Lab studies

Question 1

Rfs for CHD (13)

Answer 1

-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

Question 2

Cholesterol

Answer 2

-waxy, fat-like substance
-essntial (precursor for V D, steroid hormones)

-total <200 is DESIRABLE
200-239 borderline high
>240 high

Question 3

Cholesterol

transport carrier molecule?
limited what

Answer 3

-nonpolar, limited solubility in blood
-effective transport needs carrier molecule—> lipprotein
(lipos vary in density, and size-HDL,LDL,VLDL)

Question 4

Lipid panel

Answer 4

-Total cholesterol is a calculated quantity (HDL+DLD+trig)

LDL= total - HDL - trig /5
Lipid panel is all of this present in blood

Question 5

HDL

Answer 5

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

Question 6

LDL

Answer 6

-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)

Question 7

LDL

norm fasting ranges
plaque formation is …

Answer 7

plaque formation is self propagating (increase risk CV disease)

LDL calculated

norm fasting ranges (100 or less) LESS better

Question 8

VLDL

Answer 8

-estimated as % of triglyceride value
-high levels associated with developing plaque deposits on artery walls

Question 9

Lipprotein A

Answer 9

-Independent rf for CAD
-above 50 = increased risk of CV disease

Question 10

Cholesterol ratios

Answer 10

Total/HDL
200/50= 4 or 4:1 ratio total to HDL

lower the ratio= lower risk of HD

recommend 5 or less

Question 11

Triglycerides

Answer 11

-glycerol molecule plus 3 fatty acids

-high levels in bloodstream have been linked to atherosclerosis and risk of HD and stroke

Question 12

Types triglycerides: sat

Answer 12

Sat fats: fat molecules no double bonds- saturated with hydrogen
-high levels in blood increase risk of HD and stroke

Question 13

Types triglycerides: unsat

Answer 13

Fat molecules where there are 1+ double bonds
-Monounsaturated (1 double bond0
-polyunsaturated
-low melting point- liquid at room temp

Question 14

CIS fatty acids

Answer 14

unsat
good
naturally occuring
cardioprotectant

Question 15

trans fatty acids

Answer 15

type of unsat fats
uncommon but common produced from vegetable fats
-increased intake associated with increased risk for CVD
not good

Question 16

Ranges triglyceride

Answer 16

Norm: <150
150-199 border
200-499 high
>500 very

mx by meds (statins) and lifestyle

Question 17

Patho CVD in DM

Answer 17

-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

Question 18

Characteristics of DM heart

Answer 18

-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

Question 19

Cardiac enzymes

Answer 19

-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

Question 20

Types of CPK

Answer 20

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)

Question 21

CPK after injury/insult

Answer 21

after injury/ MI :

rise: 4-6hrs
peak: 12-24hrs
remain elevated: 4-5 days

0-175 norm range

Question 22

Troponin

Answer 22

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

Question 23

Gold standard cardiac enzyme

Answer 23

CPK

troponin is also with muscle damage

Question 24

Myoglobin

Answer 24

-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

Question 25

Why is liver panel of interest post MI

Answer 25

when heart pump is limited- liver bloodflow is limited so liver starts to get damage liver and kidneys go ary first

Question 26

ANP

Answer 26

-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

Question 27

BNP

Answer 27

-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)

Question 28

BNP physio actions

Answer 28

pee out more salt (RAAS) these levels are increased in proportion to the amount of HF (increase HF= increase LVEDV)

Question 29

BNP values

Answer 29

norm: <100 >700 acute cardiac decomp 100-700 chronic compen

Question 30

NY Heart assoc levels of HF

Answer 30

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

Question 31

CRP

Answer 31

-produced in liver- increased in inflamm states (infec, CA, etc) higher number not heart issues 1-3 high risk heart

Question 32

serum creatone

Answer 32

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