Johns Hopkins Chapter 31 Acid-Base Disorders And Rta And Chapter 32 (Electrolyte Disorders)

Front 1

Anion gap is calculated as

Back 1

Na+ − (Cl− + HCO3- )

Front 2

The normal anion gap

Back 2

12 ± 2

Front 3

components of anion gap

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made of phosphates, sulfates, organic acids, and negatively charged plasma proteins

Front 4

labs to consider with HAGMA

Back 4

evaluation of serum ketones, serum lactate, toxicology screen, and salicylate level should be considered

Front 5

define MUDPILES

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methanol, uremia, DKA or alcoholic ketoacidosis or drugs (metformin, NRTIs), Phosphate or paraldehyde,ischemia or INH or iron toxicity, lactate, ethylene glycol, starvation or salicylatse

Front 6

in a normal AGMA, what is the anion that is increased

Back 6

chloride

Front 7

mnemonic for most common causes of normal AGMA

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DURHAM - diarrhea, ureteral diversion, RTA, hyperalimentation, Addison disease, acetazolamide, ammonium chloride, miscellaneous (chloridorrhea, ampho B, toluene etc)

Front 8

helpful in evaluating normal anion gap metabolic acidosis to differentiate renal tubular acidoses (RTAs) from other causes of normal anion gap metabolic acidosis

Back 8

calculation of urine AG

Front 9

how does urine AG help narrow cause of normal AGMA?

Back 9

Normal kidney response to acidosis is to excrete acid in the form of NH4+, which is balanced by increases in urine chloride, so urine chloride is a marker of urine acid excretion. In type 1 or type 4 RTA, NH4+ excretion does not occur, and urine chloride is low.

Front 10

Formula for urine anion gap:

Back 10

Urine (Na + K − Cl)

Front 11

how to interpret urine anion gap?

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NAGMA without RTA, <0; if >0, type 1 or type 4 RTA is likely

Front 12

differentials for low AGMA

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hypoalbuminemia, multiple myeloma, ingestion of bromide

Front 13

how can one determine if MA is caused by more than one process?

Back 13

compare incraese in AG with decrease in HCO3, in pure AGMA, decrease in HCO3 = inc in AG; if HCO3 dec signif more than AG inc then coexisiting NAGMA

Front 14

how does one determine the osmolar gap?

Back 14

difference between the measured osmolality and the calculated osmolality; in normal host, difference between measured and calculated osmolality is less than 10

Front 15

implication if osmolar gap is >10?

Back 15

there are extra osmotically active compounds in the blood;

Front 16

osmotically active toxins and their associated symptoms

Back 16

methanol (associated with papilledema and retinal hemorrhages), ethylene glycol (associated with calcium oxalate crystals in the urine), toluene (presents first with anion gap metabolic acidosis, then metabolized resulting in normal anion gap metabolic acidosis)

Front 17

does isopropyl alcohol associated with an acid-base disorder?

Back 17

Isopropyl alcohol ingestion also results in an osmolar gap, although no acid-base disorder is associated

Front 18

What is Winter's formula?

Back 18

formula to predict PCO2 (1.5 HCO3 + 8 +/- 2 = PCO2

Front 19

what if winter's formula measured PCO2 is equal to actual PCO2?

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If the Pco2 is less than predicted, second disorder is respiratory alkalosis; If the Pco2 is higher than predicted, second disorder is respiratory acidosis

Front 20

two states favor maintenance of alkalosis by the kidney

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volume depletion and hypermineralocorticoid states

Front 21

normal respiratory compensation in primary metabolic alkalosis

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Pco2 rises 0.5 to 1 mm Hg for every 1-unit increase in serum HCO3- from a baseline of 24 mmol/L

Front 22

maximum Pco2 in compensation

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55-60

Front 23

Causes of a saline-responsive alkalosis (urine chloride <10 mEq/L)

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NG suction, vomiting, diuretics, post hypercapnia

Front 24

Causes of a saline-resistant alkalosis (urine chloride >10 mEq/L)

Back 24

Primary aldosteronism, Cushing disease, renal artery stenosis, renal failure plus alkali administration; Hypomagnesemia, severe hypokalemia, Bartter syndrome, NaHCO3 administration, licorice ingestion

Front 25

Prediction of pH and HCO3- in respiratory acidosis

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Acute: for every 10 mmHg increase in PCO2, pH decreases by 0.08 and serum HCO3 increases by 1; in chronic: 10:0.03:3-4

Front 26

Prediction of HCO3- in respiratory alkalosis

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Acute: for every 10 decrease in PCO2, HCO3 decreases by 2.5; in chronic, 10:5

Front 27

maximum compensation of HCO3

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15

Front 28

DDx if respiratory alkalosis

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Systemic (sepsis, salicylates, liver failure, hyperthyroidism, pregnancy, high altitude, hypotension), central causes (CVA, tumor, infection, progesterone, anxiety,fever) pulmonary (PE, RLD, hypoxemia)

Front 29

RTA type: Distal renal tubular defect in NH4+ excretion

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type 1

Front 30

RTA type: Proximal tubular defect in rHCO3- esorption

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type 2

Front 31

RTA type: Hyporeninemic hypoaldosteronism

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type 4

Front 32

which RTA responds to NAHCO3

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type 1

Front 33

which RTA presents with high serum potassium?

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type 4, (type 1 and 2 have low K)

Front 34

which RTA is unable to acidify urine to pH < 5.5

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type 1

Front 35

how is RTA Type 1 diagnosed?

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Diagnosis is made on clinical grounds and confirmed by ammonium chloride (NH4Cl) administration, which will result in worsening systemic acidosis without drop in urine pH below 5.5; UAG >0

Front 36

treatment of type 1 RTA

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NaHCO3-

Front 37

how is type 2 RTA diagnosed?

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Administration of NaHCO3 results in alkaline urine despite systemic acidosis because renal HCO3- resorption does not occur

Front 38

treatment of type 2 RTA

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not indicated

Front 39

distinguishing feature of type 4 RTA

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inability of the kidney to excrete potassium, leading to high serum potassium (types 1 and 2 RTAs are usually hypokalemic)

Front 40

most common cause of type 4 RTA

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DM

Front 41

other common causes of type 4 RTA

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mineralocorticoid deficiency (including Addison disease); therapy with NSAIDs, heparin, or angiotensin-converting enzyme inhibitors

Front 42

treatment for type 4 RTA

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if indicated, may give mineralocorticoid or furosemide

Front 43

Number of particles (osmoles, Osm) dissolved in solution

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Osmolality

Front 44

Predominant effective osmole

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sodium

Front 45

Ineffective osmole (does not induce fluid shift)

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urea

Front 46

formula for estimating serum osmolalit

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2Na + BUN+ glu

Front 47

aldosterone effects

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Major actions are to stimulate Na+ reabsorption and potassium (K+) secretion in the renal collecting tubule. Hydrogen (H+) secretion is increased due to the electronegative lumen generated by Na+ reabsorption

Front 48

actiona of ADH

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increases water reabsorption from the collecting duct lumen back into the circulation

Front 49

define pseudohypernatremia

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Hyperlipidemia and hyperproteinemia can cause an artifactual decrease in measured serum Na+. The true serum Na+ concentration is normal.

Front 50

how does high osmolality cause hyponatremia

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Osmotically active particles may pull water into the extracellular space, creating a dilutional hyponatremia (gucose, mannitol, maltose)

Front 51

urine indices suggesting hypovolemia / hypervolemia

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UNa <10 FENA <1%, Uosm>Posm

Front 52

urine indices Suggestive of euvolemia or recent diuretic use

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UNa >20 mEq/L

Front 53

findings in SIADH

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euvolemic, UNa >20 UOsm>POsm

Front 54

causes of SIDH

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pulo disease, SCLC, infections (meningitis, enceph, abscess, VZV) vascular (SAH< CVA, temporal arteritis) severe n/v; drugs (SSRIs narcotics cyclophosphamide, chlorprpamide) ecstasy ingestion< HIV, prlactinoma, waldenstrom, Shy-Drager syn, DT, oxytocin, marathon runner

Front 55

treatment of hypoosmolar hyponatremia

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hypovolemic (NS) hypervolemic (fluid restrict, diurese, dialyze), euvolemic (fluid restric, consider V2 receptor antagonists, address medical condition)

Front 56

MOA of vaptans

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Block the V2 ADH receptor in collecting duct; Results in aquaresis without significant natriuresis

Front 57

an older therapy to antagonize ADH action that is rarely used

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demeclocycline

Front 58

treatment for seizure or obtundation in hyponatremia

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Raise Na+ concentration 1 to 2 mEq/L/hr with 3% saline until symptoms abate

Front 59

rate of correction for chrnoic hyponatremia (>24-48h)

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Raise Na+ concentration 0.5 to 1 mEq/L/hr and no more than 8 to 10 mEq/L in 24 hours

Front 60

rate of correction for acute hyponatremia (<24-36h)

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Can raise 1 to 2 mEq/L/hr usually without the need for 3% saline unless severe CNS symptoms are present

Front 61

clinical presentation of hypernatremia

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restlessness, irritability, lethargy, muscle twitching, hyperreflexia, spasticity, and, in severe cases, intracranial hemorrhage

Front 62

describe DI

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Insufficient ADH action leads to polyuria and free water loss (Central fro mlack of ADH production, nephrogenic from renal resistance to ADH)

Front 63

major causes of DI

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pituitary tumor or apoplexy, lithium, hypercalcemia, hyperkalemia, and pregnancy

Front 64

serum Na and Uosm findings in DI

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High-normal to high serum Na+ concentration with low urine osmolality (<300 mOsm/kg)

Front 65

formula for free water deficit

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TBW x [(Na/140)-1)]

Front 66

rate of correction for hypernatremia

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Decrease serum Na+ concentration approximately 0.5 mEq/L/hr and no more than 8 to 10 mEq/L in 24 hours

Front 67

what causes increased renal K excretion

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aldosterone, increased Na and water delivery to distal nephron

Front 68

serum K levels and correlation with clinical SSx

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tetany or rhabdomyolysis at K+ less than 2.5 mEq/L and then paralysis when less than 2 mEq/L

Front 69

hypokalemic periodic paralysis etiology

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Autosomal dominant inheritance—mutations in CACNA1S (Ca2+ channel) or SCN4A (Na+ channel)

Front 70

acquired form of hypokalemic periodic paralysis

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from thyrotoxicosis

Front 71

lab findings in renal etiology of K wasting

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Urine K+ concentration greater than 25 to 30 mEq/day or spot greater than 20 mEq/L in the presence of normal urine output

Front 72

lab findings in extrarenal etiology of K wasting

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Urine K+ concentration less than 25 to 30 mEq/day or spot less than 15 mEq/L in the presence of normal urine output

Front 73

in hypokalemia, at what levels to give PO or IV potassium?

Back 73

3-3.5 - oral repletion; <3 IV potassium with cardiac monitorring

Front 74

serum K levels in hyperkalemia and associated clinical manifestations

Back 74

Greater than 6.5 mEq/L: Progressive weakness, muscle aches, areflexia, paresthesias, electrocardiogram (ECG) changes

▪ Greater than 7 mEq/L: Paralysis, respiratory failure, life-threatening arrhythmias

Front 75

define peaked T waves

Back 75

height .5 mm

Front 76

ECG findings in hyperkalemia correlated to the level of hyperkalemia

Back 76

6 to 7 mEq/L: Peaked T waves (height >5 mm); 7 to 8 mEq/L: Widening of QRS complex, prolonged P–R interval with flattening of P wave; Greater than 8 mEq/L: Atrial standstill, progressive QRS widening and fusion with T wave to form sine wave pattern, ventricular tachycardia and fibrillation

Front 77

causes of pseudo hyperkalemia (3)

Back 77

Hemolysis during venipuncture; Leukocytosis greater than 100,000 cells/mm3 or thrombocytosis greater than 500,000 cells/mm3. Plasma (as compared to serum) K+ should be normal. Familial pseudohyperkalemia (autosomal dominant)

Front 78

etiology of hyperkalemic periodic paralysis

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Autosomal dominant inheritance—mutation in SCN4A Na+ channel

Front 79

how to evaluate for mechanisms of impaired renal excretion of potassium?

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Calculate transtubular potassium gradient ; Uk/Pk / Uosm/Posm

Front 80

interpretation of TTKG numbers

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Value less than 5 suggests hypoaldosteronism or K+ secretory defect in setting of urine Na+ greater than 25 mEq/L and urine osmolality greater than plasma osmolality

Front 81

when to treat with calcium gluconate in hyperkalemia

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K+ greater than 6.5 mEq/L or in the presence of ECG changes

Front 82

how much SPS to give in hyperkalemia?

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One gram binds approximately 1 mEq K+ in vivo.

Front 83

SPS will not work in these patients

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SPS is ineffective in patients with prior colectomy