Hematology and Oncology Flashcards

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1
Q

Primary source of EPO synthesis

A

Renal cortex by the interstitial cells in the peritubular capillary bed

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2
Q

Ectopic sources of EPO synthesis (2)

A

Renal cell carcinoma

hepatocellular carcinoma

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3
Q

Reticulocyte blue appearance microscopically after the application of the Wright-Giemsa stain

A

Reticular (mesh-like) network of residual ribosomal RNA

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4
Q

Corrected reticulocyte count

A

Hct/45 x reticulocyte count

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5
Q

Corrected reticulocyte count in the presence of polychromatic erythroblasts

A

[(Hct/45) x reticulocyte count] / 2

Polychromatic erythroblasts contain nuclei and residual ribosomal RNA

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6
Q

Clinical implications of extramedullary hematopoiesis (2)

A
  1. Expansion of the bone marrow within the skull bones (“chipmunk facies,” “hair-on-end” radiograph
  2. Impaired bone growth, pathologic fractures 2/2 expanding mass of progenitor cells in the bone marrow thinning the bony cortex
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7
Q

Cardiac murmur a/w anemia

A

Pulmonary valve flow murmur 2/2 decreased blood viscosity

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8
Q

Cardiac pathology a/w anemia

A

High-output cardiac failure 2/2 decreased blood viscosity

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9
Q

Size variation of RBCs

A

Anisocytosis

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10
Q

Shape variation of RBCs

A

Poikilocytosis

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11
Q
Iron deficiency anemia:
(Low/normal/high)
- Ferritin
- TIBC
- Serum iron
- Iron saturation
- MCHC
- RDW
- Free erythrocyte protoporphyrin (FEP)
A
Iron deficiency anemia:
(Low/normal/high)
- Ferritin = low
- TIBC = high
- Serum iron = low
- Iron saturation = low
- MCHC = low
- RDW = high
- FEP = increased
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12
Q
Anemia of chronic disease:
(Low/normal/high)
- Ferritin
- TIBC
- Serum iron
- Iron saturation
- MCHC
- RDW
- Free erythrocyte protoporphyrin (FEP)
A
Anemia of chronic disease:
(Low/normal/high)
- Ferritin = high
- TIBC = low
- Serum iron = low
- Iron saturation = low
- MCHC = high
- RDW = normal 
- FEP = increased
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13
Q
Sideroblastic anemia:
(Low/normal/high)
- Ferritin
- TIBC
- Serum iron
- Iron saturation
- MCHC
- RDW
- Free erythrocyte protoporphyrin (FEP)
A
Sideroblastic anemia:
(Low/normal/high)
- Ferritin = high
- TIBC = low
- Serum iron = high
- Iron saturation = high
- MCHC = low
- RDW = normal 
- FEP = normal
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14
Q

Ferritin

A

Soluble iron-binding storage protein

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15
Q

Source of ferritin synthesis (2)

A

Bone marrow macrophages and hepatocytes (liver)

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16
Q

Primary storage site for iron/ferritin

A

Bone marrow macrophages

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17
Q

Inflammatory markers that increase ferritin synthesis

A

IL-1, IL-6, TNF-a

Ferritin is an acute phase reactant

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18
Q

Hemosiderin

A

Insoluble product of ferritin degradation in lysosomes

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19
Q

Hemosiderin

  • Special stain
  • Color
A
  • Prussian blue

- Blue

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20
Q

Source of iron bound to ferritin

A

Bone marrow macrophages phagocytose senescent RBCs

21
Q

Transferrin

A

Iron-binding protein/carrier in the blood

22
Q

Source of transferrin synthesis

A

Hepatocytes (liver)

23
Q

Correlate of transferrin concentration

A

TIBC

24
Q

Source of iron bound to transferrin?

A

Bone marrow macrophages (ferritin), dietary iron

25
Q

Site in GI tract where iron is absorbed

A

Duodenum

26
Q

Role of gastric acid in iron absorption

A

Gastric acid frees elemental iron from heme and nonheme proteins

  • Achlorhydria decreases availability of iron for reabsorption
27
Q

Two sources of dietary iron

A

Vegetable-derived nonheme iron (Fe3+)

Meat-derived heme iron (Fe2+)

28
Q

Duodenal enzyme that reduces nonheme iron (Fe3+) to Fe2+

A

Cytochrome b

29
Q

Transporter that carries nonheme iron (Fe3+) that was reduced to Fe2+ into duodenal enterocyte

A

Divalent metal transporter (DMT1)

30
Q

Transporter that carries heme iron (Fe2+) into duodenal enterocyte

A

Heme carrier protein 1 (HCP1)

31
Q

Two fates of Fe2+ iron absorbed into duodenal enterocyte

A
  1. Stored as ferritin in duodenal enterocyte

2. Shuttled across enterocyte cytoplasm to basolateral membrane for transport into the blood

32
Q

Transporter that carries Fe2+ from duodenal enterocyte into blood

A

Ferroportin 1

33
Q

Enzyme that immediately oxidizes Fe2+ to Fe3+ once transported from enterocyte into blood

A

Hephaestin (ferroxidase activity)

34
Q

Fate of iron once transported from enterocyte into blood and oxidized

A

Binds transferrin

35
Q

Two destinations for iron-bound transferrin

A
  1. Bone marrow erythroblasts - to incorporate iron into Hb
  2. Bone marrow and liver macrophages - to incorporate into ferritin for storage

All have transferrin receptors (TfR)

36
Q

Iron sensor cells

A

Immature enterocyte precursors

37
Q

Master regulator of iron regulation

  • Name
  • Source of synthesis
A

Hepcidin synthesized in liver

Controls whether dietary iron is absorbed or not absorbed in the duodenum

Controls whether iron is released or not released from stores in macrophages

38
Q

Mechanism by which hepcidin limits iron absorption/release

A

Hepcidin inhibits ferroportin 1 on duodenal enterocytes and macrophages, thereby limiting iron absorption/release

39
Q

Inflammatory marker that increases hepcidin synthesis

A

IL-6

Hepcidin is an acute phase reactant

40
Q

Iron deficiency anemia

  • MCC adult males
  • MCC adult females
  • MCC adults > 50 years
A
  • MCC adult males = peptic ulcer disease
  • MCC adult females = menorrhagia
  • MCC adults > 50 = polyps/colorectal cancer
41
Q

Two helminths (multicellular parasites) that cause iron deficiency anemia

A

Ancylostoma duodenale
Necator americanus
(Hookworms)

42
Q

MOA by which hookworms enter body

A

Larvae enter via skin

43
Q

MOA by which hookworms cause anemia

A

Latch to intestinal wall and suck blood, causing microcytic anemia

44
Q

Hookworm treatment (3)

A

Albendazole, Mebendazole, Pyrantel pamoate

45
Q

MOA of albendazole/mebendazole

A

Inhibits synthesis of microtubules required for glucose uptake
(interferes with muscular activity)

46
Q

MOA of pyrantel pamoate

A

interfere with synaptic transmission

ganglionic nicotinic cholinergic agonists –> Muscular tetany

47
Q

Plummer-Vinson syndrome

A

Chronic iron deficiency anemia
Esophageal webs
Glossitis, angular cheilosis (inflammation of tongue and corner of mouth, respectively)

Anemia, dysphagia for solids, beefy red tongue

48
Q

MOA by which thrombocytosis develops in chronic iron deficiency anemia

A

Reactive phenomenon to increase platelets to increase blood viscosity and decrease risk of high-output cardiac failure