- •Content
- •Сontent module 11: blood system physiology
- •Lesson 31
- •Blood physical-chemical features investigation
- •2. Study aims:
- •3.1.Basic knowledge, skills, experiences, necessary for study the topic:
- •3.2.Topic content
- •Introduction
- •Variations in plasma protein level
- •Increase in all fractions
- •Materials for auditory self-work.
- •Task 1. To get acquainted with blood taking technology for analysis performance.
- •Task 2. To determine erythrocytes osmotic resistance.
- •Task 3. Velocity sedimentation rate (vsr) determining.
- •2. Literature recommended:
- •Materials for self-control:
- •Lesson 32
- •Erythrocytes number and hemoglobin concentration investigation
- •Introduction and normal value
- •Variations in number of red blood cells
- •Variations in size of red blood cells
- •Variations in shape of red blood cells
- •In postnatal life and in adults
- •2. Hormones:
- •1. Vitamin b12 (Cyanocobalamin)
- •2. Intrinsic Factor of Castle
- •3. Folic Acid
- •Neural-humoral erythropoiesis regulation
- •Erythropoiesis inhibitors
- •Iron metabolism
- •Task 1. To determine erythrocytes amount in blood.
- •Task 2. Hemoglobin content determining in blood.
- •Task 3. To estimate blood color index.
- •Lesson 33
- •Blood groups belonging investigation
- •2. Study aims:
- •Table 2. The blood groups with their genotypes and their constituent agglutinogens and agglutinins
- •Materials for auditory self-work
- •4.1. List of study practical tasks necessary to perform at the practical class.
- •Task 2. To determine rhesus-factor while express-method usage.
- •Task 3. To perform probe on individual compatibility.
- •Literature recommended:
- •Materials for self-control:
- •Lesson 34
- •Leucocytes number, leucocytic formule investigation
- •2. Study aims:
- •Variations in the count of white blood cells
- •Innate immunity
- •Introduction
- •Immunization
- •1. Interleukins
- •2. Interferons
- •Acquired immunodeficiency syndrome (aids)
- •Differentiated leucocytes ageing changing in children
- •Leucocytes functions significance in dentistry
- •Materials for auditory self-work
- •Task 1 Leucocytes estimation in Goryaev’s chamber
- •5. Literature recommended:
- •Lesson 35
- •Platelets and vascular-platelet hemostasis investigation
- •1. The topic studied actuality.
- •Complications after teeth extraction in patients with microcirculative hemostasis disorders
- •2. Study aims:
- •Error: Reference source not found
- •4 Forms of platelets:
- •Hemostasis
- •Platelet plug formation
- •Vascular-platelet hemostasis
- •Vessels temporary spasm:
- •Vessels injury
- •Adhesion
- •Platelets
- •Releasing reaction
- •4. Materials for auditory self-work
- •4.1. List of study practical tasks necessary to perform at the practical class.
- •Task 1. Bleeding duration determining (by Duke).
- •Task 2. Aggregatogram analysis principle.
- •5. Literature recommended:
- •6. Materials for self-control:
- •Lesson 36
- •Blood coagulation investigation
- •Physiological bases of measurements at prolonged bleeding after tooth extraction
- •Physiological basement of patients preparation to tooth extraction at blood diseases
- •Complications occurring after tooth extraction in patients with blood coagulation disorders
- •2. Study aims:
- •3.1.Basic knowledge, skills, experiences, necessary for study the topic:
- •Topic content
- •Plasma blood coagulation factors
- •Materials for auditory self-work
- •Task 1. To study thromboelastogram.
- •5. Literature recommended:
- •6. Materials for self-control:
- •Lesson 37
- •Differentiated coagulogram. Disseminated intravascular coagulation (dic) syndrome
- •2. Study aims:
- •3.1.Basic knowledge, skills, experiences, necessary for study the topic:
- •Topic content
- •Main pathological processes and influences accompanied by dic-syndrome development (dic ethiology)
- •Dic types:
- •4. Materials for auditory self-work
- •4.1. List of study practical tasks necessary to perform at the practical class.
- •Task 1. Coagulogram for dic-syndrome (disseminated intravascular coagulation) diagnostics
- •Task 2. To assess hematomic hemorrhagia type.
- •Task 3. To assess microcirculative (petekchio-spotted) haemorrhagia type
- •Task 4. To assess mixed (microcirculative-haematomic) bleeding type
- •Task 5. To get acquainted to doctor tactics at vasculite-purpure and microangiomatose bleedings types
- •5. Literature recommended:
- •6. Materials for self-control:
- •Lesson 38
- •Fibrinolysis and anticoagulants. Blood coagulation and fibrinolysis regulation
- •2. Study aims:
- •3.1.Basic knowledge, skills, experiences, necessary for study the topic:
- •3.2. Topic content
- •Table 5. Main primary physiological anticoagulants
- •Plasminogen
- •Hageman-dependent
- •Hageman-independent
- •Plasmin
- •Task 1. Blood fibrinolytic activity determining.
- •Task 2. Fibrinolytic bleeding laboratory diagnostics principles.
- •Task 3. Getting acquaintance with some tests characterizing hemostasis anticoagulant link
- •5. Literature recommended:
- •6. Materials for self-control:
- •Lesson 39
- •Total blood
- •2. Study aims:
- •3.1.Basic knowledge, skills, experiences, necessary for study the topic:
- •3.2. Topic content
- •Coagulogram changes in children
- •In mature new-borned
- •In immature new-borned:
- •Total blood
- •4. Literature recommended:
- •Lesson 40
- •Practical skills on blood system physiology
- •Glossary
- •Blood system physiology
- •Tests on blood physiology
Lesson 35
Platelets and vascular-platelet hemostasis investigation
1. The topic studied actuality.
Haemostatic reactions are relatively constant during human life. Such reactions are provided by neuro-endocrine regulation complex mechanism as well as organs producing both activators and inhibitors of this process.
Important role in such a complicated regulatory system play salivary glands secreting and releasing with saliva in oral cavity haemostatic factors influencing on its vascular-platelet and coagulational-fibrinolytic link.
Particularly, saliva influences on platelets aggregation. Under its influence: latent period and aggregation velocity are accelerated, aggregates become bigger. Saliva also influences on platelet thrombus and fibrin clot retraction. It testifies to existence in it such substances like thrombostenin. Besides, this process acceleration can also be delt with calcium existence in saliva. Finally, aggregation can be caused by thromboxane B2 which is one of pro-aggregators (it is more powerful than thromboxane A2 though it has less time period comparatively to A2).
Saliva influence on platelets aggregation can also depend on antiaggregational features of salivary glands and parodont tissues. Parodont possesses mainly proaggregatory features.
Correlation between these substances (of anti- and proaggregational nature) in parodont, salivary glands, oral mucosa, saliva will define microcirculative haemostasis in a given part of alimentary tract. At proaggregational features enforcement microcirculatory hemostasis disorder can occur in mentioned substrates. Such enforcement will encourage parodontitis, syaloadenites and will influence also on interrelations between oral mucosa tissues and denturing materials in course of orthopedic treatment.
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:
the mother experiences excessive bleeding after delivery because of decreased platelet function;
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.
