Hemodynamic Disorders Flashcards

1
Q

____ delivers oxygen and nutrients to tissues and removes wastes

A

blood circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The functions of circulation include:

A
  1. Delivers oxygen & nutrients
  2. Wastes are removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Blood clotting that prevents excess bleeding after blood vessel damage:

A

hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Inappropriate clotting:

A

thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

migration of clots:

A

embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

active process, arteriolar dilation and increased blood inflow:

A

hyperemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the color of blood associated with hyperemia:

A

Red color- due to oxygenated hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the color of blood associated with congestion:

A

blue/red color (cyanosis)- deoxygenated hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperemia is a ____ process

Congestion is a ____ process

A

Hyperemia- active
Congestion- passive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

_____% of body weight is water, ___ intracellular

A

60%; 2/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

interstitial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

around ___% blood plasma is found in the body

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

accumulation of interstitial fluid in tissues

A

edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Edema is the accumulation of ___ in tissues

A

interstitial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

extravascular fluid that collects in body cavities:

A

effusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effusions are ___ that collects in body cavities

A

extravascular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Effusion in the pleural cavity:

A

hydrothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Effusion in the pericardial cavity:

A

hydropericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Effusion in the peritoneal cavity:

A

hydroperitoneum or ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Anasarca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What may cause increased hydrostatic pressure that leads to edema? (2)
1. impaired venous return 2. arteriolar dilation
26
- 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:
impaired venous return (leading to increased hydrostatic pressure which is a cause of edema)
27
- Heat - Neurohumoral dysregulation These are examples of:
components leading to arteriolar dilation (which leads to increased hydrostatic pressure which is a cause of edema)
28
- Protein-losing glomerulopathies (nephrotic syndrome) - Liver cirrhosis (ascites) - Malnutrition - Protein-losing gastroenteropathy These are all conditions leading to:
reduced plasma osmotic pressure (hypoproteinemia) (which is a cause of edema)
29
-Inflammatory - Neoplastic - Postsurgical - Postirradiation These are all conditions leading to:
lymphatic obstruction (which is a cause of edema)
30
- Excessive salt intake with renal insufficiency - Increased tubular reabsorption of sodium - Renal hypperfusion - Increase renin-angiotensin-aldosterone secretion These are all conditions leading to:
sodium retention (which is a cause of edema)
31
- Acute inflammation - Chronic inflammation - Angiogenesis These are all conditions leading to:
inflammation (which is a cause of edema)
32
What is responsible for dictating fluid movement between vascular and interstitial spaces?
- vascular hydrostatic pressure - colloid osmotic pressure (plasma proteins)
33
What causes colloid osmotic pressure?
plasma proteins
34
vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins) dictate fluid movement between:
vascular and interstitial spaces
35
Arterial outflow is normally balanced by:
inflow at the venous end
36
____ is normally balanced by inflow at the venous end
arterial outflow
37
Arterial outflow is normally balanced by inflow at the venous end: Results in small net ____ --> drained by ___
outflow of fluid in interstitial space; lymphatics
38
Capillary hydrostatic and osmotic forces are normally balanced so their is little net movement of fluid into the:
interstitium
39
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:
extravascular fluid accumulation (edema)
40
Increased _____ or diminished ____ leads to extravascular fluid accumulation (edema)
hydrostatic pressure; plasma osmotic pressure
41
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
thoracic duct; tissue edema
42
Usually caused by disorders that impair venous return:
increased hydrostatic pressure
43
Disorders that can cause impaired venous return: (2)
1. Deep venous thrombosis 2. Congestive heart failure
44
Increased hydrostatic pressure is usually caused by disorders that:
impair venous return
45
Reduced plasma albumin concentration will lead to:
reduced plasma osmotic pressure
46
Reduced plasma albumin concentration may result from:
loss in circulation or reduced synthesis
47
Nephrotic syndrome and severe liver disease are both causes for:
reduced plasma albumin concentration (which reduces plasma osmotic pressure)
48
Fill in the highlighted portions:
A: heart failure B: malnutrition C: decreased hepatic synthesis D: nephrotic syndrome E: renal failure F: edema
49
Fill in the highlighted portions:
Green: DECREASED plasma albumin Blue: DECREASED plasma osmotic pressure
50
Fill in the highlighted portions:
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
51
Pathways leading to _____ can result form heart failure, renal failure, or reduced plasma osmotic pressure
systemic edema
52
Compromises resorption of fluid from interstitial spaces --> edema:
lymphatic obstruction
53
What conditions can lead to lymphatic obstruction? (3)
1. inflammatory conditions 2. neoplastic conditions 3. congenital lymphedema
54
What does lymphatic obstruction compromise?
resorption of fluid from interstitial spaces (ultimately leading to edema)
55
Stage of lymphedema in which the lymphatic system experiences abnormal flow but no fluid build-up; (asymptomatic):
stage 1
56
Stage of lymphedema which is due to an accumulation of lymph fluid that may subside when elevated; (swelling):
stage 2
57
Stage of lymphedema categorized by permanent swelling that cannot be relived through elevation, accompanied by changes in the skin (fibrosis):
stage 3
58
Stage of lymphedema characterized by lymphostatic elephantiasis, or the deformation of a limb due to extensive swelling, skin thickening and scarring:
Stage 4
59
extravasation of blood from vessels:
hemorrhage
60
Defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic condition, inherited/aquired defects are all causes of:
hemorrhage
61
Hemorrhage manifestations include: (4)
1. hematoma 2. ecchymoses 3. purpura 4. petechiae
62
Large collection of hemorrhage in a tissue:
hematoma
63
1-2cm subcutaneous hemorrhage (bruises):
ecchymoses
64
3-5mm hemorrhages:
purpura
65
1-2 mm minute hemorrhage:
petechiae
66
Often a consequence of thrombocytopenia or vitamin C deficiency:
petechiae
67
What can be seen in this image?
petechiae
68
Clot formation steps include: (4)
1. vasoconstriction 2. platelet plug formation 3. fibrin deposition 4. clot stabilization & resorption
69
____ are the primary regulations of hemostasis though changes in expression of procoagulaant or anticoagulation factors
endothelial cells
70
Endothelial cells are the primary regulators of hemostasis through changes in expression of ___ or ___ factors
procoagulant; anticoagulant
71
Disk-shaped, enucleate fragments of megakaryocytes:
platelets
72
Platelet adhesion is mediated by:
von willebrand factor
73
Congenital deficiency of receptors or molecules may lead to:
bleeding disorders
74
Functions as adhesion bridge between subednothelial collagen and glycoprotein Ib (Gp1b) platelet receptor
VWF
75
Platelet aggregation is accomplished by ____ binding to platelet ____ on different platelets
fibrinogen; GpIIb-IIIa
76
Deficiency due to Gp2b-3a complex:
Glanzmann thrombasthenia
77
Deficiency due to Gp1b:
Bernard-Soulier syndrome
78
Von willebrand factor deficiency:
Von Willebrand disease
79
A serious of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot:
coagulation cascade
80
The coagulation cascade is also known as:
secondary hemostasis
81
Coagulation cascade pathway that is spontaneous and occurs when there is internal injury to vascular endothelium
intrinsic pathway
82
Coagulation cascade pathway that is activated by external trauma:
extrinsic pathway
83
Contact activation due to a damaged surface occurs with what coagulation cascade pathway?
intrinsic pathway
84
Label the following steps of the coagulation cascade pathways:
1. Intrinsic pathways 2. Common pathway 3. Extrinsic pathway
85
The intrinsic pathway of the coagulation cascade is activated by:
contact activation - (damaged surface)
86
The extrinsic pathway of coagulation is activated by ____.
injury
87
Factors from the intrinsic pathway & factors from the extrinsic pathway that converge: What do they act on?
5A- They form the prothrombinase complex to act on prothrombin and convert it to thrombin
88
What is the ultimate result of the various pathways of the coagulation cascade?
clot formation
89
A coagulation cascade assay is:
an evaluation of coagulation function
90
___ evaluates the intrinsic pathway factors:
Partial prothrombin time (PTT)
91
PTT evaluates ___ pathway factors including: (8)
intrinsic; XII, XI, IX, VIII, X, V, Prothrombin (II), Fibrinogen (I)
92
___ evaluates the extrinsic pathway factors:
Prothrombin time (PT)
93
Prothrombin time evaluates the ___ pathway factors including: (5)
extrinsic; VII, X, V, Prothrombin (II), Fibrinogen (I)
94
Important for regulation of coagulation, and plays a key role in synthesis of factors II, VII, IX & X:
Vitamin K
95
Vitamin K plays a key role in the synthesis of factors:
II, VII, IX, X
96
Vitamin K helps synthesize protein ___ and ___. What are these proteins important for?
C and S; important for negative feedback regulation of clotting cascade
97
Vitamin K deficiency results in:
increased bruising & bleeding
98
Anticoagulant medication, antagonist for vitamin K:
Warfarin
99
Warfarin is a ___ medication that is an antagonist for ___ and functions to inhibit ___
anticoagulation; antagonist; clotting
100
List some foods rich in vitamin K: (10)
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
MOST important coagulation factor:
Thrombin
102
Thrombin is responsible for the conversion of:
fibrinogen into cross-linked fibrin
103
Responsible for conversion of fibrinogen into fibrin:
Thrombin
104
What activates platelets?
Thrombin
105
The effects of thrombin can be described as:
Pro-inflammatory effects & Anti-coagulation effects
106
Thrombin displays anti-coagulation effects after encountering:
normal endothelium
107
Factors limiting coagulation include:
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
Fibrinolytic cascade limits the size of the but ___ activation is essential for this.
plasmin
109
The ____ serves as a barrier to platelets resulting in lack of access to ___ & ___
endothelium; VWF & collagen
110
Release of nitric oxide, prostacyclin, and adenosine diphosphate by the endothelium result in:
barrier to platelets - coagulation limitation
111
The endothelium expresses factors that inactivate ___ resulting in ___
thrombin; anticoagulant effects
112
Synthesis of tissue plasminogen activator (tPA) is considered a _____ effect
fibrinolytic (busts up the clot I think)
113
Coronary artery disease, MI and chronic inflammation are a result of:
endothelial injury leading to thrombosis
114
Endothelial injury can cause:
Thrombosis
115
Physical injury, infectious agents, abnormal blood flow, inflammatory mediators, toxins=
chronic inflammation (may lead to thrombosis)
116
Abnormal blood flow promotes endothelial procoagulant activity leading to:
thrombosis
117
Abnormal blood flow can lead to stasis which allows:
platelets and leukocytes to associate with endothelial cells (leading to thrombosis)
118
Abnormal blood flow can lead to stasis which slows:
removal of activated clotting factors, and impedes inflow of clotting factor inhibitors (leading to thrombosis)
119
abnormally high tendency for blood to clot:
hypercoagulability
120
What is an important risk factor for venous thrombosis?
hypercoagulability
121
Hypercoagulability may be classified as:
Primary (genetic) or Secondary (acquired)
122
Hypercoagulability that is genetic in nature:
primary disorder
123
Hypercoagulability that is acquired:
secondary disorder
124
Virchow's triad in thrombosis:
1. endothelial injury 2. abnormal blood flow 3. hypercoagulability
125
What is the most important factor in thrombosis?
Endothelial integrity
126
Abnormalities of procoagulatants or anti-coagulants can tip the balance in favor of:
thrombosis
127
____ (____) can lead to hypercaogulability directly and also indirectly through endothelial dysfunction
Abnormal blood flow (stasis or turbulence)
128
Where can thrombi develop?
anywhere in the cardiovascular system
129
What type of thumb often occur at sites of injury?
arterial thrombi
130
What type of thrombi occur in heart chambers or aorta:
cardiac mural thrombi
131
What type of thumb occur often at sites of stasis?
venous thrombi
132
Observed both grossly and microscopically; differentiates antemortem clots from postmortem clots:
Lines of Zahn - is the beech dead or alive
133
Thrombi occurring in heart chambers or aortic lumen:
cardiac mural thrombi
134
Thrombi typically rich in platelets, often formed by endothelial injury:
arterial trhombi
135
Venous thrombi may also be called:
phlebothrombosis
136
Thrombi that contain high volumes of red blood cells:
Venous thrombi
137
____% of venous thrombi occur in the ___
90%; legs
138
Fate of thrombi includes: (4)
1. Propagation 2. Embolization 3. Dissolution 4. Organization and recanalization
139
What fate of thrombi are being described below? Clot enlarges
propagation
140
What fate of thrombi are being described below? clot dislodged and moved by circulatory system
embolization
141
What fate of thrombi are being described below? activations of fibrinolytic factors
dissolution
142
What fate of thrombi are being described below? older thrombi are reorganized to facilitate some function
organization & recanalization
143
Clot in the leg that is described as "local congestion and swelling from impaired blood flow:
Superficial vein clot
144
Give an example of a superficial vein:
varicose veins
145
Deep venous thrombosis occurs in larger veins called:
deep veins
146
What are two risks with deep venous thrombosis?
1. may be asymptomatic in 50% of patients 2. may embolism to lungs
147
What is major cause of arterial and cardiac thrombosis?
atherosclerosis
148
atherosclerosis results in ____ which leads to:
results in loss of endothelial integrity and abnormal blood flow; leads to MI & ischemia to organs (especially brain, kidneys, and spleen)
149
DIC:
disseminated intravascular coagulation
150
DIC- Disseminated Intravascular Coagulation can be described as:
widespread thrombosis & microcirculation
151
Disseminated Intravascular Coagulation (DIC) involves the consumption of:
platelets and clotting factors
152
DIC may occur from:
complications in obstetrics, injuries, cancer, and more
153
The net result from DIC:
excessive clotting and bleeding
154
May be a solid, liquid or gaseous mass, carried by the blood from its point of origin to a distant site:
embolism
155
Most common embolism:
pulmonary embolism
156
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:
pulmonary embolism
157
Most pulmonary embolisms are small an then progressively become organized but larger ones can cause ____, and multiple emboli over time causes ____ and ____
sudden death; pulmonary hypertension & right ventricular failure
158
May arise from intracardiac mural thrombi (80%). Can embolism to lower extremities most frequently, CNS, intestines, kidney and spleen:
Systemic thromboembolism
159
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:
Fat embolism
160
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:
Amniotic fluid embolism
161
Gas in circulation can come together to obstruct vascular flow- example decompression sickness in scuba divers
Air embolism
162
How does a pulmonary embolism form? (3)
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
Area of ischemic necrosis caused by occlusion of vascular supply to the affected tissue:
infarction
164
Most infarctions are caused by:
arterial thrombosis or embolism
165
What are the most common complications of infarctions?
involvement of the heart and brain
166
Infarctions are classified based on:
color
167
Infarct that contains hemorrhage:
red infarct
168
A red infarct can be caused by:
- venous occlusion - loose tissue - tissue with dual circulation -previously congested tissue - reperfusion injury
169
Infarct that is an arterial occlusion in solid organs:
white infarct
170
A white infarct can occur in the:
heart, liver, or spleen
171
A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and lead to cellular hypoxia:
shock
172
Prolonged shock leads to:
irrreversible tissue injury
173
Three types of shock include:
1. cardiac shock 2. hypovolemic shock 3. septic shock
174
Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow resulting in shock:
cardiogenic shock
175
Inadequate blood or plasma volume resulting in shock:
hypovolemic shock
176
Peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades resulting in shock:
septic shock
177
- Myocardial infarction - Ventricular rupture - Arrhythmia - Cardiac tamponade - Pulmonary embolism These are all potential causes of:
cardiogenic shock
178
- Hemmorhage - Fluid loss (vomiting, diarrhea, burns, trauma) These are all potential causes of:
hypovolemic shock
179
- overwhelming microbial infections - gram-negative sepsis - gram-positive septicemia - fungal sepsis - superantigens (toxic shock syndrome) These are all potential causes of:
septic shock
180