1-2. overview of circ. system & edema

characteristics of arteries

• rapid blood flow & high pressure

• large lumen with minimal resistance

• thick walls of smooth muscle and elastin

  • expand and passively contract to maintain pressure and flow of blood

characteristics of veins

• slow blood flow and low pressure

• thin layers of muscle and elastin (don’t want much stretch)

• valves help prevent “backflow”

• skeletal muscle contraction → helps get blood back to the heart

• increased pressure gradient

interstitium

• space between cells and microcirculation

• composed of extracellular matrix → mostly collagen

continuous capillary

• no molecules can pass through (other than gases)

• e.g. blood-brain barrier

fenestrated capilary

• some molecules can pass through (ex. small proteins)

• e.g. renal glomeruli

discontinuous capillary

• most molecules can pass freely

• e.g. liver sinusoids

endothelium functions

• barrier

• important mediator of fluid distribution, hemostasis, inflammation and healing

characteristics of healthy endothelium

antithrombotic and profibrinolytic → prevents clotting and breaks down fibrin

characteristics of injured endothelium

prothrombotic and antifibrinolytic

edema

imbalance of fluid between the interstitium, cells, and intravascular space resulting in swelling of body tissues due to fluid accumulation

dependent edema

ventral accumulation of edema fluid (due to gravity)

pitting edema

subcutaneous edema which leaves a dent in the tissue when pushed with a finger

anasarca

whole body edema (common in frogs/toads)

non-inflammatory effusions

• low cellularity and often low [protein] effusions — clear and colorless or pale yellow-red

• causes:

  • increased hydrostatic pressure

  • decreased oncotic pressure

  • lymphatic obstruction

inflammatory effusions

• high(er) cellularity and often high(er) [protein] effusions — opaque, turbid, colored 

• causes:

  • loss of vascular integrity

  • lymphatic obstruction

  • (or chemotactic factors i.e. inflammatory stimulus)

what are the major mechanisms of increased net fluid within the extravascular space? (4)

1. increased hydraulic/hydrostatic pressure

2. decreased oncotic pressure

3. decreased lymphatic drainage

4. increased vascular permeability

causes of increased hydraulic/hydrostatic pressure

• pulmonary hypertension

• portal (liver) hypertension

• venous obstruction

• fluid overload

ascites

fluid in abdominal cavity

causes of decreased oncotic pressure

• decreased albumin production

  • liver disease (albumin produced by liver)

  • severe malnutrition

• excessive albumin loss

  • protein losing nephropathy/enteropathy

  • cutaneous burns

• water intoxication

causes of decreased lymphatic absorption/removal

• obstruction or compression (often due to masses)

• congenital lymphatic diseases

• intestinal lymphangiectasia (abnormally dilated lymphatics)

• lymphangitis

causes of increased vascular permeability

• infectious (viral, bacterial, rickettsial diseases)

• immune-mediated

• anaphylaxis

• toxins

• inflammatory mediators (e.g. cytokines) → allows vessels to let proteins and leukocytes into interstitial space