26. FUN THINGS TO FIND: Lumen, Fibrous cap (fibrous plaque), Lipid core, External Elastic Membrane thinning/destruction, Calcification, Neovascularization www.freelivedoctor.com
40. www.freelivedoctor.com A very well constructed graphic understanding of the pathogenesis of atherosclerosis. Please be expected to not only KNOW these five items, but their correct ORDER too.
104. Diagnosis of vascular neoplasms may require the use of endothelial cell markers such as Factor VIII or CD-31, especially if clear cut vascular spaces are difficult to see, especially if the tumor is UNDIFFERENTIATED enough to the degree that endothelial lined spaces are NOT clearly seen. www.freelivedoctor.com
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Editor's Notes
Please note that the “NONSPECIFIC” reactions to injury, are very closely paralleling the process we call “atherosclerosis”, also note that these processes seem to be more typical of arteries rather than veins.
Because of the simple geometric fact that smooth muscle cells are arranges axially to the axis of the blood vessel, constriction of the smooth muscle cell results in constriction of the vessel.
Intimal thickening is a NON-specific response to vascular (chiefly arterial) injury, and is they KEY feature in atherosclerosis as well.
CT Angiogram
Atherosclerosis and arteriosclerosis are often used so interchangeably, it is hardly worth differentiating them anymore, other than to know they are different!
Atherosclerosis is a LIFELONG, even childhood, process. This chart is worth knowing.
The streaks are more noticeable at the ostia of the aorta because that is where PRESSURE is the greatest. This simple observation makes it easier to understand the relationship between hypertension and atherosclerosis
These should all be household words in your vocabulary.
“ Framingham” data. Please remember that these are the ONLY four MAJOR risk factors. If somebody tells you there is anything else which is a MAJOR risk factor, nominate that joker for a Nobel prize.
Needle shaped washed out spaces in arteries, are cholesterol clefts, and can be nothing else, and like all other fat, yellow grossly, white microscopically.
Risk factors vs. ischemic heart disease
It is easy for a smoker to FORGET that cigarettes cause atherosclerosis. i.e., MAJOR risk factor. I hope YOU do not forget.
Like the sequence of events described in acute inflammation, atherosclerosis is its own Cecil B. DeMille saga! Not only should you all be familiar with these processes, but their ORDER as well. * This may be the first (i.e., earliest) microscopic and gross finding.
A very well constructed graphic understanding of the pathogenesis of atherosclerosis. Please be expected to not only KNOW these five items, but their correct ORDER too.
A simplified (nothing is TOO or OVERLY simplified, imho) concept of atherosclerosis.
Degeneration/Neoplasm/Inflammation link!
Note that classically topics of arterial diseases are divided into 1) atherosclerosis and 2) everything else.
Know ALL the ways angiotensin II increases blood pressure!
Know the difference between a TRUE (endothelial expansion) and FALSE (NO endothelial expansion) aneurysm
Dissection (i.e., blood or hemorrhage disrupting the wall of a large artery) can be both a cause or an effect of an aneurysm.
Nuclear “dust” from neutrophils, i.e., leukocyto”clasia” is the hallmark.
Mortality has improved significantly, but flare-ups, i.e., recurrences, are still the main concern.
A “mycotic” aneurysm is any aneurysm that has become secondarily infected, usually by bacteria. Hence the name “mycotic” is a misnomer.
SEVERE VARICOSITIES
Blockage of the thoracic duct is the usual cause of chylothorax
“ -ectasia” is a generic term meaning dilation and is primarily used with regard to veins rather than arteries.
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