PATHOLOGY- Blood vessel disorders Flashcards
What human disease has the highest rate of mortality/morbidity
Vascular disease
What are the 3 layers of blood vessels from innermost to outermost
Tunica intima
Tunica media
Tunica externa/adventitia
What is the tunica intima and media divided by
Internal elastic lamina
What divides the tunica media and externa
External elastic lamina
Why does the tunica media in the aorta have a high proportion of elastic fibres (2)
Aorta exposed to high pressures, allows it to expand and contract
Allows it to recoil helping with propulsion of the blood
In muscular ateries why is the media more muscular
Allows them to contract and dilate, controlling the flow of blood, therefore controls blood pressure
How does the structure of veins differ to that of arteries
Thinner media, allowing for pulling of blood
What is the role of capillaries
Nutrient and gas exchange
Describe the structure of capillaries
Thin single layer of endothelial cells with supporting cells called pericytes
What is the role of the left side of the heart
Oxygenated blood travels from left side of the heart around the body to the tissues
What is the role of the right side of the heart
Deoxygenated blood passes through the venous system in to the RHS heart which in turn passes in to the lungs for oxygenation
Why do muscular arteries have more smooth muscle in their walls
Allows for vasoconstriction and vasodilation
What does age related vascular change mean
Arterial vessels become worse with age
List 4 features of age related vascular changes
- fibrous thickening of intima
- fibrosis/scarring of muscular/elastic media
- fragmentation of elastic laminae
- calcification (deposition of calcium)
What are the 4 features of age related vascular changes as a collective known as
Arteriosclerosis
What is arteriosclerosis frequently associated with
High blood pressure
Define atherosclerosis
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
What does atherosclerosis result in
Results in elevated / occlusive intimal-based lesions (plaques) - lipids, inflammatory cells, proliferating smooth muscle cells and extra-cellular matrix.
Why is atherosclerosis significant
Underlying pathogenesis for coronary / IHD, cerebral and peripheral vascular disease - up to 50% all deaths in West
What are the risk factors for atherosclerosis (4 nonmodifiable and 5 modifiable)
Nonmodifiable (Constitutional)
Genetic abnormalities
Family history
Increasing age
Male gender
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
Inflammation
Where does atherosclerosis occur generally
Give examples
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
Why is the posterior aorta prone to atherosclerosis
High amounts of turbulence
Explain how the process of atheroscleris occurs (pathogenesis)
- insult causes endothelial damage. This increases permeability and leukocyte adhesion
- Permeability allows lipids (LDL) to seep in to the intimal wall, gradually accumulating. This attracts monocytes which results in platelelt adhesion
- 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
- Macrophages/ smooth muscle take up lipids becoming foam cells (which are lipid rich macropahges). These accumulate in the wall forming a fatty streak
- 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
What do atherosclerotic plaques usually have on them
fibrous cap
why may an atheromatous plaque disturb blood flow
because it is an initmal lesion protuding in to the lumen
what are fatty streaks
what they they made up of
- Early manifestation of process
- Mainly accumulations of lipid laden foamy macrophages
- Not all progress to advanced AS plaques
what are athersclerotic plaque
fibrofatty plaque
what happens to a fibrofatty plaque that is stable
- not liable to rupture
- will therefore get progressively larger
- blood flow impaired, tissue affected through hypoxia
- leads to critical stenosis (which can cause angina)
what can happen to a fibrofatty plaque that isnt stable
- weakening of the vessel wall
- aneurysm and rupture
what can happen to a fibrofatty plaque that is vulnerable (thin fibrous cap)
- cap can rupture
- exposes content of the plaque to blood contents
- initiates hemostasis and coagulation cascade
- causes thrombosis and sudden occlusion
what can follow with athersclerosis clinically
- Gradual mechanical obstruction to flow -> e.g. angina
- Sudden plaque rupture -> Thrombosis -> sudden occlusion e.g. sudden death
- Weakening of vessel wall -> Aneurysm
what are some major clinical consequences of athersclerosis occuring in coronary arteries
IHD -> Angina, myocardial infarction, arrhythmias, sudden death
what are some major clinical consequences of athersclerosis occuring in carotid/cerebral arteries
Cerebrovascular disease (stroke)
what are some major clinical consequences of athersclerosis occuring in the aorta
aortic aneurysm and possible rupture
what are some major clinical consequences of athersclerosis occuring in the mesentric arteries
bowel ischaemia
what are some major clinical consequences of athersclerosis occuring in the lower extremities
peripheral vascular disease
what types of plawues are more vulnerable to rupture
those with thin caps
define hypertension
persistently raised arterial blood pressure
what is hupertension a major risk factor for
stroke, myocardial infarction, heart failure, chronic kidney disease, cognitive decline and premature death
what does hypertension promote
athersclerosis
what does hypertension do to vessels
causes degenerative changes
what is pressure needed for
to deliver oxygenated blood to tissues
what is adequate pressured needed for
to pass resistance in the systemic circulation and capillary beds to reach tissues
what is systole
what does it do to arterial walls
what does it do in terms of pressure
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)
what is diastole
what does it do in terms of pressure
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)
which one is the low and high figure from systolic and diastolic blood pressure
diastolic- low
systolic- high
what can low blood pressure lead to
hypotension
tissue hypoperfusion
hypoxic injury
cell injury / death
what can high blood pressure lead to
hypertension
vessel/end-organ damage/ atherogenesis
list 5 exmaples of hypertensive vascular injury and what they can lead to
- 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
In terms of systolic / diastolic BP what is
hypertension
systolic bp equal to or above 140mmHG
diastolic bp equal to or above 90mmHG
anything below 140/90 is considered normal
what is optimal bp
<120/<80
what 4 things can be used to classify hypertension
severity
aetiology
pathology
anatomy
how can hypertension be classified through aetiology
primary/essential (90%)
secondary
how can hypertension be classified through patholigical
Benign
. “Malignant” / Accelerated
how can hypertension be classified through anatomical
- Systemic
- Pulmonary
- Portal
what does primary hypertension mean
how common is it
Meaning?
* IDIOPATHIC i.e. UNKNOWN CAUSE
* AKA ESSENTIAL HYPERTENSION
Common?
* 90-95% Cases
what is the meaning of seocndary hypertension
how common is it
Process ocurring in
* RENAL
* ENDOCRINE
* CARDIOVASCULAR
* NEUROLOGICAL
5-10% cases
what are the factors involed in primary hypertension
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.
How does renal artery stenosis cause secondary hypertension
- Decreased perfusion of kidneys (JGA cells)
- Renin produced -> activation of renin angiotensin system
- Retention of sodium / water + vasoconstriction
- BP increases
what else can cause renin to increase causing hypertension
Renin secreting tumors
3 features of benign hypertension
- Asymptomatic
- Often incidental finding
- Organ damage gradual
what is malignant (accelerated) hypertension
what % of patients does it affect
what is the BP of someone with it
what can it lead to
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
what is portal hypertension
what condition does it commonly occur in
increased pressure in portal venous system
liver cirrhosis
what is pulmonary hypertension
increased pressure in pulmonary circulation
list the pathological effects of hypertension
ACCELERATES ATHEROSCLEROTIC DAMAGE
HYALINE ARTERIOLOSCLEROSIS
HYPERPLASTIC ARTERILOSCLEROSIS
what is hyaline arteriolosclerosis
who is it common in
Pink amorhous material forms around vessels with narrow lumen
Common in elderly, esp. kidneys - nephrosclerosis
What is hyperplastic arteriolosclerosis
malignant hypertension causing extracellular matrix to form around vessel wall
list lifestyle modifictaions that can be made in treating hypertension
if bp is not too high
if bp is high
- 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
define vasculitis
inflmmation of the vessel walls
what is chapel hill nomenclature in term sof vasculitis
specific types tend to affect specific vessels
what does vasculitis look like microscopically
lots of blue dots in a blood vessel indicate vasculitis
what is the most common form of vasculitis and why is this type significant
giant cells arteritis (GCA)
Giant-cell arteritis is a medical emergency requiring prompt recognition and treatment - early recognition is VITAL!
who does GCA predominantly affect
elderly individuals in west
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
Chronic granulomatous inflammation
Large to medium-sized arteries
Esp. in the head (e.g. temporal arteries - AKA temporal arteritis)
Vertebral and ophthalmic arteries
If there is GCA in ophthalmic arteries, what can it lead to
permenant blindness
what is GCA in the aorta called
giant cell aortitis
3 morpholigcal features of GCA that can be seen microscopically
- Intimal thickening- reduces the lumenal diameter
- Med. granulomatous inflammation (granulomas forming in the media) - elastic lamina fragmentation
- Multinucleated giant cells- 75% of adequately biopsied
who is GCA rare in
< 50 years
what is the main symtom of GCA
Facial pain or headache
- Superficial temporal artery (painful to palpation)
- Jaw claudication (pain in temporal region when chewing)
How do you diagnose GCA
Biopsy and histological diagnosis
What length of artery do you need when doing a bipsy for GCA and why
2-3cm lenght of artery
GCA is a segmental disease, therefore some areas of artery may be unaffected
What is the treatment of GCA usually
in refractory cases
Cortiocosteroids
anti-TNF therapy in refractory cases
define aneurysm
localised, permanent, abnormal dilations of a blood vessel
what can aneurysms be classified by
Shape
* Saccular (small sack sticking out)
* Fusiform (bulging on both sides)
* Dissecting
Ateiology
* Atherosclerotic
* Dissecting
* Berry
* Microaneurysms
* Syphilitic
* Mycotic
* False
what is the most common type of anerysm and who do they occur in
athersclerotic aneurysm
elderly
what is commonly secondary to athersclerosis
abdonaminal aortic aneurysm
what is the main risk factor for athersclerotic aneurysms rupturing
the size (bigger=more risk)
if an aneurysm is above 6cm, what is the % of it rupturing
25%
how can athersclerotic anuerysm be detcted
ultrasounds
how can athersclerotic anuerysms be repaired
surgically
endovascularly
what are the 2 main complications with atherscleortic anuerysms
- rupture casuing retroperioneal haemorrhage
- embolisation causing limb ischaemia
what is a dissecting aneurysm
tear in intimal wall causing blood to track down between intimal and medial layers
what is the classical symptom of dissecting aneurysm
tearing pain in chest radiating to upper left shoulder
where do dissecting aneurysms usally occur q
thoracic aorta secondary to systemic hypertension
what 2 things does a dissecting aneurysm cause
progressive vascular occlusion and haemopericardium (accumulation of blood in the pericardial cavity surrounding the heart)
what can a dissecting anerysm without tx lead to
death (high mortality)
what are berry aneurysms
where do they form
- Small, saccular lesions that develop in the Circle of Willis
- Develop at sites of medial weakness at arterial bifurcations (where arteries join other arteries)
who are berry aneurysms commonly found in
young hypertensive patients
berry aneurysms that rupture cause what
subarachnoid haemorrhage (SAH)
where do charcot-bouchard aneurysms occur
what do they cause
intracerebral capillaries in hypertensive disease
intracerebral haemorrhage (i.e. stroke)
diabetes can cause what type of micro aneurysms to occur and what does it cause
retinal microaneurysms
diabetic retinopathy
tertiary syphilis causes what
ascending (thoracic) aorta aneurysms
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
- 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
what is false anerysm
Blood filled space around a vessel, usually following traumatic rupture or perforating injury
describe the structure of a false aneurysm
The adventitial fibrous tissue contains the haematoma, intitma and media ruptured
when are false aneurysms seen in
following femoral artery puncture during angiography/angioplasty
what are the 3 main causes of arterial occlusion
embolus
thrombosis
trauma
what are the 6 P’s associated with acute ischaemia
- Pale
- Pulseless
- Painful
- Paralysed
- Paraesthetic (tingly)
- Perishing Cold
2 symptoms of critical limb ischaemia (increasing in severity)
pain when resting
tissue loss
what is haemangioma
where is it common
beinign tumour of blood vessels
head, neck and thorax
give an example of an intermediate grade/borderline tumour of the blood vessels
kaposi sarcoma
kaposi sarcoma is a result from what
HHV8 (Human herpesvirus 8)
what is angiosarcoma
what is it associated with
maligannt tumour of the blood vessels
lymphoedema, radiation exposure
what type of patients would you see kaposi sarcomas in
immunosuppressed
AIDS
HIV
