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1. . ү ұң ә . Etiology and pathogenesis of disorders of bone development ( )

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ү қ ү - ү ң

ү қ құ ү: ә ү ү

Remodeling of bone tissue is the breakdown and renewal of bone that are responsible for skeletal maintenance
үң Resorbtion is the process of
           

үң қ құ өң 󳠠 ә қ mineral component and organic matrix breakdown
- үң ғ қ қ Osteoid is nonmineralyzed intercellular organic matrix of the bone
(. osteon + patos- , ) ( ө Osteon-ү + patos- , ) қғ ү үң - қ Osteopathya (osteon bone + pathos - suffering, illness) any defeats of bone system without specification of their character
(. osteon + malakia ; : ) . , ( ө Osteon -ү + malakia- ұққ; : үң ұ) ү ә ұң үң ұ Osteomalacia is defect in matrix mineralization due to decreased contents of Ca- and P salts/ Osteoid is formatted? But there is no mineralization
( . osteon + poros - ) . , . ( . osteon ү + poros - ) ү ғғң ө. ү ә ң ө Osteoporosis is a disease characterized by increased porosity of the skeleton resulting from reduced bone mass.
- - -қ қң ә 򳠠 ң қ. Arthritic syndrome is the combination of several subjective and objective signs of musculoskeletal system damage
, ң, қғң қ Arthritis is a joint inflammation. In the heart of it there is synovitis
, (c) Құқ () қ ә үң ү қ , қ құқ қ Rheumatoid arthritis (RA) is a autoimmune rheumatic disease of unknown etiology is characterized by chronic erosive arthritis (synovitis) and systemic defeats of many tissues and organsskin, blood vessels, heart, lungs, and muscles
Құқ ()- G Rheumatoid factor - is blood and synovial fluid protein, is


, G. 70 - 80% ( ) қ қ ң ә қ ұқң ә. Құқ қ ң 70-80 % қ ( құқ ). antibody against Ig. Is determined in 70-80% patients with Rheumatoid arthritis (seropositive Rheumatoid arthritis)
(. annus , ) - ( pannus ққ, () құқ қ ғ () ғ Pannus is aggressive granulation tissue rich in inflammatory cells, enzymes, mediators. It produces sustained, irreversible cartilage destruction and erosion of subchondral bone
(ankylos , ) (ankylos- ү, қ)- ң - қ- қғң Ankylosis - is a stiffness of a joint due to abnormal adhesion and rigidity of the bones of the joint, which may be the result of injury or disease
( ) - . , , , , ( ә )- ң - қ қ Osteoarthritis is degeneration of cartilage. There is secondary damage to subchondral bones, sinovia, ligaments, capsule and muscles
(. derma ; ) (堠 ; , , .). ( derma- )- ң әү ұққ, ү ғ; ққ қ, қ ң Dermatoses is common definition of different diseases of different etiology and pathogenesis (inherited and acquired, inflammatory, diastrophic, allergic ets.)
- 蠠 ⠠ - қ қ ә қ. Dermatitis is skin inflammation due to direct contact with exogenous pathogenic factors
( . yon , derma - ) , ( ө pyon-ң, derma- )- ң ң Pyodermitis - are purulant skin diseases due to pyogenous microbes. Are divided into staphylodermias,

젠 . 80% , 30%. ࠠ , , ң ң . ң -80%, - 30% құ. ғ, ғ, ү ө streptodermias, miscellanies.
- - ң ң қ Hidradenitis is purulant inflammation of apocrine glands
- , - ңқұқ ғ . Mycosis is skin disease due to fungal infection
, , , Candida - Candida ңқұқң ққң, ғң, қң қ Candidosis is defeat of mucous membranes, organs, nails, caused by Candida fungi
, 젠 ࠠ (I - ). - қ үң қ ( ә 񠠠 қ ң 1 ү ү). Urticaria (hives) is allergic disease, is a kind of skin rash notable for pale red, raised, itchy bumps (Allergic reactions of the I type - reagenic)
ꠠ 堠 - ң ң қ . Quincke's edema is the rapid swelling (edema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis (Allergic reactions of the I type -reagenic).
( , . ichthy - ) , 蠠 , - ( ,ichty- қ ө ққ)- ң әү үң ү ң (ң) ү үң Ichthyosis (from the Greek root ichthy -, meaning fishy) is the group of genetically inherited disorders associated with excessive keratin build-up (hyperkeratosis) that results clinically in fishlike scales

. , ұ . қң ққ ү, ққ ә  
( .eczema , ) 堠 , - 堠 - (eczema- қ, қ қ ө ғ)- үꠠ қ, ғ - қ, ң қң қ Eczema (The Greek word eczema, means "to boil over") is skin inflammation of neuro allergic origin, has chronic current. It is characterized by red, papulovesicular, oozing, and crusted lesions early on that, with persistence, develop into raised, scaling plaques. In time, acute spongiotic dermatitis may evolve to a more chronic form in which epidermal hyperplasia and excessive scale, rather than blistering, dominate the clinical and histologic picture
頠 , 頠 , , - ққ - ң ө ө, , ұ, ғ қ Psoriasis is a common chronic inflammatory dermatosis. Psoriasis is characterized by proliferation of epidermatic cells, disorders of keratinization, dermatitis. The most typical lesion is a well- demarcated, pink to salmon- colored plaque covered by loosely adherent scales that are characteristically silver-white in color
, 蠠 ⠠ - ү ғ ң қ. Toxicodermitis is skin disease caused by hematogenous invasion by toxins or allergens
(vitiligo , ) , . (vitiligo- , )- ң әү ө ү қ ө . Vitiligo is a chronic disorder characterized by partial or complete loss of pigment- producing melanocytes within the epidermis.
, - (құ) ң ө ғ Malassezia furfur. Seborrhoeic dermatitis (also

ү seborrheic dermatitis AmE,
㳠 ң seborrhea) (also known as
қң ұ. "seborrheic eczema") is an
. , , inflammatory skin disorder
Malassezi furfur affecting the scalp, face, and
ңқұғң torso. The probable cause is
  Malassezia furfur. Malassezia
    hydrolyze human sebum
    releasing a mixture of non-
    uniform structure saturated and
    unsaturated fatty acids which
    breach the skin's barrier
    function. This barrier breach
    induces an irritation response,
    leading to dandruff and
    seborrheic dermatitis.
Photodermatitis is skin disease
() ()- ү sometimes referred to as sun
, ә堠 қң poisoning or photoallergy, is a
ғ form of allergic contact
. dermatitis in which the
.   allergen must be activated by
    light to sensitize the allergic
    response

6.1.6. :

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1. : . / .. .. .. - .: -, 2., 2013. - . 716-731

2. .. + . 4- . ., 2010. .448-450

3. қ : .. 2010

4. V.Kumar, A. Abbas, J. C. Aster. Pathologic basis of disease/Elsevier.- 2015.- Ch.20

 

5. // . .. : . .., 2006..146-147, 214-216

6. : . / .. .. - .: . 2006.- . 337-340

7. // . .. .: , 2006. - 176

8. // . .., .. .: , 2008. - 176

 

6.1.7.

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