Complications after teeth extraction in patients with microcirculative hemostasis disorders



In patients with platelet-vascular hemostasis disorders (thrombocytopenias) one can register cases of abundant and prolonged bleedings from alveole of extracted tooth. Such bleedings character and duration are determined by local (volume and degree of tissues injure) and general (vessels and homeostasis diseases) reasons.

Aspirin and other non-steroid anti-inflammatory medicines belong to rather widely-spread practically in all branches of medicine. That is why doctors must know further information about them. Aspirin inhibits the cyclooxygenase enzyme that catalyzes the conversion of arachidonic acid (a cyclic fatty acid) into prostaglandins, and thereby inhibits the release reaction and consequent formation of a platelet plug. Since platelets lack nuclei and are not complete cells, they cannot regenerate new enzymes. Therefore, the enzymes remain inhibited for the life of the platelets. The ingestion of excessive amounts of aspirin can thus significantly prolong bleeding time for several days, which is why blood donors and women in the last trimester of pregnancy are advised to avoid aspirin. Sight inhibition of platelet aggregation by low doses of aspirin, however, can reduce the risk of atherosclerotic heart disease, and such a regimen is often recommended for patients diagnosed with this condition. Because aspirin inhibits prostanglandin synthesis, the production of thromboxanes, which are derived from prostaglandins, is also inhibited, resulted in reduced platelet activation. If an expectant mother ingests aspirin near the end of pregnancy, prostanglandin synthesis is inhibited, with several effects. Two of these effects are:

1) the mother experiences excessive bleeding after delivery because of decreased platelet function;

2) the baby can exhibit numerous localized hemorrhages over the surface of its body as a result of decreased platelet function.

If the quantity of ingested aspirin is large, the infant, mother, or both may die as a result of bleeding.

On the other hand, in a heart attack or stroke, platelet plugs and clots can form in vessels and be life-threatening. Studies of individuals who are at risk from the development of clots, such as people who had a previous heart attack, indicate that taking small amounts of aspirin daily can reduce the likelihood of clot formation and another heart attack. It is not currently recommended, however, that everyone should take aspirin daily. 

Primary (vascular-platelet) hemostasis disorders are the reason of almost 80% of bleedings and 95% cases of thromboses.

Hemorrhagic syndrome can be present is a patient of any age. But this problem is the most actual in pediatry because significant amount of innate and acquired hemorrhagic diseases have early expression. Rate of thrombocytopathies (diseases with platelets dysfunction) are rather spread in a human population. For example, fon Willebrandt disease (innate adhesive thrombocytopathy) rate is fluctuated from 1/800 to 1/500 and is inherited by autosome-recessive way. Fon Willebrandt factor, adhesion agent, releasing is disturbed at this disease. Scientists deal this pathology with the 12th chromosome where the gene of mentioned factor is located.

 

2. Study aims:

To know: platelets structure, functions, number, vascular-platelet hemostasis mechanism, its importance in general medicine and dentistry, thrombocytopoiesis and its regulation.

To be able to: to determine bleeding time (by Duke), to perform aggregatogram analysis and to assess the indexes received.

 

Pre-auditory self-work materials.

3.1.Basic knowledge, skills, experiences, necessary for study the topic:

Subject To know To be able to
Biology and Medical Genetics Inheritance main ways Analyze primary thrombocytopathies inheritance ways
Pathophysiology Vascular-platelet hemostasis reasons, disorders classification, ethiology, pathogenesis, clinics, blood analysis changes Interpret data received about platelets amount, adhesion, aggregation (in part aggregatogram), bleeding time by Duke
Pediatry with Neonatology Platelets and vascular-platelet hemostasis peculiarities in children of different age, thrombocytopoiesis and its regulation Say about thrombocytopenies and thrombocytopathies in children
Internal Diseases Platelets structure, function, number, vascular-platelet hemostasis mechanism, its importance in general medicine Tell about ethiology, pathogenesis, treatment and prophylaxy of primary hemostasis disorders
Surgery About ethiology, pathogenesis, treatment and prophylaxy of primary hemostasis disorders To prevent and to liquidate complications after bleedings in patients with microcirculative hemostasis disorders
Dentistry Oral cavity organs role in primary hemostasis, complications after teeth extraction in patients with microcirculative hemostasis disorders To prevent and to liquidate complications after teeth extraction in patients with microcirculative hemostasis disorders

Topic content

Platelets are 2 – 4 µ in diameter, volume is 6-9 mcm3; they are the smallest blood cells. They are developed from giant cells called megakaryocytes.

 

 

FIGURE 10. Platelets in blood smear.

FIGURE 11. Intact and activated (with pseudopodias) platelets

THROMBOCYTES STRUCTURE

n Spherical, oval, or rod-shaped colorless bodies.

Diameter is between 2 to 4 м. They are activated in course of side surface, many (up to 10) processes are appeared in them as a result of which their diameter is increased in 5-10 times. There are integrines on platelet membrane serving as receptors. They participate in thrombocytes interaction one to another and to injured vessel. They have glycoprotein nature expressing fibrinogen, collagen, Willebrandt factor (FW) and other substances.

n When unstimulated, under Electron Microscopy they appear as:

· Flattened discs

· Having a cell membrane

· And a Cytoplasmic matrix.

· Microtubules encircle the thrombocyte just below it’s surface membrane.

n Do not have nuclei.

n Can not reproduce.

n But behave functionally as whole cells.

n Cytoplasm includes active proteins such as:

· Actin.

· Myosin.

· Thrombasthenin.

n Cell Organelles in thrombocytes include:

· Lysosomal granules.

· Dense bodies: about 50 – 100 in number.

· Mitochondria & Enzyme systems which produce:

1) ATP

2) ADP

· Enzyme systems producing:

1) Prostaglandins – Local hormones.

· Fine Glycogen granules.

n Microvesicles.

n Microtubules.

n Filaments.

n Granules.

n Internal Membranous systems:

· Open Canalicular System:

1) Sponge-like invaginations

2) Provide multiple channels for:

a) Taking up Calcium ions

b) Secreting granule contents.

· Dense Tubular System:

1) Channels of S.E.R.

2) Serves as an intracellular store for Calcium ions.

 

PLATELETS PHYSIOLOGY

· Have a half life of 8 – 12 days.

· Eliminated from circulation by the Tissue Macrophage system.

· Thrombocytes are active structures.

· About half of them are removed by the Macrophages in the Spleen.

· Platelet surface membrane has Phospho lipids, Cholesterol & Glycolipids

Platelets contain many granules with great number of biologically active substances. One can differentiate:

1) Alpha-granules – contain more than 30 proteins delt with haemostasis and other reactions:

· platelet factor 4;

· fibrinogen;

· thrombostenin and so on.

2) Dense granules – they contain biologically active substances delt with vascular tone and hemostasis:

· ADP;

· epinephrin;

· serotonin;

· thromboxans et al.

3) Lysosomal granules:

· kinases;

· enzymes.

 

Platelet number under norm is:

· in adults - 180-320 x 109/l; (boardering – 150 – 400 x 109/l);

· in new-borns - 200 x 109/l (in average – fluctuations 100-400 x 109/l);

· 7-10th days – 150-200 x 109/l;

· 14th day – like in adulthood;

· 1-5 years: boys – 217-407 x 109/l, girls – 229-553 x 109/l;

· 10-15 years: boys – 156-408 x 109/l, girls – 154-442 x 109/l;

· 16-20 years: guys – 140-392 x 109/l, girls – 154-386 x 109/l.

  4 forms of platelets:

· junior 0-0,8%;

· mature – 90,3-95,1%;

· old – 2,2-5,6%;

· degenerative – 0-0,2%;

· irritation forms – 0,8-2,3%.

 

AMOUNT CHANGING

 Thrombocytosis (more than 500 x 109/l) - their amount increasing:

1) Physiological:

· pain (noceoceptive);

· stressogenic;

· muscular (in course of physical loading).

2) Pathological:

· spleen pathology;

· spleen removal.

 

Thrombocytopenia (less than 140 x 109/l) – as a rule, is pathology sign and is observed at:

· radiation disease;

· congenital blood diseases;

· acquired blood diseases.

But in women on course of menstruation period platelets amount may be reduced though they are seldom out of normal limits. But it should be mentioned that even at strong thrombocytopenia reaching up to 50 x 109/l, there is no any bleedings and women mustn’t be under medication at these situations. Only when reaching critical ziphras – 25-30 x 109/l - light bleedings may occur at which treaty measures are essential. It testifies that platelets amount in blood is excessive.

 

PLATELETS FUNCTIONS:

1. Participation in vascular-thrombocytic and coagulational haemostasis (properly blood coagulation).

2. Angiotrophyc function – vascular walls feeding (15 per cent of all thrombocytes daily). At this function disorders: vascular wall permeability increasing and resistance decreasing.

3. Protective function:

· phagocytosis;

· contain immunoglobulins;

· lysozyme source;

· they are essential for reparation;

· cytokines source.

 

THROMBOCYTOPOIESIS REGULATION

1. Specific:

· thrombocytopoietins;

· interleukines-3,6,7,9,11,13.

2. Non-specific:

a) hormones:

· adrenocorticothropic;

· adrenaline;

b)food products:

· nettle;

· fungus puff-ball;

c) sympathetic nervous system excitement.

 

HEMOSTASIS

Hemostasis – is the reactions complex aimed at the blood loss stopping as well as blood liquid state maintaining in vascular bed. Hemocoagulation – hemostasis system part directed to bleeding stoppage. But here we will use the term “hemostasis” in its narrow aspect – in meaning of hemocoagulation. In fact the significance of hemostasis system is much more complicated and far exceeds the limits of fighting with blood loss.

The main tasks of the hemostasis are the following: the fluid blood state storage, the transcapillary exchange, the vessel wall resistance regulation and the influence on the reparation processes and so on.

They distinguish the vessel-platelet hemostasis and blood coagulation (clotting). Speaking about the first case the question is about the blood loss stopping from the small vessels with low blood pressure; the second one is connected with the blood loss fighting at the arteries and veins rupture. Such a division is rather conditional as both at small and large vessels rupture together with the thrombocyte plug forming the blood coagulation is occurred. On the other hand such a division is very suitable for clinical practice because at the vessel-platelet hemostasis disorders the finger skin puncture (or the ear lobe) is accompanied by prolonged coagulation time whereas the bleeding time remains normal (for example at haemophilia because of normal platelet count in hemophiliac). Hemophilia is a wide-spread hereditary pathological state. It is the excessive bleeding caused by a congenital lack of a substance (plasma coagulation factor VIII, IX, X or XI) necessary for blood clotting. Treatment consists of administration of the deficient factor.

Vessel-platelet or vascular platelet hemostasis (or so-called primary one) comes to the platelet plug (or thrombus) forming.

 

PLATELET PLUG FORMATION

· It can by itself stop blood loss, if the rent is small.

· Many such minute ruptures occur thousands of times every day in minute blood vessels.

· Platelets manage to plug these very well, all by themselves.

Vascular-platelet hemostasis

The 1-st stage

vessels temporary spasm:

Vessels injury

           

         ADP

        collagen                                                 Vessels primary spasm

        epinephrine

       thromboxan A2

Epinephrine and norepinephrine                             platelets

increasing in blood                                                  activation

 


The 2-nd stage                   Glycoproteids expression

platelets adhesion
Platelet plug formation

Platelets aggregation (primary, reversible)
                                         ADP                                                       fibrinogen

 

                                        Willebrand’s                                         platelets

                                                  factor                                              activation

                                                                                                              factor

                                                                                                               thrombin

                                                                                                               fibronectin

                                                                                    

                                                       Releasing reaction

                                                                               

optically-densed granules: ADP, epinephrine, serotonin, thromboxane A2,
б -granules: factor 4, fibrinogen, thrombosteninne
Lysosomes: kinases, enzymes    
                                                                                                  

 

 


                                       

 

                                                                                   

                                                                                                             

 

Platelets aggregation (repeated, irreversible)


                                                                              

 

 

 

 The 3rd stage:                                                        Vessels secondary spasm

platelet plug retraction                                    Retraction

 


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