قراءة
عرض

Prof. DR.MAHA SHAKIR



In this system we will discuss the following:

Hyperemia and Congestion
Hemorrhage
Edema
Thrombosis
Disseminated Intravascular Coagulation
Embolism
Infarction
Shock







Hypermia and Congestion
Definition:
Both of them can be defined as a local increase in volume of blood in a particular tissue.



Hyperemia

It is an active process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of:
exercising skeletal muscle
or acute inflammation


Hyperemic tissues are redder than normal

because of engorgement with oxygenated blood.



Congestion

Congestion is a passive process resulting from impaired outflow of venous blood from a tissue. It can occur:

systemically, as in cardiac failure,
or locally as a consequence of an isolated venous obstruction.







• Congested tissues have an abnormal blue-red color (cyanosis) that stems from the accumulation of deoxygenated hemoglobin in the affected area.






In long-standing chronic congestion, inadequate tissue perfusion and persistent hypoxia may lead to:
parenchymal cell death.
secondary tissue fibrosis.
the elevated intravascular pressures may cause edema or sometimes rupture capillaries forming focal hemorrhage.







Hemodynamic Disorders, Thromboembolism, and Shock






MORPHOLOGY

Cut surfaces of hyperemic or congested tissues
feel wet and
typically ooze blood.
• Pulmonary congestion:
Acute
chronic



1.Acute pulmonary congestion:

Alveolar capillaries engorged with blood
variable degrees of alveolar septal edema and intraalveolar hemorrhage.



2.Chronic pulmonary congestion

Thickened & fibrotic septa
Alveolar spaces contain hemosiderin-laden macrophages (“heart failure cells”) derived from phagocytosed red cells.








Hemodynamic Disorders, Thromboembolism, and Shock








Hemodynamic Disorders, Thromboembolism, and Shock








Hemodynamic Disorders, Thromboembolism, and Shock


Hemodynamic Disorders, Thromboembolism, and Shock









Hemodynamic Disorders, Thromboembolism, and Shock




Fibrosed wall

Hemodynamic Disorders, Thromboembolism, and Shock




b) Hepatic congestion

1-Acute hepatic congestion:
the central vein and sinusoids are distended with blood,
and there may even be necrosis of centrally located hepatocytes.
The periportal hepatocytes, better oxygenated???WHY




because of their proximity to hepatic arterioles, experience

less severe hypoxia and may develop only reversible fatty change.



2- Chronic passive congestion of liver:

Gross examination
the central regions of the hepatic lobules, viewed, are red-brown and slightly depressed
the surrounding zones of uncongested tan, sometimes fatty, liver (nutmeg liver)



Microscopic findings

centrilobular hepatocyte necrosis,
hemorrhage
hemosiderin-laden macrophages.








Hemodynamic Disorders, Thromboembolism, and Shock

necrosiss

Normal hepatocyte


Hemodynamic Disorders, Thromboembolism, and Shock




Hemorrhage

Hemorrhage, defined as the extravasation of blood from vessels, is most often the result of:
damage to blood vessels
or defective clot formation.




capillary bleeding can occur in chronically congested tissues.

Trauma,
atherosclerosis,
or inflammatory or neoplastic erosion of a vessel wall also may lead to hemorrhage,
• Bleeding may be extensive if the affected vessel is a large vein or artery.





• The risk of hemorrhage is increased in a wide variety of clinical disorders collectively called:
• hemorrhagic diatheses.
• Including: inherited or acquired defects in:
vessel walls,
platelets,
or coagulation factors,


Hemorrhage may be manifested by different appearances and clinical consequences.

• Hemorrhage may be external or accumulate within a tissue as a hematoma, which ranges in significance from trivial to fatal.
• Large bleeds into body cavities are described variously according to location
hemothorax,
hemopericardium,
hemoperitoneum,
or hemarthrosis (in joints).




Petechiae

are minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces causes include :
low platelet counts (thrombocytopenia),
defective platelet function,
and loss of vascular wall support, as in vitamin C deficiency.



Purpura

are slightly larger (3 to 5 mm) hemorrhages.
Purpura can result from:
the same disorders that cause petechiae,
Trauma
vascular inflammation (vasculitis), and increased vascular fragility.








Ecchymoses
are larger (1 to 2 cm) subcutaneous hematomas (colloquially called bruises).
Extravasated red cells are phagocytosed and degraded by macrophages; the characteristic color changes of a bruise result from the enzymatic conversion of hemoglobin (red-blue color) to bilirubin (blue-green color) and eventually hemosiderin (golden-brown).



The clinical significance of any particular hemorrhage depends on:

the volume of blood that is lost
the rate of bleeding..
The site of hemorrhage also is important;
• chronic or recurrent external blood loss culminates in iron deficiency anemia



• By contrast, iron is efficiently recycled from phagocytosed red cells,

• so internal bleeding (e.g., a hematoma) does not lead to iron deficiency.









رفعت المحاضرة من قبل: Ali Ahmed
المشاهدات: لقد قام عضو واحد فقط و 123 زائراً بقراءة هذه المحاضرة








تسجيل دخول

أو
عبر الحساب الاعتيادي
الرجاء كتابة البريد الالكتروني بشكل صحيح
الرجاء كتابة كلمة المرور
لست عضواً في موقع محاضراتي؟
اضغط هنا للتسجيل