LABS Flashcards
URINALYSIS COLLECTION
50% midstream collection F contamination (>10 epithelial cells/HPF)
infection from catheterized specimen: 1-3%
20% if elderly or debilitated
Urine Dipstick basic U/A
Urine Microscopy Cells
urinary sediment
Cells: white, red, squamous cells, others
Labs
Urgent care and ED only
Leukocyte esterase
Enzyme produced by neutrophils
50% of pts with bacteriuria do not have pyuria
May be vaginal/penile contaminant, not diagnostic
Nitrite
Gram negative bacteria convert nitrate to nitrite. E. Coli most common
UTI
Send urine for microscopic analysis, +/- culture
RBC’s / heme
Rhabdomyolysis- myoglobin
lysed RBC
Free hemoglobin
intact Erythorocytes
Blood usually Cancer or menstral cycle
Specific gravity
Concnetrated_Hydration, solutes
Protein
Transietn common. Renal Fx
Seen w/ exercise
Bilirubin
Liver FX
Ketones
hydration/nutrition status, diabetes; product of ketone metabolism
glucose
usually none. Present = renal tubules overwhelmed
>200 HIGH glucose if seen in urine
Urine Microspy Cast
Fat laden histiocytes (oval fat bodies / macrophages) : nephrotic syndrome and proteinuria
Nephropathies or non-glomerular renal dz
Crystals
Casts – “active sediment” indicates renal disease
Erythrocyte casts = glomerular nephritis
Leukocyte casts = interstitial disease
Normal crysals- uric acicd, Ca, Phos
Abnorma- cholestrol, acylovir, sulfa
Urine Microspy Crystals
Urate, phosphate, oxalate, cystine crystals: stone formers
Uric acid crystals: gout
Urine Cultures
Obtained if infection unknown, at risk or “special” pt, sick patient
Collection method is key – females vs catheterization
Infection species significant/cause if >100K colony
2-3 days results
Treat all pts presumptively for gram neg infection; send cultures on all resistant/recurrent/”special” infections
Microscopy B4 culture
Erythrocytes: RBC’s
Normal = 80-100 oxygen transport from lungs to tissues protein: hemoglobin survive 120d Absolute number counted MCV = Mean Corpuscular Volume
Ht: Hgb 3:1 (if nt acute blood loss)
Hematocrit
Males: 38-50%, Females 34-44% (kids age variable)
Percent of blood volume occupied by erythrocytes
Derived from (MCV and total RBC count)
Hemoglobin
Males 14-18 g/dL
Females 12-16g/dL (pregnant 11-14g/dL, kids
Unique for its ability to carry and unload O2
defines anemia
Blood Smears
not common-Information on red cell size, morphology, variation, hypochromia
cell types
% immature cells; i.e. bands, stabs
Presence of precursor cells usually restricted to marrow (blasts, nucleated erythrocytes)
Helpful for abn anemia, anemia not improving w/ tx, or Ht:Hgb ratio off
Döhle bodies
are intra-cytoplasmic structures composed of agglutinated ribosomes;
inflammation and increased granulocytopoiesis
toxic neutrophils.
Heinz bodies
inclusions within RBC’s composed of denatured hemoglobin .
hemolytic anemia
Howell-Jolly bodies
are spherical blue-black inclusions of red blood cells seen on Wright-stained smears.
condensed DNA,
hemolytic anemias, dysfunctional spleens, splenectomy.
Iron deficiency
Thalassemias
Hemolytic anemia
Lyme dz
Microcytic Anemia: MCV < 80
Hemorrhage
Chronic disease
Bone marrow failure
Lead poisoning
Normocytic Anemia: MCV 80-100
Vitamin B12 deficiency
Folate deficiency
Hypothyroidism
Hepatic failure
Macrocytic Anemia MCV > 100
Leukocytes
4.5 – 11k
WBC counts and differential evaluate bacterial infection
Elevated neutrophil (PMN’s) count Inc. in the proportion of immature neutrophils (bands)= key sign of bacterial infection (left shift- more immature WBC seen)
Monitor w/ chemotherapy
RA, chronic inflam- 11-13K
Platelet Count
Formation critical for effective hemostasis w/vessel injury
150-400
Thrombocytopenia < 100
< 50 severe bleeding from trauma
< 10 spontaneous cerebral hemorrhage
Chemistry Panels
electrolyte metabolism, fluid balance, acid-base status, renal function – from venous blood draw
Na+
N-135 – 145
Holds water in extracellular fluid space
Regulated by the kidneys in response to hormonal, neural, and vascular signals reflecting intravascular fluid volume
hypo-osmolarity
hyper-osmolarity
Hypertonic Hyponatremia
Extracellular osmotic substance accumulates causing water to shift from intracellular to extracellular space lowering Na
correct the sugar 1st, sodium low bc glucose is high Every inc (100 mg/d)l in glucose above normal multiply by 1.6 to add the corrected mEq of Na.
Corrected sodium for the pt in head while correct sugar :
7 x 1.6 = 11.2 + 124 = 135 (normal total body sodium)
Causes-
hyperglycemia, mannitol (diuretic)
Normal water excretion: low solute load in extracellular space from added water
Hypotonic hypernatremia
Psychogenic polydipsia – huge water intake
Massive beer drinking (Potomania)
Impaired water excretion – kidney issue
Volume loss: diuretics, GI loss, bleeding
Edematous states: cirrhosis, CHF
Renal failure
Cortisol deficiency: adrenal / hypopituitary:
Severe hypothyroidism
SIADH
Hypernatremia
Dehydration – hypertonic hyperosmolar
water loss :Fever, hyperthermia, diaphoresis, loss of thirst sensation, burns, hyperventilation
Neurogenic diabetes insipidus- no antidiuretic hormone
Nephrogenic diabetes insipidus- kidney dont respond to antidiuretic hormone
Osmotic diuresis-glycosuria, mannitol, high protein intake
K+
N 3.5 - 5.0 extracellular levels (6-7 no s/s lab handling, RBC lyis)
intracellular ion exchange
INC or DEC =life threatening electrolyte issue
Chem 7
chemistry metabolic panel Basic
Na, K, BUN, Creatine, Glucose, CO2, HCO3
Chem 12_16-20
Basic + LFTs (AST, ALT, PHos, bilirubin) Albumin, Ca
CBC w. differential
Common, cheap
CBC basic- Hg, Ht, RDW, MCV, MCH, WBC
Diff: neutrophils, lymphocytes, basophils, eosinophils
used when looking for particular infection.
Hyperkalemia
Levels > 6.0 myocardial irritability and fatal arrhythmias
Common causes
Renal failure
Release of intracellular K+ into the extracellular space
Metabolic acidosis, massive tissue breakdown, insulin deficiency
Inc. Potassium
Potassium Abnormal? Think: Get an EKG!
Hyperkalemia
Peaked T waves
Widened PR and QRS intervals
Flattening / loss of P waves
Hypokalemia U waves Flat or inverted T waves ST depression Decreased QRS voltage
Low Potassium
Hypokalemia
Question is-True body loss vs. shift to intracellular
Decreased dietary intake/nutrition – alcoholics
Diarrhea / vomiting
Diuretics
Chloride
N 98 – 109 mEq/l extracellular
Major role as anion companion to Na +
Changes in Cl – reflect changes in other extracellular ions* bicarb
N 20-30 mEq/l
major extracellular buffer
disorders of the acid/base balance
Serum CO2/HCO3 is ~5% higher then arterial bicarbonate (ABG – arterial blood gas)
very sick if off
Bicarbonate
Blood Urea Nitrogen
Normal 10 – 20
Urea = end product of protein metabolism
related to -dietary protein, liver disease, tissue breakdown, dec renal blood flow, renal pathology
1/2 renal function lost before BUN or creatinine inc.
Azotemia (early renal failure) = elevated BUN
If dec. enough to cause a rise in BUN / creatinine then U/A will reveal proteinuria and abnormal urinary sediment
Decreased renal blood flow = increased BUN
BUN/creatinine ratio 10-15
Creatinine
Normal 0.6 – 1.2 mg/dl
#1 indicator of renal function
End product of metabolism of creatine,
Produced in liver, stored in muscle, phosphocreatine; storage for high energy phosphate
Daily muscle cell metabolism= excretion of 1g creatinine/d
Inc= loss of glomerular filtration
2x inc= indicates half of renal function
Decision to begin dialysis Tx made on clinical symptoms rather than absolute #’s
Chronic RF pts may tolerate creat > 20 mg/dl;
Acute RF pt may not tolerate creat > 6
Bilirubin- LFT
End product of heme metabolism breakdown of RBC’s
conjugated in the liver and secreted into bile
Increased conjugated
(direct) 0.1-0.5 nml
Liver dx. hepatic obstruction inc. level, w/ bilirubinuria)
Increased unconjugated
(indirect) 0.3-1.9 nml
hemolysis or congenital defects in bilirubin transport (no associated bilirubinuria)
LFT-ALT Alanine Tranferase
Hepatocyte enzyme
Normal 3 – 35
Specific: elevation seen in pts with liver disease
Normal 10 – 40
Enzyme present in large concentration in liver, heart, skeletal tissue
Less specific than ALT for liver disease
*Significant elevation in pts with massive hepatic necrosis, MI, Rhabdo
LFT Aspartate Aminotransferase (AST)
LFT-ALT/AST
ALT and AST elevated in liver dz. ratio ALT : AST= > 1
alcoholic hepatitis and massive hepatic necrosis the ratio of ALT : AST =< 1
N 25 – 100
Monophosphate concentrated in hepatocytes, bone, gut, lung
Inc.= obstruction anywhere in the biliary tract
pulmonary, renal, splenic infarction / inflammation, carcinoma
LFT- ALP Alkaline Phos
LFT- Albumin
Normal 3.5 - 5.0
abundant protein in blood plasma; 40-60% of total protein
“acid”
Dec : Primary liver disease Tissue damage / inflammation Malnutrition Malabsorption syndrome Renal failure
Ca+
ELEVATED
N- 8.5-10.5
Hyperparathyroidism *Malignancy Thyrotoxicosis Vitamin D intoxication Sarcoidosis
Renal disease
Vitamin D deficiency
Hypoparathyroidism
Mg deficiency
Ca+ DECREASED
Magnesium
INCREASED
Renal failure
Iatrogenic ingestion
Adrenal insufficiency
Magnesium DECREASED
Decreased intake Diarrhea Alcoholism Hyperthyroidism SIADH (sydrome of inappro ADH) Some diuretics
Imminent renal failure
Hypoparathroidism
Acromegaly
Vitamin D intoxication
Phosphorous
INCREASED
Phosphorous
DECREASE
Primary hyperparathyroidism Mg deficiency Vitamin D deficiency Alcoholism Soda Osteoporosis
Creatinine kinase 38-120 ng/ml
Myoglobin <85-90
Found in heart/skeletal muscle. Presence = damage
Not specific.
Used much less since advent of troponin
Cardiac Markers
Troponin
nl <0.01 – 0.03 ng/mL (Lab/method dependent) #1 Gold Standard for cardiac ischemia
cardiac protein controls calcium mediated interaction of actin/myosin;
Inc= degradation of actin and myosin filaments in the area of myocardial damage. “Trop leak”
Rises 4-6 hours after MI
At least two serial serum levels 6 hours apart are required to r/o acute MI in pt’s w/ acute CP
If last episode of CP >6hrs prior – single troponin acceptable
elevated for as long as 10 days after myocardial injury.
BNP
Brain Natriuretic Peptide
Normal: <100pg/ml
response to left ventricular stretching and increased wall tension
predict prognosis/death in heart failure in Pts w/ sx
Not a screening test
High negative predictive value = if test is negative, rules out heart failure better than a positive test predicts it
affect this test: HTN drugs, exercise, etc
Useful and expensive (>$200)
Lipid Panel
Total cholesterol, HDL, TGS
LDL calculated (not good lipids, indirectly)
TC <200
HDL >35
TG< 150 (while fasting) > 400 inaccurate LDL
LDL depends on CV
Finger prick or Lab
lactic Acid
N < 2.0
2.0-3.9- consider sepsis
>4.0 sepsis
- Gold stardard for use of TX w/ severe infection
Shock/sepsis= anerobic, O2 delivery inadequate. By product Lactic acidosis=hypoeffusion, hypoxia
Not routine test- IN Pt or ED
PT Prothrombine Time
N 10-13s
injured vessles release thromboplasin, activates exrinisit pathways for coagulation
Assess for anticoag TX
Vit K deficiency
INR international normalized Ratio
N 0.5-1.2 If anticoag drugs 2-3.5 #1 monitor for anticoag TX INT= Pts PT/control PT Warfarin ordered w/ PT
Ammonia
N 30-70 ug/dl
Indicates hepatic parenchymal damage Liver dz Asterixis- hepatic encephalopathy (can't convert NH3 to urea, damages CNS) Cirrohis Alcholics Not routin LFT