Lecture 7 Blood: RBCs, Anemia and Blood Typing (Ch. 33, 36) Flashcards

1
Q

55% of the blood is plasma; what are the different components of plasma?

A

Albumin, Globulins, Fibrinogens (& Miscellanous)

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2
Q

At age 30, where does the production of RBCs occur?

A

Vertebra, Sternum and Ribs

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3
Q

RBCs are viable for ~120 days. How are they discarded?

A

Aged RBCs are enlarged and trapped by the spleen and the liver. They’re then digested by macrophages & processed for reuse or excretion.

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4
Q

What globins chains are present in our blood postnatal (~12 weeks and onward)?

A

Alpha chain 1, Alpha chain 2, Beta chain 1, Beta chain 2

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5
Q

What are the 3 categories of hemolytic anemias?

A

Transfusion reaction, immunity-based RBC destruction and genetic

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6
Q

What are the differences in the processes that encourage Pluripotent Hematopoetic Stem Cell (PHSC) maturation?

A

Growth inducers promote proliferation (interleukin-3), and differentiation inducers drive the cell to maturation (ex. PHSC+erythropoetin ->RBC; PHSC+cytokines/lymphokines->WBC)

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7
Q

Give two examples that reflect the adaptivity of hematopoiesis?

A

Hypoxia will increase erythropoiesis and RBCs

Infection/inflammation will increased WBC production

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8
Q

Describe the hormonal stimulation of RBC production.

A

Hypoxia triggers eryhtropoietin (EPO) synthesis in the kidney.
EPO stimulates RBC production in bone marrow.

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9
Q

Describe the two types of polycythemia pathology.

A

Physiologic secondary polycythemia is when the RBC’s are elevated due to being in high altitudes.
Compensatory polycythemia can occur with lung disease due to inadequate ventilation, and in heart failure, due to inadequate blood flow to the heart.

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10
Q

During which stages of RBC maturation does hemoglobin synthesis occur, and what physiologic changes reflect this?

A

Hemoglobin synthesis occurs from the proerythroblast to the reticulocyte stage. Reticulocyte retraction expels the endoplasmic reticulum and Golgi apparatus, decreasing Hgb synthesis

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11
Q

Compare erythropoietin synthesis in normal O2 and low O2 conditions.

A
In normoxia (normal O2 conditions), HIF-alpha is hydroxylated by prolyl-4lhydroxylase (PHD) and FIH-1. HIF-1 is targeted for destruction by ubiquitin.
In hypoxia (low O2 conditions), PHD and FIH-1 are inhibited by hypoxia. HIF-1 translocates to the nucleus and bind HIF-1beta ->  Transcription of target genes including EPO
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12
Q

Describe the general pathophysiology of anemia

A
  1. tissue hypoxia and necrosis (lethargy, shortness of breath), high metabolic tissue (brain, heart, kidney) most affected
  2. reduced osmolarity: edema
  3. reduces blood viscosity (low blood pressure): increases heart rate and may cause cardiac failure
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13
Q

What determines ABO blood classification, and what are the names of the different blood types?

A

glycoproteins on RBCs that are antigenic and produce antibodies.
Blood types: O, A, B, AB

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14
Q

What is physiologic secondary polycythemia?

A

RBCs are elevated because of high altitude

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15
Q

How long are RBCs viable?

A

~120 days

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