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89 Cards in this Set
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Define "specific"/Granulomatous lymphadenitis and list causes
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• Lymphadenitis;; TB or the other fungi (coccidiomycocsis, Histoplamosis) are the causes of specific Granulomatous lymphadenitis. the other causes are foreign body granuloma
• Enlarge in response to infections, cell debris or antigen |
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List causes and clinical features of acute nonspecific lymphadenitis
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• Bacterial, painful enlargement of lymph nodes, localized to draining region
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Describe mesenteric lymphadenitis. What is the common cause?
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• Causes acute abdominal pain, looks like acute appendicitis. Do your CT and you would see enlarged lymph nodes. Most common cause is Yersinia enterocolitica
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Describe clinical features and list causes of chronic nonspecific lymphadenitis
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• Clinical: Nontender, reactive, benign
• Causes- 3 morphological patterns: follicular, paracortical, sinus histiocytosis |
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Describe major morphologic features and list causes of follicular hyperplasia of lymph nodes
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• Two must know: HIV, enlarged lymph nodes in RA and other autoimmune disease
• B-cell proliferation;; tingible bodies;; prominent cortical follicles with germinal centers |
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List causes of paracortical hyperplasia of lymph nodes. What is the major morphologic feature?
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• IM and EBV; cat scratch; vaccination
• T-cell hyperplasia;; Bartonella infection; |
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What are the associations of sinus histiocytosis of lymph nodes?
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• Lymphocytes draining antigen and the example is benign lymph nodes draining cancers. (not metastatic= they’re benign)
• Response to antigen;; Morphology: distended sinusoids with engorgement by macrophages |
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What special studies are used in lymphoma diagnosis?
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• Best one is PCR for gene rearrangement= proves its lymphoma
• Sito genetic specific translocations =proves its lymphoma • CD marker/immunophenotype= what kind of lymphoma • Immunochemistry to see where different antigens are expressed • Immunophenotype essential for categorization; determines treatment, establishes prognosis;; k or lamba light chain restriction;; Gene arrangement: establish clonality in uncertain diagnosis ;; Causes immunodeficiency;; herpes zoster;; graft vs. Host disease • Hodgkin lymphoma spreads in a orderly fashion;; Needle biopsy acceptable for deep lesions |
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For the following lymphomas, what age group is affected, what tissue locations/clinical findings, what are the immunophenotype and cytogenetics? Associations, if any? General microscopic morphology (key descriptive words- not necessary to recognize photomicrograph.) Prognosis?
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Follicular lymphoma
• B (CD 19:20 on all B) • Nodal=nodes, adult, indulant, incurable, • Marker=bcl 2;; translocation=t14:18=bcl 2 • t (14:18)--> overexpression of BCL2;; males=females; immuno=always b cell; CD119, CD20, CD 5 negative;; resistent to chemotherapy and blocks apoptosis;; micro=oval follicles or nodules composed neoplastic cells;; morph: lymph nodes enlarged, matted mases;; Diffuse large B cell lymphoma. • B • Most aggressive;; nodal or extranodal • Favorite extranodal is Ring; tonsils; CNS • Marker=besides CD20 also bcl 6 • all ages; neoplastic b cells are EBV infected;; advanced HIV;; rapidly enlarging; bone tumors (not bone marrow); waldeyers ring (tonsils, adenoids); rapidly fatal if untreated; prognosis: related to extent; 1/2 cured, remission in up to 80% Burkitt lymphoma • B • Myc, t 8:14 • Morph: starry sky • Aggressive but curable • African/Endemic: maxillary, mandible, 100% EBV; endemic=in environment • Nonendemic=sporadic American type not associated w/ EBV tends to be children, always extranodal, abdomen and small intestine, iliocecal valve region, and other viscera • HIV: 25% are EBV • morph: starry sky pattern of apoptotic bodies, benign macrophages;; african=endemic (EBV), sporadic=nonendemic (ileocecal mass is most common in children);; age=any and young;; Mantle cell lymphoma • B • T 11:14; bcl 1; cyclin D (most important) • Intermediate prognosis, low cure rates MALT/Marginal zone lymphoma • B • Helicobacto pylori (in stomach) • Lymphoma of autoimmune disease (Sjorgen and hashimoto thyroiditis) • Can be nodal • Not just one marker (so don’t need to know) • Indulent and curable, treat helicon in stomach =more than 50% resolve • MALT: middle-aged adults; nodal disease=marginal zone lymphoma;; Anaplastic large cell lymphoma • T (all have CD 3) • CD3+, children, good prognosis, ALK marker • ALK gene; T cell lyphoma Adult T cell leukemia / lymphoma • Cd3+ cd4, HTLV1, hypercalcemia, skin and neurologic lesions, • Adult:; fatal in months to 1 year; Mycosis fungoides/Sezary syndrome • Sezary=malignant cell=cd4, skin involvement always • Mycosis fungoides= looks like fungus but malignant cells infiltrate skin, patch, plaque then becomes leukemic (takes years) • Sezary starts as leukemia of cells=red man syndrome (red exfoliative skin) • Mycosis: patch stage=looks like fungal; tumor; bone marrrow;; exfoliative erythroderma=red man;; leukemia of sezary cell (cerebriform nuclei);; Extranodal NK cell lymphoma • Lethal midline granuloma of nasopharynx; associated with EBV • Extranodal: site=, skin, testes; ischemic necrosis; t cell lymphoma ***large granular cell lymphoma=cd8*** |
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Plasma cell dyscrasias: List types
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• Most common =MGUS
• Multiple myeloma- most common malignant one • MGUS=monoclonal gammopathy of undetermined significance |
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Describe the clinical and morphologic features of multiple myeloma. What are the diagnostic criteria? Prognosis?
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• Most common malignancy of bone
• Diagnostic: Need monoclonal gammopathy or M-Protein, spep (serum protein electrophoresis) • Need Benz Jones protein in the urine (monoclonal light chain) • Need Plasmacytosis of bone marrow-makes punched out bone lesion • Present with backpain and bone pain • Bone lesions are Lytic due to cytokines , which releases calcium-Hypercalcemia • They get myeloma Kidney renal disease • Anemia • IgG, IgA, IgD or light chain • Skeletal defects: generalized osteoporosis; skull, vertebral column • Myeloma kidney: tubules are plugged from accumulation of light chains • Bone marrow plasmacytosis: russell bodies • Systemic amyloidosis: wall of blood vessels • Clinical: recurrent bacterial infections; amyloidosis; hyperviscosity syndrome; atypical plasma cells • Diagnostic: CRAB= hypercalcemia, renal insufficiency; anemia; bone lesions • Lab: peripheral blood cytopenias=rouleaux;; • Incurable;; treatment if candidate for stem cell transplantation |
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What are the locations and significance of solitary plasmacytoma?
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• Nose, outside bone is curable by surgery in nose
• Localized tumor of plasma cells;; may occur in bone marrow; may be extraosseous |
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What is the frequency and significance of MGUS?
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• Precancer for myeloma, don't know when or if they'll have multiple myeloma
• Extremely Common (5%) • Can't have bone lesion, can’t have anemia or renal disease or any other criteria..only thing is monoclonal immunoglobulin • MGUS=monoclonal gammopathy of undetermined significance • M protein is asymptomatic individual: no other evidence of myeloma (diagnosis of exclustion);; incidence=most common monoclonal gammapathy |
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What are the clinical features and neoplasm related to Waldenstrom's macroglobulinemia/
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• Lymphoplasmocytic lymphoma
• Nodal, doesn't cause punched out bone lesion • Protein is monoclonal IgM • Problem is Hyperviscosity and cryoglobulin (cold) • Causes headache, platelet dysfunction, abnormal bleeding • Death in 4 years, it's incurable • Bleeding;; cryoglobulinemia (Raynauds phenomenon) |
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What is the defining cell of Hodgkin lymphoma? Recognize its morphology.
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• Reed-Sternberg cells (owls eye nuclei);; cross eyed (cell w/ two nuclei) cd15:30 + in everything but lymphocyte predominant type
• Hodgkins lymphoma is nodal |
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What are the peak age and general clinical findings of Hodgkin lymphoma?
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• Teens through 30, peak age= 32 (common);
• nontender enlarged lymph nodes • most common is Horse collar, midaxillary then mediastinal • Stage with ann arbor • EBV implicated; RS cell produces cytokines; • Enlarged lymph nodes w/wo systemic syndromes; cervical node enlargement="horse collar"; cervical then axilla then inguinal; medistinal=nodular sclerosing; generalized pruritis; bone marrow pain late; cutaneous anergy; A=absent, B=present and poorer prognosis |
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Be able to use the Ann Arbor system to stage Hodgkin lymphoma.
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• I=single group; II two groups or more on same side of diaphragm; III=crosses diaphragm, prognosis falls IV=other organs and lymph nodes
• III=disease of both sides of diaphragm, splenic involvement; IV=multifocal involvement of extralymphatic organs (bone marrow, liver) |
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List the types of Hodgkin lymphoma. Which has the best prognosis? Worst prognosis? Most associated with EBV? Least associated with EBV? Immunophenotype of RS cell in each type?
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• Nodular sclerosis 70% (most common by far), lacunar type of reed Sternberg cell which is cd15:30; lymphoid depleted is worse prognosis (also cd15:30);
• Mixed type with lymphocytes and still has Reed Sternberg • Lymphocytic deplete is strongly associated with EBV;; nodular sclerosis is +- • Lymphocyte predominate type: two characteristics LH type of Reed Sternberg CD 15:30 -, EBV – (can be in mediastinum) |
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What are the morphologic and clinical features of nodular sclerosis Hodgkin lymphoma?
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• Mediastinal mass (if see this think nodular sclerosis); starts in lymph nodes above diaphragm, reed-sternberg lacunar type; cd15:30 +; survival over 90%
• Young adults; cervical lymph nodes;; Collagen bands forms nodules; lacunar type of RS cells |
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List the four stages of infant/childhood development. What are the three major causes of death in the first twelve months? (Table 10-1) What is the major cause of injury for all three age groups above one year?
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• Neonatal is the first 4 weeks of life which is most critical
• Infancy 5-14 • Causes: short gestation, low birth weight, congenital anomalies, SIDS • Above one year: Injuries and accidents |
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What do the terms AGA, SGA and LGA stand for? At what gestational age is an infant preterm? Post-term?
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• Definitions
• AGA = appropriate for gestational age • SGA=small for gestational age • LGA=large for gestational age (diabetic mom) • Pre=37 weeks • Post after 42 wk |
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Prematurity is defined as what gestational age? What are the four major risk factors for prematurity?
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• 37 wks
• 4: premature rupture of membranes, infection, morphologic abnormalies of infant, multiple gestation |
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What does FGR (IUGR) stand for and what are the three main groups of factors that cause FGR?
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• Fetal growth reduction
• 3: fetal, placental, maternal (don’t go into a lot of detail) |
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When do alveoli begin to differentiate in the lung? When do Type I and Type II pneumocytes appear?
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• Alveolar cells that make surfactant aren't present until 26 weeks (main take home!)
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Describe the morphologic features of the immature brain.
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• Soft, gelatinous, easily pliable
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What is physiologic jaundice and what is it due to?
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• Liver isn't mature so it can't keep up
• Within first week of postnatal life due to breakdown of fetal red cells and inadequate biliary excretory function |
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What are the five parameters used for an APGAR score? What are the approximate mortality rates for an APGAR of 0-1 versus 4 versus 7 or better?
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• Know 4 vs 7
• 10 is perfect, we like 7-9 • 0 at 1-5 minutes • Low apgar after 5 minutes=higher mortality • Chances of survival • 0-1=most likely to die; 4=better; 7=almost 0% mortality |
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Define malformation, deformation, disruption, sequence and syndrome. What is the most common important birth injury?
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• Disruption: amniotic band
• Sequence*** = Potter, oligohydramnios • Intracranial hemorrhage=most common important birth injury • Malformation: intrinsic abnormality during development process • Disruption: secondary disruption or interference with an organ or body region that was previously normal in development (amniotic band) • Deformation: club foot; arise later in fetal life represent alterations in form or structure resulting from mechanical factors; uterine constraint • Sequence: pattern of cascade anomalies, some can be explained on basis of a single, localizing , initiating defect (Potter oligohydramnios sequence) • Syndrome: constellation of congenital anomalies believed to be pathologically related, can't be explained by single initiating event (virus, chromosome abnormality) |
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What features are associated with the oligohydramnios sequence (Fig. 10-3)
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• Sequence*** = Potter, oligohydramnios
• Decreased amniotic fluid due to any number of causes • No kidney or no urine output is when you get amniotic fluid • Features: Flattened facies, positional abnormalities of hands and feet, lungs hyperplastic |
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What are the three main causes of congenital malformations (Table 10-2)?
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• Genetic , environmental , multifactorial , unknown
• • Genetic (karyotype abnormality, Downs syndrome , environmental (rubella =cataracts, heart defects, deafness, mental retardation), multifactorial (congenital defects of hip), unknown |
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What is the at risk period for CMV? Rubella? What are the fetal defects seen in CMV, Rubella?
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• Cause major fetal defects, timing is different
• Rubella: really, 1st trimester, 50% the first month, earlier the worst. tetrad of defects • Rubella= cataracts, heart defects, deafness, mental retardation • CMV: 2nd trimester, CNS, mental retardation, microcephaly, hepatosplenomegaly |
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What are the two phases of intrauterine development? During what weeks is the embryo very susceptible to teratogens? What is the fetus susceptible to during the fetal period? (Fig. 10-5)
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• Pic of embryo, teratogens are a big problem =red; red=embryonic=first 9 weeks (just know red is the embryonic period)
• Embryonic=first 9 weeks of pregnancy;; Fetal= terminates at birth • 1st 3 weeks=death or abortion; Weeks 3 to 9 = very susceptible to teratogens • Fetal period: increased susceptibility to growth retardation or injury to organs |
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What are the two major routes for perinatal infections
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• Transcercially (ascending): most bacterial
• Transplacentally (descending/hematologic): parasitic and viral • Transcercially (ascending): most bacterial and a few viral acquired • Transplacentally (descending/hematologic): parasitic and viral; few bacterial |
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What does TORCH stand for? What are the common clinical and pathologic manifestations associated with the diseases?
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• Torch= toxoplasma, others (HIV), rubella, cytomegalovirus, Herpesvirus
• Cause same features in infants, so you know what infection the mom had • Fever, encephalitis, chorioretinitis, pneumonitis, hepatosplenomegaly, hemolytic anemia |
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What is another term for respiratory distress syndrome? What is the fundamental deficiency in RDS? Is the infant preterm? AGA? What sex, what maternal condition and what type of delivery are associated with RDS? Describe the clinical scenario of RDS in an untreated infant (no surfactant)? What is the characteristic microscopic finding in the lungs? The incidence of RDS is inversely proportional to what?
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• Preterm baby, 25 weeks (90% chance will have it), neonatal respiratory distress=hyaline membrane disease in adult
• Not with c-section: doesn't have pressure/pushing (affects lungs) • Clinical: no treatment, start out ok, respiratory becomes worse, ground glass, O2 helps, if they don’t recover they get cyanotic, either going to die or survive for 3-4 days. • Inversely proportional to gestational age= goes down as the age goes up • Also known as: Hyaline membrane disease • Defect: Deficiency of pulmonary surfactant • Preterm and AGA: yes • Morph: hyaline membrane;; lungs solid airless and reddish purple • diabetes in mother, C-section, male sex;; • ground glass, O2 helps, O2 becomes not helpful, they aren't going to survive the 3-4 days • Clinical: breathing well, 30 minutes breathing is difficult, retraction of lower rib and sternum on inspiration, expiratory grunt;; hours respiratory distress worsens, cyanosis develops, fine rales heard;;; X-ray: ground glass |
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What are the two cornerstones of therapy for RDS? What are the two complications of oxygen therapy? What three major complications is an infant who recovers from RDS at risk for? What are the two major ways to control RDS in an at risk fetus?
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• Oxygen and surfactant for the baby, give mom steroids
• Complications: Eye, retinolental fibroplasia- that’s the blindiness due to excess O2 they used to use • 3: necrotizing enterocolitis, intraventricular hemorrhage , and long term bronchodysplasia • 2: try to get mom stuff, then baby stuff |
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What are the clinical symptoms of NEC? What do abdominal X-rays show? What are the two treatment options? What complication may occur?
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• Premature infant, more disease the younger the child is and visa versa
• Symptoms after first feeding (intestinal ischemia) • Treat: Conservative or surgery • Know it's a complication of the premature ***Add Intraventicular Hemorrhage (what is it, prone to occur in preterm infant, can be fatal) |
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What is the classic deficiency in PKU? What does the deficiency lead to an accumulation of? What does an increased level of phenylalanine do in the infant within weeks? How is the damage manifested in the infant? How can the damage be avoided? What can be done to identify infants with PKU at birth? What odor is associated with infants who have PKU and what is it due to?
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• Abnormality but don't have enzyme, phenylalanine hydroxylase, it's built up
• Causes: Severe mental retardation • Manifest: within 6 months will see mental retardation • Avoid: diet • Identify: Heel stick screening • Odor: musty;; Severe lack of phenylalanine hydroxylase leading to hyperphenlalaninemia and PKU;; avoided by restricting phenylalanine intake |
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An infant born to a clinically normal PKU female who has discontinued dietary treatment will likely have what syndrome? Does dietary restriction help the infant? How can the syndrome be avoided?
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• Child get teratogenic effect from the phenylalanine. Child has abnormalities and you can't do anything about it
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In the more common variant of galactosemia what is lacking? What product accumulates in the tissues? What three organs are affected by the disease and what are the clinical manifestations related to these organs? How does an infant present? What is demonstrated in the urine? What specific tests can be done to diagnose the disease? How can most of the morphologic changes be prevented?
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• Lacking: enzyme that breaks down galactose
• Organs: liver , eye, and brain • Present: jaundice, hepatomegaly, then cataracts then mental retardation • You can screen for it, urine has reducing substances other than glucose (this isn’t the way you will do it, you’ll go to lab); Look for transferase • Prevented by diet (usually only have for the first 2 years of life) • Fail to thrive, vomiting diarrhea within few days of milk ingestion |
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What is the fundamental defect in cystic fibrosis? Cystic fibrosis is the most common lethal ______? What is the mode of genetic transmission? What if the CFTR gene? What does it code for? What chromosome is it located on?
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• Defect in CFTR channel, chromosome 7, encodes chloride ion channel protein and some others.
• Lethal: White population, autosomal recessive • Fatal in childhood and young adult life;; Defect: ion transport • Ion transport in epithelial cells affecting fluid secretion in exocrine glands and the epithelial lining of respiratory, GI and reproductive tracts • Mom detects salty sweat |
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Understand the different clinical phenotypes as they relate to a positive or negative sweat chloride test and the molecular phenotype using Fig. 10-20 as your guide.
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• Much more likely to have positive sweat chloride test when you are up in “this range”
• There is mild vs severe; mild is just one or two things and not recognized at all at birth or at child. |
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What are the major clinical features of classic cystic fibrosis?
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• On picture with triangles
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What happens to the ducts in the pancreas and what does it lead to morphologically?
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• Pancreas-mucus plugging, lose ducts, and lose ability for stuff to come out of the pancreas (pancreas and non-functional)
• At birth look for meconium ileus (can’t go to the bathroom, at surgery find bowels obstructed, with meconium) • Pancreas= ducts plugged with mucus, atrophy of exocrine glands, fibrosis;; impairs fat absorption |
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What happens to the submucosal glands in the lung and what does it lead to? What are the final resultant changes morphologically in the lungs? What are the three most common organisms causing infections?
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• Its Mucus secretion, then obstruction, infection…looks just like bronchiectasis
• Pseudomonas: because expresses alginate (helps mucoid stuff grow, keep you from getting it with antibiotics, find in autopsy) |
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What is the common finding in men which results in azoospermia and infertility?
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• Have congenital absence (possible carrier of gene)
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What finding is seen in a small percentage of infants at birth
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Meconium ileus
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What are the cardiorespiratory complications are the single most common cause of death in CF?
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• Its just a statement not a question
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What are the methods for diagnosing CF? What is the gold standard?
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• Sweat choride, if negative do genotyping.
• Gold: genotyping (could just look like fatty stools) (she talked about failure to thrive, respiratory infections) |
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What are the current treatment options for CF?
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• Bilateral lung transplants, give them enzymes to replace pancreatic enzymes so they can absorb, compression vests; lung most common transplant, lungs don't have all the mucus pluggins
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Define SIDS. At what age do the majority of the deaths occur? Where and when do the majority die? What do most infants have minor manifestations of what prior to the fatal event? What does ALTE stand for?
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• Unexplained after thorough investigation, Sudden death under 1 year of age,
• Age: between 2-4 months, 90% in first 6 months, • Usually die at home, after period of sleep • Have minor respiratory infections (doesn’t have to be) • Leading cause of death between age 1 month and 1 year in US;; • ALTE=apparent life threatening event (if it witnessed and resuscitated) |
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What is the most common nonspecific finding at autopsy? Why is the postmortem exam important?
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• Peticheae, also see Brainstem changes (has to do with homeostasis)
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Know the major risk factors for parental, infant and environment from table 10-7.
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• Parental: young age, maternal smoking, drug abuse, multiple children close together, low socioeconomic group, late/no prenatal care
• Infant: premature, male, multiple birth, SIDS in prior sibling • Environment: prone sleep (not sleeping on stomach for the first 6 months), • sleep on soft surface, hyperthermia, |
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List associations of poor dental hygiene
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• Carries, gingivitis, cysts (from carries)
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How does periodonitis differ from gingivitis? What are the associations and complications of periodontitis?
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• Periodonitis not associated with hygiene but with flora shift
• Downs syndrome, HIV, diabetes mellitus; infiltrates of leukemia • Comp: bacteremia, infective endocarditis, brain abscess, adverse pregnancy outcomes • Inflammation involving peridontal ligaments, alveolar bone and cementum; sequelae= loose/lost teeth=alveolar bone destroyed; independent of gingivitis • Usally occurs without associations;; AIDS, acute leukemia, |
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Describe the appearance, clinical and possible sequela of pyogenic granuloma.
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• Know picture (16-3 or 16-15, lymph node pictures, expect to see), see in mouth; pyogenic granuloma=pregnancy tumor. Look for cases where it’s a child or she’s pregnant; gum line, elevated, bleeds
• Clinical: Can become ossifying fibroma • FIGURE 16-3 Pyogenic granuloma. Erythematous, hemorrhagic, and exophytic mass arising from the gingival mucosa |
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List all associations of aphthous ulcers. Recognize morphology and clinical.
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• Shallow ulcer with red rim, painful, increased in HIV, systemic lupus erythematosis, self limited
• Canker sores; painful shallow ulcer;; Chocolate and walnuts • FIGURE 16-4 Aphthous ulcer. Single ulceration with an erythematous halo surrounding a yellowish fibrinopurulent membrane. |
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List causes of glossitis. Recognize morphologic description.
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• Case studies, iron deficiency anemia; plummer-vincent (iron deficiency, glossitis, esophageal webs, risk of squamous carcinoma)
• Deficiencies: B12, pyridoxine, riboflavin • Morph: thinned epithelium with loss of papillae (not always inflammation) • beefy red tongue or inflammation; mucosa thin; ulcerations may occur |
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Review associations of black hairy tongue
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• Drugs, mostly antibiotics, antipsychotics, seen in smokers
• Defective desquamation; reactive Associat: medications=bismuth-containing, antibiotics;; dehydration, hyposalivation; |
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What types of disease are associated with herpes simplex infection of head and neck?
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• Herpetic gingival stomatitis, 20% infants (whole mouth is inflamed)
• Recurrent reactivation last 7 days, limited to lip or inside mouth • Reactivation from cold (“cold sores”), URI, UV exposure • Prolonged with HIV • HSV 1 and 2; age 2-4; Tzanck test |
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List fungal infections of oral cavity. What are their associations?
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• Infections from lungs can get into mouth, coccidiomycosis, Histoplamosis, aspergillus (associated with neutropenia)
• Most important is candida=thrush, white plaque that scrapes off, not a problem in neonates (immune system isn’t ready yet), but you see it in diabetes mellitus, HIV, and post antibiotics |
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Define Ludwig's angina.
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• Cellulitis, floor of mouth, surgical emergency, poor dental hygiene, extension of infection in mouth, floor of mouth into chest
• Infectious process involving the submental, sublingual, and submandibular species |
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Know the oral cavity lesions associated with systemic disease (table 16-1)
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• Some are infection, some aren’t infection
• Not infection=pigmentation of mouth=peutz-Jegher=hammertomatis polyps of GI tract;; also pigmentation with Addisons disease • Leukemia infiltrates with acute monocytic leukemia • Infections= scarlet fever (strawberry and raspberry tongue) • Measles, the oral lesions=Koplic spots opposite 2nd molar • Diphtheria: dirty white membrane on throat • Mono: exudates • HIV: thrush, candida, herpes simples, and hairy leukplakia • HIV association: aphthous ulcers, |
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Describe hairy leukoplakia as to cause and morphology.
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• EBV infection of tongue in someone with HIV
• Morph: filoform or hair like from lateral tongue • Predicts progression of HIV to AIDS • Immunosuppression;; White confluent patches of fluffy thickenings; |
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What is the significance of leukoplakia (standard type)? Erythroplakia?
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FIGURE 16-6 Leukoplakia. Clinical appearance of leukoplakias is highly variable and can range from (A) smooth and thin with well-demarcated borders, (B) diffuse and thick, (C) irregular with a granular surface, to (D) diffuse and corrugated.
• White plaque that doesn't scrap off (Thrush is in differential diagnosis ) • Precancerous or have cancer in it;; Biopsy it for leukoplakia • Erythoplakia=velvety, red plate plaque, has cancer in mouth and doesn't have to be in the red spot • Radiate the whole mouth |
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What is the pathogenesis/all causes of squamous cell carcinoma of head and neck/oral cavity? Three genes are frequently involved. Know these genes.
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• Identical to esophagus; Smoking and alcohol combined is pathogenesis (most important when combined)
• Two pathways: Cigarrette/ alcohol and the HPV pathway (which you don’t get in esophagus) • Genes: cyclin D , p16, p53 |
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Review the distribution of squamous cell carcinomas of head and neck; correlate with prognosis
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• Most common location is under tongue = 50/50 prognosis of death
• Lip is best prognosis and is associated with cigar and pipe or semite • Worst=tonsil region, oropharynx, base of tongue; further back is worse prognosis |
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What are the associations of :
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Dentigerous cyst=impacted molar
*Odontogenic keratocyst*=most important; associated with hereditary Gorlin syndrome or Nevoid basal cell carcinoma; cystic and lined by squamous epitheliuim (kerato part of name) Periapical cyst=caries, become abscesses |
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What are the name and morphology of the neoplasms and hamartoma of dental structures?
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• Ameloblastoma=neoplasm of dental apparatus, most in jaw, benign and malignant version, squamous, indulent, cystic
• Hamar: making a tooth, but it’s disorganized, odontoma |
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What are the associations and defining features of nasal polyps?
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• Atopic, allergic but don't' have asthma (except those associated with aspirin)
• Defining= Eosinophils, nonneoplastic polyps, allergies • Aspirin sensitive=nasal polyps, asthma when they ingest aspirin |
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What are the complications of rhinitis and sinusitis?
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• Can involve brain by direct extension (most serious that can happen)
• Sinusitis= associated with asthma |
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List necrotizing lesions of nose and upper airways.
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• Natural killer cell lymphoma, wagner, mutiform, aspergillus,
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Briefly describe important features of nasal/nasopharyngeal:
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Angiofibroma=unilateral, postpubertal male, recurrent nose bleeds
Inverted, Schneiderian Papilloma= benign, can grow into brain, aggressive Olfactory neuroblastoma= cribriform plate, aggressively malignant Solitary plasmacytoma=not associated with monoclonal gammopathy , curable with surgery |
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What are the associations of nasopharyngeal carcinoma?
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• High yield;; EBV, more common in Asia; squamous cells are malignant with intense lymphocytic infiltrate, extensive by the time diagnosis is made
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Describe laryngeal nodules as to pathogenesis and etiology.
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• Singers, From abuse of voice (cheerleaders, politicians), harsh, non neoplastic
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List causes and behavior of squamous papilloma of the larynx.
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• HPV, type 6 and 11
• In kids can reoccur and suffocate them, adults they are usually solitary and not a problem |
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What are the etiologic factors implicated in laryngeal carcinoma
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• (we already know from oral carcinoma and esophageal carcinoma); Smoking and drinking (together it’s most common); HPV rarely
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What is the clinical presentation behavior of intrinsic laryngeal carcinoma?
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• Horseness, intrisinic=has better prognosis than others
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List complications of otitis media? What is a cholesteatoma?
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• Mastoiditis, and cholesteatoma (cyst, lined by squamous epithelium, from ruptured tympanic membrane, epithelium grows and cyst enlarges, the mass can be destructive, it’s benign and non neoplastic)
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Describe otosclerosis as to clinical features, including etiology, and pathogenesis.
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• Conduction hearing loss, fuses to oval window and doesn’t vibrate anymore, acquired (abuse, rock concerts) and hereditary (autosomal dominant=adulthood, recessive=in youth)
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List two cysts of the neck. Describe location, morphology and clinical.
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• Lymphoepithelial/branchial: lateral at angle of jaw (young adults) ; midline cyst is thyroglossal tract cyst (shows up childhood to early adulthood)
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What are the derivation and other names of the carotid body tumor?
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• Carotid body tumor is a paraganglioma, chemodectoma, paraganglion cells= parasympathetic nervous system
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Define sialadenitis; sialothiasis and describe associations.
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• Siala = salivary gland;; sialadenitis = Inflammation of salivary gland
• Sialothiasis = stone in duct of salivary gland, rapid enlargement of thyroid when you salivate • Start with acute inflammation and end up with stone, or have a stone blocking the duct and end up with acute sialadenitis • Salivary enlarges rapidly in both and is painful • Chronic=autoimmune disease; sjorgens syndrome |
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Define mucocele and ranula. What is the cause?
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• Mucocele= trauma to salivary gland, cyst filled with mucus, (know picture of lip 16-15)
• Ranula = mucocele under the tongue, frog like from enlargement |
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List the most common tumors of the salivary gland. Which is most common? Which is the most common malignancy?
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• Most common pleomorphic adenoma, then warthin tumor, then mucoepidermoid carcinoma
• Adenoidocytic=malignant; acinic cell=malignant |
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Describe pleomorphic adenoma as to clinical, morphology, behavior.
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• Most common salivary gland tumor; common location= parotid; benign with tendency to recur with incomplete excision; with recurrence it's more aggressive; painless slow growing
• Morph: two cells type from single germ cell layer; mesenchymal (like cartilage) and gland areas |
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What are the associations and morphology of Warthin tumor?
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• Risk of bilaterality, benign, smoking, adult males;; Morph: Lymphocytes and oncocytes
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What are the morphology and clinical associations of mucoepidermoid carcinoma?
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• Most common malignancy, associated with radiation of head and neck, malignant gland=muco, epidermoid=malignant squamous cells
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List the associations of each of the following:
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Developmental disorders of the thymus
Hyperplasia of the thymus Thymomas What are the morphologic types of thymoma? |
