wk 10 lec 2 Flashcards
volatile vs non volatile acids
volatile= can breath off as carbon dioxide
- via bicarbonate buffer (non volatile can also be buffered by bicarbonate to minimize large pH changes but cant breath off- still need to secrete protonated part via kidneys)
non volatile- cant breath off
examples of nonvolatile acids
lactic acid, ketone bodies, sulphuric acid, HcL from protein metabolism or consumptions
orange juice vs cranberry juice acids
cranberry- non volatile bc benzoic acid
orange juice is citric acid which turns into citrate into CO2 so its volatile
3 mechanisms of hydrogen ion regulation
- fluid chemical buffers (IC and EC)
–> rapid: bicarbonate, phosphate, ammonia, proteins - respiratory system
–> rapid, Co2, NOT nonvolatile - renal system
–> slower, non-volatile, secrete H+, reabsorb and generate new HCO3-
phosphate, proteins, bicarbonate, ammonia
where are theses buffer systesm
phospahte: renal tubular
proteins: intracellular (i.e. hemoglobin)
bicarbonate: ECF
ammonia: renal tubular
protein intraceullar buffer
donate or accept amino acids (bind or release H+)
most important amino acids at physiological pH
histidine and cysteine
why is hemoglobin a good intraceullar buffer
38 histidine residues
carries CO2 through blood when O2 is low
move co2/hco3 across RBC membrane
phosphate buffer system for
intraceullar buffer
urinary buffer to stabilize pH
most important ECF buffer
bicarbonate
normal values for HCO3, CO2 and pH
HCO3= 24 (22-26)
CO2= 40 (35-45)
pH= 7.40 (7.35-7.45)
what to carry H+ out into urine
ammonia (regulated)
also a bit of phospahte
where is ammonia made
proximal tubule
then secreted into tubular urine
ammonium reaborbed
NH4+ reabsorbed in thick ascending limb
pH of tubular urine along tubule
what happens in collecting duct and via what
continues to decrease (get more acidic)
NH3 goes into acidic collecting duct and trapped as NH4+ and eliminate H+
how does 80% of HCO3 get reabsorbed in proximal tubule
not directly (bc not permeable to luminal membranes)
combines with H+ to make H2CO3 via carbonic anhydrase and then dissociate to CO2 and H2o
then secrete H+ via Na/H countertrasnprot
production of new HCO3 via what amino acid and what process
in PCT make new bicarbonate and ammonia
from glutamine metabolism
ammonia to carry H+
gluconeogenesis – PEP from
glutamine is converted to
glucose
how to excrete lots of acid at pH of 4.5 and not too acidici
buffer with phospahte and ammonium
how to make urine acidic
which ion
which part
in collecting duct
H+ ATPase
and H2CO3 dissociate to HCO3 and H+
produce ammonium if ECF to acidic. where
PCT
urinary buffer
ammonia in PCT (to balance H+)
alpha and beta intercalated cells in collecting duct impacts
alpha (acidosis) secret H+, reabsorb HCO3- (and exchange K+ for H+ too)
beta (alkalosis): secret HCO3, absorb H+
acidosis vs alklosis
acid:: <7.35 pH
alk: >7.45 pH
respiratory acidosis
examples
pCO2 >45
hypoventilate –> decrease pH
not exhaling CO2 enough
apnea, obstructive lung disease, V/Q mismatching, right to left shunts
respiratory alkalosis
examples
pCO2 <35mmHg
hyperventilate –> increase pH
anxiety, aspirin, stroke, oxygen deficiency from high altitude or pulmonary disease
metabolic acidosis causes
low pH from loss of HCO3- or cant deal with new non-volatile acids
kidney failure to excrete metabolic acids (renal tubular acidosis)
form excess metabolic acids (diabetes, lactic acid)
add metabolic acids via ingestion (aspirin)
loss of base from body fluids (diarrhea, vomit)
metabolic alkalosis examples
increase HCO3- (or loss of H+)
diuretics, excess aldosterone, vomit, alkaline drugs
how do kidneys and lungs response if respiratory or metabolic alkalosis/acidosis
i.e. if respiratory acidosis then kidneys will excrete more H+
respiratory alkalosis then kidneys increase HCO3- excretion
ie. if metabolic acidosis alveolar hyperventilate so kidneys can increase H+ excretion
anion gap
normal: 10-12mmol/L
from Cl- and HCO3-
to find cause of metabolic acidosis –> if too high might have too many acids i.e. ketones, lactate, salicylates (conjugate bases)
causes of normal and high anion gap for metabolic acidosis
normal: diarrhea, renal tubular acidosis
high: uremia, lactic acid, ketoacidosis, methanol intoxication
where is most of potasium
intracellular
dont want extraceullarl
what 5 things shift potassium into cells
insulin (via Na+/K+ pump post prandial)
aldosterone
beta-adrenergic stimulation (NE, and epinephrine increase NA/K pump)
acid base imbalance (alkalosis shift K+ into cells, acidosis is out)
hyperkalemia (an increase in K+ in ECF shifts in via na/k pump)
what 3 things shift potassium out of cell
cell lysis
strenuous exercise
increase ECF osmolarity
acidosis
early vs late K+ shifts
early: Na/K pump activated by insulin, catecholamines, aldosterone
late: aldosterone via principal cells for renal excretions of K+
PCT absorbption of k+
65%
K+ handing in tubules
reabsorb 90%
in distal nephron secrete it depending on aldosterone and pH
K+ in PCT
reabsorb, link to Na+ and H2O (solvent drag)
ROMK channel on basolateral side
–> via decerase intraceullar ATP
–> also increase Na/K pump
K+ in thick ascending limb
K+ and Cl- permeable, paraceullar
NKCC channel pull K+ into cell
K+ in dif parts of tubule
PCT- ROMK channel
thick ascending limb: NKCC channel
distal: principal cells and alpha itnercalated, ENaC channel
K+ in distal nephon
principal cells
aldosterone fro K+ secretion and Na+ reasborb
increase ENaC, Na/K pump
KCC transporter
alpha intercalated cells rescue K+ if hypokalemia
(H+/K+ countertrasnport via ATP, alkalosis)
potassium excretory region
Most daily variation in potassium excretion is
caused by changes in potassium secretion in
distal convoluted tubule and early collecting
tubules/ducts
cells for K+ and Na+ fine-tune via aldosterone
principal cells in collecting duct
also alpha intercalated cells
luminal Na+ and K+ secretion
principal cells
secrete K+ and absorb Na+ in collecting duct
increase K+ secretion
osmotic diuresis, volume
expansion, loop diuretics
Na+ depreviation
increases aldosterone secretion
but K+ doesnt drop that much because theres decreasedGFR –> slow tubular fluid delivery –> less K+ washout
pH impacting K+
alkalosis increases K+ transport into cells (hypokalemia)
acute acidosis reduced K+ secretion, but chronic increases it
