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Pathology > Ch4: Hemodynamic Diseases > Flashcards

Ch4: Hemodynamic Diseases Flashcards

1
Q

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

A

Cardiovascular disease (35-40% of deaths)

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2
Q

What % of lean body weight is water

A

60%

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3
Q

2/3 body water is where?

A

Intracellular

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4
Q

Remainder of body water is where?

A

ECF (interstitium)

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5
Q

What percentage of water is in blood plasma?

A

5%

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6
Q

Movement of water and solutes is controlled primarily by what?

A

Opposing effect of vascular hydrostati cpressure and plasma osmotic pressure

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7
Q

What is hydrostatic pressure?

A

Pressure that pushes things out of capillary into interstitium

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8
Q

What is plasma colloid osmotic pressure?

A

Pressure pulling things into capillary

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9
Q

Micro edema is what?

A

Clearing and separation of the extracellular matrix and subtle cell swelling

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10
Q

Edema is commonly seen where? (3)

A
  1. subcutaneous tissue
  2. lungs
  3. brain
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11
Q

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

A

Gravity

Dependent edema

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12
Q

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

A

pitting edema

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13
Q

Edema is the result of what?

A

renal dysfunction

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14
Q

If edema is in the eyelids it is called?

A

Periorbital edema

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15
Q

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

A

2-3X

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16
Q

Edema in the brain can present in what two ways?

A

Localized or generalized

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17
Q

Five pathophysiologic categories of edema

A
  1. Increased hydrostatic prssure
  2. Reduced plasma osmotic pressure
  3. Lymphatic obstruction
  4. Sodium retention
  5. Inflammation
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18
Q

Increased hydrostatic pressure results from what?

A

Impaired venous return

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19
Q

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

A
  1. CHF
  2. Constrictive pericarditis
  3. Ascites
  4. Venous obstruction or compression
  5. Arteriolar dilation
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20
Q

Reduced plasma osmotic pressure is known as what?

A

Hypoproteinemia

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21
Q

What can cause hypoproteinemia? 4

A
  1. Glomerulopathies
  2. Cirrhosis
  3. Malnutrition
  4. Protein-losing gastroenteropathy
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22
Q

Lymphatic obstruction can be of what 4 types?

A

Inflammatory
Neoplastic
Postsurgical
Postirradiation

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23
Q

Two causes of sodium retention?

A

Excessive salt intake with renal insufficiency

Increased tubular reabsorption of sodium

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24
Q

What can cause increased tubular reabsorption of sodium? 2

A

Renal hypoperfusion

Increased renin-angiotensin-aldosterone secretion

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25
Q

Three inflammations that can cause edema?

A

Acute inflammation
Chronic inflammation
Angiogenesis

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26
Q

Edema simply means?

A

abnormal Increase in interstitial fluid

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27
Q

If edema is in chest it is called?

A

Hydrothorax

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28
Q

If edema is in heart, it is called?

A

Hydropericardium

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29
Q

If edema is in the peritoneum, it is called?

A

Hydroperitoneum

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30
Q

What is anasarca?

A

severe generalized edema with widespread subcutaneous tissue swelling

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31
Q

What is transudate?

A

Protein-poor fluid

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32
Q

What is exudate?

A

Protein-rich fluid

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33
Q

Regional increases in hydrostatic pressure can result from what?

A

Focal impairment such as DVT

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34
Q

Generalized increases in venous pressure with systemic edema is the result of what?

A

CHF

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35
Q

Main cause of reduced plasma osmotic pressure?

A

Albumin not synthesized in correct amount or lost from circulation

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36
Q

3 causes of albumin discrepancies?

A

Nephrotic syndrome (generalized edema)
Severe liver disease
Protein malnutrition

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37
Q

What does reduced plasma osmotic pressure lead to?

A

Decreased renal perfusion

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38
Q

Sal retention occurs when?

A

Renal function is compromised (CHF)

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39
Q

Primary retention of water is produced by what?

A

Release of ADH

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40
Q

Inappropriate releases of ADH can be the result of what? (2)

A
  1. malignancies

2. pituitary disorders

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41
Q

What does inappropriate release of ADH lead to?

A
  1. Hyponatremia

2. Cerebral edema

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42
Q

What will happen to patient with hyponatremia if you correct salt balance too quickly?

A

Patient will get central pontine myelinolysis which causes damage to myelin sheath in pons

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43
Q

Impaired lymphatic drainage leads to what?

A

Lymphedema

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44
Q

Causes of lymphedema? (5)

A 
chronic inflammation with fibrosis, 
invasive malignant tumors, 
physical disruption, 
radiation damage, 
infectious agents
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45
Q

parasitic lymphatic obstructure is called what?

Results in what disease?

A

Filariasis

Elephantiasis

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46
Q

Severe edema of the upper extremity may hamper what procedure?

A

Removal or irradation of breast and lymph nodes in patients with breast cancer

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47
Q

Carcinoma of the breast that obstructs lymphatic presents as what?

A

Peau d’orange

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48
Q

What does subcutaneous tissue edema signal? (2)

A
  1. Cardiac disease

2. Renal disease

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49
Q

Subcutaneous edema can impair what? 2

A
  1. Impair wound healing

2. Clearance of infection

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50
Q

When is pulmonary edema most frequently seen?

A
  1. LV failure
  2. renal failure
  3. ARDS
  4. pulmonary inflammation/ifection
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51
Q

How serious is brain edema?

A

Life threatening

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52
Q

What is hyperemia?

A

active process of ↑ blood flow due to arteriolar dilation

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53
Q

What is congestion?

A

passive process resulting from reduced outflow of blood from a tissue

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54
Q

Cause of local congestion?

A

Isolated venous obstruction

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55
Q

Cause of systemic congestion?

A

Cardiac failure

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56
Q

Tissue color in congestion?

A

Cyanosis

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57
Q

What does congestion lead to?

A

Edema

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58
Q

Chronic passive congestion leads to what?

A

Chronic hypoxia

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59
Q

Acute pulmonary hyperemia results from what?

A

engorged alveolar capillaries often with alveolar septal edema and focal intra-alveolar hemorrhage

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60
Q

Pulmonary congestion results from what?

A

thickened & fibrotic septa

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61
Q

Main sign of chronic pulmonary congestion

A

alveoli often contain numerous hemosiderin-laden macrophages (called heart failure cells)

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62
Q

What happens in hepatic hyperemia?

A

central vein and sinusoids are distended; centrilobular ischemia

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63
Q

What happens in hepatic congestion?

A

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)

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64
Q

What is hemorrhage?

A

extravasation of blood into extravascular spaces

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65
Q

What is a hematoma

A

Accumulated blood

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66
Q

What is petechiae?

A

1- to 2-mm hemorrhages into skin, mucous membranes, or serosal surfaces

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67
Q

Cause of petechiae? 3

A

increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function

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68
Q

What is purpura?

A

: > 3mm hemorrhages

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69
Q

Causes of purpura? 6

A 
increased intravascular pressure
low platelet counts (thrombocytopenia)
defective platelet function
Trauma
Vasculitis
Increased vascular fragility
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70
Q

What are ecchymoses?

A

larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises)

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71
Q

What causes the color changes of bruises?

A

hemoglobin (red-blue color) → bilirubin (blue-green color) → hemosiderin (gold-brown color)

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72
Q

What are some of the special names for accumulation of blood in a cavity?

A

hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis

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73
Q

Patients with extensive bleeding can develop what?

Why?

A

Jaundice

massive breakdown of RBCs and Hgb

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74
Q

Up to what rate will healthy adults not notice hemorrhage?

A

Rapid loss of up to 20% of the blood volume or slow losses of even larger amounts

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75
Q

If you go over the 20% threshold of blood lost, what will the body go into?

A

hemorrhagic (hypovolemic) shock

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76
Q

Is site important for hemorrhage?

A

Yes, for example if hemorrhage is in head, you have no margin. If an abdomen, you could probably lose quite a bit

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77
Q

Chronic or recurrent external blood loss leads to what?

What is named what?

A

Net loss in iron

Iron deficiency anemia

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78
Q

Physiologic thrombosis is called what?

A

hemostatic clot

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79
Q

Pathologic clot is called what?

A

Thrombosis

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80
Q

Three main components of thrombosis?

A
  1. vascular wall
  2. platelets
  3. coagulation cascade
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81
Q

Injury to the endothelium results in what?

What regulates this? (2)

A
  1. Transient arteriolar vasoconstriction

reflex neurogenic mechanisms and endothelin

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82
Q

Endothelial injury exposes what?

A

Highly thromobogenic subendothelial ECM

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83
Q

What is primary hemostasis?

A

Platelets adhere to wound site, become activated, aggregating to form a hemostatic plug

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84
Q

When tissue factor is endothelium is exposed, what does it do?

A

Activates coagulation cascade

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85
Q

Activation of thrombin allows it to do what?

A

converts soluble fibrinogen to insoluble fibrin (secondary hemostasis)

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86
Q

What is secondary hemostasis?

A

Polymerized fibrin and platelet aggregates form a solid, permanent plug

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87
Q

At the same time, what is going on during secondary hemostasis

A

Counter-regulatory mechanisms are set into motion to limit the hemostatic plug to the site of injury

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88
Q

How does thrombin act contradictory?

A
  1. Activates fibrinogen to fibrin to cross link clots

2. Binds to thrombomodulin to inhibit cascade

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89
Q

What determines whether thrombus formation, propagation, or dissolution occurs?

A
  1. Anti-thrombotic activities of endothelium

2. Pro-thrombotic activities of endothelium

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90
Q

What does the endothelium normally exhibit?

A

Anti-thrombotic activities (antiplatelet, anticoagulant, fibrinolytic properties)

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91
Q

What does the endothelium exhibit during injury/activation?

A

Pro-thrombotic activities

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92
Q

3 anti-platelet effects of endlthelium?

A
  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
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93
Q

4 anti-coagulant effects of endothelium?

A
  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
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94
Q

Fibrinolytic effect of endothelium?

A

Synthesis of tissue-type plasminogen activator (t-PA), promoting fibrinolysis

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95
Q

Platelet prothrombotic properties of endlthelium?

A

Produce vWF (essential cofactor for platelet binding to matrix elements)

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96
Q

Procoagulant effects of endothelium? 2

A
  1. Synthesis of tissue factor, major activator of extrinsic cascade
  2. Augment the catalytic function of activated coagulation factors IXa and Xa
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97
Q

Antifibrinolytic effects of endothelium?

A

Secrete inhibitors of plasminogen activator (PAIs)

Limits fibrinolysis and tend to favor thrombosis

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98
Q

Platelets are what type of cells?

What are they shed from?

A

Disc-shaped, anucleate cell fragments

Shed from megakaryocytes in the bone marrow

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99
Q

Function of platelets depends on what? (3)

A

Glycoprotein receptors
Contractile cytoskeleton
Cytoplasmic granules

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100
Q

Two types of cytoplasmic platelet granules?

A

alpha-granules

dense/delta granules

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101
Q

Alpha granules have what special adhesion molecule?

Also contain what? (7)

A

P-selectin

  1. Fibrinogen
  2. Fibronectin
  3. Factor V
  4. Factor VIII
  5. Platelet factor 4
  6. PDGF
  7. TGF-Beta
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102
Q

What do dense granules contain? 6

A
  1. ADp
  2. ATP
  3. Ionized Ca
  4. histmine
  5. Serotonin
  6. Epinephrine
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103
Q

After vascular injury, what do platelets encounter?

A

ECM constituents collagen and vWF

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104
Q

Upon coming into contact with collagen and vWF, what do platelets do? 3

A

Adhesion and shape change
Secretion
Aggregation

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105
Q

Platelet adhesion is mediated by what?

How exactly?

A

vWF

Bridge between the platelet surface receptor (glycoprotein Ib—GpIB) and exposed collagen

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106
Q

Platelet secretion involves what molecules?

A

alpha and dense after adhesion

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107
Q

Release of platelet dense granules is important why? 2

A
  1. calcium is required for the coagulation cascade

2. ADP is a potent activator of platelet aggregation

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108
Q

Aggregation of platelets requires what? 4

A

ADP
TxA2
Activated thrombin
Fibrinogen

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109
Q

What are steps of txA2 function? 2

A

Amplify platelet aggregation

Formation of primary hemostatic plug

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110
Q

How does thrombin activation stabilize the plug?

A

Binding to a protease-activated receptor on the platelet membrane → platelet contraction –> irreversibly fused mass of platelets

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111
Q

Most important component of platelet aggregation is what?

A

Fibrinogen

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112
Q

How does platelet bind to fibrinogen?

A
  1. activation by adp
  2. conformation change in platelet GpIIb-IIIa receptors
  3. Binding to brinogen
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113
Q

Deficiency in GpIIb-IIIa complex results in what?

A

Glanzmann thrombasthenia

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114
Q

Deficiency in GpIb results in what?

A

Bernard-Soulier syndrome

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115
Q

Deficiency in vWF leads to what?

A

Von Willebrand disease

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116
Q

What does Clopidogrel do?

A

blocks platelet by blocking ADP binding

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117
Q

Synthetic antagonists or monoclonal antibodies have what effect on platelets?

A

bind to the GpIIb-IIIa receptors

118
Q

Effect on aspirin on platelets?

A

permanently blocks platelet TxA2 synthesis; endothelial PGI2 production is also inhibited by aspirin

119
Q

How do cells overcome aspirin blockade of cascade?

A

resynthesize active cyclooxygenase

120
Q

Nitric oxide effect on platelets?

A

acts as a vasodilator and inhibitor of platelet aggregation

121
Q

What is intrinsic coagulation pathway?

122
Q

What is extrinsic coagulation pathway?

123
Q

What is the common coagulation pathway?

124
Q

What is the coagulation cascade?

A

Amplifying series of enzymatic conversions; each step proteolytically cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation

125
Q

What is the most important coagulation factor?

126
Q

Explain the changes thrombin makes on fibrinogen

A

fibrinogen → fibrin monomers → insoluble gel → secondary hemostatic plug

127
Q

What stabilizes and cross links fibrin polymers?

What activates this?

A

XIIIa

Thrombin

128
Q

Each reaciton in coagulation pathway results from what?

A

Assembly of a complex of enzyme, substrate, cofactor

129
Q

What is the enzyme in coagulation reactions?

A

Activated coagulation factor

130
Q

What is the substrate in coagulation reactions?

A

Proenzyme form of coagulation factor

131
Q

What is the cofactor in coagulation reactions?

A

Reaction accelerator

132
Q

Where does the coagulation reaction take place?

What holds it all together?

A

Phospholipid surface

Calcium ions

133
Q

Factors 2, 7, 9, and 10 binding to calcium requires what as cofactor?

134
Q

What antagonizses factors 2, 7, 9, 10 as an anti-coagulant?

135
Q

Extrinsic and intrinsic pathways converge on activation of what?

136
Q

Why is the extrinsic pathway named so?

A

it required the addition of an exogenous trigger

137
Q

What is the most physiologically relevant pathway for coagulation when vascular damage has been ocurred?

138
Q

What activates extrinsic pathway?

A

tissue factor

139
Q

What does prothrombin (PT) time measure?

A

measures VII, X, II, V, and fibrinogen

140
Q

What measures the intrinsic pathway?

A

Partial thromboplastin time (PTT) screens for the function of the proteins (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)

141
Q

Thrombin exerts what type of effects?

A

Proimflammatory

142
Q

How does thrombin modulate cellular activities?

A

Protease-activated receptors (PARs)

143
Q

What type of activities do the PAR’s through thrombin work? 3

A

I1. nduces platelet aggregation and TxA2 production

  1. Activates ECs to express adhesion molecules, and a variety of fibrinolytic (t-PA), vasoactive (NO, PGI2), and cytokine mediators (e.g., PDGF)
  2. Directly activates leukocytes
144
Q

Coagulation cascade must be restricted to where?

A

Only site of vascular injury

145
Q

Antithrombins are activated how?

A

binding to heparin-like molecules on endothelial cells

146
Q

Antithrombins act how?

A

inhibit the activity of thrombin and other serine proteases, including factors IXa, Xa, XIa, and XIIa

147
Q

How is heparin used?

A

Minimize thrombosis

148
Q

What are proteins C and S dependent on?

149
Q

What is action of proteins C and S?

A

Inactivate factors Va and VIIIa

150
Q

What is the protein produced by endothelium that inactivates tissue factor-factor VIIa complexes

151
Q

Activation of clotting cascade sets what into motion?

A

Fibrinolytic cascade

152
Q

How does the fibrinolytic cascade limit size of clot?

A

breaks down fibrin and interferes with its polymerization

153
Q

Generation of plasmin results in what?

A

fibrin split products (FSPs) can also act as weak anticoagulants

154
Q

Elevated levels of FSP’s can be used in what?

A

diagnosing abnormal thrombotic states (DIC, DVT, PE)

155
Q

The fibrinolytic system has what main reaction?

A

Enzymatic conversion of inactive precursor plasminogen to plasmin

156
Q

Two main types of plasminogen activators?

A

Tissue-type PA (t-PA) synthesized by endothelium

Urokinase-like PA (u-PA)

157
Q

Main bacterial plasminogen activator?

A

Streptokinase (bacterial enzyme

158
Q

Free plasmin is rapidly inactivated by what?

A

α2-plasmin inhibitor

159
Q

Endothelial cells also release what to inhibit plasminogen activation?

A

plasminogen activator inhibitor (PAI) which inhibits t-PA

160
Q

Abnormalities that lead to thrombus formation are together known as what?

A

Virchow’s triad

161
Q

What are the 3 components of Virchow’s triad

A

Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability of the blood

162
Q

Endothelial injury is important factor in what?

A

heart or the arterial circulation (normally high flow rates might otherwise impede clotting)

163
Q

Does the endothelium need to be physically disrupted to contribute to thrombosis?
Why?

A

no

Abnormality in the balance of prothrombotic and antithrombotic activities of endothelium can influence local clotting events

164
Q

What can induce endothelial dysfunction? (6)

A 
Hypertension
Turbulent blood flow
Bacterial endotoxins
Radiation injury
Metabolic abnormalities (homocystinemia, hypercholesterolemia)
Toxins  (cigarette smoke)
165
Q

Turbulence leads to what?

A

endothelial injury or dysfunction

Can form countercurrents and local areas of stasis

166
Q

What is main contributor in development of venous thrombi?

167
Q

Normal blood flow is described how?

A

Laminar

platelets and blood cellular components flow centrally separated from the endothelium by slower moving plasma

168
Q

Stasis promotes activation of what?

How

A

Endothelial activation

Flow-induced changes in endothelial cell gene expression

169
Q

Stasis disrupts flow and brings what into contact with endothelium?

170
Q

What does stasis prevent?

A

dilution of activated clotting factors

171
Q

Atherosclerotic plaques are involved in thrombosis how?

A

expose subendothelial ECM and cause turbulence

172
Q

Aneurysms are involved in thrombosis how?

A

Local stasis

173
Q

Acute MI’s are involved in thrombosis how?

A

areas of noncontractile myocardium and sometimes cardiac aneurysms→ formation of cardiac mural thrombi

174
Q

Rheumatic mitral valve stenosis is involved in thrombosis how?

A

left atrial dilation

175
Q

Hypoviscosity is involved in thrombosis how?

A

increases resistance to flow and causes small vessel stasis

176
Q

Sickle cell anemia is involved in thrombosis how?

A

vascular occlusions→ stasis → thrombosis

177
Q

What will hypercoagulability contribute to?

A

Thrombotic states

178
Q

Primary hypercoagulability is due to what?

A

Point mutations in the factor V gene and prothrombin gene are the most common

179
Q

Secondary hypercoagulability is due to what?

180
Q

Factor V Leiden is found in what population

A

2% to 15% of Caucasians carry a single nucleotide mutation in factor V

181
Q

Mutation in Factor V Leiden results in what?

A

factor V resistant to cleavage by protein C

182
Q

Prothrombin mutation results in what?

A

Increased levels of prothrombin with an almost threefold increased risk of venous thromboses

183
Q

Elevated levels of homocysteine contribute to what?

A

Contribute to arterial and venous thrombosis as well as the development of atherosclerosis

184
Q

Why do mild elevated levels of homocysteine occur?

A

Variant form of 5,10-methylenetetrahydrofolate reductase

185
Q

Markedly elevated homocysteine levels can be caused by what?

A

inherited deficiency of cystathione β-synthetase

186
Q

What can reduce plasma homocysteine concentration?

A

Folic acid, pyridoxine, and/or vitamin B12

187
Q

Rare inherited causes of increase risk in thrombosis are due to deficiencies in what?

A

Antithrombin III
Protein C
Protein S

188
Q

Some causes of acquired thrombophilia

A
  1. Oral contraceptive use
  2. Hyperestrogenic state of pregnancy
  3. Dissemianted cancers
  4. Reduced endothelial PGI2 in age
  5. Smoking
  6. Obesity
189
Q

Why do oral contraceptive use or hyperestrogenic state of pregnancy cause thrombosis? 2

A

increased hepatic synthesis of coagulation factors and reduced anticoagulant synthesis

190
Q

What is heparin-induced thrombocytopenia syndrome?

A

After adminstration of unfractionated heparin, there is Induction of the appearance of antibodies that recognize complexes of heparin and platelet factor 4

191
Q

Result of heparin-induced thrombocytopenia syndrome?

A
  1. platelet aggregation
  2. Platelet activation
  3. platelet consumption
192
Q

What will alleviate heparin-induced thrombocytopenia syndrome

A

Low-molecular weight heparin

193
Q

Antiphospholipid syndrome is known as what?

A

lupus anticoagulant syndrome

194
Q

How does antiphopholipid syndrome present clinically? 4

A

Recurrent venous or arterial thrombi
Repeated miscarriages
Cardiac valvular vegetations
Thrombocytopenia

195
Q

Antiphospholipid syndrome is mediated by what?

A

binding of antibodies to epitopes on plasma proteins that are induced by phospholipids

196
Q

What does antiphospholipid syndrome present as on serologic test?

197
Q

What is secondary antiphospholipid syndrome?

A

individuals with a well-defined autoimmune disease

198
Q

What is primary antiphospholipid syndrome?

A

patients with a hypercoagulable state with no evidence of other autoimmune disorders

199
Q

Thrombi can develop where in the CV system?

A

Everywhere

200
Q

Size and shape of thrombi depend on what?

A

site of origin and cause

201
Q

Thrombi are attached to what?

A

Underlying vascular surface

202
Q

Arterial thrombi grow what direction?

A

Retrograde (toward heart)

203
Q

Venous thrombi grow what way?

A

Direction of blood flow (toward heart)

204
Q

What are Lines of Zahn

A

pale platelet and fibrin deposits alternating with darker red cell–rich layers

205
Q

What do lines of Zahn signify?

A

thrombus formed in flowing blood

206
Q

Mural thrombi occur where?

A

heart chambers or in the aortic lumen

207
Q

What promotes cardiac mural thrombi? 2

A 
Abnormal mycardial contraction (arrhythmia, MI)
Endomyocardial injury (myocarditis)
208
Q

Arterial thrombi has what characteristics? 3

A
  1. Occlusive
  2. Superimposed on a ruptured atherosclerotic plaque
  3. Seen with other vascular injuries
209
Q

Common sites of arterial thrombi?

A

Coronary, cerebral, femoral arteries

210
Q

Venous thrombosis has what characteristics? 2

A
  1. Occlusive with thrombus forming a long cast of lumen

2. More enmeshed red cells and few platelets

211
Q

Thrombi of veins normally occur where?

Where else (4)

A

Lower extremities

  1. upper extremities
  2. Perioprostatic plexus
  3. ovarian
  4. periuterine veins
212
Q

Posmortem clots appear how? 3

A

Gelatinous with a dark red dependent portion
Yellow upper portion “chicken fat”
Not attached to the underlying wall

213
Q

Thrombi on heart valves are known as?

A

Vegetations

214
Q

What is infective endocarditis?

A

bacteria or fungi adhering to previously damaged valves or directly causing valve damage; formation of large thrombotic masses

215
Q

What is nonbacterial thrombotic endocarditis?

A

sterile vegetations on noninfected valves in persons with hypercoagulable states

216
Q

What is sterile, verrucous endocarditis/Libman-Sacks endocarditis?

A

Seen in setting of SLE

217
Q

What is propagation?

A

thrombi accumulate additional platelets and fibrin

218
Q

What is embolization?

A

thrombi dislodge and travel to other sites in the vasculature

219
Q

What is dissolution?

A

fibrinolysis with rapid shrinkage and disappearance of recent thrombi

220
Q

What is organization and recanalization?

A

ingrowth of endothelial cells, smooth muscle cells, and fibroblasts; capillary channels eventually form that re-establish the continuity of the original lumen

221
Q

Where do most venous thrombosis (phlebothrombosis) occur?

A

Superficial or deep veins of leg

222
Q

Characteristics of superficial venous thrombosis?

A

local congestion, swelling, pain, and tenderness; rarely embolize

223
Q

Characteristics of DVT?

A

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
Q

Lower extremeties DVT’s are associated with what?

Common predisposing factors?

A

hypercoagulable states

Bed rest and immobilization
Congestive heart failure
Trauma, surgery, and burns
Advanced age

225
Q

What is trousseau syndrome?

Due to what?

A

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
Q

Major cause of arterial thromboses?

A

Atherosclerosis

227
Q

Can cardiac and aortic mural thrombi embolize peripherally?

228
Q

Targets of cardiac and aortic mural thrombi?

A

Brain, kidneys, and spleen are particularly likely targets because of their rich blood supply

229
Q

Disseminated intravascular coagulation is seen when?

A

obstetric complications to advanced malignancies

230
Q

What happens in Disseminated intravascular coagulation?

A

Sudden or insidious onset of widespread fibrin thrombi in the microcirculation

231
Q

Result of Disseminated intravascular coagulation?

A

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
Q

DIC is a complication of any condition associated with what?

A

widespread activation of thrombin

233
Q

What is an embolism?

A

Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

234
Q

Almost all emboli represent what?

A

some part of a dislodged thrombus (thromboembolism)

235
Q

Emboli will inevitably lodge where?

A

in vessel too small to permit further passage (causing partial or completely vascular occlusion)

236
Q

A major consequence of an embolism is what?

A

Ischemic necrosis

237
Q

A major consequence of embolism is what?

A

Ischemic necrosis (infarction)

238
Q

Pulmonary embolism usually results from what?

A

leg DVT’s

239
Q

Occlusion of main pulmonary artery bifurcation is what?

A

Saddle embolus

240
Q

What is a pardoxical embolism?

A

embolus can pass through an interatrial or interventricular defect and gain access to the systemic circulation

241
Q

Do most PE’s have symptoms?

A

Nope, too small

242
Q

If more than 60% of pulmonary circulation is obstructed, what will happen?

A

Sudden death, right heart failure, or CV collapse

243
Q

Embolic obstruction of medium-sized pulmonary arteries result in what?

A

pulmonary hemorrhage but not usually infarction

244
Q

Embolic obstruction of small end-arteriolar pulmonary branches result in what?

A

hemorrhage or infarction

245
Q

Multiple emboli in PE overtime results in what?

A

pulmonary hypertension and right ventricular failure

246
Q

What is systemic thromboembolism?

A

Emboli in the arterial circulation

247
Q

Most arterial emboli arise from where?

A

intracardiac mural thrombi

248
Q

2/3 of arterial emboli are associated with what?

A

left ventricular wall infarcts

249
Q

1/4 of arterial emboli are associated with what?

A

left atrial dilation and fibrillation

250
Q

Remainder of arterial emboli arise from what?

A

thrombi on ulcerated atherosclerotic plaques, aortic aneurysms, or fragmentation of a valvular vegetation, or paradoxical emboli

251
Q

Sites for arterial emboli to lodge? and their percentage

A

Lower extremities: 75%
Brain: 10%
Intestines, kidneys, spleen

252
Q

What is a fat or marrow emboli?

A

Microscopic fat globules—with or without associated hematopoietic marrow elements—can be found in the circulation and in the pulmonary vasculature

253
Q

When are fat/marrow emboli seen?

A

Fractures of long bones

Vigorous cardiopulmonary resuscitation

254
Q

Fat Embolism Syndrome is what?

A

Term applied to the minority of patients who become symptomatic

255
Q

Causes of fat embolism syndrome? 3

A

Pulmonary insufficiency
Neurologic symptoms
Anemia and thrombocytopenia

256
Q

Presentatin of symptoms in fat embolism syndrome?

A
  1. After 1-3 days, sudden onset of tachypnea, dyspnea, and tachycardia
  2. Diffuse petechial rash (thrombocytopenia)
257
Q

What is an air embolism?

A

Gas bubbles can coalesce to form frothy masses that obstruct vascular flow

258
Q

How much air is required to have a clinical effect in pulmonary circulation?

A

more than 100 cc of air

259
Q

When can an air embolism occur? (2)

A

obstetric or laparoscopic procedures or because of chest wall injury

260
Q

What is decompression sickness due to?

A

Sudden decreases in atmospheric pressure and Gas (particularly nitrogen) dissolves in the blood and tissues

261
Q

What are the bends?

A

– rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints

262
Q

What are the chokes?

A

respiratory distress where gas bubbles in the lungs cause edema, hemorrhage, and focal atelectasis or emphysema

263
Q

Treatment for decompression sickness?

A

Compression chamber

264
Q

Caisson disease is a chronic form of what?

A

Decompression sickness

265
Q

Caisson disease is what?

A

Gas emboli in bones

Ischemic necrosis of femoral head, tibia and humerus

266
Q

Why is amniotic fluid embolism so serious?

A

80% mortality rate and fifth most common cause of maternal mortality worldwide

267
Q

What happens in amniotic fluid embolism?

A

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
Q

Result of amniotic fluid embolisM?

A

severe dyspnea, cyanosis, and shock followed by neurologic impairment

Pulmonary edema and DIC

269
Q

Findings in amniotic fluid embolism?

A

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
Q

What is ischemic necrosis?

A

Occlusion of arterial supply or venous drainage

271
Q

Nearly all infarcts result from what?

A

thrombotic or embolic arterial occlusions

272
Q

Infarction is classified according to what?

A

Color, presence of infection

273
Q

3 types of infarctions

A

Red or hemorrhagic infarcts
White or anemic infarcts
Septic or bland

274
Q

Red infarcts are most commonly caused where?

275
Q

Characteristics of places where red infarcts occur?

A

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
Q

When do white infarcts occur?

A

arterial occlusion in solid organs with end-arterial circulation (heart, spleen, kidney)

277
Q

Tissue density has what effect on white infarct

A

limits the seepage of blood from adjoining capillary beds into the necrotic area

278
Q

Wedge-shaped infarct is what?

A

Occluded vessel at the apex and the periphery of the organ forming the base

279
Q

Dominant histologic characteristic of infarct is what?

A

ischemic coagulative necrosis

280
Q

Most infarcts are replaced by what?

281
Q

In brain how do infarcts present?

A

Liquefactive necrosis

282
Q

Septic infarcts may lead to what?

283
Q

Factors that influence development of an infarct? 4

A
  1. Nature of vascular supply
  2. Rate of occlusion development
  3. Vulnerability to hypoxia
  4. Oxygen content of blood
284
Q

What is common pathway for potentially lethal clinical events?

285
Q

What can cause shock? (5)

A

Severe hemorrhage, extensive trauma or burns, large MI, massive PE, microbial sepsis

286
Q

Shock is characterized by what?
Due to what? (2)

Which results in what?

A

Systemic hypotension

  1. Reduced CO
  2. Reduced effective circulating blood volume
  3. Impaired tissue perfusion
  4. Cellular hypoxia
287
Q

Three main categories of shock

A

Cardiogenic
Hypovolemic
Septic

288
Q

Cardiogenic shock is due to what?

A

low CO due to myocardial pump failure

289
Q

What can cause cardiogenic shock?

A

MI, ventricular arrhythmias, external compression (cardiac tamponade), outflow obstruction (PE)

290
Q

What is hypovolemic shock?

Due to what? 2

A

low CO due to loss of blood or plasma volume

Hemorrhage, severe burns

291
Q

Septic shock is due to what?

A

Vasodilation and peripheral pooling of blood as part of a systemic immune reaction to bacterial or fungal infection

Pathology (36 decks)

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