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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What is hemostasis?

A

blood clotting that prevents excess bleeding after blood vessel damage

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2
Q

What is inappropriate clotting?

A

thrombosis

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3
Q

What is migration of clots?

A

embolism

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4
Q

What is hyperemia? Where is it often seen?

A
  • active process, arteriolar dilation & increased blood inflow
  • RED - oxygenated Hb
  • sites of inflammation or active sk. m.
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5
Q

What is congestion? When is it seen?

A
  • passive process, impaired outflow of venous blood from a tissue
  • blue/red (cyanosis) - deoxygenated Hb
  • cardiac failure or isolated venous obstruction
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6
Q

What does chronic congestion in the liver look like?

A

dark marks = nutmeg liver
necrosis / mush

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7
Q

What is edema?

A

accumulation of interstitial fluid in tissues

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8
Q

How much fluid in each compartment?

A

60% bw is water & 2/3 is intracellular
remaining is interstitial fluid
5% in blood plasma

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9
Q

What is an effusion? examples?

A

extravascular fluid that collects in body cavities
- hydrothorax (pleural cavity)
–> CHF
- hydropericardium
- hydroperitoneum / ascites
–> severe liver dx

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10
Q

What is anasarca?

A

severe, generalized edema due to fluid retention in tissues & cavities
–> weight gain & organ failure

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11
Q

What can cause anasarca?

A

severe kidney dx, malnutrition

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12
Q

What factors dictate fluid movement between vascular & interstitial spaces?

A
  • colloid osmotic pressure (proteins)
  • vascular hydrostatic pressure
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13
Q

How to manipulate factors to increase fluid seeping out into interstitial space?

A
  • increase hydrostatic pressure
  • decrease colloid osmotic pressure
    *capacity of lymphatic drainage is exceeded by fluid leakage
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14
Q

What typically causes increased hydrostatic pressure?

A
  • disorders impairing venous return
    –> deep vein thrombosis, CHF
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15
Q

What typically causes decreased plasma osmotic pressure?

A
  • reduced plasma albumin from loss in circulation OR reduced synthesis
    –> nephrotic syndrome (capillaries destroyed & albumin accumulation in urine/less in circulation)
    –> severe liver dx (reduced synthesis)
    –> malnutrition
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16
Q

What can cause lymphatic obstruction & edema?

A
  • inflammatory conditions (bacteria, etc)
  • neoplastic conditions (cancer)
  • congenital lymphedema
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17
Q

What are the stages of lymphedema?

A

1: asymptomatic, abnormal flow, no fluid build up
2: swelling, accumulation of fluid, may reverse when elevated
3: permanent swelling, not relieved along with fibrosis of skin
4: lymphostatic elephantiasis, deformation of limb due to swelling & fibrosis

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18
Q

What is hemorrhage?

A

extravasation of blood from vessels

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19
Q

What causes hemorrhage?

A
  • defective clot formation
  • trauma
  • atherosclerosis
  • inflammatory
  • neoplastic condition
  • inherited/acquired defects
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20
Q

List hemorrhage manifestations in order of increasing size.

A
  • petechiae
  • purpura
  • ecchymoses
  • hematoma
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21
Q

What often causes petechiae?

A
  • thrombocytopenia
  • vitamin C deficiency
  • infectious mononucleosis
  • trauma: coughing
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22
Q

What are the primary regulators of hemostasis?

A

endothelial cells

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23
Q

4 basic steps of thrombus formation & dissolution?

A
  • vasoconstriction
  • platelet plug
  • fibrin deposition
  • clos stabilization & resorption
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24
Q

Describe the vasoconstriction step of clot formation in detail.

A
  • occurs immediately to reduce blood flow
  • mediated by neurogenic reflex
  • endothelial cells secrete endothelin
    –> transient reflex allows platelet activation
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25
Q

What occurs during primary hemostasis?

A
  • formation of platelet plug
  • disruption of endothelium exposes BM collagen & VW factor
    –> conformational change of platelet when interact/adhere with vW factor
    –> release secretory granules to recruit more platelets & form a plug
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26
Q

What occurs during secondary hemostasis?

A
  • activation of clotting factors & fibrin
  • Tissue Factor is exposed & released: procoagulant glycoprotein on subendothelial cells
  • clotting cascade started –> thrombin converts fibrinogen to fibrin (mesh)
  • stabilizes clot & further activates platelets to aggregate
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27
Q

What occurs in clot resorption?

A
  • Tissue plasminogen activator from endothelial cells expressed (t-PA)
    –> limits clotting & resorbs clot (fibrinolysis)
  • thrombomodulin blocks coagulation cascade as counter regulatory mechanism to only affect site of injury
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28
Q

What are platelets?

A
  • disk-shaped, anucleate fragments of megakaryocytes
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29
Q

What mediates platelet adhesion?

A

vW factor

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30
Q

What are some congenital deficiencies that lead to bleeding disorders?

A
  • vW factor deficiency (adhesion to wall affected)
    –> gene mutation
    –> less produced (severity differs)
  • Glanzmann thrombasthenia
  • Bernard-Soulier syndrome
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31
Q

What is the coagulation cascade?

A
  • series of amplification enzymatic rxns leads to deposition of insoluble fibrin clot
  • secondary hemostasis
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32
Q

What are the two coagulation cascade pathways?

A
  • intrinsic: spontaneous, internal injury
  • extrinsic: activated by external trauma
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33
Q

What activates intrinsic & extrinsic pathways?

A

intrinsic = damaged endothelial surface
extrinsic = tissue factor

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34
Q

What test evaluates intrinsic / extrinsic paths?

A

PT = extrinsic
PTT = intrinsic

35
Q

What is the common path?

A

prothrombin –> thrombin
fibrinogen –> fibrin

36
Q

Importance of vitamin K?

A
  • regulation of coagulation / key role in synthesis of many factors
  • synthesize protein C & S –> negative feedback regulation
37
Q

What occurs with vitamin K deficiency?

A
  • increased bruising & bleeding
38
Q

What is Warfarin & what does it do?

A
  • anticoagulant medication
  • antagonist for vitamin K
    –> inhibits clotting
39
Q

What is the most important coagulation factor?

A

thrombin

39
Q

What is the function of thrombin?

A

converts fibrinogen to fibrin
activates platelets
pro-inflammatory
anti-coagulation effects (prevent clotting after vascular repair)

40
Q

What are the factors limiting coagulation?

A
  • dilution of blood past site of injury
  • negatively charged phospholipids required (do not bind - platelets)
  • regulation by neighboring intact endothelium
  • fibrinolytic cascade limits size of clot
    –> plasmin activation
41
Q

How does the endothelium limit coagulation?

A
  • barrier to platelets interacting with vWF & collagen
  • releases NO, prostacyclin, and adenosine diphosphate
  • anticoagulant: factors inactivate thrombin
  • fibrinolytic effects: make tPA
42
Q

What is thrombosis? Examples?

A
  • pathologic state of endothelial injury
  • coronary artery dx, MI, HTN
  • chronic injury (physical, infectious, abnormal blood flow, inflammatory mediators, toxins)
43
Q

How does abnormal flow cause thrombosis?

A
  • promote endothelial procoagulant activity
  • stasis allows platelets & leukocytes to associate with endothelium
  • stasis slows removal of activated clotting factors, impedes inflow of clotting factor inhibitors
44
Q

What is hypercoagulability?

A
  • abnormally high tendency for blood to clot
45
Q

What is an important risk factor for venous thrombosis?

A

hypercoagulability

46
Q

What are the primary/genetic hypercoagulable states?

A
  • Factor V mutation
  • prothrombin mutation
  • increased levels of factor VIII, IX, or XI or fibrinogen
47
Q

What are the secondary/acquired hypercoagulable states?

A
  • prolonged bed rest / immobilization
  • MI
  • atrial fibrillation
  • tissue injury (surgery, fracture, burn)
  • cancer
  • prosthetic cardiac valves
  • disseminated intravascular coagulation
  • heparin-induced thrombocytopenia -
  • anti-phospholipid antibody syndrome
48
Q

Where do thrombi develop?

A
  • anywhere in cardiovascular system
    –> arterial: sites of injury
    –> cardiac mural: heart chambers/aorta
    –> venous: sites of stasis
49
Q

What are lines of Zahn?

A
  • laminations observed grossly & microscopically in LIVING pt
  • differentiates antemortem clots from postmortem clots
50
Q

Describe arterial thrombi.

A
  • typically rich in platelets
  • often formed by endothelial injury
51
Q

Describe venous thrombi.

A

contain high volume RBC
90% in legs / lower venous circulation

52
Q

What are the fates of thrombi?

A
  • propagation: enlarges
  • embolization: dislodged & moved by circulatory system
  • dissolution: activation of fibrinolytic factors
  • organization & recanalization: older thrombi reorganized to facilitate some function
53
Q

Venous thrombosis of superficial vs deep veins?

A

superficial:
- local congestion & swelling from impaired venous flow (varicose veins)

deep:
- deep venous thrombosis, larger veins
- may be asymptomatic 50%
- may embolize to lungs
**more serious

54
Q

What are varicose veins?

A
  • superficial venous thrombosis
  • damaged valve
  • twisted, large, & painful veins
55
Q

What is a major cause of arterial & cardiac thrombosis? Why?

A
  • atherosclerosis
  • loss of endothelial integrity & abnormal flow
    –> MI, ischemia to organs (brain, kidney, spleen)
56
Q

Which organs have rich blood supply?

A
  • brain, spleen, kidneys
57
Q

What is DIC?

A
  • disseminated intravascular coagulation
  • widespread thrombosis within microcirculation
  • consumption of platelets & clotting factors
  • net result: excessive clotting & bleeding
58
Q

DIC may occur from complications in?

A

obstetrics, injuries, cancer, etc.

59
Q

Describe an embolism?

A
  • solid, liquid, or gas mass carried by blood from point of origin to distant site
60
Q

What is a common source of embolism?

A

thrombus

61
Q

What are the types of embolism?

A
  • pulmonary
  • systemic thromboembolism
  • fat
  • amniotic fluid
  • air
62
Q

What is a pulmonary embolism?

A
  • most common
  • mostly from upper deep leg veins
  • lodge in pulmonary artery / arterioles
  • multiple can occur
  • most small & progressively become organized
  • large ones can cause sudden death
  • multiple over time causes pulmonary HTN & right ventricular failure
63
Q

What is systemic thrombocytopenia?

A
  • arise from intracardiac mural thrombi (80%)
  • can embolize to lower extremities most frequently + CNS, intestines, kidney & spleen
64
Q

What is fat embolism?

A
  • Injury to bone marrow causes release of fat globules into circulation
  • rare clinical manifestations
  • <10% pulmonary prob, neuro prob, anemia, thrombocytopenia, & petechial rash
65
Q

What is amniotic fluid embolism?

A
  • severe post-birth complication
  • 80% mortality due to biochemical activation of coagulation system & immune system
  • amniotic fluid enters into mothers circulation
66
Q

What is air embolism?

A
  • gas in circulation obstructs vascular flow
    ex. decompression sickness in divers
67
Q

What is an infarction?

A
  • area of ischemic necrosis caused by occlusion of vascular supply to affected tissue
68
Q

Common organs involved in complications of infarctions?

A
  • brain & heart
69
Q

Most infarction arise from what ?

A
  • arterial thrombosis
  • embolism
70
Q

How to classify an infarction?

A

COLOR
- Red: contain hemorrhage
- White: arterial occlusion in solid organs

71
Q

Where are red infarctions?

A
  • venous occlusion
  • loose tissue (lungs)
  • tissue with dual circulation
  • previously congested tissue
  • reperfusion injury
72
Q

Where are white infarctions?

A
  • heart, liver, spleen
73
Q

What is shock?

A
  • state with diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion & leads to cellular hypoxia
74
Q

What type of shock leads to irreversible tissue injury?

A

prolonged

75
Q

What are the types of shock?

A
  • cardiac
  • septic
  • hypovolemic
  • anaphylactic
76
Q

What are examples of cardiac shock?

A
  • MI
  • ventricular rupture
  • arrhythmias
    -cardiac tamponade
  • pulmonary embolism
77
Q

What is the principal pathogenic mechanism of cardiogenic shock?

A
  • failure of myocardial PUMP from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
78
Q

What are examples of hypovolemic shock?

A
  • hemorrhage
  • fluid loss
79
Q

What is the principal pathogenic mechanism of hypovolemic shock?

A

inadequate blood or plasma volume

80
Q

What are examples of septic shock?

A
  • microbial infections
  • gram - sepsis
  • gram + septicemia
  • fungal sepsis
  • superantigens
81
Q

What is the principal pathogenic mechanism of septic shock?

A

peripheral vasodilation & pooling of blood
endothelial activation
leukocyte induced damage
disseminated intravascular coagulation
activation of cytokine cascades

82
Q

What causes anaphylactic shock ?

A

type 1 hypersensitivity

Pathology (9 decks)

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