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Unit 1: LGS > Week 7 > Flashcards

Week 7 Flashcards

1
Q

Differentiate between the systemic and pulmonary circulations

A
  • Systemic: left heart, systemic arteries, capillaries, and veins
  • Pulmonary: right heart, pulmonary arteries, capillaries, and veins.
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2
Q

Cardiac output

A

rate at which blood is pumped from either ventricle

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3
Q

Venous return

A

rate at which blood is returned to the atria from the veins

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4
Q

equation for velocity

A

v=Q/A (flow/area)

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5
Q

equation for flow

A

Q=ΔP/R (change in pressure/radius)

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6
Q

equation for resistance

A

R=8ηl/πr4 (viscosity*length/radius of vessel)

-radius of vessel is most important and causes biggest change

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7
Q

series resistance

A

-arrangement of blood vessels in a specific organ. The blood will flow into organ from an artery digressing into arteriole, into capillary, into venule, until it drains out to major vein. The total resistance of the system is equal to the sum of each individual resistance.

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8
Q

parallel resistance

A
  • distribution of blood flow among the major arteries branching from aorta and the collected at the vena cava’s. The resistance in parallel arrangement is less than any of the individual resistances
  • flow through each organ is fraction of total blood flow, which allows for no loss of pressure, and mean pressure in each major artery will be similar to mean pressure in aorta. When adding a resistance to circuit, the total resistance will decrease. When adding resistance to one of individual vessels, the total resistance will increase.
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9
Q

Compliance

A
  • volume of blood vessel can hold at given pressure.

- greater in veins which is why they can hold more

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10
Q

Local (intrinsic) control of blood flow

A
  • autoregulation
  • active hyperemia
  • reactive hyperemia
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11
Q

Autoregulation

A

maintenance of a constant blood flow to an organ in the face of changing arterial pressure. Seen in kidneys, brain, heart, and skeletal muscle.

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12
Q

Active hyperemia

A

blood flow to an organ is proportional to its metabolic activity. If metabolic activity increases, then blood flow will increase proportionately.
-due to increase in heat, BPG, CO2

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13
Q

Reactive hyperemia

A

increase in blood flowin responseto orreactingto a prior period of decreased blood flow. For example, increase in blood flow to an organ that occurs following a period of arterial occlusion. During the occlusion, an O2debt is accumulated. The longer the period of occlusion, the greater the O2debt and the greater the subsequent increase in blood flow above the preocclusion levels. The increase in blood flow continues until the O2debt is “repaid.”

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14
Q

Neural (extrinsic) control of blood flow

A

involves thesympathetic innervationof vascular smooth muscle in some tissues. The density of such sympathetic innervation varies widely from tissue to tissue.

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15
Q

steps involved in the excitation-contraction coupling of the cardiac myocyte cell

A
  1. depolarization spreads to the interior of the cell via the T tubules.
  2. Entry of Ca2+into the myocardial cell produces an increase in intracellular Ca2+concentration. This triggers the release ofmoreCa2+from stores in the sarcoplasmic reticulum through ryanodine receptors.
  3. Ca2+binds totroponinC,which binds to tropomyosin which is moved out of the way, and the interaction of actin and myosin can occur. Actin and myosin bind,cross-bridgesform and then break, the thin and thick filaments move past each other, and tension is produced.
  4. Actin and myosin bind forming cross bridge. Cross-bridge cycling, fueled by adenosine triphosphate (ATP), continues as long as intracellular Ca2+concentration is high enough to occupy the Ca2+-binding sites on troponin C.
  5. Tension produced by myocardial cells.
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16
Q

types of smooth muscle

A
  • unitary

- multiunit

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17
Q

Unitary (single unit) smooth muscle

A

Smooth muscle contracts in a coordinated fashion because the cells are linked bygap junctions. Gap junctions are low-resistance pathways for current flow, which permit electrical coupling between cells.

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18
Q

Multiunit smooth muscle

A

Each muscle fiber behaves as a separate motor unit (similar to skeletal muscle), and there is little or no coupling between cells.

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19
Q

Collaterals

A

-allow for continued blood flow with blockage in main artery

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20
Q

Relaxation of Myocardial cells

A
  • The SR will self-regulate and draw back a majority of the Ca2+, excess will leave the membrane through exocytosis
  • The reuptake of Ca causes tropomysin to block the actin binding site and the cell can no longer contract
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21
Q

Contractility through sympathetic stimulation

A
  • NE will bind to beta receptors, cause AC to activate cAMP which activates PKA.
  • PKA will phosphorylate:
    • L-type ligand gated channel and ryanodine for faster intracellular release of Ca2+ (quicker contraction)
    • Troponin C and phopholambam for faster reupatke of Ca2+(quicker relaxation)
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22
Q

Contractility through stretching

A
  • stretching of myocyte allows for more cross bridges to form which increases contraction
  • this is intrinsic mechanism
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23
Q

Contraction of smooth muscle cell

A
  • Depolarization opens up voltage-gated Ca channels in SR, flow into cell. Additional mechanisms can be used to increase intracellular concentration of Ca through IP3 and ligand gated through hormones and neurotransmiters.
  • Intracellular Ca2 binds calmodulin
  • Calmodulin binds myosin-light-chain-kinase
  • MLCK phosphorylates the myosin light chain changing the confirmation of its head and allowing it to gain access to the ATPase
  • Myosin head binds actin in cross bridge and contracts
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24
Q

Relaxation of smooth muscle

A
  • Larg + O2 = NO + cit in endo membrane
  • NO diffuses into smooth muscle, activates GC– GTP to cGMP–activates myosin light chain phosphatase–dephosphorylates myosin light chain–causes relaxation
25
Q

shear stress

A

-how fast blood flows through vessel

26
Q

Cardiac output

A

CO=HR*SV (heart rate * stroke volume)

27
Q

osmolality

A 
# molecules/amount of water
-increase in osmolality will cause influx of water to reach equilibrium
28
Q

osmotic pressure

A

pressure created by amount of solute in water and causes water movement by pulling water in to dilute solute

29
Q

oncotic pressure

A

pressure created by amount of protein in water and causes water movement by pulling water in to dilute amount of protein

30
Q

List body fluid compartments

A
  • Intracellular fluid: larger, contains 2/3 of body water

* Extracellular fluid: smaller, contains 1/3

31
Q

How does water move between IC space and EC space

A

-aquaporins; driven by osmostic pressure

32
Q

How does water move between interstitium and vasculature

A

hydrostatic pressure pushes water into interstitum on arterial side, oncotic pressure pulls water into vasculature on venous side (starling forces)

33
Q

gap junction

A

directly connect the cytoplasm of two cells, which allows various molecules, ions and electrical impulses to directly pass through a regulated gate between cells.

34
Q

tight junction

A

membranes of two neighboring cells join to form a barrier to larger molecules and water that pass between the cells

35
Q

transcellular transport

A

solutes and water transported through cell

-two step process with one step being active and the other being passive

36
Q

paracellular

A

passive transport across a tight junction

37
Q

How kidney alters urine output

A
  • water intake is low OR water loss is high the kidney will create small volume of urine that is hyperosmotic
  • water intake is high OR water loss is low kidney creates large volume of urine the is hypoosmotic
38
Q

ADH

A

-antidiuretic hormone: excreted by pituitary gland to control blood volume by binding to V1 receptors on collecting tubule of kidney, creating aquaporins which allow for water to be retained, increasing blood volume in body

39
Q

how is pituitary gland signaled to make ADH

A

-osmoreceptors detects osmolality of plasma and swell when osmolality too low, shrink when osmolality too high

40
Q

Thirst mediating AVP

A

-blood osmolality increases will increase thirst of person to drink water and dilute plasma

41
Q

Role of Kidney in vol expansion/contraction

A

vol expansion: ingestion of NaCl exceeds excretion

vol contraction: excretion of NaCl exceeds ingestion

42
Q

Positive vs Neg sodium balance

A

positive: intake exceeds excretion to balance Na
negative: excretion exceeds intake to balance Na

43
Q

How is edema formed?

A

volume fluid in interstitial exceeds ability for lymph to circulate in circulation–interstitial space is bigger than ICS and so that is where liquid pools

44
Q

SIADH

A
  • Inappropriate Antidiuretic hormone secretion
  • euvolemic hyponatremia
  • Seen in patients with pulmonary disease
45
Q

Treatment SIADH

A
  • restrict fluids

- 3% IV (hypertonic) to have Na from solution flow into ECS and cause water from cell to be driven in ECS

46
Q

Phases of Cardiac cycle

A
  1. Atrial systole
  2. Isovolumetric ventricular contraction
  3. Rapid ventricular ejection
  4. Reduced ventricular ejection
  5. Isovolumetric ventricular relaxation
  6. Rapid ventricular filling
47
Q

Atrial systole

A
  • atria contract
  • final phase of ventricles filling
  • fourth heart sound
48
Q

Isovolumetric ventricular contraction

A

-ventricles begin to contract– once ventricular pressure greater than atrial pressure the mitral and triscuspid valves closed (making first heart sound)–all valves closed

49
Q

Rapid ventricular ejection

A

-ventricle continues to contract–when ventricular pressure higher than aortic (pulmonic) pressure aortic (pulmonary) valve opens–blood is rapidly pushed into aorta increasing aortic pressure

50
Q

Reduced ventricular ejection

A

-ventricles no longer contracting–ventricles begin to repolarize–excess blood continues to flow from ventricle into aorta–atrial pressure increasing

51
Q

Isovolumetric relaxation

A

-ventricles fully repolarized- once ventricle pressure lower than aortic (pulmonic), aortic (pulmonic) valve will close (second heart sound)–all valves now closed

52
Q

Rapid ventricular filling

A

-ventricual pressure falls below atrial pressure–mitral (triscuspid) valve opens– ventricualr volume increase rapidly but pressure remains low because still relaxed (3rd heart sound)–aortic pressure decrease due to blood running into arteries

53
Q

Reduced ventricular filling

A

final portion of ventricular filling before atria contract

-affected by change in heart rate (prolonged/reduced/ eliminated)

54
Q

Ventricular changes in pressure during cardiac cycle

A

diastole: low pressure, small increase in pressure when atriums contract
systole: rapid increase as blood pushed out and then rapid decrease before diastole begins again

55
Q

Ventricular changes in blood volume during cardiac cycle

A

diastole: increase in blood volume to highest point (end diastolic volume)
systole: decrease in blood volume to lowest point (end systolic volume)

56
Q

Stoke Volume

A

=end diatolic volume-end systolic volume

57
Q

Ejection fraction

A

=stroke volume/ end diastolic volume

-normal; is 55%

58
Q

Blood pressure

A
  • systolic pressure: measures peak pressure during systole

- diastolic: measures lowest pressure during diastole

Unit 1: LGS (9 decks)

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