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

Blood Vessel Disorders Flashcards

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
Q

describe potential pathogenesis’ for systemic hypertension (4)

A
  • athersclerosis by endothelial damage
  • aortic aneurysm - death
  • cardiac hypertrophy - death
  • cerebrovascular disease - stroke/dementia
26
Q

describe the morphological features of systemic hypertension

A

hyaline arteriolosclerosis - glassy texture, pink stain
- pink material around the vessels with narrow lumen

hyperplastic arteriolosclerosis
- in malignant hypertension
- lots of extracellular matrix

27
Q

what methods are there for classifying hypertension? (5)

A
  • 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
Q

describe the aetiology classification of hypertension.

A

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
Q

renal diseases are a secondary factor for hypertension, why?

A

BP increases because..
- BP drops
- kidney secrete renin
- renin activates angiotensin system
- vasoconstriction
- retains salt and water
= BP increases

30
Q

what is ‘renal artery stenosis’? how does it lead to hypertension

A

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
Q

how can coarctation lead to increased blood pressure?

A

if there is coarctation of the aorta
- aorta narrows
- low blood pressure
- leads to renal angiotensin system activation

32
Q

what neurological process’ lead to hypertension? (4)

A

sleep apnoea
stress
increased intercranial pressure
psychogenic

33
Q

what’s the difference between the pathological causes of hypertension from benign and malignant origin?

A

benign
- asymptomatic
- organ gets damaged gradually

malignant
- rapid hypertension
- if untreated, death
- severe increase of over 180 BP
= renal failure
= retinal haemorrhage
= papillodeama

34
Q

what is the portal venous system?

A

a system which drains blood from GIT to the liver

35
Q

how can hypertension be classified anatomically?

A

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
Q

why is hypertension relevant in dentistry?

A

increased pain
increased anxieties
- difficult for extractions
- high BP can increase risk for heart attack or stroke

37
Q

define vasculitis

A

inflammation of the vessel walls

38
Q

what is the name for the classification for vasculitis?

A

Chapel Hill Nomenclature
- depends on the vessel bed and vessel size

39
Q

what does vasculitis look like?

A

blue dots in a blood vessel

40
Q

what is giant cell arteritis?

A

the most common form of vasculitis
- a chronic granulomatous inflammation affecting large-medium arteries

41
Q

describe the morphological features (4) of giant cell arteritis and what organs are involved (3)

A

features:
- intimal thickening
- granulomatous inflammation
- elastic lamina fragmentation
- multinucleate giant cells

organs:
- temporal arteries in the head
- vertebral arteries
- ophthalmic arteries

42
Q

what complications can there be with ‘giant cell arteritis’?

A

in the ophthalmic artery - can lead to permanent blindness

in the head - headache, pain on biting = jaw claudication

43
Q

how would GCA be treated?

A

with corticosteroids - anti-inflame drugs

44
Q

define ‘aneurysm’

A

a localised, permanent, abnormal dilation of a blood vessel

45
Q

how are ‘aneurysms’ classified

aetiology - are berries dark milk or fake smooth milk? (7)

A

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
Q

what is a berry aneurysm? what does the rupture cause?

A

a small, saccular lesion developing in the Circle of Willis in the brain at points of bifurcation

causes subarachnoid haemorrhage

47
Q

what are micro and syphilitic aneurysms also known as? where do they occur and what do they cause?

A

aka Charcot-Bouchard aneurysms

  • occur in intracerebral capillaries
  • cause intracerebral haemmorhage - stroke
48
Q

how can retinal microaneurysms arise? what is their pathogenesis

A

from diabetes causing diabetic retinopathy

49
Q

what are mycotic aneurysms? how does it occur in the tunica media?

A

weakening of arterial wall due to bacterial/fungal infection

  • enter tunica media from the vasa vasorum
50
Q

what aneurysm come under Charcot-Bouchard aneurysms

A

micro and syphilitic

51
Q

what is the most common infection leading to mycotic aneurysms?

A

subacute bacterial endocarditis

52
Q

what is a false aneurysm?

A

a blood filled space around a vessel usually after traumatic rupture or perforating injury

53
Q

describe a dissecting aneurysm, with symptoms and common location.

A

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
Q

where is the most common location for an aneurysm secondary to aorta

A

abdominal aortic region

55
Q

what is the main risk factor for rupture

A

the bigger the size, the more chance of rupture

56
Q

compare the pathology and complications of different aneurysms

A

cause haemorrhage or ischamia from thromboembolism

57
Q

what can be the result of ‘arterial occlusion’? (3)

A

embolism, ischaemia, infarction

58
Q

what is ‘chronic peripheral arterial occlusive disease’? state the pathological consequences

A

narrowed arteries leading to reduced blood flow to limbs
can lead to critical limb ischaemia

59
Q

what are the 3 different types of blood vessel tumours?

A

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
Q

what are the 6 P’s on acute ischaemia

A

Pale
Painful
Paralysed
Paraesthetic - tingly
Perishing Cold
Pulseless

YR 3 - Illness and Wellbeing (31 decks)

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