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PBD I Exam II > Robbins Chapter 4 - Hemodynamics > Flashcards

Robbins Chapter 4 - Hemodynamics Flashcards

1
Q

What is anasarca?

A

Generalized edema with widespread tissue swelling

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2
Q

What are the pathophysiologic categories of edema (5)?

A

Increased hydrostatic pressure, decreased plasma osmotic pressure, lymphatic obstruction, sodium retention, inflammation

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3
Q

What are two examples of disorders causing edema secondary to increased hydrostatic pressure?

A

DVT can cause regional edema through congestion.

CHF can cause systemic edema through reduced venous return.

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4
Q

What are the mechanims (2) for edema when there is decreased plasma osmotic pressure? Give Examples.

A

Loss of albumin from plasma. This occurs in nephrotic syndrome due to leaky glomerular membranes.

Reduced albumin synthesis. Malnutrition and liver disease.

However albumin is reduced the response is activation of RAAS. Leading to increased sodium and water retention. Since there are no proteins to maintain the water in the vasculature, this only worsens the edema.

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5
Q

How does edema result from increased sodium and water retention? Describe this in reference to CHF.

A

CHF causes hypoperfusion of the kidneys leading to activation of RAAS. Initially restores cardiac output and renal perfusion. However, increased sodium retention results in increased hydrostatic pressure and decreased plasma osmotic pressure causing edema, decreased VR, and a subsequent vicious cycle.

Note: CO must be restored or sodium retention eliminated to prevent spiral

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6
Q

Give an example of lymphatic obstruction resulting in edema.

A

Parasitic filariasis is the fibrosis of the inguinal lymphatic and nodes resulting in elephantiasis.

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7
Q

How does edema present microscopically?

A

Separation of ECM and cell swelling

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8
Q

What is dependent edema?

A

Edema with a distribution influenced by gravity

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9
Q

Periorbital edema is a characteristic finding of what general dysfunctionWhy is this the case?

A

Severe renal dysfunction.

This occurs because edema as a result of renal dysfunction initially effects areas with loose connective tissue.

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10
Q

How does edema present in the lungs (2)? What are common consequences (2) of this?

A

Edema will make the lungs 2-3x heavier. Presentation of a frothy, blood-tinged fluid.

Common consequences include reduced oxygen diffusion and bacterial infections

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11
Q

How does an edematous brain grossly present? What are two specific sequellae?

A

Swollen gyri with narrowed sulci. Brain may suffer herniation through foramen magnum or compression of blood supply to the brain stem.

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12
Q

How do hyperemia and congestion each occur? How would the tissues appear in each case?

A

Hyperemia is an active process that is the result of arteriolar dilation. These tissues will appear erythematous.

Congestion is a passive process that is the result of obstructed drainage from a tissue. The tissues will present bluish-red due to the presence of deoxygenated hemoglobin.

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13
Q

Describe chronic passive congestion in terms of consequences and morphology.

A

Ischemic injury will occur eventually leading to fibrosis and scarring. Also, results in rupture of capillaries. histiocytes will consume these RBCs leading to hemosiderin laden macrophages (AKA heart failure cells)

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14
Q

Describe morphologic presentation of acute pulmonary congestion (3).

A

Engorged alveolar capillaries
Alveolar septal edema
Focal intra-alveolar hemorrhage

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15
Q

Describe morphologic presentation of chronic pulmonary congestion (2).

A

Septal fibrosis with heart failure cells in alveoli

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16
Q

Describe the morphologic presentation of acute hepatic congestion (2).

A

Distension of central vein and sinusoids

Centrilobular hepatocyte ischemia

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17
Q

Describe the morphologic presentation of chronic hepatic congestion (1).

A

Nutmeg liver = centrilobular regions have become necrotic and present with depression and a red-brown color

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18
Q

What is a hematoma?

A

any accumulation of blood

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19
Q

What is petechia and what three things is it associated with?

A

Minute hemorrhages into skin, mucous membranes, and serosal surfaces.

Associated with increased hydrostatic pressure, decreased platelets, or platelet dysfunction

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20
Q

What is purpura?

A

Hemorrhages which are slightly larger than petechia.

Note: associated with same issues (increased hydrostatic pressure, decreased platelets, and platelet dysfunction), but also trauma and inflammation

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21
Q

What are echymoses? Describe the evolution of their color presentation.

A

These are bruises.

Begin blue-red (hemoglobin), but turn to blue-green (bilirubin), and finally gold-brown (hemosiderin)

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22
Q

Generally describe normal hemostasis.

A

After initial vascular injury a neurogenic response will result in transient vasoconstriction. This is augmented by the expression of endothelin from endothelium.

Platelets’ attachment to subendothelial ECM and subsequent activation leads to their aggregation and formation of primary plug.

Tissue factor from the endothelium will activate the extrinsic cascade leading to the formation of firbin polymers and the secondary plug.

Hemostasis is confined to the area of injury by counter-regulatory mechanisms.

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23
Q

Describe the anti-platelets effects (3) of the endothelium.

A

The endothelium is stimulated through the thrombin receptor to secrete NO, PGI2, and adenosine phosphatase.

NO and PGI2 inhibit platelet aggregation and cause vasodilation.

adenosine phosphatase consumes ADP preventing platelet activation.

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24
Q

Name the three anti-coagulant mechanisms of the endothelium.

A

Heparin-like molecules, thrombomodulin, and TFPI

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25
Q

Describe how heparin-like molecules inhibit coagulation

A

Heparin-like molecules bind to ATIII causing its activation. ATIII will cause the inactivation of thrombin and factors IX, X, XI, and XII.

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26
Q

Describe how thrombomodulin inhibits coagulation

A

Thrombomodulin is expressed by endothelium. It binds to thrombin allowing the complex to activate circulating protein C. Protein C complexed with protein S from the endothelium will cleave factors V and VIII.

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27
Q

Describe how TFPI inhibits coagulation

A

TFPI is a cell surface protein which directly inhibits the activities of TF-VIIa and Xa.

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28
Q

How does the endothelium effect fibrinolysis?

A

Expression of t-PA is induced by thrombin. t-PA converts plasminogen to plasmin. Active plasmin is able to lyse fibrin into fibrin-split products.

Note: fibrin-split products are weak anti-coagulants.

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29
Q

Describe how the endothelium has prothrombic properties in reference to its platelet effects (1), procoagulant effects (1), and antifibrinolytic effects (1)

A

ECM expresses vWF which causes platelet activation upon contact

Secretes TF in response to TNF and IL-1

Secretes inhibitors of plasminogen activators (PAIs)

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30
Q

Describe the intrinsic coagulation cascade from factor XII to factor Xa

A

XII is activated upon contact with negatively charged surfaces. XIIa will activate XI in the presence of calcium. XIa will activate IX in the presence of calcium.

Factor VIII is activated by thrombin (IIa). VIIIa will complex with IXa and clacium to convert X to its active form.

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31
Q

Describe the extrinsic coagulation cascade from TFto factor Xa.

A

Tissue injury will result in the production of TF (factor III), which complexes with VII. This complex is able to activate X in the presence of calcium.

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32
Q

Describe the common coagulation pathway from Xa to fibrin polymers.

A

Factor V is activated by thrombin (IIa). Va and Xa will complex and convert II (prothrombin) in the presence of calcium into IIa (thrombin).

IIa converts fibrinogen (I) to fibrin (Ia). IIa also activates XIII to XIIIa (fibrin stabilizing factor). Free Ia will polymerize. Cross-linking of fibrin is induced by XIIIa.

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33
Q

What are the mutations causing glanzmann thrombasthenia, bernard-soulier syndrome, and vonWillebrand disease?

A

GPIIb-IIIa
GPIb
vWF

all result in bleeding disorders

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34
Q

What are platelets?

A

Anucleate fragments of megakaryocytes

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35
Q

Name the contents of alpha granules (8).

A

P-selectin, PDGF, fibronectin, fibrinogen, TGF-beta, , Factors V and VIII, and pf4

Note: platelet factor 4 binds to, and inhibits heparin-like molecules

Pnemonic: Please pet furry frank tuesday-between five and eight, and probably friday at 4

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36
Q

Name the contents of delta granules (6).

A

Calcium, ADP, ATP, Histamine, Serotonin, and Epi

Word association: Delta granules = dense bodies. Contents of these granules accelerates clotting, and conDENSEation of platelets (ADP, Ca)

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37
Q

Describe the process of platelet activation to formation of the primary hemostatic plug.

A

When endothelial cell injury occcurs, the ECM is exposed. vWF bound to the ECM will bind to GPIb receptors of platelets causing activation. Shortly afterwards alpha and delta granules are released. ADP, Thrombin (via PAR) and TXA-2 cause a conformational change in the GPIIb-IIIa receptors, allowing them to bind fibrinogen creating a matrix of platelets. Platelets will also undergo contraction.

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38
Q

What is clopidogrel?

A

blocks binding of ADP

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39
Q

How does aspirin function to prevent coronary thrombosis in at risk patients?

A

Aspirin is a non-selective COX blocker. It will permanently inhibit the synthesis of TXA2 by platelets. However, it only transiently inhibits the synthesis of PGI2 by endothelial cells.

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40
Q

What are the components invloved (5) in most reactions of the clotting cascade?

A

Enzyme, substrate, cofactor, phospholipid surface, and calcium

Note: Calcium serves to hold the complex together. The requirement of all these components localizes thrombosis.

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41
Q

What do prothrombin time and partial thromboplastin time assess? What is the procedure of these test?

A

Prothrombin time = Extrinsic pathway
Addition of TF and phospholipids to citrated plasma

Partial thromboplastin time = Intrinsic pathway
Addition of ground glass to citrated plasma

42
Q

How are the pro-inflammatory effects of Thrombin mediated? What are these effects (4)

A

Through PAR

  1. Aggregation and release of TXA2 by platelets
  2. Expression of adhesion molecules by endothelium
  3. Activation of leukocytes
  4. Production of PGI2, NO, and t-PA by endothelium
43
Q

What is virchow’s triad?

A

The events leading to thrombosis. Endothelial injury, altered blood flow, and hypercoagulability

44
Q

Describe how plasminogen is converted (2) to plasmin. Name and describe the two plasminogen activators.

A

Plasminogen can either be activated by…

  1. Kalikrein activated by XIIa
  2. Plasminogen Activators (t-PA and u-PA)

t-PA = tissue plasminogen activator; most active when bound to fibrin, confining fibrinolysis

u-PA = urokinase Plamsinogen activator; active in fluid phase???

45
Q

What is bacterial streptokinase?

A

This is a bacterial enzyme which cleaves plasminogen

46
Q

What are inhibitors of plasminogen activators? How are they synthesized?

A

Inhibitors of plasminogen activators (PAIs) will bind t-PA and inhibit binding to fibrin. Production is signaled by thrombin and cytokines.

47
Q

How is free plasmin eliminated?

A

Binding of alpha2-plasmin inhibitor

48
Q

How can endothelial dysfunction result (3) in thrombosis?

A

Exposure of the ECM activates platelets
Endothelium is activated to produce pro-coagulant mediators (TF and PAIs) and decrease release of anticoagulant mediators (TM, PGI-2, and t-PA)

49
Q

Describe laminar blood flow and the consequences (3) of its disturbance by turbulence and stasis.

A

Normal blood flows in a lamellar pattern with cellular components (including platelets) towards the center of the vessel, and plasma at the periphery.

Turbulence and stasis will…
cause activation of endothelium
allow platelets to contact endothelium
prevent inhibition, washout, and dilution

50
Q

How can hyperviscosity cause alterations in blood flow?

A

Increasing viscosity increases resistance to blood flow causing stasis congestion in the smaller vessels. Seen in sickle-cell anemia and polycythemia.

51
Q

How does a leiden mutation cause primary (genetic) hypercoagulability? How frequent is it?

A

A leiden mutation makes factor Va resistant to cleavge by protein C. It is caused by the switch of glutamine to arginine at position 506. It is common.

Note: it is commonly seen in patients with recurrent DVT

52
Q

How does mutation of prothrombin cause primary hypercoagulability? How frequent is it?

A

Results in elevated prothrombin levels. It is common.

53
Q

What two mutations result in elevated homocysteine? How frequent are these mutations? How does this cause primary hypercoaulability (1)

A

Mutations of cystathione beta-synthetase (very rare) or 5,10-MeTeHyFo reductase (common) will cause this.

Homocysteine metabolites are able to form thioester bonds with fibrin.

Note: elevated homocyteine contributes to atherosclerosis, venoust thrombosis, and arterial thrombosis.

54
Q

How frequent are deficiencies in anti-coagulant mediators? What are these mediators (3)? How can they be identified?

A

These mutations involving ATIII, Protein C, and Protein S are rare. Patients will suffer venous thrombosis and recurrent thromboembolism beginning in adolescence.

55
Q

How can oral contraceptives and pregnancy cause secondary (acquired) hypercoagulability?

A

Bring the blood into a hyperestrogenic state causing the increased synthesis of procoagulation factors and decreased synthesis of ATIII.

56
Q

How can cancers induce secondary hypercoagulability?

A

Cancers release procoagulant tumor products.

57
Q

How can aging induce secondary hypercoagulability?

A

Aging causes a decrease in the endothelium’s ability to synthesize PGI2

58
Q

Describe the pathogenesis of heparin-induced thrombocytopenia.

A

Unfractionated heparin may induce antibodies to complexes of heparin and platelet factor 4 on platelets and endothelial cells. This results in platelet activation and endothelial damage.

Thrombocytopenia is a result of platelet consumption. Fractionated (LMWH) induces antibodies less frequently, but will react if they are present.

59
Q

Describe the pathogenesis of antiphospholipid antibody syndrome.

A

Antibodies against anionic phospholipids induce platelet activation and inhibit protein C activity. This can be primary (no other autoimmune disease) or secondary (simultaneous with autoimmune diseas).

Note: Antibodies are necessary but not sufficient

60
Q

How does antiphospholipid antbody syndrome present in the vascular beds of the lungs, brain, intestines, and kidneys.

A

Lungs - pulmonary embolism and pulmonary hypertension due to recurrent subclinical emboli
Brain - stroke
Kidneys - renal hypertension
intestines - ischemic bowel

61
Q

What are the general clinical manifestations of antiphospholipid antibody syndrome (4)?

A

thrombocytopenia, recurrent emboli, repeated fetal miscarriages, and cardiac valve vegetations.

62
Q

Describe the mechanism in antiphospholipid antibody syndrome which causes fetal miscarriages

A

This disorder inhibits the expression of t-PA, which is required for the trophoblastic invasion of the uterus

63
Q

Why do antibodies in antiphospholipid antibody syndrome cause a false-positive serologic test?

A

Binds to the phospholipids (cardiolipin) in the standard assay

64
Q

In which direction do arterial and venous thrombi propagate?

A

In both systems the thrombi will propagate towards the heart. In the arterial system they form against the flow of blood. In the venous system they form with the flow of blood.

Note: Propagating thrombi are prone to fragmentation

65
Q

Describe lines of zahn

A

These are microscopic and gross laminations of a clot which correlate to the alternating deposition of platelets/fibrin and RBCs. Typically occur in the arterial circulation.

Note: These are indicative of a clot forming antemortem

66
Q

What are the most frequent occlusion sites for arterial thrombi (3)?

A

Coronary>Cerebral>Femoral

67
Q

Describe the morphology of a venous thrombus

A

These thrombi tend to form long casts in the venous lumen. They will have a much higher composition of red blood cells. They are referred to as red thrombi.

68
Q

Describe the morphology of postmortem clots

A

These clots are loosely adhered to vessel walls. There is an evident red portion consisting of RBCs and an upper yellow portion (“Chicken Fat”)

69
Q

Describe how infective endocarditis leads to the development of valve vegetations

A

Microbes can adhere to a previously damaged heart valve of cause injury themselves. This will lead to EC injury and disturbance of blood flow causing vegetations.

70
Q

Describe the 4 fates of thrombi

A

Propagation - accumulation of fibrin and platelets
Embolization - fragmentation of a thrombus
Dissolution - older thrombi are less susceptible to this; this is why t-PA is only effective within hours of thrombus formation.
Organization/Recanalization - Invasion of ECs, smooth muscle cells, and fibroblasts cause the organization of the thrombus. Eventually capillary channels will re-establish continuity, and thrombi will be incorporated into the vessel wall. May become fibrous tissue.

71
Q

How does a mycotic aneurysm develop

A

Occasionally the centers of thrombi will be enzymatically degraded by the release of lysosomal enzymes from trapped platelets and leukocytes. Infection of these thrombi in the setting of bacteremia can produce an inflammatory mass, which weakens the vessel wall and causes an aneurysm.

72
Q

Describe the site, symptoms (3) and sequellae (2) of superficial venous thrombosis

A

Typically occur in the saphenous vein in the setting or varicosities. Symptoms include pain, swelling, and congestion. Local edema predisposes the site to infection in association with trauma. Also susceptible to the formation of varicose ulcers.

73
Q

What makes DVTs at or above the knee more serious?

A

These are more likely to embolize to the lungs and result in a pulmonary infarction.

74
Q

Why are DVTs commonly asymptomatic?

A

These venous obstructions can be rapidly offset by the formation of collateral channels. Still may present with pain and local edema.

75
Q

What is DIC and why is it not a primary disease?

A

DIC is the insidious or sudden onset of widespread firbin microthrombi. It is not considered a primary disease becuase it is the complication of any condition associated with the systemic activation of thrombin.

76
Q

What are the four locations where diffuse circulatory insufficiency occurs in DIC?

A

Brain, heart, lungs, kidneys

77
Q

How can DIC progress to bleeding issues?

A

The disorder begin with consumption of platelets and coagulation factors in the blood. This is followed by the activation of the fibrinolytic system.

78
Q

What is a paradoxical embolism?

A

On rare occasion an embolus can pass through a heart wall defect, gaining access to the systemic circulation.

79
Q

What are the consequences of pulmonary emboli with both minimal obstruction and large obstruction of flow?

A

Most pulmonary emboli are clinically silent. They will undergo organization and recanalization. May form a fibrous network in the capillary.

When there is obstruction of 60% of blood flow to the lungs there can be sudden death, cor pulmonale, or cardiovascular collapse.

80
Q

Even if there is pulmonary hemorrhage, why is an infarction unlikely to occur?

A

Occlusion of medium sized arteries can result in hemorrhage, but infarction is unlikely due to the dual blood supply (bronchial arteries) to the lungs.

81
Q

What are the possible origins (5) of a systemic embolism?

A

Intracardiac mural thrombi > aneurysms > atherosclerotic plaqcues > valvular vegetation > paradoxical emboli

82
Q

What is the general result of arterial emboli? At what sites (6) do they tend to become lodged?

A

The general result is infarction, but this depends on the pattern of blood supply, susceptibility to ischemia, and caliber of occluded vessel.

LE > Brain > Intestines, Kidneys, Spleen, and UE

83
Q

Describe a fat/marrow embolism. Is this of clinical consequence?

A

Pulmonary embolization of microscopic fat globules (with or without associated marrow cells) occurs after severe skeletal injuries. Typically does not cause clinically significant issues.

Note: Common finding after vigorous cardiopulmonary resuscitation

84
Q

Describe fat embolism syndrome in reference to symptoms (5-7) and pathogenesis.

A

Patients present with pulmonary insufficiency 1-3 days after injury. Also associated with neurologic symptoms including irritability and restlessness that may develop into delirium and coma. Thrombocytopenia and anemia may develop due to the aggregation of platelets and RBCs to fat globules. Petechiae may develop in relation to thrombocytopenia.

Fat microemboli will release FFAs that can cause toxic injury to ECs and activate aggregation of platelets and RBCs. Platelet activation will result in granulocyte recruitment causing further vascular injury through ROS, eicosanoids, and proteases. Emboli may also obstruct pulmonary and cerebral circulations

85
Q

Describe pathogenesis, bends, chokes, and treatment in reference to decompression sickness.

A

Pathogenesis - Air inhaled under high pressure allows for a greater amount to enter solution in the blood. If there is rapid depressurization the excess gas will dissolve from the solution and form an embolic mass.

Bends - pain in the skeletal muscle and joints as a result of gas bubbles

Chokes - Acute respiratory distress caused by gas bubbles in the pulmonary circulation. Manifests with edema, hemorrhage, and focal emphysema.

Treatment - patients are placed in a high pressure chamber and slowly decompressed

86
Q

Describe caisson disease and manifestation associated with it.

A

This is a chronic form of decompression sickness. It is associated with multiple foci of ischemic necrosis in the heads of long bones (Femur, humerus, tibia)

87
Q

Describe the cause, initial symptoms, and progressive symptoms associated with amniotic fluid embolism.

A

This is caused by an infusion of amniotic fluid or fetal tissue into the maternal circulation through a placental tear or uterine vein rupture.

Initially patients present with sudden dyspnea, cyanosis, hypovolemic shock, and neurologic impairments (headache and seizures). If the patient survives the initial phase they will experience pulmonary edema along with DIC.

88
Q

What is classic finding in the maternal pulmonary microvasculature of amniotic fluid embolism?

A

Squamous fetal cells

89
Q

Describe the five situations in which red infarcts may occur.

A
  1. Venous occlusions (ovary)
  2. Sites of dual blood supply (lungs)
  3. Loose tissues where blood can collects
  4. Tissues which became necrotic due to arterial occlusion and have been reperfused
  5. Sites of previous venous occlusion resulting in congestion
90
Q

Describe the location and morphology of white infarcts.

A

These tend to occur in solid organs with end-arterial supply.

They are wedge shaped with the occluded artery at the apex, and the base representing the periphery of the organ.

Note: when the base is a serosal surface this can result in a fibrinous exudate.

91
Q

How can septic infarctions occurs (2)?

A

Embolization of infected valvular vegetations or microbial seeding of necrotic tissues. This will form an abscess.

92
Q

Generally describe shock

A

Characterized by systemic hypotension as a result of decreased CO or ECV resulting in impaired tissue perfusion and cellular hypoxia.

93
Q

Describe the principal mechanism and give clinical examples (3) of cardiogenic shock

A

This is due to myocardial pump failure

examples = cardiac tamponade, MI, and arrhythmia

94
Q

Describe the principal mechanism and give clinical examples (4) of hypovolemic shock

A

Inadequate blood or plasma volume

Examples = vomiting, diarrhea, burns, and hemorrhage

95
Q

Describe the principal mechanism and give clinical examples (2) of septic shock

A

Vasodilation and peripheral pooling of blood due to a systemic immune reaction

Examples = superantigens and overwhelming microbial infections

96
Q

Describe the principal mechanism and give clinical examples (2) of neurogenic shock

A

Loss of vascular tone

Examples = spinal cord injury and anesthetic accident

97
Q

Describe the principal mechanism of anaphylactic shock

A

Systemic vasodilation in response to IgE hypersensitivity

98
Q

Describe the non-progressive phase of shock in reference to its mediators and net effects.

A

This phase is mediated through neurohumoral mechanisms: Baroreceptor reflexes, catecholamine release, RAAS, ADH, and sympathetic stimulation.

The net effects of these responses is tachycardia, peripheral vasoconstriction, and renal conservation of fluid. Cutaneous vasoconstriction will result in pallor of the patient. (Note: In septic shock the patient initially presents with warm and reddened skin)

Note: The coronary and cerebral arteries are minimally affected by the sympathetic innervation.

99
Q

Describe the progressive phase of shock in reference to its mediators and net effects.

A

This phase is mediated by widespread tissue hypoxia.

Tissue hypoxia will lead to the activation of anaerobic glycolysis by cells and a state of lactic acidosis. Lowered tissue pH inhibits the vasomotor response of vasoconstriction leading to peripheral pooling of the blood worsening hypoxia. Eventually hypoxia will result in EC injury and DIC.

100
Q

Describe the irreversible phase of shock. Give two examples of terminal events which can occur.

A

This is when you’re fucked. Damage has become so severe that recovery is not possible.

Renal failure can occur due to acute tubular necrosis

Ischemic bowel may also occur leading to sepsis

101
Q

Describe the general morphology of tissues

A

This is consistent with the morphologies seen in hypoxic injury

PBD I Exam II (1 decks)

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