Fluid hemodynamics disorders II

Question 1

thrombus

Answer 1

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

Question 2

Clot

Answer 2

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

Question 3

post-mortem clot composition

Answer 3

coagulation factors and erythrocyte only

Question 4

gross appearance of postmortem clot

Answer 4

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.

Question 5

thrombus gross appearance

Answer 5

heterogeneous

Question 6

arterial thrombi

Answer 6

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

Question 7

venous thrombi

Answer 7

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

Question 8

composition of thrombus

Answer 8

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)

Question 9

criteria for thromus

Answer 9

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

Question 10

criteria for PM clot

Answer 10

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

Question 11

virchow’s triad

Answer 11

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

Question 12

endothelial injury

Answer 12

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

Question 13

alterations blood flow

Answer 13

turbulence

stasis

Question 14

turbulence

Answer 14

arterial and cardiac thrombi

Question 15

stasis

Answer 15

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

Question 16

examples in alteration of blood flow

Answer 16

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

Question 17

hypercoagulability: primary

Answer 17

genetic defects/deficiencies

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

Question 18

hypercoagulability: secondary

Answer 18

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)

Question 19

fate of a thrombus

Answer 19

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

Question 20

types of thrombi

Answer 20

arterial
venous
vegetations

Question 21

arterial thombi

Answer 21

occlusive

coronary, cerebral, femoral arteries

Question 22

venous thrombosis

Answer 22

thrombophelbitis

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

Question 23

embolism

Answer 23

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

Question 24

gas embolus

Answer 24

rapid decompression > gas out of solution > gas bubbles

Question 25

parasitic embolus

Answer 25

parasites in circulation (e.x filarial nematodes)

Question 26

neoplastic embolus

Answer 26

metastasis involves entry into an dispersion by circulation

Question 27

fibrocartilaginous embolus

Answer 27

ruptured vertebral disc fragments

Question 28

amniotic fluid embolus

Answer 28

tear in placenta and infusion of amniotic cells into circulation

Question 29

foreign bodies

Answer 29

bullets, catheters, hairs

Question 30

pulmonary emboli

Answer 30

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

Question 31

why is it hard to infarct the lungs?

Answer 31

dual blood supply | -saddle embolus

Question 32

systemic emboli

Answer 32

emboli traveling in arterial circulation | -others arise from aneurysms, atherosclerotic plaques

Question 33

where do 80% of systemic emboli arise?

Answer 33

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

Question 34

infarction

Answer 34

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

Question 35

types of infarctions

Answer 35

red | white

Question 36

causes of infarcts

Answer 36

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)

Question 37

most common cause of infacrts

Answer 37

arterial thrombi/thromboemboli

Question 38

white infarcts

Answer 38

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

Question 39

red infarcts

Answer 39

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

Question 40

common sites of infarction from arterial emboli

Answer 40

``` brain retina heart (left ventricle) kidney small intestine lower leg ```

Question 41

microscopic features

Answer 41

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

Question 42

outcome of infarcts are dependent on

Answer 42

-tissue susceptibility->brain collateral circulation-> kidneys versus muscle dual blood supply: lung, liver