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Patho > Topic 7.2 - Fluid, Electolytes, pH > Flashcards

Topic 7.2 - Fluid, Electolytes, pH Flashcards

1
Q

As [H+] increased, pH ….

A

Decreases

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2
Q

What is the normal pH of blood?

A

7.35-7.45

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3
Q

pH of blood depends on which two ions?

A

Bicarbonate (HCO3-) from kidneys

Partial Pressure of carbon dioxide (PCO2) from lungs

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4
Q

What is the normal bicarbonate to carbonic acid ratio?

A

20:1

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5
Q

Which organ is responsible for converting buffering acids into bicarbonate and producing new ions to replace what is lost?

A

The kidneys

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6
Q

The kidneys have a large capacity to produce bicarbonate. What percent of nephrons must be lost before bicarbonate production is impacted?

A

70%

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7
Q

How does pH impact renal production of bicarbonate?

A

If pH drops (Acidosis), it stimulates the production of bicarbonate.

If pH rises (alkalosis), the kidneys produce less bicarbonate

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8
Q

How long does it take the renal compensatory response to change blood pH?

A

Several days - a full response can take up to a week

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9
Q

What is the normal plasma blood bicarbonate concentration?

A

22-28 mM

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10
Q

What are some possible causes of metabolic acidosis?

A

Decrease in Renal Bicarbonate Production
–> ARF, CFR, specific defects

Bicarbonate loss due to severe diarrhea

Increased Fixed Acid Production
–> Methanol, salicylate antifreeze poisoning
–> Formic acid, ketoacids, lactic acid due to hypoxemia

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11
Q

How does acidosis affect the body?

A

Brain function decreases of pH decreases
–> Disorientation and coma are main concerns

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12
Q

Adults cannot sustain a blood pH of what for more than a brief period of time before permanent brain damage occurs?

A

7.00

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13
Q

What is the anion gap? What is it usually?

A

Blood should be electroneutral, so the anion gap is difference between cations and anions in the blood. (N+ + K+) - (Cl- + HCO3-)

The difference is made up of unmeasured anions in the plasma, such as proteins, sulfate, phosphate.
Typically 6-16 mmol/L

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14
Q

Metabolic acidosis with a normal anion gap is usually caused by what?

A

Bicarbonate loss
–> Gut loss (diarrhea)
–> Renal bicarbonate loss (compensated via rise in plasma chloride)

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15
Q

Metabolic acidosis with an increased anion gap is usually caused by what?

A

Addition of an Acid
–> Lactic acid
–> Keto acids
–> Toxic alcohols
–> Aspirin

Failure to secrete acid
–> AKI or CKD is associated with retention of phosphate, sulfate, and organic anions.

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16
Q

What is the normal pCO2 range?

A

35-45mm Hg

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17
Q

How does alkalosis affect the body?

A

Brain function increases as pH increases
–> As pH approaches 7.8 individual is at risk for seizures
–> Hypoxic brain damage is a risk associated with seizures

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18
Q

What kind of pH disturbance is this Pt experiencing?
pH - 7.16
pCO2 - 23 mmHg
HCO3 - 9 mm Hg

A

Primary metabolic acidosis with compensatory respiratory alkalosis

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19
Q

You discover that your Pt has primary metabolic acidosis with compensatory respiratory alkalosis. What could cause this?

A

A history of severe diarrhea, or untreated DM.

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20
Q

What kind of pH disturbance is this Pt experiencing?
pH - 7.22
pCO2 - 80 mmHg
HCO3 - 32 mm Hg

A

Primary respiratory acidosis with compensatory metabolic alkalosis

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21
Q

What kind of pH disturbance is this Pt experiencing?
pH - 7.09
pCO2 - 80 mmHg
HCO3 - 24 mm Hg

A

Primary respiratory acidosis without compensation

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22
Q

Your patient has primary respiratory acidosis without compensation. Why might the kidneys not be compensating?

A

Respiratory disorder has recently developed and there has beeen insufficient time for a normal renal response

OR

The kidneys are abnormal and unable to compensate. Underlying metabolic acidosis.

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23
Q

How long should it take the respiratory system to compensate for metabolic alkalosis or acidosis?

A

Respiratory compensation should occur immediately.

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24
Q

What is the normal range for plasma [K]?

A

3.5 - 5.0 mM

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25
Q

Which kinds of cells regulate potassium and sodium balance in the body?

A

Principle cells in the kidney collecting ducts

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26
Q

How do kidney principle cells balance potassium and sodium?

A

Aldosterone binds to MR receptor
–> ENaC (sodium pump) inserts itself in cell membrane and begins pumping sodium from tubule lumen into cell.

ATPase pumps K into cell (which diffuses into tubule lumen) and Na back into blood

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27
Q

Why can low GFR cause hyperkalemia?

A

Flow rate or sodium coming into tubule is low in low GFR, so there is no trigger to input ENaC pumps, and the ATPase slows

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28
Q

What can be used to treat membrane potential issues caused by hyperkalemia?

A

Calcium increases the AP threshold, in combination with an elevated resting potential it can return the threshold-RMP difference to a relative normal.

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28
Q

How does hyperkalemia affect the RMP?

A

It increases the resting potential to closer to the AP threshold. If it increases too high, the cell will be unable to conduct APs.

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28
Q

Why is it so important to regulate [K]?

A

Because ECF [K] is a major determinant of membrane potential
–> Disruptions can cause muscle paralysis and cardiac arrhythmias

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29
Q

How does hypokalemia affect RMP?

A

Cells become hyperpolarized, which means they require more stimulus to initiate an AP.

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30
Q

What is a major concern in someone with hyperkalemia?

A

Cardiac arrest
–> ECG changes includes peaked T waves + widened QRS

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31
Q

What is a major concern in someone with hypokalemia?

A

Fatal arrythmia
–> Flattened T-wave + appearance of U-wave

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32
Q

Which hormones stimulate ATPases and increase K uptake?

A

Insulin and catecholamines

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33
Q

How does exercise affects K distribution?

A

It triggers K efflux from cells during repolarization

34
Q

How will a normal diet and acute renal failure affect plasma [K]?

A

It will result in hyperkalemia

35
Q

How will a normal diet and GI loss affect plasma [K]?

A

It will result in hypokalemia

36
Q

Where are N and NE released from?

A

The adrenal medulla.

37
Q

How does hyperinsulinism affect [K] in ECF?

A

Insulin stimulates the ATPase to move K into the cell. Hyperinsulinism, such as is seen in DMII, can cause hypokalemia.

Similarly, too little insulin can cause hyperkalemia.

38
Q

How do beta blockers impact ECF [K]?

A

They block catecholamine receptors –> so they do not stimulate K uptake.

39
Q

How does ECF hypertonicity affect [k]?

A

It drives efflux of water from cells, which will be followed by K

40
Q

How do cell necrosis and growth impact ECF [K]?

A

Necrosis + cell division both cause an efflux of ICF and contents. This fluid is high is K, and increases ECF [K].

41
Q

How does metabolic alkalosis affect K concentration in blood?

A

If ECF pH is high, H+ will exit cells to neutralize it.
However, cells must remain electroneutral, and will therefore intake more K as they release H+. This pushes towards hypokalemia.

42
Q

How would you treat someone who is acidotic and hyperkalemic?

A

Bicarbonate through IV
–> Binds with H+, neutralizing it.
–> As H+ concentration drops, K will rise again.

43
Q

How should hyperkalemia be treated if [K] > 6.5 and only a peaked T-wave is present?

A

Decrease K intake, stop K-sparing diuretics, and remove the cause of hyperkalemia.

44
Q

What are the most serious electrical effects of hyperkalemia?

A

Sustained, gradual depolarization
–> Causes inactivation of Na channels
–> Renders heart virtually unexcitable

45
Q

How should we treat extreme hyperkalemia? (w abnormal ECG, or [K] > 8.0)

A

–> IV Calcium to bump threshold
–> Redistribute K through insulin, glucose or bicarbonate (but only use bicarbonate in acidotic Pts)
–> Remove K from body through GI-K exchange resin or hemodialysis

46
Q

How does hypokalemia impact K channel permeability?

A

It reduces permeability and prolongs repolarization

47
Q

Does skeletal/smooth muscle paralysis occur in hyper or hypokalemia?

A

Hypokalemia

48
Q

How should hypokalemia be treated?

A

Oral administration and IV is severe (but monitor ECG if administering IV route)

49
Q

Why do K supplements have an enteric coating?

A

Because when absorbing it the stomach exchanges K for H+, which contributes to overacidity and can damage the stomach lining.

50
Q

Which kind of diuretics target the distal tubule? What kind of channel do they act on?

A

Thiazides
–> Act on a sodium/chloride cotransporter

51
Q

Which kind of diuretics target the collecting duct? What kind of channel do they act on?

A

Amiloride
–> Act on a sodium channel

52
Q

Which kind of diuretics target the thick ascending limb? What kind of channel do they act on?

A

Loop diuretics
–> Act on a sodium, potassium, and chloride channel

53
Q

What kind of diuretic is potassium sparing?

A

Amiloride

54
Q

What is Bartter’s Syndrome?

A

A genetic syndrome characterized by mutations in the thick ascending limb NKCC2
–> Inactivates channel
–> As though permanently on a loop diuretic

55
Q

What is Gitelman’s syndrome?

A

A genetic disorder characterized by a mutation in the NCC
–> Inactivation on channel
–> Mimics thiazide diuretic

56
Q

What is pseudohydoaldosteronism?

A

A genetic disorder characterized by inactivation of ENaC
–> Mimics permanent amiloride diuretic, which pushes towards hyperkaliemia
–> Mimics hypoaldosteronism, however mutation makes cell incapable of responding to aldosterone signaling

57
Q

What causes hypertonic ECF expansion?

A

High Na is plasma without a compensatory mechanism will cause water to diffuse out of the cell.

58
Q

What is normal plasma [Na]?

A

137-145 mmol/L

59
Q

What causes hypotonic ECF expansion?

A

A huge loss of fluids + electrolytes followed by fluid replacement without electrolytes can cause hyponatremia.

60
Q

What causes isotonic ECF expansion?

A

Increase in both fluids and electrolytes. Like eating a salty meal with a large glass of water.

61
Q

What does ADH promote?

A

Concentration of urine + stimulates thirst centres

62
Q

What is the major solute in ECF?

A

Na+

63
Q

What causes isotonic hyponatremia?

A

The addition of an osmotically active solute that doesn’t penetrate the cell membrane and forces water to leave the cell.
e.g., glucose

64
Q

What causes hypotonic hyponatremia?

A

–> Loss of Na in body fluids couples with fast volume replacement
–> Reduced GFR means less water secretion (dilutes sodium)
–> Excessive diuretics
–> Syndrome of Inappropriate antidiuretic hormone secretion (Too much ADH secretion all all times - leads to water reabsorption without Na)

65
Q

What are the clinical features of hyponatremia?

A

Brain edema –> lethargy, confusion, agitation, seizures, coma

Muscle cramps

66
Q

How is hyponatremia treated?

A

If body volume is high - restrict fluid/diuretics

If body volume is low –> Replace sodium + water

67
Q

What causes hypovolemic hypernatremia?

A

Loss from kidneys (diuretics)

68
Q

What causes isovolemic hypernatremia?

A

Diabetes insipidus
–> AHD insufficiency (in insensitivity)
–> Leads to producing very dilute urine.

69
Q

What might cause hypervolemic hypernatremia?

A

Renal retention due to hyperaldosteronism

70
Q

How does hypernatremia affect the brain?

A

Hyperosmolarity cause brain ells to shrink –> Seizures, muscle twitches

71
Q

How is hypernatremia treated?

A

Correction of water deficits through oral water or IV 5% dextrose.

72
Q

What are the two kinds of diabetes insipidus?

A
  1. Central
  2. Nephrogenic
73
Q

What occurs in central diabetes insipidus?

A

Insufficient secretion (deficiency) in ADH.

74
Q

What occurs in nephrogenic diabetes indipidus?

A

ADH receptors do not respond to hormone
OR
Issue with AQP2

75
Q

Describe the process of vitamin D synthesis.

A

Sunlight or dietary intake is metabolized by liver and mature vitamin D is then synthesized by kidneys.

76
Q

Which hormone is released to increase calcium uptake from the intestines and kidneys?

A

Parathyroid hormones.

77
Q

What causes hypercalcemia?

A

Hyperparathyroidism (often due to hyperplasia or malignancy)

78
Q

What are the clinical features of hypercalcemia?

A

Lethargy, weakness, depression, kidney stones, N/V
ECG changes (shortened Q-T interval)

79
Q

How can hypercalcemia be treated?

A

Loop diuretics or surgery to remove PT tissue is PTH levels are high.

80
Q

What might cause hypocalcemia?

A

Vit D deficiency
Hypoparathyroidism
Hyperphosphatemia (such as in acute pancreatitis)

81
Q

What are the clinical features of hypocalcemia?

A

Neuromuscular irritability + Muscle cramps
Prolonged Q-T interval

82
Q

How can hypocalcemia be treated?

A

IV calcium gluconate / calcium chloride
Vit D supplementation

83
Q

Why is bone disease related to CRF?

A

In CRF one is excreting too much calcium and not producing enough Vit D –> Brittle bones

84
Q

How can we treat bone disease in CKD?

A

Reduce dietary phosphate intake
GI phosphate binders (decrease plasma phosphate)
Administer Vit D by injection (expensive, very effective)

Patho (14 decks)

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