Acid Base Balance

Question 0

Mechanisms of pH homeostasis

Answer 0

Buffers-> anions and HCO3 (fast)
Ventilation
Renal (slow, used if the others don’t work)

Question 1

Sources of H gain and loss

Answer 1

Gain:
From CO2
Protein metabolism 
Loss of HCO3 
Loss:
CO2 excretion
Utilisation of H in organic ions
D and V

Question 2

Addition of new HCO3- 1

Answer 2

Ammoniagenesis 
Proximal tubule
Glutamamine-> H2O+CO2+NH4 
H2O+CO2-> H2CO3-> HCO3-+H+ 
Reabsorption of bicarbonate
Loss of H by Na/H or H+ combined with NH3, all excreted

Question 3

Ammonium Trapping

Answer 3

NH4 secreted in proximal tubule ammoniumgenesis
H+ used to Reabsorb bicarbonate
NH3 reabsorbed in ascending limb
Diffuses across to collecting duct, secreted in to lumen and excreted

Question 4

Addition of new H+ 2

Answer 4

Phosphate buffers
Distal tubule/cortical collecting duct, intercalated cells
Extra H+ that is secreted is removed by phosphate buffers
HPO4-+H+->H2PO4 then excreted
Depends on diet as lots reabsorbed early

Question 5

Respiratory acidosis

Compensation

Answer 5

Respiratory acidosis-> increase pCO2
Compensation-> increased HCO3 (metabolic-> buffers then renal)
Caused by-> hypo ventilation

Question 6

Respiratory alkalemia

Compensation

Answer 6

Decreased pCO2

Compensation-> decrease HCO3- (metabolic, buffers then renal)

Question 7

Primary disturbance

Answer 7

Changes to H+ caused by pCO2 or HCO3-

ph will still be acidic in academia and alkali in alkalemia

Question 8

Metabolic acidosis

Compensation

Answer 8

Decreased HCO3

Compensation-> decrease pCO2 (respiratory (hyperventilation)) decrease H+ and add new HCO3- (buffers and renal)

Question 9

Metabolic alkalosis

Compensation

Answer 9

Increased HCO3
Compensation-> increase pCO2 (hypo ventilation), decrease HCO3 (buffers and renal)
When caused by vomiting (loss of H+) there is also loss of H2O, HCl and KCl so hypocholramic volume depletion-> Na+ retention-> HCO3- retention so not fully compensated

Question 10

Acidosis

Answer 10

pH 5.3 respiratory cause
Metabolic compensation if [HCO3-] >24
Opposite for alkalosis

Question 11

Osmotic diuretics

Answer 11

Mannitol
Proximal tubule and descending limb
Pharmacological inert
Freely filtered
Increase osmolality of tubular fluid-> reduced diffusion of water in to lumen
Cerebral oedema, increased osmolality removes fluid from brain

Question 12

Loop diuretics

Answer 12

Furosemide, bumetanide
Loop of henle
Very powerful
Block Na/2Cl/K+ symporter-> 15-20% of filtered Na excreted
Interstitium no longer hyper osmotic so less water reabsorbed
Increased Na delivery to DCT increases K secretion
Decreased NaCl to macula densa-> increased RAA
Loss of transepithlial potential so reduced Ca and Mg reabsorption
Chronic heart failure to reduce pulmonary oedematous, renal failure

Question 13

Thiazides

Answer 13

Chlortalidene, indapamide, bendioflumethiazide
Act of DCT
Inhibit NA reabsorption and accompanying Cl
Increase osmolality of tubular fluid so decreased water reabsorption
3rd line
Mild to moderate heart failure
Renally secreted by PCT prior to acting on DCT so ineffective in moderate to severe renal impairment

Question 14

Hypo kalmia secondary to diuretics

Answer 14

Decrease in Na to macula densa causes renin release, which causes K loss
Use beta blockers in anti hypertensive therapy to inhibit renin

Question 15

K+ sparing diuretics

Answer 15

Aldosterone receptor antagonists:
Spironalactone
Antagonise aldosterone, prevent insertion of Na pumps and channels
Na channel blockers:
Amiloride, triamterene
Block luminal Na channels in late DCT and CD

Question 16

Renoprotection

Answer 16

For diabetes associated renal nephropathy

ACE’s slow renal damage by preventing inappropriate RAA

Question 17

Diuretics in practice

Answer 17

Best taken in morning 
Increased urine flow
Avoid excess salt 
Postural hypotension 
Thiazides may worsen diabetes
Thiazides and loops may worsen gout 
NSAIDs reduce the effect of loops 
Electrolyte balance should be monitored