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Lytes

Renal

QuestionAnswer
hyponatremia = Na <135 (symptoms seen at Na <125)
Etiology of hypervolemic hypotonic hyponatremia CHF, nephrotic syndrome, ARF, hepatic cirrhosis
Etiology of euvolemic hypotonic hyponatremia hypothyroid, glucocorticoid excess, SIADH, polydipsia, beer potomania
Etiology of hypovolemic hypotonic hyponatremia dehydration, diarrhea, vomiting
Hyperkalemia (K >5) etiologies ARF (most common), increased K load, metabolic acidosis, cell death, hyporeninemic hypoaldosteronism
Hypokalemia (K <3.5) nonrenal (urine K <20) etiologies GI losses (N/V/D, Z-E syndrome), metabolic alkalosis (increases K secretion)
Hypercalcemia etiologies HyperPTH (most common). Neoplasm (lung, head/neck, MM, NHL, cervical, RCC). Vit D intox. Paget. Adrenal insuff. Milk alkali syndrome. Sarcoid. ZE syndrome. Acromegaly.
Dry skin, brittle nails, mx cramps, paresthesias, laryngospasm/stridor, hyper DTRs, SOB, crackles, S3, syncope & angina = hypocalcemia (Ca <8.5); usu 2/2 CKD or hypoPTH
Hyperphosphatemia (1.0-2.5); severe (<1.0) can lead to: rhabdo, paresthesia, encephalopathy
Hypermagnesemia (2.5 mEq/L) sx/sx 1st: reduced DTRs; mx weak, hypoTN, resp depression, cardiac arrest; N/V, flushing; high bleeding time/coag
Normal range: pH: 7.40 (7.35-7.45)
Normal range: pO2: 80-100 mmHg
Normal range: pCO2: 35-45 mmHg
Normal range: HCO3: 22-26 mmol/L
Anion gap = cations (Na+) – anions (Cl- + HCO3-); Normal AG = 8-16 mmol/L
Respiratory compensation for metabolic acidosis pCO2 should fall 1.2 for every 1.0 drop in HCO3
Respiratory acidosis etiology impairment in rate of alveolar ventilation; acute medullary resp ctr depression (narcotic OD), resp mx paralysis, airway obstruction; chronic (emphysema, pickwickian)
Resp acidosis Sx/Sx metab encephalopathy: somnolence, confusion, narcosis, asterixis. Fundi: dilated, tortuous vessels, possible papilledema
Resp acidosis DDx/causes COPD, airway obstruction, CNS depression (opioids, brainstem injury), neuromx (GBS, MG, botulism), myxedema
Resp alkalosis (hypocapnia) Patho hyperventilation reduces PCO2, increases pH
Resp alkalosis Sx/Sx lightheadedness, anxiety, perioral numbness, acroparesthesias (pain hands & feet)
Resp alkalosis DDx PE, pulmo edema, PTX, ARDS, pulmo art HTN, asthma, interstitial pulmo fibrosis
NAGMA possible causes = extrarenal bicarb loss (diarrhea, renal bicarb excretion); renal tubular acidosis; chronic renal failure, carbonic anhydrase inhibitors, diuretic, primary hyperPTHism, Addison dz
AGMA: MUDPILES methanol, uremia, DKA, propylene glycol, isoniazid, lactic acidosis [shock, septicemia, hypoxemia], ethylene glycol, salicylates
AGMA: CUTE DIMPLES C for Cyanide & T for Toluene plus MUDPILES
Metab acidosis Sx/Sx CP, palpitations, HA, AMS, decreased visual acuity, N/V/abd pain, wt loss, mx weakness, bone pain; Kussmaul (profound DKA), lethargy, stupor, coma, seizures; V-tach, hypotension
Metabolic alkalosis: chloride-responsive (low urine Cl): due to: diuretic tx (contraction alkalosis) or loss of gastric secretions (2/2 vomiting or NG tube)
Metabolic alkalosis: chloride-resistant (high urine Cl): etiology Bartter or Gittelman syndrome; hyperaldosteronism; bicarb intake in CKD
Pathology of hypervolemic hypotonic hyponatremia expansion of extracellular fluid relative to amount Na present
Pathology of hypovolemic hypotonic hyponatremia 1) extrarenal. 2) renal salt/volume loss based on urine Na level
Conditions associated with isotonic hyponatremia Hyperlipidemia (familial HLD or nephrotic syndrome), hyperproteinemia (multiple myeloma, macroglobulinemia)
Isotonic hyponatremia patho Na amount in plasma stays same, but more of other solutes -> decrease in relative Na conc
Hypertonic hyponatremia etiology Hyperglycemia (100mg/dL rise -> 1.5mEq/L Na drop); hypertonic tx (eg, mannitol) -> water leaves cells, Na leaves vascular space to extracellular space
Hypernatremia defn = serum Na >145mEq/L (osmo >290)
Hypernatremia correction Free water deficit = Wt x [(Na - 140)/140]. Correct over 48h; drop Na by 1mEq/L/hr.
Hypokalemia (K <3.5) renal (urine K > 40) etiologies diuretics, renal tubular acidosis, adrenal hormones, hyperaldosteronism, Cushing/steroids, digoxin, low Mg
Hypokalemia clinical features Muscle cramps, ileus, dysrhythmia
Hypokalemia with acidosis & without HTN: suspect: RTA
Hypokalemia with high urine Cl without HTN / acidosis: suspect: Diuretics or Bartter syndrome (low urine Cl = N/V)
High dose K repletion for severe hypokalemia (<2.5 mEq/L) Max 20 mEq/L/h and max 60 mEq/L. Should be via central venous access
Dysrhythmias associated with severe hyperkalemia (>6.5) Brady, prolonged PR, peaked T waves progressing to long QRS; V-fib
Most potassium in body is found in: Intracellular
Hyperkalemia from K shift from intracellular to extracellular space may be 2/2: Burns, rhabdo, hemolysis, severe infxn, internal bleeding, extreme exercise
Hyperkalemia clinical findings Initial hyperreflexia, then flaccid paralysis; vasodilation
Hyperkalemia mgmt IV beta-agonists (salbutamol), Na bicarb, IV insulin (w/D5NS); Ca gluconate (stabilizes cardiac membrane); SPS; loop diuretics; ?HD
Ca distribution in body 99% in bone. 0.01% in body fluids. 50% of Ca bound to albumin, 10% to other, 40% free.
Hypocalcemia etiologies CKD (most common: 2/2 decreased vit D production). Low albumin. Sepsis. Acute pancreatitis. Post-thyroid surgery. hypoPTH. Blood transfusion. Medullary ca of thyroid (calcitonin secretion).
Hypocalcemia patho Low Ca (2/2 low intake/absorption or low PTH or increased Ca into bone) -> lower NM excitation threshold -> reduced contractile force in vascular smooth & cardiac mm
Symptomatic hypocalcemia mgmt. IV Ca gluconate 10% infusion, ?IV CaCl
Hypercalcemia clinical findings Weakness, polydipsia, hyporeflexia, confusion, renal calculi, N/V, constipation, ileus, nephrogenic DI, bone pain/fx
Hypercalcemia mgmt. IVF forces urinary excretion of Ca. +/- furosemide (thiazide may worsen high Ca). +/-HD.
Hypercalcemia mgmt.: underlying causes Metastatic bone dz: calcitonin +/- pamidronate (inhibit bone resorption). Sarcoid/MM/leukeumia/BrCa/vit D intox: glucocorticoids
PO4 distribution in body 70% intracellular, 29% intraskeletal, <1% serum
Hypophosphatemia etiology Decreased GI absorption, vit D def, refeeding syndrome, hyper PTH, hyperthyroid, DKA, sepsis, ASA toxicity
Severe hypophosphatemia results in: Decreased affinity of Hgb for O2
Hypophosphatemia workup Serum PO4 <2.5. Urine PO4 >20 = renal loss. PTH. Bone bx: ?osteomalacia. CK (rhabdo)
Hyperphosphatemia etiology CKD, AKI, hypoPTH, acromegaly. Increased intake, vit D, rhabdo, cell lysis, AGMA
Phosphate binders Sevelamer, lanthanum, Aluminum hydroxide
Resp alkalosis (hypocapnia) etiology Hyperventilation syndrome (?anxiety). GNR sepsis, cirrhosis, PE, CHF, ILD, PNA, pulmo edema, HAPE, CVA, anemia, PG (2/2 progesterone stim of resp ctr), acute ASA tox
Low anion gap seen in: NAGMA, myeloma, hypoalbuminemia, lithium Rx
Created by: Abarnard
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