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Pathology- fluid Hemodynamics > Fluid hemodynamics disorders II > Flashcards

Fluid hemodynamics disorders II Flashcards

1
Q

thrombus

A

pathological process
platelets+fibrin+cellular elements (RBC’s)
attached to vessel wall
mainly ante-mortem only

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2
Q

Clot

A

ante-mortem (extravascular) or post-mortem (intravascular)
RBC’s+ coagulation factors
not attached to vessel wall
NO platelet activation

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3
Q

post-mortem clot composition

A

coagulation factors and erythrocyte only

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4
Q

gross appearance of postmortem clot

A
  1. “Currant jelly clot”-> dark to red black, smooth and shiny surface, rubbery, uniform, molded to shape of vessel, NOT ATTACHED, increased RBS
  2. “Chicken-fat clot”-> yellow, results from settling and separation of RBC’s and plasma, supernatant, no/few RBC’s.
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5
Q

thrombus gross appearance

A

heterogeneous

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6
Q

arterial thrombi

A

pale, grey-tan, dry, friable, concentric layers, attached to vessel wall

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7
Q

venous thrombi

A

red (lots of red cells), friable, attached to vessel wall, can be confused with clot, often occlusive

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8
Q

composition of thrombus

A

fibrin, platelets, WBC, RBC, +/- bacteria

  • more organized than clots, attached to vessel wall
  • laminated (lines of Zahn)-> arterial thrombi, alternating layers of platelets/fibrin (pale) and RBC (dark)
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9
Q

criteria for thromus

A
  • formation: ante-mortum
  • cause: endothelial injury
  • attachment: vessel wall
  • consistency: dry
  • surface: granular, rough
  • vascular endothelium: damaged, rough
  • organization: partial
  • structure: laminated
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10
Q

criteria for PM clot

A

formation: post-mortem
cause: stagnant blood in dead animal
attachment: none
consistency: moist
surface: smooth, glistening
vascular endothelium: smooth, intact
organization: none
structure: homogenous

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11
Q

virchow’s triad

A
  1. endothelial injury/dysfunction
  2. alterations in normal blood flow
    - turbulence
    - stasis
  3. hypercoagulability
    - primary
    - secondary
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12
Q

endothelial injury

A

heart: endocardium-> infarction, infection (myocarditis), immune reactions
valves: inflammation, prostheses (on edges-> vegetations)
arteries: ulcerated, atherosclerotic plaques, vasculitis

other causes: radiation, bacterial agents, chemical agents, catheter

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13
Q

alterations blood flow

A

turbulence

stasis

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14
Q

turbulence

A

arterial and cardiac thrombi

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15
Q

stasis

A

venous thrombi
mechanism:
-flow of blood is laminar: platelets in axial stream
-stasis &turbulence disrupt laminar flow, platelets, contact endothelium
-prevent dilution of activated clotting factors by fresh blood
-retard inflow of inhibitors of coagulation, permit build-up of thrombi
-promote endothelial cell activation

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16
Q

examples in alteration of blood flow

A
  • aneurysms-> abnormal dilatation of vessels
  • MI: necrotic myofibers do not contract
  • ulcerated atherosclerotic plaques: local turbulence
  • hyperviscosity syndrome (polycthemia)-> slow blood flow
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17
Q

hypercoagulability: primary

A

genetic defects/deficiencies

  • factor V leiden
  • prothrombin mutation
  • elevated homocysteine levels
  • antithrombin III def.
  • protein C/S deficiency
  • defects in fibrinolysis
18
Q

hypercoagulability: secondary

A

acquired hypercoagulability states

  • oral contraceptives
  • cancer-> procoagulant tumor products (pancreatic cancer-> migrating thrombophlebitis)
  • aging-> increased platelet aggregation
  • heparin-induced thrombocytopenia
  • anti-phospholipid antibody syndrome (lupus)
19
Q

fate of a thrombus

A

propagation-> gets larger and moves towards heart
detachment (embolization)
lysis/dissolution
retraction-> incorporated into vessels
organization with fibrosis
recanalization: formation of capillary channels through thrombus with blood flow through lumina

20
Q

types of thrombi

A

arterial
venous
vegetations

21
Q

arterial thombi

A

occlusive

coronary, cerebral, femoral arteries

22
Q

venous thrombosis

A

thrombophelbitis

  • red, or stasis thrombi
  • more red cells, fewer platelets
  • most in deep veins of legs (pulmonary emboli)
23
Q

embolism

A

detached intravascular solid, liquid, or gaseous masses carried by the blood stream to distant sites

  • fibrinous (thrombo) emobolus-> derived from fibrin thrombus, accounts for most emboli (99% emboli)
  • deep venous thrombosis to pulmonary embolism
  • cardiac thrombi to brain
  • atheromatous debris
  • bacterial (septic) embolus
  • fat embolus: sequel to bone fracture
24
Q

gas embolus

A

rapid decompression > gas out of solution > gas bubbles

25
Q

parasitic embolus

A

parasites in circulation (e.x filarial nematodes)

26
Q

neoplastic embolus

A

metastasis involves entry into an dispersion by circulation

27
Q

fibrocartilaginous embolus

A

ruptured vertebral disc fragments

28
Q

amniotic fluid embolus

A

tear in placenta and infusion of amniotic cells into circulation

29
Q

foreign bodies

A

bullets, catheters, hairs

30
Q

pulmonary emboli

A

-often arise from thrombi in deep veins of lower legs
-most are CLINICALLY SILENT
-sequela:
sudden death
pulmonary hemorrhage
pulmonary infarction
pulmonary hypertension

31
Q

why is it hard to infarct the lungs?

A

dual blood supply

-saddle embolus

32
Q

systemic emboli

A

emboli traveling in arterial circulation

-others arise from aneurysms, atherosclerotic plaques

33
Q

where do 80% of systemic emboli arise?

A

intracranial mural thrombi
-associated with: left ventricular wall infarcts or dilated left atria
atrial fibrillation

34
Q

infarction

A

localized ischemic necrosis resulting from sudden reduction either of arterial blood supply or of venous drainage

35
Q

types of infarctions

A

red

white

36
Q

causes of infarcts

A

Arterial thrombi/thromboemboli
-local vasospams
-extrinsic vascular compression (tumor)
Expansion of antheromas with hemorrhage within plaque
Mechanical-> torsions (testis or bowel), entrapment in hernia sac
Vascular compromise by edema (anterior compartment syndrome)

37
Q

most common cause of infacrts

A

arterial thrombi/thromboemboli

38
Q

white infarcts

A

arterial occlusions in solid tissue (tissue to dense for seepage of blood into infarcted area)

  • grossly pale
  • more common
  • mainly embolic
  • well defined borders
  • if wedged-shaped-> apex points towards focus of occlusion
39
Q

red infarcts

A

hemorrhagic

  • grossly red
  • may occur with venous occlusion
  • when blood flow is re-established after arterial occlusion
  • previously congested tissue, sluggish venous outflow
  • tissue with dual blood supplies: pulmonary, small intestine, liver
  • septic infarcts
40
Q

common sites of infarction from arterial emboli

A 
brain
retina
heart (left ventricle)
kidney
small intestine
lower leg
41
Q

microscopic features

A
  • coagulative necrosis (expect brain), sharply demarcated
  • +/- occluded vessels, +/- congestion
  • congestion and leukocyte influx in adjacent tissue, later fibrosis
42
Q

outcome of infarcts are dependent on

A

-tissue susceptibility->brain

collateral circulation-> kidneys versus muscle

dual blood supply: lung, liver

Pathology- fluid Hemodynamics (4 decks)

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