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

Test 1: 10-14 Hemodynamics II Flashcards

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
Q
  1. When are fat globules common in circulation?
A

After:
Fractures of long bones
Soft tissue trauma
Burns

26
Q
  1. What happens if there is a rapid decrease in pressure (decompression)? What two disorders are in this category? What is the treatment?
A

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
Q
  1. Caisson disease occurs in people who? What happens with persistence of gas?
A

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
Q
  1. What does Amniotic emboli consist of?
A

Epithelial cells from fetal skin
Lanugo hair
Fat from venix caseosa
mucin from fetal respiratory and gastrointestinal tract

29
Q
  1. What is an infarction? In addition to thrombosis and emboli, what are its causes?
A

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
Q
  1. In infarct development, what cell type has the least, medium, or fibroblast?
A

Neuron 3-4 minutes
Myocardium 20-30 minutes
Fibroblast Hours

31
Q
  1. Red infarction occurs in what 5 examples?
A

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
Q
  1. What are white infarcts?
A

Arterial occlusions in solid organs with limitations of flow into areas of ischemic necrosis

33
Q
  1. Infarcts tend to be what shape? Where do they occlude in a vessel?
A

Infarcts tend to be wedge-shaped

Occluded vessel at apex

34
Q
  1. A septic infarct occurs when?

The major source of septic emboli is?

A

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
Q
  1. What is shock AKA? What is shock caused by? Results in what 3 symptoms?
A

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
Q
  1. What is neurogenic shock? Anaphylactic shock?
A

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
Q
  1. In the progressive stage of shock, what are signs of this?
A

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
Q
  1. In shock decreased vasomotor responses include?
A

Arterioles dilate
Pooling in microcirculation worsens cardiac output
Anoxic endothelial cell injury

39
Q
  1. Shock causes widespread cell injury. Give 3 examples
A

Widespread cell injury
Lysosmal enzyme leakage
Decreased Myocardial Contraction
Acute tubular necrosis renal failure

40
Q
  1. Give the shock morphology of the following: brain, heart, kidneys
A

Morphology
Brain: ischemic encephalopathy
Heart: coagulation necrosis/subendocardial hemorrhage, contraction band necrosis
Kidneys: acute tubular necrosis

41
Q
  1. Give the shock morphology of the following: lungs, adrenal gland, gastrointestinal tract, and liver?
A

Lungs: diffuse alveolar damage
Adrenal Gland: Cortical cell lipid depletion
Gastrointestinal tract: Mucosal hemorrhage and necrosis
Liver: Fatty change, central hemorrhagic necrosis

Pathology (6 decks)

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