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Path 2 > hemodynamics part 4 > Flashcards

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
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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
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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
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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
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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
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6
Q

What are arterial thrombi composed of

A
  • composed of:
  • -> platelets
  • -> fibrin
  • -> erythrocyte
  • -> leukocytes
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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
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8
Q

define lines of Zhan in a thrombus

A
  • alternate layering of platelets, fibrin and erythrocytes
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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
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10
Q

what are the risk factors of venous thrombosis

A
  • CHF
  • Trauma
  • surgery
  • pregnancy
  • cancer
  • -> trousseau syndrome/migratory thrombophlebitis
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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
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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)
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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
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14
Q

what are the sources of arterial emboli

A
  • atrial fibrillation
  • mitral stenosis
  • endocarditis
  • mural thombi in heart or aorta
  • paradoxical emboli
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15
Q

where do most embolism end up

A

lower extremities

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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

Path 2 (11 decks)

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