Nephrology Small Group Questions Flashcards
JD has slowly progressive chronic kidney disease (CKD). The results of 24 hr urine collections in 2008 and 2012 are given below. JD was on a similar diet and fluid intake on both occasions.
2008 2012
body weight (kg) 70 70 serum creatinine (mg/dl) 1.0 2.0 urine flow rate (ml/min) 1.0 0.8 urine creatinine (mg/dl) 100 125
What is the creatinine clearance (GFR) in 2008?
100 mL/min
Cx = (Ux x V) / Px
What does an increase in serum creatinine from 1 mg/dL to 2 mg/dL imply?
Serum creatinine doubled so GFR has decreased by approx 50% due to a loss of functioning nephrons
How is the amount of creatinine produced and excreted calculated?
for creatinine, production = urinary excretion
What determines the amt of creatine a person produces?
muscle mass (differs w/ gender and age)
What determines the amt of creatine in a person’s plasma?
muscle mass and GFR
JD has slowly progressive chronic kidney disease (CKD). The results of 24 hr urine collections in 2008 and 2012 are given below. JD was on a similar diet and fluid intake on both occasions.
2008 2012
body weight (kg) 70 70 serum creatinine (mg/dl) 1.0 2.0 urine flow rate (ml/min) 1.0 0.8 urine creatinine (mg/dl) 100 125
What is the filtered load of creatinine in 2008? In 2012?
FL = GFR x Px
2008: 1 x 100 = 1 mg/min
2012: 2 x 50 = 1 mg/min
Why does creatinine provide a good estimate of GFR?
it is not reabs and only partially secreted (<10%)
*aka the entire filtered load gets excreted
If there has been no change in _______ then a change in serum creatinine conc is due to a change in GFR
muscle mass
How is GFR estimated without 24 hr urine collections? What is a limitation of using this to est GFR?
(140 - age) / Serum Creatinine
(x 0.85 if the pt is female)
limitation: only valid in steady state conditions such as CKD. Invalid in acute kidney injury with abrupt changes in GFR (un-steady state conditions)
Describe the stages of kidney disease (1-5)
1: damage with normal or elev GFR (>90)
2: damage with mildly dec GFR (60-89)
3: moderate dec in GFR (30-59)
4: severe dec GFR (15-29)
5: kidney failure (<15 or dialysis)
What is GFR in which you start to see physical abnormalities?
60 mL/min/1.73m2
Healthy people with 1 kidney or polycystic kidney disease are considered to be stage ___ of CKD
1
An inc in serum creatinine always implies kidney disease.
F: a male body builder can have a SCr of 1.3 with stage 1 disease while a 50 year old woman can have a SCr of 1.3 with stage 3
MUSLCE MASS determines SCr for each indiv
*they have different GFRs –> diff stages of CKD
What effect does urine flow rate have on GFR?
No effect. A change in UFR is simply a reflection of the amt of water which is reabs NOT the amt of water that is filtered at the glomerulus.
T or F: GFR changes with the urine flow rate
F: GFR remains constant at different flow rates
What effect does an inc urine flow rate have on creatinine clearance?
No effect. As flow rate inc the conc of creatinine in the final urine is decreased (bc less water has been reabs) but the amount in the urine is not changed.
What is a clearance ratio? What information does it provide?
= Cx / Clearance of creatinine
It tells you the renal handling of a substance. The closer to 1 the ratio its, the substance is handled more like creatinine (no reabs and little secretion)
What does a low clearance ratio (<1) indicate?
the substance is highly reabs
What does a high clearance ratio (<1) indicate?
the substance is highly secreted
What happens to the urine flow rate and fractional excretion of Na after a hemorrhage?
Both will decrease. Na and H2O to be retained due to hypovolemic state (renin, sympathetic activ, etc)
–> inc osmolarity of urine due to dec H2O excretion
renal blood flow decreases but GFR remains normal (autoreg mech)
T or F: in a mild to moderate hypovolemic state, GFR will decrease.
F: auto-regulatory mechanisms keeps it at normal levels
T or F: in a mild to moderate qhypovolemic state, RPF will decrease.
T
What happens to the clearence of urea in a mild to moderate hypovolemic state?
it will decrease bc urea follows water (in hypovolemia, water reabs increases therefore urea reabs will inc too)
What needs to be checked when a pt is started on a drug that is excreted by the kidneys?
GFR (which assesses renal function). Need to adjust the dosing of the drug to reflect kidney function
(dec GFR/clearance = dec dosage)
A 58 year old female was admitted with moderately severe congestive heart failure. Physical examination revealed bibasilar rales, cardiac enlargement, neck vein distention, hepatomegaly, and 3+ pitting pretibial edema. The serum sodium concentration was 121 meq/l; BUN was 30 mg/dl and hematocrit 33%.
What does the information presented above tell you about total body exchangeable sodium?
nothing can be determined from looking at the serum Na conc in isolation
–> the pitting edema, cardiac enlargement, JVD, and hepatomegaly indicate inc ECFV which requires an inc in exchangeable Na.
A 58 year old female was admitted with moderately severe congestive heart failure. Physical examination revealed bibasilar rales, cardiac enlargement, neck vein distention, hepatomegaly, and 3+ pitting pretibial edema. The serum sodium concentration was 121 meq/l; BUN was 30 mg/dl and hematocrit 33%.
How do you account for the low serum sodium concentration? How is this corrected?
H2O retention that is disproportionate to the retention of Na
corrected by restricting water and salt intake and diuretic therapy
What are the mechanisms leading to the development of edema and other signs of expanded ECFV in association with hyponatremia in a patient with congestive heart failure?
CHF causes dec cardiac output/dec BP. The body senses this as an decrease in ECFV. Therefore the body signals for an inc in Na and H2O reabsorption (activation of renin-aldosterone, sympathetic activation, ADH release) to inc ECFV. WIthout correcting the heart problem, the ECFV will continue to expand.
How does ADH release affect urine osmolarity
ADH release inc Uosm
*H2O is reabs
T or F: In hypervolemia hyponatremia TB sodium is decreased
it is inc but TBW is increased more
SrNa = TB Na / TBW
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
Which of the above data are most helpful in selecting the proper therapy?
change in BW and signs of volume depletion
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
What is the most likely explanation for the disparity in BUN and serum creatinine concentration?
Urea travels with water. Therefore if more water is being reabs, urea will also be reabs and the BUN will increase. This does not happen with creatinine
Why is volume depletion often assc with an increase in BUN?
In volume depletion,water is being conserved. Urea travels with water. Therefore if more water is being reabs, urea will also be reabs and the BUN will increase.
A patient with chronic pyelonephritis and renal insufficiency was admitted because of persistent nausea and vomiting, anorexia, lethargy, and increasing somnolence. During the preceding two weeks her weight had decreased from 140 to 127 pounds (5.9 kilograms weight loss), and she had noticed dizziness and unsteadiness with ambulation. Her BUN was 80 mg/dl, serum creatinine concentration 3.7 mg/dl. Serum sodium concentration was 132 meq/l, chloride 100 meq/l, potassium 6.2 meq/l, and bicarbonate 18 meq/l. Physical examination revealed poor skin turgor and no edema.
If fluid is to be administered intravenously, how much and what type should be given? Assume that the serum sodium concentration prior to the onset of vomiting was 145 meq/l.
Math is wrong?
Prior to volume depletion:
BW= 140 pounds (63.6 kg)
TBW = 38.2 liters.
TBosm = 38.2 x 145 meq/l = 5539 meq.
After volume depletion:
BW = 140 - 5.9 =
TBW = 38.2-5.9 = 32.3 liters.
TBosm = 32.3 x 132 meq/l = 4264 meq.
Subtracting this quantity from 5539 meq reveals the total cation deficit to be 1275 meq. This is equivalent to the total body sodium deficit.
The sodium deficit can be corrected by administration of 0.9% sodium chloride intravenously over a period of 3-4 days, as determined by frequent assessment of the patient’s status by physical examination. Additional fluid administration as 0.45% sodium chloride or 5% dextrose will be necessary to replace “insensible” and continuing urinary loss of water.
A 53 year old male was admitted to the hospital after having been seen in the Nephrology Clinic with a history of persistent hyponatremia. He denied any history of shortness of breath but admitted to a 30-pack year history of cigarette smoking. The patient was thin and appeared chronically ill. Examination of the chest revealed scattered expiratory rhonchi but no cardiac enlargement. There was no hepatomegaly or ankle edema. Skin turgor was normal.
What does the physical examination tell you about the possible cause of the hyponatremia?
no physical signs of ECFV excess (no cardiac enlargement, no hepatomegaly, and no edema)
No signs of volume depetion
hyponatremia with normal volume suggests a problem in water handeling, especially if renal function is normal.
BP: 145/95 mmHg. Serum sodium: 118 meq/l potassium: 4.1 meq/l chloride: 85 meq/l bicarbonate: 25 meq/l BUN: 5 mg/dl creatinine: 0.8 mg/dl glucose: 109 mg/dl Urine osmolality: 317 mosm/kg H20 urine sodium: 88 meq/l
Which laboratory values are most helpful in assessment of the possible mechanism(s) in the development of hyponatremia?
Plasma osmolarity is too low ( SIADH
SIADH can be Dx bc…
- normal renal function (~SCr)
- no physical findings that suggest hypovolemia
- slightly elevated BP
*SIADH = inappropriate ADH secretion
What is the etiology of SIADH?
malignant tumors (esp bronchogenic carcinoma) infectious diseases Endocrinologic abnormalities (adrenal, pituitary, and thyroid probs)
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
If you are volume depleted, what happens to urine sodium?
it should be absent (bc your body is trying to conserve it)
What is the etiology of SIADH?
malignant tumors (esp bronchogenic carcinoma) infectious diseases indocrinologic abnormalities (adrenal, pituitary, and thyroid probs)
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
What is the treatment for SIADH?
fluid restriction (<1000mL/day)
*hyponatremia cannot be corrected by Na administration w/o fluid restriction
What is the most frequent cause of hypernatremia in the elderly,immobilized, or demented individuals?
inadequate fluid intake
*esp people
If the pt is inadequate fluid intake, will inc ADH restore the ECFV?
no, be there is no water present for the ADH to move
An 81 year old male with previously known dementia was admitted to hospital because of disorientation, confusion, and increasing unresponsiveness. One month earlier he had fallen at home and fractured his left hip, requiring orthopedic surgical treatment. At that time:
BW: 70 kg
Serum sodium:140 meq/l
Following this he was no longer ambulatory at home and his wife stated that it was difficult to get him to eat or drink more than small quantities of fluid. On admission to the hospital he was described as being thin and debilitated, with no edema.
BP: 120/76 mmHg
Serum sodium: 173 meq/l
Assuming no change in total body exchangeable sodium, what was the deficit in total body water on admission? What was the effect on extracellular and intracellular fluid volume?
use eq: Sr Na = TBna / TBW
t = 0:
TBW = (70)(0.6) = 42 L
ECF: (42)(1/3) = 14 L
ICF: (42)(2/3) = 28 L
TBNa = (42)(140) = 5880 meq
t = +1 month:
TBW = 173/5880 = 34 L
ECF = (34)(1/3) = 11.3 L
ICF = (34)(2/3) = 22.6 L
Tota water loss = 42 - 34 = 8 L
Both ICF and ECF dec by 19%
T or F: when hypernatermia is due to water deficit only, the percentage change in the ECF and ICF are equal
T
What is the treatment for a pt with severe hypernatremia due to water deficit only?
IV 5% dextrose given slowly (should not exceed 0.5 to 1 meq/hr)
When is an infusion of sodium containing soln indicated?
when there is a combined water and sodium deficit
when the pt is hemodynamically unstable
What is osmotic diuresis?
increase in the solute load of the tubule obligates water to be excreted
What is the osmolarity of isotonic urine?
300 mOsm
If the solute load is 785 mOsm, what would be the daily urine volume needed to excrete it isotonically?
urine volume = urine solute / urine osm
urine volume = 758/300 = 2.6 L
A 42 year old male was receiving intermittent hemodialysis three times each week for treatment of irreversible chronic renal failure. His urine output was less than 100 ml/day. Over a period of four weeks his weight increased 8 kilograms because of excessive weight gain between dialyses, and he developed bibasilar rales, cardiac enlargement, hepatomegaly, and 1+ pitting pretibial edema. His serum sodium concentration remained within a range of 132-136 meq/l.
What was the basis for this patient’s weight gain?
loss of kidney function means that he is retaining all of Na he takes in. so if he is not restricting the Na in his diet, too much will be reabs and he will expand his ECFV
A 42 year old male was receiving intermittent hemodialysis three times each week for treatment of irreversible chronic renal failure. His urine output was less than 100 ml/day. Over a period of four weeks his weight increased 8 kilograms because of excessive weight gain between dialyses, and he developed bibasilar rales, cardiac enlargement, hepatomegaly, and 1+ pitting pretibial edema. His serum sodium concentration remained within a range of 132-136 meq/l.
What was the quantity of sodium retained over the period of four weeks?
Sr Na = TBna/TBW
gained 8 lbs = 8 L of water without a change in Na serum Na = Isotonic expansion
TBna = (8)(134) = 1072 meq
In the absence of renal function, what dictates plasma osmolality?
Serum Na conc changes based on water intake and the thirst mechanism NOT vasopressin.
In the thirst mech there is a set point for osmolality and when palsma osmolality increases above it, thirst is stimulated. water is taken in and reabs and plasma osmolality is stabilized/remain constant
If a dialysis patient’s weight was 60 kg when his volume status was normal, determine his extracellular fluid volume before and after an 8 kg weight gain?
all of the water weight he gained will go exclusively to the ECF.
problem 8 D… I dont really understand their explanation, so if you do feel free to fill it in. or if i’m wrong please fix
A 45 year old male with multiple myeloma complained of polyuria and increased thirst. His urine output averaged between 3 and 4 liters per day. His BUN was 30 mg/dl, serum creatinine concentration 1.9 mg/dl, serum sodium concentration 135 meq/l, and total serum protein concentration 10 gm/dl. Restriction of water intake over an 18 hour period increased the urine specific gravity only to 1.012 and urine osmolality to 310 mosm/kg water. Administration of aqueous pitressin (vasopressin) produced no further increase in urine specific gravity or osmolality.
What is the basic defect in urine concentrating ability?
he does not respond to vasopressin = nephrogenic diabetes insipidus
= cannot concentrate urine bc the tubules are damaged
For a pt with diabetes insipidus, what would be the effect on urine volume if they increased their solute excretion?
inc sol exc –> inc urine volume
dec sol exc –> dec urine volume
*bc they have lost the ability to conserve H2O when the urine osmolarity increases
What is the treatment for a ot with nephrogenic diabetes insipidus?
restrict dietary protein and salt
What is the primary acid-base disturbance:
Cardiac temponade with sodium 137 meq/l potassium 6.8 meq/l chloride 98 meq/l bicarbonate 9 meq/l.
SAG = 30
metabolic acidosis probably due to lactate
Cardiac temponade with sodium 137 meq/l potassium 6.8 meq/l chloride 98 meq/l bicarbonate 9 meq/l.
Dx: metabolic acidosis probably due to lactate
What treatment would be appropriate?
need to treat the cardiac problem and then administer IV bicarb as needed
An 18-year-old male presented to the emergency room with an acute attack of asthma. Despite intensive bronchodilator therapy, he continued to have marked wheezing. Blood gas measurements obtained at this time revealed the following: pCO2 30 mmHg, pO2 60 mmHg, bicarbonate 22 meq/l and pH 7.47.
What is the primary acid-base disturbance?
acute respiratory alkalosis
What is a normal SAG?
10-12
What is normlal pH?
7.4
WHat is normal bicarb level?
24 meq/L
What is normal pCO2?
40 mmHg
What is normal serum Cl-?
107 meq/L
What does a serum anion gap > 20 usually indicate?
lactic acidosis/lactate in the blood
Will Cl- be low or high with a high gap metabolic acidosis?
low
*low Cl= means there is some other - charge in the serum that is also present
Why is Cl- elevated in non-gap metabolic acidosis?
the Cl- is balancing the H+ out (there is not a missing anion)
What does a positive urine ion gap indicate (with normal SAG)?
renal loss
What does a negative urine ion gap indicate (with normal SAG)?
GI loss
What are 2 lab findings that suggest renal acidification is intact?
Cl- is elevated in urine
negative antion gap
How is respiratory alkalosis determined to be acute or chronic?
for every drop in 10 mmHg of CO2, the bicarb will drop by…
2 if acute
4 if chronic
How is respiratory acidosis determined to be acute or chronic?
for every increase in 10 mmHg of CO2, the bicarb will increase by…
1 if acute
4 if chronic
What is urine Cl- used as a measure of?
urine Cl- indirectly measures NH4+ = how much H+ is excreted
*NH4 drags Cl- wherever it goes
Why is HCO3- decreased in acute respiratory alkalosis?
there is decreased production of H2CO3 and the equation shifts to the left
Hyperventilation also increases organic acid production which reduces the HCO3- conc
T or F: the renal compensatory mechanism that decreases plasma bicarbonate is more effective in response to acute respiratory alkalosis than in response to chronic respiratory alkalosis.
F: it is more effective at compensating for chronic than acute
What effect does pH have on the oxy-hemoglobin dissociation curve?
dec in pH, dec the affinity of Hgb for O2 –> more O2 delivery to tissues
–> shift to right
inc pH –> inc affinity of Hgb to O2 –> dec O2 delivery
–> shift to left
What is the treatment for lactic acidosis?
treat the underlying problem to fix acidosis
Give bicarb when pH is _____
<7.30 but give it temporarily
When CO2 is low (resp alkalosis), HCO3- levels will (inc or dec). WHy?
decrease in order to try to make more CO2
A 24-year-old female, gravida 1 para 0, in the third trimester of a normal pregnancy has the following arterial blood gas values: pH 7.41 pCO2 30 mmHg pO2 90 mmHg plasma bicarbonate 18 meq/l.
What is the primary acid-base disturbance?
chronic respiratory alkalosis
In chronic respiratory alkalosis, the decreased in serum bicarb is deot on …
renal compensatory mechanisms that decrease H+ excretion and bicarb production by renal tubular epithelium to prevent further increase in extracell pH
What is the cause of chronic respiratory alkalosis in pregnancy?>
progesterone: it directly stimulates the CNS respiratory centers to cause hyperventilation
* goes away once the baby is delivered
A 25-year-old male was found unconscious by a friend and brought to the emergency room. In the ER, he was noted to be cyanotic with very shallow respirations and had a systolic blood pressure of 110 mmHg. There was no evidence of trauma, but there were signs of “needle tracks”, consistent with intravenous drug abuse, on the forearms. Arterial blood gas measurements showed:
pH 7.15
pCO2 77 mmHg
pO2 50 mmHg
plasma bicarbonate concentration 27 meq/l
What is the primary acid-base disturbance?
acute respiratory acidosis
What can cause a decrease in pO2 with acute respiratory acidosis in the following pt?
hypoventilation –> hypoxia
What is the most likely cuase of acute respiratory acidosis
A 25-year-old male was found unconscious by a friend and brought to the emergency room. In the ER, he was noted to be cyanotic with very shallow respirations and had a systolic blood pressure of 110 mmHg. There was no evidence of trauma, but there were signs of “needle tracks”, consistent with intravenous drug abuse, on the forearms. Arterial blood gas measurements showed:
pH 7.15
pCO2 77 mmHg
pO2 50 mmHg
plasma bicarbonate concentration 27 meq/l
mis-use or overdose of agents that inhibt CNS respiratory centers (opiate and benzos)
What is the treatment for acute respiratory acidosis?
if pt has normal chest wall and lung function, place on a mechanical ventilatory to reduce CO2 levels and bring the pt back to homeostasis. also need to treat the underlying cause to make sure this condition does not return
When treating acute respiratory acidosis, the excretion of the excess CO2 can be equated with …
the excretion of acid in the urine (the conc of urinary H+ is derived from the H2CO3 formed when CO2 diffused into renal epithelium)
*when the urine acid level is corrected, the effects of the hyperventilation assc with the acute respiratory acidosis will be corrected
A 35 year-old male developed protracted diarrhea with 6-8 loose, watery stools over a 48-hour period. These symptoms developed after eating left-over cold chicken at a picnic. Laboratory evaluation, at this time, showed the following:
Plasma Na:139 meq/l Urine Na:10 meq/l
Plasma K: 3.7 meq/l Urine K: 20 meq/l
Plasma Cl: 114 meq/l Urine Cl: 35 meq/l
Plasma HCO3:15 meq/l
Urine pH: 5.5
Arterial pH: .30
Uosm 600 mosm/kg H20
What is the primary acid-base disorder?
non-gap metabolic acidosis
Under normal circumstances, what is the most abundant unmeasured anion?
albumin
What is urinary AG a measure of?
(indirectly) a measure of NH4+
Renal acidification occurs predominantly through ….
the excretion of NH4+ by the distal nephron
Proximal RTA would be a renal cause of _____ loss
direct bicarb loss
In renal acidification defect, urine NH4+ is (high or low) and UAG is (positive or negative)
low; positive
What are the kidneys doing in terms of Na and water handeling in the following pt with non-gap metabolic acidosis:
A 35 year-old male developed protracted diarrhea with 6-8 loose, watery stools over a 48-hour period. These symptoms developed after eating left-over cold chicken at a picnic. Laboratory evaluation, at this time, showed the following:
Plasma Na:139 meq/l Urine Na:10 meq/l
Plasma K: 3.7 meq/l Urine K: 20 meq/l
Plasma Cl: 114 meq/l Urine Cl: 35 meq/l
Plasma HCO3:15 meq/l
Urine pH: 5.5
Arterial pH: .30
Uosm 600 mosm/kg H20
The very low fractional excretion of sodium and increased urine osmolality suggest that the kidneys are retaining salt and water in an attempt to avoid progressive volume depletion.
A 40 year-old patient with Type II diabetes mellitus for the past 12-15 years is referred for evaluation of abnormal renal function. Blood pressure is 150/105 mmHg. There is 2+ pedal edema. There is evidence of diabetic retinopathy by funduscopic examination. Laboratory evaluation showed the following:
Urinalysis: 4+ protein Plasma Na: 140 meq/l Urine Na: 50 meq/l Plasma K: 5.6 meq/l Urine K: 18 meq/l Plasma Cl: 110 meq/l Urine Cl: 50 meq/l Urine pH: 5.0 Plasma HCO3: 20 meq/l Uosm: 320 mosm/kg H20 Arterial pH: 7.35 BUN: 35 mg/dl Creatinine: 3.0 mg/dl
What is the primary acid-base disorder?
non-gap metabolic acidosis
What is the kidney’s normal role in trying to maintain acid-base balance during non-gap metabolic acidosis?
- reabs of filtered load of bicarb at PT
2. regeneration of new bicarb in DT in order to replace the bicarb that was used in buffering the acids
Describe how ingested protein is handled by the kidneys.
Protein is broken down into acid end products that are non-volatile/cannot be converted into CO2 –> they must be excreted by kindneys
The H+ of these acid end products will be buffered by bicarb = with inc protein intake, the kidney must make more bicarb (1 meq bicarb per gram of ingested protein) = which causes more H+ to be secreted
The anions of these acid end products are poorly reabs by the kidney = they are rapidly excreted in the urine
How are protons normally eliminated in the urine?
in the form of NH4+ and some are buffered by phosphate buffers
A 10 year-old child developed cholera with massive, loose watery stools. Initial physical examination showed a weakened child with a heart rate of 120 bpm and a blood pressure of 90/60 mmHg. Initial laboratory evaluation showed a plasma bicab of 18 meq/l.
Attempts were made to rehydrate the child with oral replacement fluids. The child, however, could not tolerate the oral fluids, and the diarrhea persisted. Six hours later, the child was stuporous with a heart rate of 150 bpm and a systolic blood pressure of 70 mmHg. Laboratory evaluation, at this time, revealed a plasma bicarb of 10 meq/l.
What explains the initial bicarb drop and the second drop?
initally, it was due to direct losses in the diarrhea fluid.
With progressive and extreme in volume depletion, tissue hypoperfusion will ensure. This causes lactate to be produced, and bicarb to be used up when it is acting as a buffer (seen in the 2nd drop)
Will a pt in shock have an increased SAG?
yes, they will have lactate in their blood form hypoperfusion
When a pt has metabolic acidosis with extreme volume depletion, what is the treatment?
replace the ECFV with IV saline and K+ replacement to correct the lactic acidosis and then provide supportive care/fix the initial cause of the volume depletion
How are the different RTAs differentated based on labs?
type 1 has dec K+
type 2 has inc, normal, or dec K+
type 4 has inc K+
*all have positive urine AG
Type II RTA has labs simialar to what condition?.
diarrhea
A 38-year-old male was seen following an episode of extreme weakness lasting about 4 hours. There had been no previous episodes of this nature, although he had experienced a number of vague symptoms including numbness and tingling in his hands and feet and muscle cramps occurring especially in his hands. He also recalled having nocturia for approximately one year with relatively large night time urine volumes. His blood pressure was 180/110 mmHg. Physical examination otherwise was unremarkable with the exception of generalized hyporeflexia. The following laboratory data were obtained:
Plasma Na: 146 meq/l Plasma Cl: 106 meq/l Plasma K: 2.3 meq/l Plasma HCO3: 29 meq/l BUN: 18 mg/dl
24-hour urine potassium excretion while the patient was still hypokalemic was 55 meq.
What is the most likely diagnosis? What other diagnoses should be considered?
hyperaldosteronism
- aldo secreting tumor
- adrenal hyperplasia
- secondary due to vascular disease
diuretic induced hypokalemia/laxativ abuse
How is primary and secondary hyperaldosteronism distinguished?
give NaCl and measure both aldo and renin levels
- high renin and high aldo = renin problem/secondary
- low renin and high aldo = aldo problem/primary
What are the clinical findings for hypokalemia due to diuretic abuse?
high plasma renin low urine K+ volume depleted inc Na and Cl in stool NO HYP
How are Bartter’s syndrome and diuretic abuse distinguished?
in Bartter’s urine Cl- is ALWAYS high and with diuretic abuse it is intermittently high (goes back down after the diuretics effect wears off)
What may be the cause of euvolemic or hypovolumic hypokalemia with low Cl- in urine and plasma?
vomiting/bulimia
What type of acid-base disorder can be generated by the loss of gastic contents? Why/How does this occur?
metabolic alkalosis
*In the presence of vomiting and aspiration of gastric contents, the normal stimulus to the production of the bicarbonate is eliminated which in turn leads to increased levels of bicarbonate in the blood and thus the resulting metabolic alkalosis.
What treatment will correct hypochloremic metabolic alkalosis?
Saline –> retention of NaCl and excretion of HCO3-
The majority of K+ loss in chloride responsive metbaolic alkalosis is due to ____
renal losses
-some K+ reabs occurs thru Cl-:K+ symporters in dital nephron (without Cl- the K+ cannot be reabs)
problem
21
Type II RTA has labs simialar to what condition?.
diarrhea
A 38-year-old male was seen following an episode of extreme weakness lasting about 4 hours. There had been no previous episodes of this nature, although he had experienced a number of vague symptoms including numbness and tingling in his hands and feet and muscle cramps occurring especially in his hands. He also recalled having nocturia for approximately one year with relatively large night time urine volumes. His blood pressure was 180/110 mmHg. Physical examination otherwise was unremarkable with the exception of generalized hyporeflexia. The following laboratory data were obtained:
Plasma Na: 146 meq/l Plasma Cl: 106 meq/l Plasma K: 2.3 meq/l Plasma HCO3: 29 meq/l BUN: 18 mg/dl
24-hour urine potassium excretion while the patient was still hypokalemic was 55 meq.
What is the most likely diagnosis? What other diagnoses should be considered?
hyperaldosteronism
- aldo secreting tumor
- adrenal hyperplasia
- secondary due to vascular disease
diuretic induced hypokalemia/laxativ abuse
How is primary and secondary hyperaldosteronism distinguished?
give NaCl and measure both aldo and renin levels
- high renin and high aldo = renin problem/secondary
- low renin and high aldo = aldo problem/primary
What are the clinical findings for hypokalemia due to diuretic abuse?
high plasma renin low urine K+ volume depleted inc Na and Cl in stool NO HYP
How are Bartter’s syndrome and diuretic abuse distinguished?
in Bartter’s urine Cl- is ALWAYS high and with diuretic abuse it is intermittently high (goes back down after the diuretics effect wears off)
What may be the cause of euvolemic or hypovolumic hypokalemia with low Cl- in urine and plasma?
vomiting/bulimia
What type of acid-base disorder can be generated by the loss of gastic contents? Why/How does this occur?
metabolic alkalosis
*In the presence of vomiting and aspiration of gastric contents, the normal stimulus to the production of the bicarbonate is eliminated which in turn leads to increased levels of bicarbonate in the blood and thus the resulting metabolic alkalosis.
What treatment will correct hypochloremic metabolic alkalosis?
Saline –> retention of NaCl and excretion of HCO3-
The majority of K+ loss in chloride responsive metbaolic alkalosis is due to ____
renal losses
-some K+ reabs occurs thru Cl-:K+ symporters in dital nephron (without Cl- the K+ cannot be reabs)
problem
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