which reduces needs of the organism of insulin. ts in deficiency of insulinase
ion of insulin in blood. able 17.
Clinical manifestations: microalbuminuria, proteinuria ic renal failure.
sis of urine (in one portion) we r
20 mg/l of albuminuria, and in the urine collected with a day the contents of Albuminum is more than 30 mg
peated in 6 and 12 weeks, it is necessary to expose the diagnosis of beginning diabetic Types of diabetic (hyperglycem
1. Ketoacidotic.
.
Causes of hyp
1. Revealed for the 1st time of diabetes which was not diagnosed and treated in tim e. 2. Delayed introduction of insulin because of error of the
g of introduction of insulin.
3. Introduction of insufficient dose of insulin as in the subsequent morbid conditions the need of it is enlarged
— Intercurrent (concomitant) diseases — infectious diseases, exacerbations of chronic processes of the liver, kidneys, the cardiovascular system, and etc. — Stres
sy assimilable carbohydrates).
—Diarrhea. Hypoglycemia is a state which causes are drop nce of glycemia lev
ore than 10 mmol/l. Cau
f hypoglycem
roduced insulin and has not h
—Physical exertion
—Stressful situations.
—Development of hepatic or renal failure resul and long circulat
—Reception of alcohol.
The relative characteristic of comas in diabetes in shown in the t
Table 17 — The relative cha abetes
racteristic of comas in di
Signs Diabetic coma (ketoacidotic) Hypoglycemic coma The onset Slow Subitaneous
Con It is lost gradually, mental depression It is lost quickly, exaltation,
sciousness
can precede it delirium can precede it Tone of muscles, reflexes Hypomyotonia, flaccidity of tendon reflexes, sometimes areflexia Muscular hypertonia, muscle tension, pathological reflexes Cramps Absent Characteristic Tone of eyeglobes Lowered Normal or increased Pupils Narrowed Wide Skin Dry, acyanotic Wet
Arterial pressure r increased
Lowered Normal o
Breathing al Kussmaul, odour of acetone Superfici
Card Heart sounds are dull, tachycardia,
weak pulse Sounds are clear, bradycardia
iovascular system Dige Tongue is dry, nausea, vomiting Tongue is wet, there is no
vomiting
stive system Urine re is no glucosuria and
nuria
Glucosuria, ketonuria Theketo
Bioc
hemical analysis of blood Hyperglycemia is up to 30 mmol/l Hypoglycemia is less than 3 mmol/l
Terminology
1. Struma is augmentation of dimensions of the thyroid gland: — Diffuse — uniform augmentation of all departments of the thyroid gland.
— Nodal — presence of nodal formations in the thyroid gland. 2. Euthyroidism — production of normal quantity of thyroid hormones. id hormones.
3. Hypothyroidism — drop of production of thyroism — augmentation of production of thyroid horm
4.Hyperthyroid ones. d gland
developing in genetical predisposed to it persons, characterized by diffuse augment Etiology of diffuse toxic struma
tance nheritance is connected with a carriage of antig
essful
situa pharynx; infectious — inflammatory diseases of other
tic factors of diffuse toxic struma
5.Thyrotoxicosis — clinical manifestation of hyperthyroidism. S) is autoimmune disease of the thyroi Diffuse toxic struma (DT
ation and hyperfunction of the thyroid gland, and also by toxic changes of organs and systems owing to hyperproduction of thyroid hormones.
1.Ancestral predisposition (the basic et — multifactorial (polygenic). I iological factor). A mode of inheri-
ens HLA-B8, DR3, DW3.
2.The factors provoking development of DTS: mental traumas, str tions; diseases of naso
localizations; craniocerebral traumas. Basic pathogene
1.Ancestral deficiency of T-supressing function of lymphocytes.
2.Expression of thyreocites HLA-DR-antigens on the surface.
3.A nce of forb tes w that
p ormation of the following antibodies to receptors of thyritropic hormone: factor (it is t
function of the thyroid gland with substan ti p h
of thyroid gland.
toxic struma hyroid ho s:
ensitivity stem (tachyc pairments of he e m , rising of the l
ation of p r r). Augmentation o ying of ad nt
of glyconeogenesis and glycogeno tensifying of c ( dy weight, atrophy of muscles, thinning of skin).
—Intensifying of motility of the stomach and an intestines (abdominal pain,
,
chan
une lesion oculo rs conn fissure (the
surprised look).
3. The symptom of ubject alighting downward
—the same (the symptom of Grefe), but on
movi
ent nictitation.
7. The sy ehead on the sight upwards
ppeara
idden clones of T-lymphocy ith helping activity romotes f
— LATS
a long reacting thyreostimula or) — IgG, stimulating the
tial growth of production of T3 and T4; mulating immunoglobulins),
—GSI (growth s romoting diffuse growt
Pathogeny of basic symptoms of diffuse E
xcess of tsing s rmones cause
—Riardia, im
of the cardiovascular sy to catechyocardium olamins
art rhythm, dystrophia of th evel the of BP).
— Augment— Rising of standard metabolism. roduction of heat (sense of feve
, sweating, subfebrile feve
—
f glycemia (intensif sorption of glucose in i estines, stimulation lysis). loss of bo
— In
atabolism of fats and protein diarrhea, nausea, vomiting).
— Rising excitability of the nervous system (irritability, tearfulness geability of mood, impairment of dream).