1 / 22

ACID – BASE DISORDERS

ACID – BASE DISORDERS. M. Tatár. H + affects structure and function of proteins. . changes of cellular enzymes activity. . cellular and organ functions changes. Sources of H + in organism. a) Volatile acid CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 -. b) fixed acids

rhitchcock
Download Presentation

ACID – BASE DISORDERS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. ACID – BASE DISORDERS M. Tatár

  2. H+affectsstructure and function of proteins  changes of cellular enzymes activity  cellular and organ functions changes

  3. Sources of H+ in organism a) Volatileacid CO2 + H2O  H2CO3  H+ + HCO3- b) fixedacids H2SO4, H3PO4 c) organicacids lacticacid, ketoacids

  4. H+ balance per day

  5. Hydrogen ion [ H+ ] = from 10 - 7,44 to 10 - 7,36 = 0,000000036 - 0,000000044 mol . l-1 = 36 - 44 nmol . l-1 pH = - log [ H+] mol . l-1 pH = 7,4  0,04 mitochondria : 2 - 5 active H+

  6. H+ (nmol.l-1) 160 140 120 100 80 acidaemia 60 norm 40 basaemia 20 pH 6,8 7,1 7,4 7,7 norm acidaemia basaemia

  7. acidemia - acidosis alkalemia - alkalosis

  8. HENDERSON – HASSELBALCH equation [ H+ ] . [ HCO3-] K = --------------------- [ H2CO3] [ H2CO3] [ H+ ] = K . ---------------- [ HCO3-] 1 1 [ HCO3-] log ----- = log ----- + log ------------- [ H+ ] K [ H2CO3] [ HCO3-] pH = pK + log ------------ [ H2CO3] 24 mmol pH = 6.1 + log ----------- ( log 20 ) 30/1.5 18/0.9 1.2 mmol pH = 6.1 + 1.3 = 7,4

  9. Buffers 1 [ HCO3- ] 1. Bicarbonatesystem ------------ [ H2 CO3 ] HCl + NaHCO3  H2 CO3 + NaCl NaOH + H2 CO3  NaHCO3 + H2O Hb 2. Hemoglobinsystem--------- HbO2

  10. CO2 transport

  11. Buffers 2 proteinate- 3. Plasmaproteins--------------- H - protein HPO42- 4.Phosphatesystem---------- H2PO4- HCO3- - 53% (plasma 35%, RBC- 18%) BuffersHb - HbO2 - 35% in bloodPhosphates - 5% Plasm. prot. - 7%

  12. Proximaltubule „reabsorbed“ HCO3- Na,K,ATP-ase

  13. Distalnephron „new“ HCO3-

  14. 13.3 10.6 hypoventilation 8.0 (kPa) 6.7 Pco2 5.3 4.0 hyperventilation 2.7 7.4 7.6 7.0 7.2 pH

  15. Mechanisms of acid – base disorders metabolic metabolic 4. alkalosis 1. acidosis 2. alkalosis 3. acidosis HCO3- pH = pK + log ---------------------- PCO2 respiratory 5. acidosis 6. alkalosis

  16. Anion gap [ Na+ ] - ( [Cl-] + [ HCO3-] ) = 10 - 12 mmol.l-1 140 - ( 104 + 24 ) = 12 mmol.l-1 >  organic or fixed acids

  17. Causes of metabolic acidosis (MAC) I.Normalaniongap MAC bicarbonate loss  hyperchloremic MAC a) viathe GIT: diarrhea, smallbowel fistula b) renaltubularacidosis (reduced H+excretion) [ Na+ ] - ( [Cl-] + [ HCO3-] ) = 12 mmol.l-1 II. Highaniongap MAC gains of noncarbonic acids a)  lactic acid: hypoxia, liver insufficiency b) ketoacidosis: diabetes mellitus, starvation c) retention of fixed acids: renal failure [ Na+ ] - ( [Cl-] + [ HCO3-] ) > 12 mmol.l-1 acids

  18. Compensatory response in MAC 1. ventilation M M -----  ----- R R 2.HCO3- retentionin kidneys Clinical features - Kusmaulbreathing -  cardiaccontractility - lethargy - renalosteodystrophy - hyperkalemia - vomiting

  19. Causes of metabolic alkalosis (MAL) PrimaryCl-lost(hypochloremicalkalosis) b) kidneys: diuretics (furosemid) a) GIT: prolongedvomiting Cl- and HCO3-have a reciprocalrelationshipsto maintaineelectroneutrality of ECF [ Na+ ] - ( [Cl-] + [ HCO3-] ) = 12 mmol.l-1

  20. Compensatory response in MAL 1.Alveolarhypoventilation M M ------  ------- R R 2.Renalexcretion of theexcess HCO3- Clinical features - occasionally tetany -  risk of cardiac dysrhythmias -  afinity of Hb to O2 - hypokalemia

  21. Causes of respiratory acidosis (RAC) Respiratorydisorders CO2accumulation - alveolarhypoventilation Compensatory response HCO3- retentionin kidneys M M -------  ------- R  R Clinical features - CNS dysfunction: confusion, somnolence - cerebral vasodilation:  intracranial pressure

  22. Causes of respiratory alkalosis (RAL) Alveolarhyperventilation - respiratory centre stimulation a)the most common: anxiety and emotional stress b)hypermetabolic conditions: fever, CNS lesions, thyreotoxicosis c)hypoxia: pneumonia, pulmonary edema, high altitude Compensatory response Clinical features  renalexcretion of HCO3- M M  ------  ------- R  R  - vomiting • tetany

More Related