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42 Cards in this Set
- Front
- Back
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Barrett's esophagus |
Etiology: complication of long-standing GERD - inflammation, ulceration of squamous epithelial lining - healing through progenitor cells/re-epithelialization
Manifestations: stratified squamous mucosa --> metaplastic columnar epithelium - pink velvety mucosa - "tongues" extending up from gastroesophageal junction; circumferential band; isolated patches
Clinical significance: RISK FOR DEVELOPMENT OF ADENOCARCINOMA! (30-100x greater risk)
Epidemiology: more common in males, whites |
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Congestive heart failure (CHF) |
Etiology: increased hydrostatic pressure, decreased venous return
Manifestation: fluid (transudate) accumulates - Left side = in lungs perivascular + interstitial transudate, alveolar septa/intra-alveolar edema - Right side = in legs, extremities |
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Kwashiorkor or liver cirrhosis |
Etiology: - Kwashiorkor = malnourishment - Liver cirrhosis = liver damage (alcoholism)
Manifestations: ascites (fluid accumulation in peritoneal cavity) - plasma albumin protein reduced = osmotic gradient reduced; net movement of fluid (transudate) into interstitial tissues |
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Filariasis |
Etiology: lymphatic/LN fibrosis (scar tissue); lymphatics can't drain properly
Manifestation: edema of external genitalia + lower limbs (elephantiasis) |
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Peau d'orange (orange peel) |
Etiology: obstruction of lymphatics due to breast carcinoma
Manifestation: edema of overlying skin of breast
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Lymphedema |
Etiology: loss of lymphatic drainage (due to cancer radiation, resection, metastasis – obstruction)
Manifestation: severe edema of upper extremity |
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LAD I |
Etiology: rare autosomal recessive disease; mutation in gene coding beta-2 integrin subunit (CD18) on leukocyte - decreased firm adhesion to endothelium (neutrophil can't bind ligand)
Manifestation: - delayed separation of umbilical cord/omphalitis - recurrent bacterial infection (skin/mucosal surfaces) - gingivitis/periodontitis (later in life; lack of PMNs --> IL17 --> bone resorption) - absence of pus formation - impaired wound healing - dysplastic echar (skin sloughing off)
Diagnosis: - reduced expression of CD18 (CD11a CD11b) on neutrophils (flow cytometry) - elevated neutrophil count
Treatment: - antibiotics for recurrent infection - BM or hematopoietic cell transplant |
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LAD II |
Etiology: rare autosomal recessive disease; defect in sLeX glycoprotein (selectin ligand on neutrophil; can't bind E/P selectin) + GDP-fucose transporter - neutrophils unable to tether/roll
Manifestation: less severe than LAD I (no delay in umbilical cord separation, bacterial infection non-life threatening) - PERIODONTITIS – major persistent manifestation - some impaired pus formation - delayed motor development in children (sitting/walking) - mental retardation, short stature
Diagnosis: - mental retardation, short stature - leukocytosis (neutrophils = 10,000-40,000/mm3) - absence of sLeX expression (flow cytometry)
Treatment: - antibiotic prophylaxis (children) for recurrent infection - fucose supplementation |
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LAD III |
Etiology: rare genetic disease; defect in integrin activation by chemokines - mutation in gene for adaptor protein kindlin-3 (binds to beta-2 integrin) - also affects beta-1,3 integrins = no firm adhesion, platelet aggregation
Manifestation: similar to LAD-I - Cerebral hemorrhage at birth - Bleeding disorders
Diagnosis: - intact integrin expression but impaired activation - leukocytosis - genetic analysis for mutation in kindlin-3 gene
Treatment: - BM or hematopoietic cell transplantation - Prognosis poor unless tx in early infancy |
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Neutropenia |
Etiology: - bone marrow pathology -- congenital, malignancies, radiation, drugs (anti-cancer, antibiotics), infection (Hep A/B, measles) - decreased production of: folic acid, vit B12 - enhanced destruction of neutrophils - septicemia: most impt factor in reduced neutrophil count in blood - hypersplenism: remove neutrophils at faster rate than being produced
Manifestation: decrease in blood neutrophil count = <1500/mm3 (normal ~6000/mm3) - susceptible to infection - middle ear, perirectal area, pulmonary, oral cavity (lips, tongue, buccal mucosa; GINGIVA most affected as bacterial load greatest there --> ulceration) |
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Cyclic neutropenia |
Etiology: mutation in elastase (ELA2) gene; arrests neutrophil dev't at promyelocyte
Manifestation: intervals of neutropenia associated with opportunistic infection - neutrophils <200/mm3 - early tooth loss - tongue ulceration, stomatitis, gingivitis/periodontitis, cellulitis – may become deadly in 10%
Diagnosis: complete and sequential blood count (2-3x/week for 8 weeks)
Treatment: - antibiotics for infections - G-CSF administration to help neutrophil production - oral hygiene* (or else G-CSF is useless) |
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Agranulocytosis |
Etiology: lack of granulocytes (PMNs, basophils, eosinophils); decreased production or increased destruction - some cases idiopathic - most induced by anti-cancer chemotherapeutics (inhibit normal mitosis/division)
Manifestation: - bacterial infection frequent - oral lesions (deep necrotizing ulcers) – buccal mucosa, tongue, palate, gingiva (most susceptible)
Treatment: - if drug-induced, discontinue ASAP - antibiotics for infection - G-CSF - oral hygiene |
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Chediak-Higashi Syndrome |
Etiology: autosomal recessive disease; abnormal lysosome formation - mutation in lysosomal trafficking modulator gene (CHS1/LYST)
Manifestation: identified in infancy/childhood - oculocutaneous albinism - photophobia - gray hair - recurrent bacterial infection (defective neutrophil fxn) - gingivitis, oral ulceration, perio disease
Diagnosis: blood smear; look for characteristic degranulation in CHS cell
Treatment: - antibiotics - hematopoietic cell transplantation - gene therapy (replace mutated gene)
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Chronic granulomatous disease (CGD) |
Etiology: defect in phagocyte NAPDH oxidase (phox) that results in loss/inactivation of 1+ subunits - abnormal PMN respiratory burst = reduced H2O2/ROS production (poor NETs formation) - reduced ROS –> NF-kB activation in monocytes, reduced efferocytosis
Manifestation: - recurrent bacterial infection (most susceptible to catalase+ bacteria) - lymphadenopathy - superficial skin infections - abscesses, cellulitis, gingivitis
Diagnosis: biopsy - necrosis, monocyte infiltrates, culture grows catalase+ bacteria (no TRUE granuloma with epithelioid cells) - genetic testing
Treatment: IFN-y, gene therapy |
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Papillon-Lefevre Syndrome |
Etiology: mutation/loss of cathepsin C gene (serine protease impt for skin devt/immune response of neutrophils); autosomal recessive disease
Manifestation: - palmar/plantar keratosis - accelerated periodontitis (spontaneous exfoliation of deciduous/permanent teeth) – A. actinomycetemcomitans must be present
Diagnosis: biopsy - resembles chronic periodontitis; non-specific (CT has increased vascularity, inflammatory infiltrate)
Treatment: - retinoid (acitretin) for skin lesions - antibiotics (against AA), plaque + calculus control for periodontitis |
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Traumatic neuroma |
Etiology: NOT neoplasm; reactive proliferation of neuronal tissue after nerve bundle damage - encounter scar tissue, cannot re-establish innervation - due to trauma, extraction
Clinical significance: neurons don't regenerate, but axons/dendrites may
Manifestation: tumor-like mass develops at site of injury if can't re-establish connection - common sites – mental foramen, tongue, lower lip - painful
Treatment: surgical excision |
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Alveolar osteitis (dry socket) |
Etiology: dissolution of blood fibrin clot (plasminogen –> kinins –> clot lysis); no wound healing - extraction (mandible), oral contraceptive, trauma, smoking - deficient clot formation phase
Manifestation: - pain, foul smell
Treatment: - socket irrigation - pack with obtundent/antiseptic dressing (change every 24 h, then 2/3 days until granulation tissue covers exposed bone) - antibiotic in socket
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Proud flesh |
Etiology: unknown; exuberant granulation tissue phase
Manifestation: non-neoplastic proliferation –> excessive protruding mass of granulation tissue - erythematous, may be ulcerated, bleeds easily - histologically: lots of blood vessels; similar to granulation tissue
Treatment: cauterization with silver nitrate; surgical removal |
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Pyogenic granuloma |
Etiology: no pyogenic bacteria/pus formation actually involved; not actually a granuloma (misnomer) - exuberant granulation tissue phase - occurs due to irritation (pregnancy, young children)
Manifestation: exuberant proliferation of granulation tissue in oral tissue - may be pedunculated or sessile - usually in gingiva (70% of time) - histology – many immature blood vessels, some fibroblasts/MPs |
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Dehiscence |
Etiology: persistent coughing, vomiting, suture resorption - deficient collagen deposition phase
Manifestation: untimely rupture of healing wound - most common in abdominal wounds |
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Incisional hernias |
Etiology: insufficient collagen, inadequate cross-linking - deficient collagen deposition phase
Manifestation: protrusion of intestine, usually in abdominal wall - defect caused by surgery |
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Keloid |
Etiology: excessive collagen deposition caused by increased fibroblast proliferation/collagen synthesis - overexpression of TGF-b, VEGF; increased PDGF receptors on keloid fibroblasts - genetics? genes not yet identified (more frequent in Africans, Asians) - sometimes triggered by implantation of foreign material; burns/scalds
Manifestation: expanding scar - more immature Type III collagen
Treatment: not really effective |
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Hypertrophic scar |
Etiology: excessive collagen deposition
Manifestation: common scar - unlike keloids, hypertrophic scars flatten/regress spontaneously over months-years, do not spread beyond site of injury
Treatment: not really effective |
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Decubitis ulcer (bedsore) |
Etiology: pressure-induced ischemia (ex: on back for too long) - inadequate blood supply
Manifestation: large gaping wound
Treatment: - pressure relief - enzymatic, surgical debridement (keep wound clean/moist) - PGDF – initiate healing process; one of the first GFs produced from platelets/most pleiotropic |
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Chronic duodenal (peptic) ulcer |
Etiology: gastric acid secretion –> necrosis of surface epithelium –> acute ulcer –> acute inflammatory response tries to control; chronic ulcer (balance btwn damage/repair) |
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Bronchiectasis |
Etiology: damage to bronchial wall usually due to repeated infection or obstruction (tumor, cystic fibrosis, pneumonia)
Manifestation: non-specific chronic inflammation of bronchi - destruction of bronchial wall, permanent dilation - elastic + muscular components replaced by fibrovascular granulation tissue + collagenous fibrous tissue
Clinical significance: example of co-existing tissue damage/repair (hallmark of chronic inflammation) |
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Rheumatoid arthritis |
Etiology: autoimmune disease; T cells make cytokines that activate.... - B cells make rheumatoid factor (RF), which forms immune complex that deposits in joint –> PMNs - Fibroblasts, chondroblasts, synovial fluid –> inflammatory mediators - MPs combine to form pannus, which eventually is converted to fibrosis
Manifestation: destruction of synovial tissue
Clinical significance: example of destruction of tissue/organ (chronic inflammation) |
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Silicosis |
Etiology: inhaled silica particles produces chronic inflammatory reaction marked by fibrosis
Manifestation: silicotic nodule in lung
Clinical significance: example of fibrotic chronic inflammation (inorganic agent) |
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Periodontal disease |
Etiology: dental plaque
Manifestation: gradual destruction of periodontium - first stage is gingivitis - deepening of gingival sulcus to a perio pocket - loss of function due to BONE RESORPTION (not fibrosis) |
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Tuberculosis |
Etiology: communicable granulomatous disease; Mycobacterium tuberculosis
Manifestation: in lungs (but also other organs) - Ghon complex – granuloma forms at site of nucleation + hilar LN - miliary pattern – granulomas spreads all over lung –> cavitations - oral manifestations uncommon (chronic painless ulcer)
Diagnosis: acid-fast bacilli (AFB stain) = Tb stains red [distinguish btwn Tb/fungal infection like histoplasmosis) - M. tuberculosis granuloma (tubercle) characterized by central caseous necrosis |
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Crohn's disease |
Etiology: chronic granulomatous disease - defect in autophagy (when cell wants to conserve energy during starvation periods) - mutation of certain gene causes pannus of intestine to have no/little granular content; remove normal defense mechanism of epithelial cells - MPs produce more IL-1B and cytokines –> disease
Manifestation: abdominal cramping, diarrhea, nausea; mainly in small intestine (also large bowel, anus, LNs) - oral lesions precede in 20-30% cases: facial/lip swelling, oral ulceration, cobblestone-like thickening of buccal mucosa causing fissures/hyperplastic folds, erythematous enlarged granular gingiva
Diagnosis: non-caseating, loosely-aggregated granulomas; transmural inflammation, fissures, lymphoid aggregations - leads to widespread fibrosis (bowel obstruction)
Treatment: - sulfasalazine - metronidazole - prednisone |
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Sarcoidosis |
Etiology: unknown; chronic granulomatous disease
- lung – 90%; dyspnea, dry cough, chest pain, fever - cutaneous – 25%; lupus pernio (chronic, violaceous, indurated lesions) on nose, ears, lips, face - if salivary gland/LN excluded, clinical oral manifestations uncommon - multiple erythematous macules of hard palate + central hyperkeratosis of lower labial mucosa
Diagnosis: - radiographic evidence of bilateral hilar lymphadenopathy or pulmonary fibrosis - biopsy of tissue – non-caseating granulomas; Schaumann bodies, asteroid bodies - increased serum levels of ACE - positive Kveim test (take sarcoid tissue from another person, sterilize, inject under pt skin; not used anymore)
Treatment: 60% resolve within 2 years; don't know exact cause so tx difficult - corticosteroids (for inflammation) - methotrexate - TNF-a antagonists |
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Orofacial granulomatosis
(Melkersson-Rosenthal Syndrome, cheilitis granulomatosa/Miescher's syndrome) |
Etiology: - MRS:
Manifestation: - MRS: unilateral facial paralysis, lip swelling, fissured tongue - CG/MS: lip swelling only
Diagnosis: - biopsy shows non-caseating granulomas - superficial edema, focal accumulations of lymphocytes
Treatment: don't know exact cause so tx difficult - intra-lesional steroids, antibiotics, surgical recontouring |
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Chemotaxis – endogenous, exogenous products |
Exogenous: from pathogen - N-formyl-methionyl peptide (and bacterial products)
Endogenous: from host - C3a/C5a (complement) - LTB4 (leukotriene B4 = lipid-derived mediator) - cytokines (chemokines like IL8) |
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Dentinal sclerosis |
Etiology: caries (antigenic/bacterial metabolites diffuse through dentinal tubules)
Manifestation: increased calcification; dentinal tubules filled with mineral deposits – caries crystals (apatite) or continued peritubular dentin (reparative/tertiary dentin) - develops at periphery of almost all caries; shield pulp from irritation - vital odontoblast processes must be present in tubules
*actually a PROTECTIVE fxn! |
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Periapical abscess
Phoenix abscess, parulis |
Etiology: infection, necrotic pulp
Manifestation: accumulation of purulent exudate at apex of non-vital tooth - clinical: pain, swelling, tooth elevation; sensitive to percussion; fever, malaise - radiographic: early = thickening of PDL; late = diffuse bone loss ("moth-eaten") - histologically: dense infiltrates of PMNs, liquefactive necrosis
Diagnosis: no response to thermal, EPT
Treatment: drain, culture sensitivity/antibiotics
*Phoenix abscess: acute periapical abscess that develops in pre-existing granuloma; due to changes in microbial flora/host defenses - presents with radiolucency *Parulis: gum boil; small sessile nodule on mucosa adjacent to affected tooth; signifies sinus tract communicating with periapical abscess - chronic inflammatory tissue through which pus flows (yellow); swells/ruptures in repeated cycles
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Ludwig's angina |
Etiology: infection
Manifestation: swelling of tissues (may block airway); difficulty breathing/swallowing, drooling, earache, unusual speech (hot potato voice), feeling of strangling (no chest pain unless infection spreads into retrosternal space)
4 cardinal signs: - involvement of 1+ tissue space - gangrene with serosanguinous, putrid infiltration having almost no pus - CT but no glandular structure involvement - spread of infection via fascial continuity (not through lymph)
Treatment: antibiotics, pain meds as needed |
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Periapical granuloma |
Etiology: necrotic pulp
Manifestation: accumulation of granulation tissue at apex of non-vital tooth (NOT true granuloma); 75% of apical inflammatory lesions - clinical: asymptomatic; no mobility/sensitivity to percussion - radiograph: radiolucency/thickening of PDL (identical to periapical cyst)
Diagnosis: no EPT response
Treatment: root canal, periapical surgery (lesion >2 cm), extraction (same as periapical cyst) - if not treated, gradually will turn into periapical cyst |
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Periapical (radicular) cyst |
Clinical significance: most common cyst of jaw
Etiology: - epithelial cell proliferation/migration – tissue breakdown - mass of epithelial cells desquamate –> increased osmotic pressure in lumen (release protein)
Manifestation: - clinical: asymptomatic unless acute inflammation exacerbated - radiograph: identical to periapical granuloma
Diagnosis: no EPT response - albumin protein test in surrounding tissue
Treatment: root canal, periapical surgery (lesion >2 cm), extraction (same as periapical granuloma) |
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Acute osteomyelitis |
Etiology: infection (directly from infected teeth, jaw fracture, gunshot wounds) - uncommon in healthy pts (usually in pts suffering malnutrition, old age, immune deficiency)
Manifestation: - clinical: severe pain, fever, leukocytosis, lymphadenopathy; loose tooth, sore to percussion - histo: sequestra (bone w/o osteocytes), dense PMN infiltration of marrow spaces, liquefactive necrosis - radiograph: ill-defined radiolucency, sequestration of necrotic bone
Treatment: difficult (bone infection) - culture/sensitivity - high-dose, long-term antibiotics - remove dead bone? varying opinions on this
*if left untreated, can develop into chronic osteomyelitis
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Chronic osteomyelitis |
Etiology: infection
Manifestation: inflammation less intense, milder clinical symptoms - clinical: swelling, pain, sinus formation, pus, tooth loss, pathologic fracture, acute exacerbations - histo: soft tissue consists of chronic inflammatory cells, fibrous tissue, sequestra, "pockets of abscess" - radiograph: patchy (moth-eaten) ill-defined radiolucency with central radio-opaque sequestra
Treatment: even more difficult than acute (dead bone/pathogens shielded by fibrous tissue; liimited blood suplly) - high-dose, long-term IV antibiotics - surgical intervention mandatory! remove all infected tissues, may need re-section with immediate reconstruction |
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Condensing osteitis |
Etiology: long-standing, low-grade pulp infection
Manifestation: reactive hyperplasia of bone - more common in pts <30 y.o.; usually mand 1st molar - clinical: no pain - radio: localized radio-opaque area at periapical region
Diagnosis: negative pulp test
Treatment: endo or extraction |
