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CRRAB II- Week 1 > Popham- Kalemic > Flashcards

Popham- Kalemic Flashcards

(47 cards)

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1
Q

How much K is normally stored in an adult?

A

3000-4000 mEq

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2
Q

What is the daily intake and excretion of K?

A

4-120 mEq

Excretion min= 15-25 mEq

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3
Q

What percent of K is intracellular?

A

98%

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4
Q

How much K is extracellular?

A

4-5 mEq/L

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5
Q

How much K is normally in the serum?

A

4-5 mEq/L

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6
Q

What defines a body deficit vs. excess of K?

A

Deficet: decrease by 1 mEq/L = 200-400 mEq

Excess: increase by 1 mEq/L = 100-200 mEq

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7
Q

What are the functions of K?

A

Prot and glycogen synthesis
Maintains RMP via Na/K ATPase
Determines membrane excitability
Allows AP generation

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8
Q

What are sxs of LOW or HIGH K?

A

Unable to get an AP in muscles
Cramps
Muscle weakness/paralysis
EKG changes and arrythmias

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9
Q

How does hypercalcemia affect AP?

A

increases threshold potential and protects against hyperkalemia, which has decreased resting potential

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10
Q

What exacerbates hyperkalemia?

A

Metabolic acidosis

Causes K to be released form cells as HCl is buffered into cells

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11
Q

What drug potentiates risk of hypokalemia?

A

Digoxin

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12
Q

What can potentiate the risk of hyperkalemia?

A

Hyponatremia

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13
Q

What effects K distribution into cells and ECF?

A
  1. concentration dependent

2. Acid-base dependent

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14
Q

What happens if you drink 40 meq of OJ?

A

40 meq> 17 ECF > increase K by 2.4 meq/l

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15
Q

What increases K distribution into cells?

A
  1. Catecholamines and insulin increase Na/KATPase activity> uptake K into skeletal muscle and liver
  2. HIGH CONC causes passive movement of K into cells
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16
Q

What happens to K in acidemia vs alkalosis?

A

Acidemia: K+ moves OUT of cells as H+ is buffered into cells

Alkalosis: K+ moves INTO cells as H+ is buffered into the extracellular fluid

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17
Q

What determines excretion of K by the kidney?

A
  • Plasma K+ concentration
  • Urine flow in distal tubule (permissive)
  • Aldosterone: causes K+ secretion by principal cells of collecting tubule
  • Outer medulla, cortical & inner medulla
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18
Q

What influences K handling in the renal tubule?

A
  • K is filtered at glomerulus
  • Reabsorbed proximal tubule, following water and sodium
  • Reabsorbed loop of Henle (thick ascending limb), via NaK2Cl carrier in luminal membrane
  • Secreted distally: distal tubule, collecting tubule via principal cells
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19
Q

Where can K be reabsorbed in cases of severe hypokalemia?

Study These Flashcards
A

Collecting duct by intercalated cells

20
Q

How is K secreted in the distal tubule?

Study These Flashcards
A

Principal cells
• Luminal membrane: Na+ & K+ channels
• Basolateral membrane: Na-K ATPase

Aldosterone
• Released in response to 0.1 meq/l increase in K+
• Increases # of open Na+ & K+ channels
• Increases activity of Na-K ATPase

K concentration in blood: gradient

Distal flow is permissive

21
Q

What usually causes hypo/hyperkalemia?

Study These Flashcards
A

adrenal glands or kidneys

NOT diet

22
Q

What shifts K from extracellular to intracellular?

Study These Flashcards
A

– Insulin
– Catecholamines
– Concentration gradient
– Acid-base status

23
Q

What are the major determinants of K excretion by the kidney?

Study These Flashcards
A

– K concentration
– Aldosterone
– Distal tubular urine flow (permissive)

24
Q

What is a MAJOR toxicity of both hypo and hyperkalemia?

Study These Flashcards
A

cardiac arrythmias

25
What causes hypokalemia?
1. Decreased intake (rare) 2. Increased entry into cells – met alk, hyperinsulinemia, 3. catechol/β-agonists 4. Increased GI losses 5. Increased urinary losses – impaired H20/salt reabsorp, hypercalcemia, mineralcorticoid excess (aldosterone), hypomagnesemia 6. Increased sweat losses 7. Dialysis
26
How do you evaluate hypokalemia?
1. Determine if loss is GI or renal 2. GI losses should be obvious, except in cases of anorexia/bulemia/laxative abuse 3. 24 hour urine K+ when hypokalemic a. Kidney can decrease urine excretion of K+ to 25-30 meq in 24 hours b. If urine K is low, then loss is not from kidney 4. Acid/base status: acidosis or alkalosis
27
What can cause LOW urinary K and acidosis?
LOWER GI losses from laxatives/villous adenoma
28
What can cause low urinary K and Alkalosis?
Upper GI loss vomiting
29
What causes high urinary K and acidosis?
Ketoacidosis, type I or II RTA
30
What causes high urinary K and alkalosis?
Normotensive: vomiting (GI loss, but high urinary K due to urinary bicarb excretion with metabolic alkalosis) diuretics (early), Bartter’s syndrome (Inherited) Hypertension 1. High renin: diuretics,renovascular disease, reninoma, Cushings 2. Low renin: measure aldosterone
31
What does low vs high aldosterone indicate in situations when there is low renin?
low- exogenous mineralcorticoid high- adrenal adenoma or hyperplasia
32
What complications can occur with hypokalemia?
1. Muscle weakness, cramps, cardiac arrhythmias 2. Rhadomyolysis (K+ < 2.5 meq/l) 3. Renal dysfunction: a. loss of urinary concentrating ability b. Increase in urinary NH3 and NH4+ production/excretion c. Hypokalemic nephropathy/Interstitial fibrosis 4. Hypertension: low K+ diet causes uptake of Na+
33
How do you treat hypokalemia?
1. Replace to get patient out of danger initially, then more gradually replace entire K deficit 2. K+ deficit can only be approximated: a. Roughtly 200-400 meq for each 1 meq/l drop in K+ b. Below 2, K+ deficit can be much greater due to shifts out of cells to compensate 3. Treat underlying cause of low potassium 4. Potassium replaced orally or intravenously
34
What causes hyperkalemia?
1. Increased Intake: oral or IV 2. Shift: Movement from cells into extracellular fluid – muscle/tissue breakdown, insulin deficiency w/ hyperglycemia, met acidosis 3. Decreased urinary excretion – MCC = renal failure, hypoaldosteronism
35
What causes hypoaldosteronism?
1. Secondary decrease in aldosterone due to decreased activity of renin-angiotensin system 2. Primary decrease in adrenal synthesis of aldosterone 3. Aldosterone resistance
36
What causes secondary decreases in aldosterone?
i. Hyporeninemic hypoaldosteronism (diabetics with CKD) ii. Drugs: ACEi, NSAID’s, cyclosporine iii. HIV disease/clinical AIDS
37
What causes aldosterone resistance?
Drugs: K+ sparing diuretics, Trimethoprim Pseudohypoaldosteronism
38
How do you diagnose hyperkalemia?
DX = Transtubular K Gradient (TTKG) <7
39
How do you calculate TTKG?
[Urine K+ / (Uosm/Posm] | /Plasma K+
40
What should you do if K is 6.5-7 meq/l and there are no EKG changes?
check for pseudohyperkalemia
41
What should you do if there are EKG changes and you suspect hyperkalemia?
Start treatment immediately *Monitor on telemetry
42
What can potentiate K toxicity?
Concomitant acidemia or hyponatremia
43
How do you treat hyperkalemia?
Antagonize K+ effects (seconds/minutes) a. Calcium IV Shift K+ into cells (minutes) a. Glucose & insulin b. NaHCO3 c. Beta-agonists: albuterol nebs d. 3% NaCl if hyponatremia present Remove excess K+ (hours) a. Loop diuretics if patient makes urine b. Cation-exchange resins (kayexalate): avoid rectal use c. Hemodialysis/peritoneal dialysis
44
What EKG changes are associated with hypokalemia?
1. PR interval prolongation 2. ST depression 3. Flattened/ inverted T waves 4. U-waves 5. QRS widening
45
What ST changes are associated with hyperkalemia?
1. PR interval prolongation 2. Elevated T waves 3. Widened QRS
46
How should you treat EKG changes seen with hypokalemia?
* Concomitant digoxin use increases risk * Treat to get out of danger, replace losses, and prevent further losses * Check for hypomagnesemia
47
How should you treat EKG changes seen with hyperkalemia?
* Antagonize membrane effects: Calcium IV * Shift K+: insulin/glucose/NaHCO3 * Remove K+: diuretics, Kayexylate, dialysis

CRRAB II- Week 1 (7 decks)

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