Lab studies Flashcards
Rfs for CHD (13)
-older age
-family hx
-males
-uncontrolled HTN
-elevated total cholesterol (low concen HDL, high concen LDL, elevated triglycerides)
-uncontrolled DM
-smoking
-inactivity
-overweight-obese(BMI)
-postmenopausal
-pro-inflamm state
-uncontrolled stress
poor diet
-alcy
Cholesterol
-waxy, fat-like substance
-essntial (precursor for V D, steroid hormones)
-total <200 is DESIRABLE
200-239 borderline high
>240 high
Cholesterol
transport carrier molecule?
limited what
-nonpolar, limited solubility in blood
-effective transport needs carrier molecule—> lipprotein
(lipos vary in density, and size-HDL,LDL,VLDL)
Lipid panel
-Total cholesterol is a calculated quantity (HDL+DLD+trig)
LDL= total - HDL - trig /5
Lipid panel is all of this present in blood
HDL
Good cholesterol
Men: >60 good, <40 at risk
W: >60 good, <50 at risk
HDL is inversely associated with risk of CHD
Aerobic exercise increases this
LDL
-causal rf for developing MI and arthero CV disease
LDLs invade tunica interna and form an atheroma
-WBC move in and cause inflam
-smooth muscle cells enter
-fibrous connective tissue accumulates
-macrophages attracted
forms swelling in artery called atherosclerotic plaque (from fixing little tears)
LDL
norm fasting ranges
plaque formation is …
plaque formation is self propagating (increase risk CV disease)
LDL calculated
norm fasting ranges (100 or less) LESS better
VLDL
-estimated as % of triglyceride value
-high levels associated with developing plaque deposits on artery walls
Lipprotein A
-Independent rf for CAD
-above 50 = increased risk of CV disease
Cholesterol ratios
Total/HDL
200/50= 4 or 4:1 ratio total to HDL
lower the ratio= lower risk of HD
recommend 5 or less
Triglycerides
-glycerol molecule plus 3 fatty acids
-high levels in bloodstream have been linked to atherosclerosis and risk of HD and stroke
Types triglycerides: sat
Sat fats: fat molecules no double bonds- saturated with hydrogen
-high levels in blood increase risk of HD and stroke
Types triglycerides: unsat
Fat molecules where there are 1+ double bonds
-Monounsaturated (1 double bond0
-polyunsaturated
-low melting point- liquid at room temp
CIS fatty acids
unsat
good
naturally occuring
cardioprotectant
trans fatty acids
type of unsat fats
uncommon but common produced from vegetable fats
-increased intake associated with increased risk for CVD
not good
Ranges triglyceride
Norm: <150
150-199 border
200-499 high
>500 very
mx by meds (statins) and lifestyle
Patho CVD in DM
-DM is a disease of hyperglycemia
-creates pro-inflam state (adipose tissue) -this causes platelet activation and increases risk stroke and ischemic injury
-Dyslipidemia (bad lipid profile) often present (drives atherogenesis and atherosclerosis-> increase arterial stiffness
-increases risk HF and other CV pathos
Characteristics of DM heart
-fibrosis
-hypertrophy
-impaired perfusion
-mitochondria dysfunc
-inpaired Ca handling
commonly exhibit LV diastolic dysfunc
DM cardiomyopathy should be known as Diabetic HD or DM associated HF
Cardiac enzymes
-identified biomarkers whose blood values increase with occurrence of an MI
ischemic insult-> cell injury and death->disrupt sarcolemma -> movement of cell contents into interstitial space and blood
WE DONT NORMALLY SEE THESE THINGS IN BLOOD -creatine kinase
Types of CPK
Creatine kinase = creatine phosphokinase
catalyzes conversion of creatine and ATP into PCr and ADP
PCr-immediate energy source
CPK-MB (myocardial band)
CPK-MM (heart and skeletal muscle)
CPK-BB (brain)
CPK after injury/insult
after injury/ MI :
rise: 4-6hrs
peak: 12-24hrs
remain elevated: 4-5 days
0-175 norm range
Troponin
Norm: 0-3.0
-group of proteins found in striated muscle cells bound to actin filament
TnC: binds Ca
TnI: inhibits action between actin and myosin
TnT: links troponin to tropomyosin
T has more latency in peak than I
Gold standard cardiac enzyme
CPK
troponin is also with muscle damage
Myoglobin
-found in all muscle tissue
-recent dx tool for acute MI
-peaks 3-15 hrs
requires r/o skeletal muscle injury
norm: 25-72
peaks way more quickly than other tests
Why is liver panel of interest post MI
when heart pump is limited- liver bloodflow is limited so liver starts to get damage
liver and kidneys go ary first
ANP
-hormone secreted in response to atrial distention -too much stretch= too much preload
so increase GFR and reduce Na and H2o reabsorption
serum levels increase with increasing severity of HF- inhibits cardiac hypertrophy and fibrosis
BNP
-produced in VENTRICLES and released in response to excess stretching
BNP levels elevated in people with HF
GOLD STND for HF (both comp and uncomp HF)
BNP physio actions
pee out more salt (RAAS)
these levels are increased in proportion to the amount of HF
(increase HF= increase LVEDV)
BNP values
norm: <100
>700 acute cardiac decomp
100-700 chronic compen
NY Heart assoc levels of HF
1: no limit activity. ordinary exercise may cause some sxs
2: any acttivity causes sxs
3: comfy at rest
4: no matter what hard to func
CRP
-produced in liver- increased in inflamm states (infec, CA, etc)
higher number not heart issues
1-3 high risk heart
serum creatone
norm: <1.5
filtered by kidneys
blood levels reflect kidney func
HF-> decreased CO-> decreased renal perfusion
this elevated may be independent predictor of CV mortality
