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General Pathology > Alterations of Blood Flow > Flashcards

Alterations of Blood Flow Flashcards

1
Q

Hyperemia

A
  • An active, increased flow of blood into the microvasculature with normal outflow
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2
Q

Physiologic hyperemia

A
  • Increased flow to the skin for heat loss
  • Increased GI flow following a meal
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3
Q

Pathologic hyperemia

A
  • Inflammation
  • initial vascular response
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4
Q

Hyperemia Morphology and Significance

A
  • Blood vessels are bright red and engorged
  • Affected areas are warmer than normal
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5
Q

Congestion

A
  • A passive accumulation of blood in a vessel usually due to decreased outflow, with normal inflow
  • Can be localized or generalized
    • localized congestion occurs due to acute or chronic occlusion of a vein
    • Generalized is usually due to heart failure
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6
Q

Localized Congestion

A
  • Localized Congestion can be due to either intralumenal blockage or occlusion due to external pressure
    • Venous thrombi can cause total venous obstruction
    • External pressure can occur from inflammatory or neoplastic masses, organ displacement, or localized fibrosis
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7
Q

Generalized Congestion: Heart Failure

A
  • Right Sided Heart Failure:
    • Liver and abdominal vasculature are primarily congested
  • Left Sided Heart Failure:
    • Pulmonary circulation is primarily congested
  • Once one side of the heart fails, the other side will follow soon after
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8
Q

Congestion Morphology

A
  • Vessels are dark red and engorged
  • Pulmonary congestion:
    • Edema occurs concurrently (due to increased intravascular hydrostatic pressure)
      • Red cells lost to alveoli are phagocytosed resulting in “heart failure cells” hemosiderin-laden macrophages)
  • Hepatic Congestion:
    • Centrilobular sinusoids are initially affected resulting in a “nutmeg” appearance
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9
Q

Congestion Significance

A
  • Congested tissue is usually hypoxic
    • if prolonged, can result in tissue injury
  • Increased hydrostatic pressure associated with congestion often results in edema
  • Congested tissue is usually cool
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10
Q

Tissue perfusion

A
  • Normal homeostatic mechanisms maintain adequate flow and perfusion to tissues based on their need
  • Ischemia occurs when perfusion becomes inadequate to meet the metabolic needs of the tissue
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11
Q

Ischemia Causes

A
  • Usually involves some form of vascular occlusion
    • Atrial lumenal blockage (thrombus or emboli)
    • Prolonged arteriolar vasoconstriction
    • Venous intralumenal occlusion (thrombus) or external pressure
    • Capillary intralumenal occlusion or external pressure
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12
Q

Ischemia Characteristics

A
  • Severity determined by:
    • Local vascular anatomy
      • degree of anastomoses, collateral circulation and number of capillaries
    • Extent of the decreased perfusion
    • Rate of decreased perfusion
      • rapid is more damaging than slow, progressive
    • Metabolic needs
      • Brain and heart are most susceptible
      • Organs receiving large amounts of blood flow are relatively resistant (lungs, liver, kidneys)
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13
Q

Ischemia Outcome

A
  • Return to Normal:
    • Most common
    • ATP of ischemic tissue is degraded to adenosine, a potent vasodilator
  • Reperfusion injury
    • After prolonged ischemia, return of blood flow can produce additional detrimental effects
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14
Q

Cardiogenic Shock

A
  • Reduced cardiac output most commonly due to cardiac disease
    • failure of the central pump
  • Predisposing problems include:
    • Myocardial infarction
    • myocardial arrhythmia
    • pulmonary embolism
    • Cardiomyopathy
  • Decrease in both stroke volume and cardiac output
  • Compensatory mechanisms attempt to increase SV, contractility, HR, and total output
    • success depends on the nature of the problem
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15
Q

Reperfusion Injury

A
  • HyTissue damaged by ischemia doesn’t function properly
    • affected vessels are leaky
      • increased interstitial hydrostatic pressure and and additional vessel compression
    • Damaged tissue releases tissue factor to activate coagulation
    • Ischemic cells produce hypoxanthine from ATP
      • When combined with O2 hypoxanthine is converted into urates and O2 radicals (H2O2 and superoxide anions)
    • O2 radicals can produce additional damage to the already compromised tissue
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16
Q

Infarction

A
  • A local area of peracute ischemia that undergoes coagulative necrosis (liquefactive in nervous tissue)
    • Caused by sudden reduction in blood and O2 supply to the tissue
    • Could be caused by obstruction of arterial flow, or reduction in venous flow
  • Usually the result of thrombosis
17
Q

Influencing Factors of Infarction

A
  • Susceptibility of the tissue to ischemia
    • High susceptibility: Myocardium, brain renal tubular epithelium
    • Low susceptibility: connective tissues
  • Vascular acatomy
    • Functional end arteries
    • Parallel vascular supply
    • Dual blood supply
  • Decreased cardiovascular function
  • Anemia
18
Q

Infarction Characteristic

A
  • Variable
  • Based on
    • Type and size of the occluded vessel
    • Tissue affected
    • Duration of the occlusion
    • Status and vitality of the tissue prior to the infarct
      • pre-existing damage/disease increase likelihood of ischemia progressing to infarction
19
Q

How does type and size of the occluded vessel affect the characteristics of Infarction?

A
  • Arterial vs venous
    • Complete arterial obstruction results in immediate infarction
    • Venous obstruction usually preceded by venous congestion and edema
  • Large vs small
    • Obstruction of larger vessels generally affects more tissue
20
Q

How does the type of tissue affect the characteristics of Infarction

A
  • Tissues with minimal anastomoses (brain, heart, kidney) are more predisposed to infarction
  • Tissue with parallel blood supplies with numerous anastomoses (skeletal muscle, GIT) are relatively resistant to infarction
  • Tissues with dual blood supplies (liver, lung) are relatively resistant to infarction
21
Q

Infarction Morphology

A
  • Appearance mainly depends on type of vessel occluded and the tissue affected
    • White (anemic)
    • Red (hemorrhagic)
  • Other factors, like age of infarct, affect appearance
  • Most are red soon after occurance due to hemorrhage into the damaged tissue
    • cells swell and undergo necrosis, some blood is forced out
  • As healing occurs, infarcts become pale, contracted scars
22
Q

White Infarcts Morphology

A
  • Occur most commonly with arterial thrombi/emboli in solid tissues with minimal anastomoses
    • Solidity of the tissue limits the amount of blood that can seep back into the necrotic area
    • There is general a red zone of hemorrhage, and later inflammation that surrounds the necrotic tissue
23
Q

Red Infarct Morphology

A
  • These occur in a variety of situation:
    • Venous stasis or obstruction
    • Arterial obstruction in loose tissues
    • Tissues with dual blood supply or extensive anastomoses
    • Reperfused necrotic tissues
24
Q

Infarction Significance

A
  • Clinical significance depends on location and size
    • Infarcts involving vital organs can be serious
    • Infarcts in non-vital tissues or tissues with large functional reserves are better tolerated
25
Q

Shock

A
  • A circulatory dyshomeostasis
    • Circulating blood volume and the volume of of the circulatory system that needs to be filled are disproportionate
      • systemic vascular collapse
      • May be a loss of circulating blood volume, reduced cardiac output or inappropriate peripheral vascular resistance
  • Failure leads to widespread tissue hypoxia and altered metabolism due to decreased delivery of nutrients and removal of waste products
    • initially reversible, but rapidly become progressive and irreversible
26
Q

Types of Shock

A
  • Cardiogenic
  • Hypovolemic
  • Peripheral pooling (blood maldistribution)
27
Q

Hypovolemic Shock

A
  • Not enough blood in circulation
  • Predisposing factors include fluid loss due to:
    • severe hemorrhage
    • Vomiting
    • Diarrhea
    • Burns
  • Decreased vascular pressure, and decreased tissue perfusion
  • Compensation includes peripheral vasoconstriction and fluid movement into the plasma to increase vascular pressure
    • Vascular pressure can be maintained with loss of 10% of blood volume
    • Losses of 35-45% of blood volume can result in dramatic decreases in vascular pressure
  • Blood flow to critical tissues is prioritized
28
Q

Blood Maldistribution

A
  • Decreased peripheral resistance results in pooling of blood in peripheral tissues
    • Cased by neural or cytokine-induced systemic vasodilation
  • More capillary beds are open than can be filled
    • Blood volume is normal, but the amount of vasculature needing to be filled is increased
  • There are 3 categories of blood maldistribution
    • Anaphylactic shock
    • Neurogenic shock
    • Septic shock
29
Q

Anaphylactic shock

A
  • Generalized Type 1 hypersensitivity
    • Mast cell degranulation results in systemic release of histamine and other vasoactive mediators
    • Systemic vasodilation nd increased permeability result in decreased vascular pressure and tissue hypoperfusion
  • Causes Include:
    • Allergens (plants and insect products)
    • Drugs and vaccines
30
Q

Neurogenic shock

A
  • Autonomic nervous discharges result in peripheral vasodilation
    • cytokines do not mediate this
  • Causes include:
    • Trauma
    • Electrocution
    • Fear or distress
31
Q

Septic Shock

A
  • Excessive release of vasoactive and pro-inflammatory mediators result in systemi vasodilation
  • This is he most common type of blood maldistrbution syndrome
  • Bacterial/fungal products are the most common cause
    • Endotoxin (LPS)
    • Peptidoglycans
    • Lipoteichoic acid
32
Q

LPS in Septic Shock

A
  • LPS activates
    • Cells (endothelium, leukocytes)
      • cell activation includes interaction of LPS-binding protein, CD14 and Toll-like receptor-4
    • Protein pathways (complement)
  • Endothelial activation results in decreased production of anticoagulant substances
33
Q

Effects of LPS

A
  • Activation of Factor Xlla-related pathways
    • Intrinsic coagulation, kinins, fibrinolysis, complement
  • Activation of complement pathways
    • C3a and C5a
  • Decreased endothelial production of anticoagulants and enhanced expression of leukocyte adhesion molecules
  • TNF and IL-1 released leukocytes
    • Secondary effects of TNF and IL-1 include activation of extrinsic coagulation (TF release), PAF release, endothelial activation, production of arachidonic acid products
34
Q

Shock Pathogenesis

A
  1. Compensation (non-progressive) stage
  2. Progressive stage
  3. irreversible stage
35
Q

Compensation Stage

A
  • Reflex mechanisms are activated to maintain adequate circulating blood volume and pressure
    • HR increases
    • Peripheral Vasoconstriction
    • ADH and angiotensin II release to increase blood volume
    • Diversion of blood flow to vital tissues
  • If the initiating cause is mild, compensation usually increases vascular pressure and there is a return to normal
36
Q

Shock: Progression Stage

A
  • Compensatory mechanisms are inadequate and tissue hypoperfusion occurs
    • Metabolism shifts to anaerobic
    • Cellular and systemic acidosis
    • Host mediators accumulate (Cytokines & other inflammatory.coagulant substances
  • Peripheral vasoconstriction gives way to vasodilation as local hypoxia occurs
    • Blood pools and stagnates in the capillary beds
37
Q

Shock: Irreversible

A
  • Hypoperfusion, tissue hypoxia, and hemodynamic dysfunction result in irreversible cell damage
    • cell energy stores are depleted
    • Cell membrances deteriorate
  • There is systemic activation of platelets and coagulation factors
    • Disseminated intravascular coagulation
  • Multiple organ failure occurs
    • Failure of one system contributes to failure o another
38
Q

Shock: Morphology

A
  • Changes observed with shock depend on it’s underlying cause and stage
  • Basic changes include:
    • Hemorrhage and edema
    • Microtromosis
    • Necrosis
  • Major tissues affected:
    • Heart, lungs, liver, kidney, brain, intestines, adrenal glands, pancreas
39
Q

Shock: Significance

A
  • Shock can be rapidly progressive and life-threatening
    • Rapid and ggressive therapy is needed to prevent progression
  • Clinical features include:
    • Hypotension and weak pulse
    • Tachycardia and hyperventilation
    • Cool extremities and cyanosis
    • In later stages, multi-system organ failure

General Pathology (34 decks)

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