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68 Cards in this Set

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