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Acid/Base and Electrolytes > Potassium Disorders > Flashcards

Potassium Disorders Flashcards

1
Q

Potassium DiBartola

A
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2
Q

Is potassium the major intrscellular or extracellular cation?

A

intracellular

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3
Q

What percentage of total body potassium is located within cells

A

Asmuch as 95% ormore of total
body potassium is located within cells,

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4
Q

What is the most important role of potassium in the body?

A

Generation of resting membrane potentials

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5
Q

The Resting Membrane Potential

A
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6
Q

What maintains normal ECF and ICF potassium concs

A

Na+/K+ Atpase
Sodium out –. Potassium in
3Na:2K

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7
Q

What is the major determinant of the resting membrane potential?

A

The ratio of intracellular to extracellular potassium

Sodium out, potassium in by then Na/K ATPASE
But then potassium diffuses out along it’s conc gradient (very diffusible) until electrical gradient makes it stop diffusing. This sets the RMP

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8
Q

When is the threshold potential reached?

A

when
sodium permeability increases to the point that sodium
entry exceeds potassium exit, depolarization becomes
self-perpetuating, and an action potential develops.

The excitability of a
tissue is determined by the difference between the resting
and threshold potentials (the smaller the difference, the
greater the excitability).

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9
Q

How does hypokalaemia effect the RMP

A

makes it more negative - hyperpolarising the cell

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10
Q

How does hyperkalaemia effect the RMP

A

Makes it less negative - initially makes cells easier to excite

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11
Q

What effect does calcium have on the action potential?

A

Hypocalcaemia - lowers threshold potential
Hypercalcaemia - increases threshold potential

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12
Q

Potassium Balance

A
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13
Q

How does potassium enter the animal

A

All ingested - passively absorbed in the stomach and actively absorbed in the colon (may also be excreted by colon)

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14
Q

How much potassium is excreted by the kidneys

A

90-95%

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15
Q

How is an acute potassium load handled?

A

1/2-2/3rds excreted by the kidneys in 4-6hrs
In the mean time it is shifted intracellularly. by endogenous insulin release and B2 agonism from epi

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16
Q

Acid-Base on Potassium

A
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17
Q

How does acid base status affect K+

A

Mineral acidosis causes increase in potass as H+ moves intracellularly
Alkalosis causes decrease

However amount of potassium movement is very variable

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18
Q

Renal Handling of Potassium

A
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19
Q

What percentages of potassium are resorbed at what portion of the kidney?

A

70% with water and sodium in the proximal
tubule. An additional 10% to 20% of filtered potassium
is reabsorbed in the ascending limb of Henle’s loop.
Finally, 10% to 20% of the filtered load is delivered to the distal nephron, where final adjustments are made

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20
Q

What portion of the kidney is responsible for net potassium movement?

A

Distal tubules, cortical and medullar collecting duct.

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21
Q

How is potassium absorbed in the proximal tubule

A

at the start: lumen negative, nil active transport, is absorbed via solvent drag (?) paracellularly
Water resorption overcomes the electrical gradient and causes potassium movement
At the end: lumen pos - absorbed down an electrochemical gradient

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22
Q

How absorbed in thick ascending loop of henle?

A

lumen strongly pos - paracellular and cellular

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23
Q

How is K handled in the distal convoluted tubule?

A

Na/Cl co transporter (both in) and the K+/Cl (Both out) transporter. result in recycling of chloride and and net secretion of K+

24
Q

What are the three main factors affecting potassium excretion in the distal nephron?

A

the magnitude of the chemical concentration
gradient for potassium between the tubular cells and tubular
lumen, the tubular flow rate, and the transmembrane
potential difference across the luminal membranes of the
tubular cells.

25
Q

What is the most important hormone affecting potassium handling?

A

Aldosterone
Increases renal Na+ resorption, causes secretion of K and H in distal nephron

Its primary effect is to increase the number of open Na channels in the luminal membranes of the principal cells. it generates electronegativity in the tubular
lumen). This electronegativity can be dissipated either
by K or H ion secretion or by Cl reabsorption in
the distal nephron.
Also opens more K channels to cause secretion

26
Q

How does an increase in distal tubular flow affect potassium excretion?

A

It enhances it by creating a ‘potassium sink’ constantly allowing potassium to move down the electrochemical gradient created by the principle cells

27
Q

Why does metabolic alkalosis promote K excretion?

A

More HCO3- in the tubule = more neg = more potassium movement

28
Q

FACTORS INFLUENCING RENAL
POTASSIUM EXCRETION

A
29
Q

How does sodium intake potassium handling?

A

High sodium intake = more potass secretion in the connecting and cortical tubules, tubular cells kick excess sodium out into the peritubular ECF in exchange for potassium. Potass is then excreted into the tubular lumen.
Increased Sodium also = increased fluid movement = more potassium sink
Decreased Na+ intake = decreased potass excretion

30
Q

How does potassium intake influence potassium handing?

A

increased intake = increased excretion from increased aldosterone activity
Decreased intake = decreased excretion

31
Q

How does aldosterone influence potassium movement

A

In the cortical collecting duct - more excretion.
Principal cells more uptake from interstitium and increased sodium from lumen = more neg lumen + opens more luminal potass channels
All together means more potass moves into lumen.

32
Q

How does acute acidosis affect renal potassium handling?

A

May decrease K+ excretion -> as less K+ in cells due to H+/K+ movement
However a decrease delivery of HCO3- may cause an increased lumenal sodium and water this increases tubular flow–> K+ sink –> more excreted

33
Q

How do diuretics affect renal handling

A

Decrease due to increased distal tubular flow

34
Q

What is serum potassium often higher than plasma potassium

A

As K+ is released by platelets during clot formation. K+ also increases with plt count

35
Q

What are the most common clinical signs of hypokalemia ?

A

Muscular weakness, polyuria, polydipsia, and
impaired urinary concentrating capacity are the clinical
signs most likely to be recognized in dogs and cats with
symptomatic hypokalemia

36
Q

What are examples of causes of hypokalaemia?

A

Decreased Intake
- Alone unlikely to cause hypokalemia unless diet is aberrant
- Administration of potassium-free (e.g., 0.9% NaCl, 5% dextrose in water) or deficient fluids (e.g., lactated Ringer’s solution over several days)
- Bentonite clay ingestion (e.g., cat litter)
Translocation (ECF ! ICF)
- Alkalemia
- Insulin/glucose-containing fluids
- Catecholamines
- Hypothermia
- Hypokalemic periodic paralysis (Burmese cats)
- Albuterol overdosage
Increased Loss
- Gastrointestinal (FEK <4%-6%)
- -Vomiting of stomach contents
- - Diarrhea
-Urinary (FEK >4%-6%)
– Chronic renal failure in cats
–Diet-induced hypokalemic nephropathy in cats
–Distal (type I) renal tubular acidosis (RTA)
–Proximal (type II) RTA after NaHCO3 treatment
–Postobstructive diuresis
–Dialysis
–Mineralocorticoid excess
—-Hyperadrenocorticism
—-Primary hyperaldosteronism (adenoma, adenocarcinoma, hyperplasia)
-Drugs
–Loop diuretics (e.g., furosemide, ethacrynic acid)
–Thiazide diuretics (e.g., chlorothiazide, hydrochlorothiazide)
–Amphotericin B
–Penicillins
-Unknown mechanism
–Rattlesnake envenomation

37
Q

Effects of Hypokalaemia on Acid-Base Balance

A
38
Q

What acid-base affect does pure potassium depletion cause?

A

Metabolic acidosis - through distal tubular acidification

39
Q

What effect does hypokalaemia have on MSK?

A

MSK weakness <3
CK increase <2.5
Frank Rhabdo <2.0
Ventroflexion, HL weakness, respiratory paralysis. Ileus in humans, has not been observed in veterinary patients

Potassium is released from muscle cells during exercise,
causing Vasodilatation and increased blood flow.106
This release of cellular potassium is impaired in states of
potassium depletion, resulting in muscle ischemia. Muscle
blood flow and potassium release increased markedly
during exercise in normal but not in potassium-depleted
dogs (serum potassium concentration, 2.3 mEq/L), and
exercise caused rhabdomyolysis characterized by focal
necrosis and inflammatory cell infiltration in potassium depleted
dogs.

40
Q

Why does hypokalaemia cause cardiac disturbances?

A

delays repolarisation, increases the duration of action potential and increases automaticity.

41
Q

What ECG changes may be noted?

A

Human patients (e.g., decreased amplitude T waves, ST segment depression, and U waves) not consistently observed in dogs and cats
- supraventricular and ventricular arrhythmias may occur.
- Prolongation of the QT–interval and U waves have been reported in a dog with
severe hypokalemia (2.0 mEq/L) caused by chronic
vomiting and in dogs with experimentally induced potassium depletion (serum potassium concentration, 2.2 mEq/L).

The appearance of T waves in normal dogs is variable (e.g., positive, negative, and biphasic), and interpretation of the effects of hypokalemia on ventricular repolarization is difficult unless a baseline electrocardiogram has been obtained previously.

42
Q

How may hypokalaemia affect the utility of class 1 antiarrhythmics?

A

Make myocardium refractory to them .
K should be normalised during treatment

43
Q

What renal affects does hypokalaemia have?

A

Renal vasoconstriction
Reduced GFR
PU/PD due to insensitivity to ADH due to defective AQP2 channels

May result in hypokalaemic nephropathy

44
Q

Is decreased intake likely to result in hypokalemia alone?

A

No

45
Q

How much potassium should maintence fluids contain?

A

15-30mEq/L

46
Q

Why does alkalemia result in decreased potassium?

A

translocation intracellular for H+

47
Q

Why may diuretics result in hypokalaemia?

A

Administration of loop or thiazide diuretics may cause
hypokalemia as a result of increased flow rate in the distal
tubules and increased secretion of aldosterone secondary
to volume depletion

48
Q

Hypokalaemia Treatment

A

Treat the cause
Start orals
no more than 0.5mEq/kg/hr IV
Can cause pain on iv

49
Q

HyperKalaemia

A
50
Q

WHat is chronic hyperkalaemia almost always associated with

A

Renal impairment

51
Q

What ECG changes may be seen with hyperkalamia

A

Tented T waves
shortened QT - reflecting abnormal repolarisation
Prolonged PR interval and widened QRS - due to slow conduction
absence of P wave due to a lack of atrial conduction
Sinoventricular rhythm, Sine wave, vfib

Decreased atrial conduction, slowed conduction and reentry phenomenon

52
Q

What are the broad causes of hyperkalaemia and examples of each?

A

Increased Intake
- Unlike but can occur iatrogenically with supplementation
Translocation (ICF –> ECF)
- Acute tumour lysis syndrome
- Acute mineral acidosis (e.g., HCl, NH4Cl)
- Insulin deficiency (e.g., diabetic ketoacidosis)
Decreased Urinary Excretion
- Urethral obstruction
- Ruptured bladder
- Anuric or oliguric renal failure
- Hypoadrenocorticism
- Preg

53
Q

What may happen if an animal with chronic kidney disease encounters an acute potassium load?

A

They are less able to excrete it - often requiring longer to return to normokalaemia

54
Q

Why is AKI associated with hyperkalaemia

A

Not enough time for renal compensation for nephron loss.
Inadequate distal flow
Increased potassium release from tissues

55
Q

In pseudoadisonian situations what is the suspected cause of hyperkalemia (preg, chylous effusion, whipworm, salmonella)

A

volume depletion resulting in decreased distal tubular flow

56
Q

Treatment of hyperkalaemia

A

Treat the cause
Re-establish renal perfusion
Calcium
sodium bicarb - 1-2 mEq/kg
insulin 0.1-0.25IU/Kg followed by glucose
beta agonists
Dialysis

Acid/Base and Electrolytes (12 decks)

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