Patho17(hemodynamics file16+17) Flashcards
What is hemorrhage?
Extravasation of blood from vessels
What are the causes of hemorrhage?
Damage to blood vessels or defective clot formation, trauma, atherosclerosis, inflammatory or neoplastic erosion of a vessel wall, hemorrhagic diatheses
Define hemorrhagic diatheses.
Diverse causes, including inherited or acquired defects in vessel walls, platelets, or coagulation factors
What can hemorrhage result in? It can be location
External bleeding or accumulation of blood within a tissue as a hematoma
The hematoma ranges in importance/significance?
from trivial (e.g., a bruise) to fatal (e.g., a massive retroperitoneal hematoma resulting from rupture of a dissecting aortic aneurysm).
Names of large bleeds into body cavities in plural cavity, pericardial cavity, peritoneal cavity, joints
hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis.
What can extensive hemorrhages occasionally result in?
Jaundice from massive breakdown of red cells and hemoglobin/mainly in newborns
Describe each picture related to hemorrhage
Hematoma strong/large bleed in joint cavity/hematoma fetal in brain / hematoma trivial
What is the clinical significance of a hemorrhage depend on with explain ?
the volume of blood lost and the rate of bleeding /site of hemorrhage
* Rapid loss of up to 20% of the blood volume, or slow losses of even larger amounts, may have little impact in healthy adults; greater losses, however, can cause hemorrhagic (hypovolemic) shock.
The site of hemorrhage also is important; bleeding that would be trivial in the subcutaneous tissues can cause death if located in the brain.
What is the consequence of chronic or recurrent external blood loss? And in which condition it happens?
iron deficiency anemia as a consequence of a loss of iron in hemoglobin./ due to peptic ulcer, menstrual bleeding
What are petechiae?
Minute hemorrhages (1 to 2 mm) into skin, mucous membranes, or serosal surfaces
What are some causes of petechiae?
Low platelet counts (thrombocytopenia), defective platelet function, loss of vascular wall support (as in vitamin C deficiency)
Define purpura.
Slightly larger (3 to 5 mm) hemorrhages, same disorders that cause petechiae, trauma, vascular inflammation (vasculitis), increased vascular fragility
What are ecchymoses?
Larger (1 to 2 cm) subcutaneous hematomas /causes mainly trauma and platelet not involved just coagulation cascade
What causes the characteristic color changes of a bruise ( ecchymoses)?
Extravasated red cells are phagocytosed and degraded by macrophages;
Enzymatic conversion of hemoglobin (red-blue color) to bilirubin (blue-green color) and eventually hemosiderin (golden-brown)
What is the definition of normal hemostasis?
a series of regulated processes that culminate in the formation of a blood clot that limits bleeding from an injured vessel.
What is the pathologic counterpart of hemostasis?
thrombosis, the formation of a blood clot within non-traumatized, intact vessels.
What occurs immediately after an injury to reduce blood flow?
Arteriolar vasoconstriction
What mediates arteriolar vasoconstriction?
reflex neurogenic mechanisms and augmented by the local secretion of factors such as endothelin.
What are the main components of normal hemostasis ?
platelets, clotting factors, and endothelium.
What is the transient response in normal hemostasis?
Arteriolar vasoconstriction
What is the main mediator cause vasoconstriction?
endothelin (potent endothelium-derived vasoconstrictor)
What is primary hemostasis?
Formation of the platelet plug
What happenes during the primary hemostasis(steps)?
- Platelet adhesion: interactions with subendotheial VWF, which acts as a bridge between the platelet surface receptor glycoprotein Ib (Gplb) and exposed collagen.
- platelet activation:(Thrombin activates platelets through a special type of G-protein-coupled receptor referred to as a protease-activated receptor (PAR) and by collagen and ADP.Shape change (from small rounded discs to flat plates with spiky protrusions “sea urchins” that markedly increased surface area, and the release of secretory granules.
*Recruit additional platelets»»(aggregation)to form a primary hemostatic plug.
How platelet activation will help in the following steps ( aggregation/secondery Hemostasis)?
In platelet activation step:*the shape change of platelet accomnanied with
1) alterations in glycoprotein (IIb,IIIa)»»that increase its affinity for fibrinogen that important to aggregation
2) translocation of negatively charged phospholipids to the platelet surface»»Phospholipids bind calcium and serve as nucleation sites for the assembly of coagulation factor complexes.
* granules produce the prostaglandin thromboxane A2 (TXA2) and others >potent inducer of platelet aggregation.
What are the 3 bleeding disorders related to primary Hemostasis?
1(von Wilbrand disease)= Genetic deficiencies of vWF common in Jordan
2(BernardSoulier syndrome)=GPIb
3*(Glanzmann thrombasthenia)= Inherited deficiency of Gpllb-Illa
What is secondary hemostasis?
Deposition of fibrin
What happenes during the secondary hemostasis(steps)?
*coagulation cascade:
1)extrinsic and intrinsic pathway >to activate factor 10 (X) > generates thrombin
* Thrombin cleaves circulating fibrinogen into insoluble fibrin, a potent activator of platelets.
How coagulation cascade occurs ( steps)?
صورة
After secondary hemostasis which step ? And how it’s occer?
Clot stabilization / Polymerized fibrin and platelet aggregates undergo contraction to form a solid, permanent plug that prevents further hemorrhage.
After clot stabilization which step+ the aim of it ?
Counterregulatory mechanisms that :
1) inhibit thrombosis by : *inactive the factors in coagulation cascade
* inhibit platelets aggregation
2) activate fibrinolysis
3) clot resorption and tissue repair.
All this happens in normal endothelial cells (platelet inhibitory effects.
/Anticoagulant effects/ Fibrinolytic effects.)
Counterregulatory mechanisms In detail?
صورة
What is platelets ( shape,origin)?
Disc-shaped/anucleate cell fragments that are shed from megakaryocytes in the bone marrow into the bloodstream.
What do platelets depend on for their function?
Glycoprotein receptors, a contractile cytoskeleton, and two types of cytoplasmic granules;
Alfa/ dense gamma granules
What are the components involved in each reaction step of the coagulation cascade?
Enzyme (activated coagulation factor), substrate (inactive proenzyme form of a coagulation factor), and cofactor (reaction accelerator).
Where are the components assembled in the coagulation cascade?
On a negatively charged phospholipid surface.
What does the prothrombin time (PT) assay assess?
The function of the proteins in the extrinsic pathway (factors VII, X, V, II (prothrombin), and fibrinogen).
What does the partial thromboplastin time (PTT) assay screen?
The function of the proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen).
What are the functions of thrombin?
Conversion of fibrinogen into crosslinked fibrin, platelet activation, proinflammatory effects, and anti-coagulant effects.
What is fibrinolysis?
The enzymatic activity of plasmin, which breaks down fibrin and interferes with its polymerization.
How is plasmin generated?
inactive circulating precursor plasminogen converted to plasmin by enzymatic catabolism :
1) either by a factor 12(XII)–dependent pathway
2) plasminogen activators (t-PA) that made by endothelial cells/urokinase
**( alpha2 -Anti-plasmin) that regulate fibrinolysis by inhibiting plasmin function
What are the elevated levels of breakdown products of fibrinogen called?
Fibrin-derived D-dimers.
