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Lab Dx 2 > week 5- blood chemistry > Flashcards

week 5- blood chemistry Flashcards

1
Q

What are normal and critical K values?

A 
o	Adult/Elderly: 3.5 – 5.2 mEq/L
o	Optimum: 4.0-4.5 
o	Child: 3.4 - 4.7 
o	Infants (7 d– 1 yr): 4.1-5.3 
o	Neonates (0-7 d): 3.7 - 5.9 
o	Critical Values: < 2.5; > 6.5 to 8.0 (depends on lab, text)
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2
Q

• What factors can interfere with K values?

A

o Hemolysis releases K+ from RBCs → ↑
o Cells sitting in serum, separate, → leakage of K+ from RBCs → ↑
o “Pumping” hand prior to venipuncture ↑ K+ (esp w tourniquet)

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3
Q

• What pts should have K monitored? Why?

A

o serious illness
o diuretics or heart medications
o Minor changes in serum concentration → major physiological consequences

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4
Q

• What can cause hyperkalemia? Value?

A 
o	Serum K+ > 5.5 mEq / L
o	renal dz
o	Massive cellular trauma
o	Insulin def
o	Addison’s dz 
o	K sparing diuretics
o	↓ blood pH
o	Exercise causes K+ to move out of cells
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5
Q

• What are clinical manifestations of hyperkalemia?

A

o Early: hypertonicity, paresthesia
o Late: Muscle weakness, flaccid paralysis
o Change in ECG pattern
o Dysrhythmias
o Bradycardia, heart block, cardiac arrest

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6
Q

• What can cause hypokalemia? Value?

A

o Serum K+ < 3.5 mEq /L
o DM: Insulin gets K+ into cell
o Ketoacidosis: H+ replaces K+ → lost in urine
o Β-adrenergic drugs, epi
o Decreased intake
o Increased K+ loss: chronic diuretics, acid/base imbalance, trauma and stress, ↑aldosterone, redistribution between ICF and ECF

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7
Q

• What are clinical manifestations of hypokalemia?

A 
o	Neuromuscular dos: weakness, flaccid paralysis, respiratory arrest, constipation
o	Dysrhythmias, U wave
o	Postural hypotension
o	Cardiac arrest
o	Glucose intolerance
o	Renal damage
o	↑ BP in both normo and hypertensive
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8
Q

• What is work-up for hypo- and hyper-kalemia?

A

o Hypo: urine K, BP, aldosterone, plasma HCO3, renin

o Hyper: GFR, renal K excretion, aldosterone, renin

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9
Q

• What is Calcium’s role in body?

A

o 99% stored in bone and teeth, 1% ECF; very stable levels
o Nerve transmission, bone formation, enzymes (+P, Mg)
o 50% in serum is ionized, rest bound to protein (albumin) or salts
o Only ionized (=active form) for cardiac function, clotting, muscular contraction, nerve impulse transmission

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10
Q

• What are 3 main mechanisms of Ca2+ homeostasis? Other factors?

A

o PTH ↑ mobilization from bone (PTH inhibited by hypercalcemia)
o PTH ↑ renal reabsorption
o Active vit D ↑ absorption from intestines
o Calcitonin: from thyroid, bone formation, ↑ renal excretion
o Also: estrogens, androgens, blood pH
o Inverse relationship bw serum Ca2+ and P

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11
Q

• What are normal and critical Ca values?

A

o Adult: 8.8 - 10.4 mg/dl
o Child: Varies with age
o Optimum: 9.2 – 10.0
o Critical: < 7.0

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12
Q

• What causes hypercalcemia?

A 
o	Hyperparathyroidism 
o	Hypothyroid 
o	Renal dz
o	Excessive intake of vit D
o	Milk-alkali syndrome
o	drugs
o	Malignant tumors (products promote bone breakdown, in bone causes Ca leech)
o	Hypophosphatemia
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13
Q

• What are ssx of hypercalcemia?

A 
o	Nonspecific: fatigue, weakness, lethargy
o	↑ kidney and pancreatic stones
o	Muscle cramps
o	Bradycardia, cardiac arrest
o	Pain
o	GI activity 
o	Nausea, abdominal cramps
o	Diarrhea, constipation
o	Metastatic calcification
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14
Q

• What is work-up for hypercalcemia?

A

o CMP, vit D, PTH, TSH, ESR

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15
Q

• What are ssx of hypocalcemia?

A 
o	Hyperactive neuromuscular reflexes and tetany
o	Convulsions (severe)
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16
Q

• What causes hypocalcemia?

A

o Renal failure
o ↓ vitamin D
o ↓ parathyroid function
o ↑ calcitonin
o Malabsorption states
o Abnormal intestinal acidity and acid/ base balance
o Widespread infection or peritoneal inflammation

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17
Q

• What is the ionized calcium test?

A

o must be ordered specifically and separately
o NOT affected by serum albumin levels
o Mb more specific indicator of hyperparathyroidism than total __??
o For open heart and organ transplant surgeries

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18
Q

• What is magnesium’s role in the body?

A

o 50% in bone, 50% in cells of tissues/organs, 1% in blood (constant)
o Regulate blood sugar, normal BP, energy metabolism , protein synthesis
o Escreted in kidney
o >300 biochemical rxns
o Normal muscle/nerve fxn, heart rhythm, immune system, bones strong

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19
Q

• What is the Mg test?

A

o Not in CMP

o Separate test

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20
Q

• What is the significance of the hydration shells of Ca and Mg?

A

o Ca has 1, can shed it to fit into a structure

o Mg has 2, must shed 2, which consumes a lot of energy

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21
Q

• How are Mg levels maintained in body? Normal?

A 
o	absorbed in SI, some by LI (24%-76%)
o	more Absorbed when body levels are lo
o	Excreted in urine and feces
o	Renal excretion may vary from 0.5-70%
o	N= 1.8-3.0 mg/dL
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22
Q

• What are 4 ways to measure Mg?

A

o Serum Mg: most common, doesn’t rep body stores
o RBC levels: higher than serum, doesn’t rep body stores
o 24-hr urine: to asses Mg wasting by kidneys
o Mg retention: more sens than serum for true Mg def; detects bone def

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23
Q

• What causes hypomagnesemia?

A

o ↓dietary intake: malnutrition, malabsorption, chronic diarrhea
o ↑renal loss: Congenital or acquired tubular
o Drugs
o Endocrine: 1st and 2nd hyperaldosteronism, DM
o Other: stress, alcoholism, ↑ lactation, heat, ↑ exercise, burns    

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24
Q

• What are ssx of hypomagnesemia?

A

o muscle irritability, contractility, tetany (neuromuscular integration)
o hyperactive DTRs
o ↑BP, dysrhythmias; or hypotension/tremor
o Positive Chvostek’s and Trousseau’s signs
o Memory loss, emotional lability, confusion, hallucinations, sz
o Often mistaken for hypokalemia, which can occur simultaneously

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25
Q

• What causes hypermagnesemia?

A

o Renal failure

o Excessive intake (OTC supplements)

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26
Q

• What are ssx of hypermagnesemia?

A

o Sedates NMJ, ↓muscle excitability; hypoactive DTRs
o Hypotension, bradycardia, cardiac arrest, ↓resp
o Lethargy, drowsiness
o “Warmth” in body

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27
Q

• What is the role of chloride in the body?

A

o The major extracellular anion
o NaCl or HCl
o indicates acid-base balance w other electrolytes
o reflects Na+ levels to maintain electrical neutrality (& HCO3)

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28
Q

• how are chloride levels regulated?

A

o ↑ in metabolic acidosis (bicarbonate loss)
o Aldosterone: Na+ reabsorption from renal tubules, water and Cl follow
o →influences acid-base balance, osmotic pressure, water balance

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29
Q

• What are normal and critical values of Cl?

A

o Adults/elderly/children: 96-108 mEq/L
o Infants: 96-113
o Optimal: 100-106
o Critical: < 70 or > 120

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30
Q

• What causes hyperchloremia?

A 
o	Dehydration
o	Metabolic acidosis
o	Renal tubular acidosis
o	Acute Renal failure
o	DI (can’t reabsorb WATER (like dehydration)→hypernatremia=hyperchloremia)
o	Cushing’s 
o	Hypoparathyroidism
o	Eclampsia
o	Excess saline IV infusion
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31
Q

• What causes hypochloremia?

A 
o	Excess water intake
o	SIADH (salt-losing disease)
o	Excess sweating
o	CHF (edematous states)
o	Vomit, diarrhea lose HCl)
o	Metabolic alkalosis 
o	Respiratory acidosis (COPD)
o	Addison’s dz
o	Hypokalemia
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32
Q

• What is role of phosphorus in body?

A

o Main ICF anion
o in all tissues, 85% combined w Ca in bones and teeth
o energy storage; carb, protein, fat metabolism
o hydrogen buffer
o every major organ system
o formation of RBC enzyme to take O2 to tissues

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33
Q

• how are P levels regulated?

A

o Serum levels influenced by intestinal absorption and PTH control of bone reabsorption
o Kidneys excrete and re-absorption.
o Can easily ↑ w high diet intake (unlike Ca)

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34
Q

• What are normal P values? Test?

A

o N: 2.5-4.5 mg/dL

o Not in CMP, separate

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35
Q

• What are effects of hypophosphatemia?

A

o tissue hypoxia → hyperventilation, bruising/bleeding dt plt dysfunction, muscle weakness, tremors, paresthesia, hyporeflexia,
o GI: anorexia and dsyphagia.

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36
Q

• Effects of hyper-P?

A

o few specific sxs
o Muscle weakness, paresthesia, tingling around mouth, muscle spasms, hyperactive DTRs, tetany → hypocalcemia 2nd to ↑ serum P
o ↓ formation vit D in kidneys, ↓ blood Ca → ↑PTH
o ↓ urinary Ca excretion

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37
Q

• What is CO2 content?

A

o H2CO3 (carbonic acid)
o HCO3- (bicarbonate ion)- regulated by kidneys and liver
o Dissolved CO2 gas (Hgb)- reg by lungs
o to evaluate acid-base status and electrolyte balance

38
Q

• what are normal and critical CO2 values?

A

o Adults: 23-30 mEq/L
o Children: 20-28
o Optimal: 26-31
o Critical: < 6

39
Q

• What causes hypercapnia?

A

o Severe Vomiting
o Aldosteronism (↑ H loss w Na retention → metabolic alkalosis)
o Mercurial diuretics
o COPD (primary disturbance resp acidosis)(emph, bronch, asthma)
o Metabolic alkalosis (compensatory response)

40
Q

• What causes hypocapcia?

A 
o	Chronic diarrhea (lose HCO3)
o	Renal failure (acute & chronic)
o	Renal tubular acidosis
o	Diabetic ketoacidosis (DKA): HCO3 “used up” trying to buffer increased organic acids (ketones)
o	Starvation
41
Q

• What are interfering factors with CO2 levels?

A

o ↓ dt evaporation: Tube Underfilling (red, green, tiger top) allows escape from serum/plasma; Open tube sits on machine
o ↑: Barbiturates, bicarbonates, hydrocortisone, loop diuretics
o ↓: Methicillin, nitrofurantoin, tetracycline, thiazide diuretics

42
Q

• What is anion gap?

A

o difference bw cations & anions in plasma
o = anions in ECF not routinely measured
o “normal” = small amounts of organic & inorganic acids (lactate, sulfate, proteins, ketone bodies, phosphates)
o eval acid-base disorders
o ↑: metabolic acidosis, need to identify cause
o total # of cations must = the total # of anions

43
Q

• What is the formula for AG?

A

o =(Na + K) – (Cl + CO2)

o Some labs: Na – (Cl + CO2)

44
Q

• What can cause ↑ AG (metabolic acidosis)?

A 
o	Lactic acidosis
o	DKA
o	Starvation
o	Renal Failure
o	Inc HCO3 loss
o	Hypochloremia
o	Poisoning w salicylate, methanol, ethylene glycol
45
Q

• What causes ↓ AG?

A 
o	Excess alkali intake (eg milk alkali syndrome)
o	Multiple myeloma (dt ↑ IgG)
o	Hypercalcemia
o	Hyperaldosteronism
o	Hyponatremia
46
Q

• 84 yo F. ER. cachectic, confused, sagging skin folds, extremely dry skin. ↑Na, ↑K, ↑Cl, ↑HCT

A

o Dehydration

47
Q

• What is the blood sugar test?

A

o Glucose
o Most frequently ordered blood chem test
o Test plasma/serum = 10-15% higher than whole blood levels

48
Q

• How are blood glucose levels regulated?

A

o 1st: insulin and glucagon
o Lo: pancreas alpha cells → glucagon → liver release glucose to blood
o Hi: pancreas beta cells →insulin → fat cells take in glucose from blood
o 2nd: ACTH, adrenal corticosteroids, epi, thyroxine

49
Q

• What are the classifications of diabetes?

A

o Type 1: B-cell destruction →insulin def
o Type 2: progressive insulin secretory defect, cellular resistance
o Genetic defects in β-cell function, insulin action
o Dzs of exocrine pancreas (CF)
o Drug or chem induced (tx HIV, tr ansplant)
o Gestational DM

50
Q

• What is fasting glucose?

A

o > 8 hr fast
o DM = > 126 mg/dl (7.0mM) 2x
o Pre-Diabetes = 100 - 125 (impaired)

51
Q

• What are the normal and critical values for fasting glucose?

A 
o	> 2 years - Adult: 70-100 mg/dl
o	Optimal: 80-100 
o	< 2 years: 60-100 
o	Infant: 40-65 
o	>50: ↑ 1/yr
o	Critical: > 400
52
Q

• What factors interfere with glucose test?

A 
o	Stress 
o	Caffeine
o	Pregnancy may → glucose intolerance
o	Too long to separate serum from cells → continue glucose metabolism → false ↓
o	IV fluids w dextrose
o	Drugs
53
Q

• What is casual plasma glucose?

A

o Don’t need to fast
o > 200 mg/dl (11.1mM) = DM sxs
o Polyuria, polydipsia, unexplained weight loss
o Confirm w fasting or oral glucose tolerance test

54
Q

• What is glucose tolerance testing?

A

o For adults w impaired FBG, prego if at risk
o 8 hr fast
o Drink 75g glucose
o Test blood glucose 2 hrs later

55
Q

• What are significant values of glucose tolerance test?

A

o DM = 200 mg/dl
o Pre-DM (impaired) = >140 - 199
o normal = < 140

56
Q

• What is HbA1c (glycosylated Hb)? Levels?

A

o Amount of blood glucose attachedto Hb in RBC
o Represents avg daily blood glucose for past 3 mos
o Normal: 5%
o DM: goal 200
o 10% = 240 (not good)
o 13% = dangerous

57
Q

• What are the dx criterial for DM?

A

o HbA1c > 6.5
o OR FPG > 126 (7 mMol)
o OR tolerance > 200 (11.1)
o OR casual > 200

58
Q

• What are criteria for pre-DM?

A

o = risk factors, not clinical dx
o FPG 100-125 (5.6-6.9 mMol)
o OR OGTT 140-199 (7.8-11)
o OR HbA1c 5.7-6.4%

59
Q

• Who should be screened for gestational DM?

A

o 1st prenatal visit w risk factors, use dx criterial (=overt, not gestational)
o Everyone: 24-28 wks, OGTT (=GDM)
o GDM Post-partum: 6-12 wks, any test but A1c
o Hx GDM: lifelong every 3 yrs

60
Q

• How is GDM dx?

A

o More strict dt greater impact on neanate
o Fasting ≥92 (5.1)
o OGTT 1 h ≥180 (10.0)
o 2 h ≥153 (8.5)

61
Q

• What does google have for glucose?

A

o Smart soft contact lenses
o Non-invasive glucometer
o Sensor (tears), chip, antenna (receives power and sends info)

62
Q

• What is BUN (blood urea nitrogen)?

A

o directly related to metabolic function of liver, renal blood flow, excretory function of kidney
o Liver protein metabolism → urea
o Protein → amino acids → NH3 → Urea
o →general circulation → kidneys → urine

63
Q

• What are normal and critical BUN values?

A 
o	Adult: 6 – 20 mg/dl
o	> 60: 8-23 
o	Children: 5 –18 
o	Optimal: 10 – 18 
o	Critical:	> 50 = serious impaired renal function
o	Panic: >100
64
Q

• What is azotemia? Pre-renal?

A

o ↑ BUN
o Pre-renal azotemia most common cause (kidneys not involved)
o ↓ renal blood flow (shock, injury,illness)→ ↓ excretion, ↑retention

65
Q

• What are renal and post-renal azotemia?

A

o Renal: kidney dz/damage; ↓excretion

o Post: obstructed ureters (kidney stone), bladder neck (eg BPH); ↓excretion, regurg BUN into blood vessels

66
Q

• What can cause ↓ BUN?

A

o Liver failure (cirrhosis)
o Over hydration
o Negative nitrogen balance (malnutrition, starvation)
o Early Preg: ↑ water retention
o Nephrotic Syndrome: protein loss thru kidneys (edema, urine protein)

67
Q

• What can interfere with BUN measurement?

A

o Changes in protein intake, muscle mass
o Pregnancy
o Over hydration, dehydration
o Drugs

68
Q

• What is creatinine?

A

o creatine phosphate metabolite in muscle
o Little daily fluctuation
o Slight diurnal variation: lo 7am, hi 7pm
o 100% excreted by kidneys= good for kidney function and GFR
o Hepatic function doesn’t affect values
o rise later than BUN in renal disease
o 2x = 50% ↓GFR

69
Q

• What can increase or decrease creatinine?

A

o Inc: renal dz, acromegaly, rhabdomyolysis, MD, myasthenia gravis, UT obstruction, high meat diet
o Dec: ↓ mm mass, ↓ diet protein, small stature

70
Q

• What can interfere with creatinine measurement?

A

o High meat diet = transient ↑
o High ascorbic acid: false ↑
o Ketoacidosis: ↑
o Drugs: Nephrotoxic drugs (cisplatin, gentamicin, cephalosporins): ↑

71
Q

• What are normal and critical creatinine values?

A 
o	Adult males: 0.8-1.3 mg/dl
o	Adult females: 0.6-1.1 
o	3-18: 0.6-1.1 
o	0-3: 0.3-0.7 
o	Elder: ↓ w ↓ mm mass (w/o renal dz)
o	Optimal: 0.8 – 1.1 
o	Critical: > 4
72
Q

• What is the significance of the BUN/creatinine ratio?

A

o 10:1 Normal
o 20:1 Pre-renal azotemia
o 10:1 Renal azotemia (both rise in proportion)
o 20:1 Post-renal azotemia
o mb ↓ratio in severe liver dz, over hydration, SIADH, prego

73
Q

• what is total protein?

A

o both serum albumin & globulins
o Albumin (made in liver) = 60% total protein in serum
o Globulins made by RES (Igs), some in liver
o No known pathologic conditions associated w ↑ albumin
o ↑ TP either dt dehydration or ↑ globulins

74
Q

• What is TP used for clinically?

A 
o	Liver dysfunction
o	Nutritional status
o	Chronic edema
o	Immune system dos
o	Collagen-vascular dzs (SLE)
o	Protein wasting from kidneys and intestines
o	CA
75
Q

• What is normal TP? Interfering factors?

A

o 6.4 – 8.3 g/dl
o ↑ w prolonged tourniquet
o drugs ↑: anabolic steroids, GH, insulin, progesterone
o dDrugs ↓: OCPs, estrogen, hepatotoxic, nephrotoxic
o overhydration ↓, dehydration ↑

76
Q

• What is blood albumin? Value?

A

o Only made liver = reflects functional reserve of liver
o good measure of hepatic function
o maintains vascular colloidal oncotic pressure
o transport drugs, hormones, enzymes, Ca2+
o Normal: 3.5 – 5.0 g/dl

77
Q

• What causes ↓ albumin?

A

o Liver dz, protein-losing enteropathies (Crohn’s, sprue), nephrotic syndrome, ascites, burns, increased capillary permeability (SLE), over hydration, inflammation, Familial Idiopathic Dysproteinemia, malnutrition

78
Q

• What are globulins? Value?

A

o Form abs, glycoproteins, lipoproteins, clotting factors, acute-phase reactants
o Serum level reflects damage of RES in liver
o Alpha & Beta globulins made in liver; Gamma by WBC’s
o Normal: 2.3 – 3.4 g/dl

79
Q

• What can ↑ globulins?

A 
o	Multiple myeloma
o	Waldenstrom’s macroglobulinemia
o	Acute inflammation
o	Chronic inflammatory dzs (SLE, RA)
o	Cirrhosis
o	acute & chronic infectious dzs
o	Dehydration
o	AI hepatitis
80
Q

• What can ↓ globulins?

A

o Genetic immune do affecting Ab production
o Secondary immune deficiencies (steroids, nephrotic syndrome, lymphoma, leukemia, severe gram negative infx)
o Over-hydration

81
Q

• What is the A/G ratio (albumin/globulin)?

A

o Normal: >1 (A>G)
o ↓: conditions that ↓ albumin or ↑ globulins
o SLE: albumin lost from blood vessels dt ↓ capillary permeability, but globulins too large → ↓A/G

82
Q

• What is total bilirubin?

A

o both indirect & direct bilirubin
o Direct = Conjugated, Indirect = Unconjugated
o eval liver fxn, hemolytic anemia, neonatal jaundice
o Hepatic Panel: Includes Total & Direct.
o Indirect is a calculation
o CMP: Total only
o If ↑: request Direct to calc fractions

83
Q

• What is the pathway including bilirubin metabolism?

A

o old RBC’s sequestered in spleen → Heme to biliverdin → unconjugated bilirubin → albumin transport to liver → glucuronic acid added to bilirubin (UDP-glucuronyl transferase) → conjugated bilirubin → secreted in bile → intestines → most eliminated in feces (stercobilin), small amount in urine (urobilinogen →urobilin in kidney)

84
Q

• what are normal and critical bilirubin values?

A 
o	Total: 0.3 – 1.0 mg/dl
o	Indirect: 0.2 – 0.8 
o	Direct: 0.1 – 0.3 
o	Newborn (total): 1 – 12 
o	Critical Adult: > 12 
o	Critical Neonate: > 15
85
Q

• What can interfere with bilirubin values?

A

o Hemolysis & lipemia affect spectrophotometric test (light destroy/CONVERT bilirubin)
o Air bubbles or shaking specimen may destroy bilirubin
o Prolonged fasting and anorexia ↓
o Drugs

86
Q

What are hepatic and pre-hepatic causes of ↑indirect (unconj) bilirubin?

A

o Pre-hepatic: any type of hemolytic anemia, HDN, resolution of large hematoma, CHF, hemorrhagic pulmonary infarcts
o Hepatic: hepatitis, cirrhosis, drugs, Gilbert’s dz (genetic), Crigler-Najjar Disease (gen), neonatal Jaundice

87
Q

What can ↑ direct (conj) bilirubin?

A

o Intrahepatic obstruction: CA, hepatitis, TB, sarcoidosis, sepsis, 1o biliary cirrhosis, oral hypoglycemics, OCPs, preg (3rd tri), cholangitis
o Congenital intrahepatic: Dubin-Johnson Syndrome, Rotor Syndrome
o Post-hepatic obstruction: gallstones, head of pancreas CA, bile duct spasm, spasm of Sphincter of Oddi, Pancreatitis

88
Q

• What is neonatal jaundice?

A

o Most common reason neonates need medical attention
o “Physiologic jaundice” = normal phenomenon during transition
o Progressive rise in total bilirubin 48-120 hrs post-natal (peaks 72-96)
o dt higher postnatal load bilirubin, lower amount liver conjugating enzyme (UGT) activity
o Occurs in virtually every newborn to some degree

89
Q

• What are clinical outcomes of neonatal hyperbilirubinemia?

A

o concerning if continue to rise = unconj bilirubin is neurotoxic
o jaundice in skin and mucus membranes (>5-6 mg/dL) (if older, apparent at >2); progress cranial-caudal
o →brain (acute bilirubin encephalopathy)
o →permanent neuronal damage (kernicterus)
o CAUTION: Visual assessment is subjective, inaccurate, dependent on observer experience!

90
Q

• What causes neonatal jaundice (unconj)?

A

o Dos of production: ↑ RBC destruction
o Hb-opathy
o RBC defects: G6PD, pyruvate kinase deficiency
o RBC abn structure: spherocytosis, elliptocytosis, infantile pyknocytosis
o HDN (aka isoimmunization)
o Infx: bacterial, viral, protozoal
o Sequestration: bruising, cephalohematomas, hemangiomas
o Polycythemia: IDM (infant of diabetic mother), delayed cord clamping

91
Q

What is follow-up for neonatal jaundice?

A

o Often: Blood type & Rh mother and infant, DAT/Coombs infant, CBC (reticulocyte count, blood smear)
o St: Albumin, LFTs, thyroid FTs, Liver/GB US, HIDA (hepatobiliary iminodiacetic acid) scan (r/o biliary atresia)

Lab Dx 2 (8 decks)

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