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Common Mechanisms of Disease-2 > Hemodynamics- Things From Robbins Q's > Flashcards

Hemodynamics- Things From Robbins Q's Flashcards

1
Q

What is edema?

A

Swelling of tissue due to increased fluid in interstitial tissue spaces. It can be localized or generalized.

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2
Q

What is fluid in the pleural cavity ?

A

Hydrothorax, the fluid is called pleural effusion

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3
Q

What is fluid in the abdominal cavity?

A

Ascites, which is also called peritoneal effusion.

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4
Q

What is generalized edema?

A

Anasarca

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5
Q

What is the most common cause of generalized edema?

A

Heart failure.

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6
Q

What is the first sign of nephrotic syndrome?

A

Periorbital Edema

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7
Q

What is it called when you can poke edema with your finger

A

Pitting Edema which makes up 99% of edema

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8
Q

What is hyperemia ?

A

(Erythema) An active increase in arterial blood flow.

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9
Q

What is congestion ?

A

Passive decrease in venous outflow

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10
Q

What is hemorrhage ?

A

Extravasation of blood due to a vessel rupture

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11
Q

What is a hematoma ?

A

Hemorrhage enclosed within tissue

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12
Q

What is Petechiae

A

Tiny hemorrhages due to platelet deficiency

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13
Q

What is hemostasis?

A

The maintenance of blood in a free flowing liquid state in normal blood vessels and the formation of a blood clot (Hemostatic plug) at a site of vascular injury

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14
Q

What are platelets?

A

A-nucleate cellular components of blood important in initiation and propagation of clotting

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15
Q

What is thrombosis?

A

Inappropriate formation of blood clot in a blood vessel ( Usually occlusive)

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16
Q

What is hypercoagulability

A

The abnormal tendency to form blood clots.

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17
Q

What is a coagulapathy?

A

An abnormal tendency to bleed

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18
Q

What is embolism ?

A

A detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin.

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19
Q

What are the 4 fates of a thrombus ?

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and Recanalization
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20
Q

What is propagation of a thrombus ?

A

The thrombus enlarges through the accretion of additional platelets and fibrin increasing the odds of vascular occlusion.

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21
Q

What is dissolution ?

A

Activation of fibrinolytic factors may lead to tis rapid shrinkage and complete disssolution. This is not likely in older thrombus because of the level of cross linking.

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22
Q

What is organization and recanalization ?

A

Older thrombi become organized by ingrowth of endothelial cells, smooth muscle cells and fibroblasts into the fibrin rich thrombus.

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23
Q

What places you at high risk for deep venous thrombosis ?

A

DVT’s are associated with stasis and hypecoaguable states. The factors for this are bed rest, right heart failure, and immobilization.

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24
Q

What are thrombi on heart valves ?

A

Vegetation. Thrombus on the walls of the heart of murals.

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25
Q

What is hypercoagulability?

A

Hypercoagulability is any alteration in of the coagulation pathways that predisposes affected persons to thrombosis and can be divided into primary and secondary disorders.

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26
Q

What is a lieden mutation ?

A

A mutation in factor V making it resistant to protein C. In this case an anti-thrombotic counter regulatory mechanism is lost.

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27
Q

What is an embolism ?

A

Intracascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. Thromboembolism is the highest risk

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28
Q

What is fat embolism ?

A

Results from ruptured marrow or sinusoids causing fat to be released into the blood stream that will cause biochemical injury and mechanical obstruction.
**Clinical Presentation 1-3 days after event. Tachypenia anemia, thrombocytopenia.

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29
Q

What makes up the most common systemic embolizations ?

A

Intercardiac mural thrombi associated with left ventricular infarcts and aortic infarctions.

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30
Q

Where do venous emboli end up most of the time ?

A

In the lung. Arterial emboli can literally go anywhere.

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31
Q

When would you get amniotic fluid embolism ?

A

A complication of labor in the immediate postpartum period. Tears in the vaginal wall will allow squamous cells, fat, and mucin from the placenta can enter maternal

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32
Q

What is air embolization

A

When gas is precipitated in an artery or vein. They will obstruct venous flow

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33
Q

What does heparin do ?

A

Halts clot propagation- It binds to antithrombin and inactivates thrombin.

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34
Q

What are the inhibitors of the coagulation cascade?

A
  1. Heparin Like Molecules- enhance the inactivation of thrombin
  2. Thrombomodulin- Binds to
  3. Tissue Factor Pathway Inhibitor-
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35
Q

Sinosis ?

A

Blue do the accumulation of deoxygenated blood.

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36
Q

What is endocarditis ?

A

An infection of the heart valves, especially one that is malformed. You will haev turbulant flow which will promote clot thrombus formation

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37
Q

What is Heparin Induced Thrombocytopenic syndrome ?

A

This occurs in 5 % of patients that are treated with unfractionated heparin. This results in the development of autoantibodies that bind complexes of heparin and platelets and destroy them. The Ab’s may also bind similar complexes present on platelet activation aggregation and consumption.

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38
Q

Where do arterial thrombus travel ?

A

Toward the periphery.

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39
Q

What will the increase in procoagulatns and anti-fibrinolytic pathways result in ?

A

Microvascular thrombus (DIC) which will lead to tissue ischemia.

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40
Q

What does PDGF do ?

A

IT is stored on platelets and released upon activation. PDGF causes migration and proliferation of fibroblasts and smooth muscle cells and might contribute to the migration of macrophages.

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41
Q

What is a red infarct ?

A

A red infarct is due to a venous occlusion in loose tissue where blood can collect in the infarcted zones in tissues with ductal circulations (lung and small intestine) where inadequate perfusion by collateral arterial supply is typical. In previously congested tissues **Organs with dual blood supply,

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42
Q

What is a white infarct ?

A

Occurs with arterial occuusions in solid organs with end arterial circulations ( heart spleen and kidney ) where tissue density will limit the seepage of blood from the site of the occlusion
Organs with single blood supply Brain. Clot busting drugs will turn a white infarct into a red infarct.

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43
Q

What is the main histologic finding associated with infarcts ?

A

Ischemic coagulative necrosis with inflammatory responses

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44
Q

What is a line of Zhan ?

A

Thrombi that have grossly apparent laminations. These represent

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45
Q

What are all the functions of Thrombin ?

A
  1. Stimulates platelet aggravation
  2. Activates Monocytes and endothelial cells
  3. Increases neutrophil activation
  4. Causes Fibrin activation & Crosslinking
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46
Q

What does Tissue Pathway Factor Inhibitor do ?

A

A protein secreted by the endothelium that inactivates factor Xa and VIIa factors in the coagulation cascade.

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47
Q

What do Protein C and S do ?

A

They are vitamin K dependent proteins that act in a complex to proteolytically inactivate cofactors Va and VIIIa
**Thrombomodulin activates protein C

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48
Q

What molecule is responsible for fibrinolysis?

A

Plasmin which breaks down fibrin and interferes with its polymerization.

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49
Q

How is plasmin activated ?

A

Plasmin is activated from plasminogen by factor XII or by plasminogen activating factors.

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50
Q

What is the sequence of factor activation in the intrinsic pathway of coagulation ?

A

XII–> XII –> IX + VIII –> X + Va + Ca –> 2 –> activation of Fibrin

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51
Q

Ho is fibrin stabilized and what is responsible for this ?

A

Cross linking mediated by XIII

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52
Q

Is DIC a bleeding problem or a clotting problem?

A

A bleeding problem. You will have decreased platelet counts. Decreased Hemoglobin by hemolysis.

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53
Q

What determines the fluid movement between vascular and interstitial spaces ?

A

Hydrostatic pressure and colloid osmotic pressure. The excess fluid is normally removed by lymphatic drainage.

54
Q

What are petechiae and what do they mean

A

Minute hemorrhages into skin, mucous membranes, or serosal surfaces,

**Menas low latelet counts (Thrombocytopenia) defective platelet function, loss of vascular wall support (Vitamin C Deficency)

55
Q

What are Purpura and what do they mean?

A

They are hemorrhages due to vasculitis. The causes are the same as Petechiae, (Low platelet count ( Thrombocotypenia) defective platelet function or loss of vascular wall support.

56
Q

What are Ecchymoses and what do they mean ?

A

They are small subcutaneous henorrhages that go from red-blue to blue-green and are frequently called bruises.
**Color changes are due to extravasation of RBC’s that are degraded by macrophages and the Fe left over causes the color change.

57
Q

What is Protein C and what does it do?

A

Protein C inhibits clotting by by cleaving and inactivating two procoagulants, Factor Va and Factor VIIIa.

58
Q

How is protein C normally activated ?

A

When Thrombin binds to thrombomodulin it is activated, and with Factor S it will inhibit Va and 8a

59
Q

When an arteriole is knicked what happens in the first few seconds.

A

Neurogenic vasoconstriction will temporariy halt the bleeding as well as augment the secretion of endothelin

60
Q

What is endothelin

A

A potent endothelial derived vasoconstrictor

61
Q

What is the other pro-coagulant glycoprotein that is secreted when a vessel in injured?

A

Tissue Factor which activates the extrinsic coagulation pathway

62
Q

Describe platelet aggregation

A

Follows platelet adhesion and activation and is stimulated by some of the same fators taht induce activation such as thromboxane.

63
Q

What actually causes aggregation ?

A

Interactions between fibrinogen and GP2a/3b receptors on the platelets

64
Q

Describe platelet activation

A

Platelet adhesion leads to an irreversible shape change and secretion of both granules.
The shape change is characterized by long smooth projections as well as an increase in phospholipids on their cell membranes. This allows them to bind Ca and coagulation factors as well as activates GP2b / 3a

65
Q

What does Gp2b / 3a bind to ?

A

Fibrinogen

66
Q

What is thromboxane

A

A prostaglandin that increases platelet aggregation

67
Q

What happens if Gp2a-3b is inactivated ?

A

Platelets will not be able to aggregate

68
Q

What is platelet concurrent activation ?

A

Concurrent activation of the coagulation cascadegenetares thrombin which stabilizes the platelet plug… All done by THROMBIN

69
Q

What does thrombin do in concurrnet activation

A

Activate platelet surface receptors which concert with ADP and thromboxane to further increase aggregation, Platelet contraction follows which is irreversible

70
Q

How do leukocytes adhere to activaed platelets?

A

P-Selectins and stick to the endothelium through selectin molecules

71
Q

What do leukocytes do in active clotting?

A

They promote the inflammatory response. Thrombin promotes inflammation by stimulating neutrophil and monocyte adhesion.

72
Q

What is the main way that platelets and endothelial cells work together to mantain a sort of clot homeostasis ?

A

Endothelial cells synthesize prostagandin PGI2 which is a potent vasodialator and inhibits platelet aggregation. Platelets synthesize the thromboxane TxA2 which is a vasoconstrictor and promotes platelet aggregation.

73
Q

What causes endothelial cells to produce tissue factor ?

What else will TNF and IL-1 do ?

A

Il-1 and TNF and bacterial endotoxins

TNF and Il-1 will up regulate the endothelial cell surface adhesion molecules. They also recruit leukocytes to the site of inflammation.

74
Q

How do activated platelets inhibit fibrinolysis ?

A

They secrete plasminogen activator inhibitors which limit fibrinolysis

75
Q

What is prothrombin time ?

A

Screens the activity of coagulation proteins in the extrinsic pathway. used for evaluation of patients with Vitamin K antagonists because this inhibits factor 7

76
Q

What is partial prothrombin time ?

A

It is used to determine the activity of coagulation proteins in the intrinsic pathway. This is used to determine the anticoagulant properties of heparin. You add factor 12 and phospholipids to the patients plasma and measure time to coagulation.

77
Q

What do protease activated receptors do ?

A

Once activated they are G-Proteins that are activated by thrombin and enhance the adhesion of leukocytes.

78
Q

What happens if the activated platelets can not display Gp2b/3a on their surfaces ?

A

You will bleed out because they will not be able to aggregate before concurent activation. At this stage fibrinogen binds to Pg2b/3a before being converted to fibrin. This is Glandsmans thrombasthenia

79
Q

What is the clinical significance of a vegetation.

A

Clots on the heart valves are most often associated with nonbacterial endocaditis. The bigger the vegitation the more likely that it will become infected and some are associated with autoimmune disease susch as libman sacks endocarditis .

80
Q

What can vegitations cause ?

A

Thromboemboli- Right Heart will go to the lung and Left heart will go to the brain spleen or kidney

81
Q

What is chronic passive congestion ?

A

Capillary or sinusodial or venous stasis of blood within an organ.

82
Q

How does cancer correlate with coagulation ?

A

Cancer will place you at a higher risk for hypercoagulable states which will most likely result in arterial and venous thrombosis.

83
Q

What is phlebothrmbosis ?

A

Stasis in large veins that promotes hemorrhage.

84
Q

What will chronic passive congestion do to the liver

A

Tan and red congested fatty liver. There will be hemorrhage and hemosiderin laden macrophages.
**Severe hepatic congestion is most likely associated with right heart failure.

85
Q

What chronic pulmonary congestion do ?

A

Bloop engorged alveolar capillaries. There will be an increased number of macrophages in the alveoli and when degraded there will be hemosiderin from the RBC’s they have degraded.

86
Q

What will acute hepatic congestion do ?

A

The central vain and sinusoids will be congested with blood and there will be hepatocyte dropout due to loss of blood.

87
Q

What causes congestion ?

A

Impaired venous outflow from a tissue resulting in cyanosis. Chronic congestion will result in inadequate tissue perfusion and persistant hypoxia

88
Q

Describe the edema associated with a DVT versus the edema that will be associtated with congestive heart failure

A

Congestive heart failure will cause generalized edema due to increased hydrostatic pressure in the entire venous system. DVT’s will impede local venous return and thus the edema will only be localized to the extremity.

89
Q

If you have a patient under 50 what should you consider if she has a coagulation disease?

A

Patients under 50 will be most likely to inherit a coagulation deficiency or autoimmune disease

90
Q

What is heparin induced thrombocytopenic syndrome ? (HIT)

A

HIT syndrome- happens in patients who are treated with unfractionated heparin.

  • Charaterized when patients develop autoantibodies that bind complexes of heparin and platelet membrane protein. This will cause thrombocytopenia which is platelet consumption.
  • *Overall pro-thrombotic state
91
Q

What is anti-phospholipitd antibody syndrome?

A

The syndrome has protein manifestations including recurrent thrombosis. miscarriages, valve vegitations, and thrombocytopenia. They develop autoantibodies against anionic phospholipids. Induces a hypercoagulable state that activates platelets and comlement directly
**LUPUS ERYTHMATOSUS

92
Q

How does antiphoso=pholipid antibody syndrom induce hypercoagulation when it binds to phospholipids on platelets.

A

IT causes their activation as well as complement activation. IT will yield a serological false positive for syphilis

93
Q

How are HIT and Anti-phospholipid syndrome different

A

HIT binds to heparin and platelet factor-4.

94
Q

What is DIC

A

Widespread thrombosis in microcirculation. These consume platelets and coagulation factors while at the same time activating fibrinolytic cascades. **Widespread bleeding and catastrophe. Associated with conditions of widespread activation of thrombin

95
Q

What does a factor 5 mutation cause

A

Renders factor 5 resistant to protein C which means a counter regulatory mechanism is lost.

96
Q

Hypercholesterolemia

A

Will not affect coagulation but will cause vasoocclusion and potentially turbulent flow. More of a risk of infarction than anything

97
Q

Lupus Anticoagulant

A

Autoimmune form of antiphospholipid syndrome.

98
Q

Von Willibrand Disease

A

Vwf acts as a glue that binds Collagen in the ECM and GP2b/3a on the surface of the platelets. Vwf disease there is a deficiency in these factors that will cause excessive bleeding.

99
Q

False Serum (+) … what disease

A

LUPUS, you want more …? LUPUS LUPUS LUPUS. Memorize this shit now because the PANDA said so

100
Q

What will hypercholesterolemia do to thrombosis ?

A

It will not alter the coagulation cascade but will injure the endotheluim and cause stenosis.
**Artherosclerotic plaque can embolus from vegetations

101
Q

Is Heprin an active or passive clot inhibitor and how does it work ?

A

Heparin is passive. It works by binding to antithrombin 3 and the complex inhibits thrombin from forming fibrin polymerization.

102
Q

How does Tissue Type Plasminogen Activator work ?

A

It is synthesized by the endothelial cells. It is a protease that cleaves plasminogen to plasmin which will cleave fibrin and degrade clots.

103
Q

What does aspirin do ?

A

This will inactivate platelets and prevent secretion of thromboxane A2 from platelets which will prevent activation and vasoconstriction. This will shift the balance of prostacyclin - thromboxane and let prostacyclin do its thing ( vasodilatation )

104
Q

What clotting factors will tisssue factor pathway inhibitor inhibit ?

A

10a and 9a

105
Q

If you have a patient 30min post acute MI who is at risk for vasogenic shock what will you give and why ?

A

Tissue plasminogen activator which will activate plasmin. This will actively degrade clots whereas asprin will prevent newly formed clots.

106
Q

Where will a venous thromboembolus most likely end up?

A

In the lung.

107
Q

What is an air embolus ?

A

It is a bubble of gas that can occlude vascular flow causing distal ischemic injury

108
Q

What causes pain in decompression sickness

A

Precipitation of air bubbles in muscles and supporting tissues.

109
Q

What will cause respiratory distress in decompression sickness ?

A

Precipitation of gas in the lungs.

110
Q

What are the fatal aspects of decompression sickness ?

A

Very large venous emboli (Greater than 100ml) can cause cardiac arrest.

111
Q

What medical procedures can place a patient at risk for an air embolus

A

Spine procedure in the sitting position. Bypass surgery

112
Q

What kind of pulmonary emboli will lead to infarction

A

Left Heart failure. If there is simply a pulmonary embolus you will get dyspnia and chest pain due to an increase in CO2. But with left heart failure you will not pump oxygenated blood so the bronchiole will infarct.

113
Q

What is the limiting reagent of the extrinsic coagulation pathway

A

Factor 7, Vitamin K dependent. Coumaden will inactivate 7.

114
Q

What can inhibit plasmin ?

A

Antiplasmin A2

115
Q

What does antithrombin 3 bind to ?

A

Heparin like molecules. –> It will inactivate Thrombin 9a and 10a.

116
Q

How will a hyperestrogenic state, from pregnancy or oral contraceptives increase the likelihood of thrombosis

A

Estrogen will cause the synthesis of clotting factors to increase as well as decrease the synthesis of Antithrombin 3. This combined with smoking is a big problem .

117
Q

What will a factor 5 mutation cause ?

A

Loss of control of coagulation due to factor 5 not being inhibited by Protein C. This is prevalent in adolescents with recurrent thromboembolism and venous thrombosis.

118
Q

What type of edema is due to an increase in hydrostatic pressure?

A

Protein poor transaudate

119
Q

What type of fluid will comprise the edema in increased permeability?

A

Protein rich exaudate

120
Q

When will platelets express a greater number of negatively charged phospholipids?

A

Upon activation. The phospholipids are a binding site for numerous coagulation factors and calcium

121
Q

What does Gp2a/3b bind to ?

A

Fibrinogen

122
Q

What happens if Gp2a/3b is nonfunctional

A

You will have an inability for platelets to aggregate and will result in bleeding. It is called Glandmands thromboblastoemia.

123
Q

What factor sdoes antithrombin 3 regulate ?

A

9, 10, 11, 12,

124
Q

What is factor 8 and what does it do ?

A

factor 8 and factor 5 act as cofactors or reaction accelerators for the coagulation cascade

125
Q

What is responsible for platelet aggregation ?

A

Thromboxane and ADP

126
Q

What factor promotes fibrin polymerization

A

13

127
Q

What process leads to acute respiratory distress syndrome ?

A

HIgh levels of cytokinesand secondary mediators can reduce cardiac output and decrease myocardial contractility , blunting cardiac output, increased vascular permeability and endothelial injury in the pulmonary circulation leading to ARDS

128
Q

What is Shocked Lung

A

After a patient has undergone extensive trauma or had lots of blood loss. The hypovolemic shock that will ensue can cause diffuse alveolar damage and will thus cause shocked lung.

129
Q

In shock the general consequences of endothelial activation include what ?

A
  1. Thrombosis
  2. Increased Vascular Permeability
  3. Vasodialation
130
Q

What happens immediately after the activation of PAMPS in Sepsis ?

A

The innate immune mechanisms that drive sepsis are activated TNF and IL-1 PAF Prostaglandins, Complement activation (C3a and C5a) Mast Cell Degranulation, ROS

131
Q

What would cause endotoxic shock

A

Lysis of gram - bacteria will release endotoxins.

Common Mechanisms of Disease-2 (24 decks)

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