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AMK > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What are the 5 steps of Hemostasis / Haemostasis ?

A
  1. Vascular spasm
  2. platelet plug formation - (primary hemostatic plug)
  3. Coagulation cascade - (secondary hemostasis )
  4. Clot formation and repair
  5. Fibrinolysis
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2
Q

What is hemostasis?

A

Stopping the flow of blood . To prevent bleeding- keep blood within damaged BV.

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3
Q

What the mechanism that keep the blood thin usually?

A
  1. Nitric Oxide and PGI2 (prostacyclin)
    (epithelium releases these and they inhibit platelets and inactivate them.)
  2. heparin sulfate, antithrombin 3
    (A.T3 binds to herapin and inactivates factor 2,9,10)
  3. Thrombomodulin - Thrombin , Protein C, Protein S
    (thrombomodulin is on epithelial surface, thrombin binds and this activating Protein C. Protein C and S inactivate Factor 5 and 8.
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4
Q

What happens during Vascular spasm phase ?

A

Vasoconstriction and Contraction

  1. Endothelin released by epithelial cell.
    Endothelin causes :
    0 Smooth muscle contraction - (binds to receptors on SM cell causing contraction.)
  2. Myogenic mechanism - (damage to SM causes it to contract)
  3. Inflammation in the area causes contraction - (increased pressure presses against nociceptor or cytokines stimulate pain which cause contraction. )

(TXA2 AND Serotonin -(released in primary hemostatic plug )bind to SMC and cause contraction -enhancing Vascular spasm. )

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5
Q

What happens during platelet plug formation?

A

injured BV- damaged Epithelial cells - dont secrete Nitric Oxide, PGI and missing heparin sulphate.

  1. Secretion of Von- Willebrand factor by epithelial cells and platelets causes platelet aggregation.
    (platelet binds to Gp1B on VWF surface becoming activated)
  2. Platelet degranulation - release TXA2, ADP and serotonin.
    • TXA2 and ADP - binds to circulating platelets and activates and recruits them to the site of injury.
    • TXA2 and Serotonin - bind to SMC.

Platelets bind together through GP2B/3A and form aggregate at the injury site with VWF forming plug.

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6
Q

What happens in Coogulation cascade ?

A

Intrinsic pathway .

Phosphatidylserine on surface of activated platelets is negatively charged.

Negative charge —-> Factor 12a —–> Factor 11a ——> Factor 9a .
Activated factor 9 and 8 form complex with PF3 and Ca2+.
Complex —–> Factor 10a.

Extrinsic pathway

Factor 3 (Tissue factor ) ——> factor 7a ——–> factor 10a or factor 9a.

Tissue factor released form damaged epithelial cell. factor 7 can join in with common pathway (factor 10 —->factor 10a ) which happens in both intrinsic and extrinsic.

Factor 10 forms complex with factor 5 , PF3 and CA2+.
complex —–> activates prothrombin activator ——> (prothrombin activated into Thrombin (Factor 2)—–> (Fibrogen to Fibrin - Factor 1)——>Factor 13

 Thrombin polymerises soluble fibrogen into insoluble fibrin.  Factor 13 cross link Fibrin and forms fibrin mesh.
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7
Q

What happens during Clot retraction and repair ?

A
  1. Platelet contraction - platelet secrete compounds causing the edges of damaged epithelial cells to be pulled together.
  2. Activated platelet in clot secrete VEGF(vascular epithelium growth factor) and PDGF (platelet derived GF)
    • VEGF - repairs damaged epithelial cells
    • PDGF - repairs damaged SMC- cause proliferation of SMC and produces collagen patches to repair damaged collagen layer.
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8
Q

What happens during fibrinolysis?

A

Removing clot to prevent it breaking off and occluding BV - forming embolus.

  1. PLasminogen binds to Tissue plasminogen activator (T.M.A) ON Epithelial cells .(Plasminogen ——> Plasmin)

Plasmin breaks down fibrin mesh release D-dimer and fibrinogen.

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9
Q

What is the significance OF d-DIMER?

A

Released form clot when it is broken down by plasmin.

Used as a diagnostic tool to determine if someone has some kind of clot. Elevated levels suggest this.

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10
Q

What is the medical significance of T.P.A?

A

T.P.A - can be given to patients who have had a stroke - prevent occlusion of Cerebral BV.

Needs to be given within hours (acute reponse)

Aspirin can be given.

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11
Q

Types of Anti - coagulants ?

A

Warfarin - inactivates factor 2, 7, 9, 10 ( Vitamin K dependent Factors)
(inhibits enzyme which pushes Vitamin k Into these factors enabling it to be functional.

Heparin - inhance A.T3 activity leading to enhanced inactivation of factor 2,9,10.
2 forms -
unfractionated - heavier and longer chains
LMW- light molecular weight- shorter.

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12
Q

difference between Unfractionated and LMW Heparin?

A

Both forms of Heparin can inactivate F 2, ,10 -especially LMW.

However, Unfractionated can inactivated 9, 11 and 12
.

The different action is due to UF heparin being longer and has the ability to form chains with at least 18 disaccharide units.

18 units or more is needed to form complex with Thrombin and antithrombin 3 (with heparin molecule) to inactive thrombin.

LMW forms short molecules and these can form complexes with antithrombin 3 and inactive 10.

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13
Q

What is Thrombocytopenia ?

A

Abnormally low platelet level - immune mediated.

Groups particularly at risk - elderly, cardiac patients, patients undergoing orthopaedic surgery.

-If it occurs happens within 5-10 days of taking heparin.

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14
Q

What does protamine Sulfate do?

A

Drug used to treat Heparin overdose. Given IV.

reverse effects of Heparin.

Not used often as action of Heparin disappears by itself.

usually used to quickly terminate heparin activity after cardiac surgery.

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15
Q

What has to be considered when using Warfarin ?

A

When starting Wafarin therapy:

  • Coagulation can get temporarily get worse as as protein C and S are also Vitamin K dependent so are inactivated.
  • Another anti-coagulant needs be given with Warfarin at the start of treatment as takes time for circulation existing Vitamin K dependent factors to be degraded . So Heparin given to ensure that patient has some form of anti-coagulant cover.
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16
Q

What are antiplatelets and what do they do?

A

Decrease Platelet aggregation.

Aspirin - inhibits COX blocking production of TXA2.  (TXA2 secreted by activated platelets and cause aggregation and requirement of circulating platelets)

Clopidogrel - Inhibit P2Y12 receptor which ADP binds to you - so inhibits ADP.
- prasugrel
- ticagrelor
(do the sames as Clopidogrel)
-Glycoprotein IIb/IIIa inhibitors (for example, abciximab, eptifibatide, and tirofiban) block the binding of fibrinogen to glycoprotein IIb/IIIa receptors on the platelet.

-Dipyridamole — this has both antiplatelet and vasodilatory properties. It inhibits uptake of adenosine into erythrocytes, platelets, and endothelial cells, resulting in an increased extracellular concentration of adenosine, which is a potent inhibitor of platelet activation and aggregation.

17
Q

Anti-platelets and primary prevention of CVD - cardiovascular disease

A

0 Do not routinely prescribe antiplatelet treatment for the primary prevention of cardiovascular disease (CVD).

0 Consider prescribing aspirin in people with a high risk of stroke or myocardial infarction.

In deciding whether to treat or not treat with aspirin consider the following:

    - Aspirin is not licensed for the primary prevention of CVD.
    - People may be able to reduce their CVD risk through other means such as stopping smoking or starting a statin.
18
Q

Side effects of Antiplatelets?

A

Irritate GI lining and can cause indigestion (GORD) , stomach aches and lead to gastric ulcers.

Treatment -
- antacid or an alginate to use ‘as required’ for relief of dyspeptic symptoms.

- If taking low-dose aspirin consider treatment with a full-dose PPI for 1 month or test and treat for Helicobacter pylori (if the person's status is unknown) - .If symptoms recur after PPI treatment or eradication treatment, prescribe the lowest dose of PPI to control symptoms.

0
Avoid co-prescribing omeprazole or esomeprazole with clopidogrel — use an alternative PPI, or consider prescribing an H2-receptor antagonist (H2RA) for 1 month (for example, ranitidine [avoid cimetidine]).
Review maintenance treatment at least annually.

GI symptoms are not the only symptoms.

19
Q

Anti-platelets and secondary prevention of CVD

A

Antiplatelet treatment should be prescribed for the secondary prevention of cardiovascular events in people with:
(cardiovascular event - incidents which may cause damage to heart msuclest seg
0 Acute coronary syndrome (ACS).

0Angina.
    0Atrial fibrillation (AF) — in these people 
    anticoagulants are more usually prescribed. 
0Peripheral arterial disease (PAD).

Antiplatelet treatment should also be prescribed for the secondary prevention of cardiovascular events in people after:

- Myocardial infarction (MI).
- Stent implantation.
- Stroke or transient ischaemic attack (TIA).
20
Q

Anti-platelet treatment - Angina

A

0 Aspirin 75mg daily - unstable and stable Angina
0 Clopidogrel 75 mg daily - if Aspirin contraindicated.

Consider prescribing aspirin 75 mg daily for people with stable angina, taking into account the risk of bleeding and comorbidities.

  • Aspirin 75 mg - Unstable Angina- as soon as possible to all people, continue indefinitely, unless contraindicated by bleeding risk or aspirin hypersensitivity.
  • Aspirin contraindicated - consider clopidogrel 75 mg daily.
21
Q

Antiplatelet - Atrial Fibrillation

A

Given to prevent stroke - stroke more likely in AF patients.

Dual antiplatelet therapy (DAPT) of aspirin 75 mg daily and clopidogrel 75 mg daily may be suitable for people who are unable or unwilling to take anticoagulants.

22
Q

Antiplatelet - Acute coronary syndrome (ACS)

A

Acute coronary syndromes encompass a spectrum of conditions which include unstable angina, and myocardial infarction with or without ST-segment elevation.

Prescribe DAPT — aspirin 75 mg daily plus ticagrelor 90 mg twice a day for 12 months.
-Ticagrelor is the preferred choice (even in those previously treated with clopidogrel) unless the bleeding risk outweighs the benefit.

      - For people at high risk of bleeding, continue DAPT for at least one month. 
      - For people with MI at high ischaemic risk who have tolerated DAPT without a bleeding complication, consider treatment with DAPT (ticagrelor 60 mg twice daily) in addition to aspirin for longer than 12 months and up to 36 months.
     - If ticagrelor is not suitable, consider clopidogrel 75 mg daily (as well as aspirin) for longer than 12 months.
23
Q

Stroke, or transient ischaemic attack (TIA) and Antiplatelet drugs

A

1st Line - Clopidogrel 75 mg daily

Modified–release dipyridamole (200 mg twice a day) with low dose Aspirin- Clopidogrel contraindicated or not tolerated, -

Aspirin alone- Clopidogrel and modified-release dipyridamole are contraindicated or not tolerated.

Modified-release dipyridamole alone- Clopidogrel and aspirin are contraindicated or not tolerated,

Note: Prasugrel should not be given to people with a history of stroke or TIA.

24
Q

Peripheral arterial disease (PAD), or multivascular disease

A

Clopidogrel 75 mg daily is the preferred antiplatelet medication.
If clopidogrel is contraindicated or not tolerated, give low dose aspirin alone.

25
Q

Fibrinolytics

A

Enhance the activation of plasminogen to plasmin which degrades fibrin mesh in clot.

  • Streptokinase - enzyme secreted by streptococci
    indications - DVT, Acute MI, PE -Pulmonary embolus, acute aterial thromboembolism.

-Alteplase- enzyme

Acute MI, PE, acute ischeamic stroke etc

1st dose given within 6-12 hours of symptom onset . for stroke before 4.5hrs. .

26
Q

special case of streptokinase

A

Streptokinase can not be given after 4days after first dose.

Bacteria product so by 4 days body will have amassed antibodies - risk of allergic reaction.

-1st does should given with 12 hours of symptom onset. ideally within 1hr.

27
Q

antifibrinolytics

A

Make blood clot more.

inhibit activation of plasminogen to plasmin. reduce bleeding quickly

0 Tranexamin acid - used when risk of haemorrhage is high.

0 epsilon- aminocaproic acid

28
Q

What is Haemophilia ?

A

Blood clots for longer- so bleed for longer as the have less clotting factors.

Haemophilia A - factor 8 deficiency - treatment - OCTOCOG ALFA recombinant coagulation factor VIII(replacement therapy) & Desmopressin

Haemophilia B - Factor 9 deficiency - NONACOG ALFA recombinant coagulation factor IX

Haemophilia C - Factor 11 deficiency

Von Willebrand disease - VWF deficiency
Treatment - Desmopressin - vasopressin/ADH analogue but was found to increase level of factor 8 and VWF

29
Q

NOAC- Non Vitamin K/ novel oral anticoagulants

A

0 Rivaroxaban
0 Apixaban
(inhibit factor 10a - so prothrombin not activated to thrombin)

0 Dabigatran
(inhibits factor 11a - prevents activation of fibrinogen to fibrin)

30
Q

What is Thrombophilla ?

A

A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS

Protein C and S deficiency - degrades F5 AND 8)

Factor V Leiden - gene mutation csause activated protein c resistance- poor coagulation response to active PC- F5 slowly degraded. Most common cause of APCR.

Prothrombin mutation

Antithrombin (AT) deficiency

31
Q

Types of Thrombi

A

White - rich in platelets (arterial )

red - rich in RBC - (venous)

32
Q

What are thrombotic and thrombo-embolic defects?

A

Are common and has severe consequences, including myocardial infarction, stroke, deep vein thrombosis and pulmonary embolus.

33
Q

Arterial thrombosis vs venous thrombosis ?

A 
Arterial - linked to atherosclerosis - build up of plaque. 
Risk of AT - Age
Smoking
Male sex
Hypertension
Strong family history
Hyperlipidemia
Diabetes mellitus
Raised fibrinogen

Venous Thrombosis -thrombosis in the vein ex - DVT (happens in deep veins - lower leg, thigh, pelvis can happen in arm)

Age
Immobility - slow blood flow
Obesity
Oral contraceptive pill - increased oestrogen 
Trauma/Surgery -injury to vein
Pregnancy - increased oestrogen
Malignancy

Virchow’s triad – Factors favouring Venous thrombosis

Hypercoagulable states

Circulatory changes (stasis, turbulence)

Vascular wall injury/dysfunction

34
Q

What are hypercoagulable states? - Inherited

A

inherited hypercoagulable conditions include:

  • Factor V Leiden (the most common)
  • Prothrombin gene mutation
  • Deficiencies of natural proteins that prevent clotting (such as antithrombin, protein C and protein S)
  • Elevated levels of homocysteine - high levels damage BV
  • Elevated levels of fibrinogen or dysfunctional fibrinogen (dysfibrinogenemia)
  • Elevated levels of factor VIII (still being investigated as an inherited condition) and other factors including factor IX and XI
  • Abnormal fibrinolytic system, including hypoplasminogenemia, dysplasminogenemia and elevation in levels of plasminogen activator inhibitor (PAI-1 )
35
Q

What are hypercoagulable states? - Acquired

A

Acquired hypercoagulable conditions include:

  • Cancer
  • Some medications used to treat cancer, such as tamoxifen, bevacizumab, thalidomide and lenalidomide

Recent trauma or surgery - damage to BV

  • Central venous catheter placement
  • Obesity
  • Pregnancy - increased oestrogen
  • Supplemental estrogen use, including oral contraceptive pills (birth control pills)
  • Hormone replacement therapy
  • Prolonged bed rest or immobility (stasis)
  • Heart attack, congestive heart failure, stroke and other illnesses that lead to decreased activity
  • Heparin-induced thrombocytopenia (decreased platelets in the blood due to heparin or low molecular weight heparin preparations)

-Antiphospholipid antibody syndrome
(Autoimmune condition - immune system attacks proteins on phospholipids )

-Previous history of deep vein thrombosis or pulmonary embolism

Myeloproliferative disorders such as polycythemia vera (blood cancer - bone marrow releases too much RBC which then thicken the blood) or essential thrombocytosis - (body produces too many platelets)

-Paroxysmal nocturnal hemoglobinuria - (RBC hemolysis due to missing protein by body immune system - characterised by hemolytic aneamia , thrombosis and impaired bone marrow function (not making enough of the three blood components).

  • Inflammatory bowel syndrome
    HIV/AIDS
  • Nephrotic syndrome (too much protein in the urine)

AMK (92 decks)

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