Blood Vessels Flashcards
Hypertension:
Essential:
-What is involved
- Sodium.
- Renin-angiotensin-aldosterone system.
- Vessel wall tone / structure.
Atherosclerosis:
-Risk Factors
Non-modifiable:
* Genetics.
* FHx.^
* Increasing age.
* Male.
Modifiable:
* Hyperlipidaemia (mainly LDL).
* HTN.
* Smoking.
* Diabletes.
* Inflammation.
* Hyperhomocystienaemia.
* Lipoprotein a (altered LDL).
* Factors affecting haemostasis (e.g. plasminogen activator inhibitor 1).
^Most important risk factor
Which layer is atherosclerotic plaque found?
Intima
Structure of an Atherosclerotic Plaque
- Fibrous cap (smooth muscle cells, macrophages, foam cells,^ lymphocytes, collagen, elastin, proteoglycans, neovascularisation).
- Necrotic centre (cell debris, cholesterol crystals, foam cells, calcium).
^Foam cells = macrophages which have phagocytosed lipid.
Difference between Vulnerable plaques and Stable
Vulnerable:
- Thin fibrous cap.
- Large lipid / necrotic core.
- Inflammation ++.
Stable:
- Thickened, densely collagenous fibrous cap.
- Thinner lipid / necrotic core.
- Minimal inflammation.
What are the consequences of atherosclerosis in the coronary arteries?
Ischaemic heart disease:
* Angina.
* MI.
* Sudden cardiac death.
* Chronic HF.
What is an aneurysm
- Localised abnormal dilation of a blood vessel or the heart.
- Can be congenital or acquired.
- Can be saccular or fusiform.
What is a dissection
- Blood filled channel within the wall of the vessel.
- Blood separates blood vessel layers (dissects BV wall).
- Can occur from luminal tear or by ruputr of vessls of the vasa vasorum within the media.
- Usually occurs in medial or medial-adventitial planes.
Pathogenesis of aneurysm and dissection
Defects in synthesis or breakdown of connective tissue.
Due to either:
- Faulty intrinsic quality of the vascular connective tissues (e.g defective type III collagen as seen in Ehlers-Danlos).
- Excessive TGF-beta signalling –> decrease in extracellular matrix integrity (particularly in ascending aorta) (e.g. Marfan syndrome, Loeys-Dietz syndrome).
- Increased collagen degradation due to inflammation-driven rise in Matrix MetalloProteinases (MMPs) and/or decrease in Tissue Inhibitors of Metalloproteinases (TIMPs) –> elastic fibre loss. (e.g. atherosclerosis, aortitis).
- Ischaemia –> loss of smooth muscle cells or inappropropriate synthesis of non-collagenous / non-elastic ECM (e.g. atherosclerosis, HTN).
Vasculitis
-Definition
- Inflammation of the blood vessel walls.
- Site-specific signs and symptoms.
Broad causes of vasculitis and pathogenesis
- Infectious - direct invasion of vascular walls by pathogen.
- Non-infectious / Immune-mediated - inflammation.
Vasculitis:
Immune-mediated (non-infectious) vasculitis:
What are the main mechanisms underlying this vasculitis
- Immune complex deposition (e.g. SLE, drug-hypersensitivity).
- Antineutrophil cytoplasmic antibodies (ANCAs).
- Anti-endothelial cell antibodies.
- Autroreactive T cells.
Giant cell / Temporal Arteritis:
-What is it, who it affects, what is the mechanism, and what is the treatment
What it is:
- Large vessel vaculitis / granulomatous inflammation of arteries.
- Mainly aorta, temporal and ophthalmic arteries.
Who:
- Adults > 50 yo.
Mechanism:
- T cell mediated immune response (TNF involved).
Treatment:
- Steroids.
- Anti-TNF.
Takayasu Arteritis:
-What is it, who it affects, what is the mechanism, what can it cause, and what is the treatment
What it is:
- “Pulseless” disease - cannot feel distal pulses.
- Large vessel vasculitis / Granulomatous inflammation of larger arteries.
- Affects aortic arch and major branches (Pulmonary artery ~50% cases).
Who:
- Young (< 50 yo).
Mechanism:
- T cell mediated.
Can cause:
- Blindness.
Treatment:
- Immunosuppressants.
Polarteritis Nodosa (PAN):
-What is it, and what is the mechanism
What it is:
- Medium vessel vasculitis.
- Necrotising vasculitis with mixed inflammatory infiltrate.
- Involves kidney, heart, liver, GI.
Mechanism:
- Usually following Hep B infection (1/3 cases) –> HBsAg immune complexes.
Atherosclerosis Stages
- Normal artery.
- Endothelial dysfunction.
- Fatty Streak Formation.
- Stable (Fibrous) plaque formation.
- Unstable plaque formation.
What is Arteriosclerosis, what are the four general patterns, and which vessels does each pattern affect.
What it is:
- “Hardening of the arteries”.
- Generic term for arterial wall thickening AND loss of elastacity.
4 patterns:
- Arteriolosclerosis.
- Monckeberg medial sclerosis.
- Fibromuscular intimal hyperplasia.
- Atherosclerosis (most common).
Vessels affected:
- Small arteries and arterioles.
- Muscular arteries.
- Muscular arteries larger than arterioles.
- Coronary, cerebral and peripheral arteries.
What are the three layers found in all blood vessels except capillaries
- Intima (innermost endothelial layer).
- Media (middle smooth muscular layer, thickness varies on vessel type).
- Adventitia (outer supportive layer).
Arteriosclerosis:
Arteriolosclerosis:
-What is it caused by, what are the two anatomical variants, what are their histology, and what does it cause
Caused by:
- HTN.
- Diabetes.
Anatomical variants:
- Hyaline.
- Hyperplastic (seen in severe or malignant HTN).
Histology:
- Thickened wall that is pink, homogenous, and glassy in appearance (from protein deposits). Luminal narrowing.
- “Onion-skinning” - Concentric, laminated wall thickening (from smooth muscle cells) with no-narrow lumen. May have fibrinoid deposits and necrosis.
Causes:
- Ischaemia.
Arteriosclerosis:
Monckeberg medial sclerosis:
-What is it, who does it affect, and what does it cause
What it is:
- Calcifications of the media layer of muscular arteries.
- Typically commences along the internal elastic lamina.
Affects:
- People > 50 yo.
Causes:
- Non-obstructive calcification.
- Usually not clinically significant.
Arteriosclerosis:
Fibromuscular intimal hyperplasia:
-What is it , what causes it, and what does it cause
What it is:
- Hyperplasia of intima (increased number of cells).
- Secondary to “healing response”.
Caused by:
- Inflammation from healed arteritis or transplant-associated arteriopathy.
- Mechanical injury (associated with stents or balloon angioplasty).
Causes:
- Stenosis.
What is hypertension
- Diastolic pressure > 80 mmHg.
- Systolic pressure > 120 mmHg.
Hypertension:
-Causes
Essential HTN (i.e. primary / ideopathic; ~90% of all HTN).
Secondary HTN (~10% of all HTN):
- Renal.
- Endocrine.
- Cardiovascular.
- Neurologic.
Hypertension:
-Clinical consequences
- Arteriosclerosis.
- Atherosclerosis.
- IHD.
- Stroke.
- LVH –> failure.
- Vascular dementia.
- Aortic dissection.
