Term
| What is the most common inherited hyper-coagulable state (5% of whites)? |
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Definition
| Factor V Leiden Mutation- heterozygotes have 5x greater risk of venous thrombosis |
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Term
| What are "white thrombi"? What about "red thrombi"? What are "Mural thrombi"? |
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Definition
White= arterial (rich in platelets)
Red= Venous (rich in erythrocytes)
Mural= cardiac wall |
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Term
| Distinguish between "mural thrombi" and "vegetations." |
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Definition
| Both are thrombi. Mural are in the heart walls and vegetations are in the heart valves. |
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Term
| What are the 4 fates of thrombi? |
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Definition
1) Dissolution
Natural breaking up
2) Propagation
Spreading
3) Embolization
Pulmonary are common and dangerous. Medium-sized cause hemorrhagic infarctions and Large ones can cause acute right heart failure and sudden death.
4) Organization and Re-canalization
(in-growth of fibroblasts that convert thrombus to fibrous tissue which can become vascularized. |
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Term
| Distinguish between "saddle emboli" and "paradoxical emboli" |
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Definition
1) Saddle Emboli are in pulmonary trunk
2) Paradoxical emboli pass through patent foramen ovale or atrial septal defect to go to organs other than lungs (it is a "paradox," because these passages should not even exist!) |
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Term
| What are some surgical concerns relating to Thrombosis? |
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Definition
1) Surgery causes hyper-coagulable state, but anticoagulation carries risk of bleeding.
2) Clots always form around catheters (the larger the cath the larger the clot)
3) Centrally-inserted catheters can cause clots to embolize as they are removed. |
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Term
| Distinguish between "white anemic" infarcts and "red hemorrhagic" infarcts. |
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Definition
1) White anemic- solid organs with end-arterial circulation (heart, spleen, kidney)
2) Red hemorrhagic- venous occlusion (ovarian torsion), dual or anastomosing blood supply (lung or intestine) or with re perfusion |
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Term
| What factors determine the likelihood of infarction and how is it recognized histologically? |
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Definition
1)
- Organ vulnerability to hypoxia (neurons are 4 min)
- Rate of vascular occlusion (collateral circulation can develop),
- Blood supply (dual is protective in liver)
- Blood oxygen content.
2)
- Coagulative necrosis is most common form and is apparent after 12-18 hours usually with inflammation.
- Neutrophil response is 1-2 days after and followed by fibroblasts and macrophages
- In Brain, ischemic necrosis is "liquifactive" |
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Term
A patient presents with blackening and shrinkage of their left 2nd and 3rd toes. When they arrived in the hospital, the toes were dry, but after 2 days, they became wet.
What is going on and how do you treat? |
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Definition
Gangrene (coagulative necrosis) with a superimposed bacterial infection 2 days after admittance (turns dry into wet).
Unfortunately, the only viable option is surgical removal. |
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Term
| Why might a patient with acute pancreatitis present with chalky, white, "soap-like" stool? |
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Definition
Pancreatic enzymes are leaking out and digesting peri-pancreatic fat instead of diet-supplied fat.
Released fatty acids bind calcium and cause this appearance. |
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Term
| What causes an ulcer to form and how is it different than an "erosion"? |
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Definition
Ulcers are excavations (local defect) in the surface of organs or tissues and are produced by sloughing of inflamed necrotic tissue.
Erosion is an area of denuded epithelium with intact BM and deeping layers |
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Term
| Distinguish between "regeneration" and "healing" |
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Definition
Regeneration requires intact connective tissue scaffolding and can only occur in superficial injuries (involves fully functional replacement of dead tissue).
Healing involves fibrous patching that lack functional capacity, but that hold things together.
Remember, "Granulation Tissue" is healing tissue with cell debris, macrophages, lymphocytes, angiogenesis, fibroblasts and new collagen. It is pink-red and soft with a grainy surface. |
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Term
| What should you think of in Pathology, when you see the word "organization." |
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Definition
This fibroblasts!
"Organization" involves conversion of dead tissue or clots to fibrous tissue. |
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Term
| What are some local and systemic factors that inhibit wound healing? |
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Definition
Systemic- Diabetes, Vascular disease, Malnutrition, Steroids
Local- Infection, Early motion, foreign bodies. |
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Term
What is "Dehiscence?"
What are "Adhesions"? |
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Definition
These are both complications of healing.
1) Dehiscence is rupture of surgical wound or anastomosis. Can be caused by increased intra-abdominal pressure from vomiting, ileus, coughing (rare in laproscopic surgery)
2) "Adhesions" are abnormal connections b/w two things from surgery (fibrous is worse than fibrinous). Solved AND caused by surgery. |
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Term
| Why might you be concerned if a patient has defects in stromelysin-1? |
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Definition
It prevents "Contractures"!
This is MMP-3 and it is important to protect against excessive wound contractions leading to impaired motion |
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Term
| Why do myofibroblasts persist in Keloid scars? |
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Definition
| Remember, Keloids are hypertrophic scars that exceed original wound. Autocrine production of TGF-B causes persistent myofibroblasts in between collagen bundles. |
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Term
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Definition
Also called "fibromatosis," desmoid tumors are rare disorders involving proliferatino of myofibroblasts and production of collagen that occur in rectus abdominis muscle incisions.
Unlike Keloids, Desmoid tumors infiltrate, but do not metastasize and spread to discontinuous sites, so they can be surgically excised. |
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