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Y3 IWB > PATHOLOGY- Blood vessel disorders > Flashcards

PATHOLOGY- Blood vessel disorders Flashcards

1
Q

What human disease has the highest rate of mortality/morbidity

A

Vascular disease

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2
Q

What are the 3 layers of blood vessels from innermost to outermost

A

Tunica intima
Tunica media
Tunica externa/adventitia

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3
Q

What is the tunica intima and media divided by

A

Internal elastic lamina

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4
Q

What divides the tunica media and externa

A

External elastic lamina

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5
Q

Why does the tunica media in the aorta have a high proportion of elastic fibres (2)

A

Aorta exposed to high pressures, allows it to expand and contract
Allows it to recoil helping with propulsion of the blood

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6
Q

In muscular ateries why is the media more muscular

A

Allows them to contract and dilate, controlling the flow of blood, therefore controls blood pressure

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7
Q

How does the structure of veins differ to that of arteries

A

Thinner media, allowing for pulling of blood

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8
Q

What is the role of capillaries

A

Nutrient and gas exchange

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9
Q

Describe the structure of capillaries

A

Thin single layer of endothelial cells with supporting cells called pericytes

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10
Q

What is the role of the left side of the heart

A

Oxygenated blood travels from left side of the heart around the body to the tissues

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11
Q

What is the role of the right side of the heart

A

Deoxygenated blood passes through the venous system in to the RHS heart which in turn passes in to the lungs for oxygenation

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12
Q

Why do muscular arteries have more smooth muscle in their walls

A

Allows for vasoconstriction and vasodilation

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13
Q

What does age related vascular change mean

A

Arterial vessels become worse with age

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14
Q

List 4 features of age related vascular changes

A
  • fibrous thickening of intima
  • fibrosis/scarring of muscular/elastic media
  • fragmentation of elastic laminae
  • calcification (deposition of calcium)
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15
Q

What are the 4 features of age related vascular changes as a collective known as

A

Arteriosclerosis

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16
Q

What is arteriosclerosis frequently associated with

A

High blood pressure

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17
Q

Define atherosclerosis

A

Slow, progressive (chronic) degenerative intimal disease of large to medium-sized muscular and elastic arteries

chronic inflammatory/healing response of arterial wall to endotheilal in

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18
Q

What does atherosclerosis result in

A

Results in elevated / occlusive intimal-based lesions (plaques) - lipids, inflammatory cells, proliferating smooth muscle cells and extra-cellular matrix.

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19
Q

Why is atherosclerosis significant

A

Underlying pathogenesis for coronary / IHD, cerebral and peripheral vascular disease - up to 50% all deaths in West

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20
Q

What are the risk factors for atherosclerosis (4 nonmodifiable and 5 modifiable)

A

Nonmodifiable (Constitutional)
Genetic abnormalities
Family history
Increasing age
Male gender

Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
Inflammation

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21
Q

Where does atherosclerosis occur generally

Give examples

A

Specific points in elastic and muscular vessels that relate to points of exaggerated hemodynamic disturbance

Branches of vessels
Ostia (where vessels join other vessels)
Posterior aorta

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22
Q

Why is the posterior aorta prone to atherosclerosis

A

High amounts of turbulence

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23
Q

Explain how the process of atheroscleris occurs (pathogenesis)

A
  1. insult causes endothelial damage. This increases permeability and leukocyte adhesion
  2. Permeability allows lipids (LDL) to seep in to the intimal wall, gradually accumulating. This attracts monocytes which results in platelelt adhesion
  3. Monocytes turn in to marophages. The macrophages migrate in to the area where all the lipid has accumulated and become activated. Platelet/macrophages recruit smooth muscle cells in to the area
  4. Macrophages/ smooth muscle take up lipids becoming foam cells (which are lipid rich macropahges). These accumulate in the wall forming a fatty streak
  5. This process progresses with a further increase in smooth muscle/ extracellular matrix forming an atheromatous plaque/athersclerotic plaque

summarised
* Endothelial damage
* Monocvte / platelet adhesion
* Migrate into intima
* Growth factors -> SMCs
* Take up lipid -> foam cells
* SMC / ECM proliferation
* Progressive enlargement

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24
Q

What do atherosclerotic plaques usually have on them

A

fibrous cap

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25
Q

why may an atheromatous plaque disturb blood flow

A

because it is an initmal lesion protuding in to the lumen

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26
Q

what are fatty streaks
what they they made up of

A
  • Early manifestation of process
  • Mainly accumulations of lipid laden foamy macrophages
  • Not all progress to advanced AS plaques
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27
Q

what are athersclerotic plaque

A

fibrofatty plaque

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28
Q

what happens to a fibrofatty plaque that is stable

A
  • not liable to rupture
  • will therefore get progressively larger
  • blood flow impaired, tissue affected through hypoxia
  • leads to critical stenosis (which can cause angina)
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29
Q

what can happen to a fibrofatty plaque that isnt stable

A
  • weakening of the vessel wall
  • aneurysm and rupture
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30
Q

what can happen to a fibrofatty plaque that is vulnerable (thin fibrous cap)

A
  • cap can rupture
  • exposes content of the plaque to blood contents
  • initiates hemostasis and coagulation cascade
  • causes thrombosis and sudden occlusion
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31
Q

what can follow with athersclerosis clinically

A
  • Gradual mechanical obstruction to flow -> e.g. angina
  • Sudden plaque rupture -> Thrombosis -> sudden occlusion e.g. sudden death
  • Weakening of vessel wall -> Aneurysm
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32
Q

what are some major clinical consequences of athersclerosis occuring in coronary arteries

A

IHD -> Angina, myocardial infarction, arrhythmias, sudden death

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33
Q

what are some major clinical consequences of athersclerosis occuring in carotid/cerebral arteries

A

Cerebrovascular disease (stroke)

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34
Q

what are some major clinical consequences of athersclerosis occuring in the aorta

A

aortic aneurysm and possible rupture

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35
Q

what are some major clinical consequences of athersclerosis occuring in the mesentric arteries

A

bowel ischaemia

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36
Q

what are some major clinical consequences of athersclerosis occuring in the lower extremities

A

peripheral vascular disease

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37
Q

what types of plawues are more vulnerable to rupture

A

those with thin caps

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38
Q

define hypertension

A

persistently raised arterial blood pressure

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39
Q

what is hupertension a major risk factor for

A

stroke, myocardial infarction, heart failure, chronic kidney disease, cognitive decline and premature death

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40
Q

what does hypertension promote

A

athersclerosis

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41
Q

what does hypertension do to vessels

A

causes degenerative changes

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42
Q

what is pressure needed for

A

to deliver oxygenated blood to tissues

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43
Q

what is adequate pressured needed for

A

to pass resistance in the systemic circulation and capillary beds to reach tissues

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44
Q

what is systole
what does it do to arterial walls
what does it do in terms of pressure

A

cardiac contraction- when the ventricles contarct, ejecting blood out of the ventricles in to the aorta/pulmonary circulation
causes dilation/ stretch of arterial walls
pressure rises (systolic blood pressure)

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45
Q

what is diastole
what does it do in terms of pressure

A

recoil of the aterial wall -> expulsion of blood from arterila system in to the capillary beds and venous circulation

pressure falls, atrial fillig (diastolic blood pressure)

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46
Q

which one is the low and high figure from systolic and diastolic blood pressure

A

diastolic- low
systolic- high

47
Q

what can low blood pressure lead to

A

hypotension
tissue hypoperfusion
hypoxic injury
cell injury / death

48
Q

what can high blood pressure lead to

A

hypertension
vessel/end-organ damage/ atherogenesis

49
Q

list 5 exmaples of hypertensive vascular injury and what they can lead to

A
  • Endothelial injury / damage -> promotion of thrombosis
  • Atherosclerosis -> Coronary artery / peripheral vascular disease
  • Cardiac hypertrophy -> LV hypertrophy -> hypertensive HD -> sudden death
  • Cerebrovascular disease -> dementia / stroke
  • Aortic aneurysm -> rupture -> death
50
Q

In terms of systolic / diastolic BP what is
hypertension

A

systolic bp equal to or above 140mmHG
diastolic bp equal to or above 90mmHG

anything below 140/90 is considered normal

51
Q

what is optimal bp

A

<120/<80

52
Q

what 4 things can be used to classify hypertension

A

severity
aetiology
pathology
anatomy

53
Q

how can hypertension be classified through aetiology

A

primary/essential (90%)
secondary

54
Q

how can hypertension be classified through patholigical

A

Benign
. “Malignant” / Accelerated

55
Q

how can hypertension be classified through anatomical

A
  • Systemic
  • Pulmonary
  • Portal
56
Q

what does primary hypertension mean
how common is it

A

Meaning?
* IDIOPATHIC i.e. UNKNOWN CAUSE
* AKA ESSENTIAL HYPERTENSION
Common?
* 90-95% Cases

57
Q

what is the meaning of seocndary hypertension
how common is it

A

Process ocurring in
* RENAL
* ENDOCRINE
* CARDIOVASCULAR
* NEUROLOGICAL

5-10% cases

58
Q

what are the factors involed in primary hypertension

A

GENETIC
* Twin studies
* Single gene disorders can cause hypertension
* Genome wide studies - ~60 areas of genome may influence BP

DECREASE IN RENAL SODIUM EXCRETION

VASCOCONSTRICTIVE INFLUENCES e.g. STRUCTURAL CHANGES

ENVIRONMENTAL FACTORS
* Modify genetic effect
* Stress, smoking, obesity, physical inactivity etc.

59
Q

How does renal artery stenosis cause secondary hypertension

A
  • Decreased perfusion of kidneys (JGA cells)
  • Renin produced -> activation of renin angiotensin system
  • Retention of sodium / water + vasoconstriction
  • BP increases
60
Q

what else can cause renin to increase causing hypertension

A

Renin secreting tumors

61
Q

3 features of benign hypertension

A
  • Asymptomatic
  • Often incidental finding
  • Organ damage gradual
62
Q

what is malignant (accelerated) hypertension
what % of patients does it affect
what is the BP of someone with it
what can it lead to

A

Rapid increase in hypertension
5%
Severe increase in BP to 180/120 mmH or higher
Often > 220 mmHg / diastolic > 120 mmHg
Renal failure, retinal haemorrhages / exudates / +/- papilloedema

63
Q

what is portal hypertension

what condition does it commonly occur in

A

increased pressure in portal venous system

liver cirrhosis

64
Q

what is pulmonary hypertension

A

increased pressure in pulmonary circulation

65
Q

list the pathological effects of hypertension

A

ACCELERATES ATHEROSCLEROTIC DAMAGE
HYALINE ARTERIOLOSCLEROSIS
HYPERPLASTIC ARTERILOSCLEROSIS

66
Q

what is hyaline arteriolosclerosis
who is it common in

A

Pink amorhous material forms around vessels with narrow lumen
Common in elderly, esp. kidneys - nephrosclerosis

67
Q

What is hyperplastic arteriolosclerosis

A

malignant hypertension causing extracellular matrix to form around vessel wall

68
Q

list lifestyle modifictaions that can be made in treating hypertension
if bp is not too high
if bp is high

A
  • Maintain normal weight for adults (body mass index 20-25 kg/m2)
  • Reduce salt intake to <100 mmol/day (<6g NaCI or <2.4 g Na*/day)
  • Limit alcohol to <3 units/day for men and <2 units/day for women
  • Regular exercise for ≥30 minutes per day at least three days / week
  • Five portions/day of fresh fruit and vegetables
  • Reduce the intake of total and saturated fat

all of above and drug tretament

69
Q

define vasculitis

A

inflmmation of the vessel walls

70
Q

what is chapel hill nomenclature in term sof vasculitis

A

specific types tend to affect specific vessels

71
Q

what does vasculitis look like microscopically

A

lots of blue dots in a blood vessel indicate vasculitis

72
Q

what is the most common form of vasculitis and why is this type significant

A

giant cells arteritis (GCA)
Giant-cell arteritis is a medical emergency requiring prompt recognition and treatment - early recognition is VITAL!

73
Q

who does GCA predominantly affect

A

elderly individuals in west

74
Q

what is giant cell arteritis
what size of arteries does it affect
where does it affect these arteries the most
which other arteries can be affected

A

Chronic granulomatous inflammation
Large to medium-sized arteries
Esp. in the head (e.g. temporal arteries - AKA temporal arteritis)
Vertebral and ophthalmic arteries

75
Q

If there is GCA in ophthalmic arteries, what can it lead to

A

permenant blindness

76
Q

what is GCA in the aorta called

A

giant cell aortitis

77
Q

3 morpholigcal features of GCA that can be seen microscopically

A
  • Intimal thickening- reduces the lumenal diameter
  • Med. granulomatous inflammation (granulomas forming in the media) - elastic lamina fragmentation
  • Multinucleated giant cells- 75% of adequately biopsied
78
Q

who is GCA rare in

A

< 50 years

79
Q

what is the main symtom of GCA

A

Facial pain or headache
- Superficial temporal artery (painful to palpation)
- Jaw claudication (pain in temporal region when chewing)

80
Q

How do you diagnose GCA

A

Biopsy and histological diagnosis

81
Q

What length of artery do you need when doing a bipsy for GCA and why

A

2-3cm lenght of artery
GCA is a segmental disease, therefore some areas of artery may be unaffected

82
Q

What is the treatment of GCA usually
in refractory cases

A

Cortiocosteroids
anti-TNF therapy in refractory cases

83
Q

define aneurysm

A

localised, permanent, abnormal dilations of a blood vessel

84
Q

what can aneurysms be classified by

A

Shape
* Saccular (small sack sticking out)
* Fusiform (bulging on both sides)
* Dissecting

Ateiology
* Atherosclerotic
* Dissecting
* Berry
* Microaneurysms
* Syphilitic
* Mycotic
* False

85
Q

what is the most common type of anerysm and who do they occur in

A

athersclerotic aneurysm
elderly

86
Q

what is commonly secondary to athersclerosis

A

abdonaminal aortic aneurysm

87
Q

what is the main risk factor for athersclerotic aneurysms rupturing

A

the size (bigger=more risk)

88
Q

if an aneurysm is above 6cm, what is the % of it rupturing

A

25%

89
Q

how can athersclerotic anuerysm be detcted

A

ultrasounds

90
Q

how can athersclerotic anuerysms be repaired

A

surgically
endovascularly

91
Q

what are the 2 main complications with atherscleortic anuerysms

A
  • rupture casuing retroperioneal haemorrhage
  • embolisation causing limb ischaemia
92
Q

what is a dissecting aneurysm

A

tear in intimal wall causing blood to track down between intimal and medial layers

93
Q

what is the classical symptom of dissecting aneurysm

A

tearing pain in chest radiating to upper left shoulder

94
Q

where do dissecting aneurysms usally occur q

A

thoracic aorta secondary to systemic hypertension

95
Q

what 2 things does a dissecting aneurysm cause

A

progressive vascular occlusion and haemopericardium (accumulation of blood in the pericardial cavity surrounding the heart)

96
Q

what can a dissecting anerysm without tx lead to

A

death (high mortality)

97
Q

what are berry aneurysms
where do they form

A
  • Small, saccular lesions that develop in the Circle of Willis
  • Develop at sites of medial weakness at arterial bifurcations (where arteries join other arteries)
98
Q

who are berry aneurysms commonly found in

A

young hypertensive patients

99
Q

berry aneurysms that rupture cause what

A

subarachnoid haemorrhage (SAH)

100
Q

where do charcot-bouchard aneurysms occur
what do they cause

A

intracerebral capillaries in hypertensive disease
intracerebral haemorrhage (i.e. stroke)

101
Q

diabetes can cause what type of micro aneurysms to occur and what does it cause

A

retinal microaneurysms
diabetic retinopathy

102
Q

tertiary syphilis causes what

A

ascending (thoracic) aorta aneurysms

103
Q

what are mycotic aneurysms
how common are they
how do they happen
what is the most common underlying infection
where do they occur
what can increase their risk of rupturing

A
  • Weakening of arterial wall secondary to bacterial / fungal infection
  • rare
  • Organisms enter media from the vasa vasorum
  • Subacute bacterial endocarditis is the most common underlying infection
  • Often in the cerebral arteries
  • Infection of AAAs - risk rupture
104
Q

what is false anerysm

A

Blood filled space around a vessel, usually following traumatic rupture or perforating injury

105
Q

describe the structure of a false aneurysm

A

The adventitial fibrous tissue contains the haematoma, intitma and media ruptured

106
Q

when are false aneurysms seen in

A

following femoral artery puncture during angiography/angioplasty

107
Q

what are the 3 main causes of arterial occlusion

A

embolus
thrombosis
trauma

108
Q

what are the 6 P’s associated with acute ischaemia

A
  • Pale
  • Pulseless
  • Painful
  • Paralysed
  • Paraesthetic (tingly)
  • Perishing Cold
109
Q

2 symptoms of critical limb ischaemia (increasing in severity)

A

pain when resting
tissue loss

110
Q

what is haemangioma
where is it common

A

beinign tumour of blood vessels
head, neck and thorax

111
Q

give an example of an intermediate grade/borderline tumour of the blood vessels

A

kaposi sarcoma

112
Q

kaposi sarcoma is a result from what

A

HHV8 (Human herpesvirus 8)

113
Q

what type of patients would you see kaposi sarcomas in

A

immunosuppressed
AIDS
HIV

113
Q

what is angiosarcoma
what is it associated with

A

maligannt tumour of the blood vessels

lymphoedema, radiation exposure

Y3 IWB (31 decks)

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