A comprehensive summary covering all of systems pathology, namely Inflammation and Repair, Hemodynamic Disorders, Neoplasia, Blood Vessels, Heart, Lung, Kidney and its Collecting System, GIT, Liver, Gallbladder, Endocrine, Skin, CNS, PNS, Bones.
ANP Theme 2 Summary
Unit 2.1. Blood Vessels
Vascular disease develops through two principal mechanisms:
1. Narrowing or complete obstruction of the lumen either
progressively or acutely
2. Weakening of the vessel wall causing dilation and/or rupture
Endothelial cells create a continuous lining known as the endothelium.
Systemic and local blood pressure must be maintained within a
narrow range to maintain health. Low blood pressure (hypotension)
results in inadequate organ perfusion, organ dysfunction, and
sometimes tissue death. Conversely, high blood pressure
(hypertension) causes vessel and end-organ damage and is one of the
major risk factors for atherosclerosis.
,Hypertensive vascular disease is correctly classified
The aetiology, pathogenesis, basic morphological changes (vascular wall changes) and clinical
manifestations of the different types of hypertensive vascular diseases are correctly explained
Essential hypertension
• Aetiology
o Gene defects in enzymes involved in aldosterone metabolism
▪ Aldosterone synthase
▪ 11-beta-hydroxylase
▪ 17-alpha-hydroxylase
o Mutations in proteins that affect sodium resorption
o Although the specific triggers are unknown, it appears that both
altered renal sodium handling and increased vascular resistance
contribute to essential hypertension
• Pathogenesis
o Reduced renal sodium excretion causes an obligatory increase in fluid volume and
increase in cardiac output, thereby elevating blood pressure
▪ At the new high blood pressure, the kidneys excrete additional sodium, thus a
new steady state of sodium excretion is achieved but at the expense of elevated
blood pressure
o Increased vascular resistance may stem from vasoconstriction or structural changes in
vessel walls
o Genetic factors
o Environmental factors such as stress, obesity, smoking, physical inactivity and high levels
of salt consumption modify the impact of genetic determinants
• Vascular wall changes of small vessels
o Three histological forms of arteriosclerosis may occur
▪ Hyaline
▪ Concentric/hyperplastic
▪ Necrotizing
o The type of arteriosclerosis that occurs depends on how the intima and media respond
to injury and the intensity of the response
Secondary hypertension (in most cases) develops from:
,Malignant hypertension is associated with renal failure and retinal hemorrhages, with or without
papilledema. It can arise de novo, but most commonly it is superimposed on preexisting benign
hypertension.
Hypertension mainly affects the arterial system (known as arteriosclerosis), which can be divided into
the:
• Large elastic arteries (atherosclerosis)
• Medium muscular arteries (atherosclerosis)
• Small arteries and arterioles (arteriosclerosis)
Hyaline arteriosclerosis
• Associated with benign hypertension
• The vessel wall is thickened and has a waxy appearance
• The vessel lumen is narrowed and occurs due to leakage of plasma proteins into the vessel wall
and ECM production by SMCs
Hyperplastic Arteriosclerosis
• Associated with severe hypertension
• Occurs due to rhythmic, concentric smooth muscle hyperplasia, giving the vessel wall an onion
skin appearance histologically
, Necrotizing Arteriosclerosis
• Associated with malignant hypertension
• The acute onset of severe hypertension results in arteriolar wall necrosis and subsequent fibrin
escape into the vessel wall
Basic concepts of endothelial cell physiology are correctly described
• They line the entire vascular system and differ genetically, and therefore have different
functions in different areas of the vascular system
o Fenestrations in ECs lining hepatocyte cords, renal glomeruli and choroid plexuses
facilitate filtration
• They have interendothelial junctions
o In most regions these junctions are impermeable, however these junctions open under
the influence of hemodynamic stress and/or vasoactive agents
Possible causes of endothelial cell injury are correctly
named
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