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Immunology & hematology > Hematology > Flashcards

Hematology Flashcards

1
Q

How many iron atoms are in one molecule of hemoglobin? Under what form?

A

4 iron atoms (one per heme = one per chain)

Iron under ferrous form Fe2+

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2
Q

What is the action of hepcidin? Where is it produced?

A

Hepcidin binds and inactivates ferroportin (which is normally responsible for increasing duodenal absorption of iron and release of iron by macrophages and liver) -> decreases iron availability

Produced in the liver

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3
Q

Under what form is iron transported in plasma? Under what form is it in cells?

A

Transported bound to transferrin

Present in cells as free Fe2+ or as ferritin or hemosiderin

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4
Q

What regulates the secretion of hepcidin

A
  • Erythropoietic activity (erythroblasts) inhibit secretion
  • Decreased iron stores stimulate secretion
  • Inflammatory cytokines stimulate secretion (over-ride the other regulators)
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5
Q

What is the average lifespan in circulation of erythrocytes / platelets / neutrophils in cats and dogs

A

RBC: 104 days in dogs, 73 days in cats

Neutrophils: < 24h (~6-8h)

Platelets: 5-7 days

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6
Q

What are the mechanisms leading to increased preload in anemia? Which one predominates in hypovolemic anemia and which on in normovolemic anemia?

A
  • Decreased O2 delivery -> sympathetic response -> venoconstriction -> increased venous return (+ increased contractility and HR)
    –> predominates in hypovolemic anemia
  • Anemia -> reduced blood viscosity -> increased preload (and decreased afterload)
    –> predominates in normovolemic anemia
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7
Q

What are indicators of RBC regeneration on CBC?

A
  • Reticulocytes (in cats, aggregate reticulocytes only)
  • Polychromasia (polychromatophils)
  • Anisocytosis / red cell distribution width
  • Metarubricytosis (nucleated red cells)
  • MCV (mean corpuscular volume): often macrocytic when regenerative
  • MCHC (mean corpuscular hemoglobin content): often hypochromic when regenerative
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8
Q

What are the 2 types of immune-mediated bone marrow anemia?

A
  • Precursor directed immune-mediated anemia (targeting reticulocytes, with erythroid hyperplasia still)
  • Pure red cell aplasia (targeting earlier precursors)
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9
Q

What is the normal COHb?

A

Up to 1%

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10
Q

What is the affinity of CO for Hb compared to O2?

A

200-240 times the affinity

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11
Q

What are the 2 consequences of CO toxicity on Hb?

A
  • CO binds 2 of the 4 available hemes ->reduces O2 carrying capacity by 50%
  • CO shifts the Hb curve to the left -> decreased O2 release to tissues
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12
Q

What is MetHb? What is a normal MetHb fraction?

A

Hemoglobin where the iron has been oxidized to Fe3+

Normal <3%

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13
Q

What is the consequence of MetHb on O2 transport?

A
  • The hemes that are in ferric form (Fe3+) cannot bind O2
  • MetHb increases affinity of the other hemes (in ferrous form) for O2 (left shift of Hb dissociation curve) leading to decreased release to tissues
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14
Q

What is sulfhemoglobin? What are consequences on O2 transport?

A

Hemoglobin where the ferrous iron has been oxidized to ferric by binding of a sulfur atom (from drugs - rare)

Sulfhemoglobin cannot bind O2, but shifts Hb dissociation curve to the right ->very decreased O2 transport but increased delivery to tissues

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15
Q

What are the anti-oxidant mechanisms found in RBC

A
  • Superoxide dismutase
  • Catalase
  • Glutathione peroxidase
  • Glutathione
  • MetHb reductase (using NADH to reduce MetHb into Hb)
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16
Q

What are Heinz bodies? Why are they more frequently identified in cats? What is a consequence of their presence in RBC?

A
  • Aggregates of denatured / precipitated Hb from metabolized MetHb or oxidation of the sulfhydryl (SH) groups of Hb
  • Heinz bodies lead to disruption of anion transport and decreased membrane deformability + aggregation of membrane proteins acting as autoantibodies -> RBC destruction by intravascular hemolysis (ghost cells) or extravascular hemolysis
  • Cats are more susceptible because they have 8 SH groups instead of 4 + their spleen is inefficient at removing RBCs with Heinz bodies
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17
Q

List causes of MetHb

A
  1. Toxic:
    - Acetaminophen
    - Topical benzocaine products
    - Nitrites and nitrates
    - Skunk musk
    - Hydroxycarbamide = hydroxyurea
    - Also reported with nitroprusside / nitroglycerin in humans
  2. Congenital:
    - MetHb reductase deficiency
  3. Secondary to disease:
    - Sepsis (due to increased NO)
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18
Q

List causes of Heinz bodies anemia

A
  1. Toxic:
    - Allium plants
    - Zinc
    - Propylene glycol
    - Methylene blue
    - Naphthalene (moth balls)
    - Propofol in cats
    - Copper
  2. Secondary to disease (cats):
    - Hyperthyroidism
    - Lymphoma
    - Diabetes mellitus (especially DKA)
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19
Q

What level of MetHb / COHb is necessary to have clinical signs

A
  • 20% for MetHb
  • 15% for COHb but individual dependent
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20
Q

List 3 dyshemoglobins

A
  • COHb
  • MetHb
  • SulfHb
21
Q

What is the SpO2 reading in the presence of significant MetHb or SulfHb

A

85% for both (they have the same spectral peak)

22
Q

What hematological finding is commonly associated with MetHb

A

Heinz bodies (can be delayed)

23
Q

What is an adverse effect of methylene blue therapy for MetHb

A

Heinz body anemia (can develop up to 4 days after administration)

24
Q

What should be suspected in a patient who presents with signs suggestive of MetHb but does not improve with treatment? What is the treatment?

A

Sulfhemoglobinemia

There is no treatment - the sulfur will remain on Hb for the lifespan of RBC. Can transfuse RBC as needed.

25
Q

How long does it take after onset of anemia for regeneration to be noticeable

A

3 days in dogs and 5 days in cats
(erythropoiesis into mature RBCs is 5-7 days)

26
Q

What morphological changes can be seen in RBCs in patients with hemolysis? What do they indicate regarding the cause of hemolysis?

A
  • Spherocytes -> immune mediated
  • Schistocytes = schizocytes (+/- acanthocytes and keratocytes) -> fragmentation / mechanical damage (microangiopathic hemolysis)
  • Heinz bodies (+/- eccentrocytes and pyknocytes) -> oxidative damage

+/- parasites: Mycoplasma, Babesia

  • Anisocytosis (= regenerative anemia) with no other changes -> Heritable hemolysis
27
Q

Name 3 heritable conditions that can cause hemolysis (+ 1 breed)

A
  • Osmotic fragility (Abyssinian and Somali cats)
  • Phosphofructokinase deficiency (Springer Spaniel)
  • Pyruvate kinase deficiency (Basenji, Beagle)
28
Q

What infectious agents can cause hemolytic anemia

A
  1. RBC pathogens
    - Mycoplasma haemofelis
    - Babesia spp (mostly Babesia gibsoni in North America)
    - Cytauxzoon felis
  2. Systemic pathogens
    - FeLV
    - FIV
    (- Leptospirosis)
    (- E Coli with secondary hemolytic-uremic syndrome)
29
Q

Differentials for hemolytic anemia

A
  1. Fragmentation hemolysis
    - DIC
    - Splenic torsion / neoplasia
    - Vasculitis
    - Caudal caval syndrome
    - Heart valve disease
  2. Toxic = oxidative
    - Onion / garlic
    - Acetaminophen
    - Zinc, copper
    - Propylene glycol
    - Skunk musk
    - Naphthalene
    - Benzocaine
    - Methylene blue
    - Propofol in cats
  3. Immune-mediated
    - Non-associative
    - Associative: neoplasia, infection, drugs (penicillins, cephalosporins, sulfonamides, methimazole)
    - Neonatal isoerythrolysis
    - Transfusion reaction
  4. Heritable hemolysis
    - Phosphofructokinase deficiency
    - Osmotic fragility syndrome
    - Pyruvate kinase deficiency
  5. Infection-related hemolysis
    - Mycoplasma haemofelis
    - Babesia
    - Cytauxzoon felis
    - FIV
    - FeLV
    - Leptospirosis
  6. Miscellaneous
    - Hypophosphatemia
    - Osmolarity changes (iatrogenic)
    - Envenomation
    - Hystiocytic neoplasia (hemophagocytic histiocytic sarcoma)
30
Q

Differentials for decreased-production anemia

A
  1. Medullary causes
    Primary:
    - Aplastic anemia
    - Myelodysplastic syndromes
    - Neoplasia (leukemia, multiple myeloma)

Secondary:
- Infectious: FIV, FeLV, Parvo
- Immune mediated: non-regenerative IMHA, pure red cell aplasia
- Neoplastic: lymphoma, histiocytic disease, Sertoli cell tumor
- Toxins / drugs: chemotherapy, azathioprine, phenobarbital, estrogens, fenbendazole

  1. Extra-medullary causes
    - Renal disease (EPO deficiency)
    - Hypothyroidism
    - Inflammatory / chronic disease
    - Cobalamin deficiency
    - Iron deficiency
31
Q

What are typical blood smear findings in a cat with FeLV infection

A
  • No polychromasia (non-regenerative)
  • Macrocytic normochromic RBC
  • Increased nucleated red blood cells
32
Q

How are platelets assessed on a blood smear (magnification and location on the smear)? What is the normal number of platelets on a smear?

A

Assessed at the 100x oil immersion in the monolayer (+ check for platelet clumps in feather edge and lateral edges at 10x objective)

Should have 8-15 platelets per 100x field

33
Q

At what level of neutropenia are prophylactic antibiotics recommended

A

Neutrophils ≤ 0.75x10^9/L

Antibiotics can be considered when neutrophils ≤ 1.0x10^9/L if other risk factors and are recommended if neutrophils ≤ 1.0x10^9/L and fever is present

34
Q

What chemotherapeutic drugs cause the most severe myelosuppression

A
  • Lomustine
  • Doxorubicin
  • Carboplatin
  • Vincristine / vinblastine
  • Cyclophosphamide
35
Q

When is neutropenia typically encountered following chemotherapy

A

6-8 days following chemo (but can be much longer for some drugs)

36
Q

Differentials for erythrocytosis / polycythemia

A
  1. Relative polycythemia (dehydration, should correct with fluid therapy)
  2. Secondary appropriate polycythemia: chronic hypoxemia (chronic respiratory disease, right-to-left shunt, altitude)
  3. Secondary inappropriate polycythemia:
    - Underlying tumor (often renal)
    - Hyperthyroidism
    - Acromegaly
    - Hyperadrenocorticism
  4. Primary polycythemia = polycythemia vera
37
Q

How are EPO levels in polycythemia vera

A

Low (EPO-independent erythropoiesis having negative feedback on EPO production)

38
Q

What is the oxygen extraction ratio?

A

VO2/DO2

39
Q

What impact does anemia have on the oxyhemoglobin dissociation curve?

A

Rightward shift mediated by increase in 2,3-DPG in dogs (feline hemoglobin contain very little 2,3-DPG)2

40
Q

Hematology characteristics of a chronic GI bleed

A

Microcytic, hypo chromic non regenerative anemia

Thrombocytosis

41
Q

Role of N-acetylcystein in acetaminophen toxicity

A

Augments endogenous glutathione stores as it is hydrolyzed to cysteine

42
Q

What is the most essential regulator of RBC production?

A

Tissue oxygenation –> hypoxia causes a marked increase in erythropoietin production and the erythropoietin in turn enhances red blood cell production until the hypoxia is relieved.

43
Q

Hormones that stimulate erythropoietin production

A
  • Mainly from hypoxia-inducible-factor-1 (HIF-1)
  • Norepinephrine
  • Epinephrine
  • Several prostaglandins
44
Q

What is a degenerative left shit?

A

When granulocytic precursors outnumber mature neutrophils in circulation

45
Q

What is demmargination of neutrophils and in which scenarios is these seen?

A

Normally marginated neutrophils are not normally part of the measured neutrophil concentration (not circulating). Demargination of these cells dramatically increases neutrophil concentration

  1. Corticosteroid response
  2. Epinephrine response
46
Q

What factors can increase synthesis / release of neutrophils and macrophages

A
  • Granulocyte - Colony Stimulating Factor (G-CSF) can increase neutrophils
  • Granulocyte-macrophage colony stimulating factor (GM-CSF) can increase neutrophils and macrophages
47
Q

Define myelophthisis

A

Infiltration of the bone marrow by abnormal tissue (neoplastic cells, collagen = myelofibrosis, osteoid tissue = osteosclerosis, inflammatory tissue = severe osteomyelitis) leading to impaired hematopoiesis

48
Q

How will the bone marrow appear in a patient with myelodysplastic syndrome

A

Hyperplastic (abnormally high number of blasts) - numerous cells dividing from mutant progenitor but who are never released in circulation

49
Q

What causes myoglobinemia and what are consequences of this?

A

Excess myoglobin in the blood resulting from the damage to the cell membrane of myocytes.

Can be caused by a direct injury that damages the cells or metabolic disturbances

Consequences:
- Hypovolemia (lots of fluid in myocytes)
- Hyperkalemia, hyperphosphatemia (released from myocytes)
- AKI (direct tubular injury, cast formation, hypovolemia)

Immunology & hematology (3 decks)

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