Ch4: Hemodynamic Diseases Flashcards
(291 cards)
1
Q
What is most important cause of morbidity and mortality in Western society?
A
Cardiovascular disease (35-40% of deaths)
2
Q
What % of lean body weight is water
A
60%
3
Q
2/3 body water is where?
A
Intracellular
4
Q
Remainder of body water is where?
A
ECF (interstitium)
5
Q
What percentage of water is in blood plasma?
A
5%
6
Q
Movement of water and solutes is controlled primarily by what?
A
Opposing effect of vascular hydrostati cpressure and plasma osmotic pressure
7
Q
What is hydrostatic pressure?
A
Pressure that pushes things out of capillary into interstitium
8
Q
What is plasma colloid osmotic pressure?
A
Pressure pulling things into capillary
9
Q
Micro edema is what?
A
Clearing and separation of the extracellular matrix and subtle cell swelling
10
Q
Edema is commonly seen where? (3)
A
- subcutaneous tissue
- lungs
- brain
11
Q
Subcutaneous edema distribution is usually affected by what?
What is this called
A
Gravity
Dependent edema
12
Q
What is it called if in a subcutaneous edema, finger pressure can displace interstitial fluid and leave a depression?
A
pitting edema
13
Q
Edema is the result of what?
A
renal dysfunction
14
Q
If edema is in the eyelids it is called?
A
Periorbital edema
15
Q
How much can the weight of lungs change in pulmonary edema?
A
2-3X
16
Q
Edema in the brain can present in what two ways?
A
Localized or generalized
17
Q
Five pathophysiologic categories of edema
A
- Increased hydrostatic prssure
- Reduced plasma osmotic pressure
- Lymphatic obstruction
- Sodium retention
- Inflammation
18
Q
Increased hydrostatic pressure results from what?
A
Impaired venous return
19
Q
Impaired venous return can be caused by what? (5)
A
- CHF
- Constrictive pericarditis
- Ascites
- Venous obstruction or compression
- Arteriolar dilation
20
Q
Reduced plasma osmotic pressure is known as what?
A
Hypoproteinemia
21
Q
What can cause hypoproteinemia? 4
A
- Glomerulopathies
- Cirrhosis
- Malnutrition
- Protein-losing gastroenteropathy
22
Q
Lymphatic obstruction can be of what 4 types?
A
Inflammatory
Neoplastic
Postsurgical
Postirradiation
23
Q
Two causes of sodium retention?
A
Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium
24
Q
What can cause increased tubular reabsorption of sodium? 2
A
Renal hypoperfusion
Increased renin-angiotensin-aldosterone secretion
25
Three inflammations that can cause edema?
Acute inflammation
Chronic inflammation
Angiogenesis
26
Edema simply means?
abnormal Increase in interstitial fluid
27
If edema is in chest it is called?
Hydrothorax
28
If edema is in heart, it is called?
Hydropericardium
29
If edema is in the peritoneum, it is called?
Hydroperitoneum
30
What is anasarca?
severe generalized edema with widespread subcutaneous tissue swelling
31
What is transudate?
Protein-poor fluid
32
What is exudate?
Protein-rich fluid
33
Regional increases in hydrostatic pressure can result from what?
Focal impairment such as DVT
34
Generalized increases in venous pressure with systemic edema is the result of what?
CHF
35
Main cause of reduced plasma osmotic pressure?
Albumin not synthesized in correct amount or lost from circulation
36
3 causes of albumin discrepancies?
Nephrotic syndrome (generalized edema)
Severe liver disease
Protein malnutrition
37
What does reduced plasma osmotic pressure lead to?
Decreased renal perfusion
38
Sal retention occurs when?
Renal function is compromised (CHF)
39
Primary retention of water is produced by what?
Release of ADH
40
Inappropriate releases of ADH can be the result of what? (2)
1. malignancies
| 2. pituitary disorders
41
What does inappropriate release of ADH lead to?
1. Hyponatremia
| 2. Cerebral edema
42
What will happen to patient with hyponatremia if you correct salt balance too quickly?
Patient will get central pontine myelinolysis which causes damage to myelin sheath in pons
43
Impaired lymphatic drainage leads to what?
Lymphedema
44
Causes of lymphedema? (5)
```
chronic inflammation with fibrosis,
invasive malignant tumors,
physical disruption,
radiation damage,
infectious agents
```
45
parasitic lymphatic obstructure is called what?
| Results in what disease?
Filariasis
| Elephantiasis
46
Severe edema of the upper extremity may hamper what procedure?
Removal or irradation of breast and lymph nodes in patients with breast cancer
47
Carcinoma of the breast that obstructs lymphatic presents as what?
Peau d'orange
48
What does subcutaneous tissue edema signal? (2)
1. Cardiac disease
| 2. Renal disease
49
Subcutaneous edema can impair what? 2
1. Impair wound healing
| 2. Clearance of infection
50
When is pulmonary edema most frequently seen?
1. LV failure
2. renal failure
3. ARDS
4. pulmonary inflammation/ifection
51
How serious is brain edema?
Life threatening
52
What is hyperemia?
active process of ↑ blood flow due to arteriolar dilation
53
What is congestion?
passive process resulting from reduced outflow of blood from a tissue
54
Cause of local congestion?
Isolated venous obstruction
55
Cause of systemic congestion?
Cardiac failure
56
Tissue color in congestion?
Cyanosis
57
What does congestion lead to?
Edema
58
Chronic passive congestion leads to what?
Chronic hypoxia
59
Acute pulmonary hyperemia results from what?
engorged alveolar capillaries often with alveolar septal edema and focal intra-alveolar hemorrhage
60
Pulmonary congestion results from what?
thickened & fibrotic septa
61
Main sign of chronic pulmonary congestion
alveoli often contain numerous hemosiderin-laden macrophages (called heart failure cells)
62
What happens in hepatic hyperemia?
central vein and sinusoids are distended; centrilobular ischemia
63
What happens in hepatic congestion?
centrilobular regions grossly red-brown and slightly depressed because of cell death (nutmeg liver)
Microscopically: centrilobular hemorrhage, hemosiderin-laden macrophages, and degeneration of the hepatocytes
Centriolbular area is prone to undergo necrosis (distal end of the blood supply)
64
What is hemorrhage?
extravasation of blood into extravascular spaces
65
What is a hematoma
Accumulated blood
66
What is petechiae?
1- to 2-mm hemorrhages into skin, mucous membranes, or serosal surfaces
67
Cause of petechiae? 3
increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function
68
What is purpura?
: > 3mm hemorrhages
69
Causes of purpura? 6
```
increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function
Trauma
Vasculitis
Increased vascular fragility
```
70
What are ecchymoses?
larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises)
71
What causes the color changes of bruises?
hemoglobin (red-blue color) → bilirubin (blue-green color) → hemosiderin (gold-brown color)
72
What are some of the special names for accumulation of blood in a cavity?
hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
73
Patients with extensive bleeding can develop what?
| Why?
Jaundice
massive breakdown of RBCs and Hgb
74
Up to what rate will healthy adults not notice hemorrhage?
Rapid loss of up to 20% of the blood volume or slow losses of even larger amounts
75
If you go over the 20% threshold of blood lost, what will the body go into?
hemorrhagic (hypovolemic) shock
76
Is site important for hemorrhage?
Yes, for example if hemorrhage is in head, you have no margin. If an abdomen, you could probably lose quite a bit
77
Chronic or recurrent external blood loss leads to what?
| What is named what?
Net loss in iron
Iron deficiency anemia
78
Physiologic thrombosis is called what?
hemostatic clot
79
Pathologic clot is called what?
Thrombosis
80
Three main components of thrombosis?
1. vascular wall
2. platelets
3. coagulation cascade
81
Injury to the endothelium results in what?
| What regulates this? (2)
1. Transient arteriolar vasoconstriction
reflex neurogenic mechanisms and endothelin
82
Endothelial injury exposes what?
Highly thromobogenic subendothelial ECM
83
What is primary hemostasis?
Platelets adhere to wound site, become activated, aggregating to form a hemostatic plug
84
When tissue factor is endothelium is exposed, what does it do?
Activates coagulation cascade
85
Activation of thrombin allows it to do what?
converts soluble fibrinogen to insoluble fibrin (secondary hemostasis)
86
What is secondary hemostasis?
Polymerized fibrin and platelet aggregates form a solid, permanent plug
87
At the same time, what is going on during secondary hemostasis
Counter-regulatory mechanisms are set into motion to limit the hemostatic plug to the site of injury
88
How does thrombin act contradictory?
1. Activates fibrinogen to fibrin to cross link clots
| 2. Binds to thrombomodulin to inhibit cascade
89
What determines whether thrombus formation, propagation, or dissolution occurs?
1. Anti-thrombotic activities of endothelium
| 2. Pro-thrombotic activities of endothelium
90
What does the endothelium normally exhibit?
Anti-thrombotic activities (antiplatelet, anticoagulant, fibrinolytic properties)
91
What does the endothelium exhibit during injury/activation?
Pro-thrombotic activities
92
3 anti-platelet effects of endlthelium?
1. Intact endothelium keeps platelets off the subendothelial ECM
2. PGI2 and NO produced by endothelial cell impede platelet adhesion
3. Also elaborate adenosine diphosphatase (degrades ADP) and further inhibits platelet aggregation
93
4 anti-coagulant effects of endothelium?
1. Membrane heparin-like molecules (interact with ATIII to inactivate thrombin)
2. Thrombomodulin: a thrombin receptor (converts thrombin to an anticoagulant → activates protein C)
Protein C inactivates factors Va and VIIIa
3. Protein S (cofactor for Protein C)
4. Tissue factor pathway inhibitor (TFPI) Inhibits VIIa and Xa
94
Fibrinolytic effect of endothelium?
Synthesis of tissue-type plasminogen activator (t-PA), promoting fibrinolysis
95
Platelet prothrombotic properties of endlthelium?
Produce vWF (essential cofactor for platelet binding to matrix elements)
96
Procoagulant effects of endothelium? 2
1. Synthesis of tissue factor, major activator of extrinsic cascade
2. Augment the catalytic function of activated coagulation factors IXa and Xa
97
Antifibrinolytic effects of endothelium?
Secrete inhibitors of plasminogen activator (PAIs)
| Limits fibrinolysis and tend to favor thrombosis
98
Platelets are what type of cells?
| What are they shed from?
Disc-shaped, anucleate cell fragments
| Shed from megakaryocytes in the bone marrow
99
Function of platelets depends on what? (3)
Glycoprotein receptors
Contractile cytoskeleton
Cytoplasmic granules
100
Two types of cytoplasmic platelet granules?
alpha-granules
| dense/delta granules
101
Alpha granules have what special adhesion molecule?
| Also contain what? (7)
P-selectin
1. Fibrinogen
2. Fibronectin
3. Factor V
4. Factor VIII
5. Platelet factor 4
6. PDGF
7. TGF-Beta
102
What do dense granules contain? 6
1. ADp
2. ATP
3. Ionized Ca
4. histmine
5. Serotonin
6. Epinephrine
103
After vascular injury, what do platelets encounter?
ECM constituents collagen and vWF
104
Upon coming into contact with collagen and vWF, what do platelets do? 3
Adhesion and shape change
Secretion
Aggregation
105
Platelet adhesion is mediated by what?
| How exactly?
vWF
Bridge between the platelet surface receptor (glycoprotein Ib—GpIB) and exposed collagen
106
Platelet secretion involves what molecules?
alpha and dense after adhesion
107
Release of platelet dense granules is important why? 2
1. calcium is required for the coagulation cascade
| 2. ADP is a potent activator of platelet aggregation
108
Aggregation of platelets requires what? 4
ADP
TxA2
Activated thrombin
Fibrinogen
109
What are steps of txA2 function? 2
Amplify platelet aggregation
| Formation of primary hemostatic plug
110
How does thrombin activation stabilize the plug?
Binding to a protease-activated receptor on the platelet membrane → platelet contraction --> irreversibly fused mass of platelets
111
Most important component of platelet aggregation is what?
Fibrinogen
112
How does platelet bind to fibrinogen?
1. activation by adp
2. conformation change in platelet GpIIb-IIIa receptors
3. Binding to brinogen
113
Deficiency in GpIIb-IIIa complex results in what?
Glanzmann thrombasthenia
114
Deficiency in GpIb results in what?
Bernard-Soulier syndrome
115
Deficiency in vWF leads to what?
Von Willebrand disease
116
What does Clopidogrel do?
blocks platelet by blocking ADP binding
117
Synthetic antagonists or monoclonal antibodies have what effect on platelets?
bind to the GpIIb-IIIa receptors
118
Effect on aspirin on platelets?
permanently blocks platelet TxA2 synthesis; endothelial PGI2 production is also inhibited by aspirin
119
How do cells overcome aspirin blockade of cascade?
resynthesize active cyclooxygenase
120
Nitric oxide effect on platelets?
acts as a vasodilator and inhibitor of platelet aggregation
121
What is intrinsic coagulation pathway?
a
122
What is extrinsic coagulation pathway?
a
123
What is the common coagulation pathway?
a
124
What is the coagulation cascade?
Amplifying series of enzymatic conversions; each step proteolytically cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation
125
What is the most important coagulation factor?
Thrombin
126
Explain the changes thrombin makes on fibrinogen
fibrinogen → fibrin monomers → insoluble gel → secondary hemostatic plug
127
What stabilizes and cross links fibrin polymers?
| What activates this?
XIIIa
Thrombin
128
Each reaciton in coagulation pathway results from what?
Assembly of a complex of enzyme, substrate, cofactor
129
What is the enzyme in coagulation reactions?
Activated coagulation factor
130
What is the substrate in coagulation reactions?
Proenzyme form of coagulation factor
131
What is the cofactor in coagulation reactions?
Reaction accelerator
132
Where does the coagulation reaction take place?
| What holds it all together?
Phospholipid surface
| Calcium ions
133
Factors 2, 7, 9, and 10 binding to calcium requires what as cofactor?
Vitamin K
134
What antagonizses factors 2, 7, 9, 10 as an anti-coagulant?
Coumadin
135
Extrinsic and intrinsic pathways converge on activation of what?
Factor X
136
Why is the extrinsic pathway named so?
it required the addition of an exogenous trigger
137
What is the most physiologically relevant pathway for coagulation when vascular damage has been ocurred?
Extrinsic
138
What activates extrinsic pathway?
tissue factor
139
What does prothrombin (PT) time measure?
measures VII, X, II, V, and fibrinogen
140
What measures the intrinsic pathway?
Partial thromboplastin time (PTT) screens for the function of the proteins (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)
141
Thrombin exerts what type of effects?
Proimflammatory
142
How does thrombin modulate cellular activities?
Protease-activated receptors (PARs)
143
What type of activities do the PAR's through thrombin work? 3
I1. nduces platelet aggregation and TxA2 production
2. Activates ECs to express adhesion molecules, and a variety of fibrinolytic (t-PA), vasoactive (NO, PGI2), and cytokine mediators (e.g., PDGF)
3. Directly activates leukocytes
144
Coagulation cascade must be restricted to where?
Only site of vascular injury
145
Antithrombins are activated how?
binding to heparin-like molecules on endothelial cells
146
Antithrombins act how?
inhibit the activity of thrombin and other serine proteases, including factors IXa, Xa, XIa, and XIIa
147
How is heparin used?
Minimize thrombosis
148
What are proteins C and S dependent on?
Vitamin K
149
What is action of proteins C and S?
Inactivate factors Va and VIIIa
150
What is the protein produced by endothelium that inactivates tissue factor-factor VIIa complexes
TFPI
151
Activation of clotting cascade sets what into motion?
Fibrinolytic cascade
152
How does the fibrinolytic cascade limit size of clot?
breaks down fibrin and interferes with its polymerization
153
Generation of plasmin results in what?
fibrin split products (FSPs) can also act as weak anticoagulants
154
Elevated levels of FSP's can be used in what?
diagnosing abnormal thrombotic states (DIC, DVT, PE)
155
The fibrinolytic system has what main reaction?
Enzymatic conversion of inactive precursor plasminogen to plasmin
156
Two main types of plasminogen activators?
Tissue-type PA (t-PA) synthesized by endothelium
| Urokinase-like PA (u-PA)
157
Main bacterial plasminogen activator?
Streptokinase (bacterial enzyme
158
Free plasmin is rapidly inactivated by what?
α2-plasmin inhibitor
159
Endothelial cells also release what to inhibit plasminogen activation?
plasminogen activator inhibitor (PAI) which inhibits t-PA
160
Abnormalities that lead to thrombus formation are together known as what?
Virchow's triad
161
What are the 3 components of Virchow's triad
Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability of the blood
162
Endothelial injury is important factor in what?
heart or the arterial circulation (normally high flow rates might otherwise impede clotting)
163
Does the endothelium need to be physically disrupted to contribute to thrombosis?
Why?
no
Abnormality in the balance of prothrombotic and antithrombotic activities of endothelium can influence local clotting events
164
What can induce endothelial dysfunction? (6)
```
Hypertension
Turbulent blood flow
Bacterial endotoxins
Radiation injury
Metabolic abnormalities (homocystinemia, hypercholesterolemia)
Toxins (cigarette smoke)
```
165
Turbulence leads to what?
endothelial injury or dysfunction
| Can form countercurrents and local areas of stasis
166
What is main contributor in development of venous thrombi?
Stasis
167
Normal blood flow is described how?
Laminar
| platelets and blood cellular components flow centrally separated from the endothelium by slower moving plasma
168
Stasis promotes activation of what?
| How
Endothelial activation
| Flow-induced changes in endothelial cell gene expression
169
Stasis disrupts flow and brings what into contact with endothelium?
Platelets
170
What does stasis prevent?
dilution of activated clotting factors
171
Atherosclerotic plaques are involved in thrombosis how?
expose subendothelial ECM and cause turbulence
172
Aneurysms are involved in thrombosis how?
Local stasis
173
Acute MI's are involved in thrombosis how?
areas of noncontractile myocardium and sometimes cardiac aneurysms→ formation of cardiac mural thrombi
174
Rheumatic mitral valve stenosis is involved in thrombosis how?
left atrial dilation
175
Hypoviscosity is involved in thrombosis how?
increases resistance to flow and causes small vessel stasis
176
Sickle cell anemia is involved in thrombosis how?
vascular occlusions→ stasis → thrombosis
177
What will hypercoagulability contribute to?
Thrombotic states
178
Primary hypercoagulability is due to what?
Point mutations in the factor V gene and prothrombin gene are the most common
179
Secondary hypercoagulability is due to what?
Acquired
180
Factor V Leiden is found in what population
2% to 15% of Caucasians carry a single nucleotide mutation in factor V
181
Mutation in Factor V Leiden results in what?
factor V resistant to cleavage by protein C
182
Prothrombin mutation results in what?
Increased levels of prothrombin with an almost threefold increased risk of venous thromboses
183
Elevated levels of homocysteine contribute to what?
Contribute to arterial and venous thrombosis as well as the development of atherosclerosis
184
Why do mild elevated levels of homocysteine occur?
Variant form of 5,10-methylenetetrahydrofolate reductase
185
Markedly elevated homocysteine levels can be caused by what?
inherited deficiency of cystathione β-synthetase
186
What can reduce plasma homocysteine concentration?
Folic acid, pyridoxine, and/or vitamin B12
187
Rare inherited causes of increase risk in thrombosis are due to deficiencies in what?
Antithrombin III
Protein C
Protein S
188
Some causes of acquired thrombophilia
1. Oral contraceptive use
2. Hyperestrogenic state of pregnancy
3. Dissemianted cancers
4. Reduced endothelial PGI2 in age
5. Smoking
6. Obesity
189
Why do oral contraceptive use or hyperestrogenic state of pregnancy cause thrombosis? 2
increased hepatic synthesis of coagulation factors and reduced anticoagulant synthesis
190
What is heparin-induced thrombocytopenia syndrome?
After adminstration of unfractionated heparin, there is Induction of the appearance of antibodies that recognize complexes of heparin and platelet factor 4
191
Result of heparin-induced thrombocytopenia syndrome?
1. platelet aggregation
2. Platelet activation
3. platelet consumption
192
What will alleviate heparin-induced thrombocytopenia syndrome
Low-molecular weight heparin
193
Antiphospholipid syndrome is known as what?
lupus anticoagulant syndrome
194
How does antiphopholipid syndrome present clinically? 4
Recurrent venous or arterial thrombi
Repeated miscarriages
Cardiac valvular vegetations
Thrombocytopenia
195
Antiphospholipid syndrome is mediated by what?
binding of antibodies to epitopes on plasma proteins that are induced by phospholipids
196
What does antiphospholipid syndrome present as on serologic test?
Syphilis
197
What is secondary antiphospholipid syndrome?
individuals with a well-defined autoimmune disease
198
What is primary antiphospholipid syndrome?
patients with a hypercoagulable state with no evidence of other autoimmune disorders
199
Thrombi can develop where in the CV system?
Everywhere
200
Size and shape of thrombi depend on what?
site of origin and cause
201
Thrombi are attached to what?
Underlying vascular surface
202
Arterial thrombi grow what direction?
Retrograde (toward heart)
203
Venous thrombi grow what way?
Direction of blood flow (toward heart)
204
What are Lines of Zahn
pale platelet and fibrin deposits alternating with darker red cell–rich layers
205
What do lines of Zahn signify?
thrombus formed in flowing blood
206
Mural thrombi occur where?
heart chambers or in the aortic lumen
207
What promotes cardiac mural thrombi? 2
```
Abnormal mycardial contraction (arrhythmia, MI)
Endomyocardial injury (myocarditis)
```
208
Arterial thrombi has what characteristics? 3
1. Occlusive
2. Superimposed on a ruptured atherosclerotic plaque
3. Seen with other vascular injuries
209
Common sites of arterial thrombi?
Coronary, cerebral, femoral arteries
210
Venous thrombosis has what characteristics? 2
1. Occlusive with thrombus forming a long cast of lumen
| 2. More enmeshed red cells and few platelets
211
Thrombi of veins normally occur where?
Where else (4)
Lower extremities
1. upper extremities
2. Perioprostatic plexus
3. ovarian
4. periuterine veins
212
Posmortem clots appear how? 3
Gelatinous with a dark red dependent portion
Yellow upper portion “chicken fat”
Not attached to the underlying wall
213
Thrombi on heart valves are known as?
Vegetations
214
What is infective endocarditis?
bacteria or fungi adhering to previously damaged valves or directly causing valve damage; formation of large thrombotic masses
215
What is nonbacterial thrombotic endocarditis?
sterile vegetations on noninfected valves in persons with hypercoagulable states
216
What is sterile, verrucous endocarditis/Libman-Sacks endocarditis?
Seen in setting of SLE
217
What is propagation?
thrombi accumulate additional platelets and fibrin
218
What is embolization?
thrombi dislodge and travel to other sites in the vasculature
219
What is dissolution?
fibrinolysis with rapid shrinkage and disappearance of recent thrombi
220
What is organization and recanalization?
ingrowth of endothelial cells, smooth muscle cells, and fibroblasts; capillary channels eventually form that re-establish the continuity of the original lumen
221
Where do most venous thrombosis (phlebothrombosis) occur?
Superficial or deep veins of leg
222
Characteristics of superficial venous thrombosis?
local congestion, swelling, pain, and tenderness; rarely embolize
223
Characteristics of DVT?
in the larger leg veins
More serious
More often embolize to the lungs and give rise to pulmonary infarction
Can cause local pain and edema
DVTs are asymptomatic in approximately 50% of affected individuals
224
Lower extremeties DVT's are associated with what?
| Common predisposing factors?
hypercoagulable states
Bed rest and immobilization
Congestive heart failure
Trauma, surgery, and burns
Advanced age
225
What is trousseau syndrome?
| Due to what?
Migratory thrombophlebitis
Tumor-associated inflammation and coagulation factors (tissue factor, factor VIII) and procoagulants (e.g., mucin) released from tumor cells all contribute to the increased risk of thromboembolism in disseminated cancers
226
Major cause of arterial thromboses?
Atherosclerosis
227
Can cardiac and aortic mural thrombi embolize peripherally?
Yes
228
Targets of cardiac and aortic mural thrombi?
Brain, kidneys, and spleen are particularly likely targets because of their rich blood supply
229
Disseminated intravascular coagulation is seen when?
obstetric complications to advanced malignancies
230
What happens in Disseminated intravascular coagulation?
Sudden or insidious onset of widespread fibrin thrombi in the microcirculation
231
Result of Disseminated intravascular coagulation?
Can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart, and kidneys
Widespread microvascular thrombosis results in platelet and coagulation protein consumption and at the same time the fibrinolytic mechanisms are activated
232
DIC is a complication of any condition associated with what?
widespread activation of thrombin
233
What is an embolism?
Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
234
Almost all emboli represent what?
some part of a dislodged thrombus (thromboembolism)
235
Emboli will inevitably lodge where?
in vessel too small to permit further passage (causing partial or completely vascular occlusion)
236
A major consequence of an embolism is what?
Ischemic necrosis
237
A major consequence of embolism is what?
Ischemic necrosis (infarction)
238
Pulmonary embolism usually results from what?
leg DVT's
239
Occlusion of main pulmonary artery bifurcation is what?
Saddle embolus
240
What is a pardoxical embolism?
embolus can pass through an interatrial or interventricular defect and gain access to the systemic circulation
241
Do most PE's have symptoms?
Nope, too small
242
If more than 60% of pulmonary circulation is obstructed, what will happen?
Sudden death, right heart failure, or CV collapse
243
Embolic obstruction of medium-sized pulmonary arteries result in what?
pulmonary hemorrhage but not usually infarction
244
Embolic obstruction of small end-arteriolar pulmonary branches result in what?
hemorrhage or infarction
245
Multiple emboli in PE overtime results in what?
pulmonary hypertension and right ventricular failure
246
What is systemic thromboembolism?
Emboli in the arterial circulation
247
Most arterial emboli arise from where?
intracardiac mural thrombi
248
2/3 of arterial emboli are associated with what?
left ventricular wall infarcts
249
1/4 of arterial emboli are associated with what?
left atrial dilation and fibrillation
250
Remainder of arterial emboli arise from what?
thrombi on ulcerated atherosclerotic plaques, aortic aneurysms, or fragmentation of a valvular vegetation, or paradoxical emboli
251
Sites for arterial emboli to lodge? and their percentage
Lower extremities: 75%
Brain: 10%
Intestines, kidneys, spleen
252
What is a fat or marrow emboli?
Microscopic fat globules—with or without associated hematopoietic marrow elements—can be found in the circulation and in the pulmonary vasculature
253
When are fat/marrow emboli seen?
Fractures of long bones
| Vigorous cardiopulmonary resuscitation
254
Fat Embolism Syndrome is what?
Term applied to the minority of patients who become symptomatic
255
Causes of fat embolism syndrome? 3
Pulmonary insufficiency
Neurologic symptoms
Anemia and thrombocytopenia
256
Presentatin of symptoms in fat embolism syndrome?
1. After 1-3 days, sudden onset of tachypnea, dyspnea, and tachycardia
2. Diffuse petechial rash (thrombocytopenia)
257
What is an air embolism?
Gas bubbles can coalesce to form frothy masses that obstruct vascular flow
258
How much air is required to have a clinical effect in pulmonary circulation?
more than 100 cc of air
259
When can an air embolism occur? (2)
obstetric or laparoscopic procedures or because of chest wall injury
260
What is decompression sickness due to?
Sudden decreases in atmospheric pressure and Gas (particularly nitrogen) dissolves in the blood and tissues
261
What are the bends?
– rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints
262
What are the chokes?
respiratory distress where gas bubbles in the lungs cause edema, hemorrhage, and focal atelectasis or emphysema
263
Treatment for decompression sickness?
Compression chamber
264
Caisson disease is a chronic form of what?
Decompression sickness
265
Caisson disease is what?
Gas emboli in bones
| Ischemic necrosis of femoral head, tibia and humerus
266
Why is amniotic fluid embolism so serious?
80% mortality rate and fifth most common cause of maternal mortality worldwide
267
What happens in amniotic fluid embolism?
infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of the uterine veins
268
Result of amniotic fluid embolisM?
severe dyspnea, cyanosis, and shock followed by neurologic impairment
Pulmonary edema and DIC
269
Findings in amniotic fluid embolism?
Presence of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or GI tract in the maternal microvasculature
marked pulmonary edema, diffuse alveolar damage, and presence of fibrin thrombi in many vascular beds due to DIC
270
What is ischemic necrosis?
Occlusion of arterial supply or venous drainage
271
Nearly all infarcts result from what?
thrombotic or embolic arterial occlusions
272
Infarction is classified according to what?
Color, presence of infection
273
3 types of infarctions
Red or hemorrhagic infarcts
White or anemic infarcts
Septic or bland
274
Red infarcts are most commonly caused where?
Lungs
275
Characteristics of places where red infarcts occur?
Venous occlusions (ovary)
Loose tissues when blood can collect in the infarcted zone (lung)
Tissues with dual circulation (lung, small intestine)
Tissues previously congested by sluggish venous outflow
Flow is re-established to a site of previous arterial occlusion and necrosis
276
When do white infarcts occur?
arterial occlusion in solid organs with end-arterial circulation (heart, spleen, kidney)
277
Tissue density has what effect on white infarct
limits the seepage of blood from adjoining capillary beds into the necrotic area
278
Wedge-shaped infarct is what?
Occluded vessel at the apex and the periphery of the organ forming the base
279
Dominant histologic characteristic of infarct is what?
ischemic coagulative necrosis
280
Most infarcts are replaced by what?
Scar
281
In brain how do infarcts present?
Liquefactive necrosis
282
Septic infarcts may lead to what?
Abscess
283
Factors that influence development of an infarct? 4
1. Nature of vascular supply
2. Rate of occlusion development
3. Vulnerability to hypoxia
4. Oxygen content of blood
284
What is common pathway for potentially lethal clinical events?
Shock
285
What can cause shock? (5)
Severe hemorrhage, extensive trauma or burns, large MI, massive PE, microbial sepsis
286
Shock is characterized by what?
Due to what? (2)
Which results in what?
Systemic hypotension
1. Reduced CO
2. Reduced effective circulating blood volume
1. Impaired tissue perfusion
2. Cellular hypoxia
287
Three main categories of shock
Cardiogenic
Hypovolemic
Septic
288
Cardiogenic shock is due to what?
low CO due to myocardial pump failure
289
What can cause cardiogenic shock?
MI, ventricular arrhythmias, external compression (cardiac tamponade), outflow obstruction (PE)
290
What is hypovolemic shock?
| Due to what? 2
low CO due to loss of blood or plasma volume
Hemorrhage, severe burns
291
Septic shock is due to what?
Vasodilation and peripheral pooling of blood as part of a systemic immune reaction to bacterial or fungal infection
