Hematology and Oncology Flashcards

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

24
Q

Source of iron bound to transferrin?

A

Bone marrow macrophages (ferritin), dietary iron

25
Site in GI tract where iron is absorbed
Duodenum
26
Role of gastric acid in iron absorption
Gastric acid frees elemental iron from heme and nonheme proteins - Achlorhydria decreases availability of iron for reabsorption
27
Two sources of dietary iron
Vegetable-derived nonheme iron (Fe3+) | Meat-derived heme iron (Fe2+)
28
Duodenal enzyme that reduces nonheme iron (Fe3+) to Fe2+
Cytochrome b
29
Transporter that carries nonheme iron (Fe3+) that was reduced to Fe2+ into duodenal enterocyte
Divalent metal transporter (DMT1)
30
Transporter that carries heme iron (Fe2+) into duodenal enterocyte
Heme carrier protein 1 (HCP1)
31
Two fates of Fe2+ iron absorbed into duodenal enterocyte
1. Stored as ferritin in duodenal enterocyte | 2. Shuttled across enterocyte cytoplasm to basolateral membrane for transport into the blood
32
Transporter that carries Fe2+ from duodenal enterocyte into blood
Ferroportin 1
33
Enzyme that immediately oxidizes Fe2+ to Fe3+ once transported from enterocyte into blood
Hephaestin (ferroxidase activity)
34
Fate of iron once transported from enterocyte into blood and oxidized
Binds transferrin
35
Two destinations for iron-bound transferrin
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
Iron sensor cells
Immature enterocyte precursors
37
Master regulator of iron regulation - Name - Source of synthesis
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
Mechanism by which hepcidin limits iron absorption/release
Hepcidin inhibits ferroportin 1 on duodenal enterocytes and macrophages, thereby limiting iron absorption/release
39
Inflammatory marker that increases hepcidin synthesis
IL-6 | Hepcidin is an acute phase reactant
40
Iron deficiency anemia - MCC adult males - MCC adult females - MCC adults > 50 years
- MCC adult males = peptic ulcer disease - MCC adult females = menorrhagia - MCC adults > 50 = polyps/colorectal cancer
41
Two helminths (multicellular parasites) that cause iron deficiency anemia
Ancylostoma duodenale Necator americanus (Hookworms)
42
MOA by which hookworms enter body
Larvae enter via skin
43
MOA by which hookworms cause anemia
Latch to intestinal wall and suck blood, causing microcytic anemia
44
Hookworm treatment (3)
Albendazole, Mebendazole, Pyrantel pamoate
45
MOA of albendazole/mebendazole
Inhibits synthesis of microtubules required for glucose uptake (interferes with muscular activity)
46
MOA of pyrantel pamoate
interfere with synaptic transmission ganglionic nicotinic cholinergic agonists --> Muscular tetany
47
Plummer-Vinson syndrome
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
MOA by which thrombocytosis develops in chronic iron deficiency anemia
Reactive phenomenon to increase platelets to increase blood viscosity and decrease risk of high-output cardiac failure