Test 1: 10-14 Hemodynamics I Flashcards
(86 cards)
1
Q
- 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
2
Q
- What two things can happen with failure hemostasis mechanisms?
A
Excessive bleeding or vessel occulusion by excessive blood clot formation (thrombosis)
3
Q
- 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
4
Q
- 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
5
Q
- 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
6
Q
- 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>
7
Q
- 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
8
Q
- Edema is increased hydrostatic pressure which is an indication of? What does it produce?
A
Congestive heart edema <br></br>
Dependent edema<br></br>
9
Q
- 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>
10
Q
- What is responsible for maintaining colloid osmotic pressure?
A
Albumin <br></br>
11
Q
- 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>
12
Q
- What does ascites result from?
A
Advanced liver cirrhosis
13
Q
- 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>
14
Q
- 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
15
Q
- Salt and water retention is secondary after?
A
Renin-Angiotensin-Aldosterone system activation
16
Q
- Edema inflammation is localized unless?
A
Result of systemic inflammatory response (e.g. allergic reaction)
17
Q
- Lymphatic obstruction/impaired drainage results in? Is this localized or systemic?
A
Lymphedema, usually localized
18
Q
- Elephantitis (a lymphedema) is due to?
A
Wuchereria bancrofti (roundworms block lymph vessels)
19
Q
- What does the microscopic appearance of edema depend on?
A
Amount of protein in exudate
20
Q
- 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>
21
Q
- How does the histologic appearance of subcutaneous edema appear?
A
Subtle, with increased spaces between cells
22
Q
- 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
23
Q
- What is the most common cause of edema?
A
Heart problems
24
Q
- Left ventricular failure causes back up to?
A
Atrium, pulmonary veins, and lungs
25
25. Noncardiogenic pulmonary edema causes increased permeability leading to?
i. Alveolar hypoxia
ii. Acute respiratory distress syndrome
iii. Inhalation of toxic agents
iv. Pulmonary infections
v. Therapeutic radiation of the lungs
vi. Head injury
vii. Renal failure
viii. Hypersensitivity
ii. Acute respiratory distress syndrome
iii. Inhalation of toxic agents
iv. Pulmonary infections
v. Therapeutic radiation of the lungs
vi. Head injury
vii. Renal failure
viii. Hypersensitivity
26
26. Clinical manifestations of pulmonary edema include? Characteristics of each manifestation?
i. Dyspnea
ii. Cough
iii. Pulse
iv. Breath sounds
v. Engorged neck vessels
ii. Cough
iii. Pulse
iv. Breath sounds
v. Engorged neck vessels
27
27. Dyspnea’s characteristics in pulmonary edema?
i. Sudden
ii. Orthopnea
iii. Cyanotic (central)
iv. Air hunger
v. Tachypnea
ii. Orthopnea
iii. Cyanotic (central)
iv. Air hunger
v. Tachypnea
28
28. Clinical manifestations cough in pulmonary edema?
i. Copious sputum
ii. Frothy
iii. Blood tinged
ii. Frothy
iii. Blood tinged
29
29. Clinical manifestations of pulse, breathe sounds, and vessels in pulmonary edema?
a. Pulse: Tachycardic, bounding
b. Breath sounds: crackles, fine -> course
c. Engorged neck veins
b. Breath sounds: crackles, fine -> course
c. Engorged neck veins
30
30. What are four appearance characteristics of interstitial pulmonary edema? Alveolar pulmonary edema?
Heart and pleural cavity?
a. interstitial pulmonary edema
i. Poorly defined pulmonary vessels
ii. Visible lung fissures
iii. Septal lines
iv. Thick bronchial walls
b. Alveolar pulmonary edema
i. Bilateral symmetric perihilar lung consolidation
c. Enlarged heart and pleural effusion
i. Poorly defined pulmonary vessels
ii. Visible lung fissures
iii. Septal lines
iv. Thick bronchial walls
b. Alveolar pulmonary edema
i. Bilateral symmetric perihilar lung consolidation
c. Enlarged heart and pleural effusion
31
31. Cerebral edema is serious because? Parenchymal edema may move? If edema is more localized causes?
a. Brain swells, skull prevents expansion and so tissue is compressed
b. Parenchymal edema may shift brain due to high pressure and may push the brainstem down into the foramen magnum (tonsillar herniation)
c. One part of the brain herniates into adjacent compartments tearing brain tissue
b. Parenchymal edema may shift brain due to high pressure and may push the brainstem down into the foramen magnum (tonsillar herniation)
c. One part of the brain herniates into adjacent compartments tearing brain tissue
32
32. Give 3 localized causes of cerebral edema
| Give 4 Generalized causes of cerebral edema
a. Localized
i. Abscess
ii. Neoplasm
iii. Trauma
b. Generalized
i. Encephalitis
ii. Hypersensitive crisis
iii. Obstruction of venous outflow
iv. Trauma
i. Abscess
ii. Neoplasm
iii. Trauma
b. Generalized
i. Encephalitis
ii. Hypersensitive crisis
iii. Obstruction of venous outflow
iv. Trauma
33
33. Grossly a swollen brain in cerebral edema appears?
Appears with distended, flattened gyri and narrowed sulci
34
34. What is hyperemia? Give 3 examples of it
a. Active process in which arteriolar dilatation causes increased flow of blood to tissue
b. Skeletal muscle during exercise, inflammation, and blushing
b. Skeletal muscle during exercise, inflammation, and blushing
35
35. What is the term that describes tissue with engorgement with oxygenated blood?
Erythematous
36
36. What is congestion?
Give an example for systemic and local congestion Color and why?
Congestion and edema occur separate or together?
Give an example for systemic and local congestion Color and why?
Congestion and edema occur separate or together?
a. Congestion is a passive process due to impaired outflow of blood from a tissue
b. Systemic: congestive heart failure (CHF), local: local venous obstruction
c. Blue-red color due to accumulation of deoxygenated hemoglobin (cyanosis)
d. Congestion and edema usually occur together
b. Systemic: congestive heart failure (CHF), local: local venous obstruction
c. Blue-red color due to accumulation of deoxygenated hemoglobin (cyanosis)
d. Congestion and edema usually occur together
37
37. What are the consequences of long term congestion in chronic passive congestion?
Causes a stasis of poorly oxygenated blood, may lead to cellular degeneration and death
38
38. If there is capillary rupture, breakdown and phagocytosis of the red cell debris cause?
Accumulation of hemosiderin-laden macrophages at the site
39
39. Give characteristics of acute pulmonary congestion and chronic pulmonary congestion?
a. Acute pulmonary congestion
i. Alveolar capillaries engorged with blood
ii. Alveolar septal edema
iii. Focal intraalveolar hemorrhage
b. Chronic pulmonary congestion
i. Thickened and fibrotic septa
ii. Heart failure cells aka hemosiderin-laden macrophages in alveolar spaces
i. Alveolar capillaries engorged with blood
ii. Alveolar septal edema
iii. Focal intraalveolar hemorrhage
b. Chronic pulmonary congestion
i. Thickened and fibrotic septa
ii. Heart failure cells aka hemosiderin-laden macrophages in alveolar spaces
40
40. Nutmeg liver’s gross appearance is? Where does it appear?
Central regions of hepatic lobules are grossly red/brown and depressed (due to cellular loss) surrounded by unaffected areas
Chronic hepatic congestion
Chronic hepatic congestion
41
41. In chronic hepatic congestion, microscopically what is centrilobular necrosis? What results in long standing hepatic congestion?
a. Centrilobular necrosis; hepatocellular death and accompanying hemorrhage with hemosiderin laden macrophages
b. Hepatic fibrosis
b. Hepatic fibrosis
42
42. Hemorrhages are? Hemorrhages classifications?
a. Extravasation of blood due to ruptured vessels
| b. Internal or external
| b. Internal or external
43
43. Hemorrhages result from? Name 6
i. trauma
ii. atherosclerosis
iii. aneurysm
iv. neoplasia/inflammation
v. capillary bleeding
vi. hemorrhagic diathesis
ii. atherosclerosis
iii. aneurysm
iv. neoplasia/inflammation
v. capillary bleeding
vi. hemorrhagic diathesis
44
44. In the hemorrhagic diathesis, give 3 characteristics
i. Fragility of vessels
ii. Platelet dysfunction (petechiae, purpura)
iii. Coagulation defect (hematoma, bleeding)
ii. Platelet dysfunction (petechiae, purpura)
iii. Coagulation defect (hematoma, bleeding)
45
45. What is petechiae? What do DDX – angiomas and DDX – vasculitis do?
a. 1-2 mm foci of hemorrhage in skin, mucous membranes, or serosal surfaces
b. DDX – angiomas: Do not blanch (whiten) with pressure DDX – vasculitis: not palpable
b. DDX – angiomas: Do not blanch (whiten) with pressure DDX – vasculitis: not palpable
46
46. What size do foci of hemorrhage have to be for purpura?
≥3 mm foci of hemorrhage
47
47. Ecchymoses usually occurs? However it is used as a first sign of what disorder?
a. Ecchymotic hemorrhages usually due to trauma
| b. First sign of acute myelogenous leukemia due to low platelet count (thrombocytopenia)
48
48. Give four clinical significance of hemorrhage
i. Rapid blood loss (20%) insignificant to healthy person but can be fatal in compromised patient
ii. Sites where bleeding occurs has significant prognostic value
iii. Chronic or repeated bleeding leads to iron deficiency
iv. Internal blood loss may allow resuse of iron
ii. Sites where bleeding occurs has significant prognostic value
iii. Chronic or repeated bleeding leads to iron deficiency
iv. Internal blood loss may allow resuse of iron
49
49. Hemostasis occurs as a result of?
A well regulated/balanced process of maintaining blood in a fluid state while allowing for controlled and focused clotting to prevent blood loss
50
50. What are the 3 general components contribute to homeostasis?
```
Endothelium/Vascular wall
Platelets (bricks)
Coagulation cascade (fibrin – cement)
```
51
51. What are the 5 sequences of clot formation
i. Initial injury causes brief vasoconstriction
ii. Endothelial damage exposes subendothelium, causing endothelial death, causing platelets activated/adhere
iii. Tissue factor is released activates coagulation cascade forming fibrin
iv. Platelet activation furthers coagulation
v. Fibrin and platelets form a clot thereby plugging to prevent blood loss
52
52. Endothelium has what kind of function in hemostasis? What factors activate endothelium and shift the function to procoagulant?
```
a. Both anticoagulant and procoagulant functions
b. Factors: Infectious Agents
Hemodynamic forces
Cytokines
Plasma mediators
```
a. Both anticoagulant and procoagulant functions
b. Factors: Infectious Agents
Hemodynamic forces
Cytokines
Plasma mediators
```
53
53. What two compounds inhibit platelet aggregation?
Thrombin and several cytokines stimulate PGI2 and NO synthesis
54
54. What degrades ADP and what does this do?
Adenosine diphosphatase degrades ADP thereby inhibiting platelet aggregation
55
55. In the anticoagulant activities of the endothelium, what do heparin-like molecules do? What does thrombomodulin covert? Fibrinolytic endothelial cells make?
a. Cofactors to antithrombin
b. Thrombomodulin coverts thrombin to anticoagulant
c. Tissue plasminogen activator (tPA)
b. Thrombomodulin coverts thrombin to anticoagulant
c. Tissue plasminogen activator (tPA)
56
56. In normal conditions endothelial cells’ role is? What happens if there are injury/activation of endothelial cells?
a. Inhibit platelet adherence and blood clotting
| b. Procoagulant state
| b. Procoagulant state
57
57. What is the size of non-activated platelets? Shaped? Derived from? Contain?
57. What is the size of non-activated platelets? Shaped?
Derived from? Contain?
Derived from? Contain?
58
58. After endothelial injury what four things do platelets encounter?
Collagen, von Willibrand factor, tissue factor and thrombin
59
59. Three steps that ensue after platelets encounter other factors?
i. Adhesion
ii. Secretion and activation
iii. Aggregation
ii. Secretion and activation
iii. Aggregation
60
60. 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. Subendothelial ECM (NOT firm)
b. Subendothelial ECM to glycoprotein Ib receptors on platelets (Firm)
c. Release of their granules
b. Subendothelial ECM to glycoprotein Ib receptors on platelets (Firm)
c. Release of their granules
61
61. Platelet activation granule contents are released.
What are the contents and their function(s)?
What are the contents and their function(s)?
Calcium: critical for coagulation cascade
ADP: mediates platelet aggregation which increases platelet aggregation at the site
Platelet factor 4: binds to heparin results in its inactivation Serotonin: induces vasoconstriction
ADP: mediates platelet aggregation which increases platelet aggregation at the site
Platelet factor 4: binds to heparin results in its inactivation Serotonin: induces vasoconstriction
62
62. In platelet aggregation ADP and thromboxane released by platelets have what effect?
Further platelet aggregation
63
63. In platelet aggregation, what links fibrinogen to platelets?
What protease also binds to the platelet surface?
What does platelet activation cause?
What protease also binds to the platelet surface?
What does platelet activation cause?
a. GpIIb-IIIa
b. Thrombin
c. Expression of phospholipid complexes on the surface of platelets which act as surfaces to bind coagulation factors and calcium, thereby promoting coagulation
b. Thrombin
c. Expression of phospholipid complexes on the surface of platelets which act as surfaces to bind coagulation factors and calcium, thereby promoting coagulation
64
64. Draw the drawing on platelet adhesion and aggregation on slide 67 of hemodynamics I PPT
Drawing
65
65. What happens in the following steps of platelet adhesion and aggregation:
1. Vascular spasm
2. Platelet plug formation
3. Coagulation
1. Vascular spasm: smooth muscle contracts, causing vasoconstriction
2. Platelet plug formation: injury to vessel lining shows collagen fibers; platelets adhere here. Platelets release chemicals that make close
3. Coagulation: fibrin forms mesh that traps RBCs and platelets forming a clot
2. Platelet plug formation
3. Coagulation
1. Vascular spasm: smooth muscle contracts, causing vasoconstriction
2. Platelet plug formation: injury to vessel lining shows collagen fibers; platelets adhere here. Platelets release chemicals that make close
3. Coagulation: fibrin forms mesh that traps RBCs and platelets forming a clot
66
66. Coagulation: General Concepts
a. Coagulation factors are a sequential enzyme cascade whose activation causes?
b. These inactive serine proteases (e.g. prothrombin) are converted to “activated enzymes/proteins” by?
c. Assembly of the complex of coagulation factors, which requires cofactors and Ca, takes place on?
d. Thrombin converts fibrinogen to fibrin monomer, but also effects?
e. Fibrin monomer cross-linked to fibrin forms?
a. Fibrin clot
b. Limited proteolysis
c. Phospholipid surface
d. “Glue” for platelet plug
b. These inactive serine proteases (e.g. prothrombin) are converted to “activated enzymes/proteins” by?
c. Assembly of the complex of coagulation factors, which requires cofactors and Ca, takes place on?
d. Thrombin converts fibrinogen to fibrin monomer, but also effects?
e. Fibrin monomer cross-linked to fibrin forms?
a. Fibrin clot
b. Limited proteolysis
c. Phospholipid surface
d. “Glue” for platelet plug
67
67. Important things to remember about coagulation:
a. What is the intrinsic factor?
b. What is the extrinsic factor?
c. Both pathways merge at factors?
d. What do the factors need to be bound to for maximum activity?
e. What element is necessary for coagulation?
f. What is the end result of what is formed in coagulation?
a. What is the intrinsic factor?
b. What is the extrinsic factor?
c. Both pathways merge at factors?
d. What do the factors need to be bound to for maximum activity?
e. What element is necessary for coagulation?
f. What is the end result of what is formed in coagulation?
a. Hagerman factor (XII)
b. Tissue factor
c. Factors IX and X
d. A phospholipid surface
e. Calcium
f. Cross-linked fibrin
b. Tissue factor
c. Factors IX and X
d. A phospholipid surface
e. Calcium
f. Cross-linked fibrin
68
68. Prothrombin time (PT): extrinsic is prolonged by?
| Partial thromboplastic time (PTT): intrinsic is prolonged by?
| Partial thromboplastic time (PTT): intrinsic is prolonged by?
i. Prolonged by warfarin (Coumadin)
| ii. Prolonged by heparin
| ii. Prolonged by heparin
69
69. Blood clotting must be limited to the site of injury or the clot will?
Clot to grow block patency of vessel (i.e. thrombosis
70
. Antithrombin III
i. Directly inactivates?
ii. Name two
iii. Potentiated by?
b. Protein C
i. Inhibits (cleaves) the cofactors?
ii. Significantly decreases?
iii. Requires?
c. Plasmin
i. Role?
i. Directly inactivates?
ii. Name two
iii. Potentiated by?
b. Protein C
i. Inhibits (cleaves) the cofactors?
ii. Significantly decreases?
iii. Requires?
c. Plasmin
i. Role?
a. Antithrombin III
i. Serine proteases
ii. Thrombin and Xa
iii. Heparin
b. Protein C
i. cofactors Va and VIIIa
ii. rate of clot formation
iii. activation
c. Plasmin
i. Breaks down fibrin
i. Serine proteases
ii. Thrombin and Xa
iii. Heparin
b. Protein C
i. cofactors Va and VIIIa
ii. rate of clot formation
iii. activation
c. Plasmin
i. Breaks down fibrin
71
71. In restriction of plasmin activity, where is activity of plasmin optimized?
What inactivates free plasmin?
tPA is inactivated by?
How do endothelial cells modulate
coagulation/anticoagulation balance? What increases this?
What inactivates free plasmin?
tPA is inactivated by?
How do endothelial cells modulate
coagulation/anticoagulation balance? What increases this?
a. Fibrin deposition
b. α2 antiplasmin
c. PAI (plasminogen activator inhibitor)
d. Releasing PAI, thrombin and various cytokines increase PAI
b. α2 antiplasmin
c. PAI (plasminogen activator inhibitor)
d. Releasing PAI, thrombin and various cytokines increase PAI
72
72. In plasminogen activation, what prevents the vascular bed from being clogged with clots?
What is plasminogen activated into? Whose role is?
Name 3 substances that inactivate plasminogen
What is plasminogen activated into? Whose role is?
Name 3 substances that inactivate plasminogen
a. Breakdown of fibrin clots
b. Plasmin which breaks down fibrin
c. Urokinase, tPA (tissue plasminogen activator), streptokinase
b. Plasmin which breaks down fibrin
c. Urokinase, tPA (tissue plasminogen activator), streptokinase
73
73. Understand the drawing on slide 80 of Hemodynamics I
Drawing
74
74. Antithrombotic agents and their actions
i. Anticoagulants: prevent clot formation and extension
ii. Antiplatelet drugs: interfere with platelet activity
iii. Thrombolytic agenst: dissolve existing thrombi
ii. Antiplatelet drugs: interfere with platelet activity
iii. Thrombolytic agenst: dissolve existing thrombi
75
75. Anticoagulant Drugs:
Name two traditional anticoagulants
What is a thrombus?
What is an embolus?
Name two traditional anticoagulants
What is a thrombus?
What is an embolus?
a. Heparin and warfarin
b. Thrombus
c. Embolus
b. Thrombus
c. Embolus
76
76. What produces heparin and what is its role?
What does heparin not disintegrate?
How is heparin commonly given?
Heparin binds and activates antithrombin III, it performs this by inhibiting what?
What does heparin not disintegrate?
How is heparin commonly given?
Heparin binds and activates antithrombin III, it performs this by inhibiting what?
a. Basophils and mast cells to prevent blood clots
b. Clots that have already formed
c. Heparin commonly given intravenously by subcutaneous injection
d. Thrombin, factor IXa, factor Xa
b. Clots that have already formed
c. Heparin commonly given intravenously by subcutaneous injection
d. Thrombin, factor IXa, factor Xa
77
77. Warfarin (Coumadin) is a synthetic derivate of? Role?
Coumarin, decreases blood coagulation by interfering with vitamin K metabolism
78
78. What are the vitamin K-dependent clotting factors?
Factors VII, IX, X, II
79
79. Give 5 new anticoagulation drug types/species
```
Direct thrombin
Direct factor Xa inhibitors
Synthetic pentasaccharide inhibitors of factor Xa
Activated Protein C
Tissue Factor Pathway Inhibitor
```
Direct factor Xa inhibitors
Synthetic pentasaccharide inhibitors of factor Xa
Activated Protein C
Tissue Factor Pathway Inhibitor
```
80
80. An important thrombin inhibitor is?
| Give two director factor Xa inhibitors
| Give two director factor Xa inhibitors
a. Dabigatran
| b. Rivaroxaban and apixaban
| b. Rivaroxaban and apixaban
81
81. Know table on slide 92 be able to draw. Table is role of PT and PTT: Warfarin/Heparin monitoring
Drawing
82
82. What are two contraindications to warfarin therapy?
Pregnancy
| Situations where risk of hemorrhage is greater outweighs benefits
| Situations where risk of hemorrhage is greater outweighs benefits
83
83. The most common areas for Warfarin necrosis are?
| Patients with warfarin necrosis have low levels of?
| Patients with warfarin necrosis have low levels of?
a. The thighs, breasts, and buttocks
| b. Protein C
| b. Protein C
84
84. What may happen if warfarin is given to a patient with low levels of protein C?
A transient hypercoagulable state can develop causing local thrombosis of dermal vessels
85
85. What does tiny fibrin thrombi do to the body?
Depletes supply of platelets and coagulation factors such that the patient is now in danger of bleeding
86
86. In the diagnosis of DIC by Measurement of D-DIMER, what does the assay measure?
What does it indirectly measure?
What does it indirectly measure?
a. Plasmin-cleaved insoluble cross-linked fibrin
| b. Since thrombin is needed for fibrin to form, it indirectly measures the plasmin and thrombin activity
| b. Since thrombin is needed for fibrin to form, it indirectly measures the plasmin and thrombin activity
