What are normal and critical K values?
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)
• What factors can interfere with K values?
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)
• What pts should have K monitored? Why?
o serious illness
o diuretics or heart medications
o Minor changes in serum concentration → major physiological consequences
• What can cause hyperkalemia? Value?
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
• What are clinical manifestations of hyperkalemia?
o Early: hypertonicity, paresthesia
o Late: Muscle weakness, flaccid paralysis
o Change in ECG pattern
o Bradycardia, heart block, cardiac arrest
• What can cause hypokalemia? Value?
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
• What are clinical manifestations of hypokalemia?
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
• What is work-up for hypo- and hyper-kalemia?
o Hypo: urine K, BP, aldosterone, plasma HCO3, renin
o Hyper: GFR, renal K excretion, aldosterone, renin
• What is Calcium’s role in body?
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
• What are 3 main mechanisms of Ca2+ homeostasis? Other factors?
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
• What are normal and critical Ca values?
o Adult: 8.8 - 10.4 mg/dl
o Child: Varies with age
o Optimum: 9.2 – 10.0
o Critical: < 7.0
• What causes hypercalcemia?
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
• What are ssx of hypercalcemia?
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
• What is work-up for hypercalcemia?
o CMP, vit D, PTH, TSH, ESR
• What are ssx of hypocalcemia?
o Hyperactive neuromuscular reflexes and tetany o Convulsions (severe)
• What causes hypocalcemia?
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
• What is the ionized calcium test?
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
• What is magnesium’s role in the body?
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
• What is the Mg test?
o Not in CMP
o Separate test
• What is the significance of the hydration shells of Ca and Mg?
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
• How are Mg levels maintained in body? Normal?
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
• What are 4 ways to measure Mg?
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
• What causes hypomagnesemia?
o ↓dietary intake: malnutrition, malabsorption, chronic diarrhea
o ↑renal loss: Congenital or acquired tubular
o Endocrine: 1st and 2nd hyperaldosteronism, DM
o Other: stress, alcoholism, ↑ lactation, heat, ↑ exercise, burns
• What are ssx of hypomagnesemia?
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
• What causes hypermagnesemia?
o Renal failure
o Excessive intake (OTC supplements)
• What are ssx of hypermagnesemia?
o Sedates NMJ, ↓muscle excitability; hypoactive DTRs
o Hypotension, bradycardia, cardiac arrest, ↓resp
o Lethargy, drowsiness
o “Warmth” in body
• What is the role of chloride in the body?
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)
• how are chloride levels regulated?
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
• What are normal and critical values of Cl?
o Adults/elderly/children: 96-108 mEq/L
o Infants: 96-113
o Optimal: 100-106
o Critical: < 70 or > 120
• What causes hyperchloremia?
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
• What causes hypochloremia?
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
• What is role of phosphorus in body?
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
• how are P levels regulated?
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)
• What are normal P values? Test?
o N: 2.5-4.5 mg/dL
o Not in CMP, separate
• What are effects of hypophosphatemia?
o tissue hypoxia → hyperventilation, bruising/bleeding dt plt dysfunction, muscle weakness, tremors, paresthesia, hyporeflexia,
o GI: anorexia and dsyphagia.
• Effects of hyper-P?
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
• What is CO2 content?
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
• what are normal and critical CO2 values?
o Adults: 23-30 mEq/L
o Children: 20-28
o Optimal: 26-31
o Critical: < 6
• What causes hypercapnia?
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)
• What causes hypocapcia?
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
• What are interfering factors with CO2 levels?
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
• What is anion gap?
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
• What is the formula for AG?
o =(Na + K) – (Cl + CO2)
o Some labs: Na – (Cl + CO2)
• What can cause ↑ AG (metabolic acidosis)?
o Lactic acidosis o DKA o Starvation o Renal Failure o Inc HCO3 loss o Hypochloremia o Poisoning w salicylate, methanol, ethylene glycol
• What causes ↓ AG?
o Excess alkali intake (eg milk alkali syndrome) o Multiple myeloma (dt ↑ IgG) o Hypercalcemia o Hyperaldosteronism o Hyponatremia
• 84 yo F. ER. cachectic, confused, sagging skin folds, extremely dry skin. ↑Na, ↑K, ↑Cl, ↑HCT
• What is the blood sugar test?
o Most frequently ordered blood chem test
o Test plasma/serum = 10-15% higher than whole blood levels
• How are blood glucose levels regulated?
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
• What are the classifications of diabetes?
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
• What is fasting glucose?
o > 8 hr fast
o DM = > 126 mg/dl (7.0mM) 2x
o Pre-Diabetes = 100 - 125 (impaired)
• What are the normal and critical values for fasting glucose?
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
• What factors interfere with glucose test?
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
• What is casual plasma glucose?
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
• What is glucose tolerance testing?
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
• What are significant values of glucose tolerance test?
o DM = 200 mg/dl
o Pre-DM (impaired) = >140 - 199
o normal = < 140
• What is HbA1c (glycosylated Hb)? Levels?
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
• What are the dx criterial for DM?
o HbA1c > 6.5
o OR FPG > 126 (7 mMol)
o OR tolerance > 200 (11.1)
o OR casual > 200
• What are criteria for pre-DM?
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%
• Who should be screened for gestational DM?
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
• How is GDM dx?
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)
• What does google have for glucose?
o Smart soft contact lenses
o Non-invasive glucometer
o Sensor (tears), chip, antenna (receives power and sends info)
• What is BUN (blood urea nitrogen)?
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
• What are normal and critical BUN values?
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
• What is azotemia? Pre-renal?
o ↑ BUN
o Pre-renal azotemia most common cause (kidneys not involved)
o ↓ renal blood flow (shock, injury,illness)→ ↓ excretion, ↑retention
• What are renal and post-renal azotemia?
o Renal: kidney dz/damage; ↓excretion
o Post: obstructed ureters (kidney stone), bladder neck (eg BPH); ↓excretion, regurg BUN into blood vessels
• What can cause ↓ BUN?
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)
• What can interfere with BUN measurement?
o Changes in protein intake, muscle mass
o Over hydration, dehydration
• What is creatinine?
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
• What can increase or decrease creatinine?
o Inc: renal dz, acromegaly, rhabdomyolysis, MD, myasthenia gravis, UT obstruction, high meat diet
o Dec: ↓ mm mass, ↓ diet protein, small stature
• What can interfere with creatinine measurement?
o High meat diet = transient ↑
o High ascorbic acid: false ↑
o Ketoacidosis: ↑
o Drugs: Nephrotoxic drugs (cisplatin, gentamicin, cephalosporins): ↑
• What are normal and critical creatinine values?
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
• What is the significance of the BUN/creatinine ratio?
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
• what is total protein?
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
• What is TP used for clinically?
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
• What is normal TP? Interfering factors?
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 ↑
• What is blood albumin? Value?
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
• What causes ↓ albumin?
o Liver dz, protein-losing enteropathies (Crohn’s, sprue), nephrotic syndrome, ascites, burns, increased capillary permeability (SLE), over hydration, inflammation, Familial Idiopathic Dysproteinemia, malnutrition
• What are globulins? Value?
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
• What can ↑ globulins?
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
• What can ↓ globulins?
o Genetic immune do affecting Ab production
o Secondary immune deficiencies (steroids, nephrotic syndrome, lymphoma, leukemia, severe gram negative infx)
• What is the A/G ratio (albumin/globulin)?
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
• What is total bilirubin?
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
• What is the pathway including bilirubin metabolism?
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)
• what are normal and critical bilirubin values?
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
• What can interfere with bilirubin values?
o Hemolysis & lipemia affect spectrophotometric test (light destroy/CONVERT bilirubin)
o Air bubbles or shaking specimen may destroy bilirubin
o Prolonged fasting and anorexia ↓
What are hepatic and pre-hepatic causes of ↑indirect (unconj) bilirubin?
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
What can ↑ direct (conj) bilirubin?
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
• What is neonatal jaundice?
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
• What are clinical outcomes of neonatal hyperbilirubinemia?
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!
• What causes neonatal jaundice (unconj)?
o Dos of production: ↑ RBC destruction
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
What is follow-up for neonatal jaundice?
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)