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FBS2 PPoS > vasculature > Flashcards

vasculature Flashcards

1
Q

3 main layers of muscular artery (lumen outwards)

A

tunica intima
tunica media
tunica adventita

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2
Q

describe the structure of a capillary (layers)

A

endothelial cells
basal lamina - fibrous proteins supporting endothelium
pericytes

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3
Q

what happens to venules near a site of infection

A

become more permeable to leukocytes - allow to enter tissues for immune response

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4
Q

what facts affect vascular tone and act on only smooth muscle

A

noradrenaline - constrict
angiotensin II - constrict
adrenaline - B2 receptor = dilate

-pressure - increase=constrict (myogenic response)

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5
Q

what factors affect vascular tone and act on only endothelium

A

flow - vasodilate

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6
Q

what factors affect vascular tone and act on both smooth muscle and endothelium

A
  • tissue metabolites: dilators. Cause endothelium to release NO and activate endothelium-dependent hypopolarisation (EDH)
  • local hormones: constrict. autocoids
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7
Q

describe how an active complex is formed to cause muscles to contract

A

myosin light chain kinase + calmodulin bind to Ca2+.

phosphorylate myosin –> actin -> crossbridge cycle

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8
Q

describe how a phosphorylated myosin may be dephosphorylated

A

enzyme myosin phosphatase.
-activated by NO via. cGMP - promote relaxation
Ca desensitisation

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9
Q

what may inhibit the enzyme myosin phosphatase

A

agonists via. rho kinase = Ca sensitisation

contract

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10
Q

what is NO released by and when

A 
in response to increasing Ca
bradykinin
ATP
histamine
H+
CO2
ACh
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11
Q

what does endothelium release to vasodilate/constrict

A
  • prostacyclin (PGI2) - vasodilate and inhibit platelet aggregation
  • endothelin - vasoconstrict
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12
Q

describe NO-mediated vasodilation

A
  1. NO enters smooth muscle
  2. activates guanylate cyclase which breaks down GTP –> cGMP
  3. cGMP activates Ca pump - Ca out of cells via. SERCA and PMCA (plasma membrane Ca ATPase)
  4. myosin dephosphatase - Ca desensitisation
  5. open K channels = hyperpolarise = VGCC close
  6. phosphodiesterase - stop breakdown of GMP
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13
Q

what is angiogenesis and what structure is involved

A

growth of new blood vessels

endothelium

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14
Q

layers of an arterial vessel

A 
endothelial cells
internal elastic lamina
smooth muscle cells
external elastic lamina
tunica adventitia: blood vessel, collagen, symp nerves, fibroblasts
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15
Q

role of pericyte

A

regulate capillary diameter in CNS

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16
Q

what’s the relationship between pressure and venous volume

A

small changes in pressure/tone changes volume greatly

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17
Q

diameter of veins and composition

A

5mm

tunica media with sparce smooth muscle

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18
Q

what kinase does cGMP activate

A

protein kinase G

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19
Q

what is oxidative stress and what does it do

A

overproduction of reactive oxygen species
associated with CV disease
-cause contraction, raise BP

20
Q

examples of reactive species

A

super oxide - O2-

hydrogen peroxide - H2O2

21
Q

what do superoxides do

A

react with NO = peroxynitrate which prevents NO-mediated vasodilation

22
Q

what is an alternative mechanism of vasodilation which uses cAMP

A
  • activate B2, PGI2 and adenosine receptors on vascular SMC
  • stimulates adenylate cyclase which synthesises cAMP –> PKA activate
  • PKG and PKA= vasodilate
23
Q

what are some acids released by endothelium to cause vasodilation

A

epoxyeicosatrieonic acids (EETS)

24
Q

what do EETS do

A

activate K channels on SMC = hyperpolarisation = relax

released by endothelium

25
Q

what is autoregulation

A

constant blood flow over wide range of pressures e.g. in renal, coronary, cerebral

26
Q

what is autoregulation caused by

A

myogenic response

effects of flow on local conc of metabolites

27
Q

how does the myogenic response keep change in flow to a minimum

A

slow constriction

28
Q

how are the concentrations of metabolites prevented from building up

A

increase in metabolites = vasodilation influence.

  • increases blood flow which washes out metabolites.
  • redices dilation = increase tone and local resistance
29
Q

what is metabolic hyperaemia

A

increased metabolism produces vasodilation factors.

important in cardiac and skeletal muscle

30
Q

what is reactive hyperaemia and when does it occur

A

If local blood flow is cut off, metabolites build up which causes vasodilation until flow is resumed. Flow is enhanced after this to ensure all metabolites are washed out

static (isometric) exercise

31
Q

what are the 3 types of endothelium and where is each found

A
  • continuous - blood brain barrier (tight junctions)
  • fenestrated - kidney, joints, intestinal mucosa
  • sinusoidal - liver, bone marrow, spleen
32
Q

5 routes across a capillary wall

A

-transcellular
-paracellular & fenestral
for larger lipophilic molecules:
-vesicular transport
-trans-endothelial channel
-wide intracellular gap

33
Q

what creates a barrier to diffusion in a membrane

A

glycocalyx and narrow clefts between endothelial cells

-dependent on size of species

34
Q

what route does water mainly flow though

A

intracellular clefts (paracellular)

35
Q

what are the 3 most permeable substances

A

o2
h20
nacl

36
Q

what are the 3 of the least permeable substances

A

glucose
INULIN
albumin

37
Q

formula for the oncotic osmotic pressure

A

[blood plasma] - [interstitium] = 2.7-10 mmHg

38
Q

what is the reflection coefficient

A

if it can get through the intracellular cleft
harder = higher coefficient
proteins have a high value 0.9

39
Q

what is the starling eqn

A

net movement of fluid (Jr) is proportionate hydrostatic - (oncotic x reflection coefficient)

40
Q

what happens to reabsorption when arterioles are contracted

A

reduce capillary hydrostatic pressure so reabsorption is more important.
reduce pressure

41
Q

what happens to P(cap) - capillary pressure - during standing

A

lower extremities - increases

reflexes: cause arteriolar constriction so Pcap is reduced = compensate for rise in filtration

42
Q

4 functions of lymphatic system

A
  1. preserve fluid balance
  2. transfer fat absorbed in small int to circulation
  3. transport foreign material to lymph nodes
  4. transport lymphocytes in blood
43
Q

what pathway is in lymph capillaries and what is it driven by

A

intercellular clefts. one way entry

tissue compression

44
Q

what’s a lymphangion and why are they important

A

a unit of lymph vessel between 2 valves

-each has a pacemaker to pump fluid forwards. afferent lymph trunks contain smooth muscle - contract

45
Q

how much to lymphangions need to compress to avoid pumping

A

40-50mmHg

46
Q

describe the Tavel of lymphocytes

A

blood –> lymph glands –> blood

47
Q

what occurs at lymph nodes, and glands

A
  • reabsorption of some lymph fluid (node)

- activation of lymphocytes (glands)

FBS2 PPoS (9 decks)

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