hypokalemia
TRANSCRIPT
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Approach to etiology of Hypokalemia
Dr.M.Emmanuel Bhaskar
Associate Professor in Medicine
Sri Ramachandra Medical College
Chennai,India
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Approach……???????
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Approach to hypokalemia
All you need to do is to have a CLOSER LOOK!
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Learning objectives
1.To understand a concept based clinical approach to diagnose cause of hypokalemia
2.Understand the clinical relevance of common investigations used in the setting of hypokalemia
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Plan for Interaction
Brief Introduction
Presentation of scenario
Discussion by audience
Discussion by presentor
Questions by audience
Answers by the faculty ?
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How does body maintain a normal serum K?
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Gennari et al NEJM 1998;339:451-458
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Case-1
36 year old male admitted with pneumonia with septic shock. Admission labs shows Na-142, K-3, Cl-98, Hco3- 19. On Imipemem,nor-epinephrine,dopamine, pantoprazole , enoxaparin, I.V 0.9% Saline at 125cc/hr.
Day 5 develops Na-138,K-2.2,Cl-106,Hco3-17. Urine K- 30 meq/l .ABG- Ph-7.36 , Hco3-15, Pco2-26mmHg.. Mg-1.2 , Ca-9.6
K-improved to 3.2 with 80 meq /dy of i.v Kcl.
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Case-1: Issues ?
Approach?
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Case-1: Issues
Septic shock on Ionotropes and saline
Hospital acquired hypokalemia
Urinary K-excretion- ?
Metabolic acidosis with resp alkalosis
Marginally low serum Mg with normal Na,Cl,Ca
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Diagnostic protocol based on our observation in 76 cases of hypokalemia [ K<2 meq/l]
Study period: May 2005-May 2009
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5 Questions to fix the cause of Hypokalemia !
Is there an obvious gastro-intestinal loss
Is it drugs
How is renal handling of K
Unexplainable Metabolic acidosis/alkalosis
How is serum Mg, Na, Cl, Calcium
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Case 1
Is there an obvious gastro-intestinal loss
Is it drugs ???
How is renal handling of K- ??loss
Unexplainable Metabolic acidosis/alkalosis
How is serum Mg [?low] ,Na,Cl,Calcium
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Case 1
Is it drugs ???
Renal loss ???
Hypomagnesemia???
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Drugs and Hypokalemia ?
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Drugs and Hypokalemia
Insulin
Salbutamol, Theophylline
Diuretics
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Drugs and Hypokalemia
Insulin
Salbutamol, Theophylline
Diuretics
Nor-Epinephrine, high dose dopamine
Fludrocortisone, high dose corticosteroids
Amphotericin-B , Beta-lactum antibiotics
Bicarbonate therapy
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Case 1
Is it drugs ??? - YES
Renal loss ???
Hypomagnesemia???
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How to assess renal handling of K?
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Renal loss of K
Intrinsic renal disorders: Inherited/acquired
Hormonal effects : Hyperaldosteronism
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How to assess renal handling of K?
Urinary K excretion- spot or 24 hours
Urinary K / Urinary creatinine ratio
TTKG [ Trans-tubular potassium gradient]
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Urinary potassium excretion
A normal kidney should retain most of
the potassium in the setting of hypokalemia.
Spot K <10-15meq/l is normal
Spot K >20 meq/l indicates renal loss
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Spot Urinary Potassium excretion
Limitations Poor validity in critically ill patients when considered in isolation due to highpreval of secondary hyperaldosteronism
Extra-renal loss may be associated with elevated spot urinary K !
Reimann et al. Nephrol dial transpt 1999;14:2957-2961
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Urinary K/Urinary creatinine ratio
More meaningful test.
Excretion rates are similar during ↓K Ratio <1.5 indicates renal conservation of KRatio > 1.5 indicated renal wasting of K
Factors interfering creatinine secretion.Unclear role in critical illness
Groeneveld et al . Q J Med 2005;98:305-316
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What is TTKG?
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What is TTKG?
Most disliked term in the chapter on hypokalemia !
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What is TTKG?
Soriano et al.J Am Soc Nephrol 2002;13:2160-2170
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TTKG
Ratio between K concentration in the collecting duct and the peri-tubular cap
Tells about the behaviour of distal nephron during hypokalemia .
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TTKG
Based on one time sample
Most useful test
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TTKG
Based on one time sample
Most useful test
NOT AVAILABLE IN MOST CENTRES
TEST REQUIRES OSMOMETER
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How to assess renal handling of K?
Urinary K excretion
Urinary K / Urinary creatinine ratio
TTKG [ Trans-tubular potassium gradient]
ALL HAVE SIGNIFICANT LIMITATIONS
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How to assess renal handling of K?
Urinary K excretion
Urinary K / Urinary creatinine ratio
TTKG [ Trans-tubular potassium gradient]
ALL HAVE SIGNIFICANT LIMITATIONS
Interpretation in isolation may lead to
CONFUSION
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Potassium wasting Renal disorders……loose potassium
They often also loose chloride,
sodium,bicarbonate,magnesium,
water and calcium
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Potassium wasting renal disorders
Look beyond urinary K !
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Case 1
Is it drugs ???- YES
Renal loss ???- ? YES [ ?aldosterone]
Hypomagnesemia???
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Case 1
Is it drugs ???- YES
Renal loss ???- ? YES [ ?aldosterone]
Hypomagnesemia???
Secondary hyperaldosteronism produces
↓K much earlier than Met.alkalosis
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How to identify clinically significant hypomagnesemia
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How to identify clinically significant Hypomagnesemia?
Hypokalemia refractory to therapy
Serum Mg <1 mg/dl
Associated hypocalcemia [ < 7 mg/dl]*
Metabolic alkalosis
*Agus et al J Am Soc Nephrol 1999;10:1616-1622
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What is the relation between magnesium and calcium
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What is the relation between magnesium and calcium?
Hypomagnesemia causes impaired PTH release and increased PTH resistance.
Impaired PTH leads to renal loss of Mg
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Resolution -Case 1
Is it drugs - YES [ Noradrenaline]
Renal loss ??? – ?YES[?aldosterone]
Hypomagnesemia??? - NO
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Case 2
A 23 year old female presented with fatigue
for 3 months which worsened over the last
10 days. Clinical exam was unremarkable
except for a power of 4/5 in all limbs. Labs
showed a Na-134 meq/L,K-1.8 meq/l, Cl-110
meq/l and Hco3-15 meq/l. S.Creatinine-1.1
mg/dl, BUN-14 mg/dl, ABG: Ph- 7.31, Pco2-
30 mmHg, Hco3-14 meq/l, S.Mg-1.1mg/dl
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Ca-8.8 mg/dl , Spot urine K-60 meq/l . ECG
showed U waves with QRS widening. Urine
Ph-6, Sp-gravity-1.010, sugar-nil,prot-nil, 5-6
pus cells and no casts.
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Case 2 issues ?
Approach?
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Case 2 issues
Hypokalemia
Partially compensated metabolic acidosis
Elevated spot urine K-80 meq/l
Mild hypomagnesemia, high normal Cl
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5 Questions to fix the cause of Hypokalemia !
Is there an obvious gastro-intestinal loss
Is it drugs
How is renal handling of K
Unexplainable Metabolic acidosis/alkalosis
How is serum Mg, Na, Cl, Calcium
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Case 2 :Where to begin?
Is there an obvious gastro-intestinal loss
Is it drugs
How is renal handling of K- loss
Metabolic acidosis/alkalosis
How is serum Mg↓, Na, Cl↑, Calcium
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Case 2 :Where to begin?
Is there an obvious gastro-intestinal loss
Is it drugs
How is renal handling of K- loss
Metabolic acidosis/alkalosis
How is serum Mg, Na, Cl, Calcium
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Hypokalemia with metabolic acidosis
Possibilities to consider
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Hypokalemia with metabolic acidosis
Acute and chronic diarrheal disorder
Recovery phase of acute tubular necrosis
Renal tubular acidosis [distal , proximal]
Acetazolamide therapy
Met acidosis unrelated to hypokalemia
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How to evaluate possible RTA?
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Evaluation of possible RTA
Early morning first void urine pH
Confirm kidneys ability to acidify urine
Check for glycosuria, hypophosphatemia
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Evaluation of urine pH
Good screening test
Urine ph >5.5 : possible distal [type-1] RTA
Urine ph <5.5 : possible proximal
[type-2]RTA
Analyzed Ideally within 30 minutes
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Evaluate kidneys ability to acidify urine
Acid load test : ideal but rarely done
Frusemide test
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Frusemide test for RTA-1
Principle
Frusemide increases distal delivery of Na
A normal distal nephron secretes H ion in response to this producing acidic urine
Type-1 RTA nephron fails to do this
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Frusemide test: Protocol
Test urine pH
Administed 40 mg of frusemide preferably i.v
Repeat urine pH 1 to 2 hour later
Failure to produce acid urine indicates
Distal [type-1] RTA
Soriano et al. J Am Soc Nephrol 2002;13:2160-2170
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Proximal[type-2]RTA
Often associated with additional tubular loss of glucose, phosphate and uric acid
Osteomalacia and rickets may occur
Urinary acidification intact
Isolated proximal bicarbonate loss possible
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Case 2
Urine ph in routine sample- 6
Urine pH in first void sample-7
Frusemide test was abnormal
DISTAL RENAL TUBULAR ACIDOSIS
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Often there is a diagnostic delay in RTA
Metabolic acidosis is often mild
Becomes severe only during intercurrent illness
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Case 3
A 45 year old male presented with confusion
And irritablity for 7 days which was not
associated with fever. Patient is a known
diabetic for 8 years on OHAs. Current
alcoholic and smoker.On exam vitals were
stable and marked disorientation was
present. Labs showed a Na-141 meq/L,
K-1.4 meq/l, Cl-78 meq/l and Hco3-32 meq/l.
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S.Creatinine-0.9 mg/dl, BUN-18 mg/dl,
ABG: Ph- 7.49, Pco2- 49 mmHg, Hco3-32
meq/l, S.Mg-0.7mg/dl,Ca-6.4 mg/dl , Spot
urine K-80 meq/l . ECG showed ST
depression ,T-U waves with QRS widening.
Urine Ph-5, Sp-gravity-1.010, sugar-nil,prot-
nil, 5-6 pus cells and no casts.
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Case 3 issues?
Approach?
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Case 3 issues?
Diabetic , alcoholic
Altered mentation
Hypokalemia, Elevated urinary K loss
Metabolic alkalosis
Hypochloremia,hypomagnesemia,
hypocalcemia, normal Na
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Case 3 : Where to begin?
Diabetic , alcoholic
Altered mentation
Hypokalemia, Elevated urinary K loss
Metabolic alkalosis
Hypochloremia,hypomagnesemia,
hypocalcemia, normal Na
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Case 3 : Where to begin?
Diabetic , alcoholic
Altered mentation
Hypokalemia, Elevated urinary K loss
Metabolic alkalosis
Hypochloremia,hypomagnesemia,
hypocalcemia, normal Na
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Hypokalemia with metabolic alkalosis
Possibilities to consider
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Hypokalemia with metabolic alkalosis
Vomiting
Diuretics
Secondary hyperaldosteronism
Acquired Hypomagnesemia
Barters/Gittelman/Liddle syndrome
Hypokalemia per se
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Hypokalemia with metabolic alkalosis
Vomiting
Diuretics
Secondary hyperaldosteronism
Acquired Hypomagnesemia
Barters/Gittelman/Liddle syndrome
Hypokalemia per se
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What are the acquired causes of Hypomagnesemia?
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Acquired causes of ↓Mg
Alcoholism , Diabetes
Chronic diarrhea , vomiting, diuretic use
Diuretic phase of ATN
Rapid refeeding
Amphotericin B, Aminoglycosides
Vit D deficiency
Late pregnancy
Agus et al. J Am Soc Nephrol 1999;10:1616-1622
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Hypomagnesemia:features
Serum value may not reflect real picture
CNS effects
Hypokalemia refractory to therapy
Metabolic alkalosis, hypochloremia
Hypocalcemia
Sodium not affected in acquired causes
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Inherited tubular disorders
A birds eye view
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NEJM 1999;340:1177-1187
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Inherited tubular disorders vs Acquired Hypomagnesemia
Disorder Bp ↓Mg Na ↓Ca U .Ca
Barter N or low Yes-mild low variable
N or High
Gittel man N or low Yes-sev low no Low
Liddle High no N or High no N
↓ Mg N - N yes variable
Scheinmann NEJM 1999;340:1177-1187
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Inherited tubular disorders vs Acquired Hypomagnesemia
Disorder Bp ↓Mg Na ↓Ca U .Ca
Barter N or low Yes-mild low variable N or High
Gittel man N or low Yes-sev low N Low
↓ Mg N - N yes variable
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Inherited tubular disorders vs Acquired Hypomagnesemia
Disorder Bp ↓Mg Na ↓Ca U .Ca
Barter N or low Yes-mild low variable N or High
Gittel man N or low Yes-sev low N Low
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Case 3:resolution
Severe Hypomagnesemia [acquired]
1. risk factors- alcoholism, diabetes
2. Hypokalemia which was refractory
3. Hypocalcemia
4. Metabolic alkalosis, normal Na
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Case 4
A 25 year old female presented acute
weakness of all extremities .She had 2
similar episodes in the past. On exam vitals
were stable.Power was 1/5 all limbs. Labs
showed a Na-138 meq/L, K-1.6 meq/l, Cl-98
meq/l and Hco3-25 meq/l. S.Creatinine-0.9
mg/dl, BUN-18 mg/dl,ABG: Ph- 7.38, Pco2-
38 mmHg, Hco3-22 meq/l,
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S.Mg-1.7mg/dl,Ca-9 mg/dl , Spot
urine K-8 meq/l . ECG showed ST
depression ,T-U waves with QRS widening.
Urine Ph-5, Sp-gravity-1.010, sugar-nil,prot-
nil, 5-6 pus cells and no casts.
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Case 4: issues?
Approach?
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Case 4: Issues
Hypokalemia
Extremity weakness
Normal renal handling of K
Normal acid-base status
Normal Na,Cl,Mg and Ca
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Case 4: Where to begin?
Hypokalemia
Extremity weakness
Normal renal handling of K
Normal acid-base status
Normal Na,Cl,Mg and Ca
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Case 4: Where to begin?
Hypokalemia
Extremity weakness
Normal renal handling of K
Normal acid-base status
Normal Na,Cl,Mg and Ca
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Hypokalemic paralysis with normal acid-base status
Possibilities
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Two patients with serum K-1.5
One having paralysis and the other having normal power .Is it
possible?
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Two patients with serum K-1.5
One having paralysis and the other having normal power .Is it
possible?............yes
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The serum K level does not primarily decide occurrence of
weakness!
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What decides weakness in hypokalemia?
Ratio of ICF/ ECF
Normal 38/1
Conditions that lower both cellular and extracellular K may not produce weakness
Conditions rapidly shift large amount of K
into the cells ↑ ratio and cause weakness
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Severe hypokalemia with paralysis and normal ABG
Periodic paralysis [familial or sporadic]
Thyrotoxic periodic paralysis
Suicidal Insulin over dose
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Groeneveld et al . QJM;2005;98:305-316
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Case 4
Sporadic periodic paralysis
1. Recurrence
2. Normal renal handing of K
3. Normal acid-base status
4. Normal thyroid function
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In summary………
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5 Questions to fix the cause of Hypokalemia !
Is there an obvious gastro-intestinal loss
Is it drugs
How is renal handling of K
Unexplainable Metabolic acidosis/alkalosis
How is serum Mg, Na, Cl, Calcium
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Conclusion
Do not consider urinary K excretion in isolation
ABG is a desirable starting point while evaluating mod-severe hypokalemia
Look at Na,Cl,Mg and Ca
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My guide and mentor…….
Prof.S.Shivakumar M.D
Prof & HOD of Medicine[retd]
Govt.Stanley Medical College
Chennai
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Questions?????