Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fellowship Exam > Ch 7 Haemostasis > Flashcards

Ch 7 Haemostasis Flashcards

1
Q

where platelets from?

A

derived and released from progenitor megakaryocytes in the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do platelets release

major agonist of coagulation (2)

A

platelets synthesize prostanoids, notably thromboxane A2 (TxA2), from arachidonic acid.

ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Primary haemostasis (4)

A
  1. adherencce: endothelial disruption > Platelets adhere to subendothelial collagen, either directly or via collagen-bound von Willebrand factor (vWF)
  2. resulting in a shape change and activation

3.activation = release of agonists (Txa2 + ADP) from granules and via arachidonic acid metabolism

(4). Agonists recruit and activate additional platelets

(5) and alter the avidity and affinity of fibrinogen binding receptors, leading to aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

secondary haemostasis

cascade

A

 Intrinsic and extrinsic pathways
* Extrinsic – initiated by tissue factor
* Intrinsic – initiated through contact activation of fXII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

A Cell-Based Model of Coagulation

3 PHASES

A

(1) tissue factor = primary physiologic initiator of coagulation
(2) coagulation is localized to, and controlled by, cellular surfaces

3 overlapping phases
Initiation (on tissue factor-bearing cells)
vascular damage allows contact between plasma and tissue factor
fVII binds to TF (activated)
fVIIa-TF complex activates fX.
fX (cell surface) combines with fVa to produce thrombin.
fVIIa-TF complex also activates fIX, which diffuses into cell

amplification
platelets are fully activated, with cofactors V and VIII bound to their surfaces
thrombin amplifies the original signal

propagation (on platelets)
large scale thrombin generation occurs
fXI binds and activated by thrombin,
fXa generates fIXa.
fIXa complexes with fVIIIa to activate fX fXa-Va complexes activate prothrombin to produce burst of thrombin necessary to produce large quantities of fibrin.

Fibrin then complexed to form fibrin polymers and a stable thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Regulation of hemostasis (3)
A
  1. Platelets do not express tissue factor; coagulation can proceed only when extravascular tissue factor exposed

2.platelets are activated, markedly increases the speed of coagulation reactions > Prostacyclin limits the platelet response to TxA2,  Ecto-ADPase metabolizes ADP released

  1. anticoagulant pathways:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. anticoagulant pathways
A

:

  • **Antithrombin AT **
    inactivates coagulation proteins that escape into the circulation from a site of injury
    exerts potent antiinflammatory effect
  • thrombin-thrombomodulin complex activates protein C
    inactivate cofactors fVa and fVIIIa, and this slows the rate of thrombin
    enhances fibrinolysis inactivation of plasminogen activator inhibitor-1 (PAI- 1)
  • Tissue factor pathway inhibitor inhibits tissue factor
    abrogates the initiation complex of factor VIIa-TF, as well as factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • Fibrinolysis

2 plasminogen activators?

A

o Plasminogen activators proteolytically convert the proenzyme, plasminogen, to plasmin
o Plasmin degrades fibrin into soluble degradation products

 tissue-type plasminogen activator (t-PA
urokinase-type plasminogen activator (u-PA

plasminogen activator inhibitor-1 (PAI- 1)
 stored in platelet α-granules
 PAI-1 inhibits both tPA and uPA
 α2-antiplasmin, synthesized in the liver, inhibits plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • Platelet Enumeration and Estimation
A

Multiply average number of platelets per HPF by 15,000

o Pseudothrombocytopenia is a common artifact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • Buccal Mucosal Bleeding Time

prolonged by? 3

A

o 1-mm deep incisions in the mucosa of the upper lip
o Normal ranges are 1.7 to 4.2 minutes in the dog, and 1.4 to 2.4 minutes in the cat
o prolonged with thrombocytopenia, thrombopathia, and vasculopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • Prothrombin Time and Activated Partial Thromboplastin Time
A

o Prolongation of the PT indicates defective extrinsic and/or common pathways
o aPTT prolongation indicates defective intrinsic and/or common pathways

o short half-life of factor VII, the PT is very sensitive to vitamin K deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Activated Clotting Time
A

diatomaceous earth, which serves as a contact activator of factor XII

o normal ACT is less than 110 seconds for the dog, and less than 75 seconds for the cat

affected by: severe thrombocytopenia (<15,000/μL) or thrombopathia, anemia, altered blood viscosity, and assay incubation temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • d-Dimers
A

neo-epitope produced when soluble fibrin is crosslinked by fXIIIa

indicate the activation of thrombin and plasmin, and are specific for active coagulation and fibrinolysis

sensitive indicator of thrombotic conditions, such as DIC and thromboembolism

o excellent negative predictive value in that few dogs with DIC or thromboembolism have normal d-dimer concentrations

not specific; DIC, thromboembolism, neoplasia, hepatic disease, renal failure, cardiac failure, or internal hemorrhage, and following surgical procedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Fibrinogen
A

endpoint of all clotting assays (PT, aPTT, ACT) is based on the formation of a fibrin clot

prolongation indicating hypofibrinogenemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Viscoelastic Testing: Thromboelastography

global assessment of hemostatic system in whole blood

A

o reaction time (R) represents the enzymatic portion of coagulation (secondary hemostasis

o The clotting time (K) represents clot kinetics, largely determined by clotting factors, fibrinogen, and platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Causes of Surgical Bleeding

o 4 Technical, disorders

A

o 4 Technical
 Inadequate repair of vessels

 Occult injury to vasculature

 Damage to organs within surgical field

 Damage to organs remote from surgical site

Primary – result from decreased circulating platelet numbers (thrombocytopenia), from platelet dysfunction (thrombopathia) or rarely, from vascular anomaly (vasculopathy)
Secondary – low conc or activity of coag factors
 Acquired disorders usually affect both to variable degrees, inherited usually only affect one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

primary haemostatic disease

A

decreased production

increased destruction (IMT, 1st - evans and idiopathic and 2nd- drugs, neoplasia)

cosumption (DIC, splenic dz, severe haemorrhage)

aquired (organi dz, drugs )
inherited (vWF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

secondary hemostatic disease

A

Aquired
* 1. 1. * Vit K def
* 1. 1. * hepatic dz
* 1. 1. * DIC
* 1. 1. * Drugs
* 1. 1. * shock/acid/hypothermia

inherited
haemophillia A (FVIII)
Hameophillia B (FIX)
recessive sex-linked traits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

predisposing factors for coagulopathies (6)

A
  1. trauma/haemorrhage - tissue injury > TPA release which inhibits PAI-1
  2. Hemodilution: hypofibronigenemia thrombocytopenia and reduced factors, also triggered by massive transfusions (1 blood volume in 24 hours or 1/2 blood volume in 3 hours)
  3. Hypothermia: platelet adhesion effected

4..Acidemia:

  1. Shock: anticoagulant and hyperfibrinolytic state due to unknown mechanisms
  2. Critically ill patients:
20
Q
  • Preoperative Hemostatic Assessment
A

Patient-associated factors:
breed, diseased

Procedure bleeding risk

Tests and Their Limitations
* Routine hemostatic screening tests include the basic coagulogram (platelet count, PT, and aPTT) and/or the buccal mucosal bleeding time

21
Q

Clinical signs of primary vs secondary haemostasis

A

 Primary: ecchymoses, spontaneous bleeding from mucosal surfaces, Petechiae (more indicative of thrombocytopenia then pathia)

 Secondary: hematomas, bleeding into body cavities, SQ, joints, or muscles

22
Q
  • Operative and Postoperative Bleeding
A

 Blood loss of 25% to 30% of blood volume generally results in tachycardia and vasoconstriction

23
Q

what % needs transfusion

A

 blood pressure can be preserved until as much as 40% blood volume loss

24
Q

determining cause of coagulopathies

A

 Perform coag studies
* Normal TEG > indicates a technical cause of bleeding
 Check for hypothermia and acidosis
 Review medications
 Review history
 Additional coag studies : platetelt dysfunction with BMBT/smear. consider hyperfibrinolysis

25
Q

management for coagulopathies

prevent bleeding

A

 treat shock
 Rule out technical
 Restore normal hemostasis with medications and transfusions
 Monitor coag parameters
 Monitor for ongoing blood loss
 Monitor for complications

 “Damage control resuscitation” – aggressive correction of coagulopathies, while reducing hypoperfusion, hemodilution, and hypothermia
 “Hypotensive resuscitation therapy”

26
Q

Plasma transfusion options (3)

A

FFP: all (factors, Vwf, albumin)

cryoprecipitate: (vWf, fVII, fibrinogen)

crysupernatant: all but (vWf, fVII, fibrinogen)

27
Q

o Platelet Transfusion

A

FWB: 10ml/kg

Platelet rich plasma: short self life, limited availability

28
Q

hemostatic agents

A

 Desmopressin: induces release of vWF via V2 receptors.
lasts 2 hours. (type 1 Wonvillibrands); 1-4 ug/kg SQ

 Antifibrinolytics: aminocaproic acid and treanexamic acid (block activation of plasminogen)

 Recombinant factor VIIa-

29
Q

o Thrombocytopenia

A

 Spontaneous bleeding generally does not occur until platelet counts fall below 50,000/μL

IMT

 nonpathologic thrombocytopenia is reported in Cavalier King Charles Spaniels
 majority of thrombocytopenic cats have underlying disease,

30
Q

von Willebrand Disease

Dx: prolonged BMBT + normal platelet count.
Antigen assay (VWF:Ag (below 50%) are predicted at risk)
genetic test

type 1,2,3

A

 multimeric plasma glycoprotein that facilitates platelet adhesion to exposed subendothelium
 participates in platelet aggregation and binds fVIII

Hereditary VWD is an autosomal trait. 1 x abnormal gene increase risk. Antigen screening test required > * <50% are considered deficient

Type 1
all multimers, but in reduced concentrations
Doberman Pinschers, Poodles, Shetland Sheepdogs, GSD

Type 2
disproportionate loss of high-molecular-weight multimers
GSP

Type 3
quantitative deficiency, almost complete absence of vWF (<0.1%)
* Shetland Sheepdogs, Scottish Terriers

Tx: FFP, cryopreciptate (4hr life) desmopressin b4 surgery

31
Q

o Other Thrombopathies

A

requires the administration of platelets

32
Q

o Vitamin K Deficiency

anticoagulant rodenticide toxicity

A

factors II, VII, IX, and X, as well as for the synthesis of proteins C and S

 PT prolongation occurs first, reflecting the short half-life of fVII (4 to 6 hours).
 aPTT follows when other factors are depleted (approximately 2 days

 Vitamin K1 therapy is initiated at 2.5 to 5.0 mg/kg SC or IM

33
Q

o Hepatic Disease

A

 synthesizing clotting factors (with the exception of fVIII), coagulation inhibitors (AT, protein C), and fibrinolytic protein

significantly decreased functional hepatic mass (>70%)

 Vitamin K deficiency due to malabsorption of fat-soluble vitamins or biliary obstruction

 Hyperfibrinolysis + Thrombocytopenia

80-90% have bleeding anomoly, but unpredicatble bleeding risk

34
Q

THROMBOEMBOLIS

venous or arterial

A

macrovascular obstruction by a thrombus that develops locally (primary thrombosis), or that translocates from a distant site (embolism).

Arterial > aortic (FATE)
Venous > PTE, hepatic/portal, caudal venacava

35
Q

Virchow’s triad

risk factors for thromboembolism

A
  1. abnormalities of the vessel wall (endothelial injury)
  2. abnormalities of blood flow (vascular stasis)
  3. abnormalities of blood constituents (hypercoagulability)
36
Q

Hypercoagulability

A

imbalance between prothrombotic and anticoagulant activities

  • Hypoalbuminemia increases TxA2 synthesis
  • Acquired AT deficiencies
  • Activated protein C deficiency,
37
Q

hypercoagulable state

causes

A

IMHA and surgery > venous thromboembolism

others: Neoplasia, pancreatitis, HyperA, sepsis, DM

TEG ~ diagnosis of hypercoagulability

38
Q
  • Postoperative Thromboembolism

82% THR have PTE

A

 imaging studies
 (1) the exclusion of other potential causes; (2) laboratory evidence of hypercoagulability, if possible; and (3) identification of an underlying disorder

39
Q

Pulmonary Thromboembolism

pulmonary hypertension
> heart failure, reduced CO and death

A

xray
radiolucency, hypovascular lung regions

blood gas
increased A-a gradient, hypoxemia, hypocapnia, and decreased oxygen responsiveness

d-dimer increased

Dx: CT pulmonary angiography (CTPA)

Tx: Antiplatelet drugs
aspirin: irreversible functional defect in platelets by inactivating COX-1
* ultralow-dose standard primary thromboprophylaxis

Anticoagulants: inhibit 2nd hemostasis, venous thromboprophylaxis
* Unfractionated Heparin (needs monitoring)
* Low-molecular-weight heparin
* Warfarin

oxygen supplementation (patient support)

reduce sx risk: minimise trauma, hypoperfusion and compression

40
Q

DISSEMINATED INTRAVASCULAR COAGULATION

A

systemic activation of coagulation, leading to widespread microvascular thrombosis that compromises organ perfusion and can contribute to organ failure > progress to consumption and bleeding

CS: organ dysfunction
Dx: hypercaog (TEG), thrombocytopaenia, increased PT, aPTT, hypofibrinogen, and d-dimers

Tx: underying dz, o Adequate perfusion must be restored and maintained via appropriate fluid therapy +/- transfusion

41
Q

Preoperative autologous blood donation and transfusion in
dogs undergoing elective surgical oncology procedures with
high risk of hemorrhage
Sharma 2020 Vet Surg

A

Study design: Prospective study.
Animals: Twelve dogs.

minimum of 6 days

mandibulectomy, maxillectomy,
chest wall resection, and liver lobectomy

Ten of the 12 dogs received autologous transfusion.

No dog developed transfusion-related complications

42
Q
A
43
Q

Prospective evaluation of the utility of cross-matching prior to first transfusion in cats: 101 cases
Humm 2020

A

Transfusion reactions occurred in 20 cats, most commonly febrile non-haemolytic transfusion reactions (n = 9) and haemolytic transfusion reactions (n = 7)

44
Q

Twelve autologous blood
transfusions in eight cats
with haemoperitoneum
Cole 2019

A

retrospective descriptive study

Autologous transfusion appears to be a safe and effective technique for stabilising cats with haemoperitoneum.

45
Q

Xenotransfusion of canine blood to cats: a review of 49 cases and their outcome
Gal 2020

A

Xenotransfusion of canine packed red blood cells to cats is possible but haemolysis should be expected between 1 and 6 days after transfusion

Fellowship Exam (134 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions