Midterm Flashcards
(116 cards)
1
Q
Give examples of pre-analytical lab errors
A
patient factors, wrong tube type, wrong sample, sample handling
2
Q
Give examples of analytical lab errors
A
equipment and reagent problems, pipetting error, calculation error
3
Q
Give examples of post-analytical errors
A
reporting errors
4
Q
quality assurance
A
Lab procedures that monitor and improve all aspects of lab performance, seeks to minimize pre, post, and analytical errors
5
Q
quality control
A
lab procedures that monitor analytical performance of instruments detecting analytic error
6
Q
internal quality control
A
instrument functions built in (system checks, calibration checks, set by manufacturer)
7
Q
external quality control
A
running controls, best test for analytical error as it tests everything
8
Q
external quality assurance
A
comparability testing, 4 times a year or whenever you test it
9
Q
potassium EDTA contamination in chemistry
A
hyperkalemia, hypocalcemia, ALP falsely decreased, hypomagnesemia
10
Q
delay in separating cells for chemistry
A
hypoglycemia, hyperkalemia, hyperphosphatemia, hypermagnesemia, increased AG
11
Q
stroma components
A
reticular cells/fibroblast, adipocytes, vascular cells, collagen/proteoglycan/BM
12
Q
hematopoietic envt of megakaryocytes
A
lie outside vascular sinus and dump platelets into circulation
13
Q
hematopoietic envt of RBC progenitors
A
develop in erythroid islands around nurse cells/macrophages
14
Q
hematopoietic envt of granulocytes
A
develop in paratrabecular regions away from vascular sinuses
15
Q
HSC vs. HPCs
A
HSCs are capable of proliferation into any cell line and long-term self-renewal/differentiation. HPCs are common lymphoid/myeloid progenitors. They form colones in bone marrow culture but do not have long-term self-renewal capacities. HPCs usually express CD34.
16
Q
causes of stem cell failure
A
toxin, drug-mediated, infectious (parvo, FeLV, Ehrlichia), insufficient stimulation by cytokines/GFs, damage to stem cell niche
17
Q
early-acting HGFs
A
trigger development of dormant, primitive HSCs to begin cycling, turn into common myeloid or lymphoid progenitors.
Stem cell factor/c kit ligand
G-CSF
TPO
FLT3L
18
Q
intermediate-acting HGFs
A
broad, supports proliferation of multipotent HPCs
IL-3
GM-CSF
IL-4
19
Q
late-acting HGFs
A
more restrictive specificity, effects on committed progenitor cells and later stages of development when cell lines can be recognized morphologically
EPO TPO IL-5 M-CSF G-CSF
20
Q
aggregate reticulocytes
A
earlier, polychromatophilic, large amount of RNA, indicative of recent release, mature to punctate in 1 day
21
Q
punctate reticulocytes
A
later, ribosomal material decreases until only a few basophilic specks are seen, but not polychromatophilic, can be in circulation for up to 14 days, found in blood of normal cats
22
Q
cytokines in neutrophil production
A
GM-CSF, G-CSF, IL-3, IL-6
23
Q
cytokines in eosinophil production
A
IL-5, IL-3, GM-CSF
24
Q
cytokines in basophil production
A
IL-5, IL-3, GM-CSF, TGF-B
25
cytokines in monocyte production
IL-3, GM-CSF, M-CSF, IL-34
26
cytokines in lymphocyte production
SCG, IL-7 (IL-15 and IL-2 for NK cells)
27
cytokines in platelet production
TPO, IL-6, EPO
28
spectrin
alpha and beta, most abundant protein in RBC cytoskeleton. Anchored to protein in bilayer made of actin (4.1 protein), affixed to inner leaflet via ankyrin, bound to band 3
29
band 3
membrane protein, anion transporter. Cl/HCO exchange to increase capacity of blood to carry CO2 from tissue to lungs
30
increased 2,3 DPG
coincides with increased temp, increased CO2, decreased pH- less affinity for O2, more readily released in tissues
31
decreased 2,3 DPG
coincides with decreased temp, decreased CO2, increased pH- more affinity for O2, less readily released in tissues
32
stimulation of 2,3 DPG
anemia, inorganic phosphate, increased blood pH
33
haptoglobin
used to bind free hemoglobin in circulation, cleared by hepatocytes/macrophages- MAJOR
34
hemopexin
highest affinity for heme in plasma protein leads to hydrolysis of MetHb to ferric heme and globin- MINOR
35
serum iron
not measurement of free iron, all is bound to transferrin
36
transferrin
negative acute phase protein, serum iron bound to this
37
total iron binding capacity
total amount of Fe bound to transferrin, increased due to artifact (hemolysis, lipemia), iron overload, decreased due to inflammation and PLN/PLE
38
ferritin
positive acute phase protein, better indicator of total body iron stores, reflects iron store if inflammation not present, increased due to inflammation, overload of iron, liver disease
39
hepcidin
positive acute phase protein, downregulates ferroportin
40
pathways RBCs use to make ATP
Emden-Meyerhoff pathway (anaerobic), pentose phosphate pathway
41
protection against oxidative injury
hexose monophosphate shunt- produces reducing compound NADPH
methemoglobin reductase/cytochrome B5 reductase- re-reduces iron so that it can carry O2
42
PFK deficiency in dogs
rate-limiting enzyme in Emben-Meyerhoff pathway, decreased 2,3 DPG and ATP (increased O2 affinity), muscle PFK, RBCs alkaline fragile, strongly regenerative anemia
43
PFK deficiency breed
English Springer Spaniel
44
PK deficiency in dogs
below the shunt, increased 2,3 DPG, decreased affinity for O2, highly regenerative, progressive myelofibrosis and osteosclerosis, die of anemia or hepatic failure
45
PK deficiency breed
Basenjis, Westies, Beagles
46
PK deficiency in cats
Abyssinian, Somali, DSH, no osteosclerosis or myelofibrosis, chronic anemia, not life-limiting
47
cytochrome b5 reductase/metHb reductase
re-reduces Fe3 to Fe2 within Hb to allow it to carry O2. FAD is cofactor
48
glucose-6-phosphate dehydrogenase
in hexose monophosphate shunt, re-reduces NADP to NADPH to take hit for oxidative damage
49
flavin adenine dinucleotide/FAD
coenzyme for glutathione, hexose monophosphate shunt, and metHb pathway
50
hereditary spherocytosis
disorder of vertical interactions- band 3 and anchorin, leads to osmotic fragility, hemolytic anemia, splenomegaly
51
hereditary elliptocytosis
oval and elongated, defect in horizontal interactions, beta spectrin mutation. Decreased stability of RBCs when subjected to stress. Protein 4.1 deficiency
52
hereditary stomatocytosis
Bowl shape, slit like appearance. Miniature schnauzers- no clinical disease.
familial stomatocytosis and hypertrophic gastritis- Drentse partijshound, disorder of lipid metabolism and altered membrane phospholipid concentration
53
poodle macrocytosis
toy and miniature, no C/S
blood smear: macrocytosis, HJ bodies, hypersegmented giant neutrophils
bone marrow: nuclear bridging
54
cobalamin deficiency
non-regenerative, normocytic, normochromic anemia. Giant schnauzers don't have cubilin in ileal mucosa.
blood smear: metarubricytosis, HJ bodies, hypersegmented neutrophils, giant platelets
bone marrow: giant band neutrophils, metamyelocytes
55
congenital dyserythropoiesis
English springer spaniels- polymyopathy and cardiac dz as well
bone marrow: erythroid hyperplasia
also seen in polled Hereford calves
56
neutrophil hypersegmentation causes
glucocorticoid administration, chronic inflammation, aged neutrophils, myeloid neoplasia, leukocyte adhesion deficiency, amphetamine toxicity, idiopathic in quarter horses, heatstroke (botryoid nuclei)
57
ddx for marked leukocytosis
Hepatozoonosis, leukocyte adhesion deficiency, immune-mediated disorders, chronic myeloid leukemia, paraneoplastic, tissue necrosis, purulent inflammatory conditions, early estrogen toxicity
58
Chediak-Higashi syndrome
granules and inclusions issue
large pink/purple granules
persians, mink, foxes, whales
neutrophils have decreased mobility, increased susceptibility to infection, due to mutation in lysosomal trafficking regulator gene, abnormal platelet function (lack normal granules)
inhibition of platelet aggregation- prolonged bleeding
59
leukocyte adhesion deficiency
inherited neutrophil disorder
beta 2 integrin (Irish setters, Holstein, 1 cat)- recurrent infections
kindlin 3 (GSD)- critical for beta 2 activation, impairs platelet aggregation
decreased neutrophil adhesion, impaired chemotaxis
60
cyclic hematopoiesis
inherited neutrophil disorder
Grey collie syndrome
autosomal recessive, abnormal hair pigment, neutrophil count fluctuates at 12-14 day intervals. Often die by 6 months of age
61
Birman cat anomaly
granules and inclusions
small pink/red granules within neutrophils, but neuts have normal function. Differentiate from storage dz and toxic granulation
62
Pelger-Huet anomaly
leukocyte morphology changes
hyposegmentation
Australian shepherds
autosomal dominant
not bands!
63
May-Hegglin anomaly
granules and inclusions
mutation in muscle myosin heavy chain II gene (MYH9).
large blue inclusions in cytoplasma
thrombocytopenia (macroplatelets)
Pugs
64
toxic neutrophil granulation
granules and inclusions
magenta granules in horses
will have other indicators of toxicity
65
lysosomal storage dz
granules and inclusions
results in accumulation of undegraded substances in lysosomes
66
acute lymphoid leukemia
young to middle age, short clinical course, poor px, cats often T cell and FeLV positive, dogs B, T, NK, or null (B most common)
moderate to severe non-regenerative anemia often seen with neutropenia and/or thrombocytopenia.
immature large lymphocytes in peripheral blood
Positive for CD34
not associated with solid tumors
67
acute myeloid leukemia
young to middle age, short clinical course and poor px
large myeloid blasts in peripheral blood. BM > 20% myeloblasts. Can be difficult to differentiate blasts
due to genetic mutations that prevent cell maturation
promotion of proliferation leads to myelophthisis
68
leukemic phase of lymphoma/stage V lymphoma
variable clinical presentation, moderate to severe enlargement of lymphoid organs, small or well-differentiated neoplastic lymphoma cells
CD34 negative
69
chronic myeloproliferative neoplasia
genetic mutation causes differentiation, this also causes proliferation- high counts of involved cell lineage
myeloid hyperplasia < 20% blasts
70
myelodysplastic syndrome
ineffective hematopoiesis and abnormal maturation in > 1 cell line
preleukemia- can progress to AML
clonal proliferation
<20% blasts
71
immunophenotyping
using antibodies to detect antigens on the surface or in the cytoplasm or nucleus of cells
each hematopoietic cell expressed unique markers during differentiation and maturation
flow cytometry- use monoclonal ab's for array of proteins expressed on cell surfaces
more ab's for lymphoid than myeloid lineages in vet med
can't distinguish neoplastic from normal neutrophils, eosinophils, or monocytes. Can't distinguish myeloid from lymphoid lineage if cells aren't expressing any lineage antigens other than CD34
can distinguish stage V lymphoma from acute leukemia (CD34 positive acute leukemia
T vs. B cell
72
clonality
PARR
best to distinguish between reactive and neoplastic causes of lymphocytosis and confirming lymphoma vs. reactive
can't phenotype, Ehrlichia and Lyme can cause clonal expansion
don't need fresh tissue
73
What's the pathway of a platelet?
1. HSC
2. CMP
3. MEP
4. MkP
5. Platelets
74
How long before megakaryoblasts turn into platelets?
4-5 days
75
TPO
megakaryocyte production and differentiation produced by liver
TPO binds to MPL receptors on PLTs (inactive)
free TPO is active
IL-3 increases TPO production
TPO increases number of megakaryocytes, increased size, and increased ploidy
76
structure of a platelet
Phospholipid bilayer- resting platelet is neutral
extracellular neutral
intracellular negative
translocase
- flipase- PE, PS in
- flopase- PC out
lipid rafts- enhance signaling in initial phases of activation
77
open canalicular system
internalized membrane, granule release, particle uptake, eversion increases surface area
78
microtubules and cytoplasmic actin network
maintains shape of platelet
79
dense tubular system
SER remnant, PG synthesis (TXA2)
80
mitochondria (anaerobic vs. aerobic)
resting anaerobic
| activated aerobic
81
alpha granules
vWF
82
dense granules
70% of calcium stored here
83
overall platelet process (3 steps) primary hemostasis
1. initiation/adhere
2. extension/activate
3. stabilization/perpetuation/aggregate
84
extrinsic factors
1. concentration of platelet agonists
2. type of adhesive surface
3. local rheology
4. platelet interactions
85
intrinsic factors
1. platelet size and volume
2. levels of membrane receptors
3. levels of cytoplasmic, granular, or cytoskeletal proteins
4. platelet age
86
3 major platelet agonists
1. ADP- high shear, weak agonist, inhibited by cox
2. TXA2- synthesized by platelets, activates platelets under low shear, short half-life
3. thrombin- most potent activator, all conditions
87
vWF
1. bind to GPIb-V-IX
2. high shear
3. synthesized by megakaryocytes (alpha granules) , endothelial cells (Weibel Palade bodies)
4. clipped by ADAMST13
88
platelet disorder characteristics
1. petechiae
2. ecchymoses
3. epistaxis
4. hyphema
5. mucosal bleeding
6. spontaneous bleeding
89
True or false: inter-endothelial junctions loosen with thrombocytopenia
True and then RBCs squeeze through
90
primary thrombocytosis
1. essential thrombocytosis/thrombocythemia
- myeloproliferative dz
- unlcear MOA
- dx of exlucsion
2. megakaryoblastic leukemia
91
secondary thrombocytosis
1. reactive
- neoplasia
- inflammation (IL-6)
- endocrine dz
- regenerative anemia
2. rebound
- splenectomy
- mgmt ITP
3. other
- splenic contraction in horses
- vincristine
92
hereditary macrothrombocytopenia
1. CKCS, terriers, Akitas
big platelets
93
vWF dz
1. Dobies
normal platelets, increased BMBT
94
Glanzmann's thrombasthenia
1. Pyrenees, otterhound
95
P2Y12 (ADP) receptor defect
1. Greater swiss mountain dogs
2. prolonged bleeding
3. platelet aggregation following ADP stimulation impaired
96
dense granule effect
1. Cocker spaniels
decreased ADP, N ATP, serotonin
97
CalDAG-GEFI mutation
1. Bassets, Landseers, Eskimo spitz
2. mucosal hemorrhage
3. decreased response ADP, delayed response to thrombin
98
Kindlin 3 disorders
impaired clot retraction
defective platelet aggregation
99
Scott syndrome breed
GSD
issues with PS, platelets cannot externalize it
100
hemophilia A
1. F VIII
2. PTT increase
3. most common inherited
101
hemophilia B
1. F IX
| 2. PTT increase
102
factor X
1. increased PT/PTT
2. usually lethal in utero
3. severe epistaxis, hemorrhage if survive
103
factor XI
1. hemophilia C
2. increased PTT
3. mild bleeding, usually after surger, delayed
104
factor XII
1. Hageman factor
2. increased PTT
3. cats, no C/S of bleeding
105
factor VII
1. Beagles- mild bleeding
| 2. increased PT
106
factor XIII
1. normal PT/PTT
| 2. recurrent bleeding
107
hypofibrinogenemia
1. TCT increased clotting time
2. fibrinogen decreased
3. PT/PTT increased with dysfunctional fibrinogen and severe deficiency
108
factor II
1. prothrombin
| 2. PT/PTT increase
109
prekallikrein
1. increased PTT
| 2. no clinical bleeding
110
Which increases with heparin therapy, PT or PTT?
PTT
111
d-dimers
degradation of cross-linked fibrin, indicative of fibrinolysis. If increased, PTE, DIC
112
TCT
direct measure of functional fibrinogen
can be increased with deficiency of fibrinogen or abnormal fibrinogen, heparin therapy
113
thrombin-antithrombin complex measurement
decreased- decreased production (liver, inflam, elspar), increased consumption in DIC, increased loss- PLE/PLN, third spacing
114
DIC findings
1. thrombocytopenia
2. prolonged PT/PTT
3. hypofibrinogenemia
4. high d-dimers
5. decreased TCT
115
common causes for hyperfibrinolytic states
1. predisposition to hemorrhage
2. neoplasia
3. infection- angiostrongylus, parvovirus
4. liver dz
5. trauma
6. delayed fibrinolysis in greyhounds?
116
common causes for prothrombotic states
1. IMHA/PIMA
2. loss of antithrombin
3. HAC
4. DM
5. inflammatory states (pancreatitis, sepsis, parvo, HW dz)
6. neoplasia
7. endocarditis
