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General Pathology > Exam #2: Hemodynamics IV > Flashcards

Exam #2: Hemodynamics IV Flashcards

1
Q

What is Virchow’s Triad?

A

Virchow’s Triad outlines the three primary abnormalities that lead to thrombus formation:

1) Endothelial Injury
2) Stasis
3) Hypercoaguable state

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2
Q

What is the dominant influence on thrombosis formation?

A

Endothelial injury

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3
Q

Why is endothelial injury especially important for thrombus formation in the heart & arterial circulation?

A

High flow rates impede platelet adhesion & washout clotting factors; thus, endothelial injury is the major factor leading to thrombus formation in these high flow areas

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4
Q

List the difference sources of endotheial injury & dysfunction.

A

1) DM
2) HTN
3) Smoking
4) Oxidtive stress
5) LDL cholesterol
6) Homocysteine ADMA

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5
Q

List the consequences of endothelial dysfunction.

A

1) Vasoconstriction
2) Increased leukocyte adhesion & infiltration
3) Platelet aggregation & thrombosis
4) Vascular smooth muscle cell proliferation
5) Lipid accumulation

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6
Q

What is the difference between primary and secondary hypercoaguable states?

A

Primary= genetic mutation leading to hypercoagulation
- Factor V Leiden

Secondary= acquired alterations leading to hypercoagulation i.e.

  • stasis
  • bed rest
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7
Q

What is a Factor V Leiden deficiency?

A
  • Factor V is a clotting factor
  • Normally broken down by protein C
  • Mutation in Factor V prevents the removal of Factor V by protein C–>hypercoaguable state

Specifically, a glutamine residue is substituted for arginine in the 506 position, and prevents cleavage by protein C

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8
Q

What is the typical presentation of Factor V Leiden deficiency?

A

Recurrent DVTs without secondary risk factors

- More common in caucasians

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9
Q

What is antiphospholipid antibody syndrome?

A

Serum antibody directed against anionic phospholipid

  • In vitro there is INHIBITION of clotting due to interference with assembly of phospholipid complexes
  • In vivo= HYPERCOAGUABLE state
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10
Q

What is antiphospholipid antibody syndrome associated with?

A

Autoimmune diseases, especially, SLE

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11
Q

What are the clinical manifestations of antiphospholipid antibody syndrome?

A
  • Recurrent venous or arterial thrombi
  • Repeated miscarriage
  • Cardiac valve vegetations
  • Thrombocytopenia
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12
Q

What is the effect of turbulence in the vasculature?

A

Disruption of normal laminar flow

  • In normal laminar flow, platelets flow centrally & are separated from the endothelium by slower moving plasma
  • Stasis & turbulence:

1) Disrupts laminar flow & brings platelets in contact with endothelium
2) Prevents dilution of clotting factors
3) Promotes endothelial cell activation

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13
Q

List the causes of turbulence in the vasculature?

A
  • Ulcerated atherosclerotic plaque
  • Aneurysms
  • MI
  • Mitral valve stenosis
  • Hyperviscosity syndrome i.e. polycythemia
  • Sickle cell anemia
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14
Q

Describe the morphology of thrombi. What is the difference between aterial & venous thrombi?

A

Arterial= usually occur at sites of endothelial cell injury
- Grey-white and friable

Venous= more commonly caused by stasis/ low-flow
- Red, slower blood flow= higher accumulation of RBCs

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15
Q

What are the complications of arterial thrombi?

A

May cause local obstruction or distant embolization leading CVA, MI, and PAD

Risk Factors

  • MI
  • Rheumatic heart disease
  • A-fib
  • Atherosclerosis
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16
Q

What are arterial thrombi composed of?

A

Platelets
Fibrin
Erythrocyte
Leukocytes

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17
Q

Describe the relative incidence of arterial thrombi i.e. where do they occur most commonly?

A

Coronary arteries
Cerebral arteries
Femoral arteries

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18
Q

Where does rupture of a thrombis typically occur?

A

“Shoulder region”

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19
Q

What is an abdominal aortic aneurysm?

A

Outpouching of the wall of the abdominal aorta that is at risk for rupture
- Layered thrombus is in the lumen

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20
Q

What are “Lines of Zahn?”

A

Alternating layering of pale platelets & fibrin with darker erythrocytes

*****Note that these are important for distinguishing between antemortem & postmortem thrombosis

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21
Q

Where are venous thrombi most commonly seen?

A

90% involve LE veins, but other less common sites include:

UE
Periprostatic plexus
Ovarian & periuterine veins

22
Q

Where do venous thrombi typically form?

A

In valve pockets of the deep veins

23
Q

What is phlebothrombosis?

A

Superficial thrombi that rarely embolize

24
Q

In what percentage of patients are DVTs asymptomatic?

A

50%

**This is important! In roughly 50% of affect patients, collateral circulation may mask symptoms of a DVT i.e. the patient is asymptomatic.

25
Q

What are the risk factors for venous thrombosis?

A 
CHF 
Trauma 
Surgery 
Pregnancy 
Cancer
26
Q

What is Trousseau Syndrome?

A

This is a “migrating thrombophlebitis” caused by a serine protease released by malignant tumors that activates Factor X

  • Tumor cells release plasma membrane vesicles exhibiting procoagulant activity
  • Tissue thromboplastin is released from a necrotic tumor e
27
Q

What are the different fates of a thrombus?

A

1) Resolution
2) Embolization
3) Organization and incorporation into the wall
4) Organization & recannulization

28
Q

What is an embolus?

A

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

  • Lodge is vessels that are too small for migration to continue
  • Unless otherwise specified, embolus is assumed to be a “THROMBOEMBOLUS”
29
Q

List the sources of aterial emboli.

A
  • A-fib
  • Mitral stenosis
  • Endocarditis
  • Mural thrombi in heart or aorta*
  • Paradoxical emboli
30
Q

What is the most common source of emboli that migrate within the arterial circulation?

A

Intracardiac mural thrombi

31
Q

What is a paradoxical emboli?

A

Rare condition in which an embolus originating from the VENOUS circulation passes through a VSD and into the systemic circulation

E.g. a DVT that causes a stroke

32
Q

What is the most common cause of a pulmonary thromboembolism?

A

95% arise from deep leg vein thrombi ABOVE THE KNEE

33
Q

Where can a pulmonary thromboembolism occlude?

A
  • Main pulmonary artery
  • Saddle= across vessel bifurcation
  • Smaller braching arterioles

*Can cause sudden death via acute RVH

34
Q

What is cor pulmonale?

A

Chronic/ recurrent pulmonary embolism that leads to pulmonary HTN

35
Q

How are pulmonary embolism diagnosed?

A
  • 2D echo
  • V/Q scan
  • CT chest
  • MRI
  • Venogram
36
Q

What causes a fat embolism?

A

Long bones contain fatty marrow. In 90% of long bone fractures/ skeletal trauma, there is embolism of this fatty marrow, leading to a fat embolism. However, on 10% of patients actually develop clinical findings i.e. most are ASYMPTOMATIC

37
Q

What is fat embolism syndrome?

A

This is the term applied to the minority of patients with a fat embolism that become symptomatic. Typically 1-3 s/p injury:

1) Dyspnea, tachypnea, & tachycardia
2) Irritability & restlessness
3) Progression to delirium & coma

38
Q

What is an air embolism?

A

Coalesced gas bubbles in the circulation–>obstruction of vascular flow

39
Q

Outline the pathophysiology of decompression sickness or the Bends.

A
  • Sudden change in atmospheric pressure i.e. diving
  • Nitrogen inspired at high pressure (deep under water) dissolves in blood
  • Rapid decrease in pressure i.e. rapid ascent, nitrogen comes out of solution & forms gas bubbles in the circulation
40
Q

What is the difference between “the bends” and “the chokes?”

A

Bends= dissolution of nitrogen in muscles, bones, and joints leads to a painful condition called, “the bends”

Chokes= dissolution of nitrogen in the lung vasculature leading to edema, hemorrhage, and focal atelectasis–>respiratory distress

41
Q

What is the treatment for decompression sickness?

A

Hyperbaric oxygen therapy=

  • Forces gas back into solution
  • Allows for slow & controlled decompression
42
Q

What is an amniotic fluid embolism?

A

Breach of the placental membranes & uterine veins causes infusion of amniotic fluid into maternal circulation. This is a very ominous diagnosis and leads to:

  • Sudden severe dyspnea
  • Cyanosis
  • Shock
  • Neurologic impairment (headache, seizures–>coma)

IF the patient survives the initial crisis, pulmonary edema and DIC follow.

43
Q

Describe the pathophysiology of an amniotic fluid embolism.

A

Tear in the placental membranes or rupture of the uterine veins leads to amniotic fluid or fetal tissue into the maternal circulation

44
Q

List the contents of an amniotic fluid embolism. What is important about the contents?

A

Squamous cells from fetal skin
Lanugo hair
Fat from vernix caseosa
Mucin from fetal respiratory or GI tract

*****All are procoagulative

45
Q

What is the definition of infarction?

A

Death of tissue due to the interruption in blood supply

46
Q

What can cause infarction besides thrombosis & emboli?

A
  • Vasopasm e.g. cocaine–>MI
  • Hemorrhage within athersclerotic plaque
  • Extrinsic compression of vessel
  • Twisting of a vessel e.g. testicular torsion or intestinal volvulus
47
Q

What is the major factor in tissue damage from infarction?

A

Availability of alternative blood supply

48
Q

What cells are the most vulnerable to hypoxia?

A 
Neurons= 3-4 min
Myocardium= 20-30 min
Fibroblasts= Hours
49
Q

Describe the general morphology of an infarct.

A
  • Wedge-shaped
  • Poorly defined
  • Over time delineated by a rim of hyperemia
50
Q

What is the difference between a red and white infarct?

A 
Red= venous occlusion 
White= arterial occlusion

General Pathology (33 decks)

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