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From Flashcardlet > Pathology: Abnormalities of Blood Supply I and II > Flashcards

Pathology: Abnormalities of Blood Supply I and II Flashcards

1
Q

Edema

A

The accumulation of fluid in interstitial tissue spaces or any of the various body cavities

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2
Q

Edema occurs when (4)

A
  • Hydrostatic pressure is increased
  • Oncotic pressure is decreased
  • Lymphatics are blocked
  • Increased vascular permeability associated with inflammation
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3
Q

Localized edema occurs as a result of (4)

A

o Inflammation
o Allergic reaction
o Venous obstruction
o Lymphatic obstruction

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4
Q

Systemic edema occurs as a result of (3)

A

o Congestive heart failure
o Renal disease
o Hypoproteinemia

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5
Q

Transudate (6)

A
  • Non-inflammatory edema caused by:
    o Increased hydrostatic pressure
    o Decreased oncotic pressure
    o Lymphatic obstruction
  • No change in vascular permeability
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6
Q

Exudate (2)

A
  • Result of an inflammatory response

* Increased vascular permeability due to inflammatory mediators or direct vascular damage

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7
Q

Similarities between hyperemia and congestion

A

In both, blood vessels of microciruclation contain an increased volume of blood

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8
Q

Hyperemia

A

Active process in which arteriolar vasodilation leads to increased blood flow

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9
Q

Transudate will not result in edema unless

A

The amount produced exceeds local lymphatic drainage capacity

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10
Q

Congestion

A

Passive process due to impaired venous outflow of tissue

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11
Q

Hemostasis (2)

A
  • Arrest of blood flow

- Refers to the specific process responsible arresting bleeding or hemorrhage in an injured vessel

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12
Q

Hemostasis depends on the interaction between (3)

A
  • The injured vessel wall
  • Platelets
  • The coagulation cascade
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13
Q

Hemostasis process (7)

A
  1. Injury
  2. Exposure to subendothelial collagen
  3. Platelet binding and activation
  4. Platelets adhere and aggregate at site of injury to form a primary platelet plug
  5. Simultaneously, endothelial injury causes activation of coagulation cascade
  6. prothrombin –> thrombin
  7. Thrombin cleaves fibrinogen –> fibrin –> platelet plug
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14
Q

Protein pathways involved in hemostasis (3)

A
  • Coagulation
  • Fibrinolytic
  • Anticoagulation (regulation)
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15
Q

Coagulation pathway

A

Participates in creation of definitive platelet plug

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16
Q

Fibrinolytic pathway (2)

A
  • Activated upon completion of platelet plug

* Ensures containment of coagulation

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17
Q

Anticoagulation pathway

A

Group of proteins that regulate actions between coagulation and fibrinolytic systems

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18
Q

Hemorrhage

A

Escape of RBCs across intact vessels or from vascular rupture

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19
Q

Hematoma

A

Abnormal localized collection of blood outside the blood vessels, usually in liquid form within the tissue

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20
Q

Coagulopathy

A

Bleeding disorder in which there is a problem with the body’s blood clotting process

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21
Q

Thrombus- definition

A

A solid mass formed from blood constituents within the vascular system or the heart in a living individual

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22
Q

Thrombosis- definition

A

Dysregulation or imbalance between pro and anti-coagulation mechanisms

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23
Q

Factors that promote thrombosis (3)

A
  • Endothelial injury
  • Stasis or turbulence of blood flow
  • Blood hypercoagulability
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24
Q

Principle factor in pathogenesis of thrombosis

A

Endothelial injury

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25
Q

How does endothelial injury lead to thrombosis

A

Exposure of highly thrombogenic subendothelial ECM to blood –> platelet adherence and aggregation

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26
Q

How does stasis or turbulence of blood flow lead to thrombosis?

A

Stasis/turbulence disrupts laminar flow and increases the chances of contact between platelets and the underlying vessel wall –> accumulation of activating clotting factor

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27
Q

Stasis of blood flow causes

A

venous thrmobi

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28
Q

Turbulent blood flow causes

A

arterial thrombi

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29
Q

Blood hypercoagulability arises when

A

there is an alternation in hemostatic regulation that predisposes to thrombus

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30
Q

Arterial thrombosis occurs as a result of

A

atherosclerotic vessel disease

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31
Q

Arterial thrombi grow in

A

retrograde direction (against blood flow)

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32
Q

Arterial thrombi are predominantly composed of (4)

A
  • Platelets
  • Fibrin
  • Trapped leukocytes
  • Fewer RBCs
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33
Q

Atherogenesis (7)

A

• Chronic inflammatory, fibroproliferative process that results from

       - endothelial injury to large and medium-sized elastic and muscular arteries -->
       - retention of LDL and endothelial activation -->
       - LDL oxidation -->
       - Formation of foam cells and propagation of a chronic inflammatory response -->
       - Endothelial dysfunciton -->
       - Healing by SMCs
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34
Q

Cardiac thrombi may develop as a result of (4)

A
  • MI
  • Left atrial dilation
  • Atrial fibrillation
  • Valvular disease
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35
Q

Aortic thrombi arise as a result of (2)

A
  • Atherosclerosis

- Aneurysm formation

36
Q

Main distinction between DVT and SVT

A

DVTs are prone to embolization, SVTs are not

37
Q

DVTs vs. arterial thrombi

A

DVT grows in the direction of blood flow and are not as firmly attached to underlying endothelium

38
Q

Fate of thrombus/outcomes of thrombus development (4)

A
  • Dissolution
  • Propagation
  • Organization/recanlization
  • Embolization
39
Q

Dissolution

A

Removal of thrombus by fibrinolytic system

40
Q

Propagation

A

Accumulation of more fibrin and platelets

41
Q

Organization/recanlization

A

Conversion to a vascularized mass of connective tissue (scarring) with potential reestablishment of blood flow

42
Q

Embolization

A

Detachment and transport to distant site in vasculature

43
Q

Last step in thrombus formation

A

Generation of fibrin from fibrinogen

44
Q

Plasmin (2)

A
  • The fibrinolytic protein responsible for hydrolyzing fibrin and dissolves the blood clot/thrombus
  • Formed from enzymatic cleavage of plasminogen (precursor form)
45
Q

DIC

A

Disseminated Intravascular Coagulation

46
Q

DIC: What two features cause hemorrhage (3)

A
  • Depletion of normal clotting constituents

- Formation of thrombi results in activation of fibrinolytic system as counterbalancing mechanism

47
Q

Major mechanisms that activate DIC (2)

A
  • Release of thromboplastic substances into circulation

- Widespread injury of endothelial cells

48
Q

Thromboplastin (3)

A

o Tissue factor

o Membrane-bound lipoprotein produced by many different cells in response to tissue injury

o Activates one of the coagulation pathways

49
Q

Major mechanisms that trigger DIC by release of thromboplastic substances into circulation (4)

A

o Endotoxin in gram-negative sepsis

o Obstetric complications

o Certain malignant tumors

o Traumatized or necrotic tissue

50
Q

Major mechanisms that trigger DIC by widespread injury to enodthelial cells (3)

A

o Endotoxin in gram-negative sepsis

o Antigen-antibody complexes

o Temperature extremes

51
Q

Common lab findings of DIC (4)

A
  • Thrombocytopenia
  • Prolonged bleeding time
  • Elevated fibrin split products
  • Anemia
52
Q

DIC Treatment

A

Heparin with platelet and clotting factor replacement

53
Q

Emoblism- definition

A

Partial or complete vascular occlusion that results when a detached solid, liquid or gaseous mass enters circulation at one location and is carried within bloodstream to a distant location until it becomes lodged within a vessel

54
Q

All emboli originate from

A
  • Previously formed thrmobi
55
Q

Systemic thromboemboli

A

Thromboemboli that travel in arterial circulation

56
Q

Source of pulmonary emboli

A

Deep leg vein thrombosis

57
Q

Ischemia

A

Inadequate blood supply to a tissue relative to its metabolic needs

58
Q

Local ischemia is always produced by

A

Arterial obstruction

59
Q

Generalized ischemia is caused by

A

cardiac failure that results in decreased tissue perfusion throughout the body

60
Q

Main causes of arterial obstruction (3)

A
  • Atherosclerosis
  • Thrombosis
  • Embolism
61
Q

Obstruction of end arteries results in

A

infarction

62
Q

Major organs that possess a double blood supply (2)

A
  • Lung

- Liver

63
Q

___ has greater collateral availability than ___

A

Venous circulation has greater collateral availability than arterial circulation

64
Q

Ischemia can be caused by

A

Arterial or venous obstruction

65
Q

Infarction

A

An area of ischemic tissue necrosis caused by arterial or venous obstruction

66
Q

Almost all cases of infarction result from (2)

A
  • Arterial thrombosis OR

* Embolism

67
Q

White vs. red infarction refers to

A

the degree of hemorrhage observable in necrotic tissue

68
Q

Conditions that have red infarctions (3)

A
  • all venous infarcts
  • tissues possessing dual blood supply or marginal collateral circulation
  • Necrotic tissue in which fragmentation or lysis of the obstruction permits re-perfusion of the necrotic area
69
Q

Wedge shaped vs. irregular infarction refers to (2)

A
  • shape of the area of necrosis

- Is a reflection of the underlying vascular anatomy

70
Q

Wedge-shaped infarction occurs in

A

Organs receiving their blood supply through a hilum

71
Q

Shock- definition

A

Clinical state characterized by prolonged systemic hypoperfusion resulting from insufficient cardiac output or reduction in the effective circulating blood volume

72
Q

Types of shock (3)

A
  • Hpovolemic
  • Cardiogenic
  • Generalized vasodilation
73
Q

Hopovolemic shock occurs from

A

a sufficiently large reduction of intravascular blood volume

74
Q

Hypovolemic shock is caused by (3)

A
  • Whole blood loss
  • Fluid loss
  • Plasma loss
75
Q

Cardiogenic shock occurs from

A
  • heart pump failure
76
Q

Cardiogenic shock is caused by (2)

A
  • Associated complications of MI

- Massive pulmonary embolism

77
Q

Shock by generalized vasodilation occurs in 3 different ways: (3)

A
  • Anaphylactic shock
  • Neurogenic shock
  • Spetic shock
78
Q

Nerugoenic shock

A
  • Impairment of neural control of vasomotor tone
79
Q

Septic shock (2)

A
  • Caused by a number of different infectious agents that get into the bloodstream
  • Associated with endotoxin-producing gram negative bacilli
80
Q

Stages of shock (3)

A
  • Stage of compensation
  • Stage of impaired tissue perfusion
  • Stage of decompensation
81
Q

Antithrombin III gene (2)

A
  • Major inactivator of thrombin

- Mutation leads to severe prothrombotic defect that requires anticoagulation therapy for life

82
Q

Thrombus vs. Blood Clot- causes

A

Thrombus = result of coagulation cascade + platelet activation

Blood clot = result of activation of coagulation cascade only

83
Q

Thrombus vs. Blood Clot- location

A

Thrombus develops in vascular system or heart of living person

Blood Clot develops in extravasuclar areas, in vitro, after death

84
Q

Thrombus vs. Blood clot- relationship to underlying endothelium

A

thrombus = attached to underlying endothelium

Blood clot = not attached to underlying endothelium

85
Q

Thrombus vs. blood clot- organization

A

Thrombus = orderly layering of platelets and fibrin

Blood clot = randomly oriented fibrin with passively entrapped platelets and RBCs

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