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Robbins Pathology MOD1 (Chptr 1-6) > Chapter 4 > Flashcards

Chapter 4 Flashcards

1
Q

What is cor pulmonale and what causes it

A

Right side heart failure, and occurs when an emboli obstructs 60% or more of the pulmonary circulation

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2
Q

What is the result of the parasite filariasis

A

Induces fibrosis of lymphatic channels and nodes leading to lymphatic obstruction

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3
Q

What is the general steps that decreased oncotic pressure leads to edema

A

1) Reduced intravascular volume
2) Renal hypoperfustion
3) Increased aldosterone secretion (secondary hyperaldosteronism)
4) Water and salt retention leads to further edema

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4
Q

What are the three main factors that limit blood clotting

A

1) Dilution of blood taking factors away
2) Requirement of negative charge phospholipids only seen on activated platelets
3) Factors expressed by healthy epithelium to restrict activation

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5
Q

What are the factors that are expressed by endothelial cells to prevent coagulation

A

1) Thrombomodulin
2) Endothelial protein C receptor
3) Heparin like molecules
4) tissue factor pathway inhibitor

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6
Q

What occurs following a loss of blood >20% of blood volume

A

Hemorrhagic (hypovolemic) shock

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7
Q

Which condition is the usual cause of pulmonary edema

A

Most commonly with left ventricular failure, but can also be with renal failure, or acute respiratory distress syndrome

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8
Q

What occurs immediately following injury to a blood vessel

A

Vasoconstriction in order to reduce blood flow to injured area

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9
Q

Septic shock is most commonly triggered by which pathogen

A

Gram positive bacteria

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10
Q

What will acute pulmonary congestion present with morphologically

A

Enlarged alveolar capillaries, alveolar septal edema, and focal intraalveolar hemorrhage

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11
Q

What are the most common inherited causes of hypercoagulability

A

1) Point mutations in factor 5 gene

2) Point mutations in Prothrombin gene

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12
Q

Where is the process of clotting occurring

A

On the negatively charged phospholipid surface of platelets

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13
Q

What is the role of endothelial protein C receptor

A

Hold protein C, so bound thrombin to thrombomodulin, can inactivated factors 5a and 8a

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14
Q

Of people with DVTs, what percent are associated with factor 5 Leiden mutation

A

60%

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15
Q

During platelet aggragation, what is the significance in the changes to complex 2B/3a

A

Allows the binding of fibrinogen, and subsequent bridging of adjacent platelets

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16
Q

How is the level of plasmin regulated

A

Alpha2-plasmin inhibitor (PAI) which bind to and inactivate free plasmin

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17
Q

What are the conditions that can lead to impaired venous return and subsequent increases in hydrostatic pressure

A

CHF, constrictive pericarditis, ascites (liver failure), venous obstruction or compression, arterial dilation

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18
Q

What condition with patients regularly receive a false positive for during antiphospholipid antibody Syndrome

A

Syphilis, due to binding to cardiolipin

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19
Q

What is the main enzyme responsible of for fibrinolysis

A

Plasmin

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20
Q

What is the most important activator of factor 10

A

9a/8a

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21
Q

For the PTT test, what are the materials added

A

Negative charged particles (beads)
Phospholipids
Calcium

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22
Q

What is the cause of congestion

A

Reduction in the outflow of blood from a tissue as in cardiac failure or venous obstruction

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23
Q

How will cardiac and hypovolemic shock present in clinic

A

Hypotension, weak but rapid pulse, tachypnea, cool but clammy skin

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24
Q

What is the general order of events in primary hemostasis

A

1) von Willebrand factor and collagen are exposed
2) Platelets adhere and activate, become spiky balls
3) Platelets degranulate and release factors
4) Platelets aggregate

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25
Q

What are the three general mechanisms that disruption in laminar flow can lead to thrombin activation

A

1) Promotes endothelial activation and adhesion of proinflamatory factors
2) Brings platelets in contact with the epithelium
3) prevents washout and dilution of Activated Factors

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26
Q

Rapid loss up to which percent of blood volume can normally occur without effects

A

20%

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27
Q

What are the characteristics of subcutaneous edema

A

Accumulate in the areas with high hydrostatic pressure, which is usually determined by areas influenced by gravity (legs when standing) aka dependent edema

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28
Q

What is trousseau syndrome, aka migratory thrombophlebitis

A

Increased risk of thromboembolism due to tumor associated inflammation and coagulation factors released from tumors

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29
Q

What is the result of increased salt retention

A

1) increased hydrostatic pressure due to increased intravascular fluid volume
2) Decreased vascular oncotic pressure due to dilution

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30
Q

What is the condition of thrombophilia

A

Hypercoagulability and predisposes patient to thrombi

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31
Q

What do the antibodies in antiphospholipid antibody Syndrome bind to

A

Bind to proteins that are somehow induced by phospholipids (Beta2 glycoprotein 1

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32
Q

What are the conditions leading to lymphatic obstructions

A

1) Inflammation
2) Neoplasticism
3) Postsurgical
4) Postirradiation

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33
Q

What are usual defects in secondary hemostasis

A

Coagulation defects

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34
Q

What two conditions stem from increased blood volumes within tissues

A

Hyperemia and congestion

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35
Q

What are the conditions associated with antiphospholipid antibody Syndrome

A

Recurrent thrombosis, repeated miscarriages, cardiac valve vegetations, thrombocytopenia

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36
Q

How does an MI lead to increased risk of thrombi

A

Results in areas of noncontractile myocardium, which create areas of stasis and mural thrombi

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37
Q

What are the two factors that lead to increase movement of fluid out of vessels and into tissues

A

1) Increased hydrostatic pressure

2) Decreased colloid osmotic pressure

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38
Q

During platelet activation, what are the two factors that are released to cause coagulation

A

Thrombin and ADP

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39
Q

Following platelet activation, what complex undergoes a change

A

Gp2b/3a

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40
Q

How does administration of aspirin affect platelet activation

A

Prevents TxA2 production by COX1, which is a platelet aggregation induced

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41
Q

What are the symptoms of fat embolism syndrome

A

Pulmonary insufficiency, neuro symptoms, anemia, and thrombocypenia, tachycardia, dyspnea, tachypnea, and diffuse

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42
Q

The prothrombin time (PT) assays asses which proteins of which pathway

A

Extrinsic pathways

Factors 2,5,7,10, and fibrinogen

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43
Q

What is the risk of developing thrombi with a mutation in the prothrombin gene

A

3x more likely

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44
Q

Where is stasis commonly found and what are the conditions that can increase it

A

Generally found in venous system and is triggered by atrial fibrillation and bed rest

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45
Q

What are the ways that plasmin is activated

A

1) Factor 12 pathway

2) plasminogen activators (tPA) and urokinase

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46
Q

How does polycythemia Vera (hyper-viscosity) lead to thrombi

A

Increased resistance to flow causes small vessel, leading to stasis

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47
Q

What are the factors that posses a gamma-carboxylase glutamic acid

A

Factor 2,7,9,10

Protein C & S

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48
Q

Defects in primary hemostasis usually result in which symptoms

A

1) Epistaxis (nose bleeds)
2) GI bleeding
3) Excessive menstruation (menorrhagia)

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49
Q

What are the most common sites of edema

A

Subcutaneous tissues, lungs and brain

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50
Q

What are petechiae

A

Small bleed 1-2 mm

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51
Q

What is the difference between primary and secondary antiphospholipid antibody syndrome

A

Primary- no association with any autoimmune diseases

Secondary- Associated with autoimmune diseases, especially Lupus

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52
Q

What is the effect of aneurysms in disruption of blood flow

A

A result of aortic and arterial dilation that result in local stasis

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53
Q

What will chronic passive hepatic congestion present with morphologically

A

Nutmeg liver, which are depressed and red areas

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54
Q

Bloodborne bacteria can affect valves of the heart how?

A

Adhereing to damaged valves, or by causing damage to heart valves known as infective endocarditis

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55
Q

What is the source of the majority of systemic emboli

A

80% arise from intracranial mural thrombi (2/3 are from LV0

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56
Q

What is the affect of administering Coumadin

A

Antagonizes the use of vitamin K as a cofactor in the reactions producing gamma-glutamic acid

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57
Q

Epithelial injury most often occurs in what location and what is the rate of blood flow

A

High rate of blood flow, usually in the heart and arterial circulation

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58
Q

What is factor 11 deficiency associated with

A

Mild bleeding

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59
Q

What are purpura

A

Small bleeds >3mm

60
Q

What are the procoagulant changes seen in Activated epithelial cells

A

Down regulation of thrombomodulin, protein C and tissue factor inhibitors

61
Q

Following platelet activation, what does the change in the complex cause

A

Increased affinity for fibrinogen

62
Q

What is the most important activator of factor 9

A

Factor 7a/Tissue factor

63
Q

What is the cause of heparin-Induced thrombocytopenia (HIT) syndrome

A

Administration of fractionated heparin, which leads to antibodies against heparin and platelet factor 4 on platelets, causing aggregation

64
Q

What is the function of tissue factor pathway inhibitor (TFPI)

A

Binds and inhibits tissue factor/factor 7a complexes

65
Q

What are vegetations

A

Thrombi on heart valves

66
Q

How does antiphospholipid antibody Syndrome lead to repeated miscarriages

A

Antibody mediated interference with the growth and differenation of trophoblasts, leading to failure of placentation

67
Q

What is the general order of secondary hemostasis

A

1) Tissue Factor is deposited at the site of injury
2) Activation of factor 7
3) Thrombin activation occurs
4) Thrombin causes the activation of fibrin
5) Fibrin polymerization occurs and the more permanent plug is formed

68
Q

What is the diseases associated with a defect in vWF

A

Von Willebrand Disease (a bleeding disorder)

69
Q

What is the condition of caisson disease

A

Chronic decompression sickness, with necrosis generally at the heads to the femur, tibia, and humeri

70
Q

What will acute hepatic congestion present with morphologically

A

Central vein and sinusoids are distended. Centrilobular (distal end of blood Supply) undergo necrosis while the periportal hepatocytes undergo fatty changes

71
Q

Antiphospholipid antibody syndrome is present in what percent of the population without any symptoms

A

5-15%

72
Q

What is the result of factor 5 Leiden mutation

A

Resistant to cleavage and inactivation via protein C

73
Q

How will septic shock present in clinic

A

Warm and flushed due to peripheral vasodilation

74
Q

Enzyme reactions that produce gamma-glutamic acid require which vitamin

A

Vitamin K

75
Q

Immediate vasoconstriction at the site of injury is due to which factor and where is it derived from

A

Local secretion of endothelin, which is derived from endothelium

76
Q

What is the difference between primary and secondary hypercoagulabilty disorders

A

Primary is genetic while secondary is acquired

77
Q

What is the mutation in the factor 5 Leiden

A

Glutamine residue is substituted with arginine at position 506

78
Q

What are the conditions leading to reduced plasma oncotic pressure aka hypoproteinemia

A

1) Protein losing glomerularphathies (nephrotic syndrome)
2) Liver failure (cirrhosis or ascities)
3) Malnutrition
4) Protein losing gastroenteropathy

79
Q

How does rheumatic mitral valve stenosis lead to thrombi

A

Results in left atrial dilation, and in conjunction with atrial fibrillation leads to stasis

80
Q

What will acute hepatic congestion present with morphologically

A

Septa are thickened and fibrotic, with macrophages (aka heart failure cells) full of hemosiderin. Usually caused by heart failure

81
Q

What is the result of renal failure on platelet count and coagulation

A

1) Renal failure leads to increase in uric acid (uremia)
2) Uremia inhibits platelet formation
3) Leads to defects in primary hemostasis

82
Q

What is the condition of nonbacertial thrombotic endocarditis

A

Sterile vegetation’s on heart valves in patients in a hypercoagulability state

83
Q

What are the four general steps in coagulation

A

1) Arterial constriction
2) Primary Hemostasis plug
3) Secondary hemostasis plug
4) Clot stabilization and resorption

84
Q

What are the conditions that lead to fluid retention

A

Compromised renal function, and cardiovascular disorders (such as congestive heart failure)

85
Q

What is the respiratory distress known as the chokes associated with

A

The bends

86
Q

What are the associated symptoms with amniotic fluid embolism

A

Dyspnea, cyanosis, and shock, diffuse alveolar damage, pulmonary edema due to DIC

87
Q

What are the some of the factors that can lead to acquired thrombophilia

A

1) Oral contraceptives
2) hyperestrogenic state
3) Coagulants from cancer tumors
4) Heparin induced
5) antiphopspholipid antibody syndromes

88
Q

What is the phospholipid composition change on activated platelets and what is the significance

A

Negatively charged phospholipids (phosphotidylserine) moves to surface, which allows the binding of Calcium, serving as assembly sites for factor complexes

89
Q

What is the role of thrombomodulin

A

Binds thrombin, which removes it ability to activate platelets, and instead causes it to cleave and activate protein C, which is anti coagulative

90
Q

Where is turbulent flow commonly found and what are the conditions that can cause it

A

Usually found in arterial and cardiac thrombosis. Commonly due to narrowing of vessels secondary to atherosclerosis

91
Q

What is a feared complication of thrombocytopenia

A

Intracerebral hemorrhage

92
Q

What is the result of mutations in the prothrombin gene that lead to coagulation

A

Increased levels of thrombin in circulation

93
Q

Subcutaneous edema is usually a sign of what conditions

A

Renal or cardiac disease

94
Q

What is the mutation in the prothrombin gene that is common

A

Single nucleotide change (G20210A) in the 3 prime untranslated region

95
Q

What is the mechanism that thrombin activates platelets

A

GPCR known as protease-activated receptor (PAR), which is activated by the cleavage of thrombin

96
Q

What is periorbital edema usually indicative of

A

Renal dysfunction

97
Q

What are the general causes of increased hydrostatic pressure

A

Disorders that impair venous return

98
Q

What are Thrombin’s most important functions

A

1) Conversion to fibrinogen to crosslinked fibrin
2) Platelet Activation (via PARs, and TxA2)
3) Proinflammatory effects (neutrophil adhesion and monocyte activation)
4) Anticoagulant effects (yes this is right)

99
Q

What is the fucntion of heparin like molecules

A

Bind and activate antithrombin 3, which then inhibits:

Thrombin, 9a,10a,11a,12a

100
Q

What conditions are generally associated with secondary hemostasis defects

A

1) Bleeds into soft tissue
2) Bleeding into joints (hemarthrosis)

Commonly occur after minor trauma that wouldn’t be an issue

101
Q

What is endothelial activation or dynfunction caused by

A

Physical injury, infection, Ab normal blood flow, metabolic conditions, hypercholesterolemia, homocystinuria, toxins (smoke)

102
Q

When is t-PA most active

A

When it is bound to fibrin, so the presence of a clot will lead to the increase activation of plasmin (only at the site of the recent thrombus)

103
Q

What is the mechanism of amniotic fluid embolism

A

Biochemical activation of coagulation factors and innate immune factors by substances in the amniotic fluid

104
Q

What are the contents of dense granules

A

ADP, ATP, ionized calcium, serotonin and epinephrine

105
Q

What are the anticoagulant receptors that require Protein S

A

1) Protein C

2) Tissue Factor Pathway inhibitor (TFPI)

106
Q

What is the disease associated with a defect in Gp1b

A

Bernard-Soulier syndrome (bleeding disorder)

107
Q

Is prothrombin defects compatible with life

A

Nopers

108
Q

How are leukocytes usually entrapped in a secondary plug

A

Due to adherence to P selectins located on the activated platelets

109
Q

What diseases is associated with a defect in the Gp2b/3a Complex

A

Glanzmann thrombasthenia (a bleeding disorder)

110
Q

What is the mechanism of elevated levels of homocysteine leading to thrombi

A

Thioester linkages formed between homocysteine metabolites and proteins, including fibrinogen.

111
Q

What is the epidemiology of the mutation in the prothrombin gene

A

1-2% of the population

112
Q

How are the complex components held together in the clotting cascade

A

Via calcium ions, which are required for the reaction to work

113
Q

What are the vast majority of emboli from

A

Dislodged thrombi, aka thromboembolism

114
Q

What are the conditions leading to sodium retention

A

1) Excesive sodium intake without renal compensation

2) Increased tubular reabsorption (renal hypofusion or increased RAA secretion

115
Q

What is the result of HIT syndrome when there is heparin present and low levels of platelets

A

Will still cause aggregation and a prothrombin state

116
Q

What is the clinical significance of D-Dimers

A

Byproduct of the breakdown of fibrinogen, so can be measured to get a relative thrombotic state estimate

117
Q

What are the general results seen from lymphatic obstruction

A

Edema in the external genitalia and lower limbs. Can also become so pronounced that it will cause elephantiasis. May require irrational on axillary lymph and breasts if in the upper limb

118
Q

What is the mechanism of thrombin creating fibrin

A

1) Cleaves fibrinogen (soluble) into fibrin (insoluble)
2) Amplifies pathways (via activation of cofactor 5, 8,11)
3) Stabilizes plug with activation of factor 13, which covalently crosslinks fibrin

119
Q

What are the three primary abnormalities that lead to thrombosis

A

1) Epithelial injury
2) Stasis or turbulent flow
3) Hypercoagability

120
Q

What is the common cause for the decrease in plasma oncotic pressure

A

Inadequate synthesis of albumin, or increased los of albumin from circulation

121
Q

What is added to the prothrombin time (PT) assay

A

Tissue factor, phospholipids, and calcium

122
Q

What are peritoneal effusions aka ascites generally associated with

A

Portal hypertension, and are prone to bacteria leading to fatal infection

123
Q

What percentage of PEs come from leg DVT

A

95%

124
Q

What are the three main substances that are released by endothelial cells to prevent coagulation

A

1) Prostacyclin (PGI2)
2) Nitric oxide (NO)
3) ADPase (breaks down ADP)

125
Q

What is the cause of hyperemia and what is the color

A

Active process in which arterial dilation leads to increase in bloodflow. Tissue will be red due to the increase in blood flow

126
Q

What is the epidemiology of factor 5 Leiden

A

2-15% of Caucasians carry the mutation

127
Q

What factors are associated with moderate to severe bleeding disorders

A

5,7,8,9,10

128
Q

Arterial thrombi are usually result in what

A

Obstruction of:

1) Coronary artery
2) Cerebral artery
3) Femoral artery

129
Q

In the platelet reaction complexes, what ion is required and what does it bind to

A

Calcium is required to bind to gamma-carboxylase glutamic acid

130
Q

What is the mechanism that will lead to damage via a fat embolism

A

Biochemically, due to the release of free fatty acids from the fat globules, leading to inflammation and platelet activation

131
Q

What is the Hageman factor and which pathway is it in

A

Factor 12, and associated with the intrinsic pathway

132
Q

What is factor 12 defects associated with

A

Inability to bleed and increased risk of thrombosis

133
Q

What is the rate of risk for venous thrombi in homozygotes and heterozygotes for mutation in factor 5 Leiden

A

Hetero- 5x more likely

Homo-50x more likely

134
Q

Where do phlebothrombosis commonly occur

A

Aka venous thrmobosis, which occurs in the deep and superficial veins of the legs

135
Q

For the partial thromboplastin time (PTT) assay, which factors of which pathway are being tested

A

Intrinsic pathway

Factors 2,5,8,9,10,11,12, and fibrinogen

136
Q

What is required for the activation of protein C to begin cleaving

A

1) Binding to thrombin to thrombomodulin
2) Cleavage by thrombin bound to thrombomodulin
3) Vitamin K
4) Protein S

137
Q

When does Libman-sacks endocarditis occur

A

Sterile endocarditis in which occurring secondary to Lupus

138
Q

What are the factors that are mediating platelet adhesion

A

1) vWF, which bridges 2) Gp1b (on platelet) and exposed 3)collagen

139
Q

What are the content so the alpha granules

A

1) P selectin

2) Coagulative Factors (fibrinogen, Factor 5, vWF, fibronectin, platelet factor 4, PDGF, and TGF-beta)

140
Q

How does sickle cell anemia lead to thrombi

A

Impedes blood flow through small vessels and result in stasis

141
Q

When should hypercoagulability be considered in young patients

A

In patients less than 50 who present with thrombosis, even if acquired risks are present

142
Q

What is chronic passive congestion associated with

A

Chronic hypoxia may lead to injury and scarring. Capillary rupture is also very common, leading to small hemorrhages and hemosiderin laden macrophages

143
Q

Non inflammatory edema is assocaited with which conditions

A

Heart failure, liver failure, renal disease, and nutritional disorders

144
Q

What is the results if elevated levels of homocysteine

A

Increased risk of arterial and venous thrombi

145
Q

What are the antifibrinolytic effects seen in Activated epithelial cells

A

Secrete plasminogen activator inhibitors (PAIs), down regulate t-PA

Robbins Pathology MOD1 (Chptr 1-6) (10 decks)

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