Hemodynamic disorders Flashcards

1
Q

fluid homeostasis requires:

A
  • vascular wall integrity
  • control of intravascular volume, pressure, protein
  • normal clotting mechanisms
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2
Q

Edema

A

increased fluid in tissue interstitial spaces

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3
Q

Pleural effusion/hydrothorax

A

-fluid accumulation in pleural space

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4
Q

ascites

A
  • fluid accumulation in the abdominal cavity

- aka hydroperitoneum

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5
Q

pericardial effusion

A
  • hydropericardium

- edema fluid accumulation in pericardial sac

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6
Q

anasarca

A

serve and generalized edema w/ diffuse involvement of all interstitial tissues and grossly evident subQ swelling

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7
Q

Categories of edema

A
  • increased hydrostatic pressure/impaired venous return
  • decreased plasma oncotic pressure (hypoproteinemia)
  • lymphatic obstruction
  • sodium retention
  • inflammation
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8
Q

hyperemia

A
  • active process
  • arterioles dilate and let blood into tissue
  • erythema
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9
Q

congestion

A
  • passive process
  • decreased outflow of blood
  • cyanotic (blue-ish red) color
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10
Q

Hemorrhage

A
  • extravasation of blood due to vessel rupture
  • vascular injury
  • vascular disease +/- minor trauma
  • defects in clotting mechanism + minor trauma
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11
Q

hematoma

A

-blood accumulation in a space or tissue (coagulates)

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12
Q

petechiae

A
  • small (1-2mm) punctate hemorrhages
  • seen on skin or mucosal/serosal surfaces
  • low platelets (thrombocytopenia)
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13
Q

Purpura

A
  • slightly larger (>3mm) hemorrhages
  • low platelets
  • small vessel vasculitis
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14
Q

hemostasis

A
  • rapid formation of localized plug at site of vascular disruption
  • requires: vascular wall, platelets, and coagulation proteins
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15
Q

events leading to hemostasis

A
  • arteriolar vasoconstriction
  • platelet adherence, activation, and aggregation (von wilebrand factor) (primary hemostasis)
  • generation of thrombin and fibrin, w/ polymerization of fibrin and platelet aggregates (secondary hemostasis)
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16
Q

thrombosis

A

-pathologic activation of hemostatic mechanism (clot occurs inside blood vessel)

17
Q

Virchow triad

A
  • predispose to thrombosis
  • endothelial injury
  • hypercoagulability (genetic or acquired)
  • abnormal blood flow (stasis or turbulence)
18
Q

potential fates of thrombus

A
  • keep growing-propagate towards heart
  • resolution-gets broken down
  • pushed to one side
  • recanalization
  • pieces can break off-embolus
19
Q

embolus

A

-an intravascular solid, liquid, or gaseous mass that is detached from the vascular wall and is carried by the blood to a site distant from point of origin

20
Q

thromboembolus

A

-an embolus made up thrombosed blood (vast majority)

21
Q

pulmonary thromboembolism

A
  • most common type of embolism

- over 95% of these originate in deep venous system of lower limbs (DVT)

22
Q

saddle embolus

A

obstruct entire pulmonary inflow-block both arteries-rapidly fatal

23
Q

air embolism

A
  • causes: trauma, obstetrics

- generally at least 100ml necessary for clinical manifestations

24
Q

paradoxical embolism

A

-venous thromboembolism passing through an atrial or ventricular heart defect to lodge in the systemic arterial system

25
infarct
an area of ischemic necrosis caused by occlusion of arterial supply or venous drainage -nearly all result from arterial thrombosis or thromboembolism
26
hemorrhagic infarct
blood leaks back into tissue (dual blood supply)
27
anemic infarct
infarcted tissue never regains blood flow (end arterial)
28
factors that influence development of infarct
- nature of vascular supply - rate of occlusion of vascular supply - O2 content of blood - susceptibility of tissue to infarction
29
shock
cardiovascular collapse resulting in systemic hypoperfusion
30
hypovolemic shock
- substantial loss of intravascular volume - hemorrhage - plasma loss (burns, diarrhea, vomiting, dehydration
31
cardiogenic shock
- failure of pump | - MI, cardiac tamponade, saddle embolus
32
sepsis
- presence of various pus-forming or other pathogenic organisms, or their toxins, in blood or tissues - widespread infection w/ systemic inflammatory response
33
disseminated intravascular coagulation
- widespread activation of coagulation w/in blood vessels - consumption of coagulation factors as well as widespread activation of fibrinolytic system leads to excessive bleeding - hemorrhage and thrombosis at same time
34
acute respiratory distress syndrome (ARDS)
- shock lung - pulmonary dysfunction caused by diffuse alveolar capillary damage - endothelial damage in lungs leads to protein leakage across walls -> creates a hyaline membrane that blocks gas exchange - histologic change = diffuse alveolar damage (DAD)
35
multisystem organ failure
- terminal complication in fatal cases of septic shock | - hypoxemia/acidosis, oliguria/anuria, and confusion, ischemic complications