Role diabetes mellitus. Role homocystine diabetes, hypertension, homocystine, infection. clinical aspects and complications …
Cardio lect 2
12 Sept 03
8-9am
Pathology of Atherosclerosis II - Dr Papa Khin
Notetaker: Pearly
I AHA Classification of Atheroma from yesterday
A Type I - Mac Foam Cells
B Type II - Intracellular Lipid
C Type III - Extra
D Type IV - Extralcellular Lipid Core
E Type V - Multiple cores w/ fibrosis and calcification
F Type VI - Complicated plaques and effects
II Pathogenesis of Atherosclerosis
A Hyperlipidemia call for NEW RISK FACTORS
1 but not only reason for atherosclerosis
B Toxins: cigarette smoke, hypoxia, homocystine, endotoxin, viruses
a These damage endothelial cells
C Hemodynamic disturbances stresses and strains put on endothelial
walls
1 eg Hypotension, branches of arteries, disturbances laminar flow
D Role hypertension
E Role diabetes mellitus
F Role homocystine
III Role of Hypertension major area of development of
atherosclerosis
A Mechanical stresses EC injury
B HT alters
EC permeability of endothelial cells
1 endothelial cells, if normal, protect from fatty deposits
2 once damaged increased permeability and cant control deposition
of fatty material cholesterol
3 increased lysosomal enzyme activity
C Inc media, and connective tissue
D Most of time when you have atherosclerosis, its associated w/
hypertension
1 can get this even in pulmonary vessels
IV Role of Diabetes Mellitus
A Diabetes cellular dysfxn
1 glucose level in blood very high goes to all cells in body
excess causes metabolic defect in all cells in body, particularly
ENDOTHELIAL cells
2 EC dysfxn inc atherogenesis
B Platelet dysfxn deposition becomes sticky
C Sorbitol osmotic derangements
1 formed in DM
2 this is a different form of glucose will also deposit in various
parts of body kid, brain, subendothelium damages endothelial
cells aggravates atherosclerosis
3 artificial sugar little packets used in coffee
D glycosylation AGEs traps LDLs
1 proteins get attached by glucose glycosylation of proteins
produces abnormal features of AGEs Advanced
Glycosylation
Endproducts
a AGEs aggravates atherosclerosis
V Role of Homocystine
A Abnormal methionine amino acid metabolism
1 occurs particularly w/ HT
2 makes homocystine hyperhomocystine causes atherosclerosis
3 homocys Measurement just as important as cholesterol
B Folic acid deficiency aggravates atherosclerosis
C Homocystine toxic to ECs
D Dec anticoagulant activity of ECs coagulation
E Inc aggregation of platelets coagulation
F An INDEPENDENT risk factor for atherosclerosis
VI Clinical Features of Atherosclerosis first heading under
arteriosclerosis
A Asymptomatic for decades up to 30-40s if theres 75 obstruction
of vessel, nothing really happens as long as youre sitting downmow
your lawn and youll DROP DEAD
B Symptoms incl
1 ischemia gangrene
2 thrombosis coronary As MI
3 cerebral stroke/organs infarcts
4 embolism infarcts
5 weakening BV wall aneurysm rupture
6 remember brain attack, heart attack, gangrene and rupure
a early stages of blockage in hrt angina pectoris
b in skeletal Ms
claudication
c get clots on top of blockage infarction coronary thrombosis
in heart MI
VII Monckeberg Arteriosclerosis second heading under arteriosclerosis
LEAST important, b/c see only in elderly or incidental finding
A 50yrs increases w/ advancing age
B band-like calcifications in medium arteries bracial, popliteal, etc
C etiology unknown / unrelated to atheroma
1 best thing to do is NOT GET OLD Hehehe
D No narrowing of lumen
E Thats about it for Monckeberg usually used as a distractor in your
multiple choice questions
VIII Arteriolosclerosis ALS little arteries affected
A This is an EFFECT of hypertension
1 hypertension review
a benign slow, goes for long time 10-30yrs but still KILLS
b malignant severe - nothing to do w/ cancer comes on very
rapidly kills very rapidly
c differentiating the two
i B9 systolic 140, diastolic 90 same thing as systemic
hypertension
1 Asymptomaticdont know til you go to the doctor
ii Malignant could follow B9 or is de novo
1 Diastolic 120 systolic doesnt matter
2 YOUR EYES SHOULD
POP OUT this pt needs immediate attn
and Tx otherwise youll have a DEAD pt in your hands
B Affects small arteries / arterioles
C Hyaline ALS arteriolosclerosis B9 HT
1 two changes that happen in any arteriole, but MOST COMMON IN
KIDNEYS aka nephrosclerosis this name isnt important tho
a hyaline thickening
b elastosis proliferation of vessel wall elastic tissue
D Hyperplastic ALS MALIGNANT HT
1 two changes as well
a onion-skin thickening self explanatory wall looks like an
onion very narrow lumen
b fibrinoid necrosis
i look at vessel under scope very DARK RED appearance of
vessels seen in kidney in transplant rejection and SLE
ii necrotic areas in vessel dead areas cant control much
iii diastolic 120 then systolic must be through the roof
bvs rupture hemorrhages all over the place Pretty bad
situation if I do say so myself
IX REVIEW OF ARTERIOSCLEROSIS side note
A Atherosclerosis
1 atheroma for short
2 maj and min risk factors
3 most imp Morphologic finding COMPLICATED PLAQUE
calcification,
ulceration, thrombosis, hemorrhage
4 diabetes, hypertension, homocystine, infection
5 clinical aspects and complications
B Monckeberg just went over this
C Arteriolosclersosis just went over this
1 EFFECT of hypertension
X ROLE OF INFECTION this isnt in the textbooks, but AHA talking about
this not great importance for exam but HUGE IMPORTANCE FOR YOUR FUTURE
PRACTICE
A traditional risk factors cant explain completely
B 50 HA victims normal cholesterol levels
C repeated call for NEW RISK FACTORS
D paradigm shift in atherosclerosis research
E overwhelming evidene infection/inflammation
F Chlamydia pneumoniae, HSV, oral pathogens
1 CHLAMYDIA PNEUMONIAE MOST IMPORTANT
2 those who get antibiotics after HA do much better than those who
dont
G CRP C-reactive protein: better to predict HAs than cholesterol
H Top-to-bottom rethinking etiology CAD
I Revolutionary departure standards of cardiology
J Entirely different way of preventing and treating
K Inflammation and infection essentially missed b/c of our focus solely
on Cholesterol
L CDC AHA meeting new federal guidelines
1 have to check other things if cholesterol isnt at top of the list
eg CRP
THATS ALL FOLKSTHANX FOR LISTENINGAND NOW ONTO HEART ATTACKS WOO
HAA
Source:nova.edu
