Hemodynamic Flashcards
Effect of high hydrostatic pressure and low colloid pressure
Fluid out of vessels
Hydrostatic push out H2O and Na
Osmotic pull in H2O and Na
Cause of low osmotic pressure
Low synthesis (liver, malnutrition)
Loss (renal)
Effect of CHF on sodium/water retention
CHF -> hypoperfusion of kidneys -> active renin-angiotensin-aldosterone axis -> retention of Na et H2O = hausse blood volume -> edema and effusion
Hyperemia vs congestion
Hyperemia = active process, arterial dilation, oxygenated blood
Congestion = passive process from reduced venous outflow (cardiac, obstruction) = cyanosis = deozygenated hemoglobin
Sequence of event of hemostasis
- Arterial vasoC = reduce blood flow
- Primary hemostasis (platelet plug)
- Secondary hemostasis (depot of fibrin)
- Clot stabilization and resorption
Steps of primary hemostasis
- Platelet adhesion via GpIb-R to vWF exposed on ECM
- Shape change
- Granule release (ADP, TxA2) -> induce platelet aggregation via GpIIb-IIIa-R binding fibrinogen = platelet plug
Steps of secondary hemostasis
- Exposition of tissue factor
- Phospholipid-coag factor complexes
- Thrombin activation
- Fibrin polymerization (secondary plug)
Antithrombic events
Release of t-PA (fibrinolysis) -> plasmin break down fibrin -> D-dimers (marker for thrombolytic states(
Thrombomodulin = binds thrombin and converts to anticoag
Anti-thrombin III (activity enhanced by heparin-like molecules expressed on endothelial cells
Activation mechanism of platelets secretion of granules
Triggered by thrombin (PAR-1) and ADP (P2Y1 et 12)
What evaluates prothrombin PT time
Function of extrinsic pathway
7-10-5-2-fibrinogen
2 = prothrombin
What evaluates thromboplastin time PTT
Function of intrinsic pathway
12-11-8-9-fibrinogen
(12, 11.98)
Roles of thrombin
Conversion of fibrinogen into cross-linked fibrin (second plug)
Platelet activation = active PAR-1= induce platelet aggregation and TxA2 production
Active endothelial cells = express adhesion molecules and cytokines (PDGF)
Directly activates leucocytes
Molecules in endothelium maintaining an anti-coag state
- Heparin-like molecules + anti-thrombin III = inactive thrombin, factor 9 and 10
- Tissue-factor pathway inhibitor = inactive TF-VIIa complex
- Thrombomodulin = binds thrombin -> prot C active and with protS inative factors 5 et 8
- Release of PGI2, NO, ADP = inhibe platelet aggregation
- Release tPA = activates fibrinolysis
Virchow triad
Endothelial injury
Abnormal blood flow
Hypercoagulability
Flow of arterial and venous thrombi
Arterial = retrograde
Venous = in direction of blood flow to the heart
Lamination = lines of Zahn = flowing blood = ante vs post mortem
Where do pulmonary embolism originate?
Deep veins (DVT)
Red vs white infarct
Red = venous occlusion
White = arterial occlusion
Pathogenesis of septic shock
- Initiate inflamm response : TLR recognize PAMPs and DAMPs, GCR detect bact peptides and C-type lectin
- Active nuclear translocation of NF-kB = increase gene expression encoding inflammation mediators
- Mediators : TNF, IL1, IL12, IL18, IFNy, HMGB1
- Elevation of C-reactive protein, procalcitonin, ROS, PAF
- Active complement -> anaphylotoxin C3a, C5a and opsonin C3b
- Microbial components activates coag via factor 12
- Hyperinflamm state -> immunosuppressive mechanisms -> Th1 shift to Th2 -> anti-inflamm mediators (TNF-R, IL1-R antagonist, IL10, lympho apoptosis)
Pathogenesis of hyperglycemia and insulin resistance in septic shock
TNF, IL1, glucagon, growth hormones, GC, cathecholamines -> drive gluconeogenesis -> hyperglycemia decrease neutrophils fct
Promote insulin resistance by proinflamm cytokines = impair GLUT4
Where do capillaries have continuous endothelium? What passes through?
Brain
Muscle
Lung
Bone
Exchange O2, CO2, small molecules via pinocytosis and transcytosis
Where do capillaries have fenestred endothelium? What passes through?
Renal glomeruli
Intestinal villi
Endocrine glands
Choroid plexuses
Ciliary processes of the eye
Small molecules and proteins
Where do capillaries have discontinuous endothelium? What passes through?
Liver sinusoids
Spleen sinusoids
Bone marrow
Lymph nodes
Plasma proteins, red and white blood cells
Endothelial vasodilator
NO
PGI2
Endothelial-derived hyperpolarizing factor
C-type natriuretic peptide
Endothelial vasocontrictor
Endothelin
ROS
Angiotensin II
TxA2
Anticoagulant substances (endothelial)
PGI2 (vascular relax, inhibit platelet aggregat)
NO (vascular relax, moins aggregat, suppress thrombin)
Heparan sulfate (concentrate ATIII on endo surface)
ADPase and ATPase
Protein S (with protC inhibe activation of 8 and 10)
Thrombomodulin (active protein C)
TPA (fibrinolysis)
TFPI = inactive VII-TF complex
Components for fibrinolysis
Urokinase plasmonogen activator-R, tPA, PAI1, Annexin II
Procoagulant (endothelial)
Tissue factor, vWF
PAI-1 (reduce fibrinolyse by inhibing tPA and uPA)
PARs (active R for endo activation)
Platelets procoagulant
TxA2 (vasoC, platelet aggregation)
ADP (platelet aggregation and activation)
Calcium (coag rx)
Thrombospondin
Fibrinogen
Factor 5-11-13
VWF
PAI (inhibe plasminogen activator tPA, active prot C)
Serotonin (vasoC)
PARs
Platelets anticoag
ATP (inhib platelet aggregation)
Protease Nexin II
TFPI
Protein S
Factor I (fibrinogen) deficiency
Rare
Mild bleeding tendencies in dogs, more severe in goats
Factor II (prothrombin) deficiency
Rare
Mild-bleeding in adults
Epistaxis and umbilical cord bleeding in puppies
Factor VII deficiency
Rare
Mild, more easily bruised
Factor X deficiency
Rare
Relatively severe bleeding in most cases
Factor XII deficiency
No bleeding
Factor XI deficiency
Spontaneous hemorrhage is insignificant, can be severe after surgery
Most common hereditary coag protein in cattle
Factor IX (hemophilia B) deficiency
Variable bleeding, generally mild
Factor VIII (hemophilia A) deficiency
Bleeding can be severe
Deficiency of vWF
Mild to severe hemorrhage
Epistaxis, mucosal hemorrhage, post-cx bleeding
Most common inherited canine disorder
Vitamine-K dependent factors (2-7-9-10) deficiency
Moderate to severe and sometimes fatal hemorrhage
Prekallikrein deficiency
Post-cx bleeding
