lecture 1- hemodynamic disorders Flashcards
delivers oxygen and nutrients to tissues
wastes are removed
circulation
blood clotting that prevents excess bleeding after blood vessel damage
hemostasis
inappropriate clotting
thrombosis
migration of clots
embolism
active process, arteriolar dilation and increased blood inflow
hyperemia
oxygenated hemoglobin
red color (hyperemia)
passive process, impaired outflow of venous blood from a tissue
congestion
deoxygenated hemoglobin
blue/red (cyanosis) (congestion)
__% of body weight is water
2/3 intracellular
only ___% blood plasma
60% water
5% blood plasma
accumulation of interstitial fluid in tissue
edema
two types of edema
effusions
anasarca
extravascular fluid that collects in body cavities
pleural cavity- hydrothorax
pericardial cavity- hydropericardium
peritoneal cavity- hydroperitoneum or ascites
effusions
seve generalized edema due to fluid retention in tissues and cavities
anasarca
vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins) dictate fluid movement between vascular and interstitial spaces
capillary fluid movement
in capillary fluid movement, arterial outflow is normally balanced by:
this results in small net outflow of fluid in interstitial space-> drained by_____
inflow at the venous end
drained by lymphatics
this is usually caused by disorders that impair venous return
increased hydrostatic pressure
(deep venous thrombosis, congestive heart failure
may result from loss in circulation or reduced synthesis
reduced plasma albumin concentration
(reduced plasma osmotic pressure)
-nephrotic syndrome, severe liver disease
compromises resorption of fluid from interstitial spaces-> leads to ___
this is lymphatic obstruction
-> leads to edema
- inflammatory conditions (bacterial/parasitic infection)
- neoplastic condition (breast cancer)
- congenital lymphedema
lymphatic obstructions
extravasation of blood from vessels
hemorrhage
defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic conditions, inherited/acquired defects
hemorrhages
4 types of hemorrhage manifestations
hematoma
ecchymoses
purpura
petechiae
large collection of hemorrhage in a tissue
hematoma
1-2cm subcutaneous hemorrhage (bruises)
ecchymoses
3-5mm hemorrhages
purpura
1-2mm minute hemorrhage
-often consequences of thrombocytopenia, vitamin C deficiency
petechiae
these cells are the primary regulators of hemostasis through changes in expression of procoagulant factors
endothelial cells
(clot formation)
clot formation steps
- vasoconstriction
- platelet plug forms
- fibrin deposition
- clot stabilization
disk shaped, anculeate fragments of megakaryocytes
platelets
platelet adhesion is mediated by
von willenbrand factor
congenital deficiency of receptors or molecules may lead to bleeding disorders
platelets
series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot
-secondary hemostasis
coagulation cascade
spontaneous, internal to vascular endothelium
what pathway for coagulation cascade
intrinsic pathway
activated by external trauma
what pathway for coagulation cascade
extrinsic pathway
this evaluates intrinsic pathway factors
XII, XI, IX, VIII, X, V, prothrombin (II), fibrinogen (I)
partial prothrombin time PPT
evaluates the extrinsic pathway factors
VII, X, V, prothrombin(II), fibrinogen (I)
prothrombin time PT
important for regulation of coagulation, plays key role in synthesis
factors II, VII, IX, X
vitamin K
helps synthesize protein C and S: important for negative feedback regulation of clotting cascade
vitamin K
vitamin K deficiency does what
increased bruising and bleeding
anticoagulant mediation, antagonist for vitamin K
inhibits clotting
warfarin
most important coagulation factor
-converts fibrinogen into crosslinked fibrin
-activates platelets
-pro inflammatory effects
-anticoagulation effects
thrombin
4 factors limiting coagulation
- Dilution of blood past the site of injury
- Negatively charged phospholipids required -activated platelets
- Regulation by neighboring intact endothelium
- Fibrinolytic cascade limits size of clot (Plasmin activation essential)
- Serves as barrier to platelets
- Anticoagulant effects
- Fibrinolytic effects
endothelium and coagulation limitation
Endothelial injury
* Coronary artery disease, MI
* Chronic inflammation – physical injury, infectious agents, abnormal blood flow,
inflammatory mediators, toxins
thrombosis
- abnormal blood flow
* Promote endothelial procoagulant activity
* Stasis allows platelets and leukocytes to associate with endothelial cells
* Stasis slows removal of activated clotting factors, and impedes inflow of clotting
factor inhibitors
thrombosis
abnormally high tendency for blood to clot
* Important risk factor for venous thrombosis
* Primary (genetic) vs secondary (acquired) disorders
thrombosis
Can develop anywhere in cardiovascular system
Lines of Zahn: observed grossly and microscopically
thrombi
4 fates of thrombi
- propagation: clot enlarges
- embolization: clot dislodged and moved by circulatory system
- dissolution- activation of fibrinolytic factors
- organization and recanalization- older thrombi are reorganized to facilitate some function
most occur in veins in leg
- Superficial veins: local congestion and swelling from impaired venous flow
-Ex: varicose veins
*Deep veins: deep venous thrombosis, larger veins
-May be asymptomatic in 50% of patients
-May embolize to lungs
venous thrombosis
- Atherosclerosis is a major cause
- Results in loss of endothelial integrity and abnormal blood flow
- Leads to MI, ischemia to organs (especially brain, kidney, spleen)
arterial and cardiac thrombosis
- Widespread thrombosis within microcirculation
- Consumption of platelets and clotting factors
- May occur from complications in obstetrics, injuries, cancer, and more
- Net result: excessive clotting and bleeding
DIC- disseminated intravascular coagulation
May be a solid, liquid or gaseous mass, carried by the blood from its point of
origin to a distant site
embolism
area of ischemic necrosis caused by occlusion of the vascular supply to the
affected tissue
involvement of heart and brain is common complication
infarction
where are most infarctions
arterial thrombosis or embolism
infarctions are classified according to
color
Red infarct:
(Venous occlusion, loose tissue (ie: lungs), tissue with dual circulation, previously
congested tissue, reperfusion injury)
contain hemorrhage
white infarct
(heart, liver, spleen)
arterial occlusion in solid organs
this shock leads to irreversible tissue injury
prolonged shock
A state in which diminished cardiac output or reduced effective circulating
blood volume impairs tissue perfusion and leads to cellular hypoxia
shock
three types of shock
cardiac
hypovolemic
septic
