Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

examples of hyperemia

A

inflammation, exercise, blushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cause of hyperemia

A

vasodilation of artery leading to locally increased blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hyperemic border around necrosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cause of congestion

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what typically accompanies congestion?

A

edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

right heart failure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

left side heart failure

A

back up of blood into lungs, shortness of breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

central vein (hepatic vein to IVC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hemorrhage

A

extravasation of blood due to vessel rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hematoma

A

space occupying lesion of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

tissue hemorrhages small to big

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

thrombus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

thromboembolus

A

detached thrombus that embolizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how to identify thrombi

A

lines of zahn and adhesion to vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

virchows triad

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

important factors leading to arterial thrombi

A

endothelial cell injury and turbulent flow. atherosclerosis, inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

characteristics of arterial thrombi

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
important factors leading to venous thrombi
stasis, hypercoagulative states due to increased concentration of activated coag factors and depletion of inhibitors
26
characteristics of venous thrombi
less prominent lines of zahn due to slow blood flow, red appearance due to trapped RBCs
27
common locations of venous thrombi
superficial and deep veins of legs and pevic veins
28
important factors of cardiac chamber (mural) thrombi
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
4 general fates of thrombi
resolution, propagation, embolization, organization/recanalization
30
where do venous thromboemboli travel?
pulmonary circulation.
31
when might venous thromboemboli travel to systemic circulation? PARADOXICAL EMBOLIZATION
if there is a patent foramen ovale, ventricular septal defect, or PDA (pulmonary artery to aorta)
32
where do arterial thromboemboli travel?
lodge distally in a smaller artery
33
where do aortic thromboemboli travel?
variable distal locations in smaller branch off aorta
34
where do right cardia chamber thrombi travel?
pulmonary arterial circulation
35
where do left cardiac chamber thromboemboli travel?
systemic arterial circulation
36
organization of thrombi
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
recanalization
new vascular channels connecting end to end, allowing reestablishment of blood flow through the scar
38
what type of tissue is involved in thrombi repair?
granulation tissue
39
clinical consequences of thrombi/thromboemboli
edema, congestion, embolization, infarction
40
consequences common to venous thrombi/thromboemboli
edema, congestion, embolization
41
consequences common to arterial thrombi/thromboemboli
embolization, infarction
42
infarction
ischemic necrosis of tissue due to occlusion of arterial blood supply or venous drainage (uncommon)
43
what factors do infarctions depend upon?
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
which tissues are most susceptible to infarction
neruons
45
white (anemic) infarcts
arterial, solid organs with one blood supply. generally wedge shaped due to blood flow pattern from hilum
46
red (hemorrhagic) infarct
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
erythema
redder tissue (increased oxygenated blood). due to hyperemia
48
right sided heart failure leads to...
liver congestion (via IVC backup)
49
left sided heart failure leads to...
lung congestion (via pulmonary vein backup)
50
normal pressure differentiation along capillary (A to V)
intravascular hydrostatic pressure decreases (fluid exits artery end) and intravascular osmotic pressure increases (reabsorbed at venous end) longitudinally.
51
do venous thrombi result in congestion and edema?
might. but most of the time, collateral vessels take over so venous thrombi not usually associated with infarction
52
thrombosis and age
risk increases with increasing age
53
who is at a much greater risk for thrombosis in addition to the elderly?
hospitalized patients
54
why are hospitalized patients at a higher risk for thrombi?
cardiovascular disease and prolonged immobilization lead to stasis in the venous system and allows low levels of activated clotting factors to accumulate
55
risk factors for venous thromboembolism (VTE)
systemic diseases, inflammatory states, things that affect movement of blood through the systemic system
56
VTE prevention in hospital
mobilize patients as soon as possible, anticoagulation via heparin, mechanical compression in patients unable to tolerate anticoagulation
57
Disseminated Intravascular Coagulation (DIC)
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
clinical manifestations of DIC
patient may present with severe blessing, thrombosis, or both. acutely ill patients usually bleed, thrombosis is classically seen with cancer
59
DIC lab findings
increased PT/aPTT (used up factors), decreased platelet count (aggregated), microangiopathic hemolytic anemia (schistocytes due to fibrin RBC shearing), presence of D dimers
60
treatment of DIC
TREAT UNDERLYING CAUSE
61
most common cause of as symptomatic prolongation of PT/aPPT
antiphospholipid antibodies/lupus anticoagulants prolong aPPT in vitro but don't interfere with clotting in vivo
62
antiphospholipid antibody syndrome
presence of one or more types of antiphospholipid antibodies on at least 2 occasions 3 mos apart and thrombosis, pregnancy morbidity, possibly thrombocytopenia
63
treatment of antiphospholipid antibody syndrome
anticoagulants as prophylaxis for thrombosis, aspirin. treatment for months to lifetime depending on severity

MDTI (42 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions