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PATHOLOGY EXAM 2 > lecture 1- hemodynamic disorders > Flashcards

lecture 1- hemodynamic disorders Flashcards

1
Q

delivers oxygen and nutrients to tissues

wastes are removed

A

circulation

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2
Q

blood clotting that prevents excess bleeding after blood vessel damage

A

hemostasis

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3
Q

inappropriate clotting

A

thrombosis

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4
Q

migration of clots

A

embolism

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5
Q

active process, arteriolar dilation and increased blood inflow

A

hyperemia

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6
Q

oxygenated hemoglobin

A

red color (hyperemia)

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7
Q

passive process, impaired outflow of venous blood from a tissue

A

congestion

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8
Q

deoxygenated hemoglobin

A

blue/red (cyanosis) (congestion)

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9
Q

__% of body weight is water
2/3 intracellular

only ___% blood plasma

A

60% water
5% blood plasma

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10
Q

accumulation of interstitial fluid in tissue

A

edema

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11
Q

two types of edema

A

effusions
anasarca

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12
Q

extravascular fluid that collects in body cavities

pleural cavity- hydrothorax
pericardial cavity- hydropericardium
peritoneal cavity- hydroperitoneum or ascites

A

effusions

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13
Q

seve generalized edema due to fluid retention in tissues and cavities

A

anasarca

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14
Q

vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins) dictate fluid movement between vascular and interstitial spaces

A

capillary fluid movement

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15
Q

in capillary fluid movement, arterial outflow is normally balanced by:

this results in small net outflow of fluid in interstitial space-> drained by_____

A

inflow at the venous end

drained by lymphatics

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16
Q

this is usually caused by disorders that impair venous return

A

increased hydrostatic pressure

(deep venous thrombosis, congestive heart failure

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17
Q

may result from loss in circulation or reduced synthesis

A

reduced plasma albumin concentration
(reduced plasma osmotic pressure)
-nephrotic syndrome, severe liver disease

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18
Q

compromises resorption of fluid from interstitial spaces-> leads to ___

A

this is lymphatic obstruction

-> leads to edema

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19
Q
  1. inflammatory conditions (bacterial/parasitic infection)
  2. neoplastic condition (breast cancer)
  3. congenital lymphedema
A

lymphatic obstructions

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20
Q

extravasation of blood from vessels

A

hemorrhage

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21
Q

defective clot formation, trauma, atherosclerosis, inflammatory, neoplastic conditions, inherited/acquired defects

A

hemorrhages

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22
Q

4 types of hemorrhage manifestations

A

hematoma
ecchymoses
purpura
petechiae

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23
Q

large collection of hemorrhage in a tissue

A

hematoma

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24
Q

1-2cm subcutaneous hemorrhage (bruises)

A

ecchymoses

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25
Q

3-5mm hemorrhages

A

purpura

26
Q

1-2mm minute hemorrhage
-often consequences of thrombocytopenia, vitamin C deficiency

A

petechiae

27
Q

these cells are the primary regulators of hemostasis through changes in expression of procoagulant factors

A

endothelial cells
(clot formation)

28
Q

clot formation steps

A
  1. vasoconstriction
  2. platelet plug forms
  3. fibrin deposition
  4. clot stabilization
29
Q

disk shaped, anculeate fragments of megakaryocytes

A

platelets

30
Q

platelet adhesion is mediated by

A

von willenbrand factor

31
Q

congenital deficiency of receptors or molecules may lead to bleeding disorders

A

platelets

32
Q

series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot
-secondary hemostasis

A

coagulation cascade

33
Q

spontaneous, internal to vascular endothelium

what pathway for coagulation cascade

A

intrinsic pathway

34
Q

activated by external trauma

what pathway for coagulation cascade

A

extrinsic pathway

35
Q

this evaluates intrinsic pathway factors
XII, XI, IX, VIII, X, V, prothrombin (II), fibrinogen (I)

A

partial prothrombin time PPT

36
Q

evaluates the extrinsic pathway factors
VII, X, V, prothrombin(II), fibrinogen (I)

A

prothrombin time PT

37
Q

important for regulation of coagulation, plays key role in synthesis
factors II, VII, IX, X

A

vitamin K

38
Q

helps synthesize protein C and S: important for negative feedback regulation of clotting cascade

A

vitamin K

39
Q

vitamin K deficiency does what

A

increased bruising and bleeding

40
Q

anticoagulant mediation, antagonist for vitamin K

inhibits clotting

A

warfarin

41
Q

most important coagulation factor
-converts fibrinogen into crosslinked fibrin
-activates platelets
-pro inflammatory effects
-anticoagulation effects

A

thrombin

42
Q

4 factors limiting coagulation

A
  • Dilution of blood past the site of injury
  • Negatively charged phospholipids required -activated platelets
  • Regulation by neighboring intact endothelium
  • Fibrinolytic cascade limits size of clot (Plasmin activation essential)
43
Q
  1. Serves as barrier to platelets
  2. Anticoagulant effects
  3. Fibrinolytic effects
A

endothelium and coagulation limitation

44
Q

Endothelial injury
* Coronary artery disease, MI
* Chronic inflammation – physical injury, infectious agents, abnormal blood flow,
inflammatory mediators, toxins

A

thrombosis

45
Q
  1. abnormal blood flow
    * Promote endothelial procoagulant activity
    * Stasis allows platelets and leukocytes to associate with endothelial cells
    * Stasis slows removal of activated clotting factors, and impedes inflow of clotting
    factor inhibitors
A

thrombosis

46
Q

abnormally high tendency for blood to clot
* Important risk factor for venous thrombosis
* Primary (genetic) vs secondary (acquired) disorders

A

thrombosis

47
Q

Can develop anywhere in cardiovascular system

Lines of Zahn: observed grossly and microscopically

A

thrombi

48
Q

4 fates of thrombi

A
  1. propagation: clot enlarges
  2. embolization: clot dislodged and moved by circulatory system
  3. dissolution- activation of fibrinolytic factors
  4. organization and recanalization- older thrombi are reorganized to facilitate some function
49
Q

most occur in veins in leg

  • Superficial veins: local congestion and swelling from impaired venous flow
    -Ex: varicose veins
    *Deep veins: deep venous thrombosis, larger veins
    -May be asymptomatic in 50% of patients
    -May embolize to lungs
A

venous thrombosis

50
Q
  • Atherosclerosis is a major cause
  • Results in loss of endothelial integrity and abnormal blood flow
  • Leads to MI, ischemia to organs (especially brain, kidney, spleen)
A

arterial and cardiac thrombosis

51
Q
  • Widespread thrombosis within microcirculation
  • Consumption of platelets and clotting factors
  • May occur from complications in obstetrics, injuries, cancer, and more
  • Net result: excessive clotting and bleeding
A

DIC- disseminated intravascular coagulation

52
Q

May be a solid, liquid or gaseous mass, carried by the blood from its point of
origin to a distant site

A

embolism

53
Q

area of ischemic necrosis caused by occlusion of the vascular supply to the
affected tissue

involvement of heart and brain is common complication

A

infarction

54
Q

where are most infarctions

A

arterial thrombosis or embolism

55
Q

infarctions are classified according to

A

color

56
Q

Red infarct:

(Venous occlusion, loose tissue (ie: lungs), tissue with dual circulation, previously
congested tissue, reperfusion injury)

A

contain hemorrhage

57
Q

white infarct

(heart, liver, spleen)

A

arterial occlusion in solid organs

58
Q

this shock leads to irreversible tissue injury

A

prolonged shock

59
Q

A state in which diminished cardiac output or reduced effective circulating
blood volume impairs tissue perfusion and leads to cellular hypoxia

A

shock

60
Q

three types of shock

A

cardiac
hypovolemic
septic

PATHOLOGY EXAM 2 (6 decks)

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