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34 Cards in this Set
- Front
- Back
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pacemakers
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SA node - right atrium
AV node - interarterial septa (slower, delay for atria to finish contracting before ventricles contract) then to bundle of His, Purkinje fibers (allow for unified and stronger contraction) vagus nerve of PNS slows SA node |
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vasoconstriction
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epinephrine is powerful
large arteries have less smooth muscle per volume than smaller, therefore less affected medium sized arteries will rereoute blood under sympathetic stimulation |
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methods for materials to cross capillary walls
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pinocytosis
diffusion or transport thru capillary cell membranes movement through pores (fenestrations) in cells movement through space between cells |
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fluid exchange by capillaries dictated by:
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ratio of hydrostatic pressure to osmotic pressure
hydro>osmotic at arterial end = net fluid flow into interstitium osmotic pressure relatively constant BUT hydro drops Hydro < osmotic @ venule end = net fluid flow into capillary 10% loss of fluid to interstitium (therefore to lymph) |
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veins
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larger lumen than comparable arteries; 4X greater cross sectional area
contain far greater volume of blood = therefore act as a reservoir (64% of blood in body at rest; vs 20% in arteries, caps and systemic circ) |
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relationships between pressure, area and velocity of blood in vessels
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blood pressure increases near heart and decreases to lowest at capillaries (veins have valves and skeletal muscle to help, but major force is still heart)
total cross sectional area is highest in capillaries (because so many even tho individually are small!) since blood flow follows Q = Av well, velocity is smallest in caps where cross sectional A is large, and greatest in arteries where cross-sectional area is small (inverse relationship) |
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diaphragm and breathing
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medulla oblongota signals to contract
innervated by phrenic nerve creates negative gauge pressure |
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locations of cilia
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respiratory tract
fallopian tubes ependymal cells of SC therefore if mt problem... |
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trachea composition
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rings of cartilage
covered by ciliated mucous cells |
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inhaled vs exhaled air
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in: 79% N
21% O out 79 N 16% O 5% CO2 plus trace gases |
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partial pressures of gases in lungs
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O2 = 110mm HG
CO2 = 40 mm HG determines direction of diffusion |
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cooperativity of O2 and hemoglobin
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when one O2 molec binds with an iron atom, oxygenation of the other 3 heme groups is accelerated
similarily, release of an O2 accelerates the release of the others as O2 pressure increases, O2 saturation of Hb increases sigmoidally |
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oxyhemoglobin dissociation curve
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as O2 pressure increases, O2 saturation of Hb increases sigmoidally *** due to BPG (not seen in myoglobin)
in arteries of normal person breathing room air, O2 sat is 97% small flucs in Oxygen pressure have little effect but does depend upon CO2 pressure, pH ([H+])and temperature of blood = all shift curve to right = lowereing of Hb affinity for O2 CO has 200X greater affinity for Hb than O2 BUT shifts curve to LEFT (and doesnt get much Sat) |
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CO2 carried in blood via
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1. physical solution
2. as bicarbonate ion **10X as much than others 3. in carbamino compounds (w Hb and other proteins) |
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O2 pressure in blood
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40 mm Hg
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bicarbonate ion formation
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governed by CARBONIC ANHYDRASE in red blood cells
reversible reaction: CO2 + H2O = HCO3- + H+ |
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chloride shift
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because carbonic anhydrase is inside cells
when CO2 is absorbed in the lungs, bicarbonate ion diffuses into cells, and CHLORINE moves out to balance the electrostatic forces |
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Haldane effect
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facilitates transfer of CO2 from blood to lungs and from tissues to blood.
when Hb becomes sat. with O2, its capacity to hold CO2 decreases. reduced Hb acts as bLOOD BUFFER by accepting protons - which means greater capacity to form carbamino Hb |
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chemoreceptors
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central = located in medulla
peripheral = carotid arteries and aorta both monitor CO2 - increase breathing with levels too high peripheral also monitor O2 and pH |
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lymphatic system
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recycles interstitial fluid
transport for proteins and large particles not taken up by capillaries low soluble fate digestables to large veins of neck CNS NOT drained by lymphatics open system; one way valves and over-lapping cells (once proteins push in, cant get back out) as interstitial fluid pressure increases towards zero, lymph flow increases empties into thoracic duct (rest of body) and R lymphatic duct (R arm and head) |
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factors affecting interstitial pressure
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blood pressure
plasma osmotic pressure interstitial osmotic pressure (proteins, infection response) permeability of capillaries |
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blood parts
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IS CONNECTIVE TISSUE!
therefore cells and matrix 1. plasma (matrix = water, ions, urea, ammonia, proteins, etc) 2 buffy coat (WBC) 3. RBC - percentage of = hematocrit (normally 35-50%) |
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plasma proteins
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albumin (transport f.a. and steroids, regulate osmotic P)
immunoglobulins clotting factors made in liver (except Ig = lymph tissue) an important function= act as source of a.a. for tissue protein replacement |
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serum
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plasma in which clotting protein fibrinogen has been removed
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erythrocytes
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bags of Hb
no nucleus (lose while still in bone marrow); no organelles (lose 1-2days after leave) only live about 120 days before burst from wear and tear |
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granular vs agranular lymphocytes
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granular: neutrophils, eosinophils (acid dyes), basophils; typically deposited in tissue after 4-8 hours in blood, live for 4-5 days
agranular: monocytes, lymphocytes and megakaryocytes; live for months to years |
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platelets
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small portions of membrane-bound cytoplasm torn from megakaryocytes
no nucleus make prostaglandins etc membrane designed to avoid adherence to healthy endothelium while adhering to damaged half life 8-12 days |
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innate immunity includes
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skin
stomach acid/digestive enzymes phagocytotic cells chemicals in blood |
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inflammation response includes
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dilation of blood vessels
increased permeability of capillaries swelling of tissue cells migration of granulocytes and macrophages to area wall off effected tissue to impede spread histamine prostaglandins lymphokines |
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once Ag bound to Ab
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complement rxn
targeted by macrophages or Nk cells agglutination block chemically active portion if toxin |
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hapten
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a piece of Ag that can stimulate an immune response if person has been exposed before
antigenic determinant |
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primary and secondary immune response time
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20 days to aquire primary
5 days to get to full potential of secondary (memory B cells) |
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Rh negative mom with Rh positive fetuses
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1st fetus = mom not exposed to blood until birth
2nd fetus may be attacked by Abs of mom (small enough to pass thru placental barrier) complete replacement of fetal blood |
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types of T cells
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helper (assist B, killer and supressor = attacked by HIV)
memory suppressor (negative feedback role) killer/cytotoxic (perforin) |
