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YR 3 - Illness and Wellbeing > Blood Vessel Disorders > Flashcards

Blood Vessel Disorders Flashcards

(60 cards)

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1
Q

what is the organisation of blood vessels?

A

3 layers
- tunica externa w/ external elastic membrane
- tunica media w/ smooth muscle
—- elastic laminae separates
- tunica intima w/ internal elastic membrane

then the lumen

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2
Q

why does the aorta have a lot of elastic fibres?

A

allows the recoil and flow of large volumes and pressure of blood

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3
Q

why do muscular arteries have more smooth muscle?

A

allow vasoconstriction and vasodilation
- allows changes of blood flow to pass

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4
Q

describe the structure of capillaries.

A

single cell layer of endothelial cells
supporting sites = pericytes

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5
Q

which side does oxygenated and deoxygenated blood pass through?

A

oxygenated - through the aorta, on the left side
deoxygenated - through veins, on the right side

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6
Q

is vascular disease responsible for the highest mortality than any other human disease?

A

yes

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7
Q

what 4 age-related changes can occur in the arteries? - all come under the term of arteriosclerosis

A
  • tunica intima - fibrous thickening
  • tunica media - fibrosis/scarring
  • elastic laminae - fragmentation
  • dystrophic calcification
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8
Q

why do you get fibrous thickening as an effect of age-related changed in the vascular system?

A
  • exposure
  • activates macrophage and monocytes
  • lay down extracellular matrix
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9
Q

what is fragmentation of the elastic laminae?

A

the break down of elastic fibres
- doesn’t recoil as well

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10
Q

why do age-related changes occur in the vascular system?

A
  • long-term exposure to injurious agents, toxins and high blood pressure
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11
Q

define atherosclerosis

A
  • slow, progressive, chronic, degenerative
  • intimal disease
  • a healing response to endothelial injury on arterial wall
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12
Q

how does ‘atherosclerosis’ occur? (9)

A
  • area has haemodynamic disturbance due to risk factors
  • endothelial damage
  • permeability increases = leaky
  • lipid, macrophages and smooth muscle cell accumulation
  • macrophages take up lipids
  • accumulate in the wall
    ==== fatty streak
  • process progresses
    = atheromatous plaque
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13
Q

give 4 genetic and 5 environmental risk factors for atherosclerosis

A

genetic
- age
- males
- family history
- genetic abnormality

environmental
- hypertension
- smoking
- diabetes
- inflammation
- hyperlipidemia

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14
Q

describe the 3 pathogenesis’ of atherosclerosis

A

aneurysm and rupture - If the vessel wall weakens

occlusion by thrombus - plaque ruptures, causes thrombosis to occur

critical stenosis from stable plaque = hardened cap and mainly smooth muscle cells = not likely to rupture
- leads to occlusion, hypoxia and angina

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15
Q

what can be the end result with atherosclerosis?
- coronary, cerebral, aorta, mesenteric, lower arteries

A

in the coronary arteries:
- coronary ischaemic heart disease- angina, arrhythmias, myocardial infarction

carotid/cerebral arteries
- cerebrovascular diseases (stroke)

aorta
- aortic aneurism

mesenteric arteries
- bowel ischaemia

lower extremities
- peripheral vascular disease

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16
Q

what are the morphological features of atherosclerosis

A
  • fatty streak in the intima
  • stable plaque = hardened cap and mainly smooth muscle cells = not likely to rupture
  • gets larger into critical stenosis
  • leads to occlusion, hypoxia and angina
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17
Q

what can be the consequences of atherosclerosis

A
  • evaluated, occlusive intimal-based lesions
    AKA PLAQUES
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18
Q

what constitutes a atherosclerotic plaque? (5)

A

lipids
inflam cells
proliferating smooth muscle cell
extra-cellular matrix
fibrous cap

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19
Q

where does an atherosclerotic plaque protrude into?

A

into the lumen of the blood vessel

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20
Q

define systemic hypertension

A

persistently raised arterial blood pressure causing degenerative changes in vessels

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21
Q

why do you need pressure in the blood vessels?

A

to deliver oxygenated blood
- to pass the resistance in the circulation

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22
Q

describe the difference between systole and diastole

A

systole
- heart contracts
- raises blood pressure
arterial wall stretches

diastole
- heart relaxs
- lowers blood pressure
- fills back up again with blood
arterial wall recoils

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23
Q

give 2 outcomes of unregulated blood pressure and what they lead to.

A

hypotension - hypoxia, cell injury/death
hypertension - vessel damage, atherogenesis

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24
Q

give risk factors for systemic hypertension (4)

A
  • increasedsalt intake
  • alcohol
  • lack of exercise
  • increased fat intake
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25
describe potential pathogenesis' for systemic hypertension (4)
- athersclerosis by endothelial damage - aortic aneurysm - death - cardiac hypertrophy - death - cerebrovascular disease - stroke/dementia
26
describe the morphological features of systemic hypertension
hyaline arteriolosclerosis - glassy texture, pink stain - pink material around the vessels with narrow lumen hyperplastic arteriolosclerosis - in malignant hypertension - lots of extracellular matrix
27
what methods are there for classifying hypertension? (5)
- clinic measurement - systolic BP = >140 - diastolic BP = >90 - has 3 stages: mild, mod and severe - home ambulatory blood pressure measurement - aetiology - primary or secondary - pathological - benign or malignant - anatomical - systemic, pulmonary or portal
28
describe the aetiology classification of hypertension.
primary aka essential hypertension - idiopathic - not a specific cause, very common - mainly genetic - vasoconstrictive influences - age - stress, smoking, obesity, fitness - decrease in sodium excretion secondary - specific diseases causing hypertension - renal disease - endocrine causes - cardiovascular - neurovascular
29
renal diseases are a secondary factor for hypertension, why?
BP increases because.. - BP drops - kidney secrete renin - renin activates angiotensin system - vasoconstriction - retains salt and water = BP increases
30
what is 'renal artery stenosis'? how does it lead to hypertension
when the renal arteries are blocked through atherosclerotic process - kidney perceives decreased blood flow - renin released - angiotensin activate - vasoconstriction - water and salt retained - BP increases
31
how can coarctation lead to increased blood pressure?
if there is coarctation of the aorta - aorta narrows - low blood pressure - leads to renal angiotensin system activation
32
what neurological process' lead to hypertension? (4)
sleep apnoea stress increased intercranial pressure psychogenic
33
what's the difference between the pathological causes of hypertension from benign and malignant origin?
benign - asymptomatic - organ gets damaged gradually malignant - rapid hypertension - if untreated, death - severe increase of over 180 BP = renal failure = retinal haemorrhage = papillodeama
34
what is the portal venous system?
a system which drains blood from GIT to the liver
35
how can hypertension be classified anatomically?
systemic - pressure in the systemic circulation pulmonary - isolated pressure in the pulmonary circulation portal hypertension - pressure in the portal venous system - causes varicosities - dilations - rupture - those with liver cirrhosis can die
36
why is hypertension relevant in dentistry?
increased pain increased anxieties - difficult for extractions - high BP can increase risk for heart attack or stroke
37
define vasculitis
inflammation of the vessel walls
38
what is the name for the classification for vasculitis?
Chapel Hill Nomenclature - depends on the vessel bed and vessel size
39
what does vasculitis look like?
blue dots in a blood vessel
40
what is giant cell arteritis?
the most common form of vasculitis - a chronic granulomatous inflammation affecting large-medium arteries
41
describe the morphological features (4) of giant cell arteritis and what organs are involved (3)
features: - intimal thickening - granulomatous inflammation - elastic lamina fragmentation - multinucleate giant cells organs: - temporal arteries in the head - vertebral arteries - ophthalmic arteries
42
what complications can there be with 'giant cell arteritis'?
in the ophthalmic artery - can lead to permanent blindness in the head - headache, pain on biting = jaw claudication
43
how would GCA be treated?
with corticosteroids - anti-inflame drugs
44
define 'aneurysm'
a localised, permanent, abnormal dilation of a blood vessel
45
how are 'aneurysms' classified aetiology - are berries dark milk or fake smooth milk? (7)
shape - saccular - bulges out on one side - fusiform - bulges out both sides - dissecting - blood between intima and media aetiology - atheroslerotic - berries - dissecting - microaneurysms - false - syphlitic - mycotic
46
what is a berry aneurysm? what does the rupture cause?
a small, saccular lesion developing in the Circle of Willis in the brain at points of bifurcation causes subarachnoid haemorrhage
47
what are micro and syphilitic aneurysms also known as? where do they occur and what do they cause?
aka Charcot-Bouchard aneurysms - occur in intracerebral capillaries - cause intracerebral haemmorhage - stroke
48
how can retinal microaneurysms arise? what is their pathogenesis
from diabetes causing diabetic retinopathy
49
what are mycotic aneurysms? how does it occur in the tunica media?
weakening of arterial wall due to bacterial/fungal infection - enter tunica media from the vasa vasorum
50
what aneurysm come under Charcot-Bouchard aneurysms
micro and syphilitic
51
what is the most common infection leading to mycotic aneurysms?
subacute bacterial endocarditis
52
what is a false aneurysm?
a blood filled space around a vessel usually after traumatic rupture or perforating injury
53
describe a dissecting aneurysm, with symptoms and common location.
a tear in the wall, so blood tracks between intima and media layer symptoms - tearing pain in chest radiating to upper left shoulder common location - thoracic aorta
54
where is the most common location for an aneurysm secondary to aorta
abdominal aortic region
55
what is the main risk factor for rupture
the bigger the size, the more chance of rupture
56
compare the pathology and complications of different aneurysms
cause haemorrhage or ischamia from thromboembolism
57
what can be the result of 'arterial occlusion'? (3)
embolism, ischaemia, infarction
58
what is 'chronic peripheral arterial occlusive disease'? state the pathological consequences
narrowed arteries leading to reduced blood flow to limbs can lead to critical limb ischaemia
59
what are the 3 different types of blood vessel tumours?
Haemangioma - benign - head, neck, thorax Kaposi Sarcoma - intermediate grade, neither benign or malignant - results from infection : AIDS or HHV8 - Human Herpesvirus 8 Angiosarcoma - malignant - associated with: lymphoedema, radiation
60
what are the 6 P's on acute ischaemia
Pale Painful Paralysed Paraesthetic - tingly Perishing Cold Pulseless

YR 3 - Illness and Wellbeing (31 decks)

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