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Hemodynamic Disorders, Thromboembolism, and Shock

37 important questions on Hemodynamic Disorders, Thromboembolism, and Shock

Definition colloid osmotic pressure

Proteins suck in water to maintain their normal tertiary structure

What are the causes of increased egress of water at the capillary level?

Increased pressure at the venous end (cardiac failure, blockades)
Increased permeability (inflammation, neurogenic)
(Increased pressure arterial end (almost never!))

What are the causes of decreased return of fluid from the interstitium?

Decreased colloid osmotic pressure

What are the causes of a blocked flow of lymph?

Iatrogenic
Tumour

Transudate and exudate edema fluid

Transudate: protein poor
Exudate: protein rich

What are the types of hemorrhages?

Petechiae (up to 1 mm): thrombopenia, -pathy, vasculitis
Purpura (slightly bigger): vascular malformations, vasculitis
Ecchymoses: (1-3cm) trauma (sometimes + above), a.o.
Hematoma: Trauma, vasc. Malf. (by AC of HT)

What are the 4 outcomes of a thrombus?

Resolution
Embolization to lungs
Organized and incorporated into wall
Organized and re canalized

What are the types of emboli?

Thrombus
Fat/bonemarrow
Amniotic fluid
Tumour
Foreign body material
Parasites/eggs

Noninflammatory edema causes (4)

increased hydrostatic pressure,
decreased colloid osmotic pressure (reduced plasma albumin), l
ymphatic obstruction,
sodium retention

Which types of shock exist?

Cardiogenic shock (prognosis variable)
Hypovolemic shock (prognosis OK, if treated adequately
Septic shock (prognosis poor, 20-30% mortality)
Heterogenic rest group (incl. neurogenic shock, anaphylactic shock) (prognosis variable)

What are the signs of shock?

Rapid pulse, cold fingers/hand/toes/feet, confusion. Due to loss of circulation volume

What is the color of congested tissue?

An abnormal blue-red color (cyanosis) that stems from the accumulation of deoxygenated hemoglobin in the affected area

What are the steps of hemostasis?

Arteriolar vasoconstriction
Primary hemostasis
Secondary hemostasis
Clot stabilization and resorption

Pulmonary emboli arise from

primarly from deep venous thromboses

Describe clot stabilization and resorption

Polymerized fibrin and platelet aggregates undergo contraction to form a solid, permanent plug that prevents further hemorrhage. At this stage, counterregulatory mechanisms (e.g., tissue plasminogen activator, t-PA made by endothelial cells) are set into motion that limit clotting to the site of injury and eventually lead to clot resorption and tissue repair

Which two types of granules exist in platelets?

α-Granules and Dense (or δ) granules

What is the role of aspiring in hemostasis?

Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis

Function prothrombin time (PT) assay

It assesses the function of the proteins in the extrinsic pathway (factors VII, X, V, II (prothrombin), and fibrinogen). In brief, tissue factor, phospholipids, and calcium are added to plasma and the time for a fibrin clot to form is recorded.

Function partial thromboplastin time (PTT) assay

It screens the function of the proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen). In this assay, clotting of plasma is initiated by the addition of negative charged particles (e.g., ground glass) that activate factor XII (Hageman factor) together with phospholipids and calcium, and the time to fibrin clot formation is recorded.

3 steps primary hemostasis

1. Vascular injury exposes vWF (vonWillebrandFactor) in extracellular matrix
2. Platelets adhere trough the binding of platelet GpLb receptors to vWF
3. Adhesion leads to platelet activation, associated with secretion of platelet granule contents, changes in platelet shape and membrane composition, and conformational changes in GpIIb-IIIa receptors, which bind fibrogen, leading to platelet aggregation and fomartion of the primary hemostatic plug

Hemostatic plug (primair en secundair)

Temporary blood stolling
primary: soft and temporary, vWF and fibrogen
secundary: more stable, fibrogen becomes fibrin (by thrombin) , until vessel is healed

Systemic vs pulmonary emboli

-Systemic = arteriele circulation, meestal uit hart, infarcten en ischemie
-Pulmonary= longcircuit, meestal uit diepe venen uit de benen, ademhalingproblemen

How is coagulation restricted?

limiting enzymatic activation to phospholipid surfaces provided by activated platelets or endothelium,
circulating inhibitors of coagulation factors, such as antithrombin III, whose activity is augmented by heparin-like molecules expressed on endothelial cells
expression of thrombomodulin on normal endothelial cells, which bind thrombin and convert it into an anti-coagulant,
activation of fibrinolytic pathways (e.g., by association of tissue plasminogen activator with fibrin).

Function protein C

Inhibitor of coagulation factors Va and VIIIa

Function heparin-like molecule

Heparin-like molecules on the surface of endothelium bind and activate antithrombin III, which then inhibits thrombin and factors IXa, Xa, XIa, and XIIa.

Definition endothelial activation/dysfunction

Inflammation and other noxious stimuli can promote thrombosis by shifting the pattern of gene expression in endothelium to one that is “prothrombotic.”

With what deep venous thromboses is associated?

Stasis and hypercoagulable states

What are the consequences of gas bubbles?

They can coalesce and obstruct vascular flow and cause distal ischemic injury.

When embolus causes tissue infarction?

It depends on the site of embolization and the presence or absence of collateral circulation

When fat embolism occur?

Fat embolism can occur after crushing injuries to the bones; symptoms include pulmonary insufficiency and neurological damage

Which factors determine the damage of an occlusion?

Anatomy of vascular supply
Rate of occlusion
Tissue vulnerability to hypoxia

What are the 6 consequences of a pulmonary emboli?

nothing (very small emboli dissolve)
right sided heart failure
pulmonary hemorrhage
pulmonary infarction
pulmonary hypertension (many small emboli diminish the vasculature -> pressure increases
instant/sudden death

What is the major cause of an infarct?

Arterial occlusion.

Amniotic fluid embolism

Amniotic fluid embolism (AFE) is a rare and life-threatening complication that occurs when a pregnant woman gets amniotic fluid into their bloodstream just before, during or immediately after childbirth.

What are the major pathological factors in septic shock?

Inflammatory and counterinflammatory responses.
Endothelial activation and injury
Induction of a procoagulant state
Metabolic abnormalities
Organ dysfunction

What are the characteristics of septic shock ?

endothelial cell activation
vasodilation
edema
disseminated intravascular coagulation
metabolic derangements

Hemorrhagic vs nonhemorrhagic infarcts

Hemorrhagic (red) : there is bleeding, caused by venous occlusion or arterial conclusion in tissues in which decrease in bloodflow is partial or transient
Nonhemorrhagic (white) : absence of bleeding, blood can not seep into infarcted tissue. In tissues whit endarterial blood supplies in which the vascular obstruction is persistent

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Pathology

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