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medical school midcomp 5 > Laboratory Medicine & Anemias > Flashcards

Laboratory Medicine & Anemias Flashcards

1
Q

Anemia

A

Subnormal amount of RBC circulating in blood

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2
Q

Anemia measurement amounts for men and women

A

Hemoglobin : <13.5 for men and <12 for women
Hematocrit : <41% for men and <36% for women

Hematocrit roughly 3x hemoglobin

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3
Q

Clinical presentation of anemia

A 
Weakness
Malaise
Fatigue
Exertion
Dyspnea
Pale skin and conjunctiva
Angina pectoris and heart failure ( larger risk if person has preexisting conditions)
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4
Q

Types of Microcytic Anemia

A

Microcytic anemia - MCV<80 ( MCV average volume/size of RBC)

  1. Sideroblastic anemia
  2. Anemia of chronic disease
  3. Lead poisoning
  4. Thalassemia
  5. Iron Deficiency (late)

SALTI

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5
Q

How does Microcytic anemia occur

A

Decrease in hemoglobin production-> in order to adapt to less hemoglobin erythroblasts have one division to become normal RBC then go through an extra division..producing smaller cells

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6
Q

Iron deficiency anemia

A

Most common cause of anemia worldwide
Iron loss> iron intake

Total body iron in women is less than men…women more vulnerable to iron deficiency due to pregnancy and menses

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7
Q

Causes of iron deficiency anemia

A

No regulatory pathway for iron. Iron is only lost through 1. Bleeding 2. Epithelial cell loss from skin , gut, or genitourinary tract

Major cause of iron deficiency is 1. Blood loss or 2. Dietary deficiency

Infants -> breast feeding common cause due to lack of FE in breast milk
Children-> poor diet
Adults -> MALES: peptic ulcer disease FEMALE: menorrhagia &
Pregnancy
Elderly: western wrld:colon polyps/ carcinoma ( anytime elderly w/
Anemia is seen keep in mind to check for cancer)
Developing world: hookworm

Other causes : malnutrition, gastrectomy, malabsorption -> celiac
Disease

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8
Q

Sources of Iron

A

North American eat 10-20 mg of iron….mostly from meat Nd veggies

HEME iron- present in animal foods..20% absorbed
NON-heme iron- egg yolks and food from plants..1-2% absorbed

MILK A POOR SOURCE OF IRON…why babies need supplement

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9
Q

Where is iron absorbed in the body?

A

Iron is absorbed primarily in the duodenum

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10
Q

What is the pathway of Iron once it enters the body

A

1.Dietary iron (Fe+3) reduced to FE+2 via FERRIREDUCTASE
2.DMT1 transporter transports FE2 into enterocyte
THEN
3. FE2 stored intracellularly via ferritin
OR
3. Fe+2 released into blood stream via ferroportin-> FE2 oxidized to FE3 and loaded onto transferrin

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11
Q

Ferritin

A
  • can be found in all tissues , but mainly stores iron in liver ( parenchyma cells) for storage and bone marrow ( macrophages)
  • iron stored in these two places as either ferritin or hemosiderin ( ferritin+cellular debris)
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12
Q

Transferrin

A
  • transfers majority of iron to bone marrow for erythropoiesis
    - Around 80% of iron is recycled from senescent red blood cells
    - remaining iron delivered to other places
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13
Q

Stages of iron deficiency

A
  1. Storage iron depleted
  2. Serum iron depleted
  3. normocytic anemia
  4. microcytic/hypochromic anemia
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14
Q

Lab findings of iron deficiency anemia

A

INC: TIBC ( total iron binding capacity,transferrin conc.)
RDW(anisocytosis), AKA range in RBC size
Free erythrocytes protoporphyrin

DEC: serum iron
% saturation transferrin ( serum iron/TIBCx100)

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15
Q

Anemia of chronic disease

A

1.MC anemia seen in hospitalized patient
2. Inflammation-> inc neutrophils, granulocytes and macrophages-> secrete cytokines-> liver creates acute phase reactants such as hepcidin.
3. Hepcidin leads to iron trapping in macrophages,bone marrow,liver, and decreased iron absorption by degrading ferroportin
Cytokines suppress epo production

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16
Q

Anemia of chronic disease lab values

A

INC : ferritin
FEP ( free erythrocyte protoporphyrin)

DEC: serum iron
% saturation
TIBC

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17
Q

Sideroblastic Anemia

A
  1. Body contains enough iron but defect with protoporphyrin

Can Happen for two reasons:
1.insufficient production of protoporphyrin to use iron
Or
2. Mitochondrial function defects affecting iron pathways or impairing mitochondrial protein synthesis

18
Q

Sideroblastic Heme synthesis pathway

A

Can have congenital, acquired, or idiopathic reason

CONGENITAL- most common involves ALAS

ACQUIRED- Alcoholism-> mitochondrial poisoning
lead poisoning ->inhibit ALAD and ferrochelatase
Vit. B6 deficiency-> cofactor for ALAS
IDIOPATHIC

19
Q

Sideroblastic anemia findings

A

Accumulation of mitochondrial iron ( no protoporphyrin to bind iron ) within erythroblasts= ringed sideroblasts on Prussian blue stain

20
Q

Sideoblastic anemia lab findings

A

INC. ferritin
Serum iron
% saturation transferrin ( iron over loaded state)

DEC. TIBC

21
Q

THALASSEMIA

A
  1. NORMAL IRON STUDIES
  2. reduced/absent production of alpha or beta global chains
  3. ⬇️globin->⬇️hemoglobin-> Microcytic anemia
  4. alpha thalassemia- most common are deletions of a-globin genes
  5. beta thalassemia- most common are point mutations of b-globin genes
  6. deficiency of one global chain leads to aggregate of other-> hemolysis in bone marrow or by spleen
22
Q

Normocytic anemia

A
  1. MCV 80-100
    2.two main causes:
    A. Hemolytic- increased destruction or loss of RBC
    Intravascular hemolysis- hemolysis in blood vessels
    Extravascular hemolysis- hemolysis by RES
    B.Non-hemolytic- decreased production of normal sized RBC
    3.two can be distinguished by reticulocyte count (RCxHb/15)
  2. Normal count is 1-2%, but with properly functioning bone marrow responds to anemia by increasing RC>3%

Corrected RC>3=bone marrow working= peripheral destruction= hemolytic anemia

23
Q

Reticulocyte

A
  • immature RBC precursor
  • slightly larger than mature RBC
  • blue tint= due to remaining RNA
24
Q

Symptoms of extra/intravascular hemolysis

A

EXTRAVASCULAR: splenomegaly(increased workload)
INTRAVASCULAR: hemoglobinemia(earlier on),hemoglobinuria(earlier on), hemosiderinuria(later on)
Decreased serum haptoglobin
BOTH: anemia
Jaundice
Increased risk for bilirubin gallstones
Corrected reticulocyte count >3%

25
Hereditary spherocytosis
1. inherited red blood cell defect caused by abnormalities of proteins in RBC cytoskeleton. Involves spectrin,ankyrin,band 3, or protein 4.2 2. loss of membrane stability-> spherical instead of bioconcave->spherocytosis-> loss of central pallor-> spherocytes consumed by splenic macrophages 3. ⬆️RDW and ⬆️mean corpuscular hemoglobin conc. (MCHC)
26
Sickle cell disease
1. autosomal recessive mutation in beta hemoglobin chain 2. Hbs form w/2 abnormal genes 3. Hypoxemia,dehydration,acidic environments exacerbate hbs polymerization 4. sickling destroys rbc membrane and leads to extravascular hemolysis by RES
27
Symptoms and common findings of sickle cell
Symptoms: dactylitis, autosplenectomy,acute chest syndrome, pain crisis, encapsulates organism infection, renal papillary necrosis Common findings: howell- jolly bodies,target cells
28
Autoimmune hemolytic anemia
1. warm (37=body temp) antibody hemolytic anemia - igg antibodies bind surface of RBC->splenic sequestration - cause: idiopathic 2. Cold (0-4) antibody hemolytic anemia - IgM antibodies bind surface of RBC-> infra and extravascular hemolysis - seen in mycoplasma pneumonia infection and infectious mononucleosis
29
Coombs drug test
- test to diagnose autoimmune hemolytic anemia 1. Direct Coombs test- detect antibodies that are already stuck to the surface of RBC 2. Indirect Coombs- confirm the presence of free flowing antibodies in patients serum
30
Paroxysmal nocturnal hemoglobinuria
1. Type of intravascular hemolysis 2. defect in myeloid stem cells-> absent Glycosylphosphatidylinositol(GPI) - GPI anchors membrane DAF, which protects RBC from complement mediated damage 3. absent GPI-> absent DAF...RBC destroyed by complement 4. Shallow breathing at night->inc CO2 retention-> respiratory acidosis - > activates complement-> RBC destroyed->hemoglobinuria (cola colored urine)
31
Glucose-6 phosphate dehydrogenase deficiency
1. x linked disorder. Glutathione protects RBCs from oxidative stress like H2O2 2. Causes of O2 stress: fava beans, antimalarials, drugs(sulfa drugs,primaquine,dapsone), various infections
32
Anemia due to underproduction
1. reticulocyte count<3 2. can either involve solely RBC or other cell lines 3. Solely anemia a. Renal failure- dec EPO b. Parvovirus b19 infection- infects progenitor RBC and halts erythropoiesis. Significant anemia in those with marrow stress 4. Damage to all cell lines a. a plastic anemia( damage to hematopoietic stem cell) b. Myelophistic process ( bone marrow replaced w/fibrosis or granuloma)
33
Macrocytic anemia
- MCV >100 - occurs bcus of decreased production of DNA precursors within RBC - RBC have one less division to preserve normal dna amount - MEGALOBLASTIC ANEMIA- caused by folate of b12 deficiency
34
MEGALOBLASTIC macrocytic anemia
1. Inhibition of DNA precursor synthesis during RBC production 2. Impaired division of rapidly dividing cells that need dna precursor I.e. grnulocytes, intestinal epithelial cells 3. Impaired granulocyte division - hypersegmented neutrophils=> 5 lobes
35
Non- MEGALOBLASTIC anemia
1. RBC larger than normal, MCV>100 | Caused by alcoholism, liver disease, drugs(5-FU)
36
Folate deficiency vs b12 deficiency
Folate : Dec serum level Inc serum homocysteine NORMAL METHYLMALONIC ACID Vitamin b12: Dec serum b12 Inc serum homocysteine Inc methylmalonic acid - causes subacute combined degeneration of dorsal and lateral column * DO not give folate to b12 deficient person can worsen neurological problems BOTH: macrocytic RBC and hyper-segmented. Neutrophils, glossitis
37
Folate absorption
1. Found in green vegetable and some fruits 2. Decrease risk of birth defects ( spina bifida) 3. Absorbed in jejunum 4. minimum body stores ( deficiency develops within months) 5. Deficiency because of: - poor diet ( alcoholics and elderly) - increased demand( pregnancy, cancer, hemolytic anemia) - folate antagonists ( methotrexate)
38
Vitamin b12 absorption
- found in animal products ( meat& dairy) - takes years to develop b12 deficiency ( vegans) - absorbed by ileum - half of body stored stored in liver
39
B12 deficiency
1. Dietary deficiency ( rare except in vegans) 2. Lack of pepsin or acid ( gastritis or gastrectomy) 3. Lack of protease secretion- pancreatic insufficiency 4. Lack of parietal cells- pernicious anemia ( autoimmune attack of gastric mucosa most common cause ) 5. Damage to terminal ileum- crohnd disease 6. fish tapeworm (diphyllobothrium latum)
40
B12 absorption pathway
B12 freed from binding protein via pepsin-> b12 binds to salivary protein haptocorrin-> pancreatic proteases release b12 from haptocorrin and allow it to bind IF ( produced by parietal cells)-> complex absorbed in ileum by binding to cubilin on enterocyte - b12 binds transport protein transcobalamin II

medical school midcomp 5 (11 decks)

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