2.5 Path: Vascular disease and would healing Flashcards

1
Q

What is transudate?

A

fluid only

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2
Q

What is exudate?

A

Fluid + cells

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3
Q

What does pulmonary edema look like histologically?

A

Pink fluid in alveolar spaces

Serous fluid “Transudate”

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4
Q

With blood, what is congestion?

A

passive vascular dilatation from reduced outflow. Increased red blood cells within blood vessels.

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5
Q

What is hemorrhage?

A

leakage of red cells into tissue

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6
Q

What is liver passive congestion?

A

Congestion common in liver, generally in setting of heart failure—> R heart failure, backflow, blood pools in the liver
Passive congestion of the liver aka nutmeg liver

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7
Q

What is hemostasis? Generally, how does this occur?

A

Hemostasis= stopping blood flow (aka clotting)
Endothelial cell senses injury to self or nearby—> contrivers vasoconstriction —> IMPORTANT: activate platelets —> Platelets lay down over site on injury, forming platelet plug over damaged endothelium; if severe the signal is more intense then the Coagulation cascade is activated. This is a family of circulating proteins the quickly start forming products (eg fibrin and more) to heal defect in vessel END: form a thrombus (made of fibrin + RBCs)

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8
Q

What is thrombosis? Generally, how does this occur?

A

Why does this happen? Virchow’s triad- endothelial injury, abnormal blood flow (eg aneurism, other defect), or hypercoagulablity (can be from inflammation, immune injury, cancer).

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9
Q

What is Virchow’s triad?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability
= thrombosis

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10
Q

How do you go from oxygen depletion in tissue to thrombus?

A

Infarct—> Widespread endothelial event —> clotting cascade —> thrombus

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11
Q

Histologically, what is a thrombus? Why are they multicolored?

A

Intralumenal mass with mix of red blood cells, platelets and fibrin
Components separate into areas by molecular weight which appear alternating light and dark .

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12
Q

What are the potential fates of a thrombus?

A

Things they can do: (these options aren’t mutually exclusive)
Propagating- when a thrombus grows within the vessel
Dissolve- A natural system of fibrinolytic factors that break down clots (anti-fibrin factros) **best resolution is for body to break clots down
Reorganization and recanulazation: Eventually, the body will “take over” or “absorb” the thrombus and form a new channel through it
Embolism- Break off and travel elsewhere: typically causes the most damage

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13
Q

How does a thrombus organize and recanulize?

A

After 5-7 days, migration of fibroblasts and onset of angiogenesis within thrombus
Forms granulation tissue. “organizes”
After several days, get a response from fibroblasts outside the vessel. Angiogenesis begins. In time, new tissue “plug” is formed =granulation tissue” , and a channel can be formed through the clot. In time, the clot should remove, Depends on flow and blood access.
10-14 days, angiogenesis results in new vessels with lumens within thrombus, beginning flow or “recanulization”

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14
Q

What is en embolism? What are some common examples?

A

Detached solid, liquid or gaseous mass carried by blood to distant site from origin
Common types: Thromboembolism, Bone marrow embolism, Air Embolism

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15
Q

What is the difference between red infarct and white infact?

A

Red infarct is dead tissue that has RBCs in it because the tissue has more than once blood source. Eg lung tissue
White infarct is dead tissue absent RBCs because the one source was cut off

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16
Q

What is atherosclerosis?

A

Disorder resulting in arterial lesions called Atheroma or Atheromatous Plaques
Raised lesions in the intima which protrude into the lumen resulting in turbulent blood flow
Causes 50% of deaths in developed world
Etiology unclear..chronic inflammation/healing response?

17
Q

How does atherosclerosis form? At the tissue level.

A

Endothelial cells compromised, leak, allow cells from bloodstream esp. macrophage to enter the wall of the artery (inside wall of artery) and lipid leaks in as well (association with cholesterol). Once the macrophage is in the wall, they secrete factors that create lead to plaque development

18
Q

What is the first sign of the formation of atheromatous plaque?

A

Fatty streak: earliest lesion, lipid filled macrophages within intima

19
Q

Histologically, what is atherosclerotic plaque?

A

A complex, raised lesion with smooth muscle cells, macrophages, T cells; collagen; lipid

20
Q

What is a foam cell?

A

A macrophage filled with lipid

21
Q

What is the general sequence in wound healing?

A
Complex ordered process
Acute inflammatory response
Migration of epithelial and connective tissue
Angiogenesis
Extracellular matrix synthesis
Collagen synthesis and remodeling
22
Q

What happens in the first 24 hours after injury?

A

Acute Inflammatory Response
Neutrophil Infiltration
Erythema, Edema

23
Q

What happens 24-48 hours after injury?

A

Acute inflammatory response goes away, neutrophils die from apoptosis
Fibroblasts and microphages recruited to site- they simulate angiogenesis
See early bridging of new epithelial cells
Platelets and fibrin recruited to site- make a seal/scab.. form “fibrin cap”

24
Q

What happens on day 3 of wound healing?

A

Macrophages replace PMN’s
Granulation tissue invades wound space
Continued epithelial thickening

25
Q

What happens on day 5 of wound healing?

A

Maximal angiogenesis and granulation tissue
Collagen bridges wound
Epithelium restored

26
Q

What happens in the second week of wound healing?

A

Fibroblast proliferation and collagen synthesis
“Blanching”
Decreased vessels and edema
Resolution of inflammation Infiltrate

27
Q

What happens about a month into wound healing?

A

Cellular connective tissue
Progressive increase of tensile strength over next several months
Blood vessels have matured
Collagen lines up in a functional way to

28
Q

What is healing by first or second intention?

A

healing by 1st intention- the previous sequence, normal healing
healing by 2nd intention- more granulation, more inflmamtion, can take months to fill in , heals from outside in eg pressure sores, ulcers

29
Q

What are the characteristics of secondary healing?

A
More intense inflammation
More granulation tissue
Dramatic  wound contraction
10% of original size
Myofibroblasts