Test 3 (Units 11-15) Flashcards

(46 cards)

1
Q

Anemia-

A

decreased oxygen carrying capacity resulting in tissue hypoxia

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2
Q

Symptoms of anemia:

A
  • Fatigue and shortness of breath
    • Cravings
    • Pale, jaundice, spots on arms/legs
    • Severity depends on onset, cardiac output, severity of anemia
    • Enlarged spleen and liver
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3
Q

Describe the normal life span of a red blood cell including the percentage recycled daily.

A

Lifespan: 120 days
Daily recycling 1% of RBCs
BM releases 1% of “retics”

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4
Q

Discuss physiological adaptions found in patients with anemia.

A
EPO increased
Heart rate increased 
Respiratory rate increased
2,3 DPG increased
Too severe cardiac failure
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5
Q

Ineffective erythropoiesis: Meaning, effects and examples

A

1) RBC progenitors defective
2) -Increased precursors in BM
- Decreased Hgb in peripheral blood
- Normal or decreased retics
3) -Megaloblastic anemia
- Thalassemias
- Sideroblastic anemia

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6
Q

Insufficient erythropoiesis: Meaning, effects and examples

A

1) Insufficient amount being made
2) -Decreased precursors in BM
-Decreased RBC production
-Normal or decreased retics
3) -Iron deficiency
-EPO deficiency
-Loss of precursors due to:
Autoimmune processes
Infection
Infiltration from other cells
In BM

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7
Q

Acute Blood Loss and Hemolysis: Meaning, effects and examples

A

1) Traumatic injury/premature hemolysis
2) -BM increased productions
- Increased retics, but maybe not right away
3) -RBC membrane defects
- Enzyme deficiencies
- Extrinsic

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8
Q

List conditions resulting in premature hemolysis.

A
  • RBC membrane defects
  • Enzyme deficiencies
  • Extrinsic: antibody, mechanical, infection
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9
Q

List procedures and tests commonly performed for the detection and diagnosis of anemia.

A

CBC
Retic
Blood smear
Bone marrow

Also: 
	UA
	Stool analysis
	Renal and hepatic panels
	Iron studies
	B12
	Folate
	DAT (direct antiglobulin test)
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10
Q

Discuss the importance of the reticulocyte count in the evaluation of anemia.

A

-Tests BM response
-hemolytic anemia: increased destruction once they make it out, increased retic
As bone marrow deals with loss
-Chronic blood loss: decreased or normal retic count

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11
Q

Describe different algorithms used to classify anemias.

A

Classification based on MCV
On absolute retic count and MCV
On RDW

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12
Q

Characterize the three groups of anemias categorized based on mean cell volume (MCV) and give one example of each.

A

Microcytic- Sideroblastic anemia
Normocytic- Anemia of renal disease
Macrocytic- Folate deficiency

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13
Q

Recognize the importance of reviewing the peripheral blood film when assessing anemias and distinguish the important findings.

A

Check size, shapes and other possible abnormalities

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14
Q

Define poikilocytosis.

A

Variation in shapes

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15
Q

Diffuse basophilia: Composition, method of ID and importance

A

RNA remnants
Supravital stain-methylene blue
Normal finding but how many?

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16
Q

Basophilic stippling: Composition, method of ID and importance

A

Precipitated RNA
Wright stain
Lead poisoning or thalassemia

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17
Q

Howell-Jolly Body: Composition, method of ID and importance

A

Piece of DNA
Wright stain
Verify not a piece of dirt

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18
Q

Ringed sideroblast: Composition, method of ID and importance

A

Iron
Prussian blue (in BM)
Sideroblastic anemia

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19
Q

Pappenheimer bodies: Composition, method of ID and importance

A
Iron deposits	
Wright stain	
-After spleen removal
-Thalassemias
-Megaloblastic anemias
20
Q

Cabot ring: Composition, method of ID and importance

A

Remnant of mitotic spindle
Wright stain
Super rare, not reported

21
Q

Heinz bodies: Composition, method of ID and importance

A

Denatured hbg
Supravital stain
Thalassemias and drugs/chemicals

22
Q

4 causes of iron deficiency anemia

A

inadequate intake
increased need
impaired absorption
Chronic blood loss

23
Q

iron deficiency anemia: Inadequate intake etiology

A

Decreased intakeiron stores used up

Iron deficiencyID anemia

24
Q

iron deficiency anemia: increased need etiology

A
Increased need:
   -Periods of rapid growth like infancy,
   Childhood, adolescence 
   -Pregnancy
   -Nursing
25
iron deficiency anemia: Impaired absorption
-Diet is adequate, absorption is not -Malabsorption: celiac disease -Loss of gastric acidity (can’t convert Ferric to ferrous): gastrectomy, Bariatric surgery, antacids
26
iron deficiency anemia: pathophysiology
``` Stage 1: Hemoglobin N Serum Iron N TIBC N Ferritin Dec. Stage 2: Hemoglobin N Serum Iron Dec TIBC Inc Ferritin Dec. (Basically depleted) Stage 3: Hemoglobin Dec Serum Iron Dec TIBC Inc Ferritin Dec. ```
27
iron deficiency anemia: Chronic blood loss
Chronic blood loss - Chronic hemorrhage or hemolysis - GI bleeds - heavy menstrual bleeding - Fibroid tumors - Loss through urinary tract
28
Anemia of Chronic Inflammation: etiology
- Systemic diseases like chronic inflammatory disease or malignancies - Chronic blood loss IS NOT equal to anemia of chronic inflammation - Impaired ferrokinetics due to hepcidin - Body is inflamed so inc in hepcidin
29
Anemia of Chronic Inflammation: pathophysiology
``` Serum Iron dec *TIBC dec Transferrin saturation N or dec Serum ferritin N or inc Bone marrow N or inc ```
30
Sideroblastic Anemia: etiology
``` Acquired Primary Secondary-TB drugs, chloramphenicol, Alcohol, LEAD, chemotherapeutic agents Hereditary X linked Autosomal ```
31
Sideroblastic Anemia: pathophysiology
``` Ringed sideroblasts in BM Lead poisoning leads to hypochromic, microcytic with basophilic stipling Serum iron inc TIBC N or dec Transferrin saturation inc Serum ferritin inc (N in lead poison) ZPP inc Bone marrow N or inc ```
32
Iron Overload: etiology
Primary hereditary Hemochromatosis Secondary chronic anemia Problems with iron metabolismtoo much iron Free ironorgan damage
33
Iron Overload: pathophysiology
Serum inc x2 *Transferrin saturation inc x2 Serum ferritin inc x2 Liver function tests-see if damage has occurred
34
Describe the hemoglobin defect in thalassemias.
Quantitative defect- Structure ok, synthesis lowcompensation
35
Name the chromosomes that contain the alpha globin gene and the beta globin gene clusters and the globin chains produced by each.
``` Chromosome 11 b d g e Beta cluster Chromosome 16 A z Alpha like genes ```
36
Explain the pathophysiologic effects caused by the imbalance of globin chain synthesis in thalassemia.
``` Microcytic Hypochromic Hemolytic Unequal production Dec. in RBC production ```
37
Thalassemia minor (one normal gene): clinical features
Asymptomatic to mild anemia | Cells smaller, basophilic stippling and target cells
38
Thalassemia major: clinical features
``` Cooley’s anemia Severe Transfusion dependent Jaundice Bone changes (hair on end) Heinz bodies, basophilic stippling, Howell jolly body, elliptocyte, targets ```
39
Thalassemia intermedia: clinical features
Moderate Few transfusion requirements Polychromatophilic
40
a Thal minor: clinical features
Asymptomatic to mild Jaundice Hepatosplenomegaly
41
Hemoglobin Bart: clinical features
g4 soluble enter circulationprecipitation removal by spleen High O2 affinity-can’t get off the “bus”
42
Hemoglobin H: clinical features
``` b4 Fine, granular precipitate Mild to chronic hemolytic anemia Erythroid hyperplasia Enlarged spleen ```
43
Hgb Hydrops Fetalis: clinical features
Incompatible with life No alpha chains Can be harmful to mother
44
Alpha thalassemia: pathophysiology
Deletionsexcess g in fetuses and excess b in adults
45
Beta thalassemia: pathophysiology
Excess a chains precipitatedamage surfaces Destruction of damaged RBCs Ineffective erythropoiesis Extravascular hemolysis Ineffective production and decreased destruction
46
Describe the peripheral blood morphology associated with thalassemias.
``` H+H dec x2 RBC dec MCV dec x3 MCHC dec RDW inc ``` ``` Micro Hypo Poik- TARGET and elliptocytes Polychromasia-retics high Inclusions: basophil stippling , NRBCs TARGET CELLS MARKED MICROCYTOSIS MILD ERITHROCYTOSIS ```