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1 USMLE - Renal System > Potassium & Sodium > Flashcards

Potassium & Sodium Flashcards

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USMLE® Step 1 flashcards
1
Q

Hyper/hypokalemia symptoms

A

Cannot generate AP in muslces…

  • Cramps, muscle weakness/paralysis that starts in legs
  • EKG changes (PAC, PVC, brady, tachy, AV block, vtach/vfib, asystole
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2
Q

If a dialysis patient complain of cramps or weakness what do you do?

A

Send them to the ER IMMEDIATELY. Most likely a potassium problem - hyperkalemia

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3
Q

What are the EKG changes with hypokalemia

A 
PR interval prolongations
ST depression
Flattened or inverted T waves
U waves (another waive off of the T)
QRS widening

EKG changes are very important in the diagnosis of potassium imbalance*

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4
Q

What are the EKG changes with hyperkalemia

A

PR interval prolongation
Peaked T waves
Widened QRS

EKG changes are very important in the diagnosis of potassium imbalance*

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5
Q

What does hypercalcemia do in terms of protecting a K imbalance?

A

Protects against HYPERkalemia - hypercalcemia increase the threshold potential while hyperkalemia decreases RMP

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6
Q

What does metabolic acidosis do to potassium levels?
Alkalosis?
What is tx?

A

It exacerbates hyperkalemia - K is released from cells due to the higher positive charge inside the cell (to offset HCL (H+ actually) that is pumped into the cell) But in reality the total body potassium is most likely reduced
In alkalosis K is pumped into cells
Tx: give bicarb

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7
Q

HYPOkalemia increases what drugs toxicity?

A

Digoxin

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8
Q

Digoxin toxicity causes what potassium imbalance?

A

HYPERkalemia

Blocks Na/K pump (no more K being pumped into the cell)

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9
Q

What does insulin and catacholamines do to K?

A

Move it into cells.

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10
Q

What are the 3 things that determine potassium excretion?

A

Plasma K concentration (if high more in urine)
Urin flow in distal tubule (more channels for water pulls more K out)
Aldosterone causes K secretion by principal cells of collection tubule (only takes 0.1 mea/L increase in K** for aldosterone release)

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11
Q

Causes of hypokalemia

A

Dec intake (rare)
Increased entry to cells (alkalosis, hyperinsulinemia, increased catecholamines/beta agonists*)
GI loss (Vomiting or diarrhea, bulemia, anorexia, laxative abuse)
Urinary loss (dieuretics)
Sweat loss
Dialysis

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12
Q

If someone is hypokalemic, what else must you check the level of?

A

Mg

Hypomagnesemia affects the number of K channels (torsades de pointes)

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13
Q

How to determine what caused Hypokalemia?

A

Determine if loss is GI or Renal (GI should be obvious from Hx)

Get a 24 hour urine K+, if urine K+ is low it is NOT due to the kidney

Check acid/base status

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14
Q

Testing a pt with hypokalemia, find there is a low urinary K…What are the possibilities?

(acidosis vs alkalosis)

A

So it is a GI loss.

Acidosis - lower GI loss - diarrhea (excreting bicarb)(laxative abuse? villous adenoma)

Alkalosis - upper GI loss - vomiting (holding on to bicarb)

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15
Q

**Testing a pt with hypokalemia, find there is a high urinary K…What are the possibilities? **

(acidosis vs alkalosis)

A

So it is renal loss

Acidosis (ketoacidosis, type I or II renal tubular acidosis)

Alkalosis

  • Normotensive - vomiting (GI loss but high urinary K due to bicarb excretion in urine with metabolic alkalosis, diuretics, Bartter’s syndrome
  • Hypertension
      • High renin (diuretics, renovascular disease, reninoma, Cushings)
      • Low renin (measure aldosterone)
          • Low Aldosterone (exogenous mineral corticoid)
          • High Aldosterone (adrenal adenoma or hyperplasia)
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16
Q

Effects of Hypokalemia

A

Muscle weakness, cramps, arrythmias
Rhadomyolysis (K<2.5) CK will be elevated
Renal dysfunction
Hypertension (low K diet increases Na uptake)

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17
Q

Hypokalemia Tx

A

Replace K to get pt out of danger, then bring to normal more gradually (oral or IV)
Treat underlying cause

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18
Q

Causes of Hyperkalemia

A 
Increased intake (oral, IV, rare)
Shift (from intracellular to extra)(Muscle breakdown (burn), insulin deficiency with hyperglycemia (DKA), met acidosis)
Decreased urinary excretion - USUALLY this happens in people with RENAL DYSFUNCTION
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19
Q

What drug do you never used in patients with renal failure in terms of potassium balance?

A

Succinylcholine (paralytic)

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20
Q

What is the most common cause of hyperkalemia?

A

Renal failure*

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21
Q

Hypoaldoseronism

A

Secondary decrease in aldosterone due to decreased activity of renin-angiotensin system (hyporeninemic hypoaldoseronism)

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22
Q

Tx for hyperkalemia

A

Check EKG, if K is 6.5-7 and EKG no change, check for pseudohyperkalemia
IF EKG changes: Begin tx immediately - Calcium IV*** (instant changes),

Then shift K into cells (insulin and glucose, sodium bicarb (but NOT in DKA pts***), beta agonists (albuterol) this takes minutes

Then remove excess K (hours) loop diuretics, cation exchange (kayexalate), dyalisis

Acidemia or hyponatremia will potentiate K toxicity

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23
Q

4 ways to shift K from extracellular to intracellular?

A 
Insulin
Catecholamies
Concentration grad
Alkalosis
(acidosis shifts out)
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24
Q

Major ways for K excretion by kidney?

A

K concentration
Increased Aldosterone
Increased distal urine flow (permissive)

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25
Q

What is the MAJOR toxicity of potassium imbalance?

A

Cardiac arrythmias

26
Q

Sodium imbalance is usually a ______ problem?

A

Water

27
Q

Symptoms of hypo/hypernatremia are caused by what?

A

Alterations in plasma osmolarity causing changes in BRAIN CELLS

28
Q

Symptoms of hyponatremia

A

Brain cell swelling.

Nausa/malais
Headache/lethargy
Obtundation, seizures, coma

Usually reversible* but more sever if Na imbalance was acute*, may be asymptomatic at minimal hyponatremia if chronic

Chronic changes common in ETOH’ers or pts with liver failure

29
Q

Symptoms of hypernatremia

A

Causes brain cell dehydration/shrinkage

Lethargy, weakness, irritability, twitching, seizures, coma, death

Cerebral vessel rupture due to decreased brain volume

Common in babies who get dehydrated*

30
Q

What is ADH?

A

Antidiuretic hormone or vasopressin

Produced in hypothalamus, secreted by posterior pituitary**

31
Q

What is stimuli for ADH release?

A

Increase in plasma osmolarity**

Hypovolemia or decreased extracellular volume
Pain
Esophageal stimuli
Medications

32
Q

Mechanism of ADH?

A

Binds V2 receptor in collecting tubules, activates protein kinase, causes AQ2 channels to move into luminal membrane of collection duct***

Water moves from collecting duct BACK into blood - thus concentrated urine - urine osmolarity will be high** - water returning to blood DECREASES the serum osmolality

If ADH not present, water is NOT reabsorbed, urine osmolarity is LOW, and serum osmolarity is HIGH

33
Q

What does urine osmolarity tell you?

A

It tells you what the kidneys think about the bodies water volume status*** or if ADH is present or not.

Uosm low: kidney thinks body is dehydrated
Uosm high: kidney thinks body has HTN

34
Q

If Uosm is less than 100 then….

If Uosm is over 100…

A

ADH is NOT present

ADH IS present in varying degrees, higher Uosm the MORE ADH

35
Q

In steady state… Urinary excretion of sodium = ?

A

Daily intake of Na.

36
Q

Where in kidney is most of the Na resorbed?

A

Proximal Tubule (65%)
Loop of Henle (25-35)
Distal Tubule (5%)
Collecting (0 - 5%)

37
Q

Urine Inicies*** UNa+

If it is less than 10meq/L?
If more than 10meq/L?

A

If UNa less than 10, than low urine sodium, kidney senses low effective circulating volume (ECV) and is holding onto sodium

If UNa more than 10, high urine Na, kidney senses high ECV
or kidney can’t retain Na properly
or kidney is excreting Na in an obligate cation with something else

38
Q

Hyponatremia usually reflects what if glucose is normal?

A

Hypoosmolaligy…

Posm = 2Na + glucose/18 + BUN/2.8 = 285-300

BUN doesn’t contribute to gradient so its 0. If glucose is normal just use Posm = 2*Na

39
Q

Osmotic stimuli?

Non-osmotic stimuli?

Which is more influential?

A

ADH would maintain plasma osmolality to 1%, with out regard to ECV (effective circulating volume)

Non-osmotic: baroreceptors in kidney/carotid/heart for ADH secretion maintain ECV at expense of osmolarity*
Better to keep brain perfused than maintain plasma osmolarity*

40
Q

Hyponatremia with Uosm of less than 100 - cause and tx.

A

ADH is NOT being produced - due to appropriate response to hypoosmolarity

Due to Excessive water intake (primary polydipsia) 10-15 L/day

Tx: Restrict water intake.

41
Q

“Beer Potamania”
&
“Tea and Toast Syndrome”

A

Hyponatremia and Low urine osmolality WITHOUT excessive water intake.

Beer drinkers or old lades who only eat tea and toast… NO SALT in diet

42
Q

Hyponatremia with Uosm > 100 and UNa+ < 10 and patient is volume depleted.

Causes?

A

ADH present (Uosm >100), UNa less than 10 so kidney senses low effective circulating volume and holds onto Na (the patient is volume depleted)

GI loss (Vomiting/Diarrhea)
Skin losses (burns)
Diuretics (late)
Cortisol deficiency
43
Q

Hyponatremia with Uosm > 100 and UNa+ < 10 and patient is volume expanded.

Causes?

A

ADH present (Uosm >100), UNa less than 10 so kidneys perceive the pt is volume depleted (ECV low) but it is not true.

Happens is states of poor perfusion or edematous sates***
CHF, Cirrhosis, liver failure, nephrotic syndrome

44
Q

Hyponatremia with Uosm > 100 and UNa+ > 10 and patient is volume depleted.

Causes?

A

ADH present (Uosm >100), UNa more than 10 so kidneys perceive the ECV to be increased but it is not - this is SALT WASTING

Adrenal insufficiency
Diuretics (early)
Hypokalemia w/ met alkalosis after vomiting
Hypothyroidism

45
Q

Hyponatremia with Uosm > 100 and UNa+ > 10 and patient is volume expanded.

Causes?

A

ADH present (Uosm >100), UNa more than 10 so kidneys perceive the ECV to be expanded which is correct - this is incorrect ADH secretion**

SIADH - syndrome of inappropriate ADH secretion
CKD
Reset Osmostat

46
Q

SIADH - syndrome of inappropriate ADH secretion

A

Fixed ADH secretion without regard to osmotic or volume stimuli. Uosm fixed at HIGH level.

Tx: fluid restriction - increase osmolar load: intake of high sodium or high protein diet helps kidneys clear the excess water (not to increase salt**)

47
Q

Hyponatremia Tx

Volume depleted
Volume expanded or neutral

A

Volume depleated: Normal saline (turns off ADH, increases ECV)

Volume expanded or neutral: restrict water intake, treat underlying cause.

Can use hypertonic saline to get out of danger zone.

48
Q

Treatment of hyponatreima - Rate

A

Bring it out of danger zone over several hours - too quickly risks Central Pontine Myelinolysis/Osmotic Demyelination Syndrome

49
Q

If patient is in hyponatremic seizures?

A

3% hypertonic saline

100cc over 10 mins IV

If just neurologic sx… 30-50 cc/hour over several hours

50
Q

What drugs are ADH antagonists?

A

Vaptans
Tolvaptan: oral
Conivaptan: IV

indicated for hypervolemic hyponatremia

51
Q

Hypernatremia

A

Almost always a water problem, NOT a salt problem

Due to excessive water losses and inadequate intake - Rare

52
Q

Cause of hypernatremia with Uosm over 800?

A

Primary hypodipsia
Increases insensible losses (GI etc)
Na+ overload

53
Q

Cause of hypernatremia with Uosm under 300?

A

Sever central diabetes insipidus or nephrogenic diabetes insipidus

54
Q

Cause of hypernatremia with Uosm between 300 and 800?

A

Partial diabetes insipidus, volume depletion with diabetes insipidus, or osmotic diereses

55
Q

Central and nephrogenic diabetes insipidus

A

Central: hypothalamus/pituitary not producing/releasing ADH - cannot resorb water

Nephrogenic: collecting tubules don’t respond to ADH

Patient is always thirsty and peeing a lot - does not have concentrated urine

56
Q

How to distinguish Central from Nephrogenic DI?

A

Exogenous ADH will NOT work for nephrogenic***

It will increase Uosm if the patient has Central DI

57
Q

Big cause of nephrogenic DI?

A

Lithium, demeclocyline

58
Q

Central DI causes?

A

Trauma

59
Q

Treatment of DI?

A

Low Na diet and thiazide diuretic (diminish polyuria/polydipsia)

For central give dDAVP (ADH) desmopressin

60
Q

Treatment for hypernatremia?

A

Free water orally is best or D5W IV***

1 USMLE - Renal System (5 decks)

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