Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
161 Cards in this Set
- Front
- Back
|
study of the function of living things
|
physiology
|
|
|
study of mechanisms and processes of disease
|
pathology
|
|
|
the study of how normal physiological processes are affected by disease
|
pathophysiology
|
|
|
define normal statistically
|
95% +/- 2 SD
|
|
|
the extent to which an observation gives the same result when repeated
|
reliability
|
|
|
if a tool is measuring what it was made to measure the measurements can be considered...
|
valid
you wouldn't use a yard stick to measure the diameter of a penny |
|
|
the probability of a person with a disease testing positive for it
|
sensitivity
|
|
|
the probability of a person without a disease showing negative on the test
|
specificity
|
|
|
study of distribution of disease
|
epidemiology
|
|
|
the number of new cases arising during a specified time
|
incidence
|
|
|
the amount of existing disease at a specified time
|
prevalence
|
|
|
a term describing the effects of an illness on a person's life
|
morbidity
|
|
|
describe each level of prevention
|
primary-stop it before it starts
secondary- detect while still curable tertiary- prevent futher deterioration |
|
|
immunizations and population education would be considered what level of prevention
|
primary
|
|
|
pap smears would be an example of what level of prevention
|
secondary
|
|
|
the use of antibiotics or chemo therapy would be considered what level of prevention
|
tertiary
|
|
|
we use this value to determine the likelihood of differences between interventions occuring due to chance
|
P value; typically set at 0.05
|
|
|
list some factors that effect statistical significance
|
study population, size fo the effect, consistency of effect
|
|
|
list the steps of the epidemiologic process
|
define the problem, identify the cause, test the hypothesis, interpret the results
|
|
|
when interpreting the results of a study we should consider the possibility for these things
|
bias and confounding
|
|
|
what may cause bias in a study
|
flaws in study design, data collection, analysis, and interpretation
|
|
|
This question in a study could lead to what type of bias "Is your physician's judgment ever compromised by the use of drugs or alcohol?
|
informational bias
|
|
|
A study finding that gambling causes cancer probably has what issue
|
confounding; smoking causes cancer and occurs more often in populations that gamble
|
|
|
a disease arising abiogenically developed?
|
spontaneously
|
|
|
list several causes of cell injury
|
hypoxia, nutritional imbalance, physical, chemical, and infectious agents, genetic derangements
|
|
|
we can classify diseases as either developmental, inflammatory, neoplastic, and degenerative. Give a broad example of each
|
developmental- any genetic or congenital disease
inflammatory- trauma and infection neoplastic- cancer degen-ageing |
|
|
the father of modern pathology
|
Rudolph Virchow
|
|
|
steady state of a normal cell is referred to as
|
homeostasis
|
|
|
a cell can adapt to stress however if it does not these four things may happen
|
failure to maintain function, injury, maladaptive changes, and cell death
|
|
|
a shrinkage in size of a cell due to decreased workload, loss of innervation, inadequate nutrition, aging, and others
|
cellular atrophy
|
|
|
an increase in size, but not number of cells
|
hypertrophy
|
|
|
an increase in the number of cells
|
hyperplasia
|
|
|
a change in the type of cell as seen in the ciliated epithelium of the lungs of smokers, still reversible
|
metaplasia
|
|
|
deranged cell growth where the cells vary in size, shape, and organization, may be reversible, often a precursor to cancer
|
dysplasia
|
|
|
how does hypoxia injure cells
|
cells deprived of oxygen can no longer generate ATP or metabolize products
|
|
|
how do free radicals affect cells
|
may cause lipid peroxidation, oxidative modification of proteins, and target DNA
|
|
|
list four mechanisms of cellular injury
|
free radical formation
Hypoxia/ATP depletion disruption of calcium homeostasis membrane damage |
|
|
why are free radicals so reactive?
|
single unpaired electron in the outer orbit
|
|
|
a 5-10% decrease of ATP can cause disrupts in what vital processes
|
Na/K pump, Ca2+ and cell metabolism, protein synthesis
|
|
|
increased cytosolic Ca, loss of membrane phospholipids, and damage to cytoskeleton all may lead to what
|
membrane damage
|
|
|
for each cellular change say whether reversible or not:
atrophy hypertrophy hyperplasia dysplasia accumulations cell death |
atrophy-reversible
hypertrophy- reversible hyperplasia-reversible dysplasia- sometimes reversible accumulations-reversible cell death- not reversible |
|
|
meonpause is a physiological example of what cellular change
|
atrophy
|
|
|
faulty heart valves and hypertension are examples of what cellular change
|
pathological hypertrophy
|
|
|
liver regeneration and connective tissue in wound healing are examples of what cellular change
|
physiological hyperplasia
|
|
|
BPH and endometrial hyperplasia are physiological or pathological changes
|
pathological
|
|
|
collections of normal body substances or endogenous and exogenous products that the body cannot metabolize may lead to what
|
accumulations
|
|
|
fatty deposits on the liver and pigments like billirububin are examples of what type of accumulation
|
endogenous
|
|
|
the "blue man" has accumulations of colloidal silver. This is an example of what type of accumulation
|
exogenous
|
|
|
if a calcification occurs on dead tissue is is known as...
if it occurs on living tissue |
dystrophic
metastatic (usually due to poor metabolism) |
|
|
give an example of chemical asphyxiation
|
CO poisoning
|
|
|
what is so dangerous about the temperature extreme hypothermia
|
cellular metabolic processes are slowed and ice crystals that formed expand and destroy cells
|
|
|
what is so dangerous about hyperthermia
|
the heat denatures proteins and disrupts cell membranes
|
|
|
blast injury is a physical effect of what type of trauma
|
barotrauma
|
|
|
x rays, gamma rays, and A&B particles are examples of
|
ionizing radiation
|
|
|
infared and UV radiation are ionizing or non-ionizing
|
non-ionizing
|
|
|
describe the sequence of necrosis
|
membrane damage, lysosomal enzymes leak into cytoplasm, cellular contents leak out, inflammatory response initiated
|
|
|
this type of necrosis is characteristic of hypoxic injuries like ischemia and occurs due to acidosis
|
coagulative necrosis
|
|
|
this type of necrosis occurs when catalytic enzymes are active, typically in the brain, possibly after a stroke
|
liquefactive necrosis
|
|
|
when coagulative necrosis changes to liquifactive, most often due to loss of blood supply with subsequent infection
|
gangrenous necrosis
|
|
|
necrosis that produces soft-"cheese like" debris that persists indefinitely. Tuberculosis is a good example
|
Caseous necrosis
|
|
|
this type of necrosis is used to describe focal areas of fat destruction, fatty acids combine with calcium
|
fat necrosis
|
|
|
programmed cell death
|
apoptosis
|
|
|
list four factors that affect aging
|
Genes, diet, social conditions, and disease
|
|
|
how do cells age?
|
telomere shortening (programmed), accumlation of toxic byproducts, loss of repair mechanism, free radical injury
|
|
|
which types of cells are not subject to telomere shortening thus "immortal"
|
germ cells, cancer cells, and some stem cells
|
|
|
what enzyme is responsible for adding the repeat DNA to the 3' end, thus overcoming telomere shortening
|
telomerase
|
|
|
what are some practical uses of telomerase
|
expand cells for replacement therapies such as burns, inhibitors could selectively kill cancer cells
|
|
|
the deposition of brown atrophy pigments in vital organs
|
lipofuscin
|
|
|
the locking of actin and myosin the stoppage of calcium pumps results in what
|
rigor mortis
|
|
|
color changes associated with death are known as
|
livor mortis
|
|
|
functions to protect us from pathogens
|
immune system
|
|
|
3 R's of immune system
|
recognize intruders, respond to the threat, and remember them for a quicker attack next time
|
|
|
foreign proteins that stimulate an immune response
|
antigens
|
|
|
proteins made in response to exposure to foreing antigen
|
antibodies
|
|
|
these plasma cells develop in the bone marrow and make antibodies specific to each antigen
|
B cells (CD8)
|
|
|
these cells develop in the thymus and attack foreign and infected cells
|
t cells (CD4)
|
|
|
disease causing microorganism
|
pathogen
|
|
|
the skin, mucous, and HCL are example of what line of defense
|
innate- 1st line: non-specific barriers
|
|
|
inflammation, fever, phagocytosis, and complement are examples of what line fo defense
|
innate-2nd line: non-specifc at the cellular level
|
|
|
antibodies, b/t cells, phagocyctosis, and complement are examples of what line of defense
|
adaptive- 3rd line: specific and non specific
|
|
|
the fast, natural resistance we are born with is known as
|
innate resistance
|
|
|
the slower but more specific immunity we have that shows memory
|
adaptive/acquired immunity
|
|
|
list the five steps of inflammation
|
initial phagocytosis-> releases cytokines starting process, capillaries dilate and become more permeable (due to histamine), the foreign matter is contained, more leukocytes migrate to the area, leukocytes clear infection
|
|
|
list the four hallmarks of inflammation
|
rubor- redness (vasodilation)
calor- heat (vasodilation) tumor- swelling (edema) dolor- pain (kinins acting on neural receptors) |
|
|
what is the most common WBC
|
neutrophils (pmn's)
|
|
|
steps of chemotaxis
|
cytokines cause cells to move in, neutrophils arrive first (1hr), then macrophages (10hrs), macrophages display so that tissue macs migrate
|
|
|
cytokines traveling to the bone marrow accomplish what
|
stimulation of leukocyte proliferation
|
|
|
fever is mediated through what
|
hypothalamus
|
|
|
this cytokine activates vascular endothelium and increases vascular permeability leading to fever and mobilization of the shock metabolites
|
TNF alpha
|
|
|
this cytokine is responsible for lymphocyte activation, induces fever and acute phase proteins from the liver
|
IL6
|
|
|
this acute phase protein binds to bacterial surfaces, opsonizing and activating the complement cascade
|
C reactive protein
|
|
|
list the roles of complement proteins
|
poke holes in bacteria via MAC
stimulate histamine release opsinization |
|
|
who are the key players in our third line of defense
|
macrophages and the lymphocytes
|
|
|
these players in cell mediated immunity active B cells, T cells and macrphages
these are the "killers of the group |
T helper (CD4) cells
Tc (CD8) cells |
|
|
thse cells produce antibodies
|
B cells
|
|
|
why is HIV so devastating
|
it targets CD4 cells, the "traffic cops" of the immune system, none of the other players can be activated without these guys
|
|
|
this antigen is the most common in primary response and cannot cross the placena due to its size
|
IgM
|
|
|
This antibody is all but useless
|
IgD
|
|
|
This antibody is the most common in the blood and can cross the placenta thus is responsible for fetal immunity
|
IgG
|
|
|
This antibody is involved in allergies and is responsible for triggering histamine release
|
IgE
|
|
|
This antibody crosses mucousal sufaces and is secreted in breast milk
|
IgA
|
|
|
the universal blood donor
|
O-
|
|
|
the universal blood recipient
|
AB+
|
|
|
What should we be concerned about when an RH- woman is giving birth
|
If the Baby is RH+ and this is NOT the first birth the mother might have antibodies to the Baby's blood
|
|
|
this immune response requires weeks after 1st exposure to develop, IgM is developed followed by IgG
|
primary response
|
|
|
this immune response requires days to occur if it has been previuosly exposed. The response magnitude is greater then the primary response due to the presence of memory cells
|
Secondary response
|
|
|
this response is responsible for long term immunity, IgG response is largest
|
Secondary
|
|
|
most immunizations are examples of what type of immunity
|
passive artificial
|
|
|
immunity passed from mother to child is what type
|
passive natural
|
|
|
immunity gained from an attenuated virus vaccination is what type
|
active artificial
|
|
|
immunity gained from an actual infection is what type
|
active natural
|
|
|
anaphylaxis, asthma, and hay fever, occuring in minutes are examples of what type of hypersensitivity reaction
mediated by what |
Type I immediate
IgE |
|
|
transfusion reactions and hemolytic disease of the newborn are examples of what type of hypersensitivity reaction
mediated by what |
Type II cytotoxic
complement-IgG, IgM |
|
|
serum sickness, vasculitis, and arthus reaction are examples of what ype of hypersensitivity reaction
mediated by what |
Type III immune complex
immune complexes |
|
|
cutaneous hypersensitivity (poison oak) and graft rejections are examples of what type of hypersensitivity reaction
mediated by what |
Type IV delayed
sensitized lymphocytes |
|
|
the primary hypersensitivity response (initial phase) is characterized by what
|
vasodilation
vascular leakage smooth muscle contraction |
|
|
The secondary/late phase hypersensitivity response is characterized by what
|
eosinophil and inflammatory cell infiltration
tissue destruction |
|
|
pt reports with fever, chills, dark urine, chest and flank pain after leg surgery. What do you suspect?
|
transufusion reaction due to wrong blood type given during the surgery
|
|
|
newborn turns orange after birth, why should you be concerned
|
may be Kernicterus
the baby's liver is not able to process billirubin and may cause damage to brain |
|
|
this hypersensitivity reaction is not antibody mediated and is associated with contact dermatitis
|
Type IV- delayed
|
|
|
what type of infection is most often associated with neutrophillia
|
bacterial
|
|
|
what type of infection is most often associated with lymphocytosis
|
viral infections
|
|
|
what is shift to the left?
|
the presence of immature WBC due to overwhelming infection
|
|
|
what is the purpose of inflammation
|
eliminate the cause of injury and necrotic cells and tissues,
initiate healing and reconstruction |
|
|
what can cause inflammation
|
trauma, surgery, caustic chemicals, extreme temps, ischemia, immune response
|
|
|
this type of inflammation is the nonspecific, immediate response to injury and serves as a precursor to the immune response
|
acute inflammation
|
|
|
what are some difference between the effects of inflammation on internal organs and systemically
|
internal organs only have pain associated if there are receptors and there is no rise in temp
|
|
|
what are the two components of acute inflammation
|
the vascular and cellular stages
|
|
|
this stage of inflammation begins immediately, leads to congestion in the area, increased cap permeability, and exudation
|
vascular stage
|
|
|
this stage of inflammation begins when phagocytotic WBCs move into the area of injury and chemical mediators are released from sentinel tissue
|
cellular
|
|
|
basophils, neutrophils, and eosinophils are categorized as
|
granulocytes
|
|
|
these are the primary phagocytes, their granules resist staining and contain degrading enzymes and antibacterial substances
|
neutrophils
|
|
|
these cells stain red with acid dyes, are present in allergic responses, and granules contain proteins that are toxic to large parasitic worms
|
eosinophils
|
|
|
these cells stain blue with basic dyes. Thier granules contain histamine and other mediators of inflammation
|
basophils
(mast cells don't have granules) |
|
|
largest WBC, antigen presenting cell
|
monocyte
|
|
|
these are monocytes that have migrated to tissue and matured, they engulf foreing materials then migrate to lymph nodes
|
macrophages
|
|
|
these cells are present in mucousal surfaces and have a wide distribution in connective tissues. They are armed with IgE
|
Mast cells
|
|
|
Phases of leukocyte response
|
margination (chemcal release)
Emigration (movement into tissue, may be accompanied by RBC) chemotaxis (cytokine trail for other cells to follow) Phagocytosis |
|
|
this inflammatory mediator can cause smooth muscle relaxation, platelet antagonism, decrease leukocyte recruitment, and kill microbial agent
|
Nitric oxide
|
|
|
this inflammatory mediator is released in response to trauma and immune reactions involving IgE. High levels in circulatory platelets, basophils, and mast cells. Causes dilation and cap permeability
|
histamine
|
|
|
these inflammatory mediators cause increased cap permeability and PAIN
|
the kinins
|
|
|
Three types of plasma proteases that play a role in inflammation
|
kinins, activated complement proteins, and clotting factors
|
|
|
which arachidonic pathway leads to prostaglandins
to leukotrienes |
protaglandins= cyclooxygenase
leuko= lipoxygenase |
|
|
When you tell a patient to take aspirin, which pathway is being blocked
|
cyclooxygenase cannot produce prostaglandins
|
|
|
where do corticosteroids interact with inflammatory mediators
|
they prevent arachidonic metobolites from being produced
|
|
|
these AA metabolites induce inflammation, increase the effect of histamine, promote platelet aggregation, and vasodilation
Aspirin and other NSAIDS inhibit |
prostaglandins
|
|
|
these AA metabolites have complimentary function to histamine and induces smooth muscle contraction
|
leukotrienes
|
|
|
list the chemical mediators responsible for swelling, redness, and warmth
|
histamine, prostaglandins, leukotrienes, bradykinins, paf
|
|
|
list the chemical mediators responsible for tissue damage
|
lysosomal enzymes released from neutrohils and macrophages
|
|
|
list the chemical mediators responsible for chemotaxis
|
complement fragments
|
|
|
list the chemical mediators responsible for pain
|
prostaglandins and bradykinins
|
|
|
list the chemical mediators responsible for fever
|
IL-1, IL-6, TNF alpha
|
|
|
infiltration of macrophages and lymphocytes instead of neutrophils is a characteristic of
|
chronic inflammation
acute will have neutrophils |
|
|
list some agents of chronic inflammation
|
foreing bodies, low virulence pathogens, injured tissue (ie around a fracture)
|
|
|
type of inflammation that has mass of macrophages surrounded by lymphocytes, encapsulates foreign body
|
granulomatous inflammation
|
|
|
list characteristics of each exudate
serous hemorrhagic fibrinous membranous |
serous- watery fluid w/ low protein count
hemorrhagic- presence of RBC fibrinous- large amounts of fibrinogen forming thick sticky meshwork membranous- necrotic cell enmeshed in fibropurulent exudate (think pimples) |
|
|
a localized area of inflammation containing purulent exudate, typically has central necrotic core surrounded by layer of neutrophils
|
abcess
|
|
|
this protein is considered anti inflammatory and is responsible for neutralizing cytokines, proteases, and oxidants, levels rise in acute inflammation
|
c reactive protein
|
|
|
mast cell -> histamine, bradykinin, and lysosome components are mediators of acute or chronic inflammation
|
acute
|
|
|
t-lymphocytes, marcophages, and cytokines are mediators of acute or chronic inflammation
|
chronic
|
|
|
non-digestible organisms and non degradable foreing matter are likely to induce chronic or acute inflammation
|
chronic
|
