Acids, bases and urinary tract Flashcards
pH is equal to what? What is base excess? What is standard base excess? Acidemia? Alkalemia?
-log10{H+]
Quantity of acid required to return plasma pH to normal
Quantity of acid required to return ECF back to normal.
Low blood pH
High blood pH
What is the anion gap? Calculation?
Difference between measured anions (negative) and cations (positive)
[Na+]+ [K+]-[Cl-]-[HCO3-]
What does a wide anion gap indicate? Narrow anion gap? Normal value?
Lactic acidosis, ketoacidosis, ingest of acid, renal failure
GI HCO3- loss, renal tubular acidosis
10-16
Most common urinary buffer in proximal tubule? When all filtered HCO3- has been combined with secreted H=, what does additional H+ combine with? Increase in HCO3- plasma conc does what?
Alkaline phosphate
Non bicarbonate buffers- namely HPO4 2- to form H2PO4- which is excreted in urine
Alkalinises it
Tubular cells, mainly of proximal tubule, take up glutamine from what? Metabolise it to form what? Forms NH4+ using what? Secreted where?
Glomerular filtrate and peritubular plasma
NH3 and HCO3-
H+ from dissociation of H2CO3 or due to Na+ reabsorption
Via Na+/ NH4+ counter transport into lumen and excreted
What is respiratory acidosis? Causes? Renal compensation for this? How long does this take?
Failure to get rid of CO2 resulting in decrease in pH as CO2 builds up
Hyperventilation, COPD, any cause of respiratory failure
Increases H+ and more HCO3- into plasma–> increase in pH using ammonium buffer
Days
What is respiratory alkalosis? Causes? Renal compensation?
Too much CO2 lost resulting in increased pH
CO2 depletion due to hyperventilation, hypoxia, Type 1 resp failure
Kidneys decrease H+ secretion and decrease in HCO3- reabsorption–> increase in pH
What is metabolic acidosis? Causes? Resp compensation?
Excess acid production (by intercalated cells) resulting in pH decrease
Renal failure, GI HCO3- loss, dilution of blood, failure of H+ excretion, ketoacidosis
Enhanced respiration stimulated by lung chemoreceptors–> fall in CO2
Causes of metabolic alkalosis? Resp compensation?
Vomiting, volume depletion, alkali ingestion, hyperaldosteronism, hyperkalaemia–> increase aldosterone secretion
Inhibits lungs chemoreceptors–> reduced resp and increasing CO2
Where is erythropoietin (EPO) produced? What does it do? Increased in response to what? Decreased when?
In peritubular cells in interstitial space of renal cortex
Stimulates bone marrow- maturation of RBCs
Anaemia, altitude and cardiopulmonary disorders
Polcythaemia, renal failure
Why does urine flow through ureters to the bladder? Walls of smooth muscle in bladder known as what? Part of this at bladder neck where urethra begins functions where?
Due to contractions of ureter wall smooth muscle
Detrusor muscles
Internal urethral sphincter
Just below internal urethral sphincter ring of skeletal muscle called what? Consists of what?
External striated urethral sphincter
Slow-twitch skeletal muscle- voluntary
When the bladder is filling, what input is minimal? At same time strong sympathetic input to where? Strong input by somatic motor neurones to where?
Parasympathetic input- muscle is relaxed, internal sphincter= passively closed.
Internal sphincter
External sphincter- detrusor muscles relaxed and sphincter closed
What is the bladder stretch reflex? When is this the spinal reflex overridden?
A primitive spinal reflex- micturition is stimulated in response to stretch
During toilet training by higher brain centres
4 steps in bladder stretch reflex?
1) Bladder fills with urine and bladder walls stretch 2) Afferent sensory neurones detect stretch and transmit to the spinal cord 3) Interneurones relay the signal to parasympathetic efferents (pelvic nerve) 4) Pelvic nerve acts to contract the detrusor muscle and stimulate micturition