Interpretation of Lab Tests Flashcards
Lab Testing general principles
1-routine testing diff per facility (EKG and preg) 2-indicated testing based on patient disease states 3- timing of testing 60 considered “current”, w/ disease req closer to surgery
Hematology Testing: CBC+diff 1/2 WBC count
CBC/diff(measures diff type of leukocytes which aid in Dx, leukocytosis: appy, inflammation, dehydration vs leukopenia: bone marrow failure)
Hematology Testing: CBC+diff 2/2 RBC Count
RBC: M4.7-6.0, W4.2-5.4 -transport oxygen/CO2 inbetween tissues/lungs. “Anemia” decr by 10% of NL value: bone marrow failure, GIB, renal failure (no erythropoieten) / Erythrocytosis: dehydration, high altitude compensation, COPD compensation, congenital heart disease. Polycythemia vera = acquired disorder, uncontrolled RBCs production, incr viscosity
Indications for CBC/WBC
hemtologic disorder, vascular procedure, chemotherapy, unknown sickle cell status // leukemia/lymphoma, radiation/chemo, susp infection, aplastic anemia, hypersplenism, autoimmune disorder
Hematology Testing: Hgb
Main component of RBC. Threshold for non systemic disease patient 7g/dL.Higher threshold in systemic disease, CV disease, elderly, critical pts. M 13.5-17.5, W12-16.
Hemoglobin Characteristics
4 polypeptide chains, 2 alpha, 2 beta. Heme molecule in middle in Fe2+ state. Binding site for o2, up to 4 o2 molecules per Hgb. Elevated: COPD, CHF, dehydration, high altitudes. Decreased: anemia, hemorrhage, CRF. incr viscosity
Hematology Testing: Hct
“packed cell volume”. # of cells by %, remainder is plasma. Reflective of Hgb and RBC, Hct:Hgb = 3:1. M42-52%, W37-47%. Decreased: hemorrhage, anemia (<30 is mod-severe), leukemia, hemolytic rxn. Increased: dehydration, polycythemia, COPD, congenital heart disease.
Hematology Testing: Platelets
> 400,000 = cancer, polycythemia vera. <150,000
Indications for H&H
hematologic malignancy, recent radiation/chemo, renal disease, anticoag Rx, high EBL potential, systemic disorders
Coagulation Testing: PT (prothrombin time) (factor 2)
NL 10-14 secs, Protein made in liver, dependent on Vit K. Measures VitK dependent factors: 1,2,5,7,10. longer PT with deficient factors, monitors coumadin therapy (2-2.5 x nl). increased: liver disease, cirrhosis, hepatitis, biliary disease (limited bile for fat (vitk) metabolism.
Coagulation Testing: Ptt (activated partial thromboplastin time)
NL 25-32 secs. Monitors heparin therapy. Eval clotting factors: intrinsic path 8,9,11,12, common path1,2,5,10 Increased: liver disease, heparin therapy, hemphilia (fx 8=a, 9=b), VW disease. NO SPINAL/EPIDURAL WHILE ON HEPARIN THERAPY, must have normal aPtt.
Indications for Coag Test
leukemia, hepatis disease, bleeding disorder, anti coag threapy, severe malnutrition/absorption, baseline for post op anti coag therapy
Indications for Chemistry Test
renal disease, adrenal or thyroid disease, chemo, pituitary/hypothalamic disorder, body fluid loss/shifts (bowel prep, lasix), CNS disease
Calcium levels and fxn
Total 8.5-10.5, Ionized (non-protein bound-active form we care about, 50%) 4.4-5.4 mg/dL. Fxns: NM transmission, skeletal/cardiac contraction, coagulation, 2nd messenger H-mone release, membrane stability. Total serum levels dependent on albumin levels.
Causes // Tx of hypocalcemia
massive transfusion (citrated blood), hypervent (incr pH more pro-bound Ca), hypoPTH (no rls of Ca from bone), VitD insuff (decr GI calc absorption), CRF & hyperphospatemia (inverse to Ca) // Calc Gluc or Calc Chloride (more bio-available, burns inj) 10% over 10m, admin Vitd, monitor ECG
Causes // Tx of hypercalcemia
> 14mg/dL!! Bone dumping of calcium overloads capacity to excrete: Most commonly hyper PTH, malignancy. (acidosis shift to more active Ca) // NS infusion, loop diuretic, fix other lyte issues.
Signs and Symtpoms: Hypocalcemia
Increased nerve excitability: Paresthesia, confusion, laryngospasm, Trousseau(arm)/Chvosteks(face), Seizures, Prolong QT
Signs and Symptoms: Hypercalcemia
Depressed excitability: anorexia, n/v, polyuria, muscle weakness, imparied memory, lethargy/stupor, short QT & prolonged PR
Sodium levels and fxn (must assess balance of solute Na and solvent Water, what is the net gain loss of each comparitively)
135-148 meq/L, most abundant ECF ion. Fxn- maintain osmotic gradient, acid base balance, transmit nerve impulses. Reg by: aldosterone (renal retention), ANP (renal secretion), ADH (retain water, salt follows).
Causes // Tx hyponatremia
severe vomit/diarrhea, excessive free water intake/SIADH, ascites/peri edema, diuretics. Possibility of cerebral edema as sodium content determines vascular tonicity in brain. Tx: should eval serum osmo/urine Na to determine fluid excess:Na loss balance // fluid restriction, diuresis, poss 3% (symptomatic pts) saline 1-2 cc/kg/hr, goal of 1-2 meq/hr increase, then 10-15 mmol/24 hours.
Causes // Tx hypernatremia
dehydration & poor water intake, ID, Cushings syndrome (excess aldosterone). Tx: replacement of water deficit w/ hypotonic solutions (acute hyperNa), Isotonic solutions (chronic hyperNa) then hypotonic once euvolemic, slowed focused process similar to hypoNa tx.
Signs and Symptoms: Hyponatremia // hypernatremia
HypoNa: anorexia, n/v, cramps, weakness, confusion, agitation, Sz/coma // HyperNa: thirst, weakness, muscle twitching, irritability, disorientaiton, Sz/coma
Chloride measurement // Hypo/Hyper Causes: usually involved with metabolic derangement (r/t bicarb status)
NL 96-106. Ion follow Na, major ECF anion. Fxn: water balance, acid base balance. Hypo: vomit, gastric sxn, metabolic alkalosis (acid lost) & resp acidosis (comp) // Hyper: dehdration, metabolic acidosis (sub bicarb for Cl) and resp alkalosis (comp)
Potassium Levels and Fxn
NL 3.5-5meq/L. Major cation of ICF, K is excreted by kidneys w/o resoprtion. Imbalance creates disorder or RMP. Fxn: nerve conduction and muscle fxn, assist in controlling rate/force of cardiac contraction, helps with osmotic and acid base balances
Causes // Tx hypokalemia
<3.5 meq/L. Causes: GI loss vomit/diarrhea, acute metab alkalosis (acid shifts), hyperaldosterone (Na in, K out), diuretics (excess renal loss at loop), beta agonists (insulin also) Tx: KCL IV 10-20 meq/hr, ECG
Causes // Tx hyperkalemia
> 5 meq/L. Causes: renal failure (unable to remove), acidosis (fluid shift), K sparing diuretics, cell lysis, beta antagonists (block Na/K pump, no K back to cell) Tx: Glucose/insulin (pusk K to cell), Bicarb (for acidosis, push K into cell), Loop diuretic, kayexalate, dialysis, beta agonisits (incr Na/K pump)
Signs and Symptoms: Hypokalemia // Hyperkalemia
Hypokalemia: flat t wave, u wave (weak repolarization), wide QRS, fatigue, muscle weakness // Hyperkalemia: tall T wave, prolonged PR, widened QRS, vent dysrhythmias, cardiac arrest
Renal Function Tests: BUN, Cr
BUN = 8-20 mg/dL: directly r/t metabolic function of the LIVER & excretory function of KIDNEYs / 50-100 serious impairment, 150-250 severe impairment/renal failure // Cr = M 0.8-1.3mg/dL, W 0.6-1.2mg/dL. More specific measure of renal disease, is a by product of skeletal muscle metabolism (therefore influenced by patients’ muscle mass). Cr rises later then BUN, inverse to GFR representing chronic nature of disease. CrCl most accurate picture of renal disease.
Causes of BUN derangements
Elevated: rapid protein catabolism, impaired renal excretion, dehydration, excess protein injestion // Decreased: liver failure (poor hepatic metabolism), overhydration/fluid overload, malnutrition/malabsorption (limited protein intake)
Causes of Cr derangments
Increased: impaired kidney fxn, chronic nephritis, urinary tract obstruction // Decreased: reduced skeletal muscle mass
Fasting Blood Glucose
70-110 mg/dL, Elevated: DM, CRF, Diuretic therapy, Corticosteroid therapy / Decreased: insulin OD, hypothyroid, liver disease
Glycolated Hgb (hgb1ac)
Assess long-term compliance, check RBC glucose (3 month shelf life). Good=12%
Therapeutic Rx Levels
Digoxin: 0.5-2ng/ml Toxicity: vision changes, confusion, nausea, vent arrhythmias, AV block (risk incr with elderly, renal insuff, lyte abnls (hypokalemia) / Phenytoin: 10-20mcg/ml
