Acid Base

Front 1

Renal tubular acidosis 1

Back 1

- distal tubule
- can't secrete H+
- increase urine pH **
- low HCO3

Front 2

Renal tubular acidosis 2

Back 2

-proximal tubule can't reabsorb HCO3
-increase bicarb in urine* low urine pH during HCO3 loss
- levels out usually around blood HCO3= 15, (equilibrium) and less HCO3 is lost, urine pH becomes normal

Front 3

Renal tubular acidosis 4

Back 3

- decreased aldosterone secretion
- hyperkalemia causes decreased NH3 production, acidosis
-slightly increased creatinine and BUN

Front 4

Anion gap
- how to figure out
- when it its present/ when its not present

Back 4

Na - (Cl- + HCO3)
sometimes present during metabolic acidosis
- not present during diahhrea
- is present when there is lactic or ketoacidosis
- during renal failure, there is decreased NH4 excretion, decreases the amount of new bicarb formed, anion gap
- tubular problems - normal anion gap

Front 5

effect of vomiting

Back 5

HCO3 produced by the stomach parietal cells doesn't make it to the intestine, remains in blood --> alkalosis!

Front 6

effect of diarrhea

Back 6

there is a lot of HCO3 secretion in GI, if you increase the rate of GI mvmt (diarrhea), then there is an increased loss of HCO3 --> metabolic acidosis w/o gap

Front 7

factors that cause K+ shift from ECF to ICF

Back 7

-insulin
-beta adenergic agonists
-alkalosis

Front 8

causes of alkalosis & maintenence

Back 8

- vomiting
- diuretic use
maintenance:
- hypokalemia - causes an intracellular acidosis, stimulates NH4 excretion and HCO3 reabsorption
-volume depletion or excess aldosteronism - promotes aldosterone - stimulates H+ pump in collecting tubule, causing increased HCO3 production
AII --> na/H exchanger in prox tubule

Front 9

Buffer

Back 9

minimizes change when a strong acid or base is added to solution

Front 10

PKa

Back 10

at this pH the system has maximal buffering capacity

Front 11

volatile acid

Back 11

CO2, major acid produced by the body, eliminated as a gas by the lungs

Front 12

Fixed acids
- definition
-types, examples

Back 12

- Acids that must be buffered by the body until they can be excreted by the kidney; For every equivalent of fixed acid formed, one molecule of bicarb is lost (because it has to buffer it)
- inorganic, produced by protein and phospholipid breakdown: Hcl, sulfuric acid, phosphoric acid
- organic: lactate (hypoxia) and ketoacids (FA breakdown)

Front 13

isohydric principle

Back 13

H+ are in equilibrium with all the buffers all the time - there is an instantaneous reequilibration of acid load by with all buffer species present

Front 14

major extracellular buffers

Back 14

- CO2/HCO3
- proteins (histidine residues) - Hb & albumin
- bone

Front 15

intracellular buffer

Back 15

slower
phosphate, proteins

Front 16

titratable acid
- how its defined
- benefits

Back 16

- amt of fixed acid excreted by the kidneys
- for every equivalent of titratable acid excreted, one molecule of HCO3 is regenerated by the kidney epithelium and passed into the ECM

Front 17

ammonium ions
- where they are produced/ from what
- benefit

Back 17

- produced by the kidney from glutamine
- 1 glutamine --> 2 NH4 & 2 HCO3
- for every molecule NH4 that is excreted, one molecule of HCO3 is regenerated by the kidney

Front 18

HCO3 reabsorption in the proximal tubule

Back 18

- H+ is pumped into the lumen via the Na/ H antiporter, allows Na+ to flow down its conc gradient into the cell
- Na gradient limits the amt H+ being pumped out (no net H+ secretion)
o H enters the lumen, combines with HCO3 that has been filtered, cabonic anhydrase turns it back into CO2 and H2O which re-enters the cell (once in the cell, it is turned back into HCO3 and H+)
- bicarb is pumped out back into the blood via the Na/ HCO3 symporter (transports 3 bicarbs and 1 Na into the blood)
o net reabsorption of HCO3 and Na+
- Since there isn’t that much H+ in the lumen, CA is needed to push the equation (CO2 + H20 → HCO3+ H+) to the left to generate CO2

Front 19

common features: proximal and distal HCO3 reabsorption

Back 19

- CA is used
- H+ must be secreted into the lumen to create CO2
- CO2 enters the cell by simple diffusion
- HCO3- leaves the cell be facilitated diffusion

Front 20

HCO3 reabsorption in the distal tubule

Back 20

- an ATP H+ pump is used to pump H+ into the lumen which acidifies the urine; this also drives the reaction toward CO2 production
- bicarb is pumped back into the blood via the Cl-/ HCO3 exchanger

Front 21

Titratable acid excretion

Back 21

- same mechanisms that are used to reabsorb HCO3, except that when the H+ gets into the lumen, Phostate and other buffers are used
- one H+ is excreted
-one HCO3 is regenerated

Front 22

NH4 excretion

Back 22

2 H+ are consumed
2 HCO3 are regenerated
proximal tubular cells
regulated by acid load and K (hypokalemia stimulates and hyperkalemia decreases)

Front 23

acidosis vs acidemia

Back 23

acidosis = process that causes a pH decrease
acidemia = actual pH of the blood

Front 24

increased CO2 produced because

Back 24

exercise
fever
hyperthyroidism
anxiety
lung disease