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Oral Pathology Exam 2 > 6 Oral Manifestations of Systemic Diseases > Flashcards

6 Oral Manifestations of Systemic Diseases Flashcards

1
Q

dense collagen is deposited in the body in high amounts (immune mediated)

A

scleroderma

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2
Q
  • women 3x more than men

* adults

A

scleroderma

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3
Q
  • skin develops diffuse hard texture with a smooth surface

* localized, limited, or diffuse forms

A

scleroderma

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4
Q

Facial skin:
• increased deposition of subcutaneous collagen
• smooth, taut, masklike

A

scleroderma

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5
Q

fibrosis of lungs, heart, kidneys, GI tract —> leading to organ failure

A

scleroderma

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6
Q

In patients with scleroderma, this is the result of collagen deposition in the perioral tissues. 70% of patients have limited opening.

A

microstomia

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7
Q
  • claw-like appearance of hands
  • resorption of terminal phalanges
  • ulceration of the finger tips due to collagen deposition and lack of blood supply
A

scleroderma

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8
Q

vasoconstriction triggered by cold or emotional stress

A

Raynaud’s phenomenon (scleroderma)

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9
Q

Initially: blanching of the digits
Minutes later: bluish due to venous stasis

Warming results in increased blood flow and change to a red hue (can be painful)

A

Raynaud’s phenomenon (scleroderma)

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10
Q

Radiograph:
• widening of the PDL
• resorption of the posterior ramus, coronoid process, chin, and condyle

A

scleroderma

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11
Q

survival rate of scleroderma (2, 8, and 12 yr survival)

A

80% 2 year
30-50% 8 year
12-30% 12 year

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12
Q

tx for scleroderma

A

no tx available

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13
Q

clinical signs of jaundice

A
  • excess bilirubin in the bloodstream and accumulates in the tissues
  • yellow discoloration of the skin and mucosa

*these are NOT specific signs, require physical examination and laboratory studies to determine the precise cause

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14
Q

What is bilirubin derived from?

A

the breakdown of hemoglobin

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15
Q

process of making bilirubin

A
  • erythrocyte lifespan = 120 days
  • physiologic breakdown of hemoglobin
  • hemoglobin is degraded and processed by reticuloendothelial system
  • unconjugated bilirubin released into bloodstream
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16
Q

unconjugated vs conjugated bilirubin

A

Unconjugated—taken up by hepatocytes, conjugated with glucuronic acid

Conjugated—soluble product that can be excreted in the bile

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17
Q

physiologic vs pathological causes of jaundice

A

Physiologic
• Jaundice at birth—low level of activity of the enzyme system that conjugates bilirubin

Pathologic
• Increased production of bilirubin—RBCs broken down too fast, liver cannot keep up processing (sickle cell anemia)
• Liver function abnormality—decreased uptake of the bilirubin from circulation, decreased conjugation in the liver cells

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18
Q

2 main pathological causes of jaundice:

A

1) Liver function disturbance—forces conjugated bilirubin into the bloodstream (infection—viral hepatitis, alcoholic hepatitis, cancer)
2) Occlusion of the bile duct—gallstones, stricture, cancer

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19
Q

Tissues that have a high content of elastin and therefore attract bilirubin:

A

1) sclera—the first site at which the yellow color is noted
2) lingual frenum
3) soft palate

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20
Q

group of conditions characterized by deposition of amyloid

A

amyloidosis

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21
Q

What is amyloid?

A

extracellular proteinaceous substance

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22
Q

Amyloid can be formed in multiple ways (2)

A
  • from immunoglobulin light chains = AL

* from beta2-microglobulin = Abeta2M (protein that cannot be removed by dialysis, accumulates in plasma)

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23
Q

protein that cannot be removed by dialysis, accumulates in plasma

A

beta2-microglobulin (due to hemodialysis-associated amyloidosis)

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24
Q

All amyloid proteins form into this molecular configuration and then are deposited into tissues.

A

beta-pleated sheet

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25
Q

Two main categories of clinical presentation of amyloidosis:

A

1) Organ-limited—a solitary nodule

2) Systemic—primary, myeloma associated, secondary, hemodialysis associated, heredofamilial

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26
Q

Name the systemic amyloidosis: most common type, idiopathic

A

primary—AL

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27
Q

Name the systemic amyloidosis: excess light-chain proteins from myeloma tumor cells accumulate and are deposited in tissues

A

myeloma-associated—AL

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28
Q

Name the systemic amyloidosis: 15-20% of all amyloidosis cases

A

myeloma-associated—AL

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29
Q

Name the systemic amyloidosis: beta-2 microglobulin is a normally occurring protein that is not removed by the dialysis process —> accumulates in the plasma —> forms deposits in bones and joints (carpal tunnel, cervical spine)

*improving with better dialyzers in the future

A

hemodialysis-associated amyloidosis

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30
Q

Name the systemic amyloidosis: primarily autosomal dominant

A

heredofamilial

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31
Q

Clinical manifestations:
• average age = 65
• initial symptoms are nonspecific (fatigue, weight loss, hoarseness, orthostatic hypotension)
• eventually—carpal tunnel syndrome, hepatomegaly, mucocutaneous lesions, macroglossia (10-40% of patients)

A

primary and myeloma-associated amyloidosis

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32
Q

deposition of amyloid in the tongue, may see ulceration

A

macroglossia due to primary and myeloma-associated amyloidosis

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33
Q 
Skin lesions:
• smooth-surfaced, firm, waxy papules and plaques 
• eyelid 
• retroauricular
• neck 
• lips 
• petechia

Also:
• heart deposits
• kidney deposits

A

amyloidosis

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34
Q

biopsy of amyloidosis

A
  • rectal biopsy 80%+
  • abdominal fat aspiration 55-75%
  • labial salivary gland 80%+

Biopsy reveals amorphous acellular eosinophilic material
• stain with congo red
• polarized light = apple green color

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35
Q

tx of amyloidosis

A

depends on cause of the amyloid, many cases no tx available

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36
Q

prognosis is guarded to poor, most patients die of cardiac failure, arrhythmia, or renal disease within months to a few years after the dx

A

amyloidosis

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37
Q

possible causes of iron deficiency anemia (4)

A
  • excessive blood loss
  • increased demand for RBCs (growth, pregnancy)
  • decreased intake of iron
  • decreased iron absorption (celiac sprue)
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38
Q

Iron deficient anemia:
% of women of childbearing age
% of men (What is the main cause?)

A

11% of women

2% of men, GI disease is main cause (peptic ulcer, diverticulosis, hiatal hernia, malignancy)

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39
Q
  • fatigue, palpitations, lightheadedness
  • angular cheilitis
  • diffuse or patchy atrophy of dorsal tongue papillae
  • possible tenderness or burning sensation of oral mucosa
A

iron deficient anemia

*confirm dx with CBC

40
Q

iron-deficiency anemia in conjunction with glossitis and dysphagia

A

Plummer-Vinson syndrome

41
Q

Plummer-Vinson syndrome is associated with a high frequency of?

A

oral and esophageal SCC

*considered a premalignant process

42
Q

most patients are women of Scandinavian or Northern European background

A

Plummer-Vinson syndrome

43
Q

Systemic findings: fatigue, shortness of breath, weakness

Oral findings: burning sensation of tongue and oral mucosa, pain can be so severe that dentures cannot be worn, angular cheilitis may be severe, atrophy of the lingual papillae, smooth red appearance of the dorsal tongue

A

Plummer-Vinson syndrome

44
Q

esophageal webs—frequent difficulty swallowing (dysphasia) or pain on swallowing, endoscopy or esophageal barium reveals abnormal bands of tissue in the esophagus

A

Plummer-Vinson syndrome

45
Q

altered growth of nails (spoon-shaped, brittle) seen with Plummer-Vinson syndrome

A

koilonychia

46
Q

tx of Plummer-Vinson syndrome

A 
Dietary iron supplementation 
• resolves the anemia 
• relieves the glossodynia
• may reduce esophageal symptom severity 
• esophageal dilation if needed
47
Q

Why is a periodic evaluation for oral, pharyngeal, and esophageal cancer necessary for Plummer-Vinson syndrome?

A

5-50% prevalence of upper aerodigestive tract malignancy has been reported in affected persons

48
Q

cause of pernicious anemia

A

poor absorption of extrinsic factor/vitamin B12/cobalamin

49
Q

allows for absorption of B12, produced by parietal cells of the stomach

A

intrinsic factor

50
Q

Why are mitotically active cells the most dramatically affected by pernicious anemia?

A

B12 is required for normal nucleic acid synthesis

51
Q

Systemic symptoms:
• fatigue, weakness, SOB, headache
• tingling, numbness of extremities

A

pernicious anemia

52
Q
  • burning sensation of tongue, lips, buccal mucosa
  • patchy areas of erythema and atrophy
  • 50-60% of patients have tongue involvement
A

pernicious anemia

53
Q

How to test for pernicious anemia?

A
  • bloodwork shows macrocytic anemia and reduced serum cobalamin levels
  • serum antibodies directed against intrinsic factor—quite specific for pernicious anemia
  • Schilling test—compares absorption and excretion rates of radiolabeled cobalamin (complicated to perform, now considered obsolete)
54
Q

test for pernicious anemia that compares absorption and excretion rates of radiolabeled cobalamin (complicated to perform, now considered obsolete)

A

Schilling test

55
Q

tx for pernicious anemia

A
  • monthly IM injections of cyanocobalamin —> rapid response, reports of clearing oral lesions ~ 5 days
  • high-dose oral cobalamin therapy (equally effective)
56
Q

advantages of high dose oral cobalamin vs monthly IM injections of cyanocobalamin for treating pernicious anemia

A

cost-effectiveness, elimination of injections

57
Q

gastric carcinoma 7x more likely in patients with this

A

pernicious anemia

58
Q

increased risk of malignancy for people with pernicious anemia

A

gastric carcinoma 7x more likely

59
Q

3 parathyroid disorders:

A

hypoparathyroidism
primary hyperparathyroidism
secondary hyperparathyroidism

60
Q

results from decreased secretion of PTH

A

hypoparathyroidism

61
Q

most common cause of hypoparathyroidism

A

removal of the parathyroids during thyroidectomy

62
Q

symptoms of hypoparathyroidism (3)

A

1) hypocalcemia—causes increased neuromuscular excitability (mild tingling of hands and feet, parenthesia, muscle cramps/spasms)
2) dental related changes—if during tooth formation then pitting enamel hypoplasia, failure of tooth eruption)
3) mental effects—hyperirritability, fatigue, anxiety, mood swings/personality disturbances

63
Q

tx for hypoparathyroidism

A

oral calcium and vitamin D precursor

64
Q

syndrome caused by excessive secretion of PTH resulting from intrinsic parathyroid disease

A

primary hyperparathyroidism

65
Q

2 causes of primary hyperparathyroidism:

A

1) adenoma of the parathyroid gland (80% of cases)

2) hyperplasia parathyroid glands (15-20% of cases)

66
Q

Name the cause of primary hyperparathyroidism: dramatic enlargement of 1 of the 4 glands

A

adenoma of parathyroid gland

67
Q

tx of adenoma of parathyroid gland

A

surgical removal of the tumor

68
Q

Name the cause of primary hyperparathyroidism: develops in patients with familial multiple endocrine neoplasia types I and II, all 4 glands are involved

A

hyperplasia parathyroid glands

69
Q

> 60 yo, females 2-4x more often

A

primary hyperparathyroidism

70
Q

hypercalcemia on blood analysis

A

primary hyperparathyroidism

71
Q

Why does primary hyperparathyroidism show hypercalcemia on blood analysis?

A

increased PTH production —> excess loss of calcium from the bones —> increased serum calcium, decreased serum P

72
Q

bones, stones, moans, groans

A

primary hyperparathyroidism

73
Q

painful bones—primary hyperparathyroidism

A
  • bone resorption (finger tips) —> subperiostel resorption
  • generalized loss of the lamina dura
  • ground glass appearance of bone
74
Q

renal stones—primary hyperparathyroidism

A
  • renal tubules absorb more calcium
  • PTH stimulates the tubules to produce active vitamin D
  • active vitamin D promotes more calcium absorption from the intestines
75
Q

abdominal groans—primary hyperparathyroidism

A

duodenal ulcers, gallstones

76
Q

moans—primary hyperparathyroidism

A

depression and lethargy

77
Q

intrabony tumor called a “Brown tumor”, named because grossly tissue is deep red to brown color

A

primary hyperparathyroidism

78
Q

well-demarcated, multilocular radiolucency

A

Brown tumor (primary hyperparathyroidism)

79
Q

locations of Brown tumor

A

mandible, clavicle, ribs, pelvis

80
Q

histopathologically identical to giant cell granuloma, numerous multinucleated giant cells

A

Brown tumor (associated with primary hyperparathyroidism)

81
Q

excess secretion of PTH as a response to chronically low calcium levels (hypocalcemia)

A

secondary hyperparathyroidism

82
Q

causes of secondary hyperparathyroidism (5)

A 
Chronically low calcium levels due to: 
• kidney failure requiring dialysis (most common)—GFR falls, leads to increased phosphate retention, in turn leads to increased PTH production 
• stomach or intestine bypass surgery 
• celiac disease 
• Chron’s disease 
• severe vitamin D deficiency
83
Q

because there is not enough calcium the parathyroids go into overdrive and become hyperplastic, all 4 glands become enlarged

A

secondary hyperparathyroidism

84
Q

excess PTH production results in?

A

calcium resorbed from bones

85
Q

term specifically for bone resorption in patients with renal failure and secondary hyperparathyroidism

  • bone and joint pain
  • bone deformation and fractures at late stages
A

renal osteodystrophy

86
Q

generalized loss of lamina dura, blurring of the trabecular pattern leads to “ground glass” appearance

A

secondary hyperparathyroidism

87
Q

tx for secondary hyperparathyroidism

A
  • optimize levels of serum calcium and phosphate (dietary restriction of phosphorous and phosphate binders)
  • control PTH and vitamin D by use of vitamin D analogues
  • surgical removal of the glands
  • renal transplant if cause is renal failure
88
Q

rare metabolic bone disease due to tissue-nonspecific alkaline phosphatase deficiency

A

hypophosphotasia

89
Q

plays a role in the production of bone, precise mechanism is unknown, deficiency causes hypophosphotasia

A

alkaline phosphatase

90
Q

one of the first presenting signs of hypophosphotasia and why

A
  • premature loss of the primary teeth

* likely caused by a lack of cementum on the root surfaces

91
Q

____ distinct mutations of the gene responsible for alkaline phosphatase causing hypophosphotasia

A

150

92
Q

2 genetic causes of hypophosphotasia:

A

Homozygous autosomal recessive form
• severe manifestations
• patients usually identified in infancy

Milder forms 
• autosomal dominant or recessive 
• variable degrees of expression 
• appearing in childhood or adulthood 
• younger the age of onset = more severe
93
Q

How many types of hypophosphotasia are now recognized, depending on the severity and the age of onset of the symptoms?

A

6

94
Q

3 common factors in all types of hypophosphotasia:

A
  • reduced levels of alkaline phosphatase isozyme found in the bone, liver, and kidney
  • increased levels of blood and urinary phosphoethanolamine
  • bone abnormalities that resemble rickets
95
Q

one of the first presenting signs of childhood hypophosphotasia? why? radiographic signs?

A
  • premature loss of the primary teeth without evidence of significant inflammatory issue (incisors may be the first and only teeth involved)
  • likely caused by lack of cementum on root surfaces
  • teeth may show enlarged pulp chambers, may see alveolar bone loss
96
Q

dx of hypophosphotasia

A
  • based on the clinical manifestations
  • decreased levels of serum alkaline phosphatase
  • increased amounts of phosphoethanolamine in both the urine and blood
97
Q

tx of hypophosphotasia

A
  • alkaline phosphatase infusions are unsuccessful
  • fractures require orthopedic surgery
  • prostheses for missing teeth, implants can be used

Oral Pathology Exam 2 (8 decks)

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