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Basic Pathology > Blood Vessels > Flashcards

Blood Vessels Flashcards

1
Q

Hypertension:
Essential:
-What is involved

A
  • Sodium.
  • Renin-angiotensin-aldosterone system.
  • Vessel wall tone / structure.
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2
Q

Atherosclerosis:
-Risk Factors

A

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

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3
Q

Which layer is atherosclerotic plaque found?

A

Intima

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4
Q

Structure of an Atherosclerotic Plaque

A
  • 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.

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5
Q

Difference between Vulnerable plaques and Stable

A

Vulnerable:

  • Thin fibrous cap.
  • Large lipid / necrotic core.
  • Inflammation ++.

Stable:

  • Thickened, densely collagenous fibrous cap.
  • Thinner lipid / necrotic core.
  • Minimal inflammation.
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6
Q

What are the consequences of atherosclerosis in the coronary arteries?

A

Ischaemic heart disease:
* Angina.
* MI.
* Sudden cardiac death.
* Chronic HF.

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7
Q

What is an aneurysm

A
  • Localised abnormal dilation of a blood vessel or the heart.
  • Can be congenital or acquired.
  • Can be saccular or fusiform.
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8
Q

What is a dissection

A
  • 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.
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9
Q

Pathogenesis of aneurysm and dissection

A

Defects in synthesis or breakdown of connective tissue.

Due to either:

  1. Faulty intrinsic quality of the vascular connective tissues (e.g defective type III collagen as seen in Ehlers-Danlos).
  2. Excessive TGF-beta signalling –> decrease in extracellular matrix integrity (particularly in ascending aorta) (e.g. Marfan syndrome, Loeys-Dietz syndrome).
  3. 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).
  4. Ischaemia –> loss of smooth muscle cells or inappropropriate synthesis of non-collagenous / non-elastic ECM (e.g. atherosclerosis, HTN).
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10
Q

Vasculitis
-Definition

A
  • Inflammation of the blood vessel walls.
  • Site-specific signs and symptoms.
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11
Q

Broad causes of vasculitis and pathogenesis

A
  • Infectious - direct invasion of vascular walls by pathogen.
  • Non-infectious / Immune-mediated - inflammation.
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12
Q

Vasculitis:
Immune-mediated (non-infectious) vasculitis:
What are the main mechanisms underlying this vasculitis

A
  • Immune complex deposition (e.g. SLE, drug-hypersensitivity).
  • Antineutrophil cytoplasmic antibodies (ANCAs).
  • Anti-endothelial cell antibodies.
  • Autroreactive T cells.
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13
Q

Giant cell / Temporal Arteritis:
-What is it, who it affects, what is the mechanism, and what is the treatment

A

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.
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14
Q

Takayasu Arteritis:
-What is it, who it affects, what is the mechanism, what can it cause, and what is the treatment

A

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.
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15
Q

Polarteritis Nodosa (PAN):
-What is it, and what is the mechanism

A

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.
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16
Q

Atherosclerosis Stages

A
  1. Normal artery.
  2. Endothelial dysfunction.
  3. Fatty Streak Formation.
  4. Stable (Fibrous) plaque formation.
  5. Unstable plaque formation.
17
Q

What is Arteriosclerosis, what are the four general patterns, and which vessels does each pattern affect.

A

What it is:

  • “Hardening of the arteries”.
  • Generic term for arterial wall thickening AND loss of elastacity.

4 patterns:

  1. Arteriolosclerosis.
  2. Monckeberg medial sclerosis.
  3. Fibromuscular intimal hyperplasia.
  4. Atherosclerosis (most common).

Vessels affected:

  1. Small arteries and arterioles.
  2. Muscular arteries.
  3. Muscular arteries larger than arterioles.
  4. Coronary, cerebral and peripheral arteries.
18
Q

What are the three layers found in all blood vessels except capillaries

A
  • Intima (innermost endothelial layer).
  • Media (middle smooth muscular layer, thickness varies on vessel type).
  • Adventitia (outer supportive layer).
19
Q

Arteriosclerosis:
Arteriolosclerosis:
-What is it caused by, what are the two anatomical variants, what are their histology, and what does it cause

A

Caused by:

  • HTN.
  • Diabetes.

Anatomical variants:

  1. Hyaline.
  2. Hyperplastic (seen in severe or malignant HTN).

Histology:

  1. Thickened wall that is pink, homogenous, and glassy in appearance (from protein deposits). Luminal narrowing.
  2. “Onion-skinning” - Concentric, laminated wall thickening (from smooth muscle cells) with no-narrow lumen. May have fibrinoid deposits and necrosis.

Causes:

  • Ischaemia.
20
Q

Arteriosclerosis:
Monckeberg medial sclerosis:
-What is it, who does it affect, and what does it cause

A

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.
21
Q

Arteriosclerosis:
Fibromuscular intimal hyperplasia:
-What is it , what causes it, and what does it cause

A

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.
22
Q

What is hypertension

A
  • Diastolic pressure > 80 mmHg.
  • Systolic pressure > 120 mmHg.
23
Q

Hypertension:
-Causes

A

Essential HTN (i.e. primary / ideopathic; ~90% of all HTN).

Secondary HTN (~10% of all HTN):

  • Renal.
  • Endocrine.
  • Cardiovascular.
  • Neurologic.
24
Q

Hypertension:
-Clinical consequences

A
  • Arteriosclerosis.
  • Atherosclerosis.
  • IHD.
  • Stroke.
  • LVH –> failure.
  • Vascular dementia.
  • Aortic dissection.
25
Q

HTN patients not on medication. Normal renal angiogram, no abdominal masses, and normal renal function.
Which lab finding is most likely to be present in these patients?

A

Decreased urinary sodium.

26
Q

Patient with sudden, severe headaches for the past year. Examination reveals afebrile, HR 70 bpm, RR 14, BP 166 / 112 mmHg. Abdominal USS shows left kidney smaller than right and renal angiogram shows focal stenosis of left renal artery.
Which lab finding is most likely to be present in this patient and why?

A

High plasma renin.

Why:
Stenosis of L renal artery –> hypoperfusion of left kidney –> renin secretion to increase perfusion.

27
Q

Complications of atherosclerosis

~

A
  • Mechanical obstruction of vessel wall –> critical stenosis ~70% –> ischaemia.
  • Haemorrhage into plaque –> plaque rupture.
  • Plaque ulceration / erosion / rupture –> thrombosis –> partial / complete vascular occlusion.
28
Q

What are the consequences of atherosclerosis in the cerebral arteries?

A
  • Ischaemia.
  • Stroke.
29
Q

What are the consequences of atherosclerosis in the lower limb arteries?

A

Peripheral vascular disease.

30
Q

What is the pathogenesis of atherosclerosis

A
  1. Endothelial injury from hyperlipidaemia, HTN, smoking, homocysteine, toxins, viruses, immune reactions, haemodynamic factors.
  2. Accumulation of LDL and oxidised LDL.
  3. Endothelial dysfunction –> increased vascular permeability, leukocyte migration to injury.
  4. Monocyte adhesion to endothelium –> migration into intima (now called macrophage).
  5. Release of cytokines + oxidised LDL –> macrophage activation and recruitment of smooth muscle cells.
  6. Uptake of lipids by macrophages and smooth muscle cells –> fatty streak.
  7. Smooth muscle proliferation, collagen and other ECM deposition, T cell recruitment, extracellular and intracellular lipid accumulation.
  8. Calcification and necrosis.
31
Q

What is a fatty streak

A
  • Collection of lipid-filled (‘foamy’) macrophages in the intima of arteries.
  • Begin as small flat yellow macules.
  • Coalesce into elongated streaks 1cm or longer.
  • Not raised and do not disturb blood flow.
  • Can evolve into plaques but not always.
32
Q

In atheroma development, early lesions show increased attachment of monocytes to endothelium. The monocyte migrates into the endothelium and becomes a macrophage, where they then ingest lipid and become foam cells.
Which substance is most likely to be responsible for foam cell formation?

A

Oxidised LDL.

33
Q

Aneurysm:
-What is a saccular aneurysm

A
  • True aneurysm.
  • Focal wall bulging.
  • May be attenuated (weakened or thinned).
  • No vessel rupture.
34
Q

Aneurysm:
-What is a fusiform aneurysm

A
  • True aneurysm.
  • Circumferential dilation of the vessel.
  • No vessel rupture.
35
Q

Aneurysm:
-What is a false aneurysm

A
  • Rupture of BV wall.
  • Haematoma bounded externally by adherant extravascular tissues.
  • Gives appearance of bulging of vessel.

Basic Pathology (14 decks)

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