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Patho 1 > Chap 4- Hemodynamic disorders > Flashcards

Chap 4- Hemodynamic disorders Flashcards

1
Q

balance concept of body fluid distribution

A
  • fluid loss = fluid intake

- electrolyte loss= electrolyte intake

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2
Q

how is fluid intake regulated?

A

thirst mechanism and drinking habits

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3
Q

how is electrolyte intake regulated?

A

dietary habits

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4
Q

how is fluid output regulated?

A

kidneys

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5
Q

how is electrolyte output regulated?

A

kidneys

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6
Q

interstitium

A
  • space between cells
  • outside of capillary
  • made of collagen fibers and proteoglycan
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7
Q

what are the determinants of net fluid movement?

A
  • capillary hydrostatic pressure (Pc)
  • interstitial fluid pressure (Pif)
  • plasma colloid osmotic pressure (Pi-p)
  • interstitial fluid colloid pressure (Pi-if)
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8
Q

capillary hydrostatic pressure

A
  • Pc
  • pressure comes from heart
  • forces fluid outward through capillary membrane
  • depends on arteriole resistance and venus pressure
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9
Q

interstitial fluid pressure

A
  • Pif

- opposes filtration/ capillary pressure

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10
Q

plasma colloid osmotic pressure

A
  • Pi-p
  • causes osmosis of water inward through membrane
  • albumin in plasma creates pressure
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11
Q

interstitial fluid colloid pressure

A
  • Pi-if

- causes osmosis of fluid outward through membrane

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12
Q

flitration

A
  • getting fluid/ion/solute outside of blood

- is a positive number

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13
Q

reabsorption

A
  • get fluid/ion/solute into blood

- is a negative number

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14
Q

how to calculate net filtration pressure

A

(Pc-Pif) - (Pi-p - Pi-if)

unit is mmHg

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15
Q

hyperemia

A
  • arteriolar dilation causes increased BF
  • affected tissue turns read
  • active process
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16
Q

congestion

A
  • reduced outflow of blood from tissue
  • can be systemic or localized
  • passive process
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17
Q

Edema

A
  • swelling caused by excess fluid in interstitial space in tissues
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18
Q

pathophysiology of edema

A
  1. increased capillary hydrostatic pressure
  2. decreased plasma proteins
  3. increased capillary permeability
  4. lymphatic failure
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19
Q

ways in which capillary hydrostatic pressure can be increase

A
  • excess fluid retention by kidneys
  • decreased arterial resistance
  • increased venous pressure
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20
Q

factors that protect against edema

A
  • lymphatic flow increases
  • fluid entry will raise interstitial pressure so fluid will move back towards capillary
  • fluid entry into interstitium lowers pressure by dilution and lymphatic mediated removal of interstitial proteins
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21
Q

effusion

A
  • accumulation of fluid in body cavities

- can be transudate or exudate

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22
Q

transudate effusion

A
  • protein poor
  • fluid leaks out of capillary but protein stays
  • causes pitting edma
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23
Q

exudate effusion

A
  • protein rich

- produces swelling but no pitting

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24
Q

major causes of systemic edema

A
  • heart failure
  • renal failure
  • reduced plasma osmotic pressure
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25
pulmonary edema
- usually caused by cardiac disease - fluid builds up in alveoli - cannot exchange gases as well
26
ascites
- extra fluid in peritoneal cavity | - results in abdominal distenstion
27
main causes of non-pitting edma
- moderate to severe lymphedema | - pretibial myxedema (associated with graves disease)
28
what is normal hemostasis?
- involves platelets, clotting factors, and endothelium - occurs at site of vascular injury - results in blood clot
29
what are the general sequence of events in normal hemostasis?
- vasoconstriction - primary hemostasis - secondary hemostasis - clot stabilization and resorption
30
what is primary hemostasis?
- formation of platelet plug - disruption of endothelial cells exposes vWF and collagen - promote platelet adherence
31
what is secondary hemostasis?
- deposition of fibrin
32
what is a coagulation cascade?
series of well orchestrated enzymatic reactions that leads to deposition of insoluble fibrin clot - intrinsic pathway - extrinsic pathway - common pathway
33
prothrombin time (PT) assay
- asses function of proteins in extrinsic pathway | - VII, X, V, II and fibrinogen
34
partial thromboplastin time (PTT) assay
- asses function of proteins in intrinsic pathway | - XII, XI, IX, VIII, X, V, II and fibrinogen
35
intrinsic pathway
XII -> XI -> IX -> VIII to common pathway
36
extrinsic pathway
VII -> common pathway
37
common pathway
X -> thrombin (protrombin also acts on thrombin) -> Fibrinogen (I) -> Fibrin clot (XIII)
38
Prolonged PT but normal aPTT
- factor VII deficiency - mild vit K deficiency - liver disease - warfarin admin
39
normal PT but prolonged aPTT
- deficiencies in factors VIII, IX, or XI | - Heparin admin
40
prolonged PT and aPTT
- deficiencies of prothrombin, fibrinogen, or factors X or V | - disseminated intravascular coagulation
41
role of thrombin
- conversion of fibrinogen into cross-linked - platelet activation - pro-inflammatory effects - anti-coagulent
42
antithrombotic properties of endothelium
- platelet inhibitory effects - anticoagulant effects - fibrinolytic effects
43
what are platelet inhibitory effects of endothelial cells?
- shield platelets from vWF and collagen | - synthesize PG, NO and ADP which inhibit platelet aggregation
44
what are anticoagulant effects of endothelial cells?
- thrombomodulin binds to thrombin | - endothelial protein C receptors bind to protein C which inactivates clotting factors
45
what are fibrinolytic effects of endothelial cells?
- synthesize t-PA (tissue type plasminogen activator) | - t-PA lyses fibrin clot
46
steps of clot formation
- subendothelial exposure - adhesion - activation - aggregation - platelet plug formation - clot retraction and clot dissolution
47
thrombosis
- blood clot with non-traumatized blood vessel - clot forms when it shouldn't - pathological condition
48
causes of thrombosis
- endothelial injury - abnormal blood flow - hypercoagulability
49
primary hypercoagulable state causes
- genetic | - factor V mutation or prothrombin mutation
50
secondary hypercoagulable state causes
- prolonged immobilization - MI - tissue injury - prosthetic cardiac valve - disseminated intravascular coagulation - hyperestrogenic shock, oral contraceptive use, smoking (lower risk)
51
fate of thrombus
- propagation - embolization - dissolution - organization and recanalization
52
thrombus propagation
- pile of platelets and fibrin on top of each other | - makes blood clot expand
53
thrombus embolization
- piece of thrombus breaks off and is mobilized- can go anywhere
54
thrombus dissolution
- fibrinolytic agents help to make blood clot go away
55
thrombus organization and recanalization
- makes tunnel in midle of thrombus - due to growth of endothelial cells, SMC, and fibroblasts - lysosomal enzymes digest center - more chance of blood flow
56
arterial and cardiac thrombosis
- occlusion of critical vessel | - prone to embolism in brain, kidneys, and spleen
57
Disseminated Intravascular Coagulation (DIC)
- complication that happens in systemic circulation - thrombin is activated - rapid burst of thrombin -> bleeding - gradual amount of excess thrombin -> thrombotic complications
58
Embolism
- traveling detached intravascular mass | - can happen for variety of reasons
59
infarction
- occlusion of either arterial supply or venous drainage - causes ischemic necrosis - majority due to arterial thrombosis/ embolism
60
factors that influence infarct development
- anatomy of vascular supply - rate of occlusion - tissue vulnerability to hypoxia
61
Shock
- state of cellular and tissue hypoxia | - most common is circulatory failure
62
major classifications of shock
- cardiogenic shock - hypovolemic shock - spetic shock
63
cardiogenic shock
- results from low cardiac output as a result of myocardial pump failure (heart failure)
64
hypovolemic shock
- low cardiac output due to loss of blood supply or plasma volume
65
septic shock
- triggered by microbial infections - infection is generalized - associated with severe systemic inflammatory response syndrome (SIRS)
66
major physiologic determinants of tissue perfusion
- cardiac output | - systemic vascular resistance
67
mechanism of shock
- cellular hypoxia - cell membrane ion pump dysfunction - intracellular edema - inadequate regulation of intracellular pH due to acidosis
68
what are the causes of cellular hypoxia in shock?
- reduced tissue perfusion/ O2 delivery - increased O2 consumption - inadequate O2 utilization
69
what are the stages of shock?
- pre-shock (nonprogressive phase) - shock (progressive phase) - irreversible damage- multiple organ failure
70
sepsis
dysregulated host response to infection resulting in life-threatening organ dysfunction
71
SIRS
- caused by infectious and noninfectious diseases | - characterized by robust inflammatory response
72
pathogenesis of septic shock
- inflammatory and counterinflammatory responses- complement activation - endothelial activation and injury - induction of procoagulant state - complication of IDC - organ dysfunction -> death

Patho 1 (12 decks)

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