Homeostasis and Disease Flashcards
Pathological process
disease process, loss of homeostasis, which really forms the basis of most of the disease processes
Pathologic stimuli can be
intrinsic or innate coming from the environment-external exposures, deprivations, nutritional
Cellular adaptation
Cells are able to compensate for challenges to homeostasis through a dynamic set of processes
Cellular injury
When cell doesn’t regain homeostatsis
regulated Variables
have a physical receptor Temp, BP, glucose keep are body wnl
stimulus or signal
Afferent
means towards, consists of nerves for neurological signals and blood for endrocrine
Integrating center
hypothalmus, cardiovascular and respiratory control,compares info to a range.
Efferent pathway
carries a response towards exit out, towards periphery.
Controlled variables
Heart rate, vaso const, vaso dilate also, known as effector response
Negative feedback
bringing things back to original signal
Receptors are
thermo, baro-bp, chemo, osomo,mechanoreceptors.
regulated variables are the…
Anchor
Patho
disease causing
Genetic causes
may be inherited
Mutations
genetic changes
Acquired mutation
environmental trauma, intoxication, or deficiency- nutritional or absence of a metabolite.
Diseases usually require both
genetic and environmental
Proteins are impacted in order to
cause a disease state
Disease process causes.
inflammation, aberrant immune response.
etiology
underlying cause of disease
Metobolic and Morphological
hallmarks of disease
Severity and Duration determine
outcome
trauma, deficiency are
external, intox, deficiency
Cell injury can be
hypoxic lack of o2, hypoxic injury. emia means bld
Ischemia
insufficient bld flow
oxygen most efficient
energy prod, o2 bound to hemoglobin
Aerobic metabolism releases
lactic acid
Acids are
denaturing causing cell injury and death.
oxidative damage
One of the things that can be produced during normal metabolism is what are called reactive oxygen species or ROS
ROS
unpaired oxygen molecules that produced superoxides
ROS are produced
clean up and inactive
Excessive ROS
leads to oxidative stress
oxadative molecules come from
bursts, which are immature immune cells.
Macrophages and neutrophils are considered
bursts
Bursts are produced
from immature immune cells
Macrophages and neutrophils
try to kill off microbes
Superoxides have
unpaired electrons
Unpaired electrons interact with
protein and lipids
Unpaired electrons
damage protein and lipid cell membranes, causes cell damage under oxadative stress.
A cell can
reverse it’s course
Influx of CA+ =
cell death
hypoxia
lack of oxygen
Ischemia
reduction in bld flow
hypoglycemic state
required for good energy production
Aerobic - Anaerobic +
lactic acid
Lactic acid is
denaturing
Denaturing leads to
cell death
In a lactic acid state we have
decrease ph, that causes damage to lipids and proteins that protect cell membrane.
In anerobic conditions we
have decrease ph, and damages the cell.
Limited ATP in anerobic state
contributes to impair cell function.
Thrombus in a bld vessel is an example of
decrease oxidative phosphorylation and increase in our anaerobic process like glycolysis
End of glycolysis
under anaerobic conditions produces lactic acid.,decrease ph hat leads to denaturing, which can be seen as clumping of nuclear material like the chromatin and eventually, can lead to the breakdown of lipids in the lysosomes, which are bags of basically degradative enzymes inside of cells. And that can lead to the autodigestion or autolysis, sometimes called autolysis of the cell itself.
chromatin
clumping
lipids break down into
lysomes
lysomes
degradative enzyme inside cell, known as autolysis
Autolysis
degeneration of the cell
oxidative phosphorylation running at its full speed,
we will have a reduction in the amount of ATP that can be produced. And this is going to compromise a lot of the barriers at the membrane, such as our sodium-potassium ATPase.
Water
causes cell to swell
blebs
extension on the cell
oranelles inside cell
swell
Depending on
degree maybe reversible
Lysosomal enzymes released
causes impairment to cell membrane, ca+ comes in now=irreversable cell injury=cell death.
ROS is an ex of
superoxide
Superoxides are
free radicals
SOD converates to
superoxide and into hydrogen peroxide.
Catalase
released from opening cells acting on hydrogen peroxide-water and oxygen seeing bubbles is an evidence of catalase reaction
Refusion injury
plagues settings of transplant when we’re actually transplanting organs and tissues and that tissue is deprived for an extended period of time from blood, therefore for oxygen.
What happens is we start to see an excessive amount of reactive oxygen species being produced by those cells. And over time, we’re going to have a depletion of our cleanup system. So our SOD and catalase protection system becomes depleted.
reperfusion injury specialists that look at after transplant is that when we reperfuse that tissue, there’s an anticipation that we’re going to have additional cellular injury and potentially cell death. A
And that’s because these reactive oxygen species are produced right away, but our cleanup systems are actually delayed in getting to their full speed. So that can lead to some cellular injury or damage, and that’s referred to as reperfusion injury.
reprefusion injury is
combo of extra oxidative stress and oxidative damage
Infusing antioxidants
like superoxide dismutase or catalase to reestablish our clean up system.
Reprefusion injury occurs during
transplants and stroke
Glucose 6-phospate dehdrogenese
is a genetic mutation causing reprefusion injury
Fava beans
an example of extra oxidative stress
Extra oxadative stress
can lead to cell injury and cell death
death knell
influx of CA+
Physical injury can compromise
the cell directly
alteration in CA+ pump, altered electrolyte can
impair the pump and cause alteration in calcium homestatsis
