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CVS > 06b: Microcirculation > Flashcards

06b: Microcirculation Flashcards

1
Q

Two primary roles of capillaries.

A
  1. Deliver nutrients to tissues

2. Carry metabolites away from tissues

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2
Q

Vasomotion refers to waxing/waning of (X), to increase/decrease flow to (Y).

A 
X = arteriolar tone
Y = downstream capillaries
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3
Q

Fewer open capillary beds means (smaller/larger) diffusion distance.

A

Larger

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4
Q

Fick’s Law of Diffusion state that (X) is equal to:

A

X = Bulk Flow

D)(A)(deltaC/deltaX

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5
Q

Fick’s law: bulk flow increases with increase in which components?

A
  1. D (diffusion coefficient, which decreases with higher MW)
  2. A (surface area)
  3. DeltaC (concentration gradient)
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6
Q

Fick’s law: bulk flow increases with decrease in which components?

A

DeltaX (diffusion distance or path length)

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7
Q

The diffusion coefficient is inversely related to:

A

Square root of MW

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8
Q

Fick’s Law can be written with permeability as a factor. What’s the equation?

A

J = PAdeltaC

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9
Q

Diffusion of gases such as O2 and CO2 is primarily controlled by (X), since it takes about (Y) portion of their transit time through capillaries for exchange/equilibration to occur.

A 
X = blood flow through capillary
Y = 1/3
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10
Q

T/F: D for O2 is high, but relatively lower for CO2

A

False - high for both

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11
Q

Certain substances, such as (X) can only enter/exit capillaries through intercellular junctions. This limits the movement, because the junctions are (Y)% of total capillary (Z).

A 
X = glucose, AA
Y = 0.2-0.4
Z = surface area
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12
Q

T/F: for most nutrients, diffusion is sufficient as major mechanism to supply tissues.

A

True

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13
Q

If capillary wall is 0.3 micrometers thick, what’s the (deltaX) value in Fick’s Law?

A

Unknown - path of molecule not in straight line

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14
Q

Establishing and empirical relationship, using (X), solves the path/distance problem in Fick’s Law. (X) tells us how far molecule will move per (Y).

A 
X = Permeability
Y = unit time, unit concentration/pressure gradient, and per surface area
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15
Q

Substance moves through intercellular junction in capillary. It will have (easier/harder) time clearing its path of (X) if it’s a large molecule.

A

Harder;

X = fluid

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16
Q

(Blood/interstitium) contains high protein concentration with low permeability (proteins can’t leave). Thus, it exerts (X) pressure, which is (in sync/opposed to) hydrostatic pressure.

A

Blood;
X = oncotic
Opposed to

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17
Q

For bulk flow through capillary, which key pressure gradients should be considered?

A

Hydrostatic and Oncotic

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18
Q

If net hydrostatic pressure is greater than net oncotic pressure in capillaries, which direction is net fluid movement?

A

Out of capillaries

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19
Q

If net hydrostatic pressure is less than net oncotic pressure in capillaries, which direction is net fluid movement?

A

Into capillaries

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20
Q

Hydraulic permeability is defined as (X).

A

X = permeability of membrane to water

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21
Q

If hydrostatic pressure of interstitial fluid was negative, it would favor which movement?

A

Favor fluid movement out

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22
Q

Hydrostatic P is initially about (X) mmHg in capillary. If the value is about 4 mmHg in interstitial fluid, what’s the net hydrostatic P? Fluid moves (out/in) as it passes capillary bed.

A

X = 40;
Net: 36 mmHg

Can’t decide until you know net oncotic P

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23
Q

T/F: Oncotic P in interstitial fluid is 0 mmHg.

A

False - there is some protein in IF

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24
Q

T/F: Amount of protein in interstitial fluid depends on the tissue.

A

True

25
Q

Oncotic P is initially about (X) mmHg in capillary. If the value is about 5 mmHg in interstitial fluid, what’s the net oncotic P? Net hydrostatic is 36 mmHg. Fluid moves (out/in) as it passes capillary bed.

A

X = 25
Net: 20 mmHg

Out

26
Q

Net fluid loss out of capillaries per day is 2-4L. But we don’t lose all that fluid. Where is it going?

A

Lymphatics recaptures it (back to circulation)

27
Q

T/F: Bulk flow is enough to meet our glucose needs.

A

False - net filter only 2-5g/day, but we use 400g/day

28
Q

List the two main causes of edema.

A
  1. Increase in net filtration pressure (high hydrostatic/low oncotic P in capillaries)
  2. Blockage of lymphatics
  3. Increase in hydraulic permeability
29
Q

Hypoproteinemia will (increase/decrease) (hydrostatic/oncotic) P of (IF/capillaries), causing net filtration (in/out).

A

Decrease;
Oncotic;
Capillaries

Out (EDEMA)

30
Q

Bug bite causes local edema. Briefly explain why.

A

Toxin released that increases hydraulic permeability of capillaries

31
Q

Intercellular junctions in semipermeable membrane allow passage of (polar/nonpolar) molecules.

A

Water and small, polar solutes

32
Q

Glycocalyx lining (luminal/basal) surface of endothelial cells serves which function?

A

Luminal;

Prevents protein escape

33
Q

Beta-2 agonists (increase/decrease) permeability of endothelial junction complex. What’s the mechanism?

A

Decrease;

Increase cAMP, which increases junctional strands

34
Q

Inflammation (increase/decrease) permeability of endothelial junction complex. What’s the mechanism?

A

Increases;

Phosphorylates beta-catenin and VE-cadherin (weakens tight junctions and facilitates extravasation of WBC)

35
Q

Growing, healing, or chronically hypoxic tissue secretes (X), which stimulates (Y) growth and (increases/decreases) endothelial permeability.

A

X = VEGF;
Y = microvascular
Increases

36
Q

(Gap/tight) junctions allow rapid transmission of (X) signaling. If the signaling is between neighbor cells, it’s (Y) signaling. What’s the other type?

A

Gap;
X = chemical and electrical
Y = homo-cellular

Hetero-cellular (between endothelium and underlying vascular smooth m)

37
Q

eNO is a (short/long)-lived modulator of (X). It’s synthesized by (Y) in response to:

A

Short;
X = vascular tone
Y = eNOS (from L-Arg)

  1. Shear stress
  2. Agonists (ACh)
  3. Adenosine
  4. VEGF (hypoxia)
  5. Serotonin
38
Q

eNO causes (vasodilation/vasoconstriction) and (increases/decreases) organ perfusion.

A

Vasodilation;

Increases

39
Q

eNO (contracts/relaxes) smooth muscle. One way it does this by binding and (inhibiting/activating) (X) enzyme. Then…

A

Relaxes;
Activating
X = guanylyl cyclase

Increase cGMP, activate PKG, phosphorylation of substrates promotes relaxation

40
Q

eNO (contracts/relaxes) smooth muscle. One way it does this is by (activating/inhibiting) (X) channels. This causes (Y).

A

Activating;
X = big conductance K channels
Y = hyper polarization (and vascular relaxation)

41
Q

EDHFs, aka endothelium-derived (X), are produced in response to (Y) and (increase/decrease) smooth muscle excitability/contraction.

A

X = hyper polarization factors;
Y = agonists (bradykinin)
Decrease

42
Q

Prostacyclin is produced in response to (X) situation(s). It (increases/decreases) cAMP in smooth muscle, facilitating (Y) release.

A

X = inflammation, shear stress
Increases;
Y = eNO

43
Q

Most potent vasoconstrictor in body is (X). It’s released on (luminal/basal) side in response to agents such as (Y).

A

X = Endothelin;
Basal;
Y = Angiotensin II and ADH

44
Q

Under low BP circumstances, you’d expect (eNO, EDHF, Endothelin) to be released.

A

Endothelin

45
Q

T/F: Endothelin effect, like eNO, is short-lived.

A

False - long-lasting effect (2-3 hours contraction of vascular bed)

46
Q

Thrombin plays which two roles in regulation of hemostasis?

A
  1. Increase vWF exocytosis (platelet adhesion)

2. Increase eNO and prostacyclin production (inhibit platelet aggregation)

47
Q

Increased endothelial Ca influx causes (eNO, EDHF, Endothelin) to be released.

A

eNO and EDHFs

48
Q

Inflammatory agonists (increase/decrease) (P/E)-selectin movement to endothelial surface.

A

Increase

P-selectin

49
Q

(X) in inflamed tissue increase (P/E)-selectin, which acts for several hours to sustain “stickiness” of endothelial surface.

A

X = cytokines (IL1, TNF, interferon gamma)

E-selectin

50
Q

During “arrest” of leukocytes in inflammatory response, endothelium begins to express (X) molecules and leukocytes express (Y) molecules.

A 
X = ICAM and VCAM
Y = beta-integrins
51
Q

Diapedesis/Emigration of leukocytes is primarily dependent on high expression of (X) molecules.

A

X = ICAM and PECAM

52
Q

There’s increasing evidence that atherosclerosis formation may be tied to (X) dysfunction, such as imbalance between (Y) and (Z).

A 
X = vascular endothelial
Y = eNO
Z = endothelin
53
Q

(Endothelin/eNO) pays protective role on vascular beds, such as decreasing lesion formation. It does this by which mechanism(s)?

A

eNO;

  1. Inhibit expression of selectins/CAMs
  2. Less smooth muscle proliferation
  3. Inhibits platelet aggregation
54
Q

You’d expect (eNO/Endothelin) circulating levels to be higher in patients with atherosclerosis. And in pulmonary hypertension?

A

Endothelin higher in both cases

55
Q

Oxidative LDLs are thought to up regulate (eNO/endothelin) production by binding (X).

A

Endothelin;

X = LOX-1 receptor on endothelium

56
Q

(X) binding (Y) also produces superoxide anion, which inactivates (eNO/endothelin).

A

X = Ox-LDL and/or platelets
Y = LOX-1
eNO

57
Q

List some diseases/states that increase LOX-1 receptor.

A

HT, diabetes, hyperlipidemia, increased Ox-LDL

58
Q

(X) enzyme, which normally mediates endothelial quiescence via (Y) production, can switch its function to produce (Z).

A 
X = eNOS
Y = eNO
Z = ROS/H2O2 (promote inflammation)

CVS (11 decks)

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