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oral path 2 > metabolic syndromes > Flashcards

metabolic syndromes Flashcards

1
Q

what happens to bone in pagets disease

A

bone broken down and replaced faster than normal, where the new bone is weaker and less organized than normal bone

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2
Q

clinical features of pagets

A

multiple areas of the skeleton
enlargement of skull, jaws, facial bones, deformity of spine and long bones
increased pathologic fracture

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3
Q

you see pagets in pts over what age

A

40

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4
Q

what are you concerned about in pagets denture pts

A

enlargement of jaws and widening of the alv ridges so dentures wont fit, and there are spaces bt teeth

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5
Q

when do you see a cotton wool appearance on a radiograph

A

pagets

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6
Q

when do you see a decreased density of bone and hypercementosis on multiple teeth

A

pagets disease

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7
Q

when do you see osteoporosis circumscripta in a radiograph

A

pagets

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8
Q

howw do you verify pagets with lab values

A

increased serum alkaline phosphatase
normal calcium and phosphorus
increased urine
hydroxyproline levels

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9
Q

what can pagets cause

A

bone pain, deformity, and neurologic probs

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10
Q

tx for pagets

A

calcitonin and bisphosphonates (with increased incidence of osteosarcoma)

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11
Q

primary hyperparathyroidism

A

pth gland, hyperplasia, adenoma, carcimoma

= too much pth

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12
Q

secondary hyperparathyroidism

A

kidney disease, hypercalcemia

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13
Q

2 causes of hyperparathyroidism

A

primary (pth gland) and secondary (kidney disease)

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14
Q

hypercalcemia leads to

A 
bone and joint pain
renal calculi
peptic ulcers
cognitive impairment
painful bones, renal stones, abdominal groans, psychotic moans
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15
Q

when do you see a ground glass appearance

A

fibrous dysplasia and hyperparathyroidism

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16
Q

unlike fibrous dysplasia, hyperparathyroidism affects

A

all of the bones with no expansion

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17
Q

radiographic features of hyperparathyroidism

A

ground glass
loss of trabeculation, lamina dura, cortical plates
brown tumors

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18
Q

lab features of hyperparathyroidism

A

primary: increased calcium and pth
secondary: decreased or normal serum ca, increased pth (the gland is working fine, but the body cant absorb it)

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19
Q

microscopic evidence of hyperpth

A

giant cell lesions identical to CGCG and cherubism

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20
Q

tx of prim pth-ism

A

excision of pth gland

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21
Q

tx of secondary pth-ism

A

renal dialysis or transplant

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22
Q

cause of osteogenesis imperfecta

A

genetics leading to defective cross linking of collagen and osteoblasts produce a defective osteoid

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23
Q

t/f congenital onset of osteogenesis imperfecta is more sever than later onset

A

true

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24
Q

state of bones in osteogenesis imperfecta

A

fragile as hell

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25
Q

skeletal features of osteogenesis imperfecta

A

multiple fractures, thin cortical plates, excessive callus formation, large skull with prominent frontal bones

26
Q

orally, osteogenesis imperfecta looks like

A 
dentinogenesis imperfecta (different genes) 
opalescent teeth
27
Q

clinical features of osteogenesis imperfecta

A

blue sclerae
hearing loss
ligament laxity

28
Q

class III malocclusion is increased in pts with

A

osteogenesis imperfecta

29
Q

tx for osteogenesis imperfecta

A

none

30
Q

what happens in osteopetrosis

A

osteoclasts are unable to resorb bone

31
Q

t/f in osteopetrosis, there is a marked increase in bone density but there they have a lot of bone fratures

A

true

32
Q

what can pts with infantile osteopetrosis also present with

A

cranial nerve compressions, normocytic anemia, hepatoslenomegaly, frequent fractures,
marrow failure

33
Q

adult osteopetrosis is different than infantile how

A

marrow failure is rare, 40% asymptomatic, rare bone fractures with common nerve compression OR common bone fractures with rare nerve compressions

34
Q

2 types of ectodermal dysplasia

A

anhidrotic and hidrotic

35
Q

anhidrotic ectodermal dysplasia

A

partial or complete absence of eccrine sweat glands, sebaceous glands, and hair follicles

36
Q

face abnormalities in ectodermal dysplasia

A

midface hypoplasia

37
Q

skin and appendage abnormalities of ectodermal dysplasia

A

fine, sparse hair, scanty eyelashes and eyebrows, heat intolerance and fever

38
Q

whats happening with the teeth in pts with ectodermal dysplasia

A

cone shaped and less teeth

39
Q

oral manifestations of ectodermal dysplasia

A 
hypodontial or anodontia
hypoplasia of alv ridges
decreased vdo
protuberant lips
cone shaped teeth
unerupted teeth
xerostomia
40
Q

cherubism

A

genetic disease affecting osteoblasts and clasts

41
Q

clinical findings of cherubism

A

appears less than 10
progressive, nontender swelling of jaws
mand always involved
round, cherubic face

42
Q

radiographic findings in cherubism

A

BILATERAL radiolucent lesions
multilocular
multiple unerupted teeth

43
Q

tx for cherubism

A

lesions stabilize at puberty

surgical recontouring

44
Q

gardner sydrome

A

genetic disease with GI polyps and multiple osteomas

associated with cancer and colon/rectum carcinomas

45
Q

2 syndromes with GI polyps

A

gardners and peutz jeghers

46
Q

t/f by age 60, 100% of the intestinal polyps are malignant

A

true

47
Q

tx with garners syndrome

A

osteomas and epidermoid cysts removed

prophylactic colectomy recommended (what we’re really worried about)

48
Q

craniofacial dysostosis is also known as

A

crouzon disease (apert is also the same, but they have syndactyly - fingers and toes fuse together)

49
Q

manefestation of crouzon disease

A

synostosis (early closures of the suture)

50
Q

clinical features of crouzons

A

midface hypoplasia and exopthalamus

prominent nose

51
Q

radiographic findings of crouzons

A

beaten metal appearance

52
Q

tx of crouzons

A

craniectomy early in life to provide space for the brain

53
Q

cleidocranial dysplasia

A

genetic disease with late closure of fontanels with wormian bones
brachycephalic skull

54
Q

percent of cleidocranial dysplasia with out clavice

A

10%

55
Q

whats happening with the shoulders of cleidocranial dysplasia pts

A

aplasia, hypoplasica or thinning of clavicles

56
Q

what happening orally in cleidocranial dysplasia pts

A

high narrow palate, multiple, unerupted supernumerary teeth

57
Q

treacher collins sydrome clinical findings

A

down sloping palpebral fissures
hypooplasia of mand and malar bones
coloboma
deformed pinna - conductive hearing loss

58
Q

what syndromes that we know of have cafe au lait spots

A

neurofibromatosis, jaffe, and mccune albright

59
Q

papillon-lefevre syndrome is also known as

A

juvenile periodontosis with palmar-plantar hyperkeratosis

60
Q

what do you find clinically in pts with papillon leffevre syndrome

A

generalized aggressive periodontitis with hyperkeratotic palms and soles of feet

oral path 2 (8 decks)

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