Unit 2 Flashcards

1
Q

vascular hydro static pressure

A

pushing fluid out of vessels

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2
Q

Onconic pressure

A

drawing fluid into vessels

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3
Q

What is the purpose of the net effect of driving fluid into the vessels?

A

succeed in delivering nutrients and oxygen to the tissues

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4
Q

what is the difference in hydrostatic pressure and oncotic pressure in the arteriolar end and the venular end of the capillary bed?

A

in the arteriolar end of the capillary bed the vascular hydrostatic pressure is higher than the oncotic pressure and drives fluid into tissues, but in the venular end the vascular hydrostatic pressure is lower than the oncotic pressure and drives fluid back into vessels carying away metabolic waste products

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5
Q

Osmosis

A

tendency of fluid to move from a solution of lesser concentration to one

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6
Q

Oncotic pressure or colloid osmotic pressure

A

refers to a form of osmotic pressure exerted by proteins most notable albumin within the plasma portion of the blood

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7
Q

hydrostatic pressure

A

refers to the pressure of water influenced by the activity of the heart as a pump, the elasticity and recoil of blood vessels, the quantity of blood within a vessel

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8
Q

do hydrostatic and colloid oncotic pressure affect fluid exchange and why?

A

not really because they are near zero

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9
Q

increased hydrostatic pressure can lead to what?

A

extra vascular fluid accumulation (edema)

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10
Q

Fluid moves at _____ or _______ between endothelial cells

A

pores or junctions

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11
Q

edema

A

excess fluid in extracellular spaces

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12
Q

Edema’s are mostly seen in _______ tissue

A

subqutaneous

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13
Q

what is a localized edema?

A

insect bite, result of localized disturbance of fluid exchange mechanism in tissue

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14
Q

what is an edema of the skin?

A

pitting edema

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15
Q

effusion

A

fluid accumulates in the body cavities, pleural space, or pericardial sac or peritoneal cavity

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16
Q

Ascites

A

specific name for watery effusion in the peritonial cavity

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17
Q

Anasarca

A

indicative massive edema of the whole body

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18
Q

Pleural space

A

between surface of the lung and pleural lining of the chest wall

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19
Q

Pericardial sac

A

membrane that surrounds the heart

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20
Q

Peritonial cavity

A

abdominal cavity

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21
Q

what is the lymphatic system responsible for with local edema’s

A

removing small protein molecules which leave capillaries normally as well as a small amount of fluid which does not return to the capillaries via the onconic pressure

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22
Q

lymphatic obstuction can cause a ______ over time as well as increased _____ ________ pressure which is usually _________

A

edema, colloid onconic, zero

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23
Q

what are two important causes of localized edemas?

A

venous obstruction and lymphatic obstruction

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24
Q

what causes a generalized edema?

A

if there is ventricular failure in the heart, blood backs up in the systemic circulatory system, there is a body wide venous obstruction causing an increase in hydrostatic pressure leading to a generalized edema

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25
Q

what is a dependent edema?

A

in dependent parts of the body such as lower legs or ankles

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26
Q

what will happen if the left side of the heart starts to fail?

A

blood will accumulate in the pulmonary circultion resulting in pulmonary venous congetion

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27
Q

increased pulmonary venous hydrostatic pressure means what?

A

fluid will remain in the lungs as edema

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28
Q

pulmonary edema

A

hydrostatic pressure increased, fluid leaves capillaries and moves to to alveolar space will interfere with gas exchange

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29
Q

Dyspnea

A

laboured or difficult breathing

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30
Q

orthopnea

A

condition with difficulty breathing when lying down related to positional changes in fluid accumulation

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31
Q

is congetive hert failure a disease?

A

no its a condition or end result

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32
Q

sodium stimulates water retention by what?

A

distal tubules of the kidneys

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33
Q

_________ results in retention of salt and water in the blood

A

aldosterone

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34
Q

increased water and salt retention in the blood can in turn do what?

A
  • increase blood volume increasing vascular hydrostatic pressure
  • decrease vascular oncotic pressure by diluting the blood albumin that largely determines the vascular oncotic pressure
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35
Q

what is this:

  • caused by decrease colloid osmotic force
  • insuficient dietary intake o protein
  • decreased syntheisis of albumin in liver
A

hypoproteinemia

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36
Q

what is this:

  • low levels of serum albumin
  • low plasma osmotic pressure, decrease in plasma volume
  • decrease glomular filtration in the kidney and increased secretion of renin leading to sodium and water retention in the kidneys
A

hypoalbuminemia

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37
Q

nephrotic syndrome

A

protein losing nephropathy, generalized edema, hypoalbuminemia, marked protinuria, its a syndrome with a bunch of symptoms together

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38
Q

plasma

A

fluid part of the blood which cells are suspended, composed of water and electrolytes and proteins as well as glucose enzymes products and nucleic acid metabolism

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39
Q

serum

A

fluid that remains after blood has been aloud to clot in a tube, similar to composition to plasma except fibrinogen and other clotting factors have been depleted by clot formation

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40
Q

hemorrhage

A

presence of blood in the interstitial tissues within a body cavity

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41
Q

petechia

A

small pinpoint focal hemorrhages

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42
Q

purpura

A

multiple 3-5mm sized oval to irregular shaped hemorrhages

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43
Q

ecchymoses

A

bruises, larger areas of hemorrhage

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44
Q

hematoma

A

large blood blister, area where blood has pooled in the tissue

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45
Q

peritoneal hemorrhage

A

hemopertoneum

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46
Q

pleural hemorrhage

A

hemothorax

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47
Q

percardial hemorrhage

A

hemopericardium, causes sudden death due to blood accumulating in the pericardial space, pressure causes collapse of right atrium and ventricle and heart failure occurs

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48
Q

hyphema

A

hemorrhage into the fluids within the eye

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49
Q

spontaneous hemorrhage

A

without trauma

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50
Q

what is hemostasis

A

process of blood clotting that prevents excess bleeding after blood vessel damage

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51
Q

normal hemotasis is a balance between ________ ____________ and ______________

A

primary hemostasis, secondary hemostasis ad fibrinolysis

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52
Q

hemostasis is initially controlled by what?

A

vasoconstriction, smooth muscle contraction in the arteriolar wall

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53
Q

vasoconstriction is effective for hemostasis in _______ but not in ________

A

small vessels but not large vessels

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54
Q

what are the 4 events that generally occur for normal hemostasis?

A
  1. transient arteriolar vasoconstriction
  2. formation of hemostatic plug (primary hemostasis)
  3. secondary hemostasis including activation of the coagulation cascade that results in formation of fibrin clot
  4. formation of permanent plug with concurrent counter, regulatory mechanisms or clot reabsorption (fibrinolysis)
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55
Q

the general sequece of events for hemostasis depend on what 3 componants?

A
  1. platelets
  2. vascular wall lined with endothelial cells
  3. coagulation cascade
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56
Q

platelets are _______ than RBC’s

A

smaller

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57
Q

do platelets have nucleus?

A

no

58
Q

platelets form what?

A

the hemostatic plug

59
Q

fibrinogen

A

plasma protein, important for platelet aggregation, and connects large number of platelets together to form large aggregates

60
Q

what acts together to modulate platelet function?

A

two prostaglandins and thromboxane derived from platelets

61
Q

why is intact endothelium important?

A

critical in preventing blood clots from forming and they have antimicrobial properties

62
Q

when does the endothelium become prothrombotic?

A

when endothelium is disrupted due to blood vessel injury and ecm is exposed to the endothelium

63
Q

what are some prothrombotic properties of endothelial cells?

A
  • Synthesis of von Willebrand factor
  • Induced by cytokines or bacterial endoxin to secrete tissue factor
  • Binding to activated coagulation to augment their activities
  • secretion of inhibitors of plasminogen activators
64
Q

what does the coagulation cascade do?

A

series of enzymatic conversions that convert inactive pro enzymes into active enzymes

65
Q

blood coagulation is divided into what two pathways ?

A

extrinsic and intrinsic

66
Q

what are some factors needed to optimize coagulation?

A

calcium ions, phospholipid surface, vitamin K

67
Q

what is needed for synthesis of prothrombin and clotting factors VII, XI, X?

A

vitamin K

68
Q

what is similar between the intrinsic and extrinsic coagulation pathway?

A

 Both extrinsin and intrinsic pathway lead to the conversion of the proenzyme prothrombin to the active enzyme thrombin, which then acts to convert fibrinogen to fibrin and amplifies the cascade

69
Q

fibrin

A

polymerizes as a long insoluble strand forming a network that is the basis for a clot

70
Q

thrombin

A

critical in catalyzing the final steps of the cascade and has a variety of effects on local vessels and inflammation

71
Q

what is fibrinolysis and when does it occur?

A

along with the coagulation cascade is activated a fibrinolytic cascade that limits the extent of clot formation and helps in future dissolution

72
Q

While fibrin is being formed the proenzyme _____________ is incorporated into the developing clot

A

plasminogen

73
Q

within the clot plasminogen is formed into _________

A

plasmin/fibrinolysin

74
Q

tissue type plasminogen activator (tPA)

A

synthesized by endothelial cells, management for thrombosis

75
Q

plasmin

A

acts to break down fibrin, interferes with polymerization

76
Q

the presence of fibrin split/breakdown products indicate what?

A

thrombotic disease

77
Q

what are FSPs/FDPs?

A

weak anticlogulants

78
Q

normal hemostasis is a balance between ________ and _______

A

clot formation and fibrinolysis

79
Q

summarize how a clot forms from vessel injury

A

vessel injury occurs, transient vasoconstriction helps limit blood flow, platelets adhere to injured area, clot is formed to stop excessive bleeding, fibrinolysis prevents the clot from becoming overly large and interfering with blood flow

80
Q

coagulation disorders have two categories

A
  1. deficiency of coagulation factors

2. increased anticoagulant activity

81
Q

what are the two common gene abnormalities with deficency of coagulation factors?

A

hemophilia A and von willebrands disease

82
Q

Hemophilia A

A

Deficiency in normal functioning factor VIII, critical componant to the intrinsic pathway due to insuficient synthesis of factor VIII, Can have spontaneous bleeding in severve cases, Can be managed by plasma transfusions or by giving factor VII concentrate, to increse factor VII coagulant activity

83
Q

von willebrands disease

A

Reduced levels of circulating von willebrand factor, and the entire factor VIII complex is deficient, Disorders in platelet function also present, Bleeding tendancies related to both platelet function and coagulation

84
Q

what is an important function of vWF?

A

to facilitate platelet adhesion to damaged blood vessel walls

85
Q

epistaxis

A

nose bleeds

86
Q

what are wafarins and heparins used for?

A

anticoagulants that induce factor deficiencies and can lead to bleeding problems if not carefully minitored

87
Q

how are platelet disorders characterized?

A

small bleeds in the skin typically perechiae and purpura

88
Q

thrombocytopenia

A

decrease in platelet numbers, abnormal distribution, increased platelet destruction

89
Q

thrombocytopathia

A

abnormalities of platelet function, platelet counts normal, don’t function normally

90
Q

what can be used to alter platelet function and can be used to prevent extreme effects of heart attacks?

A

asprin

91
Q

thrombosis

A

clotting gone wrong within a vessel

92
Q

virchows triad consists of

A
  1. endothelial theory
  2. alteration in normal blood flow
  3. hypercoagulability
93
Q

acute endothelial injury

A

injuries can be caused by trauma or surgery , inflammation and lack of blood supply

94
Q

when is there an increased risk for thrombosis?

A

post surgical period

95
Q

atherosclerosis

A

example of endothelial injury, as platelets tend to stick together to rough places in the endothelium, leads to atherosclerosis one of the leading causes of thrombosis in our society, symptomatic disease, Compromise of blood flow in smaller arteries

96
Q

blood normally flows in layered ______ pattern

A

laminar

97
Q

name and describe the two changes that can occur with blood flow

A
  1. turbulance (rather than travelling in discrete columns, blood flow is fast yet erratic causing greater interaction with the endothelium)
  2. stasis or pooling (blood flow much more slowly than normal because of ; failure of forward pressure, downstream obstruction or flow, or abnormal flow qualities to the blood itself such as hyper viscosity)
98
Q

polycythemia

A

increase in RBCs, lead to viscous blood

99
Q

what are the two forms of polycythemia?

A
  1. relative (occurs in context of dehydration)

2. absolute ( blood stasis)

100
Q

what is normal polycythemia?

A

deficient oxygenation of blood such as people or animals living at high altitudes

101
Q

what is non physiologic polycythemia?

A

increased erythropoietin levels seen with certain tumours

102
Q

3 main casues of thrombosis

A

changes in blood flow (turbulence and stasis), and changes in blood itself ( alterations in clotting/fibrinolysis) and endothelial damage

103
Q

endothelial damage causes thrombosis more commonly in ______ while blood alterations with flow and composition causes thrombosis more commonly in ______

A

arteries, veins

104
Q

ischemia and infraction

A

reduction or failure of blood supply to tissues

105
Q

infarct

A

localized necrosis and inadequate blood supply and inadequate oxygen, by definition an area of ischemic necrosis

106
Q

if the blood supply fails ischemia will lead to _______

A

infraction

107
Q

anything which obstructs either the arteriole blood supply or venous drainage of the tissue can lead to what?

A

infraction where there is insufficient collateral circulation

108
Q

what occurs where myocardium is deprived of blood due to occlusion of an coronary artery?

A

death of cyocytes occurs

109
Q

myocardium

A

heart muscle

110
Q

myocardial infraction

A

death of myocytes, heart attack

111
Q

_____% or greater narrowing of lumen is considered critical

A

75%

112
Q

how are acute myocardial infractions caused ?

A

coronary artery thrombosis

113
Q

__________ ______ causes narrowing of the vessels

A

atherosclerotic plaque

114
Q

what are the 5 factors influencing the outcome of arterial obstruction?

A
  1. availibility of collateral circulation
  2. the integrity of the collateral arteries (disease?)
  3. the tissue susceptibility to ischemia
  4. tissue metabolic rate
  5. the rate of development of the obstruction
115
Q

______ is more likely to cause thrombosis in the veins

A

stasis

116
Q

idiopathic

A

disease of unknown cause

117
Q

embolism

A

an embolis is a free floating intravascular solid or gaseous mass that is carried by the blood to a site different from its point of origin

118
Q

the majority of emboli originate as what?

A

dislodged thrombus

119
Q

emboli generally obstruct what?

A

arteries and arterioles rather than veins

120
Q

what organs have dual blood supply? what are the blood supplies?

A
  1. Lungs pulmonary and bronchial artery

2. the liver both hepatic artery and portal veins supply

121
Q

dual blood supply can supply the lung or liver but cant prevent ______

A

infraction

122
Q

obstruction occurs frequently in ______

A

veins

123
Q

when the vein is obstructed hydrostatic pressure favours fluid remaining in the ________

A

interstitium

124
Q

how is further swelling limited with ischemia and infraction?

A

tissue hydrostatic forces are increased

125
Q

what happens when the hydrostatic pressure increases too much

A

capillaries can rupture and hemorrhage can occur

126
Q

what is the outcome of venous obstruction

A

local edema to congestion to hemorrhage will depend on the size of the vein obstructed, how quickly the obstruction develops and availability of collateral drainage

127
Q

whats less liekly to cause clinic problem venous or arterial obstruction?

A

venous because there is greater availibility of collateral vessels in the venous system

128
Q

torison

A

twisting of pedicle of an organ

129
Q

whats a reperfusion injury?

A

If venous outflow is impaired then any inflammatory mediators and toxic byproducts of cell death are relatively contained but If you restore blood flow to such tissue you can release all of these toxic inflammatory mediators into the bloodstream which are likely to add shock to the problem

130
Q

DIC

A

thrombohemorrhagic disorder from widespread activation of coagulation which leads to widespread systemic thrombosis in microcirculation of the body with serious and fatal complications

131
Q

is DIC a disease?

A

no its a syndrome

132
Q

How is DIC a continuum?

A

early stages its a thrombotic process but as platelets and clotting factors are consumed it becomes a hemorrhagic process

133
Q

how can DIC be triggered?

A
  1. By release of tissue factor or other thromboplastic substances into the circulation
  2. By widespread endothelial cell injury
134
Q

Name some things DIC is often associated with?

A

sepsis, malignancy (cancer), obstructed complications, severe trauma (especially cerebral trauma), and burns

135
Q

how is DIC diagnosed?

A

diagnosed by damaged RBC, RBCs are injured when passing through the fibrin stands of microthrombi, and Thrombocytopenia (thrombocytes are consumed in thrombus formation)

136
Q

what is the goal of DIC treatment?

A

stop the cycle of throbosis and fibrinolysis

137
Q

what is the pathological definition of shock?

A

physiologic state by generalized reduction in tissue perfusion related to decrease in either effective cardiac output or effective circulating blood volume

138
Q

what are the 5 causes of shock?Describe each

A
  1. Hypovolemia(decreased blood volume)
  2. Septic shock (microbial infections)
  3. Cardiogenic shock (failure of heart function)
  4. Neurogenic shock (anesthesia or spinal cord injury, loss of vascular tone)
  5. anaphlyactic shock (by immunoglobulin E mediated hypersensitivity )
139
Q

what is the common path for all 5 forms of shock ?

A

reduction of tissue perfusion

140
Q

briefly describe the stages of shock

A
  1. neuphronal reflex come sinto play
  2. decrease in blood pressure
  3. peripheral vasoconstriction helps maintain blood pressure in vital organs
  4. constriction in renal arteries which decrease blood flow to kidneys
  5. fluid retention by the kidneys and decreased urine output
  6. severe tisue hypoxia, organ failure
141
Q

what is shock lung?

A

hypoxia in the lung causes edema and hemorrhage, now termed ARDS

142
Q

ARDS

A

acute respiratory distress syndrome