Circulation and Fluid Balance Flashcards

1
Q

What is the simple system of the amoeba?

A
  • Amoeba are in direct contact with their environment to :
    • Obtain nutrients
    • Excrete wastes
  • Contractile vacuoles pump water in and out of the amoeba for these exchanges to occur
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2
Q

What does the circulatory system do?

A
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3
Q

What are the blood vessels in microcirculation?

A
  • Terminal arterioles
    • endothelium, basement membrane, muscle
  • Capillaries
    • Endothelium, basement membrane
  • Post Capillary venules
    • Endothelim, basement membrane, muscle
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4
Q

What is a Terminal arteriole

A
  • Major resistance vessel of the arterial system
  • Terminal arterioles regulate the clow of blood into a capillary bed
  • Pressure falls dramatically as blood flows thtrough the arteriole into the capillary
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5
Q

What are capillaries?

A
  • The most numerous of all vessels, but generally contain only 5-10% of blood volum
  • Blood is directed into a capillary based on tissue needs
    • At any given time most capillary beds have minimal blood flowing through them
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6
Q

What is a postcapillary venule

A
  • collect blood from a capiillary bed to begin the venous return to the heart
  • important site of cellular events associated with inflammation
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7
Q

What are the lymphatics in microcirculation?

A
  • Blind-ended lymphatic vessels originate in association with the mircrocirculation
  • Important participants in fluid balance at the microcirulatory level
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8
Q

What is the interstitium?

A
  • The space between cells and the microcirculation
  • Composed of the ECM
    • Includes:
      • Structural elements
      • Adhesive elements
      • Absorptive elements
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9
Q

What is fluid homestasis

A
  • Fluid is in constant flux between compartments of the microcirculatory environment
  • Interactions occur between:
    • cells and interstitium
    • interstitium and blood vessels
    • interstitium and lymphatic vessels
  • Fluid distribution between compartments is controlled by physical barriers, and differences in pressure and concentration of substances within the fluid
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10
Q

What is the normal water distribution in the body?

A
  • Total body water (60% body wt)
    • Extracellular water (20% body wt)
      • Plasma (4-5%)
      • Interstitium (16%)
    • Intracellular water (40%)
      • relatively stable compartment
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11
Q

How does blood and the interstitium interact?

A
  • Blood vessel wall is the barrier that separates intravascular and teh interstitial compartments
  • Capillary wall is semi-permeable membrane that allows selective movement of fluid and molecules
    • lipid soluble substanes can move through the endthelil cell
    • Water and water soluble substanes move through inter-endothelial pores
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12
Q

How does the intertitium and lyphatic vessels interact?

A
  • Lymph vessel wall separate the lymphatic and interstitial compartments
  • Lymph vessel wall functions similar to the capillary wall but is much more permeable
    • inter-endothelial gaps are large
  • Water moves freely between lymphatic vessel lumens and interstitium based on pressure gradients
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13
Q

How is the Intravascular/Interstitial fluid distribution controlled

A
  • Anatomic integrity of the circulation
  • Osmotic pressure
    • plama
    • interstitium
  • Hydrostatic pressure
    • plama
    • interstitium
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14
Q

How is water flow across the endothelium described?

A

-K * [Pcap - Pint] - σ [πcap - πint]

  • K = capillary endothelial permeability constant
  • P = hydrostatic ressure
  • σ = reflection coefficient
  • π = colloid osmotic pressure
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15
Q

Intravascular /Interstitial water distribution

A
  • Differences in hydrostatic pressure are determined mainly by teh volume of water in a compartment and any driving force acting on that volume (ex blood pressure)
  • Differences in osmotic pressure are determined manly by large protins or protein-disaccharides
    • small proteins and electrolytes account for most osmolarity, but are equally distributd between fluid compartments
      • 84% of plama osmolality is due to sodium and chloride
      • Less than 1% of plasma osmolality is due to plasma proteins
      • Protein-disaccharides contribute to interstitial osmolality
  • Intravascular and interstitial osmotic, and interstitial hydrostatic pressures are relatively constant in the normal microcirculation
  • Differences in intravascular hydrostatic pressure between arteriolar and venular ends of the microciculation are teh major actor in driving water exchange between the plasma and interstitium
    • Alternatively, water may flow from an entire capillary bed with active blood flow towards abed with minimal flow
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16
Q

What controls Fluid dristibution?

A
  • Net filtration pressue:
    • plama/interstitium pressue differential at teh arteriole
    • Net flow (nutrients) into the interstitium
  • Net absorption pressure:
    • Plasma/interstitium pressure
    • differential at the venule
    • Net flow (wastes) into the plams
  • Lymphatic vessels pick up excess fluid
17
Q

What are the the mechanism of Edema

A
  • Decreased plama osmotic pressure
  • Increased plama hydrostatic pressure
  • Decreased lymphatic drainage
  • Increased vascular permeability

more than one mechanism is often involved in clinical edema

18
Q

How is plasma osmoic pressure decreased?

A
  • Hypoalbuminemia is a common underlying factor in decreased plama osmotic pressure
    • Albumin is the major plasma protein that contributes to intravascular osmotic presure
19
Q

What causes hypoalbuminemia?

A
  • starvation
    • inadequate protein intake
  • Liver disease
    • Decreased protein production
  • Renal disese (nephrotic syndrome)
    • glomerular loss of albumin
  • GI disease
    • malabsorption
    • parasitis
  • Severe burns
20
Q

How is Edema caused by decreased plasma osmotic pressure characterized?

A
  • Due to systemic nature of hypoalbuminemia, edema tends to be generalized
    • Manifestations of generalized edema sometimes tnd to be localized (bottle jaw, brisket edema)
21
Q

How does increased plasma hydrosttic pressure cause edema?

A
  • Creates a net outflow of fluid from teh vessel to the intrstitium
    • the normal absoptive pressue at teh venule becomes a filtration pressure
      • high venula hydrostatic pressure prevents reentry of fluid from teh intersittium
22
Q

What causes increased plasma hydrostatic pressure?

A
  • Increased blood flow
    • accute inflammation
  • Passive blood accumulation
    • Venous obstruction
      • thrombi
      • Masses - inflammatory or neoplastic
      • Organ torsions
    • Heart failure
23
Q

How does heart failure cause fluid maldistribution?

A
  • Fluid maldistribution can vary depending on the nature of the failure
  • Right heart failure: blood backs up in the portal circulation
    • Fuid accumulates in the abdominal catity (ascites)
  • Left heart failure: blood backs up in pulmonary circulation
    • Fluid accumulates in the alveoli of teh lung (pulmonary edema)
  • Generaized edema from generalized heart failure can result in reduced circulating blood volume
    • ADH and aldosterone stimulate water andsodium retention to contribute to hypervolemia and increased plasma hydrostatic pressure
24
Q

How does increased plasma hydrostatic pressure cause edema?

A
  • Fluid maldistribution can be generalized or localized depending on the underlying cause
    • Generalized - heart failure
    • Local - venous obstruction
25
Q

How does Decreased lymphatic drainage cause edema?

A
  • Any decreasse in lymphatic flow prevents remol of the slight excess of fluid that normally presist in the interstitium during intravascular/interstitial fluid exchange
  • Fluid maldistribution is almost almost always localized for acquired defects in drainage
  • Congenital defects can be manifested by generalized edema
26
Q

What casues decreased lymphatic drainage

A
  • Lymphatic obstruction
    • compression from inflammatory or neoplastic masses
    • intralumenal obstruction by thrombi or emboli
  • Lymphatic anomalies
    • Congnital anasarca/lymphedema
27
Q

How does increased vascular permeability caus edema?

A
  • Decreased structual integrity alows water to move out of a vessel into teh interstitium more freely
28
Q

What causes increased vascular permeability?

A
  • Inflammation
    • endothelial contraction and cytoskeletal rearrangement results in expansion of interendothelial junctions and fluid movement to the interstitium
    • Inflamatory Meditors:
      • Immediate transient response: histamine, bradykinin, leukotrienes, C4D4E4, Platelet activating factor, substance P
      • Delayed sustained response: TNF, IL-1, gamma-IFN
  • Immunologic stimuli
    • many of the same events of inflammation are initiated
  • Direct endothelial injury
    • toxins, chemicals, or infectious agents
29
Q

How is edema caused from increased vascular permeability characterized?

A
  • Usually localized
    • increased intravscular hydrostatic pressure and increased extravascular osmotic presure also contribute to fluid loss associated with inflammation
  • In cases of systemic hypersensitivity, there can be more widespread fluid loss/edema
30
Q

What is the morphology of Edema?

A
  • Gross:
    • clear, gel-like fluid within tissue
    • tends to gravitate to ventral areas
    • Can occur in body cavities
      • Ascites - abdomen
      • hydrothorax - thoracic cavity
      • hydropericardium - pericardial sac
  • Histological:
    • Eosinophilic amorphous material within a tissue
31
Q

What is the significance of Edema?

A
  • Can be insignificant to fatal
    • SQ edema has little functional significance
    • Cerebral or pulmonary eedema are life-threatening
  • Clinical classification
    • nutritional
    • renal
    • cardic
    • parasitic