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Seminar 3

Ischemia,Congestion and Infarction
by

Sami Almutairi

on 25 June 2014

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Transcript of Seminar 3

An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage .

Which then leads to local death of the tissue.

Endothelium
Vascular endothelium is strategically located at the interface between tissue and blood.

It is important for protecting against vascular injury and maintaining blood fluidity.
Coagulation
Coagualtion :

Coagulation is a complex process by which the blood forms clots to block and then heal a lesion/wound/cut to stop the bleeding.
Coagulation involves a cellular (platelet) and protein (coagulation factor) component .
Normal conditions
The endothelial cell provides a nonthrombogenic surface that:
1) Prevent platelets or other blood cell to adhere .
2) Prevent activation of the coagulation cascade.

Injured Endothelium
Injured endothelium plays the most important role in prevention of blood loss .
Endothelium as Antithrombotic
Endotheluim as Prothrombogenic
Antithrombogenic
A) Normal endothelium releases prostacyclin and nitric oxide :
#Potent inhibitors of platelet and monocyte activation .
#Vasodilators.
B) Normal endothelial surface expresses :
5- Normal endothelium express –ve charge of glycocalyx which repels platelets and clotting factors .
1- Ecto-adenosine diphosphatase
degrades adenosine diphosphate and inhibits platelet aggregation .
2- Thrombomodulin
serves as a binding site for thrombin to activate protein C , Which initiate an essential anticoagulant pathway.
3- Heparin-like molecules
serve as a cofactor for antithrombin III.
4- Normal endothelium secretes
tissue plasminogen activator
, which activates the fibrinolysis system.
prothrombogenic
mediates platelet adhesion and shear-stress-induced aggregation.
1- Normal endothelium produces and secretes
von Willebrand factor
2- Injury to endothelium is accompanied by loss of protective molecules and expression of
A) Adhesive molecules .
B) Procoagulant activities .
# All of above mentioned substances leads to development of :
A) Thrombosis .
B) Smooth muscle cell migration and proliferation .
C) Atherosclerosis.

3) Injured endothelium releases
thromboxane A2
that will produce VC and stimulate platelets aggregations .
Hyperemia & Congestion
Hyperemia
Hyper
“excess”
Emia
“blood”
Is an active process in which arteriolar dilation leads to an increase of blood flow due to arteriolar dilation .
occure at
sites of inflammation
skeletal muscle during exercises .
or
.
Affected tissue turn
red “erythema”
due to the engorgement of vessels with oxygenated blood .
Congestion
Is a passive process resulting from reduced outflow of blood from a tissue .
It can be either due to
cardiac failure
venous obstruction.
Or
.
Congested tissue take on a dusky reddish-blue colour “cynosis” due to red cell stasis of deoxygenated hemoglobin .
A bluish discoloration of the skin due to poor circulation or inadequate oxygenation of the blood.
cyanosis :
Hyperemia & Congestion effects on the body
As a result of the increased volumes and pressures
congestion commonly leads to edema.
In longstanding chronic passive congestion, the lack of blood flow
May result in ischemic tissue injury and scarring.
causes chronic hypoxia
Hyperemia
1) Active process
2) skeletal muscle during exercise or at sites of inflammation .
3) Arteriolar dilation
4) Tissue is red
5) Due to increased tissue inflow .
3) venous outflow obstruction .
1) Passive process
2) Generalized in cardiac failure .
5) Due to impaired venous outflow .
4) Blue-red color (cyanosis) .
Congestion
Accumulation of blood in tissue .
Common
Morphology
2) Chronic Lung Congestion :
(thickened fibrous septa, Heart failure cells)
3) Chronic Liver congestion
Central areas are red and slightly depressed .
Form a Nut Meg liver pattern .
The cut surfaces of congested tissues are often discolored .
Grossly
Due to
presence of high levels of poorly oxygenated blood.
Usually physiologic except in pathologic (inflammatory) conditions .
Infarction
1) Almost all infarcts results from thrombotic or embolic arterial occlusion.

2) Local vasospasm .
3) Hemorrhage into an atheromatous plague .

4) Torsions of vessels . e.g ( Testicular torsion , Bowel volvulus )
5) Traumatic rupture .
Causes
Occure with arterial occlusion in solid organs with end-arterial circulation .





With less collateral circulaion .
White infarct
The kidneys, spleen and heart
Limited venous outflow due to
Red infarct
Red infarct of Lung
bypass channels can’t develop.
vascular obstruction
Pulmonary
e.g
# The occlusion consists more of red blood cells and fibrin strands.
Occur with venous occlusion . ( e.g , ovary )
In loose tissues (e.g , Lung )

In tissues with dual circulation > Such as Lung .
Which allow blood flow from unobstructed parallel artery into a necrotic zone .

In tissue previously congested by sluggish venous outflow .
When flow is re-established to a site of arterial occlusion .
The process of infarct formation is called as infarction.
Note Although venous thrombosis can cause infarction , the more common outcome is just congestion .
Factors of that determine the occurance of Infarction
1) The naure of blood supply .
2) The rate at which occlusion develops . e.g ( time in 5 sec or 2 min )
3) Degree of occlusion .

4) Vulnerability to hypoxia . e.g
- Highly O2 dependent : Neurons, Myocardial cells and Hepatocytes .
- Less O2 dependent : Cartlidges , Adipocytes and tendons .

5) O2 carrying cappacity . e.g ( Anemia : cell mass O2 )

6) Presence of dual blood supply or collateral circulation . e.g Lung and Heart respectively .
grossly :
The infarct is wedge-shaped
"Red"
Infarct
“These infarcts are hemorrhagic because, although the pulmonary artery is cut off, the bronchial arteries from the systemic circulation are not cut off.”
Pulmonary
"Red"
Infarct
Microscopy :
Alveoli are closed and filled with heart failure cells or transudate .

Contains air bubbles .
Outlines of alveoli are still preserved . Coagulative necrosis
contains heart failure cells (hemosiderin-laden macrophages) .
# Thus, it is a coagulative necrosis because Tissue architecture are still preserved .
Myocardial White infarction
Grossly :
Darker hyperemic boarders
With Yellowish center of necrosis .

Remaining viable parts of myocardium are reddish-brown .
Fate of Infarction
(1)Small infarct: softened, absorbed

(2)Large infarct: organization and scar formation

(3)Septic infarct: abscess formation

(4)Infarction of brain, myocardium or lung: sometimes may cause sudden death.

Endothelium is damaged
Platelets aggregate to form a plug
Cogulation cascade starts
Fibrin strands formation
1) Endothelium: prothrombogenic and antithrombogenic effects

2) Define hyperemia and congestion and give their causes, morphology and the effects they produce

3) Define infarcts and list their causes. Describe the types of infarcts. Explain the factors which determine whether an infarct will occur or not. Describe their morphology and their fate with the help of two examples of infarction.
SEMINAR 3
Topic: Ischemia, congestion and Infarction
Objectives :
Done by / Sami Abdullah Almutairi
There are 2 stages of Coagulation :
1) Primary coagulation
Platelets aggregation
2) Secondary Coaglation
Coagulation Cascade
Congestion
Hyperemia
Physiological more than Pathological
Physiological :
skeletal muscle during exercises
Vasodilatation
Redness
Pathological :
Sites of Inflammation
Vasodilation
Edema
Redness
Hotness
Microscopy
Centrilobular necrosis with degenerating hepatocytes and hemorrhage .
Grossly
Microscopy
1) Hyperemia in Pneumonia :
Alveolar capillaries engorged with blood .
alveolar septal edema .
focal minute intra-alveolar hemorrhage .
Additionaly , Most body infarcts are coagulative necrosis except in brain which is liquafactive necrosis .
Revised by /
Dr / Abdulmnem
Dr / Mostafa Khudair
<12 H # Wavy fibers
# Normal central nucleus .
# unclear striations .
<1 D # Pink contraction bands .
# cells die and release their necrotic
contents attracts neutrophils .
<1-2 D # Almost complete lose of striations .
# The contraction bands are seen clearly .
# Neutrophils are begging to infiltrate .
# Signs of extensive hemorrhages .
<3-4 D # Huge amount of of neutrophils inflitration .
# Grossly, apparent areas of hemorrhage .
Area of an infarction become a site of healing with :
# plenteous of scar tissue .
# Macrophage infiltration .
# Followed by fibroblast and granulation tissue .
The role of edothelium at normal conditions is :
Antithrombogenic
The role of an injured endotheluim in hemostasis is :
Prothrombogenic
Summary
Endothelium
Hyperemia and congestion
An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage .
Occure with arterial occlusion in solid organs with end-arterial circulation .
1) White infarct
Limited venous outflow due to
#vascular obstruction
#bypass channels can’t develop.
The occlusion consists more of red blood cells and fibrin strands.
Thus, it is called Red infarct .
e.g Lung infarct
e.g Heart infarct
Infarction
2) Red infarct
Microscopy :
Myocardial White infarction
( Robin’s Basis of Pathology textbook)

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