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Lab Dx 2 > week 8- Cardiac markers & Thyroid > Flashcards

week 8- Cardiac markers & Thyroid Flashcards

1
Q

• What are the novel cardiac biomarkers?

A

o Lp (a)
o Homocysteine
o hsCRP

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2
Q

• what is Lp(a)?

A

o Independent risk factor for CHD
o = “LDL like” Lp + glycoprotien (a) (Apo(a) structurally like plasminogen, w/o fibinolytic activity)
o role in initiation, progression and possible rupture of atheromatous plaque
o Competes w plasminogen particle and inhibits thrombolytic activity
o inhibits NOS

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3
Q

• what are risks of elevated Lp(a)?

A

o ↑ incidence CHD < 50 or > 70
o Mid-age F, >30 mg/dL assoc w 2x risk CHD
o W ↑ LDL-C →risk of angina
o Assoc w development of first MI in men

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4
Q

• What can increase Lp(a) levels?

A

o ↑ production (liver) in nephrotic syndrome

o ↓ clearance in dialysis pts

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5
Q

• What are indications of getting Lp(a) measured?

A

o premature atherosclerosis or FHx
o ↑ LDL & other risk factors
o Not recommended for first line screening

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6
Q

• What are normal and critical Lp(a) levels? Caveat?

A 
o	Optimal: < 20 mg/dl
o	Borderline High Risk: 20 – 30
o	High Risk: 31 – 50
o	Very High Risk: > 50
o	But half of all MIs occur in ppl w normal plasma lipid levels → atherosclerosis mb an inflammatory dz → so we have additional CAD risk factor biomarkers
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7
Q

• Why is hsCRP used as a CVD biomarker?

A

o Inflammation is a risk factor of CVD →cytokines in blood, assoc w risk
o = “acute phase reactant”, ↑ w inflammation from any cause
o predictive value of hsCRP is significantly higher than total cholesterol, HDL, LDL, Lp(a), and homocysteine
o = best marker dt long half life and stability
o tx inflammation → ↓CRP, representing ↓ cardiovascular risk.
o Detectable to 0.01 mg/dL (vs regular CRP)

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8
Q

• What may CRP levels indicate?

A

o > 1.5 mg/dl (RR: 0-3) = acute inflammatory response

o >10 often dt bacterial infx

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9
Q

• What is the role of CRP in atherogenesis?

A

o Unknown causative role
o present in the atherosclerotic lesion, may actively contribute to progression and/or instability of atherosclerotic plaque.

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10
Q

• What is homocysteine?

A

o Intermediary amino acid in methionine → cysteine
o Mod ↑ in 5-7% pop
o independent risk factor for development of atherosclerotic vascular disease/CVD and venous thrombosis (but less important than classic factors)
o Can result from genetic defects, drugs, vitamin deficiencies, smoking

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11
Q

• How is homocysteine directly involved in vascular injury?

A

o Cytotoxic effect on endothelial cells →damage arterial wall →lipids accumulate →plaque
o Produces ROS → LDL oxidation
o Smooth muscle hypertrophy

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12
Q

• Who should be screened for homocysteine? How? How are hi levels treated?

A

o Screening recommended w premature CVD (or unexplained DVT) and absence of other risk factors
o Use plasma from lavender tube (EDTA)
o Tx: folate, B6, B12 supplements (required in homocysteine metabolism)

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13
Q

• What are normal and critical homocysteine levels?

A 
o	Normal: 4 –17 umol/L
o	Desirable: < 10
o	borderline hi: 12-15
o	mod: 16-30
o	high: 31-100
o	very high: > 100
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14
Q

• What are inherited and acquired causes of ↑ homocysteine?

A

o I: Cystathione b-synthase def, MTHFR def or defect (in at least 43% pop), Methionine synthase defect, B12 transport defect, B12 coenzyme synthesis defect
o A: B6 B12 or folate def, Chronic dz, CRF, Hypothyroidism, Psoriasis, Malignancies, ALL, Anticonvulsants, methotrexate

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15
Q

• What are tests for determining cardiac damage?

A 
o	CK: Total Creatine Kinase
o	CK-MB: Isoenzyme of CK, myocardial-bound
o	cTnT: Cardiac Troponin T
o	cTnI: Cardiac Troponin I
o	Myoglobin 
o	AST, LDH
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16
Q

• What are cardiac markers?

A

o Located in myocardium
o Released in cardiac injury: MI, Non-Q-wave infarction, Unstable angina, Others (trauma, cardiac surgery, myocarditis etc)
o measured in blood

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17
Q

• what info can cardiac markers provide?

A

o Rule in/out acute MI
o Confirm old MI (several days)
o Monitor success of thrombolytic tx
o Risks stratification of unstable angina (if healthy, done by assess of cardiac risk factors, not markers)

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18
Q

• What determines the rate at which cardiac markers are released?

A

o Size and subcellular distribution

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19
Q

• What happens in MI that causes release of cardiac markers?

A

o Coronary artery occlusion →myocardial ischemia →anoxia →ATP pump fails, leak ions, eg K, PO4
o →lack of collateral blood flow → metabolites accumulate, leak, eg lactate, Ado
o →reversible damage → membrane damage, leak myocardial markers (enzymes, proteins)
o →irreversible damage, cell death, necrosis

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20
Q

• What are the average detection, peak, and disappearance times of cardiac markers after MI?

A 
o	Myoglobin: 1-4 h, 6-7 h, 24 h
o	CK-MB mass: 3-12 h, 12-18 h, 2-3 d
o	Total CK: 4-8 h, 12-30 h, 3-4 d
o	cTnT: 4-12 h, 12-48 h, 5-15 d
o	cTnI: 4-12 h, 12-24 h, 5-7 d
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21
Q

• what is creatine kinase (total CK)? Normal ranges?

A

o Enzyme, catalyzes ATP + creatine → ADP + phosphocreatine
o Isoenzymes in heart muscle, skeletal muscle, brain
o ↑ within 4-6 hs of acute MI, peak 18 hrs
o Returns to normal in 2-3 days
o M: 38-175 U/L
o F: 26-140

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22
Q

• What can cause ↑ CK?

A 
o	MI
o	Progressive MD
o	Dermatomyositis & polymyositis
o	Muscle trauma: Rhabdomyolysis or Myocarditis 
o	Acute cerebrovascular dz, Brain trauma
o	Surgery
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23
Q

• What are the CK isoenzyme tests that can ↑ specificity? Normal ranges?

A

o CK-BB: brain, 0%
o CK-MB: heart, st skeletal muscle, 0-6% (this one used for possible MI)
o CK-MM: skeletal & cardiac muscle, 94-100%

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24
Q

• When does CK-MB increase?

A

o 4-6 hrs post-MI, peak 12-24 hrs, normalize 24-48 hrs

o Also ↑ in: Myocardial ischemia, Muscular dystrophy, Muscle trauma, Myocarditis

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25
Q

• What are the new generation cardiac markers?

A

o Myoglobin: earliest marker, not cardio-specific, hi sensitivity
o Troponins: similar times as CK, cardio specific, hi specificity

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26
Q

• What is myoglobin? Range?

A

o The oxygen-binding protein in cardiac and skeletal muscle
o 1 heme, 1 globin
o Normal Range: 5-70 ng/ml

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27
Q

• Why is myoglobin used as cardiac marker? Caveat?

A

o early detection of MI. ↑ 2 hours post-MI. in all pts 6-10 hrs after chest pain, peak 6-9 hrs. normalize in 12-24 hrs (short half-life in plasma)
o 95% specificity for AMI if collected within 1-2 hrs
o Excellent NEGATIVE predictor of myocardial injury
o 2 samples 2-4 hrs apart with no rise in levels virtually excludes AMI
o Lo specificity b/c also from damaged skeletal mm

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28
Q

• What can cause ↑ myoglobin?

A 
o	MI
o	Muscle trauma
o	Rhabdomyolysis
o	Progressive muscular dystrophy
o	Myositis
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29
Q

• What are cardiac troponins? 3 forms?

A

o regulatory proteins on cardiac & skeletal muscle.
o Hi sensitivity and specificity for MI
o cTnT binds troponin complex to “T”ropomyosin
o cTnI “I”nhibits actin in absence of Ca2+
o cTnC binds “C”a2+

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30
Q

• when does cTnT increase? Range?

A

o 4 hrs post-MI
o Peaks 12-24 hrs (or 2-5 d, references vary)
o Normalize in 7-10 d
o Normal Range: < 0.2 ng/ml
o Problem w specificity: may also ↑ in renal failure, polymyositis, muscular dystrophy, and extensive rhabdomyolysis

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31
Q

• when does cTnI increase? Range?

A

o 4 hrs post-MI
o Peaks 12-24 hrs
o Normalize in 4-10 d
o Normal Range: < 0.35 ng/ml
o more specific to cardiac damage than cTnT
o not affected by rhabdomyolysis or skeletal muscle injury

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32
Q

• why is AST used as cardiac marker?

A

o determine timing and extent of a recent MI
o high concentrations in liver, heart muscle, kidneys, etc.
o ↑ 6-10 hrs post-MI
o Peak at 24-48 hrs
o Normalizes in 4-6 d
o 2nd rise in AST suggests extension of myocardial injury or recurrence of MI
o should do serial AST for post-MI status

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33
Q

• what is LDH? Ranges?

A

o Lactate dehydrogenase
o Catalyzes lactate ↔ pyruvate
o in most tissues: heart, kidneys, RBCs, RE system, lungs, pancreas, liver, skeletal muscle
o LD1 & LD2 predominates in heart and red cells
o Adults: 45-90 U/L
o Kids: 60-170

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34
Q

• what are the 5 isoenzymes of LDH?

A 
o	LDH1 (4H): Heart, RBCs, Kidney
o	2 (3H1M): RE system (most), heart, some lung
o	3 2H2M): Lung, pancreas, spleen & placenta
o	4 (1H3M): Liver, skeletal muscle, pancreas & placenta
o	5 (4M): Liver & skeletal muscle
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35
Q

• why is LDH used as cardiac marker?

A

o ↑ later than CK-Mb and Ck= good for delayed diagnosis
o Peaks at 48 h
o Remains ↑ for 5-6 d
o non-specific marker of tissue injury: ↑ in liver, lung, kidney, other dzs
o “LDH flip”: normally LDH1 < LDH2; LDH1 > LDH2 post MI

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36
Q

• What factors can interfere with LDH levels?

A

o ↑ w Hemolysis
o Strenuous exercise may ↑
o Drugs

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37
Q

• MB, MM; 1 > 2, both hi

A

o MI

o Could range 12-48 hrs post

38
Q

• MB, MM; 1 = 2, slightly hi

A

o MI

o Several hrs post

39
Q

• BB, MB, MM, 1>2

A

o Control to ensure test works

40
Q

• MM; hi 5

A

o Liver dz

41
Q

• MB, MM; 1>2, hi 5

A

o MI , AND:

o liver congestion OR crushing mm injury

42
Q

• lo MM; 1<2

A

o normal

43
Q

• what are the detectable, peak, and duration times of the CK, AST, LDH1/2, and troponin levels post MI?

A 
o	CK-MB: 3-10 h, 12-24 h, 1.5-3 d
o	Total CK: 5-12 h, 18-30 h, 2-5 d
o	AST: 6-12 h, 20-30 h, 2-6 d
o	LDH: 8-16 h, 30-48 h, 5-14 d
o	Cardiac troponins: 4-6 h, 12-24 h, up to 10 d
44
Q

• What is the typical ER testing on pts w chest pain?

A

o CK, CK-MB, cTnI, CBC, CMP
o PT, PTT: done prior to administration of streptokinase or TPA to dissolve the clot
o Typically, “serial testing” is done: CK, CK-MB, and cTnI are ordered on admission, repeated in 3 hrs, and in 12-24 hrs. Some MDs order them at 8-hr intervals

45
Q

• What are the functions of thyroid hormones?

A

o Metabolism: ↑ sensitivity to catecholamines, ↑ BMR, ↑ metabolism of carbs, protein, lipid
o Normal growth: ↑bone turnover
o Normal development: esp CNS (fetal brain and skeletal maturation)
o Endo: ↑ in serum glucose, ↓ cholesterol
o CV: Inotropic and chronotropic effects on heart (↑ HR, CO)
o Reproduction
o CNS: Normal brain development, regulation of synaptogenesis, neuronal integration, myelination, cell migration
o GI: Stimulates gut motility

46
Q

• What are ssx of hypothyroid?

A 
o	↓ rate of oxidative energy-releasing rxns in cells  
o	puffy skin, sluggishness, ↓ vitality, wt gain, ↓libido, cold intolerance, muscle pain and spasm, insomnia, brittle nails 
o	kids (cretinism): mental 	retardation, dwarfism, permanent sexual immaturity
47
Q

• what are ssx of hyperthyroid?

A

o abn hi body temp, profuse sweating, ↑ BP, wt loss, irritability, muscular pain and weakness
o exopthalmia: characteristic, eyeballs protrude from skull

48
Q

• what is thyroid releasing hormone, TRH?

A

o Made in Hypothalamus, circadian release → thru portal venous system to Pituitary
o Stimulates production and release of thyrotropin (TSH)
o Downregulated by T4

49
Q

• What is thyroid stimulating hormone, TSH?

A

o = major modulator of thyroid gland activity!!
o Glycoprotein, made in Anterior Pituitary → thru portal venous system to cavernous sinus, body
o Stimulates several processes: Synthesis and release of T3, T4; Growth of thyroid gland
o Upregulated by TRH
o Downregulated by T4, T3

50
Q

• Anatomy of thyroid gland:

A

o Gland consists of sacs of thyroid follicles
o Follicular epithelium produces thyroid hormones (T3/T4)
o Follicle interior contains colloid: protein rich fluid, Thyroglobulin
o bw follicles = parafollicular cells, produce hormone Calcitonin

51
Q

• what are functions of thyroid cells?

A

o Collect and transport iodine
o Make Tg, secrete into colloid
o Remove thyroid hormones from Tg, secrete into ciculation

52
Q

• How does iodine get to thyroid for hormone synthesis?

A

o Thyroxine requires iodine, absorbed from GI as iodide from food, water, meds
o Na-I ATPase concentrates I- in thyroid cells, excess secreted in urine
o Colloid: Thyroid peroxidases (TPO) oxidize Iodide to Iodine
o Thyroid/plasma concentration ratio for iodide ranges from 25:1 to 500:1.

53
Q

• How are thyroid hormones made in the colloid?

A

o Tyrosine incorporates iodine: monoiodotyrosine (MIT)
o Adds 2nd I: diiodotyrosine (DIT)
o Two DIT w Tg form L-thyroxine (T4)
o DIT & MIT w Tg form (T3) Triiodothyronine
o Tg T4:T3 ratio = 5:1
o T4 (thyroxine) is the primary hormone released into circulation.
o Large proportion of T3 is formed in liver by conversion of T4 to T3

54
Q

• What happens to T3 and T4 once in blood? Negative feedback?

A

o 98.5% T4, 1.5% T3 (greater bio acivity)
o Usu bound to proteins: thyroid binding globulin 70%, albumin 15%, transthyretin 10%
o Biologically active hormones, able to cross cell membranes into target tissues
o ↑levels → negative feedback to Hypothalamus → ↓TRH from pituitary
o → ↓TSH → ↓ production of T3 & T4 by thyroid gland

55
Q

• What are the protein carriers of thyroid hormones?

A

o <1% hormones circulate in free form (biological activity)
o = reservoir to replace free hormone fractions that have been utilized
o TBG (thyroxine binding globulin), highest binding affinity, 70% of T3 and T4
o TBPA (thyroxine-binding pre-albumin), lower affinity, 20% T4, NO T3
o Albumin, low affinity, 10% T4, 30% T3

56
Q

• What can affect the amount of thyroid hormone bound to carrier proteins?

A

o ↑TBG: ↑estrogen (preg, OCP, HRT, Tamoxifen), Liver dz (early)
o ↓TBG: Androgens or anabolic steroids, Liver dz (late)
o Binding Site Competition: NSAIDs, Furosemide IV, Anticonvulsants (Phenytoin, Carbamazepine)

57
Q

• How is T4 converted to T3? How do they affect target cells?

A

o Mainly in liver & skeletal muscle
o → bind to receptors in nucleus, stimulate DNA directed RNA synthesis
o Binding avidity of nuclear receptor is 10X greater for T3 than T4
o Biological potency of T3 much greater than T4

58
Q

• How are thyroid hormones degraded?

A

o T4 → T3 (active)
o T4 → rT3 (inactive), but measured by serum tests
o T3 → rT2 (inactive)
o All by 5’ deiodinase

59
Q

• What is the best assessment of the integrity of H-P-T axis?

A

o TSH, dt improvements in assays

60
Q

• What is RAIU?

A

o Radio Active Iodine Uptake
o measures iodine uptake by thyroid from extracellular pool, in a given time
o Useful in indicating hyperthyroid states

61
Q

• When are Tg levels increased?

A

o 10% normal

o 15-30% CA pts, best for follow-up on cancer after thyroidectomy

62
Q

• What is the significance of Total T3, T4?

A

o =bound + unbound levels

o majority is bound, so no direct correlation w metabolic state

63
Q

• what are the 3 types of hypothyroidism?

A

o Primary: dysfunction in thyroid gland
o Secondary: dysfunction in pituitary gland
o Tertiary: dysfunction in hypothalamus

64
Q

• What is the use of TSH to dx thyroid problems?

A

o single best test to screen for abn function of thyroid gland
o differentiate 1, 2, 3 hypothyroid
o Low T3 and T4 (mainly) stimulate secretion of TRH → TSH increase

65
Q

• What are TSH levels in different thyroid problems?

A

o 1 hypo: ↑ TSH (attenmpting to stimulate thyroid)

o 1 hyper: ↓ (neg feedback from T3 and T4)

66
Q

• How do you differentiate 1, 2, 3 hypothyroid?

A

o 2, 3: see pituitary or hypothalamus failure
o Plasma levels of TRH & TSH near zero despite stimulation of glands by low thyroid hormone levels
o ↓ T4, ↑TSH = thyroid problem
o ↓T4, ↓TSH = pituitary or hypothalamic problem

67
Q

• How are TSH levels regulated?

A

o Mainly T4 & T3 levels via feedback inhibition

o diurnal variation: basal levels 10am, highest 10pm (2-3X basal)

68
Q

• what are normal TSH levels? In hypo?

A

o Adult: 0.3-4.0 mU/ml
o Newborn: 1.3-19
o ND optimal: 0.5-2.0 (most ppl)
o maximum level of 2 mU/ml as cut off for hypothyroid

69
Q

• what can interfere with TSH levels?

A

o Recent radioisotope administration
o Severe illness may ↓
o Diurnal variation
o Drugs

70
Q

• What causes ↑, ↓ TSH?

A

o ↑: 1 hypo, Thyroid agenesis, Congenital cretinism, Excess iodine intake, Thyroid ablation
o ↓: 2, 3 hypo, Hyperthyroidism, Self medication w T4

71
Q

• What are dx’s with ↑ TSH, based on fT4?

A

o ↓: hypothyroid
o N: subclinical hypo
o ↑: thyroid resistance, pituitary tumor

72
Q

• What are dx’s with ↓ TSH, based on fT4?

A

o ↓: NTI or drugs
o ↑: hyperthyroid
o N: test total T3

73
Q

• ↓TSH, normal fT4, based on tT3?

A

o ↓/N: subclinical hyper

o ↑: T3 thyrotoxicosis

74
Q

• What are the different glycoforms of TSH?

A

o Base: n-acetylglucosamine, galactose, mannose
o Major pituitary: SO4 binds n-acetylgalactosamine, also fucose
o Hypothyroid: sialic acid binds, extra branches

75
Q

• What is the TRH stimulation test?

A

o ddx of hypothyroidism
o Assess responsiveness of anterior pituitary via secretion of TSH after IV injection of TRH
o 1: TSH ↑ 2-3X N
o 2: no TSH response
o 3: delayed ↑ TSH, or need multiple injections of TRH to ↑ TSH

76
Q

• What is T4, thyroxine?

A

o >90% of thyroid hormones
o 99.98% is protein bound to TBG & albumin
o 0.02% is unbound or free
o Serum T4 measures Total T4 (bound and free)
o ↑ = hyperthyroidism
o ↓ = hypothyroidism

77
Q

• What problems are associated with abn T4?

A

o Newborns screened for T4 to detect hypothyroidism
o neonatal hypothyroidism → mental retardation
o Cretinism: infants & children, dt lack of thyroid hormone

78
Q

• What can interfere with T4 levels?

A

o ↑ after iodinated X-ray contrast
o Preg: ↑ dt ↑ TBG
o Drugs

79
Q

• What are normal and critical T4 levels?

A 
o	Adult M: 4-12 ug/mL
o	Adult F: 5-12
o	>60: 5-11
o	Children/infants: great variability
o	Critical: < 2.0  myxedema coma; > 20  thyroid storm
80
Q

• What causes ↑ and ↓ T4?

A

o ↑: 1 hyper, Acute thyroiditis, Self-administered T4, Struma ovarii, ↑ TBG, Familial dysalbuminemic hyperthyroxinemia
o ↓: 1, 2, 3 hypo, Protein malnutrition, Iodine insufficiency, Drugs (Aspirin, Dilantin)

81
Q

• What is Familial dysalbuminemic hyperthyroxinemia?

A 
o	AD
o	Abn albumin, binds too much T4
o	↑ total T4, but normal free T4
o	Thus need to do both tests to r/o hyperthyroid
o	No tx required
82
Q

• What is the relationship bw T4 and TBG?

A

o T4 ↑ w ↑ TBG
o ↑ TBG: preg, OCPs → total T4 inc (false T4 elev), but FREE T4 is normal
o TBG & pre/ALB routinely measured at same time for test interpretation

83
Q

• What is T3RU?

A

o T3 resin uptake
o Indirect measure of unsaturated thyroid binding sites on TBG and TBPA
o not a measurement of T3
o Also an indirect measurement of T4
o Free labeled T3 binds to partially saturated TBG w T4
o →T3 antibodies bind all free T3
o → TBG w bound T4 and labeled T3 is isolated

84
Q

• What do T3RU values mean?

A

o ↑= ↑T4, hyperthyroidism
o ↓=↓T4, hypo
o If tT3 or tT4 go one direction, and T3RU in other = dt changes in binding capacity (secondary), not a true thyroid dysfuntion
o Ex: if binding capacity ↑ dt ↑ estrogens, labeled fT3 will ↓ → ↓T3RU

85
Q

• What is normal T3RU? Interfering factors?

A

o 25-35% resin uptake
o Recent radioisotope scans using labeled T3
o Drugs
o mostly obsolete dt ability to test for fT3, T4

86
Q

• what can cause ↑ and ↓ T3RU?

A

o ↑: Hyperthyroidism, Hypoproteinemia, Nonthyroid illnesses, Self-administer T4, Struma ovarii, Familial dysalbuminemic hyperthyroxinemia
o ↓: ↑ TBG (preg, hyperproteinemia), Hypothyroid, Hepatitis and cirrhosis

87
Q

• What is the free thyroxine index, FTI?

A

o Corrects for changes in thyroid binding proteins that affect T4 levels
o Help dx hyper and hypothyroidism
o indirect (calculated) estimate of tT4
o FTI = (T4)(T3RU)/100

88
Q

• What causes ↑ and ↓ FTI?

A

o ↑: Primary hyperthyroid, Acute thyroiditis, Self-administer T4, Struma ovarii
o ↓: Hypothyroid, Pituitary insufficiency, hypothalamic failure, Iodine deficiency

89
Q

• What is total T3 (by RIA, radio immunoassay)?

A

o To dx hyperthyroidism
o T3 toxicosis= Rare form of hyperthyroidism with normal T4 and ↑ T3
o Total = bound + unbound T3
o monitor thyroid replacement and suppressive tx
o not to dx hypo: usu normal, Severe non-thyroid dz decreases T3, Overlap bw hypothyroid and euthyroid levels

90
Q

• what is clinical significance of free T4 and T3?

A

o be most reliable tests to confirm hyper/hypothyroidism
o eval thyroid fxn w protein abnormalities that affect total hormone measurement
o 0.02 – 0.03% T4, ~0.3% T3, is unbound “free” and metabolically active

91
Q

• What is rT3 (reverse T3)?

A

o Usu ↑ in hypothyroidism
o help dx “sick thyroid” pts (who are euthyroid) from true hypothyroid cases
o in a body under stress (illness, fasting, high cortisol) T4 is deiodinized to rT3 instead of T3
o (“step down”, instead of “step up”)= (-) charge in diff spot
o Metabolic enzyme function ↓ → Stresses inhibit 5’-deiodinase → ↓ T4 to T3, ↑ rT3
o Sxs of Wilson’s (temp) syndrome: hypothyroid, ↑rT3, corrected by giving T3. (Not accepted by the mainstream.)

Lab Dx 2 (8 decks)

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