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Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

____ delivers oxygen and nutrients to tissues and removes wastes

A

blood circulation

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2
Q

The functions of circulation include:

A
  1. Delivers oxygen & nutrients
  2. Wastes are removed
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3
Q

Blood clotting that prevents excess bleeding after blood vessel damage:

A

hemostasis

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4
Q

Inappropriate clotting:

A

thrombosis

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5
Q

migration of clots:

A

embolism

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6
Q

active process, arteriolar dilation and increased blood inflow:

A

hyperemia

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7
Q

Describe the color of blood associated with hyperemia:

A

Red color- due to oxygenated hemoglobin

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8
Q

Passive process, impaired outflow of venous blood from a tissue:

A

congestion

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9
Q

Describe the color of blood associated with congestion:

A

blue/red color (cyanosis)- deoxygenated hemoglobin

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10
Q

Hyperemia is a ____ process

Congestion is a ____ process

A

Hyperemia- active
Congestion- passive

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11
Q

What is seen in this image? Is the specimen from a living or dead individual?

A

Liver with chronic passive congestion and hemorrhagic necrosis- they dead

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12
Q

_____% of body weight is water, ___ intracellular

A

60%; 2/3

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13
Q

2/3 of the 60% water comprising our body weight is:

A

intracellular

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14
Q

The remaining fluid of the body (not including the water) is comprised by mostly:

A

interstitial fluid

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15
Q

around ___% blood plasma is found in the body

A

5%

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16
Q

accumulation of interstitial fluid in tissues

A

edema

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17
Q

Edema is the accumulation of ___ in tissues

A

interstitial fluid

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18
Q

extravascular fluid that collects in body cavities:

A

effusions

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19
Q

Effusions are ___ that collects in body cavities

A

extravascular fluid

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20
Q

Effusion in the pleural cavity:

A

hydrothorax

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21
Q

Effusion in the pericardial cavity:

A

hydropericardium

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22
Q

Effusion in the peritoneal cavity:

A

hydroperitoneum or ascites

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23
Q

Severe generalized edema due to fluid retention in tissues and cavities:

A

Anasarca

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24
Q

Causes of edema include: (5)

A
  1. increased hydrostatic pressure
  2. reduced plasma osmotic pressure (hypoproteinemia)
  3. lymphatic obstruction
  4. sodium retention
  5. inflammation
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25
Q

What may cause increased hydrostatic pressure that leads to edema? (2)

A
  1. impaired venous return
  2. arteriolar dilation
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26
Q
  • CHF
  • Constrictive pericarditis
  • Ascites (liver cirrhosis)
  • Venous obstruction or compression
  • Thrombosis
  • External pressure (e.g. mass)
  • Lower extremity inactivity with prolonged dependency

These are all examples of:

A

impaired venous return (leading to increased hydrostatic pressure which is a cause of edema)

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27
Q
  • Heat
  • Neurohumoral dysregulation

These are examples of:

A

components leading to arteriolar dilation (which leads to increased hydrostatic pressure which is a cause of edema)

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28
Q
  • Protein-losing glomerulopathies (nephrotic syndrome)
  • Liver cirrhosis (ascites)
  • Malnutrition
  • Protein-losing gastroenteropathy

These are all conditions leading to:

A

reduced plasma osmotic pressure (hypoproteinemia)
(which is a cause of edema)

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29
Q

-Inflammatory
- Neoplastic
- Postsurgical
- Postirradiation

These are all conditions leading to:

A

lymphatic obstruction (which is a cause of edema)

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30
Q
  • Excessive salt intake with renal insufficiency
  • Increased tubular reabsorption of sodium
  • Renal hypperfusion
  • Increase renin-angiotensin-aldosterone secretion

These are all conditions leading to:

A

sodium retention (which is a cause of edema)

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31
Q
  • Acute inflammation
  • Chronic inflammation
  • Angiogenesis

These are all conditions leading to:

A

inflammation (which is a cause of edema)

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32
Q

What is responsible for dictating fluid movement between vascular and interstitial spaces?

A
  • vascular hydrostatic pressure
  • colloid osmotic pressure (plasma proteins)
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33
Q

What causes colloid osmotic pressure?

A

plasma proteins

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34
Q

vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins) dictate fluid movement between:

A

vascular and interstitial spaces

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35
Q

Arterial outflow is normally balanced by:

A

inflow at the venous end

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36
Q

____ is normally balanced by inflow at the venous end

A

arterial outflow

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37
Q

Arterial outflow is normally balanced by inflow at the venous end: Results in small net ____ –> drained by ___

A

outflow of fluid in interstitial space; lymphatics

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38
Q

Capillary hydrostatic and osmotic forces are normally balanced so their is little net movement of fluid into the:

A

interstitium

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39
Q

Capillary hydrostatic and osmotic forces are normally balanced so their is little net movement of fluid into the interstitium. However, increased hydrostatic pressure or diminished plasma osmotic pressure leads to:

A

extravascular fluid accumulation (edema)

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40
Q

Increased _____ or diminished ____ leads to extravascular fluid accumulation (edema)

A

hydrostatic pressure; plasma osmotic pressure

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41
Q

When extravascular fluid accumulates, tissue lymphatics drain much of the excess fluid back to the circulation by way of the ___. However, if the capacity for lymphatic drainage is exceeded, ____ results

A

thoracic duct; tissue edema

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42
Q

Usually caused by disorders that impair venous return:

A

increased hydrostatic pressure

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43
Q

Disorders that can cause impaired venous return: (2)

A
  1. Deep venous thrombosis
  2. Congestive heart failure
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44
Q

Increased hydrostatic pressure is usually caused by disorders that:

A

impair venous return

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45
Q

Reduced plasma albumin concentration will lead to:

A

reduced plasma osmotic pressure

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46
Q

Reduced plasma albumin concentration may result from:

A

loss in circulation or reduced synthesis

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47
Q

Nephrotic syndrome and severe liver disease are both causes for:

A

reduced plasma albumin concentration (which reduces plasma osmotic pressure)

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48
Q

Fill in the highlighted portions:

A

A: heart failure

B: malnutrition
C: decreased hepatic synthesis
D: nephrotic syndrome

E: renal failure

F: edema

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49
Q

Fill in the highlighted portions:

A

Green: DECREASED plasma albumin
Blue: DECREASED plasma osmotic pressure

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50
Q

Fill in the highlighted portions:

A

Green: INCREASED capillary hydrostatic pressure

Blue: INCREASED renal blood flow

Orange: activation of RNENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

Pink: retention of Na+ & H2O

Purple: INCREASED blood volume

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51
Q

Pathways leading to _____ can result form heart failure, renal failure, or reduced plasma osmotic pressure

A

systemic edema

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52
Q

Compromises resorption of fluid from interstitial spaces –> edema:

A

lymphatic obstruction

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53
Q

What conditions can lead to lymphatic obstruction? (3)

A
  1. inflammatory conditions
  2. neoplastic conditions
  3. congenital lymphedema
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54
Q

What does lymphatic obstruction compromise?

A

resorption of fluid from interstitial spaces (ultimately leading to edema)

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55
Q

Stage of lymphedema in which the lymphatic system experiences abnormal flow but no fluid build-up; (asymptomatic):

A

stage 1

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56
Q

Stage of lymphedema which is due to an accumulation of lymph fluid that may subside when elevated; (swelling):

A

stage 2

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57
Q

Stage of lymphedema categorized by permanent swelling that cannot be relived through elevation, accompanied by changes in the skin (fibrosis):

A

stage 3

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58
Q

Stage of lymphedema characterized by lymphostatic elephantiasis, or the deformation of a limb due to extensive swelling, skin thickening and scarring:

A

Stage 4

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59
Q

extravasation of blood from vessels:

A

hemorrhage

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60
Q

Defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic condition, inherited/aquired defects are all causes of:

A

hemorrhage

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61
Q

Hemorrhage manifestations include: (4)

A
  1. hematoma
  2. ecchymoses
  3. purpura
  4. petechiae
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62
Q

Large collection of hemorrhage in a tissue:

A

hematoma

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63
Q

1-2cm subcutaneous hemorrhage (bruises):

A

ecchymoses

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64
Q

3-5mm hemorrhages:

A

purpura

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65
Q

1-2 mm minute hemorrhage:

A

petechiae

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66
Q

Often a consequence of thrombocytopenia or vitamin C deficiency:

A

petechiae

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67
Q

What can be seen in this image?

A

petechiae

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68
Q

Clot formation steps include: (4)

A
  1. vasoconstriction
  2. platelet plug formation
  3. fibrin deposition
  4. clot stabilization & resorption
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69
Q

____ are the primary regulations of hemostasis though changes in expression of procoagulaant or anticoagulation factors

A

endothelial cells

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70
Q

Endothelial cells are the primary regulators of hemostasis through changes in expression of ___ or ___ factors

A

procoagulant; anticoagulant

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71
Q

Disk-shaped, enucleate fragments of megakaryocytes:

A

platelets

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72
Q

Platelet adhesion is mediated by:

A

von willebrand factor

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73
Q

Congenital deficiency of receptors or molecules may lead to:

A

bleeding disorders

74
Q

Functions as adhesion bridge between subednothelial collagen and glycoprotein Ib (Gp1b) platelet receptor

A

VWF

75
Q

Platelet aggregation is accomplished by ____ binding to platelet ____ on different platelets

A

fibrinogen; GpIIb-IIIa

76
Q

Deficiency due to Gp2b-3a complex:

A

Glanzmann thrombasthenia

77
Q

Deficiency due to Gp1b:

A

Bernard-Soulier syndrome

78
Q

Von willebrand factor deficiency:

A

Von Willebrand disease

79
Q

A serious of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot:

A

coagulation cascade

80
Q

The coagulation cascade is also known as:

A

secondary hemostasis

81
Q

Coagulation cascade pathway that is spontaneous and occurs when there is internal injury to vascular endothelium

A

intrinsic pathway

82
Q

Coagulation cascade pathway that is activated by external trauma:

A

extrinsic pathway

83
Q

Contact activation due to a damaged surface occurs with what coagulation cascade pathway?

A

intrinsic pathway

84
Q

Label the following steps of the coagulation cascade pathways:

A
  1. Intrinsic pathways
  2. Common pathway
  3. Extrinsic pathway
85
Q

The intrinsic pathway of the coagulation cascade is activated by:

A

contact activation - (damaged surface)

86
Q

The extrinsic pathway of coagulation is activated by ____.

A

injury

87
Q

Factors from the intrinsic pathway & factors from the extrinsic pathway that converge:

What do they act on?

A

5A- They form the prothrombinase complex to act on prothrombin and convert it to thrombin

88
Q

What is the ultimate result of the various pathways of the coagulation cascade?

A

clot formation

89
Q

A coagulation cascade assay is:

A

an evaluation of coagulation function

90
Q

___ evaluates the intrinsic pathway factors:

A

Partial prothrombin time (PTT)

91
Q

PTT evaluates ___ pathway factors including: (8)

A

intrinsic; XII, XI, IX, VIII, X, V, Prothrombin (II), Fibrinogen (I)

92
Q

___ evaluates the extrinsic pathway factors:

A

Prothrombin time (PT)

93
Q

Prothrombin time evaluates the ___ pathway factors including: (5)

A

extrinsic; VII, X, V, Prothrombin (II), Fibrinogen (I)

94
Q

Important for regulation of coagulation, and plays a key role in synthesis of factors II, VII, IX & X:

A

Vitamin K

95
Q

Vitamin K plays a key role in the synthesis of factors:

A

II, VII, IX, X

96
Q

Vitamin K helps synthesize protein ___ and ___. What are these proteins important for?

A

C and S; important for negative feedback regulation of clotting cascade

97
Q

Vitamin K deficiency results in:

A

increased bruising & bleeding

98
Q

Anticoagulant medication, antagonist for vitamin K:

A

Warfarin

99
Q

Warfarin is a ___ medication that is an antagonist for ___ and functions to inhibit ___

A

anticoagulation; antagonist; clotting

100
Q

List some foods rich in vitamin K: (10)

A
  1. Kale
  2. Brussel Sprouts
  3. Brocoli
  4. Asparagus
  5. Cabbage
  6. Green Snap Beans
  7. Kiwi
  8. Collard Greens
  9. Turnip Greens
  10. Spinach
101
Q

MOST important coagulation factor:

A

Thrombin

102
Q

Thrombin is responsible for the conversion of:

A

fibrinogen into cross-linked fibrin

103
Q

Responsible for conversion of fibrinogen into fibrin:

A

Thrombin

104
Q

What activates platelets?

A

Thrombin

105
Q

The effects of thrombin can be described as:

A

Pro-inflammatory effects & Anti-coagulation effects

106
Q

Thrombin displays anti-coagulation effects after encountering:

A

normal endothelium

107
Q

Factors limiting coagulation include:

A
  1. dilution of blood past the site of injury
  2. negatively charged phospholipids required- activated platelets
  3. Regulation by neighboring intact endothelium
  4. Fibrionlytic cascade limits size of clot
108
Q

Fibrinolytic cascade limits the size of the but ___ activation is essential for this.

A

plasmin

109
Q

The ____ serves as a barrier to platelets resulting in lack of access to ___ & ___

A

endothelium; VWF & collagen

110
Q

Release of nitric oxide, prostacyclin, and adenosine diphosphate by the endothelium result in:

A

barrier to platelets - coagulation limitation

111
Q

The endothelium expresses factors that inactivate ___ resulting in ___

A

thrombin; anticoagulant effects

112
Q

Synthesis of tissue plasminogen activator (tPA) is considered a _____ effect

A

fibrinolytic (busts up the clot I think)

113
Q

Coronary artery disease, MI and chronic inflammation are a result of:

A

endothelial injury leading to thrombosis

114
Q

Endothelial injury can cause:

A

Thrombosis

115
Q

Physical injury, infectious agents, abnormal blood flow, inflammatory mediators, toxins=

A

chronic inflammation (may lead to thrombosis)

116
Q

Abnormal blood flow promotes endothelial procoagulant activity leading to:

A

thrombosis

117
Q

Abnormal blood flow can lead to stasis which allows:

A

platelets and leukocytes to associate with endothelial cells (leading to thrombosis)

118
Q

Abnormal blood flow can lead to stasis which slows:

A

removal of activated clotting factors, and impedes inflow of clotting factor inhibitors (leading to thrombosis)

119
Q

abnormally high tendency for blood to clot:

A

hypercoagulability

120
Q

What is an important risk factor for venous thrombosis?

A

hypercoagulability

121
Q

Hypercoagulability may be classified as:

A

Primary (genetic) or Secondary (acquired)

122
Q

Hypercoagulability that is genetic in nature:

A

primary disorder

123
Q

Hypercoagulability that is acquired:

A

secondary disorder

124
Q

Virchow’s triad in thrombosis:

A
  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
125
Q

What is the most important factor in thrombosis?

A

Endothelial integrity

126
Q

Abnormalities of procoagulatants or anti-coagulants can tip the balance in favor of:

A

thrombosis

127
Q

____ (____) can lead to hypercaogulability directly and also indirectly through endothelial dysfunction

A

Abnormal blood flow (stasis or turbulence)

128
Q

Where can thrombi develop?

A

anywhere in the cardiovascular system

129
Q

What type of thumb often occur at sites of injury?

A

arterial thrombi

130
Q

What type of thrombi occur in heart chambers or aorta:

A

cardiac mural thrombi

131
Q

What type of thumb occur often at sites of stasis?

A

venous thrombi

132
Q

Observed both grossly and microscopically; differentiates antemortem clots from postmortem clots:

A

Lines of Zahn - is the beech dead or alive

133
Q

Thrombi occurring in heart chambers or aortic lumen:

A

cardiac mural thrombi

134
Q

Thrombi typically rich in platelets, often formed by endothelial injury:

A

arterial trhombi

135
Q

Venous thrombi may also be called:

A

phlebothrombosis

136
Q

Thrombi that contain high volumes of red blood cells:

A

Venous thrombi

137
Q

____% of venous thrombi occur in the ___

A

90%; legs

138
Q

Fate of thrombi includes: (4)

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and recanalization
139
Q

What fate of thrombi are being described below?

Clot enlarges

A

propagation

140
Q

What fate of thrombi are being described below?

clot dislodged and moved by circulatory system

A

embolization

141
Q

What fate of thrombi are being described below?

activations of fibrinolytic factors

A

dissolution

142
Q

What fate of thrombi are being described below?

older thrombi are reorganized to facilitate some function

A

organization & recanalization

143
Q

Clot in the leg that is described as “local congestion and swelling from impaired blood flow:

A

Superficial vein clot

144
Q

Give an example of a superficial vein:

A

varicose veins

145
Q

Deep venous thrombosis occurs in larger veins called:

A

deep veins

146
Q

What are two risks with deep venous thrombosis?

A
  1. may be asymptomatic in 50% of patients
  2. may embolism to lungs
147
Q

What is major cause of arterial and cardiac thrombosis?

A

atherosclerosis

148
Q

atherosclerosis results in ____ which leads to:

A

results in loss of endothelial integrity and abnormal blood flow; leads to MI & ischemia to organs (especially brain, kidneys, and spleen)

149
Q

DIC:

A

disseminated intravascular coagulation

150
Q

DIC- Disseminated Intravascular Coagulation can be described as:

A

widespread thrombosis & microcirculation

151
Q

Disseminated Intravascular Coagulation (DIC) involves the consumption of:

A

platelets and clotting factors

152
Q

DIC may occur from:

A

complications in obstetrics, injuries, cancer, and more

153
Q

The net result from DIC:

A

excessive clotting and bleeding

154
Q

May be a solid, liquid or gaseous mass, carried by the blood from its point of origin to a distant site:

A

embolism

155
Q

Most common embolism:

A

pulmonary embolism

156
Q

Most common embolism, mostly from upper deep leg veins proximal to popliteal fossa. They pass through the larger right heart vessels and lodge in the pulmonary artery or arterioles:

A

pulmonary embolism

157
Q

Most pulmonary embolisms are small an then progressively become organized but larger ones can cause ____, and multiple emboli over time causes ____ and ____

A

sudden death; pulmonary hypertension & right ventricular failure

158
Q

May arise from intracardiac mural thrombi (80%). Can embolism to lower extremities most frequently, CNS, intestines, kidney and spleen:

A

Systemic thromboembolism

159
Q

Injury to bone marrow can cause release of fat globules into circulation but rarely show clinical manifestations. Less than 10% show pulmonary problems, neurologic problems, anemia, thrombocytopenia, and petechial rash:

A

Fat embolism

160
Q

Severe post-birth complication with 80% mortality rate due to biochemical activation of coagulation system and immune system from entry of amniotic fluid into circulation system of mother:

A

Amniotic fluid embolism

161
Q

Gas in circulation can come together to obstruct vascular flow- example decompression sickness in scuba divers

A

Air embolism

162
Q

How does a pulmonary embolism form? (3)

A
  1. embolus breaks off
  2. embolus travels through vein to lung
  3. embolus travels through heart and gets lodged in blood vessel of lungs
163
Q

Area of ischemic necrosis caused by occlusion of vascular supply to the affected tissue:

A

infarction

164
Q

Most infarctions are caused by:

A

arterial thrombosis or embolism

165
Q

What are the most common complications of infarctions?

A

involvement of the heart and brain

166
Q

Infarctions are classified based on:

A

color

167
Q

Infarct that contains hemorrhage:

A

red infarct

168
Q

A red infarct can be caused by:

A
  • venous occlusion
  • loose tissue
  • tissue with dual circulation
    -previously congested tissue
  • reperfusion injury
169
Q

Infarct that is an arterial occlusion in solid organs:

A

white infarct

170
Q

A white infarct can occur in the:

A

heart, liver, or spleen

171
Q

A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and lead to cellular hypoxia:

A

shock

172
Q

Prolonged shock leads to:

A

irrreversible tissue injury

173
Q

Three types of shock include:

A
  1. cardiac shock
  2. hypovolemic shock
  3. septic shock
174
Q

Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow resulting in shock:

A

cardiogenic shock

175
Q

Inadequate blood or plasma volume resulting in shock:

A

hypovolemic shock

176
Q

Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades resulting in shock:

A

septic shock

177
Q
  • Myocardial infarction
  • Ventricular rupture
  • Arrhythmia
  • Cardiac tamponade
  • Pulmonary embolism

These are all potential causes of:

A

cardiogenic shock

178
Q
  • Hemmorhage
  • Fluid loss (vomiting, diarrhea, burns, trauma)

These are all potential causes of:

A

hypovolemic shock

179
Q
  • overwhelming microbial infections
  • gram-negative sepsis
  • gram-positive septicemia
  • fungal sepsis
  • superantigens (toxic shock syndrome)

These are all potential causes of:

A

septic shock

180
Q
A

Pathology (24 decks)

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