Test 1: lecture 8 circulatory disturbances Flashcards
function of circulatory system
Deliver nutrients to & remove waste products from cells
Circulate fluid & cells to maintain homeostasis & integrate function
breakdown of water inside the body
what is the outward pressure in blood vessels
hydrostatic
what is the pull caused by proteins called
osmotic pressure
fluid accumulation in tissues
edema
fluid accumulation in body cavities
effusion
Imbalance between intravascular & interstitial compartments cause ____
fluid accumulation in the interstitium
what does edema look like microscopically
4 causes of edema/effusion
increased vascular permeability
- increased intravascular hydrostatic pressure
- decrease plasma colloid osmotic pressure
- decrease lymphatic drainage
an increase or decrease in osmotic pressure would cause edema
decrease (osmotic pressure pulls fluid back into the blood vessels)
how does inflammation cause increased vascular permeability?
local release of inflammatory mediators such as histamine, bradykinin and leukotrienes
increased hydrostatic pressure is due to ___
increased blood volume in microvasculature
(localized or generalized)
due to impaired venous outflow
increased intravascular hydrostatic pressure is usually due to impaired ___
venous outflow (passive congestion)
2 common ways to have low protein
protein loss through the kidneys or GI
or decreased protein synthesis due to liver failure or poor nutrient
hypoproteinemia causes ___ plasma colloid osmotic pressure
decreased → leads to edema
edema caused by low osmotic pressure is usually generalized or local?
generalized (all over decrease in protein, either from loss or from decreased synthesis)
what are some causes of decreased lymphatic drainage
Compression or blockage due to trauma, fibrosis, invasive neoplasms, infectious agents, or congenital malformation (rare)
lymphatic obstruction would increase or decrease lymphatic drainage
decrease (blockage in vessel prevents it from carrying away lymph)
where are two places edema is bad
cerebral and pulmonary/thoracic
(have no place to swell)
primary hemostasis is mediated by ___
platelets
secondary hemostasis is mediated by ___
clotting factors
what happens during primary hemostasis
vasoconstriction→ tries to reduce size of injury
collagen in wall of vessel exposed and triggers vWF to cause platelets to bind and clump
what happens during secondary hemostasis
tissue factor cause coagulation cascade → thrombin formation which leads to fibrinogen into fibrin
___ is blood loss from the
circulatory system
hemorrhage
3 causes of hemorrhage
blood vessel injury
decreased platelets
decreased clotting factor
decreased number of platelets can be caused by
platelets not being made, not working right or being destroyed or used up
decreased production of platelets
increased consumption/destruction
decreased function
what kind of cells make most clotting factors
hepatocyte in the liver
many clotting factors are vitamin ___ dependent
K
needs to be recycled
hemorrhage is bad where?
___ is inappropriate clotting within the circulatory system
thrombosis
aggregate of platelets, fibrin, & other blood elements formed on
a vessel or heart wall
thrombus
If a thrombus (or fragment of a thrombus) breaks loose and enters the circulation, it becomes a ____
thromboembolus
when a piece of a blood clot breaks off and travels it is called a ___
thromboembolus
embolus
any mass (solid, liquid, or gas) carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or necrosis
___ = any mass (solid, liquid, or gas) carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or necrosis
embolus
embolism
(bone marrow in lung tissue)
what do thrombi look like
dull, rough, red/tan, friable
laminated
can be occlusive or non occlusive
difference between thrombi and postmortem blood clot
thrombi: dull, rough, red/tan, friable, laminated
postmortem: shiny, smooth, gelatinous
thrombi or post mortem clot?
thrombi → dull, rough, red/tan, friable
3 sides of virchow’s triad
endothelial injury, abnormal blood flow and hypercoagulability are all part of ___
virchow’s triad
(cause a clot)
If thrombosis is widespread, it can lead to a ___ & subsequent ___
consumptive coagulopathy
hemorrhage
(DIC- too much clotting, use up all the factors, flips and leads to uncontrolled bleeding)
Systemic ____influences help maintain adequate blood flow to the tissues
neural & hormonal
____= active engorgement of a vascular bed due to vasodilation & increased flow
hyperemia
passive engorgement of a vascular bed due to decrease outflow
congestion (blood not draining well)
hyperemia vs congestion
hyperemia: active increase of blood to an area→ vasodilation and increased blood flow
congestion: decrease in blood draining (passive) (CHF or obstruction)
CHF is an example of hyperemia or congestion
congestion (passive inability to move blood out)
blood pooling
grossly what does hyperemia look like
warm and bright red due to increased oxygenated blood to an area
(running get flushed)
grossly what does congestion look like?
cool and dark red/purple
pooling of deoxygenated blood
stagnation
Inadequate tissue perfusion
ischemia
ischemia
decreased blood flow caused by obstruction, congestion or decreased cardiac output
what three things happen during ischemia
decreased O2 delivery
decreased nutrient delivery
decreased waste removal
what organs are most susceptible to ischemia
brain and heart
high O2 need and poor collateral circulation
area of tissue necrosis due to ischemia
infract
cell death of tissues due to decreased blood flow
acute/subacute phase of infarct look ___
wedge shaped
swollen and dark red (hemorrhagic) or tan
chronic infracts grossly look ___
depressed, tan and firm
tissue has been replaced by fibrous material that shrinks during healing