Hemodynamic disorders Flashcards
(171 cards)
1
Q
Forces pushing fluid out of a vessel
A
hydrostatic pressure
2
Q
Osmotic force keeping fluid in a vessel
A
Oncotic pressure
3
Q
What is normally more than the other?
Forces keeping fluid in vessels or forces pushing/allowing fluid out?
A
Forces pushing/allowing fluid out is slightly greater
4
Q
Excess interstitial fluid
A
Edema
5
Q
Excess fluid in a cavity
A
Effusion
6
Q
Intra-abdominal effusion
A
Ascites
7
Q
3 reasons for excess fluid
A
Increased hydrostatic pressure
Decreased oncotic pressure
Increased vascular permeability
8
Q
3 reasons for increased hydrostatic pressure
A
Decreased venous return (may be local or systemic)
Increased plasma volume (kidney failure or increased Na retention)
Decreased lymphatic drainage (tumor, filariasis, scar tissue)
9
Q
2 reasons for decreased oncotic pressure
A
Decreased protein production (liver failure or malnutrition)
Increased protein loss (kidney failure or diarrheal illness)
10
Q
Fluid high in protein and cellularity
Seen in situations with high vascular permeability (inflammation, endothelial damage)
A
Exudate
11
Q
Fluid low in protein and cellularity
Seen in situations with high hydrostatic pressure or low colloid pressure (heart or liver failure)
A
Transudate
12
Q
Does high or low hydrostatic pressure lead to transudate?
A
High
13
Q
Disorder of perfusion involving increased intravascular blood due to increased inflow (inflammation)
A
Hyperemia
14
Q
Disorder of perfusion involving increased intravascular blood due to decreased outflow (heart failure)
May cause hepatomegaly
A
Congestion
15
Q
Disorder of perfusion involving blood leaving vascular space
Trauma, vascular disease, coagulopathy
A
Hemorrhage
16
Q
What is hyperemia (increased intravascular blood) due to?
A
Increased inflow
17
Q
What is congestion (increased intravascular blood) due to?
A
Decreased outflow
18
Q
Condition that makes someone vulnerable to bleeding with small injury
Can cause hemorrhages
Can involve platelets or coagulation proteins
A
Coagulopathy
19
Q
Pinpoint hemorrhage in skin or cornea
Due to microvascular rupture
A
Petechiae
20
Q
Diffuse superficial hemorrhages in skin
Often a confluence; often seen in small vessel disorders
A
Purpura
21
Q
Larger collection of blood in superficial skin
A
Ecchymosis
22
Q
Progression of bruise colors due to RBC degradation:
First to appear
A
Hemoglobin (red)
23
Q
Progression of bruise colors due to RBC degradation:
Second to appear
A
Deoxyhemoglobin (blue-red)
24
Q
Progression of bruise colors due to RBC degradation:
Third to appear
A
Biliverdin (yellow-green)
25
Progression of bruise colors due to RBC degradation:
Fourth to appear
Hemosiderin (yellow-brown)
26
Collection of blood in soft tissue of parenchymal organ
Hematoma
27
Collection of blood in anatomic space
Hemorrhagic effusion
28
Normal process to stop hemorrhage
Has three main contributing systems (vascular, platelets, coagulation)
Hemostasis
29
3 main contributing systems to hemostasis
Vascular (vascular activities slow or prevent hemorrhage)
Platelets (contribute to clot and help activate coagulation)
Coagulation (produces a fibrin meshwork)
30
Lining cell of blood vessels
Endothelium
31
Endothelium releases this which is a vasodilator that inhibits platelet aggregation
Prostacyclin (PG-I2)
32
Endothelium releases this which is a vasodilator
NO
33
Endothelium produces this which degrades platelet ADP
ADPase
34
Small disk shaped cytoplasmic buds from bone marrow megakaryocytes
Platelet
35
Platelet are small disk shaped cytoplasmic buds from these
Bone marrow megakaryocytes
36
Thrombocyte is another name for these
Platelets
37
Component with these procoagulant activities:
Provide surface phospholipid for coagulation factors
Provide ADP to activate others
Aggregate to form initial plug
Platelets
38
Platelets provide surface ______ for coagulation factors
Phospholipid
39
Coagulation system where:
Vascular injury induces vasoconstriction
Endothelium is activated to secrete vWF
Platelets adhere, activate, aggregate
Primary hemostasis
40
Coagulation system where:
Soluble coagulation factors --> fibrin
Fibrin clot forms to enmesh platelet aggregate
Secondary hemostasis
41
Coagulation system where:
Counter-regulatory measures keep it local
Tertiary hemostasis
42
3 main steps of hemostasis
1. Vasoconstriction
2. Platelet plug
3. Coagulation cascade
43
Damaged endothelium releases this, which leads to vasoconstriction
Transient effect
Promotes smooth muscle constriction
Vessel caliber decreases
Endothelin
44
Endothelin is released by this
Damaged endothelium
45
Endothelin has this effect
Vasoconstriction
46
Platelets adherence to exposed collagen (ECM) is mediated by this interaction
Glycoprotein Ib (platelet receptor) binding to von Willebrand factor (which is produced by endothelium and platelets, and binds to exposed collagen)
47
This is produced by endothelium and platelets
Binds to exposed collagen
Is bound by glycoprotein 1b on platelets
von Willebrand factor (vWF)
48
What is the role of von Willebrand factor (vWF)?
Mediates platelets adherence to exposed collagen (ECM)
Is produced by endothelium and platelets
Binds to exposed collagen
Is bound by glycoprotein 1b on platelets
49
Platelet receptor that binds to vWF during platelets adherence to exposed collagen
Glycoprotein Ib
50
This binds to platelet receptor, changing platelet shape to have "sticky ends" (starfish shape)
Thrombin (or ADP or serotonin)
51
After changing shape due to thrombin, platelet sticky ends have high density of this
Glycoprotein 2b/3a
52
4 steps of platelet activation during primary hemostasis
Platelet change shape
Glycoprotein 2b/3a concentrates on tips of filopodia
ADP/serotonin released (activate nearby platelets)
Fibrinogen released
53
Interaction that causes platelets to aggregate
Glycoprotein 2b/3a binds fibrinogen polymer to form connecting bridge between platelets
54
Role of glycoprotein 2b/3a
Binds fibrinogen polymer to form connecting bridge between platelets
Results in platelet aggregation
55
Role of glycoprotein 1b
Binds vWF --> Platelet adherence to ECM
56
Formation of fibrin clot involves a cascade of these enzymes
Serine proteases
57
Intrinsic pathway of fibrin clot formation starts with this
Begins fibrinolysis
Factor XII exposure to negatively charged surface
58
Factor XII exposure to this starts the intrinsic pathway of fibrin clot formation
Negatively charged surface
59
Factor XII activates this
XI --> XIa
60
XIa activates this
IX --> IXa
(X is skipped)
61
IXa activates this
VIII --> VIIIa
62
Extrinsic pathway of fibrin clot formation starts with this
Factor VII exposure to Tissue Factor
63
Factor VII exposure to this starts the extrinsic pathway of fibrin clot formation
Tissue Factor
64
Tissue Factor activates this
Factor VII --> VIIa
65
Convergence of the intrinsic and extrinsic pathways of fibrin clot formation
VIIIa and VIIa can both activates X to Xa
66
Xa activates this
II (Prothrombin) --> IIa (Thrombin)
67
Factor II aka
Prothrombin
68
Factor IIa aka
Thrombin
69
Prothrombin is this factor
Factor II
70
Thrombin is this factor
Factor IIa
71
Factor II (thrombin) activates these
Platelets
72
IIa activates this
Factor I (fibrinogen) --> Ia (fibrin)
73
Fibrinogen is this factor
Factor I
74
Fibrin monomer is this factor
Factor Ia
75
Factor I aka
Fibrinogen
76
Factor Ia aka
Fibrin monomer
77
Acute phase reactant that is secreted by pIt and endothelium
Produced as the end of the serine protease cascade during fibrin clot formation
Factor I = fibrin
78
These form polymers to enmesh platelets
Are cross-linked via Factor XIIIa
Fibrin
79
Fibrin is cross-linked to enmesh platelets via this
Factor XIIIa
80
Regulatory protein that inhibits Factor Va
Protein C
81
Protein C inhibits this
Va
82
Cofactor for Factor Xa
together they cleave prothrombin (factor II)
Va
83
Va is a cofactor for this
Factor Xa
together they cleave prothrombin (factor II)
84
Protein C has this cofactor
Protein S
Together they inactivate Factor Va
85
Protein S is a cofactor for this
Protein C
Together they inactivate Factor Va
86
Expressed by intact endothelium
Binds thrombin (IIa), together they activate Protein C (which inactivates V)
Thrombomodulin
87
Thrombomodulin is expressed by this
Intact endothelium
88
Thrombomodulin binds this, and together they activate Protein C
Thrombin (factor IIa)
89
Thrombomodulin binds Thrombin (IIa), and together they activate this
Protein C
90
Protein C receptor is expressed by this
Intact endothelium
91
Expressed by intact endothelium
Inhibits thrombin, Factors 9-12
Antithrombin III
92
Antithrombin III is expressed by this
Intact endothelium
93
Antithrombin III inhibits these
Thrombin, Factors 9-12
94
Factor XIIa cleaves
Plasminogen to plasmin
95
This cleaves plasminogen to plasmin
Factor XIIa
96
This is expressed by endothelium into clot and activates plasminogen to plasmin
Tissue plasminogen activator (tPA)
97
This cleaves fibrin polymers back to monomers
Clot dissolves
Plasmin
98
Mucosal bleeding, skin bleeding, severe thrombocytopenia are defects in this
Primary hemostasis
99
Soft tissue bleeds (hematomas) and hemarthroses (blood in joint space) are defects in this
Secondary hemostasis
100
Thrombosis and hypercoagulability are defect in this
Tertiary hemostasis
101
Intravascular (including intra-cardiac) blood clot formation
Thrombosis
102
Term for 3 factors that promote thrombus formation
Virchow's triad
103
Define Virchow's triad
3 factors that promote thrombus formation
(Endothelial injury, Blood stasis or turbulence, Hypercoagulability)
104
Activated endothelium (due to injury) down regulates these 3 things to promote a procoagulant state
Virchow's triad:
Thrombomodulin
Protein C receptor
Tissue plasminogen activator (tPA)
105
This is a major factor in arterial thrombosis
Endothelial injury
106
Endothelial injury is a major factor in _______ thrombosis
Arterial
107
Stasis is a major factor in _______ thrombosis
Venous
low flow state and stasis allows factor accumulation
108
Turbulence is a major factor in _______ thrombosis
Arterial or venous
109
Hypercoagulability is a major factor in _______ thrombosis
Venous
110
Example of hypercoagulability involving decreased function of anticoagulant force
Factor V Leiden (genetic mutation)
111
Example of hypercoagulability involving increased function of pro-coagulant force
Prothrombin G20210A (genetic condition)
112
Thrombi that occur in cardiac chambers, usually a result of turbulence of stasis
Mural thrombi
113
Thrombi frequently associated with atherosclerotic plaque
Often occlusive
Arterial thrombi
114
Thrombi frequently associated with stasis and hypercoagulable states
"Always" occlusive
Form lines of Zahn
Venous thrombi
115
Alternating zones of cell-rich and platelet/fibrin rich areas
Form in states of flowing blood
Form in venous thrombi
Lines of Zahn
116
This type of plaque predisposes to an arterial thrombus (produces turbulent blood flow due to plaque distorting shape of blood vessel)
Atherosclerotic
117
Thrombus propagation:
Retrograde growth from attachment site
Arterial
118
Thrombus propagation:
Anterograde growth from attachment site
Venous
119
When fragment thrombus fragment dislodges and travels downstream
Embolization
120
Thrombus obstruction involving congestion, edema, and pain due to inflammation (thrombophlebitis)
Venous thrombus obstruction
121
Thrombus obstruction involving ischemia and possible death or organ receiving blood
Arterial thrombus obstruction
122
What is thrombophlebitis?
Venous thrombus obstruction
123
Loose intravascular material carried by blood stream
Embolism
124
Detached thrombus; most common form of embolism
Thromboembolism
125
Where do venous thromboembolism end up?
Lung
(Right atrium --> right ventricle --> lung)
= Pulmonary embolism
126
Pulmonary embolism that begins in deep veins of leg
Deep vein thrombosis
127
Result of a large clot that obstructs pulmonary vasculature
Sudden death
128
Result of a smaller clot that obstructs pulmonary vasculature
Asymptomatic or chest pain
Infarction is uncommon
129
Type of embolism usually due to long bone fractures
Source = bone marrow
Multiple small emboli lodge in lung and/or systemic circulation (which could go to brain)
Produces endothelial injury and platelet aggregation (leading to low platelet counts)
Fat embolism
130
Source of fat for fat embolism
Fat embolism
131
This can occur during a fat embolism, causing respiratory distress, dyspnea, or mental status changes
Multiple small emboli lodge in lung and/or systemic circulation (which could go to the brain)
132
Type of embolism that involves platelet aggregation, leading to low platelet counts
Results in thrombocytopenia
Fat embolism
133
This is often an earlier sign of a fat embolism
Platelet aggregation, leading to low platelet counts (thrombocytopenia)
134
Introduction of gas into vasculature
Mechanisms: vessels open to air + negative pressure
Iatrogenic causes (neurosurgery, obstetrics, thoracic), or from trauma (chest wall especially) or decompression sickness
Air embolism
135
Obstetric complication where uterine vasculature opens during placental separation
Amniotic fluid enters circulation and contains baby's epithelial cells/debris
Lodged in narrowed points of circulation
Foreign material produces intravascular coagulation of mother
Amniotic fluid embolism
136
Amniotic fluid embolism causes damage when amniotic fluid enters circulation, gets lodged in narrowed points of circulation or the foreign material produces this
Intravascular coagulation of mother
137
Tissue necrosis due to ischemia
Most due to arterial atherosclerosis and/or thromboemboli
Infarct
138
This type of blood supply is more resistant to infarcts
Dual blood supply (e.g. lungs)
139
2 examples of tissues that have short duration ischemia --> infarct
CNS and myocardium
140
Tissue type that survives many hours of ischemia
Fibrous tissue
141
Infarcts are usually this shape
Wedge shaped
142
Color of infarct if end-arterial organ (e.g. spleen, bone)
Pale
143
Color of infarct if organ with dual blood supply (e.g. lung, liver)
Hemorrhagic
144
Typical type of necrosis of infarct
Coagulative necrosis
145
Infarct is hemorrhagic if due to this
Venous obstruction
146
This type of margins often occur in infarcts
Hyperemic
147
Usual result of this type of infarct is congestion and edema
Less common
Collaterals allow tissue survival
Venous infarct
Infarct occurs if enough hemorrhage occurs to obstruct arterial flow
148
2 mechanisms of ischemic injury
Lack of ATP
Generation of ROS/free radicals (mitochondrial damage or lack of O2)
149
Increased tissue damage and inflammation due to blood flow restoration
Should provide O2 to reversibly damaged cells and allow survival, but sometimes this causes increased cell death
Reperfusion injury
150
What is contraction band necrosis?
Increased Ca2+ causes contraction of actin-myosin
151
Circulatory failure with decreased perfusion and global cellular hypoxia
Shock
152
Type of shock caused by vasodilation involving bacterial infection
Septic shock
153
3 phases of shock
Compensated phase
Decompensated phase
Irreversible phase
154
Low renal blood flow results in release of this during shock
Renin
155
Renin release due to low renal blood flow has these two effects
Angiotensin release --> vasoconstrictoin
Aldosterone release --> kidneys increase sodium and water retention
156
Low hypothalamic blood flow results in release of this
ADH
157
These are symptoms of this:
Low pressure, fast pulse
Pale (parenchymal/skin vasoconstriction)
Renal vasoconstriction and renal water retention
Compensated phase of shock
158
Phase of shock involving organ hypoperfusion
Goal is to maintain cardiac output and blood pressure
Compensated phase
159
These decrease parasympathetic stimulation during the compensated phase of shock, leading to increased cardiac pumping
Baroreceptors
160
Baroreceptors lead to this characterization of the compensated phase of shock
Increased cardiac phase (fast pulse)
161
Phase of shock involving cerebral, renal, liver, cardiac, and muscle hypoperfusion
Cellular metabolism shifts to anaerobic metabolism (increased lactic acid)
Decompensated phase of shock
162
Why is there increased creatinine during the decompensated phase of shock?
Renal hypoperfusion
163
Why is there increased AST/ALT during the decompensated phase of shock?
Liver hypoperfusion
164
Why is there increased lactic acid during the decompensated phase of shock?
Cellular metabolism shifts to anaerobic metabolism
165
Phase of shock where organ damage is too extensive to reverse
Progresses to multiorgan system failure
Cardiac ischemia --> decreased cardiac output
Intestinal ischemia --> bacteremia --> sepsis
Irreversible phase
166
Especially severe form of shock due to systemic infection
Septic shock
167
Type of microorganism that most prominently causes septic shock
Gram positive > gram negative > fungal infection
168
During septic shock, there is widespread ______ activation
Endothelial
169
These are factors of this:
Microbial products activate innate immune system
Generalized cytokine release
Widespread endothelial activation (NO synthase, anticoagulant factors decreased)
Complement activation
Septic shock
170
During septic shock, these factors are decreased
Anticoagulant factors decreased, promoting a procoagulant state
171
During septic shock, a procoagulant state is promoted by these 3 things
Decreased thrombomodulin
Decreased protein C
Tissue Factor released
