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RBC pathology Flashcards

1
Q

What percentage of bone marrow is active in RBC production at birth?

A

100%

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2
Q

What are the major sites of RBC production in adulthood?

A 
Red marrow....Found in:
sternum
pelvis
ribs
skull
proximal epiphyseal portions of humerus and femur
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3
Q

What is the danger of bone fractures as it relates to the marrow?

A

Yellow marrow where fatty degeneration has occurred.

Fractures can cause a fat embolism which you can’t really tx.

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4
Q

What is responsible for the differentiation of each blood cell type from the stem cell?

A

Colony stimulating factor (CSF) - (each cell type has its own CSF; eg GM-CSF for granulocytes-macrophages

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5
Q

What are the dangerous sequelae of polycythemia?

A

too many RBCs can lead to thrombi and emboli

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6
Q

How is anemia defined?

A

decrease in number, size (Hb concentration), or both of RBCs

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7
Q

How is anemia measured?

A

decreased hematocrit

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8
Q

What are the broad spectrum reasons for low RBC numbers in anemia?

A
  • blood loss (hemorrhage)
  • impaired RBC production (hypoproliferation)
  • increased RBC destruction (hemolysis)
  • any combination of the above
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9
Q

What are the sxs of anemia?

A
  • pallor
  • increased pulse rate and weak pulse
  • shortness of breath (SOB)
  • palpitations
  • dizziness
  • fatigue
  • headaches
  • faintness or syncope
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10
Q

Would an acute or chronic anemia present as more symptomatic?

A

acute

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11
Q

What is the body’s response pattern to acute blood loss?

A
  • Hemo-dilutionlowers the hematocrit
  • decrease in oxygenation of tissues triggers the production of erythropoietin (EPO) - particularly due to decreased oxygenation of the renal juxtaglomerular JGA cells
  • BM responds by increasing erythropoiesis.
  • The bone marrow has the capacity to increase red blood production ~7-8 fold above baseline levels (presuming adequate levels of Fe are present)
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12
Q

How will a peripheral smear appear immediately after acute blood loss?

A

Normal….takes a while to pull extra fluid from the tissues in order to make more plasma.

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13
Q

As marrow replaces lost RBCs what will you find more of in the peripheral blood?

A

reticulocytes (immature RBCs)

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14
Q

What is the normal range for reticulocytes? What about after acute blood loss?

A

Normal: 0.5-1.5%

Post-hemorrhage: 10-15%

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15
Q

What is polychromasia?

A

reticulocytes stain grey-blue/purple instead of the normal red of mature RBCs.

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16
Q

How much blood is normally lost daily through the stool, etc? How much is a problematic amount?

A

Normal: 2ml/day
Problem: 10ml

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17
Q

What is generally the rate-limiter for replacing lost RBCs?

A

iron stores

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18
Q

Which organ systems are usually responsible for chronic anemia?

A 
Gastrointestinal tract
•ulcer, colitis, cancer
Gynecologic
•excessive menstrual flow, cancer
Genitourinary
•cancer or stone

‘Gee, why am I anemic?’

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19
Q

What is a hemolytic anemia? What characterizes this type of anemia?

A

RBCs are prematurely destroyed.

Anemias characterized by:
oShortened RBC life span
oHgb breakdown products accumulate
oMarked increase in BM erythropoiesis

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20
Q

What are the two classes of hemolytic anemia in terms of where RBCs are destroyed? Which is more common?

A

extravascular: hemolysis in the spleen (much more common)
intravascular: destruction w/in the blood vessels

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21
Q

What are three reasons for intravascular hemolysis?

A
  • mechanical trauma: mechanical heart valves, physical trauma (marathon running, bongo drumming)
  • antibody fixation: mismatched blood transfusion
  • toxic injury to the RBCs: malaria, septic shock
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22
Q

What will you expect to see in a peripheral smear of someone with intravascular hemolysis?

A

fragmented cells (helmet cells and schistocytes)

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23
Q

What is deformability? How is it different with extravascular hemolytic anemia?

A

Deformability: RBC’s ability to change shape (req’d to pass through endothelium)

Extravascular hemolysis results from RBCs with structural changes. These changes create less deformability of the cells.

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24
Q

What are the two classes of hemolytic anemia in terms of root cause?

A

Intrinsic (genetic and hereditary RBC diseases - expect family history) and Extrinsic (Conditions in which the abnormality is outside of or extrinsic to the RBC itself)

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25
Q

What are the features of genetic RBC conditions?

A
  • disorders of the RBC membrane
  • RBC enzyme deficiencies
  • disorders of hemoglobin synthesis
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26
Q

What are some causes of extrinsic anemias?

A
  • heart valve prosthesis and A-V shunts
  • infections such as malaria
  • chemical injury such as lead poisoning, snake venom
  • abnormal sequestration of the RBCs in the spleen (hypersplenism)
  • acquired hemolytic anemias
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27
Q

What is acquired hemolytic anemia?

A

immunologic (autoimmune) mediated RBC destruction.

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28
Q

In cases of acquired hemolytic anemia, what is the usual class of Ab? How does it lead to cell lysis?

A

IgG

  • directed against RBCs with direct cell lysis
  • react with RBC membranes to increase their susceptibility to spleen destruction
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29
Q

To what conditions might acquired hemolytic anemia be secondary?

A
  • lymphoma
  • carcinoma
  • sarcoidosis
  • collagen vascular disease -Lupus or rheumatoid arthritis.
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30
Q

What can immune hemolysis cause?

A
  • incompatible blood transfusions

* fetal maternal incompatibility

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31
Q

What are the three subtypes of intrinsic hemolytic anemia?

A
  • Abnormal hemoglobin
  • Abnormal RBC metabolism
  • Abnormal hemoglobin synthesis
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32
Q

What is the hemoglobin type during the fetal and neonatal period? What are the chains?
How long until the adult profile is achieved? What are the chains?

A

Fetal: Hb F (2 alpha, 2 gamma chains)

Adult: One year, Hb A (2 alpha, 2 beta chains)

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33
Q

Which hemoglobin type has the greatest oxygen affinity?

A

Hb F

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34
Q

Mutation in which chain causes sickle cell anemia?

A

beta chain (point mutation)

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35
Q

Under what conditions are sickle cells formed?

A 
low pH (reduces O's affinity for Hb)
low oxygen tension
36
Q

How is the life span of an RBC affected by sickling?

A

Shortened by ~20 days

37
Q

How does MCHC relate to intensity of sickle cell dz?

A

decreased MCHC (alpha-thalassemia) –pts. will have milder sxs/dz because thalassemia reduces globin synthesis…decreases the hgb conc. per cell.

38
Q

How does sickle cell anemia manifest clinically?

A

chronic hemolysis and ischemic tissue damage resulting from occlusion of small blood vessels.

39
Q

How does a direct coombs test work? Indirect?

A

The tests are used to dx autoimmune hemolytic anemias (AIHA)

Blood draw from pt with immune-mediated hemolytic anemia.

Direct: Coombs reagent (anti-human Ab) is added to patient blood.
Pos: Coombs Ab binds to the anti-RBC Ab already on the blood cells causing the complex to fall out of solution.

Indirect: Isolate anti-RBC Ab from pt’s blood, add to potential donor’s blood sample. then add Coomb’s Ab.
Pos: if pt’s anti-RBC Ab binds donor RBC, Coombs Ab will bind and the complex will fall out of solution.

40
Q

What is the most common form of AIHA? What causes it? What type of Ab is involved?

A

Warm Ab AIHA (at 37 C).

Half the cases are idiopathic, the other half are secondary to SLE, Rx or neoplastic dz (like lymphoma)

IgG binds RBCs

41
Q

What percentage of AIHA are due to Cold Agglutnin AIHA? What Ab is involved? What temp range does this occur? When do the Abs appear acutely? Chronically?

Where in the body is this likely to occur

A

Cold Ab is 15-30% of AIHA.
Involves IgM which bind to RBCs at 0-4 deg C.

Appear acutely during recovery from infx and is self-limited and usu sub-clinical.

Chronically from lymphoid neoplasms

Takes place at sites of exposure: fingers, toes, eyes and nose

42
Q

What are the only two conditions which will cause major clinical problems associated with hemolysis?

What are likely to be seen on a peripheral blood smear?

A

TTP and HUS.

Will see lots of fragmented cells.

43
Q

What are the five anemias of diminished erythropoiesis?

A
  • megaloblastic B12/Folate def.
  • Iron def.
  • anemia of chronic dz
  • anemia of renal failure
  • marrow failure
44
Q

What are the most common causes of megaloblastic/macrocytic anemias?

A
  • B-12 deficiency
  • Folic acid deficiency
  • Inadequate diet (TPN, B12) and alcoholism
  • Impaired DNA synthesis and distinctive morphological changes in the blood and bone marrow are keynotes.
  • TPN/PPN
  • Azotemia/Uremia
  • Bacteremia/ Septicemia
45
Q

Which cell types will be impacted in megaloblastic/macrocytic anemias?

A

RBC and WBC …. DNA synthesis everywhere is slowed.

46
Q

What will cause folic acid deficiency?

A
  • alcoholism (#1)
  • phenytoin
  • anti-metabolites (chemo)
  • HIV drugs
47
Q

What impact does megaloblastic anemia have on RBC size/MCV? Cell color? RDW?

A

Increased RBC size and MCV but normochromic.

Increased RDW (anisocytosis).

48
Q

What other anomalies are seen in the periphery with megaloblastic anemia? What about the marrow?

A

Reticulocytes are low and RBCs may be nucleated. PMNs will be hypersegmentd (product of incomplete DNA synth).

The marrow will be full of cells because they are almost ready to be released but aren’t able to get there.

49
Q

For what compound’s function are cobalamin and folate necessary?

A

thymidine (T)

50
Q

What happens to N:C ratio with megaloblastic anemia? Why does this occur?

A

nulceus/cytoplasm are asynchronous but nucleus doesn’t grow way out of proportion of the cytoplasm like in cancer.

because T is limited, DNA can’t reproduce, but RNA function is fine in the cytoplasm.

51
Q

What is behind pernicious anemia?

A

parietal cells of the stomach not producing intrinsic factor (IF) to absorb B12…..possible due to T cells attacking gastric mucosa

associated w/:

  • gastric atrophy
  • lost IF production
  • OTC PPI use
  • autoimmune conditions limiting saliva production (sjogren’s)
52
Q

How long will it take for a dietary deficiency of B12 to manifest?

A

At least 3 yrs

53
Q

What are the 3 types of antibody found in pernicious anemia?

A

type I: blocks B12 binding IF
type II: blocks B12-IF complex from binding receptor in ileum
type III: binds the protein pump - found in half of elderly pts w/chronic gastrits

54
Q

What are the major dietary sources of cobalamin?

A

meat and milk

55
Q

How common are anti-parietal cell Abs in patients w/pernicious anemia? General pop?

A

90% in those w/pernicious anemia

5% generally

56
Q

Patients with pernicious anemia have a 2 to 3 fold increased incidence of ________.

A

gastric carcinoma

57
Q

Adults with pernicious anemia may also have irreversible _________ and _______.

What deficiency also commonly coexists? Why?

A

gastric atrophy and achlorydia

Often see iron deficiency as well …. chloride (HCl) is required to make dietary ferric iron soluble.

58
Q

What is the gold standard of dx for pernicious anemia?

A

Bx of gastric mucosa showing depleted parietal cells.

59
Q

In pernicious anemia, what two changes are common along the alimentary tract?

A

atrophic glossitis - glazed, beefy tongue
intestinalization - gastric epithelium replaced by goblet cells (essentialy barrett’s esophagus)

these changes are due to autoimmunity so they can be treated but cancer risk can’t be lowered.

60
Q

Why are CNS lesions common with pernicious anemia?

A

decreased B12 leads to increased methylmalonic acid which leads to abnormal FAs being incorporated into neuronal lipids (bad membranes).

61
Q

What is the root cause of megaloblastic madness? What are the sxs?

A

B-12 def.

delusions, hallucinations, outbursts, and paranoid schizophrenic ideation.

can be reversed with B12 supplementation.

62
Q

What are the dx features of B12 deficiency?

A
  • Low levels in RBCs
  • MCV elevated (unless also iron deficient)
  • Jaundice (due to RBC hemoloysis - which increases Hgb turnover, which breaks down to bilirubin)
  • Inability to absorb oral B12
63
Q

What is the most common drug which may interfere with folate absorption?
What are dietary sources of folate? How much is stored in the body?

A

oral contraceptives interfere.

get folate from leafy greens and lemons, bananas, melons, and liver.

not well stored, always need a dietary supply.

64
Q

What are the major risk factors of folate deficiency?

A 
–a poor diet (seen frequently in the poor, elderly, and in people who do not eat fresh fruits/vegetables)
–overcooking food
–alcoholism
–a history of malabsorption
–pregnancy
65
Q

What are the dx factors for folate deficiency?

A
  • large RBCs in circulation and the marrow.
  • hypersegmented PMNs
  • decreased folate levels in RBCs
  • elevated homocysteine

-DO NOT have neurologic sxs of B12.

66
Q

How may pregnancies be complicated by folate deficiency?

A
  • premature birth
  • neural tube birth defects (spina bifida, cleft lip/palate)
  • increased risk of placentia previa
67
Q

What is the most common nutritional d/o worldwide? What can cause it?

A

Iron deficiency anemia

–(1) dietary lack
–(2) impaired absorption
–(3) increased requirement
–(4) chronic blood loss

68
Q

Where and why is dietary iron deficiency most common? What age groups?

A

most common in developing countries due to predominantly vegetarian diet.

occurs more often in infants, children, the poor and the elderly.

69
Q

What autoimmune condition can impair iron absorption? How will a gastrectomy do the same?

A

celiac dz

gastrectomy - decreased HCl and transit time through the duodenum

70
Q

In the western world, what is the most common cause of iron deficiency anemia?

A

•Chronic blood lossis the most common cz in the western world.

•Internal hemorrhage
–GI tract (PUD, hemorrhagic gastritis, gastric or colorectal carcinoma, hemorrhoids, parasites)
–GU (renal, pelvic or bladder tumors)
–Gyn (menorrhagia, AUB, Uterine carcinoma) depletes iron stores.

71
Q

How does iron deficiency impact cell size and Hb concentration?

A

microcytic, hypochromic (the pallor has extended beyond just central)

72
Q

What set of circumstances are required for iron deficiency anemia to appear? How does it appear clinically?

A 
•Anemia only appears when:
–Iron stores are completely depleted
–Low serum iron
–Low serum ferritin
–Low transferrin saturation

•Clinical presentation includes:
–koilonychia(nails thin and concave)
–alopecia (hair loss)
–atrophic changes in the tongue and gastric mucosa, and intestinal malabsorption.

73
Q

What lab results will lead to a dx of iron deficiency anemia?

A

–Low serum ferritin (low storage)
–Low iron levels (low circulating)
–Elevated TIBC:
total plasma iron-binding capacity (holding on tight to what it has)

74
Q

What are the three Cs of the anemia of chronic dz?

A

•Chronic infections: osteomyelitis, bacterial endocarditis, lung
abscess (bugs like Fe, somehow our body has learned to sequester it in their presence)
•Connective tissue diseases: RA, SLE, regional enteritis –crohn’s
•Cancer –Hodgkin lymphoma, lung and breast cancer also other cancers

75
Q

How does anemia of chronic dz present in terms of cell production (hyper-/hypo-/normoproliferative)?

A

•Hypoproliferative anemia:

–RBC BM precursors are deficient in their iron uptake and utilization.

76
Q

How does ACD differ from IDA lab-wise?

A

ACD is characterized by:
–Low iron levels AND Low TIBC
–With Normal or even Elevated ferritin levels

77
Q

How does ACD present on a PBS?

A

-Normocytic-Normochromic anemia

–in 1/3rd it presents as Micro-Hypochromic indicating progressive ACD dz associated WITH IDA

78
Q

What is aplastic anemia and how does it present

A

Aplastic anemia is a BM failure syndrome characterized by:
–PB Pancytopenia (peripheral blood smear shows decrease in RBC/WBC/platelets)
–BM hypOplasia - devoid of hematopoietic elements, fat cells instead

79
Q

What is the pathogenesis of aplastic anemia?

A
  • toxins activate T-cells which target and trample stem cells
  • Some marrow insult causes genetic damage that limits proliferation and differentiative capacity of stem cells.
80
Q

What are the major causes of morbidity and mortality from aplastic anemia?

A

infection and bleeding

81
Q

How might aplastic anemia manifest?

A
  • Anemia may manifest as pallor, headache, palpitations, dyspnea, and fatigue.
  • Thrombocytopenia may present as mucosal and gingival bleeding or petechialrashes.
  • Neutropenia may manifest as overt infections, recurrent infections, or mouth and pharyngeal ulcerations.
82
Q

What is the breakdown of acquired/congenital aplastic anemias?

What are the causes of acquired?

A

80:20 acquired:congenital

  • Infectious causes such as hepatitis viruses, Epstein-Barr virus (EBV), HIV, Parvo B19, and mycobacterial infections.
  • Toxic exposure to radiation and chemicals such as benzene.
  • Drugs such as chloramphenicol, sulfa, and gold, may cause aplasia of the marrow.
  • Many cases have no known etiology and are referred to as idiopathic.
83
Q

What are the causes of microcytic-hypochromic anemias?

A
  • Iron deficiency
  • Lead poisoning
  • Thalassemia
  • Hypothyroidism
  • Anemia of chronic disease
84
Q

What are the causes of macrocytic anemias?

A
  • B12 deficiency
  • Folic acid deficiency
  • ETOH abuse
  • Hyperthyroidism
85
Q

What are the causes of normocytic-normochromic anemias?

A
  • Acute hemorrhage
  • Acute lysis
  • Aplastic anemia
  • Hypothyroid
  • Anemia of chronic disease

pathology (5 decks)

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