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EEOB Exam 12

Terms in this set (40)

Vasodilation
nitric oxide
Vasoconstriction
endothelian-1

angiotensin II & vasopressin
Baroreceptors
detect BP via stretch receptors (mechanoreceptor) in large arteries

delivers info to brainstem through afferent nervous system
Short term regulation of BP
INCREASE in BP higher than it should be
more force on vessels (hydrostatic pressure)

higher frequency of APs --> goes to brain stem and compares against reflex template --> efferent response to lower BP

activates parasympathetic. inhibits sympathetic

negative feedback brings us back in range

vasodilates
Short term regulation of BP
DECREASE in BP lower than it should be
baroreceptor activity goes down

activates sympathetic. inhibits parasympathetic

vasoconstriction by endothelian-1

needs help from endocrines angiotensin II & vasopressin
Long term regulation of BP
based on blood volume (Eq. 4 PV=nRT)

too much fluid raises BP, too low fluid (dehydrated) lowers BP

adjusted by kidneys; filters blood and controls how much we take off of that as water which impacts our BP
What is taken by those with chronically high BP?
Diuretics (water pills) : kidneys dump out water and this lowers BP
Hypotension
too low of BP

often due to hemorrhaging

causes shock
Hemorrhage
Loss of fluids from the circulatory system. BP decreases. Loss of plasma fluids.

Fix by replacing the "n" in PV = nRT (water intake, IV fluids, blood transfusions)
Shock
due to visceral pain. When vital organs are in pain they send an afferent message saying the blood pressure is too low, further lowers blood pressure (Positive feedback loop)
Hypertension
Often due to a problem within the circulatory system. Problem within vessels further away from the heart. "traffic jam"

Location unknown but mostly in association with the kidneys

Heart has to work harder to push blood through = increase in BP. Peripheral resistance

If heart keeps working hard, leads to ventricular hypertrophy
Ventricular hypertrophy
heart gets bigger. this is a problem for two reasons

1) w/in a confined space = impacts lungs

2) 3D squeeze on heart. Binds up on itself. Does not = a better squeeze
Plasma (55%)
90% water
plasma proteins = albumin, immunoglobin, fibrinogen
Albumin
maintains BP and pH
Immunoglobin
antibody
Fibrinogen
(inactive) produces fibrin (active) which helps with clotting
Plasma functions
transports materials and heat, maintains BP & pH, immunity, clotting
Hematocrit (45%)
Erythrocytes (RBC) 45%

Buffy Coat (less than 1%) = leucocytes (WBC): immune system, platelets : helps with clots
Erythrocytes (RBCs)
Composition: highly specialized. small (5-7 um). no nucleus or organelles. biconcave ellipse. packed with hemoglobin which grabs onto O2

Function: transports O2, CO2, H+, CO

Lifespan: 120 days. Can't self repair
Erythropoiesis
because erythrocytes cannot divide to replenish their own numbers, the old ruptured cells must be replaced by new cells produced in the bone marrow
Rate at which erythrocytes are produced through erythropoiesis
2-3 million per second
What is needed for erythropoiesis to occur?
Fe (Iron) = allows O2 to bind to RBCs
Vit. B12 = makes hemoglobin and shapes RBCs
Folic acid = production of RBCs
Erythroprotein (EPO) = tells bone marrow to make more RBCs
Removal of RBCs through Erythropoiesis
Where: spleen & liver; screens circulating RBCs

Consequences: if too many RBCs are scanned, bilirubin from hemoglobin catabolism = causes jaundice
Anemia
decrease in oxygen carrying capacity (due to RBC or hemoglobin)
Nutritional anemia
Fe (iron) deficiency : not enough iron avail available for synthesizing hemoglobin. If no intake of essential raw foods, may not undergo erythropoiesis
Pernicious anemia
Vit. B12 absorption: vit B12 is essential for normal RBC production & maturation. Inability to absorb enough
Aplastic anemia
Bone marrow: bone marrow failing to produce enough RBCs. can also be caused by destruction of red marrow by toxic chemicals (radiation, chemo)
Renal anemia
EPO: inadequate erythroprotein secretion by diseased kidneys leads to insufficient RBC production
Hemorrhagic anemia
RBC loss: caused by losing a lot of blood. Chronic or acute
Hemolytic anemia
RBC destruction: rupture of too many circulating erythrocytes. Either because of an external factor (malaria) or because cells are defective (sickle cell disease)
Sickle cell anemia
Hemoglobin issue: hereditary abnormality or erythrocytes (crescent shaped). Blocks blood flow through small vessels = pain and tissue damage
Polycythemia
too many circulating RBCs & elevated hematocrit.

increase in oxygen carrying capacity, but blood is too viscous. flows sluggishly and reduces oxygen delivery to organs
Causes of polycythemia
Bone marrow in which EPO produces at an excessive, uncontrolled rate (hyper-responsiveness)

Increase in EPO

Response to chronically low O2 to tissues (ppl living in high altitudes, training technique)
Hemostasis
seals vessel damage to prevent blood loss. works best in small vessels but NOT arteries and veins. (hydrostatic pressure is higher in vessels closer to heart)

Three stages
1) Vascular spasm
contracting vessels (vasoconstriction) to close damaged areas.

extracellular matrix: damages collagen. vasoconstriction brings collagen back together
2) Platelet plug
activated by collagen trapping. Sticky. Platelets trapped onto sticky collagen. Release chemicals that increase vasoconstriction. Brings vessel even closer together. Platelets themselves become sticky.

Recruit other cells onto plug = positive feedback

Needs some kind of limitation...
Healthy endothelials
make sure platelet plug only goes where it's supposed to. Vasodilates by nitric oxide (saying "no")
Healthy endothelials release ________________
prostacyclin and plasminogen
Prostacyclin
strops recruitment process
Plasminogen
produces plasmin that breaks up clot
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