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Review primary disorders of metabolic/respiratory acidosis and metabolic/respiratory alkalosis.

Metabolic acidosis: decreased HCO3-, decreased pCO2 compensation
Metabolic alkalosis: increased HCO3-, increased pCO2 compensation.
Respiratory acidosis: increased pCO2, increased HCO3- compensation
Respiratory alkalosis: decreased pCO2, decreased HCO3- compensation


What are three ways of calculated compensation for metabolic acidosis?

1. Each 1 mEq/L decrease in HCO3- should have 1.2 mmHg decrease of pCO2
2. pCO2=1.5xHCO3- + 8 (+/-)2
3. pCO2= last 2 digits of pH


How can you tell if its a mixed metabolic and respiratory disorder?

-If there is deviation from the expected result (the expected magnitude and direction of compensation of the primary disturbance), then it is a mixed disorder.


What are 4 general causes of metabolic acidosis? What falls under each general cause.

1. Ingestion of acid
-ethylene glycol
-salicylic acid
2. Endogenous generation of acid
-lactic acidosis
-ketoacidosis: DM or EtOH
3. Defective acid excretion
-Renal failure
-distal renal tubular acidosis (problem in handling of acid load, NH4+ genesis)
4. Loss of alkali
-proximal RTA (problem in PT handling HCO3- reabsorption)


How do you calculate serum anion gap? Why is this significant?

-Serum anion gap is a conceptual gap since not all anions and cations are measured
-Serum anion gap=unmeasured anions-unmeasured cations = Na-(Cl+HCO3)
-normal 8-12 (due to albumin)
-unmeasured anions: albumin, PO4, SO4, lactate, pyruvate
-unmeasured cations: K, Ca, Mg, immunoglobulins*


What is the ddx for high anion gap metabolic acidosis?

-diabetic ketoacidosis
-iron and isoniazid
-lactic acidosis
-ethylene glycol and ethanol
-rhabdomyolysis and toluene abuse


What causes anion-gap acidosis?

-For example: in lactic acidosis, lactic acid generates H+ and Lactate-
-the H+ is buffered by bicarbonate, and lactate is the unmeasured anion produced


How do you calculate serum osmolal gap? What is it used for?

Osmolal gap=measured Sosm-Calculated Sosm
-Calculated Sosm: 2Na+glucose/18+ BUN/2.8
-normal is <10 mOsm/kg
-use the serum osmolal gap when you suspect toxic ingestion


What are common ddx in serum osmolal gap acidosis?

-Ethanol, ethylene glycol, propylene glycol, methanol toxic ingestion causes high osmolal gap and + anion gap
-isopropanol causes high osmolal gap and negative anion gap
-salicylates cause normal osmolal gap and +anion gap acidosis


What are main causes of non gap metabolic acidosis?

-RTA and diarrhea


What are types of renal tubular acidosis?

-Proximal Type 2: defective handling of HCO3- reabsorption. Has decreased serum K+, urine pH>5.5, high urine NH4+ and HCO3-.
-Distal Type I "Classic distal": Decreased H+ secretion. low serum K+, urine pH>5.5, low urine NH4+ and HCO3-
-Distal Type 4 Hyporeninemic hypoaldosteronism: lack of response to aldosterone or hypoaldosteronism. inadequate ammoniogenesis. high serum K+, Urine pH<5.5, low urine NH4+ and HCO3-


What are causes of RTA?

1. Proximal Type 2
-most common: multiple myeloma and heavy metals
2. Distal Type 1
-most common: autoimmune-SLE and Sjogrens
-medullary sponge
3. Distal Type 4
-sickle cell
-obstructive nephropathy


What are the general causes of metabolic alkalosis? Also specific causes?

1. Ingestion of alkali
-citrated blood (from blood transfusion, citrate is added to blood to prevent clotting)
2. Loss of Acid-GI loss
-NG suction
3. Loss of Acid- Renal loss
-diuretics "contraction alkalosis"
4. Cellular Shift
-decrease in K+: K+ exits cell and H+ enters cell


What is the ddx of hyperaldosteronism?

Hypokalemia, metabolic alkalosis and HTN
1. High aldosterone high renin
-Renal artery stenosis (decreased perfusion-->increase renin)
2. High aldosterone low renin
-Primary hyperaldosteronism
-glucocorticoid-remediable aldosteronism (GRA)
3. Low aldosterone
-Syndrome of apparent mineralocorticoid excess (AME)


What is required in the maintenance of alkalosis?

-impairment of renal excretion of excess bicarbonate even if origin of alkalosis was not renal
1. effective circulating volume depletion:
-increased PT HCO3 reabsorption
-increased distal Na reabsorption
2. Renal failure


Describe the pathogenesis of contraction alkalosis.

Loss of Cl- and water in excess of HCO3-
-There is failure of renal HCO3- excretion due to:
a. PT tubule Na+ reabsorption with HCO3-
b. secondary hyperaldosteronism with distal tubule H+ secretion


If the diagnosis is not obvious from history, may have cryptogenic metabolic alkalosis. How do you diagnose based on volume status and urine Cl-?

1. Hyperaldosteronism
-increased volume status, Urine Cl->40 mEq/L
-high Cl- in urine because of aldosterone escape, excretion of Na and Cl in urine. Pressure natriuresis.
2. Surreptitious vomiting, Urine Cl40 due to Cl- loss from diuretic


In the treatment of metabolic alkalosis, which conditions are saline-response and which are saline-resistant?

Saline responsive
-vomiting/NG suction
-edematous states
-renal failure