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LCB2 > Haemostatic disorders 2 > Flashcards

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
Q

What is Evan’s syndrome?

A

Primary (idiopathic) immune mediated haemolytic anaemia with concurrent immune mediated thrombocytopaenia

26
Q

What would indicate the presence Evan’s disease?

A

Signs of primary IMHA with melaena - melaena occurs as a result of. IMTP

27
Q

Explain why pre-renal azotaemia may be seen in IMHA

A
  • 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
Q

Explain why the use of aspirin may be indicated in the treatment of IMHA

A
  • 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

LCB2 (14 decks)

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