Lab studies Flashcards

1
Q

Rfs for CHD (13)

A

-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

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2
Q

Cholesterol

A

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

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

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3
Q

Cholesterol

transport carrier molecule?
limited what

A

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

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4
Q

Lipid panel

A

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

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

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5
Q

HDL

A

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

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6
Q

LDL

A

-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)

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7
Q

LDL

norm fasting ranges
plaque formation is …

A

plaque formation is self propagating (increase risk CV disease)

LDL calculated

norm fasting ranges (100 or less) LESS better

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8
Q

VLDL

A

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

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9
Q

Lipprotein A

A

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

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10
Q

Cholesterol ratios

A

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

lower the ratio= lower risk of HD

recommend 5 or less

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11
Q

Triglycerides

A

-glycerol molecule plus 3 fatty acids

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

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12
Q

Types triglycerides: sat

A

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

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13
Q

Types triglycerides: unsat

A

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

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14
Q

CIS fatty acids

A

unsat
good
naturally occuring
cardioprotectant

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15
Q

trans fatty acids

A

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

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16
Q

Ranges triglyceride

A

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

mx by meds (statins) and lifestyle

17
Q

Patho CVD in DM

A

-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

18
Q

Characteristics of DM heart

A

-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

19
Q

Cardiac enzymes

A

-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

20
Q

Types of CPK

A

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)

21
Q

CPK after injury/insult

A

after injury/ MI :

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

0-175 norm range

22
Q

Troponin

A

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

23
Q

Gold standard cardiac enzyme

A

CPK

troponin is also with muscle damage

24
Q

Myoglobin

A

-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

25
Q

Why is liver panel of interest post MI

A

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

26
Q

ANP

A

-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

27
Q

BNP

A

-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)

28
Q

BNP physio actions

A

pee out more salt (RAAS)

these levels are increased in proportion to the amount of HF
(increase HF= increase LVEDV)

29
Q

BNP values

A

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

30
Q

NY Heart assoc levels of HF

A

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

31
Q

CRP

A

-produced in liver- increased in inflamm states (infec, CA, etc)

higher number not heart issues

1-3 high risk heart

32
Q

serum creatone

A

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