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Heme GI > Blood smear and Neoplasia > Flashcards

Blood smear and Neoplasia Flashcards

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
Q

Sickle cells - RBC

and what is it seen with?

what is it not seen with?

A

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
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26
Q

Hemoglobin C crystals -RBC

A

seen in patients homozygous for HbC

- “gold bars”

27
Q

Nucleated RBCS (NRBC)

A

premature release of RBC from bone marrow

28
Q

Howell Jolly Body

Where is this seen?

A

nuclear remnant of DNA in RBC

- seen in postsplenectomy, hemolytic anemia, and megaloblastic anemia

29
Q

Basophilic Stippling

A

due to precipitated RNA
- seen in myelodysplastic syndromes, hemolytic anemias, and thalassemia

largely also seen to lead poisoning

30
Q

Pappenheimer Bodies

and what is it seen with?

A

clusters of granules that contain iron

- found in sideroblastic anemias, thalassemia

31
Q

Rouleaux

A

RBC’s stacked like coins

  • caused by abnormal protein that decreases repelling
  • associated with Multiple myeloma
32
Q

Agglutination in RBCs

A

irregular clusters due to IgM antibodies against RBCs

  • secondary to infections (Mycoplasma pneumonia)
  • seen in cold autoimmune hemolytic anemia
33
Q

Platelet precursor

A

Megakaryocyte

- only cell that gets larger as it matures

34
Q

Coombs Test (DAT)

A

Tells if anything is coating the RBC –> IgG or complement

35
Q

Reticulocyte count

A

proportion of young RBCs in peripheral blood

  • usually 1-2%
  • indicates the degree of effective bone marrow activity (monitor anemia)
  • stain slightly blue
36
Q

Corrected Reticulocyte count

A

(Patient Retic Ct. * Patient HCT) / Normal HCT

37
Q

Neoplasia

what is a neoplasm?

A

new growth

abnormal mass of tissue, exceeds normal and is uncoordinated –> persists after stimuli is removed

38
Q

Oncology

A

study of tumors

39
Q

What two things do all tumors have?

A

Proliferating tumor cells and supporting framework (stroma)

- stroma determines consistency

40
Q

Polyp

A

tumor protruding into the lumen of a mucosal lined organ

41
Q

How many cells do cancers result from?

What does it need to survive?

A

ONE

a nonlethal mutation

42
Q

Anaplasia

How does pleomorphism play into it?

A

lack of differentiation
- impossible to tell site of origin

Pleomorphism = variation in size/ shape, hyperchromasia

43
Q

Benign vs. Malignant Tumor

A

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
Q

Dysplasia

A

disordered growth and seen in epithelial lined structures

  • loss of normal orientation
  • no breach of basement membrane
45
Q

ABL oncogene

association and action

A

chronic myelogenous leukemia associated

  • translocated from Ch 9 to 22
  • BCR/ABL fusion
  • unregulated tyrosine kinase activity (JAK, STAT, MAPK)
46
Q

Retinoblastoma

A

TSG that allows cell cycle entry

- acts as brake until phosphorylation

47
Q

Are TSGs D or R?

A

Recessive

“two hit hypothesis”

48
Q

Li Fraumeni Syndrome

A

inherited mutant p53

  • 25% increase in cancer chance
  • loss of p53 = no DNA repair = cancer = more difficult to treat
49
Q

Familial Adenomatous Polyposis

A

loss of both APC genes

  • too much B catenin
  • too many polyps
50
Q

Warburg effect

A

Cancer cells have high glucose uptake and increased conversion of glucose to lactose (fermentation)
- provides metabolic intermediates

51
Q

Most commonly disabled in cancer: Intrinsic apoptosis or extrinsic?

A

intrinsic

52
Q

telomerase function

A

prevents telomeres shortening –> present in tumor cells

- old cells don’t die

53
Q

Principal way of killing tumor cells via immune

A

CD8 cytotoxic T cells

54
Q

Epigenetics def

A

any change to DNA besides DNA sequence

- ex: add methylation to dec transcription/lation

55
Q

Steps of chemical carcinogenesis

A

initiation and then promoter sequence

  • initiation = permanent DNA damage
  • promoters enhance proliferation = reversible, enhance proliferation of cells

MUST HAPPEN in this sequence

56
Q

Indirect carcinogens

A

require metabolic conversion to become active

57
Q

Direct carcinogens

A

require no conversion to become active

58
Q

CYP1A1 gene

A

many polymorphisms

  • high inducible activity
  • can lead to more dangerous compounds
59
Q

Asbestos can cause

A

Mesothelioma

60
Q

Vinyl chloride can cause

A

Angiosarcoma of liver

61
Q

Arsenic can cause

A

Skin cancer

62
Q

Oncogenic DNA virus

A

HPV, EBV, Hep B

63
Q

Oncogenic RNA virus

A

Human T cell leukemia virus 1

64
Q

Paraneoplastic syndrome

examples?

A

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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