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2D week 3 - acute and chronic limb ischemia > aetiology and pathogenesis of vascular disease > Flashcards

aetiology and pathogenesis of vascular disease Flashcards

1
Q

what is an aneurysm?

A

localised abnormal dilation of a blood vessel or the heart; they can be congenital or aquired

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2
Q

what does a true aneurysm involve?

A

intact attenuated arterial wall or thinned ventricular wall of the heart

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3
Q

causes of true aneurysms (4)

A

atherosclerosis; syphilis; congenital vascular aneurysms; ventricular aneurysms that follow transmural myocardial infarctions

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4
Q

types of true aneurysms (3)

A

saccular; fusiform; dissecting

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5
Q

what is an arterial dissection

A

when blood enters the arterial wall itself as a haematoma dissecting between its layers

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6
Q

what is a false aneurysm (pseudoaneurysm)

A

defect in the vascular wall leading to an extravascular haematoma; blood flow outside normal layers of arterial wall

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7
Q

characteristics of a false aneurysm (4)

A

freely communicates w the intravascular space; pulsating haematoma; surrounded by a thin fibrous capsule in communication with the lumen of a ruptured vessel; DOES NOT INVOLVE ALL THREE TUNICA LAYERS (i.e. rupture interna + media but not externa)

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8
Q

difference between a pseudoaneurysm and a dissection

A

Pseudoaneurysm: all three walls of the vessel have been broken through, and blood collects just outside the vessel, it doesn’t spread through the vessel and blood organises and become firm
Dissection: only the inner portion of the vessel wall is damaged, blood enters into that damaged area and tunnels up or down within the wall of the vessel

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9
Q

how are aneurysms generally classified?

A

shape and size

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10
Q

what are saccular aneurysms

A

spherical outpouchings involving only a portion of the vessel wall; between 5-20cm; often contain thrombus

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11
Q

what are fusiform aneurysms

A

diffuse, circumferential dilation of long vascular segment; up to 20cm in diameter and length; may involve the aortic arch, abdominal aorta, iliac arteries

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12
Q

what is the pathogenesis of aneurysms (4)

A

the intrinsic quality of the vascular wall connective tissue is poor; the balance of collagen degradation and synthesis is altered; the vascular wall is weakened through loss of smooth muscle; arteries are dynamically remodelling tissues

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13
Q

conditions associated with poor intrinsic vascular connective tissue (3)

A

Marfan’s syndrome - defective synthesis of fibrillin and progressive weakning of elastic tissue results in progressive dilation of BVs due to remodelling of inelastic media;
EDS - weak vessel walls due to defective type III collagen synthesis;
Vit C deficiency - altered collagen cross linking

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14
Q

pathogenesis of collagen degradation and aneurysms

A

local inflammatory infiltrates that produce destructive proteolytic enzymes; increased MMP production by macrophages in atherosclerotic plaques/vasculitis - these can degrade all he components of arterial walls

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15
Q

how can the vascular wall be weakened

A

loss of smooth muscle cells with inappropriate synthesis of non-collagenous/non elastic ECM

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16
Q

how does ischaemia of the inner media occur

A

atherosclerotic thickening of the intima increases the distance that oxygen and nutrients have to diffuse

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17
Q

how does ischaemia of the outer media occur

A

systemic hypertension causing narrowing of the arterioles of the vasa vasorum resulting in cystic medial degeneration

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18
Q

what is cystic media degeneration

A

degenerative changes with smooth muscle cell loss and loss of elastic fibres, inadequate ECM synthesis and production of amorphous ground substances

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19
Q

factors predisposing to weakening of arterial wall (in descending order -6)

A
  1. atherosclerosis
  2. hypertension (usually ascending aortic aneurysms)
  3. trauma
  4. vasculitis
  5. congenital defects (e.g. in the circle of Willis causing berry aneurysms)
  6. infections (mycotic aneurysms)
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20
Q

where can mycotic aneurysms originate from (3)

A

embolization of a septic thrombus (usually a complication of endocarditis); an extension of an adjacent suppurative process; circulating organisms directly infecting the arterial wall

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21
Q

how can syphilis cause aneurysms?

A

obliterative endarteritis is a characteristic of late-stage syphilis which has a predilection for small vessels which can result in ischemic injury of the aortic media and aneurysmal dilations - leads to aortic incompetence

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22
Q

pathological characteristics of AAA (3)

A

associated w atherosclerosis; atherosclerotic plaque in the intima compresses the underlying media; nutrient and waste diffusion from the vascular lumen to arterial wall is compromised; media undergoes degeneration and necrosis resulting in weakness/thinning

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23
Q

typical AAA patient

A

50+ male smoker w atherosclerosis

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24
Q

arteries usually involved in AAA

A

renal; superior/inferior mesenteric

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25
Q

consequences of AAA (5)

A
  1. rupture into peritoneal cavity/retroperitoneal tissues may result in fatal haemorrhages;
  2. obstruction og vessels leads to ischaemic injury of downstream tissues (e.g. leg, kidney);
  3. embolism from atheroma/mural thrombus
  4. impingement of adjacent structures
  5. presentation as an abdominal mass that simulates a tumour
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26
Q

what is an aortic dissection

A

when blood leaks out and separates the laminar planes of the media to form a blood-filled channel within the aortic wall

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27
Q

when can an aortic dissection be catastrophic?

A

if the dissection ruptures through the adventitia (externa) and haemorrhages into adjacent spaces

28
Q

is aortic dissection associated with aortic dilation?

A

not always, unlike aneurysms

29
Q

examples of what can cause aortic dissections (4)

A

being a 40-60yro man with antecedent hypertension; being a younger patient with abnormal connective tissues (e.g. marfan’s); iatrogenic (e.g. complicating during cannulations); during/after pregnancy

30
Q

why is dissection uncommon in the presence of atherosclerosis/ medial scarring?

A

medial fibrosis inhibits propagation of the dissecting haematoma

31
Q

pathogenesis of aortic dissection

A

a tear occurs in the intima; blood flow under systemic pressure dissects through the media - here aggressive pressure reducing therapy may be effective in limiting a dissection;

32
Q

when can an intramural haemotoma without an intimal tear occur?

A

when there is disruption to penetrating vessels of the vasa vasorum

33
Q

aortic dissection classifications

A

A - more proximal, involves either the ascending + descending aorta or just the ascending, the most common type; B - distal to the subclavian artery

34
Q

where is the most serious place to have a dissection

A

aortic valve to the arch

35
Q

Classical symptoms of aortic dissection (4)

A

sudden onset excruciating pain; beginning in the anterior chest and radiating to the back (between scapulae); moving downward as dissection progresses; changes in pulses

36
Q

most common cause of death (due to dissection)

A

outward rupture into the pericardia, pleural or peritoneal cavities

37
Q

what can retrograde dissection (into the aortic root) result in? (4)

A

disruption of the aortic valvular apparatus leading to: cardiac tamponade; aortic insufficiency; myocardial infarction

38
Q

what can extension of the dissection into large arteries result in?

A

vascular obstruction resulting is ischaemia

39
Q

what is vasculitis

A

vessel wall inflammation

40
Q

what are the two most common pathogenic mechanisms of vasculitis?

A

immune mediated inflammation; direct invasion of vascular walls by pathogens

41
Q

examples of large vessel vasculitis

A

granulomatous disease - GCA, takayasu arteritis

42
Q

examples of medium vessel vasculitis

A

polyarteritis nodosa (immune complex mediated); Kawasaki disease (anti-endothelia cell antibodies)

43
Q

examples of small vessel vasculitis (6)

A

immune complex mediated: SLE (ANA, Anti-dsDSN, Anti-smith), henoch schonlein purpura; cyroglobulin vasculitis;
ANCA associated: microscopic polynagitis (pANCA), Wegener granulomatas (cANCA), Chrug-Strauss syndrome (pANCA)

44
Q

what are the two main immunological mechanisms that initiate vasculitis

A

anti-endothelial cell antibodies; antineutrophil cytoplasmic antibodies

45
Q

what is ANCA

A

circulating antibodies that react with neutrophil cytoplasmic agents; a heterogenous group of antibodies directed against neutrophil granules, monocyte lysosome etc.

46
Q

p-ANCA target

A

anti-myeloperoxidase (MPO) - usually used to generate oxygen free radicals in phagocytosis

47
Q

c-ANCA target

A

anti-proteinase 3 (PR3) - a neutrophil azurophilic granules consitituent

48
Q

how can ANCA lead to damaged blood vessels

A

ANCA can directly activate and stimulate neutrophils to release ROS and proteolytic enzymes

49
Q

Buerger’s disease typical patient

A

under 35s who smoke heavily, usually men

50
Q

pathophysiology of Buerger’s disease (5)

A

thrombosis of medium sized arteries and veins with marked inflammatory reaction; thrombus contains microabsesses of neutrophils; tibial and radial arteries usually involved; secondary extension into veins and nerves of extremities can be seen; leads to vascular insufficiency

51
Q

pathogenesis of Buerger’s disease

A

direct endothelial cell toxicity by tobacco components; idiosyncratic immune response to tobacco agents; genetic component - increased prevalence in israeli, south asian, japanese ethnicities; association with HLA haplotypes

52
Q

clinical features of Buerger’s disease

A

cold sensitivity in hands (similar to raynauds); pain in instep of foot; severe pain even at rest (neural involvement); chronic ulcerations of toes, feet, fingers etc. (often followed by frank gangrene); dramatic relief by smoking assistance (early stages)

53
Q

what are varicose veins

A

abnormally dilated, tortuous veins produce by prolonged/increased intraluminal pressure and loss of vessel wall support (valve function loss)

54
Q

how can venous pressure increase

A

when legs are depended for prolonged periods (leads to pedal oedema and venous stasis); pregnancy; obesity

55
Q

how can chronic varicose ulcer occur? (5) pathway

A

varicose dilation renders venous valves incompetent -> stasis, congestion, oedema, pain and thrombosis occur -> disabling sequelae occur (persistent oedema in extremities, ischaemic skin changes ) -> stasis dermatitis and ulcerations occur -> poor wound healing and superimposed infections leads to chronic varicose uclers

56
Q

are varicose veins a risk for PE

A

no, embolism from superficial veins is very rare

57
Q

how do venous ulcer develop?

A

persistently high BP in the veins causes damage to skin which eventually breaks down and forms an ulcer

58
Q

what is thrombophlebitis?

A

an inflammatory process that causes a blood clot to form and block one or more veins, usually in the legs

59
Q

where does thrombophlebitis most commonly occur in men

A

periprostatic venous plexus

60
Q

where does thrombophlebitis most commonly occur in women

A

pelvic venous plexus

61
Q

what increases the risk of DVT (3)

A

prolonged immobilisation (decreases the blood flow through the veins) e.g. bed rest, airplane travel; being postoperative (esp. ortho); factors that slow venous return (pregnancy, obesity, congestive heart failure etc.)

62
Q

what increases the risk of DVT

A

prolonged immobilisation (decreases the blood flow through the veins) e.g. bed rest, airplane travel; being postoperative (esp. ortho); factors that slow venous return (pregnancy, obesity, congestive heart failure etc.)

63
Q

examples of local signs/symptoms of thrombi

A

distal oedema, cyanosis, heat, tenderness, redness, swelling, pain may be elicited or may be absent

64
Q

what is a pulmonary embolism

A

the fragmentation/detachment of the whole venous thrombus - lets lodged in the pulmonary system; it may be a complication of DVT; it can be the first manifestation of thrombophlebitis

65
Q

what causes Raynaud’s

A

exaggerated vasoconstriction of digital arteries/arterioles; temporary spasm of blood vessels in response to cold or emotional stresses

66
Q

clinical signs of Raynaud’s

A

paroxysmal pallor/cyanosis f the digits, nose, earlobes, lips etc.

2D week 3 - acute and chronic limb ischemia (4 decks)

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