Test 1: 10-14 Hemodynamics II Flashcards

(41 cards)

1
Q
  1. Give the defect and glycoprotein for Bernard-Soulier Disease and Glanzmann’s Thombasthenia
A

a. Bernard-Soulier Disease
i. Defect of platelet adhesion
ii. Glycoprotein Ib

b. Glanzmann’s thrombastenia
i. Defect of platelet aggregation
ii. Glycoprotein IIb/IIIa

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2
Q
  1. Thrombotic Thrombocytopenic Purpura (TTP) has what antibodies for which protease?
A

Von Willebrand factor cleaving protease, ADAMTS-13

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3
Q
  1. In Hemorrhagic disorders – coagulopathies, von Willebrand’s disease is a deficiency of?
A

Von Willebrand’s antigen

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4
Q
  1. Give 4 clinical presentations of von Willebrand’s disease
A

i. Easily bruised
ii. Nosebleeds
iii. Gingival bleeding
iv. Menorrhagia (heavy period)

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5
Q
  1. What is the difference between hemophilia A and B?
A

Hemophilia A: factor VIII deficiency, more common

Hemophilia B: factor IX deficiency, more rare

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6
Q
  1. Give 5 characteristics of hemophilia
A

i. Deep internal bleeding leading to swelling
ii. Joint damage (harmarthrosis/haemophillic arthropathy)
iii. Transfusion transmitted infection
iv. Adverse reactions to clotting factor treatment
v. Intracranial hemorrhage

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7
Q
  1. What pathways can be activated to produce deleterious effects?
A

The same pathways that stop hemorrhaging

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8
Q
  1. In Virchow’s triad what leads to thrombosis?
A

Endothelial injury, abnormal blood flow (or circulatory stasis), hypercoagulable state

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9
Q
  1. In heparin-induced thrombocytopenia, platelet factor 4 is released by? What does it bind to and what are results of this?
A

Released by platelets and binds heparin, thus blocking its action and promoting coagulation

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10
Q
  1. Antiphospholipid antibody syndrome is most associated with what disorder? May cause a false positive test for?
A

Systemic lupus erythematosus (SLE)

Syphilis

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11
Q
  1. Turbulence causes what kind of damage? How does it cause local pockets of stasis? Give four things turbulence does
A

a. Causes endothelial injury or dysfunction
b. By forming countercurrents causing local pockets of stasis
c. Turbulence:
i. Disrupts laminar fluid
ii. Prevents dilution of clotting factors
iii. Prevents inflow of clotting inhibitors
iv. Promote endothelial cell activation

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12
Q
  1. Give 7 causes of turbulence
A

i. Ulcerated atherosclerotic plaque
ii. Aneurysms
iii. Hyperviscosity syndrome
iv. Sickle cell anemia
v. Myocardial infarctions
vi. Mitral valve stenosis
vii. Atrial fibrillation

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13
Q
  1. Thrombi morphology
    Arterial thrombi usually occur at sites of?
    Venous thrombi usually occur as a?
    Thrombi have a point of?
A

a. Sites of endothelial injury
b. Consequence of stasis
c. Firm attachment to the vessel

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14
Q
  1. What are Lines of Zahn?
A

In a thrombus, it is alternating bands of mostly fibrin and mostly RBC

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15
Q
  1. Mural thrombi are?
A

Arterial thrombosis in cardiac chambers due to myocardial infarction, ulcerated atherosclerotic plaque or aneurysmal dilatation

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16
Q
17.	Artery thrombi are usually occlusive. What is their path in the arterial system?
How do they appear? 
What are they made of? 
May cause? 
Risk factors?
A

a. Coronary artery > cerebral artery > femoral artery
b. Grey-white and friable. Composed of platelets, fibrin, erythrocyte, and leukocytes
c. May cause local obstruction or distant embolization
d. Risk factors include
i. Myocardial infarction
ii. Rheumatic heart disease
iii. Atherosclerosis

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17
Q
  1. Venous thrombi are usually due to?
    What is their color and why?
    Mostly involve where on the body?
A

a. Usually due to stasis
b. They contain more erythrocytes and therefore are red
c. Mostly lower extremity veins but may involve other sites

18
Q
  1. Risk factors for venous thrombosis include?
A
CHF 
Trauma 
Surgery 
Pregnancy 
Cancer 
Trosseau syndrome
19
Q
  1. What happens in trousseau syndrome/migratory thrombophlebitis?
A

A serine protease released by malignant tumor cells activates factor 10
Tumor cells release plasma membrane vesicles exhibiting procoagulant activity. Tissue thromboplastin is released from necrotic tumor

20
Q
  1. What is an embolus?
A

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

21
Q
  1. Where do all emboli originate from? How long do the emboli travel? Unless otherwise specified an embolus is assumed to be a?
A

a. Dislodged thrombus
b. Until they are stuck in a vessel too small
c. Thromboembolus

22
Q
  1. Most pulmonary thromboembolism arises from?
A

Deep leg vein thrombi above knee

23
Q
  1. A pulmonary embolus may occlude in what two spaces? Where can it be lodged?
A

occlude main pulmonary artery
lodge across bifurcation
occlude smaller branching arterioles

24
Q
  1. Two sources of arterial emboli are?
A

Mural thrombi in heart or aorta

Paradoxical emboli

25
27. When are fat globules common in circulation?
After: Fractures of long bones Soft tissue trauma Burns
26
28. What happens if there is a rapid decrease in pressure (decompression)? What two disorders are in this category? What is the treatment?
a. Air bubbles form in the circulation b. The bends: Formation of gas bubbles in skeletal muscles and supporting tissues in and around joints The chokes: Gas emboli in lungs cause edema, hemorrhage atelectasis, and emphysema causing respiratory distress c. Treatment: Slow decompression allows gradual resorption and exhalation of the gases
27
29. Caisson disease occurs in people who? What happens with persistence of gas?
Persons who worked in caissons had atmospheric pressure for long periods Persistence of gas emboli in skeletal system results in multiple foci if ischemic necrosis
28
30. What does Amniotic emboli consist of?
Epithelial cells from fetal skin Lanugo hair Fat from venix caseosa mucin from fetal respiratory and gastrointestinal tract
29
31. What is an infarction? In addition to thrombosis and emboli, what are its causes?
a. Infarction -- Death of tissue due to interruption in blood supply b. Causes in addition to thrombosis and emboli: i. Vasospasm ii. Hemorrhage within atherosclerotic plaque iii. Extrinsic compression of vessel iv. Torsion of vessel
30
32. In infarct development, what cell type has the least, medium, or fibroblast?
Neuron 3-4 minutes Myocardium 20-30 minutes Fibroblast Hours
31
33. Red infarction occurs in what 5 examples?
i. Venous occlusions ii. Loose tissues iii. Tissues with dual circulation iv. Tissues previously congested due to sluggish flow v. Reestablished blood flow to a site of previous arterial occlusion and necrosis
32
34. What are white infarcts?
Arterial occlusions in solid organs with limitations of flow into areas of ischemic necrosis
33
35. Infarcts tend to be what shape? Where do they occlude in a vessel?
Infarcts tend to be wedge-shaped | Occluded vessel at apex
34
36. A septic infarct occurs when? | The major source of septic emboli is?
A septic infarct occurs when the origin of an embolus is infected tissue. The major source of septic emboli is vegetation formed by bacteria growing on heart valves in bacterial endocarditis
35
37. What is shock AKA? What is shock caused by? Results in what 3 symptoms?
a. Cardiovascular Collapse b. Shock is caused by a reduction in cardiac output or effective circulating volume c. Results in hypotension, impaired tissue perfusion and cellular hypoxia
36
38. What is neurogenic shock? Anaphylactic shock?
a. Neurogenic dysfunction causes loss of vascular tone and peripheral pooling of blood b. Generalized IgE mediated hypersensitivity response associated with vasodilatation and increased vascular permeability
37
39. In the progressive stage of shock, what are signs of this?
i. Widespread tissue hypoxia ii. Lactic acidosis iii. Decreased vasomotor responses iv. Confusion and decreased urinary output v. Irreversible Stage vi. Widespread cell injury vii. Subsequent decrease in urine output and severe fluid/electrolyte disorders occur
38
40. In shock decreased vasomotor responses include?
Arterioles dilate Pooling in microcirculation worsens cardiac output Anoxic endothelial cell injury
39
41. Shock causes widespread cell injury. Give 3 examples
Widespread cell injury Lysosmal enzyme leakage Decreased Myocardial Contraction Acute tubular necrosis renal failure
40
42. Give the shock morphology of the following: brain, heart, kidneys
Morphology Brain: ischemic encephalopathy Heart: coagulation necrosis/subendocardial hemorrhage, contraction band necrosis Kidneys: acute tubular necrosis
41
43. Give the shock morphology of the following: lungs, adrenal gland, gastrointestinal tract, and liver?
Lungs: diffuse alveolar damage Adrenal Gland: Cortical cell lipid depletion Gastrointestinal tract: Mucosal hemorrhage and necrosis Liver: Fatty change, central hemorrhagic necrosis