Terms in this set (75)
When can you see lines of Zahn
when blood is still flowing
What are lines of Zahn
layers of RBCs that have adhered to platelet and fibrin clot bc blood is flowing there is organisation of fibrin, platelets, RBCs; fibrin, platelets, RBCs; etc.
What are the microscopic hallmarks for lines of Zahn?
What are the macroscopic hallmarks for lines of Zahn?
What is haemostasis
process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury and culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding
What are the four stages of haemostasis
Explain what happens during the vasoconstriction stage of haemostasis
vasoconstriction in response to epithelial injury
•reduces blood flow
•effect is transient (eg. small knick during shaving)
-reflex neurogenic mechanism
-endothelin (and other cytokines)
Explain what happens during primary haemostasis
formation of platelet plug mediated by:
•platelet adherence (vWF)
•platelet activation (vWF)
•platelet aggregation (secretory granules)
What promotes platelet adherence?
- von Willebrand factor (vWF) and collagen
What activates platelets and what is the result?
vWF not only promotes adherence, but activates platelets too, causing a shape change (flat spiky) to increase surface area
What causes aggregation of platelets?
activated platelets release secretory granules for recruitment and aggregation
Explain what happens during secondary haemostasis
deposition of fibrin mediated by:
How is thrombin generated?
release of tissue factor (membrane-bound procoagulant glycoprotein) binds and activates factor VII this starts the ¡Coagulation Cascade! which produces thrombin
What is the result of activated thrombin (what does thrombin do?)
cleaves circulating fibrinogen into fibrin
What is the significance of fibrin?
•creates an insoluble meshwork around platelets=platelet plug
•also a potent activator of platelets, so more platelet aggregation
Explain what happens during the fibrinolysis stage of haemostasis
clot stabilization and resorption
•permanent plug: current plug contracts
-t-PA (tissue plasminogen activator)
What does t-PA do?
•limit clotting to the site of injury
•leads to clot resorption and tissue repair
Why is thrombomodulin important?
Blocks coagulation cascade (turns of the positive feedback)
What blood test can you do for clots (VTE, PAD, PVD, DVT)?
•A test for fibrin
•Not totally definitive for disease because it will show results for minor injuries
•May help form a differential diagnosis for hypothesised disease states
A localised area of necrosis arising because of persistent ischaemia, as seen in a living organism
What is the most common cause of infarctions?
Arterial thrombosis and arterial embolism are vast majority of infarctions
What are minor causes of infarctions?
•Venous embolisms (w/ or w/out paradoxical embolisation)
•Venous thrombosis often results in congestion w/ bypass channels restoring outflow to compensate for arterial inflow
•Compression (tumor, dissecting aortic aneurysm, edema, compartment syndrome)
•Vessel torsion (twisting)
•Entrapment in hernia sac
a deposit of plaque on or within the arterial wall
the transportation by the blood of abnormal material and its impaction in a vessel at a point remote from its entry into the circulation
A semi-solid mass formed from constituents of the blood that occurs inside a vessel during life (cf. clot)
Describe Virchow's triad
The 3 abnormalities leading to thrombus formation:
1. abnormal blood flow (stasis or turbulence)
2. endothelial injury
Risk factors for thrombosis and pulmonary embolism:
involuntary contraction or spasm of a blood vessel
Pain w/ passive motion,
Poikilothermia (can't regulate ones body temperature--coldness),
•The result of a severe blunt or crushing injury that causes bleeding in the muscles of the leg
•Increased pressure within a compartment compromising other structures in that same compartment
•Edema within a confined space
•Compression of the nerves and blood vessel
-Pain (always first): unrelieved with elevation or by pain medication
-Pulselessness (always last)
What are red infarcts?
•May be either septic or bland (same for white infarcts)
When and where do red infarcts occur?
1) venous occlusion
2) loose / spongy tissues (lungs)
3) tissues w/ dual circulation (lung & small intestine)
4) congested tissues (sluggish venous outflow)
5) reperfusion (angioplasty of arterial obstruction--heart after transmural infarct MI)
What are white infarcts?
•Are anemic ("why?" bc no heme (aka iron))
•May be either septic or bland (same for red infarcts)
When and where do white infarcts occur?
In solid organs:
1) without dual circulation when obstruction in arteries, often end arteries (spleen, kidney, and often non-transmural infarcts to the heart)
2) tissue density limits seepage of blood from adjoining vascular beds (same locations as #1)
Explain the wedge shape of infarcts
(Imagine a pyramid) •Both red & white infarcts
•The occluded vessel becomes the apex and the infarcted organ periphery becomes the base
When would the base of an infarct get an overlying fibrinous exudate and would this change it's shape?
•If the base is a serosal surface (outermost coat or serous layer of a visceral structure)
•The lateral margins may be irregular due to flow from adjacent vessels
What would be the appearance of an acute / fresh infarct?
1) Poorly defined / indistinct
How would an acute / fresh infarct in organs without a dual circulation appear over time?
These are white infarcts become:
2) Well defined
3) Hyperaemic / Rimmed by active congestion
4) Subsequently replaced by scar / fibrosis
Why do white infarcts appear the way they do?
so No RBCs
so No heme (iron) to convert into hemosiderin
How would an acute / fresh infarct in organs with a dual circulation appear over time?
These are red / haemorrhagic infarcts become:
2) Brown residuum
Why do red infarcts appear firm and brown?
Because extravasated RBCs are phagocytosed by macrophages & heme (iron) is converted hemosiderin.
excessive amount of blood in a part or area resulting from too much blood being delivered by the arteries (synonymous with active congestion)
What are septic infarcts?
Can be either
1) Infection of infarcted / necrotic tissue
2) Infected cardiac valve vegetations embolise (eg. infective endocarditis emboli)
3) Occur in either red or white infarcts
What is the result of septic infarct?
An abscess forms from the infarct with an enormous inflammatory response
What are bland infarcts?
Your typical uninfected red or white infarct
What is the main histological findings associated with infarcts? Are there any exceptions?
1) Ischemic coagulative necrosis (after 4-12hrs)
2) Inflammation starts at margin (hours after necrosis)
3) Inflammation well defined at margin (1-2 days)
4) Repair begins in preserved margins
5) Mostly result in scar / fibrosis (but some tissue can have parenchymal regeneration if stroma is intact)
The brain does not undergo coagulative necrosis --> liquefactive necrosis instead
What is the main pathological findings associated with infarcts?
1) Swelling and increased opacity of tissue (reversible cell injury)
2) Increased yellow/brown discolouration and opacity of infarcted area
3) Development of a hyperaemic border due to ingrowth of granulation tissue
4) Shrinkage of infarcted area due to removal of necrotic tissue
5) Formation of dense grey fibrous scar
Brain infarcts are also known as what?
What is the histological finding associated with brain (CNS) infarcts?
1) Results in liquefactive necrosis
2) Resolves to form cavity
Functional parts of an organ in the body. This is in contrast to the stroma, which refers to the structural tissue of organs, namely, the connective tissues.
Occurs through hepatocyte regeneration following liver injury
(Synonymous with hyperplasia)
What factors influence the development of an infarct?
1) Nature of blood supply (alternative vascular supply?)
2) Rate of occlusion (slow development = formation of collateral blood supply)
3) Type of affected tissue (neurons and myocardiocytes vulnerable to ischaemia)
4) Oxygen content of blood (aka hypoxaemia)
a connection between two blood vessels or tubes
When does myocardial infarction occur?
After occlusion of coronary arteries
What causes a myocardial infarction?
Coronary artery occlusion caused by the four stages of haemostasis following endothelial injury (Virchow's Triad)
When and where would you find transmural infarcts?
1) occlusion of left anterior descending = anterior transmural
2) left circumflex = left sided transmural
3) posterior descending br. of right coronary = posterior transmural
-Regional: transient/partial obstruction
-Circumferential: global HTN
-Small intramural vessel occlusions
•A Transmural infarct w/ reperfusion may act & heal to look like a Non-Transmural infarct
•Cell proteins are altered or denatured (hence coagulation)
•Loss of normal organelle structure, but preservation of cellular structural outline (due to increased lactic acid)
•Usually found following ischemia or infarction
•Typically occuring in kidneys, heart, and adrenal glands
•The histopathologic hallmark of a fresh pulmonary infarction
What are the macroscopic hallmarks of coagulative necrosis?
What are the microscopic hallmarks of coagulative necrosis?
What are the macroscopic hallmarks of liquefactive necrosis?
What are the microscopic hallmarks of liquefactive necrosis?
What are the macroscopic hallmarks of caseous necrosis?
What are the microscopic hallmarks of caseous necrosis?
What are the macroscopic hallmarks of fat necrosis?
What are the microscopic hallmarks of fat necrosis?
(Lipases attack fat --> increase in FFAs --> FFAs bind with Ca --> formation of "soaps")
What is saponification?
Formation of "soaps" from fat
How does saponification occur?
1) Lipases attack fat
2) Increase in FFAs
3) FFAs bind with Ca
4) formation of "soaps"
What are the macroscopic hallmarks of fibrinoid necrosis?
What are the microscopic hallmarks of fibrinoid necrosis?
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