Hematology Review 5/1

Know CLSI order of draw

o White, Blue, Red, Green, Purple, Grey
If a tube doesnt have enough blood, what would that do?
o You can still use the tube. It will be well anticoagulated, but the red cells may be
crenated. Hypertonic solution.
If platelet satelitism:
o Thats an artifact of EDTA. Doesnt happen in patients.
o Draw patient in citrate in order to correct. But you need to correct for the
dilution.
o To correct for the dilution:
1:10 (1 part citrate, 9 parts blood)
RBC Indices
o Rule of 3 between Hgb and Hct. (1:3)
o MCV: Mean cell volume/size
Hct/RBC x 10
o MCH:
Hgb/RBC x 10
o MCHC: Average amount of hemoglobin per red cell based on its size
Hgb/Hct x 100
High MCHC seen in (high hemoglobin in cells):
o Spherocytosis (too much hemoglobin for its size becomes
spherical)
o Cold agglutinins (a lot of cells sticking together)
Reticulocytes
o New methylene blue
Wrights Stain
o Contains methylene blue and eosin
o Dissolved in methanol, which is why you dont have to fix it first
o Leave stain on too long: Too blue (Too alkaline)
o Leave stain on not long enough: Too pink (Too acidic, or washing too much)
Bubbles in RBCs (Water artifacts)
o If the slide stains too slowly
Prussian Blue Stain
o Stains iron
Basophilic Stains
o Stains hemosiderin (insoluble storage of iron)
Hemosiderin increased in people with high RBC turnover
When RBCs burst when they are replaced, heme part is separated. Iron is
recycled, not removed from the body.
Example: People who get a lot of transfusions. Making a lot more
RBCs, using up iron faster, but generally: also getting transfusions, so
the cells burst, keep iron, but giving them more RBCs, which are
normal lifespan. BUT Broken down eventually and extra iron that
builds up.
Iron overload can cause liver issues/failure
Also seen in urine sediment
Pappenheimer bodies/Siderotic granules Both Iron
Difference between the 2: Paps can see on Wright Stain. Siderotic
only with iron stain.
Hypercellular Bone Marrow
o Polycythemia Vera: chronic myeloproliferative
o Essential Thrombocythemia
o CML
CML
o Can turn into ALL
White Count Reference Range
o Around 5-10
Left Shift
o High amount of immature cells
For Granulocytes --- Will see bands, then metas, then myelos, etc. As they
leave the marginal pool. Then from the bone marrow pool.
Example: 30% bands, 5% metas, 1% myelos
If you see pros and blasts CML
o Due to stress if non-malignant. Could be bacterial.
o Other left shifts that are malignant:
CML
Other myeloproliferative syndromes: myelofibrosis, essential
thrombocythemia
Basopenia
o Low basophils
o Very difficult to prove
Anomalies
o Pelger-Huet
Bilobed (Dumb-bells) in bands, fully mature
Function normally
o Pseudo-Pelger-Huet
Seen in hematologic disorders, like leukemias, myelodysplastic disorders
Not all the cells will appear like this.
o Chediak-Higashi
Albinism
Weird granules, platelets
o Alder-Riley
Granules are functional
o May-Heglin
Large platelets, fewer platelets
Dohle-like bodies
Coagulation Review 5/1

Primary Hemostasis
o Platelets and Vascular (Vasoconstriction)
o Resting Platelet Activated platelet after injury
1) Adheres
Form platelet plug (temporary)
Fibrin crosslinks to trap platelets in mesh
2) Aggregates
Coming together/Clumping together to each other
3) Secretes
VWF (Factor V), ADP, etc.
o Secondary Hemostasis begins after (short delay)
o Fibrin formation occurs on surfaces of platelets
Coagulation Pathway
o Intrinsic
Takes longer because starting with XII. APTT tests for Intrinsic. Slower, but
produces more.
APTT about 25 seconds
o Extrinsic
Faster. Protime. Faster, but produces less.
PT about 10 seconds
o Serine proteases
Proceeding cleaves molecule, makes available the active site becomes
active.
o NOT Serine Proteases:
V, VIII, XIII
o Extrinsic Factors:
II, V, VII, X
o Intrinsic Factors:
II, V, VIII, IX, X, XI, XII
o PT
Test for: VII, X, V
o APTT
Tests for: IX, XI, VIII
o Inhibitors
Dont want body to clot all the time.
Tissue Factor
Antithrombin (works in various places other than thrombin)
Activated Protein C works with Protein S
o Deficiency with any coag factor
Bleed more, ex. Hemophilia
Hemophilia A: VIII
Hemophilia B: IX
o Deficiency with inhibitors
Tendency to clot more
o Coumadin Antidote: Vitamin K
Ex. Rat poison consumed
o Heparin Antidote: Protamine Sulfate
o APTT
Add EACA, which skips the activation step (longest part)
Whole blood normally takes 5-10 minutes to clot normally without any
additives
Activated clotting is about 120 seconds (2 minutes)
Takes 3-7 minutes for first activating step
Eliminating this with EACA
o PT
INR purpose: for people who are anticoagulated. To make equivalent
among manufacturers.
Different kinds of thromboplastin.
o Fibrin Stabilizing Factor
Factor XIII
o Fibrinogen (Factor I)
o Prothrombin (Factor II)
o Antihemophilic Factor (Factor VIII)
o Contact Group
PK, HMWK, Factor XI, Factor XII
o Cofactors
Factor III, V, VIII, HMWK
o Vitamin K Dependent Factors
II, VII, IX, X, Protein C and S
o Fibrinolysis
Plasmin is active. Plasminogen inactive.
o Prothrombin Group
II, VII, IX, X
Made in the liver
Require calcium
Absorbed by barium sulfate
o Fibrinogen Group
Fibrin, V, VIII, XIII
Factors that are NOT Serine Proteases
o Plasmin works on fibrinogen group
I, V, VIII
o Protein C and S
Work together to inactivate V and VIII
o Factor V Liden
Also called Activated Protein C Resistance.
Normally, protein C is going to stop clotting (anticoagulant). If we have an
abnormal V (Factor V Liden) Hereditary and makes people susceptible to
clotting.
VonWillebrands Disease
o Most common hereditary bleeding disorder BESIDES low platelets (most common
bleeding disorder)
o Factor VIII is carried by VW molecule
Hemophilia A
o Most common factor deficiency disorder
o Treatment: Give factor VIII theyre missing
Dont give Cryo has stuff they dont need
DIC
o Disseminated Intracellular Coagulation
o High APTT, High PT, Low fibrinogen, Low platelets, Positive D-dimers and fibrin
split products
o Some trigger, like gram-negative sepsis, platelet clumping and fibrin formation.
Difference with TTP: Platelet problem, but coagulation is normal.
Low Molecular Weight Heparin
o Safer, usually doesnt need to be monitored.
Doesnt result in heparin-induced thrombocytopenia
o When it does need to be monitored, monitored by anti-factor Xa assay
Cant use APTT doesnt work.

Urinalysis/Body Fluid Review 5/1

Anatomy
o Afferent artery goes in, efferent artery goes out in glomerulus
Only network where it goes from artery artery
o Equivalent of plasma without large proteins and protein-bound things in Bowmans
capsule.
Blood has 6-8 grams of protein; 24-hour urine has around 80 mg. Very low.
GFR
o Rate at which the filtrate is formed per minute. Sensitive measurement.
Normal: Around 120 mL/minute
o One of the main ways that we can tell kidney function
Creatinine
BUN in blood is function of kidney disease; but not as sensitive
Doesnt accumulate in blood until GFR is less than around 20 mL/min
Microalbuminuria
o Most sensitive method for detecting
Hormones
o Renin, Angiotensin. Produced my kidneys. Response to high blood pressure
o Renin ends up in more aldosterone reabsorbs sodium. Affects blood pressure
o ADH produced by pituitary, affects mostly the collecting duct and the end of
the distal convoluted tubule. Controls water. Affects blood pressure
Creatinine Clearance
o Urine Creatinine x Volume / Plasma Creatinine
o Corrected for body surface area
1.73 / Body Surface Area
o eGRF (Estimated): calculation using plasma creatinine
Different formulas used
Oliguria
o Little urine output
Normal Urine Volume
o Around 2000 mL (2 L)
2-hours postprandial
o 2 hours after eating
o Testing to see if glucose is high If so, over renal threshold
24 hour
o Check creatinine levels to make sure the levels are around what they should be
around 24 hours of collection
Crystals
o Alkaline: Not pathogenic
o Pathogenic: Cholesterol, Cysteine
Radiographic Media
o CT Scans, etc.
o Better resolution
o Causes urine to have high specific gravity, could crystalize if refrigerated
Crystals look like cholesterol crystals or needles
pH
o 5.0 8.0
o pH isnt that diagnostic, alone
Protein
o High pH causes false positive protein results
Bases of the dipstick tests is error of indicators pH indicator, basically.
Buffered at a really acidic pH so that any change in the indicator is only
due to the protein concentration. If urine is alkaline overcomes the
buffer. Can cause false positive.
CliniTest
o Reducing sugars
o Acids (Ex. Vitamin C Ascorbic acid)
Ketones
o Breakdown of fatty acids when carbohydrates are low
Acetoacetate is what we test for in urines
Acetone
Blood
o Speckled: Intact red cells
Bilirubin
o Amber/dark yellow urine
o Protect from light
o Conjugated in urine
Add acid or OH Becomes more water soluble. Purpose of conjugating so it
can be excreted in urine
o (+) Urobili, (-) Conj Bili Pre-hepatic jaundice, ex. Hemolytic anemia
o (-) Urobili, (+) Conj Bili Post-hepatic jaundive, ex. Obstruction
Uro. Not reaching intestines Blockage.
o (+) Urobili, (+) Conj Bili
Nitrite
o (+) Bacteria that convert nitrate to nitrite, ex. E. coli
o Vitamin C interferes
Vitamin C
o Interferes anything with oxidation/reduction step
Specific Gravity
o Add 0.005 if pH > 6.5
Pad based on pH change
Pyelonephritis
o WBC Casts
Acute glomerulonephritis
o RBC Casts
If you only had one tube, what would the order be?
o Micro always go first
CSF glucose
o Should be 60-70% of blood glucose