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
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
3
Q
how do we diagnose and treat hyperpituitarism
A
- dx measure growth hormone
- tx pituitary gland surgery
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
5
Q
how do we treat hyperthyroidism
A
- hormone suppression (propylthiouracil)
- radioactive iodine
- surgery
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
7
Q
what is cretinism
A
- hypothyroidism in infants and early childhood
8
Q
what is myxedema
A
- hypothyroidism in older childhood and adults
9
Q
what are oral manifestations of hypothyroidism
A
- in infants: thickened lips, enlarged tongue, delayed eruption of teeth
- in adults: enlarged tongue
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
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
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
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
14
Q
what are the 3 Ps of type 1 diabetes
A
- polydipsia: excessive thirst
- polyuria: excessive urination
- polyphagia: excessive eating
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
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)
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
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
19
Q
what are symptoms of addison disease
A
- chronic, worsening fatigue
- inability to deal with stress
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
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
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)
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
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
25
Q
what are clinical manifestations of B12 deficiency
A
- weakness
- fatigue on exertion
- paresthesia
- oral: angular cheilitis, mucosal ulcerations (aphthous), burning tongue (depapillation)
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
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
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
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
