ORGANIC lactic acid->lactic acidosis Ketoacids (b-Hydr/ acetoacetate) = DM, ETOH, Starvation INORGANIC HCL Ammonium cloride RAPIDLY DEVELOPING ACIDOSIS

Acid Base Flashcards by O lawformonde

Primary buffer

Bicarb = extracellular

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Secondary buffer

Intracellular

Hours

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3rd step

*Lungs = minutes to hours

*Renal base-then-acid excretion
Hours to days
If too high a load, overwhelms kidney

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Formula

H + HCO3- H2CO3 CO2 + H20

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Mechanisms of acidosis

increased acid production/load
decreased acid excretion
loss of bicarb ions

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Increased acid load

ORGANIC

lactic acid->lactic acidosis
Ketoacids (b-Hydr/ acetoacetate) = DM, ETOH, Starvation

INORGANIC
*HCL
*Ammonium cloride
RAPIDLY DEVELOPING ACIDOSIS

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Decreased acid excretion

Acid = mostly from metabolism of sulfur-containing amino a
H secreted to lumen (NH3to NH4) (HPO to
Ammonium excretion UPs dramatically in respons to acid
renal failure
incre?

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Renal failure

Decrease

up NH4
down HCO3
increase unmeasured anions

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Type 1 distal renal tubular acidosis

gfr preserved, urine pH=>5.3
less H+ secreted in tubular to combine with NH4 -> less excretion = Impaired H-ATPase pump
less carbonic anhydrase
up luminal permeability to H+
DISTAL tubule = more severe
1ary = congenital,
2ndary = Meds, Sjorgen’s syndrome, RA, SLE

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3rd mech acidosis

Loss of bicarb

Big tubule = Colon (diarrhea = rich in Bicarb + sodium. Na loss, Less HCO3, more Cl, unmeasured ions to not change)
small tubule = urethra (tube disfuction- proximal renal tubule acidosis type 2 renal tubular acidosis, Down Proximal Bicarb reabsorption, will have loss unless distal tubule makes up for it)

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Clin manifestations

Metabolic acidosis

*UP ventilation
*DOWN myocardial contractility (less pH 7.2)
*Ventr arrythmia
*down vascular resistance
*GI = N/V , ab pain, DIarrhea (especially DM)
MSK
*muscle weakness, osteomalacia, hypercalcuria
CNS
*lethargy, coma
INFANTS
*impaired bone growth, listlessness

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Serum Anion Gap

UA-UC = Na - Cl + bicarb

Anion gap = UA - UC =

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Anion gap

=Na - (Cl + HCO3)

*correct AG = (4.4-ablumin) - 2.5

AG normal = 10-12
12+ abnormal AG acidosis

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High anion gap metabolic acidosis

Citrate
*Uremia
Toulene
Ethanol

*DM/ETOH/Starve ketoacidosis
Iron
Methanol
Paraldehyde
*Lactate 
Ethelyne Glycol
Salicylate

*THESE ARE NOT INGESTED

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AG acidosis

CKD

*Dietary =>sulfate ions (not reabsorbed is secreted)

STAGE 2-3 = normal AGmetabolic acidosis (defective secretion/reabsorption)

Stage 4-5 CKD = high AG M acidosi
*retention of H ions + sulfate ion, less nephron mass/GFR

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AG acidosis

DM ketoacidosis

*Insulin deficiency = UP free fatty acid = acetone production

*Glucagon excess = altered hepatic metab
Free fatty acid to ketoacids

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DKA

Renal consequences

*insulin deficiency
*more K coming out of cells
OSMOTIC DIURESIS
*Loss of hypotonic fluid
*Loss of ketoa acid ions

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AG acidosis

Lactic acidosis

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byproduct of pyruvate acidosis
if lactate up = pyruvate inbalance, or down lactate utilization
DX = lactate level, venous pH down *upCO2 cuz DOWN pulmonary blood flow (hypoperfusion)
Tx : underlying disorder

DX Acid base

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1= acidemic/alkalemic?
2= primary disorder, respiratory/metabolic?
3=respiratory (acute/chronic?)
4=Metabolic (Anion gap?)
5= Mixed? Gap/nongap?
6= compensated? If not, why?

Delta gap

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Change in AG/Change in HCO3= 1 = change in bicarb CONSISTENT with change in AG

NO NON-ION GAP PROCESS

Alkalosis

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High extracelluar PH
Primary elvation of bicarb
Respiratory compensation

Proton loss =

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Increase in bicarb concentration

GI = n/v, adenoma, ..
renal = DIURETICS, …

Loop diuretic

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Up Na delivery to Principal cell, Tubular lumen more negative, H-+ pumped

Contraction alkalosis

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Lose fluid

*higher concentration bicarb = alkalosis

Alkalosis Add Bicarb

*Nabicarb *milk-alkali syndrome *hypercalcemia *renal Bicarb reabsorption *massive blood transfusion (citrate load) CHECK HISTORY

Bicarb reabsorption in nephron

Most PCT Can malfunction in other places *Na reabsorption = Bicarb reabsorption

Alkalosis Intracellular H movmenet

Hypokalemia = K moves out cell, H in Refeeding syndrome = up increase, H + K movement into cells

Maintanence of Met Alkalosis

*kidney can’t excrete HCO3 * hypovolemia/chloremia/kalemia * mineralocorticoid excess

Volume depletion Alkalosis

Nephron main job = reabsorb Na (bicarb comes with) * ang 2 increases Na-H exchanger * low pH in PCT ups bicarb reabsoprtion Free bicarb can’t bind with H to be excreted in cell to lumen, so goes into blood

Volume depletion Alkalosi

*2ndary hyperaldosteronism???

Alkalosis Cl- depletion

* decrease Cl to macula densa = 2ndary hyperaldosteronism * UP Hatpase to mained electroneurtrality * DOWN Clbicarb exchange in intercalated cells, bicarb reabsoprted into blod Giving chloride to volume depleted tx without tx volume Cl

Hypokalemia Alkalosis

* Up KHatpase = increase H secretion * UP KH transcellur exchagne = up H secretion * Up renal NH4 generation, Up Bicarb generation

Alkalosis

*Down ventilation *ventr arrythmia *ortho HypoTN *GI = N/V *MSK = cramping, tetany CNS = confusion, seizures

Alkalosis Cl responsive

* w/ Extracellular fluid volume contraction (conserve Cl) * urine CL <20 * Tx = NaCl (mabye K repletion)

Alkalosis Cl Resistant

* w/ extracellular fluid volume expansion , HTN * depletion NaCL NOT RESPONSIBLE * urine cl high/normal >40 * NaCl doesn’thelp * treat Dz

Metabolic Acidosis - Normal AG Causes

``` H yperalimentation A cetazolamide R enal Tubular Acidosis D iarrhea U tereral diversion (neobladder) P ancreatic fistula (bicarb loss)/ Post-hypocapnea S pironolactone ```

RTA type 2

* PROXIMAL - less severe * HCO3 wasting * urine pH = variable * 1ary = congenitall * 2ary = CA inhibitor, autoimmune dz, meds

RTA type 4

* Urine pH <5.3 * HYPER K * Aldosterone deficiency (congenital/meds), Tubular resistance to aldosterone (meds, tubulointerstitial dz)

Metabolic Acidosis = High AG Causes (ingestion + non-ingestion)

``` C itrate U remia T oluene E toh R enal failure/Rhabodomyelosis ``` ``` D iabetic ketoacidosis I ron / Infxn / isoniazide M ethanol P araldehyde L actate E thylene glycol S alicylate ```

Metabolic Acidosis - High AG Non-ingestion causes

* Uremia * Ketoacidosis * Lactic Acidosis (sceptic)

Metabolic Alkalosis often w/

* Hypo Cl * Hypo K * hypovolemia * high aldosterone (?)

Kidney H/HCO3 exchange

* excrete H to bring in HCO3 = PCT | * UP in high pCO2, hypovolemia, hypokalemia

Metabolic Acidosis = High AG Mech

* Acid in blood (H + anion) dissociates | * H to bicarb, then ion accumulates in serum

Metabolic acidosis = Normal AG

* lost Bicarb replaced by Cl- * AG normal, Cl serum high * diarrhea ,RTA II = loss of Na Bicarb (?)

Acid Base Flashcards

(44 cards)