Transcript Aging of the Cardiovascular System

Anatomo-Histology
From Table
8.10
Brain atrophy,
flattening of gyri,
widening of sulci,
& cerebral ventricles
Loss of cholinergic neurons, in nucleus of Meynert,
hippocampus
& association cortices
Loss of adrenergic neurons, in locus ceruleus
Denudation of neurons, stripping of dendrites,
damage to axons
Increased microglia
Pathology
Accumulation of cell inclusions: lipofuscin, Hirano
and Lewy bodies,
altered cytoskeletal
Tau proteins,
ubiquitin
Neurofibrillary tangles, neuritic plaques with
amyloid,
Perivascular amyloid, distributed throughout the
brain, but especially in frontal,
prefrontal lobes,
Hippocampus, 
association cortices
Metabolism
Decreased oxidative metabolism, slower enzyme activity (Ch. 7)
Free-radical
accumulation (Ch. 5)
Impaired iron
homeostasis (Ch. 7)
Other minerals, zinc, aluminum
Reduced level/metabolism/ activity of neurotransmitters
Increased amyloid  peptide with accumulation of amyloid
proteins
Increased prion protein
Altered immune response
TABLE 8 - 9 Chara cteri stic s of Multi - Infarct Deme ntia
Hist ory of abrupt onset or stepwise deter ioration
Hist ory of transient ische mic at t ack or st roke
Presence of hy pertension or arrhythmia
Presence of any neurologic focal symptoms or signs
Learning at all Ages Induces
Successful Aging
T ABLE 8 - 6 Mechani sms of Effect s of
In crea sed Educat ion on Succe ssful Ag in g
Adequate income
Better access to medica l care
Better access to recreational activity
Good nu t rition
Responsible he alth behaviors
Moderate alcohol intake
Abstinence from smoking
Possibility of increased br ain reserve capacity
More dendritic branching, more synapse s
Better cerebra l blood flow
Better neura l cel l ef ficiency, adap t ability,
redundancy, su rvival and growth
T ABLE 8 - 12 Ba sic Goal s of Alzheimer’ s Disea se Man agement
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to optimiz e the pat ient’s function by tre ating underlying
medica l conditions and avoiding the use of drugs with side
ef fects on the nervo us syst em;
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to prevent stressful situations that may
exacerbat e ca t astrophic reactions;
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to identif y and ma nage complica t ions that may arise from
agitation, depression and incontinence;
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to pr ovide medica l and social information to the pat ient's
f amily in addition to any needed counseli ng.
to main t ain th e pat ient's saf et y whi le all owing as much
independence and dignity as possible;
cause or
Aging of the Cardiovascular
System
Chapter 16
P.S. Timiras
Major Functions of the
Cardiovascular System
Transports O2 & nutrients to the tissues
& returns C02 to the lungs and other products of
metabolism to the kidney
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Regulates body temperature
Distributes hormones and other agents that
regulate cell function
Major Components of the
Cardiovascular System
Heart
Pump that circulates the blood throughout the body
Vascular System
Transports blood to the body tissues
Central Nervous System (CNS)
Particularly the centers in the medulla that regulate
the function of the heart and blood vessels
Atherosclerosis
What?
Arteriosclerosis:
Sclerosis: hardening of the arterial wall
and narrowing of the arterial lumen
Atherosclerosis:
Same as arteriosclerosis PLUS presence
of artheroma (yellowish plaque
containing lipids and cholesterol) on the
arterial wall
Atherosclerosis
Universal
Progressive
Deleterious
Irreversible (?)
Fig. 16-3: Natural
history of
atherosclerosis.
Pathogenesis of
human
atherosclerotic
lesions and their
clinical
manifestations.
Myocardial
Infarction
Stroke
Aneurysm
Atherosclerosis Affects the Arteries
Arteries: the large arteries, the arterioles, & the capillaries
See Box 16-1, Fig. 16-1, Fig. 16-2 (pgs. 287-289)
Progressiveness of Atherosclerosis
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Onset at young age
Progression through adulthood
Culmination in old age with overt disease
manifestation
Consequences leading to severe disability &
death
END
Extracellular cholesterol
and cholesterol-filled
macrophages (foam cells)
accumulate in
subendothelial space.
Subsequent structural
modifications of LDL
particles render them more
atherogenic. Oxidation of
subendothelial LDL attracts
monocytes, which enter
subendothelium and
change into macrophages.
Macrophages may take up
oxidized LDL to form foam
cells.
Fibrous plaque larger than
fatty streak and occupies
more of the arterial lumen.
Thickened cap synthesized
by modified smooth muscle
cells. Central core consists
of extracellular cholesterol.
Foam cells surrounding
core derived primarily from
smooth muscle cells. Fatty
streaks may continue to
form at periphery of
plaque.
Total or partial occlusion
of coronary artery due to
plaque rupture and
thrombosis can cause
angina or frank
myocardial infarction.
Plaques likely to rupture
termed unstable. Rupture
usually occurs in lipidrich and foam cell-rich
peripheral margins and
may result in thrombosis
and arterial occlusion.
Table 16-5: General Characteristics of Atherosclerotic Lesions
Early onset -- progressive
Focal lesions
Early lesions
Advance lesions
Damage, Repair, Regression
Progression of localized lesions influenced by:
Local factors: vessel structure and metabolism, blood turbulence
Systemic factors: diabetes, hypertension, stress, genetic
predisposition