Nephrology Flashcards
1
Q
HYPERTENSION
Select patients
A
HYPERTENSION
Select patients <3 yo should have BP measured in medical settings or if predisposing condition. These patients are
- Past medical history
- Prematurity, esp born <32 weeks
- Very low birth weight
- SGA
- NICU stay
- Hx of umbilical artery catheterization
- Recurrent UTI
- Malignancy
- Bone marrow transplant
- Solid organ transplant
- Current medical conditions
- Congenital heart disease
- Genitourinary abnormalities
- Renal disease: renal or urologic malformations
- Hematuria
- Proteinuria
- Increased intracranial pressure
- Systemic illness associated with HTN: Any child w systemic/congenital illness known to result in HTN (ie tuberous sclerosis)
- Medications- Taking medications known to raise BP (ie chronic steroid therapy)
- Family Hx- Congenital kidney disease
2
Q
Diagnosis of HTN if child has BP readings >__th % on __ different visits.
A
Diagnosis of HTN if child has BP readings >95th % on 3 different visits.
3
Q
Age 1-12
- > ___% = Elevated blood pressure (Prehypertension)
- Recheck BP at a 2nd visit in __ months and discuss lifestyle changes.
- > __% = Stage I HTN.
- Recheck BP measurement in __ weeks and discuss lifestyle changes.
- > __% + ___mmHg = Stage II HTN
- If asymptomatic, recheck measurement in __ week.
- > 95% + __mmHg (urgent HTN) OR Symptomatic (end organ damage; emergent HTN)→ emergency, go to ED right away
A
Age 1-12
- > 90% = Elevated blood pressure (Prehypertension)
- Recheck BP at a 2nd visit in 6 months and discuss lifestyle changes.
- > 95% = Stage I HTN.
- Recheck BP measurement in 1-2 weeks and discuss lifestyle changes.
- > 95% + 12mmHg = Stage II HTN
- If asymptomatic, recheck measurement in 1 week.
- > 95% + 30mmHg (urgent HTN) OR Symptomatic (end organ damage; emergent HTN)→ emergency, go to ED right away
4
Q
Age >13
- <120/80 = Normal
- Between = Elevated blood pressure
- > 130/80 = Stage I HTN
- > 140/90 = Stage II HTN
A
Age >13
- <120/80 = Normal
- Between = Elevated blood pressure
- > 130/80 = Stage I HTN
- > 140/90 = Stage II HTN
5
Q
Serum osmolality = ____________
- Normal serum osmolality is ___ +/- ___
- If glucose and BUN are normal, use 2 x [Na+] to see if patient’s osmolality is ~280
- Used to differentiated euvolemia, hypovolemia, and hypervolemic hyponatremia
A
Serum osmolality = 2x [serum Na] + glucose/18 + BUN/2.8
- Normal serum osmolality is 285 +/- 10 mOsm/kg
- If glucose and BUN are normal, use 2 x [Na+] to see if patient’s osmolality is ~280
- Used to differentiated euvolemia, hypovolemia, and hypervolemic hyponatremia
6
Q
Hyponatremia
- Causes
- Net depletion of sodium or dilution of sodium
- Improper formula preparation
- Children with diarrhea, vomiting, and burns have sodium losses through the GI or skin and present with hyponatremia when the fluid replacement occurs with excess free water (eg water, juice, ginger ale, or tea). The ECF sodium is decreased with hyponatremic dehydration, and the ICF sodium is also decreased with fluids shifting from the ECF to ICF.
- Pt:
- Symptoms include CNS (headache, confusion, delirium, seizure), musculoskeletal (fatigue, muscle cramps), and GI (nausea, vomiting) findings.
- Classify:
- Hyperosmolar (Pseudohyponatremia): Glucose and mannitol shift water out of cells, diluting plasma Na OR due to elevated triglycerides
- Common presents in setting of hyperglycemia in DKA
- Tx: Treat underlying disease process
- Isoosmolar
- Artifactual decrease in serum Na associated with older lab instrument that miscalculate sodium in settings of high protein or lipid
- Tx: Artifact, no treatment
- Hypoosmolar
- Hypovolemic hyponatremia
- Diuretics
- GI losses (emesis, diarrhea)
- 3rd spacing of fluid
- Sodium-losing nephropathies
- Adrenal insufficiency (Addison disease)
- Tx: Use normal saline, watch for rapid correction
- Hypervolemia hyponatremia
- Causes: Edema-forming states: heart failure, cirrhosis, and nephrotic syndrome
- Tx: Restrict fluids and Na +/- loop diuretics
- Euvolemic hyponatremia
- ________
- Dx: Urine inappropriately concentrated/high (>250 mOsm/kg) in the setting of a low serum osmolality.
- Rule out ____ or ___ deficiency before making diagnosis as both can have low serum osmolalities and high urine osmolalities.
- Tx: ______. Refractory cases can be treated with ADH receptor antagonist (conivaptan or tolvaptan)
- ________
- Hypovolemic hyponatremia
- Hyperosmolar (Pseudohyponatremia): Glucose and mannitol shift water out of cells, diluting plasma Na OR due to elevated triglycerides
- Treatment
- Symptomatic hyponatremia:
- 0.9 NS to increase serum Na at a rate not to exceed 0.5 mEq/L/hr
- Severe symptoms (Lethargy, confusion, coma, seizures) and not hypovolemia
- 3% (hypertonic) saline. 100mL bolus to raise serum Na by 2-3 mEq/L
- __________:
- Path: If sodium concentration is raised too rapidly, cells then shrink as water rushes out of cells into the bloodstream, where the osmolality has risen
- This rare effect is more likely to occur in patient with chronic, severe hyponatremia (Na<115 mEq/L for >2 days) whose sodium is corrected rapidly (>____mEq/L over 24 hours)
- Symptomatic hyponatremia:
A
Hyponatremia
- Causes
- Net depletion of sodium or dilution of sodium
- Improper formula preparation
- Children with diarrhea, vomiting, and burns have sodium losses through the GI or skin and present with hyponatremia when the fluid replacement occurs with excess free water (eg water, juice, ginger ale, or tea). The ECF sodium is decreased with hyponatremic dehydration, and the ICF sodium is also decreased with fluids shifting from the ECF to ICF.
- Pt:
- Symptoms include CNS (headache, confusion, delirium, seizure), musculoskeletal (fatigue, muscle cramps), and GI (nausea, vomiting) findings.
- Classify:
- Hyperosmolar (Pseudohyponatremia): Glucose and mannitol shift water out of cells, diluting plasma Na OR due to elevated triglycerides
- Common presents in setting of hyperglycemia in DKA
- Tx: Treat underlying disease process
- Isoosmolar
- Artifactual decrease in serum Na associated with older lab instrument that miscalculate sodium in settings of high protein or lipid
- Tx: Artifact, no treatment
- Hypoosmolar
- Hypovolemic hyponatremia
- Diuretics
- GI losses (emesis, diarrhea)
- 3rd spacing of fluid
- Sodium-losing nephropathies
- Adrenal insufficiency (Addison disease)
- Tx: Use normal saline, watch for rapid correction
- Hypervolemia hyponatremia
- Causes: Edema-forming states: heart failure, cirrhosis, and nephrotic syndrome
- Tx: Restrict fluids and Na +/- loop diuretics
- Euvolemic hyponatremia
- SIADH (increased reabsorption of water in kidneys), but normal sodium excretion.
- Dx: Urine inappropriately concentrated/high (>250 mOsm/kg) in the setting of a low serum osmolality.
- Rule out hypothyroidism or glucocorticoid deficiency before making diagnosis of SIADH as both can have low serum osmolalities and high urine osmolalities (although more commonly seen in SIADH).
- Tx: Fluid restriction. Refractory cases can be treated with ADH receptor antagonist (conivaptan or tolvaptan)
- SIADH (increased reabsorption of water in kidneys), but normal sodium excretion.
- Hypovolemic hyponatremia
- Hyperosmolar (Pseudohyponatremia): Glucose and mannitol shift water out of cells, diluting plasma Na OR due to elevated triglycerides
- Treatment
- Symptomatic hyponatremia:
- 0.9 NS to increase serum Na at a rate not to exceed 0.5 mEq/L/hr
- Severe symptoms (Lethargy, confusion, coma, seizures) and not hypovolemia
- 3% (hypertonic) saline. 100mL bolus to raise serum Na by 2-3 mEq/L
- Osmotic demyelination syndrome (Central pontine myelinolysis):
- Path: If sodium concentration is raised too rapidly, cells then shrink as water rushes out of cells into the bloodstream, where the osmolality has risen
- This rare effect is more likely to occur in patient with chronic, severe hyponatremia (Na<115 mEq/L for >2 days) whose sodium is corrected rapidly (>10 mEq/L over 24 hours)
- Symptomatic hyponatremia:
7
Q
Hypernatremia
- Always hyperosmolar. 1st step is to determine volume status
- Hypovolemic Hypernatremia
- Low volume implies both water and total body Na loss, with the water deficit exceeding the Na deficit
- Causes: Sodium intoxication (iatrogenic, administration of baking soda), water deficit (diabetes insipidus, inadequate intake, increased insensible loss), or both water and sodium deficits (GI, cutaneous or renal losses)
- Tx: 20ml/kg NS boluses to correct volume deficit, and then hypotonic fluids / additional free water
- Hypervolemic hypernatremia
- Causes: Mineralocorticoid excess (primary hyperaldosteronism).
- Tx: Loop diuretics and free water
- Euvolemic Hypernatremia
- Most often seen in pts w ______ with reduced access to water who have not yet developed frank volume depletion.
- Typically, pts with DI who have normal access to water have normal or borderline-high serum Na levels bc they are constantly drinking water (These pts are hyperosmolar and therefore always thirsty).
- Dx: The water restriction test not only diagnoses DI but also differentiates between central and nephrogenic types.
- In a healthy person, when plasma osmolality increases to 295mOsm/kg, ADH (vasopressin) is high and urine is maximally concentrated.
- In central DI, the ADH stays low and the urine remains dilute, even with water restriction.
- In nephrogenic DI, the ADH is appropriately high, but the urine remains dilute.
- Tx:
- Resistant central DI: _____
- Nephrogenic DI: ___ or ____
- Most often seen in pts w ______ with reduced access to water who have not yet developed frank volume depletion.
- Avoid rapid decrease in serum osmolality. Rapid decrease in serum osmolality and sodium is associated with increased risk for cerebral edema bc of fluid shift from the extracellular fluid (lower osmolality after correction) to the brain cells (intracellular). If hypernatremia is corrected too quickly, water will move into these cells causing cerebral edema and seizures.
Remember: SIADH typically presents as hyponatremia with normal volume. DI commonly presents as polyuria/polydipsia, with or without hypernatremia and also with normal volume.
A
Hypernatremia
- Always hyperosmolar. 1st step is to determine volume status
- Hypovolemic Hypernatremia
- Low volume implies both water and total body Na loss, with the water deficit exceeding the Na deficit
- Causes: Sodium intoxication (iatrogenic, administration of baking soda), water deficit (diabetes insipidus, inadequate intake, increased insensible loss), or both water and sodium deficits (GI, cutaneous or renal losses)
- Tx: 20ml/kg NS boluses to correct volume deficit, and then hypotonic fluids / additional free water
- Hypervolemic hypernatremia
- Causes: Mineralocorticoid excess (primary hyperaldosteronism).
- Tx: Loop diuretics and free water
- Euvolemic Hypernatremia
- Most often seen in pts w diabetes insipidus with reduced access to water who have not yet developed frank volume depletion.
- Typically, pts with DI who have normal access to water have normal or borderline-high serum Na levels bc they are constantly drinking water (These pts are hyperosmolar and therefore always thirsty).
- Dx: The water restriction test not only diagnoses DI but also differentiates between central and nephrogenic types.
- In a healthy person, when plasma osmolality increases to 295mOsm/kg, ADH (vasopressin) is high and urine is maximally concentrated.
- In central DI, the ADH stays low and the urine remains dilute, even with water restriction.
- In nephrogenic DI, the ADH is appropriately high, but the urine remains dilute.
- Tx:
- Resistant central DI: Oral or intranasal desmopressin.
- Nephrogenic DI: Thiazide diuretics or amiloride
- Most often seen in pts w diabetes insipidus with reduced access to water who have not yet developed frank volume depletion.
- Avoid rapid decrease in serum osmolality. Rapid decrease in serum osmolality and sodium is associated with increased risk for cerebral edema bc of fluid shift from the extracellular fluid (lower osmolality after correction) to the brain cells (intracellular). If hypernatremia is corrected too quickly, water will move into these cells causing cerebral edema and seizures.
Remember: SIADH typically presents as hyponatremia with normal volume. DI commonly presents as polyuria/polydipsia, with or without hypernatremia and also with normal volume.
8
Q
Hyperkalemia
- Causes:
- Pseudohyperkalemia (falsely elevated serum potassium) is the most frequent cause of elevated potassium concentrations in the pediatric setting.
- Transcellular shifts
- _____ and _____ decrease K+ uptake → hyperkalemia (and hyperkalemia causes acidosis)
- Decreased excretion
- Renal failure
- Type ___ RTA
- TMP/SMX
- Inhibited ____ release or action increases serum K
- Potassium sparing diuretics (_____ blocks aldosterone receptor; _____ blocks channel for aldosterone to act)
- Gordon Syndrome (pseudohypoaldosteronism)- Rare genetic disorder associated with abnormalities in the renal tubules, leading to HTN.
- Serum potassium concentrations >7.0 mEq/L (mmol/L) are considered severe hyperkalemia and require urgent treatment.
- Management: 1. Recheck K, 2. Get EKG (Sequence of progressive hyperkalemia: 1) ____ wave and short QT interval (K 5.5-6.5) 2) Progressive lengthening of PR and QRS intervals (K 6.5-7.5) 3) Loss of P wave and QRS widening into sine wave (K >8) 4) _______ or cardiac standstill
- If wide QRS or absence of P waves, stabilize cardiac membranes and prevent fatal arrhythmias, as hyperkalemia leads to depolarization of cardiac membrane
- IV _____
- Shift K into cells
- _____
- _____
- ____
- Remove K from body
- ____
- _____
- ___
- If wide QRS or absence of P waves, stabilize cardiac membranes and prevent fatal arrhythmias, as hyperkalemia leads to depolarization of cardiac membrane
- If K>6.5 without symptoms or EKG changes, treat with insulin + glucose, beta-agonists, sodium bicarbonate (if acidosis), and SPS enema.
- If K <6.5, tx with loop diuretics and dietary restriction.
A
Hyperkalemia
- Causes:
- Pseudohyperkalemia (falsely elevated serum potassium) is the most frequent cause of elevated potassium concentrations in the pediatric setting.
- Transcellular shifts
- Acidosis and alpha agonists decrease K+ uptake → hyperkalemia (and hyperkalemia causes acidosis)
- Decreased excretion
- Renal failure
- Type 4 RTA
- TMP/SMX
- Inhibited aldosterone release or aldosterone action increases serum K
- Potassium sparing diuretics (spironolactone blocks aldosterone receptor; amiloride blocks channel for aldosterone to act)
- Gordon Syndrome (pseudohypoaldosteronism)- Rare genetic disorder associated with abnormalities in the renal tubules, leading to HTN.
- Serum potassium concentrations >7.0 mEq/L (mmol/L) are considered severe hyperkalemia and require urgent treatment.
- Management: 1. Recheck K, 2. Get EKG (Sequence of progressive hyperkalemia: 1) peaked T wave and short QT interval (K 5.5-6.5) 2) Progressive lengthening of PR and QRS intervals (K 6.5-7.5) 3) Loss of P wave and QRS widening into sine wave (K >8) 4) Ventricular fibrillation or cardiac standstill
- If wide QRS or absence of P waves, stabilize cardiac membranes and prevent fatal arrhythmias, as hyperkalemia leads to depolarization of cardiac membrane
- IV calcium gluconate
- Shift K into cells
- Insulin with glucose infusion
- Sodium bicarbonate
- Albuterol nebulization
- Remove K from body
- Loop diuretics
- Resin binders
- Dialysis
- If wide QRS or absence of P waves, stabilize cardiac membranes and prevent fatal arrhythmias, as hyperkalemia leads to depolarization of cardiac membrane
- If K>6.5 without symptoms or EKG changes, treat with insulin + glucose, beta-agonists, sodium bicarbonate (if acidosis), and SPS enema.
- If K <6.5, tx with loop diuretics and dietary restriction.
9
Q
Hypokalemia
- Causes: 4 general causes: 1) inadequate intake, 2) GI losses (diarrhea has high concentration of potassium leading to hypokalemia in pts with gastroenteritis; emesis has less K but contributes to hypokalemia by way of renal losses from volume depletion), 3) non-GI losses (ie renal), and 4) transcellular shift
- Increased ____ lowers serum K: Hypokalemia without obvious cause in a patient with HTN and metabolic alkalosis must cause consider hyperaldosteronism!
- Type __ RTA for unclear reasons
- Type __ RTA due to cotransport problems
- ___magnesemia
- Medications:
- Loop and thiazide diuretics
- ____ cause renal K wasting (only occurs with the sodium salt and not the potassium salt, ie PCN VK)
- ____, ___, and ____ increase K+ uptake → hypokalemia (and hypokalemia causes alkalosis)
- Pseudohyperkalemia: An artificial cause of hypokalemia can occur in pts with very elevated WBC counts
- Pt: Flattened T waves followed by ST depression and the emergence of U waves, decreased deep tendon reflexes, rhabdomyolysis, muscle weakness or cramping that may progress to paralysis, cardiac arrhythmias
- Management: 1) Recheck K 2) Check magnesium and replete (magnesium deficiency causes renal potassium wasting)
- Potassium chloride is preferred over potassium phosphate, potassium citrate, or potassium bicarbonate
- Asymptomatic hypokalemia patients with serum K 3-3.5 mEq/L (mmol/L) can be treated with increased intake of dietary K/
- In patients with no contraindication to oral intake, PO enteral administration is the preferred route for K replacement.
A
Hypokalemia
- Causes: 4 general causes: 1) inadequate intake, 2) GI losses (diarrhea has high concentration of potassium leading to hypokalemia in pts with gastroenteritis; emesis has less K but contributes to hypokalemia by way of renal losses from volume depletion), 3) non-GI losses (ie renal), and 4) transcellular shift
- Increased aldosterone lowers serum K: Hypokalemia without obvious cause in a patient with HTN and metabolic alkalosis must cause consider hyperaldosteronism!
- Type 1 RTA for unclear reasons
- Type 2 RTA due to cotransport problems
- Hypomagnesemia
- Medications:
- Loop and thiazide diuretics
- Penicillins cause renal K wasting (only occurs with the sodium salt of penicillin and not the potassium salt, ie PCN VK)
- Alkalosis, beta-agonists, and insulin increase K+ uptake → hypokalemia (and hypokalemia causes alkalosis)
- Pseudohyperkalemia: An artificial cause of hypokalemia can occur in pts with very elevated WBC counts
- Pt: Flattened T waves followed by ST depression and the emergence of U waves, decreased deep tendon reflexes, rhabdomyolysis, muscle weakness or cramping that may progress to paralysis, cardiac arrhythmias
- Management: 1) Recheck K 2) Check magnesium and replete (magnesium deficiency causes renal potassium wasting)
- Potassium chloride is preferred over potassium phosphate, potassium citrate, or potassium bicarbonate
- Asymptomatic hypokalemia patients with serum K 3-3.5 mEq/L (mmol/L) can be treated with increased intake of dietary K/
- In patients with no contraindication to oral intake, PO enteral administration is the preferred route for K replacement.
10
Q
Hypokalemia and nonanion gap metabolic acidosis without HTN
- K+ loss usually from diarrhea or RTA
- Urine anion gap differentiate causes: negative UAG in diarrhea, positive UAG in RTA
A
Hypokalemia and nonanion gap metabolic acidosis without HTN
- K+ loss usually from diarrhea or RTA
- Urine anion gap differentiate causes: negative UAG in diarrhea, positive UAG in RTA
11
Q
Hypokalemia and metabolic alkalosis with HTN
- Diuretics (most common) causing contraction alkalosis. Urine sodium is increased in spite of volume contraction.
- Hyperaldosteronism (primary or secondary)
- Cushing syndrome
- Liddle syndrome
- Adrenal hydroxylase deficiencies
A
Hypokalemia and metabolic alkalosis with HTN
- Diuretics (most common) causing contraction alkalosis. Urine sodium is increased in spite of volume contraction.
- Hyperaldosteronism (primary or secondary)
- Cushing syndrome
- Liddle syndrome
- Adrenal hydroxylase deficiencies
12
Q
Hypokalemia and metabolic alkalosis without HTN
- Bartter syndrome
- Gitelman syndrome
A
Hypokalemia and metabolic alkalosis without HTN
- Bartter syndrome
- Gitelman syndrome
13
Q
- Genetic syndromes:
- Liddle syndrome (Pseudoaldosteronism):
- ____Inheritance? condition
- Path: Mutation that causes the epithelial sodium channel in the ____ tubule to become constitutively active
- Pt: ___ blood pressure , ___kalemia, ___natremia, and metabolic ____ (high urinary chloride) with ___ aldosterone
- Tx: ______
A
- Genetic syndromes:
- Liddle syndrome (Pseudoaldosteronism):
- AD condition
- Path: Mutation that causes the epithelial sodium channel in the distal tubule to become constitutively active
- Pt: HTN, hypokalemia, hypernatremia, and metabolic alkalosis (high urinary chloride) with low aldosterone
- Tx: Amiloride or triamterene
- Bartter’s and Gittleman’s are due to abnormal solute transport in the thick ascending limb. Increased aldosterone and renin.
14
Q
- Bartter’s:
- _____Inheritance?
- Path: Primary defect in NaCl reabsorption in ascending limb of loop of Henle. Looks like taking a ____ diuretic
- Pt:
- Polyhydramnios, premature delivery
- Metabolic ___, ___kalemia, ___natremia, ___chloremia, polyuria (12-50ml/kg/day) or polydipsia, ____ blood pressure
- Associated ____. ___calciuria (may present with stones/nephrocalcinosis)
A
- Bartter’s:
- AR
- Path: Primary defect in NaCl reabsorption in ascending limb of loop of Henle. Looks like taking a loop diuretic
- Pt:
- Polyhydramnios, premature delivery
- Metabolic alkalosis, hypokalemia, hyponatremia, hypochloremia, polyuria (12-50ml/kg/day) or polydipsia, normal blood pressure WITHOUT HTN
- Associated deafness. Hypercalciuria (may present with stones/nephrocalcinosis)
15
Q
- Gitleman’s
- ____ Inheritance?
- Path: Defect in NaCl cotransporter in early distal tubule. Looks like taking _____ diuretic except that pt has severe magnesium wasting that is not understood
- Pt:
- Milder than Bartter’s and presents later in life
- ___kalemia, metabolic ___, ____ blood pressure
- ____magnesemia, ____calciuria (urine) (in contrast to Bartter syndrome, children with Gittleman have reduced ____ and ____ (more common)
A
- Gitleman’s
- AR
- Path: Defect in NaCl cotransporter in early distal tubule. Looks like taking thiazide diuretic except that pt has severe magnesium wasting that is not understood
- Pt:
- Milder than Bartter’s and presents later in life
- Hypokalemia, metabolic alkalosis, WITHOUT HTN
- Hypomagnesemia, hypocalciuria (urine) (in contrast to Bartter syndrome, children with Gittleman have reduced urinary calcium and hypomagnesemia (more common)
16
Q
- Bartter’s and Gittleman’s are due to abnormal solute transport in the thick ascending limb. Increased ____ and ____.
A
- Bartter’s and Gittleman’s are due to abnormal solute transport in the thick ascending limb. Increased aldosterone and renin.
17
Q
CALCIUM
- Calcium is regulated by parathyroid hormone and vitamin D metabolites
- Measure ionized calcium directly to get most reliable assessment of calcium status
- Calcium levels should be corrected for the ____ level, or an ionized calcium should be measured.
- Corrected Ca = _____
- Correct calcium: for each 1 g/dL decrease in albumin, increase the measured serum calcium by 0.8 mg/dL. If albumin decreases, the measured serum calcium decreases.
A
CALCIUM
- Calcium is regulated by parathyroid hormone and vitamin D metabolites
- Measure ionized calcium directly to get most reliable assessment of calcium status
- Calcium levels should be corrected for the albumin level, or an ionized calcium should be measured.
- Corrected Ca = Ca + [0.8x(4-Alb)]
- Correct calcium: for each 1 g/dL decrease in albumin, increase the measured serum calcium by 0.8 mg/dL. If albumin decreases, the measured serum calcium decreases.
18
Q
Hypercalcemia
- Causes
- Primary hyperparathyroidism (most common etiology)
- Prolonged immobilization - excess calcium release from bone suppresses PTH level
- Thiazide diuretics
- Hypercalcemia of malignancy
- Familial hypercalcemia hypocalciuria
- _____ Inheritance???
- Parathyroid glands are normal. Mildly ___ serum calcium, ____ urine calcium, inappropriately ____ PTH for calcium level (as should be suppressed in hypercalcemia)
- Tx: _____.
- Hypervitaminosis
- Multiple myeloma
- Granulomatous disease: sarcoidosis and tuberculosis
- Hypophosphatemia
- Williams syndrome
- Subcutaneous fat necrosis (self-limited panniculitis)
- Other: leukemia, thyrotoxicosis
- Hypervitaminosis A
- Milk alkali (taking too many antacids)
- Pt: ____, ____ (fatigue, weight loss, dehydration, decreased appetite), ___ (abdominal pain, constipation, vomiting), ____ (bone pain), ______ (depression, anxiety, confusion, and impairment of cognitive functioning).
- Labs: PTH level is useful to classify hypercalcemia as PTH dependent or non-PTH dependent.
- Tx:
- Most pts with significant hypercalcemia are volume depleted and need NS replacement fluid.
- ____ and _____ are now standard of care for persistent hypercalcemia.
A
Hypercalcemia
- Causes
- Primary hyperparathyroidism (most common etiology)
- Prolonged immobilization - excess calcium release from bone suppresses PTH level
- Thiazide diuretics
- Hypercalcemia of malignancy
- Familial hypercalcemia hypocalciuria
- AD
- Parathyroid glands are normal. Mildly elevated serum calcium, low urine calcium, inappropriately normal PTH for calcium level (as should be suppressed in hypercalcemia)
- Tx: None.
- Hypervitaminosis
- Multiple myeloma
- Granulomatous disease: sarcoidosis and tuberculosis
- Hypophosphatemia
- Williams syndrome
- Subcutaneous fat necrosis (self-limited panniculitis)
- Other: leukemia, thyrotoxicosis
- Hypervitaminosis A
- Milk alkali (taking too many antacids)
- Pt: Stones (kidney), moans (fatigue, weight loss, dehydration, decreased appetite), groans (abdominal pain, constipation, vomiting), bones (bone pain), psych overtones (depression, anxiety, confusion, and impairment of cognitive functioning).
- Labs: PTH level is useful to classify hypercalcemia as PTH dependent or non-PTH dependent.
- Tx:
- Most pts with significant hypercalcemia are volume depleted and need NS replacement fluid.
- Calcitonin and bisphosphates are now standard of care for persistent hypercalcemia.
19
Q
Hypocalcemia
- Neonatal hypocalcemia
- Early onset
- Most common cause is _____
- Late onset
- Often due to vitamin D deficiency with hypomagnesemia and can be treated with limited therapy
- Early onset
- Causes:
- Vitamin D deficiency
- Chronic kidney disease results in secondary hyperparathyroidism
- Severe pancreatitis
- Rhabdomyolysis
- _____magnesemia (always check magnesium level!)
- Magnesium deficiency, which can result from malabsorption syndromes, and cystic fibrosis. Hypomagnesemia is thought to cause hypocalcemia by not permitting release of PTH. This is why you always want to check magnesium when a pt’s calcium is low bc you never fix calcium until you fix the magnesium.
- Hungry bone syndrome following parathyroidectomy
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Citrate (anticoagulant in whole blood) chelates calcium in serum
- Poisoning with inorganic phosphate
- Early in the course of tx of ALL, hypocalcemia can occur due to the destruction of lymphoblasts.
- Kenny-Caffey syndrome is a condition with medullary stenosis of the long bones, short stature, delayed bone age, and eye abnormalities. It causes episodic hypocalcemia.
- Pt: Jitteriness, muscle twitching, seizures, tetany, perioral tingling, muscle twitching
- Positive ___ or ____ signs may be present.
- In more severe cases of _____, an ECG shows prolongation of the QT interval, which can lead to a fatal arrhythmia ____.
- Tx: 1) Check and correct with ___ 2) Check ionized calcium and check ___
- Mild (paresthesias): ___
- Severe (seizures, arrhythmias):___
A
Hypocalcemia
- Neonatal hypocalcemia
- Early onset
- Most common cause is prematurity
- Late onset
- Often due to vitamin D deficiency with hypomagnesemia and can be treated with limited therapy
- Early onset
- Causes:
- Vitamin D deficiency
- Chronic kidney disease results in secondary hyperparathyroidism
- Severe pancreatitis
- Rhabdomyolysis
- Hypermagnesemia (always check magnesium level!)
- Magnesium deficiency, which can result from malabsorption syndromes, and cystic fibrosis. Hypomagnesemia is thought to cause hypocalcemia by not permitting release of PTH. This is why you always want to check magnesium when a pt’s calcium is low bc you never fix calcium until you fix the magnesium.
- Hungry bone syndrome following parathyroidectomy
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Citrate (anticoagulant in whole blood) chelates calcium in serum
- Poisoning with inorganic phosphate
- Early in the course of tx of ALL, hypocalcemia can occur due to the destruction of lymphoblasts.
- Kenny-Caffey syndrome is a condition with medullary stenosis of the long bones, short stature, delayed bone age, and eye abnormalities. It causes episodic hypocalcemia.
- Pt: Jitteriness, muscle twitching, seizures, tetany, perioral tingling, muscle twitching
- Positive Chvostek or Trousseau signs may be present.
- In more severe cases of hypocalcemia, an ECG shows prolongation of the QT interval, which can lead to a fatal arrhythmia torsades de pointes.
- Tx: 1) Check and correct with albumin 2) Check ionized calcium and check magnesium
- Mild (paresthesias): Oral calcium
- Severe (seizures, arrhythmias): IV calcium gluconate while monitoring heart rates
20
Q
- Diarrhea results in metabolic ___ with a ___ bicarb.
A
- Diarrhea results in metabolic acidosis with a low bicarb.
21
Q
- Vomiting causes metabolic ____ due to loss of hydrochloric acid; would have ___ bicarb.
A
- Vomiting causes metabolic alkalosis due to loss of hydrochloric acid; would have elevated bicarb.
22
Q
- Cystic fibrosis is at high risk for _natremic, _chloremic metabolic ___ when dehydrated.
A
- Cystic fibrosis is at high risk for hyponatremic, hypochloremic metabolic alkalosis when dehydrated.
23
Q
- Alkalemia causes ______calcemia - even though serum calcium level is unchanged (= ionized + bound).
A
- Alkalemia causes an increase in the fraction of bound calcium, and the resulting decrease in ionized calcium produces these symptoms of hypocalcemia - even though serum calcium level is unchanged (= ionized + bound).
24
Q
- 1) High OG and high AG
- *Ethylene glycol (antifreeze). Toxic metabolite is glycolic acid
- Ethylene glycol (____ in urine. Metabolizes to glycolic acid and then oxalic acid)
- Tx: ____ and dialysis
- *Methanol (paint thinner, de-icing solutions/windshield wiper fluids, moonshine). Toxic metabolite is formic acid
- Visual symptoms. Metabolizes to formic acid, which is directly toxic to ___
- Tx: ____ and dialysis
- *Propylene glycol (rarely, low toxicity). Toxic metabolite is lactic acid
- Used as solvent for IV lorazepam, is approved food sweetener. Can cause severe lactic acidosis
- *Ethylene glycol (antifreeze). Toxic metabolite is glycolic acid
A
- 1) High OG and high AG
- *Ethylene glycol (antifreeze). Toxic metabolite is glycolic acid
- Ethylene glycol (Calcium oxalate crystals in urine. Metabolizes to glycolic acid and then oxalic acid)
- Tx: Fomepizole and dialysis
- *Methanol (paint thinner, de-icing solutions/windshield wiper fluids, moonshine). Toxic metabolite is formic acid
- Visual symptoms. Metabolizes to formic acid, which is directly toxic to optic nerve
- Tx: Fomepizole and dialysis
- *Propylene glycol (rarely, low toxicity). Toxic metabolite is lactic acid
- Used as solvent for IV lorazepam, is approved food sweetener. Can cause severe lactic acidosis
- *Ethylene glycol (antifreeze). Toxic metabolite is glycolic acid
25
Q
High anion gap metabolic acidosis (HAGMA)
- Anion gap acidosis occurs when an acid is added to the blood: CO2 is combined with H+, leading to low CO2, but Cl is ____
- MUDPILES
- M
- U
- D
- P, P, P
- I, I, i, I
- L
- E
- S
- Patients with metabolic acidosis often develop a compensatory respiratory alkalosis via tachypnea to normalize acid-base status.
A
High anion gap metabolic acidosis (HAGMA)
- Anion gap acidosis occurs when an acid is added to the blood: CO2 is combined with H+, leading to low CO2, but Cl is normal
- MUDPILES
- Methanol (directly toxic to optic nerve, causes vision loss, coma)
- Uremia
- DKA
- Propylene glycol (food sweetener), Propofol, Paraldehyde
- Isopropyl alcohol, Iron, isoniazid, Infection
- Lactic acidosis (ie from post seizure)
- Ethylene glycol (antifreeze, damages kidneys, calcium oxalate crystals in urine, see hypocalcemia)
- Salicylates
- Patients with metabolic acidosis often develop a compensatory respiratory alkalosis via tachypnea to normalize acid-base status.
26
Q
Normal anion gap metabolic acidosis (NAGMA)
- Occurs when HCO3- is lost.
- __chloremic acidosis that shows increase in Cl with decrease in HCO3. Cl is increased to maintain electrical neutrality
- Low bicarb with a ____ chloride
- Causes: HARDUP
- H
- A
- R
- D
- U
- P
- K
- NAGMA + Hyperkalemia: Think Type ___ RTA
- NAGMA + Hypokalemia: GI loss or RTA __ or __
- UAG
- NAGMA + positive UAG: RTA
- NAGMA + negative UAG: GI losses
A
Normal anion gap metabolic acidosis (NAGMA)
- Occurs when HCO3- is lost.
- Hyperchloremic acidosis that shows increase in Cl with decrease in HCO3. Cl is increased to maintain electrical neutrality
- Low bicarb with a high chloride
- Causes: HARDUP
- Hyperalimentation - TPN can increase the generation of NH4+ as a breakdown product of amino acids
- Acetazolamide
- Renal tubular acidosis, Renal failure - inability to excrete H+
- Diarrhea
- Urinary diversion
- Pancreatic fistula
- K
- NAGMA + Hyperkalemia: Think Type 4 RTA (hypoaldosteronism)
- NAGMA + Hypokalemia: GI loss or RTA 1 or 2
- UAG
- NAGMA + positive UAG: RTA
- NAGMA + negative UAG: GI losses
27
Q
Urine anion gap (UAG) = ________
- Estimate of unmeasured ions in the urine, the most important one being ____
- Normal value is close to 0
- Differentiates between GI loss of HCO3 (diarrhea) and RTA
- Normal/positive UAG suggests low urinary NH4 (RTA)
- Negative UAG (NeGUTive) suggests high renal excretion of H in form of NH4 (diarrhea with HCO3- loss)
A
Urine anion gap (UAG) = Na + K - Cl
- Estimate of unmeasured ions in the urine, the most important one being ammonium (NH4+)
- Normal value is close to 0
- Differentiates between GI loss of HCO3 (diarrhea) and RTA
- Normal/positive UAG suggests low urinary NH4 (RTA)
- Negative UAG (NeGUTive) suggests high renal excretion of H in form of NH4 (diarrhea with HCO3- loss)
28
Q
Metabolic Alkalosis
- ____chloremia is usually associated with metabolic alkalosis resulting from chloride loss associated with GI or renal losses
- Chloride responsive - urinary Cl- <10 mEq/L (NaCl reabsorbed to maintain intravascular volume)
- Vomiting
- Diuretics
- Posthypercapnia
- Cystic fibrosis
- Treatment: Restoration of volume with IV fluids (NaCl or KCl). Potassium correction is integral
- Chloride resistant - Urinary Cl- >10 mEq/L
- No HTN
- Bartter syndrome (hypokalemia, hyponatremia)
- Gitelman syndrome (hypomagnesemia, hypocalciuria)
- HTN
- Cushing syndrome
- Primary hyperaldosteronism
- Liddle syndrome
- 11-beta-OH deficiency
- Exogenous steroids
A
Metabolic Alkalosis
- Hypochloremia is usually associated with metabolic alkalosis resulting from chloride loss associated with GI or renal losses
- Chloride responsive - urinary Cl- <10 mEq/L (NaCl reabsorbed to maintain intravascular volume)
- Vomiting
- Diuretics
- Posthypercapnia
- Cystic fibrosis
- Treatment: Restoration of volume with IV fluids (NaCl or KCl). Potassium correction is integral
- Chloride resistant - Urinary Cl- >10 mEq/L
- No HTN
- Bartter syndrome (hypokalemia, hyponatremia)
- Gitelman syndrome (hypomagnesemia, hypocalciuria)
- HTN
- Cushing syndrome
- Primary hyperaldosteronism
- Liddle syndrome
- 11-beta-OH deficiency
- Exogenous steroids
29
Q
If there is metabolic acidosis, check the Winter’s formula to see if there is also a respiratory acidosis/alkalosis present. If there is high anion gap metabolic acidosis, check the AG vs HCO3 to see if there is a metabolic alkalosis component; also consider checking Osmolal gap if intoxicated. If there is a non-anion gap metabolic acidosis, check the urine anion gap.
A
If there is metabolic acidosis, check the Winter’s formula to see if there is also a respiratory acidosis/alkalosis present. If there is high anion gap metabolic acidosis, check the AG vs HCO3 to see if there is a metabolic alkalosis component; also consider checking Osmolal gap if intoxicated. If there is a non-anion gap metabolic acidosis, check the urine anion gap.
30
Q
- The primary treatment for all forms of RTA is ______ replacement
- Think of the type number as indicating the serum K level: Type __ = low, Type __ = low-normal, Type __ = high
A
- The primary treatment for all forms of RTA is bicarbonate replacement
- Think of the type number as indicating the serum K level: Type 1 = low, Type 2 = low-normal, Type 4 = high
31
Q
Type I Distal: Impaired distal ___ secretion into urine. _____ K
- Path: Defect of distal tubule H+ secretion by cortical collecting duct
- Causes:
- Meds (amphotericin B, toluene (glue sniffing), lithium)
- Autoimmune (sjogren’s, SLE, rheumatoid arthritis)
- Chronic active hepatitis
- Genetic disorders
- Pt:
- Urinary pH >___. ___kalemia
- Commonly causes ___ and ___, likely caused by decreased citrate excretion and hypercalcemia (citrate is a natural neutralizer of calcium crystallization)
A
Type I Distal: Impaired distal hydrogen secretion into urine. Low K
- Path: Defect of distal tubule H+ secretion by cortical collecting duct
- Causes:
- Meds (amphotericin B, toluene (glue sniffing), lithium)
- Autoimmune (sjogren’s, SLE, rheumatoid arthritis)
- Chronic active hepatitis
- Genetic disorders
- Pt:
- Urinary pH >5.5. Hypokalemia
- Commonly causes nephrocalcinosis and renal stones, likely caused by decreased citrate excretion and hypercalcemia (citrate is a natural neutralizer of calcium crystallization)
32
Q
Type 2 Proximal tubule: Poor ____ resorption. ___ K
- Path: Mechanism similar to _____ - decreasing bicarbonate reabsorption in proximal tubule
- Causes:
- Idiopathic
- ____ syndrome
- Associated with: Rickets
- Cystinosis
- Drugs: Acetazolamide, 6-mercaptopurine, expired tetracycline
- Heavy metal poisonings (lead, copper, mercury, cadmium)
- Multiple myeloma
- Disorders of protein, carbohydrate, or amino acid metabolism
- Pt:
- Urine pH
A
Type 2 Proximal tubule: Poor bicarb resorption. Low/normal K
- Path: Mechanism similar to acetazolamide - decreasing bicarbonate reabsorption in proximal tubule
- Causes:
- Idiopathic
- Fanconi syndrome
- Associated with: Rickets
- Cystinosis
- Drugs: Acetazolamide, 6-mercaptopurine, expired tetracycline
- Heavy metal poisonings (lead, copper, mercury, cadmium)
- Multiple myeloma
- Disorders of protein, carbohydrate, or amino acid metabolism
- Pt:
- Urine pH <5.5. Hypokalemia (decreased)
33
Q
Type 4 Distal: ____ resistance (or secretion problem) (defect in Na/K exchange). ___ K
- Path: Similar to ____ or hypo___
- Causes: Most commonly in pts with chronic renal failure ass w renal parenchymal injury and scarring
- Obstructive uropathy (most common)
- Interstitial renal disease (most common)
- Type 1 pseudohypoaldosteronism
- Diabetic nephropathy
- CAH / 21-hydroxylase deficiency
- Renal transplant
- Pt: Urine pH _____, ____kalemia
A
Type 4 Distal: Aldosterone resistance (or aldosterone secretion problem) (defect in Na/K exchange). High K
- Path: Similar to spironolactone or hypoaldosteronism
- Causes: Most commonly in pts with chronic renal failure ass w renal parenchymal injury and scarring
- Obstructive uropathy (most common)
- Interstitial renal disease (most common)
- Type 1 pseudohypoaldosteronism
- Diabetic nephropathy
- CAH / 21-hydroxylase deficiency
- Renal transplant
- Pt: Urine pH <5.5, hyperkalemia (elevated)
34
Q
GFR
- GFR can be estimated from creatinine clearance (using a 24-hour urine collection).
- GFR = CrCl = (UCr x V) / PCr
- Creatinine is produced by muscle tissue - the more muscle tissue there is, the more creatinine there is to be cleared from the blood
- GFR = CrCl = (UCr x V) / PCr
- Estimate GFR (Schwartz formula) = 0.413 x (height in cm/plasma creatinine in mg/dL)
- ____ is a promising and perhaps more reliable marker to estimate GFR.
A
GFR
- GFR can be estimated from creatinine clearance (using a 24-hour urine collection).
- GFR = CrCl = (UCr x V) / PCr
- Creatinine is produced by muscle tissue - the more muscle tissue there is, the more creatinine there is to be cleared from the blood
- GFR = CrCl = (UCr x V) / PCr
- Estimate GFR (Schwartz formula) = 0.413 x (height in cm/plasma creatinine in mg/dL)
- Cystatin C is a promising and perhaps more reliable marker to estimate GFR.
35
Q
An elevated BUN:Cr (LESS/GREATER THAN ___:1) can indicate prerenal azotemia
FENa is typically LESS/GREATER THAN ___ in early AGN and prerenal azotemia; LESS/GREATER THAN __ in other causes of AKI
A
An elevated BUN:Cr (>20:1) can indicate prerenal azotemia
FENa is typically <1 in early AGN and prerenal azotemia; >1 in other causes of AKI
36
Q
PROTEINURIA
Urine Dipstick
- Positive protein (Detects albumin. Does not detect amino acids or kappa/lambda)
- Trace = \_\_ mg
- 1+ = \_\_-\_\_mg
- 2+ = \_\_\_-\_\_mg. Equivalent to Pr:Cr 0.1-0.3. Need to quantify (below)
- 3+ = \_\_-\_\_\_mg
- 4+ = 1000mg
- Normal urine albumin secretion is less than ____
A
PROTEINURIA
Urine Dipstick
- Positive protein (Detects albumin. Does not detect amino acids or kappa/lambda)
- Trace = 30 mg
- 1+ = 30-100mg
- 2+ = 100-300mg. Equivalent to Pr:Cr 0.1-0.3. Need to quantify (below)
- 3+ = 300-1000mg
- 4+ = 1000mg
- Normal urine albumin secretion is <30mg/day.
37
Q
Microalbuminuria is defined as urine albumin secretion ___-300mg/day and is an important RF for end organ damage in pts with DM or HTN.
- Microalbuminuria is one the earliest signs of _____.
- Indication of early glomerular injury, including diabetic nephropathy
- Detected on Random urine Albumin:Creatinine
- __-__ mg/g suggests incipient diabetic nephropathy
- > ___ mg/g indicates overt diabetic nephropathy
- For patients with Type I DM, screen yearly for albuminuria, beginning 3-5 years after initial diagnosis. For those with Type 2 DM, screen yearly after initial diagnosis.
A
Microalbuminuria is defined as urine albumin secretion 30-300mg/day and is an important RF for end organ damage in pts with DM or HTN.
- Microalbuminuria is one the earliest signs of diabetic nephropathy.
- Indication of early glomerular injury, including diabetic nephropathy
- Detected on Random urine Albumin:Creatinine
- 30-300 mg/g suggests incipient diabetic nephropathy
- > 300 mg/g indicates overt diabetic nephropathy
- For patients with Type I DM, screen yearly for albuminuria, beginning 3-5 years after initial diagnosis. For those with Type 2 DM, screen yearly after initial diagnosis.
38
Q
Protein:Creatinine ratio
- Normal Pr:Cr = less than ____
- Proteinuria = ___ mg protein/mg creatinine on single spot urine collection
- Nephrotic range proteinuria = spot urine (preferably 1st morning sample) Pr-to-Cr ratio >___
A
Protein:Creatinine ratio
- Normal Pr:Cr = <0.2
- Proteinuria = >0.2 mg protein/mg creatinine on single spot urine collection
- Nephrotic range proteinuria = spot urine (preferably 1st morning sample) Pr-to-Cr ratio >2
39
Q
24 hour urine is most accurate
- Normal 24-hour urine protein excretion is ___ mg/m2/hour
- Proteinuria = >__ mg/m2/day
- Nephrotic range = >___ mg/m2/day
A
24 hour urine is most accurate
- Normal 24-hour urine protein excretion is 4 mg/m2/hour
- Proteinuria = >100 mg/m2/day
- Nephrotic range = >1000 mg/m2/day
