Cardiovascular: Flashcards
risk factors for coronary heart disease: non-modifiable
> male 45+
> family hx of CVD
- males under 55 - females under 65
> postmenopausal female
45-55-65 males always first and menopause starts 40-51
modifiable risk factors for coronary hert disease
>HTN >Smoking >dyslipedemia -low HDLs -elevated LDLs >diabetes mellitus >obesity >L ventricular hypertrophy
hyperlipideia has what incidence
40% approx
hyperlipidemia=
high lipid content in blood
elevated cholesterol, phospholips nd triglycerides in blood
cholesterol
is a lipid biosynthesized by animals nec to form cell membrane
what transport lipids in blood
apoproteins
whats an apoprotein + a lipid
a lipoprotein
fig 22-3
lipoproteins what are the types in order of low density to high
what is more dense fat or protein
lipoproteins all contain some triglcerides, phospholipids and cholesterol
chylomicrons transport fat into the intestine (only 2% protein)
VLDL contains lots of triglcerides and 5-10% protein
LDL isnt as bad for you as VLDL contains 25% protein
HDL is 50% protein (they transport LDLs to liver for proc and return cholesterol to liver)
osis as a suffix=
deposition of
blood vessel layers
endothelial cells>CT>internal elastic membrane>Sm muscle cell>collagen and elastic fibres (typical artery)
atheroma=
where do they form
fibrofatty lesion forms in intima of arger arteries
how do atheromas affect perfusion
they dec it>ischemia>stroke, MI or PVD
ischemia=
restricted blood flow at local level
death of tissue d/t ischemia=
infarction
what percentage of all deaths is caused by atherosclerosis
32%
3 types of lesions in atherosclerosis
initially fatty streak>fibrous atheromatous plaque>complicated lesion
initial lesion in atherosclerosis=
qualities
what does it contain
fatty streak
insidiious, subclinical
-yellowish discoloration inintima that contains defense cells and lipids
what type of lesion comes after fatty streak in atherosclerosis
what does it contain
fibrous atheromatous plaque-basic clinical lesion in intima contains: defense cells, scar tissue, smooth muscle cells
what is the third lesion in atherosclerosis
what does it do
complicated lesion
causes changes in lumen
when does atherosclerosis begin and manfest
mid to late 20s. mnfts in 50s60s
(my notes maybe use next slide?)process of atherosclerosis
endothelium gets damaged by risk factors eg smoking and lipids enter and deposit on intima
- monocytes enter intima as well as platelets.
- as lipids enter=fatty streak
- macrophages enter and release free radicals such as hydroxyl that cause damage. they also engluf lipids and turn into foam cells
- in Fibrous plaque the lipids form a core and smooth muscle begins to grow stim by foam cells releasign growth factors. at this point it would be 60% occluded
- a complicated lesion will have changes in the lumen>hemmorhaging into the plaque>thrombus inside the vessel. its 90% occluded
pathogenesis of atherosclerosis
- insidious origin w subtle endothelial injury>inflm (CRP)
- monocytes and other inflm cells bind to endothelium
- monocytes enter intima>become macrophages>release free radicals (from oxidizing the lipids) causing injury and engulf lipids to bcome foam cells
- sm muscle cells proliferate
- atheroma forms
sites of severe atherosclerosis in order of frequency
1=abdominal aorta and iliac arteries
2=proximal coronary arteries
3=thoracic aorta, femoral and popliteal arteries
4=internal carotid arteries
5=vertebral, basilar, and middle cerebral arteries
incidence of HTN
22%
HTN=
Bp=cardiac output x total peipheral resistance
4 major control systems of BP
arterial baroreceptors
RAA
vascular autoregulation
regulation of lfuid volume
R coronary circuit from aorta
aorta R coronary artery R marginal artery arterioles capillaries in myocardium venules small cardiac vein coronary sinus R atrium
L coronary circuit
L coronary artery circumflex or atrioventricular artery arterioles capillaries in myocardium venules middle or great cardiac vein
passage of blood through heart and large vessels eg aorta
deoxy blood enters R atrium via superior vena cava
passes tricuspid R atrioventricular valve into R ventricle
through pulmonary semilunar valves nto pulmonary trunk then to lungs through pulmonary arteries
after lungs the pulmonary veins carry oxygenated blood to the left atrium
past the mitral valve (L atrioventriular valve) into L ventricle
from L ventricle to body passing the aortic semilunar vve
lookup in home notes the 4 major blood pressure control systems
l
normal ranges of BP
high normal BP
120-139 AND OR 80-89
Stage I mild
140-159 or 90-99
Stage 2: moderate
160-179 or 100-109
Stage 3: severe
> 180 or >110
if you have a pt w 150/105 how would you stage their HTN? why?
use the higher value to err on the side of caution. THey would be stage 2.
diastolic and systolic are of equal importance. use the higher number
you can stage HTN by the numbers and also by _______
etiology
1’ (primary) HTN
value
etiology
>140/90 essential or idiopathic etiology is multifactorial kidneys are implicated this is more common (90% of pts have this form of HTN)
2’ (secondary) HTN
etiology
value
identifiable etiology such as renal disease
10% of those w HTN have secondary HTN
does secondary HTN follow primary?
no
why does systolic HTN mostly occur after age 50
wear and tear
At rest TPR is stable but TPR fluctuates. With aging their is change in compliance of the vessels. When heart pumps the vessels dont have the elasticity to comply. Because peripheral resistance is dec cardiac output must inc
what is white coat HTn
wc=d/t stress in health care settings
whats gestational HTn
during pregnancy
usually returns to normal after birth
eg eclampsia
malignant HTN
diastolic pressure is >120 and systolic is normal
unsure why
is edema a mnft of HTN
nope. complication
mnfts of HTN
late mnfts.
inc BP only
late: fatigue, palpitations, morning headaches, blurred vision, dizziness
palpitation=
sensation of irreg, rapid, forceful heartbeat
when is Bp lowest
2-5am
why do some get blurred vision w HTN
retina is made up of tiny blood vessels which are easily affected
if HTn isnt well managed what could happen
Progressive organ damage
- the heart because it is the pump
- the kidneys receive a large amount of blood
- vessel walls
if HTN is well managed what should manifest?
inc Bp only
Tx of HTn
lifestyle modification (diet, exercise, weight) (theyll initially take Bp, have you try the above then remeasure if still HTN then move onto drugs)
-1st line diuretic! (must maintain normal blood volum)
diuretics inc fluid loss from kidneys >dec blood volume>dec HTN. you also lose electrolytes
then, if nec add one or more of these in any order
calcium channel blocker-dec contraction of heart and on smooth muscle in blood vessels
angiotensisn II receptor blocker
ACE inhibitor
systolic HTN
systolic P >140, diastolic pressure of dec elasticity>inc systolic pressure but not diastolic pressure
