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MBBS IV - Supplementary Courses > Chemical pathology II - Potassium > Flashcards

Chemical pathology II - Potassium Flashcards

1
Q

How is K transported across intra-cellular and extra-cellular space?

A

Na/K ATPase pump

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2
Q

Effect of acid/base balance on serum K concentration?

A

Acid-base status cause transcellular
shifts for neutrality:

 HyperK (and hypermagnesemia) = acidosis

 HypoK (and hypomagnesemia) = alkalosis

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3
Q

Effect of insulin on serum K conc?

A

Insulin promotes cellular uptake of glucose together with K (and magnesium and phosphate)

> > > > serum hypoK

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4
Q

Effect of adrenaline/ catecholamine and thyroxine on serum K conc.?

A

Adrenaline (catecholamines), thyroxine stimulate cellular K+ uptake via Na+/K+-ATPase

> > > > serum HypoK

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5
Q

Effect of aldosterone on serum K conc. and acid/base balance?

A

Aldosterone action&raquo_space; renal H+, K excretion and
Na+ absorption at collecting ducts

> > alkalosis, hypokalemia, hypernatremia (e.g. Conn
syndrome)

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6
Q

Define serum and plasma K level for hyperkalemia

A

 Plasma K >5.0 mmol/L; or
 Serum K >5.5 mmol/L

Serum K higher because platelets release K in clotting

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7
Q

Can K conc. from arterial be used to define hyperK?

A

(not centrifuged = cannot detect if its hemolyzed = not reliable)

Always gives higher K value than serum and plasma K conc

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8
Q

4 clinical manifestations of HyperKalemia?

A
  • Vague muscle weakness
  • Flaccid paralysis
  • Cardiac arrhythmia
  • Paresthesia (burning or prickling sensation in hands)
  • Non-specific: malaise, vomit, nausea
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9
Q

Define the ECG changes with Hyper K at 6-7, 8-10, 11, 12mmol/L

(not important)

A

 6-7mmol/L = tall, peaked T waves
 8-10mmol/L = aberrant QRS complexes
 11mmol/L = fusion of QRS and T waves
 10-12 mmol/L = ventricular fibrillation

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10
Q

Define 4 extra-renal causes of HyperK

*****

A
  • Pseudohyperkalemia (factitious hyperkalemia)
  • Tumor lysis syndrome, tissue necrosis (trauma, burns, rhabdomyolysis): K leak from cells
  • Hyperkalemic periodic paralysis (autosomal dominant disorder)
  • drug history (IV / oral K therapy, Potassium-sparing diuretics, Digoxin/digitalis)
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11
Q

4 causes of pseudohyperkalemia

Extra-renal cause of HyperK

A

1) Hemolysed specimen (check hemolysis index):
- Elevated PO4, K, CK, AST, LDH, uric acid, Mg
- Decreased alkaline phosphatase, amylase, GGT

2) EDTA contamination (EDTA contains K; check calcium – should be low)
3) Thrombocytosis, leukocytosis(check complete blood picture, e.g. leukemia)
4) Aged samples(check sampling date and time; do the test ASAP to minimize K leakage from cells)

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12
Q

Compare hyperK and hypoK periodic paralysis clinical presentation

(Extra-renal cause of HyperK)

A

1) Hyperkalemic periodic paralysis: Acute onset of muscle weakness:
 Precipitated by exercise, cold, hyperK
 Spontaneously resolves over a few hrs

2) Hypokalamic periodic paralysis:
Attacks of flaccid paralysis (lasting 6-24 hours):
 Precipitated by rich carbohydrate diet (stimulates insulin secretion&raquo_space; hypoK)
 Spontaneously resolves

Both autosomal dominant

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13
Q

List 4 drugs that can cause serum HyperK

Extra-renal cause of HyperK

A

 IV / oral K therapy

 Potassium-sparing diuretics affect renin and aldosterone

 Digoxin/digitalis (inhibits H-K-ATPase pump&raquo_space; inhibit intracellular K+ uptake&raquo_space; hyperkalemia)

  • Insulin (rapid K uptake in cells)
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14
Q

3 risk factors for digoxin overdose?

A

 Elderly (renal failure)
 Hypothyroidism (more sensitive to side effects of digoxin)
 HypoK

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15
Q

Precaution with diabetics using insulin and K conc. imbalance?

A

Insulin activates Na+/K+-ATPases in many cells

> > flux of potassium into cells cause hypokalemia

insulin drip must be given together with K to avoid lethal hypokalemia

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16
Q

3 renal causes of HyperK?

A
  • Acute renal failure/ injury
  • End-stage Renal failure
  • Diabetic ketoacidosis
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17
Q

High plasma creatinine + HyperK

Dx?

A

renal failure (acute or end-stage renal failure)

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18
Q

Low plasma HCO3 + high anion gap + HyperK

Dx?

A 
diabetic ketoacidosis
(metabolic acidosis causes transcellular shift >>  hyperkalemia)

or Renal failure

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19
Q

2 endocrine causes of HyperK?

Explain mechanisms

A
  • Addison’s disease (primary adrenal insufficiency: no mineralocorticoid/aldosterone = hyperK)
  • Congenital adrenal hyperplasia - 21-hydroxylase deficiency (decreased synthesis of cortisol,
    aldosterone = hyperK)
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20
Q

How to use renin and aldosterone levels to d/dx HyperK causes? (4)

(kidney impairment, extrarenal causes, mineralcorticoid resistance, aldosterone dediciency)

A
  • Normal renin and aldosterone = extra-renal cause of HyperK
  • High renin and high aldosterone = Minceralcorticoid resistance/ secondary hyperaldosteronism (keep releasing aldosterone, no negative feedback to renin)
  • High renin and low aldosterone = Selective aldosterone deficiency (renin cant stimulate aldosterone release)
  • Low renin and low aldosterone = Prostaglandin inhibition
21
Q

Outline the flow of tests to d/dx hyperkalemia

A

1) Exclude all extra-renal causes of HyperK
2) Check plasma HCO3 and anion gap: low HCO3 + High anion gap = Kidney failure or Diabetic ketoacidosis
3) Check plasma creatinine: high = kidney failure
4) Check ACTH stimulation: No/ poor response = Addison’s disease or 21-hydroxylase deficiency (CAH)
5) Spot renin and aldosterone testing

22
Q

List some causes of prostaglandin inhibition (Low renin and low aldosterone)

A
  • indomethacin (NSAID inhibits prostaglandin and
    renin production)
  • interstitial nephritis
  • syndrome of hyporeninemic hypoaldosteronism
  • elderly with diabetes mellitus and mild renal impairment
23
Q

List some causes of mineralocorticoid resistance (secondary hyperaldosteronism) - High renin and high aldosterone

A

Interstitial nephritis, obstructive uropathy, amyloidosis, SLE

Pseudohypoaldosteronism (congenital)

24
Q

List some causes of selective aldosterone deficiency ( High renin and low aldosterone)

A

 Congenital: affects aldosterone synthase

 Acquired: heparin inhibits aldosterone synthesis

25
Q

Action plan for moderate and severe hyperK?

A

Moderate: <5.5mmol/L = go through diagnostic flow chart

Severe: > 6.5mmol/L = do an ECG

Save urine K +/- other blood samples before treatment
Test profiles for Renal failure, Diabetic Ketoacidosis

26
Q

Case 1:
 F/65y, HT, DM. OPD FU
 Collection time: 15/4/2011 14:05
 Arrival time: 16/4/2011 10:13

Plasma:
 Na 140 (132-144 mmol/L)
 K 5.5 (3.2-4.8 mmol/L)
 Urea 5 (3.0-8.0 mmol/L)
 Cr 125 (60-120 μmol/L)

Dx?

A

Slightly elevated creatinine + Hyper K = mild renal impairment

However, the sample is assessed very late&raquo_space; hemolysis might increase K conc.

> > Cannot determine hyperK

27
Q 
F/65y
 Plasma:
 Na 140 (132-144 mmol/L)
 K 5.5 (3.2-4.8 mmol/L)
 HCO3 15 (23-28 mmol/L) 
 Urea 5 (3.0-8.0 mmol/L)
 Cr 100 (60-120 μmol/L)

Dx?

A

HyperK
Low HCO3 - metabolic acidosis

Check anion gap > high anion gap = Renal failure or diabetic ketoacidosis

Check glucose for DM and insulin use = Extra-renal HyperK cause

28
Q 
Case 3:
 M/48, known DM, found Loss of consciousness
Plasma:
 Na 132 (132-144 mmol/L) 
 K 6.5 (3.2-4.8 mmol/L)
 Urea 23 (3.0-8.0 mmol/L)
 Cr 323 (60-120 μmol/L) 
 Glucose 18 mmol/L 
 Urine ketone ++

K deficit despite hyperK

Dx?

A

High glucose - poor DM control
High creatinine - Think renal failure or diabetic ketoacidosis
HyperK
High Urea
High urine ketone
K deficit despite hyperK - serum only accounts for 1% total body K

Renal failure causing diuresis, passing too much K

29
Q

Case 5:
 Baby/1 day old, ambiguous external genitalia, hypotensive…

Plasma:
 Na 118 (132-144 mmol/L)
 K 6.5 (3.2-4.8 mmol/L)
 Urea 9.5 (3.0-8.0 mmol/L)
 Cr 60 (30-50 μmol/L)
A

Low Na > cannot drive Na/K-ATPase > cannot excrete enough K

> > congenital adrenal hyperplasia

30
Q

Case 7a:
 M/70y, CRF with renal transplant 10 years ago, FU OPD

 Na 140 (132-144 mmol/L)
 K 9.5 (3.2-4.8 mmol/L) 
 Urea 5 (3.0-8.0 mmol/L) – normal RFT
 Cr 110 (60-120 μmol/L) – normal RFT
 Ca 0.56 (2.20-2.60mmol/L)

Dx?

A

Severe hyperK

But low Ca + Hyper K = EDTA contamination

31
Q

Case 7b:
 M/27, leukemia, just post-chemotherapy

 Na 140 (132-144 mmol/L)
 K 9.5 (3.2-4.8 mmol/L)
 Urea 5 (3.0-8.0 mmol/L)
 Cr 125 (60-120 μmol/L)
 Ca 0.56 (2.20-2.60 mmol/L)
 High PO4, urate

Dx?

A

tumour lysis syndrome

32
Q 
Case 7c:
 M/58
 Plasma:
 Na 140 (132-144 mmol/L)
 K 6.5 (3.2-4.8 mmol/L)
 Urea 5 (3.0-8.0 mmol/L)
 Cr 100 (60-120 μmol/L)
Comments: sample mishandled before analysis

Dx?

A

HyperK caused by hemolysis

> > misleading results

> > Test for free Hb in the blood to indicate hemolysis cause

33
Q

Why is serum K always higher than plasma K?

A

Serum platelets lysis release K

34
Q 
Case 8:
 M/18y, sudden onset of paralysis, but resolves after few hours
Plasma:
 Na 140 (132-144 mmol/L)
 K 5.5 (3.2-4.8 mmol/L) 
 Urea 5 (3.0-8.0 mmol/L)
 Cr 100 (60-120 μmol/L)

Dx?

A

– hyperkalemic periodic paralysis

35
Q

Hypokalemia:

Define plasma and serum levels

A

 Plasma K <3.0mmol/L

 Serum K <3.5mmol/L

36
Q

Symptoms of hypoK

A

 Anorexia, nausea
 Polyuria, polydipsia
 Muscle weakness

37
Q

2 metrics used to d/dx HypoK?

A

Paired spot urine K

Plasma HCO3-

38
Q

Outline the flow of diagnosis for HypoK

A

Plasma HCO3- normal or increased (metabolic alkalosis/ hyperkalemic alkalosis)

a) Urine K <20-40 mmol/L = non-renal loss
- Inadequate intake, intracellular shift,
- extra-renal loss (CHRONIC diarrhea, laxative abuse, PREVIOUS diuretics, colon villous adenoma)

b) Urine K >20-40 mmol/L = renal loss:
- Vomiting, emetics,
- CURRENT diuretics,
- Conn’s syndrome, Cushing’s syndrome,
- Leukemia,
- Mg depletion,
- Gentamycin
- High ACTH + High cortisol - Small cell lung cancer

Plasma HCO3- decreased (metabolic acidosis)

a) Urine K <20-40 mmol/L = Acute diarrhea
b) Urine K >20-40 mmol/L = renal loss: Renal tubular acidosis type I and II; Carbonic anhydrase inhibitor

39
Q

Causes of Plasma HCO3- normal or increased +Urine K >20-40 mmol/L

A

Urine K >20-40 mmol/L = renal loss:

  • Vomiting, emetics,
  • CURRENT diuretics,
  • Conn’s syndrome, Cushing’s syndrome,
  • Leukemia,
  • Mg depletion,
  • Gentamycin
40
Q

Causes of Plasma HCO3- normal or increased +Urine K < 20-40 mmol/L

A

Urine K <20-40 mmol/L = non-renal loss

  • Inadequate intake, intracellular shift,
  • extra-renal loss (CHRONIC diarrhea, laxative abuse, PREVIOUS diuretics, colon villous adenoma)
41
Q

Electrolyte imbalance for acute diarrhea?

A

Plasma HCO3- decreased (metabolic acidosis)
Urine K <20-40 mmol/L = Acute diarrhea
Serum HypoK

42
Q

Electrolyte imbalance for chronic diarrhea?

A

Plasma HCO3- normal or increased (metabolic alkalosis/ hyperkalemic alkalosis)
Urine K <20-40 mmol/L- extra-renal loss - CHRONIC diarrhea
Serum HypoK

43
Q

Electrolyte imbalance for vomiting

A

Plasma HCO3- normal or increased (metabolic alkalosis/ hyperkalemic alkalosis)
Urine K >20-40 mmol/L = renal loss: Vomiting

Serum HypoK

44
Q

Common causes of hypoK

A

Diuretics
Vomiting/ diarrhea
Mg deficiency

Mineralocorticoid excess
Glucocorticoid excess
Renal tubular acidosis

45
Q

Which body fluid contains the most K

A

Urine - 50mmol/L
Diarrhea fluid - 40-100mmol/L
Saliva - 15mmol/L
Gastric, pancreatic juice - 10mmol/L

46
Q

Case 9:
 M/3mo, pyloric stenosis with refractory vomiting

Plasma:
 Na 140 (132-144 mmol/L)
 K 2.5 (3.2-4.8 mmol/L)
 HCO3 30 (23-28 mmol/L)
 Urea 5 (3.0-8.0 mmol/L)
 Cr 100 (60-120 μmol/L)
A

HCO3 is high
HypoK

> > Vomiting of gastric juice causes alkalosis and loss of K

47
Q

Case 10:
 M/65, chronic smoker, weight loss and dry cough for 3 months

 Na 140 (132-144 mmol/L)
 K 2.6 (3.2-4.8 mmol/L)
 Urea 7 (3.0-8.0 mmol/L)
 Cr 110 (60-120 umol/L)
 Further investigations:
 Urine K 102 mmol/L (high)
 Cortisol 2424 umol/L
 ACTH increased
 CXR – lung mass
A

Urine K >20
HypoK
High ACTH > High cortisol

D/dx:
ectopic ACTH production (common in small cell lung cancer)
Cushing syndrome

48
Q

Case 11:
 F/70y, CA stomach on chemotherapy

Plasma:
 K 2.3 mmol/L (3.5-5.0)
 Ca 1.86 mmol/L (2.25-2.55)
 PO4 0.56 mmol/L (0.6-1.2)
 ALB 30 g/L (30-52)
 Hypocalcemia refractory to replacement
A

Chemotherapy: check Mg, especially if cisplatin cause severe hypomagnesemia <0.3mmol/L:

Cisplatin Inhibit PTH action&raquo_space;> hypoK, hypoCa

MBBS IV - Supplementary Courses (54 decks)

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