hematology Flashcards
(202 cards)
1
Q
HCT
A
hematocrit %
2
Q
HGB
A
Hb g/dL
3
Q
MCV
A
mean corpuscular volume
cystic= size of RBC
4
Q
RDW
A
RBC distribution width
5
Q
MCH
A
mean corpuscular Hb
6
Q
MCHC
A
mean corpuscular Hb concentration g/dL
chromic= color of RBC due to Hgb concentration
7
Q
microcytic anemia
A
low MCV
<80 fL
caused by iron deficiency, alpha and beta thalassemia minor
anemia of chronic disease
hypochromic (pale)
sideroblastic
decreased H & H
lead poisoning
chronic blood loss
8
Q
normalcystic anemia
A
anemia of chronic kidney disease (chronic disease anemia)
acute blood loss
hereditary spherocytosis
sickle cell
G6PD deficiency
cancer associated anemia
MCV=80-100 Fl
decreased H & H
9
Q
serum iron
A
total iron in blood
10
Q
ferritin
A
reflects the amount of stored iron in the body
11
Q
UIBC
A
unsaturated iron binding capacity
measures reserve capacity of transferrin
12
Q
total iron binding capacity
A
measurement of all proteins in the blood that are available to bind w/ iron, including transferrin
13
Q
transferrin saturation
A
calculation that is done with the iron test result
% of the transferrin that is saturated w/ iron
when iron stores are low, transferrin is high (vice versa)
14
Q
anemia
A
due to oxygen transporting capacity of blood
low blood cell mass
15
Q
macrocytic anemia
A
any condition causing marked reticulocytosis
abnormal nucleic acid metabolism (folate)
abnormal RBC maturation (B12 deficiency)
>100 fL
16
Q
CBC
A
exam RBC size and shape
Hb
hematocrit= % of RBCs in blood
peripheral blood smear
reticulocyte count= count of immature RBCs
17
Q
decreased production of RBCs
A
aplastic anemia
vitamin deficiencies
thalassemia
18
Q
increased destruction of RBCs
A
hereditary spherocytosis
G6PD deficiency
thalassemia
sickle cell disease
transfusion reactions
infections
19
Q
acute blood loss
A
hemodilution to maintain BV followed by increased erythropoiesis
normochromic and normocytic
recticulocytosis= abnormally high number of reticulocytes
20
Q
chronic blood loss
A
iron stores depleted resulting in iron deficiency anemia
21
Q
cystic
A
size of RBC
22
Q
chromic
A
color of RBC
23
Q
iron deficiency anemia
A
most common type of nutritional deficiency
decreased iron intake
malabsorption (celiac disease)
pregnancy
chronic blood loss (colon cancer, hemorrhoids, menorrhagia)
acute blood loss
low serum iron and increased iron binding capacity (IBC)
microcytic
hypochromic
spooning of nails
decreased serum ferritin, Hb, and hematocrit
increased transferrin
plummer vinson syndrome (esophageal webs and glossitis)
pica
24
Q
anemia of chronic disease
A
cytokine separation of iron into storage compartment and suppression of erythropoiesis
caused by osteomyelitis, endocarditis, lung abscess, Crohn’s, Hodgkins, lung and breast cancer, RA, IBS, DM, lupus, CKD
decreased serum iron
decreased iron binding capacity (transferrin)
increases serum ferritin
treated via erythropoietin and treating the underlying disease
25
megaloblastic anemia
impaired DNA synthesis
reduced intake of folate
decreased absorption of vit. B12
immature nucleus with mature cytoplasm
enlarged precursors in marrow
increased destruction of peripheral macrocytes
ineffective erythropoiesis
MCV>100
test via vit B12 and folate assay, bone marrow assay, peripheral blood smear
decreased platelets
26
bone marrow of megaloblastic anemia
hypercellular
megaloblasts
giant metamyeloblasts
iron accumulation
27
peripheral blood smear of megaloblastic anemia
giant platelets
hypersegmented granulocytes
pancytopenia
macroovalocytes
28
vitamin B12
large storage pool in liver and reabsorbed from the bile
29
vitamin B12 deficiency
impairs DNA synthesis by reducing available THF
neurological symptom can result in demyelination of posterolateral spinal cord
due to decreased absorption
can be caused by pernicious anemia, post gastrectomy (decreased absorption), resected ileum, Crohn's (decreased absorption), old age, dietary intake
can cause glossitis
increase in homocysteine and methylmalonic acid
30
pernicious anemia
autoantibodies in gastric juice
inhibit parietal cells leading to gastric atrophy
inhibit binding to intrinsic factor or distal ileum
megaloblastic anemia w/ reduced B12 absorption (cobalamin)
31
aplastic anemia
suppression of myeloid stem cells in bone marrow causing anemia, thrombocytopenia, and neutropenia (suppresses T cells)
can be caused by radiation, drugs, HIV, hepatitis, pregnancy, pesticides
petechiae and bruising
no splenomegaly
no reticulocytosis
myelodysplastic syndrome and aleukemic leukemia
treated via bone marrow transplant and immunosuppression
decreased platelets, decreased RBCs, decreased neutrophils (pancytopenia)
32
myelophthisic anemia
anemia/thrombocytopenia due to displacement of bone marrow
caused by tumor, TB, lipid storage disease, osteosclerosis, myelofibrosis, breast cancer
decrease in platelets
33
polycythemia
increases Hb conc. and hematocrit in peripheral blood
Hb: >16.5 (men)/ 16 (women)
hematocrit: >48 (men)/49 (women)
can lead to blood clots
34
intracorpuscular
inherent defects in RBC
inherited
35
extracorpuscular
external influences result in RBC defects
acquired
36
hemolytic anemia
increased RBC destruction
increased erythropoiesis
retention of iron
37
intravascular hemolysis
caused by malaria and transfusion reactions
mechanical trauma
complement induced injury
hemoglobinemia
hemoglobinuria
hemosiderinuria
hyperbilirubin
decreased haptoglobin
systemic hemosiderosis
in blood vessels
38
extravascular hemolysis
more common
affects liver and spleen
splenic sequestration and phagocytosis of RBCs
splenomegaly
jaundice
gallstones
decreased hapoglobin
systemic hemosiderosis
39
hereditary spherocytosis
autosomal dominant
25% autosomal recessive
intrinsic defect in RBC membrane
phagocytosed in spleen (splenomegaly)
jaundice and gallstones (40-50%)
increased osmotic fragility
treated via splenectomy
increased MCHC
40
sickle cell anemia
structurally abnormal hemoglobin (causes sickle shaped RBC)
extravascular hemolysis
heterozygous or homozygous
autosomal recessive
valine substitued for glutamic acid
41
thalassemia
reduced intracellular Hb
due to synthesis of alpha (chromosome 11) or beta (chromosome 16) chains
extravascular hemolysis
autosomal recessive
heterozygous= thalassemia minor
homozygous= thalassemia major
iron overload= heart failure
hepatosplenomegaly
high RBC count w/ low reticular count
microcytic hypochromic anemia
42
G6PD deficiency
glutathione metabolism
due to genetic variants on X chromosome
males affected the most
RBC oxidative injury w/o G6PD
reduced glutathione required to inactive oxidants (H2O2)-> denatures globin chains-> heinz bodies-> bite cells
hemolysis
43
paraoxysmal nocturnal hemoglobinuria
acquired stem cell gene mutations (piga gene)
inability to synthesize GPI
can cause infections and thrombosis
may progress to aplastic anemia or acute leukemia
absence of CD55 and CD59
hemoglobinuria
dark urine
RBCs break down at night
44
immunohemolytic anemia
due to autoimmunity or drug-induced immune hemolysis
coombs test
warm/cold hemolytic anemias
45
coombs antiglobulin test
direct=detects antibody on surface of patient RBCs
indirect=detects antibody in patient serum
46
warm hemolytic anemia
IgG opsonized RBCs phagocytosed in spleen
temps of 37 degrees
47
cold hemolytic anemia
IgM binds to RBCs at temps less than 30 degrees
Raynaud's
48
malaria
caused by plamodia protozoa
transmitted by female mosquito
fever
jaundice
hemoglobinnemia/uria
hemolytic anemia
erythroid hyperplagia
splenomegaly
brown material pigment on spleen, liver, lymph nodes, bone marrow
49
thalassemia major
microcytic hypochromic anemia
skeletal deformities
hepatosplenomegaly
systemic hemosideorsis (treated via blood transfusion, increased iron absorption, and increased erythropoiesis
frontal bossing
crew cut
50
thalassemia minor
mild microcytosis or anemia
reduced HbA and HbA2 (hemoglobin electrophoresis)
prenatal molecular diagnosis
51
relative polycythemia
hemoconcentration due decreased plasma volume
dehydration
vomiting
diarrhea
diuretics
severe burns
excessive sweating
52
absolute primary polycythemia
increase mass of RBC by mutation
proliferation of myeloid stem cells in bone marrow
due to JAK2 mutation
53
absolute secondary polycythemia
increase mass of RBC by elevated EPO
can be due to living in high altitudes which can lead to hypoxia
54
haptoglobin
protein produced by the liver that binds to free Hb in the bloodstream
prevents oxidative damage
allows liver to remove hemoglobin from body
55
heinz bodies
abnormal clumps of denatured Hb inside RBC indicating oxidative damage
56
transferrin
produced by the liver
main transporter of iron in blood
57
alpha thalassemia
1 deletion= asymptomatic
2 deletion= mild anemia
3 deletion= severe anemia (transfusion needed)
4 deletion= hydrops fetalis (death)
58
beta thalassemia
minor= asymp.
major= severe anemia
59
sickle cell treatment
treated via hydroxurea (increases in size of RBC)
60
sickle cell test findings
fatty change in heart, liver, and renal tubes
thrombosis
crew cut
proteinuria
autosplenectomy
systemic hemosiderosis
decrease in HbA seen in electrophoresis
splenic sequestration
increase in WBCs
gallstones
HCT= 18-30% beginning at 5-6 months w/ recticulocytes and hyperbilirubinemia
61
sickle cell symptoms
jaundice
painful cries
62
decreased RBC production
aplastic anemia
B12 and folate deficiency
myelophthisic
63
increased RBC destruction
sickle cell
thalassemia
immunohemolytic
64
blood
life-sustaining transport vehicle of the CV system
functions in transport, regulation, and protection
CT
65
blood transport
deliver O2 and nutrients to body cells
transports metabolic wastes to lungs and kidneys for elimination (number one metabolic waste is CO2-> 23% carried in RBC and rest in plasma)
transport hormones from endocrine organs to target organs
66
blood regulation
maintain body temp by absorbing and distributing heat
maintain normal pH using buffers (alkaline reserve of bicarbonate ions)
maintain adequate fluid volume in CV system
67
blood protection
prevent infection
prevent blood loss
68
normal hematocrit levels
males= 47% (5 SD)
females=42% (5 SD)
69
increased O2
scarlet red color
70
decreased O2
dark red color
71
normal pH of blood
7.35-7.45
72
albumin
produced by liver
makes up 60% of plasma protein
carrier of other molecules
blood buffer
maintains blood pH
major influence on plasma osmotic pressure
73
CT of blood
matrix (made up of plasma)
cells (RBCs, platelets, WBCs)
74
RBCs
45% of whole blood
most dense
have no nuclei
contribute to gas transport (increased SA)
biconcave shape
no organelles (no mitochondria)
contains spectrin
ATP production is anaerobic
Hb makes up for 97% of cell volume
normal count= 5 mil
75
buffy coat
consist of WBCs and platelets
<1% of whole blood
76
plasma
55% of blood
least dense
mostly water (90%)
77
platelets
cell fragments
78
WBCs
complete cells
79
formed elements
driven by needs of the body and chemistry (hormones, GF, O2 levels)
80
hematopoietic cells
found mostly in the bone marrow
can become RBCs, WBCs, and platelets
81
blood stem cell
myeloid stem cell-> RBCs or platelets or myeloblast->granulocytes
lymphoid stem cell->lymphoblast->lymphocyte or NK cells
82
stem cells
self-replicating
undifferentiated (no specific specialized features)
can divide and develop into cells of other types (undifferentiated->fully func.)
in leukemia, radiation treatment can also kill stem cells
stem cell transplants can also cause a immune rxn
83
EPO
produced by the kidney
causes RBCs to mature faster
testosterone enhanced EPO production (increased RBCs in males)
84
TPO
produced by the liver and kidney
85
leukocyte formation
IL-3
IL-5
G-CSF/AG-CSF
drives both myeloid and lymphoid precursor cell differentiation
86
agranulocytes
monocyte
lymphocyte
87
granulocyte
neutrophil
eosinophil
basophil
88
spectrin
gives RBCs flexibility to change shape
89
hemoglobin
4 chains (2 alpha and 2 beta)->globin protein
binds to O2 and transports it
normal levels male: 13-18 g/100 mL female: 12-16 g/100 mL
red heme pigment
contains 4 heme groups-> transports 4 O2
90
normocytic anemia
anemia of chronic disease
acute blood loss
G6PD deficiency
sickle-cell
hereditary sphereosis
91
LDH
lactate dehydrogenase
indicates hemolytic anemia
assesses tissue damage
increased LDH=hemolysis
differentiates b/w various types of anemia
tracks severity and progression of anemia
increased bilirubin
increased recticulocytes
decreased haptoglobin
92
hemocytoblasts
hematopoietic stem cells
93
erythropoiesis
process of formation of RBCs (~15 days)
hematopoietic stem cell->myeloid stem cell->proerythroblast (committed cell)-> basophilic erythroblasts (synthesizes many ribosomes)->polychromic erythroblast-> orthochromatic (eject most organelles; nucleus degrades; causes concave shape)->
recticulocytes (released into blood 1-2 days before maturation)->mature erythrocyte (within 2 days; ribosomes degrade)
## Footnote
profitable businesses pollute our rural environment
94
recticulocytosis
indicate the rate of RBC formation in bone marrow
normal range (0.5-2.5%)
95
hypoxia
too few RBCs
dietary requirements= B12 and folic acid (needed for DNA synthesis in RBCs)
EPO=increased RBCs
96
increased blood viscosity
too many RBCs
97
HIF
O2-sensitive enzymes in kidneys degrade HIF (transcription factor)
decreased O2= O2 sensitive enzymes in kidneys cannot degrade HIF
increased HIF= EPO synthesis
too many RBCs or increased O2= inhibit EPO production
98
artificial EPO
increased hematocrit (allows athletes to increase stamina and performance)
EPO can increase hematocrit from 45-65% w/ athletic dehydration concentrating blood even more
can lead to thrombosis
99
dietary requirements for erythropoiesis
AA
lipids
carbs
iron
B12
folic acid
100
iron
65% found in Hb
rest in liver, spleen, bone marrow
toxic by itself
binds to ferritin or hemosiderin and is stored in liver for reuse
supplementation can lead to constipation
101
life span of RBCs
100-120 days
macrophages in spleen engulf and breakdown/recycle dying RBCs
102
heme
bilirubin->urobilinogen-> stercobilin
103
globin
metabolized into AA and released into circulation
104
recticulocyte count
tic count
105
high recticulocyte count
hemolytics anemias
106
low recticulocyte count
iron deficiency anemia
anemia of chronic disease
sideroblastic anemia->can be caused by lead poisoning
aplastic anemia
pernicious anemia
B12 and folate deficiency
107
non megaloblastic
alcoholism
liver disease
hypothyroidism
108
hemolytic anemias
sickle cell
PNH
G6PD deficiency
blood loss
immunohemolytic anemia
hereditary spherosis
109
non-hemolytic anemias
myelophistic anemia
anemia of chronic disease
aplastic anemia
polycythemia
110
intravascular anemia
PNH
G6PD deficiency
blood loss
cold hemolytic anemia
111
extravascular anemia
warm hemolytic anemia
112
intracorpuscular anemia
sickle cell anemia
hereditary sphereosis
113
both intravascular and extravascular
sickle cell anemia
114
alpha and beta thalassemia
can cause hemolytic anemia if chains are linked up
115
renal anemia
caused by the lack of EPO
accompanied by renal disease (kidneys cannot produce enough EPO)
treated via synthetic EPO
116
hydroxurea
induces formation of fetal Hb (does not sickle)
117
NO
induces vasodilation
one of the treatments for sickle cell
118
blood doping
can cause polycythemia
119
functions in defense against disease
can leave capillaries via diapedesis
move through tissue spaces by amoeboid motion and positive chemotaxis
120
neutrophils
contain hydrolytic enzymes
or antimicrobial= defensins 50-70% WBCs
stain both via acidic and basic dyes
VERY phagocytic (kill microbes via respiratory burst)-> increase O2 consump. to then synthesize a ROS to kill pathogens
multilobed nucleus
pale red and blue cytoplasmic granules
121
granulocytes
larger and more short lived than RBCs
phagocytic
122
eosinophils
red staining granules contain digestive enzymes
bilobed nucleus
asthma and allergies
parasites
123
basophil
contain histamine
similar to mast cells
bilobed nucleus
purplish-black cytoplasmic granules
124
lymphocytes
found in lymphoid tissue
crucial to immunity
B (bacteria), T (virus and cancer)
large spherical nucleus
thin rim of pale blue cytoplasm
125
monocytes
largest
U or kidney shaped nuclei
phagocytic
activate lymphocytes and mount an immune response
126
leukopoiesis
stimulated by 2 types of chemical messengers (ILs and CSFs)
originate from hemocytoblast stem cells
127
lymphoid stem cells
produce lymphocytes and NK cells
128
myeloid stem cells
produce all other formed elements
129
granulocyte production
myeloblasts->promyelocytes (accumulate lysosomes)->myelocytes (accumulate granules)->band cells (nuclei form curved arc)->mature granulocyte (nuclei become segmented before being released in blood; 10x more are stored in BM than in blood)
130
agranulocyte production
monoblast->promonocyte->mature monocyte
131
myeloid leukemia
involves myeloid stem cells
132
lymphoid leukemia
involves lymphoid stem cells
133
acute leukemias
children
derives from stem cells
134
chronic leukemias
older people
proliferation of later cell stages
135
infectious mononucleosis
viral
aka kissing disease
caused by epstein barr virus
rest (better in 4-6 wks)
get CBC
136
chemicals involved in clotting process
serotonin
Ca2+ *
enzymes
ADP
PDGF
NO
prostacyclin from the endothelial cells lining blood vessels
137
thrombopoietin
formed in myeloid line from stage 4 megakaryoblast (stage 1)-> sends cytoplasmic projections into lumen of capillary (break off into platelet fragments)
150-400k (normal)
main regulator of thrombopoiesis
produced in liver and renal tubular epithelial cells
138
plasma cell
type of B cell
produce antibodies
139
margination
WBCs move towards vessel walls
140
diapedesis
WBCs squeeze through walls of capillaries
141
positive chemotaxis
movement of WBCs to an area of higher chem conc.
via ameboid motion
142
formation of platelets
mitosis occurs, cytokinesis does not= large stage 4 cell
143
how is pernicious anemia diagnosed?
schilling test-> shows inability to absorb vit. B12
144
what type of malaria organism is rapidly progressive and fatal?
P. falciporum
145
what can cause normocytic anemia?
cardiorenal anemia syndrome
cancer associated anemia
acquired anemia in hospitalized patients
146
hemolytic anemia
high recticulocytes
147
non-hemolytic anemia
low reticulocytes
148
lead poisoning
basophilic stippling
microcytic
149
hypothyroidism
slows DNA synthesis
slows bone marrow activity
abnormal RBC maturation
macrocytosis
150
size of nodes that need to be investigated
>1 cm
151
HIT
utilizes ELISA
152
lymphoma
chest mass
153
leukemia
painful lymph node swelling
154
primary myelofibrosis
excessive increase in collagen proteins
155
ITP
no adenopathy or splenomegaly
156
normal lymphocyte values
25-45%
157
normal monocyte values
3-8%
158
normal eosinophil values
2-4%
159
normal basophil values
0.5-1%
160
globulin proteins
alpha and beta= transport proteins in blood that bind to lipids, metal ions, and fat soluble vitamins
gamma= antibodies released by plasma cells during immune response
161
normal blood clotting time
2-7 s
162
3 steps in hemostasis
vascular spasm
platelet plug formation
coagulation
163
vascular spasm
responds to injury via SM vasoconstriction
triggered by direct to vascular SM, chemicals released by endothelial cells and platelets, pain reflexes
platelets stick to collagen fibers that are now exposed due to damage to the vessel
prostacyclins and NO prevent platelet sticking
vWF helps stabilize new platelet-collagen adhesion in damaged vessel made by endothelial cells and megakaryocytes
164
platelet plug formation
release chemical messengers ADP, vWF ad Ca2+, serotonin and thromboxane A2
165
ADP
causes more platelets to stick and release their contents
166
serotonin and thromboxane
enhance vascular spasm and platelet aggregation
167
coagulation
reinforces platelet plug with fibrin threads
blood is transformed from liquid to gel
these clots are effective in sealing larger breaks
prothrombin->thrombin->fibrinogen->fibrin->activates factor 13
168
intrinsic pathway
clotting factors are present within the blood
169
extrinsic pathway
factors needed for clotting are located outside the blood
triggered by the exposure to TF (factor 3)
faster pathway
170
anticoagulants
factors that normally dominate in blood to inhibit coagulation (heparin and protein C and S)
171
clot retraction
actin and myosin in platelets contract within 30-60 mins
contraction pulls on fibrin strands, squeezing serum from clot
draws ruptured blood vessel edges together
172
serum
plasma minus the clotting proteins
173
PDGF
released by platelets
stimulates of SM cells and fibroblasts to rebuild blood vessel wall
174
VEGF
vacular endothelial growth factor
stimulated cells to multiply and restore endothelial lining
175
fibrinolysis
clots are removed after repair is complete
begins within 2 days and continues for several days until clot is dissolved
176
plasminogen
plasma protein that is trapped in clot
converted to plasmin (fibrin-digesting enzyme)
177
antithrombin 3
inactivates any unbound thrombin that escapes into bloodstream
178
heparin
in basophil and mast cells inhibit thrombin by enhancing antithrombin 3
179
tPA
factor 12 and thrombin all play a role in this conversion process
180
factors preventing platelet adhesion
smooth endothelium of blood vessels prevents platelets from clinging
endothelial cells secrete antithrombic substances such as NO and prostacyclin
vit. E quinone, formed when vit. E react w/ O2 is a potent anticoagulant
181
thromboembolic disorders
result in undesirable clot formation
182
bleeding disorders
abnormalities that prevent normal clot formation
183
DIC
both a bleeding and thromboembolic disorders
184
thrombus
clot that develops and persists in unbroken blood vessel
may block circulation, leading to tissue death
185
embolus
clot/thrombus freely floating in bloodstream
186
embolism
embolus obstructing a BV
(pulmonary or cerebral emboli)
187
risk factors of thrombi and emboli
atherosclerosis
inflammation slowly flowing blood
blood stasis from immobility
188
anticoagulant drug
aspirin= antiprostaglandin that inhibits thromboxane A2; lowers heart attack incidence by 50%
heparin= pre- and post- operative cardiac care as well as to prevent venous thrombosis
warafin= oral; reduce risk of stroke in patients prone to A-fib in which blood pools to the heart (interferes w/ the action of vit. K)
189
impaired liver function
inability to synthesize procoagulants
causes include vit. K deficiency, hepatitis, or cirrhosis
prevent liver from producing bile which are needed to absorb fat and vit. K
190
CV system
minimizes effects of blood loss by reducing volume of affected BV ; stepping up production of RBCs
loss of 15-30% causes pallor and weakness
loss of more than 30% results in potentially fatal severe shock
death may result from low BV
191
whole blood transfusions
used only when blood loss is rapid and substantial
packed red blood cells or PRBCs are used to restore O2 carrying cap.
transfusion rxns can be fatal
blooding typing to determine blood groups
192
antigens
anything perceived as foreign that can generate an immune response
RBC antigens are referred to as agglutinogens b/c they promote agglutination
30 naturally occurring RBC antigen
193
ABO blood groups
based on presence or absence of two agglutinogens (A and B) on surface of RBCs
A=A antigen
B= B antigen
AB= A and B antigen
O= neither A or B
blood may contain performed anti-A and anti-B antibodies (agglutinin)
anti-A or anti-B in blood at about 2 months of age, reaching adult levels by 8-10 yrs of age
194
Rh blood groups
presence of D antigen
anti-Rh antibodies are not spontaneously formed in Rh- individuals
anti-Rh antibodies form if Rh- individual receives Rh+ blood, or Rh- mom is carrying Rh+ fetus
second exposure to Rh+ blood will result in typical transfusion
hemolytic disease of newborn= erythroblastosis fetalis
treated via Rhogam
195
transfusion rxns
diminished O2 carrying cap
decreased BF beyond blocked vessel
Hb in kidney tubules= can lead to renal failure
fever
chills
low BP
rapid HR
nausea
vomiting
196
type O
universal donor
197
type AB
universal recipient
198
autologous transfusions
patient predonates own blood that is stored and available if needed
199
PT and platelet counts
assess hemostasis
200
Ca2+
needed both by the intrinsic and extrinsic pathway
201
phospholipids
on surface of platelets
202
CMP
assess liver and kidney disorders
