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Titi Hem > hemost > Flashcards

hemost Flashcards

1
Q

which chemicals are secreted by the endothelium in a physiological state?

What is their purpose?

A

nitric oxide

PGI2: prostacyclin

>> inactivates platelets

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2
Q

which proteins are on the surface of endothelial cells having an impact on coagulation?

A
  • heparin sulfate
    • binding Antithrombin
    • >>> AT3 is inactivating circling coag factors:
    • 2,9,10
  • Thrombomodulin
    • binding Thrombin (= 2)
    • Thrombin activates Protein C
    • >>> inactivates 5,8
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3
Q

Name the 5 steps of hemostasis

A

vascular spasm

platelet plug formation

coagulation

clot retraction and repair

fibrinolysis

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4
Q

how does muscular spasm occur?

A
  • Endothelin is secreted by endothelium

if endothelium damaged and exposing underlying receptors

>> endothelin can bind and causes contraction of musc

  • Myogenic mechanism: automatic contraction if muscular layer is exposed
  • Nociceptor activation: activation of nociceptors under basal membrane stimulate muscle contraction
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5
Q

which factors do endothelial cells produce when they are injured?

which factors do they stop to make after injury?

what is the consequence?

A
    • Van Willebrand factor
    • nitric oxide and prostacycline (PGI2)
  • >>> binding of platelets to vWf
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6
Q

what do bound platelets secret?

A
  • ADP > chemtaxis plat
  • Thromboxin A2 > chemotax plat.
  • Serotonin
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7
Q

What are the binding sites on platelets?

A

GP 1b: binding to vWF

GP 2b/3a: binds to Fibrinogen and links platelets

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8
Q

Who is secreting Thromboxane A2 and what are its functions?

A

secreted by platelets that are activated by vWf binding

  • chemotaxis for other platelets
  • activates smooth muscle contraction together with serotonin
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9
Q

who produced factor XII and how is it activated?

A

liver

activted by clotting platelets and their negative surface charges

activates factor 9

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10
Q

what happens after factor 12 activation?

A

12 activates

  • 11
  • 9
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11
Q

What happens after activation of factor 9?

A

9 + Platelet Factor 3 + Calcium

activate 10

10 +PF3 + Calcium + Factor 5

>>>> Prothrombin Activator

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12
Q

factor 2 is also called

A

thrombin

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13
Q

What is the purpose of prothrombin activator?

A

activates factor II

so prothrombin >>> thrombin

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14
Q

who activates fibrinogen and what happens?

A

Thombin (2) activates soluable Fibrinogen and turn it into a clotlike structure: Fibrin

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15
Q

what is the purpose of thrombin and who is activated by?

A

activated by prothrombin activator

> activates fibrinogen -> fibrin

> activates factor 8

> factor 8 is the fibrin stabilator (cross linking)

> fibrinogen -> fibrin mash

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16
Q

What is the first step of the common pathway?

A

10

(10 + 5 + Calcium + PF3)

activates prothromin activator

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17
Q

what is the intrinsic pathway and how is it activated?

A

factor 12 activation by surface of bound together platelets

12 > 11 > 9 > 8

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18
Q

What is the extrinsic pathway

A

much faster than instrinsic

needs 30 seconds

  • factor 3 released from damaged tissue
  • activates factor 7
    • 7 can either activate 9 of the instrinsic pathway or
    • 7 can start common pathway
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19
Q

name the factors of the intrinsic pathway

A

contact factors, 12,10,9,8

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20
Q

name the factors of the extrinsic pathway

A

3,7

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21
Q

name the factors of the common pathway

A

10 + 5 > 2> 1

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22
Q

how can you test the extrinsic pathway?

when does it become abnormal?

A

PT

Prothrombin time: 16-20sec in horses!

(tests pathway except 3 - 3 is always there anyways)

so basically testing factor 7

time prolongs when there is <30% of factor 7 left

7 has the shorest half life of all factors!

also used to monitor Vit K deficiency

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23
Q

how can you test the instrinsic pathway?

A

PTT (partial thromboplastin time)

APTT (activated PTT): 45-66sec

more sensitive to environment like difficult venipuncture… can be false slower/faster/normal

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24
Q

clotting times in horses with DIC

A

usually long APTT

with normal PT

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25
Q

which clotting factors are Vit K dependant?

A

2,7,9,10

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26
Q

What happens during Clot retraction and repair

A
  1. platelet contraction
  2. platelets: secretion of
  • PDGF (platelet derived growth factor) >
    • helps repair connective tissue with plaques
    • proliferate smooth muscle
  • VEGF (vascular endothelial growth factor)
    • regenerate epithelial lining
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27
Q

What happens during fibrinolysis

A

= 5. step of coagulation cascade

protein on surface of endothelial cells:

tissue plasminogen activator

binds to plasminogen that is present in the blood

converts plasminogen to plasmin

PLASMIN eats FIBRIN and thereore releases

D-DIMER and fibrinogen into circulation

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28
Q

What does D-Dimer measurement help you with?

A

If there was formation of blood clots and fibrinolysis

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29
Q

what does tissue plasminogen activator do?

A

turns plasminogen into plasmin which will eat clot

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30
Q

what does heparin do?

A

enhances Antithrombin 3 activity

(AT3 inactivates 2,9,10)

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31
Q

What does aspirin do?

A

inhibits Thromboxin A2 that is normally released by platelets when they bind together to attract more platelets

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32
Q

what is warfarin?

A

Vitamin K oxide reductase inhibitor

-> inhibits interaction of Vitamin K with factor

2, 7, 9, 10, protein C

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33
Q

What does enoxaparine do?

A

inhibits ONLY factor 10 activation

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34
Q

apart from PT and APTT, which paramteres of coagulation can be measured and what do they imply?

A
  • AT - if low: risk for increased clotting, caused by GI or renal losses, consumption with hypercoagulability
  • platelet count (decreased prod, increased destruction, incr consumption)
  • D-Dimers: if high> increased fibrinolysis, implies hypercoagulative state
    • Achtung ist auch hoch in physiologischen Situationen zB Chirurgie

Fibrinogen not useful bc often high bc of inflammaation

35
Q

Name antifibrinolytics

A

E-aminocaproic acid

20-40mg/kg in 1L NaCl IV

OR

3,5mg/kg/min for 15 mins, then 0,25 CRI

inhibits plasminogen activator activity and

stimulates release of a-antiplasmin that inhibits plasmin directly

36
Q

treatments for excessive thrombosis

A
  • LMWH: 50IU/kg s.c. - inhibtis 10a
  • Unfractionated Heparin: enhances AT with all its consequences, 40-60IU IV/SC
  • Aspirin: prevents Txa production in platelets, 10-100mg/kg PO or 20mg/kg per rectum
37
Q

in equine veterinary literature, patients are considered to have subclinical DIC if…

A

abnormalities in min 3/5 tests:

  • PT
  • aPTT
  • AT
  • fibrinogen
  • D-Dimer
38
Q

Which common emergency is associated with prolonged PT time ?

A

different studies

horses with colic: 25-58% of them have prologed PT

good prognostic indicator

strangulating obstructions are associted with prol PT time

39
Q

When does thrombocytopenia occur?

A
  • increased use:
    • increased clotting f.e. sepsis, hemorrhage
  • increased destruction
    • immunmediated (IgG against thromb /megakaryocytes)
    • infections
  • decreased production:
    • neoplasia of bone marrow
    • idiopathic pancytopenia (PBZ)
40
Q

Which is the most common heriditary bleeding disorder in horses?

A

Hämophilia A (no factor 8)

only males (females are porters)

x-chromosomal rezessiv

41
Q

Name the three systems that inhibit coagulation in the physiological state

A
  • NO, PGI2
  • heparin sulfate + antithrombin III
  • thrombomodulin + thrombin (2) + Protein C
42
Q

What is the blood volume of horses

A

TB: 100ml/kg

WB: 78ml/kg

Drafts: 61ml/kg

> 6-10% of BW

43
Q

How much loss of blood volume can horses tolerate

A

15% of total blood without a problem

might tolerate up to 25-30%

44
Q

what is the donkey factor and how does it influence blood donors?

A

donkeys and mules carry this antigen on their RBCs

>>> predisposes mule foals for NI

similar antigen on their platelets predisposing foals for alloimmune thrombocytopenia

>>> donkey blood should not be given to horses

horse to donkey is ok

45
Q

which blood types are most frequently associated with transfusion reaction?

A

containing Anti Aa and anti Qa antibodies

46
Q

Calculation of blood volume needed for certain decrease in PCV

how much blood can a donor give ?

A

Blood transfusion mL =

kg × 80 mL/kg × ((desired PCV − actual PCV) /donor PCV)

~ 20% of the donor’s blood volume (8 L in a 500- kg horse) every 30 days

(give replacement if more than 15%)

47
Q

how do you store blood prior to use?

A

blood bags containing 3.2% sodium citrate at a blood-to-anticoagulant ratio of 9:1.

If blood is to be stored, citrate-phosphate-dextrose with adenine (CPDA) should be used and blood kept at 4 degrees

48
Q

How long do RBCs survive after

autologous transfer

allogeneic transfer

mild to mod crossmatch reaction

A

autologous transfer: 3 monate

allogeneic transfer: mean halflife of 30d

mild to mod crossmatch reaction:

mild: 11d half life
mod: 5 days half life

49
Q

Can horses get allergic to certain blood donors post transfusion?

A

The most antigenic group appears to be Aa,

with all Aa-negative horses developing antibodies if transfused with Aa-positive RBCs; those persisted for over a year.

Antibodies against other RBC antigens develop infrequently,

don’t seem to appear before 1 week post transfusion

can be detected 1 to 154 weeks after transfusion, and might disappear again after 4 weeks

50
Q

how quick can you transfuse?

A

begin slowly at 0.1 mL/kg for the first 15 minutes

checking vital parameters every 5 minutes.

If no adverse reactions are observed,

20 mL/kg/hr, checking vital parameters every 10 to 15 minutes

51
Q

how often do adverse effects appear after blood transfusion and what are those?

When and how should they be treated?

A

16% of horses

87.5% in crossmatchincompatible transfusions

  • hemolysis instantly-24hours after trans
  • fever
  • type 1 hypersens reactions
  • if severe, possible treatments:
    • antihistamines (hydroxyzine 0.5–1.0 mg/kg PO q12h),
    • dexamethasone 0.1 mg/kg intravenously [IV])
    • epinephrine (0.01–0.02 mL/kg of a 1:1000 solution IV; 5–10 mL for a 500-kg horse)
52
Q

autologous blood transfusion from body cavitiy

what do I need to do differnetly?

A

blood-to-anticoagulant ratio of 15:1 (0.07 mL/mL of blood)

instead of 9:1

blood in contact with serosal surfaces for longer than 1 hour becomes defibrinated and platelets and coag factors decrease

53
Q

Hemoglobin-based oxygen carriers

A

can be used for short term if no blood available

in horses (11–16 mL/kg)

a foal (22 mL/kg)

half life: 1,3-12 hours

54
Q

when do horses actively bleed from thrombocytopenia?

A

less than 30,000 to 50,000/μL is likely to be associated with clinical signs such as petechiae or epistaxis.

below 10,000/μL, active hemorrhage such as prolonged bleeding after venipuncture or hematoma formation frequently occurs

clinical signs often stabilize if you go back up to 15-30

55
Q

how to prepare and transfuse platelets? can it be stored?

how much can thrombo number go up approximately?

A

platelets remain in suspension when RBCs are allowed to settle by gravity as is commonly done for preparation of fresh equine plasma

=> platelet rich plasma

store at 22C (under 15: dysfunction)

when agitated might be stored for 5 days but bac???

extrapolation from dogs:

5L (10ml/kg) fresh whole blood for 500kg horse increases platelets by 10 000/ul

56
Q

How can the reason for intraab bleeding be established?

should you go to sx?

A

U/S

in 25% to 42% of cases an etiology cannot be established

if bleeding continues or recurs despite medical management or if the origin is surgical:

retrospective study: 19% detected origin during sx

about 42-57% of surgically managed horses survived

57
Q

How much plasma does a horse need to increase TP?

A

~ 2g/L increase through 1L Plasma

500-kg requires approx 4 to 5 L of plasma to increase TP by 10 g/L.

calculation:

Volume (L) = ([TP desired increase] × 0.05 × [kg]) ÷ TP Donor

58
Q

what is the difference between fresh frozen or just frozen plasma?

A

fresh: plasma separated from blood within 8 hours of collection and stored at −18°C for up to 1 year.

if longer than 1 year: frozen

59
Q

Reaction to commercial vs non commercial plasma

A

Reactions to commercial plasma have a reported incidence of

8.7% in foals and

0% in adults,

while the incidence with noncommercial plasma is 10%

60
Q

most common causes for hemothorax

A
  • In foals: rib fractures
  • adult horses:
    • trauma,
    • neoplasm,
    • iatrogenic injury,
    • strenous treadmill exercise
61
Q

occult fecal blood measurment in horses?

A

new lateral flow immunoassay

(SUCCEED Equine Fecal Blood Test)

detecting equine hemoglobin at concentrations of 5 to 10 μg/g of feces

(is positive 24-48 hours after rectal exam)

only really useful to rule out

62
Q

when is phenylephrine a risk factor for bleeds?

A

64-times higher risk for phenylephrine-associated bleeding was identified for horses ≥15 years old

prepare blood transfucion immediately even if only tiny bleeding (more is coming)

63
Q

Renal hemorrhage severe enough to cause anemia has been reported in horses with

A

pyelonephritis (four of seven horses were Arabians),

idiopathic hematuria, and

renal pseudoaneurysm in an Arabian colt

64
Q

which drugs might induce immune mediated hemolytic anemia?

A

Penicillin

low titers of anti–penicillin antibodies of the immunoglobulin M (IgM) class were present in 77% of horses tested.

doxycycline = also a suspect

65
Q

Treatment of IMHA refractory to corticosteroids

A

azathioprine (3.0 mg/kg PO q 24 h)

immunsuppressiv, verwendet bei Organtransplantationen

66
Q

Alloimmune Neonatal Neutropenia

which breed in the literature?

Treatment?

A

reported in a Thoroughbred and an Arabian colt.

The pathophysiology is presumed to be similar to neonatal isoerythrolysis, but the disease appears to be comparatively rare.

single injection of G-CSF (3.5–6 μg/ kg SC) resulted in a considerable increase in peripheral neutrophils

granulozyten-Kolonie stimulierender Faktor

67
Q

What is Evans Syndrome

A

characterized by the simultaneous presence of

  • IMHA,
  • thrombocytopenia, and/or
  • leukopenia

in the absence of a known underlying cause

rare, and few cases have been published in horses

68
Q

What is the cause of equine infectious anemia?

A

equine infectious anemia (EIA) virus (lentivirus)

Virus replication occurs in

  • monocytes,
  • dendritic cells,
  • tissue macrophages, and
  • endothelial cells
69
Q

Can EIA be cured?

A

Once infected, horses remain lifelong carriers.

Transmission occurs naturally via blood-feeding insects, particularly Tabanidae (horse and deer flies) or

blood-contaminated instruments or needles.

70
Q

Which are the hallmark signs of EIA?

A

Fever and thrombocytopenia

are considered to be the most reliable clinical indicators but are far from pathognomonic for EIA

Depression, weakness, hemorrhage, peripheral edema, and weight loss are commonly seen in the chronic form but can also accompany the acute stages.

71
Q
A
72
Q

EIA: Time from infection to seroconversion

A

varies widely depending on viral dose, virus strain, and test used (between 21 and 180 days).

73
Q

How to detect EIA?

Whihc

A

outbreak in Ireland: specific PCR and RT-PCR assays

  • detection of Proviral DNA integrated into the host cell
  • detection of viral RNA by RT-PCR

detection in all tissues, nasal secretions, and genital swabs, and RNA was also detected in saliva.

BLOOD testing:

agar gel immunodiffusion assay (AGID; Coggins test) is still most widely used test and detects antibodies against the major core protein p26.

100% of seropositive horses detected by serum PCR

52% of those detected by RT-PCR

74
Q

Causes of Piroplasmosis/Babesiosis

A

equine-specific hemoprotozoa:

Babesia caballi and Theileria (previously Babesia) equi

75
Q

Is Piroplasmosis/Babesiosis a lifelong disease?

A

Carrier state in untreated horses is

lifelong for T. equi whereas

B. caballi can be cleared from the horse.

As the carrier status protects against active disease and reinfection, elimination of the parasite is not desired in endemic areas.

76
Q
A
77
Q

The most sensitive test for chronic infection with Babesia/Theileria is

A

EMA (equi merozoite antigens) 1 and 2 detecting cELISA

78
Q

Treatment of Babesiosis/Piro

A

supportive

in endemic areas: no specific treatment bc carrier status is protective against reinfection

in non-endemic areas: Imidocarb diproprionate (2.2–4.4 mg/kg IM once or q 72 h for 4 doses) alongside with butylscopolamine to prevent of anticholinergic effects

79
Q

Which are the most common clinical manifestations of Leptospirosis

A

very unspecific:

  • equine recurrent uveitis,
  • abortion,
  • stillbirth or
  • premature birth,
  • neonatal disease, and
  • renal failure

RARELY: anemia and bleeding in foals

pulmonary hemorrhage in adults

80
Q

Which cells are infected in Babesiosis/Piroplasmosis?

A

B. caballi directly invades erythrocytes

whereas the first developmental stage of T. equi takes place in leukocytes.

81
Q

Hemotropic Mycoplasma Infection

A

reported in germany

infects erythrocytes of horses, dogs, cats, pigs, cattle

clinical significance unknown, might cause weight loss, depression, and mild anemia

PCR test

Treatment: tetracyclines or fluoroquinolones

82
Q

What is methemoglobinemia

A

Oxidants can damage erythrocytes by oxidizing the heme iron in hemoglobin from Fe2+ to Fe3+, forming methemoglobin and leading to anemia

-> methemoglobinemia

(also other cause fe toxic)

83
Q

Experimental feeding at the maximal voluntary intake of garlic resulted in…

0.25 g/kg PO q 12 h ->> 250g/d/500kg horse

A

mild anemia (decrease of PCV from mean 36% to 28%) with increased Heinz body formation.

excessive sweating

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