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271

Blood transfusion

  • Substitution of lost RBCs
    • Assures gas transport

272

Blood transfusion in large animals

Large animals:

  • low antibodies - no consideration needed theoretically
  • Small proportion transferred initially
  • If no incompatibility, transfusion commences

273

Blood transfusion in small animals

  • Three drops of:
    • Donor blood cells
    • Recipient's plasma
    • Physiological NaCl solution
  • Check for hemolysis or agglutination
  • Transfusion can be completed if none present

274

Blood transfusion in cats

  • In life-saving situations:
    • Blood of a donor dog can be transfused
    • Not used anymore
    • Blood typing kits now available

275

When can cat blood be donated to another cat?

After completing cross reaction tests

276

When can dog blood be donated to another dog?

After completing cross reaction tests

277

When can dog blood be donated to a cat?

In case of emergency without testing

278

Blood cell survival after transfusion of totally compatible donor and recipient

Normal lifetime (120 days)

(Figure: A)

279

Fate of blood cells after a partly compatible blood transfusion

  • Significant hemolysis
  • Enough supply for 5-10 days of normal gas transport

(Figure: B)

280

Blood cell survival after transfusion of totally incompatible donor and recipient

  • Damage is caused
  • Each RBC hemolyses immediately

(Figure: C)

281

Hemolytic illnesses of the newborn Horse

  • Rh-like antigens
  • Problem formed only postnatally
  • Epitheliochorial placenta (barely in endometrium)
  • Immunoglobulins absorbed from colostrum within 36 hours
  • Symptoms:
    • Hemolysis
    • Neonatal jaundice
  • Solution:
    • Nursing the newborn

282

Hemolytic illnesses of the newborn swine

  • Rh-like antigens
  • Postnatal problem
  • Swine antigen might cause incompatibility
  • Epitheliochorial placenta (barely in endometrium)
  • Immunoglobulins absorbed from the colostrum
  • Symptoms:
    • Hemolysis
    • Neonatal jaundice
  • Solution:
    • Nursing the newborn

283

Hemostasis

  • Blood clotting
  • Defense reaction preventing loss of blood
    • Vascular reaction
    • Aggregation of platelets
    • RBCs containing red thrombus forms
    • Held in place by fibrin fibres

 

284

How is pathological clot formation prevented in the body?

A balance of:

  • Hemostasis 
  • Self-inhibiting mechanism

285

The lack of blood coagulation

Hemophylia

286

Physiological micro-injuries

  • Number is more significant
  • Occurs constantly in all tissues
  • Hemostasis is important in the ability to immediately repair these bleeds

287

Hemostasis balance system

If something causes bleeding or coagulation and it prevails for a longer period, it has pathologic consequences

288

Imbalance of the hemostasis system

  • Decreased healing
    • hemophilia, bleeding sickness
  • Increased clot forming mechanisms +
  • Pathologically decreased clot removal
    • Thrombosis, pathological clot forming

289

Summary of the hemostasis reaction

  1. Injury
  2. Vascular reaction
  3. Thrombocyte reaction
  4. Coagulation cascade mechanism
  5. Fibrinogen-fibrin transformation
  6. Red/white thrombus formation
  7. Blood loss stops
  8. Decreased vascular reaction
  9. Cascade inactivates
  10. Fibrinolysis
  11. Thrombolysis
  12. Vessel wall repair
  13. Complete healing

 

290

Vascular reaction

  • Contraction after injury
    • Depolarisation of smooth muscle cells
    • Tissue vasoconstrictor factors
      • Causes platelet formation
  • Drop in perfusion
    • Platelet aggreagtion

291

How are platelets attracted to injured endothelial cells

Binding to negative charges of injured endothelial areas

(Primary aggregation)

292

How does von Willebrand factor assist the thrombocyte reaction?

  • Connects the injured surface with the thrombocytes
  • Aggregation increases

293

Summarise the thrombocyte reaction

  • Intima injury
  • Primary activation
    • Platelet binds to exposed collagen
  • Von willebrand factor increases primary activation
  • Secondary activation starts
  • Thrombocytes bind together
    • Secrete coagulation factors
  • Endothelial PGI2 and NO production stops
  • Thrombocyte secretion
  • Thrombin forming activates
  • Thrombocyte releases:
    • Serotonin, ADP, PF-3, TXA
  • White thrombus

294

Summarise the central 'cascade'

  1. External/internal injury
  2. Xth coagulation factor → Xa factor
  3. Prothrombin → Thrombin
  4. Fibrinogen → IA loose fibrin net
  5. Fibrine net stabilises

295

Roles of thrombin

  • Enzyme
  • Clot coagulation
  • Clot elimination
  • Self activating
  • Coagulation-anticoagulation mechanisms

296

Extrinsic way of coagulation

  • External tissue injuries
  • Inactive factor VII → Activated when plasma enters tissues
  • Factor VIIa → Activates the factor X in the central 'cascade'

297

Intrinsic way of coagulation

  • Plasma factor XII connects to the surface
  • This binds kininogen
    • Activating the enzyme kallikrein
      • Transforms factor VII to active XIIa
  • XIIa = XI → XIa → activator complex

298

Stopping blood coagulation: anticoagulation

  • Anticoagulation
    • Endothelial cells bind thrombin
    • Thrombin activates protein-C
    • Protein-C prevents activation of enzymes needed for intrinsic and extrinsic activation

299

Stopping blood coagulation: Fibrinolysis

  • Thrombin stimulates plasminogen activation
  • The produced plasmin is an enzyme which dissolves the fibrin net

300

Stopping blood coagulation: thrombolysis

  • Phagocytosis decreases the size of the thrombus
  • Increasing perfusion helps demolish the thrombus