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MAD Exam 1 > Coagulation and Hemostasis > Flashcards

Coagulation and Hemostasis Flashcards

1
Q

edema

A

abnormal fluid accumulation in tissue or body cavity
-in body cavities, we call it hydrothorax, hydropericardium, hydroperitoneum (ascites)
-can be transudate or exudate

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2
Q

transudate

A

low-protein content in edematous fluid
-mechanism usually due to increased pressures

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3
Q

exudate

A

protein-rich edematous fluids
-mechanism usually due to leaky vessels

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4
Q

anasarca

A

massive edema

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5
Q

hemorrhage

A

loss of blood from vessels

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6
Q

increased hydrostatic pressure - pathogenesis of edema

A

can lead to local or systemic edema
etiologies include:
-congestive heart disease
-portal hypertension
-venous obstruction/stasis

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7
Q

reduced plasma osmotic pressure - pathogenesis of edema

A

usually leads to systemic edema, and often associated with hypoalbuminemia (low albumin)
etiologies include:
-nephrotic syndrome
-cirrhosis/liver failure (ascites)
-protein malnutrition
-gastroenteropathy

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8
Q

lymphatic obstruction - pathogenesis of edema

A

usually leads to localized edema
etiologies include:
-inflammation
-parasites
-neoplasia
-iatrogenic/post-surgical

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9
Q

inflammation - pathogenesis of edema

A

usually leads to localized edema

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10
Q

sodium retention - pathogenesis of edema

A

usually leads to systemic edema
etiologies include:
renal insufficiency

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11
Q

hyperemia

A

increased blood in an area compared to normal, due to increased blood flow due to ARTERIAL DILATION
-active process
-organ turns red and hot, because this is increased oxygenated blood

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12
Q

congestion

A

increased blood in area compared to normal, due to impaired OUTFLOW from a tissue (constricted venules)
-passive process
-affected region is cyanotic because of increased deoxygenated blood

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13
Q

examples of congestion

A

-hepatic chronic passive congestion due to right-sided CHF (blood backup in liver)
-pulmonary chronic passive congestion due to left-sided CHF (blood backup in lungs)

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14
Q

hemorrhage

A

extravasation of blood because of vessel rupture

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15
Q

etiologies of hemorrhage

A

TRAUMA (most common), inflammatory, neoplastic

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16
Q

hematoma

A

trapped hemorrhage

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17
Q

ecchymoses

A

bruise; > 1-2 cm
-usually from trauma

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18
Q

purpura

A

> 3 mm hemorrhages
-etiologies include vasculitide, thrombocytopenia, platelet/clotting coag defects, infections

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19
Q

petechia

A

1-2 mm hemorrhages (tiny)
-etiologies include thrombocytopenia, platelet/clotting coagulation defects, capillary abnormalities
-specific locations include skin, mucous membranes, serosal surfaces

20
Q

massive hemorrhage filling a body cavity

A

hemothorax, hemopericardium, etc

21
Q

hemostasis

A

well-regulated processes to:
1) maintain blood in fluid, clot-free state AND
2) induce rapid and localized hemostatic plug at site of vascular injury

22
Q

3 components of hemostasis

A
  1. endothelial cells
  2. platelets
  3. coagulation cascade
23
Q

normal function of endothelium during hemostasis

A

inhibit thrombosis (normal endothelial cells prevent blood clotting)
-inactivates thrombin and factors Xa and IXa
-inhibit platelet aggregation

24
Q

endothelial cells after cell injury

A

favor thrombosis (tell the blood to clot)
-exposure of membrane-bound tissue factor initiates extrinsic coagulation sequence
-express vWF, which promotes platelet aggregation

25
Q

platelets and hemostasis

A
  1. adhesion and conformational shape change (exposed vWF interacts with platelet glycoprotein Ib receptor)
  2. secretion (release of pro-binding chemokines and cofactors like Ca2+; exposure of phospholipid membrane/complex)
  3. aggregation (fibrinogen links platelets via GpIIb-IIIa; secrete thromboxane, ADP, and aggregating factors)
26
Q

antithrombin III - coagulation inhibition

A

inhibits factors XIIa, XIa, Xa, IXa, and thrombin
*heparin stimulates antithrombin III

27
Q

proteins C and S - coagulation inhibition

A

proteins C and S inactivate Va and VIIIa (accelerants)
*activated by thrombin and thrombomodulin

28
Q

plasmin

A

plasminogen is activated to plasmin, which DEGRADES FIBRIN
-activated by tPA

29
Q

thrombosis

A

inappropriate activation of normal hemostasis (formation of blood clots in normal vasculature)
*pathologic opposite to hemostasis

30
Q

what causes thrombosis

A

pathologic endothelial injury (ex. atherosclerosis)

31
Q

stasis

A

venous thrombosis (ex. DVT)

32
Q

turbulence

A

arterial thrombosis
-disruption of laminar flow
*common where there is bifurcation of blood vessels

33
Q

arterial thrombi

A

common sites: coronary, cerebral, femoral
-begin at site of endothelial injury
**Lines of Zahn

34
Q

lines of Zahn

A

alternating pale layers of platelets with dark layers of trapped RBCs; imply thrombosis at site of blood flow
**characteristic of ARTERIAL thrombosis

35
Q

venous thrombi

A

common sites: veins of lower extremities and gonadal veins
-occur at sites of stasis (sluggish blood flow)
-impaired venous outflow increases hydrostatic pressure and can cause edema

36
Q

sequelae of thrombus - what can happen to a thrombus after it forms

A
  1. propagation (obstruction of a blood vessel)
  2. embolization (thrombi may dislodge and travel to other sites in vasculature)
  3. dissolution (thrombi may be removed by fibrinolytic activity)
  4. organization and recanalization (thrombi induce inflammation, fibrosis, and re-endothelialization, ultimately re-establishing vascular flow)
37
Q

embolization

A

detached intravascular solid, liquid, or gas carried by blood to distant site from point of origin
*typically caused by dislodged thrombi

38
Q

pulmonary thromboembolism

A

-usually originate from deep leg vein thrombi
-passes through the right heart into pulmonary vasculature

39
Q

systemic thromboembolism

A

-arise from/traveling within ARTERIAL circulation
-commonly from a cardiac mural thrombi (thrombus in the wall of the heart)
-travels to lower extremities, brain, etc

40
Q

fat embolism

A

common following fracture of long bones with fatty marrow

41
Q

air embolism

A

most commonly associated with chest wall injury or decompression sickness (the bends)

42
Q

tumor embolism

A

tumor enters circulation and acts like a blood clot, then pieces go wherever the blood flow goes

43
Q

amniotic fluid embolism

A

amniotic membrane tear and rupture of uterine veins
-rare complication of labor

44
Q

infarction

A

ischemic necrosis caused by occlusion of arterial supply or venous drainage

45
Q

red/hemorrhagic infarct

A

-VENOUS occlusions
-commonly impacts loose tissues or tissues with dual circulations; blood pools from other blood supplies to re-perfuse the tissue

46
Q

white/pale infarcts

A

-ARTERIAL occlusions
-commonly impact solid organs (heart, spleen, kidneys)
-no dual blood supply
-no re-perfusion

MAD Exam 1 (20 decks)

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