Nephrology Flashcards
(119 cards)
1
Q
Acidemia
A
pH <7.35
- increase [H] ion in blood
2
Q
Acidosis
A
Increasing [H] ion in arterial blood plasma (acidemia), pH <7.35
3
Q
Alkalemia
A
pH >7.45
- reduced [H] in blood
4
Q
Alkalosis
A
Reducing [H] ion in arterial blood plasma (aklalemia); pH >7.45
5
Q
Henderson equation for H+
A
H (mEq/L) = 24 x PCO2/HCO3
6
Q
Respiratory acidosis
A
pH <7.35
increased pCO2
increased HCO3
7
Q
Metabolic acidosis
A
pH <7.35
decreased pCO2
decreased HCO3
8
Q
Respiratory alkalosis
A
pH >7.45
decreased pCO2
decreased HCO3
9
Q
Metabolic alkalosis
A
pH >7.45
increased pCO2
increased HCO3
10
Q
Compensation appropriate?
A
Metabolic acidosis: HCO3 decreased by 1mmol/L, PCO2 decreased by 1.25 mmHg
Metabolic alkalosis: HCO3 increased by 1mmol/L, PCO2 increased by 0.2-0.9 mmHg
Acute respiratory acidosis: PCO2 increased by 10mmHg, HCO3 increased by 1mmol/L
Acute respiratory alkalosis: PCO2 decreased by 10mmHG, HCO3 reduced by 2.5mmol/L
Chronic respiratory acidosis: PCO2 increased by 10mmHg, HCO3 increased by 5mmol/L
Chronic respiratory alkalosis: PCO2 reduced by 10mmHG, HCO3 reduced by 5mmol/L
11
Q
Anion Gap
A
AG = Na - Cl - HCO3
normal 8-14 mEq/L
increased in AG metabolic acidosis
**always calculate to make sure no mixed disorder
AG decreases by 4 for every drop of albumin by 10g/L
12
Q
change gap
A
change HCO3 = 24 - HCO3
change AG = calculated - normal (12)
change HCO3 > change AG = simultaneous non-AG metabolic acidosis
change AG > change HCO3 = simultaneous metabolic alkalosis
change AG = change HCO3 = only AG metabolic acidosis
13
Q
Ddx respiratory acidosis & tx
A
CNS
- brainstem injury (stroke, tumor)
- central sleep apnea
- obesity hypoventilation syndrome
Resp
- upper airway obstruction: laryngospasm, epiglottitis
- lower airway obstruction: COPD, asthma, sleep apnea
- dead space ventilation: infection, pleural effusion
Muscular
- myasthenia gravis, Guillain-Barre, myopathy, ALS, hypokalemia
Drugs
- opioids
Tx- intubation, mechanical ventilation, treat underlying disease, naloxone, etc.
14
Q
Ddx AG metabolic acidosis & tx
A
MUDPILES Methanol Uremia DKA, alcoholic KA, starvation KA Paraldehyde, phenformin, metformin Iron, isoniazide Lactic acidosis Ethylene glycol Salicylates Cyanide Arsenic Toluene
Tx - correct underlying disorder; NaHCO3 if pH <7.2; HCO3 deficit (mmol) = (desired bicarb - measured bicarb) xweight (kg) x 0.6 replace 1/2 total deficit over 8-12h
15
Q
Ddx Non-AG metabolic acidosis & tx
A
USED CAR Ureteroenteric fistula Saline (IV NS) Early renal failure Diarrhea Carbonic anhydrase inhibitors (acetazolamide) Amphotericin RTA I, II, IV
Tx - correct underlying disorder; NaHCO3 if pH <7.2; HCO3 deficit (mmol) = (desired bicarb - measured bicarb) xweight (kg) x 0.6 replace 1/2 total deficit over 8-12h
16
Q
Ddx respiratory alkalosis & tx
A
Cardiopulmonary - hypoxia - pneumonia - early restrictive lung disease - mild CHF - PE - mechanical ventilation Non-cardiopulmonary - fever, sepsis, anxiety, pregnancy, hyperthyroidism, liver failure Drugs - salicylate, progesterone
Tx- underlying disorders, hyperventilation - rebreather into paperbag
17
Q
Ddx metabolic alkalosis & tx
A
Saline responders - GI loss (vomiting, NG suction) - renal loss (diuretics) - skin loss (burns, sweat) - reduced fluid intake Saline non-responders - mineralocortisolism (Conn's syndrome, Cushing syndrome) - renin production (tumor) - severe hypoK - Gitelmann syndrome - Barter syndrome - HCO3 load (sodium bicarb infusion, citrate with transfusions, acetate with TPN)
Tx - saline responses = volume repletion
- saline non responders = tx underlying issue
18
Q
Urinary Na vs. Cl re: volume status
A
- metabolic acidosis = Na better surrogate for volume status (Cl excreted in excess with NH4+)
- metabolic alkalosis = Cl better surrogate for volume status (Na excreted in excess with HCO3)
19
Q
Hypomagnesemia
A
- [Mg2+] <1.5 mEq/L pr 0.75mmol/L
(normal 1.5-2 mEq/L or 0.75-1 mmol/L or 1.7-2.4 mg/dL)
often associated with hypoK and hypoCa (chronic hypoMg = reduced PTH secretion and bone response to PTH)
1% total Mg in ECF
70% Mg filterable -> calculating FEMg = x0.7
95% filtered Mg reabsorbed
20
Q
Altered Mg excretion
A
- hyperCa, hyperMg = reduced Mg reabsorption
- reduced GFR = reduced Mg reabsorption
- phosphate depletion = increase Mg excretion
- chronic metabolic acidosis = increased Mg excretion
- chronic metabolic alkalosis = decreased Mg excretion
21
Q
Redistribution of Mg
A
- hungry bones
- referring syndrome (redistribution to bones)
- DM
22
Q
Hyperkalemia
A
Serum K >5 mEq/L
2% K extracellular
98% muscle, liver, RBCs
excretion mainly renal (minimal sweat)
23
Q
K Adaptation
A
- renal response to prolonged increase in K load
- significant increase in efficiency of renal K excretion
- mediated by enhanced activity of Na/K ATPase of renal principal cells
- gradual return of K and aldosterone levels to normal
- reabsorption of K in PCT and loop of Henle remains at constant rate
24
Q
PsuedohyperK
A
- hemolysis blood
- severe leukocytosis
- severe thrombocytosis
25
Ddx hyperK
- shifting
- increased efflux: damage to intracellular K storage, acidosis, succinylcholine, diazoxide, minoxidil, isoflurane, hyperkalemia period paralysis
- decreased influx: lack of insulin, beta-blockers, dioxin OD
- decreased excretion - reduced GFR, decreased aldosterone, volume depletion, decreased from stool/sweat
26
HyperK on ECG
- peaked T waves (tented narrow based, >10mm in precordial, >5mm in limb leads or relatively tall vs. baseline)
- shortened QT
- prolonged PR interval, then QRS
- P wave flattening then disappears
- sine wave pattern (K>8)
- ventricular standstill (flat line)
- arrhythmias (bradycardia, v-tach, v-fib)
27
Tx hyperK
```
ECG changes (K>7)
- calcium gluconate or calcium chloride (stabilize membrane)
No ECG changes (K = 6.5-7)
- insulin with glucose, B-agonist, sodium bicarb if acidotic (shifting)
No ECG changes (K <6.5)
- diuretics, caution-exchange resins, dialysis (K removal)
```
28
HypoK
Serum K <3.5 mEq/L
- often multifactorial, chronic and symptoms develop late
approx. decrease by 0.27 mEq/L = 100mEq deficit
29
Diuretics and hypoK
Loop and thiazide diuretics = Cl depletion and hypovolemia with metabolic alkalosis
K depletion via
- increased flow and delivery of NaCl to CCD
- alkalemia (redistribution)
- hypovolemia with activation of RAAS
30
Severe/life threatening HypoK
K <2.5 - 3 mEq/L
sx - weakness starts in lower extremities and progresses to upper extremities, respiratory muscle paralysis, rhabdomyolysis; ileus; arrhythmias, ECG changes
TX
-replace immediately but caution re: rebound hyperK (max K IV rate 20 mEq/h, oral 60mEq)
40-60 mEq = increase K by 1-1.5 mEq/L
31
K shifting re: hypoK
- increased Na/K ATPase activity --> insulin, b-adrenergic
- increased pH (H out, K in)
- hypoK periodic paralysis (mutation Ca channel)
- increased uptake from plasma in acute increase hematopoietic cell production
- hypothermia
- barium, caesium, chloroquine intoxication (block K channels)
- resperidone or quetiapine OD
32
Proteinuria
urinary total protein excretion >150 mg/d with >30mg/d albumin
- > risk marker for cardiovascular disease
- only albuminuria detected by urine dipstick (not reliable for microalbuminuria) -> check urine micro albumin to creatinine ratio (ACR) if risk of renal disease
- urine protein to creatinine ratio (PCR) detects all protein in urine, not sensitive at low values
severity
>2g/d - likely glomerular disease
0.15 - 2g/d - likely tubular proteinuria, overflow proteinuria, or mild glomerular disease
33
Microalbuminuria
30-300 mg/d albumin
34
Nephrotic proteinuria
>3.5g/d total protein
35
Ddx proteinuria
- benign
- transient intermittent (fever, dehydration, exercise)
- orthostatic (>50mg/8h while upright)
Persistent
- Glomerular (glomerular permeability to protein)- nephritic syndrome, glomerularnephritis, systemic disorders; nephrotic syndrome, diabetic nephropathy, FSGS
- Tubular (reduced reabsorption of filtered proteins)- tubule-interstitial disease, drugs, chronic pyelonephritis, Fanconi, sickle cell disease, etc.
- Overflow (filtered load > tubular reabsorptive capacity)- multiple myeloma, MGUS, amyloid, hemoglobinuria, myoglobinuria
36
Normally excreted proteins
40% Tamm-Horsfall mucoproteins
40% albumin
20% Igs
37
Tx primary glomerular disease
corticosteroids, diuretics, cytotoxic agents, anti-HTN, plasmapheresis as indicated
38
Tx HTN related proteinuria
BP target <125/75
| ACEI, ARBs preferred (proteinuria-reducing effect independent of anti-HTN)
39
Hyaline casts
No renal pathology - dehydration, diurectics
40
RBC casts
glomerular disease
41
Dysmorphic RBCs
upper urinary tract pathology
42
Intact RBCs
lower urinary tract pathology
43
WBCs, WBC casts, bacteria
UTI/inflammation
44
Fatty cast, oval fat bodies, free fat
Nephrotic proteinuria
45
Waxy, granular or cellular casts
Advanced chronic renal disease
46
Eosinophiluria
Acute interstitial nephritis
47
Glomerular filtration barrier
- degree of proteinuria depends on integrity of barrier (charge and size) and intraglomerular (filtration) pressure
Slit diaphragm - pores that limit passage
Visceral glomerular epithelial cell (podocyte) foot processes
GBM - limits size and negatively charged particles
Cappilary endothelial cells - limit negative charged particles; fenestrations limit size
48
Nephrotic syndromes
- proteinuria >3g/d
- edema all over
- BP, JVP normal/low
- hyaline casts, lipid droplets on urine sediment
- reduced albumin
- Cr normal/increased
Primary causes - minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, congenital nephrotic syndrome, Alport disease
Secondary causes - diabetic nephropathy, amyloidosis, lupus nephritis, membranoproliferative glomerulonephritis, secondary membranous, secondary FSGS, preeclampsia, malaria, syphilis, HIV nephropathy
49
Nephritic sydnrome
- proteinuria <3g/d
- minor edema
- increased BP, JVP
- +++ hematuria
- urine sediment: RBC, WBC, RBC casts, granular casts
- normal/mild decrease albumin
- Cr usually increased
Primary causes- IgA nephropathy, Wegener granulomatosis, antiglomerular basement membrane disease, lupus nephritis, postinfectious glomerulonephritis, endocarditis, membranoproliferative glomerulonephritis
50
HyperNa
Na > 145 mEq/L
- often when unable to experience or communicate thirst-
- unreplaced H2O losses (skin, GI, GU, insensible from airway, hypothalamic lesion re: thirst)
- sodium overload (salt poisoning, isotonic saline, hypertonic solutions, primary hyperaldosteronism)
51
Serum osmolality re: HPA
- increased plasma osmolality -> stimulate hypothalamic osmoreceptors -> ADH release -> maintain serum osmolality
52
Na correction with hyperNa
max 8mEq/L for first 24h and 10mEq/L next 24h
- overly rapid = cerebral edema
- sx = impaired mental status, headache, memory loss, seizure, coma
53
HypoNa
Na <135 mmol/L
| - severe <120 or abrupt hypoNo = increased risk neurologic complications due to cerebral edema
54
Hypovolemic hypoNa
pt lost both total body water and total body sodium but relative sodium loss, or water gain, is greater
55
Normovolemia hypoNa
normal TBNa but excess TBW
56
Hypervolemia hypoNa
increase in both TBNa and TBW, but relative excess of water
57
How do you determine if ADH is present or suppressed with hypoNa?
Urine osmolality
| - ADH surpassed if UOsm <100 most/kg, SG <1.003
58
Calculation for plasma osmolality
= 2[Na] + [glucose] + [urea]
59
Acute vs. chronic hypoNa sx
acute
- mild: asx, nausea, malaise, anorexia, headache, lethargy, weakness, confusion
- abrupt and severe: delirium, neuromuscular hyper excitability, seizure, coma, resp arrest, death
- complications - brainstem herniation, hypothalamic and posterior pituitary infarction
chronic
- cerebral adaptation - often asx
- if sx: nausea, fatigue, gait instability, amnesia, confusion, lethargy, muscle cramps
60
Management hypoNa
- plasma osmolality
- hypoosmolar - determine ECF volume
- treat hypoNa re: pt sx
- correct underlying abnormality
severe sx- 3% saline rapid correction at 1-2mmol/L/h for first 4h or sx improve
DO NOT correct >10-12 mmol/Lin first 24hr
raise Na by 4-6mEq/L within a few hours
- Captains directly inhibit ADH - can be used in euvolemic or hypervolemic pt in hospital
61
What do you do if serum Na rises by >10-12 in 24h?
Administer free water or exogenous ADH
62
Risk of increasing Na by >8 mEq in first 24h?
Osmotic demyelination - central pontine myelinolysis: dysphagia, dysarthria, delirium, spastic paraparesis or quadriparxsis, locked-in syndrome, coma, death
63
Acute renal failure
sudden, rapid, potential reversible fallen GFR leading to accumulation of nitrogenous waste products
sx - azotemia (reduced GFR, increased urea and Cr), abnormal urine volume (anuria = <100mL/24h or oliguria = 100-400mL/24h)
64
Tubuloglomerular feedback
Na delivery to macula densa regulates afferent arteriolar tone
increased delivery = vasoconstriction
65
Glomerulotubular balance
Proximal tubule tends to reabsorb constant proportion (rather than amount) of glomerular filtrate
66
Renal portal circulation
afferent arteriole -> glomerular capillaries -> efferent arteriole -> vasa recta
67
Countercurrent flow in vasa recta
PO2 higher in renal cortex and lower in renal medulla
68
What part of the kidney is most vulnerable to ischemic injury (ischemic ATN)?
Medullary portions of proximal tubule and of the TAL - highest rate of energy-dependent solute transport
69
Complications of ARF?
- intravascular overload
- hypoNa
- hyperK
- hyperphosphatemia
- hypoCa
- hyperMg
- hyperuricemia
- metabolic acidosis
Other
- anemia
- leukocytosis
- bleeding diathesis (secondary to uraemia-induced lately dysfunction)
- progress to CRF
- uremic syndrome
70
Ddx ARF
Prerenal
- renal hypoperfusion
- systemic hypo perfusion
Intrinsic
- renovascular
- glomerular
- tubular and interstitial
Postrenal/ obstructive
- renal pelvis
- ureter
- bladder
- bladder neck/ urethral
71
Chronic renal failure = chronic kidney disease
- evidence of renal damage OR moderately to severe impaired GFR (<60mL/min) for at least 3mo
target BP <130/80
72
Renal function?
- maintain ECF volume and osmolality
- produce EPO
- Ca homeostasis (via activation vit. D and tubular handling of Ca and phosphate under PTH)
- electrolyte balance
- acid-base balance (excretion H, recovery HCO3)
73
Stages of CKD
Stage 1: GFR >90 - normal to increased GFR with evidence of kidney damage
Stage 2: GFR 60-89 - mildly decreased GFR with evidence of kidney damage
Stage 3: GFR 30-58 - moderately decreased GFR
Stage 4: GFR 15-29 - severely decreased GFR
Stage 5: <15 or dialysis - ESRD or renal failure
74
Ddx CKD
Prerenal
- renal vascular disease
Renal
- glomerular disease (primary): focal segmental glomerulosclerosis, IgA nephropathy
- glomerular disease (secondary): HTN nephropathy, SLE< diabetic nephropathy, vasculitides, HIV, HBV, HCV
- tubulo-interstitial - chronic intersitial nephritis, cystic kidney disease
Postrenal
- Obstructive nephropathy
*DM (25-35%) and HTN (15-20%) most common causes of CKD
75
Hematuria
>2 RBCs per HPF
76
Microhematuria
presence of RBCs in urine without visible change in urine colour
77
Macrohematuria
red or brownish urine
78
Persistent hematuria
hematuria on at least 2 urine samples at least 1 mo apart
79
Ddx hematuria
```
Dyes: medications, food, metabolites
Pigmenturia: hemoglobin, myoglobin
True hematuria: fever, exercise
- Glomerular
- Renal
- Ureter
- Bladder
- Prostate/urethra
Mimics of hematuria - contamination of urine with menses, GI bleed, atrophic vaginitis
```
80
Investigations hematuria
- urine dipstick
- microscopy
+ labs if indicated
+ imaging if indicated
All pt should have urine culture to r/o infection and recheck urine in 6wk
No dx with cultures and imaging -> cystoscopy to r/o malignancy
81
Recurrent nephrolithiasis investigation and tx
investigations - stone analysis, 24h urine collection for urine volume, pH, calcium, phosphorus, oxalate, citrate, rate, cysteine, sodium; urine culture
tx - increase fluid intake at least 2L/d, dietary modifications, hydrochlorothiazide for hypercalciuria, citrate for hypocitraturia, allopurinol for hyperuricosuria
82
Urine dipstick
- gold standard to detect hematuria
- very sensitive
- detects dyuria
- negative in pigmenturia
83
Urine microscopy
differentiate hematuria vs. dyuria (RBCs)
84
Glomerular hematuria
- process involving glomerular structure and characterized by dysmorphic RBCs (acanthocytes), RBC casts, proteinuria, no blood clots
85
Extraglomerular hematuria
- proteinuria, blood clots
86
Polyuria
>3L urine output/24h in adults and 2L/m^2 in kids
87
Polydipsia
increased thirst and water intake
88
Ddx polyuria
- water diuresis - urine osmolality <250mOsm/kg (primary polydipsia, hypoosmolar fluid load, central DI, nephrogenic DI)
- osmotic diuresis - urine osmolality >250mOsm/kg (glucose, mannitol, urea, iso/hyperosmotic fluid loads)
89
Where is ADH produced?
By magnocellular neutrons of supraoptic and paraventricular nuclei in hypothalamus and transported via their dendrites to posterior pituitary where it is released
90
Stimulation of ADH release?
changes in blood osmolality sensed by hypothalamic osmoreceptors
91
ADH action
ADH receptors -> aquaporins released from intracellular vesicles into the luminal membrane
-> water can enter cell and be reabsorbed into blood vessels
92
Ca form in blood?
40% free ionized Ca (metabolically active)
| 60% protein bound Ca
93
How is serum Ca regulated?
PTH -> increase Ca (PTH released bc low Ca = acts on bone to increase resorption and kidney to increase reabsorption and increase Vit. D)
Vit. D -> increases intestinal Ca absorption (produced because PTH and low serum Ca)
94
What 2 blood properties can alter serum Ca?
albumin - low albumin = low Ca
pH - acidosis = reduced protein binding Ca
- often free ionized Ca same so measure ionized Ca levels
95
How do you correct Ca for albumin?
Ca falls 0.2mmol/L for every 10g/L drop in albumin
96
Ddx hyperCa
- increased bone resorption (hyperparathyroidism, malignancy, hyperthyroidism, immobilization)
- increased Ca absorption (increased intake, increased vit. D)
- decreased excretion (thiazide diuretics, familial hypocalciuric hypercalcemia)
97
HyperCa sx
Ca >3.5 mmol/L
| - confusion, stupor, coma, ARF, profound weakness
98
HyperCa tx
Pt sx and Ca >3.5
- IV rehydration, calcitonin, bisphosphonate therapy (pamidronate)
- hemodialysis if severe hyperCa and renal failure
If Vit D excess then start prednisone
99
Ddx hypoCa
PseudohypoCa
- low serum Ca but normal ionized Ca (hypoalbuminemia)
Spuriouas hypoCa
- low serum Ca after injection of gadolinium-based contest agents
True hypoCa
- excessive loss (extravascular deposition, renal losses)
- decreased absorption (vit. D deficiency, reduced PTH, PTH resistance, drugs)
100
Workup hypoCa
- true? check ionized Ca
- PTH?
low PTH - check Mg
high PTH - check GFR (low = renal failure, high = check vitamin D)
101
Symptoms hypoCa
Ca <1.9 mmol/L
- parenthesis, carpopedal spasm, tetany, seizure
- Trousseau or Chvostek sign, bradycardia
- Prolonged QT
102
What is Trousseau sign?
A sign of latent TETANY = carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes
103
What is Chvostek sign?
Twitching of the facial muscles in response to tapping over the area of the facial nerve
104
Management hypoCa
Ca <1.9 and sx?
- if prolonged QT give IV calcium gluconate 1-2g IV
- i no QT prolongation give oral calcium carbonate 1500- 2000mg daily
If hypoMg
- start Mg replacement
If Vit D deficient or hypoparathyroid
- start 1000U vit D
- use calcitriol 0.25 micrograms if renal failure
- add thiazide diuretic if hypercalciuria develops
105
Normal plasma phosphate?
1-1.5 mmol/L
| - most abundant intracellular anion
106
Where is most of total body phosphorus?
85% in bones and teeth
| 1% in extracellular fluid
107
What anion is needed for metabolic processes such as formation of high energy ATP and components of cell membranes?
Phosphorus
108
What organ is primary regulator of phosphate?
Kidneys
109
How is plasma phosphate regulated?
Humoral factors regulating renal phosphate excretion and GI phosphate absorption
- PTH (increased PTH = increased urine phosphate excretion; decreased vit D = decreased dietary phosphate absorption)
- Phosphatonins
Local factors (e.g. insulin)
110
Ddx hyperphosphatemia
- Acute high phosphate load - cell lysis (e.g. rhabdomyolysis, hemolysis), translocation of intracellular phosphate (lactic acidosis, ketoacidosis), exogenous load (phosphate-containing laxatives, IV phosphate)
- Renal failure (reduced filtration and excretion)
- Increased GI absorption (excess vit. D)
- Increased renal phosphate reabsorption (hypoparathyroidism, acromegaly, medications, familial tumoral calcinosis)
Pseudohyperphosphatemia
- interference of assay by immunoglobulins, bilirubin, hemolysis, hyperlipidemia, liposomes amphotericin B
111
Does hyperphosphatemia commonly occur with CKD?
Yes re: reduced GFR
| - dietary phosphate restriction and phosphate binders important
112
What can occur with uncontrolled hyperphosphatemia?
- secondary hyperparathyroidism
- renal osteodystrophy
- tissue calcium/ phosphate deposition
- risk factor for death
113
Investigation for hyperphosphatemia
- exclude hemolysis - bilirubin, LDH, hepatoglobin, peripheral smeal
- rhabdomyolysis - CK, myoglobinuria
- tumor lysis - uric acid (esp. with hyperK)
- lactate, ketones, PTH, Cr, BUN, Ca
114
Management hyperphosphatemia
acute should resolve in hours
- fluids may increase excretion (but avoid hypoCa)
- hemodialysis if severe hypoCa and renal dysfunction
- low phosphate diet and binding of dietary intestinal phosphate if chronic
115
Ddx hypophosphatemia
Phosphate redistribution
- refeeding syndrome, DKA, insulin secretion, hungry bone syndrome, hyperventilation with acute respiratory alkalosis
Reduced GI absorption
- poor oral intake, phosphate binding GI tract by antacid medications (Al3+, Mg2+, Ca2+)
- chronic diarrhea with malabsorption
Increased renal excretion
- hyperparathyroidism, vit D deficiency, Fanconi syndrome, oncogenic osteomalacia, hereditary hypophosphatemic rickets, diuresis
Spurious hypophosphatemia with paraproteinemia and interference with assay
116
Workup hypophosphatemia
24h urine phosphate excretion and fractional excretion phosphate - renal wasting?
117
Management hypophosphatemia
Phosphate <0.64mmol/L and asx - replete with oral phosphate, high phosphate diet
Phosphate <0.32mmol/L and pt sx or can't take PO, replete IV phosphate until >0.48mmol/L then switch to PO
- replace at half dose if pt has renal dysfunction
- potassium or sodium phosphate (no potassium phosphate in renal dysfunction)
Dipyridamole if primary urine potassium wasting
118
Risks of rapid phosphate infusion?
Calcium-phosphate precipitation
AKI
Arrhythmias
119
What causes the clinical consequences of hypophosphatemia?
Altered bone and mineral metabolism
Reduced production of cellular ATP
- often sx when <0.64 and severe <0.32
