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Physiology > Hematology Post Midterm > Flashcards

Hematology Post Midterm Flashcards

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1
Q

Hemostasis

A
  • sequence of responses that stop bleeding

- > fast, localized and carefully controlled

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2
Q

5 Steps of hemostasis

A
  1. Vascular Spasm
  2. Platelet Plug Formation
  3. Blood clot formation
  4. Healing
  5. Clot Removal (Fibrinolysis)
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3
Q

Platelets

A
  • derived from bone marrow

- fragments of megakaryocytes

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4
Q

Megakaryote fragmentation

A
  • controlled by hepatic thrombopoietin
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5
Q

Functions of Platelets

A
  • release of chemicals that promote
    1. Vasospasm
    2. Formation of Platelet Plugs
    3. Coagulation
    4. Healing
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6
Q

Concentration of Platelets

A
  • 150,000 - 300,000 per microliter (uL)
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7
Q

Content of Platelets

A
  • contractile proteins (actin and myosin)
  • > can change shape when activated
  • membrane contains several glycoproteins (inactive receptors)
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8
Q

Vasospasm

A
  • occurs immediately upon blood vessel injuury
  • > reduces blood flow and loss
  • > facilitates subsequent steps of hemostasis
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9
Q

Causes of Vasospasm

A
  1. Immediate release of endothelin from damaged endothelial cells
  2. Release of Thromboxane A2 (prostaglandin derivative) and Serotonin from activated platelets
  3. Sympathetic Stimulation
    - myogenic contraction of smooth muscle cells and pericytes/capillaries
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10
Q

Platelet Plug Formation

A
  • primary hemostasis
  • only require vWF and platelets
  • > crucial to seal off thousands of minute injuries that occur every day
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11
Q

von Willebrand Factor (vWF)

A
  • present in plasma and released from damaged endothelial and tissue cells
  • binds to damaged cell membranes and fibers
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12
Q

Bound vWF to damaged cell membranes

A
  • undergoes configurational change and exposes receptors for resting platelets
  • > loose binding/adhesion of platelets to this begins
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13
Q

Binding of Platelets to vWF

A
  • activates platelets
  • their glycoprotein receptors GP IIb, IIIa start to bind fibrinogen and enable stronger adhesion of platelets to each other
  • > aggregation
  • > platelet plug formation
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14
Q

Binding of Platelets Causes:

A
  • degranulation, or release of their factors
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15
Q

Serotonin and Thromboxane A2

A
  • released from platelets

- promote vasospasm

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16
Q

ADP and Thromboxane A2

A
  • released from platelets

- aggregation of more platelets/plug grows

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17
Q

Platelets Factors V, VIII and Calcium

A
  • more membrane receptors become activated

- binding of prothrombin and preparing for clotting

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18
Q

Secondary Hemostasis

A
  • larger injuries
  • > platelet plug not strong enough
  • clotting is initiated to stabilize the platelet plug with strong fibrin strands
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19
Q

Prothrombin

A
  • hepatic alpha globulin
  • liver synthesis is Vitamin K dependent
  • attaches to activated platelets
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20
Q

Clot formation

A
  • involves cascades of chemical reactions leading to the formation of strong fibrin threads within the platelet plug giving it more strength
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21
Q

Clot Formation Occurs in 3 Stages

A
  1. The extrinsic and intrinsic pathway lead to the formation of a prothrombin-activator complex (PAC)
  2. common pathway/PAC activates prothrombin to thrombin
  3. thrombin converts soluble fibrinogen to insoluble fibrinogen
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22
Q

Factors of clot formation

A
  • hepatic plasma factors
  • platelet factors
  • tissue factors
  • calcium
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23
Q

Extrinsic System

A
  • stimulated by injured tissue which expresses Tissue Factor (Factor III or Thromboplastin)
  • leads to the activation of PAC (Xa + Va + Calcium)
  • 15 to 30 seconds
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24
Q

Tissue Factor (Thromboplastin or Factor III)

A
  • activates Factor VII to VIIa
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25
Intrinsic System
- plasma based or contact activation - stimulated by a change in surface charge of damaged endothelial membranes and activated platelet membranes - leads to the activation of PAC (Xa + Va + Calcium) - 1 to 6 minutes
26
Intrinsic system
- binds and activates Plasma Factor XII to XIIa | - can be caused by inflammatory reactions (endotoxins); contact with glass surface (bleeding not necessary)
27
Factor XIIa
- activates an enzymatic cascade of factors XI, IX and VIII leading to activation of PAC
28
What is the function of Thrombin?
- exerts positive feedback on the extrinsic and intrinsic system - contributes to platelet aggregation - converts Fibrinogen (bound to activated platelets) to insoluble Fibrin monomers - > make platelet plug stronger
29
Intrinsic and Extrinsic Systems
- both are localized - require plasma factors, platelet factors and calcium - activated simultaneously upon injury
30
Extrinsic System
- faster and more powerful
31
Intrinsic System
- serves as an amplifier
32
The Prothrombin Activator Complex (Xa+Va+ Ca), or Common pathway
- converts the proenzyme prothrombin to the active proteolytic enzyme Thrombin
33
Thrombin
- exerts positive feedback on extrinsic and intrinsic systems causing platelet aggregation - converts fibrinogen (bound to activated platelets) to insoluble fibrin monomers
34
Fibrin Monomers
- these polymerize and are cross-linked into a strong meshwork within and around the platelet plug -> forming a stable clot - bleeding stops (within 3-6 min after injury
35
Clot retraction
- within the next 30 minutes the platelet contract more and pull fibrin threads together - > clot tightens an pulls edges of injured blood vessel together
36
Healing
- fibrin meshwork serves as a scaffolding for invading fibroblasts - wound healing and scar formation begins
37
Fibroblasts
- stimulated by platelet derived endothelial growth factor
38
Fibinolysis
- once bleeding has stopped and healing sets in this phase occurs - > clot removal - dissolution of clot and opening of blood vessel - tPA involved
39
tissue-Plasminogen Activator (tPA)
- injured tissue and endothelium slowly release this about 1-2 days after clot formation
40
tissue-Plasminogen Activator
- activates the hepatic plasma factor plasminogen to plasmin (proteolytic enzyme)
41
Plasmin
- hydrolyses fibrin fibers and clotting factors | - > FDPs (fibrin degradation products)
42
Fibrin Degradation Products (FDPs)
- removed by macrophages
43
Hemostatic Control mechanisms in Vivo
- crucial to prevent unnecessary plug and clot formation and to limit excessive clot growth
44
Prevention of hemostasis
- smoothness of endothelial cells | - Prostacyclin and Nitric oxide
45
Prostacyclin and Nitric oxide
- inhibit platelet adhesion | - secreted by intact endothelial cells and WBC
46
Prevention of excessive clot formation
1. Fibrin binds thrombin - limits fibrin formation and positive feedback 2. Antithrombin III deactivates Thrombin and other clotting factors 3. Heparin from Mast Cells and Basophils combines with Anti-thrombin III to augment its effectiveness
47
In vitro anticoagulation
- calcium binding agents - > citrate, oxalate, EDTA - heparin
48
In vivo anticoagulation
- heparin - vitamin K antagonists - prostaglandin synthesis inhibitors (NSAIDs)
49
Platelet Counts
- in counting chambers, automatic counters or via blood smears - all methods are rather inaccurate
50
Mucosal Bleeding Time
- stop time until bleeding stops after a standardized small incision into skin or mucosa -> expected time 1-5 min
51
Mucosal Bleeding Time
- measures functional ability of platelets and v. Willebrand Factor to plug minute injuries - > primary hemostasis
52
Bleeding disorders
- coagulopathies
53
Thrombocytopenia
- decreased production, increased destruction, or consumption of platelets
54
von Willebrand’s Disease (Form I,II,III)
- most common bleeding disorder in animals due to genetic lack or insufficiency of vWF - > platelets fail to adhere to sites - > spontaneous bleeding
55
von Willebrand's Disease Form I
- highest prevalence in Dobermans
56
Vitamin K deficiency
- Rodenticide poisoning | - Coumarin impairs liver synthesis of several clotting factors (VII, IX, X) including prothrombin
57
Coumarin
- Vitamin K antagonist
58
Hemphilias
- genetic deficiencies in a clotting factor | - very rare
59
Thrombosis
- clotting in an unbroken blood vessel | - > due to stasis, atherosclerosis, trauma, parasites and tumors
60
If thrombus dislodges
- embolisms, or blocking of blood vessels occur | - > causes ischemia (restriction of blood supply to tissue)
61
Saddle Thrombus/Aortic Thromboembolism
- in cats due to myocardial diseases - thrombus formation in left atrium - embolism into aorta - often lodges at caudal trifurcation and blocks the blood supply into the iliac arteries
62
Treatment of Saddle Thrombosus
- Need to dissolve embolism by giving TPA or a thrombolytic drug to avoid permanent damage to the hind limb - > Heparin would stop the clot from getting bigger, therefore can not use this
63
Clinical Signs of Saddle Thrombosus
- no blood supply to the back legs/hindlimb - they are cold - nails will turn blue - muscles will not function -> total muscle hypoxia - in a lot of pain

Physiology (6 decks)

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