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Oral Pathology > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

what is hyperpituitarism

A
  • excess hormone production by the anterior pituitary gland
  • caused most often by a benign tumor that produces growth hormone
  • gigantism results if occurs before closure of long bones
  • acromegaly results when hypersecretion occurs during adult life
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2
Q

what are clinical manifestations of hyperpituitarism

A
  • enlargement of mx and mn
  • frontal bossing
  • mx sinus – deep voice
  • separation of teeth
  • malocclusion
  • macroglossia
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3
Q

how do we diagnose and treat hyperpituitarism

A
  • dx measure growth hormone

- tx pituitary gland surgery

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4
Q

what is hyperthyroidism

A
  • over production of thyroid hormone
  • results on graves disease (autoimmune): exophthalmos, excessive sweating, weight loss
  • oral manifestations: premature exfoliation of deciduous teeth, osteoporosis, increase risk to caries and perio, burning tongue
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5
Q

how do we treat hyperthyroidism

A
  • hormone suppression (propylthiouracil)
  • radioactive iodine
  • surgery
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6
Q

what is hypothyroidism

A
  • a decreased output of thyroid hormone
  • causes include developmental disturbances, autoimmune disease, iodine deficiency, drugs and pituitary disease
  • cretinism: when it occurs in infancy and childhood
  • myxedema: when it occurs in older children and adults
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7
Q

what is cretinism

A
  • hypothyroidism in infants and early childhood
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8
Q

what is myxedema

A
  • hypothyroidism in older childhood and adults
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9
Q

what are oral manifestations of hypothyroidism

A
  • in infants: thickened lips, enlarged tongue, delayed eruption of teeth
  • in adults: enlarged tongue
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10
Q

what is hyperparathyroidism

A
  • excessive secretion of parathyroid hormone
  • parathyroid glands: calcium and phosphorus metabolism
  • hypercalcemia: increased calcium uptake from bone to blood
  • hypophosphatemia
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11
Q

what are clinical manifestations of hyperparathyroidism

A
  • joint pain/stiffness
  • bone changes: radiolucencies in jaw, generalized “ground glass” appearance, loss of lamina dura, loosening of teeth
  • dx and tx: blood levels (PTH, Ca, P). tx cause: tumor, renal disease, vitamin d deficiency. bone lesions heal
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12
Q

what is diabetes mellitus

A
  • a chronic disorder of carbohydrate metabolism characterized by abnormally high blood glucose levels
  • these result from a lack of insulin due to destruction of pancreatic beta cells, inadequate secretion of insulin by beta cells or increased insulin resistance due to obesity
  • glucose normally signals beta cells of the pancreas to make insulin
  • the hormone is then secreted into the blood stream to facilitate the uptake of glucose into fat and skeletal muscle
  • in the presence of insulin, fat and skeletal muscle cells can use glucose as an energy source
  • without insulin, tissue is broken down to provide energy and weight loss occurs. a severe hyperglycemia can lead to diabetic coma. ketone bodies can be produced by the breakdown of fatty acids. ketoacidosis lowers to pH of blood
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13
Q

why are diabetics at increased risk to infection

A
  • phagocytic activity of macrophages is reduced and neutrophil chemotaxis is delayed -> increased risk to infection
  • collagen production is abnormal -> poor healing response
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14
Q

what are the 3 Ps of type 1 diabetes

A
  • polydipsia: excessive thirst
  • polyuria: excessive urination
  • polyphagia: excessive eating
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15
Q

what drug is commonly used in type 2 diabetes

A
  • byetta
  • injectable, lowers blood sugar – no insulin
  • helps in control and improving release and resistance of insulin
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16
Q

what are clinical features of diabetes

A
  • vascular system: atherosclerosis, impaired circulation. kidney, eye – blindness, nervous system, extremities – gangrene and ulceration of feet
  • acanthosis nigrans: hyperpigmented skin plaques in folds of skin. assist in diagnosis of type 2 (usually seen in type 2)
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17
Q

what are the oral complications associated with diabetes

A
  • candidiasis
  • parotid gland enlargement
  • xerostomia
  • accentuated plaque response
  • hyperplastic and erythematous gingiva (gingival abscess)
  • slow wound healing
  • increase susceptibility to infection
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18
Q

what is addison disease

A
  • adrenal cortical insufficiency
  • decreased adrenal steroid hormones (cortisol and aldosterone)
  • autoimmune or tumors
  • increase levels of ACTH (adrenocorticotropic hormone) – stimulates melanocytes, brown macules
  • tx: steroids
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19
Q

what are symptoms of addison disease

A
  • chronic, worsening fatigue

- inability to deal with stress

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20
Q

what are anemias

A
  • red blood cell disorders
  • decrease in O2 in the blood
  • decrease in red blood cells
  • can result from:
  • iron
  • folic acid
  • b12
  • suppression of bone marrow
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21
Q

what are oral manifestations of anemias

A
  • skin and mucosal pallor
  • angular cheilitis
  • erythema
  • atrophy of oral mucosa
  • loss of filliform/fungiform papilla
  • burning tongue
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22
Q

what is iron deficiency anemia

A
  • insufficient amount of iron to bone marrow
  • RBC reproduction
  • component of Hb
  • limited Hb to carry O2
  • diet deficient
  • menstrual
  • poor absorption
  • pregnancy (increased iron required)
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23
Q

what is the diagnosis and treatment of iron deficiency

A
  • lab tests
  • low Hb
  • decrease hematocrit (volume percent of RBC)
  • smaller RBC and lighter in colour (hypochromic)
  • dietary supplementation
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24
Q

what is pernicious anemia

A
  • lack of B12
  • deficiency of intrinsic factor: in stomach, necessary for absorption of B12
  • unable to absorb
  • B12: DNA synthesis, RBC and epithelial cells affected
  • folic acid very similar; both caused by malnutrition
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25
Q

what are clinical manifestations of B12 deficiency

A
  • weakness
  • fatigue on exertion
  • paresthesia
  • oral: angular cheilitis, mucosal ulcerations (aphthous), burning tongue (depapillation)
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26
Q

how do we diagnose and treat B12 deficiency

A
  • lab: low B12. megaloblastic anemia: large, immature. cell nucleus. schilling test: ability to absorb
  • tx: B12 shots – no oral. sublingual tablets
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27
Q

what is thalassemia

A
  • inherited disorder
  • minor: heterozygous
  • major: homozygous
  • damage to RBC cell membranes
  • associated with hemolytic anemia, results from destruction of red blood cells
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28
Q

what are the clinical manifestations of thalassemia

A
  • yellow-ish skin
  • enlarged liver, spleen
  • prominent cheek
  • protrusion of max
  • flaring of max anterior
  • bone:
  • prominent trabeculae
  • blurring of others
  • “salt and pepper”
  • circular radiolucency in alveolar bone
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29
Q

how do we treat thalassemia

A
  • experimental, blood transfusions, splenectomy, supportive therapies
  • poor prognosis: extended life expectancy from early childhood to 20 years
30
Q

what is sickle cell anemia

A
  • an inherited blood disorder
  • when someone is heterozygous, it is called a sickle cell trait
  • when someone is homozygous, they are much more severely affected
  • occurs before the age of 30 and is more common in women than in men
  • the red blood cells develop a sickle shape when there is decreased oxygen
  • this can be triggered by exercise, exertion, administration of a general anesthetic, pregnancy or even sleep
31
Q

what are clinical signs of sickle cell anemia

A
  • weakness
  • short of breath
  • joint pain
  • oral
  • trabeculation
  • large spaces
  • also in skull – “hair on end” pattern
32
Q

how do we treat sickle cell anemia

A
  • bone marrow transplant
  • manage symptoms (O2, pain, blood transfusions)
  • long term heart issues (blockages)
33
Q

what is aplastic anemia

A
  • decrease in ALL blood cells - pancytopenia
  • severe depression of bone marrow
  • decrease in stem cells
  • primary (unknown cause), and secondary (chemo)
  • oral symptoms: infection, spontaneous bleeding, leukopenia (decrease of WBC), thrombocytopenia
34
Q

what are treatments for both types of aplastic anemia

A
  • primary: bone marrow transplant, transfusion

- secondary: remove cause

35
Q

what is polycythemia

A
  • increase in RBC

- 3 types: primary, secondary, relative

36
Q

what is primary polycythemia

A
  • proliferation of bone marrow stem cells
  • uncontrolled
  • headache, dizzy
  • impaired blood flow
  • decrease in platelets
  • risk to stroke, aneurism, low blood flow
37
Q

what is secondary polycythemia

A
  • decreased oxygen by physiologic cause
  • causes increase in RBC production
  • lung disease
  • high altitude
  • carbon monoxide
38
Q

what is relative polycythemia

A
  • decrease plasma volume (# of RBC stays the same but less plasma gives the appearance of increase RBC)
  • causes:
  • diuretic use and alcohol
  • vomiting
  • diarrhea
  • excessive sweating
  • very high stress (overweight, hbp, smokers, men)
  • risk: stroke, MI
39
Q

what are oral manifestations of polycythemia

A
  • mucosa:
  • deep red to purple
  • gingival swelling
  • bleed easily
  • hematomas
40
Q

how do we diagnose and treat polycythemia

A
  • lab test
  • chemo
  • phlebotomy (blood letting)
  • causal factors
41
Q

what is celiac disease/celiac sprue

A
  • sensitivity to gluten
  • ingestion = injury to intestinal mucosa
  • malabsorption of B12 and folic acid
  • clinical: painful, burning tongue. ulceration of mucosa, atrophy of papilla
  • treatment: gluten free diet
42
Q

what is leukemia

A
  • malignant neoplasms of blood forming cells
  • stem cells in bone marrow
  • excessive abnormal wbc
  • acute or chronic
43
Q

what is acute leukemia

A
  • fast onset
  • immature cells
  • lymphoblastic: lymphocytes. children, good prognosis
  • myeloblastic: PMN/granulocytes. teens and young adults. poorer prognosis
44
Q

what are clinical signs of acute leukemia

A
  • weakness
  • fever
  • enlargement of lymph nodes
  • bleeding – decrease in platelets (thrombocytopenia)
  • oral: gingival enlargement, NUG, increased bleeding
45
Q

how do we diagnose and treat acute leukemias

A
  • dx: blood test (immature wbc, elevated wbc, low platelet)

- tx: chemo, relapses, bone marrow transplant

46
Q

what is chronic leukemia

A
  • slow onset – adults
  • karyotype abnormalities
  • chronic myeloid: philadelphia chromosome – translocation between 9 and 22 (abnormally short 22)
  • chronic lymphocytic: most common
47
Q

what are clinical signs and symptoms of chronic leukemia

A
  • nonspecific fatigue, weakness
  • pallor of lips and gingiva
  • gingival enlargement and bleeding
  • dx and tx: high wbc count, chemo (short term, long term poorer prognosis, bone marrow transplant)
48
Q

what is hemostasis

A
  • cessation of bleeding

- many factors involved – vasoconstriction, platelets, fibrin (clotting factors), anticlotting to prevent blockages

49
Q

what is hemostasis dependent on

A
  • blood vessels
  • adequate platelets
  • adequate clotting factors
50
Q

what is normal platelet count

A
  • 200,000 to 400,000/mm3 = normal
  • <100,000 = thrombocytopenia (decreased # platelets)
  • <20,000 = spontaneous gingival bleeding
51
Q

what is bleeding time

A
  • adequacy of platelet function - not # of platelets
  • 1-6 mins = normal
  • > 5-10 minutes = problem
  • test is no longer easily available
52
Q

what is prothrombin time

A
  • how long to form a clot (in vitro)
  • INR = international normalized ratio
  • standardized number = more accurate
  • less than 3.0 = normal (ideal is 0.8-1.1 for pte not on anticoagulants)
  • 4-5 is concern for bleeding but patients on anticoagulants can have this value
53
Q

what is partial thromboplastin time

A
  • measures effectiveness of clot formation by measuring time it takes to form
  • intrinsic pathway: normal = 25-40 secs, no more than 50 secs
  • used to determine if blood-thinning therapy is effective
54
Q

what is purpura

A
  • reddish blue discoloration - defect or deficiency in platelets
  • skin, mucosa
  • spontaneous subepithelial bleeding
  • blood oozing from sulcus
  • purpura and ecchymoses are terms that refer to larger lesions
55
Q

what is petechiae

A
  • smaller lesions
56
Q

what is thrombocytopenic purpura

A
  • severe reduction in platelets #
  • autoimmune
  • chemo
57
Q

what is nonthrombocytopenic purpura

A
  • defect of capillary walls or platelet function
  • von-willebrand disease – autosomal dom
  • aspirin – impairment of platelet function
58
Q

what are oral manifestations of purpura

A
  • spontaneous gingival bleeding
  • petechiae
  • ecchymoses (larger lesions)
  • hemorrhagic blister
  • dx and tx: steroids, splenectomy. transfusion for platelet number low
59
Q

what is hemophilia

A
  • blood coagulation – doesn’t clot properly

- missing factors: can’t convert fibrinogen to fibrin, factor VIII or IX

60
Q

what are oral manifestations of hemophilia

A
  • spontaneous bleeding
  • petechiae, ecchymoses
  • hemhorrage post surgery
61
Q

how do we diagnose and treat hemophilia

A
  • find missing factor
  • attempt to replace
  • pt is normal
  • ptt is prolonged pathway (intrinsic pathway)
62
Q

what is radiation therapy

A
  • radiation of the head and neck
  • mucositis: painful, red, ulcerated mucosa. difficulty swallowing, eating, loss of taste
  • xerostomia: irreversible for salivary glands
  • patient often experiences mucositis during radiation therapy – mucositis begins about the second week of therapy and subsides a few weeks after its completion
  • painful, appears as an erythematous and ulcerated mucosa
  • patients may have difficulty eating, pain on swallowing, loss of taste
  • patients should have an oral evaluation before radiation therapy of the head and neck. potential sources for oral infection and teeth with a questionable prognosis should be removed
  • hygienists can help with fluoride application, patient education, frequent follow-up appts
63
Q

what is the hygienists role in patients experiencing radiation therapy

A
  • thorough med history
  • prevention: fluoride, xerostomia, OHI, limit infection, increased recall
  • see post 6-8 weeks to assess OH, compliance with fluoride, advice on future care
64
Q

what is the NADIR period

A
  • lowest point of wbc count

- usually post 7 days

65
Q

what is osteonecrosis

A
  • bone death
  • loss of blood supply – spontaneous, surgery post radiation, long term risk
  • tx: hyperbaric chamber, force oxygen into bone
66
Q

what are the 3 H’s of osteoradionecrosis

A
  • tissue hypoxia
  • hypocellularity
  • hypovascularity
  • results in tissue breakdown and non healing wounds
  • mn: more cortical bone and decreased blood supply
67
Q

what is BIONJ

A
  • bisphosphonate induce osteonecrosis of the jawbone
  • strong affinity for calcium
  • stay found to bone over 10 years
  • decrease osteoclast and increase osteoblast
68
Q

what is the IV route of bisphosphonates like

A
  • aredai, zometa
  • cancer, multiple myeloma, breast/prostate
  • contraindication to implants and dental surgery
  • all surgery and tx prior to IV drug
  • stopping drug may not prevent BIONJ
69
Q

what oral drugs exist for bisphosphonates

A
  • fosamax
  • boniva
  • actonel
  • much smaller risk
  • no contraindication for DH
  • may stop for oral surgery
70
Q

why does BIONJ happen

A
  • decrease blood supply and repair

- in jaw: direct communication with bacteria, high remodelling - 20-40x, high loading of stress

Oral Pathology (9 decks)

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