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Pathology > Test 1: 10-14 Hemodynamics I > Flashcards

Test 1: 10-14 Hemodynamics I Flashcards

1
Q
  1. Hemostasis is what kind of process? Give 2 roles
A

Highly regulated process, that maintains the fluidity of the blood and limits loss of blood from a damaged blood vessel

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2
Q
  1. What two things can happen with failure hemostasis mechanisms?
A

Excessive bleeding or vessel occulusion by excessive blood clot formation (thrombosis)

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3
Q
  1. What is seen in normal fluid hoemostasis?
A

Balance between exit of fluid at arterial end and the return of return of fluid at the venous end; with lymphatic drainage removing excess fluid

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4
Q
  1. What is an edema? When does this happen? What is a transudate?
A

a. Edema: increased fluid in the interstitial/extracellular tissue spaces <br></br>
<br></br>b. When there is greater movement of fluid out than is returned by venous absorption or lymphatic drainage
<br></br>c. The protein-poor fluid of edema

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5
Q
  1. Define the following: hydrothorax, hydropericardium, and Ascites/Hydroperitoneum
A

<br></br>Hydrothorax: fluid in pleural space
Hydropericardium: fluid in space between the heart and pericardium
<br></br>Ascites/Hydroperitoneum: fluid in peritoneal space

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6
Q
  1. Give the names of the edema that are caused each of the following sets:<br></br>
    <br></br>a. CHF, Constrictive pericarditis, ascites from liver cirrhosis, venous obstruction or compression
    <br></br>b. nephrotic syndrome, end stage liver disease, malnutrition, protein losing gastroenteropathy
    <br></br>c. Inflammation, neoplastic, surgery, postirradiation
    <br></br>d. renin angiotensin aldosterone (sodium reabsorption), renal insufficiency
    <br></br>e. Acute and chronic, angiogenesis
A

a. Elevated hydrostatic pressure <br></br>
b. Decreased plasma oncotic pressure (low protein)<br></br>
c. Lymphatic obstruction<br></br>
d. Sodium retention <br></br>
e. Inflammation <br></br>

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7
Q
  1. Draw a chart showing the relationship of edema to of the following:<br></br>
    a. heart failure<br></br>
    b. malnutrition, decreased hepatic synthesis, nephrotic syndrome <br></br>
    c. Renal failure
    <br></br>
A

Draw chart

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8
Q
  1. Edema is increased hydrostatic pressure which is an indication of? What does it produce?
A

Congestive heart edema <br></br>

Dependent edema<br></br>

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9
Q
  1. What is pitting edema and what is it due to?
A

Finger-shaped depression remains after pressing skin, due to transient fluid displacement <br></br>

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10
Q
  1. What is responsible for maintaining colloid osmotic pressure?
A

Albumin <br></br>

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11
Q
  1. Give two examples of lost/reduced synthesis of albumin
A

Decreased synthesis: Liver failure or cirrhosis <br></br>

Loss of protein: nephrotic syndrome <br></br>

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12
Q
  1. What does ascites result from?
A

Advanced liver cirrhosis

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13
Q
  1. What is anasarca? Cause? Earliest sign?
A

a. Severe generalized edema <br></br>
b. Lack of oncotic pressure<br></br>
c. Periorbital edema <br></br>

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14
Q
  1. Increased salt in circulation causes?
A

<br></br>i. Shift of fluid to intravascular space
<br></br>ii. Increased hydrostatic pressure to expansion of fluid volume
<br></br>iii. Increased plasma water content results in decreased oncotic pressure resulting from dilution of albumin

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15
Q
  1. Salt and water retention is secondary after?
A

Renin-Angiotensin-Aldosterone system activation

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16
Q
  1. Edema inflammation is localized unless?
A

Result of systemic inflammatory response (e.g. allergic reaction)

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17
Q
  1. Lymphatic obstruction/impaired drainage results in? Is this localized or systemic?
A

Lymphedema, usually localized

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18
Q
  1. Elephantitis (a lymphedema) is due to?
A

Wuchereria bancrofti (roundworms block lymph vessels)

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19
Q
  1. What does the microscopic appearance of edema depend on?
A

Amount of protein in exudate

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20
Q
  1. When looking at a microscopic appearance of edema what is usually seen? Color? Most commonly seen in what parts of the body?
A

a. Just clearing and separation of ECM parts<br></br>
b. Pink stain if enough protein <br></br>
c. Subcutaneous tissues, lungs, and brain<br></br>

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21
Q
  1. How does the histologic appearance of subcutaneous edema appear?
A

Subtle, with increased spaces between cells

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22
Q
  1. How may edema interfere with healing? Where does the severe edema compromise? It also increases the risk of?
A

a. Fluid must be removed for healing<br></br>
b. Severe edema compromises venous return, <br></br>
c. infection and ulceration

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23
Q
  1. What is the most common cause of edema?
A

Heart problems

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24
Q
  1. Left ventricular failure causes back up to?
A

Atrium, pulmonary veins, and lungs

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25
Q
  1. Noncardiogenic pulmonary edema causes increased permeability leading to?
A

i. Alveolar hypoxia<br></br>
ii. Acute respiratory distress syndrome <br></br>
iii. Inhalation of toxic agents <br></br>
iv. Pulmonary infections <br></br>
v. Therapeutic radiation of the lungs <br></br>
vi. Head injury <br></br>
vii. Renal failure<br></br>
viii. Hypersensitivity<br></br>

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26
Q
  1. Clinical manifestations of pulmonary edema include? Characteristics of each manifestation?
A

i. Dyspnea<br></br>
ii. Cough<br></br>
iii. Pulse<br></br>
iv. Breath sounds <br></br>
v. Engorged neck vessels <br></br>

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27
Q
  1. Dyspnea’s characteristics in pulmonary edema?
A

i. Sudden<br></br>
ii. Orthopnea <br></br>
iii. Cyanotic (central) <br></br>
iv. Air hunger <br></br>
v. Tachypnea

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28
Q
  1. Clinical manifestations cough in pulmonary edema?
A

i. Copious sputum <br></br>
ii. Frothy <br></br>
iii. Blood tinged

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29
Q
  1. Clinical manifestations of pulse, breathe sounds, and vessels in pulmonary edema?
A

a. Pulse: Tachycardic, bounding <br></br>
b. Breath sounds: crackles, fine -> course<br></br>
c. Engorged neck veins

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30
Q
  1. What are four appearance characteristics of interstitial pulmonary edema? Alveolar pulmonary edema?
    Heart and pleural cavity?
A

a. interstitial pulmonary edema <br></br>
i. Poorly defined pulmonary vessels<br></br>
ii. Visible lung fissures<br></br>
iii. Septal lines<br></br>
iv. Thick bronchial walls<br></br>
b. Alveolar pulmonary edema <br></br>
i. Bilateral symmetric perihilar lung consolidation<br></br>
c. Enlarged heart and pleural effusion

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31
Q
  1. Cerebral edema is serious because? Parenchymal edema may move? If edema is more localized causes?
A

a. Brain swells, skull prevents expansion and so tissue is compressed <br></br>
b. Parenchymal edema may shift brain due to high pressure and may push the brainstem down into the foramen magnum (tonsillar herniation) <br></br>
c. One part of the brain herniates into adjacent compartments tearing brain tissue

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32
Q
  1. Give 3 localized causes of cerebral edema

Give 4 Generalized causes of cerebral edema

A

a. Localized<br></br>
i. Abscess<br></br>
ii. Neoplasm<br></br>
iii. Trauma<br></br>
b. Generalized<br></br>
i. Encephalitis <br></br>
ii. Hypersensitive crisis<br></br>
iii. Obstruction of venous outflow <br></br>
iv. Trauma

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33
Q
  1. Grossly a swollen brain in cerebral edema appears?
A

Appears with distended, flattened gyri and narrowed sulci

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34
Q
  1. What is hyperemia? Give 3 examples of it
A

a. Active process in which arteriolar dilatation causes increased flow of blood to tissue<br></br>
b. Skeletal muscle during exercise, inflammation, and blushing <br></br>

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35
Q
  1. What is the term that describes tissue with engorgement with oxygenated blood?
A

Erythematous

36
Q
  1. What is congestion? <br></br>
    Give an example for systemic and local congestion
    Color and why? <br></br>
    Congestion and edema occur separate or together?
A

a. Congestion is a passive process due to impaired outflow of blood from a tissue <br></br>
b. Systemic: congestive heart failure (CHF), local: local venous obstruction<br></br>
c. Blue-red color due to accumulation of deoxygenated hemoglobin (cyanosis) <br></br>
d. Congestion and edema usually occur together

37
Q
  1. What are the consequences of long term congestion in chronic passive congestion?
A

Causes a stasis of poorly oxygenated blood, may lead to cellular degeneration and death

38
Q
  1. If there is capillary rupture, breakdown and phagocytosis of the red cell debris cause?
A

Accumulation of hemosiderin-laden macrophages at the site

39
Q
  1. Give characteristics of acute pulmonary congestion and chronic pulmonary congestion?
A

a. Acute pulmonary congestion<br></br>
i. Alveolar capillaries engorged with blood <br></br>
ii. Alveolar septal edema <br></br>
iii. Focal intraalveolar hemorrhage <br></br>
b. Chronic pulmonary congestion <br></br>
i. Thickened and fibrotic septa<br></br>
ii. Heart failure cells aka hemosiderin-laden macrophages in alveolar spaces

40
Q
  1. Nutmeg liver’s gross appearance is? Where does it appear?
A

Central regions of hepatic lobules are grossly red/brown and depressed (due to cellular loss) surrounded by unaffected areas<br></br>
Chronic hepatic congestion

41
Q
  1. In chronic hepatic congestion, microscopically what is centrilobular necrosis? What results in long standing hepatic congestion?
A

a. Centrilobular necrosis; hepatocellular death and accompanying hemorrhage with hemosiderin laden macrophages<br></br>
b. Hepatic fibrosis

42
Q
  1. Hemorrhages are? Hemorrhages classifications?
A

a. Extravasation of blood due to ruptured vessels <br></br>

b. Internal or external <br></br><br></br>

43
Q
  1. Hemorrhages result from? Name 6
A

i. trauma<br></br>
ii. atherosclerosis<br></br>
iii. aneurysm<br></br>
iv. neoplasia/inflammation<br></br>
v. capillary bleeding<br></br>
vi. hemorrhagic diathesis <br></br>

44
Q
  1. In the hemorrhagic diathesis, give 3 characteristics
A

i. Fragility of vessels<br></br>
ii. Platelet dysfunction (petechiae, purpura)<br></br>
iii. Coagulation defect (hematoma, bleeding)<br></br>

45
Q
  1. What is petechiae? What do DDX – angiomas and DDX – vasculitis do?
A

a. 1-2 mm foci of hemorrhage in skin, mucous membranes, or serosal surfaces <br></br>
b. DDX – angiomas: Do not blanch (whiten) with pressure
DDX – vasculitis: not palpable <br></br>

46
Q
  1. What size do foci of hemorrhage have to be for purpura?
A

≥3 mm foci of hemorrhage

47
Q
  1. Ecchymoses usually occurs? However it is used as a first sign of what disorder?
A

a. Ecchymotic hemorrhages usually due to trauma

b. First sign of acute myelogenous leukemia due to low platelet count (thrombocytopenia)

48
Q
  1. Give four clinical significance of hemorrhage
A

i. Rapid blood loss (20%) insignificant to healthy person but can be fatal in compromised patient <br></br>
ii. Sites where bleeding occurs has significant prognostic value <br></br>
iii. Chronic or repeated bleeding leads to iron deficiency <br></br>
iv. Internal blood loss may allow resuse of iron

49
Q
  1. Hemostasis occurs as a result of?
A

A well regulated/balanced process of maintaining blood in a fluid state while allowing for controlled and focused clotting to prevent blood loss

50
Q
  1. What are the 3 general components contribute to homeostasis?
A 
Endothelium/Vascular wall
Platelets (bricks)
Coagulation cascade (fibrin – cement)
51
Q
  1. What are the 5 sequences of clot formation
A

<br></br>i. Initial injury causes brief vasoconstriction
<br></br>ii. Endothelial damage exposes subendothelium, causing endothelial death, causing platelets activated/adhere
<br></br>iii. Tissue factor is released activates coagulation cascade forming fibrin
<br></br>iv. Platelet activation furthers coagulation
<br></br>v. Fibrin and platelets form a clot thereby plugging to prevent blood loss

52
Q
  1. Endothelium has what kind of function in hemostasis? What factors activate endothelium and shift the function to procoagulant?
A 
<br>a.	Both anticoagulant and procoagulant functions 
<br>b.	Factors:
Infectious Agents <br>
Hemodynamic forces <br>
Cytokines<br>
Plasma mediators 
<br>
53
Q
  1. What two compounds inhibit platelet aggregation?
A

Thrombin and several cytokines stimulate PGI2 and NO synthesis

54
Q
  1. What degrades ADP and what does this do?
A

Adenosine diphosphatase degrades ADP thereby inhibiting platelet aggregation

55
Q
  1. In the anticoagulant activities of the endothelium, what do heparin-like molecules do? What does thrombomodulin covert? Fibrinolytic endothelial cells make?
A

a. Cofactors to antithrombin <br></br>
b. Thrombomodulin coverts thrombin to anticoagulant<br></br>
c. Tissue plasminogen activator (tPA)<br></br>

56
Q
  1. In normal conditions endothelial cells’ role is? What happens if there are injury/activation of endothelial cells?
A

a. Inhibit platelet adherence and blood clotting <br></br>

b. Procoagulant state <br></br>

57
Q
  1. What is the size of non-activated platelets? Shaped? Derived from? Contain?
A
  1. What is the size of non-activated platelets? Shaped? <br></br>Derived from? Contain? <br></br>
58
Q
  1. After endothelial injury what four things do platelets encounter?
A

Collagen, von Willibrand factor, tissue factor and thrombin<br></br>

59
Q
  1. Three steps that ensue after platelets encounter other factors?
A

i. Adhesion<br></br>
ii. Secretion and activation<br></br>
iii. Aggregation<br></br>

60
Q
  1. Where is the platelet adhesion’s initial adherence to? What does vWF (Von Willebrand Factor) link? Which one of these adherences are firm/not firm? What does adhesion activate on the platelets?
A

a. Subendothelial ECM (NOT firm)<br></br>
b. Subendothelial ECM to glycoprotein Ib receptors on platelets (Firm) <br></br>
c. Release of their granules<br></br>

61
Q
  1. Platelet activation granule contents are released. <br></br>What are the contents and their function(s)?
A

Calcium: critical for coagulation cascade <br></br>
ADP: mediates platelet aggregation which increases platelet aggregation at the site <br></br>
Platelet factor 4: binds to heparin results in its inactivation
Serotonin: induces vasoconstriction <br></br>

62
Q
  1. In platelet aggregation ADP and thromboxane released by platelets have what effect?
A

Further platelet aggregation

63
Q
  1. In platelet aggregation, what links fibrinogen to platelets?<br></br>
    What protease also binds to the platelet surface?<br></br>
    What does platelet activation cause?<br></br>
A

a. GpIIb-IIIa<br></br>
b. Thrombin<br></br>
c. Expression of phospholipid complexes on the surface of platelets which act as surfaces to bind coagulation factors and calcium, thereby promoting coagulation

64
Q
  1. Draw the drawing on platelet adhesion and aggregation on slide 67 of hemodynamics I PPT
A

Drawing

65
Q
  1. What happens in the following steps of platelet adhesion and aggregation:
A
  1. Vascular spasm<br></br>
  2. Platelet plug formation<br></br>
  3. Coagulation <br></br>
  4. Vascular spasm: smooth muscle contracts, causing vasoconstriction<br></br>
  5. Platelet plug formation: injury to vessel lining shows collagen fibers; platelets adhere here. Platelets release chemicals that make close<br></br>
  6. Coagulation: fibrin forms mesh that traps RBCs and platelets forming a clot<br></br>
66
Q
  1. Coagulation: General Concepts
A

a. Coagulation factors are a sequential enzyme cascade whose activation causes?<br></br>
b. These inactive serine proteases (e.g. prothrombin) are converted to “activated enzymes/proteins” by?
<br></br>c. Assembly of the complex of coagulation factors, which requires cofactors and Ca, takes place on?
<br></br>d. Thrombin converts fibrinogen to fibrin monomer, but also effects?
<br></br>e. Fibrin monomer cross-linked to fibrin forms?
<br></br>a. Fibrin clot
<br></br>b. Limited proteolysis
<br></br>c. Phospholipid surface
<br></br>d. “Glue” for platelet plug

67
Q
  1. Important things to remember about coagulation:<br></br>
    a. What is the intrinsic factor?<br></br>
    b. What is the extrinsic factor?<br></br>
    c. Both pathways merge at factors?<br></br>
    d. What do the factors need to be bound to for maximum activity?<br></br>
    e. What element is necessary for coagulation?<br></br>
    f. What is the end result of what is formed in coagulation?<br></br>
A

a. Hagerman factor (XII) <br></br>
b. Tissue factor<br></br>
c. Factors IX and X<br></br>
d. A phospholipid surface<br></br>
e. Calcium<br></br>
f. Cross-linked fibrin<br></br>

68
Q
  1. Prothrombin time (PT): extrinsic is prolonged by?<br></br>

Partial thromboplastic time (PTT): intrinsic is prolonged by?

A

i. Prolonged by warfarin (Coumadin)<br></br>

ii. Prolonged by heparin

69
Q
  1. Blood clotting must be limited to the site of injury or the clot will?
A

Clot to grow block patency of vessel (i.e. thrombosis<br></br>

70
Q

. Antithrombin III<br></br>

i. Directly inactivates?<br></br>
ii. Name two<br></br>
iii. Potentiated by? <br></br>
b. Protein C<br></br>
i. Inhibits (cleaves) the cofactors?<br></br>
ii. Significantly decreases?<br></br>
iii. Requires?<br></br>
c. Plasmin <br></br>
i. Role?<br></br>

A

a. Antithrombin III<br></br>
i. Serine proteases <br></br>
ii. Thrombin and Xa <br></br>
iii. Heparin <br></br>
b. Protein C<br></br>
i. cofactors Va and VIIIa<br></br>
ii. rate of clot formation<br></br>
iii. activation <br></br>
c. Plasmin<br></br>
i. Breaks down fibrin <br></br>

71
Q
  1. In restriction of plasmin activity, where is activity of plasmin optimized?<br></br>
    What inactivates free plasmin?<br></br>
    tPA is inactivated by?<br></br>
    How do endothelial cells modulate <br></br>coagulation/anticoagulation balance? What increases this?
A

a. Fibrin deposition <br></br>
b. α2 antiplasmin <br></br>
c. PAI (plasminogen activator inhibitor)<br></br>
d. Releasing PAI, thrombin and various cytokines increase PAI<br></br>

72
Q
  1. In plasminogen activation, what prevents the vascular bed from being clogged with clots?<br></br>
    What is plasminogen activated into? Whose role is?<br></br>
    Name 3 substances that inactivate plasminogen
A

a. Breakdown of fibrin clots<br></br>
b. Plasmin which breaks down fibrin <br></br>
c. Urokinase, tPA (tissue plasminogen activator), streptokinase

73
Q
  1. Understand the drawing on slide 80 of Hemodynamics I<br></br>
A

Drawing

74
Q
  1. Antithrombotic agents and their actions<br></br>
A

i. Anticoagulants: prevent clot formation and extension<br></br>
ii. Antiplatelet drugs: interfere with platelet activity<br></br>
iii. Thrombolytic agenst: dissolve existing thrombi

75
Q
  1. Anticoagulant Drugs:<br></br>
    Name two traditional anticoagulants<br></br>
    What is a thrombus?<br></br>
    What is an embolus?<br></br>
A

a. Heparin and warfarin <br></br>
b. Thrombus <br></br>
c. Embolus <br></br>

76
Q
  1. What produces heparin and what is its role?<br></br>
    What does heparin not disintegrate?<br></br>
    How is heparin commonly given?<br></br>
    Heparin binds and activates antithrombin III, it performs this by inhibiting what?<br></br>
A

a. Basophils and mast cells to prevent blood clots<br></br>
b. Clots that have already formed<br></br>
c. Heparin commonly given intravenously by subcutaneous injection <br></br>
d. Thrombin, factor IXa, factor Xa

77
Q
  1. Warfarin (Coumadin) is a synthetic derivate of? Role?
A

Coumarin, decreases blood coagulation by interfering with vitamin K metabolism

78
Q
  1. What are the vitamin K-dependent clotting factors?
A

Factors VII, IX, X, II

79
Q
  1. Give 5 new anticoagulation drug types/species
A 
Direct thrombin<br>
Direct factor Xa inhibitors<br>
Synthetic pentasaccharide inhibitors of factor Xa<br>
 Activated Protein C<br>
Tissue Factor Pathway Inhibitor <br>
80
Q
  1. An important thrombin inhibitor is?<br></br>

Give two director factor Xa inhibitors

A

a. Dabigatran <br></br>

b. Rivaroxaban and apixaban<br></br>

81
Q
  1. Know table on slide 92 be able to draw. Table is role of PT and PTT: Warfarin/Heparin monitoring
A

Drawing

82
Q
  1. What are two contraindications to warfarin therapy?
A

Pregnancy<br></br>

Situations where risk of hemorrhage is greater outweighs benefits

83
Q
  1. The most common areas for Warfarin necrosis are?<br></br>

Patients with warfarin necrosis have low levels of?

A

a. The thighs, breasts, and buttocks<br></br>

b. Protein C

84
Q
  1. What may happen if warfarin is given to a patient with low levels of protein C?
A

A transient hypercoagulable state can develop causing local thrombosis of dermal vessels

85
Q
  1. What does tiny fibrin thrombi do to the body?
A

Depletes supply of platelets and coagulation factors such that the patient is now in danger of bleeding

86
Q
  1. In the diagnosis of DIC by Measurement of D-DIMER, what does the assay measure?<br></br>
    What does it indirectly measure?
A

a. Plasmin-cleaved insoluble cross-linked fibrin <br></br>

b. Since thrombin is needed for fibrin to form, it indirectly measures the plasmin and thrombin activity

Pathology (6 decks)

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