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Y3- I & W > Pathology: circulatory disorders > Flashcards

Pathology: circulatory disorders Flashcards

1
Q

describe artery structure

A

Three layer structure
Inner layer- tunica intima
Middle layer- tunica media
Outer layer- tunica adventitia

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2
Q

what is atherosclerosis

A

A slow progressive intimal disease of large to medium sized muscular and elastic arteries

It results in elevated or occlusive intimal based lesions
The lesions or plaques are composed of lipids, smooth muscle cells and ECM

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3
Q

what are some non modifiable risk factors for atherosclerosis

A

genetic abnormalities
family history
increasing age
male gender

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4
Q

what are some modifiable risk factors for atherosclerosis

A 
Hyperlipidaemia 
Hypertension 
Smoking 
Diabetes
Inflammation
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5
Q

what is the pathogenesis of atherosclerosis

A

1) In the first response we get monocyte/platelet adhesion
2) The monocytes-> macrophages and secret cytokines and take up lipids in the blood stream
3) The macrophage now continues to take up lipids and smooth muscle leading to the formation of a atheromatous plaque

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6
Q

what is the sequence of atherosclerosis

A 
Normal artery 
Fatty streak 
Fibrofatty artery 
Advanced vulnerable plaque 
Clinical stenosis- about 70% bloackage
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7
Q

what can atherosclerosis lead to

A

gradual mechanical obstruction to flow
plaque rupture
weakening of the vessel

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8
Q

what are major consequences in atherosclerosis

A

if in the coronary heart arteries- ischameic heart disease, angina
if in the aorta- aortic aneurysm
if in the mesenteric artery’s- bowel ischamia

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9
Q

if we get atherosclerosis in the coronary arteries what can it lead to

A

angina, MI

ischaemic heart disease

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10
Q

if we get atherosclerosis in the aorta what can it lead to

A

aortic aneurysm

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11
Q

if we get atherosclerosis in the mesenteric arteries what can it lead to

A

bowel ischaemia

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12
Q

what is age related vascular changes called

A

arteriosclerosis

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13
Q

what do we see as a patient ages in the arteries

A

thickening of the intimate
scarring of the media
fragmentation of the lamina
calcification

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14
Q

how can hyperglycaemia damage the vessel

A

• ROS formed
• Decreased NO
• Formation of advanced glycation end products
• Activation of inflammatory pathways
Promotion of thrombosis and atherosclerosis

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15
Q

what are the consequences of diabetic vascular disease

A 
Microangiopathy 
Haemorrhage 
Hypertension 
Atherosclerosis 
MI 
Nephrosclerosis 
Islet cell loss 
Gangrene 
Peripheral vascular atherosclerosis
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16
Q

what is giant cell arteritis

A

it is also known as temporal/cranial arteritis depending on the vessel
chronic vasculitis of large/medium sized vessels

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17
Q

when do we see giant cell arteritis

A

hardly ever occurs in someone less than 50

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18
Q

what are the clinical signs and symptoms of giant cell arteritis

A

new headache- temporal tenderness, enlarged artery
jaw claudication
visual symptoms- amaurosis fugax
non descriptive eg flu, body ache

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19
Q

what is amaurosis fugax

A

blindness like curtains coming down on the eyes

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20
Q

what should the GDP do if we suspect GCA

A

seek advice
treat with oral steroids glucocorticoids
40-60mg prednisolone daily

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21
Q

what are tests we can do if we suspect giant cell arteritis

A

ESR- raised over >100mm/hr
CRP raised
haematology- normochromic normocytic anaemia
temporal artery biopsy- at least 1cm or longer within 7 days of treatment

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22
Q

what can giant cell arteritis lead to

A

retinal arterial occlusion- permanent partial/complete loss of vision in one or both eyes

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23
Q

if other branches are affected what can giant cell arteritis lead to

A

cerebral ischameia
mesenteric ischaemia
aneurysms

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24
Q

what is an aneurysm

A

localised, permanent abnormal dilations of a blood vessel

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25
Q

what are the types of aneurysms

A 
Atherosclerotic 
Dissecting 
Berry 
Microaneurysms 
Syphilitic 
Mycotic 
False
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26
Q

describe atherosclerotic aneurysms

A

most common in elderly

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27
Q

what is the main risk factor for rupture of the atherosclerotic aneurysm

A

increase in the size of the aneurysm

28
Q

if the aneurysm is 4-5cm what is the percentage rupture rate

A

1%

29
Q

if the aneurysm is 5-6cm what is the percentage rupture rate

A

11%

30
Q

if the aneurysm is >6cm what is the percentage rupture rate

A

25% risk

31
Q

how can we detect an aneurysm

A

by ultrasound

32
Q

how can the aneurysm be repaired

A

endovascularly

33
Q

what are the complications of an aneurysm

A

the rupture causing retroperitoneal haemorrhage

34
Q

what is a dissecting aneurysm

A

when blood gets tracked between the layers

35
Q

what is a berry aneurysm

A

circle of willis- where small saccular lesions develop at sites of arterial bifurcations

36
Q

where is berry aneurysm found commonly

A

in hypertensive pts

37
Q

what can berry aneurysms cause

A

subarachnoid haemorrhages

38
Q

describe micro aneurysms

A

occur in hypertensive patients

rupture causes intracerebral haemorrhage

39
Q

what is a charcot bouchard aneurysm

A

occur in intracerebral capillaries in high BP pts

40
Q

what can cause diabetic retinopathy

A

retinal microanuerysms

41
Q

describe syphilitic aneurysms

A

occur in tertiary syphilis
occurs in the ascending thoracic aorta
causes ischamic medial damage fibrosis and loss of elasticity

42
Q

describe mycotic aneurysms

A

rare

weakening go the arterial wall secondary to bacterial/fungal infection

43
Q

how do organisms enter the media in mycotic aneurysms

A

from the vasa vasorum

44
Q

where is mycotic aneurysms commonly found

A

in cerebral arteries

45
Q

describe false aneurysms

A

blood filled space around the vessel following trauma

46
Q

whams in contained in the adventitial tissue in false aneurysms

A

the haematoma

47
Q

when is false aneurysms seen

A

following femoral artery puncture during angioplasty

48
Q

definition of thrombosis

A

clotting in an abnormal situation leading to harm or injury

49
Q

what is a thrombus

A

a solid mass or plug of blood constituents formed within the heart or blood vessels during life

50
Q

what factors contribute to a thrombosis formation

A

virchows triad

51
Q

what is virchows triad

A

endothelial injury
abnormal blood flow
hyper coagulability

52
Q

what is abnormal blood flow

A

non laminar blood flow

53
Q

what is venous thrombosis

A

stasis is the dominant mechanism

occurs at sites of stasis eg deep veins of legs

54
Q

describe arterial thrombosis

A

endothelial injury to turbulent blood flow

55
Q

what happens after thrombus formation

A

Propagation
Dissolution- dissolves from anti coagulation factors
Organisation- absorbed into the BV wall
Recanalization- new vascular channels open up inside the thrombus
Embolization- formation of a detached intravascular solid liquid or gas mass that is carried by the blood to a site far away from the origin leading to vascular occlusion

56
Q

what is a thromboemboli

A

Embolus derived from part of a dislodged thrombus

57
Q

what is venous emboli

A

From the venous system common legs leading to pulmonary embolism

58
Q

what is arterial systemic emboli

A

emboli leading into the Arterial system to the brain, limbs and organs

59
Q

what is a paradoxical embolism

A

Is when you have a embolus in the venous system and it lodges itself by bypassing the lungs by going through a defect in the heart

60
Q

describe pulmonary embolism

A

uptown 60000 deaths per year from this

61
Q

how does pulmonary embolism occur

A

1) Fragmentation of the DVT
2) Embolus enters the IVC
3) Passes through the right heart
4) Impaction and occlusion in pulmonary circ

62
Q

what are the causes of pulmonary embolism

A

thromboembolic in origin usually

63
Q

what is the classic history of pulmonary embolism

A

Sudden onset
Dyspnoea
Hypoxia
Tachycardic

64
Q

how do we reduce the chance of pulmonary embolism forming

A

walking around a lot
drink a lot of water
TED stockings
anti coagulants

65
Q

describe systemic thromboembolism

A

Occurs within the arterial circulation
Can come from other sources eg aortic aneurysms thrombus
Atherosclerotic thrombus
Paradoxical embolism

Y3- I & W (21 decks)

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