Hemodynamic Disorders Flashcards
what does circulation do
delivers oxygen and nutrients to tissues
- removes wastes
what is hemostasis
blood clotting that prevents excess bleeding after blood vessel damage
what is thrombosis
inappropriate clotting
what is embolism
migration of clots
what is hyperemia
-active process
- arteriolar dilation and increased blood flow
- occurs at site of inflammation or skeletal muscle movement
-red in color: oxygenated hemoglobin
what is congestion
-passive process
- impaired outflow of venous blood from a tissue
- blue/red color - deoxygenated hemoglobin
what percentage of the body weight is water
60%
where is 2/3 of water in body located
intracellular
what percentage of water is in blood plasma
5%
what is edema
accumulation of ISF in tissues
what are effusions
extravascular fluid that collects in body cavities
what is an effusion in pleural cavity called
hydrothorax
what is an effusion of the pericardial cavity called
hydropericardium
what is an effusion of the peritoneal cavity called
hydroperitoneum or ascites
what is anasarca
severe generalized edema due to fluid retention in tissues and cavities
- seen in systemic disease such as kidney disease and severe malnutrition
- causes weight gain and multiple organ failure
what diseases is ascites seen in
severe liver disease
when is hydrothorax seen
in CHF
what makes pulmonary edema distinct in a histo slide
fluid collects between the alveoli
what determines capillary fluid movement
vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins)
where is arterial outflow is normally balanced by inflow at
the venous end
why is arterial outflow balanced by inflow at the venous end
results in small net outflow of fluid in interstitial spaces -> drained by lymphatics
what pressures cause edema
increased hydrostatic pressure or plasma colloid osmotic pressure
what is increased hydrostatic pressure caused by
disorders that impair venous return such as deep venous thrombosis and CHF
what caused reduced plasma osmotic pressure
reduced plasma albumin concentration from loss in circulation or reduced synthesis
- nephrotic syndrome
- severe liver disease
how does heart failure lead to edema- mechanism
- increased capillary hydrostatic pressure -> edema
how does renal failure cause edema - mechanism
- retention of Na+ and H2O
- increase in blood volume
- edema
how does malnutrition, decreased hepatic synthesis and nephrotic syndrome cause edema
- decreased albumin-> decreased plasma osmotic pressure -> edema
how does lymphatic obstruction cause edema
- compromises resorption of fluid from interstitial spaces
what causes lymphatic obstruction
- inflammatory conditions: bacterial/ parasitic infections
- neoplastic conditions: breast cancer
- congenital lymphedma
what are the stages of lymphedema
- stage 1: asymptomatic, abnormal lymph flow but no build up
- stage 2: swelling, due to accumulation of lymph fluid that may subside when elevated
- stage 3: permanent swelling that cannot be relieved through elevation accompanied by fibrosis
- stage 4: lymphostatic elephantiasis or the deformation of a limb due to extensive swelling, skin thickening and scarring
what is a hemorrhage
- extravasation of blood from vessels
what causes a hemorrhage
- defective clot formation
- trauma
- atherosclerosis
- inflammatory
- neoplastic conditions
- inherited/acquired defects
what are the hemorrhage manifestations
- hematoma
- ecchymoses
- purpura
- petechiae
what is a hematoma
large collection of hemorrhage in a tissue
what is ecchymoses
1-2cm of subcutaneous hemorrage - bruises
what is purpura
3-5mm hemorrhages
what are petechiae
1-2mm minute hemorrhage
what are petechiae caused by
-thrombocytopenia
- vitamin C deficiency
- mononucleosis
- trauma
what are the steps in clot formation
- vasoconstriction
- platelet plug forms
- fibrin deposition
- clot stabilization and resorption
what are the primary regulators of hemostasis and how
endothelial cells through changes in expression of procoagulant or anticoagulant factors
describe vasoconstriction step in clot formation
occurs immediately to decrease blood flow
- endothelin causes the vasoconstriction
describe platelet activation and aggregation step of clot formation
- initial formation of platelet plug from endothelial cell disruption
- vWF promotes platelet adherence and causes conformational change and activates them
describe the activation of clotting factors and formation of fibrin step in clot formation
- secondayr hemostatsis
- activation of cotting factors and formation of fibrin
- exposes tissue factor expressed on subendothelial cells
-activates clotting cascade which ends in thrombin formation - thrombin converts fibrinogen into fibrin
- forms mesh work of clot
describe the clot resorption step in clot formation
- permanent plug
- t-Pa limits clotting to site of injury
describe platelets
disk shaped
- anucleate fragments of megakaryocytes
what are platelets derived from
megakaryocytes
what is platelet adhesion mediated by
vWf
what is the coagulation cascade
a series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot
- secondary hemostasis
what is the intrinsic pathway activated by
spontaneous, internal injury to vascular endothelium
what is the extrinsic pathway activated by
external trauma
what is involved in the intrinsic pathway
- factor 12
- factor 11
- factor 9
- factor 10
what is involved in the extrinsic pathway
- factor 7
- factor 10
- tisssue factor
what do the extrinsic pathway and intrinsic pathway form
- common pathway
- prothrombin converted into thrombin
- thrombin converts fibrinogen to fibrin
what does partial prothrombin time (PTT) evaluate
intrinsic pathway factors
what does prothrombin time (PT) evaluate
the extrinsic pathwya factors
what is the role of vitamin K
- regulation of coagulation, plays key role in synthesis of factors 2,7,9,10
- helps synthesize protein C and S: important for negative feedback regulation of clotting cascade
- vitamin K deficiency- increased bruising and bleeding
what is warfarin
-anticoagulant medication
- antagonist for vitamin K
- inhibits clotting
what is the most important coagulation factor
thrombin
what does thrombin do
- converts fibrinogen into fibrin
- activates platelets
- pro inflammatory effects
- anti coagulation effects
what factors limit 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
decsribe endothelium and coagulation limitation
- serves as barrier to platelets
- anticoagulant effects
- fibrinolytic effects
how does endothelium serve as a barrier to platelets
- lack of access to vWF and collagen
- release of NO, prostacyclin, adenosine diphosphate
what do anticoagulant effects do
expresses factors that inactivate thrombin
what are fibrinolytic effects
synthesis of tissue plasminogen activator (tPA)
what does thrombosis cause
- endothelial injury
- abnormal blood flow
- hypercoagulability
what is endothelial injury caused by
-coronary artery disease
- MI
- chronic inflammation - physical injury, infectious agents, abnormal blood flow, inflammatory mediators, toxins
what is abnormal blood flow caused by
- promotes 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
what is hypercoagulability
- abnormally high tendency for blood to clot
- important risk factor for venous thrombosis
what are the types of hypercoagulability
-primary (genetic)
- secondary (acquired)
what are the common primary hypercoagulable states caused by and what percentage of population is affected
- less than 1%
- factor V mutation
- prothrombin mutation
- increased levels of factor 7,9 or 11 or fibrinogen
what is considered high risk for secondary hypercoagulable staes
- prolonged bed rest or immobilization
- MI
- A fib
- tissue injury
- cancer
- prosthetic cardiac valves
- disseminated intravascular coagulation
- heparin induced thrombocytopenia
- anti phospholipid antibody syndrome
what is in Virchow’s triad in thrombosis
- endothelial injury
- abnormal blood flow
- hypercoagulability
where do thrombi occur
anywhere in the cardiovascular system
where are arterial thrombi located and describe them
often at sites of injury
- typically rich in platelets
where do cardiac mural thrombi occur
in heart chambers or aorta
where do venous thrombi occur and describe them
at sites of stasis
- contain high volume of RBCs
what are lines of Zahn
- lines observed in flowing blood clots
- differentiates antemortem clots from postmortem clots
where do 90% of venous thrombi occur
in the legs
what are the 4 fates of thrombi
- propagation: clot enlarges
- embolization: clot dislodges and moved by circulatory system
- dissolution: activation of fibrinolytic factors
- organization and recanalization- older thrombi are reorganized to facilitate some function
what are superficial venous thrombosis caused by
local congestion and swelling from impaired venous flow
decsribe deep vein thrombosis
- larger veins
- may be asymptomatic in 50% of patients
- may embolize to lungs
what is a major cause of arterial and cardiac thrombosis
atherosclerosis
what does arterial and cardiac thrombosis caused by atherosclerosis result in
loss of endothelial integrity and abnormal blood flow
- leads to MI, ischemia to organs especially brain, kidney and spleen
descibe disseminated intravascular coagulation (DIC)
- 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
describe an embolism
may be a solid, liquid or gaseous matrix carried by the blood from its point of origin to a distant site
what is a pulmonary embolism
- most common
- mostly from upper deep leg veins proximal to popliteal fossa
- pass through the larger right heart vessels and lodge in them pulmonary artery or arterioles
- multiple emboli can occur
- most are small and large ones can cause sudden death
- multiple emboli over time can cause pulmonary HTN and right ventricular failure
describe systemic thromboembolism
- may arise from intracardiac mural thrombi - 80%
- can embolize to lower extremities most frequently, CNS, intestines, kidneys and spleen
describe fat embolism
- injury to bone marrow can cause release of fat globules into circulation but rarely show clinical manifestations, but less than 10% show pulmonary problems, neurologic problems, anemia, thrombocytopenia and petechial rash
describe amniotic fluid embolism
- severe post birth complication with 80% mortality rate due to biochemical activation of coagulation system and immune system from entry of amnitoic fluid into circulation system of mother
what is air embolism
gas in circulation can come together to obstruct vascular flow
- ex: decompression sickness in scuba divers
what is an infarction
area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue
what are the most common infarctions
arterial thrombosis or embolism
- involvment of brain or heart
what are the 2 classes of infarct and describe each
- red: contain hemorrage. venous occlusion, loose tissue, tissue with dual circulation, previously congested tissue, reperfusion injury
- white infarct: arterial occlusion in solid organs, heart, liver spleen
what is shock
a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia
what does prolonged shock lead to
irreversible tissue injuryw
what are the 3 types of shock
cardiac
- hypovolemic
- septic
what are the clinical examples and pathogenic mechanisms for cardiogenic shock
- ex: MI, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolism
- mech: failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure or obstruction to outflow
what are the clinical examples and pathogenic mechanisms of hypovolemic shock
- ex: hemorrhage, fluid loss
- mech: inadequate blood or plasma volume
what are the clinical examples and pathogenic mechansim of septic shock
- overwhelming microbial infections
- gram negative sepsis
- gram positive septicemia
- fungal species
- superantigens
- mech: peripheral vasodilation and pooling of blood, endothelial activation/injury, leukocyte induced damage, disseminated intravascular coagulation, activation of cytokine cascades
