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DH Path Exam 1

DH Path Exam 1 update

QuestionAnswer
Disease caused by a healthcare worker Iatrogenic
what is the scientific study of disease Pathology
Unknown cause Idiopathic
'5' Clinical signs of Inflammation Redness, Heat Pain, Swelling loss of normal tissue functiom
Systemic signs of Inflammation Fever- pyrogen production Leukocytosis- more WBC in blood Lymphadenopathy- Hyperplasia & Hypertropy of Lymphocytes
4 stages of Mitosis Prophase, Metaphase, Anaphase, Telophase P M A T
A complete 2nd set of chromosomes (92) incompatible with life Euploid
Larger than normal, extra segment is identical to a segment of the normal chromosome Duplication
Aneuploid and extra number, but isn't an exact multiple of chromosomes
The observable appearance of an individual Phenotype
Identical Allelic Genes(genes located same level/same function) Homozygote i.e. Blood type AA
Different Allelic Genes Heterozygote
The pathological wearing away of tooth structure from repetitive mechanical habit Abrasion
Wedge shaped lesion cervical areas of tooth weakened/fatigued structure=susceptibility Abfraction
70-75% of defense pool, major antibody in the blood serum Initial Defense, (Fetal-1st passive immunity)) IgG (Immunoglobin or antibodies)
Defends body fluids from microorganisms IgA (Immunoglobin)
Activation of B lymphocytes (along w/ IgD) involved in early immune response IgM
Activates of B lymphocytes IgD
Involved in hypersensitivity reactions- release histamines IgE
level of a specific antibody Antibody Titer
link between inflammatory & immune response, act as antigen presenting cells, amplifies the immune response phagocytosis does NOT have Memory Macrophages
develop from bone marrow stem cells, reside in lymphoid tissue. Produces plasma cells and B memory cells. B lymphocytes
Pin wheel shaped nucleus, visible cytoplasm. Produces antibody proteins or Immunoglobulins Plasma Cells
develop from bone marrow stem cells, mature in the Thymus. Memory Cells, T-helper cell (T4 marker, T-Cytotoxic cells (viral surveillance) & T supressor cells (turn off B lymphocites) T8 marker T lymphocytes Cell Mediated Immunity
'B' Lymphocytes primary role and the production of Antibodies Humoral Immunity
'T' Lymphocytes assisted by macrophages are the predominant role in: (CMI) Cell Mediated Immunity
Type I hypersensitivity occurs within minutes IgE--> histamine release constricts smooth muscle in lungs swelling edema i.e. asthma, hay fever, anaphylaxis
IgG and IgM antibodies combine with antigen. Tissue destruction where antigen is present Type II hypersensitivity i.e. incompatible blood transfusions
Immune complexes formed (microorganisms+antibody) deposit in circulation, Acute inflammatory response. neutrophils->phagocytosis-> lysosomal enzymes->Tissue destruction Type III hypersensitivity (Auto Immune disease)
Delayed hypersensitivity, Cell Mediated Immunity Type IV hypersensitivity (i.e. Tuberculosis Dx, Organ Transplant rejection)
What is Uticaria? Hives, multiple well demarcated swelling w/ Itching
Arthritis, Urethritis, Conjuctivitis Antigenic marker HLA-B27 Men 10:1 Oral ulcers & tongue depapillation. lower extremities affected (knees ankles) Reiter Syndrome aka Reactive arthritis
Histocytosis X Letter-Siwe disease- Hand Schuller Christian disease Eosinophilic Granuloma of bone Langerhans Cell Disease Langerhans cell present (type of macrophage)
Acute, rapid, children under 3yrs can be fatal, oral manifestations rare Letter-Siwe disease (Langerhans)
Chronic, multifocal, children under 5yrs 'punched out' skull radiolucencies mimics advanced perio disease Hand Schuller Christian disease (Langerhans disease)
Chronic. localized older children,young adults skull & mandible commonly involved eosinophilic granuloma males affected 2x as much Solitary Eosinphilic Granuloma of the Bone (Langerhans)
Combination of dry mouth and dry eyes Sicca Syndrome
Auto-immune, Just sicca=Primary w another auto immune disease= Secondary bilateral enlarged parotid glands Sicca and Raynaud's Syndrome (fingers and toe circulation) 90% positive reaction to Rheumatoid factor Sjogren Syndrome
85% sin lesions (butterfly rash) Oral Lesions 25%, Raynaund 15% arthritis, arthralgis, kidneys possible sjorgen's present (bloodwork before dental work may need to pre-med) SLE Systemic Lupus Erythematous
confined to skin & mucous membranes mildest form: DLE Discoid Lupus Erythematous
Severe, progressive auto-immune disease affecting skin and mucous membranes.50% 1st sign in oral cavity Nikolsky's sign: gentle pressure on mucosa form bulla Epithelial cell destruction Pemphigus Vulgaris mortality now 8-10% Corticosteroids
Acantholytic or Tzanck cells- detached epithelial cells (rounded appearance)biopsy to confirm
Cicatrical Pemphigoid aka(benign) Mucous membrane pemphigoid Gingiva-most common site affects oral & genital mucosa, skin, conjuctiva Cicatrical- 'healing w/ scarring' severe eye lesions may occur desquamative gingivitis. Nikolsky's sign hard to control. corticosteroids periods of exacerberation-> remission
60yrs + lesions more extensive, painful anti-inflammatory, corticosteroids Bullous Pemphigoid
Chronic, recurrent, autoimmune disease. Avg age 30yrs, must have 2 of 3 lesions present Oral, Genital, Eye lesions, (Skin) Behcet Syndrome
60-70% of entire WBC population 1st wbc recruited by chemotaxis Main Function: Phagocytosis Neutrophils (PMN)
3-8% of entire wbc pop. 2nd to injury site longer lifespan than neutrophil function: phagocytosis, and immune response Monocyte becomes MACROPHAGE
Non specific response to injury, occurs in the same manner regardless of the nature of the injury Inflammation
Arterioles, capillaries, venules (MC) Microcirculation Constricts than Dilates during inflammation
Salivary gland stone formed by calcium salts around a central core (major and minor glands) Sialolith
Unilateral 'frog-pouch' mucocele-like lesion sublingual and submandibular glands duct obstruction likely cause Ranula
Radicular or Periapical cyst True cyst (lined w/ epithelium) most commonly occuring oral cyst epi rest of Malassez proliferation usually asymptomatic
Alveolar Osteitis 'Dry Socket' lost blood clot after tooth extraction bone surface exposed. Painful, but no inflammation because no infection exists
Trisomy 21 (Down Syndrome) most common abnormality in humans fissured/pebbly tongue, Macroglossia w/ protrusion, High arch palate, Enamel hypoplasia, microdontia, >90% Perio disease
Trisomy 13 70% live to 7mos only Bilateral cleft lip and palate small/No eyes micro/anophthalmia, supernumerary digits
Missing an 'X' chromosome short,neck webbing, hands &feet edema, broad chest, genital underdeveloped, lack the 'Barr bodies' Turner Syndrome
XXY, male phenotype Taller, wide hips, female pubic hair, >50% breasts Maxilla slighty hypoplastic, detected after puberty 1 barr body for each extra x Klinefelter Syndrome
Caused by deletions on the short arm of CH5 Mental retardation, (No Oral abnormalities) 'catlike cry' Cri du Chat Syndrome
Wolf-Hirschhorn Syndrome Deletion on CH4 Cleft Palate IQ > 30
Autosomal(non-sex chromosomes) dominant,cyclic decrease in Neutrophils 21-27dys intervals, lasting 2-3dys, Oral ulcers G-CSF Tx Cyclic neutropenia Chronic= Kotsmann Syndrome
Autosomal Recessice Inheritance Periodontal destruction, perm. tooth loss before age 14, Palmer & Plantar hyperkeratosis (retinoid Tx) Papillon-Lefevre Syndrome
Gingival Hyperkeratosis band-like, few mm in width, Free gingiva not affected
Gingival Hypertrophy, Very firm, corrugated, paler, lips may protrude Gingival Fibromatosis
Laband Syndrome Gingival Fibromatosis, nail loss,malformed nose & ears, enlarged liver & spleen, fingers/toes frog-like appearance
'Soap bubble' radiographic jaw appearance, eyes far apart, delayed eruption=pseudoanodontia Fibrous CT Cherubism
Ellis-Van Creveld Syndrome affects dwarfs, Polydactyl, toenails missing, 50% heart defects, and present natal teeth, no anterior Max. Vestibule, Conical tooth shape
> size of mand. teeth, supernumerary teeth,missing/minimal clavicles skull defects, open fontanelles Cleidocranial Dysplasia
Gardner Syndrome Osteomas (jaw,skull,long bones) and Odontaomas, Intestinal Polyps become malignant age 30+
Mandibulofacial Dysostosis (Assoc. w/ Treacher's Collins Syndrome) 'fish-like' commisures Deafness Hypoplastic mandible, Open bite, 30% high palate or cleft
Nevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome) wide spaced eyes, Jaw cysts, basal cell carcinomas,Nevi: pigmented skin lesions
Osteogenesis Imperfecta 30% W/ Family Hx, brittle bones Dentinogenesis imperfecta (dentin can't suppoprt enamel) 80% Primary teeth affected. 35% Permanent
Tori Mandibular: rare before age 15 smooth or lobulated Palate: mucosa thin, trauma easy 2:1 women > Native Americans Rare younger than 14yrs
Ehlers-Danlos Syndrome Collagen & CT defect, very elastic, joint hypermobility
Cleft palate/lip 1 in 800 births cogenital lip pits midline of lower lip vermillion border
Hereditary Hemorrhagic Telangiectasia Serious Nosebleeds (Note in DX Tx) Pinpoint/spider-like red lesions lips,eyelids,nose Tip Anterior Dorsom tongue
Multiple Mucosal Neuroma Syndrome MEN2 B Thyroid Carcinoma 75%, early Dx can become malignant oral neuromas, tip of tongue Pt: tall, large thick lips, everted eyelids
Von Recklinghausen Disease Neurofibromatosis of CNS, eyelids, nasoloabial fold (hearing/visual) Cafe au lait 105 Oral involvment
Peutz-Jeghers syndrome 98% lip & buccal mucosa lesions multiple melanin macules skin and mucosa, diminish w age GI Polyposis (rarely malignant)
White Sponge Nevus birth or after puberty white, corrugated, soft mucosa Always the buccal, never free gingiva, usually bilateral Keratin desquamates- raw mucosa
Amolgenesis Imperfecta 4 TYPES HYPO:(1)Plastic-irregular thickness,pitted(2)Calcified,yelloworange,chips easily-openbite? 3)Maturation-i.e. snowcap,soft enamel (4)Plastic-Maturation- yellow,brown pitted ALL teeth, Severe Sensitivity
Dentinogenesis Imperfecta most common AKA Hereditary Opalescent Dentin dentin soft (restorations fail), enamel chips-Attrition, NO PULP CHAMBERS, Roots are short blunt
Dentin Dysplasia Type I RADICULAR Normal crowns, Short roots-early exfoliation. half moon pulp chamber appearance. Disturbance in Hertwig's epi root sheath
Dentin Dysplasia Type II CORONAL pulp stones, Translucent/amber primary teeth Permanent: Normal crown/color, small roots no pulp chambers shown radiographically
Hypohydrotic ectodermal Dysplasia X linked recessive less hair,sweat hypo or anodontia, alveolar ridge-only if teeth present no minor salivary glands or respiratory tract mucosa soft,dry skin incisors,canines small conical
Hypophosphatasia decrease in serum alkaline phosphates (calcifies bone and cementum) bow-legged, fractures no pdl, spontaneous loss of primary teeth
Hypophosphatemic Vitamin D resistant rickets Large pulp chambers, gingival abscesses, pulpal disease, Dentin cracks, bowlegged low phosphorous serum levels
Pegged/Absent Max. Laterals primary and Secondary dentition 1-3% white 7% Asian Premolars missing 10-20%
Taurodontism Large, Pyramid Molars Large Pulp chambers, furcations, freq found in Klinefelter (XXY) Syndrome
Giant Cell Granuloma CENTRAL_Within bone, multi-nucleated giant cells only in jaw PERIPHERAL- Outside bone, Dk red, on gingiva or alveolar mucosa
Pyogenic Granuloma No pus, response to injury pregnant, teenagers, young adults
Chronic Hyperplastic Pulpitis Granulation tissue fill caries void
Increased dilation of blood vessels Kinin System
c-Reactive protein produced in liver acute & chronic > 10mg is high
Parenteral Injection
Serum sickness Drug Hypersensitivity Type III allergy i.e. horse anti-toxin (no longer done) for immunity penicillin, barbituates
Lichen Planus 1% pop almost always bilateral Wickham's Striae benign, chronic skin(lumbar), oral mucosa (buccal) desquamative gingivitis basal cell layer degeneration
Dental or Periapical granuloma painful, localized slightly extruded from socket opening in pulp canal (apex usually) thickened PDL (slight)
Focal Sclerosing Osteomyelitis aka condensing osteomitis change in bone, near apex (usually Mand 1st Molar) usually reaction to infection, asymptomatic, no tx
Created by: michelleleigh33