M2257 Lecture Notes

Flashcards for reviewing key concepts from M2257 lecture notes focusing on endocrine and renal pathophysiology to prepare for the upcoming exam.

Why are the clinical manifestations of secondary hypocorticism determined?

Lack of effects of glucocorticosteroid hormones

What are the pathogenetic principles of tertiary hypocorticism therapy?

Glucocorticosteroid hormone replacement therapy

What are the principles of retroregulation (ascending, inverse) of the hypothalamic-pituitary-adrenal axis?

Glucocorticosteroids inhibit the secretion of corticotropin. Glucocorticosteroids inhibit the secretion of corticoliberin. Corticotropin inhibits the secretion of corticotropin-releasing hormone

Patient C., who has been suffering from chronic nonspecific polyarthritis for a long time, was treated with high doses of glucocorticosteroids. Later, the X-ray revealed atrophy of both adrenal glands. What is the pathogenesis?

Exogenous glucocorticosteroids inhibit corticotropin secretion, and the lack of corticotropin causes apoptosis of adrenal cortex cells

How does vascular tone change in glucocorticosteroid hyposecretion in the lack of glucocorticoid hormones?

Vascular hypotension and arterial collapse occur. Decreases peripheral vascular resistance

How are cardiac functions modified in hypocorticism when there is a lack of glucocorticoid hormones?

Decreased systolic function. Bradycardia

What is the hormonal pattern in primary hypocorticism?

Corticotropin-releasing hormone increases, ACTH increases, cortisol decreases

What is a characteristic clinical manifestation of primary hypocorticism?

Skin hyperpigmentation

What is a characteristic clinical manifestation of secondary hypocorticism?

Skin depigmentation

What are the risks of stress for people with hypocorticism?

Hypoglycemia

One of the vital risks of stress for people with hypocorticism is arterial collapse. What is the pathogenesis?

In the absence of glucocorticosteroids, arteriole hyporeactivity to catecholamines occurs

How does the inflammatory reaction occur in people with hypocorticism?

In the hyperergic variant. Excessive exudation. Exaggerated vascular reactions

How does the inflammatory reaction occur in people with hypercorticism?

The synthesis of antibodies with humoral immunodeficiency is inhibited. Proliferation of T lymphocytes with cellular immunodeficiency is inhibited. Mixed immunodeficiency occurs – humoral and cellular

How does the inflammatory reaction occur in people with hypercorticism?

In the hypoergic version. Diminished vascular relations

In patient C. who suffers from primary hypocorticism, objective hyperpigmentation of the skin was observed. What is the pathogenesis?

Lack of glucocorticosteroid hormones – POMC hypersecretion – melanocyte stimulation – melanin synthesis

Primary hypocorticism was found in patient C. What is the possible etiology?

Autoimmune inflammation and adrenal atrophy. Adrenal tuberculosis. Hemorrhage in the adrenal glands

What is the possible cause of secondary hypercorticism?

Hormonal feedback dysregulation

What is the possible cause of secondary hypercorticism?

Somatotrophic pituitary adenoma

What is the possible cause of secondary hypercorticism?

Pituitary irradiation

What is the possible cause of secondary hypercorticism?

Pituitary resection

Why are the clinical manifestations of tertiary hypercorticism determined?

Excess glucocorticosteroid hormones

How is the immune system modified in glucocorticosteroid hypersecretion?

Decreases resistance to infectious diseases

What is the pathogenesis of adipose tissue hypertrophy in certain areas of the body in hypercorticism?

Glucorticosteroids – transport hyperlipidemia – lipogenesis from fatty acids. Glucocorticosteroids – hyperglycemia – insulin secretion – lipogenesis

How is protein metabolism modified in glucocorticosteroid hypersecretion?

The catabolism of lymphoid tissue proteins intensifies with its atrophy. The catabolism of striated myocyte proteins intensifies with their atrophy

The clinical examination of patient D. with hypercorticism demonstrates edema on the legs. What is the possible pathogenesis?

Glucocorticosteroid hormones increase sodium levels and cause hyperosmolar edema

What is the pathogenesis of secondary hyperaldosteronism in liver failure?

Liver failure - insufficient degradation of aldosterone - - hyperaldosteronism

What is the mechanism by which insulin enhances peripheral glucose utilization?

Activates GLUT receptors on striated myocytes. Activates GLUT receptors on adipocytes. Activates hepatocyte glucokinase

What are the effects of glucagon hypersecretion in type I diabetes?

Lipolysis. Transport hyperlipidemia. Glycogenolysis and hyperglycemia. Ketonemia

What are the effects and consequences of excessive hyperglycemia in type I diabetes?

Cell shrinkage. Hyperosmolar hyperglycemic coma

What are the effects and consequences of excessive hyperglycemia in type I diabetes?

Glucosuria. Hyperosmolar hyperglycemic coma

What is the pathogenesis of hyperrexia, increased appetite, in type I diabetes?

Ghrelin surplus. Reduction of leptin

What is the pathogenesis of hyperrexia, increased appetite, in type I diabetes?

Reduction of adipose tissue mass and excess ghrelin. Reduction of adipose tissue mass and leptin synthesis

What is the pathogenesis of weight loss characteristic of type I diabetes?

Muscle atrophy. Bone atrophy. Dehydration. Decrease in adipose tissue mass

Which cells are equipped with insulin- dependent Glut-4 receptors?

Striated myocyte. Adipocyte

Which cells are equipped with insulin- dependent Glut-4 receptors?

Striated myocyte. Leukocytes

Patient S. with type I diabetes mellitus complains of erectile dysfunction. What is the pathogenesis?

Atherosclerosis of the pudendal arteries

Patient S. with type I diabetes mellitus complains of erectile dysfunction. What is the pathogenesis?

Atherosclerosis of the pudendal arteries. Hypoandrogenism caused by corticosteroids

What is the cause of polydipsia in type I diabetes mellitus?

Glucosuria causes polyuria

What is the cause of polydipsia in type I diabetes?

Hypovolemia. Hyperglycemia. Hypernatremia

The hematological examination of patient C., 24 years old with type I diabetes mellitus showed: erythrocytes – 6.10 12 /L, hematocrit – 60%. What is the pathogenesis of these disorders?

Dehydration

What are the signs that differentiate type II from type I diabetes?

Onset of the disease at an older age. Obesity

What is the main pathogenetic link of secondary hypothyroidism?

Primary thyrotropin hyposecretion

What are the pathogenetic principles of secondary hypothyroidism therapy?

T4 replacement therapy

What is the hormonal pattern in secondary hypothyroidism?

High thyrotropin, low thyrotropin, low thyroid hormones

What are the clinical manifestations of tertiary hyperthyroidism?

Lack of peripheral effects of T3

The patient with hyperthyroidism has been diagnosed with Graves' disease. What type of allergic reaction does Graves' disease refer to?

Type V stimulator

Patient D., 45 years old, consulted an endocrinologist because of an enlarged thyroid gland (“goiter”). Biochemical investigations showed: increased concentration of thyroid hormones in the blood; increased concentration of TSH in the blood. Scintigraphy shows supranormal uptake of radioactive iodine uniformly throughout the thyroid parenchyma. What is the pathogenesis of this pathology?

Hypersecretion of thyrotropin

What is the mechanism of hyposecretion of antidiuretic hormone in pituitary stalk trauma?

Transport of antidiuretic hormone from the hypothalamus to the neurohypophysis is interrupted

What is the pathogenetic mechanism of glomerular hematuria?

Increased glomerular filter permeability

In what diseases is leukocyturia observed?

Inflammation of the pelvic system. Inflammation of the urethra

In which diseases is lipiduria observed?

Nephrotic syndrome. Lipid degeneration of the tubular epithelium

What factors cause the decrease in water reabsorption in the proximal renal tubules?

Increased content of osmotically active substances in primary urine. Tubular epithelial dystrophy

What factors cause the decrease in water reabsorption in the distal and collecting tubules?

Increased content of osmotically active substances in primary urine. Antidiuretic hormone insufficiency

What factors cause the decrease in distal reabsorption of Na ions?

Tubulopathies. Aldosterone deficiency

Tubular proteinuria is the result of which diseases?

Dystrophic tubulopathies. Amyloidosis

What factors cause decreased glucose reabsorption?

Hereditary deficiency of hexokinase in renal epitheliocytes. Proximal tubulopathies

What diseases cause aminoaciduria?

Inherited proximal tubulopathies. Liver disease with hyperaminoacidemia

In which pathologies is hyposthenuria observed?

Diabetes insipidus. Hyperhydration

In which pathologies is hypersthenuria observed?

Diabetes mellitus. Dehydration

In what cases is isosthenuria observed?

Chronic renal failure

What disorders does nephrotic syndrome include?

Hypoalbuminemia. Edema

What pathological phenomena does nephritic syndrome include?

Hematuria. High blood pressure

What processes cause proximal canalicular acidosis?

Bicarbonate reabsorption disorder. Fanconi syndrome

What processes cause distal canalicular acidosis?

Disorders of H ion secretion

What factors stimulate renin secretion?

Renal hypoperfusion. Hyponatremia

What are the endocrine functions of the kidney?

Erythropoietin increase. Local activation of the kallikrein-kinin system

What are the prerenal causes of acute renal failure?

Severe hypovolemia. Renal artery stenosis

What are the causes of intrinsic acute renal failure?

Massive hemolysis. Massive necrosis of skeletal muscles

What are the causes of intrinsic acute renal failure?

The action of nephrotoxic factors. Massive necrosis of skeletal muscles

What is the cause of acute renal failure of postrenal origin?

Urinary tract obstruction

What are the main syndromes in acute renal failure?

Urinary syndrome. Clinical syndrome

What are the manifestations of urinary syndrome in acute renal failure?

Oliguria. Isosthenuria

What are the manifestations of humoral syndrome in acute renal failure?

Hyperazotemia. Hyperhydration

What are the manifestations of the clinical syndrome in acute renal failure?

Respiratory rhythm disorders. High blood pressure

What are the causes of chronic renal failure?

Primary and secondary glomerular diseases. Tubulo-interstitial diseases

What is the sequence of progression of acute renal failure?

Early period, oligoanuric, polyuric, convalescence

How does the glomerular filtration rate change in glomerulopathies?

Decreases because the filtration surface area decreases

How does the glomerular filtration rate change in hypervolemia?

Increases due to the increase in effective filtration pressure. Increases due to increased intraglomerular hydrostatic pressure

How does the glomerular filtration rate change in hypovolemia?

Decreases, due to the decrease in effective filtration pressure

How does diuresis change in hypoproteinemia?

Increases as a result of decreased colloid osmotic pressure in the blood and increased effective filtration pressure

How does diuresis change in hyperproteinemia?

Decreases as a result of increased colloid osmotic pressure which decreases effective filtration pressure

How does diuresis change when cardiac output decreases?

Decreases as a result of decreased intraglomerular hydrostatic pressure. Decreases as a result of decreased pressure in the afferent arteriole

What is the mechanism of hypercoagulability in nephrotic syndrome?

Urinary loss of antithrombin III. Increased platelet aggregation

What is the mechanism of hyperlipidemia in nephrotic syndrome?

Hepatic compensatory synthesis of lipoproteins. Relative decrease in lipoprotein lipase concentration

What is the mechanism of loss of size selectivity of the renal filter:

Formation and sedimentation in glomeruli of circulating immune complexes. Activation of the complement system at the level of the glomerular filtration membrane

What is the mechanism of loss of electrostatic selectivity of the renal filter:

Minimal damage to the glomerular filtration membrane

What are the pathogenetic mechanisms of decreased GFR in acute renal failure?

Spasm of the cortical arterioles. Obstruction of the tubular lumen with squamous cells

What are the consequences of urinary tract obstruction?

Retrograde increase in pressure in Bowman's capsule. Decrease in effective filtration pressure

What are the consequences of atrophic gastritis?

Hypo and achlorhydria

What are the consequences of atrophic gastritis?

Diarrhea

What are the consequences of atrophic gastritis?

Protein maldigestion and malabsorption

What are the consequences of atrophic gastritis?

Cobalamin malabsorption

What are the mechanisms of pancreatic auto-aggression?

Intraacinar activation of zymogen granules

What are the mechanisms of pancreatic auto-aggression?

Increased plasma bradykinin levels

What is the role of alcohol in the pathogenesis of pancreatitis?

Contributes to premature activation of zymogens

What is the role of alcohol in the pathogenesis of pancreatitis?

Destabilizes the zymogen membrane

What is the role of alcohol in the pathogenesis of pancreatitis?

Activates lipid peroxidation in the acinar cell membrane

What is the role of alcohol in the pathogenesis of pancreatitis?

Alcohol increases levels of tumor-producing M2 macrophages

What are the possible consequences of sialorrhea?

Neutralization of gastric juice. Increased stomach pH. Dehydration of the body

What is one of the consequences of sialorrhea?

Excretory acidosis