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Vascular > Angiogenesis, lymphatics and oedema > Flashcards

Angiogenesis, lymphatics and oedema Flashcards

1
Q

List the layers of an artery/vein starting from the endo

A
  • endo
  • tunica intima
  • tunica media
  • tunica adventitia
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2
Q

How is blood distributed in the body?

A
  • 65% venous
  • 30% arterial
  • 5% cap
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3
Q

What are the PHYSIOLOGICAL causes of neovascularisation?

A 
Ovulation
Menstruation
Placenta formation
Wound healing
Retinal development
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4
Q

What PATHOLOGICAL causes decrease neovascularisation?

A

Pulmonary fibrosis
Emphysema
Delayed ulcer healing

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5
Q

What are the PATHOLOGICAL causes increase neovascularisation?

A 
Tumour development
Retinopathies
Psoriasis
Rheumatoid arthritis
Plaque progression?
Restenosis
Endometriosis
Vascular Malformations
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6
Q

What is neovascularisation?

A

dev of new blood vessels

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7
Q

What is vasculogen?

A

De novo formation of blood vessels from
progenitor cells
Progenitor cells in bone marrow in tissues –> Cells form blood islands –> endo differentiation –> new cap plexuses

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8
Q

What is Angiogenesis?

A

Sprouting of new capillaries from existing
capillaries
Hypoxic trigger

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9
Q

What is arteriogenesis?

A 
Enlargement of pre-existing arterial
connections to completely developed and
functional arteries
Fluid shear stress
Small vessels have a trigger e.g. fluid stress or blockage in 1 vessel inc demand on smaller vessel which causes it to stretch + get muscularised
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10
Q

Describe angiogen

A

VEGF induces blood vessel formation – causes cell migration form parent vessels
Zone I cells migrating
Zone II cells dividing
Zone III cells maturing
Gradients established by affinity of binding of VEGF to matrix

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11
Q

Describe the role of cellular chaperones

A

Monocyte macrophages interact with tip of migrating stalk of endo cells to direct, mature them etc
Macrophages + endo cells have receptors e.g. angiopoietin 1, ag2, VEGFR2 which have ligands that bind and stim the cell to prod angiogen factors etc VEGF
Cells then go through maturation

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12
Q

What regulates angiogen?

A

PROMOTERS OVERWHELM INHIBITORS –> ANGIOGENIC SWITCH

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13
Q

List promoters of angiogen

A 
VEGFs
FGFs
Angiopoietins
IGF1
TGFb
Erythropoietin
NO
Thrombin
Fibrinogen
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14
Q

List inhib of angiogen

A

Angiopoietins – difference in ratio between AG1:AG2 can be inhib or promote angiogen
Troponin-I
Soluble VEGF receptors
IL12

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15
Q

Which factors regulate vessel growth?

A

Hypoxia
Metabolic stimuli - hypoglycemia, low pH, endothelial metabolism
Mechanical factors - Flow shear stress, Stretch
Growth and inhibitory factors - VEGF, PlGF, Ang1 , Ang 2
(stress-responsive gene transcription)

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16
Q

How does hypoxia stim new vessel growth?

A

Centre of tumor becomes hypoxic as O2 can’t reach it
Hypoxic inducible factor triggers hypoxia regulator gene to produce angiogen factors e.g. VEGF to promote new blood vessel formation

17
Q

What is flow shear stress?

A

inc flow through small vessel, becomes bigger + thicker

18
Q

Describe symptoms of PAD

A 
– most is asymptomatic 
Claudication = pain on walking 
Rest pain – usually worse at night without skin changes 
Final stage is skin changes  
Gangrene can be dry or wet
19
Q

List the branches of the femoral artery

A

profunda femoris –> superficial femoral –> popliteal –> ant. Tibial –> peroneal trunk split into peroneal + post. Tibial

20
Q

How do GF induce angio/arteriogenesis?

A

Factors that mobilise progenitors e.g. GM-CSF, G-CSF, SCF

Induction of homing e.g. SDF-1

21
Q

How does cell therapy induce angio/arteriogenesis?

A

Identification of organ-specific cytokines

• Ability of cells to incorporate and function in hostile environment e.g. ischaemic muscle

22
Q

List causes of leg oedema

A
  1. Dependency/immobility
  2. Pregnancy
  3. Heart Failure
  4. Low plasma proteins
  5. Chronic venous insufficiency
  6. Deep vein thrombosis
  7. Lymphatic insufficiency
  8. Chronic renal failure
23
Q

What is chronic venous insufficiency?

A

Superficial (greater and lesser saphenous vein) and deep (femoral and popliteal) venous circ drain blood up towards heart
DVT blocks deep veins which stops BF back up to heart and damages deep vein valves –> venous hypertension + swelling of the leg

24
Q

What is Starling’s Law?

A

The stroke volume of the heart increases in response
to an increase in the volume of blood in the ventricles,
before contraction, when all other factors remain
constant.

25
Q

Describe Starling’s Law of fluid homeostasis

A

Homeostasis maintained by opposing effects of vas HP + plasma colloid oncotic P
HP of blood being pumped through arterial end forces fluid out of vessel vs venous end where osmotic P drains fluid back in tf low protein (hypoalbuminemia) inside vessel means can’t pull fluid back in

26
Q

What causes transudate?

A

inc venous HP due to venous outflow obstruction e.g. congestive cardiac failure
dec colloid osm P due to dec preotein syn (liver disease) or inc protein loss (kidney disease)
causes fluid to leak out = transudate (low protein content, few cells)

27
Q

What causes exudate?

A
  • Vessel breakdown causing fluid + protein leakage
  • inflamm –> vasodil + stasis + inc interendo spaces
  • causes fluid to leak out = exudate (high protein content, some RBCs + WBCs)
28
Q

List diff between exudate + transudate

A
  • transudate: filterate without changes in endo perm. due to physiomech factors
  • exudate: oedema of inflamed tissue –> inc vas perm, damage to serous mem
  • transudate: non-inflamm oedema
  • exudate: inflamm oedema
  • transudate: clear, pale yellow
  • exudate: cloudy, yellow/bloody
  • transudate: glucose same as plasma
  • exudate: low glucose
  • transudate: pH > 7.23
  • exudate: pH < 7.23
29
Q

List primary causes of lymphoedema

A

Syndromic primary lymphoedema: Turner’s, Noonan’s and Prader Willi. 3. Lymphoedema with overgrowth, vascular, or cutaneous manifestations: Klippel-Trenaunay 4. Congenital onset lymphoedema ( 1 year age) E.g. Milroy’s (VEGFR3 mutation): Typically present at birth and bilateral
Late onset lymphoedema (> 1 year age) E.g. Lymphoedema Distichiasis (FOXC2 mutation): Typically teenagers - Double row eyelashes #
Rare: 1.5/100,000

30
Q

List secondary causes of lymphoedema

A
  1. Radiotherapy e.g. radiotherapy of breast can affect axillary lymphatics  oedema of arm 2. Surgery 3. Cellulitis – can invade + destroy lymphatics 4. Filariasis
31
Q

What is the main diff between lymphoedema + venous oedema

A

Lymphoedema causes chronic skin changes vs venous oedema

32
Q

Management of Oedema

A
  1. Treatment of underlying cause 2. Elevation 3. Compression 4. Massage 5. Good skin care 6. Surgery

Vascular (2 decks)

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