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

A

thrombus

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
Q

three stages of shock: compensation, progressive, irreversible. defining factor of compensation

A

inc cardiac rate, slight inc in anaerobic met and decrease in nonvital circulation

26
Q

progressive stage of shock. symptoms

A

cardiac rate increases while cardiac output greatly decreases,
aerobic metabolism decreases, vital and nonvital circulation decrease

27
Q

irreversible shock symptoms

A

cardiac rate and output low
all metabolism low
circulation all low, lactic acid is high

28
Q

what is the first area of the body to suffer from hypoxia

A

central portal area in hepatic lobule. very active

29
Q

if tissue framework is damaged what occurs

A

fibrosis and scarring

30
Q

five components of fibrosis

A

inflammation, angiogenesis, fibroblast , scar formation, connective tissue remodel

31
Q

angiogenesis is important for what two things

A

formation of blood vessels. important for fibrosis and tumor growth.

32
Q

granulation tissue appearance. why

A

pink/tan shiny. new bloodvessels are leaky

33
Q

angiogenic factor. what does it do (3 things)

A

vascular endothelial growth factor (VEGF). proliferation, mobilization and survival of endothelial cells

34
Q

main differences between first intention and second intention healing.

A

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
Q

number one thing that impairs wound healing

A

infection. (also nutrition)

36
Q

contracture what does it look like? why does it happen?

A

loss of mobility due to excessive contraction of myofibroblasts. common after severe burns

37
Q

3 forms of amyloid (pathologic deposition in tissues)

A

AL, AA, AB

38
Q

which form of amyloid is associated with primary amyloidosis

A

AL, from plasma cells. neoplasia

39
Q

which form of amyloid is associated with secondard amyoidosis

A

AA. serum, from the liver. persistent inflammation

40
Q

what is the overall pathogenesis of amyloidosis

A

abnormal folding of proteins that are deposited in tissues and organs and interfere with normal cellular function

41
Q

chronic inflammation involves what amyloid

A

AA. from liver

42
Q

unknown stimuli and carcinogens involve what amyloid

A

AL. from plasma cells