Ch4: Hemodynamic Diseases Flashcards Preview

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Flashcards in Ch4: Hemodynamic Diseases Deck (291):
1

What is most important cause of morbidity and mortality in Western society?

Cardiovascular disease (35-40% of deaths)

2

What % of lean body weight is water

60%

3

2/3 body water is where?

Intracellular

4

Remainder of body water is where?

ECF (interstitium)

5

What percentage of water is in blood plasma?

5%

6

Movement of water and solutes is controlled primarily by what?

Opposing effect of vascular hydrostati cpressure and plasma osmotic pressure

7

What is hydrostatic pressure?

Pressure that pushes things out of capillary into interstitium

8

What is plasma colloid osmotic pressure?

Pressure pulling things into capillary

9

Micro edema is what?

Clearing and separation of the extracellular matrix and subtle cell swelling

10

Edema is commonly seen where? (3)

1. subcutaneous tissue
2. lungs
3. brain

11

Subcutaneous edema distribution is usually affected by what?
What is this called

Gravity

Dependent edema

12

What is it called if in a subcutaneous edema, finger pressure can displace interstitial fluid and leave a depression?

pitting edema

13

Edema is the result of what?

renal dysfunction

14

If edema is in the eyelids it is called?

Periorbital edema

15

How much can the weight of lungs change in pulmonary edema?

2-3X

16

Edema in the brain can present in what two ways?

Localized or generalized

17

Five pathophysiologic categories of edema

1. Increased hydrostatic prssure
2. Reduced plasma osmotic pressure
3. Lymphatic obstruction
4. Sodium retention
5. Inflammation

18

Increased hydrostatic pressure results from what?

Impaired venous return

19

Impaired venous return can be caused by what? (5)

1. CHF
2. Constrictive pericarditis
3. Ascites
4. Venous obstruction or compression
5. Arteriolar dilation

20

Reduced plasma osmotic pressure is known as what?

Hypoproteinemia

21

What can cause hypoproteinemia? 4

1. Glomerulopathies
2. Cirrhosis
3. Malnutrition
4. Protein-losing gastroenteropathy

22

Lymphatic obstruction can be of what 4 types?

Inflammatory
Neoplastic
Postsurgical
Postirradiation

23

Two causes of sodium retention?

Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium

24

What can cause increased tubular reabsorption of sodium? 2

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

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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

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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

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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

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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

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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

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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

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Three main categories of shock

Cardiogenic
Hypovolemic
Septic

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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