1. Hemodynamic disorders (1 of 3)
Ali Al Khader, M.D.
Faculty of Medicine
Al-Balqa’ Applied University

2. What will we discuss today?
Hyperemia & congestion
Edema
Hemorrhage
Hemostasis

3. Hyperemia & congestion
Both = increase in blood volume within a tissue
Hyperemia
Congestion
active
passive
red
blue-red
arterial
venous

4. Morphology Acute VS chronic pulmonary congestion
Acute VS chronic hepatic congestion

5. Edema, an introduction

6. Edema

7. Edema, clinical manifestations
According to the tissue involved
Can be life-threatening
Examples………?

8. Hemorrhage = extravasation of blood from vessels
Chronically congested tissues…capillary hemorrhages
Hemorrhagic diathesis…susceptibility to bleed even with minor trauma
Trauma, atherosclerosis, inflammation, or neoplasms can lead to hemorrhage

9. Hemorrhage, cont’d External or internal
From trivial (bruises) to fatal (large vessels such as aortic dissection)
Large bleeds in body cavities…give some names..

10. Hemorrhage, different sizes
Petechiae…1-2mm
…skin, mucous membranes and serosal surfaces
…problems in platelets or vessel wall (e.g., vit. C deficiency)
Purpura…3-5mm
…same causes of petechiae
…vasculitis is an important cause
Echymoses…1-2cm
…subcutaneous
…= bruises
…hemoglobin bilirubin hemosiderin

11. Hemorrhage consequences
Hypovolemic shock
Death
Iron deficiency anemia
No consequences

12. Hemostasis
A series of regulated processes that maintain blood in a fluid, clot-free state in normal vessels while rapidly forming a localized hemostatic plug at the site of vascular injury
The pathologic counterpart of hemostasis is thrombosis
3 main players:
-vascular wall
-platelets
-coagulation cascade
The endothelium can have anticoagulant functions, and can be induced to activate coagulation due to triggers such as microbes, hemodynamic forces, and inflammatory mediators
Like TNF and IL-1
By secreting tissue factor

13. Hemostasis, cont’d also activates platelets
= factor III
= thromboplastin
Degraded by adenosine diphosphatase produced by endothelial cells

14. The primary hemostatic plug is now formed
Hemostasis, cont’d
Platelets bind via glycoprotein 1b (GpIb) receptors to von Willebrand factor (vWF) on exposed extracellular matrix (ECM)
…then they are activated shape change
granule release
…Released adenosine diphosphate (ADP) and thromboxane A2 (TxA2)
additional platelet aggregation through binding of platelet GpIIb-IIIa
receptors to fibrinogen
The primary hemostatic plug is now formed

15. Hemostasis, cont’d The secondary hemostatic plug is now formed
Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids)
fibrin polymerization
The secondary hemostatic plug is now formed
larger and more stable than the primary plug and contains entrapped red cells and leukocytes

16. Homeostasis, cont’d
t-PA (tissue plasminogen activator, a fibrinolytic product)
&
thrombomodulin (interfering with the coagulation cascade)
are of the counter-regulatory mechanisms that limit the process to the site of injury

17. Some inhibitors of coagulation
Heparin-like molecules…on endothelial surface
…they are cofactors for the plasma protein
anti-thrombin III
Thrombomodulin…change thrombin activity from cleaving fibrinogen
to cleaving and activating protein C
Tissue factor pathway inhibitor…inhibits tissue factor–factor VIIa
complex and factor Xa
Inhibits factor Va and factor VIIIa
protein S is a cofactor for it

18. Abnormalities

19. We need phospholipid surface (by endothelium and platelets, and calcium ions
Coagulation cascade
The ability of coagulation factors II, VII, IX, and X to bind to calcium requires vit. K

20. Lab tests Prothrombin time (PT)…for activity
-II -V
-VII -X
-Fibrinogen
Prothrombin time (PT)…for activity
of proteins of extrinsic pathway
Partial thromboplastin time (PTT)
…for activity of intrinsic pathway
proteins
-II -V
-VIII
-IX -X
-XI
-XII
-fibrinogen
Can be used for monitoring heparin activity

21. The fibrinolytic system

22. Thank You