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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
Q

Hereditary spherocytosis

A
  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
Q

Sickle cell disease

A
  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
Q

Symptoms and common findings of sickle cell

A

Symptoms: dactylitis, autosplenectomy,acute chest syndrome, pain crisis, encapsulates organism infection, renal papillary necrosis

Common findings: howell- jolly bodies,target cells

28
Q

Autoimmune hemolytic anemia

A
  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
Q

Coombs drug test

A
  • test to diagnose autoimmune hemolytic anemia
    1. Direct Coombs test- detect antibodies that are already stuck to the surface of RBC
  1. Indirect Coombs- confirm the presence of free flowing antibodies in patients serum
30
Q

Paroxysmal nocturnal hemoglobinuria

A
  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
Q

Glucose-6 phosphate dehydrogenase deficiency

A
  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
Q

Anemia due to underproduction

A
  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
Q

Macrocytic anemia

A
  • 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
Q

MEGALOBLASTIC macrocytic anemia

A
  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
Q

Non- MEGALOBLASTIC anemia

A
  1. RBC larger than normal, MCV>100

Caused by alcoholism, liver disease, drugs(5-FU)

36
Q

Folate deficiency vs b12 deficiency

A

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
Q

Folate absorption

A
  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
Q

Vitamin b12 absorption

A
  • found in animal products ( meat& dairy)
  • takes years to develop b12 deficiency ( vegans)
  • absorbed by ileum
  • half of body stored stored in liver
39
Q

B12 deficiency

A
  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
Q

B12 absorption pathway

A

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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