Patho Exam 1

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141 Terms

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pathophysiology
study of abnormalities in physiologic functioning of living beings
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etiology
causes or reasons of disease
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pathogenesis
development or evolution of disease, from initial stimulus to ultimate expression of manifestations of the disease
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clinical manifestations
signs, symptoms, stages, and course
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idiopathic
cause is unknown
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iatrogenic
cause results from unintended or unwanted medical treatment
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sign
objective or observed manifestation of disease obtained by: clinical examination, laboratory tests, diagnostic imaging
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symptom
subjective feeling of abnormality in the body
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risk factor
factor that when present increases the likelihood of disease
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Latent stage
time between exposure of tissue to injurious agent and first appearance of signs and/or symptoms

can also refer to period during an illness when signs/symptoms temporarily become mild or silent or disappear
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subclinical stage
patient functions normally; disease processes are well established
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prodromal stage
time during which first signs and/or symptoms appear indicating onset of disease. Often nonspecific
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acute stage
disease/illness reaches its full intensity, short lived, may have severe manifestation
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chronic stage
may last months to years, sometimes following an acute course
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convalescence
stage of recovery after a disease, injury, or surgical procedure
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sequela
subsequent pathologic condition resulting from an illness
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exacerbation
sudden increase in severity of disease or signs or symptoms
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remission
decrease in severity, signs, or symptoms; may indicate disease is cured
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test sensitivity
probability that a test will be positive when applied to a person with a particular condition; failures are false negatives
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test specificity
probability that a test will be negative when applied to a person without a particular condition; failures are false positive
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validity
degree to which a measurement reflects the true value of what it intends to measure
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reliability
test’s ability to give the same results in repeated measurements
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predictive value
extent to which a test can differentiate between presence or absence of a person’s condition

negative value = probability disease is absent if test is negative

positive value = probability disease is present if test is positive
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endemic disease
native to a local region
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epidemic disease
spread to many people at the same time
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pandemic disease
spread to large geographic areas
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primary prevention
altering susceptibility or reducing exposure for susceptible persons
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secondary prevention
early detection, screening, and management of disease
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tertiary prevention
rehabilitation, supportive care, reducing disability, and restoring effective functioning
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reversible
is withstand response reversible or irreversible
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reversible
is adapt response reversible or irreversible
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irreversible
is cell death response reversible or irreversible
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reversible cell injury
hydropic swelling and accumulation of substances in cells
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hydropic swelling
cellular swelling because of accumulation of water; first manifestation of most forms of reversible cell injury
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Accumulation of substances in cells
o   Leads to injury due to toxicity, immune response, and taking up cellular space needed for cellular function

o   Caused by abnormal metabolism, defect in folding and/or transport of proteins to the outside, lack of enzyme to break substance down, ingestion of indigestible materials
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atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia
5 cellular adaptation mechanisms
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atrophy
Cells shrink and reduce their differentiation functions in response to normal and injurious factors in an effort to minimize energy consumption
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hypertrophy
Increase in cell mass accompanied by an augmented functional capacity in response to physiologic and pathophysiologic demands, usually due to increased cellular protein content
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hyperplasia
Increase in functional capacity related to an increase in cell number because of mitotic division, usually in response to increased physiologic demands or hormonal stimulation

only occur in cells capable of mitotic division
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metaplasia
conversion of one cell type to another, usually due to adaptation to persistent injury
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dysplasia
disorderly growth

disorganized appearance of cells because of abnormal variations in size, shape, and arrangement
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irreversible cell injuries
necrosis and apoptosis
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necrosis
cell rupture, spilling of contents into extracellular fluid, inflammation
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Apoptosis
occurs from injury that does not directly kill the cell but triggers
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coagulative, liquefactive, fat necrosis, caseous necrosis, gangrene
5 types of necrosis
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coagulative necrosis
most common type of necrosis

process that begins with ischemia, affected area is composed of degenerated proteins and relatively solid
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liquefactive necrosis
Rapid dissolution of dead cells by lysosomal enzymes, forms abscess or cyst from dead tissue
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fat necrosis
death of adipose tissue, usually due to trauma or pancreatitis; appears as a chalky white area of tissue
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caseous necrosis
characteristic of lung damage due to tuberculosis, resembles clumpy cheese
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gangrene
cellular death in a large area of tissue, resulting from interruption of blood supply to a particular part of the body
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dry gangrene
form of coagulative necrosis

characterized by blackened, dry, wrinkled, tissue separated by a line of demarcation from healthy tissue
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wet gangrene
form of liquefactive necrosis typically found in internal organs, can be fatal
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gas gangrene
results from infection of necrotic tissue by anaerobic bacteria like clostridium

characterized by formation of gas bubbles in damaged muscle tissue – can be fatal
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Apoptosis
occurs from injury that does not directly kill the cell but triggers “suicide,” no rupture, no inflammation, neighboring cells ingest
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externally triggered apoptosis
removal of survival signals
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internally triggered apoptosis
DNA damage beyond repair

Mitochondrial damage

high levels of p53 protein
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Cellular basis of aging
Cell death exceeds cell replacement due to progressive decline in proliferation and reparative capacity of cells and exposure to environmental factors
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ischemia and hypoxic injury
combination of disruption of oxygen supply with accumulation of metabolic waste
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ischemia
most common cause of cell injury and injures cell faster than hypoxia alone
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Nutritional injury
deficiency of fats, carbs, proteins, vitamins, or minerals needed for normal cellular function
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Infectious and Immunologic injury
o   Bacteria release exotoxins, endotoxins, or trigger body’s immune response

o   Viruses replicate inside cells and cause cell injury, some viruses can make immune system kill the cell (Hepatitis B)
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Chemical injury
toxic chemicals, poisons, or pollutants either directly injure cell or become metabolized into reactive chemicals by the body
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physical and mechanical injury
extremes in temperature, abrupt changes in atmospheric pressure, mechanical deformation, electricity, ionizing radiation
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chromosomal abnormalities
abnormal number of chromosome or alterations to structure of one or more chromosomes usually from errors of separation during meiosis
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mendelian single gene disorders
result from alterations or mutations of single genes; majority are inherited from parents
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non-mendelian single gene disorders
disorders in 3 categories: long triplet repeat mutations, mitochondrial DNA mutations, gnomic imprinting
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polygenic and multifactorial disorders
traits that develop in response to more than one gene; do not follow clear mode but tend to run in families
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autosomal aneuploidy
what are down syndrome, edwards syndrome and patau syndrome an example of
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aneuploidy and abnormal structure
categories of chromosomal abnormalities
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sex chromosome aneuploidy
what are klinefelter syndrome and turner syndrome an example of
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deletion, translocation, duplication, and inversion
4 types of abnormal chromosome structures
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deletion
cry du chat syndrome is an example of what
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autosomal dominant, autosomal recessive, and sex-linked
3 types of mendelian single gene disorders
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autosomal dominant
what are marfan syndrome and huntington disease an example of
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autosomal recessive
what are albinism, phenylketonuria, and cystic fibrosis an example of
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non-mendelian gene disorder
what is fragile X syndrome (FMR1) gene an example of
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teratogens
factors/agents that cause congenital malformations
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before third week
exposure either damages very few cells or so many that embryo can’t survive
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3-9 weeks
embryo very susceptible to teratogenesis, especially during organ development (4th and 5th week)
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after third month
affect growth or injury to already formed organs
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bengin
o   Does not have potential to kill host (may be life-threatening due to location)

o   Does not invade adjacent tissue or spread to distant sites

o   Many are encapsulated

o   More closely resembles original tissue type

o   Grows more slowly

o   Little vascularity

o   Rarely necrotic

o   Often retains original function
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malignant
o   Can kill host if untreated

o   Invades other tissues and spreads

o   Tissue-specific differentiation

o   Little resemblance to original tissue

o   Grows rapidly

o   May initiate tumor blood vessel growth (angiogenesis)

o   Frequently necrotic

o   Dysfunctional
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adenoma
benign - epithelial origin
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carcinoma
malignant - epithelial cells
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sarcoma
malignant - connective tissue
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leukemia
malignant - wbc
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malignant
lymphoma
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malignant
hepatoma
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malignant
melanoma
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benign
most -omas
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malignant
\-sarcoma

\-carcinoma
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tumor suppressor genes
loss of function genes; mutation causes underactivity of gene
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tumor supressor genes
* Rb Gene
* P53 Gene
* BRCA1 and BRCA2 Genes
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proto-oncogenes
gain-of function genes; mutation causes overactivity of gene
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growth factors (mitogens)
small cell-manufactured peptides secreted into extracellular space. They interact with receptors on target cell surface activating a signaling cascade that can produced excessive self-stimulated growth
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growth factor receptors
mutations cause excessive responsiveness by expressions of receptors that should not be there at all, excessive amounts of normally present receptors, and receptors with abnormally high affinity
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growth factor receptors
HER-2 is example of what
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cytoplasmic signaling molecules
making of excessive or abnormal components of intracellular signaling pathways; mutant proto-oncogenes can activate pathway even when no signal is received at cell surface
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transcription factors
proteins that must be assembled at the promoter area of genes begin gene transcription; mutation may cause overproduction of transcription factors or interfere with normal function of keeping them in check
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growth factors

growth factor receptors

cytoplasmic signaling molecules

transcription factors
4 types of proto-oncogenes