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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
Q

pulmonary edema

A
  • usually caused by cardiac disease
  • fluid builds up in alveoli
  • cannot exchange gases as well
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26
Q

ascites

A
  • extra fluid in peritoneal cavity

- results in abdominal distenstion

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27
Q

main causes of non-pitting edma

A
  • moderate to severe lymphedema

- pretibial myxedema (associated with graves disease)

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28
Q

what is normal hemostasis?

A
  • involves platelets, clotting factors, and endothelium
  • occurs at site of vascular injury
  • results in blood clot
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29
Q

what are the general sequence of events in normal hemostasis?

A
  • vasoconstriction
  • primary hemostasis
  • secondary hemostasis
  • clot stabilization and resorption
30
Q

what is primary hemostasis?

A
  • formation of platelet plug
  • disruption of endothelial cells exposes vWF and collagen
  • promote platelet adherence
31
Q

what is secondary hemostasis?

A
  • deposition of fibrin
32
Q

what is a coagulation cascade?

A

series of well orchestrated enzymatic reactions that leads to deposition of insoluble fibrin clot

  • intrinsic pathway
  • extrinsic pathway
  • common pathway
33
Q

prothrombin time (PT) assay

A
  • asses function of proteins in extrinsic pathway

- VII, X, V, II and fibrinogen

34
Q

partial thromboplastin time (PTT) assay

A
  • asses function of proteins in intrinsic pathway

- XII, XI, IX, VIII, X, V, II and fibrinogen

35
Q

intrinsic pathway

A

XII -> XI -> IX -> VIII to common pathway

36
Q

extrinsic pathway

A

VII -> common pathway

37
Q

common pathway

A

X -> thrombin (protrombin also acts on thrombin) -> Fibrinogen (I) -> Fibrin clot (XIII)

38
Q

Prolonged PT but normal aPTT

A
  • factor VII deficiency
  • mild vit K deficiency
  • liver disease
  • warfarin admin
39
Q

normal PT but prolonged aPTT

A
  • deficiencies in factors VIII, IX, or XI

- Heparin admin

40
Q

prolonged PT and aPTT

A
  • deficiencies of prothrombin, fibrinogen, or factors X or V

- disseminated intravascular coagulation

41
Q

role of thrombin

A
  • conversion of fibrinogen into cross-linked
  • platelet activation
  • pro-inflammatory effects
  • anti-coagulent
42
Q

antithrombotic properties of endothelium

A
  • platelet inhibitory effects
  • anticoagulant effects
  • fibrinolytic effects
43
Q

what are platelet inhibitory effects of endothelial cells?

A
  • shield platelets from vWF and collagen

- synthesize PG, NO and ADP which inhibit platelet aggregation

44
Q

what are anticoagulant effects of endothelial cells?

A
  • thrombomodulin binds to thrombin

- endothelial protein C receptors bind to protein C which inactivates clotting factors

45
Q

what are fibrinolytic effects of endothelial cells?

A
  • synthesize t-PA (tissue type plasminogen activator)

- t-PA lyses fibrin clot

46
Q

steps of clot formation

A
  • subendothelial exposure
  • adhesion
  • activation
  • aggregation
  • platelet plug formation
  • clot retraction and clot dissolution
47
Q

thrombosis

A
  • blood clot with non-traumatized blood vessel
  • clot forms when it shouldn’t
  • pathological condition
48
Q

causes of thrombosis

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
49
Q

primary hypercoagulable state causes

A
  • genetic

- factor V mutation or prothrombin mutation

50
Q

secondary hypercoagulable state causes

A
  • prolonged immobilization
  • MI
  • tissue injury
  • prosthetic cardiac valve
  • disseminated intravascular coagulation
  • hyperestrogenic shock, oral contraceptive use, smoking (lower risk)
51
Q

fate of thrombus

A
  • propagation
  • embolization
  • dissolution
  • organization and recanalization
52
Q

thrombus propagation

A
  • pile of platelets and fibrin on top of each other

- makes blood clot expand

53
Q

thrombus embolization

A
  • piece of thrombus breaks off and is mobilized- can go anywhere
54
Q

thrombus dissolution

A
  • fibrinolytic agents help to make blood clot go away
55
Q

thrombus organization and recanalization

A
  • 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
Q

arterial and cardiac thrombosis

A
  • occlusion of critical vessel

- prone to embolism in brain, kidneys, and spleen

57
Q

Disseminated Intravascular Coagulation (DIC)

A
  • complication that happens in systemic circulation
  • thrombin is activated
  • rapid burst of thrombin -> bleeding
  • gradual amount of excess thrombin -> thrombotic complications
58
Q

Embolism

A
  • traveling detached intravascular mass

- can happen for variety of reasons

59
Q

infarction

A
  • occlusion of either arterial supply or venous drainage
  • causes ischemic necrosis
  • majority due to arterial thrombosis/ embolism
60
Q

factors that influence infarct development

A
  • anatomy of vascular supply
  • rate of occlusion
  • tissue vulnerability to hypoxia
61
Q

Shock

A
  • state of cellular and tissue hypoxia

- most common is circulatory failure

62
Q

major classifications of shock

A
  • cardiogenic shock
  • hypovolemic shock
  • spetic shock
63
Q

cardiogenic shock

A
  • results from low cardiac output as a result of myocardial pump failure (heart failure)
64
Q

hypovolemic shock

A
  • low cardiac output due to loss of blood supply or plasma volume
65
Q

septic shock

A
  • triggered by microbial infections
  • infection is generalized
  • associated with severe systemic inflammatory response syndrome (SIRS)
66
Q

major physiologic determinants of tissue perfusion

A
  • cardiac output

- systemic vascular resistance

67
Q

mechanism of shock

A
  • cellular hypoxia
  • cell membrane ion pump dysfunction
  • intracellular edema
  • inadequate regulation of intracellular pH due to acidosis
68
Q

what are the causes of cellular hypoxia in shock?

A
  • reduced tissue perfusion/ O2 delivery
  • increased O2 consumption
  • inadequate O2 utilization
69
Q

what are the stages of shock?

A
  • pre-shock (nonprogressive phase)
  • shock (progressive phase)
  • irreversible damage- multiple organ failure
70
Q

sepsis

A

dysregulated host response to infection resulting in life-threatening organ dysfunction

71
Q

SIRS

A
  • caused by infectious and noninfectious diseases

- characterized by robust inflammatory response

72
Q

pathogenesis of septic shock

A
  • 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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