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Heme Final Exam > Exam 2 Highlights > Flashcards

Exam 2 Highlights Flashcards

1
Q

What are the compensatory mechanisms activated by reduced tissue oxygenation?

A
  • Hb-O2 curve shifts left in the lungs, shifts right in the tissues
  • increased temp, 2,3-DPG, CO2; decreased pH favors offloading in tissues
  • increased CO
  • increased peripheral vasoconstriction to focus blood supply to vital organs
  • BM expansion
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2
Q

Which compensatory mechanism for tissue hypoxia occurs slowly?

A
  • BM expansion; all of the others occur quickly
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3
Q

How does increased 2,3-DPG facilitate oxygen delivery to tissues?

A

produces a morphologic change to hgb favoring offloading at tissues

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4
Q

In what species is an increased 2,3-DPG effective in compensating for tissue hypoxia?

A

dogs and humans

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5
Q

In what species is increased 2,3-DPG not effective in compensating for tissue hypoxia?

A

cats and horses

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6
Q

Describe the pattern of blood loss anemia

A
  • hypoproteinemia
  • neutrophilia
  • stress leukogram
  • regenerative unless chronic
  • thrombocytopenia
  • reticulocytosis
  • rebound thrombocytosis is possible
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7
Q

What can chronic blood loss anemia present as?

A

iron deficiency anemia (microcytic hypochromic nonregenerative)

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8
Q

Describe the pattern of EV IMHA

A
  • reticulocytosis and regeneration
  • spherocytes
  • hyperbilirubinemia
  • bilirubinuria
  • icterus
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9
Q

Describe the pattern of IV IMHA

A
  • regeneration and reticulocytosis
  • ghost cells
  • hemoglobinemia
  • hemoglobinuria
  • unconjugated bilirubin
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10
Q

Describe the pattern of oxidative damage/HB anemia/maple leaf toxicity

A
  • heinz bodies
  • eccentrocytes
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11
Q

What are heinz bodies?

A

sulfhydryl groups are crosslinked and makes a nose like projection or a clearing in the cell
- denatured hgb

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12
Q

What are eccentrocytes?

A

clearing on one side of the cell because hgb aggregates toward one side and the membrane folds on itself

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13
Q

What are some causes of oxidative damage?

A
  • onions and garlic
  • propofol
  • phenothiazines
  • acetaminophen
  • vitamin K1
  • zinc
  • copper
  • DKA
  • lymphoma
  • hyperthyroidism in cats
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14
Q

What two metabolic products typically protect cells from oxidative injury?

A

NADPH and glutathione from anaerobic glycolysis

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15
Q

Describe the pattern of fragmentary anemia

A
  • schistocytes
  • keratocytes
  • acanthocytes
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16
Q

What causes fragmentary anemia?

A
  • DIC
    -IDA
  • vasculitis
  • endocarditis
  • hemangiosarcoma
  • caval syndrome (HW)
  • thrombosed catheter
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17
Q

Describe the pattern of microangiopathic hemolytic anemia

A
  • spherocytes
  • fragmentary changes
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18
Q

Describe the pattern seen with mycoplasma

A
  • acute hemolytic disorder
  • rod or coccoid strung in a line or as purple bubbles in red cells
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19
Q

What is the primary agent of mycoplasma infections in the US

A

mycoplasma haemofelis

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20
Q

What is the reservoir host of mycoplasma haemofelis?

A

bobcats

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21
Q

When can mycoplasma haemocanis cause disease?

A

immunocompromised or splenectomized patients

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22
Q

Describe the pattern of babesiosis

A
  • protozoa
  • gibsoni look like purple dots that are smaller than anaplasma and HJ bodies
  • canis can appear as large purple fluke things inside RBCs
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23
Q

Describe the pattern seen with anaplasmosis

A
  • tick borne pathogen
  • two purple dots inside RBCS (look similar to HJ bodies)
24
Q

Describe the pattern of leptospirosis

A
  • bacterial infection
  • hemolysin and phospholipases cause lysis of RBCs
25
Q

Describe the pattern of clostridium hemolyticum

A

can produce hemolysin and phospholipases that cause hemolytic anemia

26
Q

Describe the pattern seen with PK deficiency

A
  • decreased red cell life span
  • die of liver disease or anemia because of hemosiderosis
    myelofibrosis
  • reticulocytosis
27
Q

What breeds are commonly associated with PK deficiency?

A
  • Basenji
  • Abyssinian
  • Somali
28
Q

What breeds are associated with PFK deficiency?

A
  • English spring spaniel
  • cockers
  • whippets
29
Q

Describe the pattern of PFK deficiency

A
  • decreased enzymes –> susceptible to alkaline lysis –> dog pants and RBCs lyse
  • decreased 2,3-DPG
30
Q

Describe the pattern of myelophthistic anemia

A
  • neoplastic cells, fibrosis, fungal granulomas replace hematopoietic BM
  • causes pancytopenia
  • cannot be reversed
31
Q

Describe the pattern of estrogen toxicity

A
  • causes aplastic anemia - nonregenerative anemia with hypoproliferative BM
  • pancytopenia
32
Q

Describe the pattern of chronic renal failure

A
  • decreased/lack of production of EPO
  • nonregenerative anemia
  • REP cells that produce EPO are transformed into myelofibroblasts due to chronic inflammation or stressful events
  • uremic toxins and inflammatory cytokines contribute to decreased EPO
  • hepcidin increases due to decreased kidney clearance
  • reduction of RBC life span
  • blood loss b/c of uremic toxins causing intestinal ulceration
33
Q

Describe the pattern of Ehrlichia canis infection

A
  • IMHA secondary autoimmune cause –> can be nonregenerative
  • can cause aplastic anemia
34
Q

Describe the pattern associated with FeLV infection

A
  • megaloblastic anemia
  • nonregenerative anemia with hypoproliferative erythroid lineage
  • cells are too large and have a nucleus (megalocytic cells do not have a nucleus)
  • macrocytic normochromic (no polychromasia)
  • megaloblastic rubricytes and metarubricytes
35
Q

Describe the pattern of IDA

A
  • microcytic hypochromic nonregenerative anemia
  • iron stores are depleted
  • hyperproliferative BM
  • cytoplasmic maturational defect –> failure to form hgb
36
Q

What causes IDA?

A
  • nutritional (mom’s milk or parasitism)
  • chronic blood loss (serum iron and serum ferritin are decreased)
37
Q

IDA becomes nonregenerative only in what two scenarios?

A
  • chronic blood loss is prolonged and severe
  • diet is deficient
38
Q

Describe the pattern of anemia of inflammatory disease

A
  • nonregenerative anemia with hypoproliferative BM
  • PCV does not go below 20%
  • most common anemia
  • can develop in 7-10 days
  • dysregulation of iron homeostasis –> iron trapped in macs and not absorbed from GIT
  • normal/decreased serum iron, increased ferritin
  • inflammatory cytokines inhibit EPO production
  • fever shortens life span of RBCs
  • increased hemosiderin in macs
  • erythroid hypoplasia
  • EPO levels are normal to decreased
39
Q

How do you treat anemia of inflammatory disease?

A
  • tx underlying problems
  • iron or EPO administration is of little to no help
40
Q

Describe the pattern of lead toxicity

A
  • mild normocytic normochromic nonregenerative anemia
  • basophilic stippling –> pyrimidine-5’-nucleotidase
  • nRBC due to stromal damage - inappropriate numbers relative to degree of polychromasia/reticulocyte response
  • cytoplasmic maturational defect
  • leads interferes with synthesis of hgb and degradation of ribosomes
41
Q

What is the mechanism of spherocyte production?

A

IMHA –> Coomb’s positive
- extravascular splenic macrophage plucking of the red cell membrane when macs are triggered to remove Ag on cell surface
- mediated by IgG

42
Q

What can cause IMHA and spherocytosis?

A
  • inherited disorders
  • transfusion reactions
  • fragmentation anemias
43
Q

What is the mechanism of ghost cell production?

A
  • IMHA
  • IV lysis mediated by IgM –> bind and activate complement –> MAC –> hole punched into red cell –> red cell lysis –> ghost cells
44
Q

What is the mechanism of heinz body production?

A
  • oxidation of IC hgb sulfhydryl groups of red cells
  • causes nose like projections or clearings
  • caused by disruption of PPP in glycolytic pathway that normally produces NADPH and glutathione
45
Q

What is the mechanism of eccentrocyte production?

A
  • oxidation of membrane sulfhydryl groups of red cells
  • causes sulfhydryl groups to be pushed to one side of the cell –> off sided placement of hgb
46
Q

What is the mechanism of stomatocyte production?

A
  • abnormal phospholipid composition –> increased Na and water influx
  • increased permeability of membrane
  • macrocytic hypochromic
  • have a narrow elongated CP
47
Q

What breeds are known to have stomatocytes?

A
  • schauzers
  • pomeranians
  • drentse patrijshound
  • alaskan malamute (chondroplasia)
48
Q

What is the mechanism of target cell/leptocyte/codocyte production?

A
  • lloks like a bullseye
  • increased surface to volume ratio
  • greater resistance to osmotic lysis
  • balanced increased amounts of cholesterol and phospholipid in the red cell membrane
    indicates liver disease
49
Q

What is the mechanism of acanthocyte production?

A
  • irregularly spiculated red cells
  • unbalanced increased in cholesterol and phospholipid composition of the red cell membrane
  • indicates liver disease
  • classified as fragmentation injury –> hemangiosarcoma, DIC, IDA
50
Q

What is the mechanism of schistocyte production?

A
  • fragmented red cells
  • mechanical injury
  • often only in low numbers
  • DIC, vasculitis, turbulent blood flow, fragile cells, IDA
51
Q

What is the mechanism of torocyte production?

A
  • red cells with large CP and a thick hgb rim
  • usually artifact
52
Q

What is the mechanism of ovalocyte/elliptocyte production?

A
  • oval to elongated red cells
  • indicative of liver disease (hepatic lipidosis), myelofibrosis (BM scarring and red cells have to squeeze out), inherited
53
Q

What are inherited causes of ovalocytes/elliptocytes?

A
  • red cell membrane and cytoskeletal protein deficiency
  • red cell membrane band 4.1 deficiency
  • mutation in beta-spectrin
54
Q

What is the mechanism of dacrocyte production?

A
  • looks like a teardrop
  • ovalocytes and dacrocytes are diagnostic for myelofibrosis
  • red cells have to squeeze and wiggle out of scarred BM
55
Q

Start with question 6 on exam 2 review

A

IV v. EV hemolysis

Heme Final Exam (1 decks)

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