Chapter 7 Bleeding and Haemostasis Flashcards

(40 cards)

1
Q

Describe the three phases of primary haemostasis

A
  1. Adherence
  2. Activation
  3. Aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the lifespan of a canine/feline platelet?

A

6-8 days

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

Draw the cascade model of coagulation

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

What are the three phases of coagulation in the cell based model of coagulation?

A

Initiation, amplification and propagation

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

What are the two fundamental paradigm shifts in the cell based model of coagulation (vs coagulation cascade)?

A
  1. Initiator = tissue factor
  2. Coagulation localised to and contolled by cellular surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Draw the cell based model of coagulation

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

What are the three natural anticoagulant pathways?

A

antithrombin

activated protein C

tissue factor pathway inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The normal endothelium controla platelet reactivity by which three known inhibitors?

A
  1. Prostacyclin (PGI2)
  2. Ectoadenosine diphosphatase (ecto-ADPase)
  3. Nitroc oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which are the two main factors that anti-thrombin inhibits?

A

II (thrombin) and X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which two factors does activated protein C inactivate?

A

V and VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which two factors does tissue factor pathwaty inhibitor inactivate?

A

X and subsequently TF-fVII complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which molecule degrades fibrin?

A

Plasmin (pro-enzyme = plasminogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are normal BMBP times in the dog and cat?

What part of haemostasis does it reflect?

A

Dog: <3 minutes

Cat: 34-105s

Reflects in vivo primary haemostasis

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

at what deficiency level (i.e. what % remaining) does an isolated deficiency of a single factor prolong PT or APTT?

A

<25-30% of normal concentration

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

What are d-dimers?

A

Degradation products of cross-linked finrin.

Indicate the activation of thrombin and plasmin and are specific for active coagulation and fibrinolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name to two ‘tests’ that enable global assessment of the haemostatic system.

A

Thromboelastography (TEG) and rotational thromboelastometry (ROTEM)

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

What does R represent?

What does K represent?

What is angle a dependent on?

What does MA represent?

A

R = enzymatic portion of coagulation (secondary haemostasis)

K = clotting time, represents clot kinetics (clotting factors, fibrinogen, platelets)

Angle a =dependent on fibronogen (+ platelets and factors)

MA = ultimate strenght of fibrin clot, dependent primarily on platelet aggregation (+ lesser extent on fibrinogen)

18
Q

The clot shear elastic modulus (G) is a measure of overall coagulant status. What is the formula for G?

A

5000 x MA

G = ________________

(100-MA)

19
Q

List 3 broad categories of “disorders of primary haemostasis” and give a specific example of each

A
  1. Thrombocytopaenia e.g. IMTP
  2. Thrombocytopathia e.g. NSAID induced, vW disease
  3. Vascular disorders e.g. vasculitis, Ehler-Danlos
20
Q

Lost the two broad categories of “disorders of secondary haemostasis” + give a specific example of each

A
  1. Aquired e.g. Vitamin K deficiency, hepatopathy, DIC,
  2. Inherited factor deficiencies: I, II, VII (=hypoproconvertinaemia), VIII (Haemophilia A), IX (haemophilia B), X (=Stuart=Prower trait), XI (Plasma thromboplastin antecedent deficiency)
  3. (Non-pathologic e.g. factor XII deficiency = Hageman factor deficiency)
21
Q

Which 7 factor deficiencies exist and cause clinical disease?

A

1, 2, 7, 8, 9, 10, 11

12 non-pathologic

22
Q

List 6 factors that influence acute traumatic coagulopathy

A
  1. tissue injury
  2. hypoperfusion
  3. systemic inflammation
  4. acidaemia
  5. hypothermia
  6. haemodilution
23
Q

What tests are included in basic coagulogram?

A

Platelet count, PT and APTT

24
Q

By what factor do PT or APTT need to be proloned to cause haemorrhagic risk?

25
3 questions for work up of bleeding disorder?
1. Coagulopathy vs bleeding due to local factors 2. If coagulopathy, primary or secondary (primary = ecchymoses and mucosal bleeding, secondary = haematomas) 3. Inherited or aquired
26
List the constituents of fresh frozen plasma, frozen plasma, cryoprecipitate, cryosupernatant
27
What is desmopressin and what does it do? What dose?
Synthetic vasopressin analogue --\> release of subendothelial vWF (and VIII and plasminogen) 1-4 ug/kg sc or intranasally. (30 min onset of action, 2 hour duration). Used in Type 1 vW disease patients
28
At what platelet level can spontaneous bleeding occur?
\<50, 000/uL
29
Classify the three types of vW disease and give an example of a predisposed breed for each
Type 1: All monomers present but in educed concentrations. Doberman, Poodle, Type 2: Disproportionate loss of high molecular weight multimers. German pointers Type 3: Almost complete absence (\<0.1%). Shetland sheepdogs, Chesapeake bay retrievers, dutch kooikers
30
What are the viatmin k dependent coagulayion factors? N.B these are the same factors that are present in (stored) frozen plasma
2, 7, 9, 10
31
What is the name of the enzyme that recycles vitamin k?
Vitamin K epoxide reductase
32
What is Virchows triad?
1. Abnormality of vessel wall 2. Abnormal blood flow e.g. stasis 3. Abnormal blood constituents e.g. hypercoagulability)
33
Which vessels do arterial thromboembolisms tend to affect? And venous ones?
Arteria affect aorta (/branches), cerebrovascular and coronary Venous affect pulmonary (or splenic, mesenteric, portal, cava)
34
List 10 possible causes of hypercoagulability
1. IMHA 2. neoplasia 3. hyperadrenocorticism 4. corticosteroid therapy 5. sepsis 6. PLN 7. cardiac disease 8. atherosclerosis 9. diabetes ellitus 10. necrotizing pancreatitis
35
Describe initial, secondary and definitive assessment of PTE
_Initial:_ Blood gases haem + biochem TXR (pulmonary infiltrates, may see Westermark sign = regional oligemia = area of increased radiolucency. _Secondary:_ D-dimers echo (R ventricular/regional hypokinesis w sparing of cardiac apex, RA and RV dilation, pulmonary hypertension, pulmonary artery dilation, paradoxical septal wall motion, thrombus) _Defiitive:_ Selective pulmonary angiography Pulmonary scintigraphy CT angiography
36
List 2 types of anticoagulant and 2 types of anti-platelet drugs: In which scenario would you use anti-platelet and when anticoagulant?
_Anticoagulant:_ Warfarin Heparin (unfractionated or LMWH) _Anti-platelet:_ Clopidogrel Asprin Use anticoagulant in venous thrombus and anti-platelet in arterial thrombus
37
Define DIC
Syndrome characterized by systemic activation of coagulation, leading to widespread microvascular thrombosis that compromises organ perfusion and can contribute to organ failure.
38
What criteria are used to 'diagnose' DIC?
Presence of an underlying codition that could trigger DIC + 3 of the following: * thrombocytopaenia * Pt or APTT elevation * elevated fibrin split products or d-dimers * hyperfibrinogenaemia * reduced anti-thrombin activity or red blood cell fragmentation.
39
What is the cornerstone of treatment of DIC
Address underlying condition.
40