Session 6 Flashcards
A change in one pH unit represents a
10 fold change in H+ conc
PH of the urine varies between
4.5 and 8.4 depending on the bodies need to excrete H+ or HCO3-
What is the consequence of alkalemia on free calcium
Lowers free calcium by causing Ca2+ ions to come out of solution
Alkalemia = not enough H+, H+ dissociated from COOH on albumin, therefore COO- negative site for Ca2+ to bind
Consequence of lowering free calcium
Increases neuronal excitability
Fire action potentials at slightest signal
Numbness or tingling
Muscle twitches
if severe- sustained contraction (tetany) that paralyse respiratory muscles
Acidemia impact on free calcium
Increases free calcium by causing Ca2+ ions to go into solution
Acidemia= increased H+ in blood, binds to COO- on albumin, decreased negative sites for Ca2+ to bind to, more free in blood
What other impacts does Acidemia have apart from increasing free calcium
Increases plasma potassium ion concentration due to K+ H+ exchange
-Affects excitability especially in cardiac muscles- arrhythmia
Increasing H+ denatured proteins
Sources of H+
Diet, metabolism (breaking down ketones, lactic acid…)
Normal plasma pH
7.35-7.45
Buffers in body
ECF = HCO3-
Cells = proteins, Haemoglobin, phosphates
Urine = phosphates and ammonia
H+ output
Ventilation, renal
3 mechanisms to control pH of blood
Buffers, ventilation, renal regulation of H+ and HCO3-
Time frames of pH homeostasis
Renal regulation is slower than buffers and ventilation (1-2 days)
2 ways in which kidneys alter pH
Directly, by excreting or reabsorbing H+
Indirectly, by changing the rate at which HCO3- is reabsorbed or excreted
pH management at proximal tubule
Carbonic anhydrase converts H+ and HCO3- to H20 and C02, which goes into cell and is converted back to H+ and HCO3-
H+ transported into lumen with Na+ exchanger, HCO3- transported into blood with Na+ cotransporter
PH drop stimulated glutamine to break down into 2 alpha KG and then 2HCO3-, which is transported into blood, and 2NH4+ which is broken down into NH3 and diffuses into lumen to bind to H+ and form NH4+
PH control at Late DCT/CD
K+ and H+ exchanged
Acidosis can cause
Hyperkalaemia, due to XS K+ reabsorption at CD so H+ can be taken out of blood
Hyperkalaemia can cause
Acidosis
Alkalosis can cause
Hypokalaemia, Decreased K+ reabsorption in CD
More pumped into cells, less absorbed into blood, so H+ can be absorbed into blood
Hypokalaemia can cuase
Alkalosis
Respiratory acidosis occurs when
Alveolar hypoventilation results in CO2 retention and elevated pCO2
More CO2 is combined with H20 and converted into H+ and HCO3-
Any compensation must come from renal mechanisms that secrete H+ and reabsorb HCO3-
What is more common respiratory alkalosis or acidosis
Alkalosis
Respiratory alkalosis is often a result of
Hyperventilation, alveolar ventilation increases without a matching increase in metabolic CO2 production
CO2 levels fall causing levels of H+ to fall
Primary cause is excessive artificial ventilation e.g. panic attack
Compensation for respiratory alkalosis
Any compensation must come from renal mechanisms
HCO3- not reabsorbed in proximal tubule
Late DCT/CD: HCO3- secreted, H+ reabsorbed with potassium
Metabolic acidosis occurs when
Dietary and metabolic input of H+ exceeds H+ excretion (lactic acidosis, ketoacidosis)
Can also occur if body loses HCO3- (diarrhoea)
metabolic acidosis compensation
Respiratory compensation instant, increased ventilation, pCO2 decreases due to hyperventilation
Renal compensation, Late DCT/CD: secretion of H+ and potassium, reabsorption of HCO3-
What is the anion gap
Difference between measured cations and anions
Gap is increased if HCO3- is replaced by other anions
What happens to anion gap in renal causes of acidosis
Unchanged
Not making enough HCO3- but this is already replaced by Cl-
Metabolic alkalosis can be caused by
XS vomiting of acidic stomach contents and XS ingestion of bicarbonate containing antacid
Metabolic alkalosis compensation
Respiratory compensation is rapid: hypoventilation means the body retains CO2 (creates more H+ and HCO3-, restores pH but produces more HCO3-)
Renal compensation:
HCO3- not reabsorbed in proximal tubule
Late DCT/CD HCO3- secreted, H+ reabsorbed with potassium
Respiratory acidosis and alkalosis test results
Metabolic acidosis and alkalosis results
Respiratory and metabolic acidosis results
Respiratory and metabolic alkalosis results
What are the preferred terms for acute or chronic renal failure
Acute kidney injury AKI
Or chronic kidney disease CKD
What is uraemia
Term given to the clinical symptoms which arise when nitrogenous metabolic waste products accumulate in the blood (urea and creatinine)
As a result of decreased filtration by kidneys
Defining AKI
Sudden deterioration of real function over hours to days
urea and creatinine rise rapidly
Usually associated with oliguria or anuria
Usually reversible but not always
What are oliguria and anuria
Oliguria- low urine output, <500ml
Anuria- no urine output
How do you stage AKI with regards to creatinine
how do you stage AKI with regards to urine output
AKI is staged according to
The most severe classification outcome
3 different types of AKI
Pre- renal
Intrinsic renal
Post-renal
Pre renal AKI can be due to
Intrinsic renal AKI can be due to
Post renal AKI can be due to
Features of post-renal AKI due to stone
Signs of someone with AKI
Complications of AKI
Further investigations for someone with an AKI
Bedside
Bloods
Imagine
Procedures
What does these scans show
left hydroureter
What does this show
Left hydronephrotis
What does this scan show
Right hydronephrosis
What does this show
Right hydroureter
Imagine report for previous images
Short interval increase in the size of the centrally necrotic mass arising from pelvis
Mass now involved both ureters now causing bilateral hydronephrosis
Management of pre renal AKI
Management of renal/intrinsic AKI
Management of post-renal AKI
What happens in a nephrostomy
Urine is drained through nephrostomy tube
dye can be used to check
Best treatment for AKI is to
Prevent it
