lecture 7 (renal) Flashcards
(42 cards)
1
Q
what causes a low pH?
A
- metabolic acidosis (by decrease in bicarb)
- respiratory acidosis (increased pCO2)
2
Q
what is the compensation for metabolic acidosis?
A
- increased ventilation
- decreased pCO2
3
Q
what is the compensation for respiratory acidosis?
A
- increased bicarb conc
- increased H+ secretion
4
Q
what occurs with a high pH?
A
- metabolic alkalosis (increased bicarb conc)
- respiratory alkalosis (decreased pCO2)
5
Q
what is the compensation for metabolic alkalosis?
A
- increased pCO2
- decreased ventilation
6
Q
what is the compensation for respiratory alkalosis?
A
- decreased HCO3- conc
- decreased H+ secretion
7
Q
what is the primary defect in respiratory acidosis?
A
- increase in PCO2
8
Q
what is the effect of respiratory acidosis?
A
- production of too much H+ and bicarbonate
- lowers pH
- high PCO2
- high HCO3-
9
Q
what are the causes for respiratory acidosis?
A
- obstructive airway diseases
- drugs which depress respiration
10
Q
what is the primary defect in respiratory alkalosis?
A
- decrease in PCO2
11
Q
what is the effect of respiratory alkalosis?
A
- high pH
- low HCO3-
- low PCO2
12
Q
what are the causes of respiratory alkalosis?
A
- hyperventilation
- asthma
- mechanical ventilation
- salicylate overdose (aspirin)
13
Q
what is the primary defect in metabolic acidosis?
A
- decreased bicarb conc
14
Q
what is the effect of metabolic acidosis?
A
- low pH
- low bicarb conc
15
Q
what are the causes of metabolic acidosis?
A
- gain of non-volatile acid (Ketoacidosis, diabetes, lactic acid, solvent abuse)
- loss of HCO3- (diarrhoea)
- decreased renal acid secretion
16
Q
what is the primary defect in metabolic alkalosis?
A
- increase in bicarb concentration
17
Q
what is the effect of metabolic alkalosis?
A
- high pH
- high HCO3-
18
Q
what are the causes of metabolic alkalosis?
A
- increased GI loss of protons (vomitting)
- increased renal loss of protons (hyperaldosteronism)
- hypokalaemia
- administration of HCO3-/citrate IV
- liquorice (pseudohyperaldosteronism)
19
Q
how does the body recover from the acid base disturbances?
A
- buffering any excess
- respiratory compensation
- renal compensation (transcription/translation of genes etc)
- correction of defect
(work to minimise change in pH but cant correct the disorder)
20
Q
what is the compensation mechanism?
A
- making changes to allow the values to become closer to normal
21
Q
what is the acidosis respiratory compensation?
A
- increased ventilation decreases PCO2 and H+ conc
22
Q
what is the respiratory alkalosis compensation?
A
- decreased ventilation increases PCO2 and H+ conc
23
Q
what is the renal compensation for acidosis?
A
- increased H+ secretion and excretion
- all filtered HCO3- reabsorbed
- increased NH4+ excretion
- HCO3- production increased
24
Q
what is the renal compensation for alkalosis?
A
- H+ secretion inhibited
- HCO3- reabsorption reduced
- acid and NH4+ excretion reduced
- HCO3- secretion into urine
25
what transporter removes bicarbonate from the cell via the apical membrane?
- pendrin
- bicarbonate chloride transporter
26
what is pH directly proportional to?
bicarbonate concentration / partial pressure of co2
27
what is renal tubular acidosis (RTA) ?
- acidosis restyling form impaired H+ excretion from kidney
28
what aerate two types of renal tubular acidosis?
type 1 = distal renal tubule acidosis
type 2 = proximal renal tubule acidosis
29
what occurs in type 1?
- defective H+ secretion
30
what are examples causing type 1 distal tubule RTA?
- sjogren syndrome
- defective HKA
- increased nephron permeability
- distal nephron dysfunction (diabetes, drugs affecting RAAS system)
31
what occurs in type 2 RTA?
- impaired H+ secretion in PT so decreased HCO3- reabsorption
- decreased plasma HCO3- causes acidosis
32
what is the cause for type 2 RTA?
- general dysfunction
33
what is the anion gap?
- difference in measured amount of anions in serum compared to the ions that are actually present
- difference in concentration of major ECF cations and anions
34
how is the anion gap calculated?
Na+ conc - (Cl- conc + HCO3- conc)
35
what is the normal value for anion gap?
8 to 16 mEq/L
36
what is the anion gap with acidosis from acid loading ?
- larger anion gap
37
what is the anion gap with acidosis from bicarbonate loss ?
- larger anion gap
38
what does an increase in anion gap indicate?
- progression or likelihood to progress in chronic kidney disease
39
how does acidosis progress to chronic kidney disease?
- increased acid retention
- causes decreased interstitial and intracellular pH
- increased ammonia genesis ET1 and RAAS production
- activation of complement, pro inflammatory and profibriotic mediators
- tubule-interstitial injury and fibrosis
- loss of functioning nephrons
- chronic kidney disease progression
- increased acid retention (loops to cause progression of kidney disease)
40
what is the role of endothelin in kidney disease?
- podocyte foot process effacement, enhanced glomerular permeability = proteinuria
- activation of proinflamamtory factors = inflammation
- activation of fibrotic factors = fibrosis
41
how does angiotensin II contribute to chronic kidney disease?
- elevation of intra-glomerular pressure = proteinuria
- proliferation of tubular cells and fibroblasts = tubular atrophy
- activation of proinflamamtory factor = inflammation
- activation of fibrotic factors = fibrosis
- tubule interstitial injury and fibrosis
42
how does ammoniagenesis cause chronic kidney damage?
- activation of complement C3, C5b-9 and alternative complement cascade
- increased production of pro inflammatory, proliferation an profibrotic mediators
- proteinuria, inflammation, fibrosis
- tubule interstitial injury and fibrosis
