Oral glucose tolerance test (OGTT) Indications: borderline fasting or post-prandial blood glucose persistent glycosuria glycosuria in pregnant women pregnant women with a family history of diabetes mellitus and those who previously had large babies or unexplained fetal loss
Screening for diabetes with typical symptoms of diabetes __ with a first-degree relative with diabetes __ who are members of a high risk ethnic group __ who are overweight (BMI ≥ 25.0 kg/m²) __ who have delivered a baby >4.5 kg or had GDM __ who are hypertensive (≥ 140/90 mmHg) __ with raised serum triglyceride and cholesterol levels __ who were previously found to have IGT or IFG
The thyroid hormones, thyroxine (T4) and triiodothyronine (T3) are secreted under the stimulatory influence of pituitary thyrotropin (thyroid-stimulating hormone or TSH). TSH secretion is primary regulated by a dual mechanism: thyrotropin-releasing hormone (TRH); thyroid hormone. Thyroid hormone exits in circulation in both free and bound forma. The thyroid gland is the sole source of T 4 and only 20% of T 3 is secreted in the thyroid. Approximately 80% of T3 in blood is derived from peripheral tissue (mainly hepatic or renal) deiodinatoin of T4 to T3. Hypothalamus TRH stimulation inhibition Pituitary TSH stimulation Thyroid T 4 T 3 Liver Thyroid Binding proteins Free hormone Bound hormone
Diagnosis of toxic diffuse goiter I.Laboratory findings. (The diagnosis of hyperthyroidism is usually straightforward and depends on careful clinical history and physical examination, a high index of suspection, and routine thyroid hormone determination). 1.In most patients serum total T 3 and T 4 concentrations, are increased. Elevation of T 3 - resin uptake is present. 2.TSN (serum thyroid stimulating hormone) may be decreased, but it is not very sensitive assay in the assessment of thyroid hyperfunction. 3.If the diagnosis of hyperthyroidism remains unclear after these initial tests, more expensive, sophisticated and time – consuming tests may be required, e.g. A TRH test II.Ultrasonography,computed tomography, MRT
Diagnostic of hypothyroidism 1.Blood analysis: anemia; hypercholesterolemia 2.Levels of thyroid hormone: both serum T 4 and T 3 are decreased (but in 25% of patients with primary hypothyroidism may be normal circulating levels of T3), TSH hormone disturbances (in primary hypothyroidism serum levels of TSH are very high (feedback), low level of circulating TSH in secondary) 3.ECG; 4.Examination of tendon reflexes 5.Ultrasonic examination
Subclinical laboratory hypothyroidism It is a state in which we can’t find clinical features of hypothyroidism and euthyroidism is reached by compensatory increasing of TSH secretion and that’s why synthesis and secretion of such level of thyroid hormone that will be enough for organism. It is an asymptomatic state in which serum T4 and free T4 are normal, but serum TSH is elevated.
Regulation of secretion glucocorticoids’ and androgens’ secretion is regulated by hypothalamic – pituitary system
mineralocorticoids ’ secretion is regulated by the renin – angiotensin system, the level of Na+, K+ in blood, and to a lesser extent of ACTH
Laboratory findings in adrenal insufficiency. 1.A low serum Na level and a high serum P level together with a characteristic clinical picture suggest the possibility of Addison’s disease. 2.Adrenal insufficiency can be specifically diagnosed by: low levels of plasma glucocorticoids and mineralocorticoids, or urinary 17 – hydroxycorticosteroid (17 – OHCS) or 17 – ketogenic steroid (17 – KGS); demonstrating failure to increase plasma cortisol levels, or urinary 17 – OHCS or 17 – KGS excretion, upon administration of ACTH (in patients with primary adrenal insufficiency, those with secondary adrenocortical insufficiency will have a significant increase in plasma cortisol or 24 - h urinary corticosteroid levels.) 3.To distinguish between primary and secondary adrenal insufficiency, me have to find the level of plasma ACTH: primary shows increased, and secondary shows decreased level.
Catecholamines are produced from the tyrosine (organism takes it from the meal or from the phenilalanine in the liver) → dioxyphenilalanine (DOPHA) → dopamine (it goes into blood only from some neurons of the central nervous system) → norepinephrine (noradrenaline) (it goes into blood only from sympathetic teleneurons) → epinephrine (adrenaline) (it goes into blood only from adrenal medulla). The principle urinary metabolic products of epinephrine and norepinephrine are the metanephrines and vanillylmandalic acid (VMA).
Investigations of pheochromocytoma 1.An increased 3-h (24-h) urinary excretion of epinephrine, norepinephrine and their metabolic products (VMA or metanephrines). 2.Increased plasma epinephrine, norepinephrine. 3.CT scanning, MRI of the abdomen for the localization of the tumor. 4.A scan with iodine I 131–labeled metaiodobenzylguanidine (MIBG) is useful for extra – adrenal tumors.
The pituitary gland is the “master gland”, which lies in a bony structure, the sella turcica, located at the base of the skull. The gland is a small organ about I cm long; it weighs 500 mg and is divided into two parts, anterior (adenohypophysis) and posterior (neurohypophysis). The anterior pituitary secretes -corticotropin (ACTH) -Prolactin -Somatotropin (growth hormone (GH) -gonadotropins [follicle-stimulating (FSH) and luteinizing (LH) hormones] -thyrotropin (TSH) -melanocyte-stimulating hormones (MSH). In the nerve endings of the posterior pituitary are stored -Vasopressin (antidiuretic hormone, ADH) -Oxytocin
The hypothalamus plays an important role in hormone regulation by secreting a series of small peptides which stimulate or inhibit the synthesis and release of hormones by the anterior pituitary First hypothalamic releasing hormone identified in 1970 was TRH by Schalli and Guilemin who von Nobel prize in medicine for their discoveries in1977 RealisingInhibiting -CRG -TRG -LGRG -FSRG -GRH- GIH (somatostatin) -PRG- PIF (dopamine) -MRG- MIH
Regulation FEEDBACK: Hormone secretion → delivery to target cells → hormone recognition by receptors in target cells → biologic effect → hormone degradation → signal from target cells to stop further hormone secretion
Diagnosis of acromegaly : Laboratory investigations: -The level of GH (0,5 – 5,0 ng/ml) -Somatomedin-C -Test with glucose suppression of growth-hormone secretion -Test with TRH -GTT
3. Enlargement of the sella turcica (90 % of patients) X-ray, CT,MRT 4. Visual - field defects (bitemporal hemianopsia)
Diagnosis of diabetes insipidus Laboratory signs: -a specific gravity of less than 1,005 -an osmolality of less than 100 mosmol/kg -serum osmolality is increased. -level of ADH can be decreased