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My LSS- CVS > CVS 6: Blood vessel order > Flashcards

CVS 6: Blood vessel order Flashcards

1
Q

What are the three layers of blood vessels?

A
  1. Tunica Adventitia
  2. Tunica Media
  3. Tunica Intima
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2
Q

What is found in the tunica adventitia and what is its function?

A

The EXTERNAL Layer

  • contains fibrous tissue, elastin and collagen
  • helps keep shape of the blood vessel
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3
Q

What is the tunica media made of and what is its function?

A
  • Predominantly smooth muscle

- can contract or dilate based on the type of stimulus

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4
Q

What is the tunica intima made of and what is its function?

A
  • Vascular endothelium has an elastic basal lamina

- The exchange surface

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5
Q

What is the vascular endothelium?

A

A single cell layer that acs as the BLOOD-VESSEL interface

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6
Q

Give the five functions of vascular endothelium

A
  1. VASCULAR TONE- secretes and metabolises vasoactive substances (which cause vasodilation/constriction)
  2. THROMBOSTASIS- secretes anti-coagulants, prevents clotting and molecules adhering to vessel walls
  3. ABSORPTION + SECRETION
  4. BARRIER- prevents entry of pathogens and prevents atheroma formation
  5. GROWTH- mediates cell proliferation
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7
Q

What do endothelial cells contain to detect increased blood flow?

A

Mechanoreceptors

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8
Q

Name the two types of vasodilators and briefly summarise how they work.

A
  1. Nitric oxide- inhibits platelet aggregation

2. PG12 (prostacyclin)- cardioprotective molecule which also inhibits platelet aggregation

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9
Q

Name three vasoconstrictors and briefly summarise how they work.

A
  1. TXA2 (thromboxane)- produced in endothelial cells and platelets, activates other platelets–> aggregation
  2. ET-1 (endothelia 1)
  3. Angiotensin II (ANG II)
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10
Q

What controls vascular tone?

A

Balance between vasoconstriction and vasodilation

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11
Q

What is special about endothelin-1

A

Can cause vasoconstriction and vasodilation because it has different receptors on different tissues

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12
Q

What stimulates NO production and how?

A

Acetylcholine

  • It binds to the G protein coupled receptor
  • activates Phospholipase C
  • PLC converts PIP2=> IP3 and DAG
  • IP3 moves to the ER and causes Ca2+ efflux
  • A rise in IC Ca2+ up regulates endothelial nitric oxide synthase (eNOS)
  • eNOS catalyses formation of NO
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13
Q

Which reaction does eNOS catalyse?

A

L-arginine + O2==> L-citrulline + NO

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14
Q

How does NO work?

A
  • NO exits the endothelial cell and moves to the smooth muscle
  • NO in smooth muscle up-regulates Guanylyl cyclase which converts GTP to CGMP
  • cGMP up regulates Protein Kinase G
  • PKG activates potassium channels
  • membrane hyperpolarises
  • Relaxation of smooth muscle
  • Vessel dilates
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15
Q

What stimulates endothelial NO?

A

Shear stress (the force of blood going across the endothelial cells)

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16
Q

What acts as a NO donor?

A

SNP (Sodium nitroprusside)- we don’t rely on endothelial cells to produce NO. Endothelium is bypassed
Used to control high bp

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17
Q

What is used to convert phospholipids into Arachidonic acid?

A

Phospholipase A2

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18
Q

What is Arachidonic acid converted to? and using which enzyme?

A

Prostaglandin H2 (PGH2) by the COX enzymes (cyclooxygenase)- COX1 and COX2

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19
Q

Where is COX 1 found and what do an elevated levels of COX2 indicate?

A

COX1- expressed on all cells

COX2- unregulated when your body has inflammatory problems

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20
Q

What does PGH2 become and name the enzymes used…

A

PGH2==>

  1. Prostacyclin (PGI2)
    • Prostacyclin synthase
  2. Thromboxane A2 (TXA2)
    • Thromboxane synthase
  3. Other produces (PGD2, PGE2 and PGF2)
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21
Q

What is the function of some of the other products produced from PGH2?

A

Involved in the health of the epithelia and the GI tract

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22
Q

What other product might Arachidonic acid be converted to and which enzyme does this pathway use?

A

Leukotrines

Lipooxygenase enzyme cascade

23
Q

Give an example of a leukotrine and its effect in the body

A

LTD4- bronchoconstriction

LTD4 is associated with asthma

24
Q

Other than phospholipids what molecule can be used to form arachidonic acid? Which enzyme is used in this process?

A

DAG using DAG lipase

25
Q

Where is prostacyclin produced and what is it produced from?

A

Produced in endothelial cells from arachidonic acid

26
Q

What does prostacyclin bind to once it is produced in endothelial cells? What is the effect of this binding?

A
  • Binds to IP receptor on smooth muscle.
  • Activates adenylate cyclase which converts ATP to cAMP
  • cAMP up regulates PKA which causes relaxation of smooth muscle=> vasodilation
27
Q

What is the other effect of prostacyclin apart from vasodilation? How does this happen?

A
  • Has anti-platelet aggregation properties

- Has to be secreted into the blood

28
Q

Which two receptors can Thromboxane bind to?

A

Alpha- Platelets

Beta- Vascular smooth muscle cells

29
Q

How does Thromboxane bring about vasoconstriction?

A
  • TXA2 diffuses through the basement membrane
  • TXA2 binds to the TPB on VSMCs.
  • Activates PLC
  • PLC converts PIP2 into IP3
  • IP3 triggers Ca2+ influx from EC space and SER
  • Ca2+ upregulates myosin light chain kinase which causes VSMC to contract
  • vasoconstriction
30
Q

How does Thromboxane A2 bring about platelet aggregation?

A
  • TXA2 binds to TPa receptors on platelets
  • Platelets become active and produce more TXA2
  • Positive feedback response
  • Platelets aggregate
31
Q

How and where is endothelia-1 produced?

A
  • In the nucleus of endothelial cells
  • Endothelin-1 is produce from its zymogen (inactive precursor) by Endothelin Converting Enzyme (which is embedded in the membrane)
32
Q

What happens to Endothelin-1 once it has been produced in the endothelial cells?

A
  • Endothelin-1 binds to the ETA and ETB receptors on VSMCs
  • Receptors activate PLC which converts PIP2 to IP3
  • IP3 triggers Ca2+ influx
  • This causes the cell to contact ==> Vasoconstriction
33
Q

What is the alternative to Endothelin-1 binding to ETA and ETB on VSMCs?

A
  • ET-1 could bind to ETB receptor on the endothelial cell
  • triggers eNOS
  • eNOS increases NO production
  • NO diffuses to VSMC
  • Cell relaxes and vessel dilates
34
Q

What are the antagonists of ET-1 production?

A
  • Prostacyclin
  • Nitric oxide
  • ANP
  • Heparin
  • HGF
  • EGF
35
Q

What are the agonists of ET-1 production?

A
  • Adrenaline
  • ADH
  • Ang II
  • IL-2
36
Q

What is the precursor for angiotensin II? and where is it produced?

A

Angiotensinogen

Liver

37
Q

What converts Angiotensinogen to Angiotensin I? Where is this enzyme produced and under what conditions is it produced?

A
  1. Renin
  2. Produced in the kidneys
  3. Produced in response to Low blood pressure if renal perfusion decreases
38
Q

What is Angiotensin I converted to and which enzyme does this? Where is this enzyme found?

A
  1. Angiotensin II
  2. Angiotensin Converting Enzyme (ACE)
  3. Vascular endothelium
39
Q

What are the two overall effects of Angiotensin II secretion?

A
  1. Increased water retention

2. Increase in vascular resistance

40
Q

How is the increased water retention brought about by Angiotensin II?

A
  • stimulates ADH secretion
  • Increases aldosterone production
  • Increases Sodium reabsorption
41
Q

How is the increase in vascular resistance brought about?

A
  • Increased sympathetic activity

- Arteriolar vasoconstriction

42
Q

What is the effect of increasing vascular resistance and water retention?

A

Increases blood pressure

43
Q

Describe how angiotensinogen is produced from angiotensin and then goes on to affecting arterioles

A
  • Renin cleaves angiotensinogen to Ang I
  • ACE, expressed on endothelial cells in renal/ pulmonary circulation cleaves Ang I to Ang II
  • Ang II diffuses across the endothelium
  • Ang II binds to AT1 receptor on VSMC
  • Activates PLC which converts PIP2 to IP3
  • IP3 triggers Ca2+ influx
  • Ca2+ up regulates MLCK
  • increases cross-bridging
  • Cell contracts and you get vasoconstriction
44
Q

What other effect does ACE have?

A

ACE breaks down bradykinin

- NO-mediated vasodilation is reduced

45
Q

What are the three ways of increasing the diameter of blood vessels and what sort of mechanisms do the use?

A
  1. Stimulating production of NO (endothelium-dependent)
  2. Donating Nitric Oxide (endothelium- independent)
  3. Enhancing the effects of the NO that’s already there (stopping its degradation)
46
Q

Which enzyme does Viagra inhibit? Which reaction does this enzyme catalyse?

A
  1. Phosphodiesterase
  2. Involved in converting cGMP to GMP which is metabolically inactive
  3. cGMP needed for vasodilation so viagra prevents cGMP inactivation
47
Q

Which enzyme does aspirin affect?

A

Irreversible inhibition of the COX enzymes

  • COX1- inactivation
  • COX2- switches its function to generate protective lipids
48
Q

What do non-specific NSAIDs cause?

A

reversible inhibition of COX enzymes

49
Q

What is the consequence of Aspirin inhibiting the COX enzymes?

A
  • Reduce conversion of Arachidonic acid to PGH2

- less prostacyclin and thromboxane

50
Q

What is the consequence of using a low dose of aspirin on the body?

A
  • Prostacyclin levels decrease and then remain high

- Thromboxane levels continue to fall

51
Q

Why do prostacyclin levels remain high while thromboxane levels fall whilst on low dose aspirin?

A
  • Thromboxane is mainly produced in the platelets.

- Platelets don’t have nuclei so they can’t generate more mRNA to produce new proteins to build the COX enzymes again

52
Q

Why can you use drug which block VGCC without affecting the heart?

A
  • The affinity of the channel blocker to the channel is related to the membrane potential of the target cell
  • smooth muscle cells have higher membrane potentials than cardiomyocytes
53
Q

What are the effects of ACE inhibitors?

A
  • inhibit the conversion of Ang I to Ang II
  • We inhibit the breakdown of Bradykinin
  • Decreasing Bradykinin breakdown stimulates vasodilation
54
Q

What happens if the endothelium is dysfunctional?

A
  • damages
  • parts of sub-endothelial layer (collagen) is exposed
  • causes platelets to adhere
  • Platelets stick and release thromboxane
  • stimulates platelet aggregation
  • platelet plug forms

My LSS- CVS (21 decks)

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