hemodynamics part 4 Flashcards
1
Q
what are the effects of turbulence
A
- causes endothelial injury or dysfunction (disruption of normal laminar flow)
- Forms countercurrents causing local pockets of stasis
- -> disrupts laminar fluid
- -> prevent dilution of clotting factors
- -> prevent inflow of clotting inhibitors
- -> promote endothelial cell activation
2
Q
what are the causes of tubulent blood flow
A
- ulcerated atherosclerotic plaque
- aneurysm
- myocardial infarction
- mitral valve stenosis –> rheumatic fever
- atrial fibrillation
- hyperviscosity syndrome –> polycythemia
- sickle cell anemia
3
Q
what are some molecules that maintain shear stress (laminar flow)
A
- Many antithombotic agents (NO, prostacylin, tissue plasminogen activator, thrombomodulin)
- antimigration agents like NO
4
Q
describe thrombi morphology
A
- occur anywhere in cardiovascular system
- arterial thrombi usually occur at sites of ENDOTHELIAL INJURY
- venous thrombi usually occur as a consequence of stasis (LOW FLOW)
- thrombi have a point of firm attachment to the vessel
5
Q
what are the complications of arterial thrombosis
A
- may cause local obstruction or distant embolization
- risk factors include:
- -> myocardial infarction
- -> rheumatic heart disease
- -> atrial fibrillation
- -> atherosclerosis
6
Q
What are arterial thrombi composed of
A
- composed of:
- -> platelets
- -> fibrin
- -> erythrocyte
- -> leukocytes
7
Q
describe abdominal aortic aneurysm
A
- ruptured AAA mortality rate is 75%
- usually seen in older people
- stenting or surgery recommended for aneurysms greater than 5cm in diameter
- Out-pouching of the wall
8
Q
define lines of Zhan in a thrombus
A
- alternate layering of platelets, fibrin and erythrocytes
9
Q
Describe venous thrombi
A
- usually due to stasis
- -> contain more erythrocytes and therefore are red
- Mostly occur in lower extremity veins but may involve other less common sites
- Thrombi START forming in the valve pockets of the deep vein
- 50% of affected patients are asymptomatic
10
Q
what are the risk factors of venous thrombosis
A
- CHF
- Trauma
- surgery
- pregnancy
- cancer
- -> trousseau syndrome/migratory thrombophlebitis
11
Q
define Trousseau syndrome/migratory thrombophlebitis
A
- a serine protease released by malignant tumor cells activates factor 10
- tumor cells release plasma membrane vesicles exhibiting procoagulant activity
- tissue thromboplastin is released from necrotic tumor
12
Q
what is the fate of a thombus
A
- resolved (resolution)
- embolization to lungs
- organized and incorporated into wall of vessel
- organized and recanalized
- propagate towards heart (grow)
13
Q
define embolus
A
- a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
- emboli travel until they become lodged in a vessel too small for further migration to occur
- tissues distal to this blockage are at risk for infarction
14
Q
what are the sources of arterial emboli
A
- atrial fibrillation
- mitral stenosis
- endocarditis
- mural thombi in heart or aorta
- paradoxical emboli
15
Q
where do most embolism end up
A
lower extremities
16
Q
Define mural thombi
A
- arterial thombosis in cardiac chambers due to myocardial infarction, ulcerated atherosclerotic plaque or aneurysmal dilatation
17
Q
define paradoxical embolism
A
- rare condition in which an embolus originating from the venous circulation passes through an inter-atrial or inter-ventricular defect to gain access to the systemic circulation
- usually go to the leg, can go to brain
18
Q
define pulmonary thromboembolism
A
- 95% arise from deep leg vein thrombi above level of knee
- 200,000 deaths per year in the U.S.
- Pulmonay embolus may…
- -> occlude main pulmonary artery
- -> lodge across vessel bifurcation (saddle embolus) (sudden death)
- -> occlude smaller branching arterioles
19
Q
what is the result of large emboli
A
- occlude major arteries, “saddle emboli”, sudden death or acute right heart failure
20
Q
what is the result of medium sized emboli
A
- occlude medium-sized branches;
- more likely cause infarction;
- seen mainly in patients with heart or lung disease
- causes wedge like infarct in lung
21
Q
What is the result of small emboli
A
- 60-80%
- cause occlusion of peripheral vessels
- mostly SILENT
- infarctions only if compromised pulmonary circulation
- hemorrhages mainly
22
Q
what is the result of recurrent emboli
A
- 3% of cases
- pulmonary hypertension
- chronic cor pulmonale (right heart failure)
- worsening dyspnea
23
Q
describe fat embolism
A
- fat globules in the circulation are common due to:
- -> fractures of long bones
- -> soft tissue trauma
- -> burns
- 90% of people are unaffected
24
Q
Describe fat embolism syndrome
A
- 10% of people with fat emoblisms
- 1-3 days after injury
- tachypnea and dyspnea
- tachycardia
- irritability/restlessness.coma
- diffuse petechial rash
- pulmonary insufficiency
25
Q
describe air embolism
A
- due to air in the ciruclation resulting from obstetric procedures or chest wall injury
26
Q
describe decompression sickness
A
- sudden changes in the atmospheric pressure (diving)
- nitrogen inspired at high pressure dissolves in blood and tissues in greater amounts than at atmospheric pressure
- if there is a rapid decrease in pressure (decompression) nitrogen bubbles form in the circulation to form gas emboli
27
Q
what are the types of decompression sickness
A
- Bends = painful formation of gas bubbles in skeletal muscles and supporting tissue in and around joints
- Chokes = (when it affects lungs) gas emboli in lungs cause edema, hemorrhage atelectasis and emphysema causing respiratory distress
28
Q
what is the treatment of decompression sickness
A
- slow decompression allows gradual resorption and exhalation of the gases
29
Q
Describe amniotic fluid embolism
A
- amniotic fluid within the circulation
- symptoms = dyspnea, cyanosis, hypotension, shock, seizures, coma, pulmonary edema, DIC
- breach in placental membranes and uterine veins causes infusion of amniotic fluid into maternal circulation
30
Q
what comprises an amniotic fluid emboli
A
- consists of:
- -> epithelial cells from fetal skin
- -> lanugo hair
- -> fat from venix caseosa
- -> mucin from fetal respiratory and gastrointestinal tract
- *procoagulative**
31
Q
define infarction
A
- death of tissue (ischemic necrosis) due to interruption in blood supply
- usually coagulative necrosis
- venous thrombosis usually induces only congestion (infarct more likely in organs withs ingle venous outflow (testes and ovary))
- slowly developing occlusions allow for development of collateral circulation
32
Q
what are some causes of infarction
A
- thombosis and emboli
- vasospasm (cocaine addicts)
- hemorrhage within atherosclerotic plaque
- extrinsic compression of vessel
- twisting of vessel (testicular torsion/intestinal volvulus)
33
Q
what is a critical factor in determining tissue damage in infarct development
A
- Dependent on nature of vascular supply
- -> lungs = pulmonary and bronchial arteries
- -> liver = hepatic artery and hepatic vein
- -> arm = radial and ulnar arteries
- -> spleen and kindey have an END ARTERIAL SYSTEM and therefore are at increased risk of infarction
34
Q
describe the morphology of infarcts
A
- infarcts ted to be wedge-shaped with occluded vessel at apex
- -> periphery of organ forming base
- overtime the infarct is delineated by a rim of hyperemia reflecting inflammation at the edge of the lesion
35
Q
where do red (hemorrhagic) infarcts occur
A
- venous occlusions
- loose tissues
- tissue with dual circulation (lung)
- tissues previously congested due to sluggish flow
- re-established blood flow to a site of previous arterial occlusion and necrosis
36
Q
describe white (anemic) infarct
A
- typical of arterial occlusions in solid organs with limitation of blood flow into areas of ischemic necrosis
- sharply demarcated white infarct in the kidney
37
Q
describe post-infarction healing
A
- dominant histologic characteristics is ischemic coagulative necrosis (except in brain = liquefactive necrosis)
- inflammation initially occurs along the margin of an infarct within hours and becomes well defined with 1-2 days
- a reparative response follows inflammation
- most infarcts are replaced by granulation tissue followed by fibrous tissue (scar) (unless a tissue can regenerate)
38
Q
describe septic infarcts
A
- occurs when the origin of an embolus is infected tissue
- the major source of septic emboli are vegetations formed by bacteria growing on heart valves in bacterial endocarditis
- can progress to formation of an abscess
