Unit 8 - 5 Scheme

Front 1

how do buffers work

Back 1

locks up excess H ions
transforms strong acids -> weak acids which does not dissociate H as readily

Front 2

hemoglobin as a buffer

Back 2

while its intracellular, rbc are very permeable; histidine on hg has a dissociable protein

Front 3

plasma proteins buffers

Back 3

histidine is also the source o ftheir buffering

albumin, immunoglobulins, hormone binding proteins

Front 4

Phosphate buffering system

Back 4

phosphoric acid can give up 3 protons, limited buffering capacity

Front 5

main buffer intracellularly

Back 5

proteins (histidine) (best) and phosphates (less) - bound up in ATP

Front 6

conc of bicarb in blood

Back 6

24 in serum; freely filtered so conc in filtrate is 24

Front 7

how is bicarb reabsorbed

Back 7

dissociates into C02 and H20, C02 reabsorbed + H20 - CA -> HC03 (reabsorbed) + H secreted

Front 8

H gradient at distal tubule

Back 8

10000:1 = Renal lumen:Intracellullar

Thus uses ATP to pump extra protons out into lumen

if a person had a dz of collecting tubules they could not pump out the extra acid at the end

Front 9

where does ammonium come from

Back 9

glutamine -> glutamate -> a-ketoglutarate (stripping down carbons releases NH4s)

ammonia pumped into tubular lumen countertransported w/ sodium

Front 10

major cation in cell

Back 10

potassium;

sodium always wants to enter cells and cells keep pumping them out

Front 11

anion gap

Back 11

Na - Cl + HC03 = 12

144 - 108 - 24 = 12 mEq/L

Front 12

PC02 = ?

Back 12

PC02 = 1.5(HC03) + (8 +/- 2)

Front 13

normal serum osmolarity

Back 13

300

Front 14

normal chlorine levels

Back 14

108

Front 15

normal bicarb

Back 15

24

Front 16

anion gap vs delta anion gap

Back 16

what the anion gap - normal anion gap = 30 - 12 = 18

You add the anion gap to what his bicarb was before (6 + 18 = 24; since this is normal there was no other pre-existing or ongoing process)

Front 17

Aldosterone Deficiency

Back 17

Metabolic acidosis;


These patients will have a decreased reabsorption of Na+ in the distal tubule, a decreased excretion of K+ and a decreased excretion of H+. This condition will result in hyperkalemic metabolic acidosis.

Front 18

Diarrhea

Back 18

Metabolic acidosis


The loss of HCO3- in the stool results in a metabolic acidosis.
The loss of HCO3- is replaced by Cl-therefore the anion gap remains the same. This is called non-anion gap acidosis or hyperchloremic acidosis.

Front 19

Diabetic ketoacidosis

Back 19

Metabolic acidosis


In severe diabetics, the increased plasma concentration of Keto-acids (acetoacetate and beta-hydroxybutyrate) produces the acidosis.
The HCO3- levels decrease as a result of the acid that is produced and the anion gap increases.

Front 20

Carbonic anhydrase inhibitors

Back 20

Metabolic acidosis


The administration of a carbonic anhydrase inhibitor such as Diamox will result in a mild metabolic acidosis. The drug prevents the proximal reabsorption of HCO3-. This will increase the distal delivery of water and Na+ and as a result can increase K+ excretion.

Front 21

ESRD

Back 21

Metabolic acidosis


Without the kidney the body cannot rid itself of hydrogen and the pH decreases significantly, along with HCO3-. The patients will compensate with increased ventilation resulting in HCO3- levels that can decrease below 10 mEq/l.

Front 22

Anesthesia
Sedative (morphine, excessive ETOH)
Cerebral trauma (closed head injury)

Back 22

Respiratory acidosis

Front 23

mechanical respiratory acidosis

Back 23

Mechanical ventilation that is not producing an adequate air exchange and is causing the patient of retain CO2.

Front 24

Metabolic Alkalosis secondary to diuretics

Back 24

Increased distal delivery of sodium can increase the excretion of both K and H. If the patient becomes volume constricted, they will release aldosterone. The aldosterone will increase distal K excretion giving the patient hypokalemic metabolic alkalosis.

Front 25

Vomiting

Back 25

Metabolic alkalosis


You will lose HCl from the stomach. This can result in a metabolic alkalosis.
If the increased HCO3- exceeds its Tm, HCO3- along with Na+ is lost in the urine.
The final result is a volume constriction, increased aldosterone, and increased K+ excretion.
Treatment is with saline and K+

Front 26

Hyperaldosteronism

Back 26

Excess aldosterone will increase Na+ reabsorption in the distal nephron. It will also increase the excretion of both K+ and H+. This will result in hypokalemic metabolic alkalosis.

Front 27

two mcc of respiratory alkalosis

Back 27

hyperventilation due to increased altitude or hysteria

kidney secretes/excretes more HC03

compensation can be complete

Front 28

Hypoxia

Back 28

Respiratory alkalosis

Pneumonia, high altitude, hypotension, severe anemia, CHF

Front 29

Voltaile acid

Back 29

The lungs and kidneys are both involved in
maintaining acid-base homeostasis. CO2
delivered by the blood is excreted by
the lungs. It is known as a “volatile” acid.
Metabolism results in up to 15,000 mMoles
of CO2 daily.

Front 30

fixed acids

Back 30

A larger daily source is the metabolism of dietary sulfur-containing amino acids. These result in about 50-100mEq of so-called “fixed” acids, which are excreted by the kidneys.

Front 31

Acids taste sour, are corrosive to metals, change litmus (a dye extracted from lichens) red, and become less acidic when mixed with bases.
Bases feel slippery, change litmus blue, and become less basic when mixed with acids.

Back 31

eh

Front 32

hydrogen ions in pure water

Back 32

1x10&-7 ions; varies over 14 powers of ten, hence the arbitrary pH scale

Front 33

most important extracellular buffer

Back 33

This is the most important extracellular buffer, in quantity and by virtue of its dual
regulation by the lungs and the kidneys.

Front 34

why is hg considered an extracellular buffer

Back 34

Although strictly speaking it has an intracellular location, the permeability characteristics of the red blood cell membrane allow
it to be considered an extracellular fluid buffer. Its buffering
capacity comes from the side group of the amino acid histidine, which has a dissociable proton:

Front 35

what is the source of plasma proteins buffering capacity?

Back 35

histidine

Plasma proteins with buffering capacity consist albumin, immunoglobulins, and hormone-binding proteins.

Front 36

phosphate buffering system (extracellular)

Back 36

Phosphoric acid in solution can give up three protons. It has a limited bufering capacity.

Front 37

two intracellular buffers

Back 37

phosphate and proteins (note hemoglobin is considered ecb bc of rbc permeability)