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68 Cards in this Set
- Front
- Back
Specific pathological condition
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Disease
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What causes the disease
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Etiology
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What the patient experiences, subjective
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Symptom
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Objective parameter, usually quantitative, that another observer will find
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Sign
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Cluster of indications
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Syndrome
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Not normal with a particular disease
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Complication
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Normal, anticipated events that are associated with disease
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Sequelae
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Sequence of events that lead to the disease signs and symptoms
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Pathogenesis
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predicting outcomes
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Prognosis
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The total number of cases of a particular disease at one point in time
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Prevalence
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Rate, the amount of number of cases over a period of time
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Incidence
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Rapid onset, short duration
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Acute
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Generally progressive, long lasting disease state
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Chronic
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The death rate
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Mortality
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An event or sign or symptom that influences daily activities
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Morbidity
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Tightly regulated, programmed cell death; no inflammatory response
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Apoptosis
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Unregulated, enzymatic digestion of a cell; inflammatory response
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Necrosis
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Decreased cell size
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Atrophy
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Increased cell sizenty
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Hypertrophy
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Increased number of cells
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Hyperplasia
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One cell type replaced by another cell type
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Metaplasia
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deranged cell growth with differing size, shape, appearance
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Dysplasia
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Anything/person capable of sustaining growth of another organism
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Host
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Presence of an organism in or on a host; not all are detrimental
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Infection (colonization)
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Disease producing potential
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Virulence
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High virulence, always associated with disease
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Pathogen
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Normally not disease producing, but able to produce disease in immune compromised hosts
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Opportunistic pathogens
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Consequences of viruses
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Cell lysis
Latency Oncogenesis |
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Cocci
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Spherical
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Spirilla
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Helical
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Bacilli
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Elongated, rod-shaped
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Spirochetes
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Cork screw rods, movement
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Rickettsiae
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Infect arthropods transmitted via bites
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Rickettsiae and chlamydiae
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Obligate intracellular pathogens
Rigid cell wall, asexual reproduction, containing RNA and DNA (like bacteria) |
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Fungi
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Eukaryotic, normal human microflora
Usually self-limiting infections Rarely systemic disease |
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Dermaphytes
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Infection limited to skin
Superficial mycoses - ring worm, athlete's foot Systemic mycoses - transplant patient |
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Yeasts
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Normal flora of skin, GI tract, mucosa
Immune and bacterial competition keep them in check Upset in balance = overgrowth |
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Protozoa
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Unicellular with nucleus and organelles
Direct, indirect, and arthropod transmission |
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Helminths
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Worm-like, reproduce asexually
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Ectoparasites
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Infest skin, local inflammation
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Mechanisms of entry
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Penetration
Direct contact Ingestion Inhalation |
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Protracted, irregular course
Continuous or sporadic for months/years Without adequate/complete convalescent period |
Chronic infection
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Progression of infection is resolution without symptoms
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Subclinical disease
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Protracted (prolonged) prodromal stage
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Insidious disease
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Abrupt onset of symptoms with little/no prodromal stage
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Fulminant infection
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Proteins released from pathogen
Modifies/inactivates cell function or death |
Exotoxin
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Lipid and polysaccharides of cell wall
Potent activators/inducers |
Endotoxins
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How do capsules, mucous layers aid immune evasion?
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Decrease phagocytosis
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How do toxins aid immune evasion?
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Destroy phagocytic cells
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How do proteins aid immune evasion?
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Decrease antibody recognition
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How do altered cell membrane antigens aid immune evasion?
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Decrease immune recognition
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Humoral immunity
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B lymphocytes and antibodies
Primarily extracellular pathogens |
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Cell mediated immunity
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T lymphocytes
Primarily for intracellular antigens |
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Antibody effector functions
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Neutralization
Opsonization Antibody dependent cell-mediated cytotoxicity Complement activation |
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"Coating" of antigen by Ig increases efficiency of phagocytosis via Fc recfeptors on phagocytic cells
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Opsonization
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Punches hole in cell membranes
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Membrane attack complex
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Mediators of local inflammation, chemotactic for PMN, macrophages, otehrs
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By-products of complement
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Inadequate immune response
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Immunodeficiency
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Hypersensitivity reactions, autoimmune diseases
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Excessive immune response
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Autoimmune diseases
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Decreased tolerance to self antigens
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Inadequate immune response = infection
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Increased tolerance to foreign antigens
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Principle cells involved in Type 1 Hypersensitivity
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Mast cells
CD4+ T helper cells |
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Type II hypersensitivity is directed against:
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Cell surface antigens
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Type III hypersensitivity
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Immune-complex mediated
Insoluble Ag-AB complexes (where they settle) |
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Type IV hypersensitivity is mediated by
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Sensitized T cells
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Environmental factors for autoimmunity
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Decreased anergy
Release of normally sequestered antigens Molecular mimicry Superantigens |
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Graves Disease
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B cells produce thyroid stimulating IgG which mimics TSH;
Increase T3/T4 from thyroid |
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Myasthenia gravis
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Auto-antibodies against nicotinic receptors in NMJ
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