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

Topic 7.2 - Fluid, Electolytes, pH Flashcards

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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
Which kinds of cells regulate potassium and sodium balance in the body?
Principle cells in the kidney collecting ducts
26
How do kidney principle cells balance potassium and sodium?
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
27
Why can low GFR cause hyperkalemia?
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
28
What can be used to treat membrane potential issues caused by hyperkalemia?
Calcium increases the AP threshold, in combination with an elevated resting potential it can return the threshold-RMP difference to a relative normal.
28
How does hyperkalemia affect the RMP?
It increases the resting potential to closer to the AP threshold. If it increases too high, the cell will be unable to conduct APs.
28
Why is it so important to regulate [K]?
Because ECF [K] is a major determinant of membrane potential --> Disruptions can cause muscle paralysis and cardiac arrhythmias
29
How does hypokalemia affect RMP?
Cells become hyperpolarized, which means they require more stimulus to initiate an AP.
30
What is a major concern in someone with hyperkalemia?
Cardiac arrest --> ECG changes includes peaked T waves + widened QRS
31
What is a major concern in someone with hypokalemia?
Fatal arrythmia --> Flattened T-wave + appearance of U-wave
32
Which hormones stimulate ATPases and increase K uptake?
Insulin and catecholamines
33
How does exercise affects K distribution?
It triggers K efflux from cells during repolarization
34
How will a normal diet and acute renal failure affect plasma [K]?
It will result in hyperkalemia
35
How will a normal diet and GI loss affect plasma [K]?
It will result in hypokalemia
36
Where are N and NE released from?
The adrenal medulla.
37
How does hyperinsulinism affect [K] in ECF?
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
How do beta blockers impact ECF [K]?
They block catecholamine receptors --> so they do not stimulate K uptake.
39
How does ECF hypertonicity affect [k]?
It drives efflux of water from cells, which will be followed by K
40
How do cell necrosis and growth impact ECF [K]?
Necrosis + cell division both cause an efflux of ICF and contents. This fluid is high is K, and increases ECF [K].
41
How does metabolic alkalosis affect K concentration in blood?
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
How would you treat someone who is acidotic and hyperkalemic?
Bicarbonate through IV --> Binds with H+, neutralizing it. --> As H+ concentration drops, K will rise again.
43
How should hyperkalemia be treated if [K] > 6.5 and only a peaked T-wave is present?
Decrease K intake, stop K-sparing diuretics, and remove the cause of hyperkalemia.
44
What are the most serious electrical effects of hyperkalemia?
Sustained, gradual depolarization --> Causes inactivation of Na channels --> Renders heart virtually unexcitable
45
How should we treat extreme hyperkalemia? (w abnormal ECG, or [K] > 8.0)
--> 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
How does hypokalemia impact K channel permeability?
It reduces permeability and prolongs repolarization
47
Does skeletal/smooth muscle paralysis occur in hyper or hypokalemia?
Hypokalemia
48
How should hypokalemia be treated?
Oral administration and IV is severe (but monitor ECG if administering IV route)
49
Why do K supplements have an enteric coating?
Because when absorbing it the stomach exchanges K for H+, which contributes to overacidity and can damage the stomach lining.
50
Which kind of diuretics target the distal tubule? What kind of channel do they act on?
Thiazides --> Act on a sodium/chloride cotransporter
51
Which kind of diuretics target the collecting duct? What kind of channel do they act on?
Amiloride --> Act on a sodium channel
52
Which kind of diuretics target the thick ascending limb? What kind of channel do they act on?
Loop diuretics --> Act on a sodium, potassium, and chloride channel
53
What kind of diuretic is potassium sparing?
Amiloride
54
What is Bartter's Syndrome?
A genetic syndrome characterized by mutations in the thick ascending limb NKCC2 --> Inactivates channel --> As though permanently on a loop diuretic
55
What is Gitelman's syndrome?
A genetic disorder characterized by a mutation in the NCC --> Inactivation on channel --> Mimics thiazide diuretic
56
What is pseudohydoaldosteronism?
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
What causes hypertonic ECF expansion?
High Na is plasma without a compensatory mechanism will cause water to diffuse out of the cell.
58
What is normal plasma [Na]?
137-145 mmol/L
59
What causes hypotonic ECF expansion?
A huge loss of fluids + electrolytes followed by fluid replacement without electrolytes can cause hyponatremia.
60
What causes isotonic ECF expansion?
Increase in both fluids and electrolytes. Like eating a salty meal with a large glass of water.
61
What does ADH promote?
Concentration of urine + stimulates thirst centres
62
What is the major solute in ECF?
Na+
63
What causes isotonic hyponatremia?
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
What causes hypotonic hyponatremia?
--> 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
What are the clinical features of hyponatremia?
Brain edema --> lethargy, confusion, agitation, seizures, coma Muscle cramps
66
How is hyponatremia treated?
If body volume is high - restrict fluid/diuretics If body volume is low --> Replace sodium + water
67
What causes hypovolemic hypernatremia?
Loss from kidneys (diuretics)
68
What causes isovolemic hypernatremia?
Diabetes insipidus --> AHD insufficiency (in insensitivity) --> Leads to producing very dilute urine.
69
What might cause hypervolemic hypernatremia?
Renal retention due to hyperaldosteronism
70
How does hypernatremia affect the brain?
Hyperosmolarity cause brain ells to shrink --> Seizures, muscle twitches
71
How is hypernatremia treated?
Correction of water deficits through oral water or IV 5% dextrose.
72
What are the two kinds of diabetes insipidus?
1. Central 2. Nephrogenic
73
What occurs in central diabetes insipidus?
Insufficient secretion (deficiency) in ADH.
74
What occurs in nephrogenic diabetes indipidus?
ADH receptors do not respond to hormone OR Issue with AQP2
75
Describe the process of vitamin D synthesis.
Sunlight or dietary intake is metabolized by liver and mature vitamin D is then synthesized by kidneys.
76
Which hormone is released to increase calcium uptake from the intestines and kidneys?
Parathyroid hormones.
77
What causes hypercalcemia?
Hyperparathyroidism (often due to hyperplasia or malignancy)
78
What are the clinical features of hypercalcemia?
Lethargy, weakness, depression, kidney stones, N/V ECG changes (shortened Q-T interval)
79
How can hypercalcemia be treated?
Loop diuretics or surgery to remove PT tissue is PTH levels are high.
80
What might cause hypocalcemia?
Vit D deficiency Hypoparathyroidism Hyperphosphatemia (such as in acute pancreatitis)
81
What are the clinical features of hypocalcemia?
Neuromuscular irritability + Muscle cramps Prolonged Q-T interval
82
How can hypocalcemia be treated?
IV calcium gluconate / calcium chloride Vit D supplementation
83
Why is bone disease related to CRF?
In CRF one is excreting too much calcium and not producing enough Vit D --> Brittle bones
84
How can we treat bone disease in CKD?
Reduce dietary phosphate intake GI phosphate binders (decrease plasma phosphate) Administer Vit D by injection (expensive, very effective)

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