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Smith LA Medicine > Ch 37 Hematopoietic and hemolymphatics > Flashcards

Ch 37 Hematopoietic and hemolymphatics Flashcards

1
Q

What are the signs of RBC regeneration in horses vs cattle, after acute blood loss?

A

Horses: mild anisocytosis
Rum’s: polychromasia, basophilic stippling, Howell Jolly bodies, nucleated RBC’s

Within 4 d

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2
Q

How would you diagnose hemoperitoneum from a belly tap sample?

A

PCV >/= 18%, TS >/= 3.2

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3
Q

Which component of platelets enables it to provide a surface for ultimately creating thrombin?

A

Platelet factor 3

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4
Q

Very briefly, what factors initiate the extrinsic system of coagulation vs the intrinsic system?

A

Extrinsic: Lipoprotein tissue factor accessing the bloodstream

Intrinsic: Exposure of blood to a negatively charged surface (like active platelets)

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5
Q

What are the main functions of thrombin (hint, there’s 4)

A
  1. Catalyzes conversion of fibrinogen to fibrin
  2. Promotes platelet aggregation
  3. Enchances cofactor activities of factos V and VIII
  4. Activates factor XIII and protein C
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6
Q

Briefly, how does Heparin prevent coagulation?

A

It accelerates antithrombin III by 2000-fold.

AT III is the main physio inhibitor of thrombin and Xa and is 70% of plasma’s anticoag ability

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7
Q

What, overall, determines the rate of fibrinolysis?

A

The rate of fibrin formation

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8
Q

How is a vasculitis disorder definitively diagnosed?

A

Histopathology, need minimum 6mm diameter punch biopsy, in formalin and Michel’s medium

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9
Q

What is the most common histopathological inflammatory pattern on vasculitis biopsies?

A

Neutrophilic infiltration of venules in dermis and subcut, nuclear debris around vessels and fibrinoid necrosis

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10
Q

What is the major pathogenic mechanism of hypersensitivity type vasculitis?

A

Immune complex deposition in vessel walls and complement activation and chemoattractant production

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11
Q

What are the inciting factors for purpura hem. and when do they occur?

A

-Respiratory infections (strep, rhodococcus, coryne) or Strangles vaccine can incite
-Seen 2-4 weeks later

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12
Q

How is Purpura diagnosed?

A

Biopsy: Acute (non)leukocytoclastic vasculitis with blood vessel necrosis

Bloods: hyperproteinemic, anemic

Marked dermal and subcutaneous hemorrhage and dermal infarction.

Immune complex deposition

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13
Q

What kinds of immune complexes are demonstrated in purpura? What type of hypersensitivity reaction is it?

A

IgM, IgA, streptococcal M protein.
Type III

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14
Q

How is equine viral arteritis diagnosed?

A

Tests: virus isolation, PCR, or serology (shows 4-fold increase in samples 3 weeks apart), culture (semen)
Samples: Blood, semen

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15
Q

What result would flag a stallion as likely to be carrier?

A

Positive titer of 1:4

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16
Q

What type of virus is EVA?

A

enveloped, spherical, + stranded RNA virus. Arteriviridae, Nidovirales. Non arthropod borne

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17
Q

What changes (vasculitis) does EVA cause?

A

-Localizes in endothelium, medial myocytes, and pericytes
-Vasculitis with fibrinoid necrosis of tunica media
-Thrombi formation
-Lymphocytic infiltration, karyorrhexis, loss of endothelium

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18
Q

How is EVA transmitted?

A

Aerosol: resp, urinary, or repro tract secretions
Via semen from PI stallions
Horizontal transmission

19
Q

What is equine anaplasma phagocytophila? (cause, cells affected)

A

Caused by Anaplasma phagocytophila. Morulae visible under light microscopy are found in vacuoles in the cytoplasm of neutrophils and eosinophils.
From biting ticks, spread by blood or lymph

20
Q

When do A. phagocytophila antibody titres peak, how long does immunity last, and what is the incubation period for natural infection?

A

Peak at 19-81 d after Cx onset
Immunity for years
Incubation < 14 d

21
Q

How is A phagocytophila definitively diagnosed?

A

Morulae within the cytoplasm of neutrophils or eosinophils

OR

Positive PCR in buffy coat

*exposure diagnosed by > 4fold increase in IFA paired titres

22
Q

Which clotting tests are altered by thrombocytopenia?

A

Prolonged bleeding time and abnormal clot retraction
Clotting time and fibrinogen is unaffected

23
Q

At what platelet level is spontaneous bleeding more likely? When is prolonged bleeding or hematomas likely>

A

PLT < 10,000 = spontaneous bleeding
PLT < 40, 000 = small hematomas

24
Q

What is the most common overall cause of thrombocytopenia in large animals?

A

Shortened platelet life span

25
Q

How is IMTP definitively diagnosed?

A

Increased quantities of platelet-associated IgG or C or antiplatelet activity
Sample: serum

26
Q

Why is the spleen the main site of platelet phagocytosis?

A
  1. Locally secreted antiplatelet antibody
  2. more than 30% of circulating platelets are stored there
  3. Stagnant splenic blood flow
27
Q

What are the main two mechanisms by which diseases initiate DIC?

A
  1. Excessive procoagulant activity in the blood
  2. Blood contact with abnormal surfaces
28
Q

Which clotting factor can endotoxin (G-) directly stimulate?

A

Factor XII

29
Q

In a nutshell, what is the pathologic process of DIC?

A

Widespread fibrin deposition in the microcirculation and development of hemorrhagic diathesis caused by consumption of procoagulants and hyperactivity of fibrinolysis

30
Q

Vitamin K is necessary for which clotting factors?

A

II, VII, IX, and X

31
Q

What is the earliest diagnostic indicator for warfarin toxicity?

A

Prolonged PT because of short plasma t1/2 of factor VII. APTT prolongs later

32
Q

What are the parasitic causes of hemolytic anemia?

A

Anaplasmosis
Babesiosis
Hemobartonellosis
Theileriasis
Trypanosomiasis

33
Q

What are the bacterial causes of hemolytic anemia?

A

Leptospirosis
Bacillary hemoglobinuria (clostridium hemolyticum)

34
Q

What are the three main causes of heinz body anemia?

A

Wild onion
Red maple
Phenothiazine

35
Q

What is the pathogenesis of Anaplasma marginale?

A
  1. Ixodid ticks ingest Anaplasma, replicates, and then which travels via GIT to their salivary glands
  2. Tick bites animal, Anaplasma invades mature erythrocytes
  3. Bacteremia leads to leaky RBC because of peroxidation
  4. Anemia due to splenic and hepatic macrophage phagocytosis of infected RBCs. Extracellular hemolysis! No red urine!
  5. After recovery, ruminants are persistently infected
36
Q

How is A Marginale diagnosed?

A

PCR or microscopic examination.
Stain with Wright, Giemsa, or new methylene blue.
ID PI animals with serology ELISA

37
Q

What is the pathogenesis of babesiosis?

A
  1. B. bovis or B. bigemina are protozoa, ingested by Boophilus ticks, where the protozoa reproduces in feeding/female ticks
    *Larval ticks transmit bovis but must be molted to transmit bigemina
  2. Tick bites animal, infects RBCs
  3. Clinical signs 2-3 wk later
  4. INTRAVASCULAR hemolysis of RBCs by merozoites bursting out
  5. Osmotic fragility of whole RBC population drops, so even uninfected cells lyse
  6. Immune mediate condition may start, removing more RBCs
  7. Bovis is especially neuro. tachycardia, murmur, anemia, shock
  8. If they survive, can be chronic carriers
38
Q

How is babesiosis diagnosed?

A

-Giemsa stained blood smear
-Positive serology, especially for antibodies (seen less than a week after infection), especially IFA
-PCR

39
Q

Briefly, what is the pathogenesis of equine babesiosis?

A
  1. Babesia caballi or Theileria equi infect via tick bite. Transmission of Theileria is ONLY horizontally.
  2. Infected survivors stay as chronic carriers
  3. T equi is more pathogenic, causes hemoglobinuria and death
  4. Babesia causes fever and anemia
40
Q

How is equine babesiosis diagnosed?

A

cELISA test for babesia
or PCR for B or T.

41
Q

What are the three stages of Equine Infectious Anemia?

A
  1. Acute: initial viremia burst. Thrombocytopenia, then fever and malaise. Ecchymoses, petechiae
  2. Chronic: recurrent viremic episodes, in decreasing severity.
  3. Inapparent: No cx, occurs once viremia levels are immunologically contained.

*Clinical disease can progress to DIC and death at any point

42
Q

How is EIA diagnosed?

A

-Coggins test: serology
- 4 licensed ELISA tests. They detect antibody at the transmembrane glycoprotein and p26 antigen

43
Q
A

Smith LA Medicine (12 decks)

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