Quiz 2 Flashcards
Total WBC count
4.5 - 11.0 x 10^3/uL
% of neutrophil count
50-70% of WBC count
Absolute neutrophil count calculation
1.8-7.9 x 10^3/uL
Platelet count
150-450 x 10^3/uL
RBC count males
4.6-6.0 x 10^6/uL
RBC count females
3.9-5.5 x 10^6/uL
Hgb Male
13.6-17.2 g/dL
Hgb Female
12.0-15.0 g/dL
Hematocrit Male
41-50%
Hematocrit Female
35-45%
Total iron binding capacity %
66% (250-400mcg/dL)
sodium
136-142 mEq/L
potassium
3.5-5.0 mEq/L
glucose
70-110 mg/dL
BUN
8-23md/dL
Creatinine male
0.7-1.3 mg/dL
Creatinine female
0.6-1.1 mg/dL
Bilirubin (total)
0.3-1.2 mg/dL
HgbA1C
non diabetics
4.0-5.6%
HgbA1C diabetic diagnosis
greater than or equal to 6.5%
HgbA1C
poorly controlled diabetic
> 8%
HgbA1C goal for diabetic pt
7%
Troponin I
<0.03ng/mL
Troponin T
<0.1ng/mL
Cholesterol
<200mg/dL
ESR
0-20mm/hour
TSH
0.5-5.0 uIU/mL
Iron deficiency anemia
decreased iron in body
blood loss, pregnancy, poor diet, gastric bypass
most common
Vitamin deficiency anemia
low levels of B12/folate (required for erythropoesis)
poor diet
Aplastic anemia
body stops making new RBCs
chemicals, drugs, autoimmune disease
rare
Hemolytic anemia
destruction of RBCs
multiple causes (genetics, infection)
Anemia of chronic disease
decreased RBC production in bone marrow
chronic inflammatory and neoplastic states–impair RBC production
Sideroblastic anemia
abnormal production of RBCs preventing iron from binding to Hgb
multiple causes
Thalassemia
abnormal alpha/beta chain of Hgb
genetic cause
more common in certain ethnic groups
Normocytic anemia
Hgb/Hct decreased but MCV normal
acute blood loss, anemia of chronic disease
most frequently encountered anemia
Microcytic anemia
MCV decreased <80fl
thalassemia
most common cause of iron deficiency anemia
Macrocytic anemia
MCV increased >100fl
alcoholism, B12 folate deficiency, liver disease
White blood cells
monocyte eosinophil basophil lymphocyte neutrophil
WBC count purpose
measure all white blood cells
Elevated WBC count
leukocytosis
bacterial infections, steroids, smokers
Decreased WBC count
leukopenia
viral and parasitic infections, some bacterial
decreased production 2/2 cancer, chemo, B12 deficiency, alcohol abuse, poor nutrition
African American descent
WBC count fluctuations
exercise
pain
pregnancy
emotional responses
WBC w/differential
neutrophils purpose
60% of WBCs are neutrophils
important to get % as well as actual count
Elevated WBC w/diff neutrophils
leukocytosis
left shift–higher presence of immature cells (band)
occurs in infection
Decreased WBC w/diff neutrophils
leukopenia
severe neutropenia= high risk of life threatening bacterial infection
mild and moderate risks
WBC w/diff lymphocytes purpose
measure T, B, and NK cells
form body’s immunity
20-40%
Elevated WBC w/diff lymphocytes
lymphocytosis
mostly viral (mono, CMV, HIV, pneumonia, MMR, varicella)
some bacterial (pertussis, bartonella)
levels higher in infants/children
Decreased WBC w/diff lymphocytes
lymphocytopenia
bacterial/fungal sepsis
post-op state, chemo, radiation, malignancy, steroids, immunosuppressants
immature lymphocyte=blast
WBC w/diff monocytes purpose
measure monocyte level
causes of elevated WBC w/diff monocytes
bacterial, viral, parasitic infection
hematological/myeloproliferative disorder, hemolytic anemia, autoimmune
monocytes
precursor to macrophage, fxn to remove damaged/dead tissue
WBC w/diff eosinophils purpose
measure eosinophils
not really sure
Elevated WBC w/diff eosinophils
eosinophilia
parasites and allergic disorders
milde: 500-1500
Decreased WBC w/diff eosinophils
eosinopenia
acute bacterial infections
WBC w/diff basophils purpose
measure basophil count
least used part of CBC
Elevated WBC w/diff basophils
parasitic infection and allergies but uncommon
Decreased WBC w/diff basophils
uncommon
Platelets purpose
important to determine coagulation disorder
any bleeding/bruising should be thought of as platelet fxn issue
Elevated platelet count
thrombocytosis
reactive: infection, post-op, malignancy, post-splenectomy, acute blood loss
autonomous: malignancy
Decreased platelet count
thrombocytopenia
lab error, drug induced, infection, HIV, HCV, Epstein Barr, sepsis, parasites
RBC count purpose
measure RBC count
anemia
Panel includes quantity, size, weight, volume, width of RBC
Elevated RBC count
cigarette smoke, Dehydration, polycythemia (abnormally high RBC and Hgb count)
Decreased RBC count
anemia bleeding (GI and GYN) hematopoietic failure poor nutrition (lack of B6, B12, folate, iron) drug induced (abs, NSAIDs)
Hemoglobin (Hgb) purpose
HB carries O2
useful test
Elevated Hgb
tobacco, COPD, alcohol abuse
dehydration (false elevation)
increased in newborns
Decreased Hgb
acute blood loss, malnutrition, renal failure, disorders of Hgb structure (thalassemia, sickle cell)
Hematocrit (Hct)
% of whole blood made up of RBCs
packed cell volume
Mean corpuscular volume (MCV)
average volume of RBC
classify types of anemia
Elevated MCV
macrocytic
Decreased MCV
microcytic
Mean corpuscular hemoglobin concentration (MCHC)
portion of RBC taken up by Hgb
Elevated MCHC
increased Hgb
increased iron
increased color of RBC=hyperchromatic
Decreased MCHC
hypo chromatic (decreased Hgb)
less red color
Mean corpuscular hemoglobin (MCH)
weight of hemoglobin in RBC
rises and falls w/MCV
RBC distribution width (RDW)
measure variation in RBC volume
earliest manifestation of iron deficiency anemia
Anisocytosis
cells of varying size
elevated RDW
Reticulocyte count
not part of CBC
reticulocytes=immature RBCs (should be 1%)
f/u abnormal CBC
Increased reticulocyte count
hemolytic anemia
acute blood loss
severe anemia (reticulocytes released prematurely, more in circulation)
Decreased reticulocyte count
vitamin deficiency anemia, iron deficiency anemia, bone marrow failure, decreased EPO production
renal disease/failure
Hemoglobinopathies
alpha/beta thalassemia
Hb S–sickle cell
Hb C–mild anemia
Hb E–mild anemia (Asians)
Components of CMP
electrolyte fxn–sodium, potassium, chloride, carbon dioxide, anion gap
renal fxn–BUN, creatinine
liver fxn–bilirubin, alkaline phosphatase, AST, ALT
Reasons to order CMP
abdominal pain
glucose levels
potassium/renal fxn (HTN tx)
liver dysfunction/toxicity
Ion distribution
intracellular fluid: potassium
extracellular fluid: sodium
Plasma water increased
sodium and osmolality decreased
ADH secretion decreased
collecting renal tubule impermeable to water (water not reabsorbed)
Plasma water decreased
sodium and osmolality increased
ADH secretion increased
collecting renal tubule reabsorbs more water
Elevated sodium
hypernatremia
unreplaced water loss (elderly pt/people w/o free access to water)
Decreased sodium
hyponatremia
thiazide diuretics, renal insufficiency, inadequate sodium
Elevated potassium
increased intake
ACE inhibitors
crush injuries/infection
Decreased potassium
fluid/electrolyte loss
diuretics
decreased intake
Elevated glucose
diabetes acute stress response pregnancy pancreatitis corticosteroid therapy
Decreased glucose
insulinoma
insulin OD
starvation
Elevated BUN
high protein diet
GI bleed
dehydration
Decreased BUN
low protein diets
starvation
overhydration
Elevated creatinine
disorders of renal function urinary tract obstruction diabetic nephropathy rhabdomyolysis gigantism/acromegaly
Decreased creatinine
debilitation
decreased muscle mass
Elevated calcium
hypercalcemia
hyperparathyroidism
vitamin D toxicity
tumors
acromegaly
Decreased calcium
Hypocalcemia
hypoparathyroidism
vitamin D deficiency
hypoalbumin
malabsorption
Elevated serum protein
Hyperproteinemia
dehydration
malignancy
infection
over production of immunoglobulins
Decreased serum protein
Hypoproteinemia
hepatic failure/disease
malnutrition/malabsorption
renal failure/disease
Elevated albumin
hyperalbuminemia
dehydration
Decreased albumin
hypoalbuminemia
malnutrition
pregnancy
hepatic disease/failure
renal damage (kidneys spill protein)
Elevated ALP (alkaline phosphatase)
cirrhosis biliary tract obstruction liver tumors drugs toxic to liver cancers metastasizing to bone primary bone cancer
elevated in any condition of bone formation (normal or abnormal)
Decreased ALP
malnutrition state
Elevated AST (aspartate aminotransferase)
liver disease (hepatitis shoots this value through the roof)
liver tumors
mono
Elevated ALT (alanine aminotransferase)
liver abnormality
hepatitis
hepatotoxic drugs
cirrhosis
Potassium general notes
secreted but not reabsorbed by kidney
minor change has dramatic effect on membrane potential (esp in muscle cells)
important in cardiac muscle and skeletal muscle nerve excitability
Glucose levels general notes
increase after eating
cells in islets of Langerhans secrete insulin to decrease glucose level
hormones affect levels
BUN general notes
50% urea reabsorbed in renal tubule (rest excreted in urine)
reflect metabolic function of kidneys/liver, excretory function of kidneys
Creatinine general notes
secreted by kidneys at constant rate
increased level appears later in renal disease
doubling of level = 50% decrease in GFR
Calcium general notes
50% of calcium is free, rest is protein bound/complexed
Parathyroid hormone (PTH)
increases calcium levels
comes from parathyroid gland
Calcitonin
decreases calcium levels
comes from thyroid gland
Unconjugated bilirubin
indirect bilirubin
can pass through BBB (cause mental retardation/encephalopathy)
seen in newborns
Conjugated bilirubin
direct bilirubin
conjugated w/glycuronide in liver
Causes of indirect hyperbilirubinemia
hepatocellular dysfunction (hepatitis, cirrhosis, neonatal hyperbilirubinemia)
diseases increasing RBC destruction (transfusion rxn, sickle cell, hemolytic anemia)
meds
Causes of direct hyperbilirubinemia
gallstones
obstruction of extra hepatic ducts by tumor
liver metastases
Albumin general notes
60% of serum protein
regulates osmotic pressure
BMP
tests electrolytes, kidney, glucose
no liver function tests
BUN/Creatinine ratio
manually calculated, not on CMP
if both levels normal, don’t have to calculate
Normal– 10:1-20:1
Pre-renal disease
ratio >20:1
volume depletion, sepsis, hypotension, CHF
Intrarenal disease
ratio <10:1
glomerulonephritis
Postrenal disease
Early disease ratio >20:1
Late disease ratio <10:1
GGT (gamma glutamyl transpeptidase)
not included on CMP
liver disease increases level, not very specific
infants have 6-7x normal range
HgbA1C test
dx/monitor diabetes (binds most readily to sugar)
indicate glucose level over 3-4 months
determine mean plasma glucose level
Insulin level
dx insulinoma/cause of hypoglycemia
increased: insulinoma
decreased: insulin dependent diabetes
C-peptide level
determine pancreatic function/ability to make insulin
links alpha/beta chains of proinsulin (C-peptide not found on synthetic insulin)
low C-peptide
Type I diabetes
high or normal C-peptide
Type II diabetes
Amylase
elevated in acute/chronic pancreatitis, pancreatic cancer, bile duct obstruction, cholecystitis (damage to pancreas)
level back to normal in 12 hours (chronic elevation = severe disease)
Lipase
released w/pancreatic damage (see amylase)
stays elevated longer (5-7 days)–more helpful in dx
Uric acid level
increased in gout, alcohol abuse, renal failure, dehydration, increased protein/purine diet
CHF presentation
pitting edema
fluid in lungs
cardiomegaly
BNP (brain natriuretic peptide)
aid in dx of CHF (levels will be elevated in CHF, MI)
get echocardiogram in addition
released from ventricles during stretch of ventricles
Creatinine Kinase (CK)
found in high energy tissues
CK-MM (skeletal muscle, increased total CK likely due to CK-MM)
CK-BB (brain)
CK-MB (heart)
CK-MB
rises 3-6 hours post-MI
elevated for 12 hours post-MI
returns to normal 36-58 hours post-MI
not great test for MI, only indicates that damage has occurred
Troponin test
GOLD STANDARD TO DX MI
Increased sensitivity and specificity
elevated in 2-3 hours post-MI
stays elevated for 7-14 days
indicates cardiac damage/injury
Troponin I function
actin/myosin interaction
Troponin T function
binds troponin and tropomyosin
Myoglobin
released after skeletal/cardiac muscle injury
more sensitive, less specific than CK-MB
not specific for any dx
D-dimer
used to r/o DVT/PE (identify intravascular clotting, monitor thrombolytic therapy)
highly sensitive, not specific
negative predictor (r/o, not dx)
Elevated D-dimer
DIC sickle cell anemia surgery pregnancy elderly
cholesterol
HDL + LDL + VLDL
variation can exist up to 15% between tests
Triglycerides
increased level indicates triglycerides in tissue
familial hypertriglyceridemia, hyperlipidemia, increased carb diet, poorly controlled diabetes
HDL
25% of cholesterol (good)
protective against CAD (transport cholesterol from body tissues to liver)
Factors that increased HDL
genetics exercise moderate alcohol use healthier eating estrogen administration
Factors that decrease HDL
metabolic syndrome
genetics
LDL
75% of cholesterol (bad)
deposits in arterial walls/plaque
calculate by Friedewald formula
Factors that increase LDL
genetics
increased saturated fat diet
excessive alcohol consumption
Factors that decrease LDL
genetics
exercise
low fat diet
particle test of LDL
small and dense: bad (gets into blood vessels); pattern B
big and fluffy: good; pattern A
Lipid panel
screens diabetics, HTN/smokers, positive family hx
if initial test normal test every 5years
if initial test borderline test every 3 years
Pt >65 w/normal tests can stop being screened
Indications for iron studies
iron deficiency/overload
iron storage/processing (infants, kids, premenopausal women)
secondary testing after abnormal CBC (Hgb/Hct abnormal)
Iron deficient anemias
microcytic or hypo chromic
serum iron
can fluctuate at different times of day (higher in AM), or consumption of excess iron in diet, meds
don’t get level by itself
increased iron level
rare
beta-thalassemia
EtOH cirrhosis (liver damage releases iron into circulation)
high iron intake
HHC
decreased iron level
common
iron deficiency anemia, renal dz, inadequate absorption, increased loss, increased demand
have to identify where iron being lost from
Serum ferritin
gold standard to test iron deficiency anemia
ferritin levels don’t fluctuate as much
stores 15-20% of iron
acute phase reactant
distinguish b/w iron deficiency anemia and anemia of chronic disease
measure at 4 week intervals after given iron supplement
Increased ferritin
HHC
excess iron intake/poisoning
chronic hepatits
EtOH
Decreased ferritin
iron deficiency anemia
Transferrin
can bind 2 iron molecules
33% of binding sites filled normally
synthesis of transferrin in infection
increases state of iron deficiency, decreases infection (prevents bacteria from using iron to replicate/survive)
Total iron binding capacity
evaluates anemia
used w/serum iron and ferritin to evaluate and dx anemia
total amount of iron that serum proteins (transferrin) can bind to
TIBC test
radioactive iron incubated w/human serum (measure amount of iron taken up by transferrin)
TIBC in iron deficiency
TIBC level increases because there is less iron and more binding sites open
iron deficiency anemia, pregnancy
TIBC in iron overload
TIBC level decreases b/c there is too much iron and fewer binding sites open
anemia of chronic dz, HHC
Transferrin saturation
percentage of transferrin binding sites
increase indicates increase in iron absorption
serum iron/TIBC=% of iron saturation
Increased transferrin saturation
iron overload states
HHC
Decreased transferrin saturation
iron deficiency anemia
anemia of chronic dz
Lab result in iron deficiency anemia
increased TIBC
decreased MCV, serum iron, serum ferritin, % transferrin saturation
Lab result in anemia of chronic dz
Normal MCV (decreases over time) Decreased serum iron Normal/increased serum ferritin Normal/low TIBC decreased % transferrin saturation
Elevated albumin level
dehydration
Decreased albumin level
liver disease malabsorption/malnutrition abnormal loss renal dz GI loss skin loss severe burns
Prealbumin
better assessment for nutrition status (shorter half life, more sensitive to change)
not accurate in pt w/inflammation, infection, trauma
Elevated prealbumin
pregnancy
Hodgkin’s lymphoma
Decreased prealbumin
renal/liver dz malabsorption/malnutrition eating disorders Chron's dz low protein diet severe illness inflammation infection
Decreased alpha-1-antitrypsin
lungs and liver
COPD onset before 40 prolonged jaundice and hepatitis in infants liver dysfunction in kids chronic hepatitis cirrhosis hepatocellular carcinoma
Increased haptoglobulin
infection inflammation neoplastic disease pregnancy trauma
Decreased haptoglobulin
hemolytic anemia
transfusion reaction
artificial heart valves
Haptoglobulin
binds free Hgb when RBCs are destroyed, transports Hgb to liver, heme converted to bilirubin
Complement proteins
measure for autoimmune dz, recurrent infections
CH50
total complement activity (screen)
all 9 CP must be present to have normal result
if value is 0, one of pathways is totally absent
C3 and C4
investigate undetectable CH50 level
test in presence of certain fungal infections, gram negative septicemia, shock
Increased C3 and C4
cancer
UC
Decreased C3 and C4
SLE (lupus)
bacterial infection
Immunoglobulins
produced by B lymphocytes, specific against individual infectious or foreign agents
IgA
found in secretions/mucosal epithelium
present in saliva, tears, colostrum, mucus
deficiency can cause frequent respiratory infections, GI inflammation, unexplained asthma
IgD
unknown function
higher levels seen in multiple infections
IgE
key factor in allergic reactions and parasitic infections
binds to mast cells
measured in primary care
IgG
major antibody produced when antigen encountered (“I already Got Germs”
crosses placenta, can protect baby from infection
IgM
initial antibody secreted after immune challenge
half life is 10 days
indicates recent infection
“I Get Meds”
IgG and IgM
Epstein Barr Virus CMV Herpes I and II varicella measles mumps rubella
active vs past infection
Protein electrophoresis
identify cancer/precancer, immune abnormalities, dysfunction of kidney or liver
Protein electrophoresis peaks
broad peak in gamma region associated w/ infections, inflammation, reactive processes
M protein on protein electrophoresis
multiple myeloma
SLE (systemic lupus erythematosus)
butterfly facial rash (nasolabial folds unaffected) fatigue weight loss arthralgia/myalgia lymphadenopathy multiple organ involvement
Progressive systemic sclerosis (Scleroderma)
skin thickening/hardening fatigue arthralgias/myalgias digital ulcers/contractures multiple systemic manifestations
Sjogren syndrome
decreased lacrimal/salivary gland function, dry eyes/mouth/vagina, rhinitis, sinusitis, lymphoma
Erythrocyte sedimentation rate (ESR)
nonspecific marker
frequent false elevation, non-specific
Rouleaux formation 2/2 neutral environment (RBCs not repelling each other)
ESR test
Westergren tube, measure how well RBCs fall (minimal in healthy person)
Increased ESR
microcytosis
anemia
inflammatory disease, AI disease, obesity, malignancy, age, serious infection
> 100mm/hr (CALL 911–septic infection)
Decreased ESR
more RBCs
abnormally shaped RBCs
C-reactive protein (CRP)
acute phase reactant
mild, moderate, marked classifications (marked indicates bacterial infection or severe trauma)
> 50m/dL indicates bacterial infection
ANA (antinuclear antibody)
pattern and value reported
95% of SLE pt have high/positive ANA
decreased specificity but good sensitivity
Diffuse ANA
SLE
Peripheral or rim ANA
SLE
nucleolar ANA
SLE or scleroderma
speckled ANA
SLE, scleroderma, others
Rheumatoid factor
primary lab to dx RA
IgM autoantibodies directed against IgG autoantibody (Fc fragment)
most RA pt have much higher levels
IgM rheumatoid factor
good sensitivity in severe disease, less specificity
Rheumatoid arthritis vs osetoarthritis
systemic manifestations and autoantibody tissue destruction
TSH (thyroid stimulating hormone)
assess function of thyroid gland
identify origin of thyroid dysfunction
Increased T3/T4
myocardial contractility HR mental alertness ventilator drive bone turnover GI motility
Primary hyopthyroidism
defect in thyroid gland
Hashimoto’s thyroiditis (AI)
Secondary hypothyroidism
decreased TSH or TRH secretion
pituitary source (less common)
Tertiary hypothyroidism
trauma
hypothalamic tumors
uncommon
Hypothyroidism symptoms
fatigue dull mentation dry skin weight gain bradycardia constipation cold intolerance
T4 and T3
Free T3 more metabolically active
T4 converted to T3
nearly all T4 protein bound
70% of T3 protein bound
T4 in hypothyroidism
decreased
TSH in hypothyroidism
elevated
TSH and free T4 decreased
hypothalamic/pituitary failure hypothyroidism
Subclinical hypothyroidism
similar symptoms
high normal/mildly elevated TSH w/normal free T4
Hyperthyroidism
Grave’s disease (AI)
decreased TSH level (inhibits hypothalamic-pituitary axis)
Overt hyperthyroidism
low TSH
high free T4/T3
Hyperthyroidism symptoms
bulging eyes edema jittery unable to gain weight anxiety palpitations perspiration heat intolerance hyper-defectation
Subclinical hyperthyroidism
low TSH (other values normal)
non-specific symptoms
increased CV risk, a-fib
