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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
How long does it take after onset of anemia for regeneration to be noticeable
3 days in dogs and 5 days in cats (erythropoiesis into mature RBCs is 5-7 days)
26
What morphological changes can be seen in RBCs in patients with hemolysis? What do they indicate regarding the cause of hemolysis?
- 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
Name 3 heritable conditions that can cause hemolysis (+ 1 breed)
- Osmotic fragility (Abyssinian and Somali cats) - Phosphofructokinase deficiency (Springer Spaniel) - Pyruvate kinase deficiency (Basenji, Beagle)
28
What infectious agents can cause hemolytic anemia
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
Differentials for hemolytic anemia
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
Differentials for decreased-production anemia
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 2. Extra-medullary causes - Renal disease (EPO deficiency) - Hypothyroidism - Inflammatory / chronic disease - Cobalamin deficiency - Iron deficiency
31
What are typical blood smear findings in a cat with FeLV infection
- No polychromasia (non-regenerative) - Macrocytic normochromic RBC - Increased nucleated red blood cells
32
How are platelets assessed on a blood smear (magnification and location on the smear)? What is the normal number of platelets on a smear?
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
At what level of neutropenia are prophylactic antibiotics recommended
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
What chemotherapeutic drugs cause the most severe myelosuppression
- Lomustine - Doxorubicin - Carboplatin - Vincristine / vinblastine - Cyclophosphamide
35
When is neutropenia typically encountered following chemotherapy
6-8 days following chemo (but can be much longer for some drugs)
36
Differentials for erythrocytosis / polycythemia
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
How are EPO levels in polycythemia vera
Low (EPO-independent erythropoiesis having negative feedback on EPO production)
38
What is the oxygen extraction ratio?
VO2/DO2
39
What impact does anemia have on the oxyhemoglobin dissociation curve?
Rightward shift mediated by increase in 2,3-DPG in dogs (feline hemoglobin contain very little 2,3-DPG)2
40
Hematology characteristics of a chronic GI bleed
Microcytic, hypo chromic non regenerative anemia Thrombocytosis
41
Role of N-acetylcystein in acetaminophen toxicity
Augments endogenous glutathione stores as it is hydrolyzed to cysteine
42
What is the most essential regulator of RBC production?
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
Hormones that stimulate erythropoietin production
- Mainly from hypoxia-inducible-factor-1 (HIF-1) - Norepinephrine - Epinephrine - Several prostaglandins
44
What is a degenerative left shit?
When granulocytic precursors outnumber mature neutrophils in circulation
45
What is demmargination of neutrophils and in which scenarios is these seen?
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
What factors can increase synthesis / release of neutrophils and macrophages
- Granulocyte - Colony Stimulating Factor (G-CSF) can increase neutrophils - Granulocyte-macrophage colony stimulating factor (GM-CSF) can increase neutrophils and macrophages
47
Define myelophthisis
Infiltration of the bone marrow by abnormal tissue (neoplastic cells, collagen = myelofibrosis, osteoid tissue = osteosclerosis, inflammatory tissue = severe osteomyelitis) leading to impaired hematopoiesis
48
How will the bone marrow appear in a patient with myelodysplastic syndrome
Hyperplastic (abnormally high number of blasts) - numerous cells dividing from mutant progenitor but who are never released in circulation
49
What causes myoglobinemia and what are consequences of this?
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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