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MDTI > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

hyperemia

A

local increase in blood volume. increased arterial inflow due to arteriolar dilation. well oxygenated blood flowing into tissue=bright red erythema. warm. ACTIVE process

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2
Q

examples of hyperemia

A

inflammation, exercise, blushing

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3
Q

cause of hyperemia

A

vasodilation of artery leading to locally increased blood flow

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4
Q

hyperemic border around necrosis

A

white necrosis due to arterial thrombi-occlusion or thromboembolism and subsequent acute inflammatory response dilates border vessels

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5
Q

congestion

A

local increase in blood volume due to decreased venous outflow from an organ. blue-red tissue=cyanosis from increased deoxygenated blood. PASSIVE process

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6
Q

cause of congestion

A

impaired venous outflow due to compression, constriction, or functional problem of heart

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7
Q

how does congestion cause edema

A

hydrostatic pressure at venule end increases and exceeds osmotic pressure so that fluid is driven out everywhere via Starling forces and lymphatics are overwhelmed

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8
Q

what typically accompanies congestion?

A

edema

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9
Q

venous thrombosis and congestion

A

blocks blood from exiting tissue. initially there is congestion, which causes increased hydrostatic pressure in vessel and edema. but most tissues have multiple venous drainage pathways, so additional channels open and help bypass obstructed vein.

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10
Q

right heart failure

A

back up of blood into systemic veins (IVC/SVC), which commonly affects the liver.

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11
Q

left side heart failure

A

back up of blood into lungs, shortness of breath

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12
Q

where is liver congestion due to right sided heart failure found?

A

central vein (hepatic vein to IVC)

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13
Q

nutmeg liver

A

centrilobar congestion and periportal fatty change= chronic passive congestion of liver. impaired o2 delivery to hepatocytes which then accumulate fat

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14
Q

hemorrhage

A

extravasation of blood due to vessel rupture

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15
Q

hematoma

A

space occupying lesion of blood

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16
Q

tissue hemorrhages small to big

A

petechiae (1-2mm), purpura (>3mm), ecchymoses (>1-2cm)

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17
Q

thrombus

A

pathologica hemostatic plug within a blood vessel that is composed of platelets, fibrin, and trapped RBCs

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18
Q

embolus

A

intravascular solid, liquid, or gas that is carried from site of origin to a distal site in the bloodstream. doesn’t mix with aqueous portion of blood

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19
Q

thromboembolus

A

detached thrombus that embolizes

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20
Q

how to identify thrombi

A

lines of zahn and adhesion to vessel wall

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21
Q

virchows triad

A

endothelial injury, hypercoaguability, abnormal blood flow all lead to thrombi

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22
Q

important factors leading to arterial thrombi

A

endothelial cell injury and turbulent flow. atherosclerosis, inflammation

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23
Q

characteristics of arterial thrombi

A

prominent lines of zahn, white appearance (more platelets/fibrin than RBCs)

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24
Q

where are arterial thrombi more likely to occur

A

small to medium arteries (coronary, cerebral, femoral). often occlusive and present risk of infarction. less common in aorta (present as mural thrombi that stick to wall but don’t occlude. still risk embolization)

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25
Q

important factors leading to venous thrombi

A

stasis, hypercoagulative states due to increased concentration of activated coag factors and depletion of inhibitors

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26
Q

characteristics of venous thrombi

A

less prominent lines of zahn due to slow blood flow, red appearance due to trapped RBCs

27
Q

common locations of venous thrombi

A

superficial and deep veins of legs and pevic veins

28
Q

important factors of cardiac chamber (mural) thrombi

A

endocardial injury, stasis: enlarged chambers (poor contractibility=stasis), atrial fibrillation (local stasis), post myocardial infarction (stasis due to wall motion abnormality), abnormal valves. more RBCs

29
Q

4 general fates of thrombi

A

resolution, propagation, embolization, organization/recanalization

30
Q

where do venous thromboemboli travel?

A

pulmonary circulation.

31
Q

when might venous thromboemboli travel to systemic circulation? PARADOXICAL EMBOLIZATION

A

if there is a patent foramen ovale, ventricular septal defect, or PDA (pulmonary artery to aorta)

32
Q

where do arterial thromboemboli travel?

A

lodge distally in a smaller artery

33
Q

where do aortic thromboemboli travel?

A

variable distal locations in smaller branch off aorta

34
Q

where do right cardia chamber thrombi travel?

A

pulmonary arterial circulation

35
Q

where do left cardiac chamber thromboemboli travel?

A

systemic arterial circulation

36
Q

organization of thrombi

A

ingrowth of granulation tissue cells into the thrombus as mechanism of repair and gradual conversion to fibrous tissue. recanalization. followed by incorporation into vessel wall via fibrous plaques and bands

37
Q

recanalization

A

new vascular channels connecting end to end, allowing reestablishment of blood flow through the scar

38
Q

what type of tissue is involved in thrombi repair?

A

granulation tissue

39
Q

clinical consequences of thrombi/thromboemboli

A

edema, congestion, embolization, infarction

40
Q

consequences common to venous thrombi/thromboemboli

A

edema, congestion, embolization

41
Q

consequences common to arterial thrombi/thromboemboli

A

embolization, infarction

42
Q

infarction

A

ischemic necrosis of tissue due to occlusion of arterial blood supply or venous drainage (uncommon)

43
Q

what factors do infarctions depend upon?

A

susceptibility of tissue to ischemic injury, rate of occlusion development (slow=collateral formation more likely), location of thrombus (more likely arterial), arterial blood supply (1v2), venous drainage

44
Q

which tissues are most susceptible to infarction

A

neruons

45
Q

white (anemic) infarcts

A

arterial, solid organs with one blood supply. generally wedge shaped due to blood flow pattern from hilum

46
Q

red (hemorrhagic) infarct

A

venous with single drainage (0vary, testes), in organs with 2 blood supplies (lung, liver:must be secondary to impairment of other circulation like congestive heart failure or underlying lung disease), or from repercussion after white infarct since damaged vessels are leaky or via free radical injury

47
Q

erythema

A

redder tissue (increased oxygenated blood). due to hyperemia

48
Q

right sided heart failure leads to…

A

liver congestion (via IVC backup)

49
Q

left sided heart failure leads to…

A

lung congestion (via pulmonary vein backup)

50
Q

normal pressure differentiation along capillary (A to V)

A

intravascular hydrostatic pressure decreases (fluid exits artery end) and intravascular osmotic pressure increases (reabsorbed at venous end) longitudinally.

51
Q

do venous thrombi result in congestion and edema?

A

might. but most of the time, collateral vessels take over so venous thrombi not usually associated with infarction

52
Q

thrombosis and age

A

risk increases with increasing age

53
Q

who is at a much greater risk for thrombosis in addition to the elderly?

A

hospitalized patients

54
Q

why are hospitalized patients at a higher risk for thrombi?

A

cardiovascular disease and prolonged immobilization lead to stasis in the venous system and allows low levels of activated clotting factors to accumulate

55
Q

risk factors for venous thromboembolism (VTE)

A

systemic diseases, inflammatory states, things that affect movement of blood through the systemic system

56
Q

VTE prevention in hospital

A

mobilize patients as soon as possible, anticoagulation via heparin, mechanical compression in patients unable to tolerate anticoagulation

57
Q

Disseminated Intravascular Coagulation (DIC)

A

response to an injury that causes activation of normal blood clotting and fibrinolytic mechanisms. but the stimulus for activation overwhelms normal control mechanisms. Clotting exceeds factor replacement so that bleeding occurs as well

58
Q

clinical manifestations of DIC

A

patient may present with severe blessing, thrombosis, or both. acutely ill patients usually bleed, thrombosis is classically seen with cancer

59
Q

DIC lab findings

A

increased PT/aPTT (used up factors), decreased platelet count (aggregated), microangiopathic hemolytic anemia (schistocytes due to fibrin RBC shearing), presence of D dimers

60
Q

treatment of DIC

A

TREAT UNDERLYING CAUSE

61
Q

most common cause of as symptomatic prolongation of PT/aPPT

A

antiphospholipid antibodies/lupus anticoagulants prolong aPPT in vitro but don’t interfere with clotting in vivo

62
Q

antiphospholipid antibody syndrome

A

presence of one or more types of antiphospholipid antibodies on at least 2 occasions 3 mos apart and thrombosis, pregnancy morbidity, possibly thrombocytopenia

63
Q

treatment of antiphospholipid antibody syndrome

A

anticoagulants as prophylaxis for thrombosis, aspirin. treatment for months to lifetime depending on severity

MDTI (42 decks)

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