pathology exam 3 Flashcards

1
Q

causes of edema

A

increase intravascular hydrostatic pressure, decreased intravascular pressure, increased microvascular permiability, decreased lymphatic drainage

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2
Q

hyperemia vs congestion

A

hyperemia is an increase due to inflammation congestion is an increase due to a blockage not flowing

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3
Q

what causes decreased intravascular osmotic pressure and what causes that protein to do that

A

decrease in albumin. this is caused by PLE, PLN, liver failure

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4
Q

increased microvascular permeability is due to what

A

acute inflammatory vascular changes

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5
Q

two main causes of hyperemia

A

physiologic (increased demand. blood to stomach)
pathologic inflammation.

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6
Q

R cardiac infufficiency is usually due to what? what does this cause? what is the general term for it

A

Right heart cardiac insufficiency. vena cava gets backed up causes blood to accumulate in the central lobular areas of the liver. congestion and degeneration occur. nutmeg liver

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7
Q

Left cardiac insufficiency is due to what. what occurs?

A

accumulation of blood and inc hydrostatic pressure in lung. macrophages in the lungs.

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8
Q

ecchymosis

A

3mm-2cm. increased vascular fragility, secondary to trauma or petechiae. dark red centers

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9
Q

hematoma

A

hemorrhage in a focal confined space.

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10
Q

virchows triad that is needed for a thrombi

A

endothelial injury, abnormal blood flow, hypercoagulability.

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11
Q

three requirements for a thrombosis

A

blood must flow, decreased flow rate that allows for contact with the epithelium, eddies are formed

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12
Q

the _____ alteration of blood flow is a major contributor to formation of venous thrombus

A

local formation of stasis

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13
Q

which direction do thrombi form

A

away from the heart. venous grow in direction of flow arterial grow against flow

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14
Q

four things a thrombi can do

A

propagate, embolize ( travel), dissolute (remove it), organize and recanalize (incorporate into vascular wall)

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15
Q

thrombus vs blood clot

A

thrombus: dry, attached to the wall, composed of platelets, opaque, rough, from circulating blood

blood clot: moist, smooth, shiny, not attached to the wall, from fibrin, forms in stagnant blood

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16
Q

DIC

A

pathological activation of the clotting cascade. throw clots everywhere in microcirculation. consequence not a disease

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17
Q

what is the major cause of embolism

18
Q

infarct? what are these usually the result of

A

area of ischemic necrosis bc blood supply or drainage was occluded. main result of a thrombotic or embolic event.

19
Q

explain the difference betwen acute, subacute, and chronic infarcts grossly

A

acute: red, raised
subacute: level, with with red periphery
chronic: sunken in. fibrous replacement

20
Q

hypovolemic shock is caused by what? what does it do?

A

loss of blood or plasma volume. bp falls and b/v decreases. compensation is bp increases and b/v increases

21
Q

cardiogenic shock. cause, signs

A

heart pump failure. decrease in b/v and cardiac output. anaerobic glycolysis so metabolic acidosis occurs

22
Q

neurogenic shock. cause, consequence

A

injury or pain. loss of sympathetic tone. PNS takeover. vasodilation

23
Q

anaphylactic shock cause, consequence

A

IgE allergic rxn. vasodilation, inc permiability, edema

24
Q

Septic shock. cause and consequence

A

LPS generally from G- infection. TLR4 pathway. increase thrombi, organ failure, DIC, vasodilation.

25
three stages of shock: compensation, progressive, irreversible. defining factor of compensation
inc cardiac rate, slight inc in anaerobic met and decrease in nonvital circulation
26
progressive stage of shock. symptoms
cardiac rate increases while cardiac output greatly decreases, aerobic metabolism decreases, vital and nonvital circulation decrease
27
irreversible shock symptoms
cardiac rate and output low all metabolism low circulation all low, lactic acid is high
28
what is the first area of the body to suffer from hypoxia
central portal area in hepatic lobule. very active
29
if tissue framework is damaged what occurs
fibrosis and scarring
30
five components of fibrosis
inflammation, angiogenesis, fibroblast , scar formation, connective tissue remodel
31
angiogenesis is important for what two things
formation of blood vessels. important for fibrosis and tumor growth.
32
granulation tissue appearance. why
pink/tan shiny. new bloodvessels are leaky
33
angiogenic factor. what does it do (3 things)
vascular endothelial growth factor (VEGF). proliferation, mobilization and survival of endothelial cells
34
main differences between first intention and second intention healing.
1st: clean, small, epidermis returns to normal thickness, no real surface scar seen. 2nd: large, infected, wound is closed by contraction from myofibroblasts. epidermis is thinner, divot on surface is seen.
35
number one thing that impairs wound healing
infection. (also nutrition)
36
contracture what does it look like? why does it happen?
loss of mobility due to excessive contraction of myofibroblasts. common after severe burns
37
3 forms of amyloid (pathologic deposition in tissues)
AL, AA, AB
38
which form of amyloid is associated with primary amyloidosis
AL, from plasma cells. neoplasia
39
which form of amyloid is associated with secondard amyoidosis
AA. serum, from the liver. persistent inflammation
40
what is the overall pathogenesis of amyloidosis
abnormal folding of proteins that are deposited in tissues and organs and interfere with normal cellular function
41
chronic inflammation involves what amyloid
AA. from liver
42
unknown stimuli and carcinogens involve what amyloid
AL. from plasma cells