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Heme/Lymph > Intro to Anemia > Flashcards

Intro to Anemia Flashcards

1
Q

Define anemia

A

decreased O2 carrying capacity of the blood

symptom of other diseases, not a disease itself

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2
Q

How to we measure/test for anemia?

A

decreased Hb concentration of blood

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3
Q

Main Functional consequences of anemia?

A

decreased oxygen delivery to tissue

tissue hypoxia in severe cases

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4
Q

6 compensatory mechanisms in anemia

A 
increased 2,3 DPG
shunting of blood from non-vital to vital areas
increased CO
increased RR
increased red cell production
increased plasma volume
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5
Q

Main Symptoms

A

weakness, fatigue, marrow expansion/bony abnormalities, pallor, tachycardia, DOE
*symptoms more severe with rapid onset

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6
Q

Functional Classification of Anemias

A

blood loss
decreased production
accelerated destruction

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7
Q

Morphologic Classification of Anemias

A

microcytic (normo or hypochromic)
Normochromic/normocytic
macrocytic

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8
Q

Measurements related to red cell mass (3)

A

Hb, Hematocrit, RBC count

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9
Q

Measurements related to characteristics of the red cells (RBC “indices”)

A

MCV, MCH, MCHC, RDW

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10
Q

Microcytic anemia DD (3)

A

iron deficiency, thalassemia, ACD

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11
Q

Macrocytic anemia DD (2)

A

megaloblastic (impaired DNA synthesis)
-B12/folate defic, drugs, MDS
non-megaloblastic
-reticulocytosis, liver disease, hypothyroidism, drugs

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12
Q

Causes of spherocytes

A

hereditary spherocytosis, autoimmune hemolytic anemia

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13
Q

causes of target cells

A

liver disease, splenectomy, hemoglobinopathies

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14
Q

causes of elliptocytes (ovalocytes)

A

hereditary elliptocytosis, megaloblastic anemia, iron deficiency, myelofibrosis

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15
Q

causes of teardrop cells

A

megaloblastic anemia, myelofibrosis, extramedullary hematopoiesis

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16
Q

causes of sicked cells

A

sickle cell disease

17
Q

causes of fragments/schistocytes

A

TTP, DIC, malignant HTN

18
Q

causes of bite cells

A

oxidant hemolysis (ie/G6PD deficiency)

19
Q

term for red cell size variablility

A

anisocytosis

20
Q

anisocytosis, microcytosis, hypochromia

A

iron deficiency anemia

21
Q

causes of howell-jolly bodies (nuclear fragments)

A

splenectomy, megaloblastic anemia

22
Q

causes of pappenheimer bodies (iron granules)

A

splenectomy, iron overload

23
Q

causes of basophilic stippling (coarse)

A

talassemias, MDS, lead poisoning

24
Q

causes of Hb C crystals

A

HbCC disease, HbSC disease

25
Q

Cause of rouleaux

A

decreased repulsive forces between RBCs

occurs w/increased serum proteins

26
Q

Causes of aggluination

A

IgM RBC antibodies (cold agglutinins)

27
Q

Causes of hypersegmented neutrophil

A

megaloblastic anemia

28
Q

After blood loss when does reticulocyte count increase and peak?

A

increases after 2-3 days

peaks after 7-10 days

29
Q

RBC production sites throughout developments

A

embryo:yolk sac
fetus: liver
shortly after birth-rest of life: bone marrow

30
Q

Where do normoblasts obtain iron from?

A

plasma transferrin for Hb synthesis

31
Q

What gives reticulocytes their blueish tinge?

A

residual RNA

32
Q

What are causes of decreased RBC production?

A

ineffective erythropoeisis
decreased RBC precursors
anemia of chronic disease

33
Q

Ineffective erythropoiesis examples

A

iron deficiency
megaloblastic
MDS

34
Q

Ineffective erythropoiesis features

A

increased RDW
dysmaturation of precursors in marrow
decreased RC
inappropriately increased iron absorption from gut

35
Q

Decreased RBC precursors features

A

defects in proliferation, stem cell defects with adequate erythropoietin

36
Q

Decreased RBC precursors causes

A

congenital or acquired
red cell aplasia or pan aplasia
amrrow replacement, decreased EPO

37
Q

Normal RBC destruction

A

after ~120 days

intravascular: breach of membrane in circulation, low freq under normal conditions
extravascular: clearance in reticuloendothelial system as a result of RBC senescence

38
Q

Does hemolysis always cause anemia?

A

No, can have hemolysis wihout anemia if bone marrow is able to compensate

39
Q

Why does extravascular hemolysis occur?

A

due to decreased RBC deformability, can’t traverse slits in splenic cords and sinusoids, damaged by splenic cordal env, phogcytized by cordal macrophages

Heme/Lymph (18 decks)

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