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Clinical Chem II spring > Cardiac Function > Flashcards

Cardiac Function Flashcards

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1
Q

CAD
CHF
CVD
ACS

A

CAD - coronary heart disease
CHF - congestive heart failure
CVD - cardiovascular disease
ACS - acute coronary disease

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2
Q

Describe cardiovascular disease briely

Types?
c
cb
pa
aa

A

leading cause of death

4types:
CHD
cerebrovascular disease
peripheral arterial disease
Aortic artherosclerotic disease

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3
Q

What are some ways CVD begins?

A

May begin at birth or childhood
congenital heart defect or rheumatic fever

some develop overtime into adult

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4
Q

CHD overview states
an
m
h

A

angio pectoris (chest pain)
myocardial infarction (MI)
heart failure

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5
Q

Cerebrovascular disease states

A

blood supply cut off from brain
stroke/trans ischemic attack (mini)

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6
Q

Peripheral arterial disease (PAD)

A

blockage in arteries
PAD/DVTs

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7
Q

Aortic artherosclerotic
a
d

A

aneurysms widening of artery
dissection - tears in aorta

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8
Q

Describe Artherosclerosis
chronic
accum of
veins?

A

chronic inflammation
accumulation of lipid material in arteries/veins
veins narrow and harden

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9
Q

Describe Ischemia

A

lack of blood flow
localized in heart 1/3rd of deaths
can see in early as age 10

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10
Q

Describe the damage of endothelial walls in artherosclerosis
t
pl
oc/th/ru

A

turbulent blood flow
plaque formation in cycle/vessle
occlusions/thrombosis/ruptures/ combos

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11
Q

most common locations of artherosclerosis
plad
plmc
erca

A

prox. left anterior decending
prox. left main coronary
entire right coronary artery

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12
Q

When is artherosclerosis symptomatic?

A

with 75% plaque formation

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13
Q

Lack of blood supply in heart leads to?

A

ischemia

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14
Q

Classic masnifestation of cardiac ischemia/angina/HA
a
s
rad
inc

A

angina
squeezing of chest/pressure
radiates to left shoulder/neck/arm
increases in intensity

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15
Q

non classical manifestation of cardiac ischemia

A

more common in women
nausea/short breath/stabbing pain

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16
Q

Do normal ECGs rule out presents of ACS?

A

no

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17
Q

Eval of chest pain
physical exam:

chest xray

A

physical. exam: high BP cardiac valv disease
ECG chest xray

Chest xray - non cardiac source

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18
Q

Initial markers of cardiac damage explained

cell death releases..

r
s
d

A

cell death releases intracellular proteins from myocardium into circulation

1.) released rapidly/steady
2.) several day persistance
3.) detected at low levels

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19
Q

T/F if STEMI is an issue, do the EKG within 10 min

A

true

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20
Q

First cardiac markers
a/l
ck

A

AST/LD (non specific)

creatinine kinase in nearly all cells

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21
Q

CK isoenzymes

whats most reliable indicator of MI?

A

CK MB most reliable

CK-MM muscle

CK-BB brain

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22
Q

What other disease states can CK-MB be elevated in?

A

can be elevated in chronic muscle disease, end stage renal and intense excersise

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23
Q

What do troponin levels look like if the myocardium is undamaged?

A

normal

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24
Q

Cardiac troponins
complex of…

TnT
TnI
TnC

A

complex of 3 proteins, transmit calcium signals to contract muscles

TnT - binds to tropomycin
TnI - inhibits binding of actin/myosin
TnC - binds to calcium to reverse TnI

25
Q

Briefly describe tissue specific isoforms

A

slow/fast cardiac muscles

26
Q

CTnc
same..

A

same isoform for both slow twitch (T2) and cardiac

27
Q

CTnI-CTnT
unique

A

unique isoforms in fast twitch/slow and cardiac

28
Q

T/F each isoform is encoded in separate genes

A

true

29
Q

What is CTnI specific forc
detection of …. in
how many hours after onset? lasts?

widest window for detection post..
high?

A

cardiac injury
detection of myocardial cell injury acute ischemia/myocard

3-12 hr after onset/for weeks

widest window for detection post MI and high sensitivity/specificity

30
Q

Specificity/sensitiv of troponin
what kind of release?

A

slow release may not be detected when pt presents with early pain

rise and fall of troponin indicate AMI

31
Q

HS-CTn
confirms….at low []
discerns …associated with

A

can confirm myocardial injury at low concentration
discern small changes in {} delta values associated w probability of risks

32
Q

Challenges of troponin
chronic un
single rule

other diseases
unstb
struct
arth

A

chronic unhealthy people w chest pain
single rule out value due to high sensitivity
procedures and other diseases :
unstable angina
struct HD
arhterosclerosis

33
Q

Pts with kidney disease

prognosis in CKD increases? predicts?

dialysis elevation of? increases?

hemodyalisis involves filt?

A

prognosis in CKD increase troponin levels predict worse long term cardiac issues

dialysis elev in CTnT increase mortality

hemodylsis involves filt of blood of toxins diff concent of enzymes

34
Q

Myoglobin
what type of binding
released?
spcificity/half life?
used with?

A

iron oxy bind in muscles
small protein released when muscles damages
not specific short half life
used along w CK-MB and troponin

35
Q

HS-Tn can detect before?

A

myoglobin

36
Q

Cardiac injury
occurs in?
what happens?
cells removed by?
when energy fails?

reperfusion transfusions?

A

occurs in MI = cell death
apoptosis or necrosis
apoptic cells removed by macrophages - requires energy
(necorsis when enrgy fails)

Reperfusion transfusions: intravasc baloons, CABG/chem thrombosis

37
Q

Biomarkers in heart failure

descirbe heart failure

manifestations

A

heart failure: pathological condition when heart fails to inadequatly supply metabolic needs of body, decreases pumping

manifest:
retention of fluids, shortness of breath, lower extremity edema

38
Q

Reccommendations of heart failure markers

A

CTnI, CTnT, excersise stress test, X-ray

39
Q

Diagnosis and risk stratification of heart failure

most common presence of heart failure sympt?

what distinguishes cardiac vs non cardiac dspnea

what is secreted in response to inc pressure/load on heart?

A

shortness of breath most common presense of heart failure - very non specific

BNP or precursor NT-proBNP cardiac/non cardiac dyspnea

naturetic peptides secret from heart in response to incr pressure/volume load

40
Q

Reducing intravasc volume steps
promote n/d/v
inhibit sns

A

promote natr/diu/vasodilation
inhibit sympathetic nervous system signalling

41
Q

BNP/NT-ProBNP
released from ….. in response to

in what kind of pts

predicts?

A

released from myocardial cells in response to incr vol/incr pressure/hypertrophy

Both in pts with ventricular dysfunction

strong predic mortality

42
Q

BNP/NT-ProBNP continued
what is the same?
optimal?
what is being persued as target?

A

sensit/spec are same - optimal cut off vals
BNP being persued as target by manufacutures

43
Q

Cardiac troponins
diagnosis of
who else has elevations
ongoing..
impaired?

A

diagn of Myocardial injury
heart failure pts have elev as well as ongoing cell death
impaired liver

44
Q

Detection of heart failure

A

not diagnostic, stratify risk/prognosis
concomintant elev in multiple markers associated w esclating risk of effects

45
Q

Is CTnI or CTnT more common in heart failure

A

CTnI

46
Q

markers of CHD and plaque instability
m/c indicate presnce of…
predict
provide progn from…

A

MPO and CRP may indicate presence of inflam to predict mortality and provide progn from clinical risk and Hs-CTnT

47
Q

MPO
increased in …a/c

A

released when neuts gather in blood vessles
increased in ACS and chronic CAD

48
Q

CRP

A

marker of inflammation
HS-CRP progn marker of artherosclerosis/CHD
<1mg normally

49
Q

Lipoprotein A
predicts prem..

A

predict premature cardiovasc disease

50
Q

Homocystine
what kind of AA
how many forms?
total plasma HC refers to?
normal levels?
linked with?
inc risk with

A

sulfur containing AA
4 forms
total plasma HC refers to all 4 forms
norm 5-15
linked w high levels and CVD
inc risk with elevation

51
Q

hyperhomocystemia risk factor of?

inc 5 mol =

A

CVD
<40% pts w CVD have hyperhomo

increase 5mol = HD inc 20-30%

52
Q

Pulmonary embolism
embolous
puml embolism
extent?

A

embolous - mass of solid/liq/gas

pulm embolous: high risk lodged in pulm arteries impares flow

size and location affect extent

53
Q

Saddle emboli
lodged at bif…
inc h
inc incidence w
whos at higher risk?

A

lodged at bifuracation of main artery, blocks pulm blood flow
increase heart failure
incidence inc w age
women at higher risk

54
Q

Use of D dimer
when pretest prob…
cross
indicated coag..
high

A

when pretest prob of PE is low
cross linked fibrin
indicates coag indirect marker/fibrinolysis
high sensitivty/quant

55
Q

Abn levels of D dimer

A

90% of pts with PE

pts w normal levels rule out PE

56
Q

Troponin and PE
progn val w
short term?
clinic
agr

A

progn val w PE
short term mortality
clinical management
agression

57
Q

BNP with PE
evals …
neg pred values?
IDs pts with…

A

elev vals inc short term mortality
94% neg pred values
ID pts w acute PE and high risk adverse outcomes

58
Q

CHD w PE
common?
can cause?

A

uncommon substantial mortality
arhterosclerosis
can cause ischemia

Clinical Chem II spring (16 decks)

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