Haemostatic disorders 2 Flashcards

1
Q

What may disseminated intravascular coagulation occur secondary to?

A
  • Trauma
  • Electrocution
  • Sepsis
  • Heat stroke
  • Activation of platelets
  • Heart disease
  • Neoplasia
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2
Q

Describe the effect of Angiostrongylus on clotting

A
  • Abnormalities in platelet counts and clotting cascades

- Due to low grade consumptive DIC

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3
Q

What are the 2 stages of DIC?

A

1: Primary and secondary haemostatic plugs form simultaneously in many small vessels
2: Paradoxical bleeding

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4
Q

Describe the first stage of DIC

A
  • Primary and secondary haemostatic plugs form simultaneously in many small vessels
  • Leads to multiple organ microthrombosis leading to ischaemic necrosis and organ falure
  • MODS, SIRS - can be triggered by deranged blood clotting
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5
Q

Describe the appearance of the first stage of DIC on a TEG graph

A

Large clotting area

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6
Q

Describe the appearance of the second stage of DIC on a TEG graph

A

Small clotting area

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7
Q

Describe the second stage of DIC

A
  • Paradoxical bleeding
  • Consumption of platelets leading to thrombocytopaenia
  • Consumption of clotting factors
  • Consumption of anticoagulants
  • Fibrinolysis: inactivation of clotting factors, FDPs inhibit normal platelet function
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8
Q

Describe the PT and APTT values in DIC

A

Both prolonged

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9
Q

What are the 3 mechanisms of DIC?

A
  • Endothelial damage (electrocution, heat stroke, sepsis)
  • Platelet activation (mainly viral e.g. FIP, endotoxamia, neoplasia)
  • Release of tissue procoagulants e.g. (trauma, pancreatitis, bacterial infections, erythema multiforme, some neoplasms e.g haemangiosarcoma)
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10
Q

List the conditions that trigger DIC specifically in the dog

A
  • Haemaniosarcoma
  • Sepsis
  • Pancreatitis
  • Immune mediated haemolytic anaemia
  • Metastatic malignancies
  • Erythema multiforme
  • A. vasorum
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11
Q

List the conditions that trigger DIC specifically in the cat

A
  • Lymphoma (liver)
  • Cholangiosarcoma
  • Pancreatic adenocarcinoma
  • Sepsis
  • hepatic lipidosis
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12
Q

Describe the clinical features of DIC

A
  • Acute or chronic presentation
  • Profuse spontaneous bleeding
  • Signs secondary to anaemia or parenchymal organ thrombosis (i.e. end organ failure), cardiovascular collapse
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13
Q

Describe the diagnosis of DIC

A
  • No single pathognomic test
  • Serum biochem and urinalysis
  • Combination of haemostatic abnormalities notable: thrombocytopaenia, prolonged PT or APTT, D-dimers raised, antithrombin lowered, hypofibrinogenaemia
  • Schistocytes
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14
Q

Why are schistocytes present with DIC?

A

RBCs pass through disrupted vascular network

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15
Q

Outline the treatment options for DIC

A
  • Unless establish underlying cause, often hopeless
  • Heparin treatment
  • Blood/blood products
  • Increase tissue perfusion using fluid therapy
  • Prevent secondary complications
  • Euthanasia
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16
Q

Explain the use of heparin in the treatment of DIC

A
  • Only effective is sufficient antithrombin available
  • Halts intravascular coagulation and decreases activity of firbinolytic system by binding to enzyme inhibitor AT-III activating it
  • Activated ATIII then inactivates coagulation factors esp. Xa
17
Q

Outline the treatment of haemophilia where there is a small bleed contained by anatomical structures e.g. haemarthrosis

A
  • Pain relief essential

- Restrict movement

18
Q

Outline the treatment of haemophilia

A
  • Fresh plasma/FFP/whole blood transfusion to patch up factors
  • porcine factor VIII for haemophilia A (transient effect)
  • Cryoprecipitate factor VIII or cryosupernatant factor IX fine but not readily available
19
Q

List the diagnostic tests used for assessment of primary, secondary and tertiary haemostasis disorders

A
  • Primary: platelet count, BMBT, platelet function, vWF
  • Secondary: WBCT, APTT, OSPT, specific factors
  • Tertiary: D-dimers (FDPs)
20
Q

What body systems are assessed during triage?

A
  • Cardiorespiratory
  • Renal
  • Neurological
21
Q

Outline a “gold standard” diagnostic plan for the investigation of a regenerative anaemia where immune mediated disease is suspected

A
  • Blood smears for platelets, spherocytes
  • In house saline agglutination test to check for auto-agglutination
  • In house haematology
  • Biochem and urinalysis to investigate concurrent problems
  • +/- external laboratory Coomb’s test
  • Disease screening for infectious causes
  • Thoracic and abdominal radiography and abdominal ultrasound to look for underlying cause
22
Q

Outline a “value for money” diagnostic plan for the investigation of a regenerative anaemia where immune mediated disease is suspected

A
  • Thorough review of the history to determine whether there may be an inciting cause
  • In-saline agglutination
  • Blood smear
  • Haematology (incl. platelet and reticulocyte count corrected for PCV)
  • Biochem and urinalysis
  • Basic imaging
23
Q

What is elevated urea with normal creatinine, and indicative of in a patient with regenerative anaemia? Why?

A

Immune mediated haemolytic anaemia - breakdown of Hb (protein) in liver

24
Q

When investing an animal with anaemia, what does the finding of spherocytes and true in-saline aggutination indicate?

A

Immune medaited haemolytic anaemia - these results are not generally seen in any significant numbers with any other type of anaemia

25
What is Evan's syndrome?
Primary (idiopathic) immune mediated haemolytic anaemia with concurrent immune mediated thrombocytopaenia
26
What would indicate the presence Evan's disease?
Signs of primary IMHA with melaena - melaena occurs as a result of. IMTP
27
Explain why pre-renal azotaemia may be seen in IMHA
- Destruction of red blood cells so more protein in blood, conerted to urea by liver - Bleeding into GI means inermittent/continuous protein "meal", therefore high urea likely - Kidney receive less oxygen than normal, leads to pre-renal azotaemia
28
Explain why the use of aspirin may be indicated in the treatment of IMHA
- Use as anti-thrombotic, clots likely with IMHA - Platelets increase functionality in inflammatory disease including IMHA, so even with low platelets would want to use an anti-thrombotic - Clomidogrel may be better - Optimising dose of heparin difficult