Hemodynamics and Blood Vessels Flashcards Preview

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Flashcards in Hemodynamics and Blood Vessels Deck (73):
1

What does nl fluid hemostasis require?

Vessel wall integrity
Intravascular (hydrostatic ) pressure
Plasma colloid osmotic (oncotic) pressure

2

Edema

Increased fluid in interstitial tissue spaces

3

Transudate

Protein-poor fluid, typically caused by alterations in hemodynamic forces
-Specific gravity < 1.012

4

Exudate

Protein-rich fluid, typically caused by inflammation and the associated increased vascular permeability
-Specific gravity > 1.020

5

What is edema caused by?

Increased hydrostatic pressure, caused by impaired venous return
Decreased plasma colloid osmotic pressure, caused by reduction in plasma proteins
Lymphatic obstruction, caused by scarring, tumors, certain infections
Primary renal sodium retention, caused by renal failure
Increased vascular permeability, caused by inflammation

6

Hyperemia and congestion

Increased volume of blood in a particular tissue

7

Hyperemia

Active process; caused by arteriolar dilation, such as at sites of inflammation or in skeletal muscle during exercise; tissue is redder than nl (erythema)

8

Congestion

Passive process; caused by impaired venous return out of tissue; tissue is bluer than nl (cyanosis)

9

Hemorrhage

Rupture of blood vessels with loss of blood

10

Petechiae

1-2 mm, skin, mucous membranes, serosal surfaces

11

Purpura

3-5 mm, skin, mucous membranes, serosal surfaces

12

Ecchymoses

1-2 cm, subcutaneous bruises; hemoglobin (red-blue), bilirubin (blue-green), hemosiderin (golden-brown)

13

Massive hemorrhage

Blood loss, hypovolemic shock, exsangination, death

14

Hematoma

Compression of tissues

15

Intracerebral hemorrhage

Stroke, death

16

Chronic hemorrhage

Slow blood loss, iron deficiency anemia

17

Hemostasis

A nl process that maintains the blood in a fluid state and produces a local hemostatic plug at sites of vascular injury

18

Thrombosis

The pathologic form of hemostasis
Thrombosis is the formation of a blood clot (thrombus) in an uninjured or minimally injured vessel

19

What is hemostasis and thrombosis dependent on

Vascular endothelium
Platelets
Coagulation system

20

Antithrombotic properties

Antiplatelet effects
Anticoagulant properties
Fibronolytic properties

21

Prothrombic properties

Adhesion of platelets
Synthesis of von Willebrand factor (vWF)
Synthesis of tissue factor (thromboplastin)

22

Platelets

Injury of endothelial cells exposes the basement membrane extracellular matrix (ECM)
Platelets adhere to the ECM by binding to vWF and become activated
Platelets release ADP (platelet aggregation) and thromboxane A2 (platelet activation and vasoconstriction)
Formation of a primary hemostatic plug

23

Coagulation cascade

Initiated by interaction of tissue factor (on endothelial cells) and platelet phospholipids
Results in the productiono f thrombin
Thrombin cleaves circulating fibrinogen to form a longer-lasting secondary hemostatic plug

24

What does prolonged PTT indicate?

Deficiency of VI, VIII, IX, X, XI, XII, prothrombin, or fibrinogen

25

What does prolonged PT indicate?

Deficiency of V, VII, X, prothrombin, or fibrinogen

26

Where are anticoagulants produced?

At the site of endothelial injury or during activation of the coagulation cascade
-Antithrombins inhibit the activity of thrombin, and factors IXa, Xa, XIa, and XIIa
-Proteins C and S inactivate factors Va and VIIIa
-Tissue factor pathway inhibitor (TFPI) inactivates factor Xa and TF-VIIa complexes

27

Fibrinolytic cascade

Plasminogen activators (e.g., t-PA) convert plasminogen to plasmin, which breaks down fibrin

28

What are the three primary influences on thrombus formation?

Called Virchow's triad
Endothelial injury (biggest influence)
Stasis or turbulence of blood flow
Blood hypercoagulability

29

Subtle influences that alter endothelial function

Hypercholesterolemia
Radiation
Products absorbed from cigarette smoke

30

Endothelial injury

Disruption in balance between prothrombotic and antithrombotic activities of endothelial cells

31

Endothelial cell loss or injury

MI
Ulcerated plaques in atheroclerotic arteries
Trauma
Inflammation (vasculitis)

32

Turbulence and stasis in blood flow

Disruption of flow brings platelets into contact with endothelium
Prevent dilution of activated clotting factors
Retard inflow of clotting factor inhibitors
Promote endothelial cell activation

33

What causes turbulence and/or stasis?

Ulcerated atherosclerotic plaques
Aneurysms
AMI
Polycythemia

34

Hypercoagulability

Any alteration of the coagulation cascade that predisposes to thrombosis

35

Primary (inherited) hypercoagulability

Mutations in coagulation factor genes or anticoagulant genes

36

Secondary (acquired) hypercoagulability

Prolonged bedrest
MI
Tissue damage (surgery, fracture, burns)
Cancer

37

Factor V Leiden thrombophilia

Inherited disorder of blood clotting
Most common inherited form of thrombophilia
-2-15% of ppl with European ancestry
DVT
-Abnl blood clots
-Most often in legs, but occur in other parts of body
-May move to lungs- pulmonary emboli
Slightly increased risk of miscarriage
-Most women have nl pregnancies

38

Risk factors for factor V Leiden thrombophilia

Age
Obesity
Injury
Surgery
Smoking
Birth control pills
Hormone replacement therapy
Factor V Leiden mutation in combination with another mutation in the F5 gene (or other member of coagulation cascade)

39

Genetics of Factor V Leiden thrombophilia

Missense mutation in coagulation factor V (F5) gene that results in single amino acid substitution in the protein
Coagulation factor V cannot be inactivated normally by activated protein-C
Autosomal dominant gain-of-function mutation
-One allele: lifetime risk of DVT is 10%
-Two alleles: lifetime risk of DVT is 80%

40

Pathology of thrombosis

Mural thrombi of the heart-overlying myocardial infarct
Valvular thrombi of the heart- endocarditis
Arterial thrombi- atherosclerosis, aneurysms
Venous thrombi- varicose veins
Microvascular thrombi- DIC

41

Common sites of thrombus formation

Arteries: coronary cerebral femoral
Veins: femoral popliteal iliac

42

Mural thrombi

Thrombi occurring in heart chambers or in the aortic lumen

43

What could occur if the pt survives the initial thrombosis?

Propagation
Embolization
Dissolution
Organization
Recanalization

44

Propagation

Thrombus increases in size and obstructs vessel

45

Embolization

Thrombus dislodges or fragments, and moves to other locations in vessels

46

Dissolution

Thrombus is removed by fibrinolytic activity

47

Organization

Thrombus induces inflammation and fibrosis; may incorporate into vessel wall

48

Recanalization

Re-establish some degree of blood flow

49

Embolus

Any detached solid, liquid, or gaseous mass carried by the blood to a site distant from its origin
Occlude vessels resulting in varying pathology

50

Categories of emboli

Arterial: 85% arise from heart
Venous: Majority arise from leg veins

51

Pulmonary thromboembolism

Arise mainly from DVT in the legs

52

Effect of pulmonary thromboembolism

Depends on the size of the thromboembolus
60-80& are small and clinically silent
Sudden death
Right heart failure (cor pulmonale)
Pulmonary hemorrhage
Infarction

53

Systemic thromboembolism

Refers to emboli in the arterial circulation
80% arise from intracardiac mural thrombi
-LV wall infarcts
-Dilated left atria secondary to mitral valve defects
-Aortic aneurysm
-Atherosclerotic plaque

54

Major sites for arteriolar embolization

Lower extremities (75%) and brain (10%)

55

Infarct

An area of ischemic necrosis within a tissue or organ that is produced by occlusion of either its arterial supply or its venous drainage

56

Common and important cause of clinical illness- infarction

MI
Cerebral infarction
Pulmonary infarction
Bowel infarction

57

Factors that influence the development of an infarct

Availability of an alternative blood supply
Rate of development of the occlusion
Susceptibility of a tissue to hypoxia
Oxygen content of the blood

58

White infarcts (anemic)

Arterial occlusion
Solid tissues

59

Red infarcts (hemorrhagic)

Venous occlusion
Loose tissues
Dual or extensive collateral blood supply

60

What does shock cause?

Systemic hypoperfusion
-Reduced cardiac output
-Reduced circulating blood volume

61

Clinical events where shock is the final common pathway

Cardiogenic shock (heart failure)
Hypovolemic shock (blood loss)
Septic shock (infections)

62

Septic shock

Innate immune response to systemic release of endotoxins
-Gram neg bacterial cell walls
-Lipopolysaccharides (LPS)

63

Effects of septic shock

Hypotension
Decreased myocardial contractility
Endothelial injury
DIC
Fibrinolysis (plasmin)

64

What is bleeding due to in septic shock?

Consumption of coagulation factors and activation of fibrinolysis

65

Sx of septic shock

Severe hypotension
Cold, clammy skin
Edema
Somnolence, coma
Oliguria
Dyspnea
GI bleeding
Paralytic ileus

66

Morphologic features of shock

Brain: ischemic encephalopathy
Heart: subendocardial hemorrhages and necrosis
Kidneys: acute tubular necrosis or diffuse cortical necrosis
GI tract: patchy hemorrhages and necrosis
Liver: fatty change or central hemorrhagic necrosis

67

Nl blood vessels

Consist mainly of endothelial cells (ECs) and smooth muscle cells (SMCs)
Arteries
-Thick walls
-High pressure
Veins
-Large lumen
-Low pressure

68

Large (elastic) arteries

Aorta, common carotid, iliac
Lot os elastic fibers
Pulsatile

69

Medium (muscular arteries)

Coronary, renal arteries
Mostly smooth muscle cells

70

Small arteries/arterioles

All smooth muscle cells
BP controlled here

71

Capillaries

Diameter of RBC
Large numbers of them, with thin walls, slow flow
Great for exchanging oxygen, nutrients

72

Venules/veins

Large diameter, thin walls
Compressible, penetrable by tumor
Valves

73

Lymphatics

Drain excess interstitial fluid
Pass through nodes, checking for infection
Return pathogens (and tumor cells) to circulation