85. Renal acid-alkaline balance disorders

Non-gas acidosis is the most widely-spread form. 3 possible variants:

1) Glomerular acidosis or renal azotemic acidosis: it occurs due to rnal insufficiency at glomerular filtration velocity decreasing lower than 25 ml/min. It belongs to metabolic acidosis with increased anionic difference. Its development is caused by accumulation of endogenic hydrogen protons mainly in sulphates, phosphates, urinary and other acids.

2) Proxymal renal channel acidosis is a result of primary disorders in hydrocarbonate reabsorbtion in proximal convoluted channels in nephrons. It belongs to excretory acidosis with normal anionic difference (hyperchloremic).

3) Distal renal channel acidosis is caused by primary acidogenesis disorders in distal convoluted channels where hydroacrbonates are saved and urine acidification occurs. It belongs to metabolic acidosis with normal anionic difference (hyperchloremic). Urine can not accept loading with hydrogen protons. Urine pH does not reach level lower than 6.

4) Hypokaliemic (hypopotassiumemic) alkalosis can be observed at hyperaldosteronism. Aldosterone enforce K-ions secretion in distal convolent channels and cause hypopatassiumemia which in turn causes alkalosis.

86. Adrenal glands pathology. Cortex acute and chronic insuffieiency.

Subrenal glands insufficiency can be:

1) By aethiology:

a) primary – as a result of suprarenal glands injury;

b) secondary – due to hypothalamus disorders (corticoliberine deficiency) or adenohypophysis (ACTH deficiency).

2) Dependnetlt on disorders character:

a) total – all hormones production is disturbed;

b) partial – hereditary defects of separate hormones.

3) Clinically:

a) acute – expressions:

• state after adrenalectomy (suprarenal glands removal);

• haemorrhagies in suprarenal glands occurring at sepsis especially at meningococceal infection (Uoterhause-Fridericksen’s syndrome – lethality in the first days of babie’s life);

• syndrome after glucocorticoids cancellation;

b) chronic (Addisson’s or bronze disease)– expressions:

• suprarenal glands tuberculosis injury;

• autoimmune injury.

Mineralocorticoid-dependent disorders:

1) dehydration (excicosis) – due to Na loss (hyporeabsorbtion) with further water loss (polyuria);

2) arterial hypotension – as a result of circulating blood volume diminishing and excicosis;

3) haemoconcentration due to water loss and viscosity increasing; leads to microcirculation disorders and hypoxy;

4) renal circulation decreasing (due to arterial pressure decreasing) with glomerular filtration disorders and intoxication development (nitrogenemia);

5) hyperpotassiumemia - due to K-ions channel secretion decreasing and K exit from injured cells; it causes excitive tissues dysfunction;

6) distal channel acidosis;

7) gastric-intestinal bleedings (nausea, vomiting, diarrhea) – osmotic diarrhea is due to Na loss and intoxication.

Glucocorticoid-dependent disorders:

1) hypoglycemy occurring at fasting (fasting non-endurability);

2) arterial hypotension (catecholamines don’t cause arterial pressure increasing);

3) adipous tissue reaction weakening to usual lipolytic stimuli;

4) organism resistance decreasing to pathogens action - non-specific resistance (stress) disorders;

5) decreasing the ability to excrete water at watery loading (watery intoxication);

6) muscular weakness and rapid fatigueability;

7) emotional disorders (depression);

8) children growth and development retardation;

9) sensoric disorders – loosing the ability to differentiate separate shades of gustatory, olfactory, acoustic sensations;

10. distress-syndrome in new-borned (hyalinic membranosis) – due to surphactant formation disorders in lungs; lungs don’t stretched at baby birth.