Blood vessels and ischeic heart disease Flashcards
what is morbidity and mortality assoc with atherosclerosis
VIRCHOWS’
1) narrowing of vessels
2) damaged endothelial lining
3) weakened vessel walls
why is narrowing of vessels dangerous?
ischemia of tissue perfused by vessels
why is endothelial lining damage dangerous?
promotes intravascular thrombosis
why is weakened vessel walls
dangerous?
predispose to dilation/rupture
Virchow’s triad
1) abnormal blood flow = turbulence
2) hypercoagulability
3) endothelial injury
differentiate elastic vs muscular artery
elastic = accomodate/dampen pulsatile flow
muscular = regulate flow (vasconstrict/dilate)
ex of elastic artery
aorta
ex of muscular artery
renal artery
atherosclerosis is ____ to injury
response
____ is response to injury
atherosclerosis
why is atherosclerosis considered a normal response to injury
reconstituting damaged vessels
if intimal thickening increased can cause stenosis of vessels/grafts
examples of responses to vessel stenosis
1) angioplasty re-stenosis (mech)
2) transplant arteriosclerosis (immun)
3) atherosclerosis
subtypes of arterosclerosis
1) arteriolosclerosis
2) monckeberg’s
3) atherosclerosis
what is pathology of atherosclerosis
fibrofatty plaques on intima
define monckeberg’s medial calcific stenosis
calcification of MEDIA of muscular arteries
NOT AFFECT VESSEL LUMEN
what is disease assoc with calcification of media of muscular arteries
monckeberg’s medial calcific stenosis
where do you see arteriosclerosis
small arteries/arterioles
what is arteriolosclerosis assoc with
HTN
Diabetes
what are 3 major targets of atherosclerosis
1) coronary arteries –> ischemic disease
(with thrombosis –> MI)
2) cerebral arteries –> stroke, infarct, neuro
3) aorta –> AAA
4) ischemic bowel (mesenteric)
Pathogenesis of atherosclerosis
1) focal chronic endo injury
2) insudation of lipoproteins into vessel wall
3) interactions with macs and lymphs
4) incr smooth muscle prolif –> atheroma
what is a foam cell
macrophages taking up
fat globules
what is aneurysm
weakening of wall
where do you find aneurysms
1) trauma
2) local infection (mycotic aneurysm)
3) congenital defect (berry aneurysm)
4) arteriovenous aneurysm
what are major causes of aortic aneurysms (3)
1) atherosclerosis
2) cystic medial degeneration (Marfan/age)
3) syphilis
where do aortic aneurysms most commonly present
abdominal aorta, below renal
mechanism causing aortic aneurysm
1) atherosclerosis weaknes wall
2) mass effect stim tumors (compression/erosion)
what is most common co-occurrence with aortic dissection
HTN (90%)
abnormality of connective tissue
what is mechanism of aortic dissection
1) intima tear toward heart or distal
2) 2nd intimal tear, blood into lumen –> double barreled aorta
what is a double barreled aorta
2nd intimal tear when blood returns into lumen
symptoms of aortic dissection
SUDDEN EXCRUCIATING PAIN RADIATE TO BACK
Type A aortic dissection
Type B aortic dissection
Type A = ascending aorta
Type B = off great vessels
what are ascending aorta aortic dissections classified as?
type A
which is worse type A or B aortic dissections
type A because could continue into coronary arteries –> ischemia
define false aneurysm
small area in vessel wall with hematoma forming outside
Features of vasculitis in pathology
1) vessel wall inflammation
2) vessel wall damage
3) fibrinoid necrosis
what are underlying causes of vasculitis
1) localized infection (viruses)
2) radiation
3) trauma
4) arthrus rxn
5) viruses in lesion
6) SLE
which arteries do you see polyarteritis nodosa
medium to small arteries
all stages coexist
what vasculitis do you see in medium to small arteries
polyarteritis nodosa
what vessels do you see microscopic polyarteritis
arterioles
capillaries
venules
(all at same stage)
which vessels do you see temporal arteritis (giant cell arteritis)
1) temporal arteries
2) ophthalmic branches –> blindness
features of temporal arteritis
granulomatous inflammation
due to macrophages coalescing
what patient population do you see temporal arteritis
elderly (>50)
where do you find Wegener’s granulomatosis
lungs + kidneys
features of Wegener’s granulomatosis
vasculitis
granulomas
what if you don’t treat Wegener’s granulomatosis
> 90% die in 2 yrs
where do you find Takayasu’s arteritis (pulseless disease)
aorta
aortic branches
pulmonary arteries
why is Takayasu’s arteritis also known as pulseless disease
because it narrows openings of great vessels
what are symptoms of Takayasu’s arteritis
coldness
numbness of fingers and legs
what patient population do you see takayasu’s arteritis
young <40 y/o
more females
where do you find Kawasaki’s disease
coronary arteries
what patient population do you find Kawasaki’s disease
infancy
early childhood
symptoms of kawasaki’s disease
fever
erythema palms and soles
rash
where do you find Buerger’s disease
male cigarette smokers
also female incidence incr with smoking
where do you find Buerger’s disease
thrombosis of medium vessels, tibial and radial
complications of Buerger’s disease
1) gangrene
2) pain at rest (due to nerves)
where do you find thrombophlebitis
clot in deep leg veins
dangers of thrombophlebitis
death from PE (saddle embolus)
predisposing factors to thrombophlebitis
1) immobilization/bed rest
2) cancer (hypercoag)
3) trousseau’s sign
what is trousseau’s sign
clots come and go due to malignancy
2 MAJOR dangers with ischemic heart disease
1) decr blood supply due to atherosclerosis of coronary arteries
2) demand ischemia caused by hypotension from infection
when is ischemic heart disease symptomatic
> 75% stenosis
vasodilation not sufficient for O2
define angina pectoris
intermittent chest pain from reversible myocardial ischemia
define stable angina pectoris
episodic chest pain with exertion
disease assoc with episodic chest pain with exertion
stable angina pectoris
define unstable angina pectoris
incr freq and intensity with LESS EXERTION
can trigger irreversible myocardial ischemia
if you have incr freq and intensity of chest pain with less exertion
unstable angina pectoris
define prinzmetal’s angina
chest pain at rest (sleep)
what is prinzmetal’s angina due to?
vasospasm
chest pain at rest disease?
prinzmetal’s angina
define myocardial infarction
myocardial necrosis from ischemia (many hrs, not relieved by nitro)
myocardial infarction not relieved by ___
nitro
what are most myocardial infarcts caused by
clots on plaques
when does necrosis begin after MI
20-30 min after occlusion
progression of myocardial infarction
1) necrosis begin in subendocardial (under endothelial lining)
2) migrates outward
what is a full thickness necrosis known as
transmural infarction
if MI affects right dominant circulation (more common) which vessels involved
Right coronary artery
supplying posterior LV
if MI affects left dominant circulation, which vessels involved
Left circumflex coronary artery
supplying posterior LV
____ occlusion produces larger infarcts
more proximal
more proximal occlusion produces ____
larger infarcts
what happens when main vessel 100% occluded?
chronic ischemia recruits additional vessels
Gross appearance and microscopic appearance of MI at
4 hrs
gross = no change
microscopic = coagulation necrosis
what time point in MI?
gross = no change
microscopic = coagulation necrosis
4 hrs
Gross appearance and microscopic appearance of MI at
1 day
gross = pallor
micro = neutrophils
no nuclei in most myofibers
what time point in MI?
gross = pallor
micro = neutrophils
1 day
Gross appearance and microscopic appearance of MI at
1 week
gross = pallor
micro = macrophages
loss nuclei
hypereosinophilia
contraction bands
what time point in MI?
gross = pallor
micro = macrophages
1 week
Gross appearance and microscopic appearance of MI at
10 days
gross = yellow, soft, sunken
micro = granulation tissue
what time point in MI?
gross = yellow, soft, sunken
micro = granulation tissue
10 days
Gross appearance and microscopic appearance of MI at
2 months
gross = firm, grey scar
micro = fibrosis
what time point in MI?
gross = firm, grey scar
micro = fibrosis
2 months
complications of MI < 2 weeks after?
risk of rupture when mostly neutrophils and dead cells
complications of MI?
ventricular aneurysms- damaged wall
mural thrombus - damage and pooling of blood
what is sudden cardiac death most common due to?
marked atheroslcerosis
mechanism of sudden cardiac death due to atherosclerosis?
1) plaque rupture
2) clot, vasospasm
3) fatal arrhythmia or Hypertrophy
Stable vs Unstable plaque
stable angina = fixed obstruction so need more O2 delivery –> reversible ischemia
hemorrhage in clot –> may occlude remaining vessel
