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Heme GI > Blood smear and Neoplasia > Flashcards

Blood smear and Neoplasia Flashcards

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1
Q

CBC contains

A 
WBC
RBC
Hemoglobin
Hematocrit
Platelets
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2
Q

WBC differential contains

And if abnormal?

A

5 types WBC
morphology of RBC and platelets

If abnormal = manual differential

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3
Q

Absolute WBC equation

A

= total WBC count * (type of WBC %)

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4
Q

WBC estimate

A

40x objective and average number of WBC in 5 different fields –> then times by 3,000

should be between 5k-10k

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5
Q

platelet estimate

A

100x oil objective and average number platelets in 5 different fields –> x 20,000

should be between 150k-400k

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6
Q

Leukopenia

A

decrease in WBC

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7
Q

Leukocytosis

A

Increase in WBC

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8
Q

Granulocytopenia

A

decrease in granulocytic cells

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9
Q

Neutropenic

A

decrease in neutrophils

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10
Q

Neutrophilia

A

increase in neutrophils

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11
Q

Myeloblast

(Seg Neut)

A

fine nuclear chromatin with large nucleus (6:1)

  • slightly basophilic cytoplasm and no granulation
  • might see nucleoli
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12
Q

Promyelocyte

Seg Neut

A

4: 1 ratio of nucleus to cytoplasm
- basophilic cytoplasm
- large reddish primary granules

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13
Q

Myelocyte

Seg Neut

A

1: 1 ratio of nucleus to cytoplasm
- oval/round nucleus
- blueish cytoplasm
- has secondary granules

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14
Q

Metamyelocyte

Seg Neut

A

1: 1 ratio of nucleus to cytoplasm
- begin indentation of nucleus
- no nucleoli
- secondary granules

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15
Q

Dohle bodies

A

cytoplasmic inclusion of RNA remnants of rough ER

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16
Q

Plasma cells

A

not normally seen in peripheral blood –> if they are = issues usually
- seen in multiple myeloma with rouleaux in red cells

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17
Q

Anisocytosis

A

variation in size of RBC

- inc RDW on CBC report

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18
Q

Poikylocytosis

A

variation in shape of RBC

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19
Q

Spur cells -RBC
(Acanthocytes)

and what is it seen with?

A

thorn like projections and caused by free cholesterol

  • lack central pallor
  • associated with liver disease and disorders of lipid metabolism
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20
Q

Burr cells - RBC
(Echinocytes)

and what is it seen with?

A

Regular spike projections

  • central pallor observed
  • seen in liver disease, uremia, and PK def
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21
Q

Target cells - RBC

and what is it seen with?

A

caused by excess of cell membrane in RBC

- seen in thalassemia, hemaglobinopathies

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22
Q

Tear drops -RBC

and what is it seen with?

A

Occur with bone marrow replacement

- cells look like droplets

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23
Q

Schistocytes - RBC

and what is it seen with?

A

red cell fragments that hit fibrin

- seen in Microangiopathic hemolytic anemia, DIC, and TTP

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24
Q

Spherocytes - RBC

and what is it seen with?

A

Dense appearance and no central pallor

  • caused by defect in RBC membrane
  • associated with hereditary spherocytosis
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25
Sickle cells - RBC and what is it seen with? what is it not seen with?
Presence of HbS causes RBC to sickle - valine instead of glutamic acid in beta globin chain - seen in sickle cell disease, SC disease, and sickle thalassemia - NOT seen in SC trait
26
Hemoglobin C crystals -RBC
seen in patients homozygous for HbC | - "gold bars"
27
Nucleated RBCS (NRBC)
premature release of RBC from bone marrow
28
Howell Jolly Body Where is this seen?
nuclear remnant of DNA in RBC | - seen in postsplenectomy, hemolytic anemia, and megaloblastic anemia
29
Basophilic Stippling
due to precipitated RNA - seen in myelodysplastic syndromes, hemolytic anemias, and thalassemia largely also seen to lead poisoning
30
Pappenheimer Bodies and what is it seen with?
clusters of granules that contain iron | - found in sideroblastic anemias, thalassemia
31
Rouleaux
RBC's stacked like coins - caused by abnormal protein that decreases repelling - associated with Multiple myeloma
32
Agglutination in RBCs
irregular clusters due to IgM antibodies against RBCs - secondary to infections (Mycoplasma pneumonia) - seen in cold autoimmune hemolytic anemia
33
Platelet precursor
Megakaryocyte | - only cell that gets larger as it matures
34
Coombs Test (DAT)
Tells if anything is coating the RBC --> IgG or complement
35
Reticulocyte count
proportion of young RBCs in peripheral blood - usually 1-2% - indicates the degree of effective bone marrow activity (monitor anemia) - stain slightly blue
36
Corrected Reticulocyte count
(Patient Retic Ct. * Patient HCT) / Normal HCT
37
Neoplasia what is a neoplasm?
new growth abnormal mass of tissue, exceeds normal and is uncoordinated --> persists after stimuli is removed
38
Oncology
study of tumors
39
What two things do all tumors have?
Proliferating tumor cells and supporting framework (stroma) | - stroma determines consistency
40
Polyp
tumor protruding into the lumen of a mucosal lined organ
41
How many cells do cancers result from? What does it need to survive?
ONE a nonlethal mutation
42
Anaplasia How does pleomorphism play into it?
lack of differentiation - impossible to tell site of origin Pleomorphism = variation in size/ shape, hyperchromasia
43
Benign vs. Malignant Tumor
Benign: near normal N:C ratio and few normal mitotic features - slow growth rate Malignant: increased N:C ratio, numerous atypical mitoses - giant cells - invade surrounding tissue (local invasion) - lack well defined margins
44
Dysplasia
disordered growth and seen in epithelial lined structures - loss of normal orientation - no breach of basement membrane
45
ABL oncogene association and action
chronic myelogenous leukemia associated - translocated from Ch 9 to 22 - BCR/ABL fusion - unregulated tyrosine kinase activity (JAK, STAT, MAPK)
46
Retinoblastoma
TSG that allows cell cycle entry | - acts as brake until phosphorylation
47
Are TSGs D or R?
Recessive "two hit hypothesis"
48
Li Fraumeni Syndrome
inherited mutant p53 - 25% increase in cancer chance - loss of p53 = no DNA repair = cancer = more difficult to treat
49
Familial Adenomatous Polyposis
loss of both APC genes - too much B catenin - too many polyps
50
Warburg effect
Cancer cells have high glucose uptake and increased conversion of glucose to lactose (fermentation) - provides metabolic intermediates
51
Most commonly disabled in cancer: Intrinsic apoptosis or extrinsic?
intrinsic
52
telomerase function
prevents telomeres shortening --> present in tumor cells | - old cells don't die
53
Principal way of killing tumor cells via immune
CD8 cytotoxic T cells
54
Epigenetics def
any change to DNA besides DNA sequence | - ex: add methylation to dec transcription/lation
55
Steps of chemical carcinogenesis
initiation and then promoter sequence - initiation = permanent DNA damage - promoters enhance proliferation = reversible, enhance proliferation of cells MUST HAPPEN in this sequence
56
Indirect carcinogens
require metabolic conversion to become active
57
Direct carcinogens
require no conversion to become active
58
CYP1A1 gene
many polymorphisms - high inducible activity - can lead to more dangerous compounds
59
Asbestos can cause
Mesothelioma
60
Vinyl chloride can cause
Angiosarcoma of liver
61
Arsenic can cause
Skin cancer
62
Oncogenic DNA virus
HPV, EBV, Hep B
63
Oncogenic RNA virus
Human T cell leukemia virus 1
64
Paraneoplastic syndrome examples?
symptoms not explained by local/distant spread of tumor - can cause significant problems with treatment - ex: Hypercalcemia, Cushings, Acanthosis nigricans, hypertrophic osteoarthropathy, migratory thrombophlebitis, neuromyopathic (MG) helpful note: para = next to, so alongside the syndrome

Heme GI (14 decks)

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