of external resorption
Etiology, chronic inflammation
91
Radiographic appearance of external resorption
Location roots of 1° teeth
92
Histological appearance of external resorption
Radiographic blunting of red Apex to severe loss of root substance
93
Clinical features of internal resorption
Chronic pulpal inflammation
94
Radiographic appearance of internal resorption
Dental hard tissue within root or crown
95
Histological appearance of internal resorption
Round to ovoid, radiolucency in the central part of the tooth

Oral Pathology (2 decks)

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