Urinalysis

Lab Tests What its for Low Results High Results Extra Notes

Specific Gravity determine dilution dilute - brain diseases concentrated - amber - dehydrated

Renal Function
Tests
Lab Tests What its for Low Results High Results Extra Notes

Plasma Creatine Volume of blood plasma

that is cleared
concentration
BUN - Blood Urea dehydration, prerenal/renal failure urea is end product of protein
metabolism
Nitrogen
BUN/creatinine should be 1 acute tubular necrosis, decreased decreased renal perfusion,
protein intake glomerular disease, ↑protein intake
ratio

Liver Functions >70% of liver may be looking at enzyme numbers

damaged before LFT is
Test (LFT) abnormal

Lab Tests What its for Low Results High Results Extra Notes

AST - serum diagnose acute MI and Acute MI, damage to skeletal with chronic liver disease may not see
liver function muscle, kidneys, and brain tissue elevated AST or ALT
aminotransferases
ALT - serum liver damage, viral hepatitis,
mononucleosis, CHF
aminotransferases
ALP - Alkaline blocked bile ducts and increased bone formation and
liver functions obstruction of bile ducts (may have
phosphatase bile stones)
Lactic liver function liver damage abundant in RBCs -- a marker of tissue
breakdown
Dehydrogenase
(LDH)
Albumin chronic liver disease, malnutrition, dehydration and exercise maintains water in vascular and fat
starvation, advanced Cardiac Arrest, soluble vitamins bind to it and carries
CHF, Burns, Lupus to other places b/c if bound can't be
excreted
Globulins emphysema, hemolytic anemia, pregnancy, acute infection, burns,
hypocholesterolemia rheumatoid arthritis, acute MI,
diabetes mellitus
Fibrinogen clotting factor
pregnancy complications
Bilirubin detect unconjugated
bilirubin due to hemolytic
diseases or liver diseases
severe liver disease, DIC, leukemia, acute infections, inflammatory
disease, hepatitis, oral
contraceptives
sickle cell anemia, transfusion
reactions, pemicious anemia, CHF,
hepatitis
Disseminated Intravascular
Coagulation (DIC) - mini clots;
clotting cascade that run amuck so
you use all the fibrinogen up as fast as
you can -- low fibrinogen -- and can
cause hemorraging b/c no fibrinogen
to clot
is yellow breakdown product of heme
(which is found in hemoglobin) - it is
excreted from bile so increased levels
are elevated b/c of diseases that
catabolize heme (hemoglobin--in RBC)

Ammonia detect liver disorder from renal failure, malignant hypertension, hepatic failure, CHF, hepatic is toxic if not converted to urea and is
the inability of the liver to essential hypertension neuropathy, confused people a by product of gluconeogenesis
convert ammonia to Urea
Clotting factors -- to detect defects in the
blood coagulation
Factor Assay mechanism

Culture &
Sensitivity Tests
Lab Tests What its for Culture Sensitivity Extra Notes

Gram Stain method of differentiating identifies the species of bacteria to which antibiotic an organism is
bacteria into two large "sensitive" -- sensitive,
groups - gram positive and intermediate, resistnat
gram negative - based on
physical/chemical
properties of their cell wall

Complete Blood
Count (CBC)
Lab Tests What its for Low Results High Results Extra Notes

Red Blood Cell Erythrocytopenia (too little RBCs) - Erythrocytosis (too many RBCs) -
Anemia can cause thrombus formation and
sludge Polycythemia Vera
(primary) - excess RBCs are
produced as a result of an
abnormality of the bone marrow
Polycythemia (secondary) -
caused by either natural or artificial
increases in the production of
erythropoietin (hence increase in
RBCs) is resolved when underlying
cause is treated
Hemoglobin (Hb) oxygen carrying, Iron is can have high pulse ox % and low Hg should be anything with low O2 levels
needed for formation of Hg b/c pulse ox only measuring % of
hemoglobin carrying O2
Hematocrit (Hct, measure of the overhydration and anemia dehydration (increase risk of ratio in blood; not actual number of
PROPORTION or thrombus formation) Hct
PCV) percentage of RBC in total
volume of blood - so
values change with
volume/fluid changes
MCV size of RBC - normocytic - Microcytic - small size of RBC; so Macrocytic - bigger size of RBC; so useful in identifying type of Anemia
normal size of RBC lower weight and can slip through higher weight and can't get through
capillaries and don't have enough capillaries
hemoglobin in vascular
MCH amount of Hg in one RBC

MCHC proportion of the RBC

occupied by Hg
Erythrocyte non-specific test to tell if
pt is in trouble by
Sedimentation measuring the rate at
Rate (ESR) which RBCs setle to the
bottom of the tube
Reticulocyte Count measure of immature
RBCs; used to determine
the ability of the bone
marrow to produce RBCs
drugs: Aspirin, cortisone
Bone marrow depression or lack of
precursors for RBC formation (like
pernicious, vitamin B12, Folic acid,
and iron deficiency anemias)
chronic infection, inflammation, if too fast in tube then it will be too
advanced neoplasm (CA), and tissue fast in body
necrosis Also some drugs: Dextran,
oral contraceptives, methyldopa
bone marrow is producing and
releasing more RBCs in response to
Hypoxia (hemorrhage and anemia)

White Blood
Cells
Lab Tests What its for Low Results High Results Extra Notes

WBC's - Leukocytes measurs WBC count Leukopenia (low WBC) caused by
Fucntion to protect the chemotherapy (kills any proliferating
body from foreign invaders cells - bone marrow), leukemia (as
Most have very malignant cells overwhelm bone
short lifespan and need marrow), aplatic anemia (failure of
constant replenishing WBC/RBC creation which poor platelet
production), medications (minocyclen
antibiotic), infectious disease such as
flu, typhoid, malaria, HIV, and TB,
systemic lupus erythematosus
Leukocytosis (high WBC) caused by
viral, bacterial, fungal, or parasitic
infection, cancer, hemorrhage,
exposure to certain medication or
chemicals including steroids,
neoplastic growth of leukocytes
(first indication), and decrease in
RBCs b/c look at WBC %

Neutrophil Count 50% to 70% of all WBCs.
Phagocytes.
First line of defense
against microorganisms
Lymphocytes play an important role in
the immune function of
body - so a disruption will
result in altered response
to infection
Neutropenia - caused by decreased Neutrophilia - caused by bacterial
production in the bone marrow infection, acute inflammatory event
(aplastic anemia, cancer (blood), (Mis), drugs such as predinsone,
certain meds, hereditary disorders certain malignancies, and get SHIFT
(cyclic neutropenia), radiation, B12 or TO LEFT
folate deficiency, Increased
destruction (autoimmune
neutropenia, chemotherapy
treatments), Viral infections
Lymphocytopenia - caused by recent Lymphocytosis
cold, HIV, malnutrition, Rheumatoid
arthritis
Platelets cell fragments that
prevent blood loss by
(Thrombocytes) creating temporary plugs
in response to endothelial
injury in a vessel wall.
Production is stimulated in
part by thrombopoietin.
Platelets also release
serotonin and platelet
factor 3 (facilitate
coagulation), lifespan of 8
days
Prothrombin Time ratio of PT to PTT - helps
patients on coumadin
(PT) (NOT heparin)
Partial
Thromboplastin
Time (PTT) Heparin
Fibrinogen
Thrombocytopenia caused by
decrease production due to B12
deficiency, leukemia, sepsis, or
decrease production of
thrombopoietin by liver. By
increased destruction by systemic
lupus erythematosus, HIV, DIC, or
medication induced (heparin, valproic
acid, chemotheurapeutics)
DIC, liver diseases
Thrombocytosis caused by
Essential (primary) which is a
form of myeloproliferative disease
such as myelogenous leukemia,
polycythemia vera, and
myelofibrosis. Reactive
(secondary) by inflammation,
surgery, hyposplenism, and
hemorrhage or Fe deficiency
Hepatocellular diseases, obstructive
biliary disease, DIC, use of
coumadin (warfarin), patient with a
prolonged PT should be monitored
for signs and symptoms of bleeding
such as excessive bruising and
petechiae
Liver diseases, DIC, Biliary disease,
Use of heparin
Anemias
Type Information and Manifestations
Iron Deficiency Microcytic, hypochromic (low
Hg)-- Iron is needed for
Anemia (IDA) - most hemoglobin synthesis; food
common greatly reduces absorption and
can be stored as Ferritin or binds
to transferrin (2/3's is used in Hg
formation)
Vitamin B12 large number of megablast
and macrocytes; vitamin B12
(Cobalamin) needed for DNA synthesis, which
Deficiency Anemia is necessary for the formation and
maturation of rapidly proliferating
cells (RBCs); also causes WBCs
and platelet fromation by bone
marrow
Causes
Blood Loss - Trauma, menorrhagia
(prolonged/heavy menstrual
period), slow chronic blood loss
(peptic ulcer), hookworm Lack of
Fe in Diet - common in elderly
(appetite or financial related), not
eating Fe-riched foods (meat,
egges, milk) Inability to store Fe
- Fe is absorbed into your
bloodstream in your small intestine
so if have intestinal disorders like
Crohn's disease, celiac disease
(absorption issues)
Low Dietary intatke of Vitamin
B12 - vegetarians b/c no meat,
dairy, or fish Impaired
Absorption - absorbed in the
ileum so bowel resectioning or
Crohn's disease (chronic
inflammation of any part of
intestines), fish tapeworm
infestation, and liver disease
Pernicious Anemia - absence of
intrinsic factor (atrophic gastritis
and loss of gastric parietal cells -
impairs absorption of Vitamin B12
Diagnostic Tests /Manifestations
Manifestations - Brittle hair/nails,
sppon-shaped nails (due to poor
capillary circulation), Pallor,
fatigue, dyspnea, Glossitis (chronic
inflammation or infection of the
tongue), atrophy of papillae,
Cheilitis (sores in the corners of the
mouth) Diagnostics - CBC with
RBC indices will show microcytic,
hypochromic RBCs, moderately
reducted RBC count, low Hg and
low HCT, low serum Fe and Ferritin
Diagnostics - Serum level of
Vitamin B12 and Schillings Test
(to rule out Pernicious Anemia;
radioactivation to stop binding of
B12 in body tissues) - if urine test
demonstrates lack of intrinsic
factor then Pernicious Anemia; if
test is low then abnormal intestinal
absorption (impaired absorption
Manifestations - Presence of
megaloblasts, neurolgic symptoms
due to nerve demyelination,
paresthesias of the feet and
fingers, difficulty walking and
ataxia, abdominal pain, loss of
appetite, Glossitis (smooth tongue
and beefy red atrophy of papillae,
Treatment
Identify and control source of
acute or chronic loss of Fe;
Increase dietary intake of Fe,
Administer supplemental Fe like
Oral Agents: Ferrous Sulfate,
Gluconate, Fumarate (acidic
medium like OJ promotes Fe
absorption; causes GI distress
and can cause teeth staining)
Parenteral: Blood transfusion
(PRBCs), Iron Dextran
(dangerous can cause
anaphylactic rxn, muscle pain,
HA, chills, and dizziness; given in
mal-absorption or intolerance to
oral agents or severe blood
loss), Iron Sucrose (much safer;
no rxn)
Increase dietary intake of B12,
oral B12: cyanocobalamin,
hydroxochobalamin (indicated
for most people including those
with malabsorption), food
increases absorption, parental
administration: if neurologic
symptoms present
Folic Acid Deficiency Macrocytic, normochromic
RBCs, Folic Acid is required for
Anemia DNA synthesis and RBC
maturationAlcoholics get b/c they and stored in liver)
drink their calories so don't get
the need vitamins
Anemia of Chronic
Illness and
Inflammation
Sickle Cell Anemia inherited mutation of the beta
chain of the hemoglobin molecule
(autosomal recessive disorder; so
both parents have to have the
trait)
Thalassemia autosomal recessive disorder that defective synthesis of chains of Hg Alpha major is most serious of
has slow or defective synthesis of
the alpha or beta chains of Hg
G-6-PD Deficiency makes cells more vulnerable to
oxidants and causes direct
oxidation of Hg to methemoglobin.
Denaturing of Hg molecule to
form Heinz bodies which damages
the RBC resulting in hemolysis
low intake, alcoholism, intestinal
malabsorption, Celiac disease (Folic
acid is absorbed in upper intestine
chronic diseases such as AIDS,
Cancer, and Rheumatoid Arthritis
(usually mild to moderate)
Sickling Episodes/Crisis - Hypoxia
most common factor - other factors
causing are asthma, dehydration,
physical stress (trauma, physical
illness, viral or bacterial infections)
when O2 supply decreases, the Hg
distorts the RBC into a sickle shape
and becomes fragile which causes
obstruction in the microcirculation,
resulting in tissue ischemia and
necrosis (common sites are
abdominal organs, cardiac tissue,
joints, renal tissue, eyes and CNS.
Sickle cells are captured in the
spleen, where they are destroyed,
resulting in anemia
them b/c O2 can't be released to
tissue
Gene that determines this enzyme
is located on X chromosome and
defect is only expressed in males
and homozygous females
Diagnostic: Serum Folate Level
Manifestations: weakness,
fatigue, lightheadedness, difficulty
concentrating, forgetfulness,
irritability, pallor, loss of appetite
and weight loss
Manifestations - Fatigue,
dyspnea, pallor of mucous
membranes or conjunctiva If RBCs
are hemolyzed then get jaundice
and gallstones Pain (main
difference between this one and
other anemias) in legs, arms,back,
joints, and trunk (general pain),
results from hypoxia and ischemia
Folic Acid
No treatment necessary unless
symptomatic -- Erythropoietin
(glycoprotein hormone that
controls erythropoiesis, or RBC
production; in the kidneys)
Most important is help with
patient pain and then to
encourage fluid intake and rest.
Prevention - including premarital
counsiling (to know the % of
having child with sickle cell)
Palliative directly towards
symptoms management;
Sickling episode usually requires
hospitalization and may get Anti-
sickling agent (Hydroyurea), O2,
fluids, pain meds, rest, blood
transfusion (along with chelation
therapy whcih gets rid of or
avoids Iron overload from RBC
breakdown)
Blood transfusion along with Fe
chelation therapy, Splenectomy
may reduce the need for
transfusion b/c spleen filters
defective RBCs and collects Fe
from the hemoglobin and
recycles it to the bone marrow,
but in fetal produces RBCs