Lecture 12: Blood Flow Alterations, Shock Flashcards
1
Q
Primary hemostasis includes:
- Coagulation cascade
- Activation of thrombin
- Fibrinolysis
- Platelet aggregation
A
Platelet aggregation
2
Q
Brick is to mortar as platelets are to:
- Thrombin
- Factor VII
- Fibrin
- Plasminogen
A
Fibrin
Fibrin is the glue that helps stabilize the platelets
3
Q
- what is this
- How can you tell this is formed antemortem
A
- Arterial thrombus (saddle thrombus)
- firm
- Other clotted blood easily washed out
- True thrombus stays behind
- pale regions, dark red regions
4
Q
- Where is an arterial thrombus initiated at?
- does it grow upstream or downstream?
- Will it always be completely occlusive?
A
- Initiated at areas of endothelial damage
- Downstream growth (away from site of attachment)
- There’s the attachment site, and then the growth of thrombus continues away from the heart
- can be completely occlusive, but often times are not
- Remember it’s a higher pressure vessel, so blood will blast through to some degree
- If it’s a fully occlusive thrombus, then death will come rapidly
5
Q
- if a tail of an arterial thrombus breaks off and lodge in other places what will that be called?
- what does it prevent?
A
- Called a thromboembolism
- will prevent oxygenated blood from entering a site
6
Q
- What is this called?
- What distinguishes it?
- What necrosis will this be classified as?
A
- renal arterial infarct
- often have a wedge shaped outline
- Subtle elevation of the cortex here, so it’s slightly swollen,
- it’s pale
- we can still see the linear structures that represent the nephrons
- Coagulative necrosis
7
Q
- Where would venous thrombi form?
- Are they sometimes or often occlusive?
- Will it have upstream or downstream growth?
- What will it prevent?
A
- venous thrombi are most likely to occur in areas of stasis
- Blood pooling is a risk factor
- Remember there’s less pressure, less vascular tone in the venous system
- So you have the greater likelihood that the blood may pool
- Often occlusive
- Upstream growth
- Have a site of attachment, and that thrombus is going to grow in front of that attachment
- prevent the venous blood from leaving a site
8
Q
- Would this be an arterial or venous thrombi?
- why?
A
- venous thrombi
- Blood can’t escape so the Lesion will be dark red to black in color
9
Q
- what kind of infarct would this be
- why is this happening
A
- venous infarct
- there’s s twist or impingement that’s impeding the venous return
10
Q
- What kind of clot is this?
- What is in the yellowish color
- Red?
- is this normal?
A
- Chicken fat clot (post mortem, normal)
- Yellow material is a combination of fibrin, WBC, other proteins
- Red, jelly-like material - Remnants of RBC
- it is normal
11
Q
What happens in deep vein thrombosis?
A
- Sitting allows for stasis of blood to form in the long, deep veins of your leg when you sit for a long period of time,
- If you suddenly get up and start moving around, the large thrombus can break loose, will go straight to your heart, to the lungs
- Large caliber vessels, therefore really good at making large caliber thrombi
- Can be a rapid cause of death
12
Q
what are 5 other forms of emboli
A
- Bacteria - mats of fibrin seeded with bacteria makes for a great embolus
- Fat
- Cartilage - as we saw earlier this semester, can serve as an embolus if it gets into the bloodstream
- Air- from an IV apparatus
- Parasites - heartworms
13
Q
Describe the steps of what happens in DIC, disseminated intravascular coagulation
A
- Often secondary to some other primary disease
- Ex: septic, undergoing widespread metastatic event leading to
- endothelial damage (widespread)
- Allows for the formation of microthrombi
- Ischemic injury to organs
- Could lead to multiple organ failure
- Consumption of platelets and coagulation factors
- When you’re creating lots of small thrombi throughout your body, you’re also using up platelets and coagulation factors
- Which means that if you need to stop hemorrhaging somewhere, you can’t
- All the factors have been used up
- So spontaneous hemorrhage may be the next step
- Activation of fibrinolysis
- In addition, once you have the presence of thrombi in the vascular system, fibrinolysis kicks off
- Body will do what it knows to do, with is to break down thrombi
- Leads to multiple FDP, or fibrin degradation products
- Leads to hemorrhagic diathesis (diathesis = exiting of blood from a space. Nice way of saying bleeding out, or uncontrolled bleeding)
- See petechiae and ecchymoses in skin or gums, on serosal surfaces
- Ischemic injury to organs
14
Q
- What is hemorrhagic diathesis?
- What will you see grossly when this happens in DIC?
A
- diathesis = exiting of blood from a space. Nice way of saying bleeding out, or uncontrolled bleeding)
- See petechiae and ecchymoses in skin or gums, on serosal surfaces
15
Q
Can you run one test to diagnose DIC?
A
- DIC is not something we can run one test for and know that DIC is going on
- Harder to pinpoint
- More of knowing the risks, and what risk factors are present such that DIC may occur