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Pathology > Hemodynamic disorders > Flashcards

Hemodynamic disorders Flashcards

1
Q

______ delivers oxygen and nutrients to tissues & removes wastes

A

blood circulation

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2
Q

Three functions of circulation:

A
  1. delivers oxygen to tissues
  2. delivers nutrients to tissues
  3. 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 the blood associated with hyperemia:

A

red color- due to oxygenated hemoglobin

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8
Q

In hyperemia we see ______ colored blood due to ______ hemoglobin

A

red; oxygenated

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9
Q

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

A

congestion

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10
Q

Describe the color of blood associated with congestion:

A

blue/red color (cyanosis)- deoxygenated hemoglobin

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11
Q

In congestion we see _____ colored blood due to _____ hemoglobin

A

blue/red (cyanosis); deoxygenated

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12
Q

Hyperemia is a ____ process

Congestion is a ____ process

A

active; passive

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13
Q

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

A

Liver with chronic passive congestion & hemorrhagic necrosis; dead specimem

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14
Q

_____ % of the body weight is water, ______ intracellular

A

60%; 2/3

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15
Q

Two thirds of the 60% water comprising our body weight is:

A

Intracellular

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16
Q

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

A

Interstitial fluid

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17
Q

Around _____ % blood plasma is found in the body

A

5%

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18
Q

accumulation of interstitial fluid in tissues:

A

edema

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19
Q

Edema is the accumulation of ____ in tissues

A

interstitial fluid

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20
Q

Extravascular fluid that collects in body cavities:

A

Effusions

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21
Q

Effusions are _____ that collects in body cavities

A

extravascular fluid

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22
Q

Effusion in the pleural cavity:

A

hydrothorax

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23
Q

Effusion in the pericardial cavity:

A

hydropericardium

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24
Q

Effusion in the peritoneal cavity:

A

hydroperitoneum or ascites

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25
Q

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

A

anasarca

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26
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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27
Q

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

A
  1. impaired venous return
  2. arterial dilation
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28
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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29
Q

-Heat
-Neurohumoral dysregulation

These are all examples of:

A

Ateriolar dilation (leading to increased hydrostatic pressure which is a cause of edema)

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30
Q

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

These are all examples of:

A

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

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31
Q

-Inflammatory
-Neoplastic
-Postsurgical
-Postirradiation

These are all examples of conditions leading to:

A

Lymphatic obstruction (which is a cause of edema)

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32
Q

-Excessive salt intake with renal insufficiency
-Increased tubular reabsorption of sodium
-Renal hypoperfusion
-Increased renin-angtiotensin-aldosterone secretion

These are all causes of:

A

Sodium retention (which is a cause of edema)

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33
Q

-Acute inflammation
-Chronic inflammation
-Angiogenesis

Theses are all causes of:

A

Inflammation (which is a cause of edema)

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34
Q

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

A

-vascular hydrostatic pressure
-colloid osmotic pressure (plasma proteins)

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35
Q

What causes colloid osmotic pressure?

A

Plasma proteins

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36
Q

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

A

vascular & interstitial spaces

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37
Q

Arterial outflow is normally balanced by:

A

inflow at the venous end

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38
Q

_____ is normally balanced by inflow at the venous end

A

arterial outflow

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39
Q

Arterial outflow is normall 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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40
Q

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

A

Interstitium

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41
Q

Capillary hydrostatic and osmotic forces are normally balanced so there is little net movement of fluid into the interstitium. However, ________ hydrostatic pressure or _______ plasma osmotic pressure leads to extravascular fluid accumulation (edema)

A

increased hydrostatic pressure
diminished plasma osmotic pressure

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42
Q

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

A

thoracic duct; tissue edema

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43
Q

Usually caused by disorders that impair venous return:

A

increased hydrostatic pressure

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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

Disorders that can cause impaired venous return: (2)

A
  1. deep venous thrombosis
  2. congestive heart failure
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46
Q

Reduced plasma albumin concentration will lead to:

A

Reduced plasma osmotic pressure

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47
Q

Reduced plasma albumin concentration may be result from:

A

loss in circulation or reduced synthesis

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48
Q

Nephrotic syndrome and severe liver disease are both causes for:

A

Reduced plasma albumin concentration (wich reduces plasma osmotic pressure)

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49
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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50
Q

Fill in the highlighted portions:

A

Green:
DECREASED plasma albumin

Blue:
DECREASED plasma osmotic pressure

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51
Q

Fill in the highlighted portions:

A

Green:
INCREASED capillary hydrostatic pressure

Blue:
DECREASED renal blood flow

Orange:
Activation of the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

Pink:
Retention of Na+ & H2O

Purple:
INCREASED blood volume

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52
Q

Pathways leading to ______ can result from heart failure, renal failure, or reduced plasma osmotic pressure

A

systemic edema

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53
Q

Compromises resorption of fluid from interstitial spaces leading to edema:

A

Lymphatic obstruction

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54
Q

What conditions can lead to lymphatic obstruction? (3)

A
  1. inflammatory conditions
  2. neoplastic conditions
  3. congenital lymphedema
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55
Q

What does lymphatic obstruction compromise?

A

Resorption of fluid from interstitial space (ultimately leading to edema)

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56
Q

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

A

Stage 1 (asymptomatic)

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57
Q

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

A

Stage 2 (swelling)

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58
Q

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

A

Stage 3

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59
Q

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

A

Stage 4

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60
Q

Extravasation of blood from vessels:

A

Hemorrhage

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61
Q

Defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic conditions, inherited/acquired defects are all causes:

A

hemorrhage

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62
Q

Hemorrhage manifestations include: (4)

A
  1. hematoma
  2. ecchymoses
  3. purpura
  4. petechiae
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63
Q

Large collection of hemorrhage in a tissue:

A

hematoma

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64
Q

1-2 cm subcutaneous hemorrhage (bruises):

A

ecchymoses

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65
Q

3-5 mm hemorrhages:

A

purpura

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66
Q

1-2 mm minute hemorrhage:

A

petechiae

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67
Q

Often a consequence of thrombocytopenia or Vitamin C deficiency:

A

Petechiae

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68
Q

What can be seen in this image?

A

Petechiae

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69
Q

Clot formation steps include: (4)

A
  1. vasoconstriction
  2. platelet plug forms
  3. fibrin clot deposition
  4. clot stabilization and resorption
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70
Q

_______ are the primary regulators of hemostasis through changes in expression of procoagulant or anticoagulant factors

A

Endothelial cells

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71
Q

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

A

procoagulant; anticoagulant

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72
Q

Disk-shaped, enucleate fragments of megakaryocytes:

A

Platelets

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73
Q

Platelet adhesion is mediated by:

A

Von Willenbrand factor

74
Q

Congenital deficiency of receptors or molecules may lead to:

A

Bleeding disorders

75
Q

Functions as an adhesion bridge between subendothelial collagen and the glycoprotein 1b (Gp1b) platelet receptor:

A

Von Willebrand factor

76
Q

Platelet aggregation is accomplished by ____ binding to platelet Gp1b-3b receptors on different platelets

A

fibrinogen

77
Q

Deficiency due to Gp2b-3a complex:

A

Ganzmann thrombasthenia

78
Q

Deficiency due to Gp1b:

A

Bernard-Soulier syndrome

79
Q

Deficiency due to Von Willebran factor:

A

Von Willebrand disease

80
Q

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

A

Coagulation cascade

81
Q

The coagulation cascade is also known as:

A

Secondary hemostasis

82
Q

Coagulation cascade pathway that is spontaneous and occurs in response to internal injury to the vascular endothelium:

A

Intrinsic pathway

83
Q

Coagulation cascade pathway that is activated by external trauma:

A

Extrinsic pathways

84
Q

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

A

Intrinsic

85
Q

Label the following pathways of the coagulation cascade:

A
  1. Intrinsic pathway
  2. Common pathway
  3. Extrinsic pathway
86
Q

The intrinsic pathway of the coagulation cascade is activated by _____ (____)

A

Contact activation (damaged surface)

87
Q

The extrinsic pathway of the coagulation cascade is activated by ______

A

Injury

88
Q

Factors form the intrinsic pathway & factors from the extrinsic pathway merge to the common pathway at:

What do they act on?

A

5a

The form the prothrombinase complex which act on prothrombin to convert it to thrombin

89
Q

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

A

Clot formation

90
Q

A coagulation cascade assay is an:

A

evaluation of coagulation function

91
Q

_____ evaluates intrinsic pathway factors

A

Partial prothrombin time (PTT)

92
Q

PTT evaluates ____ factors including: (8)

A

Intrinsic factors: XII, XI, IX, VIII, X, V, prothrombin (II), fibrinogen (I)

93
Q

_____ evaluates the extrinsic pathway factors:

A

Prothrombin time (PT)

94
Q

PT evaluates ____ factors including: (5)

A

Extrinsic factors: VII, X, V, prothrombin (II), fibrinogen (I)

95
Q

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

A

Vitamin K

96
Q

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

A

II, VII, IX, X

97
Q

Vitamin K helps synthesize ____ & _____. What are these proteins important for?

A

Protein C & S; important for negative feedback regulation of clotting cascade

98
Q

Vitamin K deficiency results in:

A

increased bruising & bleeding

99
Q

Anticoagulant mediation; antagonist for vitamin K:

A

Warfarin

100
Q

Warfarin is a ____medication that is an antagonist for _____ and functions to inhibit _____

A

anticoagulant; antagonist; clotting

101
Q

List some foods rich in Vitamin K: (10)

A

-Kale
-green snap beans
-brussel sprouts
-kiwi
-brocoli
-collard greens
-asparagus
-turnip greens
-cabbage
-spinach

102
Q

MOST important coagulation factor:

A

Thrombin

103
Q

Thrombin is responsible for conversion of:

A

Fibrinogen into cross-linked fibrin

104
Q

Responsible for conversion of fibrinogen into cross-linked fibrin:

A

Thrombin

105
Q

What activates platelets?

A

Thrombin

106
Q

The effects of thrombin can be described as:

A

Pro-inflammatory effects & anti-coagulation effects

107
Q

Thrombin displays anti-coagulation effects after encountering:

A

normal endothelium

108
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. fibrinolytic cascade limits size of clot
109
Q

Fibrinolytic cascade limits the size of the clot but ____ activation is essential for this to occur

A

Plasmin

110
Q

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

A

Endothelium; VWF & collagen

111
Q

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

A

Barrier to the platelets- coagulation limitation

112
Q

The endothelium expresses factors that inactivate _____ resulting in _____

A

thrombin; anticoagulant effects

113
Q

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

A

Fibrinolytic effect

114
Q

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

A

Endothelial injury leading to thrombosis

115
Q

Endothelial injury can cause

A

thrombosis

116
Q

Physical injury, infectious agent, abnormal flood flow, inflammatory mediators, toxins=

A

Chronic inflammation (may lead to thrombosis)

117
Q

Abnormal blood flow promoting endothelial procoagulant activity may result in:

A

Thrombosis

118
Q

Abnormal blood flow can lead to stasis which allows:

A

Platelets & leukocytes to associated with endothelial cells (leading to thrombosis)

119
Q

Abnormal blood can lead to stasis which slows:

A

the removal of activated clotting factors, and impedes inflow of clotting factor inhibitors

120
Q

Abnormally high tendency for blood to clot:

A

Hypercoagulability

121
Q

What is an important risk factor for venous thrombosis?

A

Hypercoagulability

122
Q

Hypercoagulabiity may be classified as:

A

Primary (genetic) or Secondary (acquired)

123
Q

Hypercoagulability that is genetic in nature:

A

Primary disorder

124
Q

Hypercoagulability that is acquired:

A

Secondary disorder

125
Q

Virchow’s train in thrombosis:

A
  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
126
Q

What is the most important factor in thrombosis?

A

Endothelial integrity

127
Q

Abnormalities of procoagulants or anticoagulants can tip the balance in favor of:

A

Thrombosis

128
Q

______ (______) can lead to hypercoagulability directly and also indirectly though endothelial dysfunction

A

Abnormal blood flow (stasis or turbulence)

129
Q

Where can thrombi develop?

A

Anywhere in cardiovascular system

130
Q

What type of thrombi often occur at sites of injury?

A

Arterial thrombi

131
Q

What type of thrombi occur in the heart chambers or aorta?

A

cardiac mural thrombi

132
Q

What type of thrombi occur often at sites of stasis?

A

Venous thrombi

133
Q

Observed grossly & microscopically; differentiates antemortem clots from postmortem clots:

A

Lines of Zahn

134
Q

Thrombi occur in heart chambers or aortic lumen:

A

Cardiac mural thrombi

135
Q

Thrombi that are typically rich platelets, often formed by endothelial injury:

A

Arterial thrombi

136
Q

Thrombi that contain a high volume of red blood cells:

A

Venous thrombi

137
Q

Venous thrombi may also be termed:

A

Phlebothrombosis

138
Q

____% of venous thrombi occur in the _____

A

90% legs

139
Q

Fate of thrombi includes: (4)

A
  1. propogation
  2. embolization
  3. dissolution
  4. organization and recanalization
140
Q

What fate of thrombi is described below?

Clot enlarges:

A

Propogation

141
Q

What fate of thrombi is described below?

Clot disparaged and moved by circulatory system

A

Embolization

142
Q

What fate of thrombi is described below?

Activation of fibrinolytic factors

A

Dissolution

143
Q

What fate of thrombi is described below?

Older thrombi are reorganized to facilitate some function

A

Organization & recanalization

144
Q

Clot in the leg that is described as “local congestion & swelling from impaired venous flow”:

A

Superficial vein clot

145
Q

Give an example of a superficial vein that a clot may occur in:

A

Varicose veins

146
Q

Deep venous thrombosis occur in larger veins called:

A

Deep veins

147
Q

What are two risks with deep vein thrombosis?

A
  1. may be asymptomatic in 50% of patients
  2. may embolize to lungs
148
Q

Atherosclerosis is a major cause of:

A

Arterial & cardiac thrombosis

149
Q

What is a major cause of arterial & cardiac thrombosis?

A

Atherosclerosis

150
Q

Atherosclerosis results in ____ which leads to:

A

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

151
Q

DIC:

A

Disseminate intravascular coagulation

152
Q

DIC- Disseminated intravascular coagulation can be described as:

A

Widespread thrombosis within microcirculation

153
Q

Disseminated intravascular coagulation (DIC) involves the consumption of:

A

Platelets & clotting factors

154
Q

DIC may occur form:

A

Complications in obstetrics, injuries, cancer & more

155
Q

What is the net result of DIC?

A

Excessive clotting & bleeding

156
Q

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

A

Embolism

157
Q

Most common embolism:

A

Pulmonary embolism

158
Q

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

A

Pulmonary embolisms

159
Q

Most pulmonary embolisms are small & then progressively become organized, but large ones can cause _______, and multiple emboli over time can cause ____ & _____

A

sudden death; pulmonary hypertension; right ventricular failure

160
Q

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

A

Systemic thromboembolism

161
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

162
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

163
Q

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

A

Air embolism

164
Q

How does a pulmonary embolism form?

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
165
Q

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

A

Infarction

166
Q

Most infarctions are caused by:

A

arterial thrombosis or embolism

167
Q

What are the most common complication of infarctions?

A

Involvement of the heart & brain

168
Q

Infarctions are classified according to:

A

color

169
Q

Infarct that contains hemorrhage:

A

Red infarct

170
Q

A red infarct can be caused by:

A

Venous occlusion, loose tissue, tissue with dual circulation, previously congested tide, reperfusion injury

171
Q

Infarct that is an arterial occlusion in solid organs:

A

White infarct

172
Q

A white infarct can occur in the:

A

Heart, liver, spleen

173
Q

A state in which diminished cardiac output to reduced effective circulating blood volume impairs tissue perfusion & leads to cellular hypoxia:

A

shock

174
Q

Prolonged shock leads to:

A

Irreversible tissue injury

175
Q

Three types of shock include:

A
  1. cardiac shock
  2. hypovolemic shock
  3. septic shock
176
Q

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

A

Cardiogenic shock

177
Q

Inadequate blood flow or plasma volume resulting in shock:

A

Hypovolemic shock

178
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

179
Q

-myocardial infarction
-ventricular rupture
-arrythmia
-cardiac tamponade
-pulmonary embolism

These are all potential causes of:

A

Cardiogenic shock

180
Q

-hemorrhage
-fluid loss (vomiting, diarrhea, burns, trauma)

These are all potential causes of:

A

Hypovolemic shock

181
Q
A

Pathology (28 decks)

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