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Renal II Cumulative Final > Fluid And Electrolyte Imbalance - Na, K > Flashcards

Fluid And Electrolyte Imbalance - Na, K Flashcards

1
Q

With increased Na+ intake, what changes occur in sympathetic activity, ANP, plasma oncotic pressure, and RAS to maintain normal electrolyte concentration within the body?

A

Decreased sympathetic activity (leads to dilation of afferent arterioles and thus increased GFR —> decreased Na reabsorption in PT)

Increased ANP (leads to constriction of efferent arterioles and thus increased GFR —> decreased Na reabsorption in CDs)

Decreased plasma oncotic pressure (leads to decreased Na reabsorption in PT)

Decreased RAS (leads to decreased Na reabsorption in PT and CDs)

Overall result is increased Na+ excretion! [note that opposite would occur with decreased Na+ intake]

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2
Q

Hypovolemia independently stimulates secretion of what hormone?

A

ADH —> water retention

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3
Q

Signs/symptoms of hypovolemia

A

Decreased skin turgor

Thirst

Dry mucous membranes

Sunken eyes

Oliguria

As it worsens, may see tachycardia, hypotension, tachypnea, and confusion

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4
Q

Signs/symptoms of hypervolemia

A

Weight gain
Edema
“bounding” pulse

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5
Q

Causes of absolute, extrarenal hypovolemia

A 
Bleeding
GI fluid loss
Skin fluid loss
Resp. fluid loss
Extracorporeal ultrafiltration
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6
Q

Causes of absolute, renal causes of hypovolemia

A

Diuretics

Na+ wasting tubulopathies

Genetic or acquired tubulointerstitial dz

Obstructive uropathy/postobstructive diuresis

Hormone deficiency

Hypoaldosteronism/adrenal insufficiency

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7
Q

What does it mean to have relative hypovolemia?

A

Decreased effective circulating fluid volume with increased total body sodium

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8
Q

Extrarenal vs. renal causes of relative hypovolemia

A

Extrarenal: edematous states, heart failure, cirrhosis, anaphylaxis, drugs, sepsis, pregnancy, third-spacing

Renal: severe nephrotic syndrome

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9
Q

Causes of hypervolemia d/t primary renal sodium retention (increased ECV)

A 
Oliguric acute renal failure
Acute glomerulonephritis
Severe chronic renal failure
Nephritic/nephrotic syndrome
Primary hyperaldosteronism
Cushing syndrome
Early stage liver disease
Conn syndrome
Gordon syndrome
Liddle syndrome
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10
Q

Causes of hypervolemia d/t secondary renal sodium retention (decreased ECV)

A

Heart failure
Late stage liver disease
Nephrotic syndrome (minimal change disease)
Pregnancy

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11
Q

Hyper or hyponatremia are considered WATER problems. What is considered hyper vs. hyponatremic?

A

Hypernatremia = plasma [Na] > 145 mEq/L

Hyponatremia = plasma [Na] < 135 mEq/L

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12
Q

Most common electrolyte abnormality encountered in clinical practice

A

Hyponatremia

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13
Q

Hypervolemic etiologies of hyponatremia

A

With decreased ECV: CHF, cirrhosis, sepsis, nephrotic syndrome, pregnancy, anaphylaxis

With increased ECV: acute renal failure, advanced chronic renal failure

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14
Q

Euvolemic etiologies of hyponatremia

A

SIADH (vascular stretch receptors cause Na dumping to keep volume relatively normal)

Drugs
Glucocorticoid deficiency
Hypothyroidism
Primary polydipsia
Poor osmolar intake
Positive pressure ventilation
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15
Q

Hypovolemic etiologies of hyponatremia

A

Renal losses (indicated by U[Na]>30): diuretic excess, mineralocorticoid deficiency, salt-losing nephropathy, bicarbonaturia with RTA and metabolic alkalosis, cerebral salt wasting

Extrarenal losses (indicated by U[Na]<30): vomiting, diarrhea, third-spacing d/t burns/pancreatitis/trauma

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16
Q

Mnemonic for hyponatremia symptoms

A

SALT LOSS

Stupor/coma
Anorexia, N/V
Lethargy
Tendon reflexes decreased

Limp muscles (weakness)
Orthostatic hypotension
Seizures/HA
Stomach cramping

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17
Q

Treatment of patients with hyponatremia is based on presenting symptoms.

How would you treat a patient with Level 1, aka no or minimal symptoms, possibly including HA, irritability, inability to concentrate, altered mood, depression, falls, or unstable gait?

A

Fluid restriction

Consider a -vaptan under select circumstances like: inability to tolerate fluid restrictions, very low sodium level, need for correction to have surgery, high fracture risk with unstable gait, etc.

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18
Q

Treatment of patients with hyponatremia is based on presenting symptoms.

How would you treat a patient with Level 2, aka moderate symptoms, possibly including nausea, confusion, disorientation, or altered mental status?

A

-vaptan or hypertonic NaCl infusion, followed by fluid restriction

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19
Q

Treatment of patients with hyponatremia is based on presenting symptoms.

How would you treat a patient with Level 3, or severe symptoms, possibly including vomiting, seizures, obtundation, respiratory distress, or coma?

A

Hypertonic NaCl, followed by fluid restriction or vaptan

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20
Q

Why must correction of hyponatremia be done slowly?

A

Overly rapid correction can cause Osmotic Demyelination Syndrome

  • In acute symptomatic hyponatremia you can use a faster rate of infusion (2.5 mEq/L/h) to get to a safer zone, but do not increase more than 20 mEq/L/day
  • If chronic, rate of increase should be ~0.5 mEq/L/h until 120 mEq/Na/L with total increase not to exceed 8-12 mEq/L/day and no more than 18 in the first 48 hrs
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21
Q

Hypervolemic causes of hypernatremia

A

Administration of hypertonic saline, hypertonic sodium bicarb

Hypertonic dialysis

Hypertonic feedings

Primary hyperaldosteronism

Cushing syndrome

22
Q

Euvolemic causes of hypernatremia

A

Diabetes insipidus (central or nephrogenic) — again counterintuitive but note that vascular stretch receptors are keeping volume ~normal

Hypodipsia

Insensible dermal and skin losses (only if hypodipsic)

23
Q

Hypovolemic causes of hypernatremia

A

Lack of access to water

“Broken” thirst mechanisms

24
Q

Mnemonic for hypernatremia symptoms

A

TRIP

T - twitching, tremors, hyperreflexia

R - restlessness, irritable, confusion, etc. (d/t brain cell shrinkage)

I - intense thirst, dry mouth, decreased urine output

P - pulmonary and peripheral edema

25
Q

Treatment for hypernatremia

A

If hypovolemic, they have a sodium deficit as well as a water deficit, so use isotonic saline

In other patients, use hypotonic IV solutions (e.g., D5W, half-normal saline, quarter-normal saline)

Calculation of water deficit = 0.6% body weight (kg) x (1-[140/Na])

26
Q

Why must hypernatremia be corrected slowly?

A

If corrected too quickly can cause brain edema; so correct over 48 hours at < 0.5 mEq/L/h (i.e., <12 mEq/L/day)

27
Q

Lab values representing hyper- vs. hypokalemia

A

Hyperkalemia = plasma [K] > 5.5 mEq/L

Hypokalemia = plasma [K] < 3.5 mEq/L

28
Q

How does hyper vs. hypokalemia relate to heart rate?

A

Hyperkalemia —> bradycardia

Hypokalemia —> tachycardia

29
Q

Effects of hyperkalemia seen on ECG

A

[in order of increasing severity of hyperkalemia]

HIGH T WAVE ([K] ~ 7)

Prolonged PR interval, depressed ST segment, high T wave

Auricular standstill, intraventricular block

Ventricular fibrillation ([K] ~ 10)

30
Q

Effects of hypokalemia seen on ECG

A

[in order of increasing severity of hypokalemia]

Low T wave ([K] ~ 3.5)

Low T wave + high U wave

Low T wave + high U wave + low ST segment ([K] ~ 2.5)

31
Q

Rapid absorption of K+ in the diet (e.g., 25-50 mEq/meal) into the ECF could lead to fatal hyperkalemia if not for its rapid redistribution into the ICF; what hormone is the most important for this to occur?

A

Insulin

32
Q

If the body is in a state of acidemia, this can be buffered by ______ the ECF [K]

A

Increasing

[note that in state of alkalemia, low [H+] is buffered by lowering ECF [K]]

33
Q

Acute factors leading to enhanced cell uptake of K+

A

Insulin
Beta-catecholamines
Alkalosis

[alpha catecholamines and acidosis cause impaired cell uptake]

34
Q

What effect does hyperosmolarity have on potassium efflux?

A

Enhanced cell efflux

35
Q

What effect do chronic conditions involving thyroid, adrenal steroids, exercise, and growth have on ATP pump density?

A

Enhanced

36
Q

What effect do chronic conditions involving diabetes, potassium deficiency, or chronic renal failure have on ATP pump density?

A

Impaired

37
Q

Hyperkalemia causes what change in aldosterone levels?

A

Increased

38
Q

Effect of high Na+ intake on K+ excretion

A

K+ excretion should be unchanged, because effects of increased Na intake are balanced out

39
Q

Hypokalemia causes mnemonic

A

GRAPHIC IDEA

GI losses (vomiting/diarrhea)
Renal tubular acidosis
Aldosterone
Paralysis (periodic)
Hypothermia
Insulin excess
Cushing’s syndrome

Insufficient intake
Diuretics
Elevated beta adrenergic activity
Alkalosis

40
Q

Signs and symptoms of hypokalemia

A

CNS: drowsiness, lethargy

Neuromuscular (most prominent manifestations): skeletal muscle weakness, smooth muscle weakness —- may lead to ileus and constipation

CV: ventricular arrhythmias, hypotension, cardiac arrest

Renal: polyuria, nocturia

Metabolic: hyperglycemia

41
Q

Causes of hypokalemia in normal acid-base state

A

Redistribution: catecholamine excess, alkalosis, hypokalemic periodic paralysis, insulin administration, barium poisoning

Extrarenal losses: decreased intake (e.g., anorexia nervosa), laxative abuse

42
Q

Causes of hypokalemia in a state of metabolic acidosis

A

Extrarenal losses: diarrhea, laxative abuse

Renal losses: renal tubular acidosis, organic acidosis (lactic and ketoacidosis), carbonic anhydrase inhibitors

43
Q

Causes of hypokalemia in state of metabolic alkalosis

A

With urine K <20 mEq/L: vomiting, diuretics

With urine Cl > 20 mEq/L and normal BP: bartter syndrome, diuretics

With urine Cl > 20 mEq/L and HTN: hyperaldosteronism, essential HTN with diuretic use, hypercortisolism, apparent mineralocorticoid excess (licorice ingestion, liddle syndrome)

44
Q

Tx of hypokalemia

A

Goal is to prevent life-threatening conditions like diaphragmatic weakness, rhabdomyolysis, and cardiac arrhythmias; especially urgent if rapid K+ falls to <2.5 mEq/L

K+ replacement is mainstay of tx

Then dx/correct underlying cause: stop K+ losing diuretics, give beta blocker if evidence of increased SNS tone

45
Q

Mnemonic for causes of hyperkalemia

A

RED FETS

Renal disease: ARF, CKD, type IV RTA

Excessive intake: food, K+ IV fluids, blood transfusion

Drugs: K+ sparing diuretics, K+ salts of penicillin

Factitious: prolonged use of tourniquet, hemolysis

Endocrine: Addison’s disease

Tissue release: rhabdomyolysis, burns, hemolysis, cytotoxic therapy

Shift out of cell: acidosis, beta-antagonists, insulin deficiency, tissue damage

46
Q

Signs and symptoms of hyperkalemia

A

Cardiac (most important and most frequent): abnormal heart rhythm — BRADYCARDIA, peaked T wave, Vfib, cardiac arrest, flattened P wave, prolonged PQ interval, widened QRS, sine wave

Neuromuscular: numbness, weakness, flaccid paralysis

47
Q

Causes of pseudohyperkalemia

A

Hemolysis
Thrombocytosis
Leukocytosis

48
Q

Causes of redistribution hyperkalemia

A 
Acidosis
Decreased insulin
Beta-blockers
Arginine infusion
Succinylcholine
Digitalis overdose
Periodic paralysis
49
Q

Causes of hyperkalemia with GFR > 20 mL/min (impaired K+ secretion) and LOW aldosterone

A

Addison disease

Hyporeninemic hypoaldosteronism

Drugs: PG synthetase inhibition, Captopril

50
Q

Causes of hyperkalemia with GFR > 20 mL/min (impaired K+ secretion) and normal or HIGH aldosterone

A

Primary tubular disorders: acquired, renal transplant, lupus erythematosus, amyloid, sickle cell, obstructive uropathy

Drugs: spironolactone, triamterene, amiloride

51
Q

Emergency management of hyperkalemia (3 categories)

A
  1. Give IV calcium to antagonize cardiac effects
  2. Give insulin and glucose to redistribute K+ into cells (can also use beta agonist like albuterol)
  3. Administer K-losing diuretic to facilitate K elimination (can also consider mineralocorticoid in pts with hypoaldosteronism, cation exchange resin, or dialysis)

Then it is important to monitor intake (e.g., < 60 mEq/day), paying attention to hidden sources like abx

Renal II Cumulative Final (20 decks)

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