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B&C > SA Anemia 1-4 (Wilkinson) > Flashcards

SA Anemia 1-4 (Wilkinson) Flashcards

1
Q

Define Anemia

A

reduction in RBC mass –> reduced O2 delivery to tissue

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2
Q

O2 delivery to tissue depends on what 3 factors

A
  1. Blood flow and is distrubution to different organs
  2. O2 carrying capacity of the blood (Hgb concentration or # RBCs in circulation)
  3. Oxygen’s ability to extract the RBC into tissues
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3
Q

Body’s physiologic responses (4) to chronic anemia

A

1. Increases CO

2. Redistributes blood flow to caridac and cerebral circulation (via vasodilation) and decreases to splanchnic vascular bed (GIT, spleen, etc.) & periphery (e.g., pale gums) (via vasocinstriction)

3. Increased erythropoietin production (hormone that signals bone marrow to produce more RBCs)

4. Improved O2 extraction (via compensatory mechanism)

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4
Q

Why do animals with acute onest of anemia tend to have more severe clinical signs/exam changes than those with chronic anemia?

A

In chronicly anemic animals, the body has gotten used to its anemic state via compensatory mechanisms

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5
Q

3 main causes of anemia

A

1. Hemorrhage (hypovolemia)
2. Hemolysis (RBC destruction)
3. Hypoplasia (decreased RBC production- bone marrow dz, kidney failure)

Erythropoietin (hormone that stimulates RBC production) is produced in kidneys

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6
Q

First step in assessing anemia is determining whether it’s regenerative or non-regenerative. Define the two and what they each indicate.

A
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7
Q

Pre-regenerative anemia time period: the time period b/w anemia onset & bone marrow release of reticulocytes

A

~2-5 days

IMHA or hemorrhage: may initially present as non-regen., but b/c not enough time has lapsed, and not b/c bone marrow isn’t working properly

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8
Q

How to assess RBC regeneration

A
  • Reticulocyte count (expressed as a % of the CURRENT RBC count, so must be corrected for anemia)
  • Blood smear (polychromasia and anisocytosis; nRBCs)
  • RBC indices (MCV and MCHC)

  • Polychromasia and anisocytosis indicate presence of reticulocytes; nRBCs indicate appropriate metarubricytosis if reticulocytosis is present)
  • MCV = size of RBCs, MCHC = hemoglobin content of RBCs –> Macrocytosis and hypochromasia (not always abnormal)
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9
Q

Absolute reticulocyte count calculation

A

ARC = Reticulocyte % x RBC count

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10
Q

Values for regenerative response in dogs vs cats

A

Dogs: > 95,000/uL reticulocytes
Cats: > 60,000/uL reticulocytes

cats do not have as robust response to anemia as dogs

non-regen = less than these values

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11
Q

What is seen on blood smear of non-regen case

A

lack of polychromasia and anisocytosis; nRBCs ( = inappropriate metarubricytosis)

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12
Q

Metarubricytosis w/out reticulocytosis is associated with what?

A

Bone marrow disease or injury, splenic disease, lead poisoning

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13
Q

2 differentials for non-regen anemia:

A

Either pre-regenerative period or true hypoplasia (in bone marrow)

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14
Q

Hemorrhagic Anemia (Regenerative)

Signs of GIT blood loss

A
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15
Q

Hemorrhagic Anemia (Regenerative)

Signs of urinary or reproductive tract blood loss

A

Hematuria (gross or microscopic)

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16
Q

Hemorrhagic Anemia (Regenerative)

Signs of respiratory tract blood loss

A
  • Epistaxis
  • Hemopysis (coughing blood)
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17
Q

Hemorrhagic Anemia (Regenerative)

Where are sources of internal blood loss contributing to anemia?

A
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18
Q

Hemorrhagic Anemia (Regenerative)

3 common causes of acute blood loss

A
  1. Trauma
  2. Coagulopathy
  3. Neoplasia

Coagulopathy: 1º hemostasis defects (PLTs) or 2º hemostasis defects (clotting factors)

Neoplasia: hemangiosarcoma (liver, spleen, lung)

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19
Q

Hemorrhagic Anemia (Regenerative)

Common causes of chronic blood loss

A
  • GI tract (hookworms, ulcers, neoplasia)
  • Fleas
  • Urinary tract
  • Respiratory tract (chronic epistaxis)
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20
Q

Hemorrhagic Anemia (Regenerative)

Animals with acute hypovolemia usually have what strength of pulses and why?

A

Weak and thready pulses: they are losing large volumes of blood very quickly

loss of plasma/fluid/plasma proteins

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21
Q

Hemorrhagic Anemia (Regenerative)

Animals with hemolysis-caused anemia typically have what strength of pulse and why?

A

Hemolysis is NOT a loss of blood volume (pulses can still be strong/bounding)

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22
Q

Hemorrhagic Anemia (Regenerative)

Chronic external hemorrhage vs chronic internal hemorrhage reticulocytes

A

External chronic: present (regen) or absent (non-regen) –> NON-REGEN b/c they are losing iron in the blood –> microcytic and hypochromic anemia

Internal chronic: present (regen)

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23
Q

Hemorrhagic Anemia (Regenerative)

Relationship b/w iron & RBCs

A

Iron = essential for hemoglobin production

Iron deficiency (microcytic and hypochromic)
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24
Q

Hemorrhagic Anemia (Regenerative)

Signs of poor tissue oxygenation (5)

A

weakness, depression; tachycardia; tachypnea; bounding femoral pulses (or weak w/ acute blood loss)

Indicate start of blood transfusion

PCV < 15%: consider blood transfusion or low PCV + these clinical signs

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25
Q

Hemorrhagic Anemia (Regenerative)

What type of blood product for blood-loss anemia & cogaulopathy?

A

Fresh whole blood (prior to refrigeration):
- RBC + PLTs + all clotting factors + plasma proteins
- not usually used b/c requires another animal who can immediately donate their blood

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26
Q

Hemorrhagic Anemia (Regenerative)

Refrigerated vs non-refrigerated (stored vs fresh) whole blood products?

A
  • Refrigerated (stored): RBC + some clotting factors (no V or VIII or vWF) + plasma proteins
  • Non-refrigerated (fresh): RBC + PLTs + all clotting factors + plasma proteins

vWF clotting factor: attaches to small blood cells called platelets. This helps the platelets stick together, like glue, to form a clot at the site of injury and stop the bleeding.

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27
Q

What type of blood product for hemolytic or hypoplastic anemia?

A

Packed Red Blood Cells:
- RBC only

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28
Q

Desired PCV after blood transfusion?

A

~25%

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29
Q

Equation for blood transfusion volume

A

(BWkg x BVml/kg) x [(PCVdes - PCVpat) / (PCVdon)]

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30
Q

DEA 1.1

A

Dog Erythrocyte Antigen 1.1

a surface protein on RBC

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31
Q

When will dogs have naturally occurring antibodies against DEA 1.1?

A

If they are DEA 1.1 (-) and receive a blood transfusion

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32
Q

What blood types are most common in cats?

A

Types A, B, AB

in U.S.: 99% are type A

33
Q

Type A cats have _ anti-B antibodies

Type B cats have _ anti-A antibodies

A

Type A cats have WEAK anti-B antibodies –> these cats will have a negative rxn if given type B blood

Type B cats have VERY STRONG anti-A antibodies –> these cats will DIE if given type blood A

34
Q

What is a crossmatch

A

To assess compatibility b/w patient serum (antibody) and donor red blood cells (antigen):
take patient’s serum with donor’s RBCs and see if they react (does pt have antibodies against donor’s antigens)

35
Q

When should a crossmatch be performed?

A
  • Previous blood transfusion hx or hx is unknown
  • If given back-to-back (e.g., IMHA pt in ICU getting q12h) after ≥ 3 days following a known RBC transfusion (time it takes Abs to form)
36
Q

Blood transfusion rates:
1. first 15 mins
2. second 15 mins (if going well)
3. remainder of 4-hour window

A
  1. 1 ml/kg/hr
  2. 2 ml/kg/hr
  3. increase to rate that allows for remainder of blood to be administered within the 4-hour window

faster rates can be used if the anemia is life-threatening

TPR q15 mins first hour
TPR q30mins for remaining time

37
Q

Transfusion Reactions (2) / which is most common and which is life-threatening

A
  1. Transfusion-associated circulatory overload (non-immunologic) = pt gets fluid-overloaded
  2. Non-hemolytic febrile reaction (immunologic) = immune response to the transfused blood, very common but not life-threatening.
  3. Hemolytic transfusion reaction (immunologic) = anaphylaxic reaction which can lead to shock: febrile + tachypnea + tachycardia + vomiting + hypotension
38
Q

Hemolytic transfusion reaction

A

IV hemolysis which is completely destroying the transfused blood –> stop immediately and treat supportively (IVF, O2, corticosteroids, vasopressors). Can check PCV to see if blood is hemolyzed.

39
Q

Hemolytic Anemia (Regenerative)

EV vs IV hemolysis (mechanism + color of blood/urine)

A

CS: icterus, splenomegaly (EV), fever (IMHA, infectious anemia), bounding femoral pulses)

40
Q

Hemolytic Anemia (Regenerative)

Blood smear findings for EV vs IV hemolysis

A

EV: spherocytes
IV: ghost cells

41
Q

Hemolytic Anemia (Regenerative)

Differentials for EV hemolysis

A

1. IMHA (1º = idiopathic//most common; 2º = infection, neoplasia, drugs or vaccines)
2. Oxidant injury
3. Infectious Anemia
4. Abnormal mø activation and/or proliferation (UNCOMMON, but due to erythophagocytic histiocytic sarcoma or hemophagocytic syndrome)

EHS: møs have malignant characteristics, versus HS = too many møs present

42
Q

Hemolytic Anemia (Regenerative)

What drug classes (3) can secondarily cause IMHA?

A

Sulfonamides, penicillins, cephalosporins

43
Q

Hemolytic Anemia (Regenerative)

Most common infectious causes of IMHA in dogs (1) versus cats (3)

A

Dogs: Babesia spp.
Cats: Mycoplasma haemofelis, FeLV, FIP

44
Q

Hemolytic Anemia (Regenerative)

Autoagglutination, Spherocytosis, and positive Coombs test are strong evidence of what?

A

IMHA

  • BOTH dogs & cats will have autogluttination
  • ~75% of IMHA DOGS will have spherocytes on path review
  • Consider Coombs if ^^ are unidentified
45
Q

Hemolytic Anemia (Regenerative)

First line of treatment for IMHA

A

Corticosteroids
- Prednisone/prednisolone (rapid onset of 5-7 days for full effect)

46
Q

Hemolytic Anemia (Regenerative)

3 side effects of corticosteroids that are dose-dependent.

A

Iatrogenic hyperadrenocorticism –> adrenal gland suppression
- PU/PD, polyphagia, weight gain, panting, haircoat changes

Cats: insulin resistance –> 2º diabetes millitus

Mild-moderate elevated ALKP and GGT

47
Q

Hemolytic Anemia (Regenerative)

Azathioprine side effects (3)

an immunosuppr. that can be used in combo w/ corticosteroid

A

Bone marrow suppression
- monitor serial CBCs

Hepatotoxicity
- monitor liver enzymes

Pancreatitis

48
Q

Hemolytic Anemia (Regenerative)

Mycophenolate side effects (2)

an immunosuppr. that can be used in combo w/ corticosteroid

A

Potentially severe GI upset
- may be delaye dup to weeks after starting medication

Bone marrow suppression
- less likely than Azothioprine

49
Q

Hemolytic Anemia (Regenerative)

Cyclosporine side effects (3)

an immunosuppr. that can be used in combo w/ corticosteroid

A
  • GI upset
  • Gingival hyperplasia
  • Increased risk for opportunistic fungal infections
50
Q

Hemolytic Anemia (Regenerative)

Complications associated with IMHA?

A
  • Systemic thromboembolism
  • Acute kidney injury (AKI)
  • Disseminated intravascular coagulation (DIC)
  • Opportunistic infections (integument, UT, RT; bacterial andor fungal pathogens

Low-dose Aspirin (0.5-1.0 mg/kg SID) or Clopidogrel (1-4 mg/kg SID) should be started right when you diagnose IMHA as a preventative measure

51
Q

Hemolytic Anemia (Regenerative)

Infectious Anemia: pathogenesis and potential 2º IMHA

A

Agents directly damage RBCs –> causes hemolysis. Can activate the immune system into thinking hte RBCs are pathogens and can trigger 2º IMHA (from induced Ab formation against RBCs

52
Q

Hemolytic Anemia (Regenerative)

Hemotropic Mycoplasma and effects

A

Mycoplasma haemofelis = important organism that causes severe hemolytic anemia in cats
- Epicellular parasite of RBCs –> direct damage + triggers erythrophagocytosis (EV hemolysis)

53
Q

Hemolytic Anemia (Regenerative)

Risk factors for hemotropic myoplasma in cats

A
  • male
  • outdoor access (other cats, flea/arthropods)
  • FeLV or VIF (+)
54
Q

Hemolytic Anemia (Regenerative)

Babesiosis
Babesia canis vogeli
- pathogenesis
- transmission

A
  • large, piriform-shaped protozoan exisiting within erythrocytes (singly or paired) that causes 2º IMHA
  • brown dog tick (Rhipicephalus sanguineus)
  • subclinically infected animals can be carriers (e.g., greyhounds)

greyhouds almost always subclinically infected –> if greyhound dx with IMHA, always look for B. canis as well

55
Q

Hemolytic Anemia (Regenerative)

Babesiosis
Babesia gibsoni
- pathogenesis
- transmission

A
  • Small protozoan existing within erythrocytes with ring-like configuration
  • Bite wounds likely play a role in transmission
  • Sub-clinically infected dogs can be carriers (e.g., American pitt bulls)
56
Q

Hemolytic Anemia (Regenerative)

How is Babesiosis best diagnosed?

A

PCR (is species-specific/most sensitive)

57
Q

Hemolytic Anemia (Regenerative)

Cytauxzoonosis
Cytauxzoon felis
- transmisison
- two forms

A
  • Tick-transmitted protozoan infection of cats (Lone Star = Amblyomma americanum)
  • Forms:
    1. Tissue phase (schizont) - infects mononuclear phagocytes
    2. Erythrocyte phase (piroplasm)

Dx = blood smear or PCR

58
Q

Hemolytic Anemia (Regenerative)

Oxidant-Induced Hemolytic Anemia
- etiology

A
  • Hbg is constantly being oxidized, and is reversed by a reducing mechanism.
  • Certain toxins can cause massive/rapid oxidation –> reducing mechanism becomes overwhelmed –> Hgb damage (Heinz body formation or methemoglobinemia)
59
Q

Hemolytic Anemia (Regenerative)

Heinz bodies

A

denatured, oxidized hemoglobin –> hemolysis

60
Q

Hemolytic Anemia (Regenerative)

Culprits of Heinz Body Oxidant-Induced Hemolytic Anemia

A
61
Q

Hemolytic Anemia (Regenerative)

What toxicity that causes Heinz Body Oxidant-Induced Hemolytic Anemia can mimic IMHA? How is it diagnosed?

A

Zinc toxicity (pennies minted post 1982). Dx via abd rads!

All pts with hemolysis shoild have abd rads performed (FB)

62
Q

Hemolytic Anemia (Regenerative)

Methemoglobinemia
- etiology
- causes

A
  • Methemoglobin = oxidized heme iron
  • Is a “physiologic anemia” = normal RBC but has reduced O2 carrying capacity
  • Causes = Acetominophen
63
Q

Hemolytic Anemia (Regenerative)

Tx for Oxidant-Induced Hemolytic Anemia (3)

A
  1. Remove offending drug or toxin
  2. N-acetylcysteine (antioxidant that helps increse the reducing mechanism = increase intracellular gluthaione levels)
  3. Supportive care (Heinz body anemia = blood transfusion if indicated; Methemoglobinemia = supplemental O2)
64
Q

Hemolytic Anemia (Regenerative)

Fragmentation Hemolytic Anemia (also known as microangiopathic hemolytic anemia)
- etiology
- causes

A
  • RBC fragmentation due to contact w/ abnormal vasculature
  • HW disease, DIC, splenic torsion, hemangiosarcoma, vasculitis

Is NOT an immune response against RBCs

65
Q

Hemolytic Anemia (Regenerative)

Blood smear findings of fragmentation hemolytic anemia

A
  • Schistocytes
  • Acanthocytes
66
Q

Hypoplasia Anemia (Non-Regenerative)

Primary Hypoplasia Anemia
- definition
- causes (3)

A

Decreased production INSIDE the bone marrow
- 1º failure of erythropoiesis (RBC only)
- Aplastic anemia/pancytopenia (multiple cell lines –> e.g., PLTs or WBCs affected plus the RBCs)
- Infiltration of bone marrow w/ disease, directly affecting erythropoiesis

67
Q

Hypoplasia Anemia (Non-Regenerative)

Secondary Hypoplasia Anemia
- definition
- causes (2)

A

Disease is OUTSIDE of the bone marrow
- Hgb synthesis defect = iron deficiency (RBC only)
- 2º failure of erythropoiesis (RBC only)

68
Q

1º Hypoplasia Anemia (Non-Regenerative)

Primary failure of erythropoiesis pathogenesis

A

IMHA, but at the bone marrow level
- The precursor RBCs in the bone marrow are getting attacked
- severe anemia often present (is a chronic condition)
- other cell lines are normal (leukocytes, platelets)
- is a.k.a. pure red cell aplasia and non-regen. immune-mediated anemia

69
Q

1º Hypoplasia Anemia (Non-Regenerative)

Key difference b/w Pure Red Cell Aplasia and Non-Regenerative Immune-Mediated Anemia and traditional IMHA?

A

Pure Red Cell Aplasia and Non-Regenerative Immune-Mediated Anemia have much slower remission times than IMHA (as long as 3-4 months)

70
Q

1º Hypoplasia Anemia (Non-Regenerative)

Aplastic Anemia (Pancytopenia)

A

Peripheral blood cytopenias due to hypocellular/acellular bone marrow

71
Q

1º Hypoplasia Anemia (Non-Regenerative)

Bone Marrow Infiltration (Myelophthisis)

A

Dispalcement of bone marrow tissue by…
- neoplastic cells
- collagen (myelofibrosis) –> idiopathic, potentiallly immune-mediated; dr
- adipose tissue

72
Q

2º Hypoplasia Anemia (Non-Regenerative)

Hemoglobin synthesis defect’s CBC progression in iron deficiency

A
73
Q

2º Hypoplasia Anemia (Non-Regenerative)

What is the most common cause of non-regenerative anemia in dogs and cats? How severe is the anemia typically? Characteristics of the RBCs?

A

Anemia of chronic disease // of inflammatory disease
- mild-moderate anemia (Dogs: PCV = 20-37%, Cats: 15-26%)
- Always normocytic and normochromic anemia, all other cell lines normal

anemia resolves once underlying disease (underlying inflamm. disease) is addressed

74
Q

2º Hypoplasia Anemia (Non-Regenerative)

How does Chronic Kidney Disease lead to 2º hypoplastic anemia?

A
  • lack of erythropoietin production; GI blood loss, decreased RBC life span
75
Q

2º Hypoplasia Anemia (Non-Regenerative)

When would you expect total solids to be low?

A

Hemorrhage

76
Q

2º Hypoplasia Anemia (Non-Regenerative)

When would you expect plasma color to appear yellow or red/pink?

A

Hemolysis

77
Q

2º Hypoplasia Anemia (Non-Regenerative)

When would you expect to see Spherocytes, +/- ghost cells, on blood smear?

A

Hemolysis

78
Q

When would you not expect to see agglutination on blood smear?

A

Hemorrhage and hypoplasia; may or may not with hemolysis

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