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Nutrition > Hemodynamic > Flashcards

Hemodynamic Flashcards

1
Q

Effect of high hydrostatic pressure and low colloid pressure

A

Fluid out of vessels
Hydrostatic push out H2O and Na
Osmotic pull in H2O and Na

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2
Q

Cause of low osmotic pressure

A

Low synthesis (liver, malnutrition)
Loss (renal)

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3
Q

Effect of CHF on sodium/water retention

A

CHF -> hypoperfusion of kidneys -> active renin-angiotensin-aldosterone axis -> retention of Na et H2O = hausse blood volume -> edema and effusion

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4
Q

Hyperemia vs congestion

A

Hyperemia = active process, arterial dilation, oxygenated blood
Congestion = passive process from reduced venous outflow (cardiac, obstruction) = cyanosis = deozygenated hemoglobin

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5
Q

Sequence of event of hemostasis

A
  1. Arterial vasoC = reduce blood flow
  2. Primary hemostasis (platelet plug)
  3. Secondary hemostasis (depot of fibrin)
  4. Clot stabilization and resorption
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6
Q

Steps of primary hemostasis

A
  1. Platelet adhesion via GpIb-R to vWF exposed on ECM
  2. Shape change
  3. Granule release (ADP, TxA2) -> induce platelet aggregation via GpIIb-IIIa-R binding fibrinogen = platelet plug
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7
Q

Steps of secondary hemostasis

A
  1. Exposition of tissue factor
  2. Phospholipid-coag factor complexes
  3. Thrombin activation
  4. Fibrin polymerization (secondary plug)
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8
Q

Antithrombic events

A

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

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9
Q

Activation mechanism of platelets secretion of granules

A

Triggered by thrombin (PAR-1) and ADP (P2Y1 et 12)

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10
Q

What evaluates prothrombin PT time

A

Function of extrinsic pathway
7-10-5-2-fibrinogen
2 = prothrombin

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11
Q

What evaluates thromboplastin time PTT

A

Function of intrinsic pathway
12-11-8-9-fibrinogen
(12, 11.98)

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12
Q

Roles of thrombin

A

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

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13
Q

Molecules in endothelium maintaining an anti-coag state

A
  1. Heparin-like molecules + anti-thrombin III = inactive thrombin, factor 9 and 10
  2. Tissue-factor pathway inhibitor = inactive TF-VIIa complex
  3. Thrombomodulin = binds thrombin -> prot C active and with protS inative factors 5 et 8
  4. Release of PGI2, NO, ADP = inhibe platelet aggregation
  5. Release tPA = activates fibrinolysis
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14
Q

Virchow triad

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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15
Q

Flow of arterial and venous thrombi

A

Arterial = retrograde
Venous = in direction of blood flow to the heart
Lamination = lines of Zahn = flowing blood = ante vs post mortem

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16
Q

Where do pulmonary embolism originate?

A

Deep veins (DVT)

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17
Q

Red vs white infarct

A

Red = venous occlusion
White = arterial occlusion

18
Q

Pathogenesis of septic shock

A
  1. Initiate inflamm response : TLR recognize PAMPs and DAMPs, GCR detect bact peptides and C-type lectin
  2. Active nuclear translocation of NF-kB = increase gene expression encoding inflammation mediators
  3. Mediators : TNF, IL1, IL12, IL18, IFNy, HMGB1
  4. Elevation of C-reactive protein, procalcitonin, ROS, PAF
  5. Active complement -> anaphylotoxin C3a, C5a and opsonin C3b
  6. Microbial components activates coag via factor 12
  7. Hyperinflamm state -> immunosuppressive mechanisms -> Th1 shift to Th2 -> anti-inflamm mediators (TNF-R, IL1-R antagonist, IL10, lympho apoptosis)
19
Q

Pathogenesis of hyperglycemia and insulin resistance in septic shock

A

TNF, IL1, glucagon, growth hormones, GC, cathecholamines -> drive gluconeogenesis -> hyperglycemia decrease neutrophils fct
Promote insulin resistance by proinflamm cytokines = impair GLUT4

20
Q

Where do capillaries have continuous endothelium? What passes through?

A

Brain
Muscle
Lung
Bone
Exchange O2, CO2, small molecules via pinocytosis and transcytosis

21
Q

Where do capillaries have fenestred endothelium? What passes through?

A

Renal glomeruli
Intestinal villi
Endocrine glands
Choroid plexuses
Ciliary processes of the eye
Small molecules and proteins

22
Q

Where do capillaries have discontinuous endothelium? What passes through?

A

Liver sinusoids
Spleen sinusoids
Bone marrow
Lymph nodes
Plasma proteins, red and white blood cells

23
Q

Endothelial vasodilator

A

NO
PGI2
Endothelial-derived hyperpolarizing factor
C-type natriuretic peptide

24
Q

Endothelial vasocontrictor

A

Endothelin
ROS
Angiotensin II
TxA2

25
Q

Anticoagulant substances (endothelial)

A

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

26
Q

Components for fibrinolysis

A

Urokinase plasmonogen activator-R, tPA, PAI1, Annexin II

27
Q

Procoagulant (endothelial)

A

Tissue factor, vWF
PAI-1 (reduce fibrinolyse by inhibing tPA and uPA)
PARs (active R for endo activation)

28
Q

Platelets procoagulant

A

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

29
Q

Platelets anticoag

A

ATP (inhib platelet aggregation)
Protease Nexin II
TFPI
Protein S

30
Q

Factor I (fibrinogen) deficiency

A

Rare
Mild bleeding tendencies in dogs, more severe in goats

31
Q

Factor II (prothrombin) deficiency

A

Rare
Mild-bleeding in adults
Epistaxis and umbilical cord bleeding in puppies

32
Q

Factor VII deficiency

A

Rare
Mild, more easily bruised

33
Q

Factor X deficiency

A

Rare
Relatively severe bleeding in most cases

34
Q

Factor XII deficiency

A

No bleeding

35
Q

Factor XI deficiency

A

Spontaneous hemorrhage is insignificant, can be severe after surgery
Most common hereditary coag protein in cattle

36
Q

Factor IX (hemophilia B) deficiency

A

Variable bleeding, generally mild

37
Q

Factor VIII (hemophilia A) deficiency

A

Bleeding can be severe

38
Q

Deficiency of vWF

A

Mild to severe hemorrhage
Epistaxis, mucosal hemorrhage, post-cx bleeding
Most common inherited canine disorder

39
Q

Vitamine-K dependent factors (2-7-9-10) deficiency

A

Moderate to severe and sometimes fatal hemorrhage

40
Q

Prekallikrein deficiency

A

Post-cx bleeding

Nutrition (13 decks)

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