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KINE 3012 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is Marfan Syndrome?

A

A mutation of the extracellular matrix protein fibrilin-1

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2
Q

What are consequences of high systolic blood pressure?

A

Aneurysms and Myocardial Infartion

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3
Q

What is myocardial infarction?

A

When cardiac workload is too high and O2 demands are not met.

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4
Q

What is “afterload”?

A

The pressure that the left ventricle has to overcome in order for ventricle ejection to occur.

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5
Q

What causes decreased stroke volume during pre-compensation to high aortic pressures?

A

Shorter ventricle ejection duration.

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6
Q

What are arterioles?

A

Located within individual organs and determines blood flow to those organ, also contributing to TPR.

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7
Q

What is resistance and how does resistance increase?

A

1/r^4; increase tube length and viscosity of blood.

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8
Q

How do the arterioles regulate blood flood to the organs?

A

They vasocontrict/dilate to control flow of blood.

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9
Q

What is the composition of arterioles?

A

An inner layer of endothelial cells and an outer layer of smooth muscle.

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10
Q

What is the function of smooth muscle cells in arterioles?

A

It vasoconstricts/dilates, maintains shape and regulates local blood flow.

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11
Q

How do smooth muscles contract?

A

Constrict: Increase of actin/myosin cross bridges
Dilate: Decrease of actin/myosin cross brigdes

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12
Q

What is the function of endothelial cells?

A

They line the heart/blood vessels, prevents blood cell/platelet adherence, controls exchange of fluids/nutrients in capillaries and secretes vasodilator/constrictor substances.

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13
Q

How is nitric oxide produced by endothelial cells?

A

L-Arginine to nitric oxide through nitric oxide synthase, then nitric acid will diffuse into smooth muscle that activates guanylate cyclase producing cGMP.

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14
Q

What are two ways to regulate blow flow?

A

Locally and systemically

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15
Q

What stimuli (feedback loops) cause vasodilation/constriction

A

Active/Reactive Hyperemia and Flow Auto-Regulation.

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16
Q

What is active hyperemia?

A

It is a response to an increase in metabolic activity in the tissues; increases blood flow.

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17
Q

What is reactive hyperemia?

A

A need of blood restriction/ lack of blood.

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18
Q

How do we have reactive hyperemia responses in our hearts?

A

It is often caused by a temporary compression of blood vessels.

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19
Q

How does flow auto-regulation control local blood flow?

A

Blood flow is kept steady despite blood pressure changes.

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20
Q

What causes flow auto-regulation?

A

A myogenic response which is a reflex response of arterioles to change in blood pressure.

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21
Q

What happens when you stretch smooth muscle?

A

It activates stretch activated ion channels stimulating Ca2+ influx, which can also depolarize a membrane.

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22
Q

What is systemic control of blood flow?

A

Neural SNS and Hormones

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23
Q

How do sympathetic neurons cause vasoconstriction?

A

Sympathetic neurons will release norepinephrine which attaches to adrengeric receptors inducing vasoconstriction.

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24
Q

What are sympathetic influences on vasculature?

A
  1. Beta Adrenergic receptors that reduce vasoconstriction
  2. Metabolites overrides sympathetic vasocontriction
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25
Q

How are Active Hyperemia and Sympathetic Vasoconstriction correlated?

A

Active Hyperemia > Sympathetic Vasoconstriction

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26
Q

Why does the brain have no influence of the SNS on its blood flow?

A

It’s regulated by flow auto-regulation
Lacks alpha adrenergic receptors to react to norepinephrine

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27
Q

What happens when SNS activity is high during stress & what is blood flow like to the capillaries?

A

In Arterioles: High SNS activity causes high resistance = MAP ↑
In Capillaries: Reduced blood flow = vasoconstriction = less blood flow to lungs = less gas exchange.

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28
Q

What happens when SNS activity is high when skeletal muscle is active & what is blood flow like to the capillaries?

A

In Arterioles: Active Hyperemia > SNS on vasoconstriction = ↓ MAP
In Capillaries: Improved gas/nutrient exchange; ↑ blood flow = movement of capillaries to the organs

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29
Q

What is TPR affected by?

A

Arteriolar radius and Blood viscosity

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30
Q

What local/intrinsic controls can affect arteriolar radius?

A
  1. Local metabolic changes
  2. Flow auto regulation
  3. Histamine release
  4. Heat/cold application
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31
Q

What extrinsic controls can affect arteriolar radius?

A
  1. ↑ SNS activity
  2. Norepinephrine/Epinephrine production
  3. Vasopressin and Angiotensin II production
32
Q

Where do capillaries connect to and empty into?

A

They connect to arterioles and empty into venules.

33
Q

What is an important function of the capillaries?

A

Nutrient exchange; thin endothelial walls help with diffusion.

34
Q

How does gas exchange occur?

A

They pass through endothelial cells and require a diffusion gradient.

35
Q

How do we move substances through the capillary?

A
  1. Lipid soluble substances pass through endothelial cells.
  2. Small water soluble substances pass through the pores.
  3. Exchangeable proteins are moved across by vesicular transport.
  4. Plasma proteins gernerally cannot cross the capillary wall.
36
Q

What is capillary filtration vs. capillary absorption?

A

Capillary Filtration: Fluid exiting the capillary.
Capillary Absorption: Fluid entering the capillary.

37
Q

What is the primary function of capillary filtration/reabsorption?

A

Regulates the distribution of extracellular fluid between the plasma and interstitial fluid.

38
Q

Capillaries are the site of fluid exchange with the interstitial compartment. What are the four dictating pressures?

A
  1. Capillary hydrostatic pressure (Pc)
  2. Interstitial fluid pressure (Pif)
  3. Osmotic force (interstitial fluid proteins) (πIF)
  4. Osmotic force (plasma proteins)(πc)
39
Q

What is hydrostatic pressure?

A

It is caused by fluid exchange with the interstitial fluid.

40
Q

What is osmotic pressure?

A

The force exerted by dissolved substance to draw water towards it.

41
Q

What is the formula for net filtration pressure?

A

(Pc)+(πIF)-(Pif)-(πc)

42
Q

What is edema?

A

It is excess fluid accumulation in the extracellular/interstitial space.

43
Q

What are the lymphatic system functions?

A

Fluid balance, immune surveillance and movement of immune cells.

44
Q

How do the lymph vessels take up liquid in the interstitial space?

A

The movement of fluids through the endothelial cells.

45
Q

What do larger lymph vessels have?

A

They have smooth muscle for rhythmical contractions.

46
Q

Where are the pressures lowest in the vasculature system?

A

Pressure in veins are low because they do not need to be strong.

47
Q

What is the veins structure?

A

Thin smooth muscle walls (not contractile), valves that prevent back flow and a muscle PUMP.

48
Q

Why are veins more complaint than arteries?

A

They are thin walled and have a larger diameter and minimal matrix proteins.

49
Q

Flow formula:

A

Flow = P1 - P2 / R

50
Q

How does the body control MAP?

A

Baroreceptor reflex

51
Q

What is the muscle pump?

A

Propels blood forward is skeletal muscle pump effect

52
Q

What is the baroreceptor negative feedback loop?

A

High MAP ==> Stretch Receptor ==> CV control centre ==> ↑ PNS and ↓ SNS

53
Q

What causes changes in P1 and P2?

A

P1: ↑ sympathetic activity
↑ blood volume
↑ muscle pump
P2: ↑ inspiration

54
Q

What is the cardiac suction effect?

A

When ventricles relax, it sucks blood from atria to ventricle and decrease pressure in heart increases pressure gradient.

55
Q

What are the 5 main roles of the kidney?

A

Fluid/ion homeostasis, drug removal. waste excretion, hormone production and glucose synthesis.

56
Q

What are the two types of nephrons?

A

Juxtamedullary and Cortical Nephron

57
Q

What are the 3 main functions of the nephron?

A

Glomerular filteration, tubular reabsorption and tubular secretion.

58
Q

What is the formula for amount of solute excreted?

A

Amount Filtered - Amount Reabsorbed + Amount Secreted.

59
Q

What is the pathway for glomerular filtration?

A

Pores of endothelial cells, basement membrane matrix and podocyte filtration slits.

60
Q

What is Trans-epithelial Transport?

A

It is when substances within the tubule (filtrate) are transferred to the peritubular capillaries.

61
Q

What is renal clearance?

A

Volume of plasma that is completely removed from a substance per unit time.

62
Q

What is renal plasma flow?

A

Volume of plasma that passes through the kidney per unit of time.

63
Q

What are substances that are not reabsorbed but fully secreted?

A

H+, K+ and penicillin

64
Q

Explain the basic idea behind tubular reabsorption process?

A
  1. Na+ absorbed, creating an electrochemical gradient for anions.
  2. Ions in intersititial fluid creating a osmotic gradient.
  3. Water moves by osmosis (solute reabsorption)
  4. Solutes in the tubule become concentrated and some reabsorbed by diffusion.
65
Q

Describe the process and barriers of filtrate to plasma:

A

Luminal Cell Membrane, Cytosol, Basolateral cell membrane, Interstitial fluid and Capillary wall

66
Q

What is the purpose of the tight junction?

A

So substances can’t slip between the tubular epithelial cell

67
Q

What are the steps of Na+ reabsorption?

A
  1. Na+ enters through channels via concentration/electrochemical gradients
  2. Na+ is pumped into the basolateral side by Na+/K+ ATPase
  3. Na+ diffuses into peritubular capillaries
68
Q

What are the steps for water reabsorption?

A
  1. H2O moves through aquaporins
  2. H2O moves out of the cell by osmosis due to an Na+ gradient
  3. H2O moves into the peritubular capillaries by hydrostatic pressure and osmosis
69
Q

What is the process of glucose reabsorption?

A
  1. Na+ enters from the electrochemical gradient by SGLT-2
  2. Na+ is pumped to the basolateral side by Na+/K+ ATPase
  3. Transport of glucose through cytosol out of the cell by GLUT2 downn the gradient
  4. GLUT1 passively transports glucose into the peritubule capillaries
70
Q

What dictates the amount of glucose that is in our filtrate?

A

The amount of glucose filtrate it proportional to the plasma glucose concentration.

71
Q

What limits the absorption of glucose through the tubule to the peritubule space?

A

The number of SGLT-2 transporters

72
Q

How is tubular maximum determined by SGLT-2?

A

The number of transporters and the rate of action.

73
Q

What is renal threshold?

A

The plasma concentration of glucose that results in the saturation of the transporters detected as spillover of glucose into the urine.

74
Q

What is counter current multiplication?

A
  1. Descending loop is H2O permeable
  2. Ascending loop is H2O impermeable and has Na+Cl-K+ pumps
  3. The movement on one side will dictate the solute movement on the other
75
Q

Describe osmotic gradient:

A
  1. Ascending Na+Cl-K+ pumps moves salt into the instertitium
  2. This ↑ the osmolarity of the intersitital fluid
  3. Descending diffuses H2O out and into the intersititium following the osmotic gradient
76
Q

What is countercurrent exchange?

A

It creates high osmolarity; ↑ NaCl transport in ascending concentrates solutes in the loop which ↑ H2O reabsorption in descending.

77
Q

What is the Vasa Recta and its function?

A

It removes H2O from the medullary intersititum maintaining high osmolarity intersititium required for producing concentrated urine.

KINE 3012 (5 decks)

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