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309 Cards in this Set

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Classic Endocrinology
-blood-borne "humoral factors" first recognized with observation of effects of castration on growth and behaviors
-1st documented endocrine studies 1849
-1st successful hormone replacement therapy (thyroid hormone) 1891
-study of hormones produced in one organ, transported through the blood, and acting at a distant site"
How do cells signal/regulate one another?
-Indirect:
Paracrine (neighboring cells)
Neurocrine (synaptic through neurons and neurotransmitters)
Endocrine (Autocrine) - travel through blood and activate another target cell
How do cells signal/regulate each other?
-Cells in the body communicate using chemical messengers which pass from one cell to another
-Signals arrive at their target cells in the form of chemical messengers. The mechanisms involved in the resonse of a cell to a particular messenger depend on nature of the messenger.
-Steroid and thyroid hormones, are lipid-soluble and readily enter the cell therefore the response is initiated inside the cell
Chemical classes of hormones
-steroid family hormones: glucocorticoids, mineralcorticoids, Vitamin D, androgens
-Peptide/protein hormones: GH, insulin, PTH, ADH, Oxytocin, Releasing Hormones
-Amino Acid Hormones: thyroid hormone, Norepinephrine, epinephrine
Posterior Pituitary produces
-oxytocin: stimulates uterine contractions, mammary glands
-ADH: promotes resorption of water in kidney tubules
Anterior Pituitary produces
-Growth hormone: stimulates growth
-Prolactin: stimulates development of mammary glands and secretion of milk
-Melanocyte-Stimulating Hormone: stimulates production of melanin
-thyroid stumulating hormone (to act on thyroid)
-ACTH (to act on adrenal cortex)
-FSH, LH (gonadotropins) to act on gonads
Thyroid releases
-thyroxin: metabolic rate
Adrenal cortex releases
-cortisol: raise glucose levels in the blood
Gonads
-Sex Hormones (testosterone, estrogen, progesterone); FSH stimulates gamete production by gonads; LH stimulates sex-hormone production
Amino Acid Hormones
-synthesized from TYROSINE
-stored and secreted in bursts
Thyroid hormone
-circulates >99% bound
-very long half-life (days)
-binds to intracellular receptors (but plasma membrane transporter)
- effects through gene transcription
-SLOW
Thyroid secretes...
-secretes thyroxine (T4) and triiodothyronine (T3) which affect metabolic processes throughout body and are important to oxygen use
-secretes calcitonin that is involved with regulation of serum calcium and phosporous levels
-requires iodine for the synthesis of thyroid hormone
Thyroid development
-thyroid gland begins development at foramen caecum at the junction of the posterior one third with the anterior two thirds of the tongue and descends to its normal position in the neck during development
-on rare occasions remnants of thyroid tissue remain along the developmental path and may be seen as a lump in the midline lying at any point between foramen caecum and epiglottis, the so-called thyroglossal cyst
basic elements in regulation of thyroid function
-Hypothalamus (releases TRH- thyroid releasing hormone)
-Anterior Pituitary (releases TSH thyroid stimulating hormone)
-Thyroid gland (releases T4 and T3)
main factors interacting in the regulation of TSH syntehsis and secretion
-stress, circadian rhythym, cold, starvation, illness
Tests available that measure the thyroid hormone concentration and function...
-radioactive iodine is measured after 24 hours normal levles are 10-30% above normal = thyroid hyperfunction
-radioimmunoassays measure serum T4 and T3 concentrations in the blood with elevated levels indicating hypothyroidism and lower levels indicating hyperthyroidism
-thyroid lesions can be detected by ultrasonography or by thyroid scan after injection of I, scanner localizes areas of radioconentration
-measurement of basal serum TSH is useful for diagnosis of thyroid disease. High TSH indicates hypothyroidism and low levels of TSH indicate hyperthyroidism
Thyroid disease
-hyperthyroidism - system speeds up
-hypothyroidism -slows down
Hyperthyroidism- Clinical features
-weight loss
-heat intolerance
-thin skin
-cardiovascular- increase heart rate, atrial fib, arrhythmia
-irritable, restless
-diarrhea
-potentiates catecholamines and growth hormones
poorly controlled hyperthyroid patient
-is tachycardic and may well be in atrial fibrillation with an irregularly irregular pulse.
-fine tremor is sometimes noted and the patient may have exopthalmos with resultant diplopia. They thyroid gland itself can be enlarged
Causes of hyperthryoidism
-Graves disease
-functioning Adenoma ("hot nodule") & Toxic Multinodular Goiter (TMNG)
-excessive intake of thyroid hormones
-abnormal secretion of TSH
-thyroiditis (inflammation of the thyroid gland)
-excessive iodine intake
Graves disease
-exopthalmos and vitilligo (irregular white patches on skin)
-widened palpebral fissure, periorbital edema, proptosis, chemosis, and conjunctival infection
-pachydermia (thickening of skin)
-"pretibial myxedema" present on feets and hands, of a patient with graves disease and exopthalmos
-plummer's nails changes thinning of nail and erosion of hyponychium
Goiter
-this is a lump in the neck comprising an enlarged thyroid gland, usually due to hyperplasia caused by stimulation of TSH, secondary to a decreased level of circulating thyroid hormone
-a goiter may lead to difficulty in swallowing or even compromise the airway
-thyroid tissue may occasionally be present within the tongue- the so-called "lingual thyroid"
-all goiters should be fully investigated, particularly to exclude cancers
Thyroid cancer
-most-good prognosis
-derived from follicular cells
-presentation- enlarged thyroid may be fixed and painful, cervical nodes
-DX-family Hx. Dysphagia, hemopytsis, SOB
-test-thyroid fcn, fna biopsy, thyroid scan
-Tx-radiation surgery
Exposure to dental x-rays
-was significantly associated with an increased risk of thyroid cancer
-2x more probability of getting thyroid cancer
Dental Management
-eval thyroid as part of head and neck exam
-look for surgical scars in anterior neck
-posterior dorsal region of tongue look for nodules that could represent lingual thyroid tissue
-palpate area superior and lateral to thyroid cartilage for presence of pyramidal lobe
-have patient swallow- gland will rise
-have patient protrude tongue- nodules in thyroglossal duct will move upward
Dental considerations -what to look for on exam
-enlarged gland (goiter) feels softer than normal gland
-adenomas and carcinomas- feel firmer and will probably e isolated swellings
-hashimoto's or Reidels thyroiditis- feels firm
-thyrotoxicosis or Graves disease- upon auscultation continuous or systolic bruit heard over the hyperactive gland because of engorgement of the glands vascular system
Oral complications Hyperthyroid
-osteoporosis of alveolar bone
-increased caries and periodontal disease
-premature loss of deciduous teeth with early eruption of permanent teeth (euthyroid infants of hyperthyroid moms may present with teeth at birth)
-lingual thyroid
Hyperthyroid medical problems that will impact your tx
-adverse rxn to chatacholamines- epinephrine
-cardiac arrhythmias
-congestive heart failure
-thyrooxic crisis-secondary to infection/surgical problems
Dental treatment- thyrotoxic patient
-thyrotoxic crisis: medical aid, wet packs/ice packs, hydrocortisone (100-300mg), IV glucose solution, CPR
-Good medical tx: tx all chronic infections, avoid acute infection, normal procedures
-poorly tx/untreated: avoid surgical procedures, acute infection, epinephrine, pressor amines (in local anes, gingival retraction cordds)
-Have Dx disease: check meds, signs, symptoms, thyroid test, hx of illness
Shift of thyroid disease
-patient with graves disease development of hypothyroidism
hypothyroid patient
-will often have a bradycardia, dry skin and hair and a goitre (from earlier hyperthyroidism)
hypothyroidism clinical findings
-decreased sweating
-thickened skin
-diffuse hair
-weight gain
-bradycardia
-marcrocytic anemia
-T4 uptake low
-radioiodine uptake low
-elevated TSH
-dementia
hypothyroidism
-affects 1.4% of female population
-.1% male
-congenital 1/4000 in US
-LABS, decreased T4, T3, increased TSH
hypothyroidism
-hashimotos thyroiditis
-iatrogenic-surgery
-congenital enzyme defects or thyroid agenesis, leads to cretinism
-hypothalmic or pituitary dysfunction
Cretanism
-myxedamatous cretins secondary to hypothyroidism
Myxedema
-torpid facies
-face is puffy, and eyelids are edeamtous
-skin is thick and dry
Inflammatory thyroid disorders hashimoto's thyroiditis
-autoimmune disorder
-goiter rubbery/firm
-early euthyroid then most develop hypothyroidism
Oral complications-hypothyroid
-adults-enlarged tongue
-infants with cretanism
-thick lips
-enlarged tongue
-delayed eruption of teeth
-malocclusion
Dental treatment hypothyroid patient
-recognize myedematous coma: medical aid, hydrocortisone-100-300mg, artificial respiration
-good medical tx: tx all chronic infections, avoid acute infection, normal procedures
-poorly tx/untreated: avoid surgical procedures, acute infection, cns depressants (narcotic/barbituate)
-have dx disease: check meds, signs, symptoms, thyroid tests, hx of illness
treatment of hypothyroid patients
-often treated with synthetic levothyroxin Na LT4 or liothroxine NA LT3
-If on T4
on-anticoagulants-increased PTT-bleeding
Diabetic- need less may become hyperglycemic
stress (cold, infections, trauma) can precipitate hypothyroid coma (high mortality rate)
-Tx IV T3, steroids, artificial resp
-Who-severely hypothyroid elderly
-Untreated hyperthyroid-sensitive to narcotics, barbituates, tranquilizers- use with caution
Hypothyroid medical problems impact your practice
exagerrated response to:
sedatives
narcotic analgesic
infection
surgical procedures
CNS depressants -myxedematous coma
Adrenal Glands
-located above kidneys
-
Adrenal cortex
-involved in production of numerous hormones in each of the three zones
-Aldosterone: mineralcorticoid (salt)
-Cortisol/corticosterone- glucocorticoids (metabolism)
-adrogen/estrogen(sex steroids)
Adrenal Medulla
-hormones released after preganglionic sympathetic fibers (Ach) following pain, excitement, anxiety, hypoglycemia, cold and hemorrhage
-with "stress" stimuli release adrenaline will be accompanied by renewed synthesis
actions of primary hormones determined by receptory type and site of action
-adrenaline causes vasoconstriction in skin and viscera and vasodilation in skeletal muscle, increases metabolic rate, stimulates glycogenolysis and mobilizes free fatty acids
-adrenal medulla is postganglionic sympathetic neurons without axons
-enzyme N-methyltransferase converts most of the noradrenaline to adrenaline, therefore 80% of hormones released are in this form, 20% as noradrenaline. Enzyme is specifically induced by cortisol from the cortex
Basic releasing elements
-Hypothalamus (CRF corticotrophin releasing factor)
-Pituitary ACTH
-adrenal cortex Cortisol
Steroid family hormones
-small lipid soluble molecules derived from cholesterol
-not stored, synthesised de novo on demand
-circulate bound to globulins and other plasma proteins
-bind intracellular receptors (cytosolic & nuclear)
-effects are slow (hours), depend on gene transcription, protein synthesis etc
How steroids work
-the hormone enters the cell by passing through the membrane easily.
-steroid hormone binds to a specific receptor molecule in the cytoplasm
-the hormone/receptor complex passes into the cell nucleus binds with DNA and activates gene trasncription process.
-the messenger RNA (mRNA) produced leaves the nucleus
-mRNA promotes synthesis of specific proteins/enzymes which then change the cell's activity.
Steroid Hormones
-steroid hormones exert long term effects on their target cells; they stimulate cell growth and differentiation and regulate the synthesis of specific proteins
How is the release of steroid hormones regulated
by nervous mechanisms
adrenaline- adrenal medulla
hypercortisolism
cushing's syndrome
excess cortisol produced
virilization
acquisition of male traits in a female because of excess testosterone prodcution
feminization
acquisition of female traits in male because of excess estrogen production
precocious puberty
puberty occurring too early because of excess sex steroids produced
hyperaldosteronism
conn's syndrome
excess aldosterone leading to hypertension and low potassium
adrenogenital syndrome
excess sex steroids produced
Adrenal gland entities
hypersecretion: cushings, hyperadrenal cortisism
hyposecretion: adrenal insufficiency , addisons disease (uncommon)
Who is on Systemic Corticosteroids? Perhaps people with
-adrenal insufficiency
rheumatic disorders-rhematoid arthritis
connective tissue disease-lupus
mucocutaneous disease-pemphigus, pemphigoid
respiratory disease-COPD
hematologic disease-thrombocytopenia, hemolytic anemia
GI disease- ulcerative colitis
patient on long term steroids
-moon face, buffalo hump (excess interscapular fat)
excess fat on trunk
puple skin striae
hirsutism
tendency to acne
hypertension
diabetic tendency
osteoporosis
peripheral muscle weakness
In a cushinoid patient
-tissues are wasted, leading to peripheral myopathy and thin skin which bruises easily
-purple striae on the skin (usually abdominal) also occurs
-water retention leads to the characteristic moon face with hypertension and oedema
-there is obesity of the trunk, head and neck (buffalo hump)
hypofunction (addison's disease)
-hyperpigmentation may be seen on palmar creases and buccal mucosa
-this pigmentation is related to high circulating levles of Melanocyte Stimulating Hormone (MSH)
Oral complications of Adrenal Insufficiency
-no treatment planning modifications
-primary adrenal insufficiency: pigmentation of oral mucous membranes
-secondary adrenal insufficiency
delayed healing
increased susceptability to infection
Guidelines for Dental Management
Patients on systemic steroids
-be alert and anticipate possibility of acute adrenal crisis
-good anesthesia
-good post op pain control
-monitor blood pressure
Patients on topical/inhaled steroids
-no supplementation required
Developing recommendations for corticosteroid supplementation
-studies show that of all of the dental procedures, only extraction was associated with rise in cortisol level
-supplementation recommended for patients undergoing surgery, extensive procedures, with extreme anxiety
-need good intra and post operative analgesia
-for pts currently on steroids- consult physician- usually double daily dose, if significant post op pain expected, double next days dose as well
-monitor blood pressure- hypotension may lead to adrenal crisis
First Trimester
-emergency care - NO elective treatment
-preventative therapy and oral hygiene (includes scaling)
Second Trimester
-emergency care
-routine dental treatment (continue with prevention and OHI)
-limit radiographs only for diagnosis and treatment
Third trimester
-emergency care
-continued routine care if warranted into early stage of third trimester
-continue with prevention and OHI
Cardiovascular
-increased hormonal activity induces sodium retention, which leads to increased total body water content and increased plasma volume by 30 to 40%
-15-20% increase in red blood cell volume
-dilution anemia causes decreased oxygen carrying capacity associated with increased blood volume
-increase in cardiac output to compensate for elevated blood volume and decreased oxygen carrying capacity
Cardiovascular Changes Affecting Dental Treatment
-supine hypotensive syndrome
-can occur in later stages of pregnany
-as a result of pressure of the fetus on the inferior vena cava and aorta
Respiratory
-entire respiratory tract becomes more edematous due to capillary engorgement making breathing difficult
-residual capacity decreases due to elevation of diaphragm by uterus
-hyperventilation can occur due to these changes
Respiratory changes affecting dental treatment
-minimize stress to help prevent hyperventilation
Endocrine
-Gestational Diabetes- affects about 5% of all pregnant women
-due to inadequate insulin production
-detected between 24th and 28th weeks of pregnancy
-pathophysiology as identical to type II diabetes
-pancreatic beta cell dysfunction unable to meet increased demands
Symptom of Gestational Diabetes
-no symptoms
-increased thirst
-increased urination
-increased hunger
-blurred vision
Who is at risk for Gestational Diabetes?
-gestational diabetes in previous pregnancy
-obesity
-strong family history of type II diabetes
-glucose detected in urine
-previous delivery of large baby
-mother was large baby herself
-high blood pressure
Diagnosis Gestational Diabetes
-test performed between 24th and 28th week
-high risk women are tested earlier
-random glucose tolerance test
-1hr or 2hr oral glucose tolerance test
-fasting blood glucose
-hemoglobin A1c
Gestational Diabetes affecting dental treatment
-hyper/hypoglycemia and oral complications
Oral complications as a result of gestational diabetes
-dental caries
-periodontal disease
-xerostomia
-fungal infections
-poor wound healing
Treatment of gestational diabetes
-goal of treatment is to reduce risk of complications for the mother and baby
-eating a balanced diet
-exercise
-good oral health
-insulin
After pregnancy and gestational diabetes
-increased risk for developing gestational diabetes in future pregnancies
-there is a 30-40% chance of developing type II diabetes within 5-10 years
-the baby is susceptible to childhood and adult obesity
-the child is also at increased risk for developing type II diabetes later in life
Oral changes in pregnancy
-pregnancy gingivitis
-pyogenic granuloma
-enamel erosion
Pregnancy gingivitis
-caused by an exaggerated response to plaque during pregnancy
-gingiva becomes erythematous and teeth can even become mobile due to changes in periodontal ligament
Pyogenic Granuloma
-exaggerated inflammatory response due to local irritants
-red spherical mass protruding from gingival margins
-often pedunculated with a broad granular tumor mass
-commonly appear in canine premolar region
-generally arises during second trimester
Diagnosis Gestational Diabetes
-test performed between 24th and 28th week
-high risk women are tested earlier
-random glucose tolerance test
-1hr or 2hr oral glucose tolerance test
-fasting blood glucose
-hemoglobin A1c
Enamel Erosion
-frequent nausia and vomiting is associated with morning sickness can erode enamel
-appears as cupped out depression on the lingual surfaces of anterior dentition
Gestational Diabetes affecting dental treatment
-hyper/hypoglycemia and oral complications
other considerations for treatment of pregnant patients
-medications when prescribing always consult with physician: local anesthetics, antibiotics, analgesics, sedative agents
-radiographs
-timing
-patient education
Oral complications as a result of gestational diabetes
-dental caries
-periodontal disease
-xerostomia
-fungal infections
-poor wound healing
Treatment of gestational diabetes
-goal of treatment is to reduce risk of complications for the mother and baby
-eating a balanced diet
-exercise
-good oral health
-insulin
After pregnancy and gestational diabetes
-increased risk for developing gestational diabetes in future pregnancies
-there is a 30-40% chance of developing type II diabetes within 5-10 years
-the baby is susceptible to childhood and adult obesity
-the child is also at increased risk for developing type II diabetes later in life
Oral changes in pregnancy
-pregnancy gingivitis
-pyogenic granuloma
-enamel erosion
Pregnancy gingivitis
-caused by an exaggerated response to plaque during pregnancy
-gingiva becomes erythematous and teeth can even become mobile due to changes in periodontal ligament
Pyogenic Granuloma
-exaggerated inflammatory response due to local irritants
-red spherical mass protruding from gingival margins
-often pedunculated with a broad granular tumor mass
-commonly appear in canine premolar region
-generally arises during second trimester
Enamel Erosion
-frequent nausia and vomiting is associated with morning sickness can erode enamel
-appears as cupped out depression on the lingual surfaces of anterior dentition
other considerations for treatment of pregnant patients
-medications when prescribing always consult with physician: local anesthetics, antibiotics, analgesics, sedative agents
-radiographs
-timing
-patient education
Safely based on FDA Classification system
-5 different categories from A-E
-each category differs with regards to drugs risk to fetus based on animal and/or human studies
-A is no risk
-E is highest risk-evidence of fetal abnormalities and fetal risk exist based on human experience and the risk outweighs any possible benefit of use during pregnancy
-important note this is currently under review with regards to drug safety in pregnant patients due to its limitations to convey risk and benefit accurately and consistently
Medication use in pregnant patients
-use meds only if the expected benfits (to mother) are greater than potential risks (fetus)
-try to avoid prescribing meds during the patient's first trimester
-prescribe drugs that have been used extensively by pregnant women, not new drugs that have not been tested in pregnant patients
-prescribe minimum dose required to obtain desired effect
-recognize that the absence of data does not imply safety
Local anesthetics
-all local anesthetics cross the placenta and therefore may be at risk to fetus
-lidocaine safe to use during pregnancy (as much as .1mg can be used safely)
-mepivacaine and arcaine-should be used with caution and consult with physician
-epinephrine stimulates the cardiovascular system with proper technique should not cause any problems (ASPIRATE!!)
Antibiotics
-penicillin, cephalosporins, metronidazole and clindamycin are safe to use
-tetracycline (category D)-chelate with calcium discoloring teeth during development and inhibit bone growth - SHOULD NOT BE USED DURING PREGNANCY
Analgesics
-acetaminophen is the main pain reliever of choice in pregnant patients
-using any analgesic with a narcotic derivative is contraindicated due to respiratory depresion and may be associated with defects such as cleft lip and cardiac defects
-ibuprofen and fluriprofen. fluriprofen should be used with caution in the 2nd trimester and there could be a risk of delayed labor
Sedative agents
-any CNS depressants are contraindicated during pregnancy
-diazepam may be associated with clefts with prolonged exposure
-prolonged exposure to nitrous oxide has been associated with spontaneous abortions and reduced fertility
-non-pharmacological methods should be used to reduce anxiety
Recommended guidelines for NO2 use on pregnant patients
-minimize to 30 min
-at least 50% oxygen should be delivered to ensure adequate oxygenation at all times
-appropriate oxygenation at termination of nitrous
-repeated and prolonged exposure should be prevented
-2nd and 3rd trimesters are the safer periods for nitrous tx because organogenesis occurs during the first trimester
Radiographs
1RAD = 1 cGy (centigray)
-animal and human studies support that there is no gross congenital abnormalities or growth retardation at exposures less than 5-10cGy
-natural background radiation is .008cGy
-pan dose is .00015cGy
-full mouth series is .00001cGy
with fast exposure techniques, proper shielding, fitration and collimation these doses are of minimal risk to the fetus
Patient education
-inform patient of normal changes during pregnancy i.e. pregnancy gingivitis, pyogenic granuloma
-promote preventative care
-stress minimal risk to fetus if emergency develops
conclusion on pregnancy
-dental tx is safe for healthy pregnant patients and patients with gestational diabetes
-most of the meds prescribed by dentistis are not harmful to mother or fetus
-tx should be completed in 2nd trimester unless emergent
-apts should be kept short particularly in the 3rd trimester (minimize risk of supine hypotension)
-educate patient importance of good plaque control and fluoride use
CV facts
-2005: 80,7000,000 people in US have one or more forms of CVD
-Coronary heart disease 16,000,000
-MI 8,100,000
Angina pectoris 9,100,000
Hypertension 73,000,000
heart failure- 5,300,000
20 million americans are dental phobics
25% of population fears the dentist enough they avoid needed care
-dentist is stressful
Cardiovascular mortality
-869,724 deaths in 2004
-36.3 percent of all deaths or 1 or every 2.8 deaths
-higher than cancer, accidents or HIV
-over 148,000 americans killed by CVD in 2004 were under age 65
Ischemic Heart Disease Epidemiology
-causes more deaths and disability than any other disease in the developed world
-Most common serious, chronic, life-threatening disease in the US
-12 million people with IHD
->6 million with angina
>7 million sustained MI
Angina Pectoris
-chest discomfort described as "heaviness" "squeezing" "pressure" "crushing"
-duration usually 2-5 minutes
-patient will often localize by placing clenched fist over sternum (levine's sign)
-radiates most freqeuntly to left arm (ulnar surface of forearm)
-also radiates to back, intrascapular region, mandible and teeth, rarely above mandible or below unbilicus
-crescendo/decrescendo (get worse and better in the 2-5 min)
Classifications of Angina
-Stable angina: chest pain exacerbated by exertion and alleviated by rest
-Unstable angina: resting chest pain
-Prinzmetal's Angina: resting chest pain caused by focal coronary spasm
Class I angina
ordinary physical activity does not cause angina such as walking or climbing stairs.
Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation
Class II angina
slight limitation of ordinary activity
angina occurs on walking or climbing stairs rapidly; walking uphill' walking or stair climbing after meals; in cold or under emotional stress. Angina occurs on walking >2 level blocks and climbing >1 flight of stairs under normal conditions.
Class III angina
marked limitations of ordinary physical activity
angina occurs on walking 1 or 2 level blocks and climibing 1 flight of stairs under normal conditions
Class IV angina
inability to carry on any physical activity without dscomfort- anginal symptoms may be present at rest
Normal Cardiac vessel function
large epicardial vessels-conductance
-intramyocardial arterioles- resistance
(autoregulation-adjusts supply to meet demand)
Pathophys of Angina
Atherosclerosis: narrowing of conductance vessels by intraluminal plaque formation
Vasospasm: abnormal constriction of conductance vessels (Prinzmetal's angina)
Abnormal constriction or failure of dilation of resistance vessels (microvascular angina)
Atherosclerosis Major risk factors
diabetes melitus
smoking
hypertension
high fat diet (high LDL and low HDL)
-these all disturb normal functions of vascular endothelium
what are normal functions of vascular endothelium?
-local control of vascular tone
-maintenance of anticoagulant surface
-defense against inflammatory cells
Atherosclerosis causes vascular endothelium damage
-inappropriate constriction of coronary vessels: reduced supply to distal vasculature
-luminal clot formation: decreased flow distal to obstruction
-abnormal interactions with blood monocytes and platelets: subintimal clot/plaque gets bigger and more organized
Respiratory Structure and Function
-upper airways
-trachea, bronchi, bronchioles
-alveolar region: for gas exchange
-lymphatics: important in cancer
Trachea
-16-20 U shaped hyaline cartilages
-Begins at C6 level and ends at T4 level with bifurcation (carina)
-Right main bronchus is shorter, wider and turns at a shallower angle than left,important because foreign bodies are more likely to be in right bronchus
-Divides into 3 lobar bronchi (upper, middle, lower) and then into 10 segmental bronchi
-left main bronchus branches into two lobar bronchi (upper and lower) and then into 8-10 segments
Pleura
-serous membrane that envelops the lung and lines the thoracic cavity
- Pleura damage can allow for air to get into the membrane around the lunch and cause pneumothroax which will make the patient short of breath and cause cardiac arrhythmias
-pleuritis: visceral vs parietal
-Damage to pleura can cause spontaneous, open or tension pneumothorax
Types of pleura
-visceral Pleura
-Parietal pleura (costal, mediastinal, diaphragmatic, cervical)
-Pleural recesses (costodiaphragmatic and costomediastinal)
Tension Pneumothorax
-left lung gets moved completely to the right side
Major Manifestations of pulmonary disease
-Cough: with and without sputum, sign of irritation
-Shortness of breath
-chest pain
-hemoptysis
-Nitrous is contraindicated for spontaneous pneumothorax
Pulmonary function tests
-objective measurement of lung function
-spirometric examination
- Forced expiratory volume at 1 second (FEV1) and Functional residual capacity (FRC) are important
-albuterol a beta agonist may improve functions of some pts
Spirometry
-measures the amount and rate of air a person breathes in order to diagnose illness or determine progress in treatment
-Nose is pinched closed, blow in to a tube for 10 minutes
Oxygen saturation
-measured by pulse oximiter shines light through the nail bed
-measures the amount of oxygenated hemoglobin
-Below 90 the slope increases, little changes in the saturation of hemoglobin are big changes in oxygen partial pressure (PaO2)
-below 30 PO2 the monitor is extremely unreliable
-measurement may be affected by cold fingers, movement or nail polish
Spontaneous pneumothorax
-"lung dropped"
Disorders of ventilation: Obstructive
-limitation of expiratory flow
-reduced FEV1
-COPD
-Bronchitis
-Emphysema
-Asthma
-Difficult to get air out
Disorders of ventilation: Restrictive
-much less common
-cant get air in or out
-most involve fibrosis: lungs are sclerotic and cant get the air out
-fibrosis alveolar septa
-Low total lung capacity (TLC)
-decreased vital capacity
-difficult inhaling
-elevated Residual volume (RV)
Bronchiectasis
- abnormal permanent dilation of airways secondary to chronic infection
-Kartagner syndrome and CF
-COPD
Bronchitis
-excessive mucous production with cough
-COPD
Emphysema
-distention distal air spaces
-like a baggy balloon that keeps residual volume of unfunctional air
-COPD
Chronic obstructive pulmonary disease
-usually secondary to smoking or alpha 1 antitrypsin deficiency (problem with surfactant)
-bronchiectasis, bronchitis, emphysema
Chronic Bronchitis
-inspiration and expiration obstruction
- thickened bronchial walls
-inflammatory cell infiltrate: steroids can relieve this
-goblet cell hyperplasia
-obstruction secondary to narrowing and plugging
-similar to asthma
COPD Emphysema
-dyspnea and hypercarbia (increased carbon dioxide)
-destruction of alveolar walls, collapsed sacs
-enlarged terminal air spaces
-obstruction on expiration mostly
-increased RV, decreased FEV1
COPD Clinical Features
-chronic cough, exertional dyspnea
-elevated pCO2, decreased pO2, elevated HCT
-reduced max expiratory flow rate, FEV1 less than 70%, TLC for bronchitis is normal, while emphysema is increased, RV is increased for emphysema
-flattening of diaphragm instead of normal dome shape
-hematocrit is increased because body is trying to compensate
Medical Tx COPD
-bronchodilators: beta agonist relaxes smooth muscles
- lifestyle changes by quitting tobacco use, increasing exercise and better nutrition
-oral or inhaled steroids, and antiinflammatories
-low flow oxygen, goal SaO2 90%
What you need to ask COPD pts
-ROS: SOB, cough, URI, ox staturation
-PSH: type of anesthesia, recovery
-PMH: co-morbidities with cardiac
Dental issues with COPD pts
-avoid supine position
- need to know meds pt is taking
-local anesthetic is ok but nitrous oxide can accumulate
-care taken with sedatives
-look for oral cancer due to steroids which lower immune response
-may have to give oxygen
Asthma (reactive airway disease)
-incidence is 12-15 million americans
- unknown etiology
-triggers: infection, allergens, exercise, weather, and emotions
-variants: wheeze, shortness of breath, coughing
-obstruction, smooth muscles spasm, inflammation, mucous hyper secretion, sputum plugging
-cough, wheeze, shortness of breath, chest tightness, tachypnea, rhonchi (coarse breathing sounds) , decreased breath sounds
Mediators in Acute asthmatic response
-acetlycholine
-adeonsine
-histamine
-kinins
-leukotrienes
-neuropeptides
-nitric oxide
-Platelet activating factor
Radiographic findings of asthma
-often normal
-hyperinflation
-depression diaphragm
-pneumothorax
Severity of Asthma
-find out what meds and how often
-ask about hospitalizations
-ask about FEV1 (decreased amount of air getting out)
-Obstructive or restrictive disease
-
Mild-Intermittant Asthma
-daytime <2 times per week
-nighttime < 2 times per month
-brief exacerbations
-asymptomatic between exacerbations
-intensity of exacerbations varies
- PEF variability < 20%
FEV1>80%, PEF >80%
Mild-Persistent Asthma
-daytime >2 per week but < 1 time per day
-nighttime >2 times per month
-exacerbations may affect activity
-PEF variability range of 20-30%
- FEV1 >80%
-PEF>80%
Moderate Persistent Asthma
- daytime symptoms daily
-nighttime symptoms >1 time per week
-exacerbations affect activity
-exacerbations >2 times per week
-exacerbations last days
-daily use of inhaled short acting beta agonists
-PEV variability >30%
-FEV1>60% but <80%
-PEF>60% but <80%
Severe Persistent Asthma
-Daytime symptoms continual
-nighttime symptoms frequent
-symptoms limit physical activity
-exacerbations frequent
-PEF variability >30%
-FEV1< 60%
-PEF<60%
Intraluminal subintimal plaque formation
-when plaque occludes 75% of lumen there is a significant decrease in ability to meet increased myocardial demand caused by stress
-when >80% is occluded blood flow at rest is severely impaired and ischemia can occur
Ischemia
lack of oxygen due to inadequate perfusion of the myocardium which causes an imbalance between oxygen supply and demand
-aterosclerosis of epicardial coronary arteries is most common cause
Medical Management of IHD
-Risk reduction
-stop smoking: increase O2 demand, accelerated thrombosis development
-treat diabetes
-treat dyslipidemia: excercise, eat right and lose weight
-lose weight
obesity contributes to all of the above
Drug therapy for IHD
-Nitrates
-causes systemic venodilation reduced myocardial wall tension and O2 requirements
-absorption is most rapid through mucous membranes (sublingual tablet/spray)
-deteriorates with exposure to air and sunlight (why its in brown vial)
-prophylactic use prior to stress has been suggested
-dose: .4mg sublingual every 5 minutes (max 3 doses) until relief of symptoms
Beta Blockers
-reduce myocardial oxygen demand by inhibiting increases in heart rate, arterial pressure and myocardial contractility
-reduce mortality and reinfarction in patients with prior myocardial infarction
-ex: atenolol metoprolol, esmolol, labetolol
Calcium Channel Blockers
-coronary vasodilators that produce variable and dose-dependant reductions in myocardial oxygen demand, contractility and arterial pressure
-indicated when B blockers are contraindicated
-nifediine, verapamil, diltiazem
Antiplatelet drugs
-Aspirin: interferes with platelet activation by inhibiting platelet cyclooxygenase activity
-75-324 mg daily dose
-Clopidogrel (Plavix)
-blocks ADP receptor mediated platelet aggregation
-75 mg daily dose
-both these drugs improve coronary outcomes when given to patients 1 year after an episode of unstable angina
-both carry risk of bleeding
Coronary revascularization
-Percutaneous Coronary intervention:
-widely employed for patients with symptoms or evidence of ischemia due to stenosis of 1 or 2 vessels
-effective for more than 1/2 of patients requiring revascularization
-Coronary Artery Bypass Grafting
-for patients with stenosis of 2 or 3 vessels that are not effectively treated with med management
Hypertension
-43 million people estimated to have it defined by BP of 140/90
-risk of congestive heart failure 2-3 times higher in men and 3 times higher in women
-significantly increased risk of stroke
2.3-6.9 times risk higher for coronary heart disease
Prehypertensive
-Normal <130/85
-High-normal 130-139/85-89
Hypertension
Stage 1: 140-159/90-99
Stage 2: 160-179/100-109
Stage 3: >/=180/110
Hypertension treatment
- lose weight
-limit alcohol intake
-increase aerobic activity
-reduce sodium intake
-maintain adequate intake of dietary potassium
-maintain adequate intake of calcium and magnesium
-stop smoking and reduce intake of dietary saturated fat an cholesterol for overall cardiovascular health
Hypertension med tx
-ACE inhibitors
-Beta Blockers
-Diuretics
Acute MI
-a clinical syndrome that results form an injury to myocardial tissue that is caused by an imbalance between myocardial oxygen supply and demand
-myocyte death is generally confluent
-1.1 million people experience MI
-6 million are admitted to the hospital for consieration of the diagnosis
-460,000 people succub to coronary artery related deaths
MI pathophys
-coronary atherosclerosis is the prime instigator
-plaque rupture with subsequent thrombosis
-cardiac work exceeds the ability of the narrowed coronary artery to supply nutritive perfusion
Atypical presntations of MI
-diabetics- abdominal pain that mimics pain associated with gallstones
-elderly patients- heart failure will be predominant symptom
-by age 85 only 40% of patients will complain of chest discomfort
Medical Management of Asthma
-Inhalers: steroids and beta agonists
-oral steroids
-nebulizers
-antiinflammatories
- leukotriene modifiers: Singulair
Dental Management of Asthmatics
-avoid supine
-use inhaler, and have patient bring inhaler to appointments
-Avoid ASA and NSAIDS
-Prevent unnecessary odors and stress
-may want to use sedation dentistry if patient is anxious
-albuterol, or ep .3-.5 cc 1: 1000sc, oxygen
Pneumonia
-infectious lung issue
-bacterial/viral/fungal
-locations of lesions
-extent
Pulmonary infections
-acute bacterial pneumonia: bronchopneumonia, lobar pneumonia
-atypical pneumonia
-lung abscess
-fungal infections
-TB
Tuberculosis
-cough with thick bloody mucous
-fatigue, wt loss
-short breath
-night sweats
-tx with multidrug regimen
-pt with active TB you do not treat!
TB Dental Issues
-infection issues from airborne droplets, related to number organisms and host defenses
-Isoniazid and rifampin have drug interactions
-isoniazid interacts with acetaminophen
-Rifampin interacts with valium, biaxin, diflucan, bleeding issues
-universal precautions, active consult with MD
-Oral lesions seen on tongue
Restrictive Lung Disease
-decreased vital capacity lung
-scleroderma
-sarcoidosis
-idopathic pulmonary fibrosis
-short of breath, could have spontaneous pneumothorax
-treated with steroids
Pulmonary Fibrosis
-insidious onset breathlessness, restrictive impairment
-spontaneous pneumothorax
-tx with steroids
-mean survival 5-7 years
Sarcoidosis
-multisystem granulomatous disease
-B hilar adenopathy
-20-40, any organ system, restrictive pulmonary disease,dyspnea on exertion, cough and wheezing
-tx with steroids, 80% total remission 3 years
Pulmonary manifestations of systemic rheumatic disorders
-rheumatoid arthritis
-SLE
-Scleroderma
-sjogrens syndrome
-ankylosing spndylitis
Immediate management of MI
MONA
-M: Morphine pain control
-O: oxygen
-N: Nitroglycerine .4 mg sublingual every 5 minutes x 3
-A: asipriin antiplatelet effects and facilitates fibrinolysis platelet effects occur within 20 min
Congestive Heart Failure
-clinical syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate commensurate with the requirements of the metabolizing tissues
-basically it is just what the name implies- failure of the central pump
-leads to peripheral edema because of increased sodium retention
Heart failure epidemiology
-only cardiovascular condition that is increasing in prevalence in North America and Europe
-responsible for 1 million hospital admissions and 200,000 deaths annually
-most common in elderly therefore numbers are expected to continue to rise as life expectancy increases
-IHD responsible for 75% of all cases
Signs of Heart failure
-peripheral edema
-jugular distension - visualized 4cm above sternal angle rises with inspiration (kussmaul's sign)
-shortness of breath (dyspnea) earliest and most frequent symptom
-fatigue and weakenss particularly in the limbs
nocturia and oliguria
-cerebral symptoms
Medical tx of Heart failure
-Diuretics
thiazides act at proximal convoluted portion of renal tubule
loop diuretics inhibit active reabsorption of chlride in the medullary and cortical portion of the lop of henle (if severe)
-pottasium sparing diuretics (spironolactone) act at distal renal tubule
-ACe inhibitors
-Beta Blockers
-Inotropic agents:
-digitalis glycosides (digoxin)
-implantabe cardioverter defibrillators
-coronary revascularization
-implantable ventricular assist device
Dental Considerations for Heart failure
-patient positioning: may be unable to lie supine due to dyspnea, fluid shift from lower extremities
-medical optimization- communicate with patient physician know med
-administer supplemental oxygen
-anxiety reduction protocol
Primary Dermatologic lesions
macule, papule, nodule, wheal, vesicle, pustule, tumor
Macule
-a flat change in color
-not palpable
-macule larger than one centimeter in diameter is called an area
Example: vitiligo
Papule
-an elevated lesion
-a papule larger than .5 centimeter is called a plaque
-top of papule may be round, flat, pointed verrucous or umbilicated
example: xanthelasma
Nodule
- a raised lesion caused by a thickening of induration beneath the surface of the tissue
-example: erythema nodosum
Wheal
- a plaque in which edema of the dermis distends the epidermis. "orange peel" appearance is caused by hair follicles holding the epidermis down
example: uticaria (hives)
Vesicle (blister)
-fluid filled lesion less than .5cm in diameter
-a vesicle larger than .5cm in diameter is called a bulla
-blisters may be tense or flaccid
-blisters may be intraepidermal or subepidermal
examples: pemphigus, pemphigoid
Pustule
- a superficial collection of pus
-vesicles may evolve into pustules
example: acne vulgaris
Tumor
- a large solid growth
-the term tumor does not conote malignancy
examples: fibroma, papilloma
secondary dermatologic lesions
-scale
-crust
-excoriation
-fissure
-ulcer
-scar
Scale
-desquamating keratin
-may be described as fine, coarse, adherent or loose
example: lichen planus
Crust
-dried residue of an exudation, such as serum, pus or blood
-lay term is scab
-crust and eschar are different- eschar impllies necrosis
example: erythema multiforme
excoriation
-a linear or dug out area
-usually self inflicted
example: factitial ulcer
Fissure
- a crack in the skin extending into the dermis
-usually begins in non-viable, dehydrated, thickened stratum corneum
-often painful
Ulcer
- a loss of the pidermis and part or all of the dermis
-can heal with scarring
-an erosion is loss of the epidermis only and usually does not bleed or scar
example: diabetic ulcer
Scar
-fibrotic replacement following destruction of the skin
-may be characterized as elevated, depressed, firm or pliable
examples: acne scars, keloids
Importance of evaluating facial lesions
-orginal character of lesions, how they have changed with time
-malignant lesions typically change with time
-complexion, occupation and hobbies
-cumulative sun exposure correlates to risk
-past history of skin lesions
-past history of skin cancer correlates with future risk
Benign and Premalignant lesions
-seborrheic keratosis (senile keratosis)
-nevi (moles)
-actinic keratosis
-actinic cheilitis
Seborrheic Keratosis
-not due to sun exposure
-common on mature skin
-aymptomatic and slow growing
-begin as slightly pigmented macules then yellow to brownish-black warty plaques which appear to be "stucK" onto the skin
-surface has "greasy" appearing scale
-lesion may be flat to pedunculated
-lesions may be smooth or rough surfaced
-no malignant potential
Other assorted pulmonary issues
-pulmonary embolus
-pulmonary neoplasms
-drug induced
-genetic
-occupational
Pulmonary embolus
-pathogenesis
-increased incidence with age
-increased ventilation with no increase in O2, ventilation profuse scan, spiral CT
-tx with anticoagulants
Pulmonary Neoplasms
-28% all cancer deaths, leading cause of cancer deaths
-incidence second to breast cancer for women and prostate cancer in men
-almost 90% of lung tumors are related to smoking
-most are malignant
-central tumors are more common than peripheral
-metastases to lungs are more common than primary lung tumors
-primary lung tumors: SCC, adenocarcinomas, small cell lung carcinomas, mesothelioma
Pulmonary Neoplasm Symptoms
--causes productive cough, hemoptysis, wheezing, dyspnea, chest pain, recurrent infections
-systemic symptoms: weight loss, weakness, anorexia, pleural effusions
Paraneoplastic syndromes
-Cushing syndrome
-syndrome of Inappropriate Antidiuretic hormone release (SIADH)
-increase secretion of parathyroid hormone
-carcinoid syndromes
Lung transplant pts
-initial disease
-current medications
-medical issues
-dental issues
Drug induced interstitial lung disease
-antibiotics
-anti-inflammatory
-cardiovascular
-antineoplastic
-CNS drugs
-oral hypoglycemic
-illicit drugs
-opiates
-radiation
Cystic Fibrosis
-autosomal recessive, 1:2000 whites. 1:20 carriers
-abnormal eccrine and exocrine function, viscous secretions, insufficient pancreatic function
-lifespan is 30's or more
-frequent dental infections
-abnormal sweat glands, pancreas dysfunction, decreasing lung fx
-poor oxygenation, pulmonary HTN, obstruction of small airways
-bacterial infections, PTX, respiratory failure
Cystic Fibrosis Tx
-chest pt
-bronchodilators
-nutrition
-exercise improves cardio respiratory fitness not pulmonary function
-gene therapy
Occupational disorders
-asbestos
-coal dust
-cobalt
-silica
-talc
-parenchymal lung disease, no effective tx only support
Etiologies of facial cancer
-genetic familial
-melanin, pigmentation
-chemical, industrial
-electromagnetic radiation
-reduced immunity
-ultraviolet solar radiation
Ultraviolet radiation: sunlight
UVA tanning rays immunosupressive rays
UVB burning cancer rays
UVC bacteriocidal rays
Sun damage and facial cancers
-almost all of the premalignant lesions and facial cancers (including lips) ocur on skin already damaged by the sun
-therefore the dentist needs to pay attention to a history of sun exposure (and previous diagnosed lesions) then focus the examination of sun-damaged areas of the face and lips
Characteristics of Sun damage
-solar elastosis- coarsening and yellowing of skin
-rough, scaly and dry skin
-wrinkling- coarse and deep; rhytids around eyes and lips
-cutis rhomboidalis nuchae- deep skin lines on back of neck
-poikiloderma- atrophy, telangectasia and altered pigmentation
-venous lakes
-telangetasias
-senile or actinic purpura- macular bruising
-hyper and hypo-pigmentation
-stellate white scars
premalignant lesions
-actinic keratosis
-actinic chelitis
Actinic Keratosis
-seen on the sun damaged face due to prlonged UVB exposure
-may be only a palpable roughness
-no dermal component
-appear as multiple, pin-head sized to several cms reddish brown illdefined macules or papules
-dry adherent scale is characteristic
-when scale is picked, get a bleeding point
-induration may develop, as well as a cutaneous horn
-15% or less of actinic keratoses progress ot SCC if untreated
-even with malignant transformation metastatic potential is low
-immunosupressed patients renal transplant patients are the exceptions
Actinic Chelitis
-due to sun-damage of lips
-lower lip more commonly
- may be erythematous
-surface rough and or eroded and or scaly
-may crust and heal
- no dermal component
-ulceration or dermal component requires biopsy
Malignant lesions
-basal cell
-SCC
-melanoma
Basal Cell carcinoma
-most common neoplasma affecting light skinned persons
-ultraviolent radiation is primary cause
-rarely metastasizes, but locally destructive of tissues
-early detection and treatment to avoid cosmetic deformity and increased morbidity
Classical appearance basal cell
-appears as a nodule with pearly translucent surface and raised, rolled borders
-often telangectasias coursing up its sides
-mature lesion is unbilicated with central crusting
-bleeding is the most common presenting complaint
Nevoid basal cell carcinoma syndrome
-gorlins syndrome
-autosomial dominant
-BCC at an early age, jaw cysts, palmar-plantar pits, calcification of the falx cerebri
-bony abnormalities, defective dentition, characterisitc facies, ovarian/uterine fibromas, medulloblastoma
SCC
-arise from chronic radiation expsure, can be from viral transformation
-most SCCs arising on sun damaged skin have a low metastatic potention (2%)
-higher risk for metastasis found with sites of prior xray therapy (25%) , lower lip and temple, immunocompromised patients
SCC findings
-may be difficult to distinguish from severe actinic keratosis
-tactile sensation is one of being scaly and rough
-classically, starts as a "rough" area, then nodular which expands into a raised, lesion with a necrotic ulcerated center on an inflamed base
-indurated base is common
-crusting and attempts at "healing" common
Keratoacanthoma
-benign, self limiting lesion
-etiology unknown b ut viral and inflammatory?
-most common on face
-usually regresses, may leave scar
-appears similar to SCC and BCC and therefore NEEDS BIOPSY
Malignant Melanoma
-may evolve from lentigo maligna; appear as a superficial spreading lesion; or begin in a vertical growth phase as a nodular melanoma
-depth of invasion correlates with prognosis
-most common on loewr legs in females and on the backs of males
-classically lesions show: Assymetry, border irrgularity, colory variatio nand a diameter greater than 6mm = ABCDs of melanoma
Dental Team and Dermatology
-skin cancer is 18x more prevalent than oral cancer
-facial cancers including lips much more common tan intra oral cancers
-early recognition can prevent or minimize cosmetic disfiguration, morbidity, and mortality
-
Primay dermatologic lesions
-macule
-papule
-nodule
-wheal
-vesicle
-pustule
-tumor
Macule
-a flat change in color
-not palpable
-macule larger than 1cm in diameter is called an area
Papule
-an elevated lesion
-papule larger than .5cm is called a plaque
-top of papule may be round, flat, pointedd, verrucous or umbilicated
Nodule
-raised lesion caused by thickening or induration beneath the surface of the tissue
-not originating from superficial epithelium
Wheal
-plaque in which edema of the dermis distends the epidermis.
-Orange peel appearance is cause by hair follicles holding the epidermis down
-raised area, fluid component
-aka Hives
Vesicle
-aka blister
-fluid filled lesion less than .5cm in diameter
-vesicle larger than .5cm in diameter is called a bulla
-blisters may be tense or flaccid
-blisters may be intraepidermal or subepidermal
Pustule
-superficial collection of pus
-vesicles may evolve into pustules
Tumor
-large solid growth
-does not indicate malignancy, can be benign
Fibroma
-growth of CT
-smooth surface
Papilloma
-overgrowth of superficial epithelial layer
-irregular surface
Secondary dermatologic lesions
-scale
-crust
-excoriation
-fissure
-ulcer
-scar
Scale
-desquamating keratin
-may be described as fine, coarse, adherent or loose
Crust
-dried residue of exudation such as serum, pus or blood
-lay term is scab
-cust and eschar are different
-eschar implies necrosis
Excoriation
-linear or dug out area
-usually self inflicted
Fissure
-crack in the skin extending into the dermis
-usually begins in non-viable, dehydrated thickened stratum corneum
-often painful
Ulcer
-loss of epidermis and part or all of the dermis, into CT
-can heal with scarring
-an erosion is loss of the epidermis only and usually does not bleed or scar
Scar
-fibrotic replacement following destruction of skin
-may be characterized as elevated, depressed, firm or pliable
Evaluating lesions
-malignant lesion typically change with time
-cumulative sun exposure correlates to risk
-past history of skin cancer correlates with future risk
-fair skinned individuals are more at risk
Benign and Premalignant lesions
-seborrheic keratosis (senile keratosis)
-Nevi (moles)
-actinic keratosis
-actinic cheilitis
Seborrheic Keratosis
-not due to sun exposure
-common on mature skin
-asymptomatic and slow growing
-begin as slightly pigmented macules then yellow to brownish-black warty plaques which appear to be stuck on skin
-surface has greasy appearing scale
-lesions may be flat to pedunculated
-lesions may be smooth or rough surfaced
-no malignant potential
Nevi(Moles)
-melanocytes are being stimulated, melanin stays in localized tissue areas
-chronic
-collection of melanocytes
-can be clusters, compound, raised, smooth surface or dome shaped
-if not sure if it is changing then it is best to refer
Etiologies of Facial Cancer
-genetic, familial
-melanin, pigmentation
-chemical, industrial
-electromagnetic radiation
-reduced immunity
-UV radiation
UV Radiation: Sunlight
-UVA (3200-4000A)- tanning rays, immunosuppressive rays
-UVB (2900-3200A): burning, cancer rays
-UVC (200-2900A): bacteriocidal rays
Sun Damage and Facial Cancers
-almost all of the premalignant lesions and facial cancers (including lips) occur on skin already damaged by sun
-pay attention to history of sun exposure or previously diagnosed lesions, focus examination on sun-damaged areas of face and lips
Characteristics of Sun damage
-skin damage due to sun damage are different than those due to aging
- solar elastosis, rough scaly and dry skin, wrinkling, cutis rhomboidalis nuchae, pokiloderma, venous lakes, telangesctasia, senile or actinic purpura, hyper and hypo pigmentation, stellate white scars
Solar elastosis
-coarsening and yellowing of skin
Cutis Rhomboidalis Nuchae
-deep skin lines on back of neck
Pokiloderma
-atrophy, telangiectasia and altered pigmentation
Senile or actinic purpura
-macular bruising
-common in hands and arms
Actinic Keratosis
-seen on sun-damaged face due to prolonged UVB exposure
-may be only a palpable roughness
-no dermal component
-appears as multiple pin head sized to several cms; reddish brown ill defined macules or papuls
-dry adherent scale is characteristic
-when scale is picked, get a bleeding point
-induration may develop as well as a cutaneous horn
-check base for carcinoma
-15% or less progress to SCC if untreated
-even with malignant transformation metastatic potential is low
-immunosuppressed pts are exceptions
Actinic Cheilitis
-due to sun-damage of lips
-lower lip more commonly
-areas may be erythematous
-surface rough and/or eroded and/or scaly
-hyperplastic areas will be lighter in color
-may crust and heal
-no dermal component
-ulceration or dermal component requires biopsy
Malignant lesions
-basal cell carcinoma
-squamous cell carcinoma
-melanoma
Basal Cell Carcinoma
-most common neoplasm affecting light skinned persons
-UV radiation is primary cause
-rarely metastasizes but locally destructive of tissues
-early detection and tx to avoid cosmetic deformity and increased morbidity
-
Classical Basal Cell Carcinoma
-appears as a nodule with pearly translucent surface and raised, rolled borders
-often telangiectasis coursing up its sides
-mature lesion is umbilicated with central crusting
-bleeding is most common presenting complaint
Nevoid Basal Cell Carcinoma (Gorlin's Syndrome)
-autosomal dominant with multiple findings
-BCC's at an early age, jaw cysts, palmar-plantar pits, calcification of flax cerebri
-bony abnormalities, defective dentition, characteristic facies, ovarian/uterine fibromas, medulloblastoma
Squamous Cell Carcinoma
-arise from chronic radiation exposure or can be from viral transformation
-Most SCC's arising on sun damaged skin have a low metastatic potential (2%)
-higher risk for metastasis found with: sites of prior xray therapy (25%), lower lip and temple, immunocompromised patients
-may be difficult to distinguish from severe actinic keratosis
-tactile sensation of scaly and rough
-starts as rough area then nodular which expands into a raised lesion with a necrotic ulcerated center on an inflamed base
-indurated base is common
-crusting and attempts at healing are common
Keratoacanthoma
-benign, self-limiting lesion
-etiology unknown possibly viral or inflammatory
-most common on face
-usually regresses and may leave a scar
-appears similar to SCC and BCC and should be biopsied
Malignant Melanoma
-may evolve from lentigo maligna, appear as a superficial spreading lesion or begin in a vertical growth phase as a nodular melanoma
-depth of invasion correlates with prognosis
-most common on lower legs of females and backs of males
-classical lesions have asymmetry, border irregularity, color variation, diameter greater than 6mm
Neurological examination
-motor
-sensory
-proprioception
-cognitive ability
-emotional state/affect
Epilepsy definition
-group of disorders characterized by chronic, recurrent, paroxysmal changes in neurological function that are caused by abnormal electrical activity in the brain
-seizures may be either convulsive or manifested by other changes in neurologic fx
Classification of Seizures
-partial
-generalized
-unclassified
Partial Seizures
-focal motor
-focal sensory
-simple partial: with elemental symptoms whether they are focal motor, sensory autonomic or psychic the pt remains conscious
-complex partial
Generalized Seizures
-convulsive or non-convulsive
-absence seizures (petit mal)
-atypical absence seizures
-myoclonic seizures
-clonic seizures
-tonic seizures
-tonic-clonic seizures (grand mal)
-atonic seizures
-more global in scope and manifestations
-involve an altered consciousness state and frequently abnormal motor activity
Seizure Etiology
-genetic factors: generally not a predictable inherited entity except in rare autosomal dominant disease ex: Sturge-weber Syndrome and neurofibromatosis
-head injury: open head or closed head injury: most common cause in young adults, the more severe the injury the greater the change of seizures (50% of OHI pts)
-intracranial neoplasms
-cerebrovascular disease: most common cause of onset in pts greater than 50 yrs old
-alcoholic withdrawal: usually generalized without focal features
-hypoglycemia
-febrile illness
-idiopathic (no known cause), 1/15 can be evoked by a specific stimulus (flickering lights, monotonous sounds, loud noises)
Focal Motor seizure
-usually originates in the contralateral precentral gyrus with the first symptoms occurring in the body part controlled by that brain region
- this activity can spread to involve the whole limb and often the entire half of the body (classic jacksonian seizures)
Focal sensory
-uncommon
-originate from the postcentral gyrus and are manifested by various degrees of paresthesias or numbness
Focal sensory and motor
-mixed seizurs are found commonly
Focal psychic
-psychic symptoms include recurrent feelings of dissociation from ones body or surroundings and sudden over whelming affective symptoms like fear, anger, illusions, and complex hallucinations
Complex partial seizures
-psychomotor or temporal lobe seizures
-associated with loss or impairment of consciousness which can occur at onset or following symptoms described above for simple seizures
-may be difficult to differentiate from petit mal except for older age of onset, presence of aura, vary periods of post ictal confusion
-most common observable manifestations is the ictal automatism
Common auras
-olfactory sensations
-visceral rising sensations from the epigastrium of the throat
-overwhelming feeling of familiarity (deja vu)
Ictal automatisms
-lip smacking
-chewing movements
-fumbling movements of fingers
-inappropriate verbalizations
-complex acts
Generalized seizures
-consist primarily of tonic-clonic and absence seizures
-no onset from a focal cortical discharge, since there are no focal components the prodromal symptoms, auras, focal motor and sensory symptoms are not expected but can occur
Absence Seizures (petit Mal)
-difficult to diagnose
-usual onset is 4-10 yrs of age with frequency at puberty
-generalized tonic-clonic seizures develop at puberty in as many at 50%
-primary means of differentiation is EEG
Tonic-Clonic Seizures (Grand Mal)
-patient emits a sudden cry due to spasm in diaphragmatic muscles
-immediately looses consciousness
-Tonic phase is muscle rigidity followed by the clonic phase that consists of uncoordinated movement of the limbs and head
-incontinence of urine and feces may occur
-movement ceases and the person becomes comatose
-within minutes there is a gradual return of consciousness with stupor, headache and confusion.
-once seizure has begun the jaws and teeth are clamped tightly and cannot be pried apart
-relaxation occurs only with end of seizure
Atonic Seizures
-sudden loss of muscle tone with falling
-3-6 are usually found in childhood and with other perinatal metabolic and genetic brain diseases and have a relatively poor prognosis
Consequences of Seizure Disorder
-social stigma
-exculsion
-restriction of driver's license
-overprotection
-isolation
-depression
Dilantin
-indicated for tx of all types of seizures
-usual dose 300-400mg daily
-Side effects: visual disturbances, slurred speech, lethargy, GI distress, rashes, gingival hyperplasia, leukopenia
Dental Considerations with Dilantin
-gingival hyperplasia: maintain OH , gingivectomy prn
-leukopenia: resulting in increased incidence of microbial infection, delayed healing and gingival bleeding, CBC w/diff
-additive sedation effects with CNS depressants
Luminal(phenobarbital)
-primarily used for grand mal and cortical focal seizures
-usual dose is 60-180mg daily
-side effects: drowsiness, visual disturbances, rashes
Luminal Dental Considerations
-additive sedation effect with pain meds
-pts on this drug tend to have more refractory problems with seizures
-decreased effects of corticosteroids, doxycycline, and carbamizepine
Mysoline( primidone)
-effective against all types of seizures except absence seizures phenobarbital is one of the two metabolites of primidone
-can be used in combo with dilantin
-usual dose 750-1500mg daily
-same side effects as phenobarbital
Primidone Dental Considerations
-similar to phenobarbital
-decreased effect of acetominophen with primidone
Tegretol (carbamazepine)
-indicated for all types of seizures but absence seizures
-usual adult dose 600-1200mg daily
-Side effects: dizziness, diplopia, nystagmus, drowsiness, blurred vision
-severe side effects; aplastic anemia, liver and kidney toxicity, must monitor bone marrow fx
Tegretol Dental considerations
-xerostomia
-leukopenia and thrombocytopenia: may have increased incidence of microbial infections, delayed healing, and gingival bleeding
Tegretol drug interactions
-propoxyphene- elevated levels of tegretol with increased toxicity
-erythromycin/macrolide antibiotics: elevated levels of tegretol with toxicity
-Pb corticosteroids, benzodiazepines, phenothiazines, doxycycline=decreased effects of agents
Zarontin (ethosuximide)
-primarily for absence seizures
-usual dose up to 2000 mg daily
- side effects: nausea, vomiting, fatigue vertigo, lethargy, aplastic anemia and blood dyscrasias
Zarontin dental considerations
-taste disturbances
-lilontin and celontin are used when absence seizures are refractory to other drugs
Depakene (valproic acid) and Depakote (divalproex sodium-extended release)
-indicated for generaloized and partial seizures excluding absence, infantile spasms and atonic seizures
-usual dose up to 4000 mg daily
-Side effects: minimal sedation and CNS effects, fine tremor, alopecia, weight gain, GI upset, nausea, hepatic injury, gingival enlargement
Depakene/Depakote dental considerations
-excessive bleeding
-decreased platelet aggregation
-leukopenia and thrombocytopenia: causing increased incidence of microbial infection, delayed healing, gingival bleeding
-monitor for gingival hyperplasia
-drug interactions: Asprin, NSAIDs, avoid combination due to affects on platelet aggregation and possible hemorrhagic episodes
Valium (diazepam)
-via IV, used for status epilepticus, PO: 2nd or 3rd line agent
-usual dose: IV up to 10 mg over 2 min period, repeat every 20 min if seizure persists
-side effects: sedation, cognitive impairment, behavioral problems
Valium dental considerations
-additive sedation effects with opioids, tranquilizers and antihistamines
Klonopin (clonazepam)
-indicated for absence seizures as well as myoclonic and akinetic seizures
-up to 20mg per day (.5mg TID usual starting dose)
-side effects: sedation, cognitive impairment, xerostomia, sialorrhea
Klonopin dental considerations
-additive sedation effects
-assess salivary flow as a factor in caries, perio disease, candidiasis
Felbatol (felbamate)
-monotherapy and adjunctive therapy for absence seizures, partial seizures and atypical absence seizures
-usual dose: up to 3600mg daily
-side effects: nausea, headache, vomiting, and insomnia
-possible asplastic anemia and acute hepatic failure
Neurontin (Gabapentin)
-adjunctive tx of refractory partial seizures with or without secondarily generalized seizure
-dosage : 300-600 mg TID
-side effects: somnolence, dizziness, ataxia, fatigue, nystagmus, headache, tremor, nausea, vomiting
Other Seizure meds
-lyrica: parital seizures (dizziness/somnolence)
-lamictal: partial seizures, tonic clonic (same as above)
-Zonegran: partial seizures(somnolence, and appetite loss)
-Keppra-tonic-clonic partial seizures (somnolence and irritability
Provision of Care
-well controlled seizures usually pose no management problems
-poorly controlled seizures or poor history must have physician consult before dental tx, consider antiepileptic drug or sedative med as directed by MD
-caution with lidocaine
-caution with general anesthesia, NO, or ketamine bc may induce a seizure
-consider premed
Management of seizure
-chair back in supported position
-patient turned to side to avoid aspiration
-prevent trauma to pt: use passive restraint, clear objects
-avoid padded tongue blade
-low level of stimulation
-monitor vital signs
Status Epilepticus
-phone 911
-vital signs/O2/posture for protection
-meds: valium 5-10mg IV or IM over 2 min and repeat every 10-15 minutes, up to 30mg
-phenobarbital 5mg/kg Im up to 200mg to 300mg , 50% dextrose solution IV as indicated
-100% oxygen
Stroke Classification
-transient ischemic attacks
-reversible ischemic neurologic deficit
-stroke in evolution
-completed stroke
-ischemic or hemorrhagic
Ischemic strokes
-atherosclerosis
-embolic
-subtypes: lacunar, large vessel, brainstem stroke
Hemorrhagic strokes
-2/3 intracerebral bleeding
-1/3 aneurysmal rupture and subarachnoid
Epidemiology of Stroke
-third most common cause of death in US
-5% of population over 65 has had a stroke
-47% pts with strokes die in first month
- in US 1 stroke/min
-if pt survives: 10% with no deficit, 40% mild disability, 40% disability requiring special care, 10% institutionalized
Deficits from Stroke
-unilateral paralysis
-numbness
-sensory impairment
-dysphagia
-blindness
-diplopia
-dizziness
-dysarthria
Post stroke complications
-seizure disorder (10%)
-aspiration pneumonia
-sleep disordered breathing
-depression (50%)
-sexual difficulties
Stroke definition
-acute development of a neurologic deficit caused by a cerebrovascular accident
-results from focal necrosis of brain tissue secondary to an interruption of cerebral blood flow
-cerebral blood flow is most commonly induced by thrombosis of cerebral vessel, cerebral embolism, or intracranial hemorrhage